Peripheral vascular disease is caused by narrowing of arteries due to conditions like atherosclerosis and affects around 15% of people over 70 years old. It presents as leg pain with walking (claudication) and can progress to critical limb ischemia with rest pain, ulcers or gangrene. Treatment involves restoring blood flow through methods like thrombolysis, angioplasty or surgery as well as managing risk factors like smoking, diabetes and cholesterol. Patients with acute limb ischemia requiring inpatient care while those with stable chronic disease can often be treated as outpatients.
2. Introduction
Critical limb ischaemia
Chronic progressive peripheral artery disease with pain at rest, ulceration or gangrene
1-year mortality after onset of critical limb ischaemia is 25% and 25% of survivors require
amputation
Peripheral artery disease (ABI <0.9)
4.3% over 40yo and 15.5% over 70 years old
29% in those >50 with smoking or diabetes
In the elderly, both sexes equally affected but symptoms far more common in men
Smoking and diabetes are the most important risk factors + dyslipidaemia, hypertension,
hyperhomocysteinaemia and raised CRP
Closely linked with coronary or cerebrovascular disease
Most frequently diseased arteries are femoropopliteal, tibial, aortoiliac and
brachiocephalic vessels
3. Pathophysiology
Peripheral nerves and skeletal muscle are most sensitive to ischaemia and
irreversible changes occur within 6 hours
Reperfusion injury can occur after restoration of flow noted by muscle pain
and swelling, renal failure and peripheral muscle infarction
Often hyperkalaemia, myoglobinaemia, metabolic acidosis and raised CK ensue
Severity depends upon duration and location of obstruction, amount of collateral
flow and previous health of involved limb
1/3 of all deaths from occlusive arterial disease are due to reperfusion injury
4. Pathophysiology
Thrombosis
Most common cause of acute limb ischaemia
In lower limbs, thrombotic occlusion accounts for 80% of cases
In upper limbs, thrombotic occlusion 50%, 1/3 embolism and ¼ arteritis
Most non-embolic ischaemia is due to chronic occlusion with clinically silent or
muted symptoms due to collaterals but can be due to acute atherosclerotic plaque
rupture
Can also occur through
Propagation of clot to occlude collaterals
Ischaemia-related distal oedema leading to compartment syndrome
Fragmentation of clot into microcirculation
Oedema of microvasculature cells
5. Pathophysiology
Embolism
Less common than thrombosis due to reduced incidence of rheumatic heart disease
and anticoagulation of AF
Emboli usually originate from heart
AF in 2/3
Mural thrombus following AMI in 20% (mean 14 days post-MI)
Mechanical valve less common with adequate anticoagulation
Tumour emboli from atrial myxomas, vegetations from IE and parts of prosthetic cardiac
devices
6. Pathophysiology
Emboli
Non-cardiac sources
Thrombi from aneurysms and atheromatous plaques
Aortoiliac, femoral, popliteal and subclavian arteries most commonly
Typically cause symptoms in hands/feet (blue toe syndrome) or cerebral circulation (TIA)
Typically lodge at bifurcations of common femoral artery, popliteal or brachial artery
Other
Intra-arterial injection can lead to local vasospasm, infectious arteritis, thrombosis,
pseudoaneurysm formation and mycotic aneurysm
Inert particles or drug crystals can embolise to peripheral vessels
Prolonged use of vasopressors
Thoracic aortic dissection can propagate into subclavian or iliofemoral arteries and false lumen
may then occlude flow
7. Pathophysiology
Vasculitis
