History

The signs and symptoms of subarachnoid hemorrhage (SAH) range from subtle
prodromal events to the classic presentation. Prodromal events often are misdiagnosed,
while the classic presentation is one of the most pathognomonic pictures in all of clinical
medicine.
Prodromal events
Signs and symptoms precede ruptured cerebral aneurysm in anywhere from 10-50% of
cases. Premonitory manifestations generally appear 10-20 days prior to rupture. The
most common symptoms are as follows:
 Headache (48%)
 Dizziness (10%)
 Orbital pain (7%)
 Diplopia (4%)
 Visual loss (4%)
Signs present before SAH include the following:
 Sensory or motor disturbance (6%)
 Seizures (4%)
 Ptosis (3%)
 Bruits (3%)
 Dysphasia (2%)
Prodromal signs and symptoms usually are the result of one or more of the following:
 Sentinel leaks
 Mass effect of aneurysm expansion
 Emboli
Sentinel leaks
Sentinel, or "warning," leaks with minor loss of blood from the aneurysm are reported to
occur in 30-50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or
generalized head pain that may be severe. Sentinel headaches precede aneurysm
rupture by a few hours to a few months, with a reported mean of 2 weeks prior to
discovery of the SAH.
In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia,
malaise, or, less commonly, neck pain. These symptoms may be ignored by the
physician. Therefore, a high index of suspicion is necessary for accurate diagnosis.
Sentinel leaks usually do not generate symptoms suggestive of elevated intracranial
pressure (ICP) or meningeal irritation. Sentinel leaks usually do not occur in patients
with arteriovenous malformations.
Mass effect
Prodromal presentations occasionally are caused by the mass effect of an expanding
aneurysm and have characteristic features based on aneurysm location, as follows:
 Posterior communicating artery/internal carotid artery: focal, progressive retro-
orbital headaches and oculomotor nerve palsy
 Middle cerebral artery: contralateral face or hand paresis, aphasia (left side),
contralateral visual neglect (right side)
 Anterior communicating artery: bilateral leg paresis and bilateral Babinski sign
 Basilar artery apex: vertical gaze, paresis, and coma
  Intracranial vertebral artery/posterior inferior cerebellar artery: vertigo, components
of lateral medullary syndrome
Emboli
Emboli originating from intra-aneurysmal thrombus formation can cause transient
ischemic attacks.
Classic presentation
The central feature of classic SAH is sudden onset of severe headache (thunderclap
headache), often described as the "worst headache of my life." Less severe
hemorrhages may cause headache of moderate intensity, neck pain, and nonspecific
symptoms. Absence of headache in the setting of a ruptured intracranial aneurysm is
rare and probably represents amnesia for the event.
The headache may be accompanied by nausea and/or vomiting from increased ICP and
meningeal irritation. Symptoms of meningeal irritation, including nuchal rigidity and pain,
back pain, and bilateral leg pain, occur in as many as 80% of patients with SAH but may
take several hours to manifest. Photophobia and visual changes are common. Focal
neurologic deficits may also occur.
Sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients
as intracranial pressure (ICP) exceeds cerebral perfusion pressure. LOC often is
transient; however, approximately 10% of patients remain comatose for several days,
depending on the location of the aneurysm and the amount of bleeding.
Seizures during the acute phase of SAH occur in 10-25% of patients. Seizures result
from the sudden rise in ICP or direct cortical irritation by blood. No correlation exists
between the seizure focus and the anatomic site of aneurysm rupture.
A proposed decision rule for diagnosis of SAH focuses on the following 7
characteristics, which are strongly associated with SAH:
 Aged 40 years or older
 Witnessed loss of consciousness
 Complaint of neck pain or stiffness
 Onset of manifestations with exertion
 Arrival by ambulance
 Vomiting
 Diastolic blood pressure ≥100 mm Hg or systolic blood pressure ≥160 mm Hg
Should one or more of these be present in a patient with an acute nontraumatic
headache reaching maximum intensity within 1 hour, the possibility of SAH hemorrhage
should be investigated. [12] On the other hand, it may be possible to consider foregoing
investigation in patients with none of these characteristics. [12] This decision rule has not
yet been validated. Further study is needed before this approach can be
recommended.
Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional
strain, defecation, coitus, and head trauma contribute to varying degrees in the
remaining 60-70% of cases.
Physical Examination
Physical examination findings may be normal. About half of patients have mild to
moderate blood pressure (BP) elevation. BP may become labile as ICP increases.
Temperature elevation, secondary to chemical meningitis from subarachnoid blood
products, is common after the fourth day following bleeding. Tachycardia may be
present for several days after the occurrence of a hemorrhage.
Funduscopy may reveal papilledema. Subhyaloid retinal hemorrhage (small round
hemorrhage, perhaps with visible meniscus, near the optic nerve head) is evident in 20-
30% of patients. Other retinal hemorrhages may be seen.
Global or focal neurologic abnormalities are found in more than 25% of patients. Global
depression of neurologic function may be noted, including altered level of
consciousness and confusional state. Motor neurologic deficits occur in 10-15% of
patients, usually from middle cerebral artery aneurysms. In 40% of patients, no
localizing signs are evident. Seizures may occur.
Focal neurologic findings
Cranial nerve palsies, along with memory loss, are present in 25% of patients. The most
frequent is oculomotor nerve palsy with or without ipsilateral mydriasis, which results
from rupture of a posterior communicating artery aneurysm. Abducens nerve palsy is
usually due to increased ICP rather than a true localizing sign. Monocular vision loss
can be caused by an ophthalmic artery aneurysm compressing the ipsilateral optic
nerve.
Hemiparesis results from middle cerebral artery (MCA) aneurysm, ischemia or
hypoperfusion in the vascular territory, or intracerebral clot. Patients may also have
aphasia, hemineglect, or both. Leg monoparesis or paraparesis with or without akinetic
mutism/abulia points to anterior communicating aneurysm rupture.

