Carotid exploration for acute postoperative thrombosis.

To determine the incidence of carotid reoperation and to document operative findings and clinical results, the records of patients requiring early reoperation (after less than 24 hours) during a 10-year period were analyzed with respect to operative findings, clinical outcome, and arterial patency. Endarterectomy was performed in 920 patients, with 27 strokes (3%) and 10 deaths (1%). Early re-exploration was required for 27 patients (3%) for either expanding hematoma (6 patients) or suspected thrombosis associated with a new neurologic deficit (21 patients). Two patients bled from the arteriotomy and 4 bled from surrounding tissues. Exploration for new postoperative neurologic events confirmed thrombosis in 19 cases (91%). Two patients with patent arteries and normal operative arteriograms were felt to have distal embolization, and the arteriotomy was not opened. Causes of thrombosis were intimal flap in 6 patients and closure stenosis in 11; the cause was unknown in 2 cases. All arteries were repaired over a shunt with a patch. Follow-up studies were available for 16 arteries, all of which remained patent. Of patients explored for hemorrhage, there was one death (from myocardial infarction), no neurologic events, and no late infections. Of 21 patients who underwent a second operation for neurologic deficits, 2 died, 8 were unchanged, 2 had minor residual deficit, and 9 had completely resolved deficits. Severe contralateral disease was more common among patients with residual deficits (10 of 12) compared with patients without residual deficits (0 of 9; chi-square = 8.23, P < 0.005). Carotid re-exploration is most commonly undertaken for a new neurologic deficit, usually associated with thrombosis at the operative site. Thrombosis is more often due to arterial narrowing than to an intimal defect. Prompt repair will restore patency and result in improvement in 50% of cases. Neurologic recovery is related to the status of the contralateral artery.

Failure of thrombolytic therapy to improve long-term vascular patency.

PURPOSE: Few data are available on long-term follow-up of arterial segments subjected to thrombolysis. We reviewed all cases of vascular occlusion treated with urokinase to identify early success and determine the influence of postlysis intervention and the nature of the thrombosed segment (i.e., artery vs graft) on long-term patency. METHODS: Data on 134 cases (58 arteries, 76 grafts) treated with high-dose urokinase infusion in the lower limbs over a 7-year period were analyzed. Limbs were divided into five groups on the basis of therapy after lytic infusion to determine long-term efficacy: group I, success with no additional therapy; group II, percutaneous angioplasty alone; group III, limited surgical procedure (operative angioplasty, jump graft); group IV, extensive procedure (new bypass); and group V, revascularization after lytic failure. Long-term results were assessed by life-table analysis and groups compared by log-rank test (Mantel-Haenszel). RESULTS: Initial patency was established in 87 (64.9%) of 134 cases with 5 deaths (3.7%), 11 amputations (8.2%), and 16 complications (11.9%). Follow-up was available in 68.6% of cases for a mean of 10.9 months. No difference was seen between grafts and native arteries. Patency was analyzed at 6, 12, 18, and 24 months. The 24-month patency rate after lysis alone (group I-25.9%) was inferior (p < 0.05) to results after lysis and any subsequent intervention (groups II, III, and IV). The type of intervention did not influence subsequent patency. Twenty-four-month patency of procedures performed after failed thrombolysis (group V, 41.4%) was not different from those after successful lysis (groups I to IV). Twenty-four-month patency in groups II and III (minor interventions, 62.9%) was not significantly different from that of groups IV and V (major interventions, 53.2%) (p > 0.25). CONCLUSIONS: Operative intervention is required to produce long-term arterial patency, even after successful thrombolysis. No statistically significant benefit of thrombolysis on vascular patency was seen in our series.

Late complications of revascularization for radiation-induced arterial disease.

During a 14-year period 23 patients underwent 25 revascularizations for radiation-induced arterial obstructive disease. An average of 5000 rads was delivered, 3 to 24 (mean 9) years before arterial insufficiency, for malignancies of the following origin: gynecologic (n = 9), lymphoma (n = 7), head and neck (n = 5), testicular (n = 1), and lower extremity sarcoma (n = 1). Arterial occlusive disease occurred in the aortic arch vessels (n = 8), visceral aortic vessels (n = 1), and aortofemoral vessels (n = 16). Presenting symptoms were claudication (n = 8), rest pain or nonhealing ulcers (n = 7), transient ischemic attacks (n = 6), asymptomatic bruit (n = 1), and renal insufficiency (n = 1). Reconstructive operations included anatomic bypass (n = 10), extra-anatomic bypass (n = 4), patch angioplasty (n = 5), endarterectomy (n = 3), and resection with interposition graft (n = 1). In this group of patients there were no major perioperative wound complications or other major radiation-associated morbidity. Five patients had late graft infections that manifested from 2 to 5 years after surgery. All occurred in anatomic regions where the bypass graft passed through previously irradiated tissues. Presenting symptoms of infection included a draining groin sinus (n = 3) or soft tissue abscess (n = 2). In all cases the graft had not incorporated into the surrounding tissues when passing through the irradiated area. Treatment included graft excision and extra-anatomic bypass through nonirradiated tissue. One patient died of systemic sepsis. Vascular reconstructive surgery can safely be performed for radiation-induced arterial disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Donor iliac angioplasty and crossover femorofemoral bypass.

