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14 2
LYMPHANGITIS
CH
fever and shaking chills. History might determine whether lesions
11
induced by trauma or infection may have served as a portal of entry.
Vascular Examination
As in any comprehensive physical examination, vital signs (blood pressure, heart rate, respiratory rate) should be assessed and recorded. Blood pressure should be measured in both arms and preferably in supine, seated, and upright positions. Overall appear­ance of the patient should be noted.
The vascular examination includes inspection, palpation, and auscultation of vascular structures in many areas of the body. A systematic approach ensures a complete evaluation, so the exami­nation described in this chapter will cover principal anatomical regions that are particularly relevant to the peripheral vasculature. The heart, lungs, and neurological and musculoskeletal systems should be examined, but details of these examinations are beyond the scope of this chapter.
Limbs
PULSE EXAMINATION
The pulse examination of the arms and legs is a critical part of the vascular examination. Asymmetry, decreased intensity, or absence of pulses provide clinical evidence of PAD and indicate the location of stenotic lesions. Some examiners describe pulses as absent, diminished, or normal, or use a numerical scale (e.g., from 0 [absent] to 2+ [normal]). Bounding pulses may be evidence of aortic valve insufficiency, and dilated expansive pulses a sign of ectasia or aneurysm.
Pulses of the arms—brachial, radial, and ulnar pulses—should be palpated using two or three fingertips. The brachial pulse is superficial and in the medial third of the antecubital fossa. The radial pulse, also superficial, can be found over the stylus of the radius near the base of the thumb ( pated on the volar aspect of the wrist, over the head of the ulnar bone. Wrist support by the examiner improves pulse detection by decreasing overlying muscle tension.
Pulse examination of the leg (femoral, popliteal, posterior tibial, and dorsalis pedis pulses) should be undertaken with the patient supine. The femoral pulse is located deep, below the inguinal liga­ment, about midway between the symphysis pubis and iliac spine. Obesity may obscure local landmarks. Lateral rotation of the leg, pannus retraction, and two hands may be required for adequate palpation. On occasion, the increase in flow velocity caused by a stenosis may create a thrill in the common or superficial femoral artery that is appreciated by palpation of the femoral pulse, or a bruit that can be heard with auscultation.
Palpation of the popliteal pulse can be difficult. The leg should be straight yet relaxed to decrease overlying muscle stiffness. The popliteal pulse should be palpated with three fingers from each hand while the thumbs are applying moderate opposing force to the top of the knee ( found at the junction of the medial and lateral thirds of the fossa. In contrast to superficial pulses like the radial or dorsalis pedis pulse, the popliteal pulse is diffuse and deep. Widened popliteal pulses may be indicative of popliteal artery aneurysm.
The posterior tibial pulse can be found slightly below and behind the medial malleolus. Counterpressure with the thumb and passive dorsiflexion of the foot may increase the likelihood of
Fig. 11-2). The popliteal pulse typically can be
Fig. 11-1). The ulnar pulse is pal-
FIGURE 11-1 Palpating radial pulse. Examiner, using three or four fingers, lightly palpates the superficial radial pulse over stylus of radius near base of thumb.
FIGURE 11-2 Palpating popliteal pulse. Popliteal pulse requires moderate pressure for its appreciation. Examiner uses both thumbs for moderate opposing force while placing digits two, three, and four in lateral third of popliteal fossa. Patient's leg should be relaxed while examiner induces mild flexion. A widened popliteal artery pulse may indicate presence of aneurysm.
palpation ( absence is diagnostic for PAD. In contrast, the dorsalis pedis pulse, which can be appreciated just lateral to the extensor tendon on the dorsum of the foot, normally may be absent in 2% to 12% of persons.
Fig. 11-3). The posterior tibial pulse should be present. Its
FIGURE 11-3 Palpating posterior tibial pulse. Posterior tibial pulse resides
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slightly below and behind medial malleolus. It should be approached from the lateral aspect, with digits applied to lower curvature of malleolus. Passive foot dorsiflexion may enhance appreciation of pulse.
THE ALLEN TEST
The radial and ulnar arteries supply blood flow to the hand. Within the hand, these arteries form the superficial and deep palmar arches, enabling blood supply to the digits from either vessel; 5% to 10% of the population has a congenitally incom­plete arch. Disease states associated with interruption of the palmar arch include connective tissue diseases like the CREST variant (calcinosis, Raynaud phenomenon, esophageal dysmotil­ity, sclerodactyly, telangiectasia) of scleroderma, vasculitides like TAO, and thromboemboli. The Allen test can differentiate between a complete and incomplete palmar arch. The examiner occludes both the radial and ulnar pulses (
Fig. 11-4), and the patient then
opens and closes the fist several times, creating palmar pal­lor. Upon release of one pulse, normal skin color should return within seconds. The other artery is then tested and observed simi­larly. Persistent pallor is indicative of an incomplete palmar arch or occluded artery distal to the remaining pulse occluded by the examiner.
Nearly three quarters of all patients with TAO, will have a posi­tive Allen test, and 50% will report Raynaud phenomenon. Digital ischemia in these patients is more likely to progress and cause
persistent cyanosis and lead to digital ulcers. Patients with TAO also may develop migratory superficial thrombophlebitis, which appears as painful, tender, red nodules.
THORACIC OUTLET MANEUVERS
Thoracic outlet syndrome results from compression of the neu­rovascular bundle as it leaves the thoracic cavity. Each compo­nent of the bundle may be affected, including the brachial plexus, subclavian/axillary artery, and subclavian/axillary vein.
