Black Esophagus Research Articles

Prominent black esophagus, Wischnewsky spots, and black duodenum in a fatal hypothermia case with an underlying diabetic ketoacidosis.

Hypothermia can occur in patients with diabetic ketoacidosis (DKA), and these two conditions can exacerbate each other. Fatal hypothermia and DKA have overlapping features and findings such as Wischnewsky spots (WS), black esophagus, basal subnuclear vacuolization in the renal tubule, dehydration, and increased acetone levels. Therefore, it may be challenging to differentiate or clarify the context of these two conditions. Herein, we report a case of a 49-year-old man with type 1 diabetes who was found lying in his house in mid-winter. He experienced cardiopulmonary arrest 10h after the initial discovery and died at the hospital. On autopsy, florid left cardiac blood was observed. Black discoloration of the distal part of the esophageal mucosa, widespread WS in the gastric mucosa, and black discoloration of the duodenal mucosa were observed. Histologically, neutrophil infiltration in the esophageal mucosa, neutrophil infiltration and bleeding in the gastric mucosa, basal subnuclear vacuolization and Armanni-Ebstein lesion in the renal tubule epithelium in the kidney, and hyalinization of the islets of Langerhans were observed in the pancreas. Blood acetone and β-hydroxybutyrate levels were 538µg/mL and 8947 µmol/L, respectively. Glycated hemoglobin A1c and glucose levels were 16.2% and 883mg/dL, respectively, while C-reactive protein level was 3.64mg/dL. In conclusion, obnubilation due to DKA was assumed to be the underlying cause of hypothermia, and the combination of these two conditions led to the outcome of death. The concurrent presence of these conditions likely contributed to the conspicuous mucosal findings in the upper gastrointestinal tract.

Successful treatment of esophageal perforation due to black esophagus (acute esophageal necrosis): a case report

BackgroundBlack esophagus, or acute esophageal necrosis (AEN), is a rare disease with a poor prognosis in which the esophageal mucosa is black in color. We report a case of esophageal perforation due to AEN that was successfully treated.Case presentationAn 88-year-old woman presented to her local hospital with the chief complaint of abdominal pain. Endoscopic and radiological examinations revealed esophageal perforation due to AEN and duodenal perforation. Omental patch repair was performed for the esophageal perforation, and the duodenal ulcer perforation was treated by simple closure and gastrojejunostomy at the local hospital. Following refractory esophageal and duodenal perforations after the initial surgery, the patient was transferred to our hospital where emergent surgery was performed, comprising thoracoscopic esophagectomy, cervical esophagostomy, T-tube drainage, and omentopexy for duodenal perforation, as well as thoracic and abdominal drainage. Mucosal regeneration of the esophagostomy was confirmed endoscopically on postoperative day 19.ConclusionsAppropriate surgical intervention may be an optimal option in patients with esophageal perforation due to AEN.

Black esophagus: Massive bleeding in cirrhosis does not always mean variceal rupture

Black esophagus: Massive bleeding in cirrhosis does not always mean variceal rupture

S2723 Darkness at the End of the Tunnel: A Case of Black Esophagus Complicated by Perforation

S2723 Darkness at the End of the Tunnel: A Case of Black Esophagus Complicated by Perforation

A rare case of combined black esophagus and stomach: a case report.

Black esophagus is a relatively rare phenomenon that seems to occur in a morbid patient population, however, this entity may be more common than we currently know. Additionally, black esophagus may even be reversible in some cases. There are far fewer cases of black stomach described. The exact etiology and cause are less well known but may have similar risk factors as black esophagus. These disease pathologies are devastating to the patients they affect and can pose clinical challenges for the providers that encounter them. This case report details our experience with a moribund patient who was found to have extensive pneumomediastinum and gastric perforation secondary to black esophagus and black stomach. This was diagnosed on endoscopy following imaging that showed extensive pneumomediastinum. Initially the intent was to temporize the disease process in an attempt to stabilize the patient however at the time of diagnosis, the degree of ischemia had led to perforation and the disease process was not reversible or recoverable. He ultimately expired after comfort directed care measures were put in place. To the best of our knowledge, this case will be the first reported in current literature and will hopefully shed some light on this unusual and devastating pathology.

