The vagina is the seat of different forms of neoplasms in the various
domestic animals. Thus cystoma, lipoma, adenoma, fibroma, fibro-myoma,
sarcoma and epithelioma have been noted. They are essentially surgical
and to be dealt with as such. They are mainly important in this
connection as inducing a leucorrhœa, which in the absence of careful
examination might be mistaken for that of uterine or vaginal infective
inflammation.
PARTURITION FEVER (COLLAPSE). MILK FEVER. PARTURIENT APOPLEXY. CALVING
FEVER. PARTURITION PARESIS.
Definition. Predisposing causes: genus, breed, great milking capacity,
heredity, mature age, vigor, high feeding, powerful digestion and
assimilation, sudden plethora, drying up of milk, parturition, easy
delivery, warm season, chills, idiosyncrasy, cardiac hypertrophy,
contraction of womb, emotional excitement: Supposed causes: absorption
of toxins from womb, colostrum, Schmidt treatment its significance,
microbian infection and intoxication, effect of change of stable.
Microbiology. Nature: Theories of nervous explosion, vaso-motor
cerebral anæmia from exaggerated excitability of the uterine nerves,
or from dilatation of the portal system and womb, metro-peritonitis,
cerebral anæmia from congestion of the rete mirabile, etc., palsy of
the ganglionic nerves, plethora, intracranial arterial tension,
narcotic poisons from leucocytic or microbian source. Lesions:
variable, cerebral and spinal congestion, pulmonary congestion,
collapse, septic inhalation, bronchitis, dessication of ingesta in
omasum and large intestine, black thick blood, yellowish gelatinoid
exudates in cranium and spinal canal and under spine, glycosuria.
Symptoms: time, post parturient, plethoric subject, sudden onset,
comatose and violent forms, discomfort, restless movements,
inappetence, moaning, mental dullness, unsteady walk, muscular
weakness, compulsory recumbency, retained urine and fæces, drowsiness,
somnolence, unconsciousness, stertor, venous pulse, tympany, sudden
recovery, complete, with paralysis, fatal cases, violence, tossing
head, trembling, cramps, convulsions, temperature. Mortality.
Prevention: bleeding in plethoric, heavy milkers, purging, low diet,
exercise, comfort, milking, blisters, sucking by calf, disinfection,
iodine solution in udder. Treatment: in early stages bleeding,
purgatives, peristalsis stimulants, antiseptics, injections,
stimulants, rubefacients or cold sponging, elevation of the head,
udder massage, milking, iodine injection of the mammæ.
_Definition._ A nervous disorder which develops suddenly in plethoric
cows, heavy milkers, after calving, and is characterized by loss of
senses, of consciousness and of muscular control, by hypothermia or
hyperthermia, convulsions, coma, and mellituria.
_Causes._ While one cannot speak positively as to the essential cause of
this disease, certain conditions are so constant and prominent that they
must be given a high value as _predisposing causes_.
_Genus and Breed. Milking Capacity._ This is essentially a disease of
cows, probably largely because of all domestic animals, cows only have
been long and systematically bred to secure the greatest power of
digestion and assimilation and the highest yield of milk. It is the
disease not only of cows, but of milking breeds, and preëminently of
individuals that give the most abundant dairy product. It is rare or
unknown in scrub or common herds, while common and fatal in the best
milking breeds, in advancing ratio about as follows: short horn, red
polled, Normand, Swiss, Ayrshire, Flemish, Dutch, Alderney, Jersey,
Guernsey, and Holstein. Heredity may be claimed, as the special
predisposing qualities are hereditary.
_Age_ has a marked influence, but this is subsidiary to the milking
qualities. The disease rarely attacks a cow after the first or second
calving when the system is as yet immature, and the milk yield has not
reached its maximum: nor one that is past its prime and already failing
in vital energy and milking qualities. The following table is from
statistics compiled from veterinary records in Denmark and Bavaria:
Age, yrs Cases
—3 —8
4 21
5 65
6 160
7 171
8 202
9 117
10 124
11 44
12 70
13 78
and over.
It will be noted that it is in the period of the most vigorous, mature
life, from the 6th to the 10th year inclusive that the great majority
suffer. In a judiciously managed dairy it is the best cows that are
carried at these ages, and although the very best are kept on into old
age they show a steadily decreasing number of cases as they begin to
fail. The disease is all but unknown in primipara.
_High Feeding._ Heavy and rich feeding prior to calving and immediately
after, is a most prominent cause of the affection. This is so well known
to owners of milking breeds, that they usually hold to the principle
that the cow that is a heavy milker, should be all but starved for a
fortnight before calving and for a week after. In herds where this rule
is acted on the disease is rare and may be altogether unknown, and when
it is neglected the malady is often very destructive.
