Ann Thorac Surg 2002;73:294-296
© 2002 The Society of Thoracic Surgeons
Case report
Delayed surgical management of a traumatic aortic arch injury
Yvonne M. Carter, MDa,
Riyad Karmy-Jones, MDb,
Gabriel S. Aldea, MD*a
a Cardiothoracic Surgery, University of Washington School of Medicine, Seattle, Washington, USA
b Trauma Cardiothoracic Surgery, Harborview Medical Center, Seattle, Washington, USA
Accepted for publication April 13, 2001.
* Address reprint requests to Dr Aldea, Division of Cardiothoracic Surgery, University of Washington, 1959 NE Pacific AA115, Box 356310, Seattle, WA 98195, USA
e-mail: aldea{at}u.washington.edu
 |
Abstract
|
|---|
We report successful management of a blunt traumatic injury to the aortic arch with intentionally delayed surgical repair. The aorta was repaired after the stabilization of other, potentially fatal, traumatic injuries.
|
Introduction
|
|---|
Blunt traumatic injury of the thoracic aorta is estimated to occur in 4% of trauma patients [1], and only 3% of these involve the ascending aorta and arch [2]. The role for nonoperative therapy in the management of ascending and arch injuries has yet to be defined.
A 54-year-old male unrestrained driver was involved in a high-speed motor vehicle accident. The initial Glasgow Coma Score was 15. He was transported to a trauma center, where he acutely decompensated experiencing a decline in mental status and hypotension, mandating intubation. The brief history obtained before emergent intubation included a myocardial infarction with an angioplasty 4 years prior. The chest radiograph revealed old rib fractures, a wide mediastinum, and a left-sided apical cap, hemothorax, and pulmonary contusion (Fig 1A).
Other injuries included a right frontal subdural hematoma (SDH) with bilateral frontal cerebral contusions and hygromas (Fig 1B), and a left acetabular fracture with posterior displacement of the femoral head. The mediastinum was further evaluated with an aortogram, and demonstrated a disruption of the aortic arch with a pseudoaneurysm between the innominate and left common carotid arteries (Fig 2).
The disruption appeared to be noncircumferential and localized, without active extravasation or vessel cutoff.
View larger version (79K):
[in this window]
[in a new window]
|
Fig 1. A portable chest radiograph (A) demonstrates indeterminate mediastinum, with a hemothorax, contusion, and apical cap on the left. The small subdural hemorrhage within the right hygroma is documented by the head CT scan (B), with a maximal thickness of 7 mm. Also seen, are right and left frontal cerebral contusions and subdural hygromas.
|
|
View larger version (119K):
[in this window]
[in a new window]
|
Fig 2. The arch angiogram reveals a large pseudoaneurysm originating from the ascending thoracic aorta, between the innominate and left common carotid arteries. Both great vessels have proximal calcific stenoses. There is no evidence of active extravasation.
|
|
The presence of multiple traumatic injuries, specifically the pulmonary contusion and SDH, prompted the decision to delay surgical repair of the aorta. Following the neurosurgical consultant’s recommendation to avoid anticoagulation, nonoperative therapy with serial chest and head computed tomography (CT) scans was continued for 4 weeks. The patient was managed in the intensive care unit with antihypertensive agents (ß-blockers). Intracranial pressure (ICP; 10 to 15 mm Hg) monitoring was employed to ensure a cerebral perfusion pressure (CPP) greater than 50 mm Hg, while achieving a MAP less than or equal to 80 mm Hg. In addition to an improved mental status, the serial radiologic evaluations of the head and chest injuries demonstrated improvement and stabilization, respectively.
The aorta was repaired utilizing deep hypothermic circulatory arrest via median sternotomy. The pseudoaneurym was excised, and the anterior aortic wall was repaired with a Sulzer vaskutec gel-weave (30 mm) patch aortoplasty, with running sutures reinforced with a double rim of Teflon felt. Immediate postrepair pressures in the ascending aorta and innominate artery were normal, without a gradient. The patient’s postoperative course was uncomplicated. He was extubated on postoperative day 1, transferred out of the intensive care unit the following day, and eventually discharged to a skilled nursing facility for rehabilitative care on postoperative day 5. A 3-month follow-up chest CT scan demonstrated an intact repair.
|
Comment
|
|---|
Traumatic aortic disruptions are treated with immediate surgical intervention [1–3]. The majority of these injuries occur in the isthmus portion of the descending thoracic aorta, caused by torque or shearing forces around the ligamentum arteriosum. Blunt traumatic injuries involving the aortic root are less common and more lethal. This is perhaps due to the more severe mechanism of injury, resulting in a higher incidence of associated traumatic cardiac injuries [4, 5]. In these cases, the ascending aorta is subjected to torsion and a "waterhammer stress" with an associated shearing force on the heart [6]. The true incidence of these more proximal injuries is uncertain. Most reports appear as isolated cases in the literature.
There has been a recent trend to intentionally delay surgery in select patients with descending thoracic aorta injuries [7, 8]. Many of these patients sustain a concomitant severe closed-head injury and/or a significant lung injury. In those instances, delayed surgical intervention may be beneficial, if delaying therapy is safe. The feasibility of delaying a reparative approach depends on the location, appearance, and hemodynamic consequences of the aortic injury. Certain criteria must be met to consider such a delay. The aortic injury must be localized and contained, without evidence of circumferential involvement or compromised adjacent critical vessels. Nonoperative management is predicated on the concept that maintaining a mean arterial pressure of less than or equal to 80 mm Hg is possible, while maintaining cerebral perfusion, as it appears that free rupture is uncommon if this target can be reached. In the combined experience of over 500 patients reported in the literature treated in this manner, there have been no reported deaths due to aortic rupture when the blood pressure was safely maintained at or below normal [7–9]. ß-blockers are the preferred antihypertensive agents to use to lessen the forces that favor rupture. These drugs avoid the nitrate-induced reflex tachycardia and the increased myocardial work and oxygen consumption that occurs with the use of 
antagonist agents. Reassessment of the aortic injury to assess the lesion for progression can be achieved with serial CT scan. A possible concern of aggressive antihypertensive therapy, however, is the potential of cerebral hypoperfusion in the setting of elevated intracranial pressures. Thus, cerebral perfusion pressure monitoring is essential, and therapy must be appropriately tailored.
Prior reports of injuries at these sites support urgent surgical repair [10]. However, it may be possible to judiciously apply these principles of conservative therapy to these more proximal thoracic aortic disruptions, in selective patients with complex injuries in whom acute surgical intervention may result in significant morbidity and mortality (ie, acute cerebral hemorrhage, severe lung injury). The patient presented here suffered both cerebral and pulmonary injuries, which had the potential to impact on surgical morbidity and mortality. The aortic injury was both localized and contained, thus allowing surgical intervention to be delayed in this stable patient with an isthmus disruption [6]. Normal intracranial pressures were maintained, and the arterial pressure could be safely lowered without jeopardizing cerebral perfusion. Head and chest injuries were followed with serial CT scans, documenting improvement during the surveillance period. In this case, serial head CT scans revealed almost complete resolution of the SDH 4 weeks after the injury. Any deterioration would have been considered an indication for urgent surgical intervention. In summary, this report demonstrates that initial planned, nonoperative treatment, with careful aggressive monitoring and serial evaluations, has a role in the management of select blunt traumatic injuries involving the more proximal aorta, associated with other complex injuries.
|
References
|
|---|
-
Parmley L.F., Mattingly T.W., Manion W.C., Jahnke E.J. Nonpenetrating traumatic injury of the aorta. Circulation 1958;28:1086-1101.
-
Pretre R., Chilcott M. Blunt trauma to the heart and great vessels. N Engl J Med 1997;336:626-632.[Free Full Text]
-
Mattox K.L. Red River anthology. J Trauma 1997;42:353-368.[Medline]
-
Eddy A.C., Rusch V., Marchioro T., et al. Treatment of traumatic rupture of the thoracic aorta. Arch Surg 1990;125:1351-1356.[Abstract]
-
Markovchick V., Duffens K.R. Thoracic trauma. In: Rosen P., Barkin R.M., eds. Emergency Medicine. Concepts, and Clinical Practice. Toronto: Mosby, 1992:429-458.
-
Pezzalla A.T., Silva W.E., Lancey R.A. Cardiothoracic trauma. Curr Prob Surg 1998;35:763-771.
-
Maggisano R., Nathens A., Alexandrova N.A., et al. Traumatic rupture of the thoracic aorta: should one always operate?. Ann Vasc Surg 1995;9:44-52.[Medline]
-
Kipfer B., Leupi F., Schuepback P., et al. Acute traumatic rupture of the thoracic aorta: immediate or delayed surgical repair?. Eur J Cardiothorac Surg 1994;8:30-33.[Abstract]
-
Mattox K.L., Wall M.J. Historical review of blunt injury to the thoracic aorta. Chest Surg Clin North Am 2000;10:167-182.[Medline]
-
Cheng R., Mc Lellan B.A., Joyner C., et al. Aortic root trauma: serious injuries requiring early recognition and management. J Trauma 1999;48:525-529.
This article has been cited by other articles:
|
|
|
|
 
J. EV, G. Mundayat, K. Chunduru, J. Abraham, A. Palliyil, and D. Perimpa
Delayed surgery for traumatic rupture of aortic arch with dissection of the left anterior descending artery.
J. Thorac. Cardiovasc. Surg.,
February 1, 2008;
135(2):
428 - 430.
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Karmy-Jones, R. DuBose, and S. King
Traumatic rupture of the innominate artery
Eur. J. Cardiothorac. Surg.,
May 1, 2003;
23(5):
782 - 787.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
