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

 

 

 

Recovery from concussion – a guest blog by Kate Moores

Following our last blog on concussion, I started talking to Kate Moores via twitter (@KLM390) who had some very intersting experiences and ways of managing concussion. So, I am very pleased to introduce Kate as a guest blogger on the topic of Concussion assessment & management – we have decided to split Kates blog into 2 more manageable parts rather than one super-blog (My contribution may have been to add the occassional picture to the blog).

The original blog (here) discussed generalized pitchside assessment of a concussion, irrelevant of age. However Kate has drawn on her knowledge and experience with young rugby players to highlight in particular, the ongoing assessment of young athletes as well as adults and how it differs. Kate raises some very good points throughout but the point that really made me reflect was the consideration over “return to learn.” Looking back at concussions I’ve managed in academy football, I didn’t properly respect the impact that a day at school may have had on symptom severity or neurocognitive recovery. I was mostly interested in “have you been resting from activity?” I think this blog is an excellent resource for medical professionals, but also for teachers, coaches and parents to consider the impact of this hidden injury.

This is part 2 of Kates guest blog (part 1 here).

 

Recovery

Any player regardless of age should never return to play or training on the same day that they sustain a concussion. So when should they return? The general consensus is that players should be symptom free prior to starting their graded return to play and that youth players should have a 2 week rest period and that youth athletes should have returned to their normal cognitive activities symptom free prior to considering a return to play. It is therefore recommended that cognitive rest is adhered to for 24-48 hours post injury. This means no texting, computer games, loud music and cognitive stress. This can be difficult to get players to adhere to however research has shown that a period of cognitive rest helps to reduce the duration of symptoms.

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“They said something about no computer games”

The concern with any concussion, but increased concern with children returning to play too quickly is the risk of second impact syndrome, with well publicised cases including the tragic death of Ben Robinson a 14 year old rugby player and more recently Rowan Stringer a Canadian rugby player aged 17. Children are at a higher risk of second impact syndrome (McCory et al 2001) and this risk continues for anything up to 2/3 weeks post initial injury. This is part of the reason why an u19 rugby player can not return to play earlier than 23 days post injury unless they are being managed by a medical doctor who is experienced in managing concussions. Below is the concussion management pathway from the WRU.

WRU

Under this protocol adult athletes would be able to return within a minimum of 19 days after a concussion whereas u19s would not return before 23 days. Both groups need to be symptom free and have had a 2 week rest period prior to return. For the younger age group it does state that they must have returned to learning however there is no guidance as to how this should be staged. The graded return to play protocol consists of 6 stages which gradually increase the level of activity. Stage 2 starts with light aerobic exercise, stage 3 includes light sport specific drills, stage 4 includes more complex drills and resistance training, stage 5 is return to contact with stage 6 being return to normal activity. With children there must be 48 hours in-between stages as opposed to 24 hours with adults.

As mentioned, return to learning protocols are less well documented, there has been some proposed protocols from Oregan and Halted et al (2014) who state that a youth athlete should be able to tolerate 30-40 minutes of light cognitive activity prior to a return to school and that players should be gradually return to normal school activities prior to their graded return to play.

At present youth athletes are part managed as students and part managed as athletes, however there is an emerging theme that return to activity is potentially a far more appropriate method of managing a childs recovery from concussion. We need to do more work to align both protocols. A player may well be “fit” to return to school and therefore deemed “fit” to return to light activity and subsequently drills, however very little research has been done to look at the impact of skill acquisition in a physically challenging environment. Learning your french verbs might be fine (in isolation), gentle jogging may well be fine (in isolation) but there is no denying that trying to do the two in consecutive lessons may well be far more challenging, yet that may well be what we are expecting some of our youth athletes to do. We already know that a concussion can impact players non related injury risk for a year following a single concussion, could it is be impacting on the skill level of players we produce?

Howell et al (2014) (here) explain that traditional concussion severity scales are being abandoned in favour of individualized concussion management with multifaceted evaluation of function. For example, the SCAT3 assesses static balance as part of motor control, however Howell’s study found that up to 2 months post concussion, adolescent athletes display increased centre of mass displacement medial-lateral compared to a matched control group. Could it be that we are clearing people for activity based on a static assessment when in fact dynamic balance may take longer to recover? (a potential study for anyone interested).

