The Postero-Lateral Corner, the “Dark side of the Knee”… A guest article by Richard Norris

Now you may have been aware that I havent posted much over these last few months, for which I apologise, but things have been a little crazy recently what with my wedding and work commitments, but normal service will resume soon. However, in my temporary absense I have asked for some excellent guest writers to cover for me, and today I am very pleased to give you Richard Norris a specialist lower limb physio working in the NHS and privatley, me and Rich have been exchanging comments via twitter and I can tell you he is a smart cookie and an excellent physio, for more details on him and his clinic see here

When Adam put out the advert on twitter for guest bloggers I thought I’d use a spare evening to write about the postero-lateral corner. I sat down, started typing and soon remembered how complex the topic was. But a promise is a promise and 10 days later I’ve managed to put some stuff together, which hopefully isn’t too taxing a read. I hope you enjoy it and find it helpful but if you have any questions please feel free to contact me @richnorris00.

The postero-lateral corner (PLC) is referred to as the ‘dark side of the knee’, which denotes the fact that little is known about it: so much so that a consultant I use to work with deemed it necessary to deliver a full Star Wars themed PLC presentation at the RCSE advanced knee course in 2012. I remember first seeing the letters on some post-op notes in 2004 and assuming it was posterior cruciate ligament (PCL) scribbled incorrectly… to this day I still see patients that have been treated by their therapist having made the same wrong assumption.

The PLC’s mysterious reputation stems from the fact that the anatomy and biomechanics are complex but recent studies, most notably by Mr Robert LaPrade and his team have helped to shed some light on the subject. Robert is widely regarded as ‘Mr PLC’ and I strongly recommend reading his articles, not only for the clear explanations but the fantastic illustrations he uses. To date I haven’t found anything that summarises the PLC better than this article (http://www.jospt.org/issues/id.2450/article_detail.asp), so I will try to integrate this information with other research and the clinical experience I have gained over the years from dealing with them.

As the name suggests the PLC is a collection of tissues located at the back, outer corner of the knee rather than one individual structure. Together these tissues resist knee hyperextension, varus angulation and tibial external rotation so if a patient is conscientious enough to notice a similar mechanism at the time of the injury and complains of postero-lateral knee pain the therapist should be extremely suspicious of PLC involvement. PLC injuries most often occur with simultaneous cruciate ligament ruptures  (LaPrade & Wentorf, 2002) so overlooking or ignoring this problem may lead to chronic pain, instability, degenerative changes or surgical failure of a reconstructed cruciate ligament.  Or to loosely quote Yoda and keep with the Star Wars theme “… the dark side… leads to suffering”.

It makes sense that if the postero-lateral knee support is compromised by injury the patient may walk with a varus thrust or hyperextension thrust gait; where the knee ‘snaps’ into varus or hyperextension respectively on weight bearing. Video 1 was taken of a PLC deficient knee demonstrating a varus thrust gait and this may be the first thing you notice when you see the patient. In addition the common peroneal nerve hangs around this region of the knee and an associated injury to this nerve may lead to foot drop… so if your sense of hearing is acute enough I suppose you might hear the patient slapping their way down the corridor before you even see them.

Video 1 Varus Thrust Gait

Thus, having not even touched the patient there are five clues that the PLC may be injured

  1. The mechanism of injury
  2. The area of pain
  3. Complaints of knee instability
  4. An abnormal gait
  5. Common peroneal nerve involvement

So how do you confirm a PLC injury clinically? This is not based on findings from a double-blinded RCT but in my experience if you flex the patient’s leg as far as possible, they saw “Ow” and point at the postero-lateral crease of their knee they will either have a PLC injury or a tear of the posterior horn of the lateral meniscus.

Being slightly more scientific, Lunden et al (2010) discuss the role of ten separate structures of the PLC with the lateral/fibular collateral ligament (LCL/FCL), popliteus tendon and the popliteofibular ligament considered the most important of these (Figure1). I think we all know the LCL is the main restraint to varus movement from 0-30° of knee flexion but it also limits lateral rotation of the tibia on the femur. The popliteus tendon is an unsung hero in that it provides so much resistance to lateral rotation of the tibia that it should be regarded as a “5th major ligament” (LaPrade et al, 2010), while the popliteofibular ligament provides both varus and lateral rotation stability.

Fig 1

Figure 1: main structures of the PLC (with permission, LaPrade & Wentorf (2002)) 

Combined damage to these structures results in postero-lateral rotatory instability (PLRI) where the postero-lateral aspect of the tibial plateau translates posteriorly and rotates laterally (Kim et al, 2013) as demonstrated in figure 2. Tests that apply a varus or external rotational force on the tibia can therefore be used to assess the integrity of the PLC.

