Acute esophageal necrosis in the post-operative period: a narrative review of presentation, management, and outcomes

Introduction

Acute esophageal necrosis (AEN) is a rare clinical condition characterized by diffuse, circumferential, black mucosal discoloration of the distal esophagus. Classically the mucosal involvement stops abruptly at the gastroesophageal junction, sparing the gastric mucosa. The condition was first described by Goldenberg in 1990 as acute esophagitis, and then further defined as a distinct syndrome by Gurvits et al. in 2007 (1,2). Since then, AEN has been reported in small case series and individual case reports. The cause is likely multifactorial and can be a sequela of severe conditions including multisystem organ failure, sepsis, gastric volvulus, and trauma. Importantly, the mortality in patients with AEN has been documented to be as high as 32% (3).

Although rare, the incidence of AEN is likely underestimated, as some patients are misdiagnosed or may succumb to other injuries prior to diagnosis (4). AEN has previously been described in the post-operative period, although the etiology has not been clearly defined (5,6). It is important to further classify both the risk factors and clinical course to help aid in an early identification and successful management of these acutely ill patients. Here we provide a review of the current literature focusing on early identification and management to aid in successful treatment of AEN. In addition, we present an outline of the acute presentation of AEN in the post-operative period, showcasing key initial signs and symptoms, subsequent imaging, and procedures that demonstrate the clinical course of this rare condition (Figure 1). We present this article in accordance with the Narrative Review reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-22-1763/rc).

Figure 1 Visual abstract: presentation, diagnosis and management of a patient with acute esophageal necrosis in the post-operative period. Images used are from a patient who developed AEN in the post-operative period after resection of a pulmonary neoplasm. Focus on identification of early signs of symptoms of upper GI bleeding with hemodynamic instability followed by prompt diagnosis of esophageal necrosis on upper endoscopy. Supportive care including transfusion of blood products and crystalloid, airway protection and targeted blood pressure management. Imaging at this point is not necessary but may help guide the underlying cause of AEN and hemodynamic instability. If no improvement in 24 hours, recommend repeat upper endoscopy in the operating room and targeted intervention when application. In addition to perioperative stress, perforation of underlying duodenal ulcer contributed to development of AEN in this patient, requiring operative intervention. AEN resolved after underlying stressors were addressed. GI, gastrointestinal; AEN, acute esophageal necrosis.

Methods

A literature review of PubMed (MEDLINE) and Google Scholar was conducted 12/1/2020 and an update added from 12/1/2022. Search terms included: acute esophageal necrosis, AEN, and black esophagus (Table 1, Table S1). In combination of clinical experience with AEN, studies included consisted of case-reports, case series and reviews providing information on patient presentation, diagnosis, and management.

Key findings

Epidemiology

Black esophagus, or AEN, was first identified on autopsy in 1967, with a variable incidence reported subsequently (7). Two large retrospective studies reviewed over 100,000 endoscopies to identify cases of AEN and associated conditions. The first study found an overall incidence of 0.01% in 80,000 esophagogastroduodenoscopics (EGDs) over 16 years (8). Half of these patients recovered without recurrence and were alive and well 1 year later, whilst the other half succumbed to their injuries. The second study reviewed 10,295 endoscopies, and documented an incidence of AEN at 0.28% (9). A prospective study evaluating 3,900 endoscopies over a 1-year period found the incidence of AEN (0.2%) to be consistent with prior retrospective studies (10). The incidence is likely underrepresented as some patients may have a self-limited subclinical presentation, and early healing in which they may not present to a hospital for evaluation.

Pathophysiology

The etiology of AEN is multifactorial, linked to the combination of tissue hypoperfusion, as seen in hemodynamic compromise, decreased functional mucosal barrier, and corrosive injury due to gastric fluid (11). Vasculopathies associated with diabetes, cardiovascular disease, and renal disease may be risk factors for tissue injury and low flow states. Hypotension can lead to transient ischemic compromise of the esophagus and may play a role in the development of AEN. In addition, prolonged periods of hypotension intraoperatively may lead to transient ischemia (12). Cases of AEN have been reported in patients with malignancies, anticardiolipin antibody syndrome, and atherosclerosis, possibly due to underlying coagulopathies leading to vascular compromise (13-15).

Vasculopathy of the esophagus may explain the association with duodenal pathology that has been seen in AEN, as the blood supply is shared. Compromised blood flow through the celiac axis may lead to local tissue hypoxia in the duodenum and distal esophagus. This can lead to ulcerations, edema and inflammation of the duodenal bulb, resulting in gastric outlet obstruction, which can further contribute to the development of AEN (16). There also appears to be a link in the extent of esophageal involvement and duodenal disease. Cases of AEN with more extensive proximal and mid-esophageal involvement were associated with significant duodenal disease when compared to more mild cases involving only the distal esophagus (4). Presentation of AEN with disease extension into the mid-esophagus should prompt investigation into duodenal pathology.

