ICP Presentation by Kevin Kuo, MDGeneral ConceptsMonro-Kellie Doctrine Since the intracranial volume is fixed and as the contents are essentially non-compressible, then any increase in one volume mandates and equal volume reduction in other compartments OpenPediatrics Quick Concept Video on the Monro Kellie Doctrine Intracranial contents composed of three compartments: 1) brain / interstitial fluid (~80%) 2) intravascular blood (~10%) 3) CSF – ventricles & subarachnoid space (~10%)
 Physiologic Principles CSF functions Absorbs shock to CNS Cushions CNS from bony surroundings Helps circulate nutrients / waste Cerebral vasculature: Blood Brain Barrier and Autoregulation Starling equation: Q = K [ (Pmv - Pis) - σ (πmv - πis) ] Transcapillary fluid exchange determined by transcapillary hydrostatic & osmotic pressures & reflection coefficient Brain (intact Blood Brain Barrier and functional autoregulation) High osmotic pressure due to low permeability to crystalloids and proteins – (osmolality of CSF/ECF > plasma) Tightly autoregulated cerebral intracapillary hydrostatic pressure (CPP not critical if BBB/autoregulation intact) Most tissues (and Brain if BBB disrupted and autoregulation impaired) Low osmotic pressure due to high permeability to crystalloids (still low permeability to large proteins) Hydrostatic pressure varies with MAP (CPP critical) Autoregulation outstripped at adult CPP levels < 50 mm Hg (ischemia) or > 160 mmHg (cerebral edema) Mechanisms may be directly impaired by disease processes (and may be heterogeneous in dysfunction) Endothelial function contributes to autoregulation States of endothelial dysfunction (sepsis, MODS) can impair autoregulation Elevated ICP Normal ICP: 7-20 cm H2O (5-15 mm Hg) [Ratio is about 2/3] Harmful in 2 ways: Brain ischemia: Cerebral Perfusion Pressure (CPP) = MAP – ICP (or the CVP if it is > ICP) Herniation syndromes
Differential Diagnosis
 Signs/Symptoms of Intracranial Hypertension
“Cushing’s Triad” = Hypertension, Bradycardia, Irregular Respirations – somewhat specific but insensitive Intracranial HYPO-tension Caused by low CSF volume LP / EVD drainage CSF leak following trauma, neurosurgery, or thoracotomy (CSF-pleural fistula) Dural tear Symptoms result from the loss of buoyancy of the brain as it floats within the CSF Stretch of the dura & cortical veins (pain-sensitive structures) Headache Compensatory vasodilation, tachycardia (opposite of Cushing’s triad) ICP/CPP Monitoring Figure 2: ICP Monitoring Devices
 Herniation Syndromes Figure 3: Various Herniation Syndromes Subfalcine Herniation Cingulate gyrus & related structures herniate laterally under the falx cerebri Usually from unilateral mass lesions Usually no classic stigmata Central Herniation Downward displacement of brainstem Any mass almost anywhere with high ICP (including hydrocephalus / diffuse edema) Mild à traction on the abducens nerve (lateral rectus palsy) Severe à herniation into foramen magnum (tonsilar herniation) à medulla injury à respiratory arrest, BP instability Transtentorial/Uncal Herniation Medial temporal lobe (i.e., the uncus) herniates inferiorly through tentorial notch Causes clinical triad of “blown” pupil, hemiplegia, and coma Compression of oculomotor nerve ipsilateral (85% of cases) Initially: dilated & unresponsive pupil Later: impairment of eye movement Hemiplegia is often contralateral (compression of ipsilateral corticospinal tract in the midbrain or motor cortex) Midbrain distortion leads to decreased level of consciousness and coma
Necrosis (overt and acute energy failure with cytotoxic edema; direct disruptive trauma) Apoptosis (programmed cell death) Excitotoxicity (toxic glutamate receptor activation) ManagementManagement: Different Models Opinions differ widely on optimal intracranial hypertension therapy based on sustained versus acute increase in intracranial pressure mechanism of injury (trauma vs. metabolic vs. infectious) determination of cerebral vascular state (hypoperfusion vs. hyperemia vs. vasospasm) controversial evidence (e.g., hyperventilation, hypothermia, animal versus human models, etc.) how to tailor in setting of specific comorbidities (e.g., ventilation in ARDS, pressors in sepsis, etc.) Numerous “Schools” of thought: ICP Targeted: keep the ICP <15-20 mm Hg CPP Targeted: keep the CPP >50-70 mm Hg “Lund Concept”: (see below) Management: Applying Broad Goals in Specific Instances ICP < 15-20 mm Hg Perhaps lower <10-15 if large skull fractures/defects (avoid herniation) Perhaps higher <25-30 if global/metabolic process and other maximized therapies potentially harmful CPP > 50-70 mm Hg Set an upper limit (excessive CPP can promote cerebral edema where autoregulation is impaired) Attention to relative positions