The mechanical-vascular hypothesis of Sudeck’s atrophy: venous outflow obstruction

Abstract

Complex regional pain syndrome (CRPS), historically termed Sudeck’s atrophy, is traditionally classified as a neurogenic and sympathetically mediated disorder. However, purely neurological models fail to fully account for the rapid trophic changes of the skin and nails or the profound impact of mechanical factors observed in clinical practice. In this paper, we propose a novel mechanical-vascular hypothesis suggesting that the primary initiating driver of Sudeck’s atrophy is not neural dysfunction, but rather a mechanical venous outflow obstruction. This condition is primarily driven by the synergistic effect of rigid external cast compression and internal tissue edema following trauma. This mechanical bottleneck leads to persistent venous stasis, elevated compartmental pressure, microvascular fatigue, and rapid regional bone demineralization, while drawing a compelling pathological parallel with post-thrombotic syndrome. Importantly, this paradigm does not dismiss standard orthopedic care; rather, it integrates existing practices-such as effective pain management, targeted regional blocks to facilitate physical therapy, and muscle pump activation-with a renewed focus on early anti-edema measures and venous path clearance. Rigorous longitudinal Doppler assessments and clinical evaluations are proposed to validate this framework, offering a comprehensive dual approach to halt disease progression.