Atrial Septal Defect in a Ferret (Mustela putorius furo)

A 2-year-old, male castrated ferret (Mustela putorius furo) was presented with progressive abdominal distention and loss of muscle mass despite normal appetite. Physical examination findings included pale mucous membranes, a prolonged capillary refill time, a pulse rate greater than 300 beats/min, and severe abdominal distention. Abdominal ultrasound showed free abdominal fluid and an enlarged liver with distended hepatic veins and caudal vena cava. During the echocardiographic examination, abnormalities observed included a 2-mm-diameter left-to-right shunting atrial septal defect (ASD) with concurrent severe dilatation of the right atrium and eccentric hypertrophy of the right ventricle with mild pulmonary hypertension. All other echocardiographic measurements were within normal limits. The owner declined treatment, and the ferret was euthanized. Postmortem examination confirmed the ultrasonographic findings. The free abdominal fluid (200 mL) was a non-septic fibropurulent exudate. Decompensated right-sided heart failure due to ASD and exudative peritonitis of undetermined origin were the final diagnoses. To our knowledge, this is the first report of an ASD in a ferret.     

Clinical and pathological characterisation of primary pulmonary hypertension in a dog

Primary pulmonary hypertension was diagnosed in an eight-year-old labrador retriever on the basis of echocardiographic findings of severe right ventricular eccentric hypertrophy, abnormally high systolic and diastolic pulmonary arterial pressures calculated by applying the modified Bernoulli equation to the tricuspid and pulmonary insufficiency peak velocities, and the absence of any underlying disease known to cause secondary pulmonary hypertension. The clinical abnormalities developed gradually, from exercise intolerance starting early in life to terminal right-sided congestive heart failure. Consistent histopathological findings were severe intimal and medial thickening of small arteries and arterioles that led to vascular obliteration.     

Pulmonary hypertension as a cause of atrial fibrillation in young horses: four cases (1980-1989)

Four young horses of various breeds and suffering from atrial fibrillation died of heart failure. All had markedly high pulmonary arterial pressure, right-sided cardiomegaly, and lack of histologic lesions in the right atrium or pulmonary parenchyma. Three horses had hypertrophy and/or necrosis of the tunica media of the pulmonary vasculature. Clinical signs of disease, physiologic data, and pathologic findings indicated that these horses had primary pulmonary hypertension with secondary right-sided cardiac ventricular hypertrophy and dilatation, atrial fibrillation, and heart failure.     

Idiopathic noncirrhotic portal hypertension in dogs: 33 cases (1982-1998)

OBJECTIVE: To describe clinical signs, diagnostic findings, and outcome in dogs with idiopathic intrahepatic portal hypertension. DESIGN: Retrospective study. ANIMALS: 33 dogs. PROCEDURE: Medical records of dogs with portal hypertension of intra-abdominal origin were reviewed. Dogs with intra-abdominal portal hypertension of vascular causes or with hepatic histopathologic changes consistent with severe diffuse hepatobiliary disease were excluded. History and results of physical examination, clinicopathologic tests, diagnostic imaging studies, histologic examination, and treatment were summarized. Outcome was determined in 26 dogs. RESULTS: Dogs were referred most often because of ascites, intermittent vomiting or diarrhea, and polydipsia of several months' duration. Microcytosis, high serum alkaline phosphatase and alanine transaminase activities, hepatic dysfunction, urine specific gravity < or = 1.021, and abdominal transudate were the predominant clinicopathologic features. Microhepatia, abdominal effusion, and multiple anomalous venous anastomoses were the major findings of diagnostic imaging. Hepatic histopathologic changes were consistent with idiopathic noncirrhotic portal hypertension and were indistinguishable from those of dogs with surgically created portocaval anastomosis. Outcome was determined for 19 dogs released from hospital; 13 dogs remained healthy with mostly palliative treatment for periods of 5 months to 9 years. CONCLUSIONS AND CLINICAL RELEVANCE: The clinical signs, clinicopathologic test results, portal pressure, and gross appearance of the liver of dogs with idiopathic noncirrhotic portal hypertension may be identical to those of dogs with cirrhosis; therefore liver biopsy is crucial. Because the prognosis for idiopathic noncirrhotic portal hypertension is generally favorable, owners of affected dogs should be discouraged from choosing euthanasia.     

