Transcript Pre-Hospital Management of Traumatic Brain Injury

If I Only Had A Brain…..
Pre-Hospital Management of
Traumatic Brain Injury
Jennifer Davis, RN, MS, ANP-C,
CCRN, EMT-CC
Incidence

Traumatic Brain Injury, or TBI, is the leading
cause of death and disability in children and
adults from ages 1-44
 Most often caused by motor visual crashes,
sports injuries, or simple falls on the
playground, at work, or in the home
 Approximately 52,00 deaths occur from TBI
annually
 An estimated 1.5 million head injuries are
seen yearly in Emergency Departments
 An estimated 1.6 to 3.8 million sports related
TBIs occur each year
Facts about TBI

At least 5.3 million Americans, 2% of the US
population, currently live with disabilities
resulting from TBI
 Moderate and severe head injury
(respectively) is associated with a 2.3 and 4.5
times increased risk of Alzheimer’s disease
 Males are 2x more likely to suffer TBI that
females
 The leading causes of TBI are falls, MVC,
and assaults
Facts about TBI

TBI hospitalization rates have increased from
79% per 100,000 in 2002 to 87.9% per
100,000 in 2003
 Exposures to blasts are a leading cause of
TBI among active duty military personnel in
war zones
 Veteran’s advocates believe that between 10
and 20% of Iraq war veterans, or 150,000
and 300,000 members have some level of
TBI
 30% of soldiers admitted to Walter Reed have
been diagnosed with a TBI
Prevention

The best way to treat TBI is prevention

Bicycle helmets
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Seat belt use
Motorcycle helmets – full face
Helmets
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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 helmets
Skateboarding
Rollerblading
Scooters
At risk behaviors

Males 2 times > injury rate than females
Where does EMS fit in?
 EMS
providers are the first contact a
patient has into the trauma system
 We have the ability to prevent
secondary brain injury with the right
interventions
brain injury – the initial brain injury
sustained as a result of trauma
 Secondary injury – the injury that occurs
due to hypoxemia and hypovolemia
 Primary
Classification of TBI

Mild TBI (GCS 13-15) (MOST of what EMS
will see)
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Concussive syndrome
Reversible, temporary LOC/retrograde amnesia
Change in mental status a the time of injury only
Imaging usually normal
Moderate TBI (GSC 9-12)
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LOC and/or post amnesia of > 30 minutes but < 24
hours
GCS – 9-12
Physical, cognitive, and/or behavioral impairments
last for months or are permanent
Generally make a good recovery with treatment or
learn to compensate for deficits
Classification of TBI
 Severe
TBI (GCS 3-8)
 LOC
or post-traumatic amnesia > 24 hours
 GCS lower
 More extensive physical impairments as a
result if brain damage
 Slower course of recovery
 Clear indication of significant, permanent
deficits

What these are depend on location of injury
Classification of TBI
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Very severe/catastrophic TBI
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True comas of many weeks or months
This term is reserved for the most severely
damaged head injury
Many never regain consciousness or regain
meaningful communication with the environment
“Persistent vegetative state”
Brain Death
 Results
from a severe insult to the brain
 No cortical or brain stem activity
 No
movement to stimuli
 No brain stem reflexes
 No spontaneous breathing
 Not
diagnosed in the field
 If the brain is dead, the person is dead
Concussion
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Traumatic, REVERSIBLE neurological deficit
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Temporary LOC
Retrograde amnesia
Etiology
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Strong, rapid acceleration-deceleration injury
Blow to the head
There is a temporary cessation of the functioning
of the reticular activating system
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RAS responsible for arousal or wakefulness of the brain
Concussion
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Assessment
 Subjective Data
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HPI
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Medical Hx
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Neuro disease, recent trauma, prior head injury
Objective Data
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Mechanism, consciousness immediately after event,
duration of event, neuro events after event
Physical exam – neuro exam, memory
assessment
May have repetitive speech and questions
Diagnostics

CT scan – R/O bleed
Interventions for Concussion
 Immobilization
as necessary
 Emotional support
 High flow oxygen
Planning/Interventions for
Concussion
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Post Concussive Syndrome
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Results from repeated mild brain injuries over a
period of months or years
Can impact neurological, behavioral and cognitive
function
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“second impact syndrome” now called Chronic Traumatic
Encephalopathy or CTE


