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Module 10: Neursensory Disorders: Altered Cerebral Function and Increased
Intracranial Pressure (IICP)
Marnie Quick, RN, MSN, CNRN
Altered Cerebral Function
Etiology/Pathophysiology
1.
Normal brain physiology 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 or cerebral cortex
2)
Metabolic disorders
3)
Examples: brain lesions, cardiac (as an MI), respiratory,
kidney, diabetes, fluid and electrolyte imbalance, drugs that
suppress the CNS, and seizures.
c. Arousal/Cognition (Level of Consciousness) patho/assessment
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.
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 with understanding.
3)
Begin assessment of altered cerebral function by observing
the individual’s behavior. Call their name, if no response
then shake individual- may be asleep.
4)
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
5)
If unable to assess verbal, then assess response to
commands: Note ability to follow simple (one-part) or
complicated commands
a)
Normal- able to follow commands in absence of
paralysis
b)
Abnormal- hard to arouse, slow, falls asleep easily,
unable to perform task
6)
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 (p. 1304 Fig 40-18 &19), absence of
RNSG 2432  203
movements, or flaccid. (See ‘Motor Response’
section below)
d. Patterns of breathing
1)
The changes in respiratory pattern occur as the brainstem is
being compressed.
e. Pupillary and extraocular eye movements (EOM’s)
1)
10 of the 12 cranial nerves come off of the each side of the
brainstem and reflect compression of the brainstem.
2)
A reflex ark means that both the sensory and the motor
component must function to obtain a response.
3)
4, 6, and 8 are involved in eye movement (see Stroke)
f. Pupillary light reflex1)
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 eye
5)
Abnormal- fixed, dilated, pinpoint, slow, sluggish,
nonreative to light.
6)
Compression of the 3rd cranial nerve results in fixed dilated
pupil on the ipsilateral side
g. Dolls eyes (Oculocephalic reflex)(p. 1349 Fig 42-1)
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 oculomotor (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.
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h. Motor response
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.
Adapt motor testing as discuss in the modules SCI, CVA and
brain tumor.
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. (p. 1304 Fig 40-16/17)
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 (p. 1304 Figure 40-14) 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 (p. 1304 Figure 40-16/17) 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.
Common Manifestations/Complications
1.
Coma states and brain death
a. Irreversible coma- persistent vegetative state
1)
Permanent 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.
2)
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.
3)
Usually the result of anoxia or severe head injury.
RNSG 2432  205
2.
3.
b. Locked-in Syndrome
1)
Individual is alert and aware of the environment. Has
cognitive abilities, but unable to communicate through
speech.
2)
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.
3)
Individual can’t verbally communicate, but can
communicate with eye blinks or eye movements.
c. Brain death
1)
Irreversible loss of brain functions.
2)
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
Prognosis
a. Outcome varies according to underlying cause and pathologic
process
b. Recovery within 2 weeks associated with favorable outcome.
c. Young adults can recover from deep coma.
d. The longer the individual unconscious, the longer has absent Doll’s
eyes, the poorer the cognitive recovery
e. Residual mental problems far outweigh the physical problems
f. Glasgow coma scale at 24 hrs is a good indication of prognosis.
g. Individual usually more concerned with cognitive and memory
problems; family generally more concerned with the emotional and
personality changes.
Management includes identifying cause, preserving function and preventing
deterioration. It involves total system maintenance.
Therapeutic Interventions
1.
Diagnostic tests- to R/O and identify cause of altered LOC
a. Blood glucose- cerebral function declines rapidly when <40-50 mg/dl
(common cause of declining LOC)
b. Serum electrolytes and osmolality: hyponatremia coma Na < 115
mEq/L
c. ABG’s: hypoxemia or increased CO2
d. Serum creatinine and BUN: renal function
e. CBC: anemia or infections
f. Liver function: high ammonia interfere with cerebral metabolism
g. Toxicology: blood and urine (drug or alchol)
h. CT/MRI, EEG, Brain scan, Cerebral angiogram: identify neurologic
damage, lesions, blood flow
i. Trancranial Doppler: assess cerebral blood flow
j. Lumbar puncture with CSF analysis: infection or bleeding. Done with
care on individual with possible increased intracranial pressure, as
may cause herniation of brain
2.
