Friday, September 04, 2009
Ankle Impingement
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iCSP has posted a discussion about ankle impingement: Added by: juliephysio Hi | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
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If your patient is very keen to get back in the boat to continue rowing, you could put a heel raise in her rowing shoe to reduce the amount of dorsi flexion she'll go into at the start of her stroke so she doesn't continually irritate the impingement. Short term solution whilst working on all the other ideas??
As noted before MWMs are very useful. I find the ATFL frequently gets shortened and pulls the lateral malleolus forwards, thereby blocking DF and eversion. I would get the patient in 4-pt kneeling on the bed, (the bed is up high for you to lean on it) and the affected foot up on the bed. As they flex forwards at the ankle, simultaneously glide the malleolus backwards. If this technique is successful at improving range and decreasing pain, do it a few more times, then tape the malleolus back afterwards. I also find the exercise noted by nellmead above very useful. I.e. 4 pt kneeling and rock back onto the plantarflexed ankle. I would bias it into inversion, and instruct them to rock back until they feel it "give" but not to sit on their heels.
Hi. I have found a few techniques useful in the past for ankle impingment. One is an MWM - AP glide of talus on tibia as patient moves to end range DF in weight bearing. Another is a distraction manip in DF. Neural stretching and masses of proprioceptive work are also helpful.
I agree with the above posts re: Mulligan type techniques. A-P glide of talus in standing (using belt) can be exceptionally effective for this. I would also get on with some soft tissue work along the anterior joint line.
Anterior joint pain after Inv sprain is often due to fwd positional fault of talus or fib or both (opinion not fact). Inv MWM is very useful to improve fib positional and can sometime clear DF. If not try a W/Bing DF MWM to slide talus back into the mortise+/- fibular AP, its worth noting that sometimes relief is only gained from firm end ROM MWM,so dont be shy. The page or two on "ATFL injury" in the Mulligan textbook is well worth a read.... ATFL damage a medical fallicy??
Anterior impingements are a pain! Along with mobilisations of which using MWM would give immediate response as to its effectiveness i have recently been very impressed with Functional fascial taping especially developed for anterior impingement in ballet dancers. Basically take the rower into pain position then on the site of pain direct the skin in differing directions until you find the direction that abolishes pain. Then tape strongly into this position with half width non elastic tape.
Not sure what you've done to date regarding the capsular restriction, but the vast majority of my patients in this situation respond well to joint mobilisations - distraction of the talocrural joint (i.e. patient supine and holding onto the bed, grip calcaneus and talus and pull, grade 3 oscillations, until you feel the joint "give") followed by AP/PA glides; then I'd also palpate for subtalar joint mobility and inferior and superior tibiofibular joint glide. If your patient is still feeling impingement at EOR DF once these feel clear to you, then localise the point of impingement and stretch the foot into plantarflexion with a bias away from the impingement, to stretch the capsule at that point.
Just wondering if you had considered the possibility of osteohcondral injury. The risk of this increases with the grade of ankle sprain and reported incidence is in 40% of ankle sprains.
If you have several months to play with it may be beneficial to give the capsule a chance to settle down. We do this by imobilising the ankle in a boot for 7-10 days while on NSAIDS. The ankle can still be mobilised with conventional manual therapy techniques. If this doesn't completely irradicate symptoms steroidal injection could be considered witha similar time of imobilisation. I have found investing in that first week of immobilisation to address the synovitis beneficial to final outcome. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
20:33 Posted in Ankle/foot | Permalink | Comments (0) | Email this
Tuesday, July 21, 2009
Foot biomechanics
On the 15/07/09 I went on a course as part of my Msc module; foot biomechanics.
The day in Northampton was very interesting. I learnt how to apply orthotics for forfoot and rearfoot pronation using podiatry felt. Steve Avery took the practical session of the course. I need to buy 7mm and 5mm mixed felting with adhesive backing.
01:14 Posted in Ankle/foot, Course | Permalink | Comments (0) | Email this
Monday, March 09, 2009
New website!!
19:22 Posted in Acupuncture, Ankle/foot, Ax, Course, Cx, Elbow, Electrotherapy, Ergonomics, Guru's, Hand, Head injury, Hip, IST, Knee, Lower limb, Lx, Neurology, Occupational Health, Pain, Pathologies, PDP, Pelvis, Reflection, Research, Rheumatology, S I Joint, self referral, Shoulder, Sports Physio, Supervision, Tendon and Muscles, Tx, Vascular, Wrist | Permalink | Comments (0) | Email this | Tags: http:physiocharlie.vpweb.co.uk
Wednesday, February 04, 2009
Foot Posture Index
http://learn.clinicsinmotion.com/moodle/course/view.php?i... From the CSP conference 2008:
K. Reilly, K. Barker, M. Newman, S. Sandall
Foot Posture Index
Published 2006 Redmond et al
Free to download on the internet:
http://www.leeds.ac.uk/medicine/FASTER/FPI/FPI%20Referenc...
The measurements are of two anatomical segments taken in three planes
Gives clear indication of foot posture with a numerical score:
16:18 Posted in Ankle/foot, Knee, Research | Permalink | Comments (0) | Email this
Friday, November 28, 2008
Achillies Tendonopathy
Yesterday me and a colleague attended a module of advanced skills MSc and had a presentation on Achillies Tendonopathy by Richard Wood.
ACHILLES TENDINOPATHY
RICHARD WOOD
SPECIALIST PHYSIOTHERAPIST
UNIVERSITY HOSPITALS OF LEICESTER NHS TRUST.
OUTLINE OF PRESENTATION
THEORY OF CORE SUBJECT
ANATOMY AND PHYSIOLOGY
DIFFERENTIAL DIAGNOSIS- ACHILLES
DIFFERENTIAL DIAGNOSIS-POSTERIOR ANKLE PAIN
PREDISPOSING FACTORS TO INJURY
PREDISPOSING FACTORS TO RUPTURE
OUTLINE OF PRESENTATION
SUBJECT DEVELOPMENT
CLINICAL ASSESSMENT
RADIOLOGICAL ASSESSMENT
TREATMENT OPTIONS (EVIDENCE)
OUTLINE OF PRESENTATION
APPLICATION OF ADVANCED SKILLS RELATED TO SUBJECT
CASE STUDIES
(WHO TO SEE AND WHAT TO DO)
OUTLINE OF PRESENATION
CURRENT PRACTICE DISCUSSION
REFLECTION AND APPLICATION OF A REFLECTIVE MODEL, WORKING FROM EVIDENCE BASE.
ANATOMY AND PHYSIOLOGY
OVERVIEW
SOURCE OF PAIN?
LONG TERM PROGNOSIS
8 year follow up. Paavola et al (2000)
Follow up 83/107 patients
<6 month history at initial assessment
Follow up 8 years +/- 2 years
Questionnaire, CE, performance,muscle strength and US.
29% operation rate
84% full recovery average 8 years
94% asymptomatic
41% had symptoms in initially asymptomatic tendon
DIFFERENTIAL DIAGNOSIS ACHILLES
PARATENONITIS
ADHESIVE TENDINOPATHY
TENDINOSIS
‘TENDINITIS’
PARATENONITIS AND TENDINOSIS
PARTIAL RUPTURE OF ACHILLES
COMPLETE RUPTURE OF ACHILLES
INSERTIONAL DISORDERS (ZONE 2)
