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Intracranial Hypertension

Intracranial Hypertension. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. 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

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Intracranial Hypertension

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  1. Intracranial Hypertension Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

  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. Monroe-Kellie Doctrine • Skull is a rigid structure (except in children with fontanels) • 3 components: • Brain: 80% of total volume, tissues and interstitial fluid • Blood: 10% of total volume = venous and arterial • CSF: 10% of total volume • Vintracranial = Vbrain + VCSF + Vblood • An increase in one component occurs in the compression of another

  4. Monroe-Kellie Doctrine Copied from Rogers Textbook of Pediatric Intensive Care

  5. Brain • 80% of intracranial space = 80% water • Cell types • Neurons: Cell body, dendrites, axon, pre-synaptic terminal-neurotransmission • Astrocytes/Pericytes • Support the neurons & other glial cells by isolating blood vessels, sypnapses, cell bodies from external environment • Endothelial cells • Joined a tight junctions  form BBB • Oligodendrocytes • Myelin sheath around axons  propagates action potential  efficient transmission of information • Microglia • Phagocytes, antigen-presenting cells, secrete cytokines

  6. CSF • 10% of total volume • Choroid plexus > 70 % production • Transependymal movement fluid from brain to ventricles ~30% • Average volume CSF in child is 90cc (150cc in adult) • Rate of production: 500cc/d • Increase ICP • Decrease production • Increase absorption (up to 3X via arachnoid villa)

  7. Blood • 10% of intracranial volume • Delivered to the brain via the Circle of Willis  course through subarachnoid space before entering brain • Veins & sinuses drain into jugular veins • Cerebral blood volume (CBV) • Contributes to ICP • Cerebral blood flow (CBF) • Delivers nutrients to the brain

  8. CBF & CPP • 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

  9. CBF CBF 50 150 MAP

  10. Auto-regulation of CBF • Compensated via vascular tone in the cerebral circulation to maintain a relatively constant CBF over changes in cerebral perfusion pressure (CPP) • Brain injury causing ICP may abolish auto-regulation • CPP becomes linearly dependent on MAP

  11. CBF 125 PaCO2 CBF PaO2 0 125 CPP

  12. Auto-regulation in Newborns Narrow CPP range vs. adults, similar lower limit, upper limit ~90-100; Rogers Textbook of Pediatric Intensive Care

  13. CPP • 2003 Pediatric TBI guidelines recommend • Maintain CPP>40mmHg • Will likely be modified to titrate to age-specific thresholds • 40-50mmHg: infants & toddlers • 50-60mmHg: children • >60mmHg: adolescents

  14. Wave forms

  15. 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

  16. 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 CSF hydrostatic pressure

  17. ICP Monitoring • Intraventricular catheter • Intraparenchymal monitor • Subdural device • Epidural catheter

  18. Intraventricular Catheter - Most direct, more accurate, “gold standard” • Can re-zero • Withdraw CSF • Risk: infection, injury, bleeding, hard to place in small ventricles • Infection rate about 7% (level our after 5 days)

  19. Intraparenchymal Catheter • Placed directly into brain, easy insertion • Can’t recalibrate; monitor drifts over time • Lower risk of complication • Minimal differences between intra-ventricular & parenchymal pressures • ventricular ~2 mmHg higher

  20. 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

  21. Management Strategies • CSF • Brain • Blood

  22. Treatment: CSF • 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 • Decreasing CSF production: Acetazolamide, Furosemide • Take several days before seeing the change

  23. Treatment: Blood • Keep midline for optimal drainage • HOB >30º • MAP highest when supine • ICP lowest when head elevated • 30º in small study gave best CPP

  24. Treatment: BloodTemp Control • Lowers CMRO2 • Decreases CBF • Neuroprotective • Less inflammation • Less cytotoxicity and thus less lipid peroxidation • Mild 32-34º • Lower can cause arrhythmias, suppressed immune system

  25. Treatment: BloodSedation & NMB • Adequate sedation and NMB reduce cerebral metabolic demands and therefore CBF and hence ICP

  26. Treatment: BloodHyperventilation • 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

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

  28. Treatment: BrainOsmotic 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

  29. Treatment: BrainOsmotic agents • Hypertonic Saline • First described in 1919 • Decrease in cortical water • Increase in MAP • Decrease ICP

  30. Treatment: Decompressive craniotomy • Trend toward improved outcomes

  31. Treatment: Steroids • Not recommended • CRASH study actually showed increased morbidity and mortality

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