Blunt cardiac injury without external evidence of thoracic trauma: A report of two pediatric cases

Abstract

Objective:

To report two cases of cardiac injury following blunt thoracic trauma without external evidence of injury.

Design:

Case report and review of the literature.

Setting:

A 23-bed pediatric intensive care unit in an academic children’s hospital.

Interventions:

Two children presented following significant thoracic trauma without external evidence of injury. Cardiac injury was not initially suspected, and lack of definitive diagnostic evaluation led to a delay in diagnosis and definitive treatment.

Results:

A 4-year-old girl presented 6 months after initial injury and evaluation with massive right ventricular dilatation secondary to traumatic tricuspid regurgitation. The second patient, an 11-year-old boy, underwent a laparotomy for suspected abdominal pathology delaying diagnosis of his traumatic ventricular septal defect and definitive repair until clinical hemodynamic deterioration occurred.

Conclusion:

Clinicians should maintain a high index of suspicion for cardiac injury in patients with a significant mechanism of thoracic trauma despite external evidence. Standard screening tests are often inadequate and echocardiography should be performed for any suspected cardiac trauma.

Background

Cardiac injury following blunt chest trauma, while rare,^1,2 may be life threatening if not detected expeditiously. It is commonly associated with obvious external signs of thoracic injury, with the majority of complications being described within 48 h of the event.^1,2 We report two pediatric cases illustrating cardiac injury without external signs of thoracic trauma, one of the cases with the cardiac complication presenting temporally remote to the traumatic event.

Case reports

Case 1

A 4-year-old girl was admitted to our facility for respiratory distress following 3 days of decreased activity, intermittent vomiting, cough, and decreased oral intake. Six months prior to this visit, the patient was evaluated in a local emergency department for blunt chest and abdominal trauma suffered during a crush injury from a falling television. Evaluation at that time included chest X-ray; head, abdomen, and pelvis computed tomography (CT) scan; and urinalysis, all of which were normal. Physical examination was unremarkable, with no external signs of trauma, and the patient was discharged without scheduled follow-up.

On initial evaluation in our emergency department, a harsh, III/VI widely radiating regurgitant murmur was appreciated, and chest X-ray revealed marked cardiac enlargement, suggestive of cardiomyopathy. Echocardiogram revealed a severely dilated right ventricle with normal left ventricular size and function. There appeared to be an “unguarded” tricuspid valve with free tricuspid insufficiency secondary to rupture at the valve annulus (Figure 1). The patient was stabilized in the intensive care unit and taken for semi-urgent repair on the morning following admission.

Figure 1.

Traumatic rupture of the tricuspid valve. (a) Echocardiogram revealed a severely dilated right ventricle with normal left ventricular size and function. (b) There appeared to be an “unguarded” tricuspid valve with free tricuspid insufficiency secondary to rupture at the valve annulus.

Intraoperative findings revealed severe dilatation of both the right atrium and ventricle, with a fistulous, paravalvar communication between the tricuspid annulus and the atrioventricular wall, along with a tear from the annulus into the septal and anterior leaflets. The annulus was reconstructed and reattached to the atrioventricular groove; the leaflet tear was repaired and the atrium plicated. An unremarkable recovery led to discharge on post-operative day 3. On follow-up at 6 weeks, she was asymptomatic, with normal tricuspid valve function by transthoracic echocardiogram.

Case 2

An 11-year-old boy sustained blunt trauma to the chest wall and abdomen from a crush injury while attempting to lift a heavy park bench. Initial emergency room evaluation revealed no external evidence of trauma to the chest wall. The patient was hypotensive with poor peripheral perfusion, had a soft systolic murmur, and exhibited abdominal tenderness. Cardiac silhouette and pulmonary markings were normal on chest roentgenogram. Electrocardiogram (EKG) revealed first-degree atrioventricular block and right bundle branch block. CT of the chest and abdomen demonstrated a left-sided pulmonary contusion and free peritoneal fluid. Cardiac injury was not suspected and exploratory laparotomy revealed only a small duodenal hematoma. Post-operatively, the patient’s hemodynamic status deteriorated, and emergent echocardiogram demonstrated a large conoventricular septal defect.

