Ascites

Did You Know?

• Ascites was possibly seen as a punishment for oath-breakers among the Proto-Indo-Europeans, based on Hittite military oaths and Vedic hymns.
• A similar curse dates to the Kassite dynasty (12th century BC).
• Amounts of ascitic fluid up to 35 liters are possible.

Signs and symptoms

Mild ascites is difficult to notice, but severe ascites causes abdominal distension. Individuals typically report progressive abdominal heaviness and pressure, along with shortness of breath from mechanical pressure on the diaphragm. Physical examination may reveal flank bulging when reclining, shifting dullness on percussion, or a fluid thrill in massive ascites. Signs of the underlying cause may also appear: leg swelling, bruising, gynecomastia, hematemesis, or mental changes in portal hypertension; chronic fatigue or weight loss in cancer-related ascites; and shortness of breath, wheezing, or exercise intolerance in heart failure.

Diagnosis

Routine tests include complete blood count, basic metabolic profile, liver enzymes, and coagulation studies. Diagnostic paracentesis is recommended for new or hospital-admitted ascites; the fluid is examined for gross appearance, protein, albumin, and cell counts, with additional cultures, Gram stain, or cytopathology as indicated. The serum-ascites albumin gradient (SAAG) is preferred over older transudate-exudate measures: a gradient above 1.1 g/dL points to portal hypertension, while below 1.1 g/dL suggests a non-portal hypertensive cause. Ultrasound often precedes fluid removal, revealing organ size and shape, and Doppler studies can assess portal vein flow and detect Budd–Chiari syndrome or portal vein thrombosis. CT scan provides more accurate organ morphology. Uncomplicated ascites is graded: Grade 1 (visible only on imaging), Grade 2 (flank bulging and shifting dullness), Grade 3 (visible with fluid wave). Refractory ascites recurs or persists despite diet and diuretics, and includes diuretic-intractable and diuretic-resistant subtypes.

Pathophysiology

Ascitic fluid may be a transudate from increased portal vein pressure (over 8 mmHg, typically around 20 mmHg in cirrhosis) or an exudate from inflammation or malignancy. Exudates have high protein and lactate dehydrogenase, low pH (<7.30), low glucose, and more white blood cells; transudates have low protein (<30 g/L), low LDH, high pH, normal glucose, and fewer white cells. The serum-ascites albumin gradient is clinically most useful: a difference under 1 g/dL implies an exudate. Portal hypertension raises capillary hydrostatic pressure in the splanchnic bed. Fluid sequestration stimulates renal retention via aldosterone, sympathetic activation, and increased renin from reduced kidney perfusion, potentially leading to hepatorenal syndrome. Spontaneous bacterial peritonitis can occur due to decreased antibacterial factors like complement in the fluid.

Treatment

Treatment aims to relieve symptoms and prevent complications while investigating the underlying cause. Mild ascites is managed as an outpatient, with a weight loss goal of no more than 1.0 kg/day if peripheral edema is present, or 0.5 kg/day if ascites alone. Salt restriction is initial therapy, effective in about 15% of cases; water restriction is added if serum sodium falls below 130 mmol/L. Spironolactone, starting at 100 mg/day (max 400 mg/day), is the drug of choice, blocking the aldosterone receptor; 40% of patients respond. For nonresponders, furosemide 40 mg/day (max 160 mg/day) or another loop diuretic may be added, with a 100:40 ratio to reduce potassium imbalance. Serum potassium and renal function are monitored. Diuresis is tracked by daily weight; if weights are unavailable, urinary sodium-to-potassium ratio >1 predicts negative sodium balance. Diuretic resistance can be assessed by giving 80 mg intravenous furosemide after 3 days without diuretics; urinary sodium excretion under 50 mEq over 8 hours indicates resistance. Severe tense ascites requires hospitalization for paracentesis.