These boots are made for walking… sometimes

Image is everything in sport these days, like it or loathe it. And Aircast boots aren’t exactly en vogue. Unless you are David Beckham, who has become synonymous with the “Beckham Boot”, there aren’t many that can pull off the grey, dull, clunky boot look well.

Aircast boots / walking boots / Controlled Ankle Movement (CAM) boots… or just Beckham Boots.

This is becoming a problem, as perception of the walking boot amongst athletes, coaches and even other medical staff (unfortunately) is that the provision of a boot must equal a severe injury. Wearing one is a badge that not many people want. This worries me for a number of reasons…

Do no harm:

Whether you use POLICE or PRICE, our first thought in acute injury management is “Protect”. I’ve written about acute assessment before (here) but if you have just witnessed the injury and don’t have any immediate concerns about preservation of life or limb, then often we don’t want to rush into a diagnosis. Things can always look worse immediately after injury, so our plan is to offload, reduce risk of secondary injury or worsening of the initial injury (AKA.. “Protect”).

So, with lower limb injuries around the foot and ankle, quite often we will provide a walking boot. Cue the groans.. “I can’t be seen in this”, “Its not that bad”, “Don’t let the coach see me wearing one”.

But here are our options; walking boot, below knee cast, tubular bandage… or nothing.

Immobilise

If we are talking about doing no harm, then evidence suggests that long term immobilisation (greater than 4-6 weeks) of acute ankle sprains is detrimental when compared to “functional treatment” (to avoid an argument of what is functional, lets just call this “Optimal Load” and leave it to clinical discretion) (Here). But also no intervention could be seen as negligent. If we have enough suspicion to be weighing up “should I offload this?” then when compared to a control (wearing a normal shoe), a walking boot limits sagittal plane range around the ankle to around 4 degrees and reduces body weight in peak plantar plane surface forces (154% vs 195% BW) (Here). So if we face an option of boot vs no boot, where we know we can limit range and peak forces in an acute injury, the answer is “yes, offload it” even for a day until you can re-assess. Why wouldn’t you?

A brief period of immobilisation, “around 10 days in a below knee cast or removable boot”, along with treatment to reduce pain and inflammation is recommended (Here). In a study of fifth metatarsal fractures, those that we provided with a walking boot had better outcomes of pain and return to activity vs those immobilised in a cast (Here). This is an advantage of the boot. We can protect the foot and ankle in a boot but remove it to utilise other treatments and rehab. We can keep unaffected joints mobile – perhaps another blog but I like to use ankle injuries as an opportunity to work on detailed foot control, like great toe flexion, abduction, tibialis posterior control and so on. We can do all of this whilst limiting inversion and staying in plantar-grade if necessary. Or if its a 5th metatarsal stress, we can keep the ankle mobile. You get the point, we couldn’t do that in a cast.

Our other option was tubular bandage. In a world where we can download apps to make us look like cartoon dogs for free, we still have plain grey boots and boring beige tubigrips, I say this as an academy physio trying to make acute injury management appealing to young kids. When compared to those provided with a below knee cast & removable boot, severe ankle sprains had better clinical ankle function measures, quality of life, levels of pain and levels of activity at 3 months vs those provided with a tubigrip (Here). Perhaps a little bit unfair on the tubigrip, whose role in dealing with a severe ankle sprain is “compression” – a bit like saying an elastic band is worthless because its unable to hold sand together. But ultimately, in an acute injury, tubular bandage isn’t going to provide much protection at all.

Long term use:

Now the point of this blog is to de-sensitise reactions to using a boot for the short term, but it would be remiss not to mention their use in long term injuries. Following surgery or a fracture, the use of a walking boot is associated with a quicker return to normal gait and function (Here).

But does it come at a cost? Fixing the foot and ankle is obviously not conducive to “normal” walking, so it will change gait temporarily. In doing so, it can also create problems elsewhere. 84% of people using a boot developed or increased a secondary site of pain in the first two weeks of using the boot (Here). Now, 68% of those reported this pain made no difference to their life, but if you have someone with existing problems, especially in the low back, you might want to consider this stat as part of your clinical reasoning. Remember, part of our job is to prevent secondary injury.

If the boot fits..

There’s one option and aid we haven’t talked about and thats crutches. The reason I haven’t mentioned them is they come with the same stigma as a boot. They are obvious, they demonstrate you are “injured” so if someone doesn’t want to wear a boot, they probably aren’t going to want crutches either. But hopefully this brief blog gives you a bit more of an argument behind your reasoning to help reduce the association that wearing a boot equals a severe injury. So when we hear that a player has left the stadium in a boot, for the first couple of days, so what? It might be nothing. Something I have trialled before in a key first team player, which I admit is divisive, is to manage an athlete across 24 hours. So.. There are some injuries that can continue to train, like an inflamed sesamoid or plantar-fascia pain, but to give them the best chance of training and competing it would help to offload the structures through the rest of the day. So, instead of trying to control 1-2 hours of the day and reduce training / matches, why not try a boot to offload for the other 22 hours in a day? As the evidence above suggests, this is certainly not a long term solution. But across a couple of days, maybe? Limited evidence, but its worked twice for me.

The key to this working, was education. Ensuring that other players and staff understood that the boot didn’t mean a serious injury. But was an adjunct to help offload… or “protect”. There’s a theme here.

This is the message we need to get across, protecting an acute injury is not the same as us diagnosing or offering a prognosis. “You might only be in the boot overnight, but its a safe way of transporting you home.” We just need to help give them some good PR and make them seem less daunting, less serious…

 

Yours in sport

-Sam

 

 

 

Compex doesn’t have to be complex

compex

I should probably start by acknowledging that there are other muscle stimulation devices available… but I’m not employed by Compex, I just have some very good experiences using their product. This blog was borne out of frustration of seeing Compex machines gathering dust in treatment rooms or being used ineffectively as passive, plinth based modalities. I think a lot of people are missing the trick, you need movement!

