Case Study: Myositis Ossificans – Deadlegs aren’t just for the playground

Whether you call them a “dead leg” or a “Charlie horse” or a “cork thigh” chances are we have all had one. Mostly from the playground days where the bigger kids want to take pleasure in seeing you limp for 5 minutes. However when they happen in sport, with fully grown athletes running at full pace, a collision to the thigh can result in an injury much more serious than the one we associate with from childhood.

The reason I wanted to write this blog was that I worry  that thigh contusions are underplayed in the treatment room, potentially because we associate them with those school sports injuries that can be “run off”. This is a case study that I became involved with after initial management of the “dead leg” failed, and to this day is one I reflect on about how important initial management can be in saving severe stress in the long run. This is a case of a “routine” dead leg that is commonly seen in contact sports that resulted in 9-months of rehab to manage a secondary case of myositis ossificans.

What are we dealing with?

There are two types of “dead legs”

1. Intramuscular: blunt force trauma to the muscle that results in a haematoma, in this scenario the epimysium remains in tact and the bleeding is contained within the muscle compartment.
2. Intermuscular: the epimysium surrounding the muscle is broken along with the damage to the muscle tissue, the resulting haematoma spreads outside of the damaged muscle.

The intermuscular hematoma by far looks the worst, it’s the one where the whole thigh goes black and blue and looks pretty nasty. However, clinically these ones tend to heal quicker and they look a lot worse than they feel. The problem with the intramuscular haematoma is that because it is contained, the pressure can build up and become more painful. It is generally more debilitating as a result, with larger loss of range and more pain. It also doesn’t provide that visible diagnosis as very often you just get a small sign of bruise on the skin from the impact – this is where it can get dangerous as we like to be able to see injuries (hmmm something about invisible injuries and under diagnosis.. concussion?). We have discussed acute management before (here) but with dead legs, it is always worth monitoring for a few days and hoping that the leg goes black and blue.

In the first few days, range is a good indicator. On day 1 after the injury, if they are unable to achieve >90 degrees knee flexion, the prognosis is generally longer. For a bad intramuscular contusion, you could be looking around 6 weeks. This is where the coaches tell you it’s just a dead leg and they’ve had worse. But, it is structural damage to the tissue resulting in bleeding and should be given the same respect you would give to a tear. (Muscle injury classification via the Munich Consensus here).

Myositis Ossificans (MO):

MO is the formation of heterotrophic bone within the muscle following trauma (here) essentially following failed healing the body begins to lay down bone in an attempt to add stability and structure.

Case study:

The following case study is an example of an academy player, where an initial intramuscular trauma to the muscle was accelerated back to activity resulting in a 17cm tear of vastus lateralis (VL), consequently being diagnosed with MO that was estimated to be 3cm thick and of equal length to the tear.

Timeline:

• Day 0 – initial impact to right VL via collision in training, had to be removed.
• Day 1 – “able to squat and lunge but pain on a stretch”. Player expressed determination to train and so was allowed to.
• Day 2-3 – continued training
• Day 5 – Removed from training with “cramp / DOMS” in right leg.
• Day 8 – Sudden loss of power with running and kicking, removed from training.
• Day 30 – returned to training
• Day 31 – played in a competitive game but substituted by manager after 25 minutes due to inability to run. Assessed by doctor and head physio. Visible contained swelling in VL, palpable solid mass, loss of range and pain on contraction of quads. MRI scan demonstrates a 17cm longitudinal tear of VL. Suspicion of MO so sent for ultra sound scan which was confirmed, absent from full team training for 9 months.

Contained haematoma within the vastus lateralis muscle after 30 days of continued training post-initial injury

Management:

Surgical excision of MO is only really reserved for persistent cases that don’t respond to conservative treatment (here). A collective decision was made that we should try to reduce any form of load that may stimulate further bone growth. As a result, the player was removed from all activity of the lower limbs, no soft tissue therapy to the quads and at this stage no stretching of the affected tissues.

