Transcript Nursing Care of Clients with Neurologic Disorders

Nursing Care of Clients with
Neurologic Disorders
Client with Alzheimer’s Disease
• Form of dementia characterized by progressive,
irreversible deterioration of general intellectual
functioning
• Begins with memory loss, initially subtle until
progresses to being more noticeable; course
includes deteriorating cognition and judgment
with eventual physical decline and total inability
to perform ADL
Risk factors
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older age
female
family history
Exact cause is unknown; theories include
loss of transmitter stimulation, genetic
defects, viral and autoimmune cases
Warning signs include
• Memory loss affecting ability to function in
job
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Difficulty with familiar tasks
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Problems with language, abstract
thinking
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Disorientation, changes in mood and
personality
Types and Changes in brain
• Familial (follows inheritance pattern) and
sporadic
• Early-onset (<65)
• Older-onset (>65)
• Progressive brain atrophy
‫فیزیو پاتولوژی‬
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‫آتروفی قشر مغز بطور شدید و فراگیر بویژه در لب های گیجگاهی –‬
‫پیشانی و آهیانه‪.‬‬
‫بزرگ شدن بطن های طرفی و بطن سوم مغز‬
‫باریک شدن شکنج های قشر مخ و گشاد شدن شیار های آن‬
‫کاهش سلول های عصبی‪ -‬و کم شدن اندازه و تغییر شکل نورون ها ی‬
‫باقی مانده‬
‫پالک های پیری برون سلولی‬
‫کالفه های نورو فیبریلی درون سلولی‬
‫رسوبات آمیلوئید عروقی‬
‫• پالک های پیری بیشتر در قشر مخ‪ -‬هیپوکامپ و‬
‫آمیگدال ها پدید می آیند غالبا از یک نوع پپتید بنام‬
‫آمیلوئید بتا پروتئین ( ‪ ) A  P‬تشکیل شده اند‪ .‬ژن‬
‫مسئول سنتز پیش ساز این پروتئین در کروموزوم ‪21‬‬
‫قرار دارد‪ .‬این پالک ها افزون بر ماده فوق دارای‬
‫اجزای دیگر مانند رسوبات آلومینیوم و سلول های‬
‫نوروگلی تغییر شکل یافته هستند که احتماال در تخریب‬
‫جسم سلولی و زوائد سیتو‪.‬پالسمی نورون ها نقش‬
‫دارند‪.‬‬
Manifestations : Stage I
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Appears healthy and alert
Cognitive deficits are undetected
Subtle memory lapses, personality changes
Seems restless, forgetful, uncoordinated
Stage II
• Memory deficits more apparent
• Less able to behave spontaneously
• Wandering behavior, deterioration in orientation
to time and place
• Changes in sleeping patterns, agitation, stress
• Trouble with simple decisions
• Sundowning: increased agitation, wandering,
disorientation in afternoon and evening hours
• Echolalia, scanning speech, total aphasia at times,
apraxia, astereognosis, inability to write
• Becomes frustrated and depressed
Stage III
• Increasing dependence with inability to
communicate, loss of continence
• Progressive loss of cognitive abilities, falls,
delusion, paranoid reactions
• Average life expectancy is 7 years from
diagnosis to death, often from pneumonia,
secondary to aspiration
Collaborative Care
• No cure
• Supportive care for client and family
Diagnostic Tests
• Diagnosis by ruling out other conditions including
depression, hypothyroidism, infection, stroke
• EEG shows slow pattern in later stages of disease
• MRI and CT scan: shrinkage of hippocampus
• Positron emission tomography (PET):visualizes
brain activity and interactions
• Folstein Mini-Mental Status: instrument reflecting
loss of memory and cognitive skills
Medications
Cholinesterase inhibitors used to treat mild to
moderate dementia
• Tacrine hydrochloride (Cognex)
• Donepezil hydrochloride (Aricept)
• Rivastigmine (Exelon)
• Medications to treat depressions
• Tranquilizers for severe agitation
• Thioridazine (Mellaril)
• Haloperidol (Haldol)
• Antioxidants: vitamin E, anti-inflammatory
agents, estrogen replacement therapy in women
The mechanism of action of acetylcholinesterase
Cholinergic nerve transmission is terminated by the enzyme acetylcholinesterase (AchE). AchE is found
both on the post-synaptic membrane of cholinergic synapses and in other tissues eg red blood cells.
