CHRONIC PERIPHERAL ARTERIAL
OCCLUSIVE DISEASE( LOWER LIMB)
DR ASHOK PRADHAN
2ND YR JR
UCMS,TH
BHAIRAHAWA, NEPAL
CHRONIC LOWER LIMB ISCHEMIA
DEFINITION :
• Increased limb ischemia for more than 2 weeks
• Gradual and progressive decrease in blood flow
• Decrease in tissue perfusion
ETIOLOGY :
– ATHEROSCLEROSIS
– THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)
RISK FACTORS
DEFINITIVE
• Hypercholesterolaemia
>200mg/dl
• Hyperlipidaemia LDL
>100mg/dl; HDL<35mg/dl
• Cigarette smoking
• Hypertension
• Diabetic mellitus
RELATIVE
• Ederly
• Male predominance
• Sedentary life
• Obesity
• Family history
Atherosclerosis
• Chronic, complex inflammatory condition of elastic and
muscular arteries, involving as systemic or segmental
• Lipid plaque forms inside the arterial wall, cause
narrowing and hardening of artery
Commonly involved arteries
Infrarenal part of abdominal aorta
– Iliofemoral artery
– Poplitial arteries
Pathophysiology
• Endothelial injury by any means
• LDL enters into the tunica intima
• Monocytes enters and release free radicles
causing oxidation of LDL
• Oxidized LDL activate monocytes to become
macrophages and engulf
• Vicious cycle goes on leading to foam cell
formation
Cont.
• PDGF(platelet derived growth factor) cause
the migration of smooth muscle cell over the
foam cell leading to plaque formtion
• Covered by endothelium and over time ca++
get deposited  narrowing and hardening of
artery
• Thus atherosclerosis contain core lipid,
smooth muscle cells, and macrophages.
Aortoiliac occlusive disease
• Infrarenal aorta and iliac arteries
• Types :
– Type 1: disease localised to distal abdominal aorta
and common iliac arteries
– Type 2: wide spread aortic and iliac disease
– Type 3: multiple level disease along with
infrainguinal diseases
TYPES OF AORTOILIAC OCCLUSIVE DISEASE
Thromboangiitis Obliterans
• Nonatherosclerotic inflammatory disorder
involving medium sized and distal vessels
• Seen in smoker and tobacco user
• Young and middle age
• Male predominant
• Autoimmune disease
• Cell mediated sensitivity
to type I & III collagen.
Pathogenesis
Smoking  nicotin  interfere with NO
release but release noradrenaline  vasospasm
and at the same time nicotine irritate wall leading
to inflammation oedema  thrombosis &
obliteration of vessels (both arteries and veins)
 segmental panarteritis with involvement of
nerve (obliteration of vasa nervosum) 
features of ischemia with pain
Cont..
• Compensatory peripheral vascular disease
• Decompensatory peripheral vascular disease
(critical limb ischemia)
– Pain
– Ulceration
– Gangrene
• Smoking index (SI>300)
• Pack year index(PYI>40)
Diabetic and PAD
• High blood sugar level is source of good culture
media for bacteria to grow infection
• Diabetic microangiopathy endothelium is independent of
insulin for glucose absorption and excess glucose within vessel wall lead to formation of
O-GLCNACInterfers with phosporylation of NO synthatase
• Diabetic neuropathy
• Glycosylated hemoglobin in blood defective
oxygen dissociation
Classification of Chronic limb ischemia
Fontaine classification Rutherford classification
Grade Clinical Feature
0 Asymptomatic
1 Mild claudication
2 Moderate claudication
3 Severe claudication
4 Ischemic Rest Pain
5 Minor tissue loss
6 Major tissue loss
Stage Clinical Features
I. Asymptomatic
II a Mild claudication
II b Moderate to severe
claudication
III Ischemic rest pain
IV Ulceration or
gangrene
Clinical features
• Pain
– Intermittent caludication
– Rest pain
• Parasthesia
• Pallor
• Diminished or absent pulse
• Thinning of skin
• Loss of subcutaneous fat
• Diminished hair/ brittle nail or shining of skin
• Ulcer or gangrene
Boyd’s classification of claudication
• Grade I: Patient developed pain on walking,
but if continues to walk, pain disappears. This
is due to washing away of substance P.
