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One hundred fifty patients undergoing carotid endarterectomy were randomly assigned to receive intravenous 10% dextran 40 or placebo. Transcranial Doppler monitoring of the ipsilateral middle cerebral artery 0 to 1 hour postoperatively detected embolic signals in 57% of placebo and 42% of dextran patients, with overall embolic signal counts 46% less for dextran (p = 0.052). Two to 3 hours postoperatively, embolic signals were present in 45% of placebo and 27% of dextran patients, with embolic signal counts 64% less for dextran (p = 0.040). We conclude that dextran reduces embolic signals within 3 hours of CEA.

Cerebral ischaemia, the most frequent serious complication of carotid endarterectomy (CEA), usually occurs in the early postoperative period and is often the result of thromboembolism. We hypothesized that the early postoperative detection of microembolic ultrasonic signals (MES) with transcranial Doppler ultrasound (TCD) may be of value in identifying patients at risk of postoperative cerebral ischaemia and that the MES rate may be an important determinant in risk prediction. Sixty-five patients undergoing CEA were studied at intervals up to 24 h postoperatively with TCD insonation of the middle cerebral artery ipsilateral to the operation side. Study design was open and prospective with blinded off-line analysis of MES counts. End-points were any focal ischaemic neurological deficit and/or death up to 30 days postoperatively. MES were detected in 69% of cases during the first hour postoperatively with counts ranging from 0 to 212 MES/h (means 19 MES/h; SEM +2- 4.5; median 4 MES/h). In seven cases (10.8%) counts were > 50 MES/h. Five of these seven cases developed ischaemic neurological deficits in the territory of the insonated middle cerebral artery during the monitoring period. The positive predictive value of counts > 50 MES/h for cerebral ischaemia was 0.71. Frequent signals (> 50 MES/h) occur in approximately 10% of cases in the early postoperative phase of CEA and are predictive for the development of ipsilateral focal cerebral ischaemia.

Recurrent varicose veins may result from inadequate assessment or inadequate surgery. In this study, 110 consecutive patients (165 limbs) were assessed pre-operatively for the presence or absence of reflux at the saphenofemoral (SF) and saphenopopliteal (SP) junctions by clinical assessment and by Doppler ultrasound. The pre-operative results where then compared with findings at the time of surgery. Doppler ultrasound as a means of predicting SF and SP incompetence was superior to clinical assessment. Doppler Doppler ultrasound detected 100% (two false positives) of incompetent SF junctions, and 100% (six false positives) of incompetent SP junctions, compared to the clinical detection of 72% (no false positives) and 64% (five false positives), respectively. Short saphenous venography was performed in 36 limbs in which SP reflux was suspected on clinical assessment and/or by Doppler ultrasound. It proved valuable in demonstrating the level and mode of termination of the short saphenous vein. This guided the placement of the skin incision.

"Venous" ulceration is usually ascribed to deep venous insufficiency. We record the cases of 20 patients with 23 ulcers without a history suggestive of deep vein disease who were found to have a normal deep venous system when evaluated by Doppler ultrasound, ambulatory venous pressures, and photoplethysmography. All had gross varicose veins present for many years (mean 24 years; range 10 to 35 years), and only 14 limbs had incompetent calf perforating veins. Effective treatment is facilitated by recognition of the relationship of varicose ulcer to superficial venous disease, usually incompetence of the saphenofemoral junction, with or without the presence of incompetent calf perforating veins.

A prospective study of 125 femoro-distal vein bypass grafts (103 patients) was undertaken to assess the role of treadmill exercise testing in the detection and correction of early vein graft stenosis. Patients were followed at 1,3,6,12 months and then annually with routine clinical assessment, palpation of pulses and resting Doppler ankle/brachial index. In addition, the Doppler index was repeated after 5 minutes exercise on a treadmill set at 5 degrees and 3 km/hr. Follow-up has been carried out for a mean of 24 months (range 3-48 months) and during that time 30 vein grafts (28 patients) were submitted to angiography. This revealed vein graft stenosis in 15, native vessel disease in 11 and no morphologic abnormality in 4. One additional graft was suspected to have a stenosis but occluded before angiography could be carried out. At the time of detection by the treadmill test, 8 of the 15 (53%) confirmed vein graft stenoses, and 4 of 11 (36%) native vessel stenoses would not have been detected by clinical assessment or resting Doppler pressure measurements. The 15 vein graft stenoses which were corrected all remain patent, suggesting that treadmill testing is of value in the detection and prevention of early femoro-distal vein graft occlusion.

Twenty-one patients with severe Raynaud's phenomenon were treated on 29 occasions with prostaglandin E1 (PGE1), a potent vasodilator and pyrogen. A history of finger sepsis or necrosis was absent in 8 (group I) and present in 13 (group II). Three group I and eight group II patients had an associated connective tissue disease, and previously eight upper limbs had been sympathectomized in six group I patients and 14 upper limbs in eight group II patients. A total of 12 fingers had been amputated in six group II patients. Treatment comprised antibiotics for sepsis, PGE1 intravenously for 72 hours, and subsequent surgical debridement of septic and necrotic tissue in 30 fingers of eight group II patients under general anesthesia. Finger skin temperature measured half-hourly in a temperature-controlled ward cubicle (23.7 degrees +/- 0.7 degrees C), Doppler-detectable digital arterial flow, and finger/brachial systolic pressure index with local finger cooling to 10 degrees C were not improved by the administration of 0.9% saline for 72 hours, but were all significantly improved after PGE1 administration. Finger skin temperature was significantly elevated 11 weeks after treatment. The symptoms did not improve after PGE1 administration in group I patients but did improve in 12 of 13 group II patients. No finger deteriorated, and all debrided fingers healed after surgery. Nail bed removal in 11 fingers met with patient approval and prevented recurrent sepsis and necrosis. PGE1 provides a means of increasing finger blood flow during acute exacerbations of finger sepsis and necrosis; unlike sympathectomy, it is a minor procedure without prolonged side effects and is repeatable.