Neuro Flashcards
what is parkinsons disease
genetic defect and results in dopamin depletion
more commonly found in older adult males
parkinsons disease manifestations
tremors
rigidity
akinesia/bradykinesia: loss of ability to move your muscles voluntarily
postural instability
pill rolling tremors of the hands
fatigue
mask-like facial expression accompanied by drooling
slow-shuffling walk
difficulty rising from sitting position
echolalia
- meaningless repetition of another persons spoken words
priority goal is to prevent injury to client
parkinsons diagnostic studies
based on clients hx and clinical features
EEG
MRI
PET
parkinsons pharamcological intervnetions
goal is to provide palliative symptom managmenet and to postpone dependnece
anticholilnergics
- Benzotropine
- Procyclidine
dopamine precursors:
- levadopa-carbidopa
- levadopa
dopamine receptor antaongists:
- bromocriptine
- rotigotine patch
antiparkinsonian agents
- amantadine HcL
MAOI inhibitors;
- selegiline
- COMT inhibitors ( tolacapone)
- entacapone
parkinsons management
maintain safe environment for client and foster independence in ADLs
reinforce assistive devices
promote good nutrition and teach to eat small frequent meals and soft food
increase roughage with sufficient fluids to decrease constipation
provie emotional support to client and family members
daily exercise
safety and injury prevention
what is huntingtons disease
progressive atrophy of basal ganglia and some parts of the cerebral cortex
huntingtons disease manifestations
motor function impairement:
difficulties chewing and swallowing
chorea - jerky involuntary movements
dystonic posture
will eventually become bedridden
unable to organize, plan and do things in order
mental function will progressively decline
personality changes
no cure but palliative care
death usuall occurs 10-20 years after onset of symptoms
huntingtons diagnostic studies
clients and family history
physical exam
genetic testing
huntingtons disease care
manage symptoms promote quality of life prolong independence speech and physical therapy should be prescribed genetic counseling
psychotropic meds
tertrabenazine - decrease chorea
huntingtons management
assisitve devices
ADLs
maintain a well-balanced diet with an increased caloric intake
join support groups
what is amyotrophic lateral scerosis (ALS)
lou gehrigs disease neurological disease --> progressiv edegeneration of motor neurons of the anterior horn cells - spinal cord - brainstem - motor cortex
late middle age onset and is seen often in men than women
usually die within 2-6 years
ALS manifestations
muscle twitching
weakness in an arm or leg
muscle wasting
atrophy
spasticity
speech disorders
cognitive function and mental acuit will remain intact
voluntary and involuntary muscle function will be lost
eventually need for mechanical ventilation due to resp failure
ALS daignostic studies
client hx
physical exam
CK and EMG
loss of voice and ability to communicate can be particularly isolation and stressful for clients
ALS pharamcological interventions
muscle relaxants for spasticity
riluzole
-neuroprotector to extend life expectancy
goal is to keep client functionally independent as long as possible
speech and physial therapy can help client amintain independence
ALS mangement
provide resp care and referrals
maintain safe environment
prevent complications of immobility
balanced nutrition - enteral feedings are often required
emotional support
what is dementia
loss of brain function that occurs with certain diseases
affect memory, thinking, langauge, judgement and behvior
degenerative dementia is seen with Alzheimers disease
dementia manifesations
forgetfulness short term memor loss difficulty with many areas: - language - memory - preception or judgement
can affect higher levels of cognitive function
- ability to think abstract thoughs or perform calculations
dementia diagnostic studies
MRI
CT
neuro exam
mental status
lab tests: B12 level sblood ammonia ABG toxicology screening glucose liver enzyme
thyroid function
HIV,
syphilis
lyme titer
dementia pharamcological interventions
antipsychotics:
- haloperidol
- risperidone
- olanzapine
mood stabilizers
- fluoxetine
- imipramine
- citalopram
sertonin-affecting drugs
- trazodone
- busprione
CNS stimulants
- methyphenidate
meet clients needs
- establish a routine and promote indepdnece
- reorient them as NEEDED
alzheimers manifestations
one of more of the following will be observed:
agnosia
- difficulty naming objects
aphasia
- language disturbance
problems with organization and abstract thinking
memory impairment
apraxia
- difficulty with motor activities
cognitive difficulties are not related to other conditions
latered snesory preceptions include: illusions and hallucinations
wandering verbally or physically abusive behavior resisting care socially inappropriate behavior sundown syndrome
alzheimer early stage
- subtle personality changes include difficulty with abstract thinking
- forgetfulness and uncertainty causes anxiety, irritation and withdrawal
- difficulty making decisions, concentrating and handling work skills
