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Intracranial Hypertension Fellows Conference Sept 07.

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Presentation on theme: "Intracranial Hypertension Fellows Conference Sept 07."— Presentation transcript:

1 Intracranial Hypertension Fellows Conference Sept 07

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 CSF Choroid plexus > 70 % production Transependymal movement fluid from brain to ventricles rest Average volume CSF in child is 90cc (150cc in adult) Make about 500cc/d Rate production remains fairly constant w/ increase ICP it is absorption that changes

4 CBF 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

5 CBF MAP 50150

6 CBF Pao2 PaCO2 CPP CBF 0125

7 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

8 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 CFS hydrostatic pressure

9 Monitoring Intra-ventricular Gold standard Can re zero Withdraw CSF Infection rate about 7% Rate does not increase after 5 days

10 Monitoring Intra-parenchymal Placed directly into brain easy insertion Can’t recalibrate has drift over time Minimal differences between intra-ventricular & parenchymal pressures ventricular ~2 mmHg higher

11 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

12 Wave forms

13 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

14 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

15 Treatment Head position Keep midline for optimal drainage HOB 30 deg MAP highest when supine ICP lowest when head elevated 30 degree in small study gave best CPP

16 Treatment Sedation & NMB Adequate sedation and NMB reduce cerebral metabolic demands and therefore CBF and hence ICP

17 Treatment CSF removal 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

18 Treatment 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

19 Treatment Osmotic agents Hypertonic Saline First described in 1919 Decrease in cortical water Increase in MAP Decrease ICP

20 Treatment 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

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

22 Treatment Temp Control Lowers CMRO2 Decreases CBF Neuroprotective Less inflammation Less cytotoxicity and thus less lipid peroxidation Mild degrees Lower can cause arrhythmias, suppressed immune system

23 Treatment Decompressive craniotomy Trend toward improved outcomes

24 Treatment Steroids Not recommended CRASH study actually showed increased morbidity and mortality

25 Questions?


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