4.

Peripheral Vascular Disease

Arthur N. Steinhart, DPM

Vascular Examination
The vascular examination is conducted in a room of comfortable temperature so as to avoid inducing vasodilatation or constriction. Most of the examination is conducted with the patient supine (phlebostatic position).

Pulse Palpation
The examiners fingers are placed lightly at the site of the artery. If no pulsations are felt, the pressure used is slowly increased until the pulse is detected. Care must be used to distinguish the patients pulse from the examiners pulse. Abdominal aorta: to the left of the umbilicus Femoral: deep below the inguinal ligament at a point midway between the anterior superior iliac spine and the symphysis pubis Popliteal: deep in the popliteal fossa slightly lateral to the midline. Slightly flex the patients knee keeping the heel on the table and use both hands with the fingers coming around the medial and lateral sides of the knee. As an alternative, the patient may be in the prone position with the knee flexed Dorsalis pedis: dorsum, just lateral to the extensor hallucis longus tendon. This pulse has been reported to be congenitally absent in 8-15% of the normal population. Posterior tibial: behind and slightly below the medial malleolus The following characteristics of the pulse should be noted: Quality: the strength of the pulsation is described either qualitatively (absent, weak, normal, strong, bounding) or quantitatively (on a 0-4 scale). Exercise, anxiety, fever, and hyperthyroidism may cause bounding pulses. Weak pulses may be caused by hypovolemia and obstruction. Rhythm: Rate: indicate the beats per minute. A rate between 60-100 is considered normal. A rate below 60 is defined as bradycardia and one greater than 100 is considered tachycardia. Among the causes of bradycardia are hypothermia, hypothyroidism, drug intoxication, cardiac disease, and athletic conditioning. Among the causes if tachycardia are fever, hyperthyroidism, anemia, shock, anxiety and exercise

Other Techniques
Inspection and palpation of the skin and related structures (hair and nails): The skin should feel smooth, soft, even, and should be supple and well-hydrated. Note any atrophy of the skin and subcutaneous tissues. To test for mobility and turgor a small section of skin is pinched and released. Decreased mobility may be produced by edema and scleroderma. A decrease in turgor may be due to dehydration. Dryness of the skin may be found in hypothyroidism and diabetes. Use the backs of the fingers/hands to evaluate skin temperature and temperature gradient (the gradual change in skin temperature from the knee to the toes). The skin of the leg and foot should be warm, not hot, with a gradual drop in temperature of 10 degrees between the knee and toes. A greater than 10-degree drop is described as an increased temperature gradient and may be the result or arterial insufficiency or marked spasm. A less than 10degree drop is described as a decrease gradient and may be the result of venous insufficiency, infection, inflammation, or vasodilatation. An increase in temperature rather than a decrease is reported as a reversed gradient and may be found in more severe venous stasis, infection, inflammation, or vasodilatation.

