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).