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CME Vascular

CLI - Making the Diagnosis and Classification

Cameron Akbari, MD, MBA

Cameron Akbari, MD, MBA provides a thorough review of the PAD Classifications and their relevance in overall vascular risk stratification. Dr Akbari explains in detail the subjective and clinical indicators in differentiating claudication, rest pain and critical limb ischemia (CLI). He provides a thorough review of available non-invasive testing modalities, their role in identifying and assessing levels of vascular compromise and an understanding of the associated morbidity and mortality relates with the various levels of disease severity.

CPME (Credits: 0.5)

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Complete the 4 steps to earn your CE/CME credit:

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Goals and Objectives
  1. Recognize the various levels and classifications of Peripheral Arterial Disease (PAD)
  2. Distinguishing the differences between claudication, rest pain and CLI
  3. Appropriate use and indication for non-invasive arterial testing
  4. Appreciation for the associated morbidity and mortality rates seen with PAD and CLI
  • Accreditation and Designation of Credits
  • CPME (Credits: 0.5)

    PRESENT eLearning Systems, LLC is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine.

    PRESENT eLearning Systems, LLC has approved this activity for a maximum of 0.5 continuing education contact hours.

    Release Date: 03/16/2018 Expiration Date: 12/31/2018

  • Author
  • Cameron Akbari, MD, MBA

    Washington Hospital Center
    Washington, DC

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  • It is the policy of PRESENT e-Learning Systems and it's accreditors to insure balance, independence, objectivity and scientific rigor in all its individually sponsored or jointly sponsored educational programs. All faculty participating in any PRESENT e-Learning Systems sponsored programs are expected to disclose to the program audience any real or apparent conflict(s) of interest that may have a direct bearing on the subject matter of the continuing education program. This pertains to relationships with pharmaceutical companies, biomedical device manufacturers, or other corporations whose products or services are related to the subject matter of the presentation topic. The intent of this policy is not to prevent a speaker with a potential conflict of interest from making a presentation. It is merely intended that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts.

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    Cameron Akbari has nothing to disclose.

  • Lecture Transcript
  • Robert Frykberg: It gives me great pleasure however to bring back my good old friend Dr. Cam Akbari, who -- you are in DC right Cam, I don’t have your -- Dr. Akbari practice at the Deaconess, he was a fellow at the Deaconess and practiced there when I was still there back in Boston. We became very good friends, he is a very, very well trained vascular surgeon who has done exceptionally well in the ensuing decade or so since we first became friends. And I have asked Cam to talk about critical limb ischemia making the diagnosis and classification, some that’s critically important to us in the VA system. So let's welcome Dr. Cameron Akbari to the podium. All right Cam, so you have got twenty minutes.

    Cameron Akbari: Well thank you so much Bob for that introduction and thank you for the opportunity to be here. Today I am just going to spend a few minutes talking about critical limb ischemia and the importance of it and really how the illness falls on you, the practitioner to make the diagnosis in a timely fashion and hopefully I will be able to teach a little bit about how to make the diagnosis. I have no financial disclosures.

    The -- when we talk in general about peripheral arterial disease there is an entire spectrum and it ranges from the asymptomatic all the way to the patient with full blown gangrene and needless to say the severity increases as we go down the chain. Most patients fortunately are in the asymptomatic category, half of patients are asymptomatic who have peripheral arterial occlusive disease and only a small fraction are actually those who present with critical ischemia, about 30, 40% are stable claudication and only about 10 to 15% present with critical limb ischemia. This is the classification of peripheral arterial disease, which we generally use every day and it can be either divided, it can be divided into either the Fontaine or the Rutherford class.

    Again rating from asymptomatic all the way to tissue loss, you will note that the, that class, Fontaine class four is ulceration in Rutherford class five and six. So there are some similarities and I will get back to that in just a second. And so far as the treatment is concerned again it's also helpful to classify the severity of the disease because this also defines our treatment and again for the asymptomatic patient obviously no surgery is needed other than risk factor reduction, even in those patients with claudication not much intervention is needed other than to controlling their risk factor reduction, maybe some pharmacologic therapy, certainly some exercise therapy.

    In general revascularization is dean for these group of patients those with rest pain, ischemic ulceration and gangrene and perhaps some patients who have lifestyle disabling claudication. It does increase as we get older and certainly as we go greater than 70 age range, you can see it say high as 15% of men, maybe even higher similarly in women as well. And these of course are the well known risk factors for peripheral arterial disease and so that when a patient presents with any of these risk factors here be on the lookout for not just peripheral arterial disease but for critical limb ischemia as well.