Despite the presumed association of low flow states/vasculopathies with AEN, it is important to note the esophagus does have a rich blood supply, from arteries off the aorta, it is difficult to cause outright infarction of the esophagus. However, the lower esophagus is a potential watershed area given its supply off the terminal branches of the left gastric artery, creating a potential watershed area. This may explain the predilection of this area for local injury (17). Some studies hypothesized that esophageal spasm may also pay a role in decreased blood flow to the esophagus, contributing to necrosis (18).

Risk factors

Evaluation of approximately 100 case reports of AEN over the past twenty years has revealed some associated risk factors which may aid in diagnosis (19). Men are at higher risk, as are patients greater than 65 years of age (1,20). There is a clear association of AEN with multiple comorbidities and severe stress such as trauma and multisystem organ failure (21-23). Thirty-eight percent of patients diagnosed with AEN have a documented history of diabetes, 37% have hypertension, and 16% have chronic kidney disease (3). Alcohol abuse, coronary artery disease and hyperglycemia diabetic ketoacidosis are documented risk factors as well (24-34). Malnutrition and baseline anemia are associated with poor outcomes after AEN (35). Gastric volvulus and even paraesophageal hernias have been described in the literature as possible etiologies (36). Duodenal and/or gastric ulcer disease is seen in approximately 4% of patients, and gastroesophageal reflux in 9% (3).

While development of AEN has a strong association with multiple comorbidities, it can occur in otherwise healthy patients. Notably, we have observed this phenomenon in a healthy patient after successful resection of pulmonary neoplasm with minimal co-morbidities who presented with acute onset upper gastrointestinal bleeding (37). In these patients, it is important to look for early presenting signs and symptoms to help guide the diagnosis. Common presenting symptoms include tachycardia or hypotension, in addition to acute onset of epigastric pain and dysphagia.

Based on case reports of AEN in the post-operative period, surgery has been described as a possible trigger. This may be explained by impaired regeneration of the esophagus in response to altered cytokine environment, leading to increased susceptibility to mucosal ischemia. This, in combination with hypotension or blood loss in the peri- and intra-operative period, may explain the increased risk of tissue necrosis in this patient population (38). AEN has been reported after planned operations such as cholecystectomy and rectosigmoid resections in patients with multiple underlying comorbidities (39,40). In these cases, the patients presented with acute onset of upper gastrointestinal bleeding, were identified early, and recovered with limited long-term sequelae. Esophageal necrosis has also been reported in complex amputations associated with systemic infection (41). In that case, the patient developed multisystem organ failure and succumbed to his injuries.

Transplant patients are also at increased risk for AEN, with cases occurring in the immediate post-transplant period and other later presentations attributed to graft vs. host disease (42-46). In some cases, AEN is a consequence of opportunistic infections such as cytomegalovirus esophagitis (47). In these patients, EGD with biopsy is diagnostic, and antivirals are therapeutic (48). Thus, transplant patients represent another population that requires a higher level of suspicion, based on their altered hemodynamics and immunosuppression.

AEN is also reported during the post-operative period after oncologic lung resections (49). This is believed to be associated with the paraesophageal lymph node dissection performed during lung cancer operations (50). As previously discussed, the likelihood of devascularizing the esophagus is low; nevertheless, it is possible to cause transient changes in the microcirculation. This, in combination with potential comorbidities, perioperative changes in hemodynamics, may put these patients at higher risk. It is important to keep AEN in the differential if complications arise in the post-operative period in these patients.

Presentation and diagnosis

Black esophagus classically presents with acute upper gastrointestinal hemorrhage in patients. This primarily manifests as acute onset of hematemesis but may be more insidious with melena (51). Patients also may have abdominal pain, nausea, reflux, or syncope. Initial patient evaluation would then reveal signs of hemodynamic instability such as tachycardia and hypotension. Laboratory evaluation would show new onset anemia, secondary to acute blood loss, and possibility a reactive leukocytosis.

Endoscopic evaluation remains the gold standard in the diagnosis of AEN. The classic appearance of circumferential necrotic mucosa, affecting mostly the distal esophagus and stopping abruptly at the gastroesophageal junction, is diagnostic; proximal extension can be seen, although diffuse involvement is rare. Other associated endoscopic anomalies include signs of bleeding, duodenal ulcers, gastritis, and edema. Histologic evaluation is not necessary to make the diagnosis but may provide some benefit (52). Findings include necrotic mucosal debris, leukocyte infiltration, vascular thrombi, and other inflammatory changes. Biopsies should be sent for bacterial, viral, and fungal cultures to help narrow the differential, especially in immunocompromised patients as they are at higher risk for infections (11,53).

