Conservative management of iatrogenic pulmonary vein obstruction following transcatheter sinus venosus ASD repair: a case insight and literature review

Abstract

Background

Iatrogenic pulmonary vein obstruction (PVO) is a rare but serious complication that may occur following transcatheter correction of sinus venosus atrial septal defect (SVASD) with partial anomalous pulmonary venous connection (PAPVC) using covered stents. This procedure has gained increasing acceptance in recent years. The optimal management strategy, particularly the role of conservative therapy, remains poorly defined.

Case summary

A 42-year-old man with a 1.5 × 1.0 cm superior vena cava (SVC)-type SVASD, PAPVC, and severe pulmonary arterial hypertension (PAH) underwent transcatheter repair after six months of targeted vasodilator therapy. Under fluoroscopic and transesophageal echocardiographic (TEE) guidance, a 57 mm long Optimus-CVS PTFE-covered XXL stent (AndraTec, Germany) was deployed, internally telescoped with a 45 mm long bare-metal CP stent (NuMED, USA) for cranial anchoring. Intra-procedural TEE showed correct stent position and unobstructed pulmonary venous flow. However, 24 h later, the patient developed acute hypoxemia. Computed tomography angiography revealed complete occlusion of the anterior segment of the right upper pulmonary vein with associated thrombosis. Because the patient remained hemodynamically stable, conservative management was initiated with corticosteroids, diuretics, and therapeutic anticoagulation (apixaban plus aspirin). Within five days, oxygen saturation normalized to 90% on room air, and chest imaging confirmed resolution of pulmonary infiltrates. Follow-up at six months showed a stable stent position and no residual obstruction.

Conclusion

PVO following transcatheter SVASD repair may not be diagnosed immediately after stent deployment, as it can present with delayed onset due to progressive thrombosis formation. Normal intra-procedural imaging does not exclude subsequent PVO, and vigilant post-procedural monitoring is essential. In carefully selected, hemodynamically stable patients, conservative management with corticosteroids, anticoagulation, and diuretics can lead to complete clinical and radiographic recovery, restoring pulmonary venous drainage and potentially avoiding reintervention or surgery.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12872-026-06205-w.

Take-home message

Correction of a sinus venosus atrial septal defect using transcatheter deployment of a covered stent is feasible and safe. However, pulmonary vein obstruction (PVO) is a serious complication that may not be diagnosed immediately after stent deployment and can present up to 24 h post-procedure due to gradual thrombosis formation. Normal intra-procedural imaging does not exclude subsequent PVO. In hemodynamically stable patients, conservative management with corticosteroids, anticoagulation, and diuretics can achieve favorable outcomes without the need for reintervention.

Introduction

Iatrogenic pulmonary vein obstruction (PVO) is a rare but serious complication of transcatheter repair for SVASD with PAPVC. Although covered stent deployment across the superior vena cava–right atrium (SVC–RA) junction is an effective alternative to surgery [1–4], the close anatomical relationship between the SVC and anomalous pulmonary veins creates a risk of unintentional venous jailing. PVO occurs when the stent or post-dilation balloon encroaches upon an anomalous pulmonary vein orifice, most commonly a high-draining branch of the right upper pulmonary vein (RUPV). This iatrogenic complication is preventable with meticulous pre-procedural imaging and intra-procedural protective techniques [5]. However, data on the incidence and management of procedure-related PVO remain limited, and most reported cases have required reintervention or surgery. We present a case of acute segmental pulmonary vein obstruction involving the anterior branch of the RUPV following covered-stent repair of SVASD with severe PAH, successfully managed conservatively. This report highlights that PVO may not be immediately detectable on transesophageal echocardiography (TEE) during the procedure due to the gradual formation of thrombosis, and that conservative management may be appropriate in hemodynamically stable patients.

History of presentation

A 42-year-old man presented with exertional dyspnea (New York Heart Association functional class II) and resting oxygen saturation of 89–90%. He had no history of prior cardiac surgery, thromboembolic events, or chronic lung disease. Initial transthoracic echocardiography (TTE) revealed preserved left ventricular function (ejection fraction 55%), severe right ventricular enlargement with mild-to-moderate dysfunction, mild right ventricular hypertrophy, and severe right atrial enlargement. Estimated systolic pulmonary artery pressure (sPAP) was 90 mmHg, indicating severe PAH. Because transthoracic echocardiography (TTE) could not definitively exclude an intracardiac defect, TEE was performed, demonstrating a 1.5 × 1.0 cm SVASD with PAPVC of the right upper and middle pulmonary veins. Color Doppler imaging confirmed a left-to-right shunt (Fig. 1).

