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Journal of Clinical Images and Medical Case Reports

ISSN 2766-7820
Case Report - Open Access, Volume 5

Black esophagus: A devastating consequence - A case report and comprehensive literature analysis

Agrawal Nirav1*; Sharma Akshay1; Louis-Jean Scarlet1; Singh Sanmeet1,2

1Department of Internal Medicine, Luminis Health, Anne Arundel Medical Center, Annapolis, MD, USA.

2Department of Gastroenterology, Luminis Health, Anne Arundel Medical Center, Annapolis, MD, USA.

*Corresponding Author : Agrawal Nirav
Department of Internal Medicine, Luminis Health, Anne Arundel Medical Center, Annapolis, MD, USA.
Email: [email protected]

Received : Aug 02, 2024

Accepted : Sep 02, 2024

Published : Sep 09, 2024

Archived : www.jcimcr.org

Copyright : © Nirav A (2024).

Abstract

Acute Esophageal Necrosis (AEN) is a rare condition characterized by circumferential black discoloration and necrosis of the esophageal mucosa. This report presents a case of a 79-year-old female with metastatic cancer diagnosed with black esophagus and literature reviews of 68 cases. Our literature search highlighted common presenting symptoms were hematemesis (55%), gastrointestinal symptoms (54%), and melena (19%). And comorbidities including, malignancy (~10%) being leading cause of AEN. Age, low hemoglobin, and hypotension are associated with increased mortality. Management typically involves supportive care, but in cases of advanced malignancy, treatment may focus on symptom control and palliation.

Keywords: Acute esophageal necrosis; Black Esophagus; Malignancy; Endoscopy.

Abbreviations: AEN: Acute Esophageal Necrosis; GERD: Gastroesophageal Reflux Disease; Hb: Hemoglobin; EGD: Esophagogastroduodenoscopy; ESRD: End-Stage Renal Disease; CKD: Chronic Kidney Disease; COPD: Chronic Obstructive Pulmonary Disease; HLD: Hyperlipidemia; MEN1: Multiple Endocrine Neoplasia Type 1.

Citation: Nirav A, Akshay S, Scarlet LJ, Sanmeet S. Black esophagus: A devastating consequence - A case report and comprehensive literature analysis. J Clin Images Med Case Rep. 2024; 5(9): 3244.

Introduction

Acute esophageal necrosis, commonly known as “black esophagus,” is a rare and potentially life-threatening condition characterized by the circumferential black discoloration and necrosis of the esophageal mucosa. This condition was first described by Goldenberg et al. in 1990, and since then, numerous case reports and small case series have been published in the literature [1]. The exact pathogenesis of the black esophagus remains unclear, but it is believed to result from a combination of factors leading to compromised blood supply to the esophagus, such as low-flow states, vasculopathy, and mucosal ischemia. Proposed risk factors and associated conditions include diabetes mellitus [2], alcohol abuse, malnutrition, Gastroesophageal Reflux Disease (GERD), vascular disease, hypoperfusion states (e.g., shock, cardiac disease), and certain medications or procedures that may impair esophageal perfusion [3,4]. The clinical presentation of black esophagus is often non-specific, with upper gastrointestinal bleeding (hematemesis, melena) being the most common symptom. Other associated symptoms may include epigastric pain [5], nausea, vomiting, dysphagia, and odynophagia. Diagnosis is typically made through endoscopic evaluation [6], revealing the characteristic circumferential black discoloration and necrosis of the esophageal mucosa, often involving the distal esophagus and abruptly stopping at the gastroesophageal junction [7]. Here, we present a case report of a black esophagus in a 79-year-old female with metastatic cancer.

