Biomechanical challenges - a new model (or just an old one revisited??)

Paul vested interest extends beyond the financial. I suggest you re-read your comments here and then explain to me how you perceive yourself as having no vested interest. Any thoughts on that critical evaluation?

I take your point, but I was hoping for something rather more exciting than what can be paraphrased as "you need to diagnose the condition before you can find out what caused it". I can diagnose a hallux valgus, but that doesn't mean I could tell you what caused it. I could provide several hypotheses though.

Going back to your case examples, how do you know the cause of the conditions following ultrasound? Answer: you don't, but you can hypothesise using biomechanical theory.

Agreed.

A great point. On X-ray we see lots of heel spurs which are asymtomatic- should we be treating these? Paul intimated that resources are finite, in the UK this is exemplified by NHS services, should we now start throwing resources at asymptomatic conditions just because our imaging studies find anomolies?

 

simon, i didn't realise there was such 'oversensitivity' (http://www.thefreedictionary.com/oversensitive) and if you are quoting wikipedia, which is not your usual "top form", how about this
"..... to today, when the word has become so entrenched that few Australians and New Zealanders see any reason to avoid using the word, some even justifying the use of the word as being 'endearing'. In December 2006 the Advertising Standards Board of Australia unanimously ruled that the word "Pom" was a part of the Australian vernacular and was largely used in "playful or affectionate" terms. As a consequence, the board ruled that the word did not constitute a racial slur and could be freely used in advertising ..." (http://en.wikipedia.org/wiki/Alternative_words_for_British)

pom: short for pomegranate the skin colour usually worn by recent immigrants / tourists from england after a few days in the aussie / nz sun
....... and that "egocentric descendents of criminals", sounds like a pommy bastard to me!

 

What real benefits would a diagnostic ultrasound machine give in private practice?
Do you think that this is something that Podiatrist's NEED?
Would it change our treatment options?
FOr example in a case of plantar fasciitis -
Do you think that we need to differentiate between attinuation, fibrosis, nodule formation? WOuld it change our treatment options and more importantly the OUTCOME?

 

Hi Simon,

Thanks for these comments. I'm simplifying this some what. A more expansive article is provided in "Theories of musculoskeletal injury causation by SHRAWAN KUMAR in ERGONOMICS, 2001, VOL. 44, NO. 1, 17 ± 47".

No one is suggesting this at all. The US investigations will, and do, identify and distinguish between both symptomatic, and asymptomatic diseased and normal structures. You can identify attinuated and symptomatic structures, ie FDL tendon pathology, with inflammation (oedema is the critical idetifying feature) and without ie (ATF ligament instability and attinuation) which is asymptomatic (two examples in our data base). Obviously, the vast majority of cases we see typically have symptoms associated with the presenting complaint.

Regards

Paul

 

Sounds like very interesting stuff indeed!
I am particularly interested in the progression of these forefoot problems.
Are the asymptomatic diseased structures waiting to become symptomatic, or have they been symptomatic and progressed through this (possibly healed).
I guess the example of a flexor plate tear would likely be the clearest example where you might see this- can it be managed without surgery if completely ruptured??? I believe this is a relatively recently described pathology (I can't remember it being mentioned in university... but I can't say I remember all of university )- but it is not a new pathology.
In the past, these subjects may not have been recognised, but may have got better- do they always have a ruptured flexor plate? This should be still be apparent on u/s... perhaps it heals up?
I will have access to high quality u/s, c/t and mri...(hospital is yet to be commissioned)... hmmm possible research??? Other ideas welcome

 

Mark note how it is quoted that "few Australians and New Zealanders" see a problem with this. Hmmm. If you read the article those that object to it are those who are the target of it, not those using it - surprise surprise. For a long time none of the white South Africans could see any problems with apartheid, those who protested were "over sensitive" and were dealt with. So that meant it was fine.

