PubMed · 4537349
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L M Nashner. 1972. Vestibular postural control model.. https://doi.org/10.1007/bf00292236
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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.
Ankle instability is a frequent sequel following inversion sprain mechanisms of injury and has been estimated as occurring in approximately 20% of patients, regardless of the type of initial treatment. Mismanagement and undertreatment of this common injury contribute to the development of chronic instability symptoms with resultant tendencies toward reinjury. Loss of anatomical integrity of the injured ligamentous structures, proprioceptive deficits, or superimposed varus structural aberrations may all contribute to the chronicity of this condition. Surgical reconstruction of the insufficient ligaments can be accomplished through a variety of methods to restore stability. The more popular procedures currently being performed will be critiqued, and a new variant will be suggested that reduplicates the injured collateral ligaments more anatomically and reduces the technical complications inherent to operative procedures of this nature.
Arthrodesis of the ankle joint is commonly, performed to treat severe arthritis. Three different techniques have been biomechanically evaluated for initial stability: fusion with three isolated tibio-talar lag screws (type I), which was inaugurated by Wagner; a second fusion technique with two isolated tibio-talar lag screws and an anterior tibio-talar three-hole 3.5 mm AO compression plate (type II); and type-II fusion with an additional lag screw through the center hole of the anterior plate (type III). Ten fresh cadaver ankles were used for biomechanical evaluation. Bone stock quality was compared before fusion by CT scan and osteodensitometry. Osteopenic ankle joints (bone density less than 80% of the median density) were excluded. Each ankle fusion was stressed with 15 Nm in a universal testing machine (UTS 10, Ulm, Germany) in antero-posterior and medio-lateral directions and in a rotational torque technique. The movements at the fusion gap were recorded by computer-assisted image analysis. A video camera recorded the displacement of four active markers on both sides of the fusion line during loading in real time. A computer-assisted calculation of the dislocation at the fusion gap was performed. This technique provides comparable results except for systemic failure induced by the fixation device of the testing machine. The results revealed comparable initial stability with types I (0.063 mm/Nm) and III (0.074 mm/Nm; P = 0.95) ankle fusion. Type-II fusion was significantly less favorable concerning initial stability (0.14 mm/Nm; P < 0.01, Duncan's test for multiple comparisons). Our biomechanical results advertise isolated lag screws for ankle fusion.