Spontaneous bacterial
peritonitis (SBP), refractory
ascites,
hepatorenal syndrome (HRS),
hyponatremia and
hepatic encephalopathy are complications which frequently happen during a
clinical course of decompensated
cirrhosis. Splanchnic and peripheral vasodilatation, increased intrarenal vasoconstriction and impaired cardiac responsive function are pathological changes causing systemic and hemodynamic derangement. Extreme renal vasoconstriction leads to severe reduction of renal blood flow and glomerular filtration rate, which finally evolves into the clinical feature of HRS. Clinical manifestations of type 1 and type 2 HRS come to medical attention differently. Patients with type 1 HRS present as
acute kidney injury whereas those with type 2 HRS will have refractory
ascites as the leading problem. Prompt diagnosis of type 1 HRS can halt the progression of HRS to acute tubular
necrosis if the combined treatment of
albumin infusion and
vasoconstrictors is started timely. HRS reversal was seen in 34%-60% of patients, followed with decreasing mortality. Baseline serum levels of
creatinine less than 5 mg/dL,
bilirubin less than 10 mg/dL, and increased mean arterial pressure of over 5 mmHg by day 3 of the combined treatment of
vasoconstrictor and
albumin are the predictors of good response. Type 1 HRS can be prevented in some conditions such as
albumin infusion in SBP, prophylactic
antibiotics for upper
gastrointestinal hemorrhage,
albumin replacement after large volume paracentesis in cirrhotic patients with massive
ascites. The benefit of
albumin infusion in
infection with primary source other than SBP requires more studies.