A case report of tuberculous fibrosing mediastinitis: focusing on the diagnostic value of three-dimensional reconstruction from pulmonary contrast-enhanced CT and bronchoscopic features

Introduction

Fibrosing mediastinitis (FM) is a rare disease characterized by excessive proliferation of fibrous tissue within the mediastinum. Its clinical presentation is insidious, often leading to chronic dyspnea due to compression of airways or blood vessels (1), and it is easily misdiagnosed as a pulmonary infection or tumor (2). Tuberculosis infection is one of the most common etiologies in China (3). This article reports a case of tuberculous fibrosing mediastinitis (TFM), focusing on the diagnostic value of pulmonary contrast-enhanced computed tomography (CT) three-dimensional (3D) reconstruction with organ segmentation and the bronchoscopic finding of “anthracotic pigmentation”, providing new insights for the precise diagnosis and treatment of TFM. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-301/rc).

Case presentation

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

General information

A 69-year-old female was admitted on May 12, 2025, due to “exertional dyspnea for over 2 years, worsening for 2 months”. In early 2023, she developed exertional dyspnea without an obvious cause, requiring rest after climbing two flights of stairs, accompanied by intermittent cough and production of small amounts of white sticky sputum that was difficult to expectorate. There was no fever, night sweats, chest tightness, chest pain, or other discomforts, and she did not seek medical attention. In March 2025, a chest CT at a local hospital showed “bullae in the right upper lobe and inflammation in the right middle lobe”. Symptoms improved after anti-infective treatment with levofloxacin and cefradine, followed by one week of oral medication before discontinuation. In April 2025, dyspnea worsened again. Chest contrast-enhanced CT at the local hospital suggested “chronic inflammation in the right middle lobe, pulmonary hypertension, interstitial pulmonary edema, enlarged mediastinal lymph nodes, solid nodules in both lungs, fibrotic lesions in the lingular segment of the left upper lobe, and scattered bullae in both lungs”. Symptoms recurred after anti-inflammatory and expectorant therapy. Treatment with cefuroxime sodium (anti-inflammatory), ambroxol (expectorant), and formoterol (bronchodilator) provided slight relief, but dyspnea persisted. She was admitted to the Department of Respiratory and Critical Care Medicine at the Air Force Medical Center for further diagnosis and treatment. Past medical history included Grade 1 hypertension for 3 years (highest blood pressure 158/98 mmHg, regularly taking nifedipine controlled-release tablets with blood pressure controlled around 130/70 mmHg) and type 2 diabetes mellitus (taking metformin, blood glucose not monitored). The patient denied previous tuberculosis infection or known exposure. Interferon-gamma release assay (IGRA) was not performed.

Auxiliary examinations

Chest contrast-enhanced CT was performed on a Siemens SOMATOM Force dual-source CT scanner with a slice thickness of 0.75 mm. Contrast medium (iohexol, 350 mgI/mL) was administered at 4 mL/s. 3D reconstruction and segmentation were performed using Syngo.via VB60 software (Siemens Healthineers, Erlangen, Germany) with convolutional neural network-based vessel and bronchial segmentation followed by volume rendering.

Laboratory tests

Complete blood count, liver and kidney function, tumor markers [carcinoembryonic antigen (CEA), cytokeratin 19 fragment antigen 21-1 (CYFRA21-1), etc.], and rheumatologic immune indices [anti-nuclear antibody profile, antineutrophil cytoplasmic antibodies (ANCA), etc.] were all within normal limits.

Arterial blood gas analysis (without oxygen): pH 7.41, partial pressure of arterial oxygen (PaO₂) 66 mmHg, partial pressure of arterial carbon dioxide (PaCO₂) 38.9 mmHg, alveolar-arterial oxygen gradient 35.1 mmHg, indicating mild hypoxemia.

Echocardiography

Mitral valve calcification, estimated pulmonary artery systolic pressure (PASP) 38 mmHg (mild pulmonary hypertension), left ventricular ejection fraction 65%.

Chest contrast-enhanced CT

(I) Inflammation in the right middle lobe, few streaks in the left upper lobe; (II) multiple solid nodules in both lungs (maximum diameter 0.6 cm); (III) multiple calcifications in both lungs; (IV) localized emphysema and bullae in the anterior segment of the right upper lobe and the posterior basal segment of the right lower lobe; (V) ground-glass opacities in both lungs, considered indicative of uneven blood perfusion; (VI) multiple slightly enlarged lymph nodes in the mediastinum and bilateral hila, some with calcification. Chest CT also revealed a diffuse soft-tissue density infiltrating the mediastinum, consistent with FM.

