Posterolateral corner knee damage

Sujith Konangamparambath and Fares Haddad explain why it is important to spot posterolateral corner damage when it happens

In the past, injuries to the posterolateral corner of the knee were commonly missed. Recent research has helped improve our awareness of this complicated area at the outside back edge of the knee. And although Posterolateral corner (PLC) injuries are not common in sport, a failure to spot one can have devastating, even career-ending consequences for the affected athlete.

What is the Posterolateral corner (PLC)?

One reason for the relative obscurity of this part of the knee is that over the years there has been little academic consensus about how to define it. Currently most authors agree on a ‘three-layer’ description of the anatomy for this part of the knee(1). Within this rubric, Layer 3 describes the PLC. The three layers are:

Layer 1

* lateral fascia

* iliotibial tract

* biceps tendon

* peroneal nerve deep to the biceps femoris tendon.

Layer 2

* patellar retinaculum

* patello-femoral ligament.

Layer 3

* articular capsule

* lateral collateral ligament (LCL)

* popliteofibular ligament (PFL)

* popliteus tendon

* arcuate ligament

* fabellofibular ligament.

How injury occurs

Injury to the posterolateral knee tends to be the result of contact-sport injuries, motor vehicle accidents or falls, with one estimate attributing 40% of all Posterolateral corner (PLC) damage to sports injuries(4).

In isolation, damage to the Posterolateral corner (PLC) of the knee is rare, accounting for 1.6% of all knee injuries(2). Far more commonly, there will be some damage to the PLC in conjunction with other ligament damage – studies suggest anything between 43% and 80% occur- rence(3-5). If primary (surgical) repair of an unstable posterolateral knee is to be successful, it is essential that the injury is identified promptly(2, 4, 6, 7, 8). But prompt recognition is equally important for another reason: a delay in addressing Posterolateral corner (PLC) damage may also lead to graft failure in the attempted recon- struction of concurrent anterior and poste- rior cruciate ligament injuries(9-11).

Isolated damage to the Posterolateral corner (PLC) is typically the result of a force to a straight knee from the front and inner side, causing a hyper- extension and varus stress. More commonly, and as a part of multiple ligament injuries, there may be a varus (inward) blow to the knee with the tibia in external rotation, a hyperextension injury to the knee with the tibia internally rotated, or an obvious knee dislocation.

We have observed that sports injuries typically lead to a ‘pull off’ type of damage, where the posterolateral structures slide away from their bony insertions. By contrast, high energy injuries from road traffic accidents are often associated with disruption of the main part of the ligaments, which makes repair more difficult.

For an injury that requires surgical management, timing is critical as it can dictate whether primary repair is possible or a reconstruction is required. Repair undertaken within two to three weeks has a better outcome than a delayed reconstruction for chronic instability(2, 4, 6, 7, 8).

Grading of injury

There are two main classification systems for grading Posterolateral corner (PLC) damage:

Fanelli classification of posterolateral instability(12)

Type A:injury to the popliteofibular ligament and popliteus tendon. Shows only increased external rotation.

Type B: injury to the popliteofibular ligament, popliteus tendon and lateral collateral ligament. There is increased external rotation and mild varus opening (5 to 10 mm) to varus stress at 30 degrees of flexion.

Type C: occurs with injuries to popliteofibular ligament, popliteus tendon and lateral collateral ligament plus lateral capsular avulsion and cruciate ligament disruption. There is increased external rotation and marked varus instability at 30 degrees of knee flexion.

Hughston classification of collateral ligament injuries of the knee(13)

Grade 1+ instability:opening of the affected joint 0 to 5mm with varus stress. Grade 2+ instability: opening of 6 to 10mm. Grade 3+ instability: opening of greater than 10 mm.

Effects of PLC damage

A PLC injury can cause considerable disability. The opposing convex articulating surfaces of the lateral femur and tibia can cause the lateral side of the joint to open when the heel strikes the ground, which produces a distinctive ‘varus thrust gait’. Patients often prefer to keep their knee bent to prevent this.

Assessment

It is often the nature of the injury that will lead the clinician to suspect PLC damage. Pain in the posterolateral aspect of the knee, the knee giving way, limitation of activity, difficulty running or climbing stairs may all be indicative. In up to 15% of PLC injuries, the common peroneal nerve may be damaged(14), resulting in tingling or numbness along the leg, with or without weakness in the muscles that move the ankle and toes. Complete nerve damage, although uncommon, is usually career-ending in the sporting population.

Various clinical tests can be done to confirm damage. These include:

* external rotation recurvatum test

* varus stress test

* dial test (posterolateral rotation test)

* posterolateral drawer test

* reverse pivot shift test.

On x-ray, in the AP and lateral projections an avulsion fracture of the lateral capsule (Segond fracture), or an avulsion fracture of the fibular head (arcuate sign) may be seen. Weight-bearing long leg views may demonstrate the varus malalignment. Bilateral varus stress radiographs would show any significant lateral opening of the joint space.

A high quality MRI scan is very useful in assessing the individual structures. Arthroscopic evaluation of the lateral compartment would help identify specific damage to individual structures, preparatory to surgical operation. A positive ‘drive through’ sign, where the lateral joint line opens greater than 10mm on varus stress at arthroscopy is diagnostic.

