HEAD TRAUMA

Will/Grundy EMS
2009 2nd Trimester May CME

OBJECTIVES
Understand the divisions of the brain and their
main function.
Understand the neurological assessment and the
cranial nerve exam.
Describe primary injury vs. secondary injuries.
Describe the evolution of increased intracranial
pressure and the treatment for the brain injured
patient.
Explain the Monro-Kellie Doctrine and
autoregulatory system

NO PRESSURE

MENINGES
1) Dura Mater
2) Arachnoid
3) Pia Mater

DURA
Outermost layer
Tough, fibrous
Produces folds
Falx cerebri
Tentorium cerebelli

Dura Mater creates Potential Space

* Epidural space
* Subdural space

Epidural Hemorrhage

Subdural Hemorrhage

ARACHNOID
Avascular connective tissue
Fibrous cords (trabeculae) attached to the PIA
mater
Arachnoid Villi
Reabsorb CSF

Subrachnoid Space
Contains large blood
vessel
Contains CSF
Expanded areas-Basilar cistern, Lumbar cistern

PIA
Thin, vascular
Carries a rich supply of blood vessels
Forms the choroid plexus
Choroid plexus is found in the walls of the
ventricles
Choroid plexus produce CSF

Meninges of the Brain

CEREBRAL CORTEX

FRONTAL LOBE

Personality
Behavior
Voluntary motor function
Motor speech (Brocas),
Left side dominent
Intellectual functions, problem solving
Judgment; good/bad, right/wrong
Called the MOM portion of the Brain

PARIETAL LOBE
Primary sensory lobe; pain, pressure,
vibration, touch
Localization of stimuli
Object recognition
Position sense
Sensory association

TEMPORAL LOBE

Primary auditory lobe

Long term memory
Emotions
Cognitive speech
(Wernickes); organize language,
understand and respond to verbal input

Uncus discriminates smells

OCCIPITAL LOBE
Processing visual input

INTRACRANIAL DYNAMICS
Three substances in the cranial vault
Brain 80%
Blood 12%
CSF 8%

MONRO-KELLIE DOCTRINE
If one of these substances increase, then one or
both of the other must therefore decrease to
maintain normal pressure within the cranial vault

 Normal ICP = 5 to 10/15

Upper limits of 20 may be acceptable as long as
CPP is adequate

Cerebral perfusion pressure (CPP) = 60 to 100

The pressure needed to perfuse the brain
Ideal is 70
Calculated by subtracting ICP from MAP

Cerebral Blood Flow

Oxygen and glucose delivery are controlled
by cerebral blood flow
A function of cerebral perfusion pressure (CPP)
and resistance of the cerebral vascular bed
CPP is determined by the mean arterial pressure
(MAP) (the diastolic pressure plus one-third
pulse pressure) minus intracranial pressure

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases
Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs
Results in increased cerebral blood volume
(increasing ICP) and further cerebral
vasodilation

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases
Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs
Results in increased cerebral blood volume
(increasing ICP) and further cerebral
vasodilation

Cerebral Blood Flow

Vascular tone in the normal brain is
regulated by:
Carbon dioxide pressure (PCO2)
Oxygen pressure (PO2)
Autonomic and neurohumoral control

PCO2 has the greatest effect on

intracerebral vascular diameter and
subsequent resistance

Cerebral Blood Flow

As ICP approaches MAP:
Gradient for flow decreases
Cerebral blood flow is restricted

When ICP increases, CPP decreases

As CPP decreases, cerebral vasodilation occurs
Results in increased cerebral blood volume
(increasing ICP) and further cerebral
vasodilation

Cerebral Blood Flow

Vascular tone in the normal brain is
regulated by:
Carbon dioxide pressure (PCO2)
Oxygen pressure (PO2)
Autonomic and neurohumoral control

PCO2 has the greatest effect on

intracerebral vascular diameter and
subsequent resistance

Intracranial Pressure (ICP)

Normal range is 0-15 torr
When ICP rises above this level, the ability
to maintain CPP is compromised
Cerebral blood flow is diminished

The body attempts to compensate for the

decline in CPP by a rise in MAP
Further elevates ICP, and CSF is displaced to
compensate for the expansion

If unresolved, the brain substance herniates

CAUSES OF INCREASED ICP

Defecation
Coughing
Airway obstruction
Vomiting
PEEP
Suctioning
Muscle exertion
ROM
Isometric Exercise
Position changes
Hypercapnia PCO2 >45
Stress
Pain, noxious stimuli
Seizures
Hyperthermia
Hip flexion
Poor neck allignment

