Increased Intracranial Pressure
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Pathophysiology
Intracranial space consists of brain tissue and
extracellular fluid
Skull non-distensible cavity
If volume of one of constituents of intracranial
cavity increases, reciprocal decrease in one or both of others
Pressure rises when volume added exceeds
compensatory capacity
IICP
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Normal intracranial pressure = 10-20 mm Hg
Responds to changes in B/P, respiratory cycle,
isometric contractions, cough, Valsalva
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> 20 = life-threatening event
As ICP rises, relationship between volume and
pressure changes; small increases in volume can change ICP significantly
IICP
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Etiology
Increases in brain volume
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Mass lesions
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Cerebral edema
Cytotoxic edema Intracellular swelling of
neurons due to hypoxia and hyperosmolality
Vasogenic Break down of blood-brain barrier so
osmotically active substances leak into interstitial area and draw water from
intravascular system. Head injuries, brain tumors, abscesses
IICP
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Etiology
Cerebrovascular alterations
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Venous outflow obstructions
Neck positions compress jugular vein and inhibit
venous return, cause central venous engorgement, increase IICP. Mechanisms that
increase intrathoracic or intraabdominal pressure
Fluctuations in blood pressure
Vasodilation
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Increases in CSF fluid
IICP
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Clinical Manifestations
Decreased level of consciousness (Categories of
Consciousness, p. 276, Box 16-1)
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Earliest sign of IICP is lethargy
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Other early indicators are slowing speech and
delay in response
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Any sudden change in condition is significant
IICP
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Clinical Manifestations
Decreased motor ability
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Decortication Internal rotation and flexion of
upper extremities, plantar flexion of feet, extension and internal rotation of
lower extremities
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Decerebrate Extension and outward rotation of
upper extremities and plantar flexion and extension of lower
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Flaccidity with loss of reflexes
IICP
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Clinical Manifestations
Decreased cranial nerve function
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Any changes in pupillary size, shape, or
reactivity ominous
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In unconscious client, pupils most sensitive
sign of deterioration
Changes in vital signs
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Cushings Triad Bradycardia, Systolic
hypertension with widening pulse pressure, bradypnea
IICP
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Clinical Manifestations
Papilledema
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Common in intracranial tumors and may be first
sign
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Early changes do not cause visual acuity
problems; may be detected only with ophthalmic exam
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Prolonged pressure causes optic atrophy and
severely diminished visual acuity
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Swelling of optic disc
IICP
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Clinical Manifestations
Increasing headache
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Constant, increasing, aggravated by movement or
straining, frontal or occipital
Blurred vision
Seizure activity
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Common in intracranial tumors
IICP
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Clinical Manifestations
Vomiting
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Recurrent and projectile, not related to meals,
may have significant nausea; occurs late in IICP
Nuchal rigidity
Lateralizing signs
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Neurological findings only on one side of body
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Help localize lesion to one side of brain
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Emergency may herald herniation
IICP
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Management (Table 61-2, p. 1864)
Immediate goal
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Reduce size of brain by decreasing cerebral
volume, CSF fluid volume, or blood volume while maintaining cerebral perfusion
Mechanisms
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Osmotic diuretics (Mannitol)
Effects occur within 20 minutes; does not cross
intact blood-brain barrier; observe for rebound IICP; 0.25-1 gm/kg IV; monitor
body wt, F&E balance; Monitor CVP; foley
IICP
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Mechanisms
Corticosteroids
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Decreases cerebral edema in brain tumors
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Reduce CSF production, stabilize blood-brain
barrier and cell membranes -> overall improvement of neuronal function
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Most common is Decadron
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Needs to be weaned off
IICP
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Mechanisms
Restrict fluids
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Goal to maintain intravascular volume without
adding free water
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Strict I&O
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CO maintained to provide adequate perfusion to
brain
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Effectiveness reflected in cerebral perfusion
pressure (CPP)
CPP = MAP ICP
Ideally > 80 mm Hg
IICP
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Mechanisms
Drain CSF
