Chapter 54: Nervous System

Location and Function of the Parts of the Cerebrum

Cortical areas
 Motor
• Primary
 Precentral gyrus: controls initiation of movement on opposite side
of body
• Supplemental
 Anterior to precentral gyrus: facilitates proximal muscle activity,
including activity for stance and gait, and spontaneous movement
and coordination
 Sensory
• Somatic
 Postcentral gyrus: registers body sensations (e.g., temperature,
touch, pressure, pain) from opposite sides of body
• Visual
 Occipital lobe: registers visual images
• Auditory
 Superior temporal gyrus: registers auditory inputs
• Association areas
 Parietal lobe: integrates somatic and special sensory inputs
 Posterior temporal lobe: integrates visual and auditory inputs for
language comprehension
 Anterior temporal lobe: integrates past experiences
 Anterior frontal lobe: controls higher-order processes (e.g.,
judgment, insight, reasoning, problem solving, planning)
Language
 Comprehension
• Wernicke’s area: integrates auditory language (understanding of spoken
words)
• receptive aphasia: inability to understand spoken words
 Expression
• Broca’s area: regulates verbal expression
• expressive aphasia: inability to speak
 Dysarthria: difficult speech due to impairment of muscles involved with
production of speech
Basal ganglia: near lateral ventricles of both cerebral hemispheres – controls and
facilitates learned and automatic movements
Thalamus: below basal ganglia – relays sensory and motor inputs to cortex and other
parts of cerebrum
Hypothalamus: below thalamus – regulates endocrine and autonomic functions (e.g.,
feeding, sleeping, emotional and sexual responses)
Limbic system: Lateral to hypothalamus – influences affective (emotional) behavior and
basic drives such as feeding and sexual behavior

Chapter 55: Acute Intracranial Problems

 Factors that influence ICP under normal circumstances are changes in:
• arterial pressure
• venous pressure
• intraabdominal and intrathorasic pressure
• posture
• temperature
• blood gases, particularly CO2 levels
 Oxygen tension increased = vasodilation: increased blood flow for
oxygen
 CO2 tension increased = vasodilation
 Hydrogen ion concentration = acidosis: vasodilation
 Intracranial Pressure (ICP)
• Cerebral Edema: increased accumulation of fluid in the extravascular
spaces of the brain tissue)
• Three types of cerebral edema
 Vasogenic
♦ most common type
♦ occurs mainly in white matter and is attributed to changes
in the endothelial lining of cerebral capillaries
♦ allow leakage of macromolecules from capillaries into
extracellular space, resulting in an osmotic gradient that
favors the flow of water from the intravascular to the
extravascular space
♦ Causes: brain tumors, abscesses, and ingested toxins –
increases permeability of blood-brain barrier and produce
and increase in extracellular volume
♦ Symptoms: focal neurologic deficits to disturbances in
consciousness, including coma
 Cytotoxic
♦ swelling of brain cells – fluid and protein shift from
extracellular to intracellular
♦ occurs most often in gray matter
♦ destructive lesions or trauma to brain tissue resulting in
hypoxia or anoxia, sodium depletion, and SIADH
♦ Causes: medications
 Interstitial
 ♦ result of periventricular diffusion of ventricles in CSF in a
patient with uncontrolled hydrocephalus
♦ it can also be caused by enlargement of the extracellular
space as a result of systemic water excess (hyponatremia)

Neuro Check
 Change in LOC
• orientation to time, place, person
• speech: clear, garbled, rambling
• ability to follow commands
• if client unable to respond to verbal stimuli, apply painful stimulus by
squeezing nail bed; not response to pain
• abnormal posturing (may occur spontaneously or in response to stimulus)
 Decorticate (flexor) posture: extension of legs, internal rotation
and adduction of the arms with flexion of the elbows, wrist, and
fingers (damage to corticospinal tracts; cerebral hemispheres)
 Decerebrate (extensor) posture: back arched, rigid extension of all
four extremities with hyperpronation of arms and plantar flexion of
feet damage to upper brain stem, midbrain, and pons)
 Glasgow coma scale
• objective evaluation of LOC, motor/verbal response; a standardized
system for assessing the degree of neurological impairment in critically ill
patients
• a score of 15 indicates client is awake and oriented; the lowest score, 3, is
deep coma; a score of 7 or below is considered coma
 Change in VS
• caused by increasing pressure on the thalamus, hypothalamus, pons, and
medulla
• Cushing triad
 increased systolic pressure (widening pulse pressure)
 bradycardia with full and bounding pulse
 irregular respiratory pattern
♦ Cheyne-Stokes: regular, rhythmic alternating between
hyperventilation and apnea; cerebral dysfunction or
metabolic problems
♦ Central neurogenic hyperventilation: sustained, rapid,
regular respirations (rate of 25/min) with normal blood
oxygen levels; brainstem dysfunction
♦ Apneustic: prolonged inspiratory phase, followed by a 2 to
3 sec pause; dysfunction of respiratory center in pons
♦ Cluster breathing: clusters of irregular breathing,
irregularly followed by periods of apnea; lesions in upper
medulla and lower pons
 ♦ Ataxic breathing: completely irregular; damage to
respiratory centers in medulla
 Ocular Signs
• observe size, shape, and equality of pupils (note size in millimeters)
• reaction to light, papillary constriction
• corneal reflex: blink reflex in response to light stroking of cornea
• oculocephalic reflex (doll’s eyes) present in unconscious client with intact
brainstem; eyes stationary (midline) as the head is moved to the right or
left
• compression of oculomotor nerve (CN III) results in dilation of the pupil
ipsilateral to the mass or lesion, sluggish or no response to light, inability
to move eye upward, and ptosis of eyelid
• a fixed, unilateral dilated pupil - neurological emergency – indicates
herniation of the brain
 Motor Function
• movement of extremities (paralysis)
• muscle strength (if can follow demands)
 Headache
• compression of other intracranial structures
• often continuous but worse in morning
• straining or moving may accentuate the pain
 Vomiting
• unexpected (not associated with nausea); projectile
• pressure on vomiting center (medulla)

Complications of IICP
 inadequate cerebral perfusion
 cerebral herniation

Care for the Client with IICP

 General Information
• An increase in intracranial bulk due to an increase in any of the major
intracranial components: brain tissue, CSF, or blood.
• Increased ICP may be caused by tumors, abscesses, hemorrhage, edema,
hydrocephalus, inflammation.
• Untreated IICP can lead to displacement of brain tissue (herniation
• Presents life-threatening situation because of pressure on vital structures in
the brain stem, nerve tracts, and cranial nerves.
 Assessment Findings
• Earliest signs: decrease in LOC; progresses from restlessness to confusion
and disorientation to lethargy and coma
• Changes in vital signs (may be late sign)
  systolic blood pressure rises while diastolic pressure remains the
same (widening pulse pressure
 pulse slows
 abnormal respirations (e.g., Cheyne-Stokes)
 elevated temperature

