Posterolateral Corner Injury (PLC, 'Dark Side' of the Knee)

Posterolateral corner (PLC) of the knee, historically called the 'dark side of the knee' (Hughston) due to complex anatomy that was underrecognized for decades, comprises the structures that stabilize the posterolateral aspect of the knee against varus stress, external rotation, and posterior translation. PLC injuries are common in high-energy traumatic knee injuries and often missed acutely (delayed diagnosis 25-72% in some series), with significant consequences if untreated including failure of cruciate ligament reconstruction. Anatomy: the PLC includes static stabilizers (passive ligaments and capsular structures) and dynamic stabilizers (musculotendinous units). The three most important static stabilizers (the 'big three' for reconstruction): (1) Lateral collateral ligament/Fibular collateral ligament (LCL/FCL): runs from the lateral femoral epicondyle to the fibular head, primary restraint to varus stress at all flexion angles. (2) Popliteus tendon: arises intra-articularly from the lateral femoral condyle (just anterior and inferior to LCL origin), passes through the popliteal hiatus, and inserts on the posteromedial tibia (popliteus muscle origin) — primary restraint to external tibial rotation, secondary restraint to posterior translation. (3) Popliteofibular ligament (PFL): runs from the popliteus musculotendinous junction to the fibular styloid — restraint to external rotation. Other static stabilizers: arcuate ligament (variable structure), fabellofibular ligament (when fabella present), lateral capsule (anterior, middle, posterior thirds), oblique popliteal ligament, posterolateral capsule. Dynamic stabilizers: popliteus muscle (origin posteromedial tibia, insertion lateral femoral condyle through tendon), biceps femoris (long and short heads, insertion fibular head and lateral tibia), iliotibial band (Gerdy tubercle insertion), lateral head of gastrocnemius. Common peroneal nerve runs around the fibular neck and is at risk in PLC injuries (15% incidence of nerve injury including foot drop and sensory deficit).

Mechanism of injury: most common mechanisms include: (1) Contact varus stress: direct blow to the anteromedial knee causing varus opening and posterolateral injury. (2) Hyperextension with external rotation: knee forced into hyperextension while rotated. (3) Contact football tackles ('clipping injury'): direct lateral hit to knee with foot planted (high-energy mechanism). (4) Motor vehicle accidents and falls. (5) Knee dislocations: very high incidence of PLC injury in tibiofemoral dislocations (up to 75%). Associated injuries: ACL or PCL injury (combined in 50-75% of PLC injuries — PLC injury without cruciate injury is uncommon, so isolated PLC injury is rare). Common peroneal nerve injury (15-30% in high-grade PLC injuries) — incomplete (neuropraxia recovers in months) to complete (severe disability with foot drop and sensory deficit, may not fully recover). Vascular injury (popliteal artery) in dislocations (up to 32% in knee dislocations). Tibial plateau fractures, lateral meniscus tears (high frequency due to PLC mechanism). Clinical presentation: acute PLC injury — pain and swelling in posterolateral knee, lateral hemarthrosis or extra-articular hematoma, ecchymosis, often patient cannot weight-bear initially. Sensory deficit in superficial peroneal nerve distribution (lateral leg, dorsum of foot) and foot drop (deep peroneal nerve weakness in tibialis anterior, EHL, EDL) in cases with peroneal nerve injury — must be documented carefully on initial exam. Chronic PLC injury (more than 3-6 weeks) — varus thrust during gait (lateral opening of knee during stance phase, sometimes with audible clunk), posterolateral rotatory instability with cutting or pivoting, knee giving way, hyperextension instability, recurrent ACL/PCL graft failure if cruciate reconstruction was performed without addressing PLC. Examination of the PLC: requires comparison with contralateral knee. (1) Varus stress test at 30 degrees flexion: tests LCL/FCL — opening greater than 5-10 mm compared to contralateral side suggests LCL/FCL injury. Varus stress at 0 degrees (full extension) tests LCL/FCL plus posterolateral capsule and posterior cruciate. Grade I (3-5 mm), II (5-10 mm), III (greater than 10 mm). (2) Dial test (external rotation test): patient prone or supine, examiner externally rotates both feet at 30 and 90 degrees flexion. Increased external rotation greater than 10-15 degrees compared to contralateral side at 30 degrees only = isolated PLC injury. Increased at both 30 AND 90 degrees = combined PLC + PCL injury. Dial test is highly specific for PLC injury. (3) Posterolateral drawer test: knee at 90 degrees flexion, foot externally rotated 15 degrees, examiner applies posterior force to lateral tibia — increased posterolateral translation positive. (4) Reverse pivot shift test: from flexion with valgus stress and external rotation, slowly extending knee — positive reduction at 20-30 degrees flexion suggests PLC injury. (5) External rotation thrust test: walking with knee thrust into external rotation. (6) Hyperextension recurvatum test: lift both lower extremities by great toes — knee hyperextension and varus suggest PLC injury. (7) Detailed neurologic examination of common peroneal nerve function essential.