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Ventriculostomy Pliable catheter inserted into
lateral ventricle on nondominant side
Monitoring device and treatment modality
Flawless aseptic technique
Can remove CSF intermittently or continuously
Removal of even small amount will dramatically
decrease ICP
IICP
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Drain CSF
Subarachnoid bolt
Epidural monitor
Fiberoptic catheter
IICP
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Mechanisms
Hyperventilation
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Decreased PaCO2 causes
vasoconstriction and decreased CBF -> decreased ICP
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Maintained at 25-30 mm Hg
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Short term control
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PaO2 between 90 and 100 mm
Hg
IICP
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Mechanisms
Temperature control
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Cerebral metabolic rate directly proportional to
body temperature
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Persistent fluctuations and/or hypothermia or
hyperthermia in conjunction with head injury grave prognostic sign
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Antipyretic medications, cooling blanket
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Monitor temperature closely and observe for
shivering
IICP
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Mechanisms
Reduce cellular metabolic demands
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Patency of airway important
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Sedatives and/or neuromuscular blocking agents
if ICP monitor
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Control seizure activity
Dilantin:
15-18 mg/kg; not to exceed 50 mg/min
Valium: 5-10 mg bolus at 2 mg/min
Barbiturates (Pentobarbital & thiopental)
when not responsive to conventional therapy
IICP
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Mechanisms
Reduce cellular metabolic demands
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Paralyzing agents; CV monitoring; endotracheal
intubation; mechanical ventilation; ICP monitoring; arterial pressure
monitoring
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Lidocaine through ETT or IV
Blunts ICP spikes to stimulation
Prophylactic administration of Lidocaine before
ET suctioning widely practiced
IICP
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Nursing Process
Assessment
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LOC
Lethargy and change in LOC first signs;
restlessness
Glasgow Coma Scale
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Vital signs
Late sign
Cushings Triad
If major circulation begins to fail, pulse and
resp. increases and T inconsistently increases
IICP
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Assessment
Headache
Pupillary changes
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Check pupil reaction, size, conjugate (paired;
working together) or dysconjugate
Vomiting
IICP
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Nursing interventions
Achieve cerebral tissue perfusion
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Elevate HOB 30-45 degrees with head in neutral
position
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Cervical collar if needed to keep head neutral
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Avoid extreme hip flexion
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Avoid Valsalva maneuvers ask client to exhale
when being moved or turned
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Avoid isometric exercises that increase SBP
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Preoxygenate and hyperventilate prior to
suctioning
IICP
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Nursing interventions
Achieve cerebral tissue perfusion
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Space nursing interventions
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Avoid emotional distress and frequent arousal
from sleep
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Note abdominal distension
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Avoid high levels of PEEP
IICP
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Nursing interventions
Achieve airway clearance
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Suction to maintain patent airway
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Hyperoxygenation for suctioning
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Nasal drainage may indicate dural tear;
suctioning of nares contraindicated
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Auscultate lung fields
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No close mouth coughing
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Elevate HOB
IICP
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Nursing interventions
Attain normal respiratory pattern
Attain fluid balance
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Monitor skin turgor, mucous membranes, serum and
urine osmolality
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Monitor IVF carefully
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Observe for CHF and pulmonary edema if giving
Mannitol
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Good oral hygiene, monitor VS, monitor I&O
IICP
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Nursing interventions
Attain normal urine and bowel elimination
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Test urine for specific gravity and glucose
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Indwelling catheter
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Monitor UOP every 2-4 hours; output of > 200
ml/hr over two consecutive hours may = diabetes insipidus
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Monitor bowel sounds; abd. Distension
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Test stools for occult blood
IICP
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Nursing interventions
Hyperventilation
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PaCO2 ranged from 25-30 mm
Hg
Temperature control
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Prevent hyper- or hypothermia
B/P control
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High range normal essential for adequate