Case report

A 79-year-old female with a past medical history of type 2 diabetes mellitus, hypertension, dementia, and hyperlipidemia, presented to the emergency department with worsening abdominal swelling, and dyspnea on exertion. Her initial vitals showed hypertension 172/92 mmHg, tachycardia 104 bpm, tachypnea 22 breaths/min, temperature 97.7°F, and oxygen saturation 98% on room air. Pertinent labs were Hemoglobin (Hb) 11.2 g/dL, platelets 373 x103/μL, AST 15 U/L, ALT 5 U/L, glucose 260 mg/dL, and creatinine 1.3 mg/dL. On exam, the lungs exhibited decreased breath sounds at the bases bilaterally. Imaging revealed peritoneal carcinomatosis with a large pelvic mass measuring 12.7 x 10.8 x 16.7 cm (Figure 1). Bilateral pleural effusions and ascites were also present. Paracentesis fluid analysis showed metastatic mucin-producing adenocarcinoma, tumor cells are positive for pan cytokeratin, CK20, and CDX2. The findings were suggestive of metastatic adenocarcinoma of colorectal origin. Oncology was consulted, but no treatment options were appropriate for the patient at this time as the prognosis was very poor. And recommended a palliative care consult. On hospital day 26, she developed coffee-ground emesis, her Hb dropped to 5.6 g/dL and was hypotensive to 82/64 mmHg, requiring 2 units of packed RBCs. On day 28, she underwent an Esophagogastroduodenoscopy (EGD) revealing circumferential black discoloration of the esophagus concerning for acute necrotic esophagus (Black esophagus) (Figure 2) with biopsy showing erosive esophagitis; she was treated with intravenous proton pump inhibitors, sucralfate, and hydration. Given the patient’s overall poor prognosis in the setting of malignancy, no follow-up EGD was recommended. Her course required 4 paracenteses removing ~10L of fluid, and 1 thoracentesis for symptomatic management. As she was not a candidate for further cancer treatment, detailed goals of care discussions with the family were done. The patient was transitioned to hospice care; unfortunately, the patient passed away in the hospital before being discharged.

Results

The study involved 68 patients diagnosed with the black esophagus, with a mean age of 60.37 (16.28) years. The majority of the patients were males (67%), while females accounted for 32%. The most common presenting symptom was hematemesis (55%), followed by other gastrointestinal symptoms (54%, nausea, vomiting, diarrhea, dysphagia, dysphonia, odynophagia), abdominal pain (22%), and melena (19%). Some patients experienced loss of consciousness (7%) or altered mental status (6%). Significant comorbidities included diabetes mellitus (42%), alcohol use disorder (25%), drug addiction (16%), and gastrointestinal conditions such as GERD, cirrhosis, and hepatitis (25%). Hypertension was present in 20% of the patients, while renal comorbidities (19%, including end-stage renal disease, chronic kidney disease, and renal transplant), cardiac conditions (12%), and lung disease (4% with COPD) were also reported. Malignancy was observed in 10% of the patients, and other comorbidities, such as hyperlipidemia and multiple endocrine neoplasia type 1, were present in 4% of the cases (as Table 1). Table 2 showing acute esophageal necrosis demographic and clinical data review. As per our literature review, Figure 3 shows the prognosis of black esophagus cases over the past 2 decades where the number of cases recorded in the literature has increased, likely from more awareness, early diagnosis, and resources like EGD availability across the health care system. Moreover, there is a clear increase in survival rate in patients diagnosed with black esophagus (Represented by the green line) with a downtrend of deceased patients (Represented by the red line).

