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Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
Management of Intercranial Pressure
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Management of Intercranial Pressure

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  • 1. Intracranial Pressure and Cerebral Edema Neuro-ICU 2009 PJ Papadakos MD FCCM Director CCM Professor Anesthesiology, Surgery and Neurosurgery Rochester NY USA
  • 2. Is there a debate?
  • 3. HOW DO PATIENTS PRESENT ?HOW DO PATIENTS PRESENT ? • Obvious--motor vehicle accident, car vsObvious--motor vehicle accident, car vs pedestrian, fall from height, etcpedestrian, fall from height, etc • Less obvious--sports injuries (football), delayedLess obvious--sports injuries (football), delayed deterioration (epidural)deterioration (epidural) • Hidden--shaken baby syndrome, older childHidden--shaken baby syndrome, older child maltreatmentmaltreatment • Inter cranial HemorrhageInter cranial Hemorrhage • StrokeStroke
  • 4. CAVEATS IN BRAIN INJURYCAVEATS IN BRAIN INJURY • Neurologic examination - the mostNeurologic examination - the most important information you haveimportant information you have • Accurate history is often unavailable orAccurate history is often unavailable or inaccurateinaccurate • Potential for associated injuries or illnessPotential for associated injuries or illness (cardiovascular, respiratory,(cardiovascular, respiratory, cervical spine)cervical spine)
  • 5. CEREBRAL RESUSCITATIONCEREBRAL RESUSCITATION • Primary survey - airway, breathing, andPrimary survey - airway, breathing, and circulationcirculation • Neurologic evaluationNeurologic evaluation • Secondary survey - “head to toe”Secondary survey - “head to toe” • Neuroradiologic evaluationNeuroradiologic evaluation • Ongoing evaluation and transportOngoing evaluation and transport
  • 6. MECHANISMS OF INJURY-PRIMARYMECHANISMS OF INJURY-PRIMARY • Impact: epidural, subdural, contusion,Impact: epidural, subdural, contusion, intracerebral hemorrhage, skull fracturesintracerebral hemorrhage, skull fractures • Inertial: concussion, diffuse axonal injuryInertial: concussion, diffuse axonal injury • Hypoxic IschemicHypoxic Ischemic
  • 7. MECHANISMS OF 2MECHANISMS OF 2ndnd INJURYINJURY • GlobalGlobal – Hypoxia and ischemia of brainHypoxia and ischemia of brain – Decreased cerebral blood flow due toDecreased cerebral blood flow due to increased intracranial pressureincreased intracranial pressure • LocalLocal – impairment of cerebral blood flow or extraimpairment of cerebral blood flow or extra cellular milieu due to the presence of injuredcellular milieu due to the presence of injured brainbrain
  • 8. PATHOPHYSIOLOGYPATHOPHYSIOLOGY • Primary damage – the only treatment is byPrimary damage – the only treatment is by preventionprevention.. • Secondary damage – multifactorial andSecondary damage – multifactorial and time dependent.time dependent.