    Overall, among all patients with peripheral arterial disease as I said most are going to be asymptomatic 40% are going to have claudication and then 10% are going to be in that category of critical limb ischemic whom we are going to talk about. But just to understand a little bit about claudication in general from a PAD standpoint it is a benign condition. So that when a patient comes to you and does have leg pain with exercise, bear in mind that and so far as the leg is concerned this is generally, particularly with risk factor modification, a benign disease. And here is why three quarters of those patients will stay as a stable claudicant, only a fraction will become worse than their claudication and less than 10% will go on to either need leg bypass surgery or even smaller fraction needing an amputation. So for the most part I tell patients you will not lose your leg if you go ahead and listen to what I have to say and so far is smoking cessation.

    On the other hand it's a dangerous disease because it's a marker for overall cardiovascular morbidity and mortality. One third of patients who present with claudication are going to be dead at five years. And again looking at it from another standpoint the, if we take these patients overall, all patients need not, everybody over the age of 55 in the country 5% of the population over the age of 55 has claudication again these are the outcomes here.

    Overall another way of looking at it illustrated here, look at this two charts to your right again claudication is a benign condition and so far as the leg is concerned but it's really right up there with colorectal cancer and so far as five years mortality rates. These are just patients who have leg pain with walking; you can see quite cell brain statistics. It's also clearly the worse off the disease, the worse off the predictor of mortality, the greater predictor of mortality it is such as those patients who have a dramatic, I am sorry, who have a dramatic fall in their ankle brachial index are going to have five years survival rates of only about 30% as illustrated here.

    Overall, among all patients who then need bypass, remember this is not just the claudicant, but those patients who need bypass almost 50% of those patients are going to be dead at five years, so this is a very severe disease, a very serious disease and now of course the number one cause of death is their overall cardiovascular disease, if there is atherosclerosis effecting the legs it's going to be effecting the heart as well. Most of this is probably not news to you but it's worthwhile to reiterate here, so again to get back to the topic that we are talking about here critical limb ischemia same slide I showed you earlier these are the patient whom we defined is critical in ischemia, those patients have ischemic rest pain or tissue loss, to put in another way those patients who have Fontaine class three or four or Rutherford category four, five, six this is the group of patients that we are talking about Rutherford four, five, six; Fontaine stage three and four that is the definition of critical limb ischemia and really the absolute illness falls on you as a practitioner to differentiate those patients who have claudication versus rest pain and those patients who present with ulceration and gangrene because it's is absolutely important to ask the question and answering correctly is the ulceration due to critical limb ischemia or is it neuropathic.

    So very briefly in so far as intermittent claudication these are patient who have pain with walking not at rest. It occurs in muscles groups not in the foot so somebody who comes in who has pain in the foot with walking not a symptom of claudication. Somebody who has pain in their leg at rest not a symptom of claudication it is reproducible and it does resolve complete after they stop walking. Common size of claudication those patients who present with pain in the buttocks, hips or thighs those patients are going to have a aorta iliac disease because this is what supplies this muscle group. Those patients who have thigh and calf claudication, particularly calf claudication it's going to be in the femoral popliteal segment because again those are, that’s the muscle group supply.

    Ischemic rest pain and remember that ischemic rest pain is critical limb ischemic and it's important to recognize the symptom, the pain is going to be at rest in the foot because that represents, they are known to at rest of the body, it’s the furthest away from the heart. It's usually nocturnal, these patients who have that classic presentation of, they have to sleep with their leg dangling so that gravity can help the flow of blood to the foot. It's worse when they are in a recumbent position, it improves your dependency and again those patients who say I get pain in my calf at night when I am sleeping that is not the usually symptom of ischemic rest pain, it occurs in the foot.

    Again it's the ulceration in those patients who present with tissue loss is a due to underlying arterial occlusive disease and I submit to you that most of the time this can be diagnosed with a very good history in physical examination. The history of the ulcer has it been present, has it healed previously certainly an ulceration which has been present for two or three months should raise a red flag that there is an element of critical limb ischemia. If it has healed previously what was the time to healing, has the patient has, has the patient had a previous revascularization particularly in the contralateral leg. Other cardiovascular events or co-existing vascular risk factors which we saw earlier all should raise a suspicion of underlying PAD and critical limb ischemia as an ideology. Bear in mind that the classical symptoms of occlusive disease such as claudication of rest pain maybe diminished in those patient who have diabetes with neuropathy because again so if they come in ulcerations simply because they have never had rest pain or claudication does not rule out critical limb ischemia and PAD.

