Acute
arterial occlusion
Sudden
occlusion of an artery is commonly due to either emboli or trauma.
Embolic 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:
•
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 (Chapter 47)
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) (Fig. 15.25). Acute arterial occlusion due to an
embolus differs from atherosclerotic occlusion in that the occlusion is sudden.
Indeed, the clinical differences between these two causes of occlusion in the
lower limb are as set out in Fig 15.26 and Fig
15.27. It is essential to
differentiate between these two causes of occlusion, because they may require
different forms of treatment.
Clinical features
In the
legs, the dramatic symptoms which occur when major vessels are occluded deserve
re-emphasis — pain, pallor, paresis, loss of pulsation and anaesthesia (Fig.
15.25). 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
Treatment
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 (Fig. 15.28). 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.
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 embolism
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.
Fat embolism
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
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 (see Chapter 17) and emboli of malignant cells (e.g. hypernephroma,
see Chapter 64).
Therapeutic embolisation
This is
used to arrest haemorrhage from the gastrointestinal, urinary (Fig.
15.30) 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 (Fig.
15.31). 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
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
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
Preoperative
assessment including arteriography is valuable. It is also useful to recognise
pre-existing atherosclerotic disease.
Operative procedure
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 (Fig.
15.32). If the resection
is very limited, it maybe possible to reconstitute the vessel by direct
anastomosis of the cut
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.
Compartment syndrome (Chapter 21)
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.