• Pupillary changes
 Ipsilateral (same side) dilation of pupil with sluggish reaction to
light from compression of cranial nerve III
 pupil eventually becomes fixed and dilated
• Motor abnormities
 Contralateral (opposite side) hemiparesis from compression of
corticospinal tract
 Decorticate or decerebrate rigidity
• Headache, projectile vomiting, papilledema (edema of the optic disc)
 Nursing Care
• Maintain patent airway and adequate ventilation
 prevention of hypoxemia and hypercarbia (increased CO2)
important: hypoxia may cause brain swelling and hypercarbia
causes cerebral vasodilation, which increases ICP
 before and after suctioning, hyperventilate the client with 100%
oxygen limiting suction to 15 seconds
 assist with mechanical hyperventilation as indicated: produces
hypocarbia (decreased CO2) causing cerebral vasoconstriction and
decreased ICP
 monitor PCO2 levels (35-45)
• Monitor VS and neuro checks frequently at least every hour initially to
detect rise in ICP
• Maintain fluid balance: fluid restriction to 1200-1500 ml/day may be
ordered
• Position client with HOB elevated to 30-45 degrees and neck in neutral
position unless contraindicated (facilitates reduction of cerebral edema)
• Prevent further increases in ICP
 maintain quiet, comfortable environment
 avoid use of restraints
 prevent straining of stool; administer stool softeners and mild
laxatives as ordered
 prevent vomiting; administer antiemetics as ordered
 prevent excessive coughing
 cluster activities to minimize time disturbed
• Prevent complications of immobility
• Administer medications as ordered
 hyperosmotic agents (mannitol [Osmitrol]) to reduce cerebral
edema (pulls fluid from tissue into cells); monitor urine output
every hour (should increase)
 Diuretics (furosemide [Lasix]) to reduce cerebral edema; given 1
hour after mannitol
 Corticosteroids (dexamethasone [Decadron]); anti-inflammatory
effects reduces cerebral edema (works best if given in first 24
hours)
 Anticonvulsants (phenytoin [Dilantin]) to prevent seizures

 Analgesics for headache as needed

♦ small doses of codeine
♦ stronger opiates may be contraindicated since they
potentiate respiratory depression, alter LOC, and cause
papillary changes
• Assist with ICP monitoring when indicated
 ICP monitoring records the pressure exerted within the cranial
cavity by the brain, cerebral blood, and CSF
 Types of monitoring devices
♦ intraventricular catheter: inserted in lateral ventricle to give
direct measurement of ICP; also allows for drainage of CSF
if needed
♦ subarachnoid screw (bolt): inserted through skull and dura
mater into subarachnoid space
♦ epidural sensor: least invasive method; placed in space
between skull and dura mater for indirect measurement of
ICP
 Monitor ICP pressure readings frequently and prevent
complications
♦ Normal ICP reading 0-15 mmHg; a sustained increase
above 15 mmHg is considered abnormal
♦ use strict aseptic technique when handling any part of the
monitoring system
♦ check insertion site for signs of infection; monitor
temperature
♦ assess system for CSF leakage, loose connections, air
bubbles in lines, and occluded tubing
• Provide intensive nursing care for client treated with barbiturate therapy or
administration of paralyzing agents
 intravenous administration of barbiturates may be ordered to
induce coma artificially in the client who has not responded to
conventional treatment
♦ can not do focus neuro assessement
 ♦ IV drip – short period of time – titrate – ordered by
neurosurgeon
♦ reduces cellular metabolic demands that may protect the
brain from further injury
 paralytic agents such as vecuronium bromide (Norcuron) may be
administered to paralyze the client
 constant monitoring of the client’s ICP, arterial blood pressure,
pulmonary pressures, ABGs, serum barbiturate levels, and ECG is
necessary
 EEG monitoring as necessary
• Observe for hyperthermia secondary to hypothalamus damage

• Nutritional Needs
 increased glucose needs (TPN)
 dehydration controversial
♦ thought to be effective in reducing cerebral edema; in this
case fluids are restricted 65-75% of normal requirements
♦ concern that hypovolemia may result in a decrease in
cardiac output and BP, which may affect cerebral perfusion
and the amount of oxygen delivered to the brain

Chapter 55: pgs. 1505-1511

Head Injury
 General Information
• usually caused by car accidents, falls, assaults
• Deaths from head trauma
 immediately after injury
 2 hours after injury
 approximately 3 weeks after injury
• types
 Concussion: (minor) severe blow to the head jostles brain, causing
it to strike the skull; results in temporary neural dysfunction
 Contusion: (major) results from more severe blow that bruises the
brain and disrupts neural function
• hemorrhage
 epidural hematoma: accumulation of blood between the dura mater
and skull; commonly results from laceration of middle meningeal
artery during skull fracture; blood accumulates rapidly
  subdural hematoma: accumulation of blood between the dura and
arachnoid; venous bleeding that forms slowly; may be acute,
subacute, or chronic
 subarachnoid hematoma: bleeding in subarachnoid space
 intracerebral hematoma: accumulation of blood within the
cerebrum
• fractures: linear, depressed, comminuted, compound
 Assessment Findings
• Concussion: headache, transient loss of consciousness, retrograde or
posttraumatic amnesia, nausea, dizziness, irritability
• Contusion: neurologic deficits depend on the site and extent of damage;
include decreased LOC (loss of consciousness), aphasia, hemiplegia,
sensory deficit

• Hemorrhages
 Epidural hematoma: brief loss of consciousness followed by lucid
interval; progresses to severe headache, vomiting, rapidly
deteriorating LOC, possible seizures, ipsilateral papillary dilation
 Subdural hematoma: alterations in LOC, headache, focal
neurologic deficits, personality changes, ipsilateral papillary
dilation
 Intracerebral hematoma: headache, decreased LOC, hemiplegia,
ipsilateral papillary dilation
• Fractures
 Headache, pain over fracture site
 Compound fractures: rhinorrhea (leakage of CSF from nose);
otorrhea (leakage of CSF from ear)
• Diagnostic Tests
 Skull x-ray: reveals skull fracture or intracranial shift
 CT scan: reveals hemorrhage
 Nursing Interventions
• Maintain a patent airway and adequate ventilation (admin. O2)
• Stabilize cervical spine (assume neck injury with head injury)
• IV access – 2 large-bore needles- NS or LR (warm IV fluids); administer
fluids cautiously to prevent fluid overload and IICP
• Monitor vital signs and neuro checks; observe for changes in neurologic
status, signs of IICP, shock, seizures, and hyperthermia
• Observe for CSF leakage
 Check discharge for positive Testape or Dextrostix reaction for
glucose; bloody spot encircled by watery, pale ring “halo” on
pillowcase or sheet.
  Never attempt to clean the ears or nose of a head-injured client or
use nasal suction unless cleared by physician.
• If a CSF leak is present
 Instruct client not to blow nose
 Elevate HOB 30 degrees as ordered
 Observe for signs of meningitis and administer antibiotics to
prevent meningitis as ordered
 Place cotton ball in the ear to absorb otorrhea; replace frequently
 Gently place a sterile gauze pad at the bottom of nose for
rhinorrhea; replace frequently
• Prevent complications of immobility
• Prepare client for surgery if indicated
 Depressed skull fracture: surgical removal or elevation of
splintered bone; debridement and cleansing of area; repair of dural
tear if present; cranioplasty
 Epidural or subdural hematoma: evacuation of the hematoma

Chapter 59: pgs 1610-1634

Spinal Cord Injuries

 General Information
• Occurs most commonly in young adult males between 15-25
• Common traumatic causes: MVA, diving in shallow water, falls, industrial
accidents, sports injuries, gunshot or stab wounds
• Nontraumatic causes: tumors, hematomas, aneurysms, congenital defects
(spina bifida)

