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Peripheral Vascular Diagnostic Tests

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  #1  
Old 13th April 2008, 06:00 PM
Asher Asher is offline
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Default Peripheral Vascular Diagnostic Tests

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Hi there,

When a patient presents with concerns related to what I suspect is due to an aspect of peripheral vascular disease, I generally do an audio doppler assessment and refer back to the GP for further investigation and advice. Frequently this goes no where because either the GP is too busy (significant shortage here), doesn't care or the patient can't be bothered travelling to the capital city to take it further.

I thought that I could probably be of more use to the patient by doing some tests (that I haven't done since my uni days) and that this might also give the GP more impetus to do something about it.

So I've read up on peripheral vascular disease and in particular, the arterial insufficiency diagnostic tests of:

ABI - determines if there is any blockage by comparing the systolic pressure of the bracial pulse compared to the posterior tibial pulse. But need to be aware of vessel calcification which will distort reading (correlate with doppler sounds). 1.0 or more indicates no organic disease (atherosclerosis); 0.5-0.8 indicates one primary arterial occlusion somewhere between heart and ankle; less than 0.5 indicates multilevel occlusive disease.

Elevation-Dependency Test - Used to determine if occlusion somewhere within the lower limb. Normal is no pallor on elevation (elevation for 1 minute) and no erythema on dependency. Pallor on elevation indicates occlusive disease. If erythema is noticed on dependency, occlusive disease is mild to moderate. If no erythema, occlusive disease is severe.

5-Minute Postocclusive Reactive Hyperemia Test - Is used to determine if there is an obstruction to arterial supply to the foot, whether it is organic (atherosclerosis) or functional (vasoconstrictive disorder), gives an indication of the maximal flow that can enter the foot and takes into account the adequacy of collateral flow. Without going through how to do it, the results are:
Normal- instantaneous and uniform colour return to foot with maximum erythema within one minute and also uniform.
Functional disorder - uniform but slightly delayed (5-8 secs) colour return to foot, maximal erythema occuring between 1-2 minutes and it is marked!
Organic disease - non-uniform delayed (more than 15 secs) colour return to foot. Maximal erythema occurring after 2 minutes or not at all.

Are these tests still relevant today? I'm sure the ABI is as I have read the relevant threads on Podiatry Arena, but I haven't heard of the others since uni (15 years ago). I remember reading some time ago that the SPVPFT test is no longer used. Are there better tests that I could be doing?

Thanks in advance.

Rebecca
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Old 14th April 2008, 11:45 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Rebecca

Certainly in the UK, GPs seem to respond ABPI results - I think this is because it has a reproducible, numerical value that they can use on correspondence to Vascular Dept, who then would generally perform a duplex scan to determine the positioning of the blockage. I think to get a true reading, you are supposed to have the patient lying down for approximately 30 mins or so before the test to equalise the BP?! I hope someone will confirm or correct me....?

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Old 14th April 2008, 01:59 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Asher:

I think what you want to do is a very good thing.

Your ABI index is certainly a start on those patients that have clinical findings suggestive of PVD.
If you have a doppler, you may want to acquire some advanced training in reading and interpreting doppler waveforms (although yours may just be audible - you may need to invest in a different model)

Gotta run

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Old 25th April 2008, 12:10 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Asher

Steve mentioned interpretation of doppler waveforms which is a subject I have found suprisingly difficult to get adequate information about and properly understand.

Recently I found a great text which covers haemodynamics of most recording devices, both direct and indirect, explores chronic, acute occlusive and vasospastic arterial and venous insufficiency and thrombosis. Instrumentation covered includes CW doppler, spectrum analyser, air plethysmography, PPG, reactive hyperaemia, venous reflux testing etc. It contains info on measurement artifacts, interpretation pitfalls and limitations and case studies.

Even has a mail in CME credit MCQ exam

check it out, it gets 5 stars from me as a practical guide to what and how the technology measures and how the measurments should be interpreted.

hope this helps

cheers


Martin

http://www.unetixs.com/phys_book.html

PS (I am still working on the math thing in my minimal spare time!)

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Old 27th April 2008, 06:19 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Hello again,

I've read a lot recently about the excellent sensitivity and specificity of the ABI in predicting peripheral arterial disease (PAD). And that the toe brachial index (TBI) should be used when calcification of the tunica media of arterial walls is suspected (eg: diabetes, severe renal disease and very elderly) as calcification has much less impact on arterioles of the digits. But I am having trouble finding consensus or details of any kind of what the TBI value actually indicates - this is quite definitive with the ABI value.

Is the TBI 0.20 below the ABI value as has been suggested to me by a colleague?

Any advice or direction would be appreciated! Thanks.

Rebecca
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Old 27th April 2008, 06:31 AM
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Default Re: Peripheral Vascular Diagnostic Tests

PS: I've ordered that book Martin, thanks again.

PPS: Is there anyone that has the Hadeco Smartdop 30EX and uses all of its arterial and venous assessment capabilities - what are your thoughts / experiences with it?

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Old 29th April 2008, 10:19 PM
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Default Re: Peripheral Vascular Diagnostic Tests

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Originally Posted by Asher View Post
Hello again,

I've read a lot recently about the excellent sensitivity and specificity of the ABI in predicting peripheral arterial disease (PAD). And that the toe brachial index (TBI) should be used when calcification of the tunica media of arterial walls is suspected (eg: diabetes, severe renal disease and very elderly) as calcification has much less impact on arterioles of the digits. But I am having trouble finding consensus or details of any kind of what the TBI value actually indicates - this is quite definitive with the ABI value.

Is the TBI 0.20 below the ABI value as has been suggested to me by a colleague?

Any advice or direction would be appreciated! Thanks.

Rebecca

Hi Rebecca, you are right - TBI is very useful for digital peripheral vascular disease, however the costs of the complex machinery and equipment to take proper TBI using a "toe pressure cuff" is obscenely expensive. A great test but not so practical for a podiatry clinic!

Let me know if you find a cheap one :-)
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Old 30th April 2008, 06:51 AM
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Default Re: Peripheral Vascular Diagnostic Tests

I have to disagree with you.