Thoracic outlet maneuvers seek to elicit positional inter­ruption of arterial flow. During the examination, the physi­cian holds the radial pulse in one hand and maneuvers the arm with the other. The subclavian artery is auscultated in the supraclavicular fossa. An abnormal thoracic outlet maneu­ver is characterized by development of a subclavian bruit followed by loss of the radial pulse. Several thoracic outlet maneuvers have been described, and each may be relevant to compression at different sites in the thoracic outlet. Each side is examined in sequence. The Adson maneuver assesses the segment of the subclavian artery in the scalene triangle. The patient rotates his/her head toward the symptomatic side, extends the neck (i.e., looking up and over the shoul­der), and simultaneously performs an exaggerated inspira­tion. The costoclavicular maneuver assesses the segment of the subclavian artery coursing between the clavicle and first rib. The patient thrusts the shoulders back and inferiorly. The hyperabduction maneuver evaluates the subclavian artery as it courses near the insertion of the pectoralis major muscle. The patient is seated and the head is looking forward. The arm is abducted 180 degrees to a position along the side of the head. Abduction of the arm to 90 degrees may be combined with external rotation in evaluating symptoms suggestive of tho­racic outlet syndrome (
Fig. 11-5). This maneuver is often used
to assess subclavian venous or arterial compression during ultrasonography or angiography.
For patients in whom clinical suspicion for thoracic outlet syn­drome is present, sensitivity and specificity for these provoca­tive tests are 72% and 53%, respectively.
16
Routine application of these maneuvers is not warranted, however, since up to 50% of the population may have a positive finding. Indeed, in one study of 64 randomly selected subjects, application of these maneuvers in a nonspecific manner overdiagnosed the syndrome more than threefold. ticularly difficult group for these maneuvers and generate a false­positive rate of nearly 50%.
17
Patients with carpal tunnel syndrome present a par-
18
143
CH 11
THE HISTORY AND PHYSICAL EXAMINATION
A
FIGURE 11-4 Allen test. The Allen test determines presence or absence of a complete palmar arch. Both radial and ulnar pulses are occluded while patient opens and closes hand to create palmar pallor. Once pallor is evident, examiner releases one pulse. In this example, patient presented with persistent fifth digit and hypothenar cyanosis. A, Release of radial artery pulse results in expected hyperemia and palmar erythema. B, In contrast, release of ulnar artery pulse does not result in palmar erythema, indicating proximal occlusion in ulnar segment of palmar arch. This test is considered a positive Allen test.
B
14 4
CH
11
FIGURE 11-5 Elevated Arm Stress Test (EAST) may be used to evaluate subclavian artery as it courses near insertion of pectoralis major muscle.
Patient initially sits looking forward while arms are abducted 90 degrees, elbows are abducted 90 degrees, and patient repeatedly makes a clenched fist. During maneuver, radial pulse should be palpated while subclavian artery is auscultated. Loss of pulse or development of subclavian artery bruit is a positive study.
LIMB ISCHEMIA
ULCERS
Ischemia arising from arterial occlusive disease or emboli may cause formation of ischemic ulcers (see Chapter 60). They tend to be small, annular, pale, and desiccated (Fig. 11-6) and are usu- ally located in distal areas of the limbs (e.g., toes, heels, fingertips). Ischemic ulcers vary in size but may be as small as 3 mm in diam­eter. Arterial ischemic ulcers are tender. Neurotrophic ulcers that develop in patients with diabetes typically occur at sites of trauma, such as areas of callus formation, bony prominence, or parts of the foot exposed to mild chronic trauma caused by ill-fitting shoes. Ischemic ulcers also develop in diabetic patients with PAD and may have features of neuropathic ulcers. Without proper treatment, ulceration may progress to tissue necrosis and gangrene. Gangrene can be characterized as an area of dead tissue that blackens, mum­mifies, and sloughs.
FIGURE 11-6 Digital ulceration. Pernio is associated with persistent sensation of cold, with pain in the toes. Painful blue nodules are noted in association with a discrete ulcer.
DIGITAL VASOSPASM
It is unusual for patients with Raynaud phenomenon to present to the physician's office during an attack in which the fingers are blanched. Moreover, it is difficult to precipitate digital ischemia in these patients, even with local cold exposure, such as placing the hands in ice water. Digital ischemia may be apparent in patients with fixed obstructive lesions of the digital arteries. Persistent digital isch­emia may occur in patients with connective tissue disorders such as scleroderma or systemic lupus erythematosus, atheroemboli, TAO, or atherosclerosis. The fingers and toes are cool and appear cyanotic or pale. Fissures, pits, ulcerations, or necrosis or gangrene may be evident on the ischemic digits (see
Fig. 11-6).
LIVEDO RETICULARIS
Livedo reticularis can be described as a lacelike or netlike pattern in the skin (
Fig. 11-7). The “laces” may vary in color from red to blue
EDEMA
The most common physical findings of DVT include unilateral leg swelling, warmth, and erythema. The affected vein may be ten­der. A common femoral vein cord is detected by palpating along its course just below the inguinal ligament vein, and a femoral vein cord would be appreciated along the anteromedial aspect of the thigh. In the absence of obvious edema, a subtle clue may be unilateral absence of contours of the thigh, calf, or ankle. Muscular groups subtended by the thrombosed vein may be edematous due to poor venous drainage, conferring a boggy feeling to the affected calf or thigh muscles. Inflammation associated with a thrombosis may make the leg feel warm.
FIGURE 11-7 Livedo reticularis. Note lacelike pattern of superficial skin
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vessels surrounding a clear area.