Table 1: Demographics of all included patients with AEN.
Variables N=68
Age 60.37 (16.28)
Gender (%)
Male 67
Female 32
Presenting symptoms (n)
Hematemesis 38
Melena 13
Abdominal pain 15
Other GI symptoms* 37
Loss of consciousness 5
Altered mental status 4
Comorbidities (n)
Hypertension 14
Diabetes Mellitus 29
Drug addiction 11
Alcohol use disorder 17
GI (GERD, cirrhosis, hepatitis) 17
Cardiac 8
Renal (ESRD, CKD, Renaltransplant) 13
Lung (COPD) 3
Malignancy 7
Others (HLD and MEN1) 3
Table 2: Summary of literature review.
Sr. No Author EGD findings Biopsy Cause Treatment Prognosis
1 Porcu et al [18] N/A N/A Thoracic endoluminal aortic repair Cholecystostomy, Tazocilline,amikacin Deceased (non-BE related)
2 Akkinepally et al [19] Lower half of esophagus showedsigns of necrosis (exudates and distal blackening), DU N/A Alcoholic cirrhosis IVF, PPI, NPO Deceased (non-BE related)
3 Lee et al [20] Distal half blackening of theesophagus Reactive glandular cells withacute inflammation and necrosis. Alcohol-induced chemicalesophagitis with Achalasia and hypotensive episodes PPI, broadspectrum abx, IVF Survived
4 McLaughlin et al [21] Ischemic changes starting 25 cmfrom the incisors and ending abruptly at the gastroesophageal junction,shortened esophagus N/A N/A IVF, NG tube, broad-spectrum abx Survived
5 Carrillo et al [22] Typical blackish esophageallesions with exudates N/A Several hypotension episodes N/A N/A
6 Garas et al [23] N/A Features of ischaemia andassociated haemorrhagic necrosis N/A PPI, antiemetics, NPO Deceased
7 Altenburger et al [24] Esophagus was black with ischemicnecrosis of the mucosa, submucosa, and muscularis Diffuse acute inflammatoryinfiltrate, brown pigmentation limited to the mucosa N/A N/A Deceased
8 Singh D et al [25] Blackened esophagus, necroticappearing pale esophageal mucosa, and normal GE junction Necrotic debris, absence ofepithelium, granulation tissue, and heavy leukocytic infiltrates DKA NG tube, PPI, broad-spectrum abx,antifungal agent Survived
9 Singh D et al [25] Necrotic appearing friable areasof spontaneous bleeding N/A N/A NPO, PPI,100 units of botulinimtoxin injected at LES Survived
10 Singh D et al [25] Dusky appearance in distal 10 cmof esophagus with areas of superficial ulceration suggestive of ischemia N/A N/A NPO, PPI, TPN Deceased
11 Singh D et al [25] Diffuse blackened esophagealmucosa, friable mucosa N/A N/A PPI, broad spectrum abx Deceased
12 Singh D et al [25] Middle to distal esophagusappeared necrotic N/A DKA NPO, PPI Survived
13 Lahbabi et al [26] Lower third mucosa was black andcovered by an exudate of the same color associated with diffuse bleeding Necrotic debris, mucosalsubmucosal necrosis with a local inflammatory response N/A PPI, TPN Deceased
14 Pereira et al [27] Extensive candidiasis and ablack-appearing oesophageal mucosa compatible with necrosis at the distal 2/3of the oesophagus N/A Esophageal candidiasis,hypotension episode, alcohol abuse PPI, TPN, NPO, fluconazole Survived
15 Singh S et al [28] Extensive ulceration, sloughingand multiple areas of necrosis in the distal oesophagus and stomach N/A Dabigatran adverse effect PPI, broad spectrum abx, NG tube Survived
16 Kwon et al [29] Black macerated mucosa in the midthird of the esophagus and circumferential mucosal necrosis with a hugeadherent blood clot in the distal third of the esophagus N/A Coronary angiography complicatedwith hypotension PPI Survived
17 Shimamura et al [30] Thick black stripes involving thedistal esophagus, with a sharp demarcation at the squamocolumnar border Leukocyte infiltration withhemosiderosis. DKA IVF, PPI, NPO Survived
18 Lu et al [31] N/A N/A Foreign body ingestion Exploratory laparotomy (removedthe fish bone) Deceased
19 Zaid et al [32] Circumferential blackpigmentation, fragile esophageal necrotic mucosa, and multiple superficialulcerations in the middle and lower thirds of esophagus.The lower one-thirdof esophagus was covered with dark exudates, oozing fresh red-colored bloodwith minimal touch Focal area of ulceration. Theulcerated area was replaced by local inflammatory changes comprising necroticdebris, neutrophil exudates, hemorrhage, and background fibrinous materialdeposition. N/A IVF, PPI, NPO, analgesia, TPN Survived
20 koksal et al [33] Circumferential, black colored,necrotic distal esophageal mucosa abruptly turning to normal at thegastroesophageal junction and a giant necrotic based ulcer covering theanterior aspect of the first portion of the duodenum. N/A DM IVF, PPI, NPO,sulbactam-ampicillin N/A
