Compex doesn’t have to be complex

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

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

Its all about progress

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

Consider the tissues

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

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

Now promise me if the Compex hurts, you will turn it down. OK?

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

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

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

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

I really like Geckos. I found this Gecko a musing

Conclusion:

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

As always, thoughts and opinions are welcome.

 

Yours in sport,

Sam

Taking your time with acute injuries

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

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

Reasoning with the history:

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

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

“Do you think its grade one or two?” 

“Yes?”

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

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

Table 1: Descriptions of muscle classification systems used clinically From Mueller-Wohlfahrt et al (2012)

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

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

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

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

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

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

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

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

What about treatments?

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

Summary

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

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

 

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

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

 

Yours in sport,

Sam

 

 

 

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.

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.

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:

 

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.

 

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?

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.

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.

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

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

Introduction

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

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

Epidemiology

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

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

Adductor Related Pathologies

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

Treat the player, not the scan!

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

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

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

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

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

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

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

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

 

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

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

FAI

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

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

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

Increased loading over growth plate stimulates CAM deformity

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

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

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

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

– Low antetorision would present as decreased IR and increased ER

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

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

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

Taking this forward

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

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

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

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

Yours in sport

Sam

Pitch-side management in sport: a POV from a bucket & sponge man

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.

Key Points:

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).

 

 

As always, Yours in Sport

 

Sam

The Osgood, the bad and the ugly

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

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

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

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

What do we think we know?

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

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

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

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

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

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

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

Management:

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

Yours in sport
Sam

Cryotherapy: Therapeutic but is it clinically relevant?

ACPSEM members can access PRICE guidelines here

Try thinking of a title about Ice and avoid the temptation to put “Baby” in it!

 

The thing that I love about physiotherapy is that nothing is ever black & white. Things will come in and out of fashion and our understanding about interventions and treatment modalities will continuously evolve. One of the great debates is about the use of ice following injury. How long should we apply it? In what form should we apply it? Should we use it all?

I recently skimmed through the Physical Therapy in Sport journal under “Articles In Press” and saw two papers within that category alone that discussed the use of cryotherapy. (For anyone that is a geek like me and hasn’t got the Health Advance App by Elsevier, get it! ACPSEM members can access all the content for free here http://bit.ly/PTISaccess).

The first paper was a systematic review (Martimbianco et al 2014), which instantly lost my attention, from my point of view they combine the conclusions of a multitude of papers and varying methodologies (all with their own unique methodological flaws) to create a super-conclusion that most of the time isn’t clinically relevant or is very noncommittal. Essentially, systematic reviews are literature stereotyping. In this case, said paper based a lot of its findings on papers from in the early 1990’s. It concluded that there was not enough evidence to draw a definitive conclusion on the use of cryotherapy following ACL reconstruction.

The second paper however, provoked a bit more thought. This study was by Phil Glasgow, Roisin Ferris and Chris Bleakley – with Glasgow and Bleakley from the recent POLICE guidelines fame – who better to critique the use of ice?
Glasgows paper was a randomised trial looking at the effects of cold water immersion (CWI) comparing different temperatures and durations of immersion on Delayed Onset Muscle Soreness (DOMS). It was this paper that inspired the forthcoming discussion…

 

What do we think we know about cryotherapy?

 

The first thing to distinguish is the method of cryotherapy; in what form should ice / cold be applied? Cryotherapy comes in forms of crushed ice to blocks of ice, buckets of cold water to cold water baths, compression devices to good old-fashioned ice spray on the side of the pitch. In any form, the proposed clinical benefits encourage a pumping effect on vascular system to encourage blood flow, nutrient and waste transportation (Wilcock, Cronin & Hing 2006). Then there are psychological benefits of feeling more “awake” and less fatigued (Wilcock et al 2006). A recent Cochran review (Bleakely et al 2012) found that CWI is superior to passive intervention at reducing muscle soreness. (I know, I slate systematic reviews then use them to my advantage). The point I’m getting at is that of all the proposed benefits of cryotherapy, the most weight is behind the subjective benefits. Take Glasgows recent paper; The control groups scores of VAS pain following eccentric hamstring exercises were 20% higher than one of the intervention groups that underwent 10 minutes immersion at 6ºC (see image below source). The results were not statistically significant but they do look clinically relevant. These percentage differences do not have to be statistically significant for them to have a major benefit in elite sport, where marginal gains has now become a specialised role in itself thanks to Dave Brailsford and the British Cycling team. Everyone is looking for that extra percent to enhance performance & results.

 

Where does ice fit in the treatment room?

 

If we return to the basic scientific theory underpinning cryotherapy, we think that it decreases metabolic activity and therefore limiting secondary hypoxic damage – essentially reducing risk of secondary injury. The injury has happened, there is nothing we can do about that, but we can prevent it worsening. Secondary hypoxic damage not only weakens affected tissues, but the associated swelling can effect surrounding tissues. In steps the counter argument…

It has been found that tissue temperatures below the subcutaneous layers are very difficult to influence due to the highly sophisticated homeostatic systems in place. Bleakley, Glasgow & Webb (2012) found the changes in tissue temperature are not enough to influence metabolic activity. However we do know that CWI will reduce skin temperature, even if it doesn’t affect tissues below (Algafly & George 2007). We also know how important the skin is in feeding information back to the CNS. It plays a huge role in proprioception and nociception.

 

In our treatment room, we still advocate the use of ice despite the emergence of this new understanding. What has changed in recent years is our thought process behind what is happening as a result of the ice. Instead of using cryotherapy in isolation to limit swelling, we now combine it with compression (which is proven to assist with swelling and decreasing CK levels etc) to reduce pain. For more proximal soft tissues injuries, we have the luxury of a Game Ready machine to compress and cool affected areas. However for more distal injuries, e.g. Following an ankle sprain, we will encourage the player to submerge their foot in a bucket of 1/3 ice and 2/3 water. As soon as the foot goes numb, we begin some appropriate movements (cryokinetics) depending on injury location, structures involved etc. By doing this, we believe the hydrostatic pressure of the water will act as local compression while the ice provides appropriate analgesia. The analgesia then allows us to begin some loading of damaged structures – thinking back to the POLICE guidelines that advocate Optimal Load. Every stage of this treatment is clinically reasoned. The movements undertaken should not exceed normal ranges of movement and must be pain-free.

 

Lets wrap it up…

At the moment, cold water immersion is commonly used as a recovery modality from exercise, especially exercises that elicit DOMS, but with very little empirical evidence to support this. Despite this, we have subjective improvements in pain following any ice interventions. If we can accept that and build that into our clinical reasoning, then we have a way of removing pain from our limiting factors and enabling us to introduce movement to an injured structure. So, although we can’t clinically justify the use of cryotherapy as a recovery modality, I would advocate it as part of a treatment & rehabilitation program.

 

Yours in Sport,

 

Sam

 

Game ready professionally photographed in my kitchen