ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
Nursing Care of Clients with Life
Threatening Conditions. Acutely
Ill/Multi-Organ problems, High Acuity
and Emergency Situation
Neurologic System
• The nervous system is the major
controlling, regulatory and communicating
system in the body.
• It accounts for 3% of the total body weight,
it is the most complex organ system.
• It is the center of all mental activity,
including thought, learning and memory.
• Together with the endocrine and immune
systems, the nervous system is responsible
for regulating and maintaining homeostasis.
• Through its receptors, the nervous system
keeps in touch with the environment, both
external and internal.
NEUROLOGICAL ANATOMY AND
PHYSIOLOGY
• COMPONENTS OF THE NERVOUS
SYSTEM
• The central nervous system (CNS)
consists of the spinal cord and the brain
and is responsible for integrating,
processing and coordinating sensory data
and motor commands.
• The CNS is linked to all parts of the body
by the PNS which transmits signals to and
from the CNS.
• The human PNS is composed of 43 pairs
of spinal nerves that issue in orderly
sequence from the spinal cord, and 12 pairs
of cranial nerves that emerge from the base
of the brain.
• The peripheral nerves carry input to the
CNS via their sensory afferent fibers and
deliver output from the CNS via the efferent
fibers.
Neurons
• Are specialized cells in the nervous
system; each is comprised of a dendrite,
cell body (soma) and axon.
• The primary functional unit of the nervous
system.
• Three characteristics: (1) excitability, or
the ability to generate a nerve impulse; (2)
conductivity, or the ability to transmit an
impulse; and (3) influence, or the ability to
influence other neurons, muscle cells, or
glandular cells by transmitting nerve
impulses to them.
• A typical neuron consists of a cell body,
multiple dendrites, and an axon .
• The cell body containing the nucleus and
cytoplasm is the metabolic center of the
neuron.
• Dendrites are short processes extending
from the cell body that receive
• impulses from the axons of other neurons
and conduct impulses toward the cell body.
• The axon projects varying distances from
the cell body, ranging from several
micrometers to more than a meter. The
1 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
axon carries nerve impulses to other
neurons or to end organs. The end organs
are smooth and striated muscles and
glands.
• Many axons in the CNS and PNS are
covered by a myelin sheath, a white, lipid
substance that acts as an insulator for the
conduction of impulses.
• Axons may be myelinated or
unmyelinated. Generally, the smaller fibers
are unmyelinated.
Glial Cells
• Glial cells (glia or neuroglia) provide
support, nourishment, and protection to
neurons.
• Constitute almost half of the brain and
spinal cord mass and are 5 to 10 times
more numerous than neurons.
• Glial cells are divided into microglia and
macroglia.
• Microglia, specialized macrophages
capable of phagocytosis, protect the
neurons. These cells are mobile within the
brain and multiply when the brain is
damaged.
• Different types of macroglial cells include
the astrocytes (most abundant),
oligodendrocytes, and ependymal cells.
• Astrocytes are found primarily in gray
matter and provide structural support to
neurons. Their delicate processes form the
blood-brain barrier with the endothelium of
the blood
vessels.
• They also play a role in synaptic
transmission (conduction of impulses
between neurons).
• When the brain is injured, astrocytes act
as phagocytes for neuronal debris. They
help restore the neurochemical milieu and
provide support for repair. Proliferation of
astrocytes contributes to the formation of
scar tissue (gliosis) in the CNS.
• Oligodendrocytes are specialized cells
that produce the myelin sheath of nerve
fibers in the CNS and are primarily found in
the white matter of the CNS. (Schwann
cells myelinat the nerve fibers in the
periphery.)
• Ependymal cells line the brain ventricles
and aid in the secretion of cerebrospinal
fluid
(CSF).
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
• Neuroglia are mitotic and can replicate.
• In general, when neurons are destroyed,
the tissue is replaced by the proliferation of
neuroglial cells.
• Most primary CNS tumors involve glial
cells.
• Primary malignancies involving neurons
are rare.
Nerve Impulse
• The purpose of a neuron is to initiate,
receive, and process messages about
events both within and outside the body.
• The initiation of a neuronal message
(nerve impulse) involves the generation of
an action potential. Once an action potential
is initiated, a series of action potentials
travels along the axon.
• When the impulse reaches the end of the
nerve fiber, it is transmitted across the
junction between nerve cells (synapse) by a
chemical interaction involving
neurotransmitters.
• This chemical interaction generates
another set of action potentials in the next
neuron. These events are repeated until the
nerve impulse reaches its destination.
• Because of its insulating capacity,
myelination of nerve axons facilitates the
conduction of an action potential. Many
peripheral nerve axons have nodes of
Ranvier
(gaps in the myelin sheath) that allow an
action potential to travel much faster by
jumping from node to node without
traversing the insulated membrane
segment. This is called saltatory (hopping)
conduction.
• In an unmyelinated fiber, the wave of
depolarization travels the entire length of
the axon, with each portion of the
membrane becoming depolarized in turn.
Synapse
• A synapse is the structural and functional
junction between two neurons.
• It is the point at which the nerve impulse is
transmitted from one neuron to another.
The nerve impulse can also be transmitted
from neurons to glands or muscles.
• The essential structures of synaptic
transmission are a presynaptic terminal, a
synaptic cleft, and a receptor site on the
postsynaptic cell.
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
• Two general classes: electrical synapses
and chemical synapses.
• Electrical synapses permit direct, passive
flow of electrical current from one neuron to
another in the form of an action potential.
The current flows through gap junctions,
which are specialized membrane channels
that connect the two cells.
• Chemical synapses, in contrast, enable
cell-to-cell communication via the secretion
of neurotransmitters; the chemical agents
released by the presynaptic neurons
produce secondary current flow in
postsynaptic neurons by activating specific
receptor molecules.
Neurotransmitters
• Neurotransmitters are chemicals that
affect the transmission of impulses across
the synaptic cleft.
• Chemically, there are four classes of
neurotransmitters:
– 1. acetylcholine (ACh): the dominant
neurotransmitter in the peripheral nervous
system, released at neuromuscular
junctions and synapses of the
parasympathetic division
– 2. biogenic amines: serotonin, histamine,
and the catecholamines dopamine and
noradrenaline
– 3. excitatory amino acids: glutamate and
aspartate, and the inhibitory amino acids
gamma-aminobutyric acid (GABA), glycine
and taurine
– 4. neuropeptides: over 50 of which are
known, amino acid neurotransmitters being
the most numerous.
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

joints, viscera, and blood vessels and

enters the spinal cord by way of the dorsal
roots of the spinal nerves.
• The fasciculus gracilis and the fasciculus
cuneatus (commonly called the dorsal or
posterior columns) carry information and
transmit impulses concerned with touch,
deep pressure, vibration, position sense,
and kinesthesia (appreciation of movement,
volweight, and body parts).
• The spinocerebellar tracts carry
information about muscle tension and body
position to the cerebellum for coordination
of movement.
• The spinothalamic tractscarry pain and
Central Nervous System
temperature sensations. Therefore the
• The components of the CNS include the
ascending tracts are organized by sensory
cerebrum (cerebral hemispheres),
modality, as well as by anatomy
brainstem, cerebellum, and spinal cord.
• The spinal cord is continuous with the
Descending Tracts
brainstem and exits from the cranial cavity
• Descending tracts carry impulses that are
through the foramen magnum.
responsible for muscle movement.
• A cross section of the spinal cord reveals
• Among the most important descending
gray matter that is centrally located in an H
tracts are the corticobulbar and
shape and is surrounded by white matter.
corticospinal tracts, collectively termed the
• The gray matter contains the cell bodies of
pyramidal tract.
voluntary motor neurons, preganglionic
• These tracts carry volitional (voluntary)
autonomic motor neurons, and association
impulses from the cerebral cortex to the
neurons (interneurons).
cranial and peripheral nerves.
• The white matter contains the axons of the
• Another group of descending motor tracts
ascending sensory and the descending
carries impulses from the extrapyramidal
(suprasegmental) motor fibers.
system (all motor systems except the
pyramidal) concerned with
Ascending Tracts
voluntarymovement. It includes pathways
• The ascending tracts carry specific
originating in the brainstem, basal ganglia,
sensory information to higher levels of the
and cerebellum. The motor output exits the
CNS.
spinal cord by way of the ventral roots of
• This information comes from special
the spinal nerves.
sensory receptors in the skin, muscles and
5 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
Lower and Upper Motor Neurons
• Lower motor neurons (LMNs) are the final
common pathway through which
descending motor tracts influence skeletal
muscle.
• The cell bodies of LMNs, which send
axons to innervate the skeletal muscles of
the arms, trunk, and legs, are located in the
anterior horn of the corresponding
segments of the spinal
cord (e.g., cervical segments contain LMNs
for the arms).
• LMNs for skeletal muscles of the eyes,
face, mouth, and throat are located in the
corresponding segments of the brainstem.
• These cell bodies and their axons make
up the somatic motor components of the
cranial nerves.
• LMN lesions generally cause weakness or
paralysis, denervation atrophy, hyporeflexia
or areflexia, and decreased muscle tone
(flaccidity).
• Upper motor neurons (UMNs) originate in
the cerebral cortex and project downward.
• The corticobulbar tract ends in the
brainstem, and the corticospinal tract
descends into the spinal cord. These
neurons influence skeletal muscle
movement.
• UMN lesions generally cause weakness or
paralysis, disuse atrophy, hyperreflexia, and
increased muscle tone (spasticity).
Reflex Arc
• A reflex is an involuntary response to
stimuli.
• In the spinal cord, reflex arcs play an
important role in maintaining muscle tone,
which is essential for body posture.
• The components of a monosynaptic reflex
arc are a receptor organ, an afferent
neuron, an effector neuron, and an effector
organ (e.g., skeletal muscle).
• The afferent neuron synapses with the
efferent neuron in the gray matter of the
spinal cord.
Brain
• The term brain usually refers to the three
major intracranial components: cerebrum,
brainstem, and cerebellum.
Cerebrum
• The cerebrum is composed of the right
and left cerebral hemispheres and divided
into four lobes: frontal, temporal, parietal,
and occipital.
• The frontal lobe controls higher cognitive
function, memory retention, VOLuntary eye
movements, voluntary motor movement,
and speech in Broca’s area.
• The temporal lobe integrates somatic,
visual, and auditory data and contains
Wernicke’s speech area.
• The parietal lobe interprets spatial
information and contains the sensory
cortex.
6 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