alzheimer middle stage
impaired language, motor activity and object recognition
wandering
inability to carry out ADLs
impaired judmgeent
severe disorientation, with personality na dbehavior changes
difficulty remembering fam and friends
hallucinations and delusions
alzheimers final and terminal stage
loses ability to function physically and mentally
becomes mute, incontinent and totally dependent
alzheimer diagnostic studies
physcial exam neruo testing MRI CT scan of head lab tests: - same as dementia
alzheimers pharamcological intervention
Galantamine
- take with meals, 2x/day or every morning
- encourage fluids
donepezil
- given once a day before bed
- may be given with or without food
memantine
- in cases of moderate to severe dementia
rivastigmine
- with food twice a day
- may increase dosage at intervals
antidepressants
- SSRIs
0antipsychotics
- control hallcuination and delusions
greatest risk factor of AD is age, but age alone is not sufficient to cause AD
alzheimer disease complementary health
gingko biloba
vitamins B and E
asian ginseng
grape seed extract
no convincing evidence
alzheimers management
safe environment with structured routine and decreased stimulation
legal issue
- living will
- power of attorney
0 end of life care
nutrition needs
monitor for depression
memory aids
minimal distractions and noise
orient client as appropriate
maintain elimination routine to decredase incontinence
help family enroll the client in an identification/return program
assess for abuse/neglect
long term care
delirium
onset:
- sudden/abrupt depends on cause
- often occurs at twilight or in darkness
short diurnal fluctuation in symptoms
worse at night, in darkness and on awakening
abrupt progression
hours to less than one month of duration
reduced consciousness
alertness fluctuates, lethargic or hypervigilant
impaired attention, fluctuates
generally impaired orientation
severely varies
recent memory and immediate impaired
risk factors for stroke
uncontrolled hypertension
smoking
obestiy
incredased blood cholesterol
triglycerides
afib
transient ischemic attack
warning sign of impending stroke
produces neurologica deficits that last only minutes to hours
full functioning recovery is seen within 24-72 hours
reversible ischemic neruologic deficit
symptoms last between 24 hours and 3 weeks
visually will have a full functional recovery
partial, non progressive stroke
some neruolgical deficit but client isstabilized quickly
progressive stroke
present with a deteriorating enruological status and residula neruo deficit
completed stroke
leave client with permanent neuro deficits
ischemic stroke
slow onset
inadequate blood flow which leads to a cerebral infarction
common cause: atherosclerosis
- buidlup of fats, cholesterol and other substances
hemorrhagic stroke 4 types
- intracerebral hemorrhage
- subarachnoid hemorrhage
- epidural bleeds
- subdural bleeds
intracerebral hemorrhage
occrsuw ehn blood vessels rupture and bleed into the brain
subarachnoid hemorrhage
cuased by the rupture of a sacular intracranial aneurysm
epidural bleeds
involve cerebral arterial vessels
often a loss of consciousness for a short period of time
for epidrual bleeds = artery
- remember that “e” in epidural and “a” in artery are at the top of the alphabet
subdural bleeds
involve the veins and may not be until months after an initial trauma
for subdural bleeds = veins
- remember “s” in subdural and “v” in veins are at the bottom of the alphabet
stroke manifestations
homonymmous hemi anopsia agnosia apraxia diplopia sensory loss
brocas: difficult communicating to others, but understands
wernickes; can hear a voice or read written language, but misunderstands the meaning or takes the message too literally
global aphasia:
exhibit severe communication difficulties and may be unable to speak or comporehend the language
dysarthria
- speech disorder caused by the disturbance of mascular control, resulting in impaired pronunciation, articulation and phonation
agraphia - inability to write or spell
hemiplegia, hemiparesis
flaccidity and spasticity
emotional lability loss of social inhibtions fear anger hostility
urinary frequency and urgency
bowel and urinary incontinence
altered level of consciousness
seizure
hyperthermia
hypertension is the most important modifiable risk factor in stroke
right sided stroke
left side of the body will be affected:
could produce paralysis on left side of body
there will be problems with:
- processing visual and verbal information
- decreased cognitive skills like thinking, reading, learning, remembering
- poor judegement
- short attention span
- shorterm memory loss
left sided stroke
right side of the body will be affects
could produce paralysis on the right side of the body
problems with communication
- aphasia
- dysarthria
stroke diagnostic studies
hx and physical exam
HCP should evaluate stroke within 10 min of their arrival to hospital
CT scan should be done within 30-60 min of arrival
MRI
doppler echocardiography
carotid artery duplex doppler ultrasonography
EEG
cerebrl angiography
stroke care
