Monitoring the injured brain is important to identify secondary insults that can worsen outcomes. Common monitoring methods include measuring intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygenation (PbtO2/SJV02), microdialysis, and imaging. ICP is most accurately monitored via an intraventricular catheter but carries infection risks. PbtO2 and SJV02 monitoring provide information about brain oxygenation levels, with values below certain thresholds associated with poorer outcomes. Microdialysis samples brain fluid and detects chemical changes indicative of ischemia or cell damage. While monitoring aims to detect problems and guide treatment, the evidence for some methods like SJV02 and microdialysis remains limited

1. Monitoring the Injured BrainMonitoring the Injured Brain
Barbara Stanley FRCABarbara Stanley FRCA

2. AimsAims
 Identify the needIdentify the need
 Understand different methodsUnderstand different methods
 What is the evidence-base fo monitoringWhat is the evidence-base fo monitoring

3. The need for monitoringThe need for monitoring
 1 million annually in the US treated for TBI1 million annually in the US treated for TBI
 80,000 end up with disability80,000 end up with disability
 Death rate - 30/100,000Death rate - 30/100,000
 Source: Brain and SpinalCord.org. 2008Source: Brain and SpinalCord.org. 2008

4. Overview – why is it important?Overview – why is it important?
 Unique physiology – complex organ in aUnique physiology – complex organ in a
rigid boxrigid box
 Consequences of increased pressureConsequences of increased pressure
 Secondary insults of hypoxia andSecondary insults of hypoxia and
ischaemia have a large influence onischaemia have a large influence on
outcomeoutcome
 Restoration and preservation of adequateRestoration and preservation of adequate
cerebral blood flow essentialcerebral blood flow essential
 Risks of invasive monitoringRisks of invasive monitoring

5. MethodsMethods
 Functional – GCS and clinical neurologicalFunctional – GCS and clinical neurological
examinationexamination
 Measurement ICP - CPPMeasurement ICP - CPP
 Measurement metabolism-SJV02/ Pbr02/Measurement metabolism-SJV02/ Pbr02/
MicrodialysisMicrodialysis
 Measurement haemodynamics – TCDMeasurement haemodynamics – TCD
 Electrical activityElectrical activity
 ImagingImaging

6. ICP MeasurementICP Measurement
 Catheters placed in ventricle,Catheters placed in ventricle,
parenchyma, subdural or extraduralparenchyma, subdural or extradural
 Commonly fluid filled external strain guageCommonly fluid filled external strain guage
- often with a drain - External Ventricular- often with a drain - External Ventricular
Drain’ EVDDrain’ EVD
 Intraventricular is gold standard and moreIntraventricular is gold standard and more
reliable – CSF can be drained if ICPreliable – CSF can be drained if ICP
elevated from intraventricular catheterelevated from intraventricular catheter

7. ICP monitorsICP monitors
 Intra parenchymal –Intra parenchymal –
 Codman – resistance wires in Wheatstone bridge.Codman – resistance wires in Wheatstone bridge.
Pressure change at tip = change in resistance. NoPressure change at tip = change in resistance. No
bolt required. Can be tunneledbolt required. Can be tunneled
 Camino – Fibreoptic. Change in ICP=change in beamCamino – Fibreoptic. Change in ICP=change in beam
reflected=alters resistance in catheters circuit. Boltreflected=alters resistance in catheters circuit. Bolt
requiredrequired
 Fibreoptic – require calibration prior to insertionFibreoptic – require calibration prior to insertion
 Cannot be recalibrated once sitedCannot be recalibrated once sited
 Subdural and extadural placement give lessSubdural and extadural placement give less
reliable readingsreliable readings

8. ICP Waveform InterpretationICP Waveform Interpretation
 P1= ‘Percussive’P1= ‘Percussive’
Transmission arterialTransmission arterial
pulse from choroidpulse from choroid
plexusplexus
 P2= ‘Tidal’ brainP2= ‘Tidal’ brain
compliancecompliance
 P3= Dicrotic notch =P3= Dicrotic notch =
closure Aortic valveclosure Aortic valve

9. EVDEVD

10. Pro’s and cons - EVDPro’s and cons - EVD
 AdvantagesAdvantages
 Gold standardGold standard
 Recalibration in vivoRecalibration in vivo
 No driftNo drift
 Most accurateMost accurate
 Allows CSF drainageAllows CSF drainage
 DisadvantagesDisadvantages
 Infection risk – 6-11%Infection risk – 6-11%
(Pahl 2007)(Pahl 2007)
 Consequences ofConsequences of
misplacementmisplacement

