Abstract
The pathogenesis of the late post-traumatic rupture of the extensor pollicis longus tendon has never been satisfactorily explained. In the present series of fifty-nine ruptures two were partial, making possible an exact localization of the rupture. Microangiographic studies performed on amputated arms showed that this part of the tendon was poorly vascularized. Our study confirms earlier observations that ruptures most commonly occur after undisplaced fractures. It is suggested that increased pressure within the non-ruptured tendon sheath jeopardizes the blood flow in the already poorly vascularized parts of the tendon, leading to degeneration and rupture, usually within eight weeks. An haematoma inside the sheath interfering with the production of synovial fluid, could deprive the tendon of an alternative nutrition via diffusional pathways.