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Acute and chronic lower limb ischaemia
VASCULAR SURGERY e II
Acute and chronic lower limb ischaemia
Non-modifiable risk factors include: age gender ethnicity. Modifiable risk factors include: smoking diabetes mellitus/poor glycaemic control hypertension hyperlipidaemia hypercoagulability.
George Peach Ian M Loftus
Abstract Limb ischaemia is a common clinical condition that causes considerable morbidity and mortality and represents a major drain on healthcare resources. Peripheral arterial disease (PAD) is the leading cause of both acute and chronic limb ischaemia. Chronic limb ischaemia may also be caused by non-atherosclerotic processes such as arterial entrapment, fibrosis or arteritis. Acute limb ischaemia may be also due to embolism, thrombosis or trauma. Duplex ultrasonography, computed tomography angiography and magnetic resonance angiography are now conventional forms of arterial imaging, with catheter angiography reserved for intervention. Risk factor modification is extremely important for all these patients, since many will also have significant coronary or cerebrovascular disease. Those with claudication often improve with structured exercise and if symptoms progress they may benefit from angioplasty or stenting. Arterial bypass remains the mainstay of treatment for patients with critical limb ischaemia if they are fit enough for surgery. Acute limb ischaemia is a surgical emergency and can be treated with surgical embolectomy or catheter-directed thrombolysis (depending on local expertise). Patients with irreversible limb ischaemia should be treated with primary amputation or palliation as appropriate.
Other factors Up to 30% of young patients with PAD have high homocysteine levels (compared to 1% in the general population) and there is now evidence that this is an independent risk factor for PAD.3 Raised haematocrit, high plasma fibrinogen levels and chronic renal insufficiency also seem to be linked to an increased risk of PAD though evidence for these links being causal remains limited. Patients with both end-stage renal disease and diabetes are at extremely high risk of limb loss.4 Intermittent claudication (IC) Though many never develop symptoms, up to 15% of patients with asymptomatic PAD will develop IC within 5 years.5 Of those who do develop IC, only 20e25% are likely to experience further clinical deterioration.6 Major amputation is rare (other than in those with diabetes) and patients should be reassured accordingly. Only 1e3% of patients with IC will require major amputation within a 5-year period.6 Clinical features: intermittent claudication is an aching muscle pain, brought on by exercise, and rapidly relieved by rest. Pain arises due to increased oxygen demand of the tissues during exercise. Symptoms are determined by site of disease and since PAD most commonly affects the superficial femoral artery (SFA), pain is usually felt in the calf (i.e. distal to the arterial stenosis/ occlusion). Disease of aorto-iliac, common femoral or tibioperoneal vessels may give rise to pain in the buttock, thigh or foot respectively. The presence of bilateral symptoms may indicate aortic disease, bilateral iliac disease or non-vascular aetiology. Claudication typically comes on after walking a pain-free distance (unlike the pain of osteoarthritis etc.) and is worse when walking fast or uphill, when muscle oxygen requirements are at their highest. Though reported claudication distances are notoriously inaccurate as a measure of disease severity, serial assessment of walking ability over months can be a useful indicator of clinical improvement or deterioration. Symptoms of chronic PAD (Box 1) generally develop over months or even years, with a gradual deterioration in pain-free walking distance. Rapid deterioration of symptoms or sudden onset of claudication are important warning signs which may indicate new arterial occlusion.
Keywords Acute leg ischaemia; angioplasty; arterial bypass; limb ischaemia; peripheral artery disease
Chronic limb ischaemia The most common cause of chronic lower limb ischaemia is atherosclerotic peripheral arterial disease (PAD). PAD has an estimated worldwide prevalence of nearly 10%, rising to as much as 15e20% in those over 70 years of age and affects some 27 million people in Europe and North America alone.1 Critical limb ischaemia (CLI) e the most severe manifestation of PAD e may lead to limb loss or even death unless treated promptly. Each year, 500e1000 new cases of CLI are diagnosed per million of the population, with an estimated annual cost to the NHS of more than £200 million.2 Risk factors The development of atherosclerotic PAD is a multifactorial process involving both modifiable and non-modifiable risk factors.
George Peach MBChB MRCS is a Clinical Research Fellow at St George’s Vascular Institute, London, UK. Conflicts of interest: none declared.
Critical limb ischaemia Whilst some patients follow steady progression from asymptomatic PAD to IC and then CLI, this is the exception rather than the rule. Patients with PAD often have significant co-morbidity limiting physical activity and may develop CLI without preceding IC.
Ian M Loftus MBChB MD FRCS is Consultant Vascular Surgeon and Reader in Vascular Science at St George’s Vascular Institute, London, UK. Conflicts of interest: none declared.
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should be seen by a multidisciplinary diabetic foot team within 24 hours.8
Definitions
Clinical features: ischaemic rest pain and tissue loss (i.e. ulceration or necrosis) are key symptoms of CLI (Figure 2). True rest pain usually affects the toes or foot of the limb. It is most pronounced at night when cardiac output is at its lowest and elevation of the leg prevents gravity from assisting perfusion. Patients classically describe hanging the affected leg out of bed to ease symptoms. Arterial ulcers are typically ‘punched-out’ and have a have a white base due to the absence of healthy granulation tissue. They are often found on the dorsum of the foot or digits and usually associated with multiple stenoses or occlusions in the arterial tree.
Peripheral arterial disease (PAD) e Atherosclerosis that leads to arterial stenosis and occlusion in the major vessels supplying the lower extremities6 Intermittent claudication (IC) e Ischaemic muscle discomfort in the lower limb reproducibly produced by exercise and relieved by rest within 10 min6 Critical limb ischaemia (CLI) e Ulcers, gangrene or ischaemic rest pain for more than 2 weeks attributable to objectively proven arterial occlusive disease6 Acute limb ischaemia (ALI) e A sudden decrease in limb perfusion that threatens viability of the limb6
Non-atherosclerotic causes of chronic limb ischaemia When younger patients present with symptoms of claudication, non-atherosclerotic vascular causes should be considered. Athletic patients: popliteal artery entrapment; iliac artery endofibrosis Male heavy smokers: Buerger’s disease (thromboangiitis obliterans) Pain/pulsatile mass in buttock(s): persistent sciatic artery Young patients with no other risk factors: cystic adventitial disease; fibromuscular dysplasia
Box 1
In established CLI the prognosis is poor, so early recognition and prevention are vital. Approximately 12% of patients with CLI will require amputation within 3 months of presentation and up to 25% will die within 1 year.6 Estimated 5-year survival rate for patients with CLI is 50e60% (worse than many cancers)7 and these patients require urgent referral for specialist evaluation. Patients with PAD and diabetes are four times more likely to develop CLI and require amputation than those without diabetes. Microvascular dysfunction and poor collateralization of occluded arteries contributes to reduced peripheral blood flow (Figure 1).6 However, aetiology of ulceration in patients with diabetes is usually multifactorial with infection and neuropathy playing a significant role. ABPI readings are often artificially high in diabetic patients (due to heavy arterial calcification) and whilst 50% of diabetic foot ulcers are ischaemia related, other factors including neuropathy often play a significant role. NICE guidelines recommend that patients with diabetes and foot ulceration
Differential diagnosis: claudication-type symptoms are not always caused by atherosclerotic disease and patients with pathology of the lumbar spine often experience symptoms similar to those of PAD e so called ‘spinal claudication’. These patients differ from those with PAD in that they often report weakness as well as pain when walking and straight leg raise may reproduce their symptoms. Osteoarthritis of the hip or knee may also cause pain.