11. Evidence for ICP monitoringEvidence for ICP monitoring
 BTF – Level 2 in patients with GCS 3-8BTF – Level 2 in patients with GCS 3-8
and abnormal CT who are salvageable –and abnormal CT who are salvageable –
ICP should be monitoredICP should be monitored
 Provides useful predictive informationProvides useful predictive information
regarding worsening intracranial pathologyregarding worsening intracranial pathology
 Protocols with ICP monitoring showProtocols with ICP monitoring show
improved outcomeimproved outcome
 ICP > 20mmHg should be treatedICP > 20mmHg should be treated

12. Brain tissue OxygenationBrain tissue Oxygenation
 Non-invasive – NIRS basedNon-invasive – NIRS based
 InvasiveInvasive
SJV02SJV02
Pbr02Pbr02

13. Pbr02 - NIRSPbr02 - NIRS
 Non-Invasive skin Probes ‘INVOS’ MeasuresNon-Invasive skin Probes ‘INVOS’ Measures
regional saturation of both hemispheresregional saturation of both hemispheres
 Relies on differend light absorption spectra ofRelies on differend light absorption spectra of
oxygenated and de-oxygenated Hb at Infra redoxygenated and de-oxygenated Hb at Infra red
spectrum – 700-1000nmspectrum – 700-1000nm
 Concern over extracranial circulation contriutionConcern over extracranial circulation contriution
 Maintaining regional saturation (rS02) > 75%Maintaining regional saturation (rS02) > 75%
reduced strokes after bypass (Murkin et al,2004)reduced strokes after bypass (Murkin et al,2004)
 Correlation between low rS02 and low GCSCorrelation between low rS02 and low GCS
(Dunham 2004)(Dunham 2004)

14. The Evidence for NIRSThe Evidence for NIRS

16. Pbt02 – SJV02Pbt02 – SJV02
 SJV02 –Fibreoptic catheter measures venousSJV02 –Fibreoptic catheter measures venous
saturation of presumed dominant drainge sidesaturation of presumed dominant drainge side
 Placed in IJ – tip at level mastoid air cells = JugularPlaced in IJ – tip at level mastoid air cells = Jugular
bulbbulb
 The normal range of SjOThe normal range of SjO22, confirmed in a study of, confirmed in a study of
healthy young men, is 55%-71% (Feldman &healthy young men, is 55%-71% (Feldman &
Robertson, 1997).Robertson, 1997).
 Values below 55% reflects ischaemiaValues below 55% reflects ischaemia
 The ischemic threshold has been reported to be anThe ischemic threshold has been reported to be an
SjOSjO22 of less than 50% for at least 10 minutes, withof less than 50% for at least 10 minutes, with
multiple episodes contributing to poor outcomemultiple episodes contributing to poor outcome
(Robertson et al., 1995).(Robertson et al., 1995).

17. Decreased SJV02 valuesDecreased SJV02 values
 Decreased 02Decreased 02
deliverydelivery
 Increased ICPIncreased ICP
 ExcessiveExcessive
HypocapnoeaHypocapnoea
 HypoxiaHypoxia
 HypotensionHypotension
 AnaemiaAnaemia
 SepsisSepsis
 Increased 02Increased 02
consumptionconsumption
 SeizuresSeizures
 HyperthermiaHyperthermia
 PainPain
 Insufficient sedationInsufficient sedation

18. Increased SJV02 ValuesIncreased SJV02 Values
 Increased deliveryIncreased delivery
 Increased CPPIncreased CPP
 HypercapnoeaHypercapnoea
 HypertensionHypertension
 VasodilationVasodilation
 Increased arterial 02Increased arterial 02
 A-V malformationA-V malformation
 DecreasedDecreased
consumptionconsumption
 ComaComa
 Brain DeathBrain Death
 Deep sedationDeep sedation
 Cerebral InfarctionCerebral Infarction
 HypothermiaHypothermia
 Hyperaemic phase ofHyperaemic phase of
TBITBI

19. Evidence for SJV02Evidence for SJV02
 Only level 3 evidence for SJV02 in BTFOnly level 3 evidence for SJV02 in BTF
guidelinesguidelines
 Variable Values reported to representVariable Values reported to represent
ischaemia – 55-60%ischaemia – 55-60%
 Prompt treatment required - 10 mins =Prompt treatment required - 10 mins =
poor outcomepoor outcome (Nemani & Manley, 2004)(Nemani & Manley, 2004)
 Multiple episodes contribute to poorMultiple episodes contribute to poor
outcomeoutcome (Robertson et al., 1995)(Robertson et al., 1995)

