SUBARACHNOID
HEAMORRHAGE
The sudden onset of a
severe headache in a patient should be regarded as subarachnoid haemorrhage until proven
otherwise.
Subarachnoid
haemorrhage occurs when bleeding is primarily within the subarachnoid space rather than
into the brain itself. It represents about 5–10% of all non-traumatic intracranial haemorrhage with an
incidence of approximately 15 per 100000 population.
Apoplectic death has
been mentioned in the earliest medical writings but its relationship to intracranial haemorrhage and
cerebral aneurysm was not established until the latter part of the
seventeenth century. The introduction of cerebral angiography by Moniz
and Lima in Lisbon in 1927 allowed the diagnosis of cerebral aneurysm to be made in living
patients who had sustained subarachnoid haemorrhage. Pioneering surgery in the 1930s and
1940s, by Krayenbuhl in Switzerland and Dandy in North America, showed that aneurysms could
be treated operatively, although at that time with considerable morbidity and mortality.
Consequent improvements in microsurgical techniques and neuroanaesthesia have considerably
improved the safety of surgery.
Causes of subarachnoid haemorrhage
The most common cause of subarachnoid haemorrhage in adults is rupture
of a berry aneurysm (70%). Subarachnoid haemorrhage in children is much less common than in
the adult population and the most common paediatric cause is rupture of an arteriovenous
malformation. Rare causes of subarachnoid haemorrhage include bleeding from a
tumour, bleeding disorders, blood dyscrasias and rupture of a spinal arteriovenous malformation The
aetiology of subarachnoid haemorrhage remains undiscovered in approximately 15%
of cases after thorough clinical and radiographic study. These patients often have
associated intracranial vascular atherosclerosis and hypertension.
Subarachnoid haemorrhage— presenting features
Headache
The sudden onset of a severe headache of a type not previously
experienced by the patient is the hallmark of subarachnoid haemorrhage. A relatively small leak from an
aneurysm may result in a minor headache, sometimes referred to as the ‘sentinel headache’,
as this may be the warning episode of a subsequent major haemorrhage from the aneurysm.
Naturally, recognition of a possible minor ‘warning’ haemorrhage is essential to avert a possible
later catastrophic bleed, although many are only recognized in retrospect.
Diminished conscious state
Most patients have some deterioration of their conscious state
following subarachnoid haemorrhage. This varies from only a slight change when the haemorrhage
has been minor to apoplectic death resulting from massive haemorrhage. It is
a common cause of sudden death in young adults.
Meningism
Blood in the subarachnoid cerebrospinal fluid will cause the
features of meningism—headache, neck stiffness, photophobia, fever and vomiting. Irritation of the
nerve roots of the cauda equina, which occurs when the blood extends down to the lumbar theca, may
result in sciatica-type pain and low back discomfort.
Focal neurological signs
Focal neurological signs may occur in subarachnoid haemorrhage due to
concomitant intracerebral haemorrhage, the local pressure effects of the aneurysm itself, or
cerebral vasospasm. A cerebral aneurysm usually lies within the subarachnoid cisterns
but the aneurysm may become adherent to the adjacent brain parenchyma due to adhesions,
frequently resulting from previous leakage of blood. A haemorrhage from an aneurysm in these
circumstances may also extend into the brain and the position of the intracerebral haematoma will
determine the type of neurological deficit. A middle cerebral artery aneurysm frequently
ruptures into the temporal lobe, resulting in hemiparesis and aphasia if the dominant hemisphere
is involved (Fig. 9.1). Anterior communicating artery aneurysms may haemorrhage into the
frontal lobes with subsequent akinetic mutism (Fig. 9.2). Defective conjugate ocular
movement may result from haemorrhage into a frontal lobe, persistent deviation usually being towards
the side of the lesion and purposeful gaze defective away from that side.
Fig. 9.2 Frontal intracerebral
haematoma with blood in the Sylvian
fissure and ventricles from a ruptured anterior communicating artery aneurysm.
Occasionally, an
aneurysm may also rupture into the subdural space, resulting in a subdural haematoma and brain
compression causing lateralizing neurological signs. An arteriovenous malformation usually
lies at least partially within the brain parenchyma, so that when it ruptures intracerebral
bleeding is frequently associated with the subarachnoid haemorrhage. Focal neurological
signs may result from the position of the aneurysm itself. An aneurysm arising from the
internal carotid artery at the origin of the posterior communicating artery (known as a posterior
communicating artery aneurysm) may cause pressure on the 3rd cranial nerve. Patients with
an enlarging aneurysm in this position may present with features of a 3rd cranial nerve palsy
(ptosis, pupil dilatation, extraocular
muscle palsy) prior
to a subarachnoid haemorrhage. It is vital that the correct diagnosis of an enlarging cerebral
aneurysm is made in this situation, so as to avoid the possible catastrophic effects of
subarachnoid haemorrhage. The major differential diagnosis of the aetiology of an apparently isolated 3rd cranial
nerve palsy is an ischaemic lesion such as those resulting from diabetes mellitus or
atherosclerosis. Pupil size is a useful guide in differentiating between these causes. The pupil is
usually dilated, with an expanding aneurysm which compresses the superior aspect of
the nerve that contains the parasympathetic pupillary fibres arising from the nucleus of
Edinger–Westphal in the midbrain. An expanding aneurysm usually results in more pain than the
ischaemia associated with diabetes mellitus, although this is an unreliable guide. If there is any doubt about the cause
of the 3rd nerve palsy then angiography must be performed expeditiously. In a
patient with impaired conscious state, or in one with other abnormal neurological signs
suggesting a massive haemorrhage, 3rd cranial nerve palsy may be secondary to temporal lobe
herniation. A giant aneurysm (defined as larger than 2.5 cm in diameter)
may cause compression of adjacent neural structures resulting in focal signs (Fig. 9.3). A large aneurysm of the
internal carotid artery or anterior communicating artery will cause compression of
the optic nerve or chiasm, respectively, resulting in visual failure. Large vertebrobasilar
aneurysms may cause brainstem compression.
Cerebral vasospasm following subarachnoid haemorrhage does not
usually result in clinical manifestations for 2 or 3 days after the initial bleed so that,
although it may be the cause of subsequent focal signs resulting from brain ischaemia, it is not the cause
of focal signs immediately after the haemorrhage.
Optic fundi
Mild papilloedema is common within the first few days of
haemorrhage because of the sudden elevation of intracranial pressure resulting from hydrocephalus or
cerebral oedema. A transient communicating hydrocephalus often occurs after subarachnoid
haemorrhage due to blood blocking the arachnoid villi. In about 10% of cases the hydrocephalus
persists and is severe enough to require a CSF shunt.
Ophthalmoscopy may
reveal fundal haemorrhages, particularly in severe subarachnoid haemorrhage. Small,
scattered retinal haemorrhages usually resolve satisfactorily, although the large subhyaloid
haemorrhages may break into the vitreous, resulting in permanent visual defect.