Acetylcholine (Ach) binds to AchE and is hydrolysed to acetate and choline. This inactivates the Ach and
the nerve impulse is halted. AchE inhibitors (eg rivastigmine) prevent the hydrolysis of Ach, which
increases the concentration of Ach in the synaptic cleft; AchE inhibitors are widely used in the treatment
of Alzheimer’s disease
• Rivastigmine
The scan below is a slice through the human brain and you should imagine that you are
viewing it as if looking up from the patient's feet. Therefore, the patient's left is to the right
of the screen. The shape of the ventricles is quite distinctive and they are shown outlined in
green and orange. The presence of the third ventricle in the midline is one of the first things
to look for. If the third ventricle is either not visible, or shows signs of shift away from the
midline, this suggests that there is an abnormality. The basal cisterns is the fluid filled space
around the back of the midbrain outlined here in purple. Blood clots, or swelling of the brain
may cause this to become narrowed, or not visible altogether. Note in this scan, that the
frontal horns of the lateral ventricles are symmetrical, with the septum between them in the
midline.
Acute Subdural Haematoma
This CT scan shows a right sided acute haematoma, as well as an associated cerebral
contusion (bruising). The true midline has been outlined by yellow dots and you can see that
the frontal horns of the lateral ventricles have been pushed over to the left. In addition, the
third ventricle is now not visible and it is also extremely difficult to make out the basal
cisterns. This scan demonstrates four of the features which are included on the Early
Outcome Form, namely midline shift greater than 5mm, intracranial haematoma - non
evacuated, cortical contusion greater than 1cm in diameter and obliteration of the third
ventricle. This haematoma requires surgical evacuation, otherwise deterioration of the
patient's condition is inevitable.
Acute Subdural Haematoma
The left lateral ventricle has been compressed and the midline is deviating to the right. The
right lateral ventricle is actually slightly larger than normal and this is because the increased
pressure is preventing escape of the cerebrospinal fluid from that ventricle. Dilatation of the
contralateral ventricle like this indicates that there is very significant pressure on the brain.
This scan would be classified as "Intracranial haematoma”.
Acute Extradural Haematoma
You will note that this haematoma has a concave shape, a bit like the human lens
and this is because it is occurring between the bone and the dura and is not
actually lying on the surface of the brain itself. The points of attachment of the
dura limit the extension of this haematoma anteriorly and posteriorly. You can see
that there is shift of the midline. Look at the frontal horns in their relation to the
falx cerebri (falx cerebri is outlined on the normal scan
Diffuse Axonal Injury
The presence of petechial haemorrhages is usually an indication of a very severe primary
brain injury. Petechial haemorrhages tend to occur at the interface of grey and white matter.
It can also occur in the dorsolateral quadrant of the midbrain at the middle orange arrow, as
well as elsewhere within the brain substance. Note on this scan, that the lateral ventricles
and the third ventricle are visible and there is no midline shift. It is often a characteristic of
diffuse axonal injury, in which there are numerous petechial haemorrhages that there is no
evidence of brain swelling, or midline shift. This scan would be classified as showing one,
or more, petechial haemorrhages within the brain.
Cerebral Contusion:
Cortical contusion >1cm in diameter
This is a scan of a patient who has sustained a severe head injury. There is extensive bruising of the right
side of the brain, showing up as a large, diffuse grey area. You can also see that there are patches of white
within the grey area. This represents bleeding. The grey area represents swelling (oedema). The area of
the cortical contusion is outlined in purple. You will normally find a centimetre scale at the right hand
side of a CT scan. This scan would be classified on the Early Outcome Form as "Cortical contusion greater than 1cm in diameter.