A bidirectional doppler with PPG and printer can be bought for around $2400 in Canada which is not a place renounded for cheap medical equipment, this will have virtually no running costs and likely last decades. How else can you make good decisions regarding safety of doing digital surgery on and evaluation for foot related risk factors on your DM patients without one?


here's a study to stimulate some thought and discussion if anyone is up for it

An Evaluation of the Efficacy of Methods Used in Screening for Lower-Limb Arterial Disease in Diabetes
Dean T. Williams, MD, Keith G. Harding, MD and Patricia Price, PHD
Wound Healing Research Unit, Department of Surgery, University of Wales College of Medicine, Cardiff, U.K.



http://care.diabetesjournals.org/cgi.../9/2206?ck=nck



cheers

Martin

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Last edited by Mart : 30th April 2008 at 10:07 AM. Reason: added url for study
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Old 30th April 2008, 04:45 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Martin,

Quote:
Originally Posted by Mart View Post
I have to disagree with you.

A bidirectional doppler with PPG and printer can be bought for around $2400 in Canada which is not a place renounded for cheap medical equipment, this will have virtually no running costs and likely last decades. How else can you make good decisions regarding safety of doing digital surgery on and evaluation for foot related risk factors on your DM patients without one?


here's a study to stimulate some thought and discussion if anyone is up for it

An Evaluation of the Efficacy of Methods Used in Screening for Lower-Limb Arterial Disease in Diabetes
Dean T. Williams, MD, Keith G. Harding, MD and Patricia Price, PHD
Wound Healing Research Unit, Department of Surgery, University of Wales College of Medicine, Cardiff, U.K.



http://care.diabetesjournals.org/cgi.../9/2206?ck=nck



cheers

Martin

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I agree, that is a good paper. Another good one is by Brooks et al called TBI or not TBI: That is the question (2001). This paper investigates, among other things, what TBI value equates to each ABI value. The ABI is a very sensitive and specific test, except when arterial calcification exists, in which case the TBI is used. The agreed upon ABI values for degrees of PAD are:

0.91 or more = normal
0.71 – 0.90 = mild PAD
0.41 – 0.70 = moderate PAD
0.40 or less = severe PAD

Brooks et al found that there was about a 0.4 difference between the ABI and TBI.

ABI v TBI Interpretation
Elevated ABI>= 1.30 > TBI= 0.94
Normal ABI>= 0.90 to 1.30 TBI > 0.54 to 0.93
Reduced ABI< 0.9 TBI<= 0.54

So the magic 0.90 ABI value (below which denotes PAD) is equivalent to a 0.54 TBI value. The problem is, I can't find any paper that has attempted to confirm or refute these numbers, or any paper that actually uses this TBI value as the cutoff value. I have found TBIs of 0.60, 0.70, 0.75 and others used.

In fact, the Williams et al paper, which I believe is well thought of, use a TBI of 0.75 as the cutoff for PAD but with no reference as to where they got this number from.

Any ideas?

Rebecca
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Old 30th April 2008, 07:10 PM
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Default Re: Peripheral Vascular Diagnostic Tests

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Hi Martin,



I agree, that is a good paper. Another good one is by Brooks et al called TBI or not TBI: That is the question (2001). This paper investigates, among other things, what TBI value equates to each ABI value. The ABI is a very sensitive and specific test, except when arterial calcification exists, in which case the TBI is used. The agreed upon ABI values for degrees of PAD are:

0.91 or more = normal
0.71 – 0.90 = mild PAD
0.41 – 0.70 = moderate PAD
0.40 or less = severe PAD

Brooks et al found that there was about a 0.4 difference between the ABI and TBI.

ABI v TBI Interpretation
Elevated ABI>= 1.30 > TBI= 0.94
Normal ABI>= 0.90 to 1.30 TBI > 0.54 to 0.93
Reduced ABI< 0.9 TBI<= 0.54

So the magic 0.90 ABI value (below which denotes PAD) is equivalent to a 0.54 TBI value. The problem is, I can't find any paper that has attempted to confirm or refute these numbers, or any paper that actually uses this TBI value as the cutoff value. I have found TBIs of 0.60, 0.70, 0.75 and others used.

In fact, the Williams et al paper, which I believe is well thought of, use a TBI of 0.75 as the cutoff for PAD but with no reference as to where they got this number from.

Any ideas?

Rebecca
Hi Rebecca

My read on this is as follows;

The Gold standard to evaluate peripheral vasculature non invasively is to directly examine vessels with Color duplex imaging (CDI). Few podiatrists have the skills to do this, though it might be fun to do, we are not going to be able to act on this kind of detail and most vascular surgeons are going to want to see an arterogram anyway before making any decisions.

Williams et al study uses this standard as an index to get sensitivity, specificity and overall accuracy stats for ABPI, TPI, qualitative and quantitative waveform analysis, and pulse taking in a cohort of subjects with diabetes BUT no active foot disease, rest pain, or signs suggestive of lower-limb critical ischemia. Individuals without diabetes with and without arterial disease were used as control subjects.

The values which you notice for these indirect measurements will vary, not because they wrongly attribute a certain threshold but because they represent probability of disease actually being present. If you raise the value the sensitivity goes down but the specificity goes up and visa versa. Dont get too hung up on absolute values we are really measuring with a certain probabilty of being correct.


As podiatric clinicians we a responsible to screen our patients for risk, identify causes of problems and avoid non healing injury in our treatments.

If LEAD seems likely then refer on to vascular specialists to further evaluate our suspicions when warrented.

Although studies show pedal pulse detection has fairly good accuracy for identifying LEAD it is not as good as non-invasive vascular testing. Also if we are doing an invasive procedure and something goes wrong, having an acceptably documented indication of adequate exam is vital, I am not sure that stating that pedal pulses were palpable is really adequate.

