#Groin2014 – a not so brief summary

Any one familiar with twitter may have seen the recent hash tag for the 1st World Conference on goring pain in athletes (#Groin2014). This conference in Doha, Qatar was brilliantly orchestrated by Adam Weir (@AdamWeirSports) and his team at Aspetar. Run over three days and cram packed with information, I’m going to try and summarise the points that I found most interesting and thought provoking – please be aware these are my interpretations of what other speakers said and do not serve justice to the quality of the talks and presentations.

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

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

Introduction

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

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

Epidemiology

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

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

Adductor Related Pathologies

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

Serner
Treat the player, not the scan!

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

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

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

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

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

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

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

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

 

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

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

FAI

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

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

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

Increased loading over growth plate stimulates CAM deformity
Increased loading over growth plate stimulates CAM deformity

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

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

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

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

– Low antetorision would present as decreased IR and increased ER

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

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

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

Taking this forward

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

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

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

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

Yours in sport

Aspetar

Sam

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

bucket and sponge

Although it only forms a small percentage of our working week, the thing most people associate with physio’s working in sport is the match day, and the infamous bucket and sponge! When we watch the TV at the weekends, this is the closest we ever get to seeing a physiotherapist working in professional sport. We don’t see all the early morning meetings, assessments, rehab programs, maintenance treatments etc.

I have to admit, rightly or wrongly, it is the least enjoyable bit of my job. I can’t remember the last time I enjoyed watching a game of sport whilst I was working. Wincing at every tackle, losing track of the score back in my rugby days because I’m too busy counting the players get up from a ruck and constantly running through scenarios and management in my head. However, it is the money end of the job. The games are all about why we do what we do.

I feel bad for physiotherapists trying to break into sport, I’ve been there and done it, working evenings and weekends covering training matches and weekend games and essentially not doing very many of the skills I’ve been taught at University or on the courses I’ve dished out money for. Essentially, you are a first aider. I try and make our part time work at the club as attractive as possible in other ways, with CPD, shadowing, training clinics etc because I know its not the glamour and jazz that people think when working for a pro club.

Like it or lump it, its a huge part of the job. So, what do we do when we run on mid game? Like all aspects of our job, there should be an element of clinical reasoning behind what we do. What are we actually asking? And why do we ask it?

For the sake of keeping the blog concise and not too heavy reading, I’m going to talk about your more routine injuries, which can sometimes create harder decisions. For the management of cardiac, spinal, airway stuff make sure you go onto a proper trauma course to get your qualifications!

 

Stop ball watching

The first habit I had to break when I got into sport was to leave the armchair fan mindset at home. I started off in rugby before moving to football and was lucky to have a brilliant mentor from the start, Clare Deary, who quickly taught me to look away from the ball. Instead your watching the knees and ankles of the forwards in a line out, or checking the prop gets up after the scrum has collapsed. One of the Maddox questions we ask when we check for head injury is “what is the score?” or “who scored last” – in my early days I was asking this without knowing the answer, so if they spoke coherently that was good enough for me.

It is a little bit easier in football because there are typically only two people involved in the tackle, but still don’t get caught up in the game. It important to watch the movement of players, those with known previous injuries or knocks sustained earlier in the game. Are they worsening or improving?

The run on

Ever consciously changed your walk or run because you think people are watching you and all of a sudden you lose all motor patterns and co-ordination? Well when the game stops for an injury, everyone is watching you. If the player is rolling around on the floor screaming in pain, you already know they are conscious and their airways are well maintained, so don’t worry about your 100m sprint time for these cases. Save that for the motionless players.

Approaching the player

The location of the injury will obviously affect your approach, head or spinal injuries aside, I always approach the feet first so the player can see me and I can continuously assess their level of pain, respiratory rate, shock etc. As well as asking “where does it hurt” always make sure you double check other structures, don’t be lured by the pain. Someone landing on their shoulder could always have a neck or head injury.

“You are not trying to diagnose the problem there and then”

When questioning the player, remember its not a consultation in the clinic. You are trying to determine “is it safe for the player to continue” and “will a labouring player cost the team tactically”. If they are missing tackles that they would usually make, or misplacing passes that they normally wouldn’t you firstly run the risk of putting them into scenarios that could cause another injury as well as potentially costing the team.

BHAFC pitchside

Try to determine the irritability of the pain early on. Has it changed since the game stopped to the point of you arriving at the player? If its worsened, despite not moving, that would suggest a rapid inflammatory problem. In which case you really want to be removing the player from the field of play to reduce the risk of secondary injury. If the pain has settled or gone in the time its taken you to consciously jog perfectly across the pitch without falling over, you can probably proceed with some more vigorous testing.

Providing you’ve excluded any fractures, check what the athlete can do with the injured structures ACTIVELY before you do any passive movements. If they are reluctant or guarded with any movements thats enough of an indication for me not to do any passive movements. Why force them through a range that they consciously don’t want to go through?

