Acute arterial occlusion
An embolus is a body which is foreign to the bloodstream and which may become lodged in a vessel and cause obstruction.
Simple emboli are due to blood thrombus. The sources are most commonly mural thrombus following a myocardial infarct (a third of cases), mitral stenosis, cardiac arrhythmias (particularly atrial fibrillation) and aneurysms. Emboli may lodge in any organ with resultant ischaemia and symptoms:
• brain:the middle cerebral artery (or its branches) is most commonly affected, resulting in hemiplegia, permanent or temporary (transient ischaemic attacks);
• retina: amaurosis fugax is fleeting blindness caused by the passage into the central retinal artery of a minute thrombus emanating from an atheromatous plaque in the carotid artery. Complete obstruction causes total and permanent blindness;
• mesenteric vessels: causing engorgement and possible gangrene of the corresponding loop of intestine;
• spleen: commonly affected with local pain and enlargement;
• kidneys: resulting in loin pain and haematuria;
• lungs: pulmonary embolism is a catastrophe which may fatally interrupt convalescence after operation. Haemoptysis and dyspnoea are usual in survivors;
• lower limbs: pain, pallor, paresis, pulselessness and paraesthesia (more correctly anaesthesia). Acute arterial occlusion due to an embolus differs from atherosclerotic occlusion in that the occlusion is sudden. It is essential to differentiate between these two causes of occlusion, because they may require different forms of treatment.
Embolic arterial occlusion is an emergency, generally requiring treatment immediately the diagnosis is made.
In the legs, the dramatic symptoms which occur when major vessels are occluded deserve re-emphasis — pain, pallor, paresis, loss of pulsation and anaesthesia. The limb is cold and almost immediately the toes cannot be moved (contrast with venous occlusion when muscle function is not affected). The diagnosis can be made clinically in the majority of cases. The patient, who has no previous symptoms of claudication or limb pain and has a source of emboli, suddenly develops severe pain or numbness of the limb which becomes cold with mottled blue and white discoloration. Movement of the toes becomes progressively more difficult and sensation to touch is lost. Pulses are absent distally, but the femoral pulse may be palpable (even thrusting) if the clot is lodged in a low bifurcation of the femoral artery. This is because distal occlusion results in forceful expansion of the artery with each pressure wave, despite the lack of flow.
Because of the ensuing stasis, thrombus can extend distally and proximally to the embolus. The immediate administration of heparin 5000 units intravenously can reduce this extension and maintain patency of the surrounding (particularly the distal) vessels until the embolus can be treated. The relief of pain is essential because it is severe and constant. Embolectomy or thrombolysis are the treatments available for patients with limb emboli.
Embolectomy (and thrombectomy)
Local or general anaesthesia is used, depending upon the patient’s general condition and the scope of the proposed operation. The artery, bulging with clot, is exposed and held up by slings or fine rubber tubing. Through a longitudinal or transverse incision the clot begins to extrude and is removed, together with the embolus. Arterial clamps are applied as bleeding occurs, special note being made of the degree of retrograde bleeding (back bleeding).
Fogarty catheterisation. This is the most effective method of removing proximal and distal extension thrombus and also allows an embolus or thrombus to be removed from a vessel remote from the arteriotomy. The Fogarty catheter is like a ureteric catheter, with a balloon tip, and is introduced until it is deemed to have passed the limit of the thrombus.
The balloon is inflated and the catheter withdrawn slowly, together with the clot. The procedure is repeated until bleeding occurs. The method is valuable in patients with an aortic bifurcation embolus, since the clot and embolus can be extracted by insertion of balloon catheters via the common femoral arteries in the groin and the patient is saved from a laparotomy. Postoperatively, anticoagulant therapy is continued.
Prevention of further emboli is achieved by treatment of the cause, whenever possible, and by reducing the chance of further thrombus formation by using long-term anticoagulation with warfarin.
If ischaemia is not so severe that immediate operation is mandatory, it may be possible to treat either embolus or thrombosis by intra-arterial thrombolysis. Because of the nature of thrombosis as opposed to embolism, thrombolysis is more useful in the former condition. Indeed, it may well be the treatment of choice on many occasions.
Arteriography of the ischaemic limb is carried out (usually via the common femoral artery) in the radiology department and at the conclusion of the procedure a narrow catheter (5 French gauge) is passed into the occluded vessel and left embedded within the clot. Into this catheter a thrombolytic agent is infused over a period of several hours. In addition, heparin 250 units per hour is added to the infusatc. Intraarterial thrombolysis may be carried out in a well-staffed ward, but some workers prefer the safety of either a high dependency unit or an intensive care unit.
