ABSTRACT: Post-traumatic ventricular septal defect (VSD) is infrequent, with clinical sequelae ranging from imminent death to complete spontaneous resolution. The most appropriate management strategy is unclear. Careful observation has been advocated in the management of these patients. We demonstrate this concept by reporting two different approaches in two patients with traumatic injuries to the chest and review the English-language literature of both spontaneous and percutaneous closure of these lesions. In our case of percutaneous closure, we report a novel technique involving a transseptal approach that does not require exteriorization and formation of an arteriovenous loop, thus avoiding loop-related complications.
J INVASIVE CARDIOL 2009;21:483–487
Case Study 1. A 20-year-old male presented to the emergency room (ER) after suffering a stab wound to the left lower sternum with a systolic blood pressure of 60 mmHg and a pulse of 120 bpm. After a focused assessment with sonography for trauma (FAST) scan showed evidence of pericardial effusion, he was urgently taken to the operating room. A midline sternotomy was performed and a right ventricle (RV) laceration was noted near the interventricular septum. The laceration was sutured and the patient was taken to the cardiovascular intensive care unit. A transthoracic echocardiogram (TTE) taken on day-1 postoperatively showed a 0.6 cm by 0.8 cm muscular ventricular septal defect (VSD) (Figures 1A and B) with an echo-derived Qp:Qs of 1.3:1. This was felt to be a hemodynamically insignificant lesion. The patient recovered well from his injuries and was discharged 3 days later from the hospital. At a clinical follow-up examination 3 months later, the patient complained of increased shortness of breath with activity. A repeat TTE showed an increase in LV size and enlargement of the muscular VSD (Figures 1C and D) up to 1.5 cm with an echo-derived Qp:Qs ratio of 3:1. Given the patient’s symptoms, hemodynamic overload and the increase in size of the VSD, a decision was made to attempt to percutaneously close the VSD.
After informed consent was obtained, the patient was intubated and 6 French (Fr) and 8 Fr sheaths were inserted into the left femoral artery and the right femoral vein, respectively. A left ventriculogram was performed revealing the VSD and confirmed significant left-to-right shunting (Figure 2B). The defect was measured at 10 mm. Under transesophageal (TEE) guidance, transseptal puncture using a Mullins transseptal sheath (USCI, Billerica, Massachusetts) was successfully performed. Heparin was then administered to obtain a therapeutic activated clotting time (ACT) and was readministered as necessary throughout the procedure for a goal ACT > 250 seconds. With its balloon inflated, an Arrow Wedge catheter (Arrow International, Reading, Pennsylvania) was floated across the mitral valve, directed towards the septum, and manipulated through the VSD. A Terumo Glidewire (Terumo Medical Corp., Somerset, New Jersey) was inserted through the Arrow Wedge catheter, facilitating advancement of the Arrow balloon to the main pulmonary artery. The GlideWire was then exchanged for an extra-stiff exchange-length guidewire, which was positioned in the right pulmonary artery allowing placement of a 9 Fr AGA delivery sheath (AGA Medical Corp., Plymouth, Minnesota) across the VSD (Figure 2B). A 12 mm Amplatzer Muscular VSD Occluder (AGA Medical) was then advanced through the delivery system with a right ventricular (RV) disc of the Amplatzer VSD occluder deployed in the RV under fluoroscopic and TEE guidance. Repeat left ventriculography was performed confirming minimal residual VSD flow. The LV disc of the Amplatzer VSD Occluder was then deployed by further retraction of the delivery system (Figure 2C). The device was released and repeat imaging using TEE and ventriculography demonstrated adequate positioning of the VSD closure device with complete resolution of shunting (Figure 2D).
Case Study 2. An 18-year-old male with no previous medical history was brought to the emergency room (ER) after suffering 2 small stab wounds to the left chest. He was unresponsive, severely hypotensive and hemodynamically unstable. A FAST ultrasound in the trauma room showed cardiac tamponade. As he was being resuscitated, he had a cardiovascular arrest. A clamshell thoracotomy in the ER trauma room was performed by the cardiovascular surgeon and the tamponade relieved. A 3.5 cm laceration to the right ventricle (RV) was noted and temporized with staples. A small hole in the LV was also noted and temporized with an inflated Foley catheter. The left anterior descending (LAD) artery was lacerated just distal to the first diagonal branch. The patient regained a systolic blood pressure of 70 mmHg and was rushed to the operating room (OR) for more definite correction of his thoracic injuries.
In the OR, his right and LV lacerations were closed. As his mammary arteries were severed during the clamshell thoracotomy, a saphenous vein graft was used to bypass the injured LAD. Lung lacerations were also repaired. He was then transferred to the intensive care unit (ICU) in stable condition.’
