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Acute esophageal necrosis (AEN), also known as Gurvits syndrome, is a rare and potentially life-threatening condition characterized by necrosis of the esophageal mucosa. Acute esophageal necrosis is often associated with critical conditions, such as myocardial infarction, diabetic ketoacidosis (DKA), coronavirus disease 2019 (COVID-19) infection, or post-surgical complications. Patients typically present with nausea, hematemesis, acute dysphagia, and melena. Given its high mortality rate, prompt detection with upper endoscopy and early initiation of treatment are crucial. Most cases of Gurvits syndrome are managed conservatively using intravenous fluids, proton pump inhibitors, and antibiotics. Herein, we present a case series of AEN in the setting of DKA. Both patients received supportive care and were discharged in a stable condition. [ABSTRACT FROM AUTHOR]

A 70-year-old Italian man presented to our emergency department for dyspnea and confusion. He was affected by diabetes mellitus type 2, but he stopped his medication 10 years before. At admission, his vital signs were blood pressure of 60/50 mmHg, heart rate of 130 bpm, peripheral oxygen saturation of 94% in the Venturi Mask FiO2 40%, respiratory rate of 40/min, and body temperature of 36°C. Physical examination revealed hypoperfusion with a high Mottling Score and dark stools with a positive hydrogen peroxide reaction. He denied abdominal pain, nausea, and vomiting. Laboratory findings showed leucocytosis (White Blood Cells, WBC, 31,580/mm3; N 91.6%), Hemoglobin (Hb) 14.5 g/dL, Hematocrit Test (Hct) 49%, hyperglycaemia (>700 mg/L), and normal coagulation time. Arterial blood gas documented a metabolic acidosis with pH 6.95, Partial Pressure of Carbon Dioxide (pCO2) 27.5 mmHg, HCO3 7.1 mmol/L, lactate 8.14 mmol/L (normal value

Black esophagus or acute esophageal necrosis is characterized by circumferential black discoloration of the distal esophageal mucosa. It is a rare condition with a multifactorial pathogenesis, and its most common clinical presentation is acute upper gastrointestinal bleeding. It usually affects elderly patients with multiple comorbidities and is associated with a high mortality rate. This is a case report of a 90-year-old man with multiple comorbidities, including diabetes mellitus, atrial fibrillation with complete atrioventricular block, and a history of ischemic stroke, who presented to the emergency department for a syncopal episode followed by coffee ground emesis. Thoraco-abdominal computer tomography showed thickening of the distal esophagus and ruled out major complications such as perforation. The following esophagogastroduodenoscopy showed black circumferential necrosis of the mid and distal esophagus. Multiple irregular ulcers with black necrotic areas were also present in the bulb and second duodenal portion. During the hospitalization, the patient was treated with PPI, NPO nutrition, and broad-spectrum antibiotics with benefits. Two months later, the patient returned to the emergency department due to a new episode of hematemesis with endoscopic evidence of esophageal stricture without necrosis and recurrence of duodenal ulcers. After a few days, the patient died due to worsening of the underlying comorbidities. A black esophagus is associated with duodenal ulcers, which may recur and are possibly due to a common ischemic origin. In this case report, we explore the potential link between black esophagus and duodenal ulcers, discussing the underlying mechanisms and relevant literature supporting this association. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN) or black esophagus is a rare cause of mortality in patients with gastrointestinal bleeding. We present a case of a 54-year-old female who presented with diabetic ketoacidosis (DKA) and developed melena eventually attributed to AEN. The esophagogastroduodenoscopy (EGD) identified severe inflammation with black discoloration consistent with acute esophageal necrosis in the middle and lower esophagus. The patient was managed with intravenous pantoprazole and total parenteral nutrition (TPN) until she was able to tolerate an adequate diet. Black esophagus should be added to the differential diagnosis of patients with DKA who develop gastrointestinal bleeding. This need is stressed by the fact that early treatment is essential to reducing complications and mortality associated with the condition. [ABSTRACT FROM AUTHOR]

Background and Aims: 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. Methods: 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. Results and Conclusions: 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. [ABSTRACT FROM AUTHOR]

