NERVOUS SYSTEM
DISORDERS
And Associated Nursing Care
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Conciousness
Increased Intracranial Pressure (ICP)
Head Injury
Degenerative and Autoimmune
Nervous System Disorders
Consciousness
Consciousness
Is a condition in which the person is aware of self
and the environment and is able to respond
appropriately to stimuli (McLeaod, 2004).
Two components:
1.
Arousal: (or awakeness) reflects activity of
RAS, thalmus and upper brain stem.
2.
Content: cognitive mental functions reflects
cerebral cortex activity (thought processes,
memory, perception, problem solving, &
emotion)
Altered Consciousness

Definition: condition of being less
responsive to and aware of environmental
stimuli (Smeltzer & Bare, 2004).
Unconsciousness

Definition: physiological state in which the
client is unresponsive to sensory stimuli and
lacks awareness of self and the environment
(Hickey, 2003)
Unconsciousness


Can be brief, lasting a few second to a few
hours or longer.
To produce unconsciousness a disorder
must:
1.Disrupt the RAS which extends up to the
thalmus.
2.Significantly disrupt the function of both
cerebral hemispheres
3.Metabolically depress overall brain
function
Coma
Coma is a prolonged state of unconsciousness in which the
client is unaware of self or the environment for
sustained periods of time from hours to months.
(Hickey, 2003)
Because of:
-disorders that affect BOTH cerebral hemispheres
- disorders that affect any part of the RAS
- direct compression on parts responsible for
conciousness ie: hemorrhage, tumors
- metabolic disorders (hypoglycemia, hypoxia)
- toxins
** Duration of coma is associated with mortality &
outcome****
Major Causes and manifestations
of Altered Consciousness
Reduction in level of consciousness
may be caused by extracranial or
intracranial causes.
Intracranial Causes
Supratentorial lesions (above the cerebellum)
 A lesion must affect the cerebral hemispheres directly
and widely to cause diffuse bilateral hemispheric
dysfunction and subsequent coma (Hickey, 2003)
Infratentorial Disorders
Involve cerebellum and brain stem


Cause sudden LOC
Usually produce:
Early coma
- Abnormal respiratory patterns
- Oculorvestibulary abnormalities
- Pupillary changes
-
Extracranial Causes:
Metabolic Disorders or
Toxins
Usually produces confusion first
 Findings are symmetrical or bilateral
 Physical symptoms include tremors,
asterexis,, myoclonus & seizures.
 Pupillary response is normal unless
related to drug overdose.

Examples
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Hypoxemia
Hypercapnia/acidosis
Hypotension
Blood sugar alterations (DKA, hypoglycemic
coma)
Liver dysfunction
Fluid/electrolyte disorders
Multiorgan dysfunction
Drug effects
Psychogenic Coma


Although rare, pychogenic disorders
such as hysteria, catatonia, and severe
depression can cause alterations in
LOC
Despite outward appearances the
person is physiologically awake.
Assessment

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
Glasgow Coma Scale
Mini-mental
Diagnostic Tests
– CT and MRI
– Lumbar Puncture
– EEG
– Laboratory Tests

Tests for Abnormal Reflexes
– Oculocephalic Reflex Response
– Oculovestibular Reflex Response
The Glasgow Coma Scale
The Glasgow Coma Scale (GCS) is a
universally used neurological
assessment tool to assess degree of
consciousness impairment. CGS
measures eye, verbal, and motor
response. It is an excellent scale to
measure arousal. It is less helpful
related to content measurement.
Know the difference b/t
content & arousal
GLASGOW COMA SCALE SCORE (GCS)
Eyes
Motor
1 Closed at all times
2 Opens to pain
3 Opens to voice command
4 Open spontaneously
1 No response
2 Extension (decerebrate)
3 Flexion posturing (decorticate)
4 Flexion withdrawal
5 Localizes painful stimulus
6 Obeys commands
Verbal 1 No response
2 Incomprehensible sounds
3 Inappropriate words
4 Disoriented and converses
5 Oriented and converses
A score of 10 or
less indicates a
need for emergency
attention
15 (top score)
A score less than 7
is interpreted as
coma
*
Level
of
consciousness
is
the
*
single most important
indicator of neurological
function and change*
CONTENT
Besides orientation to time, place and person the following
cognitive abilities should also be assessed:
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Attention and vigilance
Memory – short, intermediate, long term
Language – understanding of spoken and written word
General fund of information
Construction ability
Sequencing activities
Problem solving
Abstraction
Insight and judgment
The Mini Mental Status Exam is an example of a test for
cognitive function. (Used on GARU).
Diagnostic Tests
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CT or MRI: data on structural causes such
as tumor or hemmorhage.
-Metabolic – will be unremarkable
LP: infection or bleeding (cloudy or
bloody)
EEG: structural or metabolic, seizure
activity
Lab tests: LFTs, kidney function, glucose
levels, toxicology, ABGS
Diagnostic Tests for
Abnormal Reflexes

