Neuro/Autoimmune (Module 1) Flashcards
Parkinson’s Causes (Primary)
not known, combo of genetic and environmental factors
Parkinson’s Causes (Secondary)
antipsychotic drugs or another condition such as brain tumor or trauma
Huntingtons Disease Causes
hereditary; autosomal-dominant trait at conception
PD Pathophysiology
• chronic, terminal disease
• degeneration of substantia nigra cells in basal ganglia
• LOW DOPAMINE, which normally functions to promote voluntary muscle and sympathetic nervous system control
• works opposite acetylcholine: HIGH acetylcholine, leading to smooth controlled movement and sympathetic nervous system control issue
Huntingtons Disease Pathophysiology
• chronic, terminal disease
• alterations in dopamine, gamma-aminobutyric acid (GABA), and glutamate from basal ganglia
PD Disease Course
• steady and gradual decline (10-20 years)
• cognitive, mobility, and ADL function from mild to severe
• patients die from complications of immobility
PD Cardinal Symptoms
• tremor/pill rolling tremor of fingers usually 1st sign!
• muscle rigidity (rhythmic interruption, restrictive or total resistance to movement)
• bradykinesia (slow movement, masklike expression)
• postural instability (difficulty chewing, swallowing and drooling)
• mask like face
• slow decline over 10-20 yrs
affects facial expressions, speech, bowel and bladder
Huntingtons Disease Course
• gradual decline (15 yrs)
• cognitive and neuromuscular symptoms
• progressive dementia and choreiform movements (uncontrollable rapid, jerky movements) in limbs, trunk, and facial muscles; patients usually die from complications of impaired mobility
personality changes, mood swings, depression, slurred speech, difficulty swallowing, weight loss
PD Risk Factors (Primary)
• male
• over 40
• family history (first-degree relatives)
PD Risk Factors (Secondary)
• traumatic brain injury
• brain tumor or other lesion
Huntingtons Disease Risk Factors
• dominant inheritance
• 30-50 years of age equally in men and women (when symptoms typically begin)
• caucasians higher risk
PD Etiology and Genetic Risk
• environmental and genetic factors
• exposure to chemicals and metals
• older than 40 yrs
• familial tendency
• exposure to antipsychotic meds
PD Incidence and Prevalence
• 60,000 new cases annually in people over 50
• 1 million live with PD
• 50% more men than women
PD Labs/Diagnostics
• no specific tests (may do CSF, MRI, or SPECT)
• diagnosis made by brain autopsy (Lewy bodies and neuronal loss in substantia nigra); or diagnose by clinical manifestations and ruling out other diseases
• Stage 1 (mild) to Stage 5 (severe)
Huntingtons Labs/Diagnostics
• HD genetic test (gene present?)
• computerized tomography (CT) scans- frontal horn enlargement
• magnetic resonance imaging (MRI)
• position emission tomography (PET) scanning
PD Physical Assessment
• resting tremors in UE
• rigidity assessment
• facial expression (“masklike”)
• emotional changes
• speech changes
• bowel and bladder changes
PD Meds
• Dopaminergics: levodopa/carbadopa (Sinemet)
• pramipexole (mirapex)/ropinirole (requip) (DOPAMINE AGONISTS) se is OH
• anticholinergics (trihexyphenidyl (artane), benztropine (cogentin)) for tremors
• catechol-O-methyltransferase (COMT) inhibitors (Entacapone (Comtan))
• Monoamine oxidase type B (MAO-B) inhibitors- Selegiline for 0 tyramine
• Antivirals (Amantadine)
Levodopa (PD)
converted to dopamine in the brain
Carbidopa (PD)
combined with levodopa to decrease the breakdown of levodopa
Dopamine Agonists (PD)
activate release of dopamine
can cause orthostatic hypotension, drowsiness, dyskinesias, and hallucinations
Anticholinergics (PD)
treat tremors
monitor for effects like dry mouth, constipation, urinary retention, and acute confusion
Huntingtons Meds
• tetrabenazine (xenazone)
• other antipsychotics may be used for psych symptoms
Tetrabenazine (Xenazone) (HD)
FDA approved to suppress involuntary chorea movements (SE: new/worse depression, drowsiness, nausea, restlessness)
COMT Inhibitors (Entacapone/Comtan) (PD)
taken with levodopa (decreases breakdown of levodopa)
dark urine is normal
MAO-B (Selegiline) (PD)
taken with levodopa; increases dopamine levels
helps with the wearing off effect of levodopa
avoid foods with tyramine (cheese and aged, smoked or cured foods/sausage, red wine, beer) to prevent severe headache and mega hypertension and should continue restrictions for 14 days after drug is discontinued
Amantadine (PD)
stimulate the release of dopamine and prevent its reuptake
Procedures (PD)
only for patients that haven’t responded to other therapy
• ablative procedures
• deep brain stimulation (DBS)-surgical choice
• cell transplantation
Ablative Procedures (PD)
destroys a small portion of the Globus pallidus
thalamotomy
pallidotomy
DBS (PD)
electrode implanted in the thalamus; current delivered through a generator
decreases tremors and involuntary movements
Cell Transplantation (PD)
fetal tissue transplants are experimental
Huntingtons Procedures
• no neuroprotective neurorestorative treatment available
• main medical management: supportive and symptomatic treatment
PD Complications and Nursing Care
• aspiration pneumonia (swallowing precautions, PT/OT, dietary/speech consult) maintain weight with high calorie and high protein supplements, prevent aspiration
• altered cognition (safe environment (no throw rugs, electric razor), freeze gait issue (1 step back, 2 forward), ADL/independence maintenance (exercise, assistive devices, etc.), extra time for activities, fostering communication (depression, self esteem), allow extra time for Q’s and encourage client to speak slowly and pause a lot, drug therapy, exercise programs/PT)
• OH
• DVT/embolism
• constipation
• pneumonia (increase calories and protein)
• pressure ulcers (immobility!!)
