Peripheral Arterial Disease

ABNET
 OUTLINE

 Introduction
 Epidemiology
 Risk factors
 C/presentation
 Tests
 treatment
 Prognosis
 PAD

 Is a clinical disorder in which there is a stenosis or

occlusion in aorta or arteries of limbs.

 Atherosclerosis is the leading cause in those over 40 yrs of

age.

 Majority in 6th-7th decade.

 Other causes
 Thrombosis
 Embolism
 Vasculitis

 Fibro muscular dysplasia

 Entrapment
 Cystic adventitial disease

 trauma
 Epidemiology

 Varies based on population studied and methods used.

 Most studies use ABI.

 >40-4%

 >65-15-20%

 M>F

 B>W
 Pathology

Usually large and medium sized vessels are affected

Branch points
Plaque formation
More distal vessel involvement in elderly and diabetics
Aorto-iliac -30%
Femoropopliteal-80-90%
Tibioperoneal-40-50
 Risk factors

Modifiable Non modifiable

c/smoking(2-3X) AGE
 84-90% SEX
 PAD>CAD RACE
DM(2-4X)
Dyslipidemia
HPT
 Patho phisiology

 Is due to skeletal ms oxygen demand and supply mismatch.

 Intermitent claudication –

 results due to activation of local sensory receptors by accumulation

of lactate and other metabolites
If atherosclerosis causes a stenosis, flow through the
artery is reduced.

 The pressure gradient across the stenosis increases.

 A blood pressure gradient exists at rest if the

stenosis reduces the lumen diameter by more than
50%. (exercise)
As flow through a stenosis increases, distal perfusion
pressure drops.
 local metabolites (including adenosine, nitric oxide,
potassium, and hydrogen ion) accumulate, and
peripheral resistance vessels dilate.
Perfusion pressure then drops further because the
stenosis limits flow.
Intramuscular pressure rises during exercise and may
exceed the arterial pressure distal to an occlusion,
causing blood flow to cease.
 The hemostatic system is comprised of six major components:
Platelets, vascular endothelium, procoagulant plasma protein “factors,”
natural anticoagulant proteins, fibrinolytic proteins, and
antifibrinolytic proteins. Each of these six hemostatic components must
be present in fully functional form, in adequate quantity, and at the
proper location to prevent excessive blood loss after vascular trauma
and, at the same time, to prevent pathologic thrombosis. The
hemostatic system is highly regulated and maintains a delicate balance
between a prohemorrhagic state and a prothrombotic state. Any
significant acquired or congenital imbalance in the hemostatic “scales”
can lead to a pathologic outcome.
Specific alterations in the quantitative and qualitative status of any
hemostatic cellular or protein element can lead to pathologic thrombosis. A
marked increase in the platelet count (thrombocytosis) and accentuated
platelet aggregation (“sticky platelet syndrome”) are associated with
thromboembolic events. Elevated levels of procoagulant factors such as
fibrinogen, factors VIII, IX, XI, and VII, as well as resistance to inactivation
of factor Va by APC, are recognized risk factors for vascular disease and
thrombosis. Deficiency of a natural anticoagulant protein such as protein C,
protein S, or AT is associated with venous thromboembolic disease.
Deficiency of a fibrinolytic cascade component, such as t-PA or
plasminogen, and excess plasma levels of the fibrinolytic inhibitor PAI-1
have been linked to hypercoagulability and thrombosis. It is the net balance
between the participating and, at times, opposing groups of proteins and not
the level of any individual factor that is most critical to hemostatic
regulation.
Venous thrombosis typically develops under conditions of slow blood flow
(low shear stress) and is augmented by further retardation and stagnation
of flow caused by the developing thrombus itself. Right-sided heart
failure, pre-existent venous thrombosis, extrinsic vascular compression by
tumor, and chronic venous insufficiency all promote venous stasis, blood
pooling, and a concentration of procoagulant factors.8 The anatomic
structure of venous valves results in retrograde eddy currents, which
produce pockets of stasis even in normal veins.9 The venous arcades in
the soleus muscles of the calves may represent another site of physiologic
venous stasis. These structures may enlarge and lose vascular tone with
aging.10, 11 These facts may partially explain why DVT most commonly
occurs in the valve cusps and veins of the pelvis and lower extremities,
and why older age is an important risk factor for venous thrombosis
Arterial thrombosis initially occurs under conditions of rapid blood flow
(high shear stress), a condition in which von Willebrand factor (vWF) is
critical for platelet adhesion.7 Arterial thrombi usually are composed of
tightly coherent masses of platelets, which contain small amounts of
fibrin and a few erythrocytes and leukocytes. These thrombi are the
classic “white thrombi,” which resemble, in many respects, normal
hemostatic plugs. As arterial thrombi enlarge, progressive or intermittent
deposition of new layers of platelets and fibrin produces the
characteristic lines of Zahn; partial or complete obstruction of blood
flow may produce a “tail” of “red thrombus.
 Venous thrombi are composed of large amounts of fibrin containing
numerous erythrocytes. In these loose, friable masses (the red
thrombus), the platelets and leukocytes are enmeshed in random
fashion. Venous thrombi resemble blood clots formed in vitro, and they
usually produce significant obstruction to blood flow from the outset,
but their most serious consequence is embolization. Blood flow
obstruction secondary to venous thrombosis itself promotes the further
formation of thrombus. Results of studies of clots formed in a
thromboviscometer at varying rates of shear suggest that the
differences in the structure of venous and arterial thrombi may be
mainly the result of the velocity of blood flow.
Class I
 1. A history of walking impairment, claudication, ischemic rest
pain, and/or nonhealing wounds is recommended as a required
component of a standard review of systems for adults 50 years and
older who have atherosclerosis risk factors, or for adults 70 years
and older. (Level of Evidence: C)
The five “Ps” are defined by the clinical symptoms and
signs that suggest potential limb jeopardy: pain,
pulselessness, pallor, paresthesias, and paralysis (with
polar being a sixth “P”).
Physical exam
 Key Components of the Vascular Physical Examination

Measurement of blood pressure in both arms and notation of any inter-arm

asymmetry.

