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Chapter 11:

Neurologic Emergencies
Introduction (1 of 2)

• When transporting a critical care patient with

neurologic complications, the critical care
transport professional (CCTP) faces:
– Challenges in:
• Assessment
• Management
Introduction (2 of 2)

• For the best possible outcome, the CCTP

needs an understanding of
– Underlying principles of neurologic structure,
function, dysfunction
– Various types of neurologic injuries, their
pathophysiology, and current management
Anatomy and Physiology of the
Nervous System (1 of 3)
• Most diverse and highly organized system
in the human body.
• Components are classified by location and
• Central nervous system (CNS): Brain and
spinal cord
• Peripheral nervous system (PNS): Spinal
and cranial nerves
Anatomy and Physiology of the
Nervous System (2 of 3)
• The PNS is also differentiated based on
the information that is transmitted on
certain pathways.
– Afferent pathways (ascending pathways) carry
sensory impulses toward the CNS.
– Efferent pathways (descending pathways)
carry impulses away from the CNS to effector
organs, including muscles or glands.
Anatomy and Physiology of the
Nervous System (3 of 3)
• The nervous system consists of voluntary
and involuntary divisions.
– The voluntary (somatic) nervous system is
composed of nervous system fibers that
connect the structures of the CNS with
skeletal muscles and the integument.
– The involuntary (autonomic) nervous system is
divided into the sympathetic and
parasympathetic branches.
Organization of the Nervous

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Cranial Anatomy and Physiology (1 of 2)

• The skull, or cranium, consists of the

– Neurocranium: brain box
– Viscerocranium: 14 bones that make up the
facial skeleton
• The neurocranium is the part of the skull
that encloses and protects the brain.
• Foramina are found at the base of the
Cranial Anatomy and Physiology (2 of 2)

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Meningeal Anatomy and
• The CNS is enclosed by a set of three
membranes known as the meninges.
• The cranial meninges protect the brain
and support the arteries, veins, and
venous sinuses.
• Meninges are composed of three layers
– Dura mater
– Arachnoid mater
– Pia mater
Dura Mater

• Adherent to the internal surface of the

• A two-layered membrane
– Outer layer comprises the periosteum for the
cranial bones
– Inner layer extends into the cranial space
• Four extensions of the dura mater are falx
cerebri, tentorium cerebelli, falx cerebilli,
and diapragma sellae
Arachnoid Mater

• Extremely thin and delicate layer that

loosely encloses the brain
• Closely applied to the meningeal layer of
the dura mater by the pressure of the
circulating cerebrospinal fluid (CSF)
Pia Mater

• Vascular membrane that adheres to the

surface of the brain and follows its
• Rich in small blood vessels that supply a
large volume of arterial blood to cerebral
Ventricular System and CSF (1 of 4)

• The ventricular system is filled with CSF,

which nourishes the brain and spinal cord.
• There are two lateral ventricles and
midline third and fourth ventricles
connected by the cerebral aqueduct.
Ventricular System and CSF (2 of 4)

• One lateral ventricle lies in each of the

cerebral hemispheres.
– The lateral ventricles are important structures
for intracranial pressure (ICP) monitoring, CSF
drainage, or placement of a CSF shunt.
Ventricular System and CSF (3 of 4)

• The foramen of Monro connects the two

lateral ventricles with the third ventricle.
• The cerebral aqueduct provides
communication with the fourth ventricle,
which lies between the brain stem and the
Ventricular System and CSF (4 of 4)

• Two openings at the base of the fourth

ventricle open the ventricular system into
the subarachnoid space and are essential
for the normal flow of CSF.
– Foramen of Luschka
– Foramen of Magendie

• Largest part of the brain.

• Two cerebral hemispheres are separated
by the cerebral fissure.
– Hemispheres are connected at the base of the
cerebral fissure by the corpus callosum.
– Hemispheres are separated from the brain
stem and cerebellum by the transverse
cerebral fissure.
Cerebral Cortex

• Outermost layer of the cerebrum.

• 2-5 mm thick.
• Contains billions of dendrites and neurons
called gray matter.
• Underneath the cerebral cortex are the
white matter tracts, which communicate
impulses from the cerebral cortex to other
areas of the brain.
Lobes of the Cerebrum

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Frontal Lobe

• Accounts for one third of the total

cortical tissue
• Provides control of:
– Thought
– Concentration
– Depth perception
– The ability to think abstractly
– Memory
– Autonomic nervous system response
Parietal Lobe

• Directly posterior to the frontal lobe lateral

to the central fissure
• Responsible for sensory functions,
– The integration of sensory information
– Awareness of body parts
– Interpretation of touch, pressure, and pain
– Recognition of object size, shape, and texture
Occipital Lobe

• This is the primary receptor area for vision.

Temporal Lobe

• Lies in the lateral portion of the cerebrum.

• Primary functions of this region relate to
hearing, speech, behavior, and memory.
• In the temporal lobe, the primary auditory
receptive areas receive sound impulses.
• Wernicke area: Comprehension of written
and spoken words
Limbic Lobe (Rhinencephalon)

• Borders the lateral ventricles.