Fig. 1.

Transesophageal Echocardiography (TEE) Imaging of Sinus Venosus Atrial Septal Defect (ASD) with Anomalous Drainage of the Right Upper Pulmonary Vein (RUPV) into the Right Atrium (RA). A Midesophageal TEE image without color Doppler, showing the sinus venosus ASD defect (orange arrow). B Midesophageal TEE image with color Doppler, highlighting the ASD defect (orange arrow). C TEE in the bicaval view, showing the sinus venosus ASD with the drainage of the RUPV into the RA (yellow arrow). D Pulsed-wave Doppler demonstrates pulmonary vein flow

Computed tomography angiography (CTA) confirmed a superior-type SVASD with anomalous drainage of the right upper and middle pulmonary veins into the SVC (Fig. 2). Based on a comprehensive CTA evaluation demonstrating a suitable SVC diameter and length, the multidisciplinary heart team selected a percutaneous approach for transcatheter SVASD repair.

Fig. 2.

Cardiac CT Angiography. Pre-procedural Images: Maximum intensity projection (MIP) reconstruction images demonstrate a sinus venosus atrial septal defect (ASD) (White Arrow) and the abnormal connection of the right upper and middle pulmonary veins to the superior vena cava (SVC) at different levels (Red Arrows). The most cranial red arrow labels the high right upper pulmonary A-C

Right heart catheterization confirmed severe PAH with sPAP of 80 mmHg, mean pulmonary artery pressure of 40 mmHg, pulmonary vascular resistance (PVR) of 6 Wood units, and a pulmonary-to-systemic flow ratio (Qp/Qs) of 2.5, indicating a significant left-to-right shunt. During a 10-minute oxygen challenge, PVR decreased to 5 Wood units and sPAP to 75 mmHg, with improvement in the PVR/systemic vascular resistance ratio, confirming pulmonary vascular reactivity and suitability for a treat-and-repair strategy.

Management

A treat-and-repair strategy was adopted, and pulmonary vasodilator therapy with tadalafil (10 mg BID) and macitentan (10 mg Daily) was initiated. After six months, repeat hemodynamic assessment showed improvement: sPAP reduced to 50 mmHg, PVR to 4 Wood units, and the PVR/systemic vascular resistance ratio decreased to 0.20. According to the 2020 ESC guidelines for the management of adult congenital heart disease (ACHD) [6], defect closure may be considered (Class IIb) when PVR is reduced to < 5 Wood units after targeted pulmonary arterial hypertension therapy. Our patient’s PVR decreased from 6 to 4 Wood units after six months of vasodilator therapy, with a PVR/SVR ratio of 0.20, supporting transcatheter repair.

Transcatheter repair was performed under fluoroscopic and TEE guidance. Under general anesthesia, three venous access routes were established: a 14 French, 80 cm sheath in the right femoral vein; a 12 French, 30 cm sheath in the right jugular vein; and a 6 French, 7 cm sheath in the left femoral vein.

Angiographic evaluation of the RUPV was conducted with and without balloon inflation in the SVC extending slightly into the right atrium (RA). This maneuver confirmed proper channeling of RUPV blood to the left atrium (LA) under TEE monitoring, thereby isolating the SVC from the RUPV. A multipurpose catheter was advanced via the left femoral vein across the defect to the RUPV to perform angiography in the four-chamber view before and after balloon inflation, ensuring contrast continued to drain into the LA. This was verified by agitated saline injection into the RUPV under TEE, demonstrating bubble transit from the RUPV to the LA without residual shunt. A cine fluoroscopy image captured during balloon inflation served as a reference for stent placement (Fig. 3- B).

Fig. 3.