Diagnostic workup: clinical examination is critical (can establish PLC injury based on stress tests), supplemented by imaging. (1) Plain radiographs (AP, lateral, weight-bearing both knees, sunrise/Merchant patella view): may show fibular head avulsion (arcuate sign — suggests PLC injury, present in 50% of PLC injuries), Segond fracture (anterolateral tibial avulsion, more for ACL but can be associated), tibial plateau fractures, knee subluxation. Stress radiographs: varus stress views show lateral joint space opening (greater than 2-3 mm compared to contralateral suggests LCL injury). (2) MRI: gold standard for PLC injury diagnosis. Demonstrates LCL/FCL injury (sprain, partial tear, complete tear, avulsion), popliteus tendon tear, popliteofibular ligament tear (specialized PLC MRI sequences improve sensitivity), lateral capsular injury, biceps femoris injury, posterior capsule disruption, bone edema patterns suggesting injury mechanism, and associated injuries (ACL, PCL, menisci, lateral meniscus particularly). MRI sensitivity for individual PLC structures is variable, with PFL particularly difficult to visualize (sensitivity 50-90%). (3) Stress MRI under varus stress (specialized centers). (4) Arthroscopy: provides direct visualization of intra-articular PLC structures (popliteus tendon at popliteal hiatus, lateral meniscus posterior horn) but extracapsular structures (LCL/FCL, PFL) require open surgical exploration. Schenck classification of knee dislocations with PLC involvement: KD-I (single cruciate plus collateral, less common), KD-II (both cruciates without collateral, rare), KD-III (both cruciates plus one collateral — KD-IIIM if MCL, KD-IIIL if PLC/LCL, common), KD-IV (both cruciates plus both collaterals, less common), KD-V (knee dislocation with periarticular fracture). Treatment: depends on timing (acute vs chronic), grade and structures involved, associated injuries, patient factors. Acute PLC injury (within 2-3 weeks): primary repair is preferred when possible, with screw or anchor fixation of avulsions (LCL/FCL avulsion from femur or fibular head, popliteus tendon avulsion from femoral attachment, peel-off injuries). Augmentation with allograft or autograft if midsubstance ruptures or weak repair. Combined ACL/PCL reconstruction with PLC repair in same setting if associated cruciate injury. Optimal timing within 2-3 weeks before scarring obscures planes. Chronic PLC injury (more than 3-6 weeks): anatomic reconstruction is the standard, with various techniques. (1) LaPrade anatomic reconstruction: gold standard technique, uses allograft (semitendinosus or gracilis) split into multiple limbs to anatomically reconstruct the LCL/FCL, popliteus tendon, and popliteofibular ligament with bone tunnels at anatomic insertion sites and graft fixation with interference screws. Validated biomechanically and clinically. (2) Larson modified technique: simpler reconstruction with single allograft routed through bone tunnels in fibular head and femoral epicondyle, reconstructing LCL/FCL and PFL. (3) Modified Bousquet/Hughston techniques and biceps tenodesis (less commonly used in modern era). Combined cruciate injuries: PCL plus PLC reconstruction (most common combined pattern), ACL plus PLC reconstruction, multi-ligament knee reconstruction for KD-III/IV/V. PLC reconstruction must be performed in any cruciate reconstruction with associated PLC laxity to prevent graft failure (PLC is critical biomechanical co-factor for cruciate function — untreated PLC laxity will fail ACL graft within 1-2 years, PCL graft even faster). Postoperative management: hinged knee brace in extension, non-weight-bearing for 6 weeks, then progressive weight-bearing, range of motion progression starting at 2 weeks, return to running at 6 months, return to sport at 9-12 months. Common peroneal nerve injury: observation for 3-6 months for spontaneous recovery; tendon transfers (posterior tibialis to dorsum) or ankle-foot orthotics for permanent foot drop. Outcomes: anatomic reconstruction has good outcomes with 80-90% subjective satisfaction and significant improvement in stability, although return to high-level athletics is variable (50-80%). Untreated PLC injury leads to chronic disability with varus thrust, instability, secondary cruciate failure, and progressive arthritis.