_Plethora. High Condition._ Heavy feeding and high condition usually go
together, and the majority of the victims are fat or in good flesh, yet
a certain number are actually thin. The predisposing condition is
plethora rather than fat or flesh, and this may be present in the
comparative absence of flesh. The cow that is from a stock famed as
heavy milkers, does not tend to lay on flesh, but, on succulent diet
especially, the greater part of the nutritive matter assimilated goes to
the production of milk, and she remains thin in flesh no matter how
heavily she may be fed. Many such cows never go dry, but give a liberal
yield of milk up to the day of calving, and if measures are taken to dry
them up, it is done at the expense of a sudden plethora, as the milk
giving system does not at once accommodate itself to the laying up of
fat and flesh.
The _drying up of the milk secretion_ sometime before calving in a cow
which is normally a heavy milker is therefore a potent factor.
_Parturition_ is an almost indispensable factor as the disease occurs
one to seven days after that act, and only in rare and somewhat doubtful
cases before it.
_Easy Delivery_ with little nervous outlay or loss of blood, and no
exhaustion is a special feature. The attack almost never occurs after a
difficult parturition with considerable loss of blood and much nervous
exhaustion. This should to a large extent exclude such alleged factors
as _shock_ or _wearing out of nervous energy_. The nervous prostration
which figures so prominently in the disease, seems to be less the result
of wear and tear, than of the supply of an excess of blood, which is
either over-enriched, or charged with some injurious toxic matter. At
the same time there is a manifest susceptibility at the parturient
period which is not present at other times, and the plethora or toxin
takes occasion to operate when this predisposition renders such an
attack possible. _The Warm Summer Season_ has been claimed to induce a
greater number of cases, and doubtless exposure to continuous heat,
tends to prostrate the nervous system and predispose to congestion, this
fails to take into account the still more important element of the rich
spring and early summer pastures, where the already plethoric animal is
left to feed without stint, or the tempting red clover, alfalfa and
other fodder crops, rich in albuminoids, which are fed liberally in a
succulent condition.
_Chills in cold winter weather_ have been similarly invoked as driving
the blood from the surface to collect in internal organs, including the
brain. That chills do act in this way cannot be denied, but there is no
demonstration that any number of cases have been materially affected by
cold.
_Idiosyncrasy. Constitutional Predisposition._ This must be allowed,
inasmuch as that it covers all those individual conditions, functional
and structural, which belong to the heavy milker, or the animal with
extraordinary powers of digestion and assimilation. The same shows in
the predisposition to a second attack of an animal which has survived a
first one. The structural changes in the nerve centres, which occur in
the primary attack, leave traces, which render these parts more
susceptible at the next calving. In my own experience the violence of
the disease is liable to increase with successive attacks, so that a
second or third cannot be hoped to be as mild as was the former one.
_Cardiac Hypertrophy._ Cagny draws attention to the fact that in man and
beast alike the heart undergoes hypertrophy during gestation and, above
all, during its later stages. In improved breeds of cattle, and
especially in milking breeds, a great development of the whole
circulatory system is seen, and a large heart is a constant feature of
this. This implies an increased force of cardiac systole, an increased
blood tension in the arteries and capillaries, a condition which tells
with special force on the soft tissues of the brain, as the violent
abdominal compression in the expulsive efforts of parturition, tends to
drive the blood from the great vascular viscera situated back of the
diaphragm.
_Parturition_ and the subsequent _contraction of the womb and expulsion
of the great mass of blood_, must be accorded a prominent place among
causative factors. The disease is almost restricted to the first week
after parturition, and its gravity is greater the more it is related to
the parturient act. Cases occurring in the first three days are usually
fatal. The gravid uterus contains a very large amount of circulating
blood, and when the womb contracts, the greater part of this is suddenly
thrown upon the general circulation, already plethoric to an undue
extent. As yet the mammæ are congested and there is no free depletion
through that channel, so that there is a marked temporary plethora and
vascular tension, before the system can establish free elimination and,
as it were, strike a healthy balance. In this period of transient
plethora there lies a source of great danger to the general system and,
more particularly, to the brain.
_Emotional Excitement_ connected with the removal of the calf is urged
by Günther, Jaumain, Félizet and others as a prominent cause. This,
however, must be rare, at the most; the disease does not attack the
primipara that should be most susceptible to this influence, but the
mature animal, at her third calving or later when she is already well
accustomed to this treatment; it supervenes so quickly on parturition in
many cases, that there was no opportunity for such emotion; it occurs
also in cows, the calves of which have remained with them or have
received no attention from them.
