Delcogliano A, Franzese S, Branca A, Magi M, Fabbriciani C
Istituto di Clinica Ortopedica, Università Cattolica de Sacro Cuore-Pol. A, Gemelli, Rome, Italy.
Knee Surg Sports Traumatol Arthrosc. 1996;4(4):194-9. doi: 10.1007/BF01567962.
The loss of range of motion after anterior cruciate ligament (ACL) reconstruction is one of the most common and most challenging complications of this kind of surgery. Recently, an intercondylar notch fibrous proliferation, called cyclops syndrome because of its arthroscopic appearance, has been identified as one of the specific causes of loss of extension. The incidence of cyclops syndrome is 2%-4% [17, 18], but there is still no understanding of its etiology. We speculate on the etiology and suggest some technical solutions to reduce this complication. In 180 patients submitted to arthroscopic ACL reconstruction with patellar tendon, we observed in 4 cases a fibrous nodule adherent to the neoligament that caused a loss of extension between 12 degrees and 17 degrees. In all cases, arthroscopic removal of this nodule solved completely the loss of articular motion. The nodules were subjected to light and scanning electron microscope evaluation. We observed numerous, newly formed vessels in all 4 nodules. These vessels were made up of hyperplastic and hypertrophic cells and were surrounded by bundles of disorganized fibrous tissue. No inflammatory cells or bone or cartilaginous tissue was observed. We hypothesize a microtraumatic genesis for cyclops syndrome. Repeated microtraumas expose the graft collagen fibers, which can lead to productive inflammatory process and thence to the formation of the cyclops nodule. We suggest some technical solutions to avoid graft impingement with the notch and with the tibial bone tunnel.
前交叉韧带(ACL)重建术后活动范围丧失是此类手术最常见且最具挑战性的并发症之一。最近,一种髁间窝纤维增生因其关节镜下表现被称为“独眼巨人综合征”,已被确定为伸直受限的特定原因之一。独眼巨人综合征的发生率为2% - 4%[17, 18],但其病因仍不清楚。我们推测其病因并提出一些技术解决方案以减少这种并发症。在180例行关节镜下髌腱ACL重建的患者中,我们观察到4例有纤维结节附着于新韧带,导致伸直受限12度至17度。在所有病例中,关节镜下切除该结节完全解决了关节活动丧失的问题。对这些结节进行了光学显微镜和扫描电子显微镜评估。我们在所有4个结节中均观察到大量新形成的血管。这些血管由增生和肥大的细胞组成,并被杂乱的纤维组织束包围。未观察到炎性细胞或骨或软骨组织。我们推测独眼巨人综合征的发病机制为微创伤。反复的微创伤使移植物胶原纤维暴露,这可导致增殖性炎症过程,进而形成独眼巨人结节。我们提出一些技术解决方案以避免移植物与髁间窝和胫骨骨隧道发生撞击。