Clinical Grading Scales

Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical
scales most often employed are the Hunt and Hess and the World Federation of
Neurological Surgeons (WFNS) grading systems. A third, the Fisher scale, classifies
SAH based on CT scan appearance and quantification of subarachnoid blood.
The WFNS scale is as follows:
 Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent
 Grade 2 - GCS of 13-14, motor deficit absent
 Grade 3 - GCS of 13-14, motor deficit present
 Grade 4 - GCS of 7-12, motor deficit absent or present
 Grade 5 - GCS of 3-6, motor deficit absent or present
Complications
Some complications of SAH include the following:
 Hydrocephalus
 Rebleeding
 Vasospasm
 Seizures
 Cardiac dysfunction

Rebleeding
The incidence of the complication of rebleeding is greatest in the first 2 weeks. The
peak is within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5%
per day for the next 12-13 days. Clinical factors that increase the likelihood of
rebleeding include the following:
 Hypertension
 Anxiety [5]
 Agitation
 Seizures

Vasospasm
Currently, delayed ischemia from arterial smooth muscle contraction of the large
capacitance vessels at the base of the brain is the leading cause of death and disability
following aneurysmal SAH. Vasospasm is symptomatic in 36% of patients. The
incidence of angiographic vasospasm is 30-70%; of these patients, 20-36% become
symptomatic.
Risk factors for vasospasm include the following:
 Larger volumes of blood in the subarachnoid space
 Clinically severe SAH
 Female sex
 Young age
 Smoking
Diagnostic Considerations
Missing SAH obviously carries major medicolegal consequences. [14] In the emergency
department, clinicians should err on the side of "overtapping" patients.
A good history of the current headache is essential, even in known migraineurs, and if
the presentation has any unusual aspects (eg, worst ever headache, episode of loss of
consciousness, first ever episode of diplopia), obtain a CT scan of the head and perform
a lumbar puncture even if the CT scan is negative for blood. Do not forget to measure
opening pressure and adequately check for xanthochromia.

Computed Tomography
CT without contrast is the most sensitive imaging study in SAH (see the images below).
When carried out within 6 hours of headache onset, CT has 100% sensitivity and
specificity. Sensitivity is 93% within 24 hours of onset, [17] 80% at 3 days, and 50% at 1
week. [18] Sensitivity is less on older second- or first-generation scanners, but most North
American hospitals have been using third-generation scanners since the mid 1980s.
Thin (3 mm) cuts are necessary to properly identify the presence of smaller
hemorrhages.

Magnetic Resonance Imaging

MRI is performed if no lesion is found on angiography. Its sensitivity in detecting blood
is considered equal or inferior to that of CT scan. The higher cost, lower availability, and
longer study time make it less optimal for detecting SAH. In addition, MRI is not
sensitive for SAH within the first 48 hours.
MRI is a useful tool to diagnose AVMs that are not detected by cerebral angiography or
spinal AVMs causing SAH. It can also be useful for diagnosing and monitoring
unruptured cerebral aneurysms. MRI can detect aneurysms 5 mm or larger with a high
sensitivity and is useful for monitoring the status of small, unruptured aneurysms. MRI
can be used to evaluate the degree of intramural thrombus in giant aneurysms.
One study found that cranial MRI including the brain and craniocervical region does not
provide additional benefit for the detection of bleeding sources in patients with
perimesencephalic and nonperimesencephalic SAH. However, MRI should be
considered on a case-by-case basis because rare bleeding sources are possible in
cases of nonperimesencephalic SAH.

