VASCULAR DESEASE

dr Diah Andriana, Sp.B

RSTDS
 LEARNING OBJECTIVES

1. Mahasiswa mampu menjelaskan :

- Struktur dan perjalanan Aorta
- Zona anatomi aorta menurut Criado
- Pemeriksaan penunjang untuk
mengevaluasi aorta
2. Mahasiswa mampu menjelaskan
epidemiologi etio/faktor resiko, kriteria
diagnosis :
- Aneurisma aorta
- Diseksi aorta
- Sindrom aortoarteritis
- angiopati
3. Mahasiswa mampu menjelaskan
epidemiologi etio/faktor resiko, kriteria
diagnosis :
- Penyakit oklusi arteri akut
- Penyakit oklusi arteri kronis
 EPIDEMIOLOGI
PENYAKIT JANTUNG &
PEMBULUH DARAH
 Indonesia;
HT 52,2% HT 46,5%
Stroke 13,6% Stroke 14,3%
Systemic and Pulmonary Circulation

Dr.Yoused Aljeesh Dr. Motasem Salah

 Vascular system: consist of two
interdependent system
1- Right heart pump: blood to the lung through
the pulmonary circulation.
2- Left heart pumps: blood to all body tissue
through systemic circulation.
 Adequate blood flow → adequate perfusion →
adequate O2 and nutrient to body tissue.
 Characterize: each one depend on another(pulmonary
circulation depend on systemic ) 16
Dr.Yoused Aljeesh Dr. Motasem Salah
 Arteries: distribute oxygenated blood from the
left side of the heart to the tissues [ blood
distribution]
 Veins: carry deoxygenated blood from the
tissues to the right side of the heart. [blood
collection]
 Arterioles: small arteries
 Venules: small veins
 Capillaries: microscopic vessels that carry
blood from small arteries to small veins [ from
arterioles to venules] 17
Dr.Yoused Aljeesh Dr. Motasem Salah
 Blood flow
 Left heart to aorta → arteries→ arterioles →
capillaries → venules → veins → vena cavae →
finally to the right heart.
 This unidirectional flow is caused by pressure
difference between the arterial and venous
systems.
 Arterial pressure a proximal 100 mm Hg is
greater than venous pressure a proximal 4 mm
Hg.
 Fluid flows from an area of high pressure to an
area Dr.Yoused
of low pressure.
Aljeesh
18
Dr. Motasem Salah
Illustration of the Criado landing zones, which are used to describe aortic anatomy during thoracic endovascular repair. The arch is the short segment that
includes the origins of the three brachiocephalic arteries—the innominate artery, the left common carotid artery, and the left subclavian artery. Zone 0
includes the ascending aorta and the origin of the innominate artery. Zone 1 includes the origin of the left common carotid artery. Zone 2 includes the left
subclavian artery origin. Zone 3 is a short section of the aorta that comprises the 2 cm immediately distal to the origin of the left subclavian artery, and
Zone 4 begins where Zone 3 ends. (Used with permission from Baylor College of Medicine.)
Source: Thoracic Aneurysms and Aortic Dissection, Schwartz's Principles of Surgery, 10e
Citation: Brunicardi F, Andersen DK, Billiar TR, Dunn DL, Hunter JG, Matthews JB, Pollock RE. Schwartz's Principles of Surgery, 10e; 2014
Available at: https://www.google.co.id/ Accessed: February 11, 2018
Copyright © 2018 McGraw-Hill Education. All rights reserved
Assessment of the Heart, Great vessels
of the neck, and Peripheral Vascular
system
 Great vessels of the neck
 Jugular veins
 Carotid arteries
JUGULAR VENOUS DISTENTION
JVD
 Assessment

 Position client supine

 Then head elevated at 45 degrees
 Inspection
 Chest for visible cardiac motion
 Estimate Jugular venous pressure
 Patient supine and head elevated to 15-30
degrees.
 JVP is the distance b/w highest point at
which pulsation can be seen and the
sternal angle
 Jugular venous pressure
 An indirect measure of right atrial pressure.

 Measured in centimeters from the sternal angle

and is best visualized with the patient's head
rotated to the left.

 Described for its quality and character, effects

of respiration, and patient position-induced
changes.
Palpation
 Physical Landmarks
 Suprasternal notch
 Sternum
 Manubriosternal
angle – Angle of
Louis
 Intercostals Spaces
 palpations
 Palpate for PMI; easiest if patient sits up
and leans forward
 has a diameter of  2cm and located with
10 cm of the midsternal line
 Palpate for general cardiac motion with
fingertips and patient in supine position
 Palpate for radial, carotid, brachial,
femoral, popliteal, posterior tibial And
dorsalis pedis peripheral pulses
 palpations
 See figure 4-12
 Rate strength of the pulse normal,
diminished, or absent on a scale of 0 to
+4, where 2+ is normal. See table 4-6
 Auscultation:
Auscultatory Sites
 Auscultation

 With a stethoscope
 Use diaphragm to assess higher
pitched sounds
 Needs a lot of practice and
experience
 Listen in a quiet area or to close eyes
to reduce conflicting stimuli
 See also figure 4-10 for auscultatory
Sites
Auscultatory Sites: Cont.
 Auscultatory Sites
 The auscultatory Sites are close to but not the
same as the anatomic locations of the valves.
 Aortic area2nd ICS at the right sternal border
 Pulmonic  2nd ICS at the left sternal border
 Tricuspid  lt lower sternal border
 Mitral cardiac apex
 ARTERIAL ASSESMENT

SUSTAINED HIGH ARTERIAL PRESSURE

INCREASES THE EFFECTS OF INJURY AND
DISEASE

EFFECTS OF ARTERIAL DISEASE CAUSES

TISSUE ISCHEMIA  DEATH OF TISSUE

SEVERITY OF SYMPTOMS IS DEPENDENT

UPON METABOLIC RATE & TISSUE NEEDS

SURGERY MAY RE-ESTABLISH CIRCULATION

ARTERIAL ASSESSMENT

PURPOSE: TO DETERMINE
ADEQUATE TISSUE PERFUSION
GUIDE LINES
1. COMPARE UPPER & LOWER
2. COMPARE BILATERALLY
3. COMPARE DISTAL & PROXIMAL
4. SUPINE (VS) DEPENDENT
CHANGES
 ARTERIAL ASSESSMENT

 MAJOR AREAS OF ASSESSMENT

1. CIRCULATION – PULSE MEANS
PERFUSION
2. MOTION – MUSCLES NEED
OXYGEN
3. SENSATION – PAIN, BURNING,
PROPRIOCEPTION, NUMBNESS
 ARTERIAL ASSESSMENT

 CIRCULATION
CHECK PULSE POINTS
CAROTID
RADIAL
FEMORAL
DORSALIS PEDIS
POSTERIOR TIBIAL
CAPILLARY REFILL
 ARTERIAL ASSESSMENT

 PULSES ARE BASED ON A SCALE

0 to 4+
 0 = NO PULSE
 1+ = THREADY PULSE
 2+ = NORMAL PULSE
 3+ = BOUNDING PULSE
 4+ = ANEURYSM
 ARTERIAL ASSESSMENT
 ARTERIAL INSUFFICIENCY
1. SKIN COOL, SHINY THIN, ONION
LIKE
2. PAIN /W COLD
3. PALE /W ELEVATION
4. DISTAL PULSES  OR ABSENT
5. DECREASED OR ABSENT HAIR
6. ISCHEMIC ULCERS
7. THICK NAILS
 COMMON DIAGNOSTIC
VASCULAR TESTS
 NON-INVASIVE TECHNIQUES
 DUPLEX ULTRASOUND
HELPS Dx NARROWING OR
OCCULUSION OF INTERNAL
CAROTIDS or DVT
FALSE (+) DUE TO
NO PATIENT PREP CALCIFICATION
PAINLESS & SAFE OF VESSELS