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Oculocephalic reflex
response – abnormal
if eyes remain in fixed
position when head
turned
Oculovestibular reflex
response – absence
of eye movement
when water instilled
in ear = brain death
Medical Management: goal is to
preserve brain function & prevent
further damage
– Determine Level of Involvement
– Reverse Common Causes of Coma
– Prevent Complications
Nursing Diagnoses
– Altered Tissue Perfusion
– Risk for Suffocation/Aspiration
– Altered Oral Mucous Membranes
– Risk for Impaired Skin Integrity
– Risk for Contractures
– Altered Nutrition: Less than Body
Requirements
– Fluid volume deficit
– Risk for Injury
– Altered family processes
Nursing management
–
–
–
–
–
–
Maintaining the airway
Protecting the patient
Fluid balance
Mouth care, skin and joint integrity
Corneal integrity
Thermoregulation
Nursing Assessment: Brain
Injury
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ABCDs
Maintaining airway
History if possible
Determine LOC, ability to respond to
verbal commands, reactions to tactile
stimuli, status of reflexes.
Glasgow Coma scale
Fluid and electrolyte balance
Monitoring/managing potential
complications
Increased Intracranial Pressure
Intracranial pressure

ICP is the pressure exerted by the
brain tissue, CSF, and cerebral blood
within the intracranial vault.

There is a delicate balance that exists between the
volume of the intracranial contents within this rigid
compartment (80% brain tissue, 10% blood, 10%CSF)

The normal ICP is 0-15 mmHg (15 is the upper limit).

Pressures over 20mm Hg represent severely increased
ICP, which seriously impairs cerebral perfusion.
Important Parameters
Affecting ICP

Cerebral perfusion pressure (CPP)

Cerebral blood volume (CBV)

Cerebral blood flow (CBF)
 Cerebral perfusion pressure (CPP) is the amount of
blood flow (pressure gradient ) from the systemic
circulation that is required to provide adequate oxygen
and glucose for brain metabolism.
 It is the difference between mean arterial pressure
(MAP) and ICP.
CPP = MAP – ICP
 Mean arterial pressure (MAP) represents the
average pressure during the cardiac cycle. Calculate by:
systolic pressure + 2 X diastolic
divided by 3.
Example BP 70/34. MAP= 46
 Cerebral blood volume (CBV) is dependent
on cerebral blood flow (CBF).
 If CBF increases, so does CBV. CBF
depends upon cerebral perfusion pressure
(CPP).
When MAP & ICP are equal there is no CPP
& blood flow stops!
)
Maintenance of ICP
Autoregulation is the compensatory changes in the
diameter of the intracranial blood vessels designed
to maintain a constant blood flow during changes
in systemic arterial pressure (cerebral perfusion
pressure).
Critical point may be reached when either:
1. the ICP is greater than 30 to 35 mm Hg
2. systemic blood pressure is less than 60
mm Hg
3. Systemic BP greater than 160 mm Hg.
Autoregulation is lost with increasing ICP.
After this the CBF will vary passively
with systemic blood pressure.
The Munro-Kellie Hypothesis
The Munro-Kellie Hypothesis states that a
change in volume of any of the normal
components (brain, cerebral blood volume and
cerebrospinal fluid) of the intracranial vault
must be accompanied by a reciprocal change in
one or more of the other components. If this
reciprocal change is not accomplished the
result is an increase in intracranial pressure
(ICP).
How does the body compensate for changes
in ICP?
1. Compliance

Displacement of CSF into the spinal
subarachnoid space

Increased absorption of CSF

Decreased secretion of CSF
Compensatory
mechanisms cont’d
2. Reduction of blood volume in the
brain.