Walking the green mile

So you’ve establish that they are alive, there are no fractures, they can actively and passively cope with movement, by this point the referee is probably in your ear to make a call quickly. In football, if you have entered the field of play, the player is expected to leave before kindly being invited back on by the ref. This is a good time to continue your assessment as you the leave pitch.

Can the player get themselves up from the floor unaided? Can they weight bear? Can they walk? Does walking ease the pain or make it worse? If they can walk off, assess their ability to jump / hop / run / jog on the sideline.

By this point, you have to go with your gut instinct. If any of the assessment so far has thrown you into doubt, you probably have a good reason to remove that player from the pitch. Consider the structures involved, the presence of any swelling, the compensatory movement patterns that you may have noticed leaving the pitch. I usually ask myself what I would prefer to manage out of two scenarios:

1) Substituting a player that reports to clinic the next day with no signs or symptoms of injury, but is a little p*ssed off because you wouldn’t let them play (or a peeved coach because you’ve taken their best player off the pitch).

2) Allowing a player to go back on that has given you doubts and they break down in their next sprint / action on the pitch. They walk into clinic the next day and you have to tell them they are out for 6-8 weeks.. Your coach is definitely going to be more peeved today than they would have been pitch side, I can assure you.

Vincent Kompany

This isn’t to say you remove every player from the pitch that has an injury. The mechanism of injury will have a big say in determining your thought process. For example you may be more lenient with an impact injury that is smarting a bit compared to a non-contact mechanism of injury.

Key Points:

So, chances are this has made things a lot less clear about pitch side assessment.. Unfortunately there is no algorithm to determine whether a player should continue or come off. Every individual player is different and every injury is just as individual.

  • Is it safe for the player to continue – consider secondary injuries caused by swelling / decreased proprioception, as well as the initial insult worsening.
  • Will a hampered player on the pitch cost the team tactically.
  • Whats the worst that could happen if you remove them from the pitch. This can be made easier if you are working with younger ages that perhaps have a rolling sub system, giving you more time to assess. Also, consider the implication of the game / event. A once in a lifetime shot an olympic medal may be worth the risk of a secondary injury. A community level tournament in kids rugby might make you a bit more conservative.
  • This is only discussing minor knocks and strains. If you are working pitch side and haven’t done or updated your trauma course, make sure you do! Don’t put others health at risk at the same time as your professional credentials. (lubas medical / AREA or RFU are good courses to check out)

I’d be really keen to hear peoples thoughts and experiences with this topic, I’m sure there will be some disagreement with my thinking and methods. Or perhaps people have seen some incidents of players returning to the field when they shouldn’t (I’m thinking the FIFA world cup 2014 with numerous head injuries, but concussion is a separate blog altogether I think).

 

BHAFC

 

As always, Yours in Sport

 

Sam

Case study: “Bulls Eye Lesion”

Every now and then in clinic you come across an injury that doesn’t quite fit “the norm” in terms of its recovery and management. I know every injury should be considered unique and every individual managed differently, but I thought I would share the management of this particular injury as it did prove tricky, we did fail a couple of times but eventually we got it just right.

 

Background:

This case study revolves around an 18 year old central midfielder, skeletally mature (no increase in height throughout the year / evident secondary sexual features) with a regular playing and training history prior to this injury. The presentation started in the autumn, after a complete pre-season and a good few weeks of competitive season underway. The player was in & out of training with a niggling groin / quad but with nothing substantial showing in assessment (the benefit of hindsight would be a very good money earner for any clinician that could harness it and set up a course!)

Towards the end of an under 21 game, the player was visibly struggling with pain at the top of his thigh, unable to sprint or strike a ball but 3 subs had been made, so he was inevitably staying on the pitch. At the end of the game, there was pain on palpation of the proximal rectus femoris and sartorious region. At this stage, there was nothing more to assess – there was no point, we would only aggravate something without actually learning too much more.  He presented the next morning with visible swelling in a small pocket of proximal thigh, palpable crepitus and pain with straight leg raise at 20 degrees.

 

Review of anatomy

The rectus femoris is a long fusiform muscle with TWO proximal attachments. The Direct Head attaches to the AIIS and Indirect Head attaches to the superior ace tabular ridge and the joint capsule. It has a long musculotendinous junction, as such can execute high velocity shortening as well as coping with significant length changes – remember it is a two joint muscle crossing both the hip and knee, with an action like kicking it must cope with hip extension coupled with knee extension during the pull-back of the kick, so both ends of the muscle are undergoing an eccentric load (Figure 1). The muscle structure itself is made up of mostly type II fibres so this high eccentric load makes the muscle quite prone to injury (Mendiguchia et al 2013 source).

Image
Figure 1: Demonstrating the demands on rectus femoris during a kick

 

“Bulls eye lesion”

The term “Bulls eye lesion” was coined by Hughes (1995 source) following the presentation of injury on MRI (Figure 2). The high signal signs around the tear of proximal injuries. Occasionally this causes a pseudocyst, thought to be the serous fluid in the haematoma.

