INTRODUCTION: Acute gastric necrosis is rarely encountered given the stomach's rich vascular distribution and collateral circulation. Reported causes of gastric necrosis include gastric outlet obstruction, intrathoracic herniation, ingestion of caustic substances, anorexia nervosa and bulimia, and systemic hypotension. We present a case of “black stomach” secondary to persistent shock in the setting of end-stage liver disease. CASE DESCRIPTION/METHODS: A 33-year-old female with a history of primary sclerosing cholangitis status post orthotopic liver transplant in 2017 was initially hospitalized for pneumonia complicated by worsening graft function (MELD 38). Liver biopsy confirmed recurrent PSC with cirrhosis. Her course deteriorated after developing multiple episodes of coffee-ground emesis and melena requiring pressors. Initial EGD showed mild portal hypertensive gastropathy and two, 5 mm clean-based ulcers in the gastric antrum. No esophageal varices were visualized. Despite medical therapy, her melena and hypotension continued, leading to acute renal failure requiring CVVH. Repeat EGD two days later showed an adherent clot in the gastric fundus and severe portal hypertensive gastropathy with spontaneous oozing. Despite supportive measures, she continued to have melena. A third EGD showed a large blood clot in the fundus that was unable to be removed. Friable mucosa was noted throughout, as well as a non-healing, clean-based antral ulcer. Two days later, a fourth EGD revealed mucosa in the fundus and proximal body that appeared black and diffusely necrotic with sloughing of mucosa, with normal mucosa distally. The patient was not a candidate for IR embolization, TIPS procedure or surgery. One week later, she decompensated and died of septic shock from VRE bacteremia. DISCUSSION: Our case demonstrates that persistent gastric ischemia in the setting of shock and underlying end-stage liver disease results in gastric necrosis noted endoscopically over the course of a week. It is possible that the patient's underlying decompensated graft cirrhosis predisposed her to developing segmental gastric necrosis and “black stomach” in the area supplied and drained by the left gastric vessels, which can be affected by shock and portal congestion. Despite aggressive measures and supportive care, gastric necrosis carries a high morbidity and mortality. Therefore, a high index of clinical suspicion is required to make an early diagnosis in order to guide potential therapeutic interventions in such critically ill patients.
Read full abstract