Bronchial Dieulafoy’s disease complicated by pulmonary embolism after successful hemostasis: a case report and review of the literature

Abstract

Background

Bronchial Dieulafoy’s disease (BDD) is a rare vascular anomaly characterized by a large-caliber submucosal artery that can cause sudden, massive, and potentially fatal hemoptysis. Because of its deceptively benign endobronchial appearance, the disease is frequently underrecognized and carries a high risk of catastrophic bleeding following bronchoscopic manipulation.

Case presentation

A 77-year-old woman without underlying lung disease developed massive hemoptysis and hemorrhagic shock shortly after diagnostic bronchoscopy for an indeterminate endobronchial lesion. Emergency bronchial artery embolization (BAE) achieved effective hemostasis. During recovery, pulmonary embolism was suspected and subsequently confirmed by computed tomography pulmonary angiography (CTPA); the event was classified as intermediate-risk based on right-heart strain and cardiac biomarkers, posing a major therapeutic dilemma regarding anticoagulation after recent life-threatening airway bleeding. After secure hemostasis had been confirmed by the absence of recurrent hemoptysis, stable vital signs and hemoglobin, no further transfusion requirement, and post-embolization angiographic control, anticoagulation was managed through a stepwise strategy: temporary lower-intensity low-molecular-weight heparin followed by escalation to full therapeutic anticoagulation after PE confirmation and clinical stabilization. Follow-up imaging before discharge demonstrated marked resolution of clot burden, and no recurrent hemoptysis occurred during anticoagulation.

Conclusions

This case emphasizes three practical lessons: BDD should be suspected in benign-appearing endobronchial lesions associated with unexplained hemoptysis; bronchoscopic biopsy should be avoided until a vascular lesion is reasonably excluded; and BAE can provide lifesaving hemostasis. In carefully selected patients who develop PE after secure hemostasis, stepwise anticoagulation may be considered under multidisciplinary monitoring, but this single case should be interpreted as hypothesis-generating rather than a generalizable treatment recommendation.

Background

Bronchial Dieulafoy’s disease (BDD) is an uncommon but potentially lethal cause of hemoptysis, characterized by a dysplastic, large-caliber artery running superficially within the bronchial submucosa [1, 2].

Because the overlying mucosa often appears intact and nonulcerated, the lesion may mimic benign inflammatory nodules or endobronchial tumors, leading to inadvertent biopsy and catastrophic bleeding [3, 4]. Early recognition and appropriate management are therefore critical, and pathological confirmation—when available—remains the gold standard for diagnosis, typically demonstrating a large-caliber aberrant artery located immediately beneath the bronchial epithelium without features of vasculitis or malignancy [1, 5].

Case presentation

A 77-year-old woman with no smoking history and no known underlying lung disease, including chronic obstructive pulmonary disease, bronchiectasis, or prior tuberculosis, was admitted for evaluation of lung consolidation detected on imaging. Contrast-enhanced chest computed tomography revealed a consolidation-like lesion in the left hilar region with focal enhancement and internal punctate hyperdense foci of indeterminate etiology.

Flexible bronchoscopy was performed under general anesthesia to evaluate the indeterminate left hilar consolidation and endobronchial abnormality. The procedural sequence was as follows: inspection of the left main bronchus and left lower-lobe segmental bronchi, assessment of mucosal appearance and contact bleeding, narrow-band imaging (NBI) evaluation of the lesion surface, followed by endobronchial sampling because no active bleeding or obvious superficial vascular pattern was recognized at that time. Bronchoscopy demonstrated extrinsic compression and luminal narrowing of the basal and posterior segments of the left lower lobe. A small, broad-based nodular lesion protruding from the left main bronchial wall was observed, covered by a whitish cap-like structure (“white cap”). No active bleeding was observed on gentle contact. Endobronchial biopsy, brushing, and bronchoalveolar lavage were then performed.

