Current Evidence in Tennis Elbow

Lunchtime Lecture 14th May 2012 by Dr Tim Wood, Sports Physician, Glenferrie Private Hospital, Hawthorn, Melbourne 3122  held at Albert Street Sports and Spinal Injuries Centre, Warragul

Topics discussed:

Why does tendinopathy occur?
Overload.  Trauma such as a sudden blow to the elbow (inflammatory in acute stages) - NSAIDs may be beneficial here.  Rest rarely cures the problem - we need to load the tendon at a level that it can cope with and challenge it from there.

Pathophysiology of tendinopathies - healthy tendon comprises of tight collagen fibres, tenosites and protein ?ground substance.  When the collagen breaks down, ground substance infiltrates the spaces and allows for neovessels to become embedded.  It is still uncertain what causes the pain associated with tennis elbow but perhaps the nociceptive neovessels could be responsible.  The increase in ground substance can lead to partial tears in the tendon.  Both ground substance build up and neovessels can be shown up on ultrasound, both musculoskeletal and Doppler.

Cortisone, Autologous Blood Injection, Platelet Injection & Surgery - what works well?
Less use of cortisone in sub-acute to chronic stages, unless pain is constant and severe as CSI can be an effective pain reliever.  Autologous Blook Injections are now performed in-rooms in Melbourne and also under ultrasound guide.  Platelet injection is expensive and used less regularly but provided 8-9x greater effect of blood injection than the ABI.  Surgery is now less common due to poor results.  The only surgeon in Melbourne still to perform this type of surgery is Greg Hoy at the Melbourne Orthopaedic Group.

Rehabilitation protocol:
Broomstick exercise 3x15 reps daily
Find the centre where weight is eveny distributed.  Start at that level with supination and pronation exercises and as pain allows, gradually moved hand down towards the top of the handle, 1cm by 1cm over a 12 week period.

Diagnosing Acute Knee Injuries

Presentation by Clare Walsh, Sports Physiotherapist for Clinical Edge (www.clinicaledge.com.au)


SUBJECTIVE EXAMINATION


1. Was the injury contact or non-contact?
2. Did you play on? If so, how long could you play on for?
3. Did you or anyone around you, hear a pop or a crack, or did you feel a pop?
4. Was there immediate swelling or did it take a couple of days to develop?
5. Is there any clicking, popping or giving way at the knee joint?


Giving way associated with twisting or turning which usually means that rotational instability is caused by the ACL, and also buckling in a straight line due to quads insufficiency if knee is weak or there is swelling.


If there is immediate swelling, this indicates a haemarthrosis and this can really only mean three things:
1. An ACL rupture, because of the rich blood supply to the ligament
2. Patella dislocation
3. Fracture


If milder swelling, more indicative of intra-articular pathology


OBJECTIVE EXAMINATION


Gait assessment
Squat - assess if they are able to compress the knee joint and whether WB is equal
In supine, assess the swelling with the swipe test, sweeping the fluid from the medial pocket to the lateral - a positive test will produce a pocket of fluid on the medial side


72-90% of ACL injuries are non-contact injuries
ACL rupture occurs when the athlete is decelerating and pivoting, or landing suddenly (maybe avoiding a tackle in rugby league) - the tibia moves forwards on the femur and ruptures the ACL.  This is very painful and will usually result in the athlete grabbing the flexed knee.


Lachman's - looking for an end feel with anterior drawer
Reverse Lachman's - looking for an end feel with posterior drawer (assessing integrity of PCL)


Surgery is recommended for complete ACL ruptures.  Recent studies have shown that at 8 years post injury with conservative management only, those with partial ACL tears did very well but those with compete ruptures did not have good outcomes.


Surgery is done arthroscopically, either with a hamstring tendon or patella tendon graft from the same knee, or more recently through a LARS procedure (ligament augmentation and reconstruction system) using a synthetic allograph.  The LARS procedure has a reduced recovery time as there is no donor site and therefore no specific hamstring or patella tendon healing time required


Prevention Injury and Enhanced Performance is a programme that was started in the USA and is being rolled out in Australia.  This is a warm up that has been proven to reduce ACL injury by 42% and involved neuromuscular control and proprioception exercises.


