Causes of Ascites
Cirrhosis accounts for 80-85% of all ascites cases, making it by far the most common cause, but cardiac failure, malignancy, tuberculosis, and other conditions must always be excluded through diagnostic paracentesis and serum-ascites albumin gradient (SAAG) calculation. 1, 2
Primary Etiologic Categories
Portal Hypertension-Related Causes (SAAG ≥1.1 g/dL)
Cirrhosis is the dominant cause within this category, driven by two fundamental mechanisms: portal (sinusoidal) hypertension creating increased hydrostatic pressure that forces fluid transudation into the peritoneal cavity, and sodium/water retention from activation of the renin-angiotensin-aldosterone system. 2, 3
Alcoholic liver disease represents a major subset of cirrhotic ascites and is notably reversible with abstinence—patients with Child-Pugh C alcoholic cirrhosis who stop drinking have approximately 75% 3-year survival versus 0% survival in those who continue drinking. 2, 4
Acute hepatic vein thrombosis (Budd-Chiari syndrome) causes postsinusoidal portal hypertension and is usually associated with ascites, producing high SAAG with elevated protein (>2.5 g/dL). 2, 5
Cardiac ascites from right heart failure creates portal hypertension and produces the distinctive pattern of high SAAG (≥1.1 g/dL) combined with high protein (>2.5 g/dL), distinguishing it from cirrhotic ascites which typically has low protein (<2.5 g/dL). 5
Important caveat: Patients with presinusoidal portal hypertension without cirrhosis (such as isolated chronic extrahepatic portal venous occlusion or congenital hepatic fibrosis) rarely develop ascites unless there is an additional insult to liver function like gastrointestinal hemorrhage. 2
Non-Portal Hypertension Causes (SAAG <1.1 g/dL)
Peritoneal carcinomatosis from malignancy requires ascitic fluid cytology when clinically suspected, with elevated CEA (>5 ng/mL) or alkaline phosphatase (>240 U/L) suggesting secondary peritonitis from perforated hollow viscus. 2
Tuberculous peritonitis should be suspected in high-risk patients (recent immigration from endemic areas, AIDS), with adenosine deaminase (ADA) levels >27-32 U/L showing 100% sensitivity and 93.3% specificity for diagnosis in cirrhotic patients. 2
Nephrotic syndrome produces low SAAG ascites and is one of the few non-portal hypertension causes that responds to salt restriction and diuretics. 2
Pancreatic ascites presents with ascitic amylase levels typically >1,000 mg/dL. 2
Urinary ascites from bladder or ureteral injury shows elevated urea and creatinine in ascitic fluid. 2
Mixed Ascites
Approximately 5% of patients have two or more simultaneous causes of ascites formation—most commonly cirrhosis plus peritoneal carcinomatosis or tuberculous peritonitis. 2, 3 In these cases, the sum of predisposing factors (e.g., heart failure, diabetic nephropathy, and cirrhosis) leads to sodium and water retention when each individual factor alone might not be severe enough. 2
Diagnostic Algorithm
The SAAG calculation (serum albumin minus ascitic fluid albumin) is the single best test for classifying ascites, with >97% accuracy in determining whether portal hypertension is present. 2, 1
- SAAG ≥1.1 g/dL indicates portal hypertension with 97% accuracy. 2, 5
- SAAG <1.1 g/dL indicates non-portal hypertension causes. 2
Essential initial investigations include: diagnostic paracentesis with ascitic fluid cell count and differential, ascitic fluid total protein, ascitic fluid albumin (for SAAG calculation), ascitic fluid neutrophil count and culture in blood culture bottles inoculated at bedside, and ascitic fluid amylase when pancreatic ascites is suspected. 2
Critical pitfall: Never assume the alcoholic patient has alcoholic liver disease—tests must always be directed at diagnosing the specific cause of ascites, as the underlying etiology is frequently obvious from history and examination but other causes must be systematically excluded. 2