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Original communication Society for Vascular Surgery| Volume 26, ISSUE 1, P16, July 1949

Phlegmasia cerulea dolens and gangrene associated with thrombophlebitis

Case reports and review of the literature
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      Abstract

      • 1.
        1. The occurrence, in venous thrombosis of the extremities, of clinical manifestations of arterial involvement which are so severe as to simulate acute arterial occlusion, and which even terminate in gangrene, is extremely uncommon. A review of the recent medical literature reveals only 56 cases of this condition.
      • 2.
        2. Two cases, representing the two different types of venous thrombosis (pseudoembolic phlebitis and venous thrombosis with actual gangrene of the extremity), are reported.
      • 3.
        3. The clinical manifestations follow a consistent pattern. In both forms of the disease the condition is associated with rather striking clinical manifestations which develop suddenly and progress rapidly, consisting chiefly of severe pain, edema, cyanotic violaceous discoloration, and evidence of arterial deficiency. The early course of the second form, in which gangrene occurs, may suggest a typical thrombophlebitis or phlegmasia alba dolens, with the subsequent development of fairly characteristic arterial manifestations, or the sequence of events may be reversed.
      • 4.
        4. Both conservative measures, such as the use of vasodilator drugs and procaine hydrochloride block of the regional sympathetics or periarterial sympathectomy, and operative intervention, consisting of exposure of the femoral vessels, thrombectomy, and periarterial sympathectomy, have been advocated. None has been strikingly successful.
      • 5.
        5. The prognosis in both forms of the disease is grave.
      • 6.
        6. Evidence is offered which suggests that sudden complete blockage of the circulation by venous thrombosis is the primary factor in the mechanism involved in this ischemic disturbance. Vasospasm is believed to play a secondary and contributory role in the pathogenesis of this condition.
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      2. See references 1, 5, 6, 8, 13, 14, 16, 17, 20, 21, 22–24, 31, 39, 41, 42, 45.