Guanfeng Yu

Department of Vascular Surgery

The First Affiliated Hospital of Wenzhou Medical
College

Peripheral artery disease

Arterial stenosis and

occlusion

Lerning objectives

Acute arterial occlusion

Aneurysm

Introdution
Causes and risk factors
Symptoms and signs
Physical exam
Lab and radiological
exam
Option of treatment

Background
Peripheral artery disease (PAD) is a nearly
pandemic condition that has the potential to
cause loss of limb or even loss of life.
Peripheral artery disease manifests as
insufficient tissue perfusion caused by existing
atherosclerosis that may be acutely
compounded by either emboli or thrombi.

Pathophysiology

arteriosclerosis obliterans, is primarily the

result of atherosclerosis. The atheroma
consists of a core of cholesterol joined to
proteins with a fibrous intravascular covering.
The atherosclerotic process may gradually
progress to stenosis and complete occlusion of
medium and large arteries.

Pathophysiology of
Atherosclerosis

Atheroma porridge; Sclerosis hardening

Response to endothelial injury hypothesis

Loss of barrier function, antiadhesive properties and

antiproliferative influence on underlying SMCs
Migration and proliferation of SMCs production of
ECM
Oxidized lipid accumulation in vessel walls
Recruitment( ) of macrophages and lymphocytes
Adherence of platelets to dysfunctional endothelium,
exposed matrix, and macrophages

Common Underlying Atherothrombotic

Disease Process
Atherothrombotic
Stroke

Unstable Angina

Plaque
Rupture

Platelet
Adhesion,
Activation, and
Aggregation

MI

Thrombus
Formation

Atherothrombotic Events (MI, Stroke, or CV Death)

MI, myocardial infarction; PAD, peripheral arterial disease; CV, cardiovascular.
Ness J, et al. J Am Geriatr Soc. 1999;47:1255-1256.
Schafer AI. Am J Med. 1996;101:199-209.

PAD

Atherothrombosis: A Generalized and

Progressive Process
Thrombosis
Unstable
angina ACS
MI
Ischemic
stroke/TIA

Atherosclerosis

Critical leg
ischemia
Intermitent
claudication
CV death

Stable angina/
Intermittent claudication
Adapted from Libby P. Circulation. 2001;104:365-372.

Atherothrombosis: Thrombus Superimposed on

Atherosclerotic Plaque

Adapted from Falk E, et al. Circulation. 1995;92:657-671.

Characteristics of Unstable and

Stable Plaque
Stable

Unstable

Few
SMCs

Thin
fibrous cap

Eroded
endothelium

Inflammatory
cells
More
SMCs

Thick
fibrous cap

Lack of
inflammatory
cells

Intact
endothelium
Activated
macrophages

Libby P. Circulation. 1995;91:2844-2850.

Foam cells

Plaque Rupture

Andrew Farb, MD by permission.

Peripheral Arterial Occlusive Disease

Peripheral arterial disease
PAD

Prevalence and survival

2-3% population >50y, 10% > 70y

Occurs in approximately 1/3 of patients

Strong association with CAD

Over age 70
Over age 50 who smoke or have DM
Obvious associated risk of stroke, MI, cardiovascular death

Progressive disease in 25% with progressive intermittent

claudication/limb threatening ischemia
Outcomes

Impaired QoL
Limb Loss
Premature Mortality

Prevalence and survival

Lower extremity ischemia associated with

decreased 5-yr survival

97.4 % intermittent claudication

80% claudication requiring surgery
48% limb-threatening ischemia
12% re-op for limb-threatening ischemia

Risk Factors for PAD: Framingham Heart Study

Reduced

Increased

Smoking
Diabetes
Hypertension
Hypercholesterolemia
Hyperhomocysteinemia
Fibrinogen

Mean follow-up 38 years

C- Reactive Protein
Alcohol
Relative Risk

.5

Symptoms and signs of lower limb

Intermittent claudication
Rest pain
Coldness,numbness,paraesthesia,and colour
change
Ulceration and gangrene
Temperature sensation and movement
Arterial pulsations
Arterial bruits
Venous refilling

Intermittent Claudication

Intermittent claudication (derived from the Latin word for

limp)
A reproducible discomfort of a defined group of muscles
that is induced by exercise and relieved with rest.
Supply Demand

Location depends upon the location of the disease.

