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Polina Gaisinskaya, M.D.
Internal Medicine Resident
Florida Atlantic University, United States
Disclosure information not submitted.
Adrian Artiles, M.D.
Internal Medicine Resident
Florida Atlantic University, United States
Disclosure information not submitted.
Title: Vibrio vulnificus: Acute Esophageal Necrosis Emanating from Septic Shock
Case Report Body
Introduction: Acute esophageal necrosis (AEN), also known as Gruvitis syndrome, is characterized by a circumferential black esophagus which abruptly ends at the gastroesophageal junction and most commonly presents with gastrointestinal bleeding. Underlying comorbidities predispose patients to tissue hypoperfusion, resulting in ischemic injury to the esophagus. We present a patient with septic shock secondary to Vibrio vulnificus, exacerbated by underlying adrenal insufficiency, resulting in AEN.
Description: A 67-year-old male with adrenal insufficiency secondary to pituitary apoplexy presented with diarrhea and right elbow cellulitis. He initially injured his elbow after a fall and cleaned it with ocean water. He developed nonbloody emesis and loose stools. On arrival, he was tachycardic, febrile and hemodynamically stable. Abrasions and open wounds with sloughing of the skin, erythema, and serosanguinous discharge without crepitus or fluctuance were noted on right forearm. His condition worsened with episodes of hematemesis. His pressure dropped and was nonresponsive to fluids, requiring vasopressors. He was taken for wound debridement; subsequent cultures grew Vibrio vulnificus. EGD for GI bleed revealed diffuse esophageal ulceration, exudate covering the mucosa from the esophageal cricopharyngeus to the hiatus, areas of grey mucosa, and ischemic changes. In his stomach fundus, there was an eschar area with hyperemic edges. The necrotic esophagitis was presumed to be AEN. EGD three days later revealed spontaneous healing of the necrotic esophagus.
Discussion: Vibrio vulnificus can cause disease via two different routes – ingestion from raw shellfish in a healthy person, and septicemia in persons at risk via entry through lesions in the skin with contact from ocean water. It is rare for patients without underlying liver disease to become intensely ill from a skin infection. AEN in our patient was likely multifactorial from septic shock with underlying adrenal insufficiency, disabling him from responding appropriately, leading to ischemic injury. Treatment of AEN is early hemodynamic resuscitation and controlling underlying medical comorbidities. In this case, he was given the 30cc/kg fluid bolus, vasopressors, antibiotics, and stress dose steroids with full recovery.