While I am an advocate of its use clinically, I  want to disclose that using a Compex will not make a bad exercise good. It is a bolt-on to a rehab program and is something that can make a good exercise great. That is key. The clinical reasoning, exercise selection and placement of the stimulation all underpins an effective application, so before rolling it out to all athletes or patients make sure you can reason why it has a place in your practice.

Its all about progress

Like with any intervention, the clinical reasoning behind the application of muscle stimulation can influence its use at different stages of injury and rehabilitation. In the acute stages, it is believed that muscle stimulation may modulate pain. For an interesting read on the use of electricity and pain throughout the centuries, click here. However, as we understand more about optimal loading and mechanotherapy, we probably need to limit the time an athlete sits on the plinth watching the latest Mannequin Challenge on their smart phone while their quad twitches. It is worth considering that a Compex placed on a dead body would still cause it to twitch. The key is to get them moving and use the Compex to either facilitate movement or provide an external load. Interesting that we can use the same machine and the same settings to either regress or progress an exercise… the key is in the exercise selection.

Consider the tissues

Muscle injury: It should be pretty obvious that placing a muscle stimulation device, designed to promote contraction of muscle, on a contractile tissue with a tear or micro-damage could have negative consequences. For a second, lets forget the Compex. Respect the pathology and consider if you really need to lengthen or contract that muscle to load it. Is there a way you can work that tissue as a synergist perhaps? If the hamstring was injured in the sagital plane, can we move through coronal (frontal) planes and still load the hamstring? This could possibly be a slight progression on an isometric exercise and shouldn’t change the length of the muscle that may cause pain or further damage. Certainly more beneficial than sitting on the treatment bed though. So now consider how muscle stim may benefit this stage of injury. It could possibly help with any inhibition due to swelling or pain, perhaps be used to add an increased load to unaffected tissues that you may not be able to load otherwise.

As the healing progresses and the level of activity increases, it is quite common that we see some deficits in muscle function, especially after a long acute phase (if that isn’t a paradox?! Think post surgery or fixation). A good example is post ankle reconstruction, where you have worked on regaining plantar / dorsi flexion but when you ask the athlete to do a heel raise, it’s quite an effort. It may be appropriate to use the Compex here as a little crutch to facilitate movement and contraction. But the key thing here is it is not our cadaver that we causing a contraction in, the athlete is consciously initiating the movement. (Previous blog on internal and external cues here).

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Now promise me if the Compex hurts, you will turn it down. OK?
Progressions by all definition, progress. So after working through isometric and concentric exercises, the program may require some eccentric load. This is worth trying yourself before asking a patient to do it, because a very simple exercise like a TRX squat that may have been cleared earlier in the program can dramatically increase in work with the addition of Compex. Consider a quad injury. The Compex has two phases of a cycle, a fasciculation phase that causes visible twitch and a long contraction phase (depending on the setting, the length and intensity of the contraction change). After one or two cycles for familiarisation, instruct the athlete to work against the contraction – so when the Compex wants to promote knee extension via a quad contraction, sit back and encourage knee flexion. Try this yourself for 6-8 reps and feel the fatigue induced, it usually surprises people. Again, make sure you can reason WHY you are doing this. This is usually a good bridge for someone who needs to step up their program but maybe can’t tolerate external load (confounding injuries, instability of joints, lack of technique etc etc.)

Joint Injuries: In comparison to a muscle injury, your application of Compex may be more aggressive. Because you are unlikely to affect a non-contractile tissue with the stimulation, you may use the eccentric reasoning to help reduce atrophy rates following a intracapsular injury like an ACL. Ensure you know the available range first of course.

With these injuries, the external stimulation may help with inhibition, improve proprioception lost by the ligament or capsule or it may provide stability to the joint by increasing the available contraction. Again, there will be a time and a place and it requires the clinician to reason through the application, but this may be a great addition to a program that is becoming stale.

Tendon injuries: The use of the Compex to enhance an isometric contraction or to create an eccentric contraction may be a great addition for an in-season tendinopathy as a way of managing load. The timed contraction allows clinicians to monitor Time Under Tension (TUT) which is essential for tendon management. If considering a High-Medium-Low frequency through the week, a pain free exercise that is used on a Medium day can become a High load exercise with the addition of an externally generated contraction. But consider the two things that aggravate a tendon, compression and shear. Appropriate exercise selection and range is going to be crucial, that being said, it may be that the addition of stimulation to the quads actually reduces shear through the patella tendon by changing the fulcrum of the patella (no research to back this up, just my musings).

musing
I really like Geckos. I found this Gecko a musing
Conclusion:

I think there are many options out there to enhance rehabilitation by considering the diversity of muscle stimulation. But I want to repeat for the hundredth time, it is the exercise selection that is key. The addition of a Compex will only amplify that choice.  For the patient, it adds a bit of variety to a rehabilitation program and for the clinician it is another tool to help with optimal loading of a healing tissue or structure. I am a big fan of weight training (don’t let my chicken legs fool you) but there are injuries or athletes that for one reason or another are unable to tolerate weights. This is one tool in a very large and overused metaphorical tool-box that may bridge that gap between body weight exercises and weighted exercises. I also believe there is great benefit when complimenting this with Blood-Flow Restriction Exercise or Occlusion training… but that’s another blog.

As always, thoughts and opinions are welcome.

 

Yours in sport,

Sam

Case Study: Myositis Ossificans – Deadlegs aren’t just for the playground

Whether you call them a “dead leg” or a “Charlie horse” or a “cork thigh” chances are we have all had one. Mostly from the playground days where the bigger kids want to take pleasure in seeing you limp for 5 minutes. However when they happen in sport, with fully grown athletes running at full pace, a collision to the thigh can result in an injury much more serious than the one we associate with from childhood.