PD Care Coordination and Transition Management
• home care preparation
• self management education
• health care resources
• palliative care
• neurologist
• social worker
• long term care
• PT/OT/SLP
Huntingtons: Care Coordination and Transition Management
• decisional conflict r/t whether to have children (encourage testing for family)
• aspiration pneumonia
• altered cognition (dementia, memory deficits)/mobility (Suicide prevention with depression (1), any issues with low body weight needs encouragement of 3 meals a day and necessary dietary supplements (2), eventually will need help with all ADLs, confined to bed and unable to speak; able to understand language and has awareness of family/friends (3), encourage planning for residential and EOL care (4))
• expressive dysphagia
• PT USES WHITEBOARD NOT RN
Rigidity
resistance to passive movement of the extremities; cogwheel, plastic, lead pipe
Cogwheel Rigidity
manifested by a rhythmic interruption of the muscle movement
Plastic Rigidity
mildly restrictive movement
Lead Pipe Rigidity
total resistance to movement
ALS (Lou Gehrigs) Pathophysiology
• chronic, progressive, neurodegenerative with NO CURE, UNKNOWN CAUSE/RISK
• targets the CNS and brain; loss of voluntary movement control, weakness, spasticity and flaccidity
• patients suffer from lack of physical ability
MS Pathophysiology
• chronic, progressive, neurodegenerative, NO CURE! AUTOIMMUNE NOT FATAL!
• targets brain and spinal cord (myelin sheath), demyelination of white matter leads to decreased flow of nerve impulses
• patients suffer from more cognitive dysfunction than those with ALS
sx worse in extreme heat and cold, stress, infection fatigue, pregnancy
remissions and exacerbations
MS Etiology and Genetic Risk
• multiple factors
• changes in immunity are most likely etiology
• colder climates
ALS Incidence, Disease Course, Expected Findings
• most die within 3-5 years when symptoms first start, only about 10% of people survive for 10+ yrs
• causes progressive muscle weakness and wasting, lose ability to speak, eat, move, and breathe (paralysis of respiratory muscles)
• fatigue
• muscle atrophy (wasting away and tongue) and muscle weakness by spasticity and hyperactive reflexes
• twitching (fasciculations) of face and tongue
• dysarthria (uncoordinated or slurred speech)
• dysphagia
• stiff and clumsy gait
• abnormal reflexes
MS Incidence, Disease Course, Expected Findings
• no cure, progressive; over time may progress to tetraplegia (normal life expectancy); fatigue, muscle spasticity
• blurred/double vision (diplopia)
• scotomas (patches of blindness in peripheral)
• Uhthoffs sign (temp bad vision commonly seen after exertion or heat exposure)
• nystagmus, tinnitus
• pain/parasthesia
• hypoalgesia (decreased sensitivity to pain)
• areflexic (flaccid) or spastic bladder
• decreased sexual dysfunction
• intention tremors when performing activity, changes in gait
ALS Prevalance
rare (40-60 y.o, more common in men)
MS Prevalence
ages 20-50 (1 mil in US), more common in white woman of Northern European ancestry (2x)
ALS Labs and Diagnostics
• no definitive test
• diagnosis based on med history, neuro exam, symptoms
• lab tests to rule out other metabolic conditions
MS Labs and Diagnostics
• CSF reveals elevated protein lvl, a slight increase in WBCs and IgG
• MRI plaques of brain and spine
• evoke potential testing (give stimulation and see if the sense is decreased)
ALS/MS Care Coordination and Transition Management
• continuity of care if needed
• exacerbating factors
• family coping skills
• sexual dysfunction concerns
• depression
• nutrition
• ADLs
ALS Meds
• riluzole (Rilutek)
• Edaravone (Radicava)
• muscle relaxants
Riluzole (Rilutek) (ALS)
reduces molecular stimulation preventing overstimulation and brain damage; decreases glutamate resulting in less death of brain cells
tachycardia
edema
dizziness
drowsiness
GI disturbances (liver toxicity, DIB, rash, muscle/joint pain)
Edaravone (Radicava) (ALS)
antioxidant, reduces oxidative stress
blisters
itching, skin irritation
cough
confusion
tachycardia
weakness
easy bruising
GI disturbances
DIB, A.E, glycosuria, respiratory failure
MS Meds
immunosuppressants/anti-inflammatories (secondary infections)
• interferon beta 1a/1b
• glatiramer acetate
• medical weed
• dexamethasone (Decadron)
• Muscle Relaxants: diazepam (valium benzodiazepine), dantrolene (monitor liver values, AST/ALT), baclofen (avoid stopping abruptly due to risk of seizure, hallucinations and rhabdomyolysis)
• Dalfampridine (Ampyra): improves gait/walking
• Steroids (Dexamethasone (Decadron)): used for relapses, must taper off, increased risk for infection
Interferon Beta 1a/1b (MS)
immunomodulator with antiviral effects; injectables;
WATCH OUT FOR FLU-LIKE SYMPTOMS
Glatiramer Acetate (MS)
injection site reaction (SQ) rotate injection sites!!