Venous blood may be shunted to allow
more room for expansion.
 As this ability decreases, the venous
pressure increases, & CBV and ICP rise
 This stage of compensation alters cerebral
metabolism, eventually leading to brain
tissue hypoxia and areas of ischemia.
Compensatory
mechanisms cont’d
3. Herniation
displacement of brain
tissue. Most lethal stage
of
compensation. Process
often results in death
from
brain stem compression.
Always an emergency!
Results!
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Compression
Laceration
Vascular compromise
Necrosis of structures
Blocked flow CSF
Brain compression and death
Common Causes
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Increases in tissue volume
– Space occupying lesions: brain tumor, abscess,
hemorrhage,
– Cerebral edema: infarction, interstitial edema, infection,
metab0olic disorders, toxins, electrolyte imbalances


Abscess
Increases in CSF
– hydrocephalus
– Deficient CSF absorption or overproduction of CSF
(Hogan & Hill, 2004)
Causes Cont’d

Increases in blood volume
– epidural & subdural hematoma.
– impaired blood flow to and from brain,
– CO2, O2,
– Hypertension
HYPERCAPNIA AND HYPOXIA

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Any systemic process that affects blood
levels of carbon dioxide will affect CBF,
CPP and CBV because of cerebral
vasodialation.
These conditions include respiratory
inadequacy, poor ventilation,
hyperventilation, drugs, and inadequate
amounts of oxygen.
Manifestations of
Increasing Intracranial Pressure

Any process that results in increased ICP will produce
impairment of content and arousal. Manifestations
include any alteration in level of consciousness
(restlessness, drowsiness, confusion) and a decrease in
Glasgow Coma Scale (GCS)

Clinical manifestations of increased ICP are subtle!!!
Diligent observation for changes in client’s condition.
(Porth, C., 2004)
In addition may have:
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Decreased level of
consciousness
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Behavioral changes
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Headache
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Nausea & Vomiting
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Change in speech
pattern
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Abnormal pupillary
reactions
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Changes in body
temperature
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Change in
sensorimotor status
Blurred or double
vision (diplopia)
Changes in cardiac rate
& rhythm
ataxia
Seizures
Cushing’s triad
Abnormal posturing
Nerve compression with
IICP
CUSHING’S TRIAD!
A response involving three classis signs:
 widening pulse pressure: increased systolic BP
with diastolic remaining the same or slightly
elevated.
 Bradycardia
 Slowing respirations
Cushing’s triad indicates increased
severe ICP!
Emergency Care
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ABCs
Airway maintenance, intubation with oxygenation
(PO2 > 90mmHg), mild hyperventilation – avoid
hypercapnia.
Ensure adequate fluid however avoid lowering the
blood osmolarity.
Initial neuro assessment and Glasgow Coma Scale
Etiology of the brain injury will dictate further
evaluation & treatment
Emergency Care Cont’d
osmotic diuretics (mannitol IV)
 steroids (controversial)
 vasoactive medication (100-150mmHg
systolic)
 elevate HOB (30 degrees)
 sedate as needed (barbituates IV)
 drain CSF (keep ICP < 20)
 maintain fluid status (normal serum Na &
osmolality)
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Nursing Management in Controlling ICP
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Elevate HOB (why?)
Ongoing Glasgow Coma Scale
Pulmonary management
Cardiovascular: monitor BP, CO, volume
status
Maintain head & neck in neutral alignment
(how?)
Prevent Valsalva maneuver (how?)
Nursing Management Cont’d
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Administer prescribed meds to reduce ICP:
barbituates, mannitol analgesics, narcotics
Maintain fluid balance with NaCl or RL solution
Avoid noxious stimuli (explain)
Maintain cerebral perfusion pressure >70mmHg
Maintain normal body temperature – avoid
hyperthermia
Osmotic Diuretic (Mannitol)
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Reduces cereberal edema by osmotic dehydration.
Preferred b/c it is confined to extracellular space
& does not normally cross an intact blood brain
barrier.
Carefully monitor vitals, CVP, B.P, intake &
output, catheter patency, signs of fluid overload,
eye response /acuity & electrolyte imbalance??
Why??
NOTE: If blood-brain barrier is damaged the
medication enters the brain and increases swelling!!
Types of Brain Injury
Types of Head Injury
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Scalp injury: minor injury
resulting in laceration, abrasion
& hematoma
Skull injury: may occur with
or without damage to brain.
Brain injury
Head Injuries