145
CH 11
THE HISTORY AND PHYSICAL EXAMINATION
FIGURE 11-8 Skin changes of chronic venous insufficiency. Chronic venous insufficiency and edema result in deposition of hemosiderin, causing darkening and toughening of skin and giving calf a brawny appearance. Note small superficial venous ulcers mid-calf above shin.
Homans sign is nonspecific and misses the diagnosis as com­monly as it makes it. In John Homans's essay on lower extremity venous thrombosis, he states, “The clinical signs of a deep throm­bosis of the muscles of the calf are entirely lacking when the indi­vidual lies or even reclines in bed. It is possible there may be a little discomfort upon forced dorsiflexion of the foot (tightening of the posterior muscles) but it is not yet clear whether or not this is a sign upon which to depend.”
19
Presence of thrombus just below the skin makes the diagnosis of superficial thrombophlebitis relatively easy. The patient may pres­ent with local venous engorgement, a palpable cord, warmth, ery­thema, or tenderness.
CHRONIC VENOUS INSUFFICIENCY
With chronic venous insufficiency, the physical examination may demonstrate fibrosis, tenderness, excoriation, and skin induration from hyperkeratosis, cellulitis, and ulceration (
Fig. 11-8). Chronic venous
edema may impart hemosiderin deposition in the skin and confer a brawny appearance, typically in the pretibial calf. The severity of chronic venous disease may be classified using the CEAP (clinical signs,
e
tiology, anatomy, pathophysiology) classification20 (Table 11-1).
In contrast to arterial ulcers, which are circumscribed and pallid, venous ulcers are large with irregular borders, erythematous, and moist, giving the skin a shiny appearance. They are usually located near the medial or lateral malleolus. Venous ulcers may be pain­less, but many are associated with pain.
21,22
VARICOSE VEINS
Varicose veins are dilated, serpentine, superficial veins. If they cluster, they may feel and appear like a bunch of grapes (Fig. 11-9). Varicose veins should be inspected and palpated. Areas of erythema, ten­derness, or induration may identify superficial thrombophlebitis. Varicose veins are most prominent with leg dependence (e.g., with standing). Once filled, the veins may be balloted, and a fluid wave may be detected. Venous telangiectasias, also known as spider veins,
TABLE 11-1 CEAP Clinical Classification
CLASS CLINICAL SIGNS
0 No visible or palpable signs of venous disease
1 Telangiectasis or reticular veins
2 Varicose veins
3 Edema
4 Skin changes ascribed to venous disease (e.g., pigmentation,
venous eczema, lipodermatosclerosis)
5 Skin changes as defined above, with healed ulceration
6 Skin changes as defined above, with active ulceration
CEAP, clinical signs, etiology, anatomy, pathophysiology.
are commonly confused with varicose veins. Spider veins are typi­cally small, cutaneous veins in a caput medusa pattern.
Superficial venous varicosities may be primary or result from deep venous thrombosis or insufficiency. An examiner can distin­guish between superficial venous insufficiency and deep venous insufficiency at the bedside using the Brodie-Trendelenburg test. With the patient lying supine, the leg is elevated to 45 degrees and a tourniquet applied after the veins have drained. The patient then stands. The veins below the tourniquet should fill slowly. If venous refill distal to the site of tourniquet application occurs in less than 30 seconds, this is evidence of an incompetent deep and perfora­tor system. Slower refills suggest a competent deep and perforator system. The varicose veins are examined upon tourniquet release. Superficial venous insufficiency will be confirmed with rapid ret­rograde superficial venous filling.
The Perthes test can differentiate between deep venous insuf­ficiency and a deep venous obstruction as the cause of vari­cose veins. The patient is asked to stand, and once the superficial veins are engorged, a tourniquet is applied around the mid-thigh. The patient then walks for 5 minutes. If the varicose veins col­lapse below the level of the tourniquet, the perforator veins are
14 6
CH
11
FIGURE 11-9 Varicose veins. Severe bilateral varicose veins with extension into both feet.
presumed competent and the deep veins patent. If the superficial veins remain engorged, either the superficial and/or communicat­ing veins are incompetent. If the varicose veins increase in promi­nence, and walking causes leg pain, the deep veins are occluded.
LYMPHEDEMA
Fig. 11-10). In addition, the inability to
pinch skin on the toes, the Stemmer sign, also may differentiate early lymphedema from venous edema. Subsequently, the limb becomes wooden as progressive deposition of protein-rich fluid causes indu­ration and fibrosis of affected tissues. Lymphedema increases pro­duction of subcutaneous and adipose tissue, thickening the skin. Advanced disease may be identified when the leg feels wooden, edema is no longer pitting, and the limb is enlarged; the skin may appear verrucous at the toes. Palpation for lymphadenopathy should be performed when considering secondary causes of lymphedema.
LYMPHANGITIS
Lymphangitis can usually be visualized as a red streak that extends proximally from an inciting lesion. If left untreated, the entire limb may become edematous, erythematous, and warm, without evidence of venous congestion or impairment of arterial flow. Commonly, the regional lymph nodes are indurated.
Neck Examination
The neck is inspected for any areas of swelling or asymmetry. Jugular venous pressure is assessed to investigate the possibility of a volume overloaded state or congestive heart failure. Patients typically are placed at 45 degrees and the height of jugular venous pressure estimated. If necessary, the angle of head elevation should be adjusted to see the top of the jugular venous column.
