Intracranial Hypertension

Pediatric Critical Care MedicineEmory 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

• 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:

– 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

Copied from Rogers Textbook of Pediatric Intensive Care

Monroe-Kellie Doctrine

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

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)

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• 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

CBFCBF

MAP

50 150

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

PaO2

PaCO2

CPP

CBF

0125

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

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

Monitoring• Intra-ventricular

– Gold standard– Can re-zero– Withdraw CSF– Infection rate about 7% (level our after 5 days)

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

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

Wave forms

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

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

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: 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

Treatment: BloodSedation & NMB

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

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

Treatment: BloodBarbiturate Coma

• Lower cerebral O2 consumption– Decrease demand equals decrease CBF

• Direct neuro-protective effect – Inhibition of free radical mediated lipid peroxidation

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

Treatment: Brain Osmotic agents

• Hypertonic Saline– 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