  • 9. Brain trauma BBB disruption diffuse axonal injury edema formation Eicosanoids endocannabinoids necrosis energy failure cytokines SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY apoptosis inflammation ROS polyamines CalciumAcetyl Choline ischemia Shohami, 2000 Green – pathophysiological processes; Yellow – various mediators
  • 10. Time is ImportantTime is Important
  • 11. HoursHours Days Weeks / Months Weeks/Month s Dynamic Changes Following Brain InjuryDynamic Changes Following Brain Injury Ca , Na+ Glut, ROS 8hrs 7 Necrosis Apoptosis Repair Remodeling Plasticity Functional Recovery I N J U R Y 142 Inflammation Barone &Feuerstein JCBF, 1999
  • 12. Physiology
  • 13. The Lund Concept • January 1989, Lund University Hospital Department of Neurosurgery • Protocol aimed at non- surgical reduction of ICP • Bedside measurements of CBF and vasoreactivity identified subgroup of patients with severe TBI, intractable ICP, and 100% mortality
  • 14. Lund concept • Volume-targeted therapy • Reduction of capillary hydrostatic pressure • Maintenance of colloid osmotic pressure and control of fluid balance • Reduction of cerebral blood volume • Controlled ICP
  • 15. Blood Brain Barrier in Trauma
  • 16. The Lund Concept • Avoid hyperglycemia and hyperthemia. • Avoid hypovolemia and stress response: increased baroreceptor reflex and cathacholamine release • Avoid hyperosmotic therapy: transient effects with adverse rebound and renal effects • Avoid vasopressors: vasoconstriction increases BP and CPP but may compromise brain microcirculatory perfusion (esp. pericontusional) and other organ system perfusion (ARDS)
  • 17. The Lund Concept • Stress reduction: sedatives midazolam and thiopental (0.5-3.0 mg/kg/h) combined with alpha- 2 agonism and beta-1 blockade. Avoid propofol. • Normovolemia: by normalizing plasma oncotic pressure via RBC infusion to normal S-Hb (125- 140 g/L) and albumin transfusion (20-25%) • Normalize BP: Clonidine (0.3-1.0 ug/kg X 4-6) and Metoprolol (0.04-0.08 mg/kg). Refrain from using vasopressors. Dihydroergotamine induce venous vasoconstriction with great volume in venous side. No fixed limits for CPP
  • 18. MONRO-KELLIE DOCTRINEMONRO-KELLIE DOCTRINE VVintracranialintracranial vaultvault=V=Vbrainbrain+V+Vblood +blood +VVcsfcsf
  • 19. BRAIN: CEREBRAL EDEMA-VASOGENICBRAIN: CEREBRAL EDEMA-VASOGENIC (Caused mainly by activation of NMDA receptors by glutamate)(Caused mainly by activation of NMDA receptors by glutamate)
  • 20. BRAIN: CEREBRAL EDEMA-CYTOTOXICBRAIN: CEREBRAL EDEMA-CYTOTOXIC (Caused mainly by activation of cytokines, ROS and other(Caused mainly by activation of cytokines, ROS and other pro-inflammatory mediators)pro-inflammatory mediators)
  • 21. o The brain has the abilityThe brain has the ability to control its bloodto control its blood supply to match itssupply to match its metabolic requirementsmetabolic requirements o Chemical or metabolicChemical or metabolic byproducts of cerebralbyproducts of cerebral metabolism can altermetabolism can alter blood vessel caliber andblood vessel caliber and behaviorbehavior BLOOD: CEREBRAL BLOOD FLOWBLOOD: CEREBRAL BLOOD FLOW
  • 22. BLOOD: CEREBRAL BLOOD FLOWBLOOD: CEREBRAL BLOOD FLOW (VOLUME)(VOLUME) • Increases in cerebral metabolic rateIncreases in cerebral metabolic rate – HyperthermiaHyperthermia – SeizuresSeizures – Pain, anxietyPain, anxiety
  • 23. CSF: CEREBROSPINAL FLUIDCSF: CEREBROSPINAL FLUID • 10% of intracranial volume10% of intracranial volume • Initial displacement of CSF from ventriclesInitial displacement of CSF from ventricles • Ventriculostomy to drain CSFVentriculostomy to drain CSF
  • 24. Intracranial ComplianceIntracranial Compliance • Calvarium is composed of three fluidCalvarium is composed of three fluid compartments: Cerebral Blood Volume,compartments: Cerebral Blood Volume, CSF, and cerebral parenchymaCSF, and cerebral parenchyma
  • 25. GUIDELINES – GENERAL ASPECTSGUIDELINES – GENERAL ASPECTS • Standards:Standards: accepted principles of patientaccepted principles of patient management that reflect a high degree ofmanagement that reflect a high degree of clinical certaintyclinical certainty • Guidelines:Guidelines: strategies that reflect moderatestrategies that reflect moderate clinical certaintyclinical certainty • Options:Options: unclear clinical certaintyunclear clinical certainty
  • 26. PrehospitalPrehospital
  • 27. Basic Principles: Airway • Resuscitation ABCs • Rapid sequence intubation • Retrospective studies report increased mortality: skill and optimal ventilation • Bag-valve-mask or LMA
  • 28. PREHOSPITAL AIRWAY MANAGEMENTPREHOSPITAL AIRWAY MANAGEMENT • Hypoxia must be avoided, and correctHypoxia must be avoided, and correct immediatelyimmediately . 13%-27%. 13%-27% ↓↓↓↓OO22 • Supplemental oxygen should be administeredSupplemental oxygen should be administered • No advantage of ETI (ET intubation) Vs. BVMNo advantage of ETI (ET intubation) Vs. BVM (Bag / valve / mask) ventilation for the(Bag / valve / mask) ventilation for the pre-pre- hospitalhospital airway in pediatric TBIairway in pediatric TBI 420 TBI; 115 BVM; 177 ETI420 TBI; 115 BVM; 177 ETIno change (no change (Gausche,Gausche, JAMA 2000JAMA 2000)) • TBI + ETITBI + ETI  ETCOETCO22
  • 29. RESUSCITATION OF BP AND ORESUSCITATION OF BP AND O22 AND PREHOSPITAL BRAIN-AND PREHOSPITAL BRAIN- SPECIFIC TX’S FOR SPTBI PATIENTSSPECIFIC TX’S FOR SPTBI PATIENTS • Hypotension should be identified and correctedHypotension should be identified and corrected as rapidly as possible with fluid resuscitation.as rapidly as possible with fluid resuscitation. (G)(G) • Hypotension on arrival to ERHypotension on arrival to ER (Pigula, J Ped Surg 1993)(Pigula, J Ped Surg 1993) 18% ER: mortality 61% Vs. 22%,18% ER: mortality 61% Vs. 22%, ↓↓BP+BP+↓↓OO22 –– mortalitymortality  85% !85% ! • LevineLevine (Neurosurg 1992)(Neurosurg 1992): TBI 0-4y: TBI 0-4y ↓↓BP – 32% poorBP – 32% poor outcome.outcome. • LaurssenLaurssen (J Neurosurg 1988)(J Neurosurg 1988)::↑↑BPBP ↓↓EX; WhiteEX; White (CCM(CCM 2001)2001): syst BP > 135: syst BP > 135  X19 in survival !X19 in survival !
  • 30. PREHOSPITAL TREATMENTSPREHOSPITAL TREATMENTS • No evidence of efficacy: sedation, NMB,No evidence of efficacy: sedation, NMB, Mannitol, saline 3%, hyperventilation.Mannitol, saline 3%, hyperventilation. • The prophylactic administration ofThe prophylactic administration of mannitol is not recommended.mannitol is not recommended. • Mannitol may be considered for use inMannitol may be considered for use in euvolemic patients who show signs ofeuvolemic patients who show signs of cerebral herniation or acute neurologicalcerebral herniation or acute neurological deterioration.deterioration.
  • 31. PREHOSPITAL TREATMENTSPREHOSPITAL TREATMENTS • Mild prophylactic hyperventilationMild prophylactic hyperventilation is notis not recommendedrecommended.. • Hyperventilation may be considered inHyperventilation may be considered in patients who show signs ofpatients who show signs of – Imminent cerebral herniation orImminent cerebral herniation or – acute neurological deteriorationacute neurological deterioration • After correcting hypotension or hypoxemiaAfter correcting hypotension or hypoxemia
  • 32. Pathophysiology of TBIPathophysiology of TBI • Primary injuryPrimary injury • Secondary InjurySecondary Injury • Ischemia/hypoxiaIschemia/hypoxia • ExcitotoxicityExcitotoxicity • Energy/MitochondrialEnergy/Mitochondrial failurefailure • ProinflammatoryProinflammatory mediatorsmediators • Free radical releaseFree radical release • Neuronal deathNeuronal death cascadescascades
  • 33. How do we Image
  • 34. Imaging/ Diagnosis of Head Injury • CT scan remains imaging of choice • Regional heterogeneity of brain metabolism • Need information on brain function: CBF, perfusion and metabolism in TBI • Xenon-enhanced CT in the ED setting
  • 35. Need for Portable Imaging • Transport risk of critical trauma patients • Portable CT with helical scanning capability, low radiation exposure, wireless links to imaging network, user-friendly, ability to perform perfusion studies.
