Tinjauan Pustaka

The Characteristics of
Subarachnoid Hemorrhage

Harsono
Department of Neurology, Faculty of Medicine Gadjah Mada University/
Dr. Sardjito Hospital Yogyakarta, Indonesia

Abstract: Spontaneous or non-traumatic subarachnoid hemorrhage (SAH) accounts for about

80% of cases and has a high rate of death and complications. Diagnosis of SAH can be challenging and critical. Delayed cerebral ischemia (DCI) due to cerebral vasospasm and acute hydrocephalus after SAH are major complications and continue to be the leading causes of death and
disability following SAH. Characteristics of spontaneous SAH are diverse, comprise clinical
manifestations, diagnostic procedure, specific complications, principles of management, definite treatment to the aneurysm, and prognosis. Spontaneous SAH is a major life experience that
leads to additional morbidity in up to 25% of surviving patients.
Keywords: subarachnoid hemorrhage, cerebral ischemia, acute hydrocephalus, diagnostic procedure, morbidity

Karakteristik Perdarahan Subaraknoid

Harsono
Bagian Ilmu Penyakit Saraf, Fakultas Kedokteran Universitas Gadjah Mada/
SMF Penyakit Saraf RS Dr. Sardjito Yogyakarta, Indonesia

Abstrak: Perdarahan subaraknoid spontan atau non-traumatik meliputi 80% dari seluruh kasus
perdarahan subaraknoid, mempunyai tingkat kematian dan komplikasi yang tinggi. Diagnosis
PSA bersifat sangat menantang karena berkaitan erat dengan komplikasi dan outcome. Iskemia
serebral karena vasospasme serta hidrosefalus akut merupakan penyebab utama kematian dan
disabilitas. Karakteristik perdarahan subaraknoid cukup beragam, mencakup perspektif klinik,
prosedur diagnostik, komplikasi, prinsip manajemen, terapi definitif terhadap aneurisma dan
prognosis. Para penderita perdarahan subaraknoid yang bertahan hidup akan mengalami
morbiditas yang sangat mengganggu aktivitas sehari-hari; proporsi penderita dengan morbiditas
ini mencapai 25%.
Kata kunci: perdarahan subaraknoid, iskemia serebral, hidrosefalus akut, prosedur diagnostik,
morbiditas

20

Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

The Characteristics of Subarachnoid Hemorrhage

Introduction
Subarachnoid hemorrhage (SAH) is a neurologic emergency characterized by the extravasation of blood into the
spaces covering the central nervous system that are filled
with cerebrospinal fluid. The causes of subarachnoid hemorrhage are rupture of an intracranial aneurysm and nonaneurysmal bleeding. Rupture of an intracranial aneurysm
accounts for about 80% of cases and has a high rate of
death and complications. Nonaneurysmal subarachnoid hemorrhage, including traumatic and isolated perimesencephalic
subarachnoid hemorrhage, occurs in about 20% of cases
and carries a good prognosis with uncommon neurologic
complications.1,2
In patients with aneurysmal SAH, delayed cerebral ischemia (DCI) is an important cause of poor outcome. The
pathogenesis of DCI is still poorly understood. Intracranial
vasospasm, which results from the release of vasoactive
substances, has often been incriminated. Vasospasm is often used as a synonym but is not sufficient factor because
even severe vasospasm does not always lead to secondary
ischemia. Platelet aggregation probably plays a role also.
Activation of platelet aggregation and the associated release of thromboxane B2 are increased from day 3 after the
onset of SAH. This increase is larger in patients who actually develop DCI than in patients without DCI. Data from
animal research further support the involvement of platelet
aggregation. Both rupture of an artery and the presence of
blood at the abluminal side of an intact artery activate platelet aggregation. Moreover, antiplatelet activity of the endothelium is reduces after SAH.3 Sudden death from a massive
increase in intracranial pressure occurs in approximately 1 of
10 patients (with 40% in a posterior circulation aneurysm),
and another 10% to 20% of patients who arrive at the emergency department are comatose and need immediate respiratory support.4
Characteristics of SAH are diverse; whether clinical
perspective, diagnostic procedure, specific complications,
principles of management, definite treatment to the aneurysm, and prognosis. The purpose of the following discussion on such characteristics is to describe the phenomenology related to the rupture of an intracranial aneurysm and its
clinical as well as pathological consequences. The importance of the description is to increase the physicians alertness while handling SAH, in line with the attempt to decrease morbidity as well as mortality rate.
Clinical Perspective
Blood in the subarachnoid space is a powerful meningeal irritant, which irritation that causes most of the initial signs and symptoms of SAH. Findings vary from insignificant to serious depending on the extent of hemorrhage.
The characteristic initial symptoms of patients with SAH is
sudden headache described as the most painful ever experienced.5
Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