Black Esophagus and Recurrence of Duodenal Ulcers: Two Signs of the Same Pathogenic Pathway? A Case Report

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.

Acute esophageal necrosis as a result of taking herbal Medicine

Nowadays People use herbal medicines to try to maintain or improve their health but sometimes they cause side-effects and Some herbal drug may also interact with medication. We reported a 37 -year-old man who presented to the emergency department with sever watery diarrhea, vomiting, dysphagia, bicytopenia, renal failure and Acute esophageal necrosis, also known as black esophagus which is a rare syndrome characterized by a striking diffuse circumferential black appearance of the esophageal mucosa that universally affects the distal esophagus, 2-days after use of herbal drug named suranjan . Suranjan is a herbal formulation used to treat Rheumatoid arthritis

ŒSOPHAGE NOIR : A PROPOS D’UN CAS AVEC REVUE DE LA LITTERATURE

Abstract Introduction: The black esophagus or acute esophageal necrosis is a condition of poorly understood etiology. Aim: reporter a clinical case followed by a review of the literature Clinical observation: 69-year-old patient, hypertensive, who was treated with concomitant radiotherapy, followed by abdominoperineal amputation for adenocarcinoma of the lower rectum with sphincter involvement. The patient suddenly presented on the 15th postoperative day with hematemesis of moderate abundance. Extensive necrosis of the middle and lower thirds of the esophagus without gastric or duodenal involvement was demonstrated on fibroscopy. There was no history of caustic ingestion or esophagogastric reflux. There was no transmural necrosis on the cervicothoraco-abdominal CT scan. A 7-day fast and parenteral nutrition were instituted, as well as treatment with double-dose proton pump inhibitors and an isogroup blood transfusion. The evolution was favorable with almost total disappearance of the necrosis on fibroscopy control one week later. Conclusion: Black esophagus or acute esophageal necrosis is a rare condition, most often discovered in a postoperative context. Opponents of the proton pump and resting the stomach remain effective means in their management. Keywords: acute esophageal necrosis, black esophagus.

Black esophagus: a life-threatening adverse event associated with endoscopic retrograde cholangiopancreatography.

Black esophagus: a life-threatening adverse event associated with endoscopic retrograde cholangiopancreatography.

Microvascular cutaneous flap for treatment of complications of black esophagus and complex esophageal reconstruction

Microvascular cutaneous flap for treatment of complications of black esophagus and complex esophageal reconstruction

A144 BLACK ESOPHAGUS: A PEDIATRIC PRESENTATION OF ACUTE ESOPHAGEAL NECROSIS AND MANAGEMENT OF ITS COMPLICATIONS

Abstract Background Acute esophageal necrosis (AEN), or "Black Esophagus", is a rare diagnosis in children with adult literature citing high mortality. We present a pediatric case of this unusual condition. Purpose To report the rare presentation of AEN in a child and the response to intensive endoscopic management. Method Chart and literature review of AEN presentation and management. Result(s) A 13-year-old male who presented with a one-day history of severe chest pain, worsened with swallowing, followed by coffee ground emesis. No caustic ingestion. A nasogastric (NG) tube was placed and 2L of coffee-ground aspirate drained. The patient was an ex-preterm infant (25 weeks) who presented at age 2 years with an antral ulcer that developed into an antral stricture. This resolved with successive endoscopic dilatation with no recurrence after 5 years, off acid suppression. Physical exam showed BMI 99th %ile and palpated epigastric tenderness. CT-angiogram showed diffuse circumferential thickening of the esophagus and impressive gastric dilatation. A contrast study showed stasis of contrast in the esophageal lumen. Upper endoscopy revealed a thick, white membrane followed by circumferential black mucosa in the mid to distal esophagus. Previous antral stricture was noted with easy scope passage. Biopsies were negative for fungus, bacteria, HSV, CMV and parvovirus. Inflammatory infiltrate (mainly neutrophils and scattered histocytes with occasional lymphocytes) was noted in the esophagus. Necrotic tissue was identified and a diagnosis of AEN was made. The patient remained NPO, on TPN, and morphine was used for pain control. He responded well to this, along with high dose PPI. He tolerated clear fluids and oral sucralfate. Repeat scope one week later showed resolved necrosis with remaining oedematous white plaques and an unchanged antral stricture. 10 days later he developed severe dysphagia and a 15.5 cm long 6 mm diameter distal esophageal stricture was identified. This was managed by serial balloon dilatations. Due to frequent need for dilatations, endoscopic triamcinolone injections were used in several procedures as an adjunct therapy. A total of 80 mg of triamcinolone per session was injected along the length of the stricture in 4 aliquots in five out of nine endoscopic dilations in the last seven months. The most recent procedure successfully dilated the esophagus to 18mm. Currently, the patient is now tolerating a soft oral diet and remains on PPI therapy. Image Conclusion(s) AEN is very rare in children with no literature describing the endoscopic management of AEN related stenotic complications. We report the case of this unique presentation in a teenager, resulting in severe, long-segment esophageal stenosis. Intensive endoscopic therapeutic management has resulted in a positive clinical outcome allowing oral nutrition without any stenting or surgical interventions. Early recognition and active endoscopic management likely contributed to the positive outcome. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Acute Esophageal Necrosis in Acute Pancreatitis-Report of a Case and Endoscopic and Clinical Perspective.

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.

Black esophagus as an uncommon cause of gastrointestinal bleeding.

Black esophagus (BE) or Acute esophageal necrosis (AEN) is rare clinical entity with an estimated incidence of 0.01-0.2% of patiens undergoing esophagogastroduodenoscopy (EGD). BE is characterized by circumferential blackish coloration of the mucosa, with abrupt interruption at the esophagogastric junction level, secondary to hypoperfusion and ischemia. Upper gastrointestinal hemorrhage is the most common presentation (70-90%), being a rare cause of it. We present 3 cases that were admitted in our center for hematemesis.

A Strange Case of Acute Esophageal Necrosis

Gurvits Syndrome or Acute Esophageal Necrosis (AEN) is an uncommon disease de- scribed as a “black esophagus” in Esophagogastroduodenoscopy (EGD).

Stent jako řešení perforace „černého jícnu“

Summary: “Black esophagus”, also known as acute esophageal necrosis (AEN), is a relatively rare disease characterized by black discoloration of the esophageal mucosa. The condition can be located only distally, but it can also affect the entire esophagus. Hematemesis is the most common clinical manifestation is; the condition is associated with increased lethality in high-risk groups of patients. Early diagnosis of AEN can be made by gastroscopy, the initiation of adequate treatment is crucial for a favorable patient prognosis. The most serious complications of AEN include esophageal perforation with the risk of other complications such as mediastinitis and sepsis. The nature of the disease and the affection of the esophagus and potentially the mediastinum require a multidisciplinary approach. Below we present a case report of a 68-year-old patient with a diagnosis of AEN complicated by perforation confirmed by CT and early endoscopy. An endoscopic approach with the introduction of a fully coated metal stent was chosen as the primary solution for the esophageal perforation. Nevertheless, the patient developed other complications of perforation: mediastinitis and empyema requiring chest drainage. In addition to interventional methods, the patient was treated with broad-spectrum antibiotics and a combination of parenteral and enteral nutrition. After 3 months of treatment and resolving the complications, the patient was released to outpatient care in a good clinical condition. Key words: acute esophageal necrosis – oesophageal perforation – mediastinitis – Danis stent – metallic stent

