In several previous case videos we have shown a case of traumatic ankle injury causing ankle rocker loss and subsequent knee hyperextension during sagittal gait progression, and we have shown a case of a classic Varus Thrust gait (search our site).
Today, I will shows you a case where the 2 phenomenon are connected. If you know your normal anatomy, you should be able to put this together.
Case background, video #1: *Impaired ankle rocker (severe) in action. This was a case of ankle talus dislocation while trampoline'ing :) No surgery, but ankle was bagged up for 6 weeks. This is a TIGHT and blocked ankle rocker now, better for it to be more stable than unstable since every ligament was torn completely. These are his first steps in 6 weeks. 90 ankle dorsiflexion on the table, which is insufficient for anyone to have normal gait. Here is a great view of what happens when there is insufficient ankle rocker, one scenario at least (there are several ways around an insufficient ankle rocker). Here you can see the knee hyperextension strategy at the moment the body mass attempts to pass over the ankle, the ankle says "Nope, not today bud, try throwing the knee into extension to get over me.". And so, that is what happens here. Imagine what message the hip and glutes get from that strategy ! So, you won't see this every day, but imagine all the cases of minor ankle rocker impairment you do get in a few of your clients, and the micro knee extension strategies you can't see, that are fiddling with optimal mechanics. If you do not look, you will not find. It is why I mentioned the case last week of the ankle ROM looking normal on the exam table, but it not being used during gait. Again, not everyone needs more ankle rocker, often they need more S.E.S. (skill, endurance, strength). Skill includes, proprio, balance, coordination, motor patterning, etc. Make no mistake, this fella needs more ankle rocker !
in the sagittal video below, and more obviously in a separate video further below to more clearly demonstrate a more classic Varus Thrust gait, one should be able to see the knee undergoing a sudden abrupt varus (lateral) shift during the gait loading response. The tib-femoral joint is a sagittal hinge, not a frontal-lateral plane hinge, so this is clearly pathomechanical movement. This knee will likely undergo premature knee cartilage and meniscal degeneration if the phenomenon is not resolved.
The cause of this issue is likely more simple than complicated however there may also be multiple factors coming together in a perfect storm. However, make no mistake, in order to understand a varus thrust gait, one has to understand the why and how of the gait presentation. Additionally, one must have a clinical knowledge of the restraining systems of the knee, both active and passive, and have a high degree of clinical suspicion and working knowledge of how to assess for these types of problems. It this immediate case below, with the severe ankle rocker loss (see in the first video) the client hits the loss of ankle rocker/dorsiflexion and must attempt to move forward. In video #1 we see knee hyperextension, but what you need to see on the video below is knee varus thrust. This is a soft case, it is not a TRUE varus thrust, but the mechanism is there. It is there on that left leg/knee if you know what to look for, and is in part because he is supinating the foot excessively, while moving through neutral knee and into terminal knee extension, to try and find some kind of lateral frontal plane strategy to get around the blocked ankle rocker. Remember, there is lots of medial and lateral joint play at neutral zero degree extension, and very little if any in terminal knee extension lock out. So the shift occurs mostly around the zero degree range and then is thrusted into terminal extension giving it that "sudden abrupt" appearance. Remember the knee is not a frontal plane hinge, but it does have some frontal plane wiggle room at zero degrees, test it out for yourself ! Why does this phenomenon occur in this client with zero posterolateral corner knee injury ? Well, it is simple anatomy. The medial condyle is longer and deeper than the lateral (see xray photo below showing this relationship) and with such far lateral foot supination combined with terminal knee extension, he is likely only bearing weight on the medial condyle and the joint pivots and shifts in this zero degree extension through to hyperextension lock out (not a true instability pivot-shift but the mechanism remains present) until the LCL (lateral collateral ligament) complex and iliotibial band and other lateral structures engage. Because there is no true lateral laxity, there is only a subtle lateral shift, unlike the 3rd video below of the lady walking on tiles. So, this is a case of knee hyperextension and mild varus thrust gait from a blocked ankle rocker motion joint.
