Chapter 54: Nervous System

Location and Function of the Parts of the CerebrumCortical 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 movementsThalamus: below basal ganglia – relays sensory and motor inputs to cortex and other parts of cerebrumHypothalamus: 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

involvemento 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

noseo observe for clear drainage from nose

or constant swallowing (postnasal drip); check drainage for glucose (positive results indicate CSF)

o risk for meningitis – IV ABTo treated with head elevation and rest

usually resolving in 72 hourso 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