1 Jennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC If I Only Had A Brain….. Pre-Hospital Management of Traumatic Brain InjuryJennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC
2 IncidenceTraumatic Brain Injury, or TBI, is the leading cause of death and disability in children and adults from ages 1-44Most often caused by motor visual crashes, sports injuries, or simple falls on the playground, at work, or in the homeApproximately 52,00 deaths occur from TBI annuallyAn estimated 1.5 million head injuries are seen yearly in Emergency DepartmentsAn estimated 1.6 to 3.8 million sports related TBIs occur each year
3 Facts about TBIAt least 5.3 million Americans, 2% of the US population, currently live with disabilities resulting from TBIModerate and severe head injury (respectively) is associated with a 2.3 and 4.5 times increased risk of Alzheimer’s diseaseMales are 2x more likely to suffer TBI that femalesThe leading causes of TBI are falls, MVC, and assaults
4 Facts about TBITBI hospitalization rates have increased from 79% per 100,000 in 2002 to 87.9% per 100,000 in 2003Exposures to blasts are a leading cause of TBI among active duty military personnel in war zonesVeteran’s advocates believe that between 10 and 20% of Iraq war veterans, or 150,000 and 300,000 members have some level of TBI30% of soldiers admitted to Walter Reed have been diagnosed with a TBI
5 Prevention The best way to treat TBI is prevention Bicycle helmets Not just for kids!Wearing a bicycle helmet reduces risk of TBI by 88%Only 1% of people admitted to a trauma center after a bicycling accident were wearing helmetsSeat belt useMotorcycle helmets – full faceHelmetsSkateboardingRollerbladingScootersAt risk behaviorsMales 2 times > injury rate than females
6 Where does EMS fit in?EMS providers are the first contact a patient has into the trauma systemWe have the ability to prevent secondary brain injury with the right interventionsPrimary brain injury – the initial brain injury sustained as a result of traumaSecondary injury – the injury that occurs due to hypoxemia and hypovolemia
7 Classification of TBI Mild TBI (GCS 13-15) (MOST of what EMS will see) Concussive syndromeReversible, temporary LOC/retrograde amnesiaChange in mental status a the time of injury onlyImaging usually normalModerate TBI (GSC 9-12)LOC and/or post amnesia of > 30 minutes but < 24 hoursGCS – 9-12Physical, cognitive, and/or behavioral impairments last for months or are permanentGenerally make a good recovery with treatment or learn to compensate for deficits
8 Classification of TBI Severe TBI (GCS 3-8) LOC or post-traumatic amnesia > 24 hoursGCS lowerMore extensive physical impairments as a result if brain damageSlower course of recoveryClear indication of significant, permanent deficitsWhat these are depend on location of injury
9 Classification of TBI Very severe/catastrophic TBI True comas of many weeks or monthsThis term is reserved for the most severely damaged head injuryMany never regain consciousness or regain meaningful communication with the environment“Persistent vegetative state”
10 Brain Death Results from a severe insult to the brain No cortical or brain stem activityNo movement to stimuliNo brain stem reflexesNo spontaneous breathingNot diagnosed in the fieldIf the brain is dead, the person is dead
11 Concussion Traumatic, REVERSIBLE neurological deficit Etiology Temporary LOCRetrograde amnesiaEtiologyStrong, rapid acceleration-deceleration injuryBlow to the headThere is a temporary cessation of the functioning of the reticular activating systemRAS responsible for arousal or wakefulness of the brain
12 Concussion Assessment Subjective Data Objective Data Diagnostics HPI Mechanism, consciousness immediately after event, duration of event, neuro events after eventMedical HxNeuro disease, recent trauma, prior head injuryObjective DataPhysical exam – neuro exam, memory assessmentMay have repetitive speech and questionsDiagnosticsCT scan – R/O bleed
13 Interventions for Concussion Immobilization as necessaryEmotional supportHigh flow oxygen
14 Planning/Interventions for Concussion Post Concussive SyndromeResults from repeated mild brain injuries over a period of months or yearsCan impact neurological, behavioral and cognitive function“second impact syndrome” now called Chronic Traumatic Encephalopathy or CTEMuhammad Ali, Football playersOnce a person suffers a concussion, they are four times more likely to suffer another one.