During bronchoscopy under general anesthesia, the patient suddenly developed massive hemoptysis. Initial hemostatic measures, including intravenous vasopressin, topical thrombin application, and blood transfusion, achieved only transient control. Recurrent hemorrhage occurred during transfer, and emergency bronchial artery embolization (BAE) was performed under general anesthesia on December 25, 2024. The estimated total blood loss was approximately 1500 mL.

Emergency BAE was performed as a stepwise endovascular hemostatic procedure: selective angiography was first used to identify the culprit systemic arterial supply; superselective catheterization was then performed to reduce non-target embolization; embolic agents were selected according to vessel caliber and angiographic appearance; and completion angiography was used to confirm hemostasis. Selective angiography revealed marked enlargement of the left upper bronchial artery with tortuous distal branches and focal contrast extravasation. Superselective embolization using gelatin sponge particles (560–710 μm and 710–1000 μm) and detachable coils was performed. Additional embolization was required for abnormal distal branches of the left lower bronchial artery and the left fourth to fifth intercostal arteries showing systemic–pulmonary shunting. Post-embolization angiography confirmed cessation of contrast extravasation and marked reduction of distal arterial branches.

Hemoptysis resolved promptly. Repeat bronchoscopy showed large intrabronchial clots, which were removed. The patient was transferred to the intensive care unit and later returned to the respiratory ward. She subsequently developed aspiration pneumonia and was treated with empirical broad-spectrum antibiotics.

After BAE, the patient remained critically ill with severe hypoxemia and was considered to be in the period of highest concern for rebleeding from the recently treated BDD lesion. Immediate CTPA was temporarily deferred because transfer to the CT suite was considered unsafe under high-flow nasal oxygen support and recent life-threatening airway bleeding. A reproducible interim diagnostic workflow was therefore used: (1) reassess airway and pulmonary causes of hypoxemia, including residual endobronchial clots, aspiration pneumonia, atelectasis, recurrent bleeding, and acute left-sided heart failure; (2) evaluate PE probability using clinical features and the revised Geneva score; (3) assess right-heart strain using bedside transthoracic echocardiography and cardiac biomarkers; and (4) perform CTPA once oxygenation and transport safety improved. On January 2, 2025, eight days after BAE, repeat echocardiography showed right atrial enlargement (superoinferior diameter 4.2 cm; mediolateral diameter 3.6 cm) and mild pulmonary hypertension, with sPAP increasing from 20.52 mmHg on admission to 42.81 mmHg. Cardiac troponin I was 0.122 ng/mL, NT-proBNP was 2636 pg/mL, and D-dimer was 9.471 mg/L (reference range, 0–0.243 mg/L). The revised Geneva score was at least 8 points (age > 65 years, 1 point; heart rate ≥ 95 beats/min, 5 points; hemoptysis, 2 points), indicating intermediate clinical probability. Although severe hypoxemic respiratory failure and recent massive hemoptysis could also contribute to right-heart stress, persistent high oxygen requirement after clot removal, improving inflammatory indices, absence of fever, no clinical evidence of recurrent massive hemoptysis or acute left-sided heart failure, newly increased sPAP, elevated cardiac biomarkers, markedly elevated D-dimer, prolonged bed rest, and intermediate clinical probability together supported high clinical suspicion for PE until confirmatory imaging could be safely obtained.

Anticoagulation was started only after predefined bedside safety criteria were reviewed by the treating team: no recurrent massive hemoptysis after BAE, no visible active airway bleeding during close monitoring, post-embolization angiography showing cessation of contrast extravasation, clinically stable vital signs, stable hemoglobin without ongoing transfusion requirement, and no need for rescue hemostatic intervention. Because immediate CTPA was unsafe because of the patient’s oxygenation status and transport risk, anticoagulation was cautiously initiated on January 2, 2025, eight days after BAE, with enoxaparin 60 mg (6000 IU anti-Xa) once daily as a temporary lower-intensity regimen rather than standard full-dose therapy. Dose escalation was deferred until two operational conditions were met: CTPA confirmation of PE and multidisciplinary reassessment that hemostasis remained secure. After oxygenation improved, the patient was transferred to the CT suite with a transport ventilator on January 4, 2025. CTPA confirmed acute pulmonary embolism involving the anterior and apical segments of the right upper lobe and the lingular segment of the left upper lobe, consistent with intermediate-risk pulmonary embolism. After multidisciplinary discussion with the interventional radiology team confirmed the absence of recurrent hemoptysis, stable vital signs and hemoglobin, no ongoing need for transfusion, and no evidence of active airway bleeding, anticoagulation was escalated to full therapeutic dosing (enoxaparin 60 mg every 12 h, approximately 1 mg/kg). No recurrent hemoptysis occurred after dose escalation. At discharge, anticoagulation was transitioned to rivaroxaban 15 mg twice daily for 21 days, followed by 20 mg once daily, for a total planned treatment duration of 3 months.

