Infrarenal abdominal aortic aneurysm repair: detection and treatment of associated carotid and coronary lesions.

Management of carotid or coronary lesions associated with abdominal aortic aneurysm (AAA) remains controversial. To determine the influence of these lesions on the outcome of elective infrarenal AAA repair, we review our experience between January 1978 and December 1992. A total of 345 consecutive patients underwent infrarenal AAA repair. Procedures were performed under emergency conditions in 62 patients (18%) and electively in 283 patients (82%). Carotid and coronary risk was assessed in all 283 patients undergoing elective operations. There were 259 men (91.5%) with a mean age of 68 years (range: 45-88 years) and 24 women (8.5%) with a mean age of 76 years (range: 59-92 years). Previous cardiac manifestations included myocardial infarction in 57 patients (20%), angina in 50 patients (17.6%), coronary bypass grafting in 14 patients (14.9%), and coronary transluminal angioplasty in two patients. Cerebral ischemic attacks had been observed in 11 patients (3.8%) including transient events in two cases. Carotid endarterectomy had been performed in two patients. Assessment of carotid artery risk using Doppler ultrasonography led to selective carotid angiography in six patients and carotid endarterectomy in two patients. Assessment of coronary risk using a cardiac stress test was performed in 204 patients. Results were normal or subnormal in 132 patients (46.6%), abnormal in 21 patients (7.4%), and uninterpretable in 51 patients (18%). Coronary arteriography was performed in 151 patients (53.3%) for secondary assessment after the cardiac stress testing in 72 patients (25%) and for primary assessment in 79 patients (27.9%). Significant coronary lesions were demonstrated in 52 patients (18% of the overall population; 34% of coronary arteriography procedures). In 12 cases the lesions were not considered as threatening. In four cases the lesions were deemed inoperable. In the remaining 36 cases the lesions were treated either by aortocoronary bypass grafting (34 cases) or percutaneous transluminal angioplasty (two cases). In 11 of the 36 treated cases the patient was asymptomatic and had no history of coronary disease. In all cases AAA was treated by resection graft. Eight patients (2.8 +/- 1%) died during hospitalization including two deaths related to preexisting cardiac insufficiency. No death was attributed to preoperative work-up or treatment of associated lesions. With a mean follow-up of 62 months (range: 1-14 years), late mortality involved 96 patients (33.9 +/- 3%) including 16 deaths due to cardiac causes (16.7 +/- 4%) and 10 due to stroke (10.4 +/- 3%). Actuarial survival including deaths during hospitalization was 70.5 +/- 3% at 5 years and 41.4 +/- 5% at 10 years. Comparison of these results with those previously reported supports our policy of performing carotid or coronary angiography in patients selected by noninvasive tests.

Post traumatic tracheobronchial lesions. A follow-up study of 47 cases.

This report concerns 47 ruptures of the tracheo-bronchial tree from the tracheal origin to the division of the lobar bronchi (trachea in 30 patients, main bronchus in 11, intermediate or lobar bronchus in 6). The disruption was circumferential in 24 cases and non-circumferential in 23. Injuries resulted from crush or blunt trauma in 35 cases, from seat belt or rope strangulation in 8 cases and in 4 cases, lesions were discovered following the tracheal intubation. The main symptoms were cervico-mediastinal emphysema (39), pneumothorax (31), acute dyspnea (28) and hemoptysis (11). The diagnosis was always confirmed endoscopically. In 8 patients, management of the lesions was delayed for more than 1 week due to misdiagnosis or severe associated injuries. Thirty-eight patients underwent tracheal or bronchial surgical repair associated in 13 cases with a temporary stenting, 4 patients underwent partial or total lung resection, 2 were managed by laser therapy and the 5 others received only medical care and endoscopic survey. Four patients died (8.5%), 2 from bleeding in the bronchial tree from a pulmonary artery tear, 1 from hypertensive pneumothorax under respiratory support and the last from mediastinitis due to delayed diagnosis of an associated oesophageal wound. All 43 other survived in spite of some very critical situations. This experience confirms that technical problems of surgical repair are nowadays overcome and that prognosis of tracheobronchial ruptures mainly depends on the initial control of respiratory failure and complications. Avoiding lethal anoxia or endobronchial damage in the emergency period before referring the patient to the surgeon is essential.