curs 5- traumatismele craniocerebrale

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  • Mechanisms of Injury Traumatic Brain Injury Blunt(Closed)PenetratingExplosion Fall GSW Stab Blast FragmentMotor vehicle crashes (MVC)

  • CURSTRAUMATISMELE CRANIO-CEREBRALE

  • Relative Proportion of Levels of Care for TBISource: CDC: Traumatic Brain Injury in the United States, October 2004

    50,000 Deaths235,000Hospitalizations1,111,000Emergency Department Visits???Other Medical Care or No Care

  • Military Context

  • Blast Wave PhysicsCourtesy of Keith Prusaczyk, Ph.D.

  • Types of InjuriesPrimary Injuries Scalp lacerationsSkull fractures (Linear, depressed, basiliar)Facial fractures (Le Forte 1 3)Concussion (mild traumatic brain injury): amnesiaCerebral contusionAxial / Extra-axial haematomasDiffuse axonal injury

  • ConcussionThe diagnostic sign is amnesiaTakes few months to resolveNo morphological abnormalityNo abnormalities on radiologyBeware of Second Impact Syndrome

  • Cerebral ContusionsFrontal & Temporal regions commonlyCan be multiple and bilateral An area of haemorrhage & oedemaDiagnose by CT / MRIIt is primary injury but produces secondary injury due to increased ICP

  • Diffuse Axonal InjuryRotational ForcesAcceleration Deceleration injuriesNeuronal tearing in white matterSeen on MRISuspect if many cerebral contusions on CT scan and patient has prolonged coma (>6hrs) with no evidence of a SOL.

  • Secondary InjuryCellular changesHypoxiaHypercarbiaHypotensionCerebral oedemaVasogenicCytotoxicIncreased Intra Cranial Pressure

  • Why Worry?Increasing ICPDecreased cerebral perfusion pressure causing ischaemiaMidline shift causing ventricular obstructionHerniationUncalCentralCingulate (subfalcine)Cerebellar Transcalvarial

  • HerniationUncal HerniationMedial temporal lobe (Uncus) compresses midbrain with increasing ICPPressure in the region of kernohans notch causes ipsilateral pupillary dilatation, ipsi / contralateral hemiparesis and possible posterior cerebral artery compressionDecreased level of consciousnessRespiratory pattern changeGoal is to prevent this from occuring

  • Recognition and Management of Specific Head InjuriesSkull FractureCause of Injury Most common cause is blunt trauma Signs of InjurySevere headache and nauseaPalpation may reveal defect in skullMay be blood in the middle ear, ear canal, nose, ecchymosis around the eyes (raccoon eyes) or behind the ear (Battles sign)Cerebrospinal fluid may also appear in ear and noseCareImmediate hospitalization and referral to neurosurgeon

  • Recognition and Management of Specific Eye Injuries

  • Mechanisms of Injury3 CollisionsCar hits objectHead hits windshieldBrain hits inside of skull

  • Mechanisms of Injury

  • Mechanisms of InjuryBrain movement inside the skullBase of skull is very roughMost brain movement is at the topBrain suspended by vessels and brain tissue that can be torn by movement, especially at the base

  • Mechanism of Injuries, cont.Rotational injuries injury occurs acceleration-deceleration of the brain does not follow straight linear path.Brain twists and moves at angles causing stretching and shearing of brain tissue and potential vascular injury.Penetrating include missile injuries, GSW or impalement.

  • Penetrating Mechanism

  • Response to InjuryDue to increased blood volume (not edema)Natural response to injury anywhere on your bodyBody rushes nutrients to heal injured area

  • Response to InjuryIncrease in cerebral edema (water) develops after 24-48 hours and peaks in 3-5 daysNot an acute concern, per say

  • Intracranial PressureThe pressure of the brain contents within the skull is intracranial pressure (ICP)The pressure of the blood flowing through the brain is referred to as the cerebral perfusion pressure (CPP)The pressure of the blood in the body is the mean arterial pressure (MAP)

  • Intracranial PressureMAP (Mean Arterial Pressure) can be determined by a simple formula:

    MAP = systolic + 2x diastolic 3

  • Intracranial PressureExample of MAP

    B/P is 120/80

    MAP = 120 + 160 = 280 = 93 mm/hg 3 3

  • Intracranial PressureIntracranial pressure (ICP)is measured by a device that is implanted through the skull by a surgeon

    The normal value for ICP is 0 - 10 mm/hg

  • Intracranial PressureCerebral Perfusion Pressure (CPP) can be determined by the following formula:CPP = MAP - ICP

    Normal CPP range is 60 - 150 for autoregulation to work well!

