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7/23/2019 Hetty Jurnal

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A review of progress in understanding the pathophysiologyand treatment of brain edema

Pembimbing:dr. Susatyo Pramono Hadi, Sp.S

Disusun oleh:Hetty Dwi Putri01.210.6180

FAKULTAS KEDOKTERAN

UNIVERSITAS ISLAM SULTAN AGUNG

SEMARANG



JO!"A# $D%"&$'$(A&$O"Tittle :

A review of progress i !"erst#"ig t$e

p#t$op$%siolog% # tre#t&et of 'r#i e"e&#

Fro& : Department of Neurosurgery, Virginia

Commonwealth University Medical Center, Richmond,

Virginia(riter : ANT)ON* MARMAROU+ ,)-D-

,!'lis$e" : Ne!ros!rg Fo.!s // 012:E3+ /445



)ethods. $n this paper theauthor provides a review ofprogress over the past severalde*ades in understanding thepathophysiology of the

edematous pro*ess and thesu**ess and failures oftreatment. !e*ent progressfo*used on those manus*riptsthat were published within thepast + years.

Abstract

Object. rain edema resulting

from traumati* brain in-ury &$/or is*hemia if un*ontrollede0hausts volume reserve andleads to raised intra*ranialpressure and brain herniation.



!esults. Spea1 to both the *ontrol

of produ*tion and resolution ofedema in both trauma andis*hemia are the re*ent studiesthat have fo*used on the newlydes*ribed 2water *hannels3 ora4uaporins.

Conclusions. Significant new findingshave been made in understanding the

pathophysiology of brain edema.

Aquaporin water channels offer hope formodulatin and abatin the de!astatineffects of fulminatin brain edema intrauma and stro"e.

Abstract



In the case of TBI, the swelling process has

been classified into four distinct degrees ofseverity based on studies in the Traumatic

Coma Data Bank.Of great importance is the

fact that the degree of swelling assessed on

the first computed tomography scan,

obtained soon after inury, was highly

correlated with outcome !p , "."""#$and itsuggests that therapy must be commenced

as soon as possible to avoid neurological

deterioration or even death.

I%T&OD'CTIO%



I%T&OD'CTIO%

The reason for this may be e(plained

by the e(ponential relationshipbetween IC) and brain water

content. *s edema develops, a

threshold is reached in which IC)

rises e(ponentially to small changes

in brain edema.



• #dema is an abnormalaccumulation of fluid within

the brain parenchyma$ it issubdi!ided into !asoenic andcytoto%ic types

• &asoenic edema is defined

as fluid oriinatin from blood!essels that accumulatesaround cells.

• 'ytoto%ic edema is definedas fluid accumulatin withincells as a result of in(ury. )hemost common cytoto%icedema occurs in cerebralischemia.

EDEMA



*n the case of !asoenic edema+protein e%tra!asation secondary tobarrier compromise was implicatedin the edematous process.

*t was shown that protein in the

e%tracellular space retards theclearance of fluid+but no e!idenceto date has been put forth tosubstantiate that e%tracellularprotein increases fluid entry intobrain. ,ust as protein in the

e%tracellular space has been shownto retard clearance+ lowerin the*'P enhances clearance of fluidfrom the brain+ while steroids ha!eneliible effect on the clearanceprocess

TYPES OF EDEMA



)he treatment of cellular edema is far more comple%+ i!en that

a precise identification of the processes that o!ern resolution aswell as entry of fluid into the cell is un"nown. 'ellular brain

edema is a life-threatenin complicationof cerebral infarction.

&he $mportan*e of (ellular %dema

ew dianostic methodsbased on / imain ha!e

mar"edly impro!eddianostic accuracy.

'ytoto%ic and !asoenicedema arereatest by 2 to2 hours after the ischemic

e!ent.

)hrombolytics reperfuse tissueand impro!e outcome$ when

treatment is delayed+ they canincrease edema and 333 openin.



esults of both e%perimental and clinicalstudies ha!e indicated that cerebral edemade!elops followin acute reional ischemiaand can cause mass effect and herniationthat results in a further decrease in '34.

5ith onoin ischemia+ the core reion ofimpaired metabolism e%pands+ leadin toradual infarction of the penumbra.