The reason I wanted to write this blog was that I worry  that thigh contusions are underplayed in the treatment room, potentially because we associate them with those school sports injuries that can be “run off”. This is a case study that I became involved with after initial management of the “dead leg” failed, and to this day is one I reflect on about how important initial management can be in saving severe stress in the long run. This is a case of a “routine” dead leg that is commonly seen in contact sports that resulted in 9-months of rehab to manage a secondary case of myositis ossificans.

What are we dealing with?

There are two types of “dead legs”

  1. Intramuscular: blunt force trauma to the muscle that results in a haematoma, in this scenario the epimysium remains in tact and the bleeding is contained within the muscle compartment.
  2. Intermuscular: the epimysium surrounding the muscle is broken along with the damage to the muscle tissue, the resulting haematoma spreads outside of the damaged muscle.

The intermuscular hematoma by far looks the worst, it’s the one where the whole thigh goes black and blue and looks pretty nasty. However, clinically these ones tend to heal quicker and they look a lot worse than they feel. The problem with the intramuscular haematoma is that because it is contained, the pressure can build up and become more painful. It is generally more debilitating as a result, with larger loss of range and more pain. It also doesn’t provide that visible diagnosis as very often you just get a small sign of bruise on the skin from the impact – this is where it can get dangerous as we like to be able to see injuries (hmmm something about invisible injuries and under diagnosis.. concussion?). We have discussed acute management before (here) but with dead legs, it is always worth monitoring for a few days and hoping that the leg goes black and blue.

fig2

In the first few days, range is a good indicator. On day 1 after the injury, if they are unable to achieve >90 degrees knee flexion, the prognosis is generally longer. For a bad intramuscular contusion, you could be looking around 6 weeks. This is where the coaches tell you it’s just a dead leg and they’ve had worse. But, it is structural damage to the tissue resulting in bleeding and should be given the same respect you would give to a tear. (Muscle injury classification via the Munich Consensus here).

Myositis Ossificans (MO):

MO is the formation of heterotrophic bone within the muscle following trauma (here) essentially following failed healing the body begins to lay down bone in an attempt to add stability and structure.

Case study:

The following case study is an example of an academy player, where an initial intramuscular trauma to the muscle was accelerated back to activity resulting in a 17cm tear of vastus lateralis (VL), consequently being diagnosed with MO that was estimated to be 3cm thick and of equal length to the tear.

Timeline:

  • Day 0 – initial impact to right VL via collision in training, had to be removed.
  • Day 1 – “able to squat and lunge but pain on a stretch”. Player expressed determination to train and so was allowed to.
  • Day 2-3 – continued training
  • Day 5 – Removed from training with “cramp / DOMS” in right leg.
  • Day 8 – Sudden loss of power with running and kicking, removed from training.
  • Day 30 – returned to training
  • Day 31 – played in a competitive game but substituted by manager after 25 minutes due to inability to run. Assessed by doctor and head physio. Visible contained swelling in VL, palpable solid mass, loss of range and pain on contraction of quads. MRI scan demonstrates a 17cm longitudinal tear of VL. Suspicion of MO so sent for ultra sound scan which was confirmed, absent from full team training for 9 months.

Intramuscular haematoma
Contained haematoma within the vastus lateralis muscle after 30 days of continued training post-initial injury
Management:

Surgical excision of MO is only really reserved for persistent cases that don’t respond to conservative treatment (here). A collective decision was made that we should try to reduce any form of load that may stimulate further bone growth. As a result, the player was removed from all activity of the lower limbs, no soft tissue therapy to the quads and at this stage no stretching of the affected tissues.

It is neither healthy nor beneficial (or fun!) to completely rest when you are used to training 6 days a week. Credit should go to Will Abbott (@WillAbbott_) for his contribution to the maintenance of the athletic profile for this player. A periodised program was designed to maintain metabolic and cardiovascular systems, strengthen the upper body and completely unload the lower body.

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A periodised model to demonstrate maintenance of unaffected systems with complete lower body unload (designed by Will Abbott)
The program included swimming, with multiple floats between the legs to reduce the temptation to kick. All gym based activities were performed seated or with legs supported when lying to reduce axial load through the legs during upper body lifts. Upper body metabolic sessions were implemented via high intensity interval training, with small rest periods to help maintain specific anaerobic demands relating to the sport. This was done using medicine balls, ropes, boxing pads.. anything to reduce the monotony of daily upper body training.

Each month was broken down further (as shown below), with follow-up ultra sound scans every 4 weeks. After the first 4 weeks, we observed a 2.5cm reduction in length which consolidated our thought process to continue de-loading. With limited exercise potential and treatment for the leg, we ran half days and 5 day weeks to help maintain a positive psychological presence.

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This was an opportunity to increase muscle mass in the upper body, an opportunity that would not have been possible during season if the player continued to play and train. This allowed a clear progressive pathway for increased lean mass with the following phases:

Hypertrophy –> Max strength –> Strength / power conversion –> Power

While the conditioning phases were as followed:

Aerobic base –> Max aerobic –> Supra max aerobic

There was a decrease in calcicific mass every month, although the rate of this varied each time. By the end of month-4, the mass had completely reabsorbed which meant the reintroduction of load to the lower libs.  By this point, the end of the season was 6 weeks away and therefore no realistic opportunity to play again this season, so the decision was made to start physical preparation for the following season.

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An example of the lower body periodisation
The lower body gym program was tailored as followed:

Strength endurance* –> Strength –> Max strength –> Strength & power complex training

(* This was probably more “re-introduction to the gym” rather than true strength-endurance. But this phase would have served as a gentle hypertrophy phase given the 4 months of atrophy)

Before undergoing a linear outdoor session progressing from general preparation to sport specific drills with Tom Barnden (@barnden_tom). The player completed a full pre-season and no recurrent symptoms to date.

