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Peripheral Vascular Disease and Claudication

Peripheral vascular disease can present either acutely with the sudden onset of symptoms or with a chronic and gradual progressive onset of symptoms. Classically, when we think about the acute presentation of peripheral vascular disease, we think about the five P's: pain, pulselessness, pallor, paresis and paralysis while when we think about chronic presentation, we think about or generally see a spectrum of symptoms which begin with claudication, progress to rest pain and may ultimately result in some form or element of tissue loss or nonhealing ulceration.

In terms of pathology, generally I find it useful to define the arterial pathology into one of three categories. These tend to correspond to the arterial system and they also tend to correspond to the operative or interventional management that may often be necessary for the treatment of this disease process. Angiographically, we tend to see disease involving the aorta or the iliac arteries. We may see disease involving the femoral, popliteal or tibial arteries. In the diabetic, in particular, we may see a distal disease process that involves the distal popliteal.

Pathologically we have another consideration to look at and this tends to influence the presentation. Whether someone presents acutely or chronically and if somebody presents chronically, how do they present? Specifically, is the pathology we’re dealing with a stenosis.

The goals of diagnosis when we’re dealing with peripheral vascular disease are four. (1) We’d like to determine the presence or absence of an atherosclerotic or occlusive process. (2) We would like to localize the level or levels of this disease process. (3) We would like to quantify in some way the extent of the disease process present. (4).

With respect to diagnosis, we have four primary tools. The history, the physical examination, the non-invasive laboratory and ultimately angiography. With respect to history, it is useful to get the following pieces of information.

Subjectively, how does the individual quantitate the disease process? How far can they walk? How many city blocks? How many flights of stairs can they go up? What’s the natural history of the disease process in this patient?

Before going on to non-invasive testing, I think it’s useful to make a comment about physical examination because in all honesty, physical examination may give you most of the information you need to treat the patient without necessarily having to depend upon the non-invasive laboratory if it is not available. Based on the history and physical examination, you should be able to determine the level or levels of disease and you should have some estimate of the severity of the disease process present. The pulse examination, a complete pulse examination including the carotid, brachial, femoral, popliteal, dorsalis pedis and posterior tibial arteries.

Inspection may give you some evidence of the severity of the disease process. Is there a loss of hair? Are there chronic skin changes? Does the patient have the shiny, thin-skinned characteristic of severe peripheral vascular disease?

If, however, one wants to quantify more objectively what you have observed on history and physical examination, then we can turn to the non-invasive laboratory. The common tools that are available are the measurement of an ankle-brachial index.

The ankle-brachial index is probably the most common of the vascular laboratory studies employed and also one which can easily be employed in most office situations. It is Doppler derived and so it requires a Doppler. Generally the ankle pressure is normalized.

Arteriography. I think it is useful to continue to emphasize the fact that arteriography should only be reserved for presurgical evaluation. One of the points I try to get across in this lecture is that you should be able to determine the level and extent of disease.

In terms of treatments, as I mentioned, I think it is very important to determine the viability of the patient's extremity because this is going to impact on the urgency and choice of treatment. If the individual presents with pain and mild paresthesias but grossly has intact sensation and motor function, one has the ability to proceed with anticoagulation or arteriography and potentially consider the use of lytic therapy. If the individual presents with insensate extremity and loss of motor function, oftentimes we have the ability to do a physical examination for localization, anticoagulation and then proceed directly to operative therapy employing either thrombectomy, embolectomy, intraoperative lytic therapy or bypass and reconstruction.

So, in terms of looking at these patients at the time of referral or at the time of presentation, I tend to assess the motor and sensory function. Based on the viability of the extremity, I will then make a decision regarding the role of arteriography and lytic therapy.

One could raise the question, what does one do four days following a myocardial infarction? Should one simply treat the patient with anticoagulation and accept an amputation four or five days down the road. The answer to that question is probably no. Quite simply because I can do an operative embolectomy under local anesthesia. Amputation is going to require some sort of general or regional anesthesia and is going to carry a much higher risk than is operative embolectomy. So even though the patient is 85.

The two most common problems I see in my clinic relate to the differentiation of neurologic pseudoclaudication from arteriovascular disease in terms of an etiology for lower extremity pain or discomfort that occurs with exertion. So in looking at claudication, it is very important to take a look at the elements that we discussed earlier with respect to the history. How long has it been present? How did it start? How do you describe it? What makes it better? What makes it worse? What kind of limitations do you have and what’s the natural history? Claudication, interestingly, can carry a number of descriptors. It can be described as an aching discomfort.

The symptoms are always completely relieved within a few minutes by standing at rest. It should not take an hour or two hours for the symptoms to go away. The patient should not have to sit down. The symptoms should go away relatively completely in a short period of time. So if one goes back to the two histories that we saw earlier, the first patient, onset of symptoms at half a block, relief within three to five minutes. Presence on physical examination of evidence of peripheral vascular disease is a fairly consistent and good history for claudication.

The second patient, on the other hand, has a fairly good history for pseudoclaudication or a neurologic compression of the cauda equina or distal cord. The symptoms are variable. The patient can walk half a block one day, twelve blocks the next.

Occasionally one will run up against the patient that presents a confusing history and physical examination. Once again, a 65-year-old man who presents with left leg pain on walking. After walking about half a block, the patient develops a cramping sensation in the left thigh and calf. The symptoms have been present for about six months. They are increasing in severity. They are relieved promptly with rest. It sounds like a fairly classic history of claudication, at least as you sit there listening to the patient. On physical examination, however, the femoral, popliteal, dorsalis pedis and posterior tibial pulses are 2+ of 2 bilaterally. They are all there.

What’s going on is that one is talking to the patient about a condition that occurs with exercise and yet we are examining the patient at rest. This is, in fact, a classic history of claudication. The patient does have peripheral vascular disease. When I have a patient who presents with claudication, I look at several factors. I look first at the time of initial evaluation at the extent of disability present. Next, I try to make an estimate of the pathology present on the basis of history and physical examination. If the patient presents with thigh or buttock claudication, in the absence of femoral pulses (suggesting an aortoiliac obstructive process) and if the patient has relatively little disability, one can begin with modification – lifestyle modification, risk factor modification and pharmacologic therapy. If the patient is diabetic, treat it. If the patient is hypercholesterolemic, treat it. If the patient smokes, stop.

You begin therapy with pentoxifylline which used to be a substance available as Trental. It is now available in generic form. It has been shown in a randomized prospective study to be of value in patients with claudication. I think with the presence of interventional treatments – angioplasty and stenting – there is probably also a role for early evaluation and intervention in the patient presenting with claudication and evidence of aortoiliac occlusive disease if there is a significant disability. In those situations, after discussing the options with the patient, it would not be inappropriate to proceed with angiography and early intervention. With femoropopliteal occlusive disease and claudication, generally I will always try to initiate a period of risk factor modification and pharmacologic therapy and only if that fails will I proceed to angiography and intervention, be it bypass or angioplasty.

In patients with tibial occlusive disease, fairly distal occlusive disease, I will generally only employ risk factor modification and pharmacologic therapy. In only very rare cases should such patients who present only with claudication be considered either for intervention or bypass surgery.