subarachnoid haemorrhage
TRANSCRIPT
SUBARACHNOID HAEMORRHAGE
SAMIR EL ANSARYICU PROFESSOR
AIN SHAMSCAIRO
Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY
SAH• What is it?
– Bleeding into the subarachnoid space (space between the pia & arachnoid meningeal layers) where blood vessels lie
& CSF flows
• Where does the blood come from?– An aneursym on a blood vessel in the subarachnoid space
has ruptured (~70%)– Unknown (~15%)– AVM (~10%)
– Rare causes (e.g. tumour) (~5%)
SAH
• Where does the blood go?–Anywhere where CSF goes, may get hydrocephalus if into ventricle
& causes obstruction of CSF circulation
SAH
• Higher chance if:–Female
–3rd trimester of pregnancy
–Middle-aged
–Abuse of stimulant drugs
–Connective tissue disorder
–Family history
–PCKD
What causes aneurysms to form?
• Defects in the media of the arteries
• Defects are thought to expand as a result of hydrostatic pressure from pulsatile
blood flow and blood turbulence, which is greatest at the arterial bifurcations
What causes aneurysms to rupture?
• The probability of rupture is related to the tension on the aneurysm wall
• The law of La Place states that tension is determined by the radius of the
aneurysm and the pressure gradient across the wall of the aneurysm
What causes aneurysms to rupture?
• Therefore, the rate of rupture is directly related to the size of the aneurysm
• Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas
40% of those 6-10 mm have already ruptured upon diagnosis
SAH – The Problem
• They occur in young people–80% in 40-65 year olds–15% in 20-40 year olds
• It can kill quickly–25% die within 24 hours
–50% will be dead at 6 months
SAH – The Problem
• It causes significant disability–Cognitive impairment
–Neurological disability depending on size of bleed & complications
encountered
How do they present?
•Headache–sudden onset & severe
–small leak may cause minor headache & may be warning sign
of rupture
How do they present?
• Reduced consciousness
• Meningism
–Vomiting
–Neck stiffness
–Photophobia
• Seizures
What causes symptoms & signs?
• Blood leaking from the aneurysm
• Local pressure effects of the aneurysm
• Associated ICH
• Emboli
What causes symptoms & signs?
• Blood leaking from the aneurysm
Headache
Meningism
What causes symptoms & signs?
• Local pressure effects of the aneurysm
•Visual symptoms due to optic chiasm compression
•Positive babinski
•Bilateral lower limb paresis
What causes symptoms & signs?
–MCA
•Contralateral hand & face paresis
•Contralateral visual neglect
•Aphasia (dominant side)
–ICA/Pcom
•CNIII signs
What causes symptoms & signs?
• Associated ICH
–The aneurysm usually lies within the subarachnoid cisterns
–It can become adherent to adjacent brain due to adhesions (e.g. from a previous leak)
What causes symptoms & signs?
The bleed therefore can also extend into the brain
• MCA = TL causing hemiparesis & aphasia (if dominant)
• Acom = mutism
–AVM is more likely to cause ICH as they usually lie somewhat in brain parenchyma
Headache
• A sudden onset severe headache IS caused by a SAH until you have done investigations which prove
otherwise
Sudden onset severe headache
ABCsHistory – ask about
anticoagulants
Routine bloods & coag & group &
screenIV access
Non-sedating analgesia & hold any
anticoagulants
ExaminationKeep fastingInvestigationsCT brain non-
contrastBlood on CT = SAH
Is there any other pathology on CT?
Where is the aneurysm?
CT COW +/- cerbralangiogram
For angiogram & coiling if suitable
For craniotomy & clipping if not
suitable for coiling
Meanwhile chart nimodipne, fluids,
anti-seizure medication
Monitor GCS for any changes from
admission examination
Ensure pre-op ready – consent, G&S,
check bloods, fasting
Sudden onset severe headache
History – ask about anti-coagulants
ABCsRoutine bloods & coag & group &
screenIV access
Non-sedating analgesia & hold
any anticoagulants
ExaminationKeep fastingInvestigationsCT brain non-
contrastNo blood on CT
scan
Is there any other pathology on CT?
Lumbar punctureLP = positive for
SAHDiagnosis still
uncertain CT COW +/- cerbral
angiogram
No aneurysmMay repeat
cerebral angio
Investigations
• CT scan without contrast
• Lumbar puncture
• CT COW
• Cerebral angiogram
• MRI/MRA
98% sensitive @ 12 hours80% at day 350% at day 7
Also good to see if any associated ICH or hydrocephalus. May help localise the location of the aneurysm if there is more than 1 & may also see AVM
Where is the aneurysm?
• Where is the blood on the CT scan?
–Basal cisterns – COW aneurysm
–Sylvian fissure – ICA, Pcom, MCA
–Interhemispheric or intraparenchymal- Acom
Subarachnoid
hemorrhage (SAH). There is high-attenuation
blood in the Sylvian
fissures (blue arrows) and
the interhemispheric
fissure (red arrow) seen on
this non-contrast enhanced
CT of the brain.
Do not confuse normal,
physiologic calcifications
(white and black arrows)
for blood.