acute phase: single most important point in the clients history is
- time of onset of symptoms
- last seen normal
ischemic stroke pharamcological interventions
thrombolytics
- tPA
- alteplase
must rule out hemorrhagic stroke via C scan prior to admin
antiplatelet therapy
- aspirin
- dypirdamole
platelet aggregation inhibitor
- copidogrel
- ticlopidine
steroids:
-dexmethasone
blood pressure should be managed to maintain cerebral perfusion pressure
surgery is necessary if carotid artery is stenotic or partially occluded
carotid endarterectomy or angioplasty with stenting may be performed
hemorrhagic stroke pharmacological intervention
antihypertensive agents
systemic steroids:
-dexmethasone
osmotic diuresis
- mannitol
anti-fibrinolyti agents:
- amnioocaproic acid
surgical excision of an aneurysm or clot/hematoma may be necessary
stroke acute stage management
maintain airway patency
- suctioning equipment must be available at bedside
neuro status
vitals
note seizure acitivity
adequate fluids
HOB 15-30 position, client turned or tilted to unaffected side
provide activity
perofrm passive and or active ROM
maintain propery body alignment
stroke long term management
monitor normal elimination patterns
teach about supportive devices
maintain safe environment
adequate nutrition
assist with ADls
emtoinal support provide methods of communication for clients with aphasia
what is meningitis
acute or chronic inflammation of the meninges
- the covering of the brain and spinal cord are involved
most contagious form and requires isolation
- other forms include viral and fungal meningitis
high risk clients for meningitis
infants
adults with weakened or suppressed immune system
college students esp freshmen who reside in dorms
travelers to foreign countries
- wherre disease is endemic
meningitis manifestations
nuchal rigidity
- stiff neck
positive kernigs sign and Brudzinski’s sign
positive opisthotonic position
changes in level of consciouness
seizures
meningitis diagnostic tudies
hx and physical exma
positive brudzinskis signs
- when you lift the child’s neck, their feet go up too
positive kernig’s sign
- severe stiffness of the hamstrings
- causes inability to straighten the leg when hip is flexed to 90 degrees
lumbar puncture to evaluate cerbrospinal fluid
- CSF may show signs of decreased glucose and increased protein if bacterial or fungal infection is present
- contraindicated with findings that indicate an elevated intracranial pressure
CT scan or MRi, with and without contrast, may be performed
meningitis care
cure the infection and prevent contractures
pharmacological interventions:
antibiotic therapy will depend on the type of pathogen
antifungals = if fungus is the causative agent
anticonvulsants = to prevent seizures
preventative therapy can be used for people exposed to those with meningococcal or Haemophilus influenzae
- rifampin
actions to minimize fever
prevent an increased of intracranial pressure or seizures
meningitis management
ABGs
body weight
urine volume
specific graivty and osmolality
neuro and vitals comfort measures for pain droplet precautions - haemophilus influenzae type B - neisseria meningitis
reduce external stimuli and lighting if the client is photophobic
maintain a quiet environment
monitor seizures and implement precautions
what is encephalitis
inflammation of the parenchyma of the brain and spinal cord
most common cause of encephalitis is an acute viral infection
other potential causes:
- bacterial infection
- hypoxic inflammation
- toxic substances
- arsenic
- carbon monoxide
- high level of serum ammonia due to liver failure
encephalitis manifestations
sudden fever
nuchal rigidity - stiff neck
personality changes
mild flu-like complaints
severe headache
- this can progress to stupor and then coma with seizure activitiy
altered level of consciousness
encphalitis diagnostic studies
hx and physical exam CT scan MRI EEG PCR assay cerebral spinal fluid collection to show if there is a decrease in glucose and elevated WBCs
encephalitis care
goal is to cure the infection and prevent comlications
- rest
- supportive nutrition
- fluid balance maintenance
pharamcological interventions:
- acyclovir
- antivonculsants to prevent seizures
prevent increased intracrnial pressure
mosquito control and insect repellant
encephalitis management
control clients fever and administer drugs
seizure precautions
- recommended to drive on they are 6 months seizure free
sxs of increased intracranil pressure
- headache
- blurred vision
- confusion
- shallow breathing
- voiting
ensure isolation and take airbonre or droplet precautions
maintain patent airway to prevent further hypoxia
reduce stimuli and lighting if client is photophobic
multiple sclerosis manifestations
MS can improve and worsen unpredictably
blurred vision dysphagia diploopia facial weakness and/or numbness weakness paralysis spasticity gait disturbances
dysarthria tremor incoordination ataxia vertigo
decredase in short term memory
difficulty with new information
word-finding difficulty
short attention span
urinary retention
loss of bowel incontinence
sexual dysfunction and fatigue
