Lecture 5 Subarachnoid Haemorrhage
Lecture 5 Subarachnoid Haemorrhage
Lecture 5 Subarachnoid Haemorrhage
Epidemiology NB
SAH 3% strokes + 5% stroke deaths- incidence: 10,5/ 100000 people/year
Pt. age at presentation= lower compared with other types of stroke
Frequency of aneurysm at most mortem: 5%
SAH= presents more often in women (x1.6) in Blacks (x2,1) Japanese+ Finnish (x5)
Risk factors for SAH: NB
o Having a 1st degree relative with SAH (x3-7) o Oral contraceptives
o Polycystic Kidney Disease (2 of SAH pt.’s) o Substance abuse: Cigarette smoking,
o Ehlers-Danlos Syndrome (type IV Cocaine abuse, Binge drinking
o Neurofibromatosis type 1 o Pregnancy + parturition
o Marfan syndrome o Sight increased risk with advancing age
o Hypertension
Outcome of Aneurysmal SAH
The weighted average case fatality is 51%, with 30-day mortality ~ 45% with ⅓ of
survivors which remain dependant
To break down the numbers:
o 10 15% die before reaching medical care
o Mortality is 10% within first few days
Causes of mortality
o 25% die as a result of medical complications
o 8% die from progressive deterioration from the initial haemorrhage
⅓ of survivors have moderate to severe disability
⅔ of survivors never return to the same quality of life as before the SAH
Clinical picture: NB
Clinical hallmark = sudden onset (instantaneous in 50%, seconds to minutes in 50%),
severe (“worst of my life”) headache, usually during exertion, in any area of head or
generalized. Headache can develop in: non strenuous activs./ during sleep + can persist
or resolve spontaneously or with painkillers.
½ pts have period of unresponsiveness and a third have focal signs either at onset or later
in course.
Other symptoms include vomiting (70%) and previous episodes of headache (20%)
Seizures occur in 6 16% and acute confusion in 2%, most patients also complain of
photophobia.
Signs are inconsistent and include subhyaloid haemorrhages (17%, due to obstruction of
ocular venous outflow secondary to ↑ICP) and neck stiffness (may take 3- 12 hours to
develop)
Misdiagnosis of SAH
SAH pt.’s can be misdiagnosed (±) - especially in good clinical grade
Specific misdiagnoses include: NB
o Headache of unknown origin o Ischemic stroke
o Migraine, cluster or tension headache o Hypertensive crisis
o Meningoencephalitis o Syncope
o Influenza o Arrhythmia
o Gastro enteritis o Malingering
o Viral syndrome o Alcohol intoxication
Result of misdiagnosis= pt.’s with good clinical grade= missed most likely to benefit
from tx/ develop early complications poor outcome if missed
Common factors complicating diagnosis:
o Many SAH patients may have a fall (interpreted as head injury)
o They have raised blood pressure (interpreted as hypertensive crisis)
o They have arrhythmias (up to 91%, interpreted as cardiac in origin)
Common factors leading to misdiagnosis include:
o Failure to recognize the spectrum of clinical presentations
o Limitations of CT
o Failing to perform and interpret an LP correctly
Imaging:
CT - A CT scan obtained with thin cuts (<3mm), performed parallel to the hard palate, without
contrast, performed <12hr and interpreted by neurosurgeon or neuroradiologist , has a
sensitivity of >98%
- The sensitivity declines to 95% between 12 and 24 hours and <50% by the end of the first
week.
- Reasons for decreased CT sensitivity include
Old generation scanners
Movement artifacts from restless patients
Delayed scanning (>24hrs)
CTA - Using a spinal CT and IV contrast, has sensitivity almost equal to DSA (digital
subtraction angiography). In some neurosurgical centers, surgeons operate solely based
on information obtained from this imaging modality.
- CTA is non invasive, fast and can detect 90 95% of aneurysms >2mm.
- DSA can be negative in 15 20% of aneurysmal SAH patients.
MRI - Conventional T₁W and T₂W imaging relatively insensitive to SAH. Gradient echo T₂ is
the most sensitive sequence (94% in the acute phase and ~100% in the sub acute phase)
- FLAIR MRI shows CSF hyperintense to brain and has similar sensitivity to CT at <24hr,
but increased sensitivity compared to CT in late imaging (>24hr)
MRA - Has slightly less sensitivity than CTA, requires longer time to perform, is not suitable for
agitated patients and does not demonstrate the relation of the aneurysm to the bony
anatomy, which is useful when surgery is contemplated.
DSA (Digital - Still considered the “gold standard”
Subtraction - DSA
Angiography Delineates the aneurysm neck
Identifies perforating arteries arising from the aneurysm dome
Detects multiple aneurysms
Can assess the presence of collateral circulation
Treatment:
Three factors that can predict the outcome in SAH patients:
o Neurological condition on admission= strongest prognostic factors
o Age of pt.
o Amount of blood on CT
Basic principles:
o Patients are admitted to monitored beds or to ICU according to SAH grade
o Patients should be on bed rest, maintained euvolemia and receive adequate
analgesics
o Although the administration of prophylactic phenytoin is controversial, our
department recommends it.
o Surgical and endovascular treatment are aimed at obliterating the aneurysm or
excluding it from the circulation as well as preventing and treating the potentially
severe complications
Re-bleeding
Re bleeding is the most important preventable cause of death in hospitalized patients with
SAH. 80% of patients who re bleed eventually die or remain dependant for life.
The risk is greatest within 24hr (4%) and then reduces to 1,5% per day, but accumulates
to 50% during the first month.
The overall incidence of re bleeding in SAH patients is ~15%, contributing 22% to the
mortality from SAH.
Clinical signs of a new bleed are acute neurological deterioration or sudden increase in
ICP, sudden increase in blood pressure or fresh blood coming through ventricular drains.
Risk factors for re bleeding include:
o Female gender (2x more than males)
o Older patients
o Hypertension
Vasospasms
Vasospasm is responsible for stroke and death in 15% of SAH patients. It increases by 1,5
3 x in the first 2 weeks after SAH
Types of Vasospasm:
o Angiographic vasospasm is very common (30 70% when DSA is done at day 7),
but does not always produce symptoms.
o Clinical vasospasm is less common (20 30 %) and is characterized by decrease
GCS, hemiparesis/hemiplegia or slurred speech. PET scanning in clinical
vasospasm has shown CBF<20ml/100g/min (CBF<12ml/100g/min is associated
with irreversible neurological deficits).
Vasospasm appears on day 3 4, peaks at day 7 10 and resolves between weeks 2 4.
Definitive Treatment:
Goal: to remove the aneurysm from circulation in order to treat/ ameliorate the possible
complications of SAH
Done via:
o Endovascular route
o Surgical clipping
A. Endovascular techniques to treat aneurysms:
i. Thrombosing the aneurysm
o Coiling
o Onyx gluing
ii. Trapping
iii. Proximal ligation (Hunterion ligation) – useful for giant aneurysms