Fig 2

Figure 2: PLRI (with permission LaPrade & Terry, 1997)

Numerous special tests have been proposed to quantify PLRI but the specificity and/or sensitivity for some of these tests have not been determined, making recommendations difficult. Furthermore there is uncertainty as to whether some of the tests will only be positive when other ligaments are also involved. For example the postero-lateral drawer test (Hughston & Norwood, 1980) may only be positive in combined PLC/PCL lesions (Gollehon et al, 1987), while the external rotation recurvatum test (Hughston & Norwood, 1980) may only be positive in combined PLC/ACL injuries (LaPrade et al, 2008). Although combined PLC/PCL tears occur in up to 60% of cases (Fanelli & Edson, 1995), both structures can be injured in isolation.

Fortunately what researchers do agree on is that the tibio-femoral rotation: or ‘dial’ test, assesses the PLC in isolation at 30° of knee flexion (Noyes et al, 1993) so problem solved… Just lay the patient on their back and assess how far the tibia rotates laterally with their knee bent to 30°. If it’s more on the injured side then they have a PLC injury. Right?

Well, not quite. There are a few essential components of the dial test that we need to consider… if you’re lagging then get a coffee, as this is the important bit that requires 100% concentration.

95% of people will have up to 5° difference in lateral tibial rotation between sides (Alam et al, 2013)… this is normal… and the dial test is only deemed positive when the side-to-side difference is greater than 10-15° (Bae et al, 2008). A positive test indicates that all three main PLC structures are injured OR two main PLC structures are injured in combination with the PCL. If only one or two structures are injured in total the amount of PLRI may be less than 10-15° giving a negative test (Bae et al, 2008). Therefore in cases where the history is strongly suggestive of PLC injury but dial testing is negative, further investigations (e.g. MRI) should be performed to clarify the diagnosis.

The dial test was originally performed in SUPINE at 30° and 90° degrees of knee flexion (Noyes et al, 1993) but in practice, unless you have four hands it is difficult to rotate both tibiae while simultaneously stabilising each femur for side-to-side comparison. More importantly, if the patient does have a PCL injury or their PCL is naturally ‘lax’, lying supine with the knees flexed will cause the tibia to sag posteriorly (Noyes et al, 1993). In this subluxed position the amount of available external rotation at the knee is reduced by 4.5-12° (Strauss et al, 2007) so the dial test may be negative despite a PLC injury being present.

To avoid this false negative, placing an anterior force on the tibia when the patient is supine, or performing the dial test with the patient in PRONE corrects the subluxation thereby increasing the chance of detecting a PLC injury in the presence of PCL deficiency (Strauss et al, 2007). The other advantages of performing the dial test in prone is that only 2 hands are required and the examiner can compare the side-to-side difference by rotating the feet at the same time. In either position care must be taken to avoid unwanted movement at the femur (Alam et al, 2013).

Ask anyone that has heard of the dial test and they will tell you that a positive test:

a)    at 30° indicates a PLC injury,

b)    at both 30° and 90° indicates a combined PLC/PCL injury.

While this may be true, positive tests at both 30° and 90° may also indicate medial knee injury often, but not always, in association with an ACL rupture (Hughston, 1994). Laxity in these structures causes antero-medial rotatory instability (AMRI) where the antero-medial aspect of the tibial plateau translates anteriorly and rotates laterally (Figure 3). So the tibia still rotates laterally but from a different point and it is not difficult to get confused by these two very different problems (LaPrade & Wijdicks, 2012).

Fig 3

Figure 3: AMRI (from Tibor et al, 2011).

Video 2 was taken showing a patient with a right-sided medial knee injury that had a positive dial test at 30° and 90°. Figure 4 is a screenshot using Ubersense (@ubersenseapp) showing the difference in rotation between sides; a useful guide is to look for a difference in the levels of the big toes (long yellow line).

Video 2 here

Fig 4

 Figure 4: Positive dial at 90°

Therefore, although prone dial testing makes it easier to gauge side-to-side differences and corrects tibial subluxation, when positive, the therapist should also perform the test in supine (tibia supported) with fingers on the medial and lateral tibial plateaus to determine where the subluxation is occurring (Noyes et al, 1993). In addition, medial knee injuries should be assessed by performing the valgus stress test at 0° and 30° of knee flexion (Pritsch et al, 2006) and PCL injures should be assessed by combining a posterior drawer test with the posterior sag sign (Malanga et al, 2003).