multiple sclerosis diagnostic studies
hx and physical exam
lumbar puncture
MRI
CT
multiple sclerosis pharamcological interventions
rpimary goal is to alleviate symptoms and prevent complications;
adrenocorticotropic hormone
beta interferon
immunosuppressants
antispasmodics
multiple sclerosis management
maintain clients functional independence in ADls
promote praciticng a wide base walk
prevent injury and complicationsfrom difficulties walking or immboility
avoid fatigue and stress and conserve energy
know current meds and side effects
assisitve devices correctly
maintain a diet that support nutrition and energy needs
avoid triggers such as stress, regnancy and temperature extremems
use bladder control measures during exacerbations
client with MS should NOT use hot water for a bath because of the risk of thermal injury
what is guillian barre syndrome
symmetric and ascending motor paralysis
GBS manifestations
muscle weakness if progressive, ascending and bilateral
leads to paralysis of voluntary muscles
loss of superficial and deep tendon reflexes
bulbar weakness
dysphagia
resp failure
paresthesia
burning muscle pain
paralysis vary from being partial or total paralysis
- cause fluctuations in blood pressure, heart rhythm and rate
GBS diagnostic studies
hx and physical exam
lumbar puncture will show an increase of protein in cerebrospinal
electromyography will show acute muscle denervation
GBS care
preventing complications and maintaining body functions until the reversal of paralysis
management is based o clients physiologic needs and which body systems are affected
- tracheostomy
- ventilator support
- IV fluids
- plasmapheresis
pharmacological interventions:
- immunoglobulin therapy
- morphine for apin control
GBS management
maintain care of the client on ventilator support
provide adequate pain control
monitor resp status
safe environment to minimize infection
alternate way to communicate with client
what is myasthenia gravis
progressive weakness and exhaustibility of voluntary muscles without atrophy or sensory disturbance
presents in 2 age clusters:
- women in early adulthood
- men in late adulthood
will experience myasthenic or cholinergic cristis
-cholingergic crisis differs from myasthenic risis in that is is caused by overmedication with anticholinesterase drugs
myasthenia gravis manifestations
progressive fatigue and/or weakness of the voluntary muscles but without muscular atrophy
sensation will remain intact
present with signs of restrictive lung disease
facial symptoms include: ptosis and reduced eye closure
weak smile
diplopia
blurred vision
speech and swallowing disorders
weakness of the facial muscles makes it difficult to raise eyebrows and make different faces
if nurse suspect cholinergic crisis - nurse should withhold any prescribed anticholinesterase medications
- prepare to administer atropine sulfate = antidotes
myasthenia gravis diagnostic studies
hx and physical exam
edrophonium test
- improved muscle strength after edrophnoium injection indicates a positive test for MG
single fiber electromyography and a serum assay of circulation acetylcholine receptor antibodies
myasthenia gravis pharamcological intervention
anticholineterase agents
- pyridostigmine
- neostigmine
corticosteroid therapy
immunosuppressants
- azathioprine
tplasmapheresis = separation of blood componenets
primary goal is to improve clients stregnth and endurace
management for myasthenic crisis
caused by precipitaing factors like:
- stress
- infection
- inadequate medication dose
watch for sudden inability to swallow, sepak or maintain a patent airway
edrophonium test will be performed
- positive test signal myasthenia gravis
negative test indicates cholinergic crisis that will be treated with atropine
ventilator support
management for cholinergic crisis
cause by overdose of pyridostigmine adn results in increased acetylcholine
findings include:
- profound weakness
- gastrointestinal distress
- resp failure
atropine may be administered
- stop anticholinesterase agents and restart gradually when client is stable
myasthenia gravis management
ventilator support
identify aggravating factors
give meds ordered and on time
- assist client with ADLs and feeding as indicated
support groups
emotional support
adequate rest periods
care for post-surgical if needed
energy conservation techniques
expectations, medication and side effects
signs of impending crisis
avoid or minimize stressors
avoid extremes of temperatures
avoid people with resp infections
drugs containing magnesium and morphine should be AVOIDED
- increase weakness and resp suppression
what are seizure disorders
characterized y a single event or chronic episodes of abnomral electrical activity in the brain
include cerebral lesions or biochemical alteration
can also be idioapthic
types of seizures:
- generalize
- focal
generalize seizures
clietn lses consciousness for a few seonds to several minutes
most common gernealized seizure is a tonic-clonic seizure, formerly called a grand mal seizure
during the tonic phase, the body stiffens for 10-20 seonds
