CHAPTER IV.. Depraved Appetite—Pica—the Licking Habit.

DEPRAVED APPETITE—PICA—THE LICKING HABIT.

Depraved appetite, causing animals to swallow bodies which cannot properly be described as food, is frequent. The condition is commonest in adult animals of the bovine species, in calves and in lambs. The consequences are sometimes very serious, so that although depraved appetite does not represent a well-defined morbid entity, it is important to be in a position to remedy it.

Depraved appetite does not appear under the same conditions in young and in old animals. In adults it often results from faulty feeding, or from some wasting disease which develops insidiously, or remains unrecognised; in young animals it is the result of insufficient nourishment.

Roloff & Röll hold that pica is the first symptom of osteomalacia (which see).

DEPRAVED APPETITE IN THE OX.

=Causation.= In the bovine species depraved appetite occurs in adult, debilitated animals, which are often, though not always, suffering from some well-marked digestive disturbance.

The frequency of this symptom, and the peculiarities in its occurrence, have caused it to be referred to a large number of different causes, among which may be mentioned bad hygiene, chronic gastro-enteritis, tuberculosis, osseous cachexia, pasteurellosis, gestation, etc.

It is very certain that the peculiarity in the appetite is, above all, the result of incomplete and irrational alimentation. The animal has certain special requirements, to meet which the food must be of suitable composition. If these alimentary and digestive conditions are not fulfilled, depraved appetite may occur, even in animals which appear well nourished. Certain authors refer the appearance of this condition to want of certain soda salts in the daily ration, and, in support of this opinion, they point to the frequency of the disease in mountainous regions where the geological formation is chiefly granite, as in the Black Forest. Alluvial soils are supposed not to produce it. It certainly seems more common on soils lacking in certain constituents or exhausted by repeatedly growing certain crops. Nevertheless, in France it might be urged that pica occurs equally on all kinds of soil, and a German author, Lemke, ascribes this perversion of nutrition to the want of phosphorus. Haubner and Siedamgrotsky attribute it to a nervous disorder. All causes which exhaust the organism, especially all chronic diseases of digestive origin, may induce aberration of appetite.

Permanent stabling, confinement, absence of sunlight, want of exercise and pure air contribute to the general debility which predisposes to attack. Dry seasons, by reducing the supply of food, have a similar effect.

In tuberculosis and in pasteurellosis, it is the general organic decline which produces these puzzling changes in appetite. Similarly the influence of gestation depends on the superadded demands on the organism caused by the development of the fœtus.

=Symptoms.= The symptoms may be divided into two phases.

In the first phase, the animals still preserve their appetite, but whenever they have an opportunity they eat earth, sand, manure, litter saturated with urine, plaster, etc. They lick the walls, the boarding, the mangers and the trees, and they chew and swallow linen spread out to dry.

This phase may continue for a very long time, three to four months or more, provided no acute complication results from the eating of such foreign material. There is no fever, but the appetite, although well preserved, is often capricious, and the ordinary food is eaten slowly.

In the second phase, which frequently marks the development of complications produced by the passage, contact, or prolonged sojourn of various materials in the digestive tract, fever appears, little marked as a rule, but continuous in character.

The appetite is diminished. The animal wastes; the secretion of milk diminishes, and signs of chronic gastro-enteritis may be noted. The perversion of appetite still continues; rags, decomposing or filthy materials, pieces of old shoes, etc., are eaten, and it is not surprising that such substances should have an unfavourable effect on the mucous membrane of the digestive tract.

The wasting process slowly leads to marked emaciation, and after an interval of from six months to a year, or even two years, the patients die in a state of complete exhaustion. The lesions found on post-mortem examination are those of various diseases capable of producing depraved appetite or simply lesions of chronic gastro-enteritis.

=Diagnosis.= The diagnosis presents no difficulty. The important point is to discover whether or not there exists some previously unrecognised primary disease.

=Prognosis.= The prognosis of this condition is grave, because depraved appetite is frequently only a symptom of some incurable disorder, or because the changes in the digestive mucous membrane are already too far advanced to permit of much improvement.

=The lesions= comprise: general emaciation, presence of a yellow serum in the fatty tissue, muscles pale and flabby, catarrh of the mucous membrane of the stomach and bowel. The blood seems less in quantity and coagulates feebly or not at all.

=Treatment.= The treatment should be directed against the primary cause, if such exists (osseous cachexia, pasteurellosis, gestation, etc.).

In other cases a change in management and in feeding, and the administration of food rich in mineral salts like chlorides, carbonates, and phosphates of lime, soda or potash, produces the best possible results. The leguminous foods, sainfoin, clover and lucern, are to be recommended. The animal, if formerly stabled, should be turned out and its living conditions entirely altered.

It is often useful to place a block of rock-salt in the manger; when hyperacidity of the stomach is suspected lime water, chalk, or magnesia should be given. Where digestion is weak or slow HCl, pepsin and vegetable bitters are indicated. Nevertheless, one sees cases which refuse to yield to any of the ordinary methods. In treating these, Lemke has recommended the subcutaneous injection of chloride of apomorphine, a drug which may be regarded as a true specific. The doses vary between 1½ and 3 grains, and an injection is given once a week for three weeks in succession. After this the tendency to pica is said to disappear and the general condition to improve. The treatment must be repeated every three months in countries where depraved appetite appears general and permanent.

It is difficult to understand by what mechanism this drug produces the effects attributed to it, but those who have employed it speak very highly of its action.

We may add that in addition to the different modes of treatment, it is not infrequently necessary to hastily perform gastrotomy in order to avoid fatal consequences, which would otherwise follow indulgence in this habit. When an animal has swallowed a considerable quantity of linen, for example (and Moussu has seen cases in which many pounds weight had been devoured), immediate intervention is required to avoid intestinal obstruction. Furthermore, when the history is quite clear gastrotomy allows the entire mass of foreign bodies, ingested at different times, to be removed.

DEPRAVED APPETITE IN CALVES AND LAMBS.

=Causation.= Depraved appetite is commonest in calves and lambs when the animals are insufficiently nourished, or when the mothers are suffering from chronic debilitating diseases and are therefore yielding milk poor in fat and in mineral constituents. In a few rare cases it is impossible to discover what causes the young animals to devour these foreign materials. Even fully-grown sheep, when shut up together in winter, acquire the habit of chewing each other’s wool, sometimes to the extent of virtually depilating their fellows and accumulating wool balls in their stomachs.

=Symptoms.= Calves have a tendency to lick themselves or their neighbours, and thus little by little collect a varying quantity of hair which they swallow. When this habit of licking is little marked the quantity of hair ingested may not be dangerous; but in the contrary case the hair (which cannot be digested) accumulates and is permanently retained in the abomasum. It soon becomes converted into masses, cemented together with mucus, and forms round balls, to which the name of œgagrophiles has been given. If these œgagrophiles, or hair balls, are of small size, they prove of trifling importance; but too frequently they attain considerable dimensions and obstruct the pylorus or the intestine. The young calves then refuse all nourishment, and die in twenty-four to forty-eight hours in a state of complete exhaustion or after a series of epileptiform attacks.

In lambs the complications due to depraved appetite develop in a similar way, but the wool swallowed is obtained from the mothers. The lambs first suck the locks of wool, then tear them off and swallow them. So long as these peculiarities of appetite are little marked no bad results follow; but if the shepherd is careless, and fails to note the condition of his young flock sufficiently early, accidents occur.

