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Posterolateral Corner Injury of the Knee: Evaluation and Management

Ranawat, Anil MD; Baker, Champ L. III MD; Henry, Sarah MD; Harner, Christopher D. MD

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Journal of the American Academy of Orthopaedic Surgeons: September 2008 - Volume 16 - Issue 9 - p 506-518
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Interest in the posterolateral corner (PLC) of the knee joint has increased because recent biomechanical and anatomic studies have elucidated its importance in knee stability. Improvements in imaging modalities as well as heightened suspicion during the clinical examination have led to an increased recognition of these injuries. A recent magnetic resonance imaging (MRI) analysis of surgical tibial plateau fractures demonstrated an incidence of PLC injuries in 68% of cases.1 Although isolated PLC injuries are uncommon, making up <2% of all acute knee ligamentous injuries,2,3 incidence of PLC injuries associated with concomitant anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) disruptions are much more common (43% to 80%).3-5

Prompt recognition of PLC injuries is critical for their successful treatment. Untreated PLC injuries increase the failure rates for both ACL and PCL reconstructions.6-10 Also, increased evidence supports reports of morbidity in untreated or improperly treated PLC injuries.7,11 Finally, in most cases, immediate surgical intervention on the knee has shown superior outcomes.2-5,11,12


Recent anatomic and biomechanical studies have more clearly defined the complex arrangement among the various anatomic structures composing the PLC of the knee. Initial study of the region grouped numerous structures together and referred to them as the arcuate ligament complex. Focus has now shifted to individual anatomic structures, including the lateral (ie, fibular) collateral ligament (LCL), the popliteus tendon complex, popliteofibular ligament (PFL), and the posterolateral capsule4,5,13,14 (Figure 1).

Figure 1
Figure 1:
Illustration of the anatomy of the posterolateral corner demonstrating the three major components: lateral (fibular) collateral ligament, popliteus tendon, and popliteofibular ligament. (Reproduced with permission from LaPrade RF, Ly TV, Wentorf FA, Engebretsen L: The posterolateral attachments of the knee. Am J Sports Med 2003;31:854-860.)

The LCL is the primary static restraint to varus opening of the knee.15-17 The femoral insertion is typically located just proximal and posterior to the lateral epicondyle in a small depression between the lateral epicondyle and supracondylar process. Distally, the LCL attaches to the fibular head a mean of 8.2 mm posterior to the most anterior aspect of the fibular head.18-20

The popliteus tendon complex consists of the popliteus muscletendon unit and the ligamentous connections from the tendon to the proximal fibula (ie, the popliteofibular), the tibia (ie, the popliteotibial), and the meniscus (ie, the popliteomeniscal).6 The popliteal muscle originates from the posteromedial aspect of the proximal tibia and gives rise to its tendon, which courses intra-articularly through the popliteal hiatus of the coronary ligament to insert on the popliteal saddle on the lateral femoral condyle.19 LaPrade et al19 found that the femoral insertion site of the popliteus was consistently anterior and distal to the femoral attachment of the LCL, with a mean oblique distance of 18.5 mm between them. Brinkman et al18 reported more variability in the popliteus tendon femoral insertion, with a mean distance of 11 mm distal and either anterior or posterior to the LCL. The three popliteomeniscal fascicles extend from the tendon to the lateral meniscus and assist in providing dynamic stability to the meniscus.21

The PFL is present in 94% to 100% of anatomic dissections.22,23 It arises from the myotendinous junction of the popliteus and courses distally and laterally to insert on the fibular styloid process. The PFL consistently demonstrates an anterior and posterior division, inserting from 1.6 to 2.8 mm distal to the tip of the fibular styloid.19

Other structures provide additional static and dynamic stability to the PLC. The iliotibial (IT) band is composed of multiple layers and blends with a confluence of the short head of the biceps to form an anterolateral sling about the knee.20 The long and short heads of the biceps femoris muscle provide dynamic stability, with the fabellofibular ligament being a thickening of the distal capsular edge of the short head of the biceps. The common peroneal nerve is located on the posterior border of the long head of the biceps.20 The mid third of the lateral capsular ligament is a thickening of the lateral capsule and is thought to be an important stabilizer to varus stress.13,20 Finally, the lateral meniscus increases the conformity and thus the stability of the lateral compartment, which is inherently unstable due to the convex nature of the compartment.


The structures of the PLC function primarily to resist varus rotation, external tibial rotation, and posterior tibial translation.15,17 Previous biomechanical studies, through selective sectioning of structures, provided evidence of the importance of the LCL, popliteus tendon, and PFL in resisting these movements, both singularly and in concert with the PCL.15-17,22,24,25 Current studies now focus on measuring direct forces in the individual structures during joint loading, further defining the complex interrelationships of the PLC and the primary functions of the LCL, popliteus tendon, and PFL.26

The LCL is the primary static restraint to varus opening of the knee.15-17 Direct force measurements of the LCL during an applied varus moment demonstrate loading responses at all angles of knee flexion, with the response at 30° of flexion significantly higher than at 90° of flexion.26 The individual ultimate tensile strength of the LCL has been determined to be 295 N.27 Isolated sectioning of the PCL has no effect on varus rotation; however, when the posterolateral structures are deficient, additional sectioning of the PCL produces a significant increase in varus rotation, indicating a role for the PCL as a secondary restraint.15,17

The PLC is the primarily stabilizer of external tibial rotation at all knee flexion angles. In studies by both Gollehon et al15 and Grood et al,17 isolated sectioning of the PLC produced a maximal average increase of 13° of rotation at 30° of knee flexion, which decreased to an average of 5.3° at 90°. Conversely, isolated sectioning of the PCL had no effect on external tibial rotation.15,17 Combined injury to the PCL and posterolateral structures produced significantly greater increases in external tibial rotation, especially at 90° of knee flexion (20.9°).17 These studies provide the biomechanical rationale for performing the dial test at 30° and 90° of flexion to determine the presence of an isolated PLC or combined PLC/PCL injury.28

In a recent cadaveric study, La-Prade et al26 found that the mean load responses to external rotation in the LCL were significantly higher than those of the popliteus tendon and PFL at 0° and 30° of flexion, whereas the popliteus and PFL demonstrated higher loads at higher knee flexions, peaking at 60°. The authors concluded the LCL, popliteus tendon, and PFL performed complementary roles as stabilizers to external rotation, with the LCL assuming a primary role at lower knee flexion angles and the popliteus complex assuming a primary role with higher knee flexion.