It is neither healthy nor beneficial (or fun!) to completely rest when you are used to training 6 days a week. Credit should go to Will Abbott (@WillAbbott__) for his contribution to the maintenance of the athletic profile for this player. A periodised program was designed to maintain metabolic and cardiovascular systems, strengthen the upper body and completely unload the lower body.

A periodised model to demonstrate maintenance of unaffected systems with complete lower body unload (designed by Will Abbott)

The program included swimming, with multiple floats between the legs to reduce the temptation to kick. All gym based activities were performed seated or with legs supported when lying to reduce axial load through the legs during upper body lifts. Upper body metabolic sessions were implemented via high intensity interval training, with small rest periods to help maintain specific anaerobic demands relating to the sport. This was done using medicine balls, ropes, boxing pads.. anything to reduce the monotony of daily upper body training.

Each month was broken down further (as shown below), with follow-up ultra sound scans every 4 weeks. After the first 4 weeks, we observed a 2.5cm reduction in length which consolidated our thought process to continue de-loading. With limited exercise potential and treatment for the leg, we ran half days and 5 day weeks to help maintain a positive psychological presence.

This was an opportunity to increase muscle mass in the upper body, an opportunity that would not have been possible during season if the player continued to play and train. This allowed a clear progressive pathway for increased lean mass with the following phases:

Hypertrophy –> Max strength –> Strength / power conversion –> Power

While the conditioning phases were as followed:

Aerobic base –> Max aerobic –> Supra max aerobic

There was a decrease in calcicific mass every month, although the rate of this varied each time. By the end of month-4, the mass had completely reabsorbed which meant the reintroduction of load to the lower libs.  By this point, the end of the season was 6 weeks away and therefore no realistic opportunity to play again this season, so the decision was made to start physical preparation for the following season.

An example of the lower body periodisation

The lower body gym program was tailored as followed:

Strength endurance* –> Strength –> Max strength –> Strength & power complex training

(* This was probably more “re-introduction to the gym” rather than true strength-endurance. But this phase would have served as a gentle hypertrophy phase given the 4 months of atrophy)

Before undergoing a linear outdoor session progressing from general preparation to sport specific drills with Tom Barnden (@barnden_tom). The player completed a full pre-season and no recurrent symptoms to date.

Conclusion:

Hopefully the lengthy timeline of this case study demonstrates the importance of giving each individual injury the respect it deserves. While I hope the management is interesting, the key discussion point is how do we approach “dead legs”? Should there be better education to athletes and coaches about the magnitude of injury? Essentially given the tissue damage, are they a tear? If an A4 piece of paper represented a muscle, and we tear down the middle (strain) or poke a hole through the centre of the page (blunt force trauma), that page is still affected and unable to serve as an A4 piece of paper. Why does the mechanism of damage change the management of injury? Given any loss of range or function following a blunt force trauma, always consider the magnitude of potential damage; monitor swelling, bruising and pain and have adequate timelines in the back of your mind – don’t rush to a diagnosis / prognosis on day 1. There will be times where there is impact and initial pain but full range and full strength – this is where our pitch-side assessment and reasoning comes in (here).

Yours in sport,

Sam

Clinical Updates from ISHA 2015 (International Society for Hip Arthroscopy) Conference – Ben Matthew

We are delighted to host a blog from fellow physiotherapist and twitter geek, Ben Mathew (@function2fitnes) who discusses his take home messages from last years International Hip Conference in Cambridge. Ben discusses some brilliant considerations for when conservative treatment just doesn’t work, which compliments nicely with a recent blog we wrote on trying to manage hip pathology in-season (here). Some of the points I particular like relate to the rehab after surgery. Thats enough from me…Thanks very much to Ben.

 

Clinical Updates from ISHA 2015 (International Society for Hip Arthroscopy) Conference – September 2015, Cambridge

 

Conditions like Femoro-acetabular impingement (FAI) and Acetabular Labral tears (ALT) are being recognised as the leading cause of hip and groin pain in the active population and has gained increasing attention over the past decade. In the past, these pathological process simply went undiagnosed. Surgical management, especially hip arthroscopy, can be a viable treatment option, especially when conservative management has failed.

