We performed endovascular stent grafting of a perforated descending aorta, caused by empyema after surgery for lung cancer, in a 75-year-old man. After diagnosing hemorrhage from a perforation of the proximal descending aorta, caused by left empyema, the perforation was repaired with a saphenous vein patch and a pectoralis major muscle flap. However, re-hemorrhage from the same lesion occurred 2 months postoperatively. Temporary hemostasis was achieved with gauze packing and he was transferred to our hospital for endovascular stent grafting. The infection did not resolve after fenestration, so the descending aorta was cropped out to the fenestration lesion. Therefore, endovascular stent grafting was performed on the same day. Postoperatively the bleeding stopped completely without any signs of graft infection, and he was transferred to another hospital on postoperative day 9. No re-hemorrhage or graft infection of the aortic perforative lesion occurred in the early postoperative period. However, the patient died of massive bleeding from the aorta wall of the proximal stump of the stent graft, caused by recurrence of the infection 2 months after the 2nd operation. In this situation, endovascular scent grafting provides the only chance of saving the patient's life. If endovascular stent grafting is performed as a lifesaving procedure, meticulous operative technique is imperative.

It is known that the prognosis of preductal type coarctation of the aorta is poor because cardiac malformation is frequent in these cases. There have been very few reports on adult cases of the coarctation. We have recently carried out aneurysmectomy and reconstructed the descending aorta by a 30mm Veri-Soft tube graft for one adult case of descending aortic aneurysm associated with coarctation of the aorta. The patient was 49-year-old female. Segmental stenosis 5cm in length was demonstrated in the thoracic descending aorta immediately below the bifurcation of the left subclavian artery. The poststenotic dilatation was shown at the distal portion of the segmental stenosis. The postoperative clinical course was uneventful.

During the period between January 1975 and April 1991, 37 patients with acute arterial occulusion of the extremities were admitted to our department and were classified into 2 groups according to their causative factors, including thrombosis and embolism. Among 16 thrombosis patients with involvement of 17 limbs, 4 patients died and 6 limbs were amputated at the time of discharge. On the contrary, among 21 embolism patients with involvement of 25 limbs, 2 patients died and only one limb was amputated. Sixteen of 17 limbs with thrombosis were operated on. Arterial reconstruction was carried out initially on 5 limbs, resulting in successful limb salvage; 3 of 6 limbs which had undergone thrombectomy initially were occluded again soon after the procedure. In the end, 1 limb had to be amputated. On the other hand, 22 of 25 limbs were operated on. Three arterial reconstructions, 18 embolectomies and 1 amputation were carried out initially. All arterial reconstructions and embolectomies were successful. From these results, it was concluded that arterial reconstruction must be done initially for thrombosis patients. For the embolism patients, embolectomy is preferable.

Changes of hemodynamics and chemical mediators before and after aortic clamping were investigated in 12 patients who underwent infrarenal abdominal aortic aneurysmectomy. Patients were divided into two groups; one with an aortic clamping time greater than 1 hour (the long group) and the other with aortic clamping time less than 1 hour (the short group). Cardiac output, mean pulmonary arterial pressure (MPAP), extravascular thermal volume (ETV), polymorphonuclear elastase (PMN-E), α₁ trypsin inhibitor (α₁-TI) superoxide dismutase (SOD), urine N-acetyl-β-D-glucosaminidase (NAG), were measured before and immediately after aortic clamping, immediately after, 1 and 4 hours after aortic declamping. In addition, serum GOT, GPT, creatinine and BUN were measured before and 1, 3 and 7 day after operation. These levels were expressed as ratios of the level before aortic clamping and operation. The MPAP ratio immediately after aortic clamping was 0.83±0.06 in the long group and 0.99±0.08 in the short group. There was statistical significant difference in the MPAP between both groups (p<0.01). In contrast, there was no significant difference in the cardiac output or ETV between the two groups. The PMN-E ratio immediately after aortic declamping was 2.24±0.81 in the long group and 1.19±0.45 in the short group. These ratios increased at 1 and 4 hours after aortic declamping. The PMN-E ratio following aortic clamping in the long group was greater than those in the short group (p<0.05). The SOD at 1 hour after aortic declamping was 0.78±0.13 in the long group and 1.01±0.11 in the short group (p<0.05). The NAG ratio immediately and at 1 hour after aortic declamping was significantly higher in the long group when compared with the short group (p<0.01, 0.1). Serum GOT, GPT, creatinine and BUN ratios showed no change through out this study. There was an increase in protease and a decrease of free radical scavengers in the long group. These findings are commonly known to be linked with organ damage. Through the findings of this study, we suggest that clamping time should be minimized; thus reducing the possible chance of postoperative organ damage.