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CARE of PATIENTS with NEUROLOGICAL
DISORDERS
DISEASES/ DISORDERS:
• Multiple Sclerosis
• Myasthenia Gravis
• Parkinsons DiseaseParkinsons Disease
• Guillain-Barré Syndrome
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Multiple Sclerosis• Chronic, progressive degenerative disease
affecting the myelin sheath of the white matter of the brain & spinal cord
– Plaques form on myelin sheath causing inflammation, edema, & demyelination, eventually scarring nerve transmission becomes erratic, and slows down
– Age onset: 20 -40 yrs; affects women 2:1; whites are affected more often than Hispanics, blacks or Asians.
– More prevalent in colder climates: North America & Northern Europe. Norther Australia
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Multiple Sclerosis
• Common affectation: – white matter of the spinal cord– optic nerve– brainstem– cerebrum– cerebellum
• Exacerbation and remissions.
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Multiple SclerosisETIOLOGY
– Exact cause: unknown
– Theories: some evidence suggests that an infective agent causes a predisposition to MS
– Precipitating factors: Infection, pregnancy, physical activity, emotional stress.
– Hereditary
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Multiple SclerosisCLINICAL MANIFESTATIONS
– weakness & fatigue: most common symptom– paresthesias– difficulty with coordination and balance – spastic weakness, ataxia, tremors, ↓ sensation to
temperature, foot dragging, staggering, or loss of balance
– Vision loss (optic neuritis) – Nystagmus– Bowel & bladder dysfunction: hesitancy, frequency,
loss of sensation, incontinence & retention; constipation.
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Multiple SclerosisDIAGNOSTIC TESTS
– NO single test reliable in diagnosing MS
– Lumbar Puncture• presence of oligoclonal banding – presence of IgG
antibody in CSF (provides antibody –base immunity against invading pathogens)
– MRI of brain & spinal cord• presence of MS plaques
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Multiple SclerosisNURSING DIAGNOSIS
– Impaired physical mobility related to fatigue & weakness
– Activity intolerance r/t weakness, dizziness, and unsteady gait
– Self-esteem disturbance r/t loss of health & lifestyle changes
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Multiple SclerosisMEDICAL MANAGEMENT
• Tx: for acute relapses – IV or oral corticosteroids
• Methylprednisolone, followed by oral Prednisone taper• Azathioprine (Imuran)• Cyclophosphamide (Cytoxan) Chemo drug to destroy
the Tcells
• Tx: treating exacerbations– Interferon B (Betaseron) – reduces the
production of the T cells
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Multiple SclerosisMEDICAL MANAGEMENT
• Symptomatic treatment:– Bladder dysfunction: Oxybutynin (Ditropan), Propantheline,
Urecholine, – Constipation: Psyllium hydromucilloid, Bisacodyl– Fatigue: Amantadine, Modafinil– Muscle spascity: Baclofen diazepam, Dantrolene– Tremors: Propranolol, Thenobarbial, Clonazepam– Trigeminal neuralgia: Carbamazepine, Phenytoin,
Amitriptyline– Dysesthesia: TENS (Transcutaneous Electrical Nerve
Stimulation)
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Multiple SclerosisNURSING MANAGEMENT
1. Promotes physical mobility, activity and rest
– no vigorous physical exercise– frequent rest periods– walking and gait exercises– minimize spasticity and contractures
• (warm packs, daily muscle stretching)– activities: swimming, stationary bike,
progressive weight bearing
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Multiple SclerosisNURSING MANAGEMENT
2. Minimize effects of immobility– skin integrity– cough and difficulty in breathing and expectoration
3. Promote bladder & bowel control– Urinal/bedpan readily available– PO fluids intake schedule/voiding schedule– increase fiber in diet– intermittent self-catheterization
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Multiple SclerosisNURSING MANAGEMENT
4. Improve sensory and cognitive function:– Vision
• eye patch for diplopia; prism glasses for reading; talking books
– Speech• slurred, low volume, problems with phonation – speech therapist
– Cognitive & emotional responses• forgetfulness, easily distracted, emotionally labile
5. Development of coping strengths– education about diseases process– stress relief
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Multiple SclerosisNURSING MANAGEMENT
6. Improve self care– assistive devices– raised toilet seat– shower bench– decrease physical and emotional stress– decrease exposure of extreme temperatures
7. Adapting to sexual dysfunction– counseling– plan sexual activity– willingness to experiment
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Multiple SclerosisCOLLABORATIVE MANAGEMENT
– PT for:• instruction on assistive devices• conduct ROM exercise
– For vision impairment• scan the environment, remove sources of injury
– For urological control• drink 1500 cc q day of fluids and void q 3 hrs• intermittent catherization & clean technique• neurogenic bladder (most common in MS)
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Multiple SclerosisCOLLABORATIVE MANAGEMENT
• Neurogenic bladder (most common in MS)– Refers to several bladder dysfunctions caused by
lesions of CNS/ PNS
– 5 types:• Uninhibited• Sensory paralytic (detrusor muscle hyperreflexia)• Motor paralytic (detrusor muscle areflexia)• Autonomous• Reflex
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Multiple SclerosisCOLLABORATIVE MANAGEMENT
• Tx for constipation– High-fiber diet, bulk laxatives, stool softeners, fluids > 2000
cc/ day• Laxatives & enemas should be avoided lead to dependency• Bowel program should be performed every other day
– 45 min’s after largest meal (gastrocolic reflex) give suppository
• Keep environment cool– NO hot baths– Plan activity at peak energy level– Drugs
• Amantadine (symmetrel)• Modafinil (Provigil) may alleviate fatigue
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Multiple SclerosisCOLLABORATIVE MANAGEMENT
• Require assistance with ADL’s– ADL nursing aides– assistive devices – raised toilet seat– reacher tongs
• Fear of loss of independence & fear of disability– Depressive episodes (short anti-depressant drug
therapy)
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Multiple SclerosisCOLLABORATIVE MANAGEMENT
• Knowledge Deficit– unpredictable course– remissions & exacerbations– the role of stress– National Multiple Sclerosis Society
• Discharge & Home Health Care– Medications: be sure pt understands meds.
• dosage, route, action, & side effects
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Multiple SclerosisEVALUATION
• The pt. with MS will:– Develop a realistic daily schedule that allows for
adequate rest– Achieve an activity level appropriate for the
extent of disability– Achieve bowel & bladder function– Demonstrate self-catheterization if prescribed– Verbalize and understanding of required lifestyle
changes, eg: ways to manage emotional stress, maintain a nutritious diet, avoid infection, etc
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Myasthenia Gravis• Autoimmune disorder affecting the
myoneural junction
• Antibodies directed at acetylcholine at the myoneural junction impair transmission of impulses
• Myasthenia gravis is a motor disorder
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Myasthenia Gravis
ACh receptor site in myasthenia gravisNormal ACh
receptor site
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Clinical Manifestations
– Initially, symptoms involve ocular muscles, causing conditions such as diplopia and ptosis
– Weakness of facial muscles, swallowing and voice impairment (dysphonia),
– Generalized weakness
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Myasthenia Gravis• Chronic autoimmune neuromuscular
disease characterized by weakness of voluntary muscles
• Unknown etiology• Autoimmune • Causes:
– Decreased number of ACh receptors– Thymus gland
• Females > Males• Descending weakness
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Myasthenia GravisInitial Diagnosis• Anticholinesterase test • Edrophonium chloride (Tensilon) IVAntidote• Atropine 0.4 mg should be available to
control the side effects of edrophonium:– Sweating– Cramping– Bradycardia
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Myasthenia GravisNursing Diagnosis
• Ineffective breathing pattern related to respiratory muscle weakness.
• Impaired physical mobility related to weakness of voluntary muscles.
• Risk for aspiration related to the weakness of bulbar muscles.