A ruptured cerebral aneurysm causes an unexpected,

sudden headache and may lead to loss of consciousness.
Patients describe a thunderclap headache (an unfortunate
term because no sound is heard). The patient reports the
worst headache of his or her life, more precisely, a split second, extremely intense, and overwhelming headache that fail
to subside. Many patients report feeling as if the top of my
head is blown off or as though someone hit me in the head
with a hammer, but these key elements in medical history
may be difficult to elicit in confused patients. Rarely, there
are other nonaneurysmal causes of thunderclap headache
present. These disorders include pituitary apoplexy, arterial
dissection, cerebral venous thrombosis, and hypertensive
encephalopathy. Also, thunderclap headache may be idiopathic.6
When the patient is seen hours after onset of symptoms, neurologic examination may reveal nuchal rigidity, cranial neuropathy (third or sixth cranial nerve most commonly),
or other localized neurologic deficit (aphasia, hemiparesis);
however, major neurologic signs generally are absent. Seizures may occur in a small percentage of surviving patients,
and epilepsy may develop in less than 10%, particularly in
those who had subdural hematoma or cerebral infarction
during their hospital course.7
Diagnosis
Spontaneous SAH should always be suspected in patients with a typical presentation, which includes a sudden
onset of severe headache (frequently described as the worst
ever), with nausea, vomiting, neck pain, photophobia, and
loss of consciousness. Physical examination may reveal retinal hemorrhages, meningismus, a diminished level of consciousness, and localizing neurologic signs. The latter findings usually includes third-nerve palsy (posterior communicating aneurysm), sixth-nerve palsy (increased intracranial
pressure), bilateral lower-extremity weakness or abulia (anterior communicating aneurysm), and the combination of hemiparesis and aphasia or visuospatial neglect (middle cerebral
artery aneurysm). Retinal hemorrhages should be differentiated from the preretinal hemorrhages of Tersons syndrome,
which indicates a more abrupt increase in intracranial pressure and increased mortality.2
Diagnosis SAH can be challenging. Computed tomography is the first-line diagnostic procedure in patients with
suspected SAH. Historically, CT has 90% to 95% sensitivity
for recent SAH; with modern CT equipment, sensitivity is
closer to 98%. On CT, an aneurysm is rarely seen but when
present indicates large size (more than 10 cm).1 Head CT
scanning can also demonstrate intraparenchymal hematomas, hydrocephalus, and cerebral edema and can help predict the site of aneurysm rupture, particularly in patients with
aneurysms in the anterior cerebral or anterior communicating arteries. Head CT scanning is also the most reliable test
for predicting cerebral vasospasm and poor outcome. Be21

