Mitral valve dysplasia in a cat causing reversible left ventricular hypertrophy and dynamic outflow tract obstruction

A 6-month-old male European shorthair cat was examined because of a 2/6 systolic left apical cardiac murmur. Echocardiography revealed severe concentric left ventricular hypertrophy and severe dynamic left ventricular outflow tract obstruction (pressure gradient of 85 mmHg) caused by systolic anterior motion (SAM) of the septal mitral valve leaflet. After 2 months of oral treatment with atenolol, the cardiac murmur had disappeared. Echocardiography showed only slight thickening of the interventricular septum and resolution of the pressure gradient. The cat was discharged and its owner was advised to continue atenolol lifelong. Echocardiographic findings of a combination of left ventricular concentric hypertrophy and dynamic left ventricular outflow tract obstruction can be caused by hypertrophic obstructive cardiomyopathy (HOCM) or mitral valve dysplasia in the absence of hypertension and fixed aortic stenosis. In the case of HOCM, left ventricular hypertrophy is the primary process. In the case of mitral valve dysplasia, systolic anterior motion of the mitral valve is the primary problem, which leads to dynamic left ventricular outflow tract obstruction and ultimately to left ventricular concentric hypertrophy, due to pressure overload. If the left ventricular outflow tract obstruction is reduced with an oral beta-receptor blocker the secondary left ventricular hypertrophy may resolve. This would not happen in the case of hypertrophic obstructive cardiomyopathy. To the best of the authors' knowledge, this is the first documented case of severe dynamic left ventricular outflow tract obstruction and severe left ventricular hypertrophy in a cat successfully treated with oral atenolol.     

Portal hypertension in a dog due to circumscribed fibrosis of the wall of the extrahepatic portal vein

A two-and-a-half-year-old German shepherd dog with ascites and a high concentration of blood ammonia was investigated. Sonographically, its liver was normal but the portal vein was dilated and the flow of blood within it was slow. A liver biopsy showed that the liver was normal, and did not reveal any possible cause of portal hypertension or ascites. Postmortem, the cranial part of the portal vein was dilated with a cross-striped internal surface, but the caudal part looked normal; there was a stenotic ring between the normal and dilated parts. Histology of the dilated segment revealed marked hypertrophy of both the internal circular and the external longitudinal smooth muscle layers. At the site of the stenosis, the longitudinal muscular layer was replaced by connective tissue. Circumscribed fibrosis in the wall of the portal vein was responsible for the stenosis and the subsequent prehepatic portal hypertension. The cross-striped pattern in the dilated part of the vein was the result of hypertrophy of the inner circular smooth muscle layer.     

Ultrasound-guided percutaneous drainage for treatment of pyonephrosis in two dogs

Pyonephrosis refers to suppurative destruction of the parenchyma of the kidney with complete or nearly complete loss of renal function. In dogs, nephrectomy is still the most common treatment for pyonephrosis; however, in the present report, a method for percutaneous ultrasound-guided drainage of the renal pelvis in dogs with pyonephrosis that does not require local or general anesthesia was described, and results of the procedure in 2 dogs were reported. Briefly, dogs were positioned in lateral recumbency with the affected side up, and skin overlying the affected kidney was aseptically prepared. The dilated renal pelvis was punctured percutaneously, under ultrasound guidance, with a 22-gauge needle, and a sample of material was obtained for analysis. The needle was then replaced with an IV catheter, and as much pus as possible was removed from the renal collecting system. A povidone iodine solution was then used to lavage the renal pelvis. Ultrasound-guided drainage and lavage of the renal pelvis was repeated daily until the renal pelvis was so small that it could no longer be punctured. Both dogs recovered and were reported by the owners to be healthy after the procedure.     