Postoperatively, the patient did remarkably well. However, as he was being weaned from the ventilator 36 hours post op, he was noted to have a loud holosystolic murmur best heard at the left sternal border. A TTE suggested the presence of a VSD at the mid-papillary level (Figures 3A and B). A TEE was subsequently performed, which revealed a 1.3 cm communication between the LVOT and the RV, below the level of the mitral valve. The calculated Qp:Qs was 1.6. As the patient was asymptomatic, a watchful waiting approach was undertaken for his care. A year later, the patient returned for follow up. He was completely asymptomatic and a repeat TTE showed absence of the VSD (Figures 3C and D). Right and LV size and function were within normal limits.
Discussion
VSDs may be of congenital origin, may be acquired as a result of penetrating trauma, blunt trauma, post-surgical contusion, myocardial infarction or perforation at cardiac catheterization. To understand the natural history and management of a traumatic VSD, we need to first understand the natural history of congenital VSDs. Isolated VSDs are the most commonly recognized congenital heart defect, occurring at a rate of 2 per 1000 live births.1 The natural history of VSDs may be variable, including a spontaneous decrease in defect size, development of a RVOT or LVOT obstruction, pulmonary vascular obstructive disease, aortic regurgitation or bacterial endocarditis.2 Most VSDs are small, restrictive and asymptomatic during infancy. Even with large defects, initially manifesting with significant left-to-right shunts and symptoms of congestive heart failure, a subsequent spontaneous decrease in defect size may result in decreased shunting, remission of symptoms and pressure restriction that protects the pulmonary vascular bed from significant hypertension.3
Traditional indications for VSD closure have been congestive heart failure, pulmonary hypertension, aortic valve insufficiency and prior endocarditis.4 However, these indications were determined during an era when operative mortality for VSD closure was 7.5% and there was a 20% incidence of significant residual shunt.5 The Canadian Cardiovascular Society consensus guidelines recommended VSD closure in patients with the presence of a significant VSD defined as those who are symptomatic, have a Qp:Qs of > 2:1, or pulmonary artery systolic pressure > 50 mmHg.6 A key report by Lock et al,7 in which he described percutaneous closure of VSDs in 7 patients, appeared to accelerate the interest of closure of these lesions. A plethora of reports of percutaneous closure of VSDs have appeared in the literature for both children and adults,8–18 many of whom have Qp:Qs shunts below 2:1, are asymptomatic, have no evidence of chamber enlargement or pulmonary hypertension.
Our interest and improved ability to close VSDs without sternotomy, however, may have overshadowed the obligatory scrutiny into the indications of closure. Recent evidence, for example, suggests that the majority of children with moderately large VSDs and a volume-overloaded LV without pulmonary arterial hypertension, clinical evidence of congestive heart failure or failure to thrive, remain clinically stable and experience a progressive spontaneous decrease in LV size.19 Another paradigm shift has been the recent American Heart Association guidelines that no longer recommend endocarditis prophylaxis for uncomplicated VSDs.20
Our understanding of post-traumatic VSDs has considerably more challenges than congenitally acquired VSDs. It is difficult to make any conclusions about features of traumatic VSDs, as findings from case reports are subject to reporting and selection bias. However, a few comments can be made with caution. First, up to 80% of patients who suffer penetrating cardiac injuries die before reaching the hospital,21 and of those who arrive to the hospital and require ER thoracotomy, the reported rate of survival ranges from 8–19%.22,23 In blunt trauma to the chest, the best reported estimation of prevalence of VSDs in those whose injury is not immediately fatal is 5.5%.24 The mechanisms of development of a VSD after trauma include acute laceration of the septum, deceleration injury causing myocardial infarction from an intimal coronary artery tear (resulting in spasm, thrombosis or dissection), or compression of the heart between the sternum and the spine, causing cardiac contusion.25 The contused myocardium can become necrotic and subsequently perforate. The second point, therefore, is that VSDs, particularly those incurred from blunt trauma, may occur and/or be detected hours to months after the original insult (Tables 1 and 2).
Third, where most congenital VSDs occur adjacent to the membranous septum, typically under the septal leaflet of the tricuspid valve, traumatic VSDs occur in the muscular portion of the interventricular septum. Fourth, where up to 90% of congenitally acquired VSDs spontaneously close by the age of 10 years, the natural history of traumatic VSDs is unknown. As Table 1 illustrates, several cases with large shunts (Qp:Qs ratio > 3) have been shown to spontaneously close, as documented by LV angiography and blood oxygen saturations up to 11 years later. The anatomic closure of congenital defects in the inflow portion of the ventricular septum is usually due to the ingrowth of fibrous tissue and formation of a fibrous membrane.26 Gross and histologic examination of tissue surrounding traumatic defects in the muscular interventricular septum in both human and animal studies suggests that a similar mechanism of closure may be involved in these cases.27,28 However, it is difficult to define what the predictors of closure are in such patients.