Upon presentation at our institution, chest roentgenogram showed diffuse pulmonary edema without cardiomegaly and a left-sided consolidation consistent with pulmonary contusion. Serum creatine kinase (CK) level was elevated at 718 U, with a 48% myocardial (MB) fraction. Transesophageal echocardiogram demonstrated a 1.2 cm × 1.6 cm ventricular septal defect (VSD) caused by avulsion of the membranous septum at its insertion to the aortic annulus (Figure 2). There was a large left to right shunt restrictive by 30 mmHg with hyperdynamic left ventricular function. There appeared to be limited support for the noncoronary aortic cusp with partial prolapse into the septal defect.

Figure 2.

Traumatic ventricular septal defect (VSD). (a) Transesophageal echocardiogram demonstrated a 1.2 cm × 1.6 cm VSD caused by avulsion of the membranous septum at its insertion to the aortic annulus. (b) There was a large left to right shunt restrictive by 30 mmHg with hyperdynamic left ventricular function. There appeared to be limited support for the noncoronary aortic cusp with partial prolapse into the septal defect.

Further clinical deterioration led to urgent surgical intervention 48 h after presentation. Intraoperative inspection revealed a 3 cm × 2 cm VSD extending inferiorly from the membranous septum. In addition, a previously unidentified transmural (covered only by epicardium) tear of the right ventricular free wall and partial avulsion of the pulmonary valve cusp were identified. The VSD was closed with bovine pericardium, and the right ventricular free wall defect was sutured primarily. The patient’s sternum was left open for 48 h after operation due to ventricular dysfunction on attempted primary closure. His hospital course was further complicated by sinus node dysfunction responsive to pacing. The patient’s conduction abnormalities improved after sternal closure, and follow-up EKG was significant only for right bundle branch block. The patient was discharged home on the 11th post-operative day, and at 6 months of follow-up, he has resumed normal activity and is asymptomatic.

Institutional review board review was not required for case reports at our institution at the time of case presentation and information retrieval.

Discussion

Most commonly, severe cardiac trauma presents acutely and is associated with evidence of significant chest wall injury. However, it is possible to suffer serious cardiac injury from a blunt trauma without obvious external manifestations. In one large pediatric series on cardiac trauma to date, Dowd and Krug ¹ reported on 184 cases of blunt cardiac injury in children, with 95% having simple cardiac contusion and two suffering traumatic VSD; 87.5% of these patients suffered serious multisystem injury, but only 60% had external evidence of thoracic trauma. Pulmonary contusion, presenting clinically or radiographically, which was seen in our second case, was the most frequent injury associated with blunt chest trauma and multiorgan injury is twice as frequent in these patients.^1,3 Other case reports of traumatic VSD had associated pulmonary contusions and has been shown to be a life threatening injury.^4,5 The presence of pulmonary contusion should alert the physician to the possibility of occult cardiac trauma.

Electrocardiographic abnormalities, common after pediatric cardiac trauma, appear to correlate well with the presence of traumatic VSD in the adult population (37/49 cases). ⁶ In one pediatric case of avulsed VSD after motor vehicle collision, echocardiography reported a mobile thrombus in the left ventricular outflow tract with evidence of septal wall abnormality. ⁷ The occurrence of these types of abnormalities after blunt chest trauma clearly warrants careful cardiac evaluation.

