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The conventional pathogenesis of varicose veins and their subsequent development is essentially based on primary valvular insufficiency of the main saphenous trunk and incompetence of the perforating veins. In contrast, the concept of the pathogenesis of varicose veins presented in this review is based on the presence of arteriovenous (AV) shunting that occurs primarily in the venous tributaries and rarely in the main trunks of the saphenous system. Identification of arteriovenous communications (AVCs) with varicose veins has been documented by visual observation during surgery and especially by use of high-powered microscopes or magnifying lenses. The AVCs have been found consistently to originate subfascially and to terminate in tributaries extrafascially, thus bypassing the capillary network. By means of serial arteriography it was shown that in more than 80% of varicose veins there is premature venous opacification. By means of Doppler ultrasonography, it was demonstrated that AV shunting was present in 80% of the cases. A correlative study of these parameters has shown that the initial significant pathology in varicose veins is mostly confined to the tributaries, although at an advanced stage the main trunk may also be subsequently affected to a lesser degree. In terms of management, these data strongly imply that sclerotherapy or surgical treatment (ligation or excision) should be confined to the tributaries and that high saphenofemoral ligation and stripping should be avoided except in cases where evidence shows valvular involvement and incompetency of the latter. As a result, this study strongly suggests that one could most often spare the main trunk of the saphenous vein for eventual use as a vascular graft.

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We describe herein two cases of vascular malformations, one classified as hemangioma and the other as Klippel-Trenaunay syndrome. Clinical investigation in each case failed to demonstrate the presence of arteriovenous (AV) shunting. Arteriographic findings revealed only indirect evidence of AV shunting in each case. In contrast, systematic scanning with a Doppler ultrasonographic probe of the involved extremities provided evidence of AV shunting and pinpointed it in suspected arteriographic areas. Good correlation between the two methods was confirmed in the hemangioma case both preoperatively and intraoperatively. In the case of Klippel-Trenaunay syndrome, evidence of multiple AV shunts was obtained primarily with Doppler ultrasonography. In addition to arteriography, serial phlebography, when indicated, is also necessary for complete evaluation of concomitant venous malformations. The pathogenic mechanism of these vascular malformations was briefly reviewed, emphasizing AV shunting as a common link between the various anatomicoclinical forms.

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The use of the Doppler ultrasound detector is described for the diagnosis of arteriovenous (AV) shunting in varicose veins. This investigation was carried out in 34 patients, 27 women and seven men. A total of 68 limbs with varicose veins and 48 control limbs with either no varicose veins or occlusive arterial disease are the basis for the clinical material. Twenty patients had had no prior surgery for their varicose veins and 14 had recurrent varicosities after bilateral ligation and stripping. Five patients had postphlebitic syndrome associated with varicose veins. All five had venous stasis ulcerations and edema. The Doppler flow detector uncovered AV shunting in areas outside the location of known arterial pulsations. The pulsatile venous flow was obtained at sites of "hot spots" and along markedly dilated veins. Maximum AV shunting was found in the lower third of the leg but much less often in the upper leg or thigh. The clinical implications of the role of AV shunting are discussed. The Doppler ultrasound findings appear to offer a simpler method to detect AV shunting than serial arteriography or thermography.

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Subclavian artery compression by a cervical rib is an uncommon but potentially disabling condition. A series of 12 patients with 15 arterial lesions is reviewed and a staging system proposed to provide guidelines for managing patients with this condition. Stage I lesions have only arterial stenosis and minor poststenotic dilatation and are managed by thoracic outlet decompression, usually consisting of cervical rib resection. Stage II lesions have intrinsic arterial damage usually with subclavian aneurysm formation and require rib resection, aneurysmectomy, and arterial reconstruction. Stage III lesions present with distal thromboembolic complications and require thrombectomy or embolectomy in addition to thoracic outlet decompression and arterial reconstruction. The anatomic and pathophysiologic bases of the syndrome are reviewed and clinical and angiographic examples of each stage are presented.

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In the present report, a procedure for the removal of a late occluded graft which is firmly attached to the surrounding tissues is described which consists of disrupting mechanically the perigraft fibrous capsule by means of an external metal ring passed around the graft and, thus, allowing its easy removal.