 Palpation of the carotid pulses, and notation of the carotid upstroke and amplitude,
and presence of bruits.

 Auscultation of the abdomen and flank for bruits.

 Palpation of the abdomen and notation of the presence of the aortic pulsation and
its maximal diameter.

 Palpation of pulses at peripherally palpable arteries.

Perform Allen’s test when knowledge of hand perfusion is needed.

Ausculation of both femoral arteries for the presence of bruits
 Pulse intensity should be assessed and should be
recorded numerically as follows:
 0- absent
 1- diminished
 2- normal
 3- bounding
 Inspect feet ;the color, temperature, and integrity of the
skin and intertriginous areas and presence of ulcerations.
distal hair loss, trophic skin changes, and hypertrophic
nails, should be sought and recorded .
Common Sites of Claudication

Obstruction in Ischemia in
Aorta or Buttock, hip,
iliac artery thigh

Femoral artery Thigh,

or branches calf

Popliteal artery Calf, ankle,

or distal foot
 Critical limb ischaemia (CLI)

Definition and clinical presentation

CLI is the most severe clinical manifestation of LEAD, defined as
the presence of ischaemic rest pain, and ischaemic lesions or
gangrene objectively attributable to arterial occlusive disease. It
implies a chronic condition, to be distinguished from acute limb
ischaemia (ALI) . An ankle pressure
,50 mmHg is usually recommended as a diagnostic criterion
because it includes most patients for whom rest pain or ischaemic
lesions do not improve spontaneously without intervention
. Since
healing needs additional perfusion above that required for
supporting intact skin, the ankle and toe pressure levels
needed for healing are higher than the pressures found in
ischaemic rest pain. For patients with ischaemic lesions or
gangrene, CLI is suggested by an ankle pressure of ,70 mmHg.
Toe pressure ,30 mmHg replaces the ankle pressure criteria in
case of medial calcinosis.
The investigation of the microcirculation (i.e. transcutaneous
oxygen pressure) is also helpful in some cases, not only for
diagnostic and prognostic purpose, but also sometimes to
determine the level of amputation
All patientswithCLI should be referred to a vascular specialist early
in the course of their disease, to plan revascularization. The most
significant
change in the treatment of CLI is the increasing tendency to
shift from bypass surgery to less invasive endovascular procedures
as an accepted first-choice revascularization strategy including tibial
arteries, with bypass surgery reserved as a back-up option if
necessary.
6 The main advantages of endovascular revascularization are the
low complication rates, ranging from 0.5% to 4.0%, high technical
success rates (even in long occlusions) approaching 90%, and an
acceptable short-term clinical outcome.
updates
ALI is a medical emergency and must be recognized rapidly. The time constraint is due to the period that
skeletal muscle will tolerate ischemia—roughly 4 to 6 hours (281). A rapid assessment of limb viability and
ability to restore arterial blood flow should be performed by a clinician able to either complete the
revascularization or triage the patient (282). Lower extremity symptoms in ALI can include both pain and loss
of function. The longer these symptoms are present, the less likely the possibility of limb salvage (283, 284).
Clinical assessment must include symptom duration, pain intensity, and motor and sensory deficit severity to
distinguish a threatened from a nonviable extremity (Figure 3). The bedside assessment includes arterial and
venous examination with a handheld continuous-wave Doppler because of the inaccuracy of pulse palpation
(22). The loss of Dopplerable arterial signal indicates that the limb is threatened. The absence of both arterial
and venous Doppler signal indicates that the limb may be irreversibly damaged (nonsalvageable).
Comorbidities
should be investigated and managed aggressively, but this must not delay therapy. Even in the setting of rapid
and effective revascularization, the 1-year morbidity and mortality rates ALI are high
pressures at the arms (brachial arteries) and ankles
(dorsalis pedis and posterior tibial arteries) in the supine
position by using a Doppler device. The ABI of each leg is
calculated by dividing the higher of the dorsalis pedis
pressure or posterior tibial pressure by the higher of the
right or left arm blood pressure . Segmental lower
extremity blood pressures and Doppler or
plethysmographic waveforms (pulse volume recordings)
are often performed along with the ABI and can be used
to localize anatomic segments of disease (eg, aortoiliac,
femoropopliteal, infrapopliteal)
 Diagnostic Testing
 Ankle-brachial index

 Segmental limb pressures

 Pulse volume recordings

 Doppler velocity waveform analysis

 Functional testing

 Treadmill exercise testing

 Duplex scanning

 Advanced imaging techniques

 Lower extremity segmental pressures — The patient is placed in a supine position and rested for
15 minutes. Three or four standard-sized blood pressure cuffs are placed at several positions on
the extremity. A three-cuff technique uses above knee, below knee, and ankle cuffs. A four-cuff
technique ( picture 2 ) uses two narrower blood pressure cuffs rather than one large cuff on the
thigh and permits the differentiation of aortoiliac and superficial femoral artery disease [ 32 ].

