Neurologic Trauma

Bryan E. Bledsoe, DO, FACEP

Neurologic Trauma

Neurologic Trauma
Suppose you were an
idiot. And suppose you
were a member of
Congress.
But I repeat myself.
Mark Twain

Traumatic Brain Injury (TBI)

Defined as a blow or
jolt to the head or a
penetrating head
injury that disrupts
the function of the
brain.

Statistics
1.4 million people
sustain a TBI each year
in the United States:
50,000 die,
235,000 are hospitalized,
1.1 million are treated
and released from the
ED.

Statistics
Causes:
Falls (28%)
MVCs (20%)
Struck by/against events (19%)
Assaults (11%)
Blasts are the leading cause of TBI for active
duty military personnel in war zones.

Statistics
Males are about 1.5
times more likely to
sustain a TBI as a
female.

Statistics
Highest risk for TBI:
0-4 years
15-19 years

African Americans
have the highest
death rate from TBI.

Statistics
Estimated $60 billion
lost from TBI (medical
costs and lost
productivity).*

* 2000

Anatomy

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Anatomy

Physiology
Brain Metabolism:
Like all tissues, the
brain requires a
constant supply of
oxygen and nutrients.

Physiology
Brain accounts for 2% of
total body mass.
Brain accounts for 15%
of total metabolism in the
body.
Brain metabolic rate 7.5
times the rate of other
neurological tissues.

Physiology
Almost all of the
brains energy needs
are supplied by
glucose.
Provided by
capillaries in the
brain.

Physiology
Insulin NOT
needed for
glucose delivery
to brain tissues.

Physiology
The brain is among the most oxygen
dependent organs in the body.
The brain is not capable of much
anaerobic metabolism.
Primarily due the high metabolic rate of the
neurons.

Physiology
Because of this,
sudden cessation of
blood flow to the
brain can cause
unconsciousness
within 5-10 seconds.

Physiology
Neuroglobin:
Intracellular hemeprotein.
Reversibly binds oxygen with an affinity
greater than that of hemoglobin.
Increases oxygen availability to brain tissue
and provides protection under hypoxic or
ischemic conditions, potentially limiting brain
damage.

Physiology
Brain requires:
Oxygenation
Glucose
Perfusion

Any deficit in these

results in immediate
dysfunction.

Intracranial Pressure
The cranial vault is
effectively a closed
container.
Largest opening is
the foramen magnum.
Limited room for
brain swelling.

Intracranial Pressure
There is always some
pressure in the brain.
Referred to as
intracranial pressure
(ICP).
Normal ICP:
Children: 0-10 mm Hg
Adults: 0-15 mm Hg

Intracranial Pressure
Volume of the cranial vault defined by the
Monro-Kellie doctrine:

Intracranial Volume (fixed) =

Brain Volume + CSF Volume + Blood Volume + Mass Lesion Volume

Intracranial Pressure
Normally:
Brain = 80% of cranial vault space
Blood = 10% of cranial vault space
CSF = 10% of cranial vault space

SPACE AVAILABLE FOR

BLOOD OR MASS = 0%

Intracranial Pressure
To perfuse the brain, the pressure of
blood delivered to the brain MUST be
greater than the intracranial pressure.

CPP = MAP - ICP

Intracranial Pressure
Mean Arterial Pressure:

MAP DP + 1/3 (SPDP)

Intracranial Pressure
Perfusion of the brain is driven by the
CPP.

MAP - ICP = CPP

70 - 30 = 40
CPP of 60 is the critical minimum threshold.
CPP of 40 is the critical minimum threshold
for children < 8 years of age.

Intracranial Pressure
Injury to brain tissue
causes:
Swelling
Bleeding
Edema

All cause an increase

in the size and mass
of the brain.

Intracranial Pressure
As the brain swells, it
will eventually reach
a critical volume
where ICP increases
to a point that
perfusion is
compromised.

