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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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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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

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1 4 7 10 13 16 19 22 25 28 31 34 37 40 43 46 49 52 55 58 61 64 67 70

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Glutamate during early period

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Then, Vasospasm despite continued elevated ICP

LPR response to IA nicardipine

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Glucose response to IA nicardipine

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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