Lets start making judgements on people by the colour of their skin. Begining to sound like a racist to me. Not your usual "top of the form" Mark. I think we should agree to disagree on this Mark as this is not the place for this discussion and we have both revealed our colours on this issue.

 

yep, we've definitely on the wrong forum for this discussion, all the best, mark c

 

I don't think its quite the same to compare a term related to the colour of skin following sunburn to apartheid. Being sunburned means you are stupid and therefore ripe for mockery.

Patient: Docter help, my hand is sore and red

Doctor: What did you do?

Patient: I stuck it under the grill for ten minutes and now it hurts like F***. I know they say its bad for you and causes skin cancer but i put cream on and everything and it still burned. I did the same thing for the last four years and the same thing happened then.

Doctor: Put some aloe on it. See you next year.

I love watching those travelators at airports where people go out pasty pink and come back vivid red. I always wonder if they just go round the corner, get dunked in oil and come straight back, kinda like a dougnut machine.

Personnally i'm not offended. But i would be glad if y'all would leave the whole cricket thing alone. You won, we suck, quit gloating. I'm trying to form some protective amnesia and you're not helping.

Regards
Robert

 

my lips are sealed ..........

 

LOL, Ha Ha, you guys crack me up with this crazy banter.

But picking up on the last point by Craig re Forefoot etc, plus Hylton Menz's comment in a similar thread on US inverstigation of Pl fascia Rx with steriods "Plantar fasciitis treated with local steroid... , the ff is an extremely complex structure and much of the Rx success is linked (see Hyltons thread) to accurate management of the stressed structure........hence the finding that US guided injection provided much better success rate and outcomes. We are currently running a study on similar lines (US guided injection). The finding will (hopefully) be presented in Hobart this May 2007.

 

What you are finding on US is the same we find when viewing MRI scan results. These tests often give us numerous "abnormalities", with some of them being significant and some not, relative to the pathology we are treating. Even with these tests, we still often can't arrive at a good diagnosis, but all the extra information certainly helps in most cases. Hands-on clinical testing can tell you more about the pathology than either US or MRI. The problem is that very few clinicians know how to perform or use these tests effectively.

Back to your earlier posting, I am still interested in your example of the two patients with sub 2nd metatarsal head pathology. How did you know that one of the US findings indicated shearing stress and the other did not? Is there any evidence, to your knowledge, of your contention that the plantar plate tear was not caused by shearing stress or that the other patient's pathology without a plantar plate tear was caused by shearing stress?

Also, Paul, is it common practice to perform plantar plate repairs in your country for patients who do not have digital deformities or who have not had a trial of conservative therapy? Do the surgeons you work with at your facility also go in and surgically repair all tears of the anterior talo-fibular ligament after ankle sprains? If a patient in the States had a US-confirmed diagnosis of a plantar plate tear but had no digital deformity, no treatment with orthoses, icing, and plantarflexion taping, but had a surgical repair that eventually caused a painful plantar scar, the surgeon would likely be liable for malpractice. How much conservative care did your patient have (that had the plantar plate repair) before surgery was performed?

 

Hi Kevin, Thanks for the above comments, and your touching on an important point. Re the hands-on vs US or MRI, this is not the case in our situation. Its actually the opposite. This is becasue we use the US "real-time" and in a dynamic examination method, meaning we do our physical tesing and examination, while we observe the structure/s of interest. Its absolutely phenominal the difference this is making. The immediate feedback is incredible. At a conference in NZ a couple of months ago, we demonstrated this in a neuroma case (talk to one of Australia's top pods Simon Bartold about this, the poor guy). The audience could clearly see the lesion with real-time US, while observing the clinical examination simultaneously and the Muldners compression test being performed. The lesion moved (popped) while the patient grimaced (much to the delight of the audience). A simple example I know, but equally applicable to the dozen or so FF pathologies we are distinguishing on a regular basis.

You cant do this with MRI. Static US images (the norm for most refering clinicians) are extremely limited in their value, in my opinion. Dynamic observation is completely different. A world apart.

