Acute esophageal necrosis, also known as black esophagus or acute necrotizing esophagitis is a rare condition with roughly 154 cases reported in the literature. This condition is classically diagnosed on its endoscopic findings of a circumferentially black esophagus that abruptly ends at the gastroesophageal junction and transitions to normal gastric mucosa. When present, acute esophageal necrosis potentially signifies a poor prognosis with an overall mortality up to 36%. This case report describes a critically ill patient with multiple comorbidities that was found to have acute esophageal necrosis the entire length of the esophagus secondary to ischemia/hypoperfusion that was caused by diabetic ketoacidosis. The patient had a prolonged hospitalization but was ultimately discharged in stable condition. We also review the literature of this rare esophageal condition.
We set out to investigate the mechanism(s) of hemodialysis (HD)-induced hyperthermia. We found that the increase in rectal temperature (T) during HD exceeds that due to circadian changes observed during the day off HD (0.48 versus 0.15 °C; p < 0.05). To assess the role of heat transfer from dialysate to blood, we increased dialysate T from 34 to 38 °C and observed a proportional increase in rectal T (r = 0.75). However, even when heat transfer from dialysate to blood was totally prevented rectal T still rose by 0.67 ± 0.41 (SD) °C. To assess if endogenous pyrogen could account for this increase in rectal T we performed HD with sterile dialysate (to exclude the potential contamination of standard dialysate) and during intravenous aspirin infusion (1 g before HD followed by continuous infusion of 4 mg/min) to block the effect of endogenous pyrogen on the thermoregulatory center. Both these procedures failed to prevent the increase in rectal T observed in the standard control HD. In conclusion, HD hyperthermia is not accounted for by circadian variations in body T, or by passive heat transfer from dialysate to blood. We failed to obtain indirect evidence to support the hypothesis that dialysis hyperthermia is caused by endogenous pyrogen production.
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