Brain Injury
Etiology of TBI:
Primary injury:
Damage to the brain
from mechanical effects
of trauma causing:
Ischemia
Anoxia/hypoxia
Shear injury

Brain Injury
Secondary Injury:
Results from a traumatic event and changes
in the brain or in the brain vasculature.
Hypoxia
Hypotension ( cerebral blood flow)
ICP
Hyperglycemia/Hypoglycemia
Metabolic disturbances
Seizures

Brain Injury
12-24 hours post-injury:
Hypoperfusion and decrease in CBF.
Results from increases in distal
microvascular resistance and intravascular
clot formation.

Brain Injury
1-5 days post injury:
Increased CBF > CMRO2.
Vascular engorgement
Swelling
Increased ICP
Induction of free radicals and oxidative stress.

Brain Injury
5/6-14 days post
injury:
CBF slows due to
vasospasm
Brain vulnerable to
changes in ICP.

Brain Injury
Secondary Injury:
Impaired autoregulation:
Autoregulation is the ability of the brain to maintain
CBF in light of changes in BP and CPP.

Impaired autoregulation causes:

O2 delivery to the brain and cerebral ischemia.
Cerebral metabolism altered due to loss of, or a
decrease in, CBF.
Conversion from aerobic to anaerobic metabolism.

Brain Injury
Secondary Injury (extracranial causes):
Hypotension (SBP < 90 worsens outcomes)
Hypoxia (significantly associated with
increased morbidity and mortality)
Hypocapnia:
Low CO2 causes vasoconstriction
1 mm Hg decrease on CO2 = 3% decrease in CBF.

Anemia
Hyperthermia

Brain Injury
SAH

EDH

Normal

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

MASS
BLOOD
CSF
BRAIN

Brain Injury
Compensatory
mechanisms:
Brain shifts or is
compressed.
Venous blood is
shunted to heart.
CSP shunted to
spinal SAS.

Secondary Injury
Secondary
Insults

No. of
Patients

GoodModerate
Disability

VegetativeSevere
Disability

Dead

Hypoxia

78

45%

22%

33%

Hypotension

113

26%

14%

60%

Both

52

6%

19%

75%

Signs and Symptoms

Early ( ICP):
Altered mental
status
Agitation
Nausea and/or
vomiting
Hemiparesis

Signs and Symptoms

Late ( ICP):
Coma
Hemiplegia
Posturing
Cushings Triad:
Widening pulse pressure
Bradycardia
Respiratory abnormalities

Brain Herniation
Results when ICP
increases beyond
the capability of
physiologic and
limited physical
compensation
mechanisms.

Brain Herniation
Major areas of brain
herniation syndrome:
Subfalcial (a)
Uncal (b)
Central transtentorial
(c)
External (d)
Cerebellotonsillar (e)

TBI
Mild (GCS = 14-15)
~ 80% of patients

Moderate (GCS = 913)

~ 10% of patients

Severe (GCS < 9)

~ 10 of patients

Trauma Types
Scalp Laceration:
Highly vascular
Can lead to
massive blood loss

Trauma Types
Skull Fracture:
Classified by:
Location
Pattern
Open/closed

Up to 50% of patients
with skull fracture will
NOT have LOC or
neurologic
symptoms.

Trauma Types
Concussion:
Brief and temporary loss of neurologic
function following head trauma.
May occur with or without LOC.
Symptoms:
Amnesia
Duration of amnesia predictive of injury severity.

Confusion

Concussion
Grade 1:
No LOC
Confusion without amnesia
Treatment:
Remove from event and examine immediately and every 5
minutes for the development of amnesia.
If asymptomatic > 20 minutes, can return to game.

2 Grade 1 concussions:
No sports for the day

3 or more Grade 1 concussions:

Out for season and no contact sports for 3 months

Concussion
Grade 2:
No LOC
Confusion and amnesia
Treatment:
Remove from event for the day.
Refer for exam the next day.
May return in 1 week if asymptomatic with rest/exertion.

2 Grade 2 concussions:
No play for 1 season

3 Grade 2 concussions:
Season terminated.

Concussion
Grade 3:
LOC
Treatment:
Transport to ED for evaluation
Return to sport in 1 month if asymptomatic for a 2-week
period.
2 Grade 3 concussions:
Season terminated.