Medications
a. Isotonic IV solutions- Normal saline or lactated Ringer’s solution
b. Dependent on cause- if hypoglycemic- 50% glucose; narcotic
overdose- naloxone; fluid and electrolytes- replacement; antibioticsmeningitis, etc.
206  RNSG 2432
3.
4.
Surgery
a. If indicated for a space occupying lesion, such as tumor or bleed.
Other therapeutic measures
a. Airway/mechanical ventilation
b. Treat increased intracranial pressure (refer to next section)
c. Enteral feedings—if long term, may need gastrostomy tube
placement.
Nursing Assessment Specific to Altered Level of Consciousness
1.
Terms used to describe level of consciousness. (p. 1347 Table 42-2)
2.
*Describe what you see rather than just using a ‘term’.
3.
Health history- to eliminate causes of changes in level of consciousness,
such as drugs, head injury, metabolic causes
4.
Physical exam- need to modify as to ability to cooperate. Refer to Patho
section in notes.
a. Level of consciousness (LOC)
b. Pupils: size, equality, reaction to light
c. Doll’s Eye (Oculocephalic reflex) (p. 1349 Fig 42-1)
d. Motor response: Note motor power (strength), symmetry,
coordination and involuntary movements. Check for a Babinski (p.
1304 Fig 40-15)
e. Sensory response: superficial sensation, hearing, seeing, touch
5.
Neuro Vital Signs (p. 1299 Box 40-1)
6.
Glasgow coma scale (p. 1299 table 40-4) (eye opening, motor response,
and verbal response. 3= lowest to 15= highest level of function)
Pertinent Nursing Problems and Interventions
1.
Ineffective airway clearance
a. Assess airway, cough, lungs sounds, provide care for trach
2.
Risk for aspiration
a. Assess swallowing, gag reflex, lungs, O2
b. Provide for oral hygiene, suctioning, positioning
3.
Risk for impaired skin integrity
a. Assess skin/provide basic nursing care- change position, etc
4.
Impaired physical mobility
a. ROM, splints (on 2 hrs; off 2 hrs)
5.
Risk for imbalanced nutrition
a. Monitor- daily weights, lab
b. Nutritional support- calorie count, NG/gastrostomy tube care
c. OT/speech to assess ability swallow, etc
6.
Family
a. Teach family to talk to patient- assume that individual can hear and
understand everything; individual may misinterpreted stimuli
b. Support groups, case worker evaluation
7.
Home care
a. Home evaluation, equipment at home, case worker/team evaluation,
possible placement in a nursing home
RNSG 2432  207
Increased Intracranial Pressure (IICP)
Etiology/Pathophysiology
1.
Normal brain physiology as it relates to increased intracranial pressure.
a. Monro-Kellie hypothesis
1)
The brain is surrounded by nondistenable bone and
meninges.
2)
The contents of the cranium- composed of:
a)
Brain (80%) can increase by space occupying lesions
such as tumors, hemorrhages, abscesses, or by
cerebral edema.
b)
CSF (10%) can increase by obstructive (a blockage
of the flow of CSF) or nonobstructive (increase in
CSF production) hydrocephalus.
c)
Blood vessels (10%) can dilate.
3)
As the volume of one component increases, the volume of
the other two decreases.
4)
When maximal compensation occurs and the volume
increases, the intracranial pressure rises.
b. Intracranial pressure- have a transient rise normal functions of
coughing, sneezing, straining- these increase intrathorasic pressure
1)
Normal: 5-15 mm Hg intracranial by monitor; 60-180 cm
water by lumbar puncture
2)
Abnormal: above 200 cm water; clinical symptoms appear
20-25 mg Hg; severe ICP above 40 mg Hg; level and length
of time are both important
3)
There are waveforms on monitors that reflect changes
c. Cerebral perfusion pressure (CPP)
1)
The pressure required to perfuse brain cells, essential to
life.