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Localized areas or increased temperature may be due to infection, vasodilatation, or inflammation. Localized areas of decreased temperature are the result of inadequate blood supply and may be due to blockage or vessel spasm. To evaluate for edema use a finger to firmly press the skin behind the medial malleolus, on the dorsum of the foot, and over the shin for five seconds. A depression that does not rapidly refill and return to its original shape is indicative of pitting edema. This may be reported subjectively as mild, moderate, or severe or may be graded quantitatively ranging from 1+ to 4+. 1+ when there is no visible swelling and slight pitting of no more than 2 mm is produced; 2+ when there is no apparent swelling but pressure produces pitting between 2-4 mm; 3+ when there is noticeable swelling and pitting of up to 6 mm is produced; 4+ when there is marked swelling and digital pressure induces a deep, long lasting pit. Pitting edema may be caused by right-sided heart failure, othostatic edema, and chronic venous insufficiency. When unilateral, major vein occlusion should be considered. Lymphedema or arterial disease should be considered when the swelling is non-pitting. The venous filling time and elevation-dependency color change tests are done together since both involve raising and lowering the patients legs and changing the patients position from lying to sitting. Changes in skin color with change in leg position (from the baseline horizontal position to elevated above the heart to dependent with the patient sitting up) are noted in the elevation-dependency test. The amount of time it takes for a drained vein on the dorsum of the foot to START to fill is noted in the venous filling time test. The venous filling time test is not a test of the vein but rather a test of the small vessel network (arterioles, capillaries, and veins). With the patient in the supine position a dorsal vein on each foot is marked (these are the veins that will be observed for the filling time test) and the color of the soles is noted. One leg is elevated above the level of the heart for 30-60 seconds and any change in color noted (the contralateral sole may be used for comparison if both soles were the same color prior to elevation of the test limb). The elevated limb is then lowered to its original position and the test repeated on the opposite side. Both legs are then elevated and the marked veins are allowed to empty. The patient then sits up while the legs are placed in the dependent position. The time required for each vein to start to fill is noted and the color of the soles in the dependent position (and time required for return of color if pallor developed upon elevation) is noted. Normal findings include no/minimal blanching on elevation with return of normal color in 10 seconds upon dependency. The onset of venous filling occurs in 12-15 seconds. Severe arterial insufficiency will produce blanching on elevation with a delay in return of color on dependency and a long (greater than 15 second) venous filling time. Dependent rubor with cool skin may also develop. This pallor on elevation and rubor on dependency is known as Buergers sign. Venous insufficiency may cause a rapidly developing warm dependent rubor with loss of this color on elevation. Venous filling time will be less than 12 seconds with filling occurring from the proximal side of the vein rather than the distal side that, to some, may be observable. It is because of this retrograde filling that this test becomes unreliable in the presence of varicose veins or other signs of venous insufficiency. The subpapillary venous plexus filling time (was also known as capillary filling time) is the time required for the color to return to the end of a toe that has been blanched by pressing on it. Normally, color should return almost instantaneously. Return of color will be delayed in the presence of severe arterial insufficiency or small vessel disease. The Doppler ultrasound flowmeter is a device in which high-frequency sound-waves are used to assess the status of a patients arterial and/or venous system. Testing is based upon the Doppler phenomenon in which the frequency of a soundwave is altered upon reflection from a moving object (blood cells). The depth of penetration of the transmitted signal depends upon its frequency, the lower the frequency the greater the depth of penetration. Thus, for fetal monitoring a frequency in the range of 4 MHz is used, while frequencies in the 9MHz range are most suitable for lower extremity arterial evaluation. Since ultrasound waves are not transmitted well by air a coupling gel is used to ensure transmission between the probe to the skin surface. The best signal may be obtained by holding the probe over the vessel and at a 45 angle it (not the skin surface). Thus, once a signal is located the probe should be

