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

 

 

 

“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:

Completely 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.”

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

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.

“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.

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?

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.

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)

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.

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.

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

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).

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	Physical	Emotional/ Mood	Sleep
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

“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.

Alvaro Pereria out cold in Brazil world cup

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?

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

Massage: A case for the defence

Just because we can’t prove what something does, doesn’t mean it doesn’t do anything.

The older I get, the more I read, the less I know. I know that for a fact. But recently I’ve started re-reading around the topic of massage and its place in sport and recovery. And with my critical head on, the one thing that I can consistently critique is the literature. The methodology, the participant population, but not necessarily “Massage” itself.

A good starting point for this defence would be to read the antithesis for this blog, a great blog by @AdamMeakins (There is no skill in manual therapy). Adam makes a valid point that there is not a strong background of evidence to support massage. Agreed. And its worth pointing out that a large, very large, part of my practice is exercise based rehab – I’m a strong believer of “move well, move often”. However, massage is a very well used tool in my pocket of possible treatments, so I’m going to fight for the underdog.

Below is a summary of terms / applications commonly used with recognised massage techniques (not an exclusive list).

Table 1: A summary of western massage techniques (Weerapong et al)

Technique	Definition	Suggested Application	Proposed clinical effects
Effleurage	Gliding movement over the skin in a continuous movement	Beginning & end of a session	Stimulates the parasympathetic nervous system, promotes relaxation and enhances venous return.
Pretissage	Lifting, wringing, squeezing and kneading of soft tissue.	Following effleurage	Mobilise deep muscle and subcutaneous tissue. Increases local circulation and enhances venous return
Friction	An accurate penetration of pressure applied with the fingertips	Used for specific purposes, such as reducing muscle spasm or breaking down adhesions.	Break down adhesions from old injuries
Tapotement	Various parts of the hand striking the tissues in a rhythmical but rapid rate	Before and during competition	Stimulation of tissues either by direct mechanical force or by the reflex action

 

The problem with Evidence Based Practice:

I think that all medical professions are dependent on research to ensure our practice evolves for the better. But I think sometimes we overlook the importance of anecdotal evidence. It must be considered that not all aspects of sporting competition depend on physical attributes, the mind and perceived benefits of treatment play an important role. The majority of people that go back for massages are because it made them feel better. Maybe not during, but after. A prime example, my wife never says “Can you give me an exercise program for my neck & shoulders please?” But I know that anecdotal evidence on its own doesn’t wash.

So here is where I think the literature lets massage down. The effectiveness of massage will vary depending on duration, method and depth of pressure (Drust et al) however none of these variables have been standardized making comparisons between studies very difficult (Mancinelli et al).

Jönhagen et al investigated the effects of sports massage on recovery following eccentric exercise. 16 “recreational athletes” (I have issues with this terminology for a start) were asked to complete 300 maximal eccentric contractions of their quadriceps using a Kin-Com dynamometer. Subjects received a pretissage massage once a day for 3 days before re-testing single leg long jumps to analyse “functional recovery”. SHOCK – The study found no improvement in function following massage.

@ConorMcGoldrick has been quiet on blog front, but promises he is still working hard in the gym. Trying a new technique of 300 eccentric max contractions

 

• Firstly, it may not be possible for one to truly maximally contract for such a high number of repetitions, therefore cannot be considered functional for an athlete; professional or recreational.
• Secondly, name a sport that requires 300 maximal eccentric contractions in succession. Even an eccentric dominant sport like basketball would be interspersed with periods of rest and I don’t imagine basketball players would define those eccentric actions as maximal.
• Thirdly, pretissage is a deep and firm technique, the use of which immediately following 300 eccentric contractions and continued for 3 days is more than likely going to cause mild muscle trauma. Not exactly a therapeutic choice for a tissue with acutely induced micro-trauma.

In another study investigating fatigue, Zainuddin et al studied the effects of massage on the upper limb following 60 maximal eccentric contractions of the elbow flexors of a single arm in 10 healthy subjects (5:5 M:F). The results indicated no significant change between the two arms in isometric & isokinetic strength and torque, but it did find reductions in muscle soreness and swelling. The lack of significance in the results may be due to measurements, including maximal strength, being taken before, immediately and 30 minutes after, and at 1, 2, 3, 4, 7, 10 & 14 days after, which may have been too many re-assessments of maximal strength following eccentric activity. Also, the 10 minute massage protocol consisted of 3 minutes frictions to the major muscles in the upper limb. As explained earlier, frictions are designed to promote inflammation, not to promote recovery!