perfusion pressure; too high may increase ICP; sedation and antihypertensives
IICP
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Nursing interventions
Seizure control
Monitor for complications
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Brain herniation
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Cushings stress ulcer
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Diabetes insipidus
Severe polyuria followed by polydipsia
UOP more than 9 L/day and urine osmolality of
< 100 mOsm/kg after dehydration or water restriction test require ADH
replacement (desmopressin/DDAVP)
IICP
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Nursing interventions
Monitor for complications
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Syndrome of Inappropriate Secretion of ADH
(SIADH)
High levels of ADH that result in oliguria in
the absence of normal physiologic stimuli for its release
Pituitary surgery, ectopic tumors that secrete
ADH
Monitoring ICP
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Indicated when ICP > 20 mm Hg
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Mean ICP readings taken at end of respiratory
cycle and before inspiration
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Purposes
Identify increased pressure early
Quantitate degree
Initiate appropriate therapy; monitor
effectiveness
Access CSF for sampling and drainage
Monitoring ICP
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Devices
Ventricular catheter
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Lateral ventricle of nondominant cerebral
hemisphere
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ICP monitoring and drainage of CSF
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High risk for infection
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Most accurate
Monitoring ICP
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Devices
Subarachnoid screw
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Subarachnoid space
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Pressure readings and drainage of fluid
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High risk of infection
Epidural
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Between skull and dura mater
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ICP monitoring only
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Less risk of infection, but less accurate
readings
Monitoring ICP
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Devices
Intraparenchymal Fiberoptic Prob
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Nondominant brain tissue and measures brain
tissue pressure
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Ventricle, subarachnoid space, subdural space,
brain parenchyma, or under bony flap
Monitoring ICP
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Pressure waves
A waves
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Plateau waves/ 50-100 mm Hg
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Advanced intracranial hypertension
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Generally last 15-20 minutes
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Sharp increase in ICP of 30-69 mm Hg
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Plateaus for 2-20 minutes and returns to
baseline
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May increase in amplitude and frequency before
S&S of ICP seen clinically
Monitoring ICP
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Waves
B waves
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< 50 mm Hg; correspond to respirations
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Warning of potential risk of IICP
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Sharp, rhythmic oscillations with sawtooth
appearance that occur every 30 sec to 2 minutes
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Frequently precede A waves
Monitoring ICP
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Pressure waves
C waves
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Small waves (16-20 mm Hg)
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Correlate to changes in BP and respirations
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Lack clinical significance
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Occur every 4-8 minutes
Monitoring ICP
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Nursing implications
Management of A waves directed at reduction of
high pressure and prevention of other plateau waves
Closed systems to avoid contamination and
infections
Strict aseptic technique when handling system
Inspect insertion site for signs of infection
Check all connections for leaks
Monitoring ICP
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Nursing implications
Transducer zeros at particular reference point,
usually 1 inch above ear in supine client
Ensure tubing long enough but not too long
Be careful to prevent kinks in tubing
Flush catheter if readings dampen
Monitoring ICP
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Nursing implications
If inaccurate readings
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Check for leaks in system
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Differences in height of transducer and device
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Kinks
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Client performing Valsalva maneuver
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Obstruction in system
Brain herniation syndromes
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Herniation = Protrusion of brain tissue from its
normal compartment
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Syndromes
Cingulate
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Lateral shift of tissue so frontal lobes of
cerebrum compressed
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Cerebral artery compression -> ischemia and
congestion, edema, IICP, change in LOC and mental status
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Non life-threatening but can lead to others
Brain Herniation
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Syndromes
Central or Transtentorial
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Downward shift of one or both cerebral
hemispheres
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Early indication is rapid change in LOC
