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Neurosensory: Altered Cerebral Function and Increased Intracranial pressure (IICP) Marnie Quick, RN, MSN, CNRN
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Normal brain physiology as relates to increased intracranial pressure Brain surrounded by ridged bone & meninges Falx cerebri between hemispheres Tentorium cerebelli between cerebrum and cerebellum
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Regulation & maintenance of ICP Normal intracranial pressure Essential volume components> Factors influence ICP: Arterial/venous pressure Intraabdominal & intrathoracic pressure Posture Temperature Blood gases (CO2) Normal activities that increase intrathoracic pressure cause rise in ICP
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Regulation & maintenance of ICP: Normal Compensatory adaptations Monro-Kellie Doctrine applied- any increase in one component, cause a decrease in the other two Ability to compensate is limited so when maximal compensation occurs and the volume increases> IICP Transient rises in pressure can occur with normal physiological functions
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Increased Intracranial Pressure (IICP) Cerebral edema/hydrocephalus Cerebral edema- Increases the volume of brain tissue which can cause herniation Hydrocephalus- Noncommunicating Communicating
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Subarachnoid space with arachnoid villi
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Regulation & maintenance of ICP: Measuring intracranial pressure (ICP) Measured from> Normal pressure brain 0-15 mm Hg by intracranial monitor Lumbar pressure 100- 200 mm H2O (by LP) Clinical symptoms appear 20-25 mm Hg; severe ICP >40 mmHg Level/duration important!
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Cerebral Blood Flow Autoregulation- Ability of the brain to regulate own blood flow Automatic alteration in diameter of cerebral blood vessels to maintain constant blood flow to the brain despite changes in systemic arterial BP Must have at least 50 mm Hg of MAP to work As CPP dec> autoregulation fails> CBF decreases Cerebral Perfusion Pressure (CPP) Pressure needed to ensure blood flow to brain CPP=MAP-ICP Normal 70-100 mmHg; neuronal death <50 mm Hg
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Cerebral Blood Flow Pressure changes Compliance- expandability of brain Compliance= Volume/pressure Herination occurs as brain goes greater>lesser pressure Factors affecting cerebral blood flow Blood gases (O2,CO2) an H+ CO2 potent cerebral vasodilator Cerebral O2 H+ (acidosis) result cerebral vasodilation Cardiac/respiratory arrest; systemic hemorrhage
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ICP: Cerebral edema Increase fluid extravascular space Cerebral edema Causes: Mass lesions; head inj; brain surgery; cerebral infections; vascular insult; toxic/metabolic conditions Vasogenic: Most common. Fluid in white matter Cytotoxic: Fluid in gray matter Interstitial: Fluid in extracellular space> systemic water excess/uncontrolled hydrocephalus
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ICP: Mechanisms of ICP Caused by any space occupying lesion; cerebral edema; brain inflammation; metabolic changes Progression> to right Herniation Syndromes
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Normal brain as it relates to: altered cerebral function Consciousness is a dynamic state that can fluctuate between awareness of self and environment to unawareness (coma) Etiology of altered cerebral function Lesions or injury to RAS &/or cerebral cortex Metabolic disorders Brain lesions (tumor/bleed); cardiac (MI); resp; kidney; DM; fluid electrolyte imbal
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Reticular Activating System (RAS) altered cerebral Reticular formation meshwork of gray cells within the brainstem>thalamus Controls wakefulness, arousal and alertness Injury to RAS with intact cortex results in diff with arousal which> assess cognitive function diff
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Cerebral Cortex & altered cerebral function Outer layer of gray cell bodies Controls cognition; thought processes Widespread injury with intact RAS, may respond to stimuli, but not with understanding Sleep-wake cycles
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Note cortex in brown; the black lines are 1. association fibers between hemispheres and 2. white tracks going through internal capsule
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Coma states and brain death Coma: not awake and not aware Persistent Vegetative state: Does not have functioning cerebral cortex, awake- not aware Caused by anoxia or severe brain injury Sleep-wake cycles; chew/swallow/cough, no tracking with eyes Minimally Conscious State: awake- inconsistently aware 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