Whats up doc?

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This doesn’t even make sense

Concussion management is further complicated by contradictory advice, youth concussion is not only a sporting issue, but a public health one. If GP’s or A&E do not feel able to confidently manage concussions, how can we expect them to make decisions regarding return to play? I’ve attended numerous times to A&E with players who have been told once you feel better, get back to training. With Scotlands new concussion guides they are starting to address the associated public health concerns around child concussion. It can no longer be deemed as just a sport issue or just a medical issue as the potential long term consequences go beyond these two areas.  With the Scottish guidelines being aimed across sports at a grass roots level it begins to address the disparity between the quality of concussion management across sports and levels. Whether you’re an elite athlete, a weekend warrior or a 15 year old school child you still only have one brain!

 

Prevention

Prevention is better than cure right? Non contact rugby until the age 20? I don’t think so. Considering the reaction to suggesting removing the header from football in youth sport due to concerns around sub concussive events, the suggestion we remove contact from rugby is a no go. However there are lots of benefits to playing a contact sport, from social development, self confidence and the physical benefits from contact so maybe managing the amount of contact sustained in training is one way of combating the risks of concussion and sub concussive events.

How about a helmet, monitors or head guards? Considering the issues within the NFL and concussion with players recently retiring due to concerns around concussion, it would suggest that protective headgear does little for prevention of concussion (think back to blog 1 about mechanisms within the skull). It’s widely accepted that protective headgear has a role to play in prevention of catastrophic head injuries (ie your cycle helmet) however scum caps may well give players a false sense of security which in turn increases the risk of a concussion. RFU guidelines indicate that a scrum cap must be able to compress to a certain thickness and must be made of soft, thin materials – their main purpose is to protect against lacerations and cauliflower ear, they have little to no impact on concussions.

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Following a severe head injury (skull fractures), Peter Cech has become synonomous with this head gear. It provides him with the confidence to play – but what does it do?

Every concussion needs attention. Every team has a coach or a parent watching. But not every child has access to a health care professional pitch side.

Cournoyer & Tripp (2014) (here) interviewed 334 American football players 11 high schools and found that 25% of players had no formal education on concussion. 54% were educated by their parents (but who is educating the parents?!). The following percentages represent who knew about symptoms associated with concussion:

Symptoms Consequences
Headache (97%) Persistent headache (93%)
Dizzyness (93%) Catastrophic (haemorrhage, coma, death) (60%)
Confusion (90%) Early onset dementia (64%)
Loss of Consciousness (80%) – how this is lower than headache is worrying. Early onset Alzheimers (47%)
Nausea / Vomitting (53%) Early onset parkinsons (27%)
Personality change (40%)
Trouble falling asleep (36%)
Becoming more emotional (30%)
Increased anxiety (27%)
Table 1: Frequency of concussion symptoms and consequences identified by American Football playing high school students (Cournoyer & Tripp 2014)

Education is key! Players, parents, coaches, friends, family. Everyone! The IRB has some great online learning for general public, coaches and medical professionals (here). Only by symptoms being reported, assessed and managed can we make an impact on concussion.

 

Kate is a band 6 MSK physiotherapist, having graduated in 2011 from Cardiff Univeristy. Beyond her NHS work, Kate has worked for semi-pro Rugby League teams in Wales, the Wales Rugby League age grade teams and is now in her 3rd season as lead physio for the Newport Gwent Dragons u16 squad.

Concussion Assessment – a guest blog by Kate Moores

Following our last blog on concussion, I started talking to Kate Moores via twitter (@KLM390) who had some very intersting experiences and ways of managing concussion. So, I am very pleased to introduce Kate as a guest blogger on the topic of Concussion assessment & management – we have decided to split Kates blog into 2 more manageable parts rather than one super-blog (My contribution may have been to add the occassional picture to the blog).

The previous blog discussed generalized pitchside assessment of a concussion, irrelevant of age. However Kate has drawn on her knowledge and experience with young rugby players to highlight in particular, the ongoing assessment of young athletes as well as adults and how it differs. Kate raises some very good points throughout but the point that really made me reflect was the consideration over “return to learn.” Looking back at concussions I’ve managed in academy football, I didn’t properly respect the impact that a day at school may have had on symptom severity or neurocognitive recovery. I was mostly interested in “have you been resting from activity?” I think this blog is an excellent resource for medical professionals, but also for teachers, coaches and parents to consider the impact of this hidden injury.

