Management of Peripheral Vascular Disease

Dr Binaya Timilsina BPKIHS

Nepal

Overview• Definition

• Risk factors

• Work up : lab tests and imaging

• Treatment for chronic arterial insufficiency and acute limb

ischemia

• Summary

DefinitionPeripheral artery occlusive disease or

peripheral arterial disease or

peripheral vascular disease

refers to the obstruction or deterioration

of arteries other than those supplying

the heart and within the brain.

Risk factors for symptomatic peripheral vascular disease.

EVALUATING AND TREATING THE PATIENT WITH PERIPHERAL ARTERIAL DISEASE

• History and physical examination

• Testing and Imaging

• Treatment

• Characterizing the pain divides PVD into

Chronic arterial insufficiency

Acute arterial occlusion

Chronic Arterial Insufficiency • Asymptomatic to gangrenous tissue loss • Intermittent claudication: most common presentation

Features of chronic lower limb arterial stenosis or occlusion• Intermittent claudication• Rest pain• Dependent rubor• Ulceration• Gangrene• Arterial pulsation diminished or absent• Arterial bruit• Slow capillary refilling

Intermittent claudication• Cramp-like pain felt in the muscles that is:

brought on by walking;

not present on taking the first step (unlike osteoarthritis);

relieved by standing still (unlike nerve compression from a lumbar

intervertebral disc prolapse or osteoarthritis of the spine or spinal stenosis)

Thigh Claudication

60% Upper 2/3 Calf Claudication

Lower 1/3 Calf Claudication

Foot Claudication

30% Buttock & Hip Claudication±Impotence – Leriche’s Syndrome

Sites of Intermittent claudication

Clinical Classification of Intermittent claudication;

Critical limb ischaemia (CLI)• Most severe form of PVD• Can have acute or chronic presentation

• Chronic CLI is defined as >2 weeks of rest pain, ulcer or tissue loss and characterized by

Ankle–brachial index ≤ 0.4Ankle systolic pressure ≤ 50 mmHgToe systolic pressure ≤ 30 mmHg

Work up• Lab tests• Physiological tests like ankle brachial index• ImagingDoppler ultrasonography

Duplex ultrasonography

Angiography

CT angiography

MR angiography

Lab Tests in PVD• CBC: secondary polycythemia in smoker or elevated platelet in thrombotic

disease

• Renal function test: elevated in DM,HTN. No contrast study if deranged

• Lipid profile: hyperlipidemia

• FBS and HbA1c:

• ECG:

• ESR: elevated in collagen vascular disease

• CRP: marker of worsening PVD

• Hypercoagulable state and Homocysteine: prothrombin time, partial

thromboplastin time, thrombin time, lupus anticoagulant, anti-cardiolipin

antibody, activated protein C resistance, factor V Leiden

Ankle Brachial Index (ABI)

ABIABI Inferences

>1.3 Non compressible(arteriosclerotic)

1.00-1.29 Normal

0.91-0.99 Equivocal

0.41-0.90 Mild to moderate PVD

0.31-0.40 Rest pain

<0.30 Impending gangrene

1) Segmental pressure Bp cuffs at arm, upper thigh, above knee, below knee, and above ankle

Decrease in pressure of >20 mmHg in comparison to above level indicates

occlusion

2) Digital pressure measurementMini cuff at toe base and pressure by manometer

Toe brachial index(TBI) >0.7 with pressure > 50 mmHg indicative of preserved

flow

Done if ABI>1.3 or pedal arch vessel involvement suspected

ABI

3) Exercise testing• Done in patients with claudication but pulses and ABI normal

• Patient able to walk in treadmill without symptoms or decrease in ABI :

PVD ruled out

• Drop in ABI of 0.2 or in ankle pressure of 20 mmHg which do not return to

pre exercise level within 3 min suggest PVD

ABI

• Detection of blood velocity using ultrasonography

• Normal is triphasic: peak in systole, reversal of flow in

early diastole and forward diastolic flow

• Earliest change: loss of reversal of flow so biphasic

• As obstruction increases widening of diastolic peak

occurs and flow monophasic

Doppler Ultrasonography

Duplex Ultrasonography • B mode imaging information about vessel wall and peak systolic

velocity (PSV)

