Case Presentation of Hemorrhagic Stroke (Subarachnoid Hemorrhage)
Subarachnoid Hemorrhage
Transcript of Subarachnoid Hemorrhage
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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
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What do we use at UCLA for SAH pt who is comatose?
• ICP
• cEEG
• Cerebral microdialysis
• Brain Tissue Oxygen
• TCD (intermittent)
• Xenon CBF (intermittent)
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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
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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
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SAH # 1 vital signs
• SBP 160/80
• ICP 12-15 mm Hg
• HR 84
• SaO2 99%
• Temp 37.9 C
• Na 139
• Hb 31
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EEG PAV in SAH
early before deterioration
1 – 9 - 06
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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
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EEG PAV is worse
Possibilities:
1. Vasospasm2. Deep sedation3. Sepsis due to pneumonia4. Hydrocephalus
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Get a CT, shows no hydrocephalus
PbrO2 is dropping to low values
PbtO2
PbrO2
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Angiogram shows vasospasm
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Treatment of vasospasm
• Treatment options– HHH Rx– Intraarterial vasodilators– Angioplasty– Hypothermia/ Normothermia– Hyperoxia– Metabolic Suppression
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HHH Rx is selected
Improvement in PAV
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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
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SAH # 3, clipping, edema, elevated ICP
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Elevated ICP persistent after SAH #3
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Microdialysis during metabolic suppression with high dose propofol treatment for ICP
LPR during early period of elevated ICP
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Glutamate during early period
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Then, Vasospasm despite continued elevated ICP
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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
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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
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SAH Microdialysis Monitoring of Vasospasm
MD 1
MD 2
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Microdialysis shows normal LPR, glutamate, glucose
LPR 20-25 range
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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?
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DWI while MD LPR is 25
21
MD probe locations 1 and 2
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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
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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
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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