Journal Article

Non-traumatic acute mediastinitis secondary to acute phlegmonous esophagitis: a rare case report

Journal of Surgical Case Reports, Volume 2026, Issue 10, October 2026, rjag947, https://doi.org/10.1093/jscr/rjag947
Published:
19 October 2026
Article history
Received:
03 September 2026
Revision received:
26 September 2026
Accepted:
01 October 2026
Published:
19 October 2026

Abstract

Acute mediastinitis secondary to acute phlegmonous esophagitis (APE) is an exceptionally rare, life-threatening condition with high morbidity. We report a 75-year-old diabetic female with recent severe pneumonia who presented with pleuritic chest pain, dyspnea, and elevated inflammatory markers. Computed tomography pulmonary angiography excluded embolism but revealed diffuse long-segment esophageal wall thickening with mediastinal fat stranding, aortic encasement, and pleural effusion, features consistent with APE and secondary non-traumatic mediastinitis without overt perforation. Given clinical stability, endoscopy was deferred to avoid disrupting a possible contained micro-perforation. The patient was successfully managed with 14 days of empiric broad-spectrum intravenous antibiotics (vancomycin, cefepime, metronidazole), achieving complete clinical and radiographic resolution. This case underscores that in hemodynamically stable patients without free perforation or large abscess, conservative antimicrobial therapy can be definitive. It also highlights the importance of considering APE in non-surgical patients presenting with acute chest pain.

Introduction

Acute mediastinitis is a severe, life-threatening inflammatory process involving the loose connective tissues of the mediastinum [1]. The majority of cases are iatrogenic, primarily complicating median sternotomy or esophageal perforation [2]. Non-traumatic acute mediastinitis typically stems from descending cervical necrotizing infections or direct contiguous extension from adjacent thoracic soft tissues [3].

Acute phlegmonous esophagitis (APE) is an exceptionally rare subtype of acute esophageal disease characterized by purulent bacterial inflammation within the submucosal and muscularis propria layers [4]. A 2014 literature review identified only 12 reported cases [5], and a recent 2023 systematic review of 35 cases reported a mortality rate of 8.6% [6]. Identified risk factors include uncontrolled diabetes mellitus, advanced age, immunosuppression, and malnutrition [6]. Because APE frequently manifests with retrosternal chest pain, dyspnea, fever, and leukocytosis, it is often initially mistaken for more common critical conditions such as acute coronary syndrome, aortic dissection, or pulmonary embolism [7].

When transmural bacterial transudation or occult micro-perforation occurs, APE can spread directly into the mediastinum, culminating in secondary acute non-traumatic mediastinitis [8]. Contrast-enhanced computed tomography (CT) is the gold-standard diagnostic modality for confirming mediastinal involvement [9]. Prompt recognition and multidisciplinary management are paramount, as polymicrobial mediastinal infections carry substantial hospital mortality [3]. We report a rare case of extensive non-traumatic acute mediastinitis secondary to diffuse APE successfully managed conservatively with broad-spectrum antimicrobial therapy.

Case report

A 75-year-old female presented with a 2-day history of left-sided pleuritic chest pain radiating to her back, accompanied by worsening dyspnea. Her past medical history included ischemic stroke with residual left-sided hemiplegia, type 2 diabetes mellitus, and hypertension. Four days prior, she had been discharged following a 7-day admission for severe pneumonia complicated by septic acute tubular necrosis. There was no history of dysphagia, odynophagia, dental infection, or vomiting.

On examination, vital signs revealed blood pressure 140/90 mmHg, pulse 106 beats/minute, temperature 37.9°C, and oxygen saturation 86% on room air. Respiratory examination demonstrated mild inspiratory stridor, hoarse voice, and transmitted breath sounds over the left posterior lung field. Laboratory tests showed leukocytosis (18.46 × 109/l with 80.9% neutrophils), elevated C-reactive protein (16.3 mg/dl), elevated D-dimer (3.13 mg/dl), and mild renal impairment (creatinine 1.2 mg/dl). Blood cultures yielded no growth.

CT pulmonary angiography excluded pulmonary thromboembolism but initially suggested advanced esophageal carcinoma. Upon multi-disciplinary re-review, extensive circumferential upper and middle thoracic esophageal long-segment enhancing wall thickening was identified, accompanied by loss of surrounding fat planes with the trachea, encasement of the aortic arch and descending aorta, mediastinal fat stranding, and a mild left pleural effusion, features consistent with diffuse esophagitis with secondary acute mediastinitis without overt extraluminal air or macro-perforation (Fig. 1A and B).

Two-panel computed tomography (CT) image of the chest. Panel A is an axial view showing diffuse, circumferential, long-segment thickening and enhancement of the walls of the upper and middle thoracic esophagus, marked by an arrow. There is surrounding mediastinal fat stranding, loss of the normal tissue plane between the esophagus and trachea, and encasement of the aortic arch and descending thoracic aorta. A mild left-sided pleural effusion is present. No free air or overt esophageal perforation is seen. Panel B is a sagittal view showing extensive vertical, long-segment circumferential thickening of the thoracic esophageal wall extending through the mediastinum.
Figure 1

(A) Axial CT at presentation demonstrating diffuse, circumferential long-segment enhancing wall thickening of the upper and middle thoracic esophagus (arrow) with accompanying fat stranding, loss of the normal tissue plane with the trachea, encasement of the aortic arch and descending thoracic aorta, and a mild left-sided pleural effusion. No evidence of overt esophageal macro-perforation or extraluminal gas is observed. (B) Sagittal CT at presentation highlighting extensive vertical transmural involvement and circumferential esophageal thickening extending along the thoracic esophagus.