Figure 1 (a) Typical presentation of foot ischaemia/infection in diabetes. Note generalized swelling and purulent discharge. (b) Good healing after hallux/ 2nd toe amputation (different patient).
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Examination in chronic ischaemia: physical examination should assess the entire cardiovascular system in order to identify other manifestations of cardiovascular disease. Blood pressure, heart rate and cardiac rhythm should be evaluated and the abdomen palpated for evidence of abdominal aortic aneurysm (AAA). Body mass index (BMI) should be calculated from height and weight measurements. Limb temperature and capillary refill time should also be assessed and the feet examined carefully for signs of ulceration or necrosis, with particular attention to the heels and interdigital clefts. All peripheral pulses should be palpated in order to localize the arterial stenosis/occlusion and identify other pathologies such as popliteal aneurysms. When the presence of pulses is in doubt, ankle-brachial pressure index (ABPI) can be measured using a hand-held Doppler (Box 2). However, whilst ABPI is an objective means of assessing distal limb perfusion, falsely high readings are common in patients with diabetes due to heavy arterial calcification.9 Tissue loss is the cardinal sign of CLI, but clinicians should look for other signs of chronic ischaemia such as pallor on limb elevation and hyperaemia when the leg is dependent (Buerger’s sign). This occurs due to the loss of capillary autoregulation in the ischaemic limb. ABPI measurements may be supplemented with toe-brachial pressure index, transcutaneous oxygen assessment or exercise testing. Patients with mild PAD may have a normal resting ABPI despite a good history of IC. If the ABPI is repeated immediately after exercise a significant pressure drop may be identified (a decrease of 15e20% being considered diagnostic of PAD).6
Figure 2 Appearance of a critically ischaemic foot. Note the demarcating, dry necrosis and skin rubor typical of chronic ischaemia.
Pain relieved by lumbar flexion (i.e. sitting) Degenerative lumbar spine disease Spinal canal stenosis (often associated with leg weakness) Lumbar nerve root irritation (may be exacerbated by straight leg raise)
Investigations All patients with suspected PAD should be screened for cardiovascular risk factors.
Pain elicited on joint examination Osteoarthritis of hip or knee
How to measure ankle-brachial pressure index (ABPI) Patient should be resting and supine Place sphygmomanometer cuff just above ankle Measure systolic blood pressure of dorsalis pedis (DP) and posterior tibial (PT) arteries using a hand-held Doppler device Measure systolic blood pressure of the brachial artery (bilaterally) in the same way ABPI = Highest ankle pressure (DP or PT) on that leg Highest arm pressure (right or left) Interpreting results ABPI:
>1.2 0.9-1.2 0.5-0.9 <0.5
Heavy vessel calcification (false elevation of ABPI) Normal range Peripheral arterial disease Critical limb ischaemia*
* Ulceration of the foot may occur at higher ABPIs in patients with diabetes because PAD is often only one component of a multi-factorial aetiology including infection, neuropathy and microvascular dysfunction.
Box 2
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Examination in acute limb ischaemia In assessing an acutely ischaemic limb, the main objective must be to determine the severity and reversibility of ischaemia. As for any patient with suspected arterial disease, a full cardiovascular examination should be performed before assessing for evidence of the ‘six Ps’. Hand-held Doppler should be used to assess arterial flow if pulses are not readily palpable. In the initial stages there may be only mild sensorimotor deficit and at this point the limb is likely to be salvageable if treated promptly. As ischaemia progresses, there may be signs of skin mottling or calf tenderness with tense facial compartments. These are late signs of ischaemia and suggest the limb is at risk if not treated immediately. Fixed mottling or complete loss of sensorimotor function indicates irreversible ischaemia.
All patients Random serum glucose (to exclude occult diabetes) HbA1c (to assess glycaemic control in diabetes) Full blood count (to exclude polycythaemia/anaemia/ thrombocythaemia) Serum urea and creatinine (to exclude renal dysfunction) Serum cholesterol Patients <50 years old Thrombophilia screen Serum homocysteine
Acute limb ischaemia Though PAD frequently manifests as a chronic deterioration of limb perfusion, it is also the leading cause of acute limb ischaemia (ALI), with atherosclerotic plaque rupture or in-situ thrombosis (e.g. thrombosed popliteal aneurysm) leading to arterial occlusion. Embolic occlusion has become less common as the prevalence of rheumatic heart disease has fallen, but it is still frequently encountered and is usually caused by atrial fibrillation. Emboli may also arise from aneurysms or atherosclerotic plaques in more proximal arteries. Atheroembolism can occur spontaneously, but may also be caused iatrogenically during angioplasty or bypass surgery (trash foot). This has a worse prognosis than cardiac embolization, since embolectomy and thrombolysis are less effective and small atheroemboli may pass into very distal vessels of the foot.
Investigations For those with acute ischaemia, standard preoperative blood tests should be performed along with a thrombophilia screen (prior to starting anticoagulation) and a creatine phosphokinase level to exclude rhabdomyolysis. An ECG should also be done to identify potential arrhythmias.