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Myasthenia GravisNURSING PROCESS
• Focus on patient and family teaching• Provide medication teaching and management• Implement energy conservation measures• Implement strategies to help with ocular
manifestations• Prevent and/or manage complications and avoid
crisis• Implement measures to reduce risk of aspiration• Avoid stress, infections, vigorous physical
activity, some medications, and high environmental temperatures
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Myasthenia GravisMEDICAL MANAGEMENT
Pharmacologic therapy– Cholinesterase inhibitor: pyrostigmine
bromide (Mestinon)– Immunomodulating therapy
• Plasmapheresis - blood is removed and replaced to remove the antibodies
• Thymectomy –removal of the thymus gland
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Myasthenic Crisis• Undermedication with cholinesterase
inhibitors• Result of disease exacerbation or a
precipitating event, most commonly a respiratory infection
• Severe generalized muscle weakness with respiratory and bulbar weakness (weakness of the facial and pharyngeal muscles)
• Patient may develop respiratory compromise failure
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Cholinergic Crisis• Caused by overmedication with
cholinesterase inhibitors
• Severe muscle weakness with respiratory and bulbar weakness
• Patient may develop respiratory compromise and failure
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Myastinic crisis Cholinergic crisis
Cause:Under medicationStressInfection
Manifestations:Unable to see – ptosis and diplopiaDysphagiaUnable to breathe
Management:Administer cholinesterase
Cause:Over medication
Manifestation:Flaccid ParalysisRespiratory failure
Management:Administer anticholinergic
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Management of Myasthenic Crisis
• Ensuring adequate ventilation; intubation and mechanical ventilation may be needed
• Assessment and supportive measures include:– Ensure airway and respiratory support– Take ABGs, serum electrolytes, I&O, and daily weight– If patient cannot swallow, nasogastric feeding may be
required– Avoid sedatives and tranquilizers
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Myasthenia GravisDRUG THERAPY
• Two groups of medications– Short-acting anticholinesterase
compounds• Mestinon (pyridostigmine)• Prostigmin (neostigmine)
– Corticosteriods (Prednisone)• assists in reducing the levels of serum Ach receptor
antibodies• Inform client that ther will be no immediate relief of
the symptoms
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Myasthenia GravisDRUG THERAPY
• Immunosuppressive therapy
– ↓ the level of circulating Ach receptor antibodies
Examples– Imuran (azaathioprine)– Sandimmune (cycloporine)
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Myasthenia GravisNURSING MANAGEMENT
• Improve respiratory function• Increase physical mobility• Improve communication• Provide eye care• Prevent aspiration
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Parkinson’s Disease• A progressively degenerative neurological disorder
affecting the brain centers (substantia nigra and basal ganglia) responsible for control & regulation of movement
• Occurs in 1% of pop.
• Over 50, affects men > women
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Parkinson’s DiseasePATHOPHYSIOLOGY
• depletion of dopamine levels in the basal ganglia of the mid brain
– Dopamine promotes smooth, purposeful movements of motor function
– Dopamine depletion impairment of the extrapyramidal tracts with loss of movement coordination
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Parkinson’s DiseaseETIOLOGY
• Cause: unknown– Some heredity causes
– Secondary iatrogenic PD – is drug or chemical related
• Dopamine depleting drugs: Reserpine. Phenothiazine, Metoclopromide, Butyrophenones (Droperidol & Haloperidol)
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Parkinson’s DiseaseCLINICAL MANIFESTATIONS
• 3 cardinal signs – Bradykinesia / akinesia
• slowness of movement or complete or partial loss of movement difficulty with balance
– Involuntary tremors• course, rest tremor of the fingers & thumb (pill-rolling
movement) of one hand, occurs during rest, & intensifies w/ stress, fatigue, cold, disappears during sleep, the tremor can occur in tongue, lip, jaw, chin; eventually spreads to the foot on the same side
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Parkinson’s DiseaseCLINICAL MANIFESTATIONS
– Progressive muscle rigidity to antagonistic muscle groups, causing resistance to both extension & flexion
• Flexion contractures develop in the neck, trunk, elbows, knees & hip
• Face – expressionless, mask-like appearance, drooling & ↓ tearing ability
• Propulsive gait
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Parkinson’s DiseaseCLINICAL MANIFESTATIONS
• Speech: high-pitched monotone voice & parroting the speech of others (muscles of the voice box is affected
• Hypothalmic dysfunction: ↓ perspiration, heat intolerance, seborrhea, & oil production
• Psychosocial : does not affect intellectual ability– 20% of pts will end up having dementia (Alzheimer’s)
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Parkinson’s DiseaseDIAGNOSTIC EVALUATION
• No specific tests
• History: progresses thru stages– Mild unilateral dysfunction– Mild bilateral dysfunction, expressionless face & gait
changes– Dysfunction w/ walking, initiating movements, and
maintaining equilibrium– Severe disability- difficulty in walking, & maintaining
balance & steady propulsion, rigidity
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Parkinson’s DiseaseNursing Diagnosis
• Impaired physical mobility related to the stiffness and muscle weakness.
• Self care deficit related to neuromuscular weakness, decline in strength, loss of muscle control / coordination.
