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Head Injurires presentation

Oct 06, 2015

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  • Head Trauma

  • Introduction to HeadInjuriesCommon major trauma4 million people experience head trauma annuallySevere head injury is most frequent cause of trauma deathGSW to cranium: 75-80% mortalityAt Risk populationMales 15-24InfantsYoung ChildrenElderly

  • Introduction to Head InjuriesTIME IS CRITICALIntracranial HemorrhageProgressing EdemaIncreased ICPCerebral HypoxiaPermanent Damage

    Severity is difficult to recognizeSubtle signsImprove differential diagnosisImproves survivability

  • Pathophysiology ofHead InjuryMechanism of InjuryBlunt InjuryMotor vehicle collisionsAssaultsFallsPenetrating InjuryGunshot woundsStabbingExplosions

  • Different Types of InjuryHead InjuryCranial InjuryBrain Injury

  • Head TraumaOpen Skull compromised and brain exposed

    ClosedSkull not compromised and brain not exposed*Head Trauma -

  • Scalp InjuryContusionsLacerationsAvulsionsSignificant Hemorrhage

    ALWAYS Reconsider MOI for severe underlying problems

  • Head InjuriesScalp woundHighly vascular, bleeds brisklyShock: child may developShock: adult another causeManagementNo unstable fracture: direct pressure, dressingsUnstable fracture: dressings, avoid direct pressure*Head Trauma -

  • Skull fractureLinear nondisplacedDepressedCompoundSuspect fractureLarge contusion or darkened swellingManagementDressing, avoid excess pressureHead Injuries*Head Trauma -

  • Cranial InjuryTrauma must be extreme to fractureLinearDepressedOpenImpaled Object

  • Basal SkullUnprotectedSpaces weaken structureRelatively easier to fracture

  • Cranial InjuryBasal Skull Fracture SignsBattles SignsRetroauricular EcchymosisAssociated with fracture of auditory canal and lower areas of skullRaccoon EyesBilateral Periorbital EcchymosisAssociated with orbital fractures

  • Basilar Skull FractureBattles signRaccoon eyes*Head Trauma -

  • Cranial InjuryBasilar Skull FractureMay tear duraPermit CSF to drain through an external passagewayMay mediate rise of ICPEvaluate for Target or Halo sign

  • Crainial InjuriesPenetrating trauma*Head Trauma -

  • Head Trauma -*Forces that cause skull fracture can also cause brain injury.

  • Brain InjuryAs defined by the National Head Injury Foundationa traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.

  • Brain InjuryResponse to injurySwelling of brainVasodilatation with increased blood volumeIncreased ICPDecreased blood flow to brainPerfusion decreasesCerebral ischemia (hypoxia)

    *Head Trauma -

  • Signs & Symptoms of Brain InjuryAltered Mental StatusAltered orientationAlteration in personalityAmnesiaRetrogradeAntegradeCushings ReflexIncreased BPBradycardiaErratic respirationsVomitingWithout nauseaProjectileBody temperature changesChanges in pupil reactivityDecorticate posturing

  • Signs & Symptoms of Brain InjuryPathophysiology of ChangesFrontal Lobe InjuryAlterations in personalityOccipital Lobe InjuryVisual disturbancesCortical DisruptionReduce mental status or AmnesiaRetrogradeUnable to recall events before injuryAntegradeUnable to recall events after traumaRepetitive QuestioningFocal DeficitsHemiplegia, Weakness or Seizures

  • ClassificationDirectPrimary injury caused by forces of traumaIndirectSecondary injury caused by factors resulting from the primary injury

  • Brain InjuryDirect brain injuryImmediate damage due to forceCoup and contracoupFixed at time of injuryManagement Directed at prevention*Head Trauma -

  • Direct Brain Injury TypesCoupInjury at site of impactContrecoupInjury on opposite side from impact

  • Brain InjuryIndirect brain injuryResults from hypoxia or decreased perfusionResponse to primary injuryDevelops over hoursManagementGood prehospital care can help prevent*Head Trauma -

  • Direct Brain Injury CategoriesFocalOccur at a specific location in brainDifferentialsCerebral ContusionIntracranial HemorrhageEpidural hematomaSubdural hematomaIntracerebral HemorrhageDiffuseConcussionModerate Diffuse Axonal InjurySevere Diffuse Axonal Injury

  • Focal Brain InjuryCerebral ContusionBlunt trauma to local brain tissueCapillary bleeding into brain tissueCommon with blunt head traumaConfusionNeurologic deficitPersonality changesVision changesSpeech changesResults fromCoup-contrecoup injury

