Abstract
A 47-year-old male with many years of heavy alcohol use was admitted for several days of worsening lower limb swelling, abdominal distension, jaundice, and watery diarrhea. He denied fever, chills, rigors, abdominal pain, or confusion. There was no history of intravenous drug use or the taking of prescription or over-the-counter medications. There was no family history of liver disease. Vital signs were unremarkable. Physical examination notable for jaundice, palmar erythema, numerous spider angiomata on the chest, abdominal distension with shifting dullness, and lower extremity edema extending to the thighs were noted. The patient was not confused and did not demonstrate asterixis. Laboratory studies were significant for WBCs 15.4/lL (4–10.6), INR 1.5 (0.8–1.2), potassium 2.9 mmol/L (3.5–5.1), creatinine 0.7 mg/dL (0.8–1.3 mg/dL), albumin 2 g/dL (3.5–4), ALT 84 U/L (12–78), AST 290 U/L (10–37), bilirubin 27.1 mg/dL (0.2–1) with direct fraction of 21.3 mg/dL (0.1–0.4). Tests for the presence of Wilson’s disease, hemochromatosis, viral hepatitis A, B, and C, autoimmune hepatitis, and hepatitis due to toxic substances were all negative. Alpha fetoprotein was 3.1 ng/mL (\15 ng/mL). Liver ultrasound was reported as showing hepatomegaly, splenomegaly, and ascites. Diagnostic paracentesis revealed findings consistent with non-infected portal hypertensive ascites. Stool tested positive for Clostridium difficile toxin by ELISA. The patient was diagnosed with Clostridium difficile colitis, alcoholic hepatitis (AH), and probable liver cirrhosis. The Model for End-Stage Disease (MELD) score was 23, and Maddrey’s Discriminant Function (DF) score was 39, indicating severe AH. Due to the elevated DF, pentoxifylline plus nutritional support was administered in preference to corticosteroid therapy due to the Clostridium difficile infection. Oral vancomycin was also initiated, together with furosemide and spironolactone for the ascites and the lower limb swelling. After several days of treatment, the diarrhea resolved, the lower limb swelling improved, and serum bilirubin concentrations improved to 24.3 mg/dL (0.2–1 mg/dL). He was discharged home with the plan to continue pentoxifylline for 28 days and to complete 14 days of oral vancomycin treatment for the severe Clostridium difficile infection. The patient continued to drink alcohol and over the following months had several admissions for ascites and worsening lower extremity swelling. Prednisone therapy was initiated due to the MELD score rising to 30 and DF score to 45. The use of diuretics was limited by serum creatinine rising to 2.2 mg/dL (0.8–1.3 mg/dL), necessitating serial therapeutic paracenteses. Given the poor prognosis with unlikely regression of his cirrhosis, palliative care evaluation was obtained without any hepatologic consultation with the patient electing hospice care with peritoneal drain placement for convenience. After enrollment in hospice, he was able to successfully discontinue alcohol and limit salt intake, and when evaluated several months later, his ascites had resolved, enabling K. Khirfan J. Alcorn Division of Gastroenterology and Hepatology, University of New Mexico School of Medicine, Albuquerque, NM, USA
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