The Characteristics of Subarachnoid Hemorrhage

cause of rapid clearance of blood, delayed head CT scanning may be normal despite a suggestive history, and sensitivity drops to 50% at the seven days.2
Lumbar puncture should be performed in any patient
with suspected subarachnoid hemorrhage and negative or
equivocal results on head CT scanning. Cerebrospinal fluid
(CSF) should be collected in four consecutive tubes, with
red cell count determined in tubes 1 and 4. Findings consistent with subarachnoid hemorrhage include an ele-vated
opening pressure, an elevated red-cell count that does not
diminish from tube 1 to tube 4, and xanthochromia (owing
to red-cell breakdown detected by spectrophotometry), which
may require more than 12 hours to develop.2
Moreover, examination of CSF is necessary when CT is
normal and has been reviewed for subtle areas of subarachnoid blood (posterior horns, sylvian fissure, and sulci).
Prompt ascertainment of diagnosis of SAH is warranted because a ruptures aneurysm has the highest rate of rerupture
within the initial 48 hours. However, no evidence suggests
that lumbar puncture increases the risk of aneurismal
rebleeding. Testing CSF for the presence of xanthochromia,
the yellow tinge in CSF caused by the breakdown products
of hemoglobin is the gold standard for diagnosis of SAH,
with sensitivity greater than 99%. Xanthochromia is present
as early as 6 hours after SAH and along with bilirubin remains detectable until about 2 to 3 weeks after SAH. When
gross blood is present in initial CSF specimen tube, a decrease in the quantity of red blood cells in successive specimen tubes is a frequently used (albeit unreliable) marker for
the absence of SAH. The medicolegal implications can be
substantial if cerebral angiography id deferred on the basis
of this loose criterion.6,8
Determining the presence of xanthochromia is the best
method to document disintegrated erythrocytes, but vials
should be held against a bright light and white background
to appreciate the discoloration. Visual inspection is far from
perfect. Spectrophotometry of CSF may document oxyhemoglobin or bilirubin if visual assessments of the vial with
centrifuged CSF are conflicting. Bilirubin absorbance at 473l
is diagnostic (note that iodine used during the procedure
may lead to a false-positive effects).8
The experience of an aneurysmal SAH often prompts
other family members to seek advice on screening for aneurysm. If screened on a large scale, aneurysms would be found
in approximately 7% of first degree relatives (parents, siblings, and children), with higher chance of an unruptured
aneurysm in a sibling. Screening for aneurysm is complicated and unresolved issue. The rupture risk of incidentally
detected aneurysm is low (less than 0.5% annually), but the
morbidity of surgical or endovascular repair (5%) is potentially substantial. Moreover, noninvasive imaging tests are
suboptimal for detecting unruptured aneurysm.6,9

22

Complications
Cerebral Vasospasm
Vasospasm has been described as a sustained arterial
contraction unresponsive to vasodilator drugs. This condition is commonly classified as either angiographic or clinical.
Angiographic vasospasm refers to visible narrowing of the
dye column in an artery, as shown on cerebral angiograms.
Clinical vasospasm is the functional manifestation of cerebral ischemia produced by this arterial narrowing.5
Cerebral vasospasm is a major complication and continues to be one of the leading causes of death and disability
following SAH. Vasospasm usually manifests in the first 3 to
4 days after the hemorrhage, peaks at one week, and generally resolves over the next 2 to 3 weeks. Blood products that
collect after SAH and remain in prolonged contact with the
cerebral vessel walls induce vasospasm, resulting in narrowing of the vessel lumen and compromised cerebral blood
flow and oxygenation. This can result in ischemic sequelae
manifested by the onset of confusion, a decreased level of
consciousness, speech and motor impairments, increasing
blood pressure, and a worsening headache. Approximately
7% of patients who reach neurosurgical referral centers will
die of vasospasm and another 7% will be seriously injured
because of this condition. The diagnosis of cerebral vasospasm is based on both angiographic changes and clinical
changes. Although 70% of patients may experience
angiographic vasospasm, only 20 to 30% will exhibit delayed
ischemic neurological deficits or DCI.10
The etiology and pathophysiology of cerebral vasospasm after SAH are complex and are only partially understood. Precise molecular mechanisms of vasospasm remain
to elucidated, but they include a combination of both increased dilator functions. Several theories have been offered
to explain the multifaceted process known to be involved.
Considerable evidence supports the hypothesis that oxyhemoglobin plays a primary role in the development of cerebral
vasospasm associated with aneurysmal SAH. After the initial hemorrhage, erythrocytes trapped in the subarachnoid
cisterns slowly hemolize, releasing oxyhemoglobin and other
by-products of red cell lysis (e.g., bilirubin and methemoglobin) to circulate within the subarachnoid space. These
spasminogens increase the influx calcium into the vascular
smooth muscle, altering myocyte function and causing prolonged contraction and vessel constriction.11 Spontaneous
SAH increases production of vascular extra-cellular superoxide anion. Meanwhile endogenous overexpression of extra-cellular superoxide dismutase (EC-SOD) attenuated vasospasm and oxidative stress but failed to reduce neurological deficits after SAH. Extra-cellular superoxide anion likely
plays a direct role in the etiology of vasospasm.12
Transcranial doppler ultrasonography is a noninvasive
method for monitoring development of cerebral vasospasm.

Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

The Characteristics of Subarachnoid Hemorrhage

A handled probe is used to transmit and receive a low-frequency pulsed wave through the temporal bone of the skull.
This ultrasonic wave is both range gated and directionally
sensitive, which allows for insonation of the cerebral vessels at varying depths and directions. Elevated blood flow
velocities in the middle cerebral artery are correlated with
angiographic narrowing of this vessel, although the correlation of angiographic vessel narrowing with other cerebral
vessels is less reliable.6
In contrast to the above description, several lines of
evidence cast doubt on angiographically confirmed vasospasm as the sole cause of delayed ischemic neurological
deficits (DINDs). These include the following: i) the relatively limited role that large arteries play in control of cerebral blood flow, ii) a lack of correspondence between the
sites and severity of angiographically confirmed vasospasm
and cerebral ischemia, iii) the appearance of cerebral infarcts
at autopsy, and iv) the disappointing clinical effects of vasospasm therapy. On the other hand, SAH also causes considerable injury to the vascular endothelium, resulting in
desquamation. This accompanied by the appearance of markers of endothelial activation in blood, cerebral dialisate, and
cerebrospinal fluid, blood-brain barrier dysfunction, and
platelet accumulation. The fate of microthrombi created by
either mechanic, depends on vessel size. In large arteries,
microclots are likely to embolize. Small arterioles would be
more liable to thrombose. Several investigators have demonstrated that micro-emboli can indeed cause cerebral infarction and symptomatic ischemia in animal and humans.
Hence, vasospasm and thrombo-embolism play interrelated
and additive roles in the development of DINDs, and this
interaction provides opportunities for novel therapeutic approaches.13
Acute Hydrocephalus
Normal CSF circulation may become obstructed secondary to intraventricular blood due to a thick clot in the
basal cisterns or a clot at the level of the arachnoid villi.
Certain clinical and radiographic features may predict the
occurrence of acute hydrocephalus: intracerebral extension
of hemorrhage, posterior circulation aneurysm, and reduced
Glasgow Coma Scale score on admission.6
Acute hydrocephalus after SAH is a necessary consideration in patients presenting with altered consciousness;
by CT criteria, it is present in 20% of patients. Acute neurologic deterioration in the setting of progressive ventricular
enlargement on CT is a clear indication for external ventricular drainage. However, the treatment of patients who arrive
at the hospital in a comatose state with ventricular enlargement on CT is more controversial because the neurology
impairment may be a result of the effect of the initial hemorrhage rather than due to hydrocephalus. Such patients can
be observed initially for 24 hours, and some will improve
clinically without intervention. If serial CT scans reveal proMaj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

gressive ventricular enlargement or if the neurologic condition deteriorates, external ventricular drainage is indicated.
Other clinicians may advocate early placement of external
ventricular drains and then observation for possible improvement. The most recent data suggest that external ventricular
drainage does not increase the likelihood of aneurismal
rehemorrhage when drainage is performed at moderate pressure (<10 cm H2O).6,14
Principles of Management
All patients with SAH should be evaluated and treated
on an emergency basis with maintenance of airway and cardiovascular function. After initial stabilization, patients should
be transferred to centers with neurovascular expertise and
preferably with a dedicated neurologic critical care unit to
optimize care. Once in the critical setting, the main goals of
treatment are the prevention of rebleeding, the prevention
and management of vasospasm, and the treatment of other
medical and neurologic complications i.e., cerebral vasospasm and acute hydrocephalus.2,15
Initial Treatment
The approach to initial treatment is shown in the following description. The guiding principles by organ systems
are aimed at preservation of homeostasis, use of prophylactic drugs, and preparation for definitive aneurysm treatment.6
Although surgical and endovascular therapeutic options
have substantially changed the approach to SAH, medical
treatment also has shifted considerably. On the basis of evidence from randomized trials, several therapies have been
discarded because of a serious concern of doing more harm
than good, including antifibrinolytic agents, sublingual
nifedipine, fluid restriction for hyponatremia, delayed clipping of ruptures aneurysm, and nitroprusside and other vasodilators. 16,17
The components of initial treatment of SAH consist of
airway, fluid, blood pressure, nutrition, and additional measures. Intubation and mechanical ventilation are inserted if
patients have aspiration, neurogenic pulmonary edema,
Glasgow Coma Scale motor score of withdrawal or worse.
Intravenous 0.9% NaCl is given for 2-3 L per 24 hours;
fludrocortisone acetate, 0.3 mg/dl is recommended if patients
have hyponatremia. Mean arterial pressure should be maintained within >130 mmHg. If mean arterial pressure <130
mmHg, the following antihypertensive agents can be administered: esmolol bolus (500 mg/kg in 1 minute, or intravenous
20 mg labetolol in 2 minutes, or intravenous 0.625 mg enalprilat
in 5 minutes. Meanwhile, enteric nutrition with continuous
infusion should be administered within the first 2 days. Additional measures consist of 60 mg nimodipine, 6 times a day
for 21 days. Stool softener, pneumatic compression devices,
acetaminophen with codeine or morphine(1-2 mg) or tramadol
(if no seizures) 50-100 g orally every 4 hours for pain management, and phenytoin 20 mg/kg if seizures have occurred.18
23