Elevation in serum CK MB fraction (CK-MB) is frequently present in the adult population after cardiac injury, but elevation of CK-MB appears to be a nonspecific finding in cases of pediatric chest trauma. Bromberg et al. ⁸ showed that seven of eight pediatric patients with cardiac trauma had elevated serum CK-MB, but only one had a clinically significant injury requiring intervention. Other serum assays, cardiac troponin I and cardiac troponin T, which are highly specific markers of myocardial injury, have sensitivities of only 23% and 12%, respectively, in evaluating for cardiac injury after blunt chest trauma. ⁹ Given the lack of sensitivity of frequently used screening tools, our reported cases confirm that two-dimensional echocardiography, employed as a screening tool, is the most sensitive and specific modality for diagnosis of cardiac injury after thoracic trauma.^6,10 Cardiac enzymes may be useful as an adjunct in diagnosis but cannot be relied upon to rule in or rule out significant cardiac injury.

While post-traumatic tricuspid regurgitation is quite uncommon, especially in the pediatric population,^11–14 there is a small but significant literature describing its presentation well after the inciting event, with two series reporting mean times to correction of 13 and 17 years.^15,16 Low pulmonary vascular resistance and right ventricular pressures can allow significant hemodynamic abnormalities to go unrecognized for months to years. Mild injury with resultant tricuspid insufficiency can worsen over time until overt right ventricular dysfunction occurs. The presumed mechanism of injury to the tricuspid valve is a sudden rise in right ventricular pressure due to compression of the thorax, which can lead to strain and rupture of the tensor apparatus and leaflets. ¹⁷ In all reported cases, leaflet dysfunction has been the cause of the valvular dysfunction, with most having rupture of the anterior chordae tendinae with ensuing annular dilation.^11–21 Our patient was unique in suffering separation of the leaflet along its border with the tricuspid annulus. While delayed surgical repair can result in excellent long-term results, current literature supports early diagnosis and intervention in order to avoid right ventricular dilation and failure. ²¹

The VSD here reported, located at the membranous septum, contrasts with the more posterior and apical location generally reported for the traumatic VSD. The most frequent mechanism for ventricular rupture involves a sudden, rapid, high-velocity blow to the thorax causing acute rupture of the septum, most commonly at its posterior insertion. ²² Our patient suffered a slow, crushing impact to the chest. We postulate that this crushing impact along with possible torsional forces led to a tearing of the ventricular septum from its attachments at the crux of the heart. The nearly through-and-through tear of the right ventricular free wall opposite the membranous septum supports this theory. The possibility of rupture at the level of the membranous septum or extension into the membranous septum must be considered in the preoperative evaluation of the patient with suspected ventricular rupture. Similarly, the presence of associated defects such as right ventricular free wall rupture and damage to the semilunar valves must be considered.

Optimal timing for surgical repair in the traumatic VSD remains undetermined. Some authors recommend delay in repair in order to allow for stable hemodynamics and improved tissue integrity at wound edges.^22,23 Attempted early repair in the setting of hemodynamic instability has been relatively unsuccessful in previously reported pediatric cases,^4,5 with right ventricular dysfunction contributing to poor surgical outcome in at least one patient. In the setting of progressive clinical deterioration, our patient underwent successful early repair with delayed sternal closure. It is possible that delayed sternal closure in this case may have allowed early surgical repair without subsequent hemodynamic deterioration from right ventricular dysfunction. This hypothesis is supported by recent experience with delayed sternal closure in other high-risk pediatric cardiac surgeries. ²⁴

Conclusion

A history of significant blunt thoracic trauma should lead to a high level of suspicion for cardiac injury, with hemodynamic instability, EKG abnormality, arrhythmia, or new murmur requiring prompt echocardiographic evaluation. Controversy exists regarding the utility of an echocardiogram in the evaluation of the child with thoracic trauma where the patient appears well with no external injuries but has a significant mechanism of trauma. The possibility of silent cardiac injury, as illustrated by these cases, warrants echocardiography in those patients with a history of significant thoracic trauma. While many cases with cardiac injury can be managed conservatively, detailed transthoracic (and when necessary transesophageal) echocardiograms are mandated in order to define those cases requiring intervention. Finally, significant cardiac defects may develop over time as late sequelae of thoracic trauma and should be considered by the primary care practitioner during long-term follow-up care.