S Tatebe, Y Chiba
S Tatebe, Y Chiba. Aortic Insufficiency By Blunt Chest Trauma.. The Internet Journal of Thoracic and Cardiovascular Surgery. 2009 Volume 15 Number 1.
A 76-year-old male presented with exertional dyspnea 5 months after motor vehicle accident. Preoperative echocardiography showed aortic insufficiency(AI) due to partial detachment of the non coronary cusp. He was successfully treated by valve replacement surgery. Postoperative examination of the excised aortic valve had no changes related to endocardiatis, but suggestive of traumatic AI. The issues attached to traumatic AI including lapse of time from blunt cheat trauma to onset of AI were discussed.
Cardiac injury by non penetrating blunt chest trauma occurs as pericardial rupture, myocardial contusion, rupture of the cardiac wall, and injuries to the coronary arteries, and myocardial contusion is most common. Valvular injury is an uncommon sequelae, but most of the reports were mainly a traumatic rupture of the aortic valve. We present a case of traumatic aortic insufficiency presented 5 months after blunt chest trauma, that was successfully treated by valve replacement surgery.
A 76-year-old male was brought to emergency room at our institution soon after motor vehicle collision. His medical history included acute appendicitis, colon polyp, and glaucoma, but no cardiovascular diseases. He smokes one pack a day of cigarettes. On arrival no heart murmur or signs of heart failure were found on physical examination. Radiological exam including computerized axial tomography(CAT) scan revealed normal chest but dissection of the descending aorta, and pelvic fracture. Since then one month of conservative treatment was undertaken, and no heart murmur or congestive heart failure developed. Two months after initial trauma he was found as having subdural hematoma of the head, and underwent drainage surgery. Five months after motor vehicle accident he came back due to exertional dyspnea. Echocardiography(Fig 1) showed hypokinetic ventricle and moderate aortic insufficiency from the attachment of the non coronary cusp(NCC). These findings as well as the data from the cardiac catheterization confirmed AI, possibly post-traumatic. After one month of medical treatment for congestive heart failure he underwent surgery. The heart was explored via median sternotomy, and no abnormalities were found but thin aorta. Cardiopulmonary bypass was instituted, then heart was arrested by cardioplegia. The aortic valve was explored by incision of the ascending aorta, and found nearly half of the NCC detached. Macroscopically there were no findings suggestive of endocarditis. Defect of NCC was repaired by autologous pericardium, but regurgitation persisted. No additional procedures, such as annuloplasty/commisuroplasty were undertaken due to the concern for uncontrollable bleeding which may take place on thin and fragile aortic wall. Therefore, entire aortic valve was excised, and replaced by a prosthetic valve. Postoperative course was uneventful besides repiratory complication due to pulmonary emphysema. Pathological and microbiological examination of the excised aortic valve showed free from infection, therefore diagnosed as traumatic AI.
This case report describes a case of AI developed 5 months after motor vehicle injury, and underwent valve replacement surgery. Even the patient was successfully treated, management in this case involved a number of issues, including the difficulty in preoperative diagnosis of traumatic AI.
Traumatic aortic valve rupture is thought to occur by the trauma particularly in early diastolic phase, when a tremendous pressure gradient can be generated across the aortic valve. Some patients rapidly deteriorated, and required emergent surgery, but in others there were laps of time from injury to onset of AI. Usually diagnosis is obtained base on the four criteria, 1) history of blunt chest trauma; 2) normal heart on a recent physical examination; 3) sudden onset of AI soon after the accident; 4) exclusion of other causes of AI. Our case had no history of cardiac disease, however, this case must be traumatic aortic valve rupture. Macroscopically the valve was different from the ordinary AI, and unusually torn at the annulus without changes suggestive of endocarditis, that was confirmed by microscopic examination. Some hypotheses have been presented in regard to this delay, that initially tiny tear of the cusp developed at the annulus, and then progressively extended as the result of ordinary hemodynamic stress. When the cusp becomes detached from the annulus, AI progress with a compensatory increase in the force of ejection and consequent increased hemodynamic stress to the cusp.
Surgery includes valve repair or valve replacement, that is based on the extent of injury of the cusp. In most of the cases the tear is limited in single cusp, but in severe cases, double cusp or commissure were involved. Recently better surgical results have been shown on valve replacement surgery. But the number of valve repair has been increasing and excellent outcome is increasingly reported. In this case, initially perforation was repaired with autologous pericardium, but regurgitation remained. We thought this was due to dilatation of the annulus of diseased cusp, and annuloplasty/commisuroplasty may resolve this issue. However, the aortic wall was found thin, and was thought it did not tolerate additional procedure.