• Contains the hippocampus, the uncus, the
primary olfactory cortex, and the amygdaloid
• Functions include:
– Self-preservation
– Primitive behavior
– Moods and emotion
– Short-term memory and smell
Diencephalon (1 of 4)

• Major division of the cerebrum

• Divided into four regions:
– Thalamus
– Hypothalamus
– Subthalamus
– Epithalamus
Diencephalon (2 of 4)

• Thalamus
– Acts as a relay station for motor and sensory
• Hypothalamus
– Forms the floor and anterior walls of the third
– Pituitary gland
– Several functions related to regulating and
maintaining homeostasis
Diencephalon (3 of 4)

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Diencephalon (4 of 4)

• Subthalamus
– Located below the thalamus
– Closely related to the basal ganglia in function
• Epithalamus
– Contains the pineal gland, which is thought to
play a role in physical growth and sexual
Basal Ganglia

• Several masses of nuclei located deep in

the cerebral hemispheres
• Main role is associated with fine motor
function, especially in the hands and lower
• Internal capsule is a bundle of efferent and
afferent fibers connecting subdivisions of
the brain and spinal cord

• Acts as a bridge between the cerebral

hemispheres and the spinal cord
• Consists of
– Midbrain
– Pons
– Medulla oblongata
Midbrain (1 of 2)

• Important structures include:

– The cerebral aqueduct
– The superior colliculi, inferior colliculi, and
cranial nerves III (oculomotor) and IV
– The reticular activating system
• Major function is to relay stimuli involved in
voluntary motor movement of the body
Midbrain (2 of 2)

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• Relays information to and from the brain

and spinal cord along fiber tracts
• The apneustic center is responsible for
stimulating and producing sustained
• The pneumotaxic center antagonizes the
apneustic center, inhibiting inspiration.
Medulla Oblongata

• Connects with the spinal cord at the

foramen magnum
• Also contains groups of neurons that
control involuntary functions such as:
– Swallowing
– Vomiting
– Coughing
– Vasoconstriction
– Respiration
Cerebellum (1 of 2)

• Located just superior and posterior to the

medulla oblongata
• Primary function is coordination of voluntary
• Parts include:
– Cortex, or the gray outer covering
– White matter
– Four pairs of deep cerebellar nuclei
Cerebellum (2 of 2)

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Reticular Formation

• Set of neurons that extends from the upper

level of the spinal cord through the
medulla, pons, and midbrain, and into the
thalamus and cerebral cortex
Reticular Activating System

• Diffuse system that extends from the lower

brain stem to the cerebral cortex
• Lower portion assists with control of the
sleep-wakefulness cycles and
• Upper portion allows the ability to focus
attention on a specific task
Cerebral Circulation

• The brain demands 15%-20% of total

cardiac output and 40% of the oxygen in
the available blood.
• The brain is supplied blood by two pairs of
arteries: the two vertebral arteries and the
two internal carotid arteries.
Circle of Willis
• A collection of
arteries located at the
base of the skull that
is divided into
anterior and posterior
• Fed by the internal
carotid and basilar
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Major Cerebral Arteries

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Vertebral Arteries

• Arise from the subclavian arteries and

enter the skull through the foramen
• At the pons, the two vertebral arteries join
to form the basilar artery.
– The basilar artery divides at the level of the
midbrain to form paired posterior cerebral
Internal Carotid Arteries

• Originate from the common carotid arteries

and enter the cranium through the base of
the skull.
• At the base of the brain, they connect to
the circle of Willis and then branch into the
anterior and middle cerebral arteries.
Venous Drainage (1 of 2)

• The veins of the brain enter the dural

venous sinuses, which then drain into the
internal jugular veins.
– Cerebral veins on the superolateral surfaces
of the brain drain into the superior sagittal
– Cerebral veins on the posteroinferior aspect
drain into the straight, transverse, and superior
petrosal sinuses.
Venous Drainage (2 of 2)

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Blood-Brain Barrier

• Network of endothelial cells and astrocytes

that envelop cerebral capillaries.
• The barrier regulates the transport of
nutrients, ions, water, drugs, and waste
products through the process of selective
The Spine (1 of 2)

• Usually consists of 33 irregular bones

• The vertebrae are stabilized by both
ligaments and muscles.
• Vertebrae are identified according to their
location as cervical, thoracic, lumbar,
sacral, or coccyx.
The Spine (2 of 2)

• The vertebral body, the anterior weight-

bearing structure, is made of bone that
provides support and stability.
• Components of the vertebra include:
– Lamina process
– Pedicles process
– Spinous process
The Human Vertebra

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The Spinal Cord (1 of 3)

• Originates at the base of the brain and is

the continuation of the CNS.
• This bundle of nerve fibers leaves the skull
through an opening at its base called the
foramen magnum.
• Thirty-one pairs of spinal nerves arise from
the different segments of the spinal cord.
The Spinal Cord (2 of 3)

• A cross-section of the spinal cord reveals

a butterfly-shaped central core of gray
matter that is composed of neural cell
bodies and synapses.
– This gray matter is divided into posterior
(dorsal) horns, which carry sensory input, and
anterior (ventral) horns, which innervate the
motor nerve of that segment.
The Spinal Cord (3 of 3)

• Surrounding the gray matter on each side

are three columns of peripheral white
matter composed of myelinated ascending
and descending fiber pathways.
The Spinal Cord and Its Layers

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Spinal Nerves

• The 31 pairs of spinal nerves are named

for the vertebral region and level from
which they arise.
• Nerve roots occasionally converge in a
cluster called a plexus that permits
peripheral nerve roots to rejoin and
function as a group.
Sympathetic Nervous System (1 of 3)

• Controlled by the brain’s hypothalamus.

