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.

Patients with acute esophageal necrosis often present with hematemesis and upper gastrointestinal bleeding. Our case report describes a patient\'s incidental discovery of black esophagus without recent hemodynamic instability, symptoms, or evidence of blood loss anemia. As illustrated in this case, it is important to recognize these findings in patients without classic signs and symptoms to act promptly and prevent tissue ischemia or perforation. Early recognition can also help reduce the risk of long-term complications such as stricture formation. Thus, a high index of suspicion is essential for the diagnosis of acute esophageal necrosis.

Black esophagus or acute esophageal necrosis (AEN) is a rare cause of upper gastrointestinal (UGI) bleeding usually involving distal esophagus. Proximal esophageal involvement is quite rare. We present an 86-year-old female with active coronavirus disease 2019 (COVID-19) infection who came in with newly diagnosed atrial fibrillation and was started on anticoagulation. She subsequently developed a UGI bleed, which was complicated by inpatient cardiac arrest. Following resuscitation and stabilization, UGI endoscopy showed circumferential black discoloration of proximal esophagus, with distal esophageal sparing. Conservative management was instituted and fortunately, repeat UGI endoscopy two weeks later showed improvement. This describes the first case of isolated proximal AEN in a COVID-19 patient.

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.

Acute esophageal necrosis is a rare condition, characterized by a distinctive endoscopic/necropsic image-circumferential black area of the esophagus. This paper presents a case of a 78-year-old patient with recent history of a severe form of COVID-19 (2 months previously), with multiple comorbidities, which presents sudden death in hospital. Anatomic-pathological autopsy showed extensive esophageal necrosis, pulmonary thromboses, and coronarian and aortic atherosclerosis. The histopathological examination revealed necrosis of the esophageal mucosa and phlegmonous inflammation extended to the mediastinum, chronic pneumonia with pulmonary fibrosis, viral myocarditis, papillary muscle necrosis, and pericoronary neuritis. Thromboses and necroses were identified also in the liver, pancreas, and adrenal glands. Post-COVID-19 thromboses can manifest late, affecting various vascular territories, including esophageal ones. Their clinical picture may be diminished or absent in elderly and/or diabetic patients.

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.

The \"black esophagus\" or \"acute esophageal necrosis\" is a very rare condition of the esophagus that is believed to have a multifactorial etiology and usually involves the distal esophagus. We present a case of a 66-year-old gentleman who presented with a history of retching followed by one episode of hematemesis two days after his left inguinal hernioplasty. His esophagogastroduodenoscopy showed diffuse ulceration and erosions throughout the esophagus, necrosis of the distal esophageal mucosa till the gastroesophageal junction, and a healed ulcer in the first part of the duodenum. He was managed with supportive care and discharged home in a stable condition.

Acute esophageal necrosis (AEN) is a rare and often fatal pathology of unclear etiology affecting the distal two-thirds of the esophagus. Typically, elderly patients with multiple comorbidities present with signs of upper gastrointestinal (GI) hemorrhage. On endoscopy, the mucosa is black due to ischemic necrosis, resulting in the commonly used term \"black esophagus.\" We present a rare case of a 61-year-old male presenting with shortness of breath and hematemesis diagnosed as AEN through endoscopy. This case illustrates the importance of considering AEN as part of differential diagnoses in a rising elderly population with multiple comorbidities that present with upper GI hemorrhage. Treatment should be aimed at maintaining hemodynamic stability with high-dose proton pump inhibitors.