SUPINE POSITION
 COMMON DIAGNOSTIC
VASCULAR TESTS
 NON-INVASIVE TECHNIQUES
 SEGMENTED ARTERIAL PRESSURE
MONITORING
MEASURES PRESSURE DIFFERENCE
BETWEEN EXTREMITIES AT DIFFERENT
LEVELS
USES B/P MONITOR & DOPPLER
 ANKLE/BRACHIAL INDEX
EXAMPLE:
BRACHIAL PRESSURE =120mmHg
ANKLE PRESSURE = 96mmHg
ABI = 96 / 120 = 0.8

NORMAL 0.9 - 1.2 RISK IS LOW

VASCULAR 0.6 – 0.9 MODERATE
DISEASE RISK EXISTS
SEVERE < 0.5 VERY HIGH
DISEASE RISK EXISTS
Aortic Aneurysms
 Aortic Aneurysms
Incidence

 30-60/1000
 Increasing incidence over past 3
decades

Incidence of AAA
Autopsy 1.5-3.0%
U/S Screening 3.2%
Pts with CAD 5.0%
Pts with PVD 10.0%
Pts with femoral and pop.aneurysms 50.0%
 Aortic Aneurysms
Definition

 Pseudoaneurysm

 True Aneurysm
 Definitions

 Aneurysm - Increase in diameter of

50% (1.5x) its normal diameter –
Focal region
 Ectasia - Diffuse dilatation of an
artery with increase in diameter
>50%
 Arteriomegaly - Diffuse enlargement
of an artery, but not lg. Enough to
meet criteria for an aneurysm
 Aortic Aneurysms
Associated Aneurysms

 Iliac - 41%
 Femoro-popliteal - 15%

 Pts with unilateral popliteal

aneurysms-->8% AAA
 Pts with bilateral popliteal aneurysms-
-> 30%-50% AAA
 Aortic Aneurysms
Associated Medical Conditions

 Carotid Artery Stenosis - 10% have AAA

 Smoker:Nonsmoker - 8:1
 Male:Female - 4:1
 HTN - 40% of pts with AAA have HTN
 Aortic Aneurysms
Etiology

 Atherosclerosis
 Cystic Medial Necrosis
 Dissection
 Ehlers-Danlos Syndrome
 Syphilis
 Familial Associated
 Lysyl Oxidase deficiency
 Aortic Aneurysms
Etiology

 Decrease in elastin and collagen in

arterial wall
 Elastin becomes fragmented--
>arterial elongation and dilatation
 Increase in the collagenase and
elastase activity
Aortic Aneurysms
Etiology

Multifactorial
 Aortic Aneurysms
Clinical Presentation

 Asymptomatic - 70-75%
 Symptoms:
 Early satiety, N,V
 Abd., Flank, or Back pain
 1/3 of pts experience abd. And flank
pain

 Abrupt onset of pain -->Rupture or

expansion of aneurysm
 Aortic Aneurysms
Ruptured Aneurysms

 Small tear-> pain, followed by frank

rupture
 Usually occurs postero-laterally
 Can rupture in Vena Cava creating
Aorto-Caval Fistula
 Occasionally can rupture anterior -
usually fatal
 Aortic Aneurysms
Diagnosis

 Physical Exam:
 If <5cm in diameter, then cannot be
detected by routine physical exam

 Radiographs:
 Calcified wall. Can determine size in 2/3
 Cannot rule out and AAA
 Aortic Aneurysms
Diagnosis

 Arteriography:
 Cannot determine aneurysm size because
of mural thrombus
 Indications for obtaining arteriography
 Suspicion of visceral ischemia
 Occlusive disease of iliac and femoral arteries
 Severe HTN, or impair renal function
 ? Horseshoe Kidney
 Suprarenal of TAAA component
 Femoro-Popliteal Aneurysms
 Aortic Aneurysms
Diagnosis

 Ultrasound
 Establishes diagnosis easily
 Accurately measures infrarenal diameter
 Difficult to visualize thoracic or suprarenal
aneurysms
 Difficult to establish relationship to renal
arteries
 Technician dependent
 Widely available, quick, no risk, cheap
 Aortic Aneurysms
CT Scan

 Very reliable and reproducible

 Can image entire aorta
 Can visualize relation ship to visceral
vessels
 Longer to obtain and is more costly than
U/S
 Most useful
 Requires contrast agent - renal toxicity
 Aortic Aneurysms
MRA

 Now widely available

 More expensive than CT
 No contrast agent required
 Spacial resolution less than CT
 Aortic Aneurysms
Risks
 Complications of AAA
 Thrombosis
 Distal embolization
 Rupture Size Yearly 5 Year
Rupture Rate Risk
5-6 cm 5-10% 25-50%

6-7 cm 7-15%% 30-75%

>7 cm 20-30% >90%

23.4% of aneurysms 4-5 cm will rupture

 Aortic Aneurysms
Rupture Risks

 Patients with COPD and HTN have

increased risk of rupture
 Rate of enlargement:
 0.5 cm/ year
 Survival
 50% die prior to reaching hospital, and
an additional 24% prior to repair.
 Aortic Aneurysms
Treatment Risks

 Mortality
 0.9 - 5% with current surgical
techniques
 Morbidity
 5-10% usually associated with cardiac
events

 Endovascular Techniques are

significantly reducing morbidity and
mortality associated with repair
 Aortic Aneurysms
Indications for Treatment

 Presence of an infrarenal aneurysm > 5cm

without associated co-morbid medical conditions
 Repair smaller aneurysms if rate of enlargement
is greater than expected
 Repair all symptomatic aneurysms
 If co-morbid conditions exist wait until risk of
repair and rupture are equal (approx. 6 cm)
 Aortic Aneurysms
Treatment-Surgical

 Standard Surgical Repair

 Replace diseased aorta with artificial
artery
 Requires 7 day hospital stay
 Recovery time 3-6 months
 Proven method with good long term
results
 Aortic Aneurysms
Treatment - Endovascular

 Repair through an incision in the groin

with expandable prosthesis under
fluoroscopic guidance
 Requires both surgical and radiological
assistance
 Significantly reduced m+m
 Long tern result unknown
 Hospital stay 2 days, Recovery time 1-2
weeks
AORTIC DISSECTION
 The most catastrophic disease of the aorta
 5-10 patients/ 1 milion per year
 Incidence is 0.2-0.8 % in autopsy series
 M/F: 2.5-3
 Most frequently seen 5.-6. decade of age.
 Mortality

 First 24-48 hours 20-50%

 Increases 1% every passing hour
 First 2 weeks 75%
 First 3 months 90%
 Definition

 Aortic dissection is an aortic wall disease.

