Esophagitis dissecans superficialis—clinical presentation, diagnosis, and management

Introduction

Background

Esophagitis dissecans superficialis (EDS), also known as sloughing or desquamative esophagitis, is a benign condition involving superficial necrosis and detachment of the esophageal squamous epithelium with preservation of the deeper layers (1). EDS was first described in 1892 by B Rosenberg, who reported a peeling appearance of the esophageal mucosa in a patient with chronic dyspepsia and vomiting (2). In 1935, Patterson described a series of patients with similar findings and referred to the condition as esophagitis exfoliativa (3). In the late 1990s, gastrointestinal pathologist Audrey Lazenby introduced the term sloughing esophagitis, with subsequent studies confirming that this designation refers to the same clinicopathologic entity as EDS (4).

EDS is often self-limiting and is characterized histologically by a distinctive two-toned appearance of the squamous epithelium, created by a partial or complete detachment of a superficial layer of necrotic epithelium overlying a viable deeper layer (5). This microscopic separation gives rise to the characteristic endoscopic appearance of sloughed or peeling esophageal mucosa (6,7). Diagnosis relies on correlation between endoscopic findings and histopathologic features, both of which are distinctive and, when interpreted together, allow for reliable identification of the condition (6).

Rationale and knowledge gap

Despite being recognized for more than a century, EDS remains uncommon and likely underdiagnosed. It is frequently discovered incidentally during endoscopy, and its striking mucosal appearance may be mistaken for infectious esophagitis, eosinophilic esophagitis, or neoplastic processes (8). Although prior reviews have summarized the clinical and histopathologic features of EDS, important gaps remain in understanding its underlying mechanisms, clinical spectrum, and optimal diagnostic framework. A recent study proposed distinct histologic subtypes of EDS based on the presence or absence of inflammatory infiltrates, suggesting that the condition may represent a heterogenous spectrum rather than a single unfirm entity. Emerging reports also describe rare associations with newer medication classes, including immunotherapies such as immune checkpoint inhibitors, highlighting the need to consider EDS within the context of modern treatment-related toxicities (9). In addition, optimal approaches to diagnosis and management remain incompletely defined. These gaps emphasize the need for an updated synthesis that consolidates current knowledge, underscores ongoing clinical uncertainties, and provides guidance for clinicians encountering this rare entity.

Objective

This manuscript provides a review of the clinical presentation, histopathologic and endoscopic features, associated conditions, and current management strategies for EDS, with the goal of improving recognition of this uncommon entity in clinical practice.

Clinical and epidemiologic overview

EDS is an uncommon condition most frequently reported in older adults undergoing endoscopy for a variety of upper gastrointestinal symptoms. Clinical presentation varies widely, ranging from asymptomatic incidental findings to dysphagia, odynophagia, globus sensation, nausea, vomiting, epigastric pain, reflux-related symptoms, and, less commonly, weight loss or iron deficiency anemia (6,7). Rarely, patients may expectorate or vomit tubular casts of esophageal mucosa (10).

Reported incidence of EDS is low. In a Belgian retrospective series, EDS was identified in approximately 0.03% among more than 21,000 upper endoscopies (8).

As summarized in Table 1, published case series indicate that EDS is most commonly diagnosed in older adults, with mean or median ages at diagnosis ranging from 32.9 to 76 years (5,7,8,11,12). Most cohorts report a predominance of female patients, with proportions ranging from approximately 55% to 85% (5,7,8,11,12). In contrast, Carmack et al. described a largely male cohort (92%), in a smaller single-institution series (6). This discrepancy may reflect regional or institutional differences in patient populations, referral patterns, or the limited sample size of the cohort.

Reported racial distributions are limited but predominantly Caucasian in larger U.S.-based studies (5,6), while other cohorts did not report racial demographics. Indications for endoscopy are heterogeneous and include dysphagia, abdominal pain, dyspepsia, heartburn, occult gastrointestinal bleeding, nausea, vomiting, and non-cardiac chest pain. A proportion of cases are also identified incidentally during procedures performed for unrelated gastrointestinal complaints (5,7,11).

Medication exposure and polypharmacy are frequently observed among affected patients, particularly in older populations. Psychoactive medications, nonsteroidal anti-inflammatory drugs (NSAIDs), and central nervous system (CNS) depressants have been commonly reported across several cohorts, suggesting that medication-related mucosal injury may contribute to disease development (5,7,11). Other triggers include rare toxic exposures such as transoral paraquat poisoning (12) or antibiotic exposure prior to endoscopy (8). Comorbidities such as chronic debilitation, impaired mobility, and systemic illness may further predispose to mucosal injury (7).