Staging criteria introduced in 2007 by Gurvits et al. classifies the disease progression and helps guide clinical management (1). Stage 0 is a viable and pre-necrotic esophagus. Stage 1 is the acute phase of AEN, classified by circumferential necrotic and friable mucosa with yellow exudates. As described above, these findings start at the gastroesophageal junction and extend proximally at varying lengths. Stage 2 is the healing phase, characterized by white exudates, pink mucosa, and occasional black patchy areas. The time interval from stage 1 to 2 varies from as early as 1–2 weeks after diagnosis to a month. The final phase, stage 3, is return to normal esophageal mucosa. The time required to recover varies from weeks to a month. Progression from stage 1 to stage 2 can be achieved in as early as 7 days from diagnosis and reached stage 3 in 15 days from correction of the underlying problem (Figure 2).

Figure 2 Stages of acute esophageal necrosis: visual demonstration of the phases of acute esophageal necrosis, along with the approximate time of onset and characteristic features.

Initial management

Appropriate management for patients presenting with AEN is supportive care with a focus on the driving cause of their physiologic stressor. Correction of anemia, electrolyte abnormalities, and strict nil-per-os should be implemented immediately. Medical management with intravenous proton pump inhibitors is also necessary to mitigate local damage to the gastric mucosa. The focus should then shift to the identification and management of any underlying problems. Endoscopy should be performed early and repeated to classify progression. While prophylactic antibiotics are not recommended, they should be utilized in patients with fevers or rapid decompensation where esophageal perforation is suspected. Computed tomography (CT) angiogram has not been described as necessary for diagnosis; however, it may help eliminate other differential causes of ischemia (Figure 3). Close hemodynamic monitoring in an intensive care unit setting is recommended, as this condition can quickly progress to requiring emergent and aggressive intervention.

Figure 3 CT angiogram of the thoracic and abdominal aorta with 3D reconstruction demonstrating patency of the celiac access and left gastric artery (yellow arrows). CT, computed tomography; 3D, three-dimensional.

Parenteral nutrition should be initiated once the patient has stabilized, as nutrition is importation for mucosal recovery. Surgically placed feeding tubes are not recommended in all patients, however, there are situations where they provide benefit. If the patient is not suited for oral nutrition for an extended period, a feeding tube can be a useful adjunct in optimizing nutritional status during the post-operative course. Oral nutrition can be attempted after recovery from the acute phases. If it is not tolerated, parental nutrition should be continued until the esophagus has fully recovered (54).

Sequela

Acute surgical intervention in cases of AEN is reserved for extreme cases. Esophageal perforation is seen in approximately 7% of all known cases, and is the most worrisome complication with a documented mortality rate of 40% (1,55). The AEN staging system helps guide complication potential during each phase of the disease. Perforation usually occurs during stage 1 and stricturing in stages 2 and 3 (1). In general, strictures can be managed with endoscopic dilation (56,57). Additionally, fully covered metallic stenting of the esophagus has been successfully performed to aid in controlling bleeding although embolization was also performed (58). Perforation is rare, but cases of successful surgical intervention have been reported. Akaishi et al. reported a case of perforation on day 7 after diagnosis, requiring emergent subtotal esophagectomy with esophagostomy and enterotomy (59). The patient recovered well, but did subsequently develop strictures, requiring multiple dilations and eventual reconstruction (59). Additional cases of severe strictures have been reported that eventually required esophagectomy when dilation could not safely be performed (60).

As discussed above, there has been an observed association with duodenal ulcers and inflammation with AEN (61). Recurrent AEN has been documented in patients with duodenal pathology, likely secondary to persistent inflammation and gastric outlet obstruction (35). This is important to keep in mind as a possible underlying cause in patients presenting with AEN, as their worsening clinical status may be related to progression of ulcerative disease (i.e., perforation). Initial endoscopic evaluation of patients presenting with AEN should include an examination of the duodenum for potential pathology. Although rare, AEN should be in the differential diagnoses in post-operative patients with acute onset of upper gastrointestinal bleeding, especially if they have a history of ulcerative disease.

Conclusions

AEN is a rare condition in which the mucosa of the distal esophagus becomes necrotic, usually as a response to a severe physiologic stress. Surgery is widely recognized as a physiologic stressor and as a result AEN can be seen in the post-operative period. While the reports are limited in this population, the management of AEN remains the same as in non-surgical stimuli. Identifying risk factors and trends may help diagnose this condition early, lower long-term morbidities. While AEN has been documented as having a high mortality rate, it is possible with early identification and intervention that patients can recover without long-term sequelae.

Acknowledgments

Funding: None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-22-1763/rc

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