Part 1 (of Blog 2)

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Conor McGoldricks first day at school

Children are not just little adults… a phrase commonly heard within healthcare. It’s particularly true when it comes to concussion. Children’s brains are structurally immature due to their rapid development of synapses and decreased levels of myelination, which can leave them more susceptible to the long term consequences of concussion in relation to their education and sporting activities. With adults the focus is usually on return to play, with similar protocols being used in managing youth concussions, albeit in a more protracted time frame.

However a child is physically, cognitively and emotionally different to adults, therefore is it appropriate for these return to play protocols to be used with youth athletes? Youth athletes are still children – still students as well as athletes. It is during these years that children develop & learn knowledge & skills (academic and social), in a similar way these youth athletes need to be learning the tactical knowledge and motor skills they will need for their sport. Shouldn’t “return to learning” be as much the focus in youth athletes as a “return to play” protocol?

“Youth Athletes are still children balancing studies with sports”

Assessment

So, the pitchside decision on management has been made (blog 1) and now the assessment continues in the treatment room

The use of the SCAT3 (here) and Child SCAT3 (age 5-12) (here) have been validated as a baseline test, a sideline assessment and to guide return to play decisions. O’Neil et al 2015 compared the then SCAT2 test against neuropsychological testing. They found that SCAT2 standardised assessment of concussion scores were correlated to poorer neuropsychological testing for memory, attention and impulsivity. However symptom severity scores had poor correlation with those same components. Therefore simply being symptom free may not be a good enough indicator that youth athletes are ready to return to learning or sport.

There has been recent research into the King Devick (K-D) test as another option for the assessment on concussion in children with research being done comparing SCAT scores with K-D testing (Tjarks et al 2013)

One of the benefits of using the KD test is that it has stronger links with the neurocognitive processing which may mean that it has a greater role to play with regard to return to learning as well as return to play. Another benefit is that unlike the SCAT3 tests the KD test does not require a health care professional to administer the test.

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We educate people about how robust their body is, but should we be more cautious with brain injuries?

At a club with full time staff and consistent exposure to players, the SCAT3 can be useful to compare to pre-injury tests conducted as part of an injury screening protocol. It also helps if you know that person, for some the memory tests are challenging without a concussion so post injury assessment with the SCAT3 may score badly, but is that the person or the injury? It is also important that this assessment is done in their native language. These reasons throw up some complexities if you are working part time for a club, or covering ad hoc fixtures as part of physio-pool system. Its advisable in this instance to get a chaperone in with the athlete to help your assessment – this may be a partner for an adult player or a parent / teacher for a child. A quick conversation with them to say “please just look out for anything odd in what they say or how they say it.”

Beyond the assessment tool, there is evidence now to suggest we should be asking about pre-injury sleep patterns. Sufrinko et al (2015) (here) look prospectively at 348 athletes in middle school, high school and colligate athletes across three different states in America (aged 14-23). At the start of the season the researchers grouped the athletes as those with “sleep difficulties” (trouble falling asleep, sleeping less than normal” and a control group of “no sleeping difficulties”. Following a concussion, assessment was conducted at day 2, day 5-7 and day 10-14 using the Post Concussion Symptom Scale (PCSS) and found that those with pre-injury sleep difficulties had significantly increased symptom severity and decreased neurocognitive function for longer than the control group.

woman-who-cant-sleep-article

Looking in the other direction, Kostyun et al (2014) (here) assessed the quality of sleep after a concussion and its subsequent impact on recovery. Looking at 545 adolescent athletes, the results indicated that sleeping less than 7 hours post-concussion significantly correlated with increased PCSS scores, where as sleeping over 9 hours post injury significantly correlated with worse visual memory, visual motor speed and reaction times. A word of caution with this study, the authors assumed that “normal” sleep was between 7-9 hours – but anyone who has adolescent children, or hasn’t blocked the memory of being an adolescent themselves, knows that sleep duration does increase when you are growing. Saying that, the impact of both of these studies suggests that we should be:

1) Asking about normal sleep patterns prior to injury to help us gauge recovery times (disrupted sleepers may take longer than we originally predict) and;

2) We need to keep monitoring sleep quality along with regular re-assessment as sleeping more than normal may indicate ongoing recovery from concussion.

