2. Peripheral Vaskular Disease - Dr. Muzakkir, Sp.jp

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    Peripheral Vascular Disease

    Karthik Vamanan, MD

    Asst. Prof. Dept. of SurgeryVascular and Endovascular Surgery

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    Introduction

    Vascular insufficiency

    Acute

    Chronic

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    Acute Ischemia

    Etiology

    Thrombosis

    Embolism

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    Other causes

    Causes of acute limb ischemia inatherosclerotic patients

    Thrombosis of an atherosclerotic stenoticartery

    Thrombosis of an arterial bypass graft

    Embolism from heart, aneurysm, plaque, orcritical stenosis upstream (includingcholesterol or atherothrombotic)

    Emboli secondary to endovascular procedures

    Thrombosed aneurysm (especially poplitealaneurysm)

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    Other causes

    Non atherosclerotic, non embolic causes of acute

    limb ischemia

    Arterial trauma (especially iatrogenic)

    Aortic/arterial dissection

    Arteritis with thrombosis (eg, giant cell arteritis,

    thromboangiitis obliterans)

    Spontaneous thrombosis associated with a

    hypercoagulable state

    Popliteal cyst with thrombosis

    Popliteal entrapment with thrombosis

    Vasospasm with thrombosis (e.g. ergotism)

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    Epidemiology - Acute

    Incidence = 14/100,000

    12% of operative load in vascular surgery

    units

    Mortality rate = 25%

    Morbidity rate = 20% Jivegard et al. Acute limb ischemia due to arterial

    embolism or thrombosis. J. Cardiovasc Surg 29:32-36,1988

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    Clinical Presentation - Acute

    Sudden onset of severe pain

    May be silent

    May reduce in intensity

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    H + P

    Ask about onset

    Look for previous symptoms of arterial

    disease like claudication and rest pain.

    Risk factors for atherosclerosis.

    Embolic sources - ?

    History of previous embolic episodes.

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    H + P

    Pain

    On passive extension of ischemic muscle

    Paresthesias and paralysis

    Diabetes?

    Paresthesias first, then sensory, motor last.

    Pallor

    Level of demarcation

    Cap refill

    Venous filling Poikilothermia

    Pulseless

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    Differential

    Conditions mimicking acute limb ischemia

    Heart failure (especially if associated with

    chronic occlusive disease)

    Acute DVTAcute compressive neuropathy

    Other low flow states including vasopressor

    therapy.

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    Investigation

    PE

    Non Invasive Laboratory

    Angiography / MRA / CTA

    DO NOT DELAY

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    Rx

    Percutaneous

    Thrombectomy

    Thrombolysis

    Open

    Thrombectomy

    Bypass

    Fasciotomy?

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    Treatment

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    Treatment

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    Conclusions

    Patients with acute limb ischemia face a 1-yearmortality of 10-20%

    Treatment of occluded bypass grafts has a betteroutcome than treatment of native arteries

    Risk of major bleeding increases with thrombolysiscompared with surgical revascularization

    Risk of a bleeding complication increases ascoagulopathy worsens (decreased fibrinogen,prolonged PTT)

    Risk of an intracranial bleed is approximately 1-2%with thrombolysis

    Lytic patients require fewer open surgical procedures

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    Treatment

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    Epidemiology- Chronic

    Incidence between 500 and 1000 per millionpopulation per year

    20% of these patients die annually

    5-year mortality = 70% 35% cardiovascular disease

    9% non-cardiovascular disease

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    Risk Factors

    Age

    Family history

    Trauma

    Smoking Diabetes

    Hypertension - shear forces

    Hypercholesterolemia

    Hypercoagulable syndromes

    Homocysteinemia

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    PAOD

    Spectrum of disease

    Asymptomatic Tissue Loss

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    Claudication

    Intermittent claudication is lower extremity

    muscular pain in the calves (less frequently

    the buttocks or thighs) induced by exercise

    and relieved with short periods of rest We know that for every person with

    claudication, there are at least four people

    with similar disease without symptoms

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    Claudication

    Natural History

    Associated with favorable outcome

    1 in 4 have worsening symptoms

    1-7% limb loss at 5-10 yrs Less favorable natural history if

    ABIs low

    Continues to smoke

    Poorly controlled DM

    Mortality rate at 5 years is 50%

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    Claudication

    Pathogenesis

    Arterial obstruction proximal to affectedmuscle beds

    Limits the normal exercise-induced increase inblood flow and produces transient muscle