  • Intracranial PressureExample of CPPBlood Pressure is 140/80ICP is 30CPP = 100 - 30 = 70 mm/hgIs this enough for autoregulation?What would happen if the ICP was 80?

  • Assessment FindingsCushings Triadhypertensionbradycardiaaltered respirationsLATE SIGN!

    Why do we get into Cushings Triad?

  • Assessment FindingsBP of 250/130MAP would be 170!Why is the MAP so high?The ICP is 100!Is this a good thing?Should we lower the blood pressure?

  • Concussions (Mild Head Injuries)Characterized by immediate and transient post-traumatic impairment of neural functionCause of InjuryResult of direct blow, acceleration/deceleration forces producing shaking of the brainCoup mechanismContra-coup mechanismSigns of InjuryBrief periods of diminished consciousness or unconsciousness that lasts seconds or minutesHeadache, tinnitus, nausea, irritability, confusion, disorientation, dizziness, posttraumatic amnesia, retrograde amnesia, concentration difficulty, blurred vision, photophobia, sleep disturbances

  • CareThe decision to return an athlete to competition following a brain injury is a difficult one that takes a great deal of considerationIf any loss of consciousness occurs the ATC must remove the athlete from competition With any loss of consciousness (LOC) a cervical spine injury should be assumedObjective measures (BESS and SAC) should be used to determine readiness to playA number of guidelines have been established in an effort to aid clinicians in their decisions

  • Scalp InjuriesCause of InjuryBlunt trauma or penetrating trauma tends to be the causeCan occur in conjunction with serious head traumaSigns of Injury Athlete complains of blow to the headBleeding is often extensive (difficult to pinpoint exact site)CareClean w/ antiseptic soap and water (remove debris)Cut away hair if necessary to expose areaApply firm pressure or astringent to reduce bleedingWounds larger than 1/2 inch in length should be referredSmaller wounds can be covered w/ protective covering and gauze (use extra adherent)

  • Facial LacerationsCause of InjuryResult of a direct impact, and indirect compressive force or contact w/ a sharp objectSigns of InjuryPainSubstantial bleeding CareApply pressure to control bleedingReferral to a physician will be necessary for stitches

  • CareControl bleeding and refer to a physician for X-ray,examination and reductionUncomplicated and simple fractures will pose little problem for the athletes quick returnSplinting may be necessary

  • Recognition and Management of Specific Ear Injuries

  • Rupture of the Tympanic MembraneCause of InjuryFall or slap to the unprotected ear or sudden underwater variation can result in a ruptureSigns of InjuryComplaint of loud pop, followed by pain in ear, nausea, vomiting, and dizzinessHearing loss, visible rupture (seen through otoscope)CareSmall to moderate perforations usually heal spontaneously in 1-2 weeksInfection can occur and must be continually monitoredShould not fly until condition is resolved

  • Rupture Tympanic Membrane

  • Recognition and Management of Specific Eye InjuriesOrbital Hematoma (Black Eye)Cause of Injury Blow to the area surrounding the eye Signs of InjurySigns of a more serious condition may be displayed as a subconjunctival hemorrhageSwelling and discolorationCareCold application for at least 30 minutes, 24 hours of rest if athlete has distorted visionDo not blow nose after acute eye injury may increase hemorrhaging

  • Orbital Fracture Cause of Injury Direct trauma to the eyeball Signs of InjuryBlurred visionDiplopiaRestricted eye movementDownward displacement of the eyeSoft-tissue swelling and hemorrhagingNumbness Infraorbital nerve entrapmentCareX-ray will be necessary to confirm fractureAntibiotics Decrease risk of infection (due to proximity of maxillary sinus and bacteria)Treat surgically or allow to resolve spontaneously