The Characteristics of Subarachnoid Hemorrhage

General Approach
Blood pressure should be maintained within normal limits, and if necessary, intravenous antihypertensive agents
such as labetolol and nicardipine can be used. Once the
aneurysm is secured, hypertension is allowed, but there is
no agreement on the range. Analgesia is often required, and
reversible agents such as narcotics are indicated. Two important factors that are associated with poor outcome are
hyperglycemia and hyperthermia, and both should be corrected.19-21
Prophylaxis of deep venous thrombosis should be instituted early with sequential compressive devices, and subcutaneous heparin should be added after the aneurysm
is treated. Calcium antagonists reduce the risk of poor outcome from ischemic complications, and oral nimodipine is
currently recommended. Prolonged administration of antifibrinolytic agents reduces rebleeding but is associated with
an increased risk of cerebral ischemia and systemic thrombotic events. Early treatment of aneurysms has become the
mainstay of rebleeding prevention, but antifibrinolyitic
therapy may be used in the short term before aneurysm treatment.22,23
Treatment of Cerebral Vasospasm
a. Triple H Therapy
The foundation for prevention and treatment of vasospasm is maintaining euvolemia or mild hypovolemia and
normotension or moderate hypertension.6 For patients who
become symptomatic with DCI due to vasospasm, more aggressive intravascular volume expansion (hypervolemia),
hemodilution and induced hypertension which is called
triple H therapy, are used. A hypertensive state is maintained through the use of vasopressors. Hypervolemia subsequently produces hemodilution. These maneuvers are all
designed to increase cerebral perfusion pressure, improve
blood flow to the brain, and decrease the risk of ischemia.5,24
Triple H therapy is generally started soon as the aneurysm has been secured or clipped. Occasionally, a modified
version of triple H therapy is used before securement of the
aneurysm in order to prevent rebleeding or rupture. Therapy
is continued for at least 14 days after the initial hemorrhage,
the most common period for vasospasm. Induced hypertension is designed to increase cerebral blood flow and thus
enhance perfusion pressure. In order to accomplish this goal,
target systolic blood pressure may be as high as 200 mmHg.
In addition to fluids, vasopressor and inotropic agents such
as dopamine, phenylephrine, and dobutamine are generally
required to maintain systolic blood pressure at this elevated
level. Therapeutic hypertension is only initiated once the
aneurysm has been surgically clipped or coiled. If the aneurysm has not yet been repaired surgically or is considered
inoperable, systolic blood pressure is kept between 120 and
150 mmHg to minimize the risk of rupture and rebleeding.5, 25
24

