Z Gastroenterol 2001; 39: 12
DOI: 10.1055/s-2001-919023
Supplement

© Karl Demeter Verlag im Georg Thieme Verlag Stuttgart · New York

Mars in decompensated Alcoholic Liver Disease with Multi-Organ Failure

R. Jalan1 , D. Kapoor1 , C. Steiner1 , R. Williams1
  • 1Institute of Hepatology, University College London Medical School, London
Further Information

Publication History

Publication Date:
07 October 2005 (online)

NG, a 47 year old Caucasian male with more than 15 year history of hazardous alcohol consumption (8units/day) was admitted with a history of collapse.

There was no history of seizures or alcohol binge prior to this episode. The patient had been having malaise, fatigue and deepening jaundice for 4 months and increasing, painless abdominal distension of 1 month duration prior to admission.

There was no history of intravenous drug abuse, GI bleed, fever, oligo-anuria or history of hepatic encephalopathy in the past. He had undergone L orchidectomy and nephrectomy in the late second decade of life for indications not very clear from the history.

Examination revealed pallor, deep jaundice, pedal edema, cutaneous stigmata of chronic liver disease but no flaps and a hepatosplenomegaly but no shifting dullness. He developed fever, oliguria and increasing hepatic encephalopathy on the 3rd day of hospital admission with a derangement of kidney function tests.

The blood cultures grew Bacteroides species and he became progreesively septic, encephalopathic (Gd III) and anuric with severe metabolic acidosis. He was shifted to the ITU on the 6th day of hospital admission and treated with hemofiltration, N-acetyl cysteine (3 days) and supportive measures but failed to respond to therapy. After written, informed consent from the next of kin, patient was treated with MARS. The biochemical course before and during each of the MARS sessions (6 adequate sessions) is described in Figure [1] and [2]. Clinically, his HE was significantly improved but had 3 episodes of significant sepsis. He continued to remain anuric inspite of 6 sessions of adequate MARS therapy but died about 6 weeks after the onset of MARS treatment and intensive care due to fulminant sepsis.

Figure 1 Serum bilirubin levels with serial MARS treatments.

Figure 2 Prothrombin time with serial MARS treatments.

R. Jalan

Institute of Hepatology
University College London Medical School

69-75 Chenies Mews

London WC1E 6HX

Email: r.jalan@ucl.ac