COLIC IN SOLIPEDS FROM VERMINOUS EMBOLISM. INTESTINAL CONGESTION.
Definition. Causes: presence of sclerostoma in arteries, form, habit, nature, immature, biology, life in bowel, in submucosa, in arteries, outside the mammal, pathogenesis, blood-sucking, verminous cysts, verminous aneurisms, seats of latter, coagula, embolism, stagnation of blood, œdema and thickening of intestine, mesentery, fermentations, tympany, infective inflammations, blood extravasations, infection of liver and spleen. Symptoms: sudden attack, violent colics, reckless movements, frequent defecation followed by its arrest, palsy of peristaltic movement, of pain, prostration. Course: two to twenty-four hours, death from indigestion, tympany, obstruction, hemorrhage, poisoning, recovery, sequelæ, laminitis, intestinal catarrh or atony, debility. Treatment: aneurism worms beyond reach, treat lesions, venesection, anodynes, stimulants of peristalsis, antiseptics, compresses, sinapisms. Prevention: expel intestinal worms, exclude embryos, tartar emetic, iron sulphate, arsenic, phenol, pure water, occasional vermifuges.
Definition. Congestion and spasms of the intestines in connection with blocking (thrombus or embolism) of the mesenteric arteries, and verminous aneurism.
Causes. The essential cause is the migration of the sclerostoma equinum (strongylus armatus, Rud.) into the mesenteric arteries in its agamous condition. It seems appropriate therefore to here notice the life history of this parasite.
The sclerostoma equinum (strongylus armatus) is one of the common pin worms of the horse. It is distinguished by its dull gray or reddish brown body, thickest at the cephalic end and tapering off toward the caudal, but ending in a blunt point; by the round, open mouth furnished with several firm chitinous rings, of which the outer bears six short symmetrically arranged papillæ, an intermediate row of rounded blunt tooth-like projections, and the innermost a row of fine, closely aggregated and very sharply pointed teeth for penetration of the mucosa. Male ¾ to 1½ inches long, with caudal membranous alæ in two lateral lobes, joined by a rudimentary central lobe: two delicate spicula. Female ¾ to 2 inches long, blunt pointed tail, vulva in posterior half of the body. Eggs ovoid with slightly raised ring around the centre: oviparous.
Habitats. They are found in solipeds in two stages of existence, the mature worms in the cæcum and colon, and the immature in the same organs encapsuled in little pellets of manure, and in cysts in the mucosa but also apart in the arterial system especially in the anterior mesenteric artery and other gastric or intestinal trunks.
The mature sclerostomata are found attached to the mucosa of the large intestine into which the head is sunk for the purpose of sucking the blood, and they may be gray, brown or red according to the quantity of blood which they have imbibed. The author has found them in little hernial sacs of the mucosa hanging from the peritoneal surface.
The sexually immature sclerostomata are found in little pill-like masses of ingesta in the large intestines and from which they project part of the body through a narrow opening. Another habitat is in cysts of the mucosa of the cæcum and colon and less frequently of the small intestine, individual cysts varying in size from a pin’s head to a hazel nut, and containing the young worm rolled upon itself, and varying in size but always less than the intestinal worm and always asexual. In some cases the cyst is found empty but with a small opening toward the lumen of the bowel showing the means of escape of the parasite. A third habitat of the immature worm is in the blood-vessels, especially the posterior aorta and its divisions, and still more constantly the anterior and other mesenteric arteries.