_Absorption of Toxic Matters._ The theory of a poisoning of the nerve
centres is indicated in the familiar name of _milk fever_, suggesting an
absorption, or poisonous condition of the milk. Lafosse charged the
trouble on the _uterine milk_ secreted in the cotyledons and reabsorbed
in quantity. Abadie and Kaiser attributed it to the products of
gastro-intestinal ferments, which acted on the nerve centres like a
deadly organic alkaloid. Hartenstein incriminated the products of
muscular contraction in the womb and systemic muscles during
parturition. Ehrhardt invoked a similar auto-intoxication, going on
before parturition and only reaching its climax in connection with that
act.
Allemani and Gratia attribute the disease to the absorption of the first
milk (colostrum), and there are several considerations that strongly
favor this hypothesis. The disease sets in always in connection with the
parturient development and congestion of the udder and the secretion of
the first milk. In exceptional cases it may even appear just before
parturition. Even upon the calf the colostrum operates as an irritant
and purgative. Is it wonderful that, in the parturient cow, with a high
state of plethora, a highly susceptible state of the nervous system, and
the various concurrent conditions already referred to above, a direct
poisoning of the nerve centres should appear? It is worthy of notice
that the absorption from the mammæ takes place without any metabolic
change, such as occurs in the stomach and liver in the case of materials
digested. It is to be presumed that the hypothetical mammary poison is
delivered in the brain in its pristine condition and possessed of its
full force.
The doctrine is corroborated even more strongly by the successful
results of treatment by the injection of a solution of potassium iodide
into the udder. The iodide solution may presumably act in one or more of
several ways. It is unquestionably an antiseptic, and would tend to
arrest or control microbian growth and activity, thus preventing the
further formation of toxins. It has a potent deobstruent action on
glandular tissue, tending not only to dry up the milk, but to hold in
check the leucocytic function of producing dangerous leucomaines. There
is reason to believe that with regard to some poisonous ptomaines iodine
acts as a direct antidote, probably uniting with these and forming new
and comparatively harmless compounds. It manifestly acts in this way in
the case of cryptogamic diuresis, and in cerebral congestions arising
from spoilt fodder. The iodide tends further to act as a calmative to
the nerve centres, and as a diuretic, serving to eliminate the poison
that may be present in the blood.
_Microbian Infection or Intoxication._ The doctrine has been advanced
that the disease is either a microbian infection of the nerve centres or
a process of poisoning by the absorbed toxins of microbes. Of the two
hypothesis the latter is the more acceptable, in view of the fact, that
cows in a condition of coma will sometimes recover with extraordinary
rapidity. This is more likely to occur in connection with the
elimination or exhaustion of a transient narcotic poison, than with a
deadly microbe colonized in the brain. This hypothesis is in full accord
with the acknowledged success of the iodide injections; with the
observation of Bissauge, which I can endorse, that certain villages and
hamlets habitually furnish cases of parturition fever, while neighboring
ones, with the same breeds and apparently the same management escape;
and with the observations of Russell and Wortley Axe, that the malady
will sometimes be suddenly prevented in a herd, by the simple expedient
of having the cows moved to a new and previously unoccupied stable, for
calving and the first nine days thereafter.
In support of the doctrine of a microbian origin is recalled the fact
that the disease almost invariably follows parturition, which opened the
way for the introduction of bacteria by the genital passages. This is
somewhat invalidated by the fact that it follows the easy parturition,
in which there was no chance for the introduction of germs on hands or
instruments, and does not follow dystokia in which, without question,
germs have been planted abundantly in the interior of the womb. Undue
weight should not be given to this objection, as the essential accessory
conditions of plethora, etc., are usually largely modified in cases of
dystokia.
The _microbiology_ of the affection leaves much to be desired. Coureur
and Pottiez and later Van de Velde found a streptococcus in the blood.
Trinchera, Nocard, and Cozette found the common pus cocci
(staphylococcus pyogenes aureus, citreus and albus) a streptococcus and
a colon bacillus in the liquid squeezed from the cotyledons, and in the
liquid debris on the uterine mucosa. These microbes were not found in
other organs. They grew readily in artificial cultures, but we lack the
final proof of a successful inoculation on a susceptible parturient
subject. The whole subject is therefore still a plausible theory.
We are not however limited to the womb as the only possible field of a
pathogenic microbian growth. The frequent presence of microbes in the
sphincter of the teat, in the galactophorous sinus, and in the milk
ducts inside the mammæ is absolutely proved. Guillebeau found on the
mucosa in cases of mammitis three forms of bacillus, to which he
attributed the disease. In the New York State Veterinary College we have
found mammitis usually associated with a streptococcus in the milk. In
one cow in the University herd which gave abundance of good milk, and
rarely showed any sign of congestion, streptococcus was constantly
present. In cows producing “gassy” curd, V. A. Moore and A. R. Ward
found in the milk a bacillus which morphologically and in cultures
resembled the colon bacillus (evidently one of the colon group). In the
milk and mammary gland tissue got from other (slaughtered) cows, a
micrococcus growing in yellow or buff-colored colonies predominated.