    Physical signs I do again I don’t need to run this by most of you but the location of the ulcer, the very distal, more distal location suggest PAD as an ideology, the appearance of the ulcer is granulation tissue absent, is there any bleeding with debridement, is there underlining gangrene, a very good example of somebody who has critical limb ischemia manifesting as tissue lost. Pallor with elevation, fissures, hyperkeratosis, atrophic skin multiple lesions all suggested of underlying CLI. The PAP is the most important aspect of the physical examination is the status of the foot pulse that is, is the foot pulse palpable or not and the reason why is all limb salvage efforts were failed unless there is a palpable foot pulse, the diabetic foot also requires a palpable foot pulse to heal and again the illness falls on you to make the diagnosis because you want that foot to heal.

    I want to spend a few minutes and so far as how to do a proper pulse examination, the femoral pulse is just below the inguinal ligament half way between the pubic tubercle and iliac crest, the popliteal pulse I like to palpate like this with the knee flexed fifteen degrees very relaxed you don’t want the gastrocnemius muscle to tense up and I like to palpate it with both hands starting in the midline and slowly spread my hands apart. Many of these patients have had a beta blockers so give it time, they may have a heart rate of only fifty or sixty so give it time, it takes, it takes a few minutes to do a good pulse examination.

    The posterior tibial artery pulse is located half way between the medial malleolus and the Achilles tendon in the hallow behind the medial malleolus. I like to use my contralateral hand so that my ipsilateral hand can support the foot so for the right foot I use my left hand as seen here and for the left hand, for the left foot I use my right hand and that allows me to go up and over the ankle and part my fingers directly in that hallow behind the medial malleolus. The dorsalis pedis artery is located between the first and second metatarsal, it's just lateral to the extensor hallucis tendon, I use the ipsilateral hand tear that is the right hand right foot and I use all my fingers, all the pads of my fingers are seen here to position my hand directly over line where I expect to find the artery.

    Another thing that can be done to diagnose CLI is a an ankle brachial index and this is how we do it, the blood pressure cuff is positioned at the ankle, it is inflated until the Doppler’s signal is obliterated then the cuff is deflated and the point at which the Doppler’s signal returns is recorded as the ankle pressure. The brachial pressure is derived the same way using a hand held continuous wave Doppler, the two divided and that yields an ankle brachial index. The higher the two pressures are utilized and the ABI is really quite a sensitive and specific test for PAD, it does have some limitations and I will talk about that in a second. Again some normal values 1.1 to 1.3, anything less than 0.4 or 0.3 is classified as severe disease. Bear in mind that many patients with diabetes they may ulcerate and not be able to heal with an ABI in this range and certainly always be on the lookout for non-compressible vessels in the diabetic patient. So again the diagnosis of CLI is made at the well performed history in physical it's the corner stone of evaluation but we can also perform some non-invasive testing as a useful adjunct and let me spend a few minutes talking about that.

    A variety of tests are ordered, you don’t have to order them all its costly, it can waste time in making the diagnosis which can lead to failure of limb salvage but these are, this is the menu available to you, we will spend a few minutes talking about those. Bear this in mind that all these tests have limitations in the presence of diabetes and in fact often times the interpreted results can be misleading and incorrect and applied to the diabetic lower extremity with ulceration. Doppler segmental pressures we just talked about the principle limitation is that of medial arterial calcification, I would like to think of it as my ballpoint pen, even if I put a blood pressure cuff on my pen and inflated at three hundred millimeters it will continue to write because it's got that hard rigid shell and imagine in a diabetic artery with extensive medial arterial calcification there will still be blood flow you won't be able to obliterate and so you have an artifactually elevated pressure. Present in about 60% of patients with diabetes.

    Toe pressures can be quite helpful and this is how they have performed here a small 2.5 centimeter cuff is placed, I am sorry on the toe and inflated to thirty millimeters above the brachial pressure and then the pressure is recorded with a photoplethysmograph and ones there is return of the oscillationas judged by the changes in the volume within the toe as the pressure cuff is deflated that is recorded and then that is recorded as the pressure, it can be compared to the arm such you derive a toe brachial index anything is above a 0.7 as classified as normal and really the rational from this is the idea that perhaps digital arteries are spared from medial arterial calcification so you are going to get that falsely positive artifactually elevated pressure.

    The limitations again are multiple vasoconstriction that the patient comes in from the cold, if they are a smoker anything that cause the digital vessels to constrict certainly a wrong cuff size or if there is an ulcer on the toes well you won't be able to get a toe pressure. Doppler wave form analysis can be helpful, this is based on the idea of the Doppler shift and really we insinuate a femoral, popliteal, and pedal vessels and what we are looking for is the phasicity as seen here, the normal Doppler flow wave form is triphasic with a forward flow insistently, a reversal of flow during early diastole and a late forward flow in late diastole that’s the normal triphasic waveform that is normal.

