Orthotics cause HAV...

[robertisaacs]

Alledgedly. You know i like a good contentious thread title. ;D

This was a great thread on Pod arena so i thought i'd bang it about a bit here.

What causes HAV?

Well lots of things of course. Risk factors are varied. Genetic precursors are undisputed, footwear less so. However "conventional wisdom" (that most dangerous of things) tends to say that the pronation (nobody use the O word ) is a big part of it.

I certainly get plenty of referrals from gps, other pods, even surgeons saying they need anti pronation orthotics to prevent HAV. And we all know what that means!

Can we say that with any kind of confidence?

Here's a few inconveniant truths!

A controlled prospective trial of a foot orthosis in the treatment of juvenile hallux valgus.
J.Bone Joint Surgery 1994: 76B:210-214

Showed, alarmingly, that there was a GREATER incidence of HAV in the group treated with orthotics. Frightened? I was!

The significance of pes planus in juvenile hallux valgus.
TE Kilmartin, WA Wallace - Foot Ankle, 1992
Showed NO CORRELATION between Arch height and HAV in juveniles.

Relationship between adolescent bunions and flatfeet.
V Kalen, A Brecher - Foot Ankle, 1988
Also failed to show a link.

"ahaha" i hear you cry. "thats ALL in juveniles!". What about the adults?"

Well thats a valid question. But consider this. Kiddies have some of the flattest feet you ever will see and some of the poorest joint stability to boot! If the Causal link described by root and his merrie band is as advertised why are we not seeing a good deal more juvenile HAV?

Also kiddies are an interesting study because you get at them when there is a limited amount of environmental influence (compared to adults).

Consider also the following. Whilst most studies show a link between adult HAV and lower MLA who is to say that its a causal link.

To be pretentous for a moment
Post hoc ergo propter hoc ?- Are we presuming a causal relationship where none exists?

Maybe HAV causes lowered MLA! I'm sure we could do a model for that!

What say you?

Regards
Robert

[billliggins]

Just to muddy the water even more, I cannot recall having seen a patient requiring HAV surgery who did not pronate excessively at the STJ on WB. Am I seeing an aquired forefoot supination due to the HAV or an HAV due to STJ pronation? All the paediatrics attending with HAV (and I have not seen a vast number) all presented with excessive STJ pronation but as Robert says, many youngsters do not develop HAV despite the aforesaid.

In addition to familial factors, I am beginning to look seriously at i) joint shape and stability at 1st MTPJ ii) 1st met length iii) angle of obliquity of 1st met cuneiform joint.

The problem is to carry out prospective studies over many years. Still, worth pondering over.

Bill

[robertisaacs]

In addition to familial factors, I am beginning to look seriously at i) joint shape and stability at 1st MTPJ ii) 1st met length iii) angle of obliquity of 1st met cuneiform joint.

I would certainly agree with ii. Not working with as many x rays as you i cannot really make any intelligent comment on i and iii although i do remember reading a paper about the shape of the 1st MPJ as a precursor. Flattening in the 1st met if memory serves.

As you say this is a swine of a thing to study because of just how multifactorial it is.

[glow=red,15,100]Warning, shaky rationalisation ahead[/glow]

Assuming that the resistance of the 1st met to dorsiflexion is one of the things that provides supination moments in the stj around mid stance and in late stance phase and bearing in mind that a higher IM angle increases the lever arm for the intrinsic muscles of the foot to stabilise the 1st met it would seem reasonable to assume that an increased IM angle would A: reduce the Supination moments around the STJ causing more pronation moments to be absorbed by other structures and increasing the chance of one of these structures failing to control the degree of pronation and B: By lengthening the lever arm increase the inversion moments around the long axis of the MTJ (if such a beast exists) increasing the risk of FF supinatus.

[glow=green,10,300]Shaky rationalisation ends[/glow]

I have seen paeds presentations of HAV both with and without Lowered MLA on WB.

To be quite honest i don't entirely trust myself with my own observations any more. The unconcious biases i have identified in myself, confirmation bias (where you look for data which supports your hypothesis) in particular has made me question things i took for granted.

Not least, what is an excessivly pronated foot? In this context i mean.

How do we explain the Kilmartin study where orthotics INCREASED the risk of developing HAV? Any models on offer?

