A large ventricular septal defect complicating resuscitation after blunt trauma.

A young adult pedestrian was admitted to hospital after being hit by a car. On arrival to the Accident and Emergency Department, the patient was tachycardic, hypotensive, hypoxic, and acidotic with a Glasgow Coma Scale of 3. Despite initial interventions, the patient remained persistently hypotensive. An echocardiogram demonstrated a traumatic ventricular septal defect (VSD) with right ventricular strain and increased pulmonary artery pressure. Following a period of stabilization, open cardiothoracic surgery was performed and revealed an aneurysmal septum with a single large defect. This was repaired with a bovine patch, resulting in normalization of right ventricular function. This case provides a vivid depiction of a large VSD in a patient following blunt chest trauma with hemodynamic compromise. In all thoracic trauma patients, and particularly those poorly responsive to resuscitation, VSDs should be considered. Relevant investigations and management strategies are discussed.

INTRODUCTION

A traumatic ventricular septal defect (VSD) is an uncommon complication of blunt chest injury, but when present can pose additional challenges to resuscitation. We describe the presentation and management of a large VSD in an individual with multiple injuries, diagnosed after initial attempts to stabilize the patient were unsuccessful. We include a discussion of the relevant literature, with reference to appropriate investigations and management strategies.

CASE REPORT

A 22-year-old pedestrian, with no previous medical history, was admitted to hospital after being hit by a car. On arrival to the Emergency Department, the patient was tachycardic, hypotensive, hypoxic, and acidotic with a GCS of 3. Initial investigations revealed pelvic and spinal fractures and lung contusions. An emergency laparotomy was performed, and revealed a retroperitoneal hematoma and blood within the pelvis. The pelvis was packed, but the patient went on to angiography where the left internal iliac artery was embolized. Despite these interventions, the patient remained persistently hypotensive (Systolic Blood Pressure 70-80 mmHg) and resistant to fluid resuscitation. Central venous pressures were consistently elevated to between 18 and 25 mmHg and a full Inferior Vena Cava (IVC) was confirmed using Computerized Tomography (CT). A transthoracic echocardiogram (TTE) was undertaken with a GE Vivid S6 using an M4S-RS cardiac probe [Figure 1], which demonstrated a traumatic Ventricular Septal Defect (VSD), with right ventricular strain, increased pulmonary artery pressure, and evidence of a left to right shunt [Figure 2]. The left ventricle was dilated with a reduced ejection fraction.

Figure 1

Preoperative transthoracic echocardiogram using an M4S-RS cardiac probe, demonstrating a large ventricular septal defect (red arrow)

Figure 2

Transthoracic echocardiogram demonstrating the presence of a left-to-right shunt across the defect

The patient was stabilized and monitored in the Intensive Care Unit, remaining ventilated, but undergoing no further supportive intervention. As the patient remained hemodynamically stable following initial operative and radiological procedures, intra-aortic balloon pump (IABP) therapy was not required. Open cardiothoracic surgery was performed on day nine following injury and revealed an aneurysmal septum with a single large defect. This was repaired with a bovine patch under cardiopulmonary bypass, which resulted in normalization of the right ventricular function.

DISCUSSION

Ventricular Septal Defects are uncommon complications of blunt thoracic trauma. Mechanisms for their development are thought to include compression of the heart, between the sternum and thoracic spine, and deceleration injury.[1] In the latter scenario, traumatic myocardial infarction may result from coronary artery thrombosis, spasm or dissection. The contused or infarcted myocardium may become necrotic and perforate, giving rise to a VSD if the septum is involved. As a result, the muscular portion of the interventricular septum is most commonly affected.[2] Traumatic VSDs are frequently associated with valvular injury secondary to papillary muscle rupture, and acute congestive heart failure may also result from diffuse myocardial damage.

Presentation of traumatic VSDs is variable, ranging from acute cardiac failure to detection of asymptomatic defects on routine echocardiography, several months after discharge.[3] Diagnosis in the acute phase requires a high degree of clinical suspicion, as investigation may be difficult in an unstable patient with multiple injuries. Clinical features of traumatic VSDs include tachycardia, hypotension, tachypnea, increased oxygen requirement, and signs of congestive cardiac failure. A pansystolic murmur may also be present on cardiac examination.

Evidence of cardiac injury should be sought in patients who do not respond to initial resuscitative measures and remain hemodynamically compromised, despite definitive management of other injuries, which may account for the shocked state. Electrocardiography may demonstrate ST-segment changes indicative of cardiac contusion, and conduction abnormalities may result from septal injury.[4] Bedside TTE is the most practical tool available for early diagnosis, and should be considered in all cases of blunt thoracic trauma where cardiac injury is suspected.[5] However, hemodynamically significant VSDs may be present despite a lack of anatomical evidence on TTE, and in such scenarios a CT Angiogram and cardiac MRI should be considered.

Resuscitation and preoperative stabilization of patients prior to definitive intervention is along the standard lines, although certain specific measures may also be employed. Although not required in this case, IABP therapy has been described in the context of traumatic VSDs.[6] By increasing cardiac output and coronary blood flow, IABP can assist with the acute stabilization of patients with VSDs, which may in turn facilitate a delay in surgical intervention. This helps improve the strength of a VSD repair by permitting the tissue around the defect to strengthen, and hence become more suitable for suturing. Percutaneous balloon occlusion of VSDs can also be used during stabilization of the patient before surgical intervention, although this was not performed in this case.

The most appropriate definitive management strategy in post-traumatic VSDs remains unclear, as the majority of the literature is confined to case reports subject to reporting and selection bias. Generally accepted indications for closure include the presence of heart failure, cardiogenic shock or significant left-to-right shunt as a result of the defect.[1] Careful observation has, however, been advocated as a viable management strategy in asymptomatic VSDs with low (<1.5:1) pulmonary:systemic pressure ratios, on the basis that these defects are often well-tolerated and may close spontaneously.[7] These patients should be followed up closely to detect the development of any symptoms, with regular echocardiography performed, to ensure that defect size and pulmonary : systemic pressure ratios remain favorable. In patients requiring intervention, percutaneous closure appears to be a safe and effective treatment strategy, with multiple reports of successful approaches to transcatheter closure are described in the literature.[2] Open surgical repair remains a viable option, particularly in cases where close proximity of the defect to aortic or atrioventricular valves precludes transcatheter closure.[8]

CONCLUSION

VSD are rare, but clinically important complications of thoracic trauma, which can pose significant challenges to resuscitation. A high index of suspicion is required in trauma patients with thorax injury who respond poorly to initial attempts at resuscitation. Echocardiography provides a diagnosis in the majority of cases. Stabilization of the patient prior to definitive repair is preferable, and may require invasive measures such as intra-aortic balloon pump counterpulsation. Open surgical repair and percutaneous closure are most commonly used for definitive management.