  • 36. Magnetoencephalography
  • 37. MRI • As Field Strength increases (up to 7T) see more abnormaities • Diffusion tensor imaging (DTI) • Based on fractional anisotropic movement of water molecules • Non-invasive measurement of fiber pathway structure
  • 38. CT SCANS and X-raysCT SCANS and X-rays
  • 39. Skull fractureSkull fracture
  • 40. Coup-ContrecoupCoup-Contrecoup • focal injuryfocal injury consisting ofconsisting of contusions andcontusions and hematoma at thehematoma at the site of the blow,site of the blow, opposite side of theopposite side of the brainbrain
  • 41. Hemorrage
  • 42. Intracranial HemorrhageIntracranial Hemorrhage
  • 43. Cerebral Edema
  • 44. Reversible high T2 signalReversible high T2 signal abnormalities in pre-eclampsiaabnormalities in pre-eclampsia
  • 45. Monitoring
  • 46. INDICATIONS FOR ICP MONITORING IN PATIENTSINDICATIONS FOR ICP MONITORING IN PATIENTS WITH SEVERE TBIWITH SEVERE TBI • ↑↑ICPICP ≡≡↓↓Outcome; Aggressive TxOutcome; Aggressive Tx ≡≡↑↑OutcomeOutcome • Intra-cranial pressure monitoring (ICP) isIntra-cranial pressure monitoring (ICP) is appropriate in all patients with severe traumaticappropriate in all patients with severe traumatic brain injury (TBI) (Glasgow Coma [GCS] scorebrain injury (TBI) (Glasgow Coma [GCS] score ≤≤8)8) • The presence of open fontanels and/or suturesThe presence of open fontanels and/or sutures in an infant with severe TBI does not precludein an infant with severe TBI does not preclude the development of intracranial hypertension orthe development of intracranial hypertension or negate the utility of ICP monitoring.negate the utility of ICP monitoring.
  • 47. INTRACRANIAL PRESSURE MONITORINGINTRACRANIAL PRESSURE MONITORING • STBI (GCSSTBI (GCS≤≤8) + Abnormal CT8) + Abnormal CT ≡≡ 53-63%53-63% ↑↑ICPICP (adult data).(adult data). • Intra-cranial pressure monitoring is not routinelyIntra-cranial pressure monitoring is not routinely indicated in infants and children with mild orindicated in infants and children with mild or moderate head injury.moderate head injury. • However, a physician may choose to monitorHowever, a physician may choose to monitor ICP in certain conscious patients withICP in certain conscious patients with • traumatic mass lesions ortraumatic mass lesions or – serial neurological examination is precluded byserial neurological examination is precluded by sedation, neuromuscular blockade, or anesthesia.sedation, neuromuscular blockade, or anesthesia.
  • 48. INTRACRANIAL PRESSURE MONITORINGINTRACRANIAL PRESSURE MONITORING TECHNOLOGYTECHNOLOGY • ICP monitoring: a ventricular catheter; externalICP monitoring: a ventricular catheter; external strain gauge transducer (??); catheter tip pressurestrain gauge transducer (??); catheter tip pressure transducer devicetransducer device  All accurate & reliable (O)All accurate & reliable (O) • Ventricular cath. device most accurate, reliable,Ventricular cath. device most accurate, reliable, low cost +low cost + enables therapeutic (CSF) drainageenables therapeutic (CSF) drainage.. • No report of meningitisNo report of meningitis ⇔⇔ ICP monitoring.ICP monitoring. Jensen: 7% +tip; positive > 7.5 daysJensen: 7% +tip; positive > 7.5 days
  • 49. THRESHOLD FOR TREATMENT OF INTRA-THRESHOLD FOR TREATMENT OF INTRA- CRANIAL HYPERTENSIONCRANIAL HYPERTENSION • ICP>20-40mmHgICP>20-40mmHg ≡≡ Mort. 28%; ICP>40mmHgMort. 28%; ICP>40mmHg ≡≡ 100%100% • Treatment for intracranial hypertension, defined as aTreatment for intracranial hypertension, defined as a pathologic elevation in intracranial pressure (ICP), shouldpathologic elevation in intracranial pressure (ICP), should begin at an ICPbegin at an ICP ≥≥20 mm Hg. (O)20 mm Hg. (O) • Patients may herniate at ICP < 20-25mmHg.Patients may herniate at ICP < 20-25mmHg. • Is there a lower ICP threshold for younger children ?Is there a lower ICP threshold for younger children ? • Interpretation and treatment ofInterpretation and treatment of ↑↑ICP based on any ICPICP based on any ICP threshold should be corroborated by frequentthreshold should be corroborated by frequent – clinical examinationclinical examination – monitoring of physiologic variables (CPP, Compliance)monitoring of physiologic variables (CPP, Compliance) – cranial imaging.cranial imaging.