MCL sprain occurs with a valgus force to the knee, commonly in skiing and basketball.  This can occur in isolation, or along with a medial meniscal injury.  There can be some swelling localised to the ligament itself but there will not be any effusion inside the knee joint.


Grade I: Painful but no laxity
Grade II: Painful++ and some laxity
Grade III: Obvious laxity and no end feel


Test the MCL with a valgus stress at 30 degrees flexion.  Grade II and III tears should be supported with a hinged knee brace to allow the ligament to tighten.  Knee strengthening is essential to provide some stability to the knee joint.  Straight line activity only for 4-6 weeks with grade II, possibly 8 weeks with grade III.


PCL tears usually occur with a hyperextension injury.  PCL reconstruction was the preferred choice a number of years ago, but recent research suggests that the patient can get just as good recovery, if not better, from conservative management.


To test the PCL, first assess tibial sag in crook lying.  


PCL injuries requires lots of VMO and control work to prevent patellofemoral problems from occurring.


LCL injuries are rare but occur with a varus stress to the knee joint.  The LCL is part of the postero-lateral corner of the knee, including the biceps femurs and the postero-lateral capsule and the arcuate ligament.
If there is a complete rupture of the postero-lateral corner of the knee, this will require surgery as the knee will be very unstable.  There could also be a lateral meniscus tear or a B Femoris tear in isolation.


Meniscal injuries are very common and result in an effusion that presents over a day or so, usually around the periphery/joint line, especially with a bucket handle tear.  Medial are more common than lateral, and can be diagnosed by subjective questioning, palpation and McMurray's test.  MRI can also be used to confirm diagnosis.


The McMurray's test can only be done in full flexion.  If the knee is too painful to achieve full flexion, then a diagnosis cannot be made.  The McMurray's test is done by taking the knee into full flexion then applying a varus and valgus stress to the knee.  If locking, arthroscopy will be effective.  For smaller tears in the posterior horn, a conservative approach will be tried in the first instance.  If continual swelling and pain, best to refer on to an orthopaedic surgeon for a surgical opinion.


The articular cartilage can be damaged through knee injury, especially with impact which can cause a chondral pathology.  in some cases, there may already be damage to the articular cartilage which becomes worse with impact.  Chondral injuries commonly occur with ACL injuries and meniscal injuries.  To diagnose a chondral injury, it is likely that you have ruled out any other meniscal or ligamentous damage but there is still effusion present.  MRI can diagnose this injury.


To treat the articular cartilage injuries, you can't treat the cartilage itself so treat the symptoms.  


Chondroplasty is the most common form of surgery (debridement through arthroscope) which lets the area bleed and scar over, providing a little more shock absorption at the joint.  Chondral cell implantations are being carried out but it is a drawn out process.  Chondral cells are grown in  a petri dish then implanted back into the injured site. Unfortunately, there is a long period of NWB which brings other issues.  Stem cells (greater than 10 years away before using as a regular form of treatment).


Patella dislocations present similarly to ACL ruptures.  To relocate the knee, extend the knee with hip flexed.  The patella dislocation causes a haemarthrosis and tenderness on the medial side where the retinaculum is likely to have been torn when the patella has dislocated laterally. The patella apprehension test (passive lateral glide) will be positive for apprehension. Usually tape the knee and allows a more normal gait pattern.  


Patella fracture can be treated in an extension zimmer brace for 6-8 weeks and may require K-wiring.


Tibial plateau fracture can occur with ACL tears and meniscal injuries but can also occur in isolation.  They may or may not occur internal fixation but requires a period of non-weightbearing.  


Patella tendon rupture results in the distal end of the patella tendon coming way.  Surgery is essential.

Advanced Ankle Rehab

Clinical Edge video by Russell Wright (www.clinicaledge.com.au)


ROM

Once the inflammatory stage has passed, soft tissue release techniques can be used, especially targeting the peroneals.  Slow, firm pressure is more comfortable for the patient.  The patient can self release the tension with a foam roller.  A good peroneal stretch is standing either side of a rolled up towel and going into a small squat position, keeping knees pointing forwards.  Hold 30 secs x 3.

