Cerebral Vasospasm; Delayed cerebral ischemia; subarachnoid hemorrhage; delayed ischemic neurological deficit; stroke; intra-arterial vasodilator therapy.

1. Aggressive Management of
Cerebral Vasospasm
Dhaval Shukla
Vinayak N, Hima P, Bhat DI
Dept of Neurosurgery, Dept of Neuroimaging and Intervention Radiology
National Institute of Mental Health and Neurosciences (NIMHANS)
Bangalore, India

4. Spectrum of Vasospasm, Delayed Cerebral Ischemia (DCI),
Delayed Ischemic Neurological Deterioration (DIND)
Only radiographic evidence of cerebral infarction and functional
outcome should be used as the primary outcome measures
30-70% 20-50%
15-20%

5. Medical Management DCI
• Oral Nimodipine 60 mg every 4 hours
• Serial monitoring with TCD
• “3H” therapy
• 27% use prophylactic hypervolemia.
• 12% use prophylactic induction of hypertension
• 41% use hyperdynamic therapies
• 16% patients still develop infarction
Neurocritical Care, 2011.
Complications
pulmonary edema, myocardial ischemia, hyponatremia,
cerebral haemorrhage, cerebral edema

6. Invasive interventional management of vasospasm
• Endovascular treatment (EVT) using intra-arterial vasodilators and/or
angioplasty may be considered for vasospasm related DCI
• Rescue therapy for symptoms refractory to medical treatment
• Intra-arterial vasodilator infusion therapy (IAVT)
• Regardless of the size and location of artery
• IAVT can be safely performed in awake patients
J Neurointerv Surg. 2012
Only contraindication of IAVT is systemic hypotension

7. IAVT Agents
Agent Angiographic
Improvement (%)
Clinical
Improvement (%)
Nimodipine 40-100 70-80
Verapamil 29-44 30-75 Systemic Hypotension
Nicardipine 70-100 40-90 Systemic Hypotension
Milrinone Yes ?

8. What we did?
• Retrospective analysis of aSAH managed with microsurgical clipping
• Excluded
• Unruptured aneurysms
• Neurological deterioration in the immediate postoperative period
• Delayed neurological deterioration
• Decrease in consciousness as assessed by Glasgow coma scale (GCS) or
development of motor weakness (monoparesis, hemiparesis, or paraparesis),
or development of speech and language impairment
• Head CT scan and blood investigations to exclude
• hydrocephalus, hyponatremia, seizure, hematoma, hypotension, hypoxia, or infection
• DCI due to cerebral vasospasm

9. Postoperative Management
• Oral nimodipine, phenytoin, and crystalloids to maintain euvolemia
• Normotension or permissive hypertension
• Hypotension avoided
Signs of DCI
Head CT Scan
No major arterial
territory infarction

10. Protocol for intra-arterial nimodipine therapy
• Right femoral arterial access
• 5F diagnostic catheter into ICA on side of vasospasm
• Vasospasm classified:
• none
• mild (<25 % stenosis),
• moderate (25-50% stenosis)
• severe (>50% stenosis)
• 3 mg of Nimotop (15ml) diluted with 35ml normal saline infused over 30
min
• Blood pressure monitored closely
• Intra-arterial nimodipine given daily till patient showed improvement or
developed major arterial territory infarct and fixed neurological deficit
AJNR. 2006

11. Outcome assessment
• Angiographic response
• No change in vessel diameter
• Some vasodilation
• Significant vasodilation
• Clinical response
• Improved
• No change in neurological deficits
• Worsening (progression) of neurological deficits

12. Outcome at discharge
• Favorable
• Good recovery - no neurological deficits
• Mild disability - monoplegia or hemiparesis or paraparesis with
motor power ≥3/5
• Unfavorable
• Severe disability - hemiplegia or paraplegia with motor power <3/5
• Altered sensorium
• Death

13. What we found?

14. Variable No of patients n = 106
Age in years mean ± SD (range) 51 ± 13 (12 – 72)
Males 45 (42.1%)
WFNS Grade
 I
 II
 III
 IV
 V
57 (53.8%)
23 (21.7%)
15 (14.2%)
9 (8.5%)
2 (1.9%)

15. Vasospasm
• Single vessel in 7 (26.9%).
• Unilateral 15 (57.7%)
• Bilateral 11 (42.3%)
• ICA vasospasm 4 (15.5%)

16. Intra-arterial Nimodipine
N=23
Pre nimodipine infusion vasospasm
 Mild - <25%
 Moderate - 25-50%
 Severe - >50%
8 (34.8%)
12 (52.2%)
3 (13.0%)
Number of sessions
 1
 2
 3
 4
12 (52.2%)
3 (13.0%)
4 (17.4%)
2 (28.7%)
• 3 patients did not receive intra-arterial nimodipine
• 2 patients had multiple major arterial territory infarction
• 1 IVH

17. 40/ M, AcomA aneurysm, WFNS 3
Deterioration in Sensorium 5th (8th postictal day) postop day

18. Pre-infusion Post-infusion

19. Pre-infusion Post-infusion

20. Outcome No Vasospasm
(n=80)
Vasospasm
(n=26)
Total
(n=106)
Good 62 (77.5%) 15 (57.7%) 77 (72.6%)
Mild disability 7 (8.7%) 4 (15.4%) 11 (10.4%)
Severe disability 2 (2.5%) 2 (7.7%) 4 (3.8%)
Altered sensorium 5 (6.3%) 2 (7.7%) 7 (6.6%)
Death 4 (5.0%) 3 (11.5%) 7 (6.6%)
Favorable 69 (86.2%) 19 (73.1%) 88 (83%)
Unfavorable 11 (13.8%) 7 (26.9%) 18 (17%)*
*p=0.144

21. Summary
• Traditionally endovascular intervention for symptomatic vasospasm is indicated
when medical management has failed
• We adopted direct intra-arterial nimodipine therapy
• Outcome of medical management is uncertain and associated with complications
• Clinical improvement after endovascular therapy is most often achieved when treatment is
initiated early
• Patients had good outcome with intra-arterial nimodipine therapy without
complications
• Good clinical response in 87%
• Favourable outcome in 78.3%
• Intra-arterial infusion of nimodipine is an effective therapy for clinical outcome
after SAH
• Nimodipine also has neuroprotective effects and is useful even when vasospasm is mild and
when significant vasodilation is not achieved