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Intracranial Hypertension

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

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Intracranial Hypertension

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  1. Intracranial Hypertension Fellows Conference Sept 07

  2. 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

  3. 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

  4. 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

  5. CBF CBF 50 150 MAP

  6. CBF 125 PaCO2 CBF Pao2 0 125 CPP

  7. 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

  8. 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

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

  10. 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

  11. 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

  12. Wave forms

  13. 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

  14. 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

  15. 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

  16. TreatmentSedation & NMB • Adequate sedation and NMB reduce cerebral metabolic demands and therefore CBF and hence ICP

  17. 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

  18. 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

  19. TreatmentOsmotic agents • Hypertonic Saline • First described in 1919 • Decrease in cortical water • Increase in MAP • Decrease ICP

  20. 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

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

  22. 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

  23. TreatmentDecompressive craniotomy • Trend toward improved outcomes

  24. TreatmentSteroids • Not recommended • CRASH study actually showed increased morbidity and mortality

  25. Questions?

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