Leading hip surgeons, researchers, health economists and expert physiotherapists came together for the ISHA conference at Cambridge (24 – 26 September, 2015) to discuss the latest developments and research findings in this rapidly evolving clinical speciality. I was fortunate to be there and to gain the up-to-date understanding of the complex hip and groin area, and also to listen to some top speakers. It is difficult to summarise a 3 day seminar in a short post. However, I have tried to cover some key clinical points, which might be useful for therapists, involved in hip and groin rehab. I have divided this post in three areas

 

1. Clinical Examination of Hip Related Groin Pain
2. Management of Post-op Hip Arthroscopy Patient
3. Key References which were mentioned in the lectures

 

Clinical Examination of Hip Related Groin Pain

1. Examination of Chronic hip and groin pain is challenging. It is important to have a thorough subjective assessment as part of the screening process. Some of the key subjective questions specific to the hip region are

• Childhood hip disease like Perthes, SUFE, Dysplasia (These patients are at a high Risk of secondary Osteoarthritis)
• Lower Limb Fractures and History of Stress Fractures
• Mechanical Symptoms like Clicking, Locking and Catching with pain (Highly indicative of ALT)
• History of Steroid Use (linked with Red flag Pathology like Avascular necrosis)
• Multi-joint Pain and Presence of Generalised Ligamentous Laxity (linked with capsular laxity and ligamentum teres injuries)

 

2. Use of Patient reported Scales such as the HAGOS Scale and iHOT 33 were encouraged to be used as part of the screening process, to assess the physical, functional and psychological effect of chronic hip pain.

 

3. The most provocative movements for FAI and ALT are prolonged sitting, deep squat, getting in and out of car, kicking and twisting movement. Movements which involve deep squatting or loaded rotation are usually painful in this cohort. If the patients have significant early morning stiffness, there could be an element of early osteoarthritis.

 

4. Functional testing is an important part of the objective examination. Tests such as Overhead squat, Lateral step-down and Single leg squat are impaired in chronic hip and groin pain. The most common compensation is excessive hip adduction and hip internal rotation. These impairments could be due to pain, motor control deficits or weakness. If the patient can consciously correct it, it is most likely to be motor control deficit.

 

5. It is very common to have co-existing pathologies with chronic hip pain. Some common conditions are low back pain, SIJ pain and Pubic overload syndrome

 

6. There is no specific tests to diagnose for FAI or ALT. A combination of the FAIR (Impingement test) and FABER is useful to rule out articular hip pathology. The FAIR test is not specific for FAI, but indicates internal derangement of the hip.

 

7. Strength deficits are very common in chronic articular hip pathologies. It can be bilateral. The most affected groups are hip abductors and hip external rotators.

 

8. A very useful tip to differentiate between hip related groin pain and adductor related groin pain is by isometric strength testing, using hand held dynamometer. There is reduced adductor to abductor ratio in the adductor related groin pain group than hip related groin pain.

 

9. The most important objective marker is the range of medial rotation. Generally, patients with FAI tend to have internal rotation less than 15 degrees. Patients who have less than 10 degrees of internal rotation tend to do poorly with conservative management.

 

10. Excessive ROM in internal rotation and external rotation can be indicative of structural variations such as dysplasia or capsular laxity, which is very common in the dancing and martial arts population.

 

Post-op Hip Arthroscopy Hip Patients Management 

1. There is lack of consensus on these variables following hip arthroscopy (Weight bearing status, Use of CPM, timing for manual techniques, guidance of soft tissue work, Use of brace). Therefore, it is important to liaise with the surgeon on clear guidance and precaution for optimal rehab following hip arthroscopy.

 

2. Some suggested time-lines for different types of procedures in hip arthrscopy in the conference were

• Bone Reshaping / Osteoplasty   –   Immediate WB with crutches as tolerated
• Labral Debridement / Repair       –   Immediate WB with crutches as tolerated
• Cartilage Procedures / Microfracture – 6 Weeks NWB
• Capsule Procedures / Plication          – 6 Weeks NWB

 

3. The incidence of post-op complications are very low, around 0.5% for major complications. Most post-op issues are soft tissue inflammation such as psoas tendinitis.