The dominant restraint to posterior tibial translation is the PCL. Isolated sectioning of the PCL produces increased posterior tibial translation at all angles of knee flexion, with a maximum at 90° (11.4 mm); isolated sectioning of the PLC structures also produces increased posterior tibial translation at all angles of knee flexion, with a maximum at early knee flexion.15,17 Therefore, the PLC, not the PCL, is the primary restraint to posterior tibial translation near full knee extension.17,29 Combined sectioning studies of both the PCL and PLC have demonstrated significant increases in posterior translation (21.5 mm) at 90° of flexion compared with the intact knee or knees with isolated PCL or posterolateral deficiency.15,17,24 Others have reiterated this strong functional interaction between the popliteus and the PCL; they also have shown how the popliteus acts as both a static and dynamic stabilizer of the knee.22,25,30 In a cadaveric study, Harner et al30 found that loading the popliteus in an intact knee reduced in situ forces in the PCL in response to a posterior load, whereas in a PCL-deficient model, loading of the popliteus reduced posterior translation at a maximum of 30° of knee flexion.

Biomechanical analysis of posterolateral deficiency in the setting of ACL or PCL reconstruction further demonstrates the interdependent relationship of the PLC structures and the cruciate ligaments. After sectioning the posterolateral structures, LaPrade et al31 noted increased loads in the ACL graft with application of varus and coupled varus-internal rotation moments. Because of these significantly increased loads, the authors recommend reconstruction or repair of a grade III PLC injury at the time of ACL reconstruction.

Other investigators have noted increased forces in a PCL graft in the setting of posterolateral deficiency.6,32,33 In an analysis of PCL reconstruction, Harner et al6 sectioned the posterolateral structures and, compared to knees with intact posterolateral structures, found an increased posterior tibial translation in the reconstructed knees of 6 mm at 30° and 4.6 mm at 90° of flexion, increased external rotation of up to 14°, and increased varus rotation of up to 7°. Forces on the PCL graft increased significantly by 22% to 150% under all loading conditions. Thus, failure to recognize and treat a PLC injury would result in increased stresses and possible failure in PCL reconstruction; for this reason, a combined reconstruction is recommended.6 Similarly, in a combined PCL/PLC injury model by Sekiya et al,32 reconstruction of both structures produced more nearly normal knee kinematics.

There has been a recent trend toward more anatomic reconstruction techniques, specifically, reconstructing the three most critical biomechanical structures that control varus and external rotation: the LCL, popliteus tendon, and PFL.34,35 In a cadaveric study, an anatomic reconstruction demonstrated no significant difference between the intact and reconstructed knee to varus load at 0°, 60°, and 90° of flexion or to external torque at any flexion angle.34 However, two other recent biomechanical studies, in which all three functional components were anatomically reconstructed, separately documented overconstraint of internal rotation and varus rotation, respectively.35,36

Clinical Evaluation

A correct diagnosis of posterolateral rotatory instability depends on an accurate history, including the mechanism of injury and presenting symptoms as well as an appreciation of the subtleties of a complete knee examination.5 Common mechanisms of injury include a posterolaterally directed blow to the anteromedial proximal tibia, with resultant hyperextension; a noncontact hyperextension and external rotation twisting injury; direct blow to a flexed knee; or highenergy trauma.4,5,13,14,28,37 In cases of high-energy trauma, the history may be difficult to elicit and may aid little in making the diagnosis.

Injuries to the PLC are often combined with other ligamentous injuries, especially those of the PCL.3-5 Associated instability patterns may sometimes obscure the PLC injury; therefore, the physician must maintain a high index of suspicion based on the mechanism of injury and symptoms. In a combined injury, the possibility should be considered of a knee dislocation that spontaneously reduced before evaluation. A complete neurovascular assessment should be performed, with attention paid to the integrity of the popliteal vessels and the function of the peroneal nerve. Calculation of an anklebrachial index should be done to assess the vascular status of the limb. Vascular studies (eg, arteriography) should be obtained when necessary.

Examination of the injured extremity begins with an evaluation of overall limb alignment and gait. Patients may have a standing varus alignment and demonstrate a varus or hyperextension varus thrust during the stance phase of gait.3,14,28 In the acute setting, tenderness to palpation or ecchymosis about the posterolateral aspect of the knee may be present. Ligamentous examination is performed on both knees to provide a comparison between the injured and normal state.

Specialty testing should include tests for both varus and rotational deformities. Varus testing or collateral stress testing is performed at 0° and 30° of flexion. Until proven otherwise, clinically detectable varus opening at 0° is indicative of a severe posterolateral injury and an associated cruciate injury;13,14 however, isolated cruciate injuries do not affect varus stability.15,17 Isolated injuries to the posterolateral structures usually result in maximum varus opening at 30° flexion, but PLC injury patterns do exist in which there is minimal varus deformity with significant rotational instability (eg, popliteus injury, PFL injury).

The most commonly used test to assess external rotation is the dial or posterolateral rotation test.15,17,24 The examiner places one hand behind the posterior proximal tibia for support to ensure the tibia is maintained in a reduced position. With the other hand, the examiner holds the patient’s foot and externally rotates the foot at both 30° and 90° of flexion. Veltri and Warren28 determined a 10° difference in external rotation at 30° to be evidence of pathology to the PLC. When examination at 90° of flexion reveals a decrease in the amount of external rotation compared to 30°, then injury to the PLC is isolated. When there is further increased external rotation at 90°, then a combined PCL/PLC injury is present.15,17,24

Other external rotational tests include the external rotation recurvatum, the posterolateral drawer,38 and the reverse pivot-shift.39 In the external rotation recurvatum test, a knee with a PLC injury will fall into relative hyperextension laterally, and the tibia will externally rotate into relative varus. For the posterolateral drawer test, the knee is flexed to 80°, and the foot is externally rotated while a posterior load is applied. A positive result occurs when the lateral tibial plateau rotates posteriorly and externally relative to the medial tibial plateau.38,40 Finally, the reverse pivot-shift test is performed, with the knee being taken from a position of 90° flexion into extension under a valgus load during simultaneous external rotation of the foot. A positive test result occurs when the posteriorly subluxated lateral tibial plateau abruptly reduces at 20° to 30° of flexion as the IT band changes from a flexor to an extensor of the knee.4,41 LaPrade and Terry37 found statistically significant associations between a positive reverse pivot-shift test and injury to the LCL (P = 0.01), mid third lateral capsular ligament (P = 0.02), and popliteal components (P = 0.01).