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moved proximally and distally as well as medially and laterally until the strongest signal is found. At this time the angle of the probe should be further adjusted to ensure receiving the best signal. The probe should be rested on the skin without pressure so as to avoid compromising the blood flow. Once located the signal should be evaluated as to pitch, presence of turbulence, number of sounds heard, and rate and rhythm if not noted by palpation. In the lower extremity, a normal doppler arterial signal is described as being moderately high pitched, crisp and consisting of two (and sometimes three) clear sounds. The first sound occurs during systole and is the result of the forward motion of the blood. The second sound occurs during diastole and is the result of a reversal of flow. The third sound sometimes heard is the result of arterial compliance. The initial bolus of blood moving through the artery during systole causes the vessel wall to stretch. With the drop on blood pressure during diastole this stretched position cannot be maintained and the compliant, elastic wall returns to its original position. This change in diameter of the vessel results in a forward motion of the blood producing the third sound. Lack of a third sound in the distal vessels is not abnormal. The presence of stenosis or occlusion produces changes in the detected signal. Blood distal to a stenosis or occlusion tends to move more slowly than normal so that its signal will have a lower than normal pitch. In addition, the second sound tends to be lost. Blood moving within a narrowed vessel tends to move at a greater rate than normal and will therefore have a higher than normal pitch. Turbulence will be produced by the currents set up by the moving blood striking a narrowing in the vessel and moving in many directions. Other arterial studies are performed with the Doppler flowmeter. These include determining the ankle-arm index as well as evaluating segmental blood pressures. The ankle-arm index (AAI, ankle-brachial index, ABI) is calculated by dividing the systolic pressure at the ankle by the systolic pressure of the arm. A blood pressure cuff is placed around the ankle and the Doppler signal in the dorsalis pedis located. The cuff is then inflated until the signal is lost. The cuff is then slowly deflated and the pressure at which the signal reappears is the systolic pressure. The process is repeated using the posterior tibial artery. Systolic pressure in the brachial artery is then determined (to maintain consistency the doppler flowmeter should be used) and the AAI calculated. Normally, the ankle systolic pressure will be equal to or slightly higher than the arm systolic pressure. Thus, a normal AAI should be one or slightly higher. Occlusion and/or narrowing will result in a lowering of the ankle systolic pressure indicated by an AAI of less than one. Patients will begin to experience intermittent claudication when the AAI falls to approximately 0.8. An AAI of less than 0.45 is associated with a poor prognosis for healing of a plantar ulcer. Absolute ankle pressures of less than 40 mmHg are considered to indicate a poor prognosis for ulcer healing, as are toe pressures of less than 20 mmHg. Toe pressures of greater than 40 mmHg are considered to be a favorable indication for healing. (Transcutaneous oxygen pressure of greater than 30 mmHg is felt to be a good indication for healing while pressure of less than 20mmHg is indicative of a poor prognosis.) Calcification of the vessel wall at the cuff location as occurs in Monkebergs medial calcinosis results in a higher pressure being needed to occlude the vessel (may be misinterpreted as a higher blood pressure) causing a higher AAI. The presence of this condition should be suspected in individuals with an AAI approaching two and may be confirmed by the presence of these calcifications on x-ray. It is important to note that diabetics are prone to this condition, and therefore care must be used in interpreting the results of the AAI in diabetics. It is felt that a toe-brachial index (TBI) may be more reliable since the digital vessels are not as prone to calcification. A normal TBI is 0.85. The level of narrowing or occlusion may be evaluated by obtaining segmental systolic pressures. In this study pressure cuffs are placed in several locations: high on the thigh, above the knee, below the knee, and at the ankle. There should be no more than a 30 mmHg drop in pressure from one segment to the next.

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Vascular Conditions
Aneurysm
80-90% of patients with a peripheral aneurysm have another. 80% with a popliteal aneurysm have another (60% are of the abdominal aorta; 50% have bilateral popliteal aneurysms). 20% with abdominal aorta aneurysms have a popliteal aneurysm.

Peripheral Occlusion
Peripheral arterial occlusive disease may be acute or chronic in nature. Acute peripheral occlusion may be the result of thrombolic or embolic processes and can arise in an artery already affected with chronic occlusive disease or may develop in a normal vessel. Acute thrombosis occurs most often when there is concurrent arterial occlusive disease. Here, rupture of an atherosclerotic plaque causes a thrombus to form in the already narrowed vessel, changing a chronic ischemic area into an acute ischemic area. Embolism is the most common cause of acute occlusion affecting the extremities. These emboli may originate in the heart of patients with arrhythmia, valve disease/prosthesis, or cardiomyopathy or may represent fragments of atheroma located in the arterial tree, particularly the abdominal aorta. Other causes of arterial emboli include aneurysm (popliteal), atherosclerotic plaque, injury, and vessel inflammation. Paradoxical embolism occurs when the source is a vein and the fragment passes through a septal defect in the heart. Acute occlusion is characterized by the sudden onset of pain and marked coldness of the involved extremity (or the sudden increase of symptoms in an already symptomatic extremity). The pain has been described as severe, knifelike or burning (paresthesia). Ischemia affecting the nerves in the area may result in numbness. Absence of pulses, pallor, collapsed superficial veins; sensory changes, muscle weakness and a decrease in deep tendon reflexes may all be found on physical examination. Other causes include vasospasm and aortic dissection.