Taken together, these findings suggest that EDS most often occurs in older adults undergoing endoscopy for nonspecific upper gastrointestinal symptoms, frequently in the setting of polypharmacy or chronic comorbidities. However, variability in demographic patterns across cohorts highlights the limited size of existing studies and the need for cautious interpretation of epidemiologic trends. Table 1 provides a comparative overview of study characteristics, including patient demographics, presenting symptoms, and suspected etiologic factors reported across published case series.

Endoscopic findings

Endoscopy is essential for diagnosing EDS, allowing distinction from other causes of esophageal injury, particularly infectious esophagitis. EDS is defined by sloughing or peeling of superficial esophageal mucosa, which often appears as long vertical strips or partially detached, crumpled sheets of white epithelium (Figure 1) (1,5,7,13). Occasionally, endoscopy may reveal tubular casts of sloughed esophageal mucosa. These lesions typically occur in the distal esophagus but can extend to the middle or, less commonly, the proximal third (1,5,6). The underlying mucosa usually appears normal and intact (6). Hart et al. proposed three features suggestive of EDS: strips of sloughed mucosal strips exceeding two centimeters, normal-appearing underlying mucosa, and absence of adjacent ulceration or friability (5). Rarely, chronic EDS may lead to esophageal strictures requiring endoscopic dilation (14).

Figure 1 Endoscopic findings of esophagitis dissecans superficialis. Upper endoscopy demonstrating characteristic sloughing and detachment of the superficial esophageal squamous epithelium. Longitudinal sheets of desquamated mucosa are present with preservation of the underlying mucosa and absence of deep ulceration.

Histopathologic findings

Histologically, EDS exhibits a distinct two-layered appearance of the squamous epithelium: a superficial layer of detached epithelial fragments with intraepithelial splitting, parakeratosis, and surface necrosis, often with minimal inflammation, overlying a normal or slightly basophilic basal layer reflecting basal cell hyperplasia (Figures 2,3) (6,7,15). In some cases, a thin zone of neutrophilic infiltration is observed between the two epithelial layers, ranging from scattered intraepithelial neutrophils to multifocal microabscesses or more extensive epithelial involvement (15).

Figure 2 Routine hematoxylin and eosin-stained histologic section, 100× magnification. Histology demonstrates classic two-tone squamous mucosa, with darker staining in the basal layer and lighter staining in the superficial epithelial layers.

Figure 3 Routine hematoxylin and eosin-stained histologic section, 200× magnification. The superficial squamous mucosa demonstrates epithelial sloughing and parakeratosis.

Karaaslan et al. proposed a histologic classification of EDS based on a retrospective review of 51 patients with esophageal biopsies showing sloughing of the superficial squamous mucosa. They identified two subtypes based on inflammation: sloughing esophagopathy, which lacked inflammation and correlated with endoscopic sloughing and sloughing esophagitis, which showed neutrophilic or eosinophilic infiltration with microabscesses. Both subtypes preserved the separation of the superficial squamous epithelium, producing the characteristic two-toned appearance (11).

Pathophysiology and mechanisms

The pathogenesis of EDS remains incompletely understood but appears multifactorial, involving direct epithelial injury and impaired mucosal repair. Chemical agents (e.g., NSAIDs, bisphosphonates, potassium chloride, iron) and caustic substances can compromise epithelial integrity. Thermal injury from hot liquids and mechanical trauma from vomiting, endoscopic instrumentation, or prolonged pill contact may similarly promote detachment of the superficial squamous layer while preserving the underlying epithelium (1,5-8,16).

At the tissue level, these insults disrupt intercellular adhesion and basal cell integrity, resulting in separation of the superficial layer (5,7). Karaaslan et al. noted frequent bacterial colonization of sloughed mucosa without eliciting an inflammatory response, supporting the notion that EDS arises from direct epithelial injury and impaired mucosal repair rather than an infectious process (11).

Patient-specific factors, including advanced age, chronic comorbidities, and long-term medication use, may also impair mucosal repair and increase epithelial fragility, contributing to the development of EDS (7,11). Overall, the condition is considered a benign, reactive response to mucosal stressors rather than a primary inflammatory disorder.

