Acute esophageal necrosis (black esophagus): a case report and literature review

Excerpt

A 49-year-old male patient, affected by type 2 diabetes mellitus, in oral therapy with metformin, complicated by infected diabetic foot with osteomyelitis of two fingers of the right foot, was admitted to emergency room in sleepy state, with a brief history of fever in previous days. Laboratory study revealed the presence of a septic condition characterized by increased levels of procalcitonin (16,10 ng/ml) and C-reactive protein (96,90 mg/l); lactic acidosis (pH 6.97, HCO₃ 3,4 mmol/l, pCO₂ 14,7 mmHg, pO₂ 162 mmHg, lactacidemia 10 mmol/l); acute renal impairment (creatinine 10.3 mg/dl, ureic nitrogen 299 mg/dl); neutrophilic leucocytosis (WBC 21.51 × 10³/μl, neutrophils 14.81 × 10³/μl); hyperglycemia (202 mg/dl) was also present. He was immediately admitted to intensive care unit and treated with hemodialysis by insertion of a central venous cannula. He rapidly got better, and in 2 days he was transferred to internal medicine ward. A rehydratant and empirical antibiotic treatment was started with a strict control of glycemic values with basal-bolus insulin protocol. A phlegmon of the right foot was treated on the second day by incision and wadding. The acid–base study showed moderate respiratory alkalosis. Renal function rapidly improved, without further need of dialysis. Hemodynamic condition was stable with onset of polyuria up to 4.5 l/day, treated with water and electrolytes replacement by intravenous infusions and oral intake by the patient. On the seventh day after admission, the patient reported light dysphagia. Examination of oropharynx revealed hyperemia and white patches in oral cavity, resembling oral candidiasis of tongue and soft palate. Treatment with oral antifungal gel (miconazole) was started. On the 12th day after admission, the patient had vomit of food with emission of bloody mucus. Endoscopy was performed, which revealed “widely exulcerated esophageal mucosa, from superior esophageal sphincter toward cardiac sphincter, that is relaxed. Slight hyperemia of gastric antral mucosa” (Fig. 1). The patient was placed on “nil per os,” with parenteral nutrition and I.V. proton-pump inhibitors. Therapy with antifungal drugs (I.V. fluconazole) and antivirals (I.V. acyclovir) was started. Antiviral treatment was started in consideration of the fact that in some cases esophageal necrosis may have a herpetic etiology, potentially curable.

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