The study concluded;
Qualitative waveform analysis was the most effective screening tool of all the methods tested in this study. In the absence of neuropathy its performance was as good as those of the ABPI and pulses, but in neuropathic limbs it was clearly superior to pulses and the ABPI with comparable sensitivity and marginally better specificity than the TBI. Our findings indicate that in the assessment of lower-limb perfusion in diabetes, the combination of pulse palpation and noninvasive assessment using the TBI or, ideally, qualitative waveform analysis provides effective screening for significant arterial disease. In practice, waveform analysis is a relatively quick test to perform and does not require application of tourniquets. However, further work is required to evaluate the feasibility of undertaking this form of vascular assessment in clinical practice.

In my experince - when performed and interpreted properly, Qualitative waveform analysis is fast, simple and gives you a hard copy to store which makes record keeping for a vascular exam unambiguous. Add this to TPI and ABPI even in the absence of any overt signs of ischaemia you are unlikely to miss much according to the study.

How else are you going to properly evaluate the peron with dependant edema or fatty ankles and no pulse, the diabetes mellitus patient with calcified vessels, or be reasonably sure that the pulse bearing foot is not one of the 10% of false negatives for LEAD?

This is why I was glad to find the text which I referred to in the earlier posting, it does a nice job explaining how to interpret the waveforms and what their limitations amount to (probe angulation and venous or collateral vessel interference being important factors).

Cheers

Martin

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Old 1st May 2008, 05:45 PM
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Default Re: Peripheral Vascular Diagnostic Tests

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In my experince - when performed and interpreted properly, Qualitative waveform analysis is fast, simple and gives you a hard copy to store which makes record keeping for a vascular exam unambiguous. Add this to TPI and ABPI even in the absence of any overt signs of ischaemia you are unlikely to miss much according to the study.

How else are you going to properly evaluate the peron with dependant edema or fatty ankles and no pulse, the diabetes mellitus patient with calcified vessels, or be reasonably sure that the pulse bearing foot is not one of the 10% of false negatives for LEAD?
Agreed, the combination of ABI, TBI and qualitative waveform analysis is the way to go.

The ABI has demonstrated excellent sensitivity and specificity. It was an eye-opener to read these stats:

Diagnostic test Sensitivity Specificity (Belch,J. et al. 2003.)
Pap smear 30-87% 86-100%
Fecal occult blood test 37-78% 87-98
Mammography 75-90% 90-95%
ABI 95% 100%

The TBI has the potential to be used in the same way, but it is not. Am I making an erroneous quantum leap by thinking that a certain ABI score equals a certain TBI score?

Unless the TBI value equivalent to a 0.90 ABI can be agreed upon, in the presence of arterial calcification, of what use is the TBI?

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Old 1st May 2008, 05:59 PM
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Default Re: Peripheral Vascular Diagnostic Tests

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Unless the TBI value equivalent to a 0.90 ABI can be agreed upon, in the presence of arterial calcification, of what use is the TBI?

Rebecca
Because ABI will be elevated with vessel calcification (loss of wall compliance at the site where you are applying the cuff) it will be meaningless other than to suggest calcification at this level.

Digit arteries are not likely to be effected by calcification therefore in same subject TPIs are more meaninful index of supply (no loss of compliance at toe cuff site).

hope that helps

cheers

Martin

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Last edited by Mart : 1st May 2008 at 06:04 PM. Reason: improve explaination
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Old 1st May 2008, 07:47 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Quote:
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Because ABI will be elevated with vessel calcification (loss of wall compliance at the site where you are applying the cuff) it will be meaningless other than to suggest calcification at this level.

Digit arteries are not likely to be effected by calcification therefore in same subject TPIs are more meaninful index of supply (no loss of compliance at toe cuff site).

hope that helps

cheers

Martin

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Martin,

I have no problem with the ABI and when it can't be trusted - arterial calcification. In which case, the TBI comes in.

An ABI of 0.90 is used to denote peripheral arterial disease. But when TBI is used, what equivalent value do we look for? Doesn't it strike you as odd that there is no agreement on this?

Brooks et al (2001) say TBI of 0.54
Orchard and Strandness (1993) and Rheeder et al 2004 use TBI 0.60
Others (personal communication) use TBI 0.70
Williams et al (2005) use TBI 0.75

Suzuki (2008) agrees saying "the cut-off values of TBI are arbitary and vary within the literature. In general ... a TBI of less than 0.5 to 0.75 is considered normal and anything below that is diagnostic of PAD." Big difference!

What's the deal?

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Old 1st May 2008, 10:02 PM
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Default Re: Peripheral Vascular Diagnostic Tests

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Martin,

An ABI of 0.90 is used to denote peripheral arterial disease. But when TBI is used, what equivalent value do we look for? Doesn't it strike you as odd that there is no agreement on this?

Brooks et al (2001) say TBI of 0.54
Orchard and Strandness (1993) and Rheeder et al 2004 use TBI 0.60
Others (personal communication) use TBI 0.70
Williams et al (2005) use TBI 0.75

Suzuki (2008) agrees saying "the cut-off values of TBI are arbitary and vary within the literature. In general ... a TBI of less than 0.5 to 0.75 is considered normal and anything below that is diagnostic of PAD." Big difference!

What's the deal?

Rebecca
Hi Rebecca

An ABI of 0.9 does NOT denote PVD . . . . . . it suggests that it is likely. Most tests are not unequivocal in their own right. They may be erroneus for many reasons including; operator and systemic error. If you use a cuff of different width, postion your probe angle differently, measure some one with vasospastic episode or cold feet, you will likely get a diifferent values in same subject.

I have not studied your references and agree that there seems a wide range of values used as threshold for TPI. That is the nature of scientific investigation - to test ideas and see what we might interpret from the evidence which may not be consistent and cause us to change our methods (hopefully).

From personal experience I can tell you that it can be difficult to get consitent values in a given subject using a PPG and toe cuff. What you are looking for is the first onset of a definate periodic waveform. Seeing this will depend on the sensitivity you set in your equipement. The volume of air present in the small cuff is relatively small and the control you have on rate of pressure change is less accurate than a large arm/leg cuff. Also the ratio of cuff width/toe diameter if probably more variable because of the smaller scale. I am not sure if anyone has studied this but I would think this introduces increased potential error compared to ABI.

So what to do?

For increased sensitivity use higher value, to increase specificity use lower threshold, personally I opt for higher sensitivity and let someone more expert decide if this warrants intervention.

