class 12 guillain-barre and ALS Flashcards
what is guillain-barre syndrome
an autoimmune disorder with acute attack of peripheral nerve myelin
-rapidly progressing, and potentially fatal form of polyneuritis
-symmetrical ascending paralysis with unknown cause
pathophysiology of GBS
-cellular and humoral immune reaction directed at nerves
-segmental demyelination, edema, and nerve inflammation
-transmission of nerve impulses is stopped or slowed, muscle atrophy occurs
-considered a medical emergency d/t risk of resp distress
acute stage of GBS
severe rapid weakness, decreased reflexes, numbness, pain, decreased vital capacity, facial muscle involvement
ANS involvement: bradycardia, sweating, hypotension, dysarythmias
plateau stage of GBS
2-3 weeks after inital onset, symptoms cease to change
-autonomic function stabilizes
recovery stage of GBS
symptoms improve, takes several months to 2 years to recover (usually 6m)
-muscle strength and function returns in reverse order, will need rehab
diagnostic studies for GBS
-history & clinical signs
-spinal tap (isn’t diagnostic, rules out other conditions)
-electromyography (EMG) to assess for dec in muscle transmission
-rule out other conditions
clinical manifestations of GBS
-mild to severe
-event occurs 2 weeks before s&s
-typically progress over hours to days
-symmetrical muscle weakness
-mild distal sensory symptoms of paresthesia
-absent or depressed DTR
-weakness usually begins in legs and progresses upwards (ascending)
-pain is a common symptom
complications of GBS
-respiratory distress/failure
-cardiac dysfunction
-severe pain
-immobility
-tachycardia
-UTI
-fever
-immobility
-paralytic ileus
-muscle atrophy
medical management of GBS
-requires intensive care management with continuous monitoring and respiratory support
-plasmapheresis and IVIG are used to reduce circulating antibodies
-prevent the complications of immobility (anticoags and TEDs)
assessment for GBS
-important during acute phase->can go undetected early
-vitals
-ascending paralysis
-resp function
-ABG levels
-Gag, corneal, and swallowing refexes
-may need TPN or NG for short term
nursing interventions for GBS
IV fluids/TPN/NG feeds
-ROM exercises, position changes, TEDs, SCDs
-establishing a form of communication
-frequent respiratory assessment
-diversional activities “we expect this to happen”
goals of nursing management for GBS
-improve resp function
-improve mobility
-improve nutrition status
-effective communication
-decrease fear and anxiety
-absence of complications
what is amyorophic lateral sclerosis (ALS)
“lou gehrig’s disease”
-rare progressive neurological disorder
-avg survival time is 3-5 years post dx
pathophysiology of ALS
-d/t unknown reasons, motor neurons in the brain stem and spinal cord gradually degenerate
-dead motor neurons cannot produce or transport vital signals to muscles
-electrical or chemical messages originating in the brain do not reach muscles
risk factors for ALS
-age
-family hx
-genetic aberrations now identified
-exposure to pesticides, chemicals, heavy metals (i.e. military service, athleticism, smoking, viruses)
manifestations of ALS
-depends on location of affected neurons
-fatigue, progressive muscle weakness, cramps, fasciculations, and incoordination
-progessive weakness
-dysarthria & dysphagia
-atrophy of the muscles in the arms, trunk, legs
-anal and bladder spincter function remains intact but may have accidents
early s&s of ALS
-tripping over nothing
-dropping things
-slurred or “thick” speech
-difficulty swallowing
-weight loss
-decreased muscle tone
-sob
-inc or dec reflexes
-uncontrollable laughing or crying
-feeling weak
-fatigue
-cramping/twiching
-stiffness or rigidity
death of ALS is usually d/t
-infection
-respiratory failure
-aspiration
-has the option of MAID to avoid these
signs of disease progression with ALS
-difficulty breathing
-coughing when eating or drinking
-difficulty forming works or projecting voice
-fatigue caused by muscle exhaustion
-reduced food intake and weight loss
-insomnia caused by discomfort
-excessive saliva or dry mouth
diagnostic studies for ALS
-no definitive test
-detailed hx & s&s
-electromyography (EMG), nerve conduction study (NCS), MRI to rule out mimicking diseases
how ALS is diagnosed
-clinical, electrophysical, or neuropathologic evidence of lower motor neuron degeneration
-evidence of upper motor neuron degeneration
-evidence of progressive spread of s&s within a region or to other regions
COMBINED with absence of evidence of other dx that explain’s patients neuron degenration and neuroimaging evidence of other dx that explains s&s
medical management of ALS
no cure
-riluzole (rilutek) or edaravone (radicava): glutamate antagonist slows progression by dec the amount of glutamate in the brain
-nuedexta: used to tx emotional lability
-baclofen (lioresal), dantrolene sodium (dantrium), or diazepam (valium) may be useful for patients troubled by spasticity
nursing interventions for ALS
-facilitating communication
-reduce aspiration risk
-early identification of resp insufficiency
-pain management
-dec risk of falls/injury
-support cognitive and emotional functions
-mod intensity, endurance exercises for the trunk and limbs to reduce spasticity