To be complete, a classification or grading system of the PLC must include assessment of both varus and rotational stability compared with those of the contralateral limb. In addition, the time of the injury is critical. Acute injuries are usually defined as of <3 weeks, but they can be repaired for up to 4 to 6 weeks. After this period, they are considered chronic injuries.

The most commonly used classification system, that of Hughston et al,14 defines injury severity based primarily on varus instability. Grade I injuries are sprains without tensile failure of any capsule-ligamentous structures, with little or no varus instability (0 to 5 mm). Grade II injuries are partial injuries with minimal abnormal laxity (6 to 10 mm). Grade III injuries are complete disruptions with significant laxity (>10 mm), probably representing associated injuries.14,40 Rotational instability is then defined by the dial test, with instability defined as an increase in external tibial rotation of 10° compared with that of the contralateral knee.28 A problem with this grading system is that it minimizes the importance of rotational instability; many PLC injuries may have significant rotational instability with minimal varus instability.

Fanelli and Larsen42 attempted to incorporate more fully both external rotation and varus instability by defining posterolateral instability as being of three types. Type A is an isolated rotational injury to the PFL and popliteus tendon complex. Type B is a rotational injury with a mild varus component representing an injury to the PFL and popliteus tendon complex as well as attenuation of the LCL. A type C posterolateral instability has a significant rotational and varus component secondary to complete disruption of the PFL, popliteus tendon complex, LCL, lateral capsule, and cruciate ligament or ligaments.

We commonly use the traditional grading system,14,40 but we define the grade of injury based on both rotational and varus instabilities. We believe that grade I injuries have minimal instability (either varus or rotational instability of 0 to 5 mm or 0° to 5°), grade II injuries have moderate instability (6 to 10 mm or 6° to 10°), and grade III injuries have significant instability (>10 mm or >10°). (Varus instability is measured as an absolute number, whereas rotational instability is a side-to-side difference.) Thus, a patient may have a grade III injury from primary rotation instability (eg, >15°) with minimal varus laxity. As with all PLC classification systems, this system has not been validated. For the most part, grade III injuries are treated surgically, whereas grade I and some grade II injuries are treated nonsurgically. Our treatment algorithm based on this classification system is presented in Figure 2.

Figure 2
Figure 2:
Treatment algorithm for management of posterolateral corner injury based on injury grade. Grade I injuries = minimal instability (ie, varus or rotational instability of 0 to 5 mm or 0° to 5°). Grade II injuries = moderate instability (ie, 5 to 10 mm or 5° to 10°). Grade III injuries = significant instability (>10 mm or >10°). LCL = lateral collateral ligament, PFL = popliteofibular ligament


Imaging studies are a reliable modality to help accurately diagnose PLC injuries. Although standard posteroanterior and lateral radiographs of the knee are often normal, they may show either avulsion or tibial plateau fractures. Common avulsion injuries include the “arcuate” sign (ie, fibular head fracture),43 femoral popliteus tendon avulsion, Segond fracture, or Gerdy tubercle avulsion.44 Identifying these bony avulsion injuries is critically important because, when they are recognized acutely, they may be treated by primary repair. Stress radiographs document abnormal joint space widening; oblique radiographs also may demonstrate subtle fractures. In chronic PLC injuries, a long-leg, standing, hip-to-ankle radiograph is essential to determine alignment by the use of a weightbearing line because an osteotomy may be necessary to correct varus malalignment. Chronic PLC injuries also may show signs of arthritic changes in both the medial and lateral compartments.7

MRI is helpful in elucidating the complex anatomy of the PLC. High signal (>1.5 T) MRI with standard T1-weighted, T2-weighted, proton density, fat-saturated, and gradient echo sequences with coronal, axial, and sagittal views is the primary method to assess injuries. Standard views provide accurate visualization of the LCL, popliteus, biceps femoris, gastrocnemius, and IT band. Thin-slice coronal oblique images through the entire fibular head and styloid also may be used to improve the accuracy as well as sensitivity and specificity of identifying structures of the PLC, including the popliteofibular, arcuate, and fabellofibular ligaments.44,45

The PFL is visualized by MRI in 53% to 68% of cases.43-45 PLC injuries are rarely isolated, and confirmation of associated meniscal and cruciate pathology is critical in the formulation of the treatment plan. MRI is a useful tool in the evaluation of both acute and chronic PLC injuries (Figure 3). In the acutely injured knee, an accuarate examination may be difficult to obtain; MRI helps to identify the injured structures as well as the pattern of injury.44 The use of MRI does not, however, replace a thorough physical examination, which should be the ultimate determinant of disability and the need for surgical or nonsurgical treatment.

Figure 3 A,
Figure 3 A,:
Coronal fast-spin-echo MRI scan of an acute posterolateral corner (PLC) injury, with avulsion of the popliteus (black arrow) off the femur and of the lateral collateral ligament (white arrow) and biceps (black arrowhead) off the fibula. B, Sagittal T1-weighted MRI scan of a chronic PLC injury, with an intact popliteus tendon (white arrowhead) but signs of chronic attenuation of the popliteofibular ligament (white arrow).



The natural history of PLC injuries depends on the severity or the grade of injury. In their study of grade I and II LCL injuries managed nonsurgically, Krukhaug et al11 reported good results for grade I injuries treated with early mobilization. Similarly, Kannus7 reported good results for grade II injuries managed nonsurgically with minimal radiographic changes at follow-up (mean, 8 years), despite persistent laxity. Conversely, in both studies, patients with grade III injuries treated nonsurgically reported fair functional outcomes, poor strength, and persistent instability.7,11 Up to 50% of these patients had osteoarthritic radiographic changes in both the medial and lateral compartments.7,11 These clinical studies are consistent with the rabbit model of LaPrade et al,46 in which, following creation of a grade III injury by sectioning of the LCL and popliteus tendon, medial chondromalacia was noted at 12 weeks.

