Effect of different orthotic concepts as first line treatment of plantar fasciitis

LOL.....

 

Couple of additional comments

It was counter intuitive to me after taking dissected fascia from a cadaver and “feeling” its resistance to tension with my hands that the fascia can be stretched. It is also counter intuitive that the fascia can be physically modified more effectively by doing stretching exercises compared to simply walking – Paul has mentioned this before and I agree with him.

I think though that Paul is not considering that the stiffness of the plantar aponeurosis is not constant.

I must accept that fascia has visco-elastic characteristics – this doesn’t necessarily mean that by stretching exercise its physical dimensions can be favorably lengthened and I am unaware that this has ever be demonstrated.

What it does mean though is that perhaps it can be favorably conditioned (temporarily) by stretching (to alter its stiffness temporarily).

If the predominant perpetuating factor in mechanical chronic plantar fasciosis is that rate of injury is elevated when plantar aponeurosis is at stiffest then by conditioning fascia before weight-bearing the injury rate may be reduced.

Taking this further, the value of foot orthoses intervention, if goal is to mitigate the effect of tensile loading of plantar aponeurosis, is undermined if not used when most useful ie after rest when plantar aponeurosis is at stiffest.

This idea is consistent with pathognomonic feature of worst pain on rising from bed in morning and evidence that self-administered tissue specific stretching of plantar aponeurosis is helpful.

In my experience the value of foot orthoses is undermined if not used at most likely time of injury which is after resting, exploiting this idea for several years has I believe improved outcomes enormously. I believe that part of foot orthoses value may be to reduce rate of injury by protecting fascia from tensile loading when it is at its stiffest.

I am perplexed at mention in this thread of arriving at interpretation of a “tear” using US. Anyone thinking about this please post their opinion. I use state of art US for virtually all plantar heel pain which comes through my office and whilst degeneration, neovascularization, thickening, presence of enthesites, intra-fascia calcification and occasional “core” lesions can be identified, a tear, ie a lesion which can be seen to be an opening defect with passive dorsiflexion of MTPs is extremely rare.

One finding which is interesting to me is that degenerative US signs within plantar aponeurosis are commonly asymptomatic. Also with foot orthoses use and pain resolution sonographic appearance short term is unchanged.

Whilst I find foot orthoses designed (I believe) to mitigate inner longitudinal arch excursion very effective to treat persistent plantar heel pain attributed to chronic plantar fasciosis I am curious regarding those failures.

An issue which I feel remains unclear is role of compressional stress vs tensile stress – particularly in reference to importance of enthesites at and behavior of plantar fibro-fatty pad superficial to medial process of calcaneal tuberosity.

For that reason, empirically, I have recently started adding a 7mm layer of shore 20 silicone into foot orthoses beneath medial process of calcaneal tuberosity for all those with;

• sonographically demonstrated enthesite,
• heterogeneous hypoechoic zones noted within the deep macro chambers of the calcaneal plantar fibro-fatty pad or
• Pain which is characteristically worse towards end of day rather than, or in addition to simple worst pain on rising from bed in morning.

Too early yet to have an impression of value of this but curious to know if others are thinking similarly.

Cheers

Martin

Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

Mart:

Here are 11 cases of plantar fascia tears diagnosed with ultrasound along with 2 more cases of plantar fascia tears. I see plantar fascial tears (diagnosed by history and palpation) about once a month in my practice. Certainly something as frequently reported in the literature and frequently seen by busy clinicians can't be considered "extremely rare". I would rather say that plantar fascial tears are "uncommon".:drinks

 

Thanks Kevin; I think that my practice tends to deal primarily with persistent rather than acute presentations and likely see a skewed cohort; agreed that I likely overstated what others might see in terms of tears.

In terms of the images presented in these online atlases which you posted I wanted to comment a bit about them
Image 1 from 1st site;



I think is ambiguous and is typical of plantar fasciosis with small core lesion rather than tear (as with most of the images presented in this site as tears). My criterion currently would be to seek evidence of a gapping lesion with dynamic exam in this case. This is not mentioned, nor is extent of lesion demonstrated from an axial view, or, as would be expected, evidence of signal with power Doppler imaging attributed to an acute inflammatory response if there is a frank tear. Looking at the location of this lesion; interestingly it likely corresponds to proximal extent of the enthesite.

Image 2 from 2nd site;



is what I would interpret as classic recent tear – the plantar aponeurosis is poorly visualized likely because of recent haematoma, edema, disruption of collagen orientation, and presence of signal with power Doppler imaging is obvious as would be expected.

I assume that our clinical impressions would be similar for an acute tear and would anticipate; sudden onset and often associated “pop”, constant pain worsened weight-bearing, swelling, likely ecchymosis, high VAS especially to palpation,. Image 2 is what I would see on US in these cases not image 1. I see perhaps 2-3 per year.

The reason I mention this is that I think acute onset traumatic chronic plantar fasciitis is a different entity to insidious onset fasciosis and US appearance is quite different. This is potentially important because if US is used as reliable high level evidence and cited as evidence of an entity its value is undermined if poorly or loosely interpreted. Degenerated segments of fascia do not I believe necessarily represent tears and their etiology may be quite different.

My current view of likely mechanism of chronic plantar fasciosis has been largely influenced by your posts.

Something which fascinates me is the similarity of early plantar fibromatosis (slight painless palpable mass) and suspicion of early plantar fasciosis as sonographic incidental finding (normal fascia and no pain).

What they may have in common is an initial finding of layer of edema within the plantar fibro-fatty pad intimate to the plantar aponeurosis.

