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Vascular Disease

Arteries diseases
Thoracic aortic aneurysm
Abdominal aortic aneurysm (AAA)
Aortic dissection
Peripheral arterial disease (PAD)

AORTIC ANATOMY AORTIC ANATOMY

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DEFINING THORACIC AORTIC
ANEURYSM

THORACIC AORTIC ANEURYSM


Definitions

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3
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Abdominal Aortic Aneurysm (AAA)

Aortic aneurysm rupture is the 10th


leading cause of death in men over 50.

AORTIC SCAN - To detect aneurysms that could


rupture and be fatal

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Acute Aortic Dissection
Classification
DeBakey :
Most common aortic emergency Type I:
I: involve the ascending aorta, aortic arch and the
Incidence double that of ruptured decending aorta
Type II:confined
II:confined to the ascending aorta
abdominal aortic aneurysms Type III:
III: confined to the descending aorta
Type IIIA:
IIIA: above the diaphragm
Without treatment, 36-
36-72% of patients Type IIIB:
IIIB: below the diaphragm
will die within 48 hours (one week Stanford:
Stanford:
Type A:involve
A:involve the ascending aorta
mortality of up to 91% ) Type B:
B: do not involve the ascending aorta
Acute: less than 2 weeks
Chronic: more than 2 weeks

Classification of Aortic Dissection


1. Classic with true and false lumens
separated by intimal flap
2. Medial disruption with intramural
hematoma or hemorrhage
3. Discrete/subtle aortic dissection bulge at
tear site with no hematoma
4. Plaque rupture/penetrating aortic ulcer
5. Iatrogenic and traumatic dissection
Task force on aortic dissection, European Society
of Cardiology, Eur Heart J 2001;22: 1642-
1642-81

Intramural Hematoma

In contrast to typical aortic dissection, in which


there is an intimal tear, IMH is caused by a
spontaneous hemorrhage of the vasa
vasorum of the medial layer, which weakens
the media without an intimal tear.

Clinical manifestations and the risk factors in


IMH are similar to those in typical aortic
dissection. IMH accounts for approximately
13% of the prevalence of acute aortic
dissection .

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Aortic Dissection
Classic presentation includes acute-
acute-onset,
severe chest/back pain described as tearing
or ripping
Atypical presentations are common
15% of patients report NO pain
Supportive findings include pulse deficit, new
aortic regurgitation, tamponade, and focal
neurological deficits
Majority of patients have no specific physical
findings

Clinical Presentation Clinical Presentation


Neurologic.
vaso-vagal symptoms (lightheadedness, diaphoresis,
Cardiovascular.
acute aortic regurgitation (type A)
nausea...)
acute congestive heart failure
syncope (~10%)
varying degrees of heart block
hypotension
acute MIs
near total hemispheric ischemia (stroke)
cardiac tempoande (hypotension and tachycardia)
acute paraplegia
Horners syndrome (Ptosis, Anhydrosis, Miosis,
Enophthalmos and Loss of ciliospinal reflex)

Clinical Presentation Clinical Presentation


Pulmonary. Renal.
hemoptysis refractory hypertension (renin release)
wheezing hematuria / oliguria (with back pain)
hoarseness
new onset pleural effusions Extremity ischemia.
pseudohypotension
Gastrointestinal. pulse deficits (right arm: 30%, right leg: 25%)
hematemasis duplication of pulses
dysphagia
mesenteric ischemia

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Clinical Findings(II) Ancillary Evaluation
Physical Examination Routine Lab. Tests: non-
non-specific
pulse deficits and discrepancies in BP EKG: shows LVH reflecting long-
long-standing
between limbs are key diagnostic clues hypertension
pulse deficits (50%) the EKG is useful in excluding myocardial
aortic regurgitation(50%) infarction
neurologic findings(20%): altered
sensorium,
sensorium, hemiplegia,
hemiplegia, hemianesthesia,
hemianesthesia,
gaze preference to the affected side

Radiography (I)
Chest X ray
mediastinal widening(75%)
calcium sign
sign -uncommon but highly specific, >5mm
double-
double-density appearance of the aorta
a localized bulge along a normally smooth aortic
contour
a disparity in the caliber between the descending and
ascending aorta
obliteration of the aortic knob
displacement of the trachea or nasogastric tube to the
Abnormal CXR finding a 1- 1-cm separation between the
right by the dissection
intimal calcification and the adventitial outline of the descending
descending
pleural effusions(left)
aorta (the calcium sign), consistent with aortic dissection.