If in doubt repeat measurements. Studies looking at accuracy of ABI suggest taking several readings and using the highest measured values.

Do not use a single test value in isolation, it needs to be weighted, use other tests and physical exam and Hx as parallel indicators. If I see someone with a hx of claudication pain which is consistent for a certain distance and their ABI is 0.98 I would NOT rule out ischaemic cause based on this - I would repeat test and look at other evidence.

Ultimately suspicion of occlusive artrial disease can only be confirmed by visualisation of occlusion(s) - the indirect methods we use simply give us an index of suspicion. As you have mentioned this is true of many clinical tests.

I think you will find the unetixs book helpful in getting the wider picture.

On your initial point of difficulty engaging GPs with concerns, this is something which I sometimes notice too. Developing rapport a with a vasc surgeon who gives feed back on your referals is the way to go, send a detailed report of your concerns and copy to GP.

Most important continue to think crititcally about how you practice :)

Cheers

Martin

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Old 2nd May 2008, 08:01 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Martin,

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An ABI of 0.9 does NOT denote PVD . . . . . . it suggests that it is likely.
Granted. An ABI of 0.90 provides a high level of suspicion of PAD as studies have shown the test has high sensitivity and specificity. This is not in dispute, though I should have been more clear.

Also not in dispute is the fact that ABI, TBI & qualitative waveform analysis, as a combination of tests used together, will provide good information to enable a clinician to identify patients of high likelihood of having PAD.

Again, also not in dispute is the fact that a vascular clinic will use more sophisticated and definitive methods for determining the existance of PAD.

I am trying to make a point about the fact that the TBI is not being used to its full potential, in that inspite of the best advice being that it should be used, nobody knows what a TBI actually means.

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Old 2nd May 2008, 09:47 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Rebecca

I do not understand why you seem so concerned about an absolute value.

The Index, whether it be ABI or TPI or anything else reflects a probability of detecting the condition, if it has a specificity and a sensitivity of 100% it is totally reliable but this is rare even though desirable.

I think that Williams study is good because it uses the gold standard of direct visualisation to derive its stats, I have not looked at the other studies which you cite, and it would be helpful if you could let us know if they did the same.

Williams study says this;



-------------------------------------------------------------------------------------------------------------------
Control groups.

The TBI identified all 13 limbs with arterial disease, but 5 of 21 with no arterial disease had values <0.75.

Diabetic groups.
In the groups with arterial disease, there were 15 limbs with neuropathy vs. 7 without. Mean TBI values were 0.49 and 0.58, respectively (t = 1.32, df = 20, P = 0.27). In the absence of arterial disease, of the 41 limbs with neuropathy and 25 without, mean TBI values were 0.85 and 0.82, respectively (t = –0.438, df = 64, P = 0.628). These results demonstrated that peripheral neuropathy did not influence TBI values in this study.
Of the 22 limbs with arterial disease, 2 had TBI values >0.75 (10% false-negative rate). Of the 66 limbs with no arterial disease, 23 demonstrated TBI values <0.75 (35% false-positive rate).

Continuous waveform analysis
Qualitative analysis.
In the control groups, 2 of 14 limbs with arterial disease had triphasic profiles in both foot vessels, (15% false-negative rate). One of the two limbs had a monophasic signal in one tibial vessel on CDI and no proximal disease. Of 27 limbs with no arterial disease, 1 had an absent flow in a single vessel (4% false positive rate).

In the diabetic groups, of those limbs with no detectable peripheral neuropathy or arterial disease (n = 25 limbs), 2 limbs had absent flow in a single vessel. Where flow was detected, all signals were triphasic (8% false-positive rate). However, in those limbs with no arterial disease but detectable peripheral neuropathy (n = 41 limbs), 12 limbs had at least one waveform with loss of reverse flow and 2 had undetectable flows (34% false-positive rate).

In the presence of arterial disease, the false-negative rate was 0% when any vessel waveform anomaly was regarded as indicative of the presence of arterial disease in the absence of neuropathy (n = 7). When neuropathy was present (n = 16), one limb had two triphasic signals but had diffuse atherosclerotic disease on CDI (false-negative rate of 6%).
----------------------------------------------------------------------------------------------------

That even within this study the control and the DM group had differing accuracy for all measures should make it clear that these values are not absolute. You can increase your accuracy by combining evidence from different tests and if you want to look beyond the possibilities used in this study also consider how stress testing can improve specificity.

The rational is that if occlusive disease is present a resting compensatory dilation of arteries will occur to maintain O2 supply to distal tissues. If you exercise the subject with occlusive disease there will be little or no headroom for increased supply (cause of claudication) and this is detectable with different indirect measurements. The unetixs book covers this subject nicely too.

Hope this gets you out of your bind


Cheers

Martin


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Default Re: Peripheral Vascular Diagnostic Tests

Alas, I remain bound.

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Default Re: Peripheral Vascular Diagnostic Tests

Great thread Asher (& Mart) .... so long a lot of vasc assessment has been so subjective (pedal pulses and symptoms only) amongst most of the 'rank and file' podiatrists (Yes obviously I include myself one)... I always send off a p/copy of the doppler waveform of B/tib. post. A's to the general practitioner ... they can diagnose, and I use it as a major determinant for vascular categorisation of the patient (High or Low risk) ... I don't use ABI (too invasive for me) but would DEFINITELY use TBI if available
Again, I greatly enjoy your input
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Default Re: Peripheral Vascular Diagnostic Tests

Colleagues:

Even though the paper I coauthored is fairly old, done during my surgery residency from 24 years ago, and a lot of new technology has arrived on the scene since then, the paper is on digital systolic pressure determination which seems to be a topic of interest in this thread (Kirby KA, Arkin DB, Laine W: Digital systolic pressure determination in the foot. JAPMA, 77: 340-342, 1987).

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Default Re: Peripheral Vascular Diagnostic Tests

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Alas, I remain bound.

Rebecca
Hi Rebecca

Nooooooooooo. . . . . . . . . . lets continue this thread after you have had a chance to read the unetixs book, I think that will put us on the same page, particularly understanding the inherant measurement issues with using CW dopper and PPG.