Muhammad Ali, Football players
Once a person suffers a concussion, they are four
times more likely to suffer another one.
Skull Fracture
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Types
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Linear
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Depressed
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Damages underlying cerebral tissue by compression or
laceration and by retained bony fragments
Basilar
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Most common
Account for about 70% of all types
Usually benign unless it crosses a major vascular
channel
Can occur within any of the fossae
Clinical picture depends on the area affected
Complications include infection, hematoma,
CSF leaks, loss of smell, loss of hearing,
seizures and pneumocephalus.
Skull Fracture
 Assessment
 Subjective
Data
 HPI
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Recent trauma, elapsed time, sweet or salty
taste in back of throat, post nasal drip
 Medical
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Hx
Trauma, malignancy
Skull Fracture
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Objective Data
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Physical Exam
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Surface trauma, AMS, altered pupil or motor response,
CSF leak, Raccoon eyes, Battle’s sign
Diagnostics
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Halo Test (ottorrhea or rhinorrhea)
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Using a 4X4 collect fluid leak from nose or ear
Set on the bedside table for a few minutes
Positive when there is a circular separation of blood and
clear fluid or a “halo”
Indicative of a CSF leak
Halo Sign
Depressed Skull Fx
Linear Skull Fx
Basilar Skull Fx
Basilar Skull Fx
 Battle’s
Sign
Raccoon Eyes
Diffuse Axonal Injury (DAI)

DAI is the widespread disruption of neuro
function without any focal lesions
 Characterized by microscopic damage to the
axons, diffuse white matter degeneration,
global neuro dysfunction and diffuse cerebral
edema.
 Etiology
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Acceleration-deceleration
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MVC, Pedestrian, Shaken Baby
Shear injury
DAI
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Assessment
 Subjective Data
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HPI
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Mechanism of injury, onset and duration of LOC
Medical Hx
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Neuro disease or injury
Substance abuse
Child abuse or exam doesn’t fit with mechanism of injury
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Shaken baby
DAI
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Objective Data
 Physical Exam
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Immediate LOC, lasts days to months
Increased ICP
Brain stem dysfunction
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Decortication or decerebration
Loss of brain stem reflexes – cough, gag, etc.
Hypertension
Hyperthermia
Diaphoresis
DAI
DAI
Cerebral Contusion

Cerebral contusion is an actual bruising of the
brain
 Results in focal ischemia and edema with
potential for infarction, necrosis and/or
↑ ICP
 Etiology
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Trauma, acceleration/deceleration, high velocity
blows, or rotation of the brain following a blow
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Coup – contra coup injury
Clinical picture varies depending on area
involved
Cerebral Contusion
 Assessment
 Subjective
Data
 HPI

Mechanism of injury, changes in LOC since
event
 Medical
Hx
Neuro disease or injury
 Substance abuse
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Cerebral Contusion
 Objective
Data
 Physical
exam
Altered LOC > than a few hours
 Surface trauma
 Full neuro exam
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Cerebral Contusion
Subdural Hematoma (SDH)
 SDH
is a collection of blood between
the dura matter and the subarachnoid
layer of the meninges
 Usually caused by trauma or as the
extension of an intracerebral hematoma
into the subdural space
Subdural Hematoma (SDH)
 Three
classifications
 Acute
- onset within 48 hours of
presentation
 Sub-acute – onset 2-14 days
 Chronic – more than 14 days
Subdural Hematoma (SDH)
 Assessment
 Subjective
Data
 HPI
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Mechanism of injury, time interval, trends in
neuro status
 Medical
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Hx
ETOH Abuse