The wool is not so easily converted into balls as is hair, but it soon accumulates in the pyloric region or in the intestine, and forms obstructing masses. The little patients lose appetite and lie down in corners, where they are found dead after twenty-four to forty-eight hours. The masses of wool or of hair are rarely passed with the excrement; more frequently they are vomited, but this again is exceptional; usually they become arrested at the entrance to the pylorus. The lambs show colic, tympanites of the abomasum, and attempts at vomiting, though unfortunately these are often overlooked. The quantity of wool found in the abomasum and intestine on post-mortem examination may be considerable, in relation to the size of the digestive compartments. Death results from intestinal obstruction, exactly as in the case of calves.

These aberrations of appetite in lambs have been considered as due to the want of sufficient mineral salts in the mother’s milk; and it has been stated that the lambs practise this habit because of the laxative result of the fat contained in the wool swallowed. The explanation seems very logical, though it is by no means perfectly proved. It is certain that this habit becomes particularly common after years in which forage has been scarce and among flocks in bad bodily condition. The force of example also plays a certain part, and animals probably imitate one another, and so acquire the disease. This explains the importance of early segregation.

=Diagnosis.= The diagnosis of depraved appetite, pica, or the licking habit presents no difficulty; but it can only be arrived at by the cowman or shepherd, for the symptoms can only be detected by continued watching.

The diagnosis of pyloric or intestinal obstruction is very difficult in the absence of information. It becomes easy after the first post-mortem examination has been made.

=Prognosis.= The prognosis is grave. In calves, obstruction of the bowel by hair balls inevitably causes death, and in sucking lambs the mortality may be high: as much as 15 per cent. to 20 per cent. according to the observations of several observers. The mortality occurs about the age of six weeks to two months, whilst the licking habit may begin towards the end of the second week.

=Treatment.= Prophylaxis demands that the mothers (whether cows or ewes) be well fed. An excellent precaution consists in adding to the food a sufficient quantity of salt and of phosphate of lime (2 drams to 2½ drams of each). This treatment of the mothers is necessary as soon as the tendency to licking becomes manifest.

In calves the best method of avoiding fatal results is to prevent the young animals licking one another; and the method now usually practised on well-managed farms consists in applying a simple muzzle of wicker work immediately after each meal.

In lambs treatment is more difficult. As soon as the shepherd sees any tendency to depraved appetite the lambs should only be left with their mothers whilst being suckled. The flock should be exercised in the open, and ordinary salt should be placed at a number of points on the ground occupied by the animals.

COLIC IN THE OX.

COLIC DUE TO INGESTION OF COLD WATER. CONGESTIVE COLIC.

=Causation.= Congestive colic occurs in the stable, in animals which have been doing heavy work, and, returning in a heated condition, drink large quantities of cold water. It is commoner when animals have not eaten for a considerable time, and when, therefore, the stomach is nearly empty. Under these circumstances chill of the digestive viscera is direct and immediate.

=Symptoms.= This form of colic occurs suddenly, soon after the water has been swallowed, and is characterised by violent pain. At first the animals show uneasiness, stamp, and continually move about striking themselves in the flank with the feet or horns, swishing the tail, etc. They refuse food, lie down and rise frequently, and paw the ground.

As a general rule this form of colic lasts from half an hour to one hour, and terminates in recovery. In some rare cases where death occurred Cruzel found on post-mortem examination congestion of the abomasum, and, in a few, congestion of the small intestine, with or without rupture.

=The diagnosis= is easy, on account of the suddenness of onset, rapid development and history of the disease, discovered on questioning the owner or herdsman.

=The prognosis= is not grave. This form of colic generally cures itself. Nevertheless precautions are required against possible complications, such as intestinal hæmorrhage and invagination.

The necessary preventive measures are self-evident. Animals returning from work should not be allowed to drink freely of cold water, but should first receive a little food and afterwards water at the temperature of the atmosphere.

When colic has set in, the patient can be walked about. If pain persists, the region of the abdomen may be dressed with oil of turpentine, mustard, or similar counter-irritants. The application of warm clothing is also useful. Finally, in grave cases, a moderate quantity (three, four, or five quarts) of blood may be withdrawn from the jugular. The administration of stimulants like wine, alcohol, etc., is also indicated.

COLIC DUE TO INVAGINATION.

Invagination consists in the passage of one portion of the intestine into the next-following portion. When once the condition has been set up it tends to become aggravated, the invaginated part being drawn further and further forwards. Invaginations therefore may vary in length between a few inches and sixteen to twenty inches.

Law states (Vol. II. p. 347) that in cattle and swine invagination of the large colon is almost impossible owing to the relation of the bowel with the layers of the mesentery. The anatomical arrangement is opposed to the formation of invagination, yet this accident is not uncommon in cattle and swine. The small intestine can be invaginated into the cæcum or into itself. The cæcum may become invaginated, or it may pass into the colon or rectum.

Cartwright, Veterinarian (1829), reports a case of invagination in a bull calf, and Youatt gives particulars of a similar case which was followed by sloughing and discharge per anum of the intussuscepted portion of bowel. (See also Möller and Dollar’s “Regional Surgery,” p. 328.)

=Causation.= This variety of colic is due to a number of somewhat obscure causes. In a general sense we may say that anything which increases intestinal peristalsis increases the risk of invagination. The accident may follow intestinal congestion, but is most frequent in animals suffering from intestinal worms, or in animals used for heavy work. Under the influence of violent tractive efforts the peristaltic movements are stimulated, and the intestine being in an oblique position on a plane inclined backwards, the contracted portion may slip into the dilated section behind it.

Invagination may also occur without any apparent cause, even in animals standing in the stable.

=Symptoms.= The attack always occurs suddenly, develops rapidly, and is of an extremely grave character.

Colic comes on while the animal is working, moving about, or resting, according to circumstances, and at first resembles that due to congestion. It afterwards becomes very violent; the animals paw, stamp, show great uneasiness, throw themselves violently down, and rise suddenly, only to again lie down as before. The face expresses anxiety, suffering and depression; the tail is often kept lifted, and efforts are continually made to defæcate, mucus being passed. By passing the hand into the rectum the invagination may occasionally be discovered.

Colic persists with great intensity for ten to twelve hours, interrupted only by rare periods of calm. At the end of this time, however, it may suddenly disappear, and the animal may fall into a semi-comatose state. This indicates the onset of necrosis in the invaginated section, the painful reflexes no longer being transmitted to the sympathetic system. The disappearance of colic is sometimes regarded as a sign of improvement, but this improvement is illusory. From this time onwards the animals stand stolidly, obstinately refusing both food and drink. If they lie down, it is with great care. Palpation of the right side of the abdomen is painful, and the animal actively resents it. One of the most important and constant signs at this stage is the absence of defæcation, due to obstruction of the intestine, which is occluded. The animals may survive for ten, twelve, or even fifteen days (see also Möller and Dollar’s “Regional Surgery,” loc. cit.). The invaginated, necrosed portion may even be passed with the fæces, and recovery may occur, the continuity of the intestinal tube being secured by the adhesion of the serous surfaces; but such spontaneous recoveries are exceptional. Usually after a few days death results from peritonitis.