• Processing of sight takes place in the

occipital lobe.
• The division of the cerebrum into lobes is
useful to delineate portions of the neocortex
(gray matter), which makes up the outer
layer of the cerebral hemispheres. Neurons
in specific
parts of the neocortex are essential for
various highly complex and sophisticated
aspects of mental function, such as
language, memory, and appreciation of
visual-spatial
relationships.
• The basal ganglia, thalamus,
hypothalamus, and limbic system are also
located in the cerebrum.
• The basal ganglia are a group of
structures located centrally in the cerebrum
and midbrain. The function of the basal
ganglia includes the initiation, execution,
and completion of voluntary movements,
learning, emotional response, and
automatic movements associated with
skeletal muscle activity (e.g., swinging the
arms while walking, swallowing saliva, and
blinking).
• The thalamus (part of the diencephalon)
lies directly above the brainstem and is the
major relay center for afferent inputs to the
cerebral cortex.
• The hypothalamus is located just inferior
to the thalamus and slightly in front of the
midbrain.
• It regulates the ANS and the endocrine
system.
• The limbic system is located near the
inner surfaces of the cerebral hemispheres
and is concerned with emotion, aggression,
feeding behavior, and sexual response.
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

Brainstem
• The brainstem includes the midbrain,
pons, and medulla .
• Ascending and descending fibers to and
from the cerebrum and cerebellum pass
through the brainstem.
• The nuclei of cranial nerves III through XII
are in the brainstem.
• The vital centers concerned with
respiratory, vasomotor, and cardiac function
are located in the medulla.
• Also located in the brainstem is the
reticular formation, a diffusely arranged
Cerebellum
group of neurons and their axons that
• The cerebellum is located in the posterior
extends from the medulla to the thalamus
part of the cranial fossa inferior to the
and hypothalamus. The functions of the
occipital lobe.
reticular formation include relaying sensory
• The cerebellum coordinates voluntary
information, influencing excitatory and
movement and maintains trunk stability and
inhibitory control of spinal motor neurons,
equilibrium.
and controlling vasomotor and respiratory
• The cerebellum receives information from
activity.
the cerebral cortex, muscles, joints, and
• The reticular activating system (RAS) is a
inner ear.
complex system that requires
• It influences motor activity through axonal
communication among the brainstem,
connections to the motor cortex, the
reticular formation, and cerebral cortex. The
brainstem nuclei, and their descending
RAS is responsible for regulating arousal
pathways.
and sleep-wake transitions. The brainstem
also contains the centers for sneezing,
Ventricles and Cerebrospinal Fluid.
coughing, hiccupping, vomiting, sucking,
• The ventricles are four interconnected
and swallowing.
fluid-filled cavities. The lower portion of the
fourth ventricle becomes the central canal
in the lower part of the brainstem. The
spinal canal extends centrally through the
full length of the spinal cord.

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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

Cerebrospinal fluid (CSF) by increased CSF pressure, can force

• Circulates within the subarachnoid space
that surrounds the brain, brainstem, and
spinal cord.
• This fluid provides cushioning for the brain
and the spinal cord, allows fluid shifts from
the cranial cavity to the spinal cavity, and
carries nutrients.
• The formation of CSF in the choroid
plexus in the ventricles involves both
passive diffusion and active transport of
substances. CSF resembles an ultrafiltrate
of blood.
• CSF is produced at an average rate of
about 500 mL/day, many factors influence
CSF production and absorption. The
ventricles and central canal are normally
filled with an average of 135 mL of CSF.
• Changes in the rate of production or
absorption will result in a change in the
volume of CSF that remains in the
ventricles and central canal.
• Excessive buildup of CSF results in a
condition known as hydrocephalus.
• The CSF circulates throughout the
ventricles and seeps into the subarachnoid
space surrounding the brain and spinal
cord.
• It is absorbed primarily through the
arachnoid villi (tiny projections into the
subarachnoid space), into the intradural
venous sinuses, and eventually into the
venous system.
• The analysis of CSF composition provides
useful diagnostic information related to
certain nervous system diseases. CSF
pressure is often measured in patients with
actual or suspected intracranial injury.
Increased intracranial pressure, indicated
downward (central) herniation of the brain
and brainstem.
Peripheral Nervous System
• The PNS includes all the neuronal
structures that lie outside the CNS. It
consists of the spinal and cranial nerves,
their associated ganglia (groupings of cell
bodies), and portions of the ANS.
Spinal Nerves
• The spinal cord can be seen as a series of
spinal segments, one on top of another.
• Each segment contains a pair of dorsal
(afferent) sensory nerve fibers or roots and
ventral (efferent) motor fibers or roots,
which innervate a specific region of the
body.
• This combined motor-sensory nerve is
called a spinal nerve.
• The cell bodies of the voluntary motor
system are located in the anterior horn of
the spinal cord gray matter.
• The cell bodies of the autonomic
(involuntary) motor system are located in
9 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

the anterolateral portion of the spinal cord epithelium, and those of the optic nerve are
gray matter. in the retina.
• The cell bodies of sensory fibers are
located in the dorsal root ganglia just
outside the spinal cord.
• A dermatome is the area of skin
innervated by the sensory fibers of a single
dorsal root of a spinal nerve.
• The dermatomes give a general picture of
somatic sensory innervation by spinal
segments.
• A myotome is a muscle group innervated
by the primary motor neurons of a single
ventral root.

Cranial Nerves
• The cranial nerves (CNs) are the 12
paired nerves composed of cell bodies with
fibers that exit from the cranial cavity.
• Just as the cell bodies of the spinal nerves
are located in specific segments of the
spinal cord, so are the cell bodies (nuclei)
of the CNs located in specific segments of
the brain.
• Exceptions are the nuclei of the olfactory
and optic nerves. The primary cell bodies of
the olfactory nerve are located in the nasal
Autonomic Nervous System.
• The autonomic nervous system (ANS) is
divided into the sympathetic and
parasympathetic systems.
• The ANS governs involuntary functions of
cardiac muscle, smooth muscle, and glands
through both efferent and afferent
pathways.
• The preganglionic cell bodies of the
sympathetic nervous system (SNS) are
located in spinal segments T1 through L2.

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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
The major neurotransmitter released by the
postganglionic fibers of the SNS is
norepinephrine, and the neurotransmitter
released by the preganglionic fibers is
acetylcholine.
• The preganglionic cell bodies of the
parasympathetic nervous
system (PSNS) are located in the brainstem
and the sacral spinal segments (S2 through
S4). Acetylcholine is the
neurotransmitter released at both
preganglionic and postganglionic nerve
endings.
• SNS stimulation activates the
mechanisms required for the
“fight-or-flight” response that occurs
throughout the body.
• The PSNS is geared to act in localized
and discrete regions
Cerebral Circulation
• The brain’s blood supply arises from the
internal
carotid arteries (anterior circulation) and the
vertebral arteries (posterior circulation).
• The internal carotid arteries provide blood
flow to the anterior and middle portions of
the cerebrum.
• The vertebral arteries join to form the
basilar artery and provide blood flow to the
brainstem, cerebellum, and posterior
cerebrum.
• The circle of Willis is formed by
communicating arteries that
join the basilar and internal carotid arteries.
• The circle of Willis is a safety valve for
regulating cerebral blood flow when
differential pressures or vascular occlusions
are present.
• Superior to the circle of Willis, three pairs
of arteries supply blood to the left and right
hemispheres.
• The anterior cerebra artery feeds the
medial and anterior portions of the frontal
lobes.
• The middle cerebral artery feeds the outer
portions of the frontal, parietal, and superior
temporal lobes.
• The posterio cerebral artery feeds the
medial portions
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

of the occipital an inferior temporal lobes. cerebral hemispheres from the posterior
• Venous blood drains from the brain fossa (which
through the dural contains the brainstem and cerebellum).
sinuses, which form channels that drain int • Expansion of mass lesions in the
the two cerebrum forces the brain to
jugular veins. herniate through the opening created by the
brainstem. This
• The blood-brain barrier is a physiologic is termed infratentorial herniation.
barrier between
blood capillaries and brain tissue. • The arachnoid layer is a delicate
• This barrier protects the brain from membrane that lies between
harmful agents, while the dura mater and the pia mater (the
allowing nutrients and gases to enter. delicate innermost
• Lipid-soluble compounds enter the brain layer of the meninges).
easily, whereas • The area between the arachnoid layer and
water-soluble and ionized drugs enter the the pia mater is
brain and the spinal the subarachnoid space and is filled with
cord slowly. CSF.
• Thus the blood-brain barrier affects the • Structures such as arteries, veins, and
penetration of drugs. cranial nerves passing
to and from the brain and the skull must
Protective Structures pass through the
• The meninges consist of three protective subarachnoid space.
membranes that • A larger subarachnoid space in the region
surround the brain and spinal cord: dura of the third and
mater, arachnoid, fourth lumbar vertebrae is the area used to
and pia mater . obtain CS during a
• The thick dura mater forms the outermost lumbar puncture.
layer.
• The falx cerebri is a fold of the dura that • Skull.
separates the two The skull protects the brain from
cerebral hemispheres and slows expansion external trauma. It is composed of eight
of brain tissue in cranial bones and 14 facial bones.
conditions such as a rapidly growing tumor • Vertebral Column.
or acute The vertebral column
hemorrhage. protects the spinal cord, supports the head,
• The tentorium cerebelli is a fold of dura and provides flexibility. The vertebral
that separates the column is made up of 33 individual
vertebrae: 7
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

cervical, 12 thoracic, 5 lumbar, 5 sacral system, such as head, spine, or sensory

