Traumatic Left Ventricular Aneurysm and Ventricular Septal Defect in a Child

Introduction

Presented is a case of an aneurysm of the left ventricle (LV) free wall and ventricular septum with associated ventricular septal defect (VSD) following blunt trauma in a 23-month-old girl.

Case Report

A previously healthy 23-month-old girl presented to an affiliated medical center as a trauma activation following a pedestrian versus motorcycle accident. She had a moderate concussion, grade III liver laceration, right clavicle fracture, and pulmonary contusion. The following morning, she was tachycardic (150-160 beats per minute [bpm]) with a newly noted 3 of 6 holosystolic murmur. Transthoracic echocardiogram (TTE) revealed an aneurysm of the LV free wall and the posterior ventricular septum with an associated small VSD. She was emergently transferred to our tertiary pediatric hospital cardiac intensive care unit for further management.

Upon arrival, she was normotensive with tachycardia (140-160 bpm). An electrocardiogram showed sinus tachycardia, possible right ventricular hypertrophy and inferior lead ST-segment elevation, and T-wave inversion without conduction delay. Repeat TTE showed a 22  × 17 mm aneurysm of the LV free wall and inferoposterior ventricular septum as well as a small pressure-restrictive VSD with left-to-right shunt (Figure 1). Cardiac gated computed tomography angiography (CTA) showed an aneurysm of the ventricular septum distant from the junction of the membranous and muscular septum with an associated VSD that did not involve the papillary muscles (Figure 2). Magnetic resonance angiography (MRA) revealed transmural delayed enhancement of the walls of the aneurysm, indicating myocardial necrosis.

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Figure 1.

TTE with color flow mapping: (A) apical view demonstrating septal component of LV aneurysm bulging into the right ventricular cavity; (B) modified apical view demonstrating VSD with left to right shunt; (C) modified parasternal long-axis view; (D) modified parasternal short-axis view. *  =  LV aneurysm, Arrow  =  VSD, RV  =  right ventricle, RA  =  right atrium, LA  =  left atrium.

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Figure 2.

CTA chest: (A) axial view; (B) short axis view; (C) 4-chamber view; (D) three-dimensional reconstruction. (red  =  LV, yellow  =  left atrium, blue  =  right ventricle, gold  =  right atrium); *  =  LV aneurysm.

After multidisciplinary discussions, a decision was reached to preclude immediate surgical repair due to necrotic myocardium and concerns for tissue quality. With concomitant concerns for aneurysmal rupture, she was urgently listed status 1A for a heart transplant on the postinjury day (PID) 3 with a plan to accept an ABO-incompatible heart. She was started on an esmolol infusion and transitioned to propranolol for heart rate control and to decrease the force of myocardial contraction. Aspirin was started for thromboprophylaxis. Four serial TTEs over the next 2 weeks showed stable and reassuring findings. She was transferred to the cardiac care unit on PID 5 and downgraded to status 7 for a heart transplant on PID 12. She was discharged from the hospital on PID 15 and was followed with weekly TTE. She was subsequently re-admitted to the hospital and was taken to the operating room for repair on PID 45.

Her operative course involved aorto-bicaval cardiopulmonary bypass. The aorta was cross-clamped, and myocardial preservation was achieved with antegrade Del Nido cardioplegia. The heart was elevated to expose the free wall aneurysmal sac. The myocardium was non-viable and appeared ischemic and scarred (Figure 3A). An incision was made into the aneurysmal wall which led to a large aneurysmal sac. The mouth of the aneurysm allowed entrance into the LV, and the mitral valve apparatus was well identified (Figure 3B). The mouth of the aneurysm was closed with a Dacron patch (Figure 3C). The VSD was also visible within the aneurysmal sac and was closed with interrupted pledgeted sutures. Ischemic myocardial tissue was resected in a manner to ensure no damage to nearby coronary vasculature or viable myocardium (Figure 3D). The remainder of the sac was obliterated with interrupted horizontal mattress sutures. The epicardial surface was reinforced in 2 layers. She was weaned from cardiopulmonary bypass and closed in the standard fashion. Postrepair intraoperative TEE showed no residual aneurysm or VSD with good biventricular function around the aneurysm patch.

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Figure 3.

Operative photos from surgeon’s point of view: (A) scarred myocardium of LV free wall aneurysm; (B) view of LV through ventriculotomy and VSD; (C) patch closure of neck of VSD; (D) excision of excess free wall scar tissue.

She had an unremarkable postoperative recovery and was discharged home on postoperative day 5. She was most recently seen at her 5-month follow-up and continues to do well.

Comment

Two-thirds of pediatric cardiac trauma is from blunt mechanisms. Greater than 90% of these injuries are cardiac contusions or lacerations with the remainder being coronary artery or valve injuries. ^1,2 The mortality rate for pediatric cardiac injury is high (27%-40%), ^1,2 but only a small proportion (<2%) require surgery. ¹ Accordingly, our patient had a very high-risk injury even before considering its rarity and the difficulty in surgical decision making.

Traumatic aneurysm of the interventricular septum and LV free wall with an associated VSD is unusually rare in children. Variations of this injury have been reported infrequently. ^{3 –6} Initial findings in our patient, tachycardia and a new murmur, have been reported. However, congestive heart failure, palpitations, arrhythmias, and emboli are the most common presenting symptoms of LV aneurysm. ⁶ A postulated mechanism of traumatic LV aneurysm is coronary artery injury leading to ischemic necrosis of the myocardium. ⁶

Successful delayed repair of LV aneurysm following blunt pediatric cardiac trauma has been described. ^{3 –5} However, most of these injuries were not discovered until months after the traumatic event. Delayed repair in these cases was a result of clinical presentation timing rather than surgical decision making. Moreover, the ventricular septal component of our patient’s LV aneurysm may be unique as we could find no prior reports of such an injury, further differentiating our case from prior experience.

In the acute phase, surgical repair was deemed high risk due to concerns of myocardial tissue quality as may be correlative to an adult with a postinfarct VSD. As a result, we were faced with a cardiac lesion with a high risk for rupture and sudden death without a straightforward option of immediate surgical repair. Although an immediate transplant would definitively treat her injury, it would also abandon the possibility of surgical repair and commit her to a lifetime of immunosuppression. We ultimately listed her for transplant, which allowed us to simultaneously wait for a transplant and wait for scar formation with a goal of semi-elective repair.

A traumatic aneurysm of the LV free wall and ventricular septum with VSD is a rare, high-risk injury. Discovery in the acute setting leaves surgeons with a potential surgical dilemma. We present a case of successful repair initially delayed due to concern for myocardial tissue quality in the acute phase with an interim urgent listing for transplant in a toddler. We believe this management strategy optimized our therapeutic options during each phase of the patient’s care.