 The pedal vessel (dorsalis pedis, posterior tibial) with the higher systolic pressure is used, and
the pressure that occludes the pedal signal for each cuff level is measured by first inflating the
cuff until the signal is no longer heard and then progressively deflating the cuff until the signal
resumes. The pressure at each level is divided by the higher systolic arm pressure to obtain an
index value for each level ( figure 2 ).

 A 20 mmHg or greater reduction in pressure is indicative of a flow-limiting lesion if the pressure

difference is present either between segments along the same leg or when compared with the
same level in the opposite leg (ie, right thigh/left thigh, right calf/left calf) ( figure 2 ). Well-
developed collateral vessels may diminish the observed pressure gradient and obscure a
hemodynamically significant lesion. Successive significant (>20 mmHg) decrements in the same
extremity indicate multilevel disease.
Pressure gradients may be increased in the hypertensive patient and decreased in
patients with low cardiac output. When performing serial examinations over time,
changes in index values >0.15 from one study to the next are considered significant and
suggest progression of disease.
With a four cuff technique, the high-thigh pressure should be higher than the brachial
pressure, though in the normal individual, these pressures would be nearly equal if
measured by invasive means. The four-cuff technique introduces artifact because the
high-thigh cuff is often not appropriately 120 percent the diameter of the thigh at the
cuff site. A >30 mmHg decrement between the highest systolic brachial pressure and
high-thigh pressure is considered abnormal.
A normal high-thigh pressure excludes occlusive disease proximal to the bifurcation of
the common femoral artery. If the high-thigh systolic pressure is reduced compared
with the brachial pressure, then the patient has a lesion at or proximal to the
bifurcation of the common femoral artery. If the high-thigh pressure is normal but the
low-thigh pressure is decreased, the lesion is in the superficial femoral artery. In one
prospective study, the four-cuff technique correctly identified the level of the occlusive
lesion in 78 percent of extremities
For patients with claudication, the localization of the lesion may have
been suspected from their history. The site of pain and site of arterial
disease correlates with pressure reductions seen on segmental
pressures:
Buttock, hip or thigh pain – Pressure gradient between the brachial
artery and the upper thigh is consistent with arterial occlusive disease at
or proximal to the bifurcation of the common femoral artery.
Calf pain – Pressure gradient from the high to lower thigh indicates
superficial femoral artery disease. Pressure gradient from the lower
thigh to calf reflects popliteal disease.
Low calf pain – Pressure gradient from the calf and ankle is indicative of
infrapopliteal disease.
Foot pain – Pressure gradient from the ankle and toe suggests digital
artery occlusive disease
Upper extremity segmental pressures  — Segmental
pressures may also be performed in the upper extremity.
Generally, three cuffs are used with above and below
elbow cuffs and a wrist cuff ( figure 3 ). Index values are
calculated at each level. In the patient with possible upper
extremity occlusive disease, a difference of ≥10 mmHg
between the left and right brachial systolic pressures
suggests innominate, subclavian, axillary, or proximal
brachial arterial occlusion. Differences of more than 10 to
20 mmHg between successive arm levels suggest
intervening occlusive disease
Taking into consideration the precision of this noninvasive
method and the variability in blood pressure during even short
periods, a blood pressure gradient in excess of 20 mm Hg between
successive cuffs is generally used as evidence of arterial stenosis
in the lower extremity, whereas a gradient of 10 mm Hg indicates a
stenosis between sequential cuffs in the upper extremity. Systolic
blood pressure in the toes and fingers is approximately 60% of the
systolic blood pressure at the ankle and wrist, respectively, because
pressure diminishes further in the smaller distal vessels.
 Exercise testing  —