Imaging Duplex ultrasound is the first-line imaging modality for both acute and chronic limb ischaemia, since it is non-invasive, readily available and has a sensitivity of 84e87% and a specificity of 92e98% compared to angiography.9 Although digital subtraction angiography (DSA) was traditionally considered the ‘gold standard’ for detailed arterial assessment, computed tomography angiography (CTA) (Figure 3) and magnetic resonance angiography (MRA) have largely superseded this due to their non-invasive nature. A metaanalysis of 34 studies comprising 1090 patients, found that MRA was highly accurate for assessment of arterial disease throughout the lower extremity and it is now recommended by NICE as the preferred choice of imaging in PAD.10 The role of DSA is now primarily in intervention.
Causes of acute limb ischaemia Embolic Atrial fibrillation Mural thrombus (following acute myocardial infarction) Atherosclerotic embolus Upstream aneurysm Thrombotic Atherosclerosis/plaque rupture Thrombosed bypass graft Thrombosed popliteal aneurysm Prothrombotic states (e.g. malignancy, thrombophilia, polycythaemia) Arteritis (e.g. thromboangiitis obliterans, Takayasu’s arteritis) Low flow states (e.g. due to myocardial infarction, dehydration or sepsis) Rarer causes Direct trauma Compartment syndrome Dissection HIV arteriopathy
Management of chronic limb ischaemia Risk factor modification Approximately 65% of patients with PAD will also have clinically significant cerebral or coronary artery disease and patients with PAD have a sixfold risk of death due to cardiovascular disease compared to those without PAD.11 More than 10% of patients with PAD will suffer stroke, myocardial infarction or death within 2 years of follow up.12 Risk factor modification is therefore extremely important in order to reduce the risk of life-threatening cardiovascular events as well as preventing progression of PAD.6 Smoking is the most significant modifiable risk factor for PAD.6 Smoking cessation is therefore extremely important and is best achieved through a combination of physician advice, group counselling sessions and nicotine replacement therapy (NRT). The addition of antidepressants such as buproprion has also been shown to improve cessation rates.13 For patients with diabetes, glycaemic control is very important since every 1% increase in HbA1c is associated with a 26% increase in the risk of PAD.14 PAD also progresses more rapidly in these
Clinical features: patients with embolic occlusion or acute thrombosis in an otherwise normal arterial tree typically present with severe ischaemic symptoms. The classically described signs of acute ischaemia are the ‘six Ps’ of pain, pallor, pulselessness, perishing cold, paraesthesia and paralysis, though not all of these may be present in every case.
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Figure 3 CT-angiogram images showing (a) normal lower limb arteries and (b) heavily diseased arteries with previous femoral to anterior tibial bypass.
patients and they are five to ten times more likely to require major amputation (i.e. above ankle level) than patients without diabetes. Hypertension should be treated aggressively and angiotensin converting enzyme inhibitors (ACEI) may significantly reduce the risk of cardiovascular events in patients with PAD. b-blockers can also be used safely by these patients and may reduce perioperative cardiovascular events in those requiring surgery.6 A statin should be prescribed to lower cholesterol unless contraindicated, since cardiac-related mortality is reduced by approximately 20% with every 1 mmol/litre reduction in lowdensity lipoprotein cholesterol, irrespective of initial cholesterol level.15 Use of fibrates and niacin should be reserved for those patients who have specific abnormalities of triglycerides or highdensity lipoprotein cholesterol. All patients with PAD should also be on an antiplatelet agent and clopidogrel is now considered to be safer and more effective than aspirin.16 Concurrent use of more than one antiplatelet agent
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is generally not advised for those with simple PAD, but dual antiplatelet therapy may be useful for maintaining graft patency of prosthetic bypass graft. Warfarin is not routinely advised for patients with PAD unless they have another indication for its use. Patients with a BMI greater than 25 kg/m2 should be encouraged to lose weight and take regular exercise,6 though greatest clinical benefit is derived through structured exercise programmes (discussed below). Management of claudication symptoms Exercise: exercise regimes involving at least two sessions of exercise per week may improve a patient’s walking distance by 50e200%. Structured exercise programmes appear to confer greatest benefit, with those in supervised programmes showing 30e35% greater improvement in walking distance after 3 months. NICE therefore recommends that all patients with IC should be offered a supervised exercise programme.10
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For those patients unable to comply with exercise programmes, mechanical intermittent pneumatic compression of the calf may offer some benefit, though evidence for this remains limited.
Though few studies have compared the efficacy of angioplasty and surgical bypass in the treatment of severe limb ischaemia, the BASIL trial (Bypass versus Angioplasty in Severe Ischaemia of the Leg) found no difference between groups for amputation free survival, all-cause mortality or quality of life at 2 years, though the angioplasty group had significantly higher rates of reintervention (28% vs. 17%) and many ultimately required surgery. Subgroup analysis from this study suggests that surgery may be the favoured option for fit patients with usable vein. Vein is used for the bypass whenever possible, as 5-year primary patency rates are far higher than with prosthetic grafts (70% vs. 20% for femoro-distal bypass).6 Angioplasty alone may be beneficial for patients with CLI and infra-inguinal disease who are otherwise too unfit for bypass. Though long-term patency results are poor, short-term improvements in distal perfusion may be sufficient to allow ulcer healing. When revascularization is unlikely to be successful or the patient has comorbidities that might prevent them making use of a salvageable limb, primary amputation may offer the best quality of life. The knee joint is preserved whenever possible for the sake of mobility, though this must be balanced with the need to ensure good wound healing.
Vasoactive drugs: the two drugs currently available in the UK for treatment of intermittent claudication are cilostazol and naftidrofuryl oxalate. Both of these may offer modest improvement in walking distance, though studies of their efficacy have presented very limited follow-up data and cost-effectiveness remains questionable. Though antiplatelet agents (e.g. aspirin) and vasodilators (e.g. nifedipine) are important for reducing overall cardiovascular risk, there is little compelling evidence that these drugs offer any benefit in treating the symptoms of claudication. Intervention for intermittent claudication Intervention should be considered when conservative measures have failed and PAD is severely affecting a patient’s lifestyle or becoming limb threatening. This may be either endovascular (i.e. angioplasty or stenting) or surgical. The most suitable treatment option should be determined on the basis of site/extent of the lesion, patient fitness and local expertise. Patients with focal iliac disease are more likely to be offered endovascular treatment than those with femoral disease, since intervention at iliac level is more durable (Figure 4). Metaanalysis has shown that 5-year patency is 79% after iliac angioplasty versus 55% after femoral angioplasty. However, structured exercise programmes may be just as effective as angioplasty for improving walking distance.6 Surgical bypass is generally reserved for those patients who have debilitating claudication and a pattern of disease not amenable to angioplasty.
