Ascites

Pathological accumulation of fluid within the peritoneal cavity. Cirrhosis with portal hypertension accounts for the large majority of cases in general practice, from a combination of portal hypertension driving splanchnic vasodilation, renal sodium retention, and hypoalbuminemia reducing oncotic pressure.

Other causes include malignancy (peritoneal carcinomatosis, typically an exudative, high protein ascites), heart failure and constrictive pericarditis, nephrotic syndrome, tuberculous peritonitis, and pancreatic ascites.

Abdominal distension, weight gain, discomfort, and, with large volume ascites, early satiety, dyspnea from diaphragmatic splinting, and umbilical hernia formation. Examination findings include shifting dullness (requires roughly 1.5 liters or more to detect reliably) and a fluid thrill in tense ascites. Associated features point toward cause: stigmata of chronic liver disease for cirrhotic ascites; peripheral edema, raised JVP, and orthopnea for cardiac ascites; weight loss and a fixed, irregular abdominal mass for malignant ascites; low grade fever, night sweats, and a background of TB risk for tuberculous peritonitis.

Diagnostic paracentesis is indicated for all new onset ascites and for any admission with known ascites, to characterize the fluid and exclude spontaneous bacterial peritonitis. The serum-ascites albumin gradient (SAAG, serum albumin minus ascitic albumin) is the key discriminating test: a gradient of 1.1 g/dL or greater indicates portal hypertension as the mechanism (cirrhosis, cardiac ascites, Budd-Chiari), with over 95% accuracy, while a gradient below 1.1 g/dL suggests a non-portal hypertensive cause (malignancy, tuberculosis, pancreatic ascites, nephrotic syndrome). Ascitic fluid neutrophil count above 250 cells per mm3 diagnoses spontaneous bacterial peritonitis regardless of SAAG or culture result. Additional ascitic fluid tests, guided by clinical suspicion, include cytology (malignancy), amylase (pancreatic ascites), and adenosine deaminase or culture (tuberculosis, though ascitic fluid culture sensitivity for TB is low and laparoscopic peritoneal biopsy may be needed). Abdominal ultrasound confirms and quantifies ascites and can guide safe paracentesis.

Differentials for the underlying cause are detailed above and in the Cirrhosis and Nephrotic Syndrome entries.

Cirrhotic ascites (the most common scenario) is managed with sodium restriction (below 2 g per day) and diuretics, typically spironolactone alone or in combination with furosemide in an approximately 100 to 40 mg ratio, titrated upward as tolerated with close monitoring of renal function and electrolytes. Large volume or tense ascites is managed with therapeutic paracentesis, with albumin replacement (6 to 8 g per liter removed beyond 5 liters) to prevent post-paracentesis circulatory dysfunction. Refractory ascites (not responding to maximal diuretic doses, or diuretic intolerant due to renal impairment or electrolyte disturbance) is managed with regular large volume paracentesis, TIPS in selected candidates, or liver transplant assessment. Malignant ascites is managed with therapeutic paracentesis for symptom relief, and, in selected cases, an indwelling peritoneal catheter for recurrent drainage or systemic anticancer treatment directed at the underlying malignancy. Cardiac ascites is managed by optimizing heart failure treatment (see Heart Failure entry) rather than aggressive diuresis targeted at the ascites alone. Spontaneous bacterial peritonitis, if diagnosed on paracentesis, is treated as detailed in the Cirrhosis entry, with IV antibiotics and albumin, and secondary antibiotic prophylaxis thereafter.

Referral: hepatology or gastroenterology for cirrhotic ascites, particularly if refractory; oncology for malignant ascites; urgent assessment for any patient with ascites and fever, abdominal pain, or new encephalopathy given the possibility of spontaneous bacterial peritonitis.