  • 50. CEREBRAL PERFUSION PRESSURECEREBRAL PERFUSION PRESSURE (CPP)(CPP) • A cerebral perfusion pressure (CPP) >40 mmA cerebral perfusion pressure (CPP) >40 mm HgHg
  • 51. THE ROLE OF CSF DRAINAGETHE ROLE OF CSF DRAINAGE • Cerebrospinal fluid (CSF) drainage canCerebrospinal fluid (CSF) drainage can be considered as an option in thebe considered as an option in the management of elevated ICP Drainage:management of elevated ICP Drainage: VentriculostomyVentriculostomy ±± Lumber puncture.Lumber puncture.
  • 52. Near-infrared spectroscopy • Measures complex IV cytocrome c • Mito redox state • Can detect changes in PO2/ lactate-pyruvate ratio • Potential tool for measuring cerebral aerobic metabolism
  • 53. EEG/ Bispectral Index Analysis • Continuous EEG monitoring shows that 20% of TBI patients have seizures w/in 2 wks • EEG Power spectrum analysis to monitor sedation and prevent oversedation
  • 54. Microdialysis • Measures biochemical changes in brain tissue • Increased lactate, EAA, glycerol • Decreased glucose, pyruvate • Need to collect dialysate q30 minutes for 5 days (240 samples) • Future role in target delivery of agents
  • 55. Brain Oxygen Tension Monitoring • Direct measurement of cerebral oxygen metabolism • Interpretation of PbtO2 threshold 10-20 mmHg • Placement in uninjured versus injured brain
  • 56. Treatment
  • 57. Muizelaar JP et al: Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg 59:822-828, 1983
  • 58. • Mannitol (Mannitol (2 X Class III2 X Class III) Vs. Hypertonic Saline () Vs. Hypertonic Saline (3 X Class II;3 X Class II; 1 X Class III1 X Class III).). • Mannitol is effective.Mannitol is effective. • Euvolemia + Folly catheterEuvolemia + Folly catheter • Accepted osmolarity: Mannitol < 320mOsm/L;Accepted osmolarity: Mannitol < 320mOsm/L; Hyper NS < 360mOsm/LHyper NS < 360mOsm/L • MannitolMannitol ↓↓blood viscosityblood viscosity ⇒⇒ ↓↓arteriolar diameterarteriolar diameter andand  osmotic effect.osmotic effect. • Hyper NSHyper NS  Osmolar grad; membrane pot.;Osmolar grad; membrane pot.; cellular volume;cellular volume; ↑↑ANP;ANP; ↓↓Inflammation;Inflammation; ↑↑C.O.C.O. USE OF HYPEROSMOLAR THERAPYUSE OF HYPEROSMOLAR THERAPY
  • 59. HYPEROSMOLAR THERAPYHYPEROSMOLAR THERAPY • Hypertonic saline is effective for control ofHypertonic saline is effective for control of increased ICP after severe head injuryincreased ICP after severe head injury • Effective doses: cont. infusion of 3% salineEffective doses: cont. infusion of 3% saline 0.1 - 1.0 ml/kg/h, a sliding scale.0.1 - 1.0 ml/kg/h, a sliding scale. • Goal minimum dose maintain ICP <20Goal minimum dose maintain ICP <20 mmHg.mmHg. • Mannitol bolus dose: 0.25g/Kg – 1g/Kg.Mannitol bolus dose: 0.25g/Kg – 1g/Kg.
