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Subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space surrounding


the brain, i.e., the area between the arachnoid membrane and the pia mater. It may arise
due to trauma or spontaneously, and can lead to death or severe disability even if
recognized and treated in an early stage. Treatment is with close observation, medication
and early neurosurgical intervention. Subarachnoid hemorrhage causes 5% of all strokes.
10-15% die before arriving in hospital, and average survival is 50%.1

Signs and symptoms


The classic symptom of subarachnoid hemorrhage is thunderclap headache ("most severe
ever" headache developing over seconds to minutes). 10% of all people with this
symptom turn out to have a subarachnoid hemorrhage, and is the only symptom in about
a third of all SAH patients. Other presenting features may be vomiting (non-specific),
seizures (1 in 14) and meningism. Confusion, decreased level of consciousness or coma
may be present. Intraocular hemorrhage (bleeding into the eyeball) may occur.
Subhyaloid hemorrhages may be visible on fundoscopy (the hyaloid membrane envelopes
the vitreous body).1

In a patient with thunderclap headache, none of the signs mentioned are helpful in
confirming or ruling out hemorrhage, although a seizure makes bleeding from an
aneurysm more likely. Oculomotor nerve abnormalities (affected eye looking downward
and outward, pupil widened and less responsive to light) may indicate a bleed at the
posterior communicating artery.

As a result of the bleeding, blood pressure often rises rapidly, together with a release of
adrenaline and similar hormones. As a result, substantial strain is put on the heart, and
neurogenic pulmonary edema, cardiac arrhythmias, electrocardiographic changes and
cardiac arrest (3%) may occur rapidly after the onset of hemorrhage.1

Bleeding into the subarachnoid space may occur as a result of injury or trauma. SAH in a
trauma patient is often detected when a patient who has been involved in an accident
becomes less responsive or develops hemiplegia or changed pupillary reflexes, and
Glasgow Coma Score calculations deteriorate.

Diagnosis
While the initial steps are obtaining a medical history and performing a physical
examination, the diagnosis of subarachnoid hemorrhage cannot be made on clinical
grounds alone. Medical imaging is usually required to confirm or exclude bleeding. The
modality of choice is CT scan of the brain. This has a high sensitivity (it will correctly
identify >95% of the cases), especially on the first day after the onset of bleeding. Some
data suggests that magnetic resonance imaging (MRI) may be more sensitive after several
days. In those where the CT/MRI scan is normal, lumbar puncture will identify another
3% of the cases by demonstrating xanthochromia (yellow appearance of centrifugated
fluid) or bilirubin in the CSF.1

Once a subarachnoid hemorrhage is confirmed, the next question is about its origin. CT
angiography to identify aneurysms is generally the first step, as invasive angiography
(injecting radiocontrast through a catheter advanced to the brain arteries) has a small rate
of complications but is useful if there are plans to obliterate the source of bleeding, such
as an aneurysm, at the same time.1

Causes
Spontaneous SAH is most often due to rupture of cerebral aneurysms (85%), weaknesses
in the wall of the arteries of the brain that enlarge. While most cases of SAH are due to
bleeding from small aneurysms, larger aneurysms are more likely to rupture. A further
10% of cases is due to [non-aneurysmal perimesencephalic hemorrhage], in which the
blood is limited to the area of the midbrain. Aneurysms are not generally found. The
remaining 5% are due to vasculitic damage to arteries, other disorders affecting the
vessels, disorders of the spinal cord blood vessels, and bleeding into various tumors.1

Classification
There are several grading scales available for subarachnoid hemorrhage. These have been
derived by retrospectively matching characteristics of patients with their outcomes. In
addition to the ubiquitously used Glasgow Coma Scale, three other specialized scores are
in use.2

Hunt and Hess scale

The first scale of severity, described by Hunt and Hess in 19683

• Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity.


Approximate survival rate 70%.
• Grade 2: Moderate to severe headache; nuchal rigidity; no neurologic deficit
except cranial nerve palsy. 60%.
• Grade 3: Drowsy; minimal neurologic deficit. 50%.
• Grade 4: Stuporous; moderate to severe hemiparesis; possibly early decerebrate
rigidity and vegetative disturbances. 20%.
• Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.

