Intracranial Hypertension

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Intracranial Hypertension

• Fellows Conference
• Sept 07

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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

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CSF

• Choroid plexus gt 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

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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

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CBF
CBF
50
150
MAP
6
CBF
125
PaCO2
CBF
Pao2
0
125
CPP
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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

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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

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Monitoring

• Intra-ventricular
• Gold standard
• Can re zero
• Withdraw CSF
• Infection rate about 7
• Rate does not increase after 5 days

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Monitoring

• Intra-parenchymal
• Placed directly into brain easy insertion
• Cant recalibrate has drift over time
• Minimal differences between intra-ventricular
  parenchymal pressures
• ventricular 2 mmHg higher

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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 gt 20mmHg

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Wave forms
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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

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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

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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

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TreatmentSedation NMB

• Adequate sedation and NMB reduce cerebral
  metabolic demands and therefore CBF and hence ICP

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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

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TreatmentOsmotic agents

• Mannitol
• 1st described in 50s
• 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

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TreatmentOsmotic agents

• Hypertonic Saline
• First described in 1919
• Decrease in cortical water
• Increase in MAP
• Decrease ICP

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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

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TreatmentBarbiturate Coma

• Lower cerebral O2 consumption
• Decrease demand equals decrease CBF
• Direct neuro-protective effect
• Inhibition of free radical mediated lipid
  peroxidation

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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

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TreatmentDecompressive craniotomy

• Trend toward improved outcomes

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TreatmentSteroids

• Not recommended
• CRASH study actually showed increased morbidity
  and mortality

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Questions?