The point of these studies was to investigate the use of massage in recovery from sport. Eliciting DOMs in untrained subjects and concluding that they still hadn’t returned to baseline in 3 days is not representative of the demands you will be faced with in sport. For the most part, the athletes are familiar with the exercise, so apart from pre-season or the introduction of a new exercise technique, DOMS is relatively rare throughout a season.

No blog on massage would be complete without mentioning Lactic Acid

Fatigue is believed to be determined by the accumulation of lactate in exercising muscle (Monedero & Donne). However, the notion that lactic acid (consisting of lactate ions and H⁺) is detrimental to muscle function is derived from early findings on amphibian muscles, in which acidosis is more pronounced than mammalian musculature. These early studies were conducted at 10-20°C, when they were repeated at 25-30°C the effects of acidosis were abolished (Cairns). Studies on human skeletal muscles have shown a positive correlation between increased lactic acid and muscle fatigue, but what is usually overlooked is that there is also a relationship between fatigue and a decrease in ATP, increases in inorganic phosphate and increased ADP, as well as decreased nitrous oxide and reactive oxidative species (Franklin et al) – so why do we bang on about lactate clearance all the time?!

There is now a belief that lactic acid may have ergogenic effects on performance. It is well known that acidosis stimulates the Bohr effect, whereby H⁺ causes the release of oxygen from haemoglobin, which stimulates increased ventilation, enhanced blood flow, and an increased cardiovascular drive. (Cairns). Despite this recent shift in opinion, many studies still believe lactate to be detrimental to performance, and investigations continue into the most efficient method of lactate removal.

Monedero & Donne investigated different recovery strategies after maximal exercise using 18 trained cyclists. It was concluded that a combined treatment of massage and active recovery was significant in aiding future performance compared to passive recovery, active recovery or massage alone. Despite quoting in the introduction that “the role of lactate in fatigue is questionable”, the removal of lactate forms the bulk of the conclusion as to why massage alone was not a viable treatment for recovery.

 

Judging a fish by its ability to climb trees:

I mentioned earlier that I have reservations over the term “recreational athletes” – its unclear if this is an accepted scholarly word for “weekend warrior” or if its 3-times-a-week gym goers at the local spa and health club. Even so, the use of these participant populations to make assumptions on elite sport should be taken with caution. So should the use of athletes asked to perform unfamiliar tasks. Robertson et al used cycling to exhaust 9 male subjects and found no significant effect with blood lactate clearance following 20 minutes massage. However participants were from field based backgrounds such as football, rugby and hockey.

A study by Mancinelli et al investigated the effects of massage on DOMS using female athletes. 24 volleyball and basketball players underwent a vigorous strength and conditioning training session to elicit DOMS. The study found that the massage group (n=12) had significant increases in vertical jump scores (P=0.003) and decreased levels of perceived soreness (P=0.001), while the control group significantly increased their shuttle run times (P=0.004). The study that used functional tests appropriate to the subjects sport found favourable results for massage.

More recently, in a series of studies Delextrat et al (and again here) compared the benefits of massage alone and in combination with other recovery modalities (stretching; cold water immersion) using basketball players. Again using measure specific to the sport. While I question the conclusions about different reactions between sexes (9:8 M:F), there was significant improvements in interventions compared to control groups, supporting the use of massage as a recovery modality.

So what do we think massage might do but we can’t prove?

“Massage therapy modulates the autonomic nervous system” – Franklin et al

The good thing about the Franklin paper is that it looks at potential systemic effects of massage, in particular the vascular endothelial function of the upper limb following lower limb massage – and they found a single treatment of massage had an immediate (90mins) parasympathetic nervous system response, characterised by reduced heart rate and reduced systolic blood pressure.

We think that massage, administered appropriately with appropriate techniques to suit the situation, may:

• Decrease pain (Mancinelli et al; Delextrat et al)
• Reduce swelling (Weerapong et al)
• Improve mood state (Hemmings et al; Robertson et al)
• Increase range of movement (Rushton et al)

I would question the last point – for how long does this influence last? Do we actually increase length? Or do we restore it following a loss of range (injury / pain / change in tone following exercise)? I don’t think even regular massage is enough to encourage creep deformation on tissues, but I’m more open to a change in tone to achieve an optimal length / range.

 

Conclusion:

Therapists working within a sports setting often have to adapt the duration of a massage depending on the number of athletes that require treatment, the number of clinicians available, the seniority of players (!) Clinical based MSK therapists may also be restricted by time constraints. There is also a dearth of techniques and combinations with other modalities to chose from. Two therapists performing the same technique will apply different pressures for different durations in slightly different directions possibly over different tissues. I can see this being an argument against, but its for this reason that its very difficult to measure and quantify effectiveness. To create a sturdy study design, you end up being far removed from how clinical practice actually operates. My point is, although it is important I don’t think you can base an opinion of an intervention soley on published literature.

