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Definition
The presence of blood within the subarachnoid space.
Can occur spontaneously or after head injury. The most common sites are: Anterior
communicating artery (30%)
Posterior communicating (25%),
Middle cerebral artery (20%)
Rarer sites include internal carotid,, tip of basilar artery,, pericallosal and posterior
inferior cerebellar artery, and peri-mesencephalic.
Risk Factors:
Acquired: Smoking, alcohol, hypertension,.
Inherited: Platelet glycoprotein polymorphism, Elastin deficiency (chromosome 7q
deficiency), chromosomal deletions 1p, 2p, 11q, 14q, 22xp.
Epidemiology
Major cause is due to rupture of saccular aneurysms
Other causes are, traumatic, AVM, dissections, vasculitides, amyloid angiopathy,
illicit drugs.
According to several series, 5% of general population has saccular aneurysms at
autopsy, 30% are multiple.
Presentation
30 to 50% of presentations have a warning leak preceding 6 to 20 days of bleed
Presents as the worse headache of my life
30% of the times as a headache ipsilateral to the bleed.
Rapid release of blood with arterial pressure into ventricles may raise ICP
Meningeal symptoms if presence of blood within CSF.
Classification
There are four different classifications for subarachnoid haemorhage: Hunt-Hess
(clinical but subjective); Claassen (radiological but complex); World Federation
Neurosurgery (WFNS) and Fisher scale; among these classifications, only Fisher
and WFNS are currently in use.
The Fisher scale is a radiological classification and has been correlated to the risk of
developing cerebral vasospasm Of those patients presenting with a Fisher 3 or
higher 70 % will develop radiological vasospasm, and 30% will develop clinical
vasospasm (1)
Fisher Group
1
2
3
4
Blood on CT Scan
No subarachnoid blood seen
Localised and unilateral with clot
thickness of <1mm
Bilateral clot with clot thickness of
> 1mm
Fisher
2
or
3
with
intraparenchimal
or
intraventricular blood.
WFNS
Grade 1
2
3
4
5
Clinical presentation
GCS 15 with NO motor deficit
GCS 13-14 with no motor deficit
GCS 13-14 WITH motor deficit
GCS 7-12 with or without motor deficit
GCS < 7 with or without motor deficit.
COMPLICATIONS
(a) Neurological
Early
Rebleed. Highest risk in the first 24h. Peak incidence first 6 hours.
Risk related to the amount of blood and the poor clinical presentation.
Increased ICP (secondary to hydrocephalus, cerebral swelling,
re-bleed)
Hydrocephalus (secondary to blood in CSF)
Seizures (seizures are an independent risk factor for late seizures and
a predictor of poor outcome)
Hypothalamic ischemia
Delayed
Vasospasm (symptomatic vasospasm has a 30% incidence. It is the leading
cause of disability and mortality. Presents from the 4th day to the 15th day
with a peak presentation between D7-D10). Risk factors for vasospasm
include the amount of blood on presentation (Fisher grade 3) + age < 50 years
+ hyperglycaemia.
Compatible history
Compatible examination
Investigations:
- CT head non-contrast: Diagnostic sensitivities decrease with time after onset,
being at the first 12h: 95-98%; between first 12-24h: 92-95%; within first 48h: 8086%; within first 5 days: 60-75%; after first 7 days: 40-50% (2,3)
- Lumbar Puncture: Indicated in all patients with compatible symptomatology and
history with a normal CT scan; however this should NOT be performed within 9h
of the possible bleed. This interval is necessary as it allows time for bilirubin to be
formed from metabolised hemoglobin. If performed earlier it will be impossible to
distinguish true subarachnoid blood from a traumatic tap.
TREATMENT
RESUCITATION
poor outcome of 23%. A phase III trial aiming to recruit 1200 patients over 5
years is currently in progress.
Statins: 2 meta-analysis (JAMA 2005 and Stroke 2008) showed contradictory
results. Currently recruiting STASH trial (phase III with simvastatin) aims to
finalise end 2011 and a posterior Cochrane analysis may result in a definitive
answer (6, 7,8).
Endothelin antagonists: Clazosenthan. Preliminary results from a phase II study
(9) supported the design of a current phase III study, Conscious 2 Trial -clipped
patients (10) and Conscious 3 Trial -coiled patients (11) studies are in progress.
The aim of these phase II trials is study is to demonstrate if the use of continuous
infusion of Endothelin 1A receptor antagonists, reduce the incidence and severity
of cerebral vasospasm.
KEY POINTS
1) Subarachnoid haemorrhage is a leading cause of mortality and neurological
disability, requiring early definitive management.
2) Neurological observation and daily Transcranial Doppler have shown to
achieve early detection of cerebral vasospasm, facilitating early rescue
management.
3) Preventive treatment with Statins, Clazosenthan and Magnesium are
currently subjected to multicenter RCT, results of which may offer new
evidence based therapeutic options.
QUESTIONS
Q1---A Fisher 3 SAH implies hat:
a) Blood is present unilaterally with a clot of > 1mm thickness
b) Blood is present bilaterally
c) The clot size is > 1mm thickness
d) B and c are correct
e) None of the above is correct
Q2---Among the several classifications of SAH
a) The Hunt Hess classification is currently useful and has prognostic
value
b) Hunt Hess classification is useful but Claarsen classification is obsolete
c) The WFNS has radiological prognostication value
d)
e)
Answers:
1-d
2-e
3-b
4-e
5-e
References
(1)- Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl
J Med 2006; 354(4):387-396.
Study Id : AC-054-301
(11)- ClinicalTrials.gov
identifier: NCT00940095