Conclusion:

Hopefully the lengthy timeline of this case study demonstrates the importance of giving each individual injury the respect it deserves. While I hope the management is interesting, the key discussion point is how do we approach “dead legs”? Should there be better education to athletes and coaches about the magnitude of injury? Essentially given the tissue damage, are they a tear? If an A4 piece of paper represented a muscle, and we tear down the middle (strain) or poke a hole through the centre of the page (blunt force trauma), that page is still affected and unable to serve as an A4 piece of paper. Why does the mechanism of damage change the management of injury? Given any loss of range or function following a blunt force trauma, always consider the magnitude of potential damage; monitor swelling, bruising and pain and have adequate timelines in the back of your mind – don’t rush to a diagnosis / prognosis on day 1. There will be times where there is impact and initial pain but full range and full strength – this is where our pitch-side assessment and reasoning comes in (here).

Yours in sport,

Sam

Taking your time with acute injuries

One of the benefits of working in sport is that you usually get to see injuries first hand, the mechanism, the severity, even the initial management. We have discussed pitch sidee management before (here) but what about the day, or days, following? Are we doing enough to aid the healing processes in the early stages, or perhaps too much? With our best intentions of helping an injured athlete, are we over looking the importance of “protection”?

This blog discusses the assessment of those more serious injuries – the ones that require athletes to stop in their tracks, cease the game / training. Not those little niggles that walk in at the end of the day.

Reasoning with the history:

Knowledge of the mechanism of injury can greatly aid your management throughout the later stages of your treatment. Muscular injuries for example, can be simply divided into two traumatic categories; direct (laceration and contusion) and indirect (strains) (Huard et al 2002 (here); Petersen & Holmlich 2005 (here)). Appreciating the differences in these mechanisms will certainly influence your return to train criteria later on, but what about in the acute settings? Would your treatment change on day 1 or 2 with these different mechanisms? Skeletal muscles are built of basic structural elements, myofibers. Individual myofibrils are surrounded by the endomysium and bundles of myofibrils are surrounded by the perimysium (Haurd et al 2002). Lower grade injuries such as exercise induced muscle fatigue, will only affect the myofibrils, resulting in raised creatine kinease levels (Ahmad et al 2013 here). Regardless of the mechanism, damage to the fascia and extracellular matrix would be consistent with a higher grade injury and would see the release of muscle enzymes, destruction of collagen and proteoglycans as well as the presence of inflammation (Huard et al 2002; Ahmad et al 2013). The formation of haematomas in combination with inflammation can create an ischaemic environment, increasing the risk of further muscle damage (Ahmad et al 2013).

There seems to be an false sense of urgency created in these acute situations, especially at the elite level where time lost to injury means big money and with that brings an extra level of stress and pressure to the therapist, the athlete & the coach. But the injury has happened.. we can’t change that! We can certainly make it worse though. What are we expecting to find and see with our immediate objective tests? Lets say we have just seen someone recoil, fall to the floor clutching their hamstring, unable to walk off the field of play.. is a straight leg raise or resisted knee flexion test going to tell us something we didn’t already know? OK, so maybe we want to give all parties an idea of how bad this is.

“Do you think its grade one or two?” 

“Yes?”

There are numerous injury classification systems currently used in practice, although traditional classifications can be confusing. Ahmad et al (2013) describe 3 grades of injury from mild to severe, with one set of definitions relating to clinical presentation but with differing definitions depending on the influence of Magnetic Resonance Imaging (MRI). When I was training, we used the Gr I, II & III system that was disseminated by Peetrons in 2002 (here). In 2012, the Munich consensus group (paper here) sought to clarify the term “strain” and provide a structured classification system for clinicians. Table 1 is an overview of the existing classification systems pre-2012 that are widely used in the literature as well as clinical practice.

O’Donoghue 1962 Ryan 1969 (initially for quadriceps) Takebayashi 1995, Peetrons 2002 (Ultrasound-based) Stoller 2007 (MRI-based)
Grade I No appreciable tissue tearing, no loss of function or strength, only a low-grade inflammatory response Tear of a few muscle fibres, fascia remaining intact No abnormalities or diffuse bleeding with/without focal fibre rupture less than 5% of the muscle involved MRI-negative=0% structural damage. Hyperintense oedema with or without hemorrhage
Grade II Tissue damage, strength of the musculotendinous unit reduced, some residual function Tear of a moderate number of fibres, fascia remaining intact Partial rupture: focal fibre rupture more than 5% of the muscle involved with/without fascial injury MRI-positive with tearing up to 50% of the muscle fibres. Possible hyperintense focal defect and partial retraction of muscle fibres
Grade III Complete tear of musculotendinous unit, complete loss of function Tear of many fibres with partial tearing of the fascia Complete muscle rupture with retraction, fascial injury Muscle rupture=100% structural damage. Complete tearing with or without muscle retraction
Grade IV X Complete tear of the muscle and fascia of the muscle–tendon unit X X
Table 1: Descriptions of muscle classification systems used clinically From Mueller-Wohlfahrt et al (2012)

The Munich consensus established that there was disparaging definitions amongst clinicians regarding the term “strain” and also the classification of injury. The rise of imaging to support clinical findings further added to the confusion of defining a Grade I injury that may not be present on MRI. Amongst many irregularities with the classification systems in Table 1, there was the vague nature of defining when one grade becomes another. As a result, Mueller-Wohlfahrt et al (2012) produced a new classification system that included delayed onset muscle soreness (DOMS) & contusions and allowed clinicians greater manoeuvrability in diagnosing muscle injuries. In 2014, this was taken a step further by Noel Pollock and colleagues at  British Athletics (paper here) (he explains why much better than I could, here on this BJSM podcast).