Transesophageal Echocardiography
Radiography(II) of Aortic Dissection
Echocardiography
transthoracic approach: M-M-mode & 2-
2-D=low
sensitivity and specificity
transesophageal = more accuracy and very
sensitive, can be done in ER (safer).

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Radiography (III) Radiography(IV)
Computed Tomography limitations of CT scan:
scan:
dilatation of the aorta it dose not provide information about the presence of aortic
identification of an intimal flap regurgitation
differential rates of flow in true and false lumina no information about the relationship of the dissection to the
the clear demonstration of both the true and false major arterial branches of the aorta
lumina time-
time-consuming and requires the patient to be outside ER
advantages over aortography:
aortography:
greater contrast resolution and detects small or delayed
differences in the opacification of true and false channels
may be able to detect a thrombosed false lumen despite
nonopacification
does not require arterial catheterization

Radiology(V) Radiography(VI)
Aortography
disadvantages of aortography:
aortography:
filling of a false channel or channels with or without an
most invasive, most expensive
intervening intimal flap
risks of intravenous contrast material
distortion of the true lumen by either a patent or
inadequate detection of pleural leak
thrombosed false lumen
advantages of aortography:
aortography:
thickening of the aortic wall by more than 5-
5-6 mm
accurate for determining the site of the intimal tear
caused by a thrombosed false lumen
and extent of the dissection
displaced intimal calcification
easily demonstrated aortic regurgitation
the only procedure that demonstrates the extent
and location of dissection into aortic side branches

Differential Diagnosis
Radiography(VII)
Chest pain is the most common symptom in AD
Magnetic Resonance Imaging Acute myocardial infarction
shows the site of intimal tear, type and pain is more typically pressurelike but may radiate to the
extent of dissection, presence of aortic arms or neck
pain does not typically migrate over time
insufficiency, and differential flow velocities
CK-
CK-MB levels are elevated
in the true and false channels and in the Pulmonary embolus
aortic side branches pain is generally respirophasic
advantages:
advantages: hypoxemia secondary to ventilation/perfusion mismatch
no contrast material, no ionizing radiation, Pericarditis
noninvasive pain typically changes with position
auscultation may reveal a pericardial friction rub
EKG is common diagnostic(ST-
diagnostic(ST-segment elevation
prominent in V5-
V5-6 and lead I)

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Treatment(I) Treatment(II)
Emergency Department Definite Therapy
Objective: maintaining systolic blood pressure between 100 and Type A:
A: acute aortic dissections require surgical treatment
120 mmHg the only contradiction to immediate surgical repair of a type
Antihypertensive agents: A dissection is the simultaneous occurrence of a
Sodium nitroprusside:
nitroprusside: 50-
50-100mg +D5W 500ml infused at a rate of
0.5~3 ug/min
ug/min
progressing stroke
Beta-
Beta-adrenergic blocker:reduce the heart rate to 60-60-80/m Type B : medical management mortality is 15- 15-20%(same as
Propranolol:
Propranolol: 1mg IV q 5 min, MAX initial dose < 0.15mg/kg surgery done)
Metoprolol Surgery indications: persistent pain, uncontrolled
Esmolol hypertension, occlusion of a major arterial trunk, frank aortic
Trimethaphan camsylate:
camsylate: a ganglionic blocking agent leaking or rupture, or development of a localized anerysm.
anerysm.
500mg +D5W 500ml infused at a rate of 1- 1-2 mg/min
Labetalol:both
Chronic aortic dissection: control of blood pressure using
Labetalol:both alpha and beta-
beta-blockade properties
initial bolus 10-
10-20 mg, then infuse of 1-
1-2 mg/min beta-
beta-blocking agents(most common)

Endovascular Treatment Endovascular Treatment


(Non-
(Non-endograft option)
Primary tear: cover with stent graft
Static obstruction:
Decreases pressure in false lumen
uncovered stents in
by obliterating flow
Causes thrombosis of the false origin of branches
lumen which is associated with good
long term outcome Dynamic
Should treat dynamic obstruction of
branches obstruction:
obstruction:
Can help with static obstruction of percutaneous fenestration
branches of the intimal flap
Induction of aortic remodeling

WHAT FENESTRATION DOES FENESTRATION


CONTRAINDICATIONS

CREATES HOLE IN THE FLAP SEPARATING Sever aortic insufficiency


Leaking false lumen
FALSE AND TRUE LUMEN
Coronary artery dissection with MI or
RAISES PRESSURE IN THE TRUE LUMEN right heart failure
PROMOTES FLOW IN THE FALSE LUMEN

