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

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“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

Case Study: working through the pain with Nick Atkins

Nicks 30/30 challenge

A bit of an unusual blog from us, but I hope its as popular as our previous ones due to the message it contains. A very good friend of mine is undergoing a year-long series challenges to help raise money for a cause very close to his heart.

Below is a summary of the 30 challenges that Nick Atkins is doing, having turned 30 this year.

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Nick Atkins 30 / 30 challenges

I’m sure a lot of people will question the management of some of his injuries I’m detailing here because I’ll admit its not how I would typically manage these problems, so let me explain quickly why rest is not an option here:

Nick, along with his sister Jen & brother Jon, very sadly lost their mum, Judith Atkins, to pancreatic cancer in 2013. Pancreatic cancer has the lowest survival rate of any cancer. Doctors believe there is a period of remission around 5 years that if reached, the risk of the cancer returning is negligible. Judith was a few months short of this milestone before the pancreatic cancer aggressively returned. While we are generally winning the fight against cancer, pancreatic cancer remains the outlier and part of Nicks aim is to not only raise money for research, but also awareness. (Nicks justgiving page here). For this reason, he is displaying an incredible amount of grit and determination to complete these challenges, despite his body saying otherwise.

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Nick, certified drinking athlete. Pre-challenge training

A quick background into Nick, he is what his friendship circle would describe as a “drinking athlete” and certainly not a runner. So while some endurance junkies out there may do physical challenges like these regularly, Nicks starting position was certainly not one built on endurance.

Nicks injuries to date:

 

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Disclaimer – I have permission from Nick to share these details regarding his injuries.

 

The nature of Nicks challenges meant the timeframes were dictated by inflexible dates, making it very hard to periodize any training. So load management became critical, forecasting time periods where we could off-load but maintain a crucial level of fitness.

The first problematic injury(ies) was the bilateral plantafascia pain with right sided calcaneal fat pad irritation. This was the first time we had to make decisions about the program. Previous aches and pains in the lower limbs and back were manageable and its not in Nicks nature to complain. But this pain in his foot was affecting ADL’s as well as training. Typically inflammatory in nature and progressively increasing pain, it took him to the point where he couldn’t weight bear through his heel – but was still completing physical challenges.

Controlling the controllables:

Dropping or moving a challenge was not an option, so we had to sacrifice road running training and hockey for a period of two weeks. Nick maintained fitness via swimming and cycling (a lot) in the mean time we addressed some biomechanical issues in the foot. I say this very tentatively, because in fact it was a lack of biomechanical issues that we had to address. Nick was prescribed some permanent orthotics when he was about 16 for “collapsed arches” – in fact these orthotics were probably causing more problems than solving. Nick had good active control of the medial and longitudinal arches in both feet, so no evidence of a collapsed arch. These orthotics were encouraging him to laterally weight bear via some high density medial posting of the calcaneus & preventing any medial rocking after heel-strike. We removed these, added some gel heel cushions to his work shoes to help offload the fat pad and temporarily reduced running training, which seemed to resolve the pain after two weeks. Instead, nick ramped up the swimming and cycling as part of his triathlon training.

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Nature of the beast:

There have been times recently however where we can’t modify load. Nick is currently running with right sided Achilles pain and in the last week has developed sharp pain in his left groin which is present following a rest at the end of a long run. This presented us with a problem; a month of 10k’s, with half marathons immanent and full marathons on the near horizon. Nick can’t afford to rest.

Typical management of tendon problems would be modifying load along with addressing strength. There was a dramatic difference with single leg heel raise between left & right. Temptation would be to add some exercises here to address this, but we need to acknowledge the accumulative load and consider if there would be any benefit. We decided that the back to back events could in themselves serve to maintain fitness, so we could drop a training session during the week.

The other consideration is where & when Nick is getting the pain. The Achilles pain is only present with compression, so with full plantaflexion – recreated both actively and passively, which makes me suspect a retrocalcaneal bursa involvement. We know that tendons don’t like compression but the absence of any Haglunds deformity and with adequate, well fitting running shoes there is reason to think the tendon may not be a source of symptoms. (See my previous tendon blog here with references).

The pain has stayed at the same level for over 4 weeks now, so we have identified an upcoming gap in events as a window to unload and reassess. In the mean time we can achieve short term relief with soft tissue massage to the gastrocs and some tib-fib, talocrural and subtalar mobilisations.