• Information from the brain is transmitted
through the brainstem and the cervical
spinal cord, then exits at the spine to reach
the target structures.
Sympathetic Nervous System (2 of 3)

• Thoracolumbar system provides

sympathetic stimulation to the periphery
through alpha and beta receptors.
• Alpha receptor stimulation induces smooth
muscle contraction in blood vessels and
Sympathetic Nervous System (3 of 3)

• Beta receptors respond with relaxation of

smooth muscles in blood vessels and
bronchioles, and have chronotropic and
inotropic effects on myocardial cells.
• Stimulation of sympathetic nerves without
parasympathetic input can cause
sympathetic overdrive, resulting in
autonomic dysreflexia.
Parasympathetic Nervous
• Includes fibers arising from the brain stem
and upper spinal cord that carry signals to
organs of the abdomen, heart, lungs, and
the skin above the waist.
• Disruption of the lower parasympathetic
nerves in the sacrum results in the loss of
bowel/bladder tone and sexual function.
Axonal Transport (1 of 2)

• The intracellular transport of protein and

organelle materials is essential for all
mammalian cells, especially the neuron.
• Cellular components go through a
microtubule-based transport system
composed of
– Molecular motors
– Microtubules
Axonal Transport (2 of 2)

• The type of molecular motor present

determines the direction of transport—
toward the synapse or toward the cell
• When the transport becomes disrupted,
disease can result.
– Alzheimer and related diseases, AML
Neurologic Tests (1 of 2)

• Critical patients present a variety of

examination and management challenges
during care and transport.
• Examination of the patient is the essential
starting point of the entire patient
management process.
Neurologic Tests (2 of 2)

• Some specific neurologic tests may or may

not be done in the critical care transport
– Many of these tests will have been done as
part of the initial assessment at the hospital.
– The CCTP performs evaluations as needed.
Physical Examination (1 of 4)

• Mental and emotional status

• Specific areas tested include:
– Level of consciousness
– General behavior
– Thought process, including memory, attention
and concentration, abstract thought, and
• Level of consciousness should be
performed on all patients.
Physical Examination (2 of 4)

• Awareness and arousal: Fundamental

constituents of consciousness and should
be evaluated/documented repeatedly
– Evaluation of arousal: Essentially an
assessment of the patient’s reticular activating
system and its connection with the thalamus
and cerebral cortex
Physical Examination (3 of 4)

• Arousal focuses on the patient’s ability to

respond to a variety of stimuli, and may be
described using the AVPU (awake, verbal,
painful, unresponsive) scale.
– The Glasgow Coma Scale (GCS) documents
and trends a patient’s level of arousal through
eye opening, verbalization, and movement.
AVPU Scale

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Physical Examination (4 of 4)

• The three aspects of awareness (awake,

alert, and oriented) disappear in the order
of time, place, and then person (self).
• The Mini-Mental Examination was
developed to provide a simple, easily
applied test of higher cognitive functions.
Levels of Arousal

Data from McCance K, Huether S. Pathophysiology: The Biological Basis

for Disease in Adults and Children. St. Louis, MO: Mosby; 2002.
Questions Pertaining to
Patient Orientation

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Mini-Mental Examination

Data from Fuller G. Neurological Examination Made Easy. Edinburgh, UK: Churchill Livingstone; 1999.
Speech Function

• Abnormalities of speech can

– Interfere with ability to accurately assess
higher-level functions
– Reflect dysfunction in any component or
process of communication
• The term aphasia encompasses any loss
or impairment of language function as a
result of brain damage.
Abnormalities of Speech

Data from Fuller G. Neurological Examination Made Easy.

Edinburgh, UK: Churchill Livingstone; 1999.
Assessment of Cranial Nerves (1 of 5)

• Tests require patient participation

• Olfactory nerve
– Should be assessed in patients in whom
head trauma has occurred
– Familiar odors should be used
Assessment of Cranial Nerves (2 of 5)

• Optic nerve
– Arises from cells in the retina and passes
into the orbit.
– Each eye should be evaluated individually.
• Ocular, trochlear, trigeminal, and
abducens nerves
– Usually examined as a group
– Position of the eyeball and position of the
Assessment of Cranial Nerves (3 of 5)

• Facial nerve
– Complex nerve with motor, sensory, and
parasympathetic fibers
– Instruct the patient to wrinkle the forehead,
close the eyelids, smile, and whistle.
• Vestibulocochlear nerve
– Cochlear (hearing), vestibular (balance)
– Patients complain of vertigo, nausea and
vomiting, and difficulty with balance.
Assessment of Cranial Nerves (4 of 5)

• Glossopharyngeal and vagus nerves

– Usually tested together.
– Supplies sensory components to the pharynx,
tonsils, soft palate, and posterior third of the
– Direct the patient to open his or her mouth and
say “Ah.”
Assessment of Cranial Nerves (5 of 5)

• Spinal accessory nerve

– Tested in two segments
– Trapezius muscle is palpated
– Patient turns his head to one side and pushes
his chin against the examiner’s hand
• Hypoglossal nerve
– Observe the tongue for fasciculations, atrophy,
strength, and tongue protrusion.
Assessment of Motor Function