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RISK FACTORS
Older age (> 40 years)
Male gender
Smoking
Diabetes mellitus
Hyperlipidemia
Hypertension
Hyperhomocysteinemia

When risk factors coexist, the risk increases several-


several-
fold

Am J Cardiol 2001; 87 (suppl): 3D-13D


NEJM 2001; 344: 1608-1621

Individuals With PAD Present in Clinical Practice With Distinct


Syndromes

Critical limb lschemia:


lschemia: Ischemic rest pain, nonhealing
wound, or gangrene/

Acute limb ischemia: The five Ps, defined by the


clinical symptoms and signs that suggest potential
limb jeopardy:
Pain
Pulselessness
Pallor
Paresthesias
Paralysis (& polar, as a sixth P).

INTERMITTENT CLAUDICATION (LEG


Clinical Presentations of PAD ATTACK)
~15%
Classic (Typical)
Claudication Derived from the Latin word claudicatio i.e. to
50%
limp
Asymptomatic Caused by PAD in the lower extremities
Characterized by pain, ache, cramp, tightness or
sense of fatigue in leg muscles with activity
~33% Symptoms relieved by rest
Atypical Results in reduced mobility and quality of life
Leg Pain
(functionally limited)
Drugs 2000; 59: 1057-
1057-1070

1%-2%
Critical
Limb Ischemia

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WHAT CAUSES INTERMITTENT INTERMITTENT CLAUDICATION IS
INDICATIVE OF SYSTEMIC
CLAUDICATION? ATHEROSCLEROSIS

Atherosclerosis in peripheral arteries of legs 40-


40-60% of patients with intermittent claudication
have concomitant CAD
During exercise, oxygen demand increases Prevalence of cerebrovascular disease in
intermittent claudication patients is 25-
25-50%
Muscles operate anaerobically 60% of people with PAD have CAD or
cerebrovascular disease or both
Produce lactic acid and other metabolites 40% of those with coronary or cerebrovascular
disease will also have PAD
Leg pain
Lactic acid and other metabolites washed away Am J Cardiol 2001;87(suppl):3D-13D
on rest Am J Cardiol 2001;88(suppl):43J-47J
Am J Cardiol 2001; 87 (suppl): 3D-13D

PRIMARY SITES
OF INVOLVEMENT
Femoral & Popliteal
arteries: 80-
80-90%

Tibial & Peroneal


arteries: 40-
40-50%

Aorta & Iliac arteries:


30%

Harrisons Principles of Int


Med

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HOW DOES AN INTERMITTENT
CLAUDICATION PATIENT PRESENT
CLINICALLY? DIFFERENTIAL DIAGNOSIS
CALF HIP/THIGH/BUTTOCK
Leg pain caused and reproduced by a certain Venous occlusion Arthritis
degree of exertion Tight bursting pain / dull Persistent pain, brought on
Relieved by rest ache that worsens on by variable amounts of
exercise
Not affected by body position standing and resolves Associated symptoms in
Atherosclerotic lesions usually found in arterial with leg elevation other joints
segment one level above affected muscle group Positional pain relief Spinal cord compression
Calf claudication more commonly due to disease Chronic compartment History of back pain
syndrome Symptoms while standing
in femoral arteries and less commonly due to Positional pain relief
disease in popliteal or proximal tibial or peroneal Tight bursting pain
Positional pain relief FOOT
arteries; Hip/Thigh/Buttock claudication due to Arthritis
Nerve root compression
aortoiliac disease Positional pain relief
Buerger disease
(thromboangitis obliterans)
Am J Cardiol 2001; 87 (suppl): 3D-13D Bakers cyst Am J Cardiol 2001; 87 (suppl): 3D-13D
Positional pain relief

Claudication vs. Pseudoclaudication DIAGNOSIS


Claudication Pseudoclaudication History taking
Careful examination of leg
Characteristic of discomfort Cramping, tightness, aching, Same as claudication plus
fatigue tingling, burning, numbness
Pulse evaluation
Ankle-
Ankle-brachial index (ABI):
SBP in ankle (dorsalis pedis and posterior tibial arteries)
Location of Buttock, hip, thigh, Same as ___________________________________
discomfort calf, foot claudication SBP in upper arm (brachial artery)
Exercise-
Exercise-induced Yes Variable

Distance Consistent Variable

Occurs with standing No Yes

Action for relief Stand Sit, change position Am J Cardiol 2001; 87 (suppl): 3D-13D
NEJM 2001; 344: 1608-1621
Time to relief <5 minutes 30 minutes
Also see Table 4 of Hirsch AT, et al. J Am Coll Cardiol. 2006;47:e1-e192.

