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					                         RNSG 2432 ONLINE NOTES
     Module 10: Neurosensory Disorders: Altered Cerebral Function & Increased
                           Intracranial Pressure (ICP)
                         Marnie Quick, RN, MSN, CNRN
                                Revised 1/28/09

*These notes are an expansion of the Lewis textbook and required
references. They are met to be used together.

Etiology and Pathophysiology
   1. Normal brain physiology as it relates to increased intracranial pressure.
          a. The brain is surrounded by nondistenable bone and meninges.
          b. Meninges- double fold of dura between hemispheres is falx cerebri;
             between cerebrum and cerebellum is tentorium cerebelli.
          c. Regulation and maintenance of intracranial pressure
                1)    Normal intracranial pressure
                        a) Essential volume components (Lewis 1468, Fig 57-1)
                        b) Monro-Kellie doctrine (enclosed space-brain, blood, CSF)
                        c) Factors influence ICP: arterial and venous pressure,
                            intraabdominal and intrathoracic pressure, posture,
                            temperature, blood gases (esp. CO2)
                        d) Normal body activities that increase intrathoracic
                            pressure, such as coughing, sneezing, straining will
                            cause a transient rise in ICP
                2)    Normal compensatory adaptations
                        a) Monro-Kellie doctrine applied- increase in one
                            component, causes a decrease in the other two.
                            Examples are absorption of CSF; dec CSF production;
                            displace CSF in subarachnoid space; distend dura.
                        b) Ability to compensate is limited and when maximal
                            compensation occurs and the volume increases,
                            increased intracranial pressure occurs.
                        c) Transient rises in pressure can occur with normal
                            physiological functions-coughing, sneezing, straining
                3)    Measuring ICP
                        a) Can be measured from ventricles; subarachnoid space;
                            epidural space and brain parenchyma tissue
                        b) Normal pressure in brain 0-15 mm Hg by intracranial
                            monitor (Lewis 1473 Fig 57-7)
                        c) Lumbar pressure 100-200 mm H2O (by Lumbar
                        d) Clinical symptoms appear 20-25 mm Hg; severe ICP
                            above 40mm Hg
                        e) Level and length of time (duration) are both important
                            (Lewis 1474 Fig 57-8)
          d. Cerebral blood flow
                1)    Auto regulation of cerebral blood flow
                        a) Ability of brain to regulate its own blood flow by
                            adjusting the diameter of cerebral blood vessels despite
                            changes in systemic arterial blood pressure.
                        b) Ensures a consistent CBF to provide the metabolic needs
                            of the brain tissue and maintain CPP.
                        c) Must have at least 50 mm Hg of MAP for auto regulation

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                         d) As CPP decreases, auto regulation fails and CBF
                  2)   Cerebral Perfusion Pressure (CPP)
                         a) *Pressure needed to ensure blood flow to the brain
                         b) CPP=MAP-ICP (p1468 Table 57-1)
                         c) Normal 70-100 mm Hg; neuronal death occurs <50 mm
                  3)   Pressure changes
                         a) Compliance is the expandability of the brain
                         b) Compliance= Volume/Pressure
                         c) Pressure volume curve (p1469 Fig 57-2)
                         d) Cushing’s triad can occur with loss of auto regulation
                         e) Herniation occurs as brain goes from greater to lesser
                            pressure (See below for types of herniation)
                  4)   Factors affecting cerebral blood flow
                         a) Blood gases (O2, CO2) and hydrogen ion concentration
                            affect cerebral tone
                         b) CO2 is potent cerebral vasodilator
                         c) Cerebral O2< 50 mm Hg and elevated H+ (acidosis)
                            results in cerebral vasodilatation
                         d) Cardiac/respiratory arrest; systemic hemorrhage, etc

