11/4/14 SAH 2

Lets continue on our stroke journey, learning today about SAH and vasospasm...

1) Symptomatic vasospasm occurs in 20-40% patients and is defined as a clinical deterioration due to vasospasm when other causes (seizures, hydrocephalus, edema) have been excluded.

2) Delayed cerebral ischemia: symptomatic vasospasm or new infarct on CT or MRI due to vasospasm.

3) Risk factors for vasospasm:

1. Thick blood on CT (SAH/IVH) 
2. Fever
3. Admission hypertension
4. Sentinel bleed
5. Ultra-early angiographic spasm
6. Volume depletion
7. Low cardiac output
8. Smoking

4) Cerebral angiogram is the gold standard to dg cerebral vasospasm

5) Transcranial doppler ultrasound shows elevated velocities that may precede clinical symptoms by 34-48 hrs.

6) TCD positive predictive value of MCA mean flow velocity >200 cm/s IS 87% and the negative predictive value for MCA <120 cm/s is 94%

7) Hypercalcemia can cause or exacerbate vasospasm and should be avoided or corrected

8) Nimodipine is the only medication proven in large clinical trials to improve outcome after SAH

9) Nimodipine tx: 60mg q4 hrs for SBP > 140, 30mg q 4 hrs for SBP 120-140 mmHg, and held if SBP <120 mmHg. Therapy for 21 days.

10) Treat fever aggressively and maintain normovolemia.