Management of acute lower limb ischaemia

Embolism

Until about 30 years ago, embolic disease was the underlying cause of most cases of ALI. Emboli large enough to occlude major vessels usually arise in the heart. Rheumatic mitral valve disease was the most common cause, with large emboli forming in a dilated left atrium.

Atrial fibrillation caused by ischaemic heart disease is now the cardiac origin in 80% of embolic cases; mural thrombus following acute myocardial infarction causes most of the remainder. Less commonly, embolisation originates from mural thrombi of the aorta, aortic or popliteal aneurysms and iliac arteries. Large emboli typically lodge at an arterial bifurcation, particularly in the common femoral or popliteal arteries ( Fig. 8.1 ). Patients with cardiac embolism may also have co-existing PAD as a result of the underlying process of atherosclerosis. This increases the difficulty in establishing the cause of the ischaemia and in planning revascularisation. In 20% of patients with ALI, a source for the embolus cannot be found.

Atheroembolism

Less common sources of emboli include proximal aneurysms or atherosclerotic plaques, usually located in the thoracic or abdominal aorta, or arising from popliteal artery aneurysm. Whereas cardiac embolism usually consists entirely of platelet-rich thrombus, embolism from proximal arteries can include atherosclerotic plaques or cholesterol-rich emboli. This has a much worse prognosis than cardiac embolism because embolectomy is less effective – small particles of atheroembolism can pass to very distal vessels in the foot. This digital embolism can result in the ‘acute blue toe syndrome’. In this condition, the embolic source should be identified and treated if possible. Often, this is a proximal arterial plaque that has ruptured, and the emboli are a mixture of platelet-rich thrombus and cholesterol ( Fig. 8.2 ).

Embolisation of cholesterol-rich atheroma can occur spontaneously, but also follows intra-arterial manipulation following endovascular intervention, or occasionally surgery (causing ‘trash foot’). This can be disastrous, since both large and small arteries may be occluded, and it may not be possible to revascularise with either surgery or thrombolysis. This may result in limb or end-organ damage and is sometimes fatal ( Fig. 8.3 ).

Thrombosis

In-situ thrombosis in a native artery is now the most frequent cause of ALI, commonly in patients with a high atherosclerotic burden. It may be the result of rupture of an atherosclerotic plaque or critical flow arrest at the site of an atherosclerotic stenosis. The advancing age of the population and the commensurate increase in atherosclerosis have increased the proportion of ALI caused by thrombosis. Acute native vessel arterial occlusion may also be caused by surgery (e.g., knee replacement disrupting the geniculate collateral vessels formed around a popliteal occlusion), heart failure, thrombotic tendency (polycythaemia, dehydration, malignancy, etc.) or trauma.

Acute thrombosis of a popliteal aneurysm poses the highest risk to the leg. Typically, this occurs in elderly men in association with aneurysms elsewhere (50% have an aortic aneurysm) or generalised arterial ectasia. As they enlarge, popliteal artery aneurysms can fill with lamellar thrombus, which may cause either acute thrombosis or distal embolisation that occludes the tibial vessels. The latter will place the leg in extreme jeopardy, with up to 30% risk of limb loss. It is much more common for a popliteal artery aneurysm to cause distal embolisation than to rupture.

Other CAUSES

The increasing use of both open and endovascular techniques to revascularise ischaemic limbs means that surgeons often have to deal with acute thrombosis of bypass grafts and arteries that have previously undergone endovascular treatment. Grafts occlude for a variety of reasons. Within 1 month of insertion, graft occlusion is usually the result of technical problems at the time of surgery or poor distal run-off. Graft occlusion within 1 year of placement is often caused by myointimal hyperplasia at an anastomosis or the development of stenoses within a vein graft. Occlusion after 1 year is usually caused by progression of distal atherosclerosis. Prosthetic grafts have a higher occlusion rate than autogenous vein grafts (see Chapter 7Chapter 3Chapter 7 ).

Iliac limb occlusions are observed after aorto-bifemoral bypass surgery if limbs become kinked or have poor outflow. Endovascular stent grafts used to repair abdominal aortic aneurysms (endovascular aneurysm repair [EVAR]) have similar modes of failure. Occlusion is more common when the iliac limb of the stent graft is extended into the external iliac artery. Occlusion may occur any time after implantation in up to 5% of patients.

