_Diet._ Many hepatic disorders, and especially those that are
exclusively or mainly functional may be corrected by diet alone.
Prominent among dietary influences is the abundant supply of water. The
succulent grasses of spring and early summer constitute the ideal diet,
hastening and increasing elimination, and lessening the density of the
bile, even to the extent of dissolving biliary calculi and concretions.
Upon dry winter feeding such calculi are common especially in ruminants,
whereas after a month or two at pasture they are extremely rare. In
winter the same good may be arrived at by the use of ensilage, brewer’s
grains, roots, fruits, or even scalded hay or bran. The two extremes of
highly albuminous and highly carbonaceous or saccharine food are to be
avoided or used only in limited amounts. In the one class are clover,
alfalfa, sainfoin, vetches, cowpea, lespedeza, especially in the form of
hay, beans, peas, cotton seed, gluten-meal, rape and linseed cake. In
the other are wheat, buckwheat, Indian corn, sorghum, sweet-corn and
cornstalks. Some agents like beets which are rich in saccharine matter
may be actually beneficial by reason of their laxative and cholagogue
action. In the carnivora the food should be largely of simple mush of
oatmeal, wheat seconds, or barley meal, skimmilk or buttermilk. If it is
needful to tempt the appetite in a fleshfed animal this should not be
done by rich, fat gravies, highly spiced animal food, or rich saccharine
puddings, but rather by the addition of a little pure juice of lean
meat, or some well skimmed beef tea.
It is as important to regulate the quantity as the quality of the food
as the heavy feeder will over-charge the liver as much by an excess of
otherwise wholesome food, as will the ordinary animal by the
indigestible and unwholesome articles. As a rule the improved breeds of
meat producing animals, have acquired such facility in fat production
that much of the surplus is largely and profitably disposed of in this
way, and in their short lives little obvious evil comes of the
overfeeding, but in cases in which this outlet proves insufficient, as
in horses and dogs that are highly fed on stimulating or saccharine
diet, and which are kept for the natural term of their lives, with
little exercise, the evil tends to reach a point of danger. Nursing
mothers and dairy cows find a measure of safety in the free flow of milk
and the yield of butter, but breeding cows that have been improved till
they have no longer a capacity for milking, but must have their calves
raised on the milk of other and milking strains are correspondingly
liable to suffer.
_Exercise in the Open Air._ As enforced idleness, on a full diet and in
a warm and moist environment is a main cause of hepatic disorder, so
abundant exercise in the open air and especially in a cool season is
beneficial in a marked degree. Beside the bracing effect on the
digestive organs and the improvement of the general tone of the system,
the action of the muscles in hastening the circulation greatly favors
the removal and elimination of waste matters. Still more advantageous is
the increased activity of the respiration and the aspiratory power of
the chest in at once unloading the portal system and the liver by
hastening the progress of the hepatic blood into the vena cava and right
heart, and in furnishing an abundant supply of oxygen for the
disintegration of the albuminoids and amylaceous products. Such exercise
must of course be adapted to the condition of the animal and its power
of sustaining muscular work, but judiciously employed, it is one of the
most effective agencies in correcting and improving hepatic disorder or
hepatic torpor. Idle horses, the victims of obstinate habits of
constipation, muco-enteric irritation, indigestion, nervous, urinary or
cutaneous disorders will often be greatly benefited or entirely restored
by systematic exercise. This is one of the great advantages of a run at
pasture, as the subject secures at once the laxative cholagogue diet, an
abundant supply of oxygen, a better tone of the muscular and general
system, and a more perfect disintegration of albuminoids. Sea air with
its abundance of ozone is especially advantageous.
In the carnivora while we cannot send them to grass, much can be done in
the way of systematic exercise, and in the case of city dogs a change to
the country, where they can live out of doors and will be tempted to
constant exercise and play, will go far to correct a faulty liver.
_Laxatives._ _Cholagogues._ When a free action of bowels and liver
cannot be secured by succulent food and exercise, we can fall back on
medicinal laxatives. These are advantageous in various ways. Some
laxatives like podophyllin, aloes, colocynth, rhubarb, senna, jalap, and
taraxacum act directly on the liver in increasing the secretion of bile.
These may be used for a length of time in small doses and in combination
with the alkalies. Other aperients act directly on the bowel carrying
away the excess of bile, the albuminoids and saccharine matter that
would otherwise be absorbed, and by a secretion from the portal veins,
abstracting nitrogenous and saccharine elements which would otherwise
overtax the liver to transform them. Thus indirectly these also act as
cholagogues by withholding the excess of material on which it has to
operate, and by rousing its functions sympathetically with those of the
bowels. Thus sulphates of magnesia and soda, and tartrates and citrates
of the same bases, given in the morning fasting, dissolved in a large
quantity of warm water and conjoined with sodium chloride, ammonium
chloride, sodium carbonate or other alkaline salts, or with one or more
of the vegetable cholagogues above mentioned, may be continued for a
length of time until the normal functions have been re-established, and
will maintain themselves irrespective of this stimulus.
Calomel (and even mercuric chloride in small doses), though it is not
experimentally proved to be a direct cholagogue, is one of the very best
correctives of impaired hepatic function. It expels the bile from the
duodenum and bowels generally, thereby preventing its reabsorption; it
proves antiseptic to the ingesta; it eliminates much of the peptone,
saccharine and fatty matter from the intestines and portal system thus
relieving the liver materially; and it is supposed further to modify the
other liver functions by a direct action on the hepatic cells, and by
reducing the cohesion of fibrine, and promoting the disintegration of
albumen. Certain it is that calomel gives most substantial relief in
many torpid and other disorders of the liver and as it is not in itself
an active liver stimulant but has rather a soothing action on that gland
it can be safely resorted to in states of hepatic irritation in which
the more direct cholagogues would prove more or less hurtful.
In some forms of hepatic disorder where a speedy and abundant secretion
is demanded, pilocarpin may be employed, with great caution so as not to
reduce the strength unduly by the attendant diaphoresis, diuresis,
salivation or diarrhœa.