2)
MAP-ICP= CPP
3)
Normal value is 80-100 mmHg; minimal blood flow is 50
mmHg; brain death occurs at 30 mmHg.
d. Autoregulation
1)
Compensatory mechanism in which the cerebral arterioles
change diameter to maintain cerebral blood flow when ICP
rises.
2)
It is dependent on a normal range of mean arterial pressure
3)
Types- pressure (blood pressure changes) and chemical
(carbon dioxide level change) autoregulation.
2.
Pathophysiology of intracranial hypertension (IICP)
a. Changes in the contents of cranial vault, cause the intracranial
pressure to rise (Monro-Kellie hypothesis), a loss of autoregulation
decreases the cerebral perfusion pressure depriving the brain cells of
blood.
b. Cushing reflex (increase pulse pressure by increasing systolic
pressure, and bradycardia) occurs as the brain tries to maintain
cerebral perfusion.
c. The brain shifts to attempt to compensate resulting in herniation of
the brain to a lesser pressure area –usually through the foramen
magnum which in turn compresses the brainstem (medulla), causing
death.
d. Symptoms progress in relation to these physiological changes.
208  RNSG 2432
3.
4.
5.
Cerebral edema
a. Increase in volume of brain tissue. Can occur locally around an
injured area (as in a tumor, bleed, or ischemic area) or globally
throughout the brain (as in anoxia or swirling movement of the brain
within the skull with head injury, etc) There are different types of
cerebral edema.
b. Cerebral edema increases intracranial pressure, which decreases
cerebral blood flow, causing hypoxia which in turn causes
autoregulation to dilate the blood vessels which then increases
intracranial pressure. If untreated the cycle rapidly continues until
herniation occurs.
Hydrocephalus
a. Noncommunicating- CSF circulation from the ventricles in the brain
are blocked by a tumor, edema, hematoma, etc.
b. Communicating- CSF is not effectively reabsorbed through the
arachnoid villi (as in blood from a SAH blocking reabsorption or
infection blocking) or overproduction of CSF from the choroid plexus
in the ventricles.
Brain herniation (p. 1356 Fig 42-2)
a. Cingulated herniation- shift to side
1)
cingulate gyrus slips under falx cerebri. It is seen on Xrayas a shift to the brain.
2)
It is non life-threatening.
b. Central or transtertorial hernation
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 compressing vital centers.
3)
Life-threatening
c. Uncal or lateral herniation
1)
Uncus of the temporal lobe slips through the incisura notch
of the tentorium.
2)
The third nerve becomes compressed on the same side
(ipsilateral) resulting in compression of the brainstems’
vital centers causing decreased level of consciousness (RAS
compression) and death.
3)
Life-threatening
d. Infratentorial (subtentorial) herniation
1)
Downward displacement of infratentorial structures through
the foramen magnum of the skull.
2)
Life-threatening
e. Extracranial herniation
1)
Herniation of the brain in openings in the skull, such as a
fractures.
Common Manifestations/Complications
1.
Manifestations of increased intracranial pressure (intracranial hypertension)
are the result of the compression of brain functioning.
2.
Level of consciousness is the most important/significant sign. The change
may first be seen as confusion, lethargy progressing then to coma with no
response to painful stimuli.
RNSG 2432  209
3.
4.
5.
6.
7.
The second most significant sign is pupil changes. As the third nerve
becomes compressed by the brainstem herniating downward the pupil first
becomes sluggish then nonreactive to light- fixed and dilated.
A late sign is Cushing reflex- increase systolic BP (which causes widened
pulse pressure) and decrease pulse
The speed of the symptoms is dependent on the how fast the cause
develops. (slow growing brain tumor, rapidly expanding hematoma, etc)
Other assessment findings. (Refer to box p. 1355)
The complication of IICP is permanent disability, coma or death from
compression of the vital centers in the brain stem.
Therapeutic Interventions
1.
