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J Thorac Cardiovasc Surg 1997;114:129-131
© 1997 Mosby, Inc.
BRIEF COMMUNICATIONS |
Geneva, Switzerland
Received for publication August 23, 1996 accepted for publication Sept 30, 1996. Address for reprints: Afksendiyos Kalangos, MD, PhD, University Cantonal Hospital of Geneva, Clinic for Cardiovascular Surgery, 24, rue micheli-du-Crest, 1211 Geneva, 14, Switzerland.
In civilian practice, blunt injuries to the aortic arch and its vessels are uncommon.
1 Their diagnosis and surgical management occasionally present challenging problems. This report describes the clinical picture, angiographic findings, and surgical management of an aortic arch tear that resembled an injury to the left common carotid artery (LCCA).
A 50-year-old man sustained blunt chest trauma when he was crushed against an obstacle despite efforts to stop when skiing off-piste. He was described as hemiplegic on the right side, semicomatose, and diaphoretic by the alpine emergency physician, who intubated and transferred him rapidly to the emergency room of our institution. On his arrival, he was unconscious and had right hemiplegia. Physical examination revealed a blood pressure of 150/80 mm Hg, symmetric pulses, normal findings on cardiac auscultation, and no significant external injury. The chest x-ray film disclosed no rib fractures, pneumothorax, pleural effusions, pulmonary contusion, or substantial mediastinal widening. Cerebral computed tomographic (CT) scan excluded signs of closed head injury. Chest CT scan disclosed a subadventitial hematoma along the aortic arch and excluded aortic dissection (Fig. 1, A). Therefore the patient underwent aortography to avoid neglect of a possible injury to the LCCA. Arch aortography demonstrated an anterior mediastinal extravasation of contrast material from the aortic arch, which was superposed between the origins of the innominate artery and LCCA. The LCCA was stenosed at its origin, and there was another apparent image of mediastinal contrast extravasation (Fig. 1, B).
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2 The ascending aorta was crossclamped and myocardial protection was obtained by cold blood potassium cardioplegia. Cardiopulmonary bypass was then discontinued when rectal temperature reached 25° C. The distal half of the ascending aorta was opened longitudinally, and through it the origins of the aortic arch vessels were inspected. A circumferential intimal and medial disruption of the aortic arch, running 1 cm from the origins of the innominate artery and LCCA, was hence revealed (Fig. 2). The hematoma was contained within the adventitia and periadventitial tissues of the aortic arch, thereby preventing hemorrhage. Stenosis of the LCCA, visualized by arteriography, was due to the compressive effect of a posterior subadventitial hematoma extended up to 3 cm distal to the takeoff of the LCCA from the aortic arch. No intimal disruption was detected in the innominate artery and the LCCA. The aortotomy was extended up to the left subclavian artery (LSCA) and the aortic arch was resected because of the tear between the LCCA and LSCA, leaving the latter artery attached to the distal aortic arch. A 28 mm preclotted woven Dacron prosthesis was then interposed between the distal aortic arch stump and the proximal ascending aorta. After deairing, the ascending aorta was unclamped and core rewarming started. A bifurcation graft size 20/10 mm was inserted from the aortic arch prosthesis to the innominate artery and the LCCA. The body of the bypass graft was cut close to its bifurcation, and a proximal anastomosis was performed with partial clamping of the aortic arch prosthesis. The carotid cannulas were removed after any air bubbles had been carefully evacuated from the bypass prosthesis. Microscopically, multiple sections of the aortic arch wall specimen showed no preexisting medial degenerative changes.
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Aortic arch injuries represent 8% of blunt injuries to the aorta. 3 Although the mechanisms responsible for blunt aortic arch and great vessels injuries are not well defined, we speculate that in our case the maximal shearing and torsion stresses produced by vertical deceleration, distraction, and hyperextension of the shoulder joints during stopping efforts, as well as the association of the force of impact imposed by the sudden increase of arterial blood pressure on the aorta, might have resulted in a circumferential tear of the aortic arch near the origins of the first two great vessels. Exsanguinating hemorrhage from blunt aortic trauma is the most frequent cause of clinical presentation and death. In contrast, signs and symptoms of arterial occlusion are more frequent than massive hemorrhage in blunt trauma to the aortic arch vessels. 1
Of particular interest is our patient, who had signs of injury to the LCCA rather than to the aortic arch. Controversy continues to exist regarding the best method of establishing a diagnosis of aortic arch vessel injury when bleeding, expanding hematoma, absent pulses, and shock are not obvious. Arteriography is not entirely reliable, the false negative rate being approximately 10%. 4 In our case, the only sign leading to suspicion of an aortic arch tear was the small mediastinal extravasation of the contrast material, the outline of the aortic arch and great vessels being preserved in the other areas.
Patients with aortic or great vessel tears must be treated on an urgent basis because their condition can deteriorate at any time. The literature seems to be about equally divided between those who believe strongly that the repair of cerebral vessels in the presence of a neurologic deficit is associated with a higher risk of mortality and those who do not. Our case, however, confirmed that an obvious neurologic deficit was not worsened by carotid reconstruction and neurologic recovery may even be possible. 5 We believe that cannulation of carotid arteries provides a margin of safety in patients who have acute neurologic deficit attributable to cerebral ischemia after trauma. In conclusion, severe neurologic injury after blunt trauma may be due to the aortic arch tears near the origins of the innominate artery and the LCCA. Aortography should be used more liberally in patients in whom the neurologic deficit could overshadow the vascular trauma and then delay diagnosis. With the slightest suspicion, mediastinal exploration is recommended because it will allow recognition and surgical management of occult injuries. Carotid revascularization should be attempted because the neurologic impairment may be progressively reversible.
Acknowledgments
We gratefully acknowledge the technical assistance of Michel Beux.
References
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