- followed by a jerking of extremities (clonic phase)
typically followed by a post-ictal phase where client feel stired and may sleep for several hours
- no memory of seizure
focal seizures
designated as:
simple
=- no impairment of awareness/consciousness
complez
- impairement of awareness/consciousness
what is status epilepticus
rapid sequence of seizures without interruption or pauses
MEDICAL EMERGENCY
- often occurs whena client suddenly stops their anticonvulsant medications
client is in a posti-ictal state when next seizure begins
if cerebral anoxia occurs, brain damage or death can follow
- there is a risk for severe orang and muscle hypoxia
life threatening emergenyc
- nurse should protect clients airway
- prepare to administer a benzodiazepine to stop seizures
status epilepticus diagnostic studies
hx and physical exma laboratory draws includes: -toxicology screening - ABGs - chemistry panel - anticonvulsant therapeutic drug level
EEG
CT scan
possible lumbar puncture
status epilepticus care
expected outcome will be to control or minimize the seizure activity
prevent complications by correcting underlying problem
pharamcological intervnetions:
benzodiazepines Iv
- diazepam
- lorazepam
hydration anticonvulsants
- phenytoin
- fosphenytoin for maintenance
barbituates
- phenobarbital
succinimides
- ethosuximide
vagal nerve stimulation therapy may be helpful
surgery is reserved for those wo are unresposnive to medication management
if seizure control is not achieved with single durg, then a second drug may be added
about a third need a combination regimen
status epilepticus management
administer meds as ordered
- be alert for drug interactions because htye are very common with antiepileptic medications
nurse will eduacate client on:
- wear med alert bracelet or similar identification
- understand med effects, interactions and side effects
- be aware of triggers
- develop techniques to reduce stress
- understand ho to iplement seizure care at home or at work
sinus headache
pain is behind browbone and or cheekbones
cluster headache
pain is in and around the eye
described as a sharp or stabbing pain, typically the eye area
can last up to 4 hours
tensions headache
pain is like a band squeezing the head
most common form
associated with stress, anxiety, depression or drastic changes
migraine
pain
nausea
visual changes
often run in families and have an adolescence or early adulthood onset
unilateral , throbbing pain that may be preceded by an aura or prodrome
can last from hours to days
headache manifestations
throbbing
nausea
vomiting
visual disutrbances
photophobia
- so wearing sungalsses indoors is recommended
tendereness
neck stiffness
focal neruological signs
headache diagnostic studies
hx and physical exam
CT scan
MRI
radiological exma of skull and cervical spine
lumbar puncture if inflammation of infection is suspected
alcohol is a migraine trigger and should be avoided
headache care
alleviate pain
treat underlying cause
applying pressure or a cold pack
migraine care
aspirin
acteaminophen
ibuprofen
opioid analgesics: codeine meperidine mrophine isometheptene prophylactic treatment with beta adrenergic blocking agents
serotonin agonists
imipramine
topiramiate
used to stop migraine attacks:
- frovatriptan
- rizatriptan
- sumatriptan
- zolmitriptan
ergotamine tartrate without caffeine or ergotamine with caffeine
headahce complementary health
butterbut is effective for migraine prevention
feverfew
magnesium
riboflavin
- these are maybe effective
coenzyme Q10 = possibly effective
avoid foods such as monosodium glutamate, tyramine, cheese, chocolate, aspartame, alcohol
cluster headaches interventions
inhalation of 100% oxygen is effective for about 80% of clients with cluster headaches
pharmacological intervention:
narcotics
- codeine sulfate
alpha adrenergic blocking agent:
- ergotamine tartrate
prophylactically with serotonin antagonists
tension headaches interventions
non narcotic analgesics:
- ibuprofen
- acetaminophen
- aspirin
muscle relaxants
prophylactically with antidepressants and/or dozepin
headache managment
dark environment
prompt pain management
NPO until anusea and vomiting subsides
keep a diary which can help prevent headaches by identifying triggers
discuss alternative for pain management
what is head trauma
can develop postconssuioin syndrome
- occur anywhere from 2 weeks to 2 months after injury
head trauma manifestations
persistent headache
personality and behavioral changes
changes in intellecutal ability
closed head trauma: non-penetrating
- no break in skull
open head trauma
- skull is broken, creating a direct pathway to brain tissue
mild head trauma
causes only a momentary loss of consciousness with no or minior neurological dysfunction
moderate head trauma
causes a momentary loss of consciousness witha change afterwards in neurological function
usually temporary
severe head trauma
causes a decreased level of conciousness with serious neurological impairment and dysfunction
head trauma: skull fracture
linear fraacture = simple break in the bone with no displacement of skull