Rheumatoid, lupus, polyarteritis nodosa
Raynaud’s
Rewarming, calcium channel blockers, alpha-blockers and vasodilators
Takayasu’s arteritis
Arteritis of aortic arch and branches seen in young Asian women
Thromboangiitis obliterans (Buerger’s disease)
Non-atherosclerotic segmental inflammation of small/medium vessels
Only seen in smokers
Painful nodules, ulceration and gangrenous digists in young adults 20-40yo
Hypothenar hammer syndrome
Repeated trauma to hypothenar area in laborers or vibration tools lead to narrowing of ulnar artery or
aneurysmal degeneration resulting in painful discolouration of one or more ulnar fingers with sparing of thumb
8. Pathophysiology
Popliteal artery entrapment (young males)
Surrounding musculature leads to luminal narrowing and pain in anterior aspect of
lower one third of leg with exercise
External iliac artery endofibrosis
External iliac artery fibrosis due to prolonged hip flexion
Thigh pain and numbness in cyclists and triathletes diagnosed by pre- and post-
cycling ABI
9. Clinical features
Six P’s: Pain, pallor, paralysis, pulselessness, paraesthesias and perishingly cold
Total occlusion of a severely diseased artery with well-developed collateral supply
due to chronic PAD may be clinically silent
Pain alone may be the only symptom distal to occlusion
Skin changes: Pallor, blotchy/mottled cyanosis, petechiae, blisters and finally skin
and fat necrosis
Hypo- or hyperaesthesia is a common early finding due to ischaemic neuropathy
Absence of a palpable pulse is not particular helpful if long-standing PAD unless
accompanied by skin changes
Loss of previously strong pulse suggests acute embolisation
Paralysis ensues and foreshadows impending gangrene
Preservation of light touch sensation is a good guide to tissue viability
10. Rutherford criteria
I - Viable (not immediately threatened)
No sensory loss, no muscle weakness and doppler arterial and venous signals
present
IIA - Marginally threatened (salvageable if promptly treated)
Sensory loss over toes if any, no weakness, inaudible arterial doppler but venous
doppler signal present
IIB - Immediately threatened (salvageable if immediately revascularised)
Sensory loss over more than just toes, associated with rest pain, mild/moderate
muscle weakness, inaudible arterial doppler but patent venous doppler signal
III - Irreversible
Profound/anaesthetic, profound paralysis/rigor and no doppler signal from arterial
or venous vessels
11. Clinical features
Microemboli
Pain and cyanosis in involved digit, petechiae and local muscle pain
If showering of emboli, get multiple small areas of involvement (trash foot)
Pulses are preserved (if present from the start)
12. Acute versus chronic arterial disease
Acute limb ischaemia = symptoms for <2 weeks
Pain over distal forefoot waking patient at night or requiring patient to hang legs over
bed suggests severe occlusion and warrants prompt consultation
Claudication
Localised,reproducible, resolves within 2-5 minutes of rest and recurs at consistent
walking distances
Conversely
Pain of acute limb ischaemia conversely is not well localised, is not relieved by rest or
gravity and can be a worsening of chronic pain (if thrombotic in nature)
Chronic obstructive arterial disease
Characterised by intermittent claudication, which may progress to intermittent
ischaemic pain at rest
Classical teaching suggests single-level disease results in claudication, while
multilevel disease results in rest pain or tissue loss
13. Artery-specific claudication sites
Iliac artery – Buttocks, thigh and sometimes calf. Impotence if bilateral.