Chronic SDH common in these pts secondary to
multiple falls and abnormal bleeding tendencies
secondary to impaired liver function
Subdural Hematoma (SDH)
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Medical History
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Use of blood thinners or anti-platelet agents
 Coumadin® (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
Subdural Hematoma (SDH)
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Objective Data
 Physical Exam
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Acute
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Headache, drowsiness, confusion
Steady decline in LOC
Ipsilateral , unilateral pupil dilation with lack of response
to light – LATE finding
Contra lateral hemiparesis
Chronic and sub acute
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Gradual and non-specific changes
Altered mentation
Altered motor status
Ipsilateral pupil dilation and sluggish to light
Subdural Hematoma (SDH)
Acute SDH with left to right shift
Subdural Hematoma (SDH)
Chronic SHD
(gray) with
acute SHD
component
(white)
Epidural Hematoma (EDH)
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Collection of blood between the skull and
dura
 Etiology
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Usually from a laceration of the middle meningeal
artery associated with skull fx
The arterial bleed in under high pressure – it does
not tamponade, but rather progresses to become
a space occupying lesion causing ↑↑ ICP, brain
shift and herniation
Mortality = 50% if not treated
Epidural Hematoma (EDH)
 Assessment
 Subjective
Data
 HPI
Mechanism of injury
 PATTERN of unconsciousness
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Initially unconscious, followed by a lucid period, then
followed by rapid unconsciousness
 Medical
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Hx
Previous trauma, previous head injury
Epidural Hematoma (EDH)
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Objective Data
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Physical exam
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Altered LOC, pupils with unilateral dilation, fixed and/or
dilated, contralateral paresis or paralysis which leads to
posturing
Cushing’s triad
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Abnormal respirations
Narrowing pulse pressure
Bradycardia
Diagnostics
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Rapid CT exam at trauma center
Epidural Hematoma (EDH)
Notice the
scalloping,
rather than
layering of
the blood.
EDH
 Frequent
neuro checks
 ABC’s
 Prepare
for emergency surgery
 Transport
to a facility with neurosurgery
capabilities
 TRUE
Neurosurgical emergency!
Increased ICP
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ICP is influenced by relatively fixed volumes
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The brain
The blood
The CSF
80%
10%
10%
Total volume
Monroe-Kellie Hypothesis
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to 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
Increased ICP
 Etiology
– Any condition that:
 Increases
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space occupying lesions
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SDH, masses, cerebral edema, EDH, ICB
 Increases
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blood volume
Venous outflow obstruction, hyperemia (HTN),
hypercapnia
 Increases
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brain volume
CSF
Hydrocephalus, SAH, lack of absorption of CSF
Increased ICP
 Assessment
 Subjective
Data
 HPI
Chronology
 Consciousness
 Mentation
 Personality
 Communication
 Nausea
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Pain
Seizures
Vomiting
Motor deficits
Headaches
Visual changes
Increased ICP
 Medical
History
 Neuro
disease
 Trauma
 Fainting
 Substance abuse
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Especially cocaine, heroin
 Medications
 Allergies
Increased ICP
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Objective Data
 Physical Exam
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EARLY picture of ↑ ICP
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LOC – changes may be SUBTLE. Changes in LOC may
be the FIRST sign of ↑ ICP
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Pupils – sluggish, different bilaterally
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Ipsilateral/unilateral changes
Motor function
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LISTEN to the patient’s family – they know their loved one
BEST!
Contralateral changes
Vital Signs
Increased ICP
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LATE picture of ↑ICP
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LOC
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Arouses only with deep noxious stimuli, or unresponsive
Pupils
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Motor function
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Fixed and dilated or “blown”
Hemiparesis, posturing, or flaccidity
Vital Signs
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Cushings Triad
 Bradycardia
 Narrowing pulse pressure
 Slow or irregular respirations
Hyperventilation
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Hyperventilation in Traumatic Brain
InjuryOnly used when:
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GCS < 8 plus
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Active seizure
Posturing
Increased BP and decreased pulse
Intermittent apnea
Further decrease of GCS >2 on subsequent exam
Adult – 20 breaths per minute
Child – 25 breaths per minute
Get With The Guidelines
Brain Trauma Foundation
Guidelines for the Pre-Hospital
Treatment of Traumatic Brain
Injury
Treatment for TBI
 Oxygenation
 Hypoxemia
and Blood Pressure
(<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 setting
 In children the parameters are SBP<65 (01 years old), <75 (2-5 years old), <80 (6-12
years old) and <90 (13-16 years old
Treatment for TBI
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High Flow 02 all patients
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Assist ventilations as necessary per protocol
Avoid nasal airways in those patients with facial
injury and/or suspected basilar skull fx
Raising BP in hypotensive, severe head
injury patients improves outcome in
proportion to the efficacy of the resuscitation

