Abstract
The theory of incompetent calf perforators (blow-out syndrome) according to Cockett and Jones 1 is one of the false myths within the scope of phlebological surgery. Nobody has so far confirmed by venous pressure measurements that incompetent calf perforators cause ambulatory venous hypertension; on the contrary, following objective tests, venous pressure, plethysmographic and electromagnetic flow measurements rebutted the theory of incompetent calf perforators.
Perthes 2 introduced a simple, but persuasive test. He used it to examine the patency of deep veins in the lower extremity before the era of phlebography. A tourniquet or digital compression is applied in the standing position in the thigh of varicose veins patients to interrupt great saphenous vein reflux. When the patients activate the calf muscle venous pump, the bulging varicose veins in the lower leg empty. According to the blow-out theory, they should have to fill up instead of emptying.
Bjordal 3 measured the venous pressure directly in incompetent calf perforators. The high hydrostatic pressure in the quiet standing decreased from about 90 mmHg to about 30 mmHg during the activity of the calf muscle venous pump as soon as the reflux in the great saphenous vein was interrupted by digital compression. Thus, no ambulatory venous hypertension occurred, but physiological decrease in pressure, directly the opposite than what the blow-out theory predicted.
Bjordal 3 measured the direction of flow in incompetent calf perforators by electromagnetic flowmeter. The flow had a bidirectional pattern with a prevalent inward vector into the deep vein of the lower leg. Saphenous reflux increased the inward-oriented flow vector. Hence, the flow vector in the incompetent calf perforator was oriented into the deep vein, not reversed into the superficial vein, as the blow-out theory asserted.
During each calf muscle contraction, the pressure increases in healthy persons and varicose vein patients in both deep and superficial veins of the lower leg, with a little greater increase in the deep veins. 4,5 The peak systolic pressure reached the value of 117 mmHg in the lower leg segment of the great saphenous vein during the first contraction, and 85 mmHg during the fourth one. 4 Some blood evades from the deep into the superficial veins of the lower leg via calf perforators during muscle contraction and is drained through the great saphenous vein into the common femoral vein. The pressure increase takes only a fraction of a second and is replaced by decrease in pressure during the next muscle relaxation; it does not exert any deleterious effect in either the subcutaneous or calf muscle tissues. If the venous pressure does not decrease at all in the superficial veins during calf pump activity, the severest grade of ambulatory venous hypertension occurs; in such a case, saphenous reflux is the responsible factor, not the evasion of venous blood from the deep lower leg veins via calf perforators.
Strain-gauge and air plethysmography findings in patients with primary varicose veins, strong saphenous reflux and large incompetent lower leg perforators showed severe derangement of the venous haemodynamics before operation. Selective elimination of the saphenous reflux (large incompetent perforators remained intact) normalized the haemodynamic situation, 6–8 which documents that incompetent calf perforators are haemodynamically irrelevant.