8/31/2017 Head Trauma PFN: SOMEML35
8/31/2017Head TraumaPFN: SOMEML35Hours: 3.0Instructor:JSOMTC, SWMG(A)Slide 1Terminal Learning Objective Action: Communicate knowledge of headtrauma Condition: Given a lecture in a classroomenvironment Standard: Received a minimum score of75% on the written exam IAW coursestandardsJSOMTC, SWMG(A)Slide 2References USASOC Neurocognitive Testing and Post‐Injury Evaluation and Treatment ClinicalPractice Guideline (CPG)USASOC Guidelines For Post‐ConcussionRehabilitationUSASOC mTBI Symptom Cluster TreatmentRecommendationsUSASOC Concussion Patient InformationSheetJSOMTC, SWMG(A)Slide 31
8/31/2017References Tintinalli’s Emergency Medicine, 7th edition,2010Tactical Trauma ProtocolsPHTLS, 7th edition, 2010USASOC Policy 10‐10 NeurocognitiveTesting ProgramJSOMTC, SWMG(A)Slide 4ReasonJSOMTC, SWMG(A)Slide 5Agenda Identify key definitions and epidemiologyof traumatic brain injuryIdentify the pathophysiology of traumaticbrain injuryIdentify types of head injuriesIdentify the clinical presentation andmanagement of scalp injuriesIdentify the clinical presentation andManagement of open head injuriesJSOMTC, SWMG(A)Slide 62
8/31/2017Agenda Identify the clinical presentation andmanagement of penetrating injuriesIdentify the clinical presentation andmanagement of closed skull injuriesIdentify the clinical presentation andmanagement of closed head injuriesIdentify the clinical presentation of blasthead injuriesJSOMTC, SWMG(A)Slide 7Agenda Identify the clinical presentation andmanagement of brain injuriesIdentify the Clinical Presentation andmanagement of moderate to severe TBIIdentify the Clinical Presentation andmanagement of mild TBIParticipate in a head trauma case reviewMace DemonstrationJSOMTC, SWMG(A)Slide 8Identify Key Definitions andEpidemiology of Traumatic BrainInjuryJSOMTC, SWMG(A)Slide 93
8/31/2017TBI in the Department of DefenseOver 80% of TBIsoccur in a non‐deployed settingCommon causes of TBIinclude MVA, falls,sports and recreationactivities, and militarytraining JSOMTC, SWMG(A)Slide 10TBI Epidemiology Leading cause ofdeath and disability inchildren and adultsfrom ages 1 to 44Twice as common inmenFalls, MVCs, andconcussive weapons Trimodal distribution0 to 4 years old15 to 24 years old 75 years old Mortality risescontinuously with age 20% of combatpersonnel sustain TBIJSOMTC, SWMG(A)Slide 11Traumatic Brain Injury (TBI) Impairment in brainfunction as a result ofmechanical forceCan be temporary orpermanentMay or may not result inunderlying structuralchanges in the brainClinical severity rangesfrom very mild toprofoundly impairedJSOMTC, SWMG(A)Slide 124
8/31/2017Identify the Pathophysiologyof Traumatic Brain InjuryJSOMTC, SWMG(A)Slide 13Intracranial Pressure Brain is a semisolid organ that occupies 80% of the cranialvault 20% of the body’s oxygen supply 15% of cardiac outputCranial Vault Fixed in size by outer rigid skull Contains brain tissue, blood vessels and CSFMonroe‐Kelli Doctrine Defines the relationship between the volumes of thethree compartments The expansion of one compartment MUST beaccompanied by a compensatory reduction in thevolumes of the other compartments to maintain astable intracranial pressure (ICP)JSOMTC, SWMG(A)Slide 14Primary Injury "Impact Injury" Tissue destruction that occurs as a direct resultof a physiologic trauma Very little can be done by providers toinfluence primary injury Severity and location of the primary braininjury will dictate the patients immediate levelof consciousness, metal status, and focalneurologic signsJSOMTC, SWMG(A)Slide 155