of monitoring devices (MAP at heart level, ICP at ear level, Auto-CPP calculations) Age-Apropriate targets: Infant 45-55 mm Hg Child 55-65 mm Hg Adult 60-75 mm Hg CI > 2.5-3 Maintain intravascular euvolemia or mild hypervolemia (keep left ventricle full) Optimize filling pressures to maximize starling curve of the heart without overly impeding venous return Attention to cerebral vascular state: hypoperfusion vs. hyperemia vs. vasospasm Careful selection of vasoactive substances from armamentarium Epinephrine: probably ideal for most patients, especially if low CO, low BP Dobutamine: may be optimal for global/metabolic processes, especially if normo/hypertensive β-blockers (labetolol/metoprolol) +/- α2-agonists (clonidine): may be optimal antihypertensives without causing significant cerebral vasodilatation that can lead to elevated ICP Nimodipine: may have role in vasospasm
 Figure 6: From Stochetti et al, NEJM 2014 Intracranial Volume Targeted (“Lund Concept”) Ways it’s been described: Antihypertensive and intracranial volume-targeted therapy Physiological volume regulation of the intracranial compartments Central premise: Impaired autoregulation and blood brain barrier occur in the injured brain This makes MAP and cerebral capillary hydrostatic pressure driving force behind cerebral edema, and therefore ICP Furthermore, supporting the CPP with pressors can promote more cerebral edema Therefore, a good CO with normotension and mild vasoconstriction of precapillary cerebral vessels decreases ICP The volume-targeted “Lund Strategy” has several components Reduction of stress response and cerebral energy metabolism (low dose pentothal, sedation) Reduction of capillary hydrostatic pressure with systemic antihypertensives (metoprolol and clonidine) Reduction of capillary hydrostatic pressure with precapillary vasoconstrictors (low-dose pentathol & ergotamine) Maintenance of colloid osmotic pressure and control of fluid balance Reduction of cerebral blood volume What it looks like Euvolemia to Hypervolemia Normotension using beta-blockers (metoprolol) and alpha-agonists (clonidine) Low dose pentothal and dihydroergotamine CPP typically near traditional limits, but lower CPP tolerated in preference of antihypertensive therapy ICP effectively kept <20 mm Hg most of the time Outcomes Efficacy of the protocol has been evaluated in experimental and clinical studies Surrogate physiological/biochemical improvements (lactate/pyruvate ratio in the penumbra zone by microdialysis) Non-randomized/non-controlled studies suggest significant mortality benefit Subjective clinical experiences favorable ICP Management: General & Monitoring Time is of the essence – the brain tolerates ischemia more poorly than other tissues & injury begets injury Multi-pronged approach tailored to primary cause and comorbidities of patient Serial neurologic assessments and physical examination with a short feed-back loop is critical Continuous cardio-respiratory, ICP, and CPP monitoring +/- role cerebral metabolism monitoring adjuncts (micro-dialysis, jugular venous saturation, NIRS) ICP Management: Decrease intracranial pressure Evacuate mass occupying lesions (e.g., hemorrhage, tumor, abscess, etc) Patient Positioning What: Head up 30 degrees and midline, neck position neutral and non-compressed (e.g., by cervical collar) Why: Enhance cerebral venous outflow and maximize CPP Pro: Simple, quick, well tolerated Con: Confounding injuries, comorbidities requiring movement (e.g., proning) CSF drainage What: Removal of CSF ideally through ventriculostomy (alternately an LP) Why: Decreases “volume” in the compliance equation Pro: Effective, titratable, doubles as monitor, interpretable waveform Con: Invasive, bleeding complications, infectious complications Mannitol What: 0.5 - 2 g/kg up to Osm of 320 Why: Increases intravascular oncotic pressure, rheological benefits, anti-oxidant effects Pro: Rapid onset, titratable, predictable Con: Intermittent, hypotension, hypovolemia, hypokalemia, duration hours or days, tolerance/rebound (reflection coefficient ~0.9) Hypertonic Saline: Hypertonic Saline Myths Dispelled (AJRCCM 2012) What: 5-10 ml/kg 3% NaCl up to [Na] of 145-180 meq/L – may bolus 5-10 ml/kg and start a sliding scale gtt @ 0.5-2 ml/kg/hr Why: Increases intravascular oncotic pressure, volume expander Pro: Rapid onset, titratable, continuous rx, predictable, high coefficient of reflection (reflection coefficient ~0.95), numerous others Con: Can obfuscate DI/CSW, potential renal function impairment, some concerns for effects on immune function