Studies suggest that nonsurgical treatment consisting of early mobilization results in acceptable outcomes for grade I and some grade II tears, but it leads to residual laxity and poor functional outcomes with all grade III and some grade II injuries.7,11 All grade II and III patients treated surgically in these studies were found to have improved varus stability and good functional results; therefore, grade III injuries should be treated surgically.

The ideal management of isolated grade II injuries remains unclear. Although good functional results have been reported, residual laxity remains a problem.7,11 This is likely multifactorial, dependent on individual patient factors and goals as well as the acuteness and nature of the injury. Our present protocol for nonsurgical management includes use of crutches with a hinged knee brace for 4 to 6 weeks. Early extension immobilization is then followed by progressive motion, weight bearing, and strengthening, with return to full activity in 3 to 4 months.


Acute Injuries

PLC injuries are best treated in the acute stage, before significant capsular scarring and soft-tissue stretching occur. This can be done by direct repair, with or without augmentation, or by primary reconstruction. Acute (immediate) repair generally gives more favorable results than does chronic (late) reconstruction because of the restoration of native anatomy and normal biomechanics2-5,11,12 (Figure 4). Repairs performed early (ie, <3 weeks) usually provide superior results.11,12,47-49

Figure 4
Figure 4:
Acute repair techniques of posterolateral corner (PLC) injuries. A, Injuries to the critical structures of the PLC. B, A sequential acute repair of the deep structures (popliteus complex, lateral collateral ligament, and capsule) and superficial structures (biceps and iliotibial band). (Reproduced with permission from Chhabra A, Cha PS, Rihn JA, et al: Surgical management of knee dislocations. J Bone Joint Surg Am 2005;87[1 suppl 1]:1-21.)

Some authors support reconstruction over repair in the acute setting. In a large series of 56 patients (57 PLC tears), Stannard et al50 reported that the failure rate was 37% (13/35) for the acute (immediate) repair cohort versus 9% (2/22) for the group reconstructed with a modified twotailed anatomic technique. The reason for this discrepancy may have to do with the fact that most of the cruciate injuries of these knees were not treated primarily but were staged in treatment. Both groups were started on an early aggressive physical therapy protocol, and, because acute repairs require healing, the reconstruction group may have done better because of their more rigid repair within the setting of early postoperative range of motion. Although this controversy still exists, it is generally agreed that immediate surgical intervention, with or without local soft-tissue augmentation, is superior to late reconstruction regarding the ability to restore dynamic function of the structures of the PLC.

A few basic principles exist for acute PLC primary repairs. First, one must diagnose and address all concomitant injuries.9,10,31 Second, avulsion injuries are best treated with either rigid internal fixation or sutures, depending on the nature of the avulsion. Third, although midsubstance repairs of the LCL can be performed, these are best treated acutely with a repair of the intrasubstance tear and a graft reconstruction. This is because of the inconsistent healing of the LCL, higher published failure rates (37% for acute repair versus 9% for acute reconstruction), and limited success in treating chronic LCL insufficiency.50,51 Fourth, the peroneal nerve may need to be released if there is any clinical evidence of compression or if required for safe exposure. Finally, for combined acute injuries, an attempt should be made to address all concomitant injuries at the same setting; however, this must be balanced against the increased risk of arthrofibrosis.52

Chronic Injuries

The treatment of chronic PLC injuries differs from that of acute disruptions. Beyond 4 to 6 weeks from injury, significant pericapsular scarring makes it difficult to localize and repair discrete structures; thus, reconstruction is favored. In addition, chronic injuries may become associated with significant capsular stretching, leading to a more extensive rotational instability pattern, persistent subluxation, and the development of arthrosis.4,7,11

Evaluating lower limb alignment and gait patterns in patients with chronic PLC instability is critically important. Any PLC reconstruction in the setting of untreated malalignment will have a higher failure rate as a result of the increased forces across the reconstruction.2,47,53,54 In the setting of a varus thrust and malalignment (approximately 3° of varus discrepancy, or 30% of the preoperative weight-bearing line), a high tibial opening wedge medial osteotomy is considered before any attempted reconstruction.48,54 If the patient has residual instability or pain following the osteotomy, then a PLC reconstruction can be performed in a staged fashion.

Although general consensus supports improved outcomes after PLC reconstruction for chronic injuries,2,4,9,12,47,48,55 there is no benchmark reconstructive procedure.4,40,51 PLC reconstructions can be broadly divided into two categories: nonanatomic and anatomic.40 Nonanatomic reconstructions do not directly address injured functional anatomic structures but provide primary varus support by advancement procedures in a nonisometric fashion. These reconstructions are primarily historical procedures and include biceps tenodesis, arcuate complex or proximal bone block advancements, extracapsular IT band sling, or miscellaneous augmentations.2,4,53,56,57

As reconstruction gradually began to focus on the specific anatomic structures of the PLC, Muller58 was one of the first to advocate separate reconstruction of both the LCL and popliteus with his popliteal bypass. Anatomic reconstruction can be broadly separated into fibular-based and combined tibial-fibular-based reconstructions. Larson59 was one of the first proponents of a fibular-based technique, which reconstructs both the LCL and PFL ligament (Figure 5). Similar reconstructions have also been described by Veltri and Warren12 with a two-tailed technique and other figure-of-8 reconstruction constructs. These fibular-based tech-niques were groundbreaking because they were the first ligament-specific reconstructions. They are still often used because they are less technically demanding and have good clinical outcomes compared with more anatomically accurate reconstructions.60

Figure 5
Figure 5:
Lateral view of Larson type reconstruction of the lateral (fibular) collateral ligament and the popliteofibular ligament. (Adapted with permission from Larson R, Tingstad E: Lateral and posterior instabilities of the knee in the adult, in DeLee JC, Drez D [eds]: DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice, ed 2. Philadelphia, PA: Saunders, 2003, pp 1968-1993.)