8/31/2017Secondary Brain Injury Focus of TBI treatment, to minimizesecondary brain injury ‐ can be moredamaging than primary injuryHYPOTENTSION AND HYPOXIA are the twomost acute and easily treatable mechanismof secondary injuryContinues for an indefinite period of timeJSOMTC, SWMG(A)Slide 16Secondary Brain Injury Systemic Insults Hypoxia (PaO2 90) Mortality of TBI pts with hypoxia doubled Increases brain cell death and edema Hypotension (SBP 90 mmHg) Hypotension Cerebral Perfusion CerebralIschemia Doubles Mortality Anemia 2/2 Blood Loss ( Oxygen Carrying Capacity) Hypocapnia ( pCO2)/Hypercapnia ( pCO2retention) Hyperven la on pCO2 Levels Serum pH Cerebral Vasoconstric on Cerebral Blood FlowJSOMTC, SWMG(A)Slide 17Secondary Brain InjuryOther Systemic Cause Anemia (impair oxygendelivery to the brain)Hypotension (impair oxygendelivery to the brain)Increased or decreasedblood glucose (Brain cellscannot function without it)Seizures (seen in 30%–40%of patients with penetratingbrain injuries)JSOMTC, SWMG(A)Intracranial CauseCerebral edema Hematomas Increased intracranialhypertension (ICP) Slide 186
8/31/2017Increased Intracranial Pressure Most frequent cause of death and disability after severe headinjuryDelayed cerebral swelling is the major cause of raised ICP anddeathWhen ICP rises: CPP decreases PO2 decreases PCO2 levels increase cerebral vasodilation cerebral blood volumeincreases further increased ICPJSOMTC, SWMG(A)Slide 19PathophysiologyJSOMTC, SWMG(A)Slide 20Identify Types of Head InjuriesJSOMTC, SWMG(A)Slide 217
8/31/2017Head Injuries Scalp Injuries Open (puncture, laceration,avulsion)Closed (contusion)Closed Head Injuries Blunt Diffuse Axonal Injury (DAI)Intracranial hemorrhagesCerebral contusions Skull Fractures Open Head Injuries Penetrating Primary Blast Overpressure centralnervous system injuriesJSOMTC, SWMG(A)Slide 22Identify the ClinicalPresentation andManagement of Scalp InjuriesJSOMTC, SWMG(A)Slide 23Scalp InjuryInjury to the overlying skin of the scalp, which may be incombination with injury to the skull, brain and/or face Causes Penetratingtrauma (rifle,impaledobjects,missilewounds) Blunt trauma(MVA, blast)JSOMTC, SWMG(A) Closed (contusion)Open (puncture,laceration, or avulsion) Can lead to massiveblood loss andhypovolemic shockSlide 248
8/31/2017Scalp Injury Hemorrhage controlDirect pressure or pressuredressings Donut ring Lidocaine with epinephrineinfiltration Clamp or ligate vessels Assess for fracturePrevent contaminationRepair galeal defectsJSOMTC, SWMG(A)Slide 25Identify the ClinicalPresentation and Managementof Open Head InjuriesJSOMTC, SWMG(A)Slide 26Open Head Injuries CausesPenetrating trauma Blunt trauma Signs and Symptoms JSOMTC, SWMG(A)Profuse bleeding no matterhow minor the injuryCrepitusEdemaDepressionsDeformitiesVisualize skull or bonyfragmentsSlide 279
8/31/2017Identify the Clinical Presentationand Management of PenetratingInjuriesJSOMTC, SWMG(A)Slide 28Penetrating Injury Missiles and stabwoundsAssociated injuriesSkull fractureDamage to cerebralvasculature Intracranialhemorrhage Complications includeinfection and post‐traumatic epilepsyJSOMTC, SWMG(A)Slide 29Penetrating InjuryA. Lateral skull film of a 19-year-old male who sustained multiple stab wounds to thehead, demonstrating extensive pneumocephalus. B. A CT scan of the head of the samepatient demonstrates numerous pockets of air in the sulci with marked subarachnoidpneumocephalus.JSOMTC, SWMG(A)Slide 3010
8/31/2017Identify the ClinicalPresentation and Managementof Closed Skull InjuriesJSOMTC, SWMG(A)Slide 31Skull FracturesJSOMTC, SWMG(A)Slide 32Classification of Skull Fractures Open versus closedLocation Specific skull bone (i.e.temporal)BasilarPattern LinearDepressedComminutedJSOMTC, SWMG(A)Slide 3311
