Early Stabilization of Traumatic Aortic Transection and Mitral Valve Regurgitation

Abstract

We report a case of life-threatening aortic transection with concomitant mitral papillary muscle rupture and severe lung contusion caused by a failed parachute jump.

This blunt thoracic injury was treated by early stabilization with extracorporeal membrane oxygenation followed by successful delayed graft repair of the descending aorta and mitral valve replacement with a mechanical prosthesis. (Tex Heart Inst J 2003;30:65–7)

In August 1998, a 32-year-old man experienced a serious deceleration trauma during a parachute jump when the parachute only partially opened. The patient was transferred immediately to a local hospital where artificial ventilation was started. Chest radiography showed a widened mediastinum with obscuring of the aortic knob. Other findings were lung contusion, especially in the upper part of the left lung, and fractures of the left clavicle, left maxilla, and left rib cage. Computed tomography of the chest revealed aortic transection at the level of the isthmus, surrounded by a large hematoma; pericardial and bilateral pleural effusion; and left lung contusion (Fig. 1). Computed tomography of the head revealed a discrete hemorrhage in the right capsula interna. Neurologic evaluation was difficult in this fully sedated patient.

Fig. 1 Computed tomographic scan of the chest shows transection of the isthmus of the aorta with periaortic hematoma and left lung contusion.

Within a few hours of admission to the hospital, the patient was transferred to our department in hemodynamically stable condition. Aspiration from the endotracheal tube revealed continuous active bleeding up to 800 mL/h. In view of the patient's respiratory distress, lung bleeding, and cerebral injuries, we decided to delay the aortic repair. However, arterial blood gas values, with a fraction of inspired oxygen (FIO₂) of 1.0 and with maximal positive end-expiratory pressure (PEEP) support, showed an oxygen tension of 43.7 mmHg, a carbon dioxide tension of 66.4 mmHg, and a pH of 7.15. These findings suggested severe respiratory failure.

Emergency bronchoscopy showed severe diffuse lung bleeding, especially from the lower right and upper left bronchi. Despite repeated broncho-aspirations and instillation of epinephrine, the diffuse lung bleeding, although reduced, could not be stopped.

A transesophageal echocardiogram showed normal left ventricular size and function, a small amount of pericardial fluid (3 mm), and grade 1–2/4 mitral valve insufficiency. The respiratory condition continued to deteriorate, and it was impossible to regain adequate ventilation and oxygenation. We decided to place a percutaneous extracorporeal membrane oxygenation (ECMO) system. Vascular access was achieved percutaneously in the right femoral vein and left femoral artery. A heparin-coated system with a centrifugal pump (Biomedicus BP 80, Medtronic Biomedicus Inc.; Eden Prairie, Minn) and a membrane oxygenator with integrated heat-exchanger (Maxima plus PRF, Medtronic Cardiopulmonary; Anaheim, Calif) were used. No heparin was given.

Adequate flows of 4 to 5 L/min were immediately obtained with the ECMO system. The oxygen saturation increased from 61% to 94%. During the next 2 days, the patient maintained good oxygen saturation levels, averaging 97%, with an FIO₂ of 0.8 and moderate PEEP. Bilateral chest drains were placed for relief of hemothorax. After 3 days, an attempt to decrease the ECMO flow resulted in massive pulmonary edema, and the oxygen saturation levels dropped to less than 80%.

A repeat transesophageal echocardiogram, in contrast with the 1st one, showed severe mitral valve insufficiency (grade 3/4), with prolapse of the anterior leaflet caused by a traumatic rupture of the anterior papillary muscle. We then decided that surgical correction was necessary.

