Merck Manual

Please confirm that you are a health care professional

honeypot link

Portal Hypertension and Ascites in Small Animals


Sharon A. Center

, BS, DVM, DACVIM, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University

Last full review/revision May 2015 | Content last modified Jun 2016

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.

Hepatic Disease in Small Animals
Overview of Hepatic Disease in Small Animals
Hematology in Hepatic Disease in Small Animals
Coagulation Tests in Hepatic Disease in Small Animals
Enzyme Activity in Hepatic Disease in Small Animals
Other Serum Biochemical Measures in Hepatic Disease in Small Animals
Hepatic Function Tests in Small Animals
Imaging in Hepatic Disease in Small Animals
Cholecystocentesis in Hepatic Disease in Small Animals
Liver Cytology in Small Animals
Liver Biopsy in Small Animals
Pathologic Changes in Bile in Small Animals
Nutrition in Hepatic Disease in Small Animals
Fulminant Hepatic Failure in Small Animals
Hepatic Encephalopathy in Small Animals
Portal Hypertension and Ascites in Small Animals
Portosystemic Vascular Malformations in Small Animals
Acquired Portosystemic Shunts in Small Animals
Other Hepatic Vascular Disorders in Small Animals
Hepatotoxins in Small Animals
Infectious Diseases of the Liver in Small Animals
Feline Hepatic Lipidosis
Biliary Cirrhosis in Small Animals
Canine Cholangiohepatitis
Canine Chronic Hepatitis
Lobular Dissecting Hepatitis in Small Animals
Canine Vacuolar Hepatopathy
Metabolic Diseases Affecting the Liver in Small Animals
Hepatocutaneous Syndrome in Small Animals
Nodular Hyperplasia in Small Animals
Hepatic Neoplasia in Small Animals
Miscellaneous Liver Diseases in Small Animals
Diseases of the Gallbladder and Extrahepatic Biliary System in Small Animals
Cholecystitis in Small Animals
Canine Gallbladder Mucocele
Other Disorders of the Gallbladder in Small Animals
Other Disorders of the Bile Ducts in Small Animals
Extrahepatic Bile Duct Obstruction in Small Animals
Cholelithiasis in Small Animals
Biliary Tree Rupture and Bile Peritonitis in Small Animals
Feline Cholangitis/Cholangiohepatitis Syndrome
Hepatobiliary Fluke Infection in Small Animals
Others also read
Download the Manuals App iOS ANDROID
Download the Manuals App iOS ANDROID
Download the Manuals App iOS ANDROID
Test your knowledge
Dental Development
Ruminants (cattle, sheep, and goats) lack which of the following teeth?
Become a Pro at using our website 

Also of Interest

Become a Pro at using our website