Hypervolemia is produced by infusing intravenous

crystalloids or colloids sufficient to optimize a patients Starling curve. To ensure appropriate intravascular volume and
cardiac output in symptomatic patients, invasive monitoring
in the form of right atrial or pulmonary artery catheterization
is recommended. Determining the point at which optimization occurs requires careful hemodynamic assessment. General parameters include pulmonary artery wedge pressure of
14 to 20 mmHg, cardiac index (calculated as cardiac output in
liters per minute divided by body surface area in square
meters) of 2.2 or greater, and central venous pressure of 10 to
12 mmHg.5
b. Nimodipine
Nimodipine is a calcium channel antagonist of the 1,4dihydripiridine class. It acts primarily by preventing the flux
of calcium ions through voltage-dependent and receptor
operated slow channels of the cell membrane and hence
relaxes vascular smooth muscle. Compared with nifedipine,
nimodipine is more lipophilic, a more potent cerebral vasodilator and more rapidly and widely distributed in cerebral tissue, and can lead to improvement in long-term outcomes
after SAH.5,26 Nimodipine, a calcium channel antagonists with
a relatively selective vasodilatory effect on cerebral blood
vessels, has been approved for improvement of neurologic
deficits due to spasm following SAH. Nimodipine has low
oral bioavailability (2.7-27.9%), a short half-life (2 hours), is
highly protein bound (98-99%), and is hepatically metabolized.27
Because nimodipine is lipid soluble, it easily crosses
the blood-brain barrier. This leads to decreased smoothmuscle contraction as well as decreased release of vasoactive substances from the endothelium, resulting in reduced
arterial narrowing. Nimodipine may also have some direct
neuroprotective properties, including blockage of free-radical attack on the intraneuronal mitochondria, improvement
of carbon dioxide reactivity and cerebral oxygen metabolism,
or reduction of tissue damaged caused by calcium overload
in ischemic neurons.26
Nimodipine has been used extensively in the treatment
of the prevention of vasospasm related to SAH. After hemorrhage, patients are prophylactically given oral nimodipine
at a dosage of 60 mg, every 4 hours, for 21 days. Of note, the
drug does not increase the caliber of narrowed cerebral arteries on cerebral angiography. Several randomized controlled
trials have been conducted. In a meta-analysis of a number
of published randomized trials, the evidence in favor of routine prophylactic use of nimodipine is strong. Nicardipine
has also been the subject of several controlled trials. Although the largest trial showed a considerably lower rate of
ischemic deficits secondary to cerebral vasospasm, the overall
outcome was not improved.5, 24,28
In a rabbit model of chronic cerebral vasospasm, the
results indicate that selective intra-arterial (IA) nimodipine
Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

The Characteristics of Subarachnoid Hemorrhage

treatment is effective in reversing vasospasm in experimental SAH. IA nimodipine infusion was found more effective
than its intrathecal (IT) application in basilar artery. This
probably due to the limited diffusion of the drug in IT application. IA and IT applications of nimodipine were equally
effective in vertebral artery, which demonstrates the potent
vasodilator effect of the drug. IA nimodipine infusion was
found more effective than IA papaverine infusion in both
vertebral and basilar arteries. Selective IA nimodipine treatment can be considered as an alternative technique for the
treatment of vasospasm due to SAH. However, further studies are needed to implement this treatment option into clinical practice.29
Treatment Options for Aneurysm
Currently, the two main therapeutic options for securing a ruptured aneurysm are microvascular neurosurgical
clipping and endovascular coiling. Historically, microsurgical clipping has been the preferred method of treatment. Although the timing of surgery has been debated, most neurovascular surgeon recommends early operation. Evidence
from clinical trials suggests that patients undergoing early
surgery have a lower rate of rebleeding and tend to fare
better than those treated later. Securing the ruptured aneurysm will also facilitate the treatment of complications such
as cerebral vasospasm. Although many neurovascular surgeons use mild hypothermia during microsurgical clipping
of aneurysms, it has not proved to be beneficial in patients
with lower grades of subarachnoid hemorrhages.30
When vasospasm becomes refractory to maximal medical management consisting of induced hypertension, hypervolemia, and administration of calcium channel antagonists,
endovascular therapies should be considered. Endovascular
treatment of aneurysm has been available as an alternative
to surgical therapy for the past 15 years. Coils are made of
platinum and are attached to a delivery wire. Once proper
position within the aneurysm is achieved, coils are detached
from the wire. Multiple coils of various length and diameter
are often packed into the aneurysm to exclude it from the
circulation.2,10
The International Subarachnoid Aneurysm Trial (ISAT)
prospectively examined patients with ruptured aneurysms
who were considered equally suitable for either endovascular
coiling or microsurgical clipping. The authors found that for
this particular subgroup of patients, a favorable outcome,
which was defined as survival free of disability at one year,
occurred significantly more often in patients treated with
endovascular coiling than with surgical placement clips. The
risk of epilepsy was substantially lower in patients who underwent endovascular coiling, but the risk of rebleeding was
higher. Also, in patients who underwent follow-up cerebral
angiography, the rate of complete occlusion of the aneurysm was greater with surgical clipping.31,32

Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009

Outcomes in Survivors
Optimal outcome after aneurysmal SAH depends on
careful assessment and management of patients throughout
the course of hospitalization. Critical care nurses play a crucial role in this process. Efforts continue to understand the
cascade of events that lead to cerebral vasospasm and to
develop more effective treatment.5
Spontaneous SAH is a major life experience that leads
to additional morbidity in up to 25% of surviving patients.
Many patients do not return to work, retire early, and are
unable to function at the same intellectual level as before the
rupture. Numerous clinical factors may influence outcome
after SAH, including the presenting clinical condition of the
patient, age older than 65 years, presence of posterior distribution aneurysms, rupture, intracerebral extension, and development of cerebral vasospasm or cerebral infarctions.
Pre-existing medical conditions and aneurysm size do not
appear to affect outcome. Recovery in young patients may
be protracted and better than expected. The most important
clinical factor in predicting poor patient outcome after SAH
is the presenting level of consciousness. The natural history of such patients is dismal with higher than 90% mortality. Population-based studies that eliminate the selection bias
of referral centers have estimated that approximately 30% of
patients have poor outcome after SAH.6
Summary
Subarachnoid hemorrhage should always be suspected
in patients with a sudden onset of typical presentation,
which includes a sudden onset of severe headache (frequently described as the worst ever or a thunderclap
headache), with nausea, vomiting, neck pain, photophobia,
and loss of consciousness. Diagnosis of SAH can be challenging. Computed tomography is the first-line diagnostic
procedure in patients with suspected SAH. However, lumbar puncture should be performed in any patient with suspected subarachnoid hemorrhage and negative or equivocal
results on head CT scanning
The most dangerous complications of SAH are cerebral
vasospasm and acute hydrocephalus. These complications
should be kept on mind and predicted earlier, soon after the
onset. Triple H therapy is generally started soon as the aneurysm has been secured or clipped. The calcium channel
antagonist nimodipine has strong evidence in preventing
cerebral vasospasm related to SAH. When vasospasm becomes refractory to maximal medical management,
endovascular therapies should be considered.
References
1.
2.
3.

van Gijn J, Rinkel GJ. Subarachnoid hemorrhage: diagnosis, causes

and management. Brain.2001;124:249-78.
Suarez JI, Tarr RW, Selam WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med 2006;354:387-96.
Dorhout Mees SM, Rinkel GJE, Hop JW, Algra A, van Gijn J.

25

The Characteristics of Subarachnoid Hemorrhage

4.

5.
6.

7.

8.

9.
10.

11.
12.

13.

14.

15.

16.

17.

18.
19.

26

Antiplatelet therapy in aneurysmal subarachnoid hemorrhage: a

systematic review. Stroke. 2003;34:2285-89.
Huang J, van Gelder JM. The probability of sudden death from
rupture of intracranial aneurysms: a meta-analysis. Neurosurgery.2002;51:1101-05.
Oyama K, Criddle L. Vasospasm after aneurismal subarachnoid
hemorrhage. Critic Care Nurse.2004;24(5):58-67.
Wijdicks EFM, Kalmes DF, Manno EM. Subarachnoid hemorrhage: neurointensive care and aneurysm repair. Mayo Clin Proc
2005;80(4):550-59.
Claassen J, Peery S, Kreiter KT, Hirsch LJ, Du EY. Predictors and
clinical impact of epilepsy after subarachnoid hemorrhage. Neurology.2003;60:208-14.
Beetham R, Fahie-Wilson MN, Holbrook I, Thomas P, Ward
AK. CSF spectrophotometry in the diagnosis of subarachnoid
hemorrhage. J Clin Pathol. 2002;55:479-80.
Wadlaw JM, White PM. The detection and management of
unruptured intracranial aneurysms. Brain.2000;123:205-21.
Sayama CM, Liu JK, Couldwell WT. Update on endovascular
therapies for cerebral vasospasm induced by aneurismal subarachnoid hemorrhage. Neurosurg Focus.2006;21(3):E12.
Macdonald RL. Pathophysiology and molecular genetics of vasospasm. Acta Neurochir Suppl.2001;77:7-11.
McGirt MJ, Parra A, Sheng H, Higuchi Y, Oury TD, Laskowitz
DT, et al. Attenuation of cerebral vasospasm after subarchnoid
hemorrhage in mice overexpressing extracellular superoxide
dismutase. Stroke.2002;33:2317-23.
Stein SC, Levine JM, Nagpal S, LeRoux PT. Vasospasm as the
sole cause of cerebral ischemia: how strong is the evidence?
Neurosurg Focus 2006;21(3):E2.
McIver JI, Friedman JA, Wijdicks EFM, Piepgras DG, Pichelman
MA, Toussaint LG3rd, et al. Preoperative ventriculostomy and
rebleeding after aneurysmal subarachnoid hemorrhage. J Neurosurg
2002;97:1042-44.
Suarez JI, Zaidat OO, Suri MF, Feen ES, Lynch G, Hickman J, et
al. Length of stay and mortality in neurocritically ill patients:
impact of a specialized neurocritical care team. Crit Care Med
2004;32:2311-17.
Wijdicks EFM, Vermeulen M, Hijdra A, van Gijn J. Hyponatremia and cerebral infarction in patients with ruptured intracranial
aneurysms: is fluid restriction harmful? Ann Neurol.1985;17:13740.
Wijdicks EFM, Hasan D, Lindsay KW, Brouwers PJ, Hatfield R,
Murray GD, et al. Short-term tranexamic acid treatment in aneurismal subarachnoid hemorrhage. Stroke.1989;20:1674-79.
Wijdicks EFM. The Clinical Practice of Critical Care Neurology:
Oxford, England; Oxford University Press; 2003.
Bambakidis NC, Selman WR. Subarachnoid hemorrhage. In: Suarez
JI, ed. Critical care neurology and neurosurgery. Totowa, N.J:
Humana Press; 2004.p.365-77.

