Comparative pathology of heart and liver lesions of broiler chickens that died of ascites, heart failure, and others.

Pathologic changes of 120 dead broilers from a flock of 1000 birds were compared. Macroscopically, the changes were divided into three pathologic types: ascites (retention of ascitic fluid), heart failure (right heart dilation and/or hydropericardium without retention of ascitic fluid), and others (without ascites or heart failure). The rates of ascites, heart failure, and others were 55.8% (67/120), 33.3% (40/120), and 10.8% (13/120), respectively. Histologically, cardiac histologic changes (myocardial degeneration with calcification and epicardial fibrosis) were seen in 40 of 67 (59.7%) ascites cases. Hepatic histologic changes (hepatocytic degeneration/necrosis and hepatic capsule fibrosis) were seen in 64 of 67 (95.5%) ascites cases. Cardiac histologic changes were seen in 24 of 40 heart failure cases (60.0%). Hepatic histologic changes were seen in 36 of 40 (90.0%) heart failure cases. Six of 13 others had hepatic histologic changes, but the remaining seven birds had no significant histologic changes. Ascites and heart failure cases had almost the same percentages of hepatic and cardiac histologic changes. This study indicates that two pathologic types, ascites and heart failure, may be closely related conditions and that hepatic histologic changes may be common and fundamental lesions in the pathogenesis of these pathologic types.     

Kinking of the intrathoracic caudal vena cava in five dogs

Five dogs with kinking of the intrathoracic caudal vena cava (CVC) were studied. One dog had neither clinical nor laboratory abnormalities associated with the kinked CVC, and the cause was unknown. The other four dogs had evidence of post-sinusoidal obstruction of venous flow characterized by high protein ascites (modified transudate). Causes of the kinked CVC were automobile trauma (two dogs), cardiomegaly with ascites, and a large neoplastic lung mass. Surgical removal of the kinked caval segment was successful in the two dogs injured by automobiles. Medical therapy with a diuretic was associated with a decrease in ascites, straightening of the CVC, and improvement in clinical condition of the dog with cardiomegaly and ascites. Surgical removal of the neoplastic lung mass in one dog resulted in straightening of the CVC, but it later died of respiratory failure associated with pulmonary neoplasia.     

Hepatic cirrhosis in a five-month-old dog

The clinicopathological features of an unusual case of a five-month-old male Spanish mastiff, which was presented with clinical signs indicative of severe hepatic failure, are reported. Fluid replacement therapy, colloid plasma expanders, antibiotics and diuretic drugs were unsuccessful in improving the animal's general condition, and euthanasia was elected by the owner. On necropsy, ascites and severe cirrhosis, with extensive periacinar necrosis, was found. Cirrhosis is a rare lesion in young dogs. The most common causes are circulatory disturbances, hereditary metabolic disorders or poisoning, such as aflatoxicosis and anticonvulsant therapy. The possible involvement of canine adenovirus in this case is discussed.     

Diet‐associated hepatic failure and immune‐mediated hemolytic anemia in a Weimaraner

Objective: To describe the medical and nutritional management of a 4‐year‐old Weimaraner with acute hepatic failure and immune‐mediated hemolytic anemia (IMHA) associated with consuming a commercial dog food. Case summary: A 4‐year‐old male castrated Weimaraner developed signs of IMHA, hepatic failure, disseminated intravascular coagulopathy, and malnutrition after consuming a commercial dog food. During the course of hospitalization, medical management included immunosuppressive therapy and supportive care. Nutritional support consisted of both enteral and parenteral nutrition. The dog was discharged after 19 days of hospitalization and fully recovered by 6 months. An investigation by the Food and Drug Administration was not able to determine the exact cause of the acute hepatic failure and IMHA. New information provided: This is the first case report documenting the medical and nutritional management of a critically ill animal associated with ingestion of this commercial dog food.     

Circulatory disorders of the liver in dogs and cats

Summary

This paper presents a review of the literature on hepatic circulation and circulatory disorders of the liver in the dog and cat, and also includes a number of our own not previously published data. Circulatory disorders of the liver are frequently observed in dogs and cats. These disorders can be divided into congenital portosystemic shunts, disorders associated with outflow disturbances, and disorders associated with portal hypertension. Outflow disturbances result in passive congestion of the liver and in both species are mainly due to cardiac failure. Portal hypertension with resultant portosystemic collateral circulation and ascites mainly results from chronic liver disease, particularly cirrhosis. The main vascular disorder resulting in portal hypertension and ascites in the dog is primary hypoplasia of the portal vein.     

