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Title: Text book of veterinary medicine, Volume I (of 5)
Author: Law, James
Language: English
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MEDICINE, VOLUME I (OF 5) ***
TEXT BOOK
OF
VETERINARY MEDICINE
BY
JAMES LAW, F.R.C.V.S.
Director of the New York State Veterinary College Cornell University,
Ithaca, N. Y.
VOL. I
ITHACA
PUBLISHED BY THE AUTHOR
1896
Copyright by
JAMES LAW
1896
PRESS OF
ANDRUS & CHURCH
ITHACA, N. Y.
PREFACE.
During a long experience in teaching veterinary medicine and surgery in
Cornell University, the author felt the urgent need of a compend on the
subject, written from the American standpoint and having special
reference to the American live stock industry. This led to the
production of the Farmer’s Veterinary Adviser, which has been well
received, and has, up to the present, passed through ten editions in the
United States, besides the unauthorized editions published in Canada and
Great Britain.
In entering upon a larger field as Director of the New York State
Veterinary College, and professor of medicine and sanitary science, he
aims at producing a work which will meet the needs of the American
student and practitioner. The special phases of animal pathology in
America, the diseases peculiar to our soil, and the parasites that
prevail here, but are unknown in Europe, demand consideration from the
American point of view. The special features of our breeding, grazing
and feeding industries, and of the dairy, over our great extent of
territory, and the varying influence of soil, water, climate, altitude
and traffic, the scope and limitations of our interstate traffic, and
our special relation to the old world in the matter of meat products,
combine with other conditions in demanding a somewhat different
treatment of the subject from that which we find in European
publications. Then, too, the recent extraordinary advances in the field
of bacteriology and sanitary science, which have virtually
revolutionized modern medicine, and are an earnest of still greater
advances in the near future, demand a work which shall, as far as
possible, set forth the present advanced status, and thus lay a solid
foundation to intelligently follow, if not to lead, in the imminent
advance. As a contribution to this, the present volume, the first of a
series, is offered to students, practitioners and scientists by their
friend,
THE AUTHOR.
New York State Veterinary College,
Cornell University.
October, 1896.
CONTENTS
PREFACE.
CONTENTS.
OBJECTS AND METHODS OF STUDY.
ETIOLOGY CAUSES OF DISEASE.
MEDICAL DIAGNOSIS.
SYMPTOMATOLOGY. SEMEIOLOGY.
PROGNOSIS.
PROPHYLAXIS. PROPHYLACTICS. PREVENTION.
THERAPEUTICS. TREATMENT.
HYPERÆMIA. CONGESTION.
INFLAMMATION. PHLOGOSIS. PHLEGMASIA.
FEVER.
DISEASES OF THE RESPIRATORY ORGANS.
DISEASES OF THE NOSE.
RHINITIS. CORYZA. NASAL CATARRH. COLD IN THE HEAD.
SIMPLE CORYZA IN CATTLE.
CHRONIC NASAL, CATARRH. NASAL GLEET. OZŒNA IN THE HORSE.
COLLECTION OF PUS IN THE NASAL SINUSES.
ABSCESS OF THE FALSE NOSTRIL OR TURBINATED BONES.
NASAL DISCHARGE FROM CARIOUS TEETH, ETC.
COLLECTIONS OF PUS IN THE GUTTURAL POUCHES.
NEOPLASMS IN THE HORSE’S NOSE.
CATARRH OF THE FRONTAL SINUSES IN CATTLE. CATARRH FROM TRAUMATISM.
CHRONIC CATARRH OF CATTLE.
MALIGNANT CATARRH OF CATTLE.
PARASITIC DISEASES OF THE NOSE.
COCCIDIAN CATARRH IN RABBITS.
LARVA OF ŒSTRUS OVIS (GRUB) IN THE NASAL SINUSES OF SHEEP.
NASAL CATARRH IN DOG AND HORSE FROM LINGUATULA (PENTASTOMA) TAENIOIDES.
RHINARIA TAENIOIDES.
AFFECTIONS OF THE THROAT.
LARYNGITIS IN THE HORSE.
PHARYNGO-LARYNGITIS IN CATTLE.
LARYNGITIS IN SHEEP.
LARYNGITIS IN PIG.
LARYNGITIS IN THE DOG.
PHARYNGITIS. SORE THROAT.
CROUP.
PHARYNGEAL AND LARYNGEAL POLYPI.
DYSPNŒA LARYNGEA. ROARING. HEMIPLEGIA LARYNGEA.
ŒDEMA GLOTTIDIS.
LARYNGEAL HYPERÆSTHESIA. CONVULSIVE COUGH.
INFECTIOUS DISEASES OF THE THROAT.
GUTTUROMYCOSIS OF SOLIPEDES.
DISEASES OF THE CHEST.
RELATIVE POSITION OF THE LUNGS, HEART AND OTHER ORGANS IN THE DIFFERENT
DOMESTIC ANIMALS.
PERCUSSION.
AUSCULTATION.
DISEASES OF THE LUNGS.
BRONCHITIS.
CHRONIC BRONCHITIS IN THE HORSE. BRONCHIAL CATARRH.
BRONCHITIS IN THE OX.
BRONCHITIS IN THE DOG.
CROUPOUS BRONCHITIS IN CATTLE AND SHEEP.
ACUTE CONGESTION OF THE LUNGS. PULMONARY HYPERÆMIA.
PULMONARY ŒDEMA.
ATELECTASIS. COLLAPSE OF LUNG.
HÆMOPTYSIS.
PULMONARY APOPLEXY. HÆMORRHAGIC INFARCTION.
PNEUMONITIS; PNEUMONIA; INFLAMMATION OF THE LUNGS.
ACUTE CROUPOUS PNEUMONIA. PNEUMONITIS IN THE HORSE.
CROUPOUS PNEUMONIA IN THE OX.
CROUPOUS PNEUMONIA IN SHEEP.
PIG. PNEUMONIA.
DOG. PNEUMONIA.
ACUTE PLEURISY IN THE HORSE. PLEURITIS.
PLEURISY IN CATTLE.
PLEURISY IN SHEEP.
DOG. PLEURISY.
PLEURO-PNEUMONIA. BRONCHO-PNEUMONIA. BRONCHO-PLEURO-PNEUMONIA.
HYDROTHORAX.
PNEUMOTHORAX. AIR OR GAS IN THE PLEURA.
PYO-PNEUMOTHORAX, EMPYEMA.
CHRONIC PLEURISY.
PLEURODYNIA.
BRONCHIAL ASTHMA IN THE DOG.
ASTHMA. BROKEN WIND. HEAVES. DYSPNŒA.
POLYPUS OF THE BRONCHIAL TUBES.
DISEASES OF THE BRONCHIAL AND MESENTERIC GLANDS.
PARASITES OF THE AIR PASSAGES, LUNGS, AND PLEURA.
DISEASES OF THE HEART AND ORGANS OF CIRCULATION.
PALPITATIONS.
ANGINA PECTORIS. BREAST PANG.
FUNCTIONAL IRREGULARITY IN THE RYTHM OF THE HEART.
CONGENITAL MALFORMATIONS AND DISPLACEMENTS OF THE HEART.
HYPERTROPHY OF THE HEART.
ATROPHY.
DILATATION OF THE HEART.
INFLAMMATIONS IN THE HEART.
PERICARDITIS.
ENDOCARDITIS.
CARDITIS. MYOCARDITIS.
CHRONIC VALVULAR DISEASE OF THE HEART.
FATTY DEGENERATION OF THE HEART.
NEW FORMATIONS IN THE HEART. TUMORS. PARASITES.
RUPTURE OF THE HEART.
DISEASES OF ARTERIES.
THROMBOSIS AND EMBOLISM.
ANEURISM.
ARTERIO-SCLEROSIS.
ANGEIOMA. CIRCOID ANEURISM. ANEURISM BY ANASTOMOSIS. VENOUS TUMOR.
NŒVUS.
PHLEBITIS.
VARICOSE VEINS. DILATED VEINS WITH ALTERED WALLS.
PHLEBOLITES. CALCAREOUS BODIES IN THE VEINS.
HÆMORRHAGE.
HÆMOPHILIA.
DISEASES OF THE BLOOD.
PLETHORA. POLYÆMIA.
HYDROÆMIA. ANÆMIA OLIGÆMIA.
PROGRESSIVE PERNICIOUS ANÆMIA. IDIOPATHIC ANÆMIA.
CHRONIC ANÆMIA. DROPSY IN CATTLE AND SHEEP.
MELANÆMIA. BLACK PIGMENT IN BLOOD.
LEUKÆMIA. LEUCOCYTHÆMIA.
LYMPHADENOMA. HODGKIN’S DISEASE.
ACUTE LYMPHANGITIS OF PLETHORA IN HORSE. ANGEIOLEUCITIS.
INFECTIVE LYMPHANGITIS. TRAUMATIC LYMPHANGITIS.
LYMPHANGIECTASIS. DILATED LYMPHATICS.
LYMPHORRHŒA. LYMPHORRHAGIA. DISCHARGE OF LYMPH THROUGH WOUNDS OR SORES.
LYMPHADENITIS. INFLAMMATION OF THE LYMPH GLANDS.
INDEX.
VETERINARY MEDICINE.
OBJECTS AND METHODS OF STUDY.
Pathology—general—special. Morbid anatomy. Pathological chemistry;
Disease. Health. Death—Somatic—partial—necrosis. Syncope. Apuœa.
Asphyxia. Coma. Death from old age.
The principles and practice of Veterinary Medicine should embrace all
that is known of the causes, nature, symptoms, prevention and cure of
disease in domestic animals. Incidentally it includes diagnosis and
prognosis.
=Pathology= is the science which tells of the causes, and nature of
disease, and the functional and structural changes by which it is
characterized. In modern usage the term pathology is understood to refer
to the intimate nature of disease, but this necessarily involves an
enquiry into its sources and the predispositions to its occurrence; its
phenomena whether in changes of function or structure; and its results
in the form of perverted function, structural changes, degenerations,
dependent disorder, etc. The field of pathology is further divided into
general pathology and special pathology.
=General Pathology= treats of disease processes in their generic form,
and as they appear in many different diseases. Thus inflammation and
fever are the prominent phenomena in a great many different diseases
which differ in their seats, their causes, manifestations and results.
Inflammation and fever are therefore subjects of general pathology.
Similarly all forms of degeneration—fatty, fibrous, calcic, amyloid,
etc., are disease processes found in many different organs and under
very varied conditions and they are accordingly included in general
pathology. Hypertrophy and atrophy are also possible in every organic
tissue irrespective of kind or seat, they belong therefore to this
particular field.
=Special Pathology= on the contrary is confined to a particular disease
and not only elucidates the causes, phenomena and results of such
disease, but seeks to do this in such a way as to differentiate this
malady from all others however closely related to it. Thus inflammation
of a bone is known under the general name of osteitis, this may be due
to a great variety of different causes, and each would have its own
special pathology. The osteitis of simple mechanical injury is
essentially different from the osteitis of rheumatism, of purulent
infection, of tuberculosis, of actinomycosis. So with the inflammations
of every other tissue. Each may suffer from a variety of inflammations,
springing from different causes, attended with characteristically unlike
tissue changes and tending to different issues, and every one of these
forms has therefore its own special pathology.
=General Pathology= may be said to deal with typical disease processes
to a large extent irrespective of the individual disease in which they
may appear, while =Special Pathology= deals with the morbid phenomena
which distinguishes the individual malady from all other diseases
however closely allied to it.
=Pathological (Morbid) Anatomy= deals with structural changes, the
cause, the accompaniment or result of disease. These morbid changes are
microscopic or macroscopic. Both constitute morbid anatomy, but the
microscopic alterations come under the special name of morbid
(pathological) histology.
=Pathological Chemistry= is that branch of pathology which treats of
chemical changes produced by disease in the blood, lymph, tissues,
secretions and excretions. It demands a previous knowledge of the
condition of these tissues and fluids in health, in the particular genus
of animal and under the same dietary and environment. Physiological
Chemistry is therefore an essential prerequisite to pathological
chemistry, just as anatomy, physiology and histology are indispensable
to the appreciation of pathology and morbid anatomy.
=Disease= is an injurious deviation from the normal function or
structure. The morbid process resulting in disease is usually in the
nature of a modification of the normal or physiological condition, so
that it is often difficult to set the exact limits of health and
disease. What is a purely physiological process under given conditions,
would be distinctly pathological under others. The free kidney secretion
of cold weather and the profuse perspiration of a hot season are both
purely physiological and in the main balance each other. Each under its
special environment fulfills an essential work in eliminating from the
system toxic materials which would prove hurtful if retained, and thus
each is not only physiological but beneficial. If, however, they
occurred, not in this mutually compensatory manner, but simultaneously
in this profusion, they might well be dreaded as morbid conditions.
Again if either were to occur apart from its normal causative
environment, if for example the polyuria appeared in hot weather and the
perspiration in cold, the phenomenon might fairly be called
pathological. In any case if the excessive secretion induced a lowering
of the general tone of health the process would be essentially a morbid
one. In pronouncing therefore upon a morbid process one must take fully
into account the corresponding physiological process, the attendant
conditions, and whether the result is injurious or otherwise.
The same is true of structural changes. What under given conditions
would be essentially a morbid structure, might under other conditions be
a simple adaptation to an unwonted environment, and a means of
protection from injuries that would otherwise accrue. Excessive growth
of cuticular tissue in the epithelioma, wart or corn is injurious and
essentially pathological, while the callus on the camel’s knee or the
workman’s palm is purely protective and physiological. The local
development of a mass of fatty tissue in the average man or beast is a
disease, but the tendency to the uniform deposition of fat in the
connective tissue of the improved breeds of meat producing animals, is
the happy culmination of a long continued and skillful selection and
regimen, without which the live stock industry of today would be a
grievous failure. To constitute disease, therefore, modified function
must be permanent, and not simply a compensating increase, decrease, or
other change, and it must be in some way injurious to the animal
economy. Similarly to constitute disease modified structure must be
other than a simple protection or beneficial change, it must not be a
simple evolution in the nature of accommodation to the environment but
it must be a cause of injury to function or a distinct deformity.
=Health= may be said to be the harmonious exercise and mutual balance of
all the bodily functions, and any interference with such mutual exercise
or balance may be said to constitute disease. But as health passes into
disease by insensible gradations, there is of necessity an extensive
borderland which often cannot be allotted to one condition or the other,
but which must often be left a disputed territory.
Again certain animal constitutions are innately strong and robust, while
others are weak and feeble, yet the delicacy of the latter cannot be set
down as actual disease, and by maintaining a due balance between the
functions, a fair measure of health and even long life may be secured.
=Death= as the result of disease may be either _partial_ or _somatic_.
=Partial= or =local death= may be _molecular_ as in =ulceration=, or it
may affect an organ or part of an organ, as in =necrosis=, =sphacelus=,
or =sloughing=. =Somatic death= is a loss of vitality of the entire body
and is manifested by a complete cessation of the bodily functions,
including that of nutrition. Usually the arrest begins with one of the
great vital processes, in advance of the others, and thus in different
cases, we have _death beginning at the heart, at the lungs, and at the
brain_.
=Death from syncope or fainting, begins at the heart=, which loses its
irritability or contractility, or is seized with a tonic spasm. If there
has been lack of contractility, the heart is found after death in a
flabby, soft condition, and quite frequently filled with blood. If
heart-spasm, it is contracted, firm, and empty or nearly so. Syncope may
result from severe nervous shock (emotional), from the electric current,
from insolation, or from heart sedatives like chloroform, or nicotine.
It may, however be but the culmination of a gradually advancing
debility, from exhausting diseases, from fatty degeneration of the
cardiac muscles, or from starvation, or anæmia. Again the exhaustion
coming from profuse hæmorrhage, or from violent over-exertion is a cause
of fatal syncope.
In =death beginning at the lungs= (apnœa, asphyxia, or suffocation), the
blood failing to receive oxygen and to give up its carbon dioxide is
unable to maintain the various functions of the body and the arrest of
the other vital processes speedily follows. The arrest of the
respiratory process may occur from nervous shock, but more commonly it
results from choking, strangulation, drowning, or the action of
irrespirable gases. In diseases of the heart and lungs it is liable to
occur from the obstruction of the pulmonary circulation and from the
depression of the respiratory nervous centres. After death the lungs are
found gorged with dark red—almost black—blood, which likewise distends
the right heart and systemic veins, and all mucous and serous membranes
have a dark red, congested aspect. When breathing has been arrested by
mechanical violence there are, first, active contractions of the
respiratory muscles, but no loss of consciousness; then as the brain
becomes charged with venous blood, consciousness and volition are lost
and convulsive movements ensue. Later still there is no respiratory
effort nor convulsions, but the heart continues to beat for two or three
minutes longer.
=In death beginning at the brain= (Coma) the sensory functions fail
first, as evidenced by drowsiness, stupor, or complete insensibility,
while the movement of heart and lungs are still temporarily continued.
Pressure on the brain by a fractured bone or blood clot, or in cases of
violent congestion or the rapid growth of tumors, usually operates in
this way. It may also result from the direct action of certain poisons,
like opium, belladonna, or chloroform, or the ptomaines or toxins of
bacteria. Causes acting on the brain may, however, lead to death by
syncope or asphyxia when the nerve centres presiding over circulation or
respiration are the first to feel the full effects of the pressure or
poison.
=Death from old age=, with a gradual failure of the natural processes of
nutrition and tissue-growth, and the occurrence of atrophy and various
degenerations of the organs is not a common occurrence in domesticated
animals, so that it may be dismissed without further notice.
_Actual somatic death_ is marked by the cessation of breathing and
pulse, the dilated pupils and semi-closed eyelids, the coldness and
pallor of the visible mucous membranes and skin, and the clenching of
the jaws with slight protrusion of the tongue. Yet these symptoms may be
present in syncope and it may even be impossible to detect the beats of
the heart, though the subject still lives. Pressure of the finger on a
white portion of the skin or on a mucous membrane may give a further
indication. If the indentation made by the finger is slowly effaced and
if the blood again slightly reddens the part the presumption is against
death. Even this is not infallible, since by pressure of gas in the
internal cavities or deeper blood vessels, the blood may be forced back
into the surface capillaries giving an appearance of circulation, after
actual death. On the other hand any exudation or œdema will retain the
imprint of the finger even in life. The general relaxation of the
muscles and their lack of response to electric stimulation, and the
setting in of cadaveric rigidity, and later still of putrefaction give
more conclusive evidence of dissolution.
ETIOLOGY: CAUSES OF DISEASE.
Causes—simple—complicated: Proximate; Remote: Predisposing—race,
genus, family, heredity, individual, environment, food, age, sex,
temperament, idiosyncrasy, debility, plethora, interdependence of
organs, embolism, mechanical influence. Exciting causes, intrinsic,
extrinsic, inherent, acquired, heredity, dentition, heat, cold,
atmospheric conditions, electricity, moisture, dryness, dust,
darkness, light, soil, food, water, inaction, over-exertion,
mechanical causes, poisons,—mineral—vegetable—animal, microbes,
contagious, infectious, epizootic, enzootic, sporadic, panzootic,
zymotic, mediate contagion, bacterial poisons.
The causes of disease are simple or complicated, and in the latter case
a single factor may be altogether harmless unless associated with
another which also may have been innocuous alone. For example: the
infecting germ of glanders (Bacillus Mallei) is harmless to the ox which
lacks the predisposition to the disease:—feeding buckwheat is harmless
to the dark-skinned animal, but is injurious to the white-skinned, if
exposed to sunshine:—the chicken can bear with impunity exposure to cold
or to the bacillus anthracis, but it cannot endure these two etiological
factors combined. It follows that one cannot predict the same result
from the same cause in every case. Yet with all concurrent conditions
the same the result will follow with mathematical certainty. This will
serve to illustrate the value of thoroughness in etiological knowledge,
as the basis of a sound pathology.
Etiology is primarily divided into =proximate= and =remote=. _Remote_
causes are again divided into =predisposing= and =exciting=.
=Predisposing Causes= are such as induce a condition of the system or of
a particular organ or group of organs which renders them specially
susceptible to a disease. This may be a characteristic of the _race_ or
_genus_ of animal, thus the genus bovis alone suffers from lung plague,
the genus equus from dourine, and ruminants from Rinderpest. It may be a
_family trait_, (_hereditary_) hence we see certain families of both men
and cattle cut off by tuberculosis, while other adjacent ones largely
escape. It may be an _individual peculiarity_, thus some subjects have a
congenital insusceptibility to a given disease, from which others of the
same family suffer, and one who has passed through a self-limiting
disease like measles, cowpox or anthrax is rarely attacked a second
time. Again predisposition may be due to _environment_ as when we find
herds in damp and exposed localities obnoxious to rheumatism, and horses
in dark mines exposed to specific ophthalmia. It may be the result of
_food_ as when the flesh-fed fox or rat resists anthrax and the
farina-fed one falls a ready victim. _Age_ may predispose, early youth
being remarkably susceptible to parasitism and bacteridian infection,
and old age to fractures and degenerations. _Sex_ is inevitably a cause
of limitation of disease as the females and males can only suffer from
disease of their respective =sexual= organs. Again of diseases common to
both sexes certain nervous and digestive disorders are common in
connection with gestation, and certain calculous diseases in connection
with the long and narrow urethra of the male. _Temperament_ has a marked
influence, thus the sanguineous or nervous race horse or hound shows a
marked predisposition to diseases of the heart, lungs and brain, and to
a sthenic type of inflammation and fever, while the heavy lymphatic
draught horse has a proclivity to diseases of the lymphatics and skin.
_Idiosyncrasy_ is closely allied to temperament, but the condition may
be less manifest, and the peculiarity is only recognized by the results,
as when a man is poisoned by sound fish or raspberries. _Debility_
whether from deficiency or poor quality of food, on the one hand, or
from overwork, filth, dampness or disease on the other must be looked
upon as strongly predisposing to certain diseases, such as tuberculosis
and glanders. _Plethora_ which charges the blood and tissues in a
different way with effete organic products, lays the system especially
open to certain diseases like black quarter in young cattle, and
parturition fever in cows. _Disease of one organ_ often predisposes
another organ through interdependence of function, as when torpid or
congested liver leads to portal and intestinal congestion, diseased
teeth to digestive disorder, imperfect hæmatosis to kidney trouble; in
other cases blood clots or bacteria from one pathological centre may be
arrested in the blood vessels of a distant organ and start new foci of
disease (embolism, metastasis); in still other cases the impairment of
the healthy function in one organ acts injuriously on another, as when
emphysema or other disease of the lungs forces the blood back upon the
heart causing dilation with atrophy of the walls. _Previous disease in a
tissue_ leaves for a time an impairment of structure and function which
may become the essential predisposing cause of the effective operation
of a morbific factor. _Mechanical_ action on a part may predispose to
disease, as for example, by reducing its circulation and nutrition and
thereby directly impairing its power of resistance to other inimical
agencies. Not infrequently a pus microbe lies deep in the cuticle or
even in the tissues without harm, until there occurs a bruise, or a bony
fracture when it at once develops a focus of purulent infection
(abscess).
=Exciting Causes= are the immediate causes of particular diseases. Like
the predisposing causes they may be _intrinsic_ or _extrinsic_, and the
first may be =inherent= or =acquired=.
Among =inherent= causes are certain of those already named as
predisposing causes, but which have come to be forcible enough to
develop disease without the intervention of any other observable factor.
Thus a _hereditary_ monstrosity (redundancy or defect), will appear in
successive generations without any apparent additional cause. The
appearance of white calves in herds of black cattle, after the
whitewashing of their stables shows a similar hereditary operation
though the result is not in this case pathological. The birth of blind
foals from blind sires or dams, or of foals with distorted feet from
mares suffering from severe chronic foot lameness are true pathological
sequences, in which the exciting cause is hereditary and operates during
intrauterine life. _Dentition_, as an attendant on early life is often a
directly exciting cause, from direct injury by entangled or retained
teeth that should have been shed, by fever aroused by the active local
changes, or imperfect mastication or insalivation leading to consequent
indigestion; in puppies and kittens convulsions are not uncommon as a
result.
=Extrinsic Causes= are such as operate through the environment. _Heat_,
if excessive and prolonged, relaxes and exhausts the system and exerts a
direct influence on the process of sanguification so that it may become
the direct cause of a variety of diseases. As the result of extensive
burns, dangerous congestions of internal organs are liable to occur, and
even the prolonged heat of summer often superinduces hepatic and gastric
disorder, diarrhœa and dysentery. Fat cattle in uncovered cars or yards
under a hot sun and with no breeze suffer extensively from insolation,
the temperature of their bodies rising to 110° to 112° Fah. and even
higher. _Cold_ is equally potent. With a temperature below zero Fah.,
the iron bit will freeze the buccal mucous membrane, and cause extensive
erosion of the mouth. The cold of salted snow or ice will freeze the
feet, causing sloughing of the skin above and around the coronet and
shedding of the hoofs, and predisposing to fatal septic infection of the
wounds. On the system at large, cold causes retrocession of the blood
upon the internal organs, and endangers the occurrence of acute disease
in any structure which is already debilitated or otherwise susceptible.
The nervous effect of the chilling of the skin is often the unbalancing
factor which sways the scale in favor of disease, which the system was
able to resist until this disturbing element was introduced. The sudden
chill from passing out of the warm barn into the frosty air, from
plunging into icy water, from standing in cold rain or sleet, from
standing in a draught of cold air especially when perspiring, is a
fruitful source of many diseases. In the cow, lying with the udder on a
cold stone may be the starting point of mammitis. The effect of sudden
chill is well exemplified in the great prevalence of diseases of the
respiratory organs at the change of the seasons in spring and autumn
when the vicissitudes of temperature are greatest, and the system
unprepared by habit, to bear the sudden change. Again it must be noted
that exposure to cold has a tendency to cause disintegration and
solution of the red blood globules, and that certain animals are
especially susceptible to this influence. _The condition of the
atmosphere_ is often a direct cause of disease as when charged with
offensive or irritating gases, the result of decomposition of organic
matter, with sewer or cesspool emanations, with deleterious gases from
chemical works, telluric sources, or fires. A low state of health, a
local irritation in some part of the air passages, or even a speedy
asphyxia may be the outcome of such atmospheric conditions. Again the
presence of solid particles of a more or less irritant, septic or
infecting kind prove the starting point of various diseases. The stone
cutters’ phthisis, and the sand granule ophthalmia are familiar examples
of the irritant, which often acts through the dust of the highway. Of
the infecting particles we have the germs of cattle lung plague, of
infective ophthalmias, and of tuberculosis carried with the dry dust and
inhaled. Of toxic agents borne on the atmosphere we see the compounds of
arsenic, mercury and lead. Moisture and dryness of the air induce
respectively a lymphatic constitution and low tone of health, and a
nervous constitution and a tendency to neurosis, ophthalmias, and skin
diseases. The pressure of the atmosphere has a profound effect on animal
health as seen in the extreme troubles of the heart and circulation in
the diving bell, and the respiratory, hæmorrhagic and brain affections
of high attitudes. A low barometer is attended by nervous disorders
(neuralgia) (S. Weir Mitchell). Surgical operations do best with a high
or rising barometer (Adinell, Hewson). The electrical tension of the
atmosphere shows familiarly, in man, in the feeling of heaviness,
dullness and malaise that precedes the bursting of a thunderstorm and
the relief that follows its termination. To this influence many of the
domestic animals are incomparably more sensitive than man, as witnessed
in the disposition of swine to hide in their pens or under litter on the
approach of the storm, the nervous disturbance even to abortion of
certain ewes which are heavy in lamb, and the great discomfort and even
piteous cries of some domestic felines on such occasions. The greatest
electric tension is seen in the drier climates, where the air, robbed of
its moisture, proves a poor conductor and equalizer, and the positive
and negative electricity get stored up separately in air, cloud and
soil. The presence of ozone in the air, as a habitual concomitant of
electric discharges, has been supposed to be a disturbing influence,
since it is distinctly irritating to the mucous membrane when present in
excess, but such excess apart from its artificial production is highly
improbable. As habitually met with it is antiseptic and health giving.
_Darkness_ always deteriorates the general health, producing
bloodlessness and pallor. _Light_ is usually invigorating, yet bright
sunshine falling upon the eyes from a window in front of the stall, or
in the open air when the face is turned up by an overdraw check rein, or
reflected from white dust and, above all, from snow, will often induce
inflammation and blindness. _Soils_ are often potent etiological
factors. Dense, damp, cold, undrained soils, are habitually covered by a
stratum of cold air, saturated with moisture, which greatly lowers the
vital stamnia. Damp clays, and waterlogged soils of various kinds, rich
in organic debris, are the natural homes of various pathogenic microbes,
such as those of ague, anthrax, milk sickness, actinomycosis and yellow
fever. Well drained sandy or gravelly soils are usually healthy, unless
they contain a great excess of decomposing organic matter. Again soils
with an excess of alkaline or other mineral matter may prove
deleterious, and those on the magnesian limestone often harbor the
poison of goitre, and cretinism, and favor the occurrence of urinary
calculus. _Faulty food and feeding_ in the domestic animals are
chargeable with many diseases. Stock often fall off in condition, in the
hands of one feeder, when the same food given with regularity and
judgment by a more careful feeder would keep them in the highest health.
Hay and grain which is musty and filled with cryptogams and their
products, are common causes of disorder of the stomach, the kidneys, the
nervous system or of general nutrition. Smut and ergot at certain stages
of their growth or grown under given conditions cause nervous disorders,
abortions, and gangrene of the extremity. A long list of vegetable
poisons may mix with fodders, and animal poisons with the food of the
Carnivora. A number of standard fodders may be poisonous at certain
stages of growth, as partially ripened perennial rye grass, millet,
Hungarian grass, vetches, etc. _Water and deprivation of water_ are
fertile causes of illness. Ruminants cannot chew the cud when deprived
of water, hence impaction of the first and even of the third stomach
with fermentations, tympany and other disorders. Horses suffer more from
a full drink of water after a feed of grain, the unchanged albuminoids
being carried on into the intestines, and both gastric and intestinal
indigestion induced. Sheep suffer fatal fermentations after drinking the
alkaline water of the Plains; cattle have diarrhœa and dysentery from
selenitions, or from stagnant and putrid water; and the water from the
dolomite is the usual channel of the goitre poison. Certain germs like
the plasmodia of malaria, and comma bacillus have their natural home in
impure water, and others like anthrax bacillus survive in the mud and
silt at the bottom of wells, ponds, and rivers and enter the system in
the water. _Compulsory rest_ in a stall often induces torpor of liver
and bowels, general muscular debility, and fatty degeneration especially
of the liver and heart. A few months of the swill feed, hot atmosphere
and absolute rest in a distillery stable usually ruins cattle for stock
purposes. _Overexertion_ on the other hand is prolific of illness.
Exhaustion of the muscles, congestion, inflammation, cramps, congested
lungs, heart failure or rupture, apoplexies and other hæmorrhages are
among the resultant maladies. Auto-poisoning is another result shown in
equine hæmoglobinæmia, and the fever of leucomaines. The excessive
development of sarcolactic acid from muscular work may render an
insusceptible animal susceptible to the anthrax bacillus. _Mechanical
causes_ would include over-exertion, in the production of strains,
fractures, and other injuries. They would also include impaction by
foreign bodies, calculi, and ingesta, friction of folds of skin or by
harness and other objects and pressure which leads to absorption and
atrophy. To these must be added _poisons of vegetable, mineral and
animal origin_ and the _microörganisms_ which act as injurious ferments
within the animal body. These will be treated more fully later on. Of
the microörganisms it may be said here, that they are almost certainly
the cause of all transmissible diseases. These diseases are variously
named on the basis of different ideas. They are =enthetic=, that is
implanted as a seed is planted in the ground to grow and multiply. They
are =zymotic= or fermentative because the essential cause multiplies and
is propagated like a ferment. They are =contagious= because propagated
by contact mediate or intermediate. They are =infectious= when
transmitted, not alone by contact but through the atmosphere. They are
=epizootic= because they tend to attack animals generally or a given
genus or family of animals generally when these are exposed to the
infection. They are =enzootic= when confined to the animals in a given
locality, the soil or conditions of which are favorable to the
preservation of the germ in pathogenic potency, or to the production of
a special susceptibility in the animal system. They are =sporadic= when
each case occurs without any casual relation to another. They are called
=panzootic= when they attack all animals without apparent preference.
The term _panzootic_ is also used to describe those recrudescences of a
disease or cycles of exalted pathogenesis which are observed in
contagious diseases, which frequently last for years and again give
place to a period of benignancy. Such cycles, of malignancy and
benignancy, may be due to modified environment acting either on the
disease germ or the animal system, or on both simultaneously.
The terms =enthetic=, =zymotic=, and =contagious= best express modern
views of the nature of these maladies. The term =infectious= when used
to express a gaseous or otherwise intangible (unorganized) body, or
influence transmitted through the air, necessarily excludes the
particulate, living, self-propogating germ upon which the
transmissibility of the disease depends. A chemical, electrical, or
other body or influence generated outside the animal body, cannot well
be conceived of as reproducing itself within the animal body but must
act like any other ectogenous poison, according to the size of the dose
and the frequency of its exhibition. This might create an _enzootic_
disease but would lack all the qualities of a contagious affection since
it could not spread from a victim when taken elsewhere and turned among
animals which would prove equally susceptible if placed within the
infecting area. Suppose on the other hand we apply the term _infectious_
to diseases in which the levity of the particulate living germ allows of
its being inhaled into the body of the susceptible animal, the case
becomes one of simple _mediate contagion_, the air acting as the
intermediate bearer.
The term =zymotic= conveys a clear idea of the method of increase of the
disease germ in the body by the ordinary process of generation. The old
doctrine of fermentation by a continuous change, due to contact with
dead fermenting matter, as an inflammable body continues to burn by
contact with the incandescent portion, has been definitely disproved by
the investigations of Pasteur and others, and today we must recognize
that every fermentation is the result of the propogation and vital
activity of living organisms. This does not ignore that the chemical
products or enzymes which are constructed by the vital activity of the
microbes, will dissolve or transform organic matter, but in the absence
of the microbe no such enzyme can reproduce nor multiply itself and its
action must therefore be exactly limited by its amount. The living germ
itself is therefore the one effective factor, by which the contagious
disease may be maintained and propagated. In its turn the living germ
can only come from a pre-existing living germ. To the scientist of today
the doctrine of spontaneous generation is a thing of the past and the
aphorism _omnis ovum ex ovo_ is dominant. The argument drawn from the
saccharizing of starch in the germinating seed by the operation of
diastase is inapplicable, as the diastase is produced by the living
cells of the germinal part of the seed, which are thus the counterpart
of the disease germ. No such glycogenic action occurs in the seed that
has been boiled or otherwise robbed of its vitality. So with the
arguments drawn from the ptyaline of the saliva, the pepsin of the
gastric juice, and the trypsin of the pancreatic juice; each of these is
the product of the living cells of the gland by which it is secreted,
and cannot increase its own substance in the absence of these cells.
Like the enzyme of the bacteridian ferment, these gland products can
break down or digest certain organic matters, but in all alike, the only
source of the chemical solvent is the living bacterium or gland cell
from which the particular product is derived. The toxins of a virulent
liquid, after the sterilization of the latter may still produce most of
the lesions and morbid phenomena of the disease, but, although death
were to ensue, the body of the victim would not be infecting to other
susceptible animals. The parallel between the functions of the secreting
animal cells and the disease germs may thus be put in tabular form:
Living Source. Chemical Product. Result.
Salivary gland cells = Ptyaline = Starch changed to
Sugar.
Peptic gland cells = Pepsin = Albuminoids changed
to peptones in acid
solutions.
Pancreatic gland cells = Trypsin = Albuminoids changed
to peptones in
alkaline solutions.
Disease germ = Toxin: Enzyme = Morbid phenomena.
Disease germ = Contagious disease.
Further consideration of pathogenic microörganisms will be found in
connection with contagious diseases.
MEDICAL DIAGNOSIS.
Means of diagnosis. Usual health of the subject. History of the
attack. Objective symptoms, interdependent disease, fever, diseases
that may be confounded, subsidiary disease, diagnostic signs, organ
involved, pathological test injections, course of disease, sporadic or
zymotic, result of treatment.
Diagnosis is the determination of the seat and nature of a given disease
and its distinction from other morbid conditions. Its importance to the
practitioner cannot be overestimated as it occupies the pivotal position
between causes, nature, morbid phenomena, and symptoms on the one hand,
and prognosis, prevention, and treatment on the other. Unless the
conclusions are sound as to causes, nature, lesions, and symptoms, there
can be no certain diagnosis, and without a correct diagnosis, prognosis,
prevention, and treatment can have no intelligent or scientific basis.
The practitioner who finds a dropsical condition and who is satisfied to
pronounce it dropsy and institute treatment is abusing his trust. He
must find whether this dropsy results from disease of the kidneys,
heart, bloodvessels, lymphatics, liver, lungs, bowels, or the structures
in which it is shown; whether it is due to parasites or imperfect
sanguification or to other morbid conditions, before he dare prescribe
treatment and predict results. So in every other affection; the failure
to make a correct diagnosis opens to the practitioner many doors of
error, and he is happy indeed if he can escape the injuring of his
patient.
In seeking a sound diagnosis we must attend to the following among other
indications:
1st. The habitual state of health of the subject. The genus, breed, age,
environment, habits, (pet dog, watch dog, hound, sheep-dog, ox, bull,
cow, milch cow, sheep in the field or housed, pig in pen or at large,
diet, regimen, water, race horse, draught horse, work, exposure, etc.)
as well as the personal equation of temperament, idiosyncrasy, heredity,
etc., must all be carefully considered.
2d. The history of the present illness as to its apparent cause, mode of
invasion, duration and progress.
3d. The objective symptoms by which it is manifested. All that can be
ascertained in the way of symptomatology, local and general, the
probable existence of interdependent disease, and all actual structural
lesions and disorders of function should be thoroughly investigated. As
supplementary to the more prominent objective symptoms any fever or
other constitutional disorder must be sought for; a mental list must be
made of the diseases which resemble this one, and these must be excluded
one by one by careful attention to the differential symptoms; other
diseases which are probably subsidiary to this, should be similarly
investigated and excluded; any really diagnostic sign of the suspected
disease must be carefully established and the diagnosis finally placed
on a solid foundation. The discovery of a constitutional (febrile)
disease to which a distinctive name can be given is by no means the end
of the diagnosis; the structural lesions of the disease may be largely
localized in an unimportant organ where they may remain circumscribed
without compromising life, or they may be seated in a vital organ which
will render the disease grave to the last degree or necessarily fatal.
For example: Anthrax of a dense, dry part of the skin may be a mild
local disease; anthrax of an internal organ is usually fatal. Every
local complication therefore, should be as carefully diagnosed as the
connected constitutional disorder.
But diagnosis cannot always be certain. In the early stages of certain
fevers two forms may be as yet indistinguishable and a day or two may be
required to develop differential symptoms. In some occult forms of
disease all differential symptoms may fail us. A method of diagnosis
which has hitherto been applied only to tuberculosis and glanders is
manifestly capable of much wider application, to diseases attended with
a febrile reaction. This consists in a hypodermic injection of a minimum
dose of the sterilized and filtered products of the culture of the
disease germ, which produces no effect on the healthy system but causes
febrile reaction or local inflammation, or both, in the diseased. This
will be treated more fully under the respective diseases.
In connection with such a method, but above all when no such resort has
been had, the obscure case should be seen frequently, the course,
duration, and termination of the disease should be noted, also its
tendency—sporadic or epizootic, and finally the result of treatment.
This last resort may often secure diagnosis and cure at once as when a
course of iodine cures an obscure actinomycosis.
SYMPTOMATOLOGY. SEMEIOLOGY.
Definition. Symptom. Sign. Constitutional symptoms—local, objective,
subjective, direct—idiopathic, indirect—symptomatic, premonitory.
Anamnesis. Position. Movements. Decubitus. Acute. Chronic. Fever.
Sthenic. Asthenic. State of limbs, muzzle, nose, snout, palmar-pad,
hoof, bill, digits, mouth. Thermometry. Normal temperature, in doors,
in field, at work, in hot season, in nervous subject, in thirst, in
youth—age, starvation, plethora, cold, sleep, rest, stimulants,
suppressed perspiration, eliminants, antipyretics. Fever temperature,
morning, evening, transient elevation, persistent rise, sudden
fall—collapse, crisis. Fatal elevation. Rise during defervescence.
Pulse. Respiration. Skin, staring coat, pallor, coldness, dryness,
harshness, mellowness, pliancy, hidebound, yolk, clapped wool, scurfy,
lesions, itchiness, tenderness, loss of hair, emphysema, anasarca,
sweat, sebum. Expression, life, dullness, paralysis, dropsy,
jaundiced, eye, discolorations, photophobia, amaurosis, pinched face.
Nasal mucosa, red, violet, etc., nodules, polypi, osseous disease,
pentastoma, œstrus, discharge from teeth—sinuses—actinomycosis—tumors.
State of the bowels, kidneys, nervous system.
The usual basis of diagnosis must be a clear and intelligent observation
of the symptoms of disease. A _symptom_ is an appreciable evidence of
disease. A _symptom_ however may indicate illness, without affording the
means of diagnosis, while the term sign is often used for a
pathognomonic symptom—one by which the disease can be identified. Used
in this sense a _sign_ may be said to be a diagnostic symptom.
1. =Constitutional Symptoms= are such as affect the entire system, like
a rise of body temperature, or a shivering fit.
2. =Local Symptoms= are confined to a definite area as redness,
tenderness, swelling, ulceration.
3. =Objective Symptoms= include all that can be recognized by the senses
of the observer. These alone are available in dealing with the lower
animals.
4. =Subjective Symptoms= can only be felt by the patient himself, as
pain, giddiness, cold, heat, blindness, numbness. Such symptoms are
therefore only obtainable from the human patient who can tell how he
feels. In the lower animals they can only be matter of inference, thus
pain may be inferred from lameness or wincing on pressure, and giddiness
from unsteady gait. The fact that the veterinarian is restricted to
objective symptoms renders his task a specially difficult one, yet this
has its compensation, as this very restriction tends to train the
observant practitioner to greater skill.
5. =Direct Symptoms= (=idiopathic=) are those which are connected with
the seat of disease, as the redness, exudation, and swelling of
inflammation.
6. =Indirect= (=sympathetic=, =dependent=) =Symptoms= are observable at
a distance from the actual disease:—as when headache attends on
dyspepsia, or lameness in the right shoulder upon disease of the liver.
7. =Premonitory= or =precursory symptoms= precede the diagnostic
symptoms of some diseases, thus dullness and languor often heralds an
approaching fever, and the strangles of young horses is often preceded
by a general unthrifty appearance, poor appetite and indisposition to
exertion.
In observing symptoms as in other things, some have far greater natural
ability than others, but in all a careful training will do much to
develop and improve the power and habit. A most important thing in such
habits is the strict maintenance of a system, not to be followed as a
cast iron rule but to be constantly kept in mind and strictly carried
out except when sound judgement and experience show it to be
unnecessary.
=Anamnesis.= As a rule the first thing to be learned about a patient is
his history, and personal and hereditary characteristics. What are his
general health, temperament, previous attacks, hereditary
predisposition, environment? Is the site of the building, its condition
as regards soil, springs, drainage, structure, ventilation, light,
cleanliness such as would favor any particular disorder or class of
disorder? Is the patient in high, low, or moderate condition, robust or
debilitated, alert and lively or dull and stupid? Have other animals
suffered recently, or at a corresponding season, or under similar
conditions in apparently the same manner? How long has the patient
suffered, were there any premonitory indications of illness, what were
the first symptoms, and what symptoms have followed up to the present?
Has there been any change of food, water or management that might throw
light on the cause? Has there been any change of weather or unwonted
exposure to cold, storm, overwork, compulsory abstinence or enforced
retention of some secretion? If a female is she pregnant?
Having exhausted this method, using such lines of inquiry as promise
good results in the particular case, the veterinarian is prepared to
bring his own powers of observation to bear more directly.
=Position= and =movements= will often furnish valuable data. The _horse_
which lies on his ribs, stands obstinately in chest diseases, or
whenever there is much interference with breathing. The ruminants and
carnivora on the other hand which lie on their smooth or padded sternum,
can breath with comfort in this position and only stand up persistently
in the worst cases. The habit of standing day and night is also
characteristic of anchylosed back or loins in the solipede. Roached back
may be natural, or the result of overwork and slight sprains or injuries
of the loins, of anchylosis, of intestinal or renal inflammation, or of
certain injuries to the limbs. The extension of the head on the neck may
suggest sore throat, chest disease, tumors around the throat, abscess
(fistula) of the pole, sprain or spasm of the extensors of the neck,
disease of the axoido-atloid joint, tetanus, or cervical rheumatism.
Dropping of head and neck might suggest paresis, mechanical injury to
the levator muscles or cervical ligament, extreme debility, or
prostration from a profoundly depressing fever or poisoning. Inability
or indisposition to back, might indicate sprain or fracture of the back,
anchylosis, laceration of the sublumbar muscles, paresis, cerebral or
spinal inflammation, softening or other lesion, tetanus, laminitis,
dislocated patella and certain other affections. Swaying or unsteadiness
in walking or turning would similarly suggest sprain or fracture of the
back, paresis and other nervous and locomotor injuries. The solipede
with peritonitis arches the back and draws the hind feet forward under
the belly, with impacted colon or obstruction to urination he will often
stretch with fore limbs advanced and hind limbs retracted. The mode of
decubitus may be significant. With peritonitis, enteritis, metritis or
acute nephritis or hepatitis the solipede lies down slowly and with
caution: with spasmodic colic he throws himself down as if reckless of
possible injury. Lying well up on the costal cartilages and side of the
breast bone suggests a slight affection of the air passages; lying on
the side, disease of other parts. Rolling on the back may indicate
simple intestinal spasm, but also blocking by intussusception,
impaction, volvulus or otherwise. Sitting on the haunches may suggest a
similar trouble or it may imply ruptured stomach or diaphragm. The dog
may sit on his haunches in health, or with dyspnœa in acute affections
of the respiratory organs, asthma and heart affections. Decubitus on the
belly with hind legs extended backward, may imply paraplegia, or acute
inflammation of the abdominal organs. Lying with the nose in the flank
or turning the head toward the flank, though a normal position of rest,
often indicates abdominal suffering. Turning of the head to one side
may, however, suggest injury, spasm or rheumatism of the cervical
muscles, or disease on the corresponding side of the brain. Animals, at
liberty, lie more frequently on the side on which the heaviest internal
organs are lodged, thus ruminants, pigs, and dogs rest on the right (the
side of the liver) though in cattle with a heavily loaded rumen the
condition may be reversed. Decubitus on the abdomen, with the limbs
extended and abducted implies profound nervous disorder or shock.
Habitual decubitus often indicates severe suffering in legs or feet.
Resting one limb more than another implies injury to that limb. Standing
with the pastern of one limb more upright than the others has the same
meaning. Extension of one fore foot in advance of its fellow with
flexion of the pastern and fetlock denotes suffering in the posterior
part of the foot or in the flexors. Flexion of carpus and fetlock
without advance of the foot probably bespeaks injury to shoulder or
elbow. Inability to bear weight on the fore limb, without knuckling at
the knee, should call for examination of the olecranon and joints
especially the elbow. Inability to extend the carpus should lead to
investigation of the flexor muscles and tendons, the joints and the
heel. Movement of the hind limb without flexure of the tarsus would
suggest injury to that joint, the stifle or the flexor metatarsi tendon.
Inability to extend stifle and hock, should demand examination of the
tendo-Achillus and olecranon, of the triceps extensor cruris and of its
nerves.
Atrophy of a muscle or group would require scrutiny of its tendons and
its nerve and blood supply.
More precise indications of injury of the locomotor system must be found
under surgery.
After posture, the general or constitutional disorder may claim
attention. Is the illness acute or chronic? Is fever present? Has the
animal had a rigor? Does the coat stare in patches (along the spine) or
generally? Is there perspiration? Is there full, clear, somewhat
congested eye (=sthenic=) or drooping lids over a dull brownish
sclerotic (=asthenic=). Are the lower parts of the limbs and other
extremities cold, and the roots of the horns or ears hot? Is there
significant heat and dryness of the muzzle (ox), nose (dog), snout
(pig), palmar-pad (carnivora), hoof (solidungala, bisulcates), bill and
digits (birds)? Has the mouth the hot burning feeling of fever? Finally
is the temperature as indicated by the thermometer abnormally high? To
estimate this with any degree of certainty one must be well acquainted
with the normal temperature.
=Normal temperature.= As taken indoors under ordinary conditions, the
normal temperature taken in the rectum may be: fowl, 107°–110°F.; swine,
103°–106°F.; goat and sheep, 103°–104°F.; ox, 100°–102°F.; dog,
99°–100°F.; horse, 99°–99.6°F. Ranging in the fields, at work, or on
forcing or stimulating feeding, it may be 1° higher than when at rest
indoors. A whole herd may be raised 2° by a three miles drive in warm
weather. In our summer heats a rise of 1° is common. In nervous animals
any change in management may raise the temperature, for example, 1° to
2° after failure to water at the usual time, or from retaining the milk
in the udder when the milker had been changed. Young animals are
normally .5° to 1° warmer than old ones though more sensitive to the
action of cold. Half starved animals, when put on abundant and
nutritious food may have a rise of 1° or more. Females in heat, in
advanced pregnancy and at the time of parturition are usually 1° to 3°
above the natural temperature. Among the agencies lowering temperature
are: cold, (1° to 2°); sleep, (1° to 2°); rest; starvation; alcoholic
and other circulatory stimulants which fill the cutaneous capillaries
and thereby cool the whole mass of blood; suppression of insensible
perspiration (retention of waste matters) as by varnishing the skin
which lowers the temperature to 25°; purgatives and diuretics (1°);
certain drugs like antipyrin, acetanilid, etc., which act on the heat
producing centres and retard metabolic changes.
=Temperature in disease.= Comparative temperatures should be taken at
the same hours on successive days, bearing in mind that the morning
temperature is usually slightly lower and the evening one slightly
higher. Where possible both morning and evening temperature should be
taken. With elevated temperature, repeat sooner to see that it is not
transient. A transient rise of 1° to 2° is unimportant. A permanent rise
of 2° or 3° indicates fever. A sudden additional rise of several degrees
in the progress of fever is grave. A persistence of the high evening
temperature to morning shows aggravation. A persistence of the low
morning temperature to the evening bespeaks improvement. A sudden
extreme fall to much below the normal (4° or 5°) indicates collapse.
This is usually attended with other symptoms of extreme prostration and
sinking. A sudden considerable fall to near the normal, without untoward
attendant symptoms, may indicate a _crisis_ and a more or less speedy
improvement may be hoped for. This sudden fall often attends the period
of eruption of certain exanthemata, as cowpox, horsepox, sheeppox,
aphthous epizootic, etc. A sudden extensive fall of temperature may
result from some transient accidental cause, as a prolonged deep sleep,
a hemorrhage, the relief of constipation, or of enuresis. A sudden rise
may supervene on such suppressed function or other cause of nervous
irritation or on toxin poisoning, but it does not persist more than
twelve or twenty-four hours after the cessation of the morbific cause.
A rise of 10° or 12° above the normal standard is usually promptly
fatal.
A continued high temperature indicates persistent disease, and a
considerable rise during defervescence implies a relapse and in the
absence of any error in diet or nursing is grave.
=Pulse.= Before the introduction of the clinical thermometer, the
indications furnished by the pulse were held to be of the highest value.
Though largely superseded by the usually more reliable thermometer, yet
they should not be discarded, but employed as symptoms corroborative of
the thermometric indications. In many cases the pulse will furnish
criteria, when in the absence of fever, the heat of the body will tell
of nothing amiss. This is especially true of diseases of the heart, the
large blood vessels, and of the nervous system, and in cases of
poisoning. For special indications furnished by the pulse, see diseases
of the heart.
=Respirations.= The morbid activity or inactivity of the respiration,
its modified rythm, the pathological significance of the altered
breathing sounds and of the superadded sounds, the indications furnished
by percussion, palpation, mensuration, succussion, sneezing, snorting,
yawning, cough, moan, grunt, stertor, discharge, etc., afford material
of inestimable value to the diagnostician. See under diseases of the
chest.
=Skin Symptoms.= The erection of the hair of carnivora in rage or fear
implies a profound nervous disturbance, and a similar erection (staring
coat) in the larger herbivora especially, implies a corresponding
nervous disorder, due however to a different cause. The pallor and
coldness of (white) skin and extremities the retrocession of blood
toward the internal organs, the contraction of the involuntary muscles
of the hair bulbs, the sense of cold, and the actual shivering all come
from the fundamental nervous disorder. The loss of lustre and gloss in
the hair and the dryness, rigidity and mobility (mellowness) of the skin
imply lack of nutrition. The mellow feeling of the skin under the
pressure of the finger, soft and yielding by reason of the lax
connection tissue and fatty layer in the thrifty animal, is in marked
contrast with the dry, hard, tough, unyielding hide firmly adherent to
the parts beneath (hidebound), which denotes the unhealthy or unthrifty
animal, or from the thin, attenuated, mobile, bloodless skin of the
debilitated subject, the victim of lung, liver, or intestinal worms. In
sheep in parallel conditions there is a lack of _yolk_ in the wool,
which is dry, lustreless and brittle and often flattened (clapped) on
the skin. In fowls ruffling of the plumage indicates the nervous
disorder and chill. The skin may be scurfy in conditions of low health
or in connection with the presence of vegetable or animal parasites.
Ringworm has excessive scurf, and tends usually to a circular form, and
to complete shedding of the hair from the spots. The hairs split up
before dropping. In acariasis there may be scurf, scab, abrasion and
sore of many kinds, but the outline is not necessarily circular, nor
strictly limited, isolated hairs remain even on the bare patches, and
itching is extreme as shown by the movement of the body and especially
of the lips or foot when the part is scratched.
The hair may be freely shed during convalescence from debilitating
diseases, a condition that must not be confounded with the yearly
shedding of the winter coat and the moulting of birds, which is a
perfectly normal process. Yet even the spring shedding and the growth of
the new coat makes a great drain on the system, and must always be taken
into account as a probable cause of derangement of health.
The lesions of the skin in the different cutaneous affections must be
remanded to the special chapter on skin diseases. The following however
may be named as having a general bearing.
Emphysema may be due to a local wound, (elbow, trachea, rib); it may
indicate black quarter, or it may occur subcutaneously in cattle without
marked impairment of health.
Anasarca, from diseased blood, heart, liver or kidneys is denoted by
swellings, often painless, or a general infiltration which pits on
pressure. It often shows primarily in the lower parts of the hind limbs.
Warty looking elevations must be carefully discriminated, having in mind
primarily papilloma, tubercle (grapes), actinomycosis, condyloma (in
dogs), cancer, melanosis. The secretions of the skin (sweat, sebum) may
be suppressed, or in excess, producing at times a special odor, as in
thrush and canker of the horse, cowpox and sheeppox, and rheumatism.
Before death the cadaveric odor may be marked, and attracts crowds of
flies to the victim.
=Facies.= The countenance may be expressive. Between the bright, full,
clear, prominent eye of health, and the dull, sunken, lifeless,
semi-closed eye of serious disease the contrast is extreme. The drooping
lids (ptosis) may be paralytic and even unilateral, in which case
drooping ear, and flaccid lips and alæ nasi complete the picture. With
paralyzed lips there is usually drivelling of saliva, and dropping of
half chewed morsels in the manger and stall. The eye may show dropsical
lids in kidney or liver disease and in anæmic conditions like
distomatosis in sheep. It may show the upper lid bent at an angle in
recurrent ophthalmia of solipedes. The mucosa may be red in ophthalmia,
yellow in jaundice, dusky brown in Southern cattle fever, anthrax,
cerebral meningitis, and other fevers attended with destruction of red
globules and liberation of their hæmatin. The pupils may be all but
closed in internal ophthalmias, or widely dilated and irresponsive to
light in amaurosis. The iris may lack its normal lustre or may be
distorted or torn in various ways from adhesions. Opacities of the
cornea, lens, or vitreous may be recognized.
The facial muscles may be flaccid and devoid of expression in palsy, and
prostrating diseases; they may be firm, giving the bright, intelligent
look of health; or they may be painfully drawn in the agonized
expression of spasmodic colic or enteritis.
=Nasal Mucosa.= The pituita is bright red in sthenic fevers, simple
acute coryza, strangles, laryngitis and inflammation of the larger
bronchia. It assumes a violet hue in capillary bronchitis, pulmonary
congestion, glanders, and petechial fever. Petechiæ appear in the last
named affection, and in a number of bacteridian diseases, such as
anthrax, swine plague, hog cholera, the red fever of swine etc.; a
yellow tinge in shown in jaundice. Millet-like or pea-like nodules, or
elevated patches, and ulcers show in glanders and may be felt by the
fingers. In cattle hard millet-like nodules appear in a chronic coryza
with hypertrophy of the mucosa. The orifice of the lachrymo-nasal duct,
seen in the horse on the floor of the chamber at the friction of the
mucosa with the skin of the false nostril and in ass and mule on the
outer ala near the upper commissure, is sometimes plugged with
inspissated mucus. Among other lesions of the nasal chamber may be named
polypi—soft and calcareous,—thickening and obstruction in purpura
hemorrhagica, osteoporosis and hypertrophy of bone, and
parasites—pentastoma denticulata (in the horse and dog), and the larva
of the œstrus (in sheep and buffalo). Disease of the upper molars and
abscess of the fronto-maxillary sinus may be manifested by swelling
beneath and on the inner side of the eye, fœtid discharge from the nose,
and obstruction of the air current. Dullness on percussion will show the
filling of the sinuses. These conditions must be carefully
differentiated from actinomycosis, sarcoma and other morbid growths in
the same situation.
Costiveness with fœtor and lack of the normal color in the stools may
suggest _liver torpor_ or inflammation, while fatty stools may suggest
pancreatic disease. The uneasy movements of colic, should lead to a
careful investigation of the chylo-poietic organs (see digestive
organs). Weakness of the hind parts, tenderness of the loins, and
altered condition of the urinary discharge should demand a close enquiry
into the state of the _kidneys_ and _bladder_. Satyriasis or nymphomania
would suggest disease of the _generative organs_ or the nerve centres
that preside over them. The same is true of impotence, sterility and
abortion.
In eruptions on the skin (erythema, eczema, pustule, squama) a cause may
be found in the local action of heat, friction, or other direct
irritant, but in the absence of any such manifest cause, an enquiry
should be made into the functions of sanguification, digestion,
urination and the action of the liver. It may further suggest parasitism
(ring worm, phthiriasis, fleas, acariasis, verminous disease, etc.)
Symptoms of _nervous disorder_ are too numerous to be here traced to
local lesions. Motor paralysis of one limb may, however, suggest injury
to its motor nerves, to the same side of the spinal cord, or of the
opposite half of the cerebrum. Paraplegia almost always indicates injury
to the cord. Sensory paralysis of one side may depend on disease of the
opposite corpus striatum. The animal moves in a circle when a tumor
(coenurus in sheep) exists in the roof of the lateral ventricle
presumably pressing on the ganglia on its floor. An animal rolls on its
axis when there is a lesion of the median cerebral peduncles, of the
supero-external portion of these peduncles, of the posterior part of the
encephalon, or of different parts of the hemisphere. Amaurosis suggests
disease of the corpora quadrigeminia. Loss of coördination of muscular
movement usually implies some lesion of the cerebellum. Vertigo may
imply disease of the encephalon (congestion, anæmia, inflammation,
dropsy, hæmorrhage, tumor, abscess); it may be disease of the internal
ear; it may be digestive disorder connected often with cryptogamic
poisoning; it may be heart disease with obstruction of the jugular
veins; it may be parasites in the nasal sinuses; or it may be disease of
the eye. Coma occurs in most congestions and pressures on the
encephalon, and like vertigo in poisoning by alcohol, solanine, monoxide
of carbon, etc. In acting on any ganglionic centre the agent may,
according to its degree, operate positively or negatively, producing
spasms, or paralysis as the case may be. As in the case of other
visceral affections the specific diseases must be referred to for
particular symptoms.
For the more precise points in diagnosis, including chemical, physical,
electrical and instrumental methods, etc., the reader is referred to the
special diseases.
PROGNOSIS.
Definition. Demands on the veterinarian, the question of economy.
Basis of Prognosis. Cause of the illness, internal or external, vital
or nonvital organ, enzootic, fatigue, infection, in one or two
symmetrical vital organs, regular or irregular in its course,
persistence, relapse, complications, effect of treatment, appetite,
temperature, pulse, breathing, youth, age, debility, previous disease,
breeding, climate, season.
Prognosis is a more complicated question for the veterinarian than for
the physician. The latter must pronounce on the malady, whether it is
likely to follow a regular or irregular course, whether it will last
short or long, whether it will be curable or incurable, and if curable
whether recovery would be complete or partial. For the veterinarian
there is in addition the question of economy. The veterinary patient is,
as a rule, of value, only if he can be rendered sound, and a partial
recovery may be even worse than a fatal result, since the subject
remains as a ruinous charge on his owner. The veterinarian must
pronounce on the prompt and perfect curability of the case, on the
outlay that will be requisite for treatment, on the depreciation which
will be entailed on the patient, and whether, in certain lesions that do
not harm the carcass, it would not be more judicious to butcher the
subject. The physician is expected to do the best he can for life and
health, and even a very imperfect recovery brings him a mead of
gratitude. The veterinarian on the other hand must be an expert not only
on disease, but on animal values, and if his treatment, however skillful
it may be, results only in the prolonging of the life of an useless
animal, the owner may charge him with imposing upon him an unnecessary
outlay. The soundest judgment and highest skill are often necessary to
secure the interests of an employer in such circumstances. In certain
cases the recommendation to destroy is of much more value to the
employer than the most skillful, and partially effective, curative
treatment. On this basis, the reputation of a skillful man may be
securely built. He can deceive no one if his prediction of recovery is
not justified, while if he advises destruction and the patient recovers,
he is at once discredited.
To give a sound prognosis the practitioner must have a thorough
knowledge of pathology, he must have acute powers of observation, and he
must be quick to appreciate every point that makes for or against the
patient in the particular case.
The _causes_ of the trouble must be carefully considered. Are they
transient or permanent? Are they removable or irremovable? Are they
external or internal? As a rule an internal cause is the more
redoubtable. Some lesions are necessarily fatal, as a needle penetrating
the heart or an attack of rabies or milk sickness. Is the cause an
enzootic one? If so can the patient be removed from the locality? Is it
a fatigue fever or an infectious one? Is it a simple inflammation or an
infecting one? The latter are usually much more grave. In case of
contagious disease, can its propogation be prevented? Is it of a fatal
or non-fatal type? Is it situated in a tissue favorable to a fatal
extension, (anthrax in lung) or in one unfavorable (anthrax in the tip
of the tail)? Disease in a single vital organ like the heart is
necessarily much more grave than in one of a symmetrical pair (kidneys,
lungs) one of which can carry on the functions. The regular progress of
the disease and especially an uninterrupted improvement, following on a
critical perspiration or urination, is a good prognostic sign, whereas
unevenness of temperature, pulse and respiration, with temporary
aggravations of the general symptoms, should demand a less hopeful
prognosis. The persistence of the malady is also an unfavorable
indication. A relapse after partial recovery is a serious indication
unless due to some obvious and easily removable cause, and unless the
former convalescent condition is speedily restored on its removal. A
complication is a serious indication whether it consists in an embolism,
or new centre of the same disease, or the supervention of a second
disease upon the first. The system has just so much more to contend with
and the very supervention of the second focus or malady argues a special
susceptibility, debility, or lessened power of resistance.
The prompt success or entire insuccess of treatment proves valuable.
The preservation of appetite, the slow, uniform descent of the
temperature, and the improvement of pulse and breathing are among the
most valuable indications.
Something may be deduced from the condition of the patient. If very
young or old, debilitated by overwork, bad or insufficient food,
previous disease, or any other cause, the prognosis is less hopeful, as
it is also as a rule, during gestation, in the parturient state, or if
abortion ensues. A hereditary predisposition to the malady in question
is equally unfortunate.
Climate may be an important factor. Thus liver diseases are far more to
be dreaded in a damp tropical or semi-tropical region, and rheumatism
and catarrhal affections in winter and in cold northern localities.
Acclimatization should also be considered. The bovine animal, raised on
the Gulf Coast is likely to make a good recovery from Southern Cattle
Fever while the northern beast would almost certainly die.
All in all the question of prognosis cannot always be judiciously
decided at a first visit, and for the sake of his own reputation, it is
well that the practitioner should give only a qualified opinion at first
until he can certify himself as to the probable outcome of the disease.
PROPHYLAXIS. PROPHYLACTICS. PREVENTION.
A test of public sentiment. Soil. Water. Exposure. Buildings. Local
hygiene. Breeding. Diet. Work. Harness. Ventilation.
With advancing knowledge of veterinary medicine the subject of
prophylaxis is steadily assuming a more important place, and especially
in the classes of enzootic and epizootic diseases. Indeed for the fatal
infectious diseases of animals one can fairly estimate the medical
intelligence of the people by the extent to which therapeutic treatment
is still allowed. With economy as the great central object of veterinary
medicine, the problematical recovery of the few can never balance the
assured preservation of the many. But this subject belongs to contagious
diseases to which the reader is referred.
In enzootic affections, improvements in soil, water, exposure,
buildings, and other local unhygienic conditions, are the final ends to
be sought, according to the particular nature of the prevailing disease.
So in sporadic diseases the correction of faults in breeding, hygiene,
diet, water, work, harness, exposure, buildings, ventilation, etc., are
called for in different cases as will be noted under the individual
diseases.
THERAPEUTICS. TREATMENT.
Definition. Mechanical and Medicinal Therapeutics. Adaptation to each
case of disease.
The ultimate object of all medicine is to prevent disease or when it
cannot be prevented, to cure. The term therapeutics covers all measures
applied with curative object. Therapeutics are naturally divided into
=Mechanical= and =Medicinal=. To mechanical therapeutics pertains the
whole domain of surgery. Medicinal therapeutics has to do especially
with internal medicine. Each of them, however, encroaches more or less
on the other. Modern surgery is essentially aseptic or antiseptic, and
antisepsis is secured by medicinal agents. In medicine when cups are
applied we adopt an essentially mechanical treatment. Both methods then
must remain open to physician and surgeon. Another and no less important
branch of treatment which is open to physician and surgeon alike is diet
and general hygiene. The same care must be given to the use of these in
the treatment of disease as in its prevention, and in many cases a
judicious use of these may almost entirely obviate the necessity for
medicine.
It would be useless to enter here into the subject of therapeutics.
Suffice it to say that the choice of a system and of individual agents
must be determined by the particular conditions of the case, its cause,
and nature, the strength, vigor, and genus of the patient, the organ
involved, the extent and stage of the disease, the existence of a
relapse, or complication, and all other circumstances that would affect
the action of the remedy. Specific statements must be made with the
several diseases.
HYPERÆMIA. CONGESTION.
Definition. Forms, active—arterial, passive—mechanical—venous.
Determination of blood. Causes of active congestion. Vaso-motor
nerves. Lesion of spinal cord; or of sympathetic nerve. Reflex
irritation. Central cause. Physiological hyperæmia. Medicinal
hyperæmia. Bacteridian (toxic) hyperæmia. Arterial obstruction.
Thrombus, tumor. Cold, chill. Removal of pressure. Cardiac
hypertrophy. Symptoms, bright red color, swelling, dropsy, migration
of cells. Rise of local temperature. Tenderness. Altered function.
Causes of passive congestion. Obstructions in the lungs, heart, veins.
Diminished force of circulation from age, debility, arterial disease,
distance from the heart, decubitus, vaso-motor disorder.
Gravitation—hypostatic congestion. Tumors. Paresis. Symptoms.
Cyanosis. Distended veins. Coldness. Transudation—watery. Hæmorrhage.
Thrombus. Hyperplasia. Atrophy. Postmortem lesions. Treatment. Remove
Cause. Correct injurious gravitation. Correct any fault in blood
pressure. Derivation. Constringe or support part. Massage.
Electricity. Improve general health.
_Definition._ An excess of blood in a part. It is distinguished from
inflammation by the absence of that tissue reaction, which leads to or
constitutes the special phenomenon of that morbid process.
Hyperæmia is divided into =active= or =arterial= and =passive=,
=mechanical= or =venous=. A capillary form has also been described but
usually capillary congestion is seen in both the arterial and venous
types.
I. =Active= or =Arterial Determination of blood=. In this form the
arteries are dilated under a direct nervous influence. _Causes._ In all
the regular functions of the body, the flow of blood is under the direct
control of the vaso-motor nerves which proceed from the spinal cord,
through the branches of the sympathetic to be distributed with the blood
vessels. The hard pulse of pleurisy is due to rigid contraction of the
constrictor muscles under the action of the vaso-motor nerves, and the
blush of shame is due to their relaxation. Some claim an active
dilatation of the arterial muscular coats, others look more simply upon
the dilatation as a mere yielding of the coats under the blood pressure,
when the constrictor muscles are relaxed. This vaso-motor paresis may be
induced: 1st, by any lesion of the spinal cord. 2d, by the cutting of a
sympathetic trunk, that of the abdomen, for example, which leads to
active congestion of the abdominal viscera, or the section of the
cervical sympathetic which leads to watering of the eye, sweating,
congestion, and scabbing on the corresponding half of the face. 3d, by
reflex irritation through the sensory nerves, as in congestion through
friction, heat or cold to the skin, or that resulting from excessive use
of an organ such as the mammary gland. 4th, by causes acting directly
through the brain as in emotional blushing or the facial congestion of
violent rage.
Physiologically we see the operation of this nervous control in the
congestion of the gums during dentition, of the salivary glands during
mastication, of the stomach and bowels during digestion, of the womb
during gestation, of the mammæ at parturition, and of erectile organs in
copulation.
Medicinal agents act in the same way, opium or alcohol producing active
dilatation, and belladonna and ergot causing active contraction of the
arterial walls.
Bacteridian poisons act in the same way, tuberculin and a number of
others causing active dilatation.
The obstruction of one artery by thrombus, tumor, or ligature, causes
increased tension in the collateral branches coming off just above and
an active congestion in the parts to which these are distributed. While
this is directly due to increased local pressure, it is also an instance
of the lack of balance between the blood pressure and the resistance of
the vascular walls. In this case there is increase of pressure, in the
other a diminished resistance.
If there is a superficial anæmia, as from cold or chill, there is of
necessity, an internal hyperæmia. This contributes to the production of
internal congestions and inflammations, though the seat of election of
such inflammation is usually determined by the nervous sympathy between
the part chilled and the deeper organ affected.
Another cause of congestion is the lessening of pressure by the parts
surrounding the vessel. Thus in cupping, there is prompt cutaneous
congestion, and a similar result occurs in pericardium, pleura, or
peritoneum on the withdrawal of the liquid of hydropericardium,
hydrothorax or ascites.
Another cause of congestion is found in hypertrophy of the heart and
increased force of the blood flow (blood tension). In such cases those
organs become congested in which there is some previous debility or
disease of the blood vessels.
_Symptoms and results._ The symptoms are a bright vermillion redness,
tension or swelling, heat and tenderness. Pulsation is stronger in the
vessels leading into the part, secretions tend to increase but may give
place to a serous effusion or hæmorrhage. The bright redness is
attributed to the rapid circulation of the red globules which have not
time to give up their oxygen to the tissues. It is sharply circumscribed
where the affected arterioles have no free anastomosis with those of
neighboring parts, diffuse where anastomosis is abundant, and when on
the skin it is liable to rise in knots or buttons as in urticaria. When
pressed the redness entirely disappears unlike the redness of
inflammation.
The swelling may be due to the simple turgescence of the bloodvessels,
but also often to transudation of serum as in and around the cow’s udder
at parturition. The occasional migration of globules, and their escape
through minute lacerations in the vascular walls add alike to color and
turgescence.
The elevated temperature, (rising sometimes 3° C.) in the congested
area, is attributed to the more active circulation, and Schiff prevented
its appearance after section of the cervical sympathetic, by tying the
carotid and vertebral arteries on the same side.
The tenderness of the congested parts varies inversely as the looseness
of texture and the facility for swelling. It may be scarcely perceptible
in the mammary region, and intense under the horn or hoof.
The functions in the congested organ are often seriously interfered
with, secretions appearing in excess or entirely altered. When the
congestion lasts it may cause hypertrophy, induration or hyperplasia,
these are however rather sequels than lesions of the condition. Simple
congestion is usually quite transient, and if prolonged, often merges
into inflammation.
II. =Passive or Venous Congestion.= In this there is no excess of blood
entering the part, but the regular supply is delayed in the veins by
some obstruction, and these vessels and, later, the capillaries are
gorged with black blood.
_Causes._ 1st, Mechanical obstruction to the onward flow of blood, as in
the case of disease of the lungs hindering the flow of blood from the
right heart; disease of the right heart allowing a reflux of blood into
the veins; or pressure by tumors or otherwise on the great or small
venous trunks. If in the heart or lungs the whole systemic venous system
becomes the seat of passive congestion; if in a single venous trunk then
only the parts the venous radicles of which are tributary to this. We
find examples of this in phlebitis, in compression by the swellings of
strangles, in the result of a bandage or ligature tied round a limb at
some distance from its extremity, and in the compression of the iliac
veins by a gravid womb.
2d. Diminished force of the blood current in the veins, as from old age
or great debility and especially from weakness of the heart’s action.
Also from disease of the arterial coats which impairs their tonicity.
The force being too weak to force the blood actively through the
capillaries and veins, it becomes unduly charged with carbon dioxide and
other products of tissue waste, so that nutrition suffers and the walls
of the capillaries lose their vital force. This condition is aggravated
in the hind limbs by the distance from the heart, and the dependent
position, and in decubitus by the compression of the vessels of the
limbs. Also by injuries to the vaso-motor nerve supply as œdema appeared
in the hind limb after tying of the femoral vein in animals the
abdominal sympathetic of which had been cut, but not in animals in which
this nerve was left in its normal condition (Ranvier).
3d. Gravitation in weak states of the circulation must be looked upon as
a cause of venous congestion. This is seen in the examples of hypostatic
congestion and œdema seen in the lungs and other internal organs in low
conditions and in the advanced stages of debilitating diseases, and in
certain cases of stocking of the limbs in horses.
4th. Valvular insufficiency of the left heart and tumors or aneurisms
interfering with circulation through the aorta, cause passive congestion
of the pulmonary veins and œdema of the lung.
5th. Tumors and diseases of the liver determine passive congestion of
the portal system and ascites.
6th. Passive congestion is very liable to take place in an organ the
functions of which are impaired as in a paralyzed part. In this the
hyperæmia may start in the capillaries and extend to the veins or even
to the arteries.
_Symptoms and results._ If on a mucous membrane or white skin the color
becomes dark red, or violet (cyanotic) with evident distension of the
capillaries and veins, the latter of which may stand out as knots or
cords, there is an appearance of swelling or enlargement and sometimes
coldness of the part. Soon the watery part of the blood transudes in
excess, constituting dropsy, with increased swelling and pitting on
pressure. On the mucous surfaces it determines an abundant serous
secretion. The color is deepened by the escape from the vessels of red
globules as well as white. The transudation contains little albumen and
only exceptionally fibrine. In connection with the marked deoxidation
and high carbonization of the blood, the nutrition of the part is
largely arrested together with the functions, secretory, motor or
otherwise. The imperfectly nourished vessels may give way, leading to
hæmorrhage, or nutrition may be definitely arrested producing moist
gangrene or ulceration. Sometimes a thrombus is formed in a congested
vein. The changes in the affected organs depend much on the degree and
duration of the hyperæmia. If slight and lasting it causes permanent
induration and thickening, from connective tissue hyperplasia as
frequently seen in the hind limbs of the horse. In case of blood
transudations the altered coloring matter gives the various shades of
gray, brown or black. If long continued the organ may shrink and atrophy
occur from defective nutrition and contraction of the fibrous
hyperplasia.
In making post mortem examinations mistakes may be made through the
occurrence of changes after death. Thus a hvperæmia which was quite
considerable during life may virtually disappear through the contraction
of the arterial and capillary coats forcing the blood on into the veins.
A minute point of extravasation here and there may be the only
macroscopic lesion left. Again a marked venous and capillary hvperæmia
in a dependent part of the body or of an organ may be entirely due to
hypostatic conditions, the blood having settled into the lowest part of
the vessels since the death of the animal. To avoid this source of error
one must always carefully note the position of the carcass after death.
Under other circumstances the superficial veins and capillaries may fill
up with blood through the occurrence of decomposition and the evolution
of gases in the internal cavities, which empty the splanchnic and
parietal vessels by compression.
_Treatment._ The general principles of treatment may be stated thus:
1st. Remove the cause of the hyperæmia if possible, especially any
mechanical cause; 2d. Secure the influence of gravitation in favor of
the return of blood to the heart; though not so available in animals as
in man, it is of great value in congestions of the head, ears, tail, and
to a less extent of other parts; 3d. Correct any fault of blood
pressure, excess or deficiency, which may act so as to cause active or
passive hyperæmia; 4th. Establish derivation by cupping, leeches,
fomentations, pediluvia, sinapisms, etc.; 5th. Apply cold, astringents,
bandages, to empty the hyperæmic vessels, or kneading, rubbing, or
electricity, to hasten the flow of blood; 6th. To improve the quality of
the blood and general health, in plethora by low diet, purgatives and
diuretics, in anæmic or debilitated conditions by iron, bitters,
nourishing food, fresh air, sunshine and exercise.
It is especially important to check passive congestion in febrile
diseases, and mechanical congestion at an early stage of its progress
(Roberts).
INFLAMMATION. PHLOGOSIS. PHLEGMASIA.
Definitions. Relations to active hyperæmia. Redness. Heat. Pain.
Swelling. Forms: in vascular tissues: in nonvascular. Changes in
tissue elements. Death of cells. Cloudy swelling. Granular
degeneration. Cell proliferation. Karyokinesis. Embryonic cells.
Amœboid functions. Migration of leucocytes. Red cells escaping.
Changes in innervation. Vaso-motor disorders. Fever. Changes in
circulation. Contraction of capillaries, dilatation, rapid flow, tardy
flow, stasis, oscillations, thrombus, collecting of white globules in
periphery of current, migration of leucocytes, blood plates, and red
globules, massing of red globules, exudation, softening of the
capillary walls, nutrient artery more rigid and transmits more blood,
heart contracts more forcibly, increase of fibrine, increase of waste
products. Buffy coat, physiological causes. Microbes. Ptomaines.
Toxins. Chemiotaxis. Phagocytosis. Polynuclear and mononuclear
leucocytes. Exudates, unlike dropsies. Mucous exudate. Serous exudate.
Fibrinous exudate. Blood exudations. Croupous exudation. Chyliform
exudate. Results and Products. Resolution. Delitescence. Metastasis.
New formations. Suppuration. Pus microbes. Pus. Healing by 1st
intention. Healing by 2nd intention, granulation. Granule corpuscles.
Interstitial neoplasia. Degenerations in lymph. Fatty degeneration,
melanotic. Softening. Ulceration. Gangrene.
Inflammation has been variously defined as “perverted nutrition,” as a
“protective reaction of the organism against irritant agents” and in
other terms that express at once too much and too little, without
actually defining the morbid process. Older definitions dealt with the
manifest disorders of circulation, of innervation or of tissue change
too often exalting the importance of one set of changes at the expense
of another and thus giving in the main a one sided view of the morbid
process.
Some modern bacteriologists are inclined to refuse the title to any
morbid process that is not caused by the presence of microbes or their
toxic products. To them the changes occurring in an aseptic wound or in
a simple fracture in process of healing are purely reparatory and
partake no more of the nature of inflammation than do the developmental
changes in the growing embryo. While to a large extent true, this
exclusive view implies exceptions, since if the chemical poisons derived
from the bacteria can develop inflammation, the same must be admitted as
possible for chemical irritants drawn from other sources.
As a matter of fact inflammation, occurring as it does in very different
tissues, vascular and nonvascular, fibrous, cellular, parenchymatous,
etc., and in connection with a great variety of irritants, must be held
to include a large group of morbid processes, bearing to each other a
strong family relationship and resemblance, and yet differing in many
important details. Each irritant (heat, cold, electricity, chemical
irritant, incised, punctured, lacerated or contused wound, rupture,
fracture, foreign body, parasite, microbe, toxin, etc.,) has its own
special character and mode of irritation; each tissue has its own
special method of succumbing or reacting and its own amount of blood
supply; and each system and organ has its own native or acquired power
of resistance and reaction.
Inflammation agrees with active hyperæmia in the tendency to dilation of
the vessels and an increased flow of blood to the part or if the
irritated part is nonvascular like the cornea or articular cartilage,
then to the parts adjacent. It differs, however, in the more active cell
proliferation, and in the nature of the liquid transudation which is
richer in albumen fibrine, cells and phosphates. Abstractly the inflamed
part retains very active vital processes, trophic and exudative, but
these, are largely changed from the normal and are, it is claimed,
perverted, yet they preside over the processes of cell growth and decay,
the removal of injured or useless tissue, and later, over the building
up of new material, and repair of loss. Active hyperæmia on the other
hand is mainly a circulatory disorder, and when it advances so as to
determine changes in the cells and tissues it is held to have merged
into inflammation.
The term inflammation (from inflammo, I set on fire), is suggestive of
the local heat of the inflamed part, just as fever (febris) indicates an
elevation of the temperature of the body at large. Celsius enumerated
the features of rubor, calor, dolor and tumor (redness, heat, pain and
swelling) which have come down to our own time as at least suggestive of
inflammation. But any diagnosis, based on these alone, would be today
woefully inadequate. Redness occurs in the transient blush, heat in the
febrile state, though no inflammation can be recognized, pain is present
in neuralgic and other nervous affections, and swelling in dropsy and
tumor. On the other hand redness is entirely absent, for a time, after
the outset of inflammation in nonvascular tissues (cornea, articular
cartilage), the heat of the inflamed part may be actually lowered when
there is much exudation around the capillary vessels and lessened flow
of blood, pain may be absent in some circumscribed inflammations of the
lungs, and swelling is not at first visible in the inflamed cornea or
compact bony tissue. These phenomena which are so common in inflammation
and, in general so characteristic of it, cannot therefore be accepted as
infallible evidence of its existence, nor can their absence be held as
absolutely implying its nonexistence.
=Forms of Inflammation.= This morbid process might be divided almost
indefinitely according to the organ invaded, the cause, and type, yet it
will be more convenient to deal with it generically and notice
=inflammation in nonvascular and vascular tissues= respectively, and the
different types of =granular degeneration=, =exudative inflammation= and
=croupous inflammation=. It will be requisite further to notice an
=acute= and a =chronic= type.
By dealing first with the changes in the anatomical elements of the
tissues and in the innervation, we shall virtually cover the phenomena
observed in nonvascular tissues, and later the changes in connection
with the circulatory system will give the additional characteristics of
inflammation in vascular tissues.
CHANGES IN THE TISSUE ELEMENTS.
=Death of cells and tissue.= By the application of an irritant (acid,
heat, etc.,) a certain thickness of tissue with its enclosed cells is
killed, and a thin layer of necrosis is usually produced. This does not
constitute inflammation, but it acts as a foreign body, often septic, in
producing inflammation in the parts adjacent.
=Cloudy Swelling, Granular Degeneration.= This may occur in the inflamed
area surrounding the necrosed tissue in the seat of a burn or other
injury, it is exceedingly common in the cells of inflamed parenchymatous
tissue (liver, kidney), in the muscle of the heart, in the
gastro-intestinal mucosa, in febrile affections and in poisoning with
arsenic, phosphorus, or mineral acids. The gross appearance of the
tissue is that of swelling, with a dull grayish color and a loss of its
normal translucency. The cells of the affected organs are seen under the
microscope to be filled with small albuminous granules which may be so
abundant as to completely conceal the cell structure. The granules are
insoluble in ether, but disappear under acetic acid. This condition of
the cells is often associated with the exudative forms of inflammation.
=Cell Proliferation and Change.= In the nonvascular organ attacked by
inflammation the multiplication of tissue cells and their resumption of
amœboid movements is a constant phenomenon. Virchow insisted on the
fundamental relation of the cell to the morbid process, and Goodsir and
Redfern showed the rapid increase of the cells of articular cartilage in
attacks of arthritis. There is first a sensible increase of the nucleus
of the cartilage cell which shows a more extended and deeper staining in
carmine or aniline; then by a special method of division (karyokinesis)
the cell and nucleus divide in two; by a similar process these divide in
four and so on in regular order. Meanwhile the cartilaginous substance
becomes softened and finally dissolves and disappears, leaving in the
place a mass of closely aggregated cells.
In the nonvascular transparent cornea, the membrane of Descemet, the
epithelium of serous membranes and in the epidermis a similar cell
multiplication occurs, also in the lateral cartilages of the horse’s
foot.
To follow the indirect cell division by karyokinesis, we must note the
cell as a semi-solid mass, formed of protoplasm and nucleus, each having
as its framework a network of exceedingly fine inter-crossing filaments,
much finer in the nucleus than in the cell protoplasm. The nuclear
filaments stain with hæmatoxylon and safranin and are called _chromatin_
threads. The intervening non-staining material is _achromatine_. The
nucleus has a membranous envelope in two layers, of which the inner only
stains. When about to divide two poles are formed in the cell protoplasm
opposite to each other and near the nucleus the filaments concentrating
to the poles. The chromatin threads in the nucleus thicken, become
convoluted, split and multiply, and draw into their substance the
chromatin layer of the envelope. Next the chromatin threads form long
loops directed toward an achromatine centre or pole like a star, and
this is followed by the progressive division of the star-shaped mass
into two equal parts.
Finally they separate, together with the cell protoplasm, forming two
daughter cells.
This cell proliferation under the action of an irritant is common to the
vegetable kingdom in which galls, and tumors are formed in this way. It
is a remarkable feature of these multiplying cells that they not only
lose their power of developing the tissue in which they formerly lay,
and have all their vital powers devoted to proliferation, but they
acquire the amœboid power of their ancestors, the embryonic cells, which
they further resemble in size. Indeed these cells are freely spoken of
as embryonal cells, and the tissue formed by their massing together as
embryonal tissue, and there is a widespread impression that they revert
entirely to the form and characters of the embryonic cell. In some
respects, however, they are unlike. The modified tissue cell of
inflammation presents a nucleus of horseshoe outline, or after division
of the nuclei they together retain this semi-circular outline; it has
the power of actively digesting the adjacent tissues as the embryonic
cells do not, and again it does not possess the power of differentiation
into widely different tissues as does the early embryonic cell. It may
be called a reversion, in the direction of the embryonic cell, however,
since it reacquires a number of its functions.
=Migration of white blood cells.= This is another, and in vascular
tissues the main source of the great cell accumulation in the inflamed
tissue. This process was observed by Waller in 1846, but was given its
true importance through the later observations of Cohnheim. The
migration takes place through the walls of the capillaries and veins
only, and the migrating cells are largely of the polynuclear variety of
leucocytes. These remaining adherent to the inner wall of the blood
vessel may be seen to have a small portion of their substance projected
through the wall and appearing as a small buttonlike projection on the
outer side. This gradually increases, while the remaining portion of the
cell on the inner side of the wall correspondingly decreases until the
whole cell is lodged in the tissue outside the vascular wall. The time
occupied in passing through is very varied. It may be wholly
accomplished in half a minute, and again hours may be required for the
complete passage of a single leucocyte. The explanation of this
migration has been sought in the supposed existence of stigmata
(openings) in the vascular walls (Arnold), in the effect of the blood
pressure within the inflamed vessels, in softening of the vascular walls
and, in the contractility of the leucocyte which is strongly attracted
by the pressure of certain bacteria and other irritants (chemiotaxis).
The migrated leucocyte assumes in the tissues the same habit as the
altered tissue nucleus. It multiplies rapidly, assists in the solution
and removal of the inflamed tissue, contests the ground with infective
microbes (phagocytosis), and subserves the purpose of assisting in
building up new tissue, or of degenerations.
=Red Cells.= The red blood globules follow the active current in the
centre of the blood vessel, yet a few of these also become adherent to
the softened walls and pass through them (diapedesis). When stasis of
blood takes place in the vessels, they become packed more closely with
red globules which then pass outward into the tissues in much larger
numbers.
=Changes in innervation.= As shown under hyperæmia the vaso-motor system
of nerves exerts a potent influence on the circulation and is largely
instrumental in bringing about circulatory disorders. The increase in
the number and force of the contractions of the heart, and the rigid
contraction of the walls of the arteries proceeding to an inflamed part,
are distinctly the result of a reflex nervous action. The implication of
the second eye when one has been violently inflamed from a mechanical
injury is another example of this kind. The loss of power of the
vaso-motor nerves is however even more characteristic. Experimentally
the cutting of the cervical sympathetic or crushing of the superior
cervical ganglion causes congestion and finally inflammation of the
structures on that side of the head; the crushing of the semilunar
ganglion similarly affects the abdominal viscera; and the cutting of the
pelvic plexus, the structures of the hind leg. The contraction and
dilatation of the inflamed capillaries is largely a nervous phenomenon.
A certain number of irritants, like warm water, mustard, or ammonia
cause contraction followed by dilatation of the capillaries, while
others like dilute mineral acids, alkalies, chloroform, or sodium
chloride and sugar in concentrated solution produce dilatation at once.
Some poisons act variously on different parts, eucalyptol causing
dilatation of the arteries and contraction of the veins, while corrosive
sublimate causes contraction of the arteries and dilatation of the
veins.
So with certain microbian toxins. Introduced into the general
circulation they produce active congestion or inflammation in the seat
of colonization of the microbe from which they were derived, as
witnessed in the use of tuberculin or mallein. Finally the chill and
febrile reaction which attends on extensive inflammation is essentially
a nervous phenomena in its inception and progress.
=Changes in the circulation.= The usual changes in the bloodvessels of
the inflamed part may be thus succinctly stated: 1. Contraction of the
capillary vessels of the affected part and hastening of the current of
blood through them. 2. The succeeding dilatation of the capillaries and
the slowing of the blood stream, which still flows uniformly throughout
the diseased tissue. 3. The flow of blood becomes irregular, at points
tardy, and at others oscillating or even recoiling between the pulse
beats when it has been forced into a vessel already blocked by coagulum.
4. In the still pervious vessels the red blood globules occupy the
centre of the vessel where the current is rapid, while the white
globules roll slowly along the inner surface of the walls where the
current is slow and become adherent to the walls and stationary, while
the general current rolls on. This is a direct abstraction of the white
globules from the circulating blood and greatly favors the coagulation
of the blood in the capillaries. The blood plates equally collect in the
periphery of the vessel and escape. 5. The adherent white globules
migrate in large numbers through the capillary and venous walls into the
tissues. The red globules migrate to a less extent at first. 6. Small
coagula form in the affected capillaries, forming minute red points
which cannot be pressed out by the finger. 7. The red globules in the
area of stagnation back of these capillary emboli adhere to each other
by their flat surfaces and form rolls which pack into the vessel and are
enveloped in a fibrinous clot. 8. The liquid part of the blood rapidly
exudes into the tissues leaving the red globules relatively much more
abundant in the liquid which remains inside the vessel. 9. The walls of
the capillaries become softened and allow a readier transudation of
liquor sanguineous, and escape of the globules through the walls of the
vessels. 10. The arteries leading to the inflamed part have their
muscular coats more rigid and unyielding and transmit much more blood
than the corresponding artery leading to the healthy part. 11. The heart
is equally roused to more rapid and often more forcible contractions,
which modify the pulse both in number and rhythm. 12. The circulating
blood is found to have received a great increase in the fibrine formers,
the fibrine in the shed blood amounting to 6, 8, or 10 parts per 1000 in
place of 3 parts as is normal. The contraction of this causes a
depression on the surface of the clot. 13. The red globules become
viscous and adhere together by their flat surfaces to form rolls, which
precipitate much more rapidly than single globules and leave the
coagulated blood with a straw-colored upper stratum (buffy coat). 14.
Increase of waste products, urea, uric acid, hippuric acid, etc.
Other changes in the blood are alleged, like lessening of the albumen,
as balancing the increase of fibrine, and lipæmia, but the constancy of
these in all cases of inflammation is uncertain.
By way of comment and explanation of the above changes in the
circulation the following may be advanced: The primary contraction of
the capillaries is by no means a necessary condition of inflammation,
and contractions and dilatations within certain limits occur in health
and as a purely physiological act. The dilatation of the capillaries and
the increased flow of blood to the part are related to each other as in
part cause and effect, yet both are due to a reflex act from the seat of
irritation which inhibits contraction in the capillaries and determines
a more rigid contraction in the walls of the arteries running to the
part. A rigid inelastic vessel of the same calibre and under the same
pressure transmits more liquid than the one with elastic walls. The
movement of the white globules to the walls of the vessel depends in
part on their levity, light bodies passing into the outer slow moving
layer, which is less dense, from the central stream where the force and
density are greater. The epithelial cells of the intima undergo cloudy
swelling and are often detached, allowing the readier migration of the
globules through the openings of the lymphatics and the softened and
friable walls. When the capillaries are blocked the pressure necessarily
increases on the arterial side, favoring laceration of the friable walls
and the escape of minute masses of blood. The formation of the buffy
coat is characteristic of the normal equine blood; in inflammation it
becomes more abundant. In the other genera a buffy coat apart from
inflammation may be shown in: (a) anæmia or oligocythæmia in which the
blood is deficient in red globules; (b) in plethora in which there is an
excess of blood solids; (c) in pregnancy in which there is an excess of
white and small red globules; (d) in violent exertion or
over-excitement, in which the blood has circulated with extraordinary
rapidity. The all-sufficiency of the tissue cells in determining
inflammation may be deduced from the following experiment. A ligature is
tied around a frog’s thigh so tightly as to arrest circulation, and the
leg amputated above the ligature; mustard is then applied to the web of
the foot and a blister rises precisely as though circulation continued.
MICROBES, DIAPEDESIS AND PHAGOCYTOSIS.
The rôle of =microbes= in inflammation is much greater than was formerly
supposed. It is now demonstrated that a large class of inflammations are
directly caused by the colonization of microbes in the tissue and by the
local irritation caused by their ptomaines and toxins. We must also
admit the direct action of the latter on the heat producing and
vaso-motor nervous centres, as a factor more or less potent in different
cases in the causation and maintenance of inflammation. No less
important is the relation of the microbe to the migration of the
globules and the subsequent results of the inflammation. This influence
microbes share with certain chemical agents. Migration may be greatly
checked even in inflamed parts by the hypodermic or intravenous
injection of sulphate of quinia, eucalyptol, salicylic acid, or
iodoform. Some have thought these acted by a chemiotactic attraction,
but quinia is otherwise found to repel the leucocytes. Their action on
the leucocytes or capillary walls is problematic.
=Chemiotaxis= is that power by which a microbe or any element attracts
or repels the leucocytes. When it attracts the chemiotaxis is said to be
positive, when it repels it is negative. Among negative chemiotactic
agents are quinia, solutions of sodium chloride (10%), and potassium
salts, lactic acid, alcohol (10%), chloroform, glycerine, jequirity, and
bile. To some agents, (creatine, creatinine, allantoin, peptone,
phlorydzine,) leucocytes are indifferent. To gluten, wheat casein, pea
legumin and the great majority of pathogenic microbes, leucocytes are
positively attracted. As microbes exercise a great influence in
producing local inflammation, so they are important factors in procuring
an abundant emigration of leucocytes. Some of the most fatal of
microbian diseases, like fowl cholera, repel leucocytes, and the benefit
of their defensive work is to a large extent lost. The toxins of the
chemiotactic microbe filtered from the bacteria exert the same influence
as the living bacteria, as shown by Gabritchevski, Massart and Bordet.
But chemiotaxis may be exerted from within the bloodvessel as well as
from without. Bouchard, Massart and Bordet have shown that a tube
containing a culture of bacillus pyocyanus, introduced beneath the skin
of a rabbit attracts in a few hours a great number of leucocytes. But
if, immediately after its introduction, ten cubic centimetres of a
sterilized culture of the same bacillus are injected into a vein, very
few leucocytes enter the tube inserted under the skin. The chemiotaxis
seems to operate in this case from within the blood, and the desires of
the leucocytes are satisfied without leaving the vessel. It would seem
that in such cases the migration and protective work of the leucocytes
is best exerted at the outset of the illness and before the toxic
products have been poured into the blood in any quantity, whereas in the
advanced stages when the blood is charged with ptomaines and toxins
migration and phagocytosis would be likely to be limited and
ineffective. The same consideration would forbid the use of drugs that
check migration in all cases of attacks by microbes for which leucocytes
have a positive chemiotaxis.