Intra-procedural angiographic images demonstrating sequential steps of transcatheter SVASD repair. A Contrast injection into the superior vena cava (SVC) and right upper pulmonary vein (RUPV) to delineate the defect. The arrow indicates the catheter positioned within the RUPV. B Balloon sizing of the SVC–right atrial junction to determine appropriate stent diameter and landing zone. The arrow shows the sizing balloon inflated at the SVC–right atrial junction. C Deployment of an Optimus-CVS covered stent (57 XXL) across the SVC–right atrial junction to close the interatrial communication. The arrow indicates the covered stent during deployment. D Post-dilation of the covered stent using an Atlas 22 × 50 mm balloon, followed by inferior flaring with an Andra 28 × 60 mm balloon to optimize pulmonary venous redirection. The arrow shows the post-dilation balloon inflated within the covered stent. E Placement of a second CP stent (8-zig, 45 mm) within the mid-portion of the Optimus stent to provide additional stabilization and serve as an anchoring platform. The arrow indicates the second CP stent positioned within the Optimus stent. F Post-dilation of the second CP stent with an Andra 28 × 60 mm balloon to finalize stent positioning and ensure optimal flow. The arrow shows the final post-dilation balloon inflated within the two-stent construct

A 57 mm long Optimus-CVS PTFE-covered XXL stent (AndraTec, Germany) delivered via jugular access was deployed across the SVC–RA junction, followed by post-dilation with an Atlas 22 × 50 mm balloon (Bard, USA). The stent’s distal end was flared within the RA using an Andra 28 × 60 mm balloon (AndraTec, Germany) to optimize pulmonary venous redirection. Because the Optimus-CVS stent had limited cranial anchoring and insufficient radial force for the large-diameter SVC wall, and given the patient’s large SVC diameter (15 mm) combined with a high-flow state (Qp/Qs 2.5), a 45 mm long bare-metal CP stent (8-zig) (NuMED, USA) was placed within the mid-portion of the Optimus stent, extending slightly cranially, to provide additional radial force and serve as an anchoring platform. This was followed by post-dilation with an Andra 28 × 60 mm balloon. This two-stent construct was designed to ensure secure fixation and prevent late stent migration (Fig. 3-E) [7]. Intra-procedural TEE confirmed correct stent position and unobstructed redirection (mean gradient 1 mmHg) of the pulmonary veins into the LA.

Immediately following stent deployment, the patient received aspirin 80 mg daily (300 mg loading dose pre-procedurally, continued indefinitely) and clopidogrel 75 mg daily (300 mg loading dose pre-procedure).

The patient was initially stable and transferred to the intensive care unit. However, 24 h later, oxygen saturation dropped to 75%. TTE confirmed the correct stent position (Fig. 4). Chest X-ray revealed new infiltrates in the right upper and middle lung zones, corresponding to the RUPV drainage territory (Fig. 5-A).

Fig. 4.

Postprocedural Transthoracic Echocardiography (TTE). TTE in subgastric view with color Doppler: (A) 2D TTE image showing the proper position of the covered stent (orange arrow) and absence of residual flow from the sinus venosus atrial septal defect (ASD). B Color Doppler TTE image demonstrating no residual flow from the ASD, confirming the successful closure of the defect

Fig. 5.

Postprocedural Chest X-ray (CXR). A Chest X-ray showing right upper lobe congestion with associated pulmonary infiltrates (blue arrow) following the procedure. B Chest X-ray showing complete resolution of the pulmonary congestion after conservative management, demonstrating full recovery

CTA demonstrated patent SVC stents, but complete occlusion of the anterior segment of the RUPV with associated thrombosis, along with alveolar infiltration and mild pleural effusion. On procedural review, this complication likely resulted from the second stent and its subsequent post-dilation with the 28 × 60 mm Andra balloon (Fig. 6). The stent induced partial mechanical jailing of the RUPV, which was not immediately detectable by TEE. Over the next 24 h, progressive thrombosis formation at the site of partial compression led to complete occlusion of the anterior segment of the RUPV.

Fig. 6.

Cardiac CT Angiography. Post-procedural Images: MIP reconstruction reveals the location of the stents within the SVC (Black Arrow). The uppermost pulmonary vein is occluded by the stent (Yellow Arrow), which has resulted in pulmonary hemorrhage and infarction D-F

Given hemodynamic stability, conservative management was pursued with corticosteroids (hydrocortisone 200 mg three times daily) and intravenous furosemide (40 mg twice daily). Clopidogrel was discontinued to reduce the bleeding risk associated with prolonged triple antithrombotic therapy after initiation of apixaban. Apixaban 5 mg twice daily was initiated for therapeutic anticoagulation, while aspirin 80 mg daily was continued with close monitoring. Oxygenation improved progressively, and by day 5, oxygen saturation normalized to 90% on room air. Follow-up chest X-ray showed resolution of infiltrates (Fig. 5-B). The patient was discharged in stable condition on dual-pathway inhibition (aspirin plus apixaban) for 3 months; apixaban was then discontinued, and aspirin monotherapy (80 mg daily) continued.