A lot of the literature with non-significant findings will question the use of massage in clinical application, but I can’t think of any occasions where the intervention has caused a detrimental effect! This leads me back to my first sentence.

“Just because we can’t prove what something does, doesn’t mean it doesn’t do anything.“

Remember that the field I practice in means I’m exposed to athletes for long periods of time through the day and through the week. As a proportion of that day, massage does not make up a large percentage of treatment time. Gym based, movement optimisation does. So I’m not saying we should all go and massage every athlete and patient that requests it. Like everything I think there are certain individuals that benefit from certain techniques and methods. Given time restraints in an outpatients clinic, it may not feature at all as part of my treatment. But regardless of the size this cog plays in the treatment machine, I believe its a valuable one.

 Yours in sport

Sam

#Groin2014 – a not so brief summary

Any one familiar with twitter may have seen the recent hash tag for the 1st World Conference on goring pain in athletes (#Groin2014). This conference in Doha, Qatar was brilliantly orchestrated by Adam Weir (@AdamWeirSports) and his team at Aspetar. Run over three days and cram packed with information, I’m going to try and summarise the points that I found most interesting and thought provoking – please be aware these are my interpretations of what other speakers said and do not serve justice to the quality of the talks and presentations.

Yes, I was the only delegate in shorts and flip-flops

I have themed the findings into 3 main categories: Epidemiology; Adductor related pathologies & Femoral Acetabular Impingement (FAI) (Not an exclusive list of things discussed at the conference)

Introduction

What quickly became clear through the presenters was that even in 2014, we categorise injuries far too broadly. Consider the structures involved in the “Groin” and its no wonder why this area of the body see’s such huge injury occurrences.  Also, our terminology needs to be more accurate. Per Holmich (@PerHolmich) brilliantly said “Pubalgia is as specific as saying Kneealgia” we need to be more concise with our terms if we are going to understand the pathologies and management better.

That said, a lot of the current research into epidemiology does categories pathologies into hip /groin. So we have to go with the stats that are in front of us. And what are they…

Epidemiology

Of 110 multi-sport athletes assessed by Andreas Serner (@aserner), 76% of these injuries occurred in football-code sports. Markus Walden’s (@MarkusWalden) systematic review of 12 papers found that “Groin injuries” accounted for 9-18% of all injuries in mens football, with greater time loss of injury seen in tournament football compared to the regular season. Is this because of better monitoring at club level? Where medical teams know the players in a detail that international staff can’t due to limited exposure to players? Or as Walden says, is it due to the acute nature of injuries in tournaments due to reduced recovery and increased fatigue?

Both Walden and John Orchard (@DrJohnOrchard) found a greater incidence of groin injuries in men compared to women. It was suggested that the anatomical variance in womens hips puts them at more risk of lateral hip and knee pain rather than groin pain. The inguinal canal deficiency is also greater in men than womens.

Adductor Related Pathologies

Walden reports that 64% of groin related injuries are adductor related. This was supported by Serners paper with adductor longus being the most frequently injured of the adductor muscles. The picture below demonstrates Serners findings that 1/4 of all diagnosed injuries are negative on imaging, and that clinical presentations of rectus femoris & iliopsoas especially, often appear different on imaging.

Treat the player, not the scan!

Looking at risk factors for adductor pathologies, Jackie Whittaker (@jwhittak_physio) highlighted the basic but fundamental fact that previous injury is the biggest risk factor for future adductor pathology. Secondary to this, isolated adductor strength is a good indicator – ability to perform a squat is not! (Useful for those collating Injury Screening tools). Building on from Whittaker, Andrea Mosler (@AndreaBMosler) agreed that reduced strength coupled with positive pain on 45 degree adductor squeeze highlighted strong evidence for future groin pathology. Mosler summarised the following battery of tests for risk factors with adductor related groin pain:

Adductor strength – Strong evidence that low scores indicate future groin pain

BKFO (Bent knee fall out) – strong evidence that less flexible patients have greater risk of pathology

IR (Internal Rotation) – moderate evidence between decreased IR range and pathology

ER (External Rotation) in neutral – NO evidence to link decreased range and pathology. (Despite this lack of evidence, Geoff Verrall (@GeoffreyVerrall) does highlight a loss of ER in sport due tightening of the pubofemroal ligament and shortening of the adductors – improving this ER will help with force dissipation – so assessment is still valid!)