=Phagocytosis= is the act by which the leucocytes englobe and dissolve
the invading microbe. By its amœboid movement the leucocyte flows
around, and envelopes the microbe for which it has a positive
chemiotaxis, and then begins the struggle of vitality between the two
living germs. If the poison (leucomaine antitoxin,) and digestive
ferment (enzyme) of the leucocytes are more deadly to the invading germ,
than its ptomaines, toxins and enzymes are to the leucocyte, the white
cell comes off the victor, and recovery takes place, but if the converse
obtains the triumph is on the side of the microbe. As a rule much
depends on the more or less deadly nature of the products of the
invading microbe, on the numbers of the germ, the rapidity of its
proliferation, and the consequent amount of its toxic products thrown
into the system, on the one hand: And on the other the potency of the
chemiotaxis of the leucocyte for the invading germ, the number of white
cells that emigrate into the inflamed tissue and engage in the work of
phagocytosis, and on whether the particular animal system and its white
cells have sustained a previous attack by the same germ and has thereby
been educated to produce a greater amount of the defensive proteids
(leucomaine, antitoxin, enzyme) than it naturally would (acquired
immunity).
Even with an abundant emigration of the leucocytes into the inflamed or
invaded tissue, a number, greater or less, are usually destroyed by the
bacterial poisons and pass into degeneration or liquefaction, as in the
formation of pus, and yet the attacking germ may be overcome, destroyed
and devoured by the rapidly increasing survivors. In general terms the
migration of the cells is in inverse ratio to the susceptibility of the
animal to the microbe or the disease which it causes.
The positive and negative chemiotaxis, which determine phagocytosis or
prevent it, may be seen in the action of the leucocytes toward the germs
of two diseases, to one of which the animal is susceptible and to the
other of which it is not. Thus the leucocytes of the pigeon take in the
bacillus anthracis and suffer nothing apparently, whereas the same white
cells of the dove are repelled by the bacteria of fowl cholera which are
not therefore found in their interior.
The leucocytes that migrate from the bloodvessels are in the main, the
most numerous, (the neutrophile or polynuclear) form; the mononuclear
leucocytes with horseshoe shaped nucleus also migrate but in much fewer
numbers and are as a rule less occupied in phagocytosis. At the same
time, these two forms may show each a preference for a particular
microbe, the polynuclear cell sometimes devouring one which the
mononuclear cell rejects, and the mononuclear cell taking in one which
the polynuclear refuses.
The small round white cells (lymphocytes) and the eosinophile leucocytes
take no prominent part in phagocytosis.
EXUDATION.
In inflamed vascular tissues one of the most important results is the
exudation. This is not, however, a mere transudation of the liquid parts
of the blood, as takes place in dropsy, but it is to a large extent a
selective process determined apparently by the condition of the
capillary walls, and the nature of the inflammation is stated according
to the character of the exudate. The dropsical effusion contains little
albumen, fibrine or cell forms, and does not coagulate. The inflammation
exudate contains abundance of fibrine, cells and other solids and
coagulates spontaneously in contact with inflamed tissue, or when
removed from the body, by reason of the transforming leucocytes.
Inflammatory exudate usually contains 6 to 8 per cent. of solids whereas
the normal canine lymph contains 4 to 6. The exudate varies not only in
different inflammations, but in successive stages of the same
inflammation. The exudate may be mucous, serous, fibrinous or
hæmorrhagic.
=Mucous Exudate.= In inflammation on a mucous or synovial surface the
inflammatory exudation, mingled with the more or less altered secretion
of the mucous glands, and the epithelial cells and leucocytes forms a
viscid fluid, rich in mucin, and characterizing the _mucous_ or
_catarrhal inflammation_. The nature of the discharge varies greatly,
the serous character predominating at the start of the inflammation, and
a thick, opaque creamy or semi-solid muco-purulent material appearing as
the disease advances. It contains filaments of precipitated mucin
insoluble in acetic acid or alcohol and cells in all stages of change
from the exudation leucocyte and mucous cell to the pus corpuscle, the
latter being characterized by its bipartite or tripartite nucleus
rendered visible by contact with weak acetic acid.
=Serous Exudate.= This consists of the liquid elements of the blood with
only a limited amount of fibrine formers and consequently little
tendency to clot firmly. The presence of fibrinogen however serves to
distinguish it from the liquid of mechanical dropsy, as does also the
greater quantity of cells and nuclei of common salt and phosphates. It
is usually straw colored in mass, but is sometimes slightly opalescent
by reason of the numbers of cells and floating filaments of fibrine.
Serous exudations take place in the early stages of inflammations (as in
catarrh) and in inflammations of serous membranes (pleura, peritoneum,
joints), in strong, vigorous subjects. They constitute the liquid
contents of blisters whether raised by medicinal irritants, chafing, or
heat. They clot under heat and nitric acid with a firmness proportionate
to the amount of albumen.
These effusions are dangerous by reason of their interference with the
functions of organs by pressure as with the dilatation of the lungs, the
movements of the heart, the action of joints, or the integrity of the
brain or spinal cord. When the causative disease has subsided they are
usually speedily reabsorbed, the cells passing into the lymph vessels,
or becoming degenerated, liquefied, and absorbed. Yet serous effusions
often remain as permanent accumulations. For the blood staining of
serous effusions and their clearing up, see under pleurisy.
=Fibrinous Exudate.= This is characterized by the amount of fibrinogen
and fibro-plastin in its composition and by the comparative absence of
leucocytes. It oozes through the vessels and coagulates in the tissues
or on the surface of inflamed serous or mucous membranes. The more
liquid part separating from the coagulum escapes from the free surface
or accumulates in the lower part of the serous cavity. The coagulation
is doubtless caused by the fibrine ferment derived from the rapidly
proliferating cells and degenerating leucocytes. It usually occurs
promptly in or on an inflamed tissue, but in contact with healthy
structures only (as in a serous sac) it may remain fluid for an
indefinite length of time. This exudate constitutes the false membranes
that form on the pleura, pericardium or arachnoid, the coagulum of
fibrinous pneumonia, and the plastic lymph on the surface of a
granulating wound. It is especially injurious by reason of its
enveloping organs (lungs, heart, bowels, iris) and subjecting to
permanent compression by reason of its contracting, also by binding them
to adjacent structures by false membranes. In coagulating it becomes
first fibrillar then granular and finally undergoes molecular
degeneration (Cornil and Remvier), or development into new tissue
(Paget). When organized it usually takes the form of the adjacent tissue
from which its trophic cells are derived. Thus in divided tendons, in
serous membranes and in granulating wounds it is fibrous, and between
the ends of a broken bone it is osseous. If however, the adjoining
tissue is a highly organized one, like nerve or muscle it may be
replaced by a simpler (fibrous, osseous).
Fibrinous inflammations are especially found in connection with inflamed
fibrous tissues and in strong vigorous subjects.
=Blood Exudations.= In all inflammations there is some migration of
blood globules (red as well as white) but seldom in quantity sufficient
to stain the tissues materially. Minute ruptures of the capillary
vessels are not uncommon, with punctiform clots in the tissues, but
extensive escape of blood is mainly seen in penetrating or contused
wounds of the loose, subcutaneous connective tissue, and in infective
inflammations (anthrax, Rinderpest, swine plague, petechial fever,
malignant catarrh, snakebites) with destruction of blood globules or
extreme changes in the walls of the capillaries. Newly formed vessels in
friable neoplasm are subject to blood effusions. In acute inflammations
of serous membranes the exudate is usually of a dark port wine hue at
first. In such cases it may pass in succession through all the stages of
dark red, brick red, yellow, reddish, and chocolate color, before
becoming milky and finally transparent.
=Croupous Exudate.= Croupous inflammation usually occurs on or near a
mucous surface and is characterized by an exudation consisting mainly of
fibrinous material entangling white cells, epithelium, a few pus
corpuscles and some form of bacteria. In true diphtheria of children
this is the Löffler bacillus, in the pseudodiphtheria, attending on
scarlatina, etc., it is streptococcus pyogenus, in the diphtheria of
calves it is bacillus diphtheriæ vitulorum, and in that of chickens and
pigeons it is the bacillus diphtheriæ columbarum (Löffler).
Pseudo-membranous inflammations therefore constitute a group agreeing in
the nature of the exudate but differing essentially in the cause. This
difference in the cause has a most material effect on the course and
gravity of the disease. One form like true diphtheria in man not only
extends into the tissues, and tends to necrotic changes, but also
poisons the nerve centres by the toxic materials absorbed inducing
troublesome paralysis, while another like croup of children establishes
a violent but essentially superficial disease and when that recovers it
leaves no ulterior ill effects elsewhere.
A =Chyliform exudate= has been noted in peritonitis in the dog the milky
whiteness being due to fatty granules.
RESULTS AND PRODUCTS OF INFLAMMATION.
As nearly all inflammations have significant exudations it is well to
follow these in their subsequent progress through reabsorption and
removal, development into new tissues, necrosis, suppuration and
ulceration.
=Resolution.= If an inflammation, slight in character and with only a
moderate exudation, subsides and is followed by a rapid liquefaction of
the cells and fibrinous coagula and a reabsorption of the exudate, so as
to leave the part in its primary healthy condition structurally and
functionally, it is said to have terminated by “_resolution_.” If this
occurs with extraordinary rapidity it is said to have ended by
“_delitescence_.” This is not always an unalloyed good, as often in
delitescence, coagula and infecting material may be carried on by the
circulation, to block the next set of capillaries in its course and set
up new centres of inflammation. This is one form of “_metastasis_”
though a more definite _metastasis_ is in rheumatism where the disease
attacks one joint today and a distant one to-morrow.
=Inflammatory New Formations.= Of the growths in lymph there are two
principal kinds: first, _the plastic_, _fibrinous_, _granular_ or
_molecular_; and second, _the aplastic_ or _corpuscular_. The first form
tends to develop into new structure, the second to disintegrate and
decay. The tendency to one or other form depends largely on the strength
or weakness of the system’s health, on the deficiency or excess of
corpuscles in the exuded fluid, and on the distance of the latter from
living tissues and blood supply. Much also depends on the predisposition
of the genus, the tendency to suppuration in lymph being in a descending
series from horse, ass, and mule, through ox and sheep, to dog, pig, and
finally, the bird, in which latter suppuration is quite exceptional.
=Suppuration.= In inflammations of a high type, in those occurring on
the skin or mucous membranes in which there is an extraordinary increase
of nuclei and embryonal cells, and in lymph thrown out in excess at one
point, so that its central parts are far from vascular tissue and
nourishment, the cell elements undergo a rapid increase and degradation
into pus-corpuscles, and its solidified intercellular lymph undergoes
granular decay and liquefaction into pus.
While the above conditions are favorable to the formation of pus, the
process of suppuration must now be recognized as an infective process
due to the propogation of bacteria (mainly chain forms—_Streptococcus
pyogenes_—cluster groups—_Staphylococcus py__ogenes_—and rod
forms—_Bacillus pyogenes_). These or other bacteria are found in the pus
of acute abscesses, and when absent in chronic abscesses are to be
considered as having perished since the abscess was recent and active.
Inoculation of a rabbit with an excess of the pus of an acute abscess
produces general purulent infection (pyæmia) and early death; from a
medium dose an abscess is produced; while from a small dose there is no
effect whatever. In the latter case the bacteria are overcome and
devoured by the abundance of vitally potent white blood globules and
tissue cells. This pus-forming action of these bacteria explains the
great difference in results in wounds exposed to the air and those in
the interior of the body and far removed from air and its floating
bacteria. A broken bone, with no wound in the skin and little injury to
parts around the fracture, is readily repaired without any formation of
pus, if merely kept still and immovable; whereas a broken bone,
continuous with a wound through the skin, always tends to form pus or
become otherwise infected, and is extremely dangerous even to life. The
tendency of every open sore is to form pus on its surface but this may
be arrested and avoided by preventing the access of germs, or by a free
use of disinfectants and a covering which shall arrest and filter out
the germs. Similarly in an abscess, evacuation followed by the injection
of disinfectants, without the formation of any perceptible permanent
opening to the outer air, will put a stop to the pus-formation. The
subjection of an inflamed part to the control of these pus-forming
bacteria is dependent on the lowered vitality and power of resistance of
the inflamed tissues, and of the white cells of their circulating blood.
Healthy parts can successfully resist them, though they are constantly
present in surrounding air and on objects, but in this as in all other
cases, of bacterial infection, so soon as the tissue is injured,
inflamed and lowered in its power of vital resistance, the pyogenic
bacteria assail it successfully. Hence, too, the more abundant
exudations of lymph, the centres of which are farthest removed from the
healthy tissues and from nourishment, are the most prone to suppuration.
That the germs can make their way to such deep-seated exudations in the
substance of solid tissues is to be accounted for by their gradual
advance through the inflamed and weakened structures from the adjacent
skin or mucous membrane, or in some instances by reason of their
presence in small numbers in the blood. It is further noteworthy that
those animals in which suppuration does not occur readily are such as
have a special power of resistance to some other organic poisons. Thus
the hog, which is supposed to be proof against snake-bite, is also, to a
large extent, proof against the pus-forming bacteria.
=Pus.= This is a white, or yellowish white, creamy-looking product,
composed of a clear, transparent fluid, rendered opaque by numerous
floating pus-corpuscles. These pus-corpuscles have the same size as the
white globules of the blood (¹⁄₂₅₀₀ to ¹⁄₃₀₀₀ inch) and are peculiar in
that each shows within it three or more nuclei, which become visible on
the addition of a drop of water or acetic acid. Each of the common
embryonal cells found in the inflamed tissue usually contains two
nuclei, the indication of the active increase by division into two, but
when the supply of nutriment is checked the nuclei continue to divide,
while the cells remain unchanged, and thus every cell comes to contain
several nuclei in addition to fatty granules, and constitute
pus-corpuscles.
When pus is formed in a well-maintained system and tissue, the outer
layer of the lymph is developed into a fibrous sac enclosing the liquid
pus and constituting an _abscess_. In an unhealthy system, or when the
inflammation depends on some injurious poison, like that of erysipelas,
this sac may not be formed, and the pus, burrowing into and between
different organs, destroys the connections and substance—_diffuse
suppuration_. When an abscess has formed in soft tissues its investing
sac shrinks as it assumes the fibrous character, and the confined pus
being incapable of compression, presses the membrane outward on the side
in which the surrounding tissues are most loose and least resistant,
hence, usually, though not always, in the direction of the skin; the
soft tissues become absorbed and removed in the track of the advancing
pus; and, finally, the latter reaches a free surface and escapes. Thus,
an abscess usually bursts through the skin, but also, at times, through
a mucous membrane into the lungs, bowels, etc., or through a serous
membrane into chest, abdomen, etc. When an abscess is formed in bone or
dense fibrous tissues which press equally on all sides, it may remain
imprisoned for months and years after all inflammation has subsided,
constituting an _indolent_ or _cold abscess_. When the imprisoned pus is
inclosed by thick fibrous or resistant tissues at all points but one, it
will make its way along the narrow passage of yielding tissue, but as
the resulting outlet is constricted, long, and tortuous, the contents
cannot readily escape through it nor the walls of the abscess contract
so as to expel the confined pus, and the latter goes on forming and
discharging through the narrow outlet for months or years. This is a
_fistula_ or _sinus_.
=Healing by Adhesion or First Intention=. When a clean-cut wound has the
blood staunched and its lips brought together without exposure to the
air (or contact with pyogenic germs), they adhere at once and heal
without pus or almost any appreciable formation of new tissue. Here the
lymph thrown out on the cut surfaces agglutinates them, and the cells,
multiplying, form a thin layer of embryonic tissue which gradually
develops into a fibrous structure and repairs the breach without any
perceptible scar.
=Healing by Second Intention. Granulation.= When a wound has caused
destruction of tissue, or when a simple incision is left exposed to the
air, the breach is filled up by new tissue through the process known as
granulation. The superficial layer of lymph thrown out on the raw
surface becomes oxidized and degenerates into pus, while the deeper
layers become solid, fibrillated, the seat of cell growth, and are
finally transformed into a fibrous structure. New bloodvessels form in
loops in the developing lymph and constitute the bright red
granulation-points which cover the raw surface. The fibrous tissue into
which the lymph is transformed undergoes gradual contraction in
development, and thus, day by day, the edges of the adjacent healthy
skin are drawn in, so as to cover the wound more or less perfectly, and
a slight scar only is left when healing has been accomplished.
=Granule Corpuscles and Masses.= This is another degenerative
transformation in lymph and, is seen mainly in inflamed glands and brain
and lung tissue. The cells found in the exuded lymph are made up of
granules ¹⁄₁₀₀₀₀ inch in diameter, and besides these, large, irregularly
shaped masses of granules are extended along the capillary bloodvessels.
After the lymph has coagulated these granular masses soften and liquefy
preliminary to reabsorption and removal, and the restoration of the
tissue to a healthy condition. When in excess this softens and
disintegrates the tissues, leading to permanent loss of substance. See
_granular_ degeneration.
=Interstitial Development of Lymph into Tissue.= This is equivalent to
what takes place in the formation of the sac of the abscess or of
granulation-tissue. The liquid lymph in coagulating, becomes fibrillar,
and the cells and nuclei of the adjacent tissue, having an abundant
supply of blood and nutriment, multiply first as simple, rounded
embryonic cells, then deposit around them new tissue, becoming
elongated, spindle-shaped, branching, etc., and thus get imbedded in a
fibrous material of their own formation. These new formations are
usually of a low type of organization, like white fibrous tissue or
bone, and hence, although breaches in the higher structures like muscle,
nerve, gland, skill, are filled up, it is usually only by the drawing
together of the remaining healthy parts by these new formations without
the restoration of any of the original tissue which has been destroyed.
The cicatrix (scar), alone is made up of new material.
Lymph developing in this way may undergo any degeneration to which
normal tissues are subject. Thus it may undergo black pigmentary
(_melanotic_) degeneration, it may become impregnated with lime-salts
(_calcified_), it may wither up into a hard _gelatiniform_ or _horny_
mass, or it may undergo _fatty_ degeneration.
=Fatty degeneration= is the most common form, and consists in the
excessive deposit of fatty granules, first in the cells which are in
excess or badly nourished, and next in the adjacent tissue, the normal
elements of which are replaced by fatty granules.
=Softening= is an almost constant result of inflammation. The exudate
infiltrates and separates the tissue elements, destroying their
cohesion; the liquefaction of these elements impairs this still further,
and the more or less perfect transformation of the tissue into embryonic
tissue entails the loss of its rigidity and power of resistance. Thus
the inflamed brain-tissue may become a mere pulp, and the inflamed bone
may be cut with a knife.
=Ulceration= is closely allied to softening. On the surface of a sore
there is an excessive exudation of lymph, which loosens and
disintegrates the layer of lymph that is already in process of
development, and also a part of the tissue beneath. The cells in these
parts fail to develop naturally and to build up good tissue; they become
fatty, die, and together with the tissue in which they lie, break down
and pass off as a pulpy debris. Thus the sore constantly deepens and
widens, or at least refuses to contract and heal. It is usually the
result of bacterial infection.
=Gangrene= or =death of a part= is another effect of inflammation. It
results usually from the cutting off of the blood supply through the
obstruction of the bloodvessels; by the pressure of excessive exudation
in unyielding structures, as in bone, or under the hoof; by implication
of the inner coats of the bloodvessels in the inflammation, when the
contained blood will clot and obstruct them; or by blocking with the
blood clots that have been formed at a distance and washed on in the
blood current to be arrested when they reach vessels too small to admit
them. Like suppuration, gangrene is associated with and often caused by
a bacterial growth. The dead mass remains as an irritant, and is slowly
separated by the formation around it of embryonal tissue, granulations
and pus. A second form is _molecular gangrene_, in which the cells and
minute elements of the tissue die, and are cast off, leading to
phagedenic (eating, extending) sores, as noted above under Ulceration.
When gangrene occurs on an exposed surface, that may be altered from the
normal color into shades of yellow, brown, green, red, or black,
according to the amount of blood and the stage of decomposition, and may
be cut without pain, if the subjacent parts are not pressed upon; it may
be soft, may pit on pressure, may crackle under the hand from the
evolved gases of decomposition, and may be covered with blisters
(_phlyctenæ_) with red, grumous liquid contents (_moist gangrene_);
again, it may be white, as after freezing, or it may be dark colored,
dry, and horny, as from ergotism (_dry gangrene_).
FEVER.
Definition. Symptomatic. Idiopathic. Symptoms. Contagion. Incubation.
Premonitory symptoms. Chill, rigor. Reaction, hot stage.
Defervescence. Crisis. Lysis. Natural temperature. Fever temperature.
Retention of water in the system. Production of waste materials.
Typhoid condition. High fever, low, hectic. Treatment in vigorous
subject, in weak one. Regimen. Solipedes. Ruminants. Carnivora. Drink.
Rest. Clothing. Air. General and local bleeding. Cupping. Warm baths,
tepid, compresses, derivatives. Cold. Diaphoretics. Laxatives.
Diuretics. Sedatives. Alkalies. Antipyretics. Stimulants. Tonic
refrigerants. Tonics. In low fever. No depletion. Judicious
elimination. Stimulants. Refrigerants. Antiseptics. Diet. Local
treatment of inflammation. Cold. Astringents. Antiseptics. Warm
applications. Stimulating embrocations. Blisters. Firing. Massage.
Suppuration.
_Definition. Whether occurring as an accompaniment of inflammation or
independently of it, fever is an unnatural elevation of the
temperature of the body, the direct result of an excess of destructive
chemical change in the blood and tissues, and more remotely of
disordered nervous function._
Of all extensive inflammations fever is the constant result and
accompaniment, rising as the inflammation rises or extends, and
subsiding as the inflammation subsides. It also occurs as a distinct
affection, as in all the infectious diseases, as the result of a
specific irritating poison in the system, and then is the manifestation
of the disease, while a local inflammation may or may not be present as
a special secondary feature of the malady or as an accidental
complication.
_Symptoms of Fever._ Fever is marked by certain definite stages, each of
which has its own special manifestations. In the cases due to a specific
disease germ, or _contagium_, these are, however, preceded by a period
of _latency_ or _incubation_ in which no symptoms whatever are manifest,
but during this time the germ is rapidly multiplying in the system, and
it is only when it has gained a certain increase that it disorders the
nervous system, wastes the tissues, raises the temperature of the body,
and induces the other phenomena of fever. The same may be said to hold
in the fever attending on inflammation. The slight and circumscribed
inflammation is at first productive of no fever, and it is only when it
gains a certain extent that the nerves and nutrition are disordered so
as to bring about a feverish condition.
_Premonitory Symptoms._ These usually last but a few hours and are often
entirely absent or unnoticed. There is a lack of the customary vigor and
spirit, an indisposition to exertion, a loss of clearness and vivacity
of the eye, a manifest dullness, with hanging of the head, and frequent
shifting of the limbs as if fatigued. Appetite is less sharp and
ruminants chew the cud less heartily or persistently.
_Cold Stage._ These are soon succeeded by the _chill_, _rigor_, or
_shivering fit_, in which the hair, especially that along the back,
stands erect (staring coat), the skin is cold and adherent to the
structures beneath (hidebound), the extremities (legs, tail, ears,
horns, nose) are cold, and the frame is agitated with slight tremors, or
even a shivering so violent that a wooden floor or building is made to
rattle. The back is arched, the legs brought nearer together
(crouching), the mouth is cool and clammy, the breathing hurried, the
pulse weak, and it may be rapid, but with a hard beat, the bowels
costive, and the urine higher colored than natural. The temperature of
the interior of the body, taken by a thermometer in the rectum, is
already found above the normal, the excessive destruction of tissue
having begun, and the blood driven from the cooler surface, and
accumulating in the hot interior, at once favors tissue change and
maintains the extra heat thereby produced. In cattle the end of the tail
is soft and flaccid from this stage onward. The _cold stage_ lasts a few
minutes, or one or two days in different cases.
_Hot Stage._ The hot stage appears as a reaction from the chill, the
contraction in the minute vessels of the skin giving place to
dilatation, so that the whole surface, including the extremities,
becomes hot and burning, but still dry and parched. The burning is
especially noticeable in the more vascular parts, like the roots of the
horns and ears, the muzzle or snout, the mouth, the hoofs, the bare
parts of the paws in carnivora, and the mammæ (udder) in suckling
animals. The mucous membranes lining the nose and mouth become hot and
red, the breathing freer, but not less rapid, the pulse softer but
accelerated, appetite (and rumination) greatly impaired or lost, thirst
great, costiveness increased, urine diminished and of a higher color,
the flow of milk greatly impaired or entirely arrested, and the dullness
and prostration greatly increased.
The hot stage lasts longer than the cold one, usually persisting until
death or convalescence. It may alternate with chills throughout the
whole course of the illness, and in the fever of inflammation the
interruption of the _hot stage_ by a chill usually implies either a
considerable extension of the inflammation or the occurrence of
suppuration.
_Defervescence._ The decline of the fever may take place by a sudden
reduction of the body temperature to the natural standard, or near it,
and a sudden and general improvement in the symptoms (crisis), or by a
slow improvement from day to day through a more or less tedious
convalescence (lysis).
_Fever Temperature._ A temporary rise of one or two degrees is
unimportant, but a permanent rise indicates fever. A rise of ten or
twelve degrees is usually fatal. A sudden fall to or below the natural,
unless with general improvement in the symptoms indicates _sinking_. A
similar fall, with a free secretion (perspiration, urination, relaxed
bowels) and general improvement in symptoms, betokens recovery. For
normal and febrile temperature see Semeiology.
_Retention of water in the fevered system_ is as significant as the
elevated temperature. The patient drinks greedily but all the secretions
are arrested or diminished, and liquids go on accumulating in the
system. The sudden bursting forth of secretions (especially sweating)
implies that the fever has, at least temporarily, given way.
_The production of waste matters in the system_ is necessarily
proportionate to the amount of tissue destroyed. This appears in the
blood mainly as urea, the organic acid of urine (hippuric in herbivora,
uric in carnivora), together with phosphates, sulphates, and chlorides.
These thrown off by the urine give it its high density. If not thus
thrown off they remain as poisons in the circulation and bring about
that prostrate, sunken, debilitated condition which characterizes the
advanced stages of all severe and continued fevers—_the typhoid
condition_. This is not to be confounded with the specific _typhoid
fever_, in which a special fever germ expends itself, mainly on the
bowels, and that runs through a regular course. The _typhoid condition_
is that state in which an animal system, already greatly weakened by a
severe disease, and perhaps further prostrated by a specific
disease-poison, is subjected to a species of poisoning by the retained
chemical products of the waste of the tissues.
_Types of Fever._ These are as characteristic as the types of
inflammation, and of the same kind. The _strong_ type of fever which
attends on an acute inflammation in an otherwise healthy vigorous
system, is spoken of as a _high_ or _inflammatory_ fever. The _weak_
type which occurs in a broken down or debilitated system, or in
connection with the action of a specific disease germ, or with the
saturation of the system by waste chemical products is known as _low_,
_typhoid_ (better _typhous_), or _adynamic_ fever. That form which
persists in the utterly debilitated system, where the power of
assimilation is practically lost, is known as _hectic_.
TREATMENT OF INFLAMMATION AND FEVER.
Treatment will be guided very largely by the type of the attendant
fever. If that is of a high type, with a hard, full, rapid pulse, bright
red mucous membranes, a clear eye, and well sustained strength in a
strong, vigorous animal, what is known as antiphlogistic (depleting,
depressing) treatment is admissible at the outset. But in many cases
with a low type of fever, a weak, rapid pulse, pallid, yellow, or livid
mucous membranes, a coated tongue, a dull or sunken eye, much depression
and prostration, swaying on the limbs in walking, pendant head, ears,
eyelids and lips, and varying and irregular temperature of the limbs,
etc., such measures are forbidden from the first, and tonics and
stimulants are demanded from the outset. Between the two extremes there
are many grades, which demand a judiciously adjusted intermediate
treatment. The general principles only of each characteristic form of
treatment can be here formulated, it being understood that no two cases
can be most advantageously treated in precisely the same way, but that
according to its special grade each case will demand its own specific
management applied according to the skill of the physician.
_Regimen._ An antiphlogistic diet will consist in a moderate or very
sparing amount of non-stimulating food of easy digestion (wheat bran or
oil meal in warm, sloppy mash, carrots, turnips, beets, potatoes,
apples, pumpkins; fresh, tender, green grass or in winter a little
scalded hay, may be taken as examples). _Ruminants_ should have no food
necessitating chewing of the cud; thus the roots, etc., should be pulped
or boiled, and hay and even grass must be interdicted until rumination
is re-established. When food is absolutely refused for days in
succession well-boiled gruels of oatmeal, barley-meal, linseed meal,
bran, etc., may be given from a bottle or by injection. _Dogs_ and
_cats_ should have only vegetable mush (unbolted flour, barley, or
oatmeal) with just enough beef-juice to tempt the animal to eat a
little. Milk with an admixture of oxide of magnesia, or even lime water
is often at once palatable and cooling. _Drink_ should be pure water,
cool, if kept constantly fresh before the animal, but warmed to
something less than tepid if supplied only at long intervals, so that
the thirsty patient is not tempted to drink to excess and chill himself.
_Rest_ in a clean, well-aired building, free from draughts of cold air
and with a southern exposure, is desirable, especially in winter. The
best temperature is usually sixty degrees to seventy degrees, especially
in inflammations in the chest, and extremes of temperature are to be
avoided. _Clothing_ will depend on the weather. In warm weather it may
be often discarded, while in winter it should always be sufficient to
obviate the access of _chill_ and consequent aggravation of the disease.
Whenever the atmosphere can be kept warm only at the expense of impurity
it is better to secure the comfort of the patient by the requisite
clothing than to subject him to impure air. As the extremities are the
first to suffer from cold, loose flannel bandages to the limbs are often
imperative.
_Remedies._ _General bleeding_, a great resort of our fore-fathers, has
been long all but discarded from modern practice. Today it is rarely
resorted to, except to save from an urgent and extreme danger, as in the
plethoric cow merging into parturient apoplexy, or the fat and
overdriven horse, gasping for breath and life, in general acute
congestion of the lungs. There are other cases of extensive acute and
dangerous congestions, especially in a strong, vigorous, and plethoric
patient, in which general bleeding in beneficial in warding off
threatened death; but sound, discriminating judgment is necessary to its
safe employment. When resorted to at all, the blood should be drawn from
a large orifice, in a full stream, to secure the desired depressant
effect with the smallest loss of blood, and the patient should be kept
especially quiet and apart from all excitement which would tend to
counteract the sedative action.
_Local bleeding_ is more extensively applicable than _general_, as it
usually effects the same purpose without the permanently weakening
effect. It acts in two ways, first, by emptying and contracting the
vessels in the skin over the inflamed organ, it solicits a sympathetic
contraction of the capillary vessels in that organ itself, and thus
inaugurates a progress toward recovery; and second, by so much as it
draws blood to the surface it diminishes the blood pressure on the
deeper inflamed organ, and affords a better opportunity for the
restoration of the healthy circulation and function. Local bleeding may
be practiced by simple scarification or leeches, or better, by cupping
with or without scarification. To apply leeches, the skin must first be
shaved. To cup, it must at least be greased. As a cup, an ordinary large
drinking-glass may be used, the air contained in it being driven out by
a lighted taper, and then the taper being withdrawn, the mouth of the
cup is instantly and accurately applied on the skin and held there,
until, as it cools, it draws up the skin within it and clings like a
sucker. A number of these may be applied according to the extent of the
inflammation, and, if desired, they may be removed, the part scarified,
and the cup reapplied. The cupping usually effects more than a mere
local attraction of blood; it very commonly causes a free circulation in
the whole skin, a generally diffused warmth, and even perspiration. Thus
we may secure the derivation of blood from the inflamed part, the
cooling of a large mass of blood in the extensive cutaneous circulation,
the cooling of the entire system by the return of this blood internally,
the elimination of injurious waste matters through the skin, the
lowering of the febrile heat and tension, and a better functional
activity of all the organs of the body.
Similar good results are obtained from all remedies that induce surface
warmth and vascularity and a free secretion from the skin.
_Warm baths_, for animals to which they can be applied, abstract blood
temporarily from the inflamed internal organs, diminish the blood
pressure, and really cool the system, beside securing elimination from
the skin and other secreting surfaces. They may be commenced warm (80°
F.) and gradually cooled down to 65° F. after the skin has become freely
active. In the larger quadrupeds, in which the warm bath is too often
practically impossible, the same revulsion of blood and warmth to the
skin may be secured by _rags wrung out of hot_ (_almost scalding_)
_water_, wrapped tightly round the body, covered with two or more dry
blankets, and kept tightly applied against the surface by elastic
circingles. The legs may be rubbed with straw wisps till warm, and then
loosely bandaged, or applications of red pepper, ammonia, or mustard,
may be made prior to bandaging. In place of hot water rugs, bags loosely
filled with bran, chaff, or other light agent, heated to 110° F., may be
applied round the body, or, where it is available, a Turkish or steam
bath may be resorted to. These hot cutaneous applications, to produce
glow and perspiration, are especially valuable in the chill that heralds
a violent inflammation, and if that can be suddenly checked by this
means the inflammation will often be warded off, or at least rendered
slight and easily controllable. After perspiring for half an hour the
patient may be gradually uncovered, rubbed dry, and covered with a dry,
warm blanket. If the skin is still glowing, a slight sponging with cool
or cold water may beneficially precede the rubbing and drying.
_Cold Baths._ In cases of very high fever a full cold bath (68° F.) may
be employed for fifteen minutes, and repeated as often as the
temperature rises. In many cases of parturition fever in cows great
benefit accrues from sponging the body with cold water and allowing it
to evaporate from the burning skin. In the extreme fever of heat
apoplexy (sunstroke), with a temperature of 110° F. and upward, a strong
current of cold water from a hose directed on the head and body often
gives the best results. In ordinary fevers in large animals the _cold
pack_ will often serve a good purpose. Wring a blanket out of water
(cold or tepid, according to the height of the fever and the strength
and power of reaction of the patient), wrap it round the body, cover it
with several dry blankets so that no part is exposed, and keep the whole
in close contact with the skin by elastic circingles. In fifteen minutes
the skin should be glowing and perspiring, and in half an hour the
wrappings should be removed, a little at a time, the parts rubbed dry
and covered with a dry woolen blanket. It may be repeated as often as
the fever rises.
_Diaphoretics._ Besides these remedial methods of inducing a revulsion
and glow in the skin with perspiration, _medicinal diaphoretics_ may be
resorted to. Among these may be included _copious drinks and injections
of warm water_, _acetate of ammonia_, _antimony_, _ipecacuan_, or
_pilocarpin_, or one of the sedatives, _aconite_, _veratrum_, or
_opium_, etc. Many a threatened acute inflammation has been to a great
extent cut short and nipped in the bud—the stage of chill—by warm
clothing, active hand rubbing, and such an apparently unscientific
nauseant as tobacco.
When the preliminary stage has passed and the hot stage of the fever has
set in, cooling and eliminating agents are especially called for.
_Laxatives._ In many cases, and especially in those with marked
constipation or bowels loaded with indigestible materials, a laxative is
beneficial. For the horse, aloes, or, often better, sulphate of soda,
and for cattle or sheep, the latter, or Epsom salts, will at once remove
an irritant, cool the general system, draw off much blood and nervous
energy to the bowels, and secure a considerable depletion and
elimination from the intestines. For swine, dogs, and cats castor oil or
salts may be used, and for fowls castor oil. If the mucous membranes are
yellow, the tongue furred, and feces scanty, hard, and fœtid, a dose of
calomel (horse or ox, one drachm; sheep or pig, one scruple; dog, three
grains; chicken, one-half grain) with tartar emetic (horse or ox, two
drachms; sheep, twenty grains; swine, one-half grain; dog, one-fourth
grain; chicken, one-eighth grain) may be given and followed in ten hours
by one of the laxatives named above.
_Diuretics._ In the absence of any manifest disorder of the digestive
organs, the laxative may be omitted and refrigerant diuretics resorted
to. Acetate of ammonia or potassa, nitre, tartrate of potassa,
carbonates of potassa or soda, may be used along with sedatives.
In cases of infectious disease with poisoning by ptomaines and toxins
the elimination of these by the bowels and kidneys is of the greatest
importance.
_Sedatives._ Of the sedatives, aconite, bromide of potassium, veratrum,
hyoscyamus, or chloral hydrate may be used according to the special
indications.
_Alkalies._ _Resolvents._ When the organ inflamed is a serous membrane
in which dangerous adhesions or other functional disorders are likely to
occur from newly formed false membranes, their formation should be
counteracted as far as possible by the free use of alkalies (carbonates
of soda, potash, or ammonia, nitre, iodide of potassium, muriate of
ammonia, etc.), and in the same conditions excessive effusion should be
controlled by free action on the kidneys.
_Antipyretics._ To reduce the febrile temperature and especially, when
caused by the ptomaines and toxins of bacterial infection, agents like
acetanilid, antipyrin, exalgin, analgene, benzanilide, salicylate of
soda, and quinine have been largely employed and will usually lower the
temperature several degrees in a few hours. They nearly all depress the
vital forces, or hinder reparatory processes, so that their use is to be
carefully guarded. Quinine which is less depressing than the others
hinders migration of the leucocytes and thus stands in the way of
successful phagocytosis. With a dangerously high temperature they may be
temporarily admissible, but they should be suspended as soon as
possible. In all ordinary cases they are probably better avoided. A
judicious use of the cold or tepid bath, or of wet compresses is
incomparably safer and more generally applicable.
_Stimulants._ When the disease results in great prostration or when
symptoms of septic or ptomaine poisoning set in stimulants are often
required to sustain the flagging heart and circulation. These may be
alcoholic, ammoniacal, etherial, camphor, digitalis, etc.
_Tonic Refrigerants._ Later, when both inflammation and fever have been
somewhat reduced, temperature, breathing, and pulse rendered more
moderate, eye clearer, and even appetite perhaps slightly improved, the
sedatives may give place to refrigerating tonics, such as mineral acids
(nitric, muriatic, sulphuric, or phosphoric), in combination with
bitters (quassia, cascarilla, calumba, gentian, salicin), without as yet
the suspension of refrigerant diuretics. Thus for the horse the
following Recipe: Pharmaceutical nitric acid, two drams; infusion of
gentian, ten ounces; nitrate of potassa, two ounces. Dissolve. Give one
ounce every six hours.
_In Convalescence._ When convalescence has fairly set in, the fever has
subsided, and there remains merely some debility with a remnant of the
inflammatory exudation to be removed or organized into tissue, or when
an abscess has developed and burst, the tonics must be even more freely
given, the mineral acids may even give place to preparations of iron or
cod-liver oil, and the diet must be made increasingly liberal. But
throughout the whole progress of the disease the bowels should be
carefully watched. Costiveness may quickly undo all that has been
gained, hence any indication of this should be met by laxative food
(boiled flaxseed, etc.), or, this failing, by injections or laxatives.
Similarly, if a freer action of the kidneys seems to be necessary for
elimination of waste matters or to reduce fever, diuretics should be
continuously kept up.
TREATMENT OF ADYNAMIC INFLAMMATION AND FEVER. In treating _low asthenic_
or _adynamic inflammation_ all depression and depletion is to be
carefully avoided. Even _laxatives_ must be employed with extreme
caution. If absolutely necessary it is best to give them in small (half)
doses and supplement their action by liberal injections of hot water.
Elimination of waste matter from the blood and system is still to be
sought, but it must be by _stimulating diuretics_ (sweet spirits of
nitre, carbonate, acetate, or muriate of ammonia, digitalis), and direct
_stimulants_ and _tonics_ must be given from the first (ammonia, wine,
strong ale, whisky, brandy, ether, gentian, calumba, nux vomica). For
the horse the following may serve as an example: Recipe: Sweet spirits
of nitre, four ounces; sulphuric ether, two ounces; tincture of gentian,
ten ounces; digitalis, one dram. Mix. Dose, two ounces in a pint of cool
water four times a day. When there is great debility and prostration
ammoniacal and alcoholic stimulants must be given freely, while if the
fever heat rises very unduly the cooling diuretics (citrate, tartrate,
or acetate of potassa, or nitre, etc.), and even sedatives (bromide of
potassium, hydrobromic acid, chloral hydrate, salicin, salicylate of
soda), must be resorted to. If there is any indication of a special
depressing poison in the system, or of the absorption of septic or other
noxious matter from a wound, antiseptics (hydrochloric acid, or
salicylic acid, sulphite of soda, quinia, or chlorate of potassa) may be
advantageously added to the prescription.
In these cases of asthenic inflammation, as in the advanced and
debilitated stages of sthenic inflammation, the diet should be as good
as the patient can digest. Boiled oats, barley, or flaxseed, rich,
well-boiled gruels, and beef-tea (even for herbivora,) may frequently be
resorted to with advantage.
_Local Treatment of Inflammation._ In all forms of superficial
inflammation the local treatment occupies an important place. The
persistent application of _cold_ (cold water in a stream, icebags,
freezing mixtures) will sometimes overcome the tendency to inflammation
or arrest it. This is especially sought when a violent inflammation (as
in a wounded joint) threatens to destroy an important organ. If adopted,
it must be persisted in, as if it is suspended too soon the reaction is
likely to make matters worse than ever. _Cold astringent applications_
have a similar tendency. Sugar-of-lead, one-half ounce; laudanum, one
ounce; water, one quart, may be kept applied by means of a linen
bandage. The water may often be advantageously replaced by extract of
witch-hazel. If the inflamed part is superficial the lotion may be made
_antiseptic_ (carbolic acid, one dram; or sulphurous acid solution, five
ounces; water, one quart). _Hot applications_, _fomentations_,
_poultices_ are nearly always appropriate but they should be made
antiseptic to prevent bacterial development. When adopted they should
like _cold_ ones be kept up as continuously as possible. These soothe
alike the superficial and deeper parts, the latter through sympathy,
producing first a relaxation of vessels and tissues, and later a
contraction of the former attended by pallor of the surface. They
greatly favor suppuration when that is already inevitable, though in
other cases they may obviate it by checking at an early stage the acute
inflammatory process on which it depends. Any bland agent that will
retain heat and moisture will make an excellent poultice, though
flaxseed-meal is the type of a soothing demulcent application. Very
slight inflammation may be successfully treated at the outset with a
_stimulating embrocation_ (alcohol or camphorated spirit), yet in the
more violent type of acute inflammation all local excitants tend to
aggravate the disease. In these violent forms the activity of the
disease should be first abated by local soothing and general sedative
measures, and then the part over the inflamed organ may be safely
treated with a stimulating liniment or even a blister. In such cases the
liniment first acts as a derivative of blood and nervous energy from the
inflamed part, and later and still more beneficially by securing in it a
sympathetic healing process, like that set up in the skin. It is further
probable that the absorbed albuminoids, which have been modified in the
congested part often exercise a decided effect on the inflamed tissue.
In raw sores where inflammation has been set up the granulations may
become dropsical or excessive, bulging beyond the adjacent skin as
_proud flesh_. This should be repressed by touching it gently with some
mild caustic (lunar caustic), so as to produce a thin, white film, and
the remote cause of the inflammation (often a local irritant) should be
sought and removed. In some unhealthy sores tending to excessive
granulation, the compound tincture of myrrh and aloes may be applied
daily with great benefit. When the granulations become excessive they
may be scraped down to the level of the skin and then treated with an
antiseptic (iodoform, boric acid, acetanilid, aristol).
_Blistering._ In subacute and chronic inflammations and in those acute
forms in which the violence of the inflammatory action has been already
subdued by soothing measures, blisters and other counterirritants may be
employed to counteract the remaining inflammatory action. These act
primarily by drawing off blood and nervous energy from the inflamed
organ to the skin, and secondarily, by establishing a sympathetic
healing process in the diseased part, simultaneously with the work of
recovery in the skin, when the blister has spent its action. But if
applied above a part which is still violently inflamed, there is apt to
be serious aggravation, through this same sympathy with the part
suffering under the rising of the blister. In this way great and
irreparable injury is often done through the laudations of particular
blisters for the cure of given diseases, without any reference to the
stage or grade of such disease. The value of a blister depends far more
on the time of its application than on the ingredients of which it may
be composed.
_Firing._ This acts in nearly the same manner as a blister, and demands
similar caution in its application. It is especially available in
subacute and chronic diseases of the joints, bones, and tendons, and may
be made more or less severe according to the nature and obstinacy of the
disease. It is applied in points or in lines at intervals of one-half to
one inch, and penetrating one-third, one-half, or entirely through the
skin. The hotter the iron the less the pain, but the greater the danger
of destruction of the intervening skin by the excess of radiating heat.
Hence the contact of the heated iron with any one part must be
judiciously graduated to the heat of the iron and the delicacy of the
skin, and should not exceed the fraction of a second.
_Massage, Rubbing._ In chronic inflammation and even in some acute
forms, with considerable exudation, rubbing or massage is of great
value. It hastens the progress of the blood through the veins, tends to
restore the normal circulation in the stagnant or partially obstructed
capillaries, moves on the exuded liquids in the lymphatic plexus,
rendering the absorption more active, and at once prevents the process
of disintegration of the tissues and obviates, the necessity for their
solution and removal. This may be largely accomplished by the use of the
brush or rubber, or by careful manipulation especially in the direction
of the veins. If the inflammation is near the surface the use of
antiseptic and deobstruent agents will heighten the good effect.
Iodoform, iodide of potassium, boric acid may serve as examples.
_Suppuration._ _Abscess._ The great variety of the causes and forms of
suppuration would forbid any extended notice of its treatment in this
place. It seems preferable to refer the reader to the subject of pyæmid
and the various surgical and medical diseases in which suppuration takes
place.
DISEASES OF THE RESPIRATORY ORGANS.
Importance of diseases of the respiratory organs—in horses and dogs.
Proclivity through over-exertion, through extent and delicacy of the
mucosa, through changes of temperature, through weather, through air
pollution, through kind of diet, through change of latitude, through
nervous sympathy, through debilitation of the lung tissue, through
suppression of perspiration, through a high dew point, through
bacteria and other germs, through youth and change of habits.
These are among the most frequent and grave of all affections of the
domestic animals. They are especially important however in the case of
animals that depend on the soundness of their wind. In horses and dogs
accordingly any permanent injury to the organs of respiration will
seriously impair the value, not only because of the diminished
usefulness of the affected animal, but also because of the probable
deterioration of their progeny. The rapid paces demanded of these
animals and the strain to which the respiratory organs are subject are
potent causes of respiratory disorder. In all animals, however, the
extent of the respiratory surface and its extreme delicacy and tenuity
especially predispose it to disease. Hales estimates that the mucous
membrane covering all the air sacs and air cells is, in the calf, no
less than 250 square feet. As the chest of the horse is at least double
that of the calf, and as it contains much less connective tissue, and is
made up of minute air cells from ¹⁄₇₀–¹⁄₂₀₀ inch in diameter and
separated from each other by walls so attenuated that the contained
capillary bloodvessels are equally exposed to the air on both sides, in
two adjacent air cells, the estimate for the average horse must be
considerably above 500 square feet. This membrane, incomparably the most
delicate and susceptible in the animal economy, is constantly in contact
with the air in all its variable conditions, and is necessarily affected
by these variations.
The severe changes of temperature are not without their influence on
this sensitive membrane. If these changes are sudden, as for example in
our northern states where the temperature will vary from 50° to 70°
Fah., in a single day, the danger of injury becomes imminent, and the
lungs require to be strong indeed to resist their effects. Sudden
transition from the hot close atmosphere of the barn or stable to the
chilling winds of winter is equally hurtful. But it is not alone the
transition from warmth to cold that is injurious. The general relaxation
attendant on the sudden change from a cold bracing atmosphere to one
unduly hot is even more injurious. How frequently do human beings suffer
from colds as the result of a close sultry period at once supervening on
a clear cold one? How extensively do chest diseases prevail among horses
brought from the clear pure atmosphere of the field, and shut up in
close, hot stables? Here, no doubt, there is superadded the impurity of
the too often infected air, the change of diet, of exercise and of
general care yet we find that affections of the air passages are to a
great extent in ratio with the heat of the building. Hence their
constant presence in dealer’s stables where it is thought desirable to
keep the horses warm to hasten the improvement in the coat.
The suddenness of the transition is usually a principal cause of injury.
Where the climate changes slowly the animal economy becomes habituated
to it and resists successfully the injurious influences. Thus when
spring merges gradually into summer and autumn into winter, diseases of
this kind are far less frequent. But on the other hand a sudden and
extreme variation of temperature, whether in the ordinary course of the
season or from a wide change of latitude, is notoriously attended with
diseases of the air passages. Ayrshire, shorthorn and Jersey cattle,
when first imported into the Northern States of America, contract colds,
consumption and other chest diseases to a far greater extent than the
native races, though their progeny or even they themselves after
acclimatization, exhibit powers of resistance nearly equal to the native
stock. Sheep that have been shorn in midwinter or early spring often
repay the inhumanity of their owners by dying of inflamed lungs.
Southdown and Leicester sheep, sent from England to the north of
Scotland, demand at first the greatest care to protect them against the
increased rigor of the climate. The army veterinary statistics of France
show that horses transported from the southern parts of the country to
the more northern stations, suffer largely from pulmonary affections.
But if the change is effected slowly the requisite powers of resistance
are acquired and the novel conditions of life cease to be injurious.
That this varied power of resistance is not confined to the higher
animals would appear from the experiments of W. Edwards on cold blooded
animals. He subjected them in winter and in summer respectively to a
very low temperature and found that whereas in summer their temperature
declined 3° to 6° Cent., in winter they had a greater resistance and
barely declined ⁴⁄₁₀ths of a degree.
The action of cold on the surface of the body often leads to morbid
states of the air passages as the result of nervous sympathy. A beast is
subjected to a keen cold wind, is attacked with shivering, and
inflammation of the chest supervenes. The result is rendered more
certain if the wind is associated with rain and if the animal has been
previously in a state of perspiration. A heavy coat of hair, a profuse
perspiration, and a cold draught often combines effectively to produce
respiratory disease.
It must be added that the chilling debilitates the nuclei of the animal
tissues, and lessens their power of resistance to noxious influences.
The excess of cold in the freezing of a part, is followed by congestion
and even violent inflammation with perhaps sloughing after it has been
thawed. The persistence of such tissue debility is familiar to us all in
the example of chillblains. A less extreme application of cold affects
the tissues and nuclei less powerfully, but none the less surely. The
increased liability to disease of the chilled system is strikingly
illustrated in the experiment of Pasteur with anthrax. The chicken which
had proved refractory to an ordinary dose of anthrax virus, was dipped
in water at ordinary temperature until the heat of its body was reduced,
and then it fell an easy victim to the anthrax bacillus. In the same way
the person who recklessly exposes himself to wet and chill falls a ready
victim to intermittent or yellow fever from which he would otherwise
have escaped. Debility from another cause, such as bruise or laceration,
favors deep-seated invasion by pus cocci, and a resulting abscess, from
which the patient would have remained free, but for such traumatism.
But the effect of cold is not confined to the sympathy between the skin
and respiratory mucous membrane, nor the revulsion of the blood toward
internal organs, nor to the debilitating of the tissues. The application
of cold constringes the vessels and lessens the freedom of the
circulation and suppresses the normal cutaneous exhalation. A somewhat
similar condition may be induced by prolonged exposure to the rays of a
burning sun, the skin becomes hot, dry and rigid, and incompatible with
the maintenance of the respiratory function. In either case there is a
retention of effete and deleterious matters in the circulation which it
was the function of the skin to have eliminated. The danger of such
retention may be best exemplified by noting the result of the complete
repression of perspiration in the remarkable experiments of Fourcault
and Bouley. The former covered dogs and other small animals with an
impermeable varnish which induced death after some days or in some cases
in a few hours. Bouley shaved three horses and covered the skin with
tar. There resulted dullness, torpor, deep, slow breathing, weak and
diminishing pulse, muscular tremors, manifest cooling of the body and
expired air, and deep violet color of the mucous membranes. They died
respectively on the seventh, ninth and tenth days. A fourth horse
covered with a layer of strong glue and then with tar perished nine
hours after the application. The bodies were like those of animals that
had died of suffocation. The mucous membrane of the stomach and bowels
was gorged with black blood, the lungs violently congested—dark red and
heavy—the air tubes filled with frothy material, and the lining membrane
of the heart had dark spots of blood extravasation. It is no longer then
matter for surprise that temporary suppression of the insensible
perspiration should be followed by diseases of the chest or abdomen,
that extensive burns of the surface of the body should be speedily
followed by inflammations of internal organs or that extensive and
severe cutaneous inflammations should be associated with internal
lesions.
Since the days of Hippocrates it has been universally acknowledged that
moist seasons and localities are less salubrious than dry ones. As
already observed moisture in a cold atmosphere intensifies its effect.
In a hot, close atmosphere it strongly conduces to putrefaction in dead
organic matter, and the air becomes loaded as a consequence with noxious
gases, and in its lower strata with bacteria in a state of active
growth. This condition is most intense in close, unventilated stables,
and manifestly operates in both predisposing to and exciting those
diseases of the chest and other parts, so frequent in such places. Winds
raise and carry such germs, but also sooner rob them of virulence. (See
Zymotic Diseases). Susceptible, young animals, newly housed, usually
suffer the most severely from these injurious conditions. Often in their
case frequent, extreme and sudden changes, and great atmospheric
impurity, are combined with a diet to which they have been hitherto
altogether unaccustomed. In young horses there are superadded the
exertions—too often extreme—connected with training or work. There are
the heats and chills, the soaking perspiration and the frigid winds and
rain, the general exhaustion, but particularly the overwork of the
respiratory organs, each of itself calculated to superinduce disease.
Percivall justly remarks that among young horses, newly stabled and put
to work, the prevailing diseases are “catarrh, sore throat, strangles,
bronchitis, pneumonia and pleurisy.” His tables of the diseases
attacking the horses of his own regiment (1st Life Guards), are so
instructive that I here reproduce them:
A TABLE (COMPILED FROM EXTRACTS FROM A “REGISTER OF SICK HORSES”
LIMITED TO A GIVEN PERIOD) SHOWING THE COMPARATIVE AGES AT WHICH HORSES
APPEAR MOST DISPOSED TO CERTAIN ORGANIC DISEASES.
─────────────────┬────────┬────────┬────────┬────────┬────────┬────────
│ │ │ │ No. 10 │ │
│ │ │ No. │ Years │ │
│ │ │above 5 │ and │ │
│ No. of │ No. in │ Years │Upwards │ No. 20 │
│Patients│ Their │ and │ but │ Years │
│Under 5 │ 5th │ Under │ under │ and │
│ Years. │ Year. │ 10. │ 20. │Upwards.│ Total.
─────────────────┼────────┼────────┼────────┼────────┼────────┼────────
Disease of the │ │ │ │ │ │
lungs │ 170│ 50│ 20│ 50│ 10│ 300
Disease of the │ │ │ │ │ │
bowels │ 10│ 20│ 40│ 70│ 20│ 160
Disease of the │ │ │ │ │ │
brain │ 4│ 2│ 5│ 14│ 2│ 27
Disease of the │ │ │ │ │ │
eyes │ 30│ 10│ 70│ 35│ 5│ 150
─────────────────┴────────┴────────┴────────┴────────┴────────┴────────
It will be seen that nearly one-half of the sicknesses, occurring among
the horses of the regiment, were chest diseases, and that nearly
three-fourths of these were in animals under five years old, or in those
newly purchased from the country.
The subjoined table shows the relative prevalence of disease in
different months of the year, deduced from the Register above referred
to:
───────────────────────┬───────────┬───────────┬───────────┬───────────
│Disease of │Disease of │Disease of │Disease of
│the Lungs. │the Bowels.│the Brain. │ the Eyes.
───────────────────────┼───────────┼───────────┼───────────┼───────────
January │ 20│ 12│ 1│ 10
February │ 25│ 8│ ...│ 9
March │ 23│ 11│ 1│ 7
April │ 19│ 10│ 6│ 10
May │ 13│ 3│ 3│ 9
June │ 14│ 16│ 1│ 13
July │ 13│ 13│ 3│ 19
August │ 11│ 23│ 3│ 17
September │ 11│ 5│ 10│ 19
October │ 24│ 3│ 3│ 9
November │ 19│ 10│ 3│ 9
December │ 16│ 9│ 1│ 4
───────────────────────┼───────────┼───────────┼───────────┼───────────
Totals │ 208│ 123│ 35│ 135
───────────────────────┴───────────┴───────────┴───────────┴───────────
In this table the extraordinary prevalence of lung diseases in spring
and autumn is very noticeable. There only remains to notice the number
of deaths occurring in the same regiment from pulmonary and other
diseases.
Deaths from pulmonary disease 77
Deaths from other diseases (Glanders and Farcy and accidents 57
excepted)
It is thus seen that though individually less dangerous than many
affections of the abdomen, brain, etc., yet by reason of their greater
frequency chest diseases induce the greatest mortality among this class
of stock.
In treating of the diseases of this class of organs they will be
sub-divided according as they affect the _nose_, the _throat_, the
_neck_, and the _chest_.
DISEASES OF THE NOSE.
EPISTAXIS. BLEEDING FROM THE NOSE.
Epistaxis as a primary and secondary affection. Causes—mechanical,
over-exertion, blood pressure, new formations, diseased mucosa,
disease of the nasal venous plexus, disease of heart or lungs, in
blood diseases, in hæmorrhagic constitution, in bacteridian diseases
of the respiratory organs. Symptoms. Often one nostril, blood bright,
red, clotted, sneezing, (not retching, acid, nor cough). _Treatment._
Mechanical, astringent, cold, plugging in solipedes and other animals:
hæmostatics.
As a primary affection this occurs more frequently in the horse than in
any other domestic animal, though as a symptomatic disease it is common
in all farm animals.
_Causes._ The most common causes are mechanical injury of the
Schneiderian membrane, violent congestion of this membrane during
extraordinary excitement or exertions, as in coughing, in a closely
contested race, in a trying hunt, in drawing heavy loads, especially if
uphill and with a tight collar. It may coincide with congestion of the
brain acting to some extent as a vicarious discharge, or with the
formation of new structures as polypus, or cancer, in which, from the
looseness and friability of their texture, the vessels readily give way.
The softened membrane is equally liable to laceration or rupture during
the progress of inflammation and particularly when fibrinous (croupous)
exudations are being detached. In all these cases animals of a strong,
vigorous constitution and with a full or plethoric habit are most liable
to be attacked. Various congestions of the mucosa in diseases of the
heart or lungs are additional causes. Disease or injury of the cervical
branch of the sympathetic nerve, and varicosity of the pituitary venous
plexus must be accepted as occasional causes.
Epistaxis is also met with in states of general weakness and with
deteriorated blood, as in anæmia, in the course of various fevers and in
those hemorrhagic constitutions in which the altered blood appears to
find an easy passage through the debilitated or ruptured coats of the
bloodvessels. Thus it is seen in the so-called _purpura hemorrhagica_ in
the horse, in _small-pox_ in sheep, in anthrax, and in _swine plague_
and hog cholera. _Hering_ records the case of a number of pigs suffering
from a scorbutic affection and which bled profusely from the nose. In
bleeders (hæmophilia) and in leucocythæmia it is liable to appear.
The ulcerations of the mucous membrane occurring in _glanders_ and
_chronic catarrh_ have proved exciting causes of the hemorrhage. Lastly
the intense heats of summer and prolonged exposure to the direct rays of
the sun induce a general relaxation and a determination of blood to the
surface which rouses to activity the latent tendency.
_Symptoms._ The bleeding, usually from one nostril only, falls in a
succession of drops, (rarely in a stream), collects in clots around the
nostril, and bespatters surrounding objects as it is expelled forcibly
in sneezing. It is usually of a bright crimson hue or, in fevers or
poisoned conditions of the blood, of a dark or blackish color. It is
distinguished from pulmonary hemorrhage by the absence of cough and of a
frothy condition, and from bleeding from the stomach by the absence of
the blackened clots and acid odor which indicate the presence of the
gastric juice.
It is usually to be further distinguished from these in all animals,
save solipedes, by the absence of blood in the mouth.
_Treatment._ Nasal hemorrhage often stops spontaneously, but if the
discharge is profuse or long continued, and especially in weak or anæmic
conditions it must be treated energetically. Care should be taken,
however, to ascertain first, whether it is not vicarious of some other
and more dangerous condition like cerebral congestion.
The head should be placed in an elevated position by tying it up to the
rack, and cold water or ice kept applied over the head and neck. Matico
powder may be blown into the affected nostril during inspiration, or a
solution of alum (4 drachms to 1 pint of water) or other astringent may
be thrown in by means of a syringe. A tablespoonful of peroxide of
hydrogen thrown into the nose with an ordinary syringe will give
immediate relief. (Gillette.)
Plugging the affected nostril with a pellet of tow covered with matico,
tannin, tincture of chloride of iron (1:10 or 20) or other astringent
may be employed when other means fail. By means of a cord attached to
the plug it may be withdrawn after all danger is past. In solipedes, if
both nostrils must be plugged, wrap the tow around two elastic
caoutchouc tubes and introduce these, or in the absence of these perform
tracheotomy.
Any tendency to recurrence may be met by the internal administration of
gallic acid (horse and cow ½–1 drachm), acetate of lead (horse and cow
½–1 drachm) or, in anæmic conditions, tincture of the perchloride of
iron (horse and cow ½ oz.) in water.
RHINITIS. CORYZA. NASAL CATARRH. COLD IN THE HEAD.
Coryza in the horse: Causes, wet, cold after perspiration, damp
climate, stable, soil, new buildings, hygroscopic building materials,
youth, age, poverty, nervous sympathy, local irritants, iodine,
specific disease poisons. Symptoms, dry congestion, watery discharge,
muco-purulent discharge, eyes involved, chill, fever, circulatory and
breathing disturbance, defecation, urine, glandular swelling.
Inflammation of the sinuses, the severe effects. Duration in slight
cases, in severe, in sinus complication. Treatment, hygienic, nursing,
dietary, steam, sulphur dioxide, febrifuges, insufflation,
electricity, solvent, antiseptic, stimulant.
Under this head will be considered simple inflammation of the nasal
mucous membrane. This disease might be considered as a mild febrile
affection with the local manifestation in the nose, but it is more
convenient to treat of it here as a malady of the nasal chambers.
CORYZA IN THE HORSE.
The chief _causes_ are exposure to wet and cold and especially when the
subject is exhausted and the skin relaxed and covered with perspiration.
In these circumstances a piercing wind, a cold drizzling rain, or a
draught in the stable is particularly dangerous. Sudden alternations of
temperature and especially a change to a warm stable when the general
effect is aggravated by the impurity of the atmosphere and the irritant
emanations from dung and urine. Damp climates are more injurious than
those that are clear, dry, and bracing, and so are equally damp stables
whether the moisture is due to the nature of the soil, such as a cold
impervious and undrained clay, or of the building which, from its
newness, may retain a dangerous amount of moisture in the plaster, or
because of the hygroscopic properties of the building materials which
draw moisture from the surrounding soil. It mainly attacks young horses
after they have passed out of the hands of the breeder or dealer, and
have been placed in new conditions of life alike as regards feeding,
stabling and work. Old and ill-conditioned animals are more susceptible
than the strong and vigorous, and the changes of the coat in spring and
autumn prove strong predisposing causes. Nervous causes are potent in
causing engorgement of the erectile tissue covering the turbinated
bones, and local irritants, like septic dust, lime, ipecacuanha, pollen
of certain plants, smoke, and irritating fogs may precipitate it. Iodine
in large doses produces temporary catarrh. The weakness of the mucosa
from a previous attack predisposes to a second. Occasionally the disease
sweeps over a country, assuming the form of an _epizootic_ when it may
perhaps be preferably considered as a catarrhal fever, strangles or mild
type of _influenza_, _which see_.
_Symptoms._ In the _milder forms_ of _coryza_ the symptoms may be almost
exclusively local, consisting in redness and dryness of the membrane
lining the nose and sneezing, soon followed by the bilateral discharge
of a thin transparent watery liquid, succeeded by a turbid flow
(epithelial cells in excess) and after two or three days by a thick,
white, flocculent, puriform fluid (suppuration diapedesis). With the
supervention of the purulent discharge, comes an abatement of the local
inflammation and the freer the discharge the greater usually is the
relief obtained and the more rapid the recovery. The eyes are usually
red and watery and sometimes the eyelids are swollen. This implies the
continuity of the inflammation through the lachrymo-nasal duct, and the
obstruction to the flow of tears into the nose.
When _constitutional disturbance_ exists a rough or staring coat appears
as one of the first symptoms, the sneezing is more violent, the nasal
mucous membrane is more reddened and swollen, the eyes more dull, sunken
and watery, the mouth hot and clammy, the temperature of the body
raised, the pulse more frequent and having a sharper beat, the impulse
of the heart may often be felt by applying the hand to the chest just
behind the left elbow, the appetite is fastidious and the secretions of
the bowels and kidneys are diminished, the latter being denser and more
highly colored, from the absorption of irritating or infecting matters
the glands under the throat are swollen and the swelling of the mucous
membrane may be such as to impair breathing and even to threaten
suffocation. In severe cases in which the inflammation extends to the
nasal sinuses there is heat and tenderness over the forehead and the
pain and weight are manifested by the pendent head and the red sunken,
watery eyes and tumefied eyelids. When it extends to the throat, the
cough, the difficulty in swallowing and the local tenderness on handling
are characteristic.
_Course._ With the occurrence of suppuration, improvement commences and
if the inflammation does not extend beyond the nasal chambers, and if it
is not kept up by a repetition or continuance of the cause the disease
will have terminated in recovery in eight or ten days. For ulterior
consequences in bad cases see _chronic catarrh_, _conjunctivitis_,
_abscess of the nasal sinuses_, _laryngitis_, _stomatitis_,
_staphylitis_.
_Treatment._ In slight cases the simplest treatment only is required.
Place the animal in a dry, airy, loose box, clear of draughts, and with
uniform temperature of 55° to 60° Fah., if obtainable. In the cold
season blanket warmly, and hand-rub and loosely flannel bandage the
legs. Feed on sloppy bran mashes only and add half an ounce to an ounce
of powdered nitrate of potash daily. Give fresh water _ad libitum_,
solicit the action of the bowels by giving injections of warm water
three times a day, and encourage the nasal discharge by causing the
patient to inhale steam for half an hour or an hour twice daily. This
may be done by giving scalded bran in a nose-bag or by keeping the head
over a bucket containing hay with boiling water poured over it, the
steam being meanwhile directed by a bag open at both ends one of which
is fixed around the animal’s nose and the other round the mouth of the
bucket. As a local astringent, tonic and antiseptic the fumes of sulphur
(burned behind the animal and no more concentrated than can be breathed
with comfort) will do much to cut short the attack. It is more soothing
if combined with steam. Shut doors and windows, add a few drops of
alcohol to some pinches of sulphur and burn on paper laid on a clean
shovel or piece of sheet iron. When enough has been used extinguish by
covering with a cup or other object. Repeat several times a day. Under
this treatment recovery may be completed in three or four days.
In severe cases attended with fever, besides the above a dose of
laxative medicine may be given (three or four drachms of aloes), with
this precaution, that if the fever is of a low type or the malady
epizootic, half the dose only can be safely allowed (2 dr.) on account
of the danger of superpurgation. The nostrils must be more assiduously
steamed and linseed tea may advantageously replace fresh water as a
beverage. If there is much swelling and tenderness of the glands a
poultice should be applied to the throat and between the jaws, and
sulphur fumes as advised above, or anodyne astringent insufflation
powder may be resorted to. Morphia chlorate two grains, bismuth nitrate,
six drachms and finely powdered gum arabic three drachms may be blown
into the nostril during inspiration, or the astringent anodyne injection
advised below for chronic catarrh may be used. Cocaine spray is often
very helpful, or the same agent may be used in the liquid form on cotton
wool inserted in the nasal chamber. If this is without effect a weak
continuous current of electricity will cause constriction and give
prompt relief. It may be repeated every few hours. In the absence of
this the emanations from a weak solution of ammonia or from carbonate of
ammonia may be used. In cases with excessive and persistent
muco-purulent discharge, with presumptive infection from outside
sources, or in the young, from the diseased maternal passages,
insufflation with calomel, painting with a two grains to the ounce
solution of nitrate of silver, or injection with some other germicide
may be resorted to.
In case the fever is of a low type, liquor of the acetate of ammonia (4
ozs.), salammoniac (¼ oz.), or even carbonate of ammonia (½ oz.), may be
given several times a day, with sweet spirits of nitre (½ oz.) and
tincture of gentian (1 oz.) Alcoholic stimulants are often used.
Inhalations of iodine and iodide of potassium with ether and chloroform
are often successful.
SIMPLE CORYZA IN CATTLE.
Coryza mild in cattle. General treatment. Coryza in sheep from
exposure, intemperate seasons, clipping. Acute and chronic. Wholesale
treatment in flocks. Coryza in pigs. Coryza in dogs, simple,
secondary. Treatment, food, laxative, febrifuge, nauseating,
expectorant, antiseptic, gaseous, electric.
This is usually a very simple malady when confined to the nasal
chambers, and not of infective origin. When, on the other hand, it
attacks the sinuses it becomes a disease of extreme gravity. (See
Catarrh of the Sinuses). Symptoms are as seen in the horse, but the
discharge may be overlooked because of the animal licking it out with
his tongue. Treatment does not essentially differ from that laid down
above, and recovery may be expected in seven or eight days. If a
laxative is wanted give from one to two pounds Epsom salts.
SIMPLE CORYZA IN SHEEP.
_Coryza_ is usually slight and is manifested by sneezing and running
from the nose. It occurs in animals clipped or badly sheltered during
the more inclement seasons. In the worst cases the discharge becomes
persistent and emaciation ensues so that it is necessary to interfere.
Valuable animals may be treated on the same principles as oxen, and in
the case of large flocks by shelter in a warm, dry, cleanly and airy
place and fumigations of steam and the fumes of burning sulphur repeated
daily, together with nourishing diet, such as boiled barley or other
grain, and quarter ounce doses of nitre and common salt.
CORYZA IN THE PIG.
Hogs are not very subject to this disease and are easily treated by
warm, sloppy food, and as a laxative three or four croton beans,
according to size, powdered and given in the aliment.
CORYZA IN DOGS.
Dogs are rarely the subjects of simple coryza, though it is constant in
distemper. It sometimes proves troublesome in puppies and old dogs. A
laxative (½–1 ounce castor oil) may be followed in strong and very
feverish cases by tartar emetic (¼—½ grain) three times a day. Spraying
or sponging the nose with a weak solution of chlorate of potass, common
salt, or potassium permanganate will greatly relieve. Inhalation from
burning sulphur, or from carbonate of ammonia, or both may be used when
sponging or spraying is difficult. In inveterate cases, the weak
electric current sent through the cheeks, or the insufflation of
acetanilid, iodoform or calomel may be tried. As a rule, saltpeter in
five grain doses, given in the water, will prove helpful, and in weak
conditions wine, tincture of gentian or nux vomica may be used.
CHRONIC NASAL, CATARRH. NASAL GLEET. OZŒNA IN THE HORSE.
Chronic catarrh in horse, simple form, loss of tone, inflammation,
nature of discharge, glandular swellings, differentiation from
glanders. Treatment, astringent, tonic, stimulant, hygienic, locally
astringents, antiseptics, injections.
A chronic discharge from the nose is often seen in the horse as a sequel
of _coryza_ or _sore throat_, or as an attendant on other affections of
the upper air passages, and the different conditions productive of this
symptom may here be noticed.
1ST. SIMPLE NASAL CATARRH. NASAL GLEET. OZŒNA.
In long standing _coryza_ the nasal mucous membrane becomes relaxed,
fails to acquire its lost tone and continues to pour out a muco-purulent
product. This is really a persistence of inflammation of a low type,
under the influence of which the membrane secretes pus in place of its
normal mucus. The discharge is white, thick, creamy, has little
tenacity, and flows uninterruptedly. There may be slight enlargement of
the submaxillary glands, and if the case is of long standing and the
patient in low condition sores may appear on the mucous membrane. These
ulcers are distinguished from those of _glanders_ by the absence of the
unhealthy angry aspect and excavated borders of the latter, by the
absence of the small nodular deposits on the mucosa, by the less viscid
nature of the secretion, and by the absence of submaxillary swellings,
or if these exist, by their being less nodular, less indurated and less
firmly attached to surrounding parts. The coincidence of ulcers and
submaxillary swellings is always, however, matter for the gravest
suspicion, and such cases should, as a rule, be subjected to the mallein
test. (See Glanders and Farcy).
_Treatment._ In simple nasal catarrh, due alone to the relaxation of the
mucous membrane, the internal use of tonics and the local application of
astringent solutions to the nose rapidly restore the parts to a healthy
state.
Among _stimulants_, cubebs, cayenne pepper and copaiba have a
stimulating and styptic effect on the mucous membrane and each of these
has been successfully used in such cases. _Cantharides_, in five grain
doses, have proved even more successful, (Vines, Percivall). _Sulphate
of Copper_ in drachm doses in mucilage night and morning has proved very
efficient (Sewell, Percivall). _Arsenious Acid_ has been employed with
still better results. The dose, of five grains may be intimately mixed
with a scruple of bicarbonate of soda and given daily in food.[1]
Footnote 1:
In giving this agent, any redness or watering of the eyes, or colicy
pain should be carefully watched for, and when these premonitory
symptoms of poisoning are noticed the medicine should be at once
suspended to be commenced a few days later in smaller doses.
But the most efficient tonic in these cases is arseniate of strychnia.
Its good effects may be secured by combining with the above mentioned
powders of arsenious acid and bicarbonate of soda, half a drachm of
powdered nux vomica for each dose.[2] These powders will usually be
taken in food, and may be continued for a month, or until the discharge
ceases.
Footnote 2:
Whenever nux vomica or its alkaloids, strychnia or brucia, are given,
increased irritability and nervousness should be carefully watched for
and especially any involuntary twitching of the muscles. On their
appearance the agent must be suspended and commenced a few days later
in half the former doses.
In all cases the general health must be carefully attended to. Keep the
patient in a dry, clean, airy building without draughts of cold air;
give moderate exercise in the open air; and good grooming; and allow
nutritious food of mildly laxative properties,—as occasional bran mashes
and roots in winter and succulent grasses in summer.
_Local Applications._ These are the most important remedial measures and
usually of themselves succeed in reestablishing a healthy condition.
The agents proving most useful are of an astringent nature and in
obstinate cases one may be substituted for another as the last appears
to lose its effect. Sulphate of Zinc or Sulphate of Copper in the
proportion of half a drachm of either to a quart of water, may be used,
or if there is much fœtor, a solution containing a drachm each of
carbolic acid and carbonate of potash in a quart of water is to be
preferred. In either case the addition of an ounce of pure glycerine
renders the lotion at once more soothing and more efficient. The
solution must be rendered tepid before injecting it, to obviate the
irritation attending on the contact of a cold fluid with the delicate
membrane of the nose. Among other agents may be named creolin, creosol,
creosote, acetate of lead, potassium permanganate, and silver nitrate.
Peroxide of hydrogen may be used either as injection or in spray.
The mode of injection is a matter of no small moment. It has been done
in some instances by means of a large syringe but the irritation
attendant on such a process is an insuperable objection to its use. A
better instrument is that introduced by Professor Rey of Lyons. It
consists in a tube bent on itself at an angle of 35° so as to form two
arms of unequal lengths. The longer fifteen inches in length, one and a
half in diameter and widening into a funnel at its free end;—the shorter
about five inches long and tapering towards its free end where its
aperture is only two-thirds of an inch across. The instrument is made of
block tin or extemporaneously of gutta percha. Over the shorter arm is
placed a tightly fitting leather ring four and a half inches in diameter
on which is applied some wet tow to adapt it to the nostril and
effectually close it. The nose having been drawn in so as to place the
head in a vertical position, the short arm of the instrument is
introduced into the affected nostril, and the liquid being gently poured
into the long arm rises slowly in the nose until it is filled and the
liquid flows from the nostril on the opposite side. In introducing the
tube care must be taken that it may not irritate the inner wall of the
nose on the one hand, nor pass into the blind pouch, known as the _false
nostril_, on the other.
The greatest gentleness and tact are requisite in thus injecting the
nostrils, though in troublesome animals it is sometimes necessary to
resort to blindfolding or even to the application of a twitch on the
ear, or finally to strapping the animal (head included) to a smooth firm
vertical surface (operating table).
COLLECTION OF PUS IN THE NASAL SINUSES.
Nasal Sinuses, position, orifice, suppuration, symptoms, treatment,
tonics, astringents, antiseptics, trephining, significance of the
fœtor, mode of recovery.
In severe _coryza_ the nasal sinuses become implicated as shown by the
intensity of the symptoms, the prostration, the hanging head, and the
heat and sometimes tenderness between the eyes and immediately beneath
them on the side of the upper jaw. These sinuses are large spaces filled
with air, situated between the superficial and deep plates of the bones
of the face and opening into the nostrils by a narrow orifice in the
upper part of the nasal chambers. When pus is largely formed in these it
fails to flow out as rapidly as produced, parts with a portion of its
liquid elements, increases in consistency and sometimes even undergoes
decomposition, so that the discharge from the nostril has a putrid odor.
The most distinctive symptoms of this form of _nasal gleet_ are obtained
by percussing the sinuses, and in those cases in particular in which the
accumulation is confined to one side of the head, the contrast between
the two sides is unmistakable. By gently tapping the forehead with the
middle finger from one eye to the other the flat solid sound on the
diseased side is easily distinguished from the clear drum-like resonance
on the healthy one. By tapping on the bone beneath each eye and just
above the ridge on the side of the upper jaw, the difference between the
two sides will be recognized in the same way. In some old standing cases
increased tenderness and slight bulging of the bones over the affected
sinuses are often superadded to the other symptoms. The eye on the
affected side is usually retracted so as to seem smaller.
_Treatment._ In some cases the use of tonics and astringent injections
as recommended for the treatment of _ozœna_ will prove successful, but
more usually it is needful to open and inject the sinuses.
For this the following articles are required: scissors, a knife,
forceps, a trephine or circular saw from half to three-fourths of an
inch in diameter and a whalebone or metallic prob.
The horse is thrown and made fast with the diseased side of the head
uppermost. A point is then selected on a line drawn between the centres
of the two eyeballs and an inch to one side the median line of the
forehead; the hair is closely removed with the scissors, and a
semi-circular flap of skin over an inch in diameter is dissected from
the bone and turned back toward the poll. The trephine is next applied
on the bone and a circular portion, having been cut through, is pulled
out by the forceps, when the imprisoned pus will commonly ooze from the
opening. A second point is chosen just above the lower end of the bony
ridge of the upper jaw already referred to and opposite the third molar
tooth, counting from before; the hair is removed as before, a flap of
the skin raised upward and backward and the bone trephined to open the
second sinuse. The point of election for this orifice is more important
than that of the first. If it is too near the eye the lower part of the
sinus, which is separated from the upper by an imperforate bony plate,
is not opened and may continue to keep up the discharge from the nose.
If on the contrary it is made too low down, the lower sinuse only is
opened and the upper being imperfectly washed out from the wound in the
forehead will keep up the discharge. Either then this plate must be
struck with the trephine or it must be afterward perforated to secure a
favorable result. The prob introduced by the wound in the forehead
should further appear at the lower orifice.
The cavities are to be washed out first with clear tepid water, and
thereafter daily with an astringent solution such as that used for
injecting the nose. If the discharge does not escape freely by the lower
orifice its exit may be facilitated by drawing a tape through the
sinuses, from the upper to the lower, and retaining it there by a knot
on each end.
Marked fœtor of the wound will usually indicate necrosis at the edge of
the wound, and demands the use of bone forceps or chisel to remove the
offending bone.
A cure is affected by the restoration of the membrane to its natural
state, or in other cases by the filling up and obliteration of the
cavity by granulation.
ABSCESS OF THE FALSE NOSTRIL OR TURBINATED BONES.
Structure of turbinated bones: suppuration or abscess, obstructed
breathing, treatment, puncture, plugging, injection, trephining.
The turbinated bones are two fragile bony structures attached to the
outer wall of each nasal chamber. The posterior half of each bone closes
the corresponding nasal sinuse; the anterior half is rolled upon itself
as a sheet of paper might be, and is accordingly open along one side. In
this latter a collection of pus may result from severe inflammatory
action and the resulting discharge may become somewhat chronic. The flow
is greatest after the nose has been raised, from the pus having
previously gravitated into a sac in the lower end of the bone. The pus
may moreover pass backward into the larnyx from the raising of the head
and induce a violent fit of coughing. Sometimes the inflammation has
extended to the bones covering the nose which are bulging and tender.
The thin turbinated bone gives way under the distension, bulges into the
nose, and often stops the passage of air through that side. This symptom
and the appearance of the swelling cause a close approximation in
symptoms to nasal polypus. The facts that it supervened on a severe
_coryza_, that it fluctuates on pressure if within reach of the finger,
and that pus escapes when it is punctured, exclude the idea of polypus.
_Treatment._ Puncture of the abscess inside the nose, plugging and daily
astringent injections will usually rapidly cure. Gamgee, Jessen and
others, recommend trephining of the bone above the nose and washing it
out daily, adding that an extensive removal of the bone will correct any
existing bulging and deformity.
NASAL DISCHARGE FROM CARIOUS TEETH, ETC.
Ulceration into sinus from caries, loss of molar, overgrown molar.
Fœtor, tenderness. Foreign body in the nose.
In cases of a diseased molar tooth in the upper jaw, food getting firmly
impacted in the hollow space, irritates the pulp in the fang and the
adjacent bone until the progress in ulceration reaches the nasal chamber
or sinuse and a nasal discharge is established. If an upper molar tooth
is lost the molar formerly opposed to it in the lower jaw grows out and
sets up the same train of symptoms. In all cases then in which nasal
gleet is associated with much fœtor and with difficulty in eating, a
careful examination of the teeth should be made. (See Diseases of the
Teeth).
FOREIGN BODY IN THE NOSE.
Professor Gamgee records the destruction of an animal for glanders in
which the cause of the discharge was afterwards found to be a physic
ball coughed up into the posterior part of the nose and firmly impacted
there.
COLLECTIONS OF PUS IN THE GUTTURAL POUCHES.
Structure, position and opening of pouches, inflamed by extension.
Symptoms, discharge intermittent with pendent head, swallowing,
pasturing, cough, roaring, dyspnœa, inhalation of food, parotid
swelling, glandular enlargement. Nature of contents. Treatment,
pasturage, blister, tonics, irrigation, puncture, injection.
Though this is commonly a result of severe sore throat or strangles, yet
as it causes a chronic discharge from the nose liable to be confounded
with those properly due to diseases of the nasal chamber, it is noticed
in this place.
The guttural pouches are two mucous sacs peculiar to solid footed
animals. They lie side by side above the throat, and in direct contact
with the lower surface of the superior bones of the head and the first
bone of the neck. They are properly speaking dilatations of the
Eustachian tubes which in all animals establish a communication between
the pharynx and the middle ear. The opening into the pharynx is at the
anterior extremity of the pouch and close to the posterior opening of
the nostril, hence the discharge takes place chiefly or exclusively when
the head is lowered, since gravitation then favors the escape of the
fluid.
Frequently implicated in severe sore-throat the walls of the guttural
pouches pour out pus as readily as other mucous membranes in a state of
inflammation. As the escape of this product is hindered alike by the
narrowness of the orifice and, in the elevated position of the head, by
gravitation, it frequently becomes imprisoned and inspissated and proves
a permanent source of irritation and discharge. In the early stages the
contents are glairy with whitish or yellowish clots; later they are
creamy, caseous or even cretaceous. The mucosa, at first red, congested
and tumefied, becomes in chronic cases, hard, thick, puckered and
adherent to adjacent structures. It sometimes ulcerates and the contents
escape in mass, through the pharynx and nose, or externally behind the
angle of the lower jaw. In the last case water swallowed may escape
through the opening. More commonly the pus remains pent up, and
thickens, and may dry and roll into round or oval pellets from the
movements of deglutition. The discharge may be arrested for weeks or
months when such masses block the outlet.
_Symptoms._ The nasal discharge is intermittent or irregular, being
often partially or wholly suppressed by keeping the head elevated, and
reappearing or becoming profuse when it is lowered. Feeding from the
ground, nibbling roots, or pasturing increases the discharge, as the
dependent position of the outlet, the jerking and shaking of the head
and the movements of deglutition all favor its exit. Swelling of the
parotidean region, a flatness instead of resonance on percussion, and
the flattening and discharge and sometimes gurgling by manipulation are
characteristic. There is cough, roaring during active exertion,
sometimes dyspnœa, and, in bad cases, food may be drawn into the
bronchia with serious and even fatal results. When the orifice is
blocked and the pouch filled with gas the elastic swelling and
resilience are characteristic, and pressure may flatten it with a
gurgling sound. These symptoms serve to differentiate it from
peripharyngeal abscess. The submaxillary lymphatic glands are usually
swollen but less than in glanders and not so hard.
_Treatment._ In mild and recent cases in which the contents of the pouch
have not yet become thick and dry, a cure may be effected; _in winter_
by feeding the animal from the ground and largely with roots; _and in
summer_, by turning out to grass. In either case the matter is allowed
to escape almost as soon as formed and the irritated membrane tends to
resume its healthy functions. This result will be favored by giving a
course of tonics as recommended in _simple ozœna_, and the application
of a mild blister to the throat.
Should this fail an operation must be resorted to. Günther, of Hanover,
uses an instrument in the form of a tube a yard long, half an inch in
diameter, slightly curved for two inches at one end which is blind, and
having an orifice on one side close to this extremity. This tube having
been introduced through the chamber of the nose on the affected side and
its curved end having been carried into the narrow opening of the
Eustachian pouch, tepid water is pumped in and the pouch thoroughly
cleaned out. Astringent solutions are then employed. The introduction of
the tube is, however, a very difficult operation and one quite
impossible to any one who has not the most accurate knowledge of the
parts in question.
A second mode of operating is by external incision. For this purpose are
wanted scissors, knife, artery forceps, iron probe bent in the form of
the letter S, and a tape. The horse having been thrown and fastened and
the head extended, the hair is removed from a surface in front of the
prominent border of the first bone of the neck, and an incision made
between this border and the parotid gland. The incision is made
immediately beneath a tendon which may be felt as a flattened cord
crossing the border of the bone in its upper third, and it should be
carried downward one and a half inches parallel to the margin of the
bone. In this preliminary stage the operator has to carefully avoid
injury to the parotid gland and the posterior auricular artery and vein.
The skin and fascia having been divided the index finger of the left
hand is pushed inward and forward until the prominent angle of the large
cornu of the hyoid bone is felt, together with the muscle (stylo-hyoid)
inserted into this bone above the angle referred to. The next step is
important since crossing on the inner side of this muscle and bone at
their point of union is the (internal carotid) artery which becomes
subsequently enveloped in a fold of the membranous wall of the guttural
pouch. The slightest variation in the position of the artery may here
prove fatal unless the greatest caution is used. With the knife guarded
by the index finger of the right hand the muscle is cut through from
behind forward and the pulsation of the artery felt for beneath.
Avoiding its position the knife, with its cutting edge turned forward
and its point directed toward the horse’s nose, is pushed through the
walls of the sac. The curved prob is now introduced and carried downward
until it is felt beneath the skin just behind the angle of the lower
jaw. This may be safely cut down upon with the knife as important parts
(vessels and nerves) have been turned aside by its pressure. A tape
attached to the prob is now drawn through the pouch and retained by a
knot on each end. Tepid water must be injected through the lower orifice
daily for three weeks, astringent antiseptic injections thrown in
occasionally and the horse fed from the ground. At the end of this
period the tape may be removed, and the wounds allowed to heal. During
the course of treatment it is always advisable to change the tape
several times by cutting the knot off one end of the old one, stitching
the new one to it and drawing it through.
_Puncture of the pouch at its lower part_ is a very simple operation
when the accumulation of pus is abundant and chronic. The distended
pouch gravitates downward largely separating the parotid from the deeper
vessels and nerves, and finally fluctuates toward the lower end of the
gland. In extreme cases it even opens and discharges. When fluctuation
can be felt the sac may be incised with a bistoury or abscess knife and
treated like a common sore. Opening with a pointed or olive-shaped
cautery has the advantage of checking hæmorrhage and securing more
perfect drainage. When there is no fluctuation the incision must be made
just beneath the lower border of the parotid, the parotidoauricularis
being first cut through, then the gland dissected from the deeper parts
when the distended sac can usually be felt and opened. If not felt at
once it can easily be reached by a careful dissection upward through the
loose subparotidean connective tissue, with the finger nail or handle of
the scalpel. A free opening may be made and the wound injected daily
with a weak antiseptic solution.
ABSCESS OF THE FALSE NOSTRIL.
In young horses as the result of injury from the bridle or severe
_coryza_, a circumscribed swelling sometimes appears on the outer flap
of the nostril, at first firm, hot and tender, with a surrounding pasty
infiltration, then forming into a tense elastic ovoid mass, the size of
a pigeon’s or chicken’s egg. It may become chronic and remain for an
indefinite period comparatively insensible to touch and only slightly
interfering with the movements of the nostrils. As soon as the elastic
tension betrays the presence of pus it should be evacuated by a free
incision made from inside the nostrils and the wound plugged with
medicated tow and allowed to heal by granulation.
NEOPLASMS IN THE HORSE’S NOSE.
Nasal fibrous polypus, connection, form, size, bony distortion,
obstructed breathing, abrasion, ulceration, sloughing, submucous
polypus, structure, degeneration. Symptoms, sneezing, snuffling,
discharge, palpation, bony swelling, tenderness. Treatment, forceps,
hook, ecraseur, knife, saw. Actinomycosis. Sarcoma, Carcinoma.
Consistency, structure, fœtor, glandular swelling. Treatment.
Recurrence. Fatty tumors. Bony tumors: cancellated or compact tissue,
localized or extended. Cysts. Strongyli. Angioma. Varicosity. Color,
obstruction to breathing, hæmorrhage, cicatrization.
These are essentially surgical diseases yet as they induce Chronic
Catarrh they may be profitably noticed here.
I. =Fibrous Nasal Polypus.= These are connected to the mucosa by a
pedicle or broad base, and vary in size from a pea to a mass which fills
the entire nasal chamber, projects from the nostrils and presses outward
the septum and facial bones. At times they weigh one or more pounds.
They may cause whistling or rattling in breathing, or may completely
obstruct the passage of air on the affected side. In time they may cause
bulging or even attenuation and perforation of the bony walls,
projecting through the hard palate or on the face. Sometimes the surface
becomes the seat of granulation, ulceration, or sloughing, causing more
or less fœtor. The large polypi make their main growth forward and
backward, moulding themselves to the form of the chamber, and displacing
the turbinated bones. They commence to grow under the mucous membrane
and as they grow and become more loosely attached they carry this as an
outer covering and pedicle. When incised they show a structure of
interlacing bundles of fibres, with cell elements more or less abundant,
according to the rapidity of growth. Gravitz found amyloid degeneration
of the walls of the blood vessels and mucous follicles and of the
fibres.
_Symptoms_ are difficult breathing, snuffling, a smaller current of air
on the affected side, or none, sneezing, a watery, purulent, bloody, or
fœtid discharge, and the appearance of the polypus when the nasal
chamber is examined in a good light. If beyond reach of vision the
polypus may often be felt by the finger. Care must be taken not to
mistake the red, angry surface of the turbinated bones in Catarrh for a
polypus. If beyond the reach of the finger, the flat sound on percussion
of the nasal and frontal bones on the affected side, and the
persistently diminished flow of air may serve for diagnosis. Tenderness
shown on percussion is common to this and abscess of the sinuses.
_Treatment._ The horse having been cast with the diseased side uppermost
and the head turned to the light, the tumor is seized with the fingers,
the forceps, or hook, and drawn gently outward. The chain of the
_ecraseur_ may be passed over it and slowly tightened upon the pedicle
until it is cut through. This will usually obviate any laceration of the
turbinated bones and consequent bleeding. In case of serious hæmorrhage
check by cold water, ice, the actual cautery, or by plugging. Polypi
with a broad base may be removed with a prob-pointed knife, curved on
the flat, and furnished with a long handle. The mass is seized with a
vulsella and detachment made by passing the knife with the concave side
toward the tumor. In cases where the tumor cannot be seen or reached
some have resorted to slitting up the outer wall of the nostril as far
as the angle of union of the nasal and maxillary bones, care being taken
to make the incision outside the upper end of the cartilage of the ala
nasi. If too high to be satisfactorily reached in this way the nasal or
frontal bone may be trephined over the body of the tumor as indicated by
the flatness on percussion, and the operation performed through the
opening thus made.
II. =Actinomycosis.= Though much more common in cattle than horses, yet
the occasional occurrence of this in the face of the solipede must not
pass unnoticed.
III. =Sarcoma= and =Carcinoma.= These are found growing from the
periosteum, or even starting in the cancellated tissue and projecting
into the nose, where they give rise to symptoms like those of fibrous
polypi. Being much softer in texture and more liable to ulceration and
degeneration they are likely to cause a much more offensive discharge.
There is also more tendency to the implication of the submaxillary
lymphatic glands. The only treatment is surgical and recurrence is
always to be feared. (See Diseases of the Orbit.)
IV. =Fatty Tumors= of the nose are described by Röll and Gurlt as
existing on the septum and in the sinuses. Being simple, they can be
removed with great confidence as to nonrecurrence.
V. =Osseous Tumors of the Nasal walls.= These are described by Röll as
osteophytes in the maxillary sinus in chronic catarrh, and by Gamgee as
osteomata attached to the outer wall of the nasal chamber, which had to
be detached by saw and bone forceps. I have found these latter of a soft
porous structure easily detached by the knife, and in other cases dense
and requiring, chisel, saw and forceps. In one instance the tumor grew
from a dense hypertrophy of the maxillary bone which could not be
entirely removed because the molar alveoli were implicated.
VI. =Cysts= named by Röll and others as present in the mucosa of the
ethmoid cells in solipedes often contain larva of the strongylus
armatus.
VII. =Angioma= may be but an exaggerated development of the abundant
venous plexus and erectile tissue on the surface of the turbinated
bones. There appears to be at other times an actual increase of the
vascular tissue. As might be expected it has no abrupt margin, but
gradually shades off into the healthy tissue. The prominent centre has a
bluish red or brownish hue. It obstructs breathing, is apt to bleed
under violent exertions in draught, or in contested races, and readily
ulcerates with a bloody discharge. If it subsides and heals, it is
followed by a whitish puckering like the so-called _cicatrix_ of
glanders.
CATARRH OF THE FRONTAL SINUSES IN CATTLE. CATARRH FROM TRAUMATISM.
Extent of sinuses in cattle. Causes, blows, unequal teams, locking
horns, fracture. Pathology. Congestion, exudation, suppuration,
swelling and closure of outlet, prostration, fever, agalactia, septic
infection, ulceration, exclusion of oxygen. Symptoms. Crimson
hæmorrhage, disturbed breathing, appetite, rumination, position of
head and eyelids, percussion and temperature of forehead, fever.
Chronic form. Slow progress, emaciation, anorexia, facial expression,
hide, discharge, breath heavy or fœtid. Duration. Prognosis. Lesions
in sinuses and glands. Treatment. Cold irrigation, icebags, elevation
of head, laxatives, diuretics, dehorning, trephining, injections,
astringent, antiseptic, blister, tonics.
The gravity of this affection is a consequence of the great extent of
the delicate mucous membrane which lines the frontal sinus. This cavity
not only occupies the whole forehead from beneath the eyes up to the
frontal crest, but extends, in the mature horned animal, into the
tapering bony process which forms the basis of support for the horn. The
mucosa is rendered all the more extensive by the numerous pillars and
septa that pass from the outer bony plate to the inner, giving great
strength to the part for purposes of offense and defence. Inflammation
of this membrane is usually the result of blows on the horns, and these
are much more common among working oxen than dairy cows. The immediate
cause is violent contact with the yoke when the head is lowered at
pasture, and from blows of a club in the hands of the driver. In
countries where the yoke is a broad padded board hung from the horns and
resting on the forehead traumatic injuries are much more common. The
active and vigorous animal gets the greater part of the work, and the
wrench and jar may induce hæmorrhage and catarrh. If the yoke is
ill-made or badly fitted the case is worse. The blows sustained by horn
or forehead in an ordinary fight, may also be the cause, and a partial
or complete fracture of the bony support is especially hurtful when the
detached horn is replaced so as to close in the cavity. Blows on the
frontal crest are also dangerous.
The _pathology_ of the disease consists in an inflammation of the mucosa
of the sinus, and the filling of that cavity with blood or, later, with
a muco-purulent fluid, the escape of which is prevented by the closure
of the nasal outlet by swelling. This of itself produces violent
headache and much nervous disorder as witnessed by the drooping head,
closed eyelids, prostration, high fever, anorexia, and in cows
suppression of the milk secretion. But there is reason to believe that
this is aggravated by the septic germs, which inspired with the air,
were already present in the sinus, and which in the comparative absence
of oxygen, in a rich culture medium and in contact with injured and
debilitated tissues, assume an enhanced pathogenic rôle. This may serve
to explain the ulceration of the mucosa of the sinus found in subjects
that have suffered for some time. It further explains the notorious fact
that the free access of air (oxygen) to the inflamed sinus is one of the
most helpful therapeutic measures.
