Ascites develops secondary to portal hypertension and low albumin concentrations. Physiologic responses triggered to maintain euvolemia and splanchnic perfusion pressure signal systemic conservation of sodium and water.
Portal hypertension represents circulatory dynamics thwarting craniad flow of blood through the liver. Prehepatic causes include stenosis, stricture, or thrombi involving the extrahepatic portal vein. Intrahepatic causes include the sequela of chronic hepatitis resulting in collagenization and capillarization of hepatic sinusoids, accumulation of connective tissue encircling portal triads or the hepatic venule (centrilobular area), architectural remodeling of the liver by formation of regenerative nodules (cirrhosis), vascular occlusion of hepatic or portal veins (eg, thrombi, neoplasia, vasculitis), or diffuse dissemination of neoplastic cells within sinusoids or storage materials (amyloid, glycogen) within hepatocytes. Rarely, arterialization of the hepatic parenchyma by an intrahepatic arteriovenous fistula leads to portal hypertension and ascites. Post-hepatic causes include obstruction of blood flow out of the liver through the hepatic vein; this can begin at the level of the heart (eg, right heart failure, cor triatriatum dexter, hemangiosarcoma involving the right atrium), pericardium (eg, restrictive pericarditis, pericardial tamponade), or vena cava (eg, thrombi, congenital kink, heartworm vena cava syndrome).
In all cases of hepatic portal hypertension, intrahepatic portal hypoperfusion associates with hepatic arterialization. Hepatic arterial perfusion compensates to maintain organ circulation and causes hepatofugal (backward) flow of blood in the portal circulation and formation of acquired portosystemic shunts.
(APSS). Compensatory imbalance in sodium and water homeostasis usually becomes clinically apparent with onset of portal hypertension associated with a subnormal albumin concentration. Ascitic effusion associated with hepatic disease is usually characterized as a modified or pure transudate (serum albumin <1.8 g/dL).
The first step in control of ascites is dietary sodium restriction. An intake of ≤100 mg/100 kcal (25 mg/kg/day; <0.1% dry matter basis in food) is recommended. However, sodium-restricted diets alone are often insufficient and too slow in onset for efficient management. Thus, diuretics are usually recommended. Diuretic therapy should slowly reduce ascites without causing dehydration, metabolic alkalosis, or hypokalemia. Reducing ascites by ≤1.0–1.5% of total body wt/day is recommended. Dual therapy with furosemide (1–2 mg/kg, PO, bid) and spironolactone (loading dose 2–4 mg/kg × 2–3 doses, then 1–2 mg/kg, PO, bid) is initially recommended. Reevaluation every 7–10 days allows for careful upward titration of diuretic dosages. Combining a loop diuretic with spironolactone reduces risk of iatrogenic hypokalemia.
If ascites is slow to resolve, measuring the urinary fractional excretion of sodium can help determine whether dietary restriction and diuretic dosing are adequate. If ascites causes tense abdominal distention, compromising ventilation, appetite, and patient comfort, a therapeutic abdominocentesis is recommended. Fluid administration (hetastarch) reduces risk of post-diuresis circulatory dysfunction developing ~12-hr after effusion removal when body fluids undergo re-equilibration (hypotension, worsening hypoalbuminemia). However, Hetastarch infusion increases risk of bleeding because of reduced platelet aggregation. As little ascitic fluid as possible should be removed to keep the animal comfortable. Reducing abdominal pressure increases renal perfusion and cardiac output and improves response to diuretic therapy. In many cases, once fluid is mobilized, diuretics can be used intermittently as long as a attention to dietary sodium restriction is maintained.
Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM