Back To Search Results

Esophageal Necrosis

Editor: Fatima Anjum Updated: 5/22/2023 10:27:33 PM


Acute esophageal necrosis (AEN), also known as the black esophagus, Gurvit syndrome, or acute necrotizing esophagitis, is a rare and life-threatening condition. It is characterized by either partial or total circumferential blackening of the esophagus that stops abruptly at the gastro-esophageal junction, as seen on an upper GI endoscopy. AEN was first documented in 1990 by Goldberg et al., and the exact cause remains unclear but tends to follow a pattern of acute ischemia in association with a topical insult to the esophagus.[1]

It is strongly associated with medical comorbidities and most commonly presents between the ages of 60 and 80 in the male population. The management of AEN is primarily medical but can include surgical intervention in the event of complications such as perforation and mediastinitis.  Overall mortality associated with AEN is approximately 30%; however, mortality specific to AEN is closer to 5%.


Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care


The etiology of AEN remains unclear. The main developing theory is the two-hit hypothesis, the combination of a hemodynamic compromise in conjunction with an increase in metabolic requirement from local insult leading to necrosis.[2][3] 

The majority of AEN occurs in the distal esophagus (approximately 60% to 90% of cases).[4][5][6] The distal third of the esophagus derives its blood supply from the left gastric or inferior phrenic arteries and has the poorest blood supply with the poorest collateral support compared to the proximal two-thirds.[7][8] The distal third is closest to the stomach and most at risk from gastric acid reflux. Gastric acid increases esophageal mucosal blood flow and oxygen requirement in normal physiological conditions.[9] 

Significantly increased volumes of gastric acid, for example, as a result of gastric outlet obstruction, have been shown to cause AEN.[2][3] The cause appears to be the combined effect of pre-existing vasculopathy, an acute low flow state, and increased oxygen demand. Contrary to this, there have been cases of AEN in the absence of other medical conditions or a low flow state.[10][11] However, in all cases, at least two of the following are present; acute ischemia, chronic vascular disease, and significant topical injury.


AEN is a rare but potentially underdiagnosed condition. In a review of published cases, only 88 patients existed over forty years.[2] In this series of published cases, just under 80% occurred in males (70 of 88), with only 20% occurring in females. In an autopsy series, the prevalence of blackening of the esophagus, a symptom of AEN, was 2%.[12] However, this may have occurred post-mortem as opposed to in vitro. In endoscopic studies, prevalence appears to be between 0.1 to 0.3%, with the average age of occurrence between 70 and 80 years. Overall, it is approximately four times more likely to occur in males.[12][13][14][15][16]

In a more recent literature review, the average age of occurrence was sixty-two, with 70% of patients being male [6].  Contrary to the above studies, one study from Japan found a prevalence of approximately 6% of patients on who they performed endoscopies; their other most common findings were a hiatus hernia and NSAID usage.[17] This implies that AEN may be more common and present transiently in patients with an upper GI bleed.[17]

Risk factors for AEN include:[2][3][4][5][6][14][16][18]

  • Type two diabetes (approximately 40%)
  • Hypertension (approximately 35%)
  • Ischaemic heart disease (12%)
  • Alcoholism (approximately 25%)
  • Chronic kidney disease (approximately 15%)
  • Chronic liver disease (approximately 15%)
  • Solid-organ malignancy (approximately 10%)
  • Peripheral vascular disease (approximately 10%)
  • Chronic obstructive pulmonary disease (approximately 5%)
  • Poor nutritional state

History and Physical

In most case studies, AEN cases initially present symptoms of an upper GI bleed, with haematemesis/melaena (70% to 85% of cases) and hemodynamic instability.[2][6] Patients are typically aged 60 to 80, male, and have numerous co-morbidities.[4] 

On examination, the patient may have epigastric tenderness, pallor, and peripheral hypoperfusion. Vital signs often show low-grade pyrexia, hypotension, tachycardia, and in more severe cases, hypoxia. As AEN often presents as a result of hemodynamic instability, whatever is causing this may well confound the clinical picture.[19][20][21] Cases of AEN have been seen as a result of sepsis, Cardiogenic shock, hemorrhage from either planned operation or trauma, or other medical conditions including DKA and diarrhea, and vomiting.[22][23][24][21]


Blood tests will likely show a raised white cell count, anemia, and lactic acidosis.[7] If upper GI bleeding is present and gastroscopy is performed, the typical presentation of AEN is a diffuse circumferential black discoloration of the esophageal mucosa that stops abruptly at the gastroesophageal junction.[7] 

As stated previously, it is most common in the distal third of the esophagus. However, it can extend proximally to involve the whole esophagus in 36% of cases in one literature review.[5] Other pathology may well also be present such as hiatus hernias, active bleeding, gastric ulceration, blood clots, or gastric outlet obstruction.[3] 

Tissue biopsy is not required for diagnosis however is often useful to exclude other causes of the black esophagus. Imaging is typically not performed in cases reviewed except in diagnostic uncertainty or concerns over an esophageal perforation, in which case CT scanning of the chest showed air in the mediastinum.[4][17]

Treatment / Management

In isolation, AEN has a poor prognosis. When AEN is observed as one of the multiple symptoms (it should be view as a poor prognostic factor), initial efforts should be made to treat the underlying cause. Treatment for AEN typically involves fluid resuscitation with accompanying blood transfusion if there is significant anemia.[4][25] In addition to this, patients should be placed NPO ("nil-per-os’ or nothing by mouth), and intravenous proton pump inhibitors should be given to reduce local insult to the vulnerable esophagus.[5][7][26] (B2)

Sucralfate has also been used to further reduce local insult to the esophagus. Due to an often lengthy period of NPO, there has been some evidence for total-parenteral nutrition improving outcomes.[3][27] Nasogastric tubes should not be inserted due to the risk of esophageal perforation.[26] Antibiotics should be given in the presence of sepsis or evidence of esophageal perforation but are otherwise not required [3].(B3)

Acute complications include upper GI bleeding and esophageal perforation, which may be present at the time of presentation to healthcare or during the first few days in the hospital. Localized bleeding is controllable with an adrenaline injection during a gastroscopy or by metallic stent insertion.[28] The incidence of esophageal perforation as a result of AEN appears to be approximately 5%.[5][26][29][5](B3)

If there is evidence of perforation, surgery is the primary treatment. Surgery occurred in approximately 4% of cases in one analysis.[5] This involves an initial emergency esophagectomy followed by elective esophageal reconstruction following recovery from the initial event.[30] In one case, stent insertion in the initial phase is effective but required subsequent intervention to correct stent migration.[31] One case used a combination of video-assisted thorascopic surgery (VATS) and drain placement which was reportedly successful.[32](B3)

Differential Diagnosis

Differential diagnoses of AEN include:

  • Malignant melanoma[33]
  • Acanthosis nigricans[34]
  • Coal dust deposition[35]
  • Psuedomelanosis[36]
  • Melanosis of the esophagus[37]
  • Black dye ingestion[38]
  • Direct caustic injury[1]

The majority of the above conditions follow a longer-term, more insidious course and are often found during elective gastroscopy rather than in an emergency scenario. The exceptions to this are dye ingestion or direct caustic injury, for which history will be key to determining the underlying cause of black esophagus. If there is doubt over the pathogenesis of a black esophagus, then histology can be performed following an upper GI endoscopy. If it is the result of AEN, then this will show mucosal and submucosal necrosis, necrotic debris, and localized inflammatory response.[14][39][40]


AEN itself is a poor prognostic factor that results from other conditions. The mortality rate in the most recent literature review stands at just under 30%.[6] This is similar to earlier reviews which put estimated mortality at 32%.[2][5] Due to AEN’s association with other conditions, it can be difficult to distinguish which condition is responsible for the death. Taking this into account, AEN-specific mortality has been noted to be as low as 5%.[2]


Acute complications, as listed above, include localized bleeding and esophageal perforation. Upper GI bleeding is commonly present in ~85% of cases [6]. The perforation rate is thought to be 5% to 7%.[2][5] Middle to long-term complications includes esophageal strictures and trachea-esophageal fistulas. There is a complication rate of approximately 12% in one literature review, with 70% of these patients developing strictures and the other 30% of patients developed fistulas.[6] 

These complications do not develop until at least 2 weeks after the initial event. Management of strictures is not well documented in the literature, but iterative balloon dilatation is an effective treatment.[41] The majority of patients who recover will do so without complication; however, a follow-up endoscopy is recommended at approximately 1 month to rule out other sequelae.[7]

Deterrence and Patient Education

As AEN is a multifactorial condition and primarily a prognostic marker rather than an isolated pathology, prevention should center on reducing comorbidities such as vascular disease, liver disease, and renal disease. Lifestyle factors would include the moderation of alcohol consumption, smoking cessation, regular exercise, and maintaining a healthy weight. Medical prevention for AEN has not been documented in the literature.

Enhancing Healthcare Team Outcomes

Acute esophageal necrosis is an uncommon condition that can present in a number of different ways include upper GI bleeding, signs of sepsis, or peripheral hypoperfusion. Medically co-morbid patients presenting with epigastric pain and hemodynamic compromise should raise concern for urgent investigation and treatment. Early recognition and subsequent resuscitation form the cornerstone of management for these patients, regardless of diagnostic uncertainty.

Upper gastrointestinal endoscopy is vital for diagnosis and should be performed as soon as possible. This may require liaising closely with the endoscopy department or even the operating theatre if the patient is not considered stable enough. Evidence of perforation will need surgical input, and long-term parental nutrition, guided by the dieticians, should be instigated early on. Nursing staff can coordinate and liaise activities between various clinicians, other professionals such as the dietician and the patient. Interprofessional care and communication with prolonged rehabilitation are clearly required in such cases to ensure a positive outcome.



Goldenberg SP, Wain SL, Marignani P. Acute necrotizing esophagitis. Gastroenterology. 1990 Feb:98(2):493-6     [PubMed PMID: 2295407]

Level 3 (low-level) evidence


Gurvits GE, Shapsis A, Lau N, Gualtieri N, Robilotti JG. Acute esophageal necrosis: a rare syndrome. Journal of gastroenterology. 2007 Jan:42(1):29-38     [PubMed PMID: 17322991]

Level 3 (low-level) evidence


Dias E, Santos-Antunes J, Macedo G. Diagnosis and management of acute esophageal necrosis. Annals of gastroenterology. 2019 Nov-Dec:32(6):529-540. doi: 10.20524/aog.2019.0418. Epub 2019 Sep 26     [PubMed PMID: 31700229]


Augusto F, Fernandes V, Cremers MI, Oliveira AP, Lobato C, Alves AL, Pinho C, de Freitas J. Acute necrotizing esophagitis: a large retrospective case series. Endoscopy. 2004 May:36(5):411-5     [PubMed PMID: 15100949]

Level 2 (mid-level) evidence


Abdullah HM, Ullah W, Abdallah M, Khan U, Hurairah A, Atiq M. Clinical presentations, management, and outcomes of acute esophageal necrosis: a systemic review. Expert review of gastroenterology & hepatology. 2019 May:13(5):507-514. doi: 10.1080/17474124.2019.1601555. Epub 2019 Apr 16     [PubMed PMID: 30933549]


Schizas D, Theochari NA, Mylonas KS, Kanavidis P, Spartalis E, Triantafyllou S, Economopoulos KP, Theodorou D, Liakakos T. Acute esophageal necrosis: A systematic review and pooled analysis. World journal of gastrointestinal surgery. 2020 Mar 27:12(3):104-115. doi: 10.4240/wjgs.v12.i3.104. Epub     [PubMed PMID: 32218893]

Level 1 (high-level) evidence


Gurvits GE. Black esophagus: acute esophageal necrosis syndrome. World journal of gastroenterology. 2010 Jul 14:16(26):3219-25     [PubMed PMID: 20614476]


Moretó M, Ojembarrena E, Zaballa M, Tánago JG, Ibánez S. Idiopathic acute esophageal necrosis: not necessarily a terminal event. Endoscopy. 1993 Oct:25(8):534-8     [PubMed PMID: 8287816]


Sandler AD, Schmidt C, Richardson K, Murray J, Maher JW. Regulation of distal esophageal mucosal blood flow: the roles of nitric oxide and substance P. Surgery. 1993 Aug:114(2):285-93; discussion 293-4     [PubMed PMID: 7688153]

Level 3 (low-level) evidence


Katsinelos P, Pilpilidis I, Dimiropoulos S, Paroutoglou G, Kamperis E, Tsolkas P, Kapelidis P, Limenopoulos B, Papagiannis A, Pitarokilis M, Trakateli C. Black esophagus induced by severe vomiting in a healthy young man. Surgical endoscopy. 2003 Mar:17(3):521     [PubMed PMID: 12488997]

Level 3 (low-level) evidence


Katsinelos P, Christodoulou K, Pilpilidis I, Papagiannis A, Xiarchos P, Tsolkas P, Vasiliadis I, Eugenidis N. Black esophagus: an unusual finding during routine endoscopy. Endoscopy. 2001 Oct:33(10):904     [PubMed PMID: 11571691]

Level 3 (low-level) evidence


Sandhu S, Wang T, Prajapati D. Acute esophageal necrosis complicated by refractory stricture formation. JGH open : an open access journal of gastroenterology and hepatology. 2021 Apr:5(4):528-530. doi: 10.1002/jgh3.12520. Epub 2021 Mar 1     [PubMed PMID: 33869789]


Ramos R, Mascarenhas J, Duarte P, Vicente C, Casteleiro C. [Acute esophageal necrosis: a retrospective case series]. Revista espanola de enfermedades digestivas. 2008 Sep:100(9):583-5     [PubMed PMID: 19025311]

Level 2 (mid-level) evidence


Ben Soussan E, Savoye G, Hochain P, Hervé S, Antonietti M, Lemoine F, Ducrotté P. Acute esophageal necrosis: a 1-year prospective study. Gastrointestinal endoscopy. 2002 Aug:56(2):213-7     [PubMed PMID: 12145599]


Julián Gómez L, Barrio J, Atienza R, Fernández-Orcajo P, Mata L, Saracibar E, de la Serna C, Gil-Simón P, Vallecillo MA, Caro Patón A. [Acute esophageal necrosis. An underdiagnosed disease]. Revista espanola de enfermedades digestivas. 2008 Nov:100(11):701-5     [PubMed PMID: 19159174]

Level 2 (mid-level) evidence


Singh D, Singh R, Laya AS. Acute esophageal necrosis: a case series of five patients presenting with "Black esophagus". Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology. 2011 Feb:30(1):41-5. doi: 10.1007/s12664-011-0082-z. Epub 2011 Mar 3     [PubMed PMID: 21369835]

Level 3 (low-level) evidence


Yasuda H, Yamada M, Endo Y, Inoue K, Yoshiba M. Acute necrotizing esophagitis: role of nonsteroidal anti-inflammatory drugs. Journal of gastroenterology. 2006 Mar:41(3):193-7     [PubMed PMID: 16699852]

Level 2 (mid-level) evidence


Ullah W, Mehmood A, Micaily I, Khan MS. Comprehensive review of acute oesophageal necrosis. BMJ case reports. 2019 Feb 26:12(2):. doi: 10.1136/bcr-2018-227967. Epub 2019 Feb 26     [PubMed PMID: 30814100]

Level 3 (low-level) evidence


Talebi-Bakhshayesh M, Samiee-Rad F, Zohrenia H, Zargar A. Acute Esophageal Necrosis: A Case of Black Esophagus with DKA. Archives of Iranian medicine. 2015 Jun:18(6):384-5     [PubMed PMID: 26058936]

Level 3 (low-level) evidence


Kim YH, Choi SY. Black esophagus with concomitant candidiasis developed after diabetic ketoacidosis. World journal of gastroenterology. 2007 Nov 14:13(42):5662-3     [PubMed PMID: 17948944]

Level 3 (low-level) evidence


Unuma K, Harada K, Funakoshi T, Uemura K. Sudden death of an alcoholic elderly man with acute esophageal necrosis (black esophagus). Forensic science international. 2011 Oct 10:212(1-3):e15-7. doi: 10.1016/j.forsciint.2011.05.024. Epub     [PubMed PMID: 21684699]

Level 3 (low-level) evidence


Lahbabi M, Ibrahimi A, Aqodad N. Acute esophageal necrosis: a case report and review. The Pan African medical journal. 2013:14():109. doi: 10.11604/pamj.2013.14.109.2000. Epub 2013 Mar 19     [PubMed PMID: 23717723]

Level 3 (low-level) evidence


Wallberg ME, Young P, Finn BC, Thomé M, Chueco AA, Villarejo F. [Black esophagus due to acute necrotizing esophagitis: report of one case]. Revista medica de Chile. 2009 May:137(5):672-4     [PubMed PMID: 19701557]

Level 3 (low-level) evidence


Sakatoku Y, Fukaya M, Miyata K, Nagino M. Successful bypass operation for esophageal obstruction after acute esophageal necrosis: a case report. Surgical case reports. 2017 Dec:3(1):4. doi: 10.1186/s40792-016-0277-8. Epub 2017 Jan 4     [PubMed PMID: 28054280]

Level 3 (low-level) evidence


Gurvits GE, Cherian K, Shami MN, Korabathina R, El-Nader EM, Rayapudi K, Gandolfo FJ, Alshumrany M, Patel H, Chowdhury DN, Tsiakos A. Black esophagus: new insights and multicenter international experience in 2014. Digestive diseases and sciences. 2015 Feb:60(2):444-53. doi: 10.1007/s10620-014-3382-1. Epub 2014 Oct 9     [PubMed PMID: 25297468]

Level 3 (low-level) evidence


Shafa S, Sharma N, Keshishian J, Dellon ES. The Black Esophagus: A Rare But Deadly Disease. ACG case reports journal. 2016 Jan:3(2):88-91. doi: 10.14309/crj.2016.9. Epub 2016 Jan 20     [PubMed PMID: 26958555]

Level 3 (low-level) evidence


Brar TS, Helton R, Zaidi Z. Total Parenteral Nutrition Successfully Treating Black Esophagus Secondary to Hypovolemic Shock. Case reports in gastrointestinal medicine. 2017:2017():4396870. doi: 10.1155/2017/4396870. Epub 2017 Jun 18     [PubMed PMID: 28702267]

Level 3 (low-level) evidence


Messner Z, Gschwantler M, Resch H, Bodlaj G. Use of the Ella Danis stent in severe esophageal bleeding caused by acute necrotizing esophagitis. Endoscopy. 2014:46 Suppl 1 UCTN():E225-6. doi: 10.1055/s-0034-1365384. Epub 2014 May 7     [PubMed PMID: 24806369]

Level 3 (low-level) evidence


Burtally A, Gregoire P. Acute esophageal necrosis and low-flow state. Canadian journal of gastroenterology = Journal canadien de gastroenterologie. 2007 Apr:21(4):245-7     [PubMed PMID: 17431514]

Level 3 (low-level) evidence


Wu MH, Wu HY. Incremental change in acute esophageal necrosis: report of two cases. Surgery today. 2014 Feb:44(2):363-5. doi: 10.1007/s00595-013-0526-4. Epub 2013 Mar 6     [PubMed PMID: 23463535]

Level 3 (low-level) evidence


Sato H, Ishida K, Sasaki S, Kojika M, Endo S, Inoue Y, Sasaki A. Regulating migration of esophageal stents - management using a Sengstaken-Blakemore tube: A case report and review of literature. World journal of gastroenterology. 2018 Jul 28:24(28):3192-3197. doi: 10.3748/wjg.v24.i28.3192. Epub     [PubMed PMID: 30065565]

Level 3 (low-level) evidence


Groenveld RL, Bijlsma A, Steenvoorde P, Ozdemir A. A black perforated esophagus treated with surgery: Report of a case. World journal of gastrointestinal surgery. 2013 Jun 27:5(6):199-201. doi: 10.4240/wjgs.v5.i6.199. Epub     [PubMed PMID: 23805365]

Level 3 (low-level) evidence


Lasota J, Kowalik A, Felisiak-Golabek A, Zięba S, Waloszczyk P, Masiuk M, Wejman J, Szumilo J, Miettinen M. Primary malignant melanoma of esophagus: clinicopathologic characterization of 20 cases including molecular genetic profiling of 15 tumors. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc. 2019 Jul:32(7):957-966. doi: 10.1038/s41379-018-0163-y. Epub 2019 Feb 13     [PubMed PMID: 30760858]

Level 3 (low-level) evidence


Kozlowski LM, Nigra TP. Esophageal acanthosis nigricans in association with adenocarcinoma from an unknown primary site. Journal of the American Academy of Dermatology. 1992 Feb:26(2 Pt 2):348-51     [PubMed PMID: 1569256]

Level 3 (low-level) evidence


Khan HA. Coal dust deposition--rare cause of "black esophagus". The American journal of gastroenterology. 1996 Oct:91(10):2256     [PubMed PMID: 8855776]

Level 3 (low-level) evidence


Kimball MW. Pseudomelanosis of the esophagus. Gastrointestinal endoscopy. 1978 Feb:24(3):121-2     [PubMed PMID: 305381]

Level 3 (low-level) evidence


Sharma SS, Venkateswaran S, Chacko A, Mathan M. Melanosis of the esophagus. An endoscopic, histochemical, and ultrastructural study. Gastroenterology. 1991 Jan:100(1):13-6     [PubMed PMID: 1983815]


Day A, Sayegh M. Acute oesophageal necrosis: a case report and review of the literature. International journal of surgery (London, England). 2010:8(1):6-14. doi: 10.1016/j.ijsu.2009.09.014. Epub 2009 Oct 1     [PubMed PMID: 19800431]

Level 3 (low-level) evidence


Nagri S, Hwang R, Anand S, Kurz J. Herpes simplex esophagitis presenting as acute necrotizing esophagitis ("black esophagus") in an immunocompetent patient. Endoscopy. 2007 Feb:39 Suppl 1():E169     [PubMed PMID: 17614059]

Level 3 (low-level) evidence


Altenburger DL, Wagner AS, Li S, Garavaglia J. A case of black esophagus with histopathologic description and characterization. Archives of pathology & laboratory medicine. 2011 Jun:135(6):797-8     [PubMed PMID: 21631276]

Level 3 (low-level) evidence


Maubert A, Frey S, Rahili A, Filippi J, Benizri E. Acute esophageal necrosis: Case report of an unknown entity. International journal of surgery case reports. 2019:61():188-190. doi: 10.1016/j.ijscr.2019.07.041. Epub 2019 Jul 22     [PubMed PMID: 31376741]

Level 3 (low-level) evidence