IMAGING DIAGNOSIS--ACUTE MESENTERIC ISCHEMIA ASSOCIATED WITH HYPERTROPHIC CARDIOMYOPATHY IN A CAT.

A middle-aged cat was presented with vomiting, diarrhea, and pelvic limb paresis. Radiography showed cardiomegaly, interstitial pulmonary infiltration, distended intestinal loops, and portal venous gas. Hypertrophic cardiomyopathy (HCM) was confirmed. On CT, thrombi were identified at the abdominal aorta, superior mesenteric artery, bilateral renal arteries, and cauda vena cava at the level of the iliac vein bifurcation. Dilated and gas-filled loops of bowel with a "paper thin wall" were observed on CT images and were considered indicative of necrotic bowel. This case report describes the CT findings of acute mesenteric ischemia associated with HCM in a cat.

Postsurgical segmental mesenteric ischemic thrombosis in a horse.

A 16-year-old, Lusitanian stallion was admitted to the Veterinary Teaching Hospital with a 12-hour history of signs of abdominal pain. Exploratory celiotomy was performed due to an inguinal hernia, and a second celiotomy was performed in response to the abdominal pain. The horse was euthanized and mesenteric venous thrombosis was diagnosed and considered likely due to peritonitis and systemic inflammatory response syndrome (SIRS).

Thrombose ischémique mésentérique segmentaire post-chirurgicale chez un cheval. Un étalon Lusitanien âgé de 16 ans a été admis à l'hôpital d'enseignement vétérinaire avec une anamnèse de 12 heures de douleurs abdominales. Une coeliotomie exploratoire a été réalisée en raison d'une hernie inguinale et une deuxième coeliotomie a été réalisée en réponse à la douleur abdominale. Le cheval a été euthanasié et une thrombose de la veine mésentérique a été diagnostiquée et considérée probablement attribuable à une péritonite et au syndrome de la réaction inflammatoire systémique (SRIS).(Traduit par Isabelle Vallières).

Mesenteric vascular thrombosis associated with disseminated abdominal visceral hemangiosarcoma in a cat.

An adult castrated male cat was evaluated because of a 4 day history of lethargy and partial anorexia. Physical examination revealed abdominal pain with a palpable fluid wave. Cytologic and biochemical analyses of peritoneal effusion were suggestive of septic peritonitis. On surgical exploration of the abdomen, the mesenteric vessels had no palpable pulses and they contained gross thromboses. The intestines were white with no visible peristalsis. Necropsy findings included disseminated, poorly differentiated hemangiosarcoma throughout the abdomen. Mesenteric arterioles contained fibrin thrombi. To the author's knowledge, no previous reports exist of complete mesenteric vascular thrombosis associated with disseminated abdominal visceral hemangiosarcoma in a cat.

Mesenteric vein thrombosis in a dog.

A four-year-old, male cocker spaniel was presented for vomiting and anorexia of two days' duration. An elongated abdominal mass was palpated, and abdominal pain was noted. On exploratory laparotomy, a jejunal segment was found to be infarcted transmurally. Histopathology confirmed the diagnosis of mesenteric vein thrombosis. The dog recovered uneventfully following resection of the affected bowel.

Thrombosis resulting in rectal perforation in a horse.

A 12-year-old Quarter Horse gelding was admitted to the veterinary medical teaching hospital with a 2-day history of signs of abdominal pain. Initial findings on physical examination included signs of lethargy, dehydration, diarrhea, and gastric reflux. Results of laboratory testing indicated that the horse had panleukopenia with neutrophilic toxic changes, was dehydrated, and was hypocalcemic. During the first 48 hours of hospitalization, 1 abdominal palpation per rectum and 3 analyses of peritoneal fluid were performed; abnormalities were not detected. A preliminary diagnosis of enterocolitis was made. Salmonella anatum was isolated from the feces. The horse's condition improved during a 5-day period, although left jugular thrombosis did develop. On day 8 of hospitalization, the gelding was found dead. Necropsy revealed acute severe fibrinous peritonitis as the result of vasculitis and thrombosis of the caudal mesenteric artery and its cranial rectal branch with rectal infarction and perforation. Immediate classification of rectal tears and perforation as iatrogenic should be avoided. Ischemic vascular disease is a consideration, and horses with thromboembolic disorders may be at risk for rectal perforations.

Effects of U-74389G, a novel 21-aminosteroid, on small intestinal ischemia and reperfusion injury in horses.