Trauma Types
Cerebral contusion:
Most frequent type of TBI
Most common in:
Subfrontal cortex
Frontal lobe
Temporal lobe
Occipital (less common)

Often associated with SAH.

Trauma Types

Contusion

Trauma Types
Subarachnoid
hemorrhage:
Disruption of
subarachnoid vessels.
1/3 of all patients with
moderate to severe TBI
have traumatic SAH.

Trauma Types
Epidural hematoma:
Collection of blood between the dura and the
skull.
Arterial bleed.
Incidence:
0.5-1.0% of all head-injured patients.
<10% of head-injured patients who are comatose.

Almost all associated with skull fracture.

80% will progress to uncal herniation.

Epidural Hematoma

Epidural Hematoma
Signs and Symptoms:
Classis syndrome (<20% of cases):
Immediate LOC.
Patient awakens and has a lucid interval.
Loses consciousness as hematoma expands.

Most commonly:
Most patients either never lose consciousness or
never regain consciousness.

Trauma Types
Subdural hematoma:
Collection of blood
between the dura and
the SAM.
Venous bleed.
Associated with
sudden acceleration
and/or deceleration.
Tears bridging veins.

Subdural Hematoma

Subdural Hematoma
Usually more brain parenchymal injury
than epidurals.
Classified as:
Acute (< 3 days)
Subacute (3-14 days)
Chronic (> 14 days)

Trauma Types
Diffuse Axonal Injury (DAI):
Interruption of axonal fibers in the white
matter and brain stem.
Shearing forces (usually deceleration) cause
injury.
Adults: MVCs
Babies: Shaken baby syndrome

Injury occurs immediately and is usually

irreversible.

Diffuse Axonal Injury

Trauma Types
Intracerebral
Hemorrhage:
Usually caused by
shearing forces.
Severity depends upon
location and size.
Secondary injury
common.

Trauma Types
Penetrating Injury:
Severity of injury
related to:
Kinetic energy of
injury
Location of injury

Infection a common
complication.

Trauma Types
Probably mortal.

TBI Signs and Symptoms

Anxiety/nervousness
Behavioral changes:
Disinhibition
Impulsiveness
Inappropriate laughter
Irritability

Diplopia
Depression
Trouble concentrating

Aphasia
Dysphagia
Dizziness
Headache
Uncoordination of
movements
Lightheadedness
Ataxia
Amnesia

TBI Signs and Symptoms

Muscle
stiffness/spasm
Seizures
Sleep disorders
Slurred or slowed
speech
Tingling
Numbness
Pain

Vertigo
Localized weakness
Nausea
Vomiting
Body temperature
changes
Coma
Posturing
Pupillary abnormality

TBI Signs and Symptoms

SIGNS AND SYMPTOMS

IN TBI
ARE EXTREMELY
VARIABLE

Assessment/Treatment
Airway (with cspine control)
Breathing
Circulation
Disability
Exposure

Assessment/Treatment
Palpate skull, facial bones and neck
Assess rate, depth and quality of
respirations.
Consider tachypnea at the following rates a
sign of deterioration:
Infant: 40 breaths per minute
Child: 30 breaths per minute
Adult: 20 breaths per minute

Assessment/Treatment
Assess pupils carefully:
Pupil size
Symmetry
Reactivity to light

Assessment/Treatment
Pupillary assessment:
Bilateral symmetry (asymmetric pupils differ
more than 1 mm).
Reactivity to light (a fixed pupil shows <1mm
change in response to bright light).
Dilation (greater than or equal to 4mm
diameter in adults)

Assessment/Treatment
Single fixed and dilated pupil:
45% poor outcome

Bilateral fixed and dilated pupils:

82% poor outcome

Assessment/Treatment
Mid-position fixed and
dilated pupil:
Suggests brain stem
herniation.
Indicative of mass on
same side.
Treat hypoxia and
hypotension, if present.
Treat increased ICP per
practice parameters.

