On the mechanism of action of pneumatic compression devices: Combined magnetic resonance imaging and duplex ultrasound investigation.

Objective: This study investigated the relationships between the interface pressure produced by intermittent pneumatic compression (IPC) devices, the deformation of extremity tissues produced by this pressure, and changes in venous blood flow associated with this deformation by use of magnetic resonance imaging (MRI) and duplex ultrasound (DUS) imaging in addition to the pressure measurement.

Methods: The calf garments of two IPC devices (WizAir, Medical Compression Systems, Inc, Ltd, Or-Akiva, Israel; VenaFlow, AirCast Inc, Summit, NJ) were tested in five healthy volunteers. The interface pressure was measured with Tactilus Human Body Interface sensor system (Sensor Products Inc, Madison, NJ). Changes in tissue volumes were assessed with MRI. Velocity and flow changes in the great saphenous vein (GSV) and femoral veins (FV) were evaluated by DUS scans.

Results: The spatial distribution of interface pressure differed substantially between the two devices. These differences were in the location and percentage of calf surface area to which different pressure was applied. Both devices produced the tissue compression consistent with each device's unique pattern of the interface pressure distribution. Compression by the IPC devices was associated with a measurable decrease in the volume of subcutaneous tissue under the garment, the total volume of superficial veins, and the volume of the GSV. No measurable changes occurred in subfascial volume of the calf. Compression was associated with significant increase in flow velocities in the GSV and FV. The increase of volume flow was significant in FV, but not in GSV. Comparing hemodynamic data with MRI data showed that the flow velocity increase in FV and GSV caused by IPC highly correlated with decrease in volume of superficial veins and subcutaneous tissue measured by MRI, but not with changes in subfascial volume. A single strongest predictor of venous flow increase was the change in subcutaneous veins volume.

Conclusions: This methodology provides means for the investigation of relationships between the pressure in the garment, interface pressure, tissue deformation, and hemodynamic respond to IPC. The clinical efficacy of IPC should not be explicitly attributed to the magnitude of the pressure in the garment. Similar hemodynamic responses to IPC can be produced by different spatial distributions of pressure resulting in different patterns of tissue compression. Further investigation of biomechanical mechanisms of IPC is needed to guide the development of better engineering solutions for mechanical devices aimed at prevention of venous thrombosis.