Abstract Background Acute esophageal necrosis (AEN), commonly referred to as Gurvits syndrome or “black esophagus”, is a rare clinical disease. We present a case of AEN associated with diabetic ketoacidosis (DKA). Case presentation A 66-year-old male came to our hospital with coffee-ground emesis, dyspnea, and general malaise. He was treated for type 2 diabetes mellitus using insulin and had not been taking his medication, including insulin, for several days. Laboratory analysis revealed severe hyperglycemia (730 mg/dL), normocytic anemia (hemoglobin level, 7.7 g/dL; mean corpuscular volume, 100.4 fL), high serum potassium (7.6 mEq/L), and a high level of blood urea (98.7 mg/dL). Ketones and glucose were detected in the urine, and serum β-hydroxybutyrate was elevated (2132 µmol/L). Arterial blood gas analysis confirmed metabolic acidosis (pH, 7.29; HCO3, 10.5 mmol/L). Collectively, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient’s condition improved with intravenous fluids, and he received intravenous insulin to treat DKA. According to these findings, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient underwent esophagogastroduodenoscopy (EGD) which revealed a circumferential necrosis of the middle and distal esophagus, immediately proximal to the gastroesophageal junction. The patient was then treated with an intravenous proton pump inhibitor. The patient continued to improve with conservative treatment and was subsequently discharged in a stable condition. An EGD repeated 14 days after discharge showed complete healing of the necrotic-like mucosal change without stricture formation of the esophagus. Conclusions AEN is rare but potentially life-threatening case of upper gastrointestinal bleeding. Therefore, a clinician should be aware of AEN as a potential cause of upper gastrointestinal bleeding in elderly patients with poorly controlled diabetes and significant comorbidities.

Esophageal stroke, also known as acute esophageal necrosis or Gurvits syndrome, is an entity that has gained more and more recognition in the last two decades. It is also named "black esophagus" because of striking black discoloration of the esophageal mucosa, with an abrupt transition to normal mucosa at the gastroesophageal junction. Its most common clinical presentation is represented by upper gastrointestinal bleeding and esophagogastroduodenoscopy is the main diagnostic tool. Among the etiopathogenetic and multiple predisposing factors described are hypovolemia, shock state, ischemia, congestive heart failure, acute renal failure, infections, trauma, and diabetes mellitus. Current management of this condition consists of treating the underlying pathology, nil per os, and antacid administration in uncomplicated cases. Although most of the cases have favorable prognosis, complications such as pneumomediastinum or esophageal stricture may occur and fatal cases are a consequence of underlying comorbidities. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis, also known as the black esophagus, is a rare pathology diagnosed by endoscopy that shows a black-looking esophageal mucosa. Its cause is unknown, but a multifactorial origin is attributed to it. An esophageal lesion of ischemic origin should be considered. We present the case of a 56-year-old patient with respiratory symptoms suggestive of a severe infectious process, with a rapidly progressive clinical picture and requirement of airway security, multimodal vasopressor, and organic support, and an endoscopic study due to clinical symptoms of upper digestive tract bleeding with evidence of lesions compatible with acute esophageal necrosis. Despite multimodal management in the intensive care unit, the patient died 34 days after hospital admission. [ABSTRACT FROM AUTHOR]

‘Black esophagus’or acute esophageal necrosis is a rare condition, frequently affecting the distal esophagus with a sharp transition to normal-appearing mucosa at the gastroesophageal junction. It is characterized by circumferential blackish discoloration and necrosisof the mucosa due to severe hemodynamic compromise.The pathogenesis of black esophagus is unclear, but a “two-hit” hypothesis for a dominant mucosal necrosis has been described - a low-flow vascular setting followed by an altered reparative ability of the mucosal barrier systems. The etiology is usually multifactorial, triggered by an acute event. It is associated with a high mortality rate of 31.8%−50%, most of the deaths caused by underlying illnesses. Mortality specific to acute esophageal necrosis is approximately 6%.We report a case of 72-year-old hypertensive male patient presenting with perforated gastric ulcers and sepsis. Distal gastrectomy revealed two candidial perforations. Patient expired on second post- operative day. Autopsy revealed a diffuse circumferential blackish discoloration of distal one third of the esophageal mucosa abruptly stopping at the gastro esophageal junction. On microscopy, the esophageal mucosa was ulcerated, and covered by necro-inflammatory exudate and blackish pigment extending upto the muscularis propria. Many submucosal vessels showed fresh fibrin thrombi. Special stains for fungus were negative. The diagnosis of black esophagus or acute esophageal necrosis was made. Other findings included fungal peritonitis, ischemic heart disease and chronic pyelonephritis with right-sided nephrolithiasis. The cause of death was related to septicaemia.

