Cerebrovascular
diseases include some of the most common and devastating disorders: ischemic
stroke, haemorrhagic stroke, and cerebrovascular anomalies such as intracranial
aneurysms and arteriovenous malformations (AVMs). Most cerebrovascular diseases
are manifest by the abrupt onset of a focal neurologic deficit, as if the
patient was “struck by the hand of God” (Smith et al 2008).
Between
5% and 10% of stroke are due to subarachnoid haemorrhage (Aminoff 2007). Subarachnoid
haemorrhage typically presents with a sudden severe “thunder clap”
headache (often occipital) which lasts for hours or even days, often
accompanied by vomiting. There may be loss of consciousness at the onset, so
subarachnoid haemorrhage should be considered if a patient is found comatose. Since
1 patient in 8 with a sudden severe headache has had a subarachnoid
haemorrhage, clinical vigilance is necessary to avoid a missed diagnosis. All
patients with a sudden severe headache require investigation to exclude a
subarachnoid haemorrhage (Allen et al 2006).
Forty
five percent of patients die with in the first 30 days following subarachnoid
haemorrhage, nearly two third die as a result of the initial haemorrhage and
most within first two days (Parr et al 1996). Of those who survive more than
half are left with major neurologic deficits as a result of the initial
haemorrhage, cerebral vasospasm with infraction or hydrocephalus. If the
patient survives but the aneurysm is not obliterated the annual rebleed rate is
about 3% (Smith et al 2001).
Despite
vigorous therapeutic efforts, the mortality rate from subarachnoid haemorrhage
remains high. So the major therapeutic emphasis is on preventing the
predictable early complications of the rupture which in turn depends upon early
diagnosis and prompt therapeutic intervention. A greater understanding of the
basic mechanisms and pathology of subarachnoid haemorrhage may lead to more
effective prevention and therapeutic strategies. Early diagnosis of
subarachnoid haemorrhage requires good knowledge about clinical features and
using necessary investigating tools at an earlier and appropriate time.
The
aim of writing this review article on subarachnoid haemorrhage is to understand
the details of subarachnoid haemorrhage including its pathophysiology, disease
presentation, management of such patients and future thinking.
Arteries of the
brain(Snell 1997)
The brain is
supplied by the two internal carotid and the two vertebral arteries (Fig.1). Four
arteries remain within the subarachnoid space and their branches anatomies on
the inferior surface of the brain to form the circle of Willis.
Fig.1.
The arteries at the base of the brain. The right temporal pole and most of the
right hemisphere of the cerebellum have been removed. Verifications in the
pattern of these vessels are common. Source: Gray’s anatomy (38th edn).
INTERNAL CAROTID ARTERY
Branches
of the cerebral portion:
The opthalmic artery: It supplies the eye and other orbital
structures, frontal area of the scalp, the ethmoid and frontal sinus and
the dorsum of the nose.
Posterior communicating artery: It is a small vessel, forming part of the circle
of Willis.
Choroidal artery: It is a small artery, ends in the choroid plexus
also gives off small branches to crus cerebri, the lateral geniculate
body, the optic tract, and the internal capsule.
Anterior cerebral artery: It is connected with it opposite anterior
cerebral artery by anterior communicating artery; the cortical branches
supply all the medial surface of the cerebral cortex as far back as the
parieto-occipital sulcus. They also supply a strip of cortex about 1 inch
wide on the adjoining lateral surface. A group of central branches supply
parts of the lentiform, caudate nuclei and the internal capsule.
VERTEBRAL ARTERY
The
vertebral artery is a branch of the first part of the subclavian artery. It
inters the skull through the foramen magnum. At the lower border of the pons,
it joins the vessel of the opposite side to form the basilar artery.
Branches
of the cranial portion:
Posterior spinal artery
Anterior spinal artery
Posterior inferior cerebella artery: It supplies the inferior surface of the vermin.
The central nuclei of the cerebellum and the under surface of the
cereballar hemisphere, it also supplies the medulla oblongata and the
choroid plexus of the fourth ventricle.
Medullary arteries are very small branches that are distributed to
the medulla oblongata.
BASILAR ARTERY
The pontine arteries are numerous small vessels that enter the substances
of the pons.
The labyrinthine artery.
The anterior inferior cereballar artery: It supplies the superior surface of the
cerebellum. It also supplies the pons, the pineal gland and the superior
medullary velum.
The superior cerebellar artery: It supplies the superior surface of the
cerebellum. It also supplies the pons, the pineal gland, and the superior
medullary velum.
Posterior cerebral artery: Cortical branches supply the infero-lateral and
medial surfaces of the temporal lobe and the lateral and medial surfaces
of the occipital lobe. Central branches pierce the brain substance and
supply parts of the thalamus and the lentiform nucleus and the midbrain,
the pineal and the medial geniculate bodies.
subARACHnoid
space
This
is the space between the subarachnoid and the piamater, which contains CSF and
the larger arteries and veins which traverse the surface of the brain (Fig.2).
Arteries and veins are coated by a thin layer of lepto-meninges. The pia and arachnoids
mater are connects by collagenous trabecule and sheets. The piamater is
reflected from the surface of the brain and pass along with vessels in the
brain substance and disappear as the vessels become capillaries (Berry et al
1995).
Wherever
the brain and the cranium are not close to each other, there is a wide interval
between pia and arachnoid matter and form subarachnoid cisterns, like
cerebellomedullary cistern, pontine cistern, interpeduncular cistern,cistern of
lateral fossa etc. the interpeduncular cistern contains circle of Willis (Berry
et al 1995).
The
cerebrospinal fluid subarachnoid space is a modified tissue fluid and amount is
about 150 ml. The cerebrospinal fluid gives buoyancy to the brain and protects
the nervous tissue from mechanical forces applied to the skull. Inferiorly, the
subarachnoid space extends beyond the lower end of the spinal cord and invests
the cauda equine. The subarachnoid space ends below at the level of the
interval between the second and third sacral vertebrae (Snell 1997).
Fig.2.
Relationships of pia and arachnoid mater to the dura, brain and vessels.
(modified from Alcolado et al 1988 according to Zhang, Inman & Weller
1990).
Source:
Grays’ Anatomy (38th edn).
CIRCLE OF
WILLIS
The
circle of Willis lies in the interpeduncular fossa at the base of the brain. It
extends from the superior border of the pons to the longitudinal fissure. It is
formed by the anastomosis between the two internal carotid arteries and the two
vertebral arteries. The anterior communicating, anterior carotid, posterior
communicating, posterior cerebral, and basilar arteries all contribute to the circle.
The circle of Willis allows blood that enters by either internal carotid or
vertebral arteries lobe distributed to any part of both cerebral hemispheres
(Snell 1997).
Two
types of branches arise from the circle and its major branches; these are
arbitrarily divided into cortical and central and they differ from each other
in the extent of their anastomosis. The central branches are very numerous and
slender; they tend to arise in groups and immediately pierce the surface of the
brain to supply its internal parts. The largest collections of these pass
through the anterior and posterior perforated substances. They do not anatomies
to a significant extent within the brain substance. The cortical branches
ramify over the surface of the cortex and anatomies fairly freely on the
piameter. They give rise to numerous small branches which enter the cortex at
right angles and like central branches, do not anatomies in it. It follows that
blockage of an artery on the piameter may produce little if any damage to the
brain but damage to branches entering the substances of the brain leads to
destruction of brain tissue (Romanes 1986).
The
arteries of brain are liberally supplied by sympathetic nerves which run on to
them from the carotid and vertebral plexuses. They are extremely sensitive to
injury and readily react by passing into prolong spasm. This of itself may be
sufficient to cause damage to brain tissue since even the least of neurons can
not withstand absolute loss of blood supply for a period exceeding seven
minutes (Romanes 1986).
Fig.3.
Diagram of the arteries at the base of the brain, showing the constitution of
the arterial circle. The arteries constituting this so called arterial ‘circle’
are commonly asymmetrical and sometimes a constituent vessel is missing. AL=
anterolateral central branches; AM= anteromedial central branches; PL=
posterolateral central branches;
PM=
posteromedial central branches. Source: Gray’s Anatomy(38th edn)
CAUSES OF SUBARACHNOID HAEMORRHAGE
In
85% of cases of spontaneous SAH, the cause is rupture of a cerebral aneurysm—a
weakness in the wall of one of the arteries in the brain that becomes enlarged.
They tend to be located in the circle of Willis and its branches. While most
cases of SAH are due to bleeding from small aneurysms, larger aneurysms (which
are less common) are more likely to rupture (Van Gijn et al 2007).
In
15–20% of cases of spontaneous SAH, no aneurysm is detected on the first angiogram
(Rinkel et al 1993). About half of these are attributed to non-aneurysmal
perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid
spaces around the midbrain (i.e. mesencephalon). In these, the origin of the
blood is uncertain (Van Gijn et al 2007).The remainder are due to other
disorders affecting the blood vessels (such as arteriovenous malformations),
disorders of the blood vessels in the spinal cord, and bleeding into various
tumors (Van Gijn et al 2007). Cocaine abuse and sickle cell anemia (usually in
children) and, rarely, anticoagulant therapy, problems with blood clotting and
pituitary apoplexy can also result in SAH (Warrell et al 2003; Rinkel et al
1993).
INTRACRANIAL
ANEURYSM
EPIDEMIOLOGY
The
incidence and prevalence of unruptured intracranial aneurysms and aneurysmal
SAH should be considered separately. Intracranial aneurysms are found on
postmortem examination in between 1% and 6% of adults in large autopsy series
(Schievink 1997). The frequency of intracranial aneurysm seen during
angiography for patients not suspected of harboring an aneurysm is between 0.5%
and 1.0%. The overall incidence of SAH from aneurysms is approximately 7-10 per
100,000 people per year (Menghini et al 1998), but this figure includes children,
who have a very low incidence of rupture. The mean age of rupture is
approximately 50 years. Among adults older than 30 years of age, the incidence
of SAH is approximately 40-50 per 100,000 per year, and nearly one half of
these individuals die from their SAH. Various reviews have noted a slight
female predominance of SAH from aneurysms, with a mean age of haemorrhage of
approximately 50 years. Ruptured aneurysms rarely occur in children, and there
is a steady increase in the incidence of rupture from 0.3 per 10,000 persons
per year between 25 and 34 years of age to 3.7 per 10,000 persons per year for
patients 65 years of age or older.
A
special category of patients are those who have a family history of aneurysms
and SAH. Familial occurrence of intracranial aneurysms is defined by the
presence of aneurysms in two or more first to third degree relatives without
any known hereditary disease. It is not known whether the pathogenesis of
familial intracranial aneurysms differs from that of the general population (Ronkainen
et al 1998). In a community-based study from Rochester, MN, the relative risk
of SAH among first-degree relatives of patients with the familial form of SAH
was four times higher than the general population. Other studies have shown
that in patients with familial intracranial aneurysms, there is a lower mean
age at the time of rupture compared with SAH in the general population (Ronkainen
et al 1998). Screening studies, with MRA, CT angiography, for the presence of
aneurysms in this group of patients appears warranted.
ANEURYSM PATHOGENESIS AND CAUSE:
Several
classifications of aneurysms have been proposed. This was suggested by Weir
(1985).
Morphology
Saccular
Fusiform
Dissecting
Size
Approximately
90 to 95 percent of saccular aneurysm lies on the anterior part of the circle
of Willis. The four most common sites are
1.
The proximal portions of the anterior communicating artery.
