What You Should Know About Screening For PAD

We are an aging population. One can ascertain that with aging comes an increased incidence of comorbid conditions. With the vast majority of podiatric surgical cases being elective, documentation supporting the vascular system prior to surgery will protect the surgeon from postoperative complications associated with circulatory issues, or may help surgeons recognize an asymptomatic issue for appropriate intervention prior to surgery. Recognition of asymptomatic circulatory issues is of particular importance in the younger diabetic population prior to surgery.
Systemic atherosclerosis is one of the many complications of poorly controlled diabetes that results in peripheral arterial disease (PAD). The consequences of systemic atherosclerosis can end with lower extremity amputations, ischemic heart disease, cerebrovascular disease and/or death.1 Podiatric physicians can aid in the early diagnosis of PAD by familiarizing themselves with the risks and symptoms associated with the disease.
Approximately 12 million people in the United States have PAD and patients with diabetes reportedly comprise between 20 and 30 percent of the PAD population.2 However, the prevalence could be higher because many patients with diabetes demonstrate factors that would affect clinical findings. Many patients with diabetes are asymptomatic and this could very well be the result of peripheral neuropathy masking the symptoms of intermittent claudication.3 In fact, 53.8 percent of the general population with PAD is asymptomatic so looking at the pathophysiology and risk factors is essential to aid in recognizing patients who need further evaluation.4
Atherosclerosis, the primary cause of PAD, is a systemic condition caused by a chronic inflammatory condition. One may see an elevated level of C-reactive protein (CRP) among patients with atherosclerosis as well as patients with impaired glucose tolerance. This finding is associated with the development of PAD.5 High levels of CRP inhibit the vasodilatory effects of nitric oxide (NO), which subsequently produce an uncharacteristic vascular tone. Diabetes further impairs the effects of NO due to hyperglycemia, excess free fatty acids and insulin resistance.6
Not only is the vasodilation of arteries affected by diabetes but the vasoconstriction of arteries is augmented by the induction of arthrogenic pathways. This occurs via activation of protein kinase C and nuclear factor kappa-B. Protein kinase C has an adrenergic effect on vascular smooth muscle, producing vasoconstriction. Nuclear factor kappa-B resides within a cell and becomes a first-responder through gene expression to aid in an immune response to initiate inflammation.7

Overall, atherosclerosis has the same pathophysiology in non-diabetics and patients with diabetes. However, the presence of diabetes further enhances the process of atherosclerosis and more commonly involves the vessels below the trifurcation in the lower extremity.8 Accordingly, this may correlate to the increased lower limb amputations one sees in the diabetic community.

Keys To Screening For Claudication
Claudication is defined as a halt or limp in a person’s walk. Intermittent claudication is defined as pain, tension and weakness in the legs upon walking. This pain intensifies to produce lameness or inability to function, and is predictably relieved by rest. Intermittent claudication is the most common symptom of PAD. At times, it can be difficult to determine true claudication versus disuse in the sedentary patient. This point is arguable in that these symptoms, when present, indicate a potential for PAD whether the person is or is not sedentary.
We feel that the symptoms that present as claudication are significant regardless of the person’s activity level. When posing questions to the patients, it is important to try to determine how much activity it requires to produce the symptoms.
For example, ask patients how far they can typically walk before the discomfort in their legs requires them to stop and rest. This is often a question that patients cannot answer due to the slow development of the disease and the relative collateralization that develops. While the disease is present, in the early stages, it may not produce pain or discomfort, which require rest. A very good question to ask is if patients can still do the same physical activities as they could one, two or three years prior to the development of these symptoms. If they cannot do the same activities, this may be an early clue to their disease process.

Essential Questions To Cover In The Patient History

In addition to claudication, there are a variety of other possible risk factors that can contribute to the development of PAD. Accordingly, physicians should ask the following questions of patients when they have a high index of suspicion. Does the patient use or have a history of tobacco use? A common mistake is to ask the question: “Do you smoke?” The truthful answer may be no. However, bear in mind that the patient in question may have quit smoking a few years ago and previously had a 10-30 pack year history.
The current state of tobacco use is irrelevant if there is a history of use. Previously, researchers found that current smoking status had a greater effect on the development of PAD than a lifetime of smoking because of the decrease in cardiovascular complications.4 More recent evidence shows that a history of lifetime smoking is related to asymptomatic PAD.4
Does the patient have diabetes mellitus? If so, is it diabetes type 1 or type 2, and how long has the patient had the disease? Many of the associated metabolic issues that accompany diabetes mellitus can lead to the development of PAD. For patients with diabetes who meet the indications for non-invasive testing, we recommend both ankle-brachial index (ABI) and digital pressures/photoplethysmography to screen for the macro- and microvascular complications associated with the disease. We recommend screening people with diabetes over the age of 40.
Does the patient have any history of heart disease? Is there stable or unstable angina? Has the patient had a baseline stress test? Is there a history of coronary artery bypass or coronary angioplasty? Does the patient’s medication history tip you off to the presence of underlying coronary artery disease? Is there a first-degree relative with heart disease?
Does the patient have a history of stroke or transient ischemic attack involving the carotid arteries? Is the patient taking aspirin or clopidogrel bisulfate (Plavix, Bristol-Myers-Squibb)? If the patient does take the latter medication, is it to address a history of circulation problems relating to cardiac, carotid or peripheral circulation?
If you have a high index of suspicion for PAD, the most common metabolic conditions to screen for are hyperlipidemia and hypertension. Do patients know their most recent total cholesterol levels? Do they check their blood pressure regularly? Are they currently taking antihypertensive therapies or medications specific for lipid reduction?
Has the patient had any prior vascular intervention? Ask if patients have a history of carotid endarterectomy, coronary angioplasty or coronary artery bypass. Also question the history of renal artery or lower extremity artery angioplasty, or another invasive intervention.
Generally speaking, the recommendation is to screen individuals over the age of 50. However, one should screen the diabetic population over the age of 40.
Obesity is the final risk factor for the development of PAD. Of note, clinical obesity relates to a body mass index (BMI) > 30 whereas moribund obesity is a BMI > 40.