Black esophagus or acute esophageal necrosis is characterized by circumferential black discoloration of the distal esophageal mucosa. It is a rare condition with a multifactorial pathogenesis, and its most common clinical presentation is acute upper gastrointestinal bleeding. It usually affects elderly patients with multiple comorbidities and is associated with a high mortality rate. This is a case report of a 90-year-old man with multiple comorbidities, including diabetes mellitus, atrial fibrillation with complete atrioventricular block, and a history of ischemic stroke, who presented to the emergency department for a syncopal episode followed by coffee ground emesis. Thoraco-abdominal computer tomography showed thickening of the distal esophagus and ruled out major complications such as perforation. The following esophagogastroduodenoscopy showed black circumferential necrosis of the mid and distal esophagus. Multiple irregular ulcers with black necrotic areas were also present in the bulb and second duodenal portion. During the hospitalization, the patient was treated with PPI, NPO nutrition, and broad-spectrum antibiotics with benefits. Two months later, the patient returned to the emergency department due to a new episode of hematemesis with endoscopic evidence of esophageal stricture without necrosis and recurrence of duodenal ulcers. After a few days, the patient died due to worsening of the underlying comorbidities. A black esophagus is associated with duodenal ulcers, which may recur and are possibly due to a common ischemic origin. In this case report, we explore the potential link between black esophagus and duodenal ulcers, discussing the underlying mechanisms and relevant literature supporting this association.

Background: Acute esophageal necrosis (AEN), commonly referred to as Gurvits syndrome or "black esophagus", is a rare clinical disease. We present a case of AEN associated with diabetic ketoacidosis (DKA).Case Presentation: A 66-year-old male came to our hospital with coffee-ground emesis, dyspnea, and general malaise. He was treated for type 2 diabetes mellitus using insulin and had not been taking his medication, including insulin, for several days. Laboratory analysis revealed severe hyperglycemia (730 mg/dL), normocytic anemia (hemoglobin level, 7.7 g/dL; mean corpuscular volume, 100.4 fL), high serum potassium (7.6 mEq/L), and a high level of blood urea (98.7 mg/dL). Ketones and glucose were detected in the urine, and serum β-hydroxybutyrate was elevated (2132 µmol/L). Arterial blood gas analysis confirmed metabolic acidosis (pH, 7.29; HCO3, 10.5 mmol/L). Collectively, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient's condition improved with intravenous fluids, and he received intravenous insulin to treat DKA. According to these findings, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient underwent esophagogastroduodenoscopy (EGD) which revealed a circumferential necrosis of the middle and distal esophagus, immediately proximal to the gastroesophageal junction. The patient was then treated with an intravenous proton pump inhibitor. The patient continued to improve with conservative treatment and was subsequently discharged in a stable condition. An EGD repeated 14 days after discharge showed complete healing of the necrotic-like mucosal change without stricture formation of the esophagus.Conclusions: AEN is rare but potentially life-threatening case of upper gastrointestinal bleeding. Therefore, a clinician should be aware of AEN as a potential cause of upper gastrointestinal bleeding in elderly patients with poorly controlled diabetes and significant comorbidities. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN) or “black esophagus” is a rare clinical entity caused by necrosis of distal esophageal mucosa stemming from esophageal ischemia. Possible etiologies are broad but most commonly include possible triggers of low-flow vascular states in the esophagus, including infections, broad-spectrum antibiotic use, and gastric volvulus, among others. Patients most commonly present clinically with acute onset hematemesis and melena. Here, we describe a patient who initially presented with multiple nonspecific gastrointestinal symptoms, including abdominal pain and nausea, that progressed over a 10-day period, culminating in multiple episodes of hematemesis prior to presentation. Endoscopic evaluation confirmed the diagnosis of AEN and unveiled a possible paraesophageal hernia (PEH) as the causative factor. A subsequent videofluoroscopic barium swallow was utilized to better characterize the upper gastrointestinal anatomy and confirmed the PEH as a likely etiology. Esophagogastroduodenoscopy (EGD) can often identify PEH independently, but in patients with AEN secondary to a possible, but unclear, PEH on EGD, a videofluoroscopic barium swallow is an appropriate and useful next step in confirming the diagnosis. While treatment of AEN traditionally involves fluid resuscitation, intravenous protein pump inhibitors, and total parenteral nutrition, surgical intervention is often indicated in patients who have a contributing and symptomatic PEH.