Clinical assessment
The diagnosis is usually obvious when the history is obtained from the
patient, relative or friend. The classic sudden onset of severe headache with features of meningism
and decreased conscious state is characteristic of a subarachnoid haemorrhage. However, difficulty
may occur when the haemorrhage has been minor and, tragically, a subarachnoid haemorrhage
may be misdiagnosed as either migraine or tension headache. A full neurological
examination should be performed with particular attention given to the presence of neck
stiffness, altered conscious state, pupillary status and fundal haemorrhage. Clinical grading systems have
been based on the severity of the headache and neck stiffness and on the level of
conscious state. The two major systems are the Hunt and Hess classification and the World Federation
of Neurological Surgeons (WFNS) system (Table 9.3).
Investigations
The major differential diagnosis is meningitis, although a minor haemorrhage
is often misdiagnosed as migraine. Confirmation of the clinical diagnosis of
subarachnoid haemorrhage should be undertaken as soon as possible. Computerized tomography (CT)
scanning (Fig. 9.4) is the best initial investigation as it will confirm the
diagnosis in over 85% of cases. It will also provide additional
information on associated pathology such as intracerebral haemorrhage and hydrocephalus, and on the position
of the haemorrhage, which is helpful if there is more than one aneurysm. Arteriovenous
malformation causing subarachnoid haemorrhage can frequently be diagnosed on the CT scan. If
there is any doubt that subarachnoid blood is present on the CT scan, as may occur following
more minor haemorrhages, a lumbar puncture is essential. The presence of xanthochromia (yellow
staining) in the CSF will confirm subarachnoid haemorrhage.
Fig. 9.4 Blood in the Sylvian
fissure and basal cisterns indicative of subarachnoid haemorrhage.
Cerebral angiography
will confirm the cause of the subarachnoid haemorrhage and will determine the subsequent
treatment. Intra-arterial digital subtraction angiography has considerably reduced the risks of
conventional angiography and should be undertaken as soon as the diagnosis has been
confirmed and it is clear that the patient will survive the initial haemorrhage.
Cerebral aneurysm
Cerebral aneurysms are the most common cause of subarachnoid
haemorrhage in the adult population, with a maximal incidence in the 4th and 5th decades of life,
although they can occur at any age.
Surgical anatomy
The great majority of aneurysms arise at the branch points of two
vessels, usually at an acute angle, and are situated mainly on the circle of Willis and the trunks
of the large arteries which supply it. Afew arise from its immediate branches but aneurysms on
peripheral vessels are rare (Fig. 9.5). The majority of aneurysms occur in constant positions on
the circle of Willis and about 85% occur on the anterior half of the circle.
Aneurysms arise at approximately equal frequency from the internal carotid artery, anterior
communicating artery and middle cerebral artery. Those associated with the internal carotid artery most
frequently arise at the origin of the posterior communicating artery (the so-called posterior
communicating artery aneurysm), less frequently at the terminal bifurcation, and occasionally at
the origin of the ophthalmic artery, the anterior choroidal artery or in the cavernous sinus.
Middle cerebral artery aneurysms arise from the middle cerebral artery at its bifurcation or
trifurcation in the Sylvian fissure (Fig. 9.6). Less commonly an aneurysm may arise from the
pericallosal artery at the genu of the corpus callosum.
Fig. 9.5 Usual sites of
cerebral aneurysms.
Fig. 9.6 (a) Anterior cerebral
artery aneurysm. (b) Middle cerebral artery aneurysm. (c) Posterior
communicating artery
aneurysm. (d) Terminal internal carotid artery aneurysm.
Approximately 15% of aneurysms arise from the posterior half of
the circle of Willis, the most common position being the basilar artery, most frequently at the
terminal bifurcation into the posterior cerebral arteries. However, an aneurysm may arise
from any of the main branches of the vertebral or basilar arteries, in particular the
posterior inferior cerebellar artery, anterior inferior cerebellar artery or
superior cerebellar artery (Fig. 9.7).
Fig. 9.7 (a) Terminal basilar
artery aneurysm. (b) Aneurysm arising from junction of basilar artery and
superior cerebellar
artery. (c) Posterior inferior cerebellar artery aneurysm.
Multiple aneurysms occur in more than
one position in approximately 15% of cases.
Pathogenesis of cerebral aneurysms
The common type of cerebral aneurysm resulting in a subarachnoid
haemorrhage is a saccular aneurysm, which is also known as a berry or congenital aneurysm. Fusiform aneurysms occur in the intracranial
circulation, particularly the vertebrobasilar arteries or internal
carotid arteries, and are due to diffuse atheromatous degeneration of the arterial wall,
frequently associated with hypertension. Mycotic aneurysms result from septic emboli. They
may be situated on peripheral vessels, are frequently multiple and have a high risk of
haemorrhage. The saccular or berry aneurysm arises at the junction of vessels
where there is a congenital deficiency in the muscle coat. The elastic layer in cerebral arteries, in
contrast with arteries elsewhere, is limited to the internal lamina, making these vessels more
susceptible to weakening effects of degeneration. Fragmentation and dissolution of the internal
elastic membrane occurs at the site of aneurysm development. The combination of the muscle defect
and the discontinuity of the underlying internal elastic membrane is probably necessary
for the formation of a saccular aneurysm. Other factors that increase the risk of aneurysm formation
include atheroma and hypertension. There is an increased incidence of atheroma in the
vessels of the circle of Willis and hypertension in patients with ruptured aneurysms. It is
probable that these factors play a role in the growth of the aneurysm and its subsequent rupture in some
patients.
Related diseases
There is no definite
hereditary basis to the development of intracranial aneurysms, although an epidemiology study
has shown an increased incidence of approximately seven-fold in first-degree relatives of patients
who have had an aneurysmal subarachnoid haemorrhage, with a lifetime risk of 2–5% of
developing an aneurysmal subarachnoid haemorrhage. Aneurysms do occur in association with
hereditary syndromes such as Ehlers–Danlos syndrome, coarctation of the aorta and polycystic kidney
disease.
Management of ruptured cerebral aneurysm
The management of patients following rupture of a cerebral
aneurysm is determined by three major factors.
1 Severity of the initial haemorrhage.
2 Rebleeding of the aneurysm.
3 Cerebral vasospasm.
Severity of the initial haemorrhage
About 30% of all patients suffering a subarachnoid haemorrhage from a
ruptured aneurysm either have an apoplectic death or are deeply comatose as a result of the
initial haemorrhage.
Rebleeding
This occurs in about 50% of patients within 6 weeks and 25% of
patients within 2 weeks of the initial haemorrhage. About half the patients that have a subsequent
haemorrhage will die as a result of the rebleed. After the first year the risk of a further haemorrhage
from the aneurysm is about 2–3% per year.