  • Brain InjuriesCerebral contusionBruising of brain tissueSwelling may be rapid and severeLevel of consciousnessProlonged unconsciousness, profound confusion or amnesiaAssociated symptomsFocal neurological signsMay have personality changes*Head Trauma -

  • Focal Brain InjuryIntracranial HemorrhageEpidural HematomaBleeding between dura mater and skullInvolves arteriesMiddle meningeal artery most commonRapid bleeding & reduction of oxygen to tissuesHerniates brain toward foramen magnum

  • Intracranial HemorrhageAcute epidural hematoma Arterial bleedTemporal fracture commonOnset: minutes to hoursLevel of consciousnessInitial loss of consciousnessLucid interval followsAssociated symptomsIpsilateral dilated fixed pupil, signs of increasing ICP, unconsciousness, contralateral paralysis, death*Head Trauma -

  • Focal Brain InjuryIntracranial HemorrhageSubdural HematomaBleeding within meningesBeneath dura mater & within subarachnoid spaceAbove pia materSlow bleedingSuperior sagital sinusSigns progress over several daysSlow deterioration of mentation

  • Intracranial HemorrhageAcute subdural hematomaVenous bleedOnset: hours to daysLevel of consciousnessFluctuations Associated symptomsHeadacheFocal neurologic signs High-riskAlcoholics, elderly, taking anticoagulants*Head Trauma -

  • Intracranial HemorrhageIntracerebral hemorrhageArterial or venousSurgery is often not helpfulLevel of consciousnessAlterations commonAssociated symptomsVaries with region and degreePattern similar to strokeHeadache and vomiting *Head Trauma -

  • Focal Brain InjuryIntracranial HemorrhageIntracerebral HemorrhageRupture blood vessel within the brainPresentation similar to stroke symptomsSigns and symptoms worsen over time

  • Diffuse Brain InjuryDue to stretching forces placed on individual nerve cellsPathology distributed throughout brainTypesConcussionModerate Diffuse Axonal InjurySevere Diffuse Axonal Injury

  • Diffuse Brain InjuryConcussionMild to moderate form of Diffuse Axonal Injury (DAI)Nerve dysfunction without anatomic damageTransient episode ofConfusion, Disorientation, Event amnesiaSuspect if patient has a momentary loss of consciousnessManagementFrequent reassessment of mentationABCs

  • Brain InjuriesConcussionNo structural injury to brainLevel of consciousnessVariable period of unconsciousness or confusion Followed by return to normal consciousnessRetrograde short-term amnesiaMay repeat questions over and over Associated symptomsDizziness, headache, ringing in ears, and/or nausea*Head Trauma -

  • Diffuse Brain InjuryModerate Diffuse Axonal InjuryClassic ConcussionSame mechanism as concussionAdditional: Minute bruising of brain tissueUnconsciousnessMay exist with a basilar skull fractureSigns & SymptomsUnconsciousness or Persistent confusionLoss of concentration, disorientationRetrograde & Antegrade amnesiaVisual and sensory disturbancesMood or Personality changes

  • Brain InjuriesDiffuse axonal injuryDiffuse injuryGeneralized edemaNo structural lesionMost common injury from severe blunt head traumaAssociated symptomsUnconsciousNo focal deficits*Head Trauma -

  • Diffuse Brain InjurySevere Diffuse Axonal InjuryBrainstem InjurySignificant mechanical disruption of nerve cellsCerebral hemispheres and brainstemHigh mortality rateSigns & SymptomsProlonged unconsciousnessCushings reflexDecorticate or Decerebrate posturing

  • Brain Anatomy*Head Trauma -Intracranial volumeBrainCSFBlood vessel volumeDilatation with high pCO2 Constriction with low pCO2Slight effect on volume

  • Intracranial PerfusionCranial volume fixed80% = Cerebrum, cerebellum & brainstem12% = Blood vessels & blood8% = CSFIncrease in size of one component diminishes size of anotherInability to adjust = increased ICP

  • Intracranial PerfusionCompensating for PressureCompress venous blood vesselsReduction in free CSFPushed into spinal cordDecompensating for PressureIncrease in ICPRise in systemic BP to perfuse brainFurther increase of ICPICPBP

  • Factors Affecting ICPVasculature ConstrictionCerebral EdemaSystolic Blood PressureLow BP = Poor Cerebral PerfusionHigh BP = Increased ICPCarbon DioxideReduced respiratory efficiency