DIFFERENTIAL DIAGNOSIS POSTERIOR ANKLE PAIN
OSSEOUS
POSTERIOR ANKLE IMPINGEMENT
ANTERIOR ANKLE IMPINGEMENT
OS TRIGONUM SYNDROME
LOOSE BODIES
FRACTURES + AVN
TUMOUR
SEVER’S DISEASE
DIFFERENTIAL DIAGNOSIS POSTERIOR ANKLE PAIN
SOFT TISSUE
RETROCALCANEAL BURSITIS
TIBIALIS POSTERIOR TENDINOPATHY/TEAR
FHL/FDL TENDINOPATHY
PERONEAL TENDINOPATHY
GANGLIONS
PLANTAR FASCIITIS
DIFFERENTIAL DIAGNOSIS POSTERIOR ANKLE PAIN
NEURAL
SURAL NERVE ENTRAPMENT
SUP.PERONEAL NERVE ENTRAPMENT
TIBIAL NERVE ENTRAPMENT(TTS)
REFERRAL FROM Lx SPINE
DIFFERENTIAL DIAGNOSIS POSTERIOR ANKLE PAIN
OTHER
INFLAMMATORY ARTHRITIS(REITERS)
RhA/AS/CTD
GOUT
INFECTION
Abx
HYPERLIPIDAEMIA
DM
Hormone imbalance
INTRINSIC FACTORS
FOOT PRONATION/SUPINATION-STJ FUNCTION
FOOT MECHANICS
1ST MTPJ movement
TIBIAL TORSION (<25deg)
GENU VALGUM (<11 deg)
GENU VARUM
GENU RECURVATUM
INTRINSIC FACTORS
FEMORAL ANTEVERSION/RETROVERSION
LEG LENGTH (>2cm)
LENGTH OF TENDON
HYPERMOBILITY
MUSCLE IMBALANCE
AGE
BMI
HYDRATION/NUTRITION
FATIGUE
EXTRINSIC FACTORS
TYPE OF MOVEMENT
SPEED OF MOVEMENT
MOVEMENT REPETITION
FOOTWEAR
SURFACE
WEATHER
ADEQUATE MOVEMENT PATTERNS
EXTRINSIC FACTORS
TRAINING ERRORS
FREQUENCY
DURATION
INTENSITY
TECHNIQUE
APPROPRIATE REHABILITATAION (SPORT SPECIFIC)
EARLY RETURN
PREDISPOSING FACTORS TO RUPTURE
EXCESSIVE BODY WEIGHT
DIABETES
HEAVY WEIGHT LIFTING
HISTORY OR CURRENT ANABOLIC STEROID USE
HISTORY OR CURRENT STEROID INJECTIONS
JOINT IMMOBLISATION
PREDISPOSING FACTORS TO RUPTURE
MALE SEX
INFLAMMATORY ARTHROPATHIES
MUSCLE WEAKNESS AND IMBALANCE
SMOKING
SPONDYLOARTHROPATHIES
FLUOROQUINOLONE USE
GOUT
RUPTURE
SUBJECT DEVELOPMENT
CLINICAL ASSESSMENT
RADIOLOGICAL ASSESSMENT
TREATMENT OPTIONS (EVIDENCE)
CLINICAL ASSESSMENT
PUDDU(1976)
3 ZONES
ZONE 1
ZONE 2
(ZONE 3)
ZONE 1
NON-INSERTIONAL AREA
ACHILLES PARATENONITIS +/-
ACHILLES TENDINOSIS
(ACHILLES TENDINITIS)
ACHILLES TENDON RUPTURE
ADHESIVE TENDINOPATHY
ZONE 2
INSERTIONAL AREA
CALCIFIC TENDINITIS
SUPERFICIAL CALCANEAL BURSITIS
RETROCALCANEAL BURSITIS
EXOSTOSIS OF CALCANEUM
AVULSION AT CALCANEUM
‘HAGLUNDS DEFORMITY’
SEVERS DISEASE
ZONE 3
MID CALF AREA
MUSCULOTENDINOUS JUNCTION TEARS
SURAL NERVE ENTRAPMENT
SPN ENTRAPMENT
PAES
COMPARTMENT SYNDROMES
CLINICAL ASSESSMENT
RELEVANT BIOMECHANICS
GAIT
TALOCRURAL JOINT
SUBTALAR JOINT
STABILITY TESTS
SOFT TISSUE PROFILE(consider KINETIC chain)
SPECIAL TESTS
LONDON HOSPITAL ‘TEST’
VISA-A QUESTIONNAIRE
VISA-A questionnaire
Robinson et al (2001) British Journal of sports medicine.