Complementary Therapy
• Massage, herbs, ginko biloba, Coenzyme
Q10
• Art therapy, music, dance
‫درخت معبد‬
Nursing Care &Health Promotion
• Intensive, supportive nursing interventions
directed at physical and psychosocial
responses to illness
• Maintain functional abilities
• Maintain safety of client and caregiver
Nursing Diagnoses
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Impaired Memory
Include written or verbal reminders
Use cues to deal with memory loss
Chronic Confusion
Anxiety
Hopelessness
Caregiver Role Strain
Home Care
• Education regarding disease, anticipation of
needs, use of memory cues, support groups
and peer counseling
• Refer to home health agencies, family
support, group support
Client with Multiple Sclerosis
• Description
• Chronic demyelinating disease of CNS associated with
abnormal immune response to environmental factor
• Initial onset followed by total remission making diagnosis
difficult
• Most persons have disease with periods of exacerbations
and remissions
• Progression of disease with increasing loss of function
• Incidence is highest in young adults (20 – 40); onset
between 20 – 50
• Affects females more than males
• More common in temperate climates
• Occurs mainly in Caucasians
Pathophysiology
• Autoimmune response to prior viral infection
• Inflammation destroys myelin leading to axon dysfunction
• Myelin sheaths of white matter of spinal cord, brain, optic
nerve destroyed in patches called plaques
• Demyelination slows and distorts nerve conduction resulting in
absence of impulse transmission
• Neurons in spinal cord, brain stem, cerebrum, cerebellum, and
optic nerve affected
• Recurrent demyelination and plaque formation result in
scarring of glia and degeneration of axons
• Disease follows different courses, most common is the
relapsing-remitting type
• Stressors trigger MS: febrile states, pregnancy, physical
exertion and fatigue; and these also can trigger relapses
Manifestations
• Fatigue
• Optic nerve involvement: blurred vision, haziness
• Brain stem involvement: nystagmus, dysarthria
(scanning speech), cognitive dysfunctions, vertigo,
deafness
• Weakness, numbness in leg(s), spastic paresis,
bladder and bowel dysfunction
• Cerebellar: nystagmus, ataxia, hyptonia
• Blindness
Collaborative Care
Focus is on retaining optimum functioning,
limiting disability
Diagnostic Tests
• Neurological exam, careful history
• Lumbar puncture with CSF analysis: increased
number of T lymphocytes; elevated level of
immunoglobulin G (IgG)
• Cerebral, spinal optic nerve MRI: shows multifocal
lesions
• CT scan of brain: changes
• PET: measures brain activity
• Evoked response testing of visual, auditory,
somatosensory impulses show delayed conduction
Medications
• ACTH
• Glucocorticosteroids
• Immunosuppressants: azathioprine (Imuran),
cyclophosphamide (Cytoxan)
• Cychophosphamide
• Antispasmodics to treat muscle spasms
• Medications to deal with bladder problems:
anticholinergics or cholinergics depending on problem
experienced by client
Rehabilitation
• Physical therapy to maintain abilities and
deal with spasticity
Nursing Care
• Education and support of client dealing with
chronic disease with unpredictable course
Health Promotion
• Client needs to develop strategies to deal
with fatigue, exacerbations
• Prevention of respiratory and urinary tract
infections
Nursing Diagnoses
• Fatigue
• Self care deficits
Home Care
• Education
• Referral to support group and resources
• Referral to home health agencies when
condition requires
Client with Parkinson’s Disease
Progressive, degenerative
neurological disease
• characterized by tremor at rest, muscle
rigidity and akinesia (poor movement);
cause unknown
• Affects older adults mostly, mean age 60
with males more often than females
• Parkinson-like syndrome can occur with
some medications, encephalitis, toxins;
these are usually reversible
Pathophysiology
• Neurons in cerebral cortex atrophy and dopamine
receptors in basal ganglia decrease
• Decrease in dopamine, which is neurotransmitter
involved with motor function
• Disturbance between balance of dopamine and
acetylcholine
• Balance needed for smooth coordinated movement
Manifestations
Tremor at rest with pill rolling motion of thumb and
fingers
• Lessens with purposeful movement
• Worsens with stress and anxiety
• Progressive impairment affecting ability to write
and eat
Rigidity
• Involuntary contraction of skeletal muscles
• Cogwheel rigidity: jerky motion
Manifestations
Akinesia
• Slowed or delayed movement that affects
chewing, speaking, eating
• May freeze: loss of voluntary movement
• Bradykinesia: slowed movement
Abnormal posture
• Involuntary flexion of head and shoulders, stooped
