1. Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space between the brain's outermost layers caused by a ruptured aneurysm in 70% of cases. 2. Presentation includes sudden severe headache, reduced consciousness, vomiting, neck stiffness, and seizures. Investigations include CT scan and lumbar puncture to detect blood. 3. Treatment aims to prevent rebleeding through securing the aneurysm via coiling or clipping, and managing complications like hydrocephalus, vasospasm, seizures, and hyponatremia which can occur in the weeks following SAH.

1. SUBARACHNOID
HAEMORRHAGE
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO

2. Global Critical Care
https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY

3. 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%)

4. SAH
• Where does the blood go?
–Anywhere where CSF goes, may
get hydrocephalus if into ventricle
& causes obstruction of CSF
circulation

5. SAH
• Higher chance if:
–Female
–3rd trimester of
pregnancy
–Middle-aged
–Abuse of stimulant
drugs
–Connective tissue
disorder
–Family history
–PCKD

6. 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

7. 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

8. 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

9. 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

10. SAH – The Problem
• It causes significant disability
–Cognitive impairment
–Neurological disability depending on
size of bleed & complications
encountered

11. How do they present?
•Headache
–sudden onset & severe
–small leak may cause minor
headache & may be warning sign
of rupture

12. How do they present?
• Reduced consciousness
• Meningism
–Vomiting
–Neck stiffness
–Photophobia
• Seizures

13. What causes symptoms & signs?
• Blood leaking from the aneurysm
• Local pressure effects of the
aneurysm
• Associated ICH
• Emboli

14. What causes symptoms &
signs?
• Blood leaking from the
aneurysm
Headache
Meningism

15. What causes symptoms & signs?
• Local pressure effects of the aneurysm
•Visual symptoms due to optic chiasm
compression
•Positive babinski
•Bilateral lower limb paresis

16. What causes symptoms & signs?
–MCA
•Contralateral hand & face paresis
•Contralateral visual neglect
•Aphasia (dominant side)
–ICA/Pcom
•CNIII signs

17. 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)

18. 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

19. Headache
• A sudden onset severe headache
IS caused by a SAH until you have
done investigations which prove
otherwise

20. Sudden onset severe headache
ABCs
History – ask about
anticoagulants
Routine bloods &
coag & group &
screen
IV access
Non-sedating
analgesia & hold any
anticoagulants
ExaminationKeep fastingInvestigations
CT brain non-
contrast
Blood on CT = SAH
Is there any other
pathology on CT?
Where is the
aneurysm?
CT COW +/- cerbral
angiogram
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

22. Sudden onset severe headache
History – ask about
anti-coagulants
ABCs
Routine bloods &
coag & group &
screen
IV access
Non-sedating
analgesia & hold
any anticoagulants
ExaminationKeep fastingInvestigations
CT brain non-
contrast
No blood on CT
scan
Is there any other
pathology on CT?
Lumbar puncture
LP = positive for
SAH
Diagnosis still
uncertain
CT COW +/- cerbral
angiogram
No aneurysm
May repeat
cerebral angio

23. Investigations
• CT scan without contrast
• Lumbar puncture
• CT COW
• Cerebral angiogram
• MRI/MRA
98% sensitive @ 12 hours
80% at day 3
50% 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

24. 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

27. 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.

29. • A cistern where the
arachnoid extends across
between the two temporal
lobes, and encloses the
cerebral peduncles
including 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

30. 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

31. 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

32. 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

33. 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

34. 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

36. 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

37. Complications with SAH
1. Re-bleeding
2. Hydrocephalus
3. Vasospasm
4. Hyponatraemia
5. Seizures
6. VTE

38. 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)

39. 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

40. Complications with SAH
• Hydrocephalus
Communicating
• 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)

41. Complications with SAH
Vasospasm
Blood 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

42. Complications with SAH
Vasospasm
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

43. Complications with SAH
Hyponatraemia
Susceptible 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

44. Complications with SAH
Hyponatraemia
If refractory may need a
mineralocorticoid e.g. fludrocortisone
to stimulate renal reabsorption – but
this should only be used under
instructions from consultant
endocrinologist

45. Complications with SAH
Seizures
A 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

46. Complications with SAH
Seizures
Prophylaxis with phenytoin or
levetiracetam
Ensure phenytoin levels are therapeutic
Treat as seizure from any cause &
suspect re-bleed

47. Complications with SAH
VTE
On bed rest
TEDS
Prophylactic enoxaparin as soon as
consultant sees fit
Always keep VTE in the back of your
mind

48. 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
intraventricular
clots
GCS 3-6 +/-
deficit
Grade 5

49. Subdural Haematoma

50. Extra-dural haematoma

51. Extra-dural haemtoma

52. Intra-parenchymal haematoma

53. Global Critical Care
https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512
9555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY

54. GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com