21 Galtes et al [34] N/A Severe necrosis of the mucosa andsubmucosa with absence of viable squamous epithelium and an abundance ofnecrotic debris. Marked acute inflammatory infiltrates and partialdestruction of muscle fibres DKA N/A Deceased
22 Kim S et al [35] Necrotic tissue on loweresophagus, necrotic tissue from bulb to distal area of duodenum N/A Likely from COVID-19 infection NG tube, IVF, PPI, NPO, broadspectrum abx Survived
23 Pineo et al [36] N/A N/A cocaine abuse PPI, IV opioids, NG tube, G-CSF,broad-spectrum abx, exploratory laparotomy Deceased
24 Shafa et al [4] black necrotic mucosacircumferentially throughout the entire esophagus. N/A Septic shock supportive care Deceased
25 Shafa et al [4] diffuse esophageal necrosis aswell as a small segment of denuded mucosa that was actively oozing blood N/A alcohol abuse or heart failure Bleeding esophageal segment wasinjected with epinephrine, PPI, NPO, TPN Survived
26 Shafa et al [4] acute esophageal necrosis from thecricopharyngeus to the gastroesophageal junction Inflammatory exudate and necroticdebris N/A IV PPI, NPO Survived
27 Shafa et al [4] circumferential necrosisthroughout the esophagus and a mid-esophageal stricture 5 cm in length. N/A Alcohol, cocaine, cannabis abuse, DKA Surgically placed gastrostomy tubeand supportive therapy Survived
28 Shafa et al [4] pan-esophageal necrosis withcircumferential involvement distally N/A N/A Supportive care Deceased
29 Shafa et al [4] necrosis in the distal third ofhis esophagus N/A multiorgan dysfunction N/A Deceased
30 Alcaide et al [37] Esophageal lumen diffuselydilated, with submucosal hemorrhages and confluent violet-blackish areas,hiatal hernia Esophageal mucosa withmicro-hemorrhages and microscopic foci of necrosis N/a IVF, PPI survived
31 Nunes et al [38] black esophagus covered with darkfluid, hyperaemia and erosions. N/A Paraesophageal hernia and gastricvolvulus Emergency surgery repaired thediaphragmatic hernia, achieved volvulus reduction and a Nissen fundoplication survived
32 Osterman et al [39] Severe diffuse ulcerationbeginning in the mid esophagus, with continued severe ulceration throughoutthe distal esophagus, stomach and duodenum N/A re-initiating clozapine andquetiapine N/A Deceased
33 Matsuo et al [40] black esophagus with ulceratedlongitudinal necrosis in the lower esophagus N/A N/A PPI, NPO survived
34 Crescenzi et al [41] diffuse, circumferential,blackappearing mucosa in the distal third of the esophagus N/A Septic shock IVF, PPI, TPN and broad-spectrumabx survived
35 Ullah et al [42] circumferential necrotic, friableoesophagus that extended from 21 cm to 40 cm from the incisors. There wasassociated friable red mucosa N/A cocaine abuse IVF, PPI, sucralfate suspension Deceased
36 Sato et al [43] black discoloration from theesophagus to the gastric junction, esophageal perforation and blackdiscoloration in the duodenem N/A N/A thoracic cavity drain, esophagealstent (FSEMS), SBT gastric balloon, IVF survived
37 Haghbayan et al [44] circumferential black mucosa inthe distal esophagus, immediately proximal to the gastroesophageal junction N/A DKA PPI, NPO, insulin, IVF survived
38 Kondo et al [45] diffuse black discoloration of theesophageal mucosa that affected the distal esophagus and stopped abruptly atthe gastroesophageal junction Necrosis of the esophageal mucosa DKA PPI, NPO, insulin, IVF survived
39 Ullah et al [46] circumferential necrotic, friableoesophagus extending from 21 to 38 cm from the incisors N/A Dialysis-induced hypotension NG tube, IVF, PPI, IV sucralfate Deceased
40 Tomori et al [47] necrotic esophagitis in the middleand lower parts of the esophagus and duodenal erosions No findings suggestive ofesophageal necrosis Strongyloides stercoralishyperinfection and dissemination NG tube, ivermectin, broadspectrum abxkim s survived
41 Dias et al [48] friable, diffuse black-appearingdistal esophageal mucosa with an abrupt transition at the gastroesophagealjunction N/A Septic shock Percutaneous cholecystostomy, IVF,PPI, NPO, broad-spectrum abx survived
42 Uyar et al [49] diffusecircumferential black appearance throughout the entire esophagus mucosa Histologicalappearance of Candida hyphaes and necrosis in esophagus tissue N/A PPI, IVF, anti-fungal for candidain the bx N/A
43 Tanaka S et al [50] diffuse erosiveesophagitis with black discoloration predominantly affecting the loweresophagus and abruptly interrupted at the gastroesophageal junction N/A N/A PPI, IVF, abx N/A
