Selective non-operative management of a left ventricular pseudoaneurysm after penetrating cardiac wound.

Post-traumatic cardiac pseudoaneurysm (PSA) is a rare, potentially life-threatening complication after penetrating cardiac injury. Early surgical intervention has been the treatment of choice for this sequela due to the risk of rupture. Nevertheless, selective non-operative management (SNOM) has been practiced in patients with postinfarct PSA that are small and stable. We report a case of a post-traumatic cardiac PSA subjected to SNOM.

INTRODUCTION

Post-traumatic cardiac pseudoaneurysm (PSA) is a rare, potentially life-threatening complication following penetrating cardiac injury. Early prophylactic surgical aneurysmectomy has been the treatment of choice. However, in small and stable postinfarct PSA selective non-operative management (SNOM) has been practiced.[1] We report a case of a post-traumatic cardiac PSA subjected for SNOM.

CASE REPORT

A 38-year-old Hispanic male was admitted to Los Angeles County + University of Southern California Medical Center after sustaining a single stab wound to the left chest. Upon arrival the patient was bradycardic with a systolic blood pressure of 50 mmHg, and Glasgow Coma Scale (GCS) score of 3. The patient underwent simultaneous intravenous access, oral intubation and resuscitative left thoracotomy. After evacuation of 400 ml of blood and clot from the chest a pericardial wound was noted anterior to the phrenic nerve. The cardiac tamponade was rapidly decompressed and cardiac arrest was noted. A cardiac wound in the left ventricle was repaired using a 2.0 polypropylene suture. An aortic cross-clamp was applied. Cardiac massage along with intracardiac injection of epinephrine and bicarbonate resulted in sinus tachycardia. Four additional sutures were required upon restoration of sinus tachycardia to control an exsanguination in the emergency department as the full extent of the defect was not evident during asystole. Residual hemorrhage was present when the patient was taken to the operating room (OR) for definitive repair. In the OR, the cardiac wound was reinforced with four pledgeted polypropylene mattress sutures with no residual hemorrhage. Nevertheless, the left ventricular wall appeared edematous and bruised after the complex repair. The pericardium was left open. The patient continued to be hypothermic, acidotic and coagulopathic. Attempted chest closure resulted in severe bradycardia and therefore, temporary closure was obtained with a vacuum-assisted closure device and the patient was transferred to the surgical intensive care unit. In total, 24 units of packed red cells, 10 units of fresh frozen plasma, and 6 units of platelets were transfused. On the second postoperative day, chest was uneventfully closed in the OR. The early hospital course was complicated by acute renal failure (peak creatinine 6.19 mg/dL) requiring dialysis. The patient was extubated on hospital day (HD) 10 with no neurological impairment. On HD 24 a cardiac ultrasound was obtained revealing findings consistent with a pseudoaneurysms (PSA) of the left ventricle. On HD 25 a magnetic resonance imaging (MRI) confirmed a PSA in the lateral wall of the left ventricle measuring 1.0×1.6 cm without thrombi [Figure 1]. A second MRI obtained 16 days later demonstrated stabilization of the lesion. The patient was discharged home. Six-month follow-up echocardiogram confirmed normal cardiac function and there was no evidence of progression or leakage from the PSA. One-year follow-up MRI detected a 30% decrease in size of the PSA [Figure 2]. One-year follow-up echocardiogram showed overall ejection fraction of 55-60% with moderate hypokinesis of the anterolateral wall of the left ventricle without septal or valvular lesions. The patient remained physically and neurologically intact throughout the 1-year observation period. Based on the fact that the patient had a small and non-progressing PSA, definitive non-operative management was instituted.