8/31/2017Linear Skull Fracture Accounts for about80 percent of allopen head injuriesInjury does notpenetrate braintissue, most areminor and requirelittle treatmentJSOMTC, SWMG(A)Slide 34Depressed Skull Fracture Typically occurs whensignificant force isapplied over a smallareaScalp lacerationsshould undergo sterileexplorationJSOMTC, SWMG(A)Slide 35Basilar Skull Fracture May occur anywherealong the skull baseSignificant risk factor forintracranial injuryFractures to the basilararea typically do nothave localizingsymptomsIndirect signs oftendevelopJSOMTC, SWMG(A)Slide 3612
8/31/2017Battle’s Sign Retro‐auricular EcchymosisDiscoloration of the soft tissuebehind the earAssociated with fracture ofauditory canal and lower areas ofskullThis is a late sign and may not bereadily seen.JSOMTC, SWMG(A)Slide 37Raccoon Eyes Bilateral PeriorbitalEcchymosisFracture in the anteriorportion of the skull baseJSOMTC, SWMG(A)Slide 38Hemotympanum Blood behindtympanic membraneFracture linecommunicates withthe auditory canalMay have associatedvertigo, hearing loss,and CN VII palsyJSOMTC, SWMG(A)Slide 3913
8/31/2017Classify this FractureJSOMTC, SWMG(A)Slide 40CSF Leak CSF can leak from thenose (rhinorrhea) or ears(otorrhea)Dextrose or halo test canassist in confirmation, butis not reliablePatients can developmeningitisRequires surgical repairHead elevation andantibiotics are fieldtreatmentJSOMTC, SWMG(A)Slide 41Identify the ClinicalPresentation and Managementof Closed Head InjuriesJSOMTC, SWMG(A)Slide 4214
8/31/2017Closed Head InjuryMay or may not be lacerations of the scalp, but the skull is intact, andthere is no opening to the brain. Injury to the brain itself may be farmore extensive in a closed head injury because more of the injuringforce is transmitted deeper into the brain due to pressure build‐up Causes Coup‐ContrecoupBlunt TraumaSigns and Symptoms Crepitus around injury siteHeadacheNeurological symptoms:Altered LOCRestlessnessUnequal pupilsBruisingDrainage ‐ drainage of blood or CSF fluidfrom the ears, nose, or eyes.BradycardiaIncreased systolic blood pressureNausea/vomitingDecreased Respirations/Cheyne Stokesbreathing patternDeformity of the skullJSOMTC, SWMG(A)Slide 43Coup/CountrecoupFocal Brain Injury Coup The brain is injureddirectly under the areaof impactCountrecoup Brain is injured on theside opposite theimpactJSOMTC, SWMG(A)Slide 44Diffuse Axonal Injury (DAI)Diffuse Brain Injury Stretching and shearing of white matterand axonsGenerated by sudden deceleration orrotational forcesEdema develops rapidlyOften produces devastating andirreversible deficitsBlunt trauma, MVA, or Shaken BabyJSOMTC, SWMG(A)Slide 4515
8/31/2017Diffuse Axonal Injury (DAI)Diffuse Brain InjuryJSOMTC, SWMG(A)Slide 46Identify the ClinicalPresentation of Blast HeadInjuriesJSOMTC, SWMG(A)Slide 47Primary BlastA direct injury to the brain or via a force transmitted by the greatvessels of the chest to the brain Associated with:unconsciousness, confusion,headache, tinnitus, dizziness,tremors, increased startleresponse, and increasing ICPBleeding may occur frommultiple orificesMay have no external signs ofinjury and only subtle signs ofcognitive dysfunction inattention, concentration,reaction time, and balanceJSOMTC, SWMG(A)Slide 4816
8/31/2017Identify the ClinicalPresentation and Managementof Brain InjuriesJSOMTC, SWMG(A)Slide 49Direct Brain Injury Focal DiffuseOccur at a specific location inbrain Differentials Cerebral Contusion Intracranial Hemorrhage Epidural hematoma Subdural hematoma Intracerebral Hemorrhage ConcussionDiffuse Axonal Injury (DAI)JSOMTC, SWMG(A)Slide 50Cerebral ContusionFocal Brain Injury Cerebral ContusionBlunt trauma to local brain tissueCapillary bleeding into brain tissue Common with blunt head trauma Confusion Neurologic deficit Personality changesVision changesSpeech changesResults from Coup‐contrecoup injuryJSOMTC, SWMG(A)Slide 5117