 Intimal layer separates from the medial layer and this
separation continues in general to the distal of the
Aorta.
 Patogenesis

 1. Primary intimal tear theory

 Proxymal dissections 95-100%
 Distal dissections 90-95%
 2. Occurence of intramural hematoma
theory
 Vasovasorum rupture
 Rupture of penetrating atherosclerotic ulcers
 Intimal tear

 60-70% Ascending aorta

 10-20% Arcus aorta
 25% Descending aorta
Intimal tear

 Intimal layer separates

and it results in 2 lumens:
True lumen and False
lumen.
 Ethiology

 Hypertension
 Medial degenerative disease
 Genetic diseases
 Congenital heart and vascular diseases
 Atherosclerosis
 Inflammatory aortic diseases
 Travmatic injuries
 Iatrogenic injuries
 Drug abuse
 Pregnancy
 Classifications

 Clinical classification
 Topografical classification
 De Bakey
 Stanford
 Svensson
 Topografical Classification

 Stanford
Classification
 Nomenclature
DeBakey classification system
 Type I - Originates in ascending aorta,
propagates at least to the aortic arch and often
beyond it distally.
 Type II – Originates in and is confined to the
ascending aorta.
 Type III – Originates in descending aorta, rarely
extends proximally but will extend distally.

Daily (Stanford) classification system

 Divided into 2 groups; A and B depending on
whether the ascending aorta is involved.
 A = Type I and II DeBakey
 B = Type III DeBakey
Percentage 60% 10-15% 25-30%

Type DeBakey I DeBakey II DeBakey III

Stanford A Stanford B
Proximal Distal
Classification of aortic dissection
 Clinical Classification

 Acute: 0-14 days

 Subacute: 14 days- 2 months
 Chronic: After 2 months
 Rupture

 Rupture is the most frequent cause of death

and usually occurs at the site of intimal tear.
 Type A dissection Intrapericardial
 Dissection of arcus aorta Intramediastinal
 Type B dissection Left pleura
 Organ malperfusion

 Serebral ischemia
 Spinal ischemia
 Renal ischemia
 Visceral ischemia
 Lower extremity ischemia
 Cardiac ischemia
 Clinical Findings

 Pain
 Serebrovascular accidents (Syncope, stroke)
 CHF
 Acute aortic valve insufficiency
 Hypovolemia
 Cardiac tamponade
 Malperfusion signs
Pain in Acute Type A Dissection
Pain in Acute Type B Dissection
 Differential Diagnosis

 Coronary ischemia
 MI
 AI
 Aortic aneurysms
 Mediastinal tumors
 Perikarditis
 Pulmonary embolus
 Stroke
 Visceral or lower extremity ischemia
 Physical Examination

 Pale
 Anxiety
 Shock
 Hypertension 80 %
 Hypotention 20 %
 Neurologic dysorders20 %
 BP Difference
 Diagnosis

 ECG
 Low voltage
 ST-T wave changes
 Blood tests
 Diagnosis

 Chest x-ray
 CT
 MRI
 Aortography
 To whom shall we perform
angiography?

 No need for patients with Acute type A

dissection
 It can be performed to patients with Acute
type B dissection, because CAD is frequent
 It must be performed to patients with
chronic dissection
 Treatment

 Surgical treatment
 Medical treatment
 Endovascular treatment
 Hybrid treatment
 Treatment-Aim

 Stabilize the dissection

 Avoid the rupture
 Avoid organ ischemia

 Systolic BP 100-110 mmHg

 Mean BP 60-75 mmHg
 Urine output and neurologic status
should be monitorized
 Treatment-Emergency Unit

 Fluid replacement
 ECG
 Blood tests
 Chest x-ray
 O2
 Analgesia (Morphine)
 Invasive arterial monitoring
 B-blocker
 Surgical Treatment

 Acute Type A Emergent surgical treatment

 Acute Type B Endovascular or medical
treatment (surgery for rupture, intractable
sympoms or organ ischemia)
 Chronic Type A Elective surgical treatment
 Chronic Type B Surgery for aneurysmatic
aorta, organ ischemia.
In the Clinic

GIANT CELL
ARTERITIS

© Copyright Annals of Internal Medicine, 2016

Ann Int Med. 165 (5): ITC5-1.
 risk factors for GCA
 Increasing age
 Women affected more often than men
 More common among whites, people of
Nordic or Northern European
 Genetic markers: HLA-DRB1*04 (alleles
04:01, 04:04) and non-HLA gene
polymorphisms (PTPN22)
 Current smoking or history of smoking
 Possible risk factor: varicella zoster virus
 The characteristic clinical
features of GCA
 Common features related to vascular injury
(30%-80%)
 Headache
 Scalp tenderness
 Jaw claudication

 Less common features related to vascular

injury (<20%)
 Ocular symptoms, blindness
 Painful dysphagia, respiratory symptoms
continuted…

 Limb claudication
 Absent or asymmetrical pulses
 Infrequent features related to vascular injury
(<5%)
 Ischemia of the central nervous system
 Tongue claudication
 Aortic regurgitation, myocardial infarction
 Peripheral neuropathy
 Deafness
 Tissue gangrene

 Common features related to systemic

inflammation (40%-100%)
 Intense acute-phase response
 Anemia (normocytic, normochromic)
 Polymyalgia rheumatica
 physical examination include
 Careful head and neck examination
 Erythema, tenderness, nodularity,
thickening of temporal artery, decreased
pulse (vs. unaffected temporal artery)
 Eye examination
 Visual acuity and visual fields
 Optic disc and retinal vessels

 Assess pulse and blood pressure in all

4 extremities
 Listen for bruits over thoracic and
abdominal aorta
 Differential diagnosis of GCA
 Common or migraine headache
 Atherosclerosis of large vessels
 Takayasu arteritis
 Headache and temporal artery
involvement due to other forms of
vasculitis
continuted…
 Differential diagnosis of
Polymyalgia Rheumatica
 30%-50% of patients with GCA also
have PMR
 Elderly-onset rheumatoid arthritis
 Polymyositis/dermatomyositis
 Fibromyalgia
 Late onset spondyloarthritis
 Crystalline arthritis
 Cancer-associated muscle pain
 Infection-associated muscle pain
 Osteoarthritis
 Hypothyroidism
 What is the role of
laboratory testing?
 Marked elevations in ESR and CRP:
common
 Hypochromic or normochromic or
normocytic anemia and
thrombocytosis: common
 Liver function test abnormalities: may
be found

**No autoantibody tests help identify

GCA**
 What is the role of temporal
artery biopsy in diagnosis?
 Characteristic histologic lesions establish
diagnosis
 Mononuclear cell infiltrates (most in adventitia
and media)
 Lymphocytes, macrophages, dendritic cells, and
giant cells (associated with breakdown of elastic
lamina)
 Half of biopsies compatible with GCA lack these
features
 Isolated, periadventitial inflammatory
infiltrate or vasculitis of small vessels
TA biopsy findings in GCA include inflammatory infiltrates consisting of
lymphocytes, dendritic cells, macrophages, and multinucleated giant
cells
 What is the value of imaging
studies?
 Traditional ultrasound, color duplex
ultrasound of temporal artery
 Approximately 40-75% sensitivity and
79-83% specificity for diagnosis
 MRI
 May help identify biopsy-negative GCA
patients
 Catheter-directed invasive
angiography with contrast
 Good large and medium vessel
resolution, but does not specifically
evaluate vessel wall characteristics
 FDG-PET
 For uncertainty about diagnosis, follow
disease activity
 CLINICAL BOTTOM LINE: Diagnosis...
 Consider GCA in patients older than 50 years with:
 New onset, localized unilateral headache
 Ischemic symptoms in cervico-cranial and upper
extremity vascular territories
 Muscle stiffness of the neck, shoulder, pelvic girdle
 Physical exam: tenderness, swelling, and erythema over
temporal artery; flow abnormalities of large vessels
 Lab: ESR or CRP elevated in most patients
 Temporal artery biopsy: gold standard for diagnosis
 approach to treatment
 Don’t delay treating suspected GCA
while waiting for a biopsy
 High dose oral prednisone
 With visual loss: IV pulse corticosteroids
 Low-dose aspirin may reduce
blindness risk
 Methotrexate, other
immunosuppressants for repeated
flares during tapering
 If little improvement within 5 days:
revisit diagnosis and consider
comorbid conditions causing
symptoms
What is the role of steroids in
management?
 High dose oral corticosteroids
 Prednisone or prednisolone 1 mg/kg, up
to 60 mg/d
 Treat 2 to 4 weeks, followed by slow
taper after symptoms and signs of active
disease resolve
 High dose IV corticosteroids
 Methylprednisolone 1000 mg/d for 3 d
 For acute vision loss or critical organ
ischemia
 role of aspirin

