after the storm: immediate management of sah patients fileafter the storm • whol and “negative...

2018 CEREBROVASCULAR FUTURE CARE SYMPOSIUM

After the Storm:Immediate Management of SAH Patients

Eric S. Rosenthal, MDAssociate Director, MGH Neurosciences ICUBoston, MA [email protected]


After the Storm

• WHOL and “negative CT”—who to LP• Admission findings - when to worry• Rebleeding risk and identification of patients at high risk • The role of antifibrinolytics and timing of aneurysm control• Neurologic decline, vasospasm, and delayed cerebral ischemia• The role of coordinated, interdisciplinary care• Acute ICU monitoring and current cutting-edge technology• The near horizon for SAH care in the ED and ICU

SAH Overview

• 1 in 8 die in pre-hospital phase• Half of survivors have long-term functional impairment• Risks

• Rebleeding• Seizures • Hydrocephalus• Heart failure• Vasospasm/Delayed Cerebral Ischemia

• Vasospasm: 50-70%• DCI: 15% (many without vasospasm)• Interventions include induced HTN, volume resuscitation,

endovascular vasodilators

WHOL and “negative CT”—who to LP• Ottowa SAH Rules: only excluded 15% of awake patients

Perry JJ. CMAJ. 2017; 189(45):e1379-1385.

WHOL and “negative CT”—who to LP

• CT/CTA Screening (MGH experience):• Bayesian model: 0.5% probability aSAH if CT/CTA negative.• MGH experience (2001-2009): 0/181 patients had

subsequent vascular lesion identified after negative vascular imaging (10% LP complication rate).

McCormack RF Acad Emerg Med. 2010; 17(4):444-451

Admission findings - when to worry

Clinical Severity (Hunt and Hess) Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity.Grade 2: Moderate to severe headache; nuchal rigidity; +/- cranial nerve palsy.Grade 3: Drowsy; minimal neurologic deficit.Grade 4: Stuporous; mod-severe hemiparesis; +/-early decerebrate rigidity and

vegetative disturbances.Grade 5: Deep coma; decerebrate rigidity; moribund.

Clinical Severity (WFNS) Class 1: GCS (Glasgow Coma Scale) 15 Class 2: GCS 13-14 without focal neurological deficit.Class 3: GCS 13-14 with focal neurological deficit.Class 4: GCS 7-12 with or without focal neurological deficit.Class 5: GCS <7 with or without focal neurological deficit.

Admission findings - when to worryRadiologic Severity: mod Fisher GradeGrade 1: Minimal/diffuse thin SAH, - IVHGrade 2: Minimal/diffuse thin SAH, + IVHGrade 3: Thick SAH, - IVHGrade 4: Thick SAH, + IVH

Frontera J. Neurosurgery. 2006.

Impact of Severity on Vasospasm Risk


• Angio-negative Perimesencephalic SAH• 10% of SAH; 2/3 of angio-negative SAH• Commonly in those > 50 years of age• Primarily brainstem and prepontine cisterns• 10% rate of occult vascular lesion

• Angio-negative but diffuse SAH• Vasospasm and poor outcome may occur• 0.17 odds of good outcome vs. perimes SAH• 20% rate of occult vascular lesion

• Dissection, FMD, AVM, mycotic emboli, PRES, stimulants, RCVS


• MGH Composite Admission Risk Score predicts poor outcome and risk of delayed cerebral ischemia

Admission Prevalence

Rate of DCI [95%CI]

Admission Score 1, Low 20% 37% [25-50]

Admission Score 2.5, Medium 73% 58% [50-66]

Admission Score 4, High 7% 79% [61-92]

Neurosurgery. 1998;42(5):959-68.

Rosenthal ES. Ann Neurol. 2018

1. Age > 50 y2. Aneurysm size >10 mm

3. Fisher scale score >24. Hunt and Hess Grade >3

Rebleeding risk and identification of patients at high risk • Rebleeding: 4-17% in first 72 hours

• Most in first 8 h; 50% mortality• What increases risk? aneurysm size, HTN, anticoag, WFNS,

mFS, ICH.

McCormack RF Acad Emerg Med. 2010; 17(4):444-451Thomas LE. J Neurosurg. 2014; 121:24-31.Brilstra EH. Neurology. 2000. 55:1656-1660.Naidech AM. Arch Neurol. 2005. 62:410-416.Van Donkelaar. Stroke. 2015;46:2100-2106.

mFS 3-4

mFS 0-2

15%

10%

5%

WNFS V

I

IV

III

II

Rebleeding risk and identification of patients at high risk • Antifibrinolytics decrease rebleeding: RR 0.65 [0.64-1.14]

• Antifibrinolytics increase infarct risk: RR 1.41 [1.04-1.91]• Short-term treatment (<72h) appropriate if patient cannot be

treated within 24h

• The association between EVD management and rebleeding may relate to grade and drainage.• Meta-analysis:

• Ttreatment = mean 81 h• TEVD = 50 h• TEVD-Rebleed = 1 h

McCormack RF Acad Emerg Med. 2010; 17(4):444-451Thomas LE. J Neurosurg. 2014; 121:24-31.Brilstra EH. Neurology. 2000. 55:1656-1660.Naidech AM. Arch Neurol. 2005. 62:410-416.

Nornes 1973.Sundbarb and Ponten 1976Baharoglu MI. Cochrane Database of Syst Rev. 2013.Cagnazzo F. Acta Neurochi. 2017. 159:695–704.