Histopathological examination was performed on formalin-fixed, paraffin-embedded bronchoscopic biopsy tissue. Hematoxylin and eosin staining showed a markedly dilated artery located superficially within the bronchial submucosa. Elastic fiber staining (Verhoeff–Van Gieson) demonstrated a well-defined elastic lamina, and desmin immunohistochemistry highlighted concentric smooth muscle bundles within the vessel wall, confirming the arterial nature of the lesion and supporting the diagnosis of bronchial Dieulafoy’s disease [1, 5]. No EBV-related diagnostic conclusion was made in this case, and metagenomic next-generation sequencing (mNGS) was not used to establish the diagnosis; therefore, no EBV positivity threshold, sequencing platform, or mNGS reporting cutoff was applied to the diagnostic reasoning of this report.

The patient was discharged on January 23, 2025, twenty-nine days after BAE, in stable condition and without recurrent hemoptysis. She reported significant anxiety during the episode of massive hemoptysis but experienced marked relief after successful BAE. She tolerated subsequent anticoagulation therapy well and was satisfied with the overall treatment outcome. Follow-up CTPA obtained before discharge showed marked improvement of the pulmonary embolic burden. No recurrence of hemoptysis was observed during follow-up. The overall clinical timeline is summarized in Table 1; (Figs. 1, 2, 3, 4, 5).

Table 1.

Timeline of key clinical events and anticoagulation strategy

Date / timing	Key clinical events
December 24, 2024	Admission evaluation; baseline transthoracic echocardiography showed no pulmonary hypertension, with estimated sPAP of 20.52 mmHg.
December 25, 2024	Flexible bronchoscopy and biopsy were followed by massive hemoptysis and hemorrhagic shock; emergency BAE was performed, and post-embolization angiography confirmed cessation of contrast extravasation.
After BAE	Hemoptysis resolved; repeat bronchoscopy removed large intrabronchial clots; the patient was managed in the ICU with severe hypoxemia and high rebleeding concern.
January 2, 2025 (post-BAE day 8)	The patient was transferred from the ICU back to the respiratory ward. D-dimer was 9.471 mg/L, and bedside echocardiography showed mild pulmonary hypertension with estimated sPAP of 42.81 mmHg. Because CTPA was temporarily unsafe due to persistent high-flow oxygen dependence, suspected PE was treated with lower-intensity initial enoxaparin regimen (60 mg once daily).
January 4, 2025 (post-BAE day 10)	After oxygenation improved, the patient underwent CTPA with transport ventilator support; intermediate-risk PE was confirmed. After MDT discussion and confirmation of secure hemostasis, enoxaparin was escalated to full therapeutic dosing (60 mg every 12 h).
Before discharge	Follow-up CTPA showed marked improvement in embolic burden; no recurrent hemoptysis occurred during anticoagulation.
Discharge	Anticoagulation was transitioned to rivaroxaban 15 mg twice daily for 21 days followed by 20 mg once daily, with a planned total treatment duration of 3 months.

Fig. 1.