• Classified by extent, level, and mechanism of injury

 Extent of Injury
♦ may affect vertebrae column: fracture, dislocation
♦ may affect anterior or posterior ligaments, causing
compression of spinal cord
♦ may be to the spinal cord and its roots: concussion,
contusion, compression, or laceration by
fracture/dislocation or penetrating missiles
 Level of Injury: cervical, thoracic, lumbar
 Mechanisms of Injury
♦ hyperflexion
♦ hyperextension
♦ axial loading (force exerted straight up or down spinal
column as in diving)
♦ penetrating wound
  Pathophysiology: hemorrhage and edema cause ischemia, leading
to necrosis and destruction of cord
 Medical Management: immobilization and maintenance of normal spinal
alignment to promote fracture healing.
• Horizontal turning frames (Stryker frame)
• Skeletal traction: to immobilize the fracture and maintain alignment of the
cervical spine
 Cervical tongs (Crutchfield, Gardner-Wells, Vinke): inserted
through burr holes; traction is provided by a rope extended from
the center of tongs over a pulley with weight attached at the end.
 Halo traction
♦ Stainless steel halo ring fits around the head and is attached
to the skull with four pins; halo is attached to plastic body
cast or plastic vest.
♦ Permits early mobilization, decreased period of
hospitalization and reduces complications of immobility.
 Surgery: decompression laminectomy, spinal fusion
• Depends on type of injury and the preference of the surgeon
• Indications: unstable fracture, cord compression, progression of
neurologic deficits
 Assessment Findings
• Spinal shock
 Occurs immediately after the injury as a result of the insult to the
CNS
 Temporary condition lasting from several days to months
 Characterized by decreased reflexes, loss of sensation, and flaccid
paralysis below the level of injury
• Neurogenic shock
 due to loss of vasomotor tone caused by injury
 characterized by hypotension, bradycardia, and warm, dry
extremities (parasympathetic takes over)
 loss of sympathetic innervation causes peripheral vasodilation,
venous pooling, and decreased CO
 effect usually associated with a cervical or high thoracic injury
• Classification of Spinal Cord injury
 Mechanisms of injury
♦ flexion
♦ hyperextension
♦ flexion-rotation: most unstable – ligamentous structures
stabilizing spine are torn – severe neurological deficits
♦ extension-rotation
♦ compression
 Level of injury
 ♦ paraplegia: thoraco/lumbar injuries (T1-L4) cause paralysis
of the lower half of the body involving both legs
♦ Skeletal level: injury is the vertebral level where there is
most damage to vertebral bones and ligaments
♦ Neurologic level: lowest segment of spinal cord with
normal sensory and motor function on both sides of the
body
♦ Level of injury may be cervical, thoracic, or lumbar
 Cervical and Lumbar
o if cervical cord involved, paralysis of all
four extremities; quadriplegia (tetraplegia):
cervical injuries (C1-C8) cause paralysis of
all four extremities; premature death is
usually related to compromised respiratory
function
o if thoracic or lumbar cord is damaged,
paraplegia: thoraco/lumbar injuries (T1-L4)
cause paralysis of the lower half of the body
involving both legs

 Degree of Injury
♦ Complete cord involvement
 Primary injury
 complete damage
 actual physical disruption of axons resulting in total
loss of sensory and motor function below the level
of the lesion (injury)
♦ Incomplete cord involvement
 Secondary injury
 ischemia, hypoxia, microhemorrhage, and edema
 mixed loss of voluntary motor activity and
sensation and leaves some tracts intact
 extent of injury and prognosis for recovery
determined at 72 hours or more after injury
 Syndromes associated with incomplete cord
involvement
o Central cord syndrome
 damage to central spinal cord
 cervical cord region
  motor weakness and sensory loss
present in all extremities, but upper
is affected more
o Anterior cord syndrome
 damage to the anterior spinal artery
 acute compression of anterior portion
of spinal cord
 often a flexion injury
 manifestations include: motor
paralysis, loss of pain, and
temperature sensation below level of
injury
o Brown-Sequard syndrome
 damage to one half of the spinal cord
 characterized by loss of motor
function and position and vibratory
senses, as well as vasomotor
paralysis on the same side
(ipsilateral) as the lesion; The
opposite (contralateral) side has loss
of pain and temperature sensation
below the level of the lesion

 Nursing Assessment: Manifestations

• Neurologic
 Complete: Flaccid paralysis and anesthesia below level of injury
resulting in tetraplegia (for lesions above C8 or paraplegia (for
lesions below C8), hyperactive deep tendon reflexes, bilateral
positive Babinski test (after resolution of spinal shock)
 Incomplete: Mixed loss of voluntary motor activity and sensation
• Musculoskeletal: Muscle atony (in flaccid state), contractures (in spastic
state)
• Respiratory System
 Cervical injury C1-C3: apnea, inability to cough
 Cervical injury at C4: poor cough, diaphragmatic breathing (spinal
cord edema and hemorrhage can affect function of phrenic nerve
causing hyperventilation)
 Cervical injury at C5-C6: decreased respiratory reserve
 Loss of respiratory muscle function
 Mechanical ventilation required
• Cardiovascular
  Above level of T5 (decreases sympathetic nervous system)
 Bradycardia
 Hypotension/postural hypotension
 Absence of vasomotor tone
 Cardiac monitoring necessary
 Treatment
♦ heart rate < 40 – atropine (increases heart rate and prevent
hypoxemia)
♦ IV fluids or Dopamine – increases HR and BP
♦ long term bradycardia: pacemaker
• Urinary
 Retention (for lesions between T1 and L2)
 Flaccid bladder (acute stages)
 Spasticity with reflex bladder emptying (later stages)
 Neurogenic bladder
 Spinal shock
♦ bladder atonic
♦ overdistended
♦ treatment: indwelling catheter
 Postacute phase
♦ bladder may become hyperirritable, with loss of inhibition
from brain resulting in reflux emptying
♦ When stable and large amounts of IV fluids are not
required, start intermittent catheterization; this helps to
maintain bladder tone and decrease risk of infection

• GI
Decreased or absent bowel sounds

Hypomotility (paralytic ileus in lesions above T5)

Abdominal distention

Constipation

Fecal incontinence

Fecal impaction

Treatment: intermittent NG suctioning – may relieve distention;