Eamonn Delahunt (@EamonnDelahunt) presented his research findings of squeeze assessments and groin pathologies, concluding that 45 degree squeeze has the highest sEMG and strength values (mmHg) of the 3 traditional squeeze measures. Contradictory to Moslers & Delahunts assessment of the adductors, Kristian Thorborg (@KThorborg) favoured long lever assessment when assessing for strength and pain. Pain provocation tests at a 0-degree squeeze is the best assessment to “rule adductor longus in.” While Delahunt drew his conclusions from a small population of gaelic footballers over a 6 month review period, Thorborg presented around 12 of his studies looking into the assessment of groin related pathologies. What is worth considering, is what structures are being affected when testing at these different ranges. As you’ll see below, it is a very complex and integrated part of the body.

Anthony Schache emphasised the importance of understanding the anatomy of the groin, in particular the soft tissue attachments. “Antomoy books provide discrete anatomy definitions which implies discrete anatomy – but this is not true.” The image below highlights the intimate attachments of surrounding structures in the groin.

Cadaveric groin anatomy – shows distinct LACK of “discrete anatomy” especially insertions

 

Per Holmich was keen to build further on these assessments as part of a clinical diagnosis, saying that adductor pain replicated with stress tests PLUS pain on palpation of the adductor origin (must be “the patients pain”) indicates that the adductors are the main driver of pain – any one identifying factor on its own is not enough to indicate a diagnosis. But, consider what Schache said about the anatomy – we would need to ensure that our palpation skills were incredibly accurate. You can see how being a centimetre out when palpating the pubic bone for the adductor origin could be the difference between adductor longus (AL) or gracilis, or rectus abdominus. For this reason, its important to take your time when palpating this area, although it can be uncomfortable for both practitioner and patient, but confidently & slowly working your way around the attachments could help improve your diagnosis.

Of significant interest regarding the adductors is the difference in anatomy. Stephanie Woodley describes the intramuscular tendon of AL as being 23% of the femur length, compared to 11% of femur length for adductor brevis. Also significant is the decreased vascularity of AL, less than that of brevis and both of these are less than that of gracilis. If we now consider that AL is the most commonly injured structure in the groin, could this be a cause of injury rates? At any rate, it is certainly a consideration worth knowing for healing times.

FAI

Both Damian Griffin and Joanne Kemp (@JoanneLKemp) were keen to clarify the terminology of FAI. FAI relates to the pain caused by a CAM or Pincer lesion,  CAM or pincer lesions don’t necessarily mean FAI.

“Athletes will undergo increased loads and greater demands on joints (ROM) than the general public, therefore impingements that are asymptomatic with ADL’s become FAI in sporting population” Damian Griffin.

Rintje Agricola describes an increased risk of FAI in males, especially in a sporting population but most interestingly reports that FAI is not prevalent in the non-athletes – therefore are we looking at a preventable pathology?

Increased loading over growth plate stimulates CAM deformity

We believe now that CAM deformities develop around 12-13 years old (Agricola and Kemp), the same age that IGF1, key for bone development, peaks in adolescent males. ER and flexion increase weight bearing through the femoral neck and lateral femoral head, around the growth plate, so increased physical activity at this stage of development will promote bony changes on these lateral surfaces. The population most at risk would athletes specialising in one sport, say football academies, where they increase their training volume and intensities as they physically mature.

If we understand this to be true, should we now seriously start to consider activity modification for children in this stage of development? Obviously we would need to understand stages and rate of physical maturity for individuals, and then there is a bigger debate of getting coaches on side for this change in loading.

The presence of a CAM deformity may not cause FAI in all individuals. However Schache gives an example where a CAM lesion may actually provide a false positive, or exacerbate existing symptoms. If we assessing IR range through a flexed position, a CAM lesion may act as a lever on the pubic synthesis and increase stress in this area. So a detailed assessment and knowledge of individual hip morphology would help us differentiate between an impingement or pubic synthesis stress.

Staying with this thought process of structural limitations through range, Morritz Tannast explained benefits of assessing rotation in neutral and through flexion. In a neutral hip, with legs hanging off the end of the plinth, we can assess the posterior wall of the hip joint. Extra-articular impingement in this position is most likely to come from the lesser trochanter and the ischium. In prone, we can assess the degree of ante torsion of the femoral head by looking at total range of rotation, so:

– Low antetorision would present as decreased IR and increased ER

– High antetorsion would therefore present as increased IR and decreased ER

Assessing through slight flexion, abduction and ER any extra articular impingement will be from the ischium up against the greater trochanter and our old friend, a CAM lesion. Griffin advocates the use of control and low speed with impingement tests, encouraging clinicians to explore the contact surface of the acetabular ring.