The only certain way
to prevent an aneurysm rebleeding is to exclude it from the circulation. Antifibrinolytic
agents (such as epsilon amino caproic acid or tranexamic acid) decrease the risks of rebleeding but,
as they are associated with increased incidence of thrombosis (such as deep vein thrombosis
and pulmonary embolus) and an increased risk of cerebral thrombosis associated with vasospasm, these
agents are now rarely used.
Cerebral vasospasm
Angiographic vasospasm (Fig. 9.8) occurs in about 50% of patients
following subarachnoid haemorrhage and in 25% it results in serious neurological complications. There
is a direct correlation between the amount of blood noted in the basal cisterns on the
CT scan, the risk of developing vasospasm and its severity. Although the spasm may principally
affect the vessels most adjacent to the ruptured aneurysm, generalized vasospasm occurs
frequently. The clinical manifestations resulting from vasospasm will be determined by the
vessels which are most severely affected. Spasm of the internal carotid artery and middle cerebral
arteries produces hemiparesis and aphasia in the dominant hemisphere. Vasospasm of the anterior
cerebral vessels causes paralysis of the lower limbs and akinetic mutism. Severe vasospasm may
cause widespread cerebral ischaemia so that the patient may become obtunded; if the
vasospasm is sufficiently severe it will result in death. Vasospasm does not usually occur until 2 or 3
days after the initial haemorrhage and its onset is rarely delayed beyond 14 days.
Fig. 9.8 Spasm of the anterior
and middle cerebral arteries following
subarachnoid haemorrhage from an anterior communicating
artery aneurysm. (initial
angiogram, on the 3rd day and after treatment)
Until recently there has been no satisfactory treatment for
established cerebral vasospasm. If the aneurysm has been surgically occluded from the circulation then
hypertensive therapy combined with hypervolaemia may overcome the hypoperfusion due to narrowing of
the cerebral blood vessels and reverse the ischaemic effects. Calcium channel
blocking agents such as nimodopine and nifedipine are frequently used in subarachnoid haemorrhage to
prevent and treat vasospasm, although there is still doubt as to their
effectiveness.
Following the angiogram that confirms a cerebral aneurysm, a decision
is then made as to the definitive treatment of the aneurysm. This will involve either:
• surgery with clipping of the aneurysm or
• endovascular obliteration of the aneurysm.
Surgery for ruptured aneurysm
The timing of the operation is critical in obtaining optimal results
following subarachnoid haemorrhage. Although better operative results may be achieved when
the surgery is delayed, the longer the operation is deferred the greater the risk that the
aneurysm will rebleed. In general, the operation is performed as soon as possible after the cerebral
angiogram. In the past surgery was avoided when the patient had clinical or
angiographically severe vasospasm, but it is now recognized that it is
best to clip the aneurysm even in the presence of clinical or radiological
vasospasm as with the aneurysm excluded from the circulation the spasm
can be treated using hypertensive hypervolaemic therapy and endovascular techniques.
Surgery is usually not performed on patients who are comatosed or
have features of decerebrate posturing response, unless the CT scan shows a large
intracerebral haematoma resulting from the ruptured aneurysm which needs to be evacuated, or
hydrocephalus as a cause of the poor neurological state.
Preoperative management
In those patients in whom it has been elected for some reason to delay
surgery, the management should include careful attention to the following.
• Posture. The patient should lie flat in a quiet room with subdued
lighting. Every attempt should be made to avoid environmental situations which could cause
sudden elevation of the patient’s blood pressure and thus increase the risk of rupture of
the aneurysm. Sedation usingbarbiturates or diazepam may be necessary if the patient is agitated.
• Blood pressure control. The blood pressure
is frequently elevated immediately after the haemorrhage and should be
carefully controlled. Initially this should be done using intravenous medication and utilizing
vasodilating agents (such as hydralazine or glyceryl trinitrate) and betablockers. Although it is
essential to control high blood pressure, as this may lead to rupture of the aneurysm,
hypotension may result in cerebral ischaemia, particularly when vasospasm is present. The
appropriate desirable blood pressure will depend upon the premorbid level.
• Fluids and electrolytes. Correct hydration
is essential to avoid electrolyte disturbance; in addition, overhydration may
precipitate cerebral oedema and insufficient fluids may increase the risk of cerebral
thrombosis associated with vasospasm. Electrolyte disturbances may also occur following
subarachnoid haemorrhage due to inappropriate antidiuretic hormone (ADH) secretion, which results in
hyponatraemia.
• Pain relief. Simple analgesic medication or codeine phosphate is
best used for controlling the headaches resulting from subarachnoid haemorrhage.
Surgical procedures
The surgical procedures available are:
• occlusion of the neck of the aneurysm
• reinforcement of the sac of the aneurysm
• proximal ligation of a feeding vessel.
Haemorrhage from an aneurysm is due to rupture of the fundus of the
aneurysmal sac. Therefore, the best surgical procedure is to occlude the neck of the
aneurysm, thereby isolating the aneurysm from the circulation.
In brief, the
operation involves a craniotomy which is usually based on the pterion
(pterional craniotomy) for aneurysms of the anterior circulation. This type of craniotomy may
also be used for aneurysms arising from the terminal basilar artery, although some surgeons prefer
an approach under the temporal lobe via a temporal craniotomy. Microsurgical techniques, utilizing
the operating microscope and microneurosurgical instruments, are employed. Access
to the basal cisterns may be aided by withdrawing CSF either using a ventricular drain or from the
lumbar theca. The arachnoid around the basal cisterns is opened, the neck of the aneurysm
identified and dissected and a clip placed across the neck to exclude the aneurysm from the
circulation. During the dissection of the aneurysm it is essential that vital adjacent vessels,
including the perforating arteries, are not injured, as damage to these vessels may result in severe
neurological disability. Occasionally it is not possible to safely place a clip across the neck
of the aneurysm, usually as a result of branches of the parent vessel either arising from the aneurysm or
being inseparable from the fundus. In this case the wall of the aneurysm may be reinforced by
a number of techniques, including wrapping the wall with crushed muscle, gauze or cotton wool
or a combination of these. Rapidly solidifying polymer (aneurysm cement) may be poured around
the aneurysm to provide it with a solid covering.
Postoperative
management
The usual
postcraniotomy operative management applies, with special attention to be given to the neurological
state, hydration, posture, oxygenation and blood pressure. Anticonvulsant medication is
recommended for 3 months to 1 year. Steroid medication is sometimes used in the initial postoperative
course to control cerebral oedema, although its effectiveness is not proven. The major specific
postoperative problem results from delayed cerebral vasospasm. As indicated previously,
prophylactic calcium channel blocking agents may be of use in preventing this complication. The
transcranial Doppler, utilizing non-invasive ultrasound, may give useful information on the degree of
intracranial vasospasm. Symptomatic vasospasm can be treated using hypervolaemic
hypertensive therapy. This treatment entails careful monitoring and requires the transfer of the
patient to an intensive care unit. Recently, endovascular techniques to dilate the vessels in spasm or
administer intra-arterial papaverine into the intracranial vessels have been used to treat
cerebral vasospasm postoperatively with some success.