Pearls On Conducting The Physical Exam
After assessing patients for possible claudication and completing the risk factor profile, does the clinical picture of the patient match your suspicions? The lower extremity vascular tree is the most important feature of the physical exam when it comes to the presence of PAD. Are the pedal pulses diminished or absent? Are the popliteal and femoral pulses palpable?
Keep in mind that you may see an array of physical findings. These findings may include many of the trophic changes within the physical exam. Cool temperatures are not always present due to collateralization. Muscle atrophy and weakness may or may not be present.
When one suspects moderate to significant PAD, the physician should evaluate the tone and presence or absence of the gastrocnemius muscle. This is a unique muscle of the lower extremity because only the sural nerves supply the muscle with no available collateral development.
The information one gathers from the claudication assessment, the risk factor profile and the physical exam should provide a clear picture for determining whether non-invasive vascular studies are necessary. Non-invasive vascular studies provide objective, quantitative information should you need to refer the patient for an appropriate vascular consult.

How Reliable Is The ABI In Gauging PAD Risk?
The ankle brachial index is the most sensitive and reproducible test when it comes to gauging the associated risk for the development of morbidity and mortality related to the development of PAD. The American Heart Association and the American College of Cardiology have recommended practice guidelines on how to obtain a proper ABI.10
First, the patient needs to be in a supine position for 10 minutes. Proceed to measure the systolic blood pressures of both brachial arteries and use the highest one in the calculation. Then obtain the systolic blood pressure of both the dorsalis pedis and posterior tibial arteries. Use the larger value for the calculation of the ABI for the respective limb.
In regard to these values, there is much debate as to when one should refer a patient to a vascular specialist in the case of moderate PAD. Podiatric physicians should refer these patients to an internal medicine doctor, if they do not already have one, to begin a regimen of appropriate exercise therapy and/or drug therapy.
There is no debate that any patient who demonstrates critical limb ischemia (CLI) should obtain an immediate referral to a vascular specialist. These patients are at a high risk of developing ischemic ulcerations, rest pain or gangrene — if they do not already exhibit some of those signs — and tend to trend downward without intervention.
Be aware that patients who have elevated ABIs > 1.30 have incompressible arteries that decrease the specificity of the test. For these patients, the arterial Doppler can be useful for evaluating increasing levels of ischemia. Dopplers are useful in the presence of significant calcification with non-compressible vessels. The peak velocity and morphology of the waveforms become more useful for interpreting the levelof disease.

In Summary
Peripheral arterial disease is becoming more of a concern with an increasing number of people who are being diagnosed with diabetes. Many of these patients will be coming to see their podiatrist with or without ymptoms. Considering the prevalence of asymptomatic PAD, patients who are at risk need to undergo assessment.

Dr. Sefcik is a first-year resident at Pontiac Osteopathic Hospital in Pontiac, Mich.

Dr. Wilusz is a Fellow of the American College of Foot and Ankle Surgeons. He is in private practice in Clarkston, Mich.
 

References:

1. White CJ, Gray WA. Endovascular therapies for peripheral arterial disease: an evidence-based review. Circulation 116:2203-2215, 2007.
2. Marso SP, Hiatt WR. Peripheral arterial disease in patients with diabetes. J Am Coll Cardiol 47:921-9, 2006.
3. American Diabetes Association Consensus Statement. Peripheral arterial disease in people with diabetes. Diabetes Care 26(12):3333-3341, 2003.
4. Eason SL, Petersen NJ, Suarez-Almazor M, Davis B, Collins TC. Diabetes mellitus, smoking and the risk for asymptomatic peripheral arterial disease: whom should we screen? J Am Board Fam Pract 18:355-361, 2005.
5. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 97:425-428, 1998.
6. Williams SB, Cusco JA, Roddy MA, Johnstone MT, Creager MA. Impaired nitric-oxide mediated vasodilation in patients with non-insulin dependent diabetes mellitus. J Am Coll Cardiol 27:567-574, 1996.
7. Inoguchi T, Li P, Umeda F, et al. High glucose level and free fatty acid stimulate reactive protein oxygen species production through protein kinase C-dependent activation of NAD(P)H oxidase in cultured vascular cells. Diabetes 49:1939-1945, 2000.
8. Haltmayer M, Mueller T, Horvath W, Luft C, Poelz W, Haidinger D. Impact of atherosclerotic risk factors on the anatomical distribution of peripheral arterial disease. Int Angiol 20:200-207, 2001.
9. Marso SP, Hiatt WR. Peripheral arterial disease in patients with diabetes. J Am Coll Cardiol 47:921-929, 2006. Same as 1
10. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/ Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology and the ACC/AHA Task Force on Practice Guidelines. (Writing Committee to Develop the Guidelines for the Management of Patients With Peripheral Arterial Disease. J Am Coll Cardiol 47:el-192, 2006.

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