Reglan to delay gastric emptying; H2 blockers (Zantac, Pepcid)
and proton pump inhibitors (Prilosec and Prevacid) to prevent
occurrence of ulcers during initial phase
 Intraabdominal bleeding (s/s: continued hypotension, and
decreased H&H, expanded abdominal girth)
• Skin
 Thermoregulation
 ♦ Poikilothermism: unable to regulate body heat
♦ body temperature takes on temperature of environment; life
threatening – teach to control environment at normal body
temperature
 Halo: pin care
 Halo vest: no showers, no scratching, assess skin with flashlight,
can use powder
 Pressure ulcers – infection – sepsis
• Reproductive: Priapism, loss of sexual function
• Possible Findings
 Location of level and type of bony involvement on spinal x-ray:
lesions, edema, compression on CT scan and MRI; positive finding
on myelogram
 Collaborative Care: Initial
• Assess airway, breathing, circulation
 Do not move client during assessment
 If airway obstruction or inadequate ventilation exists: do not
hyperextend neck to open airway, use jaw thrust instead
• Stabilize cervical spine
• Immobilization
 Maintenance of a neutral or slight extension position
 Sand-bags, hard cervical collars, and backboards to stabilize neck
to prevent lateral rotation of cervical spine
 Immobilization of vertebral column by skeletal traction
 Body should always be correctly aligned, and turning should be as
one unit (logrolling)
• Administer oxygen with high humidity
• IV access – NS or LR as ordered
• Perform a quick head-to-toe assessment: check for LOC, signs of trauma
to the head or neck, leakage of clear fluid from ears or nose, signs of
motor or sensory impairment
• Control external bleeding
• Obtain cervical spine radiographs with cranial tongs and traction
• Maintenance of HR (atropine); and BP (dopamine)
• Administer high-dose methylprednisolone (solu-medrol) – within 8 hrs
injury – results in greater recovery of neurological function
• NG tube with intermittent suction
• Indwelling urinary catheter (to ensure continuous flow of urine to prevent
reflux of urine into kidneys)
• Stress ulcer prophylactic
• Bowel and Bladder training
 Collaborative Care: Ongoing Monitoring
• Monitor VS, LOC, O2 sats, cardiac rhythm, UO
 • Keep patient warm
• Monitor for urinary retention, HTN
• Anticipate need for intubation if gag reflux absent
 Nursing Interventions: acute care
• Maintain optimum respiratory function
 Observe for weak or labored respirations; monitor ABGs
 Prevent pneumonia and atelectasis: turn every 2 hours; cough and
deep breath every hour; use IS every 2 hours
• Maintain optimal cardiovascular function
 Monitor VS; observe for bradycardia, arrhythmias, hypotension
 Apply thigh-high elastic stockings or ace bandages
 Change position slowly and gradually – elevate HOB to prevent
postural hypotension
• Maintain fluid and electrolyte balance and nutrition
 NG tube may be inserted until bowel sounds return
 Maintain IV therapy as ordered; avoid overhydration (can
aggravate cord edema
 Check bowel sounds before feeding client (paralytic ileus
common)
 Progress slowly form clear to regular diet
 Provide diet high in protein, carbohydrates, calories (TPN and
Lipids)
• Maintain immobilization and spinal alignment always
 Turn every hour on turning frame
 Maintain cervical traction at all times if indicated
• Prevent complications of immobility; use footboard/high topped sneakers
to prevent foot drop; provide splint for quadriplegic client to prevent wrist
drop
• Maintain urinary elimination
 Provide intermittent catheterization or maintain indwelling
catheter as ordered
 Increase fluids to 3000 ml/day
 Provide acid-ash foods/fluids to acidify urine and prevent infection
• Maintain bowel elimination: administer stool softeners and suppositories
to prevent impaction as ordered
• Monitor temperature control
 Check temperature every 4 hours
 Regulate environment closely
 Avoid excessive covering or exposure
• Observe for and prevent infection
 Observe tongs or pin site for redness, drainage
 Provide tong-or-pin-site care. Cleanse with antiseptic solution as
ordered
  Observe for signs of respiratory or urinary infection
• Observe for and prevent stress ulcers
 Assess for epigastric or shoulder pain
 If corticosteroids are ordered, give with food or antacid; administer
H2 blocker as ordered
 Check NG tube contents and stools for blood
 Nursing Interventions: chronic care
• Neurogenic bladder
 Reflex or upper motor neuron bladder; reflex activity of the
bladder may occur after spinal shock resolves; the bladder is
unable to store urine very long and empties involuntary
 Nonreflexive or lower motor neuron bladder: reflex arc is
disrupted and no reflex activity of the bladder occurs, resulting in
urine retention with overflow
 Management of reflex bladder
♦ intermittent catheterization every 4 hours and gradually
progress to every 6 hours (does not need to be sterile
procedure – own flora)
♦ regulate fluid intake to 1800-2000 ml/day
♦ bladder taps or stimulating trigger points to cause reflex
emptying of the bladder
 Management of nonreflexive bladder
♦ intermittent catheterization every 6 hours
♦ Crede maneuver or rectal stretch
♦ regulate intake to 1800-2000 ml/day
• Spasticity
 Return of reflex activity may occur after spinal shock resolves;
severe spasticity may be detrimental
 Drug therapy: baclofen (Lioresal), dantorlene (Dantrium),
diazepam (Valium)
 Physical therapy: stretching exercises, warm tub baths, whirlpool
 Surgery: chordotomy
• Autonomic dysreflexia
 Massive uncompensated cardiovascular reaction mediated by the
sympathetic nervous system
 Lesions above T6 or higher
 Visceral stimulation once spinal shock is resolved with spinal cord
lesions above T7
 Rise in BP, sometimes to fatal levels
 Stimulus may be overdistended bladder or bowel, stimulation of
the skin, or stimulation of pain receptors
 If not resolved, can lead to status epilepticus, stroke, MI, and death
 Symptoms
 ♦ Sudden onset of acute headache
♦ Elevation in BP and/or reduction in pulse rate
♦ Flushed face and upper chest (above level of lesion) and
pale extremities (below level of lesion)
♦ Sweating above level of lesion
♦ Nasal congestion
♦ Feeling of apprehension (anxiety)
 Interventions
♦ elevate HOB 45 degrees or upright position to decrease BP
♦ remove the stimulus (bladder irritation (distended bladder)/
kinked urinary catheter, fecal impaction, constrictive
clothing/tight shoes)
♦ call physican if above actions unsuccessful
♦ immediate catheterization to relieve bladder distention;
Lidocaine jelly should be installed in urethra before
catheterization
♦ Digital rectal exam only after anesthetic ointment to
decrease rectal stimulation and to prevent an increase of
symptoms
♦ Monitor BP frequently
♦ administer antihypertensives (e.g., hydralazine HCl
[Apresoline] as ordered
 Efforts to decrease likelihood of autonomic dysreflexia
♦ Maintain regular bowel function
♦ Monitor UO
 Sensory deprivation
• books on tape/tv for short periods (do not over-stimulate)
• open blinds for sunlight
• allow visitors
• talk to patient
• prism glasses

 Mourning process and Nursing Interventions in Spinal Cord Injury

• Shock and Denial
 Use meticulous nursing care
 Be honest
 Use simple diagrams to explain injury
  Encourage patient to begin road to recovery
 Establish agreement to use and improve all current abilities while
not denying the possibility of future improvement
• Anger
 Coordinate care with patient and encourage self-care
 Support family members; prevent alleviation of guilt by supporting
dependency
 Use humor liberally
 Allow patient outbursts
 Do not allow fixation on injury
• Depression
 Encourage family involvement and resources
 Plan graded steps in rehabilitation to give success with minimal
opportunity for frustration
 Give cheerful and willing assistance with ADL’s
 Avoid sympathy
 Use firm kindness
• Adjustment
 Remember that patients have individual personalities
 Balance support systems to encourage independence
 Set goals with patient input
 Emphasize potentials

Chapter 56: Stroke

Cerebrovascular Accident (CVA)

 General Information
• Infarction of brain cells caused by a reduction in cerebral blood flow and
oxygen
• Caused by thrombosis, embolism, hemorrhage
• Risk factors
 HTN, DM, ateriosclerosis/atherosclerosis, cardiac disease, chronic
Afib, MI
 Lifestyle: obesity, smoking, inactivity, stress, use of oral
contraceptives

 Types of Strokes
• Ischemic stroke: results from inadequate blood flow to the brain from
partial or incomplete occlusion of an artery
  Thrombotic
♦ result of thrombosis or narrowing of blood vessel
♦ associated with HTN or DM
♦ warning (TIA
♦ onset during or after sleep
 Embolic
♦ occurs when an embolus lodges in and occludes a cerebral
artery, resulting in infarction and edema
♦ sudden onset
♦ may or may not be related to activity
• Hemorrhagic stroke: results from bleeding into brain tissue (intracerebral)
or into the subarachnoid space or ventricles
 Intracerebral
♦ bleeding into brain caused by rupture of vessel
♦ primary cause: HTN
♦ occurs during periods of activity
♦ sudden onset of symptoms, with progression over minutes
to hours (ongoing bleeding)
♦ symptoms include neurologic deficits, headache, nausea,
vomiting, decreased LOC, and HTN
 Subarachnoid
♦ occurs when there is intracranial bleeding into the
cerebrospinal fluid-filled space between the arachnoid and
pia mater
♦ commonly caused by rupture of cerebral aneurysm
♦ majority of aneurysms are located in the circle of Willis
♦ warning sign: sudden onset of severe headache “the worst
headache of one’s life”
♦ other symptoms include focal neurological deficits, n/v,
seizures, and stiff neck
• Pathophysiology
 Interruption of cerebral blood flow for 5 min. or more causes death
of neurons in affected areas with irreversible loss of function
 Modifying factors
♦ cerebral edema: develops around affected area causing
further impairment
♦ vasospasm: constriction of cerebral blood vessel may
occur, causing further decrease in blood flow
♦ collateral circulation: may help to maintain cerebral blood
flow when there is compromise of main blood supply

 Stages of Development
 ♦ Transient ischemic attack (TIA)
 warning sign of impending CVA
 brief period of neurologic deficit: visual loss,
hemiparesis, slurred speech, aphasia, vertigo
 may last less than 30 seconds, but no more than 24
hrs with complete resolution of symptoms
♦ Stroke in evolution: progressive development of stroke
symptoms over period of hours to days
♦ Completed stroke: neurologic deficit remains unchanged
for 2-3 day period
 Assessment Findings
• Headache
• Generalized signs: vomiting, seizures, confusion, disorientation, decreased
LOC, nuchal rigidity, fever, HTN, slow bounding pulse, Cheyne-Stokes
respirations
• Focal signs (related to sight of infarction): hemiplegia, sensory loss,
aphasia, homonymous hemianopsia
• Diagnostic tests
 CT and brain scan: reveal lesion
 EEG: abnormal changes
 Cerebral arteriography: may show occlusion or malformation of
blood vessels
 Nursing Interventions: Acute Stage
• Maintain patent airway and adequate ventilation
• Monitor VS and neuro checks and observe for signs of ICP, shock,
hyperthermia, and seizures
• Provide complete bedrest
• Plan nursing care activities to minimize increase in ICP
• Maintain fluid and electrolyte balance and ensure adequate nutrition
 IV therapy first few days (1500-200 ml/day)
 NG if unable to swallow
 Fluid restriction as ordered to decrease cerebral edema
 IV solutions with glucose and water are avoided because they are
hypotonic and may increase cerebral edema and ICP
• Maintain proper positioning and body alignment
 HOB elevated 30-45 degrees to decrease ICP
 Turn and reposition every 2 hours (only 20-30 min. on affected
side)
 Passive ROM every 4 hrs
 Avoid neck or extreme hip/knee flexion to avoid obstruction of
arterial and venous blood flow
• Promote optimum skin integrity: turn and apply lotion every 2 hours
 • Maintain adequate elimination
 Offer bedpan or urinal every 2 hours
 Administer stool softeners and suppositories as ordered to prevent
constipation and fecal impaction
• Provide a quiet, restful environment
• Establish a means of communicating
• Administer medications as ordered
 Hyperosmotic agents, corticosteroids to decrease cerebral edema
 Anticonvulsants to prevent or treat seizures
 Thrombolytics given to dissolve clot (hemorrhage must be ruled
out)
♦ tissue plasminogen activator (tPA, Alteplase)
 lyses the clot
 clot specific
 less likely to cause hemorrhage
 must be given 3 hrs of onset of clinical signs of
ischemic stroke
♦ streptokinase, urokinase
♦ control of BP is critical during treatment and for 24 hrs
following
♦ no anticoagulant or antiplatelet drugs are given for 24 hrs
after tPA treatment
 Anticoagulants for stroke in evolution or embolic stroke
(hemorrhage must be ruled out)
♦ heparin
♦ warfarin (Coumadin) for long term therapy
♦ aspirin and Persantine to inhibit platelet aggregation in
treating TIAs
 Antihypertensives if indicated for elevated BP
 Nursing Interventions: Rehabilitation
• Hemiplegia: results from injury to cells in the cerebral motor cortex or to
corticospinal tracts (causes contralateral hemiplegia since tracts cross in
medulla)
 To maintain optimal function of musculoskeletal
♦ Use proper positioning and repositioning to prevent
deformities (foot drop, external rotation of hip etc…)
 trochanter roll at the hip to prevent external rotation
 hand cones to prevent hand contractures/hand
splints to reduce spasticity
  posterior leg splints, footboards, or high-top shoe to
prevent foot drop
 elevate extremities to prevent edema
 provide active and passive ROM every 4 hrs

 to prevent subluxation (displacement) of shoulder

 support paralyzed arm on pillow or use sling
while out of bed
 avoidance of pulling patient by arm
• Susceptibility to hazards
 Keep side rails up at all times
 Institute safety measures
♦ sitting patient up in bed or dangling on edge of bed to
evaluate tolerance by noting dizziness or syncope
♦ transferring: chair is placed beside bed so patient can lead
with stronger arm and leg; pt. sits on side of bed, stands,
places strong hand on far wheel-chair arm, and sits down
 Prevention of skin breakdown
♦ pressure relief by turning every 2 hrs (side-back-side),
special mattress, w/c cushions
♦ good skin hygiene: emollients applied to dried skin
♦ early mobility
♦ pillows under lower extremities to reduce pressure on heels
♦ Control of pressure is single most important factor in both
the prevention and treatment of skin breakdown
• Dysphagia
 Check gag reflex before feeding by stimulating the back of throat
with tongue blade
 Maintain calm, unhurried approach
 Place in upright position with head flexed forward for the feeding
and remain upright 30 min. following
 Place food in unaffected side of mouth
 Give mouth care before to stimulate sensory awareness, salavation
and facilitate swallowing and after meals because food may collect
on affected side of mouth
 Crushed ice can be given as a stimulant
 Offer soft foods
 Puree foods – not best choice because often bland and too smooth
 Foods to avoid
♦ Thin liquids: difficult to swallow and may promote
coughing
 ♦ Milk products: tend to increase viscosity of mucus and
increase salivation
• Bowel and Bladder Problems
 Constipation
♦ prophylactic use of stool softeners and/or fiber (Metamucil)
♦ fluid intake 1800-2000 ml/day
♦ fiber intake up to 25 g/day
♦ physical activity

 Incontinence
♦ bladder retraining program
 adequate fluid intake with a majority given between
8am-7pm
 scheduling toilet every 2 hrs using bedpan,
commode, or bathroom
 males: assist patient to stand to void
 noting signs of restlessness may indicate need for
urination
• Homonymous hemianopsia: loss of right or left half of each visual field
 Approach client on unaffected side
 Place personal belongings, food, etc… on unaffected side
 Gradually teach client to compensate by scanning, i.e., turning
head to see things on affected side
• Emotional lability: mood swings, frustration
 Create a quiet, restful environment with a reduction in excessive
sensory stimuli
 Maintain calm, nonthreatening manner
 Explain to family that client’s behavior is not purposeful
• Aphasia: most common in right hemiplegics; may be receptive/expressive
 Receptive: neither sound or speech is understood
♦ give simple, slow direction
♦ give one command at a time; gradually shift topics
♦ speak with normal tone
♦ give time for patient to process information and generate a
response before repeating a question or statement
♦ use nonverbal technique of communication
 use writing board/picture board
 point at what is wanted
 Expressive: difficulty in speaking and writing
♦ let person speak – do not interrupt – allow time for
individual to complete thoughts
 ♦ listen and watch very carefully when client attempts to
speak
♦ anticipate client’s needs to decrease frustration and feelings
of helplessness; allow body contact – touch may be the
only way the patient can express feelings
♦ keep questions to “yes” or “no”
♦ allow sufficient time for client to answer
♦ do not push communication if patient is tired or upset –
aphasia worsens with fatigue and anxiety