• The muscles should be palpated through

the normal range of motion.
• Abnormalities include:
– Spasticity or undue resistance of the muscles
– Rigidity or a more constant state of resistance
– Flaccidity or a decreased muscle tone
Assessment of Sensory
• Tests the patient’s ability to perceive
various types of sensations with the eyes
• Sensory examination assesses the
receptors and the tracts of conduction.
• CCTP should examine and document
pain, temperature, and touch.
Reflex Testing

• Examination of deep tendon reflexes gives

information about the integrity of the spinal
nerves and may indicate brainstem or
spinal cord lesions.
• Tendon reflexes are increased in upper
motor neuron lesions and decreased in
lower motor neuron lesions.
Pathologic Reflexes

• Plantar response
• Babinski sign
• Oppenheim sign
• Gordon sign
• Hoffman sign
• Grasp reflex
• Superficial reflexes
Grasp Reflex

• The CCTP places his or her fingers on the

patient’s palm and pulls the hand away,
asking the patient to let go of the hand.
– A normal response is present if the patient can
let go.
– An abnormal response consists of the
involuntary flexion of the fingers.
Superficial Reflexes

• Can be performed in men as the inner

aspect of the upper thigh is stroked
downward and movement of the testicle in
the scrotum is observed.
• In transport, this test may be done on
neonatal or pediatric patients, but not on
Evaluation of Meningeal
• May result from infections caused by
bacteria, viruses, fungi, parasites, or toxins
• The causative agent acts as an irritant,
causing an inflammatory reaction around
the meninges in the arachnoid space, the
CSF, and the ventricles.
Lhermitte Phenomenon

• Forward flexion of the neck produces an

electric shock feeling, usually down the
• Presence of this sensation indicates
cervical pathology.
Vital Signs (1 of 4)

• The CCTP should obtain vital signs.

• Centers for control of vital functions are
found within the brainstem.
• Any changes provide valuable information
regarding the patient’s overall status.
• Changes include breathing or cardiac
Vital Signs (2 of 4)

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Vital Signs (3 of 4)

• Blood pressure
– Hypertension is the effect on blood pressure
most often seen because of neurologic injury,
especially in case of rising ICP.
• Cushing triad
– Widening of pulse pressure is evident in cases
of increasing ICP.
Vital Signs (4 of 4)

• Body temperature
– Alterations in body temperature possible in
neurologic injury, especially if hypothalamus is
– Neurogenic fever may occur in as many as
one third of all patients with severe traumatic
brain injury (TBI).
Neurologic Diagnostics (1 of 3)

• Computed tomography
– Provides a mathematically reconstructed
cross-sectional view of the body, including the
• Magnetic resonance imaging
– Produces images with greater detail than a
computed tomography (CT).
Neurologic Diagnostics (2 of 3)

• Cerebral angiography
– Allows visualization of the lumen of vessels
– Provides information about patency, size,
irregularities, or occlusion
• Transcranial Doppler ultrasound
– Allows monitoring of cerebral blood flow (CBF)
velocity through thinner areas of the skull
Neurologic Diagnostics (3 of 3)

• Electroencephalography
– Involves the recording of electrical impulses
generated by the brain to localize abnormal
electrical activity
– Types of waves: delta, theta, alpha, beta,
• Lumbar puncture
– Enters the subarachnoid space in the lumbar
region of the vertebral column
Laboratory Assessment

• Laboratory studies have typically not been

used in diagnosis and management of
neurologic emergencies.
• Obtain a complete blood count, basic
chemistry panel, coagulation study, and
cardiac biomarkers.
Primary Brain Injury (1 of 3)

• Can occur because of contact phenomena

and acceleration-deceleration injuries.
• Contact phenomena occur as the direct
result of trauma to the head.
• Sudden changes in velocity cause the
brain to move, resulting in damage.
Primary Brain Injury (2 of 3)

• Areas of the brain associated with rough

portions of the skull (frontal and temporal
lobes) have higher incidences of injury.
• Contrecoup injury happens when an
impact occurs on one side of the head,
causing the brain to move and hit the
opposite side of the skull.
Primary Brain Injury (3 of 3)

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Secondary Brain Injury

• Involves the more delayed mechanisms.

• After brain injury, normal protective
mechanisms fail, causing falling perfusion
pressure and other problems.
• Neuronal swelling, edema, and cerebral
hyperemia from carbon dioxide retention
combine to raise the ICP.
Scalp Injuries (1 of 2)

• Include abrasions, contusions, lacerations,

and avulsions
– Abrasions involve the top layer of the scalp,
which may be rubbed away.
– Contusions are scalp bruises with possible
accumulation of blood in the subcutaneous
Scalp Injuries (2 of 2)

• Include abrasions, contusions, lacerations,

and avulsions
– Lacerations involve the tearing of the scalp,
and a jagged opening that may extend down
to the skull.
– Avulsions occur as a result of forceful, partial,
or complete tearing away or separation of the
scalp tissue, which appears as a flap.
Skull Fractures

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Linear Skull Fractures (1 of 2)

• Characterized by a single fracture line

• Often an incidental finding on CT
• Occurs when two or more bones of the
skull separate at the suture line
Linear Skull Fractures (2 of 2)

• A linear stellate fracture is a fracture with

multiple linear fractures radiating from the
site of impact.
• Diastatic stellate fractures are described
as separation of an epiphysis relating to a
center site of impact.
Depressed Skull Fractures (1 of 2)

• Occurs when a portion of the skull is

depressed, and the scalp and/or dura
may or may not be torn
• May have soft-tissue swelling over the
site of the trauma and a bony step-off
may be felt
• May be classified as open or closed
Depressed Skull Fractures (2 of 2)