Follow-up TTE at 1 and 6 months showed a stable stent position, reduced sPAP (40 mmHg), and improved right ventricular enlargement.

Discussion and literature review

PVO is a rare but potentially serious iatrogenic complication following transcatheter covered-stent repair of SVASD with PAPVC. This case demonstrates that conservative management of acute PVO can achieve favorable clinical and radiographic outcomes in hemodynamically stable patients. Here, we discuss etiology, prevention, diagnosis, management, and follow-up of this complication, drawing on our experience and a targeted literature review.

Etiology and mechanisms of iatrogenic pulmonary vein obstruction

Iatrogenic PVO is a well-recognized but uncommon complication following transcatheter covered-stent repair of SVASD with PAPVC. PVO arises from the close anatomical relationship between the anomalous RUPV and the superior vena cava–right atrium (SVC–RA) junction. Improper stent positioning, oversizing, or excessive cranial extension may directly occlude the pulmonary venous orifice, impairing drainage from the affected lung segment [8]. Mild compression may remain clinically silent, but significant obstruction can lead to hypoxemia, pulmonary congestion, hemorrhage, or even infarction.

Multicenter registries report major PVO in 1–4% of cases, with partial obstruction observed in 5–7% [2, 9]. Although routine balloon interrogation before stent deployment has reduced the incidence of RUPV obstruction, delayed or unrecognized occlusion still occurs and has occasionally required surgical resection for recurrent hemoptysis [2, 10].

Institutional experience: At our center, 35 patients have undergone transcatheter SVASD repair with covered stents to date. The present case represents the first instance of clinically significant PVO encountered in this series, yielding an institutional incidence of approximately 2.9%, which is consistent with published multicenter registry data [1].

In our patient, implantation of a second CP stent for cranial anchoring, followed by post-dilation with a 28 × 60 mm Andra balloon, resulted in partial mechanical jailing of a high-draining RUPV branch. Retrospective review of pre-procedural CTA confirmed that this branch was clearly visible and was not initially recognized as a structure at risk. This oversight, combined with cranial extension of the anchoring stent and aggressive post-dilation, directly contributed to partial venous compression. Hemodynamically significant obstruction of the anterior RUPV branch developed gradually over 24 h due to progressive thrombosis at the site of partial jailing, which is why intra-procedural TEE did not detect the complication.

Prevention and intra-procedural strategies

Prevention of iatrogenic PVO begins with meticulous pre-procedural planning. Cross-sectional imaging with cardiac CTA or cardiac magnetic resonance (CMR), combined with three-dimensional reconstruction, is essential for defining spatial relationships among the SVC, RA, and all anomalous pulmonary venous branches. Particular attention should be given to identifying high-draining pulmonary veins and measuring their distance from the anticipated stent landing zone [4]. Functional assessment of PVR is also crucial, especially in patients with PAH, as abnormal hemodynamics may exacerbate the consequences of venous obstruction.

From a technical standpoint, inadvertent PVO is largely preventable. The current standard approach is to leave high-draining pulmonary veins freely draining into the SVC by one of two methods: (1) positioning the covered stent sufficiently caudal so that the anomalous vein remains above the stent edge, or (2) using an additional bare-metal anchoring stent whose open struts permit continued pulmonary venous flow [2, 4]. Careful pre-procedural CTA assessment and balloon test occlusion of all draining pulmonary veins are critical to avoid jailing of a high RUPV [4].

Despite ongoing debate, customized long-covered stents with PTFE covering extension adjustment are thought to help mitigate the risk of PVO during transcatheter repair of SVASD by enabling more controlled single-step implantation [1, 5, 11, 12]. Unlike standard covered stents, customized devices can be tailored to the complex anatomy, avoiding unnecessary procedural steps, stent overlap, and repeated balloon dilations, thereby distributing radial force more homogenously.