• Grade II: Pain persist on walking but can walk
with effort
• Grade III: Due to severe pain patient seeks rest
Level of Claudication According To Site
Of Obstruction
Differential Diagnosis Of Intermittent Claudication
condition Location of pain Characteristic
discomfort
Onset to exercise Effect of rest
Nerve root
compression
Rediates down
the leg, posterior
Sharp pain Soon after
exercise
Not relieved
quickly,(rest+)
Spinal stenosis Hip, thigh,
buttock
Motor weakness After standing or
walking
Releived by rest
arthritic Foot, arch Aching pain Variable degree
of exercise
Not quickly
relieved
Hip arthritis Hip, buttock,
thigh
Aching “ “
Venous
caludication
Entire leg Tight bursting
pain
After walking Subside slowly
Compartment
syndrome
Calf muscle “ After exercise Subside very
slowly
Rest pain
• Continuous and aching
• Due to ischemic change in somatic nerve
• Cry of the dying nerves and worse at night
• Aggravated by elevation of limb above the
level of heart
• Relived by hanging the leg below the level of
heart
• Most distal part-tip of toes
Examination
• Buerger’s postural test
• Capillary filling time
• Harvey’s sign
• Fuchsig’s test
Cont..
• Ankle brachial pressure index
• Segmental pressure measurement
• Trademill exercise- to unmask the preliminary
stage of arterial occlusion (disappearing
pulse)(due to exercise increase in vasodilation and collateral circulation
coz decrease in pulse)
Interpretation Of ABI
ABI INTERPRETATION
>1.3 Noncompressible
1-1.29 Normal
0.91-0.99 Boderline
0.41-0.9 Mild to moderate PAD
0.0-0.3 Severe PAD
Investigation
• Routine blood examination
• Blood sugar
• HbA1C
• Serum creatinine
• Blood lipid
• Urine for sugar
• Straight x- rays
Cont..
• Doppler scan/ Duplex imaging- Doppler shift
• Angiography(sodium ditrizoate)
– Retrograde transfemoral seldinger angiography
• Free flush arteriography
• Selective angiography
– Direct aortic angiogram
– Digital subtraction angiogram
– CT Angiogram/ MR Angiogram
Doppler
• Normal doppler arterial waveform
demonstrates triphasic flow  sharp systolic
upstroke,reversal of flow in early diastole and
low amplitude forward flow throughout
diastole
• With the obstructive disease the initial feature
systolic upstroke is lost and reversal of flow
component ie diastolic phase and further
multiphasic flow
Angiography
Digital Subtraction Angiography
• Digital subtraction angiography is a type of
fluoroscopy technique used in interventional
radiology to clearly visualize blood vessels in
bone and dense soft tissue environment.
• It is simple technique by which bone structure
images plus opacified vessels are cancelled or
subtracted from a film by computerized
system,giving unobscured image of vessel
DSA OF RIGHT COMMON ILIAC ARTERY
Baseline digital substraction angiography of (a and b) the popliteal
region and (c) leg demonstrates abrubt thromboembolic occlusion of
the popliteal artery (large white arrow in a). Typical corkscrew collateral
arteries (small white arrows in b and c) and occlusion of the run-off
vessels in concordance with Buerger's disease before intervention.
CT ANGIOGRAPHY
ADVANTAGE
• Depiction of entire artery with ability to
appreciate thrombus and calcification
• Thin slice of 0.625 mm allows three
dimensional reconstruction of vessels
Genreal Treatment
Stop smoking
Change in lifestyle
• Healthy eating habits
• Reduction of weight
• Exercise
Buerger’s position and exercise
Care of foot
Medical Therapy
Disorder Pharmacological agent Purpose for PAD
reduction
Dyslipidemia Statin
Gemfibrozil
Target LDL<100mg/dl
PAD pts with low HDL
and high TG
Hypertension Beta blocker
ACE inhibitor
Decrease risk of
cardiovascular events
Diabetics Insulin therapy or Oral
hypoglycemic agent
Proper foot care
HbA1C <7%
Atherosclerosis Aspirin
Clopidogrel
Cilostazol
Reduce the chance of
vascular events
Surgery
• Percutaneous transluminal balloon angioplasty
Indication-(stenosis less than 5cm)
– Conventional
– Subintimal
• Endarterectomy
• Indication- ( segmental block of artery)
– Open
– Semiclosed
– Wiely’s eversion endarterectomy
• Femoroplasty/Profundaplasty (segmental block)
Cont..