Endovascular procedures for ruptured aneurysms
Over the past 10 years endovascular techniques (using detachable
coils) have been used to obliterate cerebral aneurysms. These have been investigated in international
trials, and have proven to be effective in excluding the aneurysm from the circulation.
The technique is usually performed by a specialist interventional
radiologist, and almost always under general anaesthesia. As with surgery, it is recommended
that the aneurysm is ‘coiled’ as soon as possible after the angiogram has been performed to
confirm the presence of an aneurysm (Fig. 9.9).
Fig. 9.9 (a) coils for endovascular
treatment of internal carotid artery aneurysm. Figure (c) shows the aneurysm excluded from the
circulation following the endovascular insertion of coils.
The recent ISAT trial
showed the possible superiority of endovascular coiling over surgery, although there has
been some debate as to these findings. The decision as to whether an aneurysm should be ‘clipped’
by a surgeon or ‘coiled’ by an interventional neuroradiologist is best made jointly by the
treating specialist, cerebrovascular neurosurgeon and neuroradiologist. The interventional neuroradiologist will
base his decision on
• the access to the
aneurysm and
• the configuration
of the aneurysm.
Access to the
aneurysm may be impaired by stenosis or tortuosity within the carotid artery (for anterior
circulation aneurysms) and vertebrobasilar artery (for posterior
circulation aneurysms). The ‘dome to neck’ ratio is an important consideration in
deciding whether the configuration of the aneurysm is appropriate for coiling. In general,
most neuroradiologists prefer the ratio to be 2 : 1 or greater. New techniques in interventional
radiology including the use of stents and three-dimensional coils have increased the number of
aneurysms that can be treated by endovascular techniques. At present, over 80% of terminal
basilar aneurysms can be treated by endovascular techniques, but only about half of the
anterior circulation aneurysms are amenable to ‘coiling’. Most interventional
radiologists do not coil middle cerebral artery aneurysms, as there
is difficulty in obliterating the aneurysm whilst maintaining patency of the vessels.
Management of an unruptured aneurysm
Multiple aneurysms
occur in 15% of patients who present following subarachnoid haemorrhage. In general, an
unruptured aneurysm will be clipped at the same time as the surgery for the ruptured aneurysm, provided it
can be performed through the same craniotomy. The indications for surgery are controversial for
an unruptured aneurysm occurring in a patient who has suffered a subarachnoid haemorrhage from
another aneurysm, or for an unruptured aneurysm found incidentally. The debate regarding
the optimal management of patients with an unruptured aneurysm revolves around the
relative risk of rupture of the aneurysm vs. the risk of treatment, by either surgery or an
endovascular approach. In the past
the risk of haemorrhage from an unruptured aneurysm was usually
quoted at 2–3% per year.
However, in 1998 the New England Journal
of Medicine published a large study of the natural history of unruptured
intracranial aneurysms which indicated that the risk of haemorrhage was very much lower,
particularly for aneurysms less than 10 mm in diameter and those arising from the middle cerebral
artery. There has been considerable debate in the neurosurgical literature regarding the
veracity of the so-called ISUIA (International Study of Unruptured Intracranial Aneurysms) study,
with some experts questioning the methodology. In general, the risk of rupture will depend on the
size of the aneurysm, on the configuration of the aneurysm, in particular if there is a ‘daughter
sac’ attached to the fundus, on a positive family history for aneurysmal subarachnoid haemorrhage and on the
age of the patient. Symptomatic aneurysms of all sizes should be considered for
treatment.
Arteriovenous
malformation
The arteriovenous malformation is the most common vascular
malformation. Although it accounts for approximately 60% of all subarachnoid haemorrhage in
children, by the 3rd decade it is responsible for 20% and by the 5th decade for less than 5%.
Clinical presentation
Haemorrhage. This is the most frequent first symptom of an arteriovenous
malformation and, although the bleeding may be subarachnoid, there is commonly an
intracerebral component. The arteriovenous fistulous
communication results in the development of aneurysms within the lesion, enlargement of the
arteries which feed the malformation and, consequently, the possible secondary development
of saccular aneurysms on the major feeding vessels. The haemorrhage associated with an
arteriovenous malformation may quite often be due to rupture of a saccular aneurysm on the
feeding vessel.
Epilepsy. This is the second most common presenting manifestation of an
arteriovenous malformation.
Headache. Migraine characteristics are particularly associated with
headache due to arteriovenous malformation.
Progressive neurological deficit. For example, a slowly progressive
hemiparesis may occur in a large malformation due either to local ischaemia induced by the shunt
or to increasing size of the lesion.
Surgical anatomy
Most arteriovenous
malformations are situated in the cerebral hemispheres, although they may occur in the
posterior fossa involving either the cerebellum or brainstem and they show considerable variation in size.
The malformations involving the cerebral hemispheres frequently form a pyramidal
mass, the base of which may reach the cortical surface with the apex pointing towards the lateral
ventricle. There are frequently multiple, enlarged arteries feeding the malformation and arterialized
draining veins extend superficially to the superior sagittal sinus or transverse sinus or
deeply into the deep cerebral venous system.
Radiological investigations for arteriovenous malformations (Figs 9.10–9.12)
An arteriovenous malformation is often apparent on the CT scan
because of the vivid enhancement of the enlarged feeding vessel and arterialized draining veins after
intravenous contrast. Cerebral angiography is best performed using digital subtraction
angiographic techniques and is essential for adequate evaluation of the
malformation. Precise determination of the position of the major feeding and
draining vessels is vital prior to surgery. Magnetic resonance imaging is a valuable aid in determining
the exact position of the arteriovenous malformation and the vessels. Preoperative
occlusion of accessible major feeding vessels close to the malformation by an interventional
radiologist may be useful if the procedure is technically feasible. Aflow-directed catheter is
positioned in the artery, which is occluded using cyanoacrylate
glue or a polymerizing collagen mixture.
Fig. 9.10 (a) The arteriovenous
malformation enhances vividly on the CT scan after intravenous contrast and the major dilated feeding
vessels can be seen. (b) The MRI shows the position of the malformation in
coronal and axial
planes and further information about the feeding vessels and draining veins
(c).
Fig. 9.11 Cerebral angiography
(digital subtraction angiogram) demonstrates the vascular anatomy of the arteriovenous
malformation. (a) The major feeding vessels are shown on the arterial phase.
(b) The draining veins are demonstrated on the venous phase.
Management
As with cerebral aneurysms the aim of treatment is to avoid either an
initial haemorrhage or rebleed from the malformation. There has been controversy over the
risk of haemorrhage and the morbidity and mortality associated with rupture of an arteriovenous
malformation. Recent studies have shown that the chance of haemorrhage for both ruptured and
unruptured arteriovenous malformations is about 3% each year and that the combined morbidity
and mortality of each haemorrhage is at least 40%. However, unlike cerebral aneurysms,
haemorrhage from an arteriovenous malformation rarely causes symptomatic vasospasm.