Gait deficits in liver disease: Hepatic encephalopathy and hepatic myelopathy

In this issue, the unusual clinical presentation of a horse diagnosed is described with severe liver cirrhosis and hepatic encephalopathy. The horse initially presented for thoracic and pelvic limb ataxia and weakness, and signs of forebrain disease were not apparent until later in the disease process. The typical pathology of central nervous system disease associated with liver disease is related to encephalopathy and forebrain disease; however, the spinal cord is occasionally also involved. Hepatic myelopathy is a rare syndrome usually associated with surgical or acquired portosystemic shunts, liver cirrhosis and/or portal hypertension in man. Where a gliopathy is the most prominent pathological feature seen in hepatic encephalopathy, in hepatic myelopathy the most remarkable feature is demyelination of the corticospinal tracts of the distal cervical and thoracic spinal cord with occasional axon loss. The clinical signs of hepatic myelopathy are spastic paresis/paralysis with normal sensory findings and preserved sphincter function. The prognosis for hepatic myelopathy is generally poor. In summary, in severe liver disease, motor deficits can occur secondary to the encephalopathy, but motor deficits can also occur as a result of spinal cord pathology such as seen in hepatic myelopathy. In examination of horses with myelopathies, liver disease as a cause of myelopathy should be included in our list of differentials.     

Patent ductus arteriosus in an adult cat with pulmonary hypertension and right-sided congestive heart failure: hemodynamic evaluation and clinical outcome following ductal closure

Right-sided congestive heart failure (CHF) developed secondary to severe pulmonary hypertension (PH) in an 8-year-old cat with a left-to-right shunting patent ductus arteriosus (PDA). Vascular reactivity was tested prior to shunt ligation by treatment with oxygen and sildenafil. This treatment was associated with a significant decrease in pulmonary artery pressure as assessed by echocardiography. Subsequently surgical shunt ligation was planned. During thoracotomy, digital occlusion of the PDA was performed for 10 min with simultaneous catheter measurement of right ventricular pressure, which did not increase. Permanent shunt ligation resulted in a complete and sustained clinical recovery. A lung biopsy sample obtained during thoracotomy demonstrated histopathological arterial changes typical of PH. Cats can develop clinically severe PH and right-sided CHF secondary to a left-to-right PDA even at an advanced age. Assuming there is evidence of pulmonary reactivity, PDA occlusion might be tolerated and can potentially produce long-term clinical benefits.     

Acute necrotising pulmonary vasculitis and pulmonary hypertension in a juvenile dog

A five-month-old female Jack Russell terrier was presented for investigation of acute lethargy, anorexia, coughing, respiratory distress and weakness. Examination findings included cyanosis, a grade 3 of 6 systolic heart murmur and prolonged capillary refill time. Radiography and echocardiography revealed severe pulmonary hypertension, cor pulmonale and right-sided heart failure. Indirect measurement of the systolic pulmonary artery pressure estimated pressures over 100 mmHg. Despite treatment the patient died. Post-mortem examination did not identify a congenital cardiovascular anomaly. Histopathology confirmed acute necrotising pulmonary arteritis and immunohistochemistry failed to identify any immune complex or complement deposition.     

Fatal acute lung injury after balloon valvuloplasty in a dog with pulmonary stenosis

A one-year-old French Bulldog was referred for the management of a severe form of pulmonary valve stenosis (PS) complicated by right-sided congestive heart failure.Echocardiography showed severe valvular PS with right ventricular concentric hypertrophy, dilatation and severe right atrial enlargement. A pulmonary balloon valvuloplasty (PBV) was performed with a balloon-to-pulmonary annulus ratio of 1.36. Echocardiography immediately after PBV showed a significant reduction in right atrial and ventricular size, improved opening and mobility of the pulmonary valve leaflets, and a 75% reduction in the pulmonary pressure gradient from 158 mmHg pre-operative to 40 mmHg post-operative. The dog recovered well from anesthesia, but 2 h later, it suddenly showed severe respiratory distress. Focus cardiac ultrasound showed increased left cardiac size with echocardiographic signs of high left ventricular filling pressure. Bedside lung ultrasound showed diffuse numerous-to-confluent B lines, compatible with a severe alveolar-interstitial syndrome. The dog was treated with furosemide, helmet continuous positive airway pressure, and then mechanical ventilation but without success.At post-mortem evaluation, histological examination of the lung showed diffuse, severe broncho-alveolar edema with mixed leukocyte, fibrin, and red blood cell infiltrate. Moreover, severe congestion and multifocal alveolar hemorrhages were evident. All findings were compatible with fatal acute lung injury after PBV secondary to pulmonary reperfusion-ischemia injury and increased pulmonary capillary hydrostatic pressure. Based on the present case, acute lung injury should be considered as a rare but serious complication of PBV.     

