Physical Examination

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The physical examination in patients with PVD should consist of inspection, palpation, auscultation, and even percussion. Observations should note any asymmetry between the limbs, joint deformities, varicose veins, skin discoloration, absence of hair, swelling, ulcerations, tissue loss, and gangrene. Acute CLI from embolism or thrombosis typically causes pallor with decreased capillary refill that eventually leads to mottling unless adequate collateral flow can be recruited. Chronic ischemia may have a normal skin color with relatively normal or slightly delayed capillary refill, particularly if collateral flow has developed. Chronic advanced CLI can lead to dependent rubor due to chronic dilation of the postcapillary venules. The toes of the dependent limbs can become red with brisk capillary refill. This is often mistaken for hyperemia rather than a sign of severe ischemia. A cadaveric pallor on elevating the limb to greater than 45 degrees above the horizontal for 1 to 2 minutes, followed by slow venous filling with rubor after returning to a dependent position (Buerger's sign), also signals advanced CLI.

Ulcerations may be caused by chronic venous insufficiency or edema and arterial insufficiency. Chronic venous disease typically causes pigmentation of the lower legs from extravasation of red blood cells with superficial ulcers in the calves, more often medially than laterally. Arterial ulcerations are characteristically distal, involving the toes and even forefoot in advanced disease.

Palpation of the pedal pulses should be a mandatory part of the routine physical examination. Notably, even in healthy individuals, the dorsalis pedis (DP) pulse, the posterior tibial (PT) pulse, or both are unable to be palpated 8.1%, 2.9%, and 0.7% of the time, respectively (McGee and Boyko, 1998). This results from normal anatomic variation. Wide and prominent femoral or popliteal pulses may be a sign of an aneurysm. A significant temperature gradient from proximal to distal and between ipsilateral and contralateral limbs often is a sign of advanced disease. The abdomen should be palpated to assess for the presence of an abdominal aortic aneurysm. Reproduction of pain with palpation over joints is not caused by vascular disease and seems to be a sign of such orthopedic conditions as degenerative joint disease, sacroili-itis, gout, trauma, or plantar fasciitis. Reproduction of pain with palpation of muscle groups may be vascular in etiology if there is severe ischemia, but the clinician should also

Table 27-11 Differential Diagnosis of Claudication

Onset

Onset

Effect

Location of

Features of

Relative to

Relative to

Effect of

of Body

Diagnosis

Discomfort

Discomfort

Exertion

Standing

Rest

Position

Other Features

Arterial

Depends on

Aching,

Consistently

Unrelated to

Relieved

None

Gradual onset of

claudication

level of stenosis

cramping,

reproduced

standing

promptly

discomfort with

(occlusion):

weakness

with same

exercise

aortoiliac

degree of

Very reproducible

disease affects

activity

hip/thigh/

buttock, can

affect entire

limb

Infrainguinal

disease affects

calf and foot

Venous

Entire limb,

Tight, tense

After exercise

Unrelated to

Relieved slowly

Relieved

History of DVT, edema,

claudication

usually worse

sensation

standing

more

or venous congestion

in thigh and

quickly with

groin

elevation

Chronic

Always involves

Severe burning,

Worse with

Unrelated to

Improved, but

Symptoms

Gradual or subacute

critical limb

foot; symptoms

aching, but

minimal activity

standing

incompletely

may be

onset

ischemia

may be more

may be

improved

Dependent rubor

proximal with

asymptomatic

with

Elevation pallor

more proximal

in patients

dangling

Gangrene

disease

with profound

foot over

neuropathy

side of

bed while

sleeping

Acute critical

Always involves

Severe aching,

Worse with

Unrelated to

Improved, but

Symptoms

Acute onset

limb ischemia

foot; symptoms

cramping,

minimal activity

standing

incompletely

may be

Pale, cold

may be more

painful

improved

Loss of motor/

proximal with

with

sensory functions is an

more proximal

dangling

emergency

disease

foot over

side of

bed while

sleeping

Arthritis

Joints

Aching, may

Variable

Weight

Variable, may

Less pain in

Variable, may be

be sharp with

bearing

be present with

non-weight

related to weather

position change

reproduces

rest

bearing

May have effusion

pain

position

Lumbar back

Lumbar

Sharp, stabbing,

Immediate

Weight

Variable, may

Certain

History of back

pain (e.g.,

region; may

shooting

bearing

be present at

positions

problems

herniated disc,

radiate down

reproduces

rest

exacerbate

Worse with lifting

nerve root

dermatomes

pain

or alleviate

May have motor/

compression)