 

4. Most patients symptoms tend to flare-up after 3-4 weeks, following hip arthroscopy, when they start weaning off crutches and increasing activity. It is important that patient are informed that it is a very slow process of rehab and loading should be gradual.

 

5. Hydrotherapy is a very useful adjunct and can be started within 8- 14 days, once the sutures are out and the wound is healed.

 

6. Exercises such as CLAM and Active SLR are best avoided in this cohort since it irritates the hip flexors and can lead to psoas tendinits which can be very painful and limit rehab progression. (See Sams thoughts on CLAM’s here)

 

7. Regaining Hip extension is paramount in the initial stage. Manual techniques are best avoided in the first 3-4 weeks. Avoid excessive passive stretches during this period, when the capsule and labrum is vulnerable.

 

8. Local stability of the small rotators of the hip is encouraged, in the initial stage, along with hip abductor training. Global movement training such as squats, step-ups and dead-lifts are not appropriate in the initial stages.

 

9. Progression of patients should be criteria based, rather than time based. It is important to have a clear return to play screening process, before returning to contact sports. In this regard, it is similar to ACL rehab.

 

• Around 82-87% of athletic patients are able to return to playing full sports following hip arthroscopy. The average time is between 6months – 8 months. The sport with the lowest success rate is rowing (not surprising, considering the excessive flexion in the sport)

 

I hope you found this summary of the conference useful and thanks for reading.

Any thoughts/comments very welcome.

 

Ben is MSK Extended Scope Practitioner in the NHS and also in private practice. He has a special interest in lower limb, running injuries and chronic hip and groin conditions. He is passionate about application of research in clinical practice and is involved in regular teaching nationwide on multiple lower limb courses. You can follow ben on Twitter@function2fitnes

Key References

1. Adler(2015)- Current Concepts in Rehabilitation following Hip Preservation Surgery: Part 2. Sports Health. Published online – July 2015
2. Agricola(2015)- What is Femoroacetabular Impingement? BJSM, Published Online – June 2015
3. Bleakley et al (2015)- Hip Joint Pathology as a Leading Cause of Groin Pain in the Sporting Population: A 6-Year Review of 894 Cases
 Am J Sports Med published online May 11, 2015
4. Elias- Jones et al (2015)- Inflammation and Neovascularization in Hip Impingement. Not just wear and tear. The American Journal of Sports Medicine, Vol. 43, No.8
5. Frank et al (2015)- Prevalence of Femoroacetabular Impingement Imaging Findings in Asymptomatic Volunteers: A Systematic Review, Arthroscopy, Vol 31, No 6 (June), 2015
6. Hammoud et al (2014))- The Recognition and Evaluation of Patterns of Compensatory Injury in Patients with Mechanical Hip Pain. Sports Health. Mar/Apr 2014
7. Mosler(2015)- Which factors differentiate athletes with hip/groin pain from those without? A systematic review with meta-analysis, BJSM, Published online – July 2015
8. Nepple at al (2015)- What is the association between sports participation and the development of proximal cam deformity? The American Journal of Sports Medicine
9. Ross et al (2014)- Effect of changes in pelvic Tilt on range of motion to Impingement and radiographic parameters of acetabular Morphologic Characteristics. Am J Sports Med, originally published online July 24, 2014
10. Zadpoor (2015)- Etiology of Femoroacetabular Impingement in Athletes: A Review of Recent Findings, Sports Med, Published Online: 22 May 2015

 

 

 

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

 

 

 

Laboring through a Labral Tear

One skill when working in sport is learning to compromise between your clinical brain (the one that tells you that pathology and injury needs to be managed a certain way) and your performance brain (which tells you that your job is to get athletes back over the “white line” in order to do their job). In an ideal world, we try and appease both of these brains where tissues heal well and performance is optimised with the lowest risk of re-injury. But there are some pathologies that cause these two brains to clash. Ones that can be “managed” until the off season where proper interventions can take place. One such injury that I’ve been trying to learn more about is the mid-season hip labral tear.