“If you can’t help them, at least don’t hurt them” – Dalai Lama

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I’m pretty sure he just referenced the Dalai Lama…

So with all this confusion regarding classification ,what are we supposed to say to the athlete and what are we to do? Things always look bad in the initial stages. Generally if there is pain on the way to the treatment room (if they have stopped playing, then there almost certainly will be) how much more do you need to know? This is where the mechanism & history is key. It may be required to rule out any bony injury at this stage, but again, if you have seen them pull up and clutch a muscle belly then that may not be essential – a bonus of being pitch side to observe such things. What about ligamentous injuries? Well do we need to assess instability today? Is there a chance that we could make something that is stable unstable by repeatedly testing it in the early stages? Even if we think its severe, like a complete ACL, most surgeons won’t operate while there is active swelling anyway. Some specific injuries DO require this, hand injuries for example may require more immediate attention from an orthopedic surgeon. Or total syndesmosis ruptures that usually require an operation within 2 weeks. (A good discussion on this injury was had recently by the PT Inquest guys here)

In the very acute stages (I’m talking first day or two) our role is to help reduce and minimize pain, reduce risk of secondary injury and ensure the athlete is safe to mobilize at home independently. What do we gain by giving them a classification of injury there and then?

“Lets let the swelling and pain settle down, get you comfortable and in a day or two we will be able to be more accurate with our assessment and diagnosis” – I think thats a pretty reasonable thing to say on the day of an injury and I’m yet to have any complaints from athletes, providing you explain why you are doing this. I’m not going to expose myself to sensitivity and specificity of tests because I will undoubtedly get it wrong, but in the heat of the moment, when everything hurts, you will almost certainly find false positives in tests – resulting in inaccurate diagnosis.

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I’ll admit, this takes a bit of confidence. When the treatment room is full of staff, other athletes, the injured athlete themselves. To stand there and hardly do anything seems counter intuitive. But take a breath and ask yourself, “what do I NEED to know at this very moment?” It shouldn’t be, “What tests do I know that I could use here” – these two questions are very subtly different but the actions that follow them are huge. You aren’t there to show the room what assessment skills you have, not on day one. Respect the injury.

The next couple of days can also tell you a lot of information without you needing to pull and prod on the table. Whats the 24 hour pattern of pain? Any sign of inflammation? Yes? Then whats a prolonged assessment going to do other than promote more inflammation. Check Aggravating / easing factors or limiting ADLs – getting on and off the toilet seat without excruciating pain may be enough info that you don’t need to assess a squat today. Again, be comfortable treating what you do know, treat the inflammation and the pain. When that settles, we can begin to explore a bit more specifically. Will a positive test today get them back to training quicker? No.

What about treatments?

The classic PRICE guidelines have now been superseded by the POLICE (Protect, Optimal Loading, Ice, Compression, Elevation) guidelines (here). I’ve previously debated the clinical relevance of ice here and regular readers of this blog (mum and my mate Conor) are probably familiar with my interest in Optimal Loading. Regardless of if you use PRICE or POLICE, one thing we seem to overlook is the very first letter. Protect. Protect the injury from secondary damage and unnecessary pain. This may mean not doing very much at all. Consider the nociceptive input of us repeatedly prodding the injury, whether its part of assessment or treatment. Again, we go back to the pressures of sport – to have an athlete sat there doing nothing can be uncomfortable for the staff and boring for the athlete. This is where the creativity of “optimal loading” comes in handy. Protect the injury, keep the rest of the athlete busy.

Summary

I’m not suggesting we just sit and wait for weeks hoping they get better on their own, but just try and think about why you want to assess something and how is that answer going to influence your management on this day. I appreciate that objective measures are going to be beneficial, but just take the ones you need. Now obviously, if symptoms drastically improve over night, we can be a bit more direct with our assessment. It’s here we can start to expand our objective measures.

  • Don’t rush to a diagnosis or classification (have the differentials in the back of your mind or discuss them with colleagues / club doctors)
  • Don’t over assess for the sake of it (do enough to keep the athlete safe but minimize effects of injury)
  • Don’t over treat (sometimes, less is more!)

 

Remember, this isn’t aimed at those little niggly injuries that DO warrant further assessment – in these cases a thorough assessment may actually help reduce the risk of a full blown injury. Instead, this is for those injuries that you know in the back of your mind are out for a few days / weeks. If anything, the more severe (duration) the injury, the less acute assessment required perhaps? Just remember to exclude all those nasties!!

I appreciate I’ve probably given more questions than answers in this blog, but that was the aim. This wasn’t supposed to be a recipe but has hopefully sparked some questions about your clinical reasoning.

 

Yours in sport,

Sam

 

 

 

Laboring through a Labral Tear

One skill when working in sport is learning to compromise between your clinical brain (the one that tells you that pathology and injury needs to be managed a certain way) and your performance brain (which tells you that your job is to get athletes back over the “white line” in order to do their job). In an ideal world, we try and appease both of these brains where tissues heal well and performance is optimised with the lowest risk of re-injury. But there are some pathologies that cause these two brains to clash. Ones that can be “managed” until the off season where proper interventions can take place. One such injury that I’ve been trying to learn more about is the mid-season hip labral tear.

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The purpose of these blogs is to encourage me to read more around certain topics, so in order to help with this I have to say thanks to a few people that have provided me with papers and words of wisdom (Erik Meira, Nigel Tilley & Joe Collins). And thanks to whoever invented Twitter because I probably wouldn’t have this access to knowledge otherwise.

The Problem..