leaning forward position
• Equilibrium problems causing falls, and short,
accelerated steps
Manifestations
Autonomic nervous system
• Constipation and urinary hesitation or frequency
• Orthostatic hypotension, dizziness with position
change
• Eczema, seborrhea
Depression and dementia; confusion, disorientation,
memory loss, slowed thinking
Inability to change position while sleeping, sleep
disturbance
Complications
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Oculogyric crisis (fixed lateral and upward gaze)
Impaired communication
Falls
Infection related to immobility and pneumonia
Malnutrition related to dysphagia
Skin breakdown
Depression and isolation
Prognosis
• Slow progressive degeneration
• Eventual debilitation
Diagnostic Tests: No specific test
for disease
• Drug screens to determine medications or
toxins causing parkinsonism
• EEG: slowed and disorganized pattern
Medications
• Initially selegiline (Carbex), amantadine
(Symmetrel), anticholinergics
• Combination carbidopa-levodopa (Sinemet)
• Bromocriptine (Parlodel) pergolide
(Permax) inhibit dopamine breakdown
• Medications may lose their efficacy;
response to drugs fluctuates: “on-off” effect
Treatments
Electrical stimulation for tremor suppression
Surgery has sometimes been done
• Pallidotomy: destruction of involved tissue
• Stereotaxic thalamotomy: destroys specific
tissue involved in tremor
• Autologous adenal medullary transplant
Rehabilitation
• Physical therapy
• Occupational therapy
• Speech therapy
Nursing Care
• Education and support to client and family
• Maintain functioning
• Referral to home care, community resources
Health Promotion
• Fall, malnutrition, aspiration prevention
Nursing Diagnoses
• Impaired Physical Mobility
• Impaired Verbal Communication
• Impaired Nutrition: Less than body
requirements
• Disturbed Sleep Patterns
Home Care
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Medication education
Adaptation of home environment
Gait training and exercises
Nutritional teaching
Client with Huntington’s Disease
(chorea)
Progressive, degenerative
inherited neurologic disease
• characterized by increasing dementia and
chorea (rapid, jerky involuntary
movements)
• Cause unknown
• No cure
• Usually asymptomatic until age of 30 – 40
Pathophysiology
• involves destruction of cells in basal ganglia
and other brain areas, decrease in
acetylcholine
Manifestations
• Abnormal movement and progressive dementia
• Early signs are personality change with severe
depression, memory loss; mood swings, signs of
dementia
• Increasing restlessness, worsened by
environmental stimuli and emotional stress; arms
and face and entire body develops choreiform
movements, lurching gait; difficulty swallowing,
chewing, speaking
• Slow progressive debilitation and total
dependence
• Death usually results from aspiration pneumonia
or another infectious process
Collaborative Care
• almost always requires long-term care
Diagnostic Tests
• genetic testing of blood
Medications
• Antipsychotic (phenothiazines and
butyrophenones) to restore
neurotransmitters
• Antidepressants
Nursing Care
• Very challenging: physiological,
psychosocial and ethical problems
• Genetic counseling
Nursing Diagnoses
• Risk for Aspiration
• Imbalanced Nutrition: Less than body
requirements
• Impaired Skin Integrity
• Impaired Verbal Communication
Home Care
• Referral to agencies to assist client and
family, support group and organization
Client with Amyotrophic Lateral
Sclerosis (ALS)
Description
• Progressive, degenerative neurologic disease
characterized by weakness and wasting of muscles
without sensory or cognitive changes
• Several types of disease including a familial type;
onset is usually between age of 40 – 60; higher
incidence in males at earlier ages but equally post
menopause
• Physiologic problems involve swallowing,
managing secretions, communication, respiratory
muscle dysfunction
• Death usually occurs in 2 – 5 years due to
respiratory failure
Pathophysiology
• Degeneration and demyelination of motor
neurons in anterior horn of spinal cord,
brain stem and cerebral cortex
• Involves upper and lower motor neurons
• Reinnervation occurs in the early course of
disease, but fails as disease progresses
Manifestations
• Initial: spastic, weak muscles with increased DTRs
(UMN involvement); muscle flaccidity, paresis,
paralysis, atrophy (LMN involvement); clients note
muscle weakness and fasciculations (twitching of
involved muscles); muscles weaken, atrophy; client
complains of progressive fatigue; usually involves hands,
shoulders, upper arms, and then legs
• Atrophy of tongue and facial muscles result in dysphagia
and dysarthria; emotional lability and loss of control
