management of peripheral vascular disease dr binaya timilsina
DESCRIPTION
peripheral vascular diseaseTRANSCRIPT
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
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