In complex regional pain syndrome type I (CRPS-I), edema of the affected limb is a common finding. Therefore, the changes in macro- and microcirculatory parameters were investigated to elucidate the underlying pathophysiology. Twenty-four patients with post-traumatic CRPS-I and 25 gender- and age-matched healthy subjects were examined by means of an advanced computer-assisted venous congestion strain-gauge plethysmograph. The recording of the volume response of the forearm to a stepwise inflation of an occlusion cuff placed at the upper arm enabled the calculation of the arterial blood flow into the arm (Q(a)), the vascular compliance (C), the peripheral venous pressure (P(v)), the isovolumetric venous pressure (P(vi); = hydrostatic pressure needed to achieve net fluid filtration) and the capillary filtration capacity (CFC)--an index of microvascular permeability. The study revealed no difference in any of the parameters between the right and left hand of healthy subjects. In CRPS-I patients, however Q(a), P(v), P(vi) and CFC were significantly (p < 0.01/0.001) elevated in the affected arm (Q(a) 11.2 +/- 7.0 ml x min(-1) x 100 ml(-1), P(v) 20.2 +/- 8.1 mm Hg, P(vi) 24.7 +/- 4.2 mm Hg, CFC 0.0058 +/- 0.0015 ml x min(-1) x 100 ml(-1) x mm Hg(-1)) compared to the unaffected arm (Q(a) 4.2 +/- 2.4 ml x min(-1) x 100 ml(-1), P(v) 10.0 +/- 5.1 mm Hg, P(vi) 13.2 +/- 3.7 mm Hg, CFC 0.0038 +/- 0.0005 ml x min(-1) x 100 ml(-1) x mm Hg(-1)) and the values obtained in healthy controls (Q(a) 5.1 +/- 1.3 ml x min(-1) x 100 ml(-1), P(v) 10.4 +/- 4.3 mm Hg, P(vi) 15.7 +/- 3.3 mm Hg, CFC 0.0048 +/- 0.0012 ml x min(-1) x 100 ml(-1) x mm Hg(-1)). Whereas the values in the unaffected arm of CRPS-I patients revealed no difference in Q(a), P(v) and P(vi) but a lower CFC (p < 0.01) compared to those from healthy controls. These results suggest profound changes in both macro- and microvascular perfusion in the affected arm of CRPS-I patients. The high CFC contributes to the edema formation, and combined with the elevated P(vi), they are in agreement with the hypothesis of an inflammatory origin of CRPS.
Copyright 2001 S. Karger AG, Basel