Biology. The ova of the sclerostoma are segmented in the oviduct but are hatched out after they have been laid. The hatching may be effected in the intestine or in manure or water external to the body. When hatched out in the intestine they may pass out at once with the manure or they may envelop themselves in pellets of the finer ingesta and remain for a time in the bowel and finally pass out in this condition. Baillet has traced their development out of the body. In a watery or damp medium they are hatched out in a few days as a cylindroid worm ¼ to ⅓ mm. long, thick in front and with a filiform tail. In moist environment but especially in damp manure they grow to 1 mm. or 1.5 mm. and continue for months in this condition, but remain small and asexual, until taken in, in the drink or green food of the soliped. Reaching the intestine and especially the cæcum and colon they bore their way into the mucosa and encyst themselves, or if they happen to perforate a blood-vessel they make a habitat of that. In the cyst, development proceeds and when it has reached a certain stage the worm once more bores its way through the mucosa and reaching the intestine becomes sexually mature.
In this last migration the young worm is liable to perforate a blood-vessel in which case it is destined to a period of existence in the blood. It may, however, have blundered upon a blood-vessel at an earlier stage when seeking a temporary home in the mucous membrane, so that the sclerostomata of aneurisms may be derived from two separate sources. In the blood-vessels the parasite attains a length of 1 to 8 lines, whereas in the mucous cysts it does not exceed 3½ lines. Yet Neumann holds that after leaving the blood-vessels they may again encyst themselves in the mucosa before escaping into the intestine.
Several moultings take place in the asexual condition.
Other views have been advanced as to the development of the sclerostomata. Colin believed that the ova deposited in the ducts of the mucous glands and in the perforations made by the parasite in blood-sucking, hatched in this situation and the embryo at once encysted itself in the mucosa.
Leuckart imagines that the embryo found in the fæces or in water outside the body of the soliped, should pass through an intermediate host before it can return to gain sexual maturity in the horse. But no evidence of the existence of such intermediate host is furnished, and the encysted intestinal worms show no indication of a special development which would have been accomplished in such host.
Willach holds to a hermaphrodite stage passed in the intestine of the soliped. He found in the bowel small worms apparently related to the sclerostomata by the appearance of the head and the caudal membrane, but not exceeding three to five lines in length. Some were evidently females and contained not only eggs with soft shells, but in one case embryos. Others had the caudal membrane of the male, yet contained also a few eggs. There is no vulva and the embryos escape by rupture of the oviducts. These embryos he supposes are developed in the same host into the familiar mature sclerostomata.
Whatever may be said of those alleged modes, the first described series of changes and migrations may be taken as the usual and regular method of development.
Pathogenesis. Lesions. These embrace perforations of the mucosa, cysts, aneurisms, embolisms and congestions.
Irritation of the mucosa. The adult worms, like so many leeches are continually biting and sucking blood from the mucosa and when present in large numbers, hundreds, thousands, or a million create an aggregate of irritation which may determine violent indigestions and congestions.
Verminous Cysts. These are like a pin’s head, a pea or hazel nut, containing the asexual worm in a mass of purulent debris, or if empty, presenting a small orifice where it made its exit.
Verminous Aneurisms. These are perhaps the most important lesions caused by the sclerostome as they are the steppingstone to the dangerous embolisms, and too often fatal colics and congestions of the intestines. They are very common in some localities, and rare in others following the distribution of the sclerostomata. Bollinger found them in 90 to 94 per cent. of adult horses, and Ellenberger in 84 out of 85 horses dissected. They are found in all ages from six months up, and are nearly always in the short, stubby trunk of the anterior mesenteric artery. Often two or three exist in the same animal, the whole length of the posterior aorta showing patches of disease, exudations, neoplastic elevations alternating with depressions, and aneurisms and thrombosis in its different branches. In 100 horses Bollinger found 168 aneurisms, 153 in the anterior mesenteric, and its divisions, 4 in the cœliac axis and its divisions, 3 in the hepatic artery, 3 in the posterior mesenteric artery, 3 in the renal arteries and 2 in the posterior aorta.
