RNSG 2432 ONLINE NOTES
Module 10: Neurosensory Disorders: Altered Cerebral Function & Increased
Intracranial Pressure (ICP)
Marnie Quick, RN, MSN, CNRN
*These notes are an expansion of the Lewis textbook and required
references. They are met to be used together.
Etiology and Pathophysiology
1. Normal brain physiology as it relates to increased intracranial pressure.
a. The brain is surrounded by nondistenable bone and meninges.
b. Meninges- double fold of dura between hemispheres is falx cerebri;
between cerebrum and cerebellum is tentorium cerebelli.
c. Regulation and maintenance of intracranial pressure
1) Normal intracranial pressure
a) Essential volume components (Lewis 1468, Fig 57-1)
b) Monro-Kellie doctrine (enclosed space-brain, blood, CSF)
c) Factors influence ICP: arterial and venous pressure,
intraabdominal and intrathoracic pressure, posture,
temperature, blood gases (esp. CO2)
d) Normal body activities that increase intrathoracic
pressure, such as coughing, sneezing, straining will
cause a transient rise in ICP
2) Normal compensatory adaptations
a) Monro-Kellie doctrine applied- increase in one
component, causes a decrease in the other two.
Examples are absorption of CSF; dec CSF production;
displace CSF in subarachnoid space; distend dura.
b) Ability to compensate is limited and when maximal
compensation occurs and the volume increases,
increased intracranial pressure occurs.
c) Transient rises in pressure can occur with normal
physiological functions-coughing, sneezing, straining
3) Measuring ICP
a) Can be measured from ventricles; subarachnoid space;
epidural space and brain parenchyma tissue
b) Normal pressure in brain 0-15 mm Hg by intracranial
monitor (Lewis 1473 Fig 57-7)
c) Lumbar pressure 100-200 mm H2O (by Lumbar
d) Clinical symptoms appear 20-25 mm Hg; severe ICP
above 40mm Hg
e) Level and length of time (duration) are both important
(Lewis 1474 Fig 57-8)
d. Cerebral blood flow
1) Auto regulation of cerebral blood flow
a) Ability of brain to regulate its own blood flow by
adjusting the diameter of cerebral blood vessels despite
changes in systemic arterial blood pressure.
b) Ensures a consistent CBF to provide the metabolic needs
of the brain tissue and maintain CPP.
c) Must have at least 50 mm Hg of MAP for auto regulation
RNSG 2432 263
d) As CPP decreases, auto regulation fails and CBF
2) Cerebral Perfusion Pressure (CPP)
a) *Pressure needed to ensure blood flow to the brain
b) CPP=MAP-ICP (p1468 Table 57-1)
c) Normal 70-100 mm Hg; neuronal death occurs <50 mm
3) Pressure changes
a) Compliance is the expandability of the brain
b) Compliance= Volume/Pressure
c) Pressure volume curve (p1469 Fig 57-2)
d) Cushing’s triad can occur with loss of auto regulation
e) Herniation occurs as brain goes from greater to lesser
pressure (See below for types of herniation)
4) Factors affecting cerebral blood flow
a) Blood gases (O2, CO2) and hydrogen ion concentration
affect cerebral tone
b) CO2 is potent cerebral vasodilator
c) Cerebral O2< 50 mm Hg and elevated H+ (acidosis)
results in cerebral vasodilatation
d) Cardiac/respiratory arrest; systemic hemorrhage, etc
2. Increased intracranial pressure
a. Cerebral edema
1) Increase fluid in extravascular spaces of brain tissue.
2) Causes of cerebral edema (Lewis 1470 Table 57-2)
3) Vasogenic- most common; fluid in white matter
4) Cytotoxic- local disruption of gray matter (cell bodies)
5) Interstitial- fluid in extracellular space from systemic water
excess. Diffusion into ventricles hydrocephalus
b. Mechanisms of increased intracranial pressure
1) Caused by any space occupying lesion; cerebral edema; brain
inflammation; metabolic changes
2) Progression of ICP (Lewis 1470 Fig 57-3)
3) Herniation (Lewis 1471 Fig 57-4) greater to lesser pressure
3. Normal brain as it relates to altered cerebral function
a. Consciousness is a dynamic state that can fluctuate between
awareness of self and environment to unawareness.
b. Etiology of altered cerebral function:
1) Lesions/injury to the RAS (reticular activation system) or
2) Metabolic disorders
3) Examples: brain lesions- (such as tumor, hematoma), cardiac
(as an MI), respiratory, kidney, diabetes, fluid and electrolyte
imbalance, drugs that suppress the CNS, and seizures.
c. Arousal/Cognition (Level of Consciousness)
1) Reticular formation (specifically the reticular activating
system- RAS) is a meshwork of gray cell bodies within the
brainstem up to the thalamus that controls wakefulness,
arousal and alertness. Injury to the RAS with an intact
cerebral cortex results in difficulty with arousal which in turn
makes assessment of the cognitive function difficult.
264 RNSG 2432
2) Cerebral cortex is the outer layer of gray cell bodies of the
brain controls cognition; your thought processes. Widespread
injury to the cerebral cortex with an intact RAS, the individual
has sleep-wake cycles and may respond to stimuli, but not
d. Coma states and brain death
1) Coma: not awake and not aware
2) Persistent vegetative state
a) Condition where the individual has a functioning RAS in
the brainstem, but does not have a functioning cerebral
cortex where individuals thought processes normally
take place.- therefore is awake but not aware
b) Has sleep-wake cycles; can chew, swallow and cough.
Individual can move his eyes but cannot ‘track’- follow
an object or person with his eyes.
c) Usually the result of anoxia or severe head injury.
3) Minimally Conscious State: awake- inconsistently aware
4) Locked-in Syndrome (not a true coma)
a) Individual is alert and aware of the environment. Has
cognitive abilities, but unable to communicate through
b) Has functioning RAS and cortex. The disruption is at the
pons level where there is interference of the outgoing
motor nerve tracts, resulting in paralysis.
c) Individual can’t verbally communicate, but can
communicate with eye blinks or eye movements.
5) Brain death
a) Irreversible loss of brain functions.
b) Certain criteria must be met, depending on which State
the individual resides. It includes such criteria as flat
EEG, negative cerebral blood flow studies, absent ocular
and pupils response, apnea, etc
e. Prognosis of coma
1) Outcome varies according to underlying cause and pathologic
2) Recovery within 2 weeks associated with favorable outcome.
3) Young adults can recover from deep coma.
4) The longer the individual unconscious, the longer has absent
Doll’s eyes, the poorer the cognitive recovery
5) Residual mental problems far outweigh the physical problems
6) 52% of patient still in vegetative state at one month after
injury regain consciousness
7) It is impossible to predict the extent of functional
improvement. 24% of patient still in vegetative state at one
month after injury are largely independent by one year; 50%
of patients still in minimally conscious state up to 3 months
after injury are largely independent by one year
8) Individual usually more concerned with cognitive and memory
problems; family generally more concerned with the
emotional and personality changes.
9) Management of individual in a coma includes identifying
cause, preserving function and preventing deterioration. It
involves total body system maintenance.
RNSG 2432 265
Clinical Manifestations/Complications of ICP
1. Clinical manifestations of ICP
a. Compensation/decompensation stages ICP/Herniations (Lewis1471 Fig
b. Change in level of consciousness (altered cerebral function)
c. Changes in vital signs
d. Ocular signs
e. Decrease in motor function (Lewis1472 Fig 57-6)
g. Vomiting- not preceded by nausea; projectile
2. Complications of increased intracranial pressure
a. Inadequate cerebral perfusion
b. Herniation Syndromes (Lewis1471 Fig 57-4)
3. Brain herniation
a. Cingulate herniation- shift to side
1) Cingulate gyrus slips under falx cerebri. It is seen on X-rays
as a shift of the brain.
2) It is non life-threatening.
b. Central or transtertorial herination
1) Midline structures of the cerebrum or generalized cerebral
edema cause downward compression on the brainstem.
2) Decreasing level of consciousness (compression of the RAS in
brainstem) from confusion to coma. Death occurs from
compression of brainstem (medulla) compressing vital
c. Uncal or lateral herniation
1) Uncus of the temporal lobe slips through the incisural notch of
2) The third nerve becomes compressed on the same side
(ipsilateral) resulting in compression of the brainstems’ vital
centers in the medulla causing decreased level of
consciousness (RAS compression) and death.
d. Infratentorial (subtentorial) herniation
1) Downward displacement of infratentorial structures through
the foramen magnum of the skull.
e. Extracranial herniation
1) Herniation of the brain in openings in the skull, such as a
Collaborative Care for Increased Intracranial Pressure
1. Diagnostic studies (Lewis1472 Table 57-3 Diagnostic)
2. Measurement of ICP
a. Indications for ICP monitoring- examples: GCS<8; abnormal CT/MRI
b. Methods of measuring ICP (Lewis1473 Fig 57-7)(1474 Fig 57-8)
c. Infection major concern
d. Waveforms similar to arterial pressure trace
e. Any increase in intrathoracic pressures increases ICP- can see
transient rise in ICP when sneeze, cough, vomit.
