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Clinical features of acute and chronic arterial stenosis and occlusion
1. Clinical features of acute and
chronic arterial stenosis and
occlusion
Dr Sumer Yadav
MCh – Plastic and Reconstructive Surgery
Dr Sumer Yadav
MCh – Plastic and Reconstructive Surgery
sumeryadav2004@gmail.com
2. What is PVD?
Definition:
• Also known as PAD or PAOD.
• Occlusive disease of the arteries of the lower
extremity.
• Most common cause:
o Atherothrombosis
o Others: arteritis, aneurysm + embolism.
• Has both ACUTE and CHRONIC
Pathophysiology:
• Arterial narrowing Decreased blood flow =
Pain
• Pain results from an imbalance between supply
and demand of blood flow that fails to satisfy
ongoing metabolic requirements. sumeryadav2004@gmail.com
3. The Facts:
1. The prevalence: >55 years is 10%–25%
2. 70%–80% of affected individuals are asymptomatic
3. Pt’s with PVD alone have the same relative risk of death from cardiovascular causes as
those CAD or CVD
1. PVD pt’s = 4X more likely to die within 10 years than pt’s without the disease.
2. The ankle–brachial pressure index (ABPI) is a simple, non-invasive bedside tool for
diagnosing PAD — an ABPI <0.9 = diagnostic for PAD
1. Patients with PAD require medical management to prevent future coronary and
cerebral vascular events.
1. Prognosis at 1 yr in patient’s with Critical Limb Ischemia (rest pain):
• Alive with two limbs — 50%
• Amputation — 25%
• Cardiovascular mortality 25%
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4. Risk Factors:
Typical Patient:
• Smoker (2.5-3x)
• Diabetic (3-4x)
• Hypertension
• Hx of Hypercholesterolemia/AF/IHD/CVA
• Age ≥ 70 years.
• Age 50 - 69 years with a history of smoking or diabetes.
• Age 40 - 49 with diabetes and at least one other risk factor for
atherosclerosis.
• Leg symptoms suggestive of claudication with exertion or ischemic
pain at rest.
• Abnormal lower extremity pulse examination.sumeryadav2004@gmail.com
5. Chronic PVD History:
3. Critical Stenosis = >60%, impending acute ischemic limb:
- rest pain
- ischemic ulceration
- gangrene
2. Other Symptom/Signs:
• A burning or aching pain in the feet (especially at night)
• Cold skin/feet
• Increased occurrence of infection
• Non-healing Ulcers
• Asymptomatic
1. INTERMITTENT CLAUDICATION
• Derived from the Latin word ‘to limp’
• “Reproducible pain on exercise which is relieved by rest”
• Pain can also be reproduced by elevating the leg
• “my legs get sore at night and feel better when I hang them over
the edge of the bed”
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7. DDx of Leg Pain
1. Vascular
a) DVT (as for risk factors)
b) PVD (claudication)
1. Neurospinal
a) Disc Disease
b) Spinal Stenosis (Pseudoclaudication)
1. Neuropathic
a) Diabetes
1. Musculoskeletal
a) OA (variation with weather + time of day)
b) Chronic compartment syndrome
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8. Physical Examination:
Examination: What do to:
Inspection
Expose the skin and look
for:
• Thick Shiny Skin
• Hair Loss
• Brittle Nails
• Colour Changes (pallor)
• Ulcers
• Muscle Wasting
Palpation • Temperature (cool, bilateral/unilateral)
• Pulses: ?Regular, ?AAA
• Capillary Refill
• Sensation/Movement
Auscultation • Femoral Bruits
Ankle Brachial Index
(ABI)
= Systolic BP in ankle
Systolic BP in brachial artery
Buerger’s Test • Elevate the leg to 45° - and look for pallor
• Place the leg in a dependent position 90°& look for a red
flushed foot before returning to normal
• Pallor at <20° = severe PAD.
sumeryadav2004@gmail.com
10. What does the ABI mean?
ABI Clinical Correlation
>0.9 Normal Limb
0.5-0.9 Intermittent Claudication
<0.4 Rest Pain
<0.15 Gangrene
CAUTION:
Patient’s with Diabetes + Renal Failure:
They have calcified arterial walls which can falsely elevate their ABI.