Acute renal failure following Bull ant mass envenomation in two dogs

Acute renal failure was diagnosed in a German Short Haired Pointer bitch and a Kelpie cross-bred dog following envenomation by Bull ants. Both dogs had been tethered over a Bull ant nest and had experienced mass envenomation. There was local reaction at the envenomation sites and each dog had experienced vomiting that was poorly controlled by symptomatic therapy. Intensive treatment of renal failure was successful in the German Short Haired Pointer and the bitch remains well 19 months after envenomation. The Kelpie cross-bred deteriorated despite intensive treatment and was euthanased 36 hours after presentation. Necropsy examination revealed haemorrhage and necrosis of the small intestine and myocardium, bilateral nephrosis with tubular necrosis, and patchy haemorrhage of the lung alveoli, pancreas and adrenal cortices. Electron microscopy revealed necrosis of the small intestine and hydropic swelling of proximal renal tubules with necrosis of medullary tubules.     

Pathologic findings and toxin identification in cyanobacterial (Nodularia spumigena) intoxication in a dog

A 3-year-old Cairn Terrier dog that had been in contact with sea water containing cyanobacteria (blue-green algae) was euthanized because of acute hepatic failure and anuria after a 5-day illness. Histologic findings included lytic and hemorrhagic centrilobular hepatocellular necrosis and renal tubular necrosis. The cyanotoxin nodularin was detected in liver and kidney by high-performance liquid chromatography-mass spectrometry. Nodularin is a potent hepatotoxin produced by the algal species Nodularia spumigena. The intensity of algal blooms has increased during the past decades in the Baltic Sea region, thus increasing the risk for intoxications in domestic and wild animals. The authors describe the pathologic findings of cyanobacterial toxicosis in a dog with direct identification of the toxin from organ samples.     

Endocardial fibroelastosis in a dog

Endocardial fibroelastosis is an uncommon congenital heart disease in dogs that may be manifested by signs of left-sided congestive heart failure. A three-month-old, male, Fila Brasileiro dog developed signs of generalised heart failure. Physical examination revealed normal temperature, ascites, and pale and cyanotic mucous membranes. The pup died just after radiography which revealed ascites, hepatomegaly, severe cardiac enlargement and pulmonary oedema. At necropsy, serosanguineous fluid in the thorax and abdomen, pulmonary oedema, right ventricular dilatation, hypertrophy and dilatation of the left ventricle, and mitral valve incompetence were observed. The histopathological examination demonstrated that the thickening of the endocardium of the left atrium and left ventricle was due to the presence of elastic and collagen fibres, although there were no signs of an inflammatory process.     

Xylitol intoxication associated with fulminant hepatic failure in a dog

Objective: To describe a case of xylitol intoxication causing fulminant hepatic failure in a dog. Case summary: A 2.5‐year‐old castrated male English Springer Spaniel weighing 26 kg, was presented after ingestion of half of a loaf of bread containing the sweetener xylitol. Toxic effects of the xylitol in this dog included vomiting, mild hypoglycemia and fulminant hepatic failure. Clinical management of acute hepatic failure and subsequent coagulopathy with supportive care and fresh frozen plasma is described. The dog was discharged 3 days after admission after a full clinical recovery. New or unique information provided: This paper describes the clinical consequence and successful treatment of fulminant hepatic failure in a dog following ingestion of xylitol.     

Clinical and histologic outcome in a dog surviving massive hepatic necrosis

This report describes the clinical and histologic recovery of a 2‐year‐old mixed‐breed dog presented with hypovolemic shock, markedly increased serum alanine amino transferase activity, and hemoabdomen. Emergency exploratory surgery revealed a friable liver with multiple capsule hemorrhages necessitating removal of the left lateral lobe. Histologic evaluation showed acute massive hepatic necrosis with centrilobular and midzonal distribution. The dog survived, and all monitored laboratory values normalized within 7 weeks. A liver biopsy taken 8 weeks after presentation revealed normal hepatic architecture with a few, randomly distributed neutrophilic foci. Follow‐up included intermittent determination of liver variables including liver function tests for a period of 7 years. The dog's health status, and all test results remained normal during this time. Complete recovery and good long‐term quality of life after life‐threatening acute liver failure secondary to massive hepatic necrosis is possible in dogs.     