GI disturbances
weight gain
confusion/nervousness
depression
edema
difficulty swallowing
excessive sweating
rash
flu-like symptoms
Weed (MS)
decreases spasticity, muscle stiffness, pain
can cause mental decline and dizziness
Dexamethasone (Decadron) (MS)
steroid anti-inflammatory for managing relapses (infection, hyperglycemia, don’t stop abruptly)
ALS Complications and Nursing Care
• death anxiety (impending progressive loss of function leading to death)
• palliative care for symptom management, home health care, EOL planning, hospice
• psychosocial support
• ineffective breathing pattern r/t compromised respiratory function, monitor breathing!
MS Complications and Nursing Care
• neurosensory/motor function baseline (with exacerbations, may not recover 100% function)
• psychosocial support-depression, emotional liability
• UTI prevention (hydration, bathroom schedule, bowel and bladder training)
• promote cognitive function
• eye patches for diplopia
• group care and activity planning for energy conservation
• exercise planning to avoid fatigue and overheating
• swallowing precautions
• decrease risk of injuries (safe environment, no high impact activities, PT/OT)
• remains free of infection as a result of drug therapy affecting immunity or disease process
• maintains optimal mobility and function as a result of managing fatigue and pain
• maintains adequate visual acuity and cognition to function independently
• assistive devices
MS Bowel/Bladder Training
• tracking voiding schedule and gradually lengthen
• toileting training w/schedule and restroom assistance
• dietary changes
• med management
• pelvic floor exercises
Sinus Headaches
pain is behind browbone and/or cheekbones
Cluster Headaches
pain is in and around one eye
Tension Headache
pain is like a band squeezing the head
Migraine
pain, nausea, and visual changes are typical of classic form
Migraine Pathophysiology
• recurrent episodic head pain that lasts 4-72 hrs
• throbbing, intense, unilateral pain that can be accompanied by nausea, light/sound sensitivity
• genetics and triggers
• cerebral artery vasodilation leads to prostaglandins released leading to brain tissue inflammation
Migraine Manifestations
• photophobia/phonophobia
• nausea and vomiting
• stress and anxiety
• unilateral pain, often behind one ear or eye
• history of headaches
• alterations ins ADLs (4-72 hrs)
• w/aura: vision changes
• OA: aura w/o pain
Prodrome Phase (Migraine w/Aura)
• hrs to days prior to headache (aware it’s coming)
• fatigue, nausea
• irritability
• mood changes/depression
• appetite changes/food cravings
• difficulty sleeping and focusing
• photo/phonophobia
Aura Phase (Migraine w/Aura)
• 5-60 min prior to headache
• visual disturbances (light flashes, bright spots)
• acute confusion
• loss of vision
• numbness, tingling, weakness, dizziness
• speech changes
• brainstem aura
Headache Phase (Migraine)
• 4-72 hrs (third stage-dull HA)
• second stage- severe, throbbing, incapacitating
• unilateral typically
• moderate-severe
• throbbing
• light and or sound sensitivity
• n/v
• made worse with movement
Postdrome Phase (Migraine)
• 24-48 hrs following headache
• mood changes
• difficulty focusing and concentrating
• fatigue
• residual headache
• brain fog
• tiredness
Migraine Risk Factors
• all ages (women most likely) family history
• may be associated with other conditions like colds, allergies, stress, muscle tension
• overweight/obese
• fasting/ low glucose
• high BP and cholesterol
• hx of stroke or CAD
• psych disorders (depression, anxiety)
• oral contraceptives
• some drugs (opiates, barbiturates, triptans)
at risk for stroke and epilepsy
Migraine Lab Diagnostics
• neuroimaging if neuro symptoms are present or older than 50 yrs new onset
• CT/MRI/EEG (r/o other diagnoses like tumor, MS, aneurism)
• most don’t require labs or imaging
Migraine Pain Management
- prevention (trigger avoidance, preventive drugs like beta blockers)
- abortive therapy
- trigger avoidance (tyramine, preservatives, artificial sweeteners, diary with exposures and migraine history)
- complimentary and integrative health therapies
- PREVENTATIVE: BOTOX AND BETA BLOCKERS (lower BP and HR)
Abortive Therapy (Mild Migraine)
initiate during aura phase or as soon as the headache starts
NSAIDS, acetaminophen
antiemetics (metoclopramide) for n/v
Abortive Therapy (Severe Migraine)
• triptan preparations (sumatriptan, zolmitriptan, eletriptan) to produce vasoconstriction effect contraindicated in heart disease
• ergotamine preparations with caffeine to narrow blood vessels and reduce inflammation