(fused organs. If a patient
into one), and 4 coccygeal had surgery, determine the date, cause,
procedure,
• ASSESSMENT OF NERVOUS SYSTEM recovery, and current status.
Subjective Data • Growth and developmental history can be
• Important Health Information important in
• Past Health History. ascertaining whether nervous system
Consider three points when taking a dysfunction was
history of a patient with neurologic present at an early age. Specifically inquire
problems. about major
• First, avoid suggesting symptoms or developmental tasks such as walking and
asking leading questions. talking.
• Second, the mode of onset and the course • Functional Health Patterns.
of the illness are Key questions to ask a patient with a
especially important aspects of the history. neurologic problem are presented in Table
Obtain all 56-5.
pertinent data in the history of the present
illness, especially
data related to the characteristics and
progression of the
symptoms.
• Third, if the patient is not considered a
reliable historian,
confirm or obtain the history from someone
with firsthand
knowledge of the patient.
• Medications.
Obtain a careful medication history,
especially
Objective Data
the use of sedatives, opioids, tranquilizers,
• Physical Examination. The standard
and mood
neurologic examination
elevating drugs. Many other drugs can also
helps determine the presence, location, and
cause
nature of disease
neurologic side effects.
of the nervous system.
• Surgery or Other Treatments.
• The examination assesses six categories
• Inquire about any surgery involving any
of functions: mental
part of the nervous

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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
status, cranial nerve function, motor
function, sensory
function, cerebellar function, and reflexes..
• Mental Status.
Assessment of mental status
(cerebral function) gives a general
impression of how
the patient is functioning.
• It involves determining complex and
high-level
cerebral functions that are governed by
many areas
of the cerebral cortex.
The components of the mental status
examination include:
• General appearance and behavior: This
component includes level of
consciousness (awake, asleep, comatose),
motor activity, body posture,
dress and hygiene, facial expression, and
speech pattern.
• Cognition: Note orientation to time, place,
person, and situation, as well
as memory, general knowledge, insight,
judgment, problem solving, and
calculation. Common questions are “Who
were the last three presidents?”
“Does a rock float on water?” “How much
money is a quarter, two dimes,
and a nickel?” Consider whether the
patient’s plans and goals match the
physical and mental capabilities. Note the
presence of factors affecting
intellectual capacity such as cognitive
impairment, hallucinations,
delusions, and dementia.
• Mood and affect: Note any agitation,
anger, depression, or euphoria and
the appropriateness of these states. Use
suitable questions to bring out
the patient’s feelings.
• Conscious State
• Arousal and awareness are the
fundamental constituents of
consciousness and should be evaluated
and documented
repeatedly for trend analysis. Changes in
the conscious state are
the first to change in deterioration.
• Arousal assessment
• The evaluation of arousal focuses on the
ability to be able to
respond to a variety of stimuli and can be
described using the
AVPU scale or disorientated, lethargic, or
obtunded.
• The advanced trauma life support course
recommends an initial
assessment during initial resuscitation
based on the response to
stimulation: Awake, Verbal, Pain,
Unresponsive (AVPU).
• Observe the patient’s response (verbal or
motor). If there is no
response to voice or light touch, painful
stimulus is needed to
assess neurological status.
• Assessment of awareness
• If arousable, progress to assessment of
awareness using the
Glasgow Coma Scale (GCS).
• Teasdale and Jennett designed the GCS
to establish an
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 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
objective, quantifiable measure to describe
the prognosis of a
patient with a brain injury and include
scoring of separate
subscales related to eye opening, verbal
response and motor
response.
• Eye and pupil assessment
• Pupillary responses, including pupil size
and reaction to light,
are important neurological observations and
localize cerebral
disease to a specific area of the brain.
• The immediate constriction of the pupil
when light is shone
into the eye is referred to as the direct light
reflex.
• Withdrawal of the light should produce an
immediate and
brisk dilation of the pupil.
• Introduction of the light into one eye
should cause a similar
constriction to occur in the other pupil
(consensual light
reaction).
Other points to consider when conducting
pupillary observations include the following
• pinpoint non-reactive pupils are
associated with opiate
overdose
• non-reactive pupils may also be caused
by local damage
• atropine will cause dilated pupils
• one dilated or fixed pupil may be indicative
of an expanding
or developing intracranial lesion,
compressing the
oculomotor nerve on the same side of the
brain as the
affected pupil
• A sluggish pupil may be difficult to
distinguish from a fixed
pupil and may be an early focal sign of an
expanding
intracranial lesion and raised
intracranialpressure. A
sluggish response to light in a previously
reacting pupil must
be reported immediately.
• Assessment of pupillary function
focuses on three areas:
• (1) estimation of pupil size and shape;
• (2) evaluation of pupillary reaction to light;
• (3) assessment of eye movements.
• Eye and eyelid movements
• Patients who are comatose will exhibit no
eye opening.
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• In patients with bilateral thalamic damage, involvement of a cerebral hemisphere and

there may be normal the brain stem.
consciousness, but an eye opening apraxia • It is characterised by adduction of the
may mimic coma. If the shoulder and arm,
patient’s eyes are closed, the clinician elbow flexion, and pronation and flexion of
should gently raise and release the the wrist while
eyelids. Brisk opening and closing of the the legs extend. In terms of the GCS motor
eyes indicates that the pons is score, the
grossly intact. withdrawal flexor scores a higher (4/6) than
• If the pons is impaired, one or both eyelids a spastic flexor
may close slowly or not at all. movement (3/6).
• In the patient with intact frontal lobe and
brainstem functioning, the eyes, • Decerebrate (extensor) posturing is seen
when opened, should be pointed straight with severe
ahead and at equal height. If metabolic disturbances or upper brainstem
there is awareness, the patient should look lesions. It is
towards stimuli after eye characterised by extension and pronation of
opening. the arm(s) and
• Eye deviation indicates either a unilateral extension of the legs. Patients may have an
cerebral or brainstem lesion. If asymmetrical
the eyes deviate laterally, gently turn the response and may posture spontaneously
head to see if the eyes will cross or to stimuli.
the midline to the other side. A pattern of
spontaneous, slow and random • Motor tone is first assessed by flexing the
movements (usually laterally) is termed limbs and noting
roving-eye movements. This increased or absent tone. If no tone is
indicates that the brainstem oculomotor present, the hand is
control is intact but awareness is lifted approximately 30 cm above the bed
significantly impaired. and carefully
dropped while protecting the limb from
• Limb movement injury. The test is
• Assessment of extremities and body repeated with all extremities. Typically, the
movement (or motor lower the level of
response) provides valuable information consciousness, the closer to flaccid the
about the patient limb(s) will be. An
with a decreased level of asymmetrical examination may indicate a
• Decorticate (flexor) posturing is seen lesion in the
when there is contralateral hemisphere or brainstem.

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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD
• Facial symmetry
• Facial symmetry is often difficult to
appreciate in, for
example, severely ill patients due to
oedema, endotracheal
tube tape and nasogastric tubes. An
asymmetric response is
indicative of a lesion of CN VII. Complete
hemi-facial
involvement is typically seen in peripheral
dysfunction (Bell’s
palsy), whereas superior division (forehead)
sparing weakness
indicates a pontine/medullary (central)
involvement.
• Corneal reflexes
• The corneal reflex is assessed by holding
the patient’s eye
open and lightly stimulating the cornea. The
stimuli should
result in a reflexive blink, best seen in the
lower eyelid. The
traditional assessment technique involves
using a wisp of
cotton, lightly brushed along the lower
aspect of the cornea.
An alternative, and less potentially
traumatic, method is to
gently instil isotonic eye drops or saline
irrigation ampoules
onto the cornea. This reflex is dependent
upon CN V for its
sensation and CN VII for its motor
response. Loss of this reflex
is indicative of lower brainstem damage, but
may be absent
due to trauma, surgery, or long-term contact
lens usage.
• Oropharyngeal reflexes
• The oropharyngeal reflexes are controlled
by CN IX and CN X.
The gag reflex is elicited by lightly
stimulating the soft palate
with a suction catheter or tongue blade.
Clinicians should
always avoid stimulating a gag reflex by
wiggling the
endotracheal tube because doing so may
result in an
inadvertent extubation. A gag reflex is a
forceful, symmetrical
lowering of the soft palate. The cough reflex
is usually
assessed only in patients with an
endotracheal tube. This
reflex is elicited by gently passing a suction
catheter through
the tube and stimulating a cough. Loss of
these reflexes is
indicative of lower brainstem damage.
• Cranial Nerves.
Testing each CN is an essential
part of the
• neurologic examination
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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD

• A good screening test for both balance

• Motor System. and muscle strength is
The motor system examination to observe the patient’s stature (posture
includes assessment of strength, tone, while standing) and
coordination, gait. Note the pace and rhythm of the gait
and symmetry of the major muscle groups. and observe for
normal symmetric and oppositional arm
• Test muscle strength by asking the patient swing.
to push • The patient’s ability to ambulate helps to
and pull against the resistance of your arm determine the level
as it of nursing care required and the risk of
opposes flexion and extension of the falling.
patient’s
muscle. Ask the patient to offer resistance • The finger-to-nose test (having the patient
at the alternately touch
shoulders, elbows, wrists, hips, knees, and the nose, then touch the examiner’s finger)
ankles. and the
heel-to-shin test (having the patient stroke
• Test muscle tone by passively moving the the heel of one
limbs through their foot up and down the shin of the opposite
range of motion. There should be a slight leg) test
resistance to these coordination and cerebellar function.
movements. • Other tests include asking the patient to
• Abnormal tone is described as hypotonia pronate and supinate
(flaccidity) or both hands rapidly and to do a shallow
hypertonia (spasticity). Note any involuntary knee bend, first on
movements such one leg and then on the other. Note
as tics, tremor, myoclonus (spasm of dysarthria or slurred
muscles), athetosis speech because it is a sign of
(slow, writhing, involuntary movements of incoordination of the speech
extremities), muscles.
chorea (involuntary, purposeless, rapid
motions), and • Sensory System.
dystonia (impairment of muscle tone). Several modalities are tested in the somatic
sensory examination. Each modality is
• Test cerebellar function by assessing carried by a specific
balance and ascending pathway in the spinal cord
coordination. before it reaches the
sensory cortex.
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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD
• As a rule, perform the examination with
the patient’s eyes
closed and avoid providing the patient with
clues. Ask “How
does this feel?” rather than “Is this sharp?”
• Touch, Pain, and Temperature.
• Light touch is usually tested first using a
cotton wisp or light pin prick.
• Gently touch each of the four extremities
and ask the patient to indicate
when he or she feels the stimulus.
• Test pain by alternately touching the skin
with the sharp and dull end of a
pin. Tell the patient to respond “sharp” or
“dull.” Evaluate each limb
separately.
• Extinction is assessed by simultaneously
touching both sides of the body
symmetrically. Normally, the simultaneous
stimuli are both perceived
(sensed). An abnormal response occurs
when the patient perceives the
stimulus on only one side. The other
stimulus is “extinguished.”
• The sensation of temperature (only to be
tested when the response to
deep pain is abnormal) can be tested by
applying tubes of warm and cold
water to the skin and asking the patient to
identify the stimuli with the
eyes closed. If pain sensation is intact,
assessment of temperature
sensation may be omitted because both
sensations are carried by the
same ascending pathways.
• Vibration Sense.
Assess vibration sense by applying a
vibrating
tuning fork to the fingernails and the bony
prominences of the
hands, legs, and feet. Ask the patient if the
vibration or “buzz” is
felt. Then ask the patient to indicate when
the vibration ceases.
• Position Sense.
Assess position sense (proprioception) by
placing
your thumb and forefinger on either side of
the patient’s
forefinger or great toe and gently moving
his or her digit up or
down. Ask the patient to indicate the
direction in which the digit is
moved.
• Another test of proprioception is the
Romberg test. Ask the
patient to stand with feet together and then
close his or her eyes.
If the patient is able to maintain balance
with the eyes open but
sways or falls with the eyes closed (i.e., a
positive Romberg test),
vestibulocochlear dysfunction or disease in
the posterior columns
of the spinal cord may be indicated. Be
aware of patient safety
during this test.
• Cortical Sensory Functions.
Several tests evaluate cortical
integration of sensory perceptions (which
occurs in the parietal
lobes).
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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD

• Assess two-point discrimination by placing muscle) is measured as follows:

