Terlipressin-Induced Skin Necrosis and Rhabdomyolysis

Abstract

CLINICAL PRESENTATION A 54-year-old man without known cardiovascular diseases was referred for alcoholic cirrhosis with jaundice and tense ascites. Laboratory data were significant for creatinine 2.5 mg/dL, bilirubin 4.5 mg/dL, C-reactive protein 79 mg/L and international normalized ratio 2.6. After the diagnosis of spontaneous bacterial peritonitis was made, antibiotic and albumin treatments were started. The course was complicated by hepatorenal syndrome with severely suppressed natriuresis ( 5 mEq/L), and intravenous bolus terlipressin (Haemopressin, Meduna Pharmaceuticals, Isernhagen, Germany; 1 mg/6 hour) was instituted, at first-restoring urine output. After 48 hours, ischemic skin changes became apparent with numerous areas of full-blown necrosis in flanks (Figure 1A) and limbs. In addition, the scrotal skin appeared edematous and critically underperfused (Figure 1B). Diuresis declined again, and the urine turned deeply dark (Figure 1C) with an increase of creatine kinase to 15,000 U/L. Terlipressin was stopped, and dialysis was started. The skin condition gradually improved under local therapy, and creatine kinase levels normalized, but the patient finally succumbed 3 weeks later owing to septic complications. As a long-acting vasopressin analogue significantly lowering portal pressure, terlipressin is in clinical use for variceal hemorrhage and hepatorenal syndrome. Owing to its vasoconstrictory effects, ischemic complications are not uncommon, mostly affecting cardiac, splanchnic or peripheral circulation. Likely attributable to compromised tissue oxygenation by microcirculatory failure, ischemic skin and muscle injury are among the rarer but well-recognized adverse reactions to terlipressin.1,2