History
A 4-year-old 6.8-kg (15-lb) neutered male Abyssinian cat was referred because of a 1-week history of anorexia and lethargy. The cat had previously received dexamethasone (0.5 mg/kg [0.23 mg/lb], SC, q 24 h), enrofloxacin (5 mg/kg, [2.3 mg/lb], SC, q 24 h), and IV fluid therapy with saline (0.9% NaCl) solution at a rate 30 mL/kg/h (13.6 mL/lb/h) for the first 8 hours, then 3 mL/kg/h (1.4 mL/lb/h) for 4 days. Urine output was estimated to be low by the referring veterinarian.
Physical examination revealed hypothermia (body temperature, 33°C [91.4°F]), a heart rate of 190 beats/min, no heart murmur, weak femoral pulses, slow capillary refill time, tachypnea (60 breaths/min), expiratory dyspnea, diffuse harsh lung sounds, and an abdominal fluid wave.
Hematologic evaluation revealed mature neutrophilia (18.3 × 109 neutrophils/mL; reference range, 3 × 109 neutrophils/mL to 12 × 109 neutrophils/mL). Serum biochemical analysis revealed high alanine aminotransferase activity (2,227 U/L; reference range, 10 to 90 U/L) and urea nitrogen concentration (24 mmol/L; reference range, 5.4 to 10.7 mmol/L). Serum lactate concentration was moderately high at 5.9 mmol/L (reference range, 0.4 to 2.5 mmol/L1). The cat had mild hypoalbuminemia, mild hyperbilirubinemia, mild hypocalcemia, hyponatremia (130 mmol/L; reference range, 145 to 158 mmol/L), and hyperkalemia (5.1 mmol/L; reference range, 3.6 to 4.9 mmol/L).
Venous blood gas analysis revealed probable mixed metabolic acidosis and respiratory alkalosis, given a pH of 7.21 (reference range, 7.35 to 7.45), base deficit of 11 (reference range, −4 to 2), and Pco2 of 31.8 mm Hg (reference range, 38 to 51 mm Hg). Systolic arterial blood pressure measured by Doppler ultrasonography was 80 mm Hg (reference range, 110 to 160 mm Hg).
Abdominal ultrasonography revealed free abdominal fluid that was subsequently characterized as a modified transudate (total solids concentration, 23 g/L; specific gravity, 1.020), hyperechoic renal cortices, and a medullary rim sign. Thoracic radiographs were obtained (Figure 1).
Left lateral (A) and ventrodorsal (B) radiographic views of the thorax of a 4-year-old 6.8-kg (15-lb) neutered male Abyssinian cat referred for inappetence, lethargy, moderate tachypnea, and low urine output that was nonresponsive to previous fluid therapy.
Citation: Journal of the American Veterinary Medical Association 247, 8; 10.2460/javma.247.8.885
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
Generalized cardiomegaly is evident radiographically (Figure 2). The vertebral heart score is 11 vertebrae, with the craniocaudal dimension of the heart exceeding the distance from the cranial border of the fifth rib to the caudal border of the seventh rib.2 The cranial and caudal lobar arteries and veins are enlarged. Pleural fissure lines and retraction of lung lobes from the thoracic wall indicate pleural effusion; rounding of the atelectatic lung lobes indicates chronicity of the pleural effusion. The mediastinum appears enlarged, and cranial lung lobes are displaced caudally; these findings in addition to the large amount of falciform fat are attributed to obesity. A diffuse, unstructured, interstitial lung pattern and patchy increase in soft tissue opacity in the cranial lung lobes and in the left caudal and accessory lung lobes are evident. The diffuse parenchymal change might be consistent with partial atelectasis due to pleural effusion. Patchy pulmonary opacity in conjunction with cardiomegaly is suggestive of cardiogenic pulmonary edema. There is a loss of serosal detail in the abdomen consistent with the ultrasonographically reported abdominal effusion.
Same left lateral (A) and ventrodorsal (B) radiographic images as in Figure 1. Notice the generalized cardiomegaly, confirmed on the basis of the vertebral heart score (crossing arrows; vertebral heart score, 11 vertebrae); dorsal displacement of the trachea; enlargement of pulmonary vessels; diffuse interstitial pattern; patchy alveolar pattern in the cranial, caudal, and accessory lungs lobes (1; arrows); presence of pleural fissure lines (2; arrows); and loss of serosal detail in the abdomen. An enlarged vena cava (3; arrow) as well as hepatomegaly are both suggestive of hepatic congestion. The lack of contrast and cranial mediastinum enlargement are attributed to the obese condition of the cat. The heart deviation to the left was due to positioning artifact.
