Isolated Clinically Diagnosed Grades 1-2 Lateral Collateral Ligament Injuries in Elite Athletes Do Not Require Surgery

Abstract

Background:

Lateral collateral ligament (LCL) injuries can occur in isolation or as part of more extensive posterolateral corner (PLC) injury. Although excess laxity due to PLC injury is usually considered an absolute indication for repair or reconstruction, nonoperative management of isolated LCL injuries is also possible.

Purpose/Hypothesis:

The purpose of the present study is primarily to evaluate the outcome of nonoperative treatment in a consecutive series of isolated LCL injuries in elite athletes as reflected by successful return to play (RTP), performance level, and rates of continued play at 2 and 5 years after injury. Furthermore, it was hypothesized that the clinical and radiological grading of LCL injuries do not correlate.

Study Design:

Case series; Level of evidence, 4.

Methods:

A consecutive series of elite athletes with PLC injury of the knee treated by 2 sports knee surgeons between January 2015 and June 2021 was identified. Only those with isolated LCL injuries as identified on magnetic resonance imaging (MRI) and by a lack of any abnormal rotatory laxity were included. Data pertaining to clinical examination findings, radiological findings, treatment, RTP times, performance levels, and subsequent career longevity were collected.

Results:

A total of 55 professional athletes (44 soccer players), with a mean ± SD age of 24.3 ± 4.5 years, with MRI-confirmed isolated LCL injuries were included in final analysis. Of the total cohort, clinical examination findings were notable for grade 0 laxity in 7 (12.7%) athletes, grade 1 in 42 (76.4%), grade 2 in 6 (10.9%), and grade 3 in 1 (1.8%). All patients were treated with restricted activities and rehabilitation. MRI grading and clinical grading showed low correlation (r = 0.37; P = .01). RTP was 100% at a mean of 103 (0-422) days (median of 76 days [2.5 months]). At 2 years, 51 athletes (92.7%) were still playing elite sport. At 5 years, participation among the 32 athletes still playing in elite sport reduced to 84.4% (n = 27 players). All athletes returned to their preinjury level of play. No athletes stopped elite sport secondary to their LCL injury.

Conclusion:

The current data suggest that nonoperative management of isolated clinically diagnosed grades 1 and 2 LCL injury is associated with high return to preinjury level of sport (100%), reasonable recovery times (median of 76 days), and no significant residual varus laxity. There was low correlation of MRI grade of isolated LCL injury with clinical examination findings. The authors recommend these lesions be treated without surgery.

Posterolateral corner (PLC) injuries present diagnostic and treatment challenges, as they typically involve a spectrum of injuries to the lateral ligament complex.^13,27 These can range from isolated lateral collateral ligament (LCL) lesions, which cause varus laxity alone, to isolated injuries to the popliteal complex with resultant posterolateral rotatory laxity, or more commonly, a combination of both.^1,13,27 While PLC injuries account for approximately 16% of all knee ligament injuries,^24,27 isolated ruptures of the LCL are reported to occur much less frequently at 1.1%. ²⁶

The LCL has an oblique course passing posteriorly and distally from its femoral attachment at the lateral epicondyle to the fibula.^1,20,22,31 While taut in full extension, the LCL loosens in flexion, particularly from 30° due to lateral femoral “roll-back” during knee flexion.^1,33 The LCL is the primary restraint to varus stress, and in combination with the other posterolateral structures, is a secondary restraint to tibial external rotation. ¹

Because of its structure and role, PLC and LCL injuries are typically the result of a varus and/or hyperextension traumatic injury or from a forced external rotation moment.^1,27 Avulsion fractures can occur, most commonly involving the fibular insertion.^13,16

Although magnetic resonance imaging (MRI) remains the gold standard for imaging of PLC injuries, ⁷ acute MRIs are more likely to be more accurate than chronic ones. Their interpretation is challenging because of the complex anatomy of the PLC structures that cross multiple planes.^4,28 Nevertheless, the LCL itself can usually be viewed easily.