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Changes in respiratory patterns: Cheyne-Stokes
-> central neurogenic hyperventilation -> apneustic -> ataxic ->
apnea
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Small, reactive pupils -> dilated, fixed
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+ Babinski -> Decorticate -> Decerebrate
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Brain stem dies: Absent Dolls eyes and cold caloric
Brain Stem Herniation
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Syndromes
Uncal or lateral transtentorial
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Lateral and downward shift of brain tissue,
usually temporal
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Pupils sluggish -> unresponsive first in
ipsilateral pupil then in contralateral pupil
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Decreasing LOC
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Cheyne-Stokes respirations -> central
neurogenic hyperventilation
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Decorticate -> decerebrate
Brain Stem Herniation
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Syndromes
Tonsillar
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Downward shift through foramen magnum
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Compresses medulla and upper portion of spinal
cord
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Manifestations progress rapidly
Erratic changes in BP, pulse rate, breathing
Decreased LOC
Arched still neck
Quadriparesis
Brain Herniation
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Always an emergency
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Signs and symptoms
Assessment
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Glasgow Coma Scale standardized tool for
assessing client Actual numbers less meaningful than trend in scores
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LOC: Any
change early sign of neurological deterioration
Brain Herniation
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S&S
Sensorimotor Spontaneous movement, muscle
strength, muscle tone, coordination
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Responses may include localizing, withdrawing or
posturing, flaccidity
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Compare L and R sides and upper and lower
extremities
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Abnormal postures
Hemiplegia One side of body stops moving
spontaneously
Brain Herniation
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S&S
Assessment
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Abnormal postures
Decorticate Cortical, subcortical, or
diencephalon lesion
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Flexion of upper extremities and extension with
internal rotation of lower
Decerebrate Midbrain or pons lesion
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Jaw clenched, extremities fully extended,
plantar extension, forearms pronated, wrist and fingers flexed
Babinski Major pathological DTR. Sign of upper
motor neuron lesion and damage to corticospinal tract
Brain Herniation
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S&S
Sensorimotor function
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Orientation and awareness
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Ability to follow commands
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Appropriate responses are those that do not
elicit random or reflex responses
Show me your thumb, stick out your tongue
Brain Herniation
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S&S
Sensorimotor
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Acceptable noxious stimuli
Shaking arm
Pinching inner aspect of arm or leg
Nail bed pressure
Trapezius pinch
Supraorbital pressure
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Not acceptable
Sternal rub, nipple twisting or pinching
Brain Herniation
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S&S
Respiratory patterns
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Cheyne-Stokes: Rhythmic crescendo and
decrescendo of rate and depth of respiration; brief periods of apnea
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Central neurogenic hyperventilation: Deep, rapid
respirations without periods of apnea
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Apneustic: Prolonged inspiratory and/or
expiratory pause of 2-3 sec
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Cluster breathing: Cluster of irregular, gasping
breaths separated by long periods of apnea
Brain Herniation
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S&S
Respiratory patterns
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Ataxic: Irregular, random pattern of deep and
shallow respirations with irregular apneic periods
Eye function
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Pupils: Size, shape, equality, and light reflex.
Inequality of > 1 mm pathological sign
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Direct and consensual light reflex: Rate of
response important
Brain Herniation
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Vital signs
Changes occur late in course
Initially assess q 15 minutes, temp. q 2 hr
Trends in VS and respiratory pattern analyzed
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Head-to-toe progression
LOC deteriorates before any other neurological
changes; monitor closely for subtle changes
Stages of Central Herniation
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4 stages: Decreased LOC; nuchal rigidity, HA,
small reactive pupils -> fixed dilated pupils; Cheyne-Stokes; cardiac
dysrhythmias; decerebrate or decorticate posturing -> flaccid
Reflex testing
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Dolls eyes reflex (Oculocephalic)
Contraindicated before C-spine cleared
Hold eyelids of comatose client open and briskly
turn head to one side and then the other. Observe eye movement
Normal if eyes deviate to opposite direction
when head is turned
Abnormal if deviates in different directions
Absent if no deviation
Tests
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Ice Water caloric test (Oculovestibular reflex)
Tests brain stem function and more reliable
Not done in conscious client
HOB elevated 30 degrees and 30-50 cc ice water