Combined tibial-fibular-based techniques are a recent trend in PLC surgery. These techniques reconstruct all three primary functional components of the PLC—the LCL, popliteus, and the PFL—in accordance with the proper insertion site anatomy of each.18,19 Noyes and Barber- Westin61 describe an anatomic LCL and popliteus reconstruction with plication of the posterior capsule to reconstruct the PFL. Similarly, LaPrade et al34 reconstructed all three components with two separate femoral tunnels and two grafts (Figure 6). Other anatomic combined techniques that pay particular attention to the PFL have been described by Sekiya and Kurtz62 and Yoon et al.63

Figure 6
Figure 6:
Lateral view of the LaPrade anatomic reconstruction technique of the lateral (fibular) collateral ligament (LCL), popliteofibular ligament (PFL), and popliteus tendon (PLT). Note that the PFL reconstruction is situated just posterior to the head of the fibula. (Reproduced with permission from LaPrade RF, Johansen S, Wentorf FA, Engebretsen L, Esterberg JL, Tso A: An analysis of an anatomical posterolateral knee reconstruction: An in vitro biomechanical study and development of a surgical technique. Am J Sports Med 2004;32:1405-1414.)

Despite the numerous reconstructive techniques reported in the literature, data on long-term results of PLC reconstruction are limited.4,53,57 Most studies focus on combined PCL reconstructions with nonanatomic PLC techniques.60 In addition, effective comparison of clinical outcomes is difficult because of the high frequency of associated injuries, a mixed number of acute and chronic cases, and lack of consistent outcome measurements in the treatment of these injuries.

Noyes and Barber-Westin53 described a proximal advancement of the LCL and PLC in patients with definitive but lax posterolateral structures. These authors reported that 14 of 21 knees (64%) had completely stable PLCs at a mean of 42 months. Fanelli and Edson57 performed a combined PCL/PLC reconstruction in 41 knees. The PLC reconstruction consisted of a biceps tenodesis combined with a posterolateral capsular shift. At a 2- to 10-year follow-up, the authors reported significant improvements in Lysholm knee scale and Tegner activity scale scores.

Similarly, Khanduja et al60 performed a combined Larson-type procedure and a PCL reconstruction in 19 patients. Mean follow-up was 67 months. Although the authors found increases in Lysholm knee scale and Tegner activity scale scores, five patients (26%) had persistent rotational laxity.

Finally, Kim et al64 performed a modified Clancy biceps tenodesis to treat 21 patients with isolated PLC injuries and 25 patients with combined PCL/PLC injuries. Mean follow-up was 40 months. Although 76% of patients in both groups had normal or nearly normal knees, as graded by IKDC criteria, eight patients (17%) were noted to have gradual loss of postoperative rotational stability at final follow-up. Although many of the results of nonanatomic reconstruction have shown improvement in functional scores, long-term knee stability remains an issue.

Data have begun to emerge on more nearly anatomic PLC reconstructions. Latimer et al55 and Buzzi et al65 performed anatomic femoral LCL reconstructions with good results in combined cruciate injuries. Recently, Noyes and Barber-Westin al61 published their results with an anatomic PLC reconstruction in combined cruciate injuries for chronic injuries. Yoon et al63 showed improved success comparing anatomic versus nonanatomic reconstruction (Table 1). These studies show favorable short-term results for anatomic PLC reconstructions; however, it remains unclear, from both a clinical and a biomechanical perspective, which type of anatomic PLC reconstruction is superior. Potential problems with the anatomic reconstructions include increased technical difficulty and potential to overconstrain the knee.36 Nevertheless, short-term studies of these techniques demonstrate good clinical results (Table 1).

Table 1
Table 1:
Clinical Outcomes of Chronic Anatomic Reconstruction of the Posterolateral Corner

Senior Author’s Preferred Technique

Once a decision for surgical treatment has been made (Figure 2), an examination under anesthesia is performed on both extremities; stress radiography is routinely used. This is followed by an arthroscopic evaluation, with particular attention paid to a drive-through sign and the zone of injury (ie, meniscotibial versus meniscofemoral).37 Most commonly, the pattern is a chronic grade III PCL/PLC.

Following PCL reconstruction, a lateral hockey stick incision is made, paralleling the posterior edge of the IT band (Figure 7). The IT band is then split parallel to its fibers, exposing the deep structures of the LCL distally and anteriorly as well as the lateral head of the gastrocnemius muscle and underlying popliteus complex more proximally and posteriorly (Figure 8, A).

Figure 7
Figure 7:
Intraoperative photograph of the surface anatomy and skin incision for a posterolateral corner reconstruction. Note the hockey stick incision in relation to the fibula and peroneal nerve inferiorly, as well as to the Gerdy tubercle and the femoral epicondyle.
Figure 8
Figure 8:
Cadaveric dissections demonstrating the anatomy of the posterolateral corner. A, Split iliotibial band (C) with the lateral collateral ligament (A) more distal and the lateral head of the gastrocnemius (B) more proximal. F = patella. B, The threeinterval approach: iliotibial band (C), iliotibial band/biceps femoris interval (C/E), and common peroneal nerve (D) decompression. F = patella, G = patellar tendon, H = tuberosity of the tibia, I = head of the fibula. (Reproduced with permission from Alpert JM, McCarty LP III, Bach BR Jr: The posterolateral corner of the knee: Anatomic dissection and surgical approach. J Knee Surg 2008;21:50-54.)

An alternative technique is to make multiple deep intervals or windows20 (Figure 8, B). One window is created at the anterior aspect of the IT band to expose the femoral insertions of the PLC; a second is made between the IT band and biceps tendons to expose the fibular insertions. If the peroneal nerve is going to be released, then a third window is created proximally below the biceps and carried distally, as the nerve is decompressed, around the fibular neck. If needed, an arthrotomy is then made distal to the midcapsular ligament to help repair meniscotibial and meniscofemoral structures. The lateral meniscus must be repaired to the surrounding capsule by either open surgical or arthroscopic techniques.