44 Siddiqi A [51] inflammation of theepiglottis, arytenoid cartilages, and dark mucosal pigmentation of the distaltwo-thirds of the esophagus with associated hiatus hernia Fragments offibrinopurulent exudate, and necrotic tissue with predominant neutrophilinfiltration indicating severe inflammation N/A PPI, IVF, abx N/A
45 Deliwala Ss et al [52] Blacknecrotic-appearing mucosa encompassing the entire esophagus and endingabruptly at the GEJ with associated gastric erosions and proximal duodenalulcerations Acute esophagealsterile gangrenous necrosis N/A PPI, IVF, abx N/A
46 Bhattacharya et al [53] Circumferential black oesophagealmucosa extending proximally from the gastro-oesophageal junction. The duodenumcontained microscopic foci of neuroendocrine tumour consistent withgastrinoma. MEN related PPI, IVF, abx Survived
47 Kim NY et al [54] Circumferentialblack pigmentation, and edematous mucosa covered by exudates was noted at themid-lower esophagus An ulcer, andimmunohistochemistry showed negative cytomegalovirus (CMV), herpes simplexvirus (HSV-1), and HSV-2 polymerase chain reaction findings. post renal transplantation PPI, abx Survived
48 Kroner et al [55] Diffuse severemucosal changes of the middle and lower third of the esophagus characterizedby black-discoloration, erythema, and friable tissue with ulceration,sloughing and contact bleeding Biopsies wereconsistent with acute esophageal necrosis, also known as “black esophagus”. post renal transplantation PPI, and TPN Survived
49 Riascos et al [56] Extensive esophagealnecrosis from the cricopharyngeal muscle to the esophageal-gastric junctiontransmurally at 30 cm, with a perforation of approximately 15 mm at 35 cm. N/A N/A PPI, abx, fluconazole Survived
50 Laverick et al [57] A blackdiscolouration of the distal oesophagus with deep black ulcers and diffuseoozing of blood. N/A N/A PPI, abx Survived
51 Mustafa et al [58] Two large 1.5–2 cmwide-based ulcers in the distal oesophagus without active bleeding An ulceratedsquamous mucosa with extensive necrosis extending to the muscularis propria.Coccoid bacterial colonies and rare fungal forms suggestive of Candidaspecies were seen in the necrotic areas. N/A PPI, fluconazole Survived
52 Iwamoto et al [59] Entire circumferenceof the whole esophagus was shown to have turned black N/A HHS treated the HHS Survived
53 okamoto et al [60] N/A N/A N/A Survived
54 okamoto et al [60] N/A N/A N/A Survived
55 okamoto et al [60] N/A N/A N/A Survived
56 okamoto et al [60] N/A N/A N/A Survived
57 okamoto et al [60] N/A N/A N/A Survived
58 okamoto et al [60] N/A N/A N/A Survived
59 okamoto et al [60] N/A N/A N/A Survived
60 okamoto et al [60] N/A N/A N/A Survived
61 okamoto et al [60] N/A N/A N/A Survived
62 Kitawaki [61] circumferentialnecrosis of the middle and distal esophagus, immediately proximal to thegastroesophageal junction N/A N/A PPI
63 alsakarneh et al [62] severe inflammationwith black discoloration consistent with acute esophageal necrosis in themiddle and lower esophagus, and erythematous duodenitis N/A N/A PPI, sucralfate, NPO Survived
64 Jeican et al [63] N/A N/A N/A N/A Deceased
65 Ifuku [64] circumferential mucosal injury andpartial necrosis from the middle esophagus to the gastroe- sophageal junctionwith a sudden transition to normal mu- cosa at the distal portion N/A cynotic spells from co-morb PPI and NPO for 2 days Survived
66 Greco S et al [65] circumferentialblack appearance of the esophageal mucosa, as in concentric necrosis of thedistal esophagus with possible fungal superinfection. Fungal hyphae by Candida spp. N/A IV fluconazole Survived
67 Patil et al [66] Diffuse ischemic andnecrotic mucosa beginning approximately 20 cm from the teeth and extendingdistally, and a large distal esophageal perforation extending into thestomach. Gross surgicalspecimen analysis and immunohistochemistry were consistent with diffusenecrosis. N/A surgical esophagectomy andcervical esophagostomy Survived
68 Gonzalez diaz et al [67] diffuse circumferential blackmucosa covered by fibrin, affecting the middle third and distal esophagus.These changes progressively worsened from the proximal to distal esophagus,until reaching the eso- phagogastric junction N/A N/A N/A N/A
Figure 1: Computed tomography (CT) scan imaging showing peritoneal carcinomatosis with a large pelvic mass measuring 166.5 mm in size.

Figure 2: Esophagogastroduodenoscopy (EGD).
Endoscopic features of black esophagus showing diffuse esophageal necrosing in all the three images.

Figure 3: Prognosis of black esophagus cases from 2009 to 2024, per our literature review.
Demonstrates the prognosis of black esophagus cases over the past 2 decades where the number of cases recorded in the literature. Additionally, showing linear trends, blue line representing increase in total number of cases, red line indicating decrease in mortality and green line indicating improved survival.

Discussion

The findings from our literature review are consistent with the existing knowledge of black esophagus. The mean age of the patients in our study (60.37 years) aligns with the reported predominance of this condition in older adults, likely due to the presence of comorbidities and compromised vascular supply.[8] The male predominance (67%) observed in our study is also consistent with previous reports, although the underlying reason for this gender difference remains unclear [9]. The presenting symptoms and comorbidities identified in our study are in line with the established literature. Hematemesis (55%) and other gastrointestinal symptoms (54%) were the most common presenting complaints, reflecting the underlying mucosal injury and bleeding associated with black esophagus.[10] Comorbidities such as diabetes mellitus (42%), alcohol use disorder (25%), and gastrointestinal conditions (25%) are well-recognized risk factors for the development of black esophagus, as they can contribute to vascular compromise, mucosal ischemia, and esophageal injury [11,12]. In the current case report, the patient was an elderly female with multiple comorbidities, including diabetes mellitus, hypertension, and hyperlipidemia. While she did not have any known history of alcohol or drug abuse, her advanced metastatic cancer and overall poor prognosis likely contributed to a compromised vascular supply and increased susceptibility to esophageal necrosis. Similarly, a study by [13], providing a broader perspective on prognostic factors for mortality, showed that age, low hemoglobin, and hypotension were factors associated with increased mortality. Notably, my patient had all three of these risk factors, which increased her mortality risk. Interestingly, our analysis found a relatively high prevalence of malignancy (10%) among patients with black esophagus. While malignancy itself may not directly cause black esophagus, the associated treatments or complications (e.g., chemotherapy-induced mucositis, malnutrition, immunosuppression) could potentially predispose patients to this condition. This finding is particularly relevant in the context of our case report [14], where the patient’s underlying malignancy and poor prognosis likely played a significant role in the development of black esophagus. It is noteworthy that Day et al. published a case report with a review of the literature in 2009, which included most of the cases reported until 2008. In our review, we excluded those studies and focused on more recent cases [15], incorporating literature from 2009 to 2023, making our case report one of the most up-to-date compilations of black esophagus cases. The management of black esophagus typically involves supportive care, including intravenous fluid resuscitation, proton pump inhibitors, antibiotics, and nutritional support. In our case report, the patient received appropriate management with intravenous proton pump inhibitors [16], sucralfate, and hydration. However, given the patient’s overall poor prognosis due to advanced metastatic disease, no further interventions or follow-up endoscopy were pursued, aligning with the palliative care approach. It is important to recognize that black esophagus can be a manifestation of underlying systemic illness or compromised vascular supply, and prompt diagnosis and management are crucial to prevent potential complications, such as esophageal perforation, mediastinitis, or sepsis. In cases of advanced malignancy or poor prognosis [17], as in our case report, the management may be tailored toward symptom control and palliation, with careful consideration of the risks and benefits of invasive interventions.

Conclusion

Acute esophageal necrosis is an uncommon but severe condition typically affecting older individuals with underlying medical conditions that compromise blood flow to the esophagus. Rapid diagnosis through endoscopy and prompt supportive treatment, such as intravenous fluids, proton pump inhibitors, and antibiotics, are essential. However, in cases where patients have advanced malignancy or a poor overall prognosis, the management approach may focus more on palliative care and symptom relief, carefully weighing the potential risks and benefits of invasive procedures.

Acknowledgement: None.

Conflict of interest: None.

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