1. Myasthenia Gravis
An autoimmune neurologic
disorder
By Lexi Gray & Mary Kacic

2. Background
 Myasthenia gravis means “grave muscle
weakness”
 It is an autoimmune disease affecting the
myoneural junction
 About 60,000 people in the U.S. have this
disease
 Women affected more frequently than men, at
around 20-40 years of age. Men develop it
later, at around 60-70 years of age.

3. Symptoms
 Causes varying degrees of skeletal muscle
weakness
 Hallmark of the disease: muscle weakness
increases during periods of activity and improves
during rest.
 Areas that MAY be affected: eyes/eyelid
movement, facial expression, chewing, talking,
swallowing

4. Pathophysiology
 Normal communication between the nerve and muscle
is interrupted at the neuromuscular junction (where
nerve cells meet with the muscles they control)
 Normally, nerve endings release acetylcholine which
travels through the NMJ and binds to receptors, causing
muscle contraction.
 In myasthenia gravis, these receptors are blocked or
destroyed

5. Pathophysiology
 Autoimmune disease: the antibodies that attack
or block the acetylcholine receptors are produced
by the body’s own immune system
 Thymic hyperplasia or a thymic tumor is present
in 80% of people with myasthenia gravis

6. Assessment
 Onset of the disorder may be sudden
 Many times, symptoms are not immediately
recognized as being related to myasthenia gravis
 In most cases, weakness of the eye muscles is
noticed first.

7. Assessment - Severe Symptoms
 Ptosis – drooping of one or both eyelids
 Diplopia – blurred or double vision
 Bulbar symptoms – weakness of muscles of the
face & throat
 Bland facial expression
 Difficulty swallowing – increased risk of choking &
aspiration
 Dysarthia – impaired speech
 Dysphonia – voice impairment
 Weakness In arms, hands, legs, neck
 Generalized weakness also effects intercostal
muscles, resulting in decreasing vital capacity and
respiratory failure.

8. Confirming the Diagnosis
 Acetylcholinesterase Inhibitor Test
 Confirms the diagnosis of myasthenia gravis. During
this test, the breakdown of acetylcholine is stopped.
As a result, acetylcholine is able to accumulate at the
receptor sites.
 For this test, edrophoniumchloride is administered IV.
Facial muscle weakness and ptosis will resolve about
30 second after the drug is administered, if the patient
is positive for a myasthenia gravis diagnosis. This
relief lasts only 5 minutes, so it is not considered a
treatment.
 After the drug is administered, the patient's serum is
then tested for acetylcholine receptor antibodies,
which would also be consistent with the diagnosis.
 In some cases, patients with myasthenia gravis may
have an enlarged thymus gland.

9. Nursing Diagnosis #1
 Risk for aspiration R/T difficulty swallowing,
weakness of bulbar muscles
 Overall goal: No aspiration will occur
 Interventions
 Give meals with anticholinesterase meds to inhibit
breakdown of acetylcholine and increase its
concentration at the NMJ
 Raise the HOB to semi-fowler’s position, which will
ensure upper airway patency.
 Give food with a pudding-like consistency, which
can be more easily swallowed.

10. Nursing Diagnosis #2
 Deficient knowledge R/T drug therapy, potential
for crisis (myasthenic or cholinergic), and self-
care management
 Overall goal: Patient will demonstrate knowledge
of medication management, importance of rest,
coping strategies, and prevention/management of
complications
 Interventions
 Teach patient about the actions of meds, and
importance of regimen. The patient will verbalize
the consequences delaying med intake, including
S&S of myasthenic and cholinergic crisis.
 Teach strategies for patient to conserve their
energy. The patient will develop coping strategies to

11. Treatment of myasthenia gravis
 Pharmacologic Treatment
 First-line med is pyridostrigmine bromide
(Mestinon), an anticholinesterase that inhibits the
breakdown, thus improving skeletal muscle
contraction. Side effects can include fasciculations,
abdominal pain, diarrhea.
 Immunosuppressive Therapy: Corticosteroids
decrease the amount of antibody production.
Cytotoxic meds (Azathioprine) inhibits production of
T-and B-cells, and effects may not be seen for 3-12
months. Hepatotoxicity is a risk of using cytotoxic
meds.
 Some common medications exacerbate the
symptoms of myasthenia gravis, including:

12. Possible Side Effects of
Anticholinesterase Meds
Central Respiratory/ Skeletal Muscles
Nervous System Cardiovascular
Irritability Bronchial relaxation Fasciculations
Anxiety Increased bronchial Spasms
secretions
Insomnia Tachycardia Weakness
Headache Hypotension
Genitourinary
Dysarthia Frequency
Gastrointestinal
Syncope Abdominal cramps Urgency
Seizures Nausea,vomiting and
diarrhea Integumentary
Coma Anorexia Rash
Diaphoresis Increased Salivation Flushing

13. Treatments
 Plasmatheresis
 This procedure removes the patient’s plasma and
plasma components through a centrally placed
catheter. Blood cells are separated from antibody-
containing plasma. The blood cells are then mixed
with plasma substitute and reinfused. Provides
temporary treatment for severe symptoms.
 Intravenous immune globulin
 Treats exacerbations of myasthenia gravis
temporarily. This procedure does not work as
quickly as plasmatheresis.
These are treatments for myasthenia gravis, not
cures.

14. Treatments
 Surgical Treatments
 Thymectomy: Surgical removal of the thymus
gland, which may result in the production of
antigen-specific immunosuppression, which
results in clinical improvement. Results vary;
patient may have partial or complete
remission, or no remission at all.
 Nursing considerations for the patient who
received a thymectomy include monitoring
respiratory function and mechanical ventilation.

15. Myasthenia (or cholinergic) Crisis
 Exacerbation of the disease process. Signs &
symptoms include muscle/bulbar weakness.
 Causes for myasthenia crisis may include a
respiratory infection, pregnancy, or medications.
 Primary management is focused on maintaining the
airway. The nurse assesses respiratory rate, depth,
breath sounds, and pulmonary function.
Endotracheal intubation and mechanical ventilation
may be necessary.
 Assess arterial blood gases, I&O, daily weight.
 Avoid sedatives and tranquilizers.
 Bradycardia and respiratory distress (emergency
situations) are treated with atropine.

16. References
Doenges, M., Moorhouse, M., Murr, A. (2010).
Nurse’s Pocket Guide: Diagnoses, Prioritized
Interventions, and Rationales (12th ed.).
Philadelphia: F.A. Davis. ISBN: 0803622341.
Smeltzer, S. C., Bare, B. G., Hinkle, J. L. &
Cheever, K. H. (eds.) (2008). Brunner &
Suddarth's textbook of medical-surgical nursing
(11th ed.). Philadelphia: Lippincott Williams &
Wilkins.