Echocardiographic detection of pulmonic valve rupture in a horse with right-sided heart failure

Pulmonic valve rupture was determined to be the cause of severe right-sided heart failure in a 20-year-old Thoroughbred gelding. A flail in the intermediate pulmonic valve cusp was detected by 2-dimensional echocardiography. Significant pulmonic and tricuspid valvular regurgitation were confirmed by Doppler echocardiography. Despite treatment, the horse's condition deteriorated, and euthanasia was performed. At necropsy, a tear in the pulmonary artery extending into the right valve cusp and a tear at the base of the intermediate valve cusp were identified at the junction of the right and intermediate pulmonic valve cusps. Careful echocardiographic evaluation of the pulmonic valve is warranted for horses with right-sided heart failure, for which more common causes cannot be found.     

COMPARISONS OF RADIOGRAPHIC AND ELECTROCARDIOGRAPHIC ABNORMALITIES IN CANINE HEARTWORM DISEASE

Thoracic radiographs and electrocardiograms from 137 dogs with heartworm infection were independently evaluated and comparisons were made of (1) the presence or absence of right ventricular enlargement as assessed by these two diagnostic tests and (2) the presence or absence of right-sided congestive heart failure relative to the degree of right ventricular enlargement and ECG criteria of RVH.
Radiographic evidence of severe, but not moderate, right ventricular enlargement was associated with right-sided congestive heart failure. Similarly the presence of three or more, but not fewer than three, ECG criteria of RVH were associated with right-sided congestive heart failure. If either the thoracic radiographs or the ECG indicated that severe right ventricular enlargement was absent, right-sided congestive heart failure was seldom present. The most accurate correlation of the radiographic evaluation of severe right ventricular enlargement was afforded by the presence of three or more ECG criteria of RVH. ECG criteria of RVH such as R/S^v4, + T^v10 MEA^x, and S¹¹ are highly specific tests; while S^V2 is a highly sensitive but not highly specific test. The ECG is a good confirmation test of the presence of severe right ventricular enlargement and is a good exclusion test for the absence of right-sided congestive heart failure.     

Pulmonary manifestations of heartworm disease

The clinical signs associated with heartworm disease are the result of changes in the pulmonary arterial system. These clinical signs are the result of either pulmonary hypertension or lung parenchymal disease associated with vascular changes. An increase in pulmonary arterial pressure produces an increase in right ventricular afterload, which may lead to exercise intolerance, syncope, and right-sided congestive heart failure. Coughing, dyspnea, and hemoptysis are the results of pulmonary parenchymal disease.     

Endocardial fibroelastosis and tricuspid valve insufficiency in a calf

A 5-month-old Holstein heifer had clinical signs of tricuspid valve insufficiency and histopathologic evidence of endocardial fibroelastosis. The calf had a 3-week history of weight loss, abdominal distention, dyspnea, and decreased appetite. Physical examination revealed signs of right-sided heart failure, and a systolic murmur (II/VI) was heard best over the right heart base. Results of cardiac catheterization and echocardiography indicated tricuspid valve insufficiency and right-sided heart failure. The calf was euthanatized after not responding to treatment with penicillin, furosemide, and removal of fluid from the thorax and abdomen. Necropsy findings included multifocal areas of thickening and opacification of the endocardium of the left and right ventricles. Excessive elastic fibers, consistent with fibroelastosis, were seen by use of special stains applied to sections of endocardium.     

Congestive heart failure in horses: 14 cases (1984-2001)

OBJECTIVE: To identify clinical signs, underlying cardiac conditions, echocardiographic findings, and prognosis for horses with congestive heart failure. DESIGN: Retrospective study. ANIMALS: 14 horses. PROCEDURE: Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; treatment; and outcome were determined by reviewing medical records. RESULTS: All 14 horses were examined because of a heart murmur; tachycardia was identified in all 14. Twelve horses had echocardiographic evidence of enlargement of 1 or more chambers of the heart. Other common clinical findings included jugular distention or pulsation, crackles, cough, tachypnea, and ventral edema. Nine horses had signs consistent with heart failure for > 6 days. Underlying causes for heart failure included congenital defects, traumatic vascular rupture, pericarditis, pulmonary hypertension secondary to heaves, and valvular dysplasia. Seven horses were euthanatized after diagnosis of heart failure; 5 were discharged but were euthanatized or died of complications of heart disease within 1 year after discharge. The remaining 2 horses were discharged but lost to follow-up. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that congestive heart failure is rare in horses. A loud heart murmur accompanied by either jugular distention or pulsation, tachycardia, respiratory abnormalities (crackles, cough, tachypnea), and ventral edema were the most common clinical signs. Echocardiography was useful in determining the underlying cause in affected horses. The long-term prognosis for horses with congestive heart failure was grave.     