depressed fracture= occurs when park of the skull if pushed in
basiliar fracture = located at the base of the skull
- may extend into the orbit or ear
- the ear or nose may leak CSF
- most difficulty type to verify by x-ray
concussions occur when there is jarring or shaking of the brain
- lead to temporary loss of neurologic function with complete recovery
head trauma: bleeding related
contusion in head: bruise on the surface of the brain
intracerebral hemorrhage is caused by bleeding within the brain tissue
- occurs after invasive skull trauma/ open fracture or a hemorrhage
epidural bleeds in head trauma
occurs when blood vessels are lacerated in the space between the skull and dura meter
medical emergency ebcause of high risk of deather with arterial bleedin
g0 clients commonly lose consciousness after injury
- followed by a lucid panel
- level of consciousness drops quickly within the next 24 hours
subdural bleeds in head trauma
lacerated blood vessels crossing the subdural space
secondary to a closed head injury
acute:
findings surface in 24-72 hours after the injury, with rapid neurologic deterioration
subacute:
0- findings surface in 72 hours to 2 weeks with slower progression of feterioration
chronic:
- gradual clot formation forms over time
- possible developing over months with minimal deterioration
head trauma manifestations
initial restlessness and irritability
decreased in level of consciousness
headache
nausea
vomiting
-projectile vomiting indicates increased intracranial pressure
otorrhea
- drainage of liquid from ear
pupillary changes
seizure activity
altered vital signs cushings triad is a late sign - indicative of increased intracranial pressure - bradycardia - irregular resp - widened pulse pressure
posturing
- decorticate or decerebrate with severe head trauma
CSFk leakage from ears or nose is indicative of basilar skull fracture
head trauma care
reduce or minimize increases in intracranial pressure and to preserve brain tissue
- clients in acute phase of head injury are often admitted to ICU for close monitoring
pharmacological interventions:
osmotic diuresis
- mannitol
steroids
- dexmethasone
barbituate coma by induced
neurmuscular blocking agents
intraventricular catheter, subarachnoid screw or bolt may be used to manage and montior intracranial pressure
prevention of complications such as:
- seizures
- fever
- infection
- DVT
- stress ulcers
other therapies will include resp, physical, behavioral, speech and occupational support
- as well as nutritional
head trauma management
during acute phase:
manage/ prevent increased intracranial pressure
provide appropriate care for client being mechanically ventilated
observe for rhinorrhea, otorrhea and test for glucose
- if drainage is present
- to rule CSF leakage
balanced nutrition and fluid intake
ADLs
prevent complications of immbolility
closely monitor neuro, LOC and cranial nerve function
vital
look for abnormal resp patterns
elevate head of bed to 15-30 with clients head positioned midline
- no pillow
- avoid flexion of neck
what is trigeminal neuralgia
chronic and severe paoxysmal facial pain
affects that cranial nerve V and only involves one side of the face
can be triggered by harmless events such as breeze or hot of cold liquids
trigeminal neuralgia manifestations
intesene facial pain lasting from a few seconds to a few minutes along the nerve branches
episode may be as freuqne tas 100 times a day
infrequent as a few times a year
pain may be described as burning or shooting
trigeminal neuralgia diagnostic studies
hx and physical exam
CT to rule out other causes
trigeminal neuralgia care
relieve pain and minimize frequency
pharamcological interventions:
anticonvulsants
- carbamazepine
- phenytoin
skeletal muscle relaxant
- baclofen
antidepressnats
nerve block may be considered for temporary pain management
trigeminal neuralgia management
restful environment with scheduled rest periods
reinforce the need for balanced diet
assess for depression or suicidal thoughts
chewing on opposite side of mouth in avoiding pain is helpful
avoid any very hot or cold foods
avoid exposing their face to extreme environemntal temperatures
what is facial nerve paralysis
aka Bell’s palsy
disorder of the cranial nerve VII involving only one side of the face
often occurs during high period of stress
may also be a link to the herpes simplex virus
facial nerve paralysis (Bell’s palsy) manifestations
often occur suddenly over 10-30 minutes and occur unilaterally
exhibit ptosis with excessive tearing
inability to close orbnlink eye
lower face expierences paralysis
reports impaired ability to taste and fifciulty with eating
may exhibit flat nasolabial fold
facial nerve paralysis (Bell’s palsy) diagnostic studes
hx and physical exam
rule out stroke
facial nerve paralysis (Bell’s palsy) care
restore cranial nerve function
pharmacological intervention
- prednisone
antivirals
- acyclovir
analgesics
moistening eye drops
local and comfort measures
- heat
- massage
- electrical nerve stimulation for muscle tone
alternative therapies
- massage
- guided therapeutic imagery