• Impaired Verbal Communication related to the decline in speech and facial muscle stiffness
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Parkinson’s DiseaseDrug therapy
• Goal: enhance dopamine transmission
• Dopaminergics (Levodopa)• a synthetic metabolic precursor to dopamine• given in combination with Sinemet (Carbidopa)
– to allow more Levodopa to reach the brain – prevents peripheral metabolism of levodopa– beneficial first few years– on & off reactions
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Parkinson’s DiseaseDrug therapy
• Dopaminergics (cont.)• Sinemet
– most common drug (carbidopa-levodopa)– SE: Orthostatic hypotension, nausea,
hallucinations, dyskinesia– Nursing Considerations:
» Monitor B/P» Use TED hose to venous return» Monitor for urinary retention
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Parkinson’s DiseaseDrug therapy
• Dopaminergics (cont.)• Symmetrel (Amantadine)
– Action: causes release of dopamine in CNS– Indications: rigidity, bradykinesia– SE: dizziness, ataxia, insomnia, leg edema– Nursing Considerations:
» Monitor for postural hypotension» Do not administer at bed time
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Parkinson’s DiseaseDrug therapy
• Anticholinergic– to block the release of acetylcholine (balance
between dopamine & acetylcholine)
– to block the excitatory effects of the cholinergic system
– Examples:• Artane (trihexphenidyl)• Cogentin (benztropine)• Parsidol (ethopropazine)
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Parkinson’s DiseaseDrug therapy
• Anticholinergic – Indications: tremor, rigidity, drooling– SE: dry mouth, constipation, blurred vision,
confusion, hallucination– Nursing Considerations:
• Usually contraindicated in acute-angle glaucoma, & tachycardia
• Monitor pulse & B/P during dosage adjustments• Administer w/ meals• Do not withdraw meds suddenly
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Parkinson’s DiseaseDrug therapy
• Antihistamines• Benadryl
–Indications: tremor, rigidity, insomnia–SE: dry mouth, lethargy, confusion–Nursing Considerations:
»Use w caution in pts with seizures, hypertension, hyperthyroidism, renal disease, diabetes
»Administer w meals or antacids.
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Parkinson’s DiseaseDrug therapy
• Dopamine agonists– Parlodel (Bromocriptine)
• Action: activates dopamine receptor in the CNS, helpful for treatment of on-off reactions
• Indications: fluctuation of manifestations, dyskinesia, dystonia
• SE: hallucinations, orthostatic hypotension, confusion
• Nursing considerations: – monitor B/P & mental status
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Parkinson’s DiseaseDrug therapy
• COMT inhibitors [catechol-O-methyltransferase}– Tolcapone
• Action: enhance effect of dopamine• Indications: adjuvant treatment• SE: diarrhea• Nursing Considerations:
– Monitor liver enzymes
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Parkinson’s DiseaseDrug therapy
• MAO (Monoamine Oxydase) inhibitors– Deprenyl (Selegiline)
• Action: inhibit monoamine oxidase B, an enzyme that converts chemical byproducts in the brain into neurotoxins that prevent substantia nigra cell death
• Indications: adjuvant treatment• SE: nausea, dizziness, confusion, hallucinations, dry
mouth• Nursing considerations:
– Monitor for levodopa side effects
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Parkinsonian Crisis• Sudden or inadvertent withdrawal of anti-PK drugs
or emotional trauma
• Severe exacerbation of tremor, rigidity and bradykinesia, along w/ acute anxiety, sweating, tachycardia.
• Interventions: respiratory & cardiac support, subdued lighting, mild barbiturates, anti PK drugs
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Parkinson’s DiseaseNURSING MANAGEMENT
• Improve mobility • Exercise & stretch regularly (first thing in
morning)• Encourage daily ROM to avoid rigidity & contractures
• Enhance walking – walk erect, watch horizon, wide-based gait, heel-toe gait, long strides.
• Use cane or walker prevent falls
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Parkinson’s DiseaseNURSING MANAGEMENT
• Improve hydration & nutrition• Maintain fluid intake 2 L/24 hrs
• Monitor weight & ability to chew & swallow• Upright position to chew & swallow, offer small freq.
meals, soft foods & thick cold foods supplemental puddings
• Prevent aspiration think thru the steps of swallowing, keep lips closed, keep teeth together, chew, finish one bite before another
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Parkinson’s DiseaseNURSING MANAGEMENT
• Improve bowel elimination– Stool softeners, mild laxatives, regular routine,
fiber, raised toilet seat
• Improve communication– Speech therapy: speak slowly, use board,
mechanical voice synthesizer
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Parkinson’s DiseaseNURSING MANAGEMENT
• Enhance self-care– Extra time needed to perform ADL’s, use of side
rails, overhead trapeze.
