Ascites is the pathological accumulation of free fluid within the peritoneal cavity. It is most often a manifestation of advanced liver disease, in which cirrhosis raises sinusoidal pressure and portal hypertension drives fluid into the abdomen, compounded by splanchnic vasodilation, sodium and water retention, and …
Ascites is the pathological accumulation of free fluid within the peritoneal cavity. It is most often a manifestation of advanced liver disease, in which cirrhosis raises sinusoidal pressure and portal hypertension drives fluid into the abdomen, compounded by splanchnic vasodilation, sodium and water retention, and reduced oncotic pressure from hypoalbuminemia. Non-hepatic causes include congestive heart failure, peritoneal malignancy, infection such as tuberculosis, and renal disease, each producing fluid with distinct characteristics. Because the underlying mechanism differs, diagnostic paracentesis with calculation of the serum-ascites albumin gradient is central to distinguishing portal hypertensive from other origins, alongside cell count, culture, and cytology to detect spontaneous bacterial peritonitis or malignant involvement. In chronic liver disease, ascites marks hepatic decompensation and carries prognostic weight, while non-invasive assessment of liver stiffness and portal pressure helps characterize disease severity. Clinically, ascites presents with abdominal distension, weight gain, and discomfort, and may impair respiration when tense. Management is directed at the cause and at the fluid burden: in cirrhotic ascites this centers on dietary sodium restriction and diuretics, escalating to large-volume paracentesis, and in refractory cases to transjugular intrahepatic portosystemic shunting or consideration of transplantation. Treating reversible drivers such as viral hepatitis and heart failure, and vigilance for infection and renal dysfunction, are integral to care, since ascites reflects systemic derangements rather than an isolated abdominal finding.
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