Caudal vena cava kinking in dogs with ascites

A 9-year-old dog with spontaneous ascites was found to have hepatic vein distension and a tortuous vena cava on abdominal ultrasound. In right lateral recumbency, the caudal vena cava crossed the diaphragm and became kinked before entering into the right atrium. Following this observation, we performed an experimental study in a normal dog to determine whether kinking of the caudal vena cava could be the result and not the cause of ascites. Ascites was induced using warm saline injected through a needle inserted into the abdominal cavity. Venograms were collected from different body positions, under four conditions: before and after a total of one, two and 3 liters of saline had been injected. Caudal vena cava kinking was observed in the experimental dog after 2 liters of fluid had been injected. Vena cava obstruction may cause ascites, but we found that sometimes caudal vena cava kinking can be the result and not the cause of the peritoneal effusion.     

Kernicterus in an adult dog

A 7-year-old, spayed female, Wheaton terrier dog was icteric, lethargic, and anorexic with increased activity of hepatocellular and cholestatic liver enzymes and an extreme hyperbilirubinemia level of 609 micromol/L (reference interval: 1.0-4.0 micromol/L). Necropsy findings included profound icterus and red and yellow mottling of the liver. Yellow discoloration of the thalamic and subthalamic nuclei was detected on subgross examination of the formalin-fixed brain. Histologic examination of the brain revealed neuronal necrosis within the discolored nuclei, necrosis of Purkinje cells, and Alzheimer type II astrocytes in the cerebrocortical gray matter and in the nuclei, with gross discoloration. Histologic examination of the liver revealed extensive necrosis in a periacinar-to-bridging pattern and often extending to portal triads. A case of naturally occurring kernicterus in an adult dog secondary to extreme hyperbilirubinemia resulting from fulminant hepatic failure is reported. The few reports of this disease in domestic species involved neonates, namely 1 foal and 1 kitten.     

Chronic liver disease associated with high hepatic copper concentration in a dog

An 8-month-old dog admitted for routine castration was found to have ascites. Liver biopsy revealed inflammation, fibrosis, and a copper concentration of 1,300 ppm on a dry weight basis. As cirrhosis developed, the copper concentration decreased without chelator treatment. At necropsy, the dog had cirrhosis, but the hepatic copper concentration was only 730 ppm.     

Congenital hepatic arteriovenous fistula with intrahepatic portosystemic shunt and aortic stenosis in a dog

Examination of a 2-month-old male golden retriever presented to the hospital revealed malnutrition, ascites, cardiac murmur and hyperammonemia. Identification of subaortic stenosis and hepatic arteriovenous fistula was made through ultrasonography and angiocardiography. In addition, intrasurgical mesenteric portography showed an intrahepatic portosystemic shunt. The dog did not show portal hypertension and secondary multiple extrahepatic portosystemic shunts. Surgical correction was attempted after medical treatment. The hepatic artery branch which was connected to the hepatic arteriovenous fistula was separated, and completely ligated using silk ligature. However, the separation of the intrahepatic shunt blood vessel was unsuccessful and the dog died 15 hr postoperatively.     

Encapsulating peritoneal sclerosis associated with abnormal liver development in a young dog

A 6-month-old male miniature pinscher dog developed chronic ascites, formation of fibrous membrane covering the abdominal organs, and numerous adhesions between the intestinal loops. The membrane and adhesions were surgically removed twice, but the dog died 1 month after initial presentation. Necropsy revealed recurrence of the membrane and intestinal adhesions. The fibrous membrane was composed of a thick layer of mature collagenous connective tissue, covered by immature collagenous connective tissue with mild lymphoplasmacytic infiltration, prominent neovascularization, and fibrin exudation. Similar fibrotic lesions were observed in the serosa of the liver, spleen, stomach and intestines. These findings are consistent with encapsulating peritoneal fibrosis reported in humans and dogs. The dog also had a maldeveloped liver, which is characterized by disorganized hepatic lobules and disarranged hepatic cords.     