SIGNS & SYMPTOMS OF

INCREASED ICP
Early Signs
Change in LOC
Change in pupils
Decreased motor
Worsening headache
Change in speech
Elevation in ICP
monitoring
There may be no change
in vitals

Late Signs
Difficult to arouse
Unequal pupils
Posturing
Change in respiratory
pattern
Abnormal reflexes
Cardiac changes
Loss of cranial nerves
Cushings response

MEDICAL MANAGEMENT
Only 25% to 58% of the causes of increased ICP can be
surgically treated.(Kinney)
For those patients who are treated surgically, or those patients
who have difficulty in their autoregulatory system, the aim
is to reduce the ICP by medical means.

Respiratory support
Blood Pressure Management
Osmotic diuretics
Proper sedation
Drainage of CSF

RESPIRATORY SUPPORT
Cerebral vessels are very sensitive to PaCO2 levels.
As CO2 elevates (hypercapnia, acidemia), cerebral
vessels dilate increasing cerebral blood flow and
increasing ICP.

 Recommendations for proper ventilation

PaCO2 35 to 45
PO2 >60
PH 7.35 to 7.45

Recommendation for hyperventilation

Only to be done for short periods if patient has
signs of herniation.
This is a life saving measure only

BLOOD PRESSURE
MANAGEMENT
Keep blood pressure normotensive to slightly
hypertensive (This is for head trauma, not
aneurysms)
Hypotension causes cerebral ischemia
Hypertension may aggravate cerebral edema and
possibly bleeding
Both will lead to an increase in ICP and thus a
decrease in CPP

 Recommendations for altered BP

Hypotension treat fast treat now
Adequate fluid resuscitation

Hypertension doesnt usually happen with

trauma, but it does with aneurysms

SEDATION
Sedation and paralytics are used to decrease the
patients response to stimuli.
Decreases O2 demand
Decreases metabolic demand
Decreases ICP

Please avoid giving morphine to the brain injured

patient.
Although your patient may not be able to physically
respond to you.they may still be able to hear
and feel you.

Brain Trauma
A brain injury is a traumatic insult to the
brain capable of producing physical,
intellectual, emotional, social, and
vocational change
Categories of brain injury:

Mild diffuse injury

Moderate diffuse injury
Diffuse axonal injury
Focal injury

Edema
Significant brain injuries may result in
swelling of the brain tissue with or without
associated hemorrhage
Swelling results from humoral and
metabolic responses to injury
Leads to a marked increase in intracranial
pressure
May lead to decreased cerebral perfusion or
herniation

Ischemia
Can result from:

Vascular injuries
Secondary vascular spasm
Increased intracranial pressure
Focal or more global infarcts can result

Hemorrhage
Can occur into or around brain tissue
Epidural or subdural hematomas can
compress underlying brain tissue or
intraparenchymal hemorrhage
Often associated with cerebral contusions
and skull fractures

Classification of Skull Fractures

Linear fractures
Basilar fractures
Depressed fractures
Open vault fractures

Skull Fractures - Complications

Cranial nerve injury
Vascular involvement
Meningeal artery
Dural sinuses

Infection
Underlying brain injury
Dural defects caused by depressed bone
fragments

Linear Fractures
80% of all skull fractures
Are not usually depressed
Often occur without an overlying scalp
laceration
Generally have a low complication rate (as
an isolated injury)

Linear Skull Fracture.

Depressed Skull Fractures

Usually result from a relatively small object
striking the head at high speed
Commonly associated with scalp lacerations

Frontal and parietal bones most often

affected

Depressed Skull Fracture.

Open-Vault Fractures
Result when there is direct communication
between a scalp laceration and cerebral
substance
Often associated with multisystem trauma and a
high mortality rate
May lead to infection (meningitis)

Prehospital management

Open Vault Fracture.

BASILAR SKULL FRACTURE

Base of the skull
has irregular, sharp
bony prominences.
With a direct blow,
strains occur
Compression
Shearing
Tension

 Basilar fractures occur at the base of the

skull. They are very difficult to detect even
with the use of x-rays.
May be viewed best by CT with bone
windows
Diagnosis and treatment are based on
patients clinical presentation.