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11. Investigations:
NON INVASIVE:
Duplex Ultrasound
normal is triphasic biphasic monophasic absent
BLOOD TESTS:
1. Coagulation Studies
2. Fasting Lipids and Fasting Glucose
3. HBA1C
WHEN TO IMAGE:
1. To image = to intervene
2. Pt’s with disabling symptoms where revascularisation is considered
3. To accurately depict anatomy of stenosis and plan for PCI or Surgery
sumeryadav2004@gmail.com
12. ANGIOGRAPHY:
Non-invasive:
• CT Angiogram
• MR Angiogram
Invasive:
• Digital Subtraction Angiography
Gold Standard
Intervention at the same time
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14. Tardus et parvus = small amplitude + slow rising pulse
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15. CT Angiography Digital Subtraction Angiography
Value of angiographyValue of angiography
Localizes the obstruction
Visualize the arterial tree & distal
run-off
Can diagnose an embolus:sumeryadav2004@gmail.com
16. Treatment:
1. RISK FACTOR MODIFICATION:
a) Smoking Cessation
b) Rigorous BSL control
c) BP reduction
d) Lipid Lowering Therapy
3. MEDICAL MANAGEMENT:
a) Antiplatelet therapy e.g.
Aspirin/Clopidogrel
b) Phosphodiesterase Inhibitor e.g.
Cilostazol
c) Foot Care
2. EXERCISE:
a) Claudication exercise rehabilitation
program
b) 45-60mins 3x weekly for 12 weeks
c) 6 months later +6.5mins walking
time (before pain)
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17. PCI/Surgery:
Indications/Considerations:
•Poor response to exercise rehabilitation + pharmacologic therapy.
•Significantly disabled by claudication, poor QOL
•The patient is able to benefit from an improvement in claudication
•The individual’s anticipated natural hx and prognosis
•Morphology of the lesion (low risk + high probabilty of operation success)
PCI:
•Angioplasty and Stenting
•Should be offered first to patients with significant comorbidities who are not
expected to live more than 1-2 years
Bypass Surgery:
•Reverse the saphenous vein for femoro-popliteal bypass
•Synthetic prosthesis for aorto-iliac or ilio-femoral bypass
•Others = iliac endarterectomy & thrombolysis
•Current Cochrane review = not enough evidence for Bypass>PCI
sumeryadav2004@gmail.com
19. Mr. X presents with an acutely
painful leg:
You have had a busy day in the ED and the next
patient to see is:
Mr. X – a 60 yr old gentleman with a very painful leg.
He tells you that he woke up this morning with an
excruciating pain in his left leg and has never felt this
pain before.
? Embolism (AF/Recent Infarct/Anuerysm)
? Thrombosis of native vessel or graft
MUST RULE OUT ACUTE LIMB ISCHEMIA
sumeryadav2004@gmail.com
20. What are the features of an
acute ischemic limb?
REMEMBER THE 6 P’S:
1. PAIN
1. PALLOR
1. PULSELESNESS
1. PERISHING COLD (POIKILOTHERMIA)
1. PARASTHESIAS
1. PARALYSIS
Fixed
mottling &
cyanosis
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21. History & Exam Findings
Further Hx:
• Smokes 20cigs/day for 30 years
• 4 months of ‘leg cramps’ in BOTH legs
• 2-3 weeks of intermittent chest palpitations
Examination:
• Inspection:
: below the knee is pale/cool
• Palpation:
o Irregularly irregular pulse
Capillary return is sluggish
o No pulses palpable below L femoral artery
o All pulses palpable but appear reduced in R leg
o Normal Sensation + Movement bilaterally
Impression?
60yo male with a L Acute Ischemic limb on the background of heavy
smoking, untreated AF and symptomatic PVD.sumeryadav2004@gmail.com
22. What will you do now?
1. CALL THE VASCULAR REGISTRAR
2. ORDER INVESTIGATIONS
a) FBE
b) Coagulation Studies
c) Group and Hold
d) 12 Lead ECG
e) Chest XR
3. INITATE ACUTE MANAGEMENT:
a) Analgesia
b) Commence IV heparin
c) Call Radiology for Angiography if limb still viable
d) Discuss with registrar:
i) Thrombotic cause ?cathetar induced thrombolysis
ii) Embolic cause ?embolectomy
iii) All other measures not possible Bypass/Amputation
Simple measures to improve
existing perfusion:
• Keep the foot dependant
• Avoid pressure over the heel
• Avoid extremes of temperature
(cold induces vasospasm)
• Maximum tissue oxygenation
(oxygen inhalation)
• Correct hypotension
sumeryadav2004@gmail.com
23. Mr. X’s Complication
- Angiogram is done in radiology
- Shows acute thrombosis of L popliteal artery
- Cathetar induced urokinase and heparin infusion is started
…. 3-4 hours later
-Severe calf pain in the reperfused limb
-All pulses are present
-Leg is swollen, tense and +++ tender
REPERFUSION INJURY!