(Moore and Ward). That the colon bacillus, so constant in the intestines
and manure, is not always found in the milk ducts, would show that in
its normal condition it is not adapted to this habitat, but when a
variety appears that is so fitted, it appears to be able to maintain its
place indefinitely.
With such facts before us, we must allow the possibility of poisoning by
toxins of bacteria in the udder, or by compounds formed by the synthesis
of such toxins and the leucomaines of the expanding udder, or by the
union of the udder toxins with those from the womb. The whole subject of
microbian and leucocytic causation of parturient fever is still
hypothetical, yet enough is known to show the high probability of such
source, and to demand a thorough investigation which will place the
subject on a substantial and assured basis.
_Nature._ Theories of the nature of this disease are numerous and
varied, and are largely based upon some restricted or one-sided view of
phenomena and lesions. Coutamine considers it as the reaction of the
surplus of nerve force, which was not used up in the easy parturition.
The theory is somewhat fantastic as an explanation of the rapidly
developing asthenia and paralysis. Billings explains the cerebral anæmia
as due to vaso-constriction of the nervous capillaries produced by the
exaggerated excitability of the uterine nerves. But with the easy
parturition, and delivery, and the moderate contraction of the womb,
without violence or spasm, the theory seems rather insubstantial.
Trasbot looks on the affection as a congestion of the myelon, apparently
shutting his eyes to the far more prominent encephalic symptoms. Haubner
considers it as a cerebral anæmia induced by the vaso-dilatation in the
portal system and abdominal viscera generally, the result in its turn of
the vacuity of the abdomen, from the expulsion of the fœtus and its
connections. But the womb is often found contracted and comparatively
exsanguine, the plethoric condition of the cow, suddenly increased by
the great mass of blood from the uterine vessels, maintains a marked
general blood tension, and finally, the closed box of the cranium cannot
have its blood so completely drained from it as can a part outside such
a cavity. Stockfleth attributed the malady to a metro-peritonitis, and
the absorption of the morbid products and poisoning, but neither a
metritis nor peritonitis is a common accompaniment of the affection.
Franck who accounts for the asthenia by an anæmic condition of the
brain, explains the anæmia by a pre-existing congestion and œdema of the
rete mirabile at the base of the brain. He claims that sows which have
also a rete mirabile in this situation sometimes suffer from parturient
fever. He fails to adduce cases in the sheep and goat which also have
retia mirabilia. The pregnant sheep may die of an asthenic affection,
but usually before parturition. Franck’s theory is plausibly based on
the anatomical and physiological conditions, for the elaborate network
of vessels at the base of the brain, undergoes great distention under
increased arterial tension, and with the serous effusion, compresses the
brain and drives out its blood.
Palsy of the ganglionic system has been invoked, with succeeding
congestion of the myelon and encephalon (Barlow, Kohne, Carsten Harms,
etc.). Explanation is made that the supposed excess of nervous force
fails of distribution through a lack of conductility of the nerves, and
the nerve centres suffer. Binz has even found the spinal roots of the
sympathetic surrounded by a thick gelatinoid exudate. The theory is,
however, essentially speculative and fails to explain the origin of the
disease or its connection with the recognized conditions of its
occurrence.
_Plethora with Arterial tension_ and all conditions contributing to
this, as already set forth under causes must be allowed a prominent
place in considering the nature of the disease. The blood globules in my
experience are somewhat smaller than normal, implying the density of the
plasma, and implying a direct influence on trophic and metabolic
processes. Under these influences the congestion of the encephalic
circulation, and notably of the rete mirabile, and a serous effusion,
tend first to prostrate the nerve force, and second to render the other
intracranial structures anæmic.
The direct action of a _narcotic poison_, leucocytic or microbian,
though as yet a hypothesis merely, has much in its favor, on
considerations drawn from the observed immunity in particular buildings,
the sudden prostration, the promptitude of certain recoveries and the
favorable results of the iodine mammary injections. The presence of
sugar in the urine, most abundantly in the worst cases, implies a
profound disorder in glycogenic centres (medulla, liver), and primarily
no doubt in the bulb.
_Lesions._ These are exceedingly variable in successive cases.