Electrocardiography
All patients with SAH should have a baseline chest radiograph to serve as a reference
point for evaluation of possible pulmonary complications. All patients with SAH should
have an electrocardiogram (ECG) on admission. Patients with SAH can have
myocardial ischemia due to the increased level of circulating catecholamines or to
autonomic stimulation from the brain. Myocardial infarction is a rare complication.
ECG abnormalities frequently detected in patients with SAH include the following:
 Nonspecific ST and T wave changes
 Decreased PR intervals
 Increased QRS intervals
 Increased QT intervals
 Presence of U waves
 Dysrhythmias, including premature ventricular contractions (PVCs),
supraventricular tachycardia (SVT), and bradyarrhythmias
Approach Considerations
The traditional treatment of subarachnoid hemorrhage (SAH) from a ruptured cerebral
aneurysm included strict blood pressure control, with fluid restriction and
antihypertensive therapy. This approach was associated with a high rate of morbidity
and mortality from the ischemic complications of hypovolemia and hypotension.
Current recommendations advocate the use of antihypertensive agents when the mean
arterial pressure (MAP) exceeds 130 mm Hg. Intravenous beta-blockers, which have a
relatively short half-life, can be titrated easily and do not increase intracranial pressure
(ICP). Beta-blockers are the agents of choice in patients without contraindications.
Most clinicians avoid the use of nitrates, such as nitroprusside or nitroglycerin, which
elevate ICP. Hydralazine and calcium channel blockers have a fast onset and lead to a
relatively lower increase in ICP than do nitrates. Angiotensin-converting enzyme
inhibitors have a relatively slow onset and are not first-line agents in the setting of acute
SAH.
Patients with signs of increased ICP or herniation should be intubated and
hyperventilated. Minute ventilation should be titrated to achieve a PCO2 of 30-35 mm
Hg. Avoid excessive hyperventilation, which may potentiate vasospasm and ischemia.
Other interventions for increased ICP include the following:
 Osmotic agents (eg, mannitol), which can decrease ICP dramatically (50% 30
minutes post administration)
 Loop diuretics (eg, furosemide) also can decrease ICP
 The use of intravenous steroids (eg, dexamethasone [Decadron]) for decreasing
ICP is controversial but is recommended by some authors
Patients must be admitted to the intensive care unit (ICU) with strict bed rest until the
etiology of hemorrhage is determined. Patients should not be allowed out of bed for any
reason. All patients should receive frequent neurologic evaluation. Use sedatives and
analgesics cautiously to avoid masking the neurologic examination findings.
Additional medical management is directed to prevent and treat the following common
complications of SAH:
 Rebleeding
 Vasospasm
 Hydrocephalus
 Hyponatremia
 Seizures
 Pulmonary complications
 Cardiac complications
 Ideally, management of the complications of SAH should take place in a
neurologic ICU or in an ICU similarly equipped. To minimize stimuli that may lead
to an elevation of ICP, have the patient placed in a darkened, quiet, private room
and given mild sedation if agitated. The head of the bed should be kept elevated
at 30° to ensure optimal venous drainage.
 Blood pressure must be maintained with consideration of the patient's neurologic
status. Optimally, systolic blood pressure (SBP) of no more than 130-140 mm Hg
should be the goal, unless clinical evidence of vasospasm is noted.
 Indwelling catheters include an arterial line, central venous access, and Foley
catheter. Seizure prophylaxis and calcium channel blockade are standard
medical measures. Some centers favor volume expansion to treat vasospasm
that develops days after the initial bleeding episode.
 Surgical treatment to prevent rebleeding consists of clipping the ruptured berry
aneurysm. Endovascular treatment [1] (ie, coiling) is an increasingly practiced
alternative to surgical clipping. The neurosurgeon/neurointerventionalist must be
involved early in the care of the patient with an aneurysmal SAH.


Initial Management
The initial management of patients with SAH is directed at patient stabilization. Assess
the level of consciousness and airway, breathing, and circulation (ABCs).
Endotracheal intubation should be performed for patients presenting with coma,
depressed level of consciousness, inability to protect their airway, or increased
intracranial pressure (ICP). Rapid-sequence intubation should be employed, if possible,
including the use of sedation, defasciculation, short-acting neuromuscular blockade,
and agents to blunt an increase in ICP.
Intravenous access should be obtained, including central and arterial lines. A short-
acting benzodiazepine, such as midazolam, should be administered prior to all
procedures. Monitoring should include the following:
 Cardiac monitoring
 Pulse oximetry
  Automated and/or arterial blood pressure monitoring (arterial BP monitoring is
indicated in high-grade SAH or when blood pressure is labile)
 End-tidal carbon dioxide, if applicable
 Urine output via placement of a Foley catheter
Medication Summary
The goals of treatment in patients with subarachnoid hemorrhage (SAH) are as follows:
 Blood pressure control
 Prevention of seizures
 Treatment of nausea
 Management of intracranial pressure
 Prevention of vasospasm
 Control of pain
 Maintenance of cerebral perfusion
Medications used for these purposes include analgesics, calcium channel blockers,
antiepileptic drugs, stool softeners, antihypertensive agents, antiemetics, osmotic
agents, diuretics, and general anesthetics. The use of aminocaproic acid for hemostasis
is controversial.