It is important to know that the dopper frequency shifting measured is the sum of all the flow within the reflected beam path, and therefore quite important also to select the appropriate frequency probe for the depth of the vessel - higher frequency = better selection but less penetration. This will reduce artifacts caused by picking up signal from adjacent veins, collerateral or unusually tortuous vessels etc.

PPG which is usually used for TPIs also has potential errors associtaed with contact, motion artifact, temperature, and how the amplifier gain is set on the equipement when reading etc.

The other thing is to consider Pulse Volume Recording, this is how segemental pressures are normally done in vascular labs here and is less operator skill dependant (but a more costly toy).

I think this is a worthwhile discussion but perhaps I am just not understanding you properly . . . . . geeze I think my wife said that to me ............... quite recently . . . . . . .. . . . . Noooooooooooooooooooooooooo :)

cheers

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Default Re: Peripheral Vascular Diagnostic Tests

Quote:
Originally Posted by markjohconley View Post
Great thread Asher (& Mart) .... I always send off a p/copy of the doppler waveform of B/tib. post. A's to the general practitioner ... they can diagnose, and I use it as a major determinant for vascular categorisation of the patient (High or Low risk) ... I don't use ABI (too invasive for me) but would DEFINITELY use TBI if available
Again, I greatly enjoy your input

Hi Mark

If you are recording a doppler waveform it is important that you understand how to interpret it because how you align the probe DURING the recording is crucial .

Because of the issues I mentioned in the last post you need to know what you are looking at WHILST doing the recording to get a meaningful trace.

For example it is possible to record flow in a vein ( venous fluid motion may mimic arterial in patient with CHF, bradycardia and fluid overload is possibility) and the resultant waveform could be misinterpreted as a proximally occluded PT artery.

Even if you send this to someone else to look at they need to know that you are aware of this possibility and avoided bad data. If you know how to test the signal for signs of being of venous origin (distal compression will cause momentary increased flow towards heart or valsalva will have opposite effect) your test is much more reliable.

Anyone reading this post who does doppler waveform studies and did not know this I would strongly advise to get a copy of the unetixs book. . . . . . . . . I am not on commission honest. I have learnt more about non-invasive vascular testing in this 80 page book than any other sourse. I wish it had been on my student text book list, it is very well put together.

BTW . . .. I am pretty sure that with the knowledge you can gain from this book you will allow you to make much better judgments about the circulatory status of your patients lower limbs than most primary care physicians are able to and provide them with much more useful information


good luck



Martin

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Old 2nd May 2008, 06:33 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Thanks Mart, I've already sent an email to Unetixs re purchase. All the best, Mark C
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Old 3rd May 2008, 01:48 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Martin, do you do TBIs?

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Default Re: Peripheral Vascular Diagnostic Tests

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Martin, do you do TBIs?

Rebecca
Hi Rebecca

Yes.

I have attatched a report for recent evaluation for risk of lower extremity amputation as complication of diabetes mellitus which I think illustrates how TPI measurement and doppler waveform qualitative assement may improve evalution accuracy compared to only doing ABPIs.


see what you think, if you want detail on rational for this report please let me know

hope this helps


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The St. James Foot Clinic
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Old 4th May 2008, 01:42 AM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Martin,

Many thanks for attaching your vascular assessment report! It was very interesting as I haven't seen any sort of vascular report before.

OK, I can see that you use three methods of non-invasive vascular assessment: ABI, TBI and qualitative waveform analysis. I think this is good and I will be doing the same thing (when my new doppler arrives in the next few days).

A couple of points:

1. I question the use of a TBI of 0.75 as an indicator of PAD. I expect you got this from the Williams et al study which I agree is a great study and I have taken a lot from it. But it gives no citation or rationale for using this value. The only study I have found which has investigated the TBI to produce a value is the Brooks et al study and they use a different value. All other papers / resources that I have read have either plucked the number out of thin air, or referenced someone who has plucked it out of thin air. I will be happy to be shown otherwise.

If we are going to use the TBI to be a valuable measure, it has to be investigated further.

2. Arterial wall calcification can show as an elevated ABI (you use 1.15 as the cutoff value, 1.30 is also mentioned a lot in the literature). But it can also show as a falsely normal ABI. So this makes it important to determine whether there is calcification (in that group of people where vessel calcification can occur - advanced age, diabetes mellitus and end-stage renal failure), even when a normal ABI presents.

3. Do we need TBI? Can qualitative waveform analysis provide us with the information we need to determine the status of peripheral arterial disease?

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Old 4th May 2008, 12:15 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Rebecca.

You initial reason for posting really calls into question how and why we evaluate the lower limb vascular supply as podiatrists.

Like you I have noticed that technology, knowledge and level of training has predictably changed over the 20 years since I graduated too.

I posted the report on this guy because he makes a useful illustrative case study.

At risk of making an unnecessarily pedantic post I will describe in detail my clinical reasoning for this exam, like many of us, much of what I currently do was not taught to me at school.
Anyone reading this please be critical (constructively) I regard this as an opportunity to have a peer review of my own clinical skills as well as hopefully help others and do the same and do not hold myself out to be some kind of authority ( I am really not as pompous as this sounds).

Point by point here’s what I think . . . .. . jump initial section to look at report findings if you don’t want to look at generalities . . . . . . Comments encouraged !


-----------------------------------------------------------------------------------------------------------------------

Good podiatric practice recommends annual evaluation for risk of lower extremity amputation as complication of diabetes mellitus which includes physiologic assessment of arterial supply to lower limb.

Ischemia may be considered in the differential diagnosis of non healing ulcers and foot pain; particularly rest pain, exercise induced pain which quickly resolves with rest and is predictable with level of exertion. Although clinical signs will normally be present at this stage this is not always true if compensatory vaso-dilation allows adequate perfusion for normal level of activity. Clinical signs of ischemia may exist in absence of symptoms.

