Brain edema

causes ,pathophysiology, management of brain edema

1. MarwaElhady
Lecturer of pediatrics
Faculty of medicine for girls. Al-AzharUniversity
2015

2. •Thebrainresidesinarelativelyrigidcranial
vaultwiththecranialcompliance↓withage
astheskullossificationgraduallyreplace
cartilagewithbone.
Brain
80%
CSF
10%
Blood
10%
•Intracranialdynamicsdescribesthe
interactionsofthecontents—brain
parenchyma,bloodandCSF—within
thecranium.

3. CPP = MAP -ICP
Intracranial
pressure
Blood
perfusion
pressure
Ischemic
necrosis
If

4. Cerebral blood flow
•CBF is generally independent of mean arterial
pressure but it is closely regulated by arterial
PaCO₂ systemically and locally by regional
factors such as release of endothelin and NO.

5. Factors affects cerebral blood flow (CBF)
•Autoregulation: CBF maintaied inspite of ∆ BP
•Acid-base balance of the CSF (co2 is vasodilator)
•body/brain temperature: Hyperthermia→
↑cerebral metabolic demands → cell damage
•glucose utilization: Hypoglycemia →cell death
•Hypoxemia as in prolonged siezures, HIE
•vasoactive mediators (i.e., adenosine, NO)

6. Mechanisms of BBB dysfunction
1.Physical disruption by arterial hypertension
→direct transmission of pressure to cerebral
capillary with transudation of fluid into the
extracellular fluid
2. Trauma with bleeding
3. Toxin, inflammation
4.Tumorreleaseofvasoactiveandendothelial
destructivecompoundseg.arachidonicacid,excitatory
neurotransmitters,histamine,freeradicals;vascular
endothelialgrowthfactorswhichweakensjunctionsofBBB.

7. •Cerebraledemaisalife-threatening
condition
•Brainedemaisdefinedasanabnormal
accumulationoffluidwithinthebrain
parenchyma,producingavolumetric
enlargementofthetissue.

8. Mechanism of brain edema
•changesintheBBB,bloodosmolality,
dysregulatedbloodflow,or↑capillary
pressurewillinfluencethepermeabilityofBBB
→passivediffusionofwater,ions,protiens,
andothercompoundsinthebrain.
•Itcanbeconsequenceofcerebraltrauma,
massivecerebralinfarction,hemorrhages,
abscess,tumor,allergy,sepsis,hypoxia,and
othertoxicormetabolicdisorders.

10. 1. Cytotoxic
•PermeabilityoftheBBBisnormalandedema
resultsfromadisturbanceinionichomeostasis.
•Itoccursduetoadisruptionincellular
metabolismthatimpairsATPdependantNa/K
pumpintheglialcellmembrane→cellularinflux
ofNaandwater.
•Swollenastrocytesofbothgreyandwhite
matter→lossofnormalgreywhitematter
interphase.

11. 2-Vasogenic
•duetoabreakdownofthetightendothelial
junctions→disturbBBB→↑vascular
permeability→accumulationofedemafluid
intheextracellularspaces
•Thistypeofedemaisseeninresponseto
trauma,tumors,focalinflammation,andlate
stagesofcerebralischemia.

12. Vasogenic (cont.)
•confinedtowhitemattersparescorticalgrey
matter,andpronouncesthegreywhite
matterinterphase

13. In cytotoxic edema:
influx of fluid inside
the brain cells
In vasogenicedema:
influx of fluid into
the interstitial space

14. involves both cortical grey &
white matter
loss of normal grey white
matter interphase.
confined to white matter, with
finger like projections extending
in sub cortical white matter.
Spares cortical grey matter.
Grey white matter interphase is
pronounced instead of loss.
In vasogenic edema:In cytotoxic edema:

15. 3-Interstitial cerebral edema
•Resultfromacuteobstructivehydrocephalus.
•CSFpushedintoextracellularspacein
extracellularspacesofthepreiventricular
whitematterinhydrocehalous

16. 4-Osmotic cerebral edema
•Result from dilution of blood (↓ osmolarity)
•Normally CSF and brain’s extracellular fluid
osmolality is slightly lower than plasma.
•If↓plasmaosmolarity,thebrainosmolality
willexceedtheserumosmolalitycreatingan
abnormalpressuregradientresultinwater
influxintothebraincausingedema.

17. Osmosis and semi-permeable cellular membrane
Hypo Os
Hyper Os
Hypo Os
Hyper Os
Swelling
Shrinkage

18. Osmotic cerebral edema (cont.)
•Causesincludehyponatremia,SIADH,
hemodialysis,orrapidreductionofblood
glucoseinDKA,rapidcorrectionof
hypernatremia,infusionofhypotonic
solusion.

19. 5-Hydrostatic
•Thisformofcerebraledemaisseeninacute,
malignanthypertension.
•Itisthoughttoresultfromdisturbanceof
theautoregulationofcerebralblood
circulationwithdirecttransmissionof
pressuretocerebralcapillarywith
transudationoffluidintotheECF.

