We are delighted to introduce a guest blog from Jonny King (@Jonny_King_PT), a sports physiotherapist based at Aspetar, Qatar. Jonny has experience working in professional football in the UK with both Norwich City FC and AFC Bournemouth before he made the big move East to Doha. A prevalent voice on twitter and definetely worth a follow, he provkes some intriguing questions regarding our current understanding of hamstring injuries. We hope you enjoy… P&P
Hamstring strain injury (HSI) continues to present as a huge challenge for those of us working within the sport and exercise medicine field – whether that be in a research or clinical setting. Disappointing figures have recently shown that despite an increasing body of publications over recent years and a perceived improvement in understanding of underlying causes, the epidemiology for HSI in elite sport has not changed over the past 10 years (Ekstrand, Hagglund & Walden, 2009) A worrying reality.
Some will argue that WE HAVE improved our understanding and management of hamstring injuries but the evidence base is not being applied effectively into clinical practice. (Bahr, Thornborg, EKstrand, 2015). Others will state that our ability to influence epidemiological data at elite level, has been affected by the evolution of sporting competition including increased physical application. Take professional football for example, both sprint distance (35%) and high intensity running distance (30%) have significantly increased over the past 7 years, alongside a reduction in recovery times as a result of increased fixture congestion (Barnes et al, 2014) These can all be seen as restraints to our drive for better data around HSI.
These are all factors we should appreciate, however are we missing something else?
In brief, we know those at highest risk are those with history of previous strain, weak eccentric strength and those in a fatigued state (Opar, Williams and Shield, 2012). Flexibility, neuromuscular inhibition, biomechanics and H:Q ratios have all been flirted with, but with no real hard conclusion as to their influence on HSI. Identifying those at risk is relatively straight forward these days, given increased accessibility to advanced monitoring technology, helping to identify fatigue or strength reduction. We can thank systems such as GPS and The Nordboard for this. These are for sure all very important considerations as we take a multifactorial approach to injury management and prevention. But, Is there anything else we need to consider?
One area that I feel needs further investigation with regards to HSI is the psychological harmony of the athlete. It may be difficult to account for the primary injury, but are negative beliefs, anxiety and apprehension contributing factors to high rates of re-injury?
Cognitive functioning and therapy has been discussed at length in the treatment and management of many other musculoskeletal conditions, notably chronic LBP (O’Sullivan 2012) and ACL Reconstruction , with methods such as CBT proving an effective intervention in many cases. I wonder therefore if this needs more consideration when it comes to hamstring injury treatment? Poor psychological readiness has been associated with hamstring strain re-injury (Glazer, 2009) and this would also provide a feasible explanation as to why completion of Carl Askling’s H-Test appears a strong indicator for RTP. Maybe it’s something we are missing, or not considering enough? By more thorough monitoring of anxiety and apprehension can we mitigate ‘previous HSI’ as a risk factor? Food for thought..
What about fatigue and eccentric weakness?
We know HSI is more likely to occur towards end of 1st half & throughout the 2nd half (Ekstrand 2011) and that optimal time for full physiological recovery is 72 hours (Dellal et al 2013).
We also know..
The widely documented success of the Nordic Curl programme and other eccentric lengthening programmes in reducing HSI in some populations (Arnason, 2008 and Askling 2013).
Throughout the competitive season, the clinical challenge is to address both fatigue and eccentric strength, because for me, the 2 are counterintuitive to one another. You cannot perform regular, effective eccentric strength training without inducing fatigue, therefore it becomes very difficult to address both variables during a season of heavy fixture congestion.
I do wonder if we spend too much time in-season, prescribing injury prevention programmes and exercises. I feel there is a strong argument that we are only exposing our athletes to a greater risk of injury by adding to the overall accumulative training load and fatigue.
Why are we not reducing hamstring strain injuries?
Are we trying too hard in search for that holy grail of HSI prevention? Do we just need to ease off these guys?
Ultimately, and realistically I think there has to be a fine balance between the 2 . Windows of opportunity, such as the international breaks and pre-season, should be fully utilized for specific strength training and the remainder of the season used to ensure players have adequate time to recover and prepare physiologically for upcoming competition.
No answers here, just some food for thought. Enjoy your sport =)
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).
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):
Difficulty thinking clearly
HeadacheFuzzy or blurry vision
Sleeping more than usual
Feeling slowed down
Nausea or vomiting
Sleep less than usual
Sensitivity to noise or lightBalance problems
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
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?”
“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.
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?
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!
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.
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.
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:
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.
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.
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.
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.
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)
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…
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.
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:
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.
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.
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?
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!
Although it only forms a small percentage of our working week, the thing most people associate with physio’s working in sport is the match day, and the infamous bucket and sponge! When we watch the TV at the weekends, this is the closest we ever get to seeing a physiotherapist working in professional sport. We don’t see all the early morning meetings, assessments, rehab programs, maintenance treatments etc.
I have to admit, rightly or wrongly, it is the least enjoyable bit of my job. I can’t remember the last time I enjoyed watching a game of sport whilst I was working. Wincing at every tackle, losing track of the score back in my rugby days because I’m too busy counting the players get up from a ruck and constantly running through scenarios and management in my head. However, it is the money end of the job. The games are all about why we do what we do.
I feel bad for physiotherapists trying to break into sport, I’ve been there and done it, working evenings and weekends covering training matches and weekend games and essentially not doing very many of the skills I’ve been taught at University or on the courses I’ve dished out money for. Essentially, you are a first aider. I try and make our part time work at the club as attractive as possible in other ways, with CPD, shadowing, training clinics etc because I know its not the glamour and jazz that people think when working for a pro club.