The carotid arteries are palpated between the trachea and the sternocleidomastoid muscles. In older patients especially, the carotid body may be sensitive, and carotid pulses may induce bra­dycardia and hypotension. Pulses should be symmetrical with a rapid upstroke. Pulse asymmetry may indicate a proximal carotid or brachiocephalic stenosis. Parvus and tardus pulses (decreased amplitude and a delayed slow upstroke) may indicate aortic valve stenosis or proximal occlusive disease. Stenosis of the carotid bifur­cation or internal carotid artery usually does not affect carotid pulse contour or amplitude. Occasionally, severe stenosis will cre­ate a thrill that can be appreciated by palpation.
The carotid pulses are auscultated to elicit evidence of bruits. Bruits are caused by blood flow turbulence as a result of arterial stenosis, extrinsic compression, aneurysmal dilation, or arterio­venous connection. The bell of the stethoscope is recommended to appreciate low-frequency bruits and eliminate any adventi­tious sounds heard through the diaphragm. The entire cervical portion of each carotid artery should be auscultated, including the segment near the angle of the jaw where the carotid bifurca­tion is often located ( arteries for bruits is performed in the supraclavicular fossa and between the lateral aspect of the clavicle and pectoralis mus­cle. Although the proximal location of a bruit defines the area
Fig. 11-11). Auscultation of the subclavian
FIGURE 11-10 Lymphedema. Extension of edema into foot to level of toe is a useful physical sign to differentiate between venous edema and lymphedema. Foot swelling ending abruptly at toes is called squared toe sign.
FIGURE 11-11 Auscultation of carotid artery. To appreciate low-tone bruits, examiner should use stethoscope bell and apply mild to moderate pressure. Entire length of artery should be examined, with particular attention paid to region just below jaw, at approximation of carotid artery bifurcation.
of turbulent flow, a bruit may be appreciated for an additional
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several centimeters. The sensitivity and specificity of a carotid bruit for the presence of stenosis ranges from 50% to 79% and 61% to 91%.
23
The pitch of bruits increases with worsening sever­ity. Continuation of the bruit into diastole is another marker of severity and implies advanced stenosis. Paradoxically, severe stenosis causing subtotal arterial occlusion may not evoke an audible bruit.
Abdominal Vascular Examination
Vascular examination of the abdomen is performed as the patient lies supine on the examining table, with legs outstretched. From this position, the abdominal wall should be relaxed and not rigid. Prior to palpation, the abdomen should be inspected. Engorged superficial veins in the abdomen indicate the possibility of inferior vena cava obstruction. After inspection, all four quadrants are aus­cultated with the stethoscope. The presence of bruits is indicative of aortic or branch vessel occlusive disease. Bruits may arise as a result of mesenteric, renal, or aortic disease. Following auscultation, the abdomen is palpated for masses and to detect an aortic aneu­rysm. Deepest palpation can generally be obtained by gradually increasing pressure in the midline using both hands ( asthenic patients, the aorta can be palpated. In subjects with a waist size greater than 40 inches, the likelihood of palpating an aneurysm is quite limited.
FIGURE 11-12 Abdominal palpation for aneurysm. Examiner, using progressively increasing force, palpates until aorta can be defined between both sets of fingers. Examiner should appreciate lateral pulsation with every heart beat. Aneurysm sizing is performed by estimating distance between closest fingers of each hand.
Fig. 11-12). In
Presence of an aneurysm can be determined when there is a dis­tinct and expansive pulsatile configuration to the aorta. An aneu­rysm should be sized by determining the lateral borders with both hands, and the space estimated with a measuring tape. Tenderness during the abdominal vascular examination is unusual and may suggest aneurysmal expansion, an inflammatory aneurysm, or a contained rupture. Nonaortic pathology, including appendicitis, cholecystitis, diverticulitis, and peritonitis, are more common causes of tenderness.
REFERENCES
1. Fowkes FG, Murray GD, Butcher I, et al: Ankle brachial index combined with Framingham
risk score to predict cardiovascular events and mortality: a meta-analysis, JAMA 300: 197–208, 2008.
2. McDermott MM, Greenland P, Liu K, et al: Leg symptoms in peripheral arterial disease:
associated clinical characteristics and functional impairment, JAMA 286:1599–1606,
2001.
3. McDermott MM, Liu K, Greenland P, et al: Functional decline in peripheral arterial
disease: associations with the ankle brachial index and leg symptoms, JAMA 292: 453–461, 2004.
4. Rose GA: The diagnosis of ischaemic heart pain and intermittent claudication infield
surveys, Bull World Health Org 27:645–658, 1962.
5. Coyne KS, Margolis MK, Gilchrist KA, et al: Evaluating effects of method of administration
on walking impairment questionnaire, J Vasc Surg 38:296–304, 2003.
6. Criqui MH, Denenberg JO, Bird CE, et al: The correlation between symptoms and non-
invasive test results in patients referred for peripheral arterial disease testing, Vasc Med 1:65–71, 1996.
7. Regensteiner JG, Gardner A, Hiatt WR: Exercise testing and exercise rehabilitation for
patients with peripheral arterial disease: status in 1997, Vasc Med 2:147–155, 1997.
8. Rajagopalan S, Grossman PM: Management of chronic critical limb ischemia, Cardiol Clin
20:535–545, 2002.
9. Jaffery Z, Thornton SN, White CJ: Acute limb ischemia, Am J Med Sci 342:226–234, 2011.
10. Fukumoto Y, Tsutsui H, Tsuchihashi M, et al: The incidence and risk factors of cholesterol
embolization syndrome, a complication of cardiac catheterization: a prospective study, J Am Coll Cardiol 42:211–216, 2003.
11. Olin JW: Thromboangiitis obliterans (Buerger's disease), N Engl J Med 343:864–869,
2000.