    Anything other than that such as a monophasic waveform seen here suggest proximal arterial stenosis so that a monophasic waveform at the dorsalis pedis arteries suggest occlusive disease more proximally and this is an example of that, there is loss of the flow reversal component in early diastole. The limitations of Doppler waveform is that it's essentially qualitative, there it doesn’t give you much quantitative abilities so that a monophasic waveform suggest that disease is present but it doesn’t tell you how much is present. Often times these patients have extensive bandages in the foot so it's difficult to obtain a waveform at the foot, it really can’t precisely localize the vessel being insinuated and it's limited essentially to the ankle level you cannot assess from more distal foot disease.

    Duplex ultrasonography is based on the idea that you can actually look at the vessel being insinuated and this is through the B mode or brightness mode gray scale, just like a gallbladder ultrasound. I can find the vessel and put the Doppler directly on it and then this allows me to look at things like whether it's phasic or not, here is an example of that. The B mode ultrasound localizes the femoral arteries seen here, I can then position the Doppler probe directly in the middle of the vessel giving me something called the range specificity. So now I know I am insinuating the femoral artery and then this is the normal triphasic waveform that I would like to see in a vessel without proximal arterial stenosis.

    With increasing levels of stenosis there is turbulent flow and the waveform becomes monophasic as seen here with spectral broadening and ultimately with occlusion no flow is seen so it tells me exactly what's going on in the vessel of interest. And again another example over that at the dorsalis pedis artery and at the posterior tibial artery a triphasic normal waveform and a monophasic waveform seen here, that’s how we interpret this. So again it has this own set of limitations it's operated defendant, we commonly see biphasic signals, I don’t know how to interpret that and there really are no clearly defined criteria in -- for the native vessels and so far is the velocity criteria. So there is significant variability from lab to lab.

    Pulse volume recordings quite popular at some institutions the idea behind this is that there is volume changes that occur with each heartbeat just like when we put up a blood pressure cuff you can see oscillation in the sphygmomanometer the same thing here as the volume increases to the limb through the muscle group, there is going to be changes with each heart beat. The pneumatic cuffs are placed at different levels high thigh, low thigh, calf and ankle and at the forefoot and as the limb expands with the blood there is volume changes beneath the cuff are recorded on a strip chart and here is an example of that here.

    A waveform is produced within the cuff deflections as the volume changes with the heartbeat remember you are not obliterating flow you are just sensing the flow with each heartbeat. This is normal, brisk systolic upstroke, a sharp systolic peak, a prolonged down stroke with a prominent dicrotic notch half way down the waveform. A normal waveform seen here particular note the very brisk upstroke with increasing degrees of proximal stenosis the waveform changes you can see here, there is no longer that dicrotic notch that we saw on the earlier slide here. And then ultimately the peak become rounded with delayed up stroke and then ultimately with severe abnormal waveform we classify as a flat line tracing with very low amplitude again not much volume changes with each heartbeat because there is severe proximal arterial stenosis.

    Again the test is qualitative at best only semi-quantitative. So if I order a pulse line according to see whether or not a transmit will heal there is no strict guidelines it doesn’t give me a number, it's just a matter of interpreting that waveform and again the other variables that affect the other tests also apply here. They finally TCPO2, the idea of this is that we measure the partial pressure of oxygen defusing for the skin, it's a surrogate measure of healing. The great advantage of this is that it's quantitative I get a number that’s fantastic and is unaffected by medial arterial calcification. This is how the test is done, this is with an older probe here, an interphase fluid applied and a sensor probe is applied, there is an equilibration time and normal as anything greater than 60, clearly abnormal as anything less than 20.

    Well I don’t need to tell you that there is a large gray area between 20 to 60 that exist that doesn’t really tell me whether or not healing will absolutely occur. There is probe difficulties, a probe can liftoff, there is sometimes a lack of standardization and finally as was shown several years ago diabetic patients with a non-healing foot ulcer actually have higher TCPO2 values than non-diabetic patients the reason is probably due to the AV shunting that occurs at the microvascular level. So a high TCPO2 level in a diabetic patient may not predict healing.

    At the end of the day what does this all mean well, critical limb ischemia is common particularly in the diabetic patient who presents with foot ulceration and as we know it has tremendous implications for limb amputation. Everyone in this room is probably the first to see the patient with critical limb ischemia and so it is absolutely critical to understand the disease process and make the diagnosis promptly. Really the -- in my opinion the first line to diagnose critical limb ischemia is a well performed history and physical examination. A variety of non-invasive tests are available, which can be helpful to those patients in whom the diagnoses is of a question. Thank you very much.