This is very much the essence of the soft - tissue model. With our real-time US studies we are finding and distinguishing between (just in the second met head region alone);

2nd MPJ Capsulitis
Plantar fat pad inflammation
FDL attenuation
FDL tendonitis and synovitis
FDL rupture
Bone avulsion at capsular incertion to Prox Phalanx
Bursae
Neuroma (in the inert-space)
EDL tendonitis and synovitis
plate tears
plate ruptures in isolation, or in combination with some of the above
haematoma

All of these structures have their connective tissue organised in a particular way, to perform particular functions. It seems the pathology results from stress (this is on a spectrum) being applied to specific tissues, and them failing accordingly. As we know, the risk factors are many and varied, and it may only take a one off episode (twist) to initiate irritation to the fad pad, which is subsequently irritated by activities of daily living. i.e don't need a complex biomechanical model to explain this scenario.

So, correct attributable risk is essential, and not to confuse this with observations (in my mind) of "associations", ie medially deviated STJ axis, or some other anatomical malalignment scenario (FF varus as it was refered to in the old days). This is why I would advocate the soft-tissue model, and think more emphasis needs to be placed on identifying the pathology, so this can be more readily appreciated.

Interesting, but I'm a bit confused by the comment (too many ideas in one statement).

Quick, appropriate, affordable and ethical care is what we would do. It's dependent on so many factors, but implementing a barrage of treatments & investigations (when not appropriate) says more about a lack of confidence in knowing whats going on , ie trial and error. Joe Montana had spine surgery back in the 80's and was back on the field in weeks. The answer is, it depends on the circumstance.

Regards

Paul

 

Paul,

Let me make it simpler. What types of conservative care and for what duration did the patient with the plantar plate tear have before the surgery was performed to repair the tear?

 

Kevin

In Australia it is the norm to try:

* taping the toe in a rectus position for 6 weeks +
* stiff soled shoe / post operative sandal +
* foot orthoses with dome to 2nd MT head to encourage plantarflexion of the toe

Lateral drift (Sullivan's sign), hammertoe deformity and peristent capsular pain unresponsive to a decent period of conservative care (as above) will often indicate a surgical referral.

Most commonly, direct visualisation of the tear and delayed primary repair with non-absorbable suture is performed for chronic cases. Like all foot surgery, a decent period of conservative care is always attempted in Australia, as in the USA - as failure to provide/attempt a range of conservative measures is a medicolegal nightmare waiting to happen.

LL

 

Thanks Lucky for identifying the standard of care. The impressive thing in this example was that the US demonstrated a frank rupture/tear. Even with/without minimal digital displacement, this is pretty much the "How long is a piece of string?" argument. It helps if you can at least see the string.

Regards

Paul

 

Kevin has asked Paul several times:

Paul replied:

Which doesn't really answer the question. I can sense Kevin's frustration building along with my own here. So I too will make it simple. Why can't you just be honest and say that you don't really know? Any thoughts on the critical analysis I asked about?

 

Lucky (I don't like calling you this because your comments deserve a real name):

The standards you list for Australia are very similar to what the standards are for the States. Regardless of whether a plantar plate tear is present or not, it is always in the patient's best interest to attempt conservative treatment before offering surgery since many patients with small tears end up becoming asymptomatic with appropriate conservative care.

 

Interesting discussion.

The above illustrates the difference between knowing the cause and knowing the diagnosis. A large number of those diagnoses listed above could be caused by high loads on the 2nd MPJ. Treatment is to reduce the load on the 2nd mpj. Paul, I think you have oversimplified Kevin's approach. It seems, from other comments, that you would think that Kevin would try to explain overload of the 2nd MPJ with subtalar joint rotational equilibrium theory. I don't want to put words in Kevin's mouth, but I certainly think that the tissue stress approach to foot ailments does not always have to involve the STJ. The approach that Kevin and I share is when there is stress on an anatomical structure you should reduce that stress to allow it to heel. This is not new either. Dudly Morton described 2nd metatarsal overload a long time ago. The relatively long 2nd metatarsal can lead to high loads of the 2nd which can then lead to most of the problems listed above.

