Multimodality Monitoring in SAH
Paul Vespa, MD, FCCMAssociate Professor of Neurosurgery and Neurology
Director of Neurocritical Care
Geffen School of Medicine at UCLA
New York Neurologic Emergencies and Neurocritical Care Symposium
What do we use at UCLA for SAH pt who is comatose?
• ICP
• cEEG
• Cerebral microdialysis
• Brain Tissue Oxygen
• TCD (intermittent)
• Xenon CBF (intermittent)
What are we looking for
• Seizures– 30% of SAH pts have seizures on cEEG
• Brain Ischemia– 50% of SAH pts will have some form of
vasospasm with variable amounts of ischemia
• Elevated ICP
• Brain Glucopenia
Multimodality Case 1 - SAH• 74 yo with acomm aneurysm SAH
• Confused with poor attention
• Intubated due to respiratory distress
• Not obeying, but some sedation given
• Mild left hemiparesis on exam; leg worse than arm
• cEEG and PbtO2
SAH # 1 vital signs
• SBP 160/80
• ICP 12-15 mm Hg
• HR 84
• SaO2 99%
• Temp 37.9 C
• Na 139
• Hb 31
EEG PAV in SAH
early before deterioration
1 – 9 - 06
SAH and EEG PAV
• PAV is an indicator of brain ischemia from vasospasm– Also Alpha/delta ratio is an indicator of
brain ischemia
• PAV goes down (becomes flat) with vasospasm
EEG PAV is worse
Possibilities:
1. Vasospasm2. Deep sedation3. Sepsis due to pneumonia4. Hydrocephalus
Get a CT, shows no hydrocephalus
PbrO2 is dropping to low values
PbtO2
PbrO2
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mm
Hg
Angiogram shows vasospasm
Treatment of vasospasm
• Treatment options– HHH Rx– Intraarterial vasodilators– Angioplasty– Hypothermia/ Normothermia– Hyperoxia– Metabolic Suppression
HHH Rx is selected
Improvement in PAV
Improvement in PbtO2 with HHH Rx
PbrO2
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mm
Hg
SAH case # 3
• 46 yo man with SAH with basilar aneurysm
• GCS 7, HH 4, GCS motor = 4-5
• Coiled on PBD # 2
• ICP, MD, and EEG placed
• ICP becomes elevated requiring frequent CSF drainage
SAH # 3, clipping, edema, elevated ICP
Elevated ICP persistent after SAH #3
Microdialysis during metabolic suppression with high dose propofol treatment for ICP
LPR during early period of elevated ICP
0
5
10
15
20
25
1 4 7 10 13 16 19 22 25 28 31 34 37 40 43 46 49 52 55 58 61 64 67 70
hour
LPR
Glutamate during early period
0
2
4
6
8
10
12
14
1 4 7 10 13 16 19 22 25 28 31 34 37 40 43 46 49 52 55 58 61 64 67 70
hour
uM
Then, Vasospasm despite continued elevated ICP
LPR response to IA nicardipine
0
5
10
15
20
25
30
35
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31
hour
LPR
Glutamate response to IA nicardipine
0
0.5
1
1.5
2
2.5
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31
hour
glut
amat
e uM
Glucose response to IA nicardipine
00.050.1
0.150.2
0.250.3
0.350.4
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31
hour
gluc
ose
mM
vasospasm
Microdialysis response to vasospasm and subsequent treatment
Case 4
• 58 yo woman with SAH due to Acomm
• Clipped on day 2
• Comatose with slight Right Leg weakness post operatively
• EEG PAV becomes poor on day 6
• MD monitoring started on day 3
SAH Microdialysis Monitoring of Vasospasm
MD 1
MD 2
Microdialysis shows normal LPR, glutamate, glucose
LPR 20-25 range
Uncertainty and Action
• The TCD and angio show vasospasm
• Microdialysis does not show ischemic changes
• HH therapy and intraarterial verapamil Tx done once, but persistent angio and TCD findings
• Do we return to angio? Be more aggressive?
DWI while MD LPR is 25
21
MD probe locations 1 and 2
What we did
• We continued with HH therapy and returned to angio for IA treatment
• The MD did not change from that point on
• We watched clinical exam, and EEG PAV
What did we learn?
• LPR reflected the region of interest well
• The ischemia occurred in the distal ACA territory due to distal effects of spasm
• We may need to place multiple probes in locations that are quite different than the frontal location
• We need imaging or other adjunct monitoring
Summary
• Multimodality monitoring with PbrO2, MD, and cEEG detected the ischemic response that occurred with vasospasm after SAH
• Monitoring in the ACA-MCA borderzone is good but very regional changes may occur in remote locations.
• It is unclear which method is best: PBrO2, EEG PAV, TCD, MD.
• Response to treatment can be seen