  • 60. Hypertonic saline • Efficacy in concentrations of 3%-7.5%- 23.4% in lowering ICP • Therapeutic action more effective (53.9% vs 35%) and longer lasting than mannitol • Attenuates microcirculatory disturbances (prevent secondary cerebral small vessel diameter increases and aggregation of WBCs by 90%)
  • 61. Hypertonic saline • Clinical studies show decreases in mean number and duration of intracranial hypertensive episodes • Vasoregulatory effects: prevents vasospasm • Lowers rate of clinical failure • Theoretical concerns of CPM and rapid brain shrinkage/SDH
  • 62. USE OF HYPERVENTILATION in theUSE OF HYPERVENTILATION in the ACUTE MANAGEMENTACUTE MANAGEMENT • Mild or prophylactic hyperventilation (pacoMild or prophylactic hyperventilation (paco22 <35<35 mm hg)mm hg) should be avoidedshould be avoided.. • Mild hyperventilation (pacoMild hyperventilation (paco22 30-35 mm hg) may30-35 mm hg) may be considered for longer periods for intra-be considered for longer periods for intra- cranial hypertension refractory tocranial hypertension refractory to – Sedation and analgesiaSedation and analgesia – Neuromuscular blockadeNeuromuscular blockade – Cerebrospinal fluid drainageCerebrospinal fluid drainage – hyperosmolar therapyhyperosmolar therapy
  • 63. HYPERVENTILATIONHYPERVENTILATION • Aggressive hyperventilation (PacoAggressive hyperventilation (Paco22 < 30 mm Hg)< 30 mm Hg) may be considered as a second tier option in themay be considered as a second tier option in the setting of refractory hypertension (O).setting of refractory hypertension (O). • Cerebral blood flow (CBF), jugular venous oxygenCerebral blood flow (CBF), jugular venous oxygen saturation, or brain tissue oxygen monitoring issaturation, or brain tissue oxygen monitoring is suggested to help identify cerebral ischemia in thissuggested to help identify cerebral ischemia in this setting.setting. • Aggressive hyperventilation therapy titrated toAggressive hyperventilation therapy titrated to clinical effect may be necessary for BRIEFclinical effect may be necessary for BRIEF PERIODS in cases of cerebral herniation orPERIODS in cases of cerebral herniation or acute neurologic deterioration.acute neurologic deterioration.
  • 64. High dose barbiturate therapy • For refractory intracranial hypertension • Lower cerebral metabolic rate for O2 and modulate vascular tone • Membrane stabilization and reduced lipid peroxidation • Controversial evidence as to efficacy in severe TBI • Differential effects noted between thiopental, methohexital and pentobarbital
  • 65. THE USE of BARBITURATES in the CONTROL ofTHE USE of BARBITURATES in the CONTROL of INTRA-CRANIAL HYPERTENSIONINTRA-CRANIAL HYPERTENSION • High-dose barbiturate therapy may be consideredHigh-dose barbiturate therapy may be considered in hemodynamically stable patients within hemodynamically stable patients with salvageable severe head injurysalvageable severe head injury andand refractoryrefractory intracranial hypertension.intracranial hypertension. • If high-dose barbiturate therapy is used, thenIf high-dose barbiturate therapy is used, then appropriate hemodynamic monitoring (CVP, Swan-appropriate hemodynamic monitoring (CVP, Swan- Ganz, repeated ECHOs) and cardiovascularGanz, repeated ECHOs) and cardiovascular support (Dopamine, Adrenaline) are essential.support (Dopamine, Adrenaline) are essential.
  • 66. THE USE of BARBITURATES in the CONTROL ofTHE USE of BARBITURATES in the CONTROL of INTRA-CRANIAL HYPERTENSIONINTRA-CRANIAL HYPERTENSION • Gold standard – continuous EEG to achieveGold standard – continuous EEG to achieve a state of burst suppression.a state of burst suppression. • Serum barbiturate levels are NOT GOOD forSerum barbiturate levels are NOT GOOD for monitoring that therapy.monitoring that therapy. • Prophylactic therapy is not recommendedProphylactic therapy is not recommended (side effects).(side effects).
