Acute flaccid paralysis
•
4 likes•187 views
This document provides information about acute flaccid paralysis (AFP), including its definition, anatomical localization, etiological agents, clinical features, investigations, treatment, and AFP surveillance. AFP is a lower motor neuron lesion characterized by sudden onset of weakness or paralysis in a previously normal limb in a patient under 15 years old. It can be caused by viruses, bacteria, toxins affecting different areas of the motor neuron. Clinical features vary depending on the cause but may include asymmetric weakness, sensory changes, bladder involvement and fever. Treatment involves supportive care and addressing the underlying cause. AFP surveillance is important for detecting polio cases and importation through reporting, specimen collection, identification and mapping of viruses.
More Related Content
What's hot
What's hot (20)
Similar to Acute flaccid paralysis
Similar to Acute flaccid paralysis (20)
Recently uploaded
Recently uploaded (20)
Acute flaccid paralysis
- 1. ACUTE FLACCID PARALYSIS DR. SWAPNIL C. MIRAJKAR M.D. (PAEDS)
- 2. Specific learning objectives Definition of AFP Anatomic localization Etiological agents Clinical features Investigations Treatment AFP surveillance
- 3. Definition Sudden onset of weakness or paralysis in a previously normal limb in a patient aged less than 15 years age.
- 4. AFP is a lower motor neuron lesion. LMN : lesion of the nerve fibres travelling from the anterior horn of the spinal cord to the associated muscle(s)
- 5. Anatomical localization & Etiological agents Anatomical site etiology Anterior horn cell Poliovirus, non-polio enterovirus, Japanese B encephalitis Dorsal root ganglia Herpes simplex virus, cytomegalovirus, rabies Spinal cord Acute transverse myelitis, parasitic infestations (schistosoma, cysticercus, echinococcus), space occupying lesions, anterior spinal artery syndrome, trauma, postcardiovascular surgery vascular complications
- 6. Anatomical localization & Etiological agents (continued) Anatomical site etiology Radicles & peripheral nerves Guillain barre syndrome, chronic inflammatory demyelinating polyneuropathy, HIV infection per se or associated opportunistic infections or complications (herpes simplex virus, cytomegalovirus, Epstein Barr virus, Giardia Lamblia, Toxoplasma Gondii, Mycobacterium tuberculosis, Treponema pallidum), vitamin B12 deficiency, hepatitis B, diphtheria, rabies, tick bite, hypokalemia, thyrotoxicity Neuro-muscular junction Myasthenic crisis, OPP, drugs (aminoglycoside phenytoin), botulisim, snake envenomation Muscle Polymyositis, SLE, mixed connective tissue disorder, viral (HIV, non-polio enteroviruses, human T cell lymphotropic viruses), toxoplasmosis, Lyme disease, trichinosis
- 7. Clinical features in a child presenting with acute flaccid paralysis.
- 8. Disease Onset Progressi on Topography DTRs Sens ory feat ures Bladder & Bowel involve ment Fever at onset Systemic features Etiological clues Polio & non-polio enterovir ses 2-3 weeks Hours to few days Asymmetric pure motor involvement with proximal > distal - - Rare + Meningeal signs, non- specific prodromal illness, hand foot & mouth disease in non-polio group Attack precipitate d by IM injection Rabies Mont hs to years 2-4 Symmetric, ascending, generalized - + Occasio al + Bite mark H/o animal bite GBS Hours to days 2-4 Symmetric, ascending, generalized, cranial neuropathy (Commonly 7th ), occasionally early respiratory weakness - + Occasio al +- Meningeal signs occasionally Preceding prodromal illness or vaccination
- 9. Disease Onset Progress ion Topography DTRs Senso ry featur es Bladde r & Bowel involve ment Fever at onset Systemic features Etiological clues Acute transvers Myelitis Hours to few days Hours few Symmetric, generalized, respiratory involvement in high cervical lesions Absent (in shock phase), brisk below the level of lesion later + early +- Meningeal signs occasionally Preceding prodromal illness or vaccination Post traumatic sciatic neuritis Hours to few days Maximu m deficit at onset One limb involved Absent in that limb + - - - Preceding H/o IM injections
- 10. Disease Onset Progr essio n Topography DTRs Sensory features Bladde r & Bowel involve ment Fever at onset Systemi c features Etiological clues Post diphtheritic polyneuropa thy Weeks to month s 2-4 week s Symmetric ,descending, generalized, cranial neuropathy (commonly palatal), occassionaly early respiratory weakness - + +- - Cardiom yopathy Preceding h/o fever with neck swelling (Bull neck) & membranous pharyngitis. Botulism Hours to few days Hour s to few days Symmetric, descending, generalized, cranial neuropathy (ocular & bulbar), occasionally respiratory weakness. - +- - - - - Tick bite paralysis 2-3 weeks 2-4 week s Symmetric, generalized, cranial neuropathy (occular) - - - - Bite marks h/o travel to endemic
- 11. Disease Onset Progre