Popliteal vein compression syndrome pathophysiology and correlation with popliteal compartment pressures.

Abstract

The link between obesity and popliteal vein compression syndrome (PVCS) has been documented, but thepathophysiological mechanism is unclear. The aim of this study is to understand the pathogenesis of PVCS by assessing popliteal compartment pressures (PCP). Twenty-three limbs (15 patients) were included. Eleven limbs were ultrasonically diagnosed with PVCS and underwent popliteal vein decompression. The control group consisted of 12 limbs with functional popliteal artery entrapment. Perioperatively, PCP measurements were obtained. The body mass index (BMI) was calculated and the clinical symptoms were documented (CEAP). The median BMI for the PVCS group was 32 (range, 26-45.8) compared with 28 (range, 19-31) for the control group (P= .05). In PVCS, the popliteal vein internal diameter was 9.4 mm (range, 8.0-20.0 mm) upon knee flexion, compared with 0 mm (range, 0.0-0.1 mm) upon kneeextension. Upon knee flexion, there was no difference inpressure (PVCS 10.0 [range, 4-20] vs control 11.5 [range, 3-22]; P= .95). Upon knee extension, the median PCP in the PVCS group was 53 cm H2O (range, 38-76 cm H2O) compared with 26 cm H2O (range, 17-43 cm H2O) in the control group (P< .001). PVCS is associated with high popliteal compartment pressures compared with controls. The pathophysiology of popliteal obstruction, in the absence of anatomical abnormalities, is related to an increase in popliteal compartment pressure while standing due an increase of the popliteal fat pad, related to high BMI.