• Sensory/perceptual deficits: more common in left hemiplegics;

characterized by impulsiveness, unawareness of disabilities, visual neglect
(neglect of affected side and visual space on affected side)
 Assist with self-care
 Provide safety measures
 Initially arrange objects in environment on unaffected side
 Gradually teach client to compensate by scanning, i.e., turning
head to see things on affected side
• Apraxia: loss of ability to perform purposeful, skilled acts
 Guide client through intended movement (e.g., take object such as
washcloth and guide client through movement of washing)
 Keep repeating the movement
• Nursing interventions for atypical emotional responses
 Distract patient who suddenly becomes emotional
 Explain to patient and family the reason for emotional outburst
 Maintain calm environment
 Avoid shaming or scolding the patient during emotional outbursts
• Generalizations about clients with left hemiplegia versus right hemiplegia
and nursing care
 Left hemiplegia (stroke on right side of brain)
♦ paralyzed left side
♦ perceptual, sensory deficit
♦ quick and impulsive behavior, safety problems
♦ left-sided neglect
♦ spatial-perception deficits
♦ tends to deny and minimize problems
♦ rapid performance, short attention span
♦ impaired judgment
♦ impaired time concepts
♦ Use safety measures, verbal cues, simplicities in all areas of
care
 Right hemiplegia (stroke on left side of brain)
 ♦ paralyzed right side
♦ speech-language deficits
♦ slow performance and cautious behavior
♦ impaired right and left discrimination
♦ aware of deficits: depression, anxiety
♦ impaired comprehension related to language, math
♦ Use pantomime and demonstration

Chapter 46: Endocrine System

 Endocrine Glands
• Pituitary (Hypophysis)
 Located in sella turcica at the base of the brain
 “Master Gland” of the body
♦ Anterior lobe (adenohypophysis)
 Secretes tropic hormones (hormones that stimulate
target glands to produce their hormone):
 TSH: stimulates thyroid gland to release
thyroid hormones
 ACTH: stimulates adrenal cortex to produce
and release adrenocorticoids
 FSH, LH: stimulate growth, maturation, and
function of primary and secondary sex
organs
 Also secretes hormone that have direct effect on
tissues:
 GH or somatotropin: stimulates growth of
body tissue and bones
 Prolactin: stimulates development of
mammary glands and lactation
 Regulated by hypothalamus releasing and inhibiting
factor and by negative feedback system
♦ Posterior lobe (neurohypophysis): does not produce
hormones; stores and releases
 antidiuretic hormone (ADH): regulates water
metabolism; released during stress or in response to
an increase in plasma osmolality to stimulate
reabsorption of water and decrease urine output
  oxytocin, produced by the hypothalamus:
stimulates uterine contractions during labor and the
release of milk in lactation
• Adrenal
 Two small glands, one above each kidney
 Consist of two sections
♦ Adrenal cortex (outer portion): produces
mineralocorticoids, glucocorticoids, sex hormones
 mineralcorticoids: regulate fluid and electrolyte
balance; stimulates reabsorption of sodium,
chloride, and water; stimulates potassium excretion
 glucocorticoids: increase blood glucose levels by
increasing rate of glyconeogenesis; increase protein
catabolism, increase mobilization of fatty acids;
promotes sodium and water retention; anti-
inflammatory effect; aid in body coping with stress
♦ Adrenal medulla (inner portion): produces epinephrine,
norepinephrine: function in acute stress; increase heart rate,
blood pressure; dilate bronchioles; convert glycogen to
glucose when needed by muscles for energy
• Thyroid
 Located in anterior portion of the neck
 Consists of two lobes connected by a narrow isthmus
 Produces thyroxine (T4), triiodothyronine (T3), thyrocalcitonin
♦ T3, T4: regulate metabolic rate; carbohydrate, fat, and
protein metabolism; aid in regulating physical and mental
growth and development
♦ Thyrocalcitonin: lowers serum calcium by increasing bone
deposition
• Parathyroid
 Four small glands located in pairs behind the thyroid gland
 Produce parathormone (PTH): regulates serum calcium and
phosphate levels
• Pancreas (Islets of Langerhans
 Located behind the stomach
 Has both endocrine and exocrine functions
 Islets of Langerhans (alpha and beta cells) involved in endocrine
function
♦ Beta cells: produce insulin
♦ Alpha cells: produce glucagon
• Ovaries: located in pelvic cavity, produce estrogen and progesterone
• Testes: located in scrotum, produce testosterone
Chapter 48: Endocrine Problems

Hyperpituitarism
 General Information
• Hyperfunction of the anterior pituitary gland resulting in oversecretion of
one or more hormones
• Overproduction of the GH produces acromegaly in adults and gigantism in
children (if hypersecretion occurs before epiphyseal closure)
• Usually caused by a benign pituitary adenoma
 Medical Management
• surgical removal or irradiation of the gland
 Assessment Findings
• Tumor: bitemporal hemianopia; headache
• Hormonal disturbances depending on which hormones are being excreted
in excess
• Acromegaly cause by oversecretion of GH: transverse enlargement of
bones, especially noticeable in skull and in bones of hands and feet;
features become coarse and heavy; lips become heavier; tongue enlarged
• Diagnostic tests
 Skull x-ray, CT scan reveal pituitary tumor
 Plasma hormone levels reveal increased GH, oversecretion of other
hormones
 Nursing Interventions
• Monitor for hyperglycemia and cardiovascular problems (HTN, angina,
HF) and modify care accordingly
• Provide psychological support and acceptance for alterations in body
image
• Provide care for client undergoing hypophysectomy or radiation therapy if
indicated
 Hypophysectomy:
♦ General information
 Partial or complete removal of the pituitary gland
 Indications: pituitary tumors, diabetic retinopathy,
metastatic cancer
♦ Surgical approaches
 Craniotomy: usually transfrontal
 Transphenoidal: incision made in inner aspect of
upper lip and gingiva; sella turcica is entered
through the floor of the nose and sphenoid sinuses
♦ Nursing care
 Craniotomy: observe for signs of target glands
deficiencies (diabetes insipidus, adrenal
 insufficiency, hypothyroidisms) due to total removal
of the gland or to the post-op edema
 perform hourly urine outputs and specific
gravities; alert physician if UO is > 800-900
ml/2 hours or if specific gravity is < 1.004
 administer cortisone replacement as ordered
 If transphenoidal approach used
 elevate HOB 30 degrees at all times to
decrease headache and pressure on the sella
turcica
 perform oral hygiene with soft swabs and
mouth rinses; no toothbrushing until sutures
removed and incision is healed (approx. 10
days)
 teach client to avoid bending and straining at
stool for 2 months post-op
 if gland is completely removed will have
permanent diabetes insipudis

 mild anesthesia for headaches

 life-long hormone replacement: ADH,
cortisone, thyroid hormone and replacement
of sex hormones given orally
 observe for and prevent CSF leak from
surgical site
o no coughing, sneezing, or blowing of
nose
o observe for clear drainage from nose
or constant swallowing (postnasal
drip); check drainage for glucose
(positive results indicate CSF)
o risk for meningitis – IV ABT
o treated with head elevation and rest
usually resolving in 72 hours
o if persist – spinal taps – reduces
pressure to below normal levels
allowing fossa to heal

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

 General Information
• Hypersecretion of ADH from the posterior pituitary gland even when the
client has abnormal serum osmolality
• SIADH may occur in persons with bronchogenic carcinoma or other
 nonendocrine conditions
 Medical Management
• Treat underlying cause if possible
• Diuretics
• Fluid restrictions
 Assessment Findings
• Persons with SIADH cannot excrete a dilute urine (low urinary output)
• Fluid retention and sodium deficiency
• Increased body weight
• Hyponatremia causes muscle cramps and weakness
• Other manifestations
 vomiting
 abdominal cramps
 muscle twitching
 cerebral edema as serum sodium levels continue to decline, which
leads to lethargy, anorexia, confusion, headache, seizures, and
coma