Buttock, thigh, calf or foot claudication, either singly

or in combination.

Relationship of claudication to the site of

disease

Aorticiliac

Iliac

Femoropopliteal

Distal obstruction
Ankle pulses absent

Location of obstruction

Claudication in bothbuttocks,thighs
and calves;femoral and distal
pulse(-)
Unilateral claudication in thigh and
calf and sometimes buttock
Unilateral claudication in
calf,femoral pulse palpable with
absent unilateral distal pulse
Femoral and popliteal pulses
palpable
Claudication in calf and foot

Location of claudication

Rest pain

Rest pain

Localized to metatarsal heads and toes

Worse with elevation or recumbent position
Improved with foot dependency
Worse at night
Relieved by hanging the foot out of bed or sleeping in
a chair
Coldness,numbness,paraesthesia

Physical Exam

Trophic Signs

Pulse exam

Skin atrophy, thickened nails, hair loss, dependent

rubor
Ulceration, gangrene
May miss more than 50%

Elevation and dependency test

Criqui M, et al. Circulation, 1985: 71; 516-521

Colour change
Blanched on elevation
Red speckle
Purple discolouration

Ulceration and gangrene

Vascular exam

Diminution
stenosis/occluded
Expansile arterial
pulsationdilation/aneurysm

Arterial bruites
Systolic bruitestenosis/occluded
Continuous murmur-AVF

Arterial pulsations

Radial arteries
Carotid arteries
Abdominal aorta
Femoral arteries
Popliteal arteries
Posterior tibial arteries
Dorsalis pedis arteries

Artereis to be examed

Examination of pules

Pulse intensity should be assessed and recorded

numerically as follows:

0, absent

1, diminished
2, normal
3, bounding

Use of a
standard
examination
should
facilitate
clinical
communication

Physicla exam

Venous refilling
Elevat limb for 30 seconds----laid flat on bed
Normal refilling within seconds
Reduced refilling-severe arterial insufficiency
Increased refilling -AVF

Physical Exam: Elevation and Dependency

Test

Color Return(s)

Venous Filling(s)

Normal

10

10-15

Adequate
Collaterals

15-25

15-30

Severe Ischemia

>35

>40

Halperin, Throm Res. 2002; 106: V303-311

General investigation

Full blood count

Erythrocyte sedimentation rate(ESR)
Blood and urine glucose
Blood lipid profile(triglycerides,total
cholesterol,HDL,LDL)
Chest X-ray film,plain abdominal radiography
Electrocardiogram,echocardiography

PAD

Noninvasive vascular diagnostic

laboratory

1.The ankle-brachial index

ABI =Lower extremity systolic pressure

Brachial artery systolic pressure

The ankle-brachial index is 95% sensitive and 99% specific for PAD
Establishes the PAD diagnosis
Identifies a population at high risk of CV ischemic events
Population at risk can be clinically & epidemiologically defined:

Exertional leg symptoms, non-

healing wounds, age > 70, age > 50

years with a history of smoking or
diabetes.

Toe-brachial index (TBI) useful in

individuals with non-compressible pedal
pulses

ABI algorithem

2.Segmental Pressures

Pneumatic cuffs at multiple

levels

Doppler pressure at pedal

artery
Drop >30 mm Hg between
levels
Drop >20 mm Hg between
limbs

Reflects status of artery

above drop in pressure
Inaccurate with calcified
vessels

Rose SC. J Vasc Interv Radiol. 2000; 11:1107-1114

Calibrated air
plethysmographic
wave form recording
system
Helps localize site of
obstruction
Placement of cuffs at
levels of proximal and
distal thigh, calf and
ankle

3.Duplex Doppler

Non-invasive method of evaluating the blood

vessels using sound waves, similar to
ultrasonography and echocardiography.

Can obtain both anatomic and hemodynamic

information.
Anatomical detail
vessel wall
intraluminal obstructive lesions
perivascular compressive structures

Is this enough?

