Cerebral Vasospasm

Aggressive Management of Cerebral Vasospasm

Dhaval Shukla Vinayak N, Hima P, Bhat DI

Dept of Neurosurgery, Dept of Neuroimaging and Intervention RadiologyNational Institute of Mental Health and Neurosciences (NIMHANS)

Bangalore, India

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%

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

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

IAVT AgentsAgent 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 ?

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

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

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

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

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

What we found?

Variable No of patients n = 106Age 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%)

Fisher Grade I II III IV

6 (5.7%)15 (14.2%)35 (33.0%)50 (47.2%)

Size of aneurysm ≤10 mm >10 mm

101 (95.3%)5 (4.7%)

Preoperative vasospasm 51 (48.1%)Aneurysm location ACA and AComA DACA ICA MCA Posterior circulation

53725192

Vasospasm

• Single vessel in 7 (26.9%).

• Unilateral 15 (57.7%)

• Bilateral 11 (42.3%)

• ICA vasospasm 4 (15.5%)

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 5 6

12 (52.2%)3 (13.0%)4 (17.4%)2 (28.7%)1 (4.3%)1 (4.3%)

Post nimodipine vasodilation None Some Significant

1 (4.3%)8 (34.8%)14 (60.9%)

Post nimodipine clinical response Status quo Improved Worsened

1 (4.3%)20 (87.0%)2 (8.7%)

• 3 patients did not receive intra-arterial nimodipine• 2 patients had multiple major arterial territory infarction• 1 IVH

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

Pre-infusion Post-infusion

Pre-infusion Post-infusion

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

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

Thank You