Delaloye, J.-R., Murar, J., Vieira, T. D., Franck, F., Pioger, C., Helfer, L., … Sonnery-Cottet, B. (2020). Knee Extension Deficit in the Early Postoperative Period Predisposes to Cyclops Syndrome After Anterior Cruciate Ligament Reconstruction: A Risk Factor Analysis in 3633 Patients From the SANTI Study Group Database. The American Journal of Sports Medicine, 036354651989706. doi:10.1177/0363546519897064
Cyclops syndrome is characterized by a symptomatic extension deficit attributed to impingement of a cyclops lesion within the intercondylar notch. The syndrome is an important cause of reoperation after anterior cruciate ligament reconstruction (ACLR). It has been suggested that remnant-preserving ACLR techniques may predispose to cyclops syndrome, but there is very limited evidence to support this. In general terms, risk factors for cyclops syndrome are not well-understood.
To determine the frequency of and risk factors for reoperation for cyclops syndrome in a large series of patients after ACLR.
Case-control study; Level of evidence, 3.
A retrospective analysis of prospectively collected data was performed, including all patients who underwent primary ACLR between January 2011 to December 2017. Patients undergoing major concomitant procedures were excluded. Demographic data, intraoperative findings (including the size of preserved remnants), and postoperative outcomes were recorded. Those patients who underwent reoperation for cyclops syndrome were identified, and potential risk factors were evaluated in multivariate analysis.
A total of 3633 patients were included in the study, among whom 65 (1.8%) underwent reoperation for cyclops syndrome. Multivariate analysis demonstrated that preservation of large remnants did not predispose to cyclops lesions (odds ratio [OR], 1.11; 95% CI, 0.63-1.93). The most important risk factor was extension deficit in the early postoperative period. If present at 3 weeks postoperatively, it was associated with a >2-fold increased risk of cyclops syndrome (OR, 2.302; 95% CI, 1.268-4.239; P < .01), which was increased to 8-fold if present 6 weeks after ACLR (OR, 7.959; 95% CI, 4.442-14.405; P < .0001). None of the other potential risk factors evaluated were found to be significantly associated with an increased frequency of cyclops syndrome.
Failure to regain full extension in the early postoperative period was the only significant risk factor for cyclops syndrome after ACLR in a large cohort of patients. Other previously hypothesized risk factors, such as preservation of a large anterior cruciate ligament remnant, did not predispose to the development of this debilitating postoperative complication.
The term cyclops syndrome is used to describe the clinical scenario of a symptomatic extension deficit attributed to impingement of a cyclops lesion within the intercondylar notch. The major importance of cyclops syndrome arises from the resultant morbidity. Patients experience loss of extension with snapping and catching while walking. Additionally, the associated gait disturbance is poorly tolerated, and there is some evidence to suggest that altered sagittal plane mechanics during the loading response phase of gait predisposes the patient to early medial compartment degeneration. Rates of reoperation to regain full extension after the development of cyclops syndrome are between 1.9% and 8.4% of ACLR.
The precise etiology and risk factors for the development of cyclops syndrome are incompletely defined.1 However, Pinto et al recently identified extension deficit in the early postoperative period as an important risk factor.
The final study population was composed of 3633 patients divided into 2 groups: patients with or without postoperative cyclops syndrome. Cyclops syndrome was identified in 65 patients (1.8%), who all recovered full knee extension after arthroscopic debridement of the lesion.
After univariate analysis, the following factors reached the 25% threshold of correlation with cyclops syndrome and were included in a multivariate analysis: knee extension deficit at 3 and/or 6 weeks postoperatively, body mass index .25, and the presence of bimeniscal lesions.
Indeed, patients who had a knee extension deficit at 3 and 6 weeks postoperatively had a .2-fold and 8-fold increase in the risk of postoperative cyclops syndrome, respectively, as compared with patients who presented without extension deficit (Figure 3).
The main findings of this study were that extension deficit in the early postoperative period was the most important predictor for cyclops syndrome, while preservation of large ACL remnants did not confer any increased risk of developing this complication. A further important finding was that the overall frequency of reoperation for cyclops syndrome was 1.8%.
It is not entirely clear where in the literature the concerns regarding an association between remnant preservation and cyclops syndrome have arisen, because comparative studies have not demonstrated this. However, several authors have postulated that the presence of some portion of the ACL remnant could explain the pathogenesis. Jackson and Schaefer suggested that remaining tissue around the tibial tunnel may be part of the tissue that forms the cyclops lesion. Therefore they recommended a thorough debridement around tibial tunnel. This opinion is shared by other authors as well, but is based only on personal experience rather than any scientific evidence. Delince et al observed that cyclops lesions were located at the base of the ACL graft and seemed to develop from the fibers of the ACL stump left behind. Finally, Wang hypothesized that cyclops lesions were due to an inflammatory proliferative process for which one of the possible stimulating factors could be an ACL remnant. However, no study could clearly demonstrate a correlation between ACL remnant preservation and cyclops syndrome.
It is our opinion that the findings of the current study provide a firm rebuttal against theoretical concerns that large remnants can predispose to cyclops syndrome. This study identified that the most important risk factor for the development of cyclops syndrome was knee extension deficit in the early postoperative period. This confirms the findings of Pinto et al, who reported that extension deficit at postoperative 3 and 6 weeks was associated with a significantly increased risk of cyclops syndrome. In that case-control study, 45 patients with cyclops syndrome were matched to random controls. The study design of Pinto et al did not allow an evaluation of risk factors for cyclops syndrome or a determination of whether early postoperative extension deficit remained an important predictor of cyclops syndrome in multivariate analysis. The current study confirms that extension deficit in the early postoperative period is not only a significant risk factor for cyclops syndrome but also the most important predictor. These results support the work of Jackson and Schaefer, who suggested that it is not the cyclops lesion that causes this early extension deficit but rather the extension deficit that promotes the development of the nodule in the intercondylar notch.
Despite all these precautions, 1.8% of our patients still developed cyclops syndrome, confirming that the cyclops lesion must have formed sometime after the patient was discharged from the hospital. This observation is in keeping with the findings of Gohil et al, who performed MRI evaluation at 2, 6, and 12 months after ACLR. In their prospective study including 48 patients, the initial development of cyclops lesions, as noted on MRI, was typically between 6 and 12 months. Interestingly, and consistent with our findings, the authors noted that patients who eventually had cyclops syndrome already had an extension deficit at postoperative 2 months but without MRI evidence of any cyclops lesion at that stage. The authors concluded that the early postoperative loss of extension was multifactorial and could promote the development of scar tissue in the intercondylar notch.
On the basis of the aforementioned evidence, it is apparent that the early extension deficit observed in patients who go on to develop cyclops syndrome is very unlikely to be the result of a mechanical problem. It therefore logical to suggest that the observed extension deficit that leads to an increased risk of cyclops syndrome could be related to arthrogenic muscle inhibition (AMI). AMI is a frequent but underrecognized cause of extension deficit after ACLR. It is caused by changes in the discharge of articular sensory receptors (attributed to inflammation, pain, and swelling), which in turn alter neurological pathways resulting in a hamstring contracture and a quadriceps activation failure (Figure 4). Clinically, this manifests as a passive and active extension deficit. However, further study is required to evaluate whether proven therapeutic modalities (cryotherapy and hamstring fatigue exercises) for AMI are able to reduce the risk of developing cyclops syndrome.
Failure to regain full extension in the early postoperative period was the only significant risk factor for cyclops syndrome after ACLR in a large cohort of patients. Other previously hypothesized risk factors, such as preservation of a large ACL remnant, did not predispose to the development of this debilitating postoperative complication.