Closed or blunt: blunt object damages
the brain and its coverings without actually
perforating the skull or dura.
 Penetrating: when the skull and brain
are directly lacerated by an object such as a
bullet, or piece of bone.
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Coup-Contrecoup Injuries: same
blow causes injury on opposite sides
of the brain.
Skull Fractures
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Linear Skull Fracture: is a break in the
continuity of the bone, appear as thin lines
on X-ray.
Depressed Skull Fracture - The broken
piece of skull bone is pressed towards or
embedded in the brain.
Comminuted and Compound Skull
Fracture - The scalp is cut and the skull is
splintered, multiple fractures.
Basilar Skull Fracture
The skull fracture is located at the base of
the skull and may include the opening at the
base of the skull

Basilar
fractures
Some Signs of Skull
Fractures
– CSF or fluid draining from ear (“halo”
sign)
– Blood behind tympanic membrane
– Raccoon Eyes: periorbital ecchymoses
– Battles Sign: bruise over mastiod process
– Cranial nerve and inner ear damage
Battles’ sign
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Often occurs in
fractures at base of
skull (posterior cranial
fossa).
Large "black and blue
mark" looking areas
below the ear, on the
jaw and neck.
It may include damage
to the nerve for
hearing.
CSF Otorrhea: cerebral
spinal fluid may leak
out of the ear.
Raccoon Eyes
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The skull fracture
produces "black and
blue" mark looking
areas around the
eyes.
CSF Rhinorrhea:
cerebral spinal fluid
may leak into the
sinuses and out of
nose.
Otorrhea
Traumatic Brain Injury

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Traumatic brain injury (TBI) is
an insult to the brain, caused by an
external physical force, that may
produce physical, intellectual,
emotional, social and vocational
changes.
Major causes of TBI motor vehicle
accidents, falls, acts of violence, sports
& recreational injuries, blows to head,
child abuse (shaken baby syndrome).
Mechanisms of Brain
Injury
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Acceleration injury occurs
when the immobile head is
struck by a moving object.
Deformation injury: the force
results in deformation and
disruption of the impacted part,
(skull fracture)
Mechanisms Cont’d
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Deceleration injury: head is moving
and hits an immobile object (car
accident-hitting steering wheel)
Acceleration-deceleration injury:
moving object hits immobile head and
then head hits immobile object.
Associated with rotation injury where
brain is twisted in the skull (whiplash).
Injuries

Blunt
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Penetrating

Coup-Contrecoup
Types of Brain Injury
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Concussion: is a head trauma that
may or may not result in loss of
consciousness (for 5 minutes or less)
and retrograde amnesia.
Contusion: is a severe injury in which
the brain is bruised resulting in swollen
brain tissue, areas of hemorrhage,
infarction, necrosis, edema. Results in
loss of consciousness and symptoms of
shock.
Concussion
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May experience only dizziness and feel “dazed”.
Retrograde amnesia
Treatment involves observing patient for
headache, dizziness, lethargy, irritability and
anxiety.
Client should resume normal activities slowly and
the following should be watched for: difficulty in
awakening or speaking, confusion, severe
headache, vomiting or weakness on one side of
the body.
May or may not show up on CAT scan.
Blood clot can occasionally occur causing death
Months to years to heal
Contusion
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Depends on which areas of the brain
damaged – cerebral hemispheres, brain
stem (RAS)
Can cause diffuse axonal type injury
resulting in permanent or temporary
damage
If widespread injury, abnormal eye
movement and motor function,
increased intracranial pressure and
herniation - poor outcome.
May have residual damage, seizures
Contusion resulting in
necrosis

Diffuse Axonal Injury: severe
widespread injury to axons in the
cerebral hemispheres, corpus collosum
and brain stem.
Diffuse Axonal Injury
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Extensive tearing of nerve tissue throughout
the brain causing the release of chemicals,
causing additional injury.
Immediate coma, decerebrate & decorticate
posturing, and global edema
The tearing of the nerve tissue disrupts the
brain’s regular communication and chemical
processes producing temporary or permanent
widespread brain damage, coma, or death.
A person with a diffuse axonal injury could
present a variety of functional impairments
depending on where the shearing (tears)
occurred in the brain.
Intracranial
Hemorrhage
Intracranial
hematomas are
collections of blood
that develop within
the cranial vault.
Three kinds:
epidural, subdural &
intracerebral
Types of Cerebral
Hemorrhage
Epidural
Hematoma:
mostly
Meninges
Scalp
arterial
Skull
Dura matter
Arachnoid
Pia
Brain tissue
grey
white
(blood
collects b/t
the skull &
the dura
mater of the
brain)
Scalp
Skull
Dura matter
Subdural
hemorrhage
- usually
venous (blood
collects b/t the
dura & the
arachnoid
mater). May be
classified as
acute, subacute
or chronic.
Acute & Subacute Subdural
Hematoma
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Usually result from brain or blood
vessel laceration
Symptomatic within 24 to 48 hours of
injury
Symptoms include loss or variable
levels of consciousness, headache,
irritability, increasing signs of increased
ICP (increased BP, decreased pulse,
slowing respiratory rates)
Requires prompt treatment!
Intracerebral Hematoma
Bleeding directly into the brain
tissue.
Post Head Injury