Attention is then paid to the PFL reconstruction (Figure 9). In many chronic situations, the LCL is intact; primarily, only a rotational deformity exists. Thus, only a PFL reconstruction is necessary. If the LCL is deficient, an LCL reconstruction is performed with either Achilles or bone-patellar tendon allograft, followed by a PFL reconstruction. The PFL reconstruction consists, first, of a proximal, blind femoral tunnel, which is created at the anatomic insertion site of the popliteus tendon (“saddle”), located distal to the femoral epicondyle.18,19 Next, an oblique anterior-to-posterior fibular tunnel is created and oriented similarly to the course of the ligament. The native popliteus tendon is mobilized and then advanced with a prepared anterior tibialis allograft into the blind femoral tunnel. The popliteus is fixed by a suture tied over a post (screw and washer) on the medial side of the femur. The anterior tibialis graft is then passed under the IT band and LCL into the proximal, posterior aspect of the fibular tunnel opening and out the distal, anterior opening (Figure 10). Subsequent to the final fixation, the PCL is secured on the tibia. This is followed by PLC tensioning with the knee in 30° of flexion and mild internal rotation combined with fixation via an interference screw in the fibula (Figure 11).

Figure 9
Figure 9:
Anteroposterior (A) and lateral (B) views of popliteofibular ligament reconstruction with a tibialis anterior allograft with a post fixation on the medial side of the femur and an interference screw fixation in the fibular tunnel. (Reproduced with permission from Chhabra A, Cha PS, Rihn JA, et al: Surgical management of knee dislocations. J Bone Joint Surg Am 2005;87[1 suppl 1]:1-21.)
Figure 10
Figure 10:
Intraoperative photograph of a popliteofibular ligament reconstruction with passage of a tibialis anterior allograft through the fibular tunnel distally (+) and blind femoral tunnel proximally (*).
Figure 11
Figure 11:
Anteroposterior (A) and lateral (B) postoperative radiographs following chronic posterolateral corner and double-bundle posterior cruciate ligament reconstruction. On the tibial side, two posts and two tibial tunnels represent the anterolateral and posteromedial bundles of the posterior cruciate reconstruction. On the femoral side, the three posts secure the anterolateral graft, posteromedial graft, and posterolateral corner reconstruction (popliteofibular and popliteus advancement). The popliteofibular reconstruction is fixed distally in the fibula with an interference screw.


Postoperatively, the reconstructed knee is immobilized in a hinged knee brace locked in extension. This minimizes the deleterious effects of gravity and the pull of the hamstrings. Patients usually maintain partial weight bearing, with the brace locked in extension, for the first 6 weeks. The brace is unlocked for range-of-motion exercises, including closed-chain mini squats and heel slides. Quadriceps exercises are the mainstay of rehabilitation, which includes quadriceps sets, mini squats, and straight leg raises. As range-of-motion and quadriceps strength improve, the brace is discontinued. Physical therapy continues with emphasis on restoration of normal gait, attainment of full range of motion, and gradual recovery of muscle strength, endurance, and proprioception. A safe and gradual return to work or athletic participation is achieved at approximately 10 to 12 months postoperatively.


Complications are common in the management of PLC injuries.66 Peroneal nerve dysfunction has been reported in 12% to 17% of acute cases.3,5,37 In addition to the traumatic injury, the peroneal nerve can be damaged during the surgical approach, fixation, or drilling of the fibular tunnel, or by excessive traction.66 Other potential intraoperative complications include fibula fracture, compartment syndrome from fluid extravasation, and vascular injury during concurrent PCL reconstruction. Postoperative sequelae include residual laxity, arthrofibrosis, persistent knee pain, degenerative joint disease of the medial and lateral compartments, heterotopic ossification, and reflex sympathetic dystrophy.66,67 In a recent review of failed PLC surgical procedures, Noyes et al54 identified multiple factors contributing to failure of the index operation. The most common factors were failure to successfully address and reconstruct associated cruciate ligament injuries, nonanatomic graft reconstruction, and untreated varus malalignment.


Isolated PLC injuries are rare events; combined injuries are more frequent and are increasingly recognized. A growing body of basic science literature is focused on the anatomy and biomechanics of this region and its influence on the remainder of the knee. Although no universal classification system has been adopted, attention to both varus and rotational stability is critical. Treatment emphasizes early, accurate diagnosis so that immediate surgical intervention can be performed. For chronic (ie, late) severe injuries, no benchmark reconstruction technique exists. There has been a recent trend, however, toward more nearly anatomic reconstruction, with attention paid to proper insertion site anatomy in order to restore native knee kinematics as well as possible. Reports of long-term outcomes are limited, but short-term studies demonstrate good results.


Evidence-based Medicine: There are no prospective randomized studies reported on the treatment outcomes of posterolateral corner injuries of the knee (ie, level I studies). There is one level II prospective study (reference 44). The remaining references report experience with surgical techniques in case-control cohort studies (level III) or are case reports (level IV) (references 2, 3, 6, 8, 12-43, 46-49, 51, 56, 58, 59, and 62).

Citation numbers printed in bold type indicate references published within the past 5 years.