8/31/2017Cerebral Contusion The head CT scan of ayoung male who afterbecoming intoxicatedfell to the ground,striking the left side ofhis head. Note thelarge left‐sided scalpcontusion. Also notethe right‐sidedcerebral contusion(contrecoup injury).JSOMTC, SWMG(A)Slide 52Types of Brain Hemorrhage Classified accordingto locationEpiduralSubdural Subarachnoid Intracerebral(intraparenchymal) JSOMTC, SWMG(A)Slide 53Epidural Hematoma Blood between the skull anddura materBlunt trauma to thetemporal or temporoparietalarea with an associated skullfracture and middlemeningeal arterialdisruption is the primarymechanism of injuryCan lead to herniationwithin hours after an injurybecause of high pressurearterial bleedingJSOMTC, SWMG(A)Slide 5418
8/31/2017Epidural Hematoma Classic Symptoms Transient loss ofconsciousness,followed by a lucidinterval then rapidneurologicaldecline Not common JSOMTC, SWMG(A)Lucid interval usuallylast between 6‐18hoursAs ICP rises symptomspresent, level ofconsciousnessdecreasesPatient may onlycomplain of HA anddrowsiness in earlystagesSlide 55Epidural HematomaJSOMTC, SWMG(A)Slide 56Subdural Hematoma Blood between the dura materand the surface of brain Usually bleeding from veinsthat bridge subdural spacedue to sudden accelerationand deceleration Associated contusion orlaceration of the brain isfrequently present Often the result of blunthead trauma Commonly associated withskull fractureJSOMTC, SWMG(A)Slide 5719
8/31/2017Subdural HematomaJSOMTC, SWMG(A)Slide 58Subarachnoid Hemorrhage Intracranial bleedinginto CSF resulting inbloody CSF andmeningeal irritationBleeding typicallyresults from trauma orrupture of an aneurysmClassic presentation “worst headache oflife”‐ ThunderclapNeck stiffness(meningeal irritation)JSOMTC, SWMG(A)Slide 59Intracerebral Hemorrhage 5 ml blood somewherewithin brainCauses Multiple lacerationsproduced by penetratinghead traumaHigh velocity decelerationinjuryCompression anddistortion from increasedICPOften associated withsubdural hemorrhage andskull fractureJSOMTC, SWMG(A)Slide 6020
8/31/2017Identify the Clinical Presentationand Management of Moderate toSevere TBIJSOMTC, SWMG(A)Slide 61Goals of TBI Management Three primary goals Identify other life‐threatening injuries Prevent further secondary brain injury Identify treatable mass lesions Correct or prevent hypoxia, hypotension,anemia, and hyperthermiaEvacuate intracranial masses Performed at surgical facilityJSOMTC, SWMG(A)Slide 62TBI AssessmentHistory Reconstruct the MOISAMPLE historyNausea, vomiting, headache, memoryimpairment, visual/auditory symptoms,seizures, and loss of consciousnessDrug or alcohol intoxicationJSOMTC, SWMG(A)Slide 6321
8/31/2017TBI AssessmentPhysical Examination Head Exam Scalp trauma Skull fractures Signs of basilar skull fracture Assess for other injuries C‐spine and extremities May be difficult to detect All head trauma patients are assumed to havea cervical spine injury until proven otherwiseJSOMTC, SWMG(A)Slide 64AirwayRespiration/Breathing Early establishment of adefinitive airway isimperative SuctioningPatient PositioningOPA & NPA UseEndotracheal IntubationCricothyrotomyJSOMTC, SWMG(A) Avoid hypoxia bymaintaining the oxygensaturation 90% byinitiating pulse oximetrymonitoringAvoid vasoconstriction orvasodilation bymaintaining the PaCO2between 35 and 40 mmHg.Given supplementaloxygen when available tomaintain an oxygensaturationSlide 65Circulation Hemorrhage Control Blood Pressure Maintenance Cover open head wounds securely enough to aidin the clotting process without pressing skullfragments or impaled objects inward by usingdonut o‐ring.SBP must be maintained above 90Initiate fluid bolus as indicated ‐ DO NOT LETTHE SBP GO BELOW 90 (can DOUBLE mortalityrate)JSOMTC, SWMG(A)Slide 6622