12. Mackinnon SE, Novak CB: Thoracic outlet syndrome, Curr Probl Surg 39:1070–1145, 2002.
13. Levien LJ: Popliteal artery entrapment syndrome, Semin Vasc Surg 16:223–231, 2003.
14. Wigley FM: Clinical practice. Raynaud's phenomenon, N Engl J Med 347:1001–1008, 2002.
15. Bergan JJ, Schmid-Schonbein GW, Smith PD, et al: Chronic venous disease, N Engl J Med
355:488–498, 2006.
16. Gillard J, Perez-Cousin M, Hachulla E, et al: Diagnosing thoracic outlet syndrome:
contribution of provocative tests, ultrasonography, electrophysiology, and helical computed tomography in 48 patients, Joint Bone Spine 68:416–424, 2001.
17. Warrens AN, Heaton JM: Thoracic outlet compression syndrome: the lack of reliability of its
clinical assessment, Ann R Coll Surg Engl 69:203–204, 1987.
18. Nord KM, Kapoor P, Fisher J, et al: False positive rate of thoracic outlet syndrome diagnostic
maneuvers, Electromyogr Clin Neurophysiol 48:67–74, 2008.
19. Homans J: Venous thrombosis in the lower limbs: its relation to pulmonary embolism,
Am J Surg 38:316–326, 1937.
20. Beebe HG, Bergan JJ, Bergqvist D, et al: Classification and grading of chronic venous
disease in the lower limbs, A consensus statement, Int Angiol 14:197–201, 1995.
21. de Araujo T, Valencia I, Federman DG, et al: Managing the patient with venous ulcers,
Ann Intern Med 138:326–334, 2003.
22. Nemeth KA, Harrison MB, Graham ID, et al: Pain in pure and mixed aetiology venous leg
ulcers: a three-phase point prevalence study, J Wound Care 12:336–340, 2003.
23. Magyar MT, Nam EM, Csiba L, et al: Carotid artery auscultation–anachronism or useful
screening procedure? Neurol Res 24:705–708, 2002.
147
CH 11
THE HISTORY AND PHYSICAL EXAMINATION
CHAPTER
12 Vascular Laboratory Testing
Marie Gerhard-Herman, Joshua A. Beckman, Mark A. Creager
1
Vascular testing
Limb Pressure Measurement and Pulse Volume Recordings
Limb segmental systolic blood pressure measurements and pulse volume recordings are used to confirm a clinical diag­nosis of peripheral artery disease (PAD) and further define the level and extent of the obstruction. Segmental pressures are typically measured in conjunction with segmental limb pleth­ysmography (pulse volume recordings). These techniques are used predominantly in the lower extremities, but are also appli­cable to the arms. Both procedures are performed using sphyg­momanometric cuffs appropriately sized to the diameter of the limb segment under study. The patient rests in the supine posi­tion for at least 10 minutes prior to measuring limb pressures. Commercially available machines with automatic cuff infla­tion are able to digitally store the pressures and waveforms. A continuous-wave (CW) Doppler instrument with a 4- to 8-MHz transducer frequency is used to detect the arterial flow signal. The cuff is quickly inflated to a suprasystolic pressure and then slowly deflated until a flow signal occurs. The cuff pressure at which the flow signal is detected is the systolic pressure in the arterial segment beneath the cuff. For example, if the cuff is on the high thigh and the sensor is over the posterior tibial artery at the ankle, the measured pressure is reflective of the proximal superficial and deep femoral arteries (DFAs) beneath the cuff, as well as any collateral arteries, and not the posterior tibial artery. The Doppler flow signal from an artery at the ankle is typically used for all limb measurements. It is more accurate, although less convenient, to place the Doppler transducer probe close to the cuff being inflated.
Sphygmomanometric cuffs are positioned on each arm above the antecubital fossa, on the upper portion of each thigh (high thigh), on the lower portions of the thighs above the patella (low thigh), on the calves below the tibial tubercle, and on the ankles above the malleoli. Typically, foot pressures are measured by insonating the posterior tibial and anterior tibial arteries at the ankle level. Both arm pressures at the brachial artery are deter­mined. A difference of greater than 20 mmHg between the arm pressures indicates the presence of stenosis on the side of the lower pressure. Pressure measurements are made at the high thigh, low thigh, calf, and ankle levels with a tibial or dorsalis pedis sig­nal selected as the flow indicator. A second method uses one long, contoured thigh cuff rather than two separate thigh cuffs. The lower-extremity pressure evaluation should begin at the ankle level and proceed proximally. Patients who are found to have a normal pressure measurement at rest may require a treadmill exercise test to detect PAD. If disease distal to the ankle is suspected, pedal or digital artery obstruction can be evaluated with cuffs sized appro­priately for the toes.
Segmental Doppler Pressure Interpretation
Segmental limb pressures are compared with the highest arm pressure. Ankle pressures are used to calculate the ankle-brachial indices (ABI) for each extremity. This is accomplished by dividing each of the ankle pressures by the higher of the brachial artery pressures. above 0.9 to 1.0 is borderline abnormal. ABI in healthy subjects and patients with PAD confirmed by arte­riography found that an ABI of 0.9 or lower was diagnostic of PAD with 79% to 95% specificity and 96% to 100% sensitivity. are compared between levels. A 20-mmHg or greater reduction in pressures from one level to the next is considered significant and indicates stenosis between those two levels. In healthy subjects, the high thigh pressure determined by cuff typically exceeds the brachial artery pressure by approximately 30 mmHg. A thigh/bra­chial index above 1 is interpreted as normal, and an index of 1 or less indicates stenosis proximal to the thigh ( thigh pressures are low compared with arm pressure, the site of obstruction could be in the aorta or ipsilateral iliac artery, common femoral artery (CFA), or proximal superficial femoral artery (SFA) (see chial pressure, an ipsilateral iliofemoral artery stenosis is inferred.