Non-surgical management of CLI Non-surgical treatments are generally considered to have little long-term benefit and those patients that are unsuitable for revascularization should be managed symptomatically and undergo amputation as appropriate. Prostanoids such as iloprost may improve healing of ischaemic ulcers as well as reducing pain and amputation rates in those with CLI. However, the long-term benefit remains unproven and their use is therefore limited. Spinal cord stimulation (SCS) may be useful for some patients and has been shown to improve limb salvage rates at 1 year, though the cost-effectiveness of this treatment remains in doubt and it is not widely available There is no clear evidence that lumbar sympathectomy improves limb salvage for patients with unreconstructable CLI, though it may be of use in pain control.
Intervention for critical limb ischaemia Patients with CLI typically have multi-level disease and surgical bypass is often more appropriate, though endovascular techniques may be used as adjuncts to improve flow in vessels proximal or distal to the bypass. Newer technologies such as drug-eluting balloons and stents may improve the efficacy of endovascular techniques. Endovascular techniques to re-open long-segment occlusions (such as sub-intimal angioplasty) have also demonstrated encouraging results in expert hands. TASC guidelines suggest that patients with diffuse aorto-iliac disease should be treated with surgical bypass (unless other factors such as co-morbidity prevent this) and 5-year patency of aorto-bifemoral bypass grafts is over 85% in those with CLI.6
Management of acute limb ischaemia Initial management should involve rapid resuscitation with oxygen, intravenous fluids and analgesia as necessary. Unfractionated heparin should be given intravenously (5000 units) and
Figure 4 Digital subtraction angiography images taken before (a), during (b) and after (c) angioplasty/stenting of the right common iliac artery.
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if the patient is not progressing to surgery immediately a continuous heparin infusion should be started. Diagnostic imaging is only appropriate when patients present with no sensorimotor deficit and the limb is considered to be viable. If the limb is threatened, imaging is unlikely to change management and simply delays revascularization.
found. All patients with ALI should therefore be anticoagulated for 3e6 months and those with evidence of thromboembolism should be considered for longer-term anticoagulation, or antiplatelet therapy if anticoagulation is contraindicated.6 A
Surgical revascularization Embolectomy: once the site of occlusion has been localized clinically, a Fogarty embolectomy catheter can be inserted at femoral (most common) or popliteal level and passed proximally and distally to retrieve the embolus. On-table angiography is then performed to confirm that the vessel has been cleared. If there is evidence of any residual clot, thrombolysis can be given intraoperatively.
REFERENCES 1 Belch JJF, Topol EJ, Agnelli G, et al. Critical issues in peripheral arterial disease detection and management: a call to action. Arch Intern Med 2003; 163: 884e92. 2 Hart W, Guest J. Critical limbs ischaemia: the burden of illness in the UK. Br Med Econ 1995; 8: 211e21. 3 Bønaa KH, Njølstad I, Ueland PM, et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med 2006; 354: 1578e88. 4 Jeffcoate W, Game F. Diabetes, established renal failure and the risk to the lower limb. Pract Diab Int 2006; 23: 28e32. 5 Fowkes FG, Housley E, Cawood EH, Macintyre CC, Ruckley CV, Prescott RJ. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991; 20: 384e92. 6 Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society Consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg 2007; 45: S5e67. 7 ICAI. Long-term mortality and its predictors in patients with critical leg ischaemia. The I.C.A.I. Group (Gruppo di Studio dell’Ischemia Cronica Critica degli Arti Inferiori). The Study Group of Critical Chronic Ischemia of the Lower Extremities. Eur J Vasc Endovasc Surg 1997; 14: 91e5. 8 NICE. Diabetic foot problems: inpatient management of diabetic foot Problems. Clin Guidel 2011; 119. 9 Moneta GL, Yeager RA, Antonovic R, et al. Accuracy of lower extremity arterial duplex mapping. J Vasc Surg 1992; 15: 275e87. 10 NICE. Lower limb peripheral arterial disease: diagnosis and management. Clinical Guideline 147, http://www.nice.org.uk/nicemedia/ live/13856/60426/26.pdf; 2012. 11 Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992; 326: 381e6. 12 Stansby G, Mister R, Fowkes G, et al. High risk of peripheral arterial disease in the United Kingdom: 2-year results of a prospective registry. Angiol 2011; 62: 111e8. 13 Jorenby DE, Leischow SJ, Nides MA, et al. A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 1999; 340: 685e91. 14 Selvin E, Marinopoulos S, Berkenblit G, et al. Meta-analysis: glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Intern Med 2004; 141: 421e31. 15 Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366: 1267e78. 16 Antithrombotic Triallists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Br Med J 2002; 324: 71e86. 17 STILE-Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial. Ann Surg 1994; 220: 251e66. discussion 66e8.
Arterial bypass: embolectomy is sometimes unsuccessful due to heavy atherosclerosis and these patients will require arterial bypass. Similarly, thrombosed popliteal aneurysms are not amenable to embolectomy and femoro-popliteal bypass must be performed with ligation of the native artery proximal and distal to the aneurysm to prevent embolization. Fasciotomy: if the affected limb has been severely ischaemic, reperfusion often causes significant muscle oedema and fourcompartment fasciotomies should therefore be performed to prevent compartment syndrome. Fasciotomy wounds can be allowed to heal by secondary intention or undergo split skin grafting. Catheter-directed thrombolysis When the limb is not immediately threatened, catheter-directed thrombolysis (CDT) may be used to try and clear the occlusive thrombus. Simultaneous thrombectomy (aspiration or mechanical) may also be used to improve clot dissolution. CDT is particularly useful for patients with occluded prosthetic bypass grafts for whom surgical re-intervention may be challenging. Thrombolysis is less invasive than surgery and has the advantage of clarifying the underlying lesion and allowing angioplasty if necessary. However, it can also be associated with serious complications such as bleeding, stroke or embolization. Contraindications to thrombolysis include: surgery within 2 weeks stroke or neurosurgery within 2 months recent gastrointestinal bleeding trauma. The few trials that have compared thrombolysis to surgery in acute limb ischaemia have failed to show any significant difference in limb salvage rates and its use should therefore be based on local expertise and availability.17 Amputation Up to 10% of individuals with ALI present with irreversible ischaemia and these patients should undergo primary amputation of the affected limb. Revascularization should not be attempted, as the release of toxic metabolites from the ischaemic tissue is frequently fatal. Further management Following revascularization it is important to try and identify the source of emboli, though in many cases no clear cause will be
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Acute and chronic lower limb ischaemia
Non-modifiable risk factors include: age gender ethnicity. Modifiable risk factors include: smoking diabetes mellitus/poor glycaemic control hypertension hyperlipidaemia hypercoagulability.