ANTERIOR BASILAR SKULL

FRACTURE
Presentation
Raccoon eyes
Rhinorrhea
Anosmia (damage to
CN I, olfactory)
Visual changes
(damage to CN II,
optic)
Telecanthus

MIDDLE & POSTERIOR

SKULL FRACTURES
Presentation
Otorrhea
Battles sign
Facial nerve palsy
(damage to CN
VII)
Hearing loss
(damage to CN
VIII)

Battle sign

Otorrhea

MONITOR

ABCs
LOC
Temp infection (meningitis)
Pain
Altered taste
Altered smell
Altered hearing
Bruising may not develop for a few hours
Drainage from nose or ears
Signs and symptoms of increased ICP

 Halo sign
Tests for CSF leak
Place gauze near the
area of drainage.
Allow drainage to
absorb into the pad.
A yellow ring that
appears around the
bloody drainage
would represent
CSF.

TREATMENT OF BASILAR
SKULL FRACTURES

Observe
Treat clinical presentation
Keep HOB up
Use mustache dressing to absorb drainage
Antibiotics
Avoid
Coughing, sneezing, blowing nose

Do not use nasal cannula

Do not use nasal gastric tube
Do not suction nasotracheally
Do not intubate nasotracheally

CEREBRAL CONTUSIONS
Bruising of the brain tissue that results from rapid
acceleration-deceleration movement causing
shearing of small vessels. Brain edema and mass
effect can occur
Coup injury-occurs directly below sit of impact
Countercoup injury-occurs on opposite side of
initial injury

CT with multiple cerebral

contusions

Cerebral Contusion
Bruising of the brain around the cortex or
deeper within the frontal (most common),
temporal, or occipital lobes
Produces a structural change in the brain tissue
Results in greater neurological deficits and
abnormalities than are seen with concussion

Signs and symptoms

Management

Cerebral contusions can be life threatening. If severe,

diffuse cerebral edema (secondary injury) causes
elevations in ICP.

EPIDURAL HEMATOMAS
Bleeding into the
potential space,
between dura and
skull
Usually associated
with temporal bone
fracture, resulting in
laceration of the
meningeal artery.

Because epidural
hematomas are
usually caused by
an arterial bleed
which expand
quickly, your
patient may require
emergency surgery.

SIGNS & SYMPTOMS OF

EPIDURAL HEMATOMAS
Characteristics
Brief loss of consciousness, followed by lucid
interval
Headache, increasing in severity
Vomiting, due to increased ICP
Seizure
Contralateral hemiparesis, check pronator drift
Ipsilateral pupil dilation (pressure of CN III)

SUBDURAL HEMATOMAS
Bleeding between the
dura and arachnoid
mater.
Vast majority are caused
by tearing of the bridging
veins exp: CoupContrecoup
Most common traumatic
mass lesion
Three classifications
Acute 48hrs
Subacute 2-14days
Chronic - >14days

 ACUTE Subdural Hematoma

Clinical presentation occurs
within 48-72 hrs
Gradual decrease LOC to coma
Hemiparesis
Hemiplegia
s/s are associated with rapid
expanding lesion causing
increased ICP and brainstem
compression

 SUBACUTE Subdural
Hematoma
Clinical presentations
occur within 2 days to 2
weeks
Associated with moderate
injury
Bleeding is slower
producing a steady decline
in LOC
Subacute subdural hematoma with
Sedimentation line

 CHRONIC Subdural
Hematoma
Result from low-impact
injuries-falls
Symptoms occur 2 weeks to
several months after injury
s/s are vague, but progressive
Headache
Confusion
Seizures
hemiparesis
High incidence in elderly and
ETOH abuse

 Diagnosis and Treatment

of Subdural Hematoma
Ct scan shows hypodensity
as the injury gets older
Small SDH may be treated
medically because they
frequently reabsorb
Large SDH require surgical
evacuation-craniotomy
Burr holes

INTRACEREBRAL
HEMATOMA
Bleeding develops within the
brain parenchyma
*Deep contusion
*ruptured blood vessel
May develop with other serious
injuries
Contusions, lacerations
Penetrating injuries
Depressed skull fractures

 S/S of a intracerebral hematoma will

depend on the location and extent of injury

SIGNS & SYMPTOMS OF ICH

Clinical presentation will depend on the location.
They will resemble s/s of stroke

Headache
Decreased LOC to coma
Contralateral hemiplegia
Ipsilateral dilated pupil
Speech deficits