So far through this summary, we have stayed very insular with our assessment and anatomy. Kemp encourages the clinician to consider the control of the trunk with hip pathology. An increased anterior pelvic tile will equal and increased acetabular retroversion and a decreased IR at 90 hip flexion. Sometimes, it may not be the presence of a CAM deformity reducing that range, so on this final point summarising the hip and groin, I wold encourage people to still consider the bigger picture of the patient and what role the hip / groin plays in a combination of movement patterns and dysfunctions.

Taking this forward

There is a great deal, and I mean a huge amount, that I have not discussed. Secondary cleft signs of the pubic synthesis or surgical interventions for hip & groin pathology for example. But one topic I have not discussed that is probably glaringly obvious is the treatment and management.

In terms of exercise prescription, I think this will be led by your clinical abilities to diagnose the pathology (Remember Serners findings above, don’t just treat the scan!) Hopefully this summary will encourage to you read more of the presenters own works, or maybe it has re-enforced your understanding of what is a complex structure in the body. Essentially management of this area is much like any other in the body, we identify complications or restrictions and we address them. Usually this is a global approach, looking at the whole kinetic chain  – remembering that this conference focused on a very key, but isolated area of that chain.

If you are still reading at this point, thanks for taking the time to read through what is arguably the most complex and detailed blog I’ll probably every write!

For more info, check out the Aspetar youtube channel here (updates coming soon) or follow them on twitter (@AspetarQatar) or search the has tag #Groin2014

Yours in sport

Sam

Case study: “Bulls Eye Lesion”

Every now and then in clinic you come across an injury that doesn’t quite fit “the norm” in terms of its recovery and management. I know every injury should be considered unique and every individual managed differently, but I thought I would share the management of this particular injury as it did prove tricky, we did fail a couple of times but eventually we got it just right.

 

Background:

This case study revolves around an 18 year old central midfielder, skeletally mature (no increase in height throughout the year / evident secondary sexual features) with a regular playing and training history prior to this injury. The presentation started in the autumn, after a complete pre-season and a good few weeks of competitive season underway. The player was in & out of training with a niggling groin / quad but with nothing substantial showing in assessment (the benefit of hindsight would be a very good money earner for any clinician that could harness it and set up a course!)

Towards the end of an under 21 game, the player was visibly struggling with pain at the top of his thigh, unable to sprint or strike a ball but 3 subs had been made, so he was inevitably staying on the pitch. At the end of the game, there was pain on palpation of the proximal rectus femoris and sartorious region. At this stage, there was nothing more to assess – there was no point, we would only aggravate something without actually learning too much more.  He presented the next morning with visible swelling in a small pocket of proximal thigh, palpable crepitus and pain with straight leg raise at 20 degrees.

 

Review of anatomy

The rectus femoris is a long fusiform muscle with TWO proximal attachments. The Direct Head attaches to the AIIS and Indirect Head attaches to the superior ace tabular ridge and the joint capsule. It has a long musculotendinous junction, as such can execute high velocity shortening as well as coping with significant length changes – remember it is a two joint muscle crossing both the hip and knee, with an action like kicking it must cope with hip extension coupled with knee extension during the pull-back of the kick, so both ends of the muscle are undergoing an eccentric load (Figure 1). The muscle structure itself is made up of mostly type II fibres so this high eccentric load makes the muscle quite prone to injury (Mendiguchia et al 2013 source).

Figure 1: Demonstrating the demands on rectus femoris during a kick

 

“Bulls eye lesion”

The term “Bulls eye lesion” was coined by Hughes (1995 source) following the presentation of injury on MRI (Figure 2). The high signal signs around the tear of proximal injuries. Occasionally this causes a pseudocyst, thought to be the serous fluid in the haematoma.

Figure 2: MRI scans highlighting a “Bulls-eye lesion” presentation

Predisposing factors to a proximal tear include fatigue, insufficient warm up and previous injury. From this case, we know that the pain started at the end of the game with the player in a fatigued state, and there was a history of niggling pain on and off for a couple of weeks.

 

Management:

The initial management of this injury was relatively routine, revolving around the POLICE guidelines (see Cryotherapy Blog). By day 2/3 we were addressing pelvic control exercises & posterior chain assessments. By day 5 we could achieve pain free stretching of the hip flexors and were using “Compex” to achieve isometric contractions of the quad while the player did upper body exercises.  After day 7 we were able to begin loading through a pain free range, working on co-contractions and concentric contractions of the quad.