cannot be determined because the vessels are noncompressible. An index of 1.4 or greater suggests vascular calcification artifact and makes interpretation of the pressure measurement unreliable. Presence or absence of a significant pressure gradient cannot be determined in the presence of vascular calcification artifact. In this setting, the toe brachial index (TBI) is a useful measurement. Toe brachial index is the ratio of the systolic pressure in the toe to the brachial artery systolic pressure. This should be performed in a warm room; cold-induced vasospasm may lower the digital pres­sure. To perform the procedure, a cuff is placed on a toe. Typically, the great toe is used. The pulse waveform is obtained by photoplethys­mography or Doppler. The cuff is inflated to suprasystolic pressure and then deflated. Systolic pressure is determined as the pressure at which the waveform reappears. A normal value for TBI is 0.70.
2
A normal ABI is between 1.0 and 1.4, whereas an ABI
Fig. 12-1). If only one high thigh pressure is less than the bra-
In the presence of severe vascular calcification, systolic pressures
3
Studies that evaluated the
4
Pressures
Fig. 12-1). When high
Pulse Volume Recording Interpretation
The same cuffs used to measure segmental pressures may be attached to a plethysmographic instrument and used to record the change in volume of a limb segment with each pulse, des­ignated the pulse volume. Pulse volume waveform evaluation allows assessment of arterial flow in regions of calcified vessels because the test does not rely on cuff occlusion of the calcified
5
artery.
Each cuff is inflated in sequence to a predetermined refer­ence pressure up to 65 mmHg. The change in volume in the limb segment causes a corresponding change in pressure in the cuff throughout the cardiac cycle. Interpretation of the pulse volume recording (PVR) requires calibration of the amount of air in the cuff.
A pulse volume waveform is recorded for each limb segment. Pulse volume recording analysis is based on evaluation of wave­form shape, signal, and amplitude ( the normal pulse volume waveform resembles the arterial pres­sure waveform, and is composed of a sharp systolic upstroke fol­lowed by a downstroke that contains a prominent dicrotic notch. A hemodynamically significant stenosis manifests as a change in the PVR contour toward a tardus parvus waveform. Both the slope and amplitude decrease when there is more severe disease. Severity of PAD can be defined by the slope of the upstroke and amplitude of the pulse volume (see
Fig. 12-2).
Fig. 12-2). The configuration of
14 8
PVR 66 mmHg 747cc RIGHT High Thigh
Segmental pressure
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Gain: .75 mmHg/20mm Spd: 25 Amp: 16
PVR 68 mmHg 832cc RIGHT Above Knee Gain: .75 mmHg/20mm Spd: 25 Amp: 15
and PVR study
Brachial
Right
165
1.08 178 129 0.78
1.06 175 116 0.70
0.83 137 115 0.70
Right Left
0.85 141 111DP 0.67
0.85
140 100PT 0.61
Left
162
PVR 67 mmHg 557cc LEFT High Thigh Gain: .75 mmHg/20mm Spd: 25 Amp: 25
PVR 66 mmHg 506cc LEFT Above Knee Gain: .75 mmHg/20mm Spd: 25 Amp: 27
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PVR 64 mmHg 256cc RIGHT Below Knee Gain: .75 mmHg/20mm Spd: 25 Amp: 40
PVR 65 mmHg 179cc RIGHT Ankle Gain: .75 mmHg/20mm Spd: 25 Amp: 35
PVR 56 mmHg 61cc RIGHT Metatarsal Gain: .75 mmHg/20mm Spd: 25 Amp: 13
FIGURE 12-1 Segmental pressure measurements and pulse volume recording (PVR). Right leg has a pressure drop between low thigh and calf consistent with superficial femoral/popliteal artery stenosis. Left leg has a pressure drop at level of high thigh consistent with iliofemoral artery stenosis. ABI, ankle-brachial index.
Pulse waveforms can also be obtained using photoplethysmog­raphy, recording reflected infrared light. In photoplethysmogra­phy, the signal is proportional to the quantity of red blood cells in the cutaneous circulation; it does not measure volume changes. Waveform shape is assessed in a similar fashion in pulse volume and photoplethysmography recordings. Low photoplethysmo­graphic waveforms in the toes identify increased risk of amputa­tion, in addition to the toe pressure.
5
ABI: 0.85 ABI: 0.67
shortness of breath with minimal exertion, or unstable angina. The test cannot be performed if the patient cannot walk on a treadmill.
Patients are instructed to fast for 12 hours prior to walking on the treadmill. The constant-load treadmill test is performed at a speed of 2 mph and an incline of 12%. Graded exercise protocols increase the grade and/or speed in 2- to 3-minute stages. The Gardner proto­col is the most commonly used graded protocol to evaluate walk­ing exercise capacity.
PVR 63 mmHg 237cc LEFT Below Knee Gain: .75 mmHg/20mm Spd: 25 Amp: 30
PVR 65 mmHg 165cc LEFT Ankle Gain: .75 mmHg/20mm Spd: 25 Amp: 23
PVR 54 mmHg 56cc LEFT Metatarsal Gain: .75 mmHg/20mm Spd: 25 Amp: 13
7
It begins at a speed of 2 mph and an incline
of 0%, and the grade progressively increases by 2% every 2 minutes,
Exercise Testing for Peripheral Artery Disease
Exercise testing is an adjunctive physiological test to evaluate PAD. It is useful to assess functional capacity and determine the distance patients with claudication are able to walk. Moreover, it can be used to clarify whether leg symptoms are related to PAD. This is relevant in patients with symptoms that are atypical for claudication and in those who have a history of intermittent claudication, yet normal ABIs at rest. to treadmill exercise testing for PAD include rest pain in the leg,
6
Relative contraindications
allowing for a wider range of responses to be measured. It is often used to determine clinical trial end points such as change in walk­ing time in response to therapy. Other graded exercise protocols, such as the Bruce protocol, are not commonly used because the rapid rate of speed and incline limits assessment of exercise capac­ity in claudicants.
