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.

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.

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.

BACKGROUND: Esophageal varices are a result of progressive liver disease and portal hypertension. Treatment can be performed with band ligation versus non-selective beta blockers depending on the size of varices, ability to tolerate medications and history of variceal bleeding. Band ligation is an effective intervention with rare but serious complications including bleeding, ulcers and rarely obstruction. Few cases of esophageal obstruction and necrosis caused by banding have been reported, each with varied management from conservative treatment to band removal.
METHODS: An 89 years old woman with a past medical history of nonalcoholic steatohepatitis cirrhosis presented to the hospital with an inability to swallow one day after screening esophagogastroduodenoscopy where band ligation of esophageal varices was performed for primary prophylaxis. The patient was not able to tolerate her oral secretions. Initial blood work revealed a Model of End Organ Liver Disease score of 7. She was treated with sublingual nitroglycerin for esophageal spasm, a known complication after esophageal banding. When she failed to improve, esophagogastroduodenoscopy was performed and revealed the mucosa surrounding the banded varix was necrosed and blocking the lumen of the esophagus. The band was purposefully dislodged, revealing distal ulceration and stricturing. Within 72 h after band removal, she was tolerating an oral diet. Endoscopy performed 2 wk later revealed an intrinsic stenosis, measuring 8 mm in diameter by 1 cm in length, which was dilated.
CONCLUSIONS: Esophageal obstruction is a complication of variceal banding that should be considered in patients with inability to tolerate oral diet after banding.

The ingestion of corrosive industrial chemical agents, such as caustic soda, that are mostly used for household cleaning, usually occurs accidentally or for suicidal purposes. Multiple protocols are based on documented success in preventing impending complications. In this study, we present a case of a 70-year-old man who swallowed caustic soda in a suicide attempt, causing a development of strong esophageal and gastric necrosis with subsequent gastrectomy and digiunostomy. Initially, the recommended nutritional approach was via percutaneous endoscopic jejunostomy by a polymer and high-caloric formula, with an elevated content of soluble fiber. After 5 months, the medical team removed the percutaneous endoscopic jejunostomy and the patient switched from enteral to oral nutrition. In this step, it was decided to introduce two oral, high-caloric supplements: an energy supplement in powder, based on maltodextrin, immediately soluble in foods or in hot/cold drinks and a high-energy and protein drink, enriched with arginine, vitamin C, zinc, and antioxidants. Oral administration (per os) was well tolerated by consuming homogenized food mixed in water. After 1 month, the patient was discharged from the hospital and was able to eat a regular meal.