quickly injected into ear
Slow phase eyes move toward instilled ear
Quick phase eyes make quick corrective action
opposite instilled ear
Tests
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Ice water caloric test
Showing brain stem integrity
Abnormal response indicative of severe brain
stem injury
Dysconjugate or no response = little or no
brainstem function
Contraindicated if CSF leak or perforated
tympanic
Ominous sign
Uncal Herniation
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Earliest sign is NOT DECREASED LOC but
UNILATERALLY DILATING PUPIL
Status Epilepticus
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Seizure activity of 30 minutes or more duration,
usually without return of consciousness
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Emergency condition
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Causes
Insufficient level of anticonvulsant drugs
most common
Metabolic disturbances
Status Epilepticus
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Causes
Infections
Structural CNS lesions
Familial predisposition
Status Epilepticus
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Management
Goals to stop seizures within 20 minutes
Valium 2 mg/min for total of 30 mg or Ativan IV
bolus for rapid control
Maintain seizure free
Ensure adequate cerebral oxygen
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Maintain clear airway, prevent aspiration by
positioning and suctioning, provide adequate oxygenation
Status Epilepticus
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Management
Assess client constantly; even when seizures
controlled may be unconscious for while
High risk for injury: Seizure precautions
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Padding siderails, keeping bedrails up, placing
suction equipment at bedside, keep bed at lowest level
Sensory-perceptual alteration
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Keep room quiet and dark in post-icteral period;
stimulation may cause more seizures
Status Epilepticus
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High risk for ineffective individual coping
Provide client verbal and written information
about medications; explain importance of taking medications regularly
Explain care during seizures
Help identify factors that precipitate seizures
and ways to avoid these factors
Head Injuries
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Any trauma to scalp, skull, or brain
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Scalp lacerations: Common, can be associated
with skull fractures so palpate for depressed skull fracture; very vascular
Skull Fractures
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Types
Linear Most common; bedrest and close
monitoring
Comminuted Bone fragmented into many pieces;
craniotomy
Depressed Outer table depressed below inner
table of surrounding intact skull. May be epileptogenic, may have CSF leak,
scalp bruising and tenderness
Skull Fractures
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Types
Compound Depressed fracture with added
problems of hemorrhage and avenue for infection to enter the cranial vault;
examine dura for tears and cranioplasty
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Clinical manifestations
Depend on amount and distribution of brain
injury
Skull Fractures
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Manifestations
Base of skull
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Hemorrhage from nose,pharynx, ears, conjunctiva
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Battles sign Ecchymosis over mastoid
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CSF from ears and nose
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Raccoons eyes periorbital ecchymosis from
extension of linear fracture into base of skull
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Spontaneous closure of dural tear in 7-10 days
if no infection and bony edges dont trap dura between them
Skull fractures
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Diagnostic Eval
Neurological exam
CT cornerstone of evaluation for head injuries
MRI
Cerebral angiography
Skull fractures
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Management
Nondepressed Close observation
Depressed Surgical intervention
Base of skull Check for CSF leak; keep
nasopharynx and external ear clean with plug of sterile cotton or sterile
cotton pad; no sneezing or blowing nose; HOB elevated 30 degrees; NVC and VS
frequently; no nasal suctioning; abx; surgical intervention if persistent
Concussion
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Temporary loss of neurological function from
which there is complete recovery
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Period of unconsciousness from several seconds
to an hour.
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May cause dizziness and spots in front of eyes
to complete loss of consciousness
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Retrograde amnesia; post-traumatic amnesia
Concussion
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Presents with HA, dizziness, N & V. No break
in dura or skull; no visible damage on CT
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Observation
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Postconcussion Syndrome: Develop immediately
after orientation or within few days
HA, visual disturbances, nervousness, dizziness,
confusion, gait abnormalities, poor memory, decreased info processing
Contusion
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Bruising of brain tissue with potential for
development of areas of necrosis, hemorrhage, edema
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Symptoms more marked
l
Gradually returns to normal; residual HA and
vertigo
Epidural Hematoma
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Blood in epidural space between dura and skull
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Tear of middle meningeal artery
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Altered LOC -> lucidity that can last 12
hours-> confusion, irritability; increasingly severe HA; deterioration of
LOC
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Hallmark is pupil fixed and dilated on side of
lesion
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Vomiting, possible seizures, hemiparesis
Epidural hematoma
