Commentary

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Endovascular management of these life threatening injuries has become the accepted choice of treatment at many trauma centers, but as the authors outline, there remain several unanswered questions.

First of all, which patients require any treatment? As imaging modalities have improved, most surgeons have seen minor injuries to the thoracic aorta, including small intimal tears or flaps that probably do not warrant any treatment. However, the temptation to treat such lesions with an endograft might exist for some resulting in a lower “repair threshold” for endovascular therapy than open surgery. Most published series comparing open and endovascular repair have given little information regarding the anatomic degree and severity of these injuries. This reinforces the need for a degree of injury classification system, as I suspect that most endovascular series include some patients who would not have undergone repair during the era when open surgery was the only alternative.

Trauma patients are generally younger than most patients with other thoracic aortic pathologies, and Drs Rheaume and Chen correctly remind us of the void in long-term data regarding endovascular repair. However, as Dr Casey points out, this void also exists for open repair. As with most new therapies, we have subjected endovascular repair to a more intense surveillance than the open alternative was ever subjected to, in the relative infancy of endograft technology. Regardless, anecdotal reports of reintervention following either method of repair serve to remind us of the importance of postoperative surveillance. Obviously, uncertainty remains around the duration, frequency, and method of radiologic surveillance.

The normal course of the thoracic aorta is to dilate over our lifetime,¹ and this is mentioned as an area of concern by Drs Rheaume and Chen. Potentially this dilatation could impact the durability of both an open and an endovascular repair. What remains unknown, however, is whether the placement of an endograft changes this dilatory tendency and, in fact, some animal research suggests that the inflammatory response to an endograft inhibits this dilatation.² Again, we await longer term results.

This represents an area of vascular surgery where a randomized controlled trial is unlikely and impractical so, given the current evidence, what is the preferred method of repair for those injuries of sufficient severity to require treatment? As the physiologically less stressful alternative, endovascular therapy can be offered earlier, and with a lower risk of the catastrophic complication of paraplegia and should be the first choice of therapy in those patients that require repair, the majority of which will be anatomically suitable. There remains a smaller subset of patients who will be anatomically inappropriate for endovascular repair (inadequate access, injury location, and arch anatomy) that will require open repair by a skilled surgeon.

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References 

1. Hartley MC, Langan EM, Cull DL, Taylor SM, Carsten CG, Blackhurst DW. Evaluation of the diameter of the proximal descending thoracic aorta with age: implications for thoracic aortic stent grafting. Ann Vasc Surg. 2009;23:639–644
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2. Siegenthaler MP, Celik R, Haberstroh J, Bajona P, Goebel H, Brehm K, et al. Thoracic endovascular stent grafting inhibits aortic growth: an experimental study. Eur J Cardiothorac Surg. 2008;34:17–24comment 24-5
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