Subarachnoid Hemorrhage
and It’s Complications
Diana Greene-Chandos, M.D.
Director of Neuroscience Critical Care
Assistant Professor of Neurosurgery and Neurology
The Ohio State University Wexner Medical Center
Objectives
 Describe the underlying pathology and symptoms of subarachnoid and
hemorrhagic stroke
 Identify risk factors associated with spontaneous intracerebral
hemorrhage.
 Describe the factors associated with hematoma expansion and poor
outcome.
 Understand the role and indications for surgical hematoma evacuation.
 Identify when additional imaging is needed after intracerebral
hemorrhage.
 Define stroke and understand its natural history
 Discuss the risk factors and pathogenesis of vascular disease
The Subarachnoid Space
 The interval between the arachnoid membrane and pia
mater.
More generous in the spine
Or It’s a Great Name for a Band
Bleeding in the Subarachnoid Space
 Trauma (most common etiology)
 Aneurysmal
 Benign perimesencephalic
Traumatic SAH
Traumatic SAH
 Tends to happen more commonly with moderate to
severe head trauma
 Typically associated with other types of brain injury such
as contusions, subdural hematomas and/or diffuse
axonal injury
 Typically associated with additional body or head and
neck trauma.
 Low risk of delayed ischemic deficits but can have
cerebral salt wasting syndrome
Aneurysmal SAH
 5% of population
 Rupturing is more common in women overall and in men
under the age of 40
Overall Aneurysmal SAH
Prognosis
 Among 100 typical patients with a-SAH
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33 will die before receiving medical care
20 will die or remain incapacitated from initial SAH
17 will deteriorate (50% recovering and 50% with severe
neurological deficits)
30 will do well
Cerebral Aneurysms
Most common sites for cerebral
aneurysms
Other tidbits about aneurysms
 Multiple aneurysms present 14-24% of the time
 7-20% of of pts with a ruptured aneurysm have a
first or second degree relative with an aneurysm
 If you are a first degree relative of someone with
a ruptured cerebral aneurysm risk of having an
aneurysm is 4 times higher
 Screening should occur in people with 2 or more
first degree relatives with cerebral aneurysms or
with 1 relative and tobacco abuse history +/uncontrolled hypertension.
Risks for cerebral aneurysm
formation
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Hypertension
Tobacco abuse
Polycystic Kidney Disease
Coarctation of the Aorta
Fibromuscular Dysplasia
Pseudoxanthoma Elasticum
Marfan’s syndrome
Risks for cerebral aneurysm rupture
 Surges in blood pressure
 Strenuous activity
 Size greater than 7mm
The symptoms..
 Sudden severe headache
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Usually occipital
Nuchal pain also present
Vomiting
Decreased alertness
Sentinel Hemorrhage
 31% of patients have a sentinel headache
 50% of patients with a sentinel hemorrhage are
misdiagnosed by physicians.
Focal Neurological Deficits with Cerebral
Aneurysms
 Bitemporal Hemianopsia
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Basilar bifurcation
 Weber’s Syndrome

Giant SCA
 Hemiparesis and Aphasia or Sensory Neglect

Giant MCA Aneurysms
 Third Nerve Palsy (Pupil involved):
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Intracranial ICA
PCOM
SCA
Diagnosis of Aneurysmal SAH
 Head CT is BEST….
 Do not hesitate to do an LP if there is any doubt…collect
Tube #1 and Tube #4 for cell count with differential
 Note: it may take up to 12 hours after onset of HA for
xanthrochromia to develop if just color is being looked at
 Spectrophotometry will quantify the amount of
hemoglobin and bilirubin and is independent of age of
SAH.
CT example of Aneurysmal SAH
The Fisher Grade
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I.....No blood evident on CT
II….Blood less than 1mm at maximal width on CT
III….Blood greater than 1mm maximal width on CT
IV….Any blood width with IVH or parenchymal extension
The Hunt-Hess Grade
 I…..Asymptomatic or Minimal HA and slight
nuchal rigidity
 II….Moderate to Severe HA, nuchal rigidity,
no neurological deficit other than CN
 III….Drowsiness, confusion or mild focal
deficit
 IV….Stupor, moderate to severe hemiparesis
 V….Deep coma with posturing
You’ve confirmed SAH…now what?
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Admit to NCCU…no matter what.
Keep the patient calm, quiet and pain free.
SBP must be kept below 160 systolically
Minimize procedures
Best drugs for bp
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Labetolol 10-20mg iv q 15 min prn
Hydralazine 10 mg iv q 20 min prn
If 3 doses required within 2 hours start Nicardipine
drip at 5mg/hr and titrate to goal bp
Confirmation of an Aneurysm
• CT angiography will help the angiographer know where
to focus (but avoid if there is clear SAH and significant
renal dysfunction in a patient NOT on HD)
• Cerebral Angiography is the gold standard.
• If the aneurysm is able to be coiled intravascularly, it will
be done at the time of the angiogram.
Example of CT with Corresponding
Angiography
The coiling process with microcatheter
What if it cannot be coiled?
The Titanium Clip!
The Pipeline Stent
Back to the NCCU…what’s next?
 Cerebral Edema Phase
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Days 3-5 post SAH
Utilize Hypertonic (3%) Saline to decrease
Why not Mannitol?
The Vasospasm Window
 Days 4-14
 Creates Delayed Ischemic Deficits
 Responsible for worsening outcomes in 1/3 patients
Monitoring Vasospasm
 Clinical Symptoms (HA, confusion, focal deficits)
 Clinical Signs (increasing bp, increasing urinary output,
dropping sodium levels)
 Studies:
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Transcranial Doppler
CT Angiography (95% negative predictive value)
CT Perfusion
Cerebral Angiography
EEG with Compressed Spectral Analysis
Preventing (?) Vasospam
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Nimodipine 60mg p.o. q 4 hrs for 21 days
Euvolemia
Normal Magnesium level (2.0 or greater)
Avoid hypotension
Treat abnormal LDL with statins
Treating Vasospasm (Medical)
• HHH therapy (Hypervolemia, Hypertension, and
Hypoviscosity)
• Goal Intake and Output net for every 24 hours should be
1-500cc positive
• Goal SBP 160-220 (may use neosynephrine once a
clear euvolemia to slightly hypervolemic state is reached
to achieve)
• Goal Hemoglobin is 10
Treating Vasospasm (Surgical)
 Intra-arterial injection of Calcium Channel Blockers (here
we use verapamil) at the site of vasospasm
 Direct Angioplasty (high risk)
What about AEDs?
 Use in all aneurysmal SAH until aneurysm secure.
 If a seizure has occurred, keep AED for 4 weeks
 If a seizure has occurred and an intraparenchymal
hemorrhage was also present, consider longer treatment
than 4 weeks.
 Leviteracetam or Phenytoin
What About Hydrocephalus?
 Common
 EVD should be placed in those with radiographic HCP
and high grade SAH
 Delayed Hydrocephalus (under normal pressure) can
occurred months or even years after SAH due to
scarring
What if there is an SAH and a Negative
Angiogram?
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Re-review history….? Occult trauma
Thrombosis of ruptured aneurysm
Difficult to visualize small aneurysm
Spinal AVM
Cerebral Venous Thrombosis
Vasculitis
Benign Perimesencephalic
Negative-Angiogram SAH Words to
Never Forget…..
Remember: The Onus is on us to
prove that there is no aneurysm. So if
one is not seen on the first angiogram
and there is no other etiology for the
hemorrhage found, repeat the
angiogram in 7 days.
Cardiac Effects
 Catecholamine induced subendocardial myonecrosis
 Temporary or permanent reduction in EF
 Arrythmias (typically tachyarrhythmia unless increased
ICP, then bradyarrhythmias)
 Flash pulmonary edema
Monitoring and Care
 Ideally in a high volume center
 Institutions with a dedicated Neuro-ICU with
Neuroscience Nurses are preferred and shown to
improve outcomes
My reasons to prevent a Stroke
Thank you for completing this module
 Questions?
 Diana.Greene-Chandos@osumc.edu
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