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Rapid onset
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Management Extreme emergency
Burr holes through skull, removing clot,
controlling bleeding
Dx made with CT
Careful, ongoing assessment
Lower ICP with hyperventilation
Subdural hematoma
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Collection of blood between dura and underlying
brain; surface vein torn
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Slow process in frontal or temporal lobes
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Causes
Brain trauma, falls, bleeding tendencies,
aneurysms, acceleration/deceleration, rotational forces
Subdural hematoma
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Types
Acute Occurs within 24-48 hours; serious
complication
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Similar manifestations to acute epidural
hematoma with slower onset
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Often associated with moderate or severe brain
injury
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May remain unconscious or have variable LOC
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Usually has a HA
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Irritable and confused and lapse into coma or
have fluctuating LOC
Subdural hematoma
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Acute
Subtle changes in LOC and development of
lateralizing changes
Mortality 50% if associated with injuries to
other body systems
Subdural hematoma
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Subacute Occur from 2 days to 2 weeks later
Onset slower and more subtle manifestations
Suspected in clients who fail to regain
consciousness after head trauma
Clinical symptoms similar to acute
Subdural hematoma
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Chronic Occur 2 weeks to several months later
Most common in elderly and alcoholic clients
Intermittent severe HA, alternating focal
neurological signs, personality changes, mental deterioration, focal seizures,
ipsilateral pupil dilation with sluggish reaction to light, papilledema
Tx: surgical evacuation of clot
Nursing process
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Ineffective airway clearance
Maintain adequate oxygenation; elevate HOB,
monitor ABGs, monitor ventilation, guard against aspiration
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Fluid volume deficit
Daily weights, check skin turgor, monitor
I&O
Nursing Process
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Altered nutrition
NGT feedings when stabilized unless discharge of
CSF from nose; elevate HOB; check residuals; calorie count
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High risk for violence
As emerges from coma, increased agitation;
assess adequate oxygenation and no bladder distention; padded side rails; hands
in mitts; avoid restraints; avoid opiates that decrease respirations
Nursing Process
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High risk for violence
Minimize environmental stimuli; provide adequate
lighting; do not disrupt sleep-wake cycle
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Altered thought processes
Memory deficits, decreased ability to focus and
sustain attention to task, decreased ability to process information, slow
thinking, perceiving, communicating, reading, and writing
Nursing Process
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Altered thought processes
Collaborative team work; neuropsychologist plans
program and initiates treatment or counseling; redevelop ability to devise new
problem-solving strategies
Ideal coma stimulation program Single
stimulation activity lasting no more than 10-30 minutes per session, 3-4 times
per day
Nursing Process
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Potential ineffective family coping
Dealing with physical and emotional deficits,
altered relationships, changes in temperments, behavior, and personality
Provide adequate and honest information
Encourage setting well-defined, mutual,
short-term goals
Support groups
Nursing Process
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Self-care deficit
Perform ROM exercises; provide proper alignment;
encourage to do as much for self as possible; rehabilitation focus
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Impaired verbal communication
Brocas area = expressive aphasia
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Speech produced with much effort, poorly
articulated, slow, nonfluent
Nursing Process
l
Impaired verbal communication
May be able to say 2-3 words clearly, commonly
profanity and used often
May have agraphia, dysarthria, apraxia
Muscles weakened, uncoordinated, not sequenced
in movement
Be supportive of frustration and accepting of
behaviors; allow longer response time; do not supply words; accept incorrect
words
Nursing Process
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Impaired verbal communication
Wernickes area = receptive aphasia
Unable to comprehend the spoken or written word
Speech flows, rhythmic, and articulate but makes
no sense
Speech rehab ASAP; face client when speaking;
simple sentences and common words; speak slowly and distinctly; decrease
distractions, noise
Brain Tumors
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Primary Benign or malignant tumors originating
in brain
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Secondary Tumors developing from malignancies
in other parts of the body
Brain Tumors
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Classifications
Benign or malignant
Location
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Primary intracranial intracerebral tumors
Glioma (50%)
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Grade I and II usually benign and occur in
younger
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Grade III and IV malignant
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Astrocytoma Most common presents usually
with seizure followed by mental status changes Partial resection and XRT
gives ? 5 years
Brain Tumors
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Classifications
Location
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Glioblastoma Multiforme Most common and most
lethal CNS cancer. Debulking, chemo, XRT may decrease ICP. 5-18 months from
onset of clinical symptoms