Three-dimensional reconstruction and organ segmentation revealed occlusion of the medial segmental bronchus of the right middle lobe, significant stenosis of the lateral segmental bronchus of the right middle lobe and the dorsal segmental bronchus of the right lower lobe, and extrinsic “knife-cut” like stenosis of the main right pulmonary artery (Figures 1-3). Quantitative analysis revealed a 75% stenosis of the main right pulmonary artery (minimum diameter 4 mm, reference diameter 16 mm) and >80% stenosis of the lateral segmental bronchus of the right middle lobe.

Figure 1 Chest contrast-enhanced CT scan. (A) Coronal view: streaky opacities with ill-defined borders in the right middle lobe; diffuse bilateral ground-glass opacities showing a mosaic pattern. (B) Axial view: enlargement of the right hilum, soft tissue density shadows adjacent to the bronchovascular bundles, and corresponding bronchial lumen narrowing. (C) Sagittal view: multiple slightly enlarged lymph nodes in the mediastinum and bilateral hila (some with calcification, arrow) and widened pulmonary artery. (D) Coronal view: bilateral pleural thickening with calcification (arrow). CT, computed tomography..

Figure 2 Bronchial three-dimensional imaging. (A) Anterior view: occlusion of the medial segmental bronchus of the right middle lobe (arrows); (B) lateral view: significant stenosis of the lateral segmental bronchus of the right middle lobe and the dorsal segmental bronchus of the right lower lobe (arrows).

Figure 3 Pulmonary artery three-dimensional imaging: extrinsic “knife-cut” like stenosis of the main right pulmonary artery (arrows) is visible.

Bronchoscopy

The main airway lumen was patent with smooth mucosa. Significant anthracotic pigmentation was observed on the mucosa of the left main bronchus and the upper and lower lobe bronchi. The orifice of the left upper lobe bronchus was distorted, stenotic, and occluded. The left lower lobe bronchus was distorted. The orifice of the right upper lobe bronchus was distorted, stenotic, and occluded. The medial and lateral segmental bronchi of the right middle lobe were occluded, with noticeable anthracotic changes on the mucosa, consistent with 3D reconstruction findings. The orifice of the right lower lobe was distorted and stenotic, but the distal lumen was patent. Lavage was performed 4 times in the lateral segment of the right middle lobe (30 mL of lavage fluid recovered), and brushing was performed twice. Nucleic acid detection for Mycobacterium tuberculosis complex in the lavage fluid was positive, and drug susceptibility testing (Xpert MTB/RIF Ultra and MGIT 960) confirmed susceptibility to rifampicin, isoniazid, ethambutol, and pyrazinamide. Rifampicin resistance was not detected. The patient had a 20-pack-year smoking history and reported long-term exposure to household biomass fuel (Figure 4).

Figure 4 Bronchoscopic images showing anatomical locations and findings including anthracosis and stenosis. (A) Carina: intact structure with smooth mucosa; (B) right upper lobe bronchus: distorted, stenotic, and occluded orifice with anthracotic pigmentation; (C) right intermediate bronchus: patent lumen with mild mucosal anthracosis; (D) Right middle lobe lateral segment bronchus: occluded lumen with prominent anthracotic changes; (E) left main bronchus: smooth mucosa with scattered anthracotic pigmentation; (F) left upper lobe bronchus: distorted, stenotic, and occluded orifice.

Diagnosis and treatment

Based on the patient’s history, imaging findings, and etiological results, the final diagnoses were: (I) TFM (involving bronchi and pulmonary artery); (II) pulmonary tuberculosis; (III) hypertension grade 1 (very high risk); (IV) type 2 diabetes mellitus.

Treatment regimen: (I) anti-tuberculosis therapy: isoniazid 0.3 g once daily, rifapentine 0.6 g twice weekly, pyrazinamide 1.0 g once daily, ethambutol 0.75 g once daily, levofloxacin 0.5 g once daily; the regimen followed the Chinese Tuberculosis Guidelines (2022) for FM. The patient weighed 58 kg. Planned anti-tuberculosis duration is 18 months. (II) Anti-inflammatory therapy: prednisone 30 mg once daily (tapering gradually by 5 mg every 2 weeks after the first month). (III) Control of underlying disease: valsartan amlodipine 80 mg/5 mg tablets, 1/day, blood pressure lowering, insulin subcutaneous injection to control blood glucose. After 2 weeks of treatment, the patient’s shortness of breath symptoms were reduced, and she was transferred to the local tuberculosis specialized hospital for further treatment. Three-month follow-up showed improved oxygenation (PaO₂ 78 mmHg), reduced PASP to 32 mmHg on echocardiography, and increased 6-minute walk distance from 280 to 350 m. Her symptoms were stabilized in 3 months of follow-up.

