Acute esophageal necrosis is a rare syndrome with endoscopic findings of a diffuse circumferential pattern of black mucosa. Although underlying pathogenesis is unclear, it is known to have associations with malignancy. We present a rare case of a patient with a history of metastatic urothelial carcinoma who was found to have acute esophageal necrosis.

Cocaine is an indirect-acting sympathomimetic drug that inhibits norepinephrine and dopamine reuptake in the adrenergic presynaptic cleft. Cocaine use has been associated with strokes, angina, arrhythmias, and agitation. Data on gastrointestinal complications such as mesenteric ischemia, bowel necrosis, ulceration, and perforation are scarce. Here, we present a rare case of cocaine-induced esophageal, gastric, and small bowel necrosis that contributes to the limited literature on this subject. Diagnosis of cocaine-induced gastrointestinal complications involves a combination of imaging studies, laboratory assessments, and histopathological examinations. Timely surgical resection, supported by intravenous fluids, antibiotics, and pain management, is the mainstay of treatment. The prognosis varies but is significantly influenced by the promptness and effectiveness of the intervention, underscoring the importance of vigilant clinical care in such cases.

Acute esophageal necrosis (AEN) in the setting of gastric volvulus is a rare condition with only a handful of cases reported. Volvulus may contribute to AEN by limiting tissue perfusion and promoting massive reflux of gastric contents on compromised esophageal mucosa.
We reviewed 225 original articles, literature reviews, case series, brief reports, case reports, and discuss six total cases of co-occurring esophageal necrosis and gastric volvulus.
We present the first comprehensive analysis of all reported cases in the literature to date and formulate management strategies for the co-occurrence of AEN and volvulus. Management of AEN should be directed at correcting underlying medical conditions, providing hemodynamic support, initiating nil-per-os restriction, and administering high-dose proton pump inhibitor therapy. Surgical intervention is typically reserved for cases of esophageal perforation with mediastinitis and abscess formation.

BACKGROUND: Esophageal necrosis and perforation after thoracic endovascular aortic repair (TEVAR) for ruptured traumatic aortic aneurysm is extremely rare. It is difficult to manage, and patients rarely survive without treatment. Although, there is no certain consensus in relation with the optimal treatment we present a subsequent successful management of both life-threatening conditions.
METHODS: A 52-year-old man experienced a blunt chest trauma after motor vehicle collision with mild symptoms of pain and fractured ribs. On the 12th day he had severe chest pain and computed tomography (CT) revealed a ruptured traumatic thoracic aortic aneurysm with massive mediastinal hematoma. An emergency thoracic endovascular aortic repair (TEVAR) was performed. Several days later the patient developed a fever. CT suspected a pneumomediastinum, a sign of esophageal rupture, but no confirmation from esophagography and esophagoscopy was achieved. Because of deteriorated septic condition, patient was referred for exploratory thoracotomy. The rupture was found and esophagectomy was performed, with an esophagostomy and gastrostomy to enable enteral nutrition. Almost one year after the esophagectomy, gastric conduit reconstruction through the retrosternal route was performed. The patient was still alive and symptom-free more than 1 year after the reconstruction and no infection of the stent graft was observed.
CONCLUSIONS: We successfully managed a rare case of esophageal necrosis after TEVAR for ruptured traumatic thoracic aortic aneurysm. It is essential to diagnose the esophageal necrosis at an early stage and provide appropriate treatment to increase survival.

Necrotizing esophagitis is rare and poorly understood. The etiologies reported in what little has been published (i.e., gastroesophageal reflux exacerbated by gastric outlet obstruction and low-flow ischemia) seem somewhat simplistic and lack any direct evidence. The following paper illustrates a recent clinical case while laying out arguments supporting esophageal spasm as a possible contributing factor.

暂无摘要。

BACKGROUND: To review all the reported literature on acute esophageal necrosis.
METHODS: Databases were searched using the special Medical Subject Heading (MeSH) terms. All the available reported cases of acute esophageal necrosis were analyzed.
RESULTS: A total of 154 cases were identified and 130 cases were analyzed. The mean age of presentation was 61 years, and 70% of cases were males. The most common presenting symptoms were hematemesis in 66%, shock in 36%, melena in 33%, abdominal or substernal pain in 28%. The most common comorbidities reported were diabetes in 38%, hypertension in 37%, alcohol abuse in 25%, and chronic kidney disease in 16%. On upper endoscopy, 51% had a distal disease, 36% had pan esophageal, and only 2% had a proximal disease. 84% of patients were treated with IV Proton Pump Inhibitors, 22% received transfusions, 23% got antibiotics for underlying sepsis, 14% also received sucralfate, and 4% required surgery for treatment. The mortality rate was 32%, while perforation was reported in 5% and stricture formation reported in 9% of patients.
CONCLUSIONS: Patients with acute esophageal necrosis can have a favorable outcome if treated appropriately.