Congestion and effusion in the meninges, cerebral or spinal, in the rete
mirabile and choroid plexus have been often noticed, and exceptionally
clots of extravasated blood. In certain cases congestion and pink
discoloration of portions of the brain substance (cerebral convolutions,
bulb, ganglia) with marked puncta vasculosa, are found, while in others
the greater part or the whole of the encephalon is anæmic. The puncta in
such cases, large and dark, on the surface of the section, promptly
enlarge until they may form distinct drops.
In the _lungs_ areas of collapse, and of dark red congestion and
infiltration are common, mostly as the result of the entrance of
alimentary or medicinal matters into the bronchia owing to palsy of the
pharynx. Such materials can be found in the bronchial tubes.
The _third stomach_ and the _large intestine_ may be impacted, the
contents more or less baked and glossy on the surface, and coincident
congestions of the mucosa are not uncommon. In some instances, however,
the contents are soft and pultaceous and the absence of mucous
congestions is remarkable.
The _womb_ rarely shows characters differing from the condition which is
normal to the first few days after parturition.
The _blackness and thickness of the blood_ has been noted by practically
all observers. This is partly the result of its density, but doubtless
also of the undetermined toxins which are operative in the disease.
Yellowish _gelatinoid exudates_ have been found in the subdorsal and
sublumbar regions, as well as the cranium and spinal canal.
_Glucose_ appears to be constantly present in the urine, and in excess
in the more violent and fatal cases: from 1.19 grm. per litre in slight
cases to 41.8 grms. in a fatal one (Nocard). Albumen may be present,
though probably only when local inflammation has supervened.
_Symptoms._ The conditions of the attack should be noted. This is a
disease of the first six days after parturition, rarely seen in the
second week, and never after the fourteenth day. It is very exceptional
before parturition, yet Müller quotes 47 cases in 1107 births. The
breed, condition, milking qualities, plethora, feeding, etc., of the
patient are, as already noted important data in diagnosis. The onset is
sudden without premonitory symptoms.
Two very distinct types are met with, the _comatose_ and _violent or
spasmodic_, which, however, merge into each other by insensible
gradations, and may follow each other.
From twelve to seventy hours after an easy parturition there suddenly
appear signs of discomfort. Feeding and rumination cease, the calf is
neglected, there may be plaintive moaning, the eyes seem dull and
clouded, the eyelids drooped, the conjunctiva red, the pulse normal for
parturition, sometimes extra strong, the breathing excited often with
moans or grunts. The senses are dulled, the walk is unsteady, the feet
being abducted and planted like clumps, or the legs sway, perhaps cross
each other, remain semi-bent, and soon give way leaving the animal
prostrate, resting on the sternum and abdomen, or later on the ribs,
with head extended. Attempts may still be made to rise, but this is
rarely accomplished unless when improvement sets in. This is the
condition in which the patient is usually found, being the first to be
noticed by the owner. The bowels are torpid, the urine retained in the
bladder, and the animal may remain thus in a drowsy condition, without
changing from the sterno-ventral decubitus, or dropping the head on the
ground until improvement sets in. The head rests on the shoulder or
upper flank. If held outward or forward the upper border of the neck has
an S shaped outline.
More commonly the somnolence increases, passing into a complete torpor
and insensibility, the eye may be touched without causing winking,
pricking or other injury causes no further response, the patient turns
upon its side, with its head extended on the ground. She may lie in this
condition with no sign of vital activity save pulsation and breathing,
and the latter is liable to be slow and stertorous by reason of the
paralysis of soft palate and larynx. The jugulars usually show a venous
pulse. Fermentations in the inactive paunch cause the evolution of gas
with tympany, which still further obstructs the breathing, and reacts
injuriously on the nerve centres. The normal eructations from the rumen
may continue, with liquids and floating solids, and in the paralytic
state of the throat these too often pass in part into the bronchia,
causing septic bronchitis and pneumonia. The same is liable to follow
the administration of liquids, the irritant drugs passing into the
larynx, trachea and lungs. The pulse becomes soft, small and finally
almost imperceptible. It may be 50, 60 and upward.
In favorable cases, defecation may still occur, or the rectum once
emptied may fill again through the continuance of peristalsis, the milk
continues to be secreted, and in one to four days, spontaneous
defecation and micturition may be resumed, and the patient may get on
its limbs and commence feeding. There is usually at first a little
weakness of the limbs, but this is transient and health is restored in a
very short time. The suddenness of the improvement is often as marked as
of the attack. The patient is left prostrate and insensible, without
giving any response when the eyeball is touched and in two or three
hours it is found on its feet, eating, with eyes bright and clear.
Some patients, however, are restored to ordinary sensation, intelligence
and appetite, while the hind limbs remain paralytic, or paretic, and the
station and gait both weak and uncertain for days or even weeks. In such
cases there have been presumably structural changes in the nerve
centres, which require time for repair.