Schematic timeline of the diagnostic and therapeutic workflow. The schematic summarizes the sequence of massive hemoptysis during bronchoscopy and emergency BAE on December 25, 2024; ICU monitoring and clot removal; PE suspicion on January 2, 2025 based on persistent hypoxemia, increased sPAP, elevated biomarkers, markedly elevated D-dimer, and intermediate revised Geneva score; initiation of temporary lower-intensity enoxaparin after bedside safety review; CTPA confirmation of PE on January 4, 2025; escalation to full therapeutic anticoagulation after multidisciplinary reassessment of secure hemostasis; and discharge on January 23, 2025 with transition to rivaroxaban

Fig. 2.

Bronchoscopic (white-light and NBI) and contrast-enhanced CT findings. A White-light bronchoscopy shows a small, broad-based nodular lesion protruding into the bronchial lumen (arrow). B Narrow-band imaging (NBI) view of the same lesion demonstrates no obvious abnormal superficial vascular pattern. C, D Pre-interventional contrast-enhanced chest CT demonstrates patchy consolidation in the left hilar region with punctate hyperdense foci and evident contrast enhancement. Arrows indicate enhancing tubular foci within the consolidation, likely corresponding to tortuous and dilated vascular structures. Together, these findings illustrate that a benign-appearing endobronchial lesion may still correspond to a submucosal vascular abnormality on contrast-enhanced CT

Fig. 3.

Bronchial artery embolization for massive hemoptysis. Selective angiography before bronchial artery embolization (BAE) demonstrates abnormal systemic arterial supply. A The left upper bronchial artery is markedly dilated with tortuous, disorganized distal branches and focal contrast extravasation. B The distal left lower bronchial artery shows tortuous course and intense parenchymal staining without definite contrast leakage. C Abnormal tortuous branches arising from the left fourth to fifth intercostal artery with an intercostal–pulmonary arterial fistula and increased staining, without contrast extravasation. After-embolization angiography (D–F) shows successful occlusion of the culprit vessels. D Coil embolization of the left upper bronchial artery (MWCE-18S-6/2) results in marked reduction of distal branches and disappearance of contrast extravasation. E Embolization of the left lower bronchial artery using gelatin sponge particles (560–710 μm) eliminates distal arterial opacification. F Gelatin sponge particle embolization (560–710 μm) of the intercostal artery achieves complete occlusion of abnormal distal branches. Hemoptysis improved markedly with no evidence of active bleeding. These angiographic findings identify the culprit systemic arterial supply and confirm successful endovascular hemostasis

Fig. 4.

Pulmonary embolism following bronchial artery embolization and interval improvement during anticoagulation therapy. Computed tomography pulmonary angiography (CTPA) images demonstrate acute pulmonary embolism involving the anterior and apical segments of the right upper lobe pulmonary artery (A, arrows) and the superior lingular segment of the left upper lobe pulmonary artery (B, arrows). Follow-up CTPA obtained before discharge during anticoagulation therapy shows marked interval resolution of the previously identified emboli with restoration of pulmonary arterial patency (C, D, arrows). The interval improvement indicates reduced thromboembolic burden during closely monitored anticoagulation

Fig. 5.

Histopathological features of bronchial Dieulafoy’s disease. Hematoxylin and eosin (H&E) staining (A, ×100; B, ×200) demonstrates a markedly dilated, thick-walled aberrant artery located in the subepithelial layer of the bronchial wall, in close proximity to the bronchial mucous glands (yellow arrows). The vessel shows a prominent muscular wall (black arrows), consistent with an arterial structure rather than a venous or capillary lesion. Immunohistochemical staining for desmin (C, ×200) highlights concentric smooth muscle bundles within the vascular wall (red arrows), confirming the presence of vascular smooth muscle. Elastic fiber staining (D, ×200; Verhoeff–Van Gieson) reveals a well-defined elastic lamina surrounding the vessel (white arrows), further supporting the diagnosis of an aberrant bronchial artery consistent with BDD. These pathological findings confirm a superficial aberrant bronchial artery, supporting the final diagnosis of BDD