Noninvasive lab documents presence and

severity of disease
No comprehensive anatomic information
No ability to plan interventions

Radiologic Imaging: MRA and CTA

DSA (conventional angiography) remains the

gold standard for evaluation of PVD
Newer modalities that match its accuracy are
rapidly evolving
It is a matter of time before imaging replaces
DSA, with the invasive angiographic
techniques reserved for interventional
procedures

MRA vs. DSA

MRA: Current Technique

3D gradient echo (fast

acquisition)
Gadolinium Enhanced

20-40 cc
Automated Scan delay

Renal arteries to toes

Stepping table or bolus chase
45-min exam

MRI

Limitations of MRI

Uncooperative patient
Claustrophobia(fear of closed place)
Metal artifact
Pacemakers/ICDs
Lack of visualization of calcium
(maganetic field)

CTA of PVD

Multidetector CT scanner
necessary (4+)

Iodinated contrast volume similar

to conventional angiography

Many hospitals now have 64 Slice

80-150 cc
Automated Scan Delay

Renal arteries to ankles

20-minute exam
High powered post processing
software crucial

CTA of PVD

CTA of PVD

Large volumes of data are

generated via CTA studies
and displayed in various
formats to refine the
analysis of study results

Maximum Intensity
Projection -MIP (most
common)
Shaded surface display
3D Volume rendering

CT Limitations

With significant and dense

calcifications, a false diagnosis
of patency can result.
Uncooperative patient
Pregnancy
Bad Pump
Inconsistent pedal vessel
visualization
Renal failure/contrast allergy

Digital Subtraction Angiography (DSA)

Gold standard of arterial imaging

Has almost totally replaced conventional cut film

angiography

Compares a pre contrast image with a post contrast

image using a computer, and "subtracts" elements
common to both.

Prevents images of objects like bones etc from obscuring

vascular details.
Contrast resolution is improved through use of image
enhancement software.

The Clinical Approach to the Patient with or at Risk

for PAD
Clinicians who care for individuals with PAD should be able to
provide:

Vascular review of symptoms

Vascular-focused physical examination

Noninvasive vascular diagnostic laboratory

ABI and toe-brachial index (TBI)

Exercise ABI

Duplex ultrasound

Magnetic resonance angiography (MRA)

Computed tomographic angiography (CTA)

When required, diagnostic catheter-based angiography

Diagnostic algorithem

CLASSIFICATION
Stage of severity(Fontain stages)
>Stage:asymptomatic
>Stagea:mild claudication
>Stageb: moderate to severe claudication
>Stage :ischemic rest pain
>Stage :ulceration or gangrene.

Rutherford categories
Grade 0,category0:asymptomatic
Grade,category1:mild claudication
Grade,category2:moderate claudication
Grade,category3:sever claudication
Grade,category4:ischemic rest pain
Grade , category5:minor tissue loss
Grade ,category6:major tissue loss

NON SURGICAL MANAGEMENT

General treatment

Risk factor management

Lipid-lowering therapy
Smoking cessation
Glucose control
Weight control

Supervised Exercise Programmes

Antiplatelet therapy - ASA, ticlodipine,
clopidogre(plavix)
Vasoactive - Cilostazol (Pletal),
pentoxyfilline (Trental)

Lipid lowering and antihypertension

therapy

Treatment with an HMG coenzyme-A reductase inhibitor

(statin) medication is indicated for all patients with peripheral
arterial disease to achieve a target LDL cholesterol of less than
100 mg/dl.
Antihypertensive therapy should be administered to
hypertensive patients with lower extremity PAD to a goal
of less than 140/90 mmHg (non-diabetics) or less than
130/80 mm/Hg (diabetics and individuals with chronic
renal disease) to reduce the risk of myocardial
infarction, stroke, congestive heart failure, and
cardiovascular death.

Antiplatelet therapy

Antiplatelet therapy is indicated to reduce the risk of myocardial

infarction, stroke, or vascular death in individuals with
atherosclerotic lower extremity PAD.
Aspirin, in daily doses of 75 to 325 mg, is recommended
as safe and effective antiplatelet therapy to reduce the
risk of myocardial infarction, stroke, or vascular death in
individuals with atherosclerotic lower extremity PAD.
Clopidogrel (75 mg per day) is recommended as an
effective alternative antiplatelet therapy to aspirin to
reduce the risk of myocardial infarction, stroke, or
vascular death in individuals with atherosclerotic lower
extremity PAD.

Supervised exercise

A program of supervised exercise training is

recommended as an initial treatment modality for
patients with intermittent claudication.
Supervised exercise training should be
performed for a minimum of 30 to 45
minutes, in sessions performed at least
three times per week for a minimum of 12
weeks.