20. Evidence for SJV02Evidence for SJV02
 A group of patients managed by targetingA group of patients managed by targeting
optimal SjOoptimal SjO22 levels and CPP enhancementlevels and CPP enhancement
had better outcomes than a group ofhad better outcomes than a group of
patients managed with CPP-targetedpatients managed with CPP-targeted
therapy alone (Cruz, 1998).therapy alone (Cruz, 1998).
 However-up to half reported desatHowever-up to half reported desat
episodes are false positives (Scheinbergepisodes are false positives (Scheinberg
1992)1992)

21. Pbt02 - CathetersPbt02 - Catheters
 Invasive – Pbt02 probesInvasive – Pbt02 probes
 LICOX – measures 02 and TemperatureLICOX – measures 02 and Temperature
CODMAN – measures 02, C02 and pHCODMAN – measures 02, C02 and pH
 Accurate to only 15mm squared aroundAccurate to only 15mm squared around
probe tipprobe tip

22.  Optimum depth for placement is 25-35mmOptimum depth for placement is 25-35mm
into brain. And placement in penumbra vsinto brain. And placement in penumbra vs
unaffected side of the brainunaffected side of the brain
 According to Nemani and Manley (2004),According to Nemani and Manley (2004),
placing the catheter in the contralateralplacing the catheter in the contralateral
hemisphere in a normal brain produceshemisphere in a normal brain produces
values more reflective of global brain oxygenvalues more reflective of global brain oxygen
even though it is still a regionaleven though it is still a regional
measurement.measurement.
 Nemani and Manley (2004) point out that trueNemani and Manley (2004) point out that true
"normal" values have never been determined,"normal" values have never been determined,
because the catheters have not been placedbecause the catheters have not been placed
in healthy volunteers;in healthy volunteers;

23. The Pbr02 DataThe Pbr02 Data
 Critical threshold levels where poorer outcomes have beenCritical threshold levels where poorer outcomes have been
identified differ between the two systems.identified differ between the two systems.
 In two studies using theIn two studies using the CodmanCodman system, vegetative state orsystem, vegetative state or
death resulted when PbtOdeath resulted when PbtO22 was less than 25 mm Hg or 31 mmwas less than 25 mm Hg or 31 mm
Hg, respectively (Doppenberg et al., 1998; Zauner et al.,Hg, respectively (Doppenberg et al., 1998; Zauner et al.,
1996).1996).
 In studies using the LICOX system, critical thresholds whereIn studies using the LICOX system, critical thresholds where
poor outcomes occurred varied. The PbtOpoor outcomes occurred varied. The PbtO22 threshold levelsthreshold levels
identified were below 15 mm Hg, below 10 mm Hg, and anyidentified were below 15 mm Hg, below 10 mm Hg, and any
occurrence below 6 mm Hg (van den Brink et al., 2000; Bardtoccurrence below 6 mm Hg (van den Brink et al., 2000; Bardt
et al., 1998; Valadka, Gopinath, Contant, Uzura, & Robertson,et al., 1998; Valadka, Gopinath, Contant, Uzura, & Robertson,
1998). The length of time under the particular threshold1998). The length of time under the particular threshold
measured also influenced poor outcomes.measured also influenced poor outcomes.

24. Evidence for Pbt02Evidence for Pbt02
 1996 reduced 02 reactivity correlates with1996 reduced 02 reactivity correlates with
improved outcome, pbr02 of 5mmHg orimproved outcome, pbr02 of 5mmHg or
less 24hours after injury = poor outcomeless 24hours after injury = poor outcome
 Cerebral hypoxic episodes more frequentCerebral hypoxic episodes more frequent
in those with worse outcomein those with worse outcome
 Patients with Pbt02 monitoring as well asPatients with Pbt02 monitoring as well as
ICP and CPP monitor had significantlyICP and CPP monitor had significantly
less mortality vs ICP and CPP aloneless mortality vs ICP and CPP alone
(Steifel et al 2005)(Steifel et al 2005)

25. MicrodialysisMicrodialysis
 Double-lumen probe with dialysis membrane atDouble-lumen probe with dialysis membrane at
tip. Perfused with isotonic fluidtip. Perfused with isotonic fluid
 Sample brain tissue ECF and placed inSample brain tissue ECF and placed in
penumbra = most vulnerablepenumbra = most vulnerable
 Cerebral hypoxia correlates with increasedCerebral hypoxia correlates with increased
lactate/pyruvate ratio Normal = <25lactate/pyruvate ratio Normal = <25
 Increased ratio = focal ischaemia BUT mayIncreased ratio = focal ischaemia BUT may
represent failure utilisation of 02 by mitochondriarepresent failure utilisation of 02 by mitochondria