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Observe for 24 hrs
Take to emergency if any of following::
– decreasing LOC (confusion, drowsy)
– loss of consciousness/inability to
wake
– vomiting
– convulsions
– bleeding or drainage from ears/nose
– weakness or loss of sensation in arm
or leg
– blurring of vision/slurring of speech
Medical Management
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Prompt recognition and treatment of
hypoxia & acid-base disorders (why?)
Control of increasing ICP resulting
from increased cerebral edema and
expanding hematoma
Surgical treatment
– Burr holes
– Craniotomy
Burr holes
Craniotomy (Pre)
Craniotomy
Craniotomy
Nursing Management
Nursing Management
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Maintaining airway
Monitoring fluid and electrolyte balance
Promoting adequate nutrition
Preventing injury
Maintaining body temperature
Maintaining skin integrity
Improving cognitive circulation
Preventing sleep pattern disturbance
Supporting family coping
Monitoring/managing potential
complications
Nursing Care after
Craniotomy
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Ineffective cerebral tissue perfusion r/t cerebral
edema
PC: Ineffective thermoregulation r/t damage to
the hypothalamus, dehydration, and infection.
Disturbed sensory perception r/t periorbital
edema, head dressing, e/t tube, & effects of
ICP
Body image disturbance r/t change in
appearance or physical disabilities.
Degenerative &
Autoimmune Neurological
Disorders
Disorders include:

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Alzheimer's Disease
Parkinson’s disease
Multiple Sclerosis (autoimmune)
Guillain-Barre Syndrome
(autoimmune)
PARKINSON’S DISEASE
Imbalance of dopamine and
acetylcholine in Parkinson's disease.
PARKINSON'S DISEASE
Cellular
degeneration of
dopamineproducing cells in
the part of the
basal ganglia
called the
substantia nigra,
results in
depletion of
neurotransmitter
Dopamine.
Often presence of
“Lewey Bodies”
Classic symptoms
CHARACTERISTICS
 Slowly progressive regardless of treatment
 "Shaky palsy" tremor/ rhythmic tremor
(1st symptom)
 Usually idiopathic
 150 per 100,000
 After age 50
 LE 25 yrs post onset
Manifestations
Tremor
 Rigidity
 Bradykesia
Other key symptoms
include:
 Flexed posture
 Loss of postural
reflexes
 Freezing

Bradykinesia
“ParkinsonGait”
Bradykinesis (slow
movement) makes
voluntary movements
difficult to execute.
Tremor
“Cog wheeling”
passive movement
of extremity may
lead to jerky
motion
“Pill rolling tremor”
Treatment - Common Drugs


*Levodopa: converted from L-dopa
to dopamine in basal ganglia (cause
further damage?)
Dopaminergics: (Sinemet)
levodopa/carbidopa (maximizes
benefit of levedopa
Drugs Cont’d

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Antiviral: (Amantadine) potentiates action
of dopamine
Dopamine Agonists: (Parlodel) activate
dopamine receptors
COMT Inhibitors: (Tolcapone) enhances
the effect of dopamine.
MAO Inhibitors: inhibits the breakdown of
dopamine within the brain.
Nursing Management
Adequate sleep/rest
 Maintaining/improving mobility
 Enhancing self-care
 Improving bowel elimination
 Improving nutrition
 Enhancing swallowing
 Education

Mobility

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
Trying side rails, a trapeze,
ropes or a handle to grip
Using satin sheets or pajamas
Changing to a firmer, lower or
higher mattress may help.
Consult physical therapists &
occupational therapists
Encourage daily ROM (keep
muscles flexible)
Use of assistive devices
Periodically lie prone.
Education

Educate re:
– Disease
– drugs & diet
– self-care (time & pacing)
– emotional response/depression
– Judgment
– Safety
Choking
 falling