Endovascular revasculariztion
Recommended for
1.Aortoiliac stenosis<10cm,chronic
occlusion<5cm
2.Femoropopliteal discrete stensis
<10cm,calcified stenosis <5cm
3.Infrapopliteal ensovascular Tx limited to
threatened limb loss

Percutaneus transluminal angioplasty

Iliac artery PTA+stenting

Percutaneus transluminal angioplasy

Balloon catcheter
Self-expanding Stent
Baloon-expanding stent

PTA
Stenting after or before
Stenting spontaneusly

PTA+Stenting

Surgical revasculariztion
Recommended for
1.Aortoilac: stenosis >10cm,chronic
occlusion>5cm,heavily calcified
lesion,associated with aortic aneurysm
2. Common femoral artery:lesion>10cm,heavily
calcified lesion >5cm,ostium of superficial F
involved,popliteal involved

Open surgery for PAD

CASE 1
69yr/male
MI 10Yr ago
Right foot pain 1mon
Right ABI 0.36

PTA+stenting of iliac artery

Run-in reconstruction

Femoral-distal femoral bypass

Bypass to distal superficial
femoral artery (EPTFE graft)

Proximal femoral artery

bypass

Case 2
73yr old/female
DM
Right claudication 100m
No pulse dorsalis/pt
Right ABI 0.4

Femoral-tibia bypass
Combined PTFE+auto
vein graftpopliteal
anastomosis

Femoral anastomosis

Case 3 Endarterectomy

Common femoral
artery endarteretomy

Surgery for critical limb ischemia

For individuals with combined inflow and
outflow disease with critical limb ischemia,
inflow lesions should be addressed first.

When surgery is to be undertaken, an aortobifemoral bypass is recommended for patients

with symptomatic, hemodynamically
significant, aorto-bi-iliac disease requiring
intervention.

Acute arterial occlusion

Acute embolic Disease

Acute thrombosis(based on atheroma)
Vascular trauma

Acute arterial occlusion

Embolus source:
Cardiac
atrial fibrillation
myocardial infarction
Artery
atheromatous plaque
ameurysm

Sites of Embolization

Bifurcations

Femoral - 40%
Aortic - 10-15%
Iliac - 15%

Popliteal - 10%
Upper extremities - 10%
Cerebral - 10-15%
Mesenteric/visceral - 5%

History

The onset and duration of symptoms

Pain

Sudden onset - embolic

Long-standing before acute event - thrombotic

Previous revascularization
Risk factors for atherosclerotic heart disease

5ps

Pain
Pallor
Pulselessness
Paresthesia
Paraparesis
Poikilothermia(changing temperature 6th p)

Pules and location of obstruction

Palpable Pulses
Location of
Obstruction

Femoral

Popliteal

Pedal

Aortoiliac segment

Femoral segment

++

Distal popliteal tibials

(Popliteal anerysm)

Distal popliteal tibials

Menagment

Rapid systemic anticoagulation

Arteriography

Heparin bolus/drip(5000 units i.v.)

Prevent propagation of thrombus, distal thrombosis,
venous thrombosis
Operative planning target vessel
Therapeutic thrombolysis, angioplasty
Should not delay revascularization & may be obtained
intra-operatively

Surgery- Embolectomy
Percutaneous Thrombectomy

Embolectomy

Fogarty catheter

Embolectomy

Fogarty catheter

Catheter thrombolysis
Right iliac thrombosis

24hr after catheter thrombolysis ,stenosis

PTA after thrombolysis

Stenting After Therombolysis

Ilia stent

Iliac artery
Patency
recovered

Acute Arterial Trauma

Arterial occlusion may caused by:
The lumen occluded by ,e.g. thrombosis
The wall,e.g.subintimal haematoma
The surrounding tissues,e.g. compartment
syndrome

classification

Penetrating injury(knife ,bullet)

Blaunt injury
Iatrogenic injury(cardiac catheter )

Diagnosis of Arterial Trauma

History of trauma
Wound exam
Colour,temperature,pulses of affected limb
Preoperative assessment
Angiography----leakage of contrast
/stenosis/occlusion/atheromatous lesion
Duplex ultrasound