Occasionally, trifling invaginations may become reduced spontaneously, Diarrhœa, with the passage of blood-stained material is then seen for a time, a sign which alone at this stage would justify the diagnosis of invagination.

=Diagnosis.= The intensity of the colic and the absence of defæcation for several days afterwards, justifies the diagnosis of invagination. Purgatives then remain without effect. In addition, rectal exploration offers a valuable means of diagnosis. The last portions of the intestine are found absolutely empty, and the arm when withdrawn is found to be covered with viscous blood-stained mucus, resulting from the sero-sanguinolent exudate, due to compression of the blood-vessels.

In cases of this kind accompanied by the above-mentioned symptoms abdominal exploration by the rectum should always be practised, but it rarely gives exact information. The hand, when passed towards the right flank, may sometimes reach the invaginated part, which conveys the impression of a cylindrical swelling. The invagination, however, can rarely be reached. If the operator is successful, he will find that as he displaces this cylindrical mass or attempts to grasp it, the animal shows signs of exaggerated sensitiveness.

=The prognosis= is of exceptional gravity. Apart from the rare cases where the invaginated portion becomes necrotic and is eliminated, death is inevitable. Unless an operation is performed, septic peritonitis may develop about the fifth or sixth day.

=Treatment.= The only treatment consists in surgical intervention. Some practitioners have recommended giving large doses of purgatives with the idea of causing changes in the neighbourhood of the invaginated part; but such treatment presents little chance of success. The same is true of the administration of large doses of olive oil, either in the form of draught or of enema.

Siebert attempted reduction by generating CO{2} from soda bicarbonate dissolved in water and diluted HCl, injected successively per rectum. In time fæces and CO{2} escaped, and the patient recovered. Siebert claims to have cured by this method a cow with invagination of five days’ duration; but the effect of his treatment may be doubted, as afterwards a portion of bowel was found in the cow’s dung.

When diagnosis is certain, the only treatment that can be recommended consists in performing laparotomy followed by enterotomy. One cannot, however, operate in all cases, nor do all cases offer the same chances of success. If the invagination is situated in the first portion of the small intestine, and is hidden beneath the circle of the hypochondrium, intervention is out of the question, but if it has been detected by rectal exploration in the last portion of the intestine, operation may prove successful. Only in cases of the latter description should it be attempted.

Laparotomy is performed in the right flank according to the usual method (see Möller and Dollar’s “Regional Surgery,” p. 313). After opening the peritoneal cavity, the invaginated loop of intestine must be sought. It is not always easy to discover amongst the mass of intestines present, but can be recognised by its hardness and by the congestion of neighbouring parts. After withdrawing it through the abdominal opening, the operator may then proceed by one of several methods.

(1.) Some authors recommend grasping the two ends, drawing them apart, and thus reducing the invagination. The actual manœuvre is not difficult, but even when unattended by accident or tearing of the intestine it is by no means always followed by recovery. Although the intestine may not appear gangrenous externally, necrosis often occurs eventually.

This method should only be practised during the first twenty-four hours after the appearance of colic, and even then one must always bear in mind the possible consequences just mentioned, and the chances of rapidly fatal septic peritonitis.

(2.) The second method consists in removing the invaginated portion of intestine. It is best to apply bichromatised catgut or silk ligatures to all the arteries which pass from the mesentery into the loop to be removed; after which the loop itself may be simply divided an inch or two above and below the invagination, in order to be quite certain that one is operating on healthy tissue, the divided ends being held meanwhile by an assistant. The intestine is afterwards sutured with a fine needle and bichromatised catgut or boiled silk. The form of suture will be found described in Dollar’s “Operative Technique.” It may be valuable to test the efficacy of decalcified bone tubes for uniting the ends of the intestine.

The operation is long, delicate and difficult, and it is imperative not to infect the abdominal cavity during its performance. To prevent this the liquid and solid materials present in the bowel may be thrust upwards and downwards away from the diseased part before the section is made; and in this way the wound and the operator’s hands are preserved from infection. The intestine should be kept closed during the application of sutures by means of flat clamps cautiously applied. In their absence the ends may be held by an assistant, whose hands should previously have been carefully disinfected.

(3.) In cases where the serous coats of the two portions of bowel constituting the invagination are to some extent adherent, another operation of a less perilous character may be performed. This consists in liberating the invaginated part by means of longitudinal incision, without previously disengaging the parts, and without resection. The invaginated (external) portion of intestine is divided longitudinally; the gangrenous part immediately becomes visible, and may be removed. The operator has then only to suture the longitudinal wound, an operation which is much easier and demands much less time than any circular intestinal suture whatever. These operations must not be attempted except in response to the express wish of the owner, who should be fully informed of the dangers to which they expose the animal; for after the second day of invagination local peritonitis has often developed and one is then operating on injured or infected tissues, in itself a very unfavourable modifying condition. The current formula that “the operation was very successful” is not accepted in veterinary practice when the patient dies three or four days afterwards. From the economic standpoint it is better to slaughter animals of any value, for unless secondary peritonitis has occurred, and the animal is not feverish, the meat is fit for consumption. “Volvulus,” or twist of the intestine, is said to be almost unknown in cattle, though Reichert records a case of volvulus of the ileum.

COLIC AS A RESULT OF STRANGULATION.

The symptoms of this colic differ very little from those of the preceding with which they are often confused. But in regard to its causation the condition is essentially different.

=Causation.= Strangulation of the intestine in the ox may be produced in several different ways: by the passage of a loop of intestine through a tear in the epiploon, through the diaphragm, mesentery, broad ligament of the uterus, the serous layer surrounding the spermatic cord, etc., or by strangulation of an intestinal loop by fibrous bands resulting from chronic peritonitis, etc. Of these various causes, the three principal may here be described:—

(1.) Tearing of the mesentery. As a result of mechanical violence the epiploon or mesentery becomes fissured, and the peristaltic movements cause a loop of intestine to pass through and become fixed in the fissure. If the opening is narrow, as is usually the case, the base of the intestinal loop, riding on the lower lip of the slit, becomes constricted by the margins of the opening through which it has passed.

(2.) In pelvic hernia a loop of intestine passes between the spermatic cord and the walls of the pelvis. The fissure in this case is in the serous fold which supports the large testicular arteries and the vas deferens. The fold is often ruptured during castration, especially during the practice of “bistournage,” in consequence of traction exercised on the cord.

(3.) Pseudo-ligaments and fibrous bands due to chronic peritonitis.—In local, subacute or chronic peritonitis false membranes may become organised, forming fibrous cords or folds connecting the parieto-visceral or inter-visceral surfaces. If by accident a loop of intestine insinuates itself beneath one of these fibrous bands, the passage of digestive material is first impeded and then stopped. The intestine becomes engorged, and symptoms of strangulation soon follow.

=The symptoms= appear suddenly, and are similar to those of invagination. They consist of very acute colic, which disappears after ten to twelve hours.

The peristaltic movements drive the semi-digested food, whether liquid or gaseous, towards the lower (strangulated) end, from which it cannot escape. It therefore distends the herniated loop and sets up intestinal engorgement. This constitutes the first stage of strangulation, and is accompanied by severe disturbance in the local circulation. The mucous membrane of the intestine becomes swollen and infiltrated, so that it alone soon fills the entire neck of the hernia. Necrosis of the loop of intestine is then only a matter of time.