Diagnostic tests
a. Identify cause of IICP- CT/MRI
b. Serum osmolality to monitor hydration
c. ABG’s monitor CO2 levels
2.
Medications (p. 1357 box at bottom)
a. Osmotic diuretics to draw fluid out of the edematous brain tissue.
Mannitol is the most common drug used. (p 1357 nursing resp)
b. Loop diuretics as furosemide (Lasix)
c. Antipyretics- fever increases metabolism which in turn increases ICP
(hypothermia blanket may also be used)
d. Anticonvulsants to prevent seizures
e. Antiulcer drugs to reduce stress ulcers
f. IV fluids as normal saline- keep moderately dehydrated
g. TPN for nutrition, change to NG feedings when gut returns
h. Vasoactive drugs to maintain MAP in range for adequate CPP
i. Barbiturate coma may be utilized in refractory IICP to reduce
metabolism and oxygen demand. Total nursing care is required when
this is utilized.
3.
Hypothermia- to decrease metabolism and oxygen demand, thereby
decreasing intracranial pressure
4.
Surgery
a. Remove underlying cause
b. Shunt or drainage catheter- inserted via burr hole into lateral
ventricle to drain excess CSF and decreasing hydrocephalus. External
or internal shunt to drain CSF from ventricles or lumbar drain.
c. Remove part of cranium (bone flap) to allow for brain expansionlater will do a cranioplasty to repair
5.
Mechanical ventilation
a. To prevent hypoxemia and hypercapnia
b. CO2 is a very potent vasodilator and can significantly raise ICP
6.
ICP monitoring (p. 1358 Fig 42-3)
a. Used in the ICU setting on comatose individuals to monitor
intracranial (ICP) and cerebral perfusion pressure (CPP)
b. Intraventricular catheter monitors as well is frequently used for
removal of CSF to decrease ICP. Drip chamber should be a level of
external ear canal.
c. Other monitors used include subarchnoid screw, and epidural
fiberoptic catheter and parenchyma (in the brain itself)
7.
Other monitors:
a. SjvO2-jugular venous oxygen saturation (N= 60-70%)
210  RNSG 2432
b. PbtO2- partial pressure of oxygen in brain tissue. Through burr hole
probe is placed near damaged brain tissue or for global oxygenation,
placed in opposite hemisphere from damage (N=25-50 mmHg).
Gives both cerebral oxygenation and temperature
Nursing Assessment Specific to IICP
1.
Health history
a. Assess history of brain involvement
2.
Physical exam
a. Refer to previous assessment: altered level of consciousness
b. Frequency of assessment depends on potential for developing ICPmay be every 30 min- 1 hour.
c. An early sign is change in level of consciousness (most important
sign). As pressure rises, the individual may become restless,
irritable, confusion, to coma.
d. Third nerve comes off the brainstem where it easily becomes
compressed. The pupil will change size (the ipsilateral pupil dilates)
as well as the speed of reaction to light (slow, sluggish, fixed)
e. Assess vital signs- a significant late sign is Cushing reflex-(Cushing
triad) SBP (systolic blood pressure) rises causing a widen pulse
pressure with pulse decreasing.
f. Assess other common manifestations of IICP (box on p. 1355)
headache, papilledema, projectile vomiting, vision changes,etc
Pertinent Nursing Problems and Interventions
1.
Ineffective tissue perfusion: cerebral
a. Assess/report any signs of IICP or change in monitor readings
b. Adequate airway- position, suction, humidification, evaluate need for
ventilatory support.
c. Promote venous drainage- HOB 30 degrees; avoid neck and hip
flexion; avoid PEEP
d. Control environmental stimuli- low lights; control family visits; PRN
meds for painful procedures; evaluate use of restraints
e. Plan nursing care- space procedures, don’t cluster care, especially
painful ones.
f. Avoid Valsalva’s maneuver as this increases intrathroasic pressure
which inturn IICP- assess bowels, need for restraints
g. 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.
h. Assess external shunts/drains- amount/color of drainage, etc.
2.
Risk for infection
RNSG 2432  211
212  RNSG 2432