Concerning the timing of potential closure, as our first case as well as those in Table 1 illustrate, a watchful waiting approach until patients’ symptoms develop is likely the most appropriate therapeutic strategy. Pulmonary hypertension and/or enlargement of left cavities are also indicators of significant shunting and represent appropriate indications for closure. A Qp:Qs > 2 is probably insufficient in itself to justify closure of these defects, not only because there are multiple pitfalls in the echocardiographic shunt evaluation, but also because some of these patients will improve with a conservative approach.
All the reported cases in the English-language literature of percutaneous closures of traumatic VSDs are summarized in Table 2. The indications for closure have ranged from a Qp:Qs > 2:1, symptoms or hemodynamic instability. The classic method of VSD closure was used in each case including a retrograde approach in the aorta and advancement of the wire in the pulmonary artery from the LV. An arteriovenous loop is then formed by exteriorization of the wire tip either through the femoral or the jugular vein.29 A possible untoward complication of forming loops by exteriorizing the wire is the “cheese-grating effect” — a term used to describe the sheering injury to all the cardiac structures that are in direct contact with the wire in the loop including the aorta, the ventricles and the valves (mainly aortic and tricuspid). We describe a novel technique that does not require formation of a loop, thus avoiding this complication. By placing an extra-stiff Amplatzer wire as far as possible in the right or the left pulmonary artery, there is adequate backup for deliverance of the Amplatzer Muscular VSD Occluder. Although this method requires added expertise in performing a transseptal puncture, it is a skill set that structural interventionalists should be familiar with. In addition, as VSD closures are almost always supported by intra-cardiac or TEE imaging, performing the transseptal puncture is safe and feasible. Although a transseptal approach to close a VSD has been described previously in the case of a patient with a mechanical aortic valve, an arteriovenous loop and deliverance of the device from the venous side was ultimately used to complete the procedure.30
In our case, we found that once the delivery sheath was placed across the VSD (Figure 2B), the natural curve across the atrial and then across the ventricular septum was favorable to directly deliver the occluder. Although significant kinking of the sheath has been described when attempting to deliver the device from the venous side,31 this complication is largely prevented nowadays by the use of hydrophilic braided sheaths. Releasing the device from the artery has been described in selected cases,31 but they have all been performed through a retrograde arterial approach. We do not advocate the transseptal approach for membranous VSDs, given the proximity of the defect to the aortic valve. We believe the traditional method of exteriorization of the wire by forming an arteriovenous loop is more appropriate for this lesion.
An alternative approach to a transseptal approach is crossing the defect from the RV and then deploying the device without the need to exteriorize. We do not favor this approach, first because crossing the VSD from RV to the LV is more difficult, as it is against the direction of flow. Second, due to angulation, crossing the lesion from the femoral vein access is very difficult, thus the lesion has to be crossed from the jugular vein,29 a more cumbersome approach for the operator that is associated with increased radiation exposure. Crossing the lesion from the LV is often easier because of the natural flow of blood and is ideal for lesions in the mid or apical segments of the septum.
Reported complications of percutaneous VSD closures include device embolization, hemolysis, entanglement of the device in the mitral valve, aortic valve insufficiency, injury to the tricuspid valve, cardiac tamponade and heart block. Many of these complications can be avoided with a meticulous delivery technique. Appropriate imaging by an experienced echocardiographer is also essential during the procedure to guide disc deployment, device release and post-procedure interrogation.
Conclusion
Unlike congenital VSDs, we have much to learn about the natural history of traumatic VSDs which are rare and may close spontaneously. For this reason, we favor a watchful waiting approach to look for evidence of symptoms compared to looking purely at shunt ratios in hemodynamically stable patients. For patients requiring percutaneous closure, we have presented a simplified and innovative transseptal approach made possible by the improvement of the technique and equipment.
_________________________
From the Division of Cardiology, St. Michael’s Hospital, Toronto, Canada, *Montreal Heart Institute, Montreal, Canada, and §John Hunter Hospital, Newcastle, Australia.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted September 24, 2008, provisional acceptance given October 29, 2008, final version accepted November 18, 2008.
Address for correspondence: Robert J. Chisholm, MD, Division of Cardiology, St. Michael’s Hospital, 30 Bond Street, Toronto, Ontario M5B 1W8, Canada. E-mail: ChisholmR@smh.toronto.on.ca
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