15 Skull FractureTypesLinearMost commonAccount for about 70% of all typesUsually benign unless it crosses a major vascular channelDepressedDamages underlying cerebral tissue by compression or laceration and by retained bony fragmentsBasilarCan occur within any of the fossaeClinical picture depends on the area affectedComplications include infection, hematoma, CSF leaks, loss of smell, loss of hearing, seizures and pneumocephalus.
16 Skull Fracture Assessment Subjective Data HPI Medical Hx Recent trauma, elapsed time, sweet or salty taste in back of throat, post nasal dripMedical HxTrauma, malignancy
17 Skull Fracture Objective Data Physical Exam Diagnostics Surface trauma, AMS, altered pupil or motor response, CSF leak, Raccoon eyes, Battle’s signDiagnosticsHalo Test (ottorrhea or rhinorrhea)Using a 4X4 collect fluid leak from nose or earSet on the bedside table for a few minutesPositive when there is a circular separation of blood and clear fluid or a “halo”Indicative of a CSF leak
23 Diffuse Axonal Injury (DAI) DAI is the widespread disruption of neuro function without any focal lesionsCharacterized by microscopic damage to the axons, diffuse white matter degeneration, global neuro dysfunction and diffuse cerebral edema.EtiologyAcceleration-decelerationMVC, Pedestrian, Shaken BabyShear injury
24 DAI Assessment Subjective Data HPI Medical Hx Mechanism of injury, onset and duration of LOCMedical HxNeuro disease or injurySubstance abuseChild abuse or exam doesn’t fit with mechanism of injuryShaken baby
25 DAI Objective Data Physical Exam Immediate LOC, lasts days to months Increased ICPBrain stem dysfunctionDecortication or decerebrationLoss of brain stem reflexes – cough, gag, etc.HypertensionHyperthermiaDiaphoresis
28 Cerebral ContusionCerebral contusion is an actual bruising of the brainResults in focal ischemia and edema with potential for infarction, necrosis and/or ↑ ICPEtiologyTrauma, acceleration/deceleration, high velocity blows, or rotation of the brain following a blowCoup – contra coup injuryClinical picture varies depending on area involved
29 Cerebral Contusion Assessment Subjective Data HPI Medical Hx Mechanism of injury, changes in LOC since eventMedical HxNeuro disease or injurySubstance abuse
30 Cerebral Contusion Objective Data Physical exam Altered LOC > than a few hoursSurface traumaFull neuro exam
32 Subdural Hematoma (SDH) SDH is a collection of blood between the dura matter and the subarachnoid layer of the meningesUsually caused by trauma or as the extension of an intracerebral hematoma into the subdural space
33 Subdural Hematoma (SDH) Three classificationsAcute - onset within 48 hours of presentationSub-acute – onset 2-14 daysChronic – more than 14 days
34 Subdural Hematoma (SDH) AssessmentSubjective DataHPIMechanism of injury, time interval, trends in neuro statusMedical HxETOH AbuseChronic SDH common in these pts secondary to multiple falls and abnormal bleeding tendencies secondary to impaired liver function
35 Subdural Hematoma (SDH) Medical HistoryUse of blood thinners or anti-platelet agentsCoumadin® (warfarin), Pradaxa® (dabigatran), Plavix® (clopridogrel), Effient® (prasugrel), Lovenox® (enoxaparin), Aggrenox®Many patients on blood thinners or anti-platelet agents many have minor trauma or low mechanism, but should be evaluated in ER as even very minor trauma in these patients can cause hemorrhage
36 Subdural Hematoma (SDH) Objective DataPhysical ExamAcuteHeadache, drowsiness, confusionSteady decline in LOCIpsilateral , unilateral pupil dilation with lack of response to light – LATE findingContra lateral hemiparesisChronic and sub acuteGradual and non-specific changesAltered mentationAltered motor statusIpsilateral pupil dilation and sluggish to light
37 Subdural Hematoma (SDH) Acute SDH with left to right shift
39 Epidural Hematoma (EDH) Collection of blood between the skull and duraEtiologyUsually from a laceration of the middle meningeal artery associated with skull fxThe arterial bleed in under high pressure – it does not tamponade, but rather progresses to become a space occupying lesion causing ↑↑ ICP, brain shift and herniationMortality = 50% if not treated
40 Epidural Hematoma (EDH) AssessmentSubjective DataHPIMechanism of injuryPATTERN of unconsciousnessInitially unconscious, followed by a lucid period, then followed by rapid unconsciousnessMedical HxPrevious trauma, previous head injury
41 Epidural Hematoma (EDH) Objective DataPhysical examAltered LOC, pupils with unilateral dilation, fixed and/or dilated, contralateral paresis or paralysis which leads to posturingCushing’s triadAbnormal respirationsNarrowing pulse pressureBradycardiaDiagnosticsRapid CT exam at trauma center