20. Dorhout Mees SM, van Dijk GW, Algra A, Kempink DRJ, Rinkel
GJE. Glucose levels and outcome after subarachnoid hemorrhage.
Neurology.2003;61:1132-33.
21. Commichau C, Scarmeas N, Mayer SA. Risk factors for fever in
the neurologic intensive care unit. Neurology.2003;60:837-41.
22. Roos YB, Rinkel GJ, Vermeulen M, Algra A, van Gijn J.
Antifibrinolyitic therapy for aneurysmal subarachnoid hemorrhage. A major update of a Cochrane review. Stroke 2003;34:230809.
23. Rinkel GJ, Feigin VL, Algra A, van den Bergh W, Vermeulen M,
van Gijn J. Calcium antagonists for aneurysmal subarachnoid
hemorrhage. Stroke 2005;36:1816-17.
24. Kirkpatrick PJ. Subarachnoid hemorrhage and intracranial aneurysms: what neurologist needs to know. J Neurol Neurosurg Psychiatry. 2002;73(Suppl.10):i28-i33.
25. Hob BI, Carter BS, Ogilvy CS. Risk of hemorrhage from unsecured, unruptured aneurysms during and after hypertensive
hypervolemic therapy. Neurosurgery. 2002;50:1207-11.
26. Yasuda SU, Tietze KJ. Nimodipine in the treatment of subarachnoid hemorrhage. Ann Pharmacotherapy. 1989;23(6):451-55.
27. Weekes L, Seale JP. Nimodipine: an Update. A Position statement of the NSW Therapeutic Assessment Group Inc.Australia;
1997.
28. Barker FG, Ogilvy CS. Efficacy of prophylactic nimodipine for
delayed ischemic deficit after subarchnoid hemorrhage: a metaanalysis. J Neurosurg.1996;405-14.
29. Firat MM, Gelebek V, Orer HS, Belen D, Firat AK, Balkanci F.
Selective intra-arterial nimodipine treatment in an experimental
subarchnoid hemorrhage model. Am J Neuroradiol. 2005;26:135762.
30. Todd MM, Hindman BJ, Clarke WR, Torner JC. Mild intraoperative hypothermia during surgery for intracranial aneurysm.
N Engl J Med. 2005;352:135-45.
31. Molyneux AJ, Kerr RS, Stratton I, Sandercock P. International
Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping
versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized trial. Lancet. 2002:360:126774.
32. Molyneux AJ, Kerr RS, Yu L-M, Clarke M, Sneade M, Yarnold
JA, et al International Subarachnoid Aneurysm Trial (ISAT) of
neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized comparison of effects on survival, dependency, seizures, rebleeding,
subgroups, and aneurysm occlusion. Lancet. 2005;366:809-17.

NS

Maj Kedokt Indon, Volum: 59, Nomor: 1, Januari 2009