Sub clinical ischemia may compromise healing of digits because of distal proximity in arterial tree and represents a possible problem for post surgical complications. Anecdotally I have seen poor healing post TNA in toes with foot with pedal pulses. This may because presence of pulse may yield false –ve for LEAD (consider artero-venous shunting with peripheral neuropathy) and is not sensitive for micro-vascular changes distal to pulse site.

Non-invasive vascular testing is accepted as worthwhile, ABPI being most widespread because it is relatively inexpensive and fast to perform and has lots of studies indicating it’s value.

The literature has cited problems with ABPI in diabetes mellitus subjects particularly those with peripheral neuropathy and alternatives MAY therefore useful to augment this measure.
There are variations in the literature regarding accuracy of non-invasive vascular testing measures, non are 100% reliable ie there false negatives and positives with all of them.

There are many potential sources of error associated with each of the tests used.
The measures frequently used to evaluate the probability of acute or chronic occlusive or vasospastic disease include, symptoms, clinical signs, pulses, ABPI, TPI, PPG, PVR, quantitative and qualitative waveform analysis of Doppler and PVR , stress testing, thermometry, and direct measurements using duplex US and arterography.

As a generalization if ABPI, TPI, qualitative waveform analysis suggest chronic ischaemic disease, the patient will be referred on for PVR and segmental testing, possibly stress testing and then direct testing if results remain consistent. Direct testing may be needed urgently with suspicion of acute or impending critical ischaemia.

Typically the investigation protocol should proceed according to evidence based cost/benefit ratio. My experience though suggests that it is more to do with the experience and viewpoint of the practitioner(s) who and individual happens to consult and what their financial position may be.

I offer all my diabetes mellitus patients an annual evaluation for risk of lower extremity amputation as complication of diabetes mellitus, this requires a specific appt. I spend 30 minutes on average doing this. I can comfortably do ABPI, TPI. qualitative doppler waveform, sensory evaluation, skin and structural exam, foot-wear evaluation, patient education review, and report to primary care physician within that time. Some patients decline this because they feel it is unnecessary other because of cost.

-----------------------------------------------------------------------------------------------------------------------

OK . .. . . . now for some detail of the patient who’s report I attached as .pdf file in last post.
He is type 2 diabetes mellitus diagnosed approximately 10 years ago, oral agent control, doesn’t do SMBG. He is fairly anxious, obese, doesn’t exercise, non smoker, medications for hyperlipidaemia and hypertension otherwise no reported health problems. He self amputated the tip of his right 1st toe 20 years ago with a lawn mower, it healed uneventfully, there is small flap reconstruction scar. There is significant edema and fat tissue at ankles.

This was initial evaluation for risk of lower extremity amputation as complication of diabetes mellitus.

In both feet posterior tibial pulse absent, dorsalis pedis pulse palpable (very weak and difficult to locate). He has no overt clinical signs of ischemia but sparse digital hair. He has no foot pain or skin lesions.

Epidemiologically although he is a non smoker he has significant risk factors for LEAD, ie diabetes mellitus, obesity, hypertension, hyperlipidaemia, no exercise, sex and age.
Superficially there is slight suspicion for LEAD because of posterior tibial pulse absent. However pulses may be obscured because of edema/fat or vessel calcification.

Non-invasive vascular testing is also equivocal.

To reduce measurement error I use standard protocol of: patient supine for 15 minutes prior to exam to reduce hydrostatic effects and allow extremities to equilibrate with room temperature.

His brachial systolic is elevated, is this “white coat effect”? Quite likely because he has anxious personality traits and seemed somewhat agitated by the exam.

Left side APBI slightly elevated, right side below normal. Because of the higher than normal girth of his arms I could not get my normal cuff in place properly so I used a large one for both measurements, he has short arms which made positioning the probe difficult, brachial systolic however was consistently 160mm.

Cuff artifact is possible when the pressure cuff width is < 50% of limb diameter and can elevate systolic readings or conversely wide cuff give low reading. Error on brachial may have been to underestimate systolic.

I think that it is possible that his ankle systolic measurements were erroneously low also because of cuff artifact.

TPIs were low especially right side, however right side toe was unusual because of prior trauma to distal soft tissue with scarring so PPG reading is somewhat questionable.
Doppler waveform interpretation is also questionable. I could not get a signal with an 8 Mz probe because of edema/fat tissue and had to use 4 Mhz probe to get a trace. Although waveform showed damped, monophasic, slightly elongated and disturbed shape, because the probe was possibly picking up reflections from venous and collateral vessels it also has increased likelihood of error.

In retrospect I could have got more reliable data and made a better judgment if I had looked at values using different cuff sizes, done waveform analysis on dorsalis pedis too, and also done PVR waveforms. There is a limit to what can be done in 30 mins.

This is a rather extreme example but I think illustrates my point which is that in this case no matter which TPI threshold was used the outcome of non-invasive vascular testing at this point is questionable.

I agree Rebecca that it would be wonderful to have more research data to improve evidence for which thresholds to use but as with most things we have to use best current evidence in our practice. Typically this will boil down to how we chose to review the evidence and also deciding what our priorities are.

My rational for non-invasive vascular testing is to err on the side of increased sensitivity at expense of specificity and pass responsibility of further review on to vascular specialist. My priority is to select out potential risk, not attempt unequivocal diagnosis.

Hope this long winded response spawns some benefit and look forward to some thoughtful criticism.


Cheers

Martin

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R3J 0E6
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Old 5th May 2008, 11:07 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Martin

Quote:
Originally Posted by Mart View Post
Hi Rebecca.

You initial reason for posting really calls into question how and why we evaluate the lower limb vascular supply as podiatrists.
I don't question why we evaluate the lower limb vascular supply. At the moment, I am questioning the TBI and its interpretation.

Quote:
Good podiatric practice recommends annual evaluation for risk of lower extremity amputation as complication of diabetes mellitus which includes physiologic assessment of arterial supply to lower limb.
And in non-diabetics and not just for amputation risk. Peripheral arterial disease is not just a disease of the legs, but rather evidence of disseminated arterial disease that is highly predictive of cardiovascular and cerebrovascular morbidity and mortality (Belch et al 2003).

