Papillary Muscle Rupture Due to Blunt Chest Wall Trauma Treated With Impella as a Bridge to Valve Replacement

Abstract

Severe mitral regurgitation due to papillary muscle rupture is life-threatening and rarely occurs after blunt chest wall trauma. We present a case of cardiogenic shock caused by papillary muscle rupture and severe mitral regurgitation after blunt chest wall trauma that was treated with Impella as a bridge to valve replacement.

Graphical Abstract

History of presentation

A 64-year-old male presented to the emergency department with chest pain and facial lacerations after a bike accident. Initial vital signs were blood pressure 76/52 mm Hg, pulse rate 85 beats/min, respiratory rate 25 breaths/min, and oxygen saturation 97% on room air. The physical examination was significant for Glasgow Coma Scale of 15, facial abrasions, chest wall tenderness, bilateral crackles on lung auscultation, and no audible murmur. The trauma survey showed a negative Focused Assessment with Sonography in Trauma. Chest x-ray showed no acute trauma. A computed tomography scan showed manubrium fracture, multiple rib fractures, and pulmonary contusion. Hypotension was refractory to fluid resuscitation, necessitating pressors and admission to intensive care unit.

Take-Home Messages

• •This case highlights the clinical presentation of traumatic mitral valve apparatus injury, both rare and potentially fatal.
• •Mechanical circulatory support serves as a critically important bridge to definitive intervention in acute mitral regurgitation and papillary muscle rupture.

Past medical history

The patient had a history of controlled hypertension and HIV; otherwise, past medical history was unremarkable.

Differential diagnosis

Other diagnoses might have included hemorrhagic shock, tamponade, aortic dissection, and traumatic valve injury

Investigations

Initial transthoracic echocardiogram (TTE) showed a hyperdynamic left ventricle (LV) with an ejection fraction of 70% to 75%, flail motion of the anterior leaflet of the mitral valve (MV), papillary muscle rupture, and findings consistent with acute severe mitral regurgitation (MR). Subsequent transesophageal echocardiogram (TEE) confirmed a rupture of the posteromedial papillary muscle head resulting in flail motion of the anterior leaflet of the MV and severe MR with effective regurgitant orifice area ≥0.4 cm² (Video 1, Video 2, Video 3). The patient developed flash pulmonary edema and acute hypoxic respiratory failure requiring intubation and ventilation. He also had escalating pressor requirements (Figure 1). He was taken urgently to the catheterization lab for right and left heart catheterization. Left heart catheterization showed a long segment with 70% stenosis in the middle of the right coronary artery and no significant obstruction on the left main, left anterior descending, or left circumflex arteries. Right heart catheterization showed elevated filling pressures with right atrial 17 mm Hg, pulmonary artery (PA) 57/33 mm Hg, and pulmonary capillary wedge pressure (PCWP) 26 mm Hg; PA oxygen saturation was 37%, which was consistent with a cardiac output 2.0 L/min and cardiac index 1.1 L/min/m².

Figure 1.

Initial Chest X-Ray

Chest X-ray revealing evidence of pulmonary edema (red arrow), and endotracheal tube used to intubate the patient (green arrow).

Management

Based on these findings, an Impella CP was placed. PA oxygen saturation on Impella support improved to 58% with CO 3.7 L/min and cardiac index 2.98 L/min/m²; however, the patient remained in cardiogenic shock (CS) with worsening liver and kidney function requiring renal replacement therapy. After a multidisciplinary discussion including cardiac surgery, advanced heart failure, critical care, and interventional cardiology teams, the patient received urgent MV replacement surgery. The MV was replaced with a 27-mm Mitralis bioprosthetic valve (Video 4). The Impella was left in place. The postoperative course was complicated with worsening CS with rising lactic acid and pressor requirements necessitating escalating support to venous-arterial extracorporeal membrane oxygenation (ECMO).

Hemodynamics and lactic acid improved on ECMO, and the patient was weaned off ECMO with decannulation on postoperative day 5. The Impella was removed on postoperative day 6. Pulmonary edema was shown to have improved on chest radiography (Figure 2). The patient was transitioned to intermittent hemodialysis and underwent inpatient rehabilitation. He was discharged to a long-term care facility on postoperative day 29.

Figure 2.

Postoperative Chest X-Ray

Post-operative chest x-ray revealing 27 mm mitralis bioprosthetic valve (red arrow), and improvement in pulmonary edema relative to initial chest x-ray in Figure 1.

Discussion

Papillary muscle rupture uncommonly occurs as a complication of acute myocardial infarction or infective endocarditis but is often fatal. Rarely, MV apparatus injury occurs with nonpenetrating chest wall trauma. Timely diagnosis and management improve prognosis.1, 2, 3, 4 In this case, mechanical circulatory support (MCS) was used to achieve hemodynamic stability as a bridge to a definitive surgical intervention.

In blunt chest wall trauma, tricuspid valve apparatus is most commonly involved.⁵ MV apparatus traumatic injury is rare and data on traumatic papillary muscle rupture are scarce. In 353 autopsies from a nonpenetrating cardiac trauma series, papillary muscle rupture was encountered 24 times and was mostly combined with other myocardial lesions.² This paucity of data adds to the diagnostic and therapeutic challenges of this condition.

The diagnosis of acute severe MR murmur is often missed due to rapid equalization of pressure between LV and left atrium and the atypical nature of the mitral regurgitant murmur. Diagnosis is usually established by TTE followed by TEE.³ Severe MR causes rapid increase in PCWP resulting in pulmonary edema followed by cardiac decompensation and CS. Timely diagnosis breaks the cascade to cardiac decompensation, allowing for timely stabilization and surgical intervention.⁶

Acute severe primary MR management is primarily surgical. However, when the MR causes CS, preoperative stabilization is needed. Preoperative stabilization includes afterload reduction and often MCS use as a bridge to a definitive surgical intervention. MCS offloads the LV, decreases PCWP, and improves cardiac output. MCS options include use of an intra-aortic balloon pump (IABP), ECMO, and the Impella. Escalation of MCS or combining ECMO and the Impella is sometimes needed for preoperative optimization. Literature supports the use of an IABP in acute severe MR as a bridge to surgical repair. An IABP improves hemodynamics by decreasing aortic impedance and mitral regurgitant fraction.^6,7 However, literature is lacking on Impella use in this condition. Vandenbriele et al⁸ explored using the Impella as a bridge to MitraClip in 6 patients with CS due to acute severe MR and reported a survival to discharge rate of 86%.

Follow-up

The patient followed-up in 5 months, with repeat TTE showing LV ejection fraction improved to 55% to 60%, mild MV stenosis with a mean gradient of 8 mm Hg, and overall normal bioprosthetic valve function.

Conclusions

Blunt chest wall trauma rarely causes injury to the MV apparatus. Emergent TTE and subsequent TEE are essential to establish the diagnosis. Timely surgical intervention is needed to prevent progression to CS. However, the use of MCS plays an important role in patient stabilization before surgery. Using a multidisciplinary approach by involving cardiac surgery, advanced heart failure, critical care, and interventional cardiology teams facilitates management and improves prognosis.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Transesophageal Echocardiogram 1

Video 2

Transesophageal Echocardiogram 2

Video 3

Preoperative Echocardiogram With 3-Dimensional Reconstruction

Video 4

Intraoperative Transesophageal Echocardiogram