• isometheptene (vasoconstriction) in combo with caffeine when other meds don’t work
Recovery (Migraine w/Aura)
pain and aura subsiding, increased muscle spasms and myalgia
older adult: visual migraine, aura w/o pain
Migraine w/o Aura
• pain is aggravated by physical activity
• unilateral pulsing pain as well as photophobia, phonophobia, n/v
• persists for 4-72 hrs, often occurring in early AM, during stress, premenstrual tension or fluid retention
Status Migranious
> 72 hrs
Migranious Infarction
neuro sx for >7 days, imaging may show ischemic infarction
Preventive Therapy
for frequent HA or when other therapies are ineffective
• NSAIDS
• beta blockers: take even when asymptomatic for prevention to prevent vascular changes
• botox
Migraine Complications and Nursing Care
• focus on pain management during HA (dark environment, HOB elevated, meds)
• HA diary for patterns and triggers/trigger avoidance
• avoid foods with tyramine and MSG
• manage anger and conflict
• avoid glare and flickering lights
• adequate sleep/rest
• avoid environmental triggers like odors
• yoga, meditation, exercise, acupuncture, external trigeminal nerve stimulator (wearable headband that stimulates branches associated with HA, not to be used more than 20 min/day)
SLE Pathophysiology
• chronic and progressive autoimmune disorder
• inflammatory and immune attacks occur against multiple self tissues and organs
• progressive loss of tissue integrity through excessive inflammation and overactive immunity leads to organ failure and death
arthritis and joint pain
vasculitis and rash
kidney damage to glomular and tubular basement membranes
hematologic problems
CV problems
SLE Etiology
• polygenetic susceptibility to gene-environmental interacts resulting in autoimmunity
• some will have cutaneous lupus erythematosus (CLE), but 70-80% will develop SLE
• significant multiorgan morbidity
• triggering events include infections, hormones, environmental exposures to toxins/pollutants/etc. (UV radiation)
• most common cause of death CKD and CV collapse, with good treatment patients survive 20+ years
SLE Risk Factors
• women 30-44 yr; 10x more likely than men
• incidence declines after menopause which suggests estrogen as a trigger
• black americans 8:1 to white americans
SLE Disease Course and Expected Findings
slow onset (6 yrs from first symptoms to diagnosis)
• chronic fatigue
• recurrent fevers with unknown origin
• persistent joint/muscle swelling/pain, tenderness, weakness
• alopecia
• blurred vision
• pleuritic pain (pericarditis, pleural effusions)
• anorexia, weight loss, anemia
• depression
• butterfly rash
• Raynauds
• kidney damage and hematological problems
• decreased O and protein in urine
• HTN and peripheral edema
SLE Key Features
• red, macular, facial rash over the cheeks and nose in the shape of butterfly
• coin-shaped lesions (discoid rash) on face, scalp, sun-exposed areas
• sensitivity to sunlight (photosensitivity) with rash development after exposure
• chronic lesions on mucous membranes of mouth and throat
• nonerosive arthritis of 2+ peripheral joints with pain and swelling
• inflammation of serosal membranes, especially pericarditis and pleurisy
• kidney changes with persistent casts and protein in urine
• neurologic problems like seizures/psychosis without previous history
• hematologic problems with hemolytic anemia (most common), decreased WBC (leukopenia), decreased lymphocytes (lymphopenia), decreased platelets
• immunity problems such as autoantibodies to cell nuclear structures and false-+ results of serologic tests for syphilis
• presence of antinuclear antibodies (ANAs)
SLE Labs and Diagnostics
• skin biopsy (lupus cells and cellular inflammation)
• antinuclear antibodies (ANAs) positive in 95% patients
• ESR elevated
• BUN/Creatinine elevated
• UA positive for protein, casts, RBCs
• CBC (pancytopenia)
SLE Meds
• NSAIDS (contraindicated with renal disease)
• Corticosteroids (-sone, -lone)
• Immunosuppressants (DMARDS)
• antimalarial
Corticosteroids (SLE)
prednisone is anti-inflammatory and immunosuppressant (fluid retention, HTN, impaired kidney function, hypergylcemia, skin atrophy, pathological fractures)
don’t stop abruptly (DEATH), risk for fracture, watch for hyperglycemia
caution with elderly
Immunosuppressants (SLE)
DMARDS (methotrexate), azathioprine, belimumab; monitor for infection secondary to immunosuppression and liver enzymes (AST/ALT)
reverse isolation, toxicity, bone marrow suppression, liver toxicity, hold vaccines 30 days before
Antimalarial (SLE)
hydroxychloroquine suppresses synovitis, fever, fatigue, and risk of UV related lesions (frequent eye exams)
SLE Systemic Complications
• HTN, edema
• Renal dysfunction (urine output)
• Diminished breath sounds (pleural effusion)
• Tachycardia and chest pain (pericarditis)
• rubor, pallor, cyanosis hands/feet (vasculitis, vasospasm, Raynauds)
• arthralgias/myalgias/polyarthritis (joints/connective tissue)
• changes in mental status (psychosis/paresis/seizures)
• nutritional status
• BUN, creatinine, urinary output for renal involvement
SLE Nursing Care
• pain/mobility/fatigue
• assess VSs (BP)
• systemic complications and renal impairment; pericarditis and CV impairment
• watch for Lupus Nephritis (kidneys)
• watch breath sounds
SLE Patient Education
• wide-brim hat, long sleeves/pants when outdoors
• avoid UV exposure (sunscreen)
• mild soaps/shampoos
• pat skin dry/no rubbing
• monitor for rashes/lesions and use lotion
• avoid drying agents (alcohol, scrubs, powders, cleaning products)
• steroid cream for rashes
• report peripheral/preoribital edema
• report S/S of infection (typical/atypical)
• reverse isolation
• learn the risks of pregnancy while treating SLE
• avoid large crowds
• frequent eye exams
SLE Health Promotion
• small frequent meals if anorexia/anemia is a concern and between meal supplements
• encourage a heart-healthy diet
• limit salt intake for HTN and fluid retention secondary to steroid therapy
• emotional/psychological support
• support groups
• skin protection
• exercise plan (mobility/ADLs)
• avoiding smoking/alcohol
Seizure
abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may result in a change in LOC, motor or sensory ability and/or behavior
etiologies include trauma, brain tumors, birth injuries
Epilepsy
chronic disorder in which repeated unprovoked seizure activity occurs (3/4 of cases are idiopathic; may be imbalance of electrical neuronal activity; imbalance of neurotransmitters (especially gamma aminobutyric acid (GABA)))
auras
all meds cause drowsiness, ataxia and decreased CNS
Seizures/Epilepsy Etiology and Genetic Risk: Primary
IDIOPATHIC
no specifiable cause or underlying lesion
often associated with genetics
Seizures/Epilepsy Etiology and Genetic Risk: Secondary
• underlying brain lesion (tumor or trauma)
• metabolic disorders
• acute alcohol withdrawal
• electrolyte disturbances
• high fever
• stroke
• head injury
• substance abuse
• heart disease (arrhythmias)
seizures resolve when underlying etiology resolves
Types of Seizures
• 3 broad categories (generalized (5, both hemispheres), partial (focal/local, manifestations vary based on area affected), unclassified)
Absence (Petit Mal) Seizure
individual may appear to be staring into space and/or have jerking or twitching muscles
can be precipitated by hyperventilation or flashing lights
Tonic Seizure
causes stiffening of muscles of the body, generally those in the back and extremities
Clonic Seizure
causes repeated jerking movements of muscles on both sides of the body
Myoclonic Seizure
causes jerks/twitches of the upper body, arms or legs
Atonic Seizure
causes a loss of normal muscle tone; will fall down or may drop head involuntarily
Tonic-Clonic (Grand Mal) Seizure
causes stiffening of the body and repeated jerks of the arms and/or legs as well as loss of consciousness
may be associated with biting tongue, incontinence
postictal: muscle soreness, tired
Status Epilepticus
continuous or rapidly recurring seizures; MED EMERGENCY that causes hypoxemia leading to brain damage, arrhythmias, and acidosis
seizure activity lasting longer than 5 min
IV-push lorazepam (Ativan)/diazepam (Valium) as 1st line therapy (or phenytoin (Dilantin), fosphenytoin (Cerebyx); may require endotrach for airway protection
What to do when patient starts seizing?
protect patient from injury, maintain airway (O2 therapy, suction equipment, turn patient onto their side), time the seizure
After seizure has stopped..
apply O2 and clear airway
check blood glucose
attempt to reorient patient (postictal period varies)
Seizures/Epilepsy Assessment (Recognize Cues)
• number, timing, pattern of seizures
• pre-ictal phase (does pt acknowledge an aura or presenting symptoms?)
• other med history
• substance abuse history (alcohol use-last drink?)
• diagnostics (EEG, CT, MRI, SPECT/PET, blood glucose)
Anticonvulsants
all can cause drowsiness, ataxia and CNS depression
• levetiracetam (Keppra): no need to monitor blood lvls, CBC instead
• phenytoin (Dilantin) IV
• carbamazepine (Tegretol)
• Divalproex (Depakote)
Phenytoin (Anticonvulsant) for Epilepsy
causes gingival hyperplasia, bone marrow suppression, rash, multiple drug interactions, IV vesicant
monitor blood lvl and CBC
therapeutic range: 10-20 mcg/mL (narrow!)