Common femoral artery – Thigh
Superficial femoral artery – Upper 2/3 of calf
Popliteal artery – Lower 1/3 of calf
Infrapopliteal - Foot
14. Differential diagnosis
Chronic compartment syndrome
Calf muscles, often after intense exercise, subsides slowly and relieved with elevation
Venous claudication
Whole leg, relieved by elevation and usually signs of venous congestion/previous DVT
Nerve root compression
Radiates down leg, describes as sharp lancinating pain, induced by movement, often present at rest and
improved by change in position. Worse when sitting, history of back pain and relief when supine are suspicious
Symptomatic Baker’s cyst
Hip arthritis
Aching discomfofrt, not quickly relieved, improves with sitting and rest
Spinal stenosis
Often bilateral buttocks/posterior leg with pain and weakness
Relief by lumbar spine flexion and worse with standing or extending spine
Foot/ankle arthritis
15. Examination
Sternotomy scars, murmurs, auscultation for bruits at all major vessels,
palpation for AAA
Lower limbs
Phelagmasia cerulea dolens
Phlegmasia alba dolens
Venous insufficiency – Oedema, medial malleolar ulcers
Arterial insufficiency – Foot/toe ulcers, loss of hair, muscle atrophy, thickened
nails, poor pulses
Check all pulses with doppler and check for doppler signals in veins if suspecting
acute limb ischaemia
16. Diagnosis
Acute embolism if no prior claudication, normal contralateral limb, obvious source (e.g. AF), sudden
exact time of onset
Sudden abrupt cut-off of blood flow with no collateral circulation and minimally diseased vessels on imaging
Acute thrombosis if prior claudication, marked signs of arterial disease bilaterally, no obvious source
and more gradual onset
Widespread disease with collaterals and gradual narrowing of blood flow seen on imaging
Check ABI
Ratio of SBP with cuff just above malleolus (with Doppler probe on dorsalis pedis/posterior tibial artery) and
high brachial pressure in either arm
Chronic obstructive arterial disease have ABI <0.9
<0.25 suggests acutely limb-threatening vascular disease
>1.3 suggests non-compressible vessel i.e. severe calcification
Segmental blood pressures below knee, above knee and on the high thigh can aid assessment with
Doppler on foot arteries
Difference of >30mmHg between two adjacent levels localises the site of obstruction
17. Diagnosis
Labs
CK, myoglobin, serum lactate
Chem20, FBC and coags
ECG is crucial if suspecting embolism
Imaging
If diagnosis of arterial occlusion is in question, duplex USS is very accurate for detecting
complete or incomplete obstruction
Sensitivity declines from calf down
Echo can detect embolic sources
Arteriography
CT arteriography is as sensitive as traditional angiography for larger vessels
Can determine abrupt cut-off (embolic) or gradual decline and disease (thrombosis)
18. Treatment
Restoration of blood flow and prevention of recurrent thrombosis or embolism
IV UFH 80U/kg bolus then 18U/kg/hr infusion)
May prevent clot extension, recurrent embolisation, venous thrombosis, microthrombi
distal to obstruction and re-occlusion after reperfusion
Unclear if improves outcomes in thrombosis of plaque-laden artery
LMWH 1mg/kg BD is an alternative but is less common
Aspirin may enhance clot reduction
Stratify by Rutherford criteria and consult Vascular surgeons
Stage I and IIa can undergo imaging prior to intervention
Stage IIb warrant immediate revascularisation
Stage III have irreversible damage and likely require amputation
Provide adequate analgesia, fluids and treat heart failure to improve perfusion
19. Acute management by aetiology
Suspected cardiac source
Usually large thrombi at femoral bifurcation
Present with no underlying vascular disease, absent femoral pulse on one side and
normal contralateral vascular exam
Embolectomy preferred
Distal vessel occlusion/thrombosis
Thrombolysis preferred
If history suggests chronic thrombus e.g. mural thrombus from aneurysm
Open embolectomy or transcatheter embolectomy preferred as lysis unlikely to be
helpful
20. Treatment
Subacute thrombotic occlusion with well-developed collateral often undergo medical
management
Catheter-directed intra-arterial thrombolysis is often chosen for embolic or thrombotic acute
occlusion
Long-term management
Smoking cessation
Exercise
Daily aspirin (reduces mortality 25%)
Anticoagulants if clot formation is severe or recurrent
Statins
Improving glycaemic control
Cilostazol (PDE inhibitor) for claudication with obstruction arterial disease (CI in CCF)
Pentoxyfilline is a second-line agent
21. Disposition
If chronic peripheral vascular disease without an immediate threat to limb
viability can be discharged on aspirin (if not already on it and no CI) and
referred to vascular OPD and primary care physician
If any acute or worsening chronic ischaemia, need inpatient care