Transcript Intracranial Hypertension Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta Historical Perspective • Alexander Monro 1783 described cranial vault as nonexpandable and.

Intracranial Hypertension
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Historical Perspective
• Alexander Monro 1783 described cranial vault as nonexpandable 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
Monroe-Kellie Doctrine
• Skull is a rigid structure (except in children with fontanels)
• 3 components:
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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
Monroe-Kellie Doctrine
Copied from Rogers Textbook of Pediatric Intensive Care
Brain
• 80% of intracranial space = 80% water
• Cell types
– Neurons: Cell body, dendrites, axon, pre-synaptic terminalneurotransmission
– 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
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)
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
CBF & CPP
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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
50
150
MAP
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
CBF
125
PaCO2
CBF
PaO2
0
CPP
125
Auto-regulation in Newborns
Narrow CPP range vs. adults, similar lower limit, upper limit ~90-100;
Rogers Textbook of Pediatric Intensive Care
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
Wave forms
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 CSF
hydrostatic pressure
ICP Monitoring
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Intraventricular catheter
Intraparenchymal monitor
Subdural device
Epidural catheter
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)
Intraparenchymal Catheter
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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
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
Management Strategies
• CSF
• Brain
• Blood
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
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
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
Treatment: Blood
Sedation & NMB
• Adequate sedation and NMB reduce cerebral metabolic
demands and therefore CBF and hence ICP
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
Treatment: Blood
Barbiturate Coma
• Lower cerebral O2 consumption
– Decrease demand equals decrease CBF
• Direct neuro-protective effect
– Inhibition of free radical mediated lipid peroxidation
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
Treatment: Brain
Osmotic agents
• Hypertonic Saline
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First described in 1919
Decrease in cortical water
Increase in MAP
Decrease ICP
Treatment:
Decompressive craniotomy
• Trend toward improved outcomes
Treatment: Steroids
• Not recommended
• CRASH study actually showed increased morbidity and
mortality