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Primary Intracranial Extracerebral
Meningioma Complete resection possible with
excellent prognosis. Partial resection + XRT gives 2+ years
Acoustic neuroma CN VIII, hearing loss,
dizziness, tinnitus; excellent outcome with surgery
Brain Tumors
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Location
Pituitary tumors
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Slow growing tumors; usually benign
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Manifestations: Visual field defects, irregular
or absent menstrual cycles, infertility, decreased libido, impotence, decreased
body hair, decreased production of pituitary-stimulating hormones
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Dx by test blood for stimulating hormones
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Diabetes Insipidus fairly common sequelae of
pituitary surgery IV Pitressin or inhalation of DDAVP
Brain Tumors
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Clinical Manifestations
Headache, vomiting, papilledema significant
indicators
Headaches Often severe in frontal or occipital
region; intermittent, increasing in duration, intensified by change in posture
or straining; recurrent severe HA in client previously free of them or
recurrent HA in a.m., increasing in frequency and severity
Brain Tumors
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Clinical Manifestations
N&V Late
symptom; not related to meals; marked nausea
Papilledema May
be first sign of intracranial tumors; may cause client to seek help
Seizures focal
or generalized; often first indication of tumors
Dizziness and
vertigo; mental status changes
Localized
manifestations depending on area involved
Little
relationship between size of tumor and intensity of symptoms
Brain Tumors
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Management
Neurosurgery: Debulking, palliation, prolonged
and improved lifespan, better effects of other treatment modalities, accurately
diagnosing tumors
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Stereotactic Radiosurgery: Application of
ionizing beams of radiation focused with help of intracranial guiding devices
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Craniotomy
l
Transsphenoidal Hypophysectomy Performed
through anterior upper gum or nose; nose packed to control bleeding; head
elevated; mouth care; replacement hormones
Brain Tumors
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Management
Stereotactic Radiation Therapy: Scanning device
that creates 3-dimensional map of tumor; used for implantation of radioactive
isotopes, needle biopsy, incision and aspiration. Laser to vaporize tumor
XRT Surgically implanted radioactive nuclide
in tumor
Brain Tumors
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Management
Chemotherapy: Considered after complete XRT
course, after surgical debulking in combination with XRT, for tumor recurrence.
Corticosteroids
Immunotherapy Bone marrow harvesting prior to
chemotherapy with autologous infusion 1-2 days after chemotherapy; autologous
infusion of lymphocytes intraoperatively with glioblastoma; interferon and
interleukin-2 effective
Brain Tumors
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Nursing
Pre-operatively
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Explain procedures; encourage open communication
with family; watch use of narcotics; prophylactic steroids and antibiotics
Post-operatively
l
Continuously assess neuro status and VS; use of
diuretics and CSF drainage devices
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Cardiac monitor
Brain Tumors
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Post-op
Positioning If client neurologically unstable
and ICP elevation > 20 mmHg, avoid procedures that require flat position;
support head during elevation; avoid sharp hip flexion
l
Supratentorial surgery: Elevate 30 degrees
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Intratentorial: Most common flat without HOB
elevated
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Posterior fossa: Side lying with pillow under
head for support
Brain Tumors
l
Post-op
Drainage: Inspect dressing and underlying linens
for bleeding or CSF leak
l
Assess character, estimated amount and document
prolonged oozing; increased risk of infection and managed by abx and bedrest
Monitor labs, particularly electrolytes
(glucose, sodium, K, osmolality, and Hct)
Brain Tumors
l
Post-op
Ventilation
l
Assess respiratory parameters frequently to
avoid hypercapnia and ensure maximal oxygenation
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Arterial lines and pulse ox
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Maintain airway patency but do not suction
through nose
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Monitor ABGs
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Mechanical hyperventilation
Brain Tumors
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Medications
Osmotic diuretics and steroids
Phenytoin prophylactic to manage seizures
Antacids or histamine-blockers to prevent stress
ulcer
Acetaminophen or codeine for pain relief
Brain Tumors
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Post-op
Prevent complications
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Increased ICP
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Cerebral edema
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Hematomas
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Shock
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Hydrocephalus
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Respiratory
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Infection
Brain Tumors
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Post-op
Seizures
Achieving self-acceptance
Client home education
Spinal Cord Injuries
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Mechanisms of injury
Blunt
Penetrating
Associated factors
Nontraumatic etiologies
Spinal Cord Injuries
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Management
Goal to prevent further injury and to observe
for symptoms of progressive neurological deficits
Pharmacotherapy
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Corticosteroids High dose methylprednisolone
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Histamine blockers Reduce risk of gastric and