Whilst the idea is tenuous, if chronic plantar fasciosis is caused by signaling to fibroblasts within the fascia from adjacent plantar fibro-fatty pad (caused by compressive stress or other phenomena as is suspected with plantar fibromatosis) it may be possible to witness progress of fasciosis sonographically using this sign as way to select a couple of suitable subjects for a longitudinal case study.

Currently I am validating a 3D US system and if it proves reliable may try and select a couple of cases to explore idea properly.


Cheers

Martin

Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

I would see small defects/intrasubstance longitudinal tears several times weekly in my clinical practice. Then again we do go looking for them and I would say confidently those who look more, find more! We also see a plethora of fibromas.

We see defects longitudinally from 2mm up to 20mm. I think its important to identify defect early, prior to orthotic therapy as medial ILA height irritates patients with tears. I also think it essential for any physician to identify tears early to outrule any litigation later throughout the management phase should one be found. I see no reason why these defects could not be blamed on ILA height of orthoses in some cases.

Mart I agree wholeheartedly about the "viscoelastic" properties possibly/most likely differing throughout the plantar fascia substance. I take it into account but (and I think it was on the previous page where the discussion ensued) anatomically I thought there were fibers at the insertion which had no ability to adapt to change - these are more the fiber types I am referring to.

I am specifically interested at present in tissue tensility - does anyone have any data or papers relating to plantar fascial tensility differences in adults? Do we all in fact differ? I would imagine we all would - could this tensility difference be a predictor of injury?

I think we are all on the same page - just in different paragraphs essentially - which is exactly how good books come together!

 

I have just finished a Monday at Central Queensland Uni, I have an 8.00 class. Any fan of wine knows that that is a total no-no! Now then, I am not entirely sure that words like visco-elastic can be applied to structures such as the plantar aponeurosis. Certainly they will stretch, but IMHO [my wifes tells me I do not have one.......] there is no stretch on a day-to-day timescale, apart from the expected elastic recoil that we all know about . If a biomechanist crawls out of the wood work to 1) correct me, and 2) educate me, I await.

Not sure I have helped here, but what the hell. Rob

 

There are no structures of the human body that are not viscoelastic....this includes the plantar aponeurosis.

For those of you who are unfamiliar with the term "viscoelasticity", it may be worth reading this article on the subject.

http://www.ismni.org/jmni/pdf/19/11ZHANG.pdf

 

Here is a great lecture on viscoelasticity in biologic tissues.

http://www.ewp.rpi.edu/hartford/~ernesto/F2012/MEF2/Z-Links/Papers/Viscoelasticity-KTH.pdf

Why is it so hard for some to accept that the plantar aponeurosis, like all of the body's other tissues, is viscoelastic?

 

Wow Kevin, I got out of my depth pretty fast reading that presentation!

I was going to say 'its all greek to me", but it literally IS all greek.

How much force is required to deform the plantar fasciia, and how much deformation does it exhibit before it fails? What does it's stress/ strain graph look like? Does it really stretch much, or does it just tear?

 

Phil:

Just ignore the formulas and take note of the important concepts of creep, stress relaxation and strain rate dependence. These are the hallmarks of viscoelasticity. However, the math is important also since it explains the spring-dashpot models and their force vs time curves.

I have attached the original UCBL Technical Memorandum from Wright and Rennels from October 1961 that was eventually published as a paper in JBJS in 1964 on the elastic properties of the plantar aponeurosis (Wright DG, Rennels DC: A study of the elastic properties of plantar fascia. JBJS, 46 (A):482-492, 1964). [This original UCBL Technical Memorandum was given to me by Gib Wright, the primary author of the study. I worked with Gib Wright, MD, in his medical office for about 6 months in 1985 where he was a foot and ankle orthopedic surgeon. We became friends and we had a lot of fun discussing biomechanics in the short time I worked in his office.]

If you look at page 15 of this 50+ year old study, you will see the following:

This experimental observation of a time-dependent load vs. deformation behavior of the plantar aponeurosis is caused by its viscoelastic properties.

Wright and Rennels then go onto to further describe in their discussion on page 17:

An elongation of 3.5-4.5% in a plantar fascia that is 120 mm in length means that the plantar fascia stretched 4.2-5.4 mm during their testing. Even though this isn't a lot of deformation, it is likely within the physiologic ranges seen in running and jumping sports.

Hope this helps.:drinks

 

So this obviously isn't new information! Very interesting. So we can assume at least a few mm of increase in length for normal weightbearing activities.

I notice that the second application of stress needed to achieve the same strain (change in length) was less. So maybe stretching the plantar fasciia does cause an increase in length, at least temporarily.

 

That is what I have been saying all along.

It helps to be knowledgeable of the literature when one starts discussing the load-deformation characteristics of the structural tissues of the human body.

 

Hi All- my 2 bobs worth;
How do the forces of gait (read Erdimir) let alone running compare to the relatively passive forces of isolated PF stretching? I think its a bit of a stretch (ha) to causally connect PF stretching to the onset of PF tears in the face of 10000 steps a day.
I think the same Erdimir also calculated strains of 5-7%?
Further I dont assume that the PF is the sole recipient of the stretch (muscle, nerve, ligament..). Beyond the effect to its viscoelastic properties stretching also has (difficult to quantify) effects on mechanotransduction, fluid shift, afferent discharge...
Lastly, I would think unloading tissue on a long term basis is a good way to decondition tissue designed to be loaded. Yes, respect the 'hot' phase, but down the track if a foot needs to be loaded in running and jumping, it doesnt magically conjure the tissue properties necessary to deal with such stresses without some conditioning (perhaps going off track here- but point is, load in all forms is not evil).