=The diagnosis= of colic by strangulation is difficult. The condition cannot often be recognised at an early stage, and may easily and excusably be confused with invagination. Only in rare cases will rectal and abdominal examination enable one to detect a pelvic or mesenteric hernia.

=The prognosis= is even graver than in cases of invagination. Intestinal hernia progresses very rapidly, necrosis soon sets in, and is followed by fatal consequences if the condition be not relieved.

=The treatment= is exclusively surgical. As a general rule, whenever colic is recognised as resulting from strangulated hernia, it is immediately necessary to perform laparotomy in the right flank, and after having discovered the cause of strangulation, to divide the mesentery, epiploon, serous fold supporting the testicular cord, or accidental fibrous bands, so as to free the herniated loop and avoid necrosis. If necrosis already exist, the intestine may be resected, exactly as in invagination.

DISEASES OF THE STOMACH.

In ruminants diseases of the gastric compartments are numerous, and, although they have been recognised since the earliest times, much remains to be discovered concerning at least some of them. This fact results from the imperfect state of our knowledge concerning the essential phenomena of gastric digestion in ruminants. Digestion really consists of a number of different acts—some mechanical or neuro-motor, some chemical; in addition to which must be reckoned the phenomena of sensation, concerning which patients cannot give any information.

The mechanical phenomena, consisting in the constant movement of ingested material through the different compartments, rumination, eructation, evacuation towards the intestine, etc., are well known to us; and a careful examination of diseased animals enables us to estimate the importance of changes in them.

On the other hand, the chemical phenomena are little understood. It has hitherto been considered that the rumen, reticulum, and omasum are only simple diverticula, with mechanical functions, and that the abomasum is the reservoir in which the chemical changes take place. Another view, which is perhaps not altogether justified, presupposes that the chemical transformation of the food in the abomasum takes place as in other animals, and in particular as in man, in whom the chemistry of gastric digestion has been the object of extremely careful research by certain French and other pathologists. We do not believe (for reasons too long to be explained here) that the gastric digestion of ruminants, or even of herbivora in general, can be identified with that of omnivora.

The nature of the food being totally different, the chemical reactions in the stomach and intestines are also different; in proof of which we need only cite the single fact that ptyalin is absent from the saliva. Straw and oats are not digested in the same way as a mutton cutlet.

But even supposing that the broad outlines of physiological action are the same, nothing has hitherto been discovered in veterinary surgery respecting possible variations in the chemical processes taking place in the stomach during different gastric diseases; and it appears not improbable that in this direction causes might be discovered which veterinary practitioners have hitherto sought elsewhere. Excess or insufficiency of hydrochloric acid, and variations in the quantity of the organic acids, play so important a part in the theory of gastric pathology in man, that it is scarcely surprising to find similar ideas recurring in the pathology of domestic animals. The correctness of these views remains to be proved; and without wishing actually to classify dyspeptic conditions as in man, we may assert that diseases described under other names stand in direct relation to variations in the gastric secretion or to disturbance of gastric movements—e.g., simple chronic tympanites, which, without a doubt, is often a neuro-motor dyspepsia.

The classification we shall adopt in studying the diseases of the gastric compartments is, therefore, extremely simple. In the first series we shall consider sudden, accidental, and temporary forms of indigestion, and in the second series, acute or chronic forms of gastric inflammation.

INDIGESTION.

GASEOUS INDIGESTION.

Gaseous indigestion, also described as indigestion of the rumen, is characterised by the rapid accumulation of gases (chiefly carbon dioxide, carbon monoxide, and marsh gas), due to fermentation in the upper part of the rumen. It is common in oxen and sheep, and has received the names of mephitic indigestion, acute tympanites, meteorism, etc. It occurs during or immediately after feeding.

=Causation.= Numerous causes have been invoked to explain the sudden occurrence of gaseous indigestion.

The most important is the particular condition of the animal at the moment when it has been attacked. For if external influences alone were responsible, there is no reason why all the animals of a given herd or flock, or of a particular stable, which are under similar conditions as regards feeding, etc., should not be affected in the same way.

That the external causes cited (cold, excessive heat, stormy weather, etc.) may affect different animals differently and unfavourably is beyond doubt. But the temporary morbid condition of the animal itself is the essential condition to the development of indigestion.

In all probability the animal has in every case been more or less unwell, except in those attacks of indigestion resulting from progressive poisoning during the course of a meal, such as occur when toxic plants like belladonna, veratrine, colchicum, poppies, tobacco, hemlock, etc., have been eaten. In such temporary abnormal states movement of the rumen is partly abolished, or at least is markedly retarded, and, as a consequence of vaso-motor disturbance, the mucous membrane is probably not so abundantly covered with mucus nor so freely irrigated with secretion, as usual. Under these conditions, if the animal, which may appear perfectly well, is allowed to partake of soft, wet, fermentescible food, gaseous indigestion is very likely to develop.

Cultivated grasses, like lucern, sainfoin, clover, and especially grasses grown on artificially manured fields, are regarded as particularly liable to cause gaseous indigestion. This conclusion seems justified by experience, particularly by the fact that young shoots or young, tender after-growths are very liable to fermentation.

This exaggerated tendency to fermentation of tender grasses has even been held exclusively responsible for indigestion, and the cessation of peristalsis in the rumen has been considered a secondary phenomenon, due to distension.

Whether atony of the rumen be the primary condition and abnormal fermentation secondary or inversely, whether fermentation be primary and atony secondary, is not of importance; for either view may be adopted without altering the results, and without the theory being invalidated by the objection that other animals subjected to similar influences had not contracted the condition.

We have already drawn attention to the importance of the condition of the animal’s health for the time being. Digestive peristalsis being diminished, eructation, admixture of food in the rumen, and its onward movement being impeded, fermentation proceeds rapidly. As a consequence the rumen becomes distended, and, cause and effect changing places, the distension in its turn arrests peristalsis, which had previously only been checked.

Local chills, produced by ingestion of food covered with rime, hoarfrost, or simply with dew, may favour gaseous indigestion; such conditions retard or suspend the peristaltic movements by direct local action, and probably by producing vaso-motor disturbance of the mucous membrane. In very rare cases chill has an undeniable influence, either by provoking general vaso-motor disturbance, which reacts on the secretions, or neuro-motor trouble. Gaseous indigestion is not uncommon in animals living on dry winter food, which have been moved from their ordinary quarters and sent on railway journeys or to fairs, etc. As a general rule this form of indigestion is commonest in spring, when the transition from dry winter food to grass, etc., has not been carefully effected. It is also frequent during stormy weather in full summer. Marked barometric changes seem to have an influence on the general health, and particularly on the nervous system, thus favouring organic fermentations.

=Symptoms.= The earlier symptoms of indigestion escape observation, but they soon begin to develop rapidly, and are then very easy to follow. They always exhibit the same characters, developing, however, with more or less rapidity in different cases. Soon after they commence feeding animals appear to experience special discomfort, which causes those at grass to stop grazing; even when stabled they stop feeding. From this time they show eructation, repeated yawning, restlessness, and some anxiety.

