4.7 Peripheral Vascular Disease Arthur N. Steinhart, DPM

Vascular ExaminationThe 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 examiner’s 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 patient’s pulse from the examiner’s

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 patient’s 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 bound-

ing 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 caus-

es 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 10-

degree 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 patient’s legs and changing the patient’s 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 “Buerger’s 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 patient’s 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 Monkeberg’s 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.

Medicine | Peripheral Vascular Disease 359

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:

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).

Buerger’s 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 Raynaud’s phenomenon and migratory superficial phlebitis.

Vasospasm

Livedo ReticularisLivedo 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.

Raynaud’s Phenomenon Raynaud’s phenomenon may be primary (also known as Raynaud’s 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 Raynaud’s is white-blue-red. While primary Raynaud’s phenomenon (Raynaud’s

disease) is idiopathic in nature, in secondary Raynaud’s phenomenon arteriospasm is present in conditions with

underlying occlusive disease such as occurs in collagen vascular diseases, digital atherosclerosis, Buerger’s disease,

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Area of Symptoms Site of Occlusion Foot Distal vessel (calf muscle contraction for toe off) Low calf Popliteal artery Upper calf Superficial femoral artery Calf and thigh Common femoral artery Thigh and buttock Iliac artery Bilateral calf, thigh, buttock Aorto-iliac (Leriche syndrome)

embolism, polycythemia vera, and thrombocytosis. Other conditions associated with secondary Raynaud’s

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.

AcrocyanosisThis 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 VeinsVaricose 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 Homan’s 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 Virchow’s 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, Buerger’s 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 (Milroy’s disease when

familial), arise around puberty (the most common form; lymphedema praecox, or Meige’s 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.

References1. Aronow, Wilbert S., Stemmer, Edward A., and Wilson, Samuel Eric, editors: Vascular Diseases in the Elderly.

Futura Publishing Company, 1997.

2. Arthur N. Steinhart, D.P.M., Professor, Division of Medical Sciences, New York College of Podiatric

Medicine.

3. Eton, Darwin, editor: Vascular Disease: A Multi-specialty Approach to Diagnosis and Management, 2nd

edition. Landes Bioscience, 1999.

4. Fairbairn, John F., Juergens, John L., and Spittell, John A. Jr., editors: Peripheral Vascular Diseases, 4th

edition. W. B. Saunders Company, 1972.

5. 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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