While nonsurgical management is preferred for isolated partial (clinical grades 1 and 2) LCL injuries,^15,17 treatment of clinical and MRI-based grade 3 injuries (ie, complete ruptures) is controversial. There are only limited data regarding outcomes following nonoperative treatment,^5,6,10 with most of the existing literature favoring surgical management.^{8,15,21,23,29}

The grading of medial collateral ligament injuries on MRI has been shown to poorly correlate with clinical grading. ³⁶ However, no similar studies of correlation between MRI and clinical grading for isolated LCL injury have been published. Studies have shown that stress radiography is more accurate than MRI in diagnosing significant LCL lesions. ¹⁴

The purpose of the present study is primarily to evaluate success of nonoperative treatment in a consecutive series of MRI-diagnosed isolated LCL injuries in elite athletes as reflected by successful return to play (RTP), performance level, and rates of continued play at 2 and 5 years postinjury. Furthermore, we hypothesized that the clinical and radiological grading of LCL injuries do not correlate.

Methods

A consecutive series of elite athletes with PLC injuries treated by 2 sports knee surgeons (A.W. and S.V.B.) between January 2015 and June 2021 was identified (Figure 1). Approval to complete the study was given by the institute involved in line with UK NHS Health Research Authority guidance.

Figure 1.

Flowchart of inclusion. LCL, lateral collateral ligament; MRI, magnetic resonance imaging; PCL, posterior cruciate ligament; PLC, posterolateral corner.

The medical records of all elite athletes with PLC injuries and those who had not undergone cruciate ligament surgery were reviewed to ensure all isolated LCL injuries were identified. Isolated LCL injuries were defined as those diagnosed as injured on MRI but without injury to cruciate or medial collateral ligaments and with a negative dial test on clinical examination. Athletes were included if they were >16 years of age, played elite sport, and were treated nonoperatively for an isolated LCL injury. Elite athletes were defined as those who are paid to perform their sport, or those who participate at the national/international level in an amateur sport.

Surgery for posterolateral lesions was undertaken in the following situations: (1) positive varus stress test with the knee in full extension; (2) varus laxity at 30° flexion in conjunction with a positive dial test; (3) in cases needing concomitant cruciate ligament reconstruction; and/or (4) fibular head avulsion fracture or complete soft tissue avulsion from the fibular head.

All athletes underwent MRI prior to the initial appointment with the treating surgeon, and conservative treatment amended/started immediately following the MRI. Clinical examination of the PLC included an assessment of varus laxity at 0° and 30° flexion and a dial test for external rotation stress at 30° and 90°. Clinical laxity of the LCL was defined as grade 1 if, when compared with the uninjured knee, there was an excess lateral joint opening of ≤5 mm; grade 2 if 5- to 10-mm opening; and grade 3 if >10 mm of opening on varus stress.^2,11 The dial test was deemed positive if there was an excess of external rotation of ≥10° compared with the opposite knee at 30° or 90° of flexion.

MRI was performed on all patients, and scans were evaluated independently by 2 senior sports radiologists (A.M. and J.L.) for MRI-based LCL injury classified according to Recondo et al, ³⁰ and concomitant injuries. The LCL injuries were graded as follows: grade 1, signal change within the ligament with preservation of fibrillar architecture and ligament morphology (Figure 2); grade 2, signal change plus partial loss of fibrillar architecture but preservation of ligament continuity (Figure 3); grade 3, signal change plus complete loss of fibrillar architecture plus loss of continuity (Figure 4). ³⁰ Results were compared, and if discrepancies existed, a consensus was reached following a meeting of the radiologists with reevaluation of available imaging scans.

Figure 2.

Grade 1 injury: signal change only. (A) Axial and (B) sagittal fat-saturated proton density–weighted magnetic resonance imaging of the lateral knee of a 24-year-old male professional footballer. The lateral collateral ligament returns increased signal but maintains tension and morphology. Arrows point to the ligamentous structure and its damage.

Figure 3.

Grade 2 injury. (A) Axial and (B) sagittal fat-saturated proton density–weighted magnetic resonance imaging of the lateral knee of a 24-year-old male professional footballer. The images demonstrate a longitudinal split of the ligament with minor loss of tension. The complete set of images showed continuity of the ligament from femoral to fibular attachment. Arrows point to the ligamentous structure and its damage.

Figure 4.