 Controversial whether patients with

GCA have increased risks for
cardiovascular disease
 Studies suggest that low-dose aspirin
(≤100 mg/d) diminishes risks of
cerebral or ocular and cardiovascular
events
 Prescribe low dose aspirin to patients
who have no contraindications to its
use
 other immunosuppressant
medications
 Relapses increase risk of steroid-related
complications
 Studies have examined immunosuppressives as
disease-modifying or steroid-sparing agents
 MTX: studies show questionable or modest benefit
and MTX associated with potential life-threatening
adverse events
 Tocilizumab (humanized monoclonal antibody to IL6
receptor): encouraging results for treating relapsing
GCA
 TNF-a inhibitors: not found to be beneficial for
treatment of GCA or reducing steroid requirements
 How should clinicians
monitor patients being
treated for GCA?
 Follow initially at 2- to 4-week
intervals
 Watch for unexplained increases in acute
phase reactants, symptom flares with
corticosteroid tapering
 Ask about cranial symptoms, new onset
large vessel ischemic symptoms
 Assess blood pressures in both arms and
listen for bruits
 Order aorta and branch imaging if
 What is the prognosis?
 Patients with GCA have normal life
expectancy, provided they do not develop
complications
 MI, stroke, PVD: risk is increased
 Aortic dilatation or aneurysms occur in 18%-
33%
 Aortic reconstruction or intravascular stent
placement often required to prevent rupture
or dissection
 Visual symptoms common
 Absence of aggressive treatment within 24 h
= very low likelihood of restoring functional
 How should clinicians
educate patients about GCA?
 Patients should know to notify
physician immediately when they
experience symptoms of GCA
 Especially symptoms related to organ or
regional ischemia

 Patients should know about risks and

preventive measures for
corticosteroid side effects
CLINICAL BOTTOM LINE: Treatment...
 Start corticosteroids when clinical suspicion high enough
to warrant a temporal artery biopsy
 Symptoms and acute phase reactants typically respond
promptly, but disease flares common
 Provide low-dose aspirin to decrease visual and CV
ischemic events if no contraindications
 Follow patients closely for clinical signs of relapse or LV
involvement and for corticosteroid-related complications
 Life-long surveillance advised for large vessel
involvement
 Takayasu´s arteritis

 Inflammatory and stenotic disease of

medium- and large-sized arteries
 Aortic arch and its branches
 =Aortic arch syndrome
 Incidence: 1-2 cases/million/year
 Angiography
 Frequency of angiographic
abnormalities
 Subclavian: 93%
 Common carotid: 58%
 Abdominal aorta: 47%
 Aortic arch: 35%
 Vertebral: 35%
 Pulmonary: 10-40%
 Coronary < 10%
 Clinical manifestetions

 Panarteritis with inflammatory

mononuclear cell infiltrates
 Narrowing of the lumen
 Pulses absent
 ESR↑, anemia, gammaglobulin↑
 Diagnosis

 Young woman
 Decrease or absence ofperipheral
pulses
 Discrepancies in blood pressure
 Arterial bruits
 Arteriography→irregular vessel walls,
stenosis, poststenotic dilatation,
aneurysm formation, occlusion,
evidence of increased collateral
circulation
 Treatment

 Steroid: prednisone 40-60 mg/day

 Methotrexate 25 mg/week
 Surgical correction of stenosed
arteries
 Idiopathic cutaneous
vasculitis
 =Hypersensitivity vasculitis
 =Cutaneous leukocytoclastic vasculitis
 Dermis, small vessels
 Only skin involvement→palpable purpura,
chronic urticaria
 Diagnosis: biopsy→vasculitis
 Etiology: drug, infection, underlying
disease
 Treatment:microbe→antimicrobal therapy,
steroids
 Essential mixed
cryoglobulinemia
 Cryoglobulins: cold-precipitable
monoclonal or polyclonal
immunoglobulins
 Cutaneous vasculitis, palpable
purpura, arthralgias,
glomerulonephritis
 Hepatitis C infection
 Treatment:IFN-α, Ribavirin
 Behcet´s syndrome

 Recurrent, painful aphthous oral

ulcerations in the oral cacity
 Recurrent genital ulcers
 Iritis
 Cutaneous lesions
 Treatment: topical steroids,
Prednisone
Isolated vasculitis of the CNS

 Severe headache, focal neurologic

defects
 Abnormal MRI of the brain
 Abnormal liquor
 Abnormal cerebral
angiogram→vasculitis
 Brain biopsy
 Treatment:Prednisone+Cyclophospha
mide
 Kawasaki disease

 =Mucocutaneous lymph node

syndrome
 Nonsuppurative cervical adenitis
 Children > 2 years
 Coronary artery aneurysms 25%
 Treatment:IVIG+ Aspirin
 Raynaud’s Phenomenon
 Characterized by vasospasm of the
arterioles and arteries of the upper and
lower extremities, usually unilaterally

 Raynaud's disease occurs bilaterally

 Difference in Disorders

Primary or idiopathic Raynaud’s

(Raynaud’s disease) occurs in
absence of underlying disease.
 Secondary Raynaud’s (Raynaud’s
syndrome) –
 Associated with an underlying disease
 Usually a connective tissue disorder-
systemic lupus erythematosus, rheumatoid
arthritis, or scleroderma
 Clinical Manifestations
 Classic clinical picture -- Raynaud’s
 Pallor brought on by sudden vasoconstriction.
 Skin then becomes bluish (cyanotic) -of
pooling of deoxygenated blood during
vasospasm
 As a result of exaggerated reflow
(hyperemia) due to vasodilation, a red color
(rubor) is produced when oxygenated blood
returns to the digits after the vasospasm
stops
 Color Changes –Raynaud’s

 Characteristic sequence of color

change of Raynaud’s phenomenon
 White, blue, and red
 Numbness, tingling, and burning pain
occur as the color changes
 Manifestations tend to be bilateral
and symmetric and may involve toes
and fingers
 Management
 Avoiding stimuli (e.g., cold, tobacco) that
provoke vasoconstriction
 Is a primary factor in controlling Raynaud’s
phenomenon
 Calcium channel blockers (nifedipine
[Procardia], amlodipine [Norvasc])
 May be effective in relieving symptoms
 Wear gloves when outside; avoid touching
cold items as steering wheel
If I got this ---you can too!!
 Vascular Surgery
Occlusive
Peripheral Vascular Disease
 Pathogenesis Of Blocked
Arteries
• Atherosclerosis
– Genes, hyperlipidemias
– Lifestyle
• Smoking
• High fat diet
• Lack of exercise
– Co-morbidities
• Diabetes, hypertension, hypothyroidism,
homocysteine
 Manifestations Of Blocked Arteries

• Depends on circulation affected

– Heart
• Stable angina, unstable angina, myocardial infarction
– Brain
• Transient ischemic attact, stroke
– Kidney
• Hypertension, renal failure
– Legs
• Claudication, rest pain, necrosis
 Manifestations Of Blocked Arteries