The First Tool to Establish the PAD Diagnosis:


A Standardized Physical Examination
Comprehensive Vascular Examination
Key components of the vascular physical examination include:
Pulse intensity should be assessed and should be recorded numerically
numerically
Bilateral arm blood Pulse Examination as follows:
Carotid
pressure (BP) Radial/ulnar
Cardiac examination Femoral 0, absent
Palpation of the Popliteal 1, diminished
Dorsalis pedis
abdomen for Posterior tibial 2, normal
aneurysmal disease Scale:
0=Absent
3, bounding
Auscultation for bruits 1=Diminished
Examination of legs 2=Normal Use of a standard I IIa IIb III
3=Bounding (aneurysm or AI)
and feet examination should
facilitate clinical
communication

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Ankle-
Ankle-Brachial Index Values and Ankle-
Ankle-
Clinical Classification Brachial
Index
Clinical Presentation Ankle-
Ankle-Brachial Index
Normal > 0.90
Claudication 0.50-
0.50-0.90
Rest pain 0.21-
0.21-0.49
Tissue loss < 0.20

Values >1.25 falsely elevated; commonly seen in diabetics

Am J Cardiol 2001; 87 (suppl): 3D-13D


NEJM 2001; 344: 1608-1621

Magnetic Resonance Angiography (MRA) Computed Tomographic Angiography (CTA)


MRA has virtually replaced contrast arteriography for PAD
diagnosis Requires
Excellent arterial picture iodinated
No ionizing radiation contrast
Noniodine
Noniodinebased intravenous contrast medium rarely Requires
causes renal insufficiency or allergic reaction
ionizing
~10% of patients cannot utilize MRA because of:
radiation
Claustrophobia
Produces an
Pacemaker/implantable cardioverter-
cardioverter-defibrillator excellent
Obesity arterial
Gadolinium use in individuals with an eGFR <60 mL/min
mL/min picture
has been associated with nephrogenic systemic fibrosis
(NSF)/nephrogenic fibrosing dermopathy

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The history and physical examination (pulse
evaluation and careful examination of the leg)
are usually sufficient to establish the
diagnosis

ACC/AHA Guideline for the Management of PAD:


Steps Toward the Diagnosis of PAD
Differential Diagnosis of PAD Hirsch AT, et al. J Am Coll Cardiol. 2006;47:e1-e192.

Individuals Age 50 to 69 years and history of smoking or diabetes


at risk Age 70 years
Atherosclerosis Popliteal entrapment for PAD
Abnormal lower extremity pulse examination
Known atherosclerotic coronary, carotid, or renal arterial disease
Vasculitis Cystic adventitial
Fibromuscular disease
Obtain history of walking impairment and/or limb ischemic symptoms:
Obtain a vascular review of symptoms:
dysplasia Coarctation of aorta
Leg discomfort with exertion
Leg pain at rest; nonhealing wound; gangrene

Atheroembolic disease
Vascular tumor
Thrombotic disorders
Trauma Iliac syndrome of the No leg pain Atypical
leg pain
Classic
claudication
Chronic critical
limb ischemia
Acute limb
ischemia

cyclist (CLI) (ALI)


Radiation
Popliteal aneurysm Pseudoxanthoma Perform a resting ankle-brachial index measurement
Thromboangiitis elasticum Diagnosis and Treatment of Diagnosis and Diagnosis Diagnosis Diagnosis and
obliterans (Buergers Persistent sciatic artery Asymptomatic PAD and Treatment of and and Treatment of
Atypical Leg Pain
disease) (thrombosed)
Asymptomati
c PAD and
Treatment of
Claudication
Treatment of
Critical Limb
Acute Limb
Ischemia
Atypical Leg Ischemia
Pain

ACC/AHA Guideline for the Management of PAD: WHY IS IT NECESSARY TO TREAT


Diagnosis and Treatment of Asymptomatic PAD
INTERMITTENT CLAUDICATION ?
Individual at PAD risk: No leg symptoms or atypical leg symptoms
Consider use of the San Diego Walking Impairment Questionnaire
Symptoms worsen in 25% of patients
Perform a resting ankle-brachial index measurement
Approximately 5% will require amputation
ABI 1.30 ABI 0.91 to 1.30 ABI 0.90
within 5 years
(abnormal) (borderline & normal) (abnormal) Around 5-5-10% have critical limb ischemia;
Pulse volume recording
Toe-brachial index
Measure ABI after
exercise test
risk of limb loss
(Duplex ultrasonography)
Increased risk of mortality, primarily for
Normal results: Abnormal Normal post-exercise ABI: Decreased post-exercise
cardiovascular causes
No PAD results No PAD ABI

Evaluate other causes of Confirmation of Am J Cardiol 2001; 87 (suppl): 3D-


3D-13D
leg symptoms PAD diagnosis
Hirsch AT, et al. J Am Coll Cardiol. 2006;47:e1-e192.