the two points of a – 0/5 = absent,
calibrated compass on the tips of the – 1/5 = weak response
fingers and toes. The – 2/5 = normal response
minimum recognizable separation is 4 to 5 – 3/5 = exaggerated response,
mm in the fingertips – 4/5 = hyperreflexia with clonus.
and a greater degree of separation • Clonus, an abnormal response, is a
elsewhere. This test is continued rhythmic
important in diagnosing diseases of the contraction of the muscle with continuous
sensory cortex and PNS. application of the
• Graphesthesia (ability to feel writing on stimulus.
skin) is tested by having
the patient identify numbers traced on the • ASSESSMENT OF THE INJURED
palm of the hands. BRAIN
• Stereognosis (ability to perceive the form • The primary aim of managing patients with
and nature of objects) is acute brain injury
tested by having the patient close the eyes in the critical care unit is to maintain
and identify the size cerebral perfusion and
and shape of easily recognized objects oxygenation.
(e.g., coins, keys, safety • Continuous monitoring of the central
pin) placed in the hands. nervous system in the
ICU serves three functions:
• Reflexes. • 1. determine the extent of the primary
Tendons have receptors that are sensitive injury
to stretch. • 2. early detection of secondary cerebral
• A reflex contraction of the skeletal muscle insults so that
occurs when the appropriate interventions can be instituted
tendon is stretched. In general, the biceps, • 3. monitoring of therapeutic interventions
triceps, to provide
brachioradialis, and patellar and Achilles feedback.
tendon reflexes are
tested. Brain Imaging Techniques
• Initiate a simple muscle stretch reflex by • Computed tomography
briskly tapping the • CT is the primary neuroimaging technique
tendon of a stretched muscle, usually with a in the
reflex hammer. initial evaluation of the acute brain injury
patient and
• The response (muscle contraction of the uses a computer to digitally construct an
corresponding image
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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD
based upon the measurement of the
absorption of
X-rays through the brain.
• The advantages of CT are: (1) it is rapidly
done, which is
especially important in neurological
emergencies; (2) it clearly
shows acute and sub-acute hemorrhages
into the meningeal
spaces and brain; and (3) it is less
expensive than a MRI.
• Disadvantages include: (1) it does not
clearly show acute or
sub-acute infarcts or ischemia, or brain
edema, only
established injury; (2) it does not clearly
differentiate white
from grey matter as clearly as an MRI; and
(3) it exposes the
patient to ionizing radiation. Despite these
limitations it is still
the most prevalent form of neurological
imaging.
• Magnetic resonance imaging
• The tissues of the body contain
proportionately large
amounts of protons in the form of hydrogen
and function like
tiny spinning magnets. Normally, these
atoms are arranged
randomly in relation to each other due to
the constantly
changing magnetic field produced by the
associated
electrons. Magnetic Resonance Imaging
(MRI) uses this
characteristic of protons to generate images
of the brain and
body.
• The advantages of MRI are: (1) it can be
manipulated to
visualize a wide variety of abnormalities
within the brain; and
(2) it can show a great deal of detail of the
brain in normal
and abnormal states.
• The disadvantages of MRI are: (1) it does
not show acute or
sub-acute hemorrhage into the brain in any
detail; (2) the
time frame and enclosed space required to
perform and
prepare a patient for the procedure is not
advantageous for
neurological emergencies; (3) relatively
more expensive
compared to CT; (4) the loud noise of the
procedure needs to
be considered in the patient management;
and (5) equipment
for life support and monitoring needs to be
non-magnetic due
to the magnetic nature of the procedure
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• Cerebral angiography
• Cerebral angiography involves
cannulation of cerebral vessels
and the administration of intraarterial
contrast agents and
medications for conditions involving the
arterial circulation of
the brain. This procedure also has the
benefit of using
non-invasive CT or MRI with or without
contrast to guide the
• Intracranial Pressure Monitoring
accuracy of the procedure. For example,
• Invasive measures for monitoring
intracranial
intracranial pressure (ICP)
aneurysms and arteriovenous
are commonly used in patients with a
malformations can be
severe head injury or
accurately diagnosed and repaired without
after neurological surgery.
surgical
• The normal ICP is 7–15 mmHg in a supine
intervention.
adult, 3–7 mmHg in
children, and 1.5–6 mmHg in term infants.
• Cerebral perfusion imaging techniques
The definition of
• The main imaging techniques dedicated to
intracranial hypertension depends on the
brain
specific pathology
hemodynamics are positron emission
and age, although ICP >15 mmHg is
tomography (PET),
generally considered to
single photon emission computed
be abnormal.
tomography (SPECT),
xenon-enhanced computed tomography
• Pulse waveforms
(XeCT), dynamic
• Interpretation of waveforms that are
perfusion computed tomography (PCT),
generated by the
MRI dynamic
cerebral monitoring devices is important in
susceptibility contrast (DSC) and arterial
the clinical
spin labelling (ASL).
assessment of intracranial adaptive
All these techniques give similar information
capacity (the ability of the
about brain
brain to compensate for rises in intracranial
hemodynamics in the form of parameters
volume without
such as CBF or CBV.
raising the ICP).
• Brain tissue pressure and ICP increase
with each cardiac cycle
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 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD
and, thus, the ICP waveform is a modified
arterial pressure
wave.
• The cardiac waves reach the cranial
circulation via the choroid
plexus and resemble the waveforms
transmitted by arterial
catheters, although the amplitude is lower.
• There are three distinct peaks seen in the
ICP waveform:61
• P1: the percussion wave, which is sharp
and reflects the
cardiac pulse as the pressure is transmitted
from the choroid
plexus to the ventricle;
• P2: the tidal wave, which is more variable
in nature and
reflects cerebral compliance and increases
in amplitude as
compliance decreases;
• P3: which is due to the closure of the
aortic valve and is
known as the dicrotic notch. Of recent
importance is that the
elevation of the P3 may indicate low global
cerebral
perfusion.
• Assessment of Cerebral Perfusion
• Cerebral perfusion pressure is calculated
as the
mean arterial pressure minus the
intracranial
pressure (ICP) and represents the pressure
gradient across the vessel that drives
cerebral
blood flow (CBF):
• CPP=MAP−ICP
• CPP is a pressure-based indicator of
oxygen and
metabolite delivery. There is no evidence
for the
optimum level of CPP, but 70–80 mmHg is
probably the critical
• ASSESSMENT OF CEREBRAL
OXYGENATION
• Jugular Venous Oximetry
• Jugular venous catheterization is used for
deriving oxygen
based variables.
• It facilitates the assessment of jugular
venous oxygenation
(SjvO2), cerebral oxygen extraction
(CEO2), and arteriovenous
difference in oxygen (AVDO2).
• All of these variables indicate changes in
cerebral metabolism
and blood flow, and therefore the catheter
generates
continuous data that reflect the balance
between supply and
demand of cerebral oxygen.
• Microdialysis
• Cerebral microdialysis (using a catheter
ideally placed in the
frontal lobe) is a tool for investigating the
metabolic status of
the injured brain and is part of multimodal
monitoring.
• The microdialysis probe is inserted into
the cerebral tissue
where substances in the extracellular fluid
surround the
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semipermeable membrane at the tip of the
catheter.
• Following equilibration of the tissue
metabolites with the
perfusion fluid, the dialysate can be
analyzed for
concentrations of products of energy
metabolism (glucose,
lactate, pyruvate) as indicators of hypoxia
and ischemia.
• Continuous Electroencephalography
• Electroencephalography (EEG) is the
recording of electrical
activity by sensors along the scalp
produced by the firing of
neurons within the brain.
• Continuous EEG (cEEG) has the
advantage of being
continuous, noninvasive and carrying the
potential to detect
alterations in brain physiology at a
reversible stage, which
may trigger treatment before permanent
brain injury occurs.
• Near-Infrared Spectroscopy
• Near-infrared spectroscopy (NIRS) is a
non-invasive method of
monitoring continuous trends of cerebral
oxygenated and
deoxygenated haemoglobin by utilising an
infrared light beam
transmitted through the skull. Oxygenated
and deoxygenated
haemoglobin have different absorption
spectra and cerebral
oxygenation and hemodynamic status can
be determined by
their relative absorption of near-infrared
light. NIRS allows
interrogation of the cerebral cortex using
reflectance
spectroscopy via optodes, light transmitting
and detecting
devices, placed on the scalp. Normal
saturation is 70%.
Neurological Alterations and
Management
• ALTERATIONS IN CONSCIOUSNESS
• In critical illness, impaired consciousness
is often the first sign
of a severe pathological process.
Consciousness is defined as
recognition of self and the environment,
which requires both
arousal and awareness. There are different
types of
depressed consciousness through to coma,
the most severe
form of absolute unconsciousness.
• Altered Cognition and Coma
• Coma is a state of unresponsiveness from
which the patient,
who appears to be asleep, cannot be
aroused by verbal and
physical stimuli to produce any meaningful
response;
therefore, the diagnosis of coma implies the
absence of both
arousal and content of consciousness.1
Coma must be
considered a symptom with numerous
causes, different
natural modes, and several management
modes.
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• Stupor is a state of unconsciousness from
which the patient
can be awakened to produce inadequate
responses to verbal
and physical stimuli.
• Somnolence is a state of
unconsciousness from which the
patient can be fully awakened.
• Etiology of altered cognition
• Recently gained confusion, severe apathy,
stupor or coma implies
dysfunction of the cerebral hemispheres,
the diencephalon and/or the
upper brainstem.
• Focal lesions in supratentorial structures
may damage both hemispheres,
or may produce swelling that compresses
the diencephalic activating
system and midbrain, causing transtentorial
herniation and brainstem
damage.
• Primary subtentorial (brainstem or
cerebellar) lesions may compress or
directly damage the reticular formation
anywhere between the level of
the midpons and, (by upward pressure), the
diencephalon.
• Metabolic or infectious diseases may
depress brain functions by a change
in blood composition or the presence of a
direct toxin. Impaired
consciousness may also be due to reduced
blood flow (as in syncope or
severe heart failure) or a change in the
brain’s electrical activity (as in
epilepsy).
• Concussion, anxiolytic drugs and
anesthetics impair consciousness without
producing detectable structural changes in
the brain.
• Seizures
• A seizure is an uninhibited, abrupt
discharge of ions from a
group of neurons resulting in epileptic
activity.
• Seizures are classified depending on how
they start as (a)
partial or focal seizures, (b) generalized or
full body seizures
involving both cerebral hemispheres, or (c)
partial seizures
with secondary generalization.
Etiology of seizures
• Seizures can be due to vascular,
infectious, neoplastic,
traumatic, degenerative, metabolic, toxic or
idiopathic causes.
• Factors influencing the development of
posttraumatic
epilepsy include an early posttraumatic
seizure, depressed
skull fracture, intracranial hematoma, dural
penetration, focal
neurological deficit and posttraumatic
amnesia (PTA) over 24
hours with the presence of a skull fracture
or hematoma.
• Seizures in critically ill patients are most
commonly due to
drug effects; metabolic, infectious or toxic
disorders; and
intracranial mass lesions although they may
be due to trauma
or neoplasm
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Professor: Mary Grace Suplido, RN, MD
• ALTERATIONS IN MOTOR AND
SENSORY FUNCTION
• Alterations of motor and sensory function
include skeletal
muscle weakness and paralysis. They
result from lesions in
the voluntary motor and sensory pathways,
including the
upper motor and sensory neurons of the
corticospinal and
corticobulbar tracts, or the lower motor and
sensory neurons
that leave the CNS and travel by way of the
peripheral nerve
to the muscle and sensory receptors.
• Upper motor neuron lesions produce
spastic
paralysis, and lower motor neuron lesions
produce
flaccid paralysis. Damage to the upper
motor and
sensory neurons of the corticospinal,
corticobulbar
and spinothalamic tracts is a common
component of
stroke.
• Lesions of the corticospinal and
corticobulbar tracts: result in
weakness or total paralysis of
predominantly distal voluntary
movement, Babinski’s sign (i.e. dorsiflexion
of the big toe and
fanning of the other toes in response to
stroking the outer
border of the foot from heel to toe), and
often spasticity
(increased muscle tone and exaggerated
deep tendon
reflexes).
• Disorders of the basal ganglia:
(extrapyramidal disorders) do
not cause weakness or reflex changes.
• Their hallmark is involuntary movement
(dyskinesia), causing
increased movement (hyperkinesias) or
decreased movement
(hypokinesia) and changes in muscle tone
and posture.
• Cerebellar disorders: cause abnormalities
in the range, rate
and force of movement. Strength is
minimally affected.
• Autonomic Nerve Dysfunction
• Dysfunctions of the autonomic nervous
system (ANS) or
autonomic dysreflexia are recognised by
the symptoms that
result from failure or imbalance of the
sympathetic or
parasympathetic components of the ANS
such as (i) increased
(>120/min) or decreased (<50/min) heart
rate, (ii) increased
respiratory rate (>24/min), (iii) raised
temperature (>38.5°C),
(iv) increased (>160 mmHg) or decreased
(<85 mmHg) systolic
blood pressure, (v) increased muscle tone,
(vi) decerebrate
(extensor) or decorticate (flexor) posturing,
and (vii) profuse
sweating.
29 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
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Professor: Mary Grace Suplido, RN, MD
• ALTERATIONS IN CEREBRAL
METABOLISM aND PERFUSION
• Impairment of cerebral metabolism has
been attributed to
impaired oxygen delivery, mediated by
reduced cerebral
perfusion in the swollen cerebral
parenchyma.
• Cerebral Ischemia
• Ischemia is the inadequate delivery of
oxygen, the inadequate
removal of carbon dioxide from the cell, and
an increase in
the production of intracellular lactic acid.
• Ischemia can be caused by an increase in
nutrient utilization
by the brain in a hyperactive state, a
decrease in delivery
related to either cerebral or systemic
complications, and/or a
mismatch between delivery and demand.
• Cerebral Edema
• Cerebral edema is defined as increased
brain water content.
The brain is particularly susceptible to injury
from edema,
because it is located within a confined
space and cannot
expand, and because there are no
lymphatic pathways within
the CNS to carry away the fluid that
accumulates.
• The white matter is usually much more
involved, as
myelinated fibres have a loose extracellular
space, while the
grey matter has a much higher cell density
with many
connections and much less loose
extracellular space.
• The two main subdivisions of cerebral
edema are extracellular
and intracellular.
• Intracellular (cytotoxic) oedema
• Cellular swelling, usually of astrocytes in
the grey matter, is
generally seen after cerebral ischemia
caused by cardiac
arrest or minor head injury. The blood–brain
barrier (BBB) is
intact and capillary permeability is not
impaired. The cause of
intracellular edema is anoxia and ischemia;
it is usually not
clinically significant, and is reversible in its
early phases.
• Extracellular (vasogenic) edema
• Extracellular edema involves increased
capillary permeability,
and had been termed ‘BBB breakdown’.20
Rises in brain
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water content with extracellular edema are
often quite
dramatic, because the fluid that results from
increased
capillary permeability is usually rich in
proteins, resulting in
the spread of edema and brain ischemia.
This can lead to
cytotoxic edema, and to the progressive
breakdown of both
astrocytes and neurons. Ultimately, these
changes can lead to
raised intracranial pressure and herniation.
• Hydrocephalus
• Hydrocephalus is the result of an
imbalance between the
formation and drainage of cerebrospinal
fluid (CSF). Reduced
absorption most often occurs when one or
more passages
connecting the ventricles become blocked,
preventing
movement of CSF to its drainage sites in
the subarachnoid
space just inside the skull. This type of
hydrocephalus is called
‘non-communicating’. Reduction in
absorption rate, called
‘communicating hydrocephalus’ can be
caused by damage to
the absorptive tissue.
• Hydrocephalus may be caused by:
congenital brain defects;
hemorrhage, in either the ventricles or the
subarachnoid
space; CNS infection (syphilis, herpes,
meningitis, encephalitis
or mumps); and tumors.
• Irritability is the commonest sign of
hydrocephalus in infants
and, if untreated, may lead to lethargy.
Bulging of the
fontanel, the soft spot between the skull
bones, may also be
an early sign. Hydrocephalus in infants
prevents fusion of the
skull bones, and causes expansion of the
skull.
• Symptoms of normal pressure
hydrocephalus include
dementia, gait abnormalities and
incontinence.
• Treatment includes ventriculostomy
drainage of CSF in the
short term, or a surgical shunt for those with
chronic
conditions. Either is predisposed to
blockage and infection.
• Intracranial Hypertension
• Intracranial pressure is the pressure
exerted by the contents
of the brain within the confines of the skull
and the BBB. The
Munro–Kelly hypothesis states that the
contents of the
cranium (60% water, 40% solid) are not
compressible and
thus an increase in volume causes a rapid
rise in pressure and
changes to the comensatory reserve and
pulse amplitude.
• Normal ICP is 0–10 mmHg, and a
sustained pressure of >15
mmHg is termed intracranial hypertension,
with implications
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for CBF. Areas of focal ischemia appear • Management of Intracranial Hypertension