Discussion

BDD poses a major diagnostic challenge because of its deceptively benign bronchoscopic appearance. Small, mucosa-colored nodules covered by a whitish fibrinous layer (“white cap”) are commonly described and may closely mimic nonvascular lesions [2–4]. In our patient, the absence of active bleeding and the benign appearance contributed to diagnostic biopsy, reflecting a well-recognized pitfall rather than an isolated procedural error. Notably, the absence of apparent vascular features—even when advanced imaging modalities such as narrow-band imaging (NBI) are applied—does not exclude a vascular lesion. This may relate to the optical principle of NBI, which primarily enhances superficial mucosal microvasculature with relatively limited depth penetration, whereas bronchial Dieulafoy-type lesions typically originate from a large-caliber submucosal artery that may not produce conspicuous surface vascular changes detectable by NBI [6]. Numerous reports have demonstrated that bronchoscopic manipulation or biopsy of bronchial Dieulafoy lesions can precipitate catastrophic arterial hemorrhage [1, 3, 7, 8]. This case reinforces that any broad-based endobronchial nodule associated with unexplained hemoptysis should be approached with extreme caution, and biopsy should be avoided unless a vascular lesion has been reasonably excluded. In addition, bronchial Dieulafoy’s disease should be differentiated from other rare vascular or tumor-associated conditions, such as paravertebral neurilemmoma–associated vascular anomalies, which may present with similar endobronchial appearances but differ fundamentally in pathogenesis and management [8].

Angiography plays a central role in the diagnosis and management of BDD, typically demonstrating hypertrophied and tortuous bronchial arteries with abnormal distal branching or contrast extravasation [8, 9]. Bronchial artery embolization is widely regarded as the first-line therapy for acute bleeding control and achieves high immediate success rates [9, 10]. In selected and complex cases, including pediatric or atypical presentations, multimodality imaging such as CT angiography may further facilitate early identification of the bleeding source and guide timely endovascular or bronchoscopic intervention [11]. In the present case, superselective embolization achieved effective hemostasis, with no recurrence during follow-up.

To make the literature context more explicit, previously reported BDD cases can be broadly summarized into three clinically relevant themes: diagnostic presentation, treatment strategy, and outcome. Because BDD is rare and mainly described in case reports or small series, its true incidence remains unknown. However, available reviews consistently indicate that massive hemoptysis and biopsy-related hemorrhage are the major determinants of outcome. A literature review of 88 reported cases identified 10 deaths, all related to massive hemorrhage during bronchoscopic biopsy, highlighting the importance of avoiding biopsy when a vascular lesion is suspected [12]. Recent reports further support the role of bronchial CTA/angiography and BAE as key diagnostic and therapeutic tools, although surgery remains necessary in selected cases with failed embolization, recurrent bleeding, or complex vascular anatomy [5, 8, 12, 13] (Table 2).

Table 2.

Summary of selected literature on bronchial Dieulafoy’s disease relevant to diagnosis, treatment, and outcomes

Study/source	Main focus	Key findings/outcomes	Relevance to the present case
Parrot et al. [5]	Pathological diagnosis	Large-caliber aberrant submucosal arteries; clinicopathological correlation required.	Supports pathological confirmation in this case.
Shi et al. [12]	Literature review	88 cases reviewed; 10 deaths, all biopsy-related massive hemorrhage.	Supports the biopsy-avoidance warning.
Yang et al. [8]	Diagnosis and treatment series	CTA/bronchoscopy aid diagnosis; BAE preferred when feasible.	Supports angiography and BAE.
Daboussi et al. [13]	BDD with bilateral PE	Heparin was used; embolization was insufficient and surgery was required.	Shows BDD + PE was reported, but differs from the post-BAE dilemma.
Present case	BDD with PE after successful BAE	Secure BAE hemostasis; stepwise anticoagulation without recurrent hemoptysis.	Highlights individualized post-hemostasis anticoagulation.

Taken together, the literature indicates that the clinical outcome of BDD depends less on lesion size than on early recognition, avoidance of unsafe bronchoscopic biopsy, and timely hemostatic intervention. Compared with previously reported cases, the present case adds a specific management issue: anticoagulation for acute PE shortly after successful BAE.