Grade 3 injury. (A, B) Axial and (C) sagittal fat-saturated proton density–weighted magnetic resonance imaging of the lateral knee of a 17-year-old male professional footballer. (A) is just above tear site and (B) shows absent lateral collateral ligament (LCL) at tear site. (C) shows discontinuity of the LCL. Arrows point to the ligamentous structure and its damage.

Patients with grade 2 or 3 clinical laxity were treated with a hinged range of motion brace set to block the terminal 30° of extension for 2 weeks during which time they were restricted to touch weightbearing. The logic for this is since the LCL is a nonisometric structure tightening in extension, it is quickly offloaded with flexion allowing early healing without being stressed. Following this, full weightbearing in the brace and extension to 0° was permitted for another 2 weeks after which terminal extension was allowed. There were no restrictions on flexion. Therefore, a total of 4 weeks in a brace was used. Those with lesions of clinical grades 0 and 1 were not braced and full weightbearing was permitted immediately. Early movement was encouraged. Rehabilitation reestablished neuromuscular control, strength, and balance, before progressing to sport-specific training. Progress and fitness to RTP was supervised by the athletes’ medical teams, in collaboration with the treating surgeons. Attendance for in-person follow-up and clinical examination by the treating surgeon was optional and was not mandated if the athlete, club medical team, and surgeon had no concerns.

In keeping with many previous studies, RTP was defined as playing ≥1 match or competing in ≥1 event at the professional level or national/international level in an amateur sport.^18,34,35 Time to RTP was calculated as time between date of injury and first match appearance.

RTP at the same level was defined as achieving RTP for a team in the same or higher league, or equivalent league in another country. ³ Career longevity was determined by the last available match appearance date found at the time of the study.

Statistical Analysis

Categorical variables are expressed as numbers (percentages) and continuous variables as mean ± SD. Correlation between MRI grades of injury and clinical grading was calculated using Pearson correlation test.

Results

A total of 67 athletes had isolated PLC injuries. Five required surgical treatment and were excluded. Four of them had a concomitant PCL injury and 3 had no injury to the LCL. Thus, a total of 55 athletes met the inclusion criteria of isolated LCL injuries and were treated nonsurgically.

There were 53 (96.4%) men and 2 (3.6%) women, and the mean age was 24.3 years (± 4.5 years); 44 athletes played elite-level soccer (80%), 10 played professional rugby (18.2%), and 1 was an international-level taekwondo fighter (1.8%). Mean time between injury and MRI was 6.3 ± 10.3 days. Mean time between injury and clinical examination by the treating surgeon was 13.1 ± 18.9 days. A total of 42 (76.4%) of athletes were seen within 1 week of injury. Five (9.1%) had delayed presentation of between 33 and 103 days, as an initial injury had appeared innocuous and treatment was only sought after reinjury or because of swelling or instability. Clinical and MRI findings are shown in Table 1. Follow-up for playing rates was between 2 and 9 years inclusively. Mean follow-up was 5.3 years.

Table 1.

LCL MRI and Examination Findings (N = 55) ^a

Characteristic	Clinical LCL Laxity at 30°	Patients
MRI grade 1	None	5 (9.1)
	Grade 1	6 (10.9)
	Grade 2	0
	Grade 3	0
MRI grade 2	None	1 (1.8)
	Grade 1	14 (25.5)
	Grade 2	1 (1.8)
	Grade 3	1 (1.8)
MRI grade 3	None	1 (1.8)
	Grade 1	21 (38.2)
	Grade 2	5 (9.1)
	Grade 3	0
Clinical LCL laxity at 30°	None	7 (12.7)
	Grade 1	41 (74.5)
	Grade 2	6 (10.9)
	Grade 3	1 (1.8)
Injury location on MRI	Proximal third	2 (3.6)
	Middle third	5 (9.1)
	Distal third	26 (47.3)
	Fibular insertion	22 (40.0)

^aData are presented as n (%). LCL, lateral collateral ligament; MRI, magnetic resonance imaging.

Return to Play

All athletes (100%) returned to play, at the same or higher level, at a mean of 103 ± 87 days and median of 76 days (range, 0-422 days). One athlete was able to RTP and finish the game during which he got injured, as well as compete in the subsequent games and so official diagnosis was delayed, as an MRI was not performed for 3 weeks postinjury. The time taken between injury and RTP showed significant variation.

RTP time for all soccer and rugby players is shown in Figure 5. There was a mean time between injury and first match of 96.8 ± 75.6 days. The mean RTP for rugby was 78 days and for soccer was 101 days. Nine soccer players, including the one with grade 3 laxity, took >20 weeks to RTP: 1 had subsequent fixation of an osteochondral defect, 1 had a subsequent partial lateral meniscectomy following failure of a previous lateral meniscal repair, and the others were noted to be available for selection but either did not make the team or were affected by Covid-19 sporting restrictions. The mean RTP for soccer players, excluding the 5 with known, non–LCL related reasons for delayed RTP, was 77 ± 48 days.

Figure 5.

Return to play times for soccer and rugby players.

At 2 years, 51 patients (92.7%) were still playing their elite sport; 32 athletes were >5 years postinjury; and of these, 27 (84.4%) were still playing at elite level (Figure 6).

Figure 6.

Return to play and playing rates at 2 and 5 years.

Of the total cohort, 41 (74.5%) athletes were still competing while the study was being performed. Mean career longevity after the injury was 59.3 ± 29.7 months.

Mean age at the time of retirement was 32 ± 3.3 years. The mean age of the athletes still playing was 28 ± 6.2 years. None of the athletes who had retired had done so because of sequelae caused by the LCL injury.

Correlation Between MRI and Clinical Grades

The mean time between injury and MRI was 6.4 (range, 1-49) days and between MRI and consultation was 10.1 (range, 1-56) days.

MRI grading and clinical grading demonstrated low correlation (r = 0.37; P = .01). Although 27 athletes (49.1%) had grade 3 injuries on MRI (Figure 7) only 1 had grade 3 laxity on clinical examination at the initial consultation.

Figure 7.

Magnetic resonance imaging grade 3 lateral collateral ligament tear distal third in a 23-year-old soccer player 5 days following a hyperextension injury who returned to play at 39 days from injury at the same level.

Follow-up

A total of 21 patients returned for second consultation with the treating surgeon. For the remainder, close contact with the athletes’ medical teams established that there were no ongoing issues for the players concerned, and so clinical follow-up was deemed unnecessary. Mean follow-up in the 21 cases was at 44 days. No athletes reported instability or any other symptoms.

At final clinical examination, no athlete had grade 2 or 3 laxity. Six of the 21 athletes had grade 0 clinical laxity (28.6%; all 6 athletes had initial grade 1 clinical laxity), and 15 athletes had grade 1 clinical laxity (71.4%; 1 athlete with initial grade 3 clinical laxity, 4 patients with initial grade 2 clinical laxity, and 10 athletes with initial grade 1 clinical laxity).

One patient (1.8%) suffered an LCL reinjury 42 months after the initial injury, which was again successfully treated nonsurgically.

Discussion

The most important findings of the present study are that MRI and clinically isolated LCL injuries (ie, without rotatory laxity excess) can be successfully treated nonoperatively in elite athletes and that MRI grading of injury severity has low correlation with clinical grading. The present study is believed to be the largest published series of isolated LCL injuries in any patient group. It highlights that grade 3 clinical laxity is rare in isolated LCL injuries. However, given that this is only in 1 athlete, it is not possible to draw any conclusions regarding nonoperative management of clinical grade 3 injuries.

A secondary finding is that, contrary to previous reports suggesting that most LCL injuries are at the fibular insertion,^13,16 the present study found that only 40% are at the fibular insertion but that 47.3% are in the distal third of the LCL.

Surgical management of LCL injuries became commonplace ⁹ following Kannus’ ¹⁵ review of the nonoperative treatment of injuries of the LCL with clinical grades 2 and 3 in only 23 patients, which found that clinical grade 3 LCL injuries, when treated nonsurgically, showed increased laxity. However, this is in common with other studies and included all patients with PLC injuries, not just those with isolated LCL injuries. Of the 67 patients with PLC injuries in the current study, only 5 (7.5%) patients required surgery, but 4 of these were excluded as they involved surgery to more than just the LCL. One patient was excluded because of operative treatment of an isolatetd LCL injury.

Kannus ¹⁵ found that 14 (60%) of the patients included in that study had rotatory instability, indicating that their cases were likely not truly isolated LCL tears and actually included injury to the popliteal complex, which would require surgery in any case according to the present study’s senior authors’ (A.W.) indications for surgery.