2.
At the origin of the posterior
communicating artery from the stem of the internal carotid,
3.
At the first major bifurcation of the middle cerebral artery, and
4.
At the bifurcation of the internal carotid into middle and anterior cerebral
arteries.
Other
sites include the internal carotid artery in the cavernous sinus, at the origin
of the ophthalmic artery, the junction of the posterior communicating and
posterior cerebral arteries, the bifurcation of the basilar artery, and the
origins of the three cerebeller arteries. Aneurysms that rupture in the
cavernous sinus may give rise to an arteriovenous fistula.
Fig.4.
Common sites of berry aneurysms in the circle of Willis
Source:
Robin’s Patholgy (6th edn.)
Saccular Aneurysms (Selman et al 2004)
Saccular,
or berry, aneurysms are the most common form of aneurysms and are most often
responsible for aneurysmal subarachnoid haemorrhage. Saccular aneurysms may
arise from defects in the muscular layer of cerebral arteries that occur at
vessel bifurcations and from degenerative changes that damage the internal
elastic membrane, resulting in weakness of the vessel wall. They usually occur
on the first or second order arterial branches of the vessel emanating from the
circle of Willis. Evidence suggests that both genetic and environmental factors
contribute to the development of saccular aneurysms. The evidence that genetic
factors are important comes from the documented association of intracranial
aneurysms with heritable connective tissue disorders such as autosomal dominant
polycystic kidney disease, Ehlers-Danlos syndrome type IV, neurofibromatosis
type 1, and Marfans syndrome. The familial occurrence of intracranial aneurysms
also points to a role for genetic factors. In those patients who have a first
degree relative with an aneurysmal SAH, the risk of a ruptured aneurysm is four
times higher than the risk in the general population. A role for acquired
factors in the pathogenesis of saccular aneurysm is suggested by the mean age
of 50 for patients with aneurysmal SAH, and the increased incidence of
haemorrhage occurring with age. Cigarette smoking is a risk factor in all
population studies, and a role for systemic hypertension, although not as
strong as that of cigarette smoking, in the cause of aneurysm formation appears
likely.
Saccular
aneurysms may also be caused by infection, trauma, or neoplasm. Mycotic
aneurysms results from infected emboli that lodge in the arterial intima or the
vasa vasorum and account for approximately 5% of all intracranial aneurysms.
They occur most frequently in patients with subacute bacterial endocarditis,
congenital heart disease, or a history of intravenous drug use, and are usually
located on more distal branches of the cerebral vasculature. Proper management
includes appropriate intravenous antibiotic therapy, with surgery in selected
cases. Fungal aneurysms, which are much rarer than bacterial, usually are
associated with arteritis and thrombosis and have been uniformly fatal.
Traumatic
aneurysms are rare but can be caused by either blunt or penetrating head
injury. Such aneurysms occur at sites other than bifurcations. Angiograms are
not routinely performed following head trauma, and these lesions may not be
detected, but they should be considered in patients who suffer delayed
deterioration. Early operative repair is recommended because of the high
mortality associated with these lesions.
Neoplastic
embolization, in rare cases, may produce an aneurysm in patients with choriocarcinoma,
atrial myxoma, and undifferentiated carcinoma. In forming an aneurysm, the
tumor embolus may remain viable, penetrate the endothelium, grow subintimally,
and eventually destroy the arterial wall.
Morphology (girolami et al 1999)
An
unruptured berry aneurysm is a thin-walled out pouching at arterial branch points
along the circle of Willis or major vessels just beyond. Berry aneurysms
measure a few mm to 2 to 3 cm and have a bright red, shiny surface and a thin
translucent wall. Demonstration of the site of rupture requires careful
dissection and removal of blood in the unfixed brain. Atheromatous plaques,
calcification, or thrombotic occlusion of the sac may be found in the wall or
lumen of the aneurysm. Brownish discoloration of the adjacent brain and
meninges is evidence of prior haemorrhage. The neck of the aneurysm may be
their wide or narrow. Rupture usually occurs at the apex of the sac with extravasations
of blood into the subarachnoid space, the substances of the brain, or both. The
arterial wall adjacent to the neck of the aneurysm often shows some intimal
thicking and gradual attenuation of the media as it approaches the neck. At the
neck of the aneurysm, the muscular wall and intimal elastic lamina are usually
absent or fragmented, and the wall of the sac is made up of thickened
hyalinized intima. The adventitia covering the sac is continuous with that of
the parent artery.
Fusiform Aneurysms (Selman et al 2004)
Fusiform
or dolichoectatic aneurysms are classified separately from saccular aneurysms,
although in some patients these types may overlap. The basilar artery is most
commonly affected, although these aneurysms also can be seen in the anterior
circulation. Only rarely are these lesions associated with SAH. Their
presentation is characterized by cranial nerve or brainstem dysfunction
secondary to direct compression or by embolization from intraluminal thrombus.
Dissecting Aneurysms (Selman et al 2004)
Dissecting
aneurysms result from cystic medial necrosis or a traumatic tear in the
endothelium and sub adjacent layers of the artery, allowing the formation of a
false lumen. The false lumen may connect with the true lumen distally or may
rupture through the remaining external arterial wall. Such aneurysms can occur
in any portion of the extra cranial or intracranial arterial circulation.
Trauma is a common cause in the neck and anterior circulation, but is a rare
cause in the posterior circulation. Connective tissue diseases such as Marfans
syndrome and other disorders such as fibromuscular dysplasia predispose to
arterial dissections.
PATHOLOGY AND PATHOGENESIS OF SAH
At
necropsy, subarachnoid haemorrhage is seen as a thin coating of blood in the
subarachnoid space over the surface over the surface of the brain and as a
rather thicker layer of blood around the ruptured aneurysm. The basal CSF cisterns
are often filled with blood which can be visualized by CT scan. If bleeding is
focal, it may indicate the location of an aneurysm but false localization may
occur if haemorrhage is intraventricular and has leaked through the foramen of
Luschka into the pontine cisterna around the basilar artery. Preliminary
removal of fresh blood
clot
from around the circle of Willis may reveal the aneurysm or may facilitate
dissection of the aneuryum in the fixed brain. If the blood clot around the
aneurysm is allowed to harden by fixation the aneurysm may be difficult to
locate or it may be damaged during the removal of the solidified blood clot (Sloam
et al 1990).
SAH
can alter mechanisms that control cerebral blood flow and metabolism. Chemical
control of blood flow by CO2 is altered in SAH patients (Graham 1990). Auto
regulation is commonly lost after SAH. Because the degree of impairment of auto
regulation may be different in different regions of the brain, a reduction in
cerebral perfusion pressure may cause extreme ischemia in some areas but not
others. These changes in the intrinsic control of cerebral blood flow are
particularly deleterious because several factors may operate to reduce cerebral
blood flow after SAH, including decreased cerebral perfusion pressure from the
raised intracranial pressure from the raised intracranial pressure caused by
acute hydrocephalus or clot formation (Hirashima et al 1999).
Blood
in the subarachnoid space triggers a pathological process that results in a
spasm of the vessels of the major branches of the circle of Willis. Increased
plasma platelet activating factor and antiphospholipids may contribute to the
pathogenesis of cerebral vasospasm after SAH (Endo et al 1995). In Japan, there
is a study at Tokayama, to evaluate the usefulness of measuring
anti-phospholipid antibodies (aPLs) for the occurrence of symptomatic vasospasm
and the outcome after SAH. They explained the association of antiphospholipids
with worse outcome; aPLs were detected between 7 and 13 days after SAH. The
mechanism of transient aPLs is unclear but it is more likely to occur in the
severer grade patients. The reductions in platelet count, the increased
platelet factor 4 concentrations were also observed in aPLs-positive patients
with symptomatic vasospasm (Endo et al 1995).
Delayed
cerebral vasospasm that occurs after SAH seems to be associated with both
impaired dilator and increased constrictor mechanisms in cerebral arteries.
Mechanisms contributing arteries after SAH have been intensively investigated
in recent years. Nitric oxide is produced by the endothelium and is an
important regulator of cerebral vascular tone by tonic ally maintaining the
vasculature in a dilated state. Endothelial injury after SAH may interfere with
Nitric oxide (NO) production and lead to vasoconstriction and impaired
responses to endothelium vasodilators (Sobey et al 1998).
Inactivation
of NO by Oxyhaemoglobin or superoxide from erythrocytes may also occur in the
subarachnoid space after SAH. Nitric oxide stimulates activity of soluble
guanylate cyclase in vascular in vascular muscle leading generation of cGMP and
relaxation. Subarachnoid haemorrhage appears to cause impaired activity of
soluble granylate cyclase, resulting in reduced basal levels of cGMPin cerebral
arteries to nitric oxide. Endothelin(ET) is a potent, long lasting vasoconstrictor
that may contribute to the spasm of cerebral arteries after SAH. Endothelin is
present in increased levels in the cerebrospinal fluid of SAH patients.
Pharmacological inhibition of ET synthesis or ET receptors has been reported to
attenuate cerebral vasospasm. Production of and vasoconstriction by Endothelin
may be due, in part, to the decreased activity of Nitric oxide and formation of
cGMP (Sobey et al 1998).
Protine
kinase C (PKC) is an important enzyme involved in the contraction of vascular
muscle in response to several agonists, including ET, activity of the PKC
appears to be increased in the cerebral arteries after SAH indicating that PKC may
be critical in the development of cerebral vasospasm. Recent evidence suggests
that PKC activation may occur in cerebral arteries after SAH as a result of
decreased negative feedback influence of NO/cGMP. Cerebral arteries are
depolarize after SAH, possibly due to decreased activity of potassium channels
may be due to several mechanisms, including impaired activity of Nitric oxide
(and/or cGMP) or increased activity of PKC. Thus endothelial damage and reduced
activity of Nitric oxide may contribute cerebral vascular dysfunction after SAH
(Sobey et al 1998).
Because
cerebral blood flow is inversely proportional to the fourth power of the
radius, small changes in vessel caliber can have profound effects. If regional
flow falls below the critical thresholds for membrane integrity, ischemic edema
formation and infraction can occur. Focal regions of edema can further impair
local blood flow despite on overall normal intracranial pressure. AVP (Arginine
vasopressin) plays an important role in the development of antidiuersis and
disturbance of the brain water and electrolyte imbalance after SAH ( Laszi et
al 1995).
CLINICAL SYNDROMES
Unruptured
Aneurysms
Most
unruptured intracranial aneurysms are completely asymptomatic. Aneurysms may
demonstrate evidence of their presence or of growth, before rupture, in other
ways besides headache. Premonitory manifestations depend on the
location of the aneurysm and include diplopia, visual field deficits, or facial
pain (Weir 1994).
PHYSICAL FINDINGS
Because
aneurysms can produce catastrophic haemorrhage before they reach a size that
would produce neurological deficits, the lack of clinical findings should not
preclude further diagnostic evaluation. The physical findings in patients with
unruptured aneurysms are determined in part by the size and location of the
aneurysm, although few aneurysms can be diagnosed with confidence on the basis
of clinical presentation alone. Thus aneurysms arising from the anterior
communicating artery can produce visual field defects, endocrine dysfunction,
or localized frontal headache. Aneurysms of the internal carotid artery can
produce oculomotor paresis, visual field deficits, impaired visual acuity, endocrine
dysfunction, and localized facial pain. Aneurysms of the internal carotid
artery in the cavernous sinus can produce a cavernous sinus syndrome when they
reach a sufficient size. Those of the middle cerebral artery can produce
aphasia, focal arm weakness, or paresthesias. Basilar bifurcation aneurysm can
be associated with oculomotor paresis, although the clinical features of
posterior circulation aneurysms seldom permit diagnosis before they rupture (Selman
et al 2004).