occur
• 50% of clients die within 2 – 5 years of diagnosis, often
from respiratory failure or aspiration pneumonia
Collaborative Care
• Evaluation to make the diagnosis
• Referrals for home health support;
• Client needs to make decisions regarding
gastrostomy tube, ventilator support
Diagnostic Test
• Testing rules out other conditions that may mimic
early ALS such as hyperthyroidism, compression
of spinal cord, infections, neoplasms
• EMG to differentiate neuropathy from myopathy
• Muscle biopsy shows atrophy and loss of muscle
fiber
• Serum creatine kinase if elevated (non-specific)
• Pulmonary function tests: to determine degree of
respiratory involvement
Medications
• Rilutek (Riluzole) antiglutamate
• Prescribed to slow muscle degeneration
• Requires monitoring of liver function, blood
count, chemistries, alkaline phosphatase
Nursing Care
• Help client and family deal with current
health problems
• Plan for future needs including inability to
communicate
Nursing Diagnoses
• Risk for Disuse Syndrome
• Ineffective Breathing Pattern: may require
mechanical ventilation and tracheostomy
Home Care
• Education regarding disease, community
resources for health care assistance and
dealing with disabilities
Client with Creutzfeldt-Jakob
disease
(CJD, spongiform encephalopathy)
Description
• Rapid progressive degenerative neurologic disease
causing brain degeneration without inflammation
• Transmissible and progressively fatal
• Caused by prion protein: transmission of prion is
through direct contamination with infected neural tissue
• Rare in USA affecting persons 55 - 74
• Variant form of CJD is “mad cow disease”: believed
transmitted by consumption of beef contaminated with
bovine form of disease; none identified in USA as of
yet
• Pathophysiology: spongiform degeneration of gray
matter of brain
Manifestations
• Onset: memory changes, exaggerated startle
reflex, sleep disturbances
• Rapid deterioration in motor, sensory,
language function
• Confusion progresses to dementia
• Terminal states: clients are comatose with
decorticate and decerebrate posturing
Diagnostic Tests
• Clinical pictures, suggestive changes on
EEG and CT scan
• Similar to Alzheimers in early stages
• Final diagnosis made on postmortem exam
Nursing Care
• Use of standard precautions with blood and
body fluids
• Support and assistance to client and family
Client with Myasthenia gravis
(MG)
Description
• Chronic neuromuscular disorder
characterized by fatigue and severe
weakness of skeletal muscles
• Occurs with remissions and exacerbations
• Believed to be autoimmune in origin
• Occurs more frequently in females, with
onset between ages 20 – 30
Pathophysiology
• Antibodies destroy or block neuromuscular
junction receptor sites, resulting in decreased
number of acetylcholine receptors
• Causes decrease in muscle’s ability to contract,
despite sufficient acetylcholine
• Majority of clients have hyperplasia of thymus
gland which is usually inactive after puberty;
believed that thymus is source of autoantigen
causing MG
• Associated in some clients with other autoimmune
conditions
Manifestations
Seen in the muscles that are affected
• Ptosis (drooping of eyelids), diplopia (double
vision)
• Weakness in mouth muscles resulting in dysarthria
and dysplagia
• Weak voice, smile appears as snarl
• Head juts forward
Muscles are weak but DTRs are normal
Weakness and fatigue exacerbated by stress, fever,
overexertion, exposure to heat; improved with rest
Complications
Pneumonia
Myasthenic Crisis
• Sudden exacerbation of motor weakness
putting client at risk for respiratory failure
and aspiration
• Manifestations: tachycardia, tachypnea,
respiratory distress, dysphasia
Complications
Cholinergic Crisis
• Occurs with overdosage of medications
(anticholinesterase drugs) used to treat MG
• Develops GI symptoms, severe muscle weakness,
vertigo and respiratory distress
Both crises often require ventilation assistance
Differentiation is by administration of (edrophonium
chloride) Tensilon, which will improve the muscle
weakness in myasthenic crisis and be ineffective
with cholinergic crisis
Diagnostic Tests
• Physical examination and history
• Tensilon Test: edrophonium chloride (Tensilon)
administered and client with myasthenia will show
significant improvement lasting 5 minutes
• EMG: reduced action potential
• Antiacetylcholine receptor antibody serum levels:
increased in 80% MG clients; used to follow
course of treatment
• Serum assay of circulating acetylcholine receptor
antibodies: if increased is diagnostic of MG
Medications
• Anticholinesterase medications, which act at
neuromuscular junction, allowing acetylcholine to
concentrate at receptor sites and promote muscle