Fisher grade

The Fischer Grade classifies the appearance of subarachnoid hemorrhage on CT scan:4

• Grade 1= No hemorrhage evident


• Grade 2= Subarachnoid hemorrhage less than 1 mm thick
• Grade 3= Subarachnoid hemorrhage more than 1 mm thick
• Grade 4= Subarachnoid hemorrhage of any thickness with intra-ventricular
hemorrhage (IVH) or parenchymal extension

World Federation of Neurosurgens

The World Federation of Neurosurgeons classification5

• Class 1 - GCS (Glasgow Coma Scale)15


• Class 2 - GCS 13-14 without focal neurological deficit
• Class 3 - GCS 13-14 with focal neurological deficit
• Class 4 - GCS 7-12 with or without focal neurological deficit
• Class 5 - GCS <7 with or without focal neurological deficit

Treatment
General measures

The first priority is stabilization of the patient. In those with a depressed level of
consciousness, intubation and mechanical ventilation] may be required. Blood pressure,
pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the
diagnosis is confirmed, admission to an intensive care unit (ICU) may be considered
preferable, especially given that 15% have a further episode (rebleeding) in the first hours
after admission. Nutrition is an early priority, with oral or nasogastric tube feeding being
preferable over parenteral routes. Analgesia is generally restricted to non-sedating agents,
as sedation would interfere with the monitoring of the level of consciousness. There is
emphasis on the prevention of complications; for instance, deep vein thrombosis is
prevented with compression stockings and/or intermittent pneumatic compression.1

Prevention of rebleeding

Those patients with a large hematoma, depressed level of consciousness or focal


neurology may be candidates for urgent surgical removal of the blood or occlusion of the
bleeding site. The remainder are admitted and stabilized more extensively, and undergo
an transfemoral angiogram or CT angiogram at a later stage. In those where the bleeding
is from an aneurysm (as opposed to non-aneurysmal perimesencephalic hemorrhage),
most neurosurgical centers use either coiling or clipping of the aneurysm to prevent
rebleeding. After the first 24 hours, rebleeding risk is about 40% over four weeks,
suggesting that interventions should be aimed at reducing this risk.1

Two measures are employed at repairing aneurysms. Generally, the first-line approach is
endovascular coiling. This mode relies on angiography of the cerebral arteries and
inserting platinum coils into the aneurysm to cause them to regress. Alternatively,
craniotomy and surgical clipping of the aneurysm may be performed. Recent trials
suggest a general advantage of coiling over clipping.1
Medical treatment is available to both reduce the risk of repeat bleeding, and to treat a
serious complication of SAH called vasospasm. In the case of spontaneous SAH from an
aneurysm, there is a significant risk of repeat bleeding until definitive surgical
intervention can be performed. During this waiting period medical treatments to control
blood pressure, bed rest, and a quiet environment reduce the risk of rebleed.

Vasospasm is a serious complication of SAH. It may be seen in 50% of SAH patients


studied with angiography, and is symptomatic roughly 30% of the time. This condition
can be verified by transcranial doppler or cerebral angiography, and can cause ischemic
brain injury which can cause permanent brain damage, and if severe can be fatal.
Nimodipine is an oral calcium channel blocker, that has been shown to reduce the chance
of a bad outcome, even if it does not significantly reduce the amount of angiographic
vasospasm.6

A patient who recovers without immediate intervention may receive follow-up


angiography to identify aneurysms which may be amenable to coiling to prevent
recurrent episodes of SAH.

Complications
Complications of SAH can be acute, subacute, or chronic.

• Acute:
o Coma and brainstem herniation due to increased intracranial pressure
(ICP)
o Pulmonary edema ("neurogenic pulmonary edema") as a result of the
suddenly increased ICP
o Cardiac arrhythmias and myocardial damage
o Hydrocephalus, which may also happen in the subacute time frame
• Subacute:
o Vasospasm, leading to ischemia of the brain (can be prevented partially
with the calcium channel antagonist, nimodipine)
o Hyponatremia (low sodium levels) - due to SIADH or cerebral salt
wasting syndrome
• Chronic:
o Long-term immobility
o Pneumonia and pulmonary embolism (due to immobility)
o SAH recurrence (20% within two weeks if the aneurysm is not secured by
clipping or coiling)
o Persistent neurologic deficits

Prognosis
After the SAH is treated the patients can experience prolonged, even permanently
reoccurring headaches.
Nearly half the cases of SAH are either dead or moribund before they reach a hospital. Of
the remainder, a further 10-20% die in the early weeks in hospital from rebleeding. Delay
in diagnosis of minor SAH without coma (or mistaking the sudden headache for
migraine) contributes to this mortality.

Patients who remain comatose or with persistent severe deficits have a poor prognosis.

Reference: http://wiki.cns.org/wiki/index.php/Subarachnoid_hemorrhage

Subarachnoid hemorrhage
URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/000701.htm

Subarachnoid hemorrhage is bleeding in the area between the brain and the thin tissues
that cover the brain. This area is called the subarachnoid space.

Causes
Subarachnoid hemorrhage can be caused by:

• Bleeding from an arteriovenous malformation (AVM)


• Bleeding disorder
• Bleeding from a cerebral aneurysm
• Head injury
• Unknown cause (idiopathic)
• Use of blood thinners

Injury-related subarachnoid hemorrhage is often seen in the elderly who have fallen and
hit their head. Among the young, the most common injury leading to subarachnoid
hemorrhage is motor vehicle crashes.

Subarachnoid hemorrhage due to rupture of a cerebral aneurysm occurs in approximately


10-15 out of 10,000 people. Subarachnoid hemorrhage due to rupture of a cerebral
aneurysm is most common in persons age 20 to 60. It is slightly more common in women
than men.

Risks include:

• Aneurysms in other blood vessels


• Fibromuscular dysplasia (FMD) and other connective tissue disorders associated
with aneurysm or weakened blood vessels
• High blood pressure
• History of polycystic kidney disease
• Smoking
A strong family history of aneurysms may also increase your risk.

Symptoms
The main symptom is a severe headache that starts suddenly and is often worse near the
back of the head. Patients often describe it as the "worst headache ever" and unlike any
other type of headache pain. The headache may start after a popping or snapping feeling
in the head.

Other symptoms:

• Sudden or decreased consciousness and alertness


• Difficulty or loss of movement or feeling
• Mood and personality changes, including confusion and irritability
• Muscle aches (especially neck pain and shoulder pain)
• Nausea and vomiting
• Photophobia (light bothers or hurts the eyes)
• Seizure
• Stiff neck
• Vision problems, including double vision, blind spots, or temporary vision loss in
one eye

Additional symptoms that may be associated with this disease:

• Eyelid drooping
• Eyes, pupils different size
• Sudden stiffening of back and neck, with arching of the back (Opisthotonos; not
very common)
• Seizures

Exams and Tests


A physical exam may show a stiff neck due to irritation by blood of the meninges, the
tissues that cover the brain. Except those in a deep coma, persons with a subarachnoid
hemorrhage may resist neck movement.

A neurological exam may show signs of decreased nerve and brain function (focal
neurologic deficit).

An eye exam will be performed. Decreased eye movements can be a sign of damage to
the cranial nerves. In milder cases, no problems may be seen on an eye exam.

If your doctor thinks you may have a subarachnoid hemorrhage, a head CT scan (without
dye contrast) should be immediately done. In some cases, the scan may be normal,
especially if there has only been a small bleed. If the CT scan is normal, a lumbar
puncture (spinal tap) must be performed. Patients with SAH will have blood in their
spinal fluid.

CT scan angiography (using contrast dye) may be done to look for evidence of and
aneurism.

Cerebral angiography of blood vessels of the brain is better than CT angiography to show
small aneurysms or other vascular problems. This test can pinpoint the exact location of
the bleed and can tell if there are blood vessel spasms.

Transcranial doppler ultrasound is used to look at blood flow in the arteries of the brain
that run inside the skull. The ultrasound beam is directed through the skull. It can also
detect blood vessel spasms and may be used to guide treatment.

Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) are
occasionally used to diagnose a subarachnoid hemorrhage or find other associated
conditions.

Treatment
The goals of treatment are to save your life, repair the cause of bleeding, relieve
symptoms, and prevent complications such as permanent brain damage (stroke).

If the hemorrhage is due to an injury, surgery is done only to remove large collections of
blood or to relieve pressure on the brain.

If the hemorrhage is due to the rupture of an aneurysm, surgery is needed to repair the
aneurym. If the patient is critically ill, surgery may have to wait until the person is more
stable. Surgery may involve a craniotomy (cutting a hole in the skull) and aneurysm
clipping, which closes the aneurysm, or endovascular coiling, a procedure in which coils
are placed within the aneurysm to reduce the risk of further bleeding.

If no aneurysm is found, the person should be closely watched by a health care team and
may need repeated imaging tests.

Treatment for coma or decreased alertness status may be needed. This may include
special positioning, life support, and methods to protect the airway. A draining tube may
be placed into the brain to relieve pressure.

If the person is conscious, strict bed rest may be advised. The person will be told to avoid
activites that can increase pressure inside the head. Such activities include bending over,
straining, and suddenly changing position. The doctor may prescribe stool softeners or
laxatives to prevent straining during bowel movements.
Blood pressure will be strictly controlled. This requires medicines given through an IV
line. The medicine often requires frequent adjustments. A medicine called calcium
channel blocker is used to prevent blood vessel spams.

Pain killers and anti-anxiety medications may be used to relieve headache and reduce
intracranial pressure. Phenytoin or other medications may be used to prevent or treat
seizures.

Outlook (Prognosis)
How well a patient with subarachnoid hemorrhage does depends on a number of different
factors, including the location and extent of the bleeding, as well as any complications.
Older age and more severe symptoms from the beginning are associated with a poorer
prognosis.

Complete recovery can occur after treatment, but death may occur in some cases even
with aggressive treatment.

Possible Complications
Repeated bleeding is the most serious complication. If a cerebral aneurysm bleeds for a
second time, the outlook is significantly worsened.

Changes in consciousness and alertness due to a subarachnoid hemorrhage may become


worse and lead to coma or death.

Other complications include:

• Stroke
• Seizures
• Medication side effects
• Complications of surgery

Reference: http://www.nlm.nih.gov/medlineplus/ency/article/000701.htm