An embolus consists of undissolved material which is carried in the circulation and impacts in a blood vessel, usually blocking it. The most common source of arterial embolism is the left atrium in atrial fibrillation, accounting for two-thirds of all cases. Thrombus forms because of stasis in the enlarged and fibrillating atrium, and fragments detach to enter the arterial circulation (Fig. 1) 344. Thrombi can also form on the damaged endocardium of the left ventricle after myocardial infarction, and arrhythmias cause these to detach and embolize. Other causes of emboli from the heart are shown in Table 1 196.

Emboli can arise from the aorta and its branches (Figs. 2 and 3) 345,346. Atheromatous plaques may rupture, allowing cholesterol debris to pass distally and block small arteries. Platelet thrombi forming on ulcerated atheromatous stenoses may also embolize. Thrombus forming in aneurysms due to abnormal patterns of blood flow can also form an embolism and this is a particular danger in the case of popliteal aneurysms. Table 1 196 lists the common sites of origin for arterial ‘atheroemboli’, and other rare causes of embolism. The clinical effects of small emboli are described later.

Emboli usually lodge at the bifurcations of arteries, because the diameter of each major branch is less than that of the main branching vessel.

In surgical practice most arterial emboli affect the limbs, the leg being affected six times more often than the arm (Table 2) 197. Limb emboli are considered in detail below.

The brain is a frequent site of embolism, resulting in stroke. Small emboli passing up the internal carotid artery may also enter the retinal vessels, causing temporary or permanent blindness. If carotid atheroma is the source for recurrent emboli to the eye or brain then carotid endarterectomy may be required, although many patients are treated by antithrombotic drugs such as aspirin.

The superior mesenteric artery is usually affected, with clinical features of severe abdominal pain, sometimes vomiting or diarrhoea, and evidence of an embolic source (Table 1) 196. Other features are a high white blood cell count and elevated serum amylase. A plain abdominal radiograph will show the absence of normal small bowel gas shadows centrally.

Urgent laparotomy is required and, if the bowel is still viable, embolectomy of the superior mesenteric artery can be performed. If there is doubt about bowel viability a ‘second look’ laparotomy should be performed 24 h later. In many cases the bowel is not viable and extensive resection is required. These patients require careful attention to replacement of fluid, electrolytes, and blood. If the whole small bowel has infarcted the patient will die.

The effects of an embolus blocking a major limb artery depend on the level of the obstruction and on the capacity of collateral arteries to carry blood to the distal tissues. In the absence of good collateral flow there is stasis of blood in the arteries beyond the block and propagated clotting occurs (Fig. 1) 344. Propagated clot also extends proximally to the next major branch. Reflex spasm of distal arteries is another effect of acute arterial occlusion. Clotting and spasm both make ischaemia worse.

Acute ischaemia due to an embolus causes hypoxia of the tissues and a failure to remove waste products; these are particularly damaging to muscle cells which have a rapid metabolic rate. Muscle death starts to occur after about 6 h. Initially ischaemia causes pain due to accumulation of metabolites, but as peripheral nerves become increasingly hypoxic paraesthesiae and eventually complete anaesthesia of the extremity occurs.

If the occlusion remains unresolved, venous thrombosis results from stagnation of blood flow: this is a late feature associated with a poor prognosis. ‘Fixed staining’ of the skin due to extravasation of blood into the tissues is another late sign (Fig. 4) 347. Continued neglect results in gangrene.

Diagnosis of embolism causing acute ischaemia of a limb (Fig. 5) 348

The clinical features are best remembered as the ‘six Ps’—pain, pallor, pulselessness, paraesthesiae, paralysis, and perishing cold. The onset of symptoms caused by an embolus is sudden, with pain and pallor occurring first. Colour change is variable and depends on the amount of collateral blood flow. If there are no established collaterals the extremity is white, sometimes with a bluish tinge. If some blood flow is maintained a pink colour remains, but capillary return is slower than normal. The more profound the ischaemia, the sooner paraesthesiae will be followed by anaesthesia. Loss of sensation is a serious sign and an indication for urgent treatment to restore blood flow. Paralysis is also a sign of advanced ischaemia.

Pulses distal to the occlusion are lost, while immediately proximal to the occlusion the pulse may be enhanced due to the high resistance caused by obstruction.

Acute ischaemia due to an embolus is a clinical diagnosis and special tests should not be necessary, but Doppler ultrasound investigation confirms absent or poor blood flow signals in the distal arteries, and the systolic pressure is unrecordable or low. An arteriogram is not necessary in the presence of an obvious embolic source (for example atrial fibrillation) and clear evidence of a sudden arterial occlusion, but angiography is worthwhile if there is any doubt about the diagnosis (Fig. 6) 349.