Carbamazepine (Anticonvulsant) for Epilepsy
causes bone marrow suppression
monitor blood lvl and CBC
therapeutic range is 4-12 mcg/mL
Divalproex (Anticonvulsant)
causes hepatotoxicity, bone marrow suppression
monitor blood lvls, CBC, LFTs
therapeutic range is 50-100 mcg/mL
Surgical Treatment of Epilepsy
• resection of seizure focus
• requires precise diagnosis of seizure foci
• usually hospitalized for continuous EEG monitoring
• vagal nerve stimulation (pacemaker for the brain)…
goal is to prevent seizures by sending regular, mild electrical impulses to the brain; stimulator placed under skin in upper chest and electrode surgically placed in left neck around vagus nerve
Patient Education/Med Compliance (Epilepsy)
• don’t stop anticonvulsants abruptly
• need for blood monitoring
• avoid hazardous activities
• avoid alcohol, fatigue, loss of sleep
• Medic-Alert bracelet
• Epilepsy Foundation as resource
Seizure Management
• protect pt from injury
• do not force anything into the patients mouth during seizure activity
• turn pt to side to prevent aspiration and keep airway clear
• remove any objects that might injure pt
• suction oral secretions if possible w/o force
• loosen any restrictive clothing pt has
• don’t restrain or try to stop pt movement, guide movements if necessary
• record time the seizure began and ended and frequency if necessary
• after seizure, check O2, airway and BG; reorient patient (postictal phase)
TIA
reversible cerebral ischemia, “warning sign”
usually precedes thrombotic stroke
1 in 3 people experiencing TIA eventually have a stroke, half of occur within a year
temporary neurologic dysfunction, brief interruption in cerebral blood flow that resolve in 24 hours
most common cause is CAROTID ARTERY STENOSIS
TIA Risk Factors
smoking
DM
age
inadequate nutrition
hypercholesterolemia
oral contraceptive use
excessive alcohol use
illicit drug use
Stroke Incidence and Prevalence
5th leading cause of death, women have higher incidence
“stroke belt” (8 SE states with higher mortality, 20%)
Stroke ABCS
Aspirin use when appropriate
BP control
Cholesterol management
Smoking cessation
ABCD Assessment for TIA/Stroke
Age of at least 60 years
BP of at least 140/90
Clinical TIA features
Duration of symptoms
TIA Collaborative Interventions
surgical to promote perfusion (carotid angioplasty and endarterectomy)
meds (antiplatelet drugs like aspirin or Plavix)
bp management
controlling diabetes
lifestyle changes (smoking cessation, physical activity, diet)
Stroke
an interruption of blood flow to the brain
med emergency!! (-pam first than -toin)
as certain areas of the brain become damaged or infarcted, the control of various bodily functions may be affected
Acute Ischemic (Occlusive) Stroke
most common; occur as a result of an obstruction within a blood vessel that supplies blood to the brain
thrombotic (artherosclerosis)
embolic (a fib)
CT w/o contrast; no blood means ischemic
TPA thrombolytic within 4 hrs
Hemorrhagic Stroke
interruption in blood vessel integrity leading to bleeding into brain tissue or subarachnoid space
intracerebral hemorrhage (ICH) (severe/sustained HTN)
subarachnoid hemorrhage (SAH) (ruptured aneurysms + AVM rupture)
aneurysm
arteriovenous malformation (AVM) (congenital abnormality, collection of thin walled vessels)
CT w/o contrast, if blood is present; NO TPA!
CVA Manifestations
similar to TIA but do not resolve
headaches may be present with hemorrhagic strokes due to increasing ICP
Arteriovenous Malformation (AVM)
tangled mass of abnormal blood vessels in which arterial blood flows directly into venous system, 6% of all SAH
slight male prevalence, 20-40 yrs
symptoms similar to increased ICP
treatments are surgical resection, coiling, radiation
Stroke Assessment
s/s vary depending on location of vessel involved and extent of occlusion
unilateral weakness, numbness, difficulty talking and understanding, severe headaches with no known cause
Collecting Patient History for Stroke
first priority is to ensure pt is transported to stroke center
focused/rapid assessment protocol: what do we need to know first?