To Speed up, you must be able to slow down – Bill Knowles

In the early-mid stages of rehab, we began working on movement patterns but at a painfully slow speed. Using the Bill Knowles mantra above, we progressed though different ranges of box step ups at slow pace to elicit a co-contraction of quads, hamstring and glutes (Figure 3). We slowly lowered the player through a Bulgarian split squat (Figure 4) to work on stability through range and we did some bridging variations (anti-rotational core) to encourage isometric control of the pelvis (Figure 5 – excuse the size 11 shoes taking up most of the picture!!).

Figure 3: a) Low box step up with knee drive

 

 

Figure 3: b) medium box step up

Figure 3: c) High box step up

 

 

 

 

 

 

 

 

 

 

 

Figure4: Bulgarian split squat (a & b) with progressive knee drive added later (c)

 

 

 

Figure 5: Single leg bridge (a) with ipsilateral arm fall out (b) and contralateral arm fall out (c)

 

By adding speed to the high box step up, we were able to switch the demand of the quadriceps to an eccentric action as the hip extends from a flexed position and the pelvis rapidly comes forward. We felt confident adding this eccentric component after we had cleared the player at a decent weight using the cable machine and a jacket to work though some deceleration work on the hip and knee (Figure 6).

 

Figure 6: Cable decelerations. a) start position b) end position with 3 sec hold. c to e) Dead slow step backs with weighted cable pulling posteriorly

 

The Bulgarian split squat was advanced by adding a knee drive at the top the squat, taking the back leg from a position of full hip extension through into hip flexion, a rapid concentric action. Following the model of exercise progression and regression (source) we added weight, removed the concentric component and decreased the speed again before building back up in a now weighted position.

The later stage of rehabilitation saw the player undertake more field based conditioning, working under fatigue whilst completing technical drills and building up his range of passing and shooting, all the while maintaining his gym program to supplement his rehab. This late stage rehab combined the expertise of the physiotherapy department, working alongside the strength and conditioning coach to discuss reps and sets of all drills and help periodise the weeks for the player and design the field based conditioning sessions; the sports science department was able to use GPS for all outdoor drills to help monitor load and provide up to date feedback on key information, in this case monitoring the accelerations and decelerations for the player in a fatigued state.

It was important that the stress elicited in this late stage was in line with the rest of the squad mid-competition. Rob Swire and Stijn Vandenbroucke (source) explain the importance of rehab being harder than the team training. This is because we have control over rehab, but no control of training so we must be confident that player won’t break down again in training!

The player returned just under 8 weeks later. He continued his gym program for another 4 weeks after his return to training and (touch wood) has had no recurrence of this injury since.

 

Conclusion

Knowing what I know now, I would be more cautious of this nondescript pain around the proximal thigh. The indirect head runs quite deep and typically presents as a gradual onset. The niggle the player was displaying a few weeks before was probably a worsening of this small tear, that when fatigued and put under a double eccentric load such as kicking or sprinting, was bound to “give” at some point.

I’m sure that reading this back, it seems pretty obvious that there was something wrong with the player initially. Again, another lesson learnt from this relates to the players age. He had not had a soft tissue injury prior to this, so his subjective history was vague and typically teenager-ish. Its important to remember that young players and professionals don’t necessarily understand their own body. If they play things down, its important that we as clinicians double check everything before we clear them and not just rely on their feedback alone.

 

I hope you find my reflections useful

 

Yours in sport

 

Sam

The Osgood, the bad and the ugly

One of my best sources for recent literature is via a good friend of mine, Mr Jonny King (@Jonny_King_PT). Before he shot off to Doha to have his moment in the sun, he left a multitude of articles on my desk for me to read, one of which was a study looking at that persistent pest in my clinic, Osgoods Schlatters Disease (OSD).

OSD falls under the apophysitis or enthesopathy umbrella along with severs disease and Sinding Larsen Johansen disease amongst others. In our injury audit for the last season, these injuries alone accounted for 20% of our total injuries (u9-18s).

However, with a little bit of education to players, parents and coaches we feel confident that we can manage these numbers even better.

We are very lucky to be part of an in depth, ongoing study with the brilliant and very knowledgable Jenny Strickland at the University of Greenwich. With her guidance and protocol, we are bringing the days spent on the treatment table down considerably, but ideally we want to learn about these conditions to help prevent them in the first place.

What do we think we know?

OSD is a growth related condition, we think it can be attributed to high levels of activity during periods of growth. Unlike an adult presentation of a tendinosis, the condition affects the soft cartilaginous junction between the patella tendon and the immature anterior tibial tuberosity (ATT). (See my previous blog for the BJSM about differences between adult and Paeds injury management here).

Figure 1
Demonstrating the close relationship between the enthesis, the patella tendon, the infra patella fat pad and the physis of the tibia.