Fear of Falling

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Make environment safer by taking
up scatter rugs or putting in a
nightlight
Consider the use of a walker at
night if coordinated enough
Teach to get up slowly…some
people become dizzy if they
change position too quickly.
Promote raised toilet seat… bars
Eating

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Aspiration is a huge problem!
Semi solid, pureed & thickened liquids
6 small meals
High calorie, low protein
Warming platters keep food warm
Uninterrupted
Small bites
Drugs with meals
Sit upright during & for 30 minutes
after meals
Communication

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Caregiver: don’t rush or finish
sentence
Take a breath of air before
speaking
Speak when exhaling
Slow speech … One word at a
time
Break after every 3-4 words
Practice by reading aloud
MULTIPLE
SCLEROSIS
Multiple Sclerosis
 Chronic demylinating disease that affects the
myelin sheath of neurons in the CNS
 Plaque develops on myelin causing
inflammation, edema and eventual scarring.
 Clinical course is unpredictable combinations
of sensory, motor, & coordinative disfunctions
followed by exaserbations followed by partial or
complete remission.
Manifestations





Clinical manifestations vary according to area
of demyelination and affected body system.
About 20% have a mild form with only a few
mild attacks that do not result in progression
80% of clients lead active & productive lives
Most clients are able to live a normal life
span
Cause of death is usually infection.
Manifestations






Weakness/fatigue or tingling sensations of
one or more extremities (involvement of
cerebrum or spinal cord)
Diplopia
Incoordination (cerebellar involvement)
Bowel/bladder dysfunction (spinal cord)
Constipation
Depression and/or euphoria, emotional
instability (disease or reaction?)
Manifestations Cont’d




Impaired mobility
Tremor
Pain
MS disease involvement in brain stem will
result in
– Charcot’s triad:
Nystagmus (constant involuntary
movement of eye)
 Disorder of Speech
 Altered muscle Coordinate & gait tremor

MAIN GOALS OF CARE
Multiple Sclerosis
Reduce & Manage Symptoms
Prevent Complications
Provide Support
Nursing Diagnosis
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Altered mobility r/t muscular weakness
Activity intolerance r/t fatigue
Altered comfort
Alteration in bowel elimination r/t
constipation
Bowel or bladder incontinence r/t altered
nerve innervation
Sexual dysfunction r/t altered nerve
innervation
Guillain-Barre
Syndrome
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An acute demylinating disorder of the
peripheral nervous system characterized
by progressive, usually rapid weakness &
paralysis.
One of the most common disorders of the
PNS: 1.7 per 100,000.
Cause unknown but believed to be an
altered immune response (approx 2/3 of
clients had a prior respiratory or GI
infection).
Four clinical presentations
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Ascending
– Most common, begins in legs and progresses
upward
– Symmetric motor deficits (paresis to
tetraplegia)
– Sensory deficits & diminished or absent
reflexes
– Respiratory insufficiency occurs in 50% cases
Presentation Cont’d
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Descending
– Motor deficits: initial weakness in cranial
nerves & progresses downward.
– Sensory deficits: numbness distally.
Hands>feet
– Flexes diminished or absent
– Rapid respiratory involvement
Presentations Con’t
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Miller-Fisher Variant
– Rare
– Triad of opthalmoplegia, areflexia, and
pronounced ataxia
– Usually no sensory loss
– Rarely respiratory involvement
Presentations Con’t
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Pure Motor
– Identical to ascending but sensory
manifestations are absent
– May be a mild form of ascending
– Muscle pain generally not present
Stages of Guillain-Barre
1.
Acute Stage: characterized by severe &
rapid weakness; loss of muscle strength
progressing to tetraplegia & respiratory
failure; numbness, pain, facial muscle
involvement.
2.
Stabiulizing/Plateau Stage: 2-3 weeks
after initial onset; “leveling” off of
symptoms
3.
Recovery Stage: months to years with
improvement of symptoms.
Collaborative Care
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Rapid diagnosis is important
Medication only for support: antibiotics,
morphine, anticoagulants.
Surgery: tracheotomy may be necessary
Plasmapheresis: removal of antibodies
with concurrent administration of
immunosuppressive agents
Diet: TPN or NG feeds may be necessary
Rehab: prevent complications & limit
effects of immobility (ROM, splints)
Nursing Diagnoses
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Ineffective breathing pattern
Impaired verbal communication
Anxiety & powerlessness
Altered nutrition
Impaired swallowing
Ineffective airway clearance
Risk for impaired tissue integrity
Pain
Self-care deficit
Altered protection