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GOALS OF TREATMENT
To relieve exertional symptoms and improve
walking capacity
To improve quality of life
To reduce total mortality as well as cardiac
and cerebrovascular morbidity and mortality

NEJM 2001; 344: 1608-21

MANAGEMENT MODIFICATION OF RISK FACTORS

Risk factor modification Smoking cessation


Exercise therapy Diabetes control (FBG 80-
80-120 mg/dl, PPG < 180
Antiplatelet therapy mg/dl, HbA1c < 7%)
Dyslipidemia management (LDL < 100 mg/dl, TG <
Medical therapy targeted at symptoms
150 mg/dl): Statins (RR 38%; 4S)
Revascularisation procedures Hypertension control (BP < 130/85 mmHg)
Ramipril [RR 28%; HOPE (n=4051)]

Am J Cardiol 2001; 87 (suppl): 3D-13D


NEJM 2001; 344: 1608-21
Am J Med 2002; 112: 49-57

REVASCULARISATION PROCEDURES
EXERCISE PROGRAM
Improves walking ability Incapacitating claudication
Requires motivation and personalised Limb-
Limb-threatening ischemia (pain at rest, non-
non-
supervision healing ulcers and/or infections or gangrene)
Benefits lost if not maintained on regular If symptoms persist despite medical therapy
basis
Overall effectiveness limited

NEJM 2001; 344: 1608-21 AHA guidelines 1996

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MEDICAL THERAPY USED IN PAST FOR MANAGING
INTERMITTENT CLAUDICATION SYMPTOMS
ANTIPLATELET THERAPY
Vasodilators (e.g. verapamil,
verapamil, isoxsuprine,
isoxsuprine, Aspirin
cinnarizine,
cinnarizine, xanthinol nicotinate, Clopidogrel (CAPRIE Study)
cyclandelate)
Several controlled trials have No studies have shown that
found no evidence of clinical aspirin or clopidogrel improves
efficacy of drugs of this class claudication symptoms

NEJM 2001; 344: 1608-


1608-1621
NEJM 2001; 344: 1608-21

Pharmacotherapy for Claudication Pentoxifylline

FDA Approved Drugs:


Drugs:
Drug Class: Methylxanthine
Pentoxifylline
Approved: August 1984
Cilostazol
Dosing: 400 mg tid

Pharmacologic Hemorheologic agent


There is inadequate evidence of clinical efficacy or a therapeutic role for: Properties: Some vasodilation
L-arginine, propionyl-L-carnitine, gingko biloba, oral prostaglandins,
vitamin E, or chelation therapy. Weak antiplatelet
activity

WHAT IS THE CURRENT STATUS ON


PENTOXIFYLLINE? Cilostazol

Drug Class: Phosphodiesterase III


Pentoxifylline is no longer recommended
inhibitor derivative
for first-line therapy for most patients with
Approved: January 1999
intermittent claudication
Dosing: 100 mg bid

1996 AHA Scientific Statement Pharmacologic Platelet aggregation inhibitor


Properties: Vasodilation
Am J Med 2002; 112: 49-
49-57 HDL-
HDL-cholesterol (10%)
Triglycerides (15%)
Inhibits smooth muscle cell
proliferation in vitro

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UNIQUE MECHANISM OF ACTION Contraindications to Cilostazol Use

Cilostazol Cilostazol and several of its metabolites are inhibitors of


phosphodiesterase III. Several drugs with this pharmacologic
cAMP effect have caused decreased survival compared with
placebo in patients with Class III-IV CHF. PLETAL is
contraindicated in patients with CHF of any severity.
Provisos:
Provisos:
Platelets Vascular smooth Lipoprotein lipase
CHF of any severity (systolic dysfunction)
muscle activity
Any known or suspected hypersensitivity to any of its
TG synthesis
components

Platelet Vasodilation TG
aggregation and z peripheral blood flow HDL
activation Antiproliferative effect
CHF=congestive heart failure.
Pletal (cilostazol) Package Insert. Rockville, Md: Otsuka America Pharmaceutical, Inc; 1999.