In a quarter of an hour, or less, the left flank begins to project, both laterally and vertically, so that eventually the walls of that part of the abdomen may project above the transverse processes of the lumbar vertebræ. The right flank also becomes swollen, as a consequence of the intestine being thrust out of position. The animal very rapidly shows general disturbance; the nostrils are dilated, the mucous membranes congested, respiration becomes rapid, and asphyxia threatens. The respiration soon becomes panting, for the distended rumen paralyses the diaphragm and compresses the lungs. To ease respiration the animals open the mouth, extend the neck, and stand with the front limbs spread apart; but this fails to prevent dyspnœa becoming more intense and asphyxia imminent.

The heart beats more rapidly, the superficial veins appear swollen, and the mucous membranes cyanotic. The rhythmic contractions of the rumen can no longer be detected by manual examination of the left flank; and on auscultation one neither hears the liquid nor the rolling sound, but only exaggerated crepitation. Finally, there is marked tympanitic resonance on percussion.

In cases of very grave tympanites the gaseous pressure in the interior of the rumen appears to stop the crepitation sound. The animals soon become unable to walk or even to move, suddenly fall to the ground, and die rapidly from asphyxia.

The rapidity with which gaseous indigestion develops varies greatly. Sheep and oxen may die from tympanites, within an hour or even half an hour of their arrival in the field; but more frequently the symptoms develop slowly, only becoming alarming after some hours and continuing for twelve or even twenty-four hours without causing death.

As a rule, the gas is voided by a series of eructations which empty the rumen, and recovery follows; but when distension is extreme eructation cannot occur, and gaseous indigestion then ends in asphyxia and death.

=Lesions.= It might be imagined that this form of indigestion would only appear when the rumen contains a large quantity of food; but, in point of fact, the rumen often contains very little.

On post-mortem examination the rumen is found to contain an enormous quantity of gas, which, when collected and submitted to analysis, reveals approximately the following composition:—Carbonic acid, 74 per cent.; carburetted hydrogen, 24 per cent.; sulphuretted hydrogen, 2 per cent.; nitrogen, traces. The composition of this mixture varies within certain limits, according to its origin; but carbonic acid always predominates.

Lungwitz, after elaborate experiments with different foods kept in closed vessels at the body temperature and with similar agents fed for days as an exclusive aliment to oxen provided with a fistula of the rumen for purposes of collection, found carbonic dioxide the predominating gas in all cases, though the proportion varied with the nature of the food.

Marsh gas varied from 16 to 39 per cent., being especially abundant in cases of abstinence. Hydrogen sulphide was found only in traces. Oxygen and nitrogen were present in small amount, and were attributed to air swallowed with the food. In fermentation the oxygen may be completely consumed.

The abdominal organs, particularly the intestine, are congested, as a result of impediment to the venous circulation. The thoracic organs exhibit the lesions of asphyxia.

=Pathogeny.= Death is due to carbonic acid poisoning, brought about in two different ways—viz., progressive asphyxia, caused by inability to inflate the lungs, and absorption of carbonic acid gas from the rumen; by virtue of the laws of diffusion, part of the gas contained in the rumen passes into the blood.

=The diagnosis= is always very easy, and even farm servants may recognise the condition.

=The prognosis= varies, according to the rapidity with which the disease develops. In rapid cases, where the condition is fully established in thirty minutes to one hour, asphyxia may be threatened from the beginning; but in others, e.g., when the attack follows consumption of dry food, tympanites may develop slowly, only attaining its maximum intensity after a considerable lapse of time. In general one may say that tympanites is grave in proportion to the rapidity with which the gas is generated.

=Treatment.= From the prophylactic point of view, it is necessary to avoid suddenly changing animals from dry to green food; the transition should be effected by giving mixtures of dry and green food.

Curative treatment comprises a large number of methods.

The latest, and one of the most practical, consists in massage of the left flank. The open hand is applied to the left flank and sharply pressed directly downwards, care being taken not to injure the parts. This manipulation excites reflex action, awakens the dormant contractility of the rumen, and leads to restoration of peristaltic movement. The gases pass into the omasum and abomasum, or in many cases make their way into the œsophagus. The sudden impulses sometimes cause food to be returned into the mouth, eructation recommences, and the gas accumulated in the rumen is partially and progressively evacuated. This manipulation is often practised in breeding districts, particularly in the case of sheep, in which the disease occurs with the same characters. The shepherd fixes the animal between his legs, and, thrusting the extended fingers of either hand into the flanks, makes sudden, sharp movements, which again set up eructation and get rid of the excess of gas.

In Germany cold douches are often applied to the flanks. These excite vaso-motor action and reflex peristaltic movements, which result in eructations and in the evacuation of the rumen. But this is not a very practical method, and necessitates arrangements which seldom exist on sheep farms.

The action of massage may be completed by administering stimulants like wine, alcohol, or infusions of such aromatic plants as cummin, fennel, peppermint, camomile, etc. These act first of all mechanically, by clearing the terminal portion of the œsophagus. Furthermore, they stimulate the mucous membrane of the rumen, causing reflex peristaltic contractions, and, as a consequence, circulation of the partly digested food; finally, the majority of them arrest fermentation.

With the latter object, ether and assafœtida are also given. The use of these drugs, however, entails disadvantages, and if the animal has finally to be slaughtered renders the flesh unfit for consumption.

The giving of absorbents is probably most widely practised. The ammonia which many of them contain absorbs carbonic acid, thereby diminishing the pressure of gas contained in the rumen, and therefore the distension of the first gastric reservoirs. Unfortunately this action is only temporary, and if the drug is given in too concentrated a form, the mucous membrane of the mouth, of the œsophagus, and sometimes even of the rumen and reticulum, may be irritated and inflamed, producing lesions of stomatitis, pharyngitis, œsophagitis, contraction of the œsophagus, etc., which after recovery from the acute condition may gravely affect the animal’s general health. A further drawback is that the flesh rapidly acquires an ammoniacal odour.

Perhaps the best internal treatment consists in administering purgatives such as hyposulphite or sulphate of soda or sulphate of magnesia, in doses of 10 to 20 ounces, according to the animal’s size, or, in the case of pregnant animals, in small frequently repeated doses. These check fermentation, and so arrest the evolution of gas, whilst by their purgative properties they excite contraction of the gastric reservoirs and cause eructation.

None of these methods of treatment, therefore, should be used exclusively, but all may be utilised as auxiliaries to mechanical or surgical measures, and all should be preceded by the use of the probang and puncture of the rumen.

The first of these operations, the technique of which scarcely requires description, is often of little value; for the solids and liquid contents of the rumen being permeated with gases, rise as a fermenting mass into the upper portions of the rumen, and continually obstruct the open end of the catheter, so that very little gas escapes.

Puncture of the rumen is much more effective and easier to perform. The owner himself often operates with an ordinary pocket knife, sometimes introducing a couple of fingers or a short length of elder-wood tube into the wound thus produced.

The incision should be made at one stroke, for any hesitation may cause the wall of the abdomen to recede from the rumen, which lies immediately below. Should gas escape under the skin, emphysema, which often extends to the loins and along the quarters, may be produced, and may be followed by diffuse subcutaneous suppuration, resulting from pyogenic germs entering the subcutaneous tissue.