Associated conditions and triggers

Medications

A number of medications have been implicated in EDS, likely due to direct topical injury and disruption of mucosal adhesion (5). The condition is most commonly reported in older adults, particularly those over 60 years, and is frequently associated with polypharmacy. Oral medications often cause pill-induced esophagitis, typically affecting the middle or distal esophagus (7,17). In their EDS cohort, Hart et al. reported that 73% of patients were taking psychoactive medications, with over half on selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs), and fewer exposed to bisphosphonates or NSAIDs (5). Purdy et al. similarly found that polypharmacy—defined as the use of five or more concurrent medications—was more common among patients with EDS than controls (77% vs. 32%), with many taking CNS depressants that may impair swallowing and promote mucosal irritation. Notably, the association between increased medication use and mucosal injury remained significant after adjusting for age, supporting the role of drug-related injury in EDS development (7). Rarely, newer systemic therapies, including immune checkpoint inhibitors, have also been implicated in esophageal mucosal injury, further expanding the spectrum of medication-related triggers (9). Table 2 summarizes medications associated with EDS and their proposed mechanisms.

Dermatologic and autoimmune conditions

EDS has been described in association with autoimmune blistering disorders, including pemphigus vulgaris (PV), mucous membrane pemphigoid (MMP), and, less commonly, bullous pemphigoid (6,10,18). Among these, PV can extend beyond the skin and oral mucosa to involve the pharynx, larynx, and esophagus (9). In such cases, esophageal bullae or erosions may progress to webs or strictures, highlighting the need for careful endoscopic and histopathologic correlation. In this diagnostic context, immunofluorescence can help distinguish autoimmune blistering disorders from EDS by detecting complement or immunoglobulin deposits (6,10,18). Supporting this association, Cesar et al. suggested that EDS may represent an acute manifestation of PV, independent of overall disease course (10). Beyond PV, other systemic autoimmune associations reported in literature include celiac disease with associated dermatitis herpetiformis (25), bullous systemic lupus erythematosus (26), and immunoglobulin G4 (IgG4)-related disease (27).

Other reported and rare associations

EDS has also been linked to lifestyle and physiologic stressors, such as smoking, chronic debilitation, impaired mobility, gastroesophageal reflux disease (GERD), repeated forceful vomiting, and Mallory-Weiss syndrome, as well as exposure to hot beverages, caustic substances, and prior mediastinal radiation (6-8). Iatrogenic causes include esophageal sclerotherapy with 5% ethanolamine oleate (28) and other endoscopic-related injuries, including traumatic passage of scope, sclerotherapy band ligation, and esophageal dilation (8,29,30). Immunocompromised states and other systemic conditions have also been associated with EDS, including patients with human immunodeficiency virus (HIV) infection (31), recipients of solid organ (32) or stem cell transplants (33), and those with renal failure (34). Rare toxin exposures include topical hair dye ingestion (35) and transoral paraquat poisoning (12).

EDS has been observed alongside Barrett’s esophagus, where chronic mucosal inflammation from GERD and tobacco use may contribute to epithelial injury. Liu et al. reported that EDS resolved following acid-suppressive therapy, with repeat endoscopy revealing short-segment non-dysplastic Barrett’s esophagus. They also noted that EDS may coexist with Barrett’s esophagus, potentially mimicking or obscuring underlying dysplasia and complicating histologic interpretation (36).

While many cases of EDS remain idiopathic, patient comorbidities, polypharmacy, autoimmune conditions, and local esophageal injury appear central to its development.

Diagnostic workup and differentials

Evaluation of suspected EDS typically involves a combination of endoscopic examination and histologic assessment. Endoscopy may reveal sloughed esophageal mucosa in sheets or fragments, but the appearance is often nonspecific. In their cohort, Hart et al. reported that only 41.5% of patients with histologically confirmed EDS were suspected to have the condition based on endoscopy alone (5).

EDS can mimic a variety of esophageal disorders, making histologic correlation essential for accurate diagnosis. Infectious esophagitis—including Candida, herpes simplex virus (HSV), and cytomegalovirus (CMV)—may produce superficial mucosal changes that resemble EDS, but the presence of fungal elements, viral inclusions, or specific inflammatory patterns distinguish these conditions (1,5,6). HSV typically causes small, punched-out ulcers, while CMV produces larger, shallow linear ulcerations (37). Unlike these infections, EDS does not result in true ulceration. Interestingly, Candida infection may coexist with EDS, further emphasizing the importance of biopsy for proper management (5).

Autoimmune blistering disorders, including PV, MMP, and bullous pemphigoid, can present with esophageal bullae or epithelial clefting, with immunofluorescence differentiating them from EDS. Severe gastroesophageal reflux-associated mucosal disease may also cause superficial sloughing, but histologically, reflux esophagitis is characterized by increased intercellular spaces (spongiosis) in the squamous epithelium (6).

Although formal diagnostic criteria for EDS have not been established, accurate diagnosis relies on the combination of endoscopic and histologic findings, which allow for differentiation from infections, autoimmune or dermatologic disorders, and other esophageal pathologies that require distinct management strategies.

