Successful resolution of symmetrical peripheral gangrene after severe acute pancreatitis: a case report

A 44-year-old Chinese man, who was an occasional smoker and social drinker, presented with complaints of acute pain in his upper abdomen and vomiting of particulate material resembling coffee grounds during the 24h before admission. His pain had developed 8–10h after consumption of Kaoliang liquor (3000ml of homemade liquor consisting of approximately 58% alcohol) over a period of 3 days while at home. Initially, he presented with epigastric pain, nausea, vomiting, and watery diarrhea. Because of aggravation of epigastric pain with subsequent vomiting of coffee ground–like material and passage of tarry stools, he was admitted to the emergency room by ambulance. His pain was dull, aching, and became aggravated upon eating. He had intractable vomiting approximately 30 times and subsequently vomited coffee ground–like material on the day of admission. His past medical history included two episodes of alcohol-related acute pancreatitis without mention of diabetes mellitus, claudication, cardiovascular disease, or illicit drug abuse. The patient denied steatorrhea, maldigestion, or recent body weight loss, which excluded possible chronic pancreatitis.

His initial vital signs revealed blood pressure of 74/27mmHg, heart rate of 152 beats/min, and body temperature of 38.7 °C. His clinical picture was compatible with systemic inflammatory response syndrome (SIRS) with shock status. His physical examination revealed that his abdomen was mildly distended with tenderness over the epigastric area. Chest, extremity, and other systemic examinations were unremarkable. Routine laboratory investigations revealed a hemoglobin level of 11.6g/dl, white blood cell count of 14,000/μl, amylase of 680U/L, lipase of 1125U/L, albumin of 2.0g/dl, total bilirubin of 0.61mg/dl, alkaline phosphatase of 110U/L, γ-glutamyl transferase of 70U/L, C-reactive protein of 24.49mg/dl, lactate dehydrogenase of 362U/L, and creatine phosphokinase of 489U/L. He had impaired renal function with blood urea nitrogen of 28mg/dl and creatinine of 2.3mg/dl. Impaired liver function with aspartate transaminase of 250U/L and alanine transaminase of 47U/L were also noted. He had high anion gap metabolic acidosis characterized by a lactic acid level of 5.75mmol/L, arterial blood pH of 7.058, bicarbonate level of 5.1mmol/L, anion gap of 32.1, and ethanol of 116mg/dl. His laboratory test result for serum ketone bodies was negative. His coagulation profile was consistent with SIRS with shock status and elevated D-dimer levels. His initial central venous pressure was recorded as 4mmHg. A diagnostic screen for sepsis showed unremarkable blood culture results (Table 1). His Ranson’s criteria scores were 3 on admission and 2 after 48h. Ultrasonography and computed tomography (CT) of the abdomen and abdomen revealed a picture compatible with acute pancreatitis, CT severity index grade E.

According to the revised Atlanta classification of pancreatitis, the patient was diagnosed with severe acute pancreatitis due to persistent organ failure (profound shock lasting for more than 48h and acute kidney injury with oliguria status after emergent hemodialysis).

He was treated promptly and aggressively with intravenous fluids with normal saline. His intravenous fluids were given as a 20ml/kg bolus, followed by a maintenance dose of 3ml/kg/h. He was also prescribed analgesic for pain relief. Because the patient had profound shock and a poor response to fluid resuscitation, a vasopressor was administered with intravenous norepinephrine at an infusion rate of 4μg/min for 2 days through the central venous line. This was discontinued after his blood pressure was restored. Upper GI panendoscopy was conducted because of vomitus of coffee ground material, which revealed a Mallory-Weiss tear and acute gastric ulcer with a history of recent hemorrhage. An antibiotic (ceftriaxone) and a proton pump inhibitor (omeprazole) were administered. Continuous renal replacement therapy was initiated for refractory acidosis and contrast media removal. The patient responded well to aggressive, conservative management. On the fourth day after hospitalization, a bilateral bluish discoloration of the fingers was noted. A gradual painful sensation developed 5 days after an acrocyanotic lesion was found (Fig. 1).

Dry gangrene and a limited range of motion of the fingers developed 9 days after the lesion was noted. Peripheral pulses were palpable in both the upper and lower extremities. The results of laboratory tests for SPG, comprising infection, malignancy, and the autoimmune system, were unremarkable (Table 1). Transesophageal echocardiography, carotid Doppler ultrasound, and sonography of the upper extremity vessels also were unremarkable. The patient was administered two doses of oral aspirin 75mg/day and two doses of oral pentoxifylline 400mg/day for 20 days. Because of upper GI tract bleeding noted on admission, heparin was not considered. The gangrenous lesion was kept warm and was not touched, as much as possible. The patient’s condition improved steadily over the next 7 days. His pain decreased, and his range of motion improved. Gradual desquamation of his finger skin occurred, with shedding of gangrenous scabs from the tips of his fingers and complete resolution (Fig. 2a, b). The patient was discharged from the hospital stay 26 days later. The patient responded well to the treatment and returned to his normal daily activities during outpatient follow-up.

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of written consent is available for review by the Editor-in-Chief of this journal.