Figure 1

Sagittal MRI view of the pseudoaneurysm depicting the narrow “neck”. PSA, pseudoaneurysm; LV, left ventricle

Figure 2

Sagittal MRI view of the pseudoaneurysm. One year repeated imaging shows decrease in size of the PSA. PSA, pseudoaneurysm; LV, left ventricle

DISCUSSION

Patients with penetrating cardiac injuries arriving at the hospital hypotensive with cardiac tamponade can be salvaged only with prompt surgical intervention.[2] Isolated cardiac stab wounds in patients with vital signs on admission holds the best prognosis after these life-threatening injuries.[3] Not uncommonly, atrial septal defects (ASD), ventricular septal defects (VSD), valvular insufficiency, and more rarely, development of a ventricular PSA may occur.[24] To diagnose these sequelae an echocardiogram is obtained early postoperatively.

A PSA is a rare complication resulting from a rupture of the ventricular wall, which has been contained by pericardial adhesions or the pericardial wall.[5] The wall of the PSA is composed of fibrous tissue and lacks the integrity of the normal ventricle. To date, very few cases of post-traumatic PSA have been reported in the literature[46-8] and the time from injury to diagnosis ranged between 5 days and 25 years.[48] These PSA may predispose patients to embolic sequelae, rupture and death and therefore have been subjected to prophylactic aneurysmectomy.[91011] Alternatively, percutaneous embolization has also been reported.[11] Selective non-operative management (SNOM) of this complication has been documented in asymptomatic postinfarct patients with minor (<3×3 cm) and non-progressing lesions. SNOM may also be an option in chronic PSAs (>3months). In a review of 66 patients, Natarajan and colleagues[1] observed that conservative management of a chronic postinfarct PSA was not associated with an increased risk of cardiac rupture or poor prognosis.

Septic ventricular PSA has been reported by Utley and colleagues where Staphylococcus epidermidis, Staphylococcus aureus and Salmonella have been observed to be the most common pathogens.[12] In these cases, SNOM is ill-advised. Nevertheless, in our patient, PSA was unlikely sequela of an infectious source since multiple blood cultures were negative throughout the hospital stay.

Taking into consideration the risk of stroke due to the potential embolic source associated with cardiac PSA, anticoagulation treatment has been recommended, particularly in those with arrhythmias.[13] Our case was extensively discussed with cardiac surgery service resulting in no such recommendations and the patient was discharged without anticoagulation.

We present, to the best of our knowledge, the first case of a post-traumatic ventricular PSA subjected to SNOM. Our case highlights the importance of rapid surgical intervention in penetrating cardiac trauma and the importance of thorough follow-up to detect post-traumatic complication including ventricular PSA. To make this diagnosis, postoperative screening with echocardiogram or MRI is mandatory as clinical signs and symptoms of developing PSA are generally non-specific[10] or, as seen in this present case, absent. A follow-up repeat cardiac echocardiogram at 3 months is our protocol as early edema and thrombosis may preclude detection of a minor ASD, VSD, valvular insufficiency or PSA. In this case, due to the long hospital stay and a thorough work-up with multiple MRIs confirming the PSA, no 3-month follow-up echocardiography was performed. MRI proved to be the most useful imaging modality.

The cornerstone of the management of this complication is surgical; however, there may be very selected instances whereas SNOM is applicable such as in small and stable PSAs. The current literature, however, on cardiac PSA is focused mainly on postinfarction PSAs. Nevertheless, postinfarction and post-traumatic PSAs are different entities. In this critically ill trauma patient with a small and stable PSA a trial of NOM was successfully deployed. These patients, however, should be surveyed for any signs of progression of the PSA. It is important to emphasize that the long-term complications of residual PSA after cardiac trauma is poorly understood. Therefore, more studies with longer follow-up would be required to assess the effectiveness of the non-operative management as a treatment option in selected patients. Finally, there is no role for non-operative management in enlarging PSAs or in symptomatic patients.

CONCLUSIONS

We report the first case of a post-traumatic ventricular PSA subjected to SNOM. A cardiac PSA is a rare, potentially life-threatening complication after penetrating cardiac injury. In addition to more commonly occurring cardiac complications such as ASD or VSD, PSA should be screened for in patients after an emergency cardiac repair. SNOM may be a treatment option in carefully selected patients with small and stable PSAs. Long-term outcomes after SNOM of cardiac PSA are currently lacking.