 Nursing Interventions
• Medications that stimulate ADH should be avoided or discontinued
• Administer diuretics (Lasix) as ordered to promote diuresis, but only if
serum sodium is at least 125 mEq/L, because it may promote further loss
of sodium; may need to be supplemented with potassium because lasix
increases potassium excretion
• Restrict fluids (800-1000/day) to promote fluid loss and gradual increase
in serum sodium; if severe hypernatremia fluid restriction 500 ml
• Hypertonic saline requires slow infusion rate/pump to avoid rapid rise in
sodium
• Monitor serum electrolytes and blood chemistries carefully
• I&O, daily weights
• Monitor neurologic status
• Chronic SIADH: Declomycin and lithium as ordered to block effects of
ADH on renal tubules, thereby allowing a more dilute urine

Diabetes Insipidus
 General Information
• Hypofuction of the posterior pituitary gland resulting of deficiency of
ADH or a decreased renal response to ADH
• Characterized by excessive thirst and urination (5-20 L/day)
 • Caused by tumor, trauma, inflammation, pituitary surgery
 Assessment findings
• Polydipsia (excessive thirst) and severe polyuria with low specific gravity
• Fatigue, muscle weakness, irritability, weight loss, signs of dehydration
• Tachycardia, eventually shock if fluids are not replaced
• Diagnostic tests
 Urine specific gravity < 1.005
 Water deprivation test reveals inability to concentrate urine
• After intracranial surgery, DI usually has a triphasic pattern
 acute phase with abrupt onset of polyuria
 an interphase, where urine volume apparently normalizes
 third phase, where central DI is permanent (10-14 days post-op)
 Nursing Interventions
• Maintain fluid and electrolyte balance
 Keep accurate I&O
 Weigh daily
 Monitor specific urine gravity
 Administer IV/oral fluids (hypotonic solutions) as ordered to
replace fluid losses
 Adequate fluids should be kept at bedside
• Monitor vs and observe for signs of dehydration and hypovolemia
• Monitor urine for glucose; if positive notify physican (glucosuria causes
osmotic diuresis, which increases fluid volume deficit)
• Administer hormone replacement as ordered
 Aqueous vasopressin (Pritressin) and vasopressin tannate (Pitressin
tannate in oil); given IM
♦ warm to body temperature before giving
♦ shake tannate suspension to insure uniform dispersion
 Lysine vasopressin (Diapid): nasal spray
 DDAVP (Desmopressin acetate), an analog of ADH – hormone
replacement of choice for central DI – orally or intranasal (nasal
irritation, headache, and nausea may indicate overdose, where as
failure to improve may indicate underdosage (monitor daily
weight)
• Provide client teaching and discharge planning concerns
 Life-long hormone replacement; lypressin as ordered needed to
control polyuria and polydipsia
 Need to wear Medic-Alert bracelet

Cushing’s Syndrome
 General Information
 • Condition resulting from excessive secretion of corticosteroids,
particularly the glucocorticoid cortisol
• Primary Cushing’s syndrome caused by adrenocortical tumors or
hyperplasia
• Iatrogenic: caused by prolonged use of corticosteroids (prednisone)
 Assessment Findings
• Weight gain (most common feature) caused by accumulation of adipose
• Muscle weakness, fatigue, obese trunk with thin arms and legs, muscle
wasting
• Irritability, depression, frequent mood swings
• Moon face, buffalo hump, pendulous abdomen
• Purple striae on trunk, acne, thin skin
• Signs of masculinization in women; menstrual dysfunction, decreased
libido
• Osteoporosis, decreased resistance to infection – slowed wound healing
• HTN, edema
• Diagnostic tests: cortisol levels increased, slight hypernatremia,
hypokalemia, hyperglycemia
 Nursing Interventions
• Maintain muscle tone
 Provide ROM exercises
 Assist with ambulation
• Prevent accidents or falls and provide adequate rest
• Protect client from exposure to infection

• Maintain skin integrity

 Provide meticulous skin care
 Prevent tearing of skin: use paper tape if necessary
• Minimize stress in environment
• Monitor vs; observe for HTN, edema
• Provide diet low in calories and sodium and high in protein, potassium,
calcium, and vit D; provide low-calorie, high vitamin snack
• Monitor urine for glucose and acetone; admin. insulin if ordered
• Provide psychological support and acceptance
• Prepare client for adrenalectomy if condition if condition is cased by
adrenal tumor or hyperplasia
• Provide client teaching and discharge planning concerns
 Diet modifications
 Importance of adequate rest
 Need to avoid stress and infection
 Change in medication regimen

Addison’s Disease
 General Information
• Autoimmune response (most common cause)
• Adrenocortical insufficiency; hypofunction of adrenal cortex causes
decreased secretion of the mineralcorticoids, glucocorticoids, and sex
hormones
 Assessment Findings
• Fatigue, muscle weakness
• Anorexia, n/v, abdominal pain, weight loss
• History of frequent hypoglycemic episodes
• Hypotension, weak pulse
• Bronze-like pigmentation of skin
• Decreased capacity to deal with stress
• Diagnostic tests: low cortisol levels, hyponatremia, hyperkalemia,
hypoglycemia
 Nursing Interventions
• Administer hormone replacement therapy as ordered
 Glucocorticoids (cortisone, hydrocortisone): to stimulate diurnal
rhythm of cortisol release, give 2/3 dose in early morning and 1/3
dose in afternoon
 Mineralcorticoids: fludrocortisone acetate (Florinef)
• Monitor vs
• Decrease stress in environment
• Prevent exposure to infection
• Provide rest periods; prevent fatigue
• Monitor I&O
• Weigh daily
• Provide small, frequent meals of diet high in carbohydrates, sodium, and
protein to prevent hypoglycemia and hyponatremia and provide proper
nutrition
• Provide client teaching and discharge planning concerns
 Disease process: signs of adrenal insufficiency
 Use of life-long medication regimen; never omit medications
 Need to avoid stress/infections and notify physican if these occur
for medication adjustment
 Stress management techniques
 Diet modification
 Use of salt tablet (if prescribed) or ingestion of salty food if
experiencing sweating
 Importance of alternating regular exercise with rest periods
 Avoidance of strenuous activity especially in hot weather
 Addisonian Crisis
• General Information
  Severe exacerbation of Addison’s disease cause by acute adrenal
insufficiency
 Precipitating factors
♦ strenuous activity, infection, trauma, stress, failure to take
medications
♦ Iatrogenic: surgery on pituitary or adrenal glands, rapid
withdrawal of exogenous steroids of long-term steroid
therapy
• Assessment Findings: severe generalized muscle weakness, severe
hypotension, hypovolemia, shock
• Nursing Interventions
 Administer IV fluids (5% dextrose in saline, plasma) as ordered to
treat shock
 Administer IV glucocorticoids (hydrocortisone [Solu-Cortef] and
vasopressors as ordered
 If crisis precipitated by infection, admin. ABT as ordered
 Maintain strict bedrest and eliminate all forms of stressful stimuli
 Monitor vs, I&O, daily weights
 Protect client from infection
 Provide client teaching and discharge planning: same as for
addison’s disease