Although LaPrade et al ²¹ supported surgical reconstruction for clinical grade 3 LCL injuries, only 4 of 20 patients included in that series had truly isolated LCL injuries. Geeslin and LaPrade ⁸ also reported favorable outcomes with surgical management, although only 24% (7/29 patients) had isolated PLC injuries, with the remaining 22 of 29 having concomitant cruciate ligament lesions. Further, 2 of 29 (6.9%) had isolated LCL injuries. ⁸ The surgical indications in the aforementioned studies included acute combined varus and posterolateral rotatory instability ⁸ or notable side-to-side instability during activities. ²¹ The surgical indications in the present study, however, differ from this and are mentioned above.

There is very little published literature regarding operative treatment of isolated LCL injuries and even less on their nonoperative management. Current treatment recommendations in existing literature for isolated LCL injuries are based on heterogeneous patient populations with small case numbers, concomitant pathologies (non-PLC injuries), and/or concomitant rotatory instability. The best treatment course for truly isolated LCL lesions is therefore uncertain.

In 2010 Bushnell et al ⁵ reported on 9 National Football League (NFL) elite athletes with MRI grade 3 LCL tears, comparing surgical repair and nonsurgical treatment. Five players were treated without operation. Sikka et al ³² in a review of isolated fibular collateral ligament injuries in athletes documented the outcomes of 30 NFL players based on a survey of their medical teams. Eight of these cases were MRI grade 3 injuries, 7 with a palpable defect in the LCL, but as laxity was only reported as >5 mm, it is unclear if they had grade 2 or 3 varus laxity. In both these studies, all players were able to RTP.^5,32 Bushnell et al found that the mean RTP time for the nonoperative group was 2 weeks compared with a mean of 14.5 weeks RTP time in the surgical group. ⁵ Mean RTP in the study by Sikka et al varied between 1.3 weeks for grade 1 and 4.6 weeks for grade 3 injuries. The nonsurgically treated athletes in both studies had a significantly shorter mean RTP time when compared with the present study’s patients, but they reported return to any sport, not first match appearance, which would shorten the time. In the NFL, it is also possible to compete and play while wearing a brace, which is not allowed in other sports and which would also contribute to the difference in RTP time. ⁵

Both Davenport et al ⁶ and Haddad et al ¹⁰ published single case reports of 16-year-old high-level athletes treated nonsurgically for an isolated MRI-based grade 3 LCL injury. RTP time was stated with 3.5 months from Davenport et al and with 4 months from Haddad et al. Both described RTP at previous level in a comparable time with the present study.

Outcomes reported after LCL injury have also included clinical laxity. In the study by Bushnell et al, ⁵ all the NFL athletes in the nonoperative group had residual varus laxity (4 of 1-5 mm; grade 1), and 1 had >5 mm (grades 2-3). Two (50%) of the surgically treated cases also had grade 1 laxity. In the study by Sikka et al, ³² all 8 NFL athletes with grade 3 injuries had residual grade 1 laxity. In the present study, regardless of acute postinjury laxity, of the 21 cases available for review, 15 had grade 1 laxity. This may be disproportionaly high, as follow-up with the treating surgeon was not required if the players’ medical team did not have any concerns. No cases had grade 2 or 3 clinical laxity on final follow-up.

Although other studies have reported varus laxity after operative treatment of PLC injuries, the International Knee Documentation Committee (IKDC) objective scoring system was used. As it measures laxity at 20°, it is not a direct comparison with the measurements reported in the current or previously quoted studies. Geeslin and LaPrade ⁸ published postoperative laxity data on clinical grade 3 PLC injuries treated surgically. Out of 26 patients who were followed up, 25 showed normal lateral joint laxity at 20° of flexion (IKDC A) and 1 patient had abnormal laxity (IKDC C). The IKDC system also was used by LaPrade et al ²¹ who presented IKDC A (normal) laxity at 20° of flexion after surgical treatment of PLC injuries in all 20 of their reassessed patients in their series.

The mean age in the present study was 24.3 years, and at 5 years (ie, 29 years of age), 84.4% of cases were still playing. This compares well with the rate of “average” professional soccer players in the United Kingdom still playing at the age of 29 years at 71.9%. ¹² This, and the fact that there was only 1 known repeat LCL injury in the cohort of the present study suggests that nonoperative treatment is not only effective in allowing RTP (100% in the present study) but also does not affect career longevity at all.

