These boots are made for walking… sometimes

Image is everything in sport these days, like it or loathe it. And Aircast boots aren’t exactly en vogue. Unless you are David Beckham, who has become synonymous with the “Beckham Boot”, there aren’t many that can pull off the grey, dull, clunky boot look well.

Aircast boots / walking boots / Controlled Ankle Movement (CAM) boots… or just Beckham Boots.

This is becoming a problem, as perception of the walking boot amongst athletes, coaches and even other medical staff (unfortunately) is that the provision of a boot must equal a severe injury. Wearing one is a badge that not many people want. This worries me for a number of reasons…

Do no harm:

Whether you use POLICE or PRICE, our first thought in acute injury management is “Protect”. I’ve written about acute assessment before (here) but if you have just witnessed the injury and don’t have any immediate concerns about preservation of life or limb, then often we don’t want to rush into a diagnosis. Things can always look worse immediately after injury, so our plan is to offload, reduce risk of secondary injury or worsening of the initial injury (AKA.. “Protect”).

So, with lower limb injuries around the foot and ankle, quite often we will provide a walking boot. Cue the groans.. “I can’t be seen in this”, “Its not that bad”, “Don’t let the coach see me wearing one”.

But here are our options; walking boot, below knee cast, tubular bandage… or nothing.

Immobilise

If we are talking about doing no harm, then evidence suggests that long term immobilisation (greater than 4-6 weeks) of acute ankle sprains is detrimental when compared to “functional treatment” (to avoid an argument of what is functional, lets just call this “Optimal Load” and leave it to clinical discretion) (Here). But also no intervention could be seen as negligent. If we have enough suspicion to be weighing up “should I offload this?” then when compared to a control (wearing a normal shoe), a walking boot limits sagittal plane range around the ankle to around 4 degrees and reduces body weight in peak plantar plane surface forces (154% vs 195% BW) (Here). So if we face an option of boot vs no boot, where we know we can limit range and peak forces in an acute injury, the answer is “yes, offload it” even for a day until you can re-assess. Why wouldn’t you?

A brief period of immobilisation, “around 10 days in a below knee cast or removable boot”, along with treatment to reduce pain and inflammation is recommended (Here). In a study of fifth metatarsal fractures, those that we provided with a walking boot had better outcomes of pain and return to activity vs those immobilised in a cast (Here). This is an advantage of the boot. We can protect the foot and ankle in a boot but remove it to utilise other treatments and rehab. We can keep unaffected joints mobile – perhaps another blog but I like to use ankle injuries as an opportunity to work on detailed foot control, like great toe flexion, abduction, tibialis posterior control and so on. We can do all of this whilst limiting inversion and staying in plantar-grade if necessary. Or if its a 5th metatarsal stress, we can keep the ankle mobile. You get the point, we couldn’t do that in a cast.

Our other option was tubular bandage. In a world where we can download apps to make us look like cartoon dogs for free, we still have plain grey boots and boring beige tubigrips, I say this as an academy physio trying to make acute injury management appealing to young kids. When compared to those provided with a below knee cast & removable boot, severe ankle sprains had better clinical ankle function measures, quality of life, levels of pain and levels of activity at 3 months vs those provided with a tubigrip (Here). Perhaps a little bit unfair on the tubigrip, whose role in dealing with a severe ankle sprain is “compression” – a bit like saying an elastic band is worthless because its unable to hold sand together. But ultimately, in an acute injury, tubular bandage isn’t going to provide much protection at all.

Long term use:

Now the point of this blog is to de-sensitise reactions to using a boot for the short term, but it would be remiss not to mention their use in long term injuries. Following surgery or a fracture, the use of a walking boot is associated with a quicker return to normal gait and function (Here).

But does it come at a cost? Fixing the foot and ankle is obviously not conducive to “normal” walking, so it will change gait temporarily. In doing so, it can also create problems elsewhere. 84% of people using a boot developed or increased a secondary site of pain in the first two weeks of using the boot (Here). Now, 68% of those reported this pain made no difference to their life, but if you have someone with existing problems, especially in the low back, you might want to consider this stat as part of your clinical reasoning. Remember, part of our job is to prevent secondary injury.

If the boot fits..

