ABSTRACT
Renal failure is a serious complication in patients with advanced cirrhosis. It occurs in about 20 % of patients hospitalized with cirrhosis. In about 70 % it is caused by prerenal failure, and in 30 % it is due to intrarenal causes. In about 70 % of patients with rperenal failure, renal function can be restored with fluid replacement, but the remaining 30 % are unresponsive to volume expansion. Minor increase in serum creatinine have been shown to be clinically relevant and can adversely affect survival. Therefore early efforts should be made to avoid precipitation of renal failure.Hepatorenal syndrome (HRS) is a fully reversible impairment of renal function in patients with cirrhosis unresponsive to volume expansion characterized by an acute progressive decrease in kidney function (serumcreatinin > 1,5 mg/dl) - type 1 HRS, whereas type 2 HRS features a decrease in kidney function over a long time, mostly in patients with refractory ascites. Therapy with vasoconstrictors like terlipressin to reverse splanchnic vasodilation, together with albumin is effective in 30-50 % of patients with HRS 1 and improves survival. The only effective longterm therapy is livertransplantation. An improvement of kidney fuction before transplantation is associated with a better outcome and posttransplant kidney function.
Subject(s)
Critical Care , Hepatorenal Syndrome/diagnosis , Liver Cirrhosis/complications , Liver Cirrhosis/diagnosis , Liver Failure/diagnosis , Liver Failure/therapy , Fluid Therapy , Hepatorenal Syndrome/etiology , Hepatorenal Syndrome/therapy , Humans , Kidney Function Tests , Liver Cirrhosis/therapy , Liver Transplantation , Lypressin/analogs & derivatives , Lypressin/therapeutic use , Prognosis , Serum Albumin/administration & dosage , Terlipressin , Vasoconstrictor Agents/therapeutic useABSTRACT
In a 63-year-old cirrhotic patient, recanalisation of a partial portal vein thrombosis was achieved by a low dose of rivaroxaban (10âmg daily). After anticoagulant therapy was stopped, partial vein thrombosis recurred. Restarting rivaroxaban at a dose of 10âmg led to recanalisation. The patient did not suffer any complications; in particular no bleeding occurred during 8 months of treatment.
Subject(s)
Morpholines/administration & dosage , Portal Vein/drug effects , Thiophenes/administration & dosage , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/drug therapy , Anticoagulants/administration & dosage , Dose-Response Relationship, Drug , Factor Xa Inhibitors/administration & dosage , Female , Humans , Middle Aged , Radiography , Rivaroxaban , Treatment OutcomeABSTRACT
BACKGROUND: In a pilot study, 9 patients (39-48 years) with acute decompensated heart failure and a cardiac index (CI) of 1.9 ± 0.3 l/min/m(2) were included after exclusion of an underlying hepatic disease. MATERIALS AND METHODS: The effect of levosimendan on liver blood flow and liver function was measured with the LiMON(®) system using the indocyane green plasma disappearance rate (ICG PDR). RESULTS: Levosimendan (Simdax(®)) infusion resulted in a significant increase of the CI, thus, achieving normal ranges of 2.9 ± 0.9 l/min/m(2) after 4 h and 3.3 ± 1 l/min/m(2) (p = 0.003) after 24 h. ICG PDR increased from 8.2 ± 0.8 % to 10.2 + 1.8 % after 4 h and to 11.9 ± 2.9 % after 24 h (p = 0.04). DISCUSSION: The reason for the early increase in systemic blood flow with no concomitant change in ICG PDR is not clear. A primary increase in liver blood flow with sustained low liver function might be one explanation; a low flow-mediated increased release of cytokines from liver cells with consequent deterioration of liver function is another possible explanation.