The common thrombolytic agents are streptokinase, urokinase and tissue plasminogen activator (TPA). In the UK, the most frequently used agent is now TPA, streptokinase having fallen into some disfavour owing to allergy. TPA also has a more rapid action which may be clinically useful. The speed of thrombus dissolution can be further improved by replacing the infusion technique by a pulse-spray method; this requires a special catheter and delivery system.
Whichever drug is used, regular angiograms are carried out to check on the extent of lysis. Using streptokinase, lysis was usually complete within 48 hours. TPA may achieve lysis within 24 hours and pulse-spray TPA may take less than 6 hours. Lysis should be abandoned if there is no progression of dissolution of clot with time. There are several contraindications to the technique, the most important of which are recent stroke, bleeding diathesis and pregnancy.
Mesenteric artery occlusion
Acute mesenteric occlusion can be either thrombotic (following atherosclerotic narrowing) or embolic.
Thrombotic occlusion follows progressive narrowing and so the symptoms also tend to be progressive with weight loss, abdominal pain (usually postprandial) and leucocytosis. Once the abdominal pain becomes severe, diarrhoea, systemic hypovolaemia and haemoconcentration occur. By this stage, the patient is ill out of proportion to the physical signs. Treatment is arteriography followed by percutaneous transluminal angioplasty or surgical bypass if the bowel has not already infarcted.
Embolic occlusion results in sudden, severe abdominal pain, with bowel emptying (vomiting and diarrhoea), and a source of emboli present (usually cardiac). Arteriography and embolectomy or bypass surgery can reduce the otherwise high mortality in these patients.
Air may be accidentally injected into the venous circulation, e.g. artificial pneumothorax, or sucked into an open vein. Thus venous air embolism occasionally complicates operations on the neck or axilla if a large vein is inadvertently opened, or it may be an accessory cause of death following a cut throat. The risks associated with intravenous infusion are reduced by the use of a drip chamber containing a spherical plastic float which plugs the exit when the fluid falls to a dangerous level. When air enters the right atrium it is churned up; the foam then enters the right ventricle and causes an air-lock in the pulmonary artery, which may end in right-sided heart failure.
Treatment. Trendelenburg’s position encourages air to pass into the veins of the lower half of the body and the patient is placed on the left side so that air will float into the apex of the ventricle, away from the pulmonary artery. Oxygen is administered to counteract hypoxaemia and to assist in the excretion of nitrogen. In serious cases the right ventricle should be aspirated by a needle passed upwards and backwards from below the left costal margin. If this fails, the heart is rapidly exposed for aspiration under direct vision.
Air may occasionally enter the left side of the heart, e.g. at open heart surgery, following puncture of a pulmonary vein during artificial pneumothorax or through a patent foramen ovale (paradoxical embolism). It may from there embolise coronary or cerebral arteries. Treatment is along similar lines to venous air embolism. Air embolism is also a risk following fallopian tube insufflation and following illegal abortion. The air may travel to the brain via the paravertebral veins.
This condition, which is more common than generally supposed, usually follows severe injuries with multiple or major fractures. Cases have also been recorded following electroconvulsive therapy. The fat may be derived from bone marrow or adipose tissue, but recent work suggests that it is metabolic in origin, perhaps by aggregation of chylomicrons. Symptoms are evident a day or so after injury and two more-or-less distinct types, cerebral and pulmonary, are recognised. In the cerebral type, the patient becomes drowsy, restless and disorientated (delirium tremens may be suspected). Subsequently, the patient is comatose, the pupils become small and pyrexia ensues. The pulmonary type is ushered in with cyanosis, which increases in intensity, and signs of right heart failure. White froth may occur at the mouth and nostrils. It may be mistaken for bronchopneumonia or left ventricular failure. One of the earliest signs may be emboli in the retinal arteries, which cause striate haemorrhages and ‘fluffy’ patches of exudate. The sputum should be examined for fat droplets and fat may be excreted in the urine. A fall in the haemoglobin value of the blood is a constant sign. Petechial haemorrhages often occur.
Treatment consists of oxygen, early heparinisation and intravenous low molecular weight dextran.
Other forms of emboli include infective emboli of masses of bacteria or infected clot, which may cause mycotic aneurysms, pyaemia or infected infarcts; parasitic emboli due to the ova of Taenia echinococcus and Pilaria sanguinis hominis and emboli of malignant cells (e.g. hypernephroma).