Acute esophageal necrosis syndrome, is a rare cause of gastrointestinal bleeding. It is characterized by a particular black coloration, mostly of the distal esophagus, which ends abruptly in the gastroesophageal junction. The hemorrhagic manifestation may be hematemesis, melena or both of them. It is a life-threatening condition with significant difference between the two sexes. We report a case of a 67 years old male with schizophrenia, aspiration pneumonia and sepsis who presented with hematemesis. The endoscopic finding was a black, wide linear necrosis of the esophageal mucosa which extended from the middle esophagus to the gastroesophageal junction, compatible with acute esophageal necrosis. The esophageal lesion healed progressively at the same time with the improvement of the general health condition. We must think of acute esophageal necrosis in critically ill male patients, in their sixth decade of life, with multiple comorbidities and gastrointestinal hemorrhage, because early recognition can help reducing the mortality of this rare syndrome. In conclusion, we must think of acute esophageal necrosis in critically ill male patients, in their sixth decade of life, with multiple comorbidities and gastrointestinal hemorrhage. The diagnostic is made most of the time only by the characteristic endoscopic findings. Because of the gravity of this affection, the treatment must be quick and aggressive.

Abstract A 58‐year‐old man who had the history of alcohol dependence was referred to our emergency center due to severe nausea, vomiting, and subsequent onset of chest and back pain. Esophagogastroduodenoscopy (EGD) showed black‐appearing esophagus mucosa extending from the cervical esophagus to the esophagogastric junction with clear margins, a condition typically referred to as a black esophagus. Alcohol abuse was considered an important factor associated with acute esophageal necrosis in this patient. After admission, he received fluid resuscitation and proton‐pump inhibitors, with restriction of oral intake and treatment of alcohol dependence. Follow‐up EGDs and endoscopic balloon dilation were performed for the management of esophageal narrowing before the development of severe strictures. Strictures were successfully treated endoscopically without complications such as perforation.

Acute esophageal necrosis (AEN), black esophagus, or Gurvits syndrome is a rare clinical disorder characterized by a striking endoscopic appearance of necrotic esophageal mucosa, universally affecting the distal esophagus and ending abruptly at the gastroesophageal junction. It has been gaining traction as a demonstrable cause of upper gastrointestinal bleeding in the 21st century. Its pathophysiology is multifactorial affecting men and the elderly disproportionally, with a mortality rate nearing 36%. AEN has been associated with numerous conditions in the past, and we aim to present an unusual case of AEN on the setting of chronic alcohol use.

Abstract Black esophagus is a rare medical condition, characterized by a circumferential blackish discoloration of the distal part of the esophageal mucosa, abruptly ending at the gastroesophageal junction. The etiology is multifactorial since patients suffer from multiple comorbidities. While the mortality rate specifically linked to black esophagus is only around 6%, the mortality rate linked to the underlying comorbidities amounts to 32%. A series of five cases is provided in which black esophagus was an unexpected discovery at autopsy. Black esophagus is generally considered being a challenge to the forensic pathologist. There are often no other major gross anomalies found at autopsy and information about the patient’s medical history is not always available, which complicates a correct assessment. We present a review of the literature on black esophagus, limited to reports on deceased patients. The reviewed publications are divided into autopsy and endoscopy series to correctly compare the causes of death. The aim of this review is to identify a possible divergence in causes of death in autopsy and endoscopy series and additionally to analyze the causes of these differences to enable better assessment and interpretation of black esophagus at forensic autopsies. This paper emphasizes the importance of a minimal knowledge of the victim’s comorbidities and medical record and the use of toxicology and postmortem biochemistry analysis as a valuable tool in investigating the cause of death in the setting of black esophagus.

Esophageal stroke, also known as acute esophageal necrosis or Gurvits syndrome, is an entity that has gained more and more recognition in the last two decades. It is also named “black esophagus” because of striking black discoloration of the esophageal mucosa, with an abrupt transition to normal mucosa at the gastroesophageal junction. Its most common clinical presentation is represented by upper gastrointestinal bleeding and esophagogastroduodenoscopy is the main diagnostic tool. Among the etiopathogenetic and multiple predisposing factors described are hypovolemia, shock state, ischemia, congestive heart failure, acute renal failure, infections, trauma, and diabetes mellitus. Current management of this condition consists of treating the underlying pathology, nil per os, and antacid administration in uncomplicated cases. Although most of the cases have favorable prognosis, complications such as pneumomediastinum or esophageal stricture may occur and fatal cases are a consequence of underlying comorbidities.

Acute esophageal necrosis is a gastrointestinal syndrome characterized by diffuse, circumferential, black-appearing mucosa of the distal esophagus and involves various lengths. It is a multifactorial condition involving hypoperfusion from a low flow state, large reflux of gastric contents, and a poor mucosal barrier. Complications involve esophageal stenosis or stricture and esophageal perforation. Treatment is often supportive with correction of underlying conditions, aggressive fluid resuscitation, antacid therapy, and restriction of oral intake. We present an unusual case of black esophagus in a patient with significant cardiovascular disease and rhabdomyolysis and discuss its pathogenesis, management, and outcome., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Samuel et al.)

Acute esophageal necrosis (AEN), also known as “black esophagus,” is an entity characterized by the circumferential black appearance of esophageal mucosa, usually associated with hypoperfusion and gastric outlet obstruction. This entity has a reported prevalence of up to 0.2%, affecting predominantly elderly men with multiple comorbidities. Most cases resolve with conservative treatment with no need of surgical intervention. However, the overall prognosis is poor, with mortality reaching one-third of cases due to the patient’s underlying illness. In this article we present three cases of patients with AEN.

Black esophagus is a rare condition referred from acute necrosis of the esophagus, with characteristic endoscopic finings of circumferential black appearance of the mucosa. Black esophagus is associated with systemic dysfunction, such as massive bleeding, or severe dehydration. Although the duodenal mucosa is also susceptible to ischemia, reports of black esophagus with duodenal involvement, such as bleeding or perforation, are limited. Here, we present the case of a 61-year-old male who developed the typical black esophagus with duodenal involvement following severe dehydration. The patient was treated conservatively and recovered from the acute phase. In the chronic stage, transthoracic esophagectomy was performed because of esophageal stricture, and the patient then returned to his daily life. Although the etiological mechanism of acute esophageal necrosis is unknown, it is thought to be associated with the presence of an underlying severe systemic condition. Our case is not exceptional for these systemic conditions demonstrating extreme dehydration. However, it remains unclear why our case showed duodenal involvement. Although the reason is unknown, the presence of a celiac aneurysm located near the bifurcation to duodenal blood flow might explain the impaired blood flow to the duodenum. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN) is defined as necrosis of the esophageal mucosa seen as diffuse black discoloration of the distal esophagus on an upper endoscopy. The prevalence of the disease is rare and reported to be up to 0.2% in autopsy series. The etiology of the disease is thought to be multifactorial and due to ischemic insults to the esophagus with gastric acid reflux further damaging the vulnerable mucosa. Patients are often critically ill or with significant comorbidities. Here, we present a case series of 3 patients with AEN induced by diabetic ketoacidosis.

Acute esophageal necrosis (AEN) or "black esophagus" is a rare clinical entity caused by necrosis of distal esophageal mucosa stemming from esophageal ischemia. Possible etiologies are broad but most commonly include possible triggers of low-flow vascular states in the esophagus, including infections, broad-spectrum antibiotic use, and gastric volvulus, among others. Patients most commonly present clinically with acute onset hematemesis and melena. Here, we describe a patient who initially presented with multiple nonspecific gastrointestinal symptoms, including abdominal pain and nausea, that progressed over a 10-day period, culminating in multiple episodes of hematemesis prior to presentation. Endoscopic evaluation confirmed the diagnosis of AEN and unveiled a possible paraesophageal hernia (PEH) as the causative factor. A subsequent videofluoroscopic barium swallow was utilized to better characterize the upper gastrointestinal anatomy and confirmed the PEH as a likely etiology. Esophagogastroduodenoscopy (EGD) can often identify PEH independently, but in patients with AEN secondary to a possible, but unclear, PEH on EGD, a videofluoroscopic barium swallow is an appropriate and useful next step in confirming the diagnosis. While treatment of AEN traditionally involves fluid resuscitation, intravenous protein pump inhibitors, and total parenteral nutrition, surgical intervention is often indicated in patients who have a contributing and symptomatic PEH. [ABSTRACT FROM AUTHOR]

Although esophageal stricture after acute esophageal necrosis (AEN) is often refractory to dilation therapy, there have been few reports of surgical intervention. We report two rare cases of successful subtotal esophagectomy and esophagogastrostomy for esophageal strictures after AEN using indocyanine green (ICG) fluorescence imaging. In case 1, emergent esophagogastroduodenoscopy (EGD) in a 56-year-old man with coffee-ground emesis revealed black esophageal mucosa in the middle to lower esophagus, indicating AEN. Despite conservative therapy, an esophageal stricture developed after 2 weeks. Repeated endoscopic balloon dilation (EBD) did not resolve the stenosis; esophagectomy was thus performed approximately 6 months after AEN onset. We evaluated the blood flow to the esophagus using ICG fluorescence imaging to determine the proximal surgical resection line. The postoperative course was uneventful. In case 2, an 81-year-old woman with upper gastrointestinal bleeding with hematemesis and chest pain was diagnosed with AEN by EGD and was treated with conservative therapy. An esophageal stricture developed after 3 weeks, and repeated EBD was ineffective. Approximately 2 months after AEN onset, she underwent esophagectomy using ICG fluorescence imaging. The postoperative course was uneventful. Considering that AEN is a blood flow disorder, ICG fluorescence imaging is a useful technology to prevent surgical morbidity. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN) is a condition characterized by black appearance and inflammation of the esophagus. Our patient developed AEN presenting in the setting of alcohol intoxication and extensive inferior vena cava thrombosis. Esophagogastroduodenoscopy showed blood and black discoloration of the middle and lower esophagus with oozing. To control bleeding, a self-expandable fully covered metallic esophageal stent was placed. Multiple studies and reviews agree that the initial management for AEN is supportive care, resuscitation, and proton pump inhibitors to protect the esophageal mucosa from injury from acid reflux. Our case highlights the benefits of esophageal stent placement to manage AEN with active bleeding. [ABSTRACT FROM AUTHOR]

Acute necrotizing esophagitis is a rare entity that affects mainly elderly patients. The most common clinical presentation is upper gastrointestinal bleeding. The prognosis depends on the underlying diseases, with a mortality of up to 50%. This is the case of a 77-year-old male patient who presented with melena, three episodes of hematemesis, and epigastric pain for a week. Upper endoscopy revealed mucosa with spotty necrosis and fibrin in the middle and distal esophagus. Esophageal biopsy was compatible with mucosal necrosis. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN), black esophagus, or Gurvits syndrome is a rare clinical disorder characterized by a striking endoscopic appearance of necrotic esophageal mucosa, universally affecting the distal esophagus and ending abruptly at the gastroesophageal junction. It has been gaining traction as a demonstrable cause of upper gastrointestinal bleeding in the 21st century. Its pathophysiology is multifactorial affecting men and the elderly disproportionally, with a mortality rate nearing 36%. AEN has been associated with numerous conditions in the past, and we aim to present an unusual case of AEN on the setting of chronic alcohol use. [ABSTRACT FROM AUTHOR]

Black esophagus is a rare medical condition, characterized by a circumferential blackish discoloration of the distal part of the esophageal mucosa, abruptly ending at the gastroesophageal junction. The etiology is multifactorial since patients suffer from multiple comorbidities. While the mortality rate specifically linked to black esophagus is only around 6%, the mortality rate linked to the underlying comorbidities amounts to 32%. A series of five cases is provided in which black esophagus was an unexpected discovery at autopsy. Black esophagus is generally considered being a challenge to the forensic pathologist. There are often no other major gross anomalies found at autopsy and information about the patient's medical history is not always available, which complicates a correct assessment. We present a review of the literature on black esophagus, limited to reports on deceased patients. The reviewed publications are divided into autopsy and endoscopy series to correctly compare the causes of death. The aim of this review is to identify a possible divergence in causes of death in autopsy and endoscopy series and additionally to analyze the causes of these differences to enable better assessment and interpretation of black esophagus at forensic autopsies. This paper emphasizes the importance of a minimal knowledge of the victim's comorbidities and medical record and the use of toxicology and postmortem biochemistry analysis as a valuable tool in investigating the cause of death in the setting of black esophagus. [ABSTRACT FROM AUTHOR]

