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1、CRITICALCAREThepathophysiologyandcausesofraisedintracranialpressureKathrynMayntracranialpressure(ICP)isthepressureexertedbytheintracranialIcontentsagainsttheskull.Theskull,AbstractwhichisarigidstructurewithafixedThisarticleexplainsthepathophysiologyandcausesofraisedintracranialinternal,non-compressi
2、ble,volumeofpressure(ICP),andthesignificanceofassessingandrecordingvital1400–1700mlisapproximately85%filledobservationsforallpatientswhenadmittedtohospital.Itdiscussesthebythebrain(5%extracellularfluid,45%nursingcare,treatmentandmanagementrequiredinordertominimizetheglialtissueand35%neuronaltissue),7
3、%riskoffurtherincreasesinICP.bloodand8%cerebrospinalfluidaccountKeywords:InterventionsnObservationsnPathophysiologyfortheremainingapproximate15%ofthenRaisedintracranialpressureskullcontents(LittlejohnandBader,2001).Sincetheskull’scontentsareincompressible,ifoneofthethreecomponents(brain,bloodorcereb
4、rospinalfluid)increasesinvolume,consequence;however,cerebralarterialbloodICPof25–40mmHg.WhenICPexceedsthenthismustbecompensatedforbyaflowlimitationandbrainherniationresultin40mmHg,thecerebralperfusionpressuredecreaseinthevolumeofoneormorecerebralischaemiaandinjury.decreasestoalevelthatresultsinlosso
5、ftheremainingcomponentsotherwiseAsICPrises,cerebralperfusionpressureofconsciousness(Trauma.org,2008).theICPwillincrease(theMonro-KelliefallstoapointwhenthereisnocerebralNeurologicchangesseeninincreasedICPdoctrine)(Kellie,1823;Monro,1823).bloodflow,nocerebralperfusionandaremostlyduetohypoxiaandhyper
6、capneaThenormalICPlevelis0–10mmHgbraindeath(Robertson,2001).Adireandifmasseffect(damagetothebrain(Lundberg,1960),andincreasedICPisconsequenceofincreasedICPcombinedthroughincreasedpressure)ispresent,asustainedelevationinpressureabovewithaspace-occupyingprocessisbrainwithresultingdisplacementofbraint
7、issue,20–25mmHg,causedbyanincreaseintheherniation(usuallyuncalorcerebellar),inadditionalsignsmayincludepupillaryvolumeoftheintracranialcontents.whichthebrainissqueezedpaststructuresdilatationandtheCushing’s