Atherosclerosis
Peripheral arterial occlusive disease involving the extremities occurs predominantly in males between fifty and seventy years of age, with arteriosclerosis obliterans being responsible for the majority of cases of chronic occlusive disease in the elderly. This process has been found to appear at a younger age, be more widespread, and progress more rapidly in diabetics. In addition, it has been noted that among diabetics, the condition affects women almost as frequently as men. While the condition is easily recognizable by virtue of the characteristic signs and symptoms, it should be noted that significant reduction in blood flow with resulting symptoms does not occur until the artery is approximately 75% occluded. The most characteristic and easily recognizable symptom of chronic arterial occlusive disease is intermittent claudication. Patients demonstrating intermittent claudication will complain of discomfort, usually described as cramping, arising upon exertion and relieved by rest. Other forms of discomfort may be fatigue, weakness, aching, paresthesias, or the sensation of walking on gravel (also described as the feeling that the sock or stocking is bunching up under the foot). It is important to look for the cycle of walking producing pain that is rapidly relieved by rest, only to recur upon resuming walking. The discomfort is brought upon by a set amount of exertion (as affected by speed of walking and terrain, i.e. flat or hilly) and is rapidly relieved by cessation of the activity. A change in position is not necessary to bring about relief. It is, therefore, not necessary to sit or elevate the legs to obtain relief - merely standing still is all that is required. The patient may note that by walking more slowly, stopping more frequently, or walking abducted (to avoid active calf muscle contraction for toe off) the discomfort can be prevented. Since nocturnal leg cramps are not related to diminished circulation, they are also not related to intermittent claudication.

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Once recognized as intermittent claudication, pain at a particular location provides an indication as to the level of the occlusion. Thus, when only a single occlusion is present:

Area of Symptoms Foot Low calf Upper calf Calf and thigh Thigh and buttock Bilateral calf, thigh, buttock

Site of Occlusion Distal vessel (calf muscle contraction for toe off) Popliteal artery Superficial femoral artery Common femoral artery Iliac artery Aorto-iliac (Leriche syndrome)

While usually associated with absent pedal pulses, there are some uncommon situations in which true intermittent claudication occurs in patients with palpable pulses. Among these are patients with severe anemia (low oxygen carrying), severe arteriospastic disease, popliteal artery entrapment, and amyloidosis (the main artery is patent but the branches going to the muscle are occluded). Pain resembling that of intermittent claudication has been described in neurogenic claudication (also known as claudication of the cauda equina and pseudoclaudication). In this condition, compression of the cauda equina or partial obstruction of its blood supply by a protruding disc or bone hypertrophy will produce pain, paresthesias, and/or weakness in the thigh upon bending or standing. The walk-pain-rest-relief pattern is variable in these patients. A change in body position rather than cessation of activity is necessary to bring relief. Relief does not occur as rapidly as it does in true vascular claudication. Since the atherosclerotic disease process tends to be widespread, it is most likely that if present in one area (such as the lower extremity) it is probably present elsewhere (such as the heart).

Buergers Disease (Thromboangiitis Obliterans)

This condition has a strong association with smoking. The classic patient is a young male smoker. Symptoms include intermittent claudication with progression to rest pain and gangrene. The disorder tends to affect the tibial vessels and is also associated with Raynauds phenomenon and migratory superficial phlebitis.

