sagraves traumatic brain injury
TRANSCRIPT
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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
)
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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%
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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