sagraves traumatic brain injury

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  • 8/11/2019 SAGRAVES Traumatic Brain Injury

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    Scott G Sagraves, MDProfessor, UMKC

    Trauma Medical Director, Saint Lukes Hospital

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    No financial relationships creating a conflict ofinterest to report

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    Define the anatomy and physiology ofTraumatic Brain Injury (TBI)

    Explain the concept of the Monroe-KellieDoctrine

    Interpret the Brain Trauma Foundationguidelines for EMS treatment of TBI

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    Worldwide, TBI is the leading cause of death& permanent disability

    Annually, >50,000 die

    230,000 hospitalized

    Trimodal age distribution; < 5, 15-24, > 70

    50% mortality within the first TWO hours

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    AIRWAY & C-spine Control

    BREATHINGCIRCULATION & Bleeding Control

    DISABILITY - Neurologic AssessmentEXPOSURE

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    Transient respiratory arrest after TBI

    Inability to protect airway with GCS 8

    Early intubation for adequate ventilation andoxygenation*

    Obtain a brief neurologic exam prior tosedation/intubation

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    Pre-Hospital Intubation (PHI)is Associatedwith an Increased Mortality After TBI

    2549 patients analyzed PHI vs. non-PHI Mortality 90.2% vs. 12.4%

    PHI in isolated, moderate-severe TBI patientsin associated with a nearly 5-fold increase

    in mortality.Bukur M, Kurtovic S, Berry C, et al. J Surg Res 170, e117-e121. 2011

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    Paralytics are not recommended in the urbanEMS setting for airway management

    Airway clearance/establishment to prevent

    hypoxia If using RSI/DAI in the field, monitor:

    BP

    SpO2 EtCO2

    Consider the following: BVM with nasal or oral airway

    Rescue airway (e.g. Combitube

    , King Airway

    )

    http://allemt.com/wp-content/uploads/2013/09/KINg.jpg
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    Transient respiratory arrest after TBI

    Inability to protect airway with GCS 8

    Early intubation for adequate ventilation andoxygenation*

    Obtain a brief neurologic exam prior tosedation/intubation

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    EMS Assessment Continuous monitoring for hypoxia

    Goal: SpO2> 90%

    SpO2> 90%: Mortality 14%; Morbidity 3%

    SpO260 89% Mortality 27%; Morbidity 27%

    SpO2< 60% Mortality 50%; Morbidity 50%

    http://en.wikipedia.org/wiki/File:Saturometre_2.jpg
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    Hypoxemia is damaging to injured brain, provide100% oxygen

    Ventilate at a normal rate EtCO2goal: 35-40 mmHg

    Vt: 6-7 cc/kg and rate 10 breaths/min

    Hyperventilation is a rescue maneuver and isutilized for brief periods with continuous EtCO2monitoring EtCO2< 35 should be avoided for extended periods of

    time

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    Hypotension is almost never due to braininjury or hypovolemia from brainhemorrhage.

    Exsanguination can occur from scalplaceration

    Hypotension (SBP < 90 for 5 min) doubles brain injury mortality (60% vs. 27%)

    additional hypoxia increase mortality to 75%

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    Goal:

    Maintain SBP > 90 mm Hg; MAP > 65

    Treatment Correct hypotension with isotonic fluids

    0.9% Normal Saline

    Lactated Ringers (LR)

    Consider hypertonic saline (3%) if GCS < 8

    250 mL 500 mL bolus

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    EYES OPEN4 Spontaneously3 To Verbal Command2 To Pain

    1 No Response

    BEST VERBAL RESPONSE5 Oriented and Converses4 Disoriented and Converses

    3 Inappropr iate Words2 Incomprehensible Sounds1 No response

    BEST MOTOR RESPONSE

    6 Obeys5 Localizes to Pain4 Flexion Withdrawal3 Decorticate posturing2 Decerebrate posturing

    1 No Response

    Glasgow Coma Score

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    Mild GCS 14-15 80%

    Moderate GCS 9-13 10%

    Severe GCS 3-8 10% Causes 65% of mortality in MVC

    In hospital mortality about 30%

    Full neurologic recovery rare

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    Damage to the brain caused by the

    initial insult

    Only prevention will decrease this Seatbelts

    helmets

    EMS goal to prevent secondaryinjury

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    Assess for cerebral herniation Dilated, non-reactive pupils Asymmetric pupils Posturing motor exam Progressive neurologic deterioration

    Pupil exam First rule out orbital trauma Check after resuscitated/stable Unilateral or bilateral dilated pupils

    Asymmetry

    Fixed and non-responsive

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    Pain Control

    No scientific evidence improves outcomes

    Opiates/Ketamine may INCREASE ICP Mannitol

    Osmotic diuretic

    1 gram/kg for signs of herniation Hypoglycemia

    Assess for using finger stick

    Correct hypoglycemia

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    EMS system with goal the rightpatienttothe rightplacein the rightamount of time

    Strategies Limit pre-hospital time

    Transport vehicle quickest means to closest center

    Transport to facility which has: CT scan capabilities

    ICP monitoring

    Neurosurgical Care

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    Usually bleeding from

    Middle Meningeal

    Artery Lucid interval

    Lens shaped from

    pushing the dura off

    the skull Surgery to remove

    mass

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    Usually bleeding from

    bridging veins

    Concave shapefollows skull

    Surgery to remove

    mass effect

    Associatedunderlying brain

    contusion

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    Which would you rather have?

