What are the causes and management of acute ascites?

Causes of Acute Ascites

Primary Etiologies

Cirrhosis accounts for 75-85% of all ascites cases in Western countries, making it by far the most common cause, followed by malignancy (10-15%), heart failure (3-5%), tuberculosis, and pancreatic disease. 1, 2, 3

Cirrhotic Causes (Portal Hypertension-Related)

• Alcoholic cirrhosis is the most frequent cirrhotic etiology, followed by non-alcoholic steatohepatitis (NASH), chronic viral hepatitis, and autoimmune liver diseases 1, 3
• Portal hypertension is an absolute prerequisite for ascites development in cirrhosis—ascites only occurs when portal hypertension has developed 1, 2
• The pathophysiology involves splanchnic arterial vasodilation causing decreased effective arterial blood volume, which activates the sympathetic nervous system and renin-angiotensin-aldosterone system, leading to renal sodium retention and extracellular fluid expansion 1, 2, 4

Malignant Causes

• Peritoneal carcinomatosis from primary breast, colon, gastric, or pancreatic carcinomas is the second most common cause overall 1, 2
• Massive liver metastases can also produce ascites 1, 2
• Ascitic fluid cytology has 96.7% sensitivity for detecting peritoneal carcinomatosis if three samples are processed promptly 2

Cardiac Causes

• Heart failure produces ascites distinguishable by elevated jugular venous distension and markedly elevated pro-brain natriuretic peptide (median 6100 pg/mL versus 166 pg/mL in cirrhosis) 1, 2, 3
• Alcoholic cardiomyopathy can mimic alcoholic cirrhosis but jugular venous distension is present in the former 1

Infectious Causes

• Tuberculous peritonitis is more common in endemic areas and immunocompromised patients, often requiring laparoscopy with biopsy and mycobacterial culture for diagnosis 2, 3

Other Causes

• Pancreatic ascites from pancreatitis 1, 2
• Nephrotic syndrome (renal cause) 1, 2
• Budd-Chiari syndrome and sinusoidal obstruction syndrome (vascular causes) 1, 2
• Acute liver failure 1
• Mixed ascites (approximately 5% of patients have two or more causes, usually cirrhosis plus peritoneal carcinomatosis or tuberculosis) 2, 3
• Myxedema and postoperative lymphatic leak (rare) 2

Diagnostic Approach

Essential Initial Evaluation

Diagnostic paracentesis with appropriate ascitic fluid analysis is the most rapid and cost-effective method for determining the cause of ascites and must be performed in all patients with new-onset grade 2 or 3 ascites before initiating any therapy. 1, 2, 5

Physical Examination

• Shifting dullness is the primary examination maneuver (83% sensitivity, 56% specificity) 2, 5
• At least 1,500 mL of fluid must be present before flank dullness is detectable 2, 5
• If no flank dullness is present, the patient has less than 10% chance of having ascites 5
• Abdominal ultrasound is required in obese patients to confirm ascites presence 1, 2, 5

Critical Ascitic Fluid Tests

The serum-ascites albumin gradient (SAAG) is the single most useful test to differentiate causes, with SAAG ≥1.1 g/dL indicating portal hypertension with 97% accuracy. 2, 5

• SAAG ≥1.1 g/dL indicates portal hypertension (cirrhosis, heart failure, Budd-Chiari syndrome) 2, 5
• SAAG <1.1 g/dL suggests non-portal hypertension causes (malignancy, tuberculosis, pancreatitis, nephrotic syndrome) 2, 3
• Neutrophil count >250 cells/μL indicates spontaneous bacterial peritonitis requiring immediate antibiotic therapy 2, 5
• Ascitic fluid culture, total protein, and albumin concentration should always be assessed 2, 3
• Additional tests based on clinical suspicion: cytology (for malignancy), amylase (for pancreatic ascites), tuberculosis testing 2, 3

Laboratory Assessment

• Liver function tests (AST, ALT, bilirubin, alkaline phosphatase) 5
• Renal function tests (creatinine, BUN) 5
• Serum and urine electrolytes 1
• Prothrombin time/INR and complete blood count 5

Imaging

• Abdominal ultrasound to confirm ascites and screen for hepatocellular carcinoma, portal vein thrombosis, and hepatic vein thrombosis 1

Prognostic Implications

Development of ascites marks a critical turning point, reducing 5-year survival from 80% in compensated cirrhosis to 30% in decompensated cirrhosis with ascites. 2, 3

• Approximately 15-20% of patients with ascites die within the first year after diagnosis 2, 3
• Patients with ascites should be evaluated for liver transplantation, which offers the most definitive curative treatment 1, 2, 3, 6

Management Principles

First-Line Therapy for Cirrhotic Ascites

• Sodium restriction (no more than 5 g salt per day, equivalent to one teaspoon) combined with diuretics 1, 2
• Spironolactone is the first-line diuretic, acting as an aldosterone antagonist at the distal convoluted renal tubule 7, 6
• Diuretics should be initiated at low doses and gradually increased while monitoring for complications (dehydration, electrolyte abnormalities, renal dysfunction) 1

Refractory Ascites

• Large-volume paracentesis plus albumin is the most feasible option when ascites no longer responds to diuretics 1, 4, 6
• If more than 5 L of fluid is removed, albumin infusion is required to prevent circulatory dysfunction 1
• Transjugular intrahepatic portosystemic shunt (TIPSS) is an alternative for carefully selected patients without advanced liver disease 1, 4, 6

Critical Pitfalls to Avoid

• Do not withhold paracentesis due to coagulopathy or thrombocytopenia—serious bleeding complications occur in less than 1/1000 procedures 1, 5
• Avoid ACE inhibitors and NSAIDs in cirrhotic patients with ascites as they worsen hypotension and renal function 2, 7
• Rule out spontaneous bacterial peritonitis at every hospital admission as it carries high mortality risk 1, 5