Ruptured
saccular aneurysms
With
rupture of the aneurysm, blood under high pressure is forced into the subarachnoid
space (usually in relation to the circle of Willis), and the resulting clinical
events assume one of the three patterns:
(1)
The patient is stricken with an excruciating generalized headache and vomiting
and falls unconscious almost immediately;
(2)
Headache develops in the same manner but the patient remains relatively lucid-
the most common syndrome;
(3)
Rarely consciousness is lost quickly without any preceding complaint.
Decerebrate rigidity and brief clonic jerking of the limbs may occur at the
onset of the haemorrhage, in association with unconsciousness. If the
haemorrhage is massive, death may ensue in a matter of minutes or hours, so
that ruptured aneurysm must be considered in the differential diagnosis of
sudden death. A considerable proportion of such patients probably never reach a
hospital. Persistent deep coma is accompanied by irregular respirations,
attacks of extensor rigidity, and finally respiratory arrest and circulatory
collapse. In these rapidly fatal cases, the subarachnoid blood has greatly
increased the intracranial pressure to a level that approaches arterial
pressure and caused a marked reduction in cerebral perfusion. In some instances
the haemorrhage has dissected intracerebrally and entered the ventricular
system (Ropper & Brown 2005).
Ruptured
of the aneurysm usually occurs while the patient is active rather during sleep,
and in a few instances during sexual intercourse, straining at stool, lifting
heavy objects, or other sustained exertion. Momentary valsalva maneuvers, as in
coughing or sneezing, have generally not caused aneurysmal rupture. In patients
who survive the initial rupture, the most feared complication is rerupture, an
event that may occur at any time from minutes up to 2 or 3 weeks (Ropper &
Brown 2005).
In
less severe cases, consciousness, if lost, may be regained within a few minutes
or hours, but a residuum of drowsiness, confusion, and amnesia accompanied by
severe headache and stiff neck persists for several days. It is not uncommon
for the drowsiness and confusion to last 10 days or longer. Since the
haemorrhage is confined to the subarachnoid space, there are few if any focal
neurologic signs. That is to say, gross lateralizing signs in the form of
hemiplegia, hemiparesis, homonymous hemianopia, or aphasia are absent in the
majority of cases. On occasion, a jet of blood emanating from an aneurysm may
rupture into the adjacent brain or clot in the insular cistern and produce a
hemiparesis or other focal syndrome. There may also be a focal syndrome from acute
or delayed ischemia in the territory of the aneurysm-bearing artery. Usually
this occurs several days after a large subarachnoid hemorrhage. The
pathogenesis of such manifestations is not fully understood, but a transitory
fall in pressure in the circulation distal to the aneurysm is postulated in
early cases and vasospasm is responsible for the later focal signs. Transient
deficits are not common, but they do constitute reliable indicators of the site
of the ruptured aneurysm (Ropper & Brown 2005).
Convulsive
seizures, usually brief and generalized, occur in 10 to 25 percent of cases
according to Hart et al (but far less often in our experience) in relation to
acute bleeding or rebleeding. These early seizures do not correlate with the
location of the aneurysm and do not appear to alter the prognosis (Ropper &
Brown 2005).
In
most patients the neurologic manifestations do not point to the exact sight of
the aneurysm, but it can often be inferred from the location of the main clot
on CT scan. A collection of blood in the anterior interhemispheric fissure
indicates rupture of an anterior communicating artery aneurysm; in the sylvian
fissure, a middle cerebral artery aneurysm; in the anterior perimesencephalic
cistern, a posterior communicating or distal basilar artery aneurysm; and so
on. In some instances clinical signs provide clues to its localization, as
follows:
· Third nerve palsy
(ptosis, diplopia, dilation of pupil, and divergent strabismus), as stated
above, usually indicates an aneurysm at the junction of the posterior
communicating artery and the internal carotid artery- the third nerve passes
immediately lateral to this point;
· Transient paresis
of one or both of the lower limbs at the onset of the haemorrhage suggests an
anterior communicating aneurysm that has interfered with the circulation in the
anterior cerebral arteries;
· Hemisparesis or
aphasia points to an aneurysm at the first major bifurcation of the middle
cerebral artery;
· Unilateral
blindness indicates an aneurysm lying anteromedially in the circle of Willis
(at the origin of the ophthalmic artery or at the bifurcation of the internal
carotid artery);
· A state of
retained consciousness with akinetic mutism or abulia (sometimes associated
with paraparesis) favors a location on the anterior communicating artery, with
ischemia of or haemorrhage into one or
both of the frontal lobes or hypothalamus (with or without acute hydrocephalus);
· The side on which
the aneurysm lies may be indicated by a unilateral preponderance of headache or
preretinal haemorrhage, the occurrence of monocular pain, or, rarely,
lateralization of an intracranial sound heard at the time of rupture of the
aneurysm. Sixth nerve palsy, unilateral or bilateral, is usually attributable
to raised intracranial pressure and is seldom of localizing value (Ropper &
Brown 2005).
In
summary, the clinical sequence of sudden severe headache, vomiting, collapse,
relative preservation of consciousness with few or no laterlizing signs, and
neck stiffness is diagnostic of subarachniod haemorrhage due to a ruptured
saccular aneyrysm (Ropper & Brown 2005).
The
initial clinical manifestations of SAH can be graded using the Hunt-Hess or
World Federation of Neurosurgical Societies classification schemes. For
ruptured aneurysms, prognosis for good outcomes falls as the grade increases.
For example it is unusual for a Hunt-Hess grade 1 patient to die if the
aneurysm is treated, but the mortality for grade 4 and 5 patients may be high
as 80%.
Table: Grading Scales for Subarchnoid
Hemorrage (Hemphill
& Smith 2008)
Grade
Hunt-Hess
Scale
World
Federation of Neurosurgical societies (WFNS) Scale
1
Mild
headache, normal mental status, no cranial nerve or motor findings
Glasgow
Coma Scale score 15, no motor deficits
2
Severe
headache, normal mental status, may have cranial nerve deficit
GCS
13-14, no motor deficits
3
Somnolent,
confused, may have cranial nerve or mild motor deficit
GCS
13-14, with motor deficits
4
GCS
7-12, with or without motor deficits
5
Coma,
reflex posturing or flaccid
INVESTIGATIONS
The
laboratory evaluation of patients suspected of having a rupture aneurysmal SAH
uses a combination of CT scan, magnetic resonance imaging, lumber puncture and
angiography.
CT Scan
The
blood may appear as a subtle shadow along the tentorium or in the sylvian or
adjacent fissures. A large collection of subarachnoid blood or a hematoma in
brain tissue or within the sylvian fissure indicates the adjacent location of
the aneurysm and the likely region of subsequent vasospasm, as already noted. A
high incidence of symptomatic vasospasm in the middle and anterior cerebral
arteries has been found when early CT scan shows sudarachnoid clots larger than
5*3 mm in the basal cisterns or layers of blood more than 1 mm thick in the
cerebral fissures. CT scan less reliably predicts vasospasm in the vertebral,
basilar, or posterior cerebral arteries (Ropper & Brown 2005). Also,
coexistent hydrocephalus will be demonstrable. If the CT scan documents
subarachnoid blood with certainty, a spinal tap is not necessary.
In
all other cases, where subarachnoid hemorrhage is suspected but not apparent on
imaging studies or computed tomography is unavailable but the patient is
oriented and obeying commands, a lumber puncture should be undertaken. Lumber
puncture should not be performed in patients with papilloedema or focal
neurological signs (Duffy 1982). Usually the CSF becomes grossly bloody within
30 min of the hemorrhage, with red blood cell counts up to 1 million/mm3
or even higher. With a relatively mild hemorrhage, there may be only a few
thousand cells, but it is unlikely that a severe headache syndrome from
subarachnoid hemorrhage would be associated with less than a several hundred
cells. It is also probably not possible for an aneurysm to rupture entirely
into the brain tissue without some leakage of blood into the subarachnoid
fluid. In other words, the diagnosis of ruptured saccular aneurysm (by lumber
puncture) is essentially excluded if blood is not present in the CSF. Xanthochromia
is found after centrifugation if several hours or more have elapsed from the
moment of the ictus. In a patient who reports a headache that is consistent
with subarachnoid hemorrhage but the occurrence was several days earlier, the
CT scan may be normal and xanthrochromia the only diagnostic finding. Also helpful after several days is the MRI
taken with the FLAIR sequence, with will demonstrate blood (Ropper & Brown
2005).
Fig. 5. CT scan of the
brain showing subarachnoid hemorrhage as a white area in the center
MRI Scan
Not
routinely used, but in patients with multiple aneurysms, MRI performed several
days after the bleed may provide greater
sensitivity than CT in detecting small areas
of subarachnoid clots and help determine the particular lesion
responsible (Yadav et al 1998).
Angiography
A
rupture of an intracerebral haemorrhage due to hypertension, into the
subarachnoid space or the ventricles may be difficult to distinguish from a
subarachnoid haemorrhage occurring in a hypertensive patient and invading one
cerebral hemisphere. When the diagnosis of subarachnoid haemorrhage has been
confirmed by CT scan or examination of cerebral fluid, therefore, it is
necessary to exclude a ruptured aneurysm or a bleeding angioma as its cause.
This may call for angiography, which raises the question of whether this should
be done in every case, and if so when (Yadav et al 1998).
There
is a difference of opinion about this, some surgeons recommending that carotid
angiography should be performed in every case of subarachnoid haemorrhage as
soon as the diagnosis is made while others are more selective. The rational
answer seems to be that if there is possibility that a life saving operation
may be carried out as the result of information yielded by angiography,
angiography should be performed. If on the hand this is not the case because it
is thought that the patient is too ill to stand operation or that either
angiography or the operation is fraught with greater risks than expected
treatment. As may be the case particularly in patients over the age of 60 with
evident atheroma, angiography should be postponed. There is no doubt, however,
that surgery carried out sufficient early may save lives which would otherwise
be lost (Pathirana et al 1994).
Angiography
is usually carried out at the earliest convenience, although in patients in
poor clinical condition, the clinician may prefer to delay investigation until
improvement has occurred. If a patient deteriorates from the mass effect of an
intracranial haematoma, then emergency angiography is required prior to any
decompressive operation.
Four
vessels angiography is usually performed in all patients. Anterior-posterior,
lateral and oblique views are requires for each vessel.
Carotid
angiography may show not only the site, size and shape of the aneurysm but also
whether as sometimes happens there is an associated spasm of important arteries
which may be contributing to the clinical picture (Lindsay et al 1997).
Magnetic resonance angiography
Magnetic
resonance angiography is a useful non-invasive technique for demonstrating
intracranial aneurysms but the resolution is still insufficient to ensure that small
aneurysms are not missed.
MRA
is less sensitive than conventional arteriography to visualize anomalies
(Anzalone 1995). MRA is not sensitive enough to serve as a screening procedure
after SAH. It can be used however to detect unruptured aneurysms in selected
patients (Brust 1995).