Like it or lump it, its a huge part of the job. So, what do we do when we run on mid game? Like all aspects of our job, there should be an element of clinical reasoning behind what we do. What are we actually asking? And why do we ask it?
For the sake of keeping the blog concise and not too heavy reading, I’m going to talk about your more routine injuries, which can sometimes create harder decisions. For the management of cardiac, spinal, airway stuff make sure you go onto a proper trauma course to get your qualifications!
Stop ball watching
The first habit I had to break when I got into sport was to leave the armchair fan mindset at home. I started off in rugby before moving to football and was lucky to have a brilliant mentor from the start, Clare Deary, who quickly taught me to look away from the ball. Instead your watching the knees and ankles of the forwards in a line out, or checking the prop gets up after the scrum has collapsed. One of the Maddox questions we ask when we check for head injury is “what is the score?” or “who scored last” – in my early days I was asking this without knowing the answer, so if they spoke coherently that was good enough for me.
It is a little bit easier in football because there are typically only two people involved in the tackle, but still don’t get caught up in the game. It important to watch the movement of players, those with known previous injuries or knocks sustained earlier in the game. Are they worsening or improving?
The run on
Ever consciously changed your walk or run because you think people are watching you and all of a sudden you lose all motor patterns and co-ordination? Well when the game stops for an injury, everyone is watching you. If the player is rolling around on the floor screaming in pain, you already know they are conscious and their airways are well maintained, so don’t worry about your 100m sprint time for these cases. Save that for the motionless players.
Approaching the player
The location of the injury will obviously affect your approach, head or spinal injuries aside, I always approach the feet first so the player can see me and I can continuously assess their level of pain, respiratory rate, shock etc. As well as asking “where does it hurt” always make sure you double check other structures, don’t be lured by the pain. Someone landing on their shoulder could always have a neck or head injury.
“You are not trying to diagnose the problem there and then”
When questioning the player, remember its not a consultation in the clinic. You are trying to determine “is it safe for the player to continue” and “will a labouring player cost the team tactically”. If they are missing tackles that they would usually make, or misplacing passes that they normally wouldn’t you firstly run the risk of putting them into scenarios that could cause another injury as well as potentially costing the team.
Try to determine the irritability of the pain early on. Has it changed since the game stopped to the point of you arriving at the player? If its worsened, despite not moving, that would suggest a rapid inflammatory problem. In which case you really want to be removing the player from the field of play to reduce the risk of secondary injury. If the pain has settled or gone in the time its taken you to consciously jog perfectly across the pitch without falling over, you can probably proceed with some more vigorous testing.
Providing you’ve excluded any fractures, check what the athlete can do with the injured structures ACTIVELY before you do any passive movements. If they are reluctant or guarded with any movements thats enough of an indication for me not to do any passive movements. Why force them through a range that they consciously don’t want to go through?
Walking the green mile
So you’ve establish that they are alive, there are no fractures, they can actively and passively cope with movement, by this point the referee is probably in your ear to make a call quickly. In football, if you have entered the field of play, the player is expected to leave before kindly being invited back on by the ref. This is a good time to continue your assessment as you the leave pitch.
Can the player get themselves up from the floor unaided? Can they weight bear? Can they walk? Does walking ease the pain or make it worse? If they can walk off, assess their ability to jump / hop / run / jog on the sideline.
By this point, you have to go with your gut instinct. If any of the assessment so far has thrown you into doubt, you probably have a good reason to remove that player from the pitch. Consider the structures involved, the presence of any swelling, the compensatory movement patterns that you may have noticed leaving the pitch. I usually ask myself what I would prefer to manage out of two scenarios:
1) Substituting a player that reports to clinic the next day with no signs or symptoms of injury, but is a little p*ssed off because you wouldn’t let them play (or a peeved coach because you’ve taken their best player off the pitch).
2) Allowing a player to go back on that has given you doubts and they break down in their next sprint / action on the pitch. They walk into clinic the next day and you have to tell them they are out for 6-8 weeks.. Your coach is definitely going to be more peeved today than they would have been pitch side, I can assure you.
This isn’t to say you remove every player from the pitch that has an injury. The mechanism of injury will have a big say in determining your thought process. For example you may be more lenient with an impact injury that is smarting a bit compared to a non-contact mechanism of injury.
So, chances are this has made things a lot less clear about pitch side assessment.. Unfortunately there is no algorithm to determine whether a player should continue or come off. Every individual player is different and every injury is just as individual.
Is it safe for the player to continue – consider secondary injuries caused by swelling / decreased proprioception, as well as the initial insult worsening.
Will a hampered player on the pitch cost the team tactically.
Whats the worst that could happen if you remove them from the pitch. This can be made easier if you are working with younger ages that perhaps have a rolling sub system, giving you more time to assess. Also, consider the implication of the game / event. A once in a lifetime shot an olympic medal may be worth the risk of a secondary injury. A community level tournament in kids rugby might make you a bit more conservative.
This is only discussing minor knocks and strains. If you are working pitch side and haven’t done or updated your trauma course, make sure you do! Don’t put others health at risk at the same time as your professional credentials. (lubas medical / AREA or RFU are good courses to check out)
I’d be really keen to hear peoples thoughts and experiences with this topic, I’m sure there will be some disagreement with my thinking and methods. Or perhaps people have seen some incidents of players returning to the field when they shouldn’t (I’m thinking the FIFA world cup 2014 with numerous head injuries, but concussion is a separate blog altogether I think).
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).
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.
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.
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.