GUILLAIN-BARRE SYNDROME IS AN AUTO- IMMUNE DISEASE CAUSES DE-MYELINATION OF NERVE CELLS.

1. GUILLAIN-BARRE
SYNDROME
Arvind Joshi
Nursing Officer
AIIMS Mangalagiri
03-09-2019
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2. Guillain – Barre Syndrome
• Nervous system
• GB Syndrome
• Nerve cell
• Risk Factors
• Diagnostic Evaluations
• Sign and Symptoms
• Treatment
• Prognosis
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3. Nervous System
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6. What happens ?
•Auto immune condition
•Immune system attacks nerves
•Affects peripheral nervous system
•It extends to autonomic nervous system and can
affect cranial nerves
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7. Nerve Cell
Dendrites
Cell Body
Axon Terminal
Axon
Myelin Sheath
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8. Where immune system attacks?
•Immune system attacks on myelin sheath of nerve cell
•Leads to de-myelination of nerve cell
•Transmission of nerve impulses will be obstruct.
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9. De- Myelination of Myelin sheath
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10. When Myelin Sheath is Intact
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11. When Myelin Sheath is Damaged
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12. Risk Factors
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14. Diagnostic Evaluation
• Electromyography and nerve conduction test
• It assesses for demyelination of nerve cell by determining
muscles ability to respond to nerve stimulation
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15. Lumber Puncture
Findings:-
•Elevated protein without
elevated white blood cells
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LEGS: - NUMBNESS, TINGLING DIFFICULTY IN WALKING, SYMMETRICALLY
ASCENDING SYMPTOMS, LACK OF REFLEXES,LOOSING MUSCLES TONE,
PARALYSIS OF LOWER EXTREMITIES
BLADDER AND BOWEL URINARY RETENTION, CONSTIPATION DUE
TO DECREASE PERISTALSIS
GI SYSTEM: - DYSPHAGIA, CONSTIPATION DUE TO DECREASE
GASTRIC MOTILITY CAN LEAD TO PARALYTIC ILEUS
UPPER EXTREMITIES: - NUMBNESS TINGLING LACK OF REFLEXES
RESPIRATORY SYSTEM: - DIFFICULTY IN BREATHING, PATIENT
WILL NOT BE ABLE TO TAKE DEEP BREATH , WEAK INEFFECTIVE
COUGH CONTD…..

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CRANIAL NERVES: - LOOSE CONTROL OVER FACIAL
MUSCLE, EYE BALL, SWALLOWING, SPEAKING ISSUES,
COMMUNICATION PROBLEMS
ANS INVOLVEMENT: VITALS, DYSRHYTHMIA,
TEMPERATURE IRREGULATIONS
COMPLICATIONS : - INTUBATED- TRACHEAL
INFECTION, VAP, INFECTION, BLOOD CLOTS, DVT,
PRESSURE SORES, UTI, LACK OF MUSCLE TONE

19. Treatment
3 components of management:
Monitoring, supportive and critical care.
Immunotherapy
Rehabilitation
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20. Supportive and Critical Care
Monitoring vital parameters.
Nutrition.
DVT prophylaxis.
Ventilator assistance.
Managing autonomic dysfunction.
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21. Chest and general physiotherapy.
Frequent turning and continuous skin
care.
Management of pain, constipation.
Prevention of exposure keratitis.
Constant reassurance.
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22. Immunotherapy:
• IV Ig or plasmapheresis can be initiated, as they are equally effective.
Combining these therapies has no additional benefit.
• Start treatment as soon after diagnosis as possible. Greatest effect was
observed when it was started within the first 2 weeks from onset.
• Each day counts;
• 2 weeks after the first motor symptoms, immunotherapy is only minimally
effective.
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23. • Plasmapheresis A course of plasmapheresis consists of 40–50 mL/kg
plasma exchange (PE) 4-5 times over 2 weeks.
• This therapy should ideally be administered within the first 2 weeks and
not later than 4 weeks from clinical onset.
•Immunoglobulins - IV IG is as effective as plasmapheresis, at least
in the first 2 weeks. IV Ig is preferred as initial therapy because of its
ease of administration and good safety record.
• Dose: 5 daily infusions for a total dose of 2 g/kg
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24. Prognosis
• Around 85% of patients achieve a full functional recovery
within few months to a year; minor findings (eg areflexia) may
persist for years.
• The remaining 15% have functionally important residua.
• 20% of patients not ambulant at presentation remained so
even after 6 months, despite immunotherapy. Even 3–6 years
later, GBS has a large impact on social life and the ability to
perform activities.
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