_Alkalies_ have long been recognized as of great clinical value in
hepatic disorders. Though carbonate of soda decreases the secretion of
bile, (Nasse, Röhrig), yet the alkalies generally appear to promote
oxidation, and to hasten the disintegration of albumen and the
albuminoids. They increase the disintegration of sulphur compounds
materially adding to the sulphates and urea in the urine. They further
tend to increase the hippuric acid, carbonate of soda (2 drs.) even
determining the abundant excretion of this acid in man (Nasse). It may
be concluded that the acknowledged value of alkalies in these diseases,
is largely due to their hastening of the metabolic processes in
albuminoids. Small doses of sodium carbonate further stimulate the
gastric secretion and may thus benefit by rendering the process of
digestion more complete and satisfactory.
_Chlorine, Iodine, Bromine and their Salts._ These halogens are of great
value in many hepatic disorders. The universal craving for sodium
chloride indicates the need of its elements in the animal body, and
whether this is mainly the supply of chlorine for the hydrochloric acid
of the gastric juice, or to fulfill its uses in favoring the oxidation
and disintegration of the nitrogenous matters in the blood and tissues,
or for other more or less obscure uses, it is well to recognize and act
upon the indication. The various mineral waters which are held in high
esteem in liver affections contain a large proportion of sodium
chloride. As a medicinal agent ammonium chloride maintains an equally
high position. Large doses thrice a day, so as to induce diaphoresis and
diuresis greatly relieve hepatic congestions. This agent determines a
great increase in the urea eliminated so that it is even more effective
in the same direction, than sodium chloride. Free chlorine is also
effective in hepatic torpor and congestion, and to this in part may be
attributed the great value of nitro-muriatic acid.
Bromide and iodide of potassium have been found to be effective in
reducing hepatic enlargement and thus in conducing to a more healthy
activity of the liver.
_Ipecacuanha, Euonymus, etc._ These agents are more or less hepatic
stimulants and may be found beneficial as combined with the laxative or
alkaline agents in securing a better functional activity in cases of
torpor or deranged function.
_Tonics, Bitters._ Tonics are often useful when the health has been
undermined by long continued hepatic disorder. The iron tonics are as a
rule contraindicated as tending to check secretion of bile, unless they
can be given with alkalies. Iron sulphate or chloride, combined with
sodium or potassium carbonate so as to establish a mutual decomposition
will obviate this objection. The vegetable bitters (gentian, cascarilla,
calumba, salicin, serpentaria, aloes, nux vomica) combined with alkalies
are often of great value. Quinia, like opium, checks secretion and is to
be avoided or used with judgment and in combination with cholagogues.
HÆMOGLOBINÆMIA. AZOTÆMIA. AZOTURIA. HÆMOGLOBINURIA. TOXÆMIA FROM
IMPERFECT HEPATIC FUNCTION.
Definition. Theories, of hysteria, uræmia, spinal myelitis,
myelo-renal congestion, rheumatic lumbago, myosito-myelo-nephritis,
rheumatic chill with destruction of muscle albuminoids. Yet it occurs
in our semi-tropical midsummer with a temperature of 80 or 90, in
spring and autumn, and rarely even in the cold, damp stable in
midwinter in the absence of exercise. Constant conditions: One or more
days absolute rest, preceding steady work, a strongly nitrogenous
ration, continued during the rest, sudden active exertion accelerated
breathing and unloading of peptones and proteids from portal vein and
liver into the general circulation. Sanguineous albuminuria from
excess of albuminous food, free ingestion of water, suppressed milk
secretion, forced marches. Transfusion of blood. Excess of albumen
dangerous, excess of red globules not dangerous. The blood
concentration of diuresis or diaphoresis is not dangerous. Continuous
muscle decomposition from work bars the disease. Stable miasm
untenable. Poison may be drawn suddenly from the enormous mass of
blood in the liver, spleen and portal system. The absence of icterus
antagonizes the bile theory. Benzoic acid, unaltered peptones, and
glycogen are examples of elements destructive to blood. Normal
destruction of red globules in liver, spleen and bone marrow. Sudden
access of resulting hæmoglobin to the blood. Other products of
disintegrated globules. Poisons from food, and antitoxic action of
liver in presence of glycogen. Carbon dioxide favors solution of red
globules. Theories of hæmoglobinæmia in man. Lesions: Blood black,
diffluent, iridescent, has no avidity for oxygen, with excess of urea
and extractives, serum of clot red, globules, small, pale, distorted,
not sticky, extravasations, liver, enlarged, congested, blood gorged,
spleen congested, swollen: Lumbar or gluteal muscles pale,
infiltrated, with loss of striation; bone marrow congested,
hemorrhagic; kidneys congested infarcted; urine dark brown or red,
with excess of urea and hæmoglobin. End of spinal cord has congestion
or infiltration. Symptoms: History of high condition, constant work,
high feeding, a day’s rest, then exercise and attack. To full life,
follows flagging, droops, moves one or both hind limbs stiffly,
knuckles, drags toes, crouches, trembles, perspires, breathes rapidly,
is tender on back, loins, croup or thigh, muscles firm, paretic, and
drops unable to rise. Urine retained, brown, red or black, sometimes
glairy, later may have casts. Appetite may return. In mild cases,
stiffness, lameness, with or without visible muscular lesions or
tremors. Urine glairy, dense, with excess of urea and nitrogenous
products. Recover under careful feeding and exercise, and relapse
under original causes. Progress: May recover under rest. In bad cases
accelerated breathing and recumbency forbid rest and recovery.
Recovery in a few hours or after a week. Urinary casts with renal
epithelium, imply nephritis and grave conditions. In persistent
paresis, muscles waste. Modes of death. Mortality 20 per cent.
Diagnosis, by history of onset, etc. Prevention: When highly fed and
hard worked, give daily exercise, with comparative rest, reduce
ration, and give laxative or diuretic. Plenty of water. Treatment:
Rest, sling, diffusible stimulants, bleeding, bromides, water ad
libitum, fomentations, unload liver and portal vein, purgative,
eserine, barium chloride, enemata, diuretics, for remaining paresis,
derivatives, strychnia, diet, laxative, non-stimulating, restore to
work gradually.
_Definition._ An acute auto-poisoning occurring in plethoric horse on
being subjected to active exertion after a period of idleness, and
manifested by great nervous excitement and prostration, paresis
commencing with the hind limbs and the passage of hæmoglobin in the
urine.