 HTS vs Mannitol: From Kamel et al, CCM 2011 Craniectomy What: Resect large flap of skull Why: Changes the “volume” part of the compliance equation Pro: Large sustained ICP reduction Con: Timing critical, surgical risk, tissue herniation through wound, catastrophic Hail Mary ICP Management: Decrease Cerebral Metabolic Demand Sedation & Analgesia What: Benzos, narcs, barbiturates, Lido pETT/IV; possibly premedicate before stimulation; cluster nursing activity; calm environment Why: Decrease CNS metabolic demand, dampen intrinsic catechols Pro: Easy, quick, reversible Con: Loss of neuro exam, depresses hemodynamics Seizure Control What: Agressively treat and consider prophylaxing, numerous choices of ACD (phenobarb, pentothal, dilantin) Why: Decrease CNS metabolic demand Barbiturates What: Pentothol 1-5 mg/kg to a level of 10-60 Why: Decreased CNS metabolic demand, decreased cerebral blood flow Pro: Blunts BP and respiratory fluctuations, anticonvulsant, titratable Con: Hypotension, abnormal papillary responses, duration days Antipyresis What: Tylenol, paralyzation, cooling measures, caution NSAIDS Why: Metabolic demands increase 5-10% per 1OC Hypothermia What: Pre-existing or induced redection of temperature with paralysis and active cooling measures Why: Hypothermia prior to cerebral ischemic insult protective; induced hypothermia after insult questionable Pro: Relatively simple, reversible Con: Risks of coagulopathy, arrhythmia, sepsis (usually < 33OC) ICP Management: Supportive and Indirect Ventilation: Normoventilate if able, +/- Hyperventilation temporarily if necessary What: pCO2 35-40 ideally, but 25-35 mm Hg may achieve needed ICP control (best if transient and minimal) Why: Decrease cerebral blood flow and therefore edema/ICP; hypercapnia blunts CBF autoregulation Pro: Immediate onset, well tolerated acutely Con: Brain ischemia, hypotension, requires intubation, barotrauma, duration usually hours or less Optimize Hemodynamics What: Cardiac Output >2.5-3 (e.g., inotropes, volume); CPP target; good venous return (e.g., vec, low Paw); avoid cardiac depressants Why: generate adequate oxygen/nutrient delivery and waste removal Optimize Oxygen Carrying Capacity What: PRBC, Epogen to goal Hb 8-10 Why: Deliver adequate O2 Pro: Oxygenation / DO2 Con: Hb <7-8 can impair DO2; Hb >10-11 can increase viscosity; stored PRBC are less deformable than natural RBC’s Glucose Control What: Tight glucose control with prudent dextrose administration and insulin gtt if needed Why: Hypo- and hyperglycemia in the setting of cerebral ischemia leads to enhanced anaerobic metabolism; stablize osmotic variable Pro: Relatively simple, physiologic Con: Some safety issues with inducing hypoglycemia Loop diuretics & Acetazolamide What: Furosemide, Torsemide Why: Decrease CSF production and total fluid overload Pro: quick, simple, reversible Con: Risk of dehydration and impaired CO, electrolyte & acid-base derangements Muscle Relaxants What: Vecuronium Why: Stabilize patient, decrease intrathoracic pressure (CVP) Pro: Easy, quick, reversible Con: Loss of neuro exam, weakness Corticosteroids What: Dexamethasone 1-2 mg/kg q6-24h Why: Antiinflamitory that decreases some forms of edema Pro: Effective on vasogenic edema (tumors, abscesses) Con: Less effective on cytotoxic edema (stroke or hematoma), systemic/immune/gastric side effects Other Neuroprotective Strategies to Consider More widely accepted - Literature generally neutral or is optimistic/supportive Magnesium: to levels of 2.5-3 meq/L as a calcium antagonis, vasodilator, anti-vasospasmodic Calcium channel blockers (e.g., nimodipine in vasospasm) Allopurinol: free-radical scavenger Serotonin agonists (e.g., Repinotan) Caspase inhibitors: as anti-apoptotic agents Neural stem cells Experimental - Literature highly conflicted or is generally pessimistic Carnitine Glutamate antagonists / Excitatory Amino Acid (EAA) antagonist Anti-inflammatory agents (e.g., Ibuprofen) Sodium channel blockers (e.g., dilantin) Potassium channel activator Sundry free-radical scavengers GABA Antagonists Opioid Antagonists NOS Inhibitors Gangliosides Neurotrophic factors Combination Therapy “The whole is greater than the sum of its parts” …and yet, one bad ingredient can ruin an otherwise good recipe Brain Injury is not “All or None” Neuronal drop-out is fractional: 0-100% Neuron populations heterogeneous (resilience, metabolic demands, vascular supply, etc.) Global insult classically leads to widespread partial dropout / injury of vulnerable cell populations relatively spared territories (e.g., brainstem) Focal insult classically leads to a “core” of hopeless necrosis a “penumbra” of neurons of varying injure ranging from dead to salvageable to stunned, to unaffected Think of brain injury as “irreversible” can be a self-fulfilling prophesy 1. Dr. Matthew Niedner's resident lecture: ICP |
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