 Treatment for ICH

Surgical repair of depressed fracture
Removal of clot if possible

SUBARACHNOID &
INTRAVENTRICULAR
HEMORRHAGE
Arterial blood in the
subarachnoid and
intraventricular space
Trauma
Aneurysm
Arterial venous
malformation (AVM)
Traumatic subarachnoid

SIGNS & SYMPTOMS

Sudden

severe headache

Decreased
EKG
s/s

LOC or comatose

Aneurysm

changes

of meningeal irritation

Nuchal rigidity
Photophobia
Blurred vision
N/V
Fever
Backache
Non-traumatic subarachnoid hemorrhage

 TREATMENT FOR SAH & IVH

Determine cause of injury
CT Angiography

Once cause is determined then

treatment can be determined

Emergent ICP
Possible surgery
Intensive medical management
Intensive clinical monitoring

Mild Diffuse Injury (Concussion)

A fully reversible brain injury that does not
result in structural damage to the brain
Causes
Signs and symptoms
Management

Moderate Diffuse Injury

Moderate injuries are those that result in
minute petechial bruising of brain tissue
Involvement of the brainstem and reticular
activating system lead to unconsciousness

Signs and symptoms

Management

Diffuse Axonal Injury (DAI)

Severest form of brain injury
Results from brain movement within the skull
secondary to acceleration or deceleration forces

DAI may be classified as mild, moderate, or

severe

Diffuse Axonal Injury

Mild DAI
Associated with coma of 6 to 24 hours

Moderate DAI
More common
Distinguished by coma lasting more than 24
hours and abnormal posturing

SEVERE DAI
Severe DAI (formerly known as brainstem
injury)
Involves severe mechanical shearing of many
axons in both cerebral hemispheres extending
to the brainstem

Focal Injury
Focal injuries are specific, grossly
observable brain lesions
Included in this category are lesions that
result from:

Skull fracture
Contusion
Edema with associated increased ICP
Ischemia
Hemorrhage

IMPALEMENT &
PENETRATING INJURIES
Bullets or other projectiles destroy brain
tissue along their path injuries to multiple
brain structures and vessels can occur.

 Treatment of projectile injuries

May require emergent surgery
Intense medical management
Intense clinical monitoring

 Treatment for impaled objects

DO NOT remove object

Determine injury
Surgery
Intense medical management
Intense clinical monitoring

Most common
complication of
penetrating injuries is
infection
Prophylactic
antibiotics

With any injury to the brain look for signs and

symptoms of increased intracranial
pressure.
Treatment will depend on the type of injury.
The goal being to decrease intracranial
pressure and decrease secondary injury,
through surgical techniques, or medical
treatments.

NEURO ASSESSEMENT
BASELINE ASSESSMENT IS OF GREAT
IMPORTANCE TO DETERMINE THE
HISTORY OF THE PRESENT ILLNESS
AND TO ACT AS A GUIDE FOR
FURTHER SERIAL ASSESSMENTS

LEVEL OF CONSCIOUSNESS
Glasgow coma score
Under 8, patient is considered
comatose/AIRWAY
Reasons for coma
A=ALCOHOL
E=EPILEPSY
I=INSULIN
O=OPIATES
U=URATES

T=TRAUMA
I=INFECTION
P=POISON
P=PSYCH
S=SHOCK

 Best eye opening

Degree of stimulus required to awaken the
patinet
Verbal
Tactile
Deep stimulus/Painful

Best verbal response

Assessment of the eloquent brain (speech
center)

Best motor response

Assess how a patient interprets information and
reacts to it

PUPIL RESPONSE
Size

Shape

Small
Pinpoint
Large
Dilated
Unequal

Round
Keyhole
Irregular
Ovoid

Reaction to light
Direct light reflex
Consensual light reaction
Brisk, fixed, Hippus,
sluggish, Anisocoria

VITAL SIGNS
The blood pressure and heart rate are assessed
to determine if adequate cerebral tissue
perfusion requirements are being meet.
Keep MAP ~ 80
Keep in mind that the ICP will be subtracted
from the MAP to obtain the Cerebral
Perfusion Pressure (CPP)

 Cushings Triad
Late sign of increased ICP

Increase in SBP
Widened pulse pressure
Bradycardia
Irregular respirations

What does this mean

IMPENDING HERNIATION

TEMPERATURE
Keep the patient Normothermic to mildly
hypothermic
As temperature rises the
need for increased oxygen
requirements and metabolic
demands double--bad news
for a head trauma

RESPIRATIONS
Cheyne-Stoke
Earliest and most
common alteration
in respiratory
pattern
Result of
hemispheric
compression

 Posturing
Indicates interruption of corticospinal pathways
at the internal capsule, midbrain or upper pons.

