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Transjugular intrahepatic portosystemic shunt for refractory ascites in patients with high model for end‐stage liver disease scores

Ascites is a common complication of cirrhosis, developing in approximately 50% of compensated cirrhotic patients within 10 years of diagnosis. Ascites develops as a direct result of sinusoidal portal hypertension and associated splanchnic vasodilation causing an increasing portion of the circulating blood volume to be in the splanchnic bed. This leads to effective hypovolemia and a hyperdynamic circulatory state. Arterial pressure in this state is maintained through the activation of vasoconstrictor systems, including the renin-angiotensin-aldosterone system, the sympathetic nervous system, and in later stages, hypersecretion of arginine vasopressin. Starling forces in the hepatic sinusoids drive excess sodium and water into hepatic lymph. When the capacity of hepatic lymphatics to return the lymph into circulation is exceeded, the excess sodium and water spills into the peritoneal cavity to form ascites. This detailed knowledge of the genesis of ascites provides rational targets for treatment.