)reatments for the combination of

ischemic edema and e!entual !asoenicedema secondary to barrier compromiseha!e not been successful+ and more wor"needs to be done+ not only to elucidate thepathophysioloy but to better understandthe process of cellular edema resolution

(ellular %dema in $s*hemia



%dema Development'ollowing $ntra*erebralHemorrhage

)he !asoenic and cellular

components of edema followintrauma andor ischemia are welldescribed.

Howe!er+the cause of the edemade!elopment followin

intracerebral hemorrhae remainsun"nown.



(ellular %dema in&$

esults of recent studies of )3* ha!eindicated that the predominant type ofedema in these in(uries is cellular.

)hese results ha!e been confirmed byother in!estiators that ionic dysfunctionoccurs with )3* and that e%tracellular 7is transiently increased as a result of thedepolari9ation synchronous withmechanical insult.



%ffe*t of Hypothermia on (ellular %dema

/ild hypothermia on the order of :2;' has

been shown to be neuroprotecti!e.

*t was obser!ed that hypothermia itself wascausin sinificant swellin of lial cells in adose-dependent manner.

Howe!er+ mild or moderate hypothermiafailed to pre!ent cell swellin from otherto%ins <lactic acid+ arachidonic acid+ orlutamate=+ mediatin the de!elopment ofcytoto%ic brain edema.

As a result+ it was considered that cerebralprotection by hypothermia in !i!o is mostli"ely not attributable to an inhibition ofcytoto%ic brain

edema



%ffe*t of Steroids on rain%dema

'linical trials of lucocorticoids inischemic stro"e+ intracerebralhemorrhae+ aneurysmal

subarachnoid hemorrhae+ and )3*ha!e not shown a definitetherapeutic effect.

*n clinical trials for head in(ury andstro"e+ corticosteriods ha!e notbeen shown to be effecti!e intreatin cellular edema.



)he identification of the A>Pfamily+ a water-conductinprotein-based channel consistinof 11 subtypes ubiquitouslydistributed in tissues andoranisms+ was a landmar"disco!ery. Despite a commonmolecular structure+ mammalianA>Ps ha!e been subdi!ided intothree functional roups accordinto permeabilitycharacteristics

A4uaporins and &heir Pivotal !ole in%dema



/anley et al showed in A>P-deficient mice a :?@ decrease ofcerebral edema followin middlecerebral artery occlusion+ as

measured by the percentae ofhemispheric enlarement.Alterations in the e%pression ofA>P in cultured rat astrocytesdurinhypo%ia and reo%yenationwere also noted

A4uaporins and &heirPivotal !ole in %dema



(learan*e of 5asogeni*%dema

)he processes in!ol!ed in theresolution of !asoenic edemaare better understood than thoseof cellular edema. 4luid mo!esthrouh the interstitium !ia both

bul" flowand diffusion processes.

*n !asoenic edema clearance+ )hree possiblemechanisms ha!e been considered to be responsiblefor clearance of e%tracellular water1=miration of e%tracellular water to the 'B4 by bul"flow in the presence of pressure radients2= lial upta"e of the protein components of edemafluid$:= e!erse !esicular transport from the blood !iatransendothelial passae



$maging &e*hni4ues sed in $dentifying the &ype of %dema

*t is possible with the aid of /

imain techniques to measure thediffusion of water in brain tissue.)his is usually e%pressed as theAD'. A reduction in AD' isinterpreted as a decrease indiffusion+ whereas an increase inAD' is associated with an increasein diffusion. *n cellular edema+ thewater is more closely bound andthus it would be e%pected to resultin a decreased AD'.

)o test this+ cytoto%ic edemasecondary to acute hyponatremiawas induced with intraperitonealin(ections of 2.?@ de%trose inwater and a subcutaneous in(ection

of arinine !asopressin.



Summary

5e now appreciate that the abatement ofthe edematous process will depend on thetype of edema that is contributin to tissue

swellin. #%tracellular or !aso-enic edemaproduction is dri!en by barrier dynamicsfollowin in(ury.

)reatments such as hypothermia+ which willsuppress proloned secondary openin ofthe barrier+may pro!e to be effecti!e

therapies. )he depth of hypothermia+ itsduration+ and ideal rates of rewarminha!e yet to be established

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