• Reverse saphenous vein graft –segmental block, femoropoplitial block
• Insitu saphenous vein graft – segmental block, femoropoplitial block
• Arterial graft( involvement of long segment)
• Lumber sympathectomy – for healing purpose of ulceration
• Chemical sympathctomy( caudal block)
• Omentoplasty –for healing puropse
• Amputation - gangrene
Conventional method of PTA
FEMORAL ENDARTERECTOMY(open method)
Bifurcated Dacron patch for simultaneous superficial femoroplasty and
profundoplasty
he artery.
The Y-shaped graft creates a bypass for blood to travel around the blocked section of the artery.
Bypass surgery is preferred for people who have many areas of blockage or a long, continuous
blockage in the arteries of the abdomen and/or the pelvis.
Cont..
• Lumber sympathectomy – abolish vasomotor
activity  vasodilation improve circulation
• Omentoplasty – rich in blood supply and heals
ulcers
• Amputation – depends upon extent of
gangrene, site of block and amount of
collaterals
CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

CHRONIC PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

  • 1.
    CHRONIC PERIPHERAL ARTERIAL OCCLUSIVEDISEASE( LOWER LIMB) DR ASHOK PRADHAN 2ND YR JR UCMS,TH BHAIRAHAWA, NEPAL
  • 3.
    CHRONIC LOWER LIMBISCHEMIA DEFINITION : • Increased limb ischemia for more than 2 weeks • Gradual and progressive decrease in blood flow • Decrease in tissue perfusion ETIOLOGY : – ATHEROSCLEROSIS – THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE)
  • 4.
    RISK FACTORS DEFINITIVE • Hypercholesterolaemia >200mg/dl •Hyperlipidaemia LDL >100mg/dl; HDL<35mg/dl • Cigarette smoking • Hypertension • Diabetic mellitus RELATIVE • Ederly • Male predominance • Sedentary life • Obesity • Family history
  • 5.
    Atherosclerosis • Chronic, complexinflammatory condition of elastic and muscular arteries, involving as systemic or segmental • Lipid plaque forms inside the arterial wall, cause narrowing and hardening of artery Commonly involved arteries Infrarenal part of abdominal aorta – Iliofemoral artery – Poplitial arteries
  • 6.
    Pathophysiology • Endothelial injuryby any means • LDL enters into the tunica intima • Monocytes enters and release free radicles causing oxidation of LDL • Oxidized LDL activate monocytes to become macrophages and engulf • Vicious cycle goes on leading to foam cell formation
  • 7.
    Cont. • PDGF(platelet derivedgrowth factor) cause the migration of smooth muscle cell over the foam cell leading to plaque formtion • Covered by endothelium and over time ca++ get deposited  narrowing and hardening of artery • Thus atherosclerosis contain core lipid, smooth muscle cells, and macrophages.
  • 8.
    Aortoiliac occlusive disease •Infrarenal aorta and iliac arteries • Types : – Type 1: disease localised to distal abdominal aorta and common iliac arteries – Type 2: wide spread aortic and iliac disease – Type 3: multiple level disease along with infrainguinal diseases
  • 9.
    TYPES OF AORTOILIACOCCLUSIVE DISEASE
  • 10.
    Thromboangiitis Obliterans • Nonatheroscleroticinflammatory disorder involving medium sized and distal vessels • Seen in smoker and tobacco user • Young and middle age • Male predominant • Autoimmune disease • Cell mediated sensitivity to type I & III collagen.
  • 11.
    Pathogenesis Smoking  nicotin interfere with NO release but release noradrenaline  vasospasm and at the same time nicotine irritate wall leading to inflammation oedema  thrombosis & obliteration of vessels (both arteries and veins)  segmental panarteritis with involvement of nerve (obliteration of vasa nervosum)  features of ischemia with pain
  • 12.
