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

MAP

50 150

CBF

Pao2

PaCO2

CPP

CBF

0 125

125

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 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

TreatmentHead 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

TreatmentSedation & NMB Adequate sedation and NMB reduce cerebral

metabolic demands and therefore CBF and hence ICP

TreatmentCSF 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

TreatmentOsmotic agents Mannitol

1st described in 50’s Historically thought secondary to movement of extra-

vascular 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

TreatmentOsmotic agents Hypertonic Saline

First described in 1919 Decrease in cortical water Increase in MAP Decrease ICP

TreatmentHyperventilation 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

TreatmentBarbiturate Coma Lower cerebral O2 consumption

Decrease demand equals decrease CBF Direct neuro-protective effect

Inhibition of free radical mediated lipid peroxidation

TreatmentTemp 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

TreatmentDecompressive craniotomy Trend toward improved outcomes

TreatmentSteroids Not recommended CRASH study actually showed increased

morbidity and mortality

Questions?