contraction; most commonly used medication is
pyridostigmine (Mestinon)
• Immunsuppression medications including
glucocorticoids
• Cyclosporineor azathioprine (Imuran)
Surgery
• Thymectomy is recommended in clients
<60
• Remission occurs in 40 % of clients, but
may takes several years to occur
Plasmapheresis
• Used to remove antibodies
• Often done before planned surgery, or when
respiratory involvement has occurred
Nursing Care
• Teaching interventions to deal with fatigue
• Importance of following medication therapy
Nursing Diagnoses
• Ineffective Airway Clearance
• Impaired Swallowing: plan to take
medication to assist with chewing activity
Home Care
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Avoid fatigue and stress
Plan for future with treatment options
Keep medications available
Carry medical identification
Referral to support group, community
resources
Client with Guillain-Barre
Syndrome
Description
• Acute inflammatory demyelinating disorder of peripheral
nervous system characterized by acute onset of motor
paralysis (usually ascending)
• Cause is unknown but precipitating events include GI or
respiratory infection prior, surgery, or viral
immunizations
• 80 – 90% of clients have spontaneous recovery with little
or no disabilities
• 4 – 6% mortality rate, and up to 10% have permanent
disabling weakness
• Characterized by progressive ascending flaccid paralysis
of extremities with paresthesia and numbness
• 20 % require mechanical ventilation due to respiratory
involvement
Pathophysiology
• Destruction of myelin sheath covering
peripheral nerves as result of immunologic
response
• Demyelinization causes sudden muscle
weakness and loss of reflex response
Manifestations
• Most clients have symmetric weakness beginning in
lower extremities
• Ascends body to include upper extremities, torso, and
cranial nerves
• Sensory involvement causes severe pain, paresthesia and
numbness
• Client cannot close eyes
• Paralysis of intercostals and diaphragmatic muscle can
result in respiratory failure
• Autonomic nervous system involvement: blood pressure
fluctuations, cardiac dysrhythmias, paralytic illness,
SIADH, urinary retention
• Weakness usually plateaus or starts to improve in the
fourth week with slow return of muscle strength
Collaborative Care
• Ensuring adequate respiration and
oxygenation
• Preventing complications due to immobility
Diagnostic Tests
• diagnosis made thorough history and
clinical examination; there is no specific
test
• CSF analysis: increased protein
• EMG: decrease nerve conduction
• Pulmonary function test reflect degree of
respiratory involvement
Medications
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supportive and prophylactic care
Antibiotics
Morphine for pain control
Anticoagulation to prevent thromboembolic
complications
• Vasopressors as needed
Surgery
• may need tracheostomy, if prolonged
ventilator support
Plasmapheresis
• may be helpful, if used early in the course
of disease
Dietary Management
• usually requires enteral feeding or total
parenteral nutrition
Physical and Occupational
Therapy
• usually require long-term rehabilitation to
regain maximum muscle strength
Nursing Care
• involves acute neurological and critical care
nursing and rehabilitation
Nursing Diagnoses
• Acute Pain
• Risk for Impaired Skin Integrity
• Impaired Communication
Home Care
• Clients will usually require hospitalization,
rehabilitation, and eventually discharge to
home
• Client and family will need support; support
groups
Trigeminal neuralgia
(tic douloureux)
Description
• Chronic disease of trigeminal nerve (cranial
nerve V) causing severe facial pain
• The maxillary and mandibular divisions of
nerve are effected
• Occurs more often in middle and older
adults, females more than males
• Cause is unknown
Manifestations
• Severe facial pain occurring for brief seconds to minutes
hundreds of times a day, several times a year
• Usually occurs unilaterally in area of mouth and rises
toward ear and eye
• Wincing or grimacing in response to the pain
• Trigger areas on the face may initiate the pain
• Sensory contact or eating, swallowing, talking may set
off the pain
• Often there is spontaneous remission after years, and
then condition recurs with dull ache in between pain
episodes
Diagnosis
• by physical assessment
Medications
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Anticonvulsants
carbamazepine (Tegretol)
phenytoin (Dilantin)
gabapentin (Neurotin)
Surgery
• Intractable pain may be treated by severing
the nerve root: rhizotomy
• Client may have lost facial sensation and
have loss of corneal reflex
Nursing Care
• Teaching client self-management of pain
• Maintaining nutrition