Large quantities of gas escape from the puncture, sometimes with such force as to drive out the canula. The flow of gas then ceases. In other cases the tube becomes blocked; because, as the pressure within the rumen diminishes, the gases dissolved or mixed with the partially digested food are freed, and the whole contents of the rumen become converted into an aerated, bubbling mass. Liquid or semi-liquid materials may be ejected to some distance, or may pass between the skin and the muscles, or between the walls of the rumen and the abdomen, producing various complications, like necrosis, abscess formation, etc. Such accidents can be avoided by exercising firm pressure with the fingers on the tissues surrounding the canula.

Even when the rumen has resumed its normal size recovery is not certain, and may not occur for several hours, or even several days, afterwards. The patients should therefore be kept under observation for some time, and it is usually best to leave the canula in place for one or two days, and to put the animal on low diet.

Necrosis of aponeurotic tissues, fistula formation, and local peritonitis only occur if the instrument is dirty or is introduced in a wrong direction.

IMPACTION OF THE RUMEN. INDIGESTION AS A RESULT OF OVER-EATING.

In this condition the rumen is over-distended with food. The symptoms are principally due to abnormal fermentation, the peristaltic action of the rumen being in abeyance, and the food failing to pass towards the omasum and abomasum. Rumination is generally suppressed.

The disease usually follows change of diet. When the diet has long been restricted, as occurs during years of bad harvests, and animals are afterwards set at liberty in rich pastures, they eat greedily, distend the rumen with large quantities of green fodder, and set up all the necessary conditions for this form of indigestion. Similar results follow when gluttonous animals are freely supplied with rich food. Working oxen also suffer if withdrawn from work and fed with roots, beetroot refuse, brewers’ grains, or other manufacturing residue for the purpose of fattening. These materials can only be absorbed in moderate quantity, and the large amount of water, etc., they contain is apt to disturb the animal’s digestive powers, while owing to its fine state of division such food cannot be returned to the mouth for secondary mastication, and rumination therefore remains incomplete: the food accumulates in the rumen, distending and eventually paralysing it. This is a common result of feeding on semi-liquid pulp, which in order to be ruminated should be mixed with rough forage.

Insufficiency of drinking water is another and more frequent cause, especially during the winter, because the ox-herd or cowman is often too lazy to give a regular and sufficient supply unless water is laid on in the stable itself. The dry food becomes compacted into a mass, which cannot be returned to the mouth for rumination. Moreover, less saliva is then secreted, and Colin has shown that rumination is impossible when the parotid ducts are ligatured.

=Symptoms.= As may readily be imagined, the symptoms vary, according to the quantity and digestibility of the food swallowed. In the first place the appetite falls off: animals suffering from commencing indigestion only take part of their food; later on appetite ceases, and with it rumination. Trifling colic sets in, resembling that due to congestion, and is indicated by unrest, switching of the tail, lifting of the hind legs, slight groaning, moving from side to side, and lying down and rising at short intervals. The animals seem oblivious of their surroundings, anxious, and at times semi-comatose.

When the case has been neglected for several days the animal may masticate without having any food in the mouth, and may attempt to eructate and to regurgitate food; but such attempts always fail. It then absolutely refuses food, and animals which have eaten large quantities of green forage may show tympanites. If called in at this period of the disease the veterinary surgeon finds nothing positive except signs referable to the digestive apparatus. By methodically examining the digestive tract, and in particular the stomachs, one discovers during palpation of the left flank that the rumen is distended. This is characteristic. By deep palpation it is even possible to detect marked resistance and a certain characteristic firmness resulting from accumulation of food. The percussion sounds over this region are dull, and pressure causes pain, as though the rumen and peritoneum were inflamed. When the open hand is laid flat on the rumen and thrust downwards, no peristaltic movement can be discovered. Finally, on auscultation the normal sounds, including crepitation, fermentation, and rolling sounds are all absent.

There are no well-marked general symptoms. Respiration and circulation are hardly accelerated, nor is the artery particularly tense.

=Course and Termination.= The course of the disease varies, and the condition may be divided into two forms, acute and chronic. The first develops in a single day, and may cause death by the same mechanism as acute tympanites—i.e., asphyxia or carbonic acid poisoning; the other continues for five, ten, or even twenty or thirty days, according to the promptitude with which treatment is undertaken.

In protracted cases, however, the indigestion itself ceases to be as important as the complications. Sometimes spontaneous recovery occurs, the food passing away towards the intestine, or even being vomited, though the latter conclusion is rare. Recovery may also follow from treatment. If the disease is neglected it may become complicated with gastro-enteritis.

=The diagnosis= is not very difficult. Indigestion resulting from impaction is distinguished from acute tympanites by its less rapid course and by the less marked distension of the rumen (in this case due to solid food), and from acute gastro-enteritis by the varying degree of fever which accompanies the latter condition.

=Prognosis.= The prognosis is always grave, even in cases of acute indigestion resulting from eating green food.

In this case gaseous indigestion occurs as a complication, and necessitates immediate intervention. The other forms may rapidly yield to proper treatment, or, in spite of every care, may give rise to prolonged complications.

=Lesions.= On post-mortem examination of animals which have died of complicated forms of the disease, we find certain lesions peculiar to gaseous indigestion associated with impaction of the rumen.

If death has followed the consumption of root pulps, we see signs of poisoning. As a consequence of prolonged stagnation of food in the rumen, there follows an exaggerated organic fermentation, whose products are absorbed through the stomach or intestine and pass into the circulation.

These various fermentations, which may be of the lactic, butyric, and even putrid order, produce changes in the mucous membrane of the rumen; wide tracts of the epithelium may be shed, exposing the corium, and producing enormous ulcerations, which in certain cases implicate the entire inner surface of the rumen.

=The treatment= must be varied, according to the cause, symptoms, and immediate complications. When the disease is of an acute type, such as that produced by over-gorging with lucern and green food, it is best to proceed as in gaseous indigestion, i.e., to puncture the rumen and give frequent large doses of purgatives until the stomach and bowels have been freely unloaded. The animals should then be kept for some days on small quantities of easily digested food, and should be allowed lukewarm, mucilaginous drinks.

When tympanites and impaction occur simultaneously, immediate surgical intervention becomes necessary, and gastrotomy may then be performed by a very simple method.

Two loops of cord are passed around the abdomen, one behind the hypochondriac circle, the other in front of the angle of the haunch. Assistants placed on the right side draw these loops tight, so as to immobilise the left flank. A bistoury is then thrust directly through the walls of the abdomen and rumen. As a consequence of the pressure exercised by the ropes, if not of the pressure of gas itself, the food material contained in the rumen is often expelled in a powerful stream. As the superposed tissues cannot very readily change their mutual relations, the author of this suggestion claims that there is little danger either of infectious materials passing into the subcutaneous connective tissue, or of peritonitis; but this rude treatment can only be resorted to in cases of extreme urgency, and it appears by no means without danger.

Injections of 10 to 15 centigrammes of pilocarpine and 5 to 10 centigrammes of eserine are also useful.

When impaction of the rumen assumes a less acute form, moderate doses of purgatives may be given and repeated daily, or twice a day, until the peristaltic action of the rumen is restored and resumes its normal rhythm. In certain cases, however, recovery is only apparent. The food in contact with the walls of the rumen breaks down, and passes away into the abomasum and intestine, while appetite returns. The animals then resume feeding, and some days afterwards show all their former symptoms. Low diet should therefore always be continued for some time.

