A 65-year-old man presented with acute severe pain in his right leg. Medical history revealednon-insulin-dependentdiabetesmellitusfor3yearsandamyocardialinfarc- tion (MI) some 5 years ago. The pain in the right leg developed suddenly over 6 hours without associated trauma and became worse over time. On admission, the right leg looked pale distally from the level of the knee. There was loss of light touch sensation on examinationof thefoot. The patient haddifficultiesin wiggling the toes. Plantarflexion and dorsiflexion of the toes were still possible. Palpation of the calf showed soft but tender muscles. Clinical examination of the abdomen showed no abnormalities. There was no pulsating mass. Irregular but bounding pulsations were felt in the right femoral artery. Popliteal artery and tibial artery pulsations were absent. Normal pulsations were felt in the left popliteal and posterior tibial artery.

Question 1

What is the aetiology of arterial embolism?

A.  The aetiology of arterial embolism is most frequently unknown.

B.  The most frequent cause of arterial embolism is cardiac valve destruction by rheumatic heart disease or endocarditis.

C.  The most frequent cause of arterial embolism is atrial fibrillation in association with atherosclerotic heart disease.

D.  Deep venous thrombosis might represent a rare cause of arterial embolism.

E.  Arterial embolism is most frequently seen in the presence of increased blood viscosity.

With the diagnosis of acute arterial ischaemia in mind, a full dose of intravenous heparin was administered immediately.

A. Nevelsteen

Department of Vascular Surgery, University Hospital Gasthuisberg, Leuven, Belgium

Question 2

What is the place of heparin in the treatment of arterial embolism?

A.  Heparin can dissolve an arterial embolus, avoiding the need for subsequent operation.

B.  Heparin will avoid subsequent arterial thrombosis, which can complicate treatment of arterial embolism.

C.  Heparin will avoid subsequent arterial thrombosis, which can complicate treatment of arterial embolism. In addition, heparin will prevent recurrent emboli.

D.  The use of heparin is contraindicated since it may lead to fragmentation of an arterial embolism and induce microembolisation in the peripheral arteries.

A chest film X-ray showed no abnormalities. Electrocardiogram (ECG) revealed atrial fibrillation and signs of an old MI. Laboratory studies were normal. Duplex examination showed a thrombotic occlusion of the right femoral bifurcation and the superficial femoral artery. A weak flow sign was present in the popliteal artery. The tibial arteries were not visualised.

Question 3

The preferred treatment of arterial embolism is:

A.  Local excision of the vessel and reconstruction with interposition graft. B.  Continued heparinisation and wait and see.

C.  Simple Fogarty catheter embolectomy with peroperative angiographic control.

D.  Simple Fogarty catheter embolectomy, but percutaneous aspiration thromboembolectomy might be a good alternative in selected cases.

After placement of a central venous catheter, the patient was taken to the operating theatre and the right femoral bifurcation was exposed under local anaesthesia. A transverse arteriotomy confirmed complete thrombotic occlusion of the femoral bifurcation. There was good inflow. Thrombi were removed from the femoral bifurcation, and pulsatile backflow was obtained from the profunda femoris artery.

Multiple thrombi were removed from the superficial femoral artery and the popliteal artery after several passages of Fogarty embolectomy catheters numbers 3 and 4. Intraoperative angiography showed good patency of the superficial, popliteal and peroneal arteries. The anterior tibial artery was completely occluded. The posterior tibial was patent in its first portion but occluded distally. A small catheter was inserted into the popliteal artery, and 350,000 units of urokinase were infused as a dripping infusion over 30 min. Repeated angiography showed further clearance of the posterior tibial artery to the level of the ankle joint. The anterior tibial artery was still occluded. It was decided to accept the situation. The arteries were flushed with a diluted heparinised saline solution, and the transverse arteriotomy was closed with the aid of a Dacron patch. Sodium bicarbonate was administered intravenously before reperfusion.

Question 4

Reperfusion syndrome after arterial embolectomy:

A.  Will never be seen after peripheral but only after aortic embolism. B.  Cannot be prevented medically.

C.  Will be prevented by early ambulation.

D.  Is induced by metabolic acidosis and myoglobinuria.

Postoperatively, the foot was well vascularised and the patient was able to wiggle his toes almost normally. Pulsations were felt in the posterior tibial artery. Intravenous heparin was continued. Brisk diuresis was maintained with mannitol and alkalisation of the urine. Repeated laboratory studies showed no evidence of acidosis or hyperkalaemia.

Question 5

Fasciotomy:

A.  Has become obsolete and swelling of the limb should be treated by elevation and bed rest.

B.  Is best routinely performed in any patient, treated for arterial embolism of the lower limbs.

C.  The indication to fasciotomy needs to be based on objective parameters such as the ­presence of reperfusion syndrome and postoperative compartmental pressure measurements.

D.  In daily practice, the indication for fasciotomy is most frequently based on individual preference and clinical feeling.

Six hours postoperatively, the patient developed significant limb swelling with augmentation of pain, venous hypertension and sensory impairment of the foot. A perifibular fasciotomy to decompress all four compartments was performed under general anaesthesia. Afterwards, the swelling subsided and the fasciotomy wound was closed in a delayed primary fashion after 1 week.

Question 6

With the preand peroperative diagnosis in mind:

A.  The patient should be placed under antiplatelet therapy postoperatively in order to prevent another episode of embolism.

B.  Heparin and oral anticoagulants remain the treatment of choice during the postoperative period.

C.  Subsequent investigation with regard to the source of the embolus is not necessary, because this will not change the medical treatment.

D.  Postoperative investigation with regard to the source of embolism can be limited to cardiac examinations such as echocardiography and Holter monitoring.

Abdominal ultrasound performed postoperatively showed atheromatosis of the abdominal aorta but no aneurysmal dilatation. Transthoracic and transoesophageal echocardiography revealed no ventricular aneurysm or intracardiac thrombi. Holter monitoring for 24 h confirmed atrial fibrillation. Pathological examination of the retrieved emboli was compatible with ordinary thrombotic material. Cultures were negative. The problem of atrial fibrillation was handled medically. Oral anticoagulation was initiated, and the patient was discharged after 10 days. Six months later, there were no repeat episodes of acute ischaemia.

13.1  Commentary

Acute ischaemia due to arterial embolism represents a limb-threatening event. Although the carotid or intracranial vessels may be involved in a minority of the cases, the upper or lower extremities are involved in 70–80% in most series of arterial embolisation.1 The lower extremity is involved five times as frequently as the upper extremity, and the sites of embolicocclusion are most often related to major arterial bifurcations. The common femoral bifurcation is the most frequent site of embolic occlusion, usually noted in 30–50% of all cases.2 In total, the femoral and popliteal arteries are involved more than twice as often as the aorta.

The heart is by far the predominant source of arterial emboli, seen in 80–90% of cases.3 Atrial fibrillation is present in approximately 70% of patients. Previously, it was most frequently the reflection of rheumatic heart disease. Since the incidence of rheumatic heart disease has declined steadily over the last 50 years, atrial fibrillation is now associated most frequently with atherosclerotic heart disease.

MI is the second common cause of peripheral embolisation. Left ventricular mural thrombus occurs in 30% of acute transmural infarcts. Clinically evident embolism is seen in only 5% of these patients.4 One should be aware, however, that silent MI may be present in up to 10%ofpatientswithperipheralemboli,andthatembolisationmaybethepresentingsymptom of an acute infarction. Apart from the acute period, MI may also cause emboli after longer intervals. This is usually due to areas of hypokinesis or ventricular aneurysm formation. Although most emboli occur within 6 weeks of MI, much longer intervals may be noted.

Othercardiacdiseasesareassociatedlessfrequentlywithperipheralemboli.Thromboemboli can, however, arise from prosthetic cardiac valves or from vegetations on the mitral or aortic valve leaflets. Endocarditis should certainly be ruled out. Finally, intracardiac tumours, such as atrial myxoma, may also give rise to clinically evident embolic events.