• Types of depressed skull fractures

– The true fracture is the most common, having
contact with the cranial vault.
– The flat fracture features a depressed
segment without any connection with the
cranial vault and is the least common type.
– The ping-pong ball fracture is a pediatric
greenstick fracture of the skull.
Comminuted Skull Fracture

• Fracture that occurs when the skull is

splintered or shattered into many pieces
Basilar Skull Fractures

• Involve fractures along the base of the

• Usually result from a blow to the parietal,
temporal, or occipital regions of the skull
– The temporal area is the most commonly
Facial Fractures

• As many as 60% of patients with

significant facial injuries sustain trauma to
other organ systems, including the brain.
• Usually very painful.
• Airway control is the first assessment
priority with facial injuries.
• Maxillary fractures are classified using the
Le Fort criteria.
Focal Injuries (1 of 4)

• A cerebral contusion is a bruising of the

brain tissue.
– Contusions commonly occur with rapid
deceleration injuries.
– Contusions appearing on the same side of the
impact are coup injuries; injuries on the side
opposite the impact are known as contrecoup
Focal Injuries (2 of 4)

• Lacerations that result in penetration of the

cranium may cause tearing of the cortical
surface of the brain.
• An epidural hematoma is an injury that
causes the accumulation of blood between
the inner periosteum and the dura mater.
Focal Injuries (3 of 4)

• Brain stem herniation is a primary concern

and occurs when the expanding blood
pushes the brain down the foramen
magnum, causing a shearing-type force on
the brain.
• A subdural hematoma can result from
disruption and bleeding of the bridging
veins over the crest of the brain.
Focal Injuries (4 of 4)

• Other types of brain hemorrhages

– Intracerebral hemorrhages
– Delayed traumatic intracranial hemorrhage
– Subarachnoid hemorrhage (SAH)
Diffuse Injuries (1 of 4)

• Concussion, also known as mild TBI

– Traumatically induced physiologic disruption of
brain function that occurs without structural
Diffuse Injuries (2 of 4)

• Signs and symptoms

– Any loss of consciousness
– Any loss of memory for events immediately
before or immediately after the event that
precipitated the injury
– Any alteration in mental status at the time of
the injury (eg, feeling dazed, disoriented)
Diffuse Injuries (3 of 4)

• Signs and symptoms (continued)

– Focal neurologic deficits in which the patient is
not unconscious for longer than 30 minutes.
– After 30 minutes, the patient has a GCS score
of 13-15.
Diffuse Injuries (4 of 4)

• A diffuse axonal injury (DAI) is a TBI that

occurs over a deep area of the brain.
• The mechanism for DAI is usually very
rapid acceleration-deceleration forces.
• DAI accounts for about 50% of all primary
brain injuries and 35% of TBI-related
Physiology of ICP (1 of 2)

• The normal adult ICP is 0-15 mm Hg.

• After circulating, CSF is absorbed at a rate
equal to the rate at which it is produced.
• Obstruction to venous outflow leads to an
increase in the volume of intracranial
blood, resulting in increased ICP.
Physiology of ICP (2 of 2)

• As the ICP increases, the cerebral venous

pressure also increases so that it remains
2-5 mm higher than the ICP. This prevents
collapse of the venous system.
• Increased ICP can result from changes in
CSF, edema, expansible masses, and
changes in vessel size.
Cerebral Blood Flow (1 of 2)

• The brain’s blood flow represents 15% of

resting cardiac output.
• The brain uses 1,000 L of blood every 24
• The CBF remains constant between 60 and
150 mm Hg.
Cerebral Blood Flow (2 of 2)

• For the CCTP, the following points are

– Increases in CBF as a result of hypoxia or
hypercapnia will cause an increase in ICP
once normal compensating mechanisms are
– Poor airway and ventilator control contributes
to hypoxia, hypercapnia, and hypotension
Cerebral Perfusion Pressure (1 of 2)

• Responsible for the movement of blood

through the brain and is the difference
between mean arterial pressure (MAP)
and ICP (cerebral perfusion pressure
[CPP] = MAP – ICP).
• The brain is capable of autoregulating its
blood flow, regardless of blood pressure,
by altering the resistance of cerebral blood
Cerebral Perfusion Pressure (2 of 2)

• Homeostatic mechanisms are often lost

after head trauma.
• CPP should be maintained between 70
and 90 mm Hg.
• Systemic hypotension (systolic blood
pressure less than 90 mm Hg) is
associated with poor prognosis.
Pathophysiology of Increased
• Any change that causes an increase in
volume in the skull will cause an increase
in ICP.
• Common causes include cerebral
hemorrhage, tumors, hydrocephalus, and
• Increased ICP is defined as a sustained
elevation in pressure above 20 cm H2O.
Compensatory Measures to
Maintain ICP
• Shunting of CSF into the spinal
subarachnoid space
• Increased CSF absorption
• Decreased CSF production
• Shunting of venous blood out of the skull
Cushing Triad

• Combination of increasing systolic blood

pressure, with decreasing diastolic blood
pressure and bradycardia
• Cushing triad often indicates that there is a
severe and irreversible injury in the cranial
Causes of a Rise in ICP