Negative angiography
Angiography
fails to reveal a source of the subarachnoid haemorrhage in approximately 20%
of patients. In the presence of arterial spasm, reduction in flow may prevent
the demonstration of an aneurysm and repeat angiography may be required at a
later date (Jose et al 1996).Four vessels angiography confirms the presence of
an AVM and delineates the feeding and draining vessels. Reasonably small AVMs
are difficult to detect and only early venous filling may draw attention to
their presence. In the presence of a haematoma, angiography should be delayed
until the haematoma resolves, otherwise local pressure may mask demonstration
of AVM. If the angiogram is subsequently negative, then MRI is required to
exclude the presence of a cavernous malformation (Lindsay et al 1997).
Transcranial
droppler ultrasound assessment of proximal middle, anterior and posterior
cerebral and basilar artery flow is helpful in detecting the onset of
vasospasm, even prior to symptoms and following its course and response to
therapy (Donald et al 2001).Skull radiographs sometimes reveal calcification in
the AVM or increased vascular markings in the overlying bone (Brust 1995).
Associated Systemic Changes
Acute
subarachnoid haemorrhage is associated with several characteristic responses in
the systemic circulation, water balance, and cardiac function. The ECG changes
include symmetrically large peaked T waves and other alterations suggesting
subendocardial ischemia. Also there is a tendency to develop hyponatremia; this
abnormality and its relationship to intravascular volume depletion play a key
role in treatment. Albuminuria and glycosuria may be present for a few days.
Rarely, diabetes insipidus occurs in the acute stages, but water retention or a
natriuresis is more frequent. There may be a leukocytosis of 15,000 to 18,000
cells per cubic millimeter, but the sedimentation rate is usually normal
(Ropper & Brown 2005).
Delayed
hemiplegia and other focal deficits usually appear 3 to 12 days after rupture
and rarely before or after this period. These delayed syndromes and the focal
narrowing of a large artery or arteries, seen on angiography, are referred to
as vasospasm. Fisher and coworkers (1975) have shown that spasm is most
frequent in arteries surrounded by the largest collections of clotted
subarachnoid blood. The vasospasm appears to be a direct effect of blood or
some blood product, possibly hematin or a platelet product, on the adventitia
of the artery. Areas of ischemic infraction in the territory of the vessel
bearing the aneurysm, without thrombosis or other changes in the vessel, is the
usual finding in such cases. These ischemic lesions are often multiple and
occur with great frequency, according to Hijdra and associates (1986).
After
a few days, arteries in chronic spasm undergo a series of morphologic changes.
The smooth muscle cells of the media become necrotic, and the adventitia is
infiltrated with neutrophilic leukocytes, mast cells, and red blood corpuscles,
some of which have migrated to a subendothelial position (Chyatte and Sundt). These
changes are caused by products of hemolyzed blood seeping inward from the
pia-arachnoid into the muscularis of the artery (Ropper & Brown 2005).
The
clinical features of cerebral vasospasm depend on the affected blood vessel but
typically include a fluctuating hemiparesis or aphasia and increasing confusion
that must be distinguished from the effects of hydrocephalus. In the past, an
arteriogram was required to verify the diagnosis, although it is not often
performed now because of the slight associated risk of worsening vascular spasm
and the ease with which the condition can be visualized with MRA and spiral CT
techniques. Transcranial Doppler measurements are an indirect and easier way of
following, by observations of blood flow velocity, the caliber of the main
vessels at the base of the brain. Almost all patients have a greatly increased
velocity of blood flow in the affected vessel that can be detected by this
method in the days after haemorrhage. However, progressive elevation of flow
velocity in any vessel (especially if over 175 cm/s) suggests that focal
vasospasm is occurring. There is a reasonable correlation between these
findings and the radiographic appearance of vasospasm, but the clinical
manifestations of ischemia depend on additional factors such as collateral
blood supply and the cerebral perfusion pressure (Ropper & Brown 2005).
Recurrent Hemorrhage
Recurrent
hemorrhage is a feared complication of SAH because it is a leading cause of
death or neurologic morbidity during the first 2 weeks after SAH (Roos et al
2000; Hillman et al 1998). The cumulative rate of rebleeding during the first 2
weeks after SAH is approximately 15% to 20% (Torner et al 1981). Torner and
colleagues (1981) found that the period of greatest risk for rebleeding is the
first 24 hours after the ictus; the risk peaked at approximately 4% during that
time.
Several
clinical features identify those patients at the highest risk for early
rebleeding. The most important is the level of consciousness at admission;
patient admitted in coma at the greatest risk. Rebleeding is also more common
among older people, women, and people whose systolic blood pressure exceeds 170
mm Hg. The results of the baseline CT do not predict recurrent hemorrhage.
Recurrent
haemorrhage usually causes a sudden headache and a rapid change in neurologic
condition, including a drop in consciousness. Extensor spasm s and posturing
are important early signs. A “convulsion” that occurs immediately
after SAH also can mark a recurrent haemorrhage (Hart et al 1981). However,
rebleeding in a comatose patient may be overlooked. It may be manifested only
by a sudden change in respiratory pattern or vital signs. Recurrent haemorrhage
should be sought whenever a patient experiences a new headache or worsens
neurologically (Mohr et al 2004).
The
differential diagnosis of rebleeding are vasospasm-induced brain ischemia, subacute
hydrocephalus, seizure, electrolyte imbalance, hypotension, hypoxia, medication
effects, systemic complication etc. The diagnosis of rebleeding should not be
solely on clinical features, because this approach leads to over diagnosis.
Recurrent haemorrhage can be proved most easily by the detection of additional
blood on CT scans (Mohr et al 2004).
Hydrcephalus
Hydrocephalus
is a common complication of SAH, resulting from the massive collections of
blood that fill the ventricles, block the aqueduct of sylvius, or obstruct the
fourth ventricle. Blood can fill the subarachnoid cisterns or coat the
arachnoid villi (Mohr et al 2004).
The
hydrocephalus after SAH may be classified according to its time of appearance
as (1) acute- appearing within 12 hours after aneurysmal rupture, (2) sub acute-
developing a few days after the ictus, or (3) delayed- noted as ventricular
dilation week to years later. Acute hydrocephalus is an important cause of
increased intracranial pressure and coma. Sub acute hydrocephalus is a cause of
a gradual decline in consciousness that can occur approximately 7 to 10 days
after SAH. In this situation, intracranial pressure may be modestly elevated.
Delayed hydrocephalus often manifests as a subacute dementia, gait apraxia, and
bladder incontinence. In the setting, intracranial pressure often fluctuates
and may not be consistently elevated (Mohr et al 2004).
Approximately
16% to 34% of patients have CT findings consistent with acute hydrocephalus.
Some patients with ventricular enlargement may be asymptotic, but most have
decreased consciousness. Symptoms of acute hydrocephalus in addition to decline
in alertness are bilateral motor signs, miosis, and downward deviation of the
eyes. Acute hydrocephalus predicts increased mortality and morbidity and is
correlated with subsequent development of vasospasm and ischemic stroke (Mohr
et al 2004).
MANAGEMENT OF SAH
Table
1. Factors Predicting Less Favorable Outcome after Subarachnoid Hemorrhage
(Mohr et al 2004)
Clinical
factors
Admitting level of
consciousness( coma)
Interval from
subarachnoid haemorrhage(<3 days)
Prior unrecognized
hemorrhage or warning leak
Presence of local
neurologic signs on admission
Presence of severe co
morbid disease or extraneural organ involvement
Diagnostic
results
Hyponatremia or
hypovolemia
Abnormal CT scan
Local, thick, or diffuse collection of subarachnoid blood
Intracerebral or intraventricular blood
Mass effect
Hydrocephalus
Evidence of
rebleeding detected by sequential CT scan
Vasospasm detected
by arteriography or by transcranial
Doppler ultrasonography
Aneurysm located on
anterior cerebral or vertebrobasilar arteries
Size of
aneurysm(>10mm)
ACUTE MANAGEMENT
The
patient with recent SAH is critically ill and should be evaluated and treated
urgently (Mayberg et al 1994; Wijdicks 1995). He or she should be transported
rapidly to a medical center that has the expertise to treat a patient with a
ruptured aneurysm. Acute, potentially life-threatening complications should be
anticipated. Personnel should assess the patient quickly and should measure
vital signs and assess neurologic status frequently. The heart rate and rhythm
should be monitored. The airway, breathing, and circulation should be
supported, and if necessary, supplemental oxygen, endotracheal intubation, or
ventilatory assistance should be given (Wijdicks 1995). Intravenous access is
established to expedite emergency administration of medications. Normal saline
can be given at a slow rate to maintain patency of the intravenous line.
Unfortunately, the urgent approach to acute management of SAH is often
suboptimal in emergency departments (Thomson et al 2000). Each institution
should develop a protocol for the management of SAH in the emergency
department, including plans for both acute treatment and urgent evaluation.
The
initial evaluation should include CT scan, chest radiograph, electrocardiogram,
and blood studies. CT can demonstrate subarachnoid blood and a number of other
acute intracranial complications. When CT shows intracranial bleeding, a lumber
puncture can be avoided. The findings of CT that is performed within 24 hours
after onset of symptoms with the use of third-generation scanners are normal in
approximately 2% to 7% of cases (Zouaoui 1997). If the CT findings are normal,
a cerebrospinal fluid specimen should be obtained.
Patients
should be admitted to a unit that has monitoring equipment and is staffed by
neurologically trained nurses. Acute care can be divided into general
supportive efforts and therapies aimed at preventing or controlling specific
complications (Mayberg et al 1994; Wijdicks 1995). For the first 24 hours,
blood pressure, vital signs, and neurologic status should be assessed hourly.
Thereafter, examinations can be spaced further apart in stable patients.
Cardiac monitoring and, if necessary, continuous intra-arterial or noninvasive
blood pressure monitoring are extended for at least 24 to 48 hours after
admission.
Forced
bed rest is a traditional part of management. Visitors and external stimuli are
restricted. Passive range-of-motion exercises and frequent turning are
performed. A water mattress or an alternating- pressure pneumatic bed can
reduce the risk of pressure sores and atelectasis. Patients are assisted with
self-care activities, such as bathing and eating. Black and associates (1986)
showed that external pneumatic calf compression stocking and devices reduce the
incidence of deep vein thrombosis. The use of heparin as a prophylaxis against
deep venous thrombosis is generally avoided until the ruptured aneurysm is
treated.
Gentle
pulmonary suctioning and nursing care are important for avoiding pneumonia. The
value of absolute bed rest in preventing rebleeding was tested by the
cooperative study of Intracranial Aneurysms and Subarachnoid Heamorrhage; the
cumulative rate of rebleeding was 25% during the first 14 days after SAH
(Nishioka 1981). In general, the prognosis of patients treated only with
absolute bed rest now represents the natural history of SAH.
Because
intravenously administered medications are often needed, a slow infusion of
saline is continued. Alert patients are usually given a soft, high-fiber diet
supplemented by stool softeners (Wijdicks 1995). Caffeinated beverages are
avoided. Stuporous and comatose patients are not fed during the acute treatment
period. If a seriously ill person is stable several days after SAH and the
airway is secured, nasogastric feedings can be instituted.
Symptomatic
treatment
Patients
with SAH are often confused or agitated as a result of brain injury,
hydrocephalus, or increased intracranial pressure. Pain or nausea can also lead
to irritability. Agitation raises the risk of rebleeding and aggravates
increased intracranial pressure. Control of pain or nausea can calm an upset
patient. Regular administration of diazepam or phenobarbital may be useful in
providing sedation for agitated patients.