  • Intracranial PressureRole of Carbon DioxideIncrease of CO2 in CSFCerebral VasodilationEncourage blood flowReduce hypercarbiaReduce hypoxiaContributes to ICPReduced levels of CO2 in CSFCerebral vasoconstrictionResults in cerebral anoxia

  • Pressure & Structural DisplacementIncreased pressureCompresses brain tissue

    Herniates brainstemCompromises blood supplySigns & SymptomsUpper BrainstemVomitingAltered mental statusPupillary dilationMedulla OblongataRespiratoryCardiovascularBlood Pressure disturbances

  • Signs & Symptoms of Brain InjuryPhysiological ChangesUpper Brainstem CompressionIncreasing blood pressureReflex bradycardiaVagus nerve stimulationCheyne-Stokes respirationsPupils become small and reactiveDecorticate posturingNeural pathway disruption

  • Signs & Symptoms of Brain InjuryPhysiological ChangesMiddle Brainstem CompressionWidening pulse pressureIncreasing bradycardiaCNS HyperventilationDeep and RapidBilateral pupil sluggishness or inactivityDecerebrate posturing

  • Signs & Symptoms of Brain InjuryPhysiological ChangesLower Brainstem InjuryPupils dilated and unreactiveAtaxic respirationsErratic with no patternIrregular and erratic pulse rateECG ChangesHypotensionLoss of response to painful stimuli

  • Signs & Symptoms of Brain InjuryEye SignsPhysiological IssuesIndicate pressure onCN-III (Oculomotor Nerve)Pressure on nerve causes eyes to be sluggish, then dilated, and finally fixedReduced peripheral blood flowPupil Size & ReactivityReduced Pupillary ResponsivenessDepressant drugs or Cerebral HypoxiaFixed & DilatedExtreme Hypoxia

  • Head Trauma AssessmentITLS Initial AssessmentRapid Trauma Exam Limit patient agitation, strainingContributes to elevated ICPAirwayVomiting very common within first hourEndotracheal intubation*Head Trauma -

  • Head Trauma -*Decreased level of consciousness is an early indicator of brain injury or rising ICP.

  • Reactive: ICP increasingNonreactive (altered LOC): increased ICPNonreactive (normal LOC): not from head injuryPupilsBoth dilatedNonreactive: brainstemReactive: often reversibleUnilaterally dilated*Head Trauma -Eyelid closureSlow: cranial nerve IIIFluttering: often hysteriaAnisocoria

  • Glasgow Coma ScaleSuspect severe brain injury GCS
  • Extremity PosturingDecorticateArms flexed and legs extendedDecerebrateArms extended and legs extended

    *Head Trauma -

  • Increasing ICP

    *Head Trauma -Cushings responseAs ICP increases, systolic BP increasesAs systolic BP increases, pulse rate decreases

    Vital SignChange with Increasing ICPRespirationIncrease, decrease, irregularPulseDecreaseBPIncrease, widening pulse pressure

  • Head Trauma -*Early efforts to maintain brain perfusion can be life-saving.

  • The Injured BrainHypoxiaPerfusion decrease causes cerebral ischemiaHyperventilation increases hypoxia significantly more than it decreases ICPAssist ventilationHigh-flow oxygenOne breath every 68 secondsSpO2 >95%Maintain EtCO2 at 35 mmHg*Head Trauma -

  • The Injured Brain*Head Trauma -HypotensionSingle instance increases mortality Adult (systolic
  • The Injured BrainCerebral herniation syndromeBrain forced downwardCSF flow obstructed, pressure on brainstemLevel of consciousnessDecreasing, rapid progression to comaAssociated symptomsIpsilateral pupil dilatation, out-downward deviationContralateral paralysis or decerebrate posturing Respiratory arrest, death*Head Trauma -

  • Cerebral Herniation*Is ICP severe enoughto outweigh cerebral ischemia?Head Trauma -

  • HyperventilationCerebral herniation syndromeHerniation danger outweighs hypoxiaIndications for hyperventilationTBI GCS
  • Hyperventilation Rates

    Capnography Maintain EtCO2 25 mmHg*Head Trauma -

    Age GroupNormal RateHyperventilationAdult810 per minute20 per minuteChildren15 per minute25 per minuteInfants20 per minute30 per minute

  • Advanced ProvidersHypertonic SalineIndication and Use

  • Movement of Particles vs Movement of Water

  • DiffusionMovement of particles from an area of high concentration to an area of low concentration.Moves along normal concentration gradient.PassiveSlow

  • Movement of WaterSemi-permeable membrane

  • Popcorn and Beer RuleWhere ever the salt goes, the water goes.

