Black esophagus, also called Gurvits syndrome or acute esophageal necrosis (AEN), is a rare, life-threatening condition characterized by necrosis of the esophageal mucosa. We present a 36-year-old man who presented with hematemesis and was admitted for diabetic ketoacidosis (DKA) management. He then had a further episode of hematemesis with hemodynamic instability.The esophagogastroduodenoscopy (EGD) revealed ulcerative, necrotizing, circumferential esophagitis in the middle and distal third of the esophagus. The patient was treated with intravenous fluid resuscitation, proton pump inhibitors, empiric antibiotics, and antifungals. Hematemesis in DKA should raise suspicion for black esophagus. Prompt detection of AEN allows for early management and thus reduces mortality and associated complications such as perforations and strictures.
Introduction: Acute esophageal necrosis, or black esophagus, is a rare clinical entity manifesting as upper gastrointestinal bleeding and complicating various conditions. However, black esophagus in the setting of diabetic ketoacidosis (DKA) has been rarely reported. We present a case of a 36-year-old male with black esophagus presenting as hematemesis complicating an episode of DKA. Case Description/Methods: A 36-year-old male with uncontrolled type 1 diabetes mellitus complicated by end-stage renal disease and hypertension presented to the emergency department with abdominal pain, nausea, and vomiting. Patient reported worsening abdominal pain and associated blood-tinged emesis. On presentation, patient was hemodynamically stable. Physical exam included an abdomen that was diffusely tender to palpation without peritoneal signs. Initial labs remarkable for serum glucose 1491, anion gap 41, bicarbonate 9, and hemoglobin 7.5. Patient was admitted to Critical Care for insulin drip and intravenous fluid resuscitation for DKA. Later, patient had an episode of hematemesis resulting in tachycardia, hypotension, and drop in hemoglobin to 5.6. Patient was further resuscitated with blood transfusions with improvement in hemodynamics and hemoglobin to 8.9. Continuous pantoprazole infusion was initiated. Upper endoscopy demonstrated severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding. No biopsies were taken due to concern for possible false lumen; CT chest with contrast demonstrated no signs of esophageal perforation. Following EGD, patient had several small self-limiting episodes of hematemesis and melena, while maintaining hemodynamics. He was continued on pantoprazole infusion and placed on strict nothing by mouth (NPO) precautions for 3 days with gradual advancement of diet. He received 6 days of empiric antimicrobial therapy with ampicillin-sulbactam and fluconazole. Patient reported no further episodes of hematemesis. Hemoglobin stabilized around 8.0 (Figure). Discussion: DKA is a rare but life-threatening cause of acute esophageal necrosis which may develop due to a combination of tissue hypoperfusion, impaired mucosal defenses, and gastric reflux. Upper gastrointestinal bleeding in the setting of DKA should raise suspicion for black esophagus which is a potential cause of mortality. Early diagnosis and treatment of underlying etiology are the key factors in management.
Solitary extramedullary plasmacytoma (SEP) is a rare tumor due to the monoclonal proliferation of plasma cells without bone marrow involvement. Plasmacytomas are frequently encountered in bone or soft tissue but rarely occur in the gastrointestinal (GI) tract. They can present with a multitude of symptoms depending on their site. This report describes a case of SEP diagnosed as a duodenal ulcer (DU) during esophagogastroduodenoscopy (EGD) for iron deficiency anemia.
Case Description/Methods: In this case, we present a 26-year-old male with a history of auto-brewery syndrome presenting with bilateral lower extremity paralysis, sensation loss, and neuropathy. These symptoms were similar to an episode which was inconclusive. He consumed alcohol occasionally but was sober at that time. During that stay, he was diagnosed with auto-brewery syndrome. In ED, his blood alcohol was 493mg/dL, although he was sober for 1 year, and his liver function tests were significantly elevated with AST twice the level of ALT, consistent with findings of alcoholic liver injury. There was some return of neurological and hepatic function over the hospital stay with supportive care. He was placed on a consistent carbohydrate diet and his LFTs subsequently improved. Discussion: While there is data on potential causes and causative organisms for this condition, there is little in the literature on the potential sequelae associated with auto-brewery syndrome. Chronic alcoholism and its effects are widely seen and studied. From alcohol neuropathy to cirrhosis, the effects of consistent alcohol consumption are deleterious to one's health. The question that needs to be asked is: are patients with chronic exposure to endogenous alcohol at risk for the same complications seen in chronic alcoholism? Cirrhosis, which is seen as a risk factor for ABS, may actually be a consequence of ABS. In this patient, his AST and ALT were mildly elevated, even during previous admission. Therefore, the patient may have been experiencing chronic liver injury from alcohol use while sober, placing him at increased risk for NASH and eventually cirrhosis at a much earlier onset than expected. It would be imperative in this case to ensure that the patient is on a limited intake of carbohydrates, or antifungals if necessary.
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