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U N I T 1 0
Nervous System
Aneurysmal subarachnoid hemorrhage represents
bleeding into the subarachnoid space caused by a rup-
tured cerebral aneurysm. Bleeding into the subarach-
noid space can extend well beyond the site of origin,
flooding the basal cistern, ventricles, and spinal sub-
arachnoid space. The incidence of rupture increases
with age, occurring most commonly between 40 and
60 years of age.
43
The probability of rupture increases
with the size of the aneurysm; aneurysms larger than
10 mm in diameter have a 50% chance of bleeding at
some point during the course of a year.
1
Of the various
factors that may predispose to aneurysmal subarach-
noid hemorrhage, cigarette smoking, hypertension,
and excessive alcohol intake appear to constitute the
greatest threat.
38
Rupture may occur at any time, but
often occurs with acute increases in ICP, such as with
straining at stool. The mortality rate for subarachnoid
hemorrhage is high (33% to 50%), with the major-
ity of deaths occurring within the first few days of
hemorrhage.
38
The signs and symptoms of cerebral aneurysms can
be divided into two phases: those presenting before
rupture and those presenting after rupture. Most small
aneurysms are asymptomatic; intact aneurysms fre-
quently are found at autopsy as an incidental finding.
Large aneurysms may cause chronic headache, neuro-
logic deficits, or both.
38,39
Persons with subarachnoid
hemorrhage often have a history of atypical headaches
occurring days to weeks before the onset of hemorrhage,
suggesting the presence of a small leak. These headaches
are characterized by sudden onset and often are accom-
panied by nausea, vomiting, and dizziness. Persons with
these symptoms may be mistakenly diagnosed as having
tension or migraine headaches.
The onset of subarachnoid aneurysmal rupture often
is heralded by a sudden and severe headache, described
as “the worst headache of my life.”
38
If the bleeding is
severe, the headache may be accompanied by collapse
and loss of consciousness. Vomiting may accompany
the presenting symptoms. Other manifestations include
signs of meningeal irritation such as nuchal rigidity
(neck stiffness) and photophobia (light intolerance);
cranial nerve deficits, especially CN II, and sometimes
CN III and CN IV (diplopia and blurred vision); stroke
syndromes (focal motor and sensory deficits); cerebral
edema and increased ICP; and pituitary dysfunction
(diabetes insipidus and hyponatremia). Hypertension, a
frequent finding, and cardiac arrhythmias result from
massive release of catecholamines triggered by the sub-
arachnoid hemorrhage.
The diagnosis of subarachnoid hemorrhage and intra-
cranial aneurysms is made by clinical presentation, CT
scan, lumbar puncture, and angiography.
38,39
Lumbar
puncture may reveal the presence of blood in the CSF,
whereas CT may demonstrate the location and extent
of subarachnoid blood. To identify the aneurysm at the
source of bleeding, conventional angiography, MRA,
and helical (spiral) CTA are used. Conventional catheter
angiography is the definitive diagnostic tool for detect-
ing the aneurysm.
The course of treatment after aneurysm rupture
depends on the extent of neurologic deficit. The best out-
comes are achieved when the aneurysm can be secured
early and prevention of complications initiated.
39
Persons with mild to no neurologic deficits may undergo
cerebral arteriography and early aneurysm obliteration
with surgery or endovascular coiling, usually within 24
to 72 hours. Surgery involves craniotomy and inserting
a specially designed silver clip that is tightened around
the neck of the aneurysm. This procedure offers pro-
tection from rebleeding and may permit removal of the
hematoma. The use of endovascular techniques such as
balloon embolization and platinum coil electrothrom-
bosis is an alternative to surgery, particularly in poste-
rior circulation aneurysms or poor surgical candidates.
Early outcomes and fewer complications are better with
coiling, while long-term rebleeding rates are reduced
with surgery.
39
Some persons with subarachnoid hemor-
rhage are managed medically for 10 days or more in an
attempt to improve their clinical status before surgery
or coiling.
The complications of aneurysmal rupture include
rebleeding, vasospasm with cerebral ischemia, hydro-
cephalus, hypothalamic dysfunction, and seizure activ-
ity. Rebleeding and vasospasm are the most serious and
most difficult to treat. Rebleeding, which usually occurs
on the first day after the initial rupture, results in further
and usually catastrophic neurologic deficits.
Cerebral vasospasm is a dreaded complication of
aneurysmal rupture. The condition is difficult to treat
and is associated with a high incidence of morbidity and
mortality. Usually, the condition develops within 3 to
10 days (peak, 7 days) after aneurysm rupture and
involves a focal narrowing of the cerebral artery or
arteries that can be visualized on arteriography or by
transcranial Doppler. The neurologic status gradually
deteriorates as blood supply to the brain in the region
of the spasm is decreased; this usually can be differ-
entiated from the rapid deterioration seen in rebleed-
ing. Vasospasm is treated by attempting to maintain
adequate cerebral perfusion pressure through the use
of vasoactive drugs or administration of large amounts
of intravenous fluids to increase intravascular volume
and produce hemodilution. There is risk for rebleed-
ing from this therapy. Early surgery may provide some
protection from vasospasm. Endovascular techniques,
including balloon dilation, have been developed to treat
spasmodic arterial segments mechanically. Nimodipine,
a drug that blocks calcium channels and selectively acts
on cerebral blood vessels, may be used to prevent or
treat vasospasm.
Another complication of aneurysm rupture is the
development of hydrocephalus. It is caused by plug-
ging of the arachnoid villi with products from lysis of
blood in the subarachnoid space. Hydrocephalus is
diagnosed by serial CT scans showing increasing size of
the ventricles and by the clinical signs of increased ICP.
Hydrocephalus may respond to osmotic diuretics, but
if neurologic deterioration is significant, surgical place-
ment of a shunt is indicated.