 Segmental blood pressure testing, toe-brachial index measurements and PVR

waveforms can be obtained before and after exercise to unmask occlusive disease
not apparent on resting studies. Exercise testing is a sensitive method for
evaluating patients with symptoms suggestive of arterial obstruction when the
resting extremity systolic pressures are normal.
Exercise testing is most commonly performed to evaluate lower extremity
peripheral artery disease (PAD). Exercise testing is generally not needed to
diagnose upper extremity arterial disease, though, on occasion, it may play a role
in the evaluation of subclavian steal syndrome. The discussion below focuses on
lower extremity exercise testing. The principles of testing are the same for the
upper extremity, except that a tabletop arm ergometer (hand crank) is used
instead of a treadmill.
The dynamics of blood flow across a stenotic lesion depend upon the severity of the
obstruction and whether the individual is at rest or exercising. Exercise normally
increases systolic pressure and decreases peripheral vascular resistance. The
effects of exercise on the cardiovascular system are discussed elsewhe
Exercise augments the pressure gradient across a
stenotic lesion. An arterial stenosis less than 70
percent may not be sufficient to alter blood flow or
produce a systolic pressure gradient at rest; however,
following exercise, a moderate stenosis may be
unmasked and the augmented gradient reflected as a
reduction from the resting ankle-brachial index
(ABI) following exercise. Repeat ABIs demonstrate a
recovery to the resting, baseline ABI value over time
Treadmill exercise protocols use a motorized treadmill that
incorporates
fixed or progressive speeds and angles of incline. A fixed
workload test usually maintains a constant grade of 12% and a
speed of 1.5 to 2.0 mph. A progressive, or graded, treadmill
protocol typically
maintains a constant speed of 2 mph while the grade gradually
increases by 2% every 2 to 3 minutes. Repeated treadmill test
results
have better reproducibility with progressive than with constant
grade
protocols
Interpretation  — A normal response to exercise is a slight increase or no
change in the ABI compared with baseline. If the patient develops
symptoms with walking on the treadmill and does not have a
corresponding decrease in ankle pressure, arterial obstruction as the cause
of symptoms is essentially ruled out and the clinician should seek other
causes for the leg symptoms.
A fall in ankle systolic pressure by more than 20 percent from its baseline
value, or below an absolute pressure of 60 mmHg that requires >3 minutes
to recover is considered abnormal. Severe claudication can be defined as an
inability to complete the treadmill exercise due to leg symptoms and post-
exercise ankle systolic pressures below 50 mmHg. Single-level disease is
inferred with a recovery time that is <6 minutes, while a ≥6 minute
recovery time is associated with multilevel disease, particularly a
combination of supra-inguinal and infrainguinal occlusive disease 
A 25% or greater decrease in the ABI after
exercise in a patient whose walking capacity is limited
by claudication is considered diagnostic and implicates
PAD as a cause of the patient’s symptoms.
Platinum oxygen electrodes are placed on the chest wall and legs or feet. The
absolute value of the oxygen tension at the foot or leg, or a ratio of the foot
value to chest wall value can be used. A normal value at the foot is 60 mmHg
and a normal chest/foot ratio is 0.9 . Local edema, skin temperature,
emotional state (sympathetic vasoconstriction), inflammation, and
pharmacologic agents limit the accuracy of the test.
The level of TcPO 2 that indicates tissue healing remains controversial. It is
generally accepted that in the absence of diabetes and tissue edema, wounds
are likely to heal if oxygen tension is greater than 40 mmHg [ 40 ]. A higher
value is needed for healing a foot ulcer in the patient with diabetes. Patients
with values of <20 mmHg are severely ischemic and are likely to need
revascularization for wound healing. A metaanalysis of four studies found a
more than threefold risk of developing a chronic wound healing complication
in patients with a TcPO 2 below a threshold of 20 to 30 mmHg (odds ratio
3.26, 95% CI 1.07-9.69)
 Pulse Volume Recording

Pulse volume recordings  — Modern vascular testing machines use air

plethysmography to measure volume changes within the limb, in conjunction with
segmental limb pressure measurement. The same pressure cuffs are used for each test
Cuffs are placed and inflated, one at a time, to a constant standard pressure. Volume
changes in the limb segment beneath the cuff are reflected as changes in pressure
within the cuff, which is detected by a pressure transducer and converted to an
electrical signal to produce an analog pressure pulse contour known as a pulse volume
recording (PVR).
A normal PVR waveform is composed of a systolic upstroke with a sharp systolic peak
followed by a downstroke that contains a prominent dicrotic notch . Alterations in the
pulse volume contour and amplitude indicate proximal arterial obstruction. The degree
of these changes reflects disease severity . Mild disease is characterized by loss of the
dicrotic notch and an outward “bowing” of the downstroke of the waveform . With
severe disease, the amplitude of the waveform is blunted . Pulse volume recordings are
most useful in detecting disease in calcified vessels which tend to yield falsely elevated
pressure measurements
Since the absolute amplitude of plethysmographic
recordings is influenced by cardiac output and
vasomotor tone, interpretation of these
measurements should be limited to the comparison
of one extremity to the other in the same patient and
not between patients. The dicrotic notch may be
absent in normal arteries in the presence of low
resistance, such as after exercise.
 Pulse Volume Recording

The pulse volume recording graphically illustrates the volumetric

change in a segment of the limb that occurs with each pulse. Plethysmographic
instruments, typically using strain gauges or pneumatic
cuffs, can transduce volumetric changes in the limb, which can be
displayed on a graphic recorder. These transducers are strategically
placed along the limb to record the pulse volume in its different segments, such
as the thigh, calf, ankle, metatarsal region, and toes
or the upper part of the arm, forearm, and fingers. The normal pulse
volume contour depends on both local arterial pressure and vascular
wall distensibility and resembles a blood pressure waveform. It consists
of a sharp systolic upstroke rising rapidly to a peak, a dicrotic
notch, and a concave downslope that drops off gradually toward the
baseline.
The contour of the pulse wave changes distal to a stenosis,
with loss of the dicrotic notch, a slower rate of rise, a more rounded
peak, and a slower descent. The amplitude becomes lower with
increasing severity of disease, and the pulse wave may not be recordable
at all in a critically ischemic limb. Segmental analysis of
the pulse wave may indicate the location of an arterial stenosis,
which probably resides in the artery between a normal and an
abnormal pulse volume recording. The pulse volume wave also provides
information about the integrity of blood flow when blood pressure
measurements cannot be obtained accurately because of
noncompressible vessels
 ULTRASOUND  —

