S2177 Ibuprofen Impaction: No Pill Is Too Small

Abstract

Introduction: Acute esophageal necrosis (AEN) is an emerging cause of gastrointestinal bleeding with an increasing incidence over the past two decades. It appears as a circumferential necrotic lesion encircling the distal esophagus with various proximal extensions. It is most commonly associated with exacerbations of medical co-morbidities such as diabetes, renal failure, coronary disease;however cases of AEN due to mechanical alteration in gut anatomy are exceedingly rare and its prognosis is less defined. We present a unique constellation of AEN, Cameron ulcers (CU), and gastric volvulus from a large paraesophageal hiatal hernia. Case Description/Methods: A 77-year-old female began experiencing abdominal pain and repeated emesis. She had a history of COPD, GERD, episodes of bleeding ulcers, hiatal hernia, malnutrition, and recently COVID-19. She was hemodynamically stable, ill-appearing with tenderness to abdominal palpation and a negative stool guaiac. BP 106/48 mm/Hg, HR 107, requiring oxygen. Investigations revealed WBC 18.5 k/uL, Hgb 9.8 g/dL, and acute renal failure. A CT abdomen revealed complete herniation of the stomach into the posterior mediastinum, dilated esophagus, organoaxial gastric volvulus, and gastric distension [Figure 1 - Pane A-C]. IV fluids, pantoprazole 80 mg, and ondansetron 4 mg were given. An EGD revealed a large hiatal hernia, Cameron ulcers (CU), and necrotic ulceration along the mid-to-lower third of the esophagus. The patient deferred surgical intervention and was discharged home on hospice. Discussion: These constellations represent a common underlying pathophysiologic mechanism that stems from large hiatal hernias and their effect on surrounding structures in our case, precipitated by a paraesophageal hiatal hernia that became too large causing acute gastric volvulus. In severe presentations, the stomach may herniate into the posterior mediastinum known as an upside-down stomach requiring surgery while CU represents trauma to the mucosa from the hernia sliding. In our patient, lower esophagus blood flow traversing through the lesser gastric curvature may have been compromised during gastric necrosis. Simultaneously, sudden gastric stunning from acute outlet obstruction can lead to prolonged acidic bathing of the esophageal mucosa. Often the esophagus can compensate for this by increasing blood flow, however, this is compromised in low-flow states. Limitations of our study include lack of follow-up. A systematic review of all cases of AEN and gastric volvulus are in Table 1.