• Causes and rate at which it occurs are

– Intracranial temperature or obstructive
hydrocephalus: Few or no ill effects
– Compromised CBF due to parenchymal
lesions (eg, tumors, hematomas)
– Acute hydrocephalus: No time for
Disruption of Brain Function
Secondary to ICP
• Reduction in CBF
• Transtentorial or foramen magnum
• Transtentorial herniation with brain stem
Clinical Manifestations of
Increased ICP
• Result of Cushing triad that is indicated by:
– Arterial hypertension, bradycardia, respiratory
• Respiratory changes depend on level of
brain stem involvement
– Cheyne-Stokes, sustained hyperventilation,
ataxic breathing
ICP Monitoring (1 of 2)

• Key points:
– Baseline requirements: Oxygen saturation
(SpO2), ECG, MAP, end-tidal CO2, central
venous pressure, and urine output.
– ICP and blood pressure monitoring are the
only way to reliably determine CPP and
assess cerebral hypoperfusion
ICP Monitoring (2 of 2)

• Key points:
– When ICP and CPP cannot be maintained by
standard methods:
• Use multimodality monitoring, including jugular
venous oxygen saturation, brain tissue oxygen
tension, and transcranial Doppler ultrasound
Indications for ICP Monitoring
• Severe TBI
• Intracranial hemorrhage
• Cerebral edema
• Prior craniotomy
• Space-occupying lesions
• Patients with Reye syndrome
• Encephalopathy
• Meningitis/encephalitis
• GCS score of less than 8 or a positive CT
Contraindications for ICP
• CNS infection
• Coagulation defects
• Coagulopathy
• Scalp infection
• Severe midline shift resulting in
ventricular displacement
• Cerebral edema resulting in
ventricular collapse
Complications of ICP
Monitoring (1 of 2)
• Intracranial infection
• Intracerebral hemorrhage
• Air leakage into ventricle or subarachnoid
• CSF leakage
Complications of ICP
Monitoring (2 of 2)
• Overdrainage of CSF
• Occlusion of the catheter
• Inappropriate therapy
ICP Monitoring Methods

• Noninvasive ICP monitoring involves

assessment for clinical deterioration in
neurologic status.
• Invasive methods provide a quantitative
measure of pressure, and some allow for
CSF drainage.
– Intraventricular catheter (IVC)
– Subarachnoid screw
Benefits and Problems of ICP
• Advantages of using an IVC include:
– Allows for drainage of CSF to lower ICP
– Is accurate and reliable
• Risks associated with IVC use include:
– Infection
– Injury to the brain
– Technically difficult
Precautions for ICP Monitoring
(1 of 2)

• Use aseptic technique when handling the

patient and the equipment.
• Properly level and zero the equipment.
• Avoid accidental decannulation or
disconnection of the tubing.
• Avoid flexion and hyperextension of the
neck and positioning the patient in a
Trendelenburg position.
Precautions for ICP Monitoring
(2 of 2)

• Make sure the high ICP alarm is on.

• Avoid getting the filter wet.
• Simultaneous drainage and pressure
monitoring are not recommended.
• Only a small amount of CSF should be
drained at one time.
Adverse Reactions and
Interventions for ICP Monitoring
• If a good waveform and/or accurate ICP
cannot be obtained, flush the monitoring
• Notify the physician if
– Blood is seen in the pressure tubing
– The patient has an acutely low ICP or signs of
Multimodality Monitoring

• CBF and oxygen content of the blood are

the prime parameters of concern.
– Multimodality monitoring involves using a
combination of jugular venous bulb oximetry,
brain tissue oxygen tension, and transcranial
Doppler ultrasound
Treatment Options for
Increased ICP
• Treatment: Removal of causative lesion
– First-line versus second-line management
• First line: General measures to make the
patient comfortable, effective handling of
airway, breathing, and circulation of trauma
• Second line: Involves induced cerebral
vasoconstriction, which could include:
hyperventilation; hyperosmolar therapy; the use
of barbiturates, corticosteroids, or surgery
Brain Herniation (1 of 2)

• Occurs when a portion of the brain is

displaced because of increased ICP
• Caused by brain swelling from a head
• May also be caused by a hemorrhagic
stroke or brain tumor
Brain Herniation (2 of 2)

• Most common type occurs when a portion

of the temporal lobe is displaced (uncal
• Another type occurs when part of the
cerebellum is displaced through the
foramen magnum (tonsillar herniation)
Spinal Cord Injuries (1 of 3)

• Flexion-extension injuries
– Result of rapid deceleration or from a direct
blow to the occiput
– Involve the cervical region; the spinal cord
may be injured as a result by compression in
the canal
– Hyperextension of the head and neck can
result in fractures, ligamentous injury, and
spinal cord injury (SCI).
Spinal Cord Injuries (2 of 3)

• Vertical compression
– Results from a direct blow to the crown or
rapid deceleration from a fall through the
feet, legs, and pelvis
– In falls, most injuries involve the
thoracolumbar junction.
– The lower cervical spine is often involved
with axial loads to the spinal column.
Spinal Cord Injuries (3 of 3)

• Rotation with flexion

– Often occurs in the thoracolumbar interface
– The injury patterns can involve stable or
unstable fractures and dislocations.
Primary SCI (1 of 2)

• Result of the initial trauma

• Penetrating trauma may either result in
transection of neural elements or cause
concussive injury.
• Blunt trauma may displace ligaments and
bone fragments.
Primary SCI (2 of 2)