We reviewed our experience with 99 patients who had 111 femorofemoral bypass grafts placed over a 10-year period. Mean follow-up was 36 +/- 28 months (range: 1 to 120 months). Bypass alone was performed in 89 cases (group 1). Preoperative donor iliac angioplasty was utilized in 22 cases (group 2). Overall graft failure was 21 of 89 in group 1 and 2 of 22 in group 2 (difference was not significant by chi 2: p greater than 0.05). Clinical success as calculated by life-table analysis was 95%, 83%, 75%, and 67% at 1, 3, 5, and 7 years, respectively, for group 1. Clinical success was 100% and 91% at 1 and 3 years, respectively, and 91% at 42 months for group 2. The success rates were not different for the two groups when analyzed by the log-rank test at 42 months (p greater than 0.30). We conclude that donor iliac angioplasty and femorofemoral bypass is an excellent option for patients with severe occlusive disease of one iliac artery and contralateral disease amenable to angioplasty.

Superficial femoral artery as inflow for bypass to the proximal popliteal artery.

We have obtained long term follow-up on 58 patients in whom the superficial femoral artery was used as a donor site for bypass to the proximal popliteal artery. The indication for the reconstructive procedure was intermittent claudication 36%, rest pain 34%, and gangrene 26%. All patients had angiographic evidence of a patent proximal superficial femoral artery and many had relative indications for short bypass such as limited saphenous vein availability or compromised medical condition. There was a cumulative patency rate of 79% by life table method for the series with a six year follow-up. We have observed that the superficial femoral artery is a satisfactory inflow site for proximal popliteal bypass grafts in selected patients. The procedure can maximize use of a limited segment of vein with minimal operative time and morbidity. Inflow stenosis can be revised or long bypass procedures can be offered in the event of graft failure.

Aneurysmal dilatation in saphenous vein bypass grafts.

Three patients are reported who developed aneurysmal degeneration of a saphenous vein arterial bypass graft. All three had hypercholesterolemia and two had marked elevation of triglycerides. One bypass was for occlusive disease and two for popliteal aneurysm. There was a long lag, 3 to 7 years between graft implantation and aneurysmal degeneration. The pathology was similar for all three cases with lipid laden macrophages, loss of elastic lamina, and other atherosclerotic changes in the vein wall. While atheromatous changes and aneurysm formation in saphenous vein bypass grafts are rare, this may occur especially in patients with hypercholesterolemia and hypertriglyceridemia. Careful and prolonged follow-up plus vigorous management of the hyperlipidemic state is mandatory in these patients.

Mineral metabolism of the healing arterial wall.

The mineral metabolism of healing arterial walls was studied by measuring the accumulation of several radioisotopes at the site of vascular repair in rats. Each rat was subjected to a 1-cm full-thickness aortotomy and then immediately injected by tail vein with c 5 muCi of one of the following radioisotopes: chromic chloride Cr 51 or sodium chromate Cr 51; ferrous chloride Fe 59 or ferric chloride Fe 59; manganous chloride Mn 54; selenious acid Se 75; strontium chloride Sr 85; or zinc chloride Zn 65. At intervals of 1, 2, 4, 6, and 10 days after operation and injection, groups of four rats for each radioisotope were killed, aortas dissected, and the specific radioactivity of healing vascular tissue compared with that of adjacent normal artery. There were sharp and statistically significant differences in the preferential accumulation of the radioisotopes in healing compared with normal aorta. Zinc appeared to be the element most involved in vascular repair, followed by selenium and chromium.

Development and treatment of post-traumatic pulmonary platelet trapping.

In anesthetized dogs soft tissue trauma resulting in hypovolemia was associated with pulmonary trapping of 51Cr tagged platelets. The efficacy of various forms of therapy aimed at preventing pulmonary trapping of platelets following trauma was evaluated. Lung biopsies were assayed before trauma and at hourly intervals for accumulation of autologous 51Cr tagged platelets reinfused 24 hours prior to the experiment. The study showed that pulmonary platelet trapping secondary to soft tissue trauma could be prevented by treatment with Dextran 40, Dextran 70 and methyl-prednisolone administered one hour after trauma and by pretreatment with aspirin.