The
headache of SAH is intense, and patients should receive ample doses of
analgesics (Mayberg et al 1994; Wijdicks 1995). Most alert patients require a
medication such as codeine, meperidine, or morphine. The agent is usually
administered parenterally. These medications can be combined with
acetaminophen, hydroxyzine hydrochloride, or promethazine. Some patients have
photophobia; a quiet, dark environment can help relieve some of these
conditions, which otherwise might worsen the head pain. Sedation and sleep
might also help control pain. Aspirin affects platelet aggregation and prolongs
the bleeding time; there is concern that aspirin might potentiate rebleeding.
Severe
nausea and vomiting are common and important complaints, particularly during
the first 24 hours after SAH. Nauseated patients should receive an antiemetic,
such as ondansetron, trimethobenzamide, or prochlorperazine, to control these
complaints.
ANTICONVULSANTS
Approximately
25% of patients have seizures, most of which occur within the first 24 hours
(Hart et al 1981; Rhoney et al 2000; Sundaram et al 1986). Rhoney and
colleagues (2000) reported that seizures were most common among patients with
thick cisternal clots. Most seizures happen before the patient reaches the
hospital. Hart and associates (1981) noted that 63% of the seizures happened at
the time of aneurymal rupture. However, some of these ‘seizures’ may not be
truly epileptic phenomena but may represent transient decerebrate posturing
secondary to increased intracranial pressure (Hart et al 1981; Fisher 1975).
Although
seizures occurring after hospitalization are uncommon, they can be associated
with recurrent haemorrhage. Physicians prescribe anticonvulsants to patients
who have experienced a seizure as part of SAH, but the prophylactic use of
these agents in treatment of patients who have not had a seizure is
controversial. The rationale for prophylactic of anticonvulsants is that a seizure is a dangerous event in a
person with a recent SAH. Because of the low rate of seizures after admission,
however, Hart and associates (1981) and sundaram and chow (1986) question the
necessity for routine prescription of anticonvulsants to patients with recent
SAH. However, regular use of phenytion or another parentrally administered
anticonvulsant is recommended to reduce the likelihood of seizures. No trial
has tested the value of anticonvulsants in management of patients with recent
SAH. Pending such a trail, the decision to prescribe these medications is
individualized. If a patient has had or is having convulsions, intravenous
doses of anticonvulsants are given.
Treatment of
Myocardial ischemia and cardiac arrhythmias
Cardiac
arrhythmias can be detected in almost all patients during the first few hours
after SAH; in approximately 20% of cases, the arrhythmias can be severe or
life-threatening (Di Pasquale et al 1988, Manninen et al 1995, Oppenheimer et
al 1994, Randell et al 1999). Ventricular arrhythmias are a potential cause of
sudden death after SAH. Di Pasquale and coworkers (1988)noted
torsades de points in 3.8% of 132 patients with SAH who underwent Holter
monitoring. Increased QT dispersion is a common electrocardiographic finding
after SAH (Randell et al 1997).
Changes
resembling those seen in acute myocardial ischemia can be noted in 25% to 80% of patients ( Zouaoui et al 1997, Gascon et al 1983). In fact, many
people with SAH have secondary myocardial ischemia and left ventricular
dysfunction (Sakka et al 1999, Yuki et al 1991). Elevations of the cardiac
isoenzyme creatine kinase necrosis are found among patients who died of SAH
even those without prior history of coronary artery disease. Abnormal left
ventricular function is seen most commonly among patients with elevated
creatine kinase levels. Severe left ventricular dysfunction after SAH may
necessitate a delay in aneurysm surgery. In addition, the reduction of cardiac
output after severe SAH might increase the risk of cerebral ischemia secondary
to vasospasm.
ANTIHYPERTENSIVE TREATMENT
Arterial
hypertension is common in SAH, resulting from elevations of catecholamines and
renin produced by hypothalamic disturbances (Neil-Dwyer et al 1980, Toftdahl et
al 1995) . Additionally, increased intracranial pressure can induce arterial
hypertension as a means to maintain adequate cerebral perfusion pressure.
Arterial hypertension also can be secondary to seizures, vomiting, agitation,
or pain. In addition, the patient may have preexisting hypertension.
Hypertension
after SAH has been found to correlate with increases in the risk of vasospasm
and mortality (Toftdahl et al 1995). Arterial hypertension also puts patients
at high risk for recurrent haemorrhage. Administration of antihypertensive
agents is a traditional component of early medical management of SAH (Mayberg et
al 1994, Wijdicks et al 1995). However, rapid or steep reductions in blood
pressure might be dangerous. Patients with vasospasm or increased intracranial
pressure may experience a drop in cerebral perfusion in conjunction with a
decline in blood pressure; neurologic deterrioration can result. Some antihypertensive
agents (nitroglycerin, sodium nitroprusside, fenoldopam) are potent cerebral
vasodilators, and enlargement of the cerebrovascular bed secondary to their
administration could further increase intracranial pressure.
The
blood pressure often returns to normal after the patients with SAH is admitted
to the hospital or when symptoms such as headache are treated; thus, aggressive
antihypertensive therapy might be avoided in some cases. The levels of arterial
hypertension that mandates treatment is not known. Patients with moderate
hypertension (mean arterial blood pressure lower than 120 mm Hg) probably do
not need to be treated. On the other hand, patients whose mean blood pressure
is 120 mm Hg or higher or whose systolic blood pressure is higher than 180 mm
Hg should receive medication. The goal should be to cautiously lower the blood
pressure to levels normal for the patient and to avoid inducing hypertension.
Although
alert patients with elevated blood pressures can receive oral medications, parenteral
agents have the advantage of a prompt response. Antihypertensive agents that
were used before SAH are usually continued, and they should not be stopped
abruptly. Short-acting antihypertensive agents are desirable because of the
rapid resolution of the unwanted effects of an excessive decline in blood
pressure. Because patients are often dehydrated or hyponatremic, diuretics are
avoided. B-blockers, calcium channel blockers, and angiotensin-converting
enzyme inhibitors are the oral most commonly prescribed. Nimodipine or
nicardipine may be useful antihypertensive agents in the patient with SAH.
The
patient with a markedly elevated or unstable arterial blood pressure reading
may require a continuous intravenous infusion of labetalol, sodium nitroprusside,
or fenolopam. The rate of infusion is adjusted in response to blood pressure
values. The dosage must be individuelized, because a patient may be very
sensitive to a medication, and the resulting drop in blood pressure may exceed
expectations. Doses required in patients with SAH can be lower than those
required for other hypertensive emergencies.
MANAGEMENT OF ELECTROLYTE AND FLUID
BALANCE
Disturbances
in water and sodium balance occur in approximately one third of patients with
SAH (Wijdicks et al 1985). These complications are most likely to develop in
critically ill patients with large hemorrhages. Hyponatremia and volume
depletion correlate with a poor prognosis and the subsequent development of
hydrocephalus, vasospasm, and ischemic stroke (Wijdicks et al 1985). Severe hyponatremia
can cause convulsions and is potential cause of coma.
The
primary indication for rapid correction of hyponatremia is the development of
seizures in a patient without neurologic disease; however, this indication
becomes blurred in patients with recent SAH. In the past, hyponatremia after
SAH was attributed to the syndrome of inappropriate secretion of antidiuretic hormone
(SIADH) and was treated with fluid restriction. It is now recognized, that a
more common cause of hyponatremia in patients with SAH is cerebral salt wasting
(CSW). The mechanism of water and sodium loss in CSW has been correlated with
disturbances in levels of artial natriuretic peptide, brain natriuretic
peptide, and c-type natriuretic peptide, as well as with direct neural effects
of renal function (Harrigan 2001, Sviri et al 2000, Wijdicks 1997).
The
key to diagnosis of this syndrome is the urinary excretion of large amounts of
sodium and chloride at a time when the extracellular fluid volume is contracted.
Declines in plasma volume, red blood cell mass, and total blood volume occur
(Wijdicks et al 1985, Sato et al 1999) these findings are unlike those in SIADH,
in which the patient is euvolemic or hypervolemic. In contrast to therapy for
SIADH, the appropriate therapy for CSW is replacement of salt and water rather
than fluid restriction. Assessment of volume status by means of careful
recording of inputs and outputs to calculate sodium and chloride balance, daily
body weights, or laboratory test results suggesting dehydration, such as
elevated hematocrit or blood urea nitrogen-creatinine ratio, can be useful in
choosing therapy ( Harrigan 2001,
Carlotti et al 2001).
If
the serum sodium concentration does not normalize despite a euvolemic status,
modest fluid restriction or an infusion of a hyperosmolar solution containing
sodium can be started. The serum sodium concentration should be corrected no
more rapidly than 0.7mEq/hour to avoid central pontine myelinolysis (Harrigan
2001). In 39 patients with recent SAH, Wijdicks and associates (1988)
administered 0.2 mg of fludrocortisone twice a day, combined with daily fluid
intake of at least 3L, and noted improvements in plasma volume and sodium
balance. As a result, these investigators recommend that frudrocortisone be
added to the fluid management regimen if the serum concentration of sodium is
less than 125 mmol/l. Hypokalemia after SAH probably results from vomiting but
can be secondary to elevated levels of corticosteroids, renin, or
catecholamines. Because cardiac arrhythmias can be associated with hypokalemia,
this imbalance should be corrected promptly.
Treatment of other medical complications
Gastrointestinal bleeding
can result from hemorrhage gastritis, tress gastric ulcers, or an esophageal
tear secondary to vomiting. Because of the risk of bleeding, patients are often
given intravenous histamine2-receptor antagonists or proton pump inhibitors via
nasogastric tube (Mayberg et al 1994). Sucralfate does not have central nervous
system side effects, so it has potential advantages in preventing
gastrointestinal side effects among critically ill patients prone to depression
in consciousness (Wijdicks 1988).
Obtunded
patients are at high risk for adult respiratory distress syndrome, atelectasis,
pulmonary hypoventilation, and aspiration pneumonia. Securing of the airway,
careful bronchopulmonary management, and ventilatory assistance may be
required. Events such as renal failure, hepatic dysfunction, and urinary tract
infections as well as other illness should be treated. Measures to avoid
pressure sores or orthopedic complications also are important.
Treatment of increased intracranial
pressure
A
decline in consciousness is the hallmark of increased intracranial pressure,
which, in turn, can result from a large intracerebral or intraventricular
hematoma, the mass effects of a secondary ischemic lesion, cerebral edema, or
hydrocephalus. SAH also causes vasoparalysis and loss of autoregulation;
secondary dilation of intracranial vessels might aggravate intracranial
pressure by expanding the vascular compartment. Intracranial pressure is
markedly elevated within a few minutes of aneurysmal rupture; the sudden
increase in pressure may help halt the bleeding. In addition, the elevated
intracranial pressure may transiently equal mean arterial blood pressure. A
massive rise in intracranial pressure is probably one of the causes of sudden
death after SAH. High intracranial pressure may also lead to hypoperfusion,
which induces brain ischemia. Prompt aggressive treatment of increased
intracranial pressure is one of the keys to successful management of SAH (Wijdicks
1995).
Several
medical and surgical measures are available to treat brain edema or increased
intracranial pressure. Continuous monitoring of intracranial pressure is
indicated for many patients; the results might guide the timing of surgical or
medical interventions. Continuous intraventricular drainage combined with
monitoring is an option if the patient has intraventricular haemorrhage or
acute hydrocephalus. Treatment of increased intracranial pressure consists of
(1) elevation of the head of the bed to promote venous drainage, (2) fluid
restriction, (3) correction of hyponatremia, (4) treatment of fever or
agitation, and (5) prevention of hypoventilation and secondary hypercarbia.