• Ratio of PSV at stenosis to proximal segment of 2 denotes 50%

obstruction and 4 -70%

• Non invasive, cheap has largely replaced routine use of conventional

arteriography

Angiography• Used to be gold standard test for road mapping before surgery

• Safer in recent years due to fine 3-4 F catheters

• Hematoma, arterial spasm, sub intimal dissection, infection,

pseudoaneurysm, AV fistula and embolization

• Slowly being replaced by CTA and MRA

CT Angiography• Non invasive• Still uses ionizing radiation and iodinated contrast agent absence of flow in the right • common iliac artery• (white arrow)

MR Angiography

• Shift of imaging modality due to Gd-MRI

• Better for distal small and pedal vessels as compared to

angiography

• Sensitivity 81% and specificity 92%

• Gd worsens CKD patients and precipitates nephrogenic

systemic fibrosis

Ilio-femoral arterial disease detected by contrast-enhanced MR angiography

(A) Severe stenosis at the origin of the right superficial femoral artery (arrow) also involving the origin of the profunda femoris artery. (B) Long-segment occlusion of the left superficial

femoral artery (arrowhead) and bilateral significant stenosis of the profunda femoris arteries (arrows).

Treatment of Chronic arterial insufficiency

• Risk factor modification

• Exercise therapy

• Drugs; Pentoxifyline, Cilostazole, Naftidrofuryl

• Intermittent pneumatic compression

• Revascularization by Open surgery or endovascularization

• Therapeutic angiogenesis

A. Risk factor modification1. Smoking: cessation

2. Diabetes: each 1% rise in HbA1c associated with 28% risk for PVD.

<7% treatment goal

3. Hypertension goal bp <140/90 and <130/80 if DM and renal

insufficiency

ACE inhibitors

4. Hyperlipidemia: diet modification

Statins, niacin or fibrates

5. Antiplatelet therapy

Aspirin 75-325 mg/day or clopidrogel 75mg/day or both

B. Exercise therapy

• Aids in improvement in pain free ambulation, working performance and

cardiac status

• Minimum 30-45 min/session, 3-4 times/week, for at least 12 weeks

C. Pentoxifylline

• Xanthine derivative

• Rheolytic effects on RBC wall deformability and flexibility thus reducing

viscosity and improving oxygen delivery, decreases platelet aggregation

• Dose; 400 mg TDS (max 1800mg/day)

D. Cilostazol:

Phosphodiesterase III inhibitors increases cAMP

Inhibits smooth muscle cell proliferation and contraction,

Inhibits platelet aggregation

Decreases TG and increases HDL

Dose; 50mg/day X 1 wk then 50 mg BD X 1 week then 100mg BD

E. Naftidrofuryl :

Serotonin antagonist, promotes vasodilatation

F. Intermittent pneumatic compressionInflated for 2-3 seconds, rate 3 cycle/minute

G. Revascularization

Failed medical therapy

Severe claudication

If a proximal stenotic lesion is present

Revascularization by open surgery or endovascular

technique

Surgical repair option for aortoiliac disease

A. Endarterectomy

• Opening of diseased segment and removing plaque

• Indications: in infected cases, small vessels not

amenable for endovascular or graft repair, in impotence

B. Aorto Bifemoral Bypass (ABFB)

• Using PTFE grafts or Dacron grafts (knitted/woven), iliac,

distal aortic segment and proximal femoral segment can

be bypassed by placing graft between infrarenal aorta

and B/L femoral

• End to end anastomosis better

• Patency are 90% at 5 yrs and 75-85% at 10 yrs

C. Axillo-bifemoral bypass;

• Extra anatomic repair

• Comorbidities making difficult to undergo ABFB, and failed ABFB

• Placing a subcutaneous graft between axillary artery and ipsilateral femoral

artery

• Opposite limb vascularized by femoro-femoral bypass

D. Femoro-femoral bypassIn U/L iliac artery involvement

E. Obturator bypass

Graft between iliac artery and femoral artery

through obturator membrane in infected or

distorted groin anatomy

Surgical repair option for infrainguinal disease• Autogenous grafts as great saphenous vein preferred

• Others: short saphenous vein, cephalic or basilic vein

• Cryopreserved cadaveric veins prone to thrombosis

• Very low success rate in below knee bypass if synthetic

grafts (PTFE or Daccron) used

Endovascular approach• Balloon angioplasty requires crossing the arterial

lesion transluminally with a guidewire and inflating a

balloon advanced over the wire at the lesion.