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    Bleeding insubarachnoid space

    Trauma or rupturedcerebral aneurysm

    Layers in the sulci allaround the brain

    May inducevasospasm, ischemia,or seizures

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    Blood in the tissue ofthe brain

    Diffuse axonal injury Shear injury to axons. Terrible prognosis

    May require surgery

    to remove large clotor large amount ofdamaged brain

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    The Monroe-Kellie Doctrine

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    Increased volume in a

    closed space results

    in either increased

    pressure in the space

    or loss of some

    content of the space.

    Describes the natural

    history of intracranial

    injury (early 1700s)

    Brain

    Blood

    CerebrospinalFluid

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    Small to moderatemass effect iscompensated bydecreased CSF anddecreased bloodvolume due tovenous compression

    Normal ICP

    Brain

    Blood

    CerebrospinalFluid

    Mass

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    Maximum loss ofCSF and venous

    blood

    Mass results inbrain compression

    Elevated ICP

    Brain

    Blood

    Cerebrospinal Fluid

    Mass

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    Mass causes such

    severe compression

    that arterial flow is

    lost

    Very High ICPs

    Herniation of brain

    tissue

    Brain death

    Brain

    Cerebrospinal Fluid

    Mass

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    Herniation

    Uncal herniation (2)

    Compression of CN III Dilated pupil

    Decrease level of consciousness

    Cushing reflex

    Cerebellar herniation (4) Pushed down foramen

    Rapid pulmonary failure

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    Factors which make brain injury

    worse or enlarge area of injury: Hyperglycemia

    Hyponatremia

    Hypotension

    Hypoxia

    Hyperthermia

    Hypercarbia

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    Trauma

    GCS 3-8 and abnormalhead CT

    GCS 3-8 and normalhead CT but two of thefollowing: age > 40,hypotension, posturing

    Clinical signs of

    increased intracranial

    pressure

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    Flow to the brain is the most important

    Perfusion pressure is used instead of flow

    CPP = MAP ICP

    Normal ICP < 10 cm H2o Acceptable ICP < 20 cm H2o Normal CPP > 70 cm H2o

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    Prevent Secondary Injury

    Decrease skull contents

    Decrease brain metabolic demand

    Improve CPP

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    The mass is abnormal--

    Surgical removal is

    optimal

    Subdural and Epidural

    hematomas

    Surgery may not be an

    option due to location or

    multiple small lesions

    Brain

    Blood

    CerebrospinalFluid

    Mass

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    Ventriculostomy !!!

    Brain

    Blood

    Cerebrospinal Fluid

    Mass

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    Only venous blood can bedrained without causingischemia

    Raise the head of bed

    Keep Head straight

    Loosen collar

    No Jugular lines

    Hyperventilation

    Brain

    Blood

    CerebrospinalFluid

    Mass

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    Osmolar therapy--

    increased blood

    osmolarity decreasesbrain fluid

    Mannitol -- treatment

    only, not prophylactic

    Hypertonic Saline

    Brain

    Blood

    CerebrospinalFluid

    Mass

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    Analgesia

    Sedation

    Paralysis

    Cooling

    Pentobarbital Coma

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    ICP should be controlled first, if abnormal

    If not controlled, increased MAP will provideperfusion to the brain despite high ICP{Cushings Reflex}

    Usually use Neosynephrine

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    Has been used as initial management in past.

    Works by causing hypocarbic vasoconstriction

    of cerebral blood vessels

    DECREASES CEREBRAL BLOOD FLOW

    Works only for a short time Should be used as last ditch therapy Try to keep pCO2 normal.

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    Treat Surgical lesions

    Prevent secondary injury

    Enhance venous drainage

    Provide sedation and analgesia

    Drain CSF if ventriculostomy is available

    Maximize Osmolar therapy

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    Airway protection?

    Hyperventilation??

    Head elevation with C-spine control

    ***Maintenance of blood pressure*** Permissive hypotension not applicable

    Osmotic diuresis vs. 3% Saline

    Seizure prophylaxis???

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    Steroid Administration

    Furosemide Administration

    Hemoglobin Level

    Hypothermia

    Anticonvulsant Therapy

    Never

    Theoretical

    > 10 g/dL

    Difficult

    Recommended

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    10-15% of severe head injuries will developintractable elevated ICP

    Mortality 84-100%

    Treatment Paralysis

    Pressors to enhance MAP

    Intermittent hyperventilation

    Pentobarbital coma

    Drastic measures . . . . . .

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    Remember what the dormouse said:

    Feed your Head. Feed your Head.

    --JeffersonAirplane