• A cistern where the arachnoid extends across
between the two temporal lobes, and encloses the
cerebral pedunclesincluding the structures
contained in the interpeduncular fossa.
MCA stroke - Emergency
neuroradiology. Axial CT scan at the
level of the basal cisterns shows the
"hyperdense middle cerebral artery
(MCA) sign" (arrow) representing
acute clot within the right middle
cerebral artery, accounting for the
patient's clinical symptoms
SAH & LP
• CT & LP are critical to diagnosing SAH
• No need for LP if obvious blood in subarachnoid space on CT
• Blood may not be evident on CT, especially if it is performed > few days after bleed
• LP should only be performed after 12 hours of headache onset
SAH & LP• When blood enters the CSF (e.g. from SAH or
during LP) the red cells are broken down & oxyhaemoglobin is released
• It then takes 12 hours for the oxyhaemoglobin to be converted into
bilirubin – conversion is via an enzyme found in the brain.
• Bilirubin in the CSF, therefore, tells us that blood must have been in the subarachnoid
space for at least 12 hours
SAH & LP• Blood which entered the CSF during the
LP would not encounter the enzyme & could not produce bilirubin
• The CSF will look xanthochromic(yellowish discolouration) if bilirubin is present which they will look for with
spectroscopy in the lab
What may I find on examination?
• Normal exam• Confusion/memory loss
• Aphasia• CN abnormalites
–CNII – papilloedema, usually mild initially & retinal haemorrhages
–CNIII – palsy• Hemiparesis/neglect
• Obs – HTN, tachycardic, febrile
Treatment
• Main aim is damage control – want to prevent further bleeding & try to avoid the complications that SAH patients get
• SAH patients will vary greatly from GCS 15/15 to GCS 3/15
To coil or clip?
• Coiling– Endovascular technique done in
angiography by interventional radiologists under GA
– May be best if small necked aneurysm
– Used in particularly sensitive areas e.g. basilar tip
– Must be able to access the aneurysm (e.g. any stenosis or tortuous vessels)
– Like dome:neck ratio to be 2:1 or greater
• Clipping– Craniotomy & careful
dissection using microscope to reach aneurysm & clip usually at neck
– May be performed after failed clipping
– If aneurysm can’t be reached by the endovascular root
Complications with SAH
1. Re-bleeding
2. Hydrocephalus
3. Vasospasm
4. Hyponatraemia
5. Seizures
6. VTE
Complications with SAH
Re-bleeding
80% mortality if re-bleed
Greatest risk is in the first 24 hours after the initial bleed
Aim to prevent by controlling BP to avoid dramatic changes & isolate the aneurysm
from the circulation (coil or clip)
Complications with SAH
•Hydrocephalus–Obstructive
•Blood enters the ventricles & can block the flow of CSF e.g. at the aqueduct or outlet of
the 4th ventricle
Complications with SAH
• HydrocephalusCommunicating
• Due to blood blocking reabsorption of CSF through the arachnoid granules
May need an extraventricular drain to treat
Keep head of bed at 300 (promote CSF flow & venous return)
Complications with SAH
VasospasmBlood vessel goes into spasm causing
ischaemia - stroke
To prevent keep them filled with at least 3L fluid day & nimodipine IV/PO & insert central line to monitor central
venous pressure – aiming for 8-10
Suspected with deteriorating GCS/new neurological deficit
Complications with SAHVasospasm
Treatment – Urgent CT brain to rule out a bleed as a cause of the deterioration then
urgent angiogram to diagnose & treat vasospasm
Greatest risk of vasospasm is days 4-7 but significant risk for first 3 weeks after
bleed, therefore will use preventative measures for at least 3 weeks
Complications with SAH
HyponatraemiaSusceptible due to being fluid loaded &
cerebral salt wasting
Cerebral salt wasting = renal loss of sodium due to intracranial pathology ? Cause. Loss of water & salt (whereas SIADH is loss of
salt & retention of water)
Treat with normal or hypertonic saline
Complications with SAH
Hyponatraemia
If refractory may need a mineralocorticoid e.g. fludrocortisoneto stimulate renal reabsorption – but
this should only be used under instructions from consultant
endocrinologist
Complications with SAH
SeizuresA seizure is a disturbance of sensation,
movement or consciousness
All seizures originate from the surface of the brain – cortex
Blood is an irritant to the cortex
Complications with SAH
SeizuresProphylaxis with phenytoin or
levetiracetam
Ensure phenytoin levels are therapeutic
Treat as seizure from any cause & suspect re-bleed
Complications with SAH
VTEOn bed rest
TEDS
Prophylactic enoxaparin as soon as consultant sees fit
Always keep VTE in the back of your mind
How are SAH graded?GCS 15, only CN deficit if any
Grade 1 No blood
GCS 13-14, no deficit
Grade 2 Diffuse blood, no clots & <1mm
GCS 13-14, with deficit
Grade 3 Clots & blood 1mm or more
GCS 7-12, +/-deficit
Grade 4 ICH or intraventricularclots
GCS 3-6 +/-deficit
Grade 5
Subdural Haematoma
Extra-dural haematoma
Extra-dural haemtoma
Intra-parenchymal haematoma
Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY
