GUILLAIN BARRE SYNDROME MEDICAL SURGICAL NURSING

2. GUILLAIN BARRE
SYNDROME
PRESENTED BY :
JAYANTI TAMSANG
M.Sc(N) 1ST YEAR

3. INTRODUCTION
Guillain Barre Syndrome is an Auto-immune
demyelinating disorder that leads to progressive
paralysis.

4. HISTORICAL
BACKGROUND
Discovered In 1916 by three French
physicians Guillain, Barré, and Strohl
They described two French soldiers
with motor weakness, areflexia,
cerebrospinal fluid (CSF)
albuminocytologic dissociation, and
diminished deep tendon reflexes.
The identified syndrome was later
named Guillain-Barré syndrome.

5. DEFINITION
Guillain Barre syndrome is a rare disorder in which
body's immune system attacks nerves and causes
damage to the peripheral nerves.

10. INCIDENCE
• GBS is rare, affecting approximately 1 person in every 100,000.
• It can occur at any age, but those over age 50 are at greatest
risk.
• Males are more slightly affected than females

11. ETIOLOGY
The etiology of this syndrome is unknown.
 Most cases of GBS follow viral or bacterial infection of the gastrointestinal
or upper respiratory tract.
 Cytomegalovirus is the most common viral cause. Campylobacter jejuni
gastroenteritis is the most common bacterial cause.
 Other related infections include Epstein-Barr virus, Mycoplasma
pneumonia, Haemophilus influenza,hepatitis (A, B, E), and Zika virus.
 Surgery and trauma may also trigger GBS.
 Vaccines

12. PATHOPHYSIOLOGY

13. Flaccid paralysis with muscle enervation and atrophy
Transmission of nerve impulses is stopped or slowed
Demyelination of peripheral nerves
Immune system fails to distinguish between foreign
proteins and nerve protein
Edema and inflammation of affected nerves.
Infection with organism contain amino acid that mimic
peripheral nerve myelin

14. TYPES/ CLINICAL VARIANTS
 Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) :
The most common Variant.
Includes muscle weakness that starts in the lower part of body and spreads upward.
 Miller Fisher Syndrome (MFS), in which paralysis starts in the eyes. MFS is also
associated with unsteady gait.
- Involves anti-GQ1B antibodies
-Triad of symptoms : I) Acute opthalmoplegia
II) Areflexia
III) Ataxia
- Involves no weakness

15. CLINICAL MANIFESTATIONS
 First symptoms (Occurs 1-6 weeks after post-infection)
- Begins with lower limbs
- Acroparesthesia (Pain is a common symptom in the patient with
GBS)
- Ascending weakness and paralysis( Symmetrical)
 Areflexia

16. AUTONOMIC DYSFUNCTION
 Orthostatic hypotension, hyper-tension,
 Abnormal vagal responses (bradycardia, heart block, asystole).
 Bowel and bladder dysfunction,
 Facial flushing,
 Diaphoresis.

17. CRANIAL NERVE INVOLVEMENT
 Facial weakness,
 Extraocular eye movement difficulties,
 Dysphagia.
Symptoms peaks within 2-3 weeks and resolves withing 4-6
weeks.
Monophasic in nature.

18.  Acute Motor Axonal Neuropathy (AMAN)
- Involves anti – GM1 antibodies
- Associated with C.Jejuni infections
- Normal reflexes
 Acute Motor-sensory Axonal Neuropathy (AMSAN)
- Severe form of AMAN

19. DIAGNOSTIC CRITERIA FOR GBS
REQUIRED :
• Progressive symmetric weakness
• Hyporeflexia/Areflexia
• Progression < 4weeks

20. DIAGNOSTIC STUDIES
Diagnosis is based primarily on the
patient's history and clinical signs.
 CSF analysis
- High protein with normal WBC

21. • Electro myelo graphy and Nerve Conduction Studies

22. MANAGEMENT

23. MEDICAL MANAGEMENT
 Respiratory therapy or
mechanical ventilation

24. Plasmapheresis

25.  IV Immuno-globulins
 Anticoagulant agents and anti-embolism
 Electrocardiographic (ECG) monitoring
 Short-acting medications
 IV fluid, Vasopressor agents and volume expanders
 Corticosteroids appear to have little effect on the prognosis
duration of the disease.
 Antibiotic therapy

26. NUTRITIONAL MANAGEMENT
Nutritional needs must be met in spite of possible problems.
Enteral or parenteral nutrition may be used to ensure adequate
caloric intake.

27. COLLABORATIVE MANAGEMENT
• Early referral should be made to physical, occupational, and speech
therapists.
• Counseling may help the patient adjust to the sudden disabling syndrome
and dependence on others.

28. NURSING MANAGEMENT

29. ASSESSMENT
The patient is monitored for life-threatening complications
- Respiratory failure,
- cardiac dysrhythmias,
- deep vein thrombosis [DVT])
Because of the threat to the patient in this sudden, potentially
life-threatening disease, the nurse must assess the patient’s and
family’s ability to cope and their use of coping strategies.

30. COLLABORATIVE PROBLEMS/POTENTIAL
COMPLICATIONS
Based on the assessment data, potential complications that may
develop include the following:
 Respiratory failure
 Autonomic dysfunction

31. PLANNING AND GOALS
The major goals for the patient may include
- To improve respiratory function,
- To increase mobility, improved nutritional status,
- To develop effective communication,
- To decrease fear and anxiety,
- To ensure absence of complications.

32. NURSING INTERVENTIONS
Maintaining Respiratory Function
- Incentive spirometry and chest
physiotherapy.
- Monitoring for changes
- Mechanical ventilation
- Suctioning
- Assessing Blood pressure and heart rate
frequently to identify autonomic
dysfunction

33. Enhancing Physical Mobility
- Passive range-of-motion exercises
- Position changes,
- Anticoagulation, Anti-embolism
- Adequate hydration
- Padding over bony prominences,
- Evaluate laboratory test results
- Collaborates with the physician and
dietitian

34. Providing Adequate Nutrition
- IV fluids and parenteral nutrition
- Gastrostomy tube
- Assess gag reflex and bowel sounds

35. Improving Communication
- Establishing some form of
communication
- Collaboration with the speech
therapist

36. Decreasing Fear and Anxiety
- Referral to a support group
- Family members participation
- Increase the patient’s sense of control
- Diversional activities
- Encouraging visitors, engaging visitors or volunteers

37. COMPLICATIONS
 Respiratory failure
 Respiratory infection or UTI
may occur.
 Immobility from paralysis can
cause paralytic ileus, muscle
atrophy, pressure ulcers,
orthostatic hypotension, and
nutritional deficiencies.

38. PROGNOSIS
Most patients with GBS will start to recover spontaneously at
about 28 days.
Although 80% of patients almost completely recover, the process
is slow and takes months or years.
GBS patients who have a GI infection, are older in age, have a
rapid clinical onset, have a hospital length of stay longer than
days have poor upper extremity motor strength, or need
mechanical ventilation have a poorer prognosis.