Quote:
Ischemia may be considered in the differential diagnosis of non healing ulcers and foot pain; particularly rest pain, exercise induced pain which quickly resolves with rest and is predictable with level of exertion. Although clinical signs will normally be present at this stage this is not always true if compensatory vaso-dilation allows adequate perfusion for normal level of activity. Clinical signs of ischemia may exist in absence of symptoms.

Sub clinical ischemia may compromise healing of digits because of distal proximity in arterial tree and represents a possible problem for post surgical complications. Anecdotally I have seen poor healing post TNA in toes with foot with pedal pulses. This may because presence of pulse may yield false –ve for LEAD (consider artero-venous shunting with peripheral neuropathy) and is not sensitive for micro-vascular changes distal to pulse site.

Non-invasive vascular testing is accepted as worthwhile, ABPI being most widespread because it is relatively inexpensive and fast to perform and has lots of studies indicating it’s value.

The literature has cited problems with ABPI in diabetes mellitus subjects particularly those with peripheral neuropathy and alternatives MAY therefore useful to augment this measure.
There are variations in the literature regarding accuracy of non-invasive vascular testing measures, non are 100% reliable ie there false negatives and positives with all of them.

There are many potential sources of error associated with each of the tests used.
The measures frequently used to evaluate the probability of acute or chronic occlusive or vasospastic disease include, symptoms, clinical signs, pulses, ABPI, TPI, PPG, PVR, quantitative and qualitative waveform analysis of Doppler and PVR , stress testing, thermometry, and direct measurements using duplex US and arterography.

As a generalization if ABPI, TPI, qualitative waveform analysis suggest chronic ischaemic disease, the patient will be referred on for PVR and segmental testing, possibly stress testing and then direct testing if results remain consistent. Direct testing may be needed urgently with suspicion of acute or impending critical ischaemia.

Typically the investigation protocol should proceed according to evidence based cost/benefit ratio. My experience though suggests that it is more to do with the experience and viewpoint of the practitioner(s) who and individual happens to consult and what their financial position may be.

I offer all my diabetes mellitus patients an annual evaluation for risk of lower extremity amputation as complication of diabetes mellitus, this requires a specific appt. I spend 30 minutes on average doing this. I can comfortably do ABPI, TPI. qualitative doppler waveform, sensory evaluation, skin and structural exam, foot-wear evaluation, patient education review, and report to primary care physician within that time. Some patients decline this because they feel it is unnecessary other because of cost.

-----------------------------------------------------------------------------------------------------------------------

OK . .. . . . now for some detail of the patient who’s report I attached as .pdf file in last post.
He is type 2 diabetes mellitus diagnosed approximately 10 years ago, oral agent control, doesn’t do SMBG. He is fairly anxious, obese, doesn’t exercise, non smoker, medications for hyperlipidaemia and hypertension otherwise no reported health problems. He self amputated the tip of his right 1st toe 20 years ago with a lawn mower, it healed uneventfully, there is small flap reconstruction scar. There is significant edema and fat tissue at ankles.

This was initial evaluation for risk of lower extremity amputation as complication of diabetes mellitus.

In both feet posterior tibial pulse absent, dorsalis pedis pulse palpable (very weak and difficult to locate). He has no overt clinical signs of ischemia but sparse digital hair. He has no foot pain or skin lesions.

Epidemiologically although he is a non smoker he has significant risk factors for LEAD, ie diabetes mellitus, obesity, hypertension, hyperlipidaemia, no exercise, sex and age.
Superficially there is slight suspicion for LEAD because of posterior tibial pulse absent. However pulses may be obscured because of edema/fat or vessel calcification.

Non-invasive vascular testing is also equivocal.

To reduce measurement error I use standard protocol of: patient supine for 15 minutes prior to exam to reduce hydrostatic effects and allow extremities to equilibrate with room temperature.

His brachial systolic is elevated, is this “white coat effect”? Quite likely because he has anxious personality traits and seemed somewhat agitated by the exam.

Left side APBI slightly elevated, right side below normal. Because of the higher than normal girth of his arms I could not get my normal cuff in place properly so I used a large one for both measurements, he has short arms which made positioning the probe difficult, brachial systolic however was consistently 160mm.

Cuff artifact is possible when the pressure cuff width is < 50% of limb diameter and can elevate systolic readings or conversely wide cuff give low reading. Error on brachial may have been to underestimate systolic.

I think that it is possible that his ankle systolic measurements were erroneously low also because of cuff artifact.

TPIs were low especially right side, however right side toe was unusual because of prior trauma to distal soft tissue with scarring so PPG reading is somewhat questionable.
Doppler waveform interpretation is also questionable. I could not get a signal with an 8 Mz probe because of edema/fat tissue and had to use 4 Mhz probe to get a trace. Although waveform showed damped, monophasic, slightly elongated and disturbed shape, because the probe was possibly picking up reflections from venous and collateral vessels it also has increased likelihood of error.

In retrospect I could have got more reliable data and made a better judgment if I had looked at values using different cuff sizes, done waveform analysis on dorsalis pedis too, and also done PVR waveforms. There is a limit to what can be done in 30 mins.
Thanks Martin. I can see that a thorough arterial assessment is very complex and requires a lot of skill. Being new to this, I appreciate everything you have discussed.

Quote:
This is a rather extreme example but I think illustrates my point which is that in this case no matter which TPI threshold was used the outcome of non-invasive vascular testing at this point is questionable.
I'm not sure that makes it OK.

Quote:
My rational for non-invasive vascular testing is to err on the side of increased sensitivity at expense of specificity and pass responsibility of further review on to vascular specialist. My priority is to select out potential risk, not attempt unequivocal diagnosis.
I understand.

Its interesting that the difference between your patients left ABI (1.06) / TBI (0.63) is 0.43 and right ABI (0.81) / TBI (0.38) is 0.43.

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Old 6th May 2008, 12:08 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Quote:
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Martin



I don't question why we evaluate the lower limb vascular supply. At the moment, I am questioning the TBI and its interpretation. And in non-diabetics and not just for amputation risk. Peripheral arterial disease is not just a disease of the legs, but rather evidence of disseminated arterial disease that is highly predictive of cardiovascular and cerebrovascular morbidity and mortality (Belch et al 2003).. Thanks Martin. I can see that a thorough arterial assessment is very complex and requires a lot of skill. Being new to this, I appreciate everything you have discussed. I'm not sure that makes it OK. I understand.

