Ventricular septal defect following blunt chest trauma

Abstract

We present a 32-year-old male with ventricular septal defect (VSD) following blunt chest trauma. Traumatic VSD is a rare but potentially life-threatening injury, the severity, course and presentation of which are variable. While the diagnosis of myocardial injury may be challenging, cardiac troponins are useful as a screening and diagnostic test. The proposed pathophysiological mechanisms in the development of traumatic VSD are early mechanical rupture and delayed inflammatory rupture. We conducted a literature review to investigate the pathogenesis, distribution of patterns of presentation, and the associated prognoses in patients with VSD following blunt chest trauma. We found that traumatic VSDs diagnosed within 48 hours were more likely to be severe, require emergency surgery and were associated with a higher mortality. Children with traumatic VSDs had an increased mortality risk. Smaller lesions may be managed conservatively but should be followed up to detect late complications. In both groups elective repair was associated with a good outcome.

INTRODUCTION

Blunt chest trauma may produce a variety of cardiac sequelae,[1,2] however, VSD is a particularly uncommon result.[3,4] Its severity, presentation and course are variable,[3,5–8] presenting signs are often masked by concomitant injuries,[6] and the presentation of the murmur is often delayed.[2,6,7,9]

We describe a young male who presented with a VSD following blunt chest trauma. This is followed by a literature review of the pathogenesis, patterns of injury and presentation, and associated prognoses in traumatic ventricular septal rupture.

CASE REPORT

A 32-year-old male polytrauma patient presented to the casualty of a peripheral hospital in rural KwaZulu Natal, South Africa following a motor vehicle accident. He required intubation and ventilation, and the following morning was airlifted to the Level 1 Trauma Unit at Inkosi Albert Luthuli Hospital (IALCH), in Durban, KwaZulu Natal, South Africa.

On arrival at IALCH, he had a blood pressure 110/53 mmHg, heart rate 95 beats per minute, and Glasgow Coma Scale (GCS) score E-2, M-5, V-tubed. His initial arterial blood gas on 40% oxygen showed: pO2 12.9 kPa, pCO2 6.3 kPa, pH 7.34, 98% saturation, base deficit 2.5, and lactate 2.4 mmol/L.

Clinical examination revealed significant blunt chest trauma and extensive soft tissue injuries, which included a degloving parietal scalp laceration, and deep abrasions over the right shoulder and knee. Imaging confirmed bilateral hemo/pneumothoraces (for which intercostal drains had been inserted at the peripheral hospital), fractures of the 3^rd-5^th ribs anteriorly and 6^th-10^th ribs posteriorly, with associated bilateral lung contusions. No cardiac murmur was noted on initial presentation. There were no associated brain, cervical spine, or pelvic injuries. On admission, his troponin I was 0.190 ng/ml and B-type natriuretic peptide (BNP) was 59.67 pg/ml (Siemens Advia Centaur Xp). All other blood results were normal.

The patient's soft tissue injuries were debrided on admission and again 2 days later. He was weaned off the ventilator and successfully extubated 4 days after admission. On day 2, the troponin I declined to 0.074 ng/ml. On day 7, the admitting doctor noted a new 2/6 pansystolic murmur in the left parasternal 2^nd-3^rd intercostal space. This raised the suspicion that he may have developed a ventricular septal defect (VSD) secondary to blunt chest trauma. Echocardiographic examination confirmed this diagnosis by identifying left to right flow across the peri-membranous region of the ventricular septum. In addition, a small pericardial effusion around the right ventricle and atrium was noted.

Although the possibility of a pre-existing congenital defect cannot be excluded there is strong evidence supporting the diagnosis of a post-traumatic VSD. First, the pericardial effusion and elevated BNP and troponin I clearly indicate that the patient sustained major cardiac injury. Second, the late presentation of the murmur is consistent with previously described post-traumatic VSDs, and finally, the patient gave no history of prior cardiac abnormalities.

Since this VSD was both small and asymptomatic, and the patient had remained hemodynamically stable since admission, the decision was made to manage the lesion conservatively and to schedule the patient for follow-up by the department of cardiothoracics.