 Ultrasound is the mainstay for noninvasive vascular imaging with each mode (eg, B-
mode, duplex) providing specific information. Ultrasonography is used to evaluate the
location and extent of vascular disease, arterial hemodynamics, and lesion morphology [ 
10 ].
Real-time ultrasonography uses reflected sound waves (echoes) to produce images and
assess blood velocity. Two ultrasound modes are routinely used in vascular imaging: the
B (brightness) mode and the Doppler mode (B mode imaging + Doppler flow detection =
duplex ultrasound). Duplex ultrasonography has gained a prominent role in the
noninvasive assessment of the peripheral vasculature overcoming the limitations (need
for intravenous contrast) of other noninvasive methods and providing precise anatomic
localization and accurate grading of lesion severity [ 41,42 ].
Both B-mode and Doppler mode take advantage of pulsed sound waves. Pulsed-wave
technology uses a row of crystals, each of which alternately send and receive pulse trains
of sound waves with a slight time delay with respect to their adjacent crystals. The time
and intensity differences of the transmitted and received sound waves are converted to
an image that displays depth and intensity for each crystal in the row. A pulse Doppler
also permits localization of Doppler shifts induced by moving objects (red blood cells).
Continuous wave Doppler  — A continuous wave Doppler continually transmits and
receives sound waves and, therefore, it cannot be used for imaging or to identify Doppler
shifts. It is used primarily for blood pressure measurement
The continuous wave hand-held ultrasound probe uses two separate ultrasound crystals,
one for sending and one for receiving sound waves. Continuous wave ultrasound
provides a signal that is a summation of all the vascular structures through which the
sound has passed and is limited in the evaluation of a specific vascular structure when
multiple vessels are present. However, the intensity and quality of the continuous wave
Doppler signal can give an indication of the severity of vascular disease proximal to the
probe. The quality of the arterial signal can be described as triphasic (like the heartbeat),
biphasic (bum-bum), or monophasic.
Biphasic signals may be normal in patients older than 60 because of decreased
peripheral vascular resistance; however, monophasic signals unquestionably indicate
significant pathology. Monophasic signals must be distinguished from venous signals,
which vary with respiration and increase in intensity when the surrounding musculature
is compressed (augmentation). It is often quite difficult to obtain ankle-brachial index
values in patients with monophasic continuous wave Doppler signals.
B-mode imaging  — The B-mode provides a grey
scale image useful for evaluating anatomic detail .
The quality of a B-mode image depends upon the
strength of the returning sound waves (echoes). Echo
strength is attenuated and scattered as the sound
wave moves through tissue. Angles of insonation of
90�� maximize the potential return of echoes.
Higher frequency sound waves provide better lateral
resolution compared with lower frequency waves.
Thus, high-frequency transducers are used for
imaging shallow structures at 90�� of insonation.
 Duplex scanning

 can be used to evaluate the vasculature preoperatively,

intraoperatively, and postoperatively for stent or graft surveillance and
is very useful in identifying proximal arterial disease. A meta-analysis
of 14 studies found that sensitivity and specificity of this technique for
≥50 percent stenosis or occlusion were 86 and 97 percent for aortoiliac
disease and 80 and 98 percent for femoropopliteal disease [ 43 ].
The identification of vascular structures from the B-mode display is
enhanced in the color mode, which displays movement (blood flow)
within the fiel. The shift in sound frequency between the transmitted
and received sound waves due to movement of red blood cells is
analyzed to generate velocity information (Doppler mode). Flow
toward the transducer is standardized to display as red and flow away
from the transducer is blue; the colors are semi-quantitative and do not
represent actual arterial or venous flow.
Accurate measurements of Doppler shift and,
therefore, velocity measurements require proper
positioning of the ultrasound probe relative to the
direction of flow. An angle of insonation of sixty
degrees is ideal; however, an angle between 30° and
70° is acceptable. The severity of stenosis is best
assessed by positioning the Doppler probe directly
over the lesion. The ratio of the velocity of blood at a
suspected stenosis to the velocity obtained in a normal
portion of the vessel is calculated. Velocity ratios >4.0
indicate a >75 percent stenosis in peripheral arteries
A normal arterial Doppler velocity waveform is triphasic
with a sharp upstroke, forward flow in systole with a
sharp systolic peak, sharp downstroke, reversed flow
component at the end of systole, and forward flow in late
diastole . The spectral band is narrow and a characteristic
lucent spectral window can be seen between the upstroke
and downstroke. Normal velocities vary with the artery
examined and decrease as one proceeds more distally in
an extremity . For example, velocities in the iliac artery
vary between 100 and 200 cm/s and peak systolic
velocities in the tibial artery are 40 and 70 cm/s
A delayed upstroke, blunted peak, and no second component signify progressive obstruction
proximal to the probe ( waveform 3 ), and a flat waveform indicates severe obstruction.
The pitch of the duplex signal changes in proportion to the velocity of the blood with high-
pitched harsh sounds indicative of stenosis. Proximal to a high-grade stenosis with minimal
compensatory collateralization, a thumping sound is heard.
Specific anatomic sites
Aortoiliac – Aortoiliac imaging requires the patient to fast for about 12 hours to reduce
interference by bowel gas. It is therefore most convenient to obtain these studies early in the
morning. Satisfactory aortoiliac Doppler signals ( waveform 4 ) can be obtained from
approximately 90 percent of individuals who have been properly prepared. Complete
examination involves the visceral aorta, iliac bifurcation, and iliac arteries distally.
Extremities – For the lower extremity, examination begins at the common femoral artery
and is routinely carried through the popliteal artery. The tibial arteries can also be evaluated.
In the upper extremities, the extent of the examination is determined by the clinical
indication. Visualization of the subclavian artery is limited by the clavicle. 
Any areas of stenosis are initially localized with color Doppler and then quantified
and assessed by measuring Doppler velocities. In general, the ratio of the peak
systolic velocity (PSV) within an area of stenosis is compared with the PSV in the
vessel just proximal to it to estimate the degree of stenosis. For the lower extremity,
the percent stenosis can be estimated. A PSV ratio that is 1.5 to 2.0 indicates a 50
percent arterial stenosis and a ratio >4.0 indicates >75 percent stenosis ( table 1 ).
The same general principles apply when determining the degree of stenosis within a
lower extremity bypass graft. 