if there is

pain

sensory deficits

nerve root

Reproducible with

compression

percussion

Sacroiliitis

Sacroiliac

Sharp, stabbing,

Immediate

Weight

Variable, may

Certain

Inflammatory disorder

region

shooting

bearing

be present at

positions

Reproducible with

reproduces

rest

exacerbate

palpation

pain

or alleviate

pain

Plantar fasciitis

Plantar region

sharp, stabbing,

Immediate

Weight

Immediate

Less pain in

Reproducible with

searing

bearing

relief with

non-weight-

palpation

reproduces

non-weight

bearing

pain

bearing

position

Continued

Table 27-11 Differential Diagnosis of Claudication—Cont'd

Diagnosis

Location of Discomfort

Features of Discomfort

Onset Relative to Exertion

Onset Relative to Standing

Effect of Rest

Effect of Body Position

Other Features

Peripheral neuropathy

Stocking glove distribution

Paresthesia, dysthesia, may be quite severe

Unrelated to activity

Unrelated to standing

Usually a constant sensation, unrelated to rest

Unrelated to change in position

Common in diabetics Present 24 hours a day, may interrupt sleep

Myopathy

In the muscle groups, may be systemic

Dull, aching, weakness

Immediate

Variable

Improved with less physical activity

May exacerbate discomfort

Reproducible with palpation

Statin myopathy not uncommon Inflammatory disorders rare

D]VT, Deep venous thrombosis.

Table 27-12 Differential Diagnosis of Chronic Leg Swelling

Clinical Feature

Venous

Lymphatic

CardiacOrthostatic

"Lipedema"

Consistency of swelling

Brawny

Spongy

Pitting

Noncompressible (fat)

Relief by elevation

Complete

Mild

Complete

Minimal

Distribution of swelling

Maximal in ankles and legs, feet spared

Diffuse, greatest distally

Diffuse, greatest distally

Maximal in ankles and legs, feet spared

Associated skin changes

Atrophic and pigmented, subcutaneous fibrosis

Hypertrophic, lichenified skin

Shiny, mild pigmentation, no trophic changes

None

Pain

Heavy, ache, tight or bursting

None or heavy ache

Little or none

Dull ache, cutaneous sensitivity

Bilaterality

Occasionally, but usually unequal

Occasionally, but usually unequal

Always, but may be unequal

Always

From Rutherford RB. Basic approaches to vascular problems. In Vascular Surgery, 5th ed, vol 1, p 10. Philadelphia, Saunders, 2000.

Table 27-13 Clinical Categories of Acute Limb Ischemia

Description/ Prognosis

Findings

Doppler Signals

Category

Sensory Loss

Motor Weakness

Arterial

Venous

I. Viable

Not immediately threatened

None

None

Audible

Audible

II. Threatened

a. Marginally

Salvageable if promptly treated

Minimal (toes) or none

None

Inaudible

Audible

b. Immediately

Salvageable with immediate revascularization

More than toes, associated with rest pain

Mild, moderate

Inaudible

Audible

III. Irreversible

Major tissue loss, or permanent nerve damage inevitable

Profound, anesthetic

Profound, paralysis (rigor)

Inaudible

Inaudible

From Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity Ischemia: Revised version. Reprinted with permission from The Society of Vascular Surgery.

J Vasc Surg 1

997;26:517-538, Table 1.

Table 27-14 Clinical Categories of Chronic Limb Ischemia: Fontaine's stages and Rutherford's categories consider other causes of myopathy, such as fibromyalgia, polymyalgia rheumatica, drug-induced myalgia, and trauma.

The carotid arteries, abdomen, and femoral arteries should be auscultated for bruits. Only gentle pressure should be applied with the stethoscope over the carotid and femoral arteries because pseudobruits can be created by compression of the underlying vessel. Finally, percussion over the lumbar spine may be useful in eliciting pain from sacroiliitis, lumbar disk disease, or nerve root compression.

Noninvasive Testing

Noninvasive vascular testing is useful to confirm clinical suspicion of PVD in patients with leg discomfort and to screen asymptomatic patients at risk for vascular disease, particularly diabetics. Noninvasive testing is also very helpful for the surveillance of vessel patency after percutaneous or surgical intervention.

Noninvasive Vascular Study

A complete noninvasive vascular study (NIVS) consists of the ABI, segmental BPs, and pulse-volume recordings (PVR) obtained at rest. When physically possible, the ABIs should also be ordered with exercise to assess for an ischemic response (Fig. 27-24).