  • 67. Neuromuscular blockade • For mechanically ventilated to prevent cough reflex in initial 24-48 hours • Muscle relaxants cross BBB and can activate cerebral Ach receptors causing autonomic dysfunction, weakness and seizures • Resistance due to receptor up-regulation often present so need monitoring with peripheral nerve stimulator
  • 68. Temperature Control
  • 69. Concept: Brain Thermo-Pooling Dr. Nariyuki Hayashi
  • 70. Hypothermia • Dr. Hugh Rosomoff : NIH Clinical Center 1955
  • 71. Brain Thermo-Pooling Phenomenon • Brain thermo-pooling (elevation of brain tissue temperature) with damage of blood-brain barrier (BBB). • Risk: Blood temperature higher than 38.C., systolic blood pressure lower than 90-100mmHg, and cerebral perfusion pressure (CPP) lower than 70mmHg hinders washout of brain tissue temperature by cerebral blood flow. • Recorded brain tissue temperature of 40-44 degrees Celsius.
  • 72. Temperature Control in TBI • Systemic and cerebral hyperthermia is detrimental to outcome • Up to 80% of TBI patients in ICU setting with reactive hyperthermia • Monitoring of core temperature, pyrexia identified and treated • In refractory cases electrical surface cooling blankets to prevent brain hyperthermia
  • 73. Temperature Control in TBI • Surface cooling is problematic: access, time constraints, imprecision • Multi-trauma patients with splinting • Shivering increases O2 consumption and increases ICP
  • 74. Intravascular Cooling Devices
  • 75. Alsius Cooling Catheter • Saline-filled Polyethylene balloon catheter • Combines cooling capabilities with central venous access • Products may be used with femoral, subclavian or jugular access
  • 76. InnerCool Catheters • Metallic coil heating element • Very Rapid rate of cooling (6 degrees Celsius per hour) • FDA approval for Neurosurgical ICU and recovery
  • 77. Radiant Cooling Catheter • Triple-helical coil design • Expandable to 27 Fr in IVC to increase heat exchange • 37 to 33 degrees Celsius in less than 1 hour
  • 78. Transcranial Cooling
  • 79. Intranasal cooling
  • 80. Therapeutic Hypothermia • Hypothermia neuroprotective in TBI models by decreasing EAAs, augment antioxidant activity and reduction of inflammatory markers • Randomized controlled trials have shown conflicting results • Clifton et al., showed possible outcome benefit with mild hypothermia in patients with GCS of 5-7
  • 81. Therapeutic Hypothermia • NABIS H1 (National Acute Brain Injury Study: Hypothermia): 492 patients at 5 Centers • Failed to show beneficial outcome • Intercenter variability in treatment, delay in reaching target core temp, inconsistent fluid therapy • Subgroup analysis showed beneficial effects in patients age 16-45, normotensive, GCS>4 with initial core body temp less than 35 degrees Celsius and maintained core temperature
  • 82. Neuroprotective agents • Selfotel • Cerestat • Cp101-606 • Bradycor • Dexabinol • SNX-111 • Steroids • DCppene • Trilizad • PEG-SOD • IGF-1/GH • Nimodipine • Anticonvulsants
  • 83. Neuroprotective agents • Selfotel • Cerestat • Cp101-606 • Bradycor • Dexabinol • SNX-111 • Steroids • DCppene • Trilizad • PEG-SOD • IGF-1/GH • Nimodipine • Anticonvulsants
  • 84. Calcium Channel BlockersCalcium Channel Blockers
  • 85. Ca2+ influx Voltage-Operated Ca2+ specific Receptor-Operated Ca2+ / Cation Ligand-Operated Ca2+/Cation Plasma membrane channels Ca2+ Mitochondrial Ca Uptake Sarco-/Endo-plasmic reticulum Ca Uptake Ca/Mg pumpNa-Ca exchg.