intestinal bleeding
Spinal Cord Injuries
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Management
Hypothermia
Respiratory measures Oxygen to maintain high
oxygen level. Caution to avoid flexing or extending the neck
Surgical stabilization
l
Advantage is allows earlier mobilization and
decreases complications
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Fusion, decompression, rod insertion, bone
grafting
Spinal Cord Injuries
l
Management
Manual stabilization
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Traction
Halo device
Tongs
Braces
Assessment
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ABCs
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Neurological exam Accurate assessment of
motor, sensory, and reflex function
Motor
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Assess for strength, ROM against resistance
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Evaluate and compare each side
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Flexion and extension of joints
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Ask client to spread fingers, squeeze hand, move
toes
Assessment
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Neurological exam
Sensory
l
Exact point where normal sensation felt
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Terms
Anesthesia Absence of normal sensation
Analgesia Decreased sensation of pain
Hypoesthesia Reduced sensation
Hyperesthesia Exaggerated sensation
Assessment
l
Neurological exam
Sensory
l
Cotton swab for sensation; pin prick for pain
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Begin distal and work proximal
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Proprioception tested by moving big toes and
thumbs up and down and asking client to confirm position
Reflex
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DTRs
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Peripheral reflexes
Assessment
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Neurological Exam
Spinal shock (Abates in 3-6 weeks)
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Immediate response to cord transection
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Complete loss of skeletal muscle function, bowel
and bladder tone, sexual function and autonomic reflexes
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Muscles innervated by the cord segment below the
level of lesion become completely paralyzed and flaccid; absent DTRs; no
perspiration
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Assumes environmental temperature; bradycardia;
hypotension
Diagnostic Tests
l
X-rays and CT scan
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Search for injuries especially of head and chest
l
EKG monitoring
Interventions
l
Promote adequate breathing
Observe for impending respiratory failure; ABGs
High-flow oxygen; pulse ox
Lesion C4 or above mechanical ventilation; T6
or above assistance with secretions
Prevent vaso-vagal response with suctioning
Lesion T12 or above at risk for atelectasis and
pneumonia
Interventions
l
Promote adequate breathing
Chest PT and quad-assisted coughing; exercises
to increase strength of muscles
Adequate humidification and hydration
Assess for signs of respiratory infection
Interventions
l
Promote mobility
Proper body alignment
Monitor B/P with position changes
PROM exercises
Interventions
l
Maintain skin integrity
Position changes every 2 hours
Inspect skin carefully
Keep skin clean and dry
Encourage client/family participation
ROM exercises
Interventions
l
Maintain urinary elimination
Immediately after injury, bladder atonic
No sensation of bladder distention
Intermittent catheterization or temporary foley
Record I&O, voiding pattern, residual
urines, quality of urine, unusual feelings
Interventions
l
Improve bowel function
Paralytic ileus NGT
Bowel activity usually returns in first week
High-calorie, high-protein, high fiber diet
Stool softeners
Bowel program ASAP
Interventions
l
Providing comfort measures
Tongs or calipers
l
Assess for signs of infection; pressure problems
Halo traction
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Slight HA around skull pins for several days
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Clean and observe for signs of infection
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Inspect skin under vest
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Do not wet liner of vest or use powder
Interventions
l
Monitor for complications
Thrombophlebitis
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Measure circumference of thighs and calfs
l
Anticoagulation once head and other injuries R/O
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ROM exercises, support stockings, adequate
hydration
l
At risk for up to 3 months
Interventions
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Complications
Orthostatic hypotension
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For first 2 weeks after SCI, BP unstable and low
l
Common in clients with lesion above T7
l
Close monitoring before and during position
changes
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Vasopressors for severe vasodilation problems
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Thigh-high elastic stockings or SCD
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Tilt tables help with transition
Interventions
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Autonomic
Hyperreflexia
Acute emergency
Occurs only after
spinal shock resolved
Severe, pounding
HA; paroxysmal hypertension; profuse sweating; nasal congestion; facial
flushing; bradycardia
Lesions above T6
Stimulated by
distended bladder, distended bowel, stimulation of skin, distention or
contraction of visceral organs
Management
l
Place immediately in sitting position to lower
BP
l
Empty bladder immediately
l
Examine rectum for fecal mass when sx subside
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Remove stimulus
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Ganglionic blocking agent (Apresoline) IV
Management
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Label medical record about risk
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Instruct client on preventive and management
measures
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Instruct any client with lesion above T6 event
can occur many years after initial injury