Guillan Barre Syndrome
Etiology
Antecedent events:
swine flu, influenza vaccine
GBS
Lymphoma, SLE
Viral infections like rabies swine flu
bacterial infections campylobacter jejuni, Mycoplasma pneumoniae, HIV,
Types
1 Acute Inflammatory demyelinating polyneuropathy
2 Acute motor axonal neuropathy
3 Acute motor sensory axonal neuropathy
4 Miller Fisher Syndrome
Clinical Manifestations
1 Motor symptoms
Progressive ascending symmetrical muscle weakness
Flaccid paralysis
Decreased or absent deep tendon reflexes (areflexia)
2 Sensory symptoms
Paresthesia (tingling or numbness in hands and feet)
Pain, often worse at night
Hypoesthesia (reduced sensation)
3 Autonomic symptoms
Fluctuating blood pressure (hypotension or hypertension)
Cardiac arrhythmias (tachycardia or bradycardia)
Sweating abnormalities
Urinary retention, constipation
4 Cranial Nerve Involvement
Facial weakness (e.g., bilateral facial palsy)
Difficulty swallowing (dysphagia)
Difficulty speaking (dysarthria)
Ocular muscle weakness (diplopia)
5 Respiratory Symptoms
Shortness of breath
Decreased breath sounds
Respiratory failure (requires ventilator support in 20–30% of cases)
Diagnosis
History of bacterial or viral infection
neurologic examination – Absent reflexes
CSF- low blood cell count, high protein
Change in vital capacity and negative inspiratory force
EMG
Medical Management
Plasmapheresis produces temporary reduction of circulating antibodies
Corticosteroids
Immunoglobulin
ECG monitoring and treatment of cardiac dysrhythmias
Analgesics and muscle relaxants
Mechanical ventilation and intubation.
Nursing Assessment
a. Assess pain level due to muscle spasms
b. Assess cardiac function, dysrhythmias, VTE
c. Assess respiratory status to determine closely hypoventilation due to weakness
Nursing Diagnosis
a. Ineffective Breathing Pattern related to weakness of respiratory muscles
b. Impaired Physical Mobility due to related to paralysis
c. Inadequate nutritional intake related to intubation
d. Chronic Pain related to disease
e. Anxiety related to communication difficulties
f. Impaired verbal communication
Nursing Interventions
1 Maintaining respiratory function
Monitor respiratory status through vital capacity measurements, rate and depth of
respirations and breath sounds
Monitor for impending respiratory failure; HR- above 120 or blow 70 RR – above 30,
prepar to intubate
Monitor ABGs
Respiratory function can be maximized with incentive spirometry and chest
physiotherapy
Mechanical ventilation is required if the vital capacity falls
Suctioning may be needed to maintain a clear airway
2 Enhancing Physical Mobility
Prevent VTE by ROM, position, anticoagulation , stockings, compression boots, adequate
hydration.
Assess for pressure ulcers, edema, contractures.
Padding over bony prominences, elbows, heels.
Use wheelchairs as needed.
3 Providing adequate nutrition
Assess chewing and swallowing abilities by testing CN I, V, IX and X
If function is inadequate, provide through enteral or parenteral nutrition.
Monitor for return of bowel sound
4 Improving communication
Establish some form of communication through picture cards or an eye blink system
Collaboration with speech therapist
Have conversations about the treatment
Standard call lights cannot be reached by them so stablish an adaptive call system.
5 Decreasing Fear and Anxiety
Mechanical ventilation might frighten them and patient might experience loneliness and
lack of control
Diversional activities
Patient education
Medications
Evaluation
Maintain effective respirations and airway clearance
Shows increasing mobility
Receives adequate nutrition and hydration
Myasthenia Gravis
It is a chronic autoimmune disorder affecting the neuromuscular transmission of impulses
in the voluntary muscles of the body
1. Etiology
Common associated factors:
o Thymus gland abnormalities (hyperplasia or thymoma).
o Genetic predisposition (family history of autoimmune disease).
o Triggering factors: infections, stress, pregnancy, surgery, certain drugs (e.g.,
aminoglycosides, beta blockers).
2. Pathophysiology
Normally: Acetylcholine (ACh) released from motor neurons binds to ACh receptors on
muscle cells → muscle contraction.
In MG: Autoantibodies block or destroy these receptors.
Result: ↓ ACh binding → ↓ neuromuscular transmission → muscle weakness and
fatigue.
Severity varies based on the number of receptors affected.
Fluctuating symptoms: improve with rest, worsen with activity.
3. Clinical Manifestations
Ocular symptoms (most common initial sign):
o Ptosis (drooping eyelids)
o Diplopia (double vision)
Bulbar symptoms:
o Dysphagia (difficulty swallowing)
o Dysarthria (slurred speech)
o Weak jaw or neck muscles
Generalized muscle weakness:
o Especially in proximal muscles (shoulders, hips)
o Worsens with activity; improves with rest.
Respiratory muscle weakness (in severe cases):
o Can lead to myasthenic crisis (life-threatening respiratory failure).
