have shown that raised intra-abdominal pressure increases the diameter of the external iliac vein deep to the inguinal ligament. They have concluded that this effect is dependent on there being a competent valve in the upper region of the femoral vein and that the occlusion of the femoral canal thus produced prevents femoral herniation. I wish to take issue with both conclusions.
The presence of competent valves in the iliofemoral venous segment is largely irrelevant to changes in diameter owing to raised venous pressure in uiuo. In the cadaver, there is no forward hydraulic venous flow, and therefore the closure of a competent valve will produce dilatation of the segment proximal to the valve relative to the distal segment, analogous to performing Harvey's test'. In the living subject, however, the situation is quite different. There is a constant forward venous flow resulting in a hydraulic pressure of approximately 12 cmH,O in the ileofemoral segment when supine2. Any impedence to outflow, as caused by raised intra-abdominal pressure, inevitably causes dilatation of the entire vein, irrespective of valve action. I have demonstrated this phenomenon in the iliofemoral segment of ten greyhounds in response to the Valsalva manoeuvre, and to partial and complete iliac vein occlusion (unpublished observations).
The demonstration that venous dilatation occludes the femoral canal during periods of raised intra-abdominal pressure does not justify the conclusion that femoral herniation is prevented. For this, it would be necessary to show that the pressure exerted by the femoral vein on the femoral canal exceeds the pressure exerted on the canal by any potentially herniating organ.