always a risk that LOC will change so need to prioritize information gathering
Stroke Assessment Neurological
LOC
Glasgow Coma Scale (GCS)
cranial nerves
pupils
motor and sensory
deep tendon reflexes
cerebellar function for coordination
NIH stroke scale
Stroke Assessment Cardiac and Respiratory
vitals (HR, BP)
monitor for arrhythmias
EKG
respiratory drive
rate and rhythm
Stroke Analysis
• inadequate perfusion to the brain due to interruption of arterial blood flow and possible ICP increase
• decreased mobility and possible need for assistance to perform ADLs due to neuromuscular or impaired cognition
• aphasia + dysarthria due to decreased circulation in brain (aphasia) or facial muscle weakness (dysarthria)
• sensory perception deficits due to altered neurologic reception and transmission
Stroke Diagnostics
emergent non contrast CT
may require MRI/MRA non emergently
cerebral angiogram
carotid duplex
EKG AND TEE (echocardiogram)
rule out other causes like migraine, partial seizures, subdural hematoma, brain tumor, cardiac syncope, hypoglycemia, demyelination disease
Stroke Planning and Implementation
improving cerebral perfusion
monitoring for increased intracranial pressure
promoting ADL and mobility ability
managing changes in sensory perception
Stroke ER Care
- assess ABCs and vitals
- O2 if pt is hypoxemic (<94% sat)
- IV
- blood samples for blood count, coagulation studies and glucose; give dextrose is hypoglycemic and insulin if glucose >300; give thiamine is pt has history of alcohol use or is malnourished
- assess using neurological screening assessment like NIH stroke scale
- order a CT brain scan w/o contrast and have it read quickly
- obtain 12 lead ECG and assess for arrhythmias
- don’t delay CT scan to obtain ECG, which is then taken to identify MI or arrhythmia as cause for embolic stroke (life threatening arrhythmias can happen with or follow a stroke)
- within 45 min of pt arrival, specialist must decide based on CT scan if hemorrhage is present
If hemorrhage is present…
note that the pt is NOT a candidate for fibrinolytic therapy
arrange for consultation with neurologist or neurosurgeon
consider transfer if available
If hemorrhage isn’t present…
determine if pt is a candidate for fibrinolytic therapy
repeat NIHSS
Fibrinolytic Therapy (tPA)
most important factor to determine if altephase is appropriate
period of time between symptom onset and arrival time to stroke center
FDA approved use of tPA within 3 hours of onset
American Stroke Association endorsed 4.5 hrs if no exclusion criteria are present
tPA Exclusion Criteria
age older than 80
anticoagulation therapy
baseline NIHSS score greater than 25
history of both stroke and diabetes
evidence of active bleeding
BP greater than 185 systolic or 110 diastolic
history of cerebral bleed
elevated PT/INR
Ischemic Stroke: Endovascular Interventions
- mechanical embolectomy MERCI retrieval system (for pts that don’t qualify for tPA or fail therapy; present within 8 hrs of stroke onset)
- intra-arterial thrombolysis (TPA delivered directly to thrombus within 6 hrs of onset)
- carotid artery angioplasty with stenting
Ischemic Stroke: Endovascular Nursing Care
interventional nurses are responsible for pre,peri, and postprocedural nursing care
- assessing for prevention, early identification and monitoring signs of neurological and hemodynamic incline
- ensure informed consent is signed
- administration of procedural meds
- documentation
- transition of care communication with ED, transferring organizations and ICU
- baseline neuro vascular assessment of pts extremities (pulses distal to anticipated arterial access site, capillary refill, skin color, temp; Allen/Barbeau test for baseline assessment of radial artery for trans radial approach)
Postprocedural Ischemic Endovascular Care
- document sheath removal time and time of hemostasis
- frequent vitals and neurological monitoring (every 15 min for 2 hrs, every 30 min. for 6 hrs, and every hr for 16 hrs)
- assist with hemostasis (may be achieved through manual pressure or closure device)
- monitor for vascular access complications (arterial spasms, pain, swelling, bruising, erythema, bleeding, hematoma, pulsatile mass, drainage from puncture site)
- assessment of pulses distal to arterial access site, cap refill, skin color and temp, sensation and motor function
- changes from baseline assessment are verified and communicated to proceduralist or admitting team
- frequent vascular access site and neuro vascular assessments (every 15 min for 1 hr, every 30 min for 1 hr, every hr for 4 hours)
Carotid Endarterectomy (CEA)
post procedural monitoring…
• frequent vitals
• neurological assessment (new stroke like symptoms)
• neck site for bleeding or hematomas
Stroke Expected Outcomes
• has adequate cerebral perfusion to avoid long term disability
• maintains BP and glucose within a safe and prescribed range
• performs self care and mobility activities independently w or w/o assistive devices
• learns to adapt to sensory perception changes if present
• communicates effectively or develops strategies for effective communication
• has adequate nutrition and avoids aspiration
Post-Stroke Speech Deficits
left CVA usually; can have global aphasia
Brocas area= expressive aphasia
Wernickes area= receptive aphasia
Priority Nursing Goals for Mobility
maintain ROM
position to prevent contractures
prevent foot drop
fall precautions
transfer to strong side
address functional incontinence
Nursing Care for Unilateral Neglect
place objects in pts visual field
approach pt from unaffected side
teach pt to turn head to affected side and stimulate affected side
teach pt to use mirror to survey affected side
Nursing Care for Dyspahgia
screen ALL stroke pts (assess gag reflex and swallowing function)
initiate speech consult (NPO until swallow study, barium swallow study may be indicated)
check for pocketing
modified consistency diet