Finally, when investigating the dial test Alam et al (2011) found that a lot of movement occurs at the foot/ankle complex rather than the tibia when applying a force through the grasped feet. The amount of rotation that actually occurred at the tibia was overestimated by 103% in cadavers and 136% in healthy subjects (Alam et al, 2013) when using the foot angle for measurement. The authors therefore concluded that lateral tibial rotation is more accurately measured by comparing the amount of lateral movement of the tibial tuberosity, which is only possible when the dial test is performed in supine. 

However if we are looking at subjects with 2 healthy ankles/feet it is fair to assume that the amount of movement that occurs at the foot/ankle will be similar between sides and this was confirmed in this study. Therefore, in my opinion the advantages of comparing between sides in prone outweigh those in supine, as the important measurement is the DIFFERENCE in rotation, not the exact amount of rotation that occurs. Whether a history of foot/ankle injury affects these measurements remains to be seen.

And last but not least:

Any patients that present with an acute PLC injury need to be referred onwards and time is of the essence, as surgical repairs can only be attempted within the first 2-3 weeks of the injury. By the time this window of opportunity has shut the damaged tissue may have retracted and become necrotic making it impossible to return the structures to their original anatomical position. At this point reconstruction may be required but ultimately the orthopaedic surgeon will base their decision on the time elapsed and the location of the tear.

So one of our main responsibilities is to refer the patient on immediately even if our diagnosis turn out to be wrong and we look like fools for a short period.

References:

ALAM, M., BULL, A. M., THOMAS, R. & AMIS, A. A. 2011. Measurement of rotational laxity of the knee: in vitro comparison of accuracy between the tibia, overlying skin, and foot. Am J Sports Med, 39, 2575-81.

ALAM, M., BULL, A. M., THOMAS, R. & AMIS, A. A. 2013. A clinical device for measuring internal-external rotational laxity of the knee. Am J Sports Med, 41, 87-94.

BAE, J. H., CHOI, I. C., SUH, S. W., LIM, H. C., BAE, T. S., NHA, K. W. & WANG, J. H. 2008. Evaluation of the reliability of the dial test for posterolateral rotatory instability: a cadaveric study using an isotonic rotation machine. Arthroscopy, 24, 593-8.

FANELLI, G. C. & EDSON, C. J. 1995. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy, 11, 526-9.

GOLLEHON, D. L., TORZILLI, P. A. & WARREN, R. F. 1987. The role of the posterolateral and cruciate ligaments in the stability of the human knee. A biomechanical study. J Bone Joint Surg Am, 69, 233-42.

HUGHSTON, J. C. 1994. The importance of the posterior oblique ligament in repairs of acute tears of the medial ligaments in knees with and without an associated rupture of the anterior cruciate ligament. Results of long-term follow-up. J Bone Joint Surg Am, 76, 1328-44.

HUGHSTON, J. C. & NORWOOD, L. A. 1980. The posterolateral drawer test and external rotational recurvatum test for posterolateral rotatory instability of the knee. Clin Orthop Relat Res, 82-7.

KIM, Y. H., PUREVSUREN, T., KIM, K. & OH, K. J. 2013. Contribution of posterolateral corner structures to knee joint translational and rotational stabilities: A computational study. Proc Inst Mech Eng H.

LAPRADE, R. F., LY, T. V. & GRIFFITH, C. 2008. The external rotation recurvatum test revisited: reevaluation of the sagittal plane tibiofemoral relationship. Am J Sports Med, 36, 709-12.

LAPRADE, R. F. & TERRY, G. C. 1997. Injuries to the posterolateral aspect of the knee. Association of anatomic injury patterns with clinical instability. Am J Sports Med, 25, 433-8.

LAPRADE, R. F. & WENTORF, F. 2002. Diagnosis and treatment of posterolateral knee injuries. Clin Orthop Relat Res, 110-21.

LAPRADE, R. F. & WIJDICKS, C. A. 2012. The management of injuries to the medial side of the knee. J Orthop Sports Phys Ther, 42, 221-33.

LAPRADE, R. F., WOZNICZKA, J. K., STELLMAKER, M. P. & WIJDICKS, C. A. 2010. Analysis of the static function of the popliteus tendon and evaluation of an anatomic reconstruction: the “fifth ligament” of the knee. Am J Sports Med, 38, 543-9.

LUNDEN, J. B., BZDUSEK, P. J., MONSON, J. K., MALCOMSON, K. W. & LAPRADE, R. F. 2010. Current concepts in the recognition and treatment of posterolateral corner injuries of the knee. J Orthop Sports Phys Ther, 40, 502-16.