There are no generally agreed upon criteria for determining stenosis in upper
extremity arteries, and most vascular laboratories tend to extrapolate criteria from
lower extremity arteries to upper extremity arteries.
Visceral arteries – Duplex examination of visceral arteries, especially the renal
arteries, requires the use of low frequency transducers to penetrate to the depth of
these vessels. Fasting is required prior to examination to minimize overlying bowel
gas. Validated velocity criteria for determining the degree of stenosis in visceral
vessels
 Duplex Ultrasound Imaging

Duplex ultrasound imaging provides a direct, noninvasive means of

assessing both the anatomic characteristics of peripheral arteries
and the functional significance of arterial stenoses. The methodology
incorporates gray-scale B-mode ultrasound imaging, pulsed Doppler
velocity measurements, and color coding of the Doppler shift information
. Real-time ultrasonographic scanners emit and
receive high-frequency sound waves, typically ranging from 2 to
10 MHz, to construct an image. The acoustic properties of the vascular
wall differ from those of the surrounding tissue, thus enabling
them to easily be imaged. Atherosclerotic plaque may be present and
visible on gray-scale images. Pulsed-wave Doppler systems emit ultrasound
beams at precise times and can therefore sample the reflected
ultrasound waves at specific depths to enable the examiner to determine
blood cell velocity within the lumen of the artery
Pulsed Doppler velocity measurements
can be made along the length of the artery and particularly at areas
of flow abnormalities suggested by the color images. A twofold
or greater increase in peak systolic velocity at the site of an
atherosclerotic
plaque indicates a 50% or greater stenosis (see Fig. 58-6). A
threefold increase in velocity suggests a 75% or greater stenosis. An
occluded artery generates no Doppler signal. With contrast-enhanced
angiography as a reference standard, duplex ultrasound imaging for
identification of sites of arterial stenosis has approximately 89% to
99% specificity and 80% to 98% sensitivity
 How to Perform
and Calculate the
ABI Right Arm Left Arm
Pressure: Pressure:

≥1.0 — Normal
0.81-0.90 — Mild Obstruction
0.41-0.80 — Moderate Obstruction
≤0.40 — Severe Obstruction

Pressure: Pressure:
PT PT
DP DP

Right ABI Left ABI

Higher Right Ankle Pressure = mmHg Higher Left Ankle Pressure = mm Hg
Higher Arm Pressure mm Hg Higher Arm Pressure mm Hg
lower extremity BP IS higher because pulse wave
amplification
Segmental Limb Pressure and
Pulse Volume Recordings

150 Brachial 150

170 140

158 116

154 100

152 98

1.0 0.64
AB
 Natural History of PAD
Age > 50 years

Limb
Cardiovascula
Morbidity
r Morbidity /
Mortality

Stable Worsening Critical Nonfatal Mortalit

Claudication Claudicatio Limb CV Events y 15-30%
70-80% n 10-20% Ischemia 20%
1-2%(25-
30%
amputati
on in CV Causes Non CV
ayear)
75% Causes
25%
 Does the Patient Have Intermittent
Claudication?
Claudication Pseudoclaudication

Characteristic of Cramping, tightness, Same, tingling,

discomfort aching, fatigue burning, numbness
Location of Buttock, hip, thigh,
Same
discomfort calf, foot
Exercise-induced Yes Variable
Distance Consistent Variable
Occurs with
No Yes
standing
Action for relief Stand Sit, change position
Time to relief Less than 5 minutes Up to 30 minutes
 Treatment

Goal
 Reduction in CV morbidity and mortality.

 Preserve limb viability

 Treatment of PAD
Prevent Ischemic Events
Risk factor modification Antiplatelet therapies
 Smoking cessation
 Aspirin or Clopidogrel
 Goal: complete cessation
 Goal: reduction in risk of MI,
 Lipid management
stroke, and vascular death
 Target LDL < 100 mg/dL
 Only clopidogrel is FDA
 Blood pressure control
approved
 Goal <140/90
 Many professional societies
 Blood sugar control
include ASA among first line
 Goal: HbA1c <7% agents in guidelines
All patients with
PAD should have their
serum LDL cholesterol
reduced to
,2.5 mmol/L (100 mg/dL),
and optimally to ,1.8
mmol/L
(,70 mg/dL), or ≥50% LDL
cholesterol reduction when
the
target level cannot be
reached
 Risk Factor Modification

 Dyslipidemia

 TREADMILL trial, atorvastatin (80 mg) increased pain-free

walking distance by more than 60%, compared with a 38%
increase with placebo .
 Smoking cessation

 Nonsmokers with PAD have lower rates of MI and mortality

than those who have smoked or continue to smoke.

 PAD patients who discontinue smoking have approximately

twice the 5-year survival rate of those who continue to
smoke.