Intra-procedural imaging guidance, particularly with TEE, allows real-time evaluation of stent position, pulmonary venous flow, and residual shunting. Balloon test occlusion with simultaneous venography and pressure monitoring helps confirm that the planned stent position will not compromise pulmonary venous return. When TEE visualization is suboptimal, selective pulmonary venography or intracardiac echocardiography (ICE) should be considered [5]. Additional protective strategies, such as temporary balloon or wire placement within the RUPV during stent deployment, may further reduce the risk of inadvertent obstruction. Appropriate stent sizing, careful selection of the landing zone, and controlled, gradual deployment are also essential technical steps.

Recent evidence supports the use of three-dimensional printed models or virtual simulation for complex SVASD anatomy, allowing operators to anticipate spatial relationships and test stent positions before the procedure [8]. Although not available at our center at the time, such technologies may become standard for high-risk cases.

Diagnosis of PVO

PVO typically presents within the first 24–48 h after the procedure with acute hypoxemia, dyspnea, and new pulmonary infiltrates on chest X-ray. Hemoptysis may occur in more severe cases. CTA is the diagnostic modality of choice, providing a detailed assessment of stent position, pulmonary vein patency, thrombus formation, and associated parenchymal injury (e.g., alveolar infiltration, hemorrhage, or infarction). A pulmonary vein pressure gradient of 5–10 mmHg or greater across the stenotic segment confirms hemodynamically significant obstruction.

In our patient, the diagnosis was established by CTA on post-procedural day 1, which demonstrated complete occlusion of the anterior segment of the RUPV with associated thrombosis, alveolar infiltration, and mild pleural effusion. The mean Doppler gradient of 8 mmHg and peak velocity of 1.9 m/s further supported the diagnosis of significant obstruction. These measurements were obtained by TTE using color and pulsed-wave Doppler interrogation of the obstructed anterior branch of the RUPV adjacent to the covered stent. Intra-procedural TEE immediately after stent deployment demonstrated unobstructed pulmonary venous drainage with a mean gradient of 1 mmHg. Follow-up transthoracic echocardiography at 1 and 6 months demonstrated normalization of pulmonary venous flow without residual obstruction.

Management of PVO

Management of post-procedural PVO depends on three key factors: obstruction severity, hemodynamic stability, and the presence of associated thrombosis.

Conservative management may be appropriate for hemodynamically stable patients, even in the presence of complete obstruction of one segment with thrombosis, as demonstrated in this case. Our patient received the following regimen: corticosteroids (hydrocortisone 200 mg three times daily) to reduce inflammation-mediated pulmonary congestion, diuretics (furosemide 40 mg twice daily) to manage pulmonary edema, therapeutic anticoagulation (apixaban 5 mg twice daily) for associated thrombosis, and antiplatelet therapy (aspirin 80 mg daily) for dual-pathway inhibition.

Within 48 h of initiating this regimen, the patient’s oxygenation improved significantly, and chest X-ray demonstrated progressive resolution of pulmonary infiltrates. By day 5, oxygen saturation normalized to 90% on room air, with complete radiographic resolution.

Interventional management (balloon angioplasty, stent revision, or surgical thrombectomy) is reserved for patients with severe obstruction, hemodynamic instability, or failure of conservative measures. In a recent multicenter series, the majority of clinically significant PVO cases required reintervention [2]. Our case is notable because conservative management alone led to complete clinical and radiographic recovery, without the need for invasive reintervention.

Antithrombotic considerations: When thrombosis is present, therapeutic anticoagulation should be initiated promptly. The optimal duration of therapy remains uncertain; however, based on our experience, we recommend a minimum of three months of dual-pathway inhibition (e.g., aspirin plus a direct oral anticoagulant such as apixaban), followed by long-term antiplatelet monotherapy if follow-up imaging confirms thrombus resolution and persistently patent pulmonary venous flow.

Comparison with surgical repair

Surgical correction of SVASD with PAPVC remains the gold standard, with excellent long-term outcomes and mortality rates below 1% [13]. However, transcatheter repair offers advantages including shorter hospital stays, avoidance of cardiopulmonary bypass, and reduced perioperative morbidity [14]. Importantly, venous complications—including PVO and SVC obstruction—are not exclusive to transcatheter methods; surgical series report pulmonary vein or SVC obstruction in 2.7–7.7% of patients [15]. Thus, the risk of PVO should be contextualized within the overall risk profile of both treatment modalities.