Facial and limb muscle involvement:
o Blank facial expression, difficulty smiling, weak grip.
o Snarling appearance when trying to smile
4. Diagnostic Evaluation
Edrophonium test (Tensilon test):
o IV injection of edrophonium chloride → facial muscle weakness, ptosis should
resolve for about 5 minutes, immediate improvement of muscle strength
represents a positive test
o Risk: cholinergic crisis , atropine should be available to control bradycardia,
asystole, bronchoconstriction, sweating and cramping
Serologic tests:
o Detect anti-AChR antibodies (positive in ~85% of generalized MG).
o Anti-MuSK antibodies (in seronegative MG cases).
Electromyography (EMG):
o Shows decreased muscle response with repetitive nerve stimulation.
Chest CT or MRI:
o To evaluate for thymoma (tumor of the thymus).
Pulmonary function tests (PFTs):
o To assess risk of respiratory failure, especially in severe MG.
5. Medical Management
a. Anticholinesterase drugs
Pyridostigmine (Mestinon) – first-line drug. Inhibits acetylcholinesterase. Given
multiple times/day. Side effects include diarrhea, abdominal cramps, excessive saliva.
b. Immunosuppresive drugs
Corticosteroids (Prednisone) – reduces autoimmune activity.
Azathioprine, Mycophenolate, Cyclosporine for long-term control.
c. Plasmapheresis
Removes circulating antibodies. Used during myasthenic crisis or before surgery for
short-term improvement.
d. IV Immunoglobulin (IVIG)
Temporarily blocks immune attack on NMJ. Used in crisis or severe exacerbations.
Headache migraine exacerbation aseptic meningitis and flu like symptoms
e. Thymectomy
Surgical removal of the thymus gland. Indicated if a thymoma is present or for
patients <60 years with generalized MG.
Nursing Intervention
Assessment
a. Expect the patient to complain of extreme muscle weakness and fatigue.
b. Assess cranial nerve function. Modify fatigue's ability with repetitive activity and speech.
Observe eye muscles, ptosis, ocular palsy, and diplopia.
c. Assess respiratory function, breathlessness, respiratory weakness, tidal volume, and vital
capacity measurements.
d. Assess the complications secondary to drug treatment.
e. Long-term immunomodulating therapies may predispose patients with MZ to various
complications.
f. Long-term steroid use may lead to or aggravate many conditions such as osteoporosis,
cataracts, hyperglycemia, weight gain, avascular necrosis of hip, hypertension, and
gastritis or peptic ulcer disease.
g. To decrease the risk of ulcer , the patient should take an H2 blocker or an antacid.
h. Increase risk for infection from immunomodulating therapies, especially if the patient is
in more than one agent. Such infections include tuberculosis, systemic functional
infections, pneumocystis carinii, pneumonia,
i. risk of lymphoproliferative malignancy may be increased with chronic
immunosuppression.
j. Immunosuppressive drugs may have teratogenic effects. In addition, risk of congenital
deformity is increased in offsprings of all women with severe MG. Neonates born to
women with MZ need to be monitored for respiratory failure for 1-2 weeks after birth.
Discuss these aspects with women in reproductive years prior to beginning therapy with
these drugs.
Nursing Diagnosis
1 Risk for aspiration
- Schedule meals during peak anticholinesterase effects to optimize swallowing.
- Allow rest before meals to reduce fatigue.
- Position upright with neck slightly flexed during eating.
- Offer foods with gravy or sauces for easier swallowing.
- Provide small, frequent meals earlier in the day when strength is better.
- Keep suction equipment available and teach patient/family how to use it.
- Refer to speech-language pathologist if choking occurs frequently.
- Monitor respiratory function, vital capacity, ABGs, and watch for signs of respiratory distress.
2 Impaired Physical Mobility/ Fatigue
- Educate patient to conserve energy by planning activities during peak strength times.
- Encourage frequent rest periods.
- Keep essential items within easy reach to avoid unnecessary trips. (e.g., hygiene supplies on both floors
in multi-story homes).
- Help patient identify patterns of strength/weakness using a diary; adjust activities accordingly.
3 Vision Support
- Manage ptosis/double vision with eye patching or “eyeglass crutches” to lift eyelids.
- Tape eyelids closed if incomplete closure occurs; instill artificial tears regularly to prevent
corneal injury.
4 Deficient Knowledge
- Educate patient/family on importance of strict medication schedule – delays increase risk of crisis.
- Emphasize recognizing signs of myasthenic vs cholinergic crisis.
- Teach avoidance of triggers (emotional stress, infections, heat, certain medications).
- Provide written information about medications and self-monitoring.
- Connect with support groups (e.g., Myasthenia Gravis Foundation).
5 Medication and Complications
o cholinergic crisis , atropine should be available to control bradycardia, asystole,
bronchoconstriction, sweating and cramping
o anticholinesterase side effects include diarrhea, abdominal cramps, excessive
saliva.
o IVIG side effects headache migraine exacerbation aseptic meningitis and flu like
symptoms