• Depends on speed of development of

blockage
– Slow blockage
• Permits development of collateral blood supply
so that occlusion may be asymptomatic
– Rapid blockage
• No time for development of collaterals
– Symptoms/ signs depend on adequacy of preexisting
collaterals
Duplex of carotid stenosis
Angiography
(DSA)
MRA
 Occlusive Peripheral Vascular
Disease
• Classification based upon clinical
presentation
– Acute ischemia
– Chronic ischemia
• Anatomic classifcation based upon
site(s) of disease
OPVD Anatomic Classification
• Aorto-iliac
– Le-Riche
• Femero-popliteal
• Tibio-peroneal
Acute Ischemia
 Effects Of Acute Ischemia
• Reduced blood flow
– Pulseless, pallor, perishing cold
• Nerve ischemia
– Pain, paralysis, Paresthesia
• Muscle ischemia
– Rhabdomyolysis
• Compartment syndrome
• Ischemia reperfusion syndrome
 Compartment Syndrome
• Pathophysiology
• Diagnosis
• Management
Compartment Syndrome
Pathophysiology
• Strong fascia encases the limb to aid muscle
function and return of venous blood
• Injury results in swelling
• Swelling raises pressure
• Pressure occludes lymphatic return, then
venous return, then arterial inflow
– Result is dead or severly damaged tissues due to
pressure and ischemia
 Compartment Syndrome
Diagnosis
• Strong index of suspicion
– Nature of injury and duration of ischemia
• Clinical manifestations
– Nerve and muscle dysfunction
– Decreased perfusion
– Tense compartment
• May measure compartment pressure as
adjunct to treatment > 40 mm hg
 Compartment Syndrome
Management
• Fasciotomy
 Acute Ischemia
• Causes
– Thrombosis
– Embolism
• The P’s
• Thrombosis or embolism?
• Clinical assessment of severity
• Clinical algorithm
Causes of Acute Ischemia
• Trauma
• Thrombosis
• Embolism

• Small print
– Aneurysm
– Thrombophilia
– Paradoxial embolism
– Anatomic variation
– Csytic adventitial disease
 Thrombosis
• Occlusive atherosclerosis
• Aneurysm
• Malignancy
• Thrombophilia
 Embolism
• Macro-embolism
– arterial side
– venous side (patent foramen ovale)
• Micro-embolism
– ulcerated atherosclerotic plaques
– aneurysm
 The P ’s
• No flow in artery
– Pallor
– Pulse absent
– Perishing cold
• Nerve becomes ischemic
– Pain
– Paresthesia / anesthesia
– Paralysis
 Thrombosis or Embolism?
Thrombosis Embolism
Sex Male Female
Embolic source No Yes
Onset Progressive Acute
Ischemia Milder Severe
PHx Claudication None
Other leg Abnormal Normal
 Clinical Assessment of
Severity
• Viable no immediate threat
• Threatened
– Marginally ok if treated
promptly
– Immediately ok if treated
immediately
• Irreversible dead leg
 Irreversible Ischemia
• Sensory loss Profound,
anaesthetic
• Muscle weakness Profound,
paralysis
• Arterial doppler Inaudible
• Venous doppler Inaudible

Amputation
 Viable no immediate threat
• Sensory loss None
• Muscle weakness None
• Arterial doppler Audible
• Venous doppler Audible

Restore perfusion
 Clinical Assessment of
Severity
• Viable No immediate threat
• Threatened
–marginally Ok if treated
promptly
–immediately Ok if treated
immediately
• Irreversible Dead leg
Threatened Marginally
• Sensory loss Minimal (toes)
to none
• Muscle weakness None
• Arterial doppler Inaudible
• Venous doppler Audible

Restore perfusion
Threatened Immediately
• Sensory loss More than toes,
Pain
• Muscle weakness Mild to
moderate
• Arterial doppler Inaudible
• Venous doppler Audible

Restore perfusion
 Practical Questions
• Is this ischemia? (DDx stroke, TIA, cord)
• Is the limb viable, threatened or lost?
• If threatened how long can reperfusion be
delayed?
• Is there a need for duplex or angiography?
• Should the patient be immediately
heparinised?
 acute non traumatic ischemia

Irreversible Threatened Viable

Clear embolus ?Thrombosis

Duplex
Adequate Inadequate

Angiogram

Treat

Amputation Embolectomy Thrombolyse Reconstruct

+/- PTA
 Prognosis
• Embolism
– Overall 60% dead within three years
– One episode 15-20% mortality (in hospital)
– Two episodes 40% mortality (in hospital)
• Thrombosis
– Overall 40% dead within three years
Chronic Ischemia
 LaFontaine Classification

Stage 1 claudication
Stage 2 rest pain
Stage 3 necrosis/ulceration
 Prognosis in Claudicants
• About 15% will progress to requiring
revasculartion or amputation
• Much higher risk of death from IHD and
stroke
• Rule out diabetes, hypertension and
hypercholesterolemia
• Exercise, Smoking cessation, Aspirin
and a Statin + control of risks
 Re-Vascularisation ?
• Risk factor control, aspirin, statin
• Pain control
• Dressing
• Sympathectomy (chemical, surgical)
• Iloprost
• Angioplasty +/- Stent (? Drug elute)
• Surgical
 Surgical Re-Vascularisation
• Embolectomy and Thrombolysis
• Patchplasty (synthetic/ autogenous)
• Endarterectomy (open/closed/eversion)
• Bypass with synthetic material
• Bypass with autogenous material
Thrombophlebitis and Occlusive
Arterial Disease
 Thrombophlebitis
• Formation of a venous clot depends on the
presence of of at least of one of Virchow’s
triad factors
-venous stasis
-injury to vessel wall
-hypercoagulable state
Clinical risk factors for deep vein
thrombosis
• Trauma, travel • Birth control, blood
• Hypercoagulable, group A
hormone replacement • Obesity, obstetrics
• Recreational drugs(IV • Surgery, smoking
drugs) • Immobilization
• Old (age >60y) • Sickness
• Malignancy
 Pathophysiology
• Most common cause of hereditary hemophilia is
factor V Leiden
• See Table 59.2 for other hypercoagulable states
• Thrombi usually form at the venous cusps of deep
veins where altered or static blood flow causes
clot formation
• Alternatively, clots form from intimal defects
• Clots are composed from fibrin, red cells and
platelets and cause partial/complete obstruction of
vein
 Pathophysiology
• Postphlebitic syndrome (PPS) may develop
after the resolution of a DVT
• PPS is due valvular incompetence,
persistent outflow obstruction and abnormal
microcirculation.
 Superficial Thrombophlebitis
• Thrombosis can occur in any superficial vein
primarily the saphenous vein and its tributaries
• Local pain, redness, and tenderness are
characteristic findings.
• Mild cases can be treated with warm compresses,
analgesia and elastic supports
• Severe cases can be debilitating and should be
managed by bed rest, elevation of extremity,
support stockings, and analgesia.
• Antibiotics and anticoagulants are useful in septic
thrombophlebitis
 Superficial Thrombophlebitis
• Incidence of DVT from extension of a
superficial clot is 3%.
• Most clots in great saphenous vein will
extend into a deep vein system in a week or
so thus a follow-up US is guaranteed
• Definite treatment is ligation and excision
of affected vein.
 Deep Vein Thrombosis
• Clinical exam is unreliable for detection or
exclusion of a DVT
• Pain, redness, swelling, and warmth are present in
less than half the patients with confirmed DVT.
• Pain in calf with dorsiflexion of ankle with the leg
straight (Homan’s sign) is unreliable
• See table 59.3 for predictors of deep vein
thrombosis
 Deep Vein Thrombosis
• Symptomatic DVT will be in popliteal or more
proximal veins more than 80%
• Nonextending calf DVT rarely cause PE
• Uncommon presentations of DVT include
phlegmasia cerulea dollens and phlegmasia alba
dollens
• In phlegmasia cerulea dollens, patients present
with extensive swollen and cyanotic leg due to
massive ileofemoral thrombosis which can lead to
venous gangrene.
 Deep Vein Thrombosis
• In phlegmasia alba dolens, the leg is white due to
arterial spasm secondary to massive iliofemoral
thrombosis, often mistaken for arterial occlusion.
• PPS can be difficult to differentiate from recurrent
DVT due to pain, swelling and ulceration of the
skin.
• Up to to one third of the patients with DVT can
develop PPS.
 Deep Vein Thrombosis-
Diagnosis
• All patients with any signs or symptoms
suggestive DVT should undergo an
objective diagnostic evaluation
• Venography was the historical “gold
standard” for detection of DVT with 100%
sensitivity and specificity but it is invasive
and can cause contrast-related reactions,
phlebitis and DVT (3%).
 Deep Vein Thrombosis-
Diagnosis
• Choice of test to identify DVT is ultrasound
• Ultrasound has 97% and 94% sensitivity and
specificity respectively for detecting proximal
DVT
• Ultrasound is less sensitive for pelvic DVT and
has sensitivity of 73% for a calf DVT.
• Impedance plethysmography is portable and
inexpensive but less sensitive than US
• IP measures changes in electrical resistance in
response to changes in calf volume due to
obstruction
Deep vein thrombosis-Diagnosis
• Radioisotopes have been used to diagnose DVT
but are not particularly useful in ED
• MRI is being used with increased frequency and
can detect a filling defect in entire extremity
(including calf and pelvic veins)
• D-Dimer fragments which are degradation
products of fibrin can be used to as an indicator
for the presence or absence of DVT or PE.
• The ELISA based D-Dimer has sensitivity 97 %
and specificity 35%
 Deep Vein Thrombosis-
Diagnosis
• When D-Dimer is less than 500ng/ml, the
likelihood of DVT is less than 1%.
• The latex agglutination assay D-Dimer is less
sensitive than the ELISA essay.
• Sepsis, surgery, trauma, hemorrhage, pregnancy,
cardiovascular diseases, collagen vascular disease,
liver disease, cancer are associated with elevated
d-dimer value.
 Clinical Approach to
Establishing the Diagnosis
 Treatment
• Bed rest, leg elevation and elastic stockings are of
unproven benefit in the management of DVT.
• Aggressive anticoagulation will prevent extension
of the clot.
• Early ambulation after adequate anticoagulation is
a safe approach
• Primary objective of treating DVT is the
prevention of pulmonary embolus
 Treatment
• Patients with negative ultrasound can safely
have a repeat ultrasound in a week without
anticoagulation
• Risk of PE in these patients is near 0% and
risk of forming a DVT is 1%.
• Anticoagulation is recommended for
patients with calf DVT who had PE/DVT,
immobile, have hypercoagulable state
 Treatment
• Patients with proximal DVT require
anticoagulation
• Preferred treatment is LMWH over UFH because
of the ease of administration, more predictable
anticoagulant effect, lack of need to monitor the
anticoagulation effect, lower incidence of major
bleeding and HIT
• LMWH has a preferentially inhibitory effect on
factor Xa.
 Treatment
• Because of LMWH is cleared by the kidneys, it
should be avoided in outpatients with Cr >2.03
• One need not to wait for the creatinine result
before initiating LMWH therapy.
• The ability to discharge patients from the ED after
initial dose of LMWH is cost-effective, safe,
practical and acceptable practice as long as there is
a secured 24 hr follow up with PCP.
 Treatment
• Indications for admission include inability
to ambulate, poor social support, unreliable
follow-up, difficulty with education with
drug administration, need for lysis or
invasive therapy, and an alternative serious
diagnosis under investigation or that
requires treatment(arterial ischemia,
cellulitis, pelvic mass)
 Treatment
• If LMWH is contraindicated, use UFH as 80
units/kg bolus and then 18 units/kg/hr
• Serious bleeding from LMWH cannot be
completely reversed with protamine which has
been associated with hypotension and
anaphylactoid reactions.
• If a patient has contraindication to heparin like in
pt with HIT, you can use a thrombin inhibitor like
lepirudin
 Treatment
• In pregnant pt who cannot have heparin, danaproid
should be used.
• It is acceptable to start coumadin and LMWH
simultaneously.
• Warfarin is contraindicated in pregnancy, active
bleeding, recent major surgery (thoracoabdominal,
nervous system, spine, eye)
• LMWH does not interfere with the work up of a
possible hypercoagulable state compared with
UFH.
 Treatment
• Initial hematological testing at follow-up
includes factor V leiden, prothrombin
molecular tests, screening for
antiphospholipid anticoagulants and a
fasting homocysteine level.
• Upon completion of the anticoagulation ,
further testing includes antithrombin III,
protein C, protein S, and factor VIII level
 Treatment
• Thrombolysis for DVT is indicated for
extensive iliofemoral thrombosis and upper
extremity DVT in patients with low risk for
bleeding.
• IVC filter is indicated for when
anticoagulation therapy is contraindicated,
there is embolization of DVT after 1-2
weeks of anticoagulation
 Treatment
• Thrombectomy is only indicated with ischemic leg
secondary to a massive venous clot like in
phlegmasia cerulea dolens.
• In ED , pt adequately anticoagulated who present
with new thrombus or propagation should receive
LMWH
• If the fail LMWH or there is a free-floating
thrombus an IVC should emergently inserted.
 Pelvic Vein Thrombosis
• Usually it’s an extension of a clot from the
femoral vein.
• An isolated pelvic vein thrombosis is rare and can
be a complication in the postpartum period, after
pelvic surgery or trauma.
• Septic pelvic vein thrombophlebitis is a life-
threatening condition after post-partum
endometritis and is usually diagnosed with CT or
MRI.
 Axillary and Subclavian Vein
thrombosis
• 2-4% of DVTs occur in axillary or subclavian vein
• Risks include recent central venous catheters or
pacemakers, IV drug use, malignancy,
hypercoagulable states and excessive or unusual
exercise, chronic compression(cervical rib, scalene
or web)
• PE occurs in 5-10% of cases involving axillary or
subclavian DVT
• Treatment includes anticoagulation alone or
preceded by thrombolysis.
Subclavian
Artery
Disease:

Simulation
Training
Curriculum
Subclavian Artery Stenosis
 Etiology
Incidence
Clinical manifestations
Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
Subclavian Artery Disease: Etiology

• Atherosclerosis
• Takayasu Arteritis
• Fibromuscular dysplasia
• Giant Cell Arteritis
• Radiation-induced Vascular Injury
• Thoracic Outlet Syndrome
• Neurofibromatosis
 Subclavian Artery Atherosclerosis

 Most common cause of

subclavian artery stenosis
 Predilection for the proximal part
of the artery
• The occlusion usually extends from the aortic
arch to the origin of the vertebral artery due
to poor collateral circulation
 Takayasu Arteritis
 Nonspecific inflammatory disease
 Primarily affects large arteries such as the aorta
and its branches
 Includes both occlusive and aneurysmal disease
 Occlusive disease is more prevalent in Japan, the
United States, and Europe
 Aneurysmal disease is more common in India,
Thailand, Mexico, and Africa
 The prevalence is higher in women
 Median age of onset varies from 25 years in Asia
and the United States to 41 years in Europe
 Takayasu
arteritis
presenting with
subclavian
aneurysm