  • Orbital Fracture

  • Critical Care Management in Traumatic Brain Injury Dr.(Mrs.) Bibhukalyani DasProf. & HOD Neuroanaesthesiology, Neuro ICU & Pain ClinicBangur Institute of Neuroscience & Psychiatry Kolkata

  • TBI is a global public health problem.Urbanization : Vehicles Incidence in Developing Countries. 70% victims of RTA sustain TBI 70% of RTA deaths are due to TBIMajority death occur in 72 hrs.Victims :Young males in productive age groupChildren constitute 25-30% of all TBI victimsLoss of life, Rehab of disabledSig.Econo.burdn

  • Pathophysiology:TBIA.Primary Injury (Br. damage @ impact) Minor Concussion DAI BS dysf. Followed by series of secondary events : (i) Focal hematoma / contusion (ii)Changes in CBF & CMRO2 (iii) ICP (iv) Biochemical changes @ Cellular level B.Secondary Brain Injury (hours to days)

  • TBI : Clinical Grading Duration of Unconsciousness & GCSMild : < 30 minutes 13-15Moderate: > 30 min. < 6 hours 9-12Severe : > 6 hours 8 Mortality in severe TBI is 20-25% even in neurological centers of excellence. Intensive care needed to secondary insult

  • TBI : Management ProtocolMild - Discharge with advice OR watch for 24hrs.Moderate - Admission Investigation & Imaging Conservative OR Operative management as per need.Severe - ICU Management .

  • ICU management: Severe TBI Aim is to :Optimize O2 & substrate delivery Detect harmful events. ICU management include : Intensive monitoring & Intensive therapy

  • ICU management: Severe TBI Aim is to :Optimize O2 & substrate delivery Detect harmful events. ICU management include : Intensive monitoring & Intensive therapy

  • TBI : ICU MonitoringClinical Neurological Assessment & serial CTCVS monitoring (HR, ECG, NIBP/IBP, CVP, PCWP)Respiratory : SpO2 , EtCO2, ABG, Serial chest X-rayICP monitoringJugular venous O2 saturation & ABGTranscranial Doppler monitoring Evoked potential monitoringCore Temp. monitoringMetabolic monitoring with PET, Br. Microdialysis.Fluid intake /output, Sr. electrolytes, Glucose, BUN etc.

  • TBI : ICP monitoring Importance:To predict & optimize CPP (MAP-ICP)Cl. Signs of ICH are late , nonconsistentEpisodic ICP may occur in pts. normal CT /MRI.Intraventricular Catheter Method is gold standard, but carries 1 2 % risk of Hmrge ; 8 10% risk of infectionEpidural & Subdural devices less accurate Intraparenchymal F.O. probes easy to use, infection

  • ICP monitoring(contd.)3 types of WAVES described by Lundberg -A wave : ICP>40mmHg, lasts for 5-20 mins indicates severe in IC compliance & needs aggressive management.B wave : ICP 20-25 mmHg Frequency 1-2 /min . Indicate compliance Needs treatment.C wave : No clinical significance.

  • TBI : TCD monitoringUseful non-invasive CBF monitor To diagnose Post-traumatic vasospasmIndirect estimation of ICP or CPP.MCA commonly used (75-80% IC flow)Shows Systo., Diasto., Mean CBF velocityNormal FV = 35 90 cm /sec; > 100 cm/sec in TBI ; > 200 cm/sec shows angiographic vasospasmContd. ICP Initial & then loss DCBF isolated systo.spike oscillating flow pattern (onset of IC circulatory arrest)

  • TBI : Jugular venous oxymetry The device offers 3 indices to assess CBF:1. Jugular venous oxygen saturation( SjVO2) 60-80% - Normal , > 90% -Hyperaemia < 50% -Hypoperfusion2. Cerebral arterio-venous O2 diff.(A-VDO2) A-VDO2 = CMRO2/ CBF: 5-7.5 vol% Normal 7.5 vol% Hypoperfusion3. Cerebral O2 extraction (CEO2) 20-40% Normal > 40% hypoperfusion.

  • Newer modalitiesDirect tissue oximetry : detects regional ischemia. Normal PbtO2 = 20 40 mmHg ; 8 10 mmHg criticalPbtO2 8.5 mmHg correlates 50% SjvO2Near infra red spectroscopy (NIRS) : not quantitative ; Contusion, extracereberal collection interferes.Cerebral microdialysis

    These are very expensive, not available in many centers & provide regional information.