_Nature and Causes._ The most varied conclusions as to the nature of
this disease have been put forward by different authors. In England,
Haycock called it hysteria, mistakenly supposing that it was confined to
mares, and Williams attributed it to uræmic poisoning, conveniently
ignoring the fact that the sudden manifestation of the most extreme
symptoms in an animal which just before was in the highest apparent
health and spirits contradicted the conclusion. In France (Trasbot) and
Southern Europe (Csokor) it has been looked on as a spinal myelitis, a
conclusion based on the disturbed innervation of the posterior
extremities in the great majority of cases, but which is not always
sustained by the pathological anatomy of the cord. In Germany
veterinarians have viewed the disease from widely different standpoints.
Haubner calls it myelo-renal-congestion (Nièren-Rückenmarks): Weinmann,
a rheumatic lumbago; Dieckerhoff defines it as an acute general disease
of horses, manifested by a severe parenchymatous inflammation of the
skeleton muscles, with a bloody infiltration of the bone marrow,
especially of the femur, and with acute nephritis and hæmoglobinuria. He
attributes the attack to exposure to cold. If this were the real cause
the attack would be far more common in very cold weather when the horse
is suddenly exposed to cold drafts between open doors and windows, than
when he is harnessed and driven so as to generate and diffuse animal
heat. Yet attacks in the stable are virtually unknown, and in almost
every instance the onset occurs during a short drive. Friedberger and
Fröhner say that the epithet rheumatismal may be correctly applied to
almost all cases that we meet in practice. They quote Goring as having
produced the disease experimentally by exposure to cold, and go on to
explain that rest in the stable before the attack causes the extreme
sensitiveness to cold that is generated by a warm environment. The
implication of the lumbar, pelvic and femoral muscles they explain by
the stimulation of the nutritive metamorphosis by the action of cold on
the sensitive nerves of the skin. The effect of this cutaneous
irritation is exaggerated by the heat of the stable to which they have
been previously subjected. The products of the destruction of the
albuminoids of the muscles, pass into the blood as hæmoglobin, and
produce the ulterior phenomena. The muscles of the hind quarters
especially suffer because of their greater exposure and because they are
subjected to the hardest work in propelling the animal machine. In this
connection they quote the experiments of Lassar and Nassaroff in which
sudden exposure to cold determines parenchymatous degeneration of
muscles; also the cases of paroxysmal or winter hæmoglobinuria in
certain susceptible men whenever they are exposed to an extremely low
temperature.
There are serious objections to the acceptance of this as the essential
cause, among which the following may be named:
1st. The disease is not confined to the cold season but occurs also at
midsummer when the outdoor temperature is even higher than it is in the
stable.
2d. In our Northern States it appears to be more common in spring and
autumn or early winter, when the extreme colds have either already
passed, or have not yet set in, but when the abrupt changes of weather
(rain-storms, etc.) are liable to shut up the animal indoors for a day
or more at a time.
3d. The popular names quoted with approval by these authors—Monday
disease, Easter disease, Whitsuntide disease—indicate the prevalence in
Europe also, of the malady in the milder, or more temperate seasons
rather than during the prevalence of extreme cold.
4th. The fact that the disease rarely or never occurs in the stable, no
matter how cold the season, how open the wooden walls or floor, nor how
strong the draft between doors or windows, shows that the theory of cold
as the sole or main cause must be discarded.
It is not necessary to ignore the action of cold as a concurrent factor
in certain cases, or as a stimulant to reflex vaso-motor paresis, to
muscular metamorphosis and the increase of hæmoglobin in the blood. It
is only necessary that this should be held as subordinate and
non-essential to the final result. Several other factors that are
accorded a subordinate place by these writers, are so constant and so
manifestly essential that they must be allotted a much more important
position in the list of causes.
A =period of rest= is a constant precursor of an attack. The more
extended the inquiry the more certain we become that a short rest is a
prerequisite to equine hæmoglobinæmia. The horse that is kept at daily
steady work may be said to be practically exempt. Even the
non-professional observer recognizes the fact and names the disease
after the weekly or yearly holiday or rest day which was the occasion of
it. To him it is the Monday morning disease, the disease of the day
following Thanksgiving, Christmas, New Year, or Fourth of July. It is
the disease of wet weather, of heavy snowfalls, of the blizzard, or of
the owner’s absence from home, of any time that entails one or two days
of absolute inactivity in the stall.
But again the affection does not appear in the horse that is absolutely
idle for a length of time. It is the =short period of rest in an
interval of otherwise continuous work= that determines it. In short the
subject must be in good muscular condition and with a hearty, vigorous
appetite and good digestion. The short unwonted rest interrupts the
disposal of the rich products of a vigorous digestion, and tends to
overload the portal veins, the liver, the blood and tissues with an
excess of proteids. The condition of the animal is so far one of
plethora.
Another feature that bears this out is that the attack comes only in the
animal that is =heavily fed on a strongly nitrogenous ration=. It is not
the disease of the horse kept on straw, or hay, or which receives a
limited amount only of grain. It does not occur in the animal which has
its grain suspended or materially reduced during the one or two days of
idleness. It does not select the horse that has had a laxative either in
the form of food or medicine. This last may increase the sensitiveness
to cold, but it certainly lessens the tendency to hæmoglobinæmia. The
most rational explanation appears to be that it affords this protection
by interfering with the thoroughness of digestion and absorption, by
securing elimination from the portal veins and liver, and by reducing
the amount of albuminoids in the blood.
A blood abnormally rich in albuminoids, as it is in the transient
plethora induced by a short period of rest, in the well-conditioned
working horse, without any restriction of his diet, may therefore be set
down as one of the most important factors in producing hæmoglobinæmia.
Nor is this without approximate examples in human pathology. Von
Bamberger has shown that “hæmatogenous albuminuria” will occur in
healthy individuals when there is an excess of albumen in the
blood-plasma, as after a too free use of albuminous food, or after
suppression of the milk secretion (Landois). A similar result comes from
increase of blood pressure, as after drinking freely, or when, under
emotion or violent exertion, the heart’s action is increased in force
and the blood is thrown with greater impetus into the large renal
arteries. Senator has found albuminous urine to attend and follow, for
several days, upon forced marches made by young recruits. Here the
muscular work is added to the increased blood tension superinduced by
the more active contractions of the heart.