Assessment/Treatment
Indications of herniation:
Unilateral or bilateral dilated, nonreactive
pupils.
Asymmetric pupils.
Decerebrate posturing.
No motor response to painful stimuli.

Assessment/Treatment
Monitor SpO2 and ETCO2.
Maintain SpO2 > 90%
Maintain ETCO2 between 35-37 mm Hg

Initiate IV line with saline:

Maintain adult systolic BP > 90 mm Hg
Pediatric values are lower.

Utilize Glasgow Coma Scale

Glasgow Coma Scale (Adult)

Eye Opening (E)

Verbal Response (V)

Motor Response (M)

Obeys (6)

Oriented (5)

Localizes (5)

Spontaneous (4)

Confused (4)

Withdraws (4)

Reaction to Speech (3)

Inappropriate Words (3)

Decorticate (3)

Reaction to Pain (2)

Incomprehensible
Sounds (2)

Decerebrate (2)

No Response (1)

No Response (1)

No Response (1)

TOTAL = E + V + M

Glasgow Coma Scale (Infant)

Eye Opening (E)

Verbal Response (V)

Motor Response (M)

Obeys (6)

Coos, Babbles (5)

Localizes (5)

Spontaneous (4)

Irritable Cry (4)

Withdraws (4)

Reaction to Speech (3)

Cries to Pain (3)

Decorticate (3)

Reaction to Pain (2)

Mans, Grunts (2)

Decerebrate (2)

No Response (1)

No Response (1)

No Response (1)

TOTAL = E + V + M

Assessment/Treatment
Assess blood
glucose level.

Treat Airway
Protect C-spine alignment, consider
facial trauma.
Airway support per scope of practice.
Intubate severe TBI patients.
Correct hypoxia.

When to Intubate
GCS < 9 (severe
TBI).
All patients with
respiratory failure of
apnea.

Treat Breathing
Oxygenation.
Administer supplemental oxygen by nonrebreather or BVM as appropriate.

Ventilation.
Assess rate, depth, quality, to determine the
effectiveness of respirations.
As necessary, assist ventilations with BVM
and supplemental O2.

Treat Breathing

Adult normal
Ventilation rate
=
10-12 per minute

Hyperventilation?
Hyperventilation:
Rapid PaCO2
Cerebral vasoconstriction
Decreased CBF
ICP

But, hyperventilation can CBF to the

point of ischemia.
Monitor ETCO2!

Hyperventilation?
Potential harm in patients without
evidence of brain herniation.
Short-term measure used in specific TBI
patients (herniation) until definitive
diagnostic or therapeutic can be
provided.

Hyperventilation?
Rates:
Ages 9-Adult: 20 breaths per minute:
(ETCO2 ~ 35 mm Hg).

Ages 1-8 years: 30 breaths per minute:

(ETCO2 ~ 32-35 mm Hg).

Ages < 1 year: 40 breaths per minute:

(ETCO2 ~ 32-35 mm Hg).

Fluids
Fluids to maintain SBP> 90 mm Hg.
Normal saline
Hypertonic saline?

Brain-Targeted Therapies
Glucose for hypoglycemia
Sedatives for agitation
Analgesics for pain
Paralytics for ET intubation
Controversial:
Mannitol
Lidocaine
Hypertonic Saline

Destinations
Mild (GCS 14-15): Emergency Department
Moderate (GCS 9-13): Trauma Center
Severe (GCS < 9): Trauma Center with
severe TBI management capabilities.

Take Home Messages

Clinical practice should be evidencebased.
Do early and repeated neurological
assessments.
Identify patients with severe TBI (GCS <
9).

Take Home Messages

Avoid hypoxia, keep SpO2 > 90%.
Avoid hypotension, keep SBP > 90 mm
Hg.
Hyperventilate only for clinical signs of
herniation.
Triage and transport TBI to appropriate
facilities based on severity.

The Future
Therapies to protect against secondary
injury:
Hypothermia.
Sedative-induced coma.
Metabolic therapies.
Antioxidant therapies.