An Unusual Complication of Diverticular Bleed: Dysphagia and Food Impaction from Black Esophagus Open Access

Acute esophageal necrosis, otherwise known as “black esophagus,” is a rare clinical phenomenon with an incidence less than 0.3% [1]. The typical illness script includes an older man who presents following an inciting hemodynamic event with chest and/or epigastric pain, upper GI bleeding, and dysphagia [2].

The pathophysiology of acute esophageal necrosis is unclear, but it is theorized that a background chronic condition both predisposes the esophagus to vascular compromise and decreases the local mucosal barrier mechanisms in place to help prevent significant injury [1, 3]. With this predisposition, an acute event such as hemodynamic compromise or gastric outlet obstruction can be a major trigger that leads to necrosis. The rarity of the condition is closely tied to the form and function of the esophagus; its vascular supply typically includes adequate collateral flow to prevent perfusion deficit even during a systemic hemodynamic compromise. However, the distal esophagus receives the least blood supply and for that reason is typically the first area to be observed as necrotic [3].

Dysphagia from acute esophageal necrosis could be due to several mechanisms. As the esophageal necrosis heals, stricturing can develop, causing a mechanical obstruction to solids as they pass through the esophagus. The motility of the esophagus may also be compromised if deeper layers that include neural mechanisms for peristalsis are affected by injury [1, 4].

Here, we report a case report of a patient who developed acute esophageal necrosis after a significant diverticular bleed, later complicated by dysphagia and food impaction. This case adds to the current literature on this topic as it is a variant of the typical illness script. Also, by discussing the complication of dysphagia during the recovery phase in particular, it equips readers with knowledge to better support patients as they are healing.

A 77-year-old woman with a history of coronary artery disease with recent non-ST elevation myocardial infarction and drug-eluting stent placement in November 2023 on dual antiplatelet therapy with aspirin and clopidogrel, heart failure with mid-range ejection fraction of 45%, type 2 diabetes mellitus, and stage 3 chronic kidney disease presented with a chief complaint of bloody stool on 23 December 2023 to an outside hospital. Low-dose aspirin was continued, but clopidogrel was first held in the setting of active GI bleed. She initially underwent colonoscopy on 27 December 2023 with identification of actively bleeding diverticula in the hepatic flexure that was treated with 6 endoclips. Her bleeding stopped but then recurred after restarting clopidogrel as well as intravenous heparin, which had been started after discovering bilateral deep vein thromboses. Both heparin and clopidogrel were subsequently held. A CT angiogram on 28 December 2023 showed active extravasation of contrast within the hepatic flexure at the site of previously placed clips. Arteriography demonstrated active extravasation from a branch of the middle colic artery supplying the hepatic flexure, and this vessel was successfully embolized and the bleeding resolved. After this, she remained clinically stable and only clopidogrel was resumed.

Two days after embolization, she developed severe chest pain. A repeat acute coronary syndrome workup was first performed but was unremarkable. Her chest pain improved, but over the following days she developed severe and progressive dysphagia. She ultimately underwent an EGD on hospital day 13, which revealed a black, necrotic appearing esophagus involving 15 cm of the distal esophagus terminating at the GE junction. Also present was a 5 cm sliding hiatal hernia. Esophageal biopsies were taken at the most proximal area of mucosal abnormalities to confirm the diagnosis and exclude infectious etiologies. Pathologist review of the biopsies showed active esophagitis with associated coagulative necrosis with stains negative for CMV and HSV (shown in Fig. 1).

Following her EGD, she was continued on an intravenous proton pump inhibitor bolus dosing (pantoprazole 40 mg BID) and sucralfate suspension (1 g 4 times a day) was added. A CT-A of her chest revealed no important underlying vascular cause of necrotic esophagus.

The patient was started on clear liquids the day following EGD and eventually advanced to a mechanical soft diet 3 days later. However, the following day, she complained of new dysphagia to solids, liquids, and pills. Given this, there was concern for food impaction, and a repeat endoscopy was done the same day that revealed food and liquid stasis in the distal esophagus, sloughing mucosa, and lack of peristaltic waves (shown in Fig. 1). No stricture was present. The bolus of food and debris was partially removed with a triceps grasper with the remainder passed into her stomach. On discharge 3 days later, her dysphagia had completely resolved and she was maintained on a full liquid diet only, with plan on repeat outpatient endoscopy prior to diet advancement.

Two months later, she presented to an outside hospital with complaint of dark stool at home and underwent an EGD that showed a completely healed esophagus without source of bleed. At this point, her dysphagia was completely resolved and she was tolerating a fully solid diet.

In this case, we present details of a patient with several cardiovascular comorbidities who had significant hemodynamic compromise from a lower GI diverticular bleed and subsequently developed acute esophageal necrosis, chest pain, and dysphagia with food impaction. We hypothesize that this patient’s comorbidities, including coronary artery disease, CKD, and diabetes, may have predisposed her to esophageal injury in the setting of a low-flow state during hemorrhagic shock. Previously published cases involved patients with similar comorbidities and severe hemodynamic compromise preceding the discovery of esophageal necrosis [5]. Another possibility is that her 5 cm hiatal hernia may have led to a gastric volvulus during her recovery or hiatal hernia-related gastroesophageal reflux may have compromised esophageal barrier protection and contributed to esophageal injury. Her acute episode of chest pain after embolization likely represented the esophageal injury event.

This case offers several unique clinical lessons. First, dysphagia and chest pain should be taken seriously after hemodynamic compromise, particularly in patients with pre-existing cardiovascular comorbid conditions, as esophageal necrosis remains on the differential. Second, the motility of the esophagus during the healing phases after acute esophageal necrosis can be compromised, leading to severe complications such as food impaction even in the absence of clear stricture formation. Early endoscopic evaluation if the patient has worsening dysphagia after initial diagnosis, as was done in this case, is important to consider. Diet may need to be limited to liquids and some may even require parenteral support until dysphagia related to acute esophageal necrosis has resolved. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000545171).

Ethical approval is not required for this study in accordance with local or national guidelines. Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.

The authors have no conflicts of interest to declare.

This study was not supported by any sponsor or funder.

N.N. and B.T. primarily wrote the manuscript. M.M. contributed pathology slides and descriptions. C.C, C.H., D.K., and S.M. provided manuscript edits and feedback.

The data that support the findings of this study are not publicly available due to privacy reasons but are available from the corresponding author upon reasonable request.