The question becomes, in how many of the diagnoses above does reduced force on the 2nd metatarsal head provide an an increased rate of healing? I would bet it would be most of them. The reason that I feel confident about this is the tissue stress theory. In the tissue stress theory you try to reduce stress on the injured anatomical structure. Some of the time adding supination moments to the subtalar joint will reduce stress on a structure.

Cheers,

Eric Fuller

 

Hi, thanks for these three comments (Simon, Kevin & Eric), and I'll address them individually. To "simplify" this down to a singular "causal" factor ie "shear yes/no" is just too simplistic in my view. From an epidemiological and scientific approach, we know the complex and multi-factorial nature of attributal risk factors, and their inter-relatedness. "Shear forces" occur with each and every step (as do a myriad of other stress & strains for which the foot is so well designed to manage) , so to simplify this down to the only issue of significance really fails to take account of the other (as I've contended all along), probably more significant contributory risk factor. Re the critial analysis, the literature is replete with examples of the above point. A good place to start is the text "Epidemiology, An introductory text for medical and other health science students" by David Christie et al.

I hope this reply helps to communicate my perspective a little clearer, as the intent is definately not to frustrate.

Regards

Paul.

 

Hi Kevin, I agree with all the comments here but I'd put a disclaimer on this statement......"only if it is warrented". Conservative care, if a realistic option, should be offered in the first instance. It may however, not be what the patients wants, or they feels is best for them. I'm sorry I getting off the topic with this reply, but where the diagnostic US is helpful is in differenciating, though visualisation, the extent of damage & prognosis, somethis that can't be easily achieved through clinical exam alone.

Regards

Paul.

 

Hi Eric,

Thanks for your reply and comments.

Not at all, and I apologies for that impression. One point you make however is the statement ...."A large number of those diagnoses listed above could be caused by high loads on the 2nd MPJ". I disagree with this concept, and would suggest varying "loads" in the area may be associated with symptom exacerbation, but causation can only be established if it meets the appropriate scientific criteria. As I seen the potential in the above cited examples, the patient may have had a "one off" causative event, ie a twist injury, hyper-extension of the MPJ etc which precipitates the pathology. Normal walking (not "pathomechanics") exacerbates the problem, but is not in effect the causal factor. Its an associated factor.

I certainly agree with you on this point.

My view as well.

And it could be equally argued that through plaster casting and immobilsation, all will get better, but that's not what we do. The diagnosis is critical, and needs to be viewed in combination with analysis of relevant "risk factors" and not limited to biomechanical, but focus on the relative risk associated with other know causative (from research) factors such as obesity, poor footwear, secondary muscle imbalance, one off tissue stress etc.

An interesting discussion,

Regards

Paul.

 

Here’s my 2 cents…

Paul’s original comments:

Of more recent time (mid 2006) QUT podiatry clinic has acquired a high definition ultrasound machine, which is providing us with remarkably incite into foot pathology. This system, when used real-time, is providing so much more diagnostic value that ALL the foot biomechanics theories combined. The long known difficulty in establishing a cause-effect relationship (using most biomechanical models) may have, in my opinion, proved to have been more of a "distraction" to the profession than it has been "worthwhile".

Just examining the forefoot alone (in 70 cases) we have identified 15 clear and unequivocal diagnosis of "disparate" foot pathology (hardly explained by singular biomechanical models - i.e. the oversimplified approach). The evidence is "black - (oedema) and white - (connective tissue).

Reminds me of a saying that goes something like “If all you have is a hammer, everything looks like a nail”.

I work in a running injury clinic and see plenty of FF pathology. How often would I ultrasound these patients? Hardly ever. I couldn’t agree more that you must first make a diagnosis before beginning treatment. However, if I’m ordering investigations for patients, I always think ‘how is this going to change the treatment I offer?’