Grade 1 and truly isolated Grade 2 injuries may be successfully treated non-operatively with an early range of motion rehabilitation programme(16). The need for surgical treat- ment(17)will depend on symptoms and func- tional instability, confirmed by physical examination and imaging.

Studies have shown that patients with greater than 10mm of varus laxity or greater than a 10-degree increase in external rota- tion at 30 degrees of knee flexion don’t do well without an operation. Swelling, open injuries, contaminated wounds or arterial injury may contraindicate acute repair.

Surgery

It is currently recommended that primary repair of the torn structures of the posterolateral knee should be undertaken within two weeks of the injury whenever possible(2, 4, 6, 7, 8). Where primary repair is insufficient or further stability is desired, the attachment of the repaired posterolateral structures can be strengthened by using adjacent iliotibial band and biceps femoris muscles(18, 19). In a similar fashion, one or more of the popliteus, LCL, arcuate ligament, lateral gastrocnemius tendon or capsule proximally can be attached to the lateral femoral condyle for greater stability(6).

Where primary repair is not feasible, reconstruction is the alternative. This involves using tendon grafts to reconstruct the torn structures. If there has been long- standing posterolateral instability, osteotomy (bone reshaping) may also be needed to correct the varus malalignment.

Rehabilitation

Postoperative rehabilitation is the key to a successful outcome. The protocol will vary, depending on the structures repaired/ reconstructed, the quality of the tissues and the strength of the construct obtained at the end of the operation. Most authors recommend an initial period of non-weight bearing and the knee locked into extension in a brace.

In a young, fit sportsperson, the physio- therapy regime is often aggressive. In the first two to three weeks, toe-touch weight- bearing is allowed with the hinged knee brace locked in full extension. Range of movement exercises from 0 to 90 degrees and straight leg raises are encouraged.

In the next couple of weeks, partial weight bearing with crutches is encouraged, progressing to full weight bearing without crutches at four to five weeks after the operation. The range of movement is steadily increased from 90 degrees to full, leaving the brace on but unlocked.

All being well, the brace is discontinued at three months. The physiotherapist then commences work on return to sports by training the patient to run, build up their wasted muscles and recommence sport- specific activities. Depending on progress, clearance to return to full contact sports may be given at six to eight months.

References

1. Seebacher JR, Inglis AE et al. ‘The structure of the posterolateral aspect of the knee’. J Bone Joint Surg Am. 1982;64:536-541.

2. DeLee JC, Riley MB, Rockwood CAJ. ‘Acute posterolateral rotatory instability of the knee’. Am J Sports Med. 1983;11:199-207.

3. DeLee JC, Riley MB, Rockwood CA Jr. ‘Acute straight lateral instability of the knee’. Am J Sports Med. 1983;11:404-411.

4. Chen FS, Rokito AS, Pitman MI. ‘Acute and chronic posterolateral rotatory instability of the knee’. J Am Acad Orthop Surg. 2000;8:97-110.

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. Hughston JC, Jacobson KE. ‘Chronic posterolateral rotatory instability of the knee’. J Bone Joint Surg Am. 1985;67:351-359.

7. Fleming RE, Blatz DJ, McCarroll JR. ‘Posterior problems in the knee: posterior cruciate insufficiency and posterolateral rotatory insufficiency’. Am J Sports Med. 1981;9:107-112.

8. Jakob RP, Hassler H, Staubli HU. ‘Observations on rotatory instability of the lateral compartment of the knee’. Acta Orthop Scand. 1981;191S:1-32.

9. LaPrade RF, Resig S et al. ‘The effects of grade III posterolateral knee complex injuries on anterior cruciate ligament graft force: a biomechanical study’. Am J Sports Med. 1999;27: 469-475.

10. Harner CD, Vogrin TM et al. ‘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.

11. Markolf KL, Wascher DC, Finerman GA. ‘Direct in vitro measurement of forces in the cruciate ligaments. Part II: the effect of section of the posterolateral structures’. J Bone Joint Surg Am. 1993;75:387-394.

12. Fanelli GC, Feldmann DD. ‘Management of combined ACL/PCL/posterolateral complex injuries of the knee’. Oper Tech Sports Med. 1999;7:143-149.

13. Hughston JC, Andrews JR et al. ‘Classification of knee ligament instabilities. Part II. The lateral compartment’. J Bone Joint Surg Am. 1976;58-A:173-179.

14. 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.

15. LaPrade RF. ‘Arthroscopic evaluation of the lateral compartment of knees with grade 3 posterolateral complex knee injuries’. Am J Sports Med. 1997;25:596-602.

16. Ellingson CI, Kurtz CA, Sekiya JK, ‘Nonsurgical management of lateral side injuries of the knee’, M Sports Med Arthrosc Rev 2006;14:20-22.

17. Murphy KP, Helgeson MD, Lehman, RA Jr. ‘Surgical treatment of acute lateral collateral ligament and posterolateral corner injuries sports’ Med Arthrosc Rev March 2006;14:23-27.

18. Coleman SH, Maynard MJ, Warren RF. ‘Surgical technique for knee dislocations’. In: Jackson DW, ed. Reconstructive Knee Surgery. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003:209-228.

19. Dugas JR, Cain EL, Clancy WG. ‘Posterolateral cruciate and fibular collateral ligament reconstruction’. In: Jackson DW, ed. Reconstructive Knee Surgery. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003:179-191.