8/31/2017Fluid ResuscitationGoal‐ Systolic Blood Pressure above 90 Traumatic brain injury andin shock (has a weak or absentradial pulse ) Reduces cerebral perfusion& hypoxiaInitiate IV/IO Hextend, LR,or Plasma‐Lyte AContinue until restorationof palpable radial pulse,improved mental status, orSBP 90mmHgJSOMTC, SWMG(A)Slide 67Neurological Examination Level of Consciousness (LOC)LOC is best indicator of perfusion AVPU Glasgow Coma Score (GCS) Reevaluate several times during encounter Deterioration in LOC best indicator ofincreasing ICPJSOMTC, SWMG(A)Slide 68TBI Classification Classified based patient’s LOC, not actualunderlying injuryPatients with same TBI severityclassification may have dramaticallydifferent pathophysiologyMild TBI ‐ GCS 14 to 15Moderate TBI ‐ GCS 9 to 13Severe TBI ‐ GCS 3 to 8JSOMTC, SWMG(A)Slide 6923
8/31/2017Neurological Examination Pupillary Size Reactivity Fixed Dilated Pupil Ipsilateral intracranial hematomaresulting in uncal herniation Bilateral Fixed Dilated Poor brain perfusion, bilateraluncal herniation or severe hypoxia Indicative of very poor neurological outcome Alcohol and other drugs can cause abnormal pupillary reactions Full, Complete Neurological Exam Examine for subtle neurological deficits Look for specific injury patterns: Battle’s sign, Otorrhea, Rhinorrhea, Hemotympanum, peri‐orbitalEcchymosis is indicative of skull fracture and is concerning for underlyingbrain injuryJSOMTC, SWMG(A)Slide 70Increasing ICP Clinical Presentation Early warning signs Headache Nausea and vomiting Altered level of consciousness The earliest sign of increasing ICP is a change in LOC Decline in GCS score of 2 points or moreJSOMTC, SWMG(A)Slide 71Cranial NervesCN III Oculomotor NerveControls pupil sizePressure paralyzes nerve; pupildilates and becomes unreactiveCN X JSOMTC, SWMG(A)Vagus NerveSupplies SA and AV nodesPressure on nerve stimulatesbradycardiaSlide 7224
8/31/2017Herniation SyndromesEventually some partof the brain will pushthrough an openingVarious syndromesand presentationsUncal transtentorial isthe most common JSOMTC, SWMG(A)Slide 73Increasing ICPClinical Presentation Rapidly unresponsive toverbal and painful stimuliNeurological Posturing Decorticate PosturingDecerebrate PosturingIpsilateral dilated andunreactive pupilJSOMTC, SWMG(A)Slide 74Increasing ICPClinical PresentationCushing's Reflex (triad) Acute entity seen in severelyhead injured patients withsignificant increasedintracranial pressure andimpending herniation HypertensionBradycardiaRespiratory irregularity (e.g.,Cheyne‐Stokes)JSOMTC, SWMG(A) PapilledemaUnilateral presentation isextremely rare‐ PROBABLYNOT GOING TO BE SEEN, itis a late finding in ICP andthus is not seen in acutehead injury.Slide 7525
8/31/2017Increasing ICP ManagementHead Elevation If cerebrospinal fluid(CSF) is identifiedleaking from the earsand/or nose, elevatethe head 30 to 60degrees if thecasualty’s otherinjuries permit andthe casualty ishemodynamicallystable If the casualty exhibitssigns of increased ICPand ishemodynamicallystable, considerelevating the head 30degrees to improvevenous outflow fromthe brain anddecrease ICPJSOMTC, SWMG(A)Slide 76Increasing ICP ManagementControlled Hyperventilation Temporizing measure for evidence of increasingICP and herniation ‐ NOT ROUTINEWith Capnography Ventilate to achieve pCO2 of 30‐35 mm HgWithout Capnography Ventilate at 20 BPM, tidal volume of approximately 500mlUse the highest oxygen concentration possibleJSOMTC, SWMG(A)Slide 77Increasing ICP ManagementHypertonic Saline (3%) Osmotic agent used to increase the osmotic pressuregradient between blood and tissues in order to drawwater out of the brain and reduce intracranialpressure Isolated TBI (Hemodynamically stable) Administer 3‐% HS 250 ml IV/IO Bolus TBI with controlled external hemorrhage Administer 3% HS 250 ml IV/IO Bolus plus Hextend/other fluids asper the fluid resuscitation protocol if requiredJSOMTC, SWMG(A)Slide 7826