As LL said:

As an eccentric DPM whom you know well would often say in class, "make the diagnosis, and treatment will take care of itself".

I think that same DPM also taught us to treat the patient and not the x-ray (or in this case the ultrasound).

 

Hi Kent,

Nice to hear from you. The forefoot examples cited above are purely for illustrative purposes only. The focus of the discussion is on the soft tissue model of disease, understanding causation, the limitation of existing models of biomechanical explanation of causation etc.

Regards

Paul.

 

Paul:

Here is what you wrote earlier:

I guess I am confused since you first said that the patient's "diffuse translocation of the collagen fibre matrix" indicated shear forces, which you contend are only determined by your US examination. Then you next said "To "simplify" this down to a singular "causal" factor ie "shear yes/no" is just too simplistic in my view."

So here are my questions to help clarify my understanding of what you are saying:

1. Do you or don't you think that the patient that did not have a plantar plate tear but had a "diffuse translocation of the collagen fibre matrix" had an injury caused by shear forces as you first indicated?

2. Do you think it is possible that your different US results in the two patients you described could indicate differences in the tissue characteristics in the plantar 2nd metatarsal head area between the two patients rather than what you describe as "two different causal mechanisms"?

3. How much would you charge the patient extra in a private practice situation to perform these ultrasound diagnostic tests that you are so excited about?

4. How much do these units cost?

 

Paul, like Kevin I'm a litttle confused for the reasons Kevin has outlined above. It seems initially you were confident in both identifing the injured tissue and the direction of mechanical force which caused the injury, now this is "too simplistic" ????? Also:

Paul, this isn't what I have been asking for. I was interested in the critical analysis of diagnostic ultrasound.

So if I may add to Kevin's list of questions:

1. What data do we have on the sensitivity, reliability and repeatability of this technique?

2. It has been noted in the literature that ultrasound is unable to detect whiplash injuries due to the anatomical relationships of the vertebrae, what aspects of the anatomy of the foot may create similar problems?

3. Can you list any musculoskeletal pathologies which would not be picked up on ultrasound?

4. What is the difference between the type of ultrasound you are advocating and power doppler ultrasound? Can these both be used for musculoskeletal examination and pathology identification? Which is better?

5. What potential problems are there with this technique?

 

paul b ............. THE SHARKS ARE CIRCLING!!!!!!!! ................ TOO LATE TO BAIL OUT ...... better luck next reincarnation

 

Perhaps my emphisis has been more on treatment rather than diagnosis. Reduction of force on the 2nd met head and MPJ could be shown through research to speed healing in each of those pathologies listed. Which goes to the other point, does the Ultrasound change the treatment?

Now we are talking correlation and not causation. How does obesity, or extra fat around the abdomen, cause a tear in the plantar plate. Maybe we are using a different definition of cause. Obesity could cause relatively higher loads on the 2nd met head and MPJ. Additionally poor footwear, muscle imbalance could also cause high loads on the 2nd Met/ MPJ. What is the mechanism that explains why the risk factors stated above show correlation with plantar plate tears?

From reading your posts I got a sense that you were saying, (but I'm not sure) "how can we really be sure we know anything". Well that is why we propose theories to explain why something happens. A good scientist should be willing to discard (or modify) a theory in the face of good evidence to the contrary. If you showed me a study that obesity causes plantar plate tears, I would want the follow study that showed that obese people did not have different levels of stress at the 2nd Met/MPJ than non obese people. Then you could attribute the tear to obesity and not tissue stress. Then you would have to come up with a theory on how fat cells weaken collegen or something.

Cheers,

Eric

 

You know, pretty much every one of my patients have treatment at the top of their lists of desires.

 

Cavanagh et el produced some excellent work on this, and only 12% of variability in plantar foot pressure could be explained by increases in BMI. So, while obesity does increase the force beneath the met heads, it only does so marginaly. This, like you allude to above, demonstrates the likely multifactorial nature of the event scenario (ie need stressors combining to produce the outcome).