-Restored blood flow can lead to unwanted local + systemic effects
1) Washout =
oMetabolic Acidosis
oHyperkalemia
oARF (myoglobinuria)
oNon-cardiac APO
2) Compartment Syndrome =
oMay need fasciotomy
sumeryadav2004@gmail.com
24. Learning Outcomes
1. Risk factors for PVD
2. Recognise signs and symptoms of chronic ischemia of the lower limbs
3. Differential diagnosis for leg pain
4. Examine a chronic ischemic limb
5. Understand medical/surgical of management of PVD
6. Recognise an acute ischemic limb
7. Know it is important to call the vascular registrar ASAP
8. Know what investigations to order in the ED
sumeryadav2004@gmail.com
25. ACUTE ARTERIAL OCCLUSION
• “ The operation was a success but the patient
died”
• High Morbidity and Mortality
– Emergent operations in high risk patients
– 20% mortality reported (Dale, JVS 1984)
– Endovascular approaches may lower peri-
procedural mortality while preserving
outcomes sumeryadav2004@gmail.com
26. Evolution of Atherosclerosis
• Areas of low wall shear stress
• Increased endothelial permeability
• Sub-endothelial lipid and macrophage
accumulation
• Foam cells
• Formation of Fatty Streak
• Fibrin deposition and stabilizing fibrous cap
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27. Evolution of Atherosclerosis
• Rupture of Fibrous Cap
• • Pro-thrombotic core Exposed to lumen
• • Acute thrombosis
• • Embolization of plaque materials and
thrombus
sumeryadav2004@gmail.com
28. Thromboembolism
• Embolus- greek “embolos” means projectile
• Mortality of 10-25%
• Mean age increasing – 70 years
– Rhumatic disease to atherosclerotic disease
• Classified by size or content
– Macroemboli and microemboli
– Thrombus, fibrinoplatelet clumps, cholesterol
sumeryadav2004@gmail.com
29. Macroemboli
• Cardiac Emboli
– Heart source 80-90% of thrombus macroemboli
– MI, A.fib, Mitral valve, Valvular prost hesis –
Multiple emboli 10% cases
– TEE
• Views left atrial appendage, valves, aortic root
• not highly sensitive
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30. Thromboembolism
• 75% of emboli involve axial limb vasculature
• Femoral and Polilteal – >50% of emboli
• Branch sites
• Areas of stenosis
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31. Thromboembolism
Thromboembolism Non-cardiac sources
• Aneurysmal (popliteal > abdominal)
• Paradoxical – Follows PE with PFO
• Thoracic outlet syndrome
• Cryptogenic –5-10%
• Atheroemboli (artery to artery)
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32. Atheromatous Embolization
• Shaggy Aorta – Thoracic or abdominal
• Spontaneous
• Iatrogenic – 45% of all atheroemboli
• “Blue toe syndrome”
– Sudden – Painful – cyanotic – palpable pulses
• livedo reticularis
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33. Atheromatous Embolization
• Risk factors: PVD, HTN, elderly, CAD, recent
arterial manipulation
• Emboli consist of thrombus, platelet fibrin
material or cholesterol crystals
• Lodge in arteries 100 –200 micron diameter
sumeryadav2004@gmail.com
34. Atheromatous Embolization
• Affect variety of end organs
– extremities, pelvis ,GI, kidney, brain
• Work-up:
– TEE ascending aorta, CT Angio, Angiography
• Laboratory: CRP elevated, eosinophilia
• Warfarin may destablize fibrin cap and trigger
emboli.
sumeryadav2004@gmail.com
35. Atheromatous Embolization
• Reported incidence of 0.5-1.5% following
catherter manipulation
– Advance/remove catheters over guidewire
– Brachial access?