    Cont.. • Compensatory peripheralvascular disease • Decompensatory peripheral vascular disease (critical limb ischemia) – Pain – Ulceration – Gangrene • Smoking index (SI>300) • Pack year index(PYI>40)
  • 13.
    Diabetic and PAD •High blood sugar level is source of good culture media for bacteria to grow infection • Diabetic microangiopathy endothelium is independent of insulin for glucose absorption and excess glucose within vessel wall lead to formation of O-GLCNACInterfers with phosporylation of NO synthatase • Diabetic neuropathy • Glycosylated hemoglobin in blood defective oxygen dissociation
  • 14.
    Classification of Chroniclimb ischemia Fontaine classification Rutherford classification Grade Clinical Feature 0 Asymptomatic 1 Mild claudication 2 Moderate claudication 3 Severe claudication 4 Ischemic Rest Pain 5 Minor tissue loss 6 Major tissue loss Stage Clinical Features I. Asymptomatic II a Mild claudication II b Moderate to severe claudication III Ischemic rest pain IV Ulceration or gangrene
  • 15.
    Clinical features • Pain –Intermittent caludication – Rest pain • Parasthesia • Pallor • Diminished or absent pulse • Thinning of skin • Loss of subcutaneous fat • Diminished hair/ brittle nail or shining of skin • Ulcer or gangrene
  • 16.
    Boyd’s classification ofclaudication • Grade I: Patient developed pain on walking, but if continues to walk, pain disappears. This is due to washing away of substance P. • Grade II: Pain persist on walking but can walk with effort • Grade III: Due to severe pain patient seeks rest
  • 17.
    Level of ClaudicationAccording To Site Of Obstruction
  • 18.
    Differential Diagnosis OfIntermittent Claudication condition Location of pain Characteristic discomfort Onset to exercise Effect of rest Nerve root compression Rediates down the leg, posterior Sharp pain Soon after exercise Not relieved quickly,(rest+) Spinal stenosis Hip, thigh, buttock Motor weakness After standing or walking Releived by rest arthritic Foot, arch Aching pain Variable degree of exercise Not quickly relieved Hip arthritis Hip, buttock, thigh Aching “ “ Venous caludication Entire leg Tight bursting pain After walking Subside slowly Compartment syndrome Calf muscle “ After exercise Subside very slowly
  • 19.
    Rest pain • Continuousand aching • Due to ischemic change in somatic nerve • Cry of the dying nerves and worse at night • Aggravated by elevation of limb above the level of heart • Relived by hanging the leg below the level of heart • Most distal part-tip of toes
  • 20.
    Examination • Buerger’s posturaltest • Capillary filling time • Harvey’s sign • Fuchsig’s test
  • 21.
    Cont.. • Ankle brachialpressure index • Segmental pressure measurement • Trademill exercise- to unmask the preliminary stage of arterial occlusion (disappearing pulse)(due to exercise increase in vasodilation and collateral circulation coz decrease in pulse)
  • 22.
    Interpretation Of ABI ABIINTERPRETATION >1.3 Noncompressible 1-1.29 Normal 0.91-0.99 Boderline 0.41-0.9 Mild to moderate PAD 0.0-0.3 Severe PAD
  • 23.
    Investigation • Routine bloodexamination • Blood sugar • HbA1C • Serum creatinine • Blood lipid • Urine for sugar • Straight x- rays
  • 24.
    Cont.. • Doppler scan/Duplex imaging- Doppler shift • Angiography(sodium ditrizoate) – Retrograde transfemoral seldinger angiography • Free flush arteriography • Selective angiography – Direct aortic angiogram – Digital subtraction angiogram – CT Angiogram/ MR Angiogram
  • 25.
    Doppler • Normal dopplerarterial waveform demonstrates triphasic flow  sharp systolic upstroke,reversal of flow in early diastole and low amplitude forward flow throughout diastole • With the obstructive disease the initial feature systolic upstroke is lost and reversal of flow component ie diastolic phase and further multiphasic flow
  • 26.
  • 27.
    Digital Subtraction Angiography •Digital subtraction angiography is a type of fluoroscopy technique used in interventional radiology to clearly visualize blood vessels in bone and dense soft tissue environment. • It is simple technique by which bone structure images plus opacified vessels are cancelled or subtracted from a film by computerized system,giving unobscured image of vessel
  • 28.