Pulmonary embolism in the context of BDD appears to be extremely uncommon in the available literature. A previously published case described BDD with bilateral PE, for which curative heparin therapy was prescribed [13]. However, that case differed substantially from the present one: embolization failed to achieve definitive hemostasis, and surgical intervention was ultimately required to control bleeding. In the present patient, intermediate-risk PE developed shortly after successful endovascular hemostasis had been achieved by BAE. This sequence created a distinct post-BAE management dilemma: anticoagulation was needed to prevent thromboembolic progression, whereas the recent episode of life-threatening airway bleeding created a substantial risk of recurrent hemoptysis. Therefore, the novelty of the present case should not be framed simply as the coexistence of BDD and PE, but rather as the management of PE after apparently secure BAE hemostasis using a cautious, stepwise anticoagulation strategy under close multidisciplinary monitoring.

Pulmonary embolism is not a commonly reported complication of bronchial artery embolization itself. In this patient, the thromboembolic event was likely multifactorial, related to hemorrhagic shock, prolonged immobilization, systemic inflammation, and transient hypercoagulability. Management was challenging because anticoagulation could precipitate recurrent airway bleeding after recent massive hemoptysis. Published PE guidelines and expert consensus recommend anticoagulation for suspected or confirmed acute PE, but they also emphasize individualized decisions based on hemodynamic status, bleeding risk, and the need for rapid titration or reversal [14, 15]. Importantly, no formal evidence-based protocol currently defines the optimal timing or intensity of anticoagulation after BAE for catastrophic hemoptysis. In this case, the decision to start anticoagulation was not based on a universal threshold but on a structured bedside reassessment: absence of recurrent hemoptysis, angiographic control of bleeding, clinical stability of vital signs and hemoglobin, no ongoing transfusion requirement, no need for repeat hemostatic intervention, and persistent evidence supporting PE. Low-molecular-weight heparin is generally preferred over unfractionated heparin in most hemodynamically stable patients requiring parenteral anticoagulation. However, unfractionated heparin may be considered when rapid adjustment or reversal is particularly important [14, 15]. Although unfractionated heparin might have offered a shorter half-life and easier reversal if rebleeding had occurred, LMWH was used because it was immediately available and familiar in our local practice. Therefore, the initial enoxaparin regimen of 60 mg once daily was not intended as standard therapeutic-dose anticoagulation for confirmed PE, nor did it represent conventional prophylactic dosing; rather, it was an individualized temporary lower-intensity strategy during the period of greatest concern for recurrent airway bleeding. After CTPA confirmed PE and hemostasis was reassessed as secure, anticoagulation was escalated to full therapeutic-dose enoxaparin and later transitioned to rivaroxaban for a total of 3 months, consistent with guideline-based treatment duration for acute PE associated with transient provoking factors [14, 15]. Routine repeat CTPA is not generally recommended solely to document radiographic resolution of PE or to determine anticoagulation duration [14, 15]. In our patient, however, follow-up CTPA before discharge was obtained to reassess overall pulmonary status and discharge readiness after the coexistence of massive hemoptysis, aspiration pneumonia, and acute PE during a critical illness. The interval reduction in clot burden should therefore be interpreted as supportive follow-up information rather than the basis for treatment duration planning. We also recognize that anticoagulation itself does not directly dissolve thrombus; rather, endogenous fibrinolysis contributes to clot resolution while anticoagulation prevents thrombus propagation and recurrent embolic events.

For similar cases, a concise decision framework may be useful, although it should not be interpreted as a guideline-endorsed protocol. First, PE severity should be stratified using hemodynamic status, oxygen requirement, right ventricular dysfunction, cardiac biomarkers, and clot burden. Second, when CTPA is temporarily unsafe, PE probability can be assessed with a reproducible bedside algorithm combining clinical probability scores such as the revised Geneva score, D-dimer, echocardiographic evidence of right-heart strain, and exclusion of alternative explanations for hypoxemia. Third, post-BAE hemostasis should be reassessed using operational criteria: no recurrent hemoptysis, stable hemoglobin, stable vital signs, angiographic cessation of contrast extravasation, no ongoing transfusion requirement, and no need for rescue hemostatic intervention. Fourth, if PE is high-risk or rapidly deteriorating, reperfusion or catheter-directed therapy should be discussed urgently by a multidisciplinary team. For hemodynamically stable patients with intermediate-risk PE but extreme rebleeding risk, a short stepwise approach may be considered: close monitoring, temporary lower-intensity anticoagulation during the highest-risk post-hemostatic period, confirmatory CTPA when transport is safe, and escalation to guideline-based therapeutic anticoagulation once hemostasis is secure [14, 15].