Paul

 

No No No Mark. I'm not too frightened. Much more dangerous fish called "blow fish" live in Australian waters.

PB

 

Re Q1. The plate plate, in that case, was fully in tack. The fat pad and surrounding collagen/soft tissue showed subtle oedema. Have a look at Peter Brukners new text clinical sports medicine 3rd edition page 598 has a great series of images which illustrate the disorganisation to collagen.

re Q2. The answer is yes and no. The design of the collagen matrix, and componentary (type type I, II, III, IV with varying amounts of elastin) is very dependent on the structure/function of the tissue, ie so the fat pad has a diferent structure/function when compared with the plantar plate, so it's probably different forces at play.

re Q3. In Australia, ustrasounds for MS work are about $100 per investigation. But the real value, as I see it, is as a clinical adjunct to physical examination, and guiding the clinician in terms of thinking about (a) what structure - specifically, is damaged and (b) why this has occured.

Re Q 4. The units vary from $15K second hand to $35K new (for higher definition). The top of the line systems (currently overkill in clinical podiatry, but useful in radiology clinics) are up around the $250K mark.

Regards

Paul

 

Re Q1. Simon, there are books and books and books written on this topic. A quick search will produce this information, if you have the time and interest.

Re Q2. Not sure, but we have identified hyper-echoic signals that identified small avulsion fractures missed on x-ray, lateral confirmed on open correction.

Re Q3. I'm sure there are, but in my reading of the literature, there seems to be far more indications (particularly with bone), than I'd first anticipated. Thinking these are soft-tissue instruments. Again, the big guiding factor seems to be the very, very small amounts of oedema that are being picked up on US.

Re Q4. Not sure on this one, other than the power dopper includes vascular visualisation capacity. Nice if you can afford it. I'm familiar with the higher def musculoskeletal US imaging systems.

Re Q5. Good question. I'm paranoid the head (transducer) will get dropped. These cost about $8K, so that would be an expensive mistake.

Regards

Paul.

 

Paul:

Thanks for the answers. What does an office visit cost in Australia?

It sounds like the ultrasound exam is not cheap and would add significant cost to the patient visit. How much time does the exam take in your hands, for example?

Do to the relatively high price, it sounds like US may be something that I would be interested in using in patients if they did not respond to initial conservative therapy attempts or had an obvious soft tissue tumor that needed immediate diagnosis. Is that what you recommend also considering the cost to the patient, the time it takes for you to do an exam with the US unit, and that many soft tissue injuries in the foot may be treated successfully without the relative expensive of diagnostic imaging techniques?

 

Paul I have performed searches in the usual sites, all I could come up with for systematic reviews of diagnositc ultrasound in musculoskeletal medicine was:

Seminars in Arthritis and Rheumatism
Volume 36, Issue 2, Pages 99-108 (October 2006)

Power Doppler Ultrasound in Musculoskeletal Disease: A Systematic Review

Fredrick Joshua, MBBS, FRACP?, John Edmonds, MBBS, MA, FRACP†, Marissa Lassere, MBBS(Hons), Grad Dip Epi, PhD, FRACP, FAFPHM‡
Objective
To evaluate the performance characteristics of power Doppler ultrasound as a diagnostic and monitoring tool in the assessment of musculoskeletal disease through a systematic review of the literature.

Methods
Search Strategy: We performed a literature search of PUBMED (1966 to June 2005). Selection Criteria: Only original research reports written in English involving musculoskeletal disease and power Doppler ultrasound were included. Reviews were noted but not included. Data Extraction/Reporting: The design, subjects, methods, imaging protocols, and performance characteristics studied in the research papers were reported.

Results
Of 3568 identified reports, 139 involved power Doppler ultrasound of the musculoskeletal system. Fifty-three of these reports met the inclusion criteria. Ultrasound machine settings were specified in 63% of reports. Rheumatoid arthritis was the most commonly studied musculoskeletal disease (64% of papers). Validity was the most studied performance characteristic (94% of reports), while reliability and responsiveness were studied in 17 and 34%, respectively.