Citation: Journal of the American Veterinary Medical Association 247, 8; 10.2460/javma.247.8.885
For further evaluation, echocardiography was performed (Figure 3). Enlargement of all cardiac chambers was evident. The left atrium-to-aorta ratio as measured from the right parasternal short axis view was 2.5 (reference value, < 1.5).3 A thrombus in the left auricle and another thrombus attached to the anterior papillary muscle in the left ventricle was observed. Fractional shortening was severely reduced (8%; reference range, 40% to 67%). The left ventricular internal dimension at end systole was 24 mm (reference range, 4 to 11 mm). The interventricular septum and the left ventricular wall thickness were normal in appearance. On the basis of radiographic and echocardiographic findings, the most likely differential diagnoses were dilated cardiomyopathy, end-stage hypertrophic cardiomyopathy, and cardiac lymphoma.
Right parasternal short-axis echocardiographic view at the level of the aortic valve (A) and right transthoracic parasternal short-axis M-mode echocardiographic view (B) of the cat in Figure 1. A—The left atrium-to-aorta ratio (2.5; reference value, < 1.5) is high, and a thrombus in the left auricle (arrows) is evident. Line 1 represents aortic diameter; line 2 represents left atrial diameter. B—Notice the decreased fractional shortening (8%; reference range, 40% to 67%) and the enlargement of the left ventricle in diastole and systole. The first vertical line measures left ventricle size and thickness of the interventricular septum (at the top) and of the ventricular wall (at the bottom) in diastole and the second line indicates the same measurement in systole.
Citation: Journal of the American Veterinary Medical Association 247, 8; 10.2460/javma.247.8.885
Treatment and Outcome
The cat was treated with taurine (37 mg/kg [16.7 mg/lb], PO, q 12 h), pimobendan (0.2 mg/kg [0.09 mg/lb], PO q 12 h), furosemide (4 mg/kg [1.8 mg/lb], IV, q 6 h), a constant rate infusion of dobutamine (1 μg/kg/min [0.45 μg/lb/min], increased to 3 μg/kg/min [1.4 μg/lb/min]), and active body warming with a forced-air patient warming blanket. Despite treatment, systolic arterial blood pressure did not exceed 70 mm Hg, and urine output remained low. Because of the lack of improvement after 24 hours, the cat was euthanized.
A necropsy was performed. Histopathologic findings confirmed that the cat had dilated cardiomyopathy, with myocyte necrosis and fibrosis associated with congestive heart failure. Necropsy findings included pulmonary edema, pleural effusion, centrilobular congestion of the liver, and ascites. There was evidence of remodeling of the thrombi within the heart, indicating chronicity. Moderate renal tubular necrosis and moderate periductular pancreatitis were observed.
Comments
In the cat of the present report, radiographic findings including pleural effusion, pulmonary edema, and ascites were compatible with right- and left-sided congestive heart failure.4 Pleural effusion and pulmonary edema are commonly reported4,5 for cats with dilated cardiomyopathy. Ascites is less commonly seen in cats with dilated cardiomyopathy and has been associated with a poor outcome.5
Fluid overload is usually associated with hypertension and results in cardiac hypertrophy with or without signs of congestive heart failure.6 Fluid overload that results in congestive heart failure might cause a reduction in the force-generating ability of the myocardium, which persists.6 However, this cat had received fluid therapy for a short time. This, in conjunction with persistent hypotension, the severity of the myocardial dysfunction, and the presence of a thrombus, made fluid overload unlikely as the primary cause of congestive heart failure. Fractional shortening in this cat was severely reduced and more likely consistent with dilated cardiomyopathy possibly worsened by hypothermia and acidosis. Other differential diagnoses included end-stage hypertrophic cardiomyopathy or end stage restrictive cardiomyopathy. The smooth endocardial margins and lack of history of cardiac disease make these unlikely.7,8
The cause of the dilated cardiomyopathy in the cat of the present report was unclear from the histopathologic findings. Since taurine deficiency was discovered as a common cause of dilated cardiomyopathy, dilated cardiomyopathy has become an uncommon condition in cats.8 Genetic factors and dietary taurine deficiency are still incriminated. In the case described in the present report, no signs of taurine deficiency were noted (ie, findings on fundic examination appeared normal). Response to taurine supplementation is the only way to rule out taurine deficiency; no other reliable tests have been documented.8
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6. Coulson RL, Yazdanfar S, Rubio E, et al. Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. Circ Res 1977; 40: 41–49.
7. Schober KE, Maerz I. Assessment of left atrial appendage flow velocity and its relation to spontaneous echocardiographic contrast in 89 cats with myocardial disease. J Vet Intern Med 2006; 20: 120–130.
8. Sisson DD, Knight DH, Helinski C, et al. Plasma taurine concentrations and M-mode echocardiographic measures in healthy cats and in cats with dilated cardiomyopathy. J Vet Intern Med 1991; 5: 232–238.
