Peripheral Artery Occlusive Disease Dr.mehdi hadadzadeh Cardiovascular surgeon.
-
Upload
lauren-thorpe -
Category
Documents
-
view
220 -
download
1
Transcript of Peripheral Artery Occlusive Disease Dr.mehdi hadadzadeh Cardiovascular surgeon.
Peripheral Artery Occlusive Disease
Dr.mehdi hadadzadeh
Cardiovascular surgeon
Peripheral Artery Occlusive Disease
Prevalence
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
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
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)
Estimated that of those with lower extremity arterial disease at least 10% also have CVD and 28% have CAD
Of patient with LE arterial disease 75% will die of a coronary or cerebrovascular event
History
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
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 lossSigns Muscular atrophy Decrease hair growth Thick toenails Tissue necrosis ulcers infection Absent pulses Bruits
Atypical leg pain(functionally limited)
Classic (typical) claudication
~15%
~33%
50%Asymptomatic
Critical limb ischemia
Clinical Presentations of PAD
1%–2%
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
femoropopliteal
Unilateral claudication in calf , femoral pulse palpable with absent unilateral distal pulses
Distal obstruction
Femoral & popliteal pulses palpable, ankle pulses absent, cluadication in calf & foot
Ankle Brachial Index (ABI)
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
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
Segmental Pressure Measurements Pulse Volume Recordings Duplex Scanning MRA
Segmental Pressure Measurements
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
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
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
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:
MedicalMedical
surgicalsurgical
Medical Treatments
Risk factor reduction
Exercise
Medications
How to exercise for maximal benefit?
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
Vasodilators (not effective) Antiplatelet Agents
Pentoxifylline (Trental)
Cilostazol (Pletal)
Antiplatelet Agents
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
An agent which is thought to improve erythrocyte deformability, reduce blood viscosity and decrease platelet reactivty
Effectiveness considered unknown
AHA recommends use only in cases where exercise therapy has failed or patients are unable to exercise
When to refer to vascular specialist?
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:– Lifestyle limiting claudication refractory to exercise and
pharmacotherapy– Evidence of critical limb ischemia (rest pain or tissue loss)
Percutaneous Translumenal Angioplasty
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
Generally accepted as most effective treatment for those with debilitating PAD
In some contexts surgery appears superior (infrainguinal lesions 5 yr patency 38% for PTA and 80% with surgery)
Embolism, thrombosis & vascular injury are the causes of acute lower limb ischemia.
Emboli: The Sources of arterial emboli are :
Causes
●Cardiac (90%)
Arrhythmia (atrial fibrillation)
Valvular heart diseaes. ( MS)
Prosthetic heart valves.
Hx of myocardial infarction.
Atrial myxoma.
●Arterial source (9%)Atherosclerotic aortaAneurysm
●Other (1%)Hx of medication (oral contraceptives)
WWW.SMSO.NET
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%
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.
Trauma It is important to determine a history of
arterial trauma, arterial catheterization,
intra-arterial drug induced injection, limb fractures.
Clinical Features The 6 P’s :
■ Pain.
■ Pallor.
■ Pulselessness.
■Perishing cold.
■ Paraesthesia.
■ Paralysis.
Embolism:
obvious cardiac source
No hx of cluadication
Normal pulses in contralateral limb
Angiogram: minimal atherosclerotic
Few collateral
Clinical differentiation between thrombosis & embolism
Thrombosis:
No obvious cardiac source.
history of cluadication.
abnormal pulses in contralateral
limb.
Angiogram: diffuse atherosclerotic
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 clot.
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.