2. peripheral vaskular disease - dr. muzakkir, sp.jp
TRANSCRIPT
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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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