facial paralysis of Bell’s palsy may cause a change in physical appearance
- important ofr the nurse to provide psychosocial support
- reassurance that mot clients recover within 3-6 months after onset of symptoms
facial nerve paralysis (Bell’s palsy) management
reinforce balanced nutrition witha soft diet
adminiter drugs as ordered
use medications correctly
chew on side of mouth opposite from paralysis
protectice eyewear during risk periods
use eye lubricants
remember that findings amy disappear and return in times of high stress
myopia
near sightedness
blurred distance vision but can see close
hyperopia
far sightedness
can see far but blurry for close
presbyopia
occur in middle age when lens loses elasticity with resuls of hyperopia
astigamatism
occurs when lens refracts light rays to focus on 2 different points of the retina
what is eye trauma
dmagaed caused by a direct blow to the eye
trauma may affect not only the eye, but also surrounding area, including adjacent tissue
when approrpiate, irrigate the affected eye with sterile normal saline eye irrigatn
what is corneal abrasions
disruption of the cells
loss of superficial epithelium
caused by:
- trauma
- checmical irritant
- foreign body
- lack of moisture
corneal abrasions manifestations
severe pain
blurred vision
halo around lights
teary eyes
inability to open the affected eye
photophobia
can be diagnosed using fluorescein sodium dye
corneal abrasions management
abrasions heal usually within 48 hours with no scarring or visual deficity
short acting analgesic drops
eye rest with soft or rigid eye patch
what are corneal lacerations
same causes and findings as corneal abrasions
lacerations are serious medical emergencies that require immediate attention
- srugery is often required
penetrating injury to the eye
requires immediate care
do not remove the object
do not aply pressure of any kind to the eye or object
cover the injured eye to protect mvoement of object
cover the uninjured eye with a soft or rigid eye patch to avoid movement
client will need to be seen in an emergency room immediately and surgery will be required
chmical irritants in eye
flush the eye with plenty of tap water or sterile normal saline
should immediately go to the nearest ED
ultraviolet burns in eye
occur from sun exposure or welding flames
- burns caused by looking at a welding flame without special glasses
burn irritates epithelium, which swells and scales off (desquamation)
care is the same as with lacerations
general management of eye injuries
provide copious irrigation to the affected eye
apply bilateral soft or rigid eye patch to rest both eyes y decreasing eye movement
use tinted glasses for photophobia to reduce eye discomfort from artificial lights or sunlights
avoid activities that increase intraocular pressure
- bending
- yoga
what is glaucoma
eye condition that can lead to damage to the optic nerve due to increased intraocular pressure
4 types of glaucoma
open angle (chronic) glaucoma
angle closure acute glaucoma
congenital glaucoma
secondary glaucoma
glaucoma manifestations
unaware of glaucoma until there is a disturbance in their vision
- peripheral vision loss is affected first, prior to total loss of vision
3 assessment:
- peripheral vision loss
- elevated intraocular pressure
- cupping of the optic disk
glaucoma care
reduce IOP and prevent visual field deficits
pharmacological interventions: - miotic eye drops - carbonic anhydrase inhibitors like acetazolamide - beta adrenergic blocking agents like timolol maleate ophthalmic solution use more often in emergency care
trabeculectomy
filtration or last surgery
performed when pharmacological agents are not effective
small piece of sclera containing the trabecular network is removed and an iridectomy is performed
iridectomy = procedure to remove part of the iris
may be combined with surgery to remove a cataract
trabeculectomy by traditional surgery
monitor dressing for excessive bleeding
administer antiemetics, analgesics, corticosteroids and antibiotics
assist the client with ADLs as needed
trabeculectomy by laser surgery
explain that clients vision may be blurred for first day or 2 post op
teach client to use soft or rigid eye patches or sunglasses for photphobia
discuss the use of an analgesic as ordered
glaucoma management
avoid activities that increae IOP
- bending
- stooping
- straining
- coughing
- blowing their nose
- laughing
stress the importance of eye routine exams, yearly or more often if complications aris
teach how and when to instill eye drops
- usualy recommended time is before bedtime
what is acute closed angle glaucoma
occurs wehn iris lied near the drainage channel andbulgese forward against cornea
- blocks the trabecular netowkr
- increasing IOP
medical emergency
affect more women than men, usually after age 45
acute close angle glaucoma manifestations
sudden onet of blurred vision
halos or colored rings around white lights
sudden frontal headache
sudden severe eye pain
reddening of the eye
nausea
vomiting
profuse lacrimation
mildly dilated, nonreactive pupil
cornea appears hazy
if left untreated, blindness may result in 2-5 days
acute closed angle glaucoma diagnostic studes
hx of findings
ocular pressure readings
acute closed angle glaucoma care
prevent or minimize the dmaging effects
emergency pharmacologic treatment to decrease IOP:
- intravenous osmotic agents
- topical miotic eye drops
- systemic carbonic anhydrase inhibitors
- systemic analgesics
surgery:
- iridotomy or iridectomy
- usually repeated on unaffected eye
acute closed angle glaucoma management
monitor med effectiveness
apply eye patch or sunglasses for post op photophobia
vision will often be blurred for 1-2 days post op
yearly or more frequent eye examinations
teach to avoid acitivities that increase IOP
explain correct procedure for dinstilling eye dops and then have client reutrn demonstrate
what are cataracts
clouding of the lens, whether unilaterla or bilaterla
painless, but there will be progressive loss of sight in one or both eyes
cataract diagnostic studies
hx and physical exam of eyes
cataract care
correct visual field fect
- surgical removal of cloudy lens will be performed one eye at a time
types of cataract extractions include
extracapsular cataract extraction
phacoemulsification
intrascapuslar catarct extraction
intraocular lens
extrascapular cataract extraction
lens contents are removed and posterior chamger intact
treatment of choice for cataract surgery
phacoemulsification
ultrasound fragment so the lens contents
intrascapsular cataract extraction
lens contents and lens capsulae are removed and the eye become hypermetropic
intraolcular lens
usually performed at time of extraction
what is hyphema
occurs when blooc collects in the anterior chamber of the eye
may require bed rest
wear eye patch
observe for increased IOP
- indicated by complaints of severe pain
may require prescribed miotic or cycloplegics
intraocular infection management
complaints of throbbing or pain with cloudy drainage from eye
antibiotics
avoid any actions that cause IOP
observe clients ability to apply eye drops
provide referral is if client is unable to self medicate
provide written list of complications for client to immediately report to
for 6-8 weeks after surgery, sensation of “an in the eye’ is normal
for photophobia - may be present for months to year,
client should wear sunglasses when outside or in bright light
causes of retinal detach,ent
inflammation
trauma
hemorrhage
tumor
retinal detachment manifestations
causes holes or a tear in the retina
fluid, blood or amass separates the retinas sensory layer
rapid separation gives sense of “curtain being pulled over the eye”
- client may have partial vision in affected eye
slow separation may be asymptomatic
retinal detachment diagnosti studies
hx and physical exam to confirm diagnosis
retinal detachment care
correct and/or prevent further vision loss
- vast majority of retinal detachment are successfully repaired
laser surgery/photocoagulation
= procedure tht uses a laser beam and is directe d through a dilated pupil
- effect is to seal localized breaks or rips in the retina
cryotherapy = extreme cold is applied and freezes rips in the retina
diathermy = heat applied with an ultrasonic probe to repair rips
retinal detachment pharmacologic interventions
adrenergic - mydriatic agents
cycloplegic agents
antibiotics
retinal detachment management
maintain client in proper position for bed or chair rest
apply post op rigid/soft eye patch to rest eye
suggest dark lens glasses for photophobia
administer meds as ordered
prevent acitivites that increase IOP
blindness causes
retinal degeneration glaucoma cataract amblyopic - decreased eyesight due to abnormal visual developoment
macular degeneration “central loss of vision”
blindness management
alert client when you enter room
safety emasures
orient new surrounding
use numbers on a clock to orient your client to location of furniture or food on plate
- your chicken is at 6pm
assis t with ADLs
DO NOT: grasp elbow and lead from behind
instead, instruct them to hold your elbow, as you walk slightly ahead of them
what is menieres disease
inner ear disorder
meniere disease amnifesations
attacks are intermittent and there are recurrent
vertigo with nausea nystagmus vomiting tinnitus hearing loss
meniere disease pharmacological interventions
atropine
antihistamines or decongestatns
intervetnion for remission; diuretics to decrease fluid accumulation vestibular suppressants - diazepam - meclizine
adrenergic neuron blocking agents
- epineprhine
meniere disease diagnostic studies
hx and physical exam is required
Weber and Rinne test
Ct scan
meniere disease management
during an acute attack:
keep client on bedrest in quiet, dark room
avoid unnecessary mvoement of clients, especially of their head
give general care fto clients with nausea and vomiting
restrict salt and fluid intake as prescribed
avoid tobacco and caffeine
institute precautions to prevent client from falling
hearing loss management
non-auditory modes of communication
face the client and speak
DO NOT SHOUT
tech client about danger of workplace noice, noisy tools and recreational noise
prevent falls due to vertigo