Intubation
and hyperventilation are indicated if a patient’s condition is deteriorating.
There is no evidence that dexamethasone is useful in managing brain edema after
intracranial hemorrhage. Furosemide, which can reduce intracranial pressure by
limiting the production of CSF, can be given in an emergency. However, the
diuretic effects of furosemide can lead to electrolyte disturbances and
hypovolemia. Mannitol is an osmotic agent that can be given to control
increased intracranial pressure. A response is noted within minutes, and the
duration of effect is approximately 4 to 6 hours. The dosage can be repeated as
needed. Secondary dehydration, hyperosmolarity, and a rebound increase in brain
edema are possible complications. Measurements of serum osmolality and serum
electrolytes should be performed often, especially if repeated doses of
mannitol are prescribed. Measurement of central venous or pulmonary artery
wedge pressure might be needed. Hypertonic saline has also been used in
refractory cases to lower intracranial pressure and has the advantage of
expanding intravascular volume (Qureshi & Suarez 2000).
A patient
with acute hydrocephalus can be observed, medically managed, monitored with
sequential CT studies, and treated with serial lumber punctures. Although acute
hydrocephalus may resolve spontaneously, most cases require placement of a
temporary ventriculocaval or ventriculoperitoneal catheter (Graff- Radford et
al 1989; Heros 1989). Insertion of a ventricular catheter may be difficult in a
patient with an intraventricular clot, because blood can occlude the
catheter. Continuous cisternal drainage
might relieve intracranial and expedite lavage of blood from the subarachnoid
space. Placement of a shunt is recommended for any patient with depressed
consciousness and enlarging ventricles. Shunting is not always effective.
PREVENTION OF RECURRENT HEMORRHAGE
Measures
to ameliorate recurrent hemorrhage are not effective; therefore treatment is
aimed at prevention. Choices include prolonged bed rest, induced hypotension,
antifibrinolytic agents, carotid ligation, intracranial clipping of the
aneurysm, and endovascular obliteration of the aneurysm. Occlusion of the
aneurysm is the best method for preventing rebleeding (van Gjin & Rinkel
2001). Neither absolute bed rest nor induced hypotension has been successful in
improving outcomes after SAH or in reducing the risk of recurrent haemorrhage.
Carotid ligation can be performed to prevent rebleeding from aneurysms of the
distal internal carotid artery, but because of the advances in intracranial
operative techniques and development of invasive neuroradiologic procedures,
carotid ligation now is rarely performed (Perret & Nibbelink 1981).
Antifibrinolytic therapy
The
rationale for the use of antifibrinolytic agents (aminocaproic acidor
tranexamic acid) is that the perianeurysmal clot that formed the initial
haemorrhage abuts and supports the aneurysm, thus helping to prevent its
re-rupture. Treatment would be given before surgery, to prevent rebleeding
while the patient was recovering from the acute effects of SAH.
Antifibrinolttic agents cross the blood brain barrier, but peak CSF levels of
these agents are lower than plasma levels and are also delayed. When the agents
are administered as a constant intravenous infusion, a steady state in CSF is
reached only after 36 hours. Therefore, the possible therapeutic level of agent
in the CSF may not be achieved during the period of highest risk for recurrent
haemorrhage.
Clinicians
are concerned about the safety of antifibrinolytic agents. A fulminant
myopathy, rhabdomyolysis, or myoglobulinuria can complicate prolonged use of
these medications (Brown et al 1983). Antifibrinilytic agents accentuate the
development of hydrocephalus (Graff-Radford et al 1989). Ischemic stroke is the
most feared side effects. The high rate
of ischemic stroke is the primary reason that antifibrinolytic agents are not
established as effective in the acute management of SAH (Vermeulen et al 1984).
INTRACRANIAL OPERATION
Surgery
is an important component of management of SAH. Surgical repair involves
placing a metal clip across the aneurysm neck, thereby immediately eliminating
the risk of rebleeding. This approach requires craniotomy and brain retraction,
which is associated with neurologic morbidity. Currently, surgery is the
preferred treatment for the aneurysm, but the recommendation for surgery must
still be made on a case-by-case basis. For example, the patient’s age, the
severity of neurologic injury, or the presence of a serious comorbid disease
may weigh against an intracranial operation. Although people older than 60
years tolerate intracranial operation less well than younger people, age alone
is not a reason for excluding surgery from the treatment regimen, because
outcomes in the elderly have improved over time (Johansson et al 2001).
For
most patients, the question is not whether the aneurysm should be clipped but,
rather, when is the ideal time for the operation. Some neurosurgeons advocate
delaying surgery until a patient’s condition has stabilized (Maurice-williams et
al 1997), but most neurosurgeons now favor early operation (Findlay 1997).
Early operation is preferred because the risk of rebleeding is elimination and
the operation is performed before vasospasm appears. The primary reason for
delaying surgery has been that a lag permits the patient’s condition to recover
from the initial event before the patient is subjected to the stresses
associated with early surgery. Delayed surgery leaves the aneurysm untreated
during the period of highest risk of rebleeding. In addition, the potential of
recurrent rupture of an unsecured aneurysm can complicate hypervolumic hemodilution
and induced hypertension for treatment of ischemia secondary to vasospasm.
Surgeons rightfully point out that the overall results of management, and not
just postoperative statistics, should be compared. The overall results of early
medical treatment followed by a delayed operation are not satisfactory.
Several
groups described favorable results of early operation combined with a variety
of interventions, including calcium channel blockers (Juvela et l989, LeRoux et
al1995, Nishimoto et al 1985). A small trial in Finland, demonstrated better
outcomes for early operation (Ohman and Heiskanen 1989). Although the data
favored early operation, the results were distorted by a simultaneous random
assignment of patients to receive either placebo or active treatment with
calcium channel blocking agents. Miyaoka and associates (1993) reported better
management results with early surgery in patients who were in good condition
and better results with delayed operation in patients who were seriously ill. A
large international epidemiologic study evaluated outcomes of 3521 patients
hospitalized within 3 calendar days of SAH (Kassellet al 1990). Although it was
not a randomized trial, the large numbers assured that prognostic factors were
similar in the groups that underwent early and delayed operations. Overall
management results (favorable outcomes) were similar in the two treatment
groups, but early surgery did reduce the overall risk of rebleeding. Early
surgery was not associated with a high rate of intraoperative complication,
such as a re-rupture of the aneurysm or worsening of brain edema.
ENDOVASCULAR TREATMENT
Endovascular
obliteration of the aneurysm or the parent artery is used to treat aneurysms of
the intracavernous or proximal portions of the internal carotid artery, even in
patients who have a carotid-cavernous fistula. Tandem placement of balloons in
the parent artery (trapping) can shrink the aneurysm or lead to its occlusion (Findlay
1997). This procedure is relatively effective, and the risk of ischemic stroke
is low (Larson et al 1995). However, detachable balloons can be relatively
difficult to place within the aneurysm. The sizes and shapes of the balloons
might not correspond to the contour of the aneurysmal sac. Occasionally, the
balloons can be lost and migrate into distal arteries. In addition, the
balloons can deflate, and the aneurysm can become recanalized. Finally, the
balloons might place pressure on the aneurysm’s wall and promote recurrent
rupture.
Endovascular
placement of adhesive materials can be used to occlude smaller intracranial
aneurysms. Kinugasa and associates (1995) reported success with the placement
of cellulose acetate polymer for occlusion in 9 of 12 patients with aneurysms.
Obliteration of the aneurysmal sac expedited treatment of vasospasm and allowed
the patients to become stable before the aneurysm was surgically repaired.
Development
of microcatheters and detachable coils has stimulated greater interest in
direct endovascular treatment of intracranial aneurysms (McDougall 1996).
Aneurysms that are not easily approached for direct clipping might be occluded
with endovascular treatment (McDougall 1996, Casasco et al 1993, Sinson et al
1996). In particular, aneurysms of the posterior circulation and the basilar
bifurcation can be treated with placement of coils (Birchall et al 2001). In
one multicenter trail comprising 150 patients, basilar tip aneurysms were
treated with detachable platinum coils; approximately 75% of the aneurysms were
successfully treated (Eskridge & Song 1998). The periprocedural mortality
rate was 2.7%. Complications included rupture of the aneurysm and occlution of
the parent artery. Cognard and colleagues (1998) treated 208 patients with
aneurysms (150 with SAH), achieving total occlusion of the aneurysms in 81% of
cases, and subtotal occlusion in 17%. In another study, 75 seriously ill
patients with ruptured aneurysms were treated with coils (Raymond and Roy 1997).
Success was achieved in most patients, although procedure-related mortality and
morbidity occurred in 8% of cases. Lefkowtz and coworkers (1999) placed coils
in wide-necked aneurysms in 23 patients; complete or nearly complete occlusion
was achieved in all cases. Three patients had complications. Although the
usefulness of endovascular placement of coils has not been compared with that
of surgery, this therapy has gained popularity and likely will continue to
increase in popularity in the future.
VASOSPASM AND ISCHEMIC STROKE
Removal of the subarachnoid clots
Early
intracranial operation and lavage of the subarachnoid space can remove clots
and might prevent development of vasospasm. The rationale for this procedure is
that evacuation of the clots might prevent the release of substances that
induce the arterial narrowing. Surgical removal of the clots can be difficult
in critically ill patients, however, and some of the blood collects in areas
far from the operative field. Extensive manipulation of the brain to remove the
subarachnoid clots may also injure penetrating vessels, leading to ischemic
deficits. Despite promising study did not show any reduction in the severity or
incidence of vasospasm (Kassell et al 1990). It appears that vigorous lavage of
the subarachnoid space is not a feasible way to prevent vasospasm in most
patients.
Several
small studies report the potential usefulness of intrathecal thrombolytic
therapy in the setting of acute surgical treatment of a ruptured aneurysm
(Brinker et al 1992, Mizoi et al 1993, Sasaki et al 1994, Usui et al 1994) .
Most of these studies treated only patients judged to be at very high risk for
vasospasm and ischemia. Outcomes were generally favorable, consisting of a
lower frequency of severe vasospasm and ischemic impairments (Treggiari-Venzi
et al 2001). Kodama and associates (2000) performed cisternal irrigation with
urokinase and ascorbic acid in 217 high-risk patients, and observed subsequent
symptomatic vasospasm in 6 patients. Thrombolytic agents can be instilled
safely into the basal cisterns. Thrombolytic agents can be instilled safely
into the basal cisterns. The risk of major bleeding complications, in
particular brain haemorrhage, thrombolytic agents should not be administered
until the aneurysm has been occluded. The optimal timing of treatment, the
duration of treatment, the best agent, and the best dose are not known.
Considerable research, including prospective controlled trials, is needed
before intrathecal thrombolytic agents are added to the usual care of patients
with recently ruptured aneurysms.
CALCIUM CHANNEL BLOCKING AGENTS
Influx
of extracellular calcium, an important component in sustaining contraction of
smooth muscle, is critical in the process of cellular ischemia. An agent that
inhibits calcium entry might prevent vasospasm or its cerebral ischemic
consequences. The diyhdropyridine derivatives nimodipine and nicardipine have been
tested. Although these agents can reduce the arterial blood pressure, they also
increase cerebral blood flow, including in ischemic regions. Small studies
testing the utility of oral nimodipine found that the medication reduced
mortality but it did not prevent vasospasm (Allen et al 1983, Ohman et al 1991).