8/31/2017Increasing ICP ManagementMannitol (Osmotrol) Large glucose molecule, Does not leave blood stream,Osmotic Diuretic, Effective in drawing fluid from brain Dose 1gm/kg CAUTION Forms crystals at low temperatures Reconstitute with rewarming & gentle agitation USE IN‐LINE filter & PREFLUSH lineJSOMTC, SWMG(A)Slide 79Fosphenytoin (Cerebyx )Seizure Prophylaxis Indications Prevention and treatment of seizures TMEP: Seizure Protocol TTP: Head Injury ManagementDose 18 mg/kg IV/IO at 100 to 150mg/min(over 15 mins) Repeat 100mg IV/IO Q 8 h formaintenanceJSOMTC, SWMG(A)Slide 80Fosphenytoin (Cerebyx )Seizure Prophylaxis Special Considerations WARNING ‐ Do not administer faster than 150mg/min since this may re
8/31/2017 2 JSOMTC, SWMG(A) Slide 4 References Tintinalli’s Emergency Medicine, 7th edition, 2010 Tactical Trauma Protocols PHTLS, 7thedition, 2010 USASOC Policy 10‐10 Neurocognitive Testing Program JSOMTC, SWMG(A) Slide 5 Reason JSOMTC, SWMG(A) Slide 6 Agenda Identify key definitions and epidemiology of traumatic brain injury
The assessed content included prima - ry survey, secondary survey, airway and ventilation, circulation, shock, thoracic trauma, head/spinal trauma, abdomen/pelvis trauma, musculoskeletal trauma, paediatric trauma, geriatric trauma, obstetric trauma, trans - fer of care, and other course specific inclusions.
Behind the Term: Trauma Prepared in 2016 by Development Services Group, Inc., under contract no. HHSS 2832 0120 0037i/HHSS 2834 2002T, ref. no. 283– 12–3702. 1 Behind the Term: Trauma Related terms: complex trauma, historical trauma, human-caused trauma, naturally caused trauma, trauma,
categories of trauma as a framework for trauma assessment. “Little t” trauma “Big T” trauma Complex trauma “Little t” Trauma “Little t” trauma involves events that we encounter day to day that can make life difficult but are not out of the ord
LEVEL I PEDIATRIC TRAUMA CENTER The Level I Regional Pediatric Trauma and Burn Center at Children’s Hospital Colorado is a large, multi-disciplinary program. We provide timely, comprehensive, cost- . Trauma/Burn Medical Director Trauma/Burn Program Manager Trauma Coordinators Trauma Registrars Staff Assi
Prevention of Shaken Baby Syndrome and Abusive Head Trauma PAGE 1–ABUSIVE HEAD TRAUMA Welcome to the prevention of shaken baby syndrome and abusive head trauma section of the museum. . doll. Um, they might have trouble breathing. There might even be File Size: 576KBPage Count: 19
Historical trauma - Cumulative emotional and psychological wounding from massive group trauma across generations, including lifespan Historical trauma response (HTR) is a constellation of features in reaction to massive group trauma, includes . historical unresolved grief (similar to Child of Survivors Complex re: Jewish Holocaust survivors and
Connie J. Mattera, M.S., R.N., EMT-P I. Epidemiology of chest trauma A. Incidence 1. Chest injuries are common occurrences following blunt and penetrating trauma. 2. Isolated chest trauma is uncommon; the majority of these patients will have additional injuries. 3. Prevention efforts a major key 4. Thoracic trauma accounts for ⅓ all trauma .
Kern County Emergency Medical Services Division 4 Trauma Policies and Procedures Effective Date: 07/01/2015 V. PREHOSPITAL TRAUMA SYSTEM ACTIVATION A. If a trauma patient meets the “Trauma Triage Criteria”, the Kern County Trauma Care System shall be activated as follows: 1. The following personnel are authorized to triage and then activate .