In fatal cases, death may occur quietly from apoplexy, cerebral
compression, or narcotism, or it may be preceded by a period of marked
excitement or disorderly muscular movements. Lifting of the head,
throwing it alternately on the shoulder and on the ground, trembling of
head, members and body, cramps or jerking of the limbs or of other
parts, drawing the hind limbs up against the abdomen, and again
extending them, rolling of the eyes, loud, noisy, irregular, embarrassed
breathing and a running down pulse are often marked features.
The temperature range is peculiar. At the start there may be some
hyperthermia 103° or 104°; with the advance of the disease it tends to
become lower, 98°, 96°, or 94°. When improvement sets in, it rises again
promptly to the normal.
Cadeac describes a special form which is ushered in by great
restlessness, bellowing, throwing the head to right and left, grinding
the teeth, sucking the tongue, salivation, licking of certain parts of
the body, spasms in the neck, back or limbs, and prompt recovery, or
lapse into the comatose condition as above described. It proved less
fatal than the ordinary comatose type, but seems to depend on similar
conditions.
_Prognosis. Mortality._ The disease is very deadly, the mortality in
time past having reached 40, 50 or even 60 per cent., the gravity
increasing as the disease set in nearer to parturition. Cases occurring
on the first or second day were mostly fatal, those at the end of the
first week were hopeful, and those occurring during the second week were
very hopeful. With the Schmidt (iodine) treatment the mortality is
claimed to be reduced to 16 or 17 per cent.
_Prevention._ Measures directed toward the lessening of plethora tend to
remove one of the most fruitful causes of the disease and though not
invariably successful, are yet of great value. The most direct is the
_abstraction of blood_ in the last fortnight of pregnancy, to the extent
of 6 or 8 quarts. This tends to secure a lessening of the blood tension,
and blood density, but there is the drawback of a created tendency to a
subsequent increase in blood formation to make up the loss. This measure
should be reserved for cows that are very plethoric, extra heavy milkers
and such as have already suffered from the disease.
_Purgatives_ will measurably secure the same end without the same degree
of danger. One to two pounds of Epsom or Glauber salts in the last week
of gestation, or at latest when labor pains set in, tend not only to
remove solid or impacted masses from the first and third stomachs, and
inspissated contents from the large intestines, but to secure a free
depletion from the portal system. If not before, this should always be
given immediately after parturition to cows in extra high condition,
heavy milkers, and that have had a short and easy delivery.
_Restriction of food_ for a week before and as long after parturition is
of equal importance. A very limited supply of aqueous, easily digested,
and laxative food (roots, sloppy bran mashes, fresh grass, ensilage)
will meet the demand.
_Exercise in the open air_ is of great value in giving tone to the
muscles, and especially the nervous system, and in stimulating the
emunctories and other functions.
In the cold season _protection against cold draughts and chills_ must be
seen to, and in the hot season the avoidance of an excess of solar heat
and above all of the confined impure air of the barns.
At midsummer and later, there is often great danger in the rich clover
and alfalfa pasture, or soiling crop, with which the cow will
dangerously load her stomach, and the only safe course is to remove
predisposed animals and shut them up in a bare yard or box-stall. Under
such simple precautions herds that had formerly suffered severely, have
had the disease virtually put a stop to.
In individual cases other measures are indicated. When the udder has
reached an enormous size and development, and is gorged with milk, days
before parturition, it should be systematically milked. The irritation
in the gorged gland is quite as likely to induce premature parturition,
as is milking, and, at the worst, the result is not so bad as an attack
of parturition fever.
Basing his advice on the fact that parturition fever does not follow a
case of severe dystokia, Cagny applies sinapisms on the loins, croup and
thighs of a fleshy, plethoric, heavy milking, parturient cow. Proof of
their efficacy is not obtainable.
Félizet advises leaving the calf with its dam for one week. Kohne doses
the cow with nux vomica: Harms, with tartar emetic.
In view of the probability of a bacterial infection the cow should be
taken to a clean, pure, well-aired stable a day or two before calving,
having been first cleansed from adherent filth, and sponged all over
with a 4 per cent. solution of carbolic acid.
To prevent diffusion of infection Bournay recommends antiseptic
injection of the womb immediately after calving. Bissauge adds that the
stable should be disinfected after every case of parturition fever, the
manure carefully removed and the ground scraped and well watered with a
disinfectant.
For fleshy, plethoric, predisposed cows, the iodine injection of the
udder should be applied immediately after calving. A measure of this
kind which is so successful as a curative agent, and which brings such
circumstantial evidence of the production of a poison (leucomaine or
ptomaine) in the mammary gland, can hardly fail to be even more
effective as a prophylactic than as a therapeutic resort.