Severe hemoptysis requiring advanced life-support measures has also been reported in special populations, such as pregnant patients, in whom extracorporeal membrane oxygenation combined with interventional management was successfully applied as rescue therapy [16]. These reports further underscore the extreme clinical spectrum of massive airway bleeding and the necessity of individualized, multidisciplinary decision-making when balancing hemorrhagic and thrombotic risks.

Strengths and limitations

This report has several strengths, including the rarity and educational value of the case, a clear clinical timeline, multimodal evidence from bronchoscopy, contrast-enhanced CT, angiography, CTPA, and histopathology, and a clinically important therapeutic dilemma regarding anticoagulation after recent life-threatening airway bleeding. Several limitations should also be acknowledged. First, this is a single case, and the stepwise anticoagulation strategy should not be generalized as a standard regimen. Second, the initial lower-intensity LMWH regimen was empirical and individualized rather than guideline-endorsed. Third, although selected relevant literature was summarized, the rarity of BDD and the limited number of comparable cases restrict formal comparison of outcomes across treatment strategies. Fourth, this report describes the clinically relevant pathological findings supporting BDD but does not include mNGS-based diagnostic data or EBV-related testing parameters, because these tests were not used to establish the final diagnosis.

Clinical implications

1. Bronchial Dieulafoy’s disease should be considered in patients with unexplained hemoptysis and benign-appearing endobronchial nodules, especially those with a “white cap” appearance.

2. Bronchoscopic biopsy of such lesions carries a high risk of catastrophic hemorrhage and should be avoided unless a vascular etiology has been reasonably excluded. The absence of abnormal vascular patterns on NBI does not exclude bronchial Dieulafoy’s disease, as the culprit vessel is often submucosal and beyond the effective imaging depth of NBI.

3. Bronchial artery embolization is a lifesaving first-line intervention for massive hemoptysis caused by BDD.

4. After secure hemostasis, anticoagulation for concomitant PE may be feasible in carefully selected patients, but decisions should be individualized according to PE severity, rebleeding risk, transport safety for confirmatory CTPA, and operational indicators of bleeding control, including absence of recurrent hemoptysis, stable vital signs and hemoglobin, no ongoing transfusion requirement, and no need for rescue hemostatic intervention.

5. The stepwise anticoagulation strategy should be interpreted as a case-based framework rather than a standard regimen.

Authors’ contributions

YL and RM were the primary physicians involved in the patient’s management, conceived the report, collected clinical data, performed the literature review, and drafted the manuscript. XW provided expert interpretation of CT/CTPA images. YH performed the life-saving bronchial artery embolization for hemostasis. SZ provided guidance on pathological specimen processing and interpretation of the biopsy samples. HJ coordinated nursing care. FL and FY supervised the overall clinical rescue and treatment and critically revised the manuscript. All authors read and approved the final manuscript and agree to be accountable for all aspects of the work.

Funding

This work was supported by the National Natural Science Foundation of China (Grant No. 82000043) and the Capital’s Funds for Health Improvement and Research (Grant No. 2024-2-1101).

Data availability

The data are available upon reasonable request from the corresponding author.

Declarations

Ethics approval and consent to participate

This case report was approved by the Ethics Committee of Beijing Friendship Hospital, Capital Medical University (Approval No. 2026-P2-016-01).

Consent for publication

Written and signed informed consent for publication of the clinical details and accompanying images was obtained from the patient.

Competing interests

The authors declare no competing interests.