In spite of treatment, or in consequence of treatment being too long delayed, no improvement may follow. The ingested food is not expelled. Putrid fermentation results, auto-intoxication sets in, and the temperature rises to 40° or 41° C. Unless gastrotomy is performed death is then certain.

This operation should be undertaken whenever the fever rises to 40° C., and two-thirds of the contents of the rumen removed. The rumen should not be completely emptied, as there is danger of collapse of its walls. Complications in the region of the wound can be avoided by drainage.

If the operation succeeds, the patients must be placed on very low diet or on milk for some days, and should be given lukewarm farinaceous drinks, and a little hay of good quality to excite rumination. In old milch cows this operation is seldom followed by a satisfactory recovery. Apart from the loss of milk, the animal loses condition, refuses to feed, and gradually succumbs to exhaustion.

IMPACTION OF THE OMASUM (THIRD STOMACH).

=Definition.= “A form of indigestion, of which the prominent feature is the drying and impaction of the ingesta between the folds of the third stomach. It may seem to be a primary disease, but in very many cases it occurs as a result of some acute febrile or inflammatory affection.” (Law’s “Veterinary Medicine,” Vol. II. p. 123.)

=Synonyms.= Dry murrain, clew-bound, fardel-bound, stomach staggers, grass staggers, vertigo, chronic dyspepsia, chronic indigestion.

=Causes.= Torpidity of the omasum, suppression of salivary secretion, with absence of “waves of liquid floating the finely divided food from the mouth or rumen to third stomach, are prime conditions of desiccation of the contents.” The third stomach, like the first and second, has no provision for liquid secretion, and depends for its supply on constant flushing by swallowed fluids. Therefore, if feeding and rumination are arrested and salivary secretion is suppressed, and if movements of the rumen and resulting overflow into the third stomach are checked, the ingesta of the third stomach, compressed between its folds, becomes drained of liquid and converted into a powder or dry mass. All febrile and inflammatory affections tend to this end, and more or less drying, with impaction of the contents of the omasum, is a constant feature in such cases. But in the majority of cases this condition is to be looked on as a secondary or subsidiary affection, and the real disease must be sought elsewhere.

The explanation of the susceptibility of the third stomach in constitutional troubles has been sought in the source of its innervation. Electric stimulation of the vagus rouses the movements of the first and second stomachs, but not those of the third. Action of the third stomach is excited by stimulation of the spinal cord, and of the sympathetic nervous branches going to the ganglionic cells in the walls of the omasum (Colin and Ellenberger). Its nerve supply coming from a different source, derangement of its function may occur independently of antecedent disorder of the first or second, and its motor supply coming from a source so closely related to the vaso-motor centres, perhaps affords some explanation of the connection of disorders of the omasum with febrile and inflammatory diseases.

Food is an important cause. Impaction of the omasum is a winter disease—the time of dry feeding. Dry, fibrous, innutritious fodder, and scarcity of water contribute to its production. It attacks cattle in spring or autumn on pastures in which fresh grass grows among the dead, dried, or withered stems of a previous growth. It occurs when stock are fed on corn or corn stalks (maize stalks) affected with smut or ergot, or on cereals or grasses similarly damaged, and in both cases especially when the water supply is deficient or restricted.

Sheep and goats, which habitually drink little, suffer less than do cattle, which drink freely.

=Other causes.= Fermented foods, microbian ferments and their products, which tend to induce torpidity of the omasum, fever, and lessened secretion of saliva, with diminished supply of liquid from mouth or rumen.

Pericarditis, by causing vascular stasis in the omasum, may induce torpor and impaction.

Lead poisoning paralyses action and favours impaction. Finely divided food stuffs—meal and bran—eaten greedily, may pass in quantity directly into the omasum and induce impaction. “The most acute and fatal forms occur in connection with a sudden change from dry to rich, luscious, green food in spring, the unwonted stimulus giving rise to general irritation of the whole gastric mucosa, with disordered and impaired function of all four stomachs, but especially of the third. Such cases are usually congestive and inflammatory, and the suspension of the gastric movements is a grand cause of impaction. In such cases, too, the brain or spinal cord, or both, are seriously involved, and the early death is preceded by torpor, paralysis, violent delirium or convulsions, following largely the type of acute lead poisoning.” (Law, loc. cit.)

=The symptoms= depend on the degree of impaction, and vary from simple, irregular, or suspended rumination to severe gastric and nervous disorder. The less acute cases are marked by failure to re-establish regular rumination or partial convalescence from fever or inflammation. The fever subsides, but the appetite remains capricious, the muzzle dry, eyes dull, spirits low, and breathing accelerated; the condition is sometimes accompanied by moaning. Slight tympanites may appear, and the contents of the rumen may feel solid, the mouth hot, clammy, and fœtid. The bowels are constipated, the fæces small in quantity, hard, covered with mucus or blood-streaked, and containing particles of undigested food; in other cases diarrhœa may set in, to be followed later by constipation. Alternations of constipation and diarrhœa may be repeated again and again. Exploration by pressure of the closed hand over the omasum will give an impression of solid resistance. There may be slight shivering, the ears and limbs are cold, the hair is erect in patches, dry and lustreless.

In cases occurring independently of previous disease, diarrhœa may be the first symptom observed, the malady being preceded by local irritation and congestion; but this soon gives place to constipation or diarrhœa and the symptoms above mentioned. The animal is found lying apart on its left side, with its nose in its right flank, the pulse and breathing quickened, the eyes congested; expiration is accompanied by a grunt. The patient walks with its back arched and dragging its limbs. The appetite may continue, but only in an impaired and irregular form, and as rumination ceases grinding of the teeth becomes common. The secretion of milk is diminished or arrested, emaciation advances day by day. Fœtid eructation may be a marked symptom. This form may last from ten to fourteen days, and merge finally into paralysis of the hind limbs, drowsiness and stupor, or delirium and convulsions.

“In more acute cases (from sudden access of green food, change of water, or ingestion of irritant plants), the affection partakes more or less of the nature of congestion or inflammation of the viscus (omasitis), and may run a rapidly fatal course” (Law, loc. cit.). The animal is seen apart from the herd in a characteristic recumbent position, the eyes are red and glassy, the eyelids semi-closed, the patient shows much drowsiness and stupor, but when raised may still feed in a sleepy, listless manner. The bowels are loose or confined, the pulse and breathing accelerated, the right hypochondrium is firm and tender, and the sound of fermentation absent or subdued over the omasum. Soon nervous disorder appears, the eyes glare wildly, the animal seeks relief in motion—sometimes in a straight line, sometimes to one side—and being blind and unconscious of obstacles, may fall into pits or ditches, knock against trees, fences, gates, or buildings, and continue pushing against resisting objects, breaking its horns or teeth; and otherwise sustaining injury through violent muscular contractions.

=Course.= Chronic cases may continue indefinitely, with symptoms of poor health, impaired digestion, and gradual loss of condition. After death the omasum may contain dried food which the animal consumed several months before the attack.

In cases ending in early recovery there occurs abundant diarrhœa, “the fæces are mixed with flattened, dark, solid, and polished masses, the impacted ingesta from the omasum. Tympany subsides; movement in rumen and omasum and rumbling in bowels can be heard. Appetite returns.” (Law.)

=Diagnosis.= The condition of the pulse and respiration, and the grunting with expiration may lead to confusion with pneumonia.