In common with Bushnell et al, ⁵ data presented by them support the findings of the present study of 100% RTP and that MRI grading of LCL injury does not correlate with clinical grading. All 9 patients in that study showed MRI-based grade 3 injuries, of whom 6 presented with clinical grade 1 injuries and the other 3 patients’ laxity was described as >5 mm (equivalent to a grade ≥2 injury).

The present study showed low correlation between MRI grading and clinical grading (r = 0.37), as some radiologically severe tears were not found to be associated with significant laxity. This calls into question the fundamental concept as to how complete ruptures on MRI can be associated with only minor laxity. Several of the included patients with complete tears in MRI also had ultrasound evaluations that confirmed a complete rupture. The answer to this apparent paradox is likely related to the collateral support conferred through the local anatomy. Another issue is the difficulties of imaging the LCL: it is relatively small and passes obliquely in the sagittal plane and is therefore rarely seen in a single image. The LCL lies within a tough sheath, and if this remains intact it could provide resistance to varus stress. Also, there may be consequences from the fact that the biceps tendon splits to pass both medial and lateral to the distal LCL around which there is a bursa. ³³ Perhaps the fact that the distal LCL is “gripped” by the distal biceps may be a factor in providing stability. It certainly could affect the site of LCL rupture by providing a “stress riser,” which would fit with the majority of tears occurring in the distal third of the ligament as shown in the present study. In the senior authors’ experience, in those cases needing posterolateral repair/reconstruction, a common site found for an LCL rupture is at the level where the distal LCL disappears between the limbs of the biceps tendon. In addition, it is likely that despite the small cross-sectional area of the LCL (which might suggest poor healing potential because of the LCL sheath and relationship to the distal biceps tendon, which could hold the LCL), well-aligned, nonoperative treatment of these isolated lesions do so well clinically.

Limitations

There are several limitations to the study. Besides the retrospective design of this work, a control group is missing, which could have given this study even more significance. The clinical grading of LCL injuries was based solely on the treating surgeon’s clinical examination. There were no objective measurements of clinical laxity because this is a retrospective study and instrumented laxity measurements and stress radiographs were not undertaken at the time.^19,25

Although only 21 (38.2%) athletes attended for clinical follow-up by the treating consultant, and so there can be less certainty regarding ultimate clinical laxity outcome, this is still more cases than most other reports on the management of LCL injuries.

In common with the other studies, another limitation is that no patient-reported outcomes (PROs) are described. To our knowledge, no PRO measures have been shown to be valid in this group while in nonsurgically treated ACL-injured patients, they have been shown to have a low correlation with functional performance. This suggests that RTP, which is of the most interest to the player and his or her teams, is a more appropriate outcome to be used.

Although the knowledge that 100% of cases in this high-demand group do RTP and at least to the same level is noteworthy, conclusions about RTP time are less clear-cut. Figure 5 highlights the abnormal distribution of RTP times, which can be affected by many factors unrelated to the LCL injury. In addition to the delaying factors previously discussed, RTP time can also be affected by breaks between seasons or international breaks. Players about to RTP toward the end of a competitive season often decide to wait until the next season, causing a delay in RTP of up to 8 weeks in elite soccer. Unlike other studies, RTP is based on the first match appearance rather than the return to training; therefore, a player may be fit to play but fail to be selected. Nevertheless, it is important to include these, as unexpected situations occur in real life that influence RTP time in a negative way.

Both a limitation and a strength is the restricted patient cohort of elite athletes only, meaning the results are not necessarily applicable to the general public. However, the heightened demands placed on athletes’ knees give a more robust assessment of treatments’ effectiveness, as the patients in this group test their knees far more than the general population does, and adverse outcomes would be more likely to be apparent and reported.

Conclusion

The current data suggest that nonoperative management of isolated LCL injuries is associated with high return to preinjury level of sport (100%), reasonable recovery times (median of 76 days [2.5 months]), and no significant residual varus laxity. There is a low correlation of MRI grade in isolated LCL injury with clinical examination findings. The authors recommend these lesions be treated without surgery.