Typically, hip instability injuries are seen in sports with high repetitions of rotational and axial load – football, gymnastics, hockey, tennis, martial arts.. and so on. The hip is widely accepted as being one of the most structurally stable joints in the body, with a deep acetabular socket lined by the labrum, which creates negative pressure within the joint to increase congruency of the femoral head. But what happens when this environment is disrupted? A recent review by Kalisvaart & Safran (here) explain that it takes 60% less force to distract the femoral head from the acetabulum in presence of a labral tear. (This review is great for explaining multiple causes of hip instability, not just labral tears, and also assessment techniques.)

Typically, a lack of stability is replaced by rigidity, where the surrounding soft tissues try to compensate for this increased translation (Shu & safran 2011 here and Boykin et al 2011 here). On assessment of an ongoing labral tear, its quite common to find increased tone or reduced range around adductors and hip flexors. Iliopsoas in particular plays a role to help increase congruency in the hip. (For tips on how to release iliopsoas, please tweet @Adammeakins) – one key thing when managing this condition is not to confuse high tone / over activity with being “too strong”. Chances are its the opposite, it more likely indicates a lack of control. Its not uncommon to see adductor tendinopathies secondary to labral tears as the the load around the joint increases – especially in sports like ice hockey where there is high eccentric load on the adductors (Delmore et al 2014 here).

The Intervention..

So, you’ve diagnosed the tear (clinically and / or radiographically) but other than being irritable, it isn’t affecting the athlete. (Note, not all tears can be managed conservatively, due to pain & some require mid-season surgical intervention – Philippon et al 2010 here). The key premise to your ongoing rehab should be to make the hip joint as robust as possible. Remember, “Stability – not rigidity”. Whats the difference? Can the athlete control the hip or pelvis while performing another task? Or do they lock into a position and rely on passive structures like ligaments and joints.

Consider the demands of the sport. Don’t just fall into the trap of working through what I’d call the “action man ranges” – true anatomical flexion, extension, abduction and adduction. Watch training and competitions of nearly all sports and you’ll rarely see these truly sagittal or coronal movements. They tend to be combinations accompanied by transverse movements of the body in relation to the limb. Make sure this is replicated in your rehab.

Using the three examples above, consider the role of the hip musculature throughout these movements. We don’t always have to replicate abduction in an open chain movement, sometimes its necessary for it to be closed chain and for the body to move relative to the limb. Note how none of these tasks fit the “action man ranges” but all involve some degree of traverse rotation, combined flexion and abduction or extension and adduction etc etc.

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No I can’t bench press, but my squats are awful.
Delmore et al (here) and Serner et al 2013 (here) describe some excellent exercise interventions for the adductors here. These include some good low-load isometrics for those early stage reactive tendons – with isometrics appearing to down-regulate pain associated with this acute pathology (Koltyn et al 2007 here; Rio et al 2015 here to name just two resources) . Moving forward through rehab, I’ve discussed exercise progression at length before (here), I’m not dismissing exercises that involve pure flexion, extension etc but as part of a progression, its important to combine these movements. For example, start with a single leg dead lift – can the athlete control their trunk through hip flexion and through extension back to neutral? No? Then here’s a range to work on, using regressions to help improve technique and control. Yes? Then add a rotational component at different ranges of flexion – rotation away from the standing leg will increase the demand on the adductors to control the pelvis in outer ranges. The leg itself hasn’t abducted, but relative to the trunk it is hip abduction.

Remember the bigger picture

Its important not to just focus on the affected structures. For those interested in groin pain, a summary of the 1st world conference on groin pain is here – one key message from that conference was that anatomical attachments are not as discrete as text books make them. Consider what else contributes to the hip and pelvis control. We have mentioned iliopsoas control, but also rectus abdominus. Its not just a beach muscle. Eccentric sit ups can help improve control of the hip flexors, along with some lower load exercises like dead bug regressions – a little imagination or some quick youtube research can turn this one concept into hundreds of different exercises.

We have addressed the issue of controlling abduction through range with the adductors, but also remember to maintain that abduction-adduction ratio with some external rotator & abductor muscle exercises (queue Clam rant here – clams to me are like psoas release to Meakins). Possibly the best piece of advice I was given when doing this research was from Joe Collins, who told me to consider hip joint pathologies like you would a rotator cuff injury in the shoulder. Don’t neglect those smaller, intrinsic muscles around the hip. The exercise below is an anti-rotation exercise working through ranges of hip abduction-adduction.

The athlete is tasked to resist the rotation of the femur into external rotation while slowly moving through hip abduction and back to adduction. (This example is done with a shorter lever to improve control and the bench provides feedback to keep the hips in neutral or extension, rather than the favored flexion). Anti-rotation exercises can also be incorporated into trunk / core control exercises (for any instagrammers – follow ETPI who post some great videos and snaps of golfers working on rotational control). Progress from anti-rotation into control through rotation. Some examples here:

anti-rotation plank with sagittal control

Anti-rotation plank with traverse control. Encourage the athlete to keep the pelvis still when moving the upper limb.

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Single leg bridge with arm fall outs. Can be regressed to a normal bridge if the athlete lacks lumbo-pelvic control.

Side plank with arm tucks – an example of controlled trunk rotation while isolating the lower body to stay stable. Can be combined with the adductor bridge mentioned in Serners paper to increase load through proximal adductors.

 

These are just some ideas of how to manage a labral tear mid-season; working on rotational control, analgesia via isometrics, improving congruency in the hip joint and overall hip stability via strengthening – Stability, not rigidity! The exercises mentioned here are by no means an exclusive list and I love learning about new drills and ideas, so please share any that you find useful.

