Download Intracranial Hypertension - Emory Department of Pediatrics

Intracranial Hypertension
Fellows Conference
Sept 07
Historical Perspective
 Alexander Monro 1783 described cranial vault as non
expandable and brain as non compressible so inflow
and out flow blood must be equal
 Kelli blood volume remains constant
 Cushing incorporated the CSF into equation 1926
 Eventually what we now know as Monro-Kelli
doctrine

Intact skull sum of brain, blood & CSF is constant
CSF
 Choroid plexus > 70 % production
 Transependymal movement fluid from brain
to ventricles rest
 Average volume CSF in child is 90cc (150cc
in adult)
 Make about 500cc/d
 Rate production remains fairly constant

w/ increase ICP it is absorption that changes
CBF
 Morbidity related to ICP is effect on CBF
 CPP = MAP- ICP or CPP= MAP- CVP
 Optimal CPP extrapolated from adults
 In intact brain there is auto-regulation

Cerebral vessels dilate in response to low
systemic blood pressure and constrict in
response to higher pressures
CBF
CBF
50
150
MAP
CBF
125
PaCO2
CBF
Pao2
0
125
CPP
CBF
 CBF is usually tightly coupled to cerebral
metabolism or CMRO2

Normal CMRO2 is 3.2 ml/100g/min
 Regulation of blood flow to needs mostly
thought to be regulated by chemicals
released from neurons. Adenosine seems to
be most likely culprit
Cerebral Edema
 Vasogenic
 Increased capillary permeability disruption BBB
 Tumors/abscesses/hemorrhage/trauma/ infection
 Neurons are not primarily injured
 Cytotoxic
 Swelling of the neurons & failure ATPase Na+ channels
 Interstitial
 Flow of transependymal fluid is impaired (increased
CFS hydrostatic pressure
Monitoring
 Intra-ventricular
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Gold standard
Can re zero
Withdraw CSF
Infection rate about 7%
Rate does not increase after 5 days
Monitoring
 Intra-parenchymal



Placed directly into brain easy insertion
Can’t recalibrate has drift over time
Minimal differences between intra-ventricular
& parenchymal pressures

ventricular ~2 mmHg higher
Wave forms
 Resembles arterial wave form
 Can have respiratory excursions from changes in
intrathoracic pressure
 B waves



rhythmic oscillations occurring aprox. every minute
with amplitude of up to 50mmHg
associated with unconsciousness/periodic breathing
 Plateau waves
 above baseline to a max. of 50-100mmHg
 lasting 5-20min
 associated baseline ICP > 20mmHg
Wave forms
Monitoring
 CT


Helpful if present
Good for skull and soft tissue
 MRI w/ perfusion


Assess CBF
Can detect global and regional blood flow
difference
 PET

Gold standard detect CBF
Monitoring
 Kety –Schmidt
 Uses Nitrous as an inert gas tracer and fick principle
looking at arteriovenous difference
 CO = VCO2 [ml/min]/(CO2art-CO2ven) [ml/L]
 Labor intensive not practical
 Jugular Bulb
 Global data looking at CBF w/ regard to demand
 Correlation between number of desats and outcome
 NIRS
 Measures average cerebral sats
 Usefulness not established
Treatment
Head position
 Keep midline for optimal drainage
 HOB 30 deg



MAP highest when supine
ICP lowest when head elevated
30 degree in small study gave best CPP
Treatment
Sedation & NMB
 Adequate sedation and NMB reduce cerebral
metabolic demands and therefore CBF and
hence ICP
Treatment
CSF removal
 Removing CSF is physiologic way to control
ICP
 May also have additional drainage through
lumbar drain


Considered as 3rd tier option
Basilar cisterns must be open otherwise will
get tonsillar herniation
Treatment
Osmotic agents
 Mannitol
 1st described in 50’s
 Historically thought secondary to movement of extravascular fluid into capillaries
 Induces a rheologic effect on blood and blood flow by
altering blood viscosity from changes in erythrocyte
cell compliance
 Transiently increases CBV and CBF
 Cerebral oxygen improves and adenosine levels increase
Decrease adenosine then leads to vasoconstriction
May get rebound hypovolemia and hypotension

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Treatment
Osmotic agents
 Hypertonic Saline
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First described in 1919
Decrease in cortical water
Increase in MAP
Decrease ICP
Treatment
Hyperventilation
 Decrease CO2 leads to CSF alkalosis
causing vasoconstriction and decrease CBF
and thus ICP

May lead to ischemia
 Overtime the CSF pH normalizes and lose
effect
 Use mainly in acute deterioration and not as
a mainstay therapy
Treatment
Barbiturate Coma
 Lower cerebral O2 consumption

Decrease demand equals decrease CBF
 Direct neuro-protective effect

Inhibition of free radical mediated lipid
peroxidation
Treatment
Temp Control
 Lowers CMRO2

Decreases CBF
 Neuroprotective


Less inflammation
Less cytotoxicity and thus less lipid
peroxidation
 Mild 32-34 degrees

Lower can cause arrhythmias, suppressed
immune system
Treatment
Decompressive craniotomy
 Trend toward improved outcomes
Treatment
Steroids
 Not recommended
 CRASH study actually showed increased
morbidity and mortality
Questions?