Black oesophagus, upside-down stomach and cameron lesions: cascade effects of a large hiatal hernia

Acute oesophageal necrosis, black oesophagus (BE) or Gurvits syndrome (GS) is a rare form of severe oesophagitis appearing as a striking circumferential discolouration of distal mucosa with various proximal extensions abruptly terminating at the gastro-oesophageal junction. It is most commonly associated with acute exacerbations of medical comorbidities, while associations with altered gut anatomy are rare. We present a unique constellation of BE, Cameron ulcers (CU), and gastric volvulus from a large paraesophageal hiatal hernia. Our patient recently recovered from COVID-19 and was malnourished and frail, while the expanding paraesophageal hiatal hernia turned into an acute organoaxial gastric volvulus with accompanying outlet obstruction. In low-flow post-COVID coagulopathic states, compensatory mechanisms may lack against gastric stunning and sudden massive reflux on the oesophagus. We additionally performed a systematic review and discovered additional cases with coexistent volvulus and paraesophageal hernia, although there are no previous reports of BE with CU, which makes this study the first.

Large Hiatal Hernia Associated with Cameron Ulcers and Consecutive Sideropenic Anemia: Case Presentation

BACKGROUND: Cameron lesions are seen in 5.2% of patients with hiatal hernia who undergo esophagogastroduodenoscopic examinations. The prevalence of Cameron lesions seems to be dependent on the size of the hernial sac, with an increased prevalence in the larger-sized sac. In about two-thirds of the cases, multiple Cameron lesions are noted rather than a solitary erosion or ulcer. AIM: The aim of this case report is to present the patient with Cameron ulcers associated with hiatal hernia. CASE PRESENTATION: Our patient presented with postprandial retrosternal pain, especially immediately after eating, vomiting, dyspnea, weight loss, fatigue, signs, and symptoms of severe hypochromic microcytic anemia without signs of acute gastrointestinal bleeding. No history of gastroesophageal disease. Colonoscopy was done and eliminate colic cause of anemia. The endoscopy showed a large hiatal hernia and linear erosions and ulcerations at the level of gastrodiaphragmatic contact (Cameron ulcers) and one non-sanguinant subcardial elipsoid ulceration. After conservative and operative treatment, there was significant clinically and laboratory improvement definitively, after 6 months. Cameron lesion is a rare cause of refractory sideropenic anemia. Diagnosis is very difficult in developing countries, where iron deficiency anemia is more common. A history of disease, clinical course, and laboratory findings are the important facts for diagnosis. CONCLUSION: Endoscopy is the gold standard for diagnosis, although it is not uncommon to overlook these lesions due to their unique location. There are two modalities for the treatment of Cameron lesions: Medical or surgical, which should be individualized for each patient. By severe refractory anemia and large hiatal hernia, associated with clinical signs, surgical approach is very important.