  • Multimodal Evoked Potential Functional assessment of neuronal activity Good predictor of Outcome in TBI(A) Somato sensory evoked potential (SSEP) (B) Auditory brainstem evoked potential ( ABEP ) 70-80% good outcome when EP NormalPoor prognosis when absentComplex electrical environment of ICU makes this monitoring difficult.

  • TBI : Intensive TherapyAim is to achieve optimum cerebral perfusion and prevent secondary ischaemic insultsCPP = MAP ICP : Ideally 60-70 mmHging MAP : volume expansion , ionotrops & vasopressoring ICP : head-up position, hyperventilation , diuretics , CNS depressants, drainage of CSF.

  • Intracranial Pressure (ICP) The Monro-Kellie DoctrineMonro, 1783 Constant intracranial volume Incompresible brain substanceKellie, 1824 Constant intracranial compartments because the skull is a rigid box

    Compensatory mechanisms Drainage of CSF to spinal compartmentVasoconstriction

  • Intracranial Pressure (ICP) Monitoring 1951Guillaume and Janny - continuous monitoring of ventricular pressure in humans1952Strain gauge pressure transducers and polygraph - correlation of ICP to physiologicial manipulations 1953Ryder - CSF pressure / volume curve1960Lundberg - continuous recording of ICP in patients, ICP waves1965Langfitt - volume / pressure relationship 1975Miller - volume / pressure response (brain compliance)

  • CSF pressure / volume curve

  • Intracranial Pressure (ICP)ICP WavesICP levels Severely increased 40 mm Hg Moderately increased20 -40 mm Hg Slightly increased 10-20 mm HgICP waves A waves 50-100 mm Hg, for 5-20 min headache, nausea, vomiting B waves 20-40 mm Hg, 1-2 / min periodic breathing, somnolence C waves 10-20 mm Hg, 4-8 / min BP waves

  • Pathphysiology of Increased ICP Hydrocephalus Communicating Non-communicating

    Space occupying lesion (SOL) Tumor, hematoma/blood clot, contusion

    Brain swelling - accumulation of brain water Brain edema Vasogenic Cellular (cytotoxic) Vascular congestion - increase CBV

  • Treatment of Intracranial Hypertension Oxygenation and hydration 300 head elevation Sedation and paralysis Ventricular CSF drainage Osmotic therapy - urea, mannitol Nonosmotic diuretics - furosemide Corticosteriods Hyperventilation Barbiturates, Propofol

  • The Role of Anti-Seizure Prophylaxis Following TBIHigh risk patients for developing posttraumatic seizureGCS
  • Cerebral Perfusion Pressure (CPP) CBFThe critical parameter for brain function Difficult to quantify and continuously measured CPP - estimation of CBF

    CPP = MAP - ICP

    Mean systolic BP minus intracranial pressure

  • Cerebral Blood Flow (CBF)The brain - high metabolically active organ2% of total body weight20% of cardiac output 20% of total body oxygen consumption

    Glucosethe main energy sourceGlycogenlimited energy reservesOxygenno reserves

    Constant supply of nutrients is requiredDecreases CBF causes brain ischemia

  • Cerebral Blood Flow (CBF)Threshold of CBF and Ischemia50 ml/100 g/min Normal25 ml/100 g/min Alteration in consciousnessAbnormal EEG18 ml/100 g/min Paralysis, aphasia Loss of evoked potentials Partial Na/K pump failure16 ml/100 g/min Complete pump failure Cytotoxic edema Calcium channels open 12 ml/100 g/minCell death

  • Intracranial HypertensionSigns and SymptomsHeadache, vomiting, confusion, lethargy, drowsiness, comaChanges in vital signs, medullary compressionCushings triad - experimental, rare in human and trauma,trminal stages Herniation signs - pupillary signs: ipsilateral and bilateralmydriasisHemiparesisPapilledema - in chronic elevation of ICP

  • Cerebral AutoregulationIntrinsic mechanisms control cerebral arteriolesdiameter - maintain adequate cerebral perfusion inresponse to physiological changes