George Peach Ian M Loftus
Abstract Limb ischaemia is a common clinical condition that causes considerable morbidity and mortality and represents a major drain on healthcare resources. Peripheral arterial disease (PAD) is the leading cause of both acute and chronic limb ischaemia. Chronic limb ischaemia may also be caused by non-atherosclerotic processes such as arterial entrapment, fibrosis or arteritis. Acute limb ischaemia may be also due to embolism, thrombosis or trauma. Duplex ultrasonography, computed tomography angiography and magnetic resonance angiography are now conventional forms of arterial imaging, with catheter angiography reserved for intervention. Risk factor modification is extremely important for all these patients, since many will also have significant coronary or cerebrovascular disease. Those with claudication often improve with structured exercise and if symptoms progress they may benefit from angioplasty or stenting. Arterial bypass remains the mainstay of treatment for patients with critical limb ischaemia if they are fit enough for surgery. Acute limb ischaemia is a surgical emergency and can be treated with surgical embolectomy or catheter-directed thrombolysis (depending on local expertise). Patients with irreversible limb ischaemia should be treated with primary amputation or palliation as appropriate.
Other factors Up to 30% of young patients with PAD have high homocysteine levels (compared to 1% in the general population) and there is now evidence that this is an independent risk factor for PAD.3 Raised haematocrit, high plasma fibrinogen levels and chronic renal insufficiency also seem to be linked to an increased risk of PAD though evidence for these links being causal remains limited. Patients with both end-stage renal disease and diabetes are at extremely high risk of limb loss.4 Intermittent claudication (IC) Though many never develop symptoms, up to 15% of patients with asymptomatic PAD will develop IC within 5 years.5 Of those who do develop IC, only 20e25% are likely to experience further clinical deterioration.6 Major amputation is rare (other than in those with diabetes) and patients should be reassured accordingly. Only 1e3% of patients with IC will require major amputation within a 5-year period.6 Clinical features: intermittent claudication is an aching muscle pain, brought on by exercise, and rapidly relieved by rest. Pain arises due to increased oxygen demand of the tissues during exercise. Symptoms are determined by site of disease and since PAD most commonly affects the superficial femoral artery (SFA), pain is usually felt in the calf (i.e. distal to the arterial stenosis/ occlusion). Disease of aorto-iliac, common femoral or tibioperoneal vessels may give rise to pain in the buttock, thigh or foot respectively. The presence of bilateral symptoms may indicate aortic disease, bilateral iliac disease or non-vascular aetiology. Claudication typically comes on after walking a pain-free distance (unlike the pain of osteoarthritis etc.) and is worse when walking fast or uphill, when muscle oxygen requirements are at their highest. Though reported claudication distances are notoriously inaccurate as a measure of disease severity, serial assessment of walking ability over months can be a useful indicator of clinical improvement or deterioration. Symptoms of chronic PAD (Box 1) generally develop over months or even years, with a gradual deterioration in pain-free walking distance. Rapid deterioration of symptoms or sudden onset of claudication are important warning signs which may indicate new arterial occlusion.
Keywords Acute leg ischaemia; angioplasty; arterial bypass; limb ischaemia; peripheral artery disease
Chronic limb ischaemia The most common cause of chronic lower limb ischaemia is atherosclerotic peripheral arterial disease (PAD). PAD has an estimated worldwide prevalence of nearly 10%, rising to as much as 15e20% in those over 70 years of age and affects some 27 million people in Europe and North America alone.1 Critical limb ischaemia (CLI) e the most severe manifestation of PAD e may lead to limb loss or even death unless treated promptly. Each year, 500e1000 new cases of CLI are diagnosed per million of the population, with an estimated annual cost to the NHS of more than £200 million.2 Risk factors The development of atherosclerotic PAD is a multifactorial process involving both modifiable and non-modifiable risk factors.
George Peach MBChB MRCS is a Clinical Research Fellow at St George’s Vascular Institute, London, UK. Conflicts of interest: none declared.
Critical limb ischaemia Whilst some patients follow steady progression from asymptomatic PAD to IC and then CLI, this is the exception rather than the rule. Patients with PAD often have significant co-morbidity limiting physical activity and may develop CLI without preceding IC.
Ian M Loftus MBChB MD FRCS is Consultant Vascular Surgeon and Reader in Vascular Science at St George’s Vascular Institute, London, UK. Conflicts of interest: none declared.
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should be seen by a multidisciplinary diabetic foot team within 24 hours.8
Definitions
Clinical features: ischaemic rest pain and tissue loss (i.e. ulceration or necrosis) are key symptoms of CLI (Figure 2). True rest pain usually affects the toes or foot of the limb. It is most pronounced at night when cardiac output is at its lowest and elevation of the leg prevents gravity from assisting perfusion. Patients classically describe hanging the affected leg out of bed to ease symptoms. Arterial ulcers are typically ‘punched-out’ and have a have a white base due to the absence of healthy granulation tissue. They are often found on the dorsum of the foot or digits and usually associated with multiple stenoses or occlusions in the arterial tree.
Peripheral arterial disease (PAD) e Atherosclerosis that leads to arterial stenosis and occlusion in the major vessels supplying the lower extremities6 Intermittent claudication (IC) e Ischaemic muscle discomfort in the lower limb reproducibly produced by exercise and relieved by rest within 10 min6 Critical limb ischaemia (CLI) e Ulcers, gangrene or ischaemic rest pain for more than 2 weeks attributable to objectively proven arterial occlusive disease6 Acute limb ischaemia (ALI) e A sudden decrease in limb perfusion that threatens viability of the limb6
Non-atherosclerotic causes of chronic limb ischaemia When younger patients present with symptoms of claudication, non-atherosclerotic vascular causes should be considered. Athletic patients: popliteal artery entrapment; iliac artery endofibrosis Male heavy smokers: Buerger’s disease (thromboangiitis obliterans) Pain/pulsatile mass in buttock(s): persistent sciatic artery Young patients with no other risk factors: cystic adventitial disease; fibromuscular dysplasia
Box 1
In established CLI the prognosis is poor, so early recognition and prevention are vital. Approximately 12% of patients with CLI will require amputation within 3 months of presentation and up to 25% will die within 1 year.6 Estimated 5-year survival rate for patients with CLI is 50e60% (worse than many cancers)7 and these patients require urgent referral for specialist evaluation. Patients with PAD and diabetes are four times more likely to develop CLI and require amputation than those without diabetes. Microvascular dysfunction and poor collateralization of occluded arteries contributes to reduced peripheral blood flow (Figure 1).6 However, aetiology of ulceration in patients with diabetes is usually multifactorial with infection and neuropathy playing a significant role. ABPI readings are often artificially high in diabetic patients (due to heavy arterial calcification) and whilst 50% of diabetic foot ulcers are ischaemia related, other factors including neuropathy often play a significant role. NICE guidelines recommend that patients with diabetes and foot ulceration
Differential diagnosis: claudication-type symptoms are not always caused by atherosclerotic disease and patients with pathology of the lumbar spine often experience symptoms similar to those of PAD e so called ‘spinal claudication’. These patients differ from those with PAD in that they often report weakness as well as pain when walking and straight leg raise may reproduce their symptoms. Osteoarthritis of the hip or knee may also cause pain.
