Presentation is loading. Please wait.

Presentation is loading. Please wait.

Intracranial Hypertension

Similar presentations

Presentation on theme: "Intracranial Hypertension"— Presentation transcript:

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

Download ppt "Intracranial Hypertension"

Similar presentations

Ads by Google