Mulligans MWM with the seatbelt can help improve DF range - ask the patient to put their foot on a chair, have the seatbelt around the back of their calf (mid-distal region) and the seatbelt around your hips as you kneel on the ground.  Apply an AP pressure to the talus as the patient dorsiflexes and you pull back on the seatbelt with your hips.  3x 6-10 reps.

If there is still restricted mobility, look to the deeper compartments e.g. tibialis anterior or further up the kinetic chain e.g. sacroiliac joint or hip.

STRENGTHENING

Bilateral heel raises with theraband around the injured lower leg (distal segment) - this will allow them to focus on maintaining a neutral foot position, not inverting.  The theraband will be attached to their right hand side if working on their right leg, and their left hand side if working on their left leg.  Progress accordingly into single heel raises, once again using the theraband.  Aim for 10-15 reps x 2 sets.

BALANCE

This can be started with SLS in the first week post-injury.  The wobble board can be used in the interim period between single leg stance and step to land activities, usually about 1 week.  Current evidence by Refshauge shows that the wobble board is only effect for improving proprioception at lower velocities; it does not address the prevention of ankle sprain at higher velocities/during sport specific activities.

Once the patient has mastered single leg stance, balance can be challenged further with wobble board with someone throwing a ball.  Then onto hop on the spot, hop to the spot, hop in/out of box as fast as the patient is able x 5 (each set is timed - this adds fatigue component and is a validated test for balance) and figure of 8 hopping to start power training (strength at speed).  Skipping can also be added.

ENDURANCE

Return to running as soon as the patient feels able.  Check with 50 repetition hop test.  Start with 10-15 minutes on the flat.  Heel inserts or Mulligan's fibular taping can be effective with return to running, if dorsiflexion range is still restricted.

POWER

Once the patient is able to manage 3 minutes of skipping comfortably, then progress to plyometric vertical jump.  Each jump should have a rest in-between as the patient is aiming for maximal velocity with each jump.  Then progress to lateral jumps and forwards/backwards jumps (also zig zag jumps if applicable).  If the sports demands it, progress then to single leg jump.  Can jump up to a box if more comfortable.

RETURN TO SPORT

Pass the agilities test:
1. 90% ROM compared with non-injured side or <2cm difference on dorsiflexion lunge test
2. Single leg heel raise test with theraband peroneal bias compared with non-injured side
3. Balance testing - timed figure of 8 hop test x 3 or square run x 3
4. Single leg vertical jump, using chalk as a marker
5. Motor control - SKB
6. Assessment of running gait

On returning to sport, start with slow warm up drills and ball drills and gradually progress from there.

POOR RECOVERY?

If not improving, check for:

Soft tissue impingement with meniscoid lesion at the antero-lateral joint line (MRI/referral to see if arthroscope is appropriate)

Fracture ( do not trust A&E x-ray! re-xray or CT scan then onward referral to specialist if fracture found)

Syndesmosis (high ankle sprain) which could involve the AITFL/PITFL and would lead to a longer recovery period, with possible stabilisation surgery required at the 12 week mark if there is little improvement

If a talar dome lesion is suspected with pain on weigh bearing and catching along the joint line, refer patient for MRI and seek specialist opinion after 3 months to see if an arthroscope is required.

Deltoid ligament sprain is suspected if there is more pain antero-medially.  This should be supported with taping.

Acute Ankle Inversion Injury

Subjective Examination

Important to obtain mechanism of injury - usually occurs when walking or running on uneven surface, or when pushing off laterally from an acute cutting movement

Use the OTTAWA Ankle rules and OTTAWA Foot rules (designed for emergency department originally) to determine if x-ray is required.  6 cm up the lateral or medial side of the lower leg from the malleoli, or unable to weight bear determines if ankle x-ray required.  If tender over navicular or base of 5th metatarsal, or unable to weight bear determines if foot series x-ray is required.

