Transcript ICP 2011
Intracranial Hypertension 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 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 • 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 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 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: 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 – – – – 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