Brown Nicholas M, Murray Trevor, Sporer Scott M, Wetters Nathan, Berger Richard A, Della Valle Craig J
Rush University Medical Center, 1611 West Harrison Street, Suite 300, Chicago, IL 60612. E-mail address for C.J. Della Valle:
Department of Orthopaedic Surgery, Cleveland Clinic, 9500 Euclid Avenue, A41, Cleveland, OH 44195.
J Bone Joint Surg Am. 2015 Feb 18;97(4):279-83. doi: 10.2106/JBJS.N.00759.
Extensor mechanism disruption following total knee arthroplasty is a rare but devastating complication. The purpose of this study was to report our experience with extensor mechanism allograft reconstruction for chronic extensor mechanism failure.
Fifty consecutive extensor mechanism allograft reconstructions were performed in forty-seven patients with a mean age of 67.6 years who were followed for a mean time of 57.6 months (range, twenty-four to 125 months). The operative technique included the use of a fresh-frozen, correctly sized full extensor mechanism allograft that was tensioned tightly in full extension. Patients were evaluated clinically with use of the Knee Society score, and reconstructions were considered failures if the patient had a score of <60 points or a recurrent extensor lag of >30° or if they required revision or removal of the allograft.
Nineteen reconstructions (38%) were considered failures, including four revised to a second extensor mechanism allograft due to failure of the allograft, five for deep infection, and ten considered clinical failures secondary to a Knee Society score of <60 points or an extensor lag of >30°. The mean Knee Society score improved from 33.9 to 75.9 points (p<0.0001). The estimated Kaplan-Meier survivorship with failure for any reason as the end point was 56.2% (95% confidence interval, 39.4% to 70.1%) at ten years.
Extensor mechanism disruption following total knee arthroplasty is a difficult complication to treat, with modest outcomes. Extensor mechanism allograft reconstruction is a reasonable option; however, patients must be informed regarding the substantial risk of complications, and although initial extensor mechanism function may be restored, expectations regarding longer-term outcomes are more guarded.
全膝关节置换术后伸肌机制破坏是一种罕见但极具破坏性的并发症。本研究的目的是报告我们使用伸肌机制同种异体移植重建治疗慢性伸肌机制功能障碍的经验。
对47例平均年龄67.6岁的患者连续进行了50次伸肌机制同种异体移植重建,平均随访时间为57.6个月(范围为24至125个月)。手术技术包括使用尺寸合适的新鲜冷冻全伸肌机制同种异体移植,在完全伸直位时将其紧密张紧。使用膝关节协会评分对患者进行临床评估,如果患者评分<60分、伸肌滞后复发>30°,或者需要翻修或移除同种异体移植,则认为重建失败。
19例重建(38%)被认为失败,其中4例因同种异体移植失败而翻修为第二次伸肌机制同种异体移植,5例因深部感染,10例因膝关节协会评分<60分或伸肌滞后>30°被认为是临床失败。膝关节协会平均评分从33.9分提高到75.9分(p<0.0001)。以任何原因导致的失败为终点,估计的10年Kaplan-Meier生存率为56.2%(95%置信区间,39.4%至70.1%)。
全膝关节置换术后伸肌机制破坏是一种难以治疗的并发症,预后一般。伸肌机制同种异体移植重建是一种合理的选择;然而,必须告知患者并发症的重大风险,并且尽管最初的伸肌机制功能可能恢复,但对长期预后的期望更为谨慎。