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ICP components

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-brain tissue (1400 g) -blood (75 mL) -CSF (75 mL) Volume & pressure of these 3 components are usually in a state of equilibrium

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ICP is usually measured in

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lateral ventricles of the brain

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Normal ICP pressure

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0-10 mm Hg

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Highest normal ICP

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15 mm Hg

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Monro-Kellie hypothesis states that

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because of the limited space for expansion w/i the skull, an ↑ in any one the components causes a change in the volume of others

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Because brain tissue has limited space to expand, ICP compensation is accomplished by

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-displacing or shifting CSF -↑ absorption or ↓ CSF production -↓ cerebral blood volume

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Compensation to correct ICP occurs to prevent

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↑ ICP

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Minor changes in blood & CSF volume occur as a result of

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-changes in intrathoracic pressure (coughing, sneezing, straining) -posture -BP -systemic O2 & CO2 levels

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Elevated ICP results from

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-head injury (most common) -secondary responses to : brain tumors subarachnoid hemorrhage toxic & viral encephalopathies

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Increased ICP from any cause =

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-↓ cerebral perfusion -stimulates further swelling (edema) -possible brain tissue shift resulting in herniation (freq. fatal)

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Increase ICP may reduce cerebral blood flow, resulting in

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ischemia & cell death

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In early stages of cerebral ischemia, vasomotor centers are stimulated causing

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-↑ systemic BP to maintain cerebral blood flow -slow bounding pulse -irregular respirations *These changes may suggest ↑ ICP

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↑ in PaCO2 causes

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cerebral vasodilation, leading to ↑ cerebral blood flow & ↑ ICP

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↓ in PaCO2 causes

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vasoconstriction, limiting blood flow to brain; ↓ venous outflow may also ↑ cerebral blood volume, thus ↑ ICP

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Autoregulation

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the brain's ability to change the diameter of its blood vessels to maintain a constant cerebral blood flow during alterations in systemic blood pressure

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Cerebral edema =

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↑ brain tissue volume→ ↑ ICP

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Cerebral edema compensatory mechanisms

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-autoregulation - ↓ production & flow of CSF

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Autoregulation compensatory mechanism can be impaired in pts who are experiencing a

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pathologic & sustained increase in ICP

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Brain can maintain a steady perfusion pressure if

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-arterial systolic BP= 50 to 150 mm Hg AND -ICP= <40 mm Hg

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Changes in ICP are closely linked with

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cerebral perfusion pressure (CPP)

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CPP calculation

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MAP - ICP = CPP Ex: MAP = 100 mm Hg, ICP = 15 mm Hg 100 - 15 = 85 (CPP)

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Normal CPP range

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70 to 100 mm Hg

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As ICP ↑ & autoregulation fails, CPP can

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↑ to > 100 mm Hg OR ↓ to < 50 mm Hg

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CPP < 50 mm Hg =

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irreversible neurologic damage

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CPP range to ensure adequate blood flow to the brain

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70 to 80 mm Hg

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If ICP is = to MAP

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cerebral circulation ceases

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Cushing's response

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compensatory response that attempts to provide adequate CPP in the presence of rising ICP; caused by significant ↓ of cerebral blood flow

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Cushing's reponse cycle

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heady injury→imbalance of ICP components→↑ ICP→ ↓ cerebral blood flow→ ischemia→vasomotor center triggers an ↑ in arterial pressure to try to overcome ↑ ICP →sympathetically mediated response causes ↑ in systolic BP with a widening PP & ↓ HR

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Cushing's response s/s

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-↑ SBP -Widening PP** (late sign requiring immediate intervention) -reflex ↓ of HR

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Pulse pressure (PP)

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Systolic - Diastolic = PP

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Cushing's response is a late sign that requires immediate intervention and perfusion is

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recoverable if treated rapidly

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Earliest sign of ↑ ICP =

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change in LOC

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Cushing's triad occurs when

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brain's ability to autoregulate becomes ineffective & decompensation (ischemia & infarction) occurs and pt exhibits significant changes in mental status & VS.

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Cushing's Triad s/s

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-bradycardia -hypertension -bradypnea *grave sign

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Failure to treat Cushing's Triad can lead to

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-herniation ob the brain stem -occlusion of cerebral blood flow

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Herniation refers to

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shifting of brain tissue from area of high pressure to area of low pressure; herniated tissue exerts pressure on brain & interferes w/blood supply in that area

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Cessation of cerebral blood flow results in

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ischemia→infarction→brain death

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↑ ICP s/s

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-LOC changes -severe headache -restlessness & irritability -slowness to react -dilated or pinpoint pupils -altered breathing pattern (Cheyne Stokes respirations, hyperventilation, apnea) -deterioration in motor function -abn posturing (decerebrate, decorticate, flaccidity)

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decortication

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abnormal flexion of upper extremities & extension of lower extremities

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decerebration

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extreme extnsion of the upper & lower extremities

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Diagnostic studies to determine cause of ↑ ICP

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-CT -MRI -Cerebral angiography -PET -Transcranial doppler (info about cerebral blood flow) -Electrophysiologic monitoring

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Diagnostic procedure avoided in pts w/↑ ICP

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Lumbar puncture; because sudden release of pressure in lumbar area can cause brain to herniate

