ACL Rupture After Thermal Treatment
Abstract & Commentary
Synopsis: Radiofrequency energy treatment of the normal ACL in canines appears to result in death and dissolution of the ligament and development of secondary laxity.
Source: Lopez MJ, et al. Anterior cruciate ligament rupture after thermal treatment in a canine model. Am J Sports Med. 2003;31(2):164-167.
Lopez and associates evaluated the effects of monopolar radiofrequency energy on native ACLs in 18 female research hounds. The ACL of the one extremity of the anesthetized dog was arthroscopically treated with monopolar radiofrequency energy at temperature and power settings of 70°C and 25 watts. The contralateral joint underwent a sham operative procedure. No postoperative bracing was used; however, postoperatively animals were confined to kennels.
Dogs were observed daily for signs of ACL rupture—that is, lameness, an effusion, or a positive anterior drawer sign. Gait analyses were done preoperatively and at 4, 8, 12, 16, 26, and 36 weeks postoperatively. Animals were sacrificed at 16 weeks, 26 weeks, and 36 weeks following detection of ligament failure, and their knee joints were examined. All had a mean time to rupture of 55 days post-treatment. On evaluation of the energy-treated knee joints, complete dissolution of the ACL was observed, whereas joints in which sham operative procedures had been done demonstrated normal ligament structures.
Comment by Letha Y. Griffin, MD, PhD
Although initially popularized to shrink lax collagen in loose shoulders, the idea of using radiofrequency energy to shrink loose cruciate ligaments has garnered recent interest. However, the shoulder capsule and its surrounding structures have a rich blood supply when compared with the native or reconstructed anterior cruciate ligament. Therefore, Thabit has suggested leaving the posterior aspect of the ligament untreated to allow for revascularization when performing shrinkage of the ACL with radiofrequency energy.1 In his report of 25 patients so treated with a monopolar radiofrequency device, 23 patients had only 2-mm side-to-side differences in graft laxity as measured by the KT-1000 arthrometer.
However, in 2000 Sekiya and colleagues published his case report in the Journal of Bone and Joint Surgery on autodigestion of a hamstring ACL autograft in a 16-year-old treated with a monopolar heat probe at 65°C and 40 watts of energy.2 The heat probe was used to treat laxity, which occurred following re-injury to an ACL hamstring graft, which had been in place for 5 months. Despite 12 weeks of a well-constructed postoperative rehabilitation program that emphasized graft protection, the thermally treated graft reruptured upon the athlete’s return to sport. At the time of re-operation, no remnant of the previous hamstring autograft was identified. Sekiya et al expressed concern over the use of thermal energy for treatment of ACL laxity pending further laboratory studies.
The present article seeks to more clearly understand the effects of thermal energy on normal anterior cruciate ligaments. However, Lopez et al do emphasize the study’s limitations: The entire dorsal surface of the ACL was treated (no mention was made of whether the ventral surface was also treated); no postoperative rehabilitation or immobilization was done, although the animals remained caged postoperatively; and the test species (canine) had a knee joint angle subjected to different forces than the human ACL.
Nonetheless, the study’s findings are disturbing in that all ligaments were found to be totally absent upon re-operation. Lopez et al caution against widespread adoption of radiofrequency energy to shrink injured native or reconstructed ACLs pending additional research.
References
1. Thabit G III. The arthroscopic monopolar radiofrequency treatment of chronic anterior cruciate ligament instability. Operative Techniques in Sports Medicine. 1998;6:157-160.
2. Sekiya JK, et al. Autodigestion of a hamstring anterior cruciate ligament autograft following thermal shrinkage. A case report and sentinel of concern. J Bone Joint Surg. 2000;82A:1454-1457.
Dr. Griffin is Adjunct and Clinical Faculty, Department of Kinesiology and Health, Georgia State University, Atlanta, GA.
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