A 42-year-old man, drinker of more than 100 g of ethanol per day, with no other history of interest, reported a 3-day history (coinciding with an increase in habitual alcohol intake) of fever, jaundice, abdominal pain in the right hypochondrium and abdominal distension. Physical examination revealed frank muco-cutaneous jaundice, grade I encephalopathy and ascites. No enlargement of the liver or spleen was observed. Cardiorespiratory auscultation was normal. Laboratory tests on admission showed the following results: leukocytes 26,820 per µl (neutrophils, 77%), prothrombin activity 40%, plasma creatinine 1.9 mg/dl; urea 91mg/dl; total bilirubin 21mg/dl; AST 164 U/l; ALT 103 U/l; GGT 152 UI/dl. Hepatic viral markers were negative. Chest X-ray showed a right basal alveolar infiltrate and abdominal ultrasound showed a small liver with increased echogenicity and homogeneous structure; normal bile duct; patent portal vein, splenomegaly, abundant ascites. Computed axial tomography (CT) of the abdomen showed a small liver with lobulated contour.
With the clinical diagnosis of acute alcoholic hepatitis on chronic liver disease with severity criteria and a Maddrey score of 71, he was admitted to the gastrointestinal department. Treatment was started with corticosteroids, enteral nutrition and empirical antibiotic therapy. On the fifth day of stay, progression of hepatic encephalopathy to grade III and acute renal failure in the context of type I hepatorenal syndrome was observed. Laboratory tests showed a worsening of renal function with plasma creatinine values of 4.19 mg/dl; urea 140 mg/dl and total bilirubin 35.3 mg/dl, with persistent elevated transaminase values and alteration in prothrombin time.
Pentoxifylline (as anti-TNF therapy), terlipressin and albumin (as treatment for type I SHR) and MARS were added to the treatment, after requesting informed consent.
We performed 3 sessions, every other day, with admission of the patient to the Intensive Care Unit (ICU) for each session. The approximate duration of each session was 12 hours or until filter coagulation. Femoral venous access was used exclusively for this purpose. The associated renal replacement technique was continuous veno-venous HDF. Anticoagulation was variable with epoprostenol sodium 5 ng/kg/minute, with heparin Na 5U/kg/hour or with both. The patient was haemodynamically stable during the sessions, with no notable incidents.