The groin on the other hand presents like a classic tendinopathy and we were able to exclude any pubic synthesis involvement via a series of tests. This injury was a lot more acute in nature compared to the Achilles. We tried some isometric adduction through different ranges of hip flexion and achieved some short term reductions in pain. Once again, we had to sacrifice some hockey training to try and reduce load and cutting actions in the groin, but in place of this we added isometric groin squeezes into Nicks program.

What’s next?

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Nick & his wife Cat, who has done every challenge with him so far & ironically is conducting her PhD in tendon pathology.

At the time of writing, I have my fingers crossed as Nick is running a “True Grit” obstacle course with his dedicated wife, Cat, who has done every challenge with him so far! (Except the 100 different beers in a year).

With some half marathons and marathons coming up, along with long distance treks I’m anticipating an update to this blog in the summer. Like I said, the plan now is to highlight a window of relative rest where we’ll do some detailed analysis of the right leg in particular. Overall though, I’m incredibly impressed that someone with no endurance running experience has had so little problems. It wont be typical management that’s for sure – while there are long term goals to be met, performance is not the main driver. I’m used to managing similar problems with a view of being pain free, able to perform at high level and minimising the risk of re-injury. So some of this management may not appease the purists, I understand.

For Nick, however,  there are no specific performance targets to be met, it is just essential that he finishes. He’ll do that without my help because of the level of determination he has, but my job is to try and keep a lid on the severity of injury (he insists 90 days without a hot drink is harder than any marathon or combination of marathons).

But the description of Nicks injuries & management are secondary to the fact that hopefully I’ve helped promote Nicks challenges and ultimately an awareness of Pancreatic Cancer. For that reason, if you’ve read this far please help share Nicks challenge.

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Nick & his mum, Judith.

https://www.justgiving.com/nicks3030challenge/

On behalf of Nick, yours in sport

Sam

ps – the 30th challenge is yet to be decided, Nick wants to make it something special so please send us your suggestions!!

 

#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.

Confernece
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.

Serner
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.

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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
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

Aspetar

Sam

Podcast Review: Tendons

I wonder if anyone else does this, subscribe to podcast channels and store them on your phone in an attempt to convince yourself that you’re doing CPD, but never get round to listening to them? I’ve also been known to do this with articles, printing them out then cluttering mine & my colleagues desks but never reading them.

Well I decided to catch up on a few podcasts and start listening to them in the car on the way to work. Flicking through the different channels I subscribe to, I saw 2 separate discussions about tendons. So I thought I would listen to both in succession and see what similarities or differences the experts had. These aren’t necessarily the only podcasts to talk about tendons, just 2 I had on my phone:

1) Physioedge #23: Lower Limb Tendinopathies with Dr Peter Malliaris (here)

2) The PhysioMatters Podcast session 6: Achilles Tendons with Seth O’Neil (here)

 

Revision time: 

Before we start, a quick opportunity to revise some key topics discussed below. Figure 1 demonstrates Cook & Purdhams continuum of tendinopathies.

Tendinopathy continuum
Figure 1: Cook & Purdhams Tendinopathy Continuum (click image for article)

 

Difference between Achilles and Patella Tendon:

A particularly interesting theme throughout the podcasts was the difference between Achilles and Patella tendon pathologies. None of the podcasts openly said “lets start addressing different tendons with different management” but they pretty much edged that way.

Malliaris was careful not to align himself with any particular “recipe” for tendon treatment, but did say that if he were to prescribe a protocol, he would use a different one for Achilles than he would Patella tendons. Later in the podcast, he explains his theory on not loading the patella tendon beyond 70 – 80 degrees knee flexion, explaining that there is no benefit to heavy loading into the end range for tendons… except the achilles tendon. This makes sense, if we understand that tendinopathies are a reaction to a combination of tensile and compressive loads. For the patella tendon to be lengthened, with the knee in full flexion, the patella will be acting as a fulcrum on the tendon tissues. However, when loading the achilles in a lengthened position the calcaneous doesn’t cause as much compression on the tendon (excluding Haglund’s deformity).

A quick cameo from a third podcast (BJSM Apophyseal injuries in children and adolescents with Dr Mattheiu Sailly, here) but interestingly discusses different processes between Osgood-Schlatters and Severs disease, with less tendon involvement seen in Severs. Could this paediatric presentation be similar in adult tendinopathies?

 

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Is there a benefit to deep squats with a tendinopathy?

Exercise management:

While on the topic of lengthening tendons and putting them under load, it seems apt to discuss the one exercise method that goes hand in hand with tendons, Eccentrics.

“Eccentrics are not essential – Dr Peter Malliaris”

Malliaris comes across as a big fan of eccentrics. They are a useful method of increasing time under tension (TUT) and applying a heavy load, however they do not have to be a part of every program!

If a patient is unable to perform an isometric exercise, don’t even bother attempting an eccentric exercise as they will lack the quality throughout the movement. Another example would be a program designed for a player in mid-season. In these circumstances, it could be better to provide high load isometric exercises. O’Neill supports this theory for mid-season. While we accept that eccentric exercises will help the tendon, remember that they will also fatigue the muscle and therefor could impact on performance.

It is also important to recognise the stage of tendinopathy (see Figure 1). While a degenerative tendon can be treated quite aggressively in order to increase stiffness, however most athletes are likely to present with a reactive tendinopathy. In these cases, the cellular matrix is generally intact so the management can afford to be less aggressive. In these cases, activity modification to acutely lower the load would be beneficial and combined with isometrics, which Malliaris believes have an analgesic effect.

With any program for tendons, it is important to continuously monitor pain responses. A short duration of pain following activity suggests a stable tendon, however pain for a couple days suggests a very reactive and unstable presentation. O’Neill quotes a theory based on Delayed Onset Muscle Soreness (DOMS) as the characteristics of tendon pain and DOMS are strikingly similar. He explains that fascia seems to be a source of pain as opposed to the contractile tissues. The paratenum contains most of the nerves and the structures here will suffer from the delayed onset soreness. Much like actual DOMS, the tendons respond well to loading. O’Neill uses the analogy of going for a gentle jog when you have DOMS in your legs, and feeling a bit better afterwards.Over time, changes in both central and peripheral sensititsation may cause the heightened peripheral sensitisation we see with chronic loading – hence part of our management is activity modification.

doms

Moving on from mid-season management, Malliaris discusses the off-season and the tendency of athletes to put their feet up for a few weeks after a gruelling season. This would be detrimental to a problematic tendon and as soon as they resume intense pre-season training you will spend the whole pre-season fighting fires with a reactive tendon. Therefore prescribe off-season tendon programs that include jumping, hopping, running drills to maintain control of the tendon.

 

“True tendon problems tend to be aggravated by a Stretch Shortening Cycle – Seth O’Neill”

 

In his exercise programs, Malliaris ensures that the Stretch Shortening Cycle (SSC) is as long as the “slower exercise” phases. However, these do not have to be done in simaltenous blocks. The SSC exercises should be incorporated as early as possible, providing the movement patterns are fluid and symptoms are under control (again, its important to understand and recognise a reactive or degenerative phase tendinopathy).

 

“Patella tendinopathies love intensity and loves load”

 

Summary:

Tendon management remains a complex and daunting task for physiotherapists, yet in an age where we promote individualised management of injuries we still seem keen to follow a “recipe” for tendon management. Both podcasts discuss the importance of treating the individual, with reference given to their demands and tailoring programs to suit them. However, we seem happy to discuss “tendons” as a whole. Hamstring management has its own niche, at the same time we don’t treat all ligament injuries like an ACL. Should we start discussing individual tendons separately? As mentioned at the top, Malliaris changes his stance on loading through range when managing Patella tendons and Achilles tendons. We have only discussed these two tendons, without any reference to the rotator cuff, the hamstring tendons, flexor and extensor complexes in the forearm – all of which have different roles and demands.

What is exciting is the amount of research going into tendons and our understanding is evolving very quickly. Since my short time of being a physio, we have dropped “itis” and introduced “opathy”; eccentrics fell out of favour recently and Alfredssons protocol has been dissected and critiqued to death, yet now, with the support of Malliaris and O’Neill (amongst others) we feel comfortable using eccentrics again, but as part of a bigger program.

I highly recommend listening to the above podcasts and subscribing to their channels, they are a hugely resourceful… resource!

 

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).

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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.

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

 

 

Figure 6: b) medium box step up
Figure 3: b) medium box step up
Figure 6: c) High box step up
Figure 3: c) High box step up

 

 

 

 

 

 

 

 

 

 

 

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

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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.

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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:

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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