neurosensory: altered cerebral function and increased intracranial pressure (iicp)

Neurosensory:Altered Cerebral Function and Increased intracranial pressure (IICP)

Marnie Quick, RN, MSN, CNRN

Etilogy/Patho Altered Cerebral Function: Consciousness

Dynamic state in that it fluctuates Continuum from awareness of self and

environment to unawareness Consciousness to deep coma Caused by:

lesions/injury to the reticular system or cerebral cortex

Metabolic disorders

Altered Cerebral Function: Arousal/cognition (LOC) Patho/assessment

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)

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) Respiratory- changes

occur as brainstem is being compressed

Pupillary light reflex- Sensory: CN 2 Motor: 3 Note pupil size; darken

room; shine light in and note reaction and size

Direct/consensual

Assessment Arosual/cognition (EOM’S) 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) Strength, symmetry and ability to move Order from best to worse:

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 Irreversible coma- persistent vegetative state

Does not have functioning cerebral cortex Caused by anoxia or severe brain injury Sleep-wake cycles; chew/swallow/cough, no track

Locked-in Syndrome (not true coma) Functioning RAS/cortex; pons level interference Aware, communicate with eyes

Brain death Loss of all brain function- flat EEG, no blood flow

Prognosis of individual with altered cerebral functioning

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

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 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

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 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

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 Cerebral edema-

Increases the volume of brain tissue which can cause herniation

Hydrocephalus- Noncommunicating Communicating

Subarachnoid space with arachnoid villi

Increased Intracranial Pressure (IICP) Brain Herniation Syndromes Cingulate herniation Central (transentorial) Uncal (lateral) Infratentorial herniation Extracranial herniation

Brain herniation

Normal brain and Herniation Syndromes

Increased Intracranial Pressure Common manifestations/complications

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 Diagnostic tests- to find cause; monitor hydration/O2 Medications

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

Health history- assess brain involvement Physical exam-

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

Ineffective tissue perfusion: cerebral 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