_Treatment._ With the state of plethora and congestion about the head in
the early stages the question of _bleeding_ at once arises. If early
enough while there is a full bounding pulse, and as yet no sign of great
loss of muscular control it is often very beneficial, as much as 6
quarts or more being withdrawn. It is well however to avoid cording the
neck, which must increase the vascular tension in the brain, and to
trust rather to digital compression of the vein. The blood should be
drawn from a large opening in a full free stream, and may be stopped
when the pulse softens. In the more advanced condition, with paralysis
and more or less dulling of the senses, or coma, bleeding may be
dangerous rather than useful. There is then serious pressure on the
brain, with serous effusion, and perhaps blood extravasation, and in any
case anæmia, and this latter may be dangerously or even fatally
increased by the lessening of the blood pressure, without any
compensating advantage in the way of reabsorption of the effusion. In
such cases eliminating agents are a safer resort.
_Purgatives_ commend themselves, but with the drawback of a too tardy
action. Now however with the peristaltic stimulants given hypodermically
this objection is largely obviated. Pilocarpin 1½ gr., and eserine 3
grs. will often secure a noticeable movement of the bowels in the course
of fifteen minutes, implying a corresponding motion onward in the bowels
more anteriorly, and even of the contents of the gastric cavities. If
there is already palsy of the muscles of deglutition, this may be
repeated several times at intervals of four or five hours. If however
deglutition is still well performed a purgative of one or two pounds
Epsom salts, with 10 drops croton oil, and 1 oz. oil of turpentine may
be given by the mouth. Should this operate, it will supplement and carry
on even more effectively the work of the hypodermic agents, and even
lessen the density, plasticity and tension of the blood and act as a
potent derivative from the brain.
A compromise may be made by giving aloes 2 ozs., croton oil 20 drops in
bolus; or 1 to 2 ozs. sulphate of soda in solution may be injected
subcutem.
In any case oil of turpentine or other antiseptic is of great value in
the stomach in preventing fermentation and tympany, and thereby
obviating a whole series of troubles such as: cerebral disturbance by
nervous shock and blood pressure; impaired respiration and hæmatosis by
pressure on the diaphragm; and eructations of food to the pharynx and
its inhalation or gravitation into the lungs.
It is always well to clear out the rectum by injections, when if there
is any indication of pharyngeal paralysis most of the remedies may be
given by this channel.
Stimulants (ammonia carbonate, alcohol, anise, fennel, ether, nux, etc.)
have been largely employed by the mouth and may be by the rectum. In the
absence of spasms I have relied largely on nux or strychnia.
When the skin chills, some have sought to heat it by enveloping the
posterior half of the body in cotton or wool soaked in turpentine, by
applying sinapisms, or by moving over the surface a warming-pan
containing red hot charcoal.
More generally _cold_ in the shape of cold water, ice or snow has been
applied _to the cranium and spine_. Theoretically the anæmic brain might
be thought to forbid this, but clinically it often operates well,
possibly by inducing a sympathetic contraction of the vessels in and
around the nerve centres and thus indirectly favoring the resumption of
active circulation and the reabsorption of effusions.
An _elevated position of the head_ is no less important. It favors the
return of blood from the brain by gravitation, and in this way improves
the intracranial circulation, and the resumption of normal function. A
halter, or a rope around the horns, may be tied to a beam overhead, or
the head may be laid on thick bundles of straw which will keep it up to
or above the level of the chest, and in this way not only is gravitation
ensured, but the brain is protected against the violent blows and
concussions, which come from dashing the head on the ground.
Frequent _rubbing of the udder and drawing of the milk_, is an excellent
means of depletion, a removal of a source of irritation, and presumably
an extraction of part of the offending poison. It should never be
neglected. But of all known methods of treatment the iodine injection
furnishes the greatest hope of success.
_Injection of the mammæ with Iodine._ Iodide of potassium 100 grains
(200 grs. in the case of a very large udder) are dissolved in a quart of
water which has been boiled for 15 minutes, the solution cooled to 104°
F. and injected in equal parts into the four quarters, which have been
just milked out clean. The glands are then manipulated so as to work the
solution into all the recesses of the milk tubes and follicles. If the
patient does not get on its legs at the end of twelve hours, the glands
may be milked out and injected anew. In nearly 2000 cases the recoveries
reached an average of nearly 83 per cent. In serious or advanced cases
with structural changes of a grave nature, a good result cannot be hoped
for. The injection does not forbid the concurrent use of other approved
measures.
