Spontaneous improvement of a haemodynamically significant ventricular septal defect produced by blunt chest trauma in a child

Abstract

We describe the progress of a girl aged 5 years, who suffered blunt trauma to the chest producing a ventricular septal defect of 1 centimetre in diameter. The shunt generated a mild dilation of the left-sided chambers, and exertional dyspnoea. Three months later, therapeutic catheterisation revealed important diminution in the extent of shunting. We decided, therefore, not to close the defect, and she has since remained asymptomatic.

Delayed Ventricular Septal Rupture Following Blunt Chest Trauma

“…The first postulated mechanism of VSR is acute compression of the heart with a resultant sudden rise in intracardiac pressure during the end of diastole or isovolumetric systole3) and the second postulated mechanism is that myocardial injury causes a microvascular disruption leading to infarction and liquefaction of the septum 4). The contused myocardium can become necrotic and subsequently perforate.…”

Traumatic Ventricular Septal Defect

“…If this compression occurs during the late diastolic phase, when the atrioventricular valves are closed and the ventricles filled with blood, the increased intracardiac pressure can result in acute rupture of the septum. 2,4-6,8 However, if the trauma occurs at another phase of the cycle, it may only cause a myocardial contusion. In this setting, formation of the VSD occurs later, after associated injury to the microvasculature has led to infarction, necrosis, and perforation of the interventricular septum.…”

“…2-4,6 Mechanical ventilation may become necessary, as well as positive inotropic agents such as dopamine for worsening hypotension. Physical exam usually reveals a precordial thrill and high grade, pansystolic murmur at the left sternal border 2,4-7 , but ECG findings are more variable. Either ST segment depression or elevation may be seen, with or without Q wave changes.…”

“…2 After stabilization, patients may be evaluated using cardiac MRI, which can detect the VSD itself as well as common associated injuries to the heart such as myocardial infarction, disruption of the aortic, mitral, and tricuspid valves or their corresponding papillary muscles, and myocardial contusion. 2-4,7,10 Cardiac catheterization, echocardiography, and cardiac MRI have all been used to calculate the pulmonary to systemic flow ratio (Qp:Qs) of VSDs, 2,4,5 which can play an important role in determining treatment.…”

“…Patients that experience increasing hemodynamic instability, shunts with a Qp:Qs ratio greater than 1.5-2:1, or defects larger than 1.5-2 cm usually require immediate repair of the defect. 4-6 This is often done through an open surgical approach, with cardiopulmonary bypass, venticulotomy, and patching of the VSD. There have also been successful reports of percutaneous repair with closure devices, an alternative option for patients whose critical condition precludes them from undergoing open surgery.…”