Acute management

PRICER - recent evidence shows compression to be the most important factor over the first 24-72 hours

Objective Examination

Palpation:

ATFL, CFL, anterior portion of the deltoid ligament

Anterior joint line (talus)

Peroneal tendons as they pass posterior to the lateral malleolus (longus and brevis)

Peroneal tertius as it passes anterior to the lateral malleolus, inserting onto the base of the 5th metatarsal

Tibialis posterior, FHL and FDL as they pass posterior to the medial malleolus

ROM

DF/PF/IV/EV (NWB)

Standing DF lunge when tolerated (compare to other side with %)

Supination/Pronation to eliminate midfoot injury

Strength testing

Resisted isometric tests

Bilateral heel raises as tolerated (testing peroneals in a more functional manner - if weight bearing on the lateral border, could be lengthened and weak peroneals (and/or tight tibialis).  Also look for toe grabbing which is often a compensatory thing for poor balance.

Balance

If SLS is 30 secs +, the test is too easy and so progression to the 3 point star test is merited.  The patient has 3 attempts at each of the 3 points and the best reading is taken for each point.  Use this as an outcome measure.

Ligament testing:

1. Anterior drawer test (PA glide of the talus) - compare with other side.  If excessive movement, you are suspecting rupture to the ATFL and possibly anterior fibres of deltoid lig.  If the ankle has excessive movement, but is mainly moving into inversion, then it is likely that the ATFL is the main injured ligament.

2. Talar tilt test - looking for excessive laxity at the CFL ligament

Ligament grading:

Grade I: No laxity on stability testing, tenderness over ATFL = microtrauma

Grade II: Laxity on ligament testing with anterior drawer and/or talar tilt, with end feel

Grade III: Laxity in the absence of end feel

Prognosis/Healing Times

Grade I: 2-4 weeks

Grade II: 4-6 weeks

Grade III: 6-8 weeks

TREATMENT


1. Aim to improve ROM within comfortable ranges


ROM can be limited in the early stages by swelling, increased muscle tone and possible joint subluxation. Starting with gentle dorsiflexion and plantar flexion slides in sitting, then progress to active inversion and eversion.  In order to reduce muscle tone, dry needling can be effective and is not likely to worsen the inflammation.  Mulligans MWM at the fibula (apply a posterior superior glide) can be effective in improving inversion/eversion ROM.  Maintain glide for the whole movement and complete 3 x 6-10 repetitions.  In order to improve dorsiflexion range, the MWM can also be effective.  In supine, use your anterior thigh to support the sole of the patient's foot.  Using one hand, apply an AP glide to the talus, whilst using the other hand to support under the calf.  Ask the patient to actively DF as you maintain the AP glide throughout the movement.  Ask the patient to relax as you keep the AP glide on during the return to neutral.


2. Re-activate the peroneals (excessive tone as a protective response to injury)


In sidelying, ask the patient to PF the EV against gravity.  Ensure toes are switched off and can palpate the peroneal tendons during the movement to ensure correct activation.  5x10 reps in one session per day


3. Improve balance as early as possible


Standing on one leg, with soft knee to activate gluts and quads, and core muscles switched on.  Encourage the patient to stand for as long as possible, resting when getting uncomfortable.  If too easy, progress to star excursion test


4. Function


Return to normal walking as soon as possible.  Mulligan's fibula taping can be effective in improving range of motion and reducing pain.  Using hypo fix and rigid tape, apply tape at fibula, around the back of the achilles and attaching anteriorly, using a posterior-superior glide to the fibula when applying tape.


5. Endurance


Cycling (encourage pushing through the knee) or swimming (using a pull buoy until more comfortable)

Evidence Based Practice

The Association Between Degenerative Hip Joint Pathology and Size of the Gluteus Medius, Gluteus Minimus, and Piriformis Muscles

Dr A Grimaldi et al, Manual Therapy, 14 (2009) 605-610 

This study looked at the difference in size of the abductor synergy in the control group (no OA) compared 

to mild and advanced OA of the hip using MRI.

(N = 12 with pathology, N=12 control)

The hypothesis was that there would be significant asymmetry of the GMED, GMIN and PIRI muscles at the affected hip, compared with the non-affected hip, and that the GMED, GMIN and PIRI muscles would be smaller with more advanced OA.