The special predisposition of the anterior mesenteric artery is variously accounted for: 1st. There is the obvious fact that its branches are distributed to the cæcum and double colon, the home of the mature parasite, and to the small intestines which are first reached by the young parasites that are taken in with the water and the food. These are therefore most likely to get into the branches of this vessel and to follow them up toward its origin. 2nd. The anterior mesenteric artery distributes its branches to the small intestines the most motile portion of the intestinal tract, and the cæcum and colon the most heavily loaded with solid ingesta, it is therefore the most subject to traction, and distensions, and the more so that the parent trunk is extremely short and the divisions pass in all directions and to a large extent at right angles, so that there is a dragging of the walls apart as well as an obstruction to the blood flow and an increase of internal tension. The distension, laceration, inflammation and softening of the internal coat have accordingly been regarded as the starting point of an endarteritis upon which the parasites have been implanted as a further cause of trouble. We must not forget, however, that the sharp circle of teeth of the parasite, by which it fixes itself on the intima of the vessel are quite enough to produce initial endarteritis, without any assistance from distension, traction or laceration.
The irritation of the intima from whatever cause determines here as elsewhere exudation, and coagulation, and the inflamed walls losing their tone yield more and more readily to the internal tension. Sometimes the coagulum lines the aneurism or vessel all round, leaving a narrow central passage through which the blood still flows; in other cases the clot extends into the adjacent smaller vessels, completely blocking them and disturbing circulation and innervation in the parts which they supply. As a rule the parasites are found in galleries hollowed out in the clot, and heads or tails may be seen to project into the circulating blood. Sometimes they are found imbedded in the arterial coat, or in an adjacent small abscess. The formation of aneurisms in the other arterial trunks may follow the same method.
Embolisms. These come very naturally from the formation of thrombi in the various arteries. The coagulum determined by the presence of the worms, tends to undergo retrogressive changes notably fatty degeneration, to which germs brought on the worms or in their alimentary canals contribute. This together with the movements of the parasites tends to break up the mass, and minute portions are washed on into the different smaller vessels. Soon these reach divisions which are too small to admit them, which are accordingly occluded and the circulation through them abolished. The presence of microbes as well as fibrine contributes to cause further coagulation, more absolute embolism and arrest of the circulation.
It is further alleged that the sexual instinct in the summer months (May to August) leads the worms to leave the aneurisms, to pass through the smaller divisions to the cæcum or colon where alone full sexual evolution is possible. In these migrations they cause the thrombosis of the smaller trunks and determine the verminous congestions of the bowels which are especially common in these months.
Disturbances of the Intestinal Circulation. As these usually occur in the lines of distribution of the anterior mesenteric artery a knowledge of its divisions and their destination and anastomosis, is essential to an intelligent understanding of the pathogenesis and lesions. As first pointed out by Lecoq the anterior mesenteric artery is divided into three primary bundles: (a) a left of 15 to 20 trunks which are destined to the small intestine; (b) a right which gives off cæcal branches, one to the double colon, and one to the ilium to anastomose with the last trunk of the left bundle; and (c) an anterior which gives one branch to the second division of the double colon and anastomosis with the colic branch of the right bundle at the pelvic flexure; and a second branch to the floating colon to anastomose with the posterior mesenteric artery.
The divisions of the left bundle anastomose so freely with each other in the mesentery and immediately above the intestine that the blocking of any one branch cannot entirely arrest the circulation in the corresponding part of the intestine. It may however produce a partial local stagnation in the vessels of a short loop of intestine, resulting in œdematous infiltration and thickening with resulting induration and stricture of the gut. Chronic and permanent lesions are produced by such blocking, but only rarely acutely fatal ones. Acute and fatal congestive lesions of the small intestine from verminous embolism, occur only when several adjacent divisions of the artery are blocked at once, and this is a rare occurrence.
The right bundle of branches furnishes the only two arteries which are supplied to the cæcum and the only artery furnished to the first half of the double colon. The ileo-cæcal branch is less involved, first, because being less dependent and smaller, it is less likely to receive an embolus, and, second, because any lack of blood supply is counterbalanced by the free anastomosis with the last iliac division of the left bundle. When the embolus blocks the undivided trunk of the right bundle this same principle comes into play, the free supply of blood from the posterior branch of the left bundle supplying blood through its anastomosis with the iliac and cæcal branches of the right.