• Hypoperfusion and ischemia may also

result from this type of injury to the spinal
• Spinal cord contusions are caused by
fracture, dislocation, or direct trauma.
• Cord laceration usually occurs when a
projectile or bone enters the spinal canal.
Secondary SCI

• Occurs as a result of progression of the

primary SCI
• The injury can trigger a cascade of
inflammatory responses that may result in
further deterioration.
• Some secondary SCIs are unavoidable,
but CCTPs can minimize further injury
through stabilization.
Complete SCIs

• Involves complete disruption of all tracts of

the spinal cord, with no sensory and motor
function more than three segments below
the level of injury
Incomplete Spinal Cord
Syndromes (1 of 2)
• Anterior cord syndrome
– Results from the displacement of bony
fragments into the anterior portion of the spinal
cord, often the result of flexion injuries or
• Central cord syndrome
– Hyperextension injuries to the cervical area
present with hemorrhage or edema to the
central cervical segments
Incomplete Spinal Cord
Syndromes (2 of 2)
• Brown-Sequard syndrome
– Occurs when penetrating trauma is
accompanied by hemisection of the cord and
complete damage to all spinal tracts on the
involved side
• Posterior cord syndrome
– Associated with extension injuries
Spinal versus Neurogenic
• Spinal shock
– Temporary local neurologic condition that
occurs immediately after spinal trauma and
involves impaired function of reflex arcs below
and at the level of injury
• Neurogenic shock
– Results from the temporary loss of autonomic
function, which controls cardiovascular
function, at the level of injury
Assessment for SCI (1 of 2)

• Perform a thorough assessment before

• Visually inspect the neck, looking for
deformities and feeling for crepitus or pain.
• Evaluate the patient’s airway prior to
• Assess the back for tenderness and
Assessment for SCI (2 of 2)

• Palpate the spine for tenderness and

• Assess for strength in upper and lower
extremities and for the presence of
• Provide ongoing patient assessment
Management of SCI

• CCTP should rapidly assess, treat, and

transport the patient to the closest facility
while maintaining spinal motion restriction.
– Minimize movement to prevent further injury.
• Aggressively manage hypotension/hypoxia
to prevent anoxic injury to the spinal cord.
Management Priorities (1 of 2)

• Rapid identification and correction of life-

threatening problems
• Secure and manage the airway, especially
in patients with higher-level cervical
• Monitor blood pressure by noninvasive
means or by an arterial line to alert
providers to hypotension.
Management Priorities (2 of 2)

• Provide adequate volume resuscitation

with appropriate intravenous (IV) fluids and
blood component therapy for patients with
multiple injuries.
• For patients who require monitoring to
maintain normothermia, provide warm IV
fluids, blankets, and temperature control.
Pharmacotherapy in SCI

• IV opiates can be useful for managing pain

associated with transportation, movement,
and the injury itself.
• Patients with SCIs may also have
neurogenic shock requiring vasoactive
medications to support blood pressure.
– Patients in neurogenic shock may also have
bradycardia, requiring atropine to support the
heart rate and blood pressure.
Complications of SCI (1 of 2)

• Acute-phase complications of SCI include

the potential for aspiration or respiratory
• Deep vein thrombosis and pulmonary
embolism may result from immobility and
can become life threatening.
• Pressure ulcers from immobility are
problematic in SCI.
Complications of SCI (2 of 2)

• Urinary tract infections can be reduced by

avoiding the use of Foley catheters.
• Autonomic dysreflexia, if untreated, can
cause stroke, seizures, and death.
– If the source of autonomic dysreflexia cannot
be found or minimized, reduce the patient’s
blood pressure with vasodilators.


• Mechanism of injury
– Stroke occurs when a disruption of blood
flow to the brain results in neurologic deficit
persisting for more than 24 hours.
• When deficits completely resolve within
24 hours, the event is referred to as a
transient ischemic attack.
Types of Stroke (1 of 3)

• Ischemic strokes
– Occur when CBF is decreased because of an
occlusion of a blood vessel
• Thrombotic strokes
– Result of an accumulation of atherosclerotic
plaques inside cerebral blood vessels, which
narrow the lumen of the vessel and make
blood flow difficult
Types of Stroke (2 of 3)

• Embolic strokes
– Occur when an embolus from the heart or
lower circulation travels and lodges in a
smaller cerebral vessel
• Focal ischemic strokes
– Occur when an area of marginally perfused
tissue, the ischemic penumbra, surrounds a
core of ischemic cells
Types of Stroke (3 of 3)

• Global ischemic strokes

– Result when severe hypotension or cardiac
arrest produces a drop in blood flow to all
areas of the brain
Side Effects of Stroke

• Cerebral edema occurs in 10%-20% of

patients with ischemic stroke and can
result in intracranial hypertension.
• Secondary hemorrhage at the site of an
ischemic stroke lesion is known as
hemorrhagic conversion.
• Patients who have had a stroke may have
seizures as a result of damaged neurons.
Assessment of Stroke

• The characteristic sign of stroke is the

sudden onset of focal neurologic signs
that occur in combination.
• The CCTP can use prehospital tools to
identify patients suffering from stroke:
– The Cincinnati Prehospital Stroke Scale
– The Los Angeles Prehospital Stroke Screen
Los Angeles Prehospital
Stroke Screen

*Interpretation: If criteria 1 through 6 are marked yes, the probability of a stroke is 97%.
© Jones & Bartlett Learning.
Management of Stroke (1 of 3)

• Determine the time of symptom onset.