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Prognosis of an individual in coma Outcomes vary-cause & pathologic process Longer individual unconscious, loner has absent Doll’s eyes, the poorer the cognitive recovery Residual mental problems outweigh physical problems Glasgow coma scale at 24 hrs is a good indication of prognosis Individual more concerned with cognitive and memory problems; family emotional/personality changes Management of coma includes identifying cause, preserving function and preventing deterioration. Requires total body system maintenance
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Clinical Manifestations of increased ICP
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Clinical manifestations of IICP Result of compression of brain function Level of consciousness most important sign Second- pupil changes as 3 rd nerve is compressed Speed of IICP how fast cause develops Cushing reflex late sign Complication of IICP is permanent disability, coma, death
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Complications of IICP: Inadequate CPP Herniation Syndromes Cingulate Central Uncal Infratentorial Extracranial
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Collaborative Care for increased ICP: Diagnostic tests to identify underlying cause; monitor hydration, O2 X-ray- spine/head CT/MRI Cerebral angiography EEG/EKG Brain tissue oxygenation measurement ICP measurement Transcranial doppler studies Evoked potentials PET Lab studies- blood; CSF
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Collaborative Care for increased ICP: Measurement of ICP Used guide clinical care when risk IICP GCS<8 Abnormal CT/MRI Catheters in picture> LICOX- brain tissue oxygenation catheter SjvO2 Jugular cath
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Collaborative Care for increased ICP: Measurement of ICP
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Collaborative care for IICP: Intraventricular drainage
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Collaborative care of IICP: Adequate O2; ABG analysis; may require ventilator HOB 30 degrees; head and legs in neutral position Keep blood glucose within normal range Hypothermia to decrease metabolic rate Fluid balance- normovolemic IV NS; check osmoality Nutritional therapy- hypermetabolic state- NG nutrition as soon as gut functioning
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Drug therapy Mannitol (Osmitrol) osmostic diuretic Corticosteriods- control vasogenic edema with tumors/abscesses High-dose barbiturates (coma) dec metabolic rate Antiseizure- phenytoin H2 receptor antagonist or proton pump inhibitors Surgery To remove space occupying lesions- brain tumor, abscesses, hematoma Craniectomy- bone flap
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Nursing Assessment Specific to ICP: Systematic assessment of unconscious
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Glasgow coma scale http://www.unc.edu/~rowlett/units/scales/glasgo w.htm http://www.unc.edu/~rowlett/units/scales/glasgo w.htm
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Nursing Assessment Specific to ICP: Level of consciousness (most important!) 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 Description of confusion>coma is more important than terms
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Nursing Assessment Specific to ICP: 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
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Assessment: Extroocular eye movements (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
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Animations: EOM; Dolls eyes http://cim.ucdavis.edu/eyes/version15/eyesi m.html http://cim.ucdavis.edu/eyes/version15/eyesi m.html http://library.med.utah.edu/kw/animations/ hyperbrain/oculo_reflex/oculocephalic2.ht ml http://library.med.utah.edu/kw/animations/ hyperbrain/oculo_reflex/oculocephalic2.ht ml
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Assessment: Motor Strength, symmetry and ability to move Order from best to worse: Purposeful Generalized response Posturing- abnormal flexion or extension Flaccid Planter Reflex- Babinski testing Meningeal signs- Brudzinski, nuchal rigidity
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Planter Reflex and Babinski testing
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Brudzinski Sign
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Pertinent Nursing problems/interventions for IICP Lewis p. 1479/80 NCP 57-1 Nursing Diagnosis Ineffective tissue perfusion (cerebral Decreased intracranial adaptive capacity Risk for disuse syndrome P
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Increased intracranial pressure (IICP): Pertinent Nursing Problems and Interventions Ineffective tissue perfusion: cerebral Assess/report sign IICP Adequate airway Promote venous drainage- HOB 30 no flex neck/knee Control environment stimuli Plan nursing care- don’t cluster nursing care Avoid Valsalva’s maneuver If bone flat out post op- assess should pulsate/soft Assess external shunts/drains
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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
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