Decortication>>>Decerebration>>>Flaccidity
DECORTICATION

DECEREBRATION

Assessment and Evaluation

Prehospital management of the head-injured
patient is determined by:
Mechanism and severity of injury
Patient's level of consciousness
Associated injuries

Airway and ventilation

Circulation
Neurological examination
Fluid therapy

Code 16

Page 2 of 2

ROUTINE TRAUMA CARE

SECONDARY PATIENT ASSESSMENT

1.
2.
3.
4.
5.
6.
7.

Vital Signs
GCS scoring parameters
Systematic head to toe assessment
Medications
Allergies
Reassure patient, provide comfort and loosen tight clothing
Evaluate cardiac rhythm, if indicated. (All ALS patients do not necessarily require continuous ECG
monitoring or transmission of a strip to the hospital.)
8. Contact hospital as soon as patients condition permits. Transmit assessment information and await
orders. If no radio contact can be established or patients condition requires immediate treatment,
refer to appropriate SMO and begin intervention immediately.
9. Recheck vitals and other pertinent signs at least every 15 minutes and record, noting times.
If unstable vital signs/sustained hypotension (SBP <90 on two separate readings 5 minutes apart),
vital signs should be taken and recorded every 5 minutes.
10. All patients, who, in the judgment of prehospital personnel, would benefit from care derived from a
Trauma Center, should be transported accordingly (Refer to FIELD TRIAGE PROTOCOLS CODE 14).
If unable to ventilate, transport to nearest hospital.

NOTE TO PREHOSPITAL PROVIDERS:

In a combative or uncooperative patient, the requirement to initiate initial routine trauma care, as
written, may be altered or waived in favor of rapidly transporting the patient for definitive care. Document
the patients actions or behaviors which interfered with the performance of any assessments and/or
interventions.

OUTLINE FOR RADIO REPORT (Transmit using as few words as possible)

1. Name and vehicle number of provider
2. Requested destination, closest hospital,
and estimated time of arrival
3. Age, sex, and approximate weight of patient
4. Chief Complaint, to include symptoms
and degree of distress
5. History of present illness/injury

6. Pertinent Medical History:

- Allergies
-Medications
-Past History of Current Illness
-Last Meal
-Events surrounding incident
7. Clinical condition:
-Focused and detailed patient assessment findings
8. Treatment initiated and Response

Code 18
SUSPECTED SPINAL CORD INJURY
SPINAL IMMOBILIZATION
Mechanism:
Suspected Deceleration Injuries,
Motor Vehicle Crashes, Falls, etc.

Yes

Spine pain/tenderness or
complaint of neck/spine pain
No

Yes

Physical findings suggesting neck and/or back injury

No
Other painful injury identified
(Distracting Injury)

Yes

No
Yes

Decreased or altered level of consciousness

No

Abnormal?

Motor/Sensory Exam
Patient is
Calm
Cooperative
Alert
Ambulatory without pain
No apparent distress
No suspected intoxication

Having an acute stress reaction

Suspected of being intoxicated
Have symptoms of brain injury
Acting inappropriately
Having difficulty communicating,
such as, speaks a foreign language, deaf, etc.

Reliable patient exam

Reviewed
Reviewed
Reviewed
Effective
ALS

05/01/08
06/01/06
05/01/04
05/01/98

NO IMMOBILIZATION NEEDED

IMMOBILIZE

Code 19
HEAD TRAUMA/UNCONSCIOUS PATIENT
100% OXYGEN
Assist ventilations as needed
Vomiting precautions
Immobilize C-spine
Routine Trauma Care
Yes

ALERT?

No

UNRESPONSIVE TO
VOICE AND PAIN

TRANSPORT
Pupil(s) dilated
Signs of increased
intracranial pressure
and/or
Glasgow Coma Score
8 or less

NOTE TO PREHOSPITAL PROVIDERS:

1. Do not delay transport time with multiple intubation attempts.
2. If unequal or fixed pupils and/or posturing, ventilate at 20
breaths/min.

Sedate -Refer to
MEDICATION ASSISTED
INTUBATION CODE 75a,
if indicated
ET intubation with in-line
manual stabilization
ACCELERATED TRANSPORT

Revised 05/01/08
Reviewed 06/01/06
Revised 05/01/04
Effective 05/01/98
ALS