Ultrasonographic findings in dogs with hyperammonemia: 90 cases (2000-2002)

OBJECTIVE: To determine ultrasonographic abnormalities in dogs with hyperammonemia. DESIGN: Retrospective study. ANIMALS: 90 client-owned dogs with hyperammonemia. PROCEDURE: Ultrasonography of the abdominal vessels and organs was performed in a systematic way. Dogs in which the ultrasonographic diagnosis was a congenital portosystemic shunt were included only if they underwent laparotomy or necropsy. Dogs in which the abdominal vasculature appeared normal and dogs in which the ultrasonographic diagnosis was acquired portosystemic shunts and portal hypertension were included only if liver biopsy specimens were submitted for histologic examination. RESULTS: Ultrasonography excluded portosystemic shunting in 11 dogs. Acquired portosystemic shunts were found in 17 dogs, of which 3 had arterioportal fistulae and 14 had other hepatic abnormalities. Congenital portosystemic shunts were found in 61 dogs, of which 19 had intrahepatic shunts and 42 had extrahepatic shunts. Intrahepatic shunts originated from the left portal branch in 14 dogs and the right portal branch in 5. Extrahepatic shunts originated from the splenic vein, the right gastric vein, or both and entered the caudal vena cava or the thorax. Ultrasonography revealed splenic-caval shunts in 24 dogs, right gastric-caval shunts in 9 dogs, splenic-azygos shunts in 8 dogs, and a right gastric-azygos shunt in 1 dog. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that ultrasonography is a reliable diagnostic method to noninvasively characterize the underlying disease in dogs with hyperammonemia. A dilated left testicular or ovarian vein was a reliable indicator of acquired portosystemic shunts.     

Ultrasonographic assessment of hemodynamic changes in the portal vein during surgical attenuation of congenital extrahepatic portosystemic shunts in dogs

OBJECTIVE: To determine portal hemodynamic changes associated with surgical shunt ligation and establish ultrasonographic criteria for determining the optimal degree of shunt narrowing and predicting outcome. DESIGN: Case series. ANIMALS: 17 dogs, each with a single congenital extrahepatic portosystemic shunt. PROCEDURE: Pre- and postligation flow velocities and flow directions were determined by Doppler ultrasonography intraoperatively in the shunt and in the portal vein cranial and caudal to the shunt origin. Outcome was evaluated 1 month after surgery by measuring blood ammonia concentration and performing abdominal ultrasonography. RESULTS: Hepatofugal flow was detected in 9 of 17 dogs before shunt attenuation in the portal segment that was between the shunt origin and the entering point of the gastroduodenal vein. If hepatofugal flow became hepatopetal after shunt ligation, hyperammonemia resolved. Hepatofugal portal flow was caused by blood that flowed from the gastroduodenal vein toward the shunt. Shunt attenuation converted hepatofugal flow to hepatopetal in the shunt in 12 of 17 dogs. Chronic portal hypertension developed or perioperative death occurred when the portal congestion index caudal to the shunt origin increased by > 3.6 times. CONCLUSIONS AND CLINICAL RELEVANCE: After hepatopetal flow in the cranial portal vein and the shunt is established, further shunt narrowing is contraindicated. Increase of the portal congestion index caudal to the shunt > 3.5 times should be avoided. Poor outcome because of severe hypoplasia of the portal branches can be expected if the flow direction remains hepatofugal after shunt occlusion cranial to the shunt origin.     

Reversible pulmonary hypertension associated with lungworm infection in a young cat

Two ten-week-old kittens presented with dyspnea. Two weeks later dyspnea had worsened and both kittens had developed a heart murmur. One kitten died and necropsy showed severe granulomatous pneumonia and moderate bronchi(oli)tis and peribronchi(oli)tis caused by Aelurostrongylus abstrusus. The results from echocardiography, thoracic radiography and the other kitten's fecal examination were interpreted as severe parasitic pneumonia caused by A. abstrusus infection with pulmonary hypertension. Repeated administration of milbemycine-oxime and praziquantel resulted in cessation of larvae shedding and resolution of clinical, radiographic and echocardiographic signs of bronchopneumonia and pulmonary hypertension.