ECMO: identifying tricuspid rupture behind hypoxemia

Refractory hypoxemia under VV-ECMO: the pitfall of occult cardiac lesions

Veno-venous extracorporeal membrane oxygenation (VV-ECMO) is established as the ultimate rescue therapy for severe acute respiratory failure. In the specific context of polytrauma, the management of acute respiratory distress syndrome (ARDS) is complicated by the potential presence of multi-organ injuries. This clinical case details the management of a 29-year-old patient presenting with critical refractory hypoxemia, with an initial PaO2/FiO2 ratio of 55 mmHg following a road traffic accident.

The major diagnostic challenge lies in the inability to wean the assistance despite an apparent stabilization of the lung lesions. Why does oxygenation drop abruptly as soon as the ECMO parameters are reduced? This report explores the hypothesis of a masked traumatic cardiac origin, such as a rupture of the tricuspid valve chordae, compromising the effectiveness of extracorporeal oxygenation. The objective is to demonstrate how bedside transesophageal echocardiography (TEE) becomes the pivotal tool for identifying abnormal intracardiac hemodynamics — including shunt and massive regurgitation — which invalidate conventional ventilation strategies and classic extracorporeal support.

Study design and subject

This publication is based on a clinical case report detailing the management of a 29-year-old patient who suffered severe polytrauma (Injury Severity Score of 30). The subject presented with refractory acute respiratory distress syndrome (ARDS) with an initial PaO2/FiO2 ratio of 55 mmHg, requiring support via veno-venous extracorporeal membrane oxygenation (VV-ECMO).

Implementation protocol for VV-ECMO

Circulatory support was established via peripheral cannulation: a 17 Fr drainage cannula in the right internal jugular vein and a 21 Fr return cannula in the right femoral vein. Initial parameters were calibrated as follows:

• Rotation speed: 3000 rpm.
• Blood flow: 2.76 L/min.
• Sweep gas: 5 L/min at a FiO2 of 100%.
• Anticoagulation: Continuous intravenous heparin (targets: ACT 160–200 s, APTT 60–80 s).

Surgical procedure and diagnosis

In the face of persistent hypoxemia under ECMO, an exploration by 3D transesophageal echocardiography (3D-TEE) was performed, revealing a rupture of the tricuspid valve chordae and a 2 cm atrial septal defect (ASD). On the 11th day, valve repair was performed by implantation of artificial chordae and a rigid annuloplasty ring, coupled with the closure of the ASD.

Evaluation and monitoring tools

Le suivi clinique a reposé sur une surveillance multidisciplinaire incluant la gazométrie artérielle, l'imagerie par scanner thoracique (CT) et des hémocultures répétées pour identifier d'éventuelles complications infectieuses post-décannulation.

Echocardiographic and Hemodynamic Diagnosis

Initial assessment revealed refractory hypoxemia with a PaO2/FiO2 ratio of 55 mmHg. Despite the initiation of VV-ECMO (initial flow rate of 2.76 L/min, 3000 rpm), oxygen saturation dropped upon any attempt to reduce support parameters. 3D transesophageal echocardiography (3D-TEE) identified the structural causes of this weaning failure:

• Valvular involvement: Rupture of the anterior papillary muscle chordae tendineae leading to tricuspid valve prolapse and massive regurgitation (Grade 4+).
• Septal defect: Presence of a 2 cm atrial septal defect (ASD) with bidirectional shunt.
• Cardiac dimensions: Dilation of the right atrium (58 x 48 mm) and the right ventricle (60 x 25 mm).

Surgical Procedure and ECMO Weaning

On the 11th day, a surgical procedure was performed to correct intracardiac hemodynamic anomalies. The procedure consisted of a reconstruction of the anterior leaflet using artificial chordae, stabilized by a rigid annuloplasty ring, coupled with the closure of the ASD. Immediate post-operative results showed minimal residual tricuspid regurgitation and a significant reduction in the interatrial shunt.

This correction allowed for a rapid improvement in pulmonary oxygenation, facilitating weaning from extracorporeal assistance:

Parameter	Pre-ECMO	Suture removal (D12)
FiO2 (Ventilator)	100%	40%
ECMO flow rate	2.76 L/min	1.5 L/min (before removal)
SpO2	86%	≥95%
PEEP (cm H2O)	15	6

VV-ECMO was successfully removed on the 12th day of management.