Validated
RADIOLOGICAL ASSESSMENT
X-RAY
CALCANEAL EXOSTOSIS
CALCIFICATION AT INSERTION
POSTERIOR IMPINGEMENT
MRI v’s ULTRASOUND
Khan et al (2003)
US abnormal in 37/57 sym tendons(65%)
US normal in 19/28 asym tendons (68%)
MRI abnormal in 19/34 sym tendons(56%)
MRI normal in 15/16 asym tendons (94%)
MRI v’s ULTRASOUND
Karjalainen et al (2000)
MRI only
111/118 painful tendons
Sensitivity of 94%
Specificity of 81%
(only 23% had surgery)
IMAGING SUMMARY
BOTH MRI AND US USEFUL
ABNORMAL SIGNAL DETECTED
DIFFICULT TO ALWAYS GIVE ACCURATE DIAGNOSIS
NO PROSPECTIVE STUDIES WHICH DETECT SUBTLE PATHOLOGY
ABNORMAL SCAN AND NO SYMPTOMS
Alfredson et al (2003)
TREATMENT OPTIONS
ACHILLES PARATENONITIS
ACHILLES TENDINOSIS
(ACHILLES TENDINITIS)
ACHILLES TENDON RUPTURE
ADHESIVE TENDINOPATHY
TREATMENT OPTIONS
CALCIFIC TENDINITIS
SUPERFICIAL CALCANEAL BURSITIS
RETROCALCANEAL BURSITIS
EXOSTOSIS OF CALCANEUM
AVULSION AT CALCANEUM
‘HAGLUNDS DEFORMITY’
SEVERS DISEASE
ACUTE PARATENONITIS (CHRONIC ADHESIVE TENDINOPATHY)
Welsh (1990) 4/52 relative rest to promote healing.
? immobilise
Reduce extrinsic factors (Activity)
Address intrinsic factors (Biomechanics)
Soft tissue stretching
Ice and NSAIDS (?after 3 days) and note that inflammatory cells not found even in acute tendon problems(Alfredson 2005)
?GTFM (Cook et al 2004)
ACUTE PARATENONITIS (CHRONIC ADHESIVE TENDINOPATHY)
Early intervention (Alfredson 2003)
Prevent collagen damage.
?> 6 months to improve.
ACHILLES RUPTURE
ACHILLES TENDINOSIS
ECCENTRIC EXERCISE
PODIATRY
KADER et al (2002)
12-15 mm heel wedge may be beneficial.
Obvious biomechanical dysfunctions should be targeted( a number of papers)
PODIATRY
Clement et al (1984)
109 athletes
OVERTRAINING
61% functional overpronation
41% gastroc/soleus insufficiency
PODIATRY
Kaufman et al (1999)
Hindfoot varus
Reduced dorsiflexion
PODIATRY
Kvist (1991)
Biomechanical defects in 60% athletes
Forefoot varus
Limited sub talar joint mobility
Reduced dorsiflexion
PODIATRY
Lun et al(2004)
87 Athletes
6/12 observation
79% injured
Multifactorial – no correlation with biomechanics except PFJ pain.
GTN PATCH
Paoloni et al (2004)
84 tendons
78% asymptomatic at 6/12
49% (placebo) asymptomatic at 6/12.
INJECTIONS!
Ohberg and Alfredson (2002)
US guided sclerosis (Polidocanol)
10 patients , 80 % success
O’Dowd et al (2007)
HVIGI (local anaesthetic steroid and saline-50ml)
‘Strip’Kagers fat
30 patients , 70% improved at 30/52
INJECTIONS!(Steroid)
Shrier et al (1996)+case reports
Perrypacker (2004)
Read and Motto (1992) 83 athletes/1 rupture
Speed et al (2001)
Dacruz et al (1988) 28 patients. No benefit
Lesic et al (2004) contraindicated.
Anecdotal case series
INJECTIONS!
SALINE? (Brisement)
LOCAL ANAESTHETIC?
HEPARIN?
AUTOLOGENOUS BLOOD?
OTHER TREATMENTS
Scheel et al(2004)- manage hypercholestremia. Reduce Xanthoma formation.