  • Movement of WaterOsmosis Movement of water across a semi-permeable membrane from an area of low particle concentration to an area of high particle concentration (dilute to concentrated)

  • Osmotic PressureThe force that moves water across a semi-permeable membrane

    Some energy required

    Fast process

  • Movement of Water: Capillaries

    Hydrostatic Pressure

    Colloid Osmotic Pressure

    Net Filtration

  • Hydrostatic PressureBlood pressure PUSHES water out of the capillaries (filtration)

  • Colloid Osmotic Pressure (Onconic Pressure)

    Plasma proteins (colloids) exert a PULL on water to keep it in the capillary

  • Net FiltrationHydrostatic pressure forcing out

    Osmotic pressure pulling in

    Should be equal

    Hydrostatic Osmotic = Zero

  • EdemaAccumulated water in interstitial spaceDecrease plasma proteins (colloids)Increased hydrostatic pressureIncreased capillary permeabilityBlocked drainage

  • Concentration of fluids

  • TonicityIsotonic concentration equal to the concentration of surrounding spaces; stays in the veinsi.e. blood0.9% saline (normal saline)Lactated Ringers Solution

  • Hypotonic concentration less than the concentration of surrounding spaces; water goes into the interstitial spacesFresh water5% dextrose in water0.45% saline5% D/.2 saline

  • Hypertonic concentration greater than the concentration of surrounding spaces; pulls water from the interstitial spacesProtein solutionsLipid solutions10% fructose50% mannitol3.3% saline

  • Management of Increased ICPHypertonic Solutions to pull water from the swollen brain5 cc/kg 3.3% salineCaution with packaging

  • ReviewAnswer the following questions as a group.If doing this CE individually, please e-mail your answers to:[email protected] Apr 2013 CE in subject box.You will receive an e-mail confirmation. Print this confirmation for your records, and document the CE in your PREMSS CE record book.IDPH site code 06-7100-E-1213

  • *Head Trauma -

  • ReviewWhat type of head injury is the man in the previous slide demonstrating?What 2 assessment findings confirm this injury?What is the most important initial treatment for this man?

  • ReviewYour patient has been involved in a motorcycle accident. He was not wearing a helmet. You find him unconscious, airway open and breathing 4 times per minute. His blood pressure is 180/100, pulse 64.

  • Review4. What complication of brain injury do his vital signs suggest? When you check this patients pupils what would you expect to find?How would you treat this patient?

  • ReviewWhat type of brain injury is caused from arterial bleeding?Describe the typical changes in level of consciousness in this type of injury.

  • ReviewA patient is unconscious, does not open her eyes, does not make any sounds and has no motor response to stimulation.9. What is her Glasgow Coma Scale?

  • ReviewA patient is confused, opens his eyes to verbal stimulus and can follow simple commands.10. What is his Glasgow Coma Scale?

  • ReviewAdvanced Providers OnlyYour patient has been involved in a motorcycle accident. He was not wearing a helmet. You find him unconscious, snoring respirations at a rate of 4 times per minute. His blood pressure is 180/100, pulse 50. You also observe decorticate posturing.

  • ReviewHow will you manage this patients airway?How many breaths per minute should this patient receive?What is this patients Glasgow Coma Scale?What further treatment is needed to manage this patient?What will the treatment in question 14 do for this patients injury?

  • AnswersBasilar skull fractureRaccoon eyes, blood/CSF leaking from noseOpen the airway and apply high flow oxygenIncreased intracranial pressureSmall, reactiveOpen the airway and hyperventilate at 20 breaths/min

  • AnswersEpidural hematomaInitial loss of consciousness, lucid interval followed by deteriorating level of consciousness313

  • Answers11. Intubation12. 20 breaths/min13. 514. 3.3% hypertonic saline at 5 ml/kg over 30 minutes15. Pulls water from swollen brain

    *Scalp is very vascular and bleeds freely when lacerated.Children may develop shock from briskly bleeding scalp wound. Head injuries are common in child abuse.Suspect abuse when no clear explanation of cause, if story is inconsistent with injury, or suggests child performed activity not age-appropriate. Pay attention to setting. If abuse suspected, follow procedures for your area.As a general rule, if you have an adult patient with a scalp injury who is in shock, look for another cause for shock (such as internal bleeding). However, do not underestimate blood loss from a scalp wound. Most bleeding from scalp can be easily controlled in field with direct pressure if your exam reveals no unstable fractures under wound.