1. Gardner MJ, Yacoubian S, Geller D, et al: The incidence of soft tissue injury in operative tibial plateau fractures: A magnetic resonance imaging analysis of 103 patients. J Orthop Trauma 2005;19:79-84.
2. Covey DC: Injuries of the posterolateral corner of the knee. J Bone Joint Surg Am 2001;83:106-118.
3. DeLee JC, Riley MB, Rockwood CA Jr: Acute posterolateral rotatory instability of the knee. Am J Sports Med 1983;11:199-207.
4. Hughston JC, Jacobson KE: Chronic posterolateral rotatory instability of the knee. J Bone Joint Surg Am 1985; 67:351-359.
5. Baker CL Jr, Norwood LA, Hughston JC: Acute posterolateral rotatory instability of the knee. J Bone Joint Surg Am 1983;65:614-618.
6. Harner CD, Vogrin TM, Hoher J, Ma CB, Woo SL: Biomechanical analysis of a posterior cruciate ligament reconstruction: Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med 2000;28:32- 39.
7. Kannus P: Nonoperative treatment of grade II and III sprains of the lateral ligament compartment of the knee. Am J Sports Med 1989;17:83-88.
8. LaPrade RF, Resig S, Wentorf F, Lewis JL: The effects of grade III posterolateral knee complex injuries on anterior cruciate ligament graft force: A biomechanical analysis. Am J Sports Med 1999;27:469-475.
9. Noyes FR, Barber-Westin SD, Roberts CS: Use of allografts after failed treatment of rupture of the anterior cruciate ligament. J Bone Joint Surg Am 1994;76:1019-1031.
10. O’Brien SJ, Warren RF, Pavlov H, Panariello R, Wickiewicz TL: Reconstruction of the chronically insufficient anterior cruciate ligament with the central third of the patellar ligament. J Bone Joint Surg Am 1991;73: 278-286.
11. Krukhaug Y, Molster A, Rodt A, Strand T: Lateral ligament injuries of the knee. Knee Surg Sports Traumatol Arthrosc 1998;6:21-25.
12. Veltri DM, Warren RF: Operative treatment of posterolateral instability of the knee. Clin Sports Med 1994; 13:615-627.
13. Hughston JC, Andrews JR, Cross MJ, Moschi A: Classification of knee ligament instabilities: II. The lateral compartment. J Bone Joint Surg Am 1976;58:173-179.
14. Hughston JC, Andrews JR, Cross MJ, Moschi A: Classification of knee ligament instabilities: I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am 1976;58:159- 172.
15. Gollehon DL, Torzilli PA, Warren RF: The role of the posterolateral and cruciate ligaments in the stability of the human knee: A biomechanical study. J Bone Joint Surg Am 1987;69:233- 242.
16. Shahane SA, Ibbotson C, Strachan R, Bickerstaff DR: The popliteofibular ligament: An anatomical study of the posterolateral corner of the knee. J Bone Joint Surg Br 1999;81:636-642.
17. Grood ES, Stowers SF, Noyes FR: Limits of movement in the human knee: Effect of sectioning the posterior cruciate ligament and posterolateral structures. J Bone Joint Surg Am 1988;70:88-97.
18. Brinkman JM, Schwering PJ, Blankevoort L, Kooloos JG, Luites J, Wymenga AB: The insertion geometry of the posterolateral corner of the knee. J Bone Joint Surg Br 2005;87: 1364-1368.
19. Laprade RF, Ly TV, Wentorf FA, Engebretsen L: The posterolateral attachments of the knee. Am J Sports Med 2003;31:854-860.
20. Terry GC, LaPrade RF: The posterolateral aspect of the knee: Anatomy and surgical approach. Am J Sports Med 1996;24:732-739.
21. Simonian PT, Sussmann PS, van Trommel M, Wickiewicz TL, Warren RF: Popliteomeniscal fasciculi and lateral meniscal stability. Am J Sports Med 1997;25:849-853.
22. Maynard MJ, Deng X, Wickiewicz TL, Warren RF: The popliteofibular ligament. Am J Sports Med 1996;24:311- 316.
23. Watanabe Y, Moriya H, Takahashi K, et al: Functional anatomy of the posterolateral structures of the knee. Arthroscopy 1993;9:57-62.
24. Veltri DM, Deng XH, Torzilli PA, Warren RF, Maynard MJ: The role of the cruciate and posterolateral ligaments in stability of the knee: A biomechanical study. Am J Sports Med 1995;23:436-443.
25. Veltri DM, Deng XH, Tozilli PA, Maynard MJ, Warren RF: The role of the popliteofibular ligament in stability of the human knee: A biomechanical study. Am J Sports Med 1996;24:19- 27.
26. LaPrade RF, Tso A, Wentorf FA: Force measurements on the fibular collateral ligament, popliteofibular ligament, and popliteus tendon to applied loads. Am J Sports Med 2004;32:1695-1701.
27. LaPrade RF, Bollom TS, Wentorf FA, Willis NJ, Meister K: Mechanical properties of the posterolateral structures of the knee. Am J Sports Med 2005;33:1386-1391.
28. Veltri DM, Warren RF: Anatomy, biomechanics, and physical findings in posterolateral knee instability. Clin Sports Med 1994;13:599-614.
29. Amis AA, Bull AM, Gupte CM, Hijazi I, Race A, Robinson JR: Biomechanics of the PCL and related structures: Posterolateral, posteromedial and meniscofemoral ligaments. Knee Surg Sports Traumatol Arthrosc 2003;11: 271-281.
30. Harner CD, Hoher J, Vogrin TM, Carlin GJ, Woo SL: The effects of a popliteus muscle load on in situ forces in the posterior cruciate ligament and on knee kinematics: A human cadaveric study. Am J Sports Med 1998;26:669- 673.
31. LaPrade RF, Resig S, Wentorf F, Lewis JL: The effects of grade III posterolateral knee complex injuries on anterior cruciate ligament graft force: A biomechanical analysis. Am J Sports Med 1999;27:469-475.
32. Sekiya JK, Haemmerle MJ, Stabile KJ, Vogrin TM, Harner CD: Biomechanical analysis of a combined doublebundle posterior cruciate ligament and posterolateral corner reconstruction. Am J Sports Med 2005;33:360- 369.
33. LaPrade RF, Muench C, Wentorf F, Lewis JL: The effect of injury to the posterolateral structures of the knee on force in a posterior cruciate ligament graft: A biomechanical study. Am J Sports Med 2002;30:233-238.
34. LaPrade RF, Johansen S, Wentorf FA, Engebretsen L, Esterberg JL, Tso A: An analysis of an anatomical posterolateral knee reconstruction: An in vitro biomechanical study and development of a surgical technique. Am J Sports Med 2004;32:1405-1414.
35. Nau T, Chevalier Y, Hagemeister N, Deguise JA, Duval N: Comparison of 2 surgical techniques of posterolateral corner reconstruction of the knee. Am J Sports Med 2005;33:1838-1845.