ECSWT Chen et al (2004) ?? Frequency
ELECTROTHERAPY (Evidence in animal studies)
OTHER TREATMENTS
RESTING NIGHT SPLINTS
TRANSVERSE FRICTIONS
STRETCHING (How much Dorsiflexion?)
SURGICAL TREATMENT (ZONE1)
SURGICAL TREATMENT
24% - 45%
LONG STANDING TENDINOPATHY RESULTS IN POOR OUTCOMES
VARIED SURGICAL TECHNIQUE
EXCISE FIBROTIC NODULES
REMOVE PARATENON
REMOVE DEGENERATIVE NODULES
MULTIPLE LONGITUDINAL EXCISIONS
DETACH KAGERS FAT PAD
SUCCESS 70-100%?
SURGICAL TREATMENT
Leppilahiti et al (1991) 56%excellent at 4 years. (52)
Schepsis et al (1994) follow up at 1-13 years 67%(satisfactory)
Nelen et al (1989) 80% excellent . (50)
Morberg et al (1997) 80% excellent between 1.5 and 11 years. (25)
Paavola et al (2002) 67% activity fully restored, 83% asym with strenuous exercise. (42)
SURGICAL TREATMENT
Maffuli et al (1999)
14 patients with central core degeneration
87/12 since onset of symstoms
35/12 follow up
37% excellent/good results
43% re-explored
POOR RESULTS WITH LONG DURATION and CORE DEGENERATION
SURGICAL TREATMENT
Saxena (2003)
27 athletes/37 procedures
10.6 +/- 6.3 weeks to activity (E)
15 +/- 6.2 weeks to activity (NE)
Return to competition and 100%
25/52 (E) and 27/52 (NE)
SURGICAL TREATMENT (ZONE 2)
THERE IS NO GOOD EVIDENCE FOR SURGICAL TREATMENT IN THIS AREA.
LONG RECOVERY IN CASE REPORTS.
GENERALLY MUCH POORER OUTCOMES WITH SIMILAR TREATMENTS.
APPLICATION OF ADVANCED SKILLS RELATED TO SUBJECT
CASE STUDIES
(WHO TO SEE AND WHAT TO DO)
CASE STUDIES
PRIORITISE PATIENTS
PROVISIONAL DIAGNOSIS
IMMEDIATE PLAN and WHY
PROGNOSIS AND PATIENT DISUSSION
CONSULTATION SKILLS
PRINCIPLES OF I.C.E
EXPLORE AND EXPLAIN ;
R.A.P.R.I.O.P
CURRENT PRACTICE DISCUSSION
REFLECTION AND APPLICATION OF A REFLECTIVE MODEL, WORKING FROM EVIDENCE BASE.
15:49 Posted in Ankle/foot, Course, Research | Permalink | Comments (0) | Email this
Wednesday, November 05, 2008
Tibialis posterior dysfunction
Tibialis posterior dysfunction: a common and treatable cause of adult acquired flatfoot, Kohls-Gatzoulis et al, BMJ 2004;329:1328–33
http://cms.interactivecsp.org.uk/uploads/documents/Tib%20...
http://www.bmj.com/cgi/content/full/329/7478/1328/DC1
"Adults with an acquired flatfoot deformity may present not with foot deformity but almost uniformly with medial foot pain and decreased function of the affected foot. The most common cause of an acquired flatfoot deformity in an otherwise healthy adult is dysfunction of the tibialis posterior tendon, and this review provides an outline to its diagnosis and treatment".
Causes of an adult acquired flatfoot
• Neuropathic foot (Charcot foot) secondary to: Diabetes mellitus, Leprosy, Profound peripheral neuritis of any cause
• Degenerative changes in the ankle, talonavicular or tarsometatarsal joints, or both, secondary to: Inflammatory arthropathy, Osteoarthropathy, Fractures
• Acquired flatfoot resulting from loss of the supporting structures of the medial longitudinal arch: Dysfunction of the tibialis posterior tendon, Tear of the spring (calcaneoanvicular) ligament (rare), Tibialis anterior rupture (rare)
Symptoms suggesting tibialis posterior dysfunction
• Pain and/or swelling behind the medial malleolus and along the instep
• Change in foot shape
• Decrease in walking ability and balance
• Ache on walking long distances
How to examine for tibialis posterior dysfunction
(1) Both of patient’s legs visible from knee down
(2) Observe heel alignment with patient standing with feet shoulder width apart, feet parallel. (Heel becomes valgus, arch collapses, and forefoot adducts in cases of tibialis posterior dysfunction) Also visible is the “too many toes sign,” which results from abduction of the left forefoot.