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Acute arterial thromboembolism of the upper extremity associated with the thoracic outlet syndrome is much less frequent than the neurologic manifestations, but is a potential threat to the viability of the limb if not recognized in time. The thromboembolic process originates in a damaged subclavian artery as a result of its prolonged compression, usually by congenital, much more rarely, by acquired anomalies of anatomical structures at the thoracic outlet. Major embolic complications usually occur after months or years of episodal and repetitive microemboli. A comprehensive arteriographic evaluation of the entire arterial tree in addition to other tests is essential for diagnosis. Four patterns of arterial findings are described. The scope of the surgical treatment of these manifestations it twofold: (1) decompression of the subclavian artery and (2) repair of the arterial lesions, often with additional thoracic sympathectomy. Results of management of the arterial lesions are described in three groups, based mostly on a review of data from the literature. In recent years a more aggressive approach to these lesions appears to have resulted in better management of this complex entity. A case report will illustrate some the clinical and pathological aspects of this problem. Early recognition of this unusual thromboembolic process is necessary for achieving a more complete limb salvage.

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Arterial embolism of the upper extremity is not as rare and especially not as benign in all instances as was considered in the past. Postembolic ischemic changes or frank gangrene of fingers or hand may occur in a substantial percentage of patients. This paper will attempt to update the current concepts of this problem. The clinical data and the methods for evaluation of the degree of viability of the hand or forearm will be reviewed. Arteriography is recommended more liberally than in the past. Arterial embolectomy usually performed under local anesthesia is widely applicable in view of the simplicity, safety and effectiveness of the balloon catheter technique. The overall results based on a compilation from six reports indicate that complete circulatory restoration occurred in 55% and salvage without a return of wrist pulses in 24%. Gangrene occurred in 9.3% and mortality in 11.8%. In general, mortality following embolectomy is primarily related to the gravity of the cardiopathy and least to the surgical procedure.

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In the past nine years, 1196 patients whose lower extremity was threatened because of infrainguinal arteriosclerosis have been treated at Montefiore Hospital. In the last six years, limb salvage was attempted in 679 or 90% of 755 patients. Femoropopliteal (318), small vessel (204) and axillopopliteal (29) bypasses were used along with transluminal angioplasty (128) and aggressive local operations to obtain a healed foot. Immediate (one month) limb salvage was achieved in 583 or 86% of the 679 patients in whom revascularization was possible. The 30-day mortality rate was 3%. The cumulative life table (LT) survival rate of all the patients undergoing reconstructive arterial operations was 48% at five years. The cumulative LT limb salvage rate after all reconstructive arterial operations was 66% at five years. The cumulative LT patency rate of femoropopliteal bypasses was not influenced by angiographic outflow characteristics of the popliteal artery but was increased 15% by appropriate reoperations to 67% at five years. Cumulative LT patency and limb salvage rates of small vessel and axillopopliteal bypasses were more than 50% at two years. Of patients undergoing arterial reconstruction, 88% of those who died within five years did so without losing their limbs. Of all the patients in whom limb salvage was attempted, 68% lived more than one year with a viable, useable extremity, and 54% lived over two years with an intact limb. We believe this aggressive approach to limb salvage is justified, and can be undertaken with a low cost in mortality, knee loss and morbidity.

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Metabolic complications secondary to acute arterial occlusions occurred in 7.5% of our cases. It is pointed out that the characteristic biochemical changes: 1) may already be detectable during the ischemic phase, and 2) are more pronounced after revascularization of the extremity. Their identification at the early stage is essential for preventing the serious outcome of the late stage. Amputation rates are quite high (40-50%) and mortality rates are similarly great (30-80%). The ischemic rhabdomyolysis which leads to the clinical and manifestations and biochemical alterations is the initiating pathogenic factor of this syndrome. Prophylaxis and management of these complications were reviewed.

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Acute arterial occlusions of the extremities may result, in approximately 7.5% of cases, in a severe and complex metabolic syndrome which often leads to loss of limb and life. The manifestations of this syndrome are divided into two stages: (1) the ischemic or devascularization phase, and (2) the revascularization phase. The ischemic phase includes severe clinical manifestations, of which the rigidity of the limb ("rigor mortis") is an outstanding sign, as are nephropathic-metabolic changes (oliguria, acidosis, myoglobinuria, azotemia, hyperkalemia). Their identification and correction at this phase may minimize their impact on the revascularization syndrome. The clinical and metabolic manifestations during the latter phase are more severe and may determine the outcome of the viability of the limb and the survival of the patient. Amputation rates are quite high (40% to 50%) and mortality rates range between 30% and 80%. The ischemic rhabdomyolysis appears to be the initiating event which leads to the biochemical and metabolic alterations that dominate the prognosis as to limb and life. The guiding principles of the management in these severe ischemic cases consist of early revascularization with emphasis on concurrent fasciotomy, alkalinization of the patient, reestablishment of acid-base balance, hemodialysis for renal shutdown, and often early amputation for better control of the metabolic omplications.

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