when ICP is >20 • Raised ICP is treated by removing mass
mmHg and global ischemia occurs at >50 lesions and/or
mmHg. increasing the volume available for
expansion of injured
NEUROLOGICAL THERAPEUTIC tissue. This may be achieved by reducing
MANAGEMENT one of the other
• OPTIMISING CEREBRAL PERFUSION available intracranial fluid volumes:
AND OXYGENATION • 1. CSF by ventricular drainage (as
• Intracranial hypertension and cerebral discussed previously)
ischemia are the two • 2. cerebral blood volume by
most important secondary injury processes hyperventilation, osmotic
that can be diuretic therapy or hypothermia
anticipated, monitored and treated in the • 3. brain tissue water content by osmotic
ICU. diuretic therapy
• 4. removing swollen and irreversibly
injured brain
• 5. increasing cranial volume by
craniotomy decompression.

• Hyperventilation
• Hyperventilation reduces PaCO2 and will
reduce ICP by
vasoconstriction induced by alkalosis but it
also decreases
cerebral blood flow. The fall in ICP parallels
the fall in CBV.
Hyperventilation decreases regional blood
flow to
hypoperfused areas of the brain. Thus,
generally PaCO2
should be maintained in the low normal
range of about 35
mmHg. Hyperventilation should be utilised
only when ICP
elevations are refractory to other methods
and when brain
tissue oxygenation is in the normal range.
The BTF Guidelines
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recommend hyperventilation therapy only
for brief periods
when there is no neurological deterioration
or for longer
periods when ICP is refractory to other
therapies
• Osmotherapy
• Acute administration of an osmotic such
as mannitol or
hypertonic saline produces a potent
antioedema action,
primarily on undamaged brain regions with
an intact BBB. This
treatment causes the movement of water
from the interstitial
and extracellular space into the
intravascular compartment,
thereby improving intracranial compliance
or elastance. In
addition to causing ‘dehydration’ of the
brain, osmotic agents
have been shown to exert beneficial
non-osmotic cerebral
effects, such as augmentation of cerebral
blood flow (by
reducing blood viscosity, resulting in
enhanced oxygen
delivery), free radical scavenging, and
diminishing CSF
formation and enhancing CSF reabsorption
• Normothermia
• Hyperthermia occurs in up to 40% of
patients with ischemic stroke and
intracerebral hemorrhage and in 40–70% of
patients with severe TBI or
aneurysmal subarachnoid haemorrhage.
• Hyperthermia is independently associated
with increased morbidity and
mortality after ischemic and hemorrhagic
stroke, and in subarachnoid
hemorrhage and TBI patients temperature
elevation has been linked to
raised intracranial pressure. Temperature
elevations as small as 1–2°C
above normal can aggravate ischemic
neuronal injury and exacerbate
brain edema.
• Mild hypothermia protects numerous
tissues from damage during
ischemic insult. The use of paracetamol,
cooling blankets, ice packs,
evaporative cooling and new cooling
technologies may be useful in
maintaining normothermia.
• Hyperemia (increased blood flow) may
occur during rewarming, resulting
in acute brain swelling and rebound
intracranial hypertension.
• Maintenance of body temperature at 35°C
may be optimal.
• Corticosteroids
• Excessive inflammation has been
implicated in the
progressive neurodegeneration that occurs
in multiple
neurological diseases, including cerebral
ischemia.
• The efficacy of glucocorticoids is well
established in
ameliorating edema associated with brain
tumors and in
improving the outcome in subsets of
patients with bacterial
meningitis.
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• haematoma, is accepted practice. Surgery

• Barbiturates and sedatives is also
• The BTF Guidelines state that high-dose • recommended for open compound
barbiturate therapy depressed skull
may be considered in haemodynamically fractures
salvageable severe • that cause a mass effect
TBI patients with intracranial hypertension
refractory to • CENTRAL NERVOUS SYSTEM
maximal medical and surgical interventions. DISORDERS
• The utilization of barbiturates for the • CNS disorders include brain and/or spinal
prophylactic treatment injury from trauma, infection or immune
of ICP has not been indicated. conditions.
• Barbiturates exert cerebral protective and
ICP-lowering • TRAUMATIC BRAIN INJURY
effects through alteration in vascular tone, • Head injury is a broad classification that
suppression of includes injury to the
metabolism and inhibition of free scalp, skull or brain.
radical-mediated lipid • Traumatic brain injury (TBI) is the most
peroxidation. serious form of head
• Barbiturates may effectively lower cerebral injury. The range of severity of TBI is broad,
blood flow and from concussion
regional metabolic demands. through to post coma unresponsiveness
• The lower metabolic requirements
decrease cerebral blood • Etiology
flow and cerebral volume. • Motor vehicle-related trauma accounts for
about
• Surgical interventions two-thirds of moderate and severe TBI, with
• The European TBI Guidelines suggest falls and
that operative assaults being the next most common
management causes.
• be considered for large intracerebral
lesions Pathophysiology of TBI
• within the first four hours of injury. The use • The mechanisms of injury forces inflicted
of unilateral on the head in TBI produce a complex
• craniectomy after the evacuation of a mixture of diffuse and focal lesions within
mass lesion, such the brain
• as an acute subdural haematoma or • Damage resulting from an injury can be
traumatic intracerebral immediate (primary) or secondary in nature.

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• Secondary injury results from disordered • Skull fractures

auto • Skull fractures are present on CT scans in
regulation and other pathophysiological about twothirds of
changes within the brain in the days patients after TBI. Skull fractures can be
immediately after injury. linear, depressed or
diastatic, and may involve the cranial vault
• Focal injury or skull base. In
• Because of the shape of the inner surface depressed skull fractures the bone
of fragment may cause a
the skull, focal injuries are most commonly laceration of the dura mater, resulting in a
seen in the frontal and temporal lobes, but cerebrospinal fluid
they can occur anywhere. leak.
• Basal skull fractures include fractures of
• Diffuse injury the cribriform plate,
• Diffuse (axonal) injury (DAI) refers to the frontal bones, sphenoid bones, temporal
shearing of axons and bone and occipital
supporting neuroglia; it may also traumatise bones.
blood vessels and can • The clinical signs of a basal skull fracture
cause petechial haemorrhages, deep may include: CSF
intracerebral haematomas otorrhoea or rhinorrhoea, haemotympanum,
and brain swelling. postauricular
• DAI results from the shaking, shearing ecchymoses, periorbital ecchymoses, and
and inertial effects of a injury to the cranial
traumatic impact. Mechanical damage to nerves: VII (weakness of the face), VIII
small venules as part of (loss of hearing), olfactory
the BBB can also trigger the formation of (loss of smell), optic (vision loss) and VI
haemorrhagic (double vision).
contusions. This vascular damage may
increase neuronal • Nursing Practice
vulnerability, causing post-traumatising • The surveillance and prevention of
perfusion deficits and the secondary
extravasation of potentially neurotoxic injury is the key to improving morbidity and
blood-borne substances. mortality outcomes.
• The most consistent effect of diffuse brain
damage, even when
mild, is the presence of altered
consciousness