The main differential diagnosis is acute thrombosis occurring in arteries already narrowed by atherosclerosis (often called thrombosis in situ or acute-on-chronic ischaemia). The onset of ischaemia is often less sudden than in embolism and the degree of ischaemia is less profound, with preservation of a pink colour to the skin and intact sensation, due to established collateral arteries. There may be evidence of chronic arterial disease with a history of intermittent claudication, and absence of pulses with reduced systolic pressures in the contralateral limb. The absence of an obvious embolic source also supports a diagnosis of thrombosis rather than embolism. A generalized illness with hypotension or dehydration may be evident as a precipitating cause for acute thrombosis.

The distinction between embolism and thrombosis is not always easy, and in any doubtful case an arteriogram should be performed. If arteriography suggests thrombosis, then this can be treated by low dose infusion of a thrombolytic agent (for example streptokinase) through an arterial catheter. This method of treatment requires radiological facilities and expertise, and haematological monitoring of blood clotting during the infusion of the thrombolytic agent. When the thrombus has been lysed, transluminal angioplasty or bypass grafting may be indicated for repair of the underlying arterial stenoses.

Deep vein thrombosis is sometimes confused with arterial embolism, because it causes pain, reduced ability to move the limb, and colour change. This differential diagnosis should not be difficult: the limb with a venous thrombosis is swollen, sensation is not lost, and Doppler examination will confirm a normal arterial supply. Venous thrombosis occurring as a late sequel of arterial occlusion is accompanied by florid signs of neglected ischaemia.

The first priority is relief of pain using strong analgesics such as morphine or pethidine (meperidine) given intramuscularly. An intravenous bolus of heparin should be given to reduce propagated clotting (5000–10000 units). Continuous infusion of intravenous heparin is then commenced if any delay is anticipated in definitive treatment.

The ischaemic limb should never be actively warmed—this accelerates tissue damage. Measures to cool the limb are sometimes recommended but are generally impracticable. Another traditional recommendation is to nurse the patient with the limb dependent but any improvement from such a manoeuvre is likely to be marginal. Treatment for any acute medical condition, such as cardiac failure or arrhythmias, is commenced.

After these initial steps the aim should be emergency embolectomy as soon as possible to re-establish blood flow to the extremity. Embolectomy is usually performed under a local anaesthetic because most patients are elderly and unfit. The area to be anaesthetized should be marked and a dilute local anaesthetic, for example 0.5 per cent lignocaine (lidocaine), chosen so that a large volume can be used. It is helpful, but not essential, to have an anaesthetist in attendance to monitor the patient (ECG and blood gases) and to administer oxygen or sedation if this is required. An intravenous infusion should be set up before starting the operation.

Transfemoral embolectomy is the best initial approach for all lower limb emboli, while in the upper limb exposure of the brachial artery is required. For femoral embolectomy the incision should be vertical over the femoral artery, and should allow easy access up to the inguinal ligament. The common femoral artery is controlled with a sling as high as possible. Its bifurcation is exposed and slings are passed around the superficial and profunda femoris arteries, and also around any other branches.

In the upper limb it is easiest to approach the brachial artery through a longitudinal incision over the medial aspect of the upper arm, and this usually gives a satisfactory result. An approach through the antecubital fossa allows separate embolectomy of radial and ulnar arteries. This involves an S-shaped incision (medial above the elbow, curving across the antecubital fossa to the lateral aspect of the forearm). The bicipital aponeurosis is divided to reach the brachial bifurcation.

If the artery is non-pulsatile it is opened without any clamps in place. For simple embolectomy transverse incisions in arteries allow closure without the risk of narrowing the lumen. Longitudinal arteriotomy gives greater scope for reconstructive surgery but may require closure with a patch to avoid stenosis in narrow vessels.

A balloon embolectomy catheter of appropriate size is selected (Table 3) 198 and the balloon is tested by inflating it with fluid (from a 1 ml or 2 ml syringe). The catheter is passed, proximally if it is necessary to remove clot and to ensure good inflow, and a proximal clamp is applied. After passing the catheter through an iliac clot into the aorta the contralateral limb must be checked at the end of the operation to ensure that embolic material has not been dislodged distally through the opposite iliac system.

The balloon catheter is passed distally and the clot withdrawn, adjusting the balloon inflation pressure depending on the ‘feel’ of the catheter as it is withdrawn. Balloon catheters must be used gently, especially in vessels roughened by atheroma, to avoid intimal damage. The stilette should always be removed before passing the catheter. It should be possible to pass a catheter to the foot and passages are repeated until no further thrombus or clot is withdrawn. A balloon catheter should also be passed down the profunda femoris artery in the thigh. Distal flushing with about 100 ml heparinized saline (from 500 ml normal saline containing 5000 units heparin) is then performed through a soft catheter (for example a number 6 umbilical catheter) passed into the distal artery.

