Hepatorenal syndrome treatment and management: a case report

Our aim is to report a case of a patient that came to our observation with a severe clinical picture of decompensated cirrhosis HCV and abuse of alcohol related, with ascites apparently resistant to diuretic therapy, black jaundice etc. Six months ago he has been admitted to intensive care of another hospital because of esophageal varices bleeding with hepatic encephalopathy and hepatic coma. During the hospitalizationit has been placed a transjugular intrahepatic portosystemic shunt (TIPS) and an endoprosthesis into the portal vein. At discharge the patient has been introduced to the program of hepatic transplantation. One month ago during an hepatic echography it has been highlighted thrombosis of the TIPS and endoprosthesis, into the portal system and finally of the over-hepatic veinsAt admission to our hospital he presented a large ascites, oliguria and black jaundice.In the meanwhile, with the aim to clarify better the hepatic damage and the compromise of his circulation, it was performed an abdominal angiotomography, upon pre-medication of sodium bicarbonate, that confirmed a complete thrombosis of the TIPS from the outflow into inferior cava as far as the level of splenic vein, and revealed thrombosis of over-hepatic veins, obstruction of the right branch and partial thrombosis of the portal vein with several collateral hepatofugal circulations; cholelitiasis; normal kidneys. It was established a suitable therapyfor the ascites including an antialdosteronic drug, i.e. canrenone, furosemide,and propranolol but it occurred a resistance to diuretic therapy. As we supposed an HRS we proceeded therefore to volume expansion with albumin i.v. at high doses without any effect; the introduction of dopamine did not improve renal function, while a vasoconstrictor vasopressin analog long acting drug the terlipressin, plus albumin, during a week, obtained an improvement in GFR and the reduction in serum creatinine. With the aim of keeping these results using a practical, long term, and simpler oral therapy, we discontinued the treatment with terlipressin and decided to give midodrine plus albumin (even if without octreotide) to obtain an increase of at least 15 mm Hg in mean arterial pressure, and a satisfactory, stable control of kidney function and, managing that properly, to prevent possible supine hypertension.The ideal treatment of HRS is liver transplantation, but because of the long waiting lists in the majority of transplant centers, most patients die before.Our patient won’t be able to underwent to transplantation both because of the serious compromise of his hepatic vascular bed, and of the possible evolution to malignancy: his prognosis is certainly bad at short-term, but his quality of life could be better thanks to these therapies.