Surgical excision, provided it is technically feasible and would not result
in a disabling neurological deficit, should be performed if the malformation has
haemorrhaged. Unruptured arteriovenous malformations should be considered
for excision if surgery is unlikely to produce significant neurological deficit.
Surgery for arteriovenous malformations
The principles of the operation involve isolation and occlusion of the
principal feeding arteries followed by meticulous dissection of the malformation, with occlusion and
division of the numerous small feeding vessels. The draining veins should be ligated
only after all the feeding vessels have been occluded, since premature obstruction to the arterialized
venous outflow will result in a precipitous swelling and rupture of the vascular mass.
The surgical
management of giant arteriovenous malformations is fraught with considerable risk. The lesions may
be surrounded by chronically ischaemic brain ‘steal’ by the malformation and
abrupt occlusion of the shunt through the malformation has led in some cases to oedema and
haemorrhage in the adjacent brain, a phenomenon first described by Spetzler and which was called
the ‘normal perfusion pressure breakthrough’ theory. Methods that have been employed to
avoid this complication include preoperative and intraoperative embolization and
staged excision of the malformation.
The use of radiosurgical techniques, involving either the gamma
knife (a highly focused cobalt source of irradiation) or stereotactic radiosurgery using a linear
accelerator, has been advocated for the treatment of small (less than 3 cm diameter), unruptured and surgically
inaccessible arteriovenous malformations with complete angiographic obliteration in
greater than 80% of lesions with a diameter of 3 cm or less at 3 years after radiation.
However, as the radiotherapy effect is slow, the patient remains at risk from haemorrhage for some
years.
Vein of Galen
malformation
This unusual
malformation results when arteries feed directly into the vein of Galen and produces distinct clinical
syndromes depending on the age at which the disease presents.
• Neonates present
shortly after birth with cyanosis and heart failure due to the shunt through the
malformation.
• Infants and young
children present with seizures and hydrocephalus due to obstruction of the cerebral
aqueduct.
• Adults may present
with multiple subarachnoid haemorrhage.
STROKE
Stroke is the third
most common cause of death in most Western countries and the commonest cause of chronic
adult disability. In many Western countries, there has been an impressive fall in population-based
stroke mortality over the past few decades, averaging 4–5% each year. This has been chiefly
attributed to the more effective recognition and treatment of hypertension and other risk factors.
Despite this progress, with the increasing life expectancy of the population, a marked increase in
stroke prevalence has been predicted. Stroke is generally a disease of ageing, but young adults are
also affected, with a somewhat different pathogenetic spectrum. The overall approach to stroke
has undergone a dramatic change in recent years, with important recent advances in prevention
strategies, the widespread introduction of acute stroke units, the application of new imaging
technologies and the introduction of thrombolysis for selected patients with acute ischaemic
stroke.
The term ‘stroke’ is used to describe a
sudden neurological deficit of vascular aetiology lasting more than 24 hours. A
transient ischaemic attack (TIA) indicates a transient neurological deficit of vascular
origin lasting less than 24 hours, although many patients with TIAs lasting more than minutes
have in fact suffered some neuronal damage and this time definition has been recently
challenged. Stroke is classified as cerebral infarction or ischaemic stroke, signifying ischaemic
brain damage, or cerebral haemorrhage, where the primary pathology involves vascular rupture and
extravasation of blood into the surrounding tissues. The term ‘haemorrhagic
infarction’ is used to describe an infarct into which
there has been a secondary extravasation of blood. Although subarachnoid haemorrhage (SAH) may not be
associated with a focal neurological deficit, it is usually categorized as a
stroke subtype.
Stroke prevention
Stroke prevention involves primary and secondary strategies. Primary
prevention includes lifestyle modification and treatment of risk factors in individuals who
have not experienced cerebrovascular symptoms. Risk factor management can be categorized
into the high risk approach (detecting and treating patients at high risk of stroke, such
as those with atrial fibrillation or hypertension) and the mass or population
approach (such as reducing salt intake and hence attempting to lower
blood pressure in the entire population).
Secondary prevention involves the use of strategies in a
symptomatic individual after a stroke or TIA, generally tailored to the specific type of
cerebrovascular pathology. Most stroke prevention studies have focused on a
reduction in the incidence of stroke, neurological disability and other vascular
endpoints. Recently, prevention of vascular dementia has also been recognized as an
important additional goal.
Primary prevention
Primary prevention strategies target the modifiable risk factors for
stroke (Table 10.1).
Secondary prevention
Secondary prevention strategies after stroke or TIA, unlike the
primary prevention techniques, are tailored to the underlying stroke pathology. The range of
secondary prevention strategies continues to expand (Table 10.2). These include the introduction of a
number of new antiplatelet strategies, proof of the efficacy of warfarin in non-valvular atrial
fibrillation, clarification of the indications for carotid endarterectomy and the introduction of
cerebral angioplasty/stenting.
Carotid endarterectomy
Two large trials (the North American Symptomatic Carotid
Endarterectomy Trial—NASCET and the European Carotid Surgery Trial—ECST) showed major benefits
for carotid endarterectomy over optimal medical therapy in patients with greater than 70%
carotid stenosis and either TIA or non-disabling stroke. In the NASCET study, an
absolute risk reduction of 17% over 18 months was achieved, indicating that one stroke could
be prevented for every six patients.
carotid
endarterectomy
Cerebrovascular angioplasty/stenting
Percutaneous transluminal angioplasty is increasingly used for symptomatic
and asymptomatic carotid stenosis, usually combined with endovascular
stenting. However, there is limited proof of efficacy and safety compared with
endarterectomy. One trial showed that the benefits and risks of surgery
and angioplasty/stenting were approximately equivalent. Large trials are now being conducted
in patients with symptomatic carotid stenosis, comparing stenting with endarterectomy.
Distal protection devices, which trap embolic debris at the time of the procedure, represent an
important advance. Stenting has also been used in small series of patients with symptomatic
intracranial stenoses, in whom optimal medical therapy has failed.
Acute stroke
The spectrum of
transient ischaemic attacks and stroke
Transient ischaemic attacks (TIAs) and completed cerebral infarcts are
caused by similar pathological mechanisms, most commonly large vessel
atherosclerotic disease, cardioembolism and small vessel lacunar disease. Patients
with TIAs and completed infarcts, whether large or small, have a similar
prognosis, with a 5–10-fold annual increase in stroke risk. Both conditions should be regarded as
medical emergencies. While TIAs by convention last less than 24 hours, most last
only minutes. The majority of TIAs lasting more than 1–2 hours produce tissue damage on sensitive
brain imaging techniques, such as magnetic resonance imaging. The old 24-hour
definition is therefore increasingly criticized and is not clinically
useful. The recognition of patients with minor ischaemic deficits presents a vital opportunity
for prevention of major stroke. Patients with TIAs should be urgently evaluated within 24
hours of the episode. Investigations would typically include a CT or MR scan to detect infarction
or non-vascular pathology, carotid duplex Doppler to diagnose major carotid disease, and
ECG, sometimes followed by echocardiography, to diagnose atrial fibrillation or another
cardioembolic source.
