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 within the space of Disse, fat or glycogen within hepatocytes). Rarely, arterialization of the hepatic parenchyma by an intrahepatic arteriovenous malformation leads to arterialization of the intrahepatic circulation and causes portal hypertension and ascites. Intrahepatic causes of portal hypertension are categorized as presinusoidal, sinusoidal, and postsinusoidal. Post-hepatic causes of portal hypertension include obstruction of blood flow from 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 or acquired "kink," heartworm-associated vena caval syndrome).
In all cases of hepatic portal hypertension, intrahepatic portal hypoperfusion (portal perfusion pressure is ~5–8 mmHg) is compensated by an increase in hepatic arterial perfusion that maintains organ circulation. This causes hepatofugal (backward) flow of blood into the valveless portal system and formation of acquired portosystemic shunts (APSSs).
Compensatory imbalance of sodium and water homeostasis becomes clinically apparent at the onset of portal hypertension and is typically associated with a subnormal albumin concentration. Ascitic effusion associated with hepatic disease is usually a modified or pure transudate (serum albumin < 1.8 g/dL). Consequences of portal hypertension include development of ascitic effusion, splanchnic vasodilation, risk of bleeding from APSSs, development of a portal-enteric vascuolopathy, and increased risk of septic abdominal effusion.
The standard treatment to reduce splanchnic portal hypertension in people is nonselective β-blockade using propranolol, administered to control or reduce risk of spontaneous bleeding from APSSs. Other pharmacologic interventions remain controversial and have not been shown in placebo-controlled trials to provide greater benefit. Therapeutic strategies for control of ascites include dietary sodium restriction, administration of diuretics to increase urinary sodium elimination, and therapeutic abdominocentesis (when necessary). The first step is dietary sodium restriction to an intake of ≤100 mg sodium/100 kcal diet (25 mg/kg/day; < 0.1% dry-matter basis in food). However, sodium-restriction alone is often insufficient and too slow in onset for efficient management. Thus, diuretics are usually also recommended. Diuretic therapy should slowly reduce ascites without causing dehydration, metabolic alkalosis, or hypokalemia. Reducing ascites by ≤1%–1.5% of total body wt/day is recommended by initially using combined treatment with furosemide (1–2 mg/kg, PO, bid) and spironolactone (loading dosage 2–4 mg/kg × 2–3 doses, then 1–2 mg/kg, PO, bid). Reevaluation every 7–10 days allows for careful upward titration of diuretic dosages. Combining a loop diuretic (furosemide) with spironolactone (aldosterone antagonist) reduces risk of iatrogenic hypokalemia.
If ascites is slow to mobilize, 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, or patient comfort, therapeutic abdominocentesis may be undertaken. In people, 8 g of human albumin is administered for every 5 L of effusion removed to offset the development of postdiuresis circulatory dysfunction developing ~12 hr after effusion removal. Postdiuresis circulatory dysfunction reflects reequilibration of body fluids and worsened hypoalbuminemia (removed by abdominocentesis), leading to systemic hypotension (response to redistribution of removed ascitic fluid) and splanchnic and renal vasoconstriction. The latter responses increase risk of development of the hepatorenal syndrome (reversible renal vasoconstriction associated with liver failure complicated by ascites). Because there is no access to species-specific albumin for dogs and cats, polyionic fluids may be used when therapeutic abdominocentesis to remove large amounts of ascitic fluid is performed. Large-volume abdominocentesis should never be performed without concurrent diuretic administration. In removing ascitic effusion, the goal is to remove enough volume to improve patient comfort. Rational use of therapeutic abdominocentesis reduces abdominal pressure, improves renal perfusion and cardiac output, and improves response to diuretic therapy. Once ascitic effusion is mobilized, diuretics can often be used intermittently with concurrent dietary sodium restriction.