The purpose of these blogs is to encourage me to read more around certain topics, so in order to help with this I have to say thanks to a few people that have provided me with papers and words of wisdom (Erik Meira, Nigel Tilley & Joe Collins). And thanks to whoever invented Twitter because I probably wouldn’t have this access to knowledge otherwise.

The Problem..

Typically, hip instability injuries are seen in sports with high repetitions of rotational and axial load – football, gymnastics, hockey, tennis, martial arts.. and so on. The hip is widely accepted as being one of the most structurally stable joints in the body, with a deep acetabular socket lined by the labrum, which creates negative pressure within the joint to increase congruency of the femoral head. But what happens when this environment is disrupted? A recent review by Kalisvaart & Safran (here) explain that it takes 60% less force to distract the femoral head from the acetabulum in presence of a labral tear. (This review is great for explaining multiple causes of hip instability, not just labral tears, and also assessment techniques.)

Typically, a lack of stability is replaced by rigidity, where the surrounding soft tissues try to compensate for this increased translation (Shu & safran 2011 here and Boykin et al 2011 here). On assessment of an ongoing labral tear, its quite common to find increased tone or reduced range around adductors and hip flexors. Iliopsoas in particular plays a role to help increase congruency in the hip. (For tips on how to release iliopsoas, please tweet @Adammeakins) – one key thing when managing this condition is not to confuse high tone / over activity with being “too strong”. Chances are its the opposite, it more likely indicates a lack of control. Its not uncommon to see adductor tendinopathies secondary to labral tears as the the load around the joint increases – especially in sports like ice hockey where there is high eccentric load on the adductors (Delmore et al 2014 here).

The Intervention..

So, you’ve diagnosed the tear (clinically and / or radiographically) but other than being irritable, it isn’t affecting the athlete. (Note, not all tears can be managed conservatively, due to pain & some require mid-season surgical intervention – Philippon et al 2010 here). The key premise to your ongoing rehab should be to make the hip joint as robust as possible. Remember, “Stability – not rigidity”. Whats the difference? Can the athlete control the hip or pelvis while performing another task? Or do they lock into a position and rely on passive structures like ligaments and joints.

Consider the demands of the sport. Don’t just fall into the trap of working through what I’d call the “action man ranges” – true anatomical flexion, extension, abduction and adduction. Watch training and competitions of nearly all sports and you’ll rarely see these truly sagittal or coronal movements. They tend to be combinations accompanied by transverse movements of the body in relation to the limb. Make sure this is replicated in your rehab.

UNIONDALE, NY – MARCH 05: Nik Antropov #80 of the New York Rangers warms up before playing against the New York Islanders on March 5, 2009 at Nassau Coliseum in Uniondale, New York. (Photo by Jim McIsaac/Getty Images)

Using the three examples above, consider the role of the hip musculature throughout these movements. We don’t always have to replicate abduction in an open chain movement, sometimes its necessary for it to be closed chain and for the body to move relative to the limb. Note how none of these tasks fit the “action man ranges” but all involve some degree of traverse rotation, combined flexion and abduction or extension and adduction etc etc.

No I can’t bench press, but my squats are awful.

Delmore et al (here) and Serner et al 2013 (here) describe some excellent exercise interventions for the adductors here. These include some good low-load isometrics for those early stage reactive tendons – with isometrics appearing to down-regulate pain associated with this acute pathology (Koltyn et al 2007 here; Rio et al 2015 here to name just two resources) . Moving forward through rehab, I’ve discussed exercise progression at length before (here), I’m not dismissing exercises that involve pure flexion, extension etc but as part of a progression, its important to combine these movements. For example, start with a single leg dead lift – can the athlete control their trunk through hip flexion and through extension back to neutral? No? Then here’s a range to work on, using regressions to help improve technique and control. Yes? Then add a rotational component at different ranges of flexion – rotation away from the standing leg will increase the demand on the adductors to control the pelvis in outer ranges. The leg itself hasn’t abducted, but relative to the trunk it is hip abduction.