Image
Figure 2: MRI scans highlighting a “Bulls-eye lesion” presentation

Predisposing factors to a proximal tear include fatigue, insufficient warm up and previous injury. From this case, we know that the pain started at the end of the game with the player in a fatigued state, and there was a history of niggling pain on and off for a couple of weeks.

 

Management:

The initial management of this injury was relatively routine, revolving around the POLICE guidelines (see Cryotherapy Blog). By day 2/3 we were addressing pelvic control exercises & posterior chain assessments. By day 5 we could achieve pain free stretching of the hip flexors and were using “Compex” to achieve isometric contractions of the quad while the player did upper body exercises.  After day 7 we were able to begin loading through a pain free range, working on co-contractions and concentric contractions of the quad.

To Speed up, you must be able to slow down – Bill Knowles

In the early-mid stages of rehab, we began working on movement patterns but at a painfully slow speed. Using the Bill Knowles mantra above, we progressed though different ranges of box step ups at slow pace to elicit a co-contraction of quads, hamstring and glutes (Figure 3). We slowly lowered the player through a Bulgarian split squat (Figure 4) to work on stability through range and we did some bridging variations (anti-rotational core) to encourage isometric control of the pelvis (Figure 5 – excuse the size 11 shoes taking up most of the picture!!).

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

 

 

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

 

 

 

 

 

 

 

 

 

 

 

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

 

 

 

Figure 5: Single leg bridge (a) with ipsilateral arm fall out (b) and contralateral arm fall out (c)
Figure 5: Single leg bridge (a) with ipsilateral arm fall out (b) and contralateral arm fall out (c)

 

By adding speed to the high box step up, we were able to switch the demand of the quadriceps to an eccentric action as the hip extends from a flexed position and the pelvis rapidly comes forward. We felt confident adding this eccentric component after we had cleared the player at a decent weight using the cable machine and a jacket to work though some deceleration work on the hip and knee (Figure 6).

 

Figure 6: Cable decelerations. a) start position b) end position with 3 sec hold. c to e) Dead slow step backs with weighted cable pulling posteriorly

 

The Bulgarian split squat was advanced by adding a knee drive at the top the squat, taking the back leg from a position of full hip extension through into hip flexion, a rapid concentric action. Following the model of exercise progression and regression (source) we added weight, removed the concentric component and decreased the speed again before building back up in a now weighted position.

The later stage of rehabilitation saw the player undertake more field based conditioning, working under fatigue whilst completing technical drills and building up his range of passing and shooting, all the while maintaining his gym program to supplement his rehab. This late stage rehab combined the expertise of the physiotherapy department, working alongside the strength and conditioning coach to discuss reps and sets of all drills and help periodise the weeks for the player and design the field based conditioning sessions; the sports science department was able to use GPS for all outdoor drills to help monitor load and provide up to date feedback on key information, in this case monitoring the accelerations and decelerations for the player in a fatigued state.

It was important that the stress elicited in this late stage was in line with the rest of the squad mid-competition. Rob Swire and Stijn Vandenbroucke (source) explain the importance of rehab being harder than the team training. This is because we have control over rehab, but no control of training so we must be confident that player won’t break down again in training!

The player returned just under 8 weeks later. He continued his gym program for another 4 weeks after his return to training and (touch wood) has had no recurrence of this injury since.

 

Conclusion

Knowing what I know now, I would be more cautious of this nondescript pain around the proximal thigh. The indirect head runs quite deep and typically presents as a gradual onset. The niggle the player was displaying a few weeks before was probably a worsening of this small tear, that when fatigued and put under a double eccentric load such as kicking or sprinting, was bound to “give” at some point.

I’m sure that reading this back, it seems pretty obvious that there was something wrong with the player initially. Again, another lesson learnt from this relates to the players age. He had not had a soft tissue injury prior to this, so his subjective history was vague and typically teenager-ish. Its important to remember that young players and professionals don’t necessarily understand their own body. If they play things down, its important that we as clinicians double check everything before we clear them and not just rely on their feedback alone.

 

I hope you find my reflections useful

 

Yours in sport

 

Sam

The Osgood, the bad and the ugly

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

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

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

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

What do we think we know?

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

20140607-230045-82845066.jpg
Figure 1
Demonstrating the close relationship between the enthesis, the patella tendon, the infra patella fat pad and the physis of the tibia.

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

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

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

20140607-225834-82714316.jpg
Figure 2
Classification system of the maturation status of the ATT from stages 1 to 4. ATT, anterior tibial tuberosity; B, bursa; FP, fat pad; HC, hyaline cartilage; M, metaphysic; O, ossicle; P, physis; PT, patellar.

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

Management:

20140608-095042-35442466.jpg

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

Yours in sport
Sam