 

Your in Sport,

Sam

“I’ve come here for an arguement”

I’ve recently made the move from the clinical environment into academia (despite the occasional clinical fix to satisfy my itchy feet). Part of this move was to set up some new MSc modules at the University of Brighton. The way I wanted this to run was based on me facilitating discussion rather than standing up and banging on about what I would do in different situations – no-one is going to enroll for that! But for this to work, it relies on people feeling comfortable talking about their own practice, something I’ve been surprised by the reluctance in doing so. People seem very uncomfortable disclosing what they do and how they do it.

A while back I read a blog re-tweeted by IFL Sciences (@IFLScience) about how a disagreement is different to an argument. Now rather than me eloquently blurring these definitions and confusing you more, why not allow the genius of  Monty Python to explain.. please watch this brief 3 min video (here).

The original clip goes on a bit longer and in true python fashion, gets stupider. But this clip can translate into our practice. It is perfectly reasonable and healthy to argue. We are not going to learn from each other by accepting that the other guy sat in the room, who has more experience than me, treated his ankle sprain using those exercises, so that’s what I should do.

No! Why? Why those exercises for that individual?

 

There are many roads to Derby:

imageCompletely random destination (just so happened to be one of the cities I can spell). But this image sums up what I think about clinical reasoning. It also demonstrates what I encourage our students, more so post-grad students with clinical experience, to accept when questioned about their practice.

Most of us have at some point ignored the sat-nav, right? Intentionally or not. But it simply re-routes and will eventually lead you to your destination. The same with rehab & treatment. We may all have the same goal & end point, but how we get there is different. The route we chose depends on many factors.

Letting the sat-nav make the decision:

For a relatively less experienced clinician, the situation may be this:

“I’ve only ever been to Derby once, but when I did go, that route worked pretty well for me, so I’m going for it again. Why risk otherwise?”

This is the equivalent of following a protocol or being led by a more experienced clinician. Perfectly legitimate but after a time the question will become, “have you tried other ways?” Yes that’s a pretty direct route, but sometimes it’s not about the speed you get there. An example I can think of was a player with a partial ACL injury that occurred just before christmas. We made the decision to prolong his rehab until the pre-season, despite realistically being able to get him fit for the last 2 games of the season. But there was no advantage to that, instead we were able to focus more on smaller details, enhance his “robustness” and ultimately, we had no re-injuries with him the following season. We decided to take the more scenic route and enjoy the drive. Sometimes, it shouldnt be other people asking why you have done something, but yourself. (Do this internally, arguing with yourself in a cubicle at work could have very different consequences to the intended career development).

Thanks Sat-Nav, but no thanks:

This option comes after you have driven to & from Derby a few times. Or if you insist on keeping it relevant to practice, an exposure to a certain injury with a set population. Experience may tell you that the route suggested by Sat-Nav has an average-speed check for 25 miles, so you may choose one of the alternate routes. This is the same as saying, “I wanted to use squats for his knee rehab, but it aggravates his hip so instead I used dead-lifts.” Someone has asked you why you went that route, the answer is reasoned and justified and neither party needs to be offended. But you have argued your point.

 

An argument is different to a disagreement:

An example of this not being constructive may be:

“I prefer this route because the services have Costa and not Starbucks. I hate Starbucks.” This opinion, without any justification may turn into a disagreement. “I don’t ever use a wobble cushion in my rehab, just don’t believe in them.” A genuine statement that I heard years back when I was studying myself. There was no rationale, every counter argument was met with “Nope. Dont buy it.”

opinions
This is a disagreement. Something I disagree with… Oh, balls.
Conclusion:

An argument doesn’t have to be raised voices or expletives (although people who swear more are shown to be more trustworthy and honest. If you belive that bullshit). It can be someone wanting to develop their own thinking and reasoning, therefore probing your experience – “But WHY did you chose that? (subtext = help me learn!)”

Equally it can be someone pushing you to develop. “You use that exercise for all of your patients.. why?”

I’ve started to do a little presentation at the start of our modules to explain this thinking, I will be asking “why?” A lot, but I don’t want people retreating or getting defensive. Asking Why is not a sign that I disagree with you. arguing is not a sign that I disagree with you. If you feel comfortable with those concepts, you have either done an MSc already, or you are ready to do one! For those not on twitter, firstly – how are you reading this blog? Secondly, get on there. Prime examples of arguments about clinical practice everyday and very quickly, normal jovial exchanges are resumed (I would highly commend Tom Goom (@tomgoom) for this attribute). But also, it is a good place to observe some people misunderstanding an argument and presuming it is a disagreement (I wont name people, don’t want to get in a disagreement).

 

Yours in sport,

Sam

Rehabbing teenagers can be awkward! – sensorimotor function during adolescence

There is a bit of a buzz phrase in rehab about “individualising programs” and while it is something we wholeheartedly agree with, it is a phrase that is very easy to say and yet very difficult to implement. Especially when you work with a population where said individual changes rapidly through time, like a teenager! It is a common sight on a training pitch to see a star player in their age group suddenly tripping over cones or developing a heavy touch where there was previously effortless control. Side effects of the adolescent growth spurt, where the brain is now controlling a much longer lever. It’s like giving a champion gardener a new set of garden sheers when for the past year they have used little hand-held scissors and asking to them maintain their award-winning standards. (My garden embarrassingly needs some attention and it’s affecting my analogies).

Master-Gardener-Pruner-Secateurs-Shears-Garden-Hand-plants-Shears-trim-cutter-easy-carry-Garden-Tool
The control and precision between these two instruments is influenced by the lever length of the handles…
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…Similar to a rapidly growing femur and tibia which is still being operated by muscles that have length and strength suitable for shorter levers.

 

 

 

 

 

 

 

 

Alongside the performance related issues, there is suggestion that this period of growth may coincide with increased risk of injury (Caine et al 2008). We believe that bone grows quicker than soft tissue, so we are asking a neuromuscular system to control a new, longer lever using prior proprioceptive wiring. Imagine our gardener again, for a long time he has been able to keep his pair of scissors close and controlled, now with his extra long shears the load is further away from his body, his back and shoulders are starting to ache. Not sure what I mean? With one hand hold a pencil to the tip of your nose. Now, with one hand hold a broom handle to your nose. The longer lever is harder to control. **I promise it gets a bit more sciencey than gardening and broom handles. **

Managing these growth spurts is something we have talked about before and recently contributed to a BJSM podcast on the topic (Part 1 & Part 2) and a complimentary BJSM blog about “biobanding” during periods of growth and development (here). This particular blog was inspired by a recent (2015) systematic review looking into exactly which sensorimotor mechanisms are mature or immature at the time of adolescence by Catherine Quatman-Yates and colleagues over in Cincinnati (here). The following is a combination of their summary and our examples of how these findings can influence our rehab programs.

Tailoring the program:

We have so many options for exercise programs, that’s what makes the task of designing them so fun. It challenges our creativity. When working with a teenager with sensorimotor function deficits, let’s call them “Motor Morons” for short, we don’t have to totally re-think our exercise list, just perhaps the way we deliver them. We previously spoke about motor control and motor learning (here) and how our instructions can progress just as our exercises do, but the following relates to children and adolescents in particular.

Consider the stimuli.

Children aged between 14-16 have well-developed visual perception of static objects however their perception of moving objects and visual cues for postural control continue to mature through adolescence. When very young children learn new skills such as standing and walking, they become heavily reliant on visual cues. Quatman-Yates et al suggest that puberty and growth spurts (think gardener with new shears) brings new postural challenges that causes adolescents to regress proprioceptive feedback and increase reliance on visual cues again. From a rehab perspective, we need to consider this as part of our balance and proprioception program. How many of us default to a single leg stand and throwing a tennis ball back & forth from therapist to athlete? For our Motor Moron, this may not be an optimal form of treatment in early stages, where it is commonly used, however it may incredibly beneficial to that athlete in the later stages or as part of ongoing rehab as we try to develop that dynamic perception.

Consider the amount of stimuli involved in an exercise versus what your goal of that exercise is

We should also consider the amount of stimuli we add to an exercise. Postural stability in children is believed to be affected by multiple sensory cues. If we consider that children are more dependent on visual cues than adults are, perhaps our delivery of external stimuli should be tailored also. With a multi directional running drill for example, there is sometimes an element where the athlete is given a decision making task (a red cone in one direction and a yellow cone in another) and they have to react quickly to instructions from the therapist or coach. Rather than shouting instructions like “red cone”, “yellow cone” etc, hold up the coloured cone for the corresponding drill. This way we are utilising this developed visual perception, minimising the number of stimuli and also encouraging the athlete to get their head up and look around rather than looking at their feet.

When to include unilateral exercises:

Within adult populations, it is often considered gold standard to make exercises unilateral as soon as tolerable. If they can deep squat pain free and fully weight bear through the affected side, progress them to pistol squats ASAP, or single leg knee drives. However, young children (pre-pubescent) may struggle with this for a couple of reasons.

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Difficult enough even for an adult to perform, but uncoupling the actions of the each leg & fine muscle movements to maintain balance are extra challenging for children

Firstly, we need to consider postural adjustments. Where as adults and young adults can adjust their balance with smooth control and multiple, small oscillations, children rely on larger ballistic adjustments. There is also reduced anterior-posterior control in younger athletes which suggests reduced intrinsic ankle control. Put this alongside immature structures and (if working a physio, most probably) an injury then single leg exercise become a progression that may be further down the line than an adult counterpart with the same injury. Instead, consider semi-stable exercises. Support the contralateral leg with a football or a bosu ball – something that is difficult to fixate through but provides enough stability to support the standing leg.

Secondly, we understand that coupled movements are mastered earlier in adolescence, around 12-15 years old but uncoupled movement patterns take longer to develop, 15-18 years old (Largo et al). A good example is watching a young child reach for a full cup of water at the dinner table. It is much easier and more natural for them to reach with both hands than it is with one, as coupled movements are unintended. Rarely do you see a child taking a drink with one hand filling their fork with the other – yet this is something commonly seen with adults as they are able to uncouple and segmentalise. Another example is watching a child dynamically turn, watch how the head, trunk and limbs all turn as a “block”, it is not until further down the line where dynamic movements become more fluid. The argument here is that surely running is an uncoupled movement? Or kicking a football, swinging a tennis racket, pirouetting in ballet – they are all uncoupled, segmental movement patterns that we expect kids to do, and in all they cope with. Correct, but it is usually in rehab programs for kids that we begin to introduce unfamiliar tasks and exercises that they may not have encountered before. Also, we should respect the impact of the injury on proprioception and control. So these are all considerations for starting points in exercise & if a regression is ever required.

For this reason, it is important that exercises are monitored and reviewed regularly. There is no need to hold an athlete back because of their age and making assumptions on motor function because of their age. If they can cope, then progress them. But be mindful of “over-control” where speed and variability of movement are sacrificed in place of accuracy and control (Quatman-Yates et al 2015).

Become a Motor Moron hunter

It is worth spending some time watching training, watching warm ups, watching gym sessions and talking with coaches and S&C’s trying to identify a Motor Moron as soon as possible. It’s important to minimise the chances of an immature sensorimotor mechanism ever meeting a growth spurt. It is when these two things combine that we see kids doing immaculate Mr Bean impressions and therefore increase their risk of injury.Safari-kids

Regularly re-assess your exercise programs. If things arent quite progressing as quickly as they should, it may not be failed healing of an injury, but it may be that we are providing the sensorimotor mechanism with too much information!

 

Yours in sport,

Sam

 

“The Young Athlete” conference 9-10th Oct, Brighton. Here