– controversial
• Limited Sx– Anti-coagulation/ observation
• Temporal delay up to 8 weeks before renal
symptoms sumeryadav2004@gmail.com
36. Atheromatous Embolization
Therapy
• Prevention and supportive care – Statins, prostacyclin analogs
(iloprost)
• Elimination of embolic source and reestablishing blood flow to heal
lesions
• Surgical options: endaterectomy or resection and graft placement
– Abdominal Aorta
– Aorta-bi-fem bypass
– Ligation of external iliac and extra-anatomic bypass if high risk
• Endovascular therapy
– Angioplasty & stenting
- higher rate of recurrence – Athrectomy – no datasumeryadav2004@gmail.com
37. Acute Thrombosis
• Graft thrombosis (80%)
– intimal hyperlasia at distal anastamosis (prosthetic)
– Retained valve cusp
– Stenosis at previous site of injury
• Native artery • Intra-plaque hemmorhage • Hypovolemia
• Cardiac failure • hypercoagable state • Trauma •
Arteritis, popliteal entrapment, adventitial cystic
disease
sumeryadav2004@gmail.com
38. Acute Thrombosis
Heparin Induced Thrombosis
• White Clot Syndrome
• Heparin dependent IgG anti-body against platelet factor
4
• 3-10 days following heparin contact
• Dx: thrombosis with > 50% decrease in Platelet count
• Tx: Direct throbin inhibiors: Agartroban & Hirudin
– Avoid all heparin products
• Morbity and Mortality: 7.4-61% and 1.1-23%sumeryadav2004@gmail.com
39. Other causes of Thrombosis
– Anti-thrombin III Defiency
– Protein C & S Defiency
– Factor V Leiden
– Prothrombin 20210 Polymorphism
– Hyper-homocystinemia
– Lupus Anti-coagulant (anti phospho-lipid
syndrome)
sumeryadav2004@gmail.com
41. Diagnostic Evaluation
• SVS/ISCVS Classification
• – “Rutherford Criteria”
• • Class I: Viable – Pain, No paralysis or sensory loss
• • Class 2: Threatened but salvageable
• • 2A: some sensory loss, No paralysis >No immediate threat
• • 2B: Sensory and Motor loss > needs immediate treatment
• • Class 3: Non-viable – Profound neurologic deficit, absent capillary
flow,skin marbling, absent arterial& venous signal
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42. Therapeutic Options
– Class 1 or 2A
• Anti-coagulation, angiography and elective
revascularzation
– Class 2B
• Early angiographic evaluation and intervention
• Exception: suspected common femoral emboli
– Class3
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45. Thrombotic –vs- Embolic
• Embolic
– History
• Cardiac events
• Acute onset
• Hx of emboli
– Physical
• Normal contralateral exam
– Angiographic
• meniscus Cut-off in normal vessel
• Bifurcations affected
Determination of etiology possible in 85% of cases
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46. Treatment Options
• Multiple options available
– Conventional surgery
• embolectomy
• endarterectomy
• revascularization
– Thrombolytic therapy
– Percutanious mechanical thrombectomy
• Native vessel thrombosis often require more elaborate
operations sumeryadav2004@gmail.com
47. Treatment Fundamentals
• Early recognition and anti-coagulation
– Minimizes distal propagation and recurrent emboli
• Modality of Tx depends on:
– Presumed etiology
– Location/morphology of lesion
– Viability of extremity
– Physiologic state of patient
– Available vein conduit for bypass grafting
sumeryadav2004@gmail.com
53. Indications for Thrombolysis
• Category 1-2a limbs should be considered
– Class 2b : Two schools of thought
1)“Delay in definitive Tx”
2)“Thrombolytics extend window of opportunity”
• Clots <14days most responsive
– But even chronic thrombus can be lysed
• Large clot burden
– Better response to lytic tx than surgery
– Requires longer duration of thrombolytics
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54. Technique of Thrombolysis
• Guide Wire Traversal Test (GTT)
– Abilty to traverse lesion best predictor of
success
– Use 0.035 in angled glide wire
– “knuckling-over” indicates sub-intimal plane
– Attempt pro-grade, Anti-grade, lytic bolus
sumeryadav2004@gmail.com
55. Technique of Thrombolysis
• Catheter directed delivery
1) Lace clot via catheter with side holes
2) Pulse-Spray technique (mechanical component)
• Urokinase and TPA equally effective
• 4 hr treatment followed by angiogram – 4000IU/min x4hr,
2000Iu/M=min x 48h – r-UK (TOPAS Trial) – no
improvement after 4hr >> surgery
– Continue Heparin tt
– Fibrinogen levels sumeryadav2004@gmail.com
56. Mechanical Thrombectomy
• Percutaneous aspiration embolectomy
– Viable alternative in selected patents
– Varity of devises
– Combines diagnostic and therapeutic procedure
– Removes non-lysable debris
– Effective in distal vessels
– Risk distal embolization
• Combine with lytic T x
sumeryadav2004@gmail.com
58. SUMMARY
• Thrombotic and embolic occlusions are
separate processes with different
presentations and treatments
• Treatment pathways in AAO are complex and
vary depending on clinical situation
• Catheter-based treatments preserve outcomes
with less overall morbidity
sumeryadav2004@gmail.com
There are currently insufficient data to recommend routine population screening for asymptomatic PAD using the ABPI.