The patient should be warned to expect some discomfort during balloon withdrawal and also perhaps during flushing of the extremity with cold heparinized saline.

The arteriotomy is closed with a continuous non-absorbable suture (e.g. 0000 or 00000 polypropylene), checking inflow before final closure.

On releasing clamps the extremity should rapidly regain a pink colour with return of palpable pulses. If the result is unsatisfactory (the catheter fails to pass far enough or the foot is not improved) then an immediate arteriogram should be undertaken on the operating table with a proximal clamp in place to demonstrate the state of the distal vessels. The options thereafter are exposure of the popliteal artery for embolectomy or bypass surgery, or the use of thrombolytic agents. These are best performed by a surgeon with vascular expertise. If the expertise is not available and the foot is viable, then intravenous heparin therapy should be instituted.

If the material removed from the arteries is not typical thrombus it should be sent for histology to exclude a tumour embolus.

Swelling of the leg may occur after revascularization, and this can cause increased compartmental pressure leading to muscle necrosis if untreated. If there is any suspicion of raised intracompartmental pressure, a generous fasciotomy should be done. Compartment syndromes are more common after reconstruction for vascular trauma than after embolectomy.

Embolectomy is the best treatment for arterial emboli. If in doubt about the management of an acutely ischaemic limb the artery should be explored with a view to an embolectomy. There is little to support the claim that embolectomy ‘can do more harm than good’, and an arteriogram can be performed at operation if embolectomy is not successful.

Low dose intra-arterial streptokinase or urokinase can be effective in the treatment of embolism as for arterial thrombosis. This technique should only be used if the extremity is viable (sensation preserved). The infusion should be stopped after 48 h if there is no improvement, but if sequential radiographs show lysis then the infusion may be continued for up to 5 days. This method requires good radiological support.

Intravenous heparin alone can be used for the treatment of patients with acute limb ischaemia provided the limb is viable. This is safe management, especially when the facilities or expertise for vascular work are limited, or while awaiting a vascular opinion. Heparin minimizes propagated clotting and improvement may occur through natural clot lysis and the development of collaterals. The eventual state of the circulation to the limb is likely to be less good following heparin therapy alone than after successful embolectomy.

This technique employs a specially designed catheter sheath system which can be used alone or in combination with thrombolytic drugs. The catheter is used to aspirate fragments of thrombus from the distal arteries and it is best suited to treating iatrogenic emboli resulting from intra-arterial catheterization or balloon angioplasty. This method is currently confined to specialist units.

Administration of intravenous heparin in the immediate postoperative period reduces early recurrence of emboli. Thereafter, long-term anticoagulation is traditionally instituted (warfarin by daily oral administration) in the hope of preventing further emboli. Oral anticoagulants certainly should be used in patients in atrial fibrillation, but for patients with no obvious embolic source there is conflicting evidence of effect. Nevertheless, anticoagulation seems reasonable for all patients who will take warfarin reliably and from whom regular blood samples can be obtained for clotting studies. If haematological monitoring is difficult or if patients are unlikely to comply properly then the risk of haemorrhagic complications probably outweighs the benefits of long-term anticoagulation.

Patients with emboli may present many days after the acute event. Embolectomy may be successful even after a delay of a month but is rarely successful thereafter, because thrombus adheres to the vessel wall. Thrombolytic therapy may also be successful up to 1 month after impaction of an embolus.

Thrombolysis or intravenous heparin therapy are often used for these patients who present late but whose limbs have remained viable. If the obstruction is not relieved then arterial reconstruction can be performed at a later date if required.

Patients suffering embolism are often elderly and infirm, and up to 30 per cent die in the postoperative period. Factors associated with a higher mortality are increasing age, recent myocardial infarction, proximal (aortoiliac) occlusions, poor cardiac and pulmonary function, and pre-existing arterial disease.

Amputation is an uncommon sequel to embolism and is associated with delayed presentation. Limb loss following acute ischaemia is more commonly associated with thrombosis in diseased arteries than with emboli.

The small emboli that arise from arteriosclerotic arteries or aneurysms present either as isolated ischaemic digits (Fig. 7) 350 or as ischaemic patches on an extremity. The main differential diagnoses are vasculitis and haematological disorders such as thrombocythaemia. ‘Trash foot’ is an important complication of grafting for aortic aneurysm and describes the passage of a shower of loose thrombus into the small vessels of the feet (Fig. 8) 351.

Such small distal emboli are impossible to remove surgically. During aortic grafting prevention is the most important measure—gentle handling of the aneurysm, clamping the iliac arteries first, and flushing of blood both externally and, if possible, internally at the end of the procedure so that no thrombus or clots are allowed to pass into the limb arteries. When a localized arterial stenosis or aneurysm is identified as the cause for microembolism this should be dealt with appropriately—usually by bypass grafting (Figs. 2 and 3) 345,346.

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