 Smoking cessation also lowers the risk for the development

of critical limb ischemia.
 Treatment of DM

IN DCCT trial

 intensive insulin therapy showed reduced risk of cardiovascular
events by 42%.
 6 year follow up showed lower carotid intima media
thickness in the intensive group.
 In UKPDS
 Intensive treatment with SU and insulin was ass. With a
15% reduction with MI but no decrement in PAD
incidence.
 ACCORD and ADVANCE trials didn’t show macro vascular
complication reduction with intensive glucose control.

 Target hemoglobin A1C OF<7%.

 Control of hypertension

 Reduces risk of stroke,CAD,vascular death.

 (ABCD) trial,
 intensive BP control to 128/75 mm Hg substantially reduced cardiovascular
events compared with moderate blood pressure control in patients with PAD.
 In the ACCORD study
 In patients with diabetes at high risk for cardiovascular events, there was no
difference in cardiovascular outcomes between intensive antihypertensive
therapy (<120 vs <140.)
 It is not known whether antihypertensive therapy limits the
progression of PAD.

 if clinically indicated for other conditions, beta blockers should

not be withheld in patients with PAD
HOPE study,
 the ACEI ramipril decreased the risk for vascular death,
MI, or stroke by 22%.

 44% of the patients enrolled in the HOPE trial had

evidence of PAD.

 ONTARGET (vascular disease or diabetes) both ramipril

and telmisartan reduced the rate of the composite
endpoint by 17%.(13% PAD)
 Antiplatelet Therapy

 A meta-analysis
 that included approximately 135,000 high-risk patients with
atherosclerosis including those with PAD, found that antiplatelet
therapy yielded a 22% reduction in subsequent vascular death, MI,
or stroke.
 Anti platelet other than asprin was used.
 POPADADtrial of diabetic patients with asymptomatic
PAD, found that aspirin did not decrease the risk of a
composite primary endpoint including death from
coronary heart disease or stroke, nonfatal MI or stroke,
or amputation .
 The Clopidogrel versus Aspirin in Patients at Risk of
Ischemic Events (CAPRIE) trial
 compared clopidogrel with aspirin for efficacy in preventing ischemic
events in patients with recent MI, recent ischemic stroke, or PAD.
 there was an 8.7% relative risk reduction for MI, ischemic stroke, or
vascular death in the group treated with clopidogrel.
 among the 6452 patients in the PAD subgroup, clopidogrel
treatment reduced adverse cardiovascular events by 23.8%.
 CHARISMA trial
 compared the efficacy of dual antiplatelet therapy with clopidogrel
plus aspirin to aspirin alone in patients with established CAD,
cerebrovascular disease, or PAD, as well as in patients with multiple
atherosclerotic risk factors.

 Overall, dual antiplatelet therapy produced no significant benefit

compared with aspirin alone on the primary efficacy endpoint, a
composite of MI, stroke, or cardiovascular death.
 Clopidogrel vs. Aspirin in
Prevention of Ischemic Events

Event Rate per Year Aspirin 8.7%*

16 Overall
Relative Risk
Reduction
Event Rate (%)

Aspirin
Clopidogrel
Cumulative

12 5.83%
5.32%
8 Clopidogrel

4
P = 0.045

0
0 3 6 9 12 15 18 21 24 27 30 33 36

Months of Follow-Up
*ITT analysis.
CAPRIE Steering Committee.
Lancet 1996;348:1329-1339.
 The Warfarin Antiplatelet Vascular Evaluation (WAVE)
trial
 compared combination antiplatelet and oral anticoagulant therapy
with antiplatelet therapy alone in patients with PAD.

 There was no significant difference between the two treatments on

the primary composite endpoint of MI, stroke, or cardiovascular
death.

 life-threatening bleeding occurred more frequently in patients

receiving combination antiplatelet and anticoagulant therapy
Class I
 Pharmacotherapy

 Vasodilators have o benefit unlike in CAD

 Steal phenomenon
 Already dilated vessels
 (FDA) has approved two drugs, pentoxifylline (Trental) and
cilostazol (Pletal), for the treatment of claudication in
patients with PAD
 pentoxifylline
 decreases blood viscosity and improve erythrocyte flexibility.
 It may have anti-inflammatory and antiproliferative effects.
 has marginal efficacy increasing maximum walking distance by only
14% compared with placebo in one study.(Class IIb ).
 Cilostazol
 is a quinolinone derivative that
inhibits phosphodiesterase 3,
thereby decreasing cyclic
adenosine monophosphate
degradation and increasing its
concentration in platelets and
blood vessels.
 inhibits platelet aggregation
and causes vasodilation in
experimental animals.
 improves absolute claudication
distance by 40% to 50%
compared with placebo.(class
I)
 Percutaneous Transluminal Angioplasty and Stents

 patients with lifestyle-limiting claudication, despite a trial

of exercise rehabilitation or pharmacotherapy.

 Endovascular intervention should be considered in

symptomatic patients with clinical evidence of inflow
disease.
Peripheral Artery Surgery
Algorithm for Treatment of the Symptomatic Leg
 Acute Limb Ischemia

 When an arterial occlusion suddenly reduces blood flow to the arm or

leg.

 The metabolic needs of the tissue outstrip perfusion, placing limb

viability in jeopardy.

 Depending on the severity of ischemia, patients may note disabling

claudication or pain at rest.

