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

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Presentation on theme: "Intracranial Hypertension Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta."— Presentation transcript:

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 –V intracranial = V brain + V CSF + V blood An increase in one component occurs in the compression of another

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

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 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

9 CBF MAP 50150

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 PaO 2 PaCO 2 CPP CBF 0 125

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 CBF CBF is usually tightly coupled to cerebral metabolism or CMRO 2 –Normal CMRO 2 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 –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

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 –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 –Uses Nitrous as an inert gas tracer and fick principle looking at arteriovenous difference »CO = VCO 2 [ml/min]/(CO 2 art-CO 2 ven) [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 3 rd 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 CMRO 2 –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 CO 2 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 O 2 consumption –Decrease demand equals decrease CBF Direct neuro-protective effect –Inhibition of free radical mediated lipid peroxidation

29 Treatment: Brain Osmotic Agents Mannitol –1 st 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


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