• Support the patient’s cardiopulmonary
function, monitor neurologic function, and
maintain normal blood glucose levels.
• Stroke patients are at risk for respiratory
compromise from aspiration, upper airway
obstruction, and hypoventilation.
Management of Stroke (2 of 3)

• Fibrinolytic therapy
– Used to restore circulation to ischemic brain
– Before therapy is initiated, inclusion and
exclusion criteria (refer to American Heart
Association’s criteria) for IV fibrinolytic therapy
should be reviewed.
Management of Stroke (3 of 3)

• Fibrinolytic therapy
– Exclusion criteria includes:
• History of intracranial neoplasm, arteriovenous
malformation (AVM), or aneurysm
• Bleeding concerns, in the form of either current
bleeding or a bleeding disorder
• History of stroke
Intracerebral Hemorrhage (1 of 2)

• Bleeding directly into the cerebral tissue

that causes
– Cerebral tissue destruction
– Cerebral edema
– Increased ICP
• The most common cause of spontaneous
intracerebral hemorrhage is hypertension-
induced vessel rupture.
Intracerebral Hemorrhage (2 of 2)

• Symptoms of intracerebral hemorrhage

may begin as local neurologic dysfunction
related to the area of the brain in which a
vessel has ruptured.
• As ICP continues to rise, the patient may
become unconscious.
• The time it takes for deterioration to
progress is related to the amount and
speed of bleeding.
Subarachnoid Hemorrhage (1 of 2)

• Bleeding into the subarachnoid space.

• Usually arterial in nature.
• Most are caused by rupture of a cerebral
aneurysm or AVM.
Subarachnoid Hemorrhage (2 of 2)

• Aneurysms are an outpouching of the wall

of a blood vessel that results from
weakening of the wall of the vessel.
• AVMs are tangled masses of arterial and
venous blood vessels that shunt blood
directly from arteries to veins without going
through an intervening capillary bed.
Assessment of SAH

• The patient has an abrupt onset of pain.

• A loss of consciousness, nausea,
vomiting, focal neurologic deficits,
photophobia, and nuchal rigidity may
accompany the headache.
• As ICP increases, the patient may become
comatose or die.
Management of SAH

• Maintain cardiopulmonary function.

• The patient will need airway management
and ventilatory support.
• Prevent a rise in ICP.
• Complications include rebleeding, cerebral
vasospasm, hyponatremia, and
Acute Guillain-Barré Syndrome
(1 of 2)

• A group of several immune-mediate

polyneuropathies, all with common
features often provoked by an infection.
• Patients may exhibit significant or
complete paralysis of all four extremities,
respiratory, and facial muscles.
Acute Guillain-Barré Syndrome
(2 of 2)

• Initial diagnosis is based on clinical

presentation, including progressive, mostly
bilateral muscle weakness with depressed
or absent deep tendon reflexes.
• Treatment, especially during transport, is
largely supportive.
Seizure and Epilepsy (1 of 3)

• Overactivity by excitatory transmitters or

underactivity by inhibitory transmitters can
result in a seizure.
• Can be caused by different factors
– Fever
– Glucose imbalance
– Electrolyte imbalances
– Head injuries and hemorrhagic strokes
– Toxins
Seizure and Epilepsy (2 of 3)

• Epilepsy is a recurrent seizure disorder

caused by abnormal discharges in the
brain cells.
• Management of seizure patients should
initially center on:
– Maintaining an airway
– Protecting the patient
– Providing oxygen
Seizure and Epilepsy (3 of 3)
• If the patient is actively seizing, no attempt
should be made to restrain him or her.
• An IV should be established, and the patient’s
cardiac status should be monitored.
• The patient’s glucose level should be
checked, and glucose should be administered
if indicated.
• If the patient is actively seizing, an
anticonvulsant must be administered.
Transport Considerations (1 of 4)

• Ensure all diagnostic tests and surgical

procedures are completed when possible
before transporting a patient with a
neurologic emergency.
• Equipment may need troubleshooting:
– Cardiac monitor
– Ventilator with waveform capnography
Transport Considerations (2 of 4)

• Equipment may need troubleshooting:

– Infusion pumps
– ICP monitoring
– Cerebral function monitor
Transport Considerations (3 of 4)

• The major early risks to the patient with

head injury are hypoxia and hypertension.
• The airway, breathing, and circulation are
always the first priority.
• A patient with a severe closed head injury
should be presumed to have an elevated
Transport Considerations (4 of 4)

• Some critical care transport systems

advocate the use of ear and eye protection
for the patient to prevent spikes in ICP.
• Minimum requirements for monitoring
patients during transport are:
– Continuous ECG, pulse oximetry, and the
intermittent measurement of blood pressure,
respiratory rate, and pulse rate.
Flight Considerations (1 of 3)

• If possible, have the pilot fly at altitudes

where cabin pressure can be maintained
as close to the original departure pressure
as possible.
• If the patient is intubated, the endotracheal
cuff pressure should be decreased with
Flight Considerations (2 of 3)

• The pressure inside indwelling catheters

and colostomy bags must be adjusted to
prevent breakage.
• If the patient has a drain and the ICP is
monitored, the ICP must be maintained to
less than 20 cm H2O by draining off
excess fluids.
Flight Considerations (3 of 3)

• Signs indicating herniation:

– Changes in respiratory rate or pattern
– Changes in cardiac function
• The aircraft must immediately descend to
an altitude at which the condition is