Guillain-Barre Syndrome
 General Information
• Symmetrical, bilateral, peripheral polyneuritis characterized by ascending
paralysis
• Can occur at any age; affects women and men equally
• Cause unknown; may be autoimmune process
• Precipitating factors: antecedent viral infection, immunization
• Progression of disease is highly individual; 90% of clients stop
progression in 4 weeks; recovery is usually from 3-6 months; may have
residual deficits
 Medical Management
• Mechanical ventilation if respiratory problems present
• Plasmapheresis to reduces circulating antibodies
• Continuous ECG monitoring to detect alteration in heart rate and rhythm
 • Propranolol to prevent tachycardia
• Atropine may be given to prevent episodes of bradycardia during
endotracheal suctioning and physical therapy
 Assessment Findings
• Mild sensory changes; in some clients severe misinterpretation of sensory
stimuli resulting in extreme discomfort
• Clumsiness: usually first symptom
• Progressive motor weakness in more than one limb (classically is
ascending and symmetrical)
• Cranial nerve involvement (dysphagia)
• Ventilatory insufficiency if paralysis ascends to respiratory muscles
• Absence of deep tendon reflexes
• Autonomic dysfunction
• Diagnostic tests
 CSF studies: increased protein
 EMG: slowed nerve conduction
 Nursing Interventions
• Maintain adequate ventilation
 Monitor rate and depth of respirations
 Observe for ventilatory insufficiency
 Maintain mechanical ventilation as needed; keep airway free of
secretions and prevent pneumonia
• Check individual muscle groups every 2 hours in acute phase to check for
progression of muscle weakness
• Assess cranial nerve function: check gag reflex and swallowing ability;
ability to handle secretions; voice
• Monitor vs and observe for signs of autonomic dysfunction such as acute
periods of HTN fluctuating with hypotension, tachycardia, arrhythmias
• Administer corticosteroids to suppress immune reaction as ordered
• Administer antiarrhythmic agents as ordered
• Prevent complications of immobility
• Promote comfort (especially in clients with sensory changes): foot cradle,
sheepskin, guided imagery, relaxation techniques
• Promote opimum nutrition
 Check gag reflex before feeding
 Start with purred foods
 Assess need for nasogastric tube feedings if unable to swallow
• Provide psychological support and encouragement to client/significant
others
• Refer to rehabilitation to regain strength and to treat any residual deficits

Myasthenia Gravis
 General Information
• A neuromuscular disorder in which there is a disturbance in the
transmission of impulses from nerve to muscle cells at the neuromuscular
junction, causing extreme muscle weakness
• Incidence
 Highest between ages 15-35 for women, over 40 for men
 Affects women more than men
• Cause: autoimmune process in which antibodies destroy acetylcholine
receptor sites
 Medical Management
• Drug therapy
 Anticholinesterase drugs: ambenonium (Mytelase), neostigmine
(Prostigmin), pyridostigmine (Mestinon)
♦ block action of cholinesterase and increase levels of
acetylcholine at the neuromuscular junction
♦ side effects: excessive salivation and sweating, abdominal
cramps, n/v, diarrhea, muscle twitching
 Corticosteroids: prednisone
♦ used if other drugs ineffective
♦ suppress autoimmune response
• Surgical (thymectomy)
 Surgical removal of the thymus gland (thought to be involved in
the production of acetylcholine receptor antibodies)
 May cause remission in some clients especially if preformed early
in disease
• Plasma exchange
 Removes circulating acetylcholine receptor antibodies
 Use in clients who do not respond to other types of therapy

 Assessment Findings
• Diplopia, dysphagia
• Extreme muscle weakness, increased with activity and reduced with rest
• Ptosis, mask-like facial expression
• Speech affected (weak voice, hoarseness; often fades after long
conversations)
• difficulty with chewing and swallowing food
• No sensory loss, reflexes are normal, and muscle atrophy is rare
• Exacerbations of MG can be precipitated by
  emotional stress
 pregnancy
 menses
 secondary illness
 trauma
 temperature extremes
 hypokalemia
• Diagnostic tests
 Tensilon test: IV injection of Tensilon provides spontaneous relief
of symptoms (lasts 5-10 minutes)
 Electromyography (EMG): amplitude of evoked potentials
decreases rapidly
 Presence of antiacetylcholine receptor antibodies in serum
 Nursing Interventions
• Administer anticholinesterase drugs as ordered
 Give medications exactly on time
 Give with milk/crackers to decrease GI upset
 Monitor effectiveness of drugs: assess muscle strength and vital
capacity before and after medication
 Avoid use of following drugs: morphine and strong sedatives
(respiratory suppressant effect) quinine, curare, procainamide,
neomycin, streptomycin, kanamycin and other aminoglycosides
(skeletal muscle blocking effect)
 Observe for side effects
• Promote optimal nutrition
 Mealtimes should coincide with the peak effects of the drugs: give
30 min. before meals
 Check gag reflex and swallowing ability before feeding
 Mechanical soft diet
 If client with difficult chewing and swallowing, do not leave alone
at mealtimes; keep emergency airway and suction equipment
nearby
• Monitor respiratory status frequently: rate, depth; vital capacity; ability to
deep breath and cough
• Assess muscle strength frequently; plan activity to take advantage of
energy peaks and provide frequent rest periods

• Observe for signs of Myasthenic or cholinergic crisis

 Myasthenic crisis
♦ abrupt onset of severe, generalized muscle weakness with
inability to swallow, speak, or maintain respirations
♦ caused by undermedication, physical or emotional stress,
infection
♦ symptoms will improve temporarily with Tensilon test
  Cholinergic crisis
♦ symptom similar to Myasthenic crisis and, in addition, the
side effects of anticholinesterase drugs (e.g., excessive
salivation, and sweating, abdominal cramps, n/v, and
muscle twitching
♦ Caused by overmedication with the cholinergic
(anticholinesterase) drugs
♦ Symptoms worsen with Tensilon test; keep atropine sulfate
and emergency equipment on hand
 Nursing care in crisis
♦ Maintain tracheostomy or endotracheal tube with
mechanical ventilations as indicated
♦ Monitor ABGs and vital capacities
♦ Administer medications as ordered
 Myasthenic crisis: increase doses of
anticholinesterase drugs as ordered
 Cholinergic crisis: discontinue anticholinesterase
drugs as ordered until client recovers
♦ Establish method of communication
♦ Provide support and reassurance
• Provide nursing care for the client with a thymectomy
• Provide client teaching and discharge planning concerning
 Nature of the disease
 Use of prescribed medications, their side effects, and signs of
toxicity
 Check with physician before taking new medications and OTC
drugs
 Need to avoid fatigue, stress, and people with URI
 Use of eye patch for diplopia (alternate eyes)
 Medical alert bracelet
 Myasthenia Gravis Foundation and other community agents

Medications
 Phenobarbital
• Long-acting barbiturate
• Used for grand mal (tonic clonic), partial seizures, and to control status
epilepticus
 • May be used in combination with phenytoin
 phenytoin (Dilantin)
• To treat grand mal, psychomotor, focal (simple) seizures
 edrophonium Cl (Tensilon)
• To diagnose Myasthenia gravis
• Very short acting
 ambenonium Cl (Mytelase)
• To increase muscle strength in Myasthenia gravis
• Long acting
• May be used with glucocorticoids
 neostigmine (Prostigmin)
• To increase muscle strength in Myasthenia gravis
• Short acting
• Used also to prevent or treat post-op urinary retention
 pyridostigmine bromide (Mestinon)
• To increase muscle strength in Myasthenia gravis
• Moderate acting
• Prevents the destruction of neurotransmitter acetylcholine
 vasopressin (aqueous) (Pitressin)
• To treat Diabetes insipidus
 Solu-Medrol
• For treating inflammatory conditions such as arthritis, bronchial asthma,
allergic reactions, and cerebral edema
 fludrocortisone acetate (Florinef)
• For treating adrenocortical insufficiency as in Addison’s disease
• Used only for its mineralocorticoid effects
 ethacrynic acid (Edecrin)
• For severe edema (pulmonary and peripheral)
• It is a potent diuretic and has a rapid action
• Moderate to high doses may cause ototoxicity
 cortisol (Prednisone)
• Glucocorticoid
• To decrease inflammatory occurrences; as an immunosuppressant; to treat
dermatologic disorders
• Suppression of inflammation and adrenal function
 baclofen (Lioresal)
• For muscle spasms caused by MS and spinal cord injury
• Overdose may cause CNS depression
• Drowsiness, dizziness, nausea, hypotension may occur