monro-kellie 2 - intensivistenopleidingintensivistenopleiding.nl/downloads-25/files/monro-kellie...
TRANSCRIPT
Monro-Kellie 2.0
PresentatieMDO17-08-2016L.L.A.Bisschops
Thedynamic vascular andveneuspathophysiological components ofICP
Wilson, Journal of Cerebral Blood Flow &Metabolism, 2016
1783‘Science ofICP’
AlexanderMonro1733-1817
Monro described theskull asarigid structurecontaining incompressible brain andstated thatthevolumeofblood mustremain constantunless:‘wateror other matteriseffused orsecreted from theblood-vessels’inwhich case‘aquantity ofblood,equal inbulktotheeffusedmatterwill be pressed outofthecranium’.
1824‘Science ofICP’Confirmation ofMonro’s doctrineinhuman andanimal studies:cerebral (inparticular,venous)blood volumewassimilar no matterwhat thecause ofdeath (hanging,exsanguination)was.
GeorgeKellie1720-1779
ATLSCourseManual 9thedition
Cushing doctrine:sum ofvolumeofthebrain,blood andCSFisconstant.
This description fails toexplain theimportance ofvolumeflow
Thedynamic components ofICP
StaticMonro-Kellie doctrine:Equal weighting toblood andCSFmisses thedynamic reality.
Averagemalebrain volume1473ml(brain/CSF/blood)Intracranial blood volume:100-130mlCSFvolume:75ml
Slowandsteady production ofCSF (≈0.35ml/min)Substantial,continuous blood inflow andoutflow(≈700ml/min,14%ofCO)
Thedynamic components ofICPNormal ICP≈5-15mmHg
- Greatly influenced by orthostatic postition(ICPcan be negativewhen standingup).
- Generally similar tocerebral venouspressures (if no distalobstruction).
Dynamic components:Arterial influence on ICPVenous influence on ICPExtracranial causes ofcerebral venous hypertension
Thedynamic components ofICPArterial influence on ICP
CPP=MAP- ICPICP=MAP- CPP;implies no venous involvementGuidelines:MAP>80-90,RRsyst >90mmHgHowever:Cerebral Blood Flow resulting fromanyMAPwill differ betweenindividuals (autoregulation,PaCO2)
‘static’viewoffactorsregulating ICP,andfocuson arterial inflow alone,ledtoneglect ofimportantinfluence ofcerebral veins
Thedynamic components ofICPVenous influence on ICP
CorticalDeeper (anterior)Central(thalamic)
Nomuscular wall:vulnerable tocompression
Thedynamic components ofICPArole forveinsinfluencing ICP
Failure for (intra- andextracranial)venous efferent flow toprecisely matcharterial afferent flow yields immediate anddramaticchanges inintracranialvolumeandpressure.
asCBF↑,venous drainage↑,with limited venous distension IVPwill riseupstream,andthus ICP(similar toMonro-Kellie doctrine).
Causes ofraised cerebral venouspressure
Diffusecompression ofthevenous system
Concurrentacutesubdural removementandsplenectomy
Relative venous outflow restriction
Intracraniallyisolateddiffuse
Extracranially
ConclusionBalance between cerebral inflow andoutflow isvital
Restrictions inoutflow can be assignificantasmass accumulation within thecranium
Concentration ofinterestinICP/CPP,neglect for venous side
ICPisafunction ofvenous outflow:acombination ofintra-cerebral resistance,andcervical,thoracic andabdominal pressures
If no resistance tovenous outflow:ICP=0.IVfluids to‘maintain CPP’increaseCVPandcanworsen ICP