S2421 A Dark Omen: Acute Esophageal Necrosis Associated With COVID-19

Introduction: Black esophagus, also known as acute esophageal necrosis (AEN), is a rare clinical entity with an estimated prevalence of 0.01 to 0.28 percent of cases in endoscopy series. It can present with striking endoscopic findings characterized by diffuse circumferential black discoloration of the esophagus terminating at the gastroesophageal (GE) junction. It is mostly associated with tissue hypoxia due to low flow vascular states and corrosive injury in the setting of severe illness. Patients typically present with gastrointestinal bleeding. We present a rare case of a black esophagus in the setting of severe Coronavirus-19 (COVID-19) infection. Case Description/Methods: A 75-year-old male with diabetes and chronic kidney disease presented after a mechanical fall with a prolonged down time of 13 hours. He was found to have acute on chronic renal failure with rhabdomyolysis. He was initially stable however later developed respiratory failure from COVID-19 requiring steroids and ultimately ventilator support. His course was further complicated by new onset atrial fibrillation for which he received anticoagulation, worsening renal function requiring hemodialysis and significant hypotension requiring vasopressor support. In the intensive care unit, patient was noted to have melena with a significant drop in hemoglobin, he underwent an esophagogastroduodenoscopy which showed diffuse continuous black discoloration of the esophageal mucosa with abrupt transition at the GE junction consistent with black esophagus with multiple ulcers in stomach and duodenum (Figure). Patient was kept on IV proton pump inhibitors and anticoagulation was discontinued. Given worsening multiorgan failure, he was transitioned to comfort measures only and passed away the next day. Discussion: Black esophagus or AEN is a rare but concerning finding on endoscopy which must be recognized early and managed aggressively in order to improve clinical outcomes. In our patient AEN was likely due to a combination of hypoperfusion and hypoxia in the setting of severe COVID-19 infection with multiorgan failure. AEN could be seen more frequently in patients with severe COVID-19 infections who are frequently anticoagulated due to the associated prothrombotic state with increased risk of GI bleeding. It is important for physicians to be aware of AEN as a possible etiology of GI bleeds in these patients.Figure 1.: 'Black esophagus' - Acute esophageal necrosis.

S2282 Black Esophagus Manifesting as Upper Gastrointestinal Bleeding in Diabetic Ketoacidosis: A Case Report

Introduction: Acute esophageal necrosis, or black esophagus, is a rare clinical entity manifesting as upper gastrointestinal bleeding and complicating various conditions. However, black esophagus in the setting of diabetic ketoacidosis (DKA) has been rarely reported. We present a case of a 36-year-old male with black esophagus presenting as hematemesis complicating an episode of DKA. Case Description/Methods: A 36-year-old male with uncontrolled type 1 diabetes mellitus complicated by end-stage renal disease and hypertension presented to the emergency department with abdominal pain, nausea, and vomiting. Patient reported worsening abdominal pain and associated blood-tinged emesis. On presentation, patient was hemodynamically stable. Physical exam included an abdomen that was diffusely tender to palpation without peritoneal signs. Initial labs remarkable for serum glucose 1491, anion gap 41, bicarbonate 9, and hemoglobin 7.5. Patient was admitted to Critical Care for insulin drip and intravenous fluid resuscitation for DKA. Later, patient had an episode of hematemesis resulting in tachycardia, hypotension, and drop in hemoglobin to 5.6. Patient was further resuscitated with blood transfusions with improvement in hemodynamics and hemoglobin to 8.9. Continuous pantoprazole infusion was initiated. Upper endoscopy demonstrated severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding. No biopsies were taken due to concern for possible false lumen; CT chest with contrast demonstrated no signs of esophageal perforation. Following EGD, patient had several small self-limiting episodes of hematemesis and melena, while maintaining hemodynamics. He was continued on pantoprazole infusion and placed on strict nothing by mouth (NPO) precautions for 3 days with gradual advancement of diet. He received 6 days of empiric antimicrobial therapy with ampicillin-sulbactam and fluconazole. Patient reported no further episodes of hematemesis. Hemoglobin stabilized around 8.0 (Figure). Discussion: DKA is a rare but life-threatening cause of acute esophageal necrosis which may develop due to a combination of tissue hypoperfusion, impaired mucosal defenses, and gastric reflux. Upper gastrointestinal bleeding in the setting of DKA should raise suspicion for black esophagus which is a potential cause of mortality. Early diagnosis and treatment of underlying etiology are the key factors in management.Figure 1.: Severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding.

