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Peripheral vascular disease
- 1. Peripheral vascular disease Dr AndrewCrofton ED registrar Disclaimer: https://criticalcarecollaborative.com/disclaimer/
- 2. Introduction Critical limbischaemia 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 nervesand 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 Mostcommon 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 Lesscommon 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-cardiacsources 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 arteryentrapment (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 SixP’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 chronicarterial 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 Chroniccompartment 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 embolismif 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 ofblood 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 byaetiology 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 thromboticocclusion 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 chronicperipheral 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