A British trail established the utility of nimodipine to improve outcomes after
SAH (Pickard et al 1989). The rate of
favorable outcome was increased from 67% to 80.2% with treatment. Meta-analyses
confirm the efficacy of nimodipine in treating patients with recent SAH (Barker
and Ogilvy 1996, Feigin et al 2000, Tettenborn and Dycka 1990). Although a
significant reduction in mortality is not achieved, the calcium channel
antagonists reduce the proportion of patients with ischemic deficits secondary
to vasospasm.
In
general, nimodipine is safe, and complications of its use are few. Hypotension
is a potential side effect. The exact mechanism of nimodipine’s efficacy is
unclear, but it may be neuroprotective. Patients with recently ruptured
aneurysms should receive nimodipine as part of their general medical care
(Mayberg et al 1994, Ven Gijn and Rinkel 2001). The U.S. Food and Drug
Administration have approved the use of nimodipine for this indication. The
usual oral dosage of nimodipine is 60 mg every 4 hours. Comatose patients can
receive the medication via a nasogastic tube. The usual duration of treatment
is 3 weeks after SAH, although a shorter course (10 to 14days) may be all that
is needed. If the SAH is not diagnosed until 10 to 14 days after it has
occurred, the patient has already survived the period of greatest risk for
ischemia, and nimodipine might not be needed.
Nicardipine
has similar potential theraputic actions, and it can be given parenterally. Use
of the agent in SAH was tested in a large clinical trial (Haley et al 1993). At
3 months, the actively treated and control groups had comparable rates of
favorable outcomes, but the frequency of symptomatic vasospasm was reduced with
the use of nicardipine. In another
study comparing two different doses of nicardipine, the same investigators
found that the lower dose of medication was associated with a slightly higher
rate of severe vasospasm but that outcomes were similar in the two groups (Haley
et al 1994). Shibuya and colleagues (1994), who administered nicardipine
intrathecally to 50 patients with SAH, noted declines in both symptomatic and
arteriographic vasospasm. These studies suggest that nicardipine is effective
in preventing ischemic sequelae of SAH but that the combination of aggressive
volume expansion and induced hypertension is also effective. These additional
data support the use of calcium channel blockers supplemented by hypervolemic
hemodilution and induced hypertension for prevention of ischemic stroke after
SAH.
OTHER MEDICATION TO PREVENT VASOSPASM OR
ISCHEMIC STROKE
Calcitonin
gene-related peptide (CGRP), a potent vasodilator, was tested in a small
clinical trial (Lancet 339:891-834, 1992). Hypotension was a common side effect,
and two thirds of the treated patients did not complete of the course of
treatment. Although this study was reported as having negative results for the
use of CGRP, largely because of its small size, favorable outcomes were noted
in 60% of treated patients and 60% of controls.
Clinical
studies of super selective intra-arterial administration of papaverine that
this potent vasodilator may be helpful (Clouston et al 1995). Firlik and
coworkers (1999) found that intraarterial papaverine can reverse the arterial
narrowing of vasospasm. In their series of 15 patients (32 treated arteries),
pavaverine therapy increased cerebral blood flow in 46% of cases and led to
major clinical improvement in 26%. Kaku and associates (1992) reported that
this agent should be given before the arteries lose their ability to respond.
Hypotension does not appear to be a complication of local intra-arterial
infusions. Seizures have been reported as a complication of this therapy (Carhuapoma
et al 2001). Arakawa and colleagues (2001) reported that the vasodilator
milrinone might be helpful in dilating vasospastic vessels.
Finfer
and associates (1999) used barbiturate- induced coma to protect the brain in 11
patients with severe vasospasm, 10 of whom had good outcomes. These investigators
proposed this therapy for patients who show no response to other medical
interventions. Although barbiturate-induced coma does offer benefit, it is a
very vigorous therapy that requires intensive adjunctive care. It utility has
not been established.
The
21-aminosteroids can scavenge free radicals and inhibit lipid peroxidation,
features that promote stabilization of the membranes of ischemic tissues.
Clinical trails have been conducted to test intravenously administered
tirilazed given as a supplement to oral nimodipine (Haley et al 1997, Kassell
et al 1996, Lanzino and Kassell 1999). Although the medication was well
tolerated, no major improvement in favorable outcomes was noted with treatment.
The medication has not been approved for management of patients with SAH.
HYPERVOLEMIC HEMODILUTION AND INDUCED
HYPERTENSION
Increasing
cerebral blood flow can ease ischemic symptoms and can prevent permanent
neurologic sequelae (Mayberg et al 1994, Kassell et al 1982, Mori et al 1995).
Reduction in the diameter of the vascular lumen affects the blood’s rheologic
characteristies and, thus, influences flow.
Severe losses of water and sodium result in hemoconcertration, which in
turn increases viscosity and reduces blood flow. Measures to prevent infarction
by correcting the losses of sodium and water are initiated upon the patient’s
admission to the hospital. A small randomized trial of prophylactic therapy
with hypervolemic hypertensive hemodilution therapy did not demonstrate benefit
in preventing vasospasm (Mori et al 1995).
Because
autoregulation is impaired, cerebral blood flow becomes pressure-dependent.
Cerebral perfusion pressure is altered by changes in the mean arterial blood
pressure and intracranial pressure. Improvement of venous drainage by positioning
and elevation of the head, treatment of brain edema, and control of
hydrocephalus lowers intracranial pressure and improves perfusion. When
feasible, antihypertensive agents are avoided. Nimodipine may have to be
discontinued so that the blood pressure can be effectively raised. After the
diagnosis of symptomatic vasospasm is made, more aggressive treatment of increased
intracranial pressure, including hyperventilation and mannitol, might help.
Antifibrinolytic agents should be discontinued.
Several
groups report reversal of ischemic symptoms with the combination of volume
expansion and drug induced hypertension (Kassell et al 1982, Mori et al 1995). In
some cases, neurologic signs can reappear when the therapy is discontinued (Kassell
et al 1982) Although no controlled trials of this regimen have been conducted,
the previously described trial of nicardipine demonstrates a benefit from this
aggressive therapy(Haley et al1993). Qureshi and associates (2000) found that
patients with a depressed level of consciousness at the initiation of volume
expansion therapy on blood flow and cardiac function (Lennihan et al 2000). The investigators found that hypervolemic
therapy raised cardiac filling pressures but it did not increase cerebral blood
flow. A meta -analysis of published data found that there is no sound evidence
for or against the use of volume expansion therapy in patients with SAH (Feigin
et al 2000).
If
improvement is not observed after volume expansion, a vasopressor (most
commonly dopamine or phenylephrine) is added in an attempt to increase mean
arterial blood pressure. Darby and coworkers (Darby et al 1994) noted that the
increase in cerebral blood flow after use of dopamine may be independent of
changes in blood pressure, because the dopamine might have direct
cerebrovascular effects. Although there is some disagreement about the utility
of hypervolemic hemodilution and induced hypertension to prevent ischemia after
SAH, the regimen is commonly prescribed (van Gijn & Rinkel. 2001, Oropellet
et al 1996, Ullman & Bedersom 1996).
This
therapy is vigorous, and patients need intensive observation. Arterial
pressure, cardiac rhythm, central venous pressure, or pulmonary artery wedge
pressure should be continuously monitored (Mori et al 1995). Continuous
intracranial pressure monitoring may be also needed. Frequent laboratory
assessments of serum electrolytes, serum osmolarity, blood gases, and blood
counts are needed. Complications of the therapy include congestive heart
failure, pulmonary edema, acute myocardial infraction, and cardiac arrhythmias.
Worsening of brain edema, hypertensive intracerebral hemorrhage, haemorrhagic
transformation of the infraction, and re-rupture of the aneurysm can also occur(Kassell
et al 1996). Shimoda and colleagues (1993) reported worsening of brain edema in
18 of their 94 patients undergoing hypervolemic hemodilution; 8 others had
haemorrhagic infractions. These investigators advised against the use of
hypervolemic hemodilution if a patient’s CT scan shows an ischemic lesion in
the brain, particularly if the abnormality is found within 6 days of SAH.
ANGIOPLASTY
Transluminal
angioplasty successfully dilates vasospastic arteries (Coyne et al 1994). The
development of microballoons allows for catheterization in small- to medium-sized
arteries at the base of the brain. Angioplasty does stretch and disrupt the
arterial wall (Honma et al 1995). Bejjani and associates (1998) performed angioplasty
at approximately 7 days after SAH in 31 patients, treating a total of 81
vessels. These investigators noted major clinical improvements in 12 cases and
moderate improvements in another 11. They encountered no major neurologic
complications and concluded that angioplasty is a potentially useful treatment
for patients who show no response to other therapies. Polin and coworkers
(2000) found that angioplasty is effective in reversing angiographically
confirmed vasospasm, but they did not observe clinical improvements with
treatment. At present, angioplasty is usually reserved for treatment of SAH
that does not respond to medical measures.
Arteriovenous
Malformations of the BRAIN :( ROPPER & brown 2005)
An
arteriovenous malformation (AVM) consists of a tangle of dilated vessels that
from an abnormal communication between the arterial and venous systems, really
an arteriovenous fistula. It is a developmental persistence of an embryonic
pattern of blood vessels and is not a neoplasm, but the constituent vessels may
proliferate and enlarge with the passage of time. Arteriovenous malformations
have been designated by a number of other terms, such as angioma and
arteriovenous aneurysm, but these are less appropriate; angioma suggests a
tumor, and the term aneurysm is generally reserved for the lesions described in
the preceding section. Venous malformations, consisting purely of distended
veins deep in the white matter, are a separate entity; they may be the cause of
seizures and headaches but seldom of haemorrhage. When a small haemorrhage
occurs in relation to venous malformation, it is due to an associated cavernous
malformation.
Vascular
malformations vary in size from a small blemish a few millimeters in diameter
lying in the cortex or white mater to a huge mass of tortuous channels
constituting an AV shunt of sufficient magnitude, in rare instances, to raise
cardiac output. Hypertrophic dilated arterial feeders can be seen approaching
the main lesion and to break up into a network of thin-walled blood vessels
that connect directly with draining veins. The latter often from greatly
dilated, pulsating channels, carrying away arterial blood. The tangled blood
vessels interposed between arteries and veins are abnormally thin and do not
have the structure of normal arteries or veins. Arteriovenous malformations
occur in all parts of the cerebrum, brainstem, and cerebellum (and spinal
cord), but the larger ones are more frequently found in the central part of a
cerebral hemisphere, commonly forming a wedge-shape lesion extending from the
cortex to the ventricle. Some lie on the dural surface of the brain or spinal
cord, but these most often turn out to be direct arteriovenous fistulas.
When
heamorrhage occurs, blood may enter the subarachniod space, producing a picture
almost identical to that of ruptured saccular aneurysm, but generally less
severe; since most AVMs lie within cerebral tissue, bleeding is more than
likely to be intracerebral as well, causing a hemiparesis, hemiplegia, and so
forth, or even death.
Arteriovenous
malformations are about one-tenth as common as saccular aneurysms and about
equally frequent in males and females. The two lesions-AVM and saccular
aneurysm are associated in about 5 percent of cases; the conjunction increases
with the size of the AVM and the age of the patient (Miyasaka et al 1982).
Rarely, AVMs occur in more than one member of a family in the same generation
or successive ones.