    *IMAGE: Scalp laceration. Notice linear fracture on visible skull.

    Skull injuries can be linear nondisplaced fractures, depressed fractures, or compound fractures.Suspect an underlying skull fracture in adults who have a large contusion or darkened swelling of scalp. Very little can be done for skull fractures in field except to avoid placing direct pressure upon an obvious depressed or compound skull fracture. Open skull fractures should have wound dressed, but avoid excess pressure when controlling bleeding.

    *Basilar skull fracture indicated by any of following: Bleeding from ear or noseClear or serosanguineous fluid running from nose or earSwelling and/or discoloration behind ear (Battles sign) Swelling and discoloration around both eyes (raccoon eyes)Battles sign can occur from immediately following injury to within 12 hours postinjury.Raccoon eyes are a sign of anterior basilar skull fracture.Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation. *IMAGE: Knife impaled in skull.IMAGE: X-ray of gunshot to head. Tissue destruction is seen in light area. NOTE: Reference to Mechanism of Injury (from Scene Size-up lecture). Remember: Velocity injuries (missiles) cause additional damage due to the shock wave of expanding tissues (temporary cavity).

    Penetrating objects in skull should be secured in place (impaled object) and patient transported immediately. Unless there is a clear entrance and exit wound in a perfectly linear path, assume that bullet may have ricocheted and is lodged in neck near spinal cord.

    *Forces that can cause a skull fracture can also cause a brain injury. Treat brain injury with adequate oxygenation and maintain perfusion.

    *Initial response of injured brain is to swell. Bruising or injury causes vasodilatation with increased blood flow to injured area, and thus an accumulation of blood that takes up space and exerts pressure on surrounding brain tissue. There is no extra space inside skull. Swelling of injured area increases intracerebral pressure and eventually decreases blood flow to brain that causes further brain injury.Increase in cerebral water (edema) does not occur immediately, but develops over hours. Only significant opening through which pressure can be released is foramen magnum at base, where brain stem becomes spinal cord.

    * Primary brain injury is immediate damage to brain tissue as direct result of injury force and is essentially fixed at time of injury. Most primary injuries are from blunt trauma or from movement of brain inside skull.In deceleration injuries, head strikes object such as windshield, causing sudden deceleration of skull. Brain continues to move forward, impacting first against skull in original direction of motion (coup) and then rebounding to hit (fourth collision) opposite side of inner surface of skull (contracoup). Interior base of skull is rough, and movement of brain over this area may cause various degrees of injury to brain tissue or to blood vessels supporting brain. Management of primary brain injury is best directed at prevention with such measures as better occupant restraint systems in autos, use of helmets in sports and cycling, firearms education, and so forth.

    *Good prehospital care can help prevent development of secondary brain injury. Secondary brain injury is result of hypoxia or decreased perfusion of brain tissue as result of brains response to primary injury, swelling.

    *Cerebral contusion is bruised brain tissue.Presents with a history of prolonged unconsciousness or serious alteration in level of consciousness. Example: profound confusion, persistent amnesia, abnormal behavior.May still be unconscious on arrival. May have focal neurological signs (weakness, speech problems) and appear to have suffered a cerebrovascular accident (stroke).Depending upon location of cerebral contusion, patient may have personality changes such as inappropriately rude behavior or agitation.Brain swelling may be rapid and severe.*IMAGE: Figure 10-4: Epidural hematoma (on page 149).

    Acute epidural hematoma is most often due to a tear in middle meningeal artery that runs along inside of skull in temporal region. Temporal bone (temple) quite thin and easily fractured.Arterial bleeding, so rise in ICP can occur rapidly, and death may occur quickly.History of head trauma with initial loss of consciousness often followed by a period during which patient is conscious and coherent (lucid interval).Symptoms:After a few minutes to several hours, develops signs of increasing ICP (vomiting, headache, altered mental status), lapses into unconsciousness, and develops body paralysis on side opposite of head injury.Often a dilated and fixed (no response to bright light) pupil on side of head injury. EMS may be called to evaluate after initial loss of consciousness while in lucid interval. Be suspicious of possibility of a developing epidural hematoma.*IMAGE: Figure 10-5: Subdural hematoma (on page 149).