    ischemia during exercise

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    Claudication

    Clinical Presentation

    Usually classic like the definition

    Symptoms range from severe pain and

    cramps to fatigue on exertion Level will depend on level of disease

    Initially may not be consistently reproducible

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    Claudication

    History

    Should be aimed at

    Delineation of symptoms

    Elimination of differential diagnoses Presence of risk factors

    Identification of other beds of atherosclerosis

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    Claudication

    Specific History

    Location of the pain or discomfort

    Duration of the symptom

    Whether it worsens or improves with time andwhether conservative therapy has had an

    effect

    Distance the patient can now walk before

    experiencing the discomfort

    being forced to stop

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    Claudication

    Specific History

    Elapsed time after exercise is stopped before

    the pain is relieved

    Type of rest or position of patient (standing atrest, sitting, lying) necessary to relieve the

    pain

    Whether the pain returns after the same time

    and distance if exercise is then resumed

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    Claudication

    Differential Diagnosis

    Nerve Root Compression

    Arthritis and joint problems

    DVT

    Chronic compartment syndrome

    Neuropathy Muscle strain

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    Critical Limb Ischemia

    The TransAtlantic Inter-Society Consensus(TASC) definition:

    Persistent, recurring ischemic rest painrequiring opiate analgesia for at least 2weeks,

    Ulceration or gangrene of the foot or toes,

    AND ankle systolic pressure less than50mmHg or toe systolic pressure less than

    30mmHg (or absent pedal pulses in patientswith diabetes)

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    CLI

    Natural History

    Rarely antecedent history of claudication

    Most (if not all) patients with CLI will progress

    to limb loss Mortality rate at 5 years is 70%

    Prognosis worse if

    DM

    Smoking

    Occlusive Disease below the knee

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    CLI

    History

    Prior and other history of vascular disease

    Rule out other causes of pain and ulceration

    Neuropathy Venous disease

    Infections

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    Physical Exam

    Thorough physical

    Peripheral sequelae of ischemia

    Wasting

    Thin skin

    Hair loss

    Thick nails

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    Physical Exam

    Pulse exam

    Palpate

    Presence

    Strength Character

    Auscultate

    Bruits

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    Physical Exam

    Patterns of Disease

    Inflow

    Outflow

    Combination

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    H + P

    Ischemic ulcers

    located distally (on dorsum of foot/toes)

    pain relieved by dependency, often occurring

    at night Irregular edge with poor granulation

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    H + P

    Other Ulcers

    Neurotropic

    Located at pressure points (under calluses, plantar

    aspect of 1st/5th MP joints)

    Painless

    Punched out with deep sinus

    Stasis

    Located over medial malleolus or lower third of leg

    May have mild pain relieved by elevation Shallow, irregular shape, rounded edges, granulating

    base

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    Coexistent Cardiac Disease

    20% previous myocardial infarction

    7% previous congestive heart failure

    4% previous arrhythmia

    60% abnormal EKG

    7% previous CVA

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    Investigation

    NON-INVASIVE

    ABI (ankle brachial index)

    Segmental blood pressures

    Toe pressures Pulse volume recordings

    Color flow Doppler

    MRA

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    Ankle-Brachial Index

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    Ankle-Brachial Index

    Ankle SBP/Brachial SBP

    normal is 0.9-1

    single level occlusion > 0.5

    multi level occlusion < 0.5 claudication 0.6 to 0.9

    rest pain 0.3

    Calcification can alter results

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    Segmental limb pressures

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    Segmental limb pressures

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    Toe Pressures

    Measured with cuff around digit and PPG

    (photo-plethysmography) monitor

    Not as likely affected by calcification of

    arteries Normal: 60 to 80% of ankle or brachial

    T Ph l h hi

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    Toe Photoplethysmographic

    Waveforms

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    Pulse Volume Recording

    Pneumatic cuffs measure the momentary

    volume changes with each pulse.

    Normal:

    sharp systolic peak prominent reflected wave

    Not affected by calcified vessels

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    Arterial Duplex Scan

    Duplex visualization

    Color imaging of luminal flow

    Velocity measurement of flow

    increased velocity at stenosis

    decreased velocity distal to stenosis

    spectral broadening (turbulence

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    Arterial Duplex Scan

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    MRA

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    Angiogram

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    Angiogram

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    Angiogram

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    Treatment

    Goals

    Relieve symptoms

    Pain

    Infection Tissue loss

    Preserve function

    Preserve limb

    Risk factor modification

    Improve quality of life

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    Treatment

    Medical Management

    Risk modification

    Statins

    Diabetes management Control hypertension

    Cessation of smoking

    Exercise

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    Treatment

    Drug therapy

    Antiplatelet therapy

    Aspirin

    Clopidrogel

    Ticlopidine

    Glycoprotein 11b/111a inhibitors???

    Cilostazol

    Oxypentifylline??

    Pentoxyfylline

    Antioxidants and chelation therapy???

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    Treatment

    Endovascular management

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    Treatment

    Surgical

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