Because of clinical stability and suspicion of a contained micro-perforation, upper gastrointestinal endoscopy was deferred. Empiric intravenous antimicrobial therapy was initiated using vancomycin, cefepime, and metronidazole for 14 days. By Day 6, the patient demonstrated clinical improvement: oxygen requirement decreased, inflammatory markers declined, and renal function normalized. By Day 10, vital signs stabilized. Repeat oral-contrast chest CT confirmed significant reduction in esophageal wall thickening, resolution of mediastinal fat stranding, and restoration of normal periaortic soft-tissue boundaries, with no contrast extravasation (Fig. 2A and B). Uncomplicated endoscopy on Day 11 demonstrated normal mucosal appearance. Oral feeding was resumed on Day 14. She was discharged on Day 17 after completing antibiotics.

Two-panel computed tomography (CT) image of the chest after 10 days of broad-spectrum intravenous antimicrobial therapy. Panel A is an axial view showing marked interval reduction in the thickening of the thoracic esophageal wall, with substantial resolution of surrounding mediastinal fat stranding and restoration of normal soft-tissue planes around the aorta. Panel B is a sagittal view confirming substantial improvement, with reduced esophageal wall thickening and resolution of diffuse mediastinal inflammation. No luminal stricture or contrast extravasation is seen.
Figure 2

(A) Axial CT following 10 days of targeted broad-spectrum parenteral antimicrobial therapy demonstrating significant interval reduction in esophageal wall thickening, marked resolution of surrounding mediastinal fat stranding, and restored periaortic soft-tissue boundaries. (B) Sagittal CT post-treatment confirming substantial radiological improvement and resolution of diffuse mediastinal inflammation without evidence of luminal stricture or contrast extravasation.

Discussion

Acute mediastinitis remains a condition with high morbidity and mortality, with manifestation varying widely depending on the underlying cause [10]. Non-traumatic acute mediastinitis, while rare, is diagnostically challenging and requires prompt recognition [3]. The most common causes are postoperative infection, esophageal perforation, and deep neck space infection [3, 11]. Our patient had multiple risk factors: diabetes mellitus, recent pneumonia, and cerebrovascular disease with functional impairment. Diabetes is a well-established predisposing factor for both acute mediastinitis and phlegmonous esophagitis [3, 6]; poorly controlled glycaemia has been strongly associated with descending necrotizing mediastinitis [12].

The CT findings of diffuse esophageal wall thickening with mediastinal inflammation were initially misinterpreted as advanced esophageal carcinoma, highlighting the diagnostic challenge of distinguishing APE from malignancy on imaging alone. APE is characterized by diffuse esophageal wall thickening with intramural low-attenuation areas and peripherally enhancing rims on contrast-enhanced CT [8, 13]. The absence of overt perforation on imaging may be explained by a self-healing perforation or contiguous spread from esophageal infection.

The decision to defer endoscopy was critical. In the presence of suspected contained perforation, endoscopic instrumentation risks disrupting the seal and converting a contained leak into a free perforation, with catastrophic consequences [14]. Conservative management was pursued because the patient was hemodynamically stable, had no evidence of extensive abscess formation or free air, and showed a favorable response to empiric antibiotics. The antimicrobial regimen was chosen to cover oral and gastrointestinal flora, consistent with recommended empiric therapy for mediastinitis [2, 3].

Our patient's successful outcome with conservative therapy is noteworthy, as acute mediastinitis conventionally mandates prompt invasive treatment, including surgical drainage, debridement, and sometimes resection of necrotic tissue [10, 15, 16]. In descending necrotizing mediastinitis, for example, early thoracotomy or video-assisted thoracic surgery with aggressive debridement is considered the cornerstone of management, and delayed or inadequate surgical intervention is associated with mortality rates exceeding 30%–40% [15, 17]. Similarly, mediastinitis secondary to esophageal perforation generally requires surgical repair or diversion, along with wide mediastinal drainage [16]. However, in selected hemodynamically stable patients without free perforation or extensive abscess formation, conservative medical management may be feasible [14]. The multidisciplinary approach, with early re-evaluation of imaging by multiple specialists, was instrumental in establishing the correct diagnosis and guiding therapy.

In conclusion, non-traumatic acute mediastinitis secondary to APE, though rare, should be considered in patients with acute chest pain, fever, and elevated inflammatory markers, especially those with immunocompromising conditions. In hemodynamically stable patients without evidence of free perforation or large abscess, conservative management with broad-spectrum antibiotics and multidisciplinary monitoring may achieve favorable outcomes. This case highlights the importance of maintaining a high index of suspicion and the potential role of conservative therapy in selected patients.

Acknowledgements

We thank the patient and her family for agreeing to give their consent to publish her clinical records for this case report.

Author contributions

M.H.B.: Writing—Original Draft, Conceptualization, and Visualization. E.K.D.: Writing—Original Draft, Data curation, and Conceptualization. S.Z.T.: Writing—review & editing, Investigation, Conceptualization, and Data curation. C.T.M.: Writing—review & editing, Investigation, and Data curation. E.M.A.: Writing—review & editing, and Resources. B.T.M.: Writing—review & editing, and Supervision.

Conflicts of interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

The data underlying the results presented in this work are available within the manuscript.

Ethical approval

IRB review and approval were waived for this case report.

Consent for publication

Written informed consent for publication of the clinical details and the accompanying images was obtained from the patient. The signed consent form is held by the corresponding author and can be made available to the Editor on request.

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