42 Epidural Hematoma (EDH) Notice the scalloping, rather than layering of the blood.
43 EDH Frequent neuro checks ABC’s Prepare for emergency surgery Transport to a facility with neurosurgery capabilitiesTRUE Neurosurgical emergency!
44 Increased ICP ICP is influenced by relatively fixed volumes The brain 80%The blood 10% Total volumeThe CSF 10%Monroe-Kellie Hypothesisto maintain a normal ICP, a change in the volume of one compartment must be offset by a reciprocal change in the volume of another compartment
45 Increased ICP Etiology – Any condition that: Increases brain volume space occupying lesionsSDH, masses, cerebral edema, EDH, ICBIncreases blood volumeVenous outflow obstruction, hyperemia (HTN), hypercapniaIncreases CSFHydrocephalus, SAH, lack of absorption of CSF
46 Increased ICP Assessment Subjective Data HPI Chronology Pain Consciousness SeizuresMentation VomitingPersonality Motor deficitsCommunication HeadachesNausea Visual changes
47 Increased ICP Medical History Neuro disease Trauma Fainting Substance abuseEspecially cocaine, heroinMedicationsAllergies
48 Increased ICP Objective Data Physical Exam EARLY picture of ↑ ICP LOC – changes may be SUBTLE. Changes in LOC may be the FIRST sign of ↑ ICPLISTEN to the patient’s family – they know their loved one BEST!Pupils – sluggish, different bilaterallyIpsilateral/unilateral changesMotor functionContralateral changesVital Signs
49 Increased ICP LATE picture of ↑ICP LOC Arouses only with deep noxious stimuli, or unresponsivePupilsFixed and dilated or “blown”Motor functionHemiparesis, posturing, or flaccidityVital SignsCushings TriadBradycardiaNarrowing pulse pressureSlow or irregular respirations
50 HyperventilationHyperventilation in Traumatic Brain InjuryOnly used when:GCS < 8 plusActive seizurePosturingIncreased BP and decreased pulseIntermittent apneaFurther decrease of GCS >2 on subsequent examAdult – 20 breaths per minuteChild – 25 breaths per minute
51 Get With The Guidelines Brain Trauma Foundation Guidelines for the Pre-Hospital Treatment of Traumatic Brain Injury
52 Treatment for TBI Oxygenation and Blood Pressure Hypoxemia (<90% O2 Sat) or hypotension (<90 mm Hg SBP) are significant parameters associated with a poor outcome in patients with severe head injury in the pre-hospital settingIn children the parameters are SBP<65 (0-1 years old), <75 (2-5 years old), <80 (6-12 years old) and <90 (13-16 years old
53 Treatment for TBI High Flow 02 all patients Assist ventilations as necessary per protocolAvoid nasal airways in those patients with facial injury and/or suspected basilar skull fxRaising BP in hypotensive, severe head injury patients improves outcome in proportion to the efficacy of the resuscitationIf ALS – IV NS Open until SPB >90, or up to 2 liters infused then contact Medical Control
54 Glasgow Coma Score (GCS) pre-hospital measurement of GCS is a significant and reliable indicator of severity of head injury particularly in association with repeated scoring and improvement or deterioration of the score over timeA GCS score of 3 to 5 has at least a 70% positive predictive value for poor outcome
55 GCS Best Eye Response. (4) No eye opening. Eye opening to pain. Eye opening to verbal command.Eyes open spontaneously.
56 GCS Best Verbal Response. (5) No verbal response Incomprehensible sounds.Inappropriate words.ConfusedOrientated
57 GCS Best Motor Response. (6) No motor response. Extension to pain. Flexion to pain.Withdrawal from pain.Localizing pain.Obeys Commands.
58 GCSNote that the phrase 'GCS of 11' is essentially meaningless, and it is important to break the figure down into its components, such as E3V3M5 = GCS 11.A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate injury and 8 or less a severe brain injury.Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.
