Transcript Peripheral Artery Occlusive Disease

Peripheral Artery Occlusive Disease
Dr.mehdi hadadzadeh
Cardiovascular surgeon
Peripheral Artery Occlusive
Disease
Prevalence
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Approximately 1 million Americans become
symptomatic Q year
Approximately 5% of men and 2.5% of women
complain of intermittent claudication by history
If asymptomatic disease is included (as
determined by ABI) 13% of women and 16% of
men have peripheral vascular disease
Of these only 1% have critical limb ischemia
Risk Factors
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Age
Male gender (over age 70 risk equalizes)
DM (tend to have more distal and diffuse
disease; 7 fold increase risk of amputation)
Tobacco (risk even stronger than for CAD; with
smokers experiencing IC up to 10 yrs earlier)
HTN
Hyperlipidemia
Prognosis
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Over 5-10 yrs 70% of pt’s have no change or
improve
20-30% worsen
10% require intervention
1% require amputation
In patients with IC the majority of morbidity and
mortality comes from increased risk of
CAD/CVD
Associated Risks (CAD/CVD)
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Estimated that of those with lower extremity
arterial disease at least 10% also have CVD
and 28% have CAD
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Of patient with LE arterial disease 75% will die
of a coronary or cerebrovascular event
History
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Quality (aching, numbness, weakness, fatigue)
Location (calf, buttock, or thigh)
Severity of pain and functional limitations
Typically induced by walking and relieved by rest
True claudication typically resolves in <10 minutes
after stopping activity
Nocturnal pain and pain at rest are indications of more
severe disease
Risk Factors
Physical Exam
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Condition of skin and appendages
Pulses
Check for bruits
Pallor during leg elevation
Time for color return after leg restored to
dependent position
ABI
Symptoms
 Intermittent claudication
 Rest pain
 Erectile dysfunction
 Sensorimotor impairment
 Tissue loss
Signs
 Muscular atrophy
 Decrease hair growth
 Thick toenails
 Tissue necrosis ulcers infection
 Absent pulses
 Bruits
Clinical Presentations of PAD
50%
Asymptomatic
~15%
Classic (typical)
claudication
~33%
1%–2%
Critical limb ischemia
Atypical leg
pain
(functionally
limited)
Aortoilliac Claudication of both buttoks, thighs and
calves, femoral and disal pulses
absent,bruits, impotence
Illiac
Unilateral claudication of thigh, calf
Unilateral absence of femoral and distal
pulses
femoropo Unilateral claudication in calf , femoral
pliteal
pulse palpable with absent unilateral
distal pulses
Distal
Femoral & popliteal pulses palpable, ankle
obstruction pulses absent, cluadication in calf & foot
Ankle Brachial Index (ABI)
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ABI <0.9 is 99% sensitive and 99% specific for
angiographically diagnosed PAD
Supine position
Check systolic BP in upper extremities (using
Doppler) – use highest value
Systolic BP in lower extremities – use highest
value
Divide ankle SBP by brachial SBP
May be falsely elevated in calcified vessels
(DM)
ABI
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Normal = >0.90
0.70 – 0.89 = mild disease
0.50 – 0.69 = moderate disease
<0.50 = severe disease (rest pain/tissue loss)
If strongly suspect IC but WNL, can repeat following
exercise (leg pressures only)
Other Noninvasive Testing
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Segmental Pressure Measurements
Pulse Volume Recordings
Duplex Scanning
MRA
Segmental Pressure Measurements
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Measures SBP at multiple levels (upper and
lower thigh, upper calf, ankle)
Pressure reductions between levels help to
localize occlusion
Normally pressures increase as move further
down the leg (>20mmHg gradient abnl)
Limited with calcified artery walls (ie: diabetics)
Pulse Volume Recordings
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Pneumatic cuffs placed similarly to SPM with
pulse volume recorders
Calibrated air plethysmographic wave form
recording system
Instead of SBP, measure volume of blood
entering the arterial segment during systole
Generates a waveform which normally has
rapid systolic peak and dicrotic notch
Not limited by calcifications of vessel walls
PVR
SPM and PVR
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Useful in measuring general local and severity
of obstruction
Allow for objective monitoring of patient’s
change over time through serial exams
Do not precisely localize disease or distinguish
occlusion from severe stenosis
Pre-intervention Planning
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Ultrasound—duplex scanning (also used for
follow up of patency post-intervention)
MRA (non-invasive, no ionizing radiation,
contrast dye; but more artifact)
Angiogram (gold standard; dx and rx in one
procedure):invasive
Therapeutic
Approaches:
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Medical
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surgical
Medical Treatments
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Risk factor reduction
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Exercise
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Medications
How to exercise for maximal
benefit?