_Symptoms of the Acute Form._ When the disease is traumatic the first
symptom is usually a hæmorrhage from the nose, the blood being of a
bright crimson. Respiration is hurried, and appetite diminished, yet
rumination may be imperfectly performed. The bleeding may be repeated
for days in succession, but the ox is still capable of work. On the
fifth or sixth day there is complete anorexia, rumination ceases, the
head sinks resting on the manger or soil, the ears droop forward and
downward, and may be swollen. The head inclines to the affected side,
the corresponding horn is intensely hot, and the eyes are closed. Light
percussion of the forehead on the affected side gives pain, and the
sound elicited is flat and dull as compared with that from the opposite
side. The temperature of the body rises 2° or more, the pulse becomes
frequent, full and hard and the impulse of the heart abnormally strong.
Costiveness, partially suppressed and high colored urine, and dry hot
muzzle betray the fever. Unless relieved the chronic form may supervene.
SYMPTOMS OF THE CHRONIC FORM. When this comes on slowly, working oxen
get emaciated, lose appetite, have the eyes dull and sunken, and the
lids drooping, the coat rough and staring and the skin harsh, dry, and
lacking in pliancy, the head is carried low when out of the yoke and,
after shaking the head and sneezing, a glairy, slightly fœtid matter
escapes from the nostril. The breath is fœtid and appears to be
offensive to adjacent cattle.
This may continue for months with no other change than a more constant
nasal discharge, and increasing emaciation and weakness.
_Prognosis._ This is favorable for the acute disease at the outset. But
if no relief is furnished it is liable to go on to a fatal issue. Even
the chronic form is curable unless the subject has already become
hopelessly weak and debilitated.
In _fatal cases_ the sinuses are found to be filled with a glairy fluid
and the mucosa thickened and raw or ulcerated. There may be enlargement
of the pharyngeal lymphatic glands, and there may be attendant
pharyngitis.
_Treatment._ The patient must have absolute rest and cold water
irrigation or icebags applied to the head. The bowels may be opened by a
saline, or a diuretic administered. If the head is persistently dropped
it may be kept moderately elevated by a halter tied to a higher point.
Should there be no relief at the end of twenty-four hours, no time
should be lost in securing free admission of air to the cavity. Cruzel
advises to saw off the horn at its base, as the one certain method of
securing prompt improvement and speedy recovery. If a horn and its bony
support have been broken off they should be at once removed and the head
turned up to evacuate the accumulated glairy fluid from the sinus. From
an apparently hopeless condition a few hours will suffice to restore an
appearance of good health. If the horn has not been broken and it is
desirable to save it, the bone may be trephined in front of the root of
the horn and the liquid evacuated, or less effectively and more
painfully the horn may be bored at its root by a large gimlet.
If no hæmorrhage has taken place and if active treatment has been
adopted at the outset recovery may be complete in two or three days, but
if the disease has been ushered in by a hæmorrhage which recurs several
days in succession, amputation of the horn or trephining will be
demanded. In chronic cases this should be followed by astringent and
antiseptic injections and a blister may be applied to the throat or the
side of the neck. In these cases too a course of mineral tonics is
desirable.
CHRONIC CATARRH OF CATTLE.
Catarrh, chronic, summer aggravation, thickened, roughened, mucosa,
discharge, twigs in nose. Question of parasitism. Treatment, remove
causes, antiseptic astringents.
A remarkable form of chronic catarrh with summer aggravation exists in
some of the hilly districts of New York but has not received such study
as to enable us to state its true nature.
One or two in a large herd will have a loud snuffling breathing, which
may subside so as to be entirely overlooked in winter, but reappears
when put to pasture in the spring and continues in a marked form
throughout the warm weather and until after the animal is returned to
winter quarters. There appears to be little or no fever nor
constitutional disturbance except what comes from the obstructed
breathing, and the yield of milk may be unchanged. The symptoms would
indicate a purely local disease. Yet so few are attacked out of a herd
that it cannot be actively contagious.
On close examination the nasal chambers are found to be narrowed, there
is manifest thickening of the mucosa, and its surface feels rough and
uneven, with miliary elevations. There is of course more or less glairy
discharge. If the examination is made about midsummer, the finger
introduced into the nose will usually detect the ends of twigs that have
been introduced into the cavity and broken off. When withdrawn these may
prove individually from four to eight inches long, and some force may be
required to extract them. In winter these are often absent, having been
apparently dropped one by one. The absence of these sources of
irritation sufficiently accounts for the manifest improvement during the
colder months. In spite however of the winter remissions the disease
tends to a steady advance year by year. While nothing definite is known
of its pathology, the occurrence of this disease in given localities,
its manifestly local nature, and its persistence when once established
would suggest enquiry as to the possible existence of parasitism,
bacteridian or otherwise.
Until further discovery treatment can only be of a general nature.
Removal of the foreign bodies from the nose, pasturage where there is no
brush to replace them, soiling when clean pastures cannot be found, and
the use of astringent and antiseptic agents by insufflation or injection
would be indicated.
MALIGNANT CATARRH OF CATTLE.
Local causes. Debilitation. Polluted air. Poor diet. Symptoms,
gastro-intestinal, fever, lachrymation, turbid aqueous, photophobia,
congestion of mucosæ, generally disturbed circulation, breathing,
depression, heat of forehead, buccal petechiæ, epithelial
desquamation, abrasions, ulcers, abortion, albuminuria, local
swellings, shedding of horns, dropsy, dyspnœa. Lesions, in nasal
mucosa, subcutem, cerebral, dark blood. Prognosis. Treatment,
antiphlogistic, laxative, diuretic, tonic, locally steam, antiseptic,
astringent, trephining.
This disease occurs chiefly in cold damp marshy localities where the
vital power is impaired or in cold situations exposed to severe north
and east winds. In the wet cold seasons of spring and autumn it is
especially prevalent. According to _Rychner_ it rarely attacks old cows
but prevails among young cows and oxen. In the south of France on the
contrary it appears chiefly in the hot season (June and July) and is
attributed to suppressed transpiration. It prevails especially however
in herds kept in small filthy stables, low in the roof, hot, close and
badly aired. (Festal). In New York it appears in cattle on black muck
pastures and in Minnesota on the dried up ponds.
_Symptoms._ Diarrhœa is a common premonitory symptom arising from the
irritation of the intestinal canal as it is soon followed by some degree
of costiveness, the dung becoming dark colored, firm and scanty.
Diarrhœa reappears later. The coat stares or the beast actually shivers;
the head is depressed; the roots of the horns and the forehead are hot;
the eyes are sunken, swollen and red, suffused with tears, turbid in
their anterior chamber (aqueous humor) and intolerant of light; The
muzzle dry and hot; the mouth hot but moist with abundant saliva; the
mucous membranes of the mouth, nose and vagina have a bluish red color;
the pulse is rapid and more or less full or hard; impulse of the heart
weak; the breathing is accelerated, the respiratory sound is heightened
in intensity and a cough is frequent. Temperature 104° to 107° F. The
urine is scanty and high colored. The surface of the body is alternately
hot and cold, and after some time a watery fluid begins to distil from
the nose.
At the end of twenty-four hours the symptoms are intensified or altered.
The eyelids are more swollen and the flow of tears more profuse; the
nasal discharge becomes slimy, and streaked with blood, and
accumulations take place in the frontal sinuses as indicated by the
increasing heat of the forehead and the dullness on percussion. In the
mouth appear dark red spots, from blood extravasation, over which the
epithelium sloughs off leaving raw unhealthy sores. The appetite
entirely fails; dung and urine are passed painfully and with effort, and
abortion frequently takes place in pregnant cows. The urine is
albuminous with cell forms, and casts. The limbs appear rigid and it
pains the animal to move.
From the fourth to the sixth day the ulceration appears on the mucous
membrane of the nose which has often a claret color, and the nasal
discharge becomes again more watery and irritating. The muzzle is
swollen and a dropsical infiltration appears beneath the jaws which
extends along the neck to beneath the thorax and into the limbs.
Portions of the nasal mucous membrane now slough off, and similar
sloughs are often seen on the skin of different parts of the body; the
secreting structures of the horns and hoofs even participating so that
these are easily detached or shed. Saliva flows profusely from the lips,
a fetid watery diarrhœa succeeds the constipation, the dropsy becomes
nearly general and death occurs on the eighth, ninth or tenth day of the
illness. Convulsions and symptoms of suffocation may precede death.
In a _post mortem_ section the principal lesions are found in the nasal
cavities and skin. The areolar tissue in both is the seat of an abundant
serous infiltration, which has taken place into the deeper layers of the
skin as well, rendering it thick, hard and unyielding. Besides the
sloughs and ulcerations on the skin and mucous membranes, false
membranes have been met with, on the lining membrane of the mouth and
air passages. The ulcers in the nose have in many cases reached the
bone, and from the abundant infiltration and softening, the membrane is
easily stripped from the walls of this cavity and of the sinuses. The
general infiltration appears to have reached the brain, which is
described as softened and having an undue amount of liquid in its
cavities. The blood contained in the vessels is dark colored and
numerous patches of extravasation are visible on the mucous and serous
membranes as well as in the interior of organs.
Unless the malady can be controlled in its early stages it usually
proves fatal. Patients that recover after it has been well developed at
times retain its effects in permanent blindness or palsy of the hind
limbs.
_Treatment._ Early and vigorous antiphlogistic measures are strongly
recommended by French and Italian veterinarians. Gellé and Ercolani
advocate the most copious bleedings. Festal insists that all other
measures are useless when this is neglected. Before adopting free
sanguineous depletion the history of his practice was a record of
deaths, whereas later his losses were in cases where from a failure to
recognize the disease at the outset, from the existence of diarrhœa,
from the patient being pregnant or from a fear that the milking
properties might be impaired, bleeding was deferred. He pushed the
bleeding to the extent of causing acceleration of pulse, quickened
breathing and heaving of the flanks, to effect which sixteen pounds had
to be abstracted on an average. If this were done early the engorgement
of the muzzle had usually greatly diminished if not entirely disappeared
in the course of seven or eight hours thereafter. The alleged benefit is
probably largely due to elimination.
Less heroic treatment is now generally adopted. An active purgative (one
and a half pounds Epsom salts) may be given even though apparently
contraindicated by the premonitory diarrhœa, and a further useful
derivation may be obtained by applying active friction or even
stimulating embrocations to the legs.
Steam with or without sulphur dioxide may be inhaled as for ordinary
_coryza_ and cold water or ice kept applied to the forehead.
Nitre in ounce doses daily or liquor of the acetate of ammonia in three
ounce doses may be given after the purging has ceased. Or drachm doses
of hydrochloric acid with bitters may be given thrice a day in at least
a pint of water.
Where the nasal discharge persists after the subsidence of the other
symptoms the sinuse should be trephined in front of the horn, and tepid
water and mild astringent and antiseptic lotions injected until a
healthy action has been established. Change to a dry, well drained
pasture or building is desirable for both treatment and prevention.
CONTAGIOUS DISEASES OF THE NOSE.
These are omitted here to be treated under that heading.
PARASITIC DISEASES OF THE NOSE.
Among these may be named:
LEECH BITES.
Form of wound, leeches in posterior nares, discharge of blood, mucus,
sneezing, snorting, dysphagia, anorexia, unthriftiness, anæmia.
Treatment, removal, sodium chloride, tar fumes, ether on sponge.
Though it more commonly attacks the mouth and lips yet the leech (Hirudo
Decora) will sometimes fasten itself inside the nose when that is
plunged in water. Its bite is to be recognized by its triangular shape.
When taken in by the mouth it may fasten itself in the posterior nares
where it is difficult to recognize its presence. In the anterior nares
it can be readily discovered and removed, but in the posterior nares it
may maintain its hold indefinitely. There appear in the nasal discharge
streaks or clots of blood which may also show at the corners of the
mouth. Sneezing, snorting, and difficulty of deglutition, may draw
attention to the trouble, and in protracted cases signs of anæmia,
inappetence, unthriftiness and general weakness. The most effective
treatment is to remove the leech with the fingers, but as they cannot
always be reached in this way, an injection of a strong solution of
common salt may be used. Blaise succeeded by burning tar under the nose
twice a day, and Louvigny by introducing a staff bearing a sponge soaked
in ether.
COCCIDIAN CATARRH IN RABBITS.
Coccidia in rabbit’s nose, etc., inflammation, fatality. Treatment,
sulphur dioxide.
Zurn describes a contagious catarrh of rabbits caused by the presence in
the mucosa of the nose, pharynx, Eustachian tubes and middle ears of
myriads of coccidia. They create acute irritation and prove fatal in
many cases. Embedded in the mucosa they are difficult to reach with
medicinal agents, yet the free parasites may be destroyed by frequent
fumigations with sulphurous acid, or by spraying or injecting the nose
with its solution.
LARVA OF ŒSTRUS OVIS (GRUB) IN THE NASAL SINUSES OF SHEEP.
Season of attack by fly, hibernation, botfly of sheep, mode of attack,
embryo, defensive acts of sheep, habitat of larva, mature larva, its
exit, chrysalis in soil, its transformation. Symptoms, sneezing,
snuffling, rubbing of nose, lachrymation, unsteadiness, discharge,
respiratory digestive and febrile disturbances, emaciation, septic
action. Lesions, larva, congestions of mucosa, brain. Treatment,
warmth, errhine, parasiticides, mechanical extractors, trephining,
injections. Prevention, newly turned furrow, quicklime, tar. Other
larva in nose.
Sheep are especially subject to the attacks, in summer and autumn and in
warm sunny barns even in winter, of the Œstrus (Cephalemia) Ovis, the
larva of which hibernates in the nasal sinuses or turbinated bones.
The =sheep-bot-fly= is only about four lines in length, of a light
yellowish or slightly brownish gray hue, hairy, with dull black
transverse lines on the upper surface of the thorax, and a lighter color
on the abdomen where the black lines are more broken. The transparent,
colorless wings extend beyond the body: winglets are long and cover the
poisers: abdomen is formed of five rings.
They appear during the whole summer hiding away in walls, stumps and
grass, unless when pairing or pursuing the sheep to deposit their young.
The mode of attack is difficult to follow on account of the small size,
gray color and rapid flight of the fly and fear and shyness of the
sheep. It cannot be doubted, however, that they approach and drop on the
margin of the nostril, the larva previously hatched from the egg. The
old authors describe the deposition of the egg on the margin of the
nostril and its prompt hatching by the animal heat, but the observations
of Brown, Kelly, Cockrill, Riley and Ormerod abundantly prove that the
fly is viviparous. Cockrill obtained no less than 300 live hatched larvæ
from one fly caught while pursuing a sheep.
The sheep seek to avoid the fly by resorting to dry dusty roads where
they lie with the nose close to the ground, or they stand with the nose
close to the soil and between their fore legs. At other times they will
collect in a dense phalanx with their heads directed toward the centre
of the mass and held low so that the fly cannot reach them. The moment
the fly touches the nose they shake the head, stamp with the feet, and
gallop off with the nose close to the ground, looking from side to side
to see if the fly pursues and frequently smelling at the grass as if
apprehensive of other flies hidden there. If such appear they instantly
turn and scamper to other parts of the field or take refuge in a dry
dusty place or gravel bank.
The =young larva= when deposited on the nostril speedily makes its way
up and takes refuge in the cavities of the turbinated bones and the
frontal and maxillary sinuses, where it passes the winter feeding on the
mucus and the purulent discharges determined by its presence. When
mature it leaves the nose and assumes the chrysalis form in the soil.
The =mature larva= is narrow anteriorly, broad behind: its upper surface
is prominent and rounded, lower surface flat, and furnished at the
anterior of each ring after the third, with a series of pointed
tubercles or spines: the cephalic end bears the buccal organs directed
downward, and bearing two great hooks connected with the hard framework
of the pharynx and recurved downward, backward and outward; mouth small;
antennæ thick and short placed above the buccal organs: the inferior
part of the last ring projects beyond the upper portion and is furnished
with two nodules with intervening spines: pentagonal patches of stigmata
on the last ring: very small anterior stigmata between the first and
second rings. The color is white with brown spines, stigmata and
transverse striæ. Length seven lines to one inch.
When dropped from the nostril in the course of summer they pass into
chrysalis in one or two days; and after a residence of six or eight
weeks in the soil emerge as the perfect fly.
=Morbid Symptoms Caused by the Larvæ in the Head.= =Grub in the Head.=
These bear a close relation to the number of larvæ present. If there are
only two or three no trouble may result. If many there is muco-purulent
discharge from the nose, sniffling breathing, frequent sneezing and
snorting expelling mucus and even blood; shaking of the head; rubbing of
the nose on the fore legs or other objects; weeping eyes; and occasional
unsteadiness of the gait.
In the worst cases the respiration becomes sighing, wheezing or even
snoring; the mouth open; head pendent; appetite fails; a dull, apathetic
condition ensues with grinding of the teeth rolling of the eyes, and,
rapidly advancing emaciation.
Fatal cases are not uncommon but most frequently the larvæ reaching
maturity are dropped and health is promptly re-established. Septic
poisoning from decomposition of dead larvæ and debris is a dangerous
complication.
_Lesions._ These consist in the presence of the larvæ in the sinuses,
with violently congested, purple ulcerated mucous membranes and
collections of pus. The mere presence of the grub is not conclusive as
the majority of the sheep harbor two or three from October to June.
_Treatment._ It is advised to place the sheep in a warm building to
encourage the parasites to come out of their recesses and then introduce
some agent to destroy them or to induce their expulsion by sneezing. The
value of the hot building is probably hypothetical unless the larvæ are
approaching maturity. The following agents are used:—moderately strong
solutions of salt, vinegar, carbolic acid, creosote (1 part to 100 parts
of water), or carbonate of ammonia, lime water, snuff, or even such
irritants as quick lime, oil of turpentine or hellebore. These last must
be used with caution as they are liable to induce fatal inflammation of
the air passages though no larva is present.
By passing a feather up the nostril twisting it round and then
withdrawing it some grubs can usually be withdrawn and there is no harm
in first dipping the feather in some of the milder agents mentioned
above. But the larvæ in the sinuses can never be reached in this way.
In dangerous cases it is best to trephine the outer plate of bone
covering the frontal sinuse and wash out freely with tepid water, lime
water, or benzine. The operation may be performed close in front of the
root of the horn if there is one, or to the inner side of the lower part
of the eye if there is not. A semi-circular flap of skin is to be turned
upward and backward sufficiently large to allow the use of a trephine ⅓
inch in diameter, which is to be used as for _Cœnurus Cerebralis_. The
opening being made the sinuse is to be syringed freely for some time
until the parasites come from the nose in the stream of liquid. The
wound heals very promptly. In the absence of a trephine use a gimlet.
_Prevention._ Some turn up a furrow in the pasturage, in which the sheep
may burrow their noses and evade the fly, others lay down quicklime in
covered boxes which has the further advantage of inducing sneezing and
favoring expulsion of the entering parasites. But perhaps the best plan
is to procure a log and bore a number of holes in it with a two inch
augur; place salt in the holes and smear their margins with tar, and
renew it often. The sheep then takes a protective dressing with every
lick of salt.
=Œstrus Purpureus= (Brauer) is a species which infest the nose, etc., of
the Syrian sheep, and =Cephalemia Maculata= (Wedl) one which infests the
nasal chambers of the Egyptian buffalo and camel.
NASAL CATARRH IN DOG AND HORSE FROM LINGUATULA (PENTASTOMA) TAENIOIDES.
RHINARIA TAENIOIDES.
Form. Family. Habitat when mature, and immature. Development.
Symptoms, sneezing, discharge, irritability, ill-temper, shaking the
head, rubbing nose, parasites in discharge. Treatment, injections,
trephining. Prevention.
This parasite has a worm-like body, but is closely allied to the mites
and belongs to the Arachnida. It differs from the mite in having but
four short limbs retractile and protractile and furnished with sharp
claws. The body is thickest toward the anterior end and prolonged and
narrow posteriorly; marked by about 90 rings; head rounded off abruptly,
mouth broadly open, with a horny lip; integument with numerous openings
or stigmata (respiratory); _male_ 7 lines long by a line broad in its
anterior part genital orifice on the front part of the abdomen in the
median line; _female_ 3 to 4 inches long, by 3 or 4 lines broad
anteriorly; genital opening at the end of the tail. _Reproduction_
oviparous.
_Habitat._ Nasal chambers and sinuses of the dog, wolf, goat, and horse.
_Pentastoma Denticulata._ The young partially developed _P. Taenioides_.
Has all the rings except the two first, garnished with fine sharp
recurved spines; legs more slender with accessory booklets; length 2
lines; breadth ½ line.
_Habitat._ Cysts in the lungs, liver, mesenteric glands, etc., of the
hare, porpoise, goat, sheep and other mammals, not excepting man.
_Development._ Leuckart found that the adult Pentastomata copulate in
the nasal chambers, as many as half a million of eggs being fertilized
in a single female; that these eggs are discharged with the nasal mucus
and falling on vegetables are taken in by herbivora; their shells are
digested and destroyed in the stomach, and the liberated embryos
perforate the intestinal walls and encyst themselves in various organs.
The encysted embryo varies from ¹⁄₅₀₀ to ¹⁄₄₀ inch in length, is rounded
and blunt anteriorly but very thin posteriorly with the tail slightly
curved toward the ventral aspect. It is several months before the feet,
cutaneous spine and generative organs are developed, and during this
period it undergoes several moultings. Finally it leaves its cyst and
may live free in the cavities in the body of its host, and if it does
not escape from the body it finally constructs a new cyst and then dies.
If the host is eaten by a carnivorous animal the liberated pentastomata
reach the nose either from the lips or pharynx and in a few months more
acquire their complete development. They must reach the nose of the
horse by their presence in the food or water.
_Symptoms Caused by the Pentastoma._ No morbid symptoms have been traced
to the young encysted condition of the parasite. Yet it would not be
surprising if their presence in large numbers in the mesenteric glands
and liver should give rise to troubles of assimilation, sanguification,
biliary secretion and the like. Frerichs says they are more common in
the human liver in Germany than echinococcus, but adds that they have no
clinical importance.
In their mature condition however they cause considerable irritation and
nasal discharge when present in large numbers. In dogs there is running
from the nose the discharge containing an abundance of the ova,
restless, fretful habits, sometimes a morbid readiness to bite, frequent
shaking of the head and rubbing of the face.
The _treatment_ would be to trephine the sinuses and inject lotions
impregnated with creosote, carbolic acid or naphtha. From the danger to
man of becoming infested it is important to ascertain the true nature of
any nasal discharge of the dog especially in countries like Germany and
Egypt in which this parasite is common.
_Prevention._ Deny raw offal of herbivora to dogs.
AFFECTIONS OF THE THROAT.
_Sore throat_, _Angina_, _Cynanche_—is a generic name applied to a
series of inflammatory affections of the various structures about the
throat. If the _larynx_ is specially inflamed the disease is known as
_laryngitis_, if the _pharynx_, as pharyngitis, if there are exudations
forming false membranes it is _croupous_ or _diphtheritic_, or if
associated with some general febrile affection, it takes its name
accordingly, _influenza_, _strangles_, _distemper_, or _scarlatina_, as
the case may be.
LARYNGITIS IN THE HORSE.
ANGINA LARYNGITIS, CYNANCHE LARYNGEA, ETC.
Causes, mechanical, cold, irritants, extension, diet, close stables,
infectious disease. Symptoms of acute form, head extended, throat
swollen, tender larynx, cough, in early stage, after exudation,
wheezing in inspiration, dysphagia, fever, œdena glottidis, spasms,
dyspnœa, successive discharges. Lesions, tumefaction, softening,
friability, redness (ramified or not), erosions of mucosa, œdema.
Course, duration, sequelæ, cough, roaring. Subacute form, chronic
form, in old debilitated animals, in those reined too tightly, in
those which perspire with difficulty or bear heavy coats. Symptoms,
local, in breathing, cough, effect of cold air, or water or of dust.
Sequelæ, ossified cartilages, roaring, emphysema, bronchiectasis.
Treatment, hygienic, soothing, sheepskin, compress, poultice, mustard,
sulphur dioxide, laxative, neutral salts, expectorant, sedative,
derivative, tracheotomy, with trochar and cannula, with scalpel,
tracheotomy tubes. Insufflation, injection. In chronic laryngitis,
electuaries, mustard, derivatives, astringents, caustics, tonic
inhalations.
_Causes._ These are the ordinary causes of chest diseases. As special
causes may be noted severe compression of the larynx as in roughly and
repeatedly _coughing_ an animal; the sudden contact of piercing cold
air, of irritant gases, powders or liquids with the membrane, and the
rapid, forcible and continuous current of condensed air through the
glottis during severe exertion.
Among the general causes the most fruitful are the high feeding, hot,
close stables, heats and chills, and other circumstances attendant on
domestication. Laryngitis may be an extension from coryza, pharyngitis,
bronchitis or pneumonia. It may further be but a local manifestation of
influenza or strangles, contagious pneumonia, etc. The disease is
_acute_, _subacute_, or _chronic_.
_Symptoms of acute form._ All acquainted with horses can recognize the
general symptoms of sore throat. The nose is elevated and protruded to
avoid compression of the larynx; it is carried stiffly for the same
reason. There is some swelling around the throat or beneath the root of
the ears. If the cartilages of the larynx are compressed between the
finger and thumb, or if pressure is made in the median line below upon
the connecting crico-thyroid membrane the patient instantly coughs and
throws up the head to avoid a repetition of the suffering. This
tenderness of the larynx to touch is peculiar to laryngitis and serves
to distinguish it from pharyngitis. The cough is at first very hard and
painful and only gives way to a soft mucous type when a free mucous
exudation puts an end to the tense, thickened and dry state of the
mucous membrane. The inspiratory act is accompanied by a whistling or
deep bass sound, particularly after the slightest exertion. This may be
heard at times during expiration as well, though not invariably so.
Sometimes the animal drops the food from his mouth after mastication,
because of the pain attendant on swallowing, but this is really a
symptom of coexisting pharyngitis, and its absence implies the
nonexistence of that complication. There is usually a slight pasty
swelling between the branches of the lower jaw.
There are besides the general symptoms of fever more or less marked,
such as increased temperature, accelerated pulse, red injected eyes and
nose, slightly hastened breathing, the expiration being effected by a
double lifting of the flank as in broken wind, etc.
In two or three days in favorable cases exudation takes place from the
mucous membrane, the cough becomes softer and less frequent, the local
tenderness decreases and the general symptoms subside.
If otherwise the symptoms may become more intense, and breathing may get
loud and difficult in connection with thickening and rigidity of the
mucous membrane, or a serous exudation into it and beneath it (œdema
glottidis) which by closing the glottis renders breathing almost
impossible. The same distressing symptoms may arise from spasm of the
larynx excited by the inflammatory action. As arising from thickening or
infiltration of the membrane these symptoms may come on comparatively
slowly, but in the case of spasm they appear suddenly and have periods
of intermission, reappearing on succeeding days and usually at the
earlier part of the night. In such circumstances the loud, noisy
breathing is heard at a considerable distance, the horse stands
obstinately still, the fore feet apart, his elbows turned out to allow a
firm action of the chest, the flanks working laboriously, the head low,
the nose protruded, the nostrils widely dilated, the mouth open, the
eyes standing out from their sockets red and wild looking, and the face
constrained and pinched, the whole expression being that of intense
agony from impending suffocation.
_Lesions._ In cases where death has supervened, perhaps in connection
with another disease, the laryngeal mucosa, especially on and above the
glottis, is soft, tumid, friable, with ramified or uniform redness and
petechial spots. The epithelial layer may be softened, disintegrated and
shed, leaving pointed or larger erosions, which are, however, usually
superficial. In case of œdema glottidis the mucosa and submucosa are
thickened by an abundant exudate which may extend to the connective
tissue outside the larynx as well. In aggravated cases there may be dark
red or brownish red discolorations of the mucosa.
_Course, Duration._ Fortunately these aggravated forms of the disease
are rare and unless the patient perishes during such an attack or the
inflammation extends down toward the chest, laryngitis rarely proves
fatal. Its duration is from twelve to fifteen days. Its extension to the
lungs may be suspected when the extreme tenderness of the throat
subsides without any corresponding improvement in the health.
Examination of the chest will then rarely fail to detect the presence of
disease.
But although sore throat is rarely fatal its effects are not unimportant
nor trivial. It occasionally merges into a chronic form, with a hacking
cough, tenderness to pressure and an increased liability to other
diseases of the air passages. More frequently it is followed by wasting
and fatty degeneration of the laryngeal muscles and the horse becomes a
confirmed _roarer_. In all cases it leaves a greater susceptibility to a
second attack.
=Subacute Laryngitis.= This form has been chiefly seen in young animals
and up to eight years old. At the outset its symptoms are moderate but
as it is usually associated with serous effusions in and around the
mucous membrane the symptoms above mentioned as indicating imminent
danger of suffocation may suddenly appear and life can only be preserved
by opening the trachea.
=Chronic Laryngitis.= This may follow the acute form or it may come on
independently and by slow degrees. It may accompany nasal catarrh, or
chronic bronchitis. Old animals which have had heavy draught work and
repeated attacks of sore throat, are frequent subjects of it, and as
Fergusson has pointed out it is most prevalent among horses whose
throats have been compressed by the inconsiderate use of the bearing
rein. Reynal has observed it often in horses that are sweated with
difficulty, and in those which remain long wet from the length and
thickness of their winter coats.
_Symptoms._ When acute laryngitis passes into the chronic form all the
symptoms subside except a slight nasal discharge, the cough, tenderness
of the larnyx, and _roaring_. The cough is dry, short, and hacking,
rarely soft, and is heard mainly when the animal feeds, when he leaves
the hot stable for the cold air, and after drinking cold water. During
exercise, it is equally excited, the cough becoming harder, and the
horse extending his head and neck as if to disengage some body from its
throat. The subject may in nearly all other respects maintain the
appearance of vigorous health.
_Course, etc._ This disease is liable to prove obstinate and if of old
standing, often incurable. Unless checked, the continued congestion and
irritation of the larynx, the frequent, hacking cough, and the
consequent violent distension of the lungs bring about extensive and
irreparable structural changes. Among these may be mentioned
ossification of the cartilages of the larnyx; paralysis of the left
laryngeal nerve with wasting of the muscles to which it is distributed,
and _roaring_; dilatation of the bronchial tubes, and permanent
distension and rupture of the air cells (emphysema, broken wind,
heaves).
_Treatment._ _Acute form._ Unless in the very mildest cases
unaccompanied by fever, repose is essential. If available, a roomy,
clean, dry, and airy loose box should be allowed, care being taken to
avoid draughts of cold air and to secure a soft equable temperature
neither too hot nor too cold. Blankets should be used and even flannel
bandages applied loosely to the legs if the weather is cold, or, if
there is any tendency to chills and shivering. The nostrils must be
steamed as directed for _coryza_. A piece of sheepskin with the wool
turned in may be tied around the throat and up to the ears. In very
acute cases a linseed meal poultice or wet pack may be applied to the
throat, while in the milder forms, a mustard poultice or a lotion of
Spanish flies or other stimulant may be employed. Unless the malady has
an epizootic type, with prostration and a weak, rapid pulse, the bowels
may be opened by a laxative (3 or 4 drachms, aloes), and the water or
gruel the animal daily drinks should contain ½ to 1 ounce nitre. As an
expectorant the patient may take salammoniac 1 oz. daily in the drinking
water, or this agent may be evaporated from a clean chafing dish every
two hours and inhaled. Or he may take carbonate of potash or soda, or
iodide of potassium. If the cough is troublesome, half a drachm of
Dover’s powder may be given thrice a day or 1 grain chloride of
apomorphine every hour. Bromide of potassium or sodium may also be
resorted to. Inhalations or spray of sulphurous acid, or vapor of oil of
turpentine and insufflations of calomel may benefit as local
applications. The diet must be confined to sloppy bran mashes, cut
roots, or boiled barley, or oats. Hay should be withheld in the more
acute cases until improvement appears. Under treatment such as the above
and even without the medicinal part of it, the great majority of cases
will do well.
In cases attended with high fever with strong full pulse and bright red
nasal membrane, the purgatives and diuretics are especially called for,
and the former should have their action encouraged by frequent hot water
injections. Twenty drop doses of the tincture of aconite repeated four
times a day, or ten drops every three hours, will be further useful.
When the symptoms are of such a type as portend the access of paroxysms
of threatened suffocation, bleeding has been strongly recommended, but
unless resorted to in the first twenty-four or forty-eight hours is
rarely admissible. Also in weakened constitutions and when the fever is
of a low type, with small, weak pulse and general dullness and
prostration, the temporary relief obtainable from bloodletting will not
often counterbalance the danger of increasing weakness, and the loss of
recuperative power. In all such cases the application of a strong
mustard poultice for several hours in succession, until an abundant
effusion has taken place, into the skin and beneath it, has often the
best effect by virtue of its depletive and derivative action. Active
friction of the limbs to improve their circulation and increase their
temperature is also useful.
=Tracheotomy.= When suffocation becomes imminent not a moment must be
lost in performing _tracheotomy_. This operation is always available in
threatened suffocation from obstruction to the passage of air in the
nostrils and throat.
Different methods of opening the windpipe have been resorted to. One is
by means of a cannula and trochar at least three-fourths of an inch in
diameter and about five inches long and with two large oval orifices in
the middle of the cannula, and on opposite sides. This is made to
transfix the windpipe with its investing skin and muscles from side to
side in the middle of the neck, care being taken to pass it in the
interval between two adjacent cartilaginous rings. The trochar is now
withdrawn and the orifice in the cannula corresponding to the interior
of the windpipe, the animal is enabled to breath freely through the
tube. The cannula has only then to be secured in its place by a tape
carried round the neck.
The more common plan is by introducing a tube through a circular opening
made in the trachea. For this operation are needed, scissors, knife with
a thin narrow blade, needle and thread, and tracheotomy tube. The common
tube is about an inch in diameter, four to five inches long bent upon
itself so as to fit into the trachea, and furnished with a flat shield
to slits in which cords may be attached to fix it in its place. A second
variety is only long enough to reach into the windpipe. It is provided
with a flattened shield externally and from its inner extremity projects
downwards at right angles a plate curved so as to adapt it to the form
of the interior of the trachea. There is an additional plate to fit into
the upper part of the tube, provided with two lips projecting from it at
right angles; the outer lip is screwed to the shield after the tube has
been introduced into the wind pipe and the inner lip is thus fixed
inside the ring of the trachea, immediately above the opening and
effectually prevents any displacement of the tube.
In operating the animal is kept standing with the head as nearly as
possible in the natural position. The hair is removed from the skin
beneath the windpipe between the middle and upper thirds of the neck.
The skin having been rendered tense, (without displacement) by the
fingers and thumb of the left hand, an incision is made in the median
line from above downwards, for about two inches and is carried through
the muscles so as to expose two rings of the trachea. The needle and
thread are passed through the membrane connecting the two rings, and
with the knife a semi-circular piece of cartilage is cut from each of
the two adjacent rings. The thread in the connecting membrane prevents
them from being drawn in by the rush of air. It only remains to
introduce the tube and fix it in position.
Not only does tracheotomy obviate immediate danger of suffocation, but
by removing the source of irritation in the continuous and forcible rush
of air through the narrowed and inflamed tube, and in securing for the
blood a freer æration and a purer constitution it often induces a rapid
change for the better in the character of the inflammatory action. The
wound may be daily cleansed and dressed with sodium hyposulphite.
Some veterinarians following the example of Bretonneau and Trousseau
have treated sore throat from the first by what is called the abortive
treatment. For this purpose a long whalebone prob with a pledget of tow
firmly attached to its end and covered with powdered alum is introduced
through the mouth into the pharynx and larynx even. Violent paroxysms of
coughing are induced, but cures are affected in from two to five days.
Under Delafond’s treatment calves and foals recovered in twenty-four
hours. A more modern method is to inject a solution by means of a
hypodermic syringe inserted between the upper rings of the trachea.
Milder treatment such as the inhalation for an hour several times a day,
of the fumes of burning sulphur and water vapor will be found generally
successful. The air should be impregnated with sulphur fumes only so far
as can be breathed without inducing coughing on the part of the patient.
Such measures should not divert attention from the necessity for general
care, a control of diet, clothing, air, the state of the bowels, nor
from local external applications to the throat.
=Treatment of Chronic Laryngitis.= The patient should have a loose airy
box with an equable temperature. The avoidance of work and exposure must
be sought for the time. Green food, cut roots, boiled grain, or bran
mashes, with little or no hay, or other dry food, must be given. The
bowels must be regulated. An electuary compound of linseed meal,
molasses, and a drachm of belladonna extract to every tablespoonful of
the mixture, may be given to the extent of a tablespoonful smeared on
the inner side of the cheek twice daily. A mustard poultice to the
throat has often a good effect. Light firing over the larynx is
sometimes beneficial.
If secretion is defective and cough hard and dry chloride of ammonium,
carbonates or bicarbonates of soda, potash or ammonium or borax, in
solution or in gaseous form, may be given, the various bitters being at
the same time drawn upon as tonics. If secretion is excessive, with a
loose gurgling cough, astringents are indicated like ferric sulphate or
chloride, (½ dr.), or they may be applied as spray: alum or iron alum
five grains to the ounce, zinc sulphate or sulphocarbolate two grains to
the ounce, silver nitrate one-half grain to the ounce. These may be
introduced through the nose with the head elevated, or in small genera
through the fauces. Tar, oil of turpentine, creosote, carbolic acid or
eucalyptol may be inhaled from hot water.
PHARYNGO-LARYNGITIS IN CATTLE.
Susceptibility. Causes, symptoms, cough, salivation, wheezing,
lachrymation, muzzle dry, tender throat, dysphagia, disturbed
innervation and circulation, hyperthermia. Duration. Abscess.
Treatment, laxative, local treatment, lancing.
Cattle are less subject to sore throat than horses. The skin appears
less sensitive to the influences of cold and heat. The ox is not
subjected to the same severe exertions. It is rarely seen to sweat, the
moisture passing off from the surface as insensible perspiration only.
The disease, however, recognizes the same causes as in the horse, though
these are manifestly less injurious.
_Symptoms._ The disease usually affects at once the larynx and pharynx
so that the symptoms are somewhat modified. In the simplest form there
is only a small, hacking cough, a flow of saliva from the mouth and some
loss of appetite but no fever. In more acute cases the breathing is loud
and wheezing, the cough, soft and rattling, is followed by a free
discharge of mucous from the mouth, the nostrils and eyes are red, the
muzzle dry, the pulse accelerated and full, the throat tender to the
touch, and swallowing difficult, part of the food and drink being
rejected through the nose. If the larynx is chiefly involved the loud
noise in breathing is the predominant symptom and sometimes almost the
only one.
_Course, etc._ The cough and other symptoms are usually moderated with
the access of the abundant secretion on the second or third day, and
recovery is perfect on the eighth to the fifteenth. If abscess results,
to which there is a far greater liability than in the horse, it may not
burst till the twentieth day and the case is correspondingly protracted.
This should be carefully distinguished from the deposits of tubercle
which take place around the throat in cattle. In rare cases the disease
becomes chronic.
_Treatment_ does not differ from that advised for the horse except in
the greater safety of purgatives which must in this case be saline
(Epsom or glauber salts one to two pounds), and in the greater ease with
which local treatment can be applied owing to the shortness of the soft
palate. When abscess forms it must be encouraged by poulticing and
opened with the knife or lancet as soon as it points.
LARYNGITIS IN SHEEP.
Infrequency. Causes, damp lands, storms, close buildings, clipping.
Symptoms, cough, sneezing, discharge, snuffling, oral breathing,
tender throat. Treatment, ventilation, warm water vapor, sulphur
dioxide, salines.
Sore throat is fortunately even more rare than in the larger ruminants.
It occurs chiefly where this animal, constituted to feed on the dainty
grasses of the dry mountain side, is kept on cold, marshy ground and
exposed to frequent cold, wet blasts. Sheep suffer also from hot, close,
filthy buildings in winter, and from unseasonable clipping.
The _symptoms_ are frequent coughing and sneezing, running from the
nose, working of the jaws, and breathing through the open mouth as being
easier than through the plugged nostrils. The larynx is tender and may
be swollen.
_Treatment_ is usually confined to ventilation and cleansing of the
fold, frequent fumigations with water vapor from the spout of a boiling
kettle, and with sulphur fumes, and giving tepid farinaceous gruels or
mashes containing sulphate of soda in the daily proportion of two pounds
to each hundred head of sheep. Sal ammoniac may be given in food or
drinking water.
LARYNGITIS IN PIG.
Frequency. Causes, wet, cold pens, exposure, withholding liquids.
Symptoms, prostration, dullness, cough, fever, swollen throat and
neck, dyspnœa, dark mucosa, sloughing of epithelium and epidermis,
general petechiæ, fœtid breath, great prostration. Lesions, gangrenous
patches on pharynx and fauces, ulcers, infiltrations. Treatment,
hygienic, dietetic, emetic, laxative, poultice, bandages, locally,
astringent, antiseptic, caustic, tonic.
Sore throat is common in some localities when pigs live in herds.
_Causes._ Chiefly faulty hygiene. Exposed, cold and wet piggeries, cold
blasts for which the pig has an extraordinary aversion, and the
deprivation of liquids in warm, dry seasons are frequent causes.
_Symptoms._ These have been described by M. Pradal, who divides the
disease into three stages, evidently dealing with an infectious malady.
The _first stage_ is marked by loss of appetite, dullness, slow,
listless movements, a tendency to hide under the litter; low, hoarse
grunt and cough, the last aggravated by moving the animal; pain in
swallowing; red, sunken eye, and constipation. If there is no
improvement on the second or third day it merges into the _second
stage_. This is characterized by a still hoarser grunt, painful, hard
hacking cough, difficult breathing, especially in the sunshine, and a
rapidly increasing swelling of the throat, soon extending to both ears
and as far down as the breast bone. This engorgement feels soft and
pasty though firm, tender lumps may be felt, indicating the approaching
formation of abscess. It is so abundant that suffocation may ensue in
the course of forty-eight hours. If the progress of the swelling is not
arrested it soon passes into the _third_ or _gangrenous stage_. The
breathing is more hurried; the mouth open, the protruded tongue of a
bluish black color, the cough followed by a continuous rattle, the head
unsteady, swallowing impossible, and the swelling extends to the side of
the face and beneath the chest. The swollen surface is cold and livid;
the bristles easily detached; it is bedewed by a serosity which exudes
from it, and portions of the dead skin tend to detach themselves. The
mouth and throat participate in the gangrene, the breath, saliva and
nasal discharge is fetid, and the epidermis peels off. The snout, ears
and skin generally assume a bluish black hue, the prostration is
extreme, the creature lying constantly on its side; the pain ceases and
in one or two days death ensues, preceded by a state of comparative
calmness.
On opening the throat after death the mucous membrane is engorged and
thickened, bears various hues of black, blue, livid and green, and
breaks down into a pulpy mass under slight pressure. The surrounding
(pharyngeal) muscles even are implicated in this change. In the earlier
stages there is only engorgement with blood of the tonsils and the
mucous membrane of the pharynx and larynx; serous infiltration of the
surrounding parts, and often the presence of inspissated mucus
resembling false membranes or of ulcers on the surface.
_Treatment._ In the earlier stages, hygienic measures alone may suffice
to check. A warm, dry, comfortable piggery, emollient and astringent
drinks, such as sheep’s head broth, oatmeal and other gruels acidulated
with vinegar or buttermilk, an emetic (six grains of tartar emetic); a
dose of physic (four croton beans powdered and given in the food, or
from two to three ounces of castor oil), and if the patient will permit
it a flannel bandage or piece of sheepskin round the throat. If the
symptoms are more threatening it is recommended to bleed from the ears
and tail; to apply a linseed meal poultice round the throat to hasten
the formation of abscess, or in the absence of such indications to
employ a mustard poultice made with spirits of turpentine, or rugs wrung
out of boiling water, to the same part. Local astringent and caustic
applications to the throat are the most promising, applied by means of a
whalebone prob as recommended for other animals, the mouth being held
open by a noose round the upper jaw. Sodium sulphite, silver nitrate,
potassium permanganate, hydrochloric acid diluted, and tincture of
iodine, may be employed.
When the gangrenous stage has been reached all treatment is useless.
LARYNGITIS IN THE DOG.
Sore throat is chiefly seen in pampered pets and in hunting dogs, as
the greyhound. In the latter class it is the result of chills, a cold
ducking when heated, cold damp kennels, etc. It is sometimes almost
the only manifestation of distemper.
_Symptoms._ Dullness, impaired appetite, a slight cough becoming more
frequent and paroxysmal. These paroxysms give rise to accelerated and
panting breathing, and if severe, to the ejection of a glairy yellow
(bilious) material from the stomach. There is also running from the nose
and frequent sneezing. The dull muffled bark has led to the supposition
of _rabies_ but it has no resemblance whatever to the characteristic cry
of _rabies_ while beginning like an impulsive bark merges into an
agonized and baffled howl. Accelerated pulse, elevated temperature,
reddened fauces and swollen tonsils are marked symptoms.
Sometimes a short, dry cough obstinately remains after the disease has
apparently subsided.
_Treatment._ Attend to general comfort, steam the nostrils, give a
laxative if costive, and follow with iodide of potassium or salammoniac
(5 grains) repeated thrice daily. Apply a mustard poultice to the
throat.
PHARYNGITIS. SORE THROAT.
Causes. Symptoms, larynx insensible, tender parotid and submaxillary
swelling, cough mucous, difficult swallowing with gurgling, liquids
returned by nose, buccal mucosa hot and red, salivation, chronic
cases. Treatment, medicated drinks and electuaries.
ANGINA PHARYNGEA. CYNANCHE PHARYNGEA.
Inflammation of the pharynx owes its existence to the same _causes_ as
_Laryngitis_.
_Symptoms._ The general symptoms being like those of _Laryngitis_, the
specific and distinguishing ones only will be here noticed. The larynx
is not tender to the touch nor is cough thereby excited. The glands
beneath the root of the ears (parotids) are swollen and tender and cough
is induced by handling them. The intermaxillary glands are enlarged. The
cough is loose and followed by the ejection of glairy materials by the
mouth and nose. Food and drink are swallowed with difficulty and effort,
dry grain or hay is often refused, or dropped from the mouth, after it
has been chewed, to avoid the pain of swallowing. Deglutition is
accompanied by a gurgling sound caused by the abundant secretion in the
pharynx. In swallowing liquids a portion is often rejected by the nose.
The mouth is hot, red at its back part, and filled with fetid saliva
which often drivels from between the lips in the coarser breeds of
horses. The fever varies according to the intensity of the inflammation.
This disease is rarely serious, and improvement is manifested, by a free
discharge from the nose of a white opaque color, by the ability to
swallow without pain, and the better appetite and general appearance.
Collections of pus in the _Guttural pouches_ may result from
pharyngitis. See _Chronic Nasal Catarrh_.
Reynal has seen chronic cases of this disease due to: 1st, fracture of
the large branch of the hyoid bone; 2nd, Laceration or ulceration of the
soft palate; and 3rd, an abscess of the pharyngeal mucous membrane.
The _treatment_ does not differ materially from that of laryngitis
except in the greater value of soft food, mucilaginous and acidulated
drink and of electuaries which act on the throat as they dissolve.
Subjoined is a formula:
Recipe: Extract Belladonna, four drams; potassium iodide, one ounce;
sodium hyposulphitis, three ounces; mellis, five ounces. Mix. A desert
spoonful to be smeared on the inside of the cheek thrice daily.
CROUP.
Croup: croak. Acute laryngitis, with spasms and perhaps
pseudo-membranes. Relation to diphtheria. Causes, low, damp
localities, exposure, youth, form of inflammation. Symptoms, onset
sudden, crowing inspiration, hard cough paroxysmal, fever, larynx
sensitive, dyspnœa in paroxysms or intermittent. Complications.
Duration. Lesions, intense congestion, false membranes on larynx,
fibrinous. Treatment, fomentations, ether, chloroform, chloral
hydrate, laxative saline, sedative, derivative, surgical, water vapor,
calomel, caustic, stimulants, tonics. Croup in sheep and horse.
CROUPOUS LARYNGITIS. PSEUDO-MEMBRANOUS LARYNGITIS.
_Name and Definition._ The word _croup_ by which this disease is known
over the whole of Europe and a great part of America is, essentially
_Scotch_, and is familiarly used in the Lowlands of Scotland to
signify—_to croak_. The disease consists in an acute inflammation or
high vascular irritation of the larynx, associated with spasms of its
muscles and commonly though not invariably with a firm layer of
exudation on the surface of the mucous membrane. In some cases
undoubtedly croup is but a form of the contagious pseudo-membranous
affection diphtheria, the germs of which grown on a surface freely swept
by continuous currents of pure air, retain too much of an ærobic habit
to penetrate deeply into the tissues. (See Authors, “Malignancy
mitigated by Oxygen,” Medical Record, 1881, p. 673). It does not follow,
however, that croup is always due to even a weakened germ. So far as yet
appears it may develop independently of any particular pathogenic germ,
from some violent local irritant in a predisposed subject. Croup
therefore may be treated here as a presumably noninfectious disease.
Being a very rare disease in horses its manifestation in ruminants will
first be noticed.
CROUP IN THE OX.
_Causes._ These are not well understood. Low, damp situations would seem
most liable, especially if the animals are much exposed at night. So far
indeed as can be observed it arises from the same causes as
_laryngitis_. Age affects its development. Croup is mostly seen in
animals between six months and a year old, and rarely in those over five
or six years of age. The specific cause of the formation of false
membranes and of spasms of the laryngeal muscles is a mystery, but to
these the susceptible constitution and tissues of young animals appear
to predispose. No mere grade of inflammation from the slightest
hyperæmia to the highest type of inflammatory action is of itself
sufficient to arouse the special phenomena. All of these are seen
everywhere but _croup_ may be said to be confined to certain localities
and ages.
_Symptoms._ Unless it supervenes on a pre-existant attack of catarrh,
croup is usually as sudden in its outset in the lower animals as in man.
An extremely hard _croupy_ cough, or loud, crowing, difficult breathing,
loudest in inspiration, is usually the first symptom and appears to
seize the animal in an instant and without the slightest premonition.
This is closely followed by intense fever, full, hard pulse, 80 to 100
and upward per minute, increase of bodily temperature sometimes to
107.5° F., costiveness and high colored scanty urine. The throat is
excessively tender, the slightest touch giving rise to violent paroxysms
of coughing, during which the eyes redden and protrude from their
sockets, the veins of the skin are gorged, the tongue, dry and livid, is
protruded and small portions of the contents of the stomach and white
shreds of false membrane are occasionally brought up. Sometimes in the
intervals of coughing as well the mouth is constantly open and the
tongue protruded and partly covered by a frothy but tenacious mucus.
Suffocation appears imminent in many cases and the beast may perish
suddenly in this way. On the other hand the threatening symptoms may be
present only at certain periods of the day and may be moderated
remarkably at others, especially at early morning. If complicated by any
chest affection the symptoms are more urgent and the issue more commonly
fatal. If associated with a low type of fever, a small, weak pulse, and
much prostration, as it tends to be if it continues several days without
relief, it has a more fatal tendency. The same may be said of its
occurrence epizootically.
_Duration._ Croup will often run its course and prove fatal in
twenty-four to forty-eight hours. Improvement is manifested by the cough
becoming less convulsive and painful, by the expulsion through the mouth
of shreds of false membrane, and by return of spirits and appetite.
_Postmortem Appearances._ If the animal has died suffocated, the lungs
and right side of the heart will be gorged with blood; if in a stupor
(coma), attendant on brain poisoning with venous blood, the veins will
be specially engorged. The mucous membrane of the larynx has a more
vivid arborescent redness than in ordinary laryngitis but the special
feature is the presence of false membranes. These layers of exuded
material are almost confined to the air passages. They may extend to the
soft palate and nose in an upward direction and to the trachea and
bronchial tubes in a downward, but they rarely exist in the mouth,
pharnyx, or gullet like the false membranes of diphtheria.
_Characters of the false membranes._ These are gray or yellowish white,
though they may be reddened in patches or streaks. They vary in
consistency from that of glairy mucus to a firm layer as of dense
fibrine, and become more adherent as they are of older standing.
Sometimes they are partially detached, the free end of the shreds
floating in the larynx. The deep or attached surface presents redness in
points, in streaks, or as ramifications very visible if the membrane is
held up between the eye and the light. They vary in thickness from half
to a line. Delafond has found these membranes in the lower animals to be
mostly formed of fibrine, with a little albumen, and traces of alkaline
and earthy salts.
_Treatment._ This must be prompt and energetic. Wet cloths as hot as the
hands can bear, wrapped around the throat and neck, and replaced as they
cool, will usually arrest the spasm. If this fails ether or chloroform
by inhalation or chloral hydrate by injection may be employed with
caution. The action of the bowels must be secured by salines (sulphate
of soda ½ to 1 ℔) or oil (linseed oil ½ to 1 pint) and injections of
warm water. Sulphate of soda should be thereafter given in half ounce
doses twice daily, or nitrate or acetate of potass may be substituted.
They are advantageously given in linseed decoction and may be combined
with laudanum, (½ ounce), belladonna, or other agent to check the
spasms.
A blister (mustard poultice) should be applied at first either to the
throat or breast, the windpipe being left untouched lest tracheotomy
should be required. Similar applications to the legs are useful.
If suffocation appears imminent _tracheotomy_ should be at once
performed (see under Laryngitis). This operation has been depreciated
because of the late period at which it has been employed, when the
patient was already past all hope, but the resulting wound in the neck
is more than counterbalanced by the greater freedom of breathing and the
better æration of the blood which tends to obviate the justly dreaded
low fever. It often leads to a rapid diminution of the spasms and
laryngeal irritation.
Agents applied directly to the inflamed mucous membrane are often
requisite. The air of the building should be rather warm, equable and
moistened by water vapor, if that can be conveniently done. Calomel or
alum powder may be frequently introduced into the larynx by means of a
whalebone prob and sponge as spoken of under laryngitis, or a solution
of nitrate of silver (10 grains to the ounce of water) may be applied
several times a day. These not only hasten the removal of false
membranes but counteract their production. They produce violent and
convulsive coughing at first and have to be used carefully. Delafond
blew in such agents through an opening made in the windpipe. They may be
injected with a hypodermic syringe. In prostrate conditions it may be
necessary to resort to stimulants (wine whey, carbonate of ammonia) and
tonics (gentian, Peruvian bark).
CROUP IN SHEEP.
According to Roche Lubin croup is sometimes observed in spring in lambs
and hogs. The common cause is “the shutting up of the animals for the
whole twenty-four hours in a hot confined place, the floor of which is
covered by a fine dust, and the air loaded with the same, owing to the
jostling of the sheep together, the effects being intensified by the
weight of the fleeces.”
The disease is manifested by constant working of the jaws, extreme
tension of the neck, abundant salivation, respiration hurried and
whistling, extreme pain and threatened suffocation when the slightest
pressure is made on the throat, and refusal of all food liquid or solid.
The weak, hacking, convulsive cough is associated with the discharge of
a whitish glairy mucus by the nose until the third or fourth day when
false membranes may be expected.
_Treatment_ is like that for the ox, medicine being given in about
one-fifth of the doses.
CROUP IN THE HORSE.
The rare cases of _croup_ in foals and young horses appear due to the
same general causes as in ruminants. M. Riss records two cases, and
Bouley one from breathing smoke when the straw of the stable had taken
fire. The suddenness of the attack, the spasmodic symptoms and the
duration of the disease and the treatment do not differ materially from
those given for the ox.
PHARYNGEAL AND LARYNGEAL POLYPI.
Pediculated tumors. Dyspnœa through change of position, operation by
ecraseur, snare, or cricoid incision.
Tumors of varied structure developing in or beneath the mucosa of
pharynx or larynx often become slowly detached until they hang by a
loose pedicle, and having much latitude of movement they may at times
slip between the arytenoid cartilages or even into the glottis producing
the most urgent or even fatal dyspnœa. Pediculated tumors in the
posterior nares lead to the same accident. In one case of multiple small
tumors on the pharyngeal mucosa of the horse, the largest and loosest,
attached to the front of the epiglottis, was occasionally displaced into
the larynx threatening instant asphyxia. One such attack supervened on
the opening of a suppurating guttural pouch by the writer, necessitating
prompt tracheotomy. A time was set for the removal of the polypus, but
the tracheotomy tube having been accidentally displaced during the
preceding night the patient died of suffocation. Dick mentions a polypus
growing from the interior of the larynx and causing loud _roaring_. Such
tumors may be removed by operating with the _ecraseur_ through the
mouth, or by a snare passed through a long narrow tube and used to seize
and twist through the pedicle. If the polypus grows from the laryngeal
walls, it may be best reached by incision through the cricoid cartilage
and crico-thyroid membrane as in the operation for _roaring_.
DYSPNŒA LARYNGEA. ROARING. HEMIPLEGIA LARYNGEA.
Generic name for common symptom. Low and high notes. Grunter, roarer,
whistler, piper, highblower. Pace or effort develops. Causes: of
temporary roaring, inflammations, abscess, phlebitis, choking, dropsy,
petechial fever, phlegmons along vagus. Causes of inveterate roaring,
paresis of left recurrent laryngeal nerve, fatty degeneration of left
arytenoid muscles, fracture of facial bones, polypi in air passages,
chronic thickening of mucosa, foreign bodies in passages, tumors of
lymph glands, abscess of guttural pouches, pseudo membrane, laryngeal
ulceration, ossification, distortion, fracture of cartilages, action
of forcible inspiration, leading on left side, deep origin of
recurrent nerve, effect of chest diseases and violent heart action,
examples of morbid conditions impairing innervation. Lesions in
muscles, and nerves. Facial palsy, poison (chick vetch, winter vetch,
lead, fungi, moulds). Intermittent roaring. Hereditary roaring.
Symptoms, grunting when coughed or threatened, heavy draft, gallop,
noise, laryngeal tremor, cold as a complication, roaring with
expiration, lesions. Treatment, its use. Prevention, avoid breeding
roarers, bearing reins, chick vetch, lead. Tonic medication, caustic
to mucosa, firing, setons, iodine, pad nostrils, tracheotomy,
arytenectomy, electricity.
This is the name of a symptom rather than a disease. It implies a sound
made in breathing in connection with some contraction of the air
passages. The term is however usually reserved for those conditions in
which the sound results, from chronic disease or malformation, the noise
attendant on laryngitis and other acute diseases being rarely spoken of
as _roaring_. In neither case does the noise indicate more than that
there is some impediment to the ingress and egress of air through larynx
or trachea.
The pitch of the note varies exceedingly with the causes that produce it
and with the hurried nature of the breathing. There have thus arisen the
epithets of _grunter_, _roarer_, _whistler_, _highblower_, _piper_,
_trumpeter_, _wheezer_, _etc_. The most common distinctions are those of
_roaring_ and _whistling_. The _roarer_ produces a loud deep basso sound
in inspiration, the larynx or windpipe being only slightly narrowed
while the _whistler_ or _piper_ produces a shrill blowing or sibilant
noise because of the greater constriction of the passage. The term
_grunter_ is derived from the facts that a _roarer_ usually makes a
grunting noise when struck or threatened with a cane, and that when the
upper cartilages of the windpipe are pinched between the finger and the
thumb the resulting cough is prolonged and somewhat like a _grunt_. A
_wheezer_ is usually suffering from spasmodic contraction of the
bronchial tubes, from broken wind or from chronic bronchitis. A
_highblower_ should never be spoken of in the same connection, as the
noise is made from a playful flapping of the false nostrils or soft
palate and disappears when the animal is put to the top of his speed. It
is from confounding _high-blowing_ with _roaring_ that _Eclipse_ and
other brilliant performers on the English turf have been erroneously
pronounced _roarers_.
The noise produced by the _roarer_ is not heard while he stands quiet,
nor many cases even during a short trot or gallop. Such horses are in
consequence often sold at the hammer and the purchaser is grievously
disappointed to find that what he thought a sound horse is absolutely
useless for the purpose for which he designed it.
=Causes.= Before noticing the symptoms of roaring a consideration of the
causes will be useful to enable the reader the better to understand the
signs by which the different forms are manifested.
=Causes of temporary roaring.= Whatever impedes the current of air
causes roaring. Hence inflammatory diseases of the nose, throat,
windpipe or bronchial tubes; abscess of one or the other of these parts;
inflammation of a jugular vein and pressure on the trachea or vagus
nerve by the resulting swelling; choking; the swelling in the neck
consequent on the cutting open of the gullet for the relief of choking;
thickening of the nostrils from dropsy, loss of a jugular vein, purpura
hemorrhagica etc.; and swellings pressing on the vagus nerve, and which
may be situated at the base of the brain, in the neck or in the anterior
part of the chest. Also temporary infiltration of the laryngeal mucosa.
=Causes of inveterate roaring.= The one great cause of roaring and that
which sustains the disease in nineteen cases out of every twenty is
paralysis of the left _recurrent nerve_ of the larynx and wasting of
several of the arytenoid muscles on that side. It may be well, however,
first to notice the less frequent causes and wind up with this more
common one. 1st, Fracture with distortion of the nasal bones and
narrowing of the nasal passages (Gamgee). 2nd, Polypi and other tumors
of the nose, pharynx, larynx, windpipe or bronchi. 3rd, Chronic
thickening of the nasal mucous membrane, the result of inflammation.
4th, The presence of foreign bodies in the nose, as for example balls
coughed up from the pharynx. 5th, Hering records a case resulting from
the closure of the posterior opening of one nasal chamber by a membrane.
6th, Cancerous or melanotic deposits in the lymphatic glands above and
to each side of the pharynx and larynx. 7th, Distension of the guttural
pouches by inspissated pus. 8th, Chronic thickening of the mucous
membrane of the larynx consequent on inflammation. 9th, The formation of
a projecting fold of the mucous membrane or of a new production (false
membrane) in the windpipe as the result of inflammation. Such false
membranes have been known to become detached at their median part and
remain attached at their two extremities thus constituting a band
stretching from one side of the windpipe to the other. 10th, Ulceration
of the membrane of the larynx particularly on the projecting folds
circumscribing the glottis, 11th, Ossification of the laryngeal
cartilages and loss of their elasticity. 12th, Distortion of the
cartilages of the larynx, most commonly from unduly tight reining and
pulling the nose in toward the chest. In such cases the cartilages of
the larynx and those of the windpipe adjoining being compressed slide
within each other, and the enclosed edge projecting within the air tube
materially diminishes its calibre. 13th, Fracture of one or more rings
of the trachea. This usually results from blows, as in running the neck
against the back of a cart or wagon. The cartilaginous rings are usually
broken at their median part in front and being retained together by the
investing elastic tissue which enables the pieces to move on each other
as by a hinge, and being approximated by the contraction of the
trachealis muscle above, the ring is flattened from side to side and the
channel for the passage of air correspondingly decreased. This
flattening can be easily felt by the hand in the living horse. 14th, A
peculiar congenital distortion of the trachea caused by the curling in
of one end of each cartilage of the windpipe and the straightening out
of the other. This occasionally proceeds so far that the gullet is
lodged in the interspace overlapped and hidden by the free ends of the
cartilages, the diameter of the windpipe being proportionately
diminished. Distortions and fractures are usually overlooked by
veterinarians but from the frequency with which the author has met with
them in his dissection he is convinced that they deserve greater
attention than has been awarded them. 15th, Percivall records a case of
inveterate _roaring_ in which, even tracheotomy having failed to cure,
the patient was destroyed and the lungs found to be extensively
consolidated, many of the air tubes having been so compressed as to be
almost impervious. I have known a case of roaring from the presence of a
pedunculated tumor in the lower end of the windpipe where it divides to
enter the lungs, and the same result may ensue from the partial
obstruction of the bronchial tubes by masses of tenacious mucus in
chronic bronchitis.
16th. The immediate cause of _roaring_ in the immense majority of cases
is the =paralysis and fatty degeneration of certain muscles on the left
side of the larynx=. The muscles supplied with motive power by the =left
recurrent laryngeal nerve= (Crico-arytenoideus posticus,
Crico-arytenoideus lateralis, thyro-arytenoideus, and the left half of
the arytenoideus) are those constantly and exclusively affected, while
those supplied by the _superior laryngeal nerve_ (Crico-thyroideus,
hyo-thyroideus and hyo-epiglottideus) remain unchanged. The left
recurrent nerve is also wasted and considerably attenuated as compared
with that on the opposite side. The _modus operandi_ of this paralysis
and wasting in the production of _roaring_ is beautifully seen when the
upper part of the windpipe is laid open so as to expose the interior of
the larynx in laryngectomy. The triangular opening of the glottis is
seen fairly dilated while the muscles are relaxed in the act of
expiration. As soon, however, as inspiration commences the left
arytenoid cartilage slides completely into the passage, its lower border
projecting so much to the right that it forms a prominent crest
extending beyond the median line and in some cases closely approaching
the right wall of the larynx, the superior elastic and free border of
the same cartilage meanwhile gets drawn inward by the suction power of
the air so as to block up the passage still more. The closure of the
glottis being thus seen to be largely controlled by the current of
inspired air, it becomes evident that any increase in the force of the
current will aggravate it and a decrease will lessen the extent of the
closing and alleviate the distress of breathing. This fact furnishes a
means of palliating the symptoms. (See treatment.) It explains moreover
why roaring should not be heard in quiet breathing and why it should
increase in force and in pitch as the respiration becomes more and more
hurried. It further accounts for the noise being heard only during the
act of inspiration, the outward rush of the air in the expiratory act
being of itself sufficient to carry this valvular cartilage out of the
passage and secure a free and unimpeded current.
The paralysis and wasting of the left recurrent nerve and muscles are in
their turn due to very varied morbid states.
It may commence in the larynx from distortion of its cartilages and
inflammation of the mucosa, in which case the wasting of the nerve is
probably a result of its prolonged inactivity. This mode of origin is
strongly insisted on by Percivall, and no doubt occasionally arises.
Under this explanation, however, it is difficult satisfactorily to
account for its almost invariable occurrence on the left side. The mere
fact that the horse is habitually approached on this side and more
commonly turned toward it is a most insufficient reason.
Even if admitted it utterly fails to explain the immunity of the muscles
supplied by the superior laryngeal nerve.
The fact that a horse has usually a hard and soft side of the mouth and
carries the head slightly to the latter is no better explanation, as the
tender side is not always the left.
More commonly the disease arises at some other point near the origin or
in the course of the nerve, and the changes in the larynx follow as the
consequence of deficiency or entire absence of motor innervation. Many
cases can be cited in which such an origin was unquestionable, and on
the hypothesis that this is the true and constant history of the
development of the malady, its regular occurrence in the left side, and
the absence of all signs of wasting in the muscles supplied by the
superior laryngeal nerve are alike perfectly explainable.
Let it be noted that the vagus nerves (right and left) of which the
recurrent laryngeal are branches, originate from the base of the brain,
pass down the neck beneath the jugular vein in company with the carotid
artery; that on entering the chest the right vagus nerve gives off its
recurrent branch which proceeds at once up the neck along the course of
its parent trunk till it reaches the larynx, to the muscles on the right
side of which it is distributed; that the left vagus nerve on the other
hand proceeds backward in company with the left innominate artery as far
as the base of the heart, where on about the level of the space between
the sixth and seventh ribs it gives off the left recurrent nerve; that
this left recurrent nerve closely applied at its point of origin to the
great parent arteries turns round the posterior aorta enclosing it in a
loop, and gaining the lower end of the windpipe follows its course to
the larynx. It will thus be understood how many chest diseases may
implicate the left recurrent nerve, and from which the right, which
extends no deeper than between the two first ribs, may be completely
exempt. The frequent supervention of roaring as a sequel of chest
diseases receives in this an ample explanation. Its connection with
pleurisy becomes especially probable, as the nerve lies in contact with
the surface of the pleura alike in its descending and ascending course
within the chest.
Finally the loop encircling the posterior aorta exposes the nerve to
constant stretching and shocks from the heart’s action during violent
exertions and in excited states of the circulation generally. Vaerst and
Sussdorf show that the nerve is habitually flattened between the
posterior aorta and trachea, the effect being worst when the heart’s
action is excited.
It remains to notice a few instances in which dissection established the
connection of interference with the nerve at some part of its course and
the existence of roaring.
(a.) Godine found in a roarer a tumor about the size of a chicken’s egg,
pressing on the commencement of the pulmonary artery. He attributed the
roaring to the impaired circulation of blood in the lungs by the
pressure on the artery. Considering that the tumor must have been
precisely in the situation of the left recurrent nerve at its point of
origin, it becomes much more probable that the symptom resulted from
pressure on this nerve.
(b.) The elder Bouley found in one case a considerable engorgement of
the group of lymphatic glands in the anterior part of the chest and
through the centre of which the left recurrent nerve passed.
(c.) Fergusson of Dublin dissected a roarer in which he found besides
some tumors of the lymphatic glands in the pelvic and sublumbar regions,
an indurated and enlarged gland about four inches behind the anterior
opening of the thorax. The recurrent nerve between this and the larnyx
was wasted so that its fibres could scarcely be recognized, the
laryngeal muscles on that side were atrophied, and degenerated, and the
glottis distorted and partly closed. Fergusson has in his description
made the mistake of writing the _right_ for the _left_; it is evident
that the _right recurrent nerve_ could not possibly pass through a tumor
in the situation described.
(d.) Gamgee furnishes a drawing of an immense tumor filling up the
anterior part of the chest, pressing on the vagi and recurrent nerves
and causing roaring.
(e.) The Clinique of the Alfort Veterinary School furnishes the
following among other cases of roaring consequent on inflammation of the
jugular vein. A well-bred and very fast English thoroughbred had been
used for two years by his owner who was a hard rider. In June, 1857, he
was bled as a preventive (saignée de precaution), suppurative phlebitis
was induced and was only cured at the end of six weeks. When again put
to work he proved a _roarer_ and was still affected when seen six months
later.
In connection with this it may be noted that the swelling in connection
with the inflammation of the vein extends easily to the subjacent vagus
and recurrent nerves, leading to their inflammation, functional
inactivity and atrophy. Bleeding is usually done on the left side of the
neck so that the paralysis and wasting would still be on the same side.
Happily with a more humane system of treatment, accidents of this kind
are less frequent than formerly. Glöckner furnishes a case which
followed thrombosis of the carotid.
(f) Reynal reports several cases in which _roaring_ had occurred as a
sequel of inflammations and abscess about the throat, and in which
infiltrations or gray or yellow indurations had taken place in the
areolar tissue around the vagus nerve. As nothing is more common than to
find _roaring_ resulting from severe sore throat, parotitis, etc., this
may explain its occurrence.
Mandl first carefully examined the paralyzed muscles which present to
the naked eye a flattened and wasted appearance in marked contrast to
the full well-rounded forms or those on the opposite side. They differ
no less in color. In place of the deep red of the healthy muscles those
on the diseased side are of a yellowish white hue with here and there a
pink streak indicating the position of some unchanged muscular fibre.
When placed under the microscope the healthy elements of the muscular
fibres (sarcous elements) are seen to be replaced by granules of fat.
The nerve (recurrent) is not only visibly wasted but its internal white
substance (white substance of Schwann) can no longer be recognized and
it approximates closely in character to a filament of ordinary white
fibrous tissue.
17th. Muscular paralysis due to other causes and even located in
different parts has been known to give rise to _roaring_.
Goubaux and others have noted the occurrence of roaring from paralysis
of one nostril, alike when the loss of power was special to the nasal
muscles or common to all on one side of the face.
Roaring apparently from paralysis of the laryngeal muscles has been seen
frequently in animals fed on the seeds of leguminous plants and
specially of the _Lathyrus Cicera_ (_Lathyrus Sativus Stendel_). The
whole family of the _Leguminosæ_ is open to suspicion as occasionally
containing a poisonous principle capable of inducing paralysis in
animals fed on them. The _Lathyrus Sativus_ induces paralysis in man and
the domestic animals in some parts of India (Sleeman, Irving). The
common cultivated tare (Vicia Sativa) is well known to induce general
paralysis, commencing with the hind extremities, when fed to horses at
the period of ripening in Great Britain. In France the chick vetch
(Lathyrus Cicera or Sativa) has been repeatedly noticed to lead to the
development of roaring apparently from paralysis of the laryngeal
muscles. Horses fed on 17 lbs, daily (straw and seeds) were attacked
with roaring in five days. They gained in flesh and vigor, had a smooth
shining coat and supple skin, and standing at rest presented nothing
amiss, but after ten minutes trot they were seized with roaring and if
not stopped they soon fell to the ground, with symptoms of impending
suffocation, (Delafond). Horses fed heavily on the winter vetch with cut
hay and molasses were attacked with roaring if gently exercised for one
or two minutes. It came on suddenly and threatened instant suffocation.
One horse fell and lay half an hour in a frightful state of dyspnœa.
More commonly they recovered after a few minutes rest. In the intervals
no disturbance of breathing nor any change of appetite attested the
slightest deviation from health. Reynal, Cruzel, Caffin, Motte and
Ayrault mention similar occurrences.
The paralysis of chronic lead poisoning will also cause roaring.
=Occasional or intermittent roaring.= Puzzling cases are met with in
which a horse will _roar_ at one time and not at another. In such cases
the veterinary profession has incurred an amount of odium which was by
no means deserved. Two veterinarians, equally respectable and talented,
appearing in a Court of Justice to swear to the same animal which they
had examined on different days, respectively pronounce it a roarer or a
sound horse, as it happened to be at the time of the respective
examinations. Such cases have been differently accounted for.
Slight colds or _sore throats_ may cause roaring so long as they
persist. Tight reining with the nose drawn in toward the chest induces a
stridor in certain animals by distorting the larynx and trachea. Some
horses with thick necks, badly set on heads, and in a state of obesity,
roar, yet the symptom subsides when the superfluous fat is got rid of
and they are brought into hard working condition. Stallions are very
liable to make a noise from this cause. In a case of roaring which
disappeared when the horse had been exercised for some time Leblanc
diagnosed an œdema of the glottis which was absorbed under the increased
movement of the parts. He did not test his opinion by dissection.
=Roaring sometimes hereditary.= That roaring runs in families there can
be no doubt, but the direct cause appears to be mostly the transmission
of a faulty conformation. A head with faulty shape and badly set on; a
thick, short neck, deficient in mobility, or a small, narrow chest,
predisposed to acute diseases, descends from parents to offspring,
entailing a predisposition to roaring. The large Normandy horse is
notoriously subject to roaring, but then he is equally characterized by
a big, coarse head, narrow forehead and nostrils, big jowl, and narrow
intermaxillary space. In all breeds this form is very subject to
roaring, because of the stiffness of the neck and tendency to
compression of the larynx. With the head badly set on, as it is almost
of necessity in these animals, everything is done to produce roaring.
Not only is the head cruelly reined in at work, but the horse is kept a
great part of his time in the stable in the same or even in a worse
condition, the larynx meanwhile unnaturally compressed between his
narrow jaws and the nerve compressed or the larynx distorted.
It must be added, however, that like some other acquired distortions or
alterations roaring may repeat itself in the progeny. Goodwin mentions
an instance of it on the female side through three successive
generations of thoroughbreds. Of transmission on the side of the male
the following instance is noteworthy: M. Liphaert, an extensive
proprietor in Livonia, bought a first-class English thoroughbred
stallion. His progeny were healthy until he became a roarer at ten years
old. All his foals, got after this date, followed the sire in becoming
roarers, and, it is important to observe, almost all at the age of ten
years.
_Symptoms._ These, of course, are manifest enough while the animal is
sufficiently excited to give rise to the noise. Certain indications may
be obtained even while the animal stands in the stable. If _cough_ is
excited by pinching the upper rings of the windpipe it is prolonged into
a groan. If suddenly threatened with a cane the abrupt inspiration which
results is attended by a _grunt_. The absence of these symptoms is not,
however, sufficient to establish the nonexistence of roaring. The horse
must be galloped or put to heavy draught to fully test the breathing
organs. Galloping up a steep hill is perhaps the best test. A gallop
over a recently ploughed field is about equally good. Soft pasture land
or an unpaved road is preferable to Macadam or pavement. Galloping in a
riding school on the soft tan is an excellent measure as the sound is
confined and the animal is always within earshot of the examiner. The
person examining should either ride the horse himself or have a
disinterested party, in no way connected with either buyer or seller, to
mount him. If the rider is in the interest of the seller he may contrive
to slacken the pace before he reaches the examiner, or by irritating the
horse may make it difficult to approach him immediately on his being
pulled up. If in the interest of the buyer he may succeed, by the use of
a powerful bit, in drawing the horse’s nose in to the chest, or by
compressing the larynx with a tight throat latch he may produce noise in
breathing when the animal is suddenly brought to a stand. Unless the
course is up a steep hill or over a ploughed field the horse should be
galloped for from five to ten minutes; he should be then made to pass
close to the examiner at full speed, and finally brought up suddenly by
his side and without any previous slacking of his pace. The ear should
be at once placed close to the nostrils, when the slightest abnormal
sound accompanying the inspiratory act will be at once recognized.
Draught horses are sufficiently tested by driving them in a heavy
vehicle or one with the wheels dragged. By walking alongside or keeping
the ear near to the nostrils any harsh sound additional to the normal
blowing noise of hurried breathing is easily noted.
The finger placed on the larynx detects the strong vibratory tremor, and
Friedberger notes that the left arytenoid is much more easily displaced
than the right, increasing the stridor.
If the horse is, at the time of examination, the subject of a cold, sore
throat, or other acute disease of the air passages no importance is to
be attached to any noise made in breathing, but he cannot be pronounced
a _sound_ horse until, this malady having passed off, it is found on
careful examination that no such sequel has been left.
Among the most puzzling cases are those in which the roaring occurs with
periods of intermission. If the horse has been fed for a short time on
vetches this may account for its temporary access, and unless the same
feeding is again allowed a recurrence is not to be looked for. If due to
the occasional displacement of a pedunculated tumor of the nose or
pharynx and its interference with the action of the larynx its existence
may be recognized by careful examination, diminished current of air
through one nostril, etc. But there remain some _rare_ cases in which
there are no such appreciable causes, and yet the horse would be
pronounced _sound_ or _unsound_ as examined at certain intervals. On
this subject more information is desirable.
The following varieties of roaring will be distinguished from that
of paralysis by the occurrence of the sound in both acts of
breathing (expiration and inspiration):—distortions, tumors or
foreign bodies in the nose:—tumors about the throat, in the windpipe
or bronchi:—distortion of the windpipe, from tight reining, fracture
or congenital deformity:—and the presence of a false membrane
stretching across the windpipe.
Examination by manipulation, auscultation and percussion along the whole
length of the air passages alike during rest and after exercise, may
enable one in unusual cases to recognize the structural changes that
give rise to roaring.
_Treatment._ This has long been considered as hopeless, yet preservative
and palliative measures are usually accessible, whilst even cures can be
effected in certain conditions.
_Preventive treatment._ First may be noticed the rejection for breeding
purposes of all animals possessing those conformations of head, neck and
chest already referred to as conducing to disease of the air passages or
distortion of the larynx or windpipe. Equally ought all roarers to be
set aside unless the exciting cause is accidental such as fractures of
the nasal bones, of the trachea, the existence of polypi, etc. Stallions
that make a harsh noise in breathing from an accumulation of fat about
the throat are not necessarily objectionable.
The employment of the bearing rein so as to compress and distort the
larynx is to be avoided. If bearing reins are used in horses having
short thick necks and badly set on heads and especially with
intermaxillary narrowness they should be passed through rings in the
cheek piece of the bridle or between the ears and over the forehead
(overdraw check) so that while the head is elevated the nose may be
projected forward after the Russian fashion of equitation. This measure
has indeed appeared to cure several cases of roaring. I have met with
fewer roarers in the same number of horses in America than in England,
and this I attribute to the better mode of using the bearing rein on
this side of the Atlantic.
The Chick Vetch (Lathyrus Cicera) should be excluded from the fodder of
horses or used in small proportion only. In man it is found to be
injurious when it forms a twelfth part of the bread used and gives rise
to paralysis if it amounts to a third (Aitken).
_Palliative and Curative treatment._ Medicinal treatment will prove
useless in the great majority of cases: as for example in paralysis and
degeneration of the muscles, in ossifications, fractures, or distortions
of the cartilages, etc., etc. Nevertheless where there is merely
thickening of the membrane of the larynx alterative and tonic treatment
may be successful especially if associated with iodine ointment or
active blisters applied to the throat. A case is reported by Dupuy in
which a course of arsenic cured. In these cases as well as in those due
to ulceration of the membrane the application of caustic by means of a
staff and sponge as advised in laryngitis may prove beneficial. In some
cases of this kind the application of the firing iron to the region of
the larynx has an excellent effect. Setons have proved useful in some
cases.
In cases due to tumors or enlarged glands pressing on the air passages
the internal use of iodine and other alteratives and diuretics, and the
local applications of iodine, or mercurial ointments or of blisters have
been successful. Failing in this the tumors may be removed with the
knife when accessible.
If by auscultation the existence and position of a band of lymph can be
made out, tracheotomy may be performed and the band excised. Percivall
with reason doubts the possibility of the diagnosis.
In cases due to distortion of the larynx from tight reining the bearing
reins should be dispensed with or rearranged so as to encourage
protrusion of the nose, and the horse should be bitted to the side
chains or straps in the stall several hours daily so that the head shall
be elevated and the nose protruded.
When _roaring_ depends on paralysis of the laryngeal muscles, a mode of
palliation may be adopted as practised by the London omnibus and cab
men. A strap is fixed round the nose supported by a strap passing down
the middle of the face and the cheek piece of the bridle on each side
and buckled beneath the chin. On the inner side of this strap where it
passes over the false nostrils is attached on each side a semiovoid pad
which presses on the flap of the nostril and regulates the entrance of
air. The principle on which it acts will be understood when we consider
that the paralyzed cartilage is drawn into the passage by the rush of
air and that the closure of the channel is more complete and the roaring
more marked in proportion to the force of the current. The pads by
lessening and regulating the rush of air into the lungs thus leave the
passage in reality more open and largely obviate the difficulty of
breathing and the noise.
In extreme cases with the structural lesion in the head, throat, or
upper two-thirds of the neck relief may be secured by tracheotomy.
A more radical operation is that introduced by Günther for the excision
of the left arytenoid cartilage. As improved by Möller and others this
consists in an incision through the cricoid cartilage and crico-thyroid
membrane (or even the first rings of the trachea) and the complete
extirpation of the left arytenoid cartilage and left vocal cord. The
manipulations belong to surgery. The result is satisfactory in removing
the violent dyspnœa in hurried breathing and in very favorable cases in
obviating noise altogether. More commonly some stridor remains but not
enough to interfere with pace or with heavy draft. From my personal
experience in performing the operation, I would recommend it in all
cases in which the obstruction is so great as to interfere with the use
of the horse on the track, or road, or for heavy draught. But in slight
cases, in which the disease causes little or no inconvenience beside the
noise, I would advise some less radical measure.
Another obvious line of treatment is by the use of electricity locally
and of strychnine internally. A weak current kept up for fifteen minutes
may be sent from the positive pole in the left jugular furrow to the
negative pole over the left side of the larnyx. Strychnia in the dose of
two grains may be given daily in the food or in half that amount
hypodermically over the left side of the larnyx. This would be useful
only in the early stages with little or no fatty degeneration of the
muscles.
ŒDEMA GLOTTIDIS.
Diseases Complicated by this. Seat, Abundance. Duration, Sequels,
Symptoms, sudden dyspnœa, swelling of throat, pits on pressure,
differentiation from croup. Treatment, cold, ice, astringents,
scarification, tracheotomy.
This is usually a complication of acute laryngitis, but it may be a
manifestation of other forms of local disease—tuberculosis, glanders,
purpura hemorrhagica, pseudo-membranous inflammation,—or it may be a
result of a more distant affection, like disease of the heart, lungs, or
kidneys. As a complication of local inflammation it consists in an
excessive serous exudation into the submucosa, around the base of the
epiglottis and extending to the whole larnyx and pharnyx. It may thicken
the parts by half an inch, causing complete closure of the glottis. In
favorable cases it may subside as rapidly as it rose, while in others it
may result in ulceration or abscess. The infiltration has usually a
clear watery aspect, but is sometimes a dull red. When incised an
abundance of serum escapes mixed in certain cases with pus.
_Symptoms._ In the course of one of the above named affections there
comes on suddenly extreme dyspnœa, with stertorous breathing, a
suffocative cough, and intense anxiety. The stridor is first with
inspiration and later with expiration as well. The eyes are bloodshot
and protruding, the pulse small and rapid, the movements uncertain, and
the skin moist with sweat. There is manifest swelling of the throat and
manipulation leaves the imprint of the finger.
When symptomatic of some distant affection it is at once slower in its
result and more persistent.
The local pasty swelling and the absence of any false membrane suffice
usually to distinguish it from croup which it so closely resembles in
the suddenness of its onset, and the violence of its manifestations.
The less urgent cases may be treated by application of cold water or ice
to the throat, and the injection of solutions of chloride of iron or
alum into the fauces. Or the throat may be painted with tincture of
iodine and rubbed with the palm to favor distribution and absorption of
the exudate. In dogs the mouth may be opened widely and the dropsical
membrane pricked at intervals to drain off the liquid. In the most acute
cases the prompt adoption of tracheotomy is the only means of saving
life.
LARYNGEAL HYPERÆSTHESIA. CONVULSIVE COUGH.
Convulsive cough with visible lesions—without. Excitants, cold air, or
water, rough or dusty food, irritant agents inhaled or swallowed.
Treatment, hygienic, nerve sedative, expectorant, tonics, Muriate of
ammonia, Sulphur dioxide, silver solution, ferric chloride, alum,
derivatives, elimination, aromatic, dietetic.
The chronic or paroxysmal cough may often be traced to the presence of
tumor, ulcer, local inflammation, or parasite, but in some instances no
local trouble is recognizable, the general health remains good, and yet
the throat is abnormally sensitive and a cough or fit of coughing may be
roused by passing into the cold air from a warm stable, by cold water in
drinking, by inhaling irritant gas, by the passage of rough or fibrous
food, or by handling the larnyx. There is undoubtedly a hyperæsthesia of
the larnyx and the horse and dog as being more exposed to severe demands
on the physical and nervous systems are especially liable to suffer.
_Treatment_ must be adapted to the conditions. Over-work, damp unhealthy
buildings, and all appreciable health depressing causes must be
corrected, and a course of iron and nux vomica may be tried. Borax,
bromide of potassium, and extract of hyoscyamus, made into an electuary
with molasses or honey may be smeared upon the molars four or five times
a day. In obstinate cases the inhalation of the fumes of burning
salammoniac or sulphur, or the direct application to the larnyx of
dilute solutions of silver nitrate, ferric chloride, or alum may
benefit. The throat may be blistered by cantharides or mustard. Care
should be taken to keep the functions of bowels and kidneys normally
active, to protect the patient against cold and damp, and to give
nutritive but non-stimulating and easily digested food, as for the
horse, bran mashes, roots, grass or scalded hay, and for the dog pulped
flesh, soup and mush. Sometimes benefit can be obtained from the
vegetable aromatics and stimulants as eucalyptol, tar, turpentine,
balsams of Tolu and Peru, tincture of anise, fennel, etc.
INFECTIOUS DISEASES OF THE THROAT.
Infectious throat diseases. Parasites, Leeches. Œstrus larva. Chronic
sore throat. Mechanical removal.
Infections are in many respects the most serious affections of this
region but their consideration must be sought under strangles,
distemper, diphtheria, anthrax, actinomycosis, tuberculosis, glanders,
etc.
PARASITES OF THE THROAT.
=Leeches.= These taken in with the water will sometimes fasten
themselves on the walls of the pharnyx or even on the lips of the
larnyx, producing cough, sore throat, difficulty of swallowing, bleeding
from the nose (or mouth), or dyspnœa. They are to be removed as
recommended above under parasites of the nasal chambers.
=Œstrus Larva.= =Bots.= In horses and mules the larva of the œstrus
sometimes attaches itself to the mucous membrane of the pharynx or even
of the larynx producing chronic irritation, cough and even dyspnœa. A
chronic sore throat with nasal discharge, occurring in autumn or winter,
in the absence of fever or constitutional disorder may be found to
depend on these parasites and to recover when these have been removed by
the hand.
GUTTUROMYCOSIS OF SOLIPEDES.
Aspergillus. Complications, ulceration, lesions of adjoining parts,
food in lungs, hepatization, gangrene. Treatment, by incision, sulphur
dioxide, iodine.
Rivolta and Bassi have found in the guttural pouches of horses and a
mule, an advancing ulceration of the mucosa partially covered with
crusts composed largely of the mycelium, conidia and spores of
Aspergillus or a closely allied fungus. In the mule the ulcer had opened
into the carotid artery causing a profuse epistaxis. In the three horses
there was dysphagia, and the food, descending to the lungs, had caused
pulmonary hepatization and gangrene. The description of the ulcers led
Raillet to infer the existence of glanders and that the presence of the
aspergillus was accidental, rather than a causative factor. In parallel
cases the opening of the guttural pouch and injection with sulphurous
acid solution or dilute solution of iodine would be appropriate
treatment.
DISEASES OF THE CHEST.
Cough, its artificial production, precautions, character in different
animals. Cough in disease, strong, full, ringing, weak, short, broken,
abortive, dry, rasping, croupy, small, husky, soft, humid, rattling,
mucous, paroxysmal, sympathetic, wheezing, roaring, whistling, grunt,
moan. Expectoration, nasal in horse, also buccal in other animals.
Morbid expectoration, watery, viscid, cloudy, flocculent, purulent,
rusty, cretaceous, parasitic, fœtid, varicolored, microbic. Expired
air, warm, cool, vegetable odor, acid, fœtid, heavy. Respiration,
number in health, alteration in disease, rapid, slow, tardy, short,
catching, quick, deep, labored. Position, standing, lying. Pleuritic
breathing, broken winded.
Before describing specific diseases, it is needful to consider the
methods of physical diagnosis which enable the practitioner to
differentiate the diseases of the chest. Some of the following remarks
will bear equally on diseases of the nose and throat as well.
COUGH.
The cough so varied in health and in disease deserves careful practical
study. It can usually be excited in solipedes, sheep and dogs by
pinching the first ring of the windpipe between the thumb and first two
fingers. In oxen it is best produced by compressing the anterior part of
the larynx. In old cattle it is difficult to produce coughing. In no
animal should the attempt be made rudely nor unnecessarily repeated, as
it may tend to excite or to aggravate already existing sore throat.
The cough of the healthy _horse_ is _sharp_, _loud_ and _ringing_, often
repeated two or three times and followed by a snort (clearing of
himself). It is weaker in young horses and shorter and drier in the
aged.
The usual cough of the _ox_ is _weak_, _dry_, _slightly husky_ and
_prolonged_.
That of the _sheep_, _small_, _weak_ and _dry_.
That of the _dog_, also weak and dry.
A =strong, full, deep, ringing cough= is rarely heard in disease except
in slight irritation of the larynx. In such cases the larynx is tender
and slight handling or pinching develops the cough.
A =weak cough= wanting in resonance and heard only at a short distance
from the horse, is usually associated with chronic chest diseases and
the last stages of acute thoracic inflammations.
A =short=, =broken= or =abortive cough= is one which appears to be
suddenly cut short and suppressed, from the pain it causes. It is seen
in the early stages of inflammations of the serous membranes of the
chest or abdomen, when the quick rubbing of the dry and inflamed
surfaces of these membranes on each other produces exquisite pain. It
characterizes especially the _debut_ of pleurisy, pleuro-pneumonia and
peritonitis. This cough is infrequent for the same reason that it is
short.
A =dry=, =loud=, =rasping=, or =croupous cough= is peculiar to the early
stages of laryngitis, tracheitis and bronchitis, when the membrane is
swollen, tense and dry. It is equally met with in diphtheritic and
croupous affections implicating the larynx.
A =small=, =weak=, =dry=, =husky cough= without any _rasping_ is
characteristic of broken wind (heaves) emphysema of the lungs, asthma,
or chronic bronchitis.
A =soft=, =humid= or =rattling cough= exists in the advanced stages of
laryngitis, bronchitis and pneumonia when the activity of the
inflammation has given way and a free exudation has taken place from the
mucous membrane. It is usually accompanied by a discharge, in solipedes
from the nose, and in other animals from nose and mouth.
A =soft cough= with a peculiar gurgling in the larynx is sometimes met
with in croup.
A =paroxysmal cough= is one repeated five, ten, or twenty times in rapid
succession. It is common in chronic bronchitis, early heaves, emphysema,
verminous bronchitis and influenza. In such cases it is observed chiefly
when the subject is brought out to the cold air, when he takes a drink
of cold water, or when he has just had some active exertion, or some
dusty or fibrous food.
A =symptomatic cough= is one due to disease in some other organs than
the respiratory, and which irritates the air passages through nervous
sympathy (reflex action). It is commonly small, short and dry.
Inflammation or other disease of the liver, indigestions and intestinal
worms are occasional causes of symptomatic cough. In the case of worms
it may be loud, clear and ringing.
OTHER MORBID SOUNDS.
Besides cough may be noticed the _wheezing_ breathing characteristic of
_broken wind_, _chronic bronchitis_ and _asthma_, _roaring_,
_whistling_, etc., as already described, and the sound between a _moan_
and _grunt_, produced in pneumonia especially in the ox.
EXPECTORATION.
This escapes almost exclusively by the nose in horses, because of the
length of the soft palate. It may come from the mouth of other animals,
especially when they cough. In the ox the discharge from the nose is
rarely seen because of his licking it out with his tongue. Rattles
(râles) in the larynx, trachea or bronchia, enable us to ascertain the
source of such discharges.
The nasal discharge in acute catarrh, laryngitis or bronchitis, is thin,
clear, and slightly viscid, becoming thick, whitish and flocculent as
the disease advances. It is yellowish, thick, flocculent and intermixed
with shreds of false membranes in diphtheria or in the croup of young
foals and calves. It is clear, slightly viscid and watery at the onset
of bronchitis. At the debut of pneumonia it is often reddish (rusty). It
is bright, red, frothy and bloody in hæmoptysis. It is scanty, clear,
watery, and containing minute white flocculi in pulmonary emphysema
(broken wind). It is white, thick, curdy, and devoid of viscidity in
chronic bronchitis or when a pulmonary abscess is being emptied. It is
grayish, thick and flocculent in advanced pneumonia in the horse.
Cows in the advanced stages of pulmonary tuberculosis expectorate a
yellowish, sticky matter containing minute hard masses often cretaceous.
Calves and lambs suffering from strongyli in the lungs expel these in
little pellets in the midst of a thick white material.
The expectoration is fetid, dark red and grumous in gangrene of the
lungs.
In pulmonary tuberculosis and glanders the expectoration usually
contains the respective bacilli.
CHARACTER OF THE EXPIRED AIR.
The breath is sensibly warmer in excited breathing, high fever, and
acute bronchitis and pneumonia. It is cool in most chronic diseases, in
advanced consumption and hydrothorax. Its odor is vegetable and acid in
the acute indigestions of cattle, and fetid in many chronic diseases of
the air passages attended with destruction of tissue, or the escape of
imprisoned pus, but especially fetid in gangrenous sore throat or
gangrene of the lung.
MODIFICATION OF THE RESPIRATION.
The number of respirations in a given time may afford valuable
indications in the horse but in the other domestic animals variation in
number imports little. In the ox for instance, the respirations in
health may vary from twelve to eighty per minute, according to the heat
of the cowhouse, the plentitude of the abdominal organs and other
circumstances. So in the sheep and dog slight causes, quite compatible
with health, may cause the breathing to become short, panting and
hurried.
The young horse breathes ten to twelve times per minute, the adult
animal nine to ten. Any excitement accelerates. A horse walked a few
hundred yards had the respirations increased from ten to twenty-eight
per minute; after trotting five minutes they numbered fifty-two; after
galloping five minutes sixty-five.
=Hurried breathing= occurring independently of exercise, heat of the
atmosphere, or distension of the abdomen, is indicative of fever,
especially if associated with rapid pulse and increased heat of the
body.
Infrequent respiration appears in certain brain diseases in the
intervals between the more violent paroxysms, also in poisoning by opium
and other narcotics. =Tardy or slow respirations= differ from those last
noticed in the act occupying a longer time. In infrequent breathing the
act may be short, though there are few respirations in the minute. This
is likewise seen in brain diseases and sometimes in broken wind. In the
last case there is =double action of the flank=, each act of expiration
being effected by two successive and distinct elevations of the flank.
=Quick breathing= in which the act occupies only a short time is usually
abruptly cut off, the inspiration terminating by a catch or jerk. It is
significant of the early stage of pleurisy, and arises from the desire
to avoid the pain attendant on the rubbing together of the inflamed
surfaces during deep inspirations. It is further seen in tetanus,
peritonitis, pericarditis and pleurodynia.
=Deep breathing= with great lifting of the flanks and loins is
characteristic of water in the chest, and consequent inability to
inflate the lungs.