DISCUSSION

We conducted a literature review by searching Pubmed from January 1965 to May 1, 2011 using the following search terms: ventricular septal defect and trauma. We identified 165 studies, 35 of which detailed congenital lesions, 29 described penetrating chest trauma and 13 reported iatrogenic injury following cardiac surgery. We excluded 23 studies as dealing with unrelated topics. In the remaining 65 papers, we identified 68 patients included in 62 case reports,[2–63] 2 retrospective reviews,[64,65] and 1 prospective evaluation.[66]

The pathogenesis of VSD following blunt chest trauma is unclear but is thought to be caused by either early mechanical rupture or delayed inflammatory rupture. Mechanical septal rupture has been proposed to occur as the heart is compressed during late diastole, after atrial contraction, when the ventricles are filled and the valves closed. This may occur as a result of direct cardiac impact or when the heart is compressed between the sternum and the spine.[3,5,7,8,11,15,20] It has also been suggested that a healed congenital VSD with a weakened ventricular septum may re-open with significant blunt trauma to the chest.[6] Delayed inflammatory rupture is thought to occur when cardiac injury causes localised edema with disruption of microvascular flow, leading to infarction, septal liquefaction, and perforation.[2,3,7]

The diagnosis of a VSD following blunt chest trauma may be challenging. Investigation should include elements of the history and clinical examination, as well as information gained from plain chest radiograph, cardiac enzymes, echocardiography, and nuclear imaging studies.[67]

The measurement of cardiac enzymes is fast, simple, and minimally invasive. Creatine phosphokinase myocardial band (CPK-MB) is commonly elevated in polytrauma patients due to non-myocardial sources, rendering its usefulness in the diagnosis of myocardial damage questionable.[67] Since cardiac troponins are only released following disruption of the myocardial cell membrane, they are specific indicators and therefore ideal markers of myocardial damage. Elevation in cardiac troponin I (cTnI) has been shown to be both a sensitive and specific indicator of myocardial cell necrosis,[68,69] and following blunt chest trauma, levels >1 ng/ml correlate well with trans-esophageal echocardiographic evidence of regional wall motion abnormalities.[70] Myocardial lesions not detectable on echocardiography are suggested by cTnI levels between 0.4-1 ng/ml.[70] It is therefore suggested that cTnI be routinely measured in patients sustaining blunt injury to the chest in an attempt to actively seek evidence for myocardial damage.

Patterns of Injury and Prognosis

To determine the distribution of the presentation of patients subsequently diagnosed with traumatic VSD, we separated patients into two groups according to the time of presentation of the VSD: early – within 48 hours of injury, and late – after 48 hours of injury. In 35 of the cases, the timing of diagnosis was indeterminate. In the remaining 33 cases, 17 were diagnosed early and 16 late.

Cases diagnosed early had larger and more severe VSDs, which often required emergency or elective surgical repair and were associated with a high mortality [Table 1].

Table 1.

Management of VSDs diagnosed <48 hours (n=17)

Late presentations rarely required emergency surgery although often underwent elective repair. Three late complications were reported in the group of six patients who did not have their defects corrected. These cases (one presenting with endocarditis and the other two with cardiac failure) required late defect closure [Table 2].

Table 2.

Management of VSDs diagnosed >48 hours (n=16)

Of the 16 cases diagnosed after 48 hours, only one patient required emergency repair. Ten patients, including a 4-year-old child, underwent elective repair with no documented complications, while one patient refused surgery and was lost to follow-up.

Small asymptomatic traumatic VSDs may be managed conservatively[5,37] as they often close spontaneously.[3] Surgical repair is indicated if the defect is large, if the pulmonary to systemic blood flow ratio exceeds 2:1, or if there is evidence of cardiac failure.[3,8,37] However, a persisting small lesion with chronic left to right shunting may with time result in right ventricular failure.[3]

Our identification of a bimodal pattern of presentation may reflect the two different pathophysiologies suggested in the literature. These data suggest that VSDs diagnosed within 48 hours are more likely to: be life-threatening, require emergency surgery, and be associated with a higher mortality than those diagnosed later. It is also evident that children with traumatic VSDs have an increased mortality risk.

CONCLUSION

Ventricular septal defect following blunt chest trauma is a rare but potentially life-threatening complication. Cardiac troponin I has been shown to be a valuable screening and diagnostic tool in the assessment of blunt cardiac injury. Elevated troponin levels, new onset hemodynamic instability, or the development of a new murmur must prompt further echocardiographic investigation.

While it is acceptable to manage smaller lesions conservatively, these patients should be followed up to detect the occurrence of late complications. Large or symptomatic lesions should be surgically repaired. In both the early and late groups, elective repair of the lesion is associated with a good outcome.