Carotid-territory
TIAs
These are due to
transient ischaemia in the retina or cerebral hemisphere. Transient monocular blindness (‘amaurosis fugax’) is due to a
transient reduction in retinal perfusion produced by embolism or
haemodynamic failure. The patient often describes a shade pulled down over one eye. In clinical
practice it is vital to determine whether a visual disturbance is truly monocular, indicating retinal
ischaemia, or binocular, often implicating the vertebrobasilar circulation. Hemispheric symptoms
most commonly consist of transient dysphasia and varying degrees of hemiparesis or
hemisensory disturbance, either singly or in combination.
Vertebrobasilar TIAs
These are often more
complex than carotid territory events and usually include two or more of the following
symptoms:
• binocular visual
disturbance
• vertigo
• diplopia
• ataxia
• bilateral weakness
or paraesthesiae
• deafness
• tinnitus
• amnesia.
These symptoms are
produced by transient ischaemiaof the brainstem, occipital and medical temporal lobes and
upper spinal cord.
Classification and pathogenesis of stroke
Cerebral infarction (ischaemic stroke)
Cerebral infarction accounts for approximately 80% of stroke
patients and may be classified according to anatomical location or pathogenesis. It is useful to
incorporate both classifications when considering stroke in a particular
patient.
Anatomical classification
The anatomical location refers to the specific arterial territory
(e.g. internal carotid vs. vertebrobasilar, anterior cerebral vs.
middle cerebral) or specific location within the brain (e.g. lateral medullary syndrome,
ventral pontine infarction or internal capsular infarction). Infarction most commonly occurs in
the middle cerebral arterial territory and can be classified as cortical or deep (subcortical). The
cortical middle cerebral syndromes depend on whether a small branch has been occluded, or
whether one or both of the main two divisions of the middle cerebral artery is involved, the
superior or inferior division. Subcortical infarcts occur in the territory of the deep perforating
vessels supplying the internal capsule, thalamus, basal ganglia and brainstem. The occlusion of a
single perforating vessel produces a small deep infarct, less than 1.5 cm in diameter, called a lacunar infarct, particularly if associated with one
of the five classical clinical syndromes (see below). The obstruction of the origins of several of
the deep perforating branches can produce a larger subcortical infarct termed a striatocapsular
infarct.
Pathogenetic classification
Greater emphasis is now placed on the pathogenesis of cerebral
infarction, as this is useful for the selection of secondary prevention
therapies. This classification is often referred to as the TOAST system, after the
TOAST trial.
1 Large artery atherosclerosis.
2 Cardiogenic embolism.
3 Lacunar infarction.
4 Rare causes (e.g. dissection, vasculitis, prothrombotic states).
5 Unclassified:
• despite adequate investigation
• due to inadequate investigation.
Large artery atherosclerosis (Figs 10.1–10.3)
The development of extracranial atherosclerotic plaque produces a
progressive arterial stenosis. Subsequent plaque complications include ulceration,
intraplaque haemorrhage and superimposed platelet–fibrin thrombus formation. Stroke is most often
due to the development of thrombus (Fig. 10.4) followed by propagation and distal
thromboembolism into the intracranial vessels, sometimes embolism composed of atheromatous debris,
or haemodynamic failure due to the reduction of cerebral perfusion in the arterial border zones
(borderzone or watershed infarction). Primary
intracranial atherosclerosis and atherothrombosis is rare in Caucasian populations, but more common in
African, African-American and Asian stroke patients (Fig. 10.5).
Clinical features include demonstration of relevant arterial pathology
with 50% or greater stenosis and the absence of a cardiac source. Anterior circulation infarcts
typically involve the cerebral cortex. Prodromal TIAs in the same arterial territory are another
pointer
.
Fig. 10.1 Arterial digital
subtraction angiogram demonstrating severe, proximal internal carotid artery stenosis .
Fig 10.2. carotid duplex ultrasound: high-grade
stenosis (a) and occlusion (b) of internal carotid artery
Fig. 10.3 Diffusion-weighted imaging scan (left
image) showing
large acute middle cerebral artery (MCA) cortical infarct. Magnetic
resonance angiography
(right image) shows
lack of flow in the left MCA.
Cardiogenic embolism
Avariety of cardiac diseases affecting the cardiac walls, valves or
chambers can lead to cerebral embolism. These include:
• non-valvular atrial
fibrillation (the most common)
• valvular heart disease
• myocardial infarction with ventricular thrombus formation
• post-cardiac surgery (valvular surgery or coronary artery bypass grafts)
• prosthetic cardiac valves
• infective endocarditis
• atrial myxoma
• cardiomyopathy
• septal defect with paradoxical embolism.
Clinical features include delineation of a cardiac source and lack of
evidence of large artery disease. Similarly, the cerebral cortex is usually involved.
Lacunar infarction (Fig. 10.7)
The occlusion of single deep perforating arteries supplying the
internal capsule, basal ganglia or brainstem can lead to the development of small lacunar infarcts.
These are most commonly the result of hypertensive disease, which produces localized arterial
wall pathology, termed lipohyalinosis, in these small penetrating arteries, or localized
microatheroma. Lacunar infarcts are less often due to embolism from a proximal source such as
extracranial atherosclerosis or intracardiac thrombus.
Fig. 10.7 Diffusion-weighted
imaging scan showing acute left thalamic lacunar infarct (hyperintense lesion).
Classical lacunar
syndromes include pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic
hemiparesis and the dysarthria/clumsy hand syndrome. Clinical pointers include
clinical diagnosis of one of the classical syndromes, usually exclusion of a large artery or cardiac
source and ideally neuroimaging confirmation of a small, deep infarct.
Oxfordshire
classification
Another commonly used
stroke classification, termed the Oxfordshire classification, divides ischaemic stroke into
TACI (total anterior circulation infarction), PACI (partial anterior circulation
infarction), POCI (posterior circulation infarction) and LACI (lacunar infarction). This classification
is also useful and the subtypes correlate with prognosis.
Cerebral haemorrhage (haemorrhagic stroke)
Cerebral haemorrhage is generally classified into intracerebral and
subarachnoid haemorrhage.
Intracerebral haemorrhage (Figs 10.9–10.10)
Non-traumatic (primary) intracerebral haemorrhage is most commonly due
to hypertension, which leads to rupture of deep perforating arteries in the putamen,
thalamus, central white matter, brainstem and cerebellum. The precise mechanism of this
vascular rupture is uncertain, but may be related to the development of small Charcot–Bouchard
microaneurysms on the vessel walls of these end-arteries, or direct rupture of vessels affected by
lipohyalinosis.