Colvine et al Arthritis & Rheumatism (Add Year )54, 1: 382

Subclavian Artery Stenosis
Etiology
 Incidence
Clinical manifestations
Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
Subclavian Artery Stenosis: Incidence

 Incidence of 0.5 - 2% 1

 Left : Right = 3-4 : 1 ratio

 The stenosis is usually focal and in the
proximal segment of the vessel
 Predictors:
 HTN
 Tobacco use
 Dyslipidemia
 Diabetes

1. Perrault et al, Ann Thorac Surgery 1993; 56: 927-30

Subclavian Artery Stenosis
Etiology
Incidence
 Clinical manifestations
Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
 Subclavian Steal Syndrome
The vertebral artery steals blood from the posterior
cerebral circulation

Stenosis of the subclavian artery or the

brachiocephalic trunk proximal to the vertebral
artery origin results in low-velocity and/or
retrograde flow in the ipsilateral vertebral
artery distal to the subclavian artery narrowing

Wu C et al. Radiology 2005;235:927-933

 Contrast-enhanced MR
angiogram reveals
lesion (arrow)
responsible for
subclavian steal
syndrome is seen in left
subclavian artery

Bitar et al Am J Roentg 2004; 183:1840-1

 Color MR Angiogram
Retrograde flow in
the left vertebral
artery in a patient
with a subclavian
steal is shown in blue
(arrows), indicating
opposite flow
direction. Note that
the vertebral artery is
red (arrowheads),
indicating normal
flow direction.

Aoki et al Am J Neurorad 1998; 19:691-693

 Subclavian Steal Syndrome
Clinical Manifestations

 Arm claudication or hand numbness and a

decrease of at least 20 mm Hg in blood
pressure in the upper limb on the affected
side
 Cerebral symptoms : dizziness, vertigo, and
visual disturbances. In rare cases, cerebral
ischemia may be present
Coronary - Subclavian Steal Syndrome

Reversal of internal
mammary artery flow
(arrows) with left upper
extremity activity

Coronary Ischemia

Takach et al Annal of Thoracic Surgery 2001, 71(1): 187-9

 Angiographic Evidence of
Coronary-Subclavian Steal Syndrome
A, Angiography of the left coronary
artery and LIMA in a right anterior
oblique cranial projection. The figure is a
composite of 2 images obtained during
the same injection. The arrow points to
the subclavian artery. B, Angiography of
the left subclavian artery in an anterior-
posterior projection. C,Angiography of
the left subclavian artery in an anterior-
posterior projection after stent
placement. Vert indicates vertebral
artery.

Kroll et al Circulation. 2002;105:e184

Subclavian Artery Stenosis
Etiology
Incidence
Clinical manifestations
 Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
 Subclavian Artery Disease: Diagnosis

 Obstruction of the SA is
suspected when there is a blood
pressure difference > 20mm Hg
between the two arms1
 If there is a clinical suggestion
of vasculitis: an erythrocyte
sedimentation rate (ESR) or C-
Reactive protein (CRP) should
be measured2

1. Henry et al “Angioplasty and Stenting of the Carotid and

Supra-Aortic Trunks” pg. 655-671.
2. Grossmans “Catheterization” 7th Ed. pg. 573-575
 Noninvasive Diagnostic Modalities:
Duplex Ultrasonography
 Duplex ultrasonography of the subclavian artery
and the vertebral artery can detect stenosis
greater than 50% with a moderately high
sensitivity (80% range) and an excellent
negative predictive value (> 95%)
 Duplex ultrasonography is also highly useful in
clinical follow-up of patients after
revascularization procedures

Kalaria et al J Am Soc of Echocard 2005, 18: 1107-1111

Normal subclavian artery
Duplex waveform
Abnormal subclavian artery
duplex waveform showing
elevated peak systolic
velocity, spectral
broadening, and loss of
triphasic waveform.

Kalaria et al J Am Soc of Echocard 2005, 18: 1107-1111

 Noninvasive Diagnostic Modalities
Diagnostic Imaging

The diagnostic imaging work-up of patients

should include:
- Magnetic resonance imaging (MRI) with or
without arteriography (MRA)
- Computed tomographic (CT) scan of the
brain with close evaluation of the posterior
fossa and brainstream.

Henry et al “Angioplasty and Stenting of the Carotid and

Supra-Aortic trunks” pg. 655-671.
Subclavian Artery Disease: Arteriography

 Ascending
aortography

 Selective
arteriography of
supra-aortic vessels

Kang WC et al. Circulation 2006;113:e735-737e

Severe Stenosis of Left Subclavian Artery

Baseline Angiogram Post Stenting Arteriogram

Queral R, Criado F J Vasc Surg 1996;23:368-75

Angiograms revealing total occlusions of
both subclavian arteries
Subclavian Artery Stenosis
Etiology
Incidence
Clinical manifestations
Diagnosis
 Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
 Indications for Revascularization
 Symptomatic ischemia of the posterior fossa
 Symptomatic subclavian steal syndrome
 Disabling upper extremity cludication
 Preservation of flow to LIMA/RIMA
 Preop coronary bypass surgery, where LIMA/RIMA will be
used
 Postop CABG LIMA/RIMA with ischemia (with or without
coronary-subclavian steal syndrome)
 Preservation of inflow to axillary graft or dialysis
conduit
 “Blue-digit” syndrome (embolization to fingers)
 Inability to measure blood pressure
 Progressive stenosis or thromboembolus threatening
cerebral blood supply

Grossmans “Catheterization” 7th Ed. pg. 573-575.

 Indications for Revascularization in
Asymptomatic Patients

 Angioplasty of the subclavian stenosis before

other cardiovascular intervention and
preservation of the vasculature for other
angioplasty procedures
 Preservation of the cerebral perfusion. If other
arterial lesions exist at the level of the supra-
aortic vessels, to improve cerebral flow.

Farina et al Am J Surg 1989; 58:511-14

Burke et al Radiology 1987; 164:699-704
Subclavian Artery Stenosis
Etiology
Incidence
Clinical manifestations
Diagnosis
Indications
 Treatment Options
- PTA
- Surgical
Technical Issues
Complications
Prognosis
 Subclavian Artery Stenosis: PTA

Percutaneous
revascularization with
balloon angioplasty
followed by stent
placement is the
treatment of choice.

Debries et al J Vasc Surg 2005; 41 (1) 19-23

 Subclavian Artery Stenosis: Stenting

Prevertebral Portion Postvertebral Portion

of Subclavian Artery of Subclavian Artery

Balloon expandable or self Self expanding stents to

expanding stents with avoid possibility of
good radial force postvertebral compression
by extravascular
structures at the thoracic
outlet
Subclavian Artery Stenosis:
Stenting of Ostial Subclavian
 Subclavian Artery Stenosis: Stenting

Left subclavian artery stenosis. a: Subclavian artery pre-stent. b: Stent

placement. c: Repeat angiogram post-stent placement.

Amor et al Cathet Cardiovasc Interv 2004; 63: 364-370

 Indications for Covered Stents

 Aneurysm or “pseudoaneurysm”
 Traumatic artery injury
 Spontaneous arterial rupture or dissection

Heuser R, Biamino G. Peripheral Vasc Stenting.2nd Ed. Pg:154

Subclavian Artery Stenosis: Surgery

• Carotid-subclavian
bypass
• Aortosubclavian
bypass
• Axilloaxillary bypass
Revascularization of the subclavian artery
using extrathoracic (carotid-subclavian)
bypass.