    DSA OF RIGHTCOMMON ILIAC ARTERY
  • 29.
    Baseline digital substractionangiography of (a and b) the popliteal region and (c) leg demonstrates abrubt thromboembolic occlusion of the popliteal artery (large white arrow in a). Typical corkscrew collateral arteries (small white arrows in b and c) and occlusion of the run-off vessels in concordance with Buerger's disease before intervention.
  • 30.
    CT ANGIOGRAPHY ADVANTAGE • Depictionof entire artery with ability to appreciate thrombus and calcification • Thin slice of 0.625 mm allows three dimensional reconstruction of vessels
  • 31.
    Genreal Treatment Stop smoking Changein lifestyle • Healthy eating habits • Reduction of weight • Exercise Buerger’s position and exercise Care of foot
  • 32.
    Medical Therapy Disorder Pharmacologicalagent Purpose for PAD reduction Dyslipidemia Statin Gemfibrozil Target LDL<100mg/dl PAD pts with low HDL and high TG Hypertension Beta blocker ACE inhibitor Decrease risk of cardiovascular events Diabetics Insulin therapy or Oral hypoglycemic agent Proper foot care HbA1C <7% Atherosclerosis Aspirin Clopidogrel Cilostazol Reduce the chance of vascular events
  • 33.
    Surgery • Percutaneous transluminalballoon angioplasty Indication-(stenosis less than 5cm) – Conventional – Subintimal • Endarterectomy • Indication- ( segmental block of artery) – Open – Semiclosed – Wiely’s eversion endarterectomy • Femoroplasty/Profundaplasty (segmental block)
  • 34.
    Cont.. • Reverse saphenousvein graft –segmental block, femoropoplitial block • Insitu saphenous vein graft – segmental block, femoropoplitial block • Arterial graft( involvement of long segment) • Lumber sympathectomy – for healing purpose of ulceration • Chemical sympathctomy( caudal block) • Omentoplasty –for healing puropse • Amputation - gangrene
  • 35.
  • 38.
  • 39.
    Bifurcated Dacron patchfor simultaneous superficial femoroplasty and profundoplasty
  • 41.
    he artery. The Y-shapedgraft creates a bypass for blood to travel around the blocked section of the artery. Bypass surgery is preferred for people who have many areas of blockage or a long, continuous blockage in the arteries of the abdomen and/or the pelvis.
  • 42.
    Cont.. • Lumber sympathectomy– abolish vasomotor activity  vasodilation improve circulation • Omentoplasty – rich in blood supply and heals ulcers • Amputation – depends upon extent of gangrene, site of block and amount of collaterals

Editor's Notes

  • #14 . Endothelium is independent of insulin for glucose absorption and excess glucose lead to formation of i O-GlcNAc in the blood vessels, which interefers with phosphorylation of NO synthetase, so microangiopathyleading to retinopathy, neuropathy and so on.
  • #15 1.Functional:Normal blood flow at rest but cannot increase in response to exercise leading to claudicationPain felt within muscleOccurs during walkReleived at rest. 2. critical limb ischemia Persistently recurring ischemic rest pain for more than 2 weeks which requires regular analgesics and ankle systolic pressure <50mm HgAnkle brachial pressure index (ABPI) <0.3Ulceration and gangrene of foot or toe
  • #17 Pain is brought on by build up of anaerobic metabolites and pain producing chemicals (such as Substance P) in the muscle due to inadequate arterial supply.
  • #22 Complication of arteriography: hypersensitiviy to contrast, dissection of arterial wall
  • #31 3D reconstruction is the process of capturing the shape and appearance of real objects. CARBONDIOXIDE ANGIOGRAPHY USED IN SECERE RENAL ANGIGRAPHY.
  • #33 GEMFIBROZIL-peroxisome proliferator-activated receptors- INCREASE LIPID METABOLISM (LIPOPROTEIN LIPASE ACTION), ASPIRIN- #COX-#TXA2 CLOPIDOGREL # ADP,PATHWAY OF PLATELET AGGREgation cilostazol phosphodiesterase inhibitor.#platelet aggregation