A dilemma..
Zeus: Male of undetermined age who works as King of
the Gods
HOPC: Sudden onset, excruciatingly severe headache
Precipitating factors: Straining on the toilet
PMHx: Longstanding hypertension
SHx: 40 pack year smoking Hx, regular ETOH (3-4 std.
drinks/day)
Q: What are the critical differentials you must consider
in this scenario?
Hint: There are 2..
A: Zeus is pregnant with his daughter Athena in his
head and is getting serious labour contractions
OR…
!!!!!!!!!!!!!!!!!!!!!!
Subarachnoid Haemorrhage
DEFINITION: ?
Q: What is subarachnoid haemorrhage?
Subarachnoid Haemorrhage
A: DEFINITION: Spontaneous bleeding into the
subarachnoid space of meninges. The area between the
arachnoid mater and the pia mater.
Q: This space usually contains what?
A: CSF
Zeus asks you: “So what caused this headache in the
first place?”
Q: What is the most common cause of SAH?
Causes/pathophysiology
A: 80-85% of cases result from rupture of an aneurysm,
which tend to be located in the Circle of Willis.
Risk factors for SAH include:
Familial disposition to SAH – First degree relatives of SAH
patients, are 3-7 times more likely to be afflicted.
Metabolic syndrome: hypertension, atherosclerosis
Lifestyle factors: smoking, alcohol abuse
The remainder of SAH cases are due to non-aneurysmal
disorders of blood vessels, e.g.:
Arteriovenous malformation (AVM) rupture
Angioma rupture
Neoplasmic bleeding (friable new vessels)
Cortical thrombosis
A gallery of aneurysms
Saccular (Berry) Aneurysms
Most common form of cerebral aneurysm
(>90%)
Acquired, predisposing factors of family
hx, connective tissue disorders,
hypertension.
Mycotic (Infective) Aneurysms
Account for <1% of cerebral aneurysms.
Associated with bacterial endocarditis
(left heart or right heart with PFO).
Dissecting (Traumatic) Aneurysms
Fusiform (Atherosclerotic) Aneurysms
Account for <5% of cerebral aneurysms.
Account for <5% of cerebral aneurysms.
Associated with atherosclerosis.
Associated with trauma, usually
external to brain cavity.
Rupture risk
Zeus hurls a lightning bolt at the ground in anger and
exclaims, “But why did this happen to me?!”
Q: What is the best predictor of aneurysmal rupture?
(and of AVMs?)
Rupture risk
A: Small aneurysms good, large bad.
Aneurysms with diameter less than or equal to 5mm
have a 2% risk of rupture.
Of those with diameter 6-10mm, 40% have already
ruptured upon diagnosis.
Small AVMs bad, large good.
AVMs <2.5cm rupture more frequently than AVMs
>5cm.
Q: Why are we talking about it?
A: It has very poor outcomes; death, permanent
morbidity. But also, early recognition and surgical
intervention can ALTER CLINICAL COURSE AND
PROGNOSIS.
Population is generally <60 years old; so we can make a
tangible life-year difference.
History
Zeus finishes his tantrum and then stares at you in
wonder. “But how did you know what was wrong with
me as soon as I walked in the door?”
A: What is the archetypal symptom of SAH?
History
A: Headache: Sudden onset, thunderclap, worst-ever.
At its worst in mere seconds; and can be described in
many different ways.
1) “Like someone smashed me over the head with a
hammer”
2) “Like an explosion in my head”
3) “Like a thunderclap in my head”
4) “Like someone cleaved open my head with an axe”
History
Other symptoms:
Symptoms relating to raised ICP and meningism:
Nausea, vomiting, neck stiffness, photophobia
Abnormal neurology, depending on location of bleed
and local mass effects
Decreased level of consciousness
Seizures
Q: What else could cause a sudden onset severe
headache?
Differential Diagnoses
A: More likely
Intracerebral haemorrhage (haemorrhagic stroke)
Transient Ischaemic Attack (reperfusion pain)
Malignant hypertension
Migraine headache
Less likely
Meningitis
Encephalitis
Seizure (post-ictal phase)
Examination
Haemodynamic instability
Hypertension and labile SBP
Tachycardia (bradycardia if raised ICP)
Raised ICP: Refer to previous presentation.
Meningism: Neck stiffness (Nuchal rigidity), Kernig’s sign,
Brudzinski’s sign.
Focal neurology
Cranial nerve palsies and memory loss in 25%.
Oculomotor nerve palsy most common (PcomA aneurysm).
Clinical grading
WFNS / Hunt & Hess / (Fisher – grading on imaging).
Becoming sceptical Zeus says, “Ok you’ve asked me a
whole lot of questions and made my headache worse by
moving me around, but how can you be sure what’s
going on?”
Q: What is the best first-line investigation for suspected
SAH?
Investigations
A: CT-Brain (non-contrast)
Q: If CTB shows no evidence of SAH, what is the best
2nd line investigation for detecting SAH?
Investigations
A: CT Angiography (CTA) – ( CTB + CTA gives >99%
sensitivity at ruling out SAH)
Traditionally a Lumbar Puncture is done looking for
xanthochromia (as blood can be a traumatic tap). Less
sensitive and can’t find aneurysm location, but advantage of
less radiation and have CSF to Ix other Ddx.
Other Ix include serology to inform Mx. Other imaging
includes DSA (Digital Subtraction Angiography) and MRA
(Magnetic Resonance Angiography)
Q: What are the 2 main risks of doing a lumbar puncture
without first doing a CTB?
A: Risk of coning (foramen magnum brain herniation). Risk
of further bleeding by dropping ICP and relieving the
tamponade on the ruptured aneurysm.
Just then Zeus’ wife Hera storms in and yells at you, “A mere
mortal would have died by now! Hurry up and fix him!”
Q: What should you have done as soon as Zeus stepped into
your hospital, clutching his head and feeling unwell?
Management
A: Initial management – DRSABCD LOVE (Lines O2
Vitals Extra)
Seek senior medical help ASAP if haemodynamically
unstable/concerned (and if you’re thinking SAH, you
should ALWAYS be concerned)
Maintain SBP <130mmHg, beta-blockers preferred as short
half-life, easily titrated.
Once stabilized, Ix can be performed to confirm diagnosis
If unstable, requires emergent neurosurgical treatment
You manage to stabilise Zeus and calm down Hera.
Hera then asks, “Ok, so you’ve stopped him dying, but
you still haven’t fixed him, do something!”
Q: What are the two main options for definitive
management of SAH?
Definitive Management
Surgical Clipping
Metal clip placed
across the neck of the
aneurysm.
Modern clips are MRIsafe.
Coil Embolisation
Endovascularly
delivered coils passed
into aneurysm, fill it
and cause fibrosis.
Balloon or stent used.
Definitive Management
Surgical Clipping
Hunt & Hess/WFNS
Grades 1-3
Large and giant
aneurysm
Wide-necked aneurysms
Vessels emanating from
the aneurysm dome
Mass effect or hematoma
associated with the
aneurysm
Recurrent aneurysm after
coil embolization
Coil Embolisation
Patients with poor clinical grade (i.e.,
Hunt and Hess / WFNS grades 4-5)
Patients who are medically unstable
In situations in which the aneurysm
location imparts an increased surgical
risk, such as cavernous sinus and
many basilar tip aneurysms
Small-neck aneurysms in the posterior
fossa
Patients with early vasospasm
Cases in which the aneurysm lacks a
defined surgical neck (although these
are also difficult to "coil")
Patients with multiple aneurysms in
different arterial territories if the
surgical risk is high
You come to consent Zeus for a definitive procedure
and he exclaims, “Well surely one of them is better,
which one do you think I should have?”
Q: What is the difference in outcomes between surgical
clipping and coil embolisation?
Definitive Management
A: Surgical clipping is more definitive, there is a
reduced risk of re-bleeding and of aneurysmal reformation at the clipped site.
For patients that are suitable for either surgical or
endovascular treatment, endovascular treatment has
better overall morbidity and mortality (ISAT trial).
Zeus has his procedure and is so overjoyed he gifts you
an amphora of ambrosia. Hera is less easily impressed
and asks, “So all those things on the consent form that
you said could happen after the procedure, what were
they again?”
Q: What are the three most important post-procedural
complications specific to SAH?
Complications
A: 1) Rebleed
Greatest risk of re-bleeding within 24 hours post-rupture
(4.1%), cumulative 14-day risk is 19%.
Rebleeding mortality is 70-80%.
Definitive management aims to prevent rebleeding.
Rebleeding risk can be reduced by:
Bed rest
Analgaesia
Sedation
Stool softeners (to prevent Valsalvas while straining)
Complications
2) Vasospasm
10-20% of SAH patients experience this.
Arterial territory unrelated to aneurysm location,
thought to be due to thick subarachnoid clot.
Most commonly occurs at terminal ICA and proximal
ACA and MCA.
Mx:
Traditional Mx is “Triple H”: IV fluids to achieve
Hypertension, Hypervolaemia and Haemodilution.
Evidence for Ca2+ channel blockers, esp. nimodipine.
Statins controversial, STASH trial ongoing.
Complications
3) Hydrocephalus
Caused by thrombotic blockage of CSF pathways (noncommunicating) or by toxic blockage of arachnoid
granulations (communicating).
Mx:
The presence of a CSF blockage can be detected by RISA
cisternography (nuc med scan) or echoencephalography.
Any thrombotic blockage can be evacuated and/or a
ventricular shunt placed on repeat neurosurgical
intervention.
References
1) http://brain.oxfordjournals.org/content/124/2/249.full
2) http://stroke.ahajournals.org/content/34/10/2540.full
3) http://www.patient.co.uk/doctor/subarachnoid-
haemorrhage
4) MedScape
5) OHCM
6) UpToDate