peripheral vascular disease

1. Management of
Peripheral Vascular
Disease
Dr Binaya Timilsina
BPKIHS
Nepal

2. Overview
• Definition
• Risk factors
• Work up : lab tests and imaging
• Treatment for chronic arterial insufficiency and acute limb
ischemia
• Summary

3. Definition
Peripheral 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.

4. Risk factors for symptomatic peripheral
vascular disease.

5. EVALUATINGANDTREATINGTHEPATIENT
WITHPERIPHERALARTERIALDISEASE
• History and physical examination
• Testing and Imaging
• Treatment
• Characterizing the pain divides PVD into
Chronic arterial insufficiency
Acute arterial occlusion

6. 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

7. 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)

8. 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

9. Clinical Classification of
Intermittent claudication;

10. 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 ≤ 0.4
Ankle systolic pressure ≤ 50 mmHg
Toe systolic pressure ≤ 30 mmHg

11. Work up
• Lab tests
• Physiological tests like ankle brachial index
• Imaging
Doppler ultrasonography
Duplex ultrasonography
Angiography
CT angiography
MR angiography

12. 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

13. Ankle Brachial Index (ABI)

14. ABI
ABI 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

15. 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 measurement
Mini 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

16. 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

17. • 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

18. 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

19. 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

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

21. 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

22. Ilio-femoralarterial diseasedetectedby
contrast-enhancedMR 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).

23. Treatmentof Chronic arterialinsufficiency
• Risk factor modification
• Exercise therapy
• Drugs; Pentoxifyline, Cilostazole, Naftidrofuryl
• Intermittent pneumatic compression
• Revascularization by Open surgery or endovascularization
• Therapeutic angiogenesis

24. A. Risk factor modification
1. 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

25. 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)

26. 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

27. F. Intermittent pneumatic compression
Inflated 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

28. Surgicalrepairoption for aortoiliacdisease
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

29. 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

30. D. Femoro-femoral bypass
In U/L iliac artery involvement
E. Obturator bypass
Graft between iliac artery and femoral artery
through obturator membrane in infected or
distorted groin anatomy

31. Surgicalrepairoption 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

32. 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%

33. 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 morbidity
Less interference with
daily life
Low patency rates
Longer perioperative
stay,
More complications
like bowel, ureteric
injury and impotence
Superior patency rates

34. 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

35. 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

36. Buerger’sdisease /Thromboangitisobliterans
• 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

37. •OLIN criteria for Diagnosis
1. 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

38. 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

39. Treatment of Buerger’s disease
• Tobacco cessation
• Explanation advice
• Drugs
• Direct arterial surgery
• Sympathectomy
• Omental transposition
• Amputation

40. Treatment
A. Tobacco cessation
Only proven preventing guideline
B. Explanation advice
Adjustment of lifestyle
Exercise and diet
Care of feet
Heel raise
Analgesics and position

41. 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

42. 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

43. 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%

44. 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

45. Drawbacksof Lumbarsympathectomy
• 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

46. Cervicalsympathectomy
• 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

47. 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

48. 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

49. 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

50. 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%

51. Raynaud’sphenomenon
• 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

52. ClinicalManifestations
• 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

53. 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

54. 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

55. 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

56. 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)

57. SUMMARY

58. Intermittentclaudicationtreatment algorithmAlgorithm in management of PVD

59. Treatment plan in CLI

60. THANK YOU