Remember the bigger picture

Its important not to just focus on the affected structures. For those interested in groin pain, a summary of the 1st world conference on groin pain is here – one key message from that conference was that anatomical attachments are not as discrete as text books make them. Consider what else contributes to the hip and pelvis control. We have mentioned iliopsoas control, but also rectus abdominus. Its not just a beach muscle. Eccentric sit ups can help improve control of the hip flexors, along with some lower load exercises like dead bug regressions – a little imagination or some quick youtube research can turn this one concept into hundreds of different exercises.

We have addressed the issue of controlling abduction through range with the adductors, but also remember to maintain that abduction-adduction ratio with some external rotator & abductor muscle exercises (queue Clam rant here – clams to me are like psoas release to Meakins). Possibly the best piece of advice I was given when doing this research was from Joe Collins, who told me to consider hip joint pathologies like you would a rotator cuff injury in the shoulder. Don’t neglect those smaller, intrinsic muscles around the hip. The exercise below is an anti-rotation exercise working through ranges of hip abduction-adduction.

The athlete is tasked to resist the rotation of the femur into external rotation while slowly moving through hip abduction and back to adduction. (This example is done with a shorter lever to improve control and the bench provides feedback to keep the hips in neutral or extension, rather than the favored flexion). Anti-rotation exercises can also be incorporated into trunk / core control exercises (for any instagrammers – follow ETPI who post some great videos and snaps of golfers working on rotational control). Progress from anti-rotation into control through rotation. Some examples here:

anti-rotation plank with sagittal control

Anti-rotation plank variation with weights

Anti-rotation plank with traverse control. Encourage the athlete to keep the pelvis still when moving the upper limb.

Single leg bridge with arm fall outs. Can be regressed to a normal bridge if the athlete lacks lumbo-pelvic control.

Side plank with arm tucks – an example of controlled trunk rotation while isolating the lower body to stay stable. Can be combined with the adductor bridge mentioned in Serners paper to increase load through proximal adductors.

 

These are just some ideas of how to manage a labral tear mid-season; working on rotational control, analgesia via isometrics, improving congruency in the hip joint and overall hip stability via strengthening – Stability, not rigidity! The exercises mentioned here are by no means an exclusive list and I love learning about new drills and ideas, so please share any that you find useful.

 

Your in Sport,

Sam

Recovery from concussion – a guest blog by Kate Moores

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

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

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

 

Recovery

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

“They said something about no computer games”

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

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

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

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

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

Whats up doc?

This doesn’t even make sense

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

 

Prevention

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

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

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

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

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

Symptoms	Consequences
Headache (97%)	Persistent headache (93%)
Dizzyness (93%)	Catastrophic (haemorrhage, coma, death) (60%)
Confusion (90%)	Early onset dementia (64%)
Loss of Consciousness (80%) – how this is lower than headache is worrying.	Early onset Alzheimers (47%)
Nausea / Vomitting (53%)	Early onset parkinsons (27%)
Personality change (40%)
Trouble falling asleep (36%)
Becoming more emotional (30%)
Increased anxiety (27%)

Table 1: Frequency of concussion symptoms and consequences identified by American Football playing high school students (Cournoyer & Tripp 2014)

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

 

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

Concussion Assessment – a guest blog by Kate Moores

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

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

Part 1 (of Blog 2)

Conor McGoldricks first day at school

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

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

“Youth Athletes are still children balancing studies with sports”

Assessment

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

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

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

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

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

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

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

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

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

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

 

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

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

 

 

 

 

 

 

Hamstring Injury – What are we missing? by Jonny King

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?

More brain training before RTP?

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 1^st half & throughout the 2^nd 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.

Are we doing too much?

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 =)

 

Jonny

Concussion – Pitchside management

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

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

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

George Norths contenious concussion in 2015 Six Nations

What is concussion?

The RFU describes concussion as:

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

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

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

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

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

Saying the C-Word

“He’ll be alright”

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

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

And

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

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

Making the Call

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

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

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

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

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

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

Alvaro Pereria out cold in Brazil world cup

Later, he overruled his own doctor to continue playing.

Conclusion

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

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

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

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

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

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

 

Yours in sport,

Sam

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