- In recent years, it has become evident that PAD is an important predictor of substantial coronary and cerebral vascular risk
Patients with symptomatic PAD have a 15-year accrued survival rate of about 22%, compared with a survival rate of 78% in patients without symptoms of PAD.
Patients with critical leg ischaemia, who have the lowest ABPI values, have an annual mortality of 25%
Patients at risk — Based in part upon the above observations, the 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on PAD, which were produced in collaboration with major vascular medicine, vascular surgery, and interventional radiology societies, identified the following groups at risk for lower extremity PAD
Risk Factors:
Atherosclerosis (same as RF’s for CAD and CVD)
Smoking (2.5-3x)
Diabetes 3-4x
Hypertension, increased age &gt;50, male and family history
RARE: homocysteinuria
Asymptomatic — 20 to 50 percent ** Unfortunately, however, a PAD diagnosis can be missed since nearly 50% of patients are asymptomatic or have atypical symptoms. Thus, a high index of suspicion is necessary in patients presenting with potential risk factors.
Classic claudication — 10 to 35 percent
Critical limb ischemia — 1 to 2 percent
Cramp or tingling which recurs on walking the same distance
Buttock and hip — aortoiliac disease
Thigh — aortoiliac or common femoral artery
Upper two-thirds of the calf — superficial femoral artery
Lower one-third of the calf — popliteal artery
Foot claudication — tibial or peroneal artery
Osteoarthritis of the hip or knee joints — Osteoarthritis can be distinguished clinically from aortoiliac disease because osteoarthritic pain may not disappear promptly after exercise, may be associated with weather changes, and may vary in intensity from day to day (usually worse in the morning or upon wakening)
Neurogenic claudication — Neurogenic claudication, also called pseudoclaudication, describes a pain syndrome due to lumbar neurospinal canal compression, which is usually due to osteophytic narrowing of the neurospinal canal. The clinical presentation often helps to distinguish vasculogenic (ie, true) claudication from pseudoclaudication. Unlike true claudication, which occurs with walking and is relieved by stopping, pseudoclaudication causes pain with erect posture (lumbar lordosis) and is relieved by sitting or lying down. Patients with pseudoclaudication may also find symptomatic relief by leaning forward and straightening the spine (usually done with pushing a shopping cart or leaning against a wall). (See &quot;Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis&quot;.)
Auscultate for femoral (1/2 way between the ASIS and pubic symphysis)
ULCER
associated with claudication + signs of ischaemia
occur on dorsum of foot + anterior skin
↓ pulses, cold to touch, hairless skin
Painful, punched out edge
Take the highest measurement in both limbs
low ABI is also predictive of an increased risk of all-cause and cardiovascular mortality [39,40] and of the development of coronary artery calcification
95% sensitive in detecting angiogram positive disease and around 99% specific in identifying supposedly healthy subjects
Peripheral artery wave forms: arterial form is triphasic – consists of forward flow in systolic peak, reversal of flow in early diastole and forward flow in late diastole. This becomes impaired (eliminated reverse flow due to stenosis of vessel and becomes biphasic decreased systolic peak and increase of flow in diastole)
The decision to image is a decision to intervene if a suitable lesion is identified and is only applicable to a minority of patients with intermittent claudication, and then only after risk factors have been addressed and medical management followed.