S2275 Black Esophagus Due to Severe SARS-CoV2 Infection

Introduction: Acute esophageal necrosis (AEN), also called ‘black esophagus’ due to its appearance is a rare clinical disease, recently described in medical literature. The etiology is multifactorial, often in the setting of severe systemic conditions such as sepsis and trauma, and outcomes are poor. Severe SARS-CoV2 infection can lead to overwhelming inflammation and multi-organ failure. Herein, we present a case of black esophagus with severe SARS-CoV2 infection. Case Description/Methods: A 69-year-old with rheumatoid disease, on immune suppression, was admitted to our hospital with dyspnea, coffee ground emesis and melena. He tested positive for SARS-CoV2 and was found to have acute blood loss anemia. An urgent EGD was performed which revealed a black, necrotic mucosa of the distal 2/3rd of the esophagus, consistent with AEN. Biopsies were avoided due to risk of perforation and subsequent images were negative for any perforation. Management was started with high dose PPI and supportive care in addition to recognized treatment for COVID-19. However, his hospital stay became complicated with progressive clinical decline and development of multi-organ failure. Eventually, he was transitioned to comfort care and passed away shortly after (Figure). Discussion: AEN or black esophagus, as defined by its endoscopic appearance, is a manifestation of ischemic and corrosive injury to the esophagus in the setting of severe systemic disease processes. Diffuse, circumferential, necrotic and friable esophageal mucosa, especially in the distal 2/3rd, is the hallmark. The relatively poor vascular supply of the distal esophagus makes it more susceptible to such injury. Often, a sharp demarcation is seen at the Z-line. Histology shows extensive transmural necrosis. Pathogenesis of AEN is thought to be a combination of a sudden low flow, prothrombotic state from severe systemic illness causing ischemic injury and impaired healing ability. At the same time, increased exposure to gastric content occurs from gastric hypokinesis and increased secretions which exacerbate injury. Typical presentation is upper GI bleed, and management revolves around treatment of underlying etiology and supportive measures with acid suppression and mucosal protection with PPI and sucralfate. NG tubes should be avoided due to risk of perforation, which is the most serious complication. Surgical intervention is reserved for perforation, and balloon dilation can be required in cases of stenosis or strictures.Figure 1.: Diffuse necrotic appearing esophagus with black discoloration on EGD Dilated esophagus with diffuse esophageal wall thickening on CT.

