Engkvist O, Lundborg G
Hand. 1979 Feb;11(1):76-86. doi: 10.1016/s0072-968x(79)80015-7.
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.
拇长伸肌腱创伤后晚期断裂的发病机制从未得到令人满意的解释。在本系列的59例断裂病例中，有2例为部分断裂，这使得能够精确确定断裂的位置。对截肢手臂进行的微血管造影研究表明，该部位的肌腱血管分布较差。我们的研究证实了早期的观察结果，即断裂最常发生在无移位骨折之后。有人认为，未断裂的腱鞘内压力增加会危及肌腱中原本血管分布就差的部位的血流，导致退变和断裂，通常在8周内发生。腱鞘内的血肿会干扰滑液的产生，可能会通过扩散途径使肌腱失去另一种营养来源。