If ALS – IV NS Open until SPB >90, or up to 2
liters infused then contact Medical Control
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 time
 A GCS score of 3 to 5 has at least a 70%
positive predictive value for poor outcome
GCS
 Best
Eye Response. (4)
1.No eye opening.
2.Eye opening to pain.
3.Eye opening to verbal command.
4.Eyes open spontaneously.
GCS
 Best
Verbal Response. (5)
1.No verbal response
2.Incomprehensible sounds.
3.Inappropriate words.
4.Confused
5.Orientated
GCS
 Best
Motor Response. (6)
1.No motor response.
2.Extension to pain.
3.Flexion to pain.
4.Withdrawal from pain.
5.Localizing pain.
6.Obeys Commands.
GCS
Note 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.
Pupillary Assessment
 Pupil
examination is a standard
component of the pre-hospital neuro
exam
 The pupillary exam along with the GCS
will serve as a baseline for ALL
subsequent examinations in the ER and
hospital
Pupillary Assessment
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Pre-hospital pupil exam should consist of:
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The pupil size and light reflex
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Assess and document on the PCR
The duration of the pupillary dilation and fixation
should be assessed and documented
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Brisk reaction to light
Sluggish reaction to light
No reaction to light
Anisocoria
Airway, Ventilation, and
Oxygenation

GUIDELINES
 Hypoxemia (apnea, cyanosis, Sat <90%)
MUST be avoided or corrected immediately
 Sats should be monitored, if available, on all
patients with TBI
 Hypoxemia should be treated with
supplemental O2

In NYS and Suffolk – all trauma patients should be
given high flow 02
Airway, Ventilation, and
Oxygenation

Options
 Airway should be secured in pts with GCS<9,
the inability to maintain an adequate airway,
or hypoxemia not corrected by supplemental
O2
 Endotracheal intubation is the most effective
way to maintain a difficult airway
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Intubate only if possible – i.e. teeth not clenched,
avoid prolonged attempts as this will increase ICP
In peds, BVM ventilation is just as effective as long
as you are getting chest rise
Airway, Ventilation, and
Oxygenation
 AVOID
prophylactic hyperventilation
 Patients should be maintained with
normal breathing rates (ETCO2 35-40
mmHg), and hyperventilation (ETCO2 <
35 mmHg) should be avoided unless
the patient shows signs of cerebral
herniation
Hyperventilation
 20
breaths per minute in an adult
 25 breaths per minute in a child
 30 breaths per minute in an infant less
than 1 year old
 For ALS providers:
 The
goal of hyperventilation is ETCO2 of
30-35 mmHg. Capnography is the
preferred method for monitoring ventilation
Fluid Resuscitation
 Fluid
resuscitation in patients with TBI
should be administered to avoid
hypotension and/or limit hypotension to
the shortest duration possible
 In Suffolk
 Up
to 2 large bore IV’s with NS open until
SBP >90 or up to 2 liters NS infused, then
contact with MC
 KVO for SBP > 90
Hypoglycemia
 Hypoglycemia
has been associated with
traumatic events – it exhibits signs
similar to that of patients with TBI
 I.e.
MVA secondary to low blood sugar
 Blood
sugar should be checked in all
patients with AMS of undetermined
etiology
 Treat
hypoglycemia
Transport Decisions

Patients with severe TBI and a GCS <9
should be transported to a facility with the
following capabilities:
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Immediate CT Scanning
Prompt neurosurgical care
Ability to monitor ICP and treat increased ICP
For all intents and purposes, this is a trauma
center
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GSH
SSH
BMH
UHSB
Case Study

You are dispatched to the scene of a
motorcycle vs. car – BLS ambulance
 On scene you find:
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Approximately 20 year old male lying prone
Ninja motorcycle
Full face helmet in place but not intact
Motorcycle is found approximately 50 feet from
where you find your patient
You notice bilateral femur deformities
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 protocols


Obvious depression In the occiput of the pt’s head
Using a jaw thrust, open the airway, look, listen and feel
for breathing

You determine that he is not able to maintain his airway
and that he is breathing irregularly
Case Study

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Place an oral airway
Begin BVM ventilations
Check for a distal pulse – 120 and weak
Check BP – 80/30
GCS of 6
Decerebrate posturing
You take a step back, and think to yourself…


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Oh Crap!
No – ABC’s are taken care of, now what must I do to
maintain this patient
Call for ALS to scene
While 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!!!!
Case Study

ALS – intervene enroute to trauma center

Remember the standards/guideline for prehospital management of TBI

Airway/Breathing

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Circulation

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
Is it adequate with the OPA in place, is there chest rise,
can I safely intubate this patient and not do further harm
What is the pulse and BP
IV access
NS open for SBP >90 or up to 2 liters
Hyperventilation

Do I need to do it? – In this patient, yes, mild
hyperventilation of 20 BPM is appropriate based on his
physical assessment and neuro exam
Case Study

Are my interventions helping?



Re-assess ABC’s
Re-assess GCS
Re-assess Vitals