Publication YearLo

g O

dds

Rati

o(E

VD

-Reb

leed

)

The role of antifibrinolytics and timing of aneurysm control• Management of ruptured

aneurysm• Initial SBP < 140-160 mm Hg

is reasonable but unsupported

• Coagulopathy correction• Consider anti-fibrinolytics

when aneurysm obliteration delayed• Cochrane review: RR=0.65 but

heterogeneity among 4 trials• Minimal ischemic/thrombotic

risks when used for < 72h

Hillman J. J. Neurosurg. 2002;97:771–8.Baharoglu MI. Cochrane Database Syst Rev. 2013; 8.Schuette AJ. Neurocrit Care. 2013; 19(1):48-55.Tang. PLoS One. 2014;9(6):e99536.

Neurologic decline, vasospasm, and delayed cerebral ischemia

t

100%

NeurologicFunction

Initial Injury

Neuroworsening:• Vasospasm• DCI• Seizures• Hydrocephalus• Edema• CSD

0%

Hypertension

Volume repletion

Endovascular therapy


• Prevention of vasospasm and DCI• Nimodipine, 21 days (NNT = 13)• Avoiding dehydration, hypotension, hydrocephalus• Negative results with prophylactic Triple-H therapy,

magnesium, statins, endothelin receptor antagonists, intraventricular nimodipine• Inability to select high-risk patients may be a factor

Treggiari MM. J. Neurosurg. 2003;98:978–84.Egge A. Neurosurgery. 2001;49(3):593-605.Feigin VL Cochrane Database Syst Rev. 2000;:CD000483.Feigin VL. Neurology 1998; 50:876.Hoff R. Stroke. 2009;40(7):2575.


• Causes of neurologic decline other than delayed cerebral ischemia

9.6% 8.0%11.8%

25.0%

38.0%

0%

10%

20%

30%

40%

50%

Scalp Electrodes

Sz Unsuspected

(MGH)

Scalp Electrodes

Comatose

(Columbia)

Scalp Electrodes

Sz Suspected

(MGH)

Depth Electrodes

Sz Unsuspected

(MGH)

Depth Electrodes

Comatose

(Columbia)

O'Connor KL, Westover MB, Phillips MT, Iftimia NA, Buckley DA, Ogilvy CS, Shafi MM,

Rosenthal ES. Neurocritical Care. 2014;10(4):190-203.

Claassen J et al. Ann Neurol. 2013;74(1):53-64.


• Causes of neurologic decline other than delayed cerebral ischemia

Obtunded, confused Eating, shows thumb to command, jokes

High-dose Levetiracetam

The role of coordinated, interdisciplinary care• The concept of a Clinical Practice Committee:

Donovan AL. CCM. 2018;46(6):980-990

The role of coordinated, interdisciplinary careMonitoring tools• Frequent exams: Low reliability• CT and MRI: Intermittent, late

• Daily TCDs: “Snapshot”; fair Se/Sp

• Angiography: Intermittent, invasive• EEG: Susceptible to mimics

• Near-Infrared: Scalp contamination• CBF/PbtO2 probes: Uni-regional

Acute ICU monitoring and current cutting-edge technology• Use of brain tissue oxygenation monitoring

Bijlenga P. Neurocrit Care 2010;13:17-23.

Acute ICU monitoring and current cutting-edge technology• Use of pressure autoregulation

Bijlenga P. Neurocrit Care 2010;13:17-23.

Acute ICU monitoring and current cutting-edge technology• Use of transcranial Doppler ultrasound

Risk Factor Odds of Future DCI [95% CI]

P

Mild TCD vasospasm 3.65 [1.58-8.42] <0.01

Moderate TCD vasospasm 2.73 [1.2-6.1] 0.01

Severe TCD vasospasm 1.80 [0.73-4.52] 0.14

Multimodal cEEG (any worsening)

102.5 [21.3-494] <0.01

• Use of continuous EEG

Acute ICU monitoring and current cutting-edge technology• Use of continuous EEG:

• Alpha-Delta Ratio of EEG Power


• Alpha Variability

EEG Day 2 EEG Day 4


• New epileptiform findings

L

R

L

R

Acute ICU monitoring and current cutting-edge technology• Use of continuous EEG

• Accuracy

Prediction of EEG for DCI (n=103) Low Risk[risk score=1]

Medium Risk[risk score=2.5]

High Risk[risk score=4]

Sensitivity, % 91 [81-98] 94 [88-99] 95 [87-99]

Specificity, % 83 [7193] 80 [69-90] 77 [36-99]

Pre-Test Probability of DCI, % 37 [25-50] 58 [50-66] 79 [61-92]DCI Risk (cEEG Deterioration),% 76 [58-90] 87 [79-94] 94 [79-100]DCI Risk (No cEEG Deterioration), % 6 [1-13] 10 [2-19] 9 [3-53]Number Needed to Monitor 2.6 [2.0-3.8] 3.5 [2.8-4.8] 6.7 [3.6-25.3]

The near horizon for SAH care in the ED and ICU

Prediction for DCI Prevention

The near horizon for SAH care in the ED and ICU• Personalized medicine through treatment response

Angiographic Vasodilators


Thank You!

Eric S. Rosenthal, MDAssociate Director, MGH Neurosciences ICUBoston, MA [email protected]


after the storm: immediate management of sah patients fileafter the storm • whol and “negative...

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