Management and treatment

There are no formal guidelines for treating EDS; current approaches are largely guided by case reports, case series, and strategies used for related mucosal disorders. A key first step is identifying and addressing modifiable risk factors, such as discontinuing potential causative medications, managing coexisting dermatologic, autoimmune, or systemic conditions, and implementing lifestyle modifications, including smoking cessation, to reduce esophageal irritation (6). For patients with EDS associated with dermatologic conditions such as PV, MMP, or bullous pemphigoid, follow-up with a dermatologist is recommended.

Pharmacologic management of EDS is primarily supportive, with therapy aimed at promoting mucosal healing. High-dose proton-pump inhibitors (PPIs) or histamine-2 (H2) receptor antagonists are frequently utilized, particularly in patients with concurrent GERD or mucosal irritation (1,8). Oral sucralfate may be added alongside PPIs for symptom relief (38). In one reported case, a short course of high-dose corticosteroids produced a favorable response in a patient whose EDS was refractory to PPI therapy alone (39).

Although esophageal strictures are uncommon, endoscopic dilation may be necessary in patients with severe or longstanding disease (14). EDS is generally self-limited, and routine follow-up is not required, as no formal surveillance guidelines exist. Repeat endoscopy may be considered on a case-by-case basis for persistent or worsening symptoms, such as dysphagia, though follow-up adherence may be variable (5).

Patient education is essential and should emphasize avoiding mucosal irritants, adhering to prescribed therapies, and monitoring for symptom recurrence.

Outcomes, prognosis, and recurrence

EDS is generally benign and self-limited, with most patients experiencing symptom resolution following removal of offending agents or management of underlying conditions. Data on endoscopic follow-up are limited, as not all patients undergo repeat evaluation, making the true rate of mucosal healing unclear. When performed, endoscopic follow-up has demonstrated esophageal healing in as little as eight weeks, though timelines vary with the severity of sloughing and management of comorbidities (1,5,7). In Hart et al.’s retrospective study of 41 patients, only 34% completed follow-up endoscopy at a median of four months, and 86% of these patients exhibited endoscopic resolution; no cases of esophageal malignancy were reported at a median clinical follow-up of 10 months (5). Similarly, in Carmack et al.’s cohort of 12 patients, five who underwent follow-up endoscopy after PPI therapy demonstrated complete or near-complete resolution of sloughing esophagitis (6).

Recurrence is uncommon, but patients with ongoing risk factors—such as polypharmacy, persistent GERD, or autoimmune comorbidities—may be at higher risk. Routine follow-up endoscopy is not standardized, and most patients only undergo repeat endoscopy if symptoms persist. Early recognition and differentiation from other esophageal pathologies remain important to avoid unnecessary procedures and ensure appropriate management, particularly in patients with overlapping conditions such as autoimmune disease or infections (5).

Strengths, limitations, and paucity in literature

This review details the scattered and limited literature on EDS, integrating both endoscopic and histopathologic findings to offer a cohesive overview of this uncommon condition. The endoscopic images further enhance diagnostic recognition and understanding of esophageal mucosal changes, for endoscopists, who are often visual learners. However, most available evidence consists of isolated case reports and small retrospective cohorts, with nearly all studies including fewer than 50 patients, limiting generalizability and precluding meaningful statistical analyses. Further, the lack of consistent endoscopic follow-up may underestimate true mucosal healing. Significant gaps remain in understanding the underlying mechanisms, pathogenesis, and evidence-based management of EDS. Underreporting and misdiagnosis likely contribute to the scarcity of data, highlighting the need for larger, multicenter studies and standardized diagnostic criteria to better characterize the spectrum and outcomes of this condition.

Conclusions

EDS is a rare, typically benign condition characterized by superficial sloughing of the esophageal mucosa. Its presentation can mimic other esophageal pathologies, making recognition of distinct endoscopic and histologic features essential to avoid misdiagnosis and unnecessary interventions. Most cases resolve with supportive management and removal of potential offending agents, yet accurate diagnosis remains critical to exclude infectious, autoimmune, or neoplastic conditions. Greater clinician awareness and careful correlation of endoscopic and histopathologic findings may facilitate earlier recognition and more appropriate management. Future research should focus on developing standardized diagnostic criteria and prospective multicenter registries to better define the epidemiology, risk factors, and optimal management strategies for this uncommon clinical entity.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://aoe.amegroups.com/article/view/10.21037/aoe-2025-1-45/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aoe.amegroups.com/article/view/10.21037/aoe-2025-1-45/coif). W.B. serves as an unpaid editorial board member of Annals of Esophagus from October 2025 to December 2027. J.J. is on the Speaker’s Bureau for Sanofi and Regeneron. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Disclaimer: The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the Department of Veterans Affairs or the United States government.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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