A left posterolateral thoracotomy through the 4th intercostal space was chosen. The ECMO system was left in place. The ascending aorta and right atrium were cannulated to establish cardiopulmonary bypass (CPB), and deep hypothermia was induced. When the patient's nasopharyngeal temperature was 22 °C, the heart fibrillated and circulatory arrest was begun. The thoracic aorta was clamped distal to the hematoma at the level of the 6th thoracic vertebra. Opening of the hematoma revealed complete transection of the aorta, contained only by adventitia. The tear was situated 1 cm below the left subclavian artery. The aorta was clamped distal to the left carotid artery, and CPB was restarted to perfuse the proximal part of the body. Distal perfusion was maintained by the ECMO system. The traumatic aortic rupture was repaired by interposition of a Gelsoft 18-mm-diameter graft (Vascutek; Renfrewshire, Scotland). After restoration of the native aortic circulation, the rectal temperature was raised to 28 °C. The ascending aorta was cross-clamped and 1 L of cold crystalloid cardioplegic solution was given. The mitral valve was exposed through an incision in the left atrium, starting at the left atrial auricle, anterior to the left pulmonary veins. Inspection of the mitral valve revealed a severe prolapse of the anterior leaflet caused by rupture of the anterior papillary muscle. A 31-mm St. Jude mechanical valve (St. Jude Medical, Inc.; St. Paul, Minn) was used for mitral valve replacement.

The patient was weaned from the ECMO system without any problems after 24 hours. The cardiovascular recovery was uneventful. There was progressive improvement of the neurologic deficits, with nearly complete recovery of the left hemiparesis. The patient's pulmonary recovery was delayed due to pneumonia of the right lung (Pseudomonas aeruginosa). After 3 weeks, however, he was successfully weaned from the ventilator. One week later, he was referred to a rehabilitation center. At the 1- and 3-year follow-up visits, the patient had recovered completely without neurologic sequelae.

Discussion

This report highlights the benefits of early stabilization with ECMO and delayed repair of both traumatic rupture of the thoracic aorta and mitral valve regurgitation.

The high mortality rate of traumatic rupture of the thoracic aorta, caused by blunt injuries, has been proved by autopsy studies, which have shown that death occurs in 80% to 90% of victims at the accident scene and in 30% of survivors within 24 hours. ¹ Severe blunt chest trauma, such as that caused by a failed parachute jump, can produce complete transection of all layers of the aorta, with immediate death by exsanguination, or may involve partial disruption, with injury of the intima and media. This so-called contained rupture is restricted only by a thin but strong and intact adventitia.

Acute rupture of the thoracic aorta is typically associated with other serious injuries (to the abdomen, bones, and head), which often require urgent surgery. Cardiac contusions are reported in two thirds of cases, but concomitant valve lesions are seldom reported. ²

There is considerable controversy concerning the timing of surgical repair in such cases. Acute traumatic rupture of the thoracic aorta is often considered to be an emergency requiring immediate repair. However, the risk of early rupture in patients reaching the hospital alive is overestimated, and more recent reports advocate conservative treatment in the early phase after initial stabilization. ^3,4 Priority must be given to cardiorespiratory resuscitation with strict management of hypotension. Transesophageal echocardiography is of great value, not only for identifying traumatic aortic transection, but also for providing additional information about cardiac contusion, post-traumatic myocardial infarction, and valve lesions at the bedside. This important information can be used to guide both the medical treatment and the surgical strategy. ⁵

In this patient, aortic repair was delayed because of acute respiratory failure and severe lung bleeding, which made single-lung ventilation nearly impossible and full systemic heparinization dangerous. Furthermore, lung bleeding and the unrecognized pulmonary edema caused inadequate oxygenation, and emergency use of ECMO offered the only alternative. Repeat transesophageal echocardiography, performed 3 days after the initial injury, showed severe mitral valve insufficiency with prolapse of the anterior leaflet, caused by a traumatic rupture of the anterior papillary muscle. There was a strong likelihood that severe pulmonary edema would result from the increasing mitral valve regurgitation; therefore, surgical correction was deemed necessary.

The use of extrapulmonary oxygenation in neonates for refractory hypoxemia is frequently reported in the literature with good results, whereas the efficacy in adults is more controversial. ⁶ In this patient, the FIO₂, PEEP, and inspiratory pressure were decreased without problems after the institution of ECMO. Percutaneous institution of ECMO was preferred over surgical cut-down, because it is relatively simple and can be performed easily in the intensive care unit. Finally, in this patient, ECMO enabled perfusion of the distal aorta to prevent spinal cord and renal ischemia during aortic cross-clamping.

The favorable outcome of this case is most likely attributable to the relatively young age of this patient, the early institution of ECMO, and aggressive surgical intervention after hemodynamic and respiratory stabilization.