This is used to arrest haemorrhage from the gastrointestinal, urinary and respiratory tracts, to treat arteriovenous malformations by blocking their arterial supply and to control the growth of unresectable tumours. Arterial embolisation requires accurate selective catheterisation using the Seldinger technique.
Examples. The left gastric or gastroduodenal artery may be occluded to treat a bleeding ulcer. Occlusion of the hepatic artery often relieves the pain of primary and secondary liver tumours and will usually control the endocrine effects of hormone-secreting tumours, such as metastatic carcinoid. Renal artery embolisation has been used to devascularise a renal tumour prior to surgery and to arrest persistent haemorrhage from an unresectable tumour. In patients with bleeding oesophageal varices, the portal system can be entered by percutaneous catheterisation through the liver and the veins supplying the varices can be embolised.
A wide range of materials have been used and they include blood clot, gel foam sponge, human dura, plastic microspheres, balloons, ethyl alcohol, quick-setting plastics and mechanical devices made of stainless steel coils and wool. Therapeutic embolisation is usually carried out under local anaesthesia and has a low morbidity. This is particularly useful for patients with advanced malignant disease where palliation is the aim of the procedure.
Caisson and decompression disease
These similar conditions may affect divers and those who work in compressed air chambers or who ascend in unpressurised aircraft to above 8000 m. If decompression is too rapid, bubbles of nitrogen are set free in the tissues and bloodstream, and occlude small vessels. Symptoms include pain in the muscles or joints, which may be excruciating (the ‘bends’), and neurological disturbances; if the spinal cord is affected the patient suffers from weakness of the legs and sphincters. In severe cases, the lungs may be affected, and the patient complains of tightness of the chest and a dry cough (the ‘chokes’). Caisson disease requires recompression followed by gradual decompression. The high-altitude flyer is relieved by gradual descent. Inhalation of oxygen assists the excretion of nitrogen. If the spinal cord is not permanently damaged the prognosis is good, but hypertrophic changes may persist in the ends of long bones.
Acute arterial occlusion due to trauma
Arteries (like all tubes) can be occluded as a result of changes:
• in the lumen, e.g. thrombosis;
• in the wall, e.g. subintimal haematoma;
• in the surrounding tissues, e.g. compartment syndrome.
The history of trauma should alert the clinician to check the pulses in the affected limb. There may be obvious injury, for example ‘butdher’s thigh’, when the boning knife slips and enters the groin, but sometimes in blunt injury the lack of surface changes may be misleading. Absent pulses with rest pain, or skin colour and temperature change, suggest arterial occlusion. In many Western nations, the commonest cause of arterial trauma is iatrogenic. In this group, the commonest event is femoral or brachial artery damage at cardiac catheterisation; the latter vessel is much more prone to iatrogenic complications and should be avoided if possible by those using catheter techniques.
Preoperative assessment including arteriography is valuable. It is also useful to recognise pre-existing atherosclerotic disease.
On exposing a damaged artery, an obvious laceration may be found —remember to look for a puncture wound in the back of an artery in a stabbing. If this is very small, e.g. from a needle puncture, a single suture may suffice to repair a leak. If damage is more widespread and if thrombosis forms part of the picture, it may be necessary to resect a damaged segment. If the resection is very limited, it maybe possible to reconstitute the vessel by direct anastomosis of the cut ends. In general, however, a short interposition graft (vein is best) is to be preferred. The vein should not be taken from the damaged limb because concomitant deep venous trauma may be present and superficial veins may be required to return blood centrally.
It should first be appreciated that occlusion due to trauma should never be casually ascribed to arterial spasm; ischaemia after trauma demands urgent action. Second, the results of operating on traumatised arteries are, in general, good. The outflow is not compromised by atheromatous disease in most cases. If the return of blood supply to the limb after arterial declamping is not very obvious, preoperative angiography is mandatory. Not only may there be a problem with the local arterial reconstruction but also thrombosis (from stasis) or embolism at a distal site may be present and may require separate attention.
Fractures of bone occur frequently alongside arterial injuries and require stabilisation, both in their own right and to protect the vascular repair. Stabilisation may be carried out before or after the vascular reconstruction (depending on how acute is the ischaemia) and fixation (often external) is greatly to be preferred to traction, for obvious reasons.
It must also be remembered that in the lower limb the additional problem of compression of the main artery due to haematoma or oedema in the fixed fascial compartments of the calf, especially the anterior tibial compartment, can cause distal ischaemia (and crush syndrome renal effects). The treatment is urgent fasciotomy to release the external compression on the artery.