The treadmill exercise test is terminated when the patient cannot continue owing to leg claudication or chest pain, or is limited by other symptoms such as shortness of breath or fatigue. The patient then immediately lies down on the stretcher. Ankle pressures are
150
Pr
Normal
CH
12
FIGURE 12-2 Pulse volume recording (PVR). Normal waveform has a sharp upstroke, dicrotic notch, and a period of diastasis. Mildly abnormal waveform has a delay in upstroke and a straightened downslope (blue line). Moderately abnormal waveform has a delay in upstroke (blue line), flat systolic peak, and diminished amplitude. Severely abnormal waveform has a flat systolic peak and very diminished amplitude.
Mild
Moderate
Severe
Transcutaneous Oximetry
By exploiting variations in color absorbance of oxygenated and deoxygenated hemoglobin (Hb), transcutaneous oximetry can determine the state of blood oxygenation. Oximeters use two light frequencies, red at 600 to 750 nm and infrared at 800 to 1050 nm, to differentiate oxygenated and deoxygenated Hb. Deoxygenated blood absorbs more red light, whereas oxygenated blood absorbs more infrared light. Oximeters typically employ both an emitter and receiver. Red and infrared light is emitted and passes through a relatively translucent structure such as the finger or earlobe. A photodetector determines the ratio of red and infrared light received to derive blood oxygenation. When measured continu­ously, oxygenation peaks with each heartbeat as fresh oxygen­ated blood arrives in the zone of measurement. Normal values for oxygen tension are from 50 to 75 mmHg. One probe is placed on the chest as a control to ensure that oxygen tension is from 50 to 75 mmHg. A second probe is placed on the limb in the area of interest. Measurements are obtained from the probe, which is sequentially positioned from proximal to distal segments of the limb. Normal limb Tc Transcutaneous oximetry is most often used to determine the
o
should approximate that of the chest.
2
level of amputation. A value above 20 mmHg can predict healing at the site with 80% accuracy.7 This measurement is not affected by arterial calcification.
Physical Principles of Ultrasonography
Ultrasound Image Creation
An ultrasound transducer, or probe, emits sound waves in discrete bundles or pulses into the tissue of interest. On encountering a tissue, a portion of the waves is reflected back to the transducer. The fraction of returning waves depends on density and size of the tissue examined. The depth of tissue is determined by the time required for pulse emission and return. Thus, by integrating the number of returning pulses and the time required for return, a B-mode, or gray-scale image may be created. The time for wave reflection decreases with higher ultrasound probe frequencies. Transducer probes with higher frequencies image superficial tissues better than probes with lower frequencies, but lose depth imaging because of attenuation of the returning emitted pulses.
Improvements in technology have permitted band-width widen­ing of vascular transducers, facilitating analysis of harmonics of the fundamental frequency. A harmonic represents a whole-number multiple of the emitted frequency. Because the tissue compresses and expands in response to the application of ultrasound, the fun­damental wave may become distorted, impairing image quality. The distortion, however, also creates harmonics of the original frequency that can be detected by the transducer. By detecting only the fundamental frequency and its harmonics, artifact such as speckle and reverberation may be reduced to create a clearer image.
Detection of Blood Flow
Normal blood flow is laminar in a straight segment of an artery. If thought of as a telescopic series of flow rings, blood moves for­ward most rapidly in the middle ring, and velocity decreases in the outer rings as blood comes closer to the vessel wall. The cardiac cycle, defined by its pulsatile nature of flow, causes a continual variation in blood flow velocity, highest with systole and lowest with diastole. The concentric or laminar flow of blood may be dis­turbed at a normal branching point or with abnormal vessel con­tours, such as those caused by atherosclerotic plaque. Disturbed or turbulent flow causes a much greater loss of pressure than laminar flow.
Determining flow velocity is a mainstay of vascular ultraso­nography. Abnormalities in the vessel wall cause changes in flow velocity and permit detection and assessment of stenotic regions within the vessel. Flow in a normal vessel is proportional to the difference of pressure between the proximal and distal end of the vessel. The prime determinant or limitation of flow is the radius of the vessel because volume of blood flow is determined by the fourth power of the radius. For example, a 50% reduction in vessel radius causes a greater than 90% reduction in blood flow. Thus, blood flow represents an example of Poiseuille's law, which deter­mines flow of a viscous fluid through a tube. Specifically,
8L
η
4
π×∆ ×
Q
=
where Q denotes volume of flow, D P is pressure at inflow minus the pressure at outflow, r is the radius, h is viscosity, and L is tube length. Because blood viscosity, blood vessel length, and pressure remain relatively stable, the most important determinant of blood flow is vessel lumen size.
Vascular ultrasonography can depict flow velocity by taking advantage of Doppler shift frequencies. Frequency will shift either positively or negatively, depending on direction of blood flow. Variables that determine the size of the shift include the speed of sound, speed of the moving object, and angle between the
transmitted beam and moving object. Christoph Doppler described
No frequency shift
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this relationship using the following equation:
F (2 F ·V·cos ) c
dt
where F transmitted from the probe, V is the velocity of flow, cos is the
is the Doppler frequency shift, Ft is the Doppler frequency
d
θ ÷=
cosine, q is the angle between the beam and direction of the moving object, and c is the velocity of sound.