MALANGA, G. A., ANDRUS, S., NADLER, S. F. & MCLEAN, J. 2003. Physical examination of the knee: a review of the original test description and scientific validity of common orthopedic tests. Arch Phys Med Rehabil, 84, 592-603.

NOYES, F. R., STOWERS, S. F., GROOD, E. S., CUMMINGS, J. & VANGINKEL, L. A. 1993. Posterior subluxations of the medial and lateral tibiofemoral compartments. An in vitro ligament sectioning study in cadaveric knees. Am J Sports Med, 21, 407-14.

PRITSCH, T., BLUMBERG, N., HAIM, A., DEKEL, S. & ARBEL, R. 2006. The importance of the valgus stress test in the diagnosis of posterolateral instability of the knee. Injury, 37, 1011-4.

STRAUSS, E. J., ISHAK, C., INZERILLO, C., WALSH, M., YILDIRIM, G., WALKER, P., JAZRAWI, L. & ROSEN, J. 2007. Effect of tibial positioning on the diagnosis of posterolateral rotatory instability in the posterior cruciate ligament-deficient knee. Br J Sports Med, 41, 481-5; discussion 485.

TIBOR, L. M., MARCHANT, M. H., TAYLOR, D. C., HARDAKER, W. T., GARRETT, W. E. & SEKIYA, J. K. 2011. Management of medial-sided knee injuries, part 2: posteromedial corner. Am J Sports Med, 39, 1332-40.

4 thoughts on “The Postero-Lateral Corner, the “Dark side of the Knee”… A guest article by Richard Norris

  1. Hi Adam, really enjoyed reading this blog as this is the area of the knee that I’d like to do my dissertation on. The videos and diagrams were really useful thanks mate..

    In figure 2 where you discuss the contribution of a suspected triad injury (inclusive of the medial knee structures along with an ACL rupture), do you think that if there was laxity in the coronary ligaments that attach the meniscus to the tibial plateau that they could play a role in the amount of rotation in the test also?

    Also when pain is felt in this region do you consider proximal tib/fib mobilisations as I now a lot of clinicians do it as a form of treatment? But I have struggled to find conclusive evidence to back up mobs to proximal tib/fib and its contribution to pain management of PLC of the knee. I don’t suppose you have any journals about this do you haha?

    Thanks, Matt

  2. Hi Adam

    This case study by DeLeo discusses fibular head mobs. http://www.jospt.org/search/advanced_result.asp?q=&qauthor=deleo&qYear=&qVol=&qPage=&Image2.x=-238&Image2.y=-609
    I have seen a few people with PLC injuries that have unstable superior tib fib joints so I personally wouldn’t advise mobilising those for obviously reasons. However if there is no instability mobilising the joint should theoretically maintain the small amount of joint ROM and common peroneal nerve mobility as everything heals.

    Regarding the anteromedial rotation i’d read thishttp://www.jospt.org/issues/articleID.2716,type.2/article_detail.asp

    These guys suggest the distal division of the superficial MCL which has a strong attachment to the bone is the major medial restraint to rotation. Secondary stabilisers, which only come in to play when the distal division of the superficial MCL is injured, are the proximal portion of the superficial MCL, the posterior oblique ligament and the menisco-femoral division of the deep MCL (attaches to the meniscus). So i’m not convinced that meniscal ‘laxity’ will contribute massively since there are so many attachments to bone and other soft tissue. Plus the ACL is injured in 78% of grade 3 medial knee injuries, which will contribute more to AMRI. Finally more current thinking is combined ACL/MCL injuries involve the lateral meniscus more than the medial meniscus as was previously thought.

    Shelbourne KD, Nitz PA. The O’Donoghue triad revisited: combined knee injuries involving anterior cruciate and medial collateral ligament tears. Am J Sports Med. 1991;19:474-477.

    Richard

  3. Thank you for writing this article. I am a senior Athletic Training Student at the University of Northern Colorado and had a football player experience a posterolateral corner injury which include a biceps femoris tear at the attachment on the fibular head without an avulsion fracture. Thus, it became my senior case study. This article definitely helped make this injury clearer for me to understand and learn from. I think it is a very well written article and hope to read more from you in the future! Thank you for contributing to my final project and arguably the biggest presentation I will give as a student.

    Sincerely,
    Tyler Kettner

  4. Thank you for this article. I am increasingly frustrated after 3 burst (recurring) Baker’s cysts in the course of 8 months (excruciating pain) that my ortho says nothing can be done about. Mri shows calf tears but with knee stability, doc does not feel anything can be done. Reading this confirms I need a new doc who will explore this further.

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