Santi M D, Botte M J
Department of Orthopaedic Surgery, University of California, San Diego Medical Center 92103, USA.
Foot Ankle Int. 1995 Jun;16(6):368-77. doi: 10.1177/107110079501600610.
Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.
骨骼肌的纤维化挛缩可在骨筋膜室综合征严重缺血性损伤数周或数月后出现。通常称为Volkmann缺血性挛缩，受累肢体常出现功能障碍和疼痛，且可能丧失感觉。肌肉挛缩的发病机制包括长时间缺血、肌坏死、成纤维细胞增殖、瘢痕收缩以及肌腱粘连形成。受累肌肉的缩短或过度牵拉导致僵硬和畸形。同时，初始缺血或随后软组织纤维化压迫导致的神经损伤会导致受累骨筋膜室以及更远端受其支配肌肉的肌无力或麻痹。因此，根据受影响的肌肉和神经不同，最终的畸形是不同程度挛缩和无力的组合。缺血继发的足踝部畸形和功能障碍由多种因素决定，包括：（1）受影响的腿部骨筋膜室（若有），以及外在屈肌或伸肌过度牵拉的程度；（2）因神经损伤导致足踝部外在或内在肌肉无力或麻痹的程度；（3）受影响的足部骨筋膜室（若有），以及内在过度牵拉的程度；（4）感觉神经损伤导致足部麻木、感觉减退或感觉过敏的程度。因此，小腿和足部骨筋膜室综合征后可出现多种临床表现。治疗基于对畸形病理解剖的认识。非手术治疗旨在获得或保留关节活动度、增强力量，并提供矫正支具和适应性鞋具。手术治疗通常用于治疗残留神经压迫或严重且有问题的畸形。既定的手术方案按步骤进行，包括：（1）解除残留或继发性神经压迫；（2）通过梗死切除、肌腱延长、肌肉回缩或肌腱切断术解除固定挛缩；（3）肌腱转移或关节融合术以改善功能；（4）对严重、难治性畸形进行截骨术或截肢术。
