Orishimo Karl F, Schwartz-Balle Sidse, Tyler Timothy F, McHugh Malachy P, Bedford Benjamin B, Lee Steven J, Nicholas Stephen J
Nicholas Institute of Sports Medicine and Athletic Trauma, Lenox Hill Hospital, New York, New York, USA.
Orthop J Sports Med. 2018 May 22;6(5):2325967118774031. doi: 10.1177/2325967118774031. eCollection 2018 May.
Disproportionate end-range plantar flexion weakness, decreased passive stiffness, and inability to perform a heel rise on a decline after Achilles tendon repair are thought to reflect increased tendon compliance or tendon lengthening. Since this was first noted, we have performed stronger repairs and avoided stretching into dorsiflexion for the first 12 weeks after surgery.
Using stronger repairs and avoiding stretching into dorsiflexion would eliminate end-range plantar flexion weakness and normalize passive stiffness.
Case series; Level of evidence, 4.
Achilles repairs with epitendinous augmentation were performed on 18 patients. Plantar flexion torque, dorsiflexion range of motion (ROM), passive joint stiffness, and standing single-legged heel rise on a decline were assessed at 43 ± 24 months after surgery (range, 9 months to 8 years). Maximum isometric plantar flexion torque was measured at 20° and 10° of dorsiflexion, neutral position, and 10° and 20° of plantar flexion. Passive dorsiflexion ROM was measured with a goniometer. Passive joint stiffness was computed from the increase in passive torque from 10° to 20° of dorsiflexion. Tendon thickness was measured by use of digital calipers. Plantar flexion electromyographic (EMG) data were recorded during strength and functional tests. Analysis of variance and chi-square tests were used to assess weakness and function.
Marked weakness was evident on the involved side at 20° of plantar flexion (deficit, 26% ± 18%; < .001), with no weakness at 20° of dorsiflexion (deficit, 6% ± 17%; = .390). Dorsiflexion ROM was decreased 5.5° ± 8° ( = .015), and tendon width was 8 ± 3 mm greater on the involved side ( < .001). Passive joint stiffness was similar between the involved and noninvolved sides. Only 2 of 18 patients could perform a decline heel rise on the involved side compared with 18 of 18 on the noninvolved side ( = .01). No difference in EMG amplitude was found between the involved and noninvolved sides during the strength or heel rise tests.
The use of stronger repair techniques and attempts to limit tendon elongation by avoiding dorsiflexion stretching did not eliminate weakness in end-range plantar flexion. EMG data confirmed that end-range weakness was not due to neural inhibition. Physiological changes that alter the force transmission capability of the healing tendon may be responsible for this continued impairment. This weakness has implications for high-demand jumping and sprinting after Achilles tendon repair.
跟腱修复术后，终末位跖屈力量不成比例地减弱、被动僵硬度降低以及无法在斜坡上进行足跟抬起动作，被认为反映了肌腱顺应性增加或肌腱延长。自首次发现此情况以来，我们进行了更坚固的修复，并在术后12周内避免将肌腱拉伸至背屈位。
采用更坚固的修复方法并避免拉伸至背屈位可消除终末位跖屈无力，并使被动僵硬度恢复正常。
病例系列；证据等级，4级。
对18例患者进行了带腱周增强的跟腱修复术。在术后43±24个月（范围为9个月至8年）评估跖屈扭矩、背屈活动度（ROM）、被动关节僵硬度以及在斜坡上单腿站立足跟抬起能力。在背屈20°和10°、中立位以及跖屈10°和20°时测量最大等长跖屈扭矩。用角度计测量被动背屈ROM。根据背屈从10°到20°时被动扭矩的增加计算被动关节僵硬度。用数字卡尺测量肌腱厚度。在力量和功能测试期间记录跖屈肌电图（EMG）数据。采用方差分析和卡方检验评估无力情况和功能。
在患侧，跖屈20°时明显无力（缺损26%±18%；P<.001），而背屈20°时无无力表现（缺损6%±17%；P = .390）。背屈ROM减少5.5°±8°（P = .015），患侧肌腱宽度比健侧大8±3mm（P<.001）。患侧与健侧之间的被动关节僵硬度相似。18例患者中只有2例在患侧能够在斜坡上完成足跟抬起动作，而健侧18例均能完成（P = .01）。在力量测试或足跟抬起测试期间，患侧与健侧之间的EMG幅度无差异。
采用更坚固的修复技术并试图通过避免背屈拉伸来限制肌腱延长，并未消除终末位跖屈无力。EMG数据证实终末位无力并非由于神经抑制。改变愈合肌腱力传递能力的生理变化可能是导致这种持续功能障碍的原因。这种无力对跟腱修复术后高要求的跳跃和短跑运动有影响。
