This document discusses vasospasm, a complication that can occur after subarachnoid hemorrhage from a ruptured cerebral aneurysm. Approximately 70% of patients will show angiographic evidence of vasospasm, and 30% will experience symptomatic vasospasm. The risk is highest between 4-9 days after hemorrhage. Vasospasm does not always lead to ischemia and brain injury, which depends on additional factors like microcirculatory failure. Management involves a 6 point plan: 1) nimodipine administration, 2) euvolemia, 3) induced hypertension, 4) magnesium supplementation, 5) cerebral angioplasty or intra-arterial vasodilators if needed, and 6

1. Vasospasm After SAH
PREVENTION
AND
M A N AG E M E NT

2. Prevalence
 0.5% of the population will rupture a cerebral
aneurysm
 25% of these will die
 Death is due to
 The initial catastrophic bleed
 Rebleeding
 Cerebral vasospasm

3. Vasospasm
 70% of patients will have angiographic evidence of spasm
following the haemorrhage
 30% of these cases will have symptomatic spasm
 50% of these will have DIND

4. VASOSPASM
 Delayed cerebral vasospasm typically develops
from 4 to 9 days, though earlier (3 days) or late
(3 weeks) vasospasm may be observed

5. Does spasm = ischemia?
 Not necessarily
 Many factors contribute to the development of
ischemia and infarction,
 distal microcirculatory failure,
 Poor collateral anatomy,
 genetic or physiological variations in cellular
ischemic tolerance

6. Risks for Spasm

7. Case
 50 year old woman
 Sudden onset of headache

8. ED->CTB; SAH.
Ruptured AComA aneurysm

9. Coiling

10. Progress
 EVD inserted for hydrocephalus
 Extubated on day 4.
 GCS 14 (eyes to voice) but generally drowsy
 On day 8 developed left hemiparesis
 Intubated
 DSA demonstrated severe bilateral ICA spasm
 Balloon angioplasty to RICA and MCA
 Intraarterial verapamil and papaverine

11. Progress
 Massive doses of noradrenaline and vasopressin
to maintain SBP. ICP high. Thio coma
 Angio D9... Severe spasm persists refractory to
intraarterial verapamil
 CTB; diffuse cerebral oedema. ICPs >30
 Decompressive craniectomy

13. Progress
 D10;
 Despite
decompression, ICP remain at 38.
 Unsupportable BP
 Therapy ceased

14. Diagnosis
 Neuro exam
 DSA
 TCD

Transcranial Doppler is reasonable to monitor for the
development of arterial vasospasm (Class IIa;Level of
Evidence B). (New recommendation)
 Warning Signs
 CT Perfusion

15. A=CBF B=CBV

16. Perfusion imaging can be useful to identify regions of potential brain ischaemia
(Class IIa; Level of evidence B)

17. Management

18. Management; 6 point plan

1.Nimodipine
2. Euvolemia
3. Induction of Hypertension
4. Mg
5. Cerebral angioplasty and/or selective intra-arterial
vasodilator therapy
6. Stop the boats

19. Nimodipine
 Level 1 Evidence

20. Euvolemia and Hypertensing
 Choice of fluid
 SBP aims

21. Magnesium

22. Intra-arterial therapy

24. Management of other complications due to
vasospasm
 Hyponatremia... Cerebral salt wasting
 Role
of euvolemia
 Fludrocortisone
 3% saline
 Choice of fluid

25. Fever
Independent association with high fever after SAH
and poor cognitive outcome

26. Haemoglobin
 Controversial
 Lower
threshold for transfusion in
vasospastic patients

27. Statins
 STASH Trial

28. Other
 Urokinase
 Lumbar drainage