There’s one option and aid we haven’t talked about and thats crutches. The reason I haven’t mentioned them is they come with the same stigma as a boot. They are obvious, they demonstrate you are “injured” so if someone doesn’t want to wear a boot, they probably aren’t going to want crutches either. But hopefully this brief blog gives you a bit more of an argument behind your reasoning to help reduce the association that wearing a boot equals a severe injury. So when we hear that a player has left the stadium in a boot, for the first couple of days, so what? It might be nothing. Something I have trialled before in a key first team player, which I admit is divisive, is to manage an athlete across 24 hours. So.. There are some injuries that can continue to train, like an inflamed sesamoid or plantar-fascia pain, but to give them the best chance of training and competing it would help to offload the structures through the rest of the day. So, instead of trying to control 1-2 hours of the day and reduce training / matches, why not try a boot to offload for the other 22 hours in a day? As the evidence above suggests, this is certainly not a long term solution. But across a couple of days, maybe? Limited evidence, but its worked twice for me.

The key to this working, was education. Ensuring that other players and staff understood that the boot didn’t mean a serious injury. But was an adjunct to help offload… or “protect”. There’s a theme here.

This is the message we need to get across, protecting an acute injury is not the same as us diagnosing or offering a prognosis. “You might only be in the boot overnight, but its a safe way of transporting you home.” We just need to help give them some good PR and make them seem less daunting, less serious…

 

Yours in sport

-Sam

 

 

 

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

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

 

 

 

“Has the athlete trained enough to return to play safely?” Acute:Chronic workloads and rehabilitation – a guest blog by Jo Clubb

We are delighted to have the excellent Jo Clubb agree to write a blog for us. Admittedly, this blog is a little more high-brow than our usual ramblings, so thanks to Jo for adding some class to our library. Jo has recently broken into the American sports scene, working as a sports scientist with the Buffalo Sabres NHL, bringing with her expertise from her years in football (..soccer) in the UK (previously with Chelsea & more recently with Brighton & Hove Albion FC). What makes this blog extra special to us is that Jo already has an excellent blog page of her own that is read and commended worldwide (Sports Discovery – here). Jo demonstrates how & why sports science plays a massive part in return from injury in professional sport…

Introduction:

Training Stress Balance and the Acute:Chronic Workload Ratio are real buzz words in Sports Science at the moment. They also have important implications for the Physiotherapy and Conditioning communities in terms of rehabilitation and Return To Play.

This concept is derived from Banister’s modelling of human performance back in the 1970s (and then later added to by Busso in the 1990s) that put forward an impulse-response model to predict training load induced changes in performance. If we consider a single block of training, this stimulus will have a temporary negative influence represented as ‘fatigue’ but over a longer time frame will have a positive influence, represented as ‘fitness’. Performance will consequently be a product of the Fitness Fatigue relationship (see Figure 1). Within this theoretical model of Training Theory, it is suggested that with regular training stimuli we can manipulate these processes of fitness and fatigue via training load, recovery and overcompensation, to have a positive influence on performance (see Figure 2).

Figure 1: Used with permission from Professor Aaron Coutts

 

Figure 2: Used with permission from Professor Aaron Coutts

The Acute:Chronic Workload

Whilst this concept of training stress balance has been cited since these early, groundbreaking days, it has recently been developed into the acute:chronic workload ratio by Tim Gabbett and colleagues, which they suggest is the best practice predictor of training-related injuries (Gabbett, 2015).

It has previously been represented as a % for Training Stress Balance, but the focus now seems to be on utilising it in a ratio form, for example:

= Acute workload / Chronic workload

= 3000 (Au) / 4000 (Au) = 0.75

In this example acute workload is represented as the total load over the previous one week and chronic workload is the average weekly load for the previous four weeks, both utilising an arbitary unit (Au) such as session RPE.

So a ratio below 1, as per the above example, suggests the athlete is more likely to be in a state of “freshness”; their load over the past week has been less than their average weekly load over the past four weeks.

On the other hand a ratio above 1 represents that the workload over the past week has been greater than the average weekly load over the past four weeks, so they may be more likely to be in a state of “fatigue” and potentially less prepared for that workload. Recent research has suggested a ratio greater than 1.5 represents a “spike” in workload that is related to a significantly higher risk of injury (Blanch and Gabbett, 2015 here).