Medical and Pharmacologic Treatment for CLI (Critical


limb ischemia is defined as ischemic rest pain, Options in Limb Revascularization
nonhealing wounds, or gangrene)
1. Pentoxifylline Class III(Level of evidence: B)
Parenteral administration of pentoxifylline is not useful for this treatment of Endovascular reconstruction options
CLI. Percutaneous transluminal angioplasty (PTA)
2. Prostaglandins - Class IIb (Level of evidence: A) Stents
Parenteral administration of prostaglandin E-1 or iloprost for 728 days may Surgical reconstruction options
be considered to reduce ischemic pain and facilitate ulcer healing in patients Aortoiliac/aortofemoral reconstruction
with CLI, but its efficacy is likely to be limited to a small percentage of Femoropopliteal bypass (above knee and below knee)
patients. Femorotibial bypass
- Class III (Level of evidence: B)
Oral iloprost is not an effective therapy to reduce the risk of amputation or
death in patients with CLI.
3. Angiogenic Growth Factors Class IIb (Level of evidence: C)
The efficacy of angiogenic growth factor therapy for treatment of CLI is not
well established and is best investigated in the context of a placebocontrolled
trial.

Endovascular Treatment for Claudication Endovascular Treatment for Claudication

Endovascular procedures are indicated for individuals with a


Endovascular intervention is recommended as the
vocational or lifestyle-limiting disability due to intermittent
preferred revascularization technique for TASC type A
claudication when clinical features suggest a reasonable iliac and femoropopliteal lesions.
likelihood of symptomatic improvement with endovascular
intervention and
Iliac Femoropopliteal
a. Response to exercise or pharmacologic therapy is TASC A:
inadequate, and/or (PTA recommended)

b. there is a very favorable risk-benefit ratio (e.g. focal aortoiliac


TASC B: (insufficient data to recommend)
occlusive disease)

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Endovascular Treatment for Claudication: Endovascular Treatment for Claudication
Iliac Arteries
Provisional stent placement is indicated for use in iliac arteries
as salvage therapy for suboptimal or failed result from balloon Endovascular intervention is not indicated if there is no
dilation (e.g. persistent gradient, residual diameter stenosis significant pressure gradient across a stenosis despite flow
>50%, or flow-limiting dissection). augmentation with vasodilators.

Stenting is effective as primary therapy for common iliac artery


stenosis and occlusions. Primary stent placement is not recommended in the femoral,
popliteal, or tibial arteries.
Stenting is effective as primary therapy in external iliac artery
stenosis and occlusions.
Endovascular intervention is not indicated as prophylactic
therapy in an asymptomatic patient with lower extremity PAD.

Surgery for Critical Limb Ischemia Surgery for Critical Limb Ischemia

Surgery is not indicated in patients with severe decrements in


limb perfusion in the absence of clinical symptoms of critical For individuals with combined inflow and outflow disease
limb ischemia. with critical limb ischemia, inflow lesions should be
addressed first.

Patients who have significant necrosis of the weight-


weight-
bearing portions of the foot, an uncorrectable flexion When surgery is to be undertaken, an aorto-
aorto-bifemoral
contracture, paresis of the extremity, refractory ischemic
bypass is recommended for patients with symptomatic,
rest pain, sepsis, or a very limited life expectancy due to
co-
co-morbid conditions should be evaluated for primary hemodynamically
amputation. significant, aorto-
aorto-bi-
bi-iliac disease requiring intervention.

Surgery for Critical Limb Ischemia


Surgery for Critical Limb Ischemia

Femoral-
Femoral-tibial artery bypasses should be constructed with
Bypasses to the above-
above-knee popliteal artery should be autogenous vein, including ipsilateral greater saphenous vein,
constructed with autogenous saphenous vein when possible.
or if unavailable, other sources of vein from the leg or arm.
Bypasses to the below-
below-knee popliteal artery should be
constructed with autogenous vein when possible. Composite sequential femoropopliteal-
femoropopliteal-tibial bypass, or bypass
to an isolated popliteal arterial segment that has collateral
Prosthetic material can be used effectively for bypasses to the outflow to the foot, are acceptable methods of
below knee popliteal artery when no autogenous vein from
ipsilateral or contralateral leg or arm is available. revascularization and should be considered when no other
form of bypass with adequate autogenous conduit is possible.