– Reinforce occupational & physical therapy
– Sleep on firm mattress, prevent neck contractures
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Parkinson’s DiseaseNURSING MANAGEMENT
• Support coping abilities– Feel embarrassed, depressed, lonely, bored, more
muscle rigidity & unresponsive to verbal stimuli• treat w/ dignity• do not ignore clients
– Client to be active participant– Explore feelings– Education– Services: American Parkinson’s Disease Foundation
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Parkinson’s DiseaseEvaluation
• The client is able to perform physical activity according to ability.
• The client is able to perform self care
• The client is able to maximize the ability to communicate.
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Guillain-Barré Syndrome
• Autoimmune disorder with acute attack of peripheral nerve myelin
• Rapid demyelination may produce respiratory failure and autonomic nervous system dysfunction with CV instability
• Most often follows a viral infection (respiratory/ GI: Campilobacter jejuni)
• Affects both men & women equally & of all ages.
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Guillain –Barre’ Syndrome
• also known as acute demyelinating polyneuropathy or acute idiopathic polyneuritis
• results in a temporary, flaccid paralysis lasting 4-8 weeks
• ascending
• Medical emergency, 80% will recover
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Guillain-Barré SyndromeCLINICAL MANIFESTATIONS
• variable and include: – Weakness– Paralysis– Paresthesias– Pain– diminished or absent reflexes starting with the lower
extremities and progressing upward– Cranial nerve symptoms– tachycardia, bradycardia,– hypertension, or hypotension
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Guillain-Barré SyndromeNURSING PROCESS
• Conduct ongoing assessment with emphasis on early detection of life-threatening complications of respiratory failure, cardiac dysrhythmias, and deep vein thrombosis
• Monitor for changes in vital capacity and negative inspiratory force
• Assess VS frequently/continuously including continuous monitoring of ECG
• Encourage patient and family coping
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Guillain-Barré SyndromeNURSING DIAGNOSIS
• Ineffective Breathing Pattern, related to respiratory muscle weakness or paralysis, decreased cough reflex, immobilization.
• Impaired Physical Mobility related to paralysis, ataxia.
• Risk for Impaired Skin Integrity related to muscle weakness, paralysis, impaired sensation, changes in nutrition, incontinence.
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Guillain-Barré SyndromeMEDICAL MANAGEMENT
• Requires intensive care management with continuous monitoring and respiratory support
• Plasmapheresis and IVIG (Intravenous Immunoglobulin) are used to reduce circulating antibodies
• Recovery rates vary but most patients recover completely
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Guillain-Barré SyndromeNURSING MANAGEMENT
• Enhance physical mobility and prevent DVT– Support limbs in a functional position– Perform passive ROM at least twice daily– Initiate position changes at least every 2 hours– Provide elastic compression hose and/or sequential
compression boots– Provide adequate hydration
• Administer IV and parenteral nutrition as prescribed• Assess swallowing and gag reflex and take measures
to prevent aspiration
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Guillain-Barré SyndromeNURSING MANAGEMENT
• Develop a plan for communication individualized to patient needs
• Decrease fear and anxiety– Provide information and support– Provide referral to support group– Implement relaxation measures– Maintain positive attitude and atmosphere to promote a
sense of well-being– Implement diversional activities
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Guillain-Barré SyndromeNURSING MANAGEMENT
• Develop a plan for communication individualized to patient needs
• Decrease fear and anxiety– Provide information and support– Provide referral to support group– Implement relaxation measures– Maintain positive attitude and atmosphere to promote a
sense of well-being– Implement diversional activities
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Amyotrophic Lateral Sclerosis (ALS)
• “Lou Gehrig’s disease”
• Loss of motor neurons in the anterior horn of the spinal cord and loss of motor nuclei in the brain stem
• Causes progressive weakness and atrophy of the muscles of the extremities and trunk; weakness of the bulbar muscles impairs swallowing and talking; and respiratory function is also impaired
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Amyotrophic Lateral SclerosisCLINICAL MANIFESTATIONS
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Amyotrophic Lateral SclerosisCLINICAL MANIFESTATIONS
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Amyotrophic Lateral Sclerosis (ALS)
• Course of disease – Death from pneumonia in 3-5 yrs.
• Diagnosis: – clinical signs & symptoms– EMG changes– muscle biopsies– CSF analysis– CT– MRI
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Amyotrophic Lateral Sclerosis MANAGEMENT
• Making the client as comfortable and independent as possible
• Slowing the progression of the disease: Riluzole (Rilutek)– Antibiotic– Breast-cancer drug– Antioxidant coenzyme
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Amyotrophic Lateral Sclerosis NURSING MANAGEMENT
• Physical therapy• Speech therapy• Nutritional support• Respiratory support