• Preventing injury
Bell’s Palsy
Description
• Disorder of seventh cranial nerve and
causes unilateral facial paralysis
• Occurs between age of 20 – 60 equally in
males and females
• Cause unknown, but thought to be related to
herpes virus
Manifestations
• Numbness, stiffness noticed first
• Later face appears asymmetric: side of face
droops; unable to close eye, wrinkle
forehead or pucker lips on one side
• Lower facial muscles are pulled to one side;
appears as if a stroke
Prognosis
• Majority of person recover fully in few
weeks to months
• Some persons have residual paralysis
Diagnosis
• based on physical examination
Collaborative Care
• Corticosteroids are prescribed in some cases
but use has been questioned
• Treatment is supportive
Nursing Care
• Teaching client self-care: prevent injury and
maintain nutrition
• Use of artificial tears, wearing eye patch or
taping eye shut at night; wearing sunglasses
• Soft diet that can be chewed easily, small
frequent meals
Neurologic Diseases that result
from viral infections or
neurotoxins
Postpoliomyelitis Syndrome
• Complication of previous poliomyelitis virus (epidemic
occurred in USA during 1940’s and 1950’s); persons
who recovered are re-experiencing manifestation of acute
illness in their advanced age
• Pathophysiology: Process is unknown
• Manifestations: Fatigue, muscle and joint weakness, loss
of muscle mass, respiratory difficulties, and pain
• Diagnosis: By history and physical examination
• Treatment: Involves physical therapy and pulmonary
rehabilitation
• Nursing Care: Involves emotional support and
interventions to deal with dysfunction; ADL, safety are
including in interventions
Rabies
Rhabovirus infection of CNS transmitted by
infected saliva that enters the body through
bite or open wound
• Critical illness almost always fatal
• Source often is bite of infected domestic or
wild animal
• Incubation is 10 days to years
Rabies
Manifestations occur in stages
• Prodromal: wound is painful, various paresthesias,
general signs of infection; increased sensitivity to
light, sound, and skin temperature changes
• Excitement stage: periods of excitement and quiet;
develops laryngospasm and is afraid to drink
(hydrophobia), convulsions, muscle spasms and
death usually due to respiratory failure
Rabies
Collaborative Care
• Animal that bit person is held under
observation for 7 – 10 days to detect rabies
• Sick animal are killed and their brains are
tests for presence of rabies virus
• Blood of client may be tested for rabies
antibodies
Rabies
Post-exposure treatment
• Rabies immune globulin (RIG) is administered for
passive immunization
• Client often has local and mild systemic reaction;
treatment is over 30 days
Treatment of client with rabies: involves intensive
care treatment
Health Promotion
• Vaccination of pets
• Avoid wild animals, especially those appearing ill
• Follow up care for any bites
Tetanus (lockjaw)
Disorder of nervous system caused by neurotoxin from
Clostridium tetani, anaerobic bacillus present in the soil
• Contract disease from open wound contaminated with
dirt, debris
• Has high mortality rate
Incubation is usually 8 – 12 days
Manifestations
• Stiffness of jaw and neck and dysphagia
• Spasms of jaw and facial muscles
• Develops generalized seizures and painful body muscle
spasms
• Death occurs from respiratory and cardiac complications
Tetanus (lockjaw)
Diagnosis is made on clinical manifestations
Clients with disease are treated in intensive care with
antibiotics, chlorpromazine (Thorazine) and
diazepam (Valium ) for muscles spasms
Health Promotion
• Active immunization with boosters given at time
of exposure
• Passive immunization is given to persons who are
not adequately immunized
Botulism
Food poisoning caused by ingestion of food
contaminated with toxin from Clostridium
botulinum, anaerobic bacteria found in soil
• Contracted by eating contaminated foods usually
improperly canned or cooked
• Untreated death rate is high
Pathophysiology: Bacteria produce a toxin, which
blocks release of acetylcholine from nerve endings
causing respiratory failure by paralysis of muscles
Botulism
Manifestations
• Visual disturbances
• Gastrointestinal symptoms
• Paralysis of all muscle groups
• Effecting respiration
Diagnosis
• Based on clinical picture
• Verified by laboratory analysis of client’s
serum and stool
• Testing the suspected food
Botulism
Treatment
• Administration of antitoxin
• Supportive treatment including mechanical
ventilation and systemic support in intensive care
unit
Health Promotion
• Teaching clients to process foods properly when
home canning
• Boiling foods for 10 minutes which destroys the
toxin
• Not eating spoiled foods