• Considered successful if residual stenosis

<30%

Endovascular approach Vs Surgical

• Published papers favor either of approaches

• TASC II recommends angioplasty over surgery

• BASIL trial favors surgical group

Endovascular approach Surgical approach

Shorter hospital stay

Less morbidityLess interference with daily lifeLow patency rates

Longer perioperative stay, More complications like bowel, ureteric injury and impotenceSuperior patency rates

Therapeutic angiogenesis• Gene transfer by use of 4000mg naked plasmid DNA encoding VEGF

injected directly in ischemic limbs

• Others are

Stem cells,

Autologous progenitor cells,

Growth factors such as basic fibroblast growth factor (bFGF), and

Transcription factors such as hypoxia-inducible factor-1

• Used in CLI patients who lack options for endovascular or surgical

revascularization

Amputation• Recommended in

Severe symptoms not amenable to or failed

revascularization

Gangrenous tissue/ nonfunctional

Life threatening infection

• 25% patient of CLI require amputation/yr and

25% die within 1 yr due to cardiovascular

involvement

Buerger’s disease /Thromboangitis obliterans• Non-atherosclerotic vascular disease characterized by

absence or minimal presence of atheromas,

segmental recurring and progressive vascular inflammation,

vasoocclusive phenomenon and

thrombosis of small and medium arteries and veins of hands and feet.

• Lack of unanimous diagnostic criteria: is a disease of exclusion

•OLIN criteria for Diagnosis1. Age younger than 45 years

2. Current or recent history of tobacco use

3. Presence of distal extremity ischemia (indicated by claudication, rest pain,

ischemic ulcers, gangrene) documented by non invasive vascular testing

4. Exclusion of autoimmune dis, hypercoagulable states and diabetes

5. Exclusion of proximal source of emboli by ECHO and arteriography

6. Consistent arteriographic findings in the clinically involved and non

involved limbs

Color duplex ultrasonography in TAO• Occlusion of distal calf or pedal arteries

• Occlusion of forearm, palmar arch or digital

arteries

• Normal appearing arteries proximal to lesion

• Serpigineous or corkscrew collaterals at the

site of occlusion

• Intact vessel wall in the level of thrombotic

occlusion often free of calcification

Treatment of Buerger’s disease• Tobacco cessation

• Explanation advice

• Drugs

• Direct arterial surgery

• Sympathectomy

• Omental transposition

• Amputation

Treatment A. Tobacco cessation

Only proven preventing guideline

B. Explanation adviceAdjustment of lifestyle

Exercise and diet

Care of feet

Heel raise

Analgesics and position

C. Drugs

• Prostaglandins: prostacyclin or PGI2 (iloprost) 40 times

antiplatelet and vasodilator effect as compared to PGE1

• Intra-arterial thrombolytic therapy

Intra-arterial streptokinase (bolus 10,000 U f/b 5000

units per hour

• Trental(pentoxyfiline)

• Praxiline: niftidrofuryl oxalate

• Aspirin

D. Direct arterial surgery• Revascularization surgery rarely feasible

• Arterialization of veins by creating AV fistula between artery proximal to

site of block and adjacent vein

E. Sympathectomy • Objectives

Causes vasodilatation by decreasing sympathetic vasomotor tone

Abolish pain impulses carried by sympathetic fibres

• Contraindicated in intermittent claudication by stealing blood from

ischemic muscles to skin

• Nakata et al reported ulcer healing in 58% and relief of rest pain in 64%

Methods

1. Surgical sympathectomy

Lumbar sympathectomy• Open sympathectomy by extraperitoneal approach

• In unilateral surgeries, sympathetic ganglia,L1, L2, L3 and sometimes L4

removed

• In bilateral cases L1 of one side preserved to avoid retrograde ejaculation

• Transperitoneal approach rarely used

• Laparascopic via retroperitoneal route has replaced others

Drawbacks of Lumbar sympathectomy

• Is a temporary procedure, effect rarely lasts beyond 6 months. Reasons are

Technical failure to identify lumbar chain (mistaken with lymphatic chain,

genitofemoral nerve, ureter, psoas sheath, psoas minor)