Those with mild OA tend to increase adduction at the hip during stance, and those with advanced OA tend to reduce adduction by increasing the frontal plane of the trunk.

The study concludes that there are changed in the GMED and PIRI muscles (smaller) in those with advanced OA. However, the study also concludes that the abductor synergy does not respond uniformly with changes in pathology.  The GMED, GMIN and PIRI muscles may atrophy but the TFL and Upper glut max continue to work effectively.  it has also been found that with mild pathology, GMED may actually hypertrophy rather than atrophy.

"Assessment and rehabilitation strategies should carefully consider stage of pathology and specific changes occurring within the abductor synergy. This more specific approach may improve long term outcomes of conservative intervention in the management of OA of the hip, and may provide a direction for future prevention programmes."

Lateral Hip Pain: Mechanisms and Management (Article in InTouch magazine, APA)

Written by Dr A Grimaldi

Lateral hip pain has commonly been referred to as trochanteric bursitis.  Recent evidence shows there is more bursal distension rather than acute or chronic inflammation, secondary to the compressive forces that occur along the lateral side of the hip with glut med (or min) tendinopathy.  Compression is thought to be a key factor in the development of insertional tendinopathies .  Compression of the glut med and min tendons into the lateral and anterior aspects of the greater trochanter occurs beneath the level of the ITB; with increased tightness of the ITB, compression loading and overactivity then occurs in the superficial  lateral stability system, namely TFL, upper glut max and vastus lateralis.  Sitting in saddle chairs can promote excessive static abduction, thus tightening the above structures and causing lateral hip pain in those who are largely sedentary at work.  On rising from a chair, the hips are brought into adduction, thus compressing the lateral structures, particularly glut med and min, causing pain.  

Grimaldi reports that a study by Birnbaum et al (2004) found that in neutral adduction, there is only 4N of loading over the greater trochanter.  With only 10 degrees of adduction, this rises to 36N and rises again to 106N with 40 degrees of adduction.  Therefore stretching the lateral structures can often exacerbate the problem.

Aggravating factors such as sitting for prolonged periods, sitting cross legged, sleeping on both the affected and non-affected side and standing in the positive Trendelenberg position can all affect the length-tension relationship of the lateral structures.  Excessive lengthening of the lateral structures contributes to the increased adduction in stance and thus increases the compressive force over the greater trochanter.  The increase in adduction also biases the superficial abductors and shows poor recruitment in the deeper rotators/abductors.

Other factors can predispose an athlete to this condition.  For example, pelvic obliquity with scoliosis, leg length discrepancy, hip flexor dysfunction (think soccer players striking the ball with their leg crossing the midline) and running/walking gait abnormalities, especially on the camber of a road or uneven surface like sand.

Treatment strategies are now moving away from the ice, ultrasound and stretching regime commonly associated with bursitis.  Education has been proven to be effective with exercise decompression compliance programmes and also reassures the patient that tendon recovery will take time.  Addressing negative habits such as sitting cross legged, standing hanging on one hip or sitting with feet wide and knees together will help with pain relief in the short term and reduce the pull of the TFL on the gluteal and thoracodorsal fascia.   Avoiding low chairs or using a wedge cushion to bring the hips higher than the knees can also be effective.  

Night pain is difficult to address but trying to sleep supine with a pillow under the knees can often take the pressure off the hips.  Sidelying using a pillow to keep the affected side in neutral adduction can sometimes work.

Short term relief can be achieved by dry needling, heat, massage and trigger pointing and physiotherapists can show their patients how to perform self trigger pointing.  Long term relief can only come from addressing the poor recruitment patterns and working on the muscle dysfunctions.

Lateral stability mechanism
Deepest layer is Gluteus Minimus, which attaches to the superior joint capsule, contributing to joint stability and protection.
The intermediate layer consists of all 3 sections of Gluteus Medius, and also Piriformis.  GMED comprises of anterior, posterior and superficial segments, all with separate innervation and all with independent movement patterns.


In order to maintain the pelvis in a neutral state, the gluteals contribute 70% of the workload and TFL/UGM and the ITB contribute 30% (with VL helping out).

