Neurosensory:
Altered Cerebral Function and Increased
intracranial pressure (IICP)
Marnie Quick, RN, MSN, CNRN
Etilogy/Patho Altered Cerebral Function:
Consciousness
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Dynamic state in that it fluctuates
Continuum from awareness of self and
environment to unawareness
Consciousness to deep coma
Caused by:
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lesions/injury to the reticular system or cerebral
cortex
Metabolic disorders
Altered Cerebral Function:
Arousal/cognition (LOC) Patho/assessment
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Reticular Activating System (RAS) meshwork of
gray cell within brainstem/thalamus. Controls
wakefulness, arousal and alertness.
Cerebral cortex outer layer of gray cell bodies of
brain. Controls cognition, thought process.
Reticular Activating System (RAS)
Altered Cerebral Function:
Assessment of arousal/cognition (LOC)
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Observe individual’s behavior, call name
Verbal response to person/place/time/event
If unable- how responds to commands
If unable- how responds to central pain stimuli
Assessment of arousal/cognition (Respiratory
and pupillary light reflex)
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Respiratory- changes
occur as brainstem is
being compressed
Pupillary light reflexSensory: CN 2 Motor: 3
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Note pupil size; darken
room; shine light in and
note reaction and size
Direct/consensual
Assessment Arosual/cognition (EOM’S)
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Eye movement- CN 3,4,6
In COMA- test EOM’s
Oculocephalic reflex
Doll’s eyes- Sensory- CN 8;
Motor- CN 3,4,6
Good Dolls eyes: eyes move in
opposite direction of head
movement
Bad/negative Dolls eyes: eyes
do not move head turned
Assessment arousal/cognition (Motor)
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Strength, symmetry and ability to move
Order from best to worse:
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Purposeful
Generalized response
Posturing- flexion or extension
Flaccid
Planter Reflex- Babinski testing
Meningeal signs- Brudzinski, nuchal rigidity
Decorticate posturing- abnormal flexion
Decerebrate posturing- abnormal extension
Planter Reflex and Babinski testing
Common manifestations/Complications
Coma states and brain death
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Irreversible coma- persistent vegetative state
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Locked-in Syndrome (not true coma)
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Does not have functioning cerebral cortex
Caused by anoxia or severe brain injury
Sleep-wake cycles; chew/swallow/cough, no track
Functioning RAS/cortex; pons level interference
Aware, communicate with eyes
Brain death
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Loss of all brain function- flat EEG, no blood flow
Prognosis of individual
with altered cerebral functioning
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Outcome varies according to underlying cause
and pathologic process
The longer the individual unconscious, the longer
has absent Doll’s eyes; the poorer the cognitive
recovery
Residual mental problem typically outweigh the
physical
Altered Cerebral Function
Therapeutic Interventions
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Diagnostic tests- to R/O & identify cause of
altered cerebral function
Medications- Isotonic IV; D50; treat narcotic
overdose; fluid/electrolyte replacement;
antibiotics
Surgery- to remove cause
Other- airway/vent; treat IICP; enteral feeding
Nursing assessment specific to
altered cerebral function
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Terms used to describe (p.1347)
Description more important than term
Health history- drugs/head injury/metabolic
Physical exam- modify as individual cooperation
Neuro Vital Signs (p.1299)
Glasgow coma scale (p. 1299)
Altered Cerebral Functioning:
Pertinent Nursing problems
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Ineffective airway
Risk for aspiration
Risk for impaired skin integrity
Impaired physical mobility
Risk for imbalanced nurtition
Ineffective coping- Family
Home care
Increased Intracranial Pressure (IICP)
Normal Brain
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Monro-Kellie hypothesis
Intracranial pressure:5-15 mmHg;60-180cm H2O
Cerebral perfusion pressure: MAP-ICP=CPP;
Normal: 80-100 mmHg; minimal blood flow 50;
brain death 30 mmHg
Autoregulation- cerebral arterioles change
diameter to maintain CBF when ICP rises; need
nomal range of MAP to occur; pressure (BP) and
chemical (CO2) autoregulation
Increased Intracranial Pressure
Pathophysiology of intracranial hypertension
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Monro-Kellie hypothesis
Cushing reflex- BP and Pulse
Brain shifts- herniation syndromes
Symptoms progress in relation to these
physiological changes
Increased Intracranial Pressure (IICP)
Cerebral edema/hydrocephalus
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Cerebral edemaIncreases the volume of
brain tissue which can
cause herniation
Hydrocephalus
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Noncommunicating
Communicating
Subarachnoid space with arachnoid villi
Increased Intracranial Pressure (IICP)
Brain Herniation Syndromes
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Cingulate herniation
Central (transentorial)
Uncal (lateral)
Infratentorial herniation
Extracranial herniation
Brain herniation
Normal brain and Herniation Syndromes
Increased Intracranial Pressure
Common manifestations/complications
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Result of compression of brain function
Level of consciousness most important sign
Second- pupil changes as 3rd nerve is compressed
Others- p.1355
Speed of IICP how fast cause develops
Cushing reflex late sign
Complication of IICP is permanent disability,
coma, death
Increased Intracranial Pressure (IICP):
Therapeutic Interventions
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Diagnostic tests- to find cause; monitor hydration/O2
Medications
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Osmotic/loop diuretics; antipyretics; anticonvulsants; antiulcer;
IV fluids; TPN; vasoactive drugs for MAP; barbiturate coma
Hypothermia
Surgery- remove cause; shunt/drain
Mechanical ventilation
ICP monitoring
Other monitors- Jugular venous O2; partial pressure O2 in
brain tissue
Intraventricular and subarachnoid monitoring
devices for IICP
Intraventricular drainage system
Increased intracranial pressure (IICP):
Nursing assessment specific to IICP
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Health history- assess brain involvement
Physical exam
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Altered cerebral function assessment
Frequency depends on potential IICP
Early sign- change in LOC
3rd Cranial nerve compression
Papilledema, projectile vomiting, vision changes,
seizures (p. 1355)
Late sign- Cushing VS changes– Know!
Increased intracranial pressure (IICP):
Pertinent Nursing Problems and Interventions
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Ineffective tissue perfusion: cerebral
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Assess/report sign IICP
Adequate airway
Promote venous drainage
Control environment stimuli
Plan nursing care
Avoid Valsalva’s maneuver
If bone flat out post op- assess
Assess external shunts/drains