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SPINAL CORD TRAUMA
• SCI occurs three times more often in men,
and the incidence
among those aged 15–34 years is roughly
double the rate in
those 35 years and over. More than half of
the SCIs are due
to vehicular trauma and a quarter due to
motorcycle crashes.
Falls account for nearly a third of the
injuries, with nearly half
occurring in older people.
• Recreational and sporting injuries account
for 15% of SCI, and
19% are work-related. Of all SCI cases,
51% resulted in
complete tetraplegia (loss of function in the
arms, legs, trunk
and pelvic organs). The predominant risk
factors for SCI
include age, gender, and alcohol and drug
use.
• The vertebrae most often involved in SCI
are the 5th, 6th and
7th cervical (neck), the 12th thoracic, and
the 1st lumbar.
These vertebrae are the most susceptible
because there is a
greater range of mobility in the vertebral
column in these
areas.
• Damage to the spinal cord ranges from
transient concussion
or stunning (from which the patient fully
recovers) to
contusion, laceration and compression of
the cord substance
(either alone or in combination), to
complete transection of
the cord (which renders the patient
paralysed below the level
of the injury).
• Mechanisms of Injury
• Cervical injury can occur from both blunt
and penetrating trauma but in reality is a
combination of different mechanisms of
acceleration and deceleration with and
without rotational forces and axial loading
Cervical trauma is produced by a
combination of these mechanisms as listed
below
• l Hyperflexion: These injuries usually
result from forceful decelerations
and are often seen in patients who have
sustained trauma from a head-on
motor vehicle collision (MVC) or diving
accident. The cervical region is
most often involved, especially at the
C5–C6 level.
• l Vertical compression or axial loading:
This typically occurs when a person
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lands on the feet or buttocks after falling or
jumping from a height. The
vertebral column is compressed, causing a
fracture that result in damage
to the spinal cord.
• l Hyperextension: This is the most
common type of injury. Hyperextension
injuries can be caused by a fall, a rear-end
MVC, or hit on the head (e.g.
during a boxing match). Hyperextension of
the head and neck may cause
contusion and ischaemia of the spinal cord
without vertebral column
damage. Whiplash injuries are the result of
hyperextension. Violent
hyperextension with fracture of the pedicles
of C2 and forward movement
of C2 on C3 produces the ‘Hangman’s
fracture’.
• Extension–rotation: Rotational injuries
result from forces that
cause extreme twisting or lateral flexion of
the head and
neck. Fracture or dislocation of vertebrae
may also occur. The
spinal canal is narrower in the thoracic
segment relative to
the width of the cord, so when vertebral
displacement occurs
it is more likely to damage the cord. Until
the age of , the
spine has increased physiological mobility
due to lax
ligaments, which affords some protection
against acute SCI.
Elderly patients are at a higher risk due to
osteophytes and
narrowing of the spinal canal.
• Classification of Spinal Cord Injuries
• SCIs can be broadly classified as
complete or incomplete.
• The diagnosis of complete SCI cannot be
made until spinal
cord shock resolves. If the bulbocavernosus
reflex (BCR) is
present (involuntary contraction of the rectal
sphincter after
squeezing the glans penis or clitoris or
tugging on an
indwelling urinary catheter) it indicates a
complete injury.
• If, after the return of the BCR, the patient
has some sensation
below the level of injury, he/she is
considered to be
sensory-incomplete.
• If the BCR has returned and the patient
has some motor
function and sensation below the level of
injury, he/she is
considered to be sensory- and
motor-incomplete.
There are four incomplete SCI
syndromes as follows:
• Anterior cord syndrome: Injury to the
motor and sensory
pathways in the anterior parts of the spine;
thus patients are
able to feel crude sensation, but movement
and detailed
sensation are lost in the posterior part of
the spinal cord.
Clinically, the patient usually has complete
motor paralysis
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below the level of injury (corticospinal
tracts) and loss of
pain, temperature, and touch sensation
(spinothalamic
tracts), with preservation of light touch,
proprioception and
position sense. The prognosis for anterior
cord syndrome is
the worst of all the incomplete syndrome
prognoses.
• Posterior cord syndrome: This is usually
the result of a
hyperextension injury at the cervical level
and is not
commonly seen. Position sense, light touch
and vibratory
sense are lost below the level of the injury.
• Central cord syndrome: Injury to the
center of the cervical spinal
cord, producing weakness, paralysis and
sensory deficits in the
arms but not the legs. Hyperextension of
the cervical spine is
often the mechanism of injury, and the
damage is greatest to the
cervical tracts supplying the arms. Clinically,
the patient may
present with paralyzed arms but with no
deficit in the legs or
bladder.
• Brown-Séquard syndrome: This
involves injury to the left or right
side of the spinal cord. Movements are lost
below the level of
injury on the injured side, but pain and
temperature sensation are
lost on the opposite side of injury. The
clinical presentation is one
in which the patient has either increased or
decreased cutaneous
sensation of pain, temperature and touch
on the same side of the
spinal cord at the level of the lesion. Below
the level of the lesion
on the same side, there is complete motor
paralysis. On the
patient’s opposite side, below the level of
the lesion, there is loss
of pain, temperature and touch, because
the spinothalamic
tracts cross soon after entering the cord.
Pathophysiology
• SCIs can be separated into two
categories: primary injuries
and secondary injuries.
• Primary injuries are the result of the initial
insult or trauma,
and are usually permanent. The force of the
primary insult
produces its initial damage in the central
grey matter of the
cord.
• Secondary injuries are usually the result of
a contusion or
tear injury, in which the nerve fibers begin to
swell and
disintegrate. Secondary neural injury
mechanisms include
ischemia, hypoxia and edema
• Ischemia, the most prominent post-SCI
event, may occur up to 2
hours post-injury and is intensified by the
loss of auto regulation
of the spinal cord microcirculation This will
decrease blood flow,
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which is then dependent on the systemic
arterial pressure in the
presence of hypotension or vasogenic
spinal shock.
• Edema develops at the injured site and
spreads into adjacent
areas.
• Hypoxia may occur as a result of
inadequate airway maintenance
and ventilation. Immune cells, which
normally do not enter the
spinal cord, engulf the area after a spinal
cord injury and release
regulatory chemicals, some of which are
harmful to the spinal
cord. Highly reactive oxidizing agents (free
radicals) are produced,
which damage the cell membrane and
disrupt the
sodium–potassium pump. Free-radical
production and lipid
peroxidation lead to vasoconstriction,
increased endothelial
permeability and increased platelet
activation.
• Spinal shock occurs with physiological or
anatomical
transection or near-transection of the spinal
cord; it occurs
immediately or within several hours of a
spinal cord injury
and is caused by the sudden cessation of
impulses from the
higher brain centers.
• It is characterized by the loss of motor,
sensory, reflex and
autonomic function below the level of the
injury, with
resultant flaccid paralysis.
• Loss of bowel and bladder function also
occurs
• The body’s ability to control temperature
(poikilothermia) is
lost and the patient’s temperature tends to
equilibrate with that of the external
environment.
• Neurogenic spinal shock occurs as a
result of mid-
tupper-level cervical injuries and is the
result of sympathetic vascular denervation
and peripheral vasodilation.
• The loss of spinal cord vasculature
autoregulation occurs,
causing the blood flow to the spinal cord to
be dependent on
the systemic blood pressure. Signs and
symptoms include
hypotension, severe bradycardia, and loss
of the ability to
sweat below the level of injury.
Systemic effects of spinal cord injury
• The traumatic insult causing the spinal
cord injury is
associated with an immediate stimulation of
central and
peripheral sympathetic tone.
• Initially, the elevated sympathetic activity
raises systemic
arterial blood pressure and induces cardiac
arrhythmias.
• At the stage of spinal shock with loss of
neuronal conduction,
the sympathetic excitation is closely
followed by decreases in
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systemic vascular resistance, arterial
hypotension and venous
pooling.
• Spinal cord injury may produce respiratory
failure.
• Injuries above the level of C4–C5 produce
complete paralysis
of the diaphragm, with substantial
decreases in tidal volume
and consecutive hypoxia.
• With lesions below C6, the function of the
diaphragm is
maintained and there is incomplete
respiratory failure due to
paralyzed intercostal and abdominal
musculature.
• As a consequence, arterial hypoxia and
• hypercapnia occur, both of which promote
neuronal and glial
acidosis, edema and neuroexcitation.
• Nursing Practice
• Spinal cord injury should be suspected in
patients with neck
pain, sensory and motor deficits,
unconsciousness,
intoxication, spondylitis or rheumatoid
arthritis, head injury
and facial fractures.
• If spinal cord injury is suspected or cannot
be excluded, the
patient must be placed on a spine board
with the head and
neck immobilized in a neutral position using
a rigid collar to
reduce the risk of neurological deterioration
from repeated
mechanical insults.
• Spinal injury patients are susceptible to
pressure insults, so
time must be considered when hard
surfaces are used for
immobilization. Total neck immobilization
should not
interfere with maintenance of the airway,
and inadequate
respiratory function must be avoided
• Resuscitation
• Initial treatment aims for decompression of
the spinal cord and reversal of
neurogenic shock and respiratory failure.
• Spinal shock is associated with decreases
in systemic vascular resistance,
arterial hypotension, venous pooling,
severe bradycardia and decreased
myocardial contractility.
• Treatment of neurogenic shock includes
fluid replacement using
crystalloid or colloid solutions to maintain
arterial blood pressure,
circulatory volume, renal function and tissue
oxygenation.
• Infusion of free water must be avoided, as
this decreases plasma
osmolarity and promotes spinal cord
edema.
• Atropine may be administered to reverse
bradycardia and increase cardiac
output. Administration of vasopressors (e.g.
noradrenaline) prior to
correction of the intravascular volume
status may increase systemic
vascular resistance (left ventricular
afterload) and further impair
myocardial contractility.
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• Therefore, volume replacement is the first
step, and
administration of vasopressors the second
step in the
treatment of arterial hypotension and low
cardiac output
after acute cervical spinal cord injury.
• The major early cause of death in patients
with acute cervical
SCI is respiratory failure. Tracheal
intubation may be indicated
in unconscious patients, during shock, in
patients with other
major associated injuries, and during
cardiovascular and
respiratory distress. It is also indicated in
conscious patients
presenting with the following criteria:
maximum expiratory
force below +20 cmH2O, maximum
inspiratory force below
−20 cmH2O, vital capacity below 1000 mL,
and presence of
atelectasis, contusion and infiltrate.
• Investigations and alignment
• Following the initial assessment of the
patient, detailed
diagnostic radiography defines the bone
damage and
compression of the spinal cord.
• Collaborative Management
• Patients with acute cervical spinal cord
injury require ICU
monitoring, observation and support of
ventilation, a
nasogastric tube to reduce abdominal
distension and risk of
aspiration, a urinary catheter and thermal
maintenance.
• Tracheostomy is indicated in high cervical
spine injury and
ischemia,
• Spinal alignment and immobilization
requires careful
positioning with dedicated neck support by
experienced
clinicians.
• l Shoulder and lumbar support pillows are
often prescribed.
Pressure-relief mattresses must be suitably
designed for spine
immobilization and when prescribed can be
tilted to facilitate
ventilation.
• l Meticulous integument and bowel care
are indicated with
daily protocols for regular stool softeners
and peristaltic
stimulants essential for the prevention of
autonomic
dysreflexia and autonomic nerve
dysfunction.
• Early nutritious feeding is essential,
whether oral or enteric; however,
aspiration must be prevented. The
supplementation of feeding with
high-energy protein fluids to match the
catabolic state assists with
recovery
• Hyperglycaemia is associated with
increased inflammation and must be
controlled to less than 10 mmol/Hg,
avoiding hypoglycaemia.
• The concept of pain relief and sedation in
patients with spinal cord injury
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is based on the maintenance of coupling
between metabolism and spinal
cord blood flow while achieving hypnosis,
analgesia and a ‘relaxed cord’.
This concept includes maintenance of
normal to high systemic perfusion
pressures, normoxia and normocapnia.
• Psychological and empathetic support is
essential and appropriate referral
for grieving and stress is paramount.
Rehabilitation counselling and
planning starts at the acute stage in order
to give the family unit some
future focus and hope.
• CEREBROVASCULAR DISORDERS
• Cerebral vascular disorders include
cerebrovascular disease
and cerebral vascular accidents (stroke). A
stroke (acute brain
injury of vascular origin) may be either
ischemic or
hemorrhagic and is defined as an
interruption of the blood
supply to any part of the brain, resulting in
damaged brain
tissue.
• Etiology
• Hypertension is the leading risk factor for
stroke.
• Other risk factors include diabetes,
cardiac disease, previous
cerebrovascular disease (transient ischemic
attack or stroke or
myocardial infarction), age, sex, lipid
disorders, excessive ethanol
ingestion, elevated haematocrit, elevated
fibrinogen and cigarette
smoking. Cerebral arteriosclerosis
predisposes individuals to both
ischaemic and hemorrhagic stroke.
• Smoking is the strongest risk factor for
aneurysmal SAH.
• Atrial fibrillation, endocarditis and
medications containing
supplemental estrogen are risk factors for
embolic stroke.
• Seizures develop in approximately 10% of
cases, usually appearing
in the first 24 hours and more likely to be
focal than generalized.
• Most patients with aphasia will have a
cerebral infarction in the
distribution of the left middle cerebral artery
• Ischaemic Stroke
• Ischemic stroke compromises blood flow
and energy supply to the
brain, which triggers mechanisms that lead
to cell death.
• Infarction occurs rapidly in the region of
most severe ischemia
(termed ischemic penumbra) and expands
at the expense of the
surrounding hypoxic tissue, from the center
to the periphery.
• Therapeutic strategies in acute ischemic
stroke are based on the
concept of arresting the transition of the
penumbral region into
infarction, thereby limiting ultimate infarct
size and improving
neurological and functional outcome.
Ischemic stroke can be
further categorized as middle cerebral
artery occlusion, acute
basilar occlusion, and cerebellar infarcts
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aneurysms, or certain medications (e.g.