    1) Metabolic theory - metabolic requirements 2) Myogenic / pressure theory - systemic BP controls cerebral perfusion3) Carbon dioxide (CO2) reactivity - vasodilation and vasoconstriction in response to PaCO24) Blood viscosity - rheological properties of blood are altered by blood viscosity can change CBF

  • Cerebral AutoregulationMetabolic Theory Metabolic requirements control vasomotor changes

    Coupling between metabolism and CBF in normal conditions

    High activity (seizure, fever) increased metabolism > increases CBF

    Low activity (coma, anesthesia, hypothermia) low metabolism > decreases CBF

  • Barbiturates in the Control of Intracranial HypertensionCerebral Metabolism Cerebral Metabolic Demand(glucose, oxygen)CBFCBVICPSide Effect BPCPP

  • TreatmentIntracranial pressure monitoringIntraparenchymalIntraventricularDirect CSF drainageEpidural

  • CPP managmentTarget euvolaemiaVasopressorsIf ICP is less than 20 then continue to monitor and treat patientIf ICP>20 drain CSF

    Assess patientIf ICP is greater than 20 then hyperventilate.If still then mannitolIf still consider transferConsider decompressive craniectomy (DECRA trial)If still and GCS

  • Randomised Evaluation of Surgery with Craniectomy forUncontrollable Elevation of Intra-Cranial Pressure

  • Stage 1 - initial treatment measures:Patients will be sedated, analgesed and ventilated. Patients may or may not be paralysed but this must be noted. They will be nursed head up with no venous obstruction. Invasive monitoring (central venous pressure and arterial lines as a minimum will be applied). Targets for physiological parameters will be:Cerebral perfusion pressure > 60 mmHg (central venous pressure 6-10),Oxygen saturation >97%,Arterial CO2 = 4.0-4.5 kPa,Temperature
  • Stage 2 - advanced treatment measures: In stage 2 the following measures can be considered, all of which are optional:An external ventricular drain - depending on the size of the lateral ventricles Mannitol Inotropes to increase the mean arterial pressure to maintain a cerebral perfusion pressure of >60 mmHg. Arterial carbon dioxide 3.5 to 4.5kPa (can be monitored with jugular venous oxygen saturation sensors maintaining SjvO2 >55%) Hypertonic saline Moderate cooling (35-36C) but not severe hypothermia
  • Stage 1INITIALTREATMENTMEASURES:Nurse head upVentilationSedationAnalgesia+/- ParalysisMonitoring:CVPArterial lineICPICP > 25mm Hg

    Stage 3RANDOMISEMEDICALSURGICALContinued Medical Treatment*(stage 2 options) + barbiturates permittedDecompressive craniectomy**

  • Stage 2 OPTIONS: Ventriculostomy Inotropes Mannitol Hypertonic saline Loop diuretics Hypothermia 36-34 BARBITURATES NOT PERMITTED ICP > 25 mm Hg 1-12 hours post start stage 2

  • [Summary of RESCUEicp protocol]References:Hutchinson PJ et al; Surgery for Brain Edema, Neurosurgery Focus,May 2007,15;22.Sahuquillo.J, Arikan.F; Decompressive Craniectomy for the treatment of refractory high intra-cranial pressure intraumatic brain injury, The Cochrane Collabaration, Volume(1) 2006.

    The mechanism of TBI is divided into two main categories: blunt (closed) and penetrating. Discovering the mechanism of injury is important in helping the clinician find the injuries sustained. Blunt trauma is defined as an injury produced by the wounding forces of compression and change of speed, both of which can disrupt tissue (Sanders, 2001). Common causes of blunt trauma include motor vehicle crashes, sports injuries, blast injuries, and vertical falls. A penetrating trauma is an injury that is produced by the crushing and stretching forces of an object that has caused some form of tissue disruption. The character of the penetrating object, its speed of penetration, and the type of body tissue it passes through or into determine whether crushing or stretching forces will cause injury. Gunshot and stab wounds are examples of penetrating head injury.In combat situations, shrapnel and fragments may be the etiology of penetrating brain injury. The four most common mechanisms of injury for TBI in war are: explosion or blast injury, motor vehicle crashes (MVC), falls and GSWs.