There is also a role for imaging in the small group of patients in whom there is a discrepancy between the history and objective clinical signs.
The purpose of imaging is to assess the anatomical location, morphology and extent of disease in order to determine suitability for intervention and occasionally to differentiate atherosclerotic PAD from other causes such as neurogenic claudication and entrapment.
Imaging is largely reserved for patients with disabling symptoms in whom revascularisation is planned.
In these patients, accurate depiction of the vascular anatomy is critical for clinical decision making as the distribution and severity of disease are key factors determining whether revascularisation should be by endovascular techniques or open surgery.
IV-DSA uses a computer technique which compares an x-ray image of a region of the body before and after radiopaque iodine based dye has been injected intravenously into the body. Tissues and blood vessels on the first image are digitally subtracted from the second image, leaving a clear picture of the artery which can then be studied independently and in isolation from the rest of the body.
HBA1C as close to 6.0 as possible
(Selective B-1 blockade ok Anti-hypertensive medications may worsen the PAD symptoms by reducing blood flow and supply of oxygen to the limbs, and may have long-term effects on disease progression). controversial due to the presumed peripheral haemodynamic consequences of beta blockers, leading to worsening symptoms of intermittent claudication. There is currently no evidence that beta blockers adversely affect walking distance in people with intermittent claudication. However, due to the lack of large published trials beta blockers should be used with caution if clinically indicated.
Aim LDL 2.6mmol/L with PAD
Aim LDL &lt;1.8mmol/L with ATH in other vessels
Improved endothelial dysfunction via increases in nitric oxide synthase and prostacyclin [40]. (See &quot;Endothelial dysfunction&quot;.)Reduced local inflammation that is induced by muscle ischemia by decreasing free radicals [41].Increased exercise pain tolerance [38].Induction of vascular angiogenesis [42].Improved muscle metabolism by favorable effects on muscle carnitine metabolism and other pathways [43].Reductions in blood viscosity and red cell aggregation
BEWARE HF with cilostazol (inhibits platelet aggregation and acts as an arterial vasodilator)
Two compared ACE inhibitors against placebo. In the HOPE study there was a significant reduction in the number of cardiovascular events in 168 patients receiving ramipril (OR 0.72, 95% confidence interval 0.58 to 0.91). In the second trial using perindopril in a small numbers of patients, there was a marginal increase in claudication distance but no change in ankle brachial pressure index (ABPI) and a reduction in maximum walking distance.The third trial in patients undergoing angioplasty suggested that the calcium antagonist verapamil reduced restenosis, although this was not reflected in the maintenance of a high ABPI. Another small study demonstrated no significant difference in arterial intima-media thickness with men receiving the thiazide diuretic hydrochlorathiazide compared to those receiving the alpha-adrenoreceptor blocker doxazosin.
(ie has , such as angina, heart failure, chronic obstructive pulmonary disease, or orthopedic problems).
Most procedures are performed for severe claudication but approximately 30 to 40 percent are done for limb salvage
In patients with unilateral disease with acceptable aortic inflow, procedures include iliac endarterectomy, aortoiliac or iliofemoral bypass.These procedures should be performed in conjunction with femoral-femoral bypass in bilateral iliac artery occlusive disease if the patient is not a suitable candidate for bilateral aortofemoral bypass grafting.Axillofemoral bypass should not be used for the treatment of intermittent claudication except in very limited settings, such as chronic infra-aortic occlusion associated with severe symptoms in a patient who is not a candidate for aortobifemoral bypass.For infrainguinal (outflow) disease [2]:Bypasses to the popliteal artery above or below the knee should be constructed with an autogenous vein from the ipsilateral or contralateral leg or arms, if possible.It is reasonable to use a synthetic graft to the popliteal artery below the knee only if no autogenous vein is available.The evidence is less well established for femorotibial artery bypasses with autologous vein, an approach that may be considered in rare instances.The efficacy of synthetic grafts to the popliteal artery above the knee is not well established because of reduced patency rates.Femorotibial bypasses with synthetic grafts should not be performed.
5000U bolus with 1000U/hr infusion afterwards
Heparin protocol in hospital
A cathetar inserted directly into the throbus and agents like urokinase/streptokinase or tPA used.