266 RNSG 2432
f.Inaccurate readings caused by CSF leaks; obstruction in catheter;
kinks in tubing; incorrect height of drainage system relative to
patient’s reference point
g. CSF drainage (Lewis 1474 Fig 57-9) Monitor volume of CSF drainage!
3. Therapeutic interventions of ICP (Lewis1472 Table 57-3- collaborative care)
a. Adequate oxygenation and rid body of CO2- ABG analysis guides O2
therapy; may require ventilator. PaO2 at 100 Hg or greater
b. HOB 30 degrees, head and knees in neutral position
c. ICP monitoring (see above) and cerebral oxygenation monitoring
(LICOX, SjvO2); CPP> 60 mm Hg
d. Keep blood glucose within normal range
e. Drug therapy
1) Mannitol (Osmitrol)- osmotic diurectic
2) Corticosteroids- control vasogenic edema with tumors or
abscesses. Not effective in ICP of brain injury. If receiving
need to give meds to treat GI complications. Assess need for
3) High-dose Barbiturates (coma) and hypothermia to decrease
metabolic rate. Used for refractory ICP
4) Antiseizure- phenytoin (Dilantin/cerb)
5) H2 receptor antagonist or proton pump inhibitors- GI bleed
f. Hypothermia to decrease metabolic rate
g. Nutritional therapy (Lewis1475 Evidence-based practice chart)
1) hypermetabolic and hypercatabolic state- esp seen post brain
injury. NG nutrition as soon as gut functioning.
2) increase need for glucose
3) normovolemic IV normal saline- fluid balance, osmolity
1) To remove space occupying lesions- brain tumor, abscesses,
2) Craniectomy- remove part of cranium to allow for expansion
of swollen edema brain- be sure to assess bone flap site.
Nursing Assessment Specific to ICP
1. Glasgow coma scale (Lewis 1477 Table 57-5)
2. Neurologic assessment
a. Systematic assessment unconscious (Lewis1476 Fig 57-10)
b. Level of consciousness (most important neurological sign)
1) Begin assessment of altered cerebral function by observing
the individual’s behavior. Call their name, if no response then
shake individual- may be asleep.
2) Next assess verbal response: Note response to person, place,
time, and event questions
a) Normal- appropriately responds to each area
b) Abnormal- confusion in any one of the aspects, difficulty
with memory,(immediate recall, recent, or long term
memory) document accurately
3) If unable to assess verbal, then assess response to
commands: Note ability to follow simple (one-part) or
a) Normal- able to follow commands in absence of paralysis
b) Abnormal- hard to arouse, slow, falls asleep easily,
unable to perform task
RNSG 2432 267
4) Lastly, if individual is unable to perform commands, then
apply central pain stimuli (sternal rub).
a) Normal response to central pain- purposeful
movements, tries to move stimulus away
b) Abnormal- non-purposeful movements such as random
movements, decorticate or decerebrate posturing(Lewis
1472 Fig 57-6), absence of movements, or flaccid.
c. Pupillary assessment (CN III) (Lewis1477 Fig 5711)
1) Sensory component to this reflex is the optic (2nd) cranial
nerve (from the occipital lobe); the motor component is the
occulomotor (3rd) cranial nerve (from the brainstem).
2) Begin assessment: note size of pupils and compare
3) Next darken room and shine a penlight in one eye at a time,
note reaction and size; compare pupils
4) Normal- direct pupil response- brisk contraction to direct
light. Consensual- opposite pupil contracts when shine light in
5) Abnormal- fixed, dilated, pinpoint, slow, sluggish, nonreative
6) Compression of the 3rd cranial nerve results in fixed dilated
pupil on the ipsilateral side
d. Eye movements (CN III, IV,VI) (Lewis 407 Fig 21-5)
1) Follow nurses finger in all directions (Fig 21-5)
e. Eye movements- Dolls eyes (CN III, IV, VI, VIII)
1) Used to asses eye movements (EOM’s) and brain stem
functioning in a deep comatose individual.