Conclusions
Although the majority of research reports of power Doppler ultrasound assessment of the musculoskeletal system evaluated validity, less than half reported reliability and responsiveness. Further work is needed to evaluate power Doppler ultrasound assessment of the musculoskeletal system before it can be used to guide clinical decisions or be used as an endpoint in clinical trials

Hence question 4. Perhaps you'd be good enough to offer a couple of references to those books you mentioned. Just to get me started.

Thanks for your honesty in saying that you are not sure. I'm not sure of the relevance of the above in relation to my question here. But since you draw comparative with X-ray here: Is there any pathology that would be picked up on x-ray but missed by ultrasound?

OK let me ask a different way. Are there times when you suspect a pathology and send for diagnostic imaging other than ultrasound?

See above.

Again, not really what I was asking. I meant in terms of the patients/ practitioners health and well being.

 

Kevin, I refer patients to a fully qualified ultrasonographer. Often it is the patient themselves that request this, but sometimes when the patient has an unusual presentation, I'll send them up to rule things out as much as rule things in. She charges £50 and sends back a report with her findings.

I am yet to have changed a managment strategy on the basis of one of these reports. To date my initial diagnosis based on a good old fashioned history and physical has been pretty much on the money and accurate in all of the cases, hence my initial treatment plan has not needed to be modified.

My view- it's useful in the same way that any imaging is useful- for some of the people some of the time.

 

Simon / Kevin,

These are valid points and we share a similar view. Perhaps one of the biggest differences might be the environments we work in. I’m at a university educational facility, with UG and PG podiatry students. I find it is "adjunctive" to their learning and understanding of foot pathology. It has improved my respect for the subtle differences in structures damaged, extent & amount of pathology, tissue re-organisation, collagen/elastin structure fn etc. I'm finding about 10 times more indication to use US over X-ray (bare in mind we've only been using this system for about 12 months now). Of course there are indications for all imaging techniques, but most are expensive, use ionising radiation, are invasive, or unavailable for typical in office use. It's not been until recently the quality of US technology would have, in my opinion, warranted serious consideration for more routine use (I've been monitoring this for about 8 years now). It's biggest signal advantage is its ability to identify very subtle areas of oedema, and associated tissue damage that simply are unidentifiable (with the level of precision that real-time imaging offers that needed).

Re sending out for and evaluating static US.........I still wouldn't do it for the same reasons Simon suggests, so I know where he's coming from.

Regards

Paul.

 

Paul:

As far as tissue stress is concerned, I am still not convinced that just because one plantar plate is ruptured and one is not, when comparing two patients with sub 2nd metatarsal head pain with your high definition US unit, that one can be so certain that one injury is caused mostly by shearing forces and one injury is not.

Unless you are certain that there has been single traumatic event that would indicate a certain type of internal tissue stress occurring, one can not be so certain of what type of tissue stress caused the injury in all cases. This is because one can not assume that all individuals will possess the same tissue thickness and the same elastic modulus (i.e. stress-strain curve) of tissues that would either tend to increase or decrease the likelihood of certain types of injuries occurring at a certain anatomical location in the foot/lower extremity.

Do you agree or not?

 

To simplify, let's use another example, exact same location and clinical history as previously described. The patient, on US investigation, demonstrates attinuation of the EDL tendon sub 2nd. We've seen this on US, but could not clinically distinguish it, without US. Would you be suggesting this is a result of shear forces, or force in the same axis as the collagen which has resulted in the tendon injury? The key is knowning what structure was stressed (ie fat pad v tendon). The US provides this.

Regards

Paul.

 

I would be worried if the EDL tendon was plantar to the 2nd metatarsal head. Can't you just answer my question or are we going to going around in circles endlessly on this matter??

 

Who said they were static?