 

In Part two (here), Kate continues to discuss ongoing assessment and the recovery process.

Kate is a band 6 MSK physiotherapist, having graduated in 2011 from Cardiff Univeristy. Beyond her NHS work, Kate has worked for semi-pro Rugby League teams in Wales, the Wales Rugby League age grade teams and is now in her 3rd season as lead physio for the Newport Gwent Dragons u16 squad.

 

 

 

 

 

 

Concussion – Pitchside management

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I can see the problem here – half of his face is missing

A while back, we wrote a blog about pitchside management (here) and I was very careful not to discuss concussion at the time as its potentially a topic that warrants a couple of blogs on it own (blog #2 will discuss post concussion management).

Since writing that blog, there have been a number of high-profile head injuries in the football World Cup and more recently in the IRB 6 Nations. It’s very easy to assess such scenarios from the armchair with the benefits of replays – but what these examples did do was spark positive discussions about a topic that unfortunately is glossed over within sport (not necessarily sports medicine – a few tweeters in particular that discuss the topic a bit: @PhysioRichmond, @Sophie_T_SEM, @SportsDocSkye , @KLM390).

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George Norths contenious concussion in 2015 Six Nations

What is concussion?

The RFU describes concussion as:

a functional disturbance of the brain without any associated structural pathology (as visible using current scanning technology) that results from forces transmitted to the brain (either directly or indirectly). It is generally considered part of the spectrum of traumatic brain injury (TBI)

One issue we have as clinicians is a poorly defined summary of what concussion is – where does an acute bang to the head that causes some dizziness become “concussion”? The first thing to clarify is that not all head injuries are concussions, and not all concussions result from head injuries (explained later). In fact, terming concussion a “traumatic brain injury” (TBI) may be more accurate – I am certainly not a fan of the word “mild” when discussing brain injuries.

We also have no gold standard for assessing concussion. In the updated version of the Sports Concussion Assessment Tool version 3 (SCAT3), the authors describe (here) clinical diagnosis as a combination of symptoms, physical signs and impaired cognitive function. To diagnose a concussion, some of the following symptoms should be present (via the CDC):

Thinking/
Remembering
TBI symptoms physical icon.gifPhysical TBI symptoms emotional icon.gifEmotional/
Mood
TBI symptoms sleep icon.gifSleep
Difficulty thinking clearly HeadacheFuzzy or blurry vision Irritability Sleeping more than usual
Feeling slowed down Nausea or vomiting
(early on)Dizziness
Sadness Sleep less than usual
Difficulty concentrating Sensitivity to noise or lightBalance problems More emotional Trouble falling asleep
Difficulty remembering new information Feeling tired, having no energy Nervousness or anxiety

Perhaps one reason concussion isn’t taken as seriously as it should is the lack of external signs. In some cases, it is a hidden injury. Classed as a TBI, there is undoubtably going to be swelling associated with a concussion. A swollen knee or ankle looks pretty drastic to players and coaches, its easy to point at and compare to the other limb and easy to explain why you are removing someone from the field of play. But here we are talking about something contained within the skull. There are also elements of a concussion that we won’t see in the 2 minutes we have on the pitch – such as disrupted sleep, anxiety, drastic mood swings (continued management discussed in forthcoming blog). So now we start to see some of the difficulties with assessing a head injury at pitchside..

Saying the C-Word

concussion-teen
“He’ll be alright”

So, following a clash of heads on the pitch, we rush on to survey the scene. As well as the adrenaline associated with getting on the pitch and thinking quickly about what to do & say, you probably have a referee, a handful of players, spectators and the coaching staff all asking whats going on. Lets assume there is no associated neck injury (essential to check following any head injury!!), no abrasions or lacerations – just this hidden injury within the skull. How many of those symptoms listed above should be present before you diagnose a concussion? And if they aren’t present now, how might continued swelling affect them in 1 minute, 10 minutes, 30 minutes? Some signs and symptoms may not evolve for hours (McCrory et al). The two voices in your head are saying:

“If this players gets better in a minute and I take them off, the players and coaches are going to crucify me – they’ll probably never tell me the truth about their injuries again because they think I’ll sub them every time.. Should I let them carry on for a bit?”

