A rare and threatening complication in a cirrhotic patient

Excerpt

We present the case of a 72-year-old man with alcoholic cirrhosis Child–Pugh B (9 points) complicated by esophageal variceal bleeding in the past, hepatic encephalopathy (HE), and ascites. He was admitted to our department for HE. Laboratory analysis showed pancytopenia, INR 1.4, normal liver function tests, serum creatinine 3.56 mg/dL, urea 171 mg/dL, C-reactive protein of 8.39 mg/dL, bilirubin of 3.2 mg/dL and albumin of 2.74 mg/dL. On urinalysis, a leukocyturia was found; and on urine culture, Escherichia coli was isolated. Spontaneous bacterial peritonitis was excluded. Facing a decompensated liver cirrhosis Child–Pugh C (10 points) with hepatic encephalopathy in the context of urinary tract infection and acute kidney injury stage 3, he was started on ceftriaxone 2 g/day and albumin (60 g/day). After excluding other etiologies, hepatorenal syndrome type 1 was presumed. Despite initial improvement (creatinine 3.02 mg/dL) with the administration of albumin, 10 days later his creatinine reached a level of 4.9 mg/dL. Terlipressin was instituted in a dose of 1 mg every 6 h, which was optimized to 2 mg every 6 h due to lack of improvement. The day after this dose escalation, he developed skin necrosis on the tip of the first digit of the left foot (Fig. 1a), and cyanosis of all of the fingers of the right foot with initial signs of necrosis of the third, fourth and fifth digits (Fig. 1b). These changes were most likely due to terlipressin-induced skin necrosis; therefore, this medication was immediately stopped. Ischemic features improved in a few days with the complement of surgical debridement.

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