=Labored breathing=, which is at once hurried, deep, and without
intermission, is seen in severe laryngitis, croup, capillary bronchitis,
and pneumonia, in all cases alike from the difficulty experienced in
introducing into the lungs the requisite amount of air. It is especially
marked in double pneumonia, pleuro-pneumonia, complicated with effusion
in the chest, and in old standing _broken wind_ with dilatation of the
right heart.
In all such cases where there is much interference with the æration of
blood, whether from obstruction to the circulation of blood or a
hindrance to the introduction of air, the horse invariably stands. The
fact that he has lain down may be taken as an indication that
improvement has taken place. The peculiarity is due to the sharp outline
of the horse’s sternum inferiorly so that in lying down he is compelled
to rest on his side and the whole weight of the body tends to compress
the chest. In the ox, sheep, pig and dog, which can rest on the sternum,
breathing can be carried on with comparative ease in the recumbent
position, and these animals accordingly do not necessarily stand except
in very extensive and violent affections of the chest.
The occurrence of a short inspiration suddenly checked and a prolonged
expiration characterizes pleurisy, the check to the inspiratory act
being because of the pain caused by dilating the thorax.
The double lifting of the flank in expiration:—the act appearing to be
performed by two distinct and successive acts is one of the most
prominent symptoms of broken wind, but is not peculiar to this disorder.
In the horse it exists in chronic bronchitis, dilatation of the right
heart, old standing hydrothorax, and diaphragmatic hernia. It is further
frequent in the acute diseases of the chest. In oxen it accompanies
pulmonary emphysema, pulmonary consumption, dilatation of the heart,
foreign bodies in the heart, and dropsy of the pericardium.
If accompanied by clear resonance over the chest, a permanent wheezing
noise heard over the ribs, and the small, weak wheezy cough, it
indicates emphysema (broken wind). If with strong impulse of the heart
against the ribs behind the elbows, venous pulse in the jugulars, and
modification of the second sound of the heart, it bespeaks cardiac
dilatation or other heart disease. If with paroxysmal cough, white curdy
nasal discharge and harsh rasping sounds heard at the lower part of the
trachea or along the upper part of the lungs it betrays chronic
bronchitis.
RELATIVE POSITION OF THE LUNGS, HEART AND OTHER ORGANS IN THE DIFFERENT
DOMESTIC ANIMALS.
Relative positions of thoracic organs. Diaphragm, heart, lung, in
horse, ox, sheep, pig, dog. Palpitation.
The _chest_ is that portion of the trunk closed in on each side by the
ribs, above by the bones of the back, below by the breast bone, and
behind by the diaphragm. It forms thus a cone flattened from side to
side anteriorly, and with its base, represented by the diaphragm which
slopes obliquely from above downward and forward and bulges forward in
the centre to a greater or less extent according to the plenitude of the
stomach and bowels. It results from this arrangement of the diaphragm
that a very thin layer of lung only reaches to the posterior part of the
chest, and that beneath this are solid and hollow abdominal organs which
modify the results of physical examination.
In the =Horse= the anterior third of the chest is covered laterally by
the bulky and muscular shoulders so that it cannot be satisfactorily
examined. In the median line of the chest, at a point corresponding to
the third, fourth, fifth and sixth intercostal spaces, is lodged the
heart. It deviates slightly to the left side below and by virtue of a
notch in the lower border of the lung is enabled here to reach the
surface and its beats may be felt by the hand laid on the side of the
chest just behind the left elbow.
In the =Horse= the diaphragm is attached by its outer border to the last
rib, and to the lower ends of all the asternal ribs, and the extremity
of the breast bone. A thin layer of lung accordingly extends to between
the two last ribs superiorly and down to near the lower end of the
asternal ribs. The subjacent abdominal organs are arranged as
follows:—_On the left side_, and counting from below, the large
intestines (double colon), the stomach and spleen and a portion of the
left lobe of the liver:—_on the right side_, below, the large
intestines, above, the liver and pancreas. Of these the stomach and
intestines frequently contain gases, while the liver by its solidity
gives a special solid character to the right posterior part of the
chest. The spleen is too deeply situated to affect much the results of a
physical examination. The greatest substance of lung is between the
upper and middle thirds of the thorax. The anterior third is
inaccessible on account of the shoulders, but more than usual may be
reached by raising the fore limb and drawing it forcibly forwards. The
space between the third and seventh ribs is occupied by the solid mass
of the heart, which especially modifies the result of physical
examination on the left side where a notch in the lung allows it to
approach the surface.
In the =ox= the diaphragm is only attached to the last rib for two or
three inches at its upper extremity; it is fixed to the second last rib
as far down as about one-third of its length; thereafter it is attached
in succession to the middle third of the third last, to the lower third
of the fourth last, to the lower ends of the next two in succession and
to the sternum. The result is that the lungs do not extend so far back
relatively to the ribs as they do in the horse. They are virtually
absent from the last intercostal space, present only in the upper third
of the second last, in the upper two-thirds of the third last and reach
the lower third only in the space between the ninth and tenth ribs. The
paunch alone occupies the space beneath the asternal ribs on the left
side, and the liver and the solid mass of the omasum and abomasum that
beneath the right. The shoulders in fat improved beef breeds absolutely
prevent examination of the anterior third of the chest, though in thin
animals and dairy breeds and scrubs more of this may be exposed by
raising the fore limb than in the horse. The heart corresponding in
position to the third, fourth and fifth intercostal spaces is more
completely covered by lung tissue and does not strike the left side so
forcibly as in the horse.
In the =sheep= the lung extends to the last intercostal space, nearly as
far as its lower end and the heart is covered on the left side as well
as on the right by lung tissue. The shoulder is very movable and unless
in very fat animals allows of an examination of the greater part of the
anterior third of the chest.
In the =pig= fat and indocility combine to defeat our purpose in
examination of the chest. If these can be obviated it is well to know
that the diaphragm is attached to the upper two-thirds of the last rib,
and to the next three in front above their lower third.
In the =dog= the diaphragm is attached to the upper two-thirds of the
last rib, to the lower third of the next and to the lower ends of the
two following and to the breast bone. The shoulders are so mobile and
the breast bone so thin that nearly all the chest may be satisfactorily
examined. The heart, covered on both sides by lung, lies nearly
horizontally on the breast bone, through which its position and bulk may
be clearly made out by percussion.
EXAMINATION BY TOUCH.
Pressure by the fingers in the spaces between the ribs corresponding to
the pleura will cause flinching and perhaps grunting in pleurisy. The
same result will be seen in pleurodynia. In hepatized lung and pleurisy
with adhesions there is a diminished sense of the movement felt in the
intercostal spaces of the part in health.
PERCUSSION.
Methods. Tissues as good and bad conductors of sound. Immediate,
mediate percussion. Bilateral symmetry and divergence. Effect of
building, race, etc. Horse, left side, right. Ox, left side, right.
Effect of 1st and 3d stomachs, liver, etc. Sheep, diaphragm, heart.
Pig, fat, lean, heart. Dog, method. Birds, back, ribs. In disease,
increase, decrease, absence of resonance, in large area, in patches.
Crack pot sound.
This consists in striking the walls of the chest so as to bring out the
resonance of the parts. In proportion as we tap gently with the tip of
the finger or strike forcibly with the closed fist will we elicit the
sounds from the superficial or the deeper parts of the lung. Hence
slight blows only must be used when the lung tissue is thin, to avoid
bringing out the resonance from the deeper seated organs, and both must
be resorted to when the lung is thick to ascertain its condition at the
various depths. Where a moderate force is requisite the four fingers and
thumb of the right hand are brought together in a line and the weight of
the hand as moved from the wrist is employed to bring out the sound. The
ribs being hard convey sound best from the deeper parts, and on them
percussion is usually made. Care should be taken not to mistake the
lesser resonance conveyed through the soft tissues of the intercostal
spaces for an indication of a diseased condition. In proportion too as
the ribs are covered with flesh or fat, the resonance will be diminished
and a stronger blow will be necessary to bring out the sound from the
lungs.
If the blow is made directly on the side of the chest the percussion is
called _immediate_; if made upon an elastic solid body (pleximeter) laid
on the outside of the chest it is _mediate_. The readiest and perhaps
the best pleximeter is the middle finger of the left hand which is to be
applied flat upon the side of the chest to receive the blow directed
perpendicularly to its surface. In fat or fleshy subjects it should be
pressed firmly on the surface so as to compress and condense the soft
parts and render them better conductors of sound. Some use flat pieces
of ivory, silver, caoutchouc but in employing these the nails of the
right hand must be carefully pared, lest by striking the solid body they
produce a sound which interferes with the true pulmonary resonance.
In examining the chest the two sides should be compared and if allowance
is made for the dulness felt in the lower half immediately behind the
left elbow caused by the position of the heart, and the deadness of the
sound on the last few ribs on the right side where the liver is
situated, any further deviation from a bilateral symmetry of sound is
indicative of disease. The general resonance will be decreased by a full
stomach which prevents the full inflation of the lungs, and it will be
increased if the animal stands on a wooden floor with an empty space
below. A short statement of the degrees of resonance over the different
parts of the chest in the various races of the domestic animals in a
state of health may prove useful.
=Horse.—Left side.= In the upper third the resonance is full behind the
shoulder. It diminishes from the 13th rib backward and from the
decreasing thickness of lung the blows should become less and less
powerful. In this space forcible striking brings out the drum-like
resonance of the abdominal organs.
In the middle third the sound over the 5th and 6th ribs is distinct but
not full; it increases to the 11th rib and then decreases to the last.
In the lower third a very slight resonance may be observed over the 4th
rib.; over the 5th, 6th, and 7th, where the heart approaches the surface
the sound is dead; while from this to the 13th rib a slight resonance
may be made out.
=Right side.= The upper third resembles that on left side from the
shoulder as far back as the 13th rib behind which anything above the
gentlest blows brings out a drum-like sound from the large intestine
(double colon) especially. This is clear when that is distended with
gas.
In the median third the resonance resembles that on the left side. In
the lower third it equally corresponds as far as the seventh rib behind,
which sound is dull because of the proximity of the liver.
=Ox.—Left side.= The upper third is clear in sound from the eighth to
the tenth ribs, and behind this by gentle tapping to the second last
(twelfth). Forcible striking, however, brings out the drum-like sound of
the upper sac of the paunch which always contains more or less air.
The middle third has a clear resonance as far as the seventh rib; this
diminishes to the ninth, behind which it is usually replaced by a
dullness due to the presence of food in the anterior part of the paunch.
By drawing back the limb percussion may be employed over the first and
second ribs as well.
In the lower third the first two ribs can be examined and a clear sound
should be educed. On the fourth, fifth and sixth ribs there is a full
resonance, the heart being here covered by lung tissue, contrary to the
condition in the horse. From the seventh the sound becomes duller and
the dead sound from the food in the rumen characterizes the lower fourth
of the ninth rib.
=Right side.= From the shoulder the resonance gradually decreases in the
upper third to the eleventh rib, beyond which the sounds obtained are
only from abdominal organs. In the middle third considerable resonance
is met with over the first and second ribs, it is very full and clear
over the fifth, sixth and seventh, whence it decreases and is quite lost
behind the tenth. In the lower third a clear sound can be elicited over
the first, second, fourth, fifth and sixth ribs; this is lessened over
the seventh and eighth, and completely lost behind the ninth. Any but
the slightest blows over these three last ribs brings out the dull,
solid sound from the liver.
A very full paunch greatly increases the anterior convexity of the
diaphragm, and compresses the lungs into the anterior part of the chest.
If the contents of the rumen are solid the resulting dullness on
percussion might be mistakenly supposed to indicate consolidation of the
lung. This source of error must be carefully guarded against.
=Sheep.= Percussion in the sheep differs from that in the ox chiefly in
the following particulars: The diaphragm being attached to the last rib
as in the horse, the diminishing resonance of the lung may be traced as
far back as in that animal. Thus a pulmonary sound can be obtained in
the upper third as far as the last intercostal space, in the middle as
far as the second last, and in the lower as far as the fourth from the
last. Over the lower part of the fifth and sixth ribs on the left side
the resonance is remarkably clear owing to the great relative thickness
of the anterior lobe of the left lung which here covers the heart.
=Pigs.= In fat pigs the results are almost negative. In lean animals the
middle third on each side gives out a clear resonance behind the
shoulder as far as the seventh rib, from which it diminishes to the
second last (thirteenth). The sound is less clear in the upper and lower
thirds. On the fifth intercostal space below, and on the left side the
sound is dull owing to the exposure of the heart through a slight notch
in the lung.
=Dog.= Percussion is very satisfactory in this animal because of the
amplitude of the chest, the thinness of its walls and the small bulk of
the abdominal organs. In the upper and middle thirds on both sides alike
the sound is clear and full as far back as the seventh rib, whence it
decreases to the last. In the lower third a distinct but moderate sound
marks the first eight ribs and is equally clear on the right and left
sides. The thinness of the lung in its posterior part demands that
percussion be effected by the middle finger only, without any movement
of the hand. Unless the dog is very fat, good results may be obtained by
percussion over the first and second ribs, the shoulder blade and
breastbone.
=Birds.= In these and especially in the webfooted (ducks, geese) the
sternum is so thickly covered by flesh that no result can there be
obtained. Beneath the wings, however, and upon the back percussion
through the medium of a small coin as a pleximeter and with the middle
finger alone, is valuable. Beneath the wing a clear sound may be drawn
out over nearly all the ribs and on the back over a less extent (two and
a half to four inches, according to size).
PERCUSSION IN DISEASE.
=Increase= of resonance without any perceptible modification in
character is usually partial and depends on the increased distension of
the air cells of one lung, or part of a lung, to make up for the loss of
a part or a whole lung through hepatization or pressure by false
membrane or from water in the chest. If a part of a lung is solid and
impervious it gives a dull, dead sound, contrasting strongly with the
increased clearness of the remainder. So with water in the chest, the
clearness of the upper parts contrasts unmistakably with the dullness of
the lower. By watching the advance or retirement of these symptoms the
solidification of a lung and its process of clearing up, and the
effusion of water in the chest and its removal may be equally traced
through all these stages.
If the increased clearness is confined to the upper, lower, or posterior
border of one or both lungs, the sound being natural over all other
parts, it indicates the existence of emphysema of the lungs, a condition
almost constant in broken winded horses.
If the sound is drum-like over most of the lung it is due either to
extensive emphysema or to the presence of air as well as liquid in the
cavity of the chest. In the case first noticed there will be the double
action of the flank, the weak, dry, husky cough and the wheezing
breathing; in the last there will have been the previous attack of
pleurisy, and the application of the ear to the chest will detect a
splashing sound constant or heard only at intervals or on rising. This
should be carefully distinguished from abdominal gurgling.
=Diminished= resonance, noticed over an entire lung, may be due to
congestion or œdema of the lung, to the formation of a thick false
membrane over the inner surface of the ribs or to a false membrane
enveloping the lung and preventing its due distension. Congestion will
be distinguished by the blueness of the mucous membranes and the
presence of a crepitant sound heard on auscultation. Pleurisy is known
by the tenderness on percussion or on pinching the intercostal spaces,
and by the presence in many cases of a friction sound. The sound may be
further lessened in cattle by the deposit of tubercle on the inner side
of the ribs, or the extensive deposition of miliary tubercle throughout
the substance of the lung.
=Absence= of resonance, the sound brought out by percussion being
similar to that obtained by practising it over the muscular masses of
the haunch, is always partial. It is due either to hepatization or to
water in the chest. Hepatization is distinguished by its rarely
affecting the lower thirds of both lungs at once, by the presence of a
crepitating râle round the margin of the area of dullness, and by the
increased resonance and respiratory murmur over the sound parts of the
same and the opposite lung. In water in the chest on the other hand a
friction sound and much tenderness precedes the dullness; the tenderness
continues and the dullness reaches the same height on both sides of the
chest, in the case of the horse. In the ox, water may exist on one side
of the chest only, but the tenderness on pressure and the absence of any
crepitation serve to distinguish the case from pneumonia. In the smaller
animals the position of the dulness may be altered by turning the
patient on its back as the water always gravitates to the lowest point.
The presence of extensive deposits of tubercle, of cretaceous material
in tubercular cows and sheep, and the presence of large cysts in the
lung may give rise to dullness over a circumscribed area. Such areas of
dullness are usually multiple with sound lung between.
A further modification known as the =cracked pot sound= is sometimes
heard in horses and cattle. It may be aptly represented by laying the
palms of the two hands together in such a way that they meet all round
and leave an interval filled with air right in the centre. The back of
the one hand is then struck against the knee when the noise of the air
escaping gives the characteristic sound. It occurs in consumption or in
the advanced stages of inflamed lungs when a large tubercle or abscess
has burst into a bronchial tube and the resulting cavity opens into this
tube by a narrow orifice.
AUSCULTATION.
Mediate and immediate auscultation. Methods, quiet, normal chest
sounds, tubal, bronchial, vesicular, respiratory, cardiac. Juvenile
respiratory murmur. Horse, left side, right. Ox, left side, right.
Accidental sounds, rumbling, gurgling, crepitation, friction. Sheep,
special features. Goat, force. Pig, Dog, Birds, morbid chest sounds.
Increase, general, partial. Decrease, general, partial. Absence.
Bronchial sound in excess, in improper place. Cavernous, amphoric,
mucous sounds. Râles, sonorous, sibilant, mucous, submucous,
crepitant, subcrepitant. Creaking, metallic, tinkling, gurgling,
splashing, friction. Timbre of Cough. Palpitation. Mensuration.
This is a term used in medicine to denote the mode of exploring an organ
by applying the ear over the region in which it is situated and deducing
the healthy or diseased condition by the sounds heard. First employed by
Lænnec in human medicine it was quickly availed of for the lower animals
by Delafond and Leblanc.
Auscultation is =mediate= or =immediate=. =Immediate Auscultation= is
practised by applying the ear directly upon the skin, either bare or
covered with a handkerchief. In =Mediate Auscultation= an instrument
called a stethoscope is employed to convey the sound from the surface of
the body to the ear of examiner. The common stethoscope is formed of
soft wood (cedar or ebony) or of gutta percha, is from five to seven
inches long and a quarter of an inch in the bore. The end applied on the
skin is widened into a funnel three-fourths of an inch across at the
mouth; the opposite end is flattened out to apply to the ear, is about
two inches in diameter and has a hole in the centre to convey the sound.
A flexible stethoscope is also used either with one or two ear pieces
and though less convenient in general than the common variety possesses
this advantage when the heart is being examined that it conveys the
sound without the impulse of that organ.
In mediate auscultation the ear should be closely applied to the
surface, the right ear being used for the left side and the left ear for
the right, but a preference should always be exercised in favor of that
in which the sense of hearing is most acute. If a handkerchief is used a
single fold only must be applied, otherwise the two layers may rub on
each other and produce distracting sounds. In mediate auscultation the
instrument should be held perpendicularly to the surface, accurately
applied alike to the skin and the ear, and pressed firmly on the surface
to condense the soft structures beneath the skin and render them more
conducting. If held by the hand care must be taken to avoid the
slightest movement of the fingers on the stethoscope, and long hairs
should be prevented from entering the tube as being likely to produce
additional sounds.
Among other points the following must be attended to in auscultation.
Avoid a position in which the animal can strike you with its hind limbs.
If necessary in irritable or ticklish subjects have one fore leg held
up. Select a quiet time and place, early morning or night is usually
best. Endeavor to protect the patient from the irritation of insects or
the examinations may be fruitless. Never auscultate over a contracting
muscle; the sound of muscular contraction will prevent a correct result.
If the natural sounds are indistinct increase them by exercise. The
smaller animals are examined with the greatest facility standing upon a
table or held in the upright posture with the body resting on the thighs
or on the hind feet only. Birds can be held by the wings which may be
raised and drawn inward towards the median line to expose the back and
sides of the chest.
HEALTHY CHEST SOUNDS.
In all healthy animals two distinct sounds are heard over the chest:—the
=tubal= or =bronchial= sound, and the =vesicular= or =respiratory
murmur=. The =bronchial sound= caused by the air sucking through the
larger bronchi is best heard by applying the ear to the breast over the
lower end of the windpipe or to the upper third of the chest immediately
behind the shoulder. The respiratory murmur is clear and full in the
middle third of the chest immediately behind the shoulder. It is louder
and more prolonged in inspiration than in expiration and in the right
lung than the left especially in cattle and sheep in which the former is
more capacious. It is louder in young animals than in old, hence the
name of =juvenile= respiration applied by Leblanc. In thin animals it is
better heard than in fat ones, the chest walls being thinner, firmer,
and more conducting. In animals of a nervous temperament like the
English racer it is more distinct than in the Norman, Clydesdale and
other heavier breeds. Deep, broad capacious chests emit a stronger sound
than such as are shallow, narrow and short. Exercise, fear or any
excitement accelerating the respiratory act increases the sound. A full
stomach, certain narcotics and other depressing influences lessen it.
Other things being equal the sound is lower in cattle and sheep than in
other domestic animals.
=Horse.= The ear pressed strongly upon the breast where the windpipe
enters detects a strong blowing sound referable to the lower end of the
trachea and the bronchi. In young foals a respiratory murmur is heard
when the stethoscope is applied in front of the shoulder, the limb being
meanwhile drawn backward. A similar murmur may be heard, but less
distinctly over the shoulder blade at this age.
=Left Side.= _Behind the shoulder_ in the _upper third_ of the chest the
sound is loud and somewhat harsh, the respiratory murmur being here
supplemented by the noise of the air rushing through the larger
bronchia. From the 13th rib the respiratory sound is alone heard and
becomes weaker to the second last (17th).
In the _middle third_ the respiratory murmur is moderately clear from
the 4th to the 6th rib, it becomes louder and clearer to the 9th from
which its force gradually diminishes and is lost over the 16th. In the
_lower third_ over the 4th, 5th, and 6th ribs the respiratory sound is
replaced by the sounds of the heart, each beat being distinctly divided
into two sounds, the first dull and prolonged, the second short and
quick. The respiratory murmur is heard over the 7th and 8th ribs, is
weaker on the 9th and lost over the 10th. In the middle and lower thirds
but especially towards the posterior part of the chest, abdominal sounds
are often heard. They consist chiefly in gurgling or in a noise like
that caused by the air rushing into a bottle which has been turned upon
its side when full of water. Such sounds are easily distinguishable from
those occurring in a diseased chest as they bear no relation to the
rhythmical action of breathing.
=Right Side.= In the _upper and middle thirds_ the sounds do not differ
from those of the left side. In the _lower third_ the respiratory sound
is clear from the 4th to the 7th ribs; from this it decreases and is
lost at the 10th.
=Ox.= In very lean cattle the respiratory murmur heard in front of the
shoulder and over the scapula is more distinct than in the same region
of the horse.
=Left Side.= In the _upper third_ a clear respiratory murmur is heard
over the 8th, 9th and 10th ribs but is lost about the 11th. In the
_middle third_ the vesicular sound is feeble at the lower margin of the
region and immediately behind the shoulder because of the proximity of
the base of the heart. Towards the upper margin it is loud and harsh
being complicated by the _tubal_ sound. It is full and clear over the
7th rib whence it decreases in force to be lost at the 11th above and
the 10th below. In the _lower third_ the double heart beat is alone
heard over the lower part of the 4th rib, the respiratory murmur
reappears over the 5th and 6th whence it becomes weaker and is lost at
the lower and upper margin of the region respectively over the 8th and
9th ribs.
=Right Side.= The sounds of the _upper third_ simply repeat those of the
left side. In the _middle third_ the chief difference is the greater
clearness and strength of the respiratory and tubal sounds immediately
behind the shoulder. In the _lower third_ a moderately strong
respiratory murmur is rendered harsh by a tubal sound due to the
proximity of the large bronchus going to the anterior lobe of the right
lung. The respiratory murmur continues with diminishing force to be lost
over the 8th and 9th ribs.
=Accidental but healthy Sounds.= These are more loud and frequent in the
ox than in the horse. There is the same irregular rumbling and gurgling
especially on the posterior parts of the chest. Gurgling as from a full
bottle inverted is often clearly heard over the last six ribs on the
left side, and appears due to the passage of liquids between the paunch
and honey comb bag. An occasional sound as of water falling into an
empty barrel is heard in the same region in cases of slight tympany and
after saliva has been swallowed. Rumbling sounds are chiefly heard over
the last ribs on the right side where the large and small intestines are
situated. The superadded sounds in the ox are those of _crepitation_ and
_friction_. The _crepitation_ or fine crackling due to a dryness of the
areolar tissue under the skin is frequently present in oxen in average
health. A fine _crepitation_ is also heard on the left side from the
bursting of myriads of minute bubbles of air generated among the
contents of the paunch during the process of digestion. This is
especially marked after the animal has fed on green food or potatoes. A
loud _friction_ or _rubbing_ sound, which may be imitated by placing the
back of one hand upon the ear and rubbing the palm of the opposite hand
upon it, is likewise heard over the left side after eating. It is
produced by the movements of the paunch during contraction and not being
synchronous with the respiratory acts cannot be confounded with the
friction sounds of pleurisy to be hereafter noticed.
=Sheep.= The diaphragm being attached to the last rib as in the horse
the respiratory murmur may be heard to the second last. The shoulders
being more movable than in the ox the anterior part of the chest can be
more satisfactorily examined. The vesicular murmur is heard along the
whole lower third on the left side though the heart sounds are
superadded over the 4th, 5th and 6th ribs. Crepitation from the
subcutaneous areolar tissue is rarely heard. Otherwise the sounds of the
chest and abdomen correspond to those of the ox.
=Goat.= This animal differs from the sheep mainly in the greater force
and clearness of the respiratory murmur.
=Pig.= It seems ridiculous to speak of auscultating the pig, yet he is
sometimes thin enough and quiet enough to permit of one obtaining
satisfactory results. Gentle treatment and scratching the back and
abdomen will often persuade him to be temporarily quiet and docile. The
vesicular murmur is very clear in the middle third of the chest on
either side, but diminishes gradually on the last six ribs, and
disappears on the second last. It is much less intense in the upper and
lower thirds. In the posterior part of the chest rumbling and gurgling
abdominal sounds are frequent.
=Dog.= The respiratory murmur is very clear over the whole chest. It is
most intense along the middle third and becomes less clear on the 4 or 5
last intercostal spaces. The mobility of the shoulder permits an
examination of nearly the entire chest. The respiratory murmur may be
heard over the entire length of the lower third on the left side though
the heart’s sounds are equally heard over the 4th, 5th and 6th ribs.
Rumbling and gurgling abdominal sounds are much less frequent than in
herbivora and omnivora.
=Birds.= The respiratory murmur is loud, clear and almost harsh on the
sides of the thorax, beneath the wings, and considerably softer as heard
on the back.
MORBID CHEST SOUNDS.
The close study of the healthy chest sounds upon the living animal is an
essential prerequisite to the appreciation of the morbid. The abnormal
noises are so varied, merge into each other by such imperceptible
degrees, and so coexist and complicate each other that they often prove
extremely puzzling to the unpractised ear. It is no more necessary that
the musician should educate his ear to appreciate the most delicate
gradations of musical notes, than that the auscultator should educate
his in the sounds of the healthy and diseased chest. Written
instructions are of about equal value in the two cases, they prove
auxiliaries in the acquisition of knowledge but they can never supersede
the practical study of the chest. A mere theoretical knowledge is too
often useless in the presence of the patient.
The abnormal chest sounds are either modifications of those existing in
health, or superadded sounds which have no counterpart in the healthy
chest.
_Modifications of healthy sounds._ The =vesicular= or =respiratory
murmur= may be =increased= or =diminished= in force or it may be
entirely =absent=.
=Increase of the respiratory murmur=, is merely an increase in force
without any modification in character and resembles _juvenile_
respiration. If increased equally over the entire chest it is =general=,
if only in a part it is =partial=. =General increase of the vesicular
murmur= is heard after an animal has been submitted to moderate exertion
for ten or fifteen minutes. In animals at rest it is heard in active
fevers and in the symptomatic fever which attends acute inflammations.
=Partial increase= as for example in one lung only, or in circumscribed
parts of both lungs, and especially along their superior borders, is
indicative of disease of the lungs or the pleuræ. It testifies to the
impermeability to air of some other portion of lung, from congestion,
splenisation, hepatisation, plugging of a bronchial tube with tenacious
mucous, tubercular deposits, tumors, emphysema, or hydrothorax. (See
under these names.) The healthy portion of lung in such cases takes on
the function of the whole, and the loud breathing is called
=supplementary=.
=Diminution of the respiratory murmur=, like its =increase=, may be
=partial= or =general=. =General diminution= is seen in anæmia, in low
fevers, in all very prostrate conditions from the mere want of power to
dilate the chest; in general emphysema (broken wind, heaves), in general
miliary tubercular deposit in the lungs, or in that form in cattle in
which the tubercle has been replaced by cretaceous deposits, from the
animal’s inability to fully dilate the air cells; in enteritis,
peritonitis and metritis the chest is more fully dilated because of the
pain attendant on that act, and the breathing being short and quick the
murmur is correspondingly low. In certain brain diseases with sluggish
respiration the sound is equally feeble.
=Partial diminution of murmur= is more surely indicative of lung
disease. It may arise from partial congestion when a supplementary
murmur will be observable over other parts of the lungs, and a crepitant
râle soon appears in the congested part; from local emphysema in which
there is increased resonance in percussing the part; from tubercular or
cretaceous deposit, when there will be exaggerated murmur elsewhere, or
from bronchitis with blocking up of one or more small bronchial tubes
and with louder respiratory sound in other parts.
=Absence of respiratory murmur= may be due to various causes, all of a
diseased nature. Hepatisation of lung may be recognized when this
condition is found associated with a crepitating râle around the margin
of the silent part, and when percussion shows its solidity and want of
resonance. Splenisation is associated with absence of respiratory sound
and dullness on percussion, but no surrounding crepitation. Absence of
sound in water in the chest is confined to the lower part of the chest,
keeps the same level and ratio of increase in front and behind, and in
the horse on the two sides, and has been preceded by the characteristic
catching breathing and the friction sounds of pleurisy. Large tumors and
extensive and circumscribed tubercular deposit will give rise to absence
of sound over a limited area and plugging up of one or more bronchial
tubes will lead to a similar result. Hepatisation of lung and water in
the chest are, however, the common causes of loss of respiratory murmur.
The =bronchial or tubal sound= may be increased in pitch and in
harshness in two conditions. 1st. In the early stages of bronchitis when
the lining mucous membrane of the air passages is dry, thickened and
inelastic. 2d. When that portion of lung intervening between one of the
larger tubes and the surface of the chest is solid (hepatised) and thus
proves a better conductor of sound than in the normal condition.
=Superadded abnormal sounds.= The =bronchial= sounds may be altered in
their character so as to become =cavernous=, =amphoric= or =mucous=
(rattling). The =cavernous= sound is usually caused by the presence in
the lung of the cavity left after the discharge of an abscess or
softened tubercle into a bronchial tube. It is thus preceded by cough
and white, creamy discharge from the nose. If the discharge is fetid and
grumous there has probably been circumscribed gangrene of the lung. An
approximation to the sound may be produced by blowing into a widemouthed
glass or porcelain vessel. The sound of =amphoric respiration= on the
contrary is like that made by blowing into a narrow necked bottle. It is
due to a similar cavity with a small orifice or to the existence of
pneumothorax communicating by a narrow canal with a bronchial tube. It
is rare in the lower animals, but Delafond mentions one case in the
horse and two in dogs.
=Râles.= The remaining morbid sounds are known as _râles_, or rattles.
They may either be referable to the bronchial tubes or the lung tissue.
They are called dry or humid, according as they convey the idea of air
drawn through a dry tube or one containing liquid.
The =dry râles= are due to narrowing of the bronchial tubes from the
pressure of adjacent tumors, the thickening of the mucous membrane or
the deposition on the surface of layers of tenacious mucus. The greater
the narrowing the shriller the sound, and hence the distinction of
_bronchial râles_ into =sonorous= and =sibilant= (whistling).
The =sonorous râle= has been variously exemplified by the humming of a
gnat, the cooing of a wood pigeon or the bass notes of a violin. It
commonly bespeaks the onset of bronchitis and testifies to the
thickened, dry and rigid character of the tubes, but may give place in
as short a time as three hours to a mucous râle from the occurrence of a
free secretion. It rarely extends over two or three days. Sometimes when
caused by a piece of tenacious mucus obstructing a tube, it is very
transient disappearing at once when the mucus is expelled by coughing.
Sometimes it is modified by an occasional clicking sound from the
flapping of a shred of semi-solid mucus attached to the walls of a
bronchial tube. This disappears when breathing becomes more hurried.
The =sibilant= (whistling) =râle= often acknowledges the same causes as
the sonorous, but indicates a narrower closure of the tubes. More
frequently it is heard further back on the chest and results from
pulmonary emphysema and dilatation of the smaller bronchial tubes
(broken wind, heaves). It is then heard chiefly in expiration and
coincidently with the second quick lifting of the flank. It is further
associated with the double lifting of the flank in expiration with the
short, weak, paroxysmal cough and the indigestion characteristic of
broken wind. If the whistling noise is so loud as to be heard without
applying the ear to the chest it is called wheezing.
A =mucous râle= is caused by air passing through any liquid contained in
the bronchial tubes, such as mucus, pus, or blood. It may be imitated by
blowing a large number of soap bubbles in a thick lather and noticing
them burst simultaneously or successively. It is chiefly observed in
bronchitis after the preliminary dry stage of the mucous membrane has
passed off and an abundance of mucus has been secreted. The nature of
the sound will vary according as it comes from the larger or the smaller
tubes or in other words as to whether the bubbles are large or small.
That from the smaller tubes is sometimes called a =submucous râle=.
Either of these râles may be temporary or permanent as the mucus may be
momentarily cleared away by coughing.
The =crepitant râle= is a sound of very fine crackling which has been
variously compared to the crackling of salt when put on red hot coals,
the noise of a sponge expanding in water and the rubbing of a small lock
of hair between the finger and thumb close to the ear. The existence of
the _crepitant râle_ usually denotes the existence of the early stage of
inflammation of the lungs, and the progress of hepatization in such
cases may be traced by the advance of the line of crepitation which
precedes it. So the progressive absorption of exuded matter in recover
may be equally followed by a line of crepitation gradually decreasing in
area until it meets in a point. The observations will be corroborated by
the dull sound elicited on percussing the parts. The production of the
sound has been attributed to the passage of air through the thick mucus
in the smallest bronchial tubes or more plausibly to the separation of
the walls of the air sacs and cells during inspiration, they having been
previously adherent by reason of the secretions.
_Crepitation_ is not heard in all pulmonary inflammations. In weak
animals with a low type of inflammation tending to gangrene, and in
those cases of broncho-pneumonia in which a viscid mucus blocks up the
bronchial tubes passing to the affected lobes, it may be altogether
absent.
_Crepitation_ may further occur without inflammation. Thus in pulmonary
œdema (dropsy of the lung) and capillary hemorrhage in which liquids are
effused in the smaller bronchial tubes and air sacs a crepitation is
sometimes heard.
A =modified crepitation= (=dry crepitant râle= of Delafond) is usually
heard over an emphysematous lung. The noise in this case has been
compared to that induced by handling a sheet of paper.
The =subcrepitant râle= is another modification holding a place
intermediate between the crepitant and the mucous râles. It has been
likened to the sound of a moderate effervescence in beer or other
liquid. It is referable to the presence of mucus in the smaller
bronchial tubes and indicates bronchitis or broncho-pneumonia.
Still other sounds are heard in diseased conditions of the pleuræ. These
are =friction sound=, =creaking=, =metallic tinkling=, and =gurgling= or
=splashing=.
A =friction sound= is heard in the early stages of pleurisy and is
caused by the dryness of the pleural surfaces from the absence of the
halitus or vapor which normally moistens them and the deposition of
layers of lymph by which the surfaces are rendered rough and uneven. An
approximate sound may be observed by placing the palm of the left hand
on the right ear and drawing a finger of the right softly over its back.
The sound is quick and jerking, one or a few jerks only being heard with
each inspiration as the act is cut short on account of the pain
attending the friction. It is rarely heard in expiration. It is chiefly
heard at the lowest part of the chest where the lungs have the greatest
freedom of movement. The thinness of the walls of the chest above the
breast bone in cattle and dogs permits the friction sound to be heard
more distinctly than in the horse. After the lapse of twelve,
twenty-four or forty-eight hours the friction sound disappears, the
surfaces of the pleuræ being separated by the liquid effusion, but it
may reappear when the fluid is absorbed in the process of recovery.
Sometimes the friction is further manifested by vibration of the walls
of the chest perceptible to the touch.
The =creaking sound=, as from the bending of a piece of strong leather
is caused by the movement of a thick and solid false membrane binding
the lungs to the side of the chest. This is often confounded with
crepitation.
=Metallic tinkling= is only heard when liquid and gas both exist in the
pleural sac and is due to the falling of a drop from the shreds of false
membrane above into the fluid contents below. The sound is somewhat like
the falling of drops in a closed cask half full of water, or it may be
fairly exemplified by placing the palm of the left hand flat on the
right ear and striking the back of the hand smartly with the middle
finger of the right. The sound is chiefly heard after the patient has
changed its position and especially after rising. The explanation of
this is that in the recumbent position the liquid changes its place and
bathes parts which in standing are surrounded by gaseous products only.
Drops accordingly fall into the liquid for some time with diminishing
rapidity until they cease altogether. Other explanations of the sound
but which less frequently exist are: the ascent of a bubble through the
liquid and its bursting on the surface; and the sudden recoil of air
from one wall of the plueral cavity to the other as the result of
movement or sound generated in the deeper seated solid structures.
A =gurgling= or =splashing= sound is equally indicative of the presence
of fluid and gas in the pleural sac. It is almost never heard unless
after a sudden movement on the part of the patient causing considerable
commotion in the contained liquid. Gurgling sounds transmitted from the
abdomen are too often mistaken for this. In small animals with
hydro-pneumothorax a quick shaking of the patient will develop it.
=Auscultation of the Cough= is sometimes valuable, though more difficult
and less satisfactory in the lower animals than in man, chiefly because
of the extensive movement of the ribs in the former. As conveyed through
a healthy lung to the ear applied on the side of the chest, the sound is
short, dull and indistinct. When the lung is more solid from
hepatisation, pleural exudation or other cause, or when the bronchi are
dilated the sound is loud and strong. The extent over which it may be
heard thus forcibly agrees with the area of lung in a state of
consolidation. When a considerable cavity or canal communicates with a
bronchial tube and extends to near the surface of the lung the sound is
loud and ringing. The note is specially clear and metallic when such a
cavity opens into the bronchus by a narrow orifice; an apt illustration
of this noise may be obtained by coughing into a narrow necked vessel.
The results obtained by auscultation should be confirmed by percussion
before arriving at any definite conclusion as to the state of the chest.
Consolidated lung tissue is a much better conductor of sound than the
healthy, and sounds conveyed through this may be heard at a considerable
distance from their point of origin. Thus the heart sounds are
frequently heard over any part of the right side of the chest, and
crepitation and other sounds may be heard in the centre of a hepatized
portion. On all such occasions the dull sound elicited on percussion
will not fail to correct the fallacy.
PALPATION. TOUCH.
This is chiefly useful in cases of pleurisy. As already noticed the
vibration of the chest walls which accompanies the early friction sound
is sometimes perceptible by the hand applied on the side of the chest.
Pressing firmly in the intercostal spaces at the affected part
invariably causes wincing and in cattle grunting. Pinching the back in
inflammatory chest diseases in cattle but especially in pleurisy has a
similar effect.
MENSURATION.
Measurement of the chest gives less reliable results in the lower
animals than in man. A cord four feet long should have one end placed on
a definite point on the withers and not removed until both sides have
been examined. It should be first carried down to a point in the middle
of the breast bone and the distance marked by a knot; a comparison may
be made by carrying to the same point over the opposite side. It should
next be carried successively to the lower end of the 8th rib on the two
sides and the difference marked, and lastly from the lower end of the
third rib to the lower end of the eighth. These measurements should be
made at one stage of the respiratory act, say when the chest is fully
dilated, and similar measurements when the chest is collapsed to
ascertain any difference in the expansion of the two sides of the chest.
In the smaller animals any difference in the expansion of the two sides
may be observed by inspection only, the practitioner standing directly
behind the animal and watching the movements of the two sides from this
standpoint.
A permanent dilatation of one side may be seen in water in the chest
confined to one side, and particularly if of some standing. Complete
hepatisation of one lung gives a similar result. The intercostal spaces
are observed to be wider than usual in such cases, and the movements of
the opposite side of the chest are much more extensive than of the
affected one.
A collapse with limited movement of one side is an accompaniment of
chronic disease of the lung, with wasting of its substance as in cases
of tubercular deposit.
DISEASES OF THE LUNGS.
Divisions of lung diseases. Bronchitis, pneumonia, pleurisy, their
results, nervous disorders, asthma, hiccough. Œdema. Emphysema. Morbid
growths, neoplasms. Infectious and parasitic diseases.
Inflammatory diseases of the respiratory organs situated within the
chest may be divided into: inflammation of the air tubes within the
substance of the lungs—_bronchitis_:—inflammation of the spongy tissue
of the lung—_pneumonia_:—inflammation of the covering of the lungs and
lining serous membrane of the chest—_pleurisy_:—and complicated cases in
which two or more of these conditions coexist. Beside inflammatory
diseases there are the various permanent morbid results of these
affections, such as consolidation of lung from exuded products becoming
organized; collapse (compression) of lung from organization and
contraction of false membranes, thickening or dilatation of bronchial
tubes as a result of bronchitis; also nervous affections, such as asthma
and hiccough; morbid alterations in the lung tissue independently of
inflammation, as pulmonary or pleural œdema and emphysema; specific
morbid deposits, as tubercles, glander nodes, cancer, melanosis, etc.,
and morbid states, due to parasites, as in the verminous affections of
cattle, sheep, etc.
BRONCHITIS.
Relation to other maladies of the air passages. Horse. Causes,
susceptibility, heat, cold, sudden changes, thick coat, rebreathed
air, on shipboard, in zoological gardens, in close stables, in navies,
organic matter in expired air, water vapor in expired air, effect on
the air and bacteria. Ingesta in bronchia. Medicinal liquids in
bronchia in horses and cattle. Exposed locations. Clipping. Smoke and
gaseous irritants. Symptoms, in mild cases, in severe: fever, cough in
dry stage, after secretion, auscultatory sounds, percussion,
discharge, watery, glairy, frothy, later milky, flocculent, purulent.
Convalescence. Capillary and pseudo-membranous form. Intensity of
symptoms, labored breathing, dyspnœa, violent cough, pinched
countenance, dark mucosæ, perspirations, palpitations, asphyxia.
Course, duration. Termination, difficult expectoration, blocking of
bronchia, pneumonia, bowel susceptibility, skin congestion, laminitis.
Chronic condition. Lesions, congestion and contents of bronchia, soft,
thick, friable mucosa, absence of vascular ramification, tenacious
mucus, false membranes. Collapse, atelectasis, splenisation,
emphysema, bronchiectasis. Treatment, in mild cases, in severe,
hygienic, steaming, sulphur dioxide, derivatives, guarded laxative,
neutral salts, calmatives, expectorants, alkalies, stimulant, oxygen,
peroxide of hydrogen, iodide of potassium. Diet. In advanced stages
tonics.
_Definition._ Inflammation of the mucous membrane which lines the
bronchia. It is the counterpart of _coryza_ and _laryngitis_, being but
the inflammation of another portion of the same mucous membrane which
lines the whole respiratory track. That portion of this mucous membrane
which lines the trachea is rarely or never the exclusive seat of
inflammation, so that in case of its being implicated we do not speak of
the case as one of _tracheitis_ but as _laryngitis_ or _bronchitis_,
according as the throat or bronchia form the seat of active inflammatory
action.
The bronchial mucous membrane is often inflamed in influenza, strangles,
contagious pleuro-pneumonia of cattle, distemper in dogs, and parasitic
diseases of the lungs, but the following remarks will be confined to the
simple inflammatory affection. It appears as an _acute_ and a _chronic_
affection.
HORSE. ACUTE BRONCHITIS.
This is more frequent in the horse than in other animals, and especially
so in young animals when newly stabled or put in training.
_Causes._ These are the same as those of _catarrh_ and _sore throat_. It
is but the continuation of the same mucous membrane which is affected in
all alike, and the same atmospheric changes, hot stables, noxious
inhalations and exposures to cold and wet will induce this disease
rather than the others when the bronchial mucous membrane is more
predisposed. Bronchitis often supervenes upon sore throat, by the
extension of the inflammation downward into the chest. Chilling of the
surface by exposure to cold, drenching rains, is a frequent cause, by
reason of the intimate sympathy existing between the skin and the mucous
membrane. For the same reason certain conditions of the skin will
predispose, thus a long, thick coat which keeps the animal constantly
drenched with sweat and the skin relaxed and sensitive. Williams draws
attention to the frequency and severity of bronchitis in both horses and
cattle conveyed by sea during stormy weather, and especially when the
hatches had to be fastened down. Such an experience combines in one the
evils of an overheated stall, a sudden transition often to extreme cold,
a lowering of the vitality of the whole system by the circulation of
non-ærated blood, a systemic poisoning by the retention of the waste
organic products that would otherwise have been eliminated, and the
special weakening of the lung tissue by congestion of the whole pulmonic
circulation.
But the development of bronchitis and broncho-pneumonia is the least
fatal result. The statistics of our European cattle traffic are rich in
the examples of absolute suffocation of cargoes in transit to Europe.
The following from Report of U. S. Treasury Cattle Commission is
illustrative:
“Dr. Thayer reports the case of a steamer from Boston to Liverpool, with
400 cattle on board, which encountered a storm and came through it with
only one animal surviving. Mr. Toffey, of Jersey City, lost 30 head out
of a cargo of 300 by suffocation in 1880. This happened, he informs us,
on a calm sea on a southern route with a temperature about 90° F., and
the wind astern and light so as just to keep pace with the ship. The air
on board the ship became perfectly stagnant, and there was no means of
establishing an artificial current. A still more disastrous experience
befell the steamer Thanemore, Captain Sibthorp, of the William Johnson &
Co. line. This vessel left Baltimore with 565 cattle on board, of which
228 perished by suffocation before she reached Cape Henry.”
Among animals that survive such treatment the susceptibility to lung
disease including even the contagious forms like tuberculosis is
enormously enhanced.
EFFECTS OF MODERATELY VITIATED AIR.
“When air only moderately vitiated is breathed continuously for a
greater length of time the results are still very injurious, and in the
front rank of diseases so caused stand pulmonary consumption, and other
destructive affections of the lungs. Perhaps no better example of this
can be given than that of the monkey houses of the Zoological Gardens of
London and Paris. While these houses were small and ill-ventilated the
monkeys died in large numbers from pulmonary consumption, but after they
had been enlarged and better ventilated the mortality from this cause
nearly ceased. (Arnott.)”
“Town dairy cows which are packed in close ill-ventilated buildings and
never allowed to go out are very subject to consumption, while horses
kept in no better conditions, but spending nearly half their time in the
open air, rarely have phthisis. (With lung plague it will be remembered
that the out-door exercise and mingling of herds leads to an increase of
the mortality.) Horses newly stabled suffer severely from diseases of
the lungs. The same holds true of human beings. A long list of careful
observers have noticed the essential connection of lack of ventilation
and pulmonary consumption. Baudelacque, Carmichael, Arnott, Lepelletier,
Allison, Sir James Clark, Toyubee, Guy, Greenhow, Sir Alexander
Armstrong, Parkes, and Aitken have especially insisted upon consumption
being a sequence of lack of ventilation. Dr. Cormac indeed insists with
great force that consumption is originated by rebreathed air.”
“The notorious prevalence of consumption in sailors has been directly
traced to the impure air in which they sleep, and an extensive outbreak
of lung disease (not tubercular), leading to destruction of lung tissue,
in the English Mediteranean squadron in 1860 was clearly traced by Dr.
Bryson to the contamination of the air. In a nursery hospital at Dublin
with entire neglect of ventilation, 2,944 children died in four years,
whereas after the ventilation had been improved only 279 died in the
same length of time.”
“Parkes (Practical Hygiene) says:
“‘But not only phthisis may be reasonably considered to have one of its
modes of origin in the breathing of an atmosphere contaminated by
respiration, but other lung diseases, bronchitis and pneumonia, appear
also to be more common in such circumstances. Both among seamen and
civilians working in confined, close rooms, who are otherwise so
differently circumstanced, we find an excess of the acute lung
affections.’
“In this connection, the statement of the air breathed by an ox per hour
and that supplied him on board a ship with insufficient ventilation or
none may be instructive. The ox takes in with each breath about 5 liters
of air. This is at the rate of 50 liters per minute, or 3,000 per hour =
105.9 cubic feet. This amount of air is therefore rendered all but
irrespirable by each animal in the course of an hour. And this, be it
noted, is by breathing alone, and makes no account of the contamination
by perspiration in the overheated hold, and by the emanations from the
accumulating excrement.”
“On board the steamers we have found the space allotted to each bullock
to vary from 150 to 240 cubic feet. On the steamship “Holland,” loaded
at New York, August 21, 1881, we found the stalls amidships allowed the
full space of 240 cubic feet per head. In the bow where there was less
height between the decks the space was considerably less. On the lower
deck, where 129 cattle were accommodated, the space allowed each was
217.4 cubic feet. The port-holes in the upper deck were nine inches in
diameter and there was one for each pair of stalls—central and
lateral—or for eight oxen. These being well above the water line would
be available for ventilation in ordinary weather. The port-holes in the
lower deck, similarly arranged, were about two feet above the water
line, and consequently not available for ventilation, save in
exceptionally calm weather. The temperature on the main deck of this
ship (between the outer and main deck), when only half the cattle had
been loaded, was in the neighborhood of 90° although she was lying in
the center of the North River with port-holes and hatches open, and a
fresh breeze blowing from the north.”
“On the ‘Assyrian Monarch’ the space per head was only 192 cubic feet,
but this ship was supplied with a ventilating fan or blower capable of
delivering over 50,000 cubic feet of fresh air per hour, so that her
ventilation was abundantly provided for. In some smaller ships we found
the space per head to exceed little, if at all, 150 cubic feet. In
these, accordingly, a single hour without any change of air would
threaten the life of every animal on board, and two hours would endanger
those for which even the larger space is provided. It is true that such
absolute seclusion is rarely required, and that a certain amount of
ærial diffusion is always going on through imperfectly closed hatches,
companion ways, and ventilators, yet that these are often insufficient
has been amply shown by such losses as are reported above, as well as by
the bronchitis and tuberculosis which Drs. Whitney, Lyman, and Williams
have found in the lungs of American animals arriving in England.”
“ORGANIC MATTER IN EXPIRED AIR.”
“The decomposing organic matter given off by the lungs and skin is
probably the most injurious of the animal excreta, when allowed to act
on the system for a length of time. This exhaled organic matter is
easily recognized in the air by chemical tests, or by the putrid odor
evolved when cotton wool, that has been breathed through, is left to
soak in otherwise pure water at a temperature of 70° to 80° Fahrenheit.
The experiments of Gavarret and Hammond, in which expired air had its
carbonic acid and water vapor removed, leaving only the organic matter,
showed that the latter was highly deleterious. Hammond found that a
mouse died in forty-five minutes in such an atmosphere. It has also been
again and again demonstrated that air containing a given amount of
carbonic acid as the result of respiration is far more poisonous than
air which contains the same amount of carbonic acid as a product of
combustion.”
“WATER VAPOR IN EXPIRED AIR.”
“The amount of water vapor given off by the lungs varies greatly
according as the air is already more or less saturated with water. As
the air in the stalls between decks is always saturated with water
vapor, we may take the very lowest estimate for each animal, namely, 60
ounces in 24 hours, which for a cargo of 200 head would amount to over
93 gallons. And this is in addition to the exhalations from the skin and
the bowel and kidney excretions. The air between decks is therefore
constantly saturated with moisture which condenses and runs down in
streams on every solid object. Among the ill effects of this saturation
may be noted:”
“First. The saturation of the air with water vapor increases the
exhalation of carbon dioxide from the lungs. This effect on the
excretion of carbonic acid is usually so great as to counterbalance the
tendency of warm air to reduce the production of this acid. This
saturation, therefore, with water increases the danger of suffocation by
the accumulation of the irrespirable carbon dioxide in the ship, unless
the air is being constantly removed.”
“Second. The excess of moisture in the warm atmosphere hastens the
decomposition of the organic matter derived from the lungs, skin, and
manure. Sir Alexander Armstrong, head of the medical department of the
British Navy, says: “There can be no more fertile source of disease
among seamen, or, indeed, other persons, than the constant inhalation of
a moist atmosphere, whether sleeping or waking; but particularly is this
influence injurious when the moisture exists between a ship’s decks,
where it may be at the same time more or less impure, and hot or cold,
according to circumstances.” It has become an aphorism with sanitarians
that “a damp ship is an unhealthy ship,” and many instances are adduced
in which a sufficient renewal of the air between decks, with or without
stoves to dry it, has transformed a naval pest-house into a salubrious
vessel.”
“All such considerations must emphasize the demand for such a constant
renewal of air between decks on steamers carrying cattle as shall serve
to obviate all those conditions of ill-health, with congestion and
inflammation of the lungs, as have proved in the past a serious drawback
to our foreign cattle-trade. To accomplish this and at once remove from
between decks the excess of carbon dioxide, of decomposing organic
matter, and of humidity, and to furnish air approaching in purity and
dryness that of the atmosphere outside, we can conceive of nothing more
simple and effective than thorough ventilation by fan or heat
extraction, as referred to below.” Report of the U. S. Treasury Cattle
Commission, 1882.
The above quotations were written with special reference to cattle but
the author reproduces them here as in principle applicable to horses as
well.
In both horses and cattle treated as above it is common to find ingesta
in the bronchia drawn in during the violent paroxysms of coughing. Here
we have a direct mechanical irritant and a means of septic infection,
highly calculated to induce unhealthy broncho-pneumonia. Williams quotes
the case of a horse in which vomition was caused by an over dose of
aconite, and a portion of the food entered the bronchi.
In this connection must be named the introduction into the bronchia of
liquids forcibly administered to horses and cattle. In the horse the
length of the soft palate enables him to hold liquids in the mouth
during his pleasure, and among the expedients adopted to coerce him are
the very dangerous ones of holding the nostrils and of pouring the
liquid through the nose. When the nostrils are held the urgent demand
for air leads to attempts to breathe through the mouth, and, whether he
succeeds in this or not, the usual result is the drawing of a portion of
the liquid into the lungs. When it is poured through the nose the animal
cannot protect himself except by rapid gulping, and as he must breathe,
a portion of the liquid is usually drawn into the lungs. Any irritant
taken in this way will develop bronchitis, and some bland agents like
melted lard are almost equally injurious. Cattle having a short palate
can scarcely resist swallowing liquids that are poured into the mouth,
but a cough with the succeeding quick inspiration will almost certainly
draw a portion into the bronchia. To return to the influence of cold,
exposed situations which receive the full force of cold winds, those
from the north and west on the Atlantic slope are specially conducive to
bronchitis. Exposure of newly clipped animals to stand without
protection in winter or early spring, has the same tendency. Finally the
inhalation of smoke or of heated and irritant gases and vapors, as in a
burning building, is an effective factor.
_Symptoms_: In its _mildest form_ bronchitis is a transient illness with
some dullness, impaired appetite, hot, dry mouth, redness of the visible
mucous membranes, a moderately strong, resonant cough, attended with
slight pain, slight rise of temperature, accelerated breathing and
pulse, and mucous discharge from the nose. Such an attack passes over in
a few days and without any medicinal treatment if ordinary precautions
are taken to avoid a repetition of its causes.
In _severe cases_ the symptoms are more intense from the first. Besides
the dullness and inappetence, hot, dry mouth, generally increased
temperature of the body (102° to 104° F.), accelerated and labored
breathing, and other manifestations of fever, there are more specific
symptoms. The cough is dry, hard, painful, often paroxysmal, and appears
as if it came from the very depth of the chest. A strong, harsh,
bronchial sound is heard over the lower end of the trachea and the upper
border of the middle third of the chest just behind the shoulder.
Percussion detects no change from the natural resonance of the chest,
nor auscultation any crepitating sound. Pressure in the intercostal
spaces causes no suffering. The expired air feels hot. The pulse though
accelerated is moderately soft and sometimes even weak, a condition
which marks inflammations of mucous membranes as contrasted with those
of the serous. The mucous membrane of the nose has a dark red hue,
especially when the inflammation extends to the smaller ramifications of
the bronchial tubes so as to impair the æration of the blood. In the
same state there is excessive dullness and prostration because of the
supply of partially venous blood to the brain. The head is held low, the
nose often supported upon the manger, and the eyelids are semi-closed
and injected.
From the second to the fourth day a free exudation takes place from the
surface of the mucous membrane, and the symptoms are materially changed.
The cough becomes more frequent but softer, looser, and attended with a
rattle from the air passing through the abundant mucous secretion. The
cooing or tubal sound heard at the lower end of the windpipe and behind
the shoulder has now given place to a _mucous râle_. A nasal discharge
appears at first watery, thin, of a whitish, glairy froth, but soon
becoming more opaque, white, milky and flocculent and having little
tendency to stick to the nostrils. This is often expelled with sneezing
and accompanied by movement of the jaws. With the access of free
secretion there is a great mitigation of the fever and the other
distressing symptoms, and, if no relapse nor complication supervenes,
recovery may be complete in a fortnight or three weeks from the onset.
From this time all the febrile symptoms decline and disappear, appetite
and liveliness return, the discharge rapidly diminishes and finally
disappears, when the patient may be said to have completely recovered.
=Capillary and pseudo-membranous bronchitis= are described by Reynal as
occurring in young horses recently brought into the army and subjected
to the hot and close stables in some of the French barracks. It began as
ordinary bronchitis, which in place of tending to recovery, propagated
itself to the most minute bronchial ramifications, and was frequently
complicated by the formation of false membranes. The signs of its
accession are an extreme intensity of the general symptoms, the rapid,
labored, difficult breathing, accompanied by convulsive action of the
pectoral and abdominal muscles; the frequent, painful, suffocating and
abortive cough, which violently shakes the whole body; the extended
head, open mouth, distorted nostrils, reddish brown protruding eyes; the
pinched, haggard features, and the frothy mucous, nasal discharge
striated with blood, and later interspersed with shreds of false
membrane similar to those existing in croup. In connection with these
are the symptoms of extreme oppression, partial sweats, tumultuous
action of the heart and small, weak, rapid pulse. Death resulted from
suffocation during a paroxysm of coughing.
_Course._ _Duration._ _Termination._ Bronchitis is not usually fatal,
except in very young or old or worn out animals, or unless it assumes
the _capillary_ form or is complicated by pneumonia, pulmonary abscess
or by metastasis to the bowels or feet. In the mildest cases health is
re-established in three or four days, and in the severe, about the
twelfth, fifteenth or twentieth day. In old and debilitated animals in
which pure bronchitis proves fatal, the abundant effusion into the
bronchial tubes, the influence of gravitation retaining this in the
smaller tubes, the palsy of the cilia which normally carry it outward,
and the want of power to expectorate by coughing, usually bring about
suffocation. This is favored by the non-ærated state of the blood, which
rapidly prostrates the already weakened nervous centres. The
supervention of pneumonia will be marked by a new class of symptoms,
especially labored breathing, dullness on percussion and crepitation on
auscultation. The susceptibility of the bowels is so great in some cases
of bronchitis, particularly in those associated with a low fever, that
superpurgation, enteritis and death may result from the smallest dose of
laxative medicine,—the author has seen a fatal result from the
administration of two drachms of aloes in a case of this kind. In such
circumstances the skin usually participates in an equal degree, and
though the superpurgation be checked an extension of the disease to the
feet may still prove fatal or induce such changes of structure as to
leave the animal practically worthless. In old animals or after repeated
severe attacks of bronchitis it may merge into the _chronic_ form.
_Thick wind_ is a frequent sequel of severe cases from thickening or
dilatation of the bronchial tubes, from collapse of the lung or from
emphysema.
_Postmortem appearances._ In the bodies of animals that have died of
bronchitis the air passages within the lungs are filled with a white or
greenish yellow mucus. If this is washed from the tubes by a stream of
water, the mucous membrane is often found to be injected, studded more
or less profusely with red points or with branching red lines, and with
petechia, and the mucous membrane is softened, sometimes thickened and
friable. When, however, the bronchitis has been attended by a free
purulent expectoration the mucous membrane may, when washed, show no
perceptible alteration from the healthy standard as examined by the
naked eye.
In the _capillary form_ the blocking up of the smaller tubes by a
tenacious frothy mucus, and by the false membranes which form complete
casts of many of the tubes and the partial consolidation (collapse) of
circumscribed pyriform masses of lung tissue with which such tubes
communicate form the chief features on examination after death.
This state of _consolidation_ or _collapse_ of lung is frequently seen
in simple bronchitis as well. It is then due to the blocking up of one
or more bronchia by plugs of tenacious mucus which act as valves,
preventing the entrance of air, though it may permit of its easy passage
outward. This state of lung differs materially from the consolidation
due to inflamed lung tissue (hepatisation). When cut it does not present
the granular appearance of the latter, caused by the exudation into the
minute air cells, but the cut surface has an uniform homogeneous aspect
aptly likened by Lænnec to _muscular flesh_ (splenisation). Mendelson,
Traube and Gairdner have induced artificial collapse of the lung by
introducing foreign bodies into the bronchia of animals.
_Emphysema_ of the margins of the lung is a frequent concomitant of
_collapse_. The cause is plain. The portion of lung, the subject of
collapse, emptied of its air, does not occupy a tithe of the space it
would normally fill. The rest of the lung tissue expands unduly to fill
out the vacated portion of chest and the cells become overdistended and
ruptured. The emphysematous lung is known by its lighter color, by its
irregular bulging surface, by the subsidence of these elevations when
pricked with a needle, and by a more marked crepitation when pressed.
When the cells have burst and the air escaped into the areolar tissue
between the lobes, it appears as dark lines circumscribing small
portions of pulmonary tissue and collapsing when pricked.
_Treatment._ The mildest cases will recover of themselves, especially if
care is taken to protect the patients against cold, wet, draughts of
cold air, over-exertion, and other injurious causes, and to give a part
of the food warm and sloppy. In severe cases treatment must be more
active, but it will be borne in mind that severe depletive measures are
badly endured. Bleeding dangerously increases the already existing
weakness and prostration without affording any corresponding advantage.
It is only admissible when from the severity of the symptoms in the
early stages suffocation is threatened or when the brain becomes
involved in disease.
Causing the patient to inhale water vapor from scalded bran or hay is to
be assiduously carried on for half an hour to an hour twice or thrice
daily until expectoration has been freely established and the cough and
fever alike moderated. The density of the vapor must of course be
apportioned to the particular case so as to avoid any approach to
suffocation. The addition of the fumes of burning sulphur will often by
their astringent and antiphlogistic action on the mucous membrane,
render the vaporous application more effective. A pinch put into a small
piece of paper twisted at one end to prevent burning of the fingers may
be set fire to and the fumes allowed to pervade the apartment so that
they can be breathed freely without inducing cough. A mustard poultice
to the neck and sides of the chest should also be applied and kept on an
hour or until effusion into the skin is well marked by thickening of its
substance. Injections of warm water should be given alike to check or
obviate shivering and to equalize the general temperature and to solicit
the action of the bowels. In sporadic cases with active fever and full
strong pulse a laxative dose of aloes (3 to 4 drachms) may be given, but
if with a low fever and during the prevalence of influenza not more than
half the dose should be given or enemata alone may be relied upon. As
soon as the medicine has set or at once if it is withheld, neutral salts
may be given (Liquor Ammoniæ Acetatis 2 oz. or Sweet Spirits of Nitre 1
oz. or nitrate of potass ½ oz. combined with 10 drops tincture of
aconite repeated twice or thrice daily). If the cough is troublesome and
secretion long in being established, expectorants may be used (oxymel of
squill 3 oz., powdered squill ½ oz. or liquorice 1 drachm) with half the
doses of the neutral salts.
In the early stages to hasten expectoration such preparations as the
following may be given:
Recipe: Potas. Bicarb. 2 ounces; Ammon. Carb. 2 ounces; Digitalis Pulv.
2 drams. Mix. Divide into eight powders: give one every four hours.
Recipe: Ammon. Murias. 2 ounces; Choral. Hydrat. 1 ounce; Tinct.
Hyoscam. 2 fluid ounces; Aqua 8 fluid ounces. Mix. Give two
tablespoonfuls every four hours.
Apomorphia, tartar emetic, turpentine or benzoin may be employed or even
pilocarpin, care being taken not to increase prostration unduly.
Compressed air, oxygen and peroxide of hydrogen will sometimes relieve.
With the advent of expectoration, or earlier, iodide of potassium in one
drachm dose, thrice a day will do much to obviate glandular and other
enlargement which would tend to develop _roaring_.
The diet should be laxative, non-stimulating and somewhat spare. Mashes
of wheat bran, boiled linseed or boiled barley; roots such as turnips,
carrots, beets; in summer a limited supply of fresh grass, with little
hay at any time and that scalded, may indicate the nature of the
aliments to be used. As a beverage chilled fresh water or linseed tea
may be supplied _ad libitum_.
Should the nasal discharge manifest no disposition to cease at the end
of 15 or 20 days, as will sometimes happen in young horses, stimulants
and tonics must be employed. Gentian (4 drachms), Sulphate of iron (2
drachms), Arsenious acid (5 to 10 grains) or nux vomica (1 scruple) may
be given daily as ball, electuary or powder. A full and nutritive diet
should at the same time be allowed, and open air exercise enjoined.
CHRONIC BRONCHITIS IN THE HORSE. BRONCHIAL CATARRH.
As Sequel of Acute: as result of unhygienic environment, diet and
usage. Symptoms, breathing accelerated, double expiratory act, short
breath, cough husky, or paroxysmal, excited by cold air, water,
discharge white flocculent. Percussion, drum-like patches;
Auscultation mucous and sibilant râles. Lesions, thick mucus, pale
membranes, bronchiectasis, emphysema, ulceration. Thick wind.
Treatment, stimulating, tonic, derivative, medicated vapors, careful
diet. Tar water.
This may be a sequel of the acute form, or it may appear at once as a
catarrhal discharge from the bronchial tubes and without any very marked
febrile affection, in animals debilitated by damp stables, overwork and
a faulty regimen and diet.
_Symptoms._ Respiration accelerated, and expiration effected with a
double lifting of the flank; the horse is easily blown when
moderately exercised; the cough is frequent, soft or rattling and
paroxysmal—sometimes hard and deep—is excited when brought from the
warm stable into the cold air, and is followed by a whitish,
flocculent, purulent discharge from the nostrils, consistent but not
sticky (like buttermilk). The pulse is rapid and small in volume.
Percussion manifests a healthy resonance over the greater part or all of
the chest, a drum-like sound over given areas, and auscultation over its
median part detects a bronchial rattle and in most cases a dry sibilant
râle.
_After death_ the bronchial tubes are found to contain an abundance of
thick mucus, though abnormal redness of the mucous membrane is by no
means a necessary condition. There is always more or less dilatation of
the bronchial tubes especially at their points of subdivision where they
are often twice their healthy calibre, and an emphysematous state of the
lungs is equally constant. Delafond and Rodet have noted minute ulcers
on the bronchial mucous membrane and Reynal miliary abscesses and
grayish and white indurations of the lung tissue and bronchial glands
which may have been glanderous.
It will be observed that the symptoms and lesions closely resemble those
of broken wind (heaves), and unless early and successfully treated, into
this it gradually merges. The chief distinguishing symptoms are the
abundance and nature of the discharge, the fetor of the breath, and the
presence of the mucous râle in the chest. It is one of the conditions
known by the horseman’s expression “_thick wind_.”
_Treatment._ Like its type (dilatation of the bronchia, bronchiectasis)
in man this disease obstinately resists treatment. In our efforts to
cure it the same general principles must be followed as in acute
bronchitis, with this grand qualification that the general aim must be
to stimulate and support. Stimulating liniments may be repeatedly
applied along the course of the trachea and on the sides of the chest.
An equable temperature is desirable and a dry building. Water vapor
medicated with various astringents and antiseptics (creosote, carbolic
acid, turpentine, tar, or tar vapor) is to be commended. A course of
tonic and expectorant medicine is desirable and a highly nutritious and
laxative diet is imperatively demanded.
As tonics Gentian may be given daily in 4 drachm doses combined with
quaiacum in doses of 2 scruples. In most cases it will be advisable to
add to the above or employ separately arsenious acid in doses of 5 to 10
grains combined with three times the amount of bicarbonate of soda, and
given daily for a month or longer.
The diet should be as for broken wind, nutritious, in small bulk, of a
laxative nature and given at least an hour before work. A moderate
supply of grass, roots, bran, oats or barley may be given, but hay must
be sparingly supplied and, if exclusively clover hay, dry and dusty, is
better withheld. In the north of France horses with chronic bronchitis
are maintained in a serviceable condition by a diet of cut straw and cut
hay, well sifted to remove all dust mixed with oats and molasses and set
aside in a large cask to ferment before being given to the animals. Tar
water may be the exclusive drink.
A pint of linseed, well boiled, and given daily for a length of time in
succession is often of great value.
BRONCHITIS IN THE OX.
Working oxen most susceptible. Causes, damp buildings, wet, cold,
exposed localities. Debility, overwork, poor feeding, close, foul
stables, sudden changes of temperature. Previous attacks. Symptoms,
mild form, and severe, fever, sneezing, cough, dry, later soft,
prostration, retraction of nostrils, labored breathing, hot breath,
discharge, watery, milky, purulent. Duration, Complications and
sequelæ. Chronic form. Respiratory disturbance, paroxysmal cough,
purulent discharge, mucous and sibilant râles, emaciation. Lesions.
Treatment, laxative safer, expectorant, derivative stimulant, etc., as
in horse. Bronchitis in pigs and sheep.
This is less common than the same disease in the horse, though in
working oxen, in which many of the same causes operate, it is frequently
seen. It is not infrequent in other cattle in damp buildings or in wet
cold exposed situations. Debility from overwork and poor feeding, often
brings on the chronic form of this disease. Living out in damp nights
after a hard day’s work is another frequent cause. The enervating
influence of the hot foul air of many cow houses conduces to it and is
specially injurious if alternated with a chilling atmosphere out of
doors. Previous attacks strongly predispose to future ones.
_Symptoms._ Some cases are so slight as to escape a cursory observation
and subsiding in a few days leave the animal perfectly well. Others are
severe and may prove dangerous.
The earlier symptoms are dullness, staring coat or shivering, and
sneezing, followed by reaction with hot clammy mouth, general increase
of temperature, rapid pulse, reddened nose and eyes, and suspended
rumination. The more characteristic symptoms are a hard, dry, hacking
cough, not so resonant as in the horse, and soon a mucous discharge from
the nose usually cleared away by the tongue almost as rapidly as formed.
If the case increases in severity, and in many cases almost from the
first there is great depression, hanging head, semi-closed watery eyes,
extreme movement of the nostrils, hot expired air, labored action of the
flank, complete loss of appetite, constipation, fæces covered by mucus,
cough very hard, painful, occurring in paroxysms and easily excited by
touching the larynx or trachea. This is followed by a loose cough, a
free discharge from the nose and a mucous râle on auscultation.
Percussion gives healthy resonance. The disease reaches its height on
the fifth day and recovery may be almost perfect on the eighth. Its
chief danger is from a complication with pneumonia or pleurisy, or from
its merging into the _chronic form_.
=Chronic bronchitis in the ox= is characterized by a persistent
disturbance of the respiration, paroxysms of coughing, a white
flocculent discharge from the nose, increasing emaciation, pallor of the
mucous membranes, a mucous râle over the windpipe and median part of the
chest and a cooing sound over other points. If left to itself emaciation
becomes extreme, the skin is harsh, inelastic, attached to the ribs and
covered by vermin, and death usually ensues from diarrhœa or
consumption.
_After death_ the lesions are like those seen in the horse, unless there
is the complication of tuberculous or other disease of the substance of
the lungs.
_Treatment._ Neither the general care nor the remedial treatment differs
materially from that for the horse. The principle difference is in the
lesser liability to superpurgation and in the preference to be given to
Epsom or glauber salts over aloes as a laxative. Either saline may be
given in dose of one pound combined with an ounce of ginger or other
stimulants, and followed up by similar diuretics, expectorants and
tonics, as in the horse. The _chronic form_ is to be treated as in the
horse.
=Pigs and sheep= affected with =bronchitis= must be treated on the same
general principles as the ox, only giving one-fifth the amount of the
different medicaments, and in the case of the pig oleaginous purgatives
and emetics as advised for the dog.
BRONCHITIS IN THE DOG.
Causes, damp kennels, cold and damp after hunting, pampering and
exposure, distemper. Symptoms, fever, cough hard, later soft,
discharge watery, glairy, purulent. In capillary bronchitis cough more
paroxysmal, painful and attended with vomiting. Disturbance of
breathing, pulse, temperature. Fatality in different breeds.
Treatment, laxative, expectorants, diuretics, heart tonic, calmative,
water vapor, chest jacket, stimulant expectorants, stimulants, tonics.
Diet.
This is common and severe. Hounds kept in damp kennels, much exposed to
cold and damp after being heated in hunting, or subjected to frequent
and sudden alternations of temperature are specially liable. Pampered
pets kept in warm rooms, overfed and having little open air exercise,
are equally subject to its attacks. It is an usual form in which
distemper is manifested.
_Symptoms._ There is roughness of the coat or shivering and a small,
hard cough often repeated. If confined to the bronchi the cough soon
becomes loose, a free discharge sets in, and with care recovery may be
secured in five or six days.
If the smaller bronchial tubes are involved the symptoms are more
intense and persistent. The temperature may reach 104° or 105°. To the
same early symptoms succeed, a painful cough occurring in paroxysms and
sometimes followed by vomiting of a glairy mucus. There is running from
the eyes and nose, and reddening of thin membranes. The creature stands
with his elbows turned out, his flanks heaving and his heart beating
rapidly and tumultuously. In the worst cases when the inflammation has
been propagated to the smallest bronchial tubes constituting _capillary
bronchitis_, these symptoms are seen in their most aggravated type and
the subject often dies of suffocation, or by implication of the lung
tissue. Percussion and auscultation are even more applicable than in the
larger animals, showing the clear resonance, of the lung tissue, the
tubal murmur in the early stages and the mucous rattle in the later
ones. In the _capillary form_ a distinct crepitation is heard like that
of pneumonia. Bronchitis proves most fatal to the higher bred dogs, such
as King Charles spaniels, Italian greyhounds, and English terriers, and
according to St. Cyr small dogs suffer more severely than large ones.
_Treatment._ If the bowels are costive a tablespoonful of castor oil
should be given, followed up by nauseating expectorants and diuretics
(tartar emetic two grains, nitrate of potass one drachm, and sugar one
drachm, mix thoroughly, divide into twelve powders and shake one on the
tongue thrice daily). If the cough is very troublesome two grains of
powdered digitalis may be added to each dose, or after the nasal
discharge has been freely established two to four grains of opium among
the tartar. The opiates are of great value in controlling the paroxysms
of coughing and the propagation of the disease to the smallest
ramifications of the air passages, but as they check secretion they must
be used with caution until a free discharge has been established. In the
early stages bromides, hyoscyannes or digitalis may be preferred.
Muriate or carbonate of ammonia, syrup of Tolu, senega, or gnaiac may
follow.
Inhalations of water vapor, the maintenance of an equable temperature,
and the moist chest jacket, followed by mustard poultices to the throat
and chest are not to be neglected. The diet should be simple, oatmeal or
Indian corn pudding with milk, soups and the like may be allowed, but as
a rule butcher meat is to be withheld. If the patient has previously fed
entirely on the latter it should now be given in very limited amount
only, and qualified by an admixture of farinaceous diet.
In some cases the prostration becomes so great that the patient must be
supported by tonics and stimulants (a teaspoonful each of sweet spirits
of nitre and tincture of gentian, or a teaspoonful of port wine repeated
twice daily).
In case of persistent discharge, iron, liquor arsenicalis, the same
strength as Fowler’s solution, or cod-liver oil may be used.
CROUPOUS BRONCHITIS IN CATTLE AND SHEEP.
Causes, smoke, hot air or gas, irritant inhalations, concomitant of
infectious diseases. Lesions, intense congestion covered by fibrinous
exudates. Symptoms, slowly or suddenly developed, fever, loud,
wheezing, stertorous, panting breathing, dyspnœa, dry râles and
blowing. Course. Treatment, moist jacket, soothing, expectorant,
stimulant inhalations, expectorants, derivatives.
This affection has been found in cattle and sheep from exposure to
smoke, hot air or gas, and other irritants, and even from exposure to
cold, and without any suspicion of a contagious element. Again it has
been seen as a complication in Rinderpest, lung plague and malignant
catarrh. The lesions are those of tumefaction and extreme arborescent
redness of the mucosa, and the formation of patches of a dense fibrinous
exudate of a yellowish color, in some cases completely obstructing some
of the smaller tubes.
_Symptoms._ The attack may come on slowly as in ordinary bronchitis,
while in other cases it is sudden. The respiration being loud, wheezing,
stertorous and panting and general dyspnœa supervening. Auscultation
furnishes loud, blowing sounds, dry râles and rouchi, while percussion
may show no abnormal change. A strong tremor is felt by the hand on the
trachea, and after a paroxysm of coughing false membranes may be
expelled. If there is no improvement by the second or third day death is
liable to supervene by asphyxia.
Treatment is usually unsatisfactory. The hot, moist jacket, inhalations
of vapors of warm water, of carbonate of ammonia, and of ether may be
tried, counterirritants to the chest, and internally liquor ammonia
acetatis and iodide of sodium would be indicated. When the membranes are
somewhat loosened pilocarpin, or in weaker subjects apomorphine may
assist their expulsion.
ACUTE CONGESTION OF THE LUNGS. PULMONARY HYPERÆMIA.
Active and passive congestions. Congestion of incipient pneumonia.
Congestion of over-exertion. Causes, lack of condition, fat, plethora,
gorged stomach, hot weather, cold rains, cold baths, infectious
diseases. Symptoms, dilated nostrils, labored breathing, deep lifting
of flanks, panting, pendent head, staring, fixed, bloodshot eyes,
pale—later dark red nasal mucosa, rapid pulse, palpitating heart, fine
crepitation, cold limbs, tremors, perspiration, obstinate standing,
till unable, blood from nose. Fulminant cases. Exposure cases. Course.
Termination. Resolution. Lesions, lungs black, gorged, do not
crepitate nor collapse, lessened buoyancy, cut surface, compressed
bronchioles and alveoli, right heart and veins gorged, blood black,
semi-liquid, petechiæ. Nature. Not yet inflammatory, blood
engorgement, no cell proliferation, migration, non-exudation,
pulmonary vaso-motor paresis, effect of blood pressure, of peptones,
etc., of exhaustion. Treatment, relieve respiratory muscles,
derivation to surface, stimulants, hot pediluvia and packs, relief of
vascular system, bleeding, heart stimulants, digitalis.
Congestion of the lungs occurs in all animals as the precursor of
inflammation, but as death may occur without the supervention of actual
inflammation a special notice appears to be demanded. The hyperæmia of
the lungs may be seen in two forms, active and passive, the latter form
being secondary to other diseases, such as valvular diseases of the left
heart, by reason of which the blood is forced back on the lungs and
creates mechanical congestion. The active form is a pathological process
developed in the lung itself, and which often proves fatal through
arrest of the circulation through this organ.
_Causes._ The pulmonary congestions preceding pneumonia are due to the
same causes with that disease. The most typical, acute and deadly form
of pulmonary congestion is usually due to _over-exertion in an animal
that is fat and out of condition_. The English hunting field presents
the most typical specimens. A horse that has just left the dealer’s
hands, or that is plethoric, fat, soft and flabby, is ridden over a
heavy country, and though he may perform well for a few miles, he soon
hangs heavily on the bit, slackens his pace, and if not pulled up,
staggers and falls “all of a heap.” A farm horse, taken from grass or
other soft feeding, and entirely out of condition often suffers in the
same way, in going perhaps for the veterinarian in case of urgent colic
in one of its fellows. Cruzel draws attention to similar congestions
from over-exertion in fat cattle, and Trasbot in wild stags and hogs
when beechnuts and acorns were abundant, in pampered family horses and
in plethoric farm animals generally. Excessive heat (heat apoplexy) is
invoked as a cause, and the arrest of hæmatosis and consequent
stagnation in the pulmonary capillaries are undoubtedly accessory
causes, yet the majority of cases, and the most typical and fatal, occur
in the winter season (the hunting season). On the other hand, chills
from rains or cold draughts, especially when heated and exhausted, are
common causes, and the disease often comes on more gradually, attaining
its acme after five or six hours. A horse perspiring after a hard drive
and left to face a cold blast unblanketed, or one plunged by accident
into ice cold water for ten minutes (Trasbot) are examples of this kind.
These cases are ushered in by violent rigors, whereas in those due to
over-exertion this is much less marked and is usually only suggested by
the coldness of surface and extremities. Another condition which
contributes to pulmonary congestion is a full stomach. The plentitude of
the abdominal organs leads to compression of the lungs and hampered
circulation, and when to this is added over-exertion and exhaustion
acute congestion is speedily induced.
Acute congestions are noticed as an accompaniment of other diseases, but
these are mostly either the localization in the lung of a specific
morbid process (anthrax, influenza, distemper, strangles), or it is due
to auto-poisoning, as when the cutaneous transpiration is suppressed by
a coating of glue, or to embolism.
_Symptoms._ In the horse which fails under severe exertion there are the
dilated nostrils, the labored breathing, the deep, almost convulsive
action of the flanks, the hanging on the reins, the slacking of the
pace, the unsteadiness of gait, and lastly the fall. There may now be
noticed the protruded bloodshot eyes, the agonized expression of
countenance, the extended head, the pallor, and later the blueness of
the nasal mucous membrane, the short, panting breathing, accompanied by
a roaring noise alike in inspiration and expiration, and the small,
weak, rapid pulse often imperceptible at the jaw. If the animal has been
stopped short of having fallen, or if he is able to get upon his feet,
he stands with his limbs apart to secure his stability, and with the
elbows turned out to facilitate the expansion of the chest. As the
breathing becomes panting the respirations are less deep, the ribs are
maintained permanently drawn outward, and the flanks rise and fall to a
limited extent only but with great rapidity (eighty to one hundred per
minute). Auscultation may detect at first an increase in the pitch of
the respiratory murmur, and the presence of the finest possible
_crepitation sound_. Soon the murmur decreases uniformly. The
extremities are cold, and in this coldness the general surface to some
extent participates even though it may be covered by perspiration.
Tremors or rigors are present. The heart is felt behind the left elbow
to beat tumultuously. If blood is drawn it flows in a thin, black, tary
stream.
In some cases blood more or less frothy is discharged from the nostrils
as the result of rupture of pulmonary vessels.
In the fulminant cases in =cattle= respiration is rapid, even panting,
wheezing, the expiration attended by a hoarse grunt, sometimes nasal
hemorrhage, great prostration, profuse perspiration, a stupor sets in
and the animal falls and dies, with more or less struggling.
In the cases which develop more slowly, and as the result of cold and
chill whether in horses or cattle, there is dullness, anorexia,
prostration, increasing rapidity and oppression of the breathing, a
small, frequent, hoarse cough, and at first distinct pallor of the
conjunctiva and pituitary mucosa, with more or less trembling. The head
is extended on the neck, toward an open door or window, if available,
until prostration and stupor forbid. The pulse is small, thready, often
almost imperceptible and much accelerated, while the heart beats are
strong, violent, tumultuous. For a time the respiration may be not more
than double the normal rythm, but it tends to more or less rapid
increase with wheezing or stertorous sounds and shaken by trembling of
the respiratory muscles. The nasal discharge is slight and grayish often
with streaks of blood. If it increases the cough becomes looser and
softer. Quite early the respiratory murmur decreases over the whole lung
and a blowing sound from the bronchia or larnyx is heard on the upper
middle third of the chest. This may be complicated by a mucous râle, or
when hæmorrhage has supervened by a loud rattling. Percussion shows a
lack of resonance over the whole lung, not so flat and definitely
circumscribed as in pneumonia but a partial flatness of sound over the
whole chest. In pneumonia a limited area of lung is absolutely
solidified (hepatized) while the remaining lung is practically normal,
whereas in acute congestion often the whole lung is gorged with blood
but for some time no part of it is entirely divested of air.
Another marked feature is the maintenance at first of the normal
temperature with only a slight rise of about 1°. This serves to
distinguish congestion of the lungs from sunstroke (heat anhæmatosis) in
which the temperature usually rises to 108° or 110° F or higher. The
temperature rises however as the disease advances and merges into
pneumonia. Another distinguishing feature from sunstroke is the early
pallor of the mucous membranes which in heat apoplexy are strongly
congested. In congestion they become dark red only with the advance of
the disease and the advent of asphyxia. These features serve also to
distinguish acute pulmonary congestion from contagious fevers, pneumonia
and other inflammations of internal organs.
_Course._ _Termination._ The more acute (fulminant) forms are promptly
fatal. In the exhausted system the lungs have become uniformly gorged
with blood, which can no longer be forced through the capillaries by the
right heart, the heart in turn is overdistended with blood and ceases to
beat and death ensues in a few minutes.
In the less acute cases the patient survives twenty-four hours and
upward, the whole lung not being equally implicated but only certain
lobules, usually the lower, or the congestion, if uniform in all the
lung, being less extreme.
In favorable cases recovery takes place in one or two days. There is a
return of life and appetite, a gradual improvement in pulse and
breathing, the respirations becoming deeper and longer, and in a few
hours all the more violent symptoms may have disappeared. With a more
gradual improvement recovery may still be complete in four or five days.
_Lesions._ When the subject has died suddenly the appearances are
essentially those of uniform engorgement of the pulmonary capillaries
with blood. The general aspect is a dark red, varying from reddish brown
to black, the darkest shades corresponding to circumscribed areas of
actual hæmorrhage. In the worst cases the whole mass may appear like
black currant jelly. The lungs do not collapse when the chest is opened,
they are more or less friable at various points, and different portions
will sink or float in (not on) water, according as it may be more or
less airless. A dark liquid blood exudes freely from the torn or cut
surface. Sections of the lung tissue hardened and examined under the
microscope show the alveoli and bronchioles devoid of exudate, but
having their cavities compressed and obliterated by the pressure of the
swollen mucosa, and its investing blood clot. The heart is overdistended
with fluid blood. In asphyxiated cases the general venous system is
filled with black, liquid blood, and the serosæ spotted with petechiæ.
_Nature._ The nature of this disease is variously understood. It differs
from inflammation in the absence of active cell proliferation, and
migrations of inflammatory exudation, and of fever at all proportionate
to the extent of the lesions. All these may and do supervene if the
patient survives but they are practically absent for a length of time at
the outset. Some attribute it to paresis of the vaso-motor centres for
the lungs, as the result of their over stimulation and of the
retrocession of blood from the chilled surface to the internal organs.
But congestions caused by cutting the cervical branch of the sympathetic
nerve or the sciatic plexus are not marked by a similar blood
extravasation and destruction of tissue. The delicate structure of the
lung tissue and the comparative absence of mechanical support will
account for this in part, the great force of the circulation overloading
the capillaries, under the impulse of the heart so closely adjacent, has
doubtless a certain effect, and the venous nature of the blood thus
forced into the lungs and calculated to arrest all normal function has a
potent influence. If we add to this, for the _over-exertion_ cases, the
sudden advent into the circulatory stream of unchanged peptones and
other ingredients of the portal blood of highly fed and plethoric
animals we find a sufficiently pathogenic combination. In all acute
cases however the adiposity, poor condition and susceptibility to speedy
exhaustion must be given their full share of responsibility.
_Treatment._ Girths, saddles and anything else that may hamper the
movement of the chest must be at once removed and the horse’s head
turned to the wind, an active stimulant given and the legs well rubbed
and loosely flannel bandaged. The nature of the stimulant is of less
consequence than its prompt administration. Two ounces of chloroform, of
sulphuric ether, or of sweet spirits of nitre; half a pint of whisky,
brandy or gin; or a pint of any of the more stimulating wines may be
given, diluted in warm water so as to remove their irritating qualities.
A drink of warm gruel will often go far to restore warmth to the surface
and to unload the overtaxed lungs. Frequent large injections of warm
water have a similar effect. Active hand rubbing of the legs and the
wrapping of them loosely in flannel bandages previously warmed at the
fire is equally valuable. If a roomy, well ventilated, loose box can be
obtained the horse should be led to it gently and a light but warm rug
placed upon the body. Valuable derivation may be obtained from
pediluvia, the feet and legs up to the knees and hocks being put in
buckets of water as hot as the hands can bear, and at the same time
actively rubbed. If this is impossible the legs may be wrapped in
bandages and wet with hot water every few minutes. Or this soothing
derivative agent may be applied as well to the surface of the chest. A
blanket wrung out of hot (nearly boiling) water until it no longer drops
is wrapped round the body and covered up with two or three dry rugs. A
second smaller rug is wrung and placed on the neck and covered by a
sufficiency of hoods to keep in the heat. The legs are meanwhile hand
rubbed and bandaged and the other measures above recommended carried out
to restore the circulation in the surface and extremities. The time
honored practice of bleeding freely from the jugular vein is one of the
most effective means of relieving the overcharged heart and lungs, and
should be resorted to at the earliest possible moment. The blood will at
first flow in a small, dark stream, but as the circulation obtains
relief the jet will increase in volume and the general symptoms will
improve. From four to six quarts may be taken with advantage from an
ordinary horse. This is not a pneumonia but an overloaded heart and
lungs, threatening speedy death and which the abstraction of blood
promptly relieves.
The longer the bleeding is delayed the less effective it is. It should
not supersede the other measures already recommended. There is no real
paradox in both bleeding and giving stimulants in such a case, as the
essential condition is one of weakness, and if the abstraction of blood
has been of use in relieving the clogged heart and lungs, the depression
under which these have labored may be still further overcome by agents
calculated to rouse their suspended vitality.
Trasbot strongly recommends large doses of tartar emetic and iodide of
potassium to reduce the blood pressure in the lungs, an advice which
will be received with hesitation by those who dread the already paretic
condition of the heart. His combination of iodide of potassium with
digitalis will be more confidently resorted to. One drachm of the former
may be given with a half drachm of the latter twice daily.
With the advent of marked fever and other signs of pneumonia, the
treatment for that disease should be resorted to.
PULMONARY ŒDEMA.
Causes, pneumonia, extra force of right heart or weakness of left,
insufficiency of mitral valves, deflection of blood by obstruction in
one portion of lung, pressure of tumor on pulmonary veins. Malignant
œdema. Malignant catarrh. Bright’s disease. Anæmia. Parasitism.
Symptoms, abnormal heart sound, or urinary secretion. Parasitism.
Percussion shows flat sound auscultation lowered, respiratory murmur,
heightened blowing. No crepitation. Expectoration serous. Prognosis
grave. Treatment, attacks primary disease. Posture. Elimination. Dry
capping. Heart tonic.
A dropsy of the lung tissue may supervene in weak conditions, in the
course of inflammatory disease of the lungs; it may also depend on an
imperfect balance in the forces of the right and left heart
respectively, which leads to the habitual throwing of blood pressure
back upon the lungs. Still more frequently the congestion and dropsy
depends on insufficiency of the mitral valves by reason of which a
reflux of blood toward the lungs takes place at each heart beat. The
pressure of tumors on the pulmonary veins may have a similar action.
Obstruction of circulation in one portion of lung may cause an extra
blood pressure on an adjacent one, and œdema so caused may be found
especially in cattle and pigs in which the interlobular connective
tissue is specially abundant. This may be seen in miliary tuberculosis
in cattle, and it probably contributes to produce the extraordinary
liquid collections that characterize lung plague. In cattle also
malignant œdema may affect the lung, and an œdematous condition is
sometimes met with in malignant catarrh. Bright’s disease is another
cause, the uræmic dropsy finding a favorite seat of election in the
loose lung tissue unsupported by solid tissues. The anæmia resulting
from parasitism like distomatosis may similarly affect the lung.
The _symptoms_ of pulmonary œdema will usually be complicated by those
of the affection causing it. Thus modification of the first heart sound
or of the urinary secretion, or the existence of parasitism, would
furnish valuable indications.
The _physical signs_ of lung disease vary. If pneumonia is present it is
betrayed by its characteristic symptoms. In the absence of inflammation
there is dullness on percussion over the affected area, and on
auscultation an absence of the respiratory murmur, and perhaps abnormal
clearness of bronchial, cardiac and other sounds from deeper parts. It
differs from pneumonia in the absence of fever and of any crepitation
surrounding the consolidated portion. The expectoration is serous or
watery, rather than rusty or purulent.
The _prognosis_ is always grave in proportion to the incurable nature of
the primary disease. Chronic valvular or Bright’s disease, miliary
tuberculosis or malignant tumors would render the case hopeless, while
in acute pneumonia, or nephritis or parasitism there may be some hope.
The _treatment_ will largely consist in the therapeutics of the primary
disease, yet we may also seek to relieve the dangerous symptoms of
œdema. The frequent change of position may serve to limit hypostatic
accumulation. Diuretics or purgatives in strong patients will favor
absorption. Pilocarpin more than any other agent secures temporary
absorption but cannot be continued owing to its depressing effects.
Digitalis is often valuable in improving the heart’s action, and acting
freely on the kidneys. Dry capping on the chest acts as a derivative.
ATELECTASIS. COLLAPSE OF LUNG.
Atelectasis in bronchitis, congenital, etc. Airless condition in the
absence of exudation. Causes, congenital persistence in butcher
animals. Blocking of air tubes by exudate—ball valve. Desquamation of
ciliated epithelium. Compression by hydrothorax, pneumothorax, and
false membrane. Symptoms. Percussion flatness, juvenile respiration
elsewhere, blowing sounds loud. Drum-like sounds on emphysema and
pneumothorax. Cyanosis. Lesions, depressed, flesh-like,
non-crepitating lobules or lobuletes, sink in water, dilatable.
Treatment, rouse respiratory centres, douches, cold and warm,
slapping, electricity, forced inspiration, diet, massage. Treat
attendant disease.
This has been already referred to as a result of bronchitis, but it
deserves special mention as a sequel of that affection, and in various
domestic animals, as an independent condition. The condition is one of
consolidation of lung by the complete exclusion of air, but without any
infiltration of its substance by inflammatory exudate or dropsical
effusion. The tissue remains in its normal state apart from the fact
that its bronchioles and air sacs are undilated. The affected portion
has a solid dark fleshy appearance. The collapsed portion often
represents one lobule or group of lobules which communicate with a
single bronchium.
_Causes._ In some instances the conditions remain from birth, the lobule
never having been called into use. This is seen especially in cattle and
other meat producing animals, in which active breathing is
systematically suppressed in the interests of rapid growth and the
deposition of fat. In the improved breeds the lungs remain larger than
the exigencies of the life demand, and large portions remain out of use.
In bronchitis the condition is acquired, and is mainly dependent on the
blocking of a bronchial tube with tenacious mucus or a desiccated mass.
The pathological lesions of bronchitis favor this since one of the
earliest changes in the inflamed mucosa is the desquamation of the
columnar epithelium. This removal of much of the cilia and the paralysis
of much of what is left annihilates for a time the normal method of
clearing away the secretion, and this being now produced in excess
blocks the tubes. This secretion virtually acts like a ball valve in
favoring the exit of the air during the convulsive expiration of
coughing, and hindering its entrance during the succeeding inspiration.
The bronchia and bronchioles decrease in size to near their termination,
so that, as forced out in coughing, the secretion enters the larger tube
and allows the exit of air, which as drawn back in inspiration it enters
the smaller tube and closes it against any possible ærial entrance.
Mendelssohn and Traube demonstrated this action by introducing a shot
into a dog’s lung, and in two days the left lung was found collapsed and
the right one the seat of complementary emphysema. The violence and
frequency of the cough therefore bears a ratio to the occurrence and
extent of atelectasis. Other causes are the compression of the lower
lobes of the lung by hydrothorax, by pneumothorax (developed by
lacerated lung or perforated chest wall) or by a false membrane
contracting in process of organization.
_Symptoms._ As a congenital condition in the improved meat producing
animals the condition is rarely recognized in life and cannot be said to
be a defect. The collapsed lobule being farther removed from the air may
be a more favorable field for the growth of pathogenic bacteria, but on
the other hand these do not so readily penetrate it as if the tubes were
open. When the collapse is more extensive, the contrast in the flatness
on percussion and indistinctness of the respiratory murmur on the
affected side, and the marked resonance and loud murmur on the other,
may serve to identify the affection. In extensive, traumatic cases this
contrast is much more prominently marked, as the expanded portions have
to take on extra compensatory work and are not infrequently rendered
emphysematous. The drum-like sound in percussion of such parts, and in
the upper part of the chest in pneumothorax are pathognomonic of these
conditions. Again in hydrothorax the horizontal upper level of the area
of dulness betrays a liquid cause. Severe cases are marked by cyanosis.