2) The sensory component to this reflex is the vestibulocochlear
(8th) cranial nerve; the motor components that move the eye
are occulomotor (3rd)(moves the eye up, in and down),
trochear (4th) (moves eye down and in) and abducens (6th)
(abducts the eye).
3) This reflex requires that the individual be in a very low level
of consciousness- deep coma, where they do not have
voluntary control over their eye movements.
4) *It is NOT done if the individual is suspected of having a
spinal cord injury, instead water caloric testing is used to test
EOM’s (extraocular movements) in a comatose individual.
Ruptured ear drum must be ruled out before water is instilled
Caloric testing is usually by the physician.
5) Begin assessing for Doll’s eyes by holding the individuals head
and quickly turning side to side and up and down
6) If has reflex (‘Good’ or ‘positive Doll’s eyes’): when the head
is quickly turned the eyes move in opposite direction that the
nurse is turning the head. Positive Doll’s eyes means that
there is an intact brainstem and the cranial nerves involved
with eye movement
7) If does not have reflex (‘Bad’ or ‘negative Dolls eyes’): when
the head is quickly turned the eyes do not move they remain
in a fixed position in the head.
f. Motor strength
1) To accurately assess the strength, symmetry and ability to
move in assessing motor function, the individual needs
adequate mental functioning to be able to follow commands.
268 RNSG 2432
Adapt motor testing as discuss in the modules SCI, CVA and
2) As the gray cell bodies and the white tracts in the brain
become compressed or interfered with, the individual has
difficulty with movement. At first show lack of voluntary
movement to commands, then respond only to painful stimuli.
The individual may respond purposefully as pushing the nurse
away; then the response may be more just generalized
movements, progressing to posturing (decorticate then
decerebrate) and last becomes flaccid.
3) Posturing is a nonpurposeful response to stimuli. This stimuli
maybe a sternal rub, or even just bumping the bed. The less
stimuli it takes to illicit a response the worse the condition.
a) Decorticate posturing (rigidity)- Usually indicates
interference of the cortex of the brain. The individuals’
response to the stimuli is rigid flexion of the upper
extremities with rigid extension of the lower extremities.
b) Decerebrate posturing (rigidity)- Usually indicates
interference at the midbrain level where the cardio and
respiratory centers are located. The individual’s
response to the stimuli is rigid extension of both the
upper and lower extremity.
4) Babinski testing- test by firmly stroking the lateral aspect of
the sole of the foot, across to the big toe. The Babinski
reflex is dorsiflexion of the big toe and fanning of the other
toes; whereas the planter reflex (normal reflex) is curling of
the toes. The Babinski reflex is a normal reflex in the
newborn but, indicates interference in the pyramidal tract in
the older child and adult.
5) Meningeal signs in the client with altered level of
consciousness and suspect bleeding or infection in the
subarachnoid space (meninges) test for Brudzinski sign. If
irritation is causing a positive sign the client will has pain
and resistance, flexion of hips/knees when the head is
flexed to the chest.
g. Vital signs- Respiratory patterns, Cushing’s triad
Pertinent Nursing Problems and Interventions (Nursing Process)
Lewis 1479 NCP 57-1
1. Nursing diagnosis
a. Ineffective tissue perfusion (cerebral)
b. Decreased intracranial adaptive capacity
c. Risk for disuse syndrome
2. Planning- overall goals:
a. Maintain patent airway
b. ICP within normal limits
c. Normal fluid and electrolyte balance
d. No complications secondary to immobility and decreased LOC
3. Nursing implementation
a. Respiratory function
b. Fluid and electrolyte balance
c. Monitoring ICP
d. Assess/report any signs of IICP or change in monitor readings
RNSG 2432 269
e. Adequate airway- position, suction, humidification, evaluate need for
f. Promote venous drainage- HOB 30 degrees; avoid neck and hip
flexion; avoid PEEP
g. Control environmental stimuli- low lights; control family visits; PRN
meds for painful procedures; evaluate use of restraints
h. Plan nursing care- space procedures, don’t cluster care, especially
i. Avoid Valsalva’s maneuver as this increases intrathoracic pressure
which in turn increases ICP- assess bowels, need for restraints
j. If individual has bone flap left out to relieve pressure, assess. It is
normal for it to be soft and pulsate. It should not be tight.
k. Assess external shunts/drains- amount/color of drainage, etc.
l. Body position maintained with head of bed at 30 degrees
m. Protection from injury
n. Psychological considerations- assume that an individual in a coma can
hear and understand everything; individual may misinterpret stimuli
270 RNSG 2432