At first there is no fever, tenderness is confined to the right flank; there is an absence of pulmonary crepitation, of pleural effusion, and of movement in the rumen and omasum. Signs of gastric and intestinal disorder can be detected.

=Lesions.= The omasum is gorged—it may be twice its normal size—solid, resistant, almost stony. The spaces between the leaves are packed with dried food, which, when removed, carries a layer of epithelium from the mucous membrane. (This (layer on contents) is not inconsistent with health.)

The rumen contains ingesta packed in masses, more or less offensive from putrefaction.

The abomasum is empty of food, but contains much mucus. Its mucous membrane is congested.

The small intestine is red in places, empty and collapsed.

The larger intestine contains a quantity of dry, glistening pellets, and much mucus.

=Treatment= follows the lines of impaction of rumen, though the response is usually less certain, and always slower. Flax-seed tea, several bucketfuls per day, will often succeed.

Epsom and common salts, with sol. ammoniæ, excite thirst; liquids should be supplied freely.

In obstinate cases, and in absence of gastric or cerebral congestion, 20 croton beans, or 20 drops of croton oil, may be added to the purgative. Nux vomica stimulates the nervous supply. Enemata may be given freely.

Other remedies, stimulating contractility and secretion, are: Eserine, 1½ grains; veratrine, 1 grain; barium chloride, 10 to 15 grains; or pilocarpin, 3 grains, hypodermically.

The patient may be days or even a week without alvine discharge and recover.

If fever and symptoms of gastric congestion appear, a blister may be applied to the right side over the omasum.

Nervous symptoms, such as dilated pupils, blindness, congested mucous membrane, hot horns and ears, drowsiness or excitement, are combated by applying cold water or ice to poll, etc.

When free action of the bowels is restored, laxative diet, roots (pulped), green food, plenty of common salt, and free access to drinking water should be prescribed.

During convalescence a course of tonics, including nux vomica, is advisable to help in restoring normal gastric functions.

ABOMASAL INDIGESTION.

Primary indigestion in the abomasum appears to be rare in adults, for until the present time no one has given a sufficiently characteristic description of this disease to enable it readily to be recognised. On the other hand, it is to be presumed, although final proof has certainly not been furnished, that in cases of gaseous indigestion, or of impaction of the rumen, the abomasum, whose physiological action is predominant, must simultaneously suffer.

Primary abomasal indigestion, on the contrary, is common in young animals before weaning, so that the condition has been given the name of “milk indigestion.” It could not very well be otherwise, for the abomasum is the only one of the gastric divisions which in ruminants is active during the first few weeks of life. At this period it is larger than the other gastric reservoirs; and the rumen, the reticulum, and the omasum do not undergo great development till weaning begins.

=Causation.= Milk indigestion attacks young animals, under varying conditions.

In animals suckled by the mother the disease rarely occurs, but yet when the mothers are good milkers, like the Flemish, Norman, Jersey, and Holland breeds, and when there is too long an interval between the feeds, calves, which are naturally greedy, and in addition are hungry, are apt to take too large a quantity of milk—in fact, they often gorge to the fullest possible extent. Owing to its over-distended state the abomasum either fails to secrete sufficient of the rennet ferment necessary for coagulating the milk or secretes an insufficiently active ferment. The first stage of digestion remains incomplete, giving rise to so-called “milk indigestion.”

When the cows are employed in ploughing, etc., or in drawing carts, not only are the calves fed at long intervals, but the milk is not always of proper chemical composition even in the udder. As a result of work, fatigue, over-exertion and irregular feeding, the cow’s yield of milk for the time is less digestible than the normal supply, or may even prove irritant to the calf’s stomach. Milk indigestion is thus set up.

When the cows are fed on factory waste, like beetroot-pulp or brewers’ grains, toxic or irritant products may even find their way into the milk, which then irritates the little creature’s abomasum and produces gastric indigestion. Just as in the production of congenital alcoholism in man, the young animal is then ingesting, unknown to those responsible for its well-being, chemical substances which produce various pathological changes.

But milk indigestion is commonest of all in calves fed by hand. The food usually given is a mixture of milk from the previous night, and skim milk or even butter milk. It contains lactic ferments and various microbes, some capable of producing toxic principles.

When swallowed and brought directly in contact with the mucous membrane these cause abomasal indigestion.

=Symptoms.= Soon after feeding, the little animal appears dull and somnolent, and shows moderate abdominal pain, suggesting trifling colic.

This stage is soon followed by nausea; the breathing and the heart’s action become rapid, vomiting efforts are made, and finally milk, in the form of firm or partially softened curds, depending on the time which has elapsed since the last feed was taken, are vomited. The quantity ejected varies. Pressure over the right side of the abdomen produces pain, and tympanites of the abomasum may sometimes be detected on percussion.

The sensitiveness and gaseous inflation are confined to the middle and lower zone of the hypochondrium. Soon after vomiting the animal begins to improve. The patient seems brighter, relief is very marked, and in some cases proves permanent; but more frequently a certain degree of depression persists, the mouth emits a sourish odour, and for a time the appetite remains poor. This temporary irritation of the abomasum has a tendency to become permanent; or even to extend to the intestine, in which the conditions appear more favourable to the development of microorganisms than do those in the stomach. Indigestion then becomes complicated with diarrhœic enteritis.

=The diagnosis= presents no difficulty.

=The prognosis= is not serious, provided that the young animals are carefully attended to; but such complications as diarrhœic enteritis may become very grave if neglected.

=The treatment.= To prevent recurrences:

(1) The periods of feeding should be regulated;

(2) The cows should not be worked, or should be worked as little as possible;

(3) Mixed milk, or milk which has already undergone lactic or other fermentation, should be avoided.

If the calves must be reared by hand, the mixed milk should at least be boiled or relatively pasteurised by heating to 70° or 80° C., and the buckets used for feeding should be kept scrupulously clean. These precautions become absolutely necessary when diarrhœa exists amongst the calves. Curative treatment consists in placing the animals on low diet for two or three days after the attack of indigestion, or in giving them boiled milk diluted with from one-half to two-thirds of boiled water.

The addition of a mild saline purgative like sulphate of soda, in doses of one-half to three-quarters of an ounce, usually ensures a cure. Infusions of lime-tree flowers, peppermint, camomile, etc., may advantageously be used to replace boiled water in diluting the first foods.

ACUTE GASTRIC INDIGESTION IN SWINE.

=The causes= comprise putrid food, swill, spoilt turnips, potatoes, apples, succulent vegetables, frozen food, and the admixture of caustic alkaline powders (used in washing table dishes) with the swill. Indigestible matters—hoof, horn, hair, bristles, tree bark, etc.—when not rejected by vomiting, cause gastritis and indigestion. Lastly, medicinal substances and poisons, paint and lead, sometimes produce the disease.

Among the symptoms may be mentioned dulness, arching of the back, standing with the feet brought together, erection of the bristles, hiding under the litter, grunting, uneasiness, shifting from place to place, tenseness of the abdominal wall, borborygmus; these may be followed by diarrhœa and recovery. Speedier relief is afforded by copious vomiting of irritant matters.

=The treatment= should commence with the free administration of emetics. To combat alkaline poisoning vinegar may be given, followed by a laxative. Prophylaxis calls for greater care in feeding.