Regards
Robert

[rothbart]

Rootian biomechanics taught us that forefoot hypermobility (secondary to abnormal pronation) results in the 'loose bag of bones' syndrome, and this, in turn can lead to the development of HAV. I thought this was a good explanation some 40 years ago and still do today. The more severe the pronation pattern, the greater the tendency or risk is towards developing a HAV. When it comes to understanding foot biomechanics and the resulting pathodysfunctions, Root's Model was and still is, an excellent paradigm to use.

My observations over the years have led me to the following conclusions:

(1) You see HAV developing in children who have severe abnormal pronation (e.g., the Preclinical Clubfoot Deformity)

(2) You see HAV developing in adults whose abnormal pronation is quite pronounced but not as severe as that seen in children (e.g., the Primus Metatarsus Supinatus Foot with PMs Values over 16mm)

This all makes sense when you think about the loose bag of bones theory. The looser the bag of bones, the quicker the HAV develops.

Of course, there are secondary issues that come into play. For example, the infamous stiletto heel, pointed toe shoes. (whoever designed that shoe must have been a Podiatrist looking for work).

Do orthotics exacerbate the development of HAV? They definitely can, if the wrong type of insole is used.

Prof B

[davidsmith]

Robert

First of all lets see if the statistical terminology IE Causal is the correct term to use.

Two types of statistical analysis are Correlative and causal.
Causal statistics can in general only be implied from experimental data gathering IE were the researcher changes some variable to see if it changes the parameter of interest. Correlative data is gathered from research where the researcher only gathered data about two variables and compared them. Though correlation of two variable from correlative data might suggest causation this cannot be proved by correlative data alone.
However causation does require correlation therefore, where there is a negative correlation, it might be more valid to say that where there is no correlation there is no causation. This line of reasoning has to taken cautiously though and a thorough understanding of the scientific method is required.

So Robert, I not having read any of the papers you reference ask, what type of data was analysed? Especially in the paper
'A controlled prospective trial of a foot orthosis in the treatment of juvenile hallux valgus. J.Bone Joint Surgery 1994: 76B:210-214', which inferes a positive correlation and so causation. Was there causative data in any of theses studies? or is it a case of Cum Hoc ergo procter Hoc.

Second, I believe that to say 'juvenile feet are flat so therefore they represent adult flat feet as a representative model' should be cautiously proposed.

Juvenile feet are not completely ossified and connective tissue is more elastic. Therefore equivalent 'pound for pound' 'Newton for Newton' internal forces cannot be assumed. The mechanical and material properties of the juvenile foot are too varied, when compared to the adult, for extrapolation of data to be valid.

At the end of the day it is easy to show correlation but difficult, some say impossible, to prove absolute causation.

All the best Dave

[podiathing]

Sorry, I'm really late on this. Tim Kilmartin answered this in a letter following the republication of McDonald and Kidds paper on the research on the use of foot orthoses in the BJP. His paper showed a trend towards increase of incidence of HAV, but this was not statistically significant. Or so he said anyway, and i guess he's know!

Hope this helps

Paul Harradine

[davidsmith]

Robert

Had a look at this thread this morning and I had forgotten I had contributed before in Janurary.

Anyway I read this paper
A controlled prospective trial of a foot orthosis in the treatment of juvenile hallux valgus. Kilmarten T et al J.Bone Joint Surgery 1994: 76B:210-214
And the abstract of this one -
The significance of pes planus in juvenile hallux valgus. Kilmarten et al.

There are many things to question but here are a couple of main ones.
The first paper did not specify the foot type and only the 1st MPJ angle was the inclusion criteria. whether or not they had excessive pronation in the first place is not stated. They may have had low 1st MPJ and a valgus f/foot and cavus foot. This may still result in HAV but as Prof Rothbart so correctly pointed out they may have been prescribed the entirely wrong orthosis. They may have been prescribed an orthosis that had a forefoot varus post, which might well have increased the tendency to FncHL and increased PF tension.

The second paper looked at the statistical significance of the MLA parameters but not the clinical significance. If a small change in MLA length or height resulted in a large change in PF stress then this may be significant. PF stres and strain was not investigated.

There are too many variables not included in these studies. To draw conclusions about the relationship of orthoses or MLA height to HAV is spurious in my opinion.

Cheers Dave