Historically OSD has been labelled as “growing pains” (a genuine medical entity, but no clinical similarities to OSD) and sufferers of the condition may well have been told to “just get on with it” or that “you’ll grow out of it”. Unfortunately this attitude still exists amongst some parents and, regrettably, GP’s – we see first hand evidence of this in our academy. When I first started in my role, I was guilty of just sitting a lad on the plinth with some ice, telling him to rest for a few weeks and we’ll see how we go.

OSD can almost certainly be attributed to growth spurts, where high levels of cellular activity in the growth zones of bone can’t be matched by the attaching muscles, resulting in traction on the inherently weak enthesis. Usual subjective presentation is that of an ache during, or more prominently, after activity. Gradually pain has been worsening over a period of days or weeks. Eases with rest. However, occasionally we see examples of players that have been kicked or landed on their knees in acute incidents but will display all the characteristics of OSD. But this doesn’t fit with our understanding of growth and traction…

Sailly et al (2013) looked at symptomatic adolescent male athletes competing in elite sport and using Doppler ultrasound they compared the ATT complex to gauge different stages of maturation. Within these stages of maturation, they could attribute pain scores from symptomatic athletes to determine the more vulnerable stages of growth (figure 2 below). The best descriptions for these stages that I have heard are from Sid Ahamed on his Adolescent Injuries course. He describes the enthesis as a continuum that develops with maturation from a stable state to an increasingly unstable state as the cartilage calcified with age.

Figure 2
Classification system of the maturation status of the ATT from stages 1 to 4. ATT, anterior tibial tuberosity; B, bursa; FP, fat pad; HC, hyaline cartilage; M, metaphysic; O, ossicle; P, physis; PT, patellar.

In Sailly’s study they found that no players reported pain during the “stable” first phase but increasing scores of VAS in stage 2. As the enthesis calcified and unites in stage 3 and 4, the numbers decrease again.
So what is happening in this 2nd stage of maturation? The use of Doppler ultrasound opens some new theories. In these symptomatic stage 2 patients, there was Doppler activity within the pre-patella and deep infra patella bursa, indicating the presence of neo-vessels within these structures. Recently, Seth O’Neil (physio matters podcast) explained that most of these pain inducing neovascular structures are actually present in peritendon & surrounding tissues like the bursa, fat pads and fascia. Maybe the same is true with the adolescent population.
The synovium that surrounds the enthesis is highly prone to compressive forces and as such, prone to inflammation. In the developing ATT, the patellar ligament attaches to the tibial tubercle but also to the physis of the tibial growth plate and to the periosteum of the metaphysis of the tibia (see figure 1 at top) . Sailley et al propose that this anatomical area is not only prone to traction that we normally associate with OSD, but also compression. Perhaps this explains the sudden onset OSD in the clinic alongside those rumbling insidious case loads.

Management:

As I mentioned, we now follow the Strickland protocol at our club in terms of treatment, but I still believe the key is in prevention rather cure. We regularly discuss loading with our coaches at every age group. If you consider that most of our players at school boy level will also play and train for their school, probably be selected for other sports such as cricket and rugby and will generally tear around everywhere at 100mph. Basically their day consists of sprinting, jumping, bounding and kicking. Consider the load on those immature structures (both compressive and tensile). As part of a warm up, does that player then need to do a series of hurdle drills or jumps? Could they not spend their conditioning sessions doing low impact movement patterns, balance & proprioception, or co-ordination drills for their newly elongated and uncontrollable limbs? Perhaps every now and then having a training session where the lads don’t have to strike a ball? Like basketball maybe, where you teach spacial awareness and evading the opponent? Or placing a technical bias on the session and reducing the pace?
If we can help coaches, players and parents understand that modifying activities and occasionally, resting, is the best thing in the long run for all parties, I think we will continue to see a drop in training / matches missed due to OSD.

Yours in sport
Sam

Don’t clam up over lower limb exercises

 

I regularly find myself debating this exercise with students, new staff, and part-time staff all from different clinical backgrounds and I always find myself asking them – “Why is that patient doing clams?”

For those unsure of the terminology, the “Clam” exercise is designed to activate the external rotators of the hip, performed in side lying with limited pelvic / lumbar rotation.

Firstly I’d like to make it clear that this exercise does have a place in some rehab plans and I am not adverse to including it as part of a program where necessary – but I strongly disagree with it being a mainstay in rehabilitation plans. Purely going from anecdotal evidence, people seem to use clams as a way of increasing endurance of the glutes, particularly glute med. Often prescribing high sets and reps to target the endurance component of the muscles. Previous literature has suggested that Maximum Voluntary Contraction (MVC) of greater the 50% is required to produce any strength gains in an individual muscle (Atha 1981). Figure 1 below demonstrates the EMG activation of glute med during 2 clam exercises, at 30 and 60 degrees hip flexion. Its clear from this study that the activation of glute med is below the required level to achieve any strength gains.