Management of main arterial trauma

Suture repair (punctured wound)
Resection of damaged segment
+anastomosis
+Interposition graft(vein or )
Vein repair
Stabilisation of bone fracture before or
after(depending how acute is the ischemia)

Complication of arterial reconstruction

Question: 6 hours after a femoral-tibial artery
bypass for
advanced acute ischemia, the lower leg is
swollen and painful with palpable pulse. The
likely etiology is:
A. DVT
B. Reperfusion injury
C. Thrombosis
D. Arterial spasm

The answer is

B. Reperfusion injury

Reperfusion injury

Local effects

Oxygen radicals accumulate

Compound cellular insult

Systemic effects

Acid, potassium, cytokines, cardiodepressants

accumulate in ischemic limb
Sudden cardiac arrhythmias
Renal failure
Acute lung injury

Prevention and Management

Hydration

Alkalinization of urine

Prevent myoglobin precipitation in renal tubules

Mannitol

UO 100cc/hr

Antioxidant, osmotic diuretic

Insulin/glucose
Fasciotomy

Question
Regarding compartment syndrome, which of the
following is correct?
A. The leg is divided into two compartments--anterior and
posterior
B. The most commonly affected compartment is the
posterior
C. The earliest manifestation of acute compartment
syndrome is pain
D. Patients with compartment pressures greater than 15
mm Hg should undergo fasciotomy

Compartment of leg
4 compartments:
Anterior
Lateral (Peroneal)
Deep Posterior
Superficial Posterior

Pathophysiology

CELL INJURY

TRANSUDATION
OF FLUID

CELL SWELLING

INTRACOMPARTMENT
PRESSURE
VENULAR
PRESSURE

CAPILLARY
TRANSUDATE

NO NUTRIENT FLOW

TISSUE PRES. =
CAP. HYDR. PRES.
ISCHEMIA

Signs and symptoms

Pallor and pulselessness

Not always reliable

Distal pulses may be present

Paralysis - Late symptom

Pain - Severe and out of proportion, increased on
passive motion
Paresthesia - Numbness, weak dorsiflexion,
numbness in 1st dorsal web space
Tender, swollen, tense muscle compartments

Indications for fasciotomy

Classically > 40-45 mm Hg at any point

or > 30 mm Hg for 3-4 hrs
Arterial perfusion pressure is paramount

Mean arterial pressure - interstitial pressure < 30

mm Hg is critical
Diastolic pressure - compartment pressure < 20
mm Hg is critical

Fasciotomy

Aneurysm

ANEURYSM

An abnormal dilatation of an artery

Caused by weakened vessel wall from:
Congenital defect(marfan syndrome)
Systemic disease(collagen disease)
Atherosclerosis
Infection(mycotic)
Trauma

Pathology

True aneurysm

three layer of arterial wall

Intima, media, adventia

Pseudoaneurysm

Single layer of fibrous tissue

PSEUDOANEURYSM

Injury to wall of vessel allows blood to escape

from vessel into adjacent tissue
Extravasated blood coagulates and becomes a
mass along side the vessel
This mass of blood (hematoma) gives the
impression that there is an aneurysm

Brachial artery
Pseudoaneurysm with
Axillary fat
blood clot
Axilla Pseudoaneurysm, stab wound severed brachial artery

SHAPES OF ANEURYSMS

Saccular

Fusiform

Cylindroid(circular ends and straight sides

)
Berry

Atherosclerotic Aneurysm
Atherosclerosis is the most common
cause of aortic aneurysm
Most frequently occur in males, >50
years of age
Most occur in abdominal aorta, below the
renal arteries
Complications include thrombosis,
embolism, and rupture

Atherosclerotic Abdominal Aortic Aneurysm

Syphilitic Aneurysm

Seen in tertiary stage of syphilis with

obliterative endarteritis of vasa vasorum and
aortitis
Roughening of intima: Tree barking
Involves the thoracic aorta
Complications include rupture, aortic
insufficiency, and narrowing of coronary ostia

Syphilitic Aneurysm Ascending Arch of Aorta

Mycotic Aneurysm

Bacterial infection weakens vessel wall

Associated with sepsis, bacterial endocarditis
May involve aorta or cerebral, renal,
mesenteric, and splenic arteries

Berry Aneurysm

Involve cerebral arteries at bifurcations

Probably arise at congenital points of
weakness in wall
Can rupture and result in subarachnoid
hemorrhage
Clinically may see headache, stiff neck
(meningeal irritation) and death

Dissecting Aneurysm

Entry of blood into substance of wall &

extension along the length of the vessel
Actually a form of hematoma, hence also
called dissecting hematoma
Male > female
Associated with hypertension

Dissecting Anerysm (cont.)