Symptomatic partial anomalous pulmonary venous connection in a kitten

A 3-month-old intact female American Shorthair cat, with syncope and tachypnea, underwent cardiac examination which identified no heart murmur or gallop. Thoracic radiography disclosed mild generalized enlargement of the cardiac silhouette and a bronchial and interstitial pattern throughout the lungs. Echocardiography identified tubular structures near the left atrium. After agitated saline contrast imaging, persistent left cranial vena cava with unroofed coronary sinus was suspected. Computed tomography angiography showed the right cranial, right caudal and left caudal pulmonary veins draining into the coronary sinus and flowing into the right atrium. The left cranial pulmonary vein drained normally into the left atrium. Partial anomalous pulmonary venous connection (PAPVC) was diagnosed. The kitten was treated with diuretics but died of heart failure 2 months later. Permission for necropsy was not granted. This case represents symptomatic PAPVC in a kitten. Most pulmonary veins were connected abnormally with the coronary sinus. The prognosis was grave because of refractory heart failure.     

Systemic coccidioidomycosis in a llama cria native to Missouri

A 3-mo-old male llama was examined because of a 4-wk history of lethargy and ill thrift. Clinical examination revealed subcutaneous masses in the left prescapular and right inguinal regions, mild ataxia, a slight head tilt to the right, and right ear droop. The cria died before clinical workup was complete. At autopsy, there was generalized lymphadenomegaly, a hepatic nodule, a midbrain mass causing rostral compression of the cerebellum, and internal hydrocephalus. Microscopic findings included pyogranulomatous lymphadenitis, meningoencephalitis, hepatitis, and bronchopneumonia. Intralesional fungal spherules, most consistent with Coccidioides spp., were identified in the lymph nodes, lung, and brain. Fungal culture, single-nucleotide variation genotyping real-time PCR, and DNA sequencing confirmed Coccidioides posadasii. The dam of the cria was native to Arizona and had been moved to Missouri ~2.5 y previously. Agar gel immunodiffusion assay of the herd revealed that only the dam was positive for Coccidioides spp.; 6 herdmates were negative. Computed tomography of the dam revealed multiple nodules within the lungs and liver, which were presumed to be an active coccidioidomycosis infection. This case of systemic coccidioidomycosis in a llama native to Missouri was presumably acquired by vertical transmission from the dam.     

Reversible pulmonary hypertension in a cat

A 13-year-old, neutered female domestic shorthair cat was presented for sudden respiratory distress following palliative radiotherapy and the combined administration of a single dose of carboplatin for the treatment of recurrent fibrosarcoma. Clinical and radiographic findings were suggestive of pleural effusion. Echocardiography revealed marked right-sided cardiac enlargement associated with tricuspid regurgitation and Doppler evidence of pulmonary hypertension. After 25 days of treatment for congestive heart failure and suspected pulmonary thromboembolism, clinical signs and echocardiographic and Doppler evidence of right-sided cardiac enlargement and pulmonary hypertension had completely resolved. To the best of the authors' knowledge, this is the first report of reversible pulmonary hypertension, likely secondary to pulmonary thromboembolism, in a cat.     

Total serum bile acid concentrations in dairy cows with fatty liver and liver failure

In forty-five Holstein Frisian dairy cows (1-6 weeks post partum; mean age: 5.1 +/- 1.2 years) the serum total bile acid concentrations (SBA) were measured enzymatically. In all cows a left sided abomasal displacement was corrected surgically by right side laparotomy and omentopexy three days before investigation. The liver fat content was determined in all cows histologically. Liver failure was assumed if typical clinical signs (ataxia, general depression, recumbency or coma), an increased venous plasma ammonia level (> 35 mumol/l) and a decreased plasma amino acid index (< 4.0) were found. Cows without liver failure (N = 29) were grouped according to the liver fat content as cows with mild (N = 5), moderate (N = 19) or severe hepatosteatosis (N = 5). Histological examination of liver biopsies in cows with liver failure (N = 16) revealed in twelve cases a severe fatty liver and in four cases a hydropic degeneration of the liver tissue. Although in cows without liver failure mean SBA concentrations were higher in the group with moderate (47.3 +/- 30.9 mumol/l) or severe fatty liver (32.9 +/- 21.7 mumol/l) than in that with mild lipidosis (18.0 (16.8 mumol/l), differences were not significant. The mean SBA concentration in cows with liver failure (70.5 +/- 49.5 mumol/l) was only significantly (p < 0.05) increased compared to cows with uncomplicated mild hepatic lipidosis. In conclusion, the determination of SBA concentrations is of little value in the recognition of fatty liver or even liver failure due to the considerable variance of SBA concentrations in dairy cows.