But when the emboli are lower down, in the cæcal branches of the right bundle, or in these and the colic branch, arrest of the circulation in the intestinal walls ensues, followed by paresis, passive congestion and hemorrhage. The cæcum and double colon thus become the seats of the grave and fatal lesions of verminous embolism.
The resulting lesions are to be variously accounted for. The stagnation of blood in the vessels below the embolus, determines a speedy exhaustion of its oxygen and increase of its carbon dioxide, so that it is rendered unfit to maintain the normal nutrition and functions of the part, and the capillary and intestinal walls are alike struck with atony or paresis. The blood filters into the stagnant vessels slowly from adjacent anastomosing trunks, and the liquor sauguinis exudes into the substance of the tissues and lumen of the intestine, leaving behind the greater part of the blood globules so that the stagnant blood is rendered more and more abnormal in composition. The walls of the capillaries soon lose their cohesion as well as their contractility, and giving way at different points, allow the escape of blood into the tissues, bowels and peritoneal cavity. It has been further claimed that the emboli already infected and in process of degeneration communicate this to the walls of the vessels and to the stagnant blood, hastening the process of degeneration and rupture.
Another series of circulatory disorders are liable to take place. The blocking of the vessels of the right bundle, tends to increase the blood pressure in the left bundle and the anterior one, and thus to determine congestions, paresis and inflammations in the small intestines, the second division of the double colon and the floating colon. The resulting inflammation and increased vascular tension may lead indirectly to implications of the brain and lung.
Extravasations so extensive as to appear like blood clots may be present between the layers of the mesentery or in the mucosa and submucosa, and blood, liquid or coagulated, may have accumulated in the abdominal cavity. Blood effusion into the intestine gives a dark red coloration to the contents which are further mixed with distinct clots.
The atonic bowels are always the seat of extensive fermentations and tympany. The microbes engaged in these fermentations and their toxins, are accountable for toxic changes occurring in the locally diseased parts and in distant organs. To this may be attributed the congestion and softening of the liver and the engorgements and hemorrhagic centres in the spleen.
Symptoms. An animal, perhaps known to harbor the sclerostoma equinum, is suddenly attacked with violent and persistent colic. He trembles, paws, moves his hind feet uneasily, kicks the abdomen, throws anxious looks at the flanks, crouches, lies down, rolls, gets up, and at once gets down again. The intensity of the suffering rapidly increases, the face is drawn and pinched, the eye is extremely anxious, the patient no longer lies down, but throws himself down reckless of consequences, when down he is not quiet for an instant, but now on his breast, then on his side, then on his back, the limbs struggling and jerked violently, the head turned first to one side and then to the other, he is a picture of extreme agony. If made to walk the same indications continue; he walks with head down and limbs semiflexed ready to drop at any moment, and often he will drop suddenly in spite of every effort to keep him on his feet. The pulse is at first strong and full, but as extensive effusion takes place into the bowels or abdomen, or as the animal is poisoned by toxins, it becomes small, weak, and it may be imperceptible. Breathing is quick and catching, and the mucous membranes are dark red. Sweating which shows first about the elbows or flanks or back of the ears finally becomes general, the surface cold and the limbs especially so. Fæces may be passed at first, a few dry balls at a time from the floating colon or rectum, but soon they are suppressed entirely. Some patients strain frequently to micturate but pass little at a time.
In some instances the acute pain seems to suddenly cease, but there is no general improvement, the patient stands with head depressed, eyes sunken and expressionless, ears lopped, cold perspiration, chilly limbs, unsteady gait and imperceptible pulse. It implies merely a paralysis of the affected bowels in connection with the extensive congestion and extravasation.