Figure 1 (a) Typical presentation of foot ischaemia/infection in diabetes. Note generalized swelling and purulent discharge. (b) Good healing after hallux/ 2nd toe amputation (different patient).
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Examination in chronic ischaemia: physical examination should assess the entire cardiovascular system in order to identify other manifestations of cardiovascular disease. Blood pressure, heart rate and cardiac rhythm should be evaluated and the abdomen palpated for evidence of abdominal aortic aneurysm (AAA). Body mass index (BMI) should be calculated from height and weight measurements. Limb temperature and capillary refill time should also be assessed and the feet examined carefully for signs of ulceration or necrosis, with particular attention to the heels and interdigital clefts. All peripheral pulses should be palpated in order to localize the arterial stenosis/occlusion and identify other pathologies such as popliteal aneurysms. When the presence of pulses is in doubt, ankle-brachial pressure index (ABPI) can be measured using a hand-held Doppler (Box 2). However, whilst ABPI is an objective means of assessing distal limb perfusion, falsely high readings are common in patients with diabetes due to heavy arterial calcification.9 Tissue loss is the cardinal sign of CLI, but clinicians should look for other signs of chronic ischaemia such as pallor on limb elevation and hyperaemia when the leg is dependent (Buerger’s sign). This occurs due to the loss of capillary autoregulation in the ischaemic limb. ABPI measurements may be supplemented with toe-brachial pressure index, transcutaneous oxygen assessment or exercise testing. Patients with mild PAD may have a normal resting ABPI despite a good history of IC. If the ABPI is repeated immediately after exercise a significant pressure drop may be identified (a decrease of 15e20% being considered diagnostic of PAD).6
Figure 2 Appearance of a critically ischaemic foot. Note the demarcating, dry necrosis and skin rubor typical of chronic ischaemia.
Pain relieved by lumbar flexion (i.e. sitting) Degenerative lumbar spine disease Spinal canal stenosis (often associated with leg weakness) Lumbar nerve root irritation (may be exacerbated by straight leg raise)
Investigations All patients with suspected PAD should be screened for cardiovascular risk factors.
Pain elicited on joint examination Osteoarthritis of hip or knee
How to measure ankle-brachial pressure index (ABPI) Patient should be resting and supine Place sphygmomanometer cuff just above ankle Measure systolic blood pressure of dorsalis pedis (DP) and posterior tibial (PT) arteries using a hand-held Doppler device Measure systolic blood pressure of the brachial artery (bilaterally) in the same way ABPI = Highest ankle pressure (DP or PT) on that leg Highest arm pressure (right or left) Interpreting results ABPI:
>1.2 0.9-1.2 0.5-0.9 <0.5
Heavy vessel calcification (false elevation of ABPI) Normal range Peripheral arterial disease Critical limb ischaemia*
* Ulceration of the foot may occur at higher ABPIs in patients with diabetes because PAD is often only one component of a multi-factorial aetiology including infection, neuropathy and microvascular dysfunction.
Box 2
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Examination in acute limb ischaemia In assessing an acutely ischaemic limb, the main objective must be to determine the severity and reversibility of ischaemia. As for any patient with suspected arterial disease, a full cardiovascular examination should be performed before assessing for evidence of the ‘six Ps’. Hand-held Doppler should be used to assess arterial flow if pulses are not readily palpable. In the initial stages there may be only mild sensorimotor deficit and at this point the limb is likely to be salvageable if treated promptly. As ischaemia progresses, there may be signs of skin mottling or calf tenderness with tense facial compartments. These are late signs of ischaemia and suggest the limb is at risk if not treated immediately. Fixed mottling or complete loss of sensorimotor function indicates irreversible ischaemia.
All patients Random serum glucose (to exclude occult diabetes) HbA1c (to assess glycaemic control in diabetes) Full blood count (to exclude polycythaemia/anaemia/ thrombocythaemia) Serum urea and creatinine (to exclude renal dysfunction) Serum cholesterol Patients <50 years old Thrombophilia screen Serum homocysteine
Acute limb ischaemia Though PAD frequently manifests as a chronic deterioration of limb perfusion, it is also the leading cause of acute limb ischaemia (ALI), with atherosclerotic plaque rupture or in-situ thrombosis (e.g. thrombosed popliteal aneurysm) leading to arterial occlusion. Embolic occlusion has become less common as the prevalence of rheumatic heart disease has fallen, but it is still frequently encountered and is usually caused by atrial fibrillation. Emboli may also arise from aneurysms or atherosclerotic plaques in more proximal arteries. Atheroembolism can occur spontaneously, but may also be caused iatrogenically during angioplasty or bypass surgery (trash foot). This has a worse prognosis than cardiac embolization, since embolectomy and thrombolysis are less effective and small atheroemboli may pass into very distal vessels of the foot.
Investigations For those with acute ischaemia, standard preoperative blood tests should be performed along with a thrombophilia screen (prior to starting anticoagulation) and a creatine phosphokinase level to exclude rhabdomyolysis. An ECG should also be done to identify potential arrhythmias.
Imaging Duplex ultrasound is the first-line imaging modality for both acute and chronic limb ischaemia, since it is non-invasive, readily available and has a sensitivity of 84e87% and a specificity of 92e98% compared to angiography.9 Although digital subtraction angiography (DSA) was traditionally considered the ‘gold standard’ for detailed arterial assessment, computed tomography angiography (CTA) (Figure 3) and magnetic resonance angiography (MRA) have largely superseded this due to their non-invasive nature. A metaanalysis of 34 studies comprising 1090 patients, found that MRA was highly accurate for assessment of arterial disease throughout the lower extremity and it is now recommended by NICE as the preferred choice of imaging in PAD.10 The role of DSA is now primarily in intervention.
