Subarachnoid Haemorrhage
When to screen?
Whom to treat?
ASHIS PATHAK
LEAD CONSULTANT for
VASCULAR NEUROSURGERY
HULL ROYAL INFIRMARY
SAH
• 9% of all strokes
• 75% caused by ruptured
aneurysms
• 6% by AVMs
• 6% due to bleeding diathesis
• 13% no cause
Ruptured Intra-Cranial Aneurysms
Classical presentation
• First described in Bible
• Probably first mentioned in scientific literature by
Bonet 1679
• Devastating headache, collapse, abrupt in onset,
incapacitating in severity
• Diffuse, often radiates posteriorly & down to neck
• Accompanied by blunting of consciousness,
vomiting, stiff neck, sometimes subhyaloid hges
• Headache remains for hours, more commonly days
then clears off in few weeks, survival permitting
Pathogenesis of Headache in SAH
• Initial pain
Stretching & tearing of distended vessel and adjacent
arachnoid
Sudden transmission of intra arterial pressure to the
rigid intracranial compartment
• Post-ictal pain
Chemical irritation of pain sensitive meninges by
blood
• Delayed pain
Chemical meningitis
Vasospasm
Hydrocephalus
Infarction
Sentinel bleed
• Less dramatic symptom - unusual sudden
headaches, vomiting, dizziness
• Up to 10% cases
• Indicate small bleeds
CT negative SAH
• CT positivity depends on
Grade of SAH
Time after Hge
Quality of scan
• After few days SA blood becomes isodense
• Minor leak
• Blood localised around the aneurysm
CT negative SAH
• Lumbar Puncture
Contraindications: Abnormal clotting, Raised ICP,
Spinal AVM
• CSF
Pressure normal to raised
RBC 10,000 to 50,0000 ?mm3
WBC increased in proportion to red cells
Glucose N
Proteins high (for 1000 RBC 1.5 Gm /dl proteins)
CT negative SAH
CSF to be kept at 4 0 C & centrifuged immediately
Xanthochromia - Spectrophotometry
appears within Hrs universal after 12 hours
Spectrophotometry – No haemoglobin or bilirubin
after few hours further
investigations not necessary
unless strong history
After 3 weeks - History is most important
angiography decisive
Warning leak / Bleed
Prerupture Manifestations
• III N palsy
7% -12% of aneurysm pts III N palsy prior to rupture
20-30% of isolated IIIN palsy are due to aneurysm
Mean time from onset of palsy to rupture - 29.6 days
• Patient with oculomotor palsy with headaches is an
emergency, ideally needs CT & angiogram
• Other features
Hemiparesis
Dysphasia
Visual loss
Field defect
Seizures
Atypical presentation of aneurysmal SAH
D/D
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Migraine
Systemic infection
Viral illness,
Hypertensive crisis
Cervical spinal disorders / arthritis
Herniated disc
Aseptic meningitis
Brain tumours
Sinusitis
Alcohol intoxication
Migraine
Vs
Aneurysmal SAH
Migraine
Vs
Aneurysmal
SAH
Head Injury & Aneurysmal SAH
Head Injury
&
Aneurysmal
SAH
Non Aneurysmal SAH
• 10% of SAH
• No vascular cause detected on
angiogram
• Course usually benign
• Outcome good in 90% pts
Non –aneurysmal SAH
Non –aneurysmal SAH
Exertional activity & Aneurysmal SAH
• First co-operative study on 2288 ruptured
aneurysms
One third ruptured in sleep
One third ruptured in unspecified circumstances
One third ruptured during exertional activity
e.g. Lifting, emotional strain, defaecation,
coitus, coughing, parturition
Post coital
cephalgia or SAH
SAH Or Post-coital Headaches
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Duration of headache
Vomiting
Disturbance of consciousness
Meningeal signs
Demonstraion of blood in CSF
Absence of prior sexually associated
headaches
Paediatric SAH
Pre -op
Post-op
PRE - OP
Moya Moya disease
POST- OP
Drug Abuse & Stroke
THREE WEEKS LATER
Headaches
with
Incidental Aneurysms
Patient undecided - wants to think
Patient decides for image surveillance
Patient not concerned
Needs
Intervention
Conclusion
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Awareness
History is of paramount importance
Neurological examination gives the clue
Good investigative tools are a must
Whenever in doubt – DO NOT HESITATE
Remember - There are always exceptions
Sensitivity of Cerebral Blood vessels to
pain
• Common, internal & external carotid vessels
are sensitive to pain
• Main trunk of dural arteries & veinous sinuses
are sensitive to pain Myelinated &
unmyelinated nerve fibres project from dural
arteries & veins to trigeminal nerve
• Larger areteies at Circle of Willis and upto
first CM sensitive to pain.
• But substance P has been demonstrated in
distal blood vessels also
Pattern of pain referral
• Pain from ICA is referred to ipsilateral sid
eof head
• Pain from supratentorial structures is
referred to the front of head
• Pain from infratentorial structures id
referred to posterior aspect of head due to
innervation of C2
Headaches of genereal physical exertion
• Primary ICH
• Embolism
• Thrombo-occlusive disease
Reversible cerebral vasoconstriction
syndrome (RCVS)
• Orgasmic headache (OH) is an "explosive"
headache that occurs at orgasm.
Historically, it was considered benign with
no treatment needed. Reversible cerebral
vasoconstriction syndrome (RCVS) refers
to a group of disorders characterized by
recurrent thunderclap headache (TCH) and
multifocal vasoconstriction.
Sudden catastrophic headache during
sexual intercourse
• SAH due to rupture or expansion of
intracranial aneurysm or AVM may need to
be excluded
• Lundberg & Osterman (1974)reviewed 50
patents of SAH – 6 cases 12% SAH occured
during coitus
• All cases residual pain lasted 24 hrs.
• 2 Pts became unconscious & 5 had vomiting
Physiology of sexual activity
• Increase in heart rate
& BP
• Values reach
maximum during
orgasm
• Erratic respiratory
pattern
• Valsalva with
paroxysmal Increased
intrathoracic pressure
due to closed glottis
• Phenomenon similar
to any severe
exertional efforts with
compartmental
pressure changes
Physiology of sexual activity
Benign Coital Cephalgia
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Raised intrathoracic pressure
Transmitted intracranially
Increased tension in dural matrix
Tear in dural matrix leading to leakage of
CSF
Physiology of sexual activity
• As sexual tension is
elevated individual
frowns, scowls,
grimaces and facial
muscles contract
involuntarily in
semispasm
• Jaw is clenched
spastically, neck
muscles contract rigidly
as orgasm is imminent
• There is local and
general vasodialtion
during orgasm
• This mechanism can be
cause of pre-orgasmal
headaches.
• Primary migraine can be
triggered with coitus but
occurs following coitus
but Benign Coital
Cephalgia occurs during
the act of intercourse
Physiology of sexual activity
• Gross vascular & autonomic changes during
orgasm can be causes of vascular headaches.
• During orgasm there is abrupt increase in
parasympathetic outflow.
• Sudden vasodiltion superadded with maximum
cardiac output& extreme elevation of BP
• Unique intracranial context leading to sudden
increase in intracranial blood volume or acute
failure in intracranial autoregulation