Below are some thoughts from a prior video on Varus Thrust gait (see video to the right). You must understand all of these components to help these clients fully.
Things to consider:
- old ACL/PCL and posterolateral corner damage (search our site for articles we have composed)
When the posterolateral corner complex of the knee is torn up from a blow to the knee or a torsional loading failure, the 3 components of the posterolateral corner (the lateral collateral ligament (LCL), the popliteal tendon, and the popliteo-fibular ligament complex). This complex attaches just in front of the origin of the lateral gastrocnemius tendon off the lateral femoral epicondyle. This complex can be blown out from either a PCL or ACL injury mechanism, these big player ligaments are rarely torn in isolation.
- is there a Pivot Shift phenomenon, likely. A positive Pivot Shift test will be present. One must know how to perform this test to confirm its presence, it can be a tricky test if one does not know the load vectors to apply and what the shift feels like and where it occurs during the test. This can be a very subtle positive test, again, first hand experience is everything.
- one must find this before surgery occurs for the ACL or PCL. Failure to find and address this damaged complex will likely result in rotational stability problems once return to play occurs. IT will not likely be noted in the initial post-operative months as the aggressive loading response will not be performed early on. Failure to address this problem will likely put ACL-PCL reconstruction success at a high risk.
Other critical factors to consider in the Varus Thrust Gait:
- is there medial knee osteoarthritis ?
- what is the foot type and what are the mechanics ? ie. Forefoot varus, Forefoot supinatus, rearfoot variances
- does the patient have excessive pronation challenges that create massive internal spin into the tibia ?
- is the hip frontal and rotation plane stable? Can the patient adequately control rotation at the hip level ?
- is there a Cross Over gait phenomenon with narrow based step width ? (search our blog and youtube for "gait guys crossover gait"). A narrow step width will create an "unstacked" limb and promote more rotational risk into the limb, often playing out at the least tolerable joint to rotation . . . the knee.
- Does the client have Tibial Varum ? Genu Varum, Genu Valgum ? These can promote and complicate the Varus Thrust gait.
- Does the client have Tibial torsion or Femoral Torsion variants ? These can promote and complicate the Varus Thrust gait.
- is there weakness of the lateral gastrocnemius or biceps femoris (to name just two the directly cross over this posterolateral interval and can offer joint compression/stability ? What about weaknesses in the medial leg ? Not that these are anywhere sufficient to offset a PLRI (posterolateral rotatory instability), but, they are secondary helpers/restraints.
One should clearly see now that the Varus Thrust gait is potentially complicated and multifactorial. One MUST understand:
1. many components of normal gait and normal anatomy from foot to pelvis, at least.
2. be able to assess for aberrant mechanics and pathologies within all joints of the lower limb
3. be able to assess for post operative rotational stability and laxity (*even a healed, yet partially attenuated, Posterolateral corner complex that was not noted or addressed in the ACL-PCL reconstruction can come back to haunt even the best reconstruction. Those little rotational instabiliites will build over the years and render attenuation of the other secondary posterior restraints in the knee. Like a Lisfranc injury, sometimes things take a few years to brew and blossom before the "career ender" instability shows up. Trust us, we have seen it enough times.
Rule: if one does not know it exists, one will miss it. If one does not know how to assess it, one will miss it. If one does not know normal anatomy, torsional variants, foot types and gait types, one is likely to be lost and left fumbling. Our clients deserve more.
Clinical pearl: if you are radiographically sharp, you should have noted the Pellegrini-Stieda lesion at the medial tibial epicondyle (this is not a radiograph for this case, it was used to show the longer medial condyle reach). These are ossified post-traumatic lesions near the medial femoral collateral ligament attachment. This avulsion injury of the medial collateral ligament can calcificy after a few post-trauma weeks.
- Dr. Shawn Allen, the other gait guy