Causes of acute limb ischaemia Embolic Atrial fibrillation Mural thrombus (following acute myocardial infarction) Atherosclerotic embolus Upstream aneurysm Thrombotic Atherosclerosis/plaque rupture Thrombosed bypass graft Thrombosed popliteal aneurysm Prothrombotic states (e.g. malignancy, thrombophilia, polycythaemia) Arteritis (e.g. thromboangiitis obliterans, Takayasu’s arteritis) Low flow states (e.g. due to myocardial infarction, dehydration or sepsis) Rarer causes Direct trauma Compartment syndrome Dissection HIV arteriopathy
Management of chronic limb ischaemia Risk factor modification Approximately 65% of patients with PAD will also have clinically significant cerebral or coronary artery disease and patients with PAD have a sixfold risk of death due to cardiovascular disease compared to those without PAD.11 More than 10% of patients with PAD will suffer stroke, myocardial infarction or death within 2 years of follow up.12 Risk factor modification is therefore extremely important in order to reduce the risk of life-threatening cardiovascular events as well as preventing progression of PAD.6 Smoking is the most significant modifiable risk factor for PAD.6 Smoking cessation is therefore extremely important and is best achieved through a combination of physician advice, group counselling sessions and nicotine replacement therapy (NRT). The addition of antidepressants such as buproprion has also been shown to improve cessation rates.13 For patients with diabetes, glycaemic control is very important since every 1% increase in HbA1c is associated with a 26% increase in the risk of PAD.14 PAD also progresses more rapidly in these
Clinical features: patients with embolic occlusion or acute thrombosis in an otherwise normal arterial tree typically present with severe ischaemic symptoms. The classically described signs of acute ischaemia are the ‘six Ps’ of pain, pallor, pulselessness, perishing cold, paraesthesia and paralysis, though not all of these may be present in every case.
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Figure 3 CT-angiogram images showing (a) normal lower limb arteries and (b) heavily diseased arteries with previous femoral to anterior tibial bypass.
patients and they are five to ten times more likely to require major amputation (i.e. above ankle level) than patients without diabetes. Hypertension should be treated aggressively and angiotensin converting enzyme inhibitors (ACEI) may significantly reduce the risk of cardiovascular events in patients with PAD. b-blockers can also be used safely by these patients and may reduce perioperative cardiovascular events in those requiring surgery.6 A statin should be prescribed to lower cholesterol unless contraindicated, since cardiac-related mortality is reduced by approximately 20% with every 1 mmol/litre reduction in lowdensity lipoprotein cholesterol, irrespective of initial cholesterol level.15 Use of fibrates and niacin should be reserved for those patients who have specific abnormalities of triglycerides or highdensity lipoprotein cholesterol. All patients with PAD should also be on an antiplatelet agent and clopidogrel is now considered to be safer and more effective than aspirin.16 Concurrent use of more than one antiplatelet agent
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is generally not advised for those with simple PAD, but dual antiplatelet therapy may be useful for maintaining graft patency of prosthetic bypass graft. Warfarin is not routinely advised for patients with PAD unless they have another indication for its use. Patients with a BMI greater than 25 kg/m2 should be encouraged to lose weight and take regular exercise,6 though greatest clinical benefit is derived through structured exercise programmes (discussed below). Management of claudication symptoms Exercise: exercise regimes involving at least two sessions of exercise per week may improve a patient’s walking distance by 50e200%. Structured exercise programmes appear to confer greatest benefit, with those in supervised programmes showing 30e35% greater improvement in walking distance after 3 months. NICE therefore recommends that all patients with IC should be offered a supervised exercise programme.10
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For those patients unable to comply with exercise programmes, mechanical intermittent pneumatic compression of the calf may offer some benefit, though evidence for this remains limited.
Though few studies have compared the efficacy of angioplasty and surgical bypass in the treatment of severe limb ischaemia, the BASIL trial (Bypass versus Angioplasty in Severe Ischaemia of the Leg) found no difference between groups for amputation free survival, all-cause mortality or quality of life at 2 years, though the angioplasty group had significantly higher rates of reintervention (28% vs. 17%) and many ultimately required surgery. Subgroup analysis from this study suggests that surgery may be the favoured option for fit patients with usable vein. Vein is used for the bypass whenever possible, as 5-year primary patency rates are far higher than with prosthetic grafts (70% vs. 20% for femoro-distal bypass).6 Angioplasty alone may be beneficial for patients with CLI and infra-inguinal disease who are otherwise too unfit for bypass. Though long-term patency results are poor, short-term improvements in distal perfusion may be sufficient to allow ulcer healing. When revascularization is unlikely to be successful or the patient has comorbidities that might prevent them making use of a salvageable limb, primary amputation may offer the best quality of life. The knee joint is preserved whenever possible for the sake of mobility, though this must be balanced with the need to ensure good wound healing.
Vasoactive drugs: the two drugs currently available in the UK for treatment of intermittent claudication are cilostazol and naftidrofuryl oxalate. Both of these may offer modest improvement in walking distance, though studies of their efficacy have presented very limited follow-up data and cost-effectiveness remains questionable. Though antiplatelet agents (e.g. aspirin) and vasodilators (e.g. nifedipine) are important for reducing overall cardiovascular risk, there is little compelling evidence that these drugs offer any benefit in treating the symptoms of claudication. Intervention for intermittent claudication Intervention should be considered when conservative measures have failed and PAD is severely affecting a patient’s lifestyle or becoming limb threatening. This may be either endovascular (i.e. angioplasty or stenting) or surgical. The most suitable treatment option should be determined on the basis of site/extent of the lesion, patient fitness and local expertise. Patients with focal iliac disease are more likely to be offered endovascular treatment than those with femoral disease, since intervention at iliac level is more durable (Figure 4). Metaanalysis has shown that 5-year patency is 79% after iliac angioplasty versus 55% after femoral angioplasty. However, structured exercise programmes may be just as effective as angioplasty for improving walking distance.6 Surgical bypass is generally reserved for those patients who have debilitating claudication and a pattern of disease not amenable to angioplasty.