S2278 Black Esophagus: A Striking Etiology of Gastrointestinal Bleeding

Introduction: Black esophagus, or acute esophageal necrosis (AEN), is an uncommon etiology of upper gastrointestinal bleeding with incidence 0.01%-0.2% and poor prognosis. AEN is characterized by endoscopic findings of diffuse circumferential black discoloration of distal esophageal mucosa with sharp demarcation at the GEJ. The pathophysiology of AEN is unknown, however current hypotheses implicate ischemia, thromboembolic injury, critical illness, and corrosive injury. We describe a case of black esophagus in a patient with hemorrhagic shock. Case Description/Methods: An 83-year-old woman with hypertension presented to an outside hospital after a fall with lethargy, acute hypoxic respiratory failure, and shock. CT chest revealed right sided hemothorax. The patient was intubated, resuscitated with IV fluids and blood products, initiated on vasopressors, and a chest tube was placed prior to transfer to our institution. Repeat CT chest was concerning for the right thoracostomy tube traveling through the right middle lobe parenchyma and terminating within the mediastinum between the left atrium and the distal esophagus. The chest tube was removed and replaced in the operating room. Double contrast esophogram was without esophageal leak. The patient subsequently developed melena and worsening anemia. EGD demonstrated sharply demarcated circumferential black ulceration of the distal esophagus consistent with black esophagus without obvious signs of perforation. IV PPI and therapy aimed at reversing the underlying shock was pursued. Unfortunately, after a prolonged hospital course with worsening acute respiratory distress syndrome and inability to liberate from the ventilator, the patient’s family elected to pursue comfort measures and the patient expired (Figure). Discussion: In this case, AEN was most likely caused by ischemia secondary to hemorrhagic shock. Black esophagus carries a very poor prognosis, usually related to the underlying condition. Timely recognition of AEN and treatment aimed at reversing the underlying etiology can help prevent complications such as infection, esophageal stricture, and perforation. AEN is managed with aggressive IV PPI, NPO, and avoiding passage of nasogastric tubes due to risk of perforation. In rare instances, surgical intervention may be warranted. This case highlights the need to maintain a wide differential diagnosis for gastrointestinal bleeding and the importance of early recognition and treatment of this rare condition to prevent complications.Figure 1.: EGD indicating circumferential black ulceration of the distal esophagus with clear demarcation (arrow).

S479 Acute Esophageal Necrosis in Patients With Diabetic Ketoacidosis: A Systematic Review of Diagnostic and Therapeutic Conundrums

Introduction: Acute esophageal necrosis (AEN) associated with diabetic ketoacidosis (DKA) remains an exceedingly rare clinical entity. The likely causal mechanism is related to hypoperfusion and transient hyperglycemic gastric dysmotility, potentially increasing the risk of AEN. To our knowledge, this is the first systematic review of AEN in patients with DKA. Methods: A systematic search of MEDLINE, Embase, Scopus, and Cochrane was conducted for English-only articles published between inception and June 15, 2022. Abstracts from major gastroenterology conferences and bibliography lists were also reviewed. Search terms "esophageal necrosis" and "black esophagus" were combined using the Boolean operators ‘AND’ and ‘OR’ with the terms "diabetic ketoacidosis" and "diabetes mellitus," with all permutations. Two authors independently reviewed each article for eligibility. The search yielded a total of 326 results. However, 28 articles fulfilled the inclusion criteria. Results: A total of 31 case reports only (clinical evidence level: IV) of AEN in the setting of DKA were included, dating from 2014 to 2022. The mean age of patients was 52.81 ± 13.49 years (range: 30–78 years) and 61% of cases were reported in males. Common presenting symptoms were hematemesis (58%), nausea (55%), abdominal pain (53%), vomiting (35%), and altered mental status (19%). Apart from diabetes, major comorbidities were hypertension (29%), alcoholism (23%), GERD (16%), and COPD (10%). On EGD, 58% had pan-esophageal, 26% had mid-to-distal, and 16% of patients had distal segment disease. Esophageal biopsy was documented in 29% of patients. All patients received insulin and fluid replacement therapies. PPIs in 60%, sucralfate in 32%, antifungals in 29%, and antibiotics were administered in 19% of patients. Blood transfusions were performed in 16% of patients. The mortality rate was 6.4%. AEN complications included esophageal stenosis (6%), as well as stricture formation (6%). (Figure) Conclusion: This systematic review reiterates the occurrence of AEN in association with DKA. Overt GI bleeding is a common presentation, but patients may develop nausea, abdominal pain, vomiting, and disorientation as major symptoms. Therefore, endoscopists should keep a low threshold for performing EGD in DKA patients. While the cause-and-effect relation of AEN with hyperglycemia are unclear, fluid replacement and gastric acid suppression are pertinent to the management of AEN.Figure 1.: Upper endoscopy showing necrotic-appearing black esophagus in the lower third of esophagus in a female diabetic patient.