Training and Game Loads and Injury Risk

Tim Gabbett and his colleagues have collected consistent data within the training environment, statistically modelled the relationships between workload and injury risk, applied their model to help reduce injury risk in the training environment and published this data – for me this is the gold standard process of Sports Science and a method we should strive to replicate within each of our own environments. The relationship between workloads and injury risk has included just some of the following research:

• Running loads and soft tissue injury in rugby league (Gabbett and Ullah, 2012)
• Training and game loads and injury risk in Australian football (Rogalski et al, 2013; Colby et al, 2014)
• Pitching workloads and injury risk in youth baseball (Fleisig et al, 2011)
• Spikes in acute workload and injury risk in elite cricket fast bowlers (Hulin et al, 2014)
• Acute:chronic workload ratio and injury risk in elite rugby league players (Hulin et al, 2015)

I can talk about this all day (and probably will in a number of other blogs); however the focus of this specific blog is on the application in the rehabilitation environment so I will leave it at that for now. If you do want to read more of this topic, I highly recommend reading the following OPEN ACCESS paper:

The training-injury prevention paradox: should athletes be training smarter and harder? (Gabbett, 2016) Br J Sports Med doi:10.1136/bjsports-2015-095788

 

Rehabilitation

There is plenty of application to this approach in the training environment however; it is just as important in the rehabilitation setting as highlighted in the following paper:

Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player’s risk of subsequent injury (Blanch and Gabbett, 2015).

Rehabilitation is without doubt a very complex continuum in which medical staff assist the athlete through early stage rehabilitation to the multifaceted return to train, play and performance decisions, which I have tried to tackle previously (here)  and specifically for hamstring injuries (here). Previous to the paper by Peter Blanch and Tim Gabbett much of the literature on Return to Play failed to acknowledge the consideration of the progression of load in the RTP decision.

Often the evaluation of health status that directly influences the Return To Play decision may incorporate instantaneous physical testing results such as isokinetics or force plate assessment, as well as functional on pitch activity profile targets such as peak speeds, distances, high intensity running and velocity changes. Whilst there is no doubt these have their place, there also needs to be consideration for the loading achieved throughout the rehabilitation continuum in preparation for the acute and chronic loading demands of training and matchplay.

Blanch and Gabbett present a real world example from rugby league (Figure 3) in which a player suffered a hamstring injury after an acute:chronic workload ratio of 1.6 in training week 15. After two low-minimal weeks of high speed running due to the injury, the acute:chronic workload three weeks later spiked to 1.9 (presumably as high speed running was reincorporated into the rehabilitation phase in week 18) and then suffered a reinjury. This example also reminds us to consider which measure(s) of load is most relevant to each sport, injury and individual. High speed running is no doubt important to a hamstring injury but may be of less importance with other sports and injuries. The acute:chronic workload ratio can be applied to any of the variables you collect and may represent a different picture across different metrics.

Figure 3: From Blanch and Gabbett (2015), p2.

Rod Whiteley recently gave an excellent presentation at the Aspire Monitoring Training Loads conference entitled “The conditioning-medical paradox: should service teams be working together or as enemies on the training load battlefield?” He applied Tim Gabbett’s work to rehabilitation workloads and related it to the “chronic rehabber”; s/he who never gets to build a consistently high base of chronic workload to prepare themselves for returning to the training environment, so suffers a spike in acute:chronic workload and then a reinjury (Figure 4). He called upon us to “fundamentally rethink how we’re reintroducing the athletes” as well as breaking down the traditional silo structure between medical staff and conditioning staff.

Figure 4: Presented by Rod Whiteley, Aspire Monitoring Training Load Conference February 2016

Now we obviously cannot keep athletes away from the training environment forever and nor would we want to. However, it seems avoiding spikes in acute:chronic workloads with returning athletes may help the transition into return to training and competition, and to reduce reinjury risk. This may be achieved via further progressing the load achieved prior to RTP and/or reducing the load from reintegration by using modified training (or a mixture of both). In reality it may not be as simple as that – a major challenge for the Science and Medicine team is to manage expectations of both the athlete and the coaches. I’m sure if the athlete is looking good and undergoing a substantial training load there will be pressure to incorporate them into training.

I believe this paper highlights the need firstly to consider and plan (where possible) the progression of load throughout rehabilitation, end stage and continued into training and games. Whilst the athlete may be physically prepared for the demands of a one off training session, we must also pay attention to the demands in terms of acute and chronic load. It also highlights the need to consider the consequences of each decision relating to loading of the athlete; whether that is the decision to offload the athlete for a day (which may of course be truly necessary based on the clinical presentation) or the decision of how much load to put the athlete through day to day. In another example from the Blanch and Gabbett paper the authors put forward a representation of an injured player’s Return to Play and demonstrate how the variations in load in that week directly influence the likelihood of injury – i.e. 90% acute load would return an 11% likelihood of injury, compared to 120% which would be related to 15% risk.

Whilst injuries are undoubtedly complex, multifaceted and influenced by many factors, and statistical modelling of the risk has its own limitations, it seems the evidence is strong enough to suggest that the interaction of acute and chronic load through rehabilitation and RTP is another piece of the puzzle that is worthwhile considering.

Jo Clubb (@JoClubbSportSci)

 

References

Banister EW & Calvert TW. (1975) A systems model of training for athletic performance. Aust J Sports Med; 7: 57-61.

Blanch P & Gabbett TJ. (2015) Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player’s risk of subsequent injury. Br J Sports Med;0:1–5. doi:10.1136/bjsports-2015-095445

Busso T, Hakkinen K, Pakarinen A, et al. (1990) A systems model of training responses and its relationship to hormonal responses in elite weight-lifters. Eur J Appl Physiol; 61: 48-54.

Colby MJ, Dawson B, Heasman J, et al. (2014) Accelerometer and GPS-dervied running loads and injury risk in elite Australian footballers. J Strength Cond Res; 28: 2244-52.

Fleisig GS, Andrews JR, Cutter GR, et al. (2011) Risk of serious injury for young baseball pitchers: a 10-year prospective study. Am J Sports Med; 39: 253-7.

Gabbett, TJ. (2016) The training-injury prevention paradox: should athletes be training smarter and harder? Br J Sports Med doi:10.1136/bjsports-2015-095788

Gabbett TJ & Ullah S. (2012) Relationship between running loads and soft-tissue injury in elite team sport athletes. J Strength Cond Res; 26:953-60.

Hulin BT, Gabbett TJ, Blanch P, et al. (2014) Spikes in acute workload are associated with increased injury risk in elite cricket fast bowlers. Br J Sports Med; 48: 708-12.

Hulin BT, Gabbett TJ, Lawson DW, et al. (2015) The acute:chronic workload ratio predicts injury: high chronic workload may decrease injury risk in elite rugby league players. Br J Sports Med; Published Online First: 28 Oct 2015. doi:10.1136/bjsports-2015-094817doi:10.1136/bjsports-2015-094817

Rogalski B, Dawson B, Heasman J, et al. (2013) Training and game loads and injury risk in elite Australian footballers. J Sci Med Sport; 16: 499-503.

 

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.

 

 

 

 

 

 

Rehabbing teenagers can be awkward! – sensorimotor function during adolescence

There is a bit of a buzz phrase in rehab about “individualising programs” and while it is something we wholeheartedly agree with, it is a phrase that is very easy to say and yet very difficult to implement. Especially when you work with a population where said individual changes rapidly through time, like a teenager! It is a common sight on a training pitch to see a star player in their age group suddenly tripping over cones or developing a heavy touch where there was previously effortless control. Side effects of the adolescent growth spurt, where the brain is now controlling a much longer lever. It’s like giving a champion gardener a new set of garden sheers when for the past year they have used little hand-held scissors and asking to them maintain their award-winning standards. (My garden embarrassingly needs some attention and it’s affecting my analogies).

The control and precision between these two instruments is influenced by the lever length of the handles…

…Similar to a rapidly growing femur and tibia which is still being operated by muscles that have length and strength suitable for shorter levers.

 

 

 

 

 

 

 

 

Alongside the performance related issues, there is suggestion that this period of growth may coincide with increased risk of injury (Caine et al 2008). We believe that bone grows quicker than soft tissue, so we are asking a neuromuscular system to control a new, longer lever using prior proprioceptive wiring. Imagine our gardener again, for a long time he has been able to keep his pair of scissors close and controlled, now with his extra long shears the load is further away from his body, his back and shoulders are starting to ache. Not sure what I mean? With one hand hold a pencil to the tip of your nose. Now, with one hand hold a broom handle to your nose. The longer lever is harder to control. **I promise it gets a bit more sciencey than gardening and broom handles. **

Managing these growth spurts is something we have talked about before and recently contributed to a BJSM podcast on the topic (Part 1 & Part 2) and a complimentary BJSM blog about “biobanding” during periods of growth and development (here). This particular blog was inspired by a recent (2015) systematic review looking into exactly which sensorimotor mechanisms are mature or immature at the time of adolescence by Catherine Quatman-Yates and colleagues over in Cincinnati (here). The following is a combination of their summary and our examples of how these findings can influence our rehab programs.

Tailoring the program:

We have so many options for exercise programs, that’s what makes the task of designing them so fun. It challenges our creativity. When working with a teenager with sensorimotor function deficits, let’s call them “Motor Morons” for short, we don’t have to totally re-think our exercise list, just perhaps the way we deliver them. We previously spoke about motor control and motor learning (here) and how our instructions can progress just as our exercises do, but the following relates to children and adolescents in particular.