CLINICAL FEATURES
Bleeding
or seizures are the main modes of presentation. Most AVMs are clinically silent
for a long time, but sooner or later they bleed. The first haemorrhage may be
fatal, but in more than 90 percent of cases the bleeding stops and the patient
survives. The rate of haemorrhage in untreated patients is established to be 2
to 4 percent per year, far lower than aneurysms. The mortality rate in two
major series (Crawford et al 1986, Ondra et al 1994) has been 1 to 2 percent
per year but as high as 6 to 9 percent in the immediate year following a first haemorrhage.
The matter of an increased risk of AVM rupture during pregnancy has been
disputed. The weight of evidence suggests that the risk is not raised by
pregnancy alone, but -as with saccular aneurysm- that parturition and Valsalva
activity is always a source of concern. Before rupture, chronic, recurrent
headache may be a complaint; usually the headache is of a nondescript type, but
a classic migraine with or without neurologic accompaniment occurs in about 10
percent of patients-probably with greater frequency than it does in the general
population. Most of the lesions associated with migraine-like headaches lie in
the parietal-occipital region of one cerebral hemisphere, and about two-thirds
of such patients have a family history of migraine.
Huge
AVMs may produce a slowly progressive neurologic deficit because of compression
of neighboring structures by the enlarging mass of vessels and by shunting of
blood through greatly dilated vascular channels (“intracerebral
steal”), resulting in hypoperfusion of
the surrounding brain(Homan et al 1986). When the vein of Galen is
enlarged as a result of drainage from an adjacent AVM, hydrocephalus may
result. Not infrequently one or both carotid arteries pulsate unusually forcefully
in the neck. A systolic bruit heard over the carotid in the neck or over the mastoid process or
the eyeballs in a young adult is almost pathognomonic of an AVM. However, such
bruits have been heard in fewer than 25 percent of our patients. Exercise that
increases the pulse pressure may bring out a bruit if none is present at rest.
Fully
95 percent of AVMs are disclosed by CT scans if enhanced and an ever larger
number by MRI. Magnetic susceptibility MRI shows small areas of previous
bleeding around AVMs. Arteriography is usually necessary to establish the
diagnosis with certainty and will demonstrate AVMs larger than 5 mm in
diameter; MRI may fail to reveal smaller lesions. Small ones may be obscured by
haemorrhage; even at autopsy, a careful search under the dissecting microscope
may be necessary to find them.
Treatment
The
preferred approach in most centers is surgical excision. Some 20 to 40 percent
of AVMs are amenable to block dissection, with an operative mortality rate of 2
to 5 percent and a morbidity of 5 to 25 percent. In the others, which are
inaccessible, attempts have been made to obliterate the malformed vessels by
ligation of feeding arteries or by the use of endovascular remobilization with
liquid adhesives or particular material that are injected via a balloon
catheter that has been navigated into a feeding vessel. Complete obliteration
of large AVMs is usually not possible by these methods but, they are highly
effective in reducing the size of the AVM prior to surgery.
Kjellberg and Chapman (1983) pioneered the treatment
of AVMs at the Massachusetts General Hospital using a single dose
subnecrotizing stereotactically directed proton radiation. The technique of
radiosurgery has been adopted by others using photon radiation sources, such as
a linear accelerator, gamma knife, and other modes of focused x-ray radiation,
as an accepted alternative to operative treatment of lesions situated in deep
regions, including the brainstem, or in ‘eloquent’, areas of the cortex.
Generally, malformations smaller than 3 cm diameter are treatable in this way.
Radiosurgical obliteration of AVM occurs in a delayed manner, usually with a
latency of at least 18 to 24 months after treatment. During this early period
the patient is unprotected from rebleeding.
The
likelihood of successful treatment and the nature of the risks depend on the
location and size of the AVM and the radiation dose delivered. After 2 years,
75 to 80 percent of AVMs smaller than 2.5 cm in diameter have been obliterated.
Even for those AVMs that have not been totally eliminated, the radiation effect
appears to confer some long-term protection from bleeding. Of the larger ones, majorities
are shrunken or appear less dense. The rest have shown no change at this low
dose level, but even in this group, the morbidity and mortality are lower than
in the untreated group. However, a proportion of larger AVMs that are
obliterated will recanalize, and many of these will subsequently bleed. Among
more than 250 patients whose AVMs disappeared following proton beam therapy,
there has been no recurrence of hemorrhage for up to 10 years; in larger AVMs
(approximately the last 1000 cases) treated in this way, the frequency and
severity of hemorrhage have been significantly reduced. The results of
treatment with focused gamma radiation have been about the same. In one study,
the risk of hemorrhage was reduced by 54 percent between the time of radiation
and obliteration of the malformation and by 88 percent thereafter (Maruyama et
al 2005).
Two
types of complications of radiation occur at a combined rate of approximately 2
to 4 percent. The first is delayed radiation necrosis, which is predictable
based on the radiation dose, and the second is a venous congestion that occurs
several weeks or months after treatment. The latter is indicative of the
desired effect of thrombosis of the malformation. Both cause local symptoms for
weeks or months. Radiation necrosis may be reduced by the administration of
corticosteroids but the vascular problem generally is not helped.
The
treatment of AVMs by endovascular techniques is increasingly popular but has
not been fully evaluated. Nearly every AVM has several feeding arteries, some
not reachable by catheter and some part of the AVM remains after treatment. In
most series, 25 percent
or
more of AVMs, mostly of small and medium size, could be completely obliterated,
with a mortality rate below 3 percent and morbidity of 5 to 7 percent, which
compares favorably with surgical outcomes. These techniques are also
particularly well adapted to lesions of a combined AVM and an aneurysm on the
feeding vessel.
Most
recently, combined therapy that begins with endovascular reduction of the
lesion and is followed by either surgery or radiation has been viewed most
favorably. In series of patients using this approach, over 90 percent of
lesions could be obliterated with a very low rebleeding rate over several
years. What is clear is that the plan for each patient must be individualized
based on the size, location, nature of feeding vessels, the presence of other
vascular lesions (aneurysm or additional AVM), and the age of the patient. Even
then, there will be differences of opinion based on local resources and
experience.
Finally,
if the primary problem is recurrent seizure successful treatment with reduction
or cessation of seizures is achieved in a very high proportion of cases. The
results are comparable to those from surgery and radiation, even if the AVM is
not entirely obliterated.
Dural Arteriovenous Fistulas
These
curious vascular abnormalities, occurring in both the cranial and spinal dura,
have different presentations at each site. The cranial type is being detected
with increasing frequency as refinements continue to be made in imaging of the
cerebral vessels, but its true incidence and pathogenesis are not fully known.
The defining features are radiologic -a nidus of abnormal arteries and veins
with arteriovenous shunting contained entirely within the leaflets of the dura.
The lesion is fed by dural arterial vessels derived from the internal cranial
circulation and often more prolifically, from the external cranial circulation
(external carotid artery and muscular branches of the vertebral artery). The
venous drainage is complex and is largely into the dural venous sinuses. The
rapid transit of injected angiographic dye through these fistulas account, for
the early opacification of the draining venous structures; in the case of
high-flow connections, this may not be seen unless images are taken almost
immediately after the injection. A number of potential feeding vessels must be
injected to demonstrate all the conduits into the lesion. On CT scanning and
MRI, the fistula is sometimes detected as a thickening or enhancement of a
region of dura, generally close to a large dural venous sinus. In other cases,
the dilated draining vessels may be seen only with the injection of dye or
gadolinium. Probably, many are not detected by these techniques.
The
origin of these vascular lesions has not been settled- several mechanisms may
be involved. Most evidence suggests that some of these lesions, unlike
conventional cerebral AVMs and aneurysms, are not developmental in origin. The
best-defined examples are those that arise adjacent to a venous sinus
thrombosis or in association with a vascular atresia, most often in the
transverse sigmoid sinus or adjacent to the cavernous sinus. However, it is not
clear whether the abnormality of the dural sinus is the cause or the result of
the dural fistula. In a number of cases, a dural fistula has appeared after a
forceful head injury, often in a region remote from the site of impact. A small
group is associated with the Klippel-Trenaunay or Osler-Weber-Rendu syndromes,
diseases in which frequent conjunction with AVMs is well known. Usually all of
these causes can be excluded and the largest group remains idiopathic.
Treatment
is by surgical extirpation or endovascular embolization, a painstaking
procedure because of the multitude of potential feeding vessels. Surgery seems
preferable for the smaller lesions and embolization for larger and inaccessible
ones. The issue of anticoagulation, when there is slowed flow in a venous sinus
draining a malformation, is unsettled.
Cavernous Malformafions
Vascular
malformations composed mainly of clusters of thin walled veins without
important arterial feeders and with little or no intervening nervous tissue
make up a significant group, some 7 to 8 percent of our series of AVMs.
Conventional subdivisions of this group into cavernous, venous, and
telangiectatic types have not proven useful. We have, therefore, roughly
designated them all as cavernous. They have several attributes that set them
apart. Their tendency to bleed is probably no less than that of the more common
AVMs, but far more often the haemorrhages are small and clinically silent. The
exact incidence of bleeding is uncertain but is estimated to be less than 1
percent per year per lesion. Often there are multiple lesions. They are
generally not seen in arteriograms. The diagnosis is based on their clinical
manifestations and MRI, which discloses a cluster of vessels surround by a zone
of hypodense feritin in the T1- weight images, the product of previous small
episodes of bleeding. A small but uncertain number are associated with adjacent
venous malformations, visualized by imaging studies. The lack of formation of a
mass over long period of time separates this lesion from a malignant tumor that
has bled. About one-half of all cavernous angiomas lie in the brainstem, and in
the past (before the availability of MRI), many of them were misdiagnosed as
multiple sclerosis because of a stepwise accumulation of neurologic deficits
with each haemorrhage.
About
10 percent of these lesions are multiple and 5 percent are familiar. In one of
the families we have followed of Italian-American origin, there were 29
affected members in there generations. The inheritance followed an autosomal
dominant pattern; Marchuk and coworkers (1995) have localized the abnormal gene
in other kindreds to the long arm of chromosome 7. One interesting
characteristic of this group, as pointed out by Labauge and colleagues (2001),
is the appearance over time of new lesions in one- third of patients. The
follow- up of some of our patients has documented this.
Treatment
Cavernous
angiomas on the surface of the brain, within reach of the neurosurgeon, even
those in the brainstem, can be plucked out, like clusters of grapes, with low
morbidity and mortality. Kjellberg and colleagues (1983) have treated 89 deeply
situated cavernous angiomas with low-dose proton radiation. Our impression is
that these vascular malformations, like the hemangioblastoma, respond poorly to
radiation and are not amenable to treatment by endovascular techniques.
Lesions
that cause recurrent bleeding and are surgically accessible with little risk
are often removed, but incidentally discovered angiomas and those that are
inaccessible may be left alone. Although this is the approach usually taken,
there is not adequate data on the rate and risk of bleeding to determine proper
approach.
CONCLUSION
Considerable
progress is being made in the management of SAH. Medical and surgical therapies
that effectively prevent rebreeding and vasospasm are reflected by declines in
mortality and morbidity. Still, there is considerable room for improvement.
Several promising therapies are being tested; one or more of these
interventions likely will be shown to further improve outcomes after SAH.
However, most successful therapies are based on early treatment. Thus, the
medical community must give greater attention to the early diagnosis of SAH and
the acute care of patients with SAH who are critically ill.
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