1. Intracranial Hypertension
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Lecture is prepared by Dr. Karen Walson

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 Microglia
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
Rate production remains fairly constant
w/ increase ICP it is absorption that changes (increase 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
CBF: Cerebral blood flow
CPP: Cerebral perfusion pressure, represents the pressure gradient acting across the cerbrovascular bed; important factor in the regulation of CBF

9. CBF
CBF 50
150
CBF is tightly regulated bwt MAP ; Virtually no change in CBF
Low MAP  local vessels dilate to increase/maintain CBF
Hi MAP  vasoconstricte to prevent overcirculation
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 125 CPP The effect of PaCO2 and PaO2 on CBF
CBF is linearly related to PaCo2, with an approximate 4% change in CBF/torr change in PaCO2 between ~20-80 torr.
<20 torr: this curve dramatically flattens
> torr: this relationship also more gradually flattens
The relationship between CBF and paO2 is relatively flat until the PaO2 of ~50 mmHg is reached, below which, a dramatic increase in CBF is observed
PaO2
125
CPP

12. Auto-regulation in Newborns
Figure Comparison of the relative pressure: CBF autoregulatory curves from studies of subhuman primate newborns and adults. In the adult, CBF is maintained relatively constant when arterial blood pressure is between 50 and 160 mm Hg, while in newborns, CBF is maintained over a narrower range due to a reduced upper limit of CBF autoregulation. CBF autoregulation of newborns makes them more vulnerable to hypertensive episodes. MABP, mean arterial blood pressure. From Pediatr Clin North Am
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. 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

15. Cerebral Edema Vasogenic Cytotoxic Interstitial
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
- BBB: blood brain barrier

16. Monitoring Intra-ventricular Gold standard Can re-zero Withdraw CSF
Infection rate about 7% (level our after 5 days)

17. Monitoring Intra-parenchymal
Placed directly into brain, easy insertion
Can’t recalibrate; monitor drifts over time
Minimal differences between intra-ventricular & parenchymal pressures
ventricular ~2 mmHg higher

18. 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 mmHg
lasting 5-20min
associated baseline ICP > 20mmHg

19. Wave forms

20. Monitoring CT MRI w/ perfusion PET 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. Monitoring Kety –Schmidt Jugular Bulb NIRS
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

22. Management Strategies
CSF
Brain
Blood

23. 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

24. 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

25. Treatment: Blood Temp 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

26. Treatment: Blood Sedation & NMB
Adequate sedation and NMB reduce cerebral metabolic demands and therefore CBF and hence ICP

27. Treatment: Blood 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

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

29. Treatment: Brain Osmotic 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

30. Treatment: Brain Osmotic agents
Hypertonic Saline
First described in 1919
Decrease in cortical water
Increase in MAP
Decrease ICP

31. Treatment: Decompressive craniotomy
Trend toward improved outcomes

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