Its interesting that the difference between your patients left ABI (1.06) / TBI (0.63) is 0.43 and right ABI (0.81) / TBI (0.38) is 0.43.

Rebecca
Hi Rebbeca.

Of course I agree with your comments, my post should have emphasized more that TPI is of particular interest in the DM patient with peripheral neuropathy as outlined in Williams paper, if the ABPI is elevated by calcification then it is meaningless and we should probably look at something else like TPI.

I had not noticed the identical difference in TPI and ABPI that is interesting thanks for pointing this out.

When you get to study the book, look at the section which looks at systolic peak time and gradient of this initial forward flow. Because the terminal vasculature should be highly resistive, the peak in forward velocity should occur after approximately 0.2 secs (one small division of recorded trace on report which was 5mm/sec)) with normal resting heart rate.

If you look at my patient’s peak it is considerably longer which if the trace is not being adulterated with venous or collateral flow I would put large weighting on as evidence of compensatory vasodilation which reduces peripheral resistance.

Another issue which I have been pondering over which I’d be interested in others comment concerns the nature of the relationships between time taken for significant occlusion to occur, and calcification to develop. Also if the effects of calcification are linear on elevating APBI or exponential.

We know that occlusive severity (viscous energy loses) is inversely proprtortional to 4th power of vessel radius because of the geometric relationships of a circle and viscosity mechanics. Also that stenosis needs to approach 75% of x/s area before becoming symptomatic, and that embolisation is more likely as occlusive diameter increases.

My assumption becasue of this is that the final and symptom stages of occlusive disease are likely to develop relatively rapidly hence the need for periodic evaluation particularly as risk factors increase.

I have assumed, perhaps wrongly, that the effects of calcification are not really absolute and may have a gradual increased effect in elevating ABPI. Assuming the same kind of exponential relationship exists between vessel wall stiffness and rate of calcification perhaps I am wrong and it is more likely to be sudden, which seems implied in the literature which I have looked at.


Anyone have any ideas on this?


cheers

Martin

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Last edited by Mart : 6th May 2008 at 09:58 PM. Reason: confusing sentence
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Old 8th May 2008, 01:49 AM
Asher Asher is offline
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Default Re: Peripheral Vascular Diagnostic Tests

Hi Martin,

Quote:
Originally Posted by Mart View Post
When you get to study the book, look at the section which looks at systolic peak time and gradient of this initial forward flow. Because the terminal vasculature should be highly resistive, the peak in forward velocity should occur after approximately 0.2 secs (one small division of recorded trace on report which was 5mm/sec)) with normal resting heart rate.
My book (Scissons) came today and I look forward to reading it. However, I turned straight to the TBI section. It states that a TBI of less than 0.65 is abnormal (ie: PAD). Where does this come from I wonder?

This is what I have so far in regard to TBI values to indicate high probability PAD (ie: ABI 0.90 or less):

0.54 - Brooks et al (did stastistical analyses to determine the 'agreement' between the ABI and TBI)
0.60 - Orchard and Strandness (this is the paper everyone quotes for 0.60 - I can't see where they get 0.60 from)
0.65 - Scissons (no reference for 0.65)
0.70 - Toursarkissian - in response to the Williams study (says "many vascular labs" use 0.70)
0.75 - Williams et al (no reference for 0.75)



Quote:
I have assumed, perhaps wrongly, that the effects of calcification are not really absolute and may have a gradual increased effect in elevating ABPI. Assuming the same kind of exponential relationship exists between vessel wall stiffness and rate of calcification perhaps I am wrong and it is more likely to be sudden, which seems implied in the literature which I have looked at.
I agree, in which case, it makes it important to determine if the ABI is falsely normal.

Do you think that instead of the absolute number gained by the TBI, it might be more revealing to look at the difference between the ABI and TBI to get a gauge of whether the ABI can be trusted or not (ie: calcification or not)?

Rebecca
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File Type: pdf Williams et al. Diabetes Care 2005 Vol 28 No9.pdf (121.4 KB, 37 views)
File Type: pdf TBI or not TBI full text.pdf (99.5 KB, 14 views)
File Type: pdf Orchard and Strandness Circulation 1993.pdf (2.28 MB, 32 views)
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Old 8th May 2008, 06:23 PM
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Default Re: Peripheral Vascular Diagnostic Tests

Quote:
Originally Posted by Asher View Post
Hi Martin,



My book (Scissons) came today and I look forward to reading it. However, I turned straight to the TBI section. It states that a TBI of less than 0.65 is abnormal (ie: PAD). Where does this come from I wonder?

This is what I have so far in regard to TBI values to indicate high probability PAD (ie: ABI 0.90 or less):

0.54 - Brooks et al (did stastistical analyses to determine the 'agreement' between the ABI and TBI)
0.60 - Orchard and Strandness (this is the paper everyone quotes for 0.60 - I can't see where they get 0.60 from)
0.65 - Scissons (no reference for 0.65)
0.70 - Toursarkissian - in response to the Williams study (says "many vascular labs" use 0.70)
0.75 - Williams et al (no reference for 0.75)





I agree, in which case, it makes it important to determine if the ABI is falsely normal.

Do you think that instead of the absolute number gained by the TBI, it might be more revealing to look at the difference between the ABI and TBI to get a gauge of whether the ABI can be trusted or not (ie: calcification or not)?

Rebecca

Hi Rebecca

Thanks for the refs I will try and get time to look at them over weekend.

As to the value of an ABPI/TPI comparison as an possible index of Posterior tibial incomressibility I would say maybe, so long as you could make the assumption that microvascular changes between ankle and toe were not a significant issue and and in the case of DM neuropathic subjects there is reason to think microvascular changes would be. I'd be curious to see how you feel about qualitative waveform interpretation once you have had a chance to understand it, this stikes me a useful parallel measure which although requiing a bit more skill to use should help to verify pressure measurements.

cheers

Martin
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