OBJECTIVE: To determine the effects of the 21-aminosteroid, U-74389G, on reperfusion of the equine jejunum, using total (TVO) and partial (PVO) vascular occlusion during the ischemic period. DESIGN: TVO: 16 healthy horses were randomly allotted to 3 groups-4 horses received the vehicle alone, 6 horses received a low dosage (3 mg/kg o body weight), and 6 horses a high dosage (10 mg/kg) of U-7438G. PVO: 10 healthy horses were randomly allotted to 2 groups--5 horses received the vehicle alone, and 5 horses received the low dosage (3 mg/kg) of U-74389G. PROCEDURES: TVO was induced for 1 hour followed by 2 hours of reperfusion. During PVO, blood flow was reduced to 20% of baseline for 2 hours, followed by 2 hours of reperfusion. For both models, either the vehicle alone or the drug was given 15 minutes prior to reperfusion. Samples were obtained before, during, and after ischemia for determination of myeloperoxidase (MPO) activity, malondealdehyde (MDA) concentration, concentration of conjugated dienes (PVO experiment only), and morphometric analysis. RESULTS: TVO: tissue concentration of MDA and MPO activity were not altered in any group by ischemia or reperfusion. During ischemia, mucosal volume and surface area were reduced. After reperfusion, no further reduction occurred. After initial decrease in submucosal volume during ischemia, there was a significant increase after reperfusion in the vehicle-only group (P < 0.05). PVO: there were no alterations in the concentration of either MDA or conjugated dienes. There was significant increase in the activity of MPO during ischemia and reperfusion (P < 0.05). These effects were similar for the vehicle-only and drug groups. During ischemia, there was a significant decrease in mucosal surface area and volume (P < 0.05), that was continued during reperfusion for the vehicle-only (P < 0.05). Submucosal volume increased during ischemia and reperfusion. CONCLUSIONS AND CLINICAL RELEVANCE: Reduced blood flow during ischemia (PVO group) caused continued loss in mucosal volume and surface area during reperfusion. At the dosage given, the 21-aminosteroid, U-74389G, was not effective in preventing continued reduction in mucosal volume and surface area after restoration of blood supply in the horses subjected to reduced blood flow.

Cecal torsion in a horse as a consequence of cecocolic fold hypoplasia.

Cecal torsion in horses is relatively rare. This clinical report describes cecocolic fold hypoplasia, producing increased cecal mobility, as a predisposing cause of cecal torsion in a horse.

Artificial induction of red gut in sheep.

Eight out of 10 lambs died within six to 11 hours after occlusion of the cranial mesenteric blood vessels by a snare placed around both the artery and vein. Death resulted from shock and was accompanied by post mortem findings identical to those seen in red gut. It is suggested that the cause of death in the naturally occurring disease is from arrested mesenteric blood flow following intestinal torsion.

Lesions in sheep inoculated with Sarcocystis tenella sporocysts from canine feces.

Sarcocystosis was studied in 37 sheep after oral inoculation with 10(4)-5 x 10(7) sporocysts of Sarcocystis tenella from canine feces. Two sheep inoculated with 2.5 x 10(7) and 5 x 10(7) sporocysts became moribund 16 and 19 days post-inoculation (DPI), respectively, due to occlusion of arteries of gut and mesentery by first generation meronts. Sheep inoculated with 10(7) sporocysts remained clinically normal until 21 DPI and those inoculated with 10(5)-10(6) became ill 24-28 DPI due to anemia coincident with maturation of second generation meronts. Inflammation, hepatitis and myocarditis were the main lesions of acute and subacute ovine sarcocystosis. Inflammation began to subside by the time (75 DPI) sarcocysts matured. Sarcocystis-induced encephalitis was distinguished from naturally occurring myelomalacia in sheep caused by an unidentified sporozoan.

Intestinal infarction associated with mesenteric vascular thrombotic disease in the horse.

Intestinal infarction associated with cranial mesenteric artery thrombosis, without strangulation obstruction of the intestine, was studied in 18 horses. Findings normally of value in evaluating horses with acute abdominal pain (heart rate, rectal palpation findings, gastric reflux) or classification of the degree of pain were not helpful in diagnosing the problem. Similarly, packed cell volume, plasma total protein, circulating white blood cell count, peritoneal white blood cell count, and peritoneal fluid total protein were not of value in predicting severity of the intestinal damage, location of infarction, or patient survival. In one half of the cases, peritoneal fluid color was of aid in distinguishing intestinal infarction from strangulation. Findings on gross dissection and limited histologic examination did not support the premise that thromboembolism was the major mechanism for production of infarction. In most of the horses, a thrombus or embolus was not found in the peripheral mesenteric vessels.

The pathogenesis of single experimental infections with Strongylus vulgaris in foals.

The clinical signs, pathology and clinical pathology associated with single experimental infections of Strongylus vulgaris in worm-free pony foals are described. The major clinical signs which became apparent in the infected foals during the first three weeks were pyrexia, anorexia, dullness and abdominal pain. Within the first two weeks of infection lesions were confined to the intestine and terminal branches of the intestinal arteries and consisted of mucosal, submucosal and serosal haemorrhage together with arteritis of submucosal and serosal arteries and also a marked inflammatory reaction. The main lesion seen three weeks after infection was gross thrombosis of the anterior mesenteric artery or one of its major branches. On section these affected arteries showed marked intimal thickening with infiltration of plasma cells, lymphocytes, macrophages and neutrophils. Between one and four months after infection the gross lesions were predominantly in the arteries and consisted of fibrous thickening of the arterial wall and thrombosis associated with the presence of developing fourth stage larvae. Four months after infection the arterial lesions were still prominent and microscopically there was fibrosis of the wall of the affected artery with wide-spread disruption of the intima. In the adventitia organised thrombi were apparent in the vasa vasorum and resulted in the obliteration of their lumina. The typical lesion associated with the return of fifth stage larvae to the intestine was nodule formation in close proximity to thrombosed terminal intestinal arteries and sections of parasites were seen in the intestinal wall surrounded by neutrophils and necrotic debris. By nine months after infection the arterial lesion had healed, but histologically there was fibrosis of the intima and macrophages containing haemosiderin were seen in the arterial wall. The most significant haematological findings during the experimental period were a marked polymorphonuclear leucocytosis and an increase in the number of circulating eosinophils in the infected animals. Also marked was an increase in the serum globulin levels of the infected foals.