Non-surgical management of CLI Non-surgical treatments are generally considered to have little long-term benefit and those patients that are unsuitable for revascularization should be managed symptomatically and undergo amputation as appropriate. Prostanoids such as iloprost may improve healing of ischaemic ulcers as well as reducing pain and amputation rates in those with CLI. However, the long-term benefit remains unproven and their use is therefore limited. Spinal cord stimulation (SCS) may be useful for some patients and has been shown to improve limb salvage rates at 1 year, though the cost-effectiveness of this treatment remains in doubt and it is not widely available There is no clear evidence that lumbar sympathectomy improves limb salvage for patients with unreconstructable CLI, though it may be of use in pain control.
Intervention for critical limb ischaemia Patients with CLI typically have multi-level disease and surgical bypass is often more appropriate, though endovascular techniques may be used as adjuncts to improve flow in vessels proximal or distal to the bypass. Newer technologies such as drug-eluting balloons and stents may improve the efficacy of endovascular techniques. Endovascular techniques to re-open long-segment occlusions (such as sub-intimal angioplasty) have also demonstrated encouraging results in expert hands. TASC guidelines suggest that patients with diffuse aorto-iliac disease should be treated with surgical bypass (unless other factors such as co-morbidity prevent this) and 5-year patency of aorto-bifemoral bypass grafts is over 85% in those with CLI.6
Management of acute limb ischaemia Initial management should involve rapid resuscitation with oxygen, intravenous fluids and analgesia as necessary. Unfractionated heparin should be given intravenously (5000 units) and
Figure 4 Digital subtraction angiography images taken before (a), during (b) and after (c) angioplasty/stenting of the right common iliac artery.
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if the patient is not progressing to surgery immediately a continuous heparin infusion should be started. Diagnostic imaging is only appropriate when patients present with no sensorimotor deficit and the limb is considered to be viable. If the limb is threatened, imaging is unlikely to change management and simply delays revascularization.
found. All patients with ALI should therefore be anticoagulated for 3e6 months and those with evidence of thromboembolism should be considered for longer-term anticoagulation, or antiplatelet therapy if anticoagulation is contraindicated.6 A
Surgical revascularization Embolectomy: once the site of occlusion has been localized clinically, a Fogarty embolectomy catheter can be inserted at femoral (most common) or popliteal level and passed proximally and distally to retrieve the embolus. On-table angiography is then performed to confirm that the vessel has been cleared. If there is evidence of any residual clot, thrombolysis can be given intraoperatively.
REFERENCES 1 Belch JJF, Topol EJ, Agnelli G, et al. Critical issues in peripheral arterial disease detection and management: a call to action. Arch Intern Med 2003; 163: 884e92. 2 Hart W, Guest J. Critical limbs ischaemia: the burden of illness in the UK. Br Med Econ 1995; 8: 211e21. 3 Bønaa KH, Njølstad I, Ueland PM, et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med 2006; 354: 1578e88. 4 Jeffcoate W, Game F. Diabetes, established renal failure and the risk to the lower limb. Pract Diab Int 2006; 23: 28e32. 5 Fowkes FG, Housley E, Cawood EH, Macintyre CC, Ruckley CV, Prescott RJ. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991; 20: 384e92. 6 Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society Consensus for the management of peripheral arterial disease (TASC II). J Vasc Surg 2007; 45: S5e67. 7 ICAI. Long-term mortality and its predictors in patients with critical leg ischaemia. The I.C.A.I. Group (Gruppo di Studio dell’Ischemia Cronica Critica degli Arti Inferiori). The Study Group of Critical Chronic Ischemia of the Lower Extremities. Eur J Vasc Endovasc Surg 1997; 14: 91e5. 8 NICE. Diabetic foot problems: inpatient management of diabetic foot Problems. Clin Guidel 2011; 119. 9 Moneta GL, Yeager RA, Antonovic R, et al. Accuracy of lower extremity arterial duplex mapping. J Vasc Surg 1992; 15: 275e87. 10 NICE. Lower limb peripheral arterial disease: diagnosis and management. Clinical Guideline 147, http://www.nice.org.uk/nicemedia/ live/13856/60426/26.pdf; 2012. 11 Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992; 326: 381e6. 12 Stansby G, Mister R, Fowkes G, et al. High risk of peripheral arterial disease in the United Kingdom: 2-year results of a prospective registry. Angiol 2011; 62: 111e8. 13 Jorenby DE, Leischow SJ, Nides MA, et al. A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 1999; 340: 685e91. 14 Selvin E, Marinopoulos S, Berkenblit G, et al. Meta-analysis: glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Intern Med 2004; 141: 421e31. 15 Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366: 1267e78. 16 Antithrombotic Triallists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Br Med J 2002; 324: 71e86. 17 STILE-Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial. Ann Surg 1994; 220: 251e66. discussion 66e8.
Arterial bypass: embolectomy is sometimes unsuccessful due to heavy atherosclerosis and these patients will require arterial bypass. Similarly, thrombosed popliteal aneurysms are not amenable to embolectomy and femoro-popliteal bypass must be performed with ligation of the native artery proximal and distal to the aneurysm to prevent embolization. Fasciotomy: if the affected limb has been severely ischaemic, reperfusion often causes significant muscle oedema and fourcompartment fasciotomies should therefore be performed to prevent compartment syndrome. Fasciotomy wounds can be allowed to heal by secondary intention or undergo split skin grafting. Catheter-directed thrombolysis When the limb is not immediately threatened, catheter-directed thrombolysis (CDT) may be used to try and clear the occlusive thrombus. Simultaneous thrombectomy (aspiration or mechanical) may also be used to improve clot dissolution. CDT is particularly useful for patients with occluded prosthetic bypass grafts for whom surgical re-intervention may be challenging. Thrombolysis is less invasive than surgery and has the advantage of clarifying the underlying lesion and allowing angioplasty if necessary. However, it can also be associated with serious complications such as bleeding, stroke or embolization. Contraindications to thrombolysis include: surgery within 2 weeks stroke or neurosurgery within 2 months recent gastrointestinal bleeding trauma. The few trials that have compared thrombolysis to surgery in acute limb ischaemia have failed to show any significant difference in limb salvage rates and its use should therefore be based on local expertise and availability.17 Amputation Up to 10% of individuals with ALI present with irreversible ischaemia and these patients should undergo primary amputation of the affected limb. Revascularization should not be attempted, as the release of toxic metabolites from the ischaemic tissue is frequently fatal. Further management Following revascularization it is important to try and identify the source of emboli, though in many cases no clear cause will be
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