Cross connections of chain from opposite chain

Regeneration from cut ends

Hypersensitivity of end organ receptors to circulating adrenalins

Cervical sympathectomy

• T1(lower portion of stellate ganglion), T2 and T3 removed

• Approaches

Supraclavicular route

Axillary route

Posterior approach

Transthoracic laparoscopic approach now standard treatment of choice

2. Chemical sympathectomy

• 5ml of phenol solution in water(1:16) injected beside bodies of 2nd and 4th

vertebrae

• Contraindicated in patients on anticoagulants

• Preferably under fluoroscopic or ultrasound guidance pt on lateral position

on local anesthesia

F. Omental transposition• Rich vascular supply which directly improves tissue perfusion

• Causes neovascularization

• Increases lymphatic drainage

• Based on arterial arcade formed by anastomosis of right and left

gastroepiploic artery

Steps• Midline incision

• Omentum mobilized

• Subfascial tunneling from inferior end of incision to

inguinal incision and again

to upper third of thigh

• 3-4 transverse incisions over the medial aspect of

the thigh and leg and subfascial tunnel made and

omental pedicle advanced

• Distal end of the pedicle is fixed to the

gastrocnemius with atraumatic 2-0 chromic catgut

Complications and outcomes

• Complications: gastric devascularization and necrosis, paralytic

ileus, gastric hemorrhage, omental necrosis, and wound

infection

• Singh et al reported healing in 88%, decrease in rest pain in 72%,

increase in claudication distance in 96%

Raynaud’s phenomenon

• Excessively reduced blood flow in response to cold or emotional stress,

causing discoloration of the fingers, toes, and occasionally other areas

• Raynaud's disease (also known as primary Raynaud's phenomenon),

where the cause is unknown

• Raynaud's syndrome (secondary Raynaud's phenomenon), caused by a

known primary disease, most commonly connective tissue disorders such

as SLE, Sjogrens disease, Rheumatoid arthritis, Multiple sclerosis

• Hyperactivation of sympathetic nervous system causing

extreme vasoconstriction of the peripheral blood vessels, leading to

tissue hypoxia

Clinical Manifestations

• Usually bilateral –(both arms or feet are affected)

• Pallor, coldness, numbness, cutaneous cyanosis and pain

• With longstanding or prolonged Raynaud’s disease – ulcerations can

develop on the fingertips and toes

Management

• Aimed at prevention

• Person is advised to protect against exposure to cold

• Quit smoking

• Drug therapy – calcium channel blockers, vascular smooth muscle relaxants,

vasodilators – to promote circulation and reduce pain

• Botox

• Sympathectomy to relieve symptoms in the early stage of advanced ischemia

• If ulceration/gangrene occur, the area may need to be amputated

Acute limb ischemia• Acute onset of extremity pain with absent pulses

• Cause either emboli or trauma

• Bounding water hammer pulses proximal to occlusion

• Revascularization within 6 hours critical to avoid limb loss

• Emergent arterial imaging include duplex ultrasound, CTA, MRA and

invasive angiogram

• Heparin bolus 100 U/kg followed by IV heparin infusion 15U/kg/hour with

goal PTT 60-80 sec

• Two methods of treatment: Embolectomy and

Intra-arterial thrombolysis

Embolectomy (and thrombectomy)• Local or general anesthesia

• The artery (usually the femoral), exposed and held

in slings.

• Longitudinal or transverse incision, the clot

removed, together with the embolus with Fogarthy

balloon catheter

• The catheter introduced both proximally and

distally

• Procedure repeated until bleeding occurs

Intra-arterial thrombolysis

• 5F catheter passed into occluded vessel, left embedded in clot and

thrombolysis by tissue plasminogen activator 5mg bolus with

mechanical pulse spray/ suctioning with catheter

• The method abandoned if no progression of dissolution of clot with

time (>24 hours)

SUMMARY

Intermittent claudication treatment algorithmAlgorithm in management of PVD

Treatment plan in CLI

THANK YOU