Consider the stimuli.

Children aged between 14-16 have well-developed visual perception of static objects however their perception of moving objects and visual cues for postural control continue to mature through adolescence. When very young children learn new skills such as standing and walking, they become heavily reliant on visual cues. Quatman-Yates et al suggest that puberty and growth spurts (think gardener with new shears) brings new postural challenges that causes adolescents to regress proprioceptive feedback and increase reliance on visual cues again. From a rehab perspective, we need to consider this as part of our balance and proprioception program. How many of us default to a single leg stand and throwing a tennis ball back & forth from therapist to athlete? For our Motor Moron, this may not be an optimal form of treatment in early stages, where it is commonly used, however it may incredibly beneficial to that athlete in the later stages or as part of ongoing rehab as we try to develop that dynamic perception.

Consider the amount of stimuli involved in an exercise versus what your goal of that exercise is

We should also consider the amount of stimuli we add to an exercise. Postural stability in children is believed to be affected by multiple sensory cues. If we consider that children are more dependent on visual cues than adults are, perhaps our delivery of external stimuli should be tailored also. With a multi directional running drill for example, there is sometimes an element where the athlete is given a decision making task (a red cone in one direction and a yellow cone in another) and they have to react quickly to instructions from the therapist or coach. Rather than shouting instructions like “red cone”, “yellow cone” etc, hold up the coloured cone for the corresponding drill. This way we are utilising this developed visual perception, minimising the number of stimuli and also encouraging the athlete to get their head up and look around rather than looking at their feet.

When to include unilateral exercises:

Within adult populations, it is often considered gold standard to make exercises unilateral as soon as tolerable. If they can deep squat pain free and fully weight bear through the affected side, progress them to pistol squats ASAP, or single leg knee drives. However, young children (pre-pubescent) may struggle with this for a couple of reasons.

Difficult enough even for an adult to perform, but uncoupling the actions of the each leg & fine muscle movements to maintain balance are extra challenging for children

Firstly, we need to consider postural adjustments. Where as adults and young adults can adjust their balance with smooth control and multiple, small oscillations, children rely on larger ballistic adjustments. There is also reduced anterior-posterior control in younger athletes which suggests reduced intrinsic ankle control. Put this alongside immature structures and (if working a physio, most probably) an injury then single leg exercise become a progression that may be further down the line than an adult counterpart with the same injury. Instead, consider semi-stable exercises. Support the contralateral leg with a football or a bosu ball – something that is difficult to fixate through but provides enough stability to support the standing leg.

Secondly, we understand that coupled movements are mastered earlier in adolescence, around 12-15 years old but uncoupled movement patterns take longer to develop, 15-18 years old (Largo et al). A good example is watching a young child reach for a full cup of water at the dinner table. It is much easier and more natural for them to reach with both hands than it is with one, as coupled movements are unintended. Rarely do you see a child taking a drink with one hand filling their fork with the other – yet this is something commonly seen with adults as they are able to uncouple and segmentalise. Another example is watching a child dynamically turn, watch how the head, trunk and limbs all turn as a “block”, it is not until further down the line where dynamic movements become more fluid. The argument here is that surely running is an uncoupled movement? Or kicking a football, swinging a tennis racket, pirouetting in ballet – they are all uncoupled, segmental movement patterns that we expect kids to do, and in all they cope with. Correct, but it is usually in rehab programs for kids that we begin to introduce unfamiliar tasks and exercises that they may not have encountered before. Also, we should respect the impact of the injury on proprioception and control. So these are all considerations for starting points in exercise & if a regression is ever required.

For this reason, it is important that exercises are monitored and reviewed regularly. There is no need to hold an athlete back because of their age and making assumptions on motor function because of their age. If they can cope, then progress them. But be mindful of “over-control” where speed and variability of movement are sacrificed in place of accuracy and control (Quatman-Yates et al 2015).

Become a Motor Moron hunter

It is worth spending some time watching training, watching warm ups, watching gym sessions and talking with coaches and S&C’s trying to identify a Motor Moron as soon as possible. It’s important to minimise the chances of an immature sensorimotor mechanism ever meeting a growth spurt. It is when these two things combine that we see kids doing immaculate Mr Bean impressions and therefore increase their risk of injury.

Regularly re-assess your exercise programs. If things arent quite progressing as quickly as they should, it may not be failed healing of an injury, but it may be that we are providing the sensorimotor mechanism with too much information!

 

Yours in sport,

Sam

 

“The Young Athlete” conference 9-10th Oct, Brighton. Here