• The management of an ischemic stroke anticoagulants
comprises four and amphetamines).
primary goals: restoration of cerebral blood
flow • Symptoms are produced when an
(reperfusion), prevention of recurrent aneurysm or arteriovenous
thrombosis, malformation (AVM) enlarges and presses
neuroprotection, and supportive care. on nearby cranial
nerves or brain tissue or, more dramatically,
when a blood
vessel, aneurysm or AVM ruptures, causing
intracerebral or
subarachnoid hemorrhage.
• When an aneurysm ruptures, arterial
pressure forces blood
into the subarachnoid space between the
arachnoid mater
and the surface of the brain. Free blood
then travels through
the fissures into the basal cisterns and
across the surface of
the brain.
• Haemorrhagic Stroke
• When clotted, this blood can interfere with
• Hemorrhagic strokes are caused by
the circulation
bleeding into the
and reabsorption of cerebrospinal fluid
brain tissue, the ventricles or the
(CSF), potentially
subarachnoid space.
causing obstructive hydrocephalus and
• Primary intracerebral hemorrhage from a
raised intracranial
spontaneous
pressure.
rupture of small vessels accounts for
approximately 80%
• The commonest cause is a leaking
of hemorrhagic strokes and is primarily
aneurysm in the
caused by
area of the circle of Willis or a congenital
uncontrolled hypertension.
AVM of the
• Secondary intracerebral hemorrhage is
brain. Blood in the subarachnoid space is a
associated with
powerful
arteriovenous malformations (AVMs),
meningeal irritant, and it is this irritation that
intracranial
causes

43 I KRISTINE JOY F. SASTRILLO | 4-F

 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

most of the initial signs and symptoms of Hunt-Hess SAH severity Scale III (see
SAH. Table 17.5) and greater
to manage systemic complications,
• In intracerebral hemorrhage the bleeding recognize and treat
is usually clinical deterioration, investigate the cause
arterial and occurs most commonly in the of the
cerebral haemorrhage and to treat any underlying
lobes, basal ganglia, thalamus, brainstem aneurysm or
(mostly the arteriovenous malformation.
pons) and cerebellum. • Resuscitation is directed towards
maintaining cerebral
• Normal brain metabolism is disrupted by perfusion pressure by ensuring adequate
the brain being arterial blood
exposed to blood. The sudden entry of pressure (often with the use of inotropes to
blood into the produce relative
subarachnoid space or brain parenchyma hypertension although reactive
results in a rise in hypertension is often
ICP, which then leads to compression and present), ensuring a relatively high
ischaemia resulting circulating blood volume
from the reduced perfusion pressure and (hypervolaemia), and producing relative
vasospasm that haemodilution
often accompany intracerebral and (’triple H therapy’).
subarachnoid
haemorrhage.
• Depending on the severity, clinical findings
include severe
headache, nuchal rigidity, photophobia,
nausea and vomiting,
hypertension, ECG changes, pyrexia,
cranial nerve deficits,
visual changes, sensory or motor deficits,
fixed and dilated
pupils, seizures, herniation and sudden
death.

• Subarachnoid Haemorrhage
• Admission to ICU is indicated for • Hypovolaemia occurs in 30–50% of
subarachnoid haemorrhage patients, as does excessive

44 I KRISTINE JOY F. SASTRILLO | 4-F

 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD
hyponatraemia in 30% of patients. In the
first six days, plasma
volume decreases of greater than 10% can
occur following
SAH, thus increasing the risk of vasospasm
and ischaemia.
Women have been found to have more
significant drops in
blood volume than men following SAH.
‘Third space’ loss,
insensible losses and blood loss account
for this drop in fluid
volume, as well as electrolyte disturbances.
• ICP monitoring and drainage of CSF via
ventriculostomy is indicated in SAH
but not in cerebral haemorrhage.
• SAH causes increased sympathetic
activation from the presence of
haemoglobin in the subarachnoid space.
This results in elevated
catecholamine levels, which may result in
focal myocardial necrosis,
explaining the presence of inverted T
waves, ST depression, prominent U
waves, and Q-T intervals in more than 50%
of patients.
• As cardiac function is one of the
determinants for adequate cerebral blood
flow, it is essential to identify such
occurrences early and treat them
accordingly.
• Hyponatraemia occurs from alterations in
atrial natriuretic factor (ANF) in
response to sympathetic nervous system
activation. The syndrome of
inappropriate secretion of antidiuretic
hormone (SIADH) is primarily
responsible for hyponatraemia in those with
SAH, as is cerebral
salt-wasting syndrome; however, both
mechanisms are still relatively
misunderstood
• Collaborative Management of Stroke
• Expected outcomes for patients with acute
ischaemic and
haemorrhagic stroke include prevention of
secondary injury,
of airway and respiratory complications,
and the maintenance
of haemodynamic stability.
• Timely assessment and intervention is
paramount in the
management of ischaemic stroke,
especially regarding
interventional pharmacology and prevention
of cerebral
haemorrhage.
• Atrial fibrillation and deep vein thrombosis
(DVT) prevention
(in ischaemic stroke) requires
anticoagulation control. In
haemorrhagic stroke, sequential
compression device and
stockings are indicated for DVT prophylaxis
as anticoagulants
are a risk factor for rebleeding.
Maintenance of bowel and
bladder function and prevention of
integument
complications, malnutrition, seizures and
increasing
neurological deficits are important goals.
Environmental
45 I KRISTINE JOY F. SASTRILLO | 4-F
 ILOILO DOCTORS’ COLLEGE
COLLEGE OF NURSING BATCH 2023
NCM 119 - NURSING LEADERSHIP AND MANAGEMENT
Professor: Mary Grace Suplido, RN, MD

precautions are implemented to provide a

non-stimulating
environment, preventing rises in ICP and
further bleeding.
• Sensory perceptual and motor alterations
need to be
assessed in regard to effective
communication and pain
management. Rehabilitation and
psychological support for
the patient and significant others are
integrated into the
acute care phase for a smooth transition.

46 I KRISTINE JOY F. SASTRILLO | 4-F