Non-cardiac sources of peripheral emboli are noted less frequently. Major emboli may arise from aneurysms of the aorta or less frequently from the femoropopliteal vessels.5 With upper-extremity emboli, one should be aware of unsuspected thoracic outlet syndrome and aneurysmal deformation of the subclavian artery. Paradoxical emboli might be seen with deep venous thrombosis in association with a patent foramen ovale. Primary or secondary lung tumours might invade the pulmonary veins, causing tumour emboli. Finally, apart from rare causes such as foreign body embolisation, it should be recognised that the source of embolisation will remain inapparent in some 10% of patients.2 [Q1: C, D]

The diagnosis of acute ischaemia caused by arterial embolism is usually straight-for- ward. The most typical signs are characterised by the “five Ps”: pulselessness, pain, pallor, paraesthesia and paralysis. The level of occlusion is determined by the presence or absence of palpable pulses. Once the diagnosis of acute arterial ischaemia has been made, 5,000 units of heparin are administered intravenously. This is not meant as effective treatment but it prevents the propagation and fragmentation of the thrombus. Concomitant venous thrombosis, which can occur with prolonged severe arterial ischaemia, might also be avoided. Heparin administration allows time for diagnosis, evaluation and, if necessary, treatment of cardiac disturbances. [Q2: B]

Fogarty catheter embolectomy remains the treatment of choice in most patients with peripheral embolisation.6 The procedure is usually carried out under local anaesthesia and is effective in cases of major emboli. All retrieved emboli should be sent for pathological and microbiological examination. The operative result should be checked by intraoperative fluoroscopy or angioscopy. Remaining thrombi in the distal vessels can be approached directly or by intraoperative thrombolysis.7 Thrombolytic therapy or percutaneous aspiration thromboembolectomy (Fig. 13.1) may be used as alternatives to Fogarty catheter embolectomy in selected cases with no motor dysfunction or profound sensory loss.8, 9 [Q3: C, D]

All patients undergoing revascularisation of an acutely ischaemic limb are at risk of ischaemia reperfusion syndrome. This was first emphasised by Haimovici,10 described under its most grave form as the myonephropathic-metabolic syndrome. This reperfusion syndrome is the consequence of muscular hypoxia and the associated metabolic changes. A prolonged period of ischaemia results in accumulation of potassium, lactic acid, myoglobin and other cellular enzymes, leading to a significant fall in blood pH due to anaerobic metabolism, paralysis of the sodium potassium cellular pump and rhabdomyolysis.11 Acutewashoutoftheseproductsmayleadtohyperkalaemiaandmetabolicacidosis,resulting in myocardial depression or dysrhythmias. Myoglobin and other products of skeletal muscle breakdown can precipitate within the kidney and result in acute renal failure. Myoglobinuria is the first sign. [Q4: D] These problems should be anticipated with bicarbonate and/or calcium intravenously just before reperfusion. Induction of forced diuresis with mannitol and alkalisation of the urine might avoid acute renal failure. In addition, mannitol also acts as a scavenger of oxygen-derived free radicals, which are an important intermediary in ischaemia reperfusion injury.12, 13 It is clear, therefore, that the patient should be monitored carefully postoperatively with regard to electrolyte changes, development of metabolic acidosis and urinary output.

Another problem following revascularisation of an acute ischaemic limb might be significant limb swelling. This may result in secondary muscle or nerve injury, venous compression, further oedema and compartment syndrome, leading to arterial compression and secondary ischaemia. To avoid this, the surgeon might prefer to perform a fasciotomy in conjunction with the embolectomy procedure.14 Alternatively, the extremity can be assessed immediately and at regular intervals postoperatively for evolving compartment syndrome. As described in different textbooks, there are several ways of performing an adequate fasciotomy. The most important point here is that all four compartments should be decompressed.

Although concomitant fasciotomy can be preferable in some cases of prolonged acute ischaemia, the more conservative approach might avoid unnecessary fasciotomy and

Fig. 13.1  (a) Embolic occlusion of the left popliteal artery; treatment consisted of percutaneous aspiration thromboembolectomy. (b) Normal patency of the popliteal, anterior tibial and peroneal arteries

unaesthetic scars. Since a Fogarty catheter embolectomy can easily be carried out under local anaesthesia, this wait-and-see approach eliminates the need for systematic general anaesthesia, particularly for patients in a poor general condition.15

Despitethefactthatthevalueofpostoperativecompartmentalpressuremeasurementshas been documented by several teams,16, 17 the decision regarding subsequent fasciotomy is most frequently based upon individual preferences and prior clinical experience. [Q5: D] Every effort should be made in the postoperative period to minimise the incidence of recurrentemboli.Thepatientshouldbetreatedwithheparinororalanticoagulantsuntilthe source of the embolus has been taken care of. [Q6: B] If extensive investigation fails to show any correctable source, then long-term anti-coagulation is indicated, except in the

case of major contraindications.