  • 86. Calcium Channel blockersCalcium Channel blockers • May be membrane protectiveMay be membrane protective • Affect VasospasmAffect Vasospasm
  • 87. Coronary/Cerebral StealCoronary/Cerebral Steal The detrimental redistribution of blood flow in patients with atherosclerotic disease from underperfused areas toward better perfused areas Before Vasodilator Stenosis After Vasodilator
  • 88. Dexabinol • Cannabinoid and non-competitive NMDA- receptor antagonist • Safely decreases mean time of ICP elevation above 25 mmHg and MAP <90 • Also acts as antioxidant and cytokine inhibitor • Phase III trials promising
  • 89. Anti-inflammatory agents • Anti-ICAM-1 (Enlimomab) • Anti IL1-alpha • Anti a4 integrin Ab • Chemokine inhibitor (CXC/CC types) • MEK 1 /2 (MAP/ERK kinase) inhibitor U0216 • P38 MAP kinase inhibitor SB239063 • Selective PKC inhibitor Go6976 • Caspase inhibition • Naloxone • Proteosome inhibitor PS519 • Indomethicin • Celecoxib (COX-2 selective) • Cyclosporin A • Epoeitin A
  • 90. Failure of Translational research • Rx w/in 1 hour • Single dose • Lesion/infarct size • Outcome days/wks • No adjunct therapy • Inbred rodents/male • Single mechanism of injury • Rx w/in 8 hours • Multiple dosages • GOS • Outcome mos/yrs • Multiple Rx • Variable population • Multiple mechanisms
  • 91. Future Trends in Preclinical Research • Multiple models/ complexity (secondary injury) • Different species/gender/age • Timing of interventions • Range of severities • Physiological dosages • Drug interactions (antiepileptics) • Multifaceted treatment cocktails • Surrogate biomarkers (animal ICU): ICP, SjvO2, imaging, microdialysis, etc.
  • 92. Surgical DecompressionSurgical Decompression
  • 93. DECOMPRESSIVE CRANIECTOMYDECOMPRESSIVE CRANIECTOMY • Decompressive craniectomy appears to beDecompressive craniectomy appears to be lessless effectiveeffective in patients who have experiencedin patients who have experienced extensive secondary brain insultsextensive secondary brain insults • Patients who experiencePatients who experience – Secondary deterioration on the Glasgow coma scaleSecondary deterioration on the Glasgow coma scale (GCS) and/or evolving cerebral herniation syndrome(GCS) and/or evolving cerebral herniation syndrome within the first 48 hrs after injury may represent awithin the first 48 hrs after injury may represent a favorable groupfavorable group – Unimproved GCS of 3 may represent anUnimproved GCS of 3 may represent an unfavorableunfavorable groupgroup
  • 94. THE USE OF CORTICOSTEROIDS IN THETHE USE OF CORTICOSTEROIDS IN THE TREATMENT TBITREATMENT TBI • With the lack of sufficient evidence forWith the lack of sufficient evidence for beneficial effect and the potential forbeneficial effect and the potential for increased complications and suppressionincreased complications and suppression of adrenal production of cortisol, the routineof adrenal production of cortisol, the routine use of steroids is not recommendeduse of steroids is not recommended forfor patients following severe traumatic brainpatients following severe traumatic brain injury.injury.
  • 95. NUTRITIONAL SUPPORTNUTRITIONAL SUPPORT • Replace 130-160% of resting metabolismReplace 130-160% of resting metabolism expenditure after TBI in patients. Weight-expenditure after TBI in patients. Weight- specific resting metabolic expenditurespecific resting metabolic expenditure guidelines can be found in Talbot's tables.guidelines can be found in Talbot's tables. • Based on the adult guidelines, nutritionalBased on the adult guidelines, nutritional support shouldsupport should – begin by 72 hrsbegin by 72 hrs – with full replacement by 7 days.with full replacement by 7 days.
  • 96. THE ROLE of ANTI-SEIZURE PROPHYLAXISTHE ROLE of ANTI-SEIZURE PROPHYLAXIS FOLLOWING STBIFOLLOWING STBI • Prophylactic anti-seizure therapy may beProphylactic anti-seizure therapy may be considered as a treatment option toconsidered as a treatment option to prevent increased oxygen utilizationprevent increased oxygen utilization
  • 97. Questions ?

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