In this connection it is interesting to trace the changes in the blood
after transfusion. The dilatability of the capillaries enables the
system to accommodate itself to a very great increase in the volume of
blood An increase of 83 per cent. may be borne without serious results,
but above this limit there is increasing risk and an increase of 150 per
cent. entails immediate danger to life. In the restoration of the blood
to its normal condition, the secretion of water sets in promptly leaving
an excess of albuminoids and blood globules. The next change is in the
albuminoids which in two days are almost entirely transformed into urea.
This leaves the blood abnormally rich in globules (Panum, Lesser,
Worm-Müller), the red globules break up much more slowly and may still
be in excess after the lapse of a month (Tscherjew).
In this light, temporary plethora cannot of itself be accepted as the
main or essential cause of the disease. It must be admitted to be a more
constant and important factor than the mere exposure to cold, but of
itself it is inadequate to the production of hæmoglobinæmia. In the
absence of exertion the general plethora fails to produce the specific
disease; again, after transfusion a plethora of albumen lasts for one or
two days, but hæmoglobinæmia sets in only in the first few minutes after
the animal starts out from the stable, (never after an hour or two at
work): once more, excess of globules may last for a month, but with
steady work there is no danger of this disease, after the first mile or
two has been traversed, on the first day of the resumption of labor.
A similar plethora of albuminoids and globules may be induced in a
plethoric animal by a profuse diarrhœa, diuresis or perspiration, the
blood having been robbed of its watery constituents, and concentrated
especially as regards its globules and albuminoids, but hæmoglobinæmia
never occurs as the result of such an artificial concentration. On the
contrary a free secretion by the bowels or kidneys is of the greatest
value in cutting short its progress after it has set in.
The doctrine of poisoning by hæmoglobin produced by excessive work and
disintegration of the muscles is equally insufficient to account for an
attack. Excess of muscular work and of muscle-decomposition-products,
would not reach its maximum within the first few minutes after the
animal has started from the stable, but, other things being equal, would
increase with the continuance of work and the accumulation in the blood
of a constantly increasing amount of these products. The sharp line of
restriction by which the attack is limited to the initial period of
work, while it is never seen after hard work continued for hours in
succession, rules out this from the list of essential causes. It may be
that the products of muscular decomposition aggravate the attack, but to
set them down as the cause of the attack is to beg the whole question
and to contradict the truth that continuous and severe muscular work
with its consequent increase of waste products is a direct bar to the
development of the disease. It should be noted in this connection that
the increase in the waste of nitrogenous bodies, as shown by the
increase of urea, is dependent far more on the amount of nitrogenous
matters ingested than on the muscle work or decomposition. In eleven
hours just before ascending the Faulhorn, Fick passed 21.686 grs. of
urea per hour; in eight hours ascending the hill, 12.43 grs. per hour;
and in six hours after the ascent he passed 13.39 grs. per hour.
A general survey of the field shows that it is not the simple increase
of any normal waste product in the blood which determines
hæmoglobinæmia, and on the other hand the suddenness and severity of the
attack bears all the marks of a profound poisoning. The nature of the
poison has not yet been definitely ascertained, yet one or two
hypothesis may be hazarded, as furnishing a working theory, in
anticipation of the actual demonstration which may be expected in the
early future.
The action of a _stable miasm_ as claimed by some writers is
contradicted by the fact that the disease does not develop so long as
the animal is left to inhale that _miasm_, and on leaving the stable,
the life and vigor are usually remarkable.
The morbific agent must be sought in some source from which it can be
supplied with great rapidity under the stimulus of a short but active
exertion. The chylopoietic viscera furnish such a source. The healthy
liver contains one-fourth of the entire mass of the blood. The torpid
congested liver of the vigorous high conditioned horse, after a short
period of idleness, on full, rich feeding, must hold much more than this
normal ratio. The spleen, the natural store-house or safety valve of the
portal veins, is also gorged with this liquid in the high fed, idle
animal. This organ which is always turgescent after meals, is especially
so in the over-fed horse, which for twenty-four hours has been denied
the opportunity of working off by exercise, the superfluous products of
an active digestion and absorption. Then the whole of the portal veins
and the capillaries in which they originate are surcharged with rich
blood which cannot make its way with the necessary dispatch through the
inactive liver.
In this condition there is incomparably more than a quarter of the
entire mass of blood, enriched to the highest degree in proteids, ready
to be discharged through the liver and hepatic veins into the general
circulation. Under the action of the hurried breathing and circulation,
caused by the sudden and active exertion, this whole mass of rich blood
is speedily unloaded on the right heart, the lungs and the systemic
circulation. One can hardly conceive of a more effective method of
inducing a sudden plethora, with an excess of both globules and
albuminoids.
The presence of actual poisons in such blood is not so easily certified.
The absorption of _bile_ elements and especially of taurocholic acid,
which is a solvent of the red blood globules, and would set free their
globulin might account for the characteristic condition of the blood.
The powerful aspiratory action of the chest, would speedily empty the
whole of the liver blood vessels, and lessening their tension below that
of the biliary radicals would determine an active absorption of bile or
of the more diffusible of the bile elements. A manifest objection to
this view is the absence of an icteric tint in the mucous membranes of
the affected animals. The visible mucosæ are of a brownish red hue, such
as might come from hæmoglobin dissolved in the blood serum, rather than
the yellow tint which might be expected from bile pigment. The theory of
poisoning by bile acids therefore, would require an explanation of
concurrent suppression or decomposition of the bile pigments.
Other sources, however, offer solvents for hæmoglobin, benzoic acid,
which is derived from a cellulose in the fodders, and forms the source
of hippuric acid, dissolves red globules (Landois). In the over-fed
horse with active digestion, but inactive body and liver, this must
accumulate in the liver, spleen and portal system, and when suddenly
drawn into the blood without time for oxidation in the liver it will
contribute to the condition of hæmoglobinæmia.