And

“Actually, I Couldnt care less what they think, even if they are star player and we lose, we are talking about this persons brain!”

I believe things are about to change, if they havent already, but previously just saying the word concussion in rugby ruled a player out for a minimum of 3 weeks. Two concussions in one season for the same player would rule them out for the remainder of the season. Designed to safeguard the player and the medical team, this does add a bit more pressure to on-pitch assessments.

Making the Call

There are huge benefits to being pitchside to witness injuries, especially when the injury may result in the loss of memory of said injury. Observing the mechanism of injury can give you great indicator as to potential problems. But remember, not all concussions are caused by impact injuries to the head. McCrory et al (here) define concussion as:

“An injury caused by a direct blow to the head, face, neck, or somewhere else on the body with an impulsive force transmitted to the head, resulting in a graded set of clinical symptoms”

The population you work with is going to be key here. Reduced neck musculature and head control could make younger athletes, or slighter built adult athletes, more susceptible to non-head impact concussions.

It is personal opinion, but I would say some symptoms are more severe than others. For example, ANY loss of consciousness, even seconds and the player should come straight off. We are talking about an event that is significant enough to stop the brain working. Poor terminology, but imagine the fear and anxiety if you told an athlete their back didn’t work – I’m pretty sure they would be asking for your help then (**semantic police disclaimer – I don’t recommend ever telling someone “something doesn’t work”**).

Secondly, vomiting is a pretty clear indicator of a concussion. Although the mechanisms aren’t quite clear, it’s believed to be a combination of individual intrinsic factors (Brown et al 2000), which means the absence of vomiting unfortunately doesn’t rule a concussion out, but the presence of it definitely makes the diagnosis more likely.

Finally, the third thing I would always look for, or listen for, is what they are saying and how they are saying it. If it is incoherent or in any way bizarre (depends on your athlete, you have a pre-existing level of weird that you may want to work from) then that’s a pretty good sign of a brain injury. Most people are familiar with asking your short-term memory questions with a head injury, but equally important to what they aren’t saying, is what they are saying – self-control, judgement & decision-making occurs in the frontal lobe and is one of the first skills to diminish following a brain injury. With a limb injury you may be inclined to listen to their judgement and monitor performance & function briefly, but head injuries are one example where the athlete shouldn’t be involved in the immediate decision-making process. As mentioned above, this may be an invisible injury and it may be tricky to demonstrate to a concussed athlete that they are concussed.

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Alvaro Pereria out cold in Brazil world cup
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Later, he overruled his own doctor to continue playing.

Conclusion

I think this is pretty straight forward. There is no game or event that is bigger than a persons life. Admittedly, I have never worked at a World Cup or a 6 Nations event but the level of sport you work in shouldnt matter either. This is an injury that could have serious implications on quality of life, regardless of the quality of sport. If there is any doubt in your mind about a potential concussion, they need to come off.

Look back at the RFU description of concussion – “a functional disturbance of the brain…” We are talking about THE BRAIN. It controls EVERYTHING. How a person feels, thinks, moves, sees… Do I need to go on? There is some seriously concerning data coming out from America about long-term effects of repeated concussion in the NFL with regards to depression, substance abuse and even suicide. Just this year, NFL line backer Chris Brland, aged 24, retired from the game due to fear of the effects from repeated concussions (here).

There are numerous pressures on therapists pitchside to make quick calls regarding injuries. It is pleasing to see some discussions in rugby and football about providing more time for head injury assessment, similar to a blood sub, but I would say that if there is enough doubt to request this extra time to monitor, is that sufficient doubt to suspect a traumatic brain injury?

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BOD ruled out of 3rd Lions test in 2009 with concussion

There is a whole other blog (or three) to discuss different assessment tools and post-concussion management – how it differs between adults and younger athletes, so bear with us – we’re already working on that.

For those that want to know more – The 2015 ACPSEM conference has Dr Jonathan Hansen (here) (AKA @SportsDocSkye) discussing concussion management in sport – dont miss it!

 

Yours in sport,

Sam