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Buergers disease (Thromboangitis
(Thromboangitis Histology:
obliterans)
obliterans) Localised inflammatory changes occur in walls of
arteries and veins leading to thrombosis.
Definition:
It is occlusive disease of small & medium size
Clinical picture:
arteries, thrombophlebitis of superficial or deep
The usual symptoms and signs of arterial
veins & Raynauds syndrome.
occlusive disease are present.
Gangrene of the toes and fingers is common and
It occurrs in male patients with heavy smoking &
progressive.
usually under the age of 30 years.

Thromboangitis obliterans treatment Thromboangitis obliterans treatment

Cessation smoking Prevention of complications from Buerger disease:


Prostacyclin analogue - intravenous iloprost has been
shown to be somewhat effective in improving symptoms, Use of well-
well-fitting protective footwear to prevent foot
accelerating resolution of distal extremity trophic changes, trauma and thermal or chemical injury
and reducing the amputation rate among patients with
Buerger disease. Early and aggressive treatment of extremity injuries to
Recently, Isner and colleagues reported improved protect against infections
healing of ischemic ulcers and relief of rest pain in a small
series of patients with Buerger disease using Avoidance of cold environments
intramuscular gene transfer of vascular endothelial growth
factor Avoidance of drugs that lead to vasoconstriction

Thromboangitis obliterans treatment Raynauds disease


Surgical Care
Given the diffuse segmental nature of thromboangiitis obliterans and Idiopathic condition usually occurs in young
the fact that the disease primarily affects small-
small- and medium-
medium-sized women & affects the upper extremities more
arteries, surgical revascularization for Buerger disease is usually not than lower.
feasible and is extremely rare.
Effort to improve distal arterial flow in patients with Buerger disease; Peripheral pulses are normal.
autologous vein bypass of coexistent large-
large-vessel atherosclerotic It is attributable to abnormal sensitivity in
stenoses in patients with severe ischemia who have an acceptable the direct response of the arterioles to cold.
distal target vessel.
Other proposed surgical treatments for Buerger disease are as follows:
Omental transfer
Sympathectomy
Spinal cord stimulator implantation
Ultimate surgical therapy for refractory Buerger disease (in patients
who continue smoking) is distal limb amputation for nonhealing ulcers,
gangrene, or intractable pain.

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When cooled, these vessels constrict & the part
Raynauds Disease becomes blanched & incapable of finer movements.
The capillaries then dilate & fill with slow flowing
deoxygenated blood, the digits therefore becoming
Small artery, arteriole vasospasm swollen & dusky.
White, blue, red As the attack pass off, the arterioles relax, oxygenated
blood returns into the dilated capillaries & the digits
become red.
Often accompanied by pain.

OCCLUSIVE ARTERIAL DISEASE Pathophysiology


Acute limb ischemia secondary to thrombosis or Acute limb ischemia leads to cell death and irreversible
embolus is true emergency. tissue damage.

Mortality is 25% and risk of amputation is 20%. After prolonged arterial obstruction, reperfusion may not be
fully attainable due to distal edema and thrombi forming in
11-
11-27%of elderly have peripheral arterial disease the microcirculation.

Smoking, diabetes, hyperlipidemia, hypertension and Peripheral nerves and skeletal muscle are very sensitive to
homocysteinemia are significant risk factors ischemia and irreversible damage can occur within 6 h of
anoxia
At least half of the patients with coronary or cerebrovascular
disease have PVD Non-
Non-embolic ischemia is due to atherosclerosis of the
vessels

Pathophysiology Etiology
Progression of ischemic injury can occur Thrombotic occlusion is significantly more common cause of
through several mechanisms: acute limb ischemia than is embolism.
a) propagation of clot to include collateral vessels
Emboli originate from the heart in 80-
80-90 % with atrial
b) ischemia-
ischemia-related distal edema leading to high fibrillation being the cause in two thirds of all peripheral
compartment pressures emboli.

c) fragmentation of clot in the microcirculation Mural thrombus in the ventricle after recent myocardial
infarction is the second most common cause.
d) edema of the microvasculature cells

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Etiology Etiology
Other causes of emboli include atrial myxomas, vegetations Thrombosis unrelated to atherosclerotic disease can occur
from valve leaflets, and parts of prosthetic devices such as at an area of vessel injury during invasive studies.
mechanical valves.
Peripheral arterial supply can be obstructed by vasospastic
Noncardiac causes include thrombi from aneurysms and or inflammatory conditions like Raynaud disease and
atheromatous plaques. Thromboangitiis obliterans (young smokers)

Iatrogenic embolization can happen during angiograhic Limb ischemia can also seen with central causes like
procedures of the aorta and larger vessels thoracic aortic dissection and Takayasu arteritis.