    Acute subdural hematoma is result of bleeding between dura and arachnoid and is associated with injury to underlying brain tissue.Because bleeding is venous, intracranial pressure increases more slowly, and diagnosis often is not apparent until hours or days after injury. Signs and symptoms include headache, fluctuations in level of consciousness, and focal neurologic signs (e.g., weakness of one extremity or one side of body, altered deep tendon reflexes, and slurred speech). Due to underlying brain tissue injury, prognosis is often poor. Mortality is very high (60%90%) in patients who are comatose when found. Always suspect a subdural hematoma in an alcoholic with any degree of altered mental status following a fall. Elderly patients and those taking anticoagulants are also at high risk for this injury.

    *IMAGE: Figure 10-6: Intracerebral hemorrhage (on page 149).

    Intracerebral hemorrhage is bleeding within brain tissue.Traumatic intracerebral hemorrhage may result from blunt or penetrating injuries of head. Unfortunately, surgery is often not helpful. Signs and symptoms depend upon regions involved and degree of injury. They occur in patterns similar to those that accompany a stroke; spontaneous hemorrhages of this type may be seen in patients with severe hypertension. Alteration in level of consciousness is commonly seen, though awake patients may complain of headache and vomiting.*A concussion implies no structural injury to brain that can be demonstrated by current imaging techniques. There is a brief disruption of neural function that often results in loss of consciousness, but many people will have a concussion without a loss of consciousness. Classically there is a history of trauma to head with a variable period of unconsciousness or confusion and then a return to normal consciousness. There may be amnesia following injury. This amnesia usually extends to some point before injury (retrograde short-term amnesia), so often patient will not remember events leading to injury. Short-term memory is often affected, and patient may repeat questions over and over as if he hasnt been paying attention to your answers. Patients may also report dizziness, headache, ringing in ears, and/or nausea. *Diffuse axonal injury: Most common type of injury as a result of severe blunt head trauma. Brain is injured so diffusely that there is generalized edema. Usually, there is no evidence of a structural lesion. In most cases patient presents unconscious, without focal deficits.*NOTE: Briefly review key issues of anatomy. NOTE: Point out brain stem (respiratory center) at area of foramen magnum. NOTE: Point out optic nerves would come directly from brain to pupils (pupil evaluation).Increased volume of any one of these components has to result in decrease of another component. Vasoconstriction or vasodilation influence intracranial volume. Brain normally adjusts blood flow in response to metabolic needs based on level of carbon dioxide in blood (pCO2). Normal level of pCO2 is around 40 mmHg (also commonly listed as 35 to 45 mmHg).Increased pCO2 (hypoventilation) promotes cerebral vasodilatation, which increases ICP. Lowering pCO2 (hyperventilation) causes vasoconstriction and decreases blood flow. Hyperventilation has only minimal effect on ICP.NOT, as previously thought, that hyperventilation improved cerebral blood flow by causing vasoconstriction and decreasing ICP. *Initial Assessment in head-trauma patient is to determine quickly if patient is brain injured and, if so, if patients condition is deteriorating.All observations must be recorded because later treatment is often dictated by detection of deterioration of clinical stability.Determining exact type of TBI or hemorrhage cannot be done in field. It is more important presence of brain injury be recognized and supportive measures be provided during transport.TBI patients may be difficult to manage because they are often uncooperative and may be under influence of alcohol or drugs.Remember to check blood glucose in all altered mental status.Limit patient agitation, when possible:Avoid excessive movement or jostling of patient.Limit lights and noise to the necessary.Evaluate if extra rescue personnel not directly involved in patient care in a closed environment are necessary.Consider sedation.IV lidocaine is no longer recommended. Topical lidocaine is acceptable. *Initial Assessment neurological exam is limited to level of consciousness and any obvious paralysis. History of head trauma, or if Initial Assessment reveals altered mental status, then Rapid Trauma Survey will include a more complete neurological exam.Treatment of Decreased LOC is:Establish/maintain an adequate airway.Establish adequate ventilation and oxygenation.Establish adequate perfusion.Check blood glucose.Look for and correct any complicating factors.Level of consciousness is most sensitive indicator of brain function. Evaluate and monitor patient closely for change in condition.

    *IMAGE: Abnormally dilated pupils (mydriasis).IMAGE: Anisocoria with unevenly sized pupils.IMAGE: Unilaterally dilated pupil.IMAGE: Cranial nerve III damage may cause eyelid to droop (ptosis) or close slowly. Outward and slightly downward deviation of the eye also reflects damage to cranial nerve III.

    NOTE: Asymmetry (unequal) is defined as 1 mm (or more) difference in size of pupil.NOTE: Fixed (nonreactive) is defined as no response (