Vasospasm
Livedo Reticularis Livedo reticularis is the most common of the vasospastic conditions. The skin shows a persistent reddish blue mottling, which is made worse with cold exposure affecting the extremities. The primary form tends to affect women between the ages of 20-40 and may improve with warming. Secondary livedo reticularis may be the result of embolism or be associated with systemic lupus erythematosus, polyarteritis nodosa, polycythemia vera, thrombocytosis, dysproteinemias, cold injury, neurogenic disorders, and amantadine use. Raynauds Phenomenon Raynauds phenomenon may be primary (also known as Raynauds disease) or secondary. Both conditions are clinically identical and are characterized by sudden arteriospasm associated with a three-phase color change of the skin along with pain and paresthesia. The fingers, toes, ears, and nose are most frequently affected. Exposure to cold, cigarette smoke, or emotional stress can incite the spasm with resulting marked pallor and pain. Slight breaking of the spasm with return of some blood flow results in cyanosis since there is extensive deoxygenation of the red blood cells reaching the area. Complete break in spasm results in vasodilatation with accompanying rubor. Thus, the sequence of color changes in Raynauds is white-blue-red. While primary Raynauds phenomenon (Raynauds disease) is idiopathic in nature, in secondary Raynauds phenomenon arteriospasm is present in conditions with underlying occlusive disease such as occurs in collagen vascular diseases, digital atherosclerosis, Buergers disease,

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embolism, polycythemia vera, and thrombocytosis. Other conditions associated with secondary Raynauds phenomenon include cryoglobulinemia, macroglobulinemia, cold agglutinins, cold injury, hepatitis B and C, malignancy, primary pulmonary hypertension, occupational trauma (pneumatic hammer, typing, piano playing), myxedema, pheochromocytoma, carpal tunnel syndrome, and nerve injury. Some medications such as ergot containing drugs, methylsergide, phenylpropanolamine, bleomycin, vincristine, bromocriptine, and beta-blockers have also been found to cause the condition. Acrocyanosis This condition, usually affecting young women, is characterized by a constant painless cyanosis and coldness of the hands and feet, made worse by cold exposure. The digits may become puffy and the skin may be hyperhidrotic. There is no association with arterial insufficiency in acrocyanosis and ulceration does not occur. The condition may be primary or secondary (associated with scleroderma, polycythemia vera, thrombocytosis, and propanolol). Erythromelalgia (erythermalgia) The skin of the feet (and lower legs) becomes red and warm upon warming. This may be associated with burning, itching, or tingling. Patients report the discomfort arises when the feet are covered while sleeping, and therefore sleep with the feet exposed. The condition may be primary or secondary. Secondary erythermalgia occurs in myeloproliferative disorders and may also occur in hypertension, venous insufficiency, diabetes, systemic lupus erythematosus, and rheumatoid arthritis. Aspirin and methysergide have been used as treatment.

Venous Disease
Unlike atherosclerosis, disorders of the venous system tend to affect younger individuals. The most common of these conditions is varicose veins (affecting approximately 12% of the population). Unlike the limb and/or life threatening arterial diseases, the problem associated with varicose veins is most often a cosmetic one, with most individuals being otherwise asymptomatic. Deep vein thrombosis is an exception to this due to the risks of life threatening pulmonary embolism and the subsequent development of post-phlebotic syndrome with its associated ulceration. Varicose Veins Varicose veins are more common in women and are aggravated by pregnancy. They are most commonly due to incompetent valves at the saphenofemoral junction resulting in reflux down the saphenous vein. When symptomatic, they produce feelings of a heavy, aching, tired lower leg and may be associated with ankle swelling. The vein may be tender. The symptoms are made worse by standing and tend to increase at the end of the day. Relief is obtained by elevation. Deep Vein Thrombosis (DVT) Unlike cases of superficial thrombophlebitis in which the classic signs and symptoms of swelling, redness, pain, and increased temperature and presence of a palpable cord are easily noted, most instances of deep vein thrombosis are asymptomatic. When symptomatic, the most common complaints are pain and swelling. Clotting present in the superficial femoral vein or below the knee produces swelling in the calf and foot. Involvement of the common and deep femoral veins will result in swelling to the inguinal ligament. Phlegmasia cerulea dolens, characterized by extreme leg swelling, cyanosis or rubor, pain, and loss of arterial pulses may develop when the thrombus occludes the iliofemoral outflow. This condition may progress to gangrene and has been reported to result in hypovolemic shock and death. If the limb becomes pale rather than rubrous or cyanotic, the condition is referred to as phlegmasia alba dolens. The classic Homans sign described in DVT is not as common as believed. Therefore, diagnosis based solely on clinical signs is inaccurate. Continuous wave doppler provides a sensitive and specific means to evaluate venous flow. Colorflow duplex ultrasonography is another reliable, noninvasive test useful in diagnosing DVT and has replaced venography. Initial treatment of DVT is intravenous heparin followed by oral warfarin (Coumadin).