Takach et al Annal of Thoracic Surgery 2001; 71: 187-9

 Subclavian Artery Stenosis
Anticoagulation

 Premedication with Aspirin, with

optional addition of clopidogrel
 Anticoagulation for a period of
several weeks prior to
revascularization in cases of
Subclavian occlusion

Grossmans “Catheterization” 7th Ed. pg. 573-575.

 Femoral Approach

It is used at first intention in the

majority of the cases
 Subclavian Artery Stenosis
Femoral Approach

8 Fr quiding catheter
0.035’’ steerable or hydrophilic guide wire
0.018’’ – 0.020’’ steerable guide wire Brachial approach

Failure Surgery
Success

Adjacent to vertebral Artery

Isolated stenosis
2 steerable guide wires
(Vertebral 0.014’’, subclavian 0.018’’)
Primary stenting Predilatation
Kissing balloon angioplasty

Good result Insufficient result Good result Insufficient result

Stent Stent
Henry et al “Angioplasty and Stenting of the Carotid and
Supra-Aortic trunks” pg. 655-671.
 Brachial Approach
 Recanalization of an occluded
Subclavian artery (SA)
 When the occlusion begins at
the ostium of the SA
 Severe tortuosity of the aorta
 Iliac and subclavian artery
 Bilateral occlusion of the iliac
arteries Queral R, Criado F J Vasc Surg
1996;23:368-75.)

Henry et al “Angioplasty and Stenting of the Carotid and

Supra-Aortic trunks” pg. 655-671.
 Subclavian Artery Stenosis

First Approach Brachial Approach After failure of

FemoralApproach

6 or 7 Fr long introduceur quiding catheter

0.035’’ steerable or hydrophilic guide wire
0.018’’ – 0.020’’ steerable guide wire

Success Failure

Primary stenting Predilatation Femoral Approach

Good result Insufficient result Success Failure

Stent Surgery
Henry et al “Angioplasty and Stenting of the Carotid and
Supra-Aortic trunks” pg. 655-671.
Subclavian Artery Stenosis
Etiology
Incidence
Clinical manifestations
Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
 Complications
Prognosis
 Subclavian Artery Stenting:
Complications
 Hematomas
 Subclavian thrombosis
 Axillary artery thrombosis
 Stent Migration
 Arterial rupture
 Dissection
 Distal embolization
 Restenosis
 Neurologic complications
 Transient ischemic attack , stroke, hemiplegia,
diplopia.
 Arterial Rupture

A B
Stent Migration
Thrombus
Dissection
Subclavian Artery Stenosis
Etiology
Incidence
Clinical manifestations
Diagnosis
Indications
Treatment Options
- PTA
- Surgical
Technical Issues
Complications
 Prognosis
 Favorable Predictors

 Presence of subclavian steal syndrome : it

prevents the risk of vertebral embolization 1

 Isolatated stenosis
 Recurrent angina following an internal
mammary coronary bypass 2,3

1. Hennerici et al Neurology 1988; 38: 669-673

2. Diethrich et al J Endovasc Surg 1995; 2: 77-80
3. Marques et al J cardiol 1996; 78: 687-690
Subclavian Artery Stenosis: Outcome

Percutaneous transluminal angioplasty appears

safe and efficient therapy for subclavian artery
stenoses is not only an effective initial
treatment, but also successful over the short-
and long-term results.
Buerger’s
Disease
 Buerger’s Disease

Buerger's disease (thromboangiitis obliterans)

is a rare disease characterized by a
combination of acute inflammation and
thrombosis of the arteries and veins in the
hands and feet. The obstruction of blood
vessels in the hands and feet reduces the
availability of blood to the tissues, causes pain
and eventually damages or destroys the
tissue. It often leads skin ulcerations and
gangrene of fingers and toes. Rarely, in
advanced stages of the disease, it may affect
vessels in other parts of the body.
Buerger’s Disease: Appearance

Ulcers and Gangrene caused by Buerger’s

Disease
Buerger’s Disease: Who It Affects

Buerger's disease affects approximately six out

of every 10,000 people. It almost always
affects men, ages 20 to 40, who smoke or
chew tobacco. Recently, however, more
women and men over the age of 50 have been
diagnosed with Buerger's disease. This
disorder is still very uncommon in children, but
it may occur in those with autoimmune
diseases. Buerger's disease is most common in
the Orient, Southeast Asia, India and the
Middle East, but is rare among African-
Americans.
 Buerger’s Disease:
Symptoms
 Enlarged, red, tender cord-like veins
 Pain or tenderness
 Numbness and tingling in the limbs
 Skin ulcers or gangrene of the digits

 Discoloration
 Two or more limbs affected
 Pain may increase with activity such as walking and decrease
with rest
 Pulse may be decreased or absent in the affected extremity
 Symptoms may worsen with exposure to cold or with emotional
stress
 Buerger’s Disease: The
Cause

Buerger's disease is greatly

associated with heavy to moderate
tobacco use, both cigarette and
smokeless. The disease is an
autoimmune reaction triggered by
tobacco.
 Buerger’s Disease:
Diagnosing
 Buerger's disease is often masked by a wide variety of
other diseases that cause diminished blood flow to the
hands and feet, therefore, other disorders must be ruled
out with aggressive evaluation.

Blockage of blood vessels in the hands and feet caused

by Buerger's disease may be detected by one of the
following methods:

 An angiogram or an arteriogram of the upper and lower

extremities
 A Doppler ultrasound

Skin biopsies are rarely used because of concern that the

biopsy site near an area with poor blood circulation will
not heal.
Normal and Abnormal Angiograms
 Buerger’s Disease:
Angiogram
Angiogram of the Hand

Normal In Buerger’s Disease

 Buerger’s Disease:
Prevention

To avoid the onset of Buerger's

disease, tobacco use should be
avoided, particularly by men.
 Buerger’s Disease:
Treatment

 The only method known to be an effective

treatment for Buerger's disease is
immediately quitting smoking. Patients
who continue to smoke after a diagnosis
of Buerger's disease will generally require
amputation of the fingers and toes.

 Since there is no cure for Buerger's

disease, the goal of treatment is to control
Buerger’s Disease: Symptom Control

 Gentle massage and warmth to increase

circulation
 Avoid conditions that reduce circulation to the
extremities
 Avoid sitting or standing in one position for
long periods
 Do not walk barefoot to avoid injury
 Do not wear tight or restrictive clothing
 Report all injuries to physician for appropriate
treatment
Buerger’s Disease: Prognosis

The symptoms of Buerger's disease

may disappear if tobacco use is
stopped. If the affected extremity is
to be saved, the patient must stop
smoking. If infection or gangrene
occurs, amputation of the affect
extremity may be necessary.
 Some People Just CAN’T Quit!
(Even if it costs an arm & a leg!)
 References

 Davies, Crispin; Bashir, Yaver; Shively.

Cardiovascular Emergencies. London,
GBR: BMJ Publishing Group, 2001. p151-
172
 Manning, Warren. Clinical manifestations
and diagnosis of aortic dissection.
UptoDate
 Suzuki et. al. Diagnosis of Acute Aortic
Dissection by D-Dimer. Circulation 2009;
119, 2702-2707
 References:
 Nelson’s Pediatrics
 Harrison’s Internal Medicine
 Google search for pictures
 AAP Board PREP
 CMDT 2004