Gluteus Medius Tendinopathy

University of Queensland - Dr Alison Grimaldi, currently doing PhD on lateral hip and muscle function - PhysioEdge podcast #9 January 2012 through ClinicalEdge.com.au

Little known about the deep hip muscles/stabilisers

Lateral hip pain (epidemic)

Trochanteric bursitis still occurs but perhaps not the correct term to be using in the absence of inflammation - ineffective treatment programme led to short term relief with bursectomy and removing compression from the underlying ITB tension

Current research ongoing into the pathophysiology behind the 'trochanteric bursitis' condition

Glut Med tendinopathy is described as lateral hip pain over the greater trochanter region

In the past 10 years, it has been found that the trochanteric bursa is very rarely the primary cause of lateral hip pain.  The glut medius, and in some cases minimus, are more likely primary causes.

Proliferative stage, advanced into degenerative stage by the time the patient presents to physiotherapy - changes within tendon structure, usually related to a compression issue.  ITB places too much compression around lateral hip, causing problems at the insertion point of the glut medius tendon.  Hip adduction is the aggravator.

Protoglycan matrix changes within the tendon, larger protoglycans are produced in response to the compression, which causes the thickening within the tendon and these protoglycans start breaking down causing disorganisation of the collagen fibres which weakens the tendon, predisposing the patient to a tendon tear.

Primary complaint is pain over the greater trochanter - this can often refer along the lateral leg, sometimes into the groin or buttock.  Sleeping on either side can be aggravating.  Night time is often the worst.  At times, walking uphills or standing on one leg, sitting for prolonged periods then standing up are all aggravators.  If quite severe, pain will come on with legs crossed or sitting in a low chair will aggravate.

The more hip flexion, the more compression there is over the lateral hip.  The ITB has insertions into the gluteal fascia and up into the thoraco-dorsal fascia.

The largest groups affected are the post-menopausal women (incidence 4:1 female : male).  This may be related to overweight women who start exercising from sedentary position - tendinopathy will already have been there but asymptomatic until a change in the loading on the tendons, e.g. long walks, charging uphills etc.  This condition also affects younger athletes, especially runners or people doing step aerobics, where excessive hip abduction will flare up condition.  Some males will have the condition if they sit in excessive hip abduction (habitual postures) or if they are just particularly tight along their ITB.  Spending a lot of time in saddle chairs with hip abduction + +, or cycling/running, there is an increase in loading over the lateral hip.

Predisposing factors for glut med tendinopathy include poor movement and postural habits, for example positive Trendelenberg, where hanging on the hip can increase compression over the ITB.  Spending long periods of time in this position with hip abductors lengthened causes a change in length-tension relationships and recruitment patterns.  Hip abductors are less efficient and therefore causes lateral shift and tilt of the pelvis, biasing the superficial muscle system.  The superficial part of the abductor system are over-recruited (TFL and upper glut max) and join into the ITB, causing lots of compressive loading over the lateral hip.  

Other factors like leg length difference, where one leg is in adduction and the other leg in abduction, can cause lateral hip pain.  Also, a scoliosis can cause significant pelvic obliquity and lead to similar issues.

Running around the track in the same direction all the time, age and hormonal factors (oestrogen is important in the health of collagen fibres) and weight increase are all predisposing factors.  

Assessment would begin with a functional assessment - standing posture, single leg function (increases in pelvic tilt, lateral shift (as this increases ADDuction)), walking gait and running gait if appropriate. Challenge them more by dropping their pelvis into Trendelenberg position.

Single leg stance control - 7-10 abduction is normal when measuring with goniometer from ASIS to femur

Single knee bend - significant angle when squatting (IR/add) will increase compression over lateral hip

Pain provocation tests - hip flexion, abduction and external rotation (FABER) is a passive compression test.  Always compare to the other side and check this reproduces their symptoms.  Always use palpation too.

Glut med/min are internal rotators and so a static muscle test where they are pushing the ankle out into your hand may reproduce their symptoms.

Sidelying Ober test, taking into maximum hip adduction (over the bed) then do the static muscle test, pushing up into abduction.

Old literature on trochanteric bursitis - ice, U/S then ITB stretches - will only enhance the problem by increasing the compression of the ITB over the lateral hip!! 