The injection is easily made with a caoutchouc tube of five feet long
fitted to a teat tube at one end and to a funnel at the other. The tube
is inserted in the teat, and the funnel at a height of five feet
receives the liquid, which readily passes into the teat. When ready to
pass the tube from one teat to another, an assistant pinches the
caoutchouc tube just below the funnel, until the insertion has been
made. Every precaution must be taken against sepsis. The udder, teats
and hands, must be washed with soap, and treated with a 3 per cent.
solution of lysol. The teat tube and funnel are boiled. The caoutchouc
tube is washed and irrigated with a solution of mercuric chloride
(1:1000), and then with one of boric acid (3:100).
DISEASES OF THE EYE.
DESIRABLE FEATURES IN THE EYE.
The eye in the physiognomy. Broad forehead. Full eyes. Both eyes
alike. Iris smooth, lustrous. Media translucent. Pupil sensitive to
light. Convexity median, uniform. Pupil black in ordinary light. Lids
open and mobile. Sclera light pink. Tears clear, limpid without
overflow. Lids thin, delicate, margins evenly curved. Whole eye
responsive to moving objects. Defects: small eye: semi-closed, thick,
sluggish lids; convex cornea: sunken eye: projecting eye: weeping eye:
blear eye: watch eye: irresponsive iris: dilated pupil: unequal eyes:
flat cornea; ovoid cornea.
Much of the expression of the face depends upon the eyes, and in animals
as in man it is difficult to find compensations for a forbidding
countenance. Perfect, sound, intelligent eyes are always pleasing;
imperfect, defective, sunken or lifeless eyes mar the whole expression.
The following points may be specially noted:
1st. =Ample breadth between the orbits.= This is of great importance in
the horse, in which we seek for intelligence, courage and indomitable
energy. This confirmation does not indicate the size of brain, as the
cranium is situated higher up, but by placing the eyes well outward, it
indicates a wider range of vision, and usually implies large, clear
eyes, and since interdependent parts tend to correspond in development
and quality, this commanding vision bespeaks a large, active brain,
intelligence, docility and activity.
2d. =Full, prominent eyes.= This may be excessive, either through
primary conformation or disease. Abnormal convexity of the cornea
implies myopia. But within normal limits the prominent eye suggests good
health, condition and vigor, with ample cushions of fat under the bulb
and a sound, well-developed condition of the eyeball and its muscles.
3d. =Both eyes equal in all respects.= Any variation in size, shape,
color, fullness, clearness or in any other respect is at best unsightly,
and implies not only defect but often disease as well.
4th. =The iris should be lustrous, uniform in color and even in
surface.= Whether dark brown as in the horse, or yellow as in the dog,
it should be brilliant. Any part that lacks lustre, being lighter brown,
or yellow and dull like a dead leaf, usually indicates previous disease
and a tendency to further trouble. Albinos and those in which the
pigment is congenitally absent in patches must be considered as
exceptions, yet, even in them, the peculiarity cannot be held to add to
the beauty.
5th. =All the Media (Cornea, aqueous humor, lens and vitreous) must be
perfectly clear and translucent.= The slightest cloudiness or opacity in
any of these is a serious blemish and usually indicates disease, past or
present.
6th. =The pupil should promptly and freely respond to light and darkness
by contraction and expansion.= Absence or tardiness of movement
indicates impaired vision, from disease of the eye, its nerves, or their
nerve centres.
7th. =Each cornea should have a median convexity, uniform in all
directions implying the absence of myopia, preshyopia and astigmatism.=
Any deviation from this will interfere with the perfection of sight, and
endanger shying and other troubles.
8th. =Under ordinary light the pupil should appear black throughout.= In
the larger animals such dilation of the pupil as to expose the tapetum
lucidum under such circumstances implies impaired vision (amblyopia,
amaurosis), inflammation of the iris or undue intraocular pressure. A
white color or spot shows cataract.
9th. =The lids must be open and mobile without excessive dilation.=
Tardily moving or semi-closed lids, distorted by scar or angle, everted
or inverted, are unattractive and usually imply disease in the eye,
nerves or brain.
10th. =The unpigmented portion of the sclera should be light pink.= The
dark red of congestion and the pallor of anæmia are equally
objectionable.
11th. =The tears must be clear, limpid and confined within the lower
lid.= Any milkiness, flocculency or overflow is indicative of disease.
12th. =The eyelids must be thin, delicate, evenly and uniformly curved
along the borders, and fringed by an abundance of strong, prominent and
well directed lashes.= Puffiness or swelling betrays inflammation,
dropsy, anæmia, parasitism or other disorder, angularity of the upper
lid an internal ophthalmia, and depilation or wrong direction of the
lashes, local disease.
13th. =The eye should respond instantly, by movement, to new objects and
noises, without showing undue irritability or restlessness.= The
intelligent apprehension of the objects will introduce an aspect of
calmness and docility.