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Greatest improvement in pain distances
occurred with:
1. Exercise to near maximal pain
2. At least 3 times per week
3. Duration of at least 6 months
4. Walking as exercise mode
Medications
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Vasodilators (not effective)
Antiplatelet Agents
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Pentoxifylline (Trental)
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Cilostazol (Pletal)
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Antiplatelet Agents
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Strong evidence that aspirin is benefitial both in
reducing progression of arterial occlusive
disease and in reducing vascular death (MI,
stroke)
Pentoxifylline (Trental) 400mg TID
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An agent which is thought to improve erythrocyte
deformability, reduce blood viscosity and decrease
platelet reactivty
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Effectiveness considered unknown
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AHA recommends use only in cases where exercise
therapy has failed or patients are unable to exercise
When to refer to vascular
specialist?
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Most patients can be managed with risk factor
modification, exercise and pharmacotherapy
Arteriography is not necessary for diagnostic
evaluation of patients with PAD and is indicated only
when condition requires revascularization
Therefore, referral is indicated for:
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Lifestyle limiting claudication refractory to exercise and
pharmacotherapy
Evidence of critical limb ischemia (rest pain or tissue loss)
Percutaneous Translumenal
Angioplasty
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High initial success rates of 90%
Long-term success rates vary from 51-70%
Best for stenosis (rather than occlusion), short
segment disease, larger vessels (ie: iliac), no
DM, normal renal function
Bypass Surgery
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Generally accepted as most effective treatment
for those with debilitating PAD
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In some contexts surgery appears superior
(infrainguinal lesions 5 yr patency 38% for PTA
and 80% with surgery)
Causes
Embolism, thrombosis & vascular injury are the causes of
acute lower limb ischemia.
Emboli:
 The Sources of arterial emboli are :
●Cardiac (90%)
Arrhythmia (atrial fibrillation)
Valvular heart diseaes. ( MS)
Prosthetic heart valves.
Hx of myocardial infarction.
Atrial myxoma.
●Arterial source (9%)
Atherosclerotic aorta
Aneurysm
●Other (1%)
Hx of medication (oral
contraceptives)
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Emboli usually impact at branching points in arterial
tree, particularly at the bifurcation of the aorta, the
common femoral bifurcation & popliteal trifurcation.
Sites of occlusion embloi to the lower
limb:
Femoral artery
45%
Aorta & iliac artery 26%
popliteal artery
15%
tibial artery
1%
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Thrombosis:
Thrombosis usually occur on a pre-existing atherosclerotic lesion.
 Occasionally thrombosis occur on relatively normal artery
In patients with hypercoagulabale states ex:
Pt with malignancy, polycythemia
or pt taking high doses of oestrogen.
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Trauma
It is important to determine a history of
arterial trauma, arterial catheterization,
intra-arterial drug induced injection, limb fractures.
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Clinical
Features
 The 6 P’s :
■ Pain.
■ Pallor.
■ Pulselessness.
■Perishing cold.
■ Paraesthesia.
■ Paralysis.
Clinical differentiation between
thrombosis & embolism
Embolism:
Thrombosis:
obvious cardiac source
No obvious cardiac source.
No hx of cluadication
history of cluadication.
Normal pulses in contralateral limb
abnormal pulses in contralateral limb.
Angiogram: minimal atherosclerotic
Angiogram: diffuse atherosclerotic
Few collateral
Well developed collateral
TX:Immediately
Anticoagulant with heparin to prevent propagation of
thrombus & distal thrombosis & this achieved by
giving a bolus of 10 000 units of heparin
intravenously & an infusion of about 1000 units of
heparin per hour
Example of
acute arterial
embolus
“Saddle”
Embolus of
right iliac
artery
Man Embolectomy : agement
This operation usually
performed under local
anaesthesia.
A groin incision is made & the
common femoral artery is
opened. often the clot is
found in the artery a Fogarty
balloon catheter is passed in
turn into the proximal &
distal arteries the balloon is
inflated & the catheter
withdrawn removing the
Fogarty balloon catheter
Management
Thrombolytic
therapy:
 Percutaneous intra-arterial thrombolytic therapy.
Takes approximately 12-72 hours to dissolve the clot.
 Agents used: streptokinase, urokinase & tissue
plasminogen activator.
 Mechanism:
The convert plasminogen to plasmin which the active
lytic agent.
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