Fig. 10.9 CT scan showing
hypertensive putaminal haemorrhage.
Fig. 10.10 CT scan showing frontal and occipital lobar haemorrhages in a
patient with amyloid angiopathy.
‘Lobar’ haemorrhage refers to superficial vascular rupture within the
cerebral lobes, outside these deep arterial territories. It is sometimes due to an underlying structural
lesion, such as an arteriovenous malformation, cerebral aneurysm, tumour, vasculopathies or
coagulation disorders. Amyloid angiopathy is an important cause of lobar cerebral haemorrhage in
elderly patients and is due to amyloid deposition in the walls of the cerebral arteries. These haemorrhages
may be multiple and typically occur in patients who are normotensive and may show features
of Alzheimer’s disease.
Clinical clues to ICH include the features of a sudden rise in
intracranial pressure with depressed conscious state, headache and vomiting. The mortality is much
higher than in ischaemic stroke. However, patients with ICH may be surprisingly alert and well
looking. Conversely, patients with ischaemic stroke may have early depression of
conscious state. Hence, neuroimaging, usually with CT, is mandatory in all cases
to rapidly diagnose ICH.
Subarachnoid haemorrhage is classified
according to pathological cause and site. The two most important
identifiable causes include rupture of a berry aneurysm and arteriovenous
malformation, but in up to 15% of cases no bleeding can be identified at
angiography. Some of these idiopathic bleeds are due to perimesencephalic haemorrhage.
Modern principles of acute stroke management
Key principles of acute stroke management include:
1 Urgent recognition of stroke symptoms by the patient or their
carer.
2 Urgent ambulance transport to a hospital with adequate diagnostic
facilities and organized stroke care.
3 Urgent triage and investigation in the emergency department including
CT brain scanning.
4 Assessment for acute stroke therapy, particularly thrombolysis.
5 Admission to a specialized stroke unit.
Clinical assessment of stroke
The following questions should be considered in the management of any
patient with a presumed stroke.
• Is it a stroke?
• Is it an infarct or haemorrhage?
• Is the patient eligible for thrombolytic therapy or other urgent
intervention?
• What is the arterial or anatomical localization and pathogenesis?
Stroke and pseudostroke
Non-vascular pathologies (‘pseudostroke’) such as cerebral tumour,
subdural haematoma, abscess, migraine, metabolic disturbances and epilepsy can mimic
the stroke process. All patients with suspected stroke require an urgent CT or MR scan to exclude
non-cerebrovascular disorders, as well as to differentiate between infarct and haemorrhage (Figs
10.8 and 10.9). Lumbar puncture is reserved for those cases where meningitis is
considered (usually after a CT scan) or where the diagnosis of subarachnoid haemorrhage is still contemplated
after a normal CT scan.
The distinction between infarct and haemorrhage
The distinction between cerebral haemorrhage and infarction is
vital, as some haemorrhages are considered for surgical evacuation, while patients with ischaemic stroke
may be considered for thrombolysis or anticoagulation. While there are clinical pointers
(see above) this differentiation is usually based on CT scan findings. Although CT scanning remains
the workhorse for acute stroke assessment, recent studies indicate that MRI is at least
as sensitive for intracerebral haemorrhage as CT and far more sensitive for acute ischaemia.
Patients with ischaemic stroke often have early infarct changes on CT, although these may be subtle.
MRI with diffusionweighted imaging (DWI) is increasingly used as this technique allows
a sensitive diagnosis of cerebral ischaemia (Figs 10.3 and 10.7).
Is the patient eligible for thrombolysis?
The thrombolytic agent tissue plasminogen activator (tPA) has now been
licensed in most parts of the world as the first proven stroke drug therapy, given intravenously
within 3 hours of stroke onset in selected patients with ischaemic stroke. The approval of this
acute therapy followed the positive results of a two-part pivotal trial, conducted in the USA. Other
European trials testing tPAup to 6 hours have shown a marked trend to benefit over risk,
and meta-analysis confirms the 3-hour window for tPA. Use of tPA increases the risk of symptomatic
haemorrhagic complications by three- to fourfold. Major early infarct changes on CT, for example
greater than one-third of the area of the middle cerebral artery, are associated with a higher risk of
haemorrhagic transformation. Up to 10% of ischaemic stroke patients can be treated in
well-organized centres. In contrast to the tPAtrials, three trials evaluating the role of intravenous streptokinase
produced negative results, chiefly linked to the substantial risk of intracerebral
haemorrhage associated with the drug.
Direct infusion of thrombolytics via intra-arterial catheters has been
shown to be effective in one trial up to 6 hours after middle cerebral artery occlusion.
There is interest in experimental mechanical devices which can break up thrombi, with a much lower
risk of cerebral haemorrhage.
Location and pathogenesis of infarction
Cortical infarcts (Fig. 10.3). Based on
the clinical examination, a distinction should be made between an infarction
in the carotid or in the vertebrobasilar territory. With regard to carotid territory infarction,
the presence or absence of cortical signs—dysphasia, apraxia, anosognosia (unawareness or
denial of the stroke), sensory, motor or visual agnosia (inattention), acalculia, right/left confusion,
dysgraphia or cortical sensory loss (loss of two-point discrimination, astereognosis,
dysgraphaesthesia)—suggests an embolic source from either the extracranial vessels or the heart, rather
than lacunar infarction.
Subcortical infarcts (Fig. 10.7). As
indicated earlier, lacunar infarcts (less than 1.5 cm in diameter) rely on diagnosis of
one of the classical lacunar syndromes. Cortical signs are not present. Lacunar syndromes reflect
small vessel occlusions in the internal capsule, thalamus and brainstem.
Haemorrhage
Intracerebral haemorrhage (Fig. 10.9). As
previously discussed, the rapid onset of a stroke with early depression of
conscious state favours the diagnosis of a primary intracerebral haemorrhage. Primary intracerebral
haemorrhage and aneurysmal subarachnoid haemorrhage can overlap in their
clinical presentations. For example, a berry aneurysm can rupture primarily into the brain parenchyma,
presenting as an intracerebral haemorrhage, whereas a primary brain haemorrhage can
rupture directly into the ventricular system and present with marked meningeal features
due to subarachnoid blood.
Urgent assessment in the emergency department
Rapid triage of suspected stroke patients should be performed in an
emergency department, with skilled medical evaluation and urgent investigations. These involve blood
tests, including a blood glucose measurement to exclude hypoglycaemia (which can mimic
acute stroke), and an ECG to diagnose atrial fibrillation or acute myocardial infarction, which can
reveal the cause of cerebral embolism. Most importantly, a CT brain scan must be
performed urgently in all patients to differentiate between cerebral infarction and cerebral haemorrhage.
In addition, CT scanning is essential to exclude the other brain pathologies that can simulate
stroke. As noted above, many centres are now using acute MRI with DWI and magnetic resonance angiography
(MRA). Computed tomographic angiography (CTA) is another useful tool.
