Most often due to arteriovenous malformation in children
Although rare in children, SAH is a leading cause of pediatric stroke.
ETIOLOGY
“Congenital,” saccular, or berry aneurysm rupture (80–90%):
Occur at bifurcations of major arteries
Incidence increases with age.
Aneurysms may be multiple in 20–30%.
Nonaneurysmal perimesencephalic hemorrhage (10%)
Remaining 5% of causes include:
Mycotic (septic) aneurysm due to syphilis or endocarditis
Arteriovenous malformations
Vertebral or carotid artery dissection
Intracranial neoplasm
Pituitary apoplexy
Severe closed head injury
DIAGNOSIS SIGNS AND SYMPTOMS History
Classically a severe, sudden headache:
Often described as “thunderclap” or “worst headache of life”
Headache is often occipital or nuchal, but may be unilateral.
Usually develops within seconds and peaks within minutes
Distinct from prior headaches
Headache often maximal at onset
Sentinel headaches and minor bleeding occur in 20–50%:
May occur days to weeks prior to presentation and diagnosis
Seizures, transient loss of consciousness, or altered level of consciousness occur in more than 50% of patients.
Vomiting occurs in 70%.
Syncope, diplopia, and seizure are particularly high-risk features for SAH.
Physical-Exam
Focal neurologic deficits occur at the same time as the headache in 33% of patients:
3rd cranial nerve (CN III) palsy (the “down and out” eye) occurs in 10–15%.
Isolated CN VI palsy or papillary dilation may also occur.
Nuchal rigidity develops in 25–70%.
Retinal hemorrhage may be the only clue in comatose patient.
ESSENTIAL WORKUP
Complete neurologic exam and fundoscopic exam
Emergent noncontrast head CT scan:
Diagnoses 93–98% of SAH if performed within 12 hr
Thin cuts (3 mm) through base of brain improve diagnostic yield.
CT is less sensitive after 24 hr or if hemoglobin <10 g/L.
Lumbar puncture (LP) and CSF analysis must be performed if CT negative and history suggests possibility of SAH.
Pregnancy Considerations
Incidence slightly increased in pregnancy
Workup should include CT and LP
DIAGNOSIS TESTS & NTERPRETATION Lab
Baseline CBC and differential
Electrolytes, renal function tests
Coagulation studies
Cardiac markers:
Troponin I elevated in 10–40%
CSF analysis (see below)
Imaging
Chest radiograph for pulmonary edema:
Occurs in up to 40% with severe neurologic deficit
Traditional gold standard: 4-vessel digital subtraction cerebral angiography
Spiral CT angiography:
Useful for operative planning
Quite sensitive for detection of aneurysms >4 mm, less with smaller aneurysms
MR angiography:
MRI is less sensitive for hemorrhage
Quite sensitive for detection of aneurysms >4 mm, less with smaller aneurysms
Transcranial Doppler ultrasound:
May be useful in detecting vasospasm.
Diagnostic Procedures/Surgery
LP:
Presence of erythrocytes in CSF indicates SAH or traumatic tap:
If traumatic tap suspected, LP should be performed 1 interspace higher.
Diminishing erythrocyte count in successive tubes suggests but does not firmly establish a traumatic tap.
Xanthochromia is diagnostic of SAH if performed 12 hr after onset.
An elevated opening pressure may indicate SAH, cerebral venous sinus thrombosis, or pseudotumor cerebri.
ECG:
ST-segment elevation or depression
QT prolongation
T-wave abnormalities
Often mimics ischemia or infarction
Symptomatic bradycardia, ventricular tachycardia, and ventricular fibrillation
DIFFERENTIAL DIAGNOSIS
Neoplasm
Arterial dissection
Aneurysm (unruptured)
Arteriovenous malformation
Migraine
Pseudotumor cerebri
Meningitis
Encephalitis
Hypertensive encephalopathy
Hyperglycemia or hypoglycemia
Temporal arteritis
Acute glaucoma
Subdural hematoma
Epidural hematoma
Intracerebral hemorrhage
Thromboembolic stroke
Sinusitis
Seizure disorder
Cerebral venous sinus thrombosis
Cavernous sinus thrombosis
TREATMENT PRE HOSPITAL
Initial assessment and history:
Level of consciousness
Glasgow Coma Scale score
Gross motor deficits
Other focal deficits
Patients with SAH may need emergent intubation for rapidly deteriorating level of consciousness.
IV access should be established.
Provide supplemental oxygen.
Monitor cardiac rhythm.
Patients should be transported to a hospital with emergent CT and ICU capability.
INITIAL STABILIZATION/THERAPY
Manage airway, resuscitate as indicated:
Rapid-sequence intubation
Pretreat with lidocaine and defasciculating dose of nondepolarizing paralytic to blunt increase in intracranial pressure (ICP) during intubation.
Cardiac monitoring and pulse oximetry
Establish adequate IV access
Obtain urgent neurosurgical consultation
ED TREATMENT/PROCEDURES
Prevent rebleeding:
Risk of rebleeding highest in the 1st few hours after aneurysmal rupture
Manage ICP:
Elevate head of bed to 30°.
Prevent increases in ICP from vomiting and defecation with antiemetics and stool softeners.
Treat increased ICP with controlled ventilation and mannitol.
Maintain central venous pressure >8 mm Hg and urine output >50 mL/hr
BP control:
Balance HTN-induced rebleeding vs. cerebral hypoperfusion
Goal mean arterial pressure 100–120 mm Hg, systolic BP <160:
Labetalol, hydralazine, nitroprusside, or nicardipine for hypertension
Correct hypovolemia:
Should start within 96 hr of SAH
Treat hypotension with volume expansion.
Cerebral vasospasm:
May cause secondary ischemia and infarction after SAH:
Oral nimodipine improves functional outcome:
Discuss with neurosurgeon prior to administration
Monitor with transcranial Doppler.
Adequately treat pain.
Seizures:
Manage with IV benzodiazepine
Consider prophylactic anticonvulsants in immediate posthemorrhagic period
Correct temperature, electrolyte, glucose, or pH abnormalities.
Treat coagulopathy, thrombocytopenia, and severe anemia.
Monitor for and correct pulmonary edema and cardiac arrhythmias.
Antifibrinolytic therapies:
Discuss with neurosurgeon prior to initiation
Consider administration immediately after aneurysmal rupture in patients at high risk of rebleeding when this is combined with treatment of aneurysm and monitoring for hypotension.
When patient is stable, expedited transfer to hospital with neurosurgical capabilities is mandatory.