A special group of iatrogenic occlusion of external iliac and femoral vessels is related to the maldeployment or failure of arterial closure devices. These achieve closure of arteries after endovascular intervention using percutaneously delivered sutures or plugs. Inadvertently, they can cause arrest of flow through direct closure or stenosis of the artery, or by dissection of the vessel. Presentation is usually in the early post-intervention period but may be delayed.

Spontaneous native arterial thrombosis occasionally occurs without an underlying flow-limiting stenosis and these patients should be investigated for an intrinsic clotting abnormality/thrombophilia, for example, antiphospholipid syndrome, activated protein C deficiency or malignancy.

Occasionally, acute arterial occlusion may be caused by arterial dissection, trauma, extrinsic compression or illicit drug use (cocaine and ‘crack’ cocaine). In a young patient with acute popliteal artery occlusion, either popliteal entrapment or cystic adventitial disease should be considered (see Chapter 2 on chronic limb ischaemia).

Recent changes

A number of factors may have changed the presentation of ALI. The incidence of co-existing PAD is increasing, meaning that revascularisation can be more challenging in the acute setting. Medical therapy has improved and many patients are now treated with cardioprotective drugs such as antiplatelet therapy and statins if they have risk factors for cardiovascular disease. Antiplatelet therapy probably reduces the risk of deterioration and the need for limb revascularisation in those patients with established PAD. Recent evidence suggests that low-dose (2.5 mg) rivaroxaban twice a day, in combination with low-dose (100 mg) aspirin may significantly reduce the risk of ALI when compared to aspirin alone. Similarly, patients with atrial fibrillation are often established on anticoagulation to reduce their risk of embolic complications. However, despite adequate anticoagulation, some patients do still present with ALI.

A randomised double-blind placebo-controlled trial evaluating Vorapaxar used ALI as one of the endpoints. The investigators demonstrated that, in selected patients with symptomatic PAD without atrial fibrillation, Vorapaxar reduced the incidence of ALI regardless of the cause. With further research, this protease-activated receptor 1 antagonist could be used to reduce the risk of ALI in patients with known PAD, however it has not yet been widely adopted.

Radiological investigations

Diagnostic imaging is recommended to guide treatment, unless it poses a significant delay to treatment, or if the need for primary amputation is obvious. The recent European Society for Vascular and Endovascular Surgery (ESVS) guidelines on acute limb ischaemia recommend computed tomography angiography (CTA) in the first instance. Duplex ultrasound or contrast-enhanced magnetic resonance angiography (MRA) are alternatives, depending on availability. In practice, MRA is rarely used in the acute setting because of its long acquisition time and often limited immediate availability. Concerns about the use of contrast-enhanced imaging in the context of acute renal failure may be considered a relative problem when facing this life- and limb-threatening condition. Anatomical coverage of a standard lower limb CTA should extend from the renal arteries to the feet, with a second acquisition for the crural arteries if required.

Irreversible (Rutherford category III) leg ischaemia

A small number of patients will present in a moribund state or with irreversible leg ischaemia (muscle paralysis, tense swollen fascial compartments, fixed skin staining) and terminal care should be considered. For the irreversibly ischaemic leg, revascularisation is, by definition, inappropriate and may be dangerous, owing to the risk of ischaemia-reperfusion injury and subsequent systemic inflammatory response syndrome. This includes the patient who develops ALI while being treated for another condition, usually as an inpatient on an elderly care ward. Prognosis is particularly dismal in this group. Surviving patients should be resuscitated and stabilised before considering primary amputation.

Immediately threatened (Rutherford category IIb ischaemia)

The acute white leg with sensorimotor deficit requires urgent intervention to prevent limb loss. Although the differentiation between thrombosis and embolus can be difficult, it is in this group of patients that embolism is more likely. An acute white leg with no prior history of claudication, normal contralateral pulses and a probable embolic source, such as atrial fibrillation, would indicate that embolisation is the most likely cause. Urgent revascularisation is indicated in these patients, after resuscitation. Traditionally, patients with Rutherford IIb ischaemia have been managed preferentially with an open approach given the requirement for swift restoration of blood flow, however, this dogma has been challenged recently with improvements in the ability to restore flow rapidly using a variety of advanced endovascular tehcniques. Operative approaches may include surgical thromboembolectomy, bypass, percutaneous catheter-directed thrombolysis (CDT), mechanical thrombectomy, thrombus aspiration (with or without CDT) and hybrid procedures such as thromboendarterectomy.