Follow-up protocol and surveillance

Patients complicated with PVO require intensified follow-up to confirm resolution and exclude late sequelae such as restenosis, chronic thrombus, or parenchymal scarring. While our standard follow-up after uncomplicated covered stent placement includes clinical evaluation and TTE at 1, 6, and 12 months, stent-associated thrombosis warrants additional surveillance [11].

In our case, follow-up TTE at 1 and 6 months showed a stable stent position, reduced systolic pulmonary artery pressure (40 mmHg), and improved right ventricular enlargement. No residual PV obstruction was detected. Given the history of stent-associated thrombosis, this patient is at increased risk for future thrombotic events at the stent site. Given the history of stent-associated thrombosis, continuation of long-term aspirin therapy was selected as an individualized management strategy in this patient after multidisciplinary discussion. However, the optimal duration of antiplatelet therapy following this complication remains uncertain and should be tailored according to thrombotic and bleeding risk. In our experience, continuing long-term anticoagulation (e.g., apixaban, warfarin) is more effective in patients who develop recurrent thrombosis, atrial fibrillation, or another indication for anticoagulation. The 3-month course of apixaban was sufficient to achieve complete thrombus resolution, and the risk of bleeding with indefinite anticoagulation outweighs the benefit in this stable patient.

Limitation

First, it represents a single case, and the favorable outcome with conservative management may not be generalizable to all patients with PVO. Second, ICE was unavailable at our center during the procedure. ICE could have provided superior visualization of the high-draining RUPV branch, which was located beyond the optimal imaging field of the TEE probe. Third, three-dimensional simulation and virtual printing technologies were not available at our center at the time of this procedure. Such tools could have enabled pre-procedural planning to anticipate the spatial relationship between the high-draining RUPV branch and the anticipated stent landing zone, potentially preventing this complication. These limitations highlight opportunities for quality improvement in future cases, including wider adoption of advanced imaging modalities, routine use of selective venography and balloon test occlusion for all anomalous pulmonary veins, and integration of three-dimensional simulation in cases with complex anatomy.

Conclusion

PVO is a rare but serious iatrogenic complication of transcatheter covered-stent repair for SVASD. Importantly, PVO may not be immediately detectable on intra-procedural TEE and can present with a delayed onset due to progressive thrombosis. Proper pre-procedural assessment with advanced, systematic balloon interrogation of all anomalous pulmonary veins, and intra-procedural protective strategies (selective venography, temporary wire/balloon protection, and careful stent positioning) are essential to reduce this risk. When PVO occurs, conservative management with corticosteroids, anticoagulation, and diuretics may achieve favorable outcomes in hemodynamically stable patients, potentially avoiding reintervention or surgery. This case provides valuable insights into the recognition, prevention, and management of this rare complication.

Abbreviations

SVASD

Sinus Venosus Atrial Septal Defect

PAPVC

Partial Anomalous Pulmonary Venous Connection

SVC

Superior Vena Cava

RUPV

Right Upper Pulmonary Vein

RA

Right Atrium

LA

Left Atrium

TEE

Transesophageal Echocardiography

CXR

Chest X-ray

CT

Computed Tomography

CTA

Computed Tomography Angiography

TTE

Transthoracic Echocardiography

ASD

Atrial Septal Defect

PAH

Pulmonary Arterial Hypertension

SVC-RA

Superior Vena Cava-Right Atrium

MIP

Maximum Intensity Projection

Qp/Qs

Pulmonary-to-Systemic Flow Ratio

PVR

Pulmonary Vascular Resistance

SVR

Systemic Vascular Resistance

PVO

Pulmonary Vein Obstruction

PV

Pulmonary Vein

Authors’ contributions

SS and NK wrote the main manuscript. AF and Z Kh edited the manuscript, HP prepared Figs. 1, 2, 3, 4, 5 and 6, and all authors participated in data collection, patient care, and final manuscript revision. All authors read and approved the final manuscript.

Funding

This study received no external funding. The authors did not receive financial support from any organization for the submitted work.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Ethical approval was not required for this case report, as the data were anonymized and published with the patient’s consent.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.