   2. Increased intracranial pressure
          a. Cerebral edema
                 1)   Increase fluid in extravascular spaces of brain tissue.
                 2)   Causes of cerebral edema (Lewis 1470 Table 57-2)
                 3)   Vasogenic- most common; fluid in white matter
                 4)   Cytotoxic- local disruption of gray matter (cell bodies)
                 5)   Interstitial- fluid in extracellular space from systemic water
                      excess. Diffusion into ventricles hydrocephalus
          b. Mechanisms of increased intracranial pressure
                 1)   Caused by any space occupying lesion; cerebral edema; brain
                      inflammation; metabolic changes
                 2)   Progression of ICP (Lewis 1470 Fig 57-3)
                 3)   Herniation (Lewis 1471 Fig 57-4) greater to lesser pressure
   3. Normal brain 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 (reticular activation system) or
                      cerebral cortex
                 2)   Metabolic disorders
                 3)   Examples: brain lesions- (such as tumor, hematoma), cardiac
                      (as an MI), respiratory, kidney, diabetes, fluid and electrolyte
                      imbalance, drugs that suppress the CNS, and seizures.
          c. Arousal/Cognition (Level of Consciousness)
                 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.

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       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.
d. Coma states and brain death
      1)   Coma: not awake and not aware
      2)   Persistent vegetative state
             a) 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.- therefore is awake but not aware
             b) 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.
             c) Usually the result of anoxia or severe head injury.
      3)   Minimally Conscious State: awake- inconsistently aware
      4)   Locked-in Syndrome (not a true coma)
             a) Individual is alert and aware of the environment. Has
                  cognitive abilities, but unable to communicate through
             b) 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.
             c) Individual can’t verbally communicate, but can
                  communicate with eye blinks or eye movements.
      5)   Brain death
             a) Irreversible loss of brain functions.
             b) 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
e. Prognosis of coma
      1)   Outcome varies according to underlying cause and pathologic
      2)   Recovery within 2 weeks associated with favorable outcome.
      3)   Young adults can recover from deep coma.
      4)   The longer the individual unconscious, the longer has absent
           Doll’s eyes, the poorer the cognitive recovery
      5)   Residual mental problems far outweigh the physical problems
      6)   52% of patient still in vegetative state at one month after
           injury regain consciousness
      7)   It is impossible to predict the extent of functional
           improvement. 24% of patient still in vegetative state at one
           month after injury are largely independent by one year; 50%
           of patients still in minimally conscious state up to 3 months
           after injury are largely independent by one year
      8)   Individual usually more concerned with cognitive and memory
           problems; family generally more concerned with the
           emotional and personality changes.
      9)   Management of individual in a coma includes identifying
           cause, preserving function and preventing deterioration. It
           involves total body system maintenance.

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Clinical Manifestations/Complications of ICP
    1. Clinical manifestations of ICP
           a. Compensation/decompensation stages ICP/Herniations (Lewis1471 Fig
           b. Change in level of consciousness (altered cerebral function)
           c. Changes in vital signs
           d. Ocular signs
           e. Decrease in motor function (Lewis1472 Fig 57-6)
           f. Headache
           g. Vomiting- not preceded by nausea; projectile
    2. Complications of increased intracranial pressure
           a. Inadequate cerebral perfusion
           b. Herniation Syndromes (Lewis1471 Fig 57-4)
    3. Brain herniation
           a. Cingulate herniation- shift to side
                  1)    Cingulate gyrus slips under falx cerebri. It is seen on X-rays
                        as a shift of the brain.
                  2)    It is non life-threatening.
           b. Central or transtertorial herination
                  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 (medulla) compressing vital
                  3)    Life-threatening
           c. Uncal or lateral herniation
                  1)    Uncus of the temporal lobe slips through the incisural notch of
                        the tentorium.
                  2)    The third nerve becomes compressed on the same side
                        (ipsilateral) resulting in compression of the brainstems’ vital
                        centers in the medulla 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

Collaborative Care for Increased Intracranial Pressure
   1. Diagnostic studies (Lewis1472 Table 57-3 Diagnostic)
   2. Measurement of ICP
         a. Indications for ICP monitoring- examples: GCS<8; abnormal CT/MRI
         b. Methods of measuring ICP (Lewis1473 Fig 57-7)(1474 Fig 57-8)
         c. Infection major concern
         d. Waveforms similar to arterial pressure trace
         e. Any increase in intrathoracic pressures increases ICP- can see
             transient rise in ICP when sneeze, cough, vomit.