Abstract Although white esophagus is an extremely rare disease, careful diagnosis and intensive treatment are required because of a relationship with black esophagus. Further case accumulation including duodenal and jejunum lesion is needed.

Background: Ketosis-prone diabetes (KPD) is an intermediate subtype of diabetes mellitus, usually affecting Afro-American adults, presenting with diabetic ketoacidosis (DKA), without the classic phenotype of autoimmune type 1 diabetes. Patients require insulin therapy at onset for the acute decompensation, then usually remain insulin-free for prolonged periods with diet alone or with other antidiabetic drugs. DKA can be rarely complicated by upper gastrointestinal bleeding and mucosal necrosis, a severe complication named acute esophageal necrosis (AEN) burdened by high mortality. The association of KPD presenting with DKA complicated by AEN is here reported for the first time, to the knowledge of the authors, in the medical literature., Case Presentation: Here we report an interesting case of middle-aged African woman, newly diagnosed with KPD, presenting with DKA hematemesis. The patient was first treated at Intensive Care Unit for the ketoacidosis with intravenous fluids combined with continuous insulin infusion, and then switched to subcutaneous regimen. At the same time, esophagogastroduodenoscopy (EGD) was performed to diagnose acute esophageal necrosis, which was promptly managed with proton pump inhibitors infusion, fasting, and parenteral nutrition. After the correct clinical evaluation, the patient was switched to oral antidiabetic and basal insulin at discharge and an EGD follow-up was scheduled., Conclusions: KPD remains an under-recognized and under-diagnosed type of diabetes which can present as DKA. Since DKA could be a possible trigger of AEN, a rare but potentially lifethreatening condition, that clinicians should be aware of, in patients presenting with upper gastrointestinal bleeding and ketoacidosis. The prompt management and classification of DKA, combined with the EGD execution for early AEN diagnosis and follow-up, is essential., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Acute esophageal necrosis is a rare syndrome classically characterized by a striking endoscopic image of diffuse and circumferential black mucosal discoloration of distal esophagus, with an abrupt transition at the gastroesophageal junction and variable proximal extension. The typical patient is an older male with general debilitation and multiple comorbidities presenting with hematemesis or melena. The pathophysiology usually involves a combination of esophageal ischemia, backflow injury from gastric chemical contents and impaired mucosal reparative mechanisms associated with debilitated physical states. It may arise in the setting of hemodynamic compromise, diabetic ketoacidosis, hypothermia, alcoholic intoxication, trauma, inflammatory diseases, esophageal local infection, solid organ transplantation, postoperative status, drugs or acute gastric outlet obstruction, usually in the background of a chronic debilitating process, where the concurrent presence of multiple risk factors, including diabetes mellitus, hypertension, malnutrition, malignancy or alcohol abuse, places a patient at higher risk. The characteristic endoscopic appearance establishes the diagnosis. Biopsy is supportive but not required. Management is mainly supportive and consists of correcting coexisting conditions, fluid therapy, bowel rest, intravenous proton pump inhibitor therapy and red blood cell transfusion as needed. Although this is a serious life-threatening condition, appropriate treatment may result in a favorable outcome in the majority of patients. [ABSTRACT FROM AUTHOR]

Acute esophageal necrosis (AEN) is defined as necrosis of the esophageal mucosa seen as diffuse black discoloration of the distal esophagus on an upper endoscopy. The prevalence of the disease is rare and reported to be up to 0.2% in autopsy series. The etiology of the disease is thought to be multifactorial and due to ischemic insults to the esophagus with gastric acid reflux further damaging the vulnerable mucosa. Patients are often critically ill or with significant comorbidities. Here, we present a case series of 3 patients with AEN induced by diabetic ketoacidosis. [ABSTRACT FROM AUTHOR]

Background: The term "acute esophageal mucosal lesion (AEML)" includes black esophagitis, and non-black esophagitis characterized by diffuse circumferential erosions without black-appearing mucosa. Black esophagitis is easily diagnosed, whereas non-black esophagitis is often misdiagnosed as severe reflux esophagitis (sRE). The aim of this study was to determine differences in clinical characteristics of patients with AEML and those with sRE. Methods: Thirty-nine patients with sRE and 32 patients with AEML were diagnosed on the basis of endoscopic findings from 2009 to 2016. Characteristics assessed included age, sex, medication use, coexisting endoscopic finding, comorbidities, laboratory tests results, and chief complaints. Results: In contrast with sRE, male sex, need for emergency endoscopy, presence of duodenal lesions, hypertension, and renal dysfunction were positively associated with AEML. Analysis of associations between laboratory data and AEML showed that high white blood cell count, blood urea nitrogen, and blood glucose were significantly associated with an increase OR for AEML. Conclusions: We showed that AEML differed from sRE regarding both endoscopic findings and clinicopathological features. AEML has not been widely recognized, but it should be defined as a distinct inflammatory disease of the esophagus consisting of both black and non-black esophagitis. [ABSTRACT FROM AUTHOR]

Background: To review all the reported literature on acute esophageal necrosis. Research 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. [ABSTRACT FROM AUTHOR]

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We are reporting a case of spontaneous acute esophageal necrosis "black esophagus" of unclear etiology in a kidney transplant recipient. A patient with end-stage renal disease due to IgA nephropathy received a deceased-donor kidney transplant. The surgical procedure was uneventful, without hemodynamic instability. He was started on alemtuzumab for immunosuppression induction followed by maintenance immunosuppression with intravenous methylprednisolone for 3 days, then oral prednisone, mycophenolate mofetil and tacrolimus (a target level between 8 and 10ng/ml) daily. On postoperative day (POD) 3, the patient started to develop significant gastro-intestinal symptoms: epigastric pain, dysphagia, odynophagia, eructation, pyrosis, nausea, and regurgitation of food contents. He was diagnosed with esophageal necrosis by upper endoscopy on postoperative day 4. We describe a successful treatment with supportive therapy and complete recovery despite receiving immunosuppressive therapy. To our knowledge, this case is one of the few reported cases of esophageal necrosis in kidney transplant recipients and the first case that was not associated with clinical risk factors. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Black esophagus or acute esophageal necrosis (AEN) is a rare medical disorder which is characterized by a diffuse circumferential black esophageal mucosa. The majority of patients present with signs of upper gastrointestinal bleeding. Diagnosis is made based on esophagogastroduodenoscopy. Treatment consists of intravenous fluids, proton pomp inhibitors and additional therapies to treat the underlying illness. In this article we present five cases of patients with AEN and briefly review the literature of AEN. [ABSTRACT FROM AUTHOR]

To review the entity “black esophagus” and sequela of a slipped laparoscopic adjustable band. The patient’s history, physical examination, imaging, and endoscopic findings were reviewed. Detailed review of pathophysiology, presentation, diagnosis, management, and natural history was conducted. “Black esophagus,” also known as acute esophageal necrosis (AEN), is a rare condition resulting in black discoloration of the mid to distal esophagus with less than a hundred reported cases. It has not been previously documented in bariatric surgery or following laparoscopic adjustable gastric banding. The volvulus was reduced at surgery, and the esophageal changes resolved without sequela. “Black esophagus” is an acute, ominous-appearing condition with a spectrum ranging from superficial mucosal disease to transmural involvement with perforation. Fortunately, esophageal resection is rarely required. [ABSTRACT FROM AUTHOR]

Acute necrotizing esophagitis (black esophagus) is a rare pathology that is characterized by partial or total loss of the epithelium, ulceration up to the circumferential slough of all layers of the mucosa and submucosa, frequent involvement of deep muscle layers, and frequent perforations. Its blackish appearance in endoscopic examinations has given it the name of black esophagus. Five illustrative cases, all concordant with descriptions the medical literature, are presented in this study together with a review of the literature, case descriptions and risk and prognosis factors. [ABSTRACT FROM AUTHOR]