36. Markolf KL, Graves BR: How well do anatomical reconstructions of the PLC restore varus stability to the PCL-reconstructed knee? Am J Sports Med 2007;35:1117-1122.
37. LaPrade RF, Terry GC: Injuries to the posterolateral aspect of the knee: Association of anatomic injury patterns with clinical instability. Am J Sports Med 1997;25:433-438.
38. Hughston JC, Norwood LA Jr: The posterolateral drawer test and external rotational recurvatum test for posterolateral rotatory instability of the knee. Clin Orthop Relat Res 1980; 147:82-87.
39. Jakob RP, Hassler H, Staeubli HU: Observations on rotatory instability of the lateral compartment of the knee: Experimental studies on the functional anatomy and the pathomechanism of the true and the reversed pivot shift sign. Acta Orthop Scand Suppl 1981; 191:1-32.
40. Cooper JM, McAndrews PT, LaPrade RF: Posterolateral corner injuries of the knee: Anatomy, diagnosis, and treatment. Sports Med Arthrosc 2006;14:213-220.
41. Cooper DE: Tests for posterolateral instability of the knee in normal subjects: Results of examination under anesthesia. J Bone Joint Surg Am 1991;73:30-36.
42. Fanelli GC, Larson RV: Practical management of posterolateral instability of the knee. Arthroscopy 2002;18(2 suppl 1):1-8.
43. Lee J, Papakonstantinou O, Brookenthal KR, Trudell D, Resnick DL: Arcuate sign of posterolateral knee injuries: Anatomic, radiographic, and MR imaging data related to patterns of injury. Skeletal Radiol 2003; 32:619-627.
44. LaPrade RF, Gilbert TJ, Bollom TS, Wentorf F, Chaljub G: The magnetic resonance imaging appearance of individual structures of the posterolateral knee: A prospective study of normal knees and knees with surgically verified grade III injuries. Am J Sports Med 2000;28:191-199.
45. Yu JS, Salonen DC, Hodler J, Haghighi P, Trudell D, Resnick D: Posterolateral aspect of the knee: Improved MR imaging with a coronal oblique technique. Radiology 1996;198:199-204.
46. LaPrade RF, Wentorf FA, Crum CA: Assessment of healing of grade III posterolateral corner injuries: An in vivo model. J Orthop Res 2004;22:970- 975.
47. Cooper DE, Warren RF, Warner JJ: The posterior cruciate ligament and posterolateral structures of the knee: Anatomy, function and patterns of injury. Instr Course Lect 1991;40:249- 270.
48. Noyes FR, Barber-Westin SD: Treatment of complex injuries involving the posterior cruciate and posterolateral ligaments of the knee. Am J Knee Surg 1996;9:200-214.
49. Swenson TM, Harner CD: Knee ligament and meniscal injuries: Current concepts. Orthop Clin North Am 1995;26:529-546.
50. Stannard JP, Brown SL, Farris RC, McGwin G Jr, Volgas DA: The posterolateral corner of the knee: Repair versus reconstruction. Am J Sports Med 2005;33:881-888.
51. Noyes FR, Barber-Westin SD: Surgical reconstruction of severe chronic posterolateral complex injuries of the knee using allograft tissues. Am J Sports Med 1995;23:2-12.
52. Harner CD, Waltrip RL, Bennett CH, Francis KA, Cole B, Irrgang JJ: Surgical management of knee dislocations. J Bone Joint Surg Am 2004;86:262- 273.
53. Noyes FR, Barber-Westin SD: Surgical restoration to treat chronic deficiency of the posterolateral complex and cruciate ligaments of the knee joint. Am J Sports Med 1996;24:415-426.
54. Noyes FR, Barber-Westin SD, Albright JC: An analysis of the causes of failure in 57 consecutive posterolateral operative procedures. Am J Sports Med 2006;34:1419-1430.
55. Latimer HA, Tibone JE, ElAttrache NS, McMahon PJ: Reconstruction of the lateral collateral ligament of the knee with patellar tendon allograft: Report of a new technique in combined ligament injuries. Am J Sports Med 1998;26:656-662.
56. Clancy WG Jr: Repair and reconstruction of the posterior cruciate ligament, in Chapman MW (ed): Operative Orthopaedics, ed 3. Philadelphia, PA: Lippincott, 1988, vol 3, pp 2093- 2108.
57. Fanelli GC, Edson CJ: Combined posterior cruciate ligament-posterolateral reconstructions with Achilles tendon allograft and biceps femoris tendon tenodesis: 2- to 10-year followup. Arthroscopy 2004;20:339-345.
58. Muller W: The Knee: Form, Function and Ligament Reconstruction. Berlin, Germany: Springer-Verlag, 1983.
59. Larson RV: Isometry of the lateral collateral and popliteofibular ligaments and techniques for reconstruction using a free semitendinosus tendon graft. Oper Tech Sports Med 2001;9: 84-90.
60. Khanduja V, Somayaji HS, Harnett P, Utukuri M, Dowd GS: Combined reconstruction of chronic posterior cruciate ligament and posterolateral corner deficiency: A two- to nine-year follow-up study. J Bone Joint Surg Br 2006;88:1169-1172.
61. Noyes FR, Barber-Westin SD: Posterolateral knee reconstruction with an anatomical bone-patellar tendonbone reconstruction of the fibular collateral ligament. Am J Sports Med 2007;35:259-273.
62. Sekiya JK, Kurtz CA: Posterolateral corner reconstruction of the knee: Surgical technique utilizing a bifid Achilles tendon allograft and a double femoral tunnel. Arthroscopy 2005; 21:1400.
63. Yoon KH, Bae DK, Ha JH, Park SW: Anatomic reconstructive surgery for posterolateral instability of the knee. Arthroscopy 2006;22:159-165.
64. Kim SJ, Shin SJ, Jeong JH: Posterolateral rotatory instability treated by a modified biceps rerouting technique: Technical considerations and results in cases with and without posterior cruciate ligament insufficiency. Arthroscopy 2003;19:493-499.
65. Buzzi R, Aglietti P, Vena LM, Giron F: Lateral collateral ligament reconstruction using a semitendinosus graft. Knee Surg Sports Traumatol Arthrosc 2004;12:36-42.
66. Lubowitz JH, Elson W, Guttmann D: Complications in the treatment of medial and lateral sided injuries of the knee joint. Sports Med Arthrosc 2006;14:51-55.
67. Fanelli GC, Monahan T: Complications in posterior cruciate ligament and posterolateral corner surgery. Oper Tech Sports Med 2001;9:96-99.
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