Abstract
Ascites, the pathological accumulation of fluid within the peritoneal cavity, often results from an imbalance between fluid production and absorption. This case involved a seven-and-a-half-year-old neutered female Labrador retriever presenting with abdominal distension, inappetence, weakness, and lethargy. Clinical examination revealed respiratory distress, abdominal pain, pale mucous membranes, muffled heart sounds, and a positive fluid thrill upon abdominal palpation. Hematological evaluation showed normocytic normochromic anemia, neutrophilia, leukocytosis, and thrombocytopenia. Biochemical analysis revealed hypoalbuminemia, hypoglycemia, elevated liver enzymes (ALT, AST, ALP), and increased blood urea nitrogen (BUN) and creatinine levels, indicating impaired liver and kidney function. Arterial blood gas analysis indicated hepatobiliary dysfunction, showing low pCO(2), reduced bicarbonate (HCO(3)) levels, and a negative base excess (BE), consistent with metabolic acidosis with compensatory respiratory alkalosis. Radiographic imaging showed a ground-glass appearance and pleural effusion, while ultrasonography confirmed the presence of free anechoic fluid in the peritoneal cavity, rounded liver margins, a dilated hepatic portal vein, hyperechoic liver parenchyma, ill-defined corticomedullary junctions in the kidneys, and splenomegaly. Cytological analysis of the straw-colored ascitic fluid showed fibrin strands and white blood cells. The serum-ascites albumin gradient (SAAG) was 2.4 g/dL, indicating portal hypertension as the underlying cause. The final diagnosis was ascites of hepatic origin. Treatment included diuretics, antibiotics, fluid therapy, liver supplements, and dietary modifications, including salt restriction and the provision of high-quality protein. This case underscores the importance of a comprehensive diagnostic approach that combines clinical, hematological, biochemical, and imaging findings to enable timely intervention and effective management of canine ascites.