Usually have tear in media where blood enters

the wall & blood can reenter lumen through a
second tear
Blood dissects in media as outer third & inner
third of media separates
May be associated with cystic medial necrosis
with loss of elastic and smooth muscle fibers
Can be seen in Marfans syndrome

Ascending Aorta Dissecting Aneurysm

Symtoms

Expansion
Thrombosis
Emboli
rupture

Clinic features

Expansile pulsative mass (along the couse of

artetry)
Palpable thrill
Bruit
Neighbouring or distal structures pressed

Edema-veins
Altered sensation-nerves
Obstrcuction of trachea/esophgus

Abdominal Aortic Aneurysm

The commonest aneurysm

Atherosclerosis

Genetic predisposition (weakening vs. occlusion)

Marfans, Ehlers-Danlos
Infection (Syphilis, salmonella, others)

AAA Epidemiology

15,000 Deaths per year USA

13th leading cause of death in USA
1.8-6.6% of patients in Autopsy series!
Strong male predominance 3:1 - 8:1
Racial distribution Whites > Blacks

38% patients AAAs initially detected by PE

62% found incidentally on x-ray studies done for other
indications
43 % of AAAs detected on radiologic examination had
palpable AAAs that should have been detected on PE.
23% AAAs were not palpable on preoperative PE, even when
the diagnosis was known.
Obese patients had only 15% of AAAs detected by PE, and
only 33% were palpable.

AAA: Associated conditions

Emphysema: frequent association, and

emphysema is the strongest independent risk
factor for rupture of a known AAA

Destruction of elastin matrix in lung and aortic

wall may have a common cause (e.g. alpha 1
antitrypsin deficiency)

2x increase in inguinal hernias

AAA symptom

Abdominal pain or back pain

Lower limb eschemic problem

Physical Exam: Specific exam for AAA!

Deep palpation
ABOVE umbilicus
LEFT of midline
continuous over
several heartbeats

AAA NOT detected

on exam for tenderness or lower abdominal
masses!

AAA Diagnosis

Ultrasound: low cost, reliable, fast, safe

Poor imaging above renals

CT: Excellent Dx, now able to map for

surgery
MRI/MRA: Little if any advantage over CT
Angiogram: not optimal test for diagnosis,
excellent for pre-op mapping
Flat Plate/KUB: Incidental finding of AAA

AAA

Indications for Repair

Size: 5.5 cm (NEJM)

Immediate Repair Compared with
Surveillance of Small Abdominal Aortic
Aneurysms
5.0 cm still used in common practice by many
surgeons
Rupture (Leak)
Symptoms: abdominal or back pain, to groin in
some cases. Tenderness of AAA

AAA: Risk of Rupture

Emphysema , smoking,
hypertension increase liklihood of rupture
(Cronenwett 1985)
Law of LaPlace
T = Pr/2
Larger Aneurysm more likely to rupture
<4cm: 2% rupture over 5 years
>5 cm 25-41% rupture over 5 years
6 cm rupture rate ? 50% in 5 years

AAA: Treatment Options

Observation: Small aneurysms < 5 cm

Repair

Open surgical repair

Endovascular (stent-graft) repair

Surgical repair

3-5% mortality (elective

cases)
small risk of MI,
pulmonary complications,
renal failure, limb
ischemia, hemorrhage,
colon ischemia, etc
Repair effectively
permanent

Procedure of AAA repair

Endovascular repair

Quick recovery, less

trauma, possibly lower
mortality
Endoleaks about 30%
need further procedures
Requires very tight
follow-up
Expensive procedure

Ruptured AAA

Case of ruptured AAA

Male/78yr
Abdominal pain/4days
History of stroke/5yr
Died 2 hours late
post AAA Repaire
Respratory failure

Complications of Ruptured AAA

Hemorrhage and shock

Renal Failure
Anoxic Encephalopathy
Ischemic Colitis (30%)
Limb ischemia
Pulmonary failure
Countless others