West Visayas State University

COLLEGE OF NURSING
La Paz, Iloilo City

NURSING CARE PLAN

CLUSTERED NURSING RATIONALE OUTCOME NURSING RATIONALE EVALUATION

CUES DIAGNOSIS CRITERIA INTERVENTIONS
Impaired Limitation in independent BDG will be able Assess for Bed rest or
physical mobility purposeful physical movement to increase her developing immobility promotes
related to of the body or of one or more muscle strength thrombophlebitis. clot formation.
decreased extremities. and function
efficiency of through proper Assess skin integrity. Regular examination
muscular Myasthenia gravis (MG) is a positioning, Check for signs of of the skin will allow
transmission neuromuscular disorder turning and redness and tissue for prevention or
characterized by weakness and mobility exercises ischemia. early recognition and
fatigability of skeletal muscles. by treatment of
The underlying defect is a pressure sores.
decrease in the number of BDG will maintain
available acetylcholine good skin Monitor input and Pressure sores
receptors (AChRs) at integrity through output record and develop more quickly
neuromuscular junctions due to proper positioning nutritional needs as in patients with a
an antibody-mediated and regular they related to nutritional deficit.
autoimmune attack. turning by immobility. Proper nutrition also
provides needed
In MG, the fundamental defect energy for
is a decrease in the number of participating in an
available AChRs at the exercise or
postsynaptic muscle rehabilitative
membrane. In addition, the program.
postsynaptic folds are
flattened, or "simplified." These Assess elimination Immobility promotes
changes result in decreased status. constipation.
efficiency of neuromuscular
transmission. Therefore, Assess emotional Acceptance of
although ACh is released response to disability temporary or more
normally, it produces small or limitation. permanent
end-plate potentials that may
fail to trigger muscle action
potentials. Failure of
transmission at many
neuromuscular junctions results
in weakness of muscle
contraction.
The amount of ACh released
per impulse normally declines
on repeated activity (termed
presynaptic rundown). In the
myasthenic patient, the
decreased efficiency of
neuromuscular transmission
combined with the normal
rundown results in the
activation of fewer and fewer
muscle fibers by successive
nerve impulses and hence
increasing weakness, or
myasthenic fatigue. This
mechanism also accounts for
the decremental response to
repetitive nerve stimulation
seen on electrodiagnostic
testing.
The neuromuscular
abnormalities in MG are
brought about by an
autoimmune response
mediated by specific anti-AChR
antibodies. The anti-AChR
antibodies reduce the number
of available AChRs at
neuromuscular junctions by
three distinct mechanisms: (1)
limitations can vary
widely among
individuals. Each
person has his or her
own definition of
acceptable quality of
life.
Provide positive Patients may be
reinforcement during reluctant to move or
activity. initiate new activity
due to a fear of
falling. A positive
approach allowas the
learner to feel good
baout learning
accomplishments.
Allow the patient ot Increases self-
perform the tasks at esteem and
his or her own rate. promotes recovery.
Do not rush the
patient. Encourage
independent activity
as able and safe.
Turn and position the Turning patients
patient every 2 hours optimizes circulation
or as needed. to all tissues and
relieves pressure.
Maintain limbs in Maintaining proper
functional alignment. alignment of
Support legs in extremities prevents
dorsiflexed position. contractures such as
footdrop and
excessive planter
accelerated turnover of AChRs flexion or tightness.
by a mechanism involving Heavy bed linens can
cross-linking and rapid cause improper
endocytosis of the receptors; alignment of feet.
(2) blockade of the active site
of the AChR, i.e., the site that Clean, dry and These measures
normally binds ACh; and (3) moisturize skin as reduce skin
damage to the postsynaptic needed. breakdown from
muscle membrane by the prolonged immbolity.
antibody in collaboration with
complement.
Administer
The distribution of muscle prescribed
weakness often has a medications. Antimyasthenic
characteristic pattern. The a. Mestinone Inhibits the enzyme
cranial muscles, particularly the acetylcholinesterase,
lids and extraocular muscles, thereby reducing the
are often involved early in the degradation of
course of MG, and diplopia and acetylcholine.
ptosis are common initial
complaints. Facial weakness Essential in
produces a "snarling" b. Potassium maintaining
expression when the patient supplement adequate potassium
attempts to smile. Weakness in levels in the body.
chewing is most noticeable
after prolonged effort, as in
chewing meat. Speech may
have a nasal timbre caused by
weakness of the palate or a
dysarthric "mushy" quality due
to tongue weakness. Difficulty
in swallowing may occur as a
result of weakness of the
palate, tongue, or pharynx,
giving rise to nasal
regurgitation or aspiration of
liquids or food. Bulbar
weakness is especially
prominent in MuSK antibody–
positive MG. In 85% of
patients, the weakness
becomes generalized, affecting
the limb muscles as well. If
weakness remains restricted to
the extraocular muscles for 3
years, it is likely that it will not
become generalized, and these
patients are said to have ocular
MG. The limb weakness in MG
is often proximal and may be
asymmetric. Despite the muscle
weakness, deep tendon
reflexes are preserved. If
weakness of respiration
becomes so severe as to
require respiratory assistance,
the patient is said to be in
crisis.

Sources:
Nurse’s Pocket Guide 2008 11th
Edition

Harrison’s Internal Medicine

2007 17th Edition