The _lesions_ seen in atelectasis consist in depressed areas of a dark
fleshy color on the surface of the lung, usually sharply limited by the
borders of the lobules, and in strong contrast with the bulging, light
colored lobules adjacent, which are often emphysematous. The collapsed
lobule may usually be dilated when air is forced into the bronchium, but
if it has been of some standing this is often difficult or impossible.
If it has resulted from bronchitis or compression of a previously
inflated lung it will often float in (not on) water, from a little
retained air, but in congenital atelectasis it is airless and sinks to
the bottom.
When _treatment_ is demanded it will vary according to the cause. In
congenital atelectasis the respiratory centres must be roused. The new
born animal may be sprinkled alternately with ice cold and hot water, or
the chest may be slapped with the palm of the hand or a wet towel. The
nostrils must be cleared of mucus, and the lungs inflated by blowing or
bellows, the larynx being pressed back against the gullet to prevent
inflation of the stomach. If available electricity may be applied to the
chest walls. These measures may be repeated at intervals and the
systemic weakness overcome by nourishing food, stimulants and friction
of the skin.
In acquired atelectasis we should seek to correct the disease to which
it owes its existence. In bronchitis the measures already indicated for
the liquefaction and removal of the expectoration will be in order; in
hydrothorax a judicious paracentesis and in pneumothorax the aspiration
of the gas, and the closure of any traumatic opening through which that
gas has gained access.
HÆMOPTYSIS.
Causes, over-exertion in plethoric, glanders, pulmonary tubercle,
petechial fever, embolism, aneurism, ulcerated new formations,
anthrax, septicæmia, hæmorrhagic diathesis. Symptoms. Inappetence,
cough, cold limbs, rigor, hard pulse, jugular pulse, violent heart
beats, unsteady gait. Discharge, bloody, crimson, frothy, with cough,
without acid, excited breathing, debility. Indications from
pre-existing disease. Treatment, quiet, elevated head, cold
irrigation, ice bags, acetate of lead, opium, ergot, matico, tannin,
iron, oil of turpentine, laxatives, cool stable.
The term _hæmoptysis_ (αιμα, blood, πτυω, I spit,) is now entirely
restricted to bleeding from the lungs and lower air passages. It is a
very rare complaint in the lower animals, but is sometimes seen in both
horse and ox. In very plethoric subjects the overloaded circulatory
organs give way in the delicate membrane, lining the ultimate bronchial
tubes and the air cells. The exciting cause in such cases is usually
some severe effort of draught, a violent gallop, or other unwonted
exertion. It occurs in glanders from rupture of caseated pulmonary
nodules. It does not appear to be so common in phthisis in the lower
animals as in man, but one case occurred under the eye of the writer in
which the bursting of a large tubercle in the lung of a cow involved the
rupture of a considerable vessel with a fatal result. Pulmonary embolism
and infarction, petechial fever, aneurism, ulcerated neoplasms, anthrax,
and septicæmia are additional causes. Lastly hæmoptysis sometimes takes
place in hæmorrhagic subjects without any appreciable rupture of
vessels, the blood sweating from the surface of the bronchial mucous
membrane.
Premonitory symptoms are sometimes noticed, such as dulness, and
lassitude, loss of appetite, a frequent short cough, coldness of the
limbs and surface, shivering, full, hard pulse, pulsation in the
jugulars, tumultuous action of the heart, and unsteadiness of gait.
More commonly it comes on suddenly as the result of severe muscular
strain or excitement. The blood flows from the nose, and rarely from the
mouth in solipedes, but indiscriminately from both in other animals. It
is bright red, clear, frothy, or mixed with mucus, and variable in
amount. It is easily distinguished from nasal hæmorrhage, which is not
frothy, and from bleeding from the stomach, which is clotted and
blackened, with an acid odor from the presence of the gastric juice. The
cough of hæmoptysis contrasts with the sneezing of epistaxis and the
retching of hæmatemsis. The rattling cough increases the discharge, as
does also a dependent position of the head. Besides the cough there is
usually an anxious countenance, accelerated breathing and considerable
lifting of the flank. When the loss is excessive there is weakness,
giddiness, rolling of the eyes, and pallor of the visible mucous
membranes.
The previous ill-health of the patient, the presence of tubercle as
ascertained by auscultation and percussion, and the hæmorrhagic
constitution as shown by occurrence of bleeding from other parts of the
system will lessen the chances of a favorable termination. Sometimes,
too, the flow is so profuse that the blood cannot be coughed up, and
filling the bronchial tubes it destroys life suddenly by suffocation.
_Treatment._ When brought on by severe exertion absolute quiescence will
usually check hæmoptysis. Keeping the head in an elevated position
favors its arrest. The application of cold water to the head, neck and
thorax, and the giving of iced water, strongly acidulated by vinegar or
one of the mineral acids may sometimes be required. In threatening or
obstinate cases one drachm of acetate of lead may be given thrice daily
to check by its astringent effect on the vessels, and the addition of a
drachm of opium is of great value in suppressing the cough. Ergot,
tannin, matico, and oil of turpentine have each been employed with
advantage, and when costiveness exists a saline laxative (one pound
sulphate of soda) may be usefully resorted to. The patient should be
kept in a cool, airy dwelling, and should rest for fifteen or twenty
days after an attack.
PULMONARY APOPLEXY. HÆMORRHAGIC INFARCTION.
Different forms. Embolism with infarction. Embolism from arteritis.
Rupture of bloodvessel. Changes in color. Symptoms. Repair.
Hæmorrhage into the lungs may be: 1st. Petechial in infectious diseases.
2d. _interlobular_ as from ruptured vessels. 3d. _Infarction_ or
apoplexy. _Infarction_ results from embolism of a branch of the
pulmonary artery, which may in its turn be due to clots formed in a
diseased heart or in the systemic veins and carried to the lungs in the
blood stream. It may also result from inflammation of the inner coat of
the pulmonary artery. A virtual stasis occurs beyond the embolism, and
the blood filtering in through the anastomosing capillaries fills and
blackens the affected lobule. With rupture of a considerable vessel the
blood escapes _en masse_ and appears like black currant jelly. As it
ages it becomes granular and changes to a yellow color, or it may form a
necrotic mass enclosed in a cyst as in lung plague. The symptoms, apart
from the absence of respiratory murmur and resonance, are not
diagnostic. It may take months to undergo liquefaction and absorption.
Iodide of potassium, bitters and stimulating diuretics may be given.
PNEUMONITIS; PNEUMONIA; INFLAMMATION OF THE LUNGS.
_Definition._ Inflammation of the spongy tissue of the lungs
uncomplicated by that of the bronchia or pleura.
_Divisions._ This affection has been variously divided according to
_seat_, _nature_, and _complications_: thus:
_Single Pneumonia_: Affecting one lung: _right_ or _left_.
_Double Pneumonia_: Affecting both lungs.
_Lobar Pneumonia_: Affecting one lobe or by lobes.
_Lobular Pneumonia_: Affecting by lobules.
_Acute Pneumonia_: _Subacute Pneumonia._ _Chronic Pneumonia._
_Croupous or Fibrinous_: With fibrinous exudate.
_Catarrhal_: With exudate rich in cells and granules.
_Hæmorrhagic_: With extravasation of blood.
_Purulent_: Tending to pus: abscess.
_Necrotic_: Tending to gangrene: sequestra.
_Desquamative_: With great proliferation of alveolar epithelium.
_Interstitial_. _Interlobular_: Affecting mainly the interlobular
connective tissue.
_Hypostatic_: Dependent on gravitation of the blood.
_Metastatic_: Due to embolism.
_Parasitic_: Caused by parasites. Due to wounds or foreign bodies.
_Contagious_ and _Traumatic Pneumonia_.
Many of these are, however, but localizations of the same affection and
others are manifestly microbian diseases which in the present state of
pathology it is not always easy to early distinguish sufficiently for
clinical and therapeutic purposes. For the sake of convenience therefore
pneumonia will here be treated of generally, and under the headings
devoted to etiology, pathology, therapeutics, etc., attention will be
given to distinctions. Those pneumonias that are but pulmonary
manifestations of other diseases—influenza, glanders, tuberculosis,
strangles, contagious pneumo-enteritis, lung plague, septicæmia, pyæmia,
swine plague, hog cholera, petechial fever, actinomycosis, and neoplasms
will be considered under these respective headings.
ACUTE CROUPOUS PNEUMONIA. PNEUMONITIS IN THE HORSE.
Definition. Differentiation from acute vascular congestion.
Predisposing causes, age, sex, stabling, training, diet, impure air,
low health, previous lung disease, plethora, climate, season, exciting
causes, chill, fatigue, leucomaines, sudor, draughts, plunging in or
spraying with cold water, clipping, inhalation of irritant smoke, gas,
dust, drawing of food, irritating or insoluble drugs into the lungs,
neoplasms, parasites, contusions, fractured ribs, punctures,
contagion, plurality of germs, bacillus of Friedländer, micrococcus of
Talamon and Fränkel, diplococcus pneumoniæ equina of Schütz,
diplococcus pneumoniæ equina of Cadeac. Symptoms, chill, hyperthermia,
dullness on percussion and crepitation in the lower part of the lung,
reaction, congested mucosæ, accelerated labored breathing, excited
circulation, pulse oppressed, cough deep, patient statant, elbows
everted, nose protruded, nostrils dilated, approaching door or window,
pinched countenance, skin dry, harsh, adherent, partial sweats, loins
insensible, nasal discharge rusty, dependent part of lung largely
non-resonant, with peripheral crepitation. Blowing in abnormal
situation over hepatized lung. Decubitus, its significance. Course.
Results. Favorable indications in pulse, breathing, face, temperature,
appetite, decubitus, clearing of lung. Unfavorable indications in
breathing, pulse, fever, face, uneasy movements, pawing, cold limbs,
prostration, nervousness, weakness. Sabacuto Pneumonia. Terminations
of pneumonia, death, resolution, splenisation, abscess, gangrene, red
hepatisation, gray hepatisation, fibrinous consolidation. Lesions.
Congestion, exudation and cell growth, hepatization—red and gray,
deliquescence, abscess. Blood, loss of red globules, increase of
white, excess of fibrine, glandular swelling, pleurisy, degenerations
in other organs, laminitis, rheumatism. Treatment, adapted to strength
of subject and type of disease, hygienic, anti-rigor, antiphlogistic,
expectant, stimulant, antipyretic, febrifuge, sedative, moist
compresses, derivatives, laxatives. In subacute form tonics, heart
stimulants, febrifuge. In chronic cases add rich digestible diet, and
easy open air life.
This consists in inflammation of the spongy tissue of the lung involving
mainly and primarily the walls of the alveoli and interlobular
connective tissue with their respective trophic centres (nuclei). The
acute congestion of excessive heart action and debilitated pulmonary
capillaries described above, is primarily a disease of the bloodvessels
which become over distended and may or may not lead to the inflammatory
processes in their walls and the tissues adjacent. Pneumonia on the
other hand is essentially inflammation of these tissues and nuclei, with
exudation usually of a fibrinous material into their substance.
PREDISPOSING CAUSES. =1.= =Age.= A very early age is nearly exempt, and
from 6 years upward there are fewer cases relative to the equine
population, variations that may be better accounted for by stabling,
training and acquired immunity than by the mere fact of age. Of 237
cases, 2 were 3½ years; 32 were 4 years; 19 were 5 years; 131 were 6 to
11 years; 46 were over 11 years; and 7 of uncertain age (Trasbot). =2.=
=Sex.= No visible effect. =3.= =Stabling, training, change of food.=
While the young colt at pasture is practically immune, the period of
stabling, transition to a dry and grain diet, and to the nervous
excitement attendant on training and unwonted work as shown in the
statistics of Percivall and Trasbot determine an enormous increase of
cases. In a cavalry regiment Percivall found that 56.6 per cent. of all
lung diseases occurred before the 5th year, and Trasbot found that at
the Alfort Veterinary College 13.5 per cent. of all equine pneumonias
occurred in the 4th year. =4.= =Hot Stables.= =Impure Air.= These two
conditions usually coexist and prove potent causes especially in young
horses brought from the fields. We cannot, however, separate this cause
as usually observed from the action of pathogenic germs which are
preserved and concentrated in such places. =5.= =Poor Health.=
Debilitating diseases, insufficient and poor diet, overwork, exposure to
cold draughts or darkness and any other cause which lowers the vitality
predisposes. =6.= =A Previous Attack.= This usually leaves some
structural or functional change which renders the lung more susceptible
to a subsequent invasion. Against this must be placed the immunity which
follows the contagious forms, but as this is usually exhausted in the
course of six months it does not invalidate the position that the
permanent impairment of pulmonary integrity is a predisposing cause.
=7.= =Plethora.= Tending as this does to congestion it must be accepted
also for the next pathological step—pneumonia. =8.= =Climate and
Season.= This is notoriously an important factor. At Paris, Trasbot met
with 237 cases in the nine months from October to June inclusive and but
8 cases in the summer months—July, August and September. In Great
Britain, where the vicissitudes are less severe Percivall had in the
cavalry horses in the seven months from October to April inclusive 146
cases = 20.85 Per month, and in the 5 months from May to September
inclusive 62 cases = 12.4 per month.
_Exciting Causes._ Nearly all the above causes when acting with unusual
force may become direct factors in causation. The effect of a sudden and
extreme chill is especially to be feared. Even in cases that are
unquestionably due to a microbe as the essential cause, the nervous
disorder manifested in the chill, and the clogging of the pulmonary
circulation in connection with the retrocession of blood from the
surface of the body furnishes the opportunity for the colonization of
the germ. The average horse at pasture will stand with impunity cold
storms of rain, snow, and sleet, and transitions from a warm noonday sun
to a cold night wind and dew and even frost, but under other conditions
of the system, with the fatigue and fret and sudden changes of food and
regimen attendant on domestication, or with any derangement of an
important bodily function the _chill_ is often the manifest occasion of
disturbance of the balance of health, and the supervention of pneumonia.
=Fatigue=, a system charged with =leucomanies=, and a =free
perspiration=, which is suddenly checked by exposure, at rest, to a
=cold rain=, or =snow=, to a =draught between door and window=, to
=immersion in the cold waters= of a river, or to =sponging with cold
water= is quite liable to cause pneumonia. An unduly heavy winter coat,
an individual peculiarity or determined by a cold environment in autumn
often predisposes strongly to such dangerous chills, by the frequency
and profuseness of the perspirations and general relaxation of the
system. Clipping of such subjects is a true hygienic measure though it
entails the need of extra care in blanketing. Again in the animal that
has already suffered from disease of the respiratory organs these chills
are more dangerous factors.
=Direct irritation= by inhalation of smoke and other products of
combustion; or acrid or irritant gases or dust; by the drawing of food
by aspiration into the lungs (as in paralysis of the larnyx or pharnyx,
choking, apoplexy, vomiting, etc.); by pouring irritant or insoluble
drugs (oil, lard) through the nose; by the pressure of neoplasms
(actinomycosis, tubercle, glanders, cancer); or by the presence of
parasites (strongylus, distomata, echinococci, linguatulas).
_Pneumonia_ from =Contusion= of the chest, fracture of a rib, or
puncture or laceration of the lung is recognized.
=Contagion.= The presence of a _contagium_ in pneumonia is today well
established. Clinical observation had indicated this even before the
discovery of a specific germ, but recent bacteriological investigations
and the transmission of the disease by inoculation of artificial
cultures have definitely settled the question. It does not follow that
all cases are contagious, nor equally so, but the recognition of the
contagious form satisfactorily explains the prevalence of the disease in
one stable while an adjoining one escapes, and the eruption of new cases
in a stable after an animal affected with the disease or convalescent
from it has been introduced. It has been objected that many horses stand
in the stable with pneumonia cases and escape, but so is it with
glanders, cowpox, and many other affections. It merely argues an
immunity in the case of some, and for the disease germ a very limited
transmissibility through the air. The further objection that the
existence of lesions in the lung before the onset of fever, excludes
this from the list of infectious diseases, is untenable since many
undeniably contagious diseases, like cutaneous anthrax, glanders, lung
plague, cowpox, appear locally before any constitutional disturbance
occurs, which later as the result of extensive local disease and the
circulation of toxins in the blood. It places contagious pneumonia
however in that long list of infectious diseases which develop first
locally in the seat of infection and later become more or less
generalized.
It must be admitted however that the germ of pneumonia is not the same
for all cases of the disease and for all genera of animals. It must also
be allowed that the same germ does not always maintain the same degree
of virulence, and that it may even live for a time on the buccal mucosa
of an animal belonging to a susceptible genus without any morbid result.
In short we must recognize that different germs of pneumonia may become
temporarily non-virulent or only slightly virulent, and remain
pathologically quiescent, as for example during the summer months, to
reassert itself later when the conditions become more favorable to its
pathogenesis.
BACTERIOLOGY.
a. BACILLUS OF FRIEDLÄNDER. This is a short rod with rounded ends, often
merely oval, occurring in pairs, or chains of four, and under given
circumstances surrounded by a transparent gelatinous capsule. It is
ærobic, nonmotile, does not liquefy gelatine, nor sporulate, and in
gelatine stick cultures has a nail-like growth. This was found by
Friedländer, Frobenius, Weichselbaum and Wolf in the pulmonary alveoli
in a small proportion of cases of croupous pneumonia in man. The
cultures, injected into the lungs of animals, killed one dog (out of
five), six Guinea pigs (out of eleven), and thirty-two mice (all the
injected). Lesions were intense congestion of the lungs, seropurulent
pleural effusion, and enlarged spleen, while the bacillus swarmed in the
blood and exudate.
MICROCOCCUS PNEUMONIÆ CROUPOSÆ. First found by Sternberg in his own
saliva in health, and by Pasteur in the saliva of a rabid child.
Afterward found in the great majority of lungs affected with croupous
pneumonia in man, by Talamon, Salvioli, Sternberg, Fränkel,
Weichselbaum, Netter, Gamalei, etc. Later it was found in meningitis, in
ulcerative endocarditis, in arthritis, in otitis media, and in acute
abscess in man.
It is a _spherical_ or _oval coccus_, arranged in pairs, in fours, or
exceptionally in eights or tens. Lanceolate forms are the rule in the
blood of animals, and circular in artificial cultures. It stains readily
in aniline colors and by Gram’s method, grows in ordinary culture media,
at 37° C. in the absence of free acid, and in gelatine stick cultures as
small, white colonies along the line of culture, without liquefying the
gelatine. It dies in ten minutes at 52° C. (Sternberg). Its virulence
lessens in artificial cultures, but is restored by passing through the
body of a susceptible animal.
Injection into the lungs or trachea of rabbits, mice, sheep and, less
certainly, Guinea pigs, produced distinct fibrinous pneumonia filled
with the microbe. In dogs, subcutaneously, it caused abscess, but in the
lungs an acute fibrinous pneumonia which only exceptionally proved
fatal, recovery usually taking place in ten to fifteen days.
Klemperer induced immunity, sometimes lasting six months, by intravenous
injection of filtered cultures.
DIPLOCOCCUS PNEUMONIÆ EQUINA. First found by Schütz in the lungs of
pneumonic horses in 1887. It is an oval coccus arranged usually in pairs
or in threes or fours, and surrounded by a transparent envelope. It
stains in aniline colors but not by Gram’s method. It is ærobic and
grows in gelatine at ordinary temperature without liquefying it, and in
stick cultures forms a line of small, white, separate colonies which do
not coalesce by growth. Does not grow on the surface of the gelatine
around the puncture. Line cultures on agar are in colonies like minute
transparent droplets. In bouillon it develops long chains.
Inoculated on the rabbit, Guinea pig and mouse, it produced death with
pneumonic affections (hæmorrhagic congestion or inflammation), but it
failed to take in some of the rabbits and Guinea pigs. Chickens and pigs
proved immune. Injected into the horse’s lung or as spray into the
trachea it produced true croupous pneumonia. Fiedaler and others
obtained similar results. Peter has found the fæces of pneumonic horses
virulent, an important point in connection with disinfection.
Schütz found that 20 grammes of the culture, in an equal quantity of
boiled water, injected into the horse’s trachea, produced a rise of
temperature by two or three degrees, with rigors, cough, accelerated
pulse, elevated temperature, dyspnœa and prostration, but that this
subsided in a few hours. By repeating this every thirty-six hours, the
fourth or fifth would fail to produce a reaction and the subject proved
immune.
CADEAC’S DIPLOCOCCUS PNEUMONIÆ EQUINA. In the lungs of cases of
contagious pleuro-pneumonia of the horse Cadeac found a round
noncapsulated coccus appearing in pairs, or rarely in chains, and
staining by Gram’s method. It grew slowly in bouillon and agar at 37°
C., forming on the latter in twenty-four hours, a thick, whitish, oily
drop, which, as it grew larger, assumed a silvery whiteness, and dried
in the centre. In bouillon it precipitated a powdery sediment. The
reaction of the culture medium was unchanged. It lost virulence rapidly
in artificial cultures or by a heat of 50° C., and it died in ten
minutes at a temperature of 60° C. Virulence was long retained when
dried, or even in putrid material.
This proved infecting to the ass, rabbit and Guinea pig, while the cat
and white rat proved immune. Intratracheal injection of the dog produced
a transient pneumonia. The ass inoculated with the blood of the infected
rabbit died in three days, with a hepatized lung, pleurisy, and swarms
of the microbes in the lungs, blood and internal organs. Rabbits
injected intravenously had enlarged spleen, reddish exudate in the
serous cavities, urine stained with hæmoglobin, and lungs and kidneys
congested. With intratracheal injections the lesions were exclusively
pulmonary. The pulmonary lesions were less constant in the Guinea pig.
Weakened virus caused pulmonary lesions only without septicæmia.
It has been suggested that this coccus is at least closely related to
that of pneumo-enteritis of the horse.
_Symptoms._ The onset of pneumonia is not often seen by the
veterinarian, who is called in only after the cough, loss of appetite,
hurried breathing and rigor has revealed illness to the attendants.
Hence perhaps chill and rise of temperature have been placed among the
earliest symptoms. The symptoms are more violent in the racer, trotter
and other nervous animals. Trasbot positively claims, that considerable
pulmonary inflammation and even exudation have taken place before there
is any chill or rise of temperature. This is especially the case in the
heavy lymphatic races of draught horses, which often according to this
author perform their usual work for days after inflammatory exudation
has set in. A fair counterpart of this is found in lung plague of cattle
and it would indicate that both start from a local infection, which
gradually extends until the systemic derangement is induced. As usually
seen, and especially when it follows exposure to severe cold, a staring
coat or a shivering fit usher in the disease, the degree of the chill
bearing some ratio to the coldness of the air and to the future severity
of the malady. This may be accompanied by a small, dry cough, but
without any other marked sign of lung disease. With the access of the
hot stage the characteristic symptoms of lung disease are manifested, at
first resembling those of _congested lungs_, but less severe than those
given under that head. There is a distinct increase of the body
temperature; the visible mucous membranes are suffused with a blush; the
expired air feels hot upon the hand; the breathing, 30 to 40 per minute,
is short and accompanied by much lifting of the flanks—(_labored_); the
cough is deep as if coming from the depth of the chest, but not so hard
nor so painful as in bronchitis; the legs are placed apart, the elbows
turned out and the head protruded to facilitate breathing; the nose is
turned to an open door or window if any such is available; the
contraction of the muscles of the face, the dilated nostrils and the
retracted angle of the mouth give an anxious expression to the
countenance; the eyes are semi-closed; the pulse full but
soft—(_oppressed_)—, beats from 48 to 70 per minute; the bowels are
slightly costive, the urine scanty and high colored; the skin
inelastic—_hidebound_—harsh and dry, though sweats may bedew it in
parts; the loins insensible to pinching; and if there is any discharge
from the nose it consists only in a reddish—_rusty_—colored mucus.
=Auscultation= and =percussion= complete the diagnosis. At the outset
the inflamed portion of lung, usually near its lower part, conveys a
_crepitating_ sound to the ear, but as consolidation extends the healthy
murmur and the crepitating râle are alike suppressed over the whole
extent of the hepatised portion around the margin of which a line of
crepitation betrays the limit of the advancing inflammation. A similar
line of crepitation encircles the hepatised mass even when the exuded
products are being absorbed and when the lung is being cleared up and
restored to its healthy state. Thus the advance of the inflammation, and
the progress of recovery can be equally followed by the crepitation
which, in the different circumstances, betokens active inflammation or
active absorption. When both lungs are involved the posterior parts are
chiefly implicated, while if the pneumonia is single it may attack the
anterior, median or posterior part, or the entire lung may become
consolidated. If hepatisation exists in the anterior part of the lung
the thick fleshy shoulder will forbid any satisfactory examination, but
if in the middle portion only, while the respiratory murmur is lost it
will be replaced by a strong blowing sound (bronchial respiration)
because the noise of the air rushing through the larger bronchial tubes
to the posterior healthy part of the lung is conveyed with greater force
to the ear through the consolidated lung tissue. This is audible from
the lower third of the chest to the upper limit of hepatization. The
respiratory murmur in the healthy lung is always louder than is natural.
=Percussion= confirms these results. Over the hepatised lung where no
respiratory sound remains, a dull, dead sound only is brought out by the
impulse of the fingers or closed fist, comparable to that obtained by
percussion over the muscular masses of the shoulder or haunch, and
forming a marked contrast to that obtained over the surrounding healthy
lung. There is not that tenderness on pressure in the intercostal spaces
which characterises pleurisy, but a sharp blow with the closed fist
leads to wincing and usually grunting because of the concussion to which
the diseased part is subjected. By increasing the force of such blows
the deepest parts of the lungs may be tested, since in this way dullness
due to consolidation of the deeper portions of the lungs may be detected
even though the superficial investing parts are healthy.
The nature of the symptoms will vary according to the extent and
character of the inflammation, from mild febrile reaction, with excited
breathing and slight crepitation, to the more severe varieties in which
the intensity of the symptoms are such as to threaten suffocation.
A marked feature of pneumonia in solipedes is that the patient
obstinately stands in one position and never lies down so long as the
severity of the inflammation lasts. The sharp crest on the lower border
of his breast bone compels the horse to lie on his side, and since in
this position the whole weight of the body has to be overcome in any
full dilatation of the chest, he cannot retain the recumbent posture
when any serious impediment to breathing exists. Hence it is that the
fact of a horse suffering from pneumonia having lain down and remained
so for some time is justly accepted as an indication of improvement.
_Progress and results of the disease._ The general symptoms above noted,
remain with more or less intensity throughout. After the first flush of
heat, on the occurrence of febrile reaction, the limbs become
alternately hot and cold, and in this the general surface partakes to a
less extent.
The tendency of pneumonia is to a crisis and recovery. Certain days have
been supposed to be critical and on the whole the third, seventh,
eleventh and fourteenth are those on which a favorable change is most
probable.
Among the more _favorable indications_ are the manifest abatement of the
high bodily temperature and febrile symptoms generally, the increasing
ease and regularity of the breathing, the greater force, distinctness
and slowness of the pulse, the permanent return of warmth to the limbs,
the softer and more elastic feeling of the skin, the recovery of
appetite, and above all, the turning of the nose from the open window or
the retention of the recumbent position for a length of time. These
symptoms will become more patent day by day, and the absorption of the
effused products and the clearing up of the lung may be traced by the
gradually decreasing area of dullness and of the circular line of
crepitation as ascertained by percussion and auscultation.
If on the contrary the disease takes an _unfavorable_ turn, some such
signs as the following will manifest it: Increasing rapidity and
embarrassment of the breathing; smallness and indistinctness of the
pulse, which is increased to perhaps 100 beats per minute; tumultuous
heart’s action, the impulse of which is strongly felt behind the left
elbow; a more laborious working of the flanks; frequent despondent
looking toward the flanks; pawing with the fore feet, lying down, and as
suddenly rising again; permanent coldness of the extremities; hanging
head with great dullness and despondency of expression; dull, sunken,
lusterless eye; hanging lower lip; leaden hue of the nasal mucous
membrane; convulsive twitching of the muscles of the surface; reeling in
gait, and extension of the crepitation over all the still pervious lung.
SUBACUTE PNEUMONIA. This term is employed to designate that subdued or
milder form of the disease which sometimes arises spontaneously and at
others follows the acute.
In this variety the characteristic symptoms may be much less marked and
the disease is less easily recognized. There is some acceleration and
quickness of pulse, lifting of the flanks and heat of the mouth and body
generally. There are alternations of heat and cold of the surface and
extremities, a rough, unthrifty coat, hidebound, a dull, listless moping
manner and the same symptoms on auscultation and percussion as in the
acute form.
The changes take place slowly but the disease may prove obstinate and is
often followed by permanent alterations in the lungs. Rheumatic
affections of the limbs, inflammation of the feet, and other diseases
frequently supervene during the course of this form of the affection.
The =terminations= of pneumonia are:—by =death=; =resolution= with
absorption of exuded products:—=splenisation=; =abscess=; =gangrene=;
permanent consolidation with organization of exuded products. The
disease will sometimes lapse into the chronic form.
=Death= is fortunately the least frequent issue. It may follow on
rapidly advancing and general congestion of the lung,—asphyxia; from
heart failure, the overworked organ becoming exhausted under the strain
of forcing the blood through the virtually impervious lungs; from
hyperthermia, the limit of bodily temperature 108°F. having been reached
or exceeded; or from collapse and exhaustion.
In =resolution= which is the most favorable termination the febrile and
other symptoms subside and the exudations in the effused lung undergo a
process of liquefaction and absorption until neither auscultation, nor
percussion nor even the examination of the lung after death will show
the slightest trace of the pre-existent disease. This is the most common
termination in single pneumonia in the horse.
=Splenisation= is that condition of lung already described under the
head of _pulmonary congestion_, and if affecting both lungs throughout,
necessarily destroys life by arresting the æration of the blood.
=Abscess.= Diffuse suppuration is very common in the stage of gray
hepatization. In this the affected lung becomes more or less extensively
infiltrated with pus limited by no distinct membrane like the pus of an
abscess, but exuding freely from the cut surface of the lung or escaping
from its interstices when it is pressed. It is preceded and in its early
stages associated with the formation of granular masses and corpuscles.
Its existence cannot be certainly ascertained though it may be surmised
when after hepatization of a portion of lung a _mucous râle_, a sort of
gurgling, is heard in the adjacent bronchium and an abundant
muco-purulent discharge takes place from the nose. It threatens
extensive destruction of lung tissue.
_Circumscribed suppuration_ or _abscess_ is infrequent though
occasionally met with in the horse and ox. In this case the excessive
exudation at one point liquefies and the surrounding lymph becoming
organized into a vascular membrane an abscess is formed. This may burst
into the bronchial tubes and be discharged by the nose. In less
favorable cases it makes its way toward the pleural surface and opens
into the cavity of the chest. It is impossible to detect the existence
of a pulmonary abscess though after it has burst into a bronchial tube
the existence of the cavity may be ascertained by the amphoric sound
heard on auscultation.
Animals may recover from such pulmonary suppurations or if they are too
extensive the consequent depletion may induce hectic and death.
=Gangrene= of the lung is happily rare and has appeared to be connected
with close, foul stables, previous ill-health, and work after the onset
of pneumonia. It is characterized by high temperature (106° to 108° F.)
by great dulness and prostration due to the poisoning of the nerve
centres, by weakness and unsteadiness, by complete loss of appetite, and
at length an intolerable fœtor of the breath as if from putrefying
animal matter. In rare cases recovery may take place, the dead portion
having become detached and expectorated.
=Consolidation= from =hepatization= is the condition in which the
inflamed lung is always found, in the second stage of the disease. The
lung has then the density and brownish red appearance naturally
belonging to the liver (_red hepatization_), which changes on the
occurrence of softening of the exuded products to a grayish hue (_gray
hepatization_). But after the subsidence of the acute symptoms, the
process of liquefaction and absorption is not always complete, a portion
of the exuded product becomes vascular, is developed into fibrous tissue
and remains permanently impervious to air. Such is the state of the lung
in many cases of _thick_ or _short wind_ in horses when these have
occurred as a sequel of pneumonia. A horse suffering in this way has the
breathing habitually accelerated and is thrown into a state of great
distress by any attempt to make him perform hard work such as galloping,
dragging a load up hill and the like. A _chronic cough_ may equally
accompany this condition.
=Pathological Lesions.= These differ according to the stage of the
disease. In the _first stage_, that of congestion the lung tissue is
engorged with blood as described under the head of =congested lungs=. As
early as 6 or 7 hours after artificial irritation, the alveoli of the
affected part are already filled by exudation and cell proliferation.
Until this has taken place the alveoli can still be distended by blowing
into the bronchial tube.
In the =second stage= the condition of the lung is that of =red
hepatisation=, so called from its resemblance in color and consistency
to the liver. There are gradations between congestion and red
_hepatisation_. In the earlier stages of the latter, the lung retains a
measure of its softness, elasticity and permeability to air, though it
is considerably firmer and less permeable than that which is in a state
of congestion and differs further from it in exuding from its cut
surface not a grumous, dark bloody pulp, but a clear straw colored
fluid. In the advanced _red hepatisation_ the lung is of a firm
consistency and granular liver like appearance. In color it varies from
a bright red to a dark liver hue, the darker shades being chiefly met
with in old animals or when the inflammation and fever have been intense
and prostrating. Varying shades are seen in different lobules of the
same lung. Its air cells are no longer pervious, it no longer crepitates
under the pressure of the finger, nor floats in water, and its
friability is such that it breaks down readily when the finger is thrust
into its substance. Its surface is distinctly granular from the
fibrinous plugging of the alveoli. Such a lung does not collapse when
the chest is opened but retains its bulk and shape and in some cases the
diseased portion may, by reason of the abundance of the exudation, be
really larger than the same portion of lung in a normal state of
dilatation. Its surface may thus retain the imprint of the ribs. Owing
to the stasis of the blood in the vessels a hepatised portion of lung
cannot be injected. The exudation which infiltrates the lung tissue and
obliterates the air cells contains in the vicinity of the bloodvessels
numerous granular masses and corpuscles and in the darker colored
portions blood globules, owing to the action of diapedesis the red cells
and the rupture of minute vessels. The smaller bronchial tubes stand out
white and empty showing that they have escaped the inflammatory action.
Hepatization usually extends from the anterior lobe or lower border
upward.
=Gray hepatization= is a sequel of the _red_ and presents the same
firmness, friability and usually the same granular aspect; the lack of
crepitation on pressure, and the higher density than water. From the cut
surface a fatty or purulent fluid exudes spontaneously, or in other
cases only when pressure is applied. The granular masses and corpuscles
have disappeared, and if suppuration is not so abundant as to prove
extensively destructive to lung tissue, that is gradually cleared up and
restored to health. This state is always a very perilous one.
=Abscess of the lung= sometimes met with in animals dying of pneumonia
shows a circumscribed area of inflammation and induration with the
liquid pus in the centre immediately surrounded by a vascular (limiting)
membrane. Abscess may be single or multiple though in the latter case it
is commonly a symptom of pyæmia.
In _gangrene of the lung_ the part may be in the dried condition of an
eschar; it may indicate gangrene only by its altered color, its
flaccidity, its fetid smell and the altered appearance of all its
microscopic elements; it may be denoted by a putrid softening, the
tissue easily breaking down into a stinking pulp of mixed fibrous and
granular materials; or lastly there may be merely a cavity with traces
of putrid contents, the dead mass having been detached, disintegrated
and expectorated.
_Modifications of the Blood and Distant Organs._
A marked feature of pneumonia is the destruction of red blood globules.
This is early indicated in the staining of the visible mucosæ by the
liberated hæmoglobin and by actual count they may be reduced in the
horse from 7,500,000 to 6,000,000 per cubic millimeter (Trasbot). There
is an increase of white globules, an absolute increase, not only in
ratio to the red. The hæmatoblasts are enormously increased especially
during defervescence. The fibrine (fibrine formers) is materially
increased; in the horse from 3.5 to 6.7 or 7.5 per 1,000 (Grehaut).
Albumen is diminished. Soda salts are increased. The bronchial lymphatic
glands are always congested, swollen and reddened with some serous
effusion. They may become the seat of inflammatory cell growth
(embryonic tissue) or even of suppuration. The abscess may open into the
bronchia or pleura. These are especially to be dreaded from their
tendency to implicate the inferior laryngeal nerve and induce roaring.
Pleurisy is inevitable when the inflammation reaches the surface of the
lung, hence hydrothorax is often present. Pericarditis and
hydropericardium are similarly met with. Endocarditis is occasionally
present and may be traced to strain of the valves of the laboring heart,
or to direct infection with the pneumonia microbe. Dilatation of the
right ventricle is common as a result of the obstructed pulmonary
circulation.
Fatty degeneration of the heart and congestions of the intestinal
mucosa, liver, kidneys, and spleen are further complications.
Finally laminitis and rheumatoid affections occur as complications.
_Treatment._ This must be adapted to the nature and condition of the
subject and to the character of the disease. A horse in vigorous
condition or with an acute type of inflammation may be greatly benefited
by an actively depleting treatment, whereas to the same animal in a low
state of health, or during the prevalence of an epidemic form of the
malady depletion may be destruction. It is not sought here, as is so
often done in the consideration of this disease, to ring the changes, as
to the probability of a change of type in disease, or a change of theory
on the part of physicians, having affected the practice of bloodletting.
True to our primary purpose of rendering the work eminently practical,
we shall first notice the general management applicable to all cases,
then the treatment of the two great types of the disease, acute
(sthenic), and subacute (asthenic), leaving to the enlightened judgment
of the reader to apply an appropriately modified system to that large
class of cases which occupy an intermediate position.
A pure airy box is first demanded, with the windows or doors toward the
south, or at least not turned in the direction of the prevailing cold
winds. The craving for pure air, so strikingly shown by the position
which the animal assumes, ought never to be ignored nor neglected. We do
not advocate the system of the late Professor Coleman who kept pneumonia
patients in open sheds exposed to all vicissitudes of temperature winter
or summer, and yet the fact that many recovered under such treatment as
well as under a more rigorous system, having been turned out into the
open fields amidst frost and snow, ought to open the eyes of all to the
incomparable value of fresh air in this disease. The box then must be
dry, cool and airy but without a cold exposure and without draughts of
cold air.
Next in importance to pure, cool air is the comfort of the patient. Any
tendency to chill, shivering, staring coat, or coldness of the surface
and extremities is to be counteracted as far as possible. One or more
blankets according to the condition of the patient and the temperature
of the atmosphere are valuable and for the same reason a hood may be put
on. Coldness of the limbs is to be met by active rubbing with the hand
or with wisps of dry hay and then wrapping up loosely in flannel
bandages. Some apply to the limbs ammonia and oil, spirits of
turpentine, and other stimulants and thus by a powerful derivative
action obtain an alleviation of the lung symptoms. For the same reason a
mustard poultice on the chest, or the hot wet rugs recommended for
congested lungs, often prove valuable in the earlier stages. Large
injections of warm water and the supply of warm gruels are not to be
neglected when they can be employed. Measures such as these directed to
check any chill and render the circulation free and uniform in the skin
and extremities, if adopted during the cold stages of the fever, will
sometimes succeed in bringing about a resolution of the pulmonary
congestion and warding off a threatened attack of pneumonia.
The diet should be of a non-stimulating and laxative kind. Bran mashes,
linseed, oatmeal, or other gruels, carrots, turnips, scalded hay, or
green food, if at the proper season, should be given in small quantities
so as not to satiate.
_Antiphlogistic Treatment._ Half a century ago bloodletting was
considered the remedy _par excellence_ for pneumonia and it seemed
justified by the marked relief to breathing and pulse which usually at
once followed a free bleeding. In a short time, however, the fever would
rise anew and the distressing symptoms reappear, which led the school of
Broussais to repeat the bleeding, _coup sur coup_, as often as the
exacerbation appeared. There was no respite for either age or condition,
the debilitated city toiler, the babe at the breast, and man of eighty
tottering into the grave had alike to submit to the lancet, and when the
oppressive symptoms returned, the blood had to flow anew. Broussais
himself, however, recognized his error in his later life, and remarkably
enough, his conversion was effected through veterinary practice. His two
carriage horses were successively attacked by pneumonia: the first was
treated by bleeding _coup sur coup_ and recovered: the second was put
under a more conservative treatment and also got well, but while the
first remained soft, flabby, debilitated and susceptible for a length of
time, the second was on convalescence at once able to go into active
work. The enormous abuse of bleeding, led to its more complete
abandonment than would otherwise have been probable, and the contrast
between the high mortality of cases treated by excessive bleeding, and
the lower fatality in pneumonias treated without phlebotomy on the
expectant (let alone) plan of Dietl or the stimulating method of Todd,
Bennett and others, served to hasten its abandonment. Yet in
bloodletting we have an instrument for good or evil which is not to be
judged on slight evidence. The mere lessening of the blood pressure is
to be little considered, as it requires the abstraction of nearly
one-third of the entire mass of blood to visibly affect this. The
vascular walls at once adapt themselves to the lessened amount. Nor is
the mere lessening of the volume a vital point. After moderate bleeding
this is made up in a few hours: after severe bleeding in 24 to 48 hours.
The loss of adult red globules is more lasting. Bleeding to the extent
of one per cent. of the body weight may have the number restored in
seven days. The young red globules though rapidly produced have
individually less hæmoglobin, and they can convey less oxygen to the
tissues. This should mean less oxidation, less heat, less waste, less
urea, uric acid, hippuric acid and other poisonous products in the
tissues. Yet Baur says that in anæmia there is a greater metabolism of
proteids and more excretion of urea. How easy it is to blunder in
looking from one single point of view. Again after bleeding there is a
great relative increase of the various forms of white blood globules,
most of them young and therefore with somewhat altered functions. The
paucity of red globules and excess of white are brought about by the
pneumonia and independently of bleeding, so that it is difficult to say
whether the phlebotomist is enhancing an evil, or helping a natural
therapeusis. It seems hopeless to estimate the effects of these and
other changes in the blood after bleeding, upon the metabolic processes
of nutrition, secretion and sanguification. This digression has not been
made to elucidate the results or the _modus operandi_ of bleeding, but
rather to illustrate the complexity of the problem involved and to warn
against broad and unwarranted generalizations from insufficient
premises.
Even today practitioners of the soundest judgment meet with a limited
number of cases in which they resort to bleeding with advantage. These
occur mainly in strong, robust constitutions, in individuals accustomed
to an invigorating, open air life, liberal diet and abundant exercise.
Even in these this measure is chiefly resorted to, to relieve an acute
pulmonary congestion with a dangerous distension and over charging of a
fatigued and overworked heart. In short the condition is one closely
allied to acute congestion in which the value of bleeding is all but
universally admitted. It is especially warranted early in the disease,
though it may still be adopted with caution in a similar condition which
has supervened at a later stage. A strong pulse and bright red mucous
membranes, are not as has been supposed, essential prerequisites to its
employment. The mucosæ may be pale, or more likely cyanotic, and the
pulse small and weak, from the over charging of the heart and its
tendency to failure, and it is to relieve these conditions that we adopt
this most potent of all measures for securing a temporary lessening of
the blood pressure in the right heart and pulmonary circulation. Even
the transient relief may allow this to right itself and then less
radical or dangerous measures may be relied on. Bleeding should very
rarely be resorted to save at the outset of the disease; extensive
exudation into the lung tissue strongly contra-indicates it; it cannot
be safely employed in the very young or old, in weak or debilitated
subjects, when the pneumonia has relapsed or supervened on another
serious malady, or when occurring in an unhealthy district. Delafond met
with a very high death-rate from bleeding in a damp undrained locality.
Where bleeding is permissible, the blood should be drawn from the
jugular in a full stream, from a large orifice, the finger being placed
upon the pulse, and the flow arrested as soon as the blood is felt to
pass along the vessel in a fuller, freer current, and the breathing is
seen to be relieved. It can rarely be repeated with profit or safety,
and in the vast majority of cases can be well dispensed with altogether.
_Antipyretic Treatment._ When the temperature runs dangerously high, a
temporary use of antipyrin, acetanilid, phenacetin, or other potent
antithermic remedy may be resorted to. But agents that so profoundly
affect the heat centres are not devoid of danger and should not as a
rule be continued after the dangerous excess of temperature has been
overcome. They may be looked on as valuable to temporarily obviate an
extreme danger rather than as a form of regular treatment.
The modern resort of applying ice bags to the chest may be similarly
disposed of. In very high fever they have been apparently beneficial,
but the danger of chill or injurious reaction is so great that they must
be employed with the greatest possible consideration and care.
_Refrigerant Febrifuge._ Neutral salts such as saltpeter in 2 drachm
doses every six hours may be given in the drinking water. These are
valuable for their cooling and eliminating action, and possibly in
counteracting the viscidity of the blood and exudations. Acetate of
potash, bicarbonate of soda, iodide of potassium or muriate of ammonia
may be substituted.
_Stimulants._ In debilitated subjects or with low fever or oppressed
heart the stimulating diuretics like sweet spirits of nitre or liquor of
the acetate of ammonia are to be preferred, and this is especially the
case during convalescence. They at once sustain the flagging heart and
aid in the excretion of morbid products. Digitalis is often of great
value in the same sense, and as a heart stimulant nux vomica.
Some follow Todd and Bennett in seeking stimulation from alcohol,
ammonia and its salts, ether, etc. When the circulation is weak or
flagging these are often of value and they may even act directly on the
pathogenic microbe. The inhalation of oxygen, or the solution of
peroxide of hydrogen given by the mouth has often an excellent effect.
_Sedatives._ Aconite has become too much of a domestic remedy,
nevertheless it may be used with advantage in high fever with excited
heart action, to moderate the circulation and relieve the breathing.
Veratrum, hydrobromic acid, bromide of sodium or ammonium, or chloral
hydrate may be used as alternates or substitutes.
_Compresses._ _Fomentations._ _Poultices._ No measure is safer nor more
promising, especially in the early stages, than the poultice jacket or
compress. A blanket wrung out of hot water is wrapped around the chest,
covered with a thick dry one, and held firmly attached by elastic
circingles. Or soaked cotton wool is applied and covered with a dry
blanket or a rubber sheet. The more acute the inflammation the more
valuable is this measure.
_Derivatives._ As a derivative the mustard pulp rubbed in and covered
with thick paper or rubber is especially valuable. In one hour it may
secure a free exudation and material relief to the breathing. It may be
replaced by ammonia and oil, with or without a covering, by hot water or
by cantharides. This must however be used with judgment. In the early
stage with a high type of inflammation and fever the surface irritation
may aggravate this through sympathy; in such cases therefore the
severity of the inflammation should first be moderated before using an
active counterirritant. In debilitated conditions, too with an altered
or depraved state of the blood and during the prevalence of a low type
of the disease, sloughing may ensue from incautious blistering.
The repetition of the blister is often useful, the healing process going
on simultaneously in the blistered surface and the diseased lung by
virtue of nervous sympathy.
To complete recovery a course of vegetable tonics, such as gentian, nux
vomica, calumba, may be given with iodide of potassium for a week or
more. Constipation occurring during convalescence must always be
corrected by food, (bran mashes, linseed gruel), injections, or
oleaginous, saline, or aloetic laxatives. The greatest care should be
exercised to secure pure air, comfort, sunshine, good grooming and
general hygiene, and to prevent over-exertion during convalescence.
In the _subacute_ types of pneumonia the fundamental difference in the
treatment consists in the avoidance of all depressing remedies and the
employment of stimulants and a supporting diet from the beginning. Sweet
spirits of nitre and liquor of the acetate of ammonia, carbonate of
ammonia or salammoniac with digitalis and strychnia may be used from the
first. Vegetable tonics may be resorted to at an early stage, peroxide
of hydrogen, and when expectoration is established and the fever
moderated even mineral tonics may be employed. Nourishing gruels,
mashes, roots, green food, and scalded oats may be used in turn to coax
the appetite and not to satiate. In other respects the treatment is the
same as for the acute. This form of the disease is liable to prove
obstinate and persistent, and there appears to be a greater tendency to
complications and so-called metastasis, as enteritis, laminitis or
rheumatoid affections of the back or limbs. These when they occur must
be treated as if they had arisen in ordinary circumstances, having
regard meanwhile to the remaining inflammation in the lungs, for that
has not necessarily been quite superseded but only alleviated.
CHRONIC PNEUMONIA. This has been described but if uncomplicated by
consumption it appears to be usually only that consolidation of lung,
due to the organization of exuded products into fibrous tissue, which
occasionally forms a sequel of acute inflammation of the lungs. In such
cases an access of circumscribed local congestion is liable to result
from over-exertion, or a chronic state of irritation is maintained
attended with more or less fever, inappetence, mal-assimilation, and
often in the long run hectic, under which the animal is worn out. In
such cases the chief indications are to avoid overwork or any undue
strain upon the breathing organs, to support the patient by nourishing
and easily digested food, and to control and remove any local irritation
by measures indicated under the head of acute pneumonia.
CROUPOUS PNEUMONIA IN THE OX.
Subacute in many cases. Effect of temperament, and work. Acute form.
Symptoms. Decubitus. Unfavorable symptoms. Prognosis. Suppuration
frequent: indications. Gangrene. Colliquative Diarrhœa. Lesions,
Comparison with those of lung plague. Tubercle. Treatment, bleeding,
laxatives, refrigerant salts, derivatives, stimulants, tonics. Chronic
form. Symptoms. Treatment.
In the large ruminants this disease tends more towards a subacute type
than in the horse, and coming on insidiously from ordinary causes is
liable to be confounded with the _contagious pleuro-pneumonia_ of the
bovine race. As in the horse the nervous animals show more violent
symptoms. It is rare in milch cows and young cattle and more frequent in
work oxen.
In the _acute form_ the symptoms mainly agree with those of the horse.
There is the same shivering, followed by a hot stage, hyperthermia, the
accelerated pulse, the short quick labored breathing, heaving flanks,
cough frequent, deep, hacking, and easily excited, dilating nostrils,
redness of the mucous membrane, and the same indications on auscultation
and percussion, care being taken to obviate misconception of natural
conditions in the chest of the ox. There is in addition a dry muzzle,
tenderness of the back and breast bones and wincing when they are
pinched between the fingers and thumb; suspension of the appetite and
rumination and in cows suppression of the secretion of milk; the mouth
is often opened and the tongue protruded to facilitate breathing, and in
bad cases each expiration is accompanied by a moan or grunt. In many
cases the ox can lie on his flattened breastbone and maintain the
breathing process, but when the disease is severe he stands no less
obstinately than the horse, his elbows turned out, his nose protruded
and directed towards a window or other opening.
Among the unfavorable symptoms may be mentioned increasing anxiety and
distress, a more oppressed breathing, the animal standing constantly in
one position with legs apart, elbows turned out, his nose extremely
raised, nostrils widely dilating, mouth open, tongue protruded, the
expiratory grunt deep and prolonged, the cough infrequent and so weak as
to be almost inaudible, being rather like a forced expiration, and the
pulse rapid, feeble or imperceptible. The prognosis is favorable in
moderate cases subjected to early treatment.
The termination by _suppuration_ is more frequent than in the horse. The
general symptoms are ameliorated, appetite and rumination return though
they remain capricious and irregular, there remains the double action of
the flanks, the dry, rough muzzle, the tense, inelastic skin, frequently
varying in temperature, the beast shivers at intervals, the cough is
weak and often repeated, a yellowish thick discharge takes place from
the nose, weakness and emaciation increases and the animal dies in from
twenty to thirty days.
Gangrene of the lung sometimes supervenes and is indicated by similar
symptoms as in the horse. In severe and prolonged cases a violent fetid
diarrhœa often supervenes and hastens a fatal result.
The _post mortem_ lesions are similar to those of the horse. The cut
surface of the hepatized lung, however, is divided into irregular red
spaces by intersecting yellow lines—hence the name of _marbled lung_,
from a supposed resemblance to that stone. The red spaces represent the
pulmonary lobules and the whitish lines the surrounding areolar tissue
which being especially abundant in ruminants and pigs stands out
prominently when infiltrated with the yellowish exudation. There is then
nothing specific in this appearance as has been erroneously supposed, it
is merely the result of the different conformation of the lung in these
animals and is always seen in the hepatized lung unless when from
extravasation of blood into its substance the redness is rendered
uniform. The amount of exudate into the interlobular tissue is, however,
never so great as in lung plague.
The greater frequency of suppuration in the lung of the ox, as well as
the greater tendency to tubercular deposit in prolonged cases are
additional features in the diseased lungs.
_Treatment._ Blood-letting should be employed only with precautions, as
in the horse. A saline laxative (1 lb. Epsom salts and ½ lb. molasses)
may be used with advantage and safety early in the disease though in
advanced stages it may sometimes prove dangerous from the tendency to
diarrhœa. If constipation appears at a late stage injections of warm
water and a mild laxative (6 ounces sulphate of soda) only, should be
given. The purgative may be followed by the same neutral salts and in
the same doses as for the horse. Counterirritants are of equal value. A
mustard poultice may be kept on for several hours, or a mixture in equal
parts of oil of turpentine, ammonia, and olive oil may be actively
rubbed over both sides of the chest and repeated daily until tender. In
Denmark a prompt and efficient blister is made with 1 part of Croton oil
and 10 parts each of sulphuric ether and spirits of wine. This is rubbed
actively over the chest and washed off as soon as a sufficient effect
has been produced. It must be carefully watched to prevent blemishing.
In the low types of the disease and during convalescence stimulants and
tonics are to be employed as recommended for the horse.
CHRONIC PNEUMONIA. Gellé describes a chronic form of this disease in
cows. For about a month the patient became increasingly emaciated, there
was a frequent, dry, weak cough, lifting of the flanks, and expiration
double and accompanied by a moan. All these symptoms were aggravated by
gentle exercise. Percussion detected dullness at the lower part of the
lung and auscultation a distinct crepitating râle. The pulse was weak
and rapid, the mucous membranes red and tumid, skin dry, ears and horns
cold, appetite small and capricious, rumination rare, excrements soft,
and milk almost dried up.
The _treatment_ is by diuretics with vegetable tonics and stimulants and
active counterirritation over the chest. Gellé considers the malady as
all but incurable unless active blistering is promptly employed so soon
as the malady has assumed the chronic form and before extensive
structural changes have taken place in the lungs.
CROUPOUS PNEUMONIA IN SHEEP.
Causes, damp, cold soils, inclement weather, cold rains, hard driving,
shearing or washing in cold weather, change to a cold climate, or from
a warm barn, hot barns, heavy fleeces, sudden plethora. Symptoms, in
congestive cases, in inflammatory. Treatment, preventive, hygienic,
antiphlogistic, laxative, febrifuge, derivative.
This disease is not infrequent in these animals, occurring enzootically
in low, wet pastures; or from cold storms of wind, sleet or drenching
rains, particularly after hard driving, or shearing; or from washing
during inclement weather. Dressing with mercurial ointment in cases of
_scab_ is a frequent cause of pneumonia and death in Lincolnshire and
various other English counties. Lastly M. Seron in Hurtrel d’Arboval’s
“_Dictionaire_” describes its prevalence in _Seine-Inférieure_ among low
conditioned sheep subjected abruptly to a very nutritious diet. The hot
buildings, heavy fleeces, and sudden plethora, appear to conduce to
dangerous pulmonary congestions. The _symptoms_ do not differ materially
from those seen in the ox except so far as they are modified by the fact
that the disease often terminates fatally before hepatization has been
established and the symptoms and post mortem appearances are those of
congestion and sanguineous engorgement of the lung rather than of
hepatization.
This engorged state of the lungs it is which has led Youatt and others
to describe them erroneously as “gangrenous” and shepherds to name the
disease “rot of the lights.” The condition is that of acute congestion
and analogous to that seen in congested lungs in the horse.
The _treatment_ ought to be chiefly preventive and will consist in the
avoidance of the causes above indicated.
When the disease has set in, fresh air, and general comfort, bleeding if
in the very earliest stages and in a strong patient, purging (3 ounces
sulphate of soda and ¼ lb. treacle in warm gruel) and a free supply of
nitre (about ½ an ounce daily to each) in the water or gruel supplied
are the leading indications. As a counterirritant aqua ammonia acts well
being sufficiently confined by the fleece.
PIG. PNEUMONIA.
Symptoms, chill, burrowing, hot skin, cough, disturbed breathing,
indications of exudation. Treatment, laxative, sedative, nauseant,
febrifuge, wet jacket, blister.
Hogs are not exempt from this disease. They show the same symptoms of
chill with hiding under the litter, followed by a hot stage, cough,
hurried breathing, and (if the clothing of fat is not too thick)
conclusive results on auscultation and percussion.
As _treatment_ bleeding from the ears and tail is sometimes resorted to
with questionable benefit. A laxative of three ounces of castor oil or
three or four croton beans given in the food is of value. Tartar emetic
in doses of ¼ grain and nitrate of potash in 10 grain doses should be
shaken on the tongue at least four times daily to keep up a continued
nausea and action on the urinary organs. The tartar emetic so worthless
in the larger animals is of value in the pig and dog. A damp compress or
blister may be used. The skin of the animal is difficult to blister, but
by the use of the Danish croton liniment, mentioned for the ox, of hot
water, or of a mixture of oil of turpentine and croton, 8 parts of the
former and 1 part of the latter, a sufficient effect can usually be
obtained.
DOG. PNEUMONIA.
Breeds most liable. Causes, over-exertion, cold baths, clipping,
exposure in cold, distemper. Symptoms, chill, fever, disturbed
breathing, cold extremities, cough. Treatment, dietary, nursing,
laxative, nauseant, febrifuge, moist jacket, mustard, stimulants,
tonics, heart tonics and careful nutrition during convalescence.
This is a frequent affection in hounds. In hunting or coursing dogs the
causes are like those operating in the horse. The clipping of long
haired dogs in inclement weather, swimming dogs in winter without
afterwards drying or heating them by exercise, and shutting them out of
doors at night, when accustomed to a warm dwelling are occasional
causes. It sometimes occurs epizootically and frequently supervenes
during distemper.
The chief _symptoms_ of chill, fever, and difficulty in breathing are
like as in other animals, while the results of auscultation and
percussion are more satisfactory than in any other domestic animal. The
dog sits on its haunches to facilitate breathing; his elbows turned out,
his mouth open and his tongue protruded. Coldness of the ears and a
short quick cough are usually marked symptoms.
_Treatment._ The general care applicable to other animals is equally
demanded here. The diet should consist of mild broths, or farinaceous
foods with a little gravy if necessary to render it palatable.
Bleeding from the jugular has been recommended and may be admissible at
the outset of the disease in a very few appropriate cases. If
costiveness exists a tablespoonful of castor oil may be given (more or
less according to the size of the animal), following this up by the
tartar emetic, nitre and sugar recommended for bronchitis. The poultice
jacket is of great value. Mustard poultices may later be applied to the
sides of the chest. Stimulants, tonics and nourishing diet may be
required during convalescence, or when the disease assumes a low type.
CROUPOUS PNEUMONIA IN FOWLS.
In chickens exposure and neglect are alleged causes. Foul coops and the
contrast between the warm building and cold outer air are justly blamed.
Ruffled feathers, drooping head, dark colored comb and wattles, trailing
wings, a disposition to gape, panting and cough are noticed. Under the
wings and over the back crepitations and dulness may be detected. The
patient may take a teaspoonful of castor oil, and saltpetre or iodide of
potassium may be given in the drinking water. In careful doses the other
remedial measures may be attempted.
_Pneumonia in birds._ Causes, exposure, neglect, foul coops, hot, close
houses, etc. Symptoms, erect plumage, drooping head, wings, and tail,
dark comb, gaping, panting, cough, crepitation. Treatment, hygienic,
laxative, febrifuge.
ACUTE PLEURISY IN THE HORSE. PLEURITIS.
Causes, cold, damp, soils and exposures, as with rheumatism, youth,
vigor, heavy diet, digestion, or hepatic disorder, over-exertion,
perspiration and succeeding chill, wading or swimming rivers, standing
in snow, salted snow, rain, sleet, snow, draughts between open doors
and windows, clipping, cold sponging of legs, tuberculosis, a common
cause in man and cattle is rare in horses, surface pneumonias,
cancers, actinomycosis, tumors. Traumas from broken rib, penetrating
intercostal wound, blows, contusions, ruptured pulmonary or
intercostal abscess. Irritant (infectious) exudate suggests microbes.
Symptoms, chill, reaction, partial sweats, pawing, pointing one foot,
hyperthermia, hard, jarring pulse, hurried breathing, inspiration
catching, pleuritic ridge, uneasy movements, hacking cough, tumors and
twitching of chest muscles, tender intercostals, grunting, friction
sound, subsiding with appearance of dull area below, signs of
effusion, relief, dyspnœa, lifting flanks and loins, perspirations,
stocking limbs, pasty swelling on sternum, effusion of same level on
both sides, creaking sounds, splashing, gurgling, metallic tinkling,
weakness, sinking. Signs of adhesions, compression of lung, abscess.
Duration. Lesions, early formation of false membranes, pleuritic
effusion, its composition, its color at different stages, dry
pleurisy, sero-fibrinous, sero-fibro-purulent, hydro-pneumothorax,
tubercle. Prognosis. Treatment, during the chill, warm air, clothing,
drinks, injections, compresses, pilocarpin during early inflammatory
stage, derivatives, dry cupping, mustard, cantharides, hot water, or
air, cold applications, laxatives, calmatives, antirheumatics,
alkaline agents, with bitters, diuretics, heart tonic, iodine,
mercury, thoracentesis.
_Causes._ Pleurisy is common in all domestic animals and especially so
in cold, damp, exposed localities which suffer equally from rheumatism.
It occasionally extends to the fascia of the limbs, the joints, or the
navicular or other trochlea as a rheumatic affection. The disease is
prevalent among young and vigorous horses, four or five years old, on
stimulating feeding. Here hepatic derangements and poisons,
over-exertion, perspiration and succeeding chills are especially to be
suspected. Plunging the limbs in ice cold water as in wading a river
(Fromage), standing in snow and above all in salted snow, or facing a
cold rain, sleet, or snow when perspiring or fatigued, are recognized
causes. A full drink of ice cold water when freely perspiring, and
followed by standing in the frosty air, or in a cold current indoors.
Exposure unblanketed after clipping in winter (Field, Trasbot), and even
sponging the body or legs with cold water when heated or fatigued or
both. St. Cyr found that pneumonias stood to pleurisies as 3: 1, Trasbot
as 10: 1, yet the latter draws attention to the fact that in cavalry
horses habituated to the stable and sent out into camps in the depth of
winter, the pleurisies are more numerous than pneumonias. This may
suffice to show the importance of the rôle filled by cold and chill in
the production of pleurisy. Yet many physicians look upon the chill as a
predisposition only, while the true origin of disease is microbian. And
in man a large proportion of pleurisies appear to be distinctly
tuberculous. Bowditch traced 90 cases of acute pleurisy and found that
32 had tuberculosis. The objection to generalizing too largely on this
for the lower animals is that the horse and dog, in which tuberculosis
is rare, are by far the most common subjects of pleurisy, whilst cows
which are very prone to tuberculosis show few cases of simple pleurisy.
Again we find pleurisy in the horse as the result of other diseases
localized in or adjacent to the pleura, and where there is nothing to
indicate tuberculosis. Thus it follows pneumonia approaching the surface
of the lung, cancers, actinomycosis and other tumors, and traumas—a
pulmonary abscess bursting into the pleura, a broken rib scratching and
lacerating the lung, a perforating wound of the intercostal space, or in
cattle a sharp pointed body advancing from the reticulum toward the
heart.
But the presumptive absence of the tubercle bacillus in the great
majority of pleurisies in the horse does not prove the absence of all
pathogenic microbes. Trasbot, who rejects the microbian theory, found
that the injection of a little of the exudate into the pleural cavity of
a sound horse, always determined a generalized pleurisy. Injections of
distilled water with the same antiseptic precautions, made separately by
himself and Laborde, had no pathogenic effect. Trasbot attributes the
pleurisy vaguely, to the irritant effect of the exudate, but if it
should finally be shown that this exudate contains microbes, though they
may not be those of tuberculosis, the irritant action will be much more
clearly explained. There are forms of pleurisy which are unquestionably
the result of microbes, as in lung plague, influenza, canine distemper,
glanders, tuberculosis, pneumo-enteritis, actinomycosis, and
theoretically it might be supposed that in our ordinary acute
pleurisies, other germs that have been lurking harmless in the system
may take occasion by reason of the lowered vitality induced by a chill,
or a trauma, to colonize the thoracic serosa and develop pleurisy. Under
such a theory, the predisposing and microbian element would remain
equally effectual, but only operative when conjoined, neither being
pathogenic without the other.
Until the constancy of the microbian factor is demonstrated we must
recognize the time honored doctrine, that pleurisy may be due to cold,
exposure, over exertions, to traumatic injuries, blows, concussions,
fractures, penetrating wounds, and to extension by contiguity from
adjacent diseases.
Most commonly pleurisy is unilateral on the right side but is often on
the left or on both sides.
_Symptoms._ There is the early symptom of shivering followed by a hot
stage in which the limbs participate and partial sweats bedew the
surface. There are first uneasy movements of the fore limbs with some
lifting of the flanks and this discomfort increases until the patient is
panting with pain and occasionally glancing round at his heaving flanks
and even pawing as in colic. If the pleurisy is confined to one side the
corresponding fore limb is often advanced before the other. The
temperature is 102° and upward. The pulse is quick, hard and
incompressible being usually compared to a jarred wire and beats from 48
to over 60 per minute. The breathing is highly characteristic. It is
hurried, is carried on chiefly by the abdominal muscles to avoid the
rubbing of the inflamed pleuræ on each other, and has the inspiration
short and suddenly checked by an audible closure of the glottis while
the expiration is slow and prolonged. This character of the breathing is
well observed when the ear is placed against the false nostril. The
laboring abdominal muscles stand out as a ridge from the outer angle of
the ilium along the lower ends of the last ribs (pleuritic ridge). A
tremor on this line is often noticeable in the early stages. It may also
be felt by the hand laid on the costal region. The horse does not stand
obstinately still as in pneumonia, but frequently moves as if seeking an
easier posture. The short, hacking cough contrasts with the deep, rare
cough of pneumonia. The expired air is not so hot, nor the mucous
membrane of the nose so red as in the last named disease and there is no
nasal discharge. A twitching of the muscles of the chest is sometimes
seen and if the intercostal muscles are pressed upon, the animal winces
and frequently grunts. This last symptom is likewise seen in rheumatic
disease of the intercostal muscles (pleurodynia) but the absence of the
fever, the cough, and other chest symptoms sufficiently distinguish
this. Auscultation detects in the early stages in addition to a healthy
respiratory murmur, a friction sound audible in inspiration only in
short jerks near the close of the act and comparable to the rubbing of
the palm of one hand over the other laid over the ear, but this is no
longer heard when effusion of liquid has taken place into the pleuræ.
Percussion in the early stages detects no change from the healthy chest
resonance.
If not relieved in from twenty-four to thirty-six hours, a remarkable
modification of the symptoms takes place indicating the occurrence of
effusion. The violent symptoms are suddenly relieved. The quick catching
breathing which is in many cases accompanied by a grunt, becomes easy
and though fuller than natural is comparatively regular. In particular
the inspiration is free and full and comparatively painless, the sudden
check and the grunt by which it was arrested having alike disappeared.
The tension of the abdominal muscles and the tucked up appearance of the
flanks give way; the pulse acquires a softer character, the haggard
pinched countenance is relaxed, and a general appearance of comfort and
even liveliness prevades the animal. This temporary improvement is often
so great that the horse will take to feeding as if he had all at once
recovered.
The apparent recovery is, however, only transient. Soon the pulse
becomes more frequent and loses its fulness, the breathing is more
laborious and attended with a characteristic lifting of the flanks and
loins, the nostrils are widely dilated, the limbs outstretched and the
elbows outturned, the eyes stare and project and the countenance has a
haggard appearance indicating threatened suffocation. Partial sweats may
break out on the surface, due to the state of nervous excitement and
general relaxation and supplementing in some degree the impaired
exhalation from the lungs. Auscultation over the lower region of the
chest shows a complete absence of the respiratory murmur, rising to the
same level precisely at all points. Percussion elicits no resonance on
the same region. If the effusion has taken place slowly or existed for
some time, the dulness and absence of sound will usually indicate that
the liquid rises to the same level on both sides. So thin and permeable
is the posterior mediastinum in its lower part that unless thickly
coated by new solid exudations, the effusion readily passes through it
and rises to the same height on both sides. If gas as well as liquid is
produced in the pleural sac a gurgling or splashing sound may be heard
on auscultation, and occasionally, after rising or other change of
position, a _metallic tinkling_, due to droppings from the shreds of
false membranes above into the fluid below.
As the disease proceeds dropsical effusions are observed beneath the
skin of the breast and abdomen, a mucous rattle is heard in the trachea,
the nose, ears and limbs become cold, the pulse increases in rapidity
and weakness, shows the distinct anæmic tremor or thrill, and becomes
rapidly imperceptible; the horse moves unsteadily and often falls
suddenly dead.
This early fatality is, however, only seen in the worst cases. In those
about to terminate favorably improvement is shown usually about the
fourth day. The lifting of the flanks and loins becomes moderated, the
ribs move more freely, the grunt ceases, the pulse is fuller, softer and
less frequent, and auscultation and percussion show a steady decrease in
the effusion. Appetite meanwhile returns, the horse moves more freely,
lies down for a length of time in succession, and convalescence lasts
from two to three weeks.
In the less fortunate cases structural changes more or less permanent,
keep up symptoms of illness for a variable length of time. Sometimes
after the liquid effusion has been absorbed the lung remains attached to
the side of the chest by newly formed tissue (false membrane) and while
this is undergoing a drying and organizing process, it gives rise to a
leathery, creaking sound heard on auscultation and easily mistaken for
crepitation. Sometimes an abscess forms on the surface of the pleura or
in the newly organized false membrane, and either bursts into the
pleural sac (empyema) where it serves to increase and sustain the
irritation, or it makes its way through the intercostal spaces and is
discharged externally. In this last case its advance toward the surface
is heralded by an extensive inflammatory infiltration and pasty swelling
much more tender to the touch than the dropsical swelling already
referred to. Another condition is that in which false membranes of
considerable thickness invest a lung and, following the law of all
fibrous structures in process of organization, they contract and cause a
compression and partial collapse of the contained lung tissue. A
flattening of the corresponding side of the chest and a muffled and
almost inaudible respiratory murmur is the result of this condition. In
some measure these symptoms are present during convalescence in all
cases of pleurisy since the lung never expands to its full size till
some time after apparent recovery, but it is only when the organ is
invested with false membrane that the symptoms are very apparent.
In all such cases of prolonged pleurisy from protracted structural
change there is continued illness without the violent symptoms by which
the acute form of the disease is manifested. The acute suffering, the
restlessness, the grunt, and even the catching breathing may be absent;
the temperature may be almost reduced to the healthy standard, the pulse
small and tolerably soft, the appetite considerably improved and the
different secretions tolerably normal; yet the pinching of the
intercostal spaces causes sharp pain, and measurement, auscultation and
percussion testify to the persistence of disease. The animal is
hidebound, unthrifty and unequal to any exertion. The cough is weak and
painful and sometimes accompanied by a grunt.
Besides the changes connected with exudation and effusion, and
organization or suppuration in the exuded products, _gangrene_ sometimes
results. A case of this kind is related by _Percivall_.
The _duration_ of pleurisy may thus extend from two days in very acute
cases to several weeks, or even months if we estimate it by the
continuance of _hydrothorax_ in the chronic cases.
_Post Mortem Appearances._ These consist mainly in the presence of false
membranes lining the pleura and hanging in cobweblike shreds into the
cavity of the chest, and of the liquid effusion which fills up the chest
at its most dependent part. The pericardium also contains fluid in many
cases. The periods at which exudation takes place, and when the
principal changes take place in the exuded materials have been well
investigated by Dupuy, Hamont, Delafond and St. Cyr. They induced
pleurisy by injecting irritant liquids into the chest, and noted the
regular sequence of changes.
Dupuy injected two drachms of oxalic acid dissolved in three ounces of
water. Symptoms of pleurisy at once came on, with the friction sound
characteristic of its early stages. Next day friction sound had ceased
and evidence of effusion existed. The same experiment repeated on
several horses showed that if killed at any period subsequently to this,
considerable exudation had already taken place. In one horse in which
the disease was of 50 hours’ standing the chest contained 43 pints of
citrine-colored fluid, and abundance of yellow, thick, false membrane
enveloping the costal and pulmonary pleuræ.
Hamont injected seven ounces of a weak solution of tartaric acid into
the left pleural sac, repeated the injection next morning and destroyed
the horse twenty minutes afterward. The chest opened immediately showed
a small amount of liquid on the affected side, and the pleura injected
and reddened.
Delafond made twenty-two experiments with the same general result.
Percivall found recent adhesions between the lungs and side so early as
seventeen hours after the commencement of the pleurisy.
Andral injected rabbits with acetic acid and in nineteen hours found in
the injected pleura soft, thin, false membranes traversed by red
anastomosing lines, and in certain cases a serous or puriform fluid.
W. Williams found a false membrane formed twenty-four hours after the
injection of the irritant.
St. Cyr in a series of 43 experimental and casual pleurisies in horses,
found that in a very few hours there was marked local congestion and
swelling of the pleura speedily followed by the formation of soft,
pulpy, friable false membranes, largely amorphous and granular but
impregnated with many cells and nuclei. These adhere feebly to the
pleura but may accumulate with prodigious rapidity so as to cover in
three or four days the whole pleural surface on one or both sides. The
attendant serous effusion was bloody, turbid, or lactescent. The pleural
surface under the false membrane was highly vascular and studded with
fragile, red conical elevations projecting into the membrane.
Exceptionally the sub-serous connective tissue became the seat of
exudation as well.
From the sixth to the ninth day the false membranes began to become
vascular and from the tenth to the fourteenth day commenced to organize
into the connective tissue. With the advent of this stage, the
inflammatory action tended to subside, and the reabsorption and repair
to ensue.
_Pleuritic effusion._ This varies greatly at the different stages of the
disease. As effused it has a composition resembling that of the blood:—
Water, 911 to 924
Albumen, 63.33 to 82.50
Fibrine formers, 2.16 to 12.50
Extractive matter.
Salts.
The progressive changes from the hæmorrhagic effusion to the limpid
hydrothorax and their relation to the different stages of the disease
and the subsidence of the inflammation are of the greatest importance in
deciding questions of responsibility, when the animal has recently
changed hands. St. Cyr has classified his cases in the following
instructive table:
─────────────────────┬─────────────────────────────────────────┬───────
Duration of the │ │
Disease. │ Effusions. │Total.
─────────────────────┼──────┬─────────────────┬────────┬───────┼───────
│ Port │ │Muddy or│ │
│Wine. │Sero-sanguineous.│Grayish.│Limpid.│
─────────────────────┼──────┼─────────────────┼────────┼───────┼───────
From 1st to 7th day.│ 9│ 6│ 3│ │ 18
„ 8th to 15th day. │ 2│ 3│ 4│ 6│ 15
„ 16th to 30th day. │ │ 1│ 1│ 5│ 7
After 30th day. │ │ │ │ 3│ 3
─────────────────────┼──────┼─────────────────┼────────┼───────┼───────
│ 11│ 10│ 8│ 14│ 43
─────────────────────┴──────┴─────────────────┴────────┴───────┴───────
Up to the 7th day 50 per cent. were dark red; after the 7th day only
13.3 per cent.; and after the 15th day none. Up to the 7th day 83.3 per
cent. were either dark red or sero-sanguineous and not one had attained
to translucency. After the 7th day only 8 per cent. were of port wine
hue, and by the 15th day 24 per cent. of all cases of over seven days
standing were already transparent. Of all cases of over 15 days
standing, 80 per cent. were perfectly translucent and none showed the
dark red hue. Finally after the 30th day all remaining cases were
limpid. This of course must not be applied with the same confidence in
both directions. While translucency of the effusion bespeaks seven days
standing and probably fifteen or twenty, the dark red hue must not be
held to imply a recent date for the attack. A relapse in the course of
convalescence may easily and quickly stain anew a liquid that was
already limpid, or had advanced far toward this condition.
The appearance of the lung tissue in a case of confirmed pleurisy is
characteristic. The lung is of a dull red color, shrunken, slightly
collapsed, flabby, scarcely crepitant under pressure and heavier than
water or floating in water. It is tough, not friable like hepatized
lung, and its cut surface is dry, smooth, and presents the interlobular
septa very well marked. This is due to the compression by effused
liquid, and by the organizing and contracting false membranes covering
the lung and implies nothing more than simple condensation. The air cell
may be collapsed, but contains no new product and has not parted with
its epithelium and the lung can be inflated through the bronchia.
_Differentiation according to the nature of the effusion._ Pathologists
have divided acute pleurisy into the _dry_, _sero-fibrinous_, and
_sero-fibro-purulent_.
=1. Dry or fibrinous pleurisy= has usually a more acute type and the
exudate containing an excess of the fibrinogenous elements forms a
coagulum or false membrane on the affected surface tending to bind that
to the part adjacent—the lungs to the costal pleura. The serum, small in
quantity, is in the main retained in the exudate or if set free is
actively reabsorbed by the healthy pleura.
=2. Sero-fibrinous pleurisy.= This form is usually less acute and more
extended involving perhaps an entire pleural sac, or even both sides of
the chest. This is the common form of pleurisy and is that referred to
in the experiments of St. Cyr and others above. The earliest lesions in
experimental cases (with chloride of zinc solution) in dogs are an
uniform bright red congestion, with a bright, shining surface as yet
perfectly dry. There is already shedding of patches of the endothelial
cells, swelling and proliferation of the superficial connective tissue
cells and the formation of a few pus globules. This is seen in from half
an hour to six hours after the application of the irritant.
Next follows the exudation of fibrine and serum, which respectively
coagulate as false membrane on the inflamed membrane, or drop to the
bottom of the sac as liquid. The fibrine appears as granules, little
knobs and threads between and on the endothelial cells and entangling a
few pus cells. The changes are now much more marked in the connective
tissue cells, which are more numerous, larger, nucleated and often
stellate or polygonal. Changes are well advanced in twenty-four hours.
The cells go on increasing to the fourth or fifth day, when new blood
vessels are formed into the membrane and may be injected from the
pleura. From this time, in favorable cases absorption of the liquid
proceeds, and the fibrine is organized, and by the fourteenth day is
transformed into connective tissue, the superficial cells forming
endothelium and the deeper, branching connective tissue cells. The
result is the thickening of the pleura and the formation of adhesions.
The case, however, may prove fatal, or it may be protracted through the
continued production of fibrine and serum, or it may pass into empyema.
=3. Sero-fibrino-purulent pleurisy.= =Empyema.= This is usually very
dangerous as well as complicated. It may supervene on the last described
form. It may depend on rupture into the pleura of abscess of the lung,
bronchial glands, liver, diaphragm or intercostal space and the
infection of the chest cavity. It may in the same way follow the
laceration of a bronchium by a broken rib, the perforation of the
intercostal space by a foreign body, or (in cattle) the penetration of
the chest by a sharp pointed body from the reticulum. It may follow at
once on pleurisy of a very high grade. Probably in all such cases there
is infection of the pleura by pus microbes. When there is a
communication with a bronchium, the reticulum or the external air there
are usually septic germs in addition, and the contents of the chest
become fœtid.
The purulent fluid may accumulate in the lower part of the pleural sac,
or it may be confined in abscess form in the false membrane, and extend
thence into surrounding tissues. The pus-containing pleura, or cavity
infected by the pus germs, assumes the appearance of a granulating
surface, or of the lining membrane of an abscess, and continues to
produce pus in greater or less amount.
The formation of pus in the pleura is known as _empyema_. When air
enters the pleura through a wound perforating the chest wall, or when
gas is formed in the pleura, the condition is =pneumothorax=. As liquid
is usually present as well it is =hydro-pneumothorax=.
Tubercular and other forms of pleurisy have in certain cases been
superadded to the specific local lesions, by which such diseases are
individually characterized.
_Prognosis._ Occurring in an otherwise healthy system and especially if
confined to one side of the chest, pleurisy is not frequently fatal, and
under appropriate treatment recovery is oftentimes rapid and
satisfactory. A certain number of cases merge into chronic hydrothorax,
the inflammation apparently subsiding, but reabsorption failing to take
place. The hydrothorax may last for months or even a year.
_Treatment._ If seen during the _chill_ and before inflammation has been
definitely established every effort must be directed to secure its
abortion, if possible. No time should be lost in placing the patient in
a warm comfortable stall or box, covering him with woolen blankets and
actively rubbing and loosely flannel bandaging the legs. Warm drinks and
warm injections must be given. Half an ounce or an ounce of camomile or
boneset in infusion in two or three quarts of hot water, or in the
absence of this any of the carminatives, or etherial, alcoholic or
ammoniacal stimulants may be given. Pilocarpin in 7 grain dose
hypodermically may promptly secure a revulsion of blood to the skin and
at once overcome the chill and prove a most effective derivative from
the pleura. Placing the legs in buckets of hot water, or the whole
animal in a hot air bath will often act equally well. Packing the chest
and even the abdomen in a blanket wrung out of very hot water and
covering it closely by one or two dry ones, or, better still, by a
rubber or other impermeable covering, will long retain both heat and
moisture, securing free cutaneous circulation, and soothing in a most
effective way the irritation in the chest. This may be maintained as
long as requisite to relieve the patient, and then the body may be
uncovered, a part at a time, rubbed dry and covered with a dry woolen
blanket. By using elastic circingles over the compress they are adapted
to the respiratory movements and any restriction in the movement of the
ribs is beneficial by limiting the friction, pain and irritation in the
pleura.
In the second stage, when inflammation has already set in, the same
general measures of derivation toward the skin and hot bath or soothing
derivative compress are still demanded though they may be substituted by
more stimulating derivatives. The bleeding of the patient into his own
vessels is sought in various ways. On the continent of Europe
stimulating embrocations (essential oils, ammonia and oil, mustard,
etc.) are applied to the limbs. In America and England similar agents
are more commonly applied to the walls of the chest and dry cupping in
the same region has been resorted to. Metallic cups with small mouths
and having a capacity of about a pint each, have the air rarefied by
plunging into each a spirit lamp, and, on its withdrawal, suddenly
applying the mouth of the cup on the skin of the costal region
previously well coated with lard. Another form of cup is made with a
tube and stopcock in its otherwise blind end by means of which it is
exhausted with a syringe after its mouth has been applied to the skin.
In the absence of both a narrow mouthed glass tumbler may be employed,
the air is rarefied by inserting into it a burning spill of paper or
wood for a few seconds and on its withdrawal the cup is instantly
inverted on the skin. If the animal is very hairy or very thin it may be
necessary to shave the part, and smear with oil and even to select a
very narrow mouthed cup. When applied the cup is cooled with water or
otherwise and owing to the partial vacuum the skin is strongly drawn up
into it and the blood accumulates in and under the skin. It may be kept
on for half an hour at a time and with ten or twelve cups on one side
the patient tends to profuse perspiration establishing a strong
revulsion toward the skin, and great relief. In dangerous cases three or
four applications may be required in twenty-four hours.
Next to this the mustard application is perhaps the safest and most
valuable. The best ground mustard (black by preference) is made into a
very thin pulp with tepid or cold (never hot nor boiling) water and
rubbed in against the hair so as to soak the surface of the skin; it is
then closely covered with paper and with a rubber or other impervious
covering or, in default of better, with a close blanket and left on for
two hours. By this time the skin should be thickened to the extent of at
least a quarter of an inch and the derivation and relief will be very
manifest.
Cantharides is sometimes used but like most other severe irritants, is
liable to induce sympathetic irritation in an already severely inflamed
pleura, and thus to obviate all benefit. Cantharides is also liable
through extensive absorption to irritate the kidneys. To counteract this
Bouley gave ½ drachm doses of camphor with alleged good effect.
Some practitioners make local applications of hot water and of aqua
ammonia (confined) but unless very closely watched these are liable to
destroy the hair follicles and produce permanent blemish.
The hot air, steam bath, and hot compress have the advantage over the
mere irritant derivatives that their action is from first to last
soothing and free from all risk of inducing sympathetic irritation and
yet as derivatives they are eminently efficient. Next to them in safety
and efficacy comes dry cupping.
The irritant derivatives are often the most valuable, but must be used
with great judgment. They are always dangerous when the pleural
inflammation runs very high and when the local irritation and suffering
are specially acute. Under such circumstances it is usually desirable to
adopt other measures to moderate the severity of the inflammation, and
to fall back on baths, compresses and cups until the irritation is
alleviated before vegetable or animal vesicants are resorted to. In
acute and severe attacks these latter are especially applicable to the
early stages before the inflammation has been fully formed, or after the
stage of free effusion has set in.
With high fever and no benefit from hot local applications, cold
irrigation or refrigerant compresses to the walls of the chest, have
proved useful, but considering the rôle filled by cold in causation and
the suggested relation between pleurisy and rheumatism this is not to be
followed as a general practice.
If the patient has been a hearty feeder and if there is evident
costiveness a purgative (aloes or sulphate of soda) is often desirable
at the outset, but if the disease is of a low type this is always
dangerous, owing to susceptibility of the intestinal mucosa and it is
safer to correct constipation by injections or at most by a pint of
olive oil.
When the suffering is very acute and is aggravating the fever, a
hypodermic injection of morphine will often greatly relieve and even
favor a revulsion of blood toward the skin, but as it tends to suppress
the action of both bowels and kidneys it should be avoided unless it
seems absolutely necessary, and above all it should not be given by the
stomach. Cocaine hypodermically may be used to relieve pain.
Both fever and suffering can sometimes be greatly relieved by large
doses (2 drachms 3 or 4 times daily) of salicylate of soda, which again
suggests a close relation of the disease to rheumatism. Acetanilid or
phenacetin may be used to fill the same indication.
Next come the questions of alkaline and diuretic treatment. Some cases
do well if given nitrate of potash freely in the drinking water. Some
prefer the alkaline diuretics, such as acetate of potash or ammonia,
bicarbonate of potash or soda, biborate of soda, or the vegetable
diuretics such as colchicum, squills, etc. Fraënkel found that, while
comparatively ineffective alone, these proved most efficient (in man)
when combined with cinchona or other bitter. The hint should be useful
to the veterinarian. Diuretics in the stage of effusion should be pushed
as far as the strength of the patient will warrant.
Friedberger and Fröhner recommend pilocarpin, and no agent produces an
equal secretion from the natural emunctories and an equal tendency to
reabsorption. It is however so profoundly exhausting that it must be
used with the greatest judgment and caution.
Digitalis has often an excellent effect. Though not primarily a
diuretic, it is a powerful tonic of the heart and circulation, and by
increasing the blood tension it usually produces a free flow of urine.
In combination with the diuretic salts it may be used from the first but
it is especially valuable, after effusion and when attention must be
given mainly to securing reabsorption. Care is demanded that we avoid
its cumulative action, and in place of continuous large doses, a strong
infusion applied over the loins will sometimes have a good effect. It
may also be combined with bitters and even with ferruginous tonics in
the advanced stages.
In combination with neutral salts and digitalis, iodide of potassium
would seem to be indicated. Results however do not show a great
superiority to other diuretics in favoring absorption.
Tincture of iodine, painted upon the chest over the affected parts, and
repeated until tender, acts more or less as both a derivative and
deobstruent. A liniment of iodide of potassium and soap is a convenient
form of application.
The inunction of the chest walls with mercurial ointment has strong
advocates both among physicians and veterinarians, and is combined in
such cases with the exhibition of calomel internally. Unless the good
effects are shown in a day or two it may well be abandoned.
When effusion becomes dangerous through excess, and in advanced cases
when it fails to yield to medicinal measures thoracentesis is called
for. (See under _hydrothorax_.)
PLEURISY IN CATTLE.
Milch cows and work oxen most liable. Causes. Damp buildings and
locations, sudden transitions from heat to cold, exposure when
fatigued, etc. Symptoms, rigor, reaction, cold horns and limbs, later
hot, excited pulse, catching breathing, hyperthermia, 104° to 105°,
tender chine and intercostals, friction sound, later dulness,
creaking, weaker murmur, subacute cases often tuberculous, effusion
unilateral, chronic cases. Lesions, as in horse with superficial
marbling of lung. Treatment, laxative, warm drink, compresses,
derivatives, sedatives, diuretics, heart tonics, diuretics,
thoracentesis.
This is not common in young growing cattle, but is more frequent in
milch cows and work oxen. It is due to the same causes as in the horse,
and especially to chills when heated, damp buildings and locations, cold
draughts between open windows or doors, and cold storms. The greatest
danger comes from hot, close stables, like many distillery stables,
approximating to the temperature of the animal body and from which the
stock are suddenly turned out of doors, or shipped by car or boat with a
temperature near zero, and above all if furnished ice water to drink.
Such animals taking no exercise to increase the circulation and heat,
are especially liable to shiver and contract illness. Rigors too are
easily induced in animals standing in hot buildings, when, in connection
with the cleaning, an adjacent door is thrown wide open or two on
opposite sides of the house. Working oxen heated with exercise and then
exposed to extreme cold and compulsory inaction are endangered.
_Symptoms._ The attack is manifested by the same general symptoms as in
the horse. The rigors are often very well marked, especially over the
shoulder; the tenderness of the chine and intercostal spaces is
striking; the breathing is catching but there is rarely the same
restlessness as in the horse; the bowels are costive, appetite and
rumination impaired or suspended, and the paunch is often distended with
gas. The tenderness of the intercostal spaces, the friction sound of the
pleura, and the maintenance of the respiratory murmur and the normal
resonance of the lung, become the ultimate diagnostic symptoms. The
pulse may be 70° and upward, the temperature above 104° to 105°. In some
insidious cases indeed the fever is very slight and besides the general
wasting of the animal, the indications obtained by physical examination
alone enabled us to recognize the malady. Tuberculous pleurisy which is
very common in cattle is to be suspected in such cases.
Effusion is recognized by the dulness of the lower part of the chest up
to a certain line, and often unilateral, by the softer pulse, by the
dilated nostrils, or open mouth, the contracted facial muscles, by the
glazed eye, and anxious expression, by oppressed breathing and often by
engorgement under the chest and in the limbs.
When the disease lasts over ten or twelve days it tends to pass into the
chronic form. Or a chronic pleurisy of a subacute type may begin _de
novo_ and pursue an insidious and latent course.
If the disease commences as a subacute affection there may have been for
a month, capricious appetite, general ill-health and falling away before
any other symptom is noticed. Now the breathing is manifestly excited, a
small, short cough is heard at intervals, the pulse is accelerated but
weak, and pinching auscultation and percussion detect unequivocal signs
of pleurisy. From this the symptoms become more decided though for a
length of time they are very slight, the animal meanwhile becomes
increasingly emaciated, and perishes ultimately in a state of great
weakness. Such insidious cases are always to be suspected of
tuberculosis.
The _post mortem appearances_ resemble those of the horse. The surface
of the lung beneath the diseased portions of pleura, however, often
presents a marbled appearance from the infiltration of the areolar
tissue between the adjacent pulmonary lobules. The organization of the
false membranes begins on an average about the tenth day.
_Treatment._ The same general principles must be followed as in the
horse. Bleeding can rarely be employed, partly because the disease so
often assumes a subacute form, and partly because when first seen
considerable effusion has often already taken place and severe depletive
measures are thereby contraindicated.
A laxative dose (1 ℔.) of sulphate magnesia, may be given in warm gruel,
and the same means by compresses, hot fomentations and counterirritation
adopted, and the same sedative and diuretic medicines given as in the
horse. In the advanced stages and in the low types of the disease the
stimulating diuretics (sweet spirits of nitre, and liquor of the acetate
of ammonia) and vegetable and mineral tonics are especially indicated.
The diet in these last types must be nutritive, laxative and easily
digested.
Tapping of the chest is equally applicable as in the horse, (_see
Hydrothorax_.)
In the chronic forms everything is to be done to support the general
health whether by food stimulants or tonics, and counterirritants may be
applied several times.
PLEURISY IN SHEEP.
Causes, exposure, after clipping, washing in cold weather,
alternations from hot buildings to cold fields, shedding of the wool.
Symptoms, hyperthermia, troubled breathing and pulse with catching
inspiration, tender intercostals, friction sound, and signs of
effusion. Treatment, preventive, shelter, febrifuges in food or water,
aqua ammonia to sides.
The causes of pleurisy in sheep may be largely included in the general
statement—exposure. Cold washing and exposure after clipping is
especially injurious. Devieusart saw 300 cases of pleurisy and thirty
deaths in a flock of sheep shorn in February. If kept secluded in warm
buildings sheep may be shorn in midwinter, but any reckless exposure,
and any sudden reduction of the temperature of the building is liable to
be disastrous. Scab and other skin affections which lead to a shedding
of the wool in inclement weather may also be the occasion of widespread
attacks. Otherwise the causes are essentially those of the same disease
in the larger animals.
The _symptoms_ resemble those of pneumonia, but with the peculiar sharp,
short arrest of the inspiration, and the marked tenderness of the
intercostal spaces as above described. The cough is short, dry, hacking
and infrequent or suppressed as much as possible. Auscultation and
percussion signs, corresponding to those found in other animals, are
easily got in the newly shorn sheep. In the unshorn the wool must be
parted and a stethoscope employed.
The _treatment_ is mainly _preventive_, or when the disease is present,
of a general nature applicable to flocks. A warm barn, with pure air,
blanketing, wet compresses, to which may be added extract of henbane,
and nitrate of potash in the drinking water give examples of general
medication. As a derivative, aqua ammonia and oil may be applied in
lines on the chest exposed by parting the wool or generally on the
shorn. Where the patient can receive the requisite attention further
treatment should be on lines laid down for cattle.
DOG. PLEURISY.
Causes, exposure to cold, etc. Chill, reaction, disturbed breathing,
catching inspiration, rapid, hard pulse, hyperthermia, tender chest,
friction sound, later dullness at lower part of the chest in any
position. Treatment, as in pneumonia, with antirheumatics and
diuretics freely. Thoracentesis.
This is occasionally seen in the dog as the result of exposure, and like
other diseases of the chest is easily recognized. It owns the same
causes with pneumonia.
_Symptoms._ There is first dulness, shivering and some excitement of
respiration. To this follow the more acute symptoms, the hard pulse, the
rapid, catching breathing, the animal standing or sitting on his
haunches, the open mouth, pendent tongue, the injected mucous membrane,
the costiveness, but above all the tenderness of the intercostal spaces,
the early friction sound on auscultation, the pain and normal resonance
on percussion, the muscular twitchings and the short, suppressed,
painful cough. When effusion has occurred its amount may easily be
estimated by turning the animal alternately on its feet, back and
haunches, and observing how high the dullness extends in these various
positions.
The same _treatment_ may be adopted as in _pneumonia_, with this
difference that salicin may be given freely, and when effusion has taken
place active diuretics are specially indicated, and hence tincture of
squills (a teaspoonful) may be made to replace the nitre. In advanced
and obstinate cases, or where danger exists from rapid effusion, the
liquid may be drawn off with a cannula and trochar as in other animals.
PLEURO-PNEUMONIA. BRONCHO-PNEUMONIA. BRONCHO-PLEURO-PNEUMONIA.
Though we often meet with typical forms of _bronchitis_, _pneumonia_ and
_pleurisy_, it is much more common to find them combined more or less
with each other. Thus combined inflammation of the bronchial tubes and
pulmonary substance is frequent; inflammation affecting both the lung
and its investing pleural membrane is no less common; and cases are seen
in which all three structures are involved. These conditions are to be
recognized by the presence of the symptoms of both the coexisting
maladies but particularly by the indications furnished by touch,
auscultation and percussion. The predominance of one disease over
another will decide the nature of the treatment which must be adapted to
the peculiar character of each case whether _mainly bronchitic_,
_pneumonic_, or _pleuritic_. It is these mixed cases that test the
ability and judgment of the practitioner as he must carefully
individualize each case, ascertain the different parts affected, the
grade of the inflammatory action, the nature of the attendant fever, the
presence or absence of epizootic influence, etc., and having all these
conditions in view must apply remedial measures accordingly.
It must be evident that particular directions cannot be supplied for all
of these cases. General principles only can be inculcated and their
adaptation to the varied phases of different cases left to the judgment
of the student.
HYDROTHORAX.
All animals liable. Causes, pleurisy, obstruction to pulmonary or
intercostal veins, heart disease, Bright’s disease, anæmia, parasitic
or otherwise. Effusion reddish gray or clear straw color, inflammatory
and dropsical. Symptoms, troubles of respiration, as a secondary
disease complicated by dropsies elsewhere, signs of hydrothorax
without fever, shedding of hair. Treatment, diuretic, tonic,
derivative, thoracentesis, trochar and cannula or aspiration, point of
election for puncture, method, asepsis, drainage by aspirator, or into
an antiseptic solution, eligible cases, dangers attending
thoracentesis, shock, rupture of false membranes and lung, infection
of pleura, injection of antiseptics.
