Cerebral vasospasm is a narrowing of cerebral arteries that occurs after subarachnoid hemorrhage, usually from a ruptured aneurysm. It develops in 50-90% of aneurysmal SAH cases on angiography but only 20-30% develop neurological deficits. Vasospasm typically begins 3-14 days after hemorrhage and can last up to 4 weeks. Risk is predicted by modified Fisher scale and thick subarachnoid blood. Transcranial Doppler is commonly used to screen for vasospasm. Prevention focuses on hydration, blood pressure control, nimodipine, and clot removal while treatments include "triple H" therapy and endovascular interventions like angiop

1. CEREBRAL VASOSPASM
ROSHAN KHATIWADA
Senior Resident
Neurosurgery

2. INTRODUCTION
Cerebral vasospasm is a prolonged, sometimes
severe, reversible narrowing of the cerebral
arteries that begins few days after subarachnoid
hemorrhage (SAH).
Blood clots in the subarachnoid space and
ventricles
Causes : rupture of a aneurysm, traumatic SAH,
vascular malformations or tumor bleed

3. Types
• Angiographic vasospasm : Vascular imaging :
focal, segmental, or diffuse;
– mild (<25%),
– moderate (25% to 50%)
– severe (>50%)
50-90% of aneurysmal SAH
• Clinical vasospasm : narrowing causing cerebral
ischemia with corresponding symptoms and signs
(delayed ischemic neurological deficits)
Only half of the patient with angiographic vasospasm

4. Prediction of Vasospasm
Risk Factors for Vasospasm
i. Thick subarachnoid clots
ii. Intra ventricular hematoma
iii. Persistent subarachnoid clots (slow clearance)
iv. Poor neurological condition on admission
v. Loss of consciousness associated with rupture
vi. History of cigarette smoking
vii. Pre existing hypertension
viii.Cocaine use

5. Modified Fisher Scale and
Risk for Vasospasm
 1 : Focal or diffuse thin layer of SAH, no IVH:
low risk
 2: Focal or diffuse thin layer of SAH, IVH
present: moderate risk
 3: Focal or diffuse thick layer of SAH, no
IVH: high risk
 4: Focal or diffuse thick layer of SAH, IVH
present: very high risk

6. Pathogenesis
• Smooth muscle contraction:
– Hemoglobin ---- entry and release of calcium ---
activation of calcium/calmodulin -dependent
myosin light-chain kinase --- phosphorylation of
the myosin light chain ---- actin and myosin cross-
linkage and mechanical shortening (smooth muscle
contraction).
• Endothelial Injury, decreased Nitric Oxide,
and increase Endothelin-1

7. Theories on the Pathogenesis
of Vasospasm
 Prolonged vasoconstriction
 Endothelin-1 overproduction (vasoconstrictor)
 Nitric oxide underproduction (vasodilator)
 Inflammation-mediated “remodeling” and
narrowing of the arterial wall.

8. Symptoms and Signs
• Diminished attention, changes in verbal
output, or a slight but new pronator drift of the
upper extremity.
• Increased headache and either agitation or
somnolence, change in patient behavior
 Monoparesis , hemiparesis , aphasia confusion,
drowsiness, poverty of speech, and abulia.

9. Differential Diagnosis
• Increased edema surrounding hematomas,
contusions, or infarcts
• Re-bleeding of aneurysms or aneurysmal
remnant
• Hydrocephalus
• Infection, ventriculitis
• Hyponatremia
• Hypoxemia

10. Diagnosis
• Pathologic increases in TCD velocities; there is a high
probability of significant large-artery vasospasm with
velocities >200 cm/sec
• Pathologic reductions in CBF detected by
Perfusion CT scanning
SPECT
Xenon-enhanced CT
Thermal diffusion flowmetry

11. • Detection of cerebral ischemia by
– Diffusion-weighted MRI
– Microdialysis
– Jugular venous oxygen saturation
• Vascular imaging by
– Catheter-based angiography
– CT angiography

12. Prevention of Vasospasm and
Cerebral Protection
General Measures
– Maintain euvolemia (at least 3 L of isotonic fluids
daily)
– Prevent anemia (hemoglobin <9 g/dL)
– Maintain normal to high systemic blood pressure
– Prevent high ICP (and maintain CPP) with
external ventricular drainage as necessary
– Nimodipine 60 mg by mouth or nasogastric tube
every 4 hr.

13. Investigational Treatments
Endothelin receptor antagonists
HMG-CoA inhibitors (statins)
Magnesium sulfate (intravenous infusion)
Intrathecal vasodilators (slow-release implants)
– nicardipine implants

14. CONTD…
• Augmentation of Subarachnoid Clot
Clearance
Clot lysis
Lamina terminalis fenestration
Lumbar CSF drainage
Combined treatment

15. Reversal of Vasospasm and
Cerebral Ischemia: Rescue
Treatments
• Triple-H Therapy: Hypervolemia, Hypertension, and
Hemodilution
– central venous pressure between 8 and 10 mm Hg or a
– pulmonary capillary wedge pressure in the range of 14 to 16 mm Hg
– Systolic blood pressure of 200 mm Hg or higher or CPP greater than 80 mm Hg
• Intra-aortic Balloon Counterpulsation
– placement of a transfemoral aortic balloon that inflates on aortic valve closure
with each cardiac cycle and augments diastolic flow proximally to the coronary
and cranial arteries and distally to the peripheral circulation .

16. Endovascular Reversal of
Vasospasm
Chemical Angioplasty:
Papaverine
Verapamil (≈3 mg per vessel or ≈20 mg per
patient)
nicardipine and nimodipine
Balloon Angioplasty:

17. Practical Approach
1. Ensure adequate intravascular volume with additional
isotonic crystalloid, colloid (albumin), or red blood cell
infusions as appropriate (target CVP, 8-12 mm Hg;
hemoglobin, >9 g/dL)
2. Induce hypertension with one or more of the following
agents (target systolic blood pressure, >200 mm Hg
within 2 hr):
a Dobutamine, 5-20 μg/kg/min
b Dopamine, 5-15 μg/kg/min
c Milrinone, 0.50-0.75 μg/kg/min
d Norepinephrine, 5-20 μg/kg/min
e Phenylephrine, up to 150 μg/min

18. CONTD…
3. Percutaneous TBA:
a Consider early for patients with severe deficits or fragile
cardiopulmonary status (i.e., before maximum
“triple-H” therapy)
b First rule out cerebral infarction with CT scanning
c May require ongoing hypertensive treatment of distal or untreated
vasospastic territories
4 .Chemical angioplasty (i.e., intra-arterial verapamil, ≈3 mg per
vessel):
a When TBA is unavailable
b For vasospasm in territories untreatable by TBA
c May have to be repeated
5. Intra-aortic balloon counterpulsation:
a Consider in patients with refractory vasospastic ischemia and heart
failure (and endovascular treatment
is not feasible or successful)

19. Question 1
• What is the percentage of people who develop
clinical vasospasm after a cerebrovascular
aneurysm rupture?

20. ANSWER 1
• 20-30%

21. Question 2
• What is the early onset cerebral vasospasm?

22. Answer 2
• Within 48hrs

23. Question 3
• How long can vasospasm last?

24. Answer 3
• upto 4weeks

25. Question 4
• What is the most common screening tool for
catching early vasospasm signs?

26. Answer 4
• TCD

27. THANK YOU