Traumatic Laceration of the Aorta

R a p i d deceleration, which occurs in high-velocity automobile accidents, forces passengers against the steering wheel or dashboard and produces a crushing injury to the bony thorax. Rapid deceleration also sometimes tears the thoracic aorta. This tearing usually occurs where the movable aortic arch becomes fixed to the posterior chest wall, namely, at the level of the left subclavian artery; however, such tears have been noticed elsewhere in the thoracic aorta, principally in the ascending aorta at the level of the innominate artery and in the transverse arch itself. The actual incidence of such injuries is unknown, but it is clear that they are related to the actual incidence of automobile accidents producing rapid deceleration and, therefore, are probably increasing in frequency. Aortic tears, even when circumferential, may produce hemorrhage which will be contained by the intact adventitia of the aorta in the form of a periaortic hematoma. It is now established that the natural history of these hematomas is eventual rupture into the pleural cavity, but, indeed, they may be contained for a long time and actually have been reported as existing in a contained fashion years after the occurrence of injuries. It is essential that all patients who sustain injuries due to rapid deceleration be evaluated immediately for the possibility of aortic laceration. The hematoma is usually apparent on a plain x-ray film of the chest, where it produces a widening of the mediastinal shadow. Compression of the descending thoracic aorta can ordinarily be recognized because it produces a hypertension in the brachiocephalic circulation and a diminution in pulse pressure in the lower extremities. The recognition of any of these signs indicates that emergency aortographic studies should be performed to identify the site of laceration. Aortographic demonstration of a laceration should be followed by an immediate emergency operation to repair the laceration. Only active bleeding at another site takes precedence. A variety of techniques have now been developed which permit the descending thoracic aorta to be isolated from the remainder of the aortic circulation, and thereby resected or repaired. These include the establishment of a left atrial-femoral bypass; the establishment of a femoral-femoral bypass employing a pump oxygenator; the use of temporary shunts which are relatively nonthrombogenic and permit bypass of the aorta without the use of systemic administration of heparin; and, finally, rapid repair of the aorta with cross-clamping above and below the site of injury without the aid of any bypassing technique. The use of coated shunts, which can easily be inserted into the ascending aorta and the femoral artery prior to disturbing the hematoma, is a preferred technique, since it eliminates the systemic administration of heparin in the face of multiple injuries. It has recently been demonstrated that such shunts can be inserted between the apex of the left ventricle and the femoral artery; however, if there is active bleeding into the pleural space at the time of thoracotomy, or indeed, if the shunt cannot be placed without disturbing the hematoma, rapid cross-clamping of the aorta above and below, followed by evacuation of the hematoma and repair of the aorta by simple suture or by the interposition of a prosthetic graft segment can be performed. A report by Fry and associates1 in the July issue of Chest documented a case of traumatic laceration of the aorta which produced acute left ventricular failure, and which was managed by aortic resection and graft replacement using a left atrial-femoral bypass. The appearance of acute left ventricular failure as a principal sign of a periaortic hematoma in the descending thoracic aorta is distinctly unusual. The degree of aortic narrowing at this site which is necessary to produce acute left ventricular failure is severe (probably in excess of 60 percent). Usually such hematomas are recognizable from conventional signs (such as mediastinal widening or a difference in the pressures above and below the site of aortic compression) before a significant degree of luminal narrowing occurs, which can produce left ventricular decompensation. In addition, acute left ventricular failure may be a consequence of cardiac contusion itself and not related to luminal narrowing at