Course. Duration. The more acute cases reach their acme with great rapidity, death may occur after two hours illness, and in other cases it may be delayed ten or even twenty-four hours. It may be caused by indigestion and tympany, by volvulus or invagination, by excessive hemorrhage, or by poisoning with toxic matters.
Recovery occurs when the vessel blocked is an unimportant one as a branch of the left bundle so that circulation may be reëstablished from collateral trunks; or when a more important trunk has been but partially blocked, and after a time it either clears itself, or collateral circulation comes in with sufficient compensation. There is a more or less rapid disappearance of the colics and other symptoms, a free passage of urine, the rejection of fæces, it may be in a liquid, semi-liquid or sanguineous condition, yet enough to indicate the restoration of intestinal tone. The patient begins to pick morsels of food and soon acquires his former appetite.
In some instances, however, the recovery is not complete. Trasbot has noted a case of laminitis occurring within fifteen hours after the improvement, and in other cases there remain chronic debility and catarrh of the intestines. The appetite remains poor, there are occasional colics, the bowels are irregular, loose or costive, and the fæces are dry, glossy and covered with mucus. The back is arched, the belly tucked up, strength and vigor are both lacking, and the patient spends much time in the recumbent position.
Complications of various kinds may follow as in other diseases of the intestines. After even the best recoveries, a relapse is always to be apprehended as the original cause remains and the animal is liable to be cut off at any time.
Treatment. This is very unsatisfactory as the original source of trouble, the worms, being in the blood-vessels, cannot be reached by vermifuges that would be harmless to the host, and clots blocking the smaller intestinal vessels, cannot be dissolved and removed. Moreover, although we could compass the death of the worms in the aneurisms, we would leave their dead bodies as sources of septic change, blood coagulation and embolism.
A certain number of cases, however, are not necessarily fatal, and the worms of the blood-vessels have not an indefinite period of life, so that there is some encouragement for both therapeutic and preventive treatment. During the attack we must be content to treat symptoms. French veterinarians still trust largely to general bleeding, adopted at the very outset and to the extent of 6 to 10 quarts. It will temporarily lessen the vascular tension, more permanently dilute the blood, and calm nervous excitement, and in the most violent cases, as a kind of forlorn hope, it might be tried with the view of tiding over the acute stage until a freer collateral circulation could be established.
The use of anodynes will be more generally acceptable to American practitioners. Two to four grains of sulphate of morphia or codeine may be given hypodermically in combination with 1½ gr. eserin, 7 grs. barium chloride, or 2 grs. pilocarpin, to secure a speedy movement of the bowels.
To counteract intestinal fermentation perhaps no better agent can be got than chloral hydrate, ½ oz. of which may be given by the mouth in water, and ½ oz. more by the rectum.
Wet compresses to the abdomen, or fomentations with water rather hotter than the hand can bear or even the application of mustard is sometimes useful as a soothing or derivative agent.
In the absence of morphia or chloral, laudanum, ether, chloroform, camphor or assafœtida have been recommended.
It is important to keep the patient on a soft, littered floor to prevent injury from his throwing himself down, and walking him around may be resorted to for the same purpose.
Prevention. After a non-fatal attack and in every case in which a horse is found to harbor the sclerostoma equinum in quantity, measures should be taken to expel those present in the bowels and to prevent the entry of embryos. The infested horse may be purged and put on two drachms each of tartar emetic and sulphate of iron every morning in a handful of feed half an hour before the first meal. After six doses he may take a second active purgative. In case of need the addition of 6 grains arsenious acid and a drachm of carbolic acid to each dose will render them much more effective. All water must be withheld that comes from streams running by farm-yards, from ponds or open wells in barn-yards, from uncovered cisterns and from any source which receives drainage or leaching from land occupied by solipeds or spread with their manure.
A course of vermifuge medicine should be given at intervals of two or three months to get rid of the worms which have passed in the interval from the cysts of the colon, into the intestine.