Etiology for the condition (compression issue) - no ITB or flexion/adduction stretches

Massage is beneficial over the long weak abductor system, with trigger point therapy, which is much more appropriate than stretch.  

Strengthening assessment - functional tests of SKB and gait patterns give some initial information, but can also check side lying abduction (hip may drift into hip flexion or pelvis may roll back so they can use their TFL more efficiently)  Make sure you control their pelvis to see what their active range is liked compared to their passive range.  This active-passive discrepancy is normal with 5 degrees but large lag of 20-30 degrees is reflective of what is happening in that deeper system and poor inner range function.

Abduction strength test in neutral may be normal in mid range but does not give a true picture of functional ability in the deep stabilisers.  

Palpation includes TFL and upper glut max  (superficial glut med may be activating well but deep glut med not so much - can look at this with Real Time U/S)  Without U/S, can palpate deep at the lateral hip, halfway between greater trochanter and ASIS, where behind back border of TFL but in front of glut max, before initiating slow abduction in the early recruitment phase, should get swelling in those deeper muscles (concertina effect on U/S) - excessive early activation of TFL can be palpated.

Where does the pain start from or where is the centre of the pain?  Pseudo-radicular pattern appears to come from the lumbar spine (red herring).  If starting in mid/upper buttock, more likely to come from back.  Be sure to check!  Can have coinciding lumbar spine and tendinopathy problems

Treatment


Sleeping - pillow between legs to avoid excessive adduction


Walking - avoid striding out, avoid stairs and hills to reduce tendon loading, as tolerated (does it make your night pain worse? worse the next morning?)


Education


Exercise programme


No Clams or Leg Lifts!! Open chain leg loading over recruits superficial system therefore prefer closed chain.


1. Recruit their abductors in the correct way (easier with real time ultrasound) - can palpate over gluteus med and TFL, static abduction in side lying with knees bent and pillow between legs.  Think about lifting whole shin off bed (not a clam - this can be very provocative as you are flicking the ITB down across the bone and back again)  The static contraction is aimed at recruiting the deeper part of the muscle, low load tendon loading only - this can be useful for pain relief - 10-15 secs x 10, x 2 day as long as TFL not helping out.  


2. Can also do a standing version, leaning with back against a wall first.  Legs just a little abducted, static abduction (bilateral) as if doing the splits or unilateral as if doing a hurdle (3-5 reps).  Gradually increase holding time over a few weeks, particularly in standing as there is generally poor endurance with standing.


3.  Bilateral - weight shift - unilateral.  Start with bridge to bring in glut max as well, and TA/pelvic floor. Often there is poor conditioning of gluteals.  Try not lift too high to avoid back symptoms.  Progress to off set bridge (bring one leg in front of other, loading one side more 70:30) then finally to unilateral bridge, much stronger loading for the abductors, especially anterior abductors as they are also strong internal rotators, trying not to drop the pelvis into relative external rotation (using deep rotators to keep pelvis level)


4. Mini-squat or STS patterning - keep neutral lumbar spine and use glut max, controlling the adduction/internal rotation.  Bilateral in front of the mirror then single leg work with support early on.  Try not to rush to SLS unsupported as this will only exacerbate the add/IR.  Encourage them to put their hand on the wall, focussing on thinking around the g. trochanter, suck in from the side, keeping trunk and lower limb in neutral line.  Then progress to unsupported SLS, SKB then step and land.


By controlling abduction, you can control the compression.


5. Clinical Pilates Reformer (or sliding platform) - push leg into abduction with resistance.  Working into abduction reduces compression and allows you to bias the deep muscle system (superficial muscles have difficulty working in the inner range position)


Success?
If previous failure from previous physiotherapy, usually  involves clams and ITB stretches.  Stop these exercises and educate them about compression.    Short term results with exercise programme but long term, must address the aggravating factors.  Try not to rapidly progress into higher level exercises (single leg work)


Websites
physiotech.com.au
online learning site, access theoretical information on dralisongrimaldi.com
also runs practical seminars

Femoro-acetabular Impingement (FAI) Hip