Discussion

FM, also known as sclerosing mediastinitis or mediastinal fibrosis, is characterized by inflammation and progressive fibrosis within the mediastinum, which can lead to compression of airways and blood vessels (4). The etiology of FM is diverse, with infection being a major cause. Histoplasmosis is common in Western countries (5), but in other regions, Mycobacterium tuberculosis infection is a significant cause (6).

Diagnostic reasoning and differential diagnosis

The diagnosis of TFM in this case was based on a combination of clinical, imaging, endoscopic, and etiological evidence. Although histopathological confirmation via endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) or mediastinal biopsy was not performed—which we acknowledge as a limitation—the presence of calcified mediastinal lymph nodes, bronchial distortion with anthracosis, positive Mycobacterium tuberculosis complex nucleic acid in lavage fluid, and the characteristic ‘knife-cut’ pulmonary artery stenosis on 3D reconstruction collectively support the diagnosis of TFM rather than malignancy, sarcoidosis, IgG4-related disease, or fungal infection. The absence of rapid progression, systemic symptoms, and negative tumor markers further argues against malignancy. Sarcoidosis typically presents with symmetrical lymphadenopathy without calcification, which was not seen in this case. IgG4-related disease often involves multiple organs and elevated serum IgG4, which was absent. Fungal infections such as histoplasmosis are rare in our region and were not supported by serological or cultural evidence.

TFM is a chronic granulomatous inflammation of the mediastinum triggered by Mycobacterium tuberculosis infection. Tuberculosis commonly affects the lungs but can also involve other organs, including mediastinal lymph nodes, mediastinal vessels, the trachea, and bronchi, leading to luminal stenosis or occlusion (7,8). This case involved both bronchi (distortion, stenosis/occlusion) and the pulmonary artery (imaging suggested uneven perfusion), representing a typical multi-structural involvement pattern. The pathogenesis of TFM is not fully understood but is currently thought to be related to (I) lymph node inflammation and fibrosis: tuberculosis infection of mediastinal lymph nodes causes inflammation; chronic inflammation leads to node rupture, caseous necrosis, triggering an excessive fibroproliferative response, ultimately resulting in FM; (II) immune response: the immune response to tuberculosis may cause chronic inflammation and fibrosis in mediastinal tissues; (III) direct invasion: Mycobacterium tuberculosis may directly invade mediastinal tissues, causing inflammation and fibrosis (9,10).

The clinical symptoms of FM relate to the involved structures and lack specificity. Common manifestations include: (I) respiratory symptoms (11), such as exertional dyspnea, cough, and sputum production; bronchial occlusion can lead to atelectasis or recurrent pulmonary infections. This patient primarily presented with exertional dyspnea and right middle lobe inflammation. (II) Vascular involvement: pulmonary artery compression can cause abnormal pulmonary hemodynamics, potentially leading to pulmonary hypertension (12). (III) Systemic symptoms: some patients may experience low-grade fever, night sweats, and fatigue, which may be less apparent in the chronic phase. (IV) Others: dysphagia if the esophagus is involved, hoarseness if nerves are involved (13,14).

Diagnosing FM requires comprehensive judgment based on history, imaging, endoscopy, and etiological evidence. TFM often has a history of tuberculosis or tuberculosis contact (15,16). Chest contrast-enhanced CT is a crucial diagnostic tool, showing mediastinal soft tissue shadows, calcifications (as in this case with lung and lymph node calcifications), bronchial distortion and stenosis, pulmonary artery compression, and secondary pulmonary changes (e.g., emphysema, bullae) (17,18). Compared to conventional chest contrast-enhanced CT, 3D reconstruction technology offers significant advantages. Based on thin-slice CT, it uses convolutional neural networks for vessel and bronchial segmentation and volume rendering for 3D visualization of anatomical structures. This not only clarifies the spatial relationship between bronchi and surrounding vessels but also allows more precise assessment of the degree of bronchial involvement by FM (19-21). In this case, 3D reconstruction provided superior spatial visualization of the relationship between stenotic bronchi and the compressed pulmonary artery, which was less apparent on axial or multiplanar reconstructions. This directly influenced the decision to avoid bronchoscopic intervention due to high bleeding risk from vascular involvement, favoring medical management instead. In this case, 3D reconstruction clearly revealed right middle lobe bronchial stenosis, directly related to FM’s pathological mechanism: fibrous tissue proliferation often extends along mediastinal spaces towards the hilum and peribronchial areas. Due to its anatomical proximity to the mediastinum (close connection to the right hilum and mediastinal lymph nodes), the right middle lobe bronchus is easily ensnared and tractioned by proliferating fibrous tissue, leading to luminal stenosis (22). 3D reconstruction can more accurately assess the degree of stenosis (e.g., severe stenosis or near-occlusion) and the presence of vascular compression, informing treatment decisions (23). Particularly when vascular involvement is suspected, 3D imaging helps clinicians assess potential pulmonary artery compression, guiding the choice to prioritize anti-tuberculosis therapy to control fibrosis progression and avoid blind bronchoscopic intervention, which carries increased bleeding risk if vessels are involved (1,16).

