2 CASE REPROT
A 66-year-old male presented to our hospital with coffee-ground emesis, dyspnea, and general malaise. He also had abdominal pain and nausea. His medical history included type 2 diabetes mellitus, obstructive pulmonary disease, and alcohol abuse. He had not been taking his medication, including insulin, for several days due to nausea. His vital signs were as follows: Glasgow Coma Scale, 15 (E4V5M6); body temperature, 35.5 ℃; blood pressure, 103/79 mmHg; pulse, 100 beats per minute; and percutaneous oxygen saturation with a flow rate of 2 liters per minute through a nasal cannula, 100%. A physical examination revealed pallor conjunctiva and a coffee ground-like substance around the mouth. The abdomen was mildly tender without guarding. Other physical examinations revealed no remarkable findings. Laboratory analysis revealed severe hyperglycemia (730 mg/dL), normocytic anemia (hemoglobin level, 7.7 g/dL; mean corpuscular volume, 100.4 fL), high serum potassium (7.6 mEq/L), and a high level of blood urea (98.7mg/dL). A urine sample was positive for ketones and glucose, and serum β-hydroxybutyrate was elevated (2,132 μmol/L). Arterial blood gas analysis showed metabolic acidosis (pH, 7.29; HCO3, 10.5 mmol/L) (Table 1). Collectively, the patient was diagnosed with DKA and upper gastrointestinal bleeding.
The patient was resuscitated with intravenous fluids, and administered insulin by intravenous infusion for treatment of DKA. After approximately 48 h of insulin infusion, the daily plasma glucose profile improved. The patient underwent esophagogastroduodenoscopy (EGD) which showed a circumferential necrosis of the middle and distal portions of the esophagus with an abrupt transition at the gastroesophageal junction (Figure. 1A, 1B). A chest computed tomography revealed a thickened distal esophagus but excluded the presence of esophageal perforation. EGD also revealed a gastric ulcer on the lesser curvature of the upper body of the stomach with an exposed blood vessel (Figure. 1C). The exposed blood vessel was cauterized with hemostatic forceps. From the endoscopic findings, acute necrotizing esophagitis and hemorrhagic gastric ulcer were diagnosed. The patient was then treated with an intravenous proton pump inhibitor. A second EGD, performed one day after admission, showed no remarkable findings with circumferential black discoloration at the middle and distal portion of esophagus as compared to those the day before (Figure. 2A, 2B), and hemostasis of the gastric ulcer. The patient continued to improve with conservative management and he was subsequently discharged from the hospital in a stable condition. An EGD repeated 14 days after discharge showed complete healing of the necrotic-appearing mucosal change without stricture formation of the esophagus (Figure. 3A, 3B).