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↑ ICP Complications

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-brain stem herniation -Diabetes Insipidus -Syndrome of inappropriate antidiuretic hormone (SIADH)

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Diabetes Insipidus

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result of ↓ secretion of ADH

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Diabetes Insipidus s/s

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-excessive UOP -↓ urine osmolality (excretion of mainly H20) -serum hyperosmolarity (serum has ↑ salt)

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Diabetes Insipidus tx

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-administer fluids -electrolyte replacement -Vasopressin

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SIADH

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result of ↑ secretion of ADH

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SIADH s/s

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-FVE -↓ UOP -↓ serum Na+

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SIADH tx

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-FR (<800 mL/day w/no free water) can usually correct hyponatremia -Careful admn of 3% hypertonic saline solution (severe cases only) *Na+ concentration correction rate should not exceed 1.3 mEq/L/h

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↑ ICP medical mgmt

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-Invasive ICP monitoring -Osmotic diuretics (mannitol) -FR -draining CSF -controlling fever -maintain systemic BP & oxygenation -↓ celluar metabolic demands

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↑ ICP medical mgmt goals

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-↓ cerebral edema -↓ CSF volume -↓ cerebral blood volume while maintaining cerebral perfusion

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↑ ICP nursing goals

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-Maintain patent airway -Achieve adequate breathing pattern -Optimize cerebral tissue perfusion -Maintain negative fluid balance -Prevent infection -Monitor/Manage potential complications

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Nursing interventions to maintain patent airway in ↑ ICP pt

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-Suction PRN w/care to prevent ↑ ICP -Discourage coughing -Auscultate lungs q8h for adventitious sounds or areas of congestion -Elevate HOB to aid in clearing secretions & improve venous drainage of brain

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Nursing interventions/care to achieve adequate breathing pattern in pt w/↑ ICP

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-Monitor for Cheyne-Stokes respirations (due to ↑ pressure on frontal lobes or deep midline structures) -Hyperventilation therapy to ↓ ICP (causes cerebral vasoconstriction & ↓ in cerebral blood volume) *RN collaborates w/resp therapist in monitoring PaCO2 which is usually maintained at <30 mm Hg

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Nursing interventions/care to optimize cerebral perfusion in pt w/↑ ICP

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-Proper positioning (head is kept in neutral (midline)position, maintained w/cervical collar if needed, to promote venous drainage) -HOB elevated 30-45 degrees -Extreme rotation/flexion of neck avoided because compression or distortion of jugular veins ↑ ICP -Avoid extreme hip flexion to prevent ↑ in intra-abd & intra-thoracic pressures which can ↑ ICP -Avoid Valsalva maneuver

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Nursing interventions/care to maintain negative fluid balance in pt w/↑ ICP

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-Administer osmotic, loop diuretics (promote venous return) -Corticosteroids (reduce cerebral edema) -FR -I&O *If UOP is >200mL/h for 2h could indicate diabetes insipidus -Oral care due to mouth dryness from dehydration

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Nursing interventions/care to prevent infection in pt w/↑ ICP

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-Aseptic technique when managing ICP monitoring system & changing ventricular drainage bag -Monitor for s/s of meningitis: fever, chills, nuchal rigidity, & increasing/persistent headache

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Nursing interventions/care to manage potential complications in pt w/↑ ICP

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Detect early indications of ↑ ICP by doing freq. neuro checks for: -disorientation, restlessness, confusion, ↑ resp effort, purposelss mvmts -Pupillary changes & impaired extraocular mvmts -Weakness in 1 extremity or on 1 side of body -Constant headache Detect later indications of ↑ ICP by assessing: -LOC -VS (especially widening of PP) -Altered resp patterns -Projectile vomiting -Hemiplagia or decorticate or decerebrate posturing -Loss of brain stem reflexes (pupillary, corneal, gag, swallowing) **Monitor ICP pressure

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Controlling ICP interventions

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-HOB elevated -Maintain head & neck in neutral position -Prevent Valsalva maneuver w/stool softeners -Maintain PaO2 >60 mm Hg -Maintain calm atmosphere -Avoid environmental stimuli (noise, conversation) -Maintain CPP >70 mm Hg -Use mannitol in bolus form -Administer sedation & paralytic agents before initiation of nursing activities

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Interventions to ↓ cerebral edema

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-Osmotic diuretics (mannitol) -FR -HOB elevated to 30 degrees (prevents impairment of venous return thru jugular vein) -Corticosteroids (dexamethasone) for tumors (↓ edema around tumor)

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Interventions to maintain cerebral perfusion

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-Inotropic agents: dobutamine & NE (↑ CO which is reflected in CPP which must be >70 mm Hg; lower CPP=inadequate CO)

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Interventions to ↓ CSF & intracranial blood volume

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-CSF drainage (↓ ICP and restores CPP)

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Interventions to control fever

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-Antipyretic meds (fever ↑ cereberal metabolism & rate at which cerebral edema forms) -Hypothermia blanket -Avoid shivering (↑ O2 consumption, ↑ level of catecholamines, & ↑ vasoconstriction)

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Interventions to maintain oxygenation & reducing metabolic demands

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-Monitor ABGs & SpO2 -Barbiturates-Pentobarbital (↓ brain metabolic requirements thus providing cerebral protection) -Paralyzing agent-propofol (Diprivan) ↓ metabolic & cerebral demand

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