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Once diagnosis and treatment of DVT has been established, it is necessary to determine its cause. It has long been recognized that the components of Virchows triad, slowing of blood flow (stasis), hypercoagulability, and changes in the vessel wall (trauma), are factors contributing to the development of DVT. While trauma (such as direct injury and surgery, especially pelvic surgery and surgery for hip fractures) and stasis (as associated with prolonged bed rest and compression) are easily recognized changes in coagulability may be more difficult to detect. Among conditions associated with hypercoagulability are internal malignancy, obesity, inflammatory bowel disease, Buergers disease, pregnancy, nephrotic syndrome, sepsis, cardiac disease (congestive heart failure with poor peripheral perfusion and venous stasis), ingestion of estrogen containing substances, and hypercoagulability disorders such as thrombocytosis, polycythemia vera, antithrombin III deficiency, heparin cofactor II deficiency, platelet hyperaggregability, lupus anticoagulant, protein C deficiency, and protein S deficiency. Following resolution of deep vein thrombosis, the patient will likely develop venous valvular (deep and/or communicating) incompetence with resulting post-phlebotic syndrome. This condition, the result of chronic venous stasis, is characterized by swelling, leakage of plasma proteins into the interstitial spaces, and extravasation of blood from the capillaries in the area. These contribute to the formation of skin discoloration (hemosiderin), pruritus (due to irritation caused by the hemosiderin), swelling, induration, and eventual ulceration (it should be noted that chronic ulcerations, as those associated with this condition, may undergo malignant conversion; long-standing stasis ulcers should, therefore, be biopsied at multiple sites along the edges). Patients with post-phlebotic syndrome may complain of pain, usually aching, which is relieved by leg elevation.

Lymphatic Disorders
Lower extremity swelling is a common complaint among patients and may be the result of many conditions. When the swelling is bilateral, systemic causes such as congestive heart failure, kidney disease, liver disease, malnutrition, and hypothyroidism as well as local causes such as bilateral deep vein or inferior vena cava thrombosis, venous valvular disease, and physiologic edema (due to prolonged dependency) should be considered. Unilateral swelling may occur in venous insufficiency, deep vein thrombosis, infection, and trauma. Lymphedema should be considered in both unilateral and bilateral swelling. Lymphedema, the accumulation of lymphatic fluid in the interstitial spaces, may be primary or secondary. Primary lymphedema affects females more frequently than males and may be congenital (Milroys disease when familial), arise around puberty (the most common form; lymphedema praecox, or Meiges disease when familial), or develop after the age of 35 (lymphedema tardive). Secondary lymphedema is the result of obstruction of lymphatic channels due to transection and scarring, lymph node resection, recurrent lymphangitis (elephantiasis nostras), tumor, parasitic infection (filariasis; the most common cause worldwide of secondary lymphedema), trauma, and radiation.

References
1. 2. 3. 4. 5. Aronow, Wilbert S., Stemmer, Edward A., and Wilson, Samuel Eric, editors: Vascular Diseases in the Elderly. Futura Publishing Company, 1997. Arthur N. Steinhart, D.P.M., Professor, Division of Medical Sciences, New York College of Podiatric Medicine. Eton, Darwin, editor: Vascular Disease: A Multi-specialty Approach to Diagnosis and Management, 2nd edition. Landes Bioscience, 1999. Fairbairn, John F., Juergens, John L., and Spittell, John A. Jr., editors: Peripheral Vascular Diseases, 4th edition. W. B. Saunders Company, 1972. Loscalzo, Joseph, Creager, Mark A., and Dzau, Victor J., editors: Vascular Medicine A Textbook of Vascular Biology and Diseases, 2nd edition. Little, Brown and Company, 1996.

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