The ABI is defined as the highest systolic blood pressure (SBP) of either the DP artery or PT artery divided by the higher of the SBP from either the right or left brachial artery (Table 27-15). Segmental BPs provide more specific information as to the location of the stenosis/obstruction. BP readings are obtained at the high-thigh, low-thigh, calf, ankle, metatarsal, and toe level, specifically looking for pressure gradients proximally to distally. Pulse-volume recordings are plethysmography measurements that detect changes in the blood volume flowing through the limb. A normal PVR tracing resembles a normal arterial pulse wave tracing with a rapid upstroke, prominent dicrotic notch, and rapid down-stroke. As the severity of the disease increases, the waveforms become more blunted, the dicrotic notch disappears, and ultimately the waveforms become flat.

The standard exercise protocol of walking on a treadmill for 5 minutes at 2 mph at a 12% grade (Rutherford et al., 1997) is quite modest in comparison to the workload involved in a routine Bruce protocol that is typically employed for cardiac stress testing. The purpose of the Rutherford protocol is not to induce coronary ischemia and thus is typically well tolerated from a cardiopulmonary standpoint. Relative contraindications to walking on a treadmill include severe symptomatic CAD (Canadian Cardiovascular Society Class 3 or 4), severe decompensated CHF (NYHA Class III or IV), severe symptomatic COPD, orthopedic or balance disorders that preclude safe ambulation on a treadmill, or severely depressed resting ABI (<0.5). If patients are unable to walk on a treadmill, other means of exercise may suffice, such as stationary bicycling, walking in the hallway, or toe lifts. However, these alternative forms of exercise are not standardized and may impact the diagnostic sensitivity and specificity of the study.

Some patients with mild PVD may have an ABI that is normal at rest but significantly decreased with exercise (Fig. 27-25). In fact, comparing angiography, which is the "gold standard" for diagnosing PVD, to ABIs, there actually needs to be a rather severe single stenosis, or moderate diffuse multilevel disease, to have a depression in the resting ABI. Even a mildly depressed resting ABI implies there is a considerable burden of disease. Therefore, ABIs done at rest only and not with exercise will have a relatively high false-negative rate, and many patients with a normal resting ABI will be misdiagnosed as having nonvascular limb pain when the true etiology of their discomfort is PVD. A corollary to this is that many epidemiologic studies use only resting ABI as a diagnostic criterion for PVD, which leads to underestimation of the true incidence of PVD. In fact, obtaining ABIs at rest only without exercise is similar to performing a nuclear myocardial perfusion imaging study at rest only and trying to establish a diagnosis of coronary artery disease—this is impossible. The myocardial perfusion may be normal at rest, but it is the stress images that allow one to determine whether there is reversible ischemia.

Another potential pitfall of ABIs is vascular calcification. Severe calcification of the arterial wall eventually leads to an inability to compress the blood vessels despite cuffs inflated to suprasystolic pressures. Consequently, ABIs can be falsely elevated, and caution should be used in interpreting an ABI greater than 1.3. This is particularly common in patients with diabetes and patients on chronic hemodialy-sis. In this case the toe-brachial index has been established as an adequate surrogate to the ankle-brachial index (Sahli et al., 2004).

An NIVS can provide a general region (e.g., femoropop-liteal segment) that is diseased. However, the NIVS is not precise enough to determine the exact location of the stenosis or occlusion. In other words, NIVS provides physiologic information with limited anatomic localization of disease. Arterial duplex Doppler ultrasound, computed tomography

Table 27-14 Clinical Categories of Chronic Limb Ischemia: Fontaine's stages and Rutherford's categories

Fontaine

Rutherford

Stage

Clinical

Grade

Category

Clinical

I

Asymptomatic

G

G

Asymptomatic

IIa

Mild claudication

I

1

Mild claudication

severe claudication

I

2

Moderate claudication

I

3

Severe claudication

III

Ischemic rest pain

II

4

Ischemic rest pain

III

S

Minor tissue loss

IV

Ulceration or gangrene

III

6

Major tissue loss

From Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). TransAtlantic InterSociety Consensus (TASC). J Vasc Surg 2GGG;B1:S1-S296, Table 9. Reprinted with permission from The Society of Vascular Surgery.

7/21/2005

Doppler

I-Segmental BP-1

1 Segment/Brachial Index '

I-Segmental BP-1

1 Segment/Brachial Index '

179 1.25

1.06

1.08

64 0.45

179 1.25

1.06

1.08

64 0.45

1.01

153 129

0.43

lura

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