(3) Inspect for swelling behind medial malleolus
(4) Ask patient to stand on tiptoes. Normally the heel should bend inwards. A patient with tibialis posterior dysfunction will have great difficulty standing on tiptoes, and the heel will not bend inwards
(5) Ask the patient to perform 10 unsupported heel rises on each leg. A patient with tibialis posterior dysfunction will not be able to do this
(6) Palpate along the tibialis posterior tendon for tenderness
(7) Test tibialis posterior tendon for power. Ask the patient to bring foot into an inverted and plantar flexed position from an everted and dorsiflexed position against your resistance
(8) Examine for hindfoot movement. In stages I and II, the foot is supple and the flatfoot deformity can be corrected by rotating the heel inwards (the arch of the foot will be reconstituted). In stage III and IV subtalar arthritis is present, and movement of the subtalar joint will be lessened and painful. Additionally in stage IV, ankle arthritis has set in and the ankle becomes stiff and painful
Stages of tibialis posterior dysfunction and treatment options
Stage I
Tendon inflamed, No change in foot shape, Acute: 4-8 weeks’ immobilisation; rest, ice, compression, and elevation (RICE); non-steroidal anti-inflammatory drugs (NSAIDs), Chronic lace-up, flat footwear and corrective orthosis or ankle foot orthosis (AFO), surgery; Tendon debridement combined with corrective osteotomy
Stage II
Tendon elongated, Acquired flatfoot deformity, Acute: 4-8 weeks’ immobilisation, RICE, NSAIDS, Chronic: lace-up, flat footwear and corrective orthosis, Surgery; Tendon transfer and corrective osteotomy
Stage III
Fixed deformity, Degenerative changes at subtalar joint, Lace-up, semirigid shoes or customised footwear and accommodative orthosis (AFO), Surgery; Triple arthrodesis (subtalar, calcaneo-cuboid. and talonavicular articulations)
Stage IV
Fixed deformity, Degenerative changes at subtalar and ankle joints, Lace-up, semirigid shoes or customised footwear and accommodative orthosis (AFO), Surgery; Pantalar arthrodesis (subtalar, calcaneo-cuboid, talonavicular, and ankle articulations)
Resources for patients and doctors
www.bofss.org.uk Designed for both patients and doctors and is run by the British Orthopaedic Foot Surgery Society and gives good general advice about foot care
www.orthoteers.co.uk good site for doctors. Click on flatfeet (in the paediatrics section) and then on tibialis posterior insufficiency
http://www.foothyperbook.com/elective/aaff/aaffIntro.htm website for the Blackburn Foot and Ankle Hyperbook.
12:05 Posted in Ankle/foot, Research | Permalink | Comments (1) | Email this
Wednesday, September 24, 2008
Sprains and strains
14:13 Posted in Ankle/foot, Knee, Research | Permalink | Comments (0) | Email this
Friday, September 19, 2008
Compartment syndrome/ vascular issues
I found this discussion on iCSP:
| Hi I am in search of some diagnostic help. I assessed a 44 year old woman who is a keen runner in clinic today. She is currently training for a marathon which is 5 weeks away. She has been running seriously for the past 7 years, however has a chronic problem in her right calf. She describes symptoms consistent with compartment syndrome in that her calf becomes very painful and rock hard after running approximately half a mile or when walking up a steep hill. However her symptoms are not behaving like a compartment syndrome. She is able to ease her symptoms by stopping and simply shaking her leg, pumping her ankle and then continue running for half a mile before she has to repeat this routine. She has to do this every half a mile for the 1st 3 miles and then she is able to continue running with no problems. She is up to running 16 miles at present. Can I please emphasise that this problem is not a result of an increase in training load, change of footwear or any obvious cause. This has been happening for her entire running career and nobody has been able to give her a diagnosis. She saw an orthopaedic consultant last year who palmed her off with compartment syndrome without doing any investigations or suggesting any further intervention. There has been no trauma other than a hyaline fracture many years ago, before she begun running, and healed with no dramas and has had no problems since. On examination today there appears to be no biomechanical abnormality. Leg lengths are equal, there is no over pronation/supination and she wears a neutral running shoe. She has full ROM at her ankle with no suggestion of muscle shortening. There is no localised tenderness on palpation. NAD was detected on assessing Lx. The only muscle imbalance abnormality was minimal shortening of TFL on the problematic side. I put the patient on the treadmill today to assess her gait and to try and reproduce her symptoms. To the eye there appears to be no major issues around her pelvis. I was able to reproduce her symptoms following 4 mins of incline walking (10% gradient). The lateral half of her calf became solid and very tender on palpation. Medially was relaxed with no tenderness. This settled within 60 seconds. Please correct me if I am wrong but if this was a true compartment syndrome she would not be able to continue running with no problems in the pattern she describes above. The symptoms have not worsened. But have frustrated her as she is unable to keep up with her running group for the 1st 3 miles. If its of relevance she runs 9 minute miles. I am wondering whether this could be a vascular problem but I have not come across anything like this before. Any ideas on pathology and diagnostic tests would be hugely appreciated. Regards, Math | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Hi Math, I have seen several patients with very similar symptoms, being based in the Newcastle area we see lots of people training for the Great North Run. My clinical area of interest is visceral fascial release and I have found that most of these clients have fascial restrictions around the first part if the large intestine which seems to create vascular problems of the lower limb. An obvious cause can be an appendix scar but it is not always as blatant as that. I do not, as yet, have a full physiological explanation but all of these patients have had some degree of SIJ restsritions, tight hip flexors and tight plantar flexors. Good luck with your client. Best wishes Graham
I see, yet again, physio mitch has suggested fatigue of the sympathetic nervous system as the diagnosis for this patient. If so,I wonder if you could shed some light on why her symptoms are only evident for the first 3 miles? Is her sympathetic nervous system not fatigued for the rest of her run? Math, crude as it maybe, I would look at pre and post exercise pulse palpation as a method of identifying a possible vascular origin of her symptoms. good luck
Interesting thread! . . . . Sportex Medicine published "How to recognise vascular flow problems in athletes;a clinical reasoning exercise" Taylor & Kerry Issue 35 Jan 08 That may be helpful? Cheers Alan
Hi I would agree if this was true compartment syndrome, the lady would be unable to run once the symptoms occur. It sounds vascular, there was a paper (case study) a few years ago that if my memory serves had a similar presentation. It was found that there was popliteal artery occlusion brought on only during/after exercise. Hope this helps
Hi This is anot an uncommon or odd case. The basic foundation of this problem is one of overuse. If I may, I would like you to picture this typical scenario. The end result may differ from person to person, but the underlying factors are very common. Runners, in my view, do too much running as a part of their training. Running mare than twice a week can be a form of overload/overuse. The body needs 48 hours to recover from exercise including the immune system Studies have shown white cell count to increase during exercise, reduce after exercise (to BELOW normal numbers), and then to return to normal levels 48 hours later. The scenario of a typical runner can go as follows. Please note this is my opinion after 16 years of treating runners and other sports persons: - Too much running (or any exercise for that matter) without sufficient rest in between (48hrs) can lead to fatigue of the sympathetic nervous system. This system controls the rate of blood flow through controlling the tone of the arteries and their peristaltic movements. - Fatigued nerve cells mean they cannot feed thmselves enough blood to recover and thus get stuck in a state of fatigue - This leads to slower rates of blood flow to, eg the lower limbs - This results in muscle weakness (often evident in the hips initially) and tightness of the myofascial units (stiffness and weakness go together) - This now produces a mechanical problem, with weakness in the hip abductors resulting in compensatory overuse of the thigh and calf muscles to maintain good function of the lower limb - It is this overuse that often manifests as thigh, knee or calf pain. The tightening of the calf is mostly due to a chronic loss of good blood flow rate, resulring in fascial tightening. This is why she can relieve the symptoms by stopping and moving the foot about, thus restoring some blood flow (similar to intermittant claudication, but without the physical vessel constriction). - The more she runs the more she demands increased rates of blood flow to the muscle. This stresses the sympathetics more, and the cycle goes on. Muscle fatigue is often an indication of nerve cell fatigue in the sympathic nervous system. From your explanation and from my own experience with this type of condition I would suggest she has a chronic fatigue of the sympathetic nervous system (T10 to L2) with resulting muscle weakness and fascial shortening (ITB tightness being evidence of this). Even a little tightness in ITB can be very harmful. The calf tightness is a symptom of this problem, not the cause. You will need to accurately assess hip strength, left and right, TFL strength, knee flexion/extension and ankle plantar/inversion and dorsiflexion strengths. Any weakness may be caused by poor blood flow and/or tight fascial sheaths. T10 to L2 needs to be assessed as discussed above, and any corrections made, preferably through myofascial release. She should not be running now!!! It may mean missing the marathon, but there are plenty more. She may recover in time, but running during treatment is detrimental to recovery. Rest will assist in recovery of the sympathetic nervous system, as well as some form of treatment to the affected area of the spine. Hope this helps
Originally Added by: daveharvey Hi, This ladies start of symptoms seem a bit too young to be caused by spinal stenosis if she has had these symptoms for her entire running career. Aggravation of her calf pain during uphill walking as u know I'm sure is also not classic spinal stenosis presentation. I assume she is not exhibiting any circulatory symptoms? Popliteal Artery Entrapment Syndrome is a rare but potential diagnosis for this lady as it tends to affect runners with well developed calf muscles. Check out this article... www.dirjournal.org/pdf.php3?id=52 Best test to rule out vascular probs seems to be the angiograph done whilst exercising the ankle. Clinical tests that we can do basically involve testing leg pulses pre/post producing symptoms and with ankle dorsi and then plantarflexed to see if they diminish. Good luck!
I am a taekwondo player and compete regularly and suffered from a similar problem for nearly three years. No one could tell me what was wrong. I was investigated extensively for stress fractures, medial tibial stress and for compartment syndrome and had pressure tests taken. The pain was exercise induced. After approximately 4 minutes of exercise my calves would become very tight and this would cause pins and needles and numbness into my feet with some reduced circulation. I occasionally suffered from pitting oedema around the posterior medial tibia. It got to the stage that I couldn't stand anyone touching my shins. I was under the care of three consultants, (orthopaedic, biomechanic, vascular) none of which were sure of the cause of my symptoms. By chance I attended an SIJ course. The course leader assessed me and I had quite a marked SIJ dysfunction which was causing neural tension. I had no pain in the SIJ region itself, the problems manifested itself in my shins. The course leader treated me and I have had no problems since. Maybe assess this patient's SIJ? Shirin
Originally Added by: Tim.Pigott sounds more vascular to me.... check pulses and BP at ankle vs arm if Ok at rest, get her on a treadmill until the symtoms come on, and re-test.
Originally Added by: patsuth Had a sort of similar problem with a 45yr old man some years ago. He wasn't a runner, but a keen hillwalker. He first presented with calf pain which appeared to be local in origin. I suspected Compartment Syndrome, and he went for an orthopaedic opinion. Orthopod thought it was vascular. To cut a long story short, he had Spinal stenosis. (No Hx of any back pain or injury, and Lx assessment had not been significant) Surgery alleviated the problem. Not quite your scenario, but worth considering maybe.
If as you say, this lady has had this all her running life then there is a high chance she has a unilateral congenital limb hyperplasia. There is no remedy for this pathology. It relates directly to muscle bulk. If the pulses are normal at rest there is unlikely to be an arterial issue. The only other diagnosis is a vascular abnormality, which would require a duplex scan. ABPI does not help but you should find girth of the calf larger at rest on the affected side. Send her to a vascular surgeon for confirmation. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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