Artifact
Although a highly reliable imaging modality, ultrasound does suf­fer from occasional image artifact. calcium deposits permit few sound waves to penetrate, resulting in acoustic shadowing and diminishing imaging of deeper tissues. Tissue imaging enhancement may be noted on the far side of echo­free or liquid-filled zones. Tissue interfaces may generate multiple sound wave reflections, causing “additions” to the tissue termed reverberation artifact. Refraction of the sound pulse may cause improper placement of a structure of an image and shadowing at the edge of a large structure. Highly reflective surfaces may cre­ate mirror images because the reflecting tissue alters the timing of the returning sound wave. The mirror image should be equidistant from the reflecting surface or tissue.
8
Dense objects like vessel-wall
Gray-Scale (B Mode) Imaging
Ultrasound images are generated using a pulse echo system. The position of the tissue interface is determined by the time between pulse generation and returning echo. Each returning echo is displayed as a gray dot on a video screen using a brightness mode (B mode) in which the brightness of the dot depends on the strength of the reflected wave. A two-dimensional (2D) image is created by sequentially transmitting waves in multiple directions within a single plane and combining the reflected echoes into a single display. The image can be refreshed rapidly, permitting real­time display of the gray-scale image. The surface of interest should be perpendicular to the ultrasound beam to obtain the brightest echo with B-mode imaging. This is readily achieved in vascular imaging because the neck, extremity, and visceral vessels gener­ally lie parallel to the surface of the transducer. Higher-frequency probes are used to image vessels close to the surface, and lower­frequency probes are used to image deeper vessels. Details of the vessel wall can be seen more clearly with the use of harmonics. The wide band width of transducers allows analysis of returning har­monics (whole-number multiples) of the fundamental frequency.
Spectral Doppler Waveform Analysis
Velocity recordings are obtained with an angle of 60 degrees between the Doppler insonation beam and the flow. In ultrasound practice, the optimal angle of measurement between the beam and blood flow is 60 degrees. Although maximal shift is detected at 0 degrees, this angle cannot be reliably obtained in vascular imaging because the vessels are parallel to the surface of the body. Insonation angles below and above 60 degrees influence the mea­surement such that small reductions in the insonation angle may alter velocity by 10%, whereas small increases in insonation angle may change flow velocity by 25% ( volume cursor is placed parallel to the inner wall, and a Doppler angle from 30 to 60 degrees between the wall and the insonation beam (or flow jet) is used. A normal peripheral artery Doppler waveform consists of a narrow, sharply defined tracing. This indi­cates that all blood cells are moving at an equivalent speed at any time in the cardiac cycle. as high resistance due to limited flow during diastole (e.g., nor­mal peripheral arterial Doppler velocity waveform), or low resis­tance with continuous flow during diastole, as when downstream resistance arterioles are widely dilated or there is contiguity with
Fig. 12-3). Thus, the sample-
11
Waveforms are also characterized
9,10
90°
V=(Fd·c)/2Ft cos θ)
FIGURE 12-3 Doppler angle is the angle between insonation beam and sample cursor aligned with flow. Dashed lines represent different insonation
beams. Solid arrow represents direction of flow and position of Doppler sample cursor. Velocity is determined using the Doppler equation, with the cosine (cos) in the denominator. The cos θ degrees = 1, cos 30 degrees = 0.86, cos 60 degrees = 0.5, and cos 90 degrees = 0. c, velocity of sound; Fd, Doppler frequency shift; Ft, transmitted Doppler frequency; V, velocity.
High resistance
Low resistance
FIGURE 12-4 High- and low-resistance waveforms. These two waveforms are distinguished by the absence (high resistance) and presence (low resistance) of flow during diastole.
50% of maximal shift60°
30°
low-resistance circuits (e.g., normal internal carotid artery [ICA] velocity waveform) (
Fig. 12-4). The normal high resistance wave-
form is typically triphasic. The first component is caused by ini­tial high-velocity forward flow during ventricular systole. A range of normal peak systolic velocity (PSV) measurements have been
12
defined
for each arterial segment, described later in this chapter.
The second phase of the waveform consists of early diastolic flow reversal as left ventricular (LV) pressure falls below aortic pressure prior to aortic valve closure.
13
The final or third component is a small amount of forward flow when there is elastic recoil of vessel walls. Flow is typically not uniform or laminar at bifurcations and sites of stenosis; at these sites flow becomes turbulent. For these locations, the spectral Doppler waveform reflects the fact that blood cells move with varying velocities. Instead of a narrow well-defined trac­ing (see
Fig. 12-4), spectral broadening becomes evident (Fig. 12-5) ,
with partial or complete filling-in of the area under the spectral waveform. This third, or late, diastolic component is usually absent in atherosclerotic vessels that have lost compliance or elasticity.
Color Doppler
Color Doppler is the phase or frequency shift information con­tained in the returning echoes and processed in real time to form a velocity map over the entire imaging field. shift data are available for every point imaged. This information is then superimposed on the gray-scale image to provide a com­posite real-time display of both anatomy and flow. When motion is detected, it is assigned a color, typically red or blue, determined by whether the frequency shift is toward or away from the probe. Color assignment is arbitrary and can be altered by the user, but most choose to assign the color red to arteries and blue to veins. With increasing Doppler frequency shifts, the hue and intensity of the color display change, with progressive desaturation of the color and a shift toward white at the highest detectable velocities.
14
Doppler frequency-
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