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          f.Inaccurate readings caused by CSF leaks; obstruction in catheter;
            kinks in tubing; incorrect height of drainage system relative to
            patient’s reference point
         g. CSF drainage (Lewis 1474 Fig 57-9) Monitor volume of CSF drainage!
   3. Therapeutic interventions of ICP (Lewis1472 Table 57-3- collaborative care)
         a. Adequate oxygenation and rid body of CO2- ABG analysis guides O2
            therapy; may require ventilator. PaO2 at 100 Hg or greater
         b. HOB 30 degrees, head and knees in neutral position
         c. ICP monitoring (see above) and cerebral oxygenation monitoring
            (LICOX, SjvO2); CPP> 60 mm Hg
         d. Keep blood glucose within normal range
         e. Drug therapy
                1)    Mannitol (Osmitrol)- osmotic diurectic
                2)    Corticosteroids- control vasogenic edema with tumors or
                      abscesses. Not effective in ICP of brain injury. If receiving
                      need to give meds to treat GI complications. Assess need for
                3)    High-dose Barbiturates (coma) and hypothermia to decrease
                      metabolic rate. Used for refractory ICP
                4)    Antiseizure- phenytoin (Dilantin/cerb)
                5)    H2 receptor antagonist or proton pump inhibitors- GI bleed
         f. Hypothermia to decrease metabolic rate
         g. Nutritional therapy (Lewis1475 Evidence-based practice chart)
                1)    hypermetabolic and hypercatabolic state- esp seen post brain
                      injury. NG nutrition as soon as gut functioning.
                2)    increase need for glucose
                3)    normovolemic IV normal saline- fluid balance, osmolity
         h. Surgery
                1)    To remove space occupying lesions- brain tumor, abscesses,
                2)    Craniectomy- remove part of cranium to allow for expansion
                      of swollen edema brain- be sure to assess bone flap site.

Nursing Assessment Specific to ICP
  1. Glasgow coma scale (Lewis 1477 Table 57-5)
  2. Neurologic assessment
         a. Systematic assessment unconscious (Lewis1476 Fig 57-10)
         b. Level of consciousness (most important neurological sign)
               1)    Begin assessment of altered cerebral function by observing
                     the individual’s behavior. Call their name, if no response then
                     shake individual- may be asleep.
               2)    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
               3)    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

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                  4)   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(Lewis
                              1472 Fig 57-6), absence of movements, or flaccid.
          c. Pupillary assessment (CN III) (Lewis1477 Fig 5711)
                1)     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
                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
          d. Eye movements (CN III, IV,VI) (Lewis 407 Fig 21-5)
                1)     Follow nurses finger in all directions (Fig 21-5)
          e. Eye movements- Dolls eyes (CN III, IV, VI, VIII)
                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 occulomotor (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.
          f. Motor strength
                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.

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                       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.
                         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- 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 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.
          g. Vital signs- Respiratory patterns, Cushing’s triad

Pertinent Nursing Problems and Interventions (Nursing Process)
Lewis 1479 NCP 57-1
   1. Nursing diagnosis
          a. Ineffective tissue perfusion (cerebral)
          b. Decreased intracranial adaptive capacity
          c. Risk for disuse syndrome
   2. Planning- overall goals:
          a. Maintain patent airway
          b. ICP within normal limits
          c. Normal fluid and electrolyte balance
          d. No complications secondary to immobility and decreased LOC
   3. Nursing implementation
          a. Respiratory function
          b. Fluid and electrolyte balance
          c. Monitoring ICP
          d. Assess/report any signs of IICP or change in monitor readings

                                                                       RNSG 2432  269
         e. Adequate airway- position, suction, humidification, evaluate need for
             ventilatory support.
         f. Promote venous drainage- HOB 30 degrees; avoid neck and hip
             flexion; avoid PEEP
         g. Control environmental stimuli- low lights; control family visits; PRN
             meds for painful procedures; evaluate use of restraints
         h. Plan nursing care- space procedures, don’t cluster care, especially
             painful ones.
         i. Avoid Valsalva’s maneuver as this increases intrathoracic pressure
             which in turn increases ICP- assess bowels, need for restraints
         j. 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.
         k. Assess external shunts/drains- amount/color of drainage, etc.
         l. Body position maintained with head of bed at 30 degrees
         m. Protection from injury
         n. Psychological considerations- assume that an individual in a coma can
             hear and understand everything; individual may misinterpret stimuli
   4. Evaluation

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