Duplex Doppler scanning is of value in the diagnosis of large vessel
atherosclerosis, while echocardiography (usually less urgent) can aid in
the diagnosis of intracardiac thrombi and valvular or cardiac wall kinetic
abnormalities. Transoesophageal echocardiography is superior to
transthoracic echocardiography.
Acute stroke units
One of the most
important developments in acute stroke management in recent years has been the proven value
of stroke units, based on the results of clinical trials which have compared organized expert care
in a special unit to the management of patients in general medical wards. The usual stroke unit
model involves a geographical area in the hospital, incorporating a skilled
multidisciplinary stroke team, led by a neurologist or other physician with
expertise in stroke management. Vascular surgeons and neurosurgeons should be readily
available for consultation and intervention in selected cases. In a systematic overview
of the benefits of stroke units, it was shown that mortality could be reduced by about 25%, also
with evidence of reduced disability. In addition, stroke units have been found to reduce
bed stay and hence hospital costs.
The components of
team management in the stroke unit include:
1 Acute medical,
surgical and nursing care.
2 Diagnosis of the
pathological mechanism of the stroke and the institution of tailored secondary prevention
strategies.
3 Prevention, early
detection and treatment of complications such as aspiration pneumonia, pressure sores,
hyperglycaemia, seizures and sepsis.
4 Use of measurement
instruments and stroke registers.
5 Early integrated
neurorehabilitation with evaluation of premorbid status and therapy goals.
6 Involvement,
education, and support for patient and family.
7 Early, coordinated
discharge planning.
Acute medical care
Three key, evidence-based advances include the use of tPA, aspirin
(see below) and stroke unit care. In the acute phase, close monitoring of vital and neurological
signs is paramount, given that about a third of stroke patients deteriorate after admission to
hospital. Cardiac monitoring is useful for many acute stroke patients. Initial clinical evaluation should
involve assessment of the patient’s function and clinical state before the stroke, the stroke
type and pathogenesis, documentation of the nature and severity of neurological deficits, and
comorbid diseases. Early mobilization, range of motion exercises for hemiplegic limbs,
frequent turning, fluid and nutritional maintenance, dysphasia management, avoidance of
aspiration, prevention of deep venous thrombosis (DVT) and pneumonia, management of
incontinence, treatment of urinary tract infections and other causes of fever, and maintenance of
skin integrity are all key planks in the team treatment of the acute stroke patient.
Patients should have oximetry, but there is no evidence of the value
of routine supplemental oxygen by mask or nasal prongs. Patients should be well hydrated
using normal saline rather than glucose-containing solutions, because of the hazards of even mild degrees
of hyperglycaemia. In general, blood pressure should not be acutely lowered, because this
can compromise cerebral perfusion in acute stroke. Hypertension is usual in acute stroke and
this usually settles spontaneously over 2–3 days. We routinely use compression stockings and usually
low-dose heparin, or low molecular weight heparin or heparinoid, in DVT prophylaxis.
Airway assessment should be an urgent priority to avoid aspiration pneumonia.
We generally use nasogastric feeding after 24–48 hours if the patient’s bulbar function is
compromised.
Adverse prognostic factors include advancing age, depression of
conscious state, severity of neurological deficit, conjugate gaze palsy and early urinary
incontinence. Causes of mortality in stroke patients are predominantly neurological (transtentorial
herniation) in the 1st week, and due to secondary systemic factors in the 2nd and 3rd weeks such as
pneumonia, pulmonary embolism and cardiac causes.
Progressing stroke
A deteriorating neurological deficit is seen in about one-third of
stroke patients. Cerebral oedema, with progressive elevation of intracranial pressure, is an
important cause of death. However, this oedema is generally cytotoxic and clinical trials have
demonstrated that corticosteroids are of no value in either cerebral infarction
or haemorrhage. Intravenous mannitol and glycerol are sometimes empirically
used, but their value has not been proven. In highly selected young patients with severe, early
brain oedema, surgical decompression with hemicraniectomy should be considered.
Heparin
Heparin has been the most widely used unproven therapy in most
countries. The International Stroke Trial (IST) evaluated unmonitored, subcutaneous heparin
up to 48 hours after stroke onset and showed that a slight reduction in recurrent stroke
was offset by an increased risk of haemorrhagic transformation. The rate of early,
recurrent embolism in patients with atrial fibrillation was much lower in recent trials than in a
number of earlier clinical studies.
Systematic overview of the available evidence leads to the
conclusion that heparin is not generally indicated for most patients with acute ischaemic stroke, but
heparin should be considered for selected patients with nondisabling ischaemic stroke and
a very high risk of recurrent embolism.
Acute aspirin
Two large trials (the International Stroke Trial and the Chinese Acute
Stroke Trial) both showed that, as for acute myocardial infarction, aspirin administered within
48 hours of stroke onset produced a modest improvement in outcomes at 6 months. Hence,
aspirin should be used routinely in acute ischaemic stroke, unless thrombolysis is being used.
Neuroprotective
therapies
A complex cascade of
biochemical changes occurs in stroke, secondary to the initial ischaemia. Ischaemic brain
injury is associated with elevated levels of the excitatory neurotransmitters glutamate and
aspartate. These lead to excessive stimulation of the N-methyl D-aspartate (NMDA) receptor on
the cell surface. This activation is followed initially by an influx of sodium and water into the
cells and secondly by a sudden rise in intracellular calcium. Arange of neuroprotective compounds has been
designed to inhibit various points in the excitotoxic cascade. These include calcium
channel and NMDAantagonists, glutamate release inhibitors, glycine antagonists, free radical
scavengers, inhibitors of the neutrophil influx into the ischaemic region and
various growth factors. To date, none of these compounds have proven
effective in adequately powered, Phase III clinical trials, but there are several ongoing
studies. Other approaches include the combination of thrombolysis with neuroprotective drugs.
Cerebral hemorrhage
While routine surgical evacuation of haematoma is unproven, we
consider evacuation in selected patients with cerebral haemorrhage, particularly in the cerebellum, as
well as younger patients with lobar haemorrhage. The general principles of acute stroke
management apply equally to intracerebral haemorrhage as to infarction.
Prevention of recurrent stroke—secondary stroke prevention
Patients with symptomatic high-grade carotid stenosis should be
considered for subacute carotid endarterectomy. While surgery is awaited, or if
endarterectomy is inappropriate, antiplatelet therapy should be instituted. In cardioembolic stroke,
there is uncertainty as to the optimal timing of anticoagulation, particularly in patients with
atrial fibrillation. Our approach is to employ heparin acutely if the patient has a mild deficit
and there is a high risk of recurrent embolism. Many patients with atrial
fibrillation are commenced on warfarin 7–10 days after onset, without prior
heparin, because of the risk of haemorrhagic transformation. Lacunar infarcts are less commonly
embolic and generally have a good prognosis.