20. CYTOTOXIC VASOGENICINTERSTITIALOSMOTIC HYDROSTATIC
Pathophysi
ology
#cellular
metabolism
#Na/K pump
BBB
breakdown
CSF leak ↑Osmotic
gradient
↑Hydrostatic
gradient
pathologyCell swelling↑Capillary
permeability
hydrocephalus↑ blood
osmolarity
hypertension
content Water, Na
no protein
Plasma
highprotein
CSF
Low protein
Water
no protein
Water, Na
no protein
locationGray & white
matter
White
matter
Periventricular
white matter
White
matter
White matter
ECF ↓ ↑ ↑ ↑ ↑
BBB intact disturbedintact intact intact
steroid No effect effectiveNo effect No effectNo effect
diureticsTransient
effect
Minimal
effect
Transient
effect
Minimal
effect
Transient
effect
CLASSIFICATION OF CEREBRAL EDEMA

21. Increased intracranial pressure
Brain edema

22. Clinical presentation
Manifestation of ↑ICP
–Headache
–Vomiting
–Diplopia,visualloss
Cushing triad: Hypertension, Bradycardia, Papilledema
Siezure
Disturbed conscious level
Herniationsyndromes
Clinical sings of brain edema start to appear when ICP
exceed 30mmHg

23. •ICPisderivedfromthevolumeofbrain
componentsandthebonycompliance.
•↑inICvolumecanresultfromswelling,
masses,or↑inbloodandCSFvolumes
•↑ICP→↓CPP→brainischemia
•Further↑inICP→cerebralherniation

24. cingulate herniation
uncal herniation
Central herniation
Cerebellar tonsillar herniation
Upward cerebellar herniation

25. Cerebral edema
Pathological increase in the water content of the brain
Increased intracranial pressure
Neurological deterioration
Herniation
Death

26. Management
•Treatmentofcerebral
edemaiscomplex
•Goodprognosisonlyif
thediagnosisandthe
managementdecision
aretimely.

27. General Measures for
Managing Cerebral Edema
1.Optimizing Head and Neck Positions
2.Ventilation and Oxygenation
3.Maintain Intravascular Volume and Cerebral
Perfusion
4.Seizure Prophylaxis
5.Management of Fever and Hyperglycemia
6.Nutritional Support

28. Optimizing Head and Neck Positions
•30̊elevationoftheheadinpatientsisessential
for
–AimfordecreasingCSFhydrostaticpressure.
–Butavoidingjugularcompressionandimpedanceof
venousoutflowfromthecranium
•avoidtheuseofrestrictingdevicesaroundthe
neckwhichmaycompressinternaljugularveins.
•Headpositionelevationmaybedetrimentalin
ischemicstroke,becauseitmaycompromise
perfusiontoischemictissueatrisk.

29. Ventilation and Oxygenation
•Hypoxiaandhypercapniaarepotentcerebral
vasodilator
•MaintainePaCO2>30mmHgtosupportadequate
CBForCPPtobrain
•maintenPaO2atapproximately100mmHg
•Ptshouldbeintubatedin:
1.GCSscoreslessthanorequalto8
2.Patientswithpoorupperairwayreflexesbeintubated
forairwayprotection.
3.PulmonarydisorderegARDS,aspirationpnemonia
•AvoidhighPEEP→#systemicvenousreturn,↓COP

30. Maintain Intravascular Volume and
Cerebral Perfusion
•Maintain CPP level >60 mmHg
CPP=MAP-ICP
NORMAL CPP= 70 -90 mm of Hg
•IfhypertensionavoiduseofPotent
vasodilatorseg.Nitroglycerine,Nitroprusside
astheymayexacerbatecerebraledemavia
accentuatedcerebralhyperemiaduetotheir
directvasodilatingeffectsoncerebralvs.

31. Seizure Prophylaxis
•Phenobarb and phenytoin specially in brain
trauma (used for 1-2 weeks)
Fever control
Fever → ↑O2 consumption so worsen out come

32. Maintain blood glucose
•Avoid hypoglycemia → brain cell damage
•Avoid hyperglycemia →↑ brain injury →
worse cerebral edema
Nutritional Support
•High caloric intake
•Unless CI, enteral route is preferred
•avoid free water intake →hypoosmolarstate
and worsen cerebral edema

33. Specific Measures for
Managing Cerebral Edema
1.Controlled Hyperventilation
2.Osmotherapy
3.Corticosteroid Administration
4.Therapeutic Hypothermia
5.Other Adjunct Therapies

34. Osmotherapy
•Osmotic therapy draw water out of the brain
by an osmotic gradient and help to decrease
blood viscosity.
•These changes ↓ICP and ↑CBF.
•CI of manitol ttt
–Acute tubular necrosis, Anuria
–Cerebral haemorrhage.
–Pulmonary edema, CHF

35. •Osmoticdiureticsareshort-lasting
•mayberepeatedprovidedplasmaosmolarity
doesnotexceed320mOsm.
•Theosmoticeffectcanbeprolongedbythe
useofloopdiuretics(Furosemide)afterthe
osmoticagentinfusion.

36. Corticosteroid Administration
•Usedinvasogenicedema
•steroidsdecreasecapillariespermeabilityand,in
turn,stabilizethedisruptedBBB,promotingthe
movementofNa+/K+ionsandwaterthrough
themainendothelialmembrane
•Glucocorticoids,especiallydexamethasone,are
thepreferredsteroidalagents,duetotheirlow
mineralocorticoidactivity

37. •Controlledhypothermia→↓therateof
metabolisminthebrain.
•Slightlypositivefluidbalanceshouldbe
maintainedusingcrystalloidorcolloid
(hypertonic–hyperoncotic)solutions,atthe
sametimemaintainingcerebralperfusion
pressureexceeding70mmHg.

38. •Extendedcerebraledemaistreatedsurgically
viaabilateraldecompressivecraniotomy,
whichallowsthebraintoexpandasit
continuestoswell