Glute med (if it ever did work in isolation, which I don’t think it does) would concentrically abduct the hip, isometrically stabilise the pelvis and lower limb, and eccentrically control adduction and internal rotation. The best types of activity to stimulate these actions are going to be weight bearing exercises (Figure 1); (Krause et al 2009).

There is evidence to suggest that the posterior portion of glute med is deactivated with any degree of hip flexion, with the bias for primary movement coming from gluteus maximus (Delp et al 1999). This said, Di Stefano et al’s (2009) study produced similar glute med activation at 30 and 60 degrees hip flexion. Either way, my argument is the same – clams probably aren’t working the structures you intend to target.

Reference: DiStefano 2009 here

Clinical Reasoning

My question to clinicians who regularly use clams is always “why?”. What is the purpose of this exercise? At the moment, I work with an elite athletic population. How often in their training and/or competition do they have to externally rotate a flexed hip in an open chain from a side lying position? Never. Even in standing, I can only think of them opening up their hip to control a ball in mid-air but then they are mainly using hip flexors to activate that movement – something we strictly instruct them not to do with a clam. So now that we can’t think of a transferable example for this exercise, I would ask “why are we doing high reps and sets of an exercise we don’t need to do?”

Problem solving

We have already said that the best exercises for glute med activation are weight bearing exercises and the reason for that is exactly the reason why we shouldn’t try and isolate glute med… in weight bearing, it will work as one part of a complex and brilliant kinetic chain. This was highlighted in a very interesting study recently by Kendall et al (2013) who used a nerve block on the superior gluteal nerve and then performed the Trendelmberg test. Even with a neural block to the gluteal muscles, patients maintained pelvic alignment through the step test, highlighting that in isolation, the glutes alone do not support the pelvis.

One of my preferred, early stage exercises to improve hip control / stability is a single leg isometric movement (figure 2).

Figure 2: Single leg isometric flutes (brilliantly demonstrated by @riarottner)

The patient is instructed to rest the contralateral leg against the wall for balance only. All of the body weight should be through the standing leg. Explain to the patient that their foot is superglued to the floor, but you want them to rotate their thigh out (encourage external rotation). There should be no movement from the upper body, bum should be “tucked in” with text book posture and they should hold this contraction for 10s, repeat 10 times. I promise, it will burn your glutes towards the end. Try this yourself and pay particular attention to what else happens further down the chain. You’ll see activation of the VMO and the medial arch will raise as tibialis posterior activates too. A brilliant example of the kinetic chain in action.

“Providing the patient is able to single leg balance, any exercise targeting hip control should be done unilaterally”

Now, there are examples in the patient populations where this is not an appropriate exercise. For example, early stage ACL injuries due to the torsion this creates through the femur and tibia. Instead I would adapt the exercise to something that we were all taught very early on in our physiotherapy degree – a simple small box step, placing one foot from the floor onto a step and back onto the floor – where the standing leg is the working leg. If you are strict enough with posture and lumbo-pelvic control, this is great early stage exercise for the glutes and easily progressed into a full step up, step downs, lateral steps, greater step heights etc. (For exercise progression, please see my shameless plug for my recent Model of Exercise Progression). Kendalls (2013) paper that we mentioned earlier, supports this simple trendelmberg exercise for patients with marked hip abductor weakness. Krause et al (2009) found an increased activation of glute med with single leg exercises compared to double leg stance, so providing the patient is able to single leg balance, any exercise targeting hip control should be done unilaterally.

For the non-weight bearing patients there is reasoning to perform these open chain exercises. While we have said we may not be increasing strength, we know that there is some activation occurring within the glutes so we limit an atrophy and maintain neuromuscular activation while the patient is NWB. Refer back to figure 1- the top exercise for glute med EMG is straight leg hip abduction so even with these NWB patients there are more appropriate alternatives to the clam.

Conclusion

Two of the core elements of physiotherapy is the ability to clinically reason and to provide effective exercise prescription. I would encourage people who regularly use any exercise, not just clams, as part of their mainstay exercise protocol to consider exactly why they are using them. I personally don’t think there are many examples where the clam is an appropriate exercise for sports medicine populations. The exception being NWB patients who are unable to control long lever exercises like single leg hip abduction. Therefore, there is an argument that the clam may quickly become an extinct creature.

 

Yours in sport

Sam