_Hydrothorax_ or _water in the chest_ is common to all domestic animals.
It is as we have seen one of the most ordinary results of _pleurisy_,
and may persist long after that disease has disappeared. It likewise
occurs independently of inflammation as a dropsical effusion. Thus when
the return of blood by the bronchial, pulmonary or intercostal veins, is
hindered by any cause such as tumors in the bronchial glands or
subvertebral region a passive effusion may take place through the coats
of the vessels. In imperfection of the mitral valves the regurgitation
of blood in the pulmonary veins during each cardiac systole equally
causes such transudation. Chronic disease of the kidneys (Bright’s
disease) with the retention of effete and injurious materials in the
blood leads to dropsy of the chest as in other parts of the body. Again
in many debilitated conditions parasitic and otherwise, with a tendency
to general dropsy the chest participates and a collection of fluid takes
place in the pleuræ.
The nature of the contained fluid will vary according to the conditions
in which it has been effused. If the result of inflammation there are
the different stages already indicated: _first_, of a yellow citrine
color or red from contained blood; _second_, grayish and muddy either
from contained pus or other changes taking place in the fluid; and
_third_, clear limpid and translucent as seen in the later stages. If
merely a dropsical effusion the fluid is watery clear and translucent or
with a slight straw color. The inflammatory effusion contains fibrine or
fibrinogenous elements, is associated with the formation of false
membranes, and though it may remain fluid so long as it is retained in
the chest, it coagulates rapidly when withdrawn. The dropsical effusion
rarely contains fibrine, and then only in very small amount, and it does
not coagulate when drawn off from the chest. The inflammatory effusion
usually contains a greater proportion of common salt, phosphates or
albumen than exist in the blood, and floating granules, particles and
cell forms, none of which conditions characterize the dropsical
effusions. The most prominent feature of the inflammatory effusions is
thus seen to be their power of coagulation, by virtue of the contained
fibrine, when exposed to the air.
_Symptoms._ When a sequel of pleurisy it is manifested by the symptoms
already mentioned under that head as indicating the occurrence of
effusion.
The dropsical cases may come on rapidly and present all the signs of
troubled respiration together with the results of auscultation and
percussion that characterize rapid inflammatory effusion but without the
fever and acute symptoms of pleurisy. More usually it comes on
insidiously, the lung accommodates itself to the gradual increase of the
fluid and it is only when the accumulation has become excessive that the
symptoms become prominent. In heart or kidney disease the filling of the
legs and infiltrations of the eyelids and of the skin beneath the chest
and abdomen are precursors or early concomitants of the disease, but in
all cases the accumulation in the chest is to be measured by the height
of the line of dulness on percussion and the extent of chest surface
giving forth no respiratory murmur on auscultation. As the liquid rises
on both sides of the chest, as it always does in such cases in the
horse, the breathing becomes short and labored, being chiefly effected
by the action of the diaphragm and the flanks—the ribs moving only
slightly. The nostrils are widely dilated with each breath. The
previously existing want of vigor and energy, the weak pulse, the poor
appetite and the pallor of the mucous membranes become aggravated; the
animal becomes very weak and prostrate, the loins insensible, the
permanently tucked up flanks labor tumultuously, the loins rise in
inspiration, the face is pinched and haggard, the eyeballs glazed and
protruding, and death is preceded by the same general symptoms as in
rapid effusion after pleurisy. A prominent feature of this, as of all
dropsical affections, and one usually seen in the hydrothorax of
inflammation as well, is the ease with which, even at an early stage of
the disease, the long hairs of the mane and tail may be pulled out. In
many cases they come out in handfulls when the comb or the fingers are
passed through them.
_Treatment._ The treatment must be of the actively diuretic kind
recommended for the effusion of pleurisy. It is modified however in one
respect. The inflammatory action having subsided or nearly so and the
condition being now essentially one of weakness a free use of tonics is
demanded. Many a patient dies in such circumstances from the actively
depletive treatment to which it has been subjected and the want of
attention to its need of generous diet and other support. The agents
prescribed for the advanced stage of pleurisy may be given, or the
digitalis or other diuretics and bitters may be combined with iodide of
potassium in one or two drachm doses, the amount being apportioned to
the strength of the animal. Iron in the form of sulphate, perchloride or
iodide may be freely given combined with gentian, quassia, or other
vegetable tonic, and above all a liberal and easily digested diet must
be allowed. Good will sometimes result from repeated applications of
strong iodine ointment to the sides with active friction.
When the condition is dependent on disease of the heart, kidney or other
organ, these must be attended to according to their special
requirements.
Disconnected from such complications hydrothorax will often give way to
an active treatment similar to that indicated above. In some cases
however our only hope of even temporarily prolonging life lies in the
operation for drawing off the fluid.
=Tapping the chest= or as it is technically called =thoracentesis= or
=paracentesis thoracis= has proved sufficiently successful in the lower
animals to warrant its continuance in cases that resist other modes of
treatment. It is highly probable that the larger proportion of
unsuccessful cases is due in great part to the hopelessly advanced stage
at which it is often had resort to, to the insufficient precautions
adopted in its performance, and to the want of appropriate dietetic and
medicinal treatment. Dr. Bowditch’s treatment by _paracentesis_ saved in
the human subject at the rate of about two patients in five and we ought
by availing of similar precautions to reach the same standard.
The cannula employed in veterinary practice is a silver tube two inches
in length, a quarter of an inch in diameter and furnished with a shield
of the same metal at one end. The trochar by which it is introduced is
of steel or brass. To carry out Dr. Bowditch’s system the operator must
supply himself with a syringe of a somewhat smaller bore and an
intermediate brass piece of a size adapted to fit accurately into the
cannula and supplied with a stopcock. By an instrument of this kind the
fluid can be drawn off by means of the syringe without any risk of the
introduction of ærial germs which always tend to induce suppuration and
even a putrefactive decomposition in the contained fluid.
The point selected to operate on is, in the horse, ox or dog, in front
of the anterior border of the ninth rib, at its lower end or close to
its union with the cartilage. The point of the trochar should be
directed slightly upward and forward to avoid the possibility of
injuring the diaphragm. The skin is first rendered aseptic by shaving,
followed by a thorough soapy wash and a free use of mercuric chloride
solution (1:500). It is then pricked with a lancet, then drawn aside
that the wounds in the skin and muscles may not correspond after the
cannula has been withdrawn. The trochar is then pushed steadily through
the intercostal space till all obstruction has been overcome, when it
may be concluded that the pleural sac has been reached. The trochar is
now withdrawn and the fluid allowed to flow from the cannula until there
is presumably some risk of the introduction of air, when the brass piece
is to be applied and the remainder drawn off with the syringe or
aspirator. As a substitute for the aspirator a caoutchouc tube, eighteen
inches long, put on the cannula or needle and having its lower end
plunged in a solution of boric acid will prevent the entrance of germs.
A prob has often to be introduced to prevent plugging of the cannula by
floating false membranes, and a new puncture in a different place may be
necessary. In the case of excessive accumulation it is often advisable
to draw it off at two operations, as recommended in large abscess of the
pleura and for the same reasons. The need for such a precaution will be
understood when it is stated that in bad cases the chest contains as
much as six or seven ordinary stable bucketfuls of the liquid. If,
however, it is limited in amount it may be all withdrawn at once.
The most successful cases in the horse have been upon young, vigorous
animals, from four to eight years old, during the first month of
illness, and where the pleurisy has been confined to one side.
Dr. Bowditch lays down the following rules for the adoption of
paracentesis in man (_Clinical Medicine_, by Prof. W. T. Gairdner):—
“I now never operate unless I find some distension or rounding out of
the chest, and filling up of some of the intercostal spaces, so that the
chest presents a uniform curve, and not alternate depressions and
elevations as in the healthy chest. I operate under the following
circumstances when I feel certain there is fluid:
“1. When there is _severe permanent dyspnœa_—orthopnœa—however acute the
disease if I find fluid filling the pleural cavity, or nearly filling
it.
“2. When there are occasional attacks of orthopnœa threatening death,
even if there be not sufficient to fill more than half of the cavity. If
the fluid seems to be the cause of the dyspnœa I operate, because
occasionally I have lost a patient while waiting for more extensive
physical signs. This rule I apply to acute and chronic cases.
“3. I use the trochar after three or four weeks of ineffectual
treatment, without any absorption being produced.
“4. In chronic idiopathic hydrothorax, a latent pleurisy with simply
physical signs to indicate _extensive_ effusion, but when the rational
signs are either very slight or none at all save a general malaise and
weakness.”
The use of iodide of potassium and vegetable and mineral tonics must be
perseveringly employed and the strength further supported by a generous
diet, to secure the animal against the dangers of extreme prostration,
of suppuration, or other undesirable conditions of the exuded product.
Among the dangers attending thoracentesis are fainting as a result of
shock on the sudden withdrawal of so much liquid, rupture of the false
membranes, and even of the enclosed lung tissue or of blood vessels,
under the sudden expansion of the partially collapsed lung confined by
the investing false membrane, and the introduction of pus or septic
germs into the pleural cavity. To obviate the first named dangers tight
bands (circingles) around the chest will give support and limit sudden
expansion. In case of excess of liquid the withdrawal of one-half or
two-thirds at a time will allow opportunity for accommodation.
Hæmorrhage may be met by the internal use of chloride, sulphate or
nitrate of iron, matico, hamamelis or tannic acid, and a weak solution
of boric acid or other antiseptic agent may even be injected in small
amount into the pleural cavity.
In obstinate and chronic cases the injection of a weak solution of
iodine and iodide of potassium is often of service. In other cases a
normal chloride of sodium solution (previously sterilized) may be
introduced as soon as a partial evacuation causes uneasiness, and by a
succession of such evacuations and injections the residuum liquid may be
rendered clear and largely aseptic on a single occasion.
In the smaller animals the selection of the most dependent part for
insertion of the trochar is not so essential, as the body may be turned
to facilitate the drainage.
On completion of the operation the wound may be again treated
antiseptically and coated with aristol or collodion.
PNEUMOTHORAX. AIR OR GAS IN THE PLEURA.
Causes, decomposition of liquid effusion, perforation from a
bronchium, the stomach, a thoracic wound. Symptoms, metallic tinkling,
splashing, succussion, drum-like resonance, suppressed respiratory
murmur, distance of cough sound, distress, anxiety, dyspnœa, bulging
intercostal spaces, sometimes a wound. Treatment, closure of wound,
calmatives, aspiration of gas. Treatment for pleurisy.
The collection of air or gas in the cavity of the pleura has already
been noticed as coexisting with liquid effusion in some cases of
advanced pleurisy. It may arise from other causes, among which may be
noted: 1. When a mass of pulmonary tubercle connected with a bronchial
tube has opened into the pleural sac. 2. When a communication has been
established between the pleural cavity and the alimentary canal, as in
combined rupture of the stomach and diaphragm, or of the double colon
and diaphragm. 3. When a rib is fractured and the broken end penetrates
the lung tissue and opens into one or more small bronchial tubes. 4.
When a wound has been inflicted penetrating the walls of the chest and
forming a valvular orifice through which air is drawn inward during each
inspiratory act, but out of which it cannot pass when the thorax
collapses.
The amount of gas present may be extremely slight, or in a case such as
that from a valvular wound it may cause complete collapse of the lung,
filling up the entire half of the thorax and bulging into the opposite
half.
The _symptoms_ are often very obscure. If with liquid the metallic
tinkling after rising, in small animals the splashing when shaken and
the other sounds of auscultation and percussion will point it out as
described under _pleurisy_. In the case of a broken rib the distortion,
swelling and tenderness, will lead to suspicion. A penetrating sound
will be sufficiently evident, and in the case of tubercle previous cough
and ill-health will have been manifest.
The specific signs of uncomplicated pneumothorax are: 1st, A drum-like
resonance on percussion over the seat of the gas, usually at the upper
part of the chest; 2d, A partially suppressed or distant respiratory
murmur over the same area; 3d, A muffled or suppressed sound of the
cough; 4th, Sometimes, especially if the gas is abundant, prominence of
the chest on that side; 5th, There are also more or less distress and
anxiety, difficult breathing, quick, weak, rapid pulse, and other signs
of illness.
Some cases of this kind recover spontaneously or with the liquid
effusion with which they are associated; in traumatic cases the wound is
sometimes sealed up by a pleuritic exudation which here becomes a
curative process; while in some examples of valvular wound of the lung
or walls of the chest death may ensue in a period varying from a few
minutes and upwards to weeks.
_Treatment_ is limited to the prevention of the ingress of air through
an external wound where that exists; the employment of opiates and other
agents to moderate attendant suffering; to measures calculated to
moderate the intensity of resulting pleurisy, and, in cases where there
is imminent danger from accumulation of gas, to the puncture of the
chest and the careful withdrawal of the gas by aspiration. If necessary
sterilized air may be made to replace the aspirated gas.
PYO-PNEUMOTHORAX, EMPYEMA.
Causes, septic cocci entering through wound or blood. Symptoms, those
of hydrothorax, with prostration, fœtor, and it may be issue of pus.
Treatment by antiseptic injections.
A purulent fluid in the pleural cavity may be found in ordinary
pleurisy, but is much more likely to supervene in traumatic forms, in
which the pus cocci reach the cavity through the wound of the bronchia,
alimentary canal, or chest walls.
The symptoms are essentially those of pneumothorax, with greater
prostration, and in certain cases a distinct feverish smell or fœtor of
the breath, or the escape of pus through a wound. In treatment the
difference from pneumothorax is mainly in the antiseptic character of
the injections and the freer employment of stimulants and tonics. Salt,
salicylic acid, borax, peroxide of hydrogen, aluminium acetate, or
potassium permanganate solutions may be used. Tonics (quinia) and
antiseptics (sulphites, salicylates, iron) may be given.
CHRONIC PLEURISY.
Animals liable. Causes, irritation through effusion and exudate acting
on susceptible pleura, or by other disease products in lung or pleura.
Unhygienic surroundings and management predisposes. Frequent chills in
cold water. Symptoms, unthriftiness, easily blown, fatigued, or
sweated, cough, paroxysmal under exertion, pallor of mucous membranes
becoming congested on slight exertion, difficult breathing when
recumbent, percussion and auscultation signs of pleurisy and
hydrothorax. Lesions, great liquid effusion, clotting on exposure,
with much albumen and cell forms. False membranes partially organized.
Treatment, tonic, diuretic, derivative, diet nourishing,
counterirritants, paracentesis.
In all domestic animals acute pleurisy may merge into the chronic form,
the irritation being maintained by the presence of the residuum liquid
and the false membranes and adhesions which interfere with the free
dilatation of the chest. The pleura too, having been once inflamed,
retains an increased susceptibility to such disturbing conditions. In
other cases the affection is symptomatic of other chronic affections, as
tuberculosis, glanders, and neoplasms of various kinds. It has been seen
especially in old, weak and debilitated subjects, kept in confined,
impure stables or habitually exposed to undue cold and damp. Hence dairy
cows in unhygienic conditions, and hunting dogs, which plunge in water
when heated, are among the most frequent victims.
_Symptoms_ are often obscure. The affected horse may be bright and
lively, showing little respiratory disturbance unless under exertion.
Yet there is a general appearance of unthriftiness, with erect, dry
hair, hidebound, and a small, dry cough. Under work there is hurried
breathing, early exhaustion, ready perspiration, and aggravation of the
cough which then occurs in paroxysms. Auscultation and percussion give
characteristic signs according as there may or may not be false
membranes or effusion at particular points. It is usually bilateral in
horses, unilateral in other animals.
In cows in addition to the corresponding symptoms, there is pallor of
the mucous membranes when at rest, quickly transformed into congestion
under exercise, suppression of the milk, and weak heart beats unless
when excited. In the advanced condition the animal has difficulty of
breathing when recumbent on the sound side and subcutaneous infiltration
is felt or seen beneath the sternum or in the limbs. The affected side
shows an increased dimension, vertical and longitudinal, of the chest,
and the intercostal spaces in their lower part bulge out and fluctuate.
In cows and indolent animals there may be a quiescent condition or very
slow progress, but any violent exertion is likely to give a sudden
stimulus to the morbid process.
_Lesions._ The liquid effusion, usually unilateral, except in the horse
may amount to 40 quarts in the latter animal, 30 quarts in the ox
(Rigot), and 5 to 6 quarts in the dog. Unless there has been a recent
sudden accession of inflammation it is of a pale straw color, with, in
the dog, a slight rosy tinge. It clots loosely on exposure to the air
and contains a large amount of albumen and few cell forms. The false
membranes are thick and white at some points and red and vascular at
others. In the main they are completely organized. The lung is more or
less collapsed and the right heart dilated and attenuated.
_Treatment_ must be in the main tonic, diuretic and derivative. Food
must be nourishing, digestible and in liberal amount; diuretics and
bitter tonics with digitalis and, (if there is little fever)
preparations of iron are to be pushed as far as the strength will allow;
and the counterirritants applied to the sides of the chest a number of
times in succession. Iodides may be used internally and externally, and
_paracentesis_ must be employed unless early improvement is manifested.
PLEURODYNIA.
Definition. Symptoms, stiffness, pointing of fore limb, catching
inspiration, tender intercostals, less fever, cough, and hardness of
pulse than in pleurisy, no friction sound nor signs of pleuritic
effusion. Treatment, antirheumatic, derivatives, colchicum, alkalies,
salicylate, salol, phenacetin, warm (steam) bath, warm building and
clothing.
_Definition._ Rheumatism of the intercostal muscles. This has been
occasionally observed in the horse, and is liable to be mistaken for
pleurisy, which it closely resembles in its symptoms. There are the same
stiffness of the fore limb on the affected side, the same short
breathing, the same fixed and inactive appearance of the ribs, and the
same extreme tenderness on pressure as in pleurisy; but the high type of
fever, the cough and the full hard and accelerated pulse are usually
absent; the tenderness tends to shift from one point to another, there
is no shivering nor friction sound in the early stages, and no
subsequent absence of sound and deadness on percussion over the lower
part of the chest as result from effusion. When associated with fever it
is very difficult to distinguish from pleurisy, and its recognition can
only be made by these physical signs just mentioned.
_Treatment._ This must be the same as in rheumatic attacks in general.
Rub the chest actively and repeatedly with a mixture of equal parts of
spirits of turpentine, laudanum and olive oil, give ½ drachm doses of
powdered colchicum daily and bicarbonate of potass freely in the water
drank. Or give four times a day 2 drachms of salicylate of soda, or 1
drachm of salol, or phenacetin. A warm building and warm clothing are
essential elements in treatment.
BRONCHIAL ASTHMA IN THE DOG.
Definition. Pathology, neurotic origin, bronchial spasms, swelling of
mucosa, fibrinous inflammation of bronchioles, Berkart’s
streptococcus, irritants formed in indigestion, overfeeding,
inactivity, plethora, constipation. Symptoms, obesity, sluggishness,
recurrent paroxysms of dyspnœa, hard cough, tense abdomen,
constipation, piles, depilation of skin, tartar covered teeth, fœtid
breath. Retching, vomiting, a glairy mucus, emaciation may follow.
Lesions, emphysema, fatty deposits in mediastinum, old standing
diseases of the heart, lungs and digestive organs. Treatment,
antispasmodics by lungs or rectum, stramonium, nitre fumes, emetic,
purgatives, vegetable diet, exercise, sedatives, blisters. Asthma in
the horse.
_Definition._—A neurotic affection mainly affecting the pneumogastric
nerve, and leading to paroxysms of stenosis or constriction of the
bronchioles and attacks of dyspnœa. In its initial stages it is
associated with corpulence and disordered digestion, and later with
congestion and swelling of the mucosa of the bronchioles, emphysema, and
dilatation of the right side of the heart.
_Pathology._ Asthma is generally attributed to spasm of the bronchial
muscles (Williams), and though recent observations have failed to
sustain this it must be admitted that in the majority of cases it is of
decided neurotic origin. Again it is attributed to erythematous swelling
in patches of the bronchial mucosa, (Clark). Another theory is that it
is a fibrinous inflammation of the mucosa of the bronchioles, the
tenacious exudate blocking the tubes more or less completely and relief
coming with a more diffluent secretion. Berkart found a streptococcus in
the sputa which he supposed to be the final cause. Again it has been
held to depend on the circulation in the blood of deleterious matters
introduced during digestion. Again it has been attributed to a neurosis
roused by constipation and the accumulation of irritant matters in the
intestine. Whatever local conditions may be operative, there can be no
doubt that in dogs it is almost exclusively confined to those kept
indoors, overfed, without exercise, plethoric and constipated. The
disease seems to originate in and persist by nervous disorder propagated
from the digestive organs. A change of diet or any disturbing cause may
bring on a paroxysm.
_Symptoms._ The disease is one of pet dogs, kept in towns, deprived of
exercise, fresh air, and of the opportunity to relieve the bowels at
will, and gorged with highly spiced meats, and sweets at least three
times a day. Sluggishness and obesity are marked characteristics of the
dog when first attacked though in the advanced stages the violence of
the paroxysms and their frequent recurrence may have induced extreme
emaciation.
The affection is usually ushered in by a cough, at first slight, but
soon becoming frequent, hard and sonorous, as in the early stages of
bronchitis. The cough becomes very troublesome and the breathing
habitually labored, but at irregular intervals a paroxysm comes on which
threatens death by suffocation. The dog stands or sits on his haunches
with open mouth, pendent tongue and staring eyeballs, panting for
breath, and has his condition aggravated by every change of position or
other source of excitement. By the frequency and severity of the attacks
may be estimated the danger of the patient.
An examination in the intervals of the attacks detects some disturbance
of the digestive organs. The tense and distended condition of the
abdomen usually manifests the existence of overloaded stomach and
bowels, of indigestion, tympany and constipation. Piles are often
present as a result of long continued costiveness. The skin is dry and
unthrifty, and often in patches denuded of hair. The teeth are covered
with tartar and the breath fœtid.
Retching is occasionally seen to occur during a violent access of
coughing, but only a little glairy mucus is brought up.
The cough, hurried breathing, and paroxysms of dyspnœa become
aggravated, the general health suffers largely, and death often ensues
in a state of great weakness and emaciation.
On _dissection_ of such cases the lesions of various old standing
diseases of the heart, lungs, or abdominal organs have been met with at
times, and such disorders have doubtless assisted in maintaining and
aggravating the asthma. The most constant lesions, however, are
emphysema of the lung, and accumulations of fat in the mediastinum.
=Treatment.= 1st. =During a paroxysm.= This is confined to the
administration of antispasmodics either by inhalation or as an injection
to avoid the additional suffering of swallowing. Ether or chloroform may
be inhaled from a sponge, but the employment of these should be guarded
especially in advanced cases when besides the prevailing weakness there
is reason to suspect structural changes in the heart. The same agents in
doses of one, two or three teaspoonfuls, or laudanum in double that
quantity may be thrown up as an enema, and may be combined with a couple
of ounces of castor oil when costiveness exists. The fumes from burning
stramonium or from burning brown paper which has been previously soaked
in a strong solution of nitrate of potass, will in many cases suddenly
cut short the paroxysm. If on the other hand there is reason to believe
that the stomach is overloaded the attacks will often be suddenly cut
short by giving an emetic. For this purpose a grain of tartar emetic may
be shaken upon the tongue, or a dessert spoonful of wine of ipecacuan,
or of antimony, poured over the throat. 2d. =In the intervals between
the paroxysms.= Attention must be given to counteract any inflammatory
action in the chest by which the disease may be maintained. Our chief
object, however, must be to divest the animal of its superfluous fat and
bring the digestive organs into a healthy condition. Unfortunately the
propensity to fatten in some dogs seems to be a morbid condition. The
food appears to be stored up as fat at the expense of muscular and other
tissues even when the animal is kept on the borders of starvation. All
flesh must be withheld and coarse vegetable fare alone allowed. A well
boiled pudding (porridge) made with oatmeal or Indian corn meal, water
and a little salt, with a small quantity of skimmed milk or buttermilk,
is an excellent diet in such cases. The amount must be small, though the
hitherto pampered favorite will rarely seek to fully replenish his
stomach until he has forgotten his former extravagant habits.
A good deal of open air exercise must be given, not violent, but gentle
and long continued, and this though the patient may appear physically
unfit for it. Exercise should be given three hours or more after a full
meal. Purgatives (one ounce castor oil) should be administered twice a
week. A clean bed, not too soft nor luxurious, should be allowed in a
dry, airy place. The skin should be well brushed daily and occasionally
washed thoroughly with soap, care being taken to dry the coat completely
afterwards. Sedatives should be given daily, such as a half grain each
of stramonium and tartar emetic, and in advanced stages with weakness
and emaciation vegetable tonics will be demanded.
Blaine strongly advocates a course of emetics, given every alternate
day, and Mayhew lauds frequently repeated ammoniacal blisters to the
sides. Such measures will be especially applicable when there is
irritation and discharge from the bronchial mucous membrane. Strong
subjects can alone, however, bear such treatment.
All cases of asthma in the dog are obstinate and critical and require
much judgment in treatment.
ASTHMA IN THE HORSE.
Hering records a case of _spasmodic asthma_, in a strong cart horse.
Besides the oppressed and difficult respiration, the animal was
excessively dull and had no appetite, but the pulse was almost of the
natural standard. The animal was not benefited by opening medicine but
improved under active doses of extract of hyoscyamus. Quillaume reports
two asses attacked apparently in the same way, and Delwart and Robertson
refer to other cases. They recovered under antispasmodics. These are at
least closely related to heaves, which is largely a neurosis at first.
ASTHMA. BROKEN WIND. HEAVES. DYSPNŒA.
Definition, neurotic affection with digestive and respiratory
disorders. Causes, no racial exemption, disease largely coextensive
with leafy hay from clover, alfalfa and other leguminous plants, musty
hay, cryptogams, overloading the stomach, active work on a full
stomach, overdriving, bronchitis, chronic bronchitis, emphysema.
Nature, a neurotic affection, starting with derangement of some part
of the vagus, dilatation of the right heart, congestion of the
bronchioles. Symptoms, double expiratory action, flatulence, weak,
husky cough, wheezing, glairy, grayish nasal discharge, wheezing,
increased resonance along the margins of the lungs, sibilant râle,
heart’s impulse strong, even felt on right side, aggravation with
overloaded stomach, costiveness or muggy atmosphere, improvement on
laxative (green) food. Treatment, succulent green food, natural
pastures, relieve any abnormal state of lungs or bowels, pure air,
heart tonic, diet, arsenic, special diagnosis, guard against masking
of symptoms by narcotics, privation of water, shot, lard,
recto-vaginal fistula, diagnostic signs, dilated nostrils,
auscultation and percussion signs of emphysema, relapse under hay and
water.
_Definition._ A chronic affection of the equine species, manifested by a
hurried, wheezy breathing, greatly aggravated by close, muggy weather, a
full stomach, certain kinds of diet, or by exercise; by a double lifting
of the flank with each expiration; by a small, weak, dry cough, often
occurring in paroxysms and easily excited by a drink of cold water,
exposure to cold air or a fibrous quality of food; and lastly, by a
marked disorder of the digestive organs.
_Causes._ This disease is essentially the result of faulty feeding and
working, though pre-existing diseases of the air passages and sudden
violent muscular efforts no doubt occasionally contribute to its
development.
It has been alleged that some races of horses are exempt from this
disease. Among these the Arabian, Persian, Barb, Spanish and Portuguese
are especially named but their immunity in all probability depends on
the feeding and management rather than on any peculiarity of breed. The
countries where these horses are met with are not subject to a prolonged
winter but yield green food throughout the greater part of the year, and
it is a notorious fact that no horse becomes broken winded at pasture.
The Arabians moreover “feed their horses on the scanty plants which the
borders of the deserts supply and when these are wanting they are fed on
a little barley with chopped straw, withered herbs, roots dragged from
the sands, dates when these can be obtained, and in cases of need the
milk of the camel. They drink at long intervals and in moderate
quantities,” (Low). Since an habitually overloaded stomach is the most
common cause of _heaves_ the absence of the affection in the Arab is not
surprising. But the Arab unfortunately enjoys no such security in
England or America. Concerning the Barb, Delwart remarks that after a
day’s hard work, fasting, he is fed on six or seven pounds only of
barley, and without the cut straw that the Arab is allowed in similar
circumstances.
In Spain and Portugal horses at work are fed on broken wheat and barley
straw, from twelve to twenty-five pounds, and barley from six to twelve
pounds daily, according to the size of the animal and the demands upon
his strength. The mares are constantly at pasture and according to the
rainfall they are starved or in abundance. Green food and a limited
straw and grain diet are precisely the conditions in which broken wind
does not appear. Rodriguez, veterinarian to the queen says that the
disease was unknown to Spain until the cultivation of red clover,
lucerne, and sainfoin. At Aranjuez, horses fed on the hay of these
plants, lost vigor and wind and several became decidedly broken winded.
All were, however, restored to health and vigor by a return to their
former diet. Count Cardenas found that his horses gained in flesh on the
new fodder, but that symptoms of broken wind developed themselves
rapidly.
In France, M. Demoussy records similar facts. In Segala, where the
aliment is substantially hay, broken winded horses abound, whilst in the
adjacent district of Causse where horses are fed through the winter on
straw and barley broken by the mules feet in the act of threshing or
treading out, the disease is virtually unknown.
Lucerne and sweet trefoil are indigenous and grow abundantly in Causse
and Caussergne but eaten green or after their seed has been shaken off
and the stems have acquired a dry ligneous character these are
innocuous. When however condemned to stand in the stable through a
severe winter, with their racks constantly filled with hay, they will
eat from thirty to thirty-five pounds of this daily and many become
broken winded. The breeding mares which get little hay, seldom become
affected though the plenitude of their abdomen and the impaired
respiratory function might be thought to conduce to the affection.
In England broken wind is much less prevalent than on the European
Continent and it is deserving of notice that lucerne and sainfoin hold
no place among the British green crops, that red clover hay is only
exceptionally met with owing to the amount of land that is
_clover-sick_, that natural hay is largely used, and that when horses
are largely fed on hay it is qualified by such laxative agents as
turnips, carrots, beet, etc.
All this throws light on the immunity of horses on our western prairies
and plains. Feeding on the indigenous grasses fresh or made into hay,
they are saved from the noxious influence of those artificial products
which are found in all countries to determine the development of broken
wind. It needs not that we adopt the popular notion that any special
plant growing in these pastures ensures the safety of the equine races.
It is merely a repetition in the Western Hemisphere of the experience so
long before obtained in the case of Spain. Parallel with the progress of
cultivation in our western lands, we see this malady advancing. Fifty
years ago it was virtually unknown in Michigan and adjacent states
whereas now these states can almost emulate New York in the relative
number of their victims. It must not however be supposed that this
cultivated fodder is the sole cause of the westward march of this
malady. With improved agriculture have come better roads, spring wagons
and driving at a pace which was comparatively unknown to the early
settlers.
In California the condition of Spain was for long pretty accurately
repeated. With no winter worthy of the name, troops of horses were left
at pasture throughout the whole year and those that were stabled
subsisted chiefly on natural hay in which the indigenous grasses were
commingled with white—but no red—clover. California long retained the
reputation of having no broken winded horses.
In our Eastern states where the disease was thirty years ago so
notoriously prevalent, the fields of luxuriant red clover might well
have excited the envy of the English farmer. The hay made from this,
full of seed and dust was given without stint to the farm horses, which
during the rigor of the winter were often shut up in stable for a length
of time continuously and dangerously gorged themselves with this
provender. In the Eastern States with a steady falling off in the red
clover, there is also a corresponding reduction in the number of cases
of heaves. The grain allowed them, a mixture, supposed to consist of
Indian corn, oats and buckwheat, given as a dry coarse flour, was little
calculated to counteract the effects of the clover hay, and the entire
absence of turnips and other succulent roots as a farm crop precluded
their use as a preventive of the malady. We need not forget the
prevalent ambition to possess a fast trotter, nor the effect of the
climate on the air passages (See _chronic bronchitis_) in estimating the
causes of this malady in the Eastern states.
The mere overloading of the stomach is a potent cause of the development
of heaves. The horse is above all other animals compelled to undergo
hard work on a full stomach. Coleman cites the experience of the
coaching days when each horse had 20 lbs. of oats daily and not more
than 5 lbs. of hay with no water before work. These horses were driven
fast for long stages yet they never contracted broken wind under this
treatment. Farmers’ and millers’ horses on the other hand were most
subject to the disease because gorged continually with hay chaff and
mealy food, and worked in this condition. “Nimrod” who confirms
Coleman’s statement says “I have taken some pains to ascertain this fact
by my own personal inquiries. One proprietor who has nearly fifty horses
at work—many of which are in as fast coaches as any that travel on the
road—assured me lately that he had not a broken winded horse in his
yard; whereas before he stinted them in their hay he generally had one
to five in that state.” Percivall testifies to its comparative
infrequency in the English cavalry horses, which have their diet
carefully regulated. Hay musty from bad harvesting or other cause and
such as is rank from growing in low wet localities are _caeteris
paribus_ more injurious than good hay.
Every day observation shows that driving a horse upon a full stomach
often causes broken wind and nothing will more surely aggravate it, when
it does exist. The same remark may be made of the drinking of large
quantities of water after feeding and just before going to work. Gross
feeders are above all others the subjects of the complaint.
The question arises how a disturbing cause operating directly upon the
digestive organs should affect the respiratory, in such a marked and
permanent manner. It cannot be because of the gastric and abdominal
distension since pregnant mares though in a state of much greater
plentitude, are not thereby rendered liable to broken wind, and if they
have previously suffered from this infirmity, the symptoms are usually
less marked when breeding. The explanation first advanced by Dupuy
appears to be the correct one. The lungs, the stomach, and certain other
organs derive innervation from the vagus nerve, and certain disturbances
of the stomach and intestines so impair the function of this nerve that
the lungs are affected, at first functionally and afterwards
structurally. In support of this view is the fact that broken wind is
usually associated quite as much with digestive as respiratory
derangement. The horse though a heavy feeder becomes unthrifty,
hidebound and emaciated; his dung is passed in an undigested state like
so much chopped straw, and flatus is continually passed from the bowels.
Indeed the almost incessant passage of wind and fæces, during the first
mile or two of a journey, is a disgusting evidence of the malady. The
power of doses of shot, fat and other agents to temporarily allay the
symptoms may be held to point in the same direction.
Beside causes operating on the side of the digestive organs others
undoubtedly superinduce the disease, and among these severe exertions
and chronic bronchitis ought to hold prominent positions.
Overexertion induces overdistension and rupture of the air cells by the
forced retention of air within the lungs, by the closure of the glottis,
while the chest is strongly compressed by the respiratory muscles. It is
an essential condition to all severe exertion in man that the breath
should be held, and though the horse appears equal to the same efforts
of draught after the operation of tracheotomy has deprived him of the
power of holding the breath, yet he would seem to be sooner exhausted
(Goubaux, Colin, Bouley), from which it may be inferred that this power
is frequently exercised, and it probably always is in any sudden severe
effort as in starting a heavy load, or jumping a five-bar gate. This
retention of air in the lungs during violent compression of the chest
walls is precisely the condition met with during an access of coughing,
and in both cases alike there is the tendency to overdistension of the
minute tubes and air cells until they have lost their power of
contraction, or they may even give way and allow the air to pass out and
lodge in the lung tissue.
Another mode in which violent effort injures the lungs is by the rapid
and continued inhalation of great quantities of air during rapid
breathing, so as to dilate the lungs suddenly to their fullest extent.
Sometimes from irregular distribution of the ærial current or from the
want of tone in a particular part of the lung that gives way under the
pressure and the air cells become overdistended or ruptured. This
condition is especially met in the more rapid paces. It is well
exemplified in the results of the deep breathing after cutting the vagi
nerves.
In either case the result will be more certain if the effort is made
upon a full stomach or with the functions of the vagus nerve impaired by
a previous faulty diet.
That broken wind is a frequent concomitant or sequel of _chronic
bronchitis_ is undeniable, and theoretically nothing is more likely to
cause dilatation and rupture of the air cells and consequent impairment
of the innervation and contractility of the lung than violent fits of
coughing, while the bronchial tubes have thickened and friable walls, or
are partially plugged by tenacious mucus.
Broken wind is mainly a disease of old horses, though I have seen
several cases in five-year-old animals, and Bouley records a case in a
two-year-old colt out of a badly broken winded mare. This would seem to
indicate an hereditary proclivity, and there is no doubt that the
shallow, narrow, weak chest predisposing to this as to many other
pulmonary complaints is transmitted from parent to offspring.
_Nature of the Disease._ Emphysema of the lungs is the most constant
structural change met with in the bodies of animals which have suffered
from broken wind. This condition of the horse’s lung appears to have
been noticed by the early Greek writers. It was advanced as the cause of
broken wind by Riding in 1704 (Pathologie Veterinaire), by Floyer in
England in 1761 (Treatise on Asthma in Man), by Vitet in France in 1783
(Medicine Veterinaire, Lyon), by Freutzel in Germany, and Bracy Clark in
England in 1795. It was only, however, after the admirable discoveries
of Lænnec that the question was systematically investigated by Delafond,
who has furnished the most comprehensive data on the subject. Out of
fifty-four broken winded horses dissected by him no less than forty-five
had the lungs extensively emphysematous. This emphysematous lung differs
according to whether the emphysema is _vesicular_ or _interlobular_.
In =vesicular emphysema= the smallest bronchial tubes and the air cells
have become distended beyond the natural standard and remain permanently
so, the lung tissue having lost its power of contraction. If such a lung
is inflated and dried, and a thin slice taken from the surface of the
emphysematous part the size of the minute orifices on the cut surface
will show its condition. These fine openings are only the air cells cut
across, and in their healthy state they will admit no larger object than
the point of a needle or a fine bristle. They are slightly larger in
adult and especially in old horses than they are in the young. If
affected by emphysema they will often admit a hempseed or even a small
pea. On opening a healthy chest the lung collapses, contracting on
itself and expelling the contained air; if the lung is emphysematous the
diseased portion does not collapse and if the entire lung is affected it
continues to fill the chest and may even bulge outward after it has been
opened. The color of the emphysematous lung is of a brighter red than
are the healthy portions. If a diseased lung has been left exposed to
the air for twenty-four to thirty-six hours and then cut across in all
directions, the diseased lobules may be distinguished at a glance by
this lighter shade, and such light portions if near the surface will be
found to correspond to elevations above the general level of the lung.
If the diseased lung is placed in water it floats on the surface like an
inflated bladder scarcely at all sinking into the fluid. If the lung is
blown full of air the emphysematous part is first filled causing the
bulging on the surface to be still more marked than before. Vesicular
emphysema rarely affects an entire lung; it is usually confined to the
anterior lobes and to the thin lower and posterior borders of the organ.
=Interlobular emphysema= is the extravasation of air into the connection
tissue between the lobules owing to rupture of the air cells, and
smaller bronchial tubes. It may occur independently of the vesicular
emphysema but more frequently, it is preceded by that form and results
from it. It is manifested on the surface of the lung by irregularly
formed transparent elevations movable from one place to another under
the pressure of the finger contrary to what is the case in vesicular
emphysema. These vary from the size of a pea to that of a hen’s egg.
When the air exists in the cellular tissue between the lobules, it
appears as intersecting lines circumscribing irregular spans, and
seemingly dark colored to a superficial glance but seem to be
transparent on a closer examination. Like the elevations on the surface
these collapse on being pricked.
When a lung in this state has been inflated and dried it presents on the
diseased parts the union of several air sacs into one by the rupture of
their intervening walls so that a pea may be lodged in the cavity; it
further shows wide and prolonged canals on the surface and in the
intervals between the lobules—the dilated areolæ of the connective
tissue. These abnormal conditions like the vesicular emphysema are
chiefly met with in the anterior lobes of the lungs along their free
borders and on their inner surface near the entrance of the bronchi.
One or both of these two forms of emphysema may be considered as
essential conditions in all forms of broken wind. It does not follow
that this is the primary disease; we have already seen that the cause of
the malady is usually to be sought on the side of the digestive organs,
and that impaired innervation, on the part of the vagus nerve or of the
ganglia in the brain presiding over it, leads to these functional and
structural changes in the lungs. If these changes are results and not
causes, their extent will not necessarily bear a constant proportion to
the intensity of the disease, though in reality they are generally found
to do so.
From a series of injections of lungs from broken winded horses M.
Demoussy arrived at the conclusion that the essential lesion of broken
wind was an aneurismal dilatation of the capillary vessels of the lung.
This is like the condition of the mucosa found in asthma in man and is
explainable in both cases by the impaired innervation, as dilatation of
these minute vessels is a natural consequence of the loss of vaso-motor
nervous power, and contact with air saturated with carbonic acid.
Dilatation of the smaller bronchial tubes is frequently present and
especially characterises such cases as supervene on chronic bronchitis.
These dilated tubes contain a plastic, whitish, inodorous mucus.
Another frequent concomitant of the emphysematous lung is a dilatation
of the right cavities of the heart, especially the auricle, and an
attenuation of their walls. The same condition is noticed in pulmonary
emphysema in man and like this is probably due to the slow and imperfect
circulation in the diseased lung.
Collating these structural changes with the different causes of the
disease we find that they harmonize with the theory of impaired function
on the part of the vagus nerve or its presiding ganglia, whether this
functional disturbance has its origin in disorder of the digestive
organs, as in the great majority of cases, in severe muscular efforts,
or in chronic bronchitis.
Section of the vagi nerves affords an exaggerated instance of their
paralysis and its results. These are mainly emphysema, capillary
dilatation, blood extravasation, inflammation and pulmonary collapse.
Emphysema is the first result and due to the slow, deep respiration
(Boddaert) and loss of contractibility (Longet); capillary dilatation
results from the extreme distension of the air cells and the retention
in them of air highly charged with carbonic acid (Donders); the other
lesions occur later and own very different causes.
That this is the true nature of the disease would further appear from
the occurrence of emphysema without broken wind, two cases of which are
recorded by Percivall; and from the existence of broken wind without
emphysema. Cases of this last variety have been recorded by Godine,
Volpi, Rodet, D’Arboval, and Delafond in France; and by Sewall, Dick,
Smith, Hallen and Gloag in Britain. In connection with this last class
of cases it must be noted that dilatation of the right cavities of the
heart sometimes gives rise to very similar symptoms, and that the signs
of chronic bronchitis are often scarcely distinguishable from those of
broken wind. In catarrhal bronchitis too, after the air tubes have been
washed, it is sometimes impossible to decide whether the lining membrane
has been the subject of inflammation or not.
_Symptoms._ The most prominent are the double lift of the flank with
each expiratory act, in the absence of fever, the short, weak, dry and
almost inaudible cough, the wheezing noise in breathing when that is
accelerated by exertion, and the intestinal flatulence with the frequent
passage of gas.
The =cough= usually heralds the advent of other symptoms. Often the
character of the cough draws forth the remark that an animal is becoming
broken winded and though no other symptom is seen at this time they
thereafter rapidly develop themselves. At this early stage of the
disease the cough is paroxysmal, coming on in fits during work or after
a drink of cold water. Once the disease is established the horse rarely
coughs more than once at a time. The cough is extremely short, weak and
low and followed by a sort of wheeze. So specific is it that if once
heard it can readily be recognized. The sudden effort made in coughing
usually leads to the expulsion of gas from the flatulent bowels.
The =double lifting of the flank= in expiration is not peculiar to
broken wind. It is seen as well in most diseases of the lungs and even
of other organs (enteritis, peritonitis) which interfere with the
freedom of the respiratory act. If however it is not attended by fever
but associated with the broken winded cough, the wheezing respiration,
the disordered and flatulent state of the bowels, the tumultuous beating
of the heart against the left side after exertion, and the slight flow
of clear, watery matter from the nose, it is pathognomonic. The act of
inspiration is quick and free, that of expiration is not uniform and
continuous as in health, but consists of two stages interrupted by a
momentary arrest. In the first stage the posterior part of the abdomen
is slightly raised and it falls in laterally; then comes an almost
imperceptible period of inaction, followed at once by the further
lifting of the flanks to complete the expulsion of air from the lungs.
The first stage seems the natural collapse of the walls of the chest and
forward movement of the diaphragm, the second a contraction of the
abdominal muscles partly due to an exercise of will to overcome the
obstacle to the expulsion of air.
In very bad or advanced cases these symptoms are more marked. The
inspiration is sudden and manifested by a rapid expansion of the chest,
and dropping of the belly previously supported by active contraction of
the abdominal muscles. The two stages of the expiratory act are quite
distinct. The first is manifested by a sudden falling in of the walls of
the chest so that the ribs no longer stand out prominently beyond their
interspaces; the abdomen equally rises inferiorly and falls in laterally
so that a projecting ridge is formed from the lower end of the last rib
to the point of the hip. This is specially marked during the period of
inaction, and this is succeeded by the second effort quick and almost
convulsive. These movements are so extensive that they are conveyed in a
striking degree to any vehicle to which the animal is attached,
especially if it has only two wheels, and a rider on horseback feels the
movement still more disagreeably. When a horse is in this state the
alternate rising and falling of the abdominal organs imparts a
synchronous movement of protrusion and contraction to the anus and in
thin subjects a rising and falling of the muscles on each side of the
root of the tail. The nostrils too are kept constantly dilated.
There is a _nasal discharge_, but this is very inconsiderable in the
early stages of the malady. It is a clear watery or slightly grayish
albuminous material without any visible admixture of pus globules, and
on drying it leaves a scarcely perceptible crust. At first it appears
intermittently and in minute quantities, but in bad cases it becomes
almost constant, and is especially profuse after exercise.
=Abnormal respiratory sounds= are marked symptoms in the advanced
stages. The wheezing noise of the breathing, especially when that is
excited by exertion, may be heard at a short distance from the animal.
The increased resonance on percussion along the lower border of the lung
is only heard when the emphysema is extensive. The dry sibilant or
whistling râle heard over the same parts is equally a symptom of the
advanced stages. When there is much discharge a moist rattle is often
heard over the lower end of the windpipe or immediately behind the
middle of the shoulder. The overlaying of the anterior lobe by the
thick, muscular shoulder, and the complication of results obtained at
the free border of the lung by the abdominal noises and resonance render
these results less conclusive in the earlier stages and slighter cases.
The application of the hand to the side of the chest behind the left
elbow may detect a strong impulse of the heart with each beat. If the
patient is actively exercised for some time this may be felt on the
right side as well. This symptom indicates the existence of dilatation
of the right cavities of the heart.
The symptoms of =indigestion= are also very manifest. The dung passed is
like so much chopped hay and oats, and does not at all resemble the
fæces of a healthy horse. The abdomen is tumid, tense and filled with
flatus, which is frequently passed _per-ano_, and has no doubt given
rise to the name of =broken wind=. This expulsion of gas from the rectum
usually takes place whenever the animal is excited to cough. When first
started on a journey, the frequent passage of wind and dung for the
first mile or two is one of the most disagreeable features of the
disease. When the animal has thus _emptied himself_ he usually goes much
better for the remainder of the journey.
Broken-winded horses are always greedy feeders, and if they get little
work they manage to maintain their flesh. But they are soft and flabby,
and if put to active work they fall off rapidly, becoming emaciated and
hidebound, a true indication of their impaired digestion.
The symptoms are liable to occasional aggravation. If the stomach and
bowels are overloaded they are invariably so. If the patient is kept in
a hot, close stable, the same result follows. Thick, muggy weather has
the same effect. After a more than usually severe day’s work all the
symptoms may be intensified, and this may continue for several days or a
week. Bouley attributes this to an extensive rupture of air cells and a
sudden increase of emphysema, and the gradual subsidence of the symptoms
to the partial absorption of the displaced air and the accommodation of
the lung to its new condition.
Light and laxative diet on the other hand alleviates the symptoms and a
broken winded horse usually improves at grass.
_Course._ The general tendency of broken wind is to persistent
aggravation, but by a judicious regimen many cases may be checked in
their progress and greatly relieved, or even cured.
_Treatment._ We have already seen that broken wind is virtually unknown
on natural pastures where the grass is short, green and succulent.
Turning out on such pastures will improve or even temporarily cure mild
cases. The same may be said of the laxative systems of diet. (See that
recommended for _chronic bronchitis_). Feeding on dry grain only, with a
very limited supply of water, will enable many broken winded horses to
do ordinary work with comparative ease and comfort. In such cases,
however, improvement is only due to the empty and unclogged condition of
the digestive organs and the symptoms return with all their former
intensity when the original diet is restored. By way of palliation much
may be secured by avoiding accidental causes of aggravation. If catarrh
or bronchitis has supervened it should be treated in the ordinary way.
If the stomach and bowels are overloaded and costive, a small dose of
aloes and enemata will relieve. If the stable is close a free admission
of air will be beneficial. The temporary excitement in these cases may
be further alleviated by sedatives, of which opium and digitalis have
been mostly employed. The last agent will sometimes control the
breathing to such an extent that the horse may be thought to have
completely recovered. Professor Dick believed that he had effected a
cure in one case by the administration at a single dose of a drachm each
of camphor, opium, calomel and digitalis. Temporary results only can,
however, be expected from such agents, except in the case of an
aggravation due to a cause acting for a limited time only, in which case
the partial improvement may be lasting.
By adopting such measures to check accidental complications and
confining the animal to a rigid system of diet a broken winded horse may
be worked with comfort to himself and his master. The aliment should be
principally or exclusively of oats, bran or barley, though good
succulent grass, turnips, carrots, beet, and potatoes may be allowed, as
may also wheat or oat straw in limited quantity, but no hay and above
all none prepared from red clover, alfalfa, sainfoin, or allied foreign
plants and none that is musty or otherwise injured by keeping. No food
nor water must be allowed for one or two hours before going to work, and
the pace must be slow at first and gradually increased as the horse
empties himself, and the breathing gets less embarrassed. If meadow hay,
straw or other bulky food is allowed in small quantity this must be
after the horse has returned from his day’s work.
If the food above recommended is boiled or pulped, and mixed with some
saccharine agent as molasses its restorative action is enhanced.
If, however, we add to these hygienic and dietetic measures a prolonged
course of arsenic, the symptoms generally disappear. From five to
fifteen grains of arsenic made into a powder with a drachm of
bicarbonate of soda may be given daily in the food until improvement is
noticed or symptoms of the poisonous action of the agent appear. When
these are manifested in loss of appetite, colicy pains or red and watery
eyes the medicine must be suspended and begun again some days later in
smaller doses.
The therapeutic value of arsenic in this case is probably largely due to
its action on the nervous system, which has long been recognized. As
early as the first century of the Christian Era, Dioscorides,
recommended its use in asthma and in recent times it has acquired a
considerable reputation for the treatment of neuralgia. Another—though
perhaps an allied—physiological action of arsenic no doubt adds to its
value in this equine disorder. This is its power of retarding the waste
of tissues. This property it possesses in common with tea, coffee and
some other agents, but to a greater degree. This has led to its
extensive employment by the peasants in Lower Austria, Styria, and the
mountains separating Austria from Hungary, who found that it improved
their personal appearance, increased their weight and enabled them to
sustain greater exertions in climbing without fatigue. It was the
revelations of Dr. Tschudi concerning the Styrian arsenic eaters that
first led Professor Bouley to try this agent in broken wind.
=Examination of Broken-winded Horses.= Though the symptoms enumerated
above are sufficient to detect broken wind in all ordinary cases, yet it
may not be time thrown away to caution the reader against pronouncing it
absent when the more prominent symptoms are not seen. Unscrupulous
dealers do not hesitate to avail of a variety of devices to conceal the
symptoms and make the animal pass for a sound horse. Digitalis and other
sedatives are so employed, but are mostly rejected because they render
the horse dull and sluggish. By some the bowels are unloaded by a dose
of physic, the horse is kept on a spare diet of oats, beans and other
grain, water is withheld, and on the morning of sale one or two pounds
of leaden shot or of bacon fat are administered. The inconvenience
attendant on the presence of these agents in the stomach makes the
animal desist as much as possible from moving the abdominal organs, and
the double lifting of the flank is thus more or less completely hidden.
With the veterinarian however this measure like the last defeats its own
purpose, for such horses are always intolerably thirsty and if allowed
to regale themselves at the nearest watering trough, the charm is
broken, the double lift returns and with it all the symptoms of the
malady.
A brutal practice existed among ancient farriers, of making an
artificial opening into the rectum to allow the exit of the flatus upon
which they conceived the disease to depend. This was effected either by
cutting through the sphinctor ani with a knife or by making a new
opening to one side of it with a red hot iron. According to Ferguson
this has been improved upon by the modern Irish jockey, in the case of
broken winded mares. With the knife an artificial communication is made
between the rectum and the vagina, of sufficient size to insure that it
will remain open and large enough to allow pellets of dung to pass into
the vagina. The double lifting of the flank forces the fæces through
this artificial opening, and to avoid the inconvenience of their
presence in the vagina the animal carefully refrains from this action.
This orifice further allows the free escape of any gases generated in
the rectum and thus materially relieves the flatulence. Ferguson says he
has seen broken winded mares that have been operated on in this manner,
that breathed so freely that even professional men have failed to detect
the affection.
In all cases of broken wind, no matter how masked there will be
manifest, on slight exertion, a permanent dilatation of the
nostrils—_i.e._, alike in inspiration and expiration,—and when any such
suspicious symptom is seen the horse should be carefully examined,
especially the state of his lungs as ascertained by auscultation and
percussion, his breathing after he has freely partaken of water and hay,
and, if there is suspicion of drugging, after he has stood over night in
a hot stable plentifully supplied with both hay and water.
It should be borne in mind that mares advanced in pregnancy often show
no double action of the flank though decidedly broken winded.
POLYPUS OF THE BRONCHIAL TUBES.
Like other mucous membranes, that covering the bronchial tubes, is
liable to diseased growths, which may each remain attached by a broad
base, and form a morbid elevation of the surface, or it may become
loosened and retain its connection with the mucous membrane only by a
neck or pedicle. An interesting case of the latter variety is recorded
in the _Edinburgh Veterinary Review_ for January, 1864, by Mr. Parker of
Birmingham. It was attached to the wall of the right bronchus about an
inch below the bifurcation of the trachea, and had an ovoid form
measuring 8½ inches in its longest circumference by 4½ in its shorter.
The pedicle was 1½ inch long and allowed the tumor to pass freely upward
into the lower part of the windpipe, threatening instant suffocation. It
had a fibrous structure and was continuous with the interlacing bundles
of yellow elastic tissues which cover the cartilaginous rings of the
bronchus.
From its frequent displacement upward the tumor gave rise to paroxysms
of hurried and difficult breathing apparently threatening suffocation,
but when these passed off, respiration was tolerably tranquil and easy.
The fits of dyspnœa came on after any unwonted excitement, but above all
after a cough. In such cases the tumor had been coughed up into the
lower end of the windpipe and until it slid back into its former
position, the animal seemed on the very verge of death. The paroxysms
had appeared very frequently during a period of five months that had
elapsed since her purchase, increasing steadily in severity and finally
causing death. The lungs contained many small abscesses the result
doubtless of the frequent paroxysms of dyspnœa.
Cases of this kind are not usually amenable to treatment, nevertheless
as they are pretty certain to end fatally if neglected, it would be
quite permissible to perform tracheotomy in the lower part of the neck
and attempt to snare the tumor with an elastic wire passed through a
single or double tube. The tumor might even be seized by a vulsella and
twisted off, provided it could be reached.
DISEASES OF THE BRONCHIAL AND MESENTERIC GLANDS.
These are the seat of congestions, neoplasms, and parasites, including
pentastoma, actinomycosis, tubercle, glanders, etc., which will be
treated under their respective headings.
PARASITES OF THE AIR PASSAGES, LUNGS, AND PLEURA.
Nearly all the domestic animals are subject to parasites of the lower
air passages. These give rise to verminous bronchitis in cattle, sheep,
horses, swine, goats and camels, to gapes in birds, and to pulmonary
acariasis in fowls. The lungs and pleura are invaded by distomum,
echinococcus, cysticercus, aspergillus, etc. (See parasites).
DISEASES OF THE HEART AND ORGANS OF CIRCULATION.
Susceptibility in different genera. Reasons for partial immunity of
the quadruped, special and general causes in quadrupeds, violent,
forced work, fatty degeneration, swallowing of pointed metallic
bodies, difficult diagnosis in the animal. Position of the heart in
the horse, ox, sheep, pig, carnivora, birds. Structure of the heart as
a pump. Results of imperfect structure or action. Heart walls. Table
of size of the heart. Capacity. Weight. Pulse in each healthy genus,
according to age, size, environment, temperament, proximity to
parturition. Morbid conditions of the pulse, frequent, slow, quick,
tardy, full, strong, weak, feeble, indistinct, small, hard, wiry,
thready, oppressed, leaping and receding, intermittent, unequal,
irregular, anæmic, venous. Percussion. Palpitation. Auscultation.
Healthy sounds. Morbid sounds, in unusual place, force, intensity,
rythm, repetition of 1st sound, of 2nd sound. Murmurs, synchronance
with given stages of heart movement, their significance, pericardial
murmur. General symptoms of heart disease, cold extremities, passive
congestions, dropsies of limbs, etc., shortness of breath, venous
pulse, vertigo, dulness, sluggishness, corpulence.
The lower animals are perhaps less subject to heart disease than
mankind, but the comparative immunity generally assumed for them is far
from being a real one. The horizontal position of the quadruped largely
obviates that special tax upon the heart demanded by the erect position
of man, and especially by the elevated place given to his more ample and
vascular brain. Animals too are comparatively free from those mental and
moral influences which so largely affect the regularity of the
circulation in the human subject. But on the other hand many physical
causes of heart disease affect the lower creation equally with their
lord, while some undoubtedly operate with special force on the brute.
All animals are subject to diseases of the heart as of other internal
organs, from exposure; this organ is occasionally involved from its
contiguity with other diseased structures or from interdependence of
function as we have already seen in certain diseases of the lungs
(congestion, broken wind, etc.); the tendency to heart disease
frequently runs in a particular family of animals, especially with the
rheumatic constitution, which is transmitted from parent to offspring as
surely as the color of the skin the turn of the horn or the depth and
spring of the rib. The lower animals are further subject to congenital
malformations and imperfections and to deposits of morbid material
around the heart or in its substance so as to impair its healthy action.
Horses and dogs have special predisposing causes in the violent and
prolonged exertion to which they are habitually exposed. The quiet
sluggish and nonexcitable ox and pig meet with dangers no less real
though of a different kind in the overfeeding which induces fatty
degeneration of the heart as of other muscular tissues. The larger
ruminants are further endangered by their propensity to swallow needles
and other sharp pointed bodies which ultimately reach and penetrate the
heart.
The prevalence of heart disease in animals may be deduced from the fact
that out of 150 horses, oxen and dogs dissected at Montfauçon by Leblanc
in 1840, not less than one twentieth presented cardiac lesions. The
supposition of an immunity of the lower animals has been largely due to
the heavy muscular shoulder of quadrupeds which covers the upper and
anterior regions of the heart shutting them out from physical
exploration. In man the entire heart and connecting blood vessels are so
open to examination that the physician can pronounce with the greatest
accuracy not only concerning the existence of disease, but also its
precise locality and nature. In the quadruped no such facility is open
to us, and veterinarians have too generally refused to face the
difficulty, preferring to ignore heart diseases, or still worse seeking
to cover their ignorance by the assertion that such affections rarely
exist. Now however we not only know that heart diseases are much more
frequent in the lower animals than heretofore believed, but that as a
general rule they are sufficiently manifested and recognizable by their
distinctive symptoms.
=Position and exposure of the heart.= In the horse the heart has only
its apex and a small portion of its left ventricle approached to the
surface of the chest, at a point where it is felt to beat behind the
left elbow. The apex approaches the surface in the interval between the
fifth and sixth ribs and close above the breast bone. The posterior
border of the ventricle follows a nearly vertical line upwards from this
point, while the anterior border has a direction upward and forward
crossing diagonally over the fifth rib. The part of the ventricle
exposed extends about three inches upwards from the apex, and is about
two inches in its transverse diameter. The great mass of the organ is
covered by lung substance.
In the =ox= about the same extent of heart tissue is exposed. In =sheep=
a portion about an inch in height and one and a half inches in breadth
is left uncovered by lung. In the =pig= the heart is exposed only in a
triangular space of about an inch across.
In the =carnivora= the heart lies more directly in the median line of
the chest. It appears as if tilted forward so that its apex is directed
backward and its base forward, while the body of the organ lies directly
over the breast bone. The lungs invest it on both sides preventing any
approximation to the walls of the chest laterally, and it can best be
auscultated by applying the ear over the sternum.
In =birds= the heart is situated in the centre of the chest and
enveloped by lung tissue so that its exploration is about equally
difficult at all points.
The larger blood vessels at their origin from the heart are not open to
examination in the lower animals except to a limited extent in the dog.
=Internal arrangement and structure of the heart.= In all warm blooded
animals the heart is composed of two portions, the internal cavities of
which are perfectly distinct from each other and contain blood in
different conditions; the right portion holding the impure, purple or
venous blood which has just circulated through the body, and the left
portion being filled with the bright crimson or arterial blood, which
has been ærated by circulating through the lungs. Each of these portions
is divided into two distinct cavities, an _upper_ (auricle) which
receives the blood from the veins, and a _lower_ (ventricle) which
receives the blood from the auricle and transmits it into the arteries.
The auricle is separated from the ventricle by a transverse
musculo-membranous partition having a large central orifice furnished
with valves (auriculo-ventricular), the free borders of which are turned
downward so that they allow the blood to flow freely downward from the
auricle but completely close the orifice and prevent any reflex when the
ventricle contracts. The great artery which originates from the base of
each ventricle is likewise furnished with a system of valves (semilunar)
having their free borders turned into the artery, so that they allow
blood to flow freely into that vessel during the contraction of the
ventricle, but prevent any reflux into the heart when the ventricle
again dilates. The apparatus may be likened to a force pump with two
systems of valves, one to prevent the return of any water from the pump
into the fountain; the other to hinder any reflux from the delivery pipe
into the pump. Any interference with either of these valves entails a
very serious and usually a fatal disorder of function.
These _orifices_ differ considerably in size. Those between the auricles
and ventricles are considerably larger than those at the commencements
of the great arteries. Those on the right side of the heart too are
greater than those on the left. They vary with the form of the heart.
Thus in dilatation of an auricle and ventricle on one side of the heart,
the auriculo-ventricular opening becomes equally widened and the valves
remaining disproportionately small the blood is allowed to rush back
into the auricle during ventricular contraction. The left
auriculo-ventricular opening has been known to become contracted in some
very flat and shallow chests; the blood failing to circulate freely
through the lungs and to reach the left side of the heart in a full
supply this orifice accommodates its size to the amount, and may become
so narrowed that it forms a serious obstacle to the blood flow and a
series of morbid changes result following the backward course of the
circulation. The auricle first becomes overdistended and its muscular
walls increase in thickness and consistency; the lungs tend next to
suffer from a passive congestion, and lastly the right side of the heart
becomes engorged and enlarged.
Any obstruction in the aorta which conveys the blood from the left side
of the heart equally leads to dilatation of its internal cavity and
abnormal thickness of its walls.
The imperfection of the valves is one of the most serious results of
such changes in heart structure. The sounds by which such imperfection
may be recognized will be presently noticed, meanwhile the mode of
testing this in the heart of the dead animal will be referred to. If due
to structural changes in the valves themselves, the new deposits, the
cicatrices, the lacerations, etc., will be visible to the eye. Though no
such disease-changes are seen the valves may still manifest imperfection
by failing to fulfill their normal function when put to the test. Water
is poured into one or other of the great arteries which arise from the
ventricles, the vessel being held vertically, and if it fails to descend
into the heart the valvular action is perfect. The auriculo-ventricular
valves may be equally tested by filling the ventricle and observing
whether there is a reflux into the auricle.
The =thickness of the walls of the heart= varies in disease. The
auricular walls are invariably thin and flaccid except as above noted
with diminution of the auriculo-ventricular orifice. The walls of the
right and left ventricles differ in thickness in accordance with the
distance to which they have respectively to propel the blood and the
propulsive effort demanded. Thus the walls of the _right ventricle_
which is only called upon to propel the blood through the lungs are only
about ½ an inch in thickness and are thinnest at their lower part. Those
of the _left ventricle_ which have to send the blood to the most distant
parts of the body are from 1 to 1½ inches except at the lower part where
they form the apex of the heart, and are reduced to a tenuity resembling
the walls of the auricles. They are thickest at the median part, and
diminish slightly in an upward or downward direction. The bulk of these
walls is excessively muscular, the fibres arranged as an elaborate
double spiral and connected with a layer of white fibrous tissue placed
in the interval between the auricles and ventricles and surrounding the
auriculo-ventricular openings and the orifices by which the great
arteries take their origin. It is at this point, where the muscular
fibres of the ventricles are connected with the white fibrous rings,
where rupture of the heart usually takes place.
The following measurements may be held to refer to medium sized animals
of the different kinds mentioned.
─────────┬──────────────┬───────────────────────────────┬──────────────
│ Longitudinal │ │
│ Diameter. │Transverse Diameter at the Base│Circumference.
│ Inches. │ of the Ventricles. │ Inches.
─────────┼──────────────┼────────────────┬──────────────┼──────────────
│ │Antero-Posterior│ Transverse │
│ │ Inches. │ Inches. │
─────────┼──────────────┼────────────────┼──────────────┼──────────────
Horse │ 10 │ 7½│ 5⅓│ 19½
Ox │ 9⅘│ 6⅘│ 4½│ 17½
Sheep │ 4 │ 3 │ 2 │ 7⅓
Pig │ 4½│ 3⅗│ 2⅓│ 9⅘
Dog │ 3⅘│ 3⅗│ 2 │ 8½
─────────┴──────────────┴────────────────┴──────────────┴──────────────
The =internal capacity of the ventricles= is so modified by the amount
of _post mortem_ contraction that it differs widely from the actual
capacity during life. The left ventricle of the larger domestic
quadrupeds usually admits from 3½ oz. to over 5 oz., while the right
ventricle whose walls are so much thinner and more lax will contain
double that amount. In the smaller animals about a tenth of these
quantities will be admitted.
=The weight of the heart= too can only be stated as an average or for
medium sized animals. In the _horse_ it may be from 4½ lbs. to 9 lbs.;
in the ox from 3 lbs. 5 oz. to 4½ lbs.; in the _sheep_ from 5½ oz. to 7
oz.; in the _pig_ from 9½ oz. to 14 oz.; and in the _dog_ from 5 oz. to
7 oz. This statement must be understood to apply to dogs approximating
in size to the shepherd’s.
Taking into account the size of the particular animal any considerable
deviation from these measurements and weights may be accepted as
abnormal. The ratio to the body weight is about:—horse and dog 1:100,
ox, sheep and pig 1:220. This necessarily varies with condition—fat or
lean.
The =pulse= offers valuable indications in disease of the heart.
The _number_ of the pulse in healthy full-grown animals may be set down
as follows per minute:—horse, 36 to 46; ox, 38 to 42 (with loaded paunch
or in a hot stable up to 70); sheep, goat and pig 70 to 80; dog 80 to
100; cat 120 to 140; goose 110; pigeon 136; chicken 140. In old age the
pulse is less frequent. This diminution may extend to 5 beats per minute
in the larger quadrupeds and to 20 or even 30 in the smaller. Youth and
small size again are associated with a greater rapidity of the pulse.
The pulse of the foal, at birth, is about three times that of the horse;
in the colt of six months it is double; at a year old about one and a
half times; and at two years old one and a quarter.
The smaller the animal, _caeteris paribus_, the more rapid is the pulse.
Hot buildings, exertion, fear or any other exciting cause likewise
accelerates it. It is more frequent with the nervous temperament, as for
example in the English race horse, or the greyhound, than in the dull
lymphatic cart horse or mastiff. In advanced pregnancy it is increased
in number. In the cow and mare it undergoes a monthly increase of four
or five beats per minute after the sixth month. (Delafond)
Independently of these conditions a rapid pulse indicates febrile
excitement attendant on active inflammatory or other disease, or a state
of weakness and debility. In this last condition the heart beats more
frequently to secure a more rapid circulation in the capillary blood
vessels, and thus make up to the craving tissues by frequency of
contact, what is wanting in the quantity and quality of the nutritive
fluid. This point cannot be too much insisted upon, as the fatal
doctrine that a rapid pulse indicates force of the circulation is very
misleading as to treatment.
The =force and character of the pulse= differ in the various species. In
the =horse= it is full, moderately tense and elastic. In the =ass= and
=mule= it is smaller and harder, with an inequality of force in
successive beats, and sometimes even a beat is suppressed or
imperceptible. In the =ox= the pulse is full, soft and regular,
appearing to roll forward beneath the fingers. In the =sheep= and =goat=
the pulse is small but with a peculiar quick or sharp beat. The =pig’s=
pulse is said to be firm and hard. That of the =dog= and =cat= is firm
and hard coming with a sharp impulse against the finger. In the dog,
however, successive beats are not always of the same force and an
intermission or complete absence of a beat is by no means an indication
of disease of the heart or other serious malady. It often attends the
slightest excitement in a perfectly healthy animal.
In disease the _pulsations_ may become:—=frequent= or increased in
number; =slow= or decreased in number; =quick= or striking with a sharp
impulse against the finger; =tardy= or without sharpness of stroke and
as if they rolled slowly past under the finger; =full= and =strong= when
the impulse is forcible and not easily compressed by the finger; =weak=,
=feeble= or =indistinct= in the opposite conditions; =small= when though
perfectly distinct and forcible they are wanting in fulness; =hard=,
when forcible and jarring (this is sometimes called =wiry= or, if
smaller, =thready=); =soft= when though the artery may be full the beat
is devoid of hardness and easily compressible so as to be unfelt;
=oppressed= when with a full rounded artery, the impulse is jerking
though not hard and as if the distended vessels opposed the transmission
of the impulse; =jerking and receding=—=leaping=, when with empty and
flaccid arteries the pulse seems to leap forward with each beat of the
heart—(this pulsation may be visible to the eye in the carotids);
=intermittent= when after a number of beats at regular intervals there
is a complete pause extending over that period of time which would have
been occupied by a full beat; =unequal= when some beats are strong and
others weak; =irregular= when without any distinct intermission for a
period equal to that of a single beat, the intervals between successive
beats are of varying length. The pulse further has a peculiar =thrill=
or =tremor= in states of great debility with deficiency of blood and
imperfect filling of the vessels.
Of these the =leaping=, the =intermittent=, the =unequal= and the
=irregular= pulses are of special importance in their bearing on heart
diseases.
The =jerking and receding= pulse is felt in cases of imperfection of the
semilunar valves at the commencement of the great aorta, and which
allows blood propelled into the arteries by the contraction of the
ventricle to flow back into the ventricle during its state of
relaxation. This pulse is met with in other conditions as in aneurism of
the aorta, but if from heart disease it is distinguished by the presence
of a _blowing murmur_ with the second sound of the heart.
The =intermittent= pulse indicates functional derangement of the heart
but it does not as is generally believed betoken structural disease. It
is frequently observed in healthy asses and mules, and in dogs however
slightly excited whether by fear or joy, or by the mere fact of their
being handled, it is so common as to be almost the rule rather than the
exception. It may be seen in a healthy horse as the result of
excitement. During the early stages of convalescence from inflammatory
affections of the lungs in the horse the pulse is often intermittent.
The pulsations are at the same time unequal. There is a regular cycle of
beats gradually decreasing in force and extending over a complete
respiratory act. The cycle commences with the strongest beat during or
immediately after the act of expiration, and the succeeding four or five
beats are less and less forcible until the chest is fully expanded when
there is a quiescent interval corresponding to the period of one beat.
In many such cases there is no other indication of heart disease and the
phenomenon appears due to the interference with the circulation by the
hepatized lung, to the impaired nervous energy of the heart and to its
compression between the distended lungs. A pulse simply _intermittent_
and not associated with any further sign of heart disease does not then
possess the significance generally attributed to it, but a careful
examination of the heart should invariably be made when this functional
disorder is observed. It exists or may be brought about by slight
excitement in the great majority of heart diseases.
In case of intermittent pulse it is useful to ascertain whether there is
also an intermission of the heart’s beat, since in softening of the
heart, that organ may beat without being able to transmit the impulse
along the artery.
A pulse at once =unequal and irregular= is a much more serious
indication than a merely intermittent pulse. It is observed especially
in fatty degeneration of the muscular substance, and with imperfection
of the valves on the left side of the organ, though it may be present in
other cardiac diseases independent of the existence of those lesions.
In _hypertrophy of the left ventricle_, the pulse is full and strong and
the impulse appears prolonged, because of the greater length of time
taken up by the ventricle in the act of contraction. When _dilatation_
coexists with _hypertrophy_ the impulse is still full and strong, more
blood being transmitted through the vessel; but when _dilatation_ is
combined with _attenuation_ of the ventricular walls the impulse is soft
and weak by reason of the feebleness of the contractions.
The pulse at the radial artery should be about synchronous with the beat
of the heart. If retarded it may be held to indicate the existence on
the anterior aorta or its primary divisions of an aneurism with elastic
walls or more probably an imperfection of the aortic valves, which
allows a regurgitation of the blood into the heart.
=Venous pulse.= A venous pulse seen in the lower end of the jugular
veins is common in the domestic animals. In the ox it is quite
compatible with health and is only to be judged by its amplitude and
force. In other animals it often coexists with congestion of the lungs
which impedes the circulation through the right side of the heart and
leads to engorgement of the venous system. In the absence of this
condition it frequently indicates an imperfection of the
auriculo-ventricular valves in the right heart and a reflux of blood
from the contracting ventricle which checks the descending current in
the veins.
=Percussion.= In the =horse= a dull, dead sound is emitted when
percussion is made over the left side for about four inches above the
breast bone and in the space corresponding to the lower ends and the
cartilages of prolongation of the fourth, fifth and sixth ribs. In the
ox this dulness is less marked on the level of the sixth rib. The same
results can be obtained on the right side by imparting heavier blows to
the chest walls so as to derive the sound from the deeper parts.
The area of dulness is _increased_ in cases of _hypertrophy_ or in
_dilatation_ of the heart when the enlarged organ presses aside the lung
tissue and exposes a greater amount of its substance to the chest walls.
The same result takes place in hydropericardium.
The area of dullness is _diminished_ in cases of ruptured air cells (as
in “heaves”) when the inflated and expanded lung tissue envelopes the
heart more completely and gives out its own clear resonance where the
dull sound of the heart is usually obtained.
=Application of the hand.= =Palpation.= In conditions of health and in
quietude the hand applied on the side of the chest, close behind the
left elbow only just perceives the beat of the heart with each
contraction. If the animal is excited whether from fear, joy or physical
suffering the heart’s impulse becomes more powerful and by this alone
the state of its function may be very satisfactorily ascertained. The
impulse is strong in all active fevers and extensive inflammations of
important organs, but it is especially marked in diseases of the heart
and lungs. Irregularity in the force of successive beats is seen in
various heart diseases and debilitated conditions are recognized in the
same way.
Any want of harmony between the heart’s action and the pulse may be
observed by laying the right hand over the region of the heart and
applying the fingers of the left on the radial artery. In debility and
especially if from a deficiency of blood the violent or tumultuous
action of the heart contrasts strangely with the weak jerking and
compressible pulse. The same symptoms are noticed when the valves of the
heart close their orifices imperfectly. In convalescence from lung
diseases and in certain diseases of the heart a beat may be felt by the
right hand for which no corresponding pulsation is felt in the radial
artery by the left.
When the heart is hypertrophied the impulse is stronger and is
associated with a full, strong, and rolling pulse. When it is atrophied
the impulse on the chest and pulse beat are equally weak. When water
exists in the pericardium the heart strikes the ribs with less force.
=Sounds of the Heart.= Synchronous with each beat of the heart two
distinct sounds are heard, separated by a short interval, inappreciable
to most ears, and followed by a period of silence. These sounds are
distinct alike in character and duration. The _first sound_ is dull and
prolonged; the _second_ is short and quick. Some idea of these sounds
may be formed by the pronunciation of the two syllables, _lub_—_tip_,
but an acquaintance with the sounds themselves is essential to a correct
conception of them. The period of time occupied by the first sound is
double that taken up by the second and in man and the smaller quadrupeds
the subsequent period of silence is of equal duration with the second
sound. Dividing the time belonging to one revolution of the heart into
four equal periods the first two are taken up by the first sound, the
third by the second sound and the fourth by the interval of silence. In
the horse the silence is more prolonged, and occupies the entire latter
half of the period of a revolution. The relations stand thus:—the first
sound extends over two-sixths of the time, the second sound over
one-sixth, and the silence over three-sixths.
The _first sound_, synchronous with the beat of the heart against the
ribs corresponds also in point of time with the contraction of the
ventricles, the closure and tension of the auriculo-ventricular valves
and the rush of the blood into the great arteries. The second sound
corresponds to the reflux of blood in the arteries and the closure of
the valves between them and the heart. The period of silence represents
the period of rest during which the heart is being filled from the
veins.
In the horse, at rest, the first is the only sound that can be
distinctly heard in many cases, but during the excitement of exercise,
or in febrile conditions the second is sufficiently apparent and any
deviation from the natural character is easily noted.
These sounds are most distinct over the lower end of the fifth and sixth
ribs on the left side, but they may be heard distinctly behind the
middle of the shoulder on either side when the corresponding limb is
advanced. In birds they may be heard beneath the wings but above all and
most clearly over the breastbone.
In =disease= these =sounds= may be heard in unusual situations, they may
be altered in force duration or rythm, or they may be associated with
other sounds or superseded by them.
The sounds may be heard in new situations, in displacements of the heart
from tumors or effusions in the chest, structural changes in the lungs,
pleuræ, or pericardium, aneurism of the aorta, etc., etc.
The heart sounds are clearly heard over any part of the chest when the
lung tissue intervening between that part of the surface and the heart
is solid (hepatized). They are heard distinctly behind the median part
of the right shoulder, when liquid effusion into the left pleural sac
has displaced the heart to the right; and when the right cavities of the
heart are extensively dilated as exists so commonly in the advanced
stages of “_heaves_.”
The =extent= over which the sounds may be heard is _increased_ when the
lung surrounding the heart is solidified (hepatisation, splenisation,
etc.), or when liquid effusion exists in the chest. A liquid but more
especially a solid is a better conductor of sound than the spongy lung.
Enlargement (hypertrophy) of the heart equally increases the area of
sound. The _area_ of sound is lessened by atrophy of the heart, and by
an emphysematous condition of the lungs by which the heart is more
extensively covered and further separated from the walls of the chest.
The =force= or =intensity= of the heart sounds is increased in high
fever, in acute inflammation, in increase of the muscular walls of the
heart with enlargement of the internal cavities, in functional
disturbance from fear or other exciting cause, and in palpitation. Often
in a weak and bloodless patient the heart sounds can be clearly heard at
several yards distance from the animal. The _intensity_ of the sounds is
diminished in debility when not associated with palpitation, in atrophy
of the muscular substance of the heart, in hypertrophy of the muscular
tissue of the heart with diminution of its internal cavities, in _broken
wind_ when the emphysematous lung more completely envelopes the heart,
and in cases of extensive liquid effusion into the pericardium which
prevents the apex of the heart from striking against the side of the
chest.
The regular =rythm=, normally manifested by the two sounds and the
silence, may be modified in the unequal irregular or intermittent
contractions of the heart. Küssmaul’s paradoxical pulse is one in which
the pulse is more frequent but less full during inspiration than
expiration. Seen in weak heart, during recovery from chest diseases, in
chronic pericarditis, and when fibrous bands encircle the root of the
aorta. Bigeminal and trigeminal when two or three beats follow each
other rapidly, and are separated from the preceding and succeeding beats
by longer intervals. This occurs in disease of the mitral valve, and in
other weak states of the heart. Fœtal heart rythm in which the pause is
shortened and the two sounds of the heart are almost identical, is seen
in the later stages of fevers, and in extreme dilation. A curious
aberration of rythm is the _repetition_ of either the first or second
sound. If of the first sound (anapestic bruit) each beat will be
accompanied by three sounds the first two of which resemble the first
sound of health. If the second sound is repeated (dactylic bruit, bruit
de galop) the first sound only will be prolonged and the last two sharp
and quick. The repetition of the last sound is probably due to impaired
nervous supply which allows the completion of the contraction of the
ventricle and the closure of the arterial (semilunar) valves sooner on
one side than the other. If due to diminution of the arterial orifice
which retarded the emptying of one of the ventricles, the first sound
would probably be accompanied by a blowing murmur. If the
auriculo-ventricular valves on one side were imperfect, allowing a
reflux into the auricle and a more rapid emptying of the ventricle a
blowing murmur would equally accompany the first sound. In either of
these two last mentioned cases the murmur would mask or hide the first
of two doubled sounds.
The repetition of the 1st sound is often due to dilatation of one
ventricle, which in consequence is longer in reaching the same sensation
of plenitude, and in receiving the stimulus to contraction.
=Morbid Sounds.= =Murmurs.= The distinct and superadded sounds heard in
disease are usually designated murmurs. They originate in the interior
of the heart (endocardial) or externally to the heart (pericardial). The
=endocardial= sounds mostly arise from some abnormal conditions of the
valves or orifices and consist in a blowing or rushing noise which
usually accompanies or displaces one of the heart sounds, though it may
precede or succeed these. The following table modified from that of
Bartle and Roger presents at a glance the relations of these different
sounds and their significance.
Blowing or Hissing Murmurs.
Blowing murmur before │Narrowing of the auriculo-ventricular orifice.
the first sound. │ Vegetations or coagula on the valves.
│Strongest toward the │
Blowing murmur with the│ base of the heart. │Narrowing of the aortic
first sound. │ Propagated along the │ opening.
│ great arteries. │
│Strongest toward the │Narrowing of the
│ apex of the heart. │ pulmonary artery or
│ Not propagated in the│ insufficiency of the
│ great arteries. │ auriculo-ventricular
│ │ valves.
│Double rushing sound │Insufficiency of the
Blowing murmur with the│ heard over the great │ arterial (semilunar)
second sound. │ arteries at each beat│ valves.
│ of the heart. │
│Double rushing sound in│
Blowing murmur after │ the arteries with │Aneurism (dilatation of
the second sound. │ each beat of the │ the great aorta.)
│ heart. │
From the table it will be seen that each orifice in the heart may become
the seat of two perfectly distinct and independent murmurs; one due to
constriction of the orifice in which case the sound is produced with the
onward progress of the blood wave; and one due to dilatation of the
orifice or insufficient closure of it by the valves, when the sound is
due to a recoil or regurgitation of the blood. There is a further sound
due to mere roughness of the valves in cases of disease when the sound
will be with the normal current of blood, though a second or regurgitant
hiss is often heard from the valves being at the same time insufficient
to close the orifice. Another blowing murmur is usually heard over the
heart and coincident with its first sound in the bloodless state
(anæmia). This is not necessarily connected with any diseased condition
of the heart itself.
The nature of these murmurs differs in special instances. They may
resemble the soft whisper of the words _who_ or _awe_, of the double
letter _ss_, or the single letter _r_, according as they are soft or
hard and purring.
The =pericardial murmur=, caused by the rubbing of the dry roughened
surface of the serous membrane covering the heart on the correspondingly
dry rough surface of the same membrane, reflected on the investing sac,
resembles that caused by passing the palm of the one hand over the other
which lies on the ear. It is distinguished from the friction sound of
pleurisy by its coinciding with the movements of the heart and not with
those of respiration. It is usually heard alike during the sounds of the
heart and during the period of silence or in other words during the
movements of contraction and dilatation in that organ.
=General Symptoms of Heart disease.= In the acute inflammatory
affections there are the signs of general constitutional disturbance
attending similar affections in other organs. The decision as to the
true nature of the disease must be arrived at from the special character
of the pulse, heart sounds, etc. as already noticed.
In the chronic forms of the disease however a particular class of
symptoms usually point towards the organ affected. In cattle, sheep and
pigs raised only for slaughter, and as far as possible protected against
active exertion, serious heart diseases may exist for a length of time
without making themselves manifest by any prominent symptoms. Thus in
cows, pins and other sharp pointed bodies swallowed with the food
frequently make their way to the heart and lodge for a length of time in
its vicinity without material derangement and when at last the animal
dies a sudden death they are found transfixing the walls of that organ.
In the horse or other animal subjected to exertion the symptoms are
usually very patent.
When the heart is enlarged the pulse strong and the circulation full and
free, apoplexies or hemorrhages especially on the brain or other soft
organs where the resistance is least, are liable to occur. When on the
other hand the circulation is weak from atrophy or fatty degeneration of
the heart, or from insufficiency of the valves there is a tendency to
coldness of the extremities, and to passive congestions with their
consequences:—serous effusions, dropsies, and difficult breathing. The
imperfect supply of blood to the muscles of the extremities sometimes
brings about an unsteadiness of gait in the hind limbs when the animal
is trotted for a short distance and sometimes cramps supervene.
Continued coldness of the limbs, and a filling or thickening first of
the hind limbs then of the fore and lastly of the chest and belly and of
the skin beneath their dependent parts are useful indications.
Shortness of breath and inability to proceed when trotted or galloped on
hard ground or when walked up hill, the animal being in fair condition,
without fever or cough, but subject to cold extremities and a venous
pulse in the jugulars, almost certainly indicates insufficiency of the
auriculo-ventricular valves on the right side of the heart.
Vertigo megrims or giddiness may be caused by heart disease. The horse
without having sustained any pressure on the veins of the neck by the
collar, and having had no previous symptom of brain disease suddenly
reels in harness and perhaps falls. There are the cold and engorged
limbs or a tendency to their engorgement as in the former case. The
attacks recur, when the horse is put to the same exertion, and he proves
utterly worthless. In such cases a careful examination of the pulse and
heart sounds will complete the chain of evidence.
An almost constant feature of chronic heart disease is a condition of
dulness, sluggishness, and in many cases, curiously enough, a tendency
to lay on fat, so that although the patient is unfit to work, he appears
to enjoy excellent general health to which a period is only put by
sudden death.
Affections of the heart are primarily divisible into _functional_ and
_structural_ disorders.
PALPITATIONS.
Convulsive contraction of the heart, functional or structural
diagnostic features of these. Significance of the functional disorder,
genera most liable. Treatment, quiet, heart tonic, digitalis, correct
other disorders.
These consist in a sudden violent and convulsive beating of the heart,
not connected with any appreciable structural disease. They differ
chiefly from the palpitations of organic disease of the heart in the
absence of any apparent local change to account for their occurrence.
The following table from Bellingham furnishes a number of criteria
equally valuable in the lower animals as in man.
PALPITATION DEPENDENT ON ORGANIC │PALPITATION INDEPENDENT OF ORGANIC
DISEASE OF THE HEART. │ DISEASE OF THE HEART.
│
1. Palpitation usually comes on │1. Palpitation usually sets in
slowly and gradually. │ suddenly.
2. Palpitation constant, though │2. Palpitation not constant, having
more marked at one period than at│ perfect intermissions.
another. │
3. Impulse of the heart usually │3. Impulse neither heaving nor
stronger than natural, sometimes │ prolonged; often abrupt knocking
remarkably increased heaving and │ and circumscribed, and
prolonged; at others irregular │ accompanied by a fluttering
and unequal. │ sensation (visible jerking or
│ lifting) in the precordial region
│ or epigastrium (flank and
│ abdomen).
4. Palpitation often accompanied by│4. Auscultatory signs of diseased
the auscultatory signs of │ valves absent; bellows sound
diseased valves. │ often present in the large
│ arteries and a continuous murmur
│ in the veins.
5. Rythm of the heart regular, │5. Rythm of heart usually regular,
irregular, or intermittent; its │ sometimes intermittent; its
action not necessarily quickened.│ action generally more rapid than
│ natural.
6. Mucous membranes often reddened │6. Mucous membranes generally pale;
and congested; dropsy of hind │ dropsy of hind limbs rare.
limbs common. │
7. Palpitation increased by │7. Palpitation increased by close
exercise, by stimulants and │ confinement; by local and general
tonics, etc.; relieved by rest │ bleedings, etc.; relieved by
and frequently also by local and │ moderate exercise and by
general bleeding and an │ stimulants and tonics,
antiphlogistic regimen. │ particularly the preparations of
│ iron.
Palpitations in the lower animals not dependent on any structural
disease of the heart are usually due to some violent mental emotion,
such as fear or joy. The author once possessed a fast and clever cob,
having no sign of organic disease, and equal to the severest work on the
road without showing signs of exhaustion, but which nevertheless was
affected by palpitation when threatened with a cane in his stall, or if
he had been guilty of some wilful misdemeanor for which he dreaded
punishment. In such cases the heart’s action was accelerated and the
beating could be heard loudly for a distance of several yards. They are
especially common in dogs under strong mental emotion (joy, fear), and
in dogs and pigs suffering from digestive disorder (worms) or chest
diseases.
Percivall collects a series of cases from the _Veterinarian_ under the
head of _Spasm of the Diaphragm_, a diagnosis originating in the jerking
movement of the flank, a symptom which, as is shown in the above table,
is common to man as well. Leblanc equally collects cases from the French
veterinary journals and acknowledges their true character. One of these
observed by Coulbeaux is thus described: “The respiratory movements are
interrupted by a violent lifting of the flanks, confined to the upper
part, and so intense as to be appreciated by the hand as well as the
eye. The lifting of the flank which is limited to a few square inches of
surface precisely in the hollow of this region, is perfectly isochronous
with the beats of the heart, which cannot be appreciated but by the
ear.”
A case reported by Levrat at greater length may also be given. The
subject a mare, fifteen years old, and kept for hire, was attacked
without any known cause. “There was a jerking of the whole body produced
by the extraordinary force of the beats of the heart which struck
violently against the back towards the upper ends of the first asternal
ribs on the left side. The shock is very distinct and does not appear to
be due to any tumor interposed between the heart and the ribs; its force
is such that it causes a movement of the whole body, which can be seen
at a great distance. The beats of the heart very regular, numbering
fifty per minute, were heterochronous with the pulsations of the
submaxillary artery, which are of the same number.” (The pulsation was
evidently retarded). “The pulse was soft and regular. The breathing was
peculiar. On approaching the ear to the nostrils the animal is heard to
make three successive inspirations which coincide with the beats of the
heart; each of these inspirations is followed by an expiration so short
and feeble that the expired air can not be felt; the fourth is followed
by full expiration sustained during three beats of the heart.” This form
of respiration was continued without intermission for an entire day.
In three cases observed at the Lyons Veterinary School the disease
continued for eight days. In all these and twenty more observed by
Leblanc, the patients invariably recovered. The steady persistence of
the disease for several days and the subsequent complete recovery under
the unaided action of digitalis would seem to warrant the conclusion
that such cases were really accompaniments of structural diseases of the
heart and not mere functional disorders. Even inflammation of the lining
membrane of the heart often exists without any obvious fever or other
manifest symptom of illness, and in the dissecting rooms of medical
schools nothing is more common than to find traces of pre-existing heart
disease in patients whose whole life had been passed without the
suspicion of such a malady.
A number of such cases observed in England and on the European Continent
are adduced to prove spasm of the diaphragm or of the abdominal muscles,
(Delafond), and great importance is attached to the fact that the
convulsive movements of the abdomen and loins are heterochronous with
the beats of the heart. This lack of exact coincidence however does not
seem to amount to more than a perceptible delay after the heart beat,
just as the maxillary pulsation is delayed in case of aneurism of the
aorta. This has been my own experience with such cases. The flank
movements have been equal in number to the heart beats or have
corresponded to certain beats in the heart cycle, and have been
perceptibly retarded in accordance with the necessity for time for the
transmission of the blood wave along the posterior aorta and the
development of the reflex action which set the phrenic and abdominal
muscles in motion. We must of course accept the convulsive action of the
phrenic and abdominal muscles, only it would seem that each such
movement has its starting point in the contraction of the heart. In
cases that show no relation in number nor succession with the heart
beats, we can freely acknowledge a neurosis starting at a point
different from the heart, but in all examples which are manifestly
connected with heart movements, and readily curable by the heart-tonic
digitalis, the recognition of the cardiac derangement as an initial
factor is sound alike in pathology and practice.
Nervous and purely functional palpitations are probably confined to
cases in which they are manifested at intervals appearing under the
influence of some transient excitement, and continuing only for a few
minutes at a time.
In the anæmic or bloodless condition the palpitation of weakness is
often observed under the slightest exciting cause. It is then associated
with a pallid state of the visible mucous membranes, a weak, trickling
pulse and a blowing murmur in the larger veins.
Palpitations are much more frequent in pigs and dogs than in horses.
_Treatment._ Quietness and avoidance of all excitement are first to be
secured, then the action of the heart is to be calmed and regulated by
the use of digitalis. To the horse 15 to 30 grains of the powered leaves
may be given thrice daily, and to the dog from two to four grains at
equal intervals. When the disease is associated with anæmia this agent
may still be used in combination with the various tonic remedies
recommended, but in the smallest doses only as the heart is usually
morbidly sensitive to external influences. Chloral hydrate has been used
with success. Bromides, valerian, and belladonna may be tried in
obstinate cases. Any other deviation from a healthy condition must be
noted and corrected, especially any disordered condition of the stomach
or bowels.
ANGINA PECTORIS. BREAST PANG.
W. Williams describes a case of illness in the horse to which he gives
this name. When standing idle he had twitchings of the pectoral muscles,
and when exercised these and adjacent muscles became violently
convulsed, the left fore limb being alternately fixed by spasm, and
paralyzed so that it was useless and the animal fell if compelled to
move. There was “venous pulse, great irregularity of the heart’s action,
a loud cooing or blowing sound and strong impulse indicative of
hypertrophy and a want of correspondence between the cardiac energy and
feeble pulse.” It was unfortunate that the murmur was not associated by
the observer with a particular heart sound, and with the right or left
side of the heart, and that hypertrophy was not diagnosed by percussion,
since the case can be of little value as it stands.
Breast pang is usually associated with some disease of the heart:
obstruction (usually calcification) of the coronary arteries,
insufficiency of the aortic valves, calcareous degeneration of the
aorta, aortic aneurism, or fatty degeneration of the heart. Loomis,
basing his view on dissections made by himself and others, resolves all
of these into concurrent ischæmia of the heart, the circulation in the
coronary arteries being seriously interfered with.
“That the sudden withdrawal of a supply of blood to a part may occasion
neuralgia is shown by the intense pain in the limb which directly
follows embolism of the femoral artery. Moreover general anæmia, as is
well known, favors the recurrence of neuralgia in various situations.”
Inability of the heart to propel the blood is to be explained in the
same way.
The difficulty of endorsing Williams’ diagnosis lies in the fact that
the disease, so far as it is a distinct disease, is functional and
manifested by pain, the nature of which can only be inferred in the case
of the lower animals (not by spasms of the pectoral muscles), and that
hypertrophy of the heart is not likely to be present in case of
insufficiency of blood supply to its walls.
In true angina pectoris of the horse, treatment is useless. Absolute
rest is a prime requisite, and anodynes, stimulants, heart tonics, and
nerve tonics are indicated. But the horse at rest with no prospect of
final recovery is simply a source of expense.
FUNCTIONAL IRREGULARITY IN THE RYTHM OF THE HEART.
Associated or not with palpitation, irregularity in the force or
frequency of the heart beats is sometimes met with at intervals or
independently of any further indication of structural disease.
Particularly in the greyhound and certain other breeds of dogs the
temporary occurrence of intermitting action of the heart is a frequent
though a very transient condition. It may be excited by some emotion or
excitement such as the attentions of the owner, or the straining anxiety
in the immediate anticipation of the chase. Here again digitalis is
pronounced the great panacea though it need not be resorted to unless
the habit interferes with the usefulness of the animal. If in any degree
dependent on weakness, that must be counteracted by a systematic tonic
treatment.
CONGENITAL MALFORMATIONS AND DISPLACEMENTS OF THE HEART.
Ectopia Cordis. Cyanosis, pervious foramen ovale. Symptoms, blue
mucosæ, coldness, staring coat, unthriftiness. Unequal to exertion,
palpitations, murmur before the first heart sound. Obstructed
circulation in the lungs as a cause of cyanosis, cyanosis as a cause
of lung disease.
These have been much less frequently observed in the lower animals than
in man. The anomalies observed in mammals include the following: The
displacement of the heart to the right side of the chest; displacement
entirely out of the chest (ectopia cordis); permanent communication
between the right and left auricles (cyanosis); entire absence of heart;
two hearts; one common ventricle communicating with two auricles as in
reptiles; three ventricles; only one auricle; absence of one or several
valves; absence of the pericardium; variations in the mode of connection
of the heart and large vessels, etc.
=Displacements of the heart= have been especially studied by Hering on
calves. The breast bone remained as originally developed in two lateral
halves, and the heart remained outside connected with the interior of
the chest only by its large vessels. The heart thus exposed and covered
only by its investing membrane (pericardium) afforded an excellent
opportunity to study its action, of which Hering freely availed himself.
Animals affected in this way survived their birth but a very short time.