 Concurrent ischemia of peripheral nerves causes sensory loss and

motor dysfunction.

 The 5 p’S)
 Prognosis

Usually have co morbid cardiovascular disorders,

which may even be responsible for the ischemia.
Has a poor long-term outcome.
 The 5-year survival rate after acute limb ischemia
caused
 by thrombosis -45%
 embolism-<20%.
 The 1-month survival rate in persons older than 75 years with
acute limb ischemia is approximately 40.
 Pathogenesis

The causes of acute limb ischemia include

 arterial embolism
 thrombosis in situ

 dissection

 trauma.

 Most arterial emboli arise from thrombotic sources in the heart.

 prosthetic cardiac valves.
 ventricular thrombus resulting from MI or left ventricular
aneurysm.
 left atrial myxomas.
 Aneurysms of the aorta or peripheral arteries may
harbor thrombi.

 paradoxical embolism of venous thrombi.

 Atrial fibrillation complicating valvular heart

disease, congestive heart failure, CAD, and
hypertension accounts for approximately 50% of
cardiac emboli to the limbs
 Thrombosis in situ occurs
 in atherosclerotic peripheral arteries.

 infrainguinal bypass grafts.

 peripheral artery aneurysms.(popliteal a)

 normal arteries of patients with hypercoagulable states.

 In patients with peripheral atherosclerosis, thrombosis in situ may

complicate plaque rupture
 Treatment

 Analgesic s

 Position bed.

 Keep the room warm.

 Heparin iv

 revascularization
Findings from the individual trials
suggest that catheter-based thrombolysis is an
appropriate initial option in patients with viable or
marginally threatened limbs andwhen the ischemia is
of less than 14 days’ duration,
whereas surgical revascularization is more appropriate
in those with immediately threatened limbs and in
those whose symptoms have lasted for more
than 14 days.
Catheter-based
thrombolysis can also be considered for patients at high risk for surgical
intervention. Identification and repair of a graft stenosis after
successful thrombolysis improve long-term graft patency.125 The
thrombolytic regimens currently used include the recombinant tissue
plasminogen activators alteplase, reteplase, and tenecteplase.
Catheter-based thrombolytic therapy should generally be continued
for 24 to 48 hours to achieve optimal benefit and to limit the risk for
bleeding. Adjuvant use of platelet glycoprotein IIb/IIIa inhibitors
shortens thrombolysis time but does not improve outcome
 Prognosis
 Angiographically In the AGATHA)
significant CAD - 60% to registry,
80% of patients with PAD.  50% - CAD,
 50% - prior stroke, TIA, or
 REACH registry, carotid artery
 62% of patients had either revascularization.
or both coronary and
cerebrovascular disease.  The specificity of an
abnormal ABI to predict
 25%- MI future cardiovascular
 30% - angina events is approximately
90%.
 16%- prior stroke,15% -TIA
 Atheroembolism
From atheroma on aorta
commonly.
Less frequently from branch
arteries
Occludes artery and arterioles
of extremities (50% LE)
Men >60yo.
Blue toe syndrome.
Look for other site inv’t.
Analgesics , foot care ,surgical
removal of atheroma
Anti platelate ,statins
Anticoagulants ???
Atheroembolism refers to occlusion of arteries resulting from
detachment
and embolization of atheromatous debris, including fibrin,
platelets, cholesterol crystals, and calcium fragments. Other terms
include atherogenic embolism and cholesterol embolism.
Atheroemboli
originate most frequently from shaggy protruding atheroma of
the aorta and less frequently from atherosclerotic branch arteries.
The atheroemboli typically occlude small downstream arteries and
arterioles of the skin, extremities, brain, eyes, kidneys, or mesentery.
127 Most affected individuals are men older than 60 years with
clinical evidence of atherosclerosis.
The most notable clinical features of atheroembolism
involving the extremities include painful cyanotic toes,
a condition called blue toe syndrome . Livedo
reticularis occurs in approximately 50% of patients.
Local areas of erythematous or violaceous
discoloration may be present on the lateral aspects of
the feet and the soles, as well as on the calves. Other
findings include digital and foot ulcerations, nodules,
purpura, and petechiae. Pedal pulses are typically
present
because the emboli tend to lodge in the more distal
digital arteries and arterioles. Symptoms and signs
indicating additional organ involvement with
atheroemboli should be sought
Funduscopy can be used to visualize Hollenhorst
plaques in patients with visual loss secondary to retinal
ischemia or infarction. Renal involvement, manifested by
increased blood pressure and azotemia, commonly
occurs in patients with peripheral atheroemboli. Patients
also sometimes show evidence of mesenteric or bladder
ischemia and splenic infarction.
atheroembolism include an elevated
erythrocyte sedimentation rate, eosinophilia, and eosinophiluria.
Other findings may include anemia, thrombocytopenia,
hypocomplementemia, and azotemia. Imaging of the aorta with
transesophageal ultrasound, MRA, or computed tomography may
identify sites of severe atherosclerosis and shaggy atheroma indicating
a source of the atheroemboli. The only definitive test for atheroembolism
is pathologic confirmation on skin or muscle biopsy
specimens. Pathognomonic findings include elongated needleshaped
clefts in small arteries caused by cholesterol crystals and
often accompanied by inflammatory infiltrates composed of lymphocytes
and possibly giant cells and eosinophils, intimal thickening,
and perivascular fibrosis.
References
THANK YOU!