Infectious Complication and Clinical Outcome

After decannulation, the patient developed a febrile syndrome marked by a degradation of inflammatory markers (leukocytes at 28.17 x 10^9/L, CRP at 61.74 mg/L). TEE revealed an irregular hyperechoic mass of 18 x 7.2 mm on the anterior tricuspid leaflet, suggesting vegetations.

Blood cultures confirmed infectious endocarditis due to Burkholderia cepacia. Targeted antibiotic treatment (meropenem, ceftazidime, and sulfamethoxazole/trimethoprim) was initiated. After 72 hours, clinical improvement was observed (apyrexia, decrease in CRP to 35.59 mg/L). Following a 6-week course of antibiotic therapy, the patient was weaned from mechanical ventilation and transferred to a rehabilitation center.

Analysis: When hypoxemia persists despite VV-ECMO

This clinical case highlights a formidable therapeutic impasse: refractory hypoxemia under veno-venous extracorporeal membrane oxygenation (VV-ECMO). In this 29-year-old patient, presenting an Injury Severity Score (ISS) of 30, the initiation of ECMO for traumatic ARDS did not achieve the expected stabilization. Data analysis shows that the effectiveness of extracorporeal oxygenation was bypassed by intracardiac hemodynamic anomalies that were unrecognized during the initial management.

The persistence of SpO2 at 86% despite a gas flow rate of 5 L/min and a FiO2 of 100% is explained by the combination of massive tricuspid regurgitation (grade 4+) and a 2 cm interatrial shunt. These lesions, resulting from thoracic trauma, promoted major recirculation and a right-to-left shunt, rendering the ECMO settings ineffective. The study highlights that in this context, the problem was no longer membrane-related but mechanical, requiring surgical intervention (reconstruction using artificial chordae and septum closure) to restore oxygenation efficiency, allowing for weaning on the 12th day.

Case limits and specificities

Although the results are convincing, this is a single case report concerning a rare etiology (traumatic rupture of the tricuspid chordae). The main limitation lies in the initial diagnostic delay, as the ultrasound was not performed in the first-line facility. Furthermore, the episode of Burkholderia cepacia infective endocarditis post-decannulation highlights the immunological vulnerability of these patients, although the infection was controlled by targeted antibiotic therapy.

Implications for clinical practice

Compared to classic cases of pure ARDS, this report demonstrates that ECMO cannot compensate for structural cardiac failure. The systematic use of 3D echocardiography (TOE) was the pivot of the differential diagnosis here, revealing that the hypoxemia was not solely of pulmonary origin. Specifically, early surgical valve repair must be considered as soon as intracardiac hemodynamics compromise systemic oxygenation under ECMO.

Summary of results

This clinical case (initial PaO2/FiO2 of 55 mmHg) demonstrates that refractory hypoxemia under VV-ECMO can result from an initially undiagnosed traumatic cardiac injury. Transesophageal echocardiography (TEE), performed at the first signs of adjustment difficulties (D2-D3), revealed a rupture of the tricuspid chordae and an atrial shunt, the surgical repair of which on D11 allowed for weaning from assistance as early as D12.

In concrete terms, for the practitioner:

• Look for a cardiac cause: In the event of ineffective oxygenation under VV-ECMO, suspect massive tricuspid regurgitation or a shunt that increases flow recirculation.
• Prioritize early TOE: Echocardiography must be performed systematically within the first 48 hours in case of unstable saturation to exclude any traumatic valvular anomaly.
• Post-assistance infectious vigilance: An inflammatory rebound after cannula removal requires suspicion of infectious endocarditis, necessitating rapid ultrasound diagnosis and targeted antibiotic therapy.

The initiation of veno-venous extracorporeal membrane oxygenation (VV-ECMO) often constitutes the final resort in the face of refractory acute respiratory distress syndrome (ARDS), particularly in a polytrauma context. However, when hypoxemia persists despite optimal extracorporeal support, the clinician must imperatively consider an etiology beyond pulmonary parenchymal involvement alone. The diagnostic challenge then lies in the early identification of intracardiac anomalies potentially masked by the initial presentation.

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