Peptones, being very diffusible, are very rapidly absorbed, but they are
not found, in healthy conditions, in the portal vein (Neumeister). These
are manifestly transformed into albumen in the intestinal mucosa
(Salvioli), or taken up by the very numerous leucocytes and transformed
or carried elsewhere (Hoffmeister). But peptones injected into the blood
of the dog render it incoagulable, and in large quantity are fatal
(Landois). An excess of glycogen dissolves the red globules, and the
conditions of heavy feeding and torpid liver, are calculated to produce
this in great excess and to store it in the liver cells.
Under the extra vigorous aspiratory force of the chest, these highly
diffusible agents, present in great excess, are likely to be drawn on
through the mucosa, into the portal vein, liver, and cava, without an
opportunity for complete transformation by leucocytes or liver cells.
These would tend to rob the blood globules of their normal physiological
vigor, would unfit them for maintaining the healthy functions of lungs,
kidneys, brain or muscle, and would unfit the globules for successful
resistance to solvents and other inimical influences.
Again it is an important function of the liver, spleen and red bone
marrow to disintegrate worn out or abnormal red globules. These are
taken up by the white blood corpuscles of the hepatic capillaries, by
the cells of the spleen and the bone marrow and are stored up chiefly in
the _capillaries of the liver_, in the _spleen_, and in the marrow of
bone. They are transformed, partly into colored and partly into
colorless proteids, and are either deposited in the granular form, or
are dissolved (Landois). Quincke says: “That the normal red blood
globules and other particles suspended in the blood stream are not taken
up in this way, may be due to their being smooth and polished. As the
corpuscles grow older and become more rigid, they, as it were, are
caught by the amœboid cells. As cells containing blood corpuscles are
very rarely found in the general circulation, one may assume that the
occurrence of these cells within the spleen, liver, and marrow of bone,
is favored by the slowness of the circulation in these organs.” From
this chain of normal processes of blood disintegration, we may
reasonably infer, a greatly exaggerated work of blood destruction when,
in connection with an increased density of the plasma, and the presence
in the portal blood of poisonous products of digestion, the red globules
have been altered in density, in outline and in vitality, so that they
become ready victims of the amœboid cells of blood and tissues. Then the
stagnant condition of this altered blood in the compulsorily idle animal
favors the greatest excess of this destruction and the storing up of an
increased quantity of hæmoglobin and other products, to be poured
suddenly into the general circulation as soon as the movement of the
blood is quickened by exercise.
This destruction of the red blood globules by disintegration contributes
to the formation of numerous decomposition-products, like succinic,
formic, acetic, butyric and lactic acids, inosite, leucin, xanthine,
hypoxanthin, and uric acid, some of which are strongly toxic. The
tendency will be to lower the vitality of the red globules and thus to
render them the easier victims of the leucocytes and of the liver,
spleen and marrow cells. Even the freed hæmoglobin appears to exert a
solvent action on the red blood globules. These are, of course, most
concentrated and effective in the seat of their production, yet when
drawn suddenly in large amount, into the general circulation, by the
vigorous aspiratory action of the chest, they may prove seriously
detrimental to the blood at large.
Again a variety of toxic matters are introduced into the system in the
food and others are developed from the food in the stomach and
intestine. Brieger found in the gastric peptones a potent alkaloid
having the effect of urari, and which in excess would determine muscular
paralysis. The alkaloidal and other poisons produced by fermentations in
the intestines have to be safely disposed of. The ptomaines, if not too
abundant, are arrested or even decomposed in the liver which thus stands
as a guardian, at the outlet of the portal system, to protect the body
at large. But this antitoxic function of the liver is only exercised in
the presence of glycogen (Rogers, Landois), and forced muscular movement
soon removes all glycogen from the liver of the dog (Landois). Again
glycogenesis in the liver is now believed to be dependent on a ferment
produced by the pancreas. If therefore, the sudden active exercise and
the aspiratory action of the chest freed the liver of its glycogen, and
hurried the alkaloidal and other poisons through its capillaries too
rapidly to allow of the protective action of the liver cells, or if the
pancreas as well as the liver had become torpid and had failed to
produce the requisite amount of glycogen-ferment for the liver, the
poisoning of the blood and system at large would be imminent.
Not to mention the other toxic products which come from imperfect
metamorphosis in the liver, it may be noted that a venous condition of
the blood or an excess of carbon dioxide contributes greatly to the
solubility of the red blood globules. It also tends greatly to modify
the fibrinogenous elements. Thus the blood of a suffocated animal fails
to coagulate or coagulates loosely, and the blood of the portal vein of
a suffocated horse is strongly toxic (Sauson). Now the conditions
attendant on the onset of equine hæmoglobinæmia are such as to give free
scope to both of these inimical influences. The great mass of blood in
the portal vein, spleen and liver is venous blood strongly charged with
carbon dioxide, and by the sudden, active exertion this is forced
rapidly through the liver and lungs without time for full æration, so
that the whole mass of the circulating blood is speedily reduced below
par, and laid specially open to the action of blood solvents. By the
same action the systemic blood is charged with poisons, direct from the
food, and fermenting ingesta, and from the overworked spleen and liver
whose functions are profoundly impaired, and later from other important
organs, the healthy functional activity of which can no longer be
maintained by the deteriorated blood supplied to them.
Hæmoglobinæmia in dogs has been produced experimentally by the injection
of water into the veins the mere dilution of the plasma dissolving out
the coloring matter from the red globules (Hayem); also by the
inhalation of arseniureted hydrogen (Naunyn and Stadelman); by the
ingestion of toluylendiamine, or phosphorus (Afanassiew, Stadelman); by
snake venom, septicæmia, influenza, contagious pneumonia, petechial
fever, anthrax, etc. These cannot be looked on as causes of the acute
hæmoglobinæmia in the horse, but they serve as illustrations of changes
in the plasma, and poisons in the blood determining the escape of
hæmoglobin from the cells.
Ralfe recognizes two forms of hæmoglobinæmia in man:
1st. That in which the hæmoglobin is simply dissolved out of the blood
globules, the solution taking place chiefly in parts exposed to cold.
2d. A more severe form in which the dissolution is general and probably
attended by some destruction of red globules in the liver, spleen and
even in the kidneys. The general opinion appears to be that the attacks
are due to some nervous disturbance, which causes vaso-motor disorder
and it is supposed that there is an exaggerated sensibility of the
reflex nervous system. It has been suggested that peripheral irritation
causes irritation of the vaso-motor centre, and in turn this causes
local asphyxia in the part stimulated, under which conditions the red
globules part with their hæmoglobin (Roberts).
