Cirrhotic ascites
Cirrhotic ascites is fluid accumulation in the peritoneal cavity driven by portal hypertension and splanchnic vasodilation, confirmed by a serum-ascites albumin gradient of 1.1 g/dL or more on diagnostic paracentesis. Management proceeds from sodium restriction and combination diuretics to large-volume paracentesis with albumin and TIPS for refractory disease, with every new or worsening episode screened for spontaneous bacterial peritonitis.
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What this article covers
- Overview
Definition: cirrhotic ascites is the pathologic accumulation of fluid in the peritoneal cavity that results from portal hypertension and splanchnic arterial vasodilation in a patient with cirrhosis.
- Epidemiology
Common decompensating event: ascites occurs in about 50% of patients within 10 years of a cirrhosis diagnosis and is the most common symptom of decompensated cirrhosis.
- Risk factors
Established cirrhosis with portal hypertension: the prerequisite for cirrhotic ascites; the degree of portal pressure elevation correlates with fluid accumulation.
- Pathophysiology
Portal hypertension as the initiating event: intrahepatic fibrosis, regenerative nodules, and increased intrahepatic vascular resistance raise portal venous pressure (portal hypertension).
- Clinical features
Progressive abdominal distension: the presenting complaint in most patients, often accompanied by rapid weight gain and new or worsening peripheral edema.
- Differential diagnosis
Cardiac ascites (congestive heart failure or constrictive pericarditis): SAAG is high like cirrhotic ascites but ascitic fluid total protein is 2.5 g/dL or more (versus under 2.5 g/dL in cirrhosis), and jugular venous distension is present.
- Diagnosis
Establish the cause with the serum-ascites albumin gradient (SAAG) on diagnostic paracentesis: SAAG equals serum albumin minus ascitic fluid albumin drawn the same day; a SAAG of 1.1 g/dL or greater…
- Management
Restrict dietary sodium to under 2 g (88 mEq) per day as first-line therapy for all patients with cirrhotic ascites; this alone controls mild ascites in a meaningful minority.
- Complications
Spontaneous bacterial peritonitis: infection of ascitic fluid without a surgical source, diagnosed by PMN count 250/microL or greater, with high short-term mortality if untreated.
- Prognosis
Ascites onset marks decompensation and worsens survival, with mortality substantially higher than in compensated cirrhosis.
- Prevention
Screen for varices at diagnosis of cirrhosis: upper endoscopy in all patients with cirrhosis, repeated in 3 years if no varices are found on compensated disease (sooner if decompensation occurs).
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Related articles
- Cirrhosis
Cirrhosis is end-stage hepatic fibrosis with regenerative nodules, staged as compensated or decompensated by the onset of ascites, variceal hemorrhage, encephalopathy, or jaundice. Severity is graded by Child-Pugh class and MELD, and management centers on treating the underlying cause, surveillance for varices and hepatocellular carcinoma, and timely transplant referral once decompensation appears.
- Portal hypertension
Portal hypertension is elevated pressure in the portal venous system, most often from cirrhosis, that drives the major decompensating complications of chronic liver disease: varices, ascites, splenomegaly, and encephalopathy. Diagnosis rests on imaging and endoscopy for its downstream signs, and management combines treating the underlying cause with nonselective beta-blockade and, for refractory complications, TIPS.
- Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis is a monomicrobial infection of cirrhotic ascitic fluid without a surgical source, diagnosed by an ascitic fluid neutrophil count of 250 cells/microL or higher on paracentesis. Treatment is prompt IV third-generation cephalosporin plus IV albumin in patients with renal or hepatic dysfunction, followed by indefinite secondary antibiotic prophylaxis because recurrence is common.
- Hepatorenal syndrome
Hepatorenal syndrome is functional renal failure in a patient with cirrhosis and ascites, driven by splanchnic vasodilation and compensatory renal vasoconstriction, and it is diagnosed only after excluding shock, nephrotoxins, and structural kidney disease and after creatinine fails to improve with diuretic withdrawal and an albumin challenge. Treatment is a splanchnic vasoconstrictor (terlipressin first-line) with intravenous albumin as a bridge to liver transplantation, the only curative therapy.
- Hepatic encephalopathy
Hepatic encephalopathy is a reversible spectrum of brain dysfunction from insufficient hepatic clearance and portosystemic shunting of gut-derived toxins, graded by the West Haven criteria and almost always triggered by an identifiable precipitant such as infection, gastrointestinal bleeding, constipation, or an electrolyte disturbance. Diagnosis is clinical, and management proceeds by treating the precipitant first, then titrating lactulose and adding rifaximin for recurrence prevention.
- Gastroesophageal varices
Gastroesophageal varices are dilated portosystemic collateral veins that form as portal pressure rises in cirrhosis, and their rupture causes acute variceal hemorrhage, a GI emergency treated with vasoactive therapy, prophylactic antibiotics, and urgent endoscopic band ligation. Screening endoscopy in cirrhotics guides primary prophylaxis with a nonselective beta-blocker or ligation, and survivors of a bleed require combined beta-blocker and serial ligation for secondary prophylaxis.
- Hyponatremia
Hyponatremia is a serum sodium below 135 mEq/L, worked up by serum osmolality then volume status and urine osmolality/sodium; treatment is a 3% saline bolus for severe or acute symptomatic cases (chronic correction capped at 8 mEq/L per 24 hours), isotonic saline for hypovolemic disease, and fluid restriction plus tolvaptan or demeclocycline for SIADH.