Etiology Clinical features


6 Ps:pain, pallor, polar
Low cardiac output states like cardiogenic or hypovolemic (for cold), An area of
shock may also present with limb ischemia pulselessness, fixed cyanosis Fixed
mottling &
surrounded by
paresthesias, and reversible cyanosis
Cardiac tamponade, ischemic cardiomyopathy, valvular heart paralysis. mottling

disease can impair left ventricle function and lead to leg


Despite the belief that
ischemia in patients with existing peripheral vascular disease. the limb salvage is
possible within 4-
4-6 h,
tissue loss can occur
with significantly
shorter occlusion
times.

Investigations of acute limb ischemia


Diagnosis
Arteriography
Clinical evaluation is the most useful Patients with high clinical probability of embolic ischemia do NOT need angiography
diagnostic tool.
If the differentiation between
Capillary refill is not reliable alone embolic & thrombotic ischemia is
not clear clinically, and if the limb
A hand held Doppler can detect the condition permits,
presence or absence of a pulse. DO ANGIOGRAPHY
If a pulse is detected, then the ankle-
ankle- Value of angiography
brachial index (ABI) and segmental leg Localizes the obstruction
pressures should be checked Visualize the arterial tree & distal run-
An ABI<0.5 indicates acute arterial off

obstruction Can diagnose an embolus:


Popliteal embolism Lt. iliac embolism
Sharp cutoff, reversed meniscus or clot silhouette
If time permits, do a duplex ultrasound Reversed meniscus sign Clot silhouette

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Treatment
Goals of therapy include restoration of
blood flow, preservation of limb and life,
and prevention of recurrent thrombosis
Current practice includes UFH to prevent
clot extension, venous thrombosis, the
appearance of thrombi distal to the
obstruction, and reocclusion.
Fluid resuscitation and treatment of heart
failure and dysrhythmias are sometimes
necessary to improve limb perfusion.
Definite treatment includes surgery or
thrombolysis

Treatment of acute limb ischemia Treatment of acute limb ischemia


B Catheter directed thrombolysis Agents used: Streptokinase,
A Once you diagnose Urokinase, tissue plasminogen
Indications: activator
Immediate anticoagulation with heparin to avoid clot propagation 1. Viable or marginally threatened limb (class I, IIa)
Appropriate analgesia 2. Recent acute thrombosis (not suitable for embolism or old thrombi)
Simple measures to improve existing perfusion: 3. Avoid patients with contraindications

Keep the foot dependant Contraindications:


Contraindications:
Avoid pressure over the heal Absolute:
Absolute
1. Cerebro-vascular stroke within previous 2 months
Avoid extremes of temperature (cold induces vasospasm, heal raises the metabolic rate)
2. Active bleeding or recent GI bleeding within previous 10 days
Maximum tissue oxygenation (oxygen inhalation)
3. Intracranial trauma or neurosurgery within previous 3 months
Correct hypotension Relative:
Relative
Start treatment of other associated cardiac conditions (CHF, AF) 1. Cardio-pulmonary resuscitation within previous 10 days
2. Major surgery or trauma within previous 10 days
3. Uncontrolled hypertension

Treatment of acute limb ischemia Following revascularization:


C Surgery
The sudden return of oxygenated blood to the acutely ischemic
muscles generates & releases oxygen free radicals that causes
1- Acute embolism: Catheter embolectomy under local anesthesia cellular injury and severe edema

2- Immediate surgical revascularization is indicated in class IIb, or class I, IIa when Compartment syndrome
thrombolysis is not possible or contraindicated
& muscle necrosis
A combination of different procedures can be done:
Arterial exploration at different sites
ttt
Arterial thrombectomy
Bypass surgery based on pre-operative angiography if
available or intra-operative angiography Fasciotomy
Longitudinal incision of the skin & deep fascia to release pressure over swollen muscles

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Amputation:
Upper Extremity Ischemia
Done for irreversible ischemia with permanent tissue
damage (turgid muscles, fixed cyanosis) Upper extremity arterial occlusion is less
common.
There is a well-
well-developed collateral
The level of amputation is decided according to the level of
palpable pulse. circulation around the shoulder and elbow,
thus arterial occlusion is better tolerated.
Palpable popliteal pulse -------------- Below knee amputation
Usual causes are vasospasm, arteritis,
Absent popliteal pulse ---------------- Above knee amputation trauma, hypercoagulable state, plaque
rupture, thoracic outlet syndrome,
aneurysms.
Treatment includes heparinization and
surgical thrombectomy.

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