Anuric renal failure in a dog after red-bellied black snake (Pseudechis porphyriacus) envenomation

A case of Red-bellied Black snake envenomation resulting in intravascular haemolytic anaemia, rhabdomyolysis and anuric renal failure is described in the dog. A 12-year-old female desexed Golden Retriever was presented with a 15 hour history of profuse salivation, progressive lethargy, obtundence, inappetence and collapse. Significant findings on clinical examination were pallor, icterus, tachypnoea and dyspnoea with increased respiratory sounds and crackles in all lung fields. Generalised abdominal and muscular pain was apparent and dark red-brown urine was present around the perineal region. A diagnosis of Red-bellied Black snake (Pseudechis porphyriacus) envenomation was made and the dog was treated with intravenous fluid therapy, Tiger/Brown snake antivenom, packed red cell transfusions and Intermittent Positive Pressure Ventilation. Continued clinical deterioration occurred and a diagnosis of acute renal failure secondary to myohaemoglobinuric pigmenturia was made 12 hours after admission. Intensive treatment was attempted with diuresis and volume expansion. Oliguria and subsequent anuria ensued and the dog was euthanased due to a grave prognosis and lack of clinical response to treatment. Necropsy examination revealed muscular necrosis, accumulation of fluid in the thoracic and peritoneal cavities, and marked renal tubular necrosis with intraluminal occlusion secondary to pigmentary casts.     

Long-term palliation of right-sided congestive heart failure after stenting a recurrent cor triatriatum dexter in a 10½-year-old pug

A 10½-year-old, male neutered, pug presented with increasing ascites over two months. Echocardiography revealed cor triatriatum dexter with no concurrent cardiovascular anomalies, subsequently confirmed by computed tomography angiography. Balloon dilation of the perforated intra-atrial membrane under fluoroscopic guidance resulted in the transient resolution of all clinical abnormalities, but six months later stenosis and ascites recurred. After repeated balloon dilation, a stent was placed across the membrane. The dog remains asymptomatic fourteen months after the second procedure. One noteworthy feature of this case is the onset of congestive heart failure due to a congenital defect only at more than 10 years of age.     

Nutritional myopathy in goats

A nutritional myopathy in unweaned fibre goats aged 2 to 4 mths is described in 3 flocks from the tablelands of New South Wales. Clinically affected animals were illthrifty and in circulatory failure prior to being found dead. At necropsy, there was pronounced ascites, pulmonary congestion and marked mottling of the liver. Chalky white streaks and patches were obvious in the myocardium, particularly in the right ventricular wall. Skeletal muscles varied from grossly normal to generally pale. Histologically, the myocardium exhibited areas of severe acute myonecrosis with mineralisation and adjoining areas of phagocytosis and fibrosis. In 2 of 3 flocks, some skeletal muscles showed a mild subacute myopathy. Marked hepatic congestion extended to periacinar haemorrhage and necrosis in some areas. Dietary imbalances of selenium, vitamin E and polyunsatured fatty acids were probable factors in the pathogenesis of the condition.     

Haemolytic-uraemic syndrome in a dog

An 11-year-old female German Shepherd dog presented with lethargy and anorexia, which progressed to haemorrhagic vomiting, diarrhoea and seizures. Serum biochemistry and haematology results showed azotaemia and mild thrombocytopaenia. Euthanasia was elected and the dog was submitted for necropsy examination. There were widespread serosal and mucosal petechial and ecchymotic haemorrhages within the abdomen, with ascites and multiple renal infarcts. The renal infarcts were associated with fibrinoid necrosis and thrombosis of inter-lobular arteries and arterioles. These arterial lesions and clinical signs are consistent with haemolytic-uraemic syndrome, which has not previously been reported in dogs in Europe.     

Inherited copper toxicosis in Bedlington terriers

SUMMARY Chronic hepatitis and increased hepatic copper concentrations, from 1,600 to 6,361 fig/g dry tissue were found in 4 related, Australian-bred Bedlington terriers. Two dogs were asymptomatic and 2 were clinically ill with signs referable to liver dysfunction. Two dogs were treated with d-penicillamine. After one year there was no improvement in the histopathological liver changes in either dog or significant lowering of hepatic copper level in one dog.