The anthracotic pigmentation observed on the bronchial mucosa in this case may be related to long-term inhalation of pollutants or chronic inflammation post-tuberculosis infection (17). Although anthracosis is nonspecific, its presence in conjunction with tuberculosis-related stenosis supports chronic airway inflammation. Bronchoscopy allows direct observation of mucosal changes (distortion, stenosis, occlusion, anthracosis) and enables biopsy. Detection of Mycobacterium tuberculosis or granulomatous inflammation with caseous necrosis on biopsy confirms the diagnosis, as evidenced by the positive nucleic acid test for Mycobacterium tuberculosis complex in the lavage fluid here. The mechanism of distorted stenosis and occlusion involves the invasive and contractile nature of tuberculous granulomas and fibrous tissue, which infiltrate along the bronchial wall and traction the lumen, causing orifice distortion (24). Long-term fibrotic progression can gradually occlude the lumen (e.g., left upper lobe and right middle lobe bronchus occlusion in this case). This appearance differs from neoplastic stenosis (often eccentric, irregular) and simple tuberculous bronchitis (primarily mucosal congestion, ulceration, less commonly irreversible distortion) (25). Mucosal anthracotic changes suggest long-term chronic inflammation or a history of inhaled pollutants. In TFM, this may be associated with: (I) chronic inflammation impairing airway clearance, leading to deposition of inhaled carbon particles on the mucosa (26); (II) tuberculous inflammation damaging the bronchial mucosal barrier, increasing the risk of carbon particle adhesion. Although not specific to TFM, combined with tuberculosis-related imaging and endoscopic stenosis features, it can support the diagnosis of “chronic tuberculous airway disease” (27).

The key to differential diagnosis of TFM lies in excluding other mediastinal diseases, including malignant tumors, sarcoidosis, fungal infections, and idiopathic mediastinal fibrosis. Malignancies often present as space-occupying lesions with rapid progression and weight loss, requiring pathological confirmation (28,29). Sarcoidosis typically shows symmetric mediastinal lymphadenopathy without calcification and a negative tuberculin test. Fungal infections like histoplasmosis can be differentiated by etiological testing. Idiopathic mediastinal fibrosis lacks a clear infection history or evidence of tuberculosis and progresses slowly. TFM has a high misdiagnosis rate due to non-specific symptoms and imaging findings, as well as insufficient awareness of the disease. Symptoms like dyspnea and cough are easily mistaken for chronic obstructive pulmonary disease (COPD) or pneumonia. Imaging findings like calcification and nodules can be confused with tumors or sarcoidosis. Additionally, difficulties in obtaining etiological confirmation and limited awareness among primary care physicians contribute to misdiagnosis risk (30).

The core treatment for TFM is early anti-tuberculosis therapy, supplemented by symptomatic and supportive care. Anti-tuberculosis drugs require early, combined, regular, and full-course use, typically for 12–18 months. Bronchoscopic dilation or stenting may be considered for bronchial stenosis (16). Surgical release of fibrotic tissue may be an option for severe hemodynamic compromise due to pulmonary artery compression, but it carries a high risk. Concomitant pulmonary infections require anti-infective treatment. Patients with bullae should avoid strenuous activity. The prognosis of TFM is closely related to early diagnosis and timely treatment (31). Early diagnosis and standard treatment can effectively control fibrosis progression and improve symptoms. Delayed treatment may lead to irreversible bronchial and vascular occlusion, causing severe complications and poor outcomes. This patient already had multiple bronchial occlusions and pulmonary structural changes, necessitating long-term follow-up to monitor for complication progression (32).

Conclusions

In conclusion, TFM is a special complication of tuberculosis infection. Three-dimensional vascular reconstruction and bronchoscopy reveal the characteristics of airway and vascular involvement in TFM from different perspectives. Their combination improves diagnostic accuracy and provides an important basis for assessing disease severity, guiding treatment, and determining prognosis. Clinicians should pay attention to the association of these features with tuberculous fibrosis, aiming for early diagnosis to avoid missed diagnosis or mistreatment and improve patient outcomes.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-301/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-301/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-301/coif). The 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. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

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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