26. MicrodialysisMicrodialysis
 Glycerol – componant of cell membranesGlycerol – componant of cell membranes
Increased level = increased cell breakdownIncreased level = increased cell breakdown
Typically high in first 24hrs – late peaks fromTypically high in first 24hrs – late peaks from
seizures or ischaemiaseizures or ischaemia
 Glucose – low levels = hyperglycolysis orGlucose – low levels = hyperglycolysis or
decreased supplydecreased supply
 Glutamate – excitatory AAGlutamate – excitatory AA
Elevated earlyElevated early
Late peaks due to secondary damageLate peaks due to secondary damage

27. Microdialysis - EvidenceMicrodialysis - Evidence
 Not in BTF guidelinesNot in BTF guidelines
 Normal levels of cerebral chemicals include aNormal levels of cerebral chemicals include a
lactate - pyruvate ratio of 15-20, a glutamatelactate - pyruvate ratio of 15-20, a glutamate
level of 10 mcm, and a glycerol level of 50-100level of 10 mcm, and a glycerol level of 50-100
mcm with a 10-mm dialysis membranemcm with a 10-mm dialysis membrane
(Ungerstedt & Rostami, 2004)(Ungerstedt & Rostami, 2004)
 Increased LPR and Glycerol may predictIncreased LPR and Glycerol may predict
delayed ischaemic deficit due to vasospasm 11-delayed ischaemic deficit due to vasospasm 11-
23 hours before clinical appearance (Tisdall23 hours before clinical appearance (Tisdall
2006)2006)
 Largely research tool at presentLargely research tool at present

28. SummarySummary
 ICP monitoring via EVD is gold standardICP monitoring via EVD is gold standard
and supported by level 2 evidenceand supported by level 2 evidence
 SJV02 <50% is a level 3 recommendedSJV02 <50% is a level 3 recommended
treatment thresholdtreatment threshold
 Other monitiring modalities of varying useOther monitiring modalities of varying use
but have no recommendations from thebut have no recommendations from the
guidelinesguidelines

29. ReferencesReferences
 ‘‘Gizmos and Gadgets for the Neurointensive Care Unit’Gizmos and Gadgets for the Neurointensive Care Unit’
MK Bader Medscape Critical Care. 2007MK Bader Medscape Critical Care. 2007
 BTF Guidelines 2007 J Neurotrauma Vol 24 Suppl 1BTF Guidelines 2007 J Neurotrauma Vol 24 Suppl 1
 Continuous Monitoring of Partial Pressure of BrainContinuous Monitoring of Partial Pressure of Brain
Tissue Oxygen in Patients with Severe Head InjuryTissue Oxygen in Patients with Severe Head Injury..vanvan
Santbrink,Santbrink, Henk.; Maas, Andrew Avezaat, Cees J.J.Henk.; Maas, Andrew Avezaat, Cees J.J.
Neurosurgery. 38(1):21-31, January 1996.Neurosurgery. 38(1):21-31, January 1996.
 Traumatic Brain Injury: Management on theTraumatic Brain Injury: Management on the
Neurointensive Care Unit Clemens Pahl FRCA DICMNeurointensive Care Unit Clemens Pahl FRCA DICM
Consultant Intensivist King’s College HospitalConsultant Intensivist King’s College Hospital

30. ReferencesReferences
 Monitoring the Injured Brain. Gupta AK. JMonitoring the Injured Brain. Gupta AK. J
Postgraduate Med 2002:48;218-225Postgraduate Med 2002:48;218-225
 Reduced Mortality Rate in patients severeReduced Mortality Rate in patients severe
traumatic brain injury treated with brain tissuetraumatic brain injury treated with brain tissue
oxygen monitoring. MF Stefel et al. J Neurosurgoxygen monitoring. MF Stefel et al. J Neurosurg
103:805-811;2005103:805-811;2005
 Cerebral Microdialysis;research technique orCerebral Microdialysis;research technique or
clinical tool? BJA 2006:97;18-25clinical tool? BJA 2006:97;18-25
 Neuromonitoring. M Smith. Anaesthesia andNeuromonitoring. M Smith. Anaesthesia and
Intensive Care Medicine;9;5;2008Intensive Care Medicine;9;5;2008