Murri holds that the disease depends on an increased irritability of the
vaso-motor reflex centre, and the formation, owing to the disorder of
the blood forming organs, of corpuscles unable to withstand exposure to
cold or carbon dioxide.
While it is not assumed to point out the actual poisons of
hæmoglobinæmia in the horse the above suggestions may offer valuable
hints as to the lines of inquiry that may be followed with the best hope
of reaching definite results.
_Lesions._ These are especially found in the blood, liver, spleen,
muscles, bone marrow and kidneys. The spinal cord and nerve trunks are
occasionally affected.
The _blood_ is charged with carbon dioxide and is black, tarry,
comparatively incoagulable remaining in the veins and showing an
iridescent reflection. It does not absorb oxygen readily though exposed
to the air, and thus bears a strong general resemblance to the blood of
anthrax. It contains an abnormal proportion of urea and allied
extractive matters which greatly increase its density, and interfere
with the healthy exercise of the different cell organisms and functions.
These are not due to excessive muscular activity as stated by
Friedberger and Fröhner, but are derived mainly from the abundant
products of digestion. When the shed blood coagulates it forms a soft
clot without buff and the expressed serum is reddish from the presence
of hæmoglobin, and of hæmatoidin crystals. The uncoagulated blood drawn
over a sheet of white paper stains it deeply by reason of the same
coloring matters in solution. The red corpuscles may be paler than
natural, some even entirely colorless, and they are often notched or
broken up in various irregular forms. They have lost the natural
tendency of the shed equine blood to stick together, to collect in
rouleaux and precipitate to the bottom of the vessel, so that no buffy
coat is formed, should the blood coagulate. The white corpuscles are
relatively increased. Finally the coloring matters contained in the
plasma are imbibed by the different tissues and give a brown or reddish
tinge to such as are naturally white. Limited blood extravasations are
not uncommon especially in the more vascular organs like the muscles,
liver, spleen and kidneys.
The _liver_ is more or less congested and enlarged, friable, yellow, or
mottled yellow and red and exudes black blood freely when incised. The
bile is thick, viscid and dark green, as in cases of experimental
intravenous injection of hæmoglobin.
The _spleen_ is also swollen and congested with blood, and the pulp is
very high colored from the excess of hæmoglobin and other products of
blood destruction. The _muscles of the croup_ are usually the seat of
visible lesions. There may be pallor, œdema and swelling, but not
unfrequently there are blood extravasations varying in size from a pin’s
head upward and giving a dark red aspect to the affected tissues. Under
the microscope the affected fibres are seen to have lost their
transverse striation and to have assumed a more or less granular or
hyaline appearance. Next to the gluteal muscles, these changes are
frequently found, in the muscles of the thigh (especially the rectus
femoris, and triceps extensor cruris), and in those of the loins (psoas,
ilio-spinalis, and longissimus dorsi). Exceptionally the pectoral
muscles are involved or even the abdominal muscles. A considerable
straw-colored œdema may be found in the intermuscular connective tissue.
The _red bone marrow_ primarily of the large bones of the limbs (femur,
tibia, humerus, radius,) and less frequently of other bones, even of the
vertebræ, is often the seat of intense vascular congestion and even of
hemorrhage. The medullary matter is of a deep red or black color, and
there is an abnormal accumulation of red globules in various conditions
of growth and destruction (red nucleated corpuscles, fragments of
corpuscles, colored granules). Dieckerhoff considers the condition one
of osteomyelitis, but it seems to be rather a sudden, extraordinary
exaggeration of the processes of blood metamorphosis. Neumann found that
when the blood regeneration process is very active even the yellow
marrow may be changed into red, and this throughout all the bones of the
extremities.
The _kidneys_ are usually the seat of congestion, and black spots of
infarction, when the disease has lasted for twenty-four hours. In
rapidly fatal cases they may appear normal. There may be enlargement of
the kidneys with softening and granular degeneration of the renal
epithelium in cases that survive for some days.
The _bladder_ contains dark brown or red glairy urine of a high density
and loaded with urea, hæmoglobin, etc.
The _terminal portion of the spinal cord_ and the lumbo-sacral plexus,
or some of its branches, are sometimes blood stained, or the seat of an
exudate or surrounded by one.
_Symptoms._ In the regular type of hæmoglobinæmia in the horse the
history of the attack is highly significant. The subject is in good
working condition, he may be fat, or lean, but in either case the
muscles are firm and well developed, diet has been liberal, embracing a
large proportion of albuminoids, work has been constant up to within a
day or two preceding the attack, when the animal has been left
absolutely idle in the stall without any reduction of feed. Then finally
it has been suddenly subjected to active exertion which demands vigorous
muscular movement, and above all activity of the respiratory muscles and
the heart. This exertion usually consists in riding under the saddle or
going in harness, but may attend on casting in the stall, lounging in a
ring, or in a playful run when suddenly set at liberty.
=Severe Cases.= The attack comes on early in the course of such
exercise. The patient may not have gone more than one hundred yards from
the stable or he may have traveled for half an hour or an hour, but the
disease rarely shows itself after a longer period of work.
The horse which left the stable full of life and spirit, suddenly flags
and hangs on the bit, the ears or head may drop, and one or more limbs
usually the hind ones, are moved stiffly and awkwardly, or even stagger.
He knuckles over at the fetlocks, drags the toes on the ground, flexes
the joints imperfectly, the muscles appearing to be rigid and
uncontrollable, or he crouches, the joints remaining semiflexed the
animal in vain attempting to extend them. The patient trembles
violently, sweats profusely, breathes deeply and rapidly and assumes a
pinched, anxious, agonized expression of countenance. The heart beats
tumultuously, the pulse (in 84 per cent. Friedberger and Fröhner) is
accelerated to a variable degree, and the temperature is still normal
(in 80 per cent. Friedberger and Fröhner), or rarely exceeds 101.5°F.
There is often tenderness on percussion and sometimes even on
manipulation over the loins, short ribs, and the croup, and pinching of
the loins may cause wincing. The affected muscle or muscles (lumbar,
gluteal, crural) are usually firm, hard and tender, they may be the seat
of spasm or of œdema and paresis. These parts may, however, have their
sensitiveness lessened and even punctures or electric currents may have
little effect on them.
Soon the increasing muscular weakness is incompatible with the
maintenance of the standing position, the bending of the limbs and
crouching become extreme, the animal makes vain efforts to control the
muscles and extend the joints, and helplessly drops to the ground. When
down he moves his legs convulsively, but is unable to coördinate the
muscular movements and all efforts to rise are unavailing.
The spasms and paresis may attack other parts of the body such as the
pectoral region the shoulders and even the abdomen, but the earliest and
most persistent disorder is usually in the divisions of the lumbo-sacral
plexus affecting the supra or sublumbar muscles, the gluteals, the
patellar (triceps,) the adductors and the abductors. The caudal muscles
are exceptionally involved. In a series of ten cases Bouley noticed that
the left hind limb was always the first paralyzed (evidently a simple
coincidence).
Urine may be passed freely or the bladder may be paretic so that it must
be emptied with the catheter. In severe cases the urine is of a high
density and of a dirty brownish gray, red or almost black color. It
contains no blood clots, nor blood globules, but granular hæmoglobin,
tyrosin and other waste products contribute to produce the reddish
color. In some instances there is an abundant _metalbumen_ which renders
the liquid glairy, causing it to fall in fine threads or films. Urea is
usually present in great excess. Hippuric and even uric acid are usually
present but not in excess. When the disease has advanced to nephritis
the albuminuria is complicated by the presence of casts of the
uriniferous tubes, renal epithelium, white and even red blood globules.
During the violence of the attack there is no disposition nor leisure to
eat, but when the more violent symptoms abate appetite is usually
manifested. There may be more or less paresis of both bowels and
bladder, so that neither fæces nor urine is passed yet in other cases
both are discharged spontaneously.
The senses are preserved, excepting in the case of the affected muscles
and the integument which covers them. There may, however, be more or
less dullness and stupor in certain cases from poisoning of the cerebral
centres by the poisons circulating in the blood.
=Mild Cases.= In the mildest cases there is stiffness and lameness in
one, or less frequently in both hind limbs, coming on when put to work
after a period of idleness, and not associated with any appreciable
lesion of the limb in question. There may or may not be hardness and
swelling of the gluteal or other muscles of the quarter or loins. This
has the appearance of rigidity or spasm but may be primarily due to
œdema or exudation into the substance of the muscle. In some instances
the muscles of the breast, shoulder, or forearm are the seat of the
trouble. Muscular trembling and perspiration may be present and if the
urine is examined, it is often found to be glairy, or charged with urea,
and allied nitrogenous products. These cases are not benefited by local
applications, but they recover (temporarily) under rest and above all
under active eliminating treatment. Under gentle and progressive
exercise too they improve and get well. They recur, however, with great
readiness under a rich nitrogenous diet and a temporary rest followed by
sudden exertion.
Between the mildest and gravest cases there are infinite gradations of
severity, one-third to one-half of the worst cases usually terminating
fatally, whereas the mildest are always amenable to treatment.
_Progress._ The course of the disease depends on the severity of the
attack but also, in no small degree, on the good judgment of the driver.
Cases that develop with great suddenness, and apparently with extreme
severity may subside spontaneously if the animal is placed in a
condition of absolute rest. If, however, we can secure rest of the
muscles of progression only, while the breathing remains rapid and
labored, improvement is unlikely, as the system continues to receive
large accessions of the toxic products. When the patient is down and
unable to rise, the enforced rest may be beneficial, but too commonly,
the greater effort with which breathing is carried on in the recumbent
position, and the frequent ineffectual struggles of the limbs prevent
the requisite muscular quietude.
In some cases, and especially in the mildest, recovery may seem to have
been effected in a few hours, and in others it will be seen in
twenty-four or forty-eight hours, while in still others the paresis and
helplessness may continue for a week and yet be followed by recovery. In
these cases appetite may be retained in greater or less degree, but the
intestinal peristalsis is usually weak and imperfect, the fæces small in
quantity and dry, and the bladder atonic so that the urine may have to
be drawn off with the catheter. It usually retains the deep red color,
or improvement may be heralded by a change to a dirty grayish hue. If,
however, it shows an excess of albumen, cylindroid casts entangling
renal epithelium and white or red globules it will indicate the access
of diffuse nephritis and a prolonged or even a fatal illness.
When control of the limbs is not restored at the end of a week, the
paretic muscles usually undergo marked and rapid wasting, which may last
for months or years. This is especially common in the case of the
patellar muscles (muscle of the fascia lata, triceps extensor cruris) in
which the atrophy may become so extreme that the skin covering the inner
and outer sides of the thigh may be brought virtually in contact in
front of the femur. This entails an almost complete inability to sustain
the body on the hind limbs. When atrophy is less extreme, there is only
a weakness, stiffness, or swaying or staggering on the hind limbs in
progression.
In fatal cases death may occur early in connection with the violent
struggles, the excited breathing, pulmonary hypostasis and congestion, a
cyanotic hue of the visible mucous membranes and a gradual increase of
stupor. Though delayed for several days, there is a continuation of the
muscular struggles, and the labored breathing; the red or glairy
character of the urine persists or is exaggerated; the nervous
irritability increases, with muscular trembling; and cyanosis, or stupor
increases until death.
The _mortality_ is always high in the severe forms of the disease, the
deaths ranging from 20 per cent. upward.
After a first attack there is a strong predisposition to a second under
similar exciting conditions.
_Diagnosis._ The peculiar symptoms of this disease and the circumstances
attending its onset, are usually sufficient to distinguish it from all
others. There may be danger of confounding certain cases with thrombosis
of the posterior aorta, or of the iliac arteries or their branches, but
the absence, in such cases, of the special history of the attack and of
the morbid state of the urine, and the absence of pulsation in the
arteries distal to the thrombosis will serve to prevent confusion.
Spinal myelitis will be distinguished by the gradual nature of the
onset, by the absence of the conditions attending on the attack of
hæmoglobinæmia, and usually by the absence of hæmoglobin, urea and other
nitrogenous products in excess in the urine.
_Prevention._ The hard worked or systematically exercised horse, which
is at the same time heavily fed must not be left in a state of absolute
rest in his stall for twenty-four hours. A fair amount of exercise must
be given on every day in the week, and at the same time, the food should
be restricted in ratio with the restriction of exercise. Turning for an
hour or two daily into a yard may be a sufficient precaution. When from
any cause, rest is imperative, the diet must be materially reduced and
given in part in a laxative form (bran, roots), or a slight laxative
(Glauber salts) or diuretic (saltpeter) may be added. Cleanliness and a
free ventilation of the stable, are also of value in obviating at once
auto-intoxication and the admission of poison through the lungs. In the
same way a free allowance of drinking water is beneficial as favoring a
general elimination from the various emunctories, and a dilution of the
plethoric blood.
These precautionary measures are especially important in the case of
horses which have passed through a first attack and which are in
consequence strongly predisposed to a second. Horses fed liberally on
highly nitrogenous food (oats, beans, peas, cotton seed meal), will also
require specially careful oversight when at rest for a day or two only.
_Treatment._ The first and perhaps the most important consideration is
absolute rest. If the subject is stopped instantly on the appearance of
the first symptoms, the disease may be often aborted. It is better to
avoid the exercise of walking to a stable until such time as the
severity of the attack has somewhat moderated and then to move the
subject only in the slowest and quietest possible way. If the patient is
already down and unable to rise, he may be carried to the nearest stable
in an ambulance or on a stone-boat, and there helped to his feet and
supported in slings. Though he may be unable to continue in the standing
position without the sling, yet if he can use his limbs at all for
support, and is prevented from lying down, the breathing will be
rendered so much more free and quiet, that it may greatly lessen the
transfer of the poisonous elements into the general circulation and
materially contribute to recovery. If, however, he cannot stand on his
limbs at all, but must settle in the slings, the compression of the
chest will so excite the breathing that it will induce dyspnœa,
pulmonary congestion and a rapidly fatal result. In such a case a good
bed must be provided and the patient made as comfortable as possible in
the recumbent position.
In some cases in the earliest stages a full dose of sweet spirits of
nitre or even half a pint of whiskey has seemed to assist in aborting
the disease though the urine was already of a deep red color. It
probably acted by supporting the already oppressed heart, and securing a
prompt elimination by the kidneys.
Friedberger and Fröhner strongly recommend bleeding in all cases of
dyspnœa and excited heart action, and considering the plethoric
condition of the animal it would equally commend itself in other cases
as well. This is the most prompt sedative of the nervous and vascular
excitement, and the most speedy and certain means of removing much of
the poisons accumulated in the blood, and of diluting what remains by
reason of the absorption of liquids from every available source. This
will more than counterbalance any temporary increase of poisons drawn
from the portal system to fill up the vacuum in the systemic veins
caused by the emission of blood. When the thick tarry condition of the
blood seriously hinders a speedy abstraction both jugulars may be opened
at once.
In some cases of great nervous excitement bromides may be useful in
moderating circulatory and respiratory movement, but on the whole the
advantage is greater from an immediate resort to eliminating agents.
One of the most effective agents is water. If the patient is thirsty he
should have all he will drink, and if not, it may even be given from a
bottle, or thrown into the rectum. A still more effective resort would
be to introduce water intravenously in the form of a normal saline
solution, or even to pass it into the trachea through a small cannula or
large hypodermic needle. This serves to dilute the over dense blood, to
stimulate the kidneys and other emunctories to active secretion, and to
retain in solution the hæmoglobin, urea and other products which would
otherwise cause greater irritation. This would be especially applicable
after the blood tension had been diminished by phlebotomy.
Warm fomentations to the loins or croup are not without their influence.
They tend to soothe the irritated parts and to solicit the action of the
kidneys more particularly. The old resort of a fresh sheep skin, with
the fleshy side in, may be used as a substitute.
Perhaps the most important indication is to secure depletion from the
overloaded portal system and liver. Where nothing better offers, a pint
or quart of castor oil, or a pound of Glauber salts, or a half drachm of
podophyllin and four drachms of aloes may be given. If available 1 to 1½
grains of eserine, or 7 grains of barium chloride may be given
hypodermically in distilled water or that which has been raised to the
boiling point. This may be supplemented by frequent injections of hot
soap suds or even of laxative saline solutions. If the bowels can be
roused to free secretion the removal of toxic matters from the portal
blood and the delay in the progress of similar matters through the liver
will go far toward securing a favorable result. When free purgation has
been secured recovery can usually be counted on.
The action on the bowels must be followed up by diuretics to eliminate
the offensive matters from the general system. Colchicum has been
recommended because of its action in increasing the solids of the urine,
and this may be combined with saltpeter or other diuretic, or the latter
may be used alone and repeated twice a day. If, however, the patient
can, by the free use of common salt or otherwise, be induced to drink
freely of water, the elimination through the kidneys will be
sufficiently secured.
The muscular weakness and paralysis that remain after the acute symptoms
have subsided must be met by stimulating liniments and even blisters to
the loins or affected muscles, by the internal use of strychnia (2 grs.
twice daily) until the jerking of the muscles indicates that its
physiological action has been secured, and by an electric current daily
for ten minutes at a time through the affected nerves and muscles.
Animals that have been helpless for weeks have, in our hands, recovered
under such treatment, and even cases of several months’ standing, with
the most extensive atrophy of the triceps, and in which the animal could
barely stand, have made a satisfactory recovery.
Any remaining nephritis must be treated according to its indications.
During recovery and in the convalescent animal the diet should be
laxative and non-stimulating. Bran mashes, turnips, beets, carrots,
green fodder, ensilage and scalded hay may be allowed. Oats, corn,
beans, peas, vetches, etc., must be carefully avoided. If the food fails
to maintain the bowels in a gently relaxed condition one, two or more
ounces of sulphate of soda may be added daily.
In the mild cases a good dose of purgative medicine succeeded by a
course of diuretics will serve a good purpose.
In all cases alike work must be resumed very gradually. At first the
animal may be walked a few hundred yards, and the pace or load and
duration of exercise may be increased day by day until full work can be
safely endured. In an animal that has once suffered the same gradual
inuring to labor should be followed, after any short period of rest on a
fairly good ration.