An approach to this condition was thirty years ago made familiar to the
medical world in the person of M. Gouz, a German mechanic, the movements
of whose heart could be easily watched through a fissure in the breast
bone.
=Permanent communication between the two auricles.= =Pervious foramen
ovale.= =Cyanosis.= Previous to birth there is an opening between the
right and left auricle, allowing the blood to flow from the former into
the latter in place of, as in after life, descending into the right
ventricle and thence circulating through the lungs. At birth this is
contracted, and in a few days is completely closed in accordance with
the new life, which demands that all blood must circulate through the
lungs in order to its æration. Sometimes this fails to be effected, and
venous blood from the right side of the heart continues to mix with
arterial in the left, deteriorating it in quality and unfitting it for
nutrition, secretion, calorification, and other essential processes. The
semi-venous blood circulating in the arteries gives a bluish hue to the
visible mucous membrane, hence the name of _the blue disease_. This
blood is unfit for sustaining the vital changes essential to the
production of animal heat, so that the animal suffers from coldness of
the surface and extremities, staring coat and general unthrifty
appearance. Such subjects grow badly, and refuse to lay on flesh, but
are said to arrive at maturity in some instances and to have their
imperfection recognized only because of the short breathing, and
irregular heart’s action when subjected to exertion. A heart murmur
preceding the first sound of health is usually present, as in anæmia.
Drs. Abernethy and Wardrop draw attention to the frequency of previous
_foramen ovale_ in the human subject in connection with pulmonary
consumption, and opine that it is reopened as a consequence of this
disease. The coincidence has not been observed in the lower animals,
though if it were found to exist the question would arise whether the
deterioration of the blood and general health in open _foramen ovale_
did not also favor the deposit of tubercle in the lungs. When from
deficient ventilation the atmosphere and blood become impregnated with
carbonic dioxide the production of tubercle in man or in animals is
correspondingly frequent.
The subjects of previous foramen ovale die young or prove worthless when
they arrive at maturity. Nothing can be done to ameliorate the
condition.
HYPERTROPHY OF THE HEART.
Simple, eccentric, concentric. Ventricles chiefly affected. Causes,
increased functional activity, from obstruction to the circulation, or
continued extra exertion. Right ventricular hypertrophy-obstruction in
the pulmonary circulation; left ventricular hypertrophy-obstruction in
the systemic. Auricular hypertrophy-insufficiency of the
auriculo-ventricular valves. Pericarditis as a cause. Abnormal
weights. Symptoms, beats more forcible and prolonged, 1st sound low,
prolonged, 2nd sound clear, often doubled, increased dulness on
percussion, diagnostic signs of hypertrophy, dilatation and a
combination of the two. Simple hypertrophy rarely dangerous, with
dilatation grave, threatens congestions and apoplexies. Treatment,
rest, laxatives, sedatives, in irregular heart action digitalis,
arsenic.
An enlargement of the heart from increase of its muscular substance is
by no means uncommon in the horse. It may exist without any change in
the capacity of the cavities of the heart (simple hypertrophy) or it may
be associated with dilatation of one or more of these cavities
(hypertrophy with dilatation;—eccentric hypertrophy). A third variety
has been described in which the capacity of the cavities is decreased
but Cruveilhier and Budd have satisfactorily shown the nonexistence of
this condition except as a congenital deformity.
It is in the ventricles that the increase is chiefly observed, the
reason of which is to be found in the causes of the malady. These
usually consist in some obstruction to the circulation such as chronic
congestions in the lungs or elsewhere, rupture of air cells in the
lungs, tuberculous and other abnormal deposits in the chest and
elsewhere, tumors which by their position interfere with the circulation
through the larger vessels, and the like. Where by some such cause the
blood is impeded in its outward course, one or both ventricles are
called upon to contract more vigorously to force a sufficient amount of
blood onward and in accordance with the inherent adaptability of the
animal economy, there takes place an increase of the muscular walls of
the ventricle proportionate to the required energy of the contractions.
The condition then is essentially due to a more active nutrition and
growth of the muscular substance and finds its exact parallels in the
well-developed legs of the ballet dancer or the brawny arm of the
blacksmith. All alike occur in accordance with a general law that
whenever there is habitually demanded of any organ an unusual activity
of function, which stimulates without exhausting its power, nature adds
to the active element of such organ till the required labor can be
accomplished without the overwork of any particular part.
Keeping this in view we can easily explain the increase of one part of
the heart without immediate implication of another. The ventricles are
more commonly enlarged than the auricles because upon them devolves the
work of overcoming the obstruction, whether this exists in the lungs or
the system at large. The auricles fulfill little more than a passive
function in receiving the blood from the veins during the contraction of
the ventricles and allowing it to pass down into these when their
relaxation takes place. The closure of the auriculo-ventricular valves
during the ventricular contraction protects the auricles from the
internal tension to which the lower part of the heart is subjected and
thus all tendency to increase is obviated.
The hypertrophied part corresponds to the locality of the obstruction.
If it exists in the lungs (heaves, consumption, hepatisation, chronic
bronchitis), pulmonary artery, its valves at its origin from the heart,
or if it consists in contraction of that orifice, the enlargement takes
place primarily in the right ventricle, the right auricle remaining
unchanged so long as the auriculo-ventricular valves act perfectly. The
ventricle, however, tends to dilate as well as enlarge in thickness of
walls, and as soon as this dilatation has proceeded so far as to widen
the orifice between the auricle and ventricle and render its valves
insufficient, the auricle also begins to dilate and its walls often
increase in thickness. But the vicious chain does not end here. Should
the animal survive and the original obstruction persist, the veins
throughout the system become habitually congested because of the reflux
of blood from the right auricle and ventricle, dropsies appear in
different parts, the congestion of the veins is continued through the
capillary bloodvessels to the arteries, the difficulty of propelling the
blood comes to be experienced by the left ventricle and a corresponding
series of morbid changes taking place on that side, as have already
ensued on the right, the vicious circle is soon completed, and the
entire organ becomes diseased, each constituent part of the organ
operating injuriously on that which preceded it in the track of the
circulation, and every new change forming but a stepping stone to a more
dangerous modification.
On the other hand the obstruction may exist in the general circulation,
on the course of the aorta, or its branches, in its valves at its origin
from the heart, or in the narrowing of its orifice. Then the increase
takes place first in the left ventricle, is propagated to the left
auricle, leads to congestion of the veins, capillaries and arteries of
the lungs, and lastly to disease of the right side of the heart. Here
there is a different starting point, but the progress of the
disease-changes in a direction opposed to the course of the circulation
is the same.
The disease may, however, begin with the auricles, owing to disease of
the auriculo-ventricular valves impeding the flow of blood into the
ventricle, or to simple narrowing of the auriculo-ventricular opening.
The auricle is then primarily enlarged, the corresponding veins
congested, this is propagated to the capillaries and arteries, and
lastly the ventricle on the opposite side of the heart is involved. This
is chiefly seen with fibrinous deposits on the valves or in the case of
polypus hanging into the auriculo-ventricular opening. Aneurisms,
embolisms, neoplasms, atheroma and calcic degeneration of the arterial
walls may be effective factors.
In addition to these causes Bouilaud and Leblanc attach a high
importance to chronic inflammations of the serous membranes, which by
reason of the contiguity of the latter to the muscular structure bring
about a more abundant circulation in this and an increased nutrition.
Another cause is unintermitting hard work which necessitates excessive
exertion of the heart, to supply blood more freely to the muscular
system and the lungs. Many hunters suffer from this affection it is
believed because of their extraordinary exertions. The stallion Helenus
had a heart of 14 ℔s.
_Weight of the heart._ The heart in the horse which rarely weighs over 9
℔s. is increased from 10 ℔s. to 14 ℔s. in this disease and in one case
in a cart horse, recorded by Stephenson in the Veterinarian for 1861, it
is said to have reached 32 ℔s. Stephenson probably weighed the heart
while filled with blood. A diseased heart weighed in this way by Thomson
amounted to 34 ℔s., one by Gerlach, 19 ℔s., an ox’s heart by Herran 36
℔s. In Stephenson’s case there was further an extraordinary dilatation
of the anterior vena cara. Haycock (Veterinarian, 1850), records a case
in which though the heart only weighed 10 ℔s. 8 oz., yet the walls of
the ventricles were double the normal thickness, those of the left being
2¼ inches while those of the right were 1 inch. An estimate from the
thickness of the walls, it must be borne in mind, is not so satisfactory
as the absolute weight taken after the removal of the large vessels, the
superfluous fat and the contained blood.
The usual coincidence of other complaints supports the statement that it
is mostly due to obstruction to the circulation. A few cases will
illustrate. Dyer reports the case of a hunter in which with general
hypertrophy and dilatation of the right auricle, the pulmonary artery
was so large as to admit the fist. (Veterinarian, 1861). Halloway
relates a case in which there were extensive internal deposits of
melanotic material, especially in the mesenteric glands, liver, spleen,
and kidneys (Veterinarian, 1850). Haycock records a case with thickening
of the auriculo-ventricular valves on the right side, and of several of
their tendinous cords, also a diseased liver which had ruptured before
death (Veterinarian, 1850). Percivall publishes a case associated with
pleurisy and rheumatism (Veterinarian, 1858). Henderson furnishes a case
associated with diseased right auriculo-ventricular valves and enlarged
liver weighing 55 ℔s. (Veterinarian, 1847.)
_Symptoms._ In simple hypertrophy the heart beats are more forcible and
prolonged so that the period of silence or rest is shortened. This is
due to the greater length of time taken up in the contraction of the
ventricles. For the same reason the pulse which may or may not be
accelerated, irregular or intermittent, is full and rolling or as it
were prolonged. The first sound of the heart is prolonged and low or
muffled, sometimes almost inaudible while the second is unnaturally
loud. Sometimes when one ventricle only is enlarged that may complete
its contraction later than the other and the second sound is repeated as
in the syllables _lub_—_tip tip_. A duplication of the first sound only
is less common. If the sounds are heard over a greater extent of the
chest’s surface than is natural, the lungs being healthy, it is probably
due to hypertrophy of the heart. If very clear on the right side they
indicate increase of the right ventricle. The heart’s impulse is usually
strong and may be felt on both sides, and it may be over the whole
chest.
Percussion usually shows a more extended dulness in the region of the
heart but the blows must be pretty forcible to bring out the deeper
resonance, otherwise it will come only from the thin layer of lung.
These results are of the greatest value in the dog.
The pulse is usually regular and if excited to irregularity and
intermission quickly returns to its natural state when the patient is
left at rest.
As hypertrophy is usually associated with dilatation of the heart the
following table abridged and modified from Dr. Walshe will prove
valuable by presenting side by side the signs indicating hypertrophy
with and without dilatation, and simple dilatation.
TABLE CONTRASTING THE MAIN SYMPTOMS OF HYPERTROPHY AND DILATATION.
A. General Physical Signs.
SIMPLE HYPERTROPHY. HYPERTROPHY WITH SIMPLE DILATATION.
DILATATION.
Heart’s impulse slow Force increased, Impulse conveys a
and heaving as if sharper, more feeble undulatory
pressing steadily knocking, may impart sensation; force of
against an a shake to the body. successive beats
obstacle—in rythm May be felt on the unequal; rythm
regular, in force right side. irregular.
unequal.
First sound is dull, Sounds gain greatly in First sound short,
muffled, prolonged loudness and extent abrupt and clear.
and weakened almost of transmission, Second sound not
to extinction. Second especially if the specially affected.
sound full and valves are thickened.
clanging; period of
silence shortened.
Murmur with the first Murmur with the first Murmur with the first
sound present at one sound may be present, sound from
time and absent at from altered insufficiency of the
another. direction of the auriculo-ventricular
orifice of the aorta. valves.
B. General Functional Symptoms.
SIMPLE HYPERTROPHY. HYPERTROPHY WITH SIMPLE DILATATION.
DILATATION.
Strength unimpaired. Strength tends to Strength fails.
Power of continued become impaired.
exertion (especially
uphill) limited by
shortness of breath.
Visible mucous Purpleness and lividity Lividity of the mucous
membranes healthy or of the mucous membranes. Dropsical
of a bright red. membranes effusions of the
proportionate to the limbs and other
valvular or pulmonary dependent parts which
obstruction. pit on pressure.
Difficulty of breathing Difficulty of breathing Difficulty of breathing
occasional. occurs in paroxysms. great and constant,
with occasional
aggravations.
Pulse full, strong, Fulness of pulse Pulse small and feeble,
firm, tense, continues but much later than the
resisting and strength and power of heart beat. Regular
prolonged without resistance lost. or feeble, fluttering
jerk or thrill. and irregular. Venous
pulse in the
jugulars.
Rarely and never Indirectly and more or Palpitation frequent.
rapidly the direct less rapidly fatal. Faintness occurs from
cause of death. time to time, and may
lapse into fainting
and sudden death.
Pure hypertrophy rarely implies imminent danger unless dependent on some
pre-existing structural disease which impedes the freedom of the
circulation. If excessive, however, or if associated with dilatation the
animal is short-winded and unfit for all but the slowest work. It
predisposes to congestion or apoplexy of the lungs when its seat is the
right ventricle, and to congestions and hemorrhage in other parts of the
system, brain, kidney, lungs, liver, bowels, if in the left.
Asthma (dogs), heaves (horses), emphysema and tuberculosis in cattle are
occasional complications attended by grave symptoms.
_Treatment._ In advanced cases and such as are dependent on irremovable
structural changes in the lungs or elsewhere no treatment is of any
avail. In recent and uncomplicated cases in the horse and cow and in
some more advanced conditions in other animals, not used for work, a
palliative treatment may be profitably adopted. This consists in a
nitrogenous restricted and gently laxative diet, perfect rest in
fattening oxen and other animals, or in the horse moderate and carefully
regulated work, and as a medicament the use of digitalis or aconite. No
known remedy has any power to directly check the growth of the heart and
the utmost that can be expected of these agents is to lessen the
activity of the heart’s action and retard its growth. Digitalis may be
given as recommended for palpitation, or aconite in the form of tincture
20 drops for horses and cattle and 1 to 2 drops for dogs, repeated four
times daily. Strophanthus may replace digitalis. When depletion seems
advisable purgatives or diuretics should be given as appears most
applicable to the particular case. Iodide of potassium has been strongly
recommended.
When extreme dilatation exists with the hypertrophy, sedatives should be
given cautiously and their effects carefully watched as the heart is
often dangerously susceptible to depressing influences. When the disease
has advanced so far as to cause abundant dropsical effusions it is
futile to resort to treatment as amelioration can rarely be looked for,
not even to the extent of allowing an animal to be fattened.
The value of arsenic in most cases of broken wind (heaves) has suggested
the inquiry whether it does not operate directly on the heart. Leblanc
who advances this query might have quoted in explanation the known power
of arsenic to retard and arrest tissue change, with its natural
consequences, the diminished amount of effete matter thrown into the
blood in any given time, and the lessened necessity for an active
circulation to supply any great waste of structure. It may benefit such
cases in this way but does so probably to a far greater extent by an
influence on the nervous function analogous to its action in neuralgia
and other purely nervous disorders. Dilatation of the heart which
usually exists in _heaves_ is usually benefited by tonics which like
arsenic are destitute of stimulating properties.
ATROPHY.
Simple, eccentric, concentric. Usually eccentric. Causes, effusion in
pericardium, obstruction of coronary arteries, by false membranes,
etc., general inanition. Symptoms, beats weak, sounds loud, clear,
decreased area of dulness on percussion, pulse slow, weak, under
excitement unequal, irregular, intermittent with palpitation, dropsy
of limbs, etc., murmur with 1st sound. Treatment only in early stages
by removal of the cause.
The loss of substance in the muscular walls of the heart is either
_simple_ when there is no change in the capacity of its different
cavities:—=eccentric= when the chambers of the heart are enlarged; or
=concentric= when these chambers are reduced in size. Like hypertrophy
it may affect the walls of one chamber to the exclusion of the others.
Atrophy is much less frequent in the lower animals than hypertrophy and
in nearly all cases on record it was associated with dilatation.
The _causes_ are not always very evident. Effusion into the pericardium
is one of the most frequent, the compression of the heart impairing its
nutrition and decreasing its size. Especially is it hurtful when several
layers of false membranes deposited on the surface of the heart become
organized, preventing its sufficient dilatation and compressing its
nutrient bloodvessels. A case of this kind in a dog occurred to Leblanc;
the right auriculo-ventricular opening was surrounded by thick organized
layers of false membranes which by their contraction had largely
diminished the opening and even pressed on the coronary artery cutting
off to a great extent the supply of blood to the walls of the ventricle.
Another alleged cause is a prolonged insufficient nourishment to the
entire body. Leblanc has also observed this in dogs the subjects of long
continued wasting maladies.
_Symptoms._ In pure atrophy these are the opposite of those seen in
hypertrophy. The beats of the heart are weak or inappreciable to the
hand placed on the side of the chest behind the left elbow. The sounds
of the heart are loud and clear, their intensity being proportionate to
the thinning of the walls and the dilatation of the chambers. Percussion
so far as it can be made effectual, which is chiefly in dogs, shows a
diminished area of dulness. The pulse is slow, weak, or indistinct,
compressible, becoming accelerated, unequal, irregular, and intermittent
when the patient is excited. Palpitation is frequent, breathing is
difficult or easily embarrassed and there is a tendency to dropsy of the
limbs and dependent parts. These symptoms are usually associated with
considerable prostration and depression.
These are often complicated by symptoms of valvular disease or
dilatation.
Atrophy progresses slowly and rarely causes death in the earlier stages.
In its advanced stages when dropsy has supervened little can be done
even in its mitigation. In the earliest stages only can good be done by
employing measures calculated to remove its causes and thus put a stop
to its progress.
DILATATION OF THE HEART.
Result of obstruction to circulation. In right ventricle usually. In
auricle from narrow auriculo-ventricular opening. Pure dilatation from
sudden extreme blood pressure as in inflammations of the lungs. In fat
cattle from fatty obstructions around the heart and great vessels.
Weakness of cardiac muscles in fatty degeneration, fevers, debility,
etc. Symptoms, dyspnœa under slight exertion, unsteady walk, cold,
dropsical limbs, venous pulse, pulse small, weak, irregular,
intermittent, with palpitations. Treatment, in early stages arrest the
causes, arsenic, digitalis, fatten for butcher.
Dilatation of the right cavities of the heart is one of the most common
heart diseases of the horse. It is an almost constant condition in
advanced broken wind, and is a frequent concomitant of hypertrophy and
an occasional one of atrophy of the heart. Its usual direct cause is
some obstacle to the free escape of blood from the cavity affected. Thus
in broken wind the difficulty of the circulation through the lungs
causes accumulation in the pulmonary artery and right ventricle of the
heart, the walls of which are distended because of the unwonted internal
pressure. When the dilatation of this ventricle reaches a certain stage
the auriculo-ventricular opening is equally widened, the valves become
insufficient to close it and the right auricle and venæ cavæ participate
in turn in the internal pressure and dilatation. The right ventricle is
more often affected than the left, because of the greater frequency of
obstruction in the circulation through the lungs than in that through
the general system, and because of the thinness of its walls which more
readily give way under internal pressure. Dilatation may result from
disease of the great arteries, from diminution of their calibre by the
pressure of tumours, or by narrowing of their openings at the heart,
whether as the result of diseased valves or other morbid condition. As
affecting the auricles primarily its usual cause is narrowing of the
auriculo-ventricular opening from some abnormal deposit. The extreme
thinness of the walls of the auricles allows these to give way under
internal pressure even much more readily than the right ventricle.
The causes it will be seen are similar to those inducing hypertrophy,
and hence the frequent coexistence of the two. Pure dilatation occurs
especially when internal pressure takes place suddenly and to excess,
and while the nutritive functions are to a great extent in abeyance.
Such conditions are found in acute inflammations of the respiratory
organs, or of the inner or outer membranes of the heart, and the rapid
deposit in the lungs of tubercles or other abnormal material.
Dilatation of the right side of the heart is a common complaint in
overfed cattle, and is apparently due to the diminished power of
resistance in the walls of the heart, the muscular substance of which is
partly replaced by fatty granules, and to the obstruction offered to the
circulation by the extraordinary accumulation of fat around the base of
the heart and the commencement of the large blood vessels. Though a
diseased condition this rarely shortens life or interferes with the uses
to which cattle are put.
The heart walls are similarly weakened and yield more readily to the
internal blood pressure in endocarditis, myocarditis, pericarditis, high
fever, infectious diseases, poisonings, anæmia, and debilitating
diseases generally. Debility and incapacity to resist the blood pressure
is the essential prerequisite to dilatation.
The _symptoms_ which have been already enumerated in the table given
under the head of _hypertrophy_ are mainly these: Loss of appetite,
spirit and endurance; faintness and difficulty of breathing on the
slightest exertion; habitual coldness with a tendency to dropsy of the
extremities; loss of control over the extremities when walked or trotted
far; venous pulsation in the jugulars; heart’s impulse weak and
undulatory or tremulous, or under exertion tumultuous or palpitating;
murmur often present with the first sound; the first or more commonly
the second sound may be doubled; pulse small, weak, irregular, and often
intermittent, and frequently livid spots in the nasal mucous membrane.
Paroxysms of unsteady gait from irregular circulation in the brain is
frequent, and Dyer asserts that he has repeatedly seen blindness as a
result of this condition.
In _treatment_ the main purpose should be to put a stop to the cause of
the disease before it has been developed to a dangerous extent. When the
malady is manifested by the symptoms above enumerated the subject is
rendered permanently unfit for service and will probably die suddenly
under some slight exertion. Fattening animals in a condition of quietude
will often lay on flesh for an indefinite length of time notwithstanding
that the heart is considerably dilated. (See note on digitalis,
strophanthus and arsenious acid in dilated heart, under the head of
_hypertrophy_). To relieve the asthmatic attacks attending on an
overtaxed heart Zuill strongly recommends the combination of iodide of
potassium, digitalis, nux vomica and coca. But heart tonics are often
much more affective after the bowels and portal system have been
unloaded by a laxative.
INFLAMMATIONS IN THE HEART.
These are among the most common diseases of this organ and moreover lead
to many of the changes in structure to be hereafter noticed so that it
is convenient to treat of them here. According to their relative
frequency they may be ranged:—1st. Inflammation of the external covering
of the heart—pericarditis; 2d. Inflammation of the internal lining
membrane of the heart—endocarditis; and 3d. Inflammation of the muscular
substance of the heart—carditis.
PERICARDITIS.
Definition. Frequency in different genera. Causes, rheumatic,
traumatism, extension from pleurisy. Unwholesome buildings and
localities, debility. Symptoms, chill, reaction, pleuritic symptoms,
hyperthermia, tenderness behind left elbow only, friction sound
synchronous with heart beat, later it is lost and heart sounds are
muffled, increased area of dulness on percussion, oppressed breathing,
venous pulse, patient statant, little fever in chronic cases.
Traumatism from the stomach, digestive disorder, grunting, dropsy
under the sternum with little fever at first. Lesions, as in pleurisy,
obliteration of pericardial sac. In traumatism from stomach the
foreign body is formed in the cardiac end of a band of lymph extending
to the reticulum. Treatment, in chill, after reaction, medicinal
measures as in pleurisy, local applications to the region of the
heart. Paracentesis, insertion of needle, antiseptic precautions.
Chronic pericarditis in oxen.
_Definition._ Inflammation of the strong fibro-serous sac in which the
heart is contained and which is reflected on the muscular substance of
that organ so as to form its external covering.
This is the most common inflammatory disease of the heart and has been
met with more frequently in horses and cattle than in the smaller
quadrupeds.
_Causes._ It frequently coincides with or follows other diseases such as
_influenza_, _pleuro-pneumonia_ and above all _rheumatism_. In cattle
and goats wounds from sharp pointed bodies, (needles, pins, nails,
etc.), which have been swallowed with the food and have passed through
the walls of the second stomach, the diaphragm and pleura to the heart
constitute a frequent cause in cattle. The pericardium has been
punctured by a fractured rib and has been implicated in inflammation
attendant on an abscess or other lesion in the walls of the chest.
Besides these the general influences which cause uncomplicated attacks
of the disease are the same as those producing pleurisy, peritonitis,
rheumatism and inflammation of serous membranes generally. These are
sudden changes from heat to cold, cold winds, cold draughts, drenching,
chilling rains in animals already overheated and exhausted, or prolonged
exposure in severe weather, in low states of the system. Leblanc justly
remarks that “with the morbid influences which appear specific, there
often coincide intemperate seasons, badly arranged buildings, a want of
sufficient attention to the conditions of health, and in the case of
herbivora, wet, cold, and badly exposed pastures.” In other words
whatever deteriorates the health and vitality predisposes.
_Symptoms._ These are less characteristic than in man owing to the
smaller portion of the heart exposed, but they are usually marked enough
to permit a recognition of the disease. _Acute form._ The affection is
ushered in by chill, general fever, hyperthermia, (103° to 104°),
staring coat, hot, dry mouth, dilated nostrils, excited, difficult
breathing, double lifting of the flank with each expiration, the
existence of a prominent ridge from the lower end of the last ribs along
the flank to the outer angle of the hip bone, as in pleurisy, pinched,
anxious expression of countenance, fixed eyes, accelerated, full, hard
and often wiry pulse, and tenderness when the ribs behind the left elbow
are pinched or struck. The same tenderness is noticed particularly in
the ox and smaller quadrupeds when pressure or compression is made
beneath the breast bone. Auscultation over the lower ends of the fifth
and sixth ribs and their cartilages detects a friction or rubbing sound
in the early stages and until liquid has been thrown out into the
pericardial sac. This sound may be at first the finest possible
creaking, afterward increasing to a distinct rubbing, is synchronous
with the beat of the heart, and usually with the first sound. It is
distinguished from the friction sound of pleurisy in occurring
rythmically with the sounds of the heart and not with those of
breathing, and from sounds produced in the interior of the heart by its
absence when auscultation is made over the carotid or other large
artery. This friction sound is lost when serous effusion takes place
into the pericardium, but reappears when the liquid is absorbed in the
process of recovery. Until effusion takes place the impulse of the heart
is strong, often irregular, in force, and sometimes accompanied by a
purring tremor or, according to Leblanc, a metallic tinkle.
When effusion has taken place the pulse is weaker and softer, irregular
or intermittent, the impulse of the heart is weaker, the friction sound
is lost, and the area of dulness corresponding to the heart is
increased. Percussion shows it to extend higher than three inches above
the breast bone in the horse and more than two or two and a half inches
transversely. It is distinguished from the effusion of pleurisy in this,
that the dulness is confined to the anterior part of the chest, having
the outline of an inverted cone, and does not extend backward along a
horizontal line, and, in solipedes, in not showing equally on both
sides. In the smaller animals it may be distinguished by not always
occupying the dependent part of the chest when the animal is placed in
different positions. As the effusion increases, the heart’s sounds,
previously strong, become first muffled, then more and more distant
until they may become altogether imperceptible. The difficulty and
oppression of the breathing increases, the nose is protruded, the eyes
more rigidly fixed, and the face more haggard; a venous pulse,
apparently due to the compression of the heart and large veins by the
fluid, is seen in the lower ends of the jugulars, and the animal
obstinately stands as indeed the solipeds do all through the disease. At
this advanced stage dropsies of the limbs, sheath, and other dependent
parts of the body are frequent.
A painful cough is sometimes though by no means invariably present
throughout the disease. Emaciation takes place rapidly and in the more
acute cases death ensues in five to eight days. A fatal issue may be
delayed until after three weeks or the affection may merge into a
_chronic form_.
=Chronic Pericarditis= is sometimes seen in the ox without any preceding
acute attack. This is manifested by the local symptoms without the
accompanying acute fever. Along with a _slight_ fever, there is the
oppressed breathing aggravated by exertion, the weak irregular or
intermittent pulse, the weak or distant heart sounds, the absence of
respiratory sounds and the dullness on percussion over a space
represented by an inverted cone at the anterior part of the chest on
each side, the venous pulse in the neck and the general tendency to
dropsy.
If the _pericarditis_ has been the result of sharp pointed metallic
bodies swallowed and afterwards making their way to the heart, it is
sometimes preceded by eructations, tympany, difficulty in swallowing or
in rumination, and by dropsy under the sternum, but more frequently the
heart symptoms are the first to be noticed. It is not attended by the
high fever of other pericarditis.
_Post Mortem Appearances._ These do not differ materially from those of
pleurisy, to which accordingly the reader is referred. The effusions and
false membranes are of course localized in the sac of the pericardium. A
frequent termination is a permanent adhesion of the pericardium
throughout more or less of its extent to the surface of the heart. In
cases of death the serous effusion is commonly colored with blood though
mostly from a _post mortem_ infiltration of blood from the congested
lungs. The effusion has been known to measure fifteen litres in the
horse. It may be purulent or combined with fœtid gases, particularly in
traumatic cases. After mild attacks white patches (milk spots) are often
left extending, it may be only through the pericardium and in other
cases reaching into the muscular substance. At a less advanced stage the
false membranes are yellow, with a rough or villous surface, they may be
softened from fatty degeneration or they may be more or less completely
calcified.
When the cause has been perforation by a metallic body, it will be found
surrounded by exudate enveloping a canal or band extending to the
diaphragm or stomach.
_Treatment._ Pericarditis often proves fatal but it is by no means
invariably so in uncomplicated cases. There is especial danger when
serous effusion is excessive, when it occurs in a weak and debilitated
subject, or when it is complicated by pleurisy, influenza or rheumatism.
The preliminary chill may be met by the measures advised for the rigor
of pleurisy, but if the malady is developed other treatment is required.
The medication is still essentially as for pleurisy, only the primary
disease (rheumatism, influenza, pneumonia) must be specially attended to
when such is present. Acute pain may be met by carefully graduated doses
of opium or aconite and by the moist jacket or fomentations. Some employ
icebags to soothe at once inflammation and pain and in the absence of
rheumatism these may be resorted to. In the small animals leeches may be
applied over the cardiac region. Dry cupping is a good alternative
applicable to all.
An active purgative is demanded unless the affection is attended by a
low type of fever or has occurred during the course of an epizootic
disease (Horse 5 to 7 drachms aloes, cow 1 to 2 lbs. Epsom Salts, dog 1
oz. castor oil). After the walls of the chest have been well fomented
they may be enveloped in a large mustard poultice which must be
continued until a considerable effusion has taken place beneath the
skin. To moderate and control the heart’s action give digitalis (horse
and ox ½ drachm, dog 2 to 4 grains) four times a day. After the
purgative has acted an ounce of nitrate or acetate of potass may be
given daily to the larger quadrupeds (1½ drachms to sheep and pigs, and
20 grains to dogs) in the drinking water. These agents together with the
digitalis must be pushed to the largest doses when the effusion has
taken place abundantly and when it threatens to dangerously interfere
with the heart’s action. Pilocarpin is a dernier resort, to be used with
caution. In similar circumstances, ointment or tincture of iodine should
be freely applied over the chest in the region of the heart. Mustard and
other vesicants repeatedly applied often greatly hasten the reabsorption
of the liquids.
From the first the animal must be warmly clothed and every means
employed to obtain free circulation and warmth on the surface. The legs
must be well rubbed and wound in warm flannel bandages, or this failing,
may have mustard freely applied to them. Warm injections must be at the
same time thrown into the rectum and will benefit by soliciting the
action of the bowels as well as in raising the temperature of the
surface generally. The food allowed should be warm mashes of wheat bran,
boiled linseed and similar agents in small quantities.
If the amount of effusion threatens a fatal result, it may be drawn off
by a cannula and trochar introduced between the cartilages of the fifth
and sixth ribs, by a valvular wound and with antiseptic precaution (see
hydrothorax), care being taken to avoid puncturing the heart itself.
The trochar or aspirator needle should be pushed in a direction upward
and inward until resistance ceases or it is felt that the heart has been
touched. A caoutchouc tube may now be attached to it and allowed to
depend twelve or eighteen inches, and its lower end should be plunged in
a weak solution of boric acid or other antiseptic. This avoids the
entrance of air and insures against the introduction of ærial bacteria.
When the vital powers are being exhausted stimulants must be given to
support the animal, combined with iodide of potassium. (See advice
concerning the allied condition in _Hydrothorax_).
In the _chronic pericarditis of oxen_ the fatality is greater. Treatment
consists mainly in counterirritants and powerful diuretics employed in
doses determined by the strength of the animal, and combined with
stimulants and tonics as in the advanced stages of the acute disease.
In complicated forms of pericarditis attention must be given mainly to
the constitutional affection, thus in _influenza_ a stimulating and
supporting treatment is demanded, and in _rheumatism_ colchicum, acetate
of potass, salicylate of soda, salol and similar agents must be freely
administered, though not to the exclusion of counterirritants to the
region of the heart, and other measures demanded by the heart diseases.
ENDOCARDITIS.
Definition. Pathology and lesions, congestion of the endocardium
covering the valves, valves liable through friction and strain,
exudation in or on the serosa rendering it opaque, coagula of fibrine
on the surface, secondary endocarditis mycotic, microbes, changes in
serosa, distortions and degenerations of valves. Symptoms, as in
pericarditis, with violent heart impulse of varying force, clear
metallic sound, blowing murmurs, weak pulse decreasing in force,
irregular, intermittent, absence of local tenderness, no friction
sound, no increase in area of dulness, if lesions are in right
heart—venous pulse, venous congestion, dropsies. Valve lesions, in
mitral valve—general heart symptoms and murmur with 1st heart sound,
2d sound may be repeated and exceptionally a venous pulse—in tricuspid
valve—same with constant venous pulse, venous congestion and dropsy;
narrowing of the mitral orifice—general heart symptoms and blowing
murmur before the 1st sound; narrowing of the tricuspid orifice—same
with murmur sometimes audible on the right side; insufficiency of
aortic valves—general heart symptoms and murmur with 2d heart sound,
double rushing sound in arteries and delay of pulse beat at jaw;
lesions in pulmonary valves—same but without double rush in arteries,
or delay of pulse beat at jaw. Loose coagula. Embolism. Causes, as in
pericarditis and strain on valves, and poisons and microbes in the
blood. Prognosis grave. Treatment, as in the early stages of
pericarditis, antirheumatics and germicides more, and diuretics less
desirable. For clots iodides, alkalies.
_Definition._ Inflammation of the serous membrane lining the chambers
and covering the valves of the heart.
_Pathology and Morbid Anatomy._ The causes and symptoms will be better
understood after the diseased conditions have been comprehended. The
earliest changes are the reddening and thickening of the lining membrane
of the heart but above all of that covering the valves. The valves are
particularly exposed to inflammation by reason of the friction of the
blood when violently forced through the narrow opening in excited
conditions of the heart, by the strain thrown upon them from the violent
contractions of the heart or the recoil of blood in the arteries, and by
their susceptibility in common with all other fibrous structures to
rheumatic inflammation. The redness is of the ramified or branching kind
characteristic of inflammation, and is neither removable by washing the
surface nor does it correspond in position with the colored portion only
of a clot which the cavity in question may contain, as seen in
bloodstaining occurring after death.
There is further exudation of plastic lymph into and beneath the serous
membrane, rendering it opaque, white and thick, or on its surface
forming granular elevations, and in the case of the valves becoming
moulded into ridges or festoons by the mutual pressure of the different
flaps on each other. The inflamed surfaces are further liable to be
covered by masses of blood clot in successive layers, deposited by the
action of the fibrinogenous matter developed in the inflamed part. These
clots sometimes accumulate in considerable masses, firmly adherent to
the heart’s walls or valves by their attached surface, but soft and
filamentous on their free aspect. These clots or polypi, as they have
been called, are soft and loose on their free surface, and become firmer
toward their points of attachment. In other words their consistency is
in direct ratio to their age. If of old standing they are usually pale
yellow or white and streaked with red, while if recent they are mostly
red throughout. They vary in size from a thin film to a mass filling up
nearly the entire cavity in which they are lodged, and as they
frequently extend through the auriculo-ventricular openings or become
applied against this or the opening of the great artery, they seriously
and sometimes fatally interfere with the circulation. Leblanc asserts
that large masses of this kind may be deposited in a few days or even
hours, causing sudden deaths, and especially in dogs. He has found other
circumstances than endocarditis to cause these fibrinous deposits, and
especially the absorption of pus, or the sudden suppression of a long
standing discharge, as in catarrh of the air passages. If death does not
immediately ensue, these fibrinous deposits may become vascular, as is
the case with false membranes in the pleuræ, becoming organized into
fibrous tissue, or even degenerating into calcareous matter, necrotic
debris, or pus, several instances of which as occurring in horse and cow
are on record.
These cases illustrate _endocarditis by infection_ (_mycotic_,
_malignant_, _or ulcerative endocarditis_), which occurs independently,
or as an extension of a bacteridian disease, primarily localized
elsewhere in the system. Thus it is a secondary lesion in infectious
omphalitis, pneumonia, pleurisy, arthritis, abscess, pyæmia, etc. Beside
the general lesions of endocarditis and a great tendency to molecular
death of the new formations and the underlying tissues, there is the
presence of specific germs which have been the occasion of the disease.
Among these the staphylococcus pyogenes aureus, the streptococcus
pyogenes, and the diplococcus pneumoniæ, have been particularly noted.
In case the valves were already diseased, they become especially liable
to be colonized by any such bacteria that may be circulating in the
blood.
In the early stage there may be a mere swelling of the valves, with as
yet a smooth, unbroken surface, but with enlargement and increase of the
connective tissue cells, later fungous vegetations start out from the
surface, and on these the fibrine of the blood is deposited in layers.
Besides the formation of clots on their surfaces other changes occur on
the cardiac valves as the result of inflammation. The organization of
the exuded lymph within and upon them leads to rigidity, loss of
elasticity, unevenness of their surface, contraction and puckering so
that they can no longer approximate to each other, but leave the orifice
imperfectly closed. They may, moreover, have gristle or bone deposited
in their substance. The osseous degeneration of such new products
appears to be the most common cause of those ossifications of the heart,
of which specimens are to be found in nearly all veterinary museums.
=Chronic valve disease= is thus found to be a common result of
endocarditis, and from the obstacle presented to the flow of blood
through the different cardiac orifices by the rigid, inelastic and
distorted valves, hypertrophy of the heart frequently supervenes.
In our domestic quadrupeds ante-mortem clots and fibrinous polypi have
been chiefly formed in the right side of the heart, and diseased valves
in the left.
_Symptoms._ The general symptoms agree in many respects with those of
_pericarditis_. There are the same general symptoms of fever
(temperature 102° to 106°), the same pinched, anxious countenance, the
same shortness of breath and oppression when moved, the same violent
heart’s action, and the same rapid, excitable pulse tending to be
irregular and intermittent. Among the more specific symptoms are a very
violent impulse of the heart against the left side, varying in force,
however, in successive beats; a metallic tinkling accompanying the
impulse and sometimes heard at some little distance from the body, a
blowing murmur as soon as the changes in the valves render them
insufficient to close the orifices, and, if the obstruction exists on
the right side, venous pulse, general venous congestion, and dropsical
swellings.
The pulse may at first have considerable force but, as insufficiency of
the valves ensues, it becomes small and weak, its weakness forming a
most marked contrast to the violence of the heart’s impulse against the
side. The irregularity and intermission of the pulse is to be ascribed
at first to the impaired nervous energy of the heart though later it is
often due to the obstacle presented by clots to the flow of blood from
the heart, so that a beat sometimes takes place without a corresponding
pulsation. It may reach 80 or 160 per minute in horse or ox.
The blowing murmur when heard is one of the most characteristic symptoms
but must be carefully distinguished from other allied heart sounds. If
very loud it may be confounded with the friction sound of pericarditis,
but may be differentiated by its invariable coincidence with some
particular portion of the heart’s beat. The absence of local tenderness
is another distinctive symptom. Again in pericarditis effusion takes
place early annulling friction sound, and diminishing alike the impulse
and the sounds of the heart.
It is of less practical value to be able to distinguish the precise seat
of the murmur, yet the following data will guide to such a conclusion.
=Simple induration or insufficiency of the Left Auriculoventricular
(Mitral) valve.= Paroxysms of palpitation, oppression, and difficulty of
breathing; vertigo with loss of control over the limbs and vacillating
gait; stupor, coma; slight tremor and blowing noise with the first sound
of the heart; heart’s impulse, violent, but irregular in force,
sometimes double; pulse feeble, irregular, unequal, or intermittent;
sometimes though not at all constantly a venous pulse in the lower end
of the jugulars. In chronic induration of this valve, or in osseous, or
cartilaginous degeneration the same symptoms are shown. The more general
symptoms may, however, require exercise to develop them.
=Induration, etc., of the Right Auriculo-Ventricular (tricuspid) valve.=
The symptoms are almost identical with the last. Venous pulse is
constant, and, particularly after exertion, the veins generally are
distended. Dropsies are more common.
=Narrowing of the Mitral orifice.= In addition to the same general
symptoms as the last named lesions, there is a sighing, blowing, purring
or rasping sound, according to the degree of narrowing, heard _before_
the first sound of the heart. It is the noise of the blood rushing
through the narrowed orifice between auricle and ventricle. It is
usually loudest behind the middle of the shoulder on the left side.
Feeble pulse, frequent imminence of suffocation and filling of the
limbs, etc., are nearly constant.
=Narrowing of the Tricuspid orifice.= Symptoms nearly identical with the
last. Venous pulse more constant. Blowing murmur sometimes loudest on
the _right_ side of the chest.
=Induration or insufficiency of the aortic valves.= Blowing murmur with
the second sound of the heart. Double rushing sound in the carotid with
each heart’s beat. There is an appreciable interval between the beat of
the heart and corresponding pulsation at the jaw.
=Induration or insufficiency of the pulmonary valves.= Blowing murmur
with the second heart sound, but no corresponding double sound in the
carotid, nor any marked retarding of the pulse.
=Loose coagula in the heart= or _adherent ones_ (_polypi_) produce one
or other of the above class of symptoms, according to the particular
orifice they tend to block or the valves whose function they impair.
Anæmia and leukæmia may have blowing murmurs with the first or second
heart sound.
=Embolism.= =Plugging of arteries.= Another class of symptoms sometimes
supervenes because of loose clots being washed on into the arteries, and
blocking them when they reach those that are too small to transmit them.
These symptoms will be as varied as the organs whose arteries are
plugged. If in the brain there may be dulness, stupor, vertigo,
somnolence, delirium; if in the liver, biliary and digestive
derangement; if in the lungs, cough with the other signs of pneumonia
and abscess; and if in the limbs lameness and paralysis, (brought on or
aggravated by exercise, and often removed by a few minutes’ rest),
wasting of the muscles, etc. (_See Embolism_).
_Causes._ These are in the main the same as those of _pericarditis_.
Weak health, exposure to extremes of weather, punctures with foreign
bodies, but above all, the rheumatic constitution are common causes.
Indeed rheumatism appears more prone to attack the serous membrane
lining the heart cavities than that enveloping it externally. One reason
for this is to be found in the great and incessantly recurring strain on
the fibrous structure of the valves, and particularly in hard worked
horses and hunting dogs in which the strain is often extreme. It has
been argued that the increased blood pressure caused by digitalis is an
appreciable cause. Its frequent connection with rheumatism is shown in
the rheumatic lesions of joints and fibrous structures seen in carcasses
dead of endocarditis.
Diseases in the muscular substance of the heart as cysts, abscess, etc.,
frequently extend to the endocardium.
Among other causes must be mentioned disease-changes in the blood. These
may act on the valves directly as in the case of lactic acid injected by
Dr. Richardson, into the peritoneum with the view of producing
rheumatism and successfully as regards the lesions of the cardiac
valves; or indirectly by determining coagulation and irritation of the
lining membrane coming into contact with the clot. The very fibrinous
and plastic state of the blood in extensive inflammations is a probable
cause of the occurrence of clots in the heart, and the frequency of such
clots in the dog has been ascribed to the plasticity of his blood
(Leblanc). The injection of pus into the blood or the absorption of
microbes from diseased surfaces will sometimes produce ulcerative
disease of the valves. The same is true as regards the germs of
omphalitis, pneumonia, arthritis and other infectious diseases.
Lafosse records certain cases of endocarditis due to extension of the
disease from inflamed veins.
_Prognosis._ Endocarditis is always attended with great danger to life,
but it is more likely to terminate in chronic valvular disease which
quite unfits the animal for useful work. Mild cases may terminate in
complete recovery.
_Treatment._ This is in the main the same as that adopted in the early
stages of pericarditis. Absolute rest is of prime importance. Laxatives,
sedatives and counterirritants are to be mainly relied upon. Belladonna
and chloroform on the chest behind the left elbow may be used. As there
is not the same danger from effusion, diuretics need not be pushed to
the same extent. Digitalis must be avoided if possible until the high
fever subsides. In infective cases, quinia, salicylate of soda, salol,
or hyposulphite of soda may be given. Later give tincture of muriate of
iron.
In rhemuatic cases, treat as for an acute attack of rheumatism. Frequent
large doses of salicylate of soda or salol, large doses of acetate of
potass and colchicum, warm clothing and counterirritants to the region
of the heart are especially demanded. (See Rheumatism.)
When clots are suspected, and when endocarditis threatens to lapse into
the chronic form, it is recommended to give iodide of potassium (horse
and ox 1 drachm, dog 5 grains, twice daily) with carbonate of ammonia or
of potass and bitter tonics. A lengthened rest after apparent recovery
is essential to avoid permanent valve lesions.
CARDITIS. MYOCARDITIS.
Definition. Rare. Complicates pericarditis and endocarditis, wounds of
the heart, and tubercular and other deposits. Symptoms. Treatment.
_Definition._ Inflammation of the muscular substance of the heart.
This is a rare affection and is necessarily limited to a small portion
of the heart’s substance, otherwise, the cardiac contractions must cease
in obedience to the general law that the normal function of an inflamed
organ is for the time abolished. It is mainly seen as a concomitant of
endocarditis or pericarditis, and extends only to the superficial
muscular layers; or it results from a wound as in the penetration of the
heart by a needle or other sharp pointed body and is then equally
circumscribed. It has been seen as a complication in infectious
diseases—aphthous fever, pyæmia, septicæmia, pneumonia and tuberculosis.
The evidences of the existence of carditis are chiefly the lesions met
with after death. 1st, The existence of abscesses in the heart’s
substance associated with polypus (Gowing, Leblanc, etc.,) or otherwise
(Reynal). Also diffuse suppuration in the heart’s substance (Puze, etc.)
2nd, Softening of the muscular substance, a state occasionally met with
when an animal has died of ruptured heart. 3d, Ulceration of the walls
of the heart as reported by Mercier in a case of endocarditis. 4th,
Transformation, and induration of the heart’s substance whether into
fibrous tissue, cartilage or bone. This last condition of the walls of
the right auricle and ventricle has been repeatedly seen in old horses,
the change being in certain cases so extensive that one is left in
wonder as to how circulation could have been carried on. Three specimens
of this kind were preserved in the museum of the Alfort Veterinary
College, Paris, and the Royal Veterinary College, London. Lafosse
records two cases of gangrene of the internal layers of muscle in
endocarditis.
The _symptoms_ are those of acute heart disease generally modified
somewhat by the precise location of the inflamed spot, and _treatment_
need not differ materially from that applied for inflammation of the
investing membranes, inner and outer, and for the infectious disease
which it complicates.
CHRONIC VALVULAR DISEASE OF THE HEART.
This, as already noticed, is a common result of endocarditis, the valves
being most obnoxious to disease in such cases. The _symptoms_ are those
mentioned under endocarditis as characterizing disease of the different
valves, such as incapacity for exertion, difficult breathing,
palpitation, irregularity or intermission of pulse, venous pulse,
abnormal heart sounds, unsteadiness of the limbs when driven, and
dropsical swellings in the limbs and elsewhere. The reader is referred
to endocarditis for particulars, it being borne in mind that these
symptoms are not in this case associated with fever.
Horses affected in this way are useless. Cattle may sometimes be
partially fattened by preserving them from all sources of excitement, by
keeping the bowels regular and by combating any paroxysms with
sedatives, such as aconite, veratrum, hydrocyanic acid, or opium, and
with digitalis.
FATTY DEGENERATION OF THE HEART.
Causes, improvement in the direction of easy fattening, inactive life,
best breeds of butcher cattle and pigs suffer. Symptoms, weak,
irregular, intermittent pulse, palpitation, unfitness for exertion,
general heart symptoms.
In addition to the fibrous and bony transformations to which the
substance of the heart’s walls is subject, a fatty metamorphosis is
frequently met with. In most cases the fat accumulates in great masses
externally, but in others the muscular tissue has to a greater or less
extent lost its natural structure and fatty granules have taken the
place of the sarcous elements. In overfed oxen the right cavities of the
heart rarely escape dilatation, and this condition is very often
accompanied by the fatty change. Virchow has shown that highbred English
pigs imported into Germany are subject to a similar affection of the
heart and of the entire muscular system. It may occur during wasting
diseases and from phosphorous poisoning.
The _symptoms_ are weak, irregular and intermitting pulse, palpitation
on excitement, weakness of the heart’s impulse in the intervals,
incapacity for exertion, sighing, Cheyne-Stokes respiration, loss of
control over the limbs when hurriedly driven and tendency to dropsy. It
is often associated with dilatation, is rarely distinguishable from it
in life, and is equally beyond remedial measures. The feeding animals
most commonly affected can usually be fattened if removed from all
sources of excitement. In case of phosphorous poisoning improvement
takes place when the poison is stopped.
NEW FORMATIONS IN THE HEART. TUMORS. PARASITES.
Glanders, abscess, melanosis, tubercle, polypus, nœvus,
parasites—echinococcus, cysticercus tenuicollis, cysticercus
cellulosa, trichina, sarcocyst, filaria immitis, strongylus subulatus,
strongylus vasorum.
1st. =Deposits of Glanders.= In many cases of glanders and farcy in
horses the specific product is deposited in the heart as well as in
other internal organs. Such deposits are small but numerous,
infiltrating the muscular tissue; their cut surface is dry, finely
granular and of a yellowish white color.
2d. =Abscesses= are sometimes formed in the heart from the colonization
of microbes from suppurating surfaces.
3d. =Cancer of the heart= has been noticed chiefly in dogs by Leblanc.
It occurs only consecutively to cancer in other parts of the body, yet
it has sometimes acquired considerable dimensions and interfered
materially with the movements of the heart.
4th. =Melanosis= of the heart has been repeatedly noticed in the horse.
Some if not all such cases should be classed with cancers, as these
internal deposits of black coloring matter in solipedes, have, in our
experience, mostly possessed malignant characters, though they are
usually simple tumors as developed in the skin of the horse. These black
masses usually project beneath the pericardium or endocardium.
5th. =Tuberculous deposits= have been met with in the substance of the
heart in cases in which the lungs or other organ were the seat of this
disease.
6th. The _fibrous growths_ or _polypi_ due to the deposition and
organization of fibrinous material from the blood have been referred to
under _endocarditis_.
7th. Gamgee reports the existence of a vascular tumour of the right
ventricle of a horse in the museum of the Turin Veterinary School. It
consisted of varicose veins ramifying beneath the endocardium which in
its turn was healthy.
8th. The =parasites found in the heart= are various, _a._ One, the
=Echinococcus Veterinorum=, has been repeatedly found in the substance
of the heart or projecting from its inner or outer surface. _b._
Another, the =cysticercus tenuicollis=, has been met with in the
pericardial sac of a calf (Reed). _c._ A third, the =cysticercus
cellulosa= infests the muscular structure of the heart of measly pigs.
_d._ The heart like other voluntary muscles of hogs occasionally
contains =trichina spiralis=. _e._ =Rainey’s cysts= (=sarcocysts=) are
microscopic ovoid bodies usually found in the hearts of oxen and other
animals. _f._ A round worm, =filaria immitis=, first described as
filaria papillosa hæmatica by Delafond and Gruby, lives in the blood of
the dog, is one millimeter thick by fifteen to 30 centimeters long. It
may obstruct the pulmonary artery (Serres) or the mitral orifice
(Silvestre). It may cause various nervous disorders and even sudden
death. Its mode of entrance is unknown. _g._ =Strongylus Subulatus=, 1
to 2 mm. long by 70 to 90 μ. in thickness was found in numbers in a
nodule of a dog’s lung, and the dorsal vein of the penis of a dog
(Leisering). _h._ =Strongylus Vasorum= in the right auricle and
ventricle of a dog, in pea-like blood clots. It is 14 to 21 mm. long by
1 m. in thickness (Serres).
RUPTURE OF THE HEART.
In the lower animals ruptures of the heart have been observed as the
result of (a) extraordinary exertion, (b) violent concussion, and (c)
ulceration and degeneration. The rupture of the fatty heart in the lower
animals is not common.
=Rupture during severe exertion= occurs in the perfectly healthy heart.
The ruptures take place in the weakest point, and most commonly in the
fibrous ring which encircles the base of the heart and attaches the
great aorta. This is occasionally seen to happen in very spirited horses
during a severely contested race or when a heavy load is being dragged
up hill. Percivall mentions the case of a horse at a Woolich racing
meeting, which had just lost a heat by half a head and which died just
after passing the winning post, with ruptured right auricle.
Cases occur during coitus (Hering), tympany (Anacker, Mayer, Perdan) and
operations (Stockfleth).
=Rupture from Concussion= more frequently implicates the muscular walls
which have not the same power of resistance when they receive the blow
in a relaxed condition. Parker met with a case of rupture of the right
auricle at its base or at the line of its union with the ventricle. The
subject was a pony which ran away down hill and struck his right
shoulder violently against a cart wheel. In other instances the rupture
takes place in the posterior vena cava, and particularly if its walls
have been the seat of disease. Gamgee found rupture of the commencement
of the azygos vein in oxen killed by pithing in the slaughter houses of
Ferrara, and Professor Maffei subsequently found that out of 3095 oxen
killed in these abattoirs 57 had this vein ruptured. Gamgee’s
explanation of the occurrence is that “the instant the animals are
pithed the walls and contents of the chest become paralyzed, the heart
becomes an inert bag filled with fluid, the jerk of which as the animal
falls, causes rupture of the containing vessel at its weakest part and
this is in truth the vena azygos whose walls are thin and only protected
externally by the pleura.” Hertwig gives other cases resulting from
falls.
=Perforation of the heart from ulceration= is sometimes seen in cows
when sharp pointed metallic bodies from the stomach make their way into
its substance. An alleged case of rupture following ulceration of the
walls of the right ventricle is recorded by Gaullet.
Inflammation, softening, fatty and calcareous degeneration, dilatation,
atheroma, and the presence of parasitis in its substance render the
heart more friable and predispose to rupture.
_Lesion._ The rupture is often at the fibrous ring encircling the aorta
or pulmonary artery; in other cases in the muscular wall of ventricle or
auricle.
_Symptoms._ Death may be practically instantaneous. If delayed there is
hurried breathing, anxiety, weakness, pallor of the mucous membranes,
staggering, trembling, vertigo, stupor, and convulsions.
DISEASES OF ARTERIES.
The chief morbid conditions seen in arteries are: Wounds, inflammation,
thrombosis, embolism, degeneration, and aneurisms. Wounds belong
essentially to surgery.
ARTERITIS. EMBOLISM.
Internal and external arteritis. Thrombosis, from inflammation.
Embolism. Bruising. Stretching. Ligature. Lesions. Extension of clot,
color, consistency, adhesion, lamination. Composition of clot.
Condition of vessel. Changes in muscles. Causes: muscular tension,
embolism. Heart clots, venous clots. Infecting debris. Symptoms:
paresis or paralysis on exertion. Local suffering, tenderness, firm
swollen artery, derangement of nutrition and function, atrophy.
Chronic arteritis: Atheroma. Changes in serosa. Fibrous thickening,
atrophy, dilatation. Strongylus. Treatment: rest, anodynes, alkalies,
massage.
_Inflammation of arteries_ has been divided into _external_ and
_internal_ arteritis, according as it affects the fibrous sheath of the
artery or its inner lining membrane.
In =external arteritis= the exudation of lymph often forms a protecting
layer around the vessel, while the inner coats continuing sound the
current of blood remains unimpaired. Even when suppuration takes place
in the vicinity of a large artery, that vessel may pass through the
center of the abscess and convey the blood as freely as before. The
nutrition of the vessel thus detached from the surrounding tissues is
maintained by its accompanying nutrient artery, though if the abscess is
large there is danger of a deficient supply. The frequent presence of
such arteries traversing an abscess should make the surgeon careful how
he breaks down the bright pink bands occasionally seen to stretch across
such cavities.
=Internal arteritis=, or _inflammation of the internal coat of an
artery_ is incomparably more serious and mainly because it determines
the coagulation of the contained blood and consequent _plugging_ of the
vessel. This is but one manifestation of the general law that in
inflamed tissues the fibrine-forming elements are produced in excess,
and when blood comes in contact with these it tends to coagulate
(thrombosis). On the other hand the inflammation in the arterial coats
may ensue from the pressure of a blood clot formed in the veins or heart
and carried on with the current until it reaches an artery too small to
admit it (embolism).
The inflammation may be confined to a limited space as when an artery is
bruised, stretched so as to tear through its inner coats, or interrupted
by a ligature. It may on the other hand be diffused over a greater
extent of the vessel, and in some cases two inflamed portions are
separated by intervals of sound artery.
=Anatomical features of the inflamed artery.= In active inflammation of
the internal coats of an artery, it contains blood clots, and if the
inflamed surface is not very limited in extent the vessel is completely
plugged and the clot forms up to its nearest transverse branch on the
cardiac side, precisely as if the artery had been tied. The resulting
clot is sometimes tubular, so that an impaired circulation is still
carried on. The clot varies in length according to the extent of vessel
inflamed, or the distance from the inflamed spot to the nearest
diverging branch. The clot is usually fusiform in outline and is firmly
attached throughout more or less of its diameter, and occasionally so
firmly that it is all but inseparable from the serous membrane. The
narrowed ends of the clot mostly float free in the liquid blood and
portions from the end most distant from the heart will sometimes get
detached, and by blocking up smaller arteries give rise to new centres
of disease. This is a true instance of _embolism_ or _plugging_.
The clot has nearly always a grayish or yellowish white color in the
larger vessels, such as the posterior aorta, and an uniform pink or red
streaked with yellow in the small. It is possessed of great firmness and
elasticity. That portion of the surface which was not attached to the
arterial walls, during life, is clear, smooth and glistening, while the
portion which adhered to these walls is rough, irregular, and broken
into shreds. It is usually composed of concentric layers showing its
mode of formation.
Clots of this kind analyzed by M. M. Lassaigne and Clement were composed
of water 74 parts; fibrine and albumen 25 parts; and alkaline salts 1
part.
The vessels filled by these clots are very irregular in their outline
being thick and bulging at one point and thin and constricted at
another. The outer coat is rarely the seat of morbid change, though it
sometimes shows branching redness and thickening from exuded lymph. The
internal coat where the clot was attached is intensely and unnaturally
red, and a rough granular surface has given place to the healthy, smooth
glistening appearance. In old standing cases the clots can only be
separated from such surfaces by dissection with the knife. Other
portions of the surface than those to which the clot adheres are usually
smooth and polished, though rough granular and injected patches are
sometimes met with independently of clots.
The muscles formerly supplied with blood by the obstructed arteries are
pale, discolored, unnaturally firm, and if some time has elapsed since
the plugging their fibrillated structure is made out with difficulty.
_Causes._ The causes of arteritis are often obscure. Goubaux conceived
that it was frequently determined by extreme muscular tension. In
support of this view he adduced the facts that it has been mainly
observed in the horse, in which such stretching of the muscles is
greatest, and that its most common seats have been where the muscles and
vessels are most liable to stretching. Thus it is frequent in the
posterior aorta towards its termination or in other words where the
adjacent muscles (psoæ) are very liable to laceration from slipping
backward or from efforts to disengage the limbs when fixed in soft
ground; the femoral and auxiliary arteries are likewise frequent seats
of inflammation and are likely to be overstretched when the limbs slip
outwards.
=Embolism= or =Plugging= of the arteries must be accepted as another
cause. This is referred to under _endocarditis_, as an occasional
consequence of the detachment of clots and fibrinous substances from the
internal membrane of the heart. The detached mass in this case passes
from the heart into the aorta and thence through its divisions until it
reaches a vessel too small to receive it, when it is at once arrested
and determines inflammatory action in the plugged vessel. When arrested
in some soft organ such as the lungs, liver or brain the resulting
inflammation often gives rise to extensive suppuration and abscess. In
other situations its effects may be confined to inflammation, the
shutting off, of blood from particular parts, the impairment or loss of
their function and nutrition, and finally atrophy and degeneration.
But the heart is not always the primary source of such clots. Virchow
and others have demonstrated by _post mortem_ examinations in cases of
plugging and by a number of experiments on the lower animals, not only
that such clots may have their place of nativity in some distant and
diseased part of the body and proceed in the veins to the heart, and
thence through the arteries to other distant parts of the body where
they plug the vessels and induce a train of morbid changes; but that
such embolism arteritis and abscesses can be produced at will by the
introduction into the circulation of solid and insoluble (infecting)
bodies. Fragments of decaying and suppurating tissue and the elements of
tubercle and cancer may be thus equally carried onward in the current of
the circulation, and reproduce themselves at those points where their
course is arrested. This is a mode in which secondary deposits of these
morbid matters are determined. Embolism and arteritis in the body and
limbs occurring in this way necessarily have their point of departure in
pre-existing disease of the lungs. The clots loosened from the
capillaries or veins of the lungs are carried through the left side of
the heart into the arteries of the body at large to be arrested in some
of the smaller vessels. I have seen plugging of the digital arteries of
the hind limbs, to occur in this way in a horse that had been suffering
from inflamed lungs.
Microbes and toxins may pass harmlessly through healthy parts, including
the pulmonic circulation, to establish colonies and embolism beyond
where the tissues have become debilitated. Thus Gamgee records a case of
embolism of the anterior mesenteric, right external iliac and right
femoral arteries, supervening on an attack of strangles.
_Symptoms of acute arteritis._ These consist largely in impaired
muscular power in the part, indications of acute local suffering, such
as trembling and tenderness to the touch, if the obstructed vessel lies
within reach it can be felt as an exquisitely tender cord-like mass, and
the limb on the distal side of the embolism and dependent on the
diseased vessel for its blood supply is anæmic and cold. In the distal
portion of the embolic artery and its branches pulsation has ceased. If
the lesion is extensive there may be more or less fever, but a limited
arteritis in a small vessel may escape this complication. If the disease
is of long standing there is atrophy of the tissues formerly supplied by
the embolic vessels. The secondary derangement of nutrition and function
are as varied as the organs affected and will be noted below in the
special article on thrombosis and embolism.
=Chronic arteritis.= =Atheroma.= This is an indolent inflammation
supposed to result mainly from strain and overwork, and manifested by
thickening and clouding of the serosa, with cell proliferation,
softening and fatty degeneration. The diseased substance becomes soft,
pultaceous, slightly greasy, and under molecular degeneration it breaks
up and is even in part washed on in the blood stream. Other
degenerations may occur in the inflamed walls of the artery. The exudate
may become organized, constituting fibrous thickening. It may become the
seat of calcareous degeneration. It may yield to the blood pressure,
becoming slowly attenuated (atrophy), and even dilated (aneurism by
dilatation). As a cause of chronic internal arteritis in the horse
should be named the presence in the vessels of the larva of the
strongylus armatus. The posterior aorta and anterior mesenteric artery
which are the most commonly infested by these parasites are frequently
attenuated, dilated and calcified in this connection.
_Treatment._ Acute arteritis should be treated like any other local
inflammation, by rest, soothing applications (fomentations, astringents,
icebags), and alkaline salts. It has been proposed to manipulate the
affected artery and contained thrombus, but this can only tend to block
the smaller arteries farther on, and perhaps with even more injurious
results. The liberal use of alkalies on the other hand, if effective in
dissolving any portion of the clot, returns this to the blood stream in
a condition that will not endanger further embolism. The agents usually
employed are carbonates of ammonia, potash or soda, and iodide of
potassium.
THROMBOSIS AND EMBOLISM.
Definition. Thrombosis—clotting in the vessel. Embolism, blocking
of the vessel. Thrombus may form in any bloodvessel. Embolism
occurs in arteries. Clot follows the blood current. Causes of
clotting—fibrinogen, paraglobulin, fibrine ferment; foreign
bodies; parasites; air; blood that has been exposed, transfusion;
ærial germs; disease germs; chemical coagulants; high and low
temperatures; breaches of endothelium; congestion or inflammation
of the serosa; stasis of blood and extension of clot; ligature
near a branch vessel: deoxidation and carbonization of blood,
marasmus; neoplasms; traumas of the vascular coats. Infarction,
causes of blocking; disintegration of clots, softening,
liquefaction, ulceration, action of microbes; excess of white
globules; air; fat; parasites. Pathogenesis; complete occlusion of
vessel; infarction; sequestrum; collateral circulation; embolism
of external iliac or femoral artery; effects on pulse; during
rest; atrophy; lameness comes on with exertion; disappears under
rest; circulation inadequate to sustain active function. Embolism
of internal iliac artery; effect on pulse; on tail and pelvic
organs. Embolism of axillary artery; effect on pulse, action,
nutrition. Embolism of mesenteric artery; verminous; effects on
innervation and circulation; spasms, congestions, paresis;
involution. Treatment: expectant; alkalies; gentle exercise, time.
_Definition._ =Thrombosis= is the blocking of a blood vessel by a clot
formed in its interior by the deposition of layer above layer on its
inner coat.
=Embolism= is the blocking of a bloodvessel by a clot or other solid
body formed at a distant point of the circulation floated on in the
blood stream, and arrested when it reaches a vessel too small to
transmit it.
A _thrombus_ may be formed at any point of the circulatory apparatus
(heart, arteries, veins) whenever the conditions are such as to
determine coagulation of the blood. An _embolism_ on the contrary is a
disease of the arteries since in these the blood current, proceeding
centrifugally from the greater to the lesser, inevitably carries the
moving solid to a point too narrow to allow of its further progress.
Thus clots originating in the systemic veins or right heart pass to the
lungs and produce embolism of the pulmonary arteries whereas those
formed in the pulmonary vein or left heart are arrested in some part of
the systemic arteries. Clots formed in the portal vein however are
arrested in the hepatic vessels into which that trunk breaks up.
_Causes of Thrombus._ The production of a thrombus may be due to the
condition of the blood or of the vessels. The researches of Buchanan,
Schmidt, Hammersten and others show that two albuminoid elements,
fibrinogen and paraglobulin, present in the living blood, and a fibrine
ferment mainly derived from the white corpuscles in process of change or
destruction, determine powerfully the formation of fibrine and clot.
Hewson, Brücke and Lister have shown that blood may be maintained fluid
for many hours in an unimpaired vein, or turtle’s heart though it may
have been removed from the body, the important condition being that the
vein shall retain its vitality and suffer no derangement of its
endothelium. Lister has even shown that blood may remain fluid for many
hours in a sterilized glass tube which has been filled by passing the
tube carefully into such a vein without disturbing its lining membrane,
or imparting motion to the liquid. In such a case a thin film of
coagulum only, forms on the interior of the glass tube. In healthy
blood, without addition of any extraneous matter, and kept perfectly
still, the plasma and globules retain their integrity, and the former
its fluidity for a length of time. But if shed into a basin it
coagulates at once.
a. _Changes in the blood._ Contact with foreign bodies generally
determines this change and prompt coagulation. Transfixing the artery
with a needle, even a silver one, the entrance of parasites
(actinomycosis, strongyli, filaria), the presence of pus, and of certain
infectious microbes and their products, the introduction of solid
particles and even of air into the vessels, the transfusion of blood
which has been exposed to receive ærial germs, or which contains
microscopic clots, or the globules of which have become modified by
contact with a basin or other vessel, even the transfusion of
defibrinated blood may cause coagulation. The danger is always greater
if the blood is drawn from a different genus and unfitted to live in the
blood of the recipient. Disease germs are especially dangerous if
adapted to colonize the serosa of the vessel and destroy its epithelium.
A decrease of the density of the blood favors coagulation, a lowering of
one thousandth rendering it syrupy, and various chemical agents induce
or favor coagulation, thus acetic acid, valerianic acid, alcohol, the
salts of iron, and above all the salts of lime act in this way. Very
high and low temperatures throw down the fibrine as a grumous
precipitate, but the clot remains soft.
b. _Changes in the vessels._ Any disturbance or alteration of the
endothelium sets free the so-called fibrine ferment, and precipitates
coagulation. Lister found that contact of ammonia with the interior of
an otherwise living vein caused a thrombus. So in all endarteritis and
phlebitis coagulation takes place on the serosa and quickly blocks the
vessel. Even in the capillary vessels the same principle holds, and in
inflammation minute coagula (thrombi) form in the capillary network
throughout the whole inflamed area. This explains not only the capillary
blood stasis but the thrombosis of inflamed arteries and veins. In these
two latter the clot increases and extends in the direction of blood
stasis:—in the artery toward the heart as far as the next colateral
branch, and in the veins away from the heart as far as to the next
colateral trunk. On the distal side of the arterial thrombus the blood
flows off freely toward the capillaries, but on the proximal or cardiac
side it is absolutely stagnant up to the next branch through which it
can freely flow into the capillary plexus. Into this stagnant blood the
fibrine ferment, produced by the altered white globules in the clot
already formed, slowly extends until the whole has formed a firm
coagulum. Beyond this the actively moving blood carries off and dilutes
this ferment so rapidly that it can exert no appreciable effect on the
fibrine-forming elements. The principle is an important one in surgery,
as the clot formed entad of the ligature will be extensive in proportion
to the distance from the first colateral trunk, and in inverse
proportion to this clot will be the danger of secondary hæmorrhage. In
veins the same rule holds, with this difference that as the blood is
flowing toward the heart it empties the vessel on the cardiac side, and
stagnates on the distal side up to the next colateral branch. Hence it
is that a thrombus in a vein always extends away from the heart, while
that of the artery extends toward it.
Another cause of coagulation is the deoxidation of the blood and the
excess of carbon dioxide. This occurs in the stagnant blood in the
vessels and above all in the capillaries. The normal trophic changes in
the serosa, fail to take place in contact with blood in this state, and
the resulting changes in the white and endothelial cells set free
fibrine ferment and determine coagulation. Stasis of the blood from any
cause (ligature, pressure, embolism), tends to this condition and the
extension of the coagulum.
A thrombosis of marasmus has been observed in anæmic and debilitating
diseases, and apart from the microbian invasions in a certain number of
those affections, this may be looked on as due in part to the lessened
density and other changes in the blood and to the debility of the serosa
of the vessels.
The compression of the vascular walls or their penetration by neoplasms,
tumors and ulcers, is another cause of coagulation and thrombus, also a
varicose or aneurismal dilatation, with weakening of the vascular walls,
or dilatation of the heart with structural changes in the endocardium as
stated under that heading, or compression of the smaller vessels and
capillaries by an exudate in process of organization, or a similar
obliteration under the action of extreme cold. Injury to the serosa of
the vessel by stretching, bruising, laceration or section determines a
thrombus starting from the injured endothelium. In the smaller vessels
the thrombus is usually deep red from the entangling of a large quantity
of red globules, whilst in the larger arteries the greater part of the
globules pass on and the coagulum is largely buff or straw colored.
Again in obstruction in the smaller arteries, the inactive capillary
plexus and the tissue beyond are liable to become gorged with blood with
excess of red globules, from the adjacent capillary network,
constituting _infarction_, and ending in gangrene. In cases in which
this is prevented by the action of intense cold the part may remain
pale, as _white infarction_.
_Causes of Embolism._ As already stated embolism results from a detached
portion of a thrombus passing to a smaller vessel and obstructing it.
Such detachment is favored by molecular softening, liquefaction or
suppuration in the clot or beneath it, by the destructive action of
microbes, or by friction or manipulation of the obstructed vessel.
Excess of white globules (leukæmia) favors the formation of minute
coagula and embolism. Bubbles of air, globules of fat, or cholesterine
crystals block the fine pulmonary capillaries, and the debris from
atheromatous patches, ulcers, and tumors opening on the inner wall of
the artery form emboli in various parts. Finally parasites, especially
the larval strongyli in solipedes and filaria and spiroptera in dogs,
themselves obstruct the vessels and determine coagulation.
_Pathogenesis._ In the larger arteries (aorta, radical stump of the
mesenteric artery) clots (as from strangles) rarely produce dangerous
obstruction. In the smaller vessels stenosis is complete and anæmia and
gangrene are liable to occur unless the blood supply is partially
maintained by anastomotic vessels. When the embolism affects a number of
smaller arteries or capillaries in a vascular organ like the lungs, the
blood filters in from the adjacent capillaries, in which circulation is
still carried on, and this passes through the softened and ruptured
capillary walls so that the tissue is charged with globules and
constitutes a _black infarction_. In the lung this usually affects one
or several lobulettes, forming a pear shaped mass corresponding to the
distribution of the obstructed vessel. The cut surface is black, compact
and granular. The lymph thrown out around it forms an organized fibrous
sac, and the unclosed sequestrum undergoes a slow necrobiosis, blanching
and liquefaction into a pus-like fluid which is removed by absorption.
Such results are met with in the parenchymatous organs (lungs, liver,
spleen, kidneys, etc.) and less frequently in the limbs. The symptoms
will correspond to the particular organ invaded.
In the fore or hind limbs the result is usually less radical. The
vessels below the obstructed trunk are connected more or less freely by
anastomosing branches, so that the circulation in the tissues below,
though somewhat restricted, remains active enough to sustain a fair
measure of nutrition. Apart from the suffering, attendant on the
preliminary inflammation, the morbid phenomena are largely confined to
the absence of pulsation in the lower part of the limb and the inability
of the muscles to sustain active contraction.
=Chronic Embolism of the External Iliac or Femoral Artery.= In this
condition the pulsations in the digital arteries are imperceptible, if
it has been of long standing there may be obvious atrophy of the muscles
of the thigh, but when standing quietly or walking there is usually no
lameness. In continuous rapid walking and above all in the trot,
however, he soon begins to halt on the affected limb, and this rapidly
increases, the joints bending under his weight, the toe dragging and the
animal threatening to drop altogether. If stopped and allowed to rest
for ten or fifteen minutes he gradually recovers and may be led quietly
back to his stable without a sign of lameness. But if again trotted
fifty or one hundred paces the lameness develops anew and disappears in
the same way when left at rest. The circulation in the muscles is enough
for a moderate nutrition but altogether inadequate to sustain active
work.
=Chronic Embolism of the Internal Iliac Artery.= In this case the
control of the muscles of the limb may be perfect but there is some
indication of paresis of tail, bladder, rectum and anus. Impaction of
the rectum is liable to occur. By examination through the rectum the
pulsations are felt to be strong in the aorta and external iliac, but
imperceptible in the internal iliac blocked by the embolus.
=Chronic Embolism of the Axillary Artery.= Here there are the same
general symptoms, the absence of the radial and digital pulsations, the
wasting of the muscles of the forearm, and the intermittent lameness,
developed rapidly by exercise and recovering promptly under rest.
=Acute Embolism of the Mesenteric Arteries.= This will be fully treated
under the title of verminous colic in solipedes. The blocking of the
branches, usually of the anterior mesenteric artery, leads to
derangement of the innervation, congestions, spasms, involutions and
other disorders. The presence of the strongyli in the fæces, the general
symptoms of intestinal worms, and the recurrence of the indigestions and
spasms would serve to indicate the nature of the complaint.
_Treatment of Chronic Embolism._ As affecting the arteries of the limbs
the repair must be largely left to nature, and we must place the patient
in condition, favorable to such repair. Except in the early stages
absolute rest is not necessary. Gentle exercise stimulating to a freer
circulation solicits a slow enlargement of the anastomosing vessels
(arterial or capillary), and when this has reached a given stage, weak
pulsations may again be felt in the vessels beyond and the muscles will
once more stand moderate work without lameness. Alkalies and iodide of
potassium may be given to solicit solution of the clot, but this can
rarely be counted on to the extent of rendering the vessel once more
pervious. A small paddock in which the patient can move around quietly
is desirable, and in a few months a tolerable recovery may have taken
place.
Embolism in other organs must be treated on the same general expectant
method, and a considerable time is usually necessary to secure a fair
recovery.
ANEURISM.
Definition. Divisions, true, false, dissecting, arterio-venous, mixed,
traumatic, spontaneous. Causes, violence, rupture, debilitated
vascular walls, strains, stretching, force of blood current,
overloaded intestine, strongyli, contiguous inflammation, embolism,
microbian invasion of the walls, arteritis, concussion. Symptoms, soft
tumor pulsating with the heart, a double rushing sound, diagnosis from
abscess, nervous disorders through pressure, cramps, palpitations.
Treatment, when desirable, rest, moderate, laxative diet, iodides,
bromides, icebags, compression, ligature, galvano-puncture, wire
coils, injections.
_Definition._ A pulsating swelling on an artery, consisting of a sac
filled with arterial blood.
_Divisions._ =A true aneurism= (=aneurism by dilatation=,
=arteriectasis=) is a simple dilatation of the artery, the tumor being
surrounded on all sides by the distended arterial walls. It is usually
fusiform or cylindroid, but may have the form of a more or less rounded
sac.
=A false aneurism= is where the wall of the artery has been lacerated
and the blood is enclosed in an adjacent sac of condensed connective
tissue and communicates with the interior of the vessel. The same name
has been given to cases in which the inner coat only has given way, and
the middle and outer coats constitute the walls of the sac. From its
liability to extend and separate the tissues this is further known as a
=dissecting aneurism=. =Arterio-venous aneurism= in which an intervening
sac communicates with both artery and vein, has been found in the human
subject.
=Mixed aneurisms= are those in which a dilatation of the artery is
complicated by the presence of an outside pouch.
A distinction has also been made according to origin into _traumatic_
and _spontaneous_. The former is of necessity _false_, whereas the
latter may be _false_ or _true_.
_Causes._ Apart from rupture of the arterial coat by direct violence,
the common cause is a debility and loss of resistance in the walls. In
horses a far larger proportion of aneurisms are deep-seated than in man,
in whom forced muscular effort is less common. Yet even in horses the
most common seat—the posterior aorta—is liable to overstretching and to
inflammation and softening by reason of contiguity to dorsal sprains.
The posterior aorta too, from its size and direction on leaving the
heart, is in the direct line of the strongest blood current, and under
long continued, forced and violent efforts (as in racing, hunting, and
heavy uphill draughts), has to sustain an extraordinary blood pressure.
Bouley claims as an additional cause the pressure of a loaded colon.
This is also the point of all others where the vessels suffer from the
presence of the larval strongyli. From whatever cause originating,
congestion of the arterial coats leads to more or less attenuation,
softening or lack of cohesion, and they tend to yield under the blood
pressure. Similar conditions operate on the smaller vessels in different
parts of the body, and thus overstretching, contiguous inflammation, and
excessive blood pressure cause such lesions in the chest, trunk and
limbs.
Another cause is embolism which by blocking an artery at once increases
the tension in the vessel on the cardiac side of the obstruction, and
develops inflammation in the arterial coats, robbing them of their
cohesion and resisting power.
Eppinger has shown the importance of infectious microbes in weakening
the arterial walls and predisposing to aneurism.
The larval strongylus armatus already referred to is the most potent
factor in solipedes. They accumulate in the anterior mesenteric artery,
leading to clotting of the blood, inflammation of the serous coat, and
dilatation, so that in some verminous localities nearly every old horse
shows a lesion of this vessel.
All forms of arteritis, and disease of the vascular walls which entail
attenuation or weakening, predispose to aneurism.
Of direct traumatism may be mentioned an aneurism of the arch of the
aorta in a horse struck by a wagon pole, during a sharp descent (Jacob),
and two with aortic aneurism after violent blows on the back with shafts
of wagons.
_Symptoms._ An aneurism within reach of the hand is to be recognized
primarily by the pulsation of the swelling synchronously with the beats
of the heart, and by a double rushing sound with each beat of the heart,
observed on auscultation. An abscess over a large artery lying on a bone
may pulsate but it is to be distinguished by the presence of a single in
place of a double rushing sound on auscultation, by the possibility of
causing more or less complete collapse under pressure, and by the
history of an active phlegmonous inflammation followed by softening
which steadily extends from the centre of the previously dense mass. In
a case of aneurism of the gluteal artery of the horse reported by King
and in one observed by the author the symptoms were unmistakable. Other
similar examples on the popliteal artery and other failed to be
recognized during life though attended by lameness.
In internal aneurism the symptoms are mostly indefinite. Ollivier found
tympany and vomiting in a goat which at the necropsy showed an aneurism
of the anterior aorta as large as the closed fist and enclosing a sewing
needle. A more careful diagnosis should have detected a retarding of the
maxillary pulse and a double rush over the carotid with each beat of the
heart. Pressure on the vagus doubtless led to the symptoms noticed. In
aneurism of the posterior aorta there have been noticed a loss of life
and energy, dulness, lack of appetite and stiffness of the loins. Torpor
of the bowels, expulsion of fæces with effort and groaning, intermittent
colics, lameness in one or both hind limbs, and finally cramps in the
hind limbs, and palpitations. In one case Maillet was able to reach the
aneurismal tumor through the rectum.
_Treatment._ The treatment of internal aneurism will be seldom called
for in the lower animals, as the disease is seldom diagnosed, is beyond
reach of mechanical applications, and survival without certain power of
endurance would seldom be desirable. In some valuable breeding animals
it might be worth while to seek prolongation of life. The most promising
measures are absolute rest, and low, non-stimulating diet of a laxative
nature and in small bulk. Iodide of potassium is often useful in man,
and although in the lower animals there is not the excuse of specific
disease, yet the rest to the circulation and reduction of blood tension
are not to be undervalued. Bromides may be given with the same object.
Other measures applicable only to aneurisms, within reach and
essentially of a surgical nature include: Ice bags and compression. The
compression should as a rule begin at the distal end of the limb and be
concentrated by suitably shaped pads on the swellings. Ligature of the
diseased artery above or below or both above and below the tumor.
Galvano-puncture of the aneurism with the object of inducing
coagulation. The introduction of coils of fine wire through a hypodermic
needle with the same object in view. In both horse and dog the
persistent compression with the finger seconded as it is by the
plasticity of the blood has succeeded in checking the flow from large
arterial orifices, and offers great encouragement in the application of
this measure to aneurisms. The injection into the sac of tincture of
chloride of iron with firm compression to prevent motion of the blood is
another available resort.
ARTERIO-SCLEROSIS.
Fibrous thickening of the arterial coats and calcification are well
known lesions in the posterior aorta particularly of the horse.
Commencing in congestion or degeneration which lessens the resistance of
the vascular walls, the condition tends to dilatation, and if this is
checked by compensatory thickening, the condition of sclerosis is
induced. The combination of a slight fusiform dilatation and fibrous or
calcareous sclerosis is well known in the posterior aorta of the horse.
Unless it advances to marked aneurismal dilatation the condition is not
often recognized. If diagnosed, rest and quieting of the circulation are
especially indicated. Should it occur in other parts of the body the
symptoms would correspond to the organ invaded.
ANGEIOMA. CIRCOID ANEURISM. ANEURISM BY ANASTOMOSIS. VENOUS TUMOR.
NŒVUS.
These are forms of dilatation and elongation of the network of small
arteries, or veins, and even of the intervening capillaries. In man
these constitute the unsightly red patches and swellings that appear on
the face and hands. In animals with dark skins and hairy covering they
can only be recognized by the swelling, the feeling as of a bag of worms
when the hand is passed over it, and by the rushing sound when
auscultated. The trouble is usually subcutaneous and is essentially a
surgical one. The most promising treatment is by persistent pressure, by
electric current supplementing the pressure, by electro-puncture, and by
injections of muriate of iron. When the nœvus is not too extensive a
double thread drawn by a needle through beneath the tumor at short
intervals, then cut and each point tied separately, so as to completely
stop circulation is most effective.
PHLEBITIS.
Divisions, traumatic and idiopathic. Causes, punctures, defective
blood supply in walls, debile coats, thrombus, infection,
overstretching, injury or disease of serosa, irritants in blood,
microbic infection. Lesions, exudation, cell growth, breaches in
serosa. Adhesive phlebitis, desquamation, granulation, occlusion.
Suppurative phlebitis, infection, pyæmia, erysipelas, metritis,
ulceration, neoplasms, phlebolites. Symptoms, local, firm, corded,
swollen vein, extends entad, venous congestion, dropsy, gangrene,
diagnosis from lymphangitis. Fever, venous congestion in vicinity.
Treatment, germicide, rest, cold, antiseptics, blisters.
Inflammation of veins as seen in the lower animals has usually been a
sequel of bleeding and is hence a purely surgical lesion. Animals as
well as man however are subject to idiopathic phlebitis which as
affecting the deeper seated veins may be held to be a medical subject.
The _causes_ of =idiopathic phlebitis= are varied. Injury to the walls
like the punctures made in bleeding; if they result in the exposure of a
raw, and above all an inflamed, surface to the blood, tends to the
formation of a thrombus, and of local inflammation. Even the
inflammation of the outer coat tends in the same way to thrombosis and
phlebitis, and the experiment of Nicasse showed that the dissection of
its sheath from a vein, thus robbing it of its vascular and nervous
supply promptly induced coagulation of the blood in the denuded part.
The debilitated or devitalized walls evidently give off fibrinogen and
fibrine ferment in amount that is incompatible with the maintenance of
fluidity. All other forms of direct injury to the veins, leading to
disturbance of the endothelium or cell enlargement or exudation in the
intima, will operate in the same manner. Sometimes as in puerperal
phlebitis the inflammation extending from the adjacent tissue to the
walls of the veins, determines thrombosis, and the invasion by pus
microbes determines suppuration. Bruises, overstretching, pressure with
overdistension, and the circulation in the blood of irritant matters may
lead to changes in the wall, thrombus, and inflammation. Such irritants
may be septic or other bacterial products, or they may arise from the
colonization of bacteria on or in the venous coats with the same final
result.
The _lesions_ in the vein are often primarily of the nature of exudation
and cell growth in the coat, without at first any change in the serosa
or endothelium. Later the changes implicate those, thrombosis follows
and one of various ulterior processes.
In =adhesive phlebitis= which is most frequent as the result of purely
mechanical injury, the endothelium is desquamated and granulations from
the denuded surface extend into the clot and finally occlude the vein. A
recovery takes place by the organization of this new product and the
contraction of the vessel into a simple fibrous cord.
In =suppurative phlebitis=, which occurs especially in connection with
infection (erysipelas, metritis), the inflammation, though starting in
the same way in the vascular coats, advances rapidly to suppuration, and
the intima, lying in contact with the resulting thrombus may become
itself the seat of the suppurating process. Cases of this kind are
almost of necessity in the nature of an infection and the danger is
greatly enhanced. Small abscesses formed in the vascular coats may burst
into the vein and passing on with the blood produce general infection
(pyæmia). Even when the pus enters the vein at a point covered by the
thrombus, it may escape by the partial loosening of the clot from the
serosa, or through the interior of a honey-combed coagulum and thus lead
to general infection. This is especially liable to follow in erysipelas
and metritis, in which the tendency as in the solid tissues is to
diffuse suppuration without any investing limiting membrane. There are
other forms of bacterial colonization of the vascular walls, of
ulceration, and of the extension of morbid growths into or through the
venous walls, producing inflammation more or less localized, and leading
or not to general infection. The presence of phlebolites in the vein is
a conceivable source of phlebitis, though no such case has been so far
recorded.
The _symptoms_ in localized cases of simple adhesive phlebitis may be
purely local. The vein if within reach may be felt like a firm, rounded
cord, which extends in a direction from the heart. If there are no free
anastomosis with neighboring veins on the distal side of the thrombus,
venous congestion and dropsy of the tissues ensue, and in some cases
moist gangrene. When, however, such anastomosis is abundant these
peripheral symptoms may be absent, especially if the affected vein
returns blood from a higher level than the heart, and then the symptoms
are confined to the vein and its immediate surroundings. From
lymphangitis which shows similar hard cords, it is distinguished by the
absence of an extended network of diseased vessels, by the lack of a
diffuse, doughy swelling, and by the fact that the adjacent lymph glands
remain free from inflammation, pain and swelling. In the more extended
cases there is fever, which may be of a very high type and may merge
into pyæmia. In deep-seated cases it may be difficult to identify the
disease, but it may be suspected if in the course of erysipelas or
metritis there is a sudden increase of fever with pain and swelling, and
distension of veins leading into the part.
The _treatment_ of idiopathic phlebitis is largely that of the
particular infecting disease on which it depends. In simple cases due to
trauma absolute rest and the application of ice and antiseptic
solutions, or where these cannot be applied, the use of antiseptics
internally, will be indicated. Hyposulphite of soda and sulphide of
calcium are especially indicated. From the early days of veterinary
medicine, flying blisters of Spanish flies, over the inflamed vein or
veins have proved very successful, and under the lead of Nonat the same
was in 1858 and since adopted with gratifying success in the human
subject. Abscesses formed in accessible situations should be promptly
opened and treated antiseptically, and swelling of the affected part
should be checked by elevated position, or if that is impossible, by a
smoothly applied bandage. Rubbing and active movement are dangerous, as
tending to detach clots which float off to start new emboli and
inflammations in the lungs.
VARICOSE VEINS. DILATED VEINS WITH ALTERED WALLS.
Rare in animals. Angioma Varix. Superficial. Deep. Causes, obstructed
circulation, compression, congestion. Symptoms, enlargement,
elongation, tortuosity of veins, stiffness, lameness, complications.
Treatment, compression, coagulants, cauterization, ligature.
Varix is not so common in the lower animals as in man, and is generally
observed in the superficial veins, so that it comes under the domain of
surgery. In the form of angioma, which affects the veins, there is
extensive dilatation and elongation, but it involves a large group of
connecting and anastomosing veins, whereas varix usually affects but one
or a few connecting vessels. In the horse the most common seat of varix
is in the saphena vein, as it passes obliquely over the inner side of
the hock. Less frequently it appears on the flank or other superficial
part. In cattle the mammary veins are the most frequent seat. Varices,
however, occur also in deep-seated veins and in connection with normal
venous plexuses, as in the buccal, palatal, and peneal. Anatomically
they may be simple fusiform dilatations, as in the saphena; dilated,
elongated and tortuous, branching trunks, as in the mammary veins; or
dilated veins with thickened walls and pouch-like dilatations.
_Causes._ There is usually some obstruction to the circulation through
the affected vessel, it may be by pressure by a tumor, or a constrained
position, obliteration by a phlebitis and thrombus, extension of
inflammation from adjacent organs, increased blood pressure by
gravitation, or from diseased heart or lungs. Whether from the extension
of contiguous inflammation, from external pressure, or from blood
tension, the morbid process has much in common; the circulation and
nutrition in the vascular walls are interfered with, degenerations set
in (softening, fatty, connective tissue), which predispose to dilatation
under the blood pressure. The pouch-like dilatations of the jugular
consequent on bleeding, are essentially traumatic. The impaired
innervation which lessens the resistance of the vascular walls is not to
be forgotten. Varix of the saphena is usually an attendant or sequel of
tibio-tarsal synovitis, and is the result of combined pressure and
congestion. Mammary varices are manifestly connected with the congestion
and exudations which affect the udder and environment at the time of
parturition, or with a casual mammitis.
The _symptoms_ in superficial vessels are visible enlargement, and often
elongation and tortuous direction of the vein or veins, with or without
tenderness. Deep-seated varicosities may be attended by stiffness of the
part and a halting in progression with or without pain on pressure.
These cases may recover spontaneously as the result of adhesive
phlebitis, or they may develop phlebolites, suppuration, inflammation,
ulceration and hæmorrhage.
_Treatment._ Superficial varices have been treated by compression,
cauterization, coagulating injections, and ligature. It is not often
that interference is demanded but in such cases, pressure with elastic
bandage having failed, ligature with antiseptic precautions is
indicated.
PHLEBOLITES. CALCAREOUS BODIES IN THE VEINS.
Nature. Location. Mode of formation. Calcareous plates in two inner
coats. Phlebotomy. Altered sanguification. Treatment. Extraction.
Calcareous bodies have been repeatedly found in the veins of man and
several observations of the same kind have been made in the horse.
Spooner found them in the abdominal veins and Simmonds in the jugular.
Much difference of opinion has existed as to the mode of formation of
these bodies whether by calcareous deposit in a coagulum or by
degeneration of a neoplasm in the vascular wall. Andral held the latter
opinion, and Tiedemann and Cruveilhier found the bodies connected to the
inner coat of the vein by a fine membrane. Morton’s cut of one of
Simmonds’ specimens (Calculus Concretions) shows a structure in
successive layers having their centre at one end, evidently
corresponding to a former connection by pedicle. Cornil and Ranvier says
“sometimes there are seen in chronic varices, calcareous incrustations
in the form of plates, nodules or spheres with concentric layers ...
calcareous infiltration is seen in the form of spheres or phlebolites in
the varicose diverticula. An extensive calcareous induration several
centimetres in length, is also sometimes observed, the vein being
transformed into a calcareous tube with the ramifications also varicose.
The calcareous plates of the vein are developed in the fibrous and
internal portion of the middle coat. At the beginning they consist of
granules deposited in the fasciculi of the connective tissue or between
them; these soon unite and form transparent plates with granular striæ.”
Phlebolites in the jugular suggest a connection with the pouch-like
dilatations, and transformations in the vascular walls that have been
subjected to phlebotomy. It is probable however that there is usually a
morbid condition of sanguification and nutrition which predisposes to
their formation. In Simmonds’ case the jugular was impervious below the
bodies, there was hepatitis and arthritis of the fetlock joint.
When recognized during life these may be extracted with due antiseptic
precautions. If the vein can be dispensed with it may be ligatured above
and below, if not an attempt may be made to preserve it, extracting
through a clean cut longitudinal incision and securing as perfect
coaptation of the edges of the wound as possible.
HÆMORRHAGE.
Arterial, venous and capillary hæmorrhage belong almost exclusively to
the domain of surgery. Internal hæmorrhages will be considered in
connection with the organs in which they take place.
HÆMOPHILIA.
Definition. Causes, lack of plasticity of the blood, thin walls, blood
tension, cardiac erethism, hypertrophy and neurosis. Sex. Heredity
through the female. Treatment, depletive, styptic, astringent.
Transfusion.
This is a constitutional infirmity, usually hereditary and characterized
by the occurrence of profuse and continuous bleeding as the result of
otherwise insignificant injuries or even apart from any recognizable
lesion. It has been attributed to a slow coagulation of the blood, but
at the start of a hæmorrhage the blood is rich in corpuscles and
coagulates firmly. It has also been ascribed to extreme tenuity of the
vascular walls, but this has only been met with in a certain proportion
of the cases. Another potent factor is a permanent over-filling of the
bloodvessels (Immermann, Delafield, Prudden). The same writers attach
importance to cardiac erethism, cardiac hypertrophy, and certain
neurotic influences which temporarily increase the habitually congestive
diathesis. In man the majority of victims have been males, perhaps
because most subject to traumatisms. On the contrary the hereditary
transmission is mainly through the female members of the family. The
families are very prolific, a condition counterbalanced by the death of
the majority of the victims at an early age. Among the lower animals it
has been observed in horses consequent on castration (Siedamgrotzky,
Kohne, Friedberger and Fröhner), setoning (Kohne, Dieckerhoff), and an
ulcer of the leg (Kohne).
_Treatment_ consists in combating plethora and constipation by saline
purgatives. The subject should be carefully protected from injuries.
Locally use styptics such as matico, muriate of iron, tannin, alum with
pressure. Internally ergot, lead acetate, iron chloride, tannin, alum,
or muriate acids. Transfusion is a dernier resort.
DISEASES OF THE BLOOD.
Obscurity of blood changes. Red globules, biconcave, embryonic.
Source. Escape of immature red globules. White globules, eosinophile,
neutrophile, uninuclear, multinuclear, lymphocyte, granular amœboid,
strap-nucleated. Conditions of increase. Relation to microbes and
their products. Blood plates. Destruction of red globules in the
liver. Numbers in animals, in different vessels and conditions.
The blood is the common medium through which all nourishment is conveyed
to the tissues, all material to the glands for secretion, or
transformation, and all effete matter to the various emunctories for
elimination. It is beside the carrier of oxygen for the respiration of
the tissues, and the seat of changes, as yet little known, effected
through the white globules. The activities of the various processes,
carried on by the fixed tissue cells and nuclei would suggest, that any
disease or derangement of these processes would be at once cognizable in
changes shown in the blood. Yet so perfect is the balance of
sanguification and elimination on the one hand, and of the remaining
vital processes on the other, that it has hitherto been impossible to
detect in the blood such changes as would identify the great majority
with morbid processes. Some morbid changes are however recognizable and
it is important that the significance of these should be known.
The blood is a liquid, consisting of a plasma holding in solution serum
albumen, serum globulin, fibrine-forming elements, sugar, urea, salts,
and a variety of other soluble bodies, and floating a series of
semi-solid organized bodies, the red and white globules.
