7 GBS ERPM n.pptx gulilan baree syndrome

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1. Guillain-Barre syndrome Dr. Ruwanka De Livera

2. The group inflammatory demyelinating neuropathies It often follows 1-3 weeks after a respiratory infection or diarrohea , which may have been mild. Guillain-Barre syndrome

3. GBS - Pathophysiology Infection Organism Immune response Host neural tissue Molecular mimicry

4. Infection Viral (CMV, EBV, VZV, HIV) Campylobacter jejuni (severe GBS) Vaccines Rabies, influenza Molecular mimicry

5. Target epitopes GBS - Pathophysiology

6. Acute flaccid areflexic paralysis Self limiting 2/3 – trigger event Rapid progressive – up to 4 weeks Plateau Recovery GBS – clinical features

7. 1. Motor 2. Sensory – 3. Autonomic

8. Progression

9. Clinical CSF ………………………………. ………………………………… NCS/EMG Demyelination Axonal degeneration Changes best seen after 10-14 days GBS - diagnosis Slowed conduction velocities

10. No classical features of cardio-respiratory failure in neuromuscular failure No dysponea But saturation Also measure signs of respiratory failure – VC by spirometry

11. Poliomyelitis Myaesthenia gravis Paralytic rabies (dumb rabies) Porphyria Toxic neuropathy – OP Electrolyte imbalance ( hypokalaemia , hypomagnesaemia) Snake bite Botulism – descending Diphtheria Exclude – other causes of acute flaccid paralysis

12. Marked asymmetry of signs Sensory level Persistent bladder/bowel dysfunction Fever at onset CSF cells > 50 GBS unlikely

13. General 1/3 intensive care Respiratory support – VC<20ml/kg Specific treatment – GBS - Management

14. Monitoring Rehabilitation Prevention