59 Pupillary AssessmentPupil examination is a standard component of the pre-hospital neuro examThe pupillary exam along with the GCS will serve as a baseline for ALL subsequent examinations in the ER and hospital
60 Pupillary Assessment Pre-hospital pupil exam should consist of: The pupil size and light reflexAssess and document on the PCRThe duration of the pupillary dilation and fixation should be assessed and documentedBrisk reaction to lightSluggish reaction to lightNo reaction to light
62 Airway, Ventilation, and Oxygenation GUIDELINESHypoxemia (apnea, cyanosis, Sat <90%) MUST be avoided or corrected immediatelySats should be monitored, if available, on all patients with TBIHypoxemia should be treated with supplemental O2In NYS and Suffolk – all trauma patients should be given high flow 02
63 Airway, Ventilation, and Oxygenation OptionsAirway should be secured in pts with GCS<9, the inability to maintain an adequate airway, or hypoxemia not corrected by supplemental O2Endotracheal intubation is the most effective way to maintain a difficult airwayIntubate only if possible – i.e. teeth not clenched, avoid prolonged attempts as this will increase ICPIn peds, BVM ventilation is just as effective as long as you are getting chest rise
64 Airway, Ventilation, and Oxygenation AVOID prophylactic hyperventilationPatients should be maintained with normal breathing rates (ETCO mmHg), and hyperventilation (ETCO2 < 35 mmHg) should be avoided unless the patient shows signs of cerebral herniation
65 Hyperventilation 20 breaths per minute in an adult 25 breaths per minute in a child30 breaths per minute in an infant less than 1 year oldFor ALS providers:The goal of hyperventilation is ETCO2 of mmHg. Capnography is the preferred method for monitoring ventilation
66 Fluid ResuscitationFluid resuscitation in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possibleIn SuffolkUp to 2 large bore IV’s with NS open until SBP >90 or up to 2 liters NS infused, then contact with MCKVO for SBP > 90
67 HypoglycemiaHypoglycemia has been associated with traumatic events – it exhibits signs similar to that of patients with TBII.e. MVA secondary to low blood sugarBlood sugar should be checked in all patients with AMS of undetermined etiologyTreat hypoglycemia
68 Transport DecisionsPatients with severe TBI and a GCS <9 should be transported to a facility with the following capabilities:Immediate CT ScanningPrompt neurosurgical careAbility to monitor ICP and treat increased ICPFor all intents and purposes, this is a trauma centerGSHSSHBMHUHSB
69 Case StudyYou are dispatched to the scene of a motorcycle vs. car – BLS ambulanceOn scene you find:Approximately 20 year old male lying proneNinja motorcycleFull face helmet in place but not intactMotorcycle is found approximately 50 feet from where you find your patientYou notice bilateral femur deformities
70 Case Study Patient is unresponsive to verbal stimuli Upon rolling your patient, while maintaining cervical stabilization, of course, you open the visor of the helmet and determine that the patient is not maintaining an adequate airway and you……………………..Remove helmet per NYS protocolsObvious depression In the occiput of the pt’s headUsing a jaw thrust, open the airway, look, listen and feel for breathingYou determine that he is not able to maintain his airway and that he is breathing irregularly
71 Case Study You take a step back, and think to yourself… Place an oral airwayBegin BVM ventilationsCheck for a distal pulse – 120 and weakCheck BP – 80/30GCS of 6Decerebrate posturingYou take a step back, and think to yourself…Oh Crap!No – ABC’s are taken care of, now what must I do to maintain this patientCall for ALS to sceneWhile waiting for ALS, rapid transport decision, immobilize in c-collar and place on LBB, get patient ready for transport. Do not wait on scene for ALS!!!!
72 Case Study ALS – intervene enroute to trauma center Remember the standards/guideline for pre-hospital management of TBIAirway/BreathingIs it adequate with the OPA in place, is there chest rise, can I safely intubate this patient and not do further harmCirculationWhat is the pulse and BPIV accessNS open for SBP >90 or up to 2 litersHyperventilationDo I need to do it? – In this patient, yes, mild hyperventilation of 20 BPM is appropriate based on his physical assessment and neuro exam
73 Case Study Are my interventions helping? Re-assess ABC’s Re-assess GCS Re-assess Vitals