The red globule is however seen in two distinct forms. 1st. The
biconcave disc, non-nucleated, containing a colorless stroma, and the
coloring matter—hæmoglobin. 2d. The embryonic red globule, large,
nucleated and rarely biconcave. The latter is found in the blood of the
fœtal man or animal and persists to a slight extent for some time after
birth. These are believed to be formed from the embryonic cell and from
the cells of the embryonic liver, spleen, and marrow, whereas after
birth they are derived from the marrow cell, and in healthy conditions
pass the nucleated stage before they escape into the blood. In
pathological anæmia and after severe hæmorrhages they escape more
rapidly, probably from both spleen and marrow, and appear in the blood,
even of the adult, of the gigantic size and nucleated appearance of the
embryonic red globule.
The white blood globules (leucocytes) are spherical, about twice as
large as the red globules, and are readily divisible by the acid eosin
stain into two kinds: 1st. Cells which are deeply stained by
eosin—eosinophile; and 2d. Cells that do not take on the eosin
stain—neutrophile (Ehrlich).
Howells further divides these white globules into uninuclear and
multinuclear. Of the uninucleated he describes three varieties: _a._ The
lymphocyte which is non-granular and without amœboid movement; _b._ The
granular cell with a protoplasmic envelope and amœboid movement; and
_c._ The granular with strap-shaped, horseshoe or spiral nucleus. Like
Lovet he considers the multinucleated as on the way to disintegration.
We cannot as yet speak with confidence of the pathological significance
of these respective forms of white globules, but they increase greatly
in numbers in connection with certain diseases of lymph plexus, and
glands, of the spleen and other blood glands, and in foci of
inflammation, and they perform most important functions in connection
with the resistance of microbian invasion and in elaborating the
antitoxines which confer immunity from second attacks.
The next form of blood solids are the _blood plates_ of Bizzozero, the
hæmatoblasts of Hayem. These are nucleated (Semmer) discoid, less than
half the diameter of the red globules, and cluster together in granule
masses when the blood is drawn. Their true significance is uncertain
though it has been surmised that they are intermediate corpuscles
(Semmer), that they are the disintegrated nuclei of the leucocytes, and
that they furnish paraglobulin to the circulating blood (Schmidt,
Howell).
The liver is one centre for the destruction of red blood globules and in
the blood of the hepatic vein there may be a reduction of a million to a
million and a half of red globules per cubic centimeter, as compared
with the portal vein.
Malassez gives 4,500,000 as the number of globules in a cubic millimeter
of blood (dog and horse 7,500,000, Nocard). The white globules are to
the red in the proportion of about 1 to 300 (domestic animals 1:800,
1:1100, Nocard). The variation in different parts of the vascular system
and at different times of the day is striking and suggestive.
In the blood of the splenic vein 1:60; in the hepatic vein 1:170; in the
portal vein 1:740; in the morning, fasting 1:716; half an hour after
breakfast, 1:347; in boys 1:226; in girls 1:389; in men 1:346; in old
men 1:381; in menstruating woman 1:247; in pregnant woman 1:281,
(Stricker).
PLETHORA. POLYÆMIA.
Definition. Transitory only. Causes, kidney disease, drinking freely,
rich feeding, profuse secretion, polycythemia, hyperalbuminosa, excess
of fibrine, sugar or fat. Ratio of blood to body. Variations of
globules. Symptoms, general, local. Appearance of blood. Prevention.
Treatment.
_Definition._ An excess of blood, of the blood globules, or of the
albuminoids.
Formerly accorded an important place in pathology, plethora has been
entirely eliminated from some recent works. The actual amount of blood
varies greatly at different times, rising after a free consumption of
food or drink, and falling during a period of abstinence. A healthy
activity of the secretory and excretory organs secures a fair uniform
average in the plenitude of the circulatory system. Moreover, large
variations are not in themselves rapidly injurious. Worm-Müller and
Cohnheim introduced into dogs ten to twelve per cent. of the body weight
(fifty to eighty per cent. of their blood) of canine blood without
inducing fatal results. More than this was fatal. In non-fatal cases a
reduction to the normal standard is speedily secured.
But we cannot count on absolute immunity in all circumstances. Disease
of the kidneys, or drinking water to excess, determines a surplus of
water and urinary salts (serous plethora, polyæmia aquosa). In cases of
rapid gain in condition from rich feeding, and above all after profuse
watery secretion (diarrhœa, diuresis, perspiration), the red globules
are relatively increased (plethora polycythæmica). After hearty feeding
there is a large increase of albumins (plethora hyperalbuminosa).
Fibrine-forming elements are apparently in excess during rheumatism,
pneumonia and other acute inflammations. Sugar is in excess after a
saccharine or farinaceous meal, fat in obese individuals, after
consumption of fat, after injuries to the bone marrow, and after severe
diseases with much destruction of albumen.
The ratio of blood to the body weight is: In birds 1: 12; in Guinea pig
1: 19; in rabbit 1: 20; in cat 1: 21; in dog 1: 17; in horse 1: 18; in
sheep 1: 24; in pig 1: 26; in ox 1: 29 (Colin). As showing the variation
under even different normal conditions of the system Bollinger found the
blood but 2.2 per cent. of the body weight in a fat pig, whilst it was
13.5 per cent. in a draft horse. Colin found it 2.4 per cent. in the fat
ox instead of the usual 3.4 per cent.
The excess of red globules and usually also of albumins is seen as a
temporary condition, in lean but vigorous animals put suddenly on an
abundant diet, rich in assimilable albuminoids, in working animals, put
in confinement to feed, and above all in high conditioned cows after an
easy parturition, when the uterine blood has been suddenly thrown on the
general circulation and the emunctories have failed to establish a
balance. Also in the lymphangitis occurring after a day or two of rest,
in a horse that has been hard worked and heavily fed.
It should be borne in mind that the number of red globules varies
considerably in the different animals. In the dog it was by weight 148.3
grammes per 1000; in the pig 105.7; in the horse 102.9; in the ox 99.71,
and in the sheep 98.2 (Andral, Gavarret, Delafond). By count the horse
has 5,500,000 per cubic millimeter (7,500,000, Nocard); and the dog
5,000,000.
_Symptoms._ Under a sudden dangerous increase of the volume or the
organic elements of the blood, there are usually dulness, lassitude,
dropping of the head, strong, full, hard pulse, extra force in the heart
beats, thirst, elevated temperature, and redness of the visible mucous
membranes. At first there is no indication of local disease, but unless
relief comes by free secretion some local complication is likely to
ensue. This may be epistaxis, congestion or apoplexy of the brain,
parturition fever, lymphangitis, or congestion of some internal organ,
etc. A drop of blood colors deeply the finger or other object, it clots
firmly in three to five minutes, and shows more than usual of a buffy
coat.
_Treatment._ As dangerous plethora is usually a very transient condition
the main attention should be given to _prevention_, in keeping the diet
low and the emunctories active in high conditioned parturient cows; in
lowering the diet and securing free secretion, or in giving exercise to
high fed, hard worked horses that have been laid off work; in changing
only by slow gradations thin, vigorous animals to a rich diet, etc. When
the danger is imminent prompt relief can be secured by the liberal
abstraction of blood. Purgatives, diuretics, and restricted diet may be
applied to less urgent cases.
HYDROÆMIA. ANÆMIA OLIGÆMIA.
Definition. Causes: bleeding, watery repair, hydroæmia, repair of
globules, changes in red globules, in bone marrow. Cause of
chronicity; profuse secretions; moplasms; parasites; chronic
exhausting diseases; defective diet or hygiene; diseases of jaws or
throat; overwork; toxic substances. Symptoms: pallid mucosæ, weakness,
perspiration, soft tissues, small pulse, palpitation, anæmic
heart—arterial and venous murmurs, depilation, indigestion,
costiveness, urine clear, abundant, emaciation. Lesions: blood poor in
globules, embryonic, and other abnormal red globules, fatty
degeneration, blood clot. Treatment: remove causes, diet, hygiene,
sunshine.
_Definition._ Bloodlessness; Deficiency of blood; Lack of red blood
globules. The last named is the condition to which the term is
habitually applied.
_Causes._ Anæmia is not so much a disease, as a result of a great many
debilitating and exhausting conditions. =Hæmorrhage= the most direct
cause of anæmia determines at first an actual lack of blood (oligæmia)
and of blood pressure, which may be sufficient to cause fainting and
death. In case of survival the amount of blood is rapidly made up by
absorption from all available sources of liquid in the economy, but the
blood so restored is essentially hydroæmic having an excess of water and
a lack of globules and dissolved solids. If however the loss has been
moderate the quality may be restored in a few days. Buntzen found that
after moderate bleeding the volume is restored in a few hours; after a
profuse hæmorrhage in 24 to 48 hours. After bleeding to 1.1 to 4.4 per
cent. of the body weight the increase of the red globules may be noticed
after 24 hours, and is completed in 7 to 34 days. It is noteworthy that
during this repair the bone marrow becomes much redder and more
cellular, and that new red cells found in the blood are nucleated
(Neumann) and contain less hæmoglobin (Ott). The absence of hæmoglobin
is nearly in proportion to the amount of the hæmorrhage (Bizzozero,
Salvioli). If the hæmorrhage is slow and continuous this repair is
counterbalanced and the anæmia is much more persistent.
=Profuse secretion= as of milk (cows, goats, ewes, bitches, on poor
feeding), of liquid fæces, urine, or pus often determine a marked and
even dangerous anæmia.
The rapid growth of multiple =tumors= as of _melanosis_ in gray horses
has been noticed to cause profound anæmia (Bouley).
Perhaps no cause is more potent than the attacks of =parasites= and
especially such as live by sucking the blood. The numerous strongyli of
the lungs, stomach, and intestine, the tricocephalus, and allied round
worms, the trematodes of the liver, and the cytodites of birds furnish
striking examples of the bloodless and debilitated condition which they
may produce. In man ankylostomata causes anæmia in Egypt, Italy (St.
Gothard) and elsewhere, and bothriocephala in different countries.
=Chronic exhausting diseases= especially those which affect the
digestive organs and mesenteric glands are prolific causes. So with
Bright’s disease.
Connected with these are =defects in diet or hygiene=. Starvation,
unsuitable, innutritions, or indigestible food, too laxative food, damp,
dark, draughty or unventilated stables, and irregularity in feeding,
watering and work are all potent factors in inducing anæmia.
=Diseases of the masticatory apparatus= (broken jaw, diseased teeth,)
preventing the preparation of food, and pharyngeal troubles interfering
with deglutition are other causes. Finally overwork is not to be
forgotten.
=Toxic anæmia= may occur from the ingestion of lead, mercury, or
arsenic.
_Symptoms._ These may be little marked at the outset in slowly
developing cases. Extra pallor of the mucous membranes, fatigue and even
breathlessness on slight exertion, a small, weak, pulse, with a tendency
to become rapid, with violent heart beats, when excited.
At a more advanced stage the mucosæ, especially the buccal, are pale and
thin, the muscles are soft, flabby and weak, fatigue and perspiration
are easily induced, the feet are advanced more nearly in the median line
of the body, and the toes strike on any obstacles, the pulse is weak,
small and quick, and the heart easily excited even to palpitation, and
with an occasional anæmic murmur with the first heart sound. Arterial
and venous murmurs may be present. The hairs are easily detached.
Appetite and digestion fail, there is costiveness, a full secretion of
urine of a clear aspect, the subcutaneous fat disappears and the skin
feels thin and limp (paper skin in sheep), the hair dry and lusterless,
the wool flattened (clapped). The weakness and emaciation go on
increasing and dropsies appear in the limbs, under the trunk and jaw and
in the internal cavities.
_Pathology._ _Lesions._ Apart from the causes, the morbid conditions are
mainly found in the blood. The watery state of the blood, the lack of
red globules (even to but 2,000,000 per cubic millimeter), the absence
of albumen (76 per 1000 in place of 83), the loose coagulum with excess
of buffy coat, and the excess of serum are characteristic. The presence
of large, nucleated (myelogenous) red cells, of spherical bodies smaller
than the normal red cells (microcytes), and of irregularly shaped red
cells (poikilocytes) is characteristic, the latter especially of
pernicious anæmia. As the disease advances fatty degeneration of heart,
liver, kidneys, and other organs are complications and tend to aggravate
the disease, by counteracting repair of the globules—thus establishing a
vicious circle. All the organs are pale and flaccid, the arteries empty,
the veins contain a little blood, forming pale clots. In the cases
considered, all the result of another disease, the lack of blood and of
the solid and vital elements in that which remains, entails imperfect
function in all the vital processes, including sanguification itself,
and in this way an anæmia once established tends to perpetuate and
aggravate itself.
_Treatment._ The anæmia above considered being largely symptomatic, or
resultant from other diseases, the first consideration as regards both
prevention and treatment is to prevent or cure such diseases. Where
dietetic or hygienic, a liberal diet, and good hygiene will meet every
demand in the early stages. In the warm season an open air life is most
important. In case of a drain by over-secretion (milk) this must be
judiciously checked. In bitches it will often be needful to wean several
of the puppies. A rich and very digestible diet (oats, beans, linseed,
oil meal, milk, gruel), in small compass, and suited to the genus and
individual, with iron and bitters, and in the herbivora carminatives,
will suit many cases. Muriate of iron, with strychnine or nux vomica;
iron sulphate, sodium chloride and nux; or dialysed iron, or some other
soluble ferruginous salt, with quinia, gentian, or some other bitter
will serve a good purpose. For the dog saccharated carbonate of iron or
citrate of iron and ammonia with quinia or strychnine, in pill form, is
convenient. With poor digestion muriatic acid and pepsin may replace the
iron at first. Beef teas may often be given with advantage, even to the
herbivora, and injections of defibrinated ox blood night and morning
have proved of service. In extreme anæmia, as from hæmorrhage,
transfusion, or its equivalent, must be resorted to. A normal saline
solution (0.6 per cent. NaCl), boiled, may be thrown into the peritoneum
or subcutaneous connective tissue, or defibrinated blood, may be
injected into the peritoneum. Transfusion is the dernier resort.
PROGRESSIVE PERNICIOUS ANÆMIA. IDIOPATHIC ANÆMIA.
Definition. Causes, obscure, faulty diet, hygiene, microbes,
glycerine, pyrogallic acid, hæmoglobin, deranged sanguification,
parasitisms. Symptoms, of anæmia of obscure origin. Treatment as for
anæmia, special measures, for intestinal fermentations, dietetic.
_Definition._ Anæmia which is without any pre-existing appreciable
cause.
_Causes._ As in the corresponding disease in man the real starting point
of pernicious anæmia is unknown. Faults in diet and in general hygiene
have been adduced, and while in Berne this appears to be sustained, in
Ireland, in the poorest classes, the disease is little known, and in
Montreal, it find its victims largely in a class of well to do artisans
(Osler.) In the domestic animal it is described on all soils, and on the
most varied dietary (Bouley and Reynal). Zschokke and Friedberger and
Fröhner in cases occurring enzootically in stables, found a minute
bacillus in the patients, which would remove these cases into the list
of symptomatic anæmia. The same is true of the anæmia (Surra) of horses
and mules in India and Siberia, in which Evans, Burke, Steele and
Ignatovsky, found a motile spirilloid organism which destroys the red
globules. Other forms that are apparently purely idiopathic have been
attributed to a failure in the cytogenic processes in the bone marrow
especially. Back of this we know only of the various debilitating causes
in food, hygiene, building, location, work, etc., operating on a
specially susceptible system, in which, once started, the morbid process
tends to perpetuate itself and increase.
Ponfick induced anæmia experimentally by the intravenous injection of
glycerine, pyrogallic acid, solutions of hæmoglobin, etc., which
dissolve the blood globules. This suggests the probable pathogenesis by
the production of unidentified blood solvents in cases of deranged
sanguification, but it still leaves us in the dark as to the exact seat
of such derangements (liver, blood glands, bone marrow, etc.) and as to
the cause, parasitic or otherwise, which determines such disorder.
Pathological investigation has enabled us to differentiate, according to
their respective causes, a number of diseases (distomatosis, lung worms,
ankylostomiasis, internal acariasis, chronic trichinosis, strongyliasis,
etc.,) which were formerly classed as anæmias, and it seems altogether
probable that the onward progress of medicine will enable us to go
farther in the same direction and to allot the remaining unclassed
anæmias to their proper etiological places. Some may be unrecognized
helminthiasis, others microbian disorders, and still others, disorders
in nutrition and sanguification from different causes.
The _Symptoms_ are those of other forms of anæmia, but being more
obscure in origin and therefore less open to corrective treatment, it is
more likely to grow to an extreme development and fatal issue. The weak
pulse, irritable heart, debility, unsteady walk with the hind limbs,
hurried breathing and sweating under exercise, watery, puffy eyes,
dropsies in limbs and dependent parts of the body, progressive
emaciation, and weakness are even more marked than in symptomatic
anæmia.
The _treatment_ is in the main as for the other form alike in its
hygienic and medicinal bearing. In man recoveries have taken place under
arsenic combined with the iron. Arseniate of potash and ferrum redactum
in pill form, or tincture of chloride of iron, and Fowler’s solution in
food or water, continued for a length of time. Phosphated pepsin, and
peroxide of hydrogen have seemed to do well in some instances, and
phosphorated oil is another resort. W. Hunter attributes idiopathic
anæmia to toxins derived from microbes in the alimentary canal, as Sir
Andrew Clark ascribes chlorosis to a similar cause. He prescribes
beta-naphthol as the least soluble and best antiseptic, in a dose of 5
grains daily in mucilage for man (1 drachm for horse or ox). Hunter
further found that a farinaceous diet protected the globules against
destruction while a nitrogenous diet favored this. It may be noted that
long ago Delafond attributed anæmia in animals to the extension of the
use of artificial fodders of the natural order leguminosæ which are rich
in nitrogen.
CHRONIC ANÆMIA. DROPSY IN CATTLE AND SHEEP.
Definition. Causes, parasitic and microbian. Symptoms. Treatment.
_Definition._ A progressive anæmia in ruminants and other animals,
resulting in general anasarca, and dropsies of the internal cavities.
In veterinary works published on the European Continent this affection
is given a special place apart from the same train of symptoms which
mark distomatosis, taeniasis, and strongyliasis. The disease is
described as prevailing in wet years, after inundations, when the
vegetation is rank and aqueous, and of course largely aquatic, in
animals that are turned out in early morning before the dew has
evaporated, in the conditions, in other words, that favor the ingestion
of parasites. It prevails also in work oxen fed on the refuse of sugar
factories (beets, turnips) in which the nitrogenous materials are held
to be deficient, but in Great Britain where cattle are often fattened on
an exclusive diet of turnips, containing even a larger proportion of
water, this non-parasitic disease is unknown. It is also ascribed to
close, ill-ventilated, unwholesome buildings, and to over-kept and
tainted fodder, and so far as a separate disease exists, it seems more
reasonable to charge it to the toxins produced by bacterial ferments or
cryptogams than to causes which elsewhere appear to be inoperative.
The _symptoms_ are essentially those of distomatosis, and the
_treatment_, apart from the parasiticides, is the same. When
helminthiasis can be certainly excluded _prevention_ would include the
avoidance of the factory refuse, especially when in a state of decay.
MELANÆMIA. BLACK PIGMENT IN BLOOD.
Definition. Melanin, in normal tissues, abnormal. Melanosis.
Bisulphide of carbon subcutem. Decomposition of hæmoglobin in
leucocytes. Coloration of tissue.
_Definition._ Accumulation of granules and scales of blood pigment
(melanin) in the circulating fluid, and in various organs (spleen,
liver, bone marrow, brain, etc).
=Melanin=—C_{44.2}, H_{3}, N_{9.9}, O_{42.6}—or black pigment (a close
relative of hæmatin) occurs physiologically in epithelium (choroid,
retina, iris, in the deeper layers of epidermis, and on the surface of
the dog’s lung and of the sheep’s brain) and in connective tissue
corpuscles (lamina fusca of the choroid).
Pathologically it is found in the blood of the victims of malarious
fever, often in great abundance, and in the spleen, liver, bone marrow,
brain, lymph glands and some other organs. It is formed abundantly in
the black pigment tumors (melanosis) of man and animals, and in
extensive melanosis is present in the blood of both man and horse
(Schimmeln). So far it has not been found in connection with the
extensive destruction of red globules which takes place in anæmia.
Schwalbe has developed malanæmia experimentally by the hypodermic
injection of bisulphide of carbon in rabbits.
According to one view the melanin is produced in connection with the
destruction of red globules in the liver, spleen, etc., and is thence
carried into the blood. This is in keeping with the local formation of
the pigment in melanosis. Arnstein however urges that in malarious cases
the destruction of the red cells takes place in the blood, and that the
hæmoglobin, absorbed into the leucocytes, is transformed into melanin,
and finally deposited in the tissues by the migrating white corpuscle.
Why the hæmoglobin set free in anæmia is not similarly transformed, does
not appear. The pigmented organ may be quite black in the immediate
vicinity of the blood vessels, and in its general aspect in chronic
cases reddish brown, dark gray, or dark olive.
LEUKÆMIA. LEUCOCYTHÆMIA.
Definition. Nature. Result of other morbid processes. Leucocytes
polynuclear. Lymphatic leukæmia. Spleno-myelogenous leukæmia.
Leucocytes in each. Loss of amœboid movement. Charcot’s crystals.
Hæmatoblasts. Cell increase in bone marrow. Myelocytes. Enlarged
spleen and lymph glands. Hæmorrhages. Lymphoid growths. Susceptible
genera. Causes obscure. Symptoms, pallor, listlessness, weakness,
apnœa, sweating, thirst, emaciation, weak circulation, anæmic murmur,
enlarged spleen, bleedings, diarrhœa, dropsy, excess of white
globules, reduction of red globules, buffy coat, beaten fibrine is
granular, china-white mucosæ, hurried breathing, stertor, deranged
digestion, marasmus. Duration. Not inoculable. Treatment, not hopeful,
as for anæmia, good hygiene, tonics, stimulants, antiseptics.
_Definition._ An excessive and persistent increase of the white blood
globules, and associated with enlargement of the spleen, lymph glands or
bone marrow.
_Nature._ This must be distinguished from the leucocytosis which occurs
during digestion, or that which attends on tuberculosis, glanders,
pneumonia, and other extensive inflammations and profuse suppuration.
These forms are transient and the cells are of the polynuclear variety.
The cells of leukæmia are various in character, but bear some relation
to the particular organ which is the seat of hypertrophy or morbid
process.
“In =lymphatic leukæmia= the increase in the number of leucocytes is due
to the mononuclear lymphocytes, especially of the small form. As many as
ninety-five per cent. of the colorless cells may be of this form. In
=Spleno-Myelogenous leukæmia= the eosinophile cells may be especially
increased in number, and there are also large leucocytes coming
apparently from the marrow of the bones, and called myelocytes. These
most nearly resemble the larger lymphocytes of normal blood, but they
are usually larger. They have a single large nucleus which stains feebly
and their bodies may show neutrophile granules. Larger and smaller
nucleated red blood cells may be found in spleno-myelogenous leukæmia.
The leucocytes are frequently in a condition of fatty degeneration, and
there may be a decrease in the number of red blood cells.” (Delafield
and Prudden). In splenic leucocythæmia blood plates may be absent and in
lymphatic leucocythæmia they may be in excess.
Cafavy claims that many of the leucocytes have lost their active amœboid
movements.
Bright white crystals in the form of elongated octahedra are found not
only in the blood but in the diseased glands, spleen or marrow
(Charcot’s crystals). Clusters of discoid hæmatoblasts (blood plates)
are present in the blood in variable numbers (Schultze’s granule
masses).
The bone marrow is marked by an accumulation of spheroidal cells, which
tend to pass into a condition of fatty degeneration. Most of them are
colorless, larger than the lymphocytes of normal blood and have one
large often vesicular nucleus, staining less highly than the lymphocyte
nuclei, and with neutrophile granules in the protoplasm (=myelocytes=).
There are besides, nucleated red blood cells, spheroidal cells,
containing red blood cells, and Charcot’s crystals. The marrow may be
uniformly red, mottled gray and red, gray, grayish yellow, or puriform
(Delafield and Prudden). This may affect one or many bones. The affected
spleen is usually much enlarged, at first uniformly, later unevenly,
firm or softened, and with thickened white capsule. The cut surface is
smooth, brownish red, or yellow, with white lines (thickened trabeculæ)
and indistinct Malpighian corpuscles. It contains glutin, glycocoll,
hypoxanthin, zanthin, leucin, tyrosin, and lactic, acetic, or formic
acids.
The affected lymph glands are somewhat enlarged, red or gray,
exceptionally, softened or caseated and otherwise contain an excess of
leucocytes.
Slight hæmorrhages may appear in any of these structures. Lymphoid
growths may appear in a number of other organs as the liver, heart,
lungs, kidneys, bowels, tonsils, the different blood glands, the serosæ
and the retina.
_Genera affected._ It has been seen mainly in dogs, but also in horse,
ox, pig, cat and mouse. Nocard has collected the following cases: horse
9, cattle 6, pig 5, dog 22, cat 1.
Leisering found a horse’s spleen weighing 28 kilogrammes. Johne found a
pig’s spleen of 2.4 kilogrammes.
_Causes._ The primary causes of leukæmia are unknown. As in anæmia all
unhygienic conditions are invoked as causes. That it is not due to
simple hypertrophy or irritation of the leukogenic centers is plain, as
it does not follow on ordinary diseases and injuries of these parts, but
what is the precise nature of the morbid cause has so far eluded us.
_Symptoms._ Pallor of the visible mucous membranes, listlessness, lack
of energy and endurance, breathlessness and perspiration on the
slightest exertion, ardent thirst, rapidly advancing emaciation,
unsteady gait, stiffness or lameness, lies most of the time, walks with
pendent head, and jaws open, small, weak pulse, anæmic murmur in the
heart, enlarged lymph glands, or spleen felt beneath the left lumbar
transverse processes in the ox, or in the left hypochondrium in the
horse. Bleeding from the nose or elsewhere, slight hæmorrhage into the
conjunctiva, irritable conditions of the bowels, diarrhœa and dropsies
are suggestive. The blood when obtained in epistaxis or drawn by a
needle prick may be pale rose, brownish or grayish brown instead of red,
and under the microscope shows the enormous excess of leucocytes—the
ratio to the red being sometimes 1: 2, or even more, in the human
subject. In the domestic animals the following ratios have been made by
actual count: 1: 85 (Leblanc and Nocard), 1: 50, 1: 45 (Mauri), 1: 20
(Nocard), 1: 15 (Siedamgrotzky), 1: 12 (Forestier and Laforque). The
normal average for the domestic animal according to Nocard is 1: 900.
This great relative excess of white globules serves to distinguish this
malady from anæmia, and its persistency is a means of diagnosis from
transient leucocytosis.
The red globules are always reduced in number in the horse and dog to
5,082,000, and even 2,050,000 per cubic millimetre, while the normal is
7,500,000 (Nocard).
In clotting, the blood forms an extensive buffy coat, and in solipedes
which normally show this, the blood set in a test tube forms three
strata, the upper slightly yellow, semi-transparent and formed of
fibrine; a median of a dull, opaque white color and formed mainly of
leucocytes and blood plates, and a lower of a violet red and formed
mainly of red globules.
The amount of fibrine is variable. It becomes granular when beaten.
Albumen is variable but usually reduced.
The visible mucous membranes are bloodless and of a clear porcelain
white. The walk becomes weaker, fore feet wide apart and the hind limbs
partly flexed, head and neck extended, and breathing labored. The
breathing may be with constant stertor, the bowels torpid and
tympanitic, or loose and fœtid, dropsies and hæmorrhages ensue, and the
patient dies in complete marasmus.
_Duration._ The disease may prove fatal in less than a month, or it may
last for three, six, or eight months. It is mostly fatal.
_Not inoculable._ Many attempts have been made to transmit it by
inoculation, but in no case with success.
_Treatment_ is not successful. All hygienic measures should be adopted,
as for anæmia; open air and sunshine, with protection against chills;
the treatment of all complications; iron, bitters, phosphorus, arsenic
in particular, electricity to the spleen, massage; oxygen inhalation;
and locally, iodide of potassium or mercury, generally and locally.
LYMPHADENOMA. HODGKIN’S DISEASE.
Definition. Relation to leukæmia. Causes. Mainly accessory. State of
lymph glands, spleen, liver, bone marrow, intestine, tonsils, thymus,
kidneys, liver, lungs, bronchial mucosa, pleura, pericardium, nervous
system. Symptoms, as in leukæmia, with adenoid hyperplasia, but little
leucocythemia. Relation to glanders. Uric acid, low density, no
hippuric acid. Tuberculin and mallein tests. Treatment, as in
leukæmia. Excision in cases not constitutional. Phosphorus, phosphide
of zinc.
_Definition._ Hypertrophy of the lymphatic glands with little or no
leucocytosis. There may further be lymphoid growths in the liver,
spleen, bone marrow and other organs.
The visceral lesions in lymphadenoma do not differ in character from
those of leukæmia, and as it does often apparently merge into that
disease by the characteristic changes in the blood, it is denied by many
that it constitutes a separate pathological entity. In his admirable
monograph on leucæmia in the lower animals Nocard affirms their
identity. The main excuse for keeping up an alleged distinction, is the
frequent absence of leucocytosis, and this often supervenes after the
lymphadenoma has existed for some time.
_Causes._ As in leucæmia, no definite cause can be found in the majority
of cases. An accessory cause can sometimes be observed where a local
irritation gives rise to swelling of the adjacent lymphatic glands and
this goes on to distinct lymphadenoma.
=Lesions in the Lymph Glands.= The hyperplasia may affect but a single
group of glands, more commonly a number of groups, and often nearly all.
In one case only of leukæmia in the lower animals, a dog, has Nocard
failed to find the lymph glands affected. In the horse he has found the
sublumbar glands alone weighing 14.5 kilogrammes, 11 k. and 8 k. They
compressed the posterior aorta and vena cava and had caused extensive
ascites.
The enlarged glands are white, gray or in case of rapid growth veined or
pointed with red; they may be soft or firm according as the hyperplasia
has operated most on the trabeculæ or the cells; they are homogeneous
throughout. The scraping of the cut surface gives a more or less thick
milky juice containing a great number of nucleated or double nucleated
lymphocytes, free nuclei and granules which stain strongly.
Hardened sections show an enormous development of the follicles at the
expense of the medullary walls, and double nucleated white globules
packed in a rich reticulum of adenoid tissue, whilst the bloodvessels in
the connective tissue are crowded with white cells, and there are slight
ruptures, old or recent.
=Lesions of the Spleen.= These are nearly always present. Leisering
found a horse’s spleen over three feet long and 28 lbs. weight, and
Nocard one of 13 lbs. Bollinger found a pig’s spleen 3½ lbs.
Siedamgrotzky found dog’s spleens over 2 lbs. The consistency is usually
firm (sometimes soft in dog). Capsule thickened and white, cut surface
dry, reddish brown, granular, Malpighian bodies enlarged like a pea,
hazel nut or walnut, with contents as in the lymph follicles. The
capillaries are enlarged and crowded with white cells.
=Lesions in the Liver.= The liver is enlarged in one-half of the cases
of leukæmia in the lower animals. It has been found to weigh 20 lbs. in
the horse, and 4 lbs. in the dog. It is of a grayish brown, or yellowish
brown hue, or light red spotted with yellow, or mapped out by
anastomosing grayish white lines. There may be enlargement of the acini,
or the formation of little nodes of adenoid tissue, or most commonly in
the lower animals, there is an adenoid thickening of the bands of
connective tissue extending in from the capsule. These are filled with
white cells which stain deeply with carmine. There may also be slight
extravasations of blood and infarcts.
_Lesions in the Bone Marrow._ These noticed in the pig by Fürstenberg,
and in dogs by Siedamgrotzky, consist in increased vascularity, great
cell hyperplasia, and formation of adenoid tissue as described under
leukæmia.
=Lesions of the Intestine.= These commence in the agminated or solitary
glands, which become enlarged, causing thickening of the mucous
membrane, and later grow out into more or less rounded masses of
lymph—adenoid tissue up to an inch in thickness. They are quite subject
to ulcerations.
=Lesions of the Tonsils.= Bollinger, Nocard and Siedamgrotzky found
these enlarged in dogs in connection with adenoma of the spleen. They
were soft, friable, grayish, and consisted of a very delicate and
fragile adenoid tissue.
In one case Siedamgrotzky found adenoid hypertrophy of the thymus in a
cow, and adenoma of the kidneys similar to that of the liver has been
noticed.
Similar adenoid hyperplasia has been found in the lungs, the bronchial
mucous membrane, the pleura, the mediastinal and bronchial glands, and
the pericardium. In man this has invaded the nerve centres, and it seems
that at any point where there is a lymph gland or a lymph plexus this
adenoid hyperplasia may localize itself.
_Symptoms._ The general symptoms of failing health are as described in
leukæmia. The particular symptoms of this disease consist in the
recognition of the adenoid hyperplasia in the absence of a marked
leucocytosis. The submaxillary glands are usually the first attacked,
and the disease may, in the horse, be confounded with glanders. There
is, however, no pituitary discharge nor ulcer, the glands are enlarged
symmetrically on the two sides, and a careful search will usually
discover other groups with similar symmetrical enlargement. The
parotidean, the pharyngeal, the prepectoral, the prescapular, the
axillary, the popliteal, the prefemoral, the post and premammary, and
the inguinal should be critically examined. The enlarged mesenteric
glands may be reached and detected by the hand engaged in the rectum, or
in the small animals by external palpation, as may also the enlarged
spleen or liver.
The adenoid hyperplasia in the chest offers very obscure and uncertain
symptoms. The enlarged bronchial and mediastinal glands may seriously
interfere with the functions of the vagus nerve, causing, in cattle,
disturbed digestion and rumination and tympanies, in horses stertorous
breathing, and in the carnivora and omnivora a tendency to vomiting. In
animals generally the pressure on the cardiac nerves leads to great
irritability of the heart, and violent action under any exertion. The
prominent dyspnœa in the advanced stages may be explained by these
thoracic hyperplasiæ.
Nocard claims that the urine furnishes most important indications in its
low specific gravity (horse 1010), its constant acidity, and in the
almost entire absence in that of the horse of hippuric acid. When there
is any suspicion of tuberculosis or glanders, the tuberculin or mallein
test will decide.
_Treatment_ is essentially the same as in leukæmia, and equally
unsatisfactory. Arsenic has in the main given the best results. In the
very earliest stages when the granular hyperplasia is confined to one
group, excision is advisable. This should be avoided in all cases in
which the constitutional symptoms have developed. Phosphorus and
phosphide of zinc have seemed beneficial in certain hands. Injections
into the glands have so far proved useless.
ACUTE LYMPHANGITIS OF PLETHORA IN HORSE. ANGEIOLEUCITIS.
Definition. Symptoms and causes. Genera affected. Causes of plethora.
High feeding. Work followed by rest. Fever, hurried breathing, strong,
rapid pulse, anorexia, stiffness and swelling in a hind limb, inguinal
glands, connective tissue engorgement, corded lymphatics, suppuration
rare. Mild forms. Lesions, in lymphatic vessels and glands. Chronic
cases. Nature, plethoric, lymph excess, stasis, excess of cells and
fibrine, immunity of the fore limb. Season of prevalence. Climate.
Diagnosis, from farcy, erysipelas, etc. Treatment, exercise, friction,
resolvents, purgative, bleeding, diuretics, astringents, iodine,
pressure, diet. Prevention. Treatment of chronic cases.
_Definition._ Inflammation of the lymphatic vessels and glands of one
limb usually in connection with rest.
_Symptoms._ This affection is common in heavy draft horses of a
lymphatic temperament and kept on high feeding and at hard work. It
rarely develops however while the subject is kept at steady work. But
if, in the midst of such work, the horse is kept at rest in the stall
over one, two, or more days on the same generous diet, he is found
shivering violently, with rapid, labored, breathing, high pulse and
elevated temperature, symptoms which have been frequently mistaken for
those of pneumonia. There is complete anorexia, and often ardent thirst.
The patient is indisposed to move and if forced to it shows lameness in
one hind limb with an extraordinary abduction of the limb at each step,
and sometimes so severe as to prevent his putting his full weight upon
it. If an examination is now made high up in the groin close outside the
inguinal ring, the lymphatic glands will be found to be swollen, hot and
tender, so that under even moderate pressure the leg will be lifted and
abducted until the patient threatens to fall on the other side.
A little later the shivering may have given way to the hot stage, with
it may be general perspiration, and the swelling may have extended down
the course of the saphena vein and lymphatics, as a distinct ridge and
the lower part of the limb from the foot to the hock may be filled,
dropsical and hot. Unless checked the swelling goes on increasing till
the lower part of the limb is two or three times its natural thickness,
and the swelling has extended well up on the thigh. The swelling has a
soft œdematous feeling, easily receiving and retaining the imprint of
the finger and is not only hot, but excessively tender. From the margin
of the swelling, firm, tender, rounded cords are found to emerge passing
upward along the line of the saphena vein and its branches toward the
inguinal glands. These represent the swollen and gorged lymphatic
trunks, and may often be traced for some distance into the substance of
the general engorgement.
When the inflammation is violent, suppuration may ensue at one or
several centers, but more commonly the engorgement goes on increasing
and when the febrile attack has subsided the limb is left permanently
enlarged and correspondingly liable to a second attack.
Milder cases are met with which are perhaps even more misleading. There
may be little or no rise of temperature, loss of appetite or general
constitutional disturbance, but under some change of regimen and
particularly after one or two days of rest the subject becomes lame in
one hind limb, without any of the usual injuries to account for it.
Examination of the groin shows swelling and tenderness of the external
inguinal glands, with or without, a tender cord-like swelling running
down from them.
Between these two types may be found all grades of lymphatic
inflammation with a varied degree of attendant constitutional
disturbance.
_Lesions._ The coats of the inflamed lymphatic vessels are thickened by
exudate and the outer coat is the seat of ramified redness with minute
spots of blood extravasation. The inner coat is dull, opaque, or even
thickened. The vessel is dilated and its walls friable. The contained
lymph in the intervals between the valves has coagulated into a very
thin diffluent jelly-like clot, which in old standing cases may have
become granular. The connective tissue from which these vessels lead is
infiltrated with liquid and the lacunar spaces distended. Red patches
from blood extravasations are numerous. The external inguinal glands and
often the internal and sublumbar are swollen, congested, and the seat of
active cell hyperplasia. Abscesses are exceptionally seen.
In chronic cases the lymphatic vessels of the affected limb and
especially of the lower part which is permanently swollen, are
enormously increased in calibre (lymphangiectasis), and have their walls
correspondingly thickened. The connective tissue is the seat of
extensive fibrous hyperplasia, and its interstices are greatly enlarged.
_Causes._ _Nature._ This disease has not been sufficiently studied to
ascertain what toxic agents are produced in the plethoric condition,
under the torpid processes of nutrition and sanguification entailed by
absolute compulsory rest. A consideration, however, of the relations of
the lymph and lymph vessels and glands to other parts will in part
explain the pathology of the malady. The lymphatics take their origin in
the nuclear spaces of the various tissues, the anastomosing canals of
such pericellular spaces together with the latter forming the actual
radicles of this set of vessels. They receive, therefore, the surplus
plasma which is not used up by the tissue cells in performing their
trophic, secretory and other functions. This lymph carried on by the
_vis a tergo_, muscular compression and other movements, is delayed in
the adenoid tissue known as lymph nodes, and especially in the lymph
glands, in which the proliferation of lymph cells is mainly carried on.
Thus the lymph cells are very scarce in the lymph radicles of the
connective and other tissues, and are found in greater numbers after
passing through the lymph nodes, and in still greater after passing
through the lymph glands. But the increase of cells is also in inverse
ratio with the rapidity of the circulation of the lymph. When this is
rapid the cells are hurried on and there is little time for their
reproduction. When slow on the other hand, there is time for cell growth
and division in the glandular detention cavities, and the ratio of cells
to the plasma is materially increased. Consider next that the
multiplicity of cells determines an increase of the fibrine factors, so
that the more cells the lymph contains there is the more material for
fibrine (Landois), and we have one good reason why under enforced rest
the overcharged and congested gland may become the seat of fibrinous
coagula or lymphatic embolism. Any overdistension, toxic element, or
other cause of disturbance, which deranges the functions of the cell or
causes its rapid multiplication by division—as in inflammation—at once
sets free the fibrine ferment and determines the coagulation. In the
disease before us we have the overfeeding of an animal having a strong
digestion, we have an absolute compulsory inactivity, with a suspension
to a large extent of the functions of nutrition, sanguification,
secretion, and elimination; we have in consequence an increase of the
blood pressure, and of the solids of the blood and of the plasma of the
lymph; we have a suspension of the great motor force of lymph
circulation, namely, the muscular contraction, and we have the
consequent tardy movement of the lymph, the great increase of
lymphocytes, and the distension and engorgement of the lymph glands. As
soon as this has reached a certain stage the congestion and incipient
inflammation of the gland determines the precipitation of fibrine, the
obstruction of the gland, and of the entire circulation of lymph in the
lower part of the limb. The fever, the local swelling, and the
subsequent steps follow as a matter of course. This view is sustained by
the fact that incipient cases can be cured by muscular movement alone.
The rarity of the disease in the fore limb may be ascribed to the
greater force of the _vis a tergo_, the lesser height of the lymph
column, and the stronger action of the aspiratory power of the chest on
the lymphatic vessels.
In addition to the causes mentioned above must be noted the following:
The disease is an affection of heavy draft horses, in which the tissues
are more lax, and the lymph plexus in the connective tissue of the hind
limb is much more abundant. It is common in the heavy English, Scotch
and Belgian draft horses, and rare in the English racer, the American
trotter, and in the average light American horse. The malady is most
frequent in spring and autumn, when the work is hardest and the feeding
most abundant. It rarely attacks the horse in steady work, but appears
after an idle Sunday spent in the stable (Monday morning disease), or
after one or more days of compulsory idleness from heavy rains or other
cause. The damp climate of western Europe has probably an exciting
influence, as it has in producing the lymphatic constitution. In the
same line of thought Zundel says that many cold weather attacks would be
prevented by clipping off the heavy coat which keeps the entire system
relaxed. In some cases a sudden change of food, and in others musty oats
have been claimed as causes.
_Diagnosis._ Lymphangitis is distinguished from a simple dropsy of the
limb by the acute fever, the great local tenderness especially of the
inguinal glands, and by the tender corded lymphatics that enter these.
From cutaneous glanders (farcy) it is diagnosed by the more acute fever,
by the swelling of the inguinal glands in the early stage of the
disease, followed by the swelling of the lower limb, and by the absence
of the hard, comparatively insensible and prone to ulcerate, farcy bud.
Farcy buds usually appear on the pastern or fetlock, with more or less
swelling of the lower part of the limb, while the inguinal glands are as
yet normal in size and without tenderness. From erysipelas, with which
this has been confounded, it is distinguished, by the suddenness of the
onset, under the circumstances above described, by the high type of
fever, by absence of early cutaneous inflammation and the formation of
vesicles, and by the fact that lymphangitis commences in swelling of the
inguinal glands.
_Treatment._ In cases that are seen in the earliest stages, before the
leg has become badly swollen, recovery will usually take place under
active exertion continued for hours at a time. The pumping action inside
the hoof during exercise, and the alternate compression and relaxation
of the lymph vessels by the muscles, tend to establish a rapid current
of lymph, to break up coagula and to re-establish a healthy condition.
Friction from below upward on the lymphatic vessels and swollen limb
will greatly assist in this restoration. Different agents are employed,
such as camphorated spirits or oil, iodine, mercurial, and even
blistering ointments. These should not replace exercise when this is
possible.
When the fever has set in suddenly and runs very high, the abstraction
of four or five quarts of blood, and the administration of a purgative
(8 drs. aloes) will be in order. In cases occurring in the same stable
and in all other respects apparently identical, the subjects of
phlebotomy recovered without any permanent swelling of the limb, while
those that were not bled recovered with thickened limb.
In cases so advanced that the limb cannot be used, cold irrigation, with
friction, may be applied, and when the irrigation is intermitted one may
apply some astringent (vinegar, alum, lead acetate), or an iodine lotion
followed by an evenly applied bandage.
The purgative should be followed by full doses of diuretics (nitre,
bicarbonate of potash or soda, colchicum, iodide of potassium) until
fever and local inflammation have subsided.
As soon as the patient can use the limb, walking exercise should be kept
up for several hours forenoon and afternoon.
Throughout the disease the food should be of a light and non-stimulating
variety. When appetite returns give at first wheat bran, or roots, or
sweet grass in small amount, and do not return to a grain diet until
fully recovered and ready to go to work.
After one attack there is always an increased liability to a second, and
great care should be taken to give the subject daily exercise, or where
this is impossible, to reduce the feed, give a dose of saltpeter, and
turn into a yard or roomy loose box on the idle day.
In chronic thickening of the limb, an evenly applied elastic bandage,
extending from the hoof up, regular feeding and exercise, washing daily
with a weak iodine lotion, and the internal use of iodide of potassium
and other diuretics, with bitters and even iron tonics may be used.
INFECTIVE LYMPHANGITIS. TRAUMATIC LYMPHANGITIS.
Infection varied, through wounds, autogenous. Simple irritation,
simple lymphangitis. Causes, sun’s rays, bruises, other injuries,
lymph coagulation from heat, cold, chemical irritants, and coagulants.
Germs in blood act on debilitated tissues, lymphatic constitutions,
anæmic, overworked, or starved. Insect bites, claws, teeth of
carnivora, foul instruments, fingers or clothes. Bloodless wounds
dangerous. Distal parts of the limbs exposed. Fresh wound exposed,
granulating less so. Most microbes enter by the lymphatics. Symptoms,
extension from wound, swollen lymphatics, reticular lymphangitis,
tubular lymphangitis, farcy, tuberculous case, slough. Fever variable.
General infection. Joint infection. Chronic cases. Lesions. Diagnosis,
from phlebitis. Treatment, antiseptics, diet, eliminants,
antithermics, blisters, mercurial ointment, iodine, lancing, tonics,
massage, bandage.
Under this heading must be named not one specific disease but a group of
infections entering by the lymphatic vessels and developing inflammation
of their substance. They may be divided into two classes: those caused
by infection through external wounds and those in which the poison
already in the system becomes localized on a weak or exposed tissue.
A third class must be included, in which there is no recognizable poison
but simply a local irritation which leads to coagulation or other
alteration in the lymph, or disease of the lymphatic vessels.
This subject belongs rather to surgery than medicine but it seems
necessary to contrast it here with the plethoric form of equine
lymphangitis. Most of its forms pertain to infectious diseases and will
be treated in connection with these.
_Causes of Simple Lymphangitis._ Formerly many forms of lymphangitis
were ascribed to mere local irritation; a superficial form will occur
from exposure to the rays of the sun, and an inflammation attendant on a
bruise or other injury with unbroken skin, may cause local inflammation
of the lymph vessels and enlargement of the adjacent lymph glands. As we
have seen above coagulation of the lymph and fibrine embolism may induce
local inflammation in the walls, and this may occur in connection with
excessive heat or cold or the presence of chemical irritants and
coagulants. These cases are however rarely serious and the tendency
today is to trace nearly all cases to infection, from germs already
present in the lymph or blood, or introduced through a wound or sore.
The effect of germs already circulating was shown in the beautiful
demonstrations of Chauveau in regard to calves subjected to castration
by subcutaneous torsion (bistournage). In the healthy calf the simple
operation gave rise to little disturbance. The healthy calf injected
with septic liquids equally escaped visible trouble. But the calf
injected with septic liquids and then subjected to bistournage had a
fatal infecting inflammation. There is a strong presumption that, in
lymphangitis, starting from an injury with no external sore, the germs
were already present in the blood or tissues but were unable to do any
serious damage until the injured and weakened part or organ offered an
area of lessened resistance to their colonization. Following the same
line of thought it has been noticed that animals of a coarse texture,
and lymphatic constitution (heavy draft horses and animals raised for
the butcher), and such as are debilitated by anæmia, overwork, or poor
and insufficient nourishment are above all liable to be attacked by
lymphangitis.
The insertion of the septic poison may take place through the bites of
insects, the claws, or teeth of carnivora that have been devouring
tainted or infecting meat, through the lancet or operating instrument of
the surgeon, by his fingers or the dust from his hair or clothes. The
wound is perhaps more likely to be infecting if it leads to no effusion
of blood, but affects only the thickness of the epidermis, as there is
less chance for the washing out of germs by the flowing blood, and there
is less care to employ antiseptics. Wounds in the feet and lower parts
of the limbs are specially liable to infection by reason of their
frequent contact with manure and decomposing organic matter in the soil.
A fresh wound, in which the lymph spaces are exposed, is somewhat more
open to infection than one that has advanced to the stage of
granulation, the layer of unorganized lymph and cells acting as a slight
barrier to the passage of the microbes.
Nearly all microbian diseases make their inroad by way of the
lymphatics, where the sparse cells fail to establish as active
phagocytosis as do the numerous moving cells of the blood. Hence a
number of infectious maladies are primarily and pre-eminently diseases
of the lymphatics, as glanders, strangles, tuberculosis, cancer,
anthrax, swine-plague, etc.
_Symptoms._ The most common form is where lymphangitis extends from some
pre-existing wound—as pricked or suppurating foot, fistula of foot,
withers or poll, chafing of shoulder or back, cracked heels, boil,
sloughing bruise, etc. The swelling around the sore or injury involves
in fact the radical lymphatic plexus in the connective tissue (reticular
lymphangitis). When the swelling extends and becomes more tense, with
firm, painful sinuous cords running out of it in different directions,
and especially toward the nearest lymphatic glands, and when these
glands are slightly swollen and tender, tubular lymphangitis is
diagnosed. No more striking example can be found than in skin glanders
(farcy). The rigid cords extend from the side of the face, from the eye,
and nose down toward the submaxillary glands and with more or less
adjacent engorgement. Or on a hind limb, or some portion of the trunk, a
more or less turgid swelling with one or more firm nodes (farcy buds)
and painful, tortuous cords running towards the lymph glands is very
characteristic.
A tuberculous case may show an indolent, hard, comparatively insensible
cutaneous cord leading toward the jugular furrow, the prescapular,
precrural or inguinal glands, and at long intervals softening,
fluctuating, bursting and discharging a thick pus. In a carcinoma there
is the old, hard, nodular, and finally ulcerating swelling from which
the firm cords extend to the mass of steadily enlarging lymphatic
glands.
A simpler form is where a bruise by the harness causes a hard, thick,
slough, embracing the entire thickness of the skin, from which the firm
corded lymphatics extend in different directions. After the slow process
of detachment, the local lymphangitis usually subsides under simple
cooling or antiseptic treatment.
But the grade of such lymphangitis is as varied as the particular germ
or combination of germs present in the wound, and the susceptibility of
the animal attacked, and there will be high, moderate or no fever,
according to the severity of the case, and in some cases purely local
trouble and in others general infection with purulent or septic
localization in distant parts. There is always danger of extension to a
neighboring joint with destructive results.
A curious outbreak is described by Wiart as attacking nearly every horse
in the regiment that sustained a slight wound. A tubercle looking mass
formed in the depth of the wound was slow to heal, and the lymphatics
leading out from it became round, corded, turgid, and at long intervals
developed along their course fluctuating centres which, whether opened
spontaneously or by the lancet, showed the same indolent habit. A single
attack would last from two to six months, and the actual cautery had to
be used on the sores.
The _lesions_ are those already described in the last article for simple
lymphangitis. For infecting cases they are those of the particular
disease which may be present.
_Diagnosis._ The general diagnosis of lymphangitis is the distinction
from phlebitis. In phlebitis the vein is blocked and cannot be raised by
pressure on the side leading toward the heart; in lymphangitis it can be
so raised. The swelling and tenderness are both greater in lymphangitis.
The inflamed vein is more rectilinear, the lymph vessel somewhat
sinuous. If suppuration ensues it is more diffuse in lymphangitis; more
restricted and mixed with the elements of blood in phlebitis.
For identification of the particular forms of infecting lymphangitis,
the reference must be made to the individual infectious diseases.
_Treatment._ In general the treatment of lymphangitis is the antisepsis
of wounds. Further than this the treatment of each case is that of the
particular disease which it represents. For all cases alike it is
important to apply vigorous treatment early, so as to cut it short
before it can attain a dangerous extension.
For the simpler forms of lymphangitis the wound should first be
thoroughly cleansed and disinfected. Washing with soap suds, or
carbonate of soda will remove any greasy agent which would prevent a
thorough antisepsis. Then it may be washed with the antiseptic
lotion:—carbolic acid solution (1:20), or mercuric chloride solution
(1:500), or zinc chloride (1:400) or potassium permanganate (1:160). If
the infection has been introduced by a small or punctured wound, the
sting or bite of an insect, or the prick of a sharp instrument it should
be freely cauterized to its depth with lunar caustic incising it if need
be to reach the whole of the poison, and the surface afterward dressed
with antiseptics.
The diet should be light but nutritious and laxative, and the free
action of the bowels and kidneys should be maintained by salines. When
fever runs high give quinine, or salicylate of soda. When a large wound
has to be dressed it may be requisite to use a non-poisonous agent like
acetate of aluminium or boric acid to irrigate it thoroughly. In some
such cases packing the irrigated wound with iodoform gauze has often an
excellent effect.
When there is a firm inflamed cord, hot and painful, a fly blister along
its course followed by mercurial ointment often gives excellent results.
Or they may be repeatedly painted with tincture of iodine.
Foci of suppuration must be promptly opened and thoroughly and
persistently disinfected.
With suppuration in multiple abscesses or large open sores liberal
feeding must be enjoined and iron and other tonics should be resorted
to.
The persistent swelling of the part must be met by active rubbing or
kneading, by exercise and by uniform compression by a flannel or elastic
bandage.
LYMPHANGIECTASIS. DILATED LYMPHATICS.
Result of lymphangitis, of heart disease, of pulmonary arterial
thrombosis, of external jugular plugging. Causes, obstruction to lymph
flow, compression, increased venous blood pressure, fibrinous lymph
coagula, action of sensory nerves, of lymphadenitis, anæmia. Symptoms
like dropsy if in plexus, in large lymphatics, moniliform swelling,
sacculation, wounds discharge lymph, hyperplasia of connective tissue,
fatty deposits, lipomata. Treatment, elastic bandage, cold,
astringents, iodine, punctures, ligatures, cauterizations, tonics.
The most striking cases of dilatation of the lymphatics in the lower
animals are met with in horses that have suffered repeatedly and
severely from the lymphangitis of plethora. Then the lower part of the
shank and the pastern are enormously thickened to perhaps two or even
three feet in circumference, and skin and connective tissue are the seat
of a general dilatation of the lymphatic plexus and vessels with great
thickening of their walls. Nocard and Barrier record cases of general
dilatation of the lymphatics in dogs in connection with heart disease,
also the case of a horse with old standing thrombosis of the pulmonary
arteries, hypertrophy of the right heart, and dilatation of the thoracic
duct to the size of the arm and of the lymphatics of the mesocolon to
the diameter of half an inch to nearly an inch. Nocard records two cases
in the horse, one of a reticular lymphangioma of the sheath, and the
other of dilatation of the lymph vessels accompanying the saphena vein
on the inside of the thigh. This formed small, soft, fluctuating,
extremely irregular tumors, completely covering the vein for a space of
about four inches.
In both cases the dilatations were surrounded by a thick layer of
connective tissue filled with liquid. Virchow records a case of a
new-born calf in which a thrombosis of the external jugular vein caused
obstruction of the mouth of the thoracic duct, and a consequent extreme
distension of all the splanchnic lymph vessels with a slightly
sanguinolent fluid. The intestines especially were covered everywhere
with broad, bead-like canals, arranged so closely together that the
intervening tissue could be scarcely recognized.
The _causes_ of lymphangiectasis appear to be generally some obstruction
to the onward flow of the lymph. Any diseased condition, therefore, that
causes compression of the larger lymph vessels may cause dilatation of
the smaller ones leading into these. General distension may come from
disease of the lungs or left heart and increased venous blood pressure,
or from thrombus of the jugular, or a tumor obstructing the thoracic
duct, while local engorgements may come from the pressure of tumors, or
the occurrence of lymphangitis and formation of fibrinous coagula. In
cases of partial obstruction of the lymph vessels the increased
secretion of lymph may lead to distension and enlargement. It may be
named in this connection that irritation of the sensory nerves in dogs
has been shown to determine a larger production of lymph (Krause).
Lymphadenitis and the obstruction of the passage of lymph through the
glands is an obvious cause, and hence the disease is specially liable to
appear in connection with diseases which show a predilection for the
lymphatics (tuberculosis, glanders, strangles, carcinoma, etc.)
In his work on dilatation and occlusion of lymph channels Busey shows
that in man the majority of cases are in hospital patients in whom blood
and general health have been impoverished and reduced by unhygienic
conditions. One case gave support to the theory of maternal impression,
the pregnant mother having suffered from over-use of the right limb on a
sewing machine, and the offspring having shown extensive
lymphangiectasis in the right leg.
_Symptoms_ consist in enlargement of the lymph vessels or plexus, and
often of the glands. If of the lymph plexus it may appear like a
dropsical effusion in the part, with or without saccular dilatations at
intervals. If of the larger vessels, their tortuous anastomosing trunks
following largely the lines of the veins are usually characteristic. If
the distension is slight it is usually moniliform, as the valves are
still intact, and the intervals between them stand out as bladder-like
masses. If the structure is wounded or if it ulcerates there is the
discharge of a straw-colored fluid, often rendered milky by the presence
of fatty granules, and at times tinged with blood. There is always a
tendency to the increase and condensation of the connective tissue
surrounding the vessels, and fatty degeneration and the formation of
lipomata are not uncommon.
_Treatment._ Compression, by flannel or elastic bandage, from the foot
upward, is the simplest and most promising treatment when the limb is
affected. The local application of cold, astringents or iodine may be
added. Punctures, ligatures, and cauterization have not given
encouraging results. Ligature of the nutrient artery of the part, has
succeeded in one or two cases, but has failed in others. Tonics are to
be tried more particularly in cases due to specific debilitating
diseases. Sometimes a spontaneous recovery has been noticed when the
surrounding connective tissue has increased and contracted in connection
with inflammation.
LYMPHORRHŒA. LYMPHORRHAGIA. DISCHARGE OF LYMPH THROUGH WOUNDS OR SORES.
Result of rupture of lymphatics. Milky, fatty lymph. Treatment,
ligature, excision, cauterization, of little avail. Compression.
Tonics.
Obstruction of a lymph duct may lead to rupture and the discharge of its
fluid on the surface or into an internal cavity. Dr. Cayley records a
case of fatal peritonitis in man from rupture of the receptaculum chyli,
and the formation of lymph fistulæ has been attributed to filaria
sanguinis hominis. We are aware of no corresponding case in connection
with the blood parasites of the horse or dog. In the larger domestic
animals the great thickness and resistance of the skin offers a barrier
to the rupture of subcutaneous lymph vessels, but this no longer applies
in case of a suppurating or ulcerous wound. The escaping lymph has often
a milky hue from the admixture of fat, just as its escape in the kidneys
causes chyluria, and in the bowel fatty stools. The escape is often very
profuse and persistent, and results in marked debility. Ligature and
excision of the fistulous vessel, also caustics—actual and potential,
have been tried with rather poor success. Fitzer succeeded in an
obstinate case by the extensive application of nitrate of silver and
others by simple compression. As the victims are usually debilitated a
course of tonics is usually desirable.
LYMPHADENITIS. INFLAMMATION OF THE LYMPH GLANDS.
Result of lesions of tributary tissues. Arrest in glands of microbes
and other irritants. Trauma of gland. Inflammation. Symptoms,
swelling, stiffness, gland tender, hot, pitting envelope, corded lymph
vessels, abscess, fever. Lesions. Treatment, antiseptics, astringents,
emollients, vesicants, lancing, antiseptics, antiphlogistics,
antithermics. Chronic adenitis. Symptoms, enlarged glands without
engorgement, if simple affects a single gland, if infectious, a group.
Lesions, gland swelling, induration, shrinking, follicular distension,
pigmentation, growth of lymphocytes, caseation, calcification.
Treatment, antiphlogistic, antiseptic, iodine, chloride of calcium,
iodide of potassium.
Apart from traumatic lesions lymphadenitis virtually implies some lesion
of the tissues from which the different vessels of the glands proceed.
The glands however have been referred to as filtering agents on the
course of the lymph vessels and in this partial view of their functions
we find abundant reason why irritants carried in the lymph stream,
should be arrested with pathogenic results in the glands. A particle of
pigment gaining entrance to the lymph vessels tends to be arrested among
the trabeculæ of the gland, and contributes to the pigmentation so
common in old animals. Cells and granules from malignant tumors, and
bacteria from an infection-atrium are arrested in the glands and make
these the great centres of infection-lesions.
_Traumatic_ inflammation comes from bruises, punctures or incisions
directly implicating the glands. There result swelling, tenderness and
the other general signs of inflammation, and in the case of an open
wound possibly lymphorrhagia.
_Acute inflammation_ more commonly supervenes on inflammation in the
area drawn upon by the afferent vessels of the gland. In inflammations
generally the adjacent lymphatic glands become congested. In
lymphangitis it is so in a marked degree. In external parts we can
follow this by careful observations during life, in internal organs we
often find the glandular enlargement after death.
_Symptoms_ consist in swelling and perhaps stiffness in the region of
the gland. Manipulation shows tenderness and heat, the gland being felt
abnormally large, round, or oval, tense, loose from the skin but having
a distinct envelope of soft pitting exudate which tends to increase in a
downward direction. There may or may not be a corded feeling of the
afferent lymphatic trunks. As the pasty swelling increases, it extends
into surrounding parts, binds the gland to the skin and adjacent
structures, and may even conceal the gland in the excess of its
investing engorgement. This is especially frequent in strangles. As the
process advances softening may take place in the centre and extend
toward the circumference, and this may burst like an ordinary abscess.
In some cases the softening is very limited and tardy, and the pus may
be pent up and inspissated, or it may appear to be entirely reabsorbed
while the gland is in process of induration. Fever which may run high
during the process of suppuration, moderates when that has been
accomplished.
In the case of glands too deeply situated to be clearly felt the
occurrence of purulent fluctuation in their vicinity suggests abscess of
the glands, an important induction as the maturation and healing are
usually slow in the gland tissue.
_Lesions._ At the outset the glands are visibly enlarged, softened, and
of a dark red hue, with spots of a brighter red. The changes, mainly in
the medullary layer, consist in a great proliferation of spheroidal
cells in the follicles and also of polyhedral cells in the lymph
sinuses. The endothelial cells are swollen, the blood vessels gorged,
and extravasations of blood into the follicles and sinuses are frequent.
Abscess or fibroid hyperplasia with induration may follow. Much depends
on the particular infection (tuberculosis, glanders, carcinoma, etc.) as
the special product of each disease will be found in the affected gland.
_Treatment_ is in the main as advised for lymphangitis and will vary
with each specific causative disease. Locally antiseptics, astringents,
deobstruents, emollients, and vesicants will be requisite in different
cases. As soon as pus can be distinctly diagnosed it should as a rule be
evacuated, and the cavity treated antiseptically. General treatment may
at first be antiphlogistic and febrifuge, but must usually embrace
tonics and stimulants in the end.
=Chronic Adenitis= may be a sequel of the acute, or it may arise
independently. In the latter case it is usually the result of some other
disease (tuberculosis, glanders, carcinoma, sarcoma melanosis inveterate
disease of the skin, chronic fistula, abscess, or mucous inflammation).
The _symptoms_ are those of enlarged glands with no material surrounding
engorgement. In the infections of tuberculosis and glanders it shows a
tendency to affect the whole group, whereas in simple abscess or in
suppuration of the nasal sinuses it may implicate one gland only, the
remainder appearing normal.
_Lesions._ The gland often becomes indurated and even shrunken, the
connective tissue elements undergoing a steady increase at the expense
of the follicles and lymphoid cells. This is a common condition of
tuberculous glands (perl-knoten, grapes) of cattle, but may result from
the entrance of pigment or other cause of mild irritation. In other
cases pigment entering from without or developed from blood in the
congested gland, finds permanent lodgment in its tissue and may give it
a gray mottled or quite black aspect. In still other cases, there is a
great increase of the round lymphoid and larger polyhedral cells, many
of which degenerate becoming strongly refracting, stain feebly, or not
at all, and pass into a cheesy degeneration. This is a common condition
in tuberculosis and glanders, and the caseous centres beginning as
multiple miliary centres may coalesce to form masses of six or twelve
inches in their greatest diameter as in bovine tuberculosis. In other
cases the caseating mass becomes the seat of calcareous deposit and the
necrotic and caseated gland becomes in part calcified. Other
degenerative changes such as atrophy, amyloid, and hyaline are met with
but have received little attention.
_Treatment_ will be subordinated to the primary cause. If that is a
simple local inflammation or irritation its removal will entail a speedy
improvement in the gland, and, in the absence of too extensive
structural change, a speedy recovery. The infectious cases on the other
hand are likely to prove as inveterate as the disease on which they
depend. In case the enlargement or congestion of the gland persists
after the removal of its primary cause local deobstruents especially the
preparations of iodine are usually effective. Tincture of iodine with
soap, iodide of lead, and mercurial ointment have been severally used
with advantage. Injection of a weak solution of iodine into the gland
will at times succeed. The internal use of chloride of calcium or iodide
of potassium will often hasten recovery.
INDEX.
Abomasum, position of in ox, 156.
Abscess in adynamic inflammation, 71.
Abscess of false nostril, 92, 97.
Abscess of guttural pouches, 94.
Abscess in heart, 338, 341.
Abscess in inflammation, 71.
Abscess of the lung in pneumonia, 225.
Actinomycosis, 99.
Adynamic fever, 68.
Adynamic inflammation, 68.
Adynamic inflammation, abscess in, 71.
Adynamic inflammation, blistering in, 70.
Adynamic inflammation, firing in, 70.
Adynamic inflammation, massage in, 71.
Adynamic inflammation, suppuration in, 71.
Adynamic inflammation, local treatment of, 69.
Adynamic inflammation, treatment of, 68.
Adynamic fever, treatment of, 68.
Air, character of the expired, 153.
Air, effects of vitiated, 180.
Air in the pleura, 265.
Air passages, parasites of, 290.
Anæmia, chronic, 377.
Anæmia, idiopathic, 375.
Anæmia oligæmia, 371.
Anæmia, pernicious, 375.
Anæmia, progressive pernicious, 375.
Anamnesis, 19.
Anatomy, definition of pathological, 2.
Aneurism, 356, 359.
Aneurism by anastomosis, 359.
Angeioleucitis, 386.
Angioma, 359.
Angina, 114.
Angina pectoris, 311.
Angina pharyngea, 126.
Angioma in nose, 100.
Apoplexy, pulmonary, 211.
Arteriectasis, 356.
Arteries, diseases of, 345.
Arterio-sclerosis, 359.
Arteritis, 345.
Arteritis, external, 345.
Arteritis, internal, 345.
Asthma, 274.
Asthma in the dog, bronchial, 270.
Asthma in the horse, 273.
Asthma, pathology of, 270.
Asthma, symptoms of, 271.
Asthma, treatment of, 271.
Atelectasis, 206.
Atelectasis, causes of, 206.
Atelectasis, lesions of, 207.
Atelectasis, symptoms of, 207.
Atelectasis, treatment of, 208.
Atheroma, 349.
Atrophy, 322.
Auscultation, 164.
Auscultation of birds, 168.
Auscultation of cough, 174.
Auscultation of dog, 168.
Auscultation of goat, 168.
Auscultation of horse, 166.
Auscultation, immediate, 164.
Auscultation, mediate, 164.
Auscultation of ox, 167.
Auscultation of pig, 168.
Auscultation of sheep, 168.
Axillary artery, embolism of, 355.
Bacillus of Friedländer, 216.
Bacteriology of pneumonia, 216.
Baths, cold, 65.
Baths, warm, 64.
Birds, auscultation of, 168.
Birds, percussion in, 161.
Bleeding, in fever, 63.
Bleeding, local, 64.
Blistering in inflammation, 70.
Blood, active determination of, 33.
Blood, arterial determination, 33.
Blood, black pigment in, 378.
Blood, diseases of, 367.
Blood exudations, 52.
Blood globules, 367.
Blood globules, numbers of, 368.
Blood, modifications of in pneumonia, 226.
Blood, ratio to body weight, 370.
Bot-fly, sheep, 109.
Bots, 149.
Breast pang, 311.
Breathing, deep, 154.
Breathing, hurried, 153.
Breathing, labored, 154.
Breathing supplementary, 169.
Breathing, quick, 153.
Broken wind, 274.
Broken-winded horses, examination of, 287
Bronchial asthma in the dog, 270.
Bronchial catarrh, 191.
Bronchial glands, diseases of, 290.
Bronchial sound, 170.
Bronchial tubes, polypus of, 289.
Bronchitis, 178.
Bronchitis, acute in horse, 178.
Bronchitis, capillary, 186.
Bronchitis, chronic in horse, 191.
Bronchitis, in cattle, 197.
Bronchitis in dog, 195.
Bronchitis in ox, 193.
Bronchitis in sheep, 197.
Bronchitis, pseudo-membranous, 186
Broncho-pleuro-pneumonia, 258.
Broncho-pneumonia, 258.
Cadeac’s diplococcus pneumoniæ equina, 218.
Cancer of the heart, 341.
Carcinoma in nose, 99.
Carditis, 338.
Carious Teeth, Nasal Discharge from, 93.
Catarrh, bronchial, 191.
Catarrh, chronic, in cattle, 104.
Catarrh, chronic nasal, 87.
Catarrh, coccidian in rabbits, 108.
Catarrh, malignant, 105.
Catarrh, nasal from linguatula, 113.
Catarrh, nasal from rhinaria taenioides, 113
Catarrh, nasal in dog, 113.
Catarrh, nasal in horse, 113
Catarrh, of cattle, 105.
Catarrh of frontal sinuses in ox, 101.
Catarrh of nose, 81.
Catarrh, traumatic, 101.
Cattle, catarrh of, 105.
Cattle, chronic catarrh in, 104.
Cattle, Coryza in, 85.
Cattle, croupous bronchitis in, 197.
Cattle, pharyngo-laryngitis of, 122.
Cattle, pleurisy in, 253.
Cell change, 42.
Cell proliferation, 42.
Cephalemia maculata, 112.
Changes in circulation, 45.
Changes in innervation, 44.
Changes in tissue elements, 41.
Chemiotaxis, 47.
Chemistry, definition of pathological, 2.
Chest, 155.
Chest, accidental sounds of, 167.
Chest, bronchial sound of, 165.
Chest, diseases of, 150.
Chest, healthy sounds of, 165, 167.
Chest, mensuration of, 175.
Chest sounds, modifications of healthy, 169.
Chest, morbid sounds of, 152.
Chest percussion of in horse, 159.
Chest, percussion of in ox, 159.
Chest, contents of in horse, 155.
Chest, respiratory murmur of, 165.
Chest sounds, abnormal, 171.
Chest sounds, amphoric, 171.
Chest sounds, cavernous, 171.
Chest sounds, morbid, 169.
Chest sounds, mucous, 171.
Chest, tapping the, 261.
Chest, tubal sound of, 165.
Chest, vesicular sound of, 165.
Chronic pneumonia in the ox, 235.
Chyliform exudate, 52.
Circulation, changes in, 45.
Circulation, diseases of organs of, 291.
Clots in the heart, 337.
Cloudy swelling, 41.
Coccidian catarrh in rabbits, 108.
Cold, action of, 74.
Cold in the head, 81.
Collapse of lung, 206.
Collapse of lung, causes of, 206.
Collapse of lung, symptoms of, 207.
Collapse of lung, treatment of, 208.
Congestion, 33.
Congestion of the lungs, 198.
Congestion of the lungs, causes of, 198.
Congestion of the lungs, course of, 201.
Congestion of the lungs, lesions in, 201.
Congestion of the lungs, nature of, 202.
Congestion, passive, 35.
Congestion of the lungs, symptoms of, 199.
Congestion of the lungs, termination of, 201.
Congestion, treatment, 38.
Congestion of the lungs, treatment of, 202.
Congestion, venous, 35.
Contagious diseases, of nose, 107.
Convulsive cough, 148.
Coryza, 81.
Coryza, causes of, 82.
Coryza, course of, 83.
Coryza in cattle, 85.
Coryza in dog, 85.
Coryza in horse, 81.
Coryza in pig, 85.
Coryza in sheep, 85.
Coryza, symptoms of, 82.
Coryza, treatment of, 83.
Coryza, treatment of chronic, 90.
Cough, 150.
Cough, abortive, 151.
Cough, auscultation of, 174.
Cough, broken, 151.
Cough, convulsive, 148.
Cough, croupous, 151.
Cough, dry, 151.
Cough, humid, 151.
Cough, husky, 151.
Cough, loud, 151.
Cough of dog, 150
Cough of horse, 150.
Cough of ox, 150.
Cough of sheep, 150.
Cough, paroxysmal, 151.
Cough, rasping, 151.
Cough, rattling, 151.
Cough, short, 151.
Cough, small, 151.
Cough, soft, 151.
Cough, strong, 150.
Cough, symptomatic, 151.
Cough, weak, 151.
Crepitation, 173.
Crepitation, modified, 173.
Croup, 128.
Croup in sheep, 131.
Croup in the horse, 132.
Croup in the ox, 128.
Croupous bronchitis in cattle, 197.
Croupous bronchitis in sheep, 197.
Croupous cough, 151.
Croupous exudate, 52.
Croupous laryngitis, 128.
Croupous pneumonia, 213.
Croupous pneumonia, exciting causes, 215.
Croupous pneumonia in fowls, 238.
Croupous pneumonia in sheep, 236.
Croupous pneumonia in the ox, 233.
Croupous pneumonia, predisposing causes, 214.
Cynanche, 114.
Cynanche pharyngea, 126.
Cysticercus cellulosa in heart, 342.
Cysticercus tenuicollis in heart, 342.
Cysts in nose, 100.
Death beginning at brain, 5.
Death beginning at lungs, 4.
Death from old age, 5.
Death from syncope, 4.
Death of cells, 41.
Death of tissue, 41.
Death, molecular, 4.
Death, partial, 4.
Degeneration, fatty, 340.
Determination of blood, active, 33.
Determination of blood, arterial, 33.
Defervescence, 61.
Diagnosis, history of the attack in, 16.
Diagnosis, means of, 16.
Diagnosis, medical, 16.
Diagnosis, objective symptoms in, 16.
Diagnosis, usual state of health of subject, 16.
Diapedesis, 47.
Diaphoretics, 66.
Diaphragm, position of in dog, 157.
Diaphragm, position of in horse, 156.
Diaphragm, position of in ox, 156.
Diaphragm, position of in pig, 157.
Diplococcus pneumoniæ equina, 217.
Disease, causes of, 7.
Disease, definition of, 2.
Disease, exciting causes of, 9.
Disease, extrinsic causes of, 9.
Diseases, infectious of the throat, 149.
Diseases of nose, 107.
Diseases of the chest, 150.
Diseases of the lungs, 177.
Diseases of the nose, 78.
Diseases of the respiratory organs, 72.
Diseases, parasitic of the nose, 108.
Disease, percussion in, 161.
Disease, predisposing causes of, 7.
Distemper, 114.
Dog, auscultation of, 168.
Dog, bronchial asthma in, 270.
Dog, bronchitis in, 195.
Dog, coryza in, 85.
Dog, laryngitis in, 126.
Dog, nasal catarrh in, 113.
Dog, percussion in, 161.
Dog, position of diaphragm in, 157.
Dog, position of heart in, 157.
Dog, pleurisy in, 257.
Dog, pneumonia in, 237.
Dropsy, anæmic, 377.
Dyspnœa, 274.
Dyspnœa laryngea, 133.
Echinococcus veterinorum in the heart, 341.
Embolism, 345, 347, 350.
Empyema, 266.
Emphysema, interlobular, 280.
Emphysema, vesicular, 280.
Endocarditis, 331.
Epistaxis, 78.
Epistaxis, causes of, 78.
Epistaxis, symptoms of, 79.
Epistaxis, treatment of, 79.
Erysipelas, 361.
Etiology, 7.
Expectoration, 152.
Exudation, 49.
Facies, 25.
False nostril, abscess of, 92, 97.
Fatty degeneration, 57.
Fatty degeneration of the heart, 340.
Fatty tumors in nose, 99.
Fever, 59.
Fever, adynamic, 68.
Fever, alkalies in, 67.
Fever, antipyretics in, 67.
Fever, cold baths in, 65.
Fever, cold stage, 60.
Fever, convalescence in, 67.
Fever, defervescence, 61.
Fever, definition of, 59.
Fever, diaphoretics in, 66.
Fever, diuretics in, 66.
Fever, general bleeding in, 63.
Fever, hot stage, 60.
Fever, laxatives in, 66.
Fever, local bleeding in, 64.
Fever, premonitory symptoms of, 60.
Fever, production of waste matters in the system in, 61.
Fever, regimen, 62.
Fever, remedies, 63.
Fever, resolvents in, 67.
Fever, retention of water in the fevered system, 61.
Fever, sedatives in, 66.
Fever, stimulants in, 67.
Fever, symptoms of, 59.
Fever, temperature, 61.
Fever, tonic refrigerants in, 67.
Fever, treatment of, 62.
Fever, types of, 62.
Fever, typhoid, condition in, 61.
Fever, warm baths in, 64.
Fibrinous exudate, 51.
Filaria immitis, 342.
Filaria papillosa hæmatica, 342.
Firing in adynamic inflammation, 70.
Firing in inflammation, 70.
Flank, double action of, 153.
Foreign body in nose, 94.
Fowls, croupous pneumonia in, 238.
Frontal sinuses in cattle, catarrh of, 101.
Gangrene, 58.
Gangrene, in pneumonia, 226.
Glander nodules in heart, 341.
Glottidis, œdema, 147.
Goat, auscultation of, 168.
Granular degeneration, 41.
Granulation, 56.
Granule corpuscles, 56.
Granule masses, 56.
Grub in head, 110.
Guttural pouches, abscess of, 94.
Gutturomycosis of solipedes, 149.
Hæmophilia, 366.
Hæmoptysis, 209.
Hæmorrhage, 365.
Hæmorrhage from the nose, 78.
Hæmorrhagic infarction, 211.
Healing by adhesion, 56.
Healing by first intention, 56.
Healing by second intention, 56.
Health, definition of, 3.
Heart, abscess in, 338.
Heart, atheroma of, 344.
Heart, cancer of, 341.
Heart, calcified, 344.
Heart, cartilaginous degeneration of, 338.
Heart, chronic disease of, 339.
Heart, congenital malformations and displacements of, 313.
Heart, cysticercus cellulosa in, 342.
Heart, cysticercus tenuicollis in, 342.
Heart, diffuse suppuration in, 338.
Heart, dilatation of, 323.
Heart disease, general symptoms of, 305.
Heart, diseases of, 291.
Heart, echinococcus in, 341.
Heart, fatty degeneration of, 340.
Heart, fibrous degeneration of, 338.
Heart, filaria in, 342.
Heart, functional irregularity of, 312.
Heart, glander nodules in, 341.
Heart, hypertrophy of, 315.
Heart, induration of, 338.
Heart, inflammations in, 325.
Heart, melanosis of, 341.
Heart, morbid sounds of, 303.
Heart, neoplasms of, 341.
Heart, osseous degeneration of, 338.
Heart, polypus in, 338.
Heart, position of, 292.
Heart, position of in dog, 157.
Heart, position of in horse, 155.
Heart, position of in sheep, 157.
Heart, Rainey’s cysts in, 342.
Heart, relative position of in the domestic animals, 155.
Heart, rupture from concussion, 343.
Heart, rupture from exertion, 343.
Heart, rupture from pithing, 343.
Heart, rupture of, 343.
Heart, sarcocysts in, 342.
Heart, softening of, 338.
Heart, sounds of, 301.
Heart, strongyli in, 342.
Heart, structure of, 293.
Heart, table contrasting symptoms of hypertrophy and dilatation, 319.
Heart, table of murmurs of, 304.
Heart, thickness of the walls, 295.
Heart, trichina in, 342.
Heart, tubercle of, 341.
Heart, ulceration of, 338.
Heart, ulceration of, 343.
Heart, valvular disease of, 339.
Heart, varicose veins in, 341.
Heart, weight of, 296.
Heart, weight of, 317.
Heaves, 274.
Hemiplegia laryngea, 133.
Hereditary roaring, 141.
Hodgkin’s disease, 382.
Horse, acute bronchitis in, 178.
Horse, acute pleurisy in, 239.
Horse, asthma in, 273
Horse, auscultation of, 166.
Horse, chronic bronchitis in, 191.
Horse, croup in, 132.
Horse, laryngitis in, 115.
Horse, nasal catarrh in, 113.
Horse, percussion of chest in, 159.
Horse, pneumonitis in, 213.
Horse, position of chest in, 155.
Horse, position of diaphragm in, 156.
Horse, position of heart in, 155.
Horse, position of intestines in, 156.
Horse, position of liver in, 156.
Horse, position of lung in, 156.
Horse, position of pancreas in, 156.
Horse, position of spleen in, 156.
Horse, position of stomach in, 156.
Hydroæmia, 371.
Hydrothorax, 259.
Hydrothorax, symptoms of, 260.
Hydrothorax, treatment of, 261.
Hyperæmia, 33.
Hyperæmia, definition of, 33.
Hyperæmia, pulmonary, 198.
Hyperæmia, results of, 35.
Hyperæmia, symptoms, 35.
Hyperæsthesia, laryngeal, 148.
Hypertrophy of the heart, 315.
Iliac arteries, embolism of, 354, 355.
Induration of the heart, 338.
Infarction, hæmorrhagic, 211.
Infectious diseases of the throat, 149.
Inflammation, 39.
Inflammation, abscess in, 71.
Inflammation, adynamic, 68.
Inflammation, blistering in, 70.
Inflammation, cold applications in, 69.
Inflammation, definition of, 39.
Inflammation, firing in, 70.
Inflammation, forms of, 41.
Inflammation, hot applications in, 69.
Inflammation, local treatment of, 69.
Inflammation, massage in, 71.
Inflammation of the lungs, 212.
Inflammation, products of, 52.
Inflammation, results of, 52.
Inflammation, rubbing in, 71.
Inflammation, suppuration in, 71.
Inflammation, treatment of, 62.
Inflammatory, new formations, 53.
Influenza, 114.
Innervation, changes in, 44.
Intermittent roaring, 141.
Interstitial development of lymph into tissue, 57.
Intestines, position of in horse, 156.
Inveterate roaring, causes of, 134.
Laryngea, cynanche, 115.
Laryngea, dyspnœa, 133.
Laryngea, hemiplegia, 133.
Laryngeal hyperæsthesia, 148.
Laryngeal polypi, 132.
Laryngitis, 114.
Laryngitis, angina, 115.
Laryngitis, chronic, 117.
Laryngitis, croupous, 128.
Laryngitis in the dog, 126.
Laryngitis in the horse, 115.
Laryngitis in sheep, 123.
Laryngitis in pig, 124.
Laryngitis, pseudo-membranous, 128.
Laryngitis, subacute, 117.
Laryngitis, treatment of chronic, 121.
Laryngo-pharyngitis in cattle, 122.
Larynx, inflamed, 114.
Larva in head, morbid symptoms caused by, 110.
Larva in nasal sinuses of sheep, 109.
Larva, mature, 110.
Larva, œstrus, 149.
Larva, of œstrus ovis, 109.
Larva, young, 110.
Leeches, 149.
Leech bites, 108.
Leucocythæmia, 379.
Leukæmia, 379.
Linguatula taenioides, nasal catarrh from, 113.
Liver, position of in horse, 156.
Liver, position of in ox, 156.
Lung, abscess of in pneumonia, 225.
Lung, collapse of, 206.
Lungs, congestion of, 198.
Lungs, diseases of, 177.
Lungs, inflammation of, 212.
Lungs, parasites of, 290.
Lungs, position of in horse, 156.
Lungs, position of in ox, 156.
Lungs, position of in sheep, 157.
Lungs, relative positions of in the domestic animals, 155.
Lymphadenitis, 400.
Lymphadenoma, 382.
Lymphangiectasis, 397.
Lymphangitis, acute, 386.
Lymphangitis, infective, 392.
Lymphangitis of plethora, 386.
Lymphangitis, traumatic, 392.
Lymphatics, dilated, 397.
Lymph glands, inflammation of, 400.
Lymphorrhagia, 399.
Lymphorrhœa, 399.
Lymph, interstitial development into tissue, 57.
Malignant catarrh, 105.
Massage in adynamic inflammation, 71.
Massage in inflammation, 71.
Medical diagnosis, 16.
Melanæmia, 378.
Melanosis of the heart, 341.
Mensuration of chest, 175.
Mesenteric arteries, embolism of, 355.
Mesenteric glands, diseases of, 290.
Metritis, 361.
Microbes, 47.
Micrococcus pneumoniæ crouposæ, 217.
Migration of white blood cells, 43.
Monday morning disease, 386.
Morbid sounds, 152.
Mucous exudate, 50.
Myocarditis, 338.
Nasal catarrh, 81.
Nasal catarrh, chronic, 87.
Nasal discharge from carious teeth, 93.
Nasal gleet, 87.
Nasal mucosa, 26.
Nasal polypus, 98.
Nasal sinuses of sheep, larva in, 109.
Nasal sinuses, pus in, 90.
Neoplasms in nose, 98.
Neoplasms of heart, 341.
Nervous disorder, symptoms of, 27.
Nœvus, 359.
Nœvus in heart, 341.
Nose, angioma in, 100
Nose, bleeding from, 78.
Nose, carcinoma in, 99.
Nose, contagious diseases of, 107.
Nose, cysts in, 100.
Nose, diseases of, 78.
Nose, neoplasms in, 98.
Nose, osseous tumors in, 100.
Nose, parasitic diseases of, 108.
Nose, sarcoma in, 99.
Occasional roaring, 141.
Œdema glottidis, 147.
Œdema, pulmonary, 204.
Œstrus larva, 149.
Œstrus ovis in nasal sinuses of sheep, 109.
Œstrus ovis, larva of, 109.
Œstrus purpureus, 112.
Omasum, position of in ox, 156.
Organs, relative positions of in the domestic animals, 155.
Osseous tumors in nose, 100.
Ox, auscultation of, 167.
Ox, bronchitis in, 193.
Ox, chronic pneumonia in, 235.
Ox, croup in, 128.
Ox, croupous pneumonia in, 233.
Ox, percussion of chest in, 159.
Ox, position of abomasum in, 156.
Ox, position of diaphragm in, 156.
Ox, position of liver in, 156.
Ox, position of lungs in, 156.
Ox, position of omasum in, 156.
Ox, position of paunch in, 156.
Ozœna, 87.
Palpation, 175, 300.
Palpitations, 307.
Pancreas, position of in horse, 156.
Paracentesis thoracis, 261.
Parasites in anæmia, 372.
Parasites of the air passages, 290.
Parasites of the throat, 149.
Parasitic diseases, of the nose, 108.
Paroxysmal cough, 151.
Passive congestion, causes of, 35.
Passive congestion, results, 37.
Passive congestion, symptoms, 37.
Pathology, definition of, 1.
Pathology, definition of general, 1.
Pathology, definition of special, 2.
Paunch, position of in ox, 156.
Percussion, 158, 300.
Percussion, immediate, 158.
Percussion in birds, 161.
Percussion in disease, 161.
Percussion in dog, 161.
Percussion in pigs, 160.
Percussion in sheep, 160.
Percussion, mediate, 158.
Pericarditis, 326.
Pericarditis, chronic, 328.
Perspiration, suppressed, 75.
Phagocytosis, 47, 48.
Pharyngeal polypi, 132.
Pharyngitis, 114, 126.
Pharyngo-laryngitis in cattle, 122.
Pharynx, 114.
Phlebitis, 360.
Phlebitis, adhesive, 361.
Phlebitis, idiopathic, 360.
Phlebitis, suppurative, 361.
Phlebolites, 364.
Phlegmasia, 39.
Phlogosis, 39.
Pig, auscultation of, 163.
Pig, coryza in, 85.
Pig, laryngitis in, 124.
Pig, percussion in, 160.
Pig, pneumonia in, 237.
Pig, position of diaphragm in, 157.
Plethora, 369.
Plethora, lymphangitis of, 386.
Pleura, air in, 265.
Pleura, parasites of, 290.
Pleurisy, causes of, 239.
Pleurisy, chronic, 267.
Pleurisy, classification of cases in, 246.
Pleurisy, dry, 247.
Pleurisy, fibrinous, 247.
Pleurisy in dog, 257.
Pleurisy in cattle, 253.
Pleurisy in horse, 239.
Pleurisy in sheep, 256.
Pleurisy, pleuritic effusion in, 246.
Pleurisy, post mortem appearances in, 244.
Pleurisy, prognosis of, 249.
Pleurisy, sero-fibrinous, 247.
Pleurisy, sero fibrino-purulent, 248.
Pleurisy, symptoms of, 241.
Pleurisy, treatment of, 249.
Pleuritis, 239.
Pleurodynia, 269.
Pleuro-pneumonia, 258.
Plugging the nose, 79.
Pneumonia, 212.
Pneumonia, abscess in, 223.
Pneumonia, abscess of the lung in, 225.
Pneumonia, antiphlogistic treatment of, 228.
Pneumonia, antipyretic treatment in, 230.
Pneumonia, auscultation in, 220.
Pneumonia, bacteriology of, 216.
Pneumonia, chronic, 232.
Pneumonia, compresses in, 231.
Pneumonia, consolidation in, 224.
Pneumonia, contagion in, 216.
Pneumonia, croupous, 213.
Pneumonia, croupous in fowls, 238.
Pneumonia, death in, 223.
Pneumonia, derivatives in, 231.
Pneumonia, fomentations in, 231.
Pneumonia, gangrene in, 224, 226.
Pneumonia, gray hepatisation in, 225.
Pneumonia in the dog, 237.
Pneumonia in the ox, chronic, 235.
Pneumonia in the ox, croupous, 233.
Pneumonia in the ox, treatment of, 235.
Pneumonia in the pig, 238.
Pneumonia in the sheep, croupous, 236.
Pneumonia, modifications of distant organs in, 226.
Pneumonia, modifications of the blood in, 226.
Pneumonia, pathological lesions in, 224.
Pneumonia, percussion in, 220.
Pneumonia, poultices in, 231.
Pneumonia, progress of, 221.
Pneumonia, red hepatisation in, 224.
Pneumonia, refrigerant febrifuge in, 231.
Pneumonia, resolution in, 223.
Pneumonia, sedatives in, 231.
Pneumonia, splenisation in, 223.
Pneumonia, stimulants in, 231.
Pneumonia, subacute, 222.
Pneumonia, symptoms of, 219.
Pneumonia, treatment of, 227.
Pneumonitis, 212.
Pneumonitis in the horse, 213.
Pneumothorax, 265.
Pneumothorax, symptoms of, 265.
Pneumothorax, treatment of, 266.
Polyæmia, 369.
Polypi, laryngeal, 132.
Polypus in the heart, 338, 341.
Polypus, nasal, 98.
Polypus of the bronchial tubes, 289.
Polypi, pharyngeal, 132.
Prevention, 31.
Prognosis, 28.
Prognosis, causes of illness, 29.
Prognosis, definition of, 28.
Prophylactics, 31.
Prophylaxis, 31.
Pseudo-membranous laryngitis, 128.
Pulmonary apoplexy, 211.
Pulmonary hyperæmia, 198.
Pulmonary œdema, 204.
Pulmonary œdema, physical signs of, 205.
Pulmonary œdema, prognosis of, 205.
Pulmonary œdema, symptoms of, 205.
Pulse, 23, 296.
Pus, 55.
Pyo-pneumothorax, 266.
Rabbits, coccidian catarrh, 108.
Rainey’s cysts in the heart, 342.
Râles, 171.
Râles, bronchial, 171.
Râle, crepitant, 172.
Râle, dry, 171.
Râle, mucous, 172.
Râle, sibilant, 171, 172.
Râle, sonorous, 171.
Râle, subcrepitant, 173.
Râle, submucous, 172.
Red cells, 44.
Resolution, 53.
Resonance, absence of, 162.
Resonance, diminished, 162.
Resonance, increase of, 161.
Respiration, 24.
Respiration, Cheyne-Stokes, 340.
Respiration, creaking sound in, 174.
Respiration, friction sound in, 173.
Respiration, gurgling sound of, 174.
Respiration, juvenile, 165.
Respiration, metallic tinkling in, 174.
Respiration, modification of, 153.
Respiration, slow, 153.
Respiration, splashing sound of, 174.
Respiration, tardy, 153.
Respiratory disease, affected by age, 70.
Respiratory disease, affected by season, 77.
Respiratory diseases, general causes, 72.
Respiratory mucosa, extent of, 72.
Respiratory murmur, absence of, 170.
Respiratory murmur, diminution of, 169.
Respiratory murmur, general diminution of, 170.
Respiratory murmur, increase of, 169.
Respiratory murmur, partial diminution of, 170.
Respiratory organs, diseases of, 72.
Retention of water in the fevered system, 61.
Rheumatic endocarditis, 337.
Rhinaria taenioides, nasal catarrh from, 113.
Rhinitis, 81.
Roaring, 133.
Roaring, hereditary, 141.
Roaring, immediate cause of, 136.
Roaring, intermittent, 141.
Roaring, inveterate, causes of, 134.
Roaring, occasional, 141.
Roaring, temporary, causes of, 134.
Rupture of the heart, 343.
Sarcoma in nose, 99.
Sarcocysts in the heart, 342.
Scarlatina, 114.
Semeiology, 18.
Serous exudate, 50.
Sheep, auscultation of, 168.
Sheep-bot-fly, 109.
Sheep, coryza in, 85.
Sheep, croup in, 131.
Sheep, croupous bronchitis in, 197.
Sheep, croupous pneumonia in, 236.
Sheep, laryngitis in, 123.
Sheep, percussion in, 160.
Sheep, pleurisy in, 256.
Sheep, position of the heart in, 157.
Sheep, position of lung in, 157.
Skin symptoms, 24.
Softening, result of inflammation, 57.
Solipedes, gutturomycosis of, 149.
Sore throat, 114, 126.
Sore throat, croupous, 114.
Sore throat, diphtheritic, 114.
Spleen, position of in horse, 156.
Stomach, position of in horse, 156.
Strangles, 114.
Strongylus subulatus, 342.
Strongylus vasorum in the heart, 342.
Study, objects and methods of, 1.
Suppuration, 53.
Suppuration in adynamic inflammation, 71.
Suppuration in inflammation, 71.
Suppuration in nasal sinuses, 90.
Symptomatology, 18.
Symptomatic cough, 151.
Symptoms, constitutional, 18.
Symptoms, definition, 18.
Symptoms, direct, 19.
Symptoms, facies, 25.
Symptoms, idiopathic, 19.
Symptoms, indirect, 19.
Symptoms, local, 18.
Symptoms, movements, 20.
Symptoms, objective, 18.
Symptoms of coryza, 82.
Symptoms of nervous disorder, 27.
Symptoms, position, 20.
Symptoms, precursory, 19.
Symptoms, premonitory, 19.
Symptoms, skin, 24.
Symptoms, subjective, 18.
Symptoms, sympathetic, 19.
Tapping the chest, 261.
Temperature in disease, 22.
Temperature, normal, 22.
Temporary roaring, causes of, 134.
Therapeutics, 32.
Thoracentesis, 261.
Throat, affections of, 114.
Throat, infectious diseases of, 149.
Throat, parasites of, 149.
Thrombosis, 350.
Touch, 175.
Tracheotomy, 119, 131.
Traumatic catarrh, 101.
Treatment, 32.
Treatment of chronic coryza, 87, 90.
Treatment of epistaxis, 79.
Treatment of frontal catarrh, 102.
Trichina in the heart, 342.
Tubal sound, 170.
Tubercle in heart, 341.
Ulceration, 57.
Ulceration of the heart, 338.
Varicose veins, 363.
Veins, calcareous bodies in, 364.
Veins, varicose, 363.
Vena azygos, rupture of, 343.
Ventricles, internal capacity of, 296.
Vesicular murmur, general increase of, 169.
Vesicular murmur, partial increase of, 169.
White blood cells, migration of, 43.
Winds, carry disease, 76.
------------------------------------------------------------------------
TRANSCRIBER’S NOTES
1. P. 237, moved the entire “Pneumonia in birds” paragraph from the dog
section to the bottom of the “croupous pneumonia in fowls”
section.
2. P. 245, changed “formed twenty-fours after the injection” to “formed
twenty-four hours after the injection”.
3. Added table of Contents.
4. Silently corrected obvious typographical errors and variations in
spelling.
5. Retained archaic, non-standard, and uncertain spellings as printed.
6. Enclosed italics font in _underscores_.
7. Enclosed bold font in =equals=.
8. Denoted subscripts by an underscore before a series of subscripted
characters enclosed in curly braces, e.g. H_{2}O.
*** End of this LibraryBlog Digital Book "Text book of veterinary medicine, Volume I (of 5)" ***
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