HOB to 90°
tube feeding may be indicated if pt is aspirating
Collab Care for Stroke
PT: mobility, gait, transfer, strengthening
OT: ADLs, coping with cognitive and perceptual defects (adaptive equipment)
speech therapy: evaluating and treating aphasia, dysarthria and dysphagia
Spinal Cord Injury (SCI)
neurological deficits related to lvl and degree of injury
complete (all inner action below lvl of injury eliminated) or incomplete (some function or movement below lvl of injury)
can cause cauda equina (saddle numbness)
Mechanism for SCI
hyperflexion (accelerate forward, injury to cervical like a rear end collision)
hyperextension
axial loading/vertical compression (broken vertebral pieces from divings/falls)
excessive rotation
penetrating trauma
SCI Etiology
trauma (MOST COMMON) (MVC, falls, acts of violence, sports related)
malignancies/pathologies
SCI Incidence and Prevalence
18,009 new SCIs every year in the US
80% young white males, average age is 43 yrs old
cervical cord injuries more common than thoracic or lumbar cord injuries
Cervical SCI
above C4 requires mechanical ventilation
all cause respiratory insufficiencies (decreased cough, vital capacity and high risk of atelectasis and pneumonia)
Primary Injury SCI
initial injury/disruption of cord (spinal shock)
Spinal Shock
decreased reflexes and flaccid paralysis below level of injury due to acute SCI
complete but temporary loss of motor, sensory, reflex, and autonomic function (48 hrs-several weeks)
flaccid paralysis and bladder, paralytic ileus, loss of sensation, decreased or absent reflexes
spasticity may emerge after spinal shock resolves
Secondary SCI
on going damage from ischemia, inflammation, toxic metabolites, edema
neurogenic and hypovolemic shock
Neurogenic Shock
high risk with injury above T6; disruption of SNS
HEMODYNAMIC PHENOMENON!! (but can be present alongside spinal shock)
hypotension, bradycardia, Poikilothermia (hemo instability)
may require atropine, pacing or dopamine, potential need for acute airway management
Autonomic (Dysreflexia) Hyperreflexia
above T6; stimulus below lesion causes an imbalanced and unopposed reflex sympathetic stimulation; counter balancing from baroreceptors blocked
usually visceral/cutaneous stimuli (impaired sensation puts pt at risk)
distended bladder, fecal impaction, tight clothing, extreme temps are risks
Autonomic Hyperreflexia Symptoms
headache, blurred vision, diaphoresis, flushing, tachycardia
severe hypertensive crisis
can progress to status epilepticus or CVA, MI, cerebral hemorrhage and death
Autonomic Hyperreflexia Nursing Care
elevate HOB and remove tight clothes
monitor BP (administer meds if needed via IV)
remove noxious stimuli
close neurological assessment
SCI ER Post-Injury Care
immobilize injury with backboard and neck care
maintain ABCs
stat x-ray
spine CT/MRI
establish IV
assess LOC, head injury and other injuries
comprehensive neuro assessment (touch, pain, muscle strength)
high dose methylprednisolone (Solu-Medrol) to lower edema
maintain adequate perfusion (between 80-90, may require dopamine continuous infusion)
stabilization (application of traction/halo; surgical decompression with laminectomy and instrumentation)
Nursing Care for Acute SCI (Cardiovascular)
potential for CV instability (shock and autonomic dysreflexia) due to loss or interruption of sympathetic innervation or hemorrhage
- monitor HR and treat bradycardia (atropine for HR drop to 50-60)
- maintain MAP between 80-90 (titrate dopamine/other vasoactive drugs for acute management)
- maintain fluid volume status
- dextran (plasma expander that increases capillary blood flow within spinal cord)
- DVT prophylaxis (SCDs and Lovenox)
Nursing Care for Acute SCI (Respiratory)
potential for respiratory distress/failure due to aspiration, decreased diaphragmatic innervation and decreased mobility
- coughing and deep breathing exercises
- ventilator management
- monitor O2 sat and ABGs
Nursing Care for Acute SCI (GI)
- auscultate bowel sounds for ileus (NG tube for ileus aka gastric decompression)
- stress ulcer prophylaxis (PPI) ie pantoprozole
- TPN until begin oral feeding
- high protein/high cal diet
- initiate bowel training program
Nursing Care for Acute SCI (GU)
- catheter care (foley vs straight cath?)
- monitor output
- prevent UTI
- possibly initiate catheterization
- monitor BUN and creatinine (for and prevent bladder distention)
Nursing Care for Acute SCI (Skin Care)
risk for decreased mobility and sensory perception due to spinal cord damage and edema; high risk for pressure ulcers
- pin care for traction/halo
- infection prevention for any surgical sites
Nursing Care for Acute SCI (Psychosocial)
assess…
• grieving process
• body image, self-concept, role performance
• family dynamics?
• anger and depression
• loss of control
• sexuality, family planning?
• prepare for rehab (physical training; some rehabs for SCI also incorporate intimacy counselors)
SCI Care Coordination
home care
self management education (mobility, pressure injury prevention, ADLs, bowel/bladder training, sexuality education, prevention of autonomic dysreflexia)
health care resources (interdisciplinary, specialized SCI center, maximize independence)
SCI Health Promotion
prevention
education (reduce high risk behaviors, implement safety precautions)
rehab (restoration of function, level of independence, vocational rehab)
SCI Expected Outcomes
• exhibits no deterioration in neurologic status
• maintains a patent airway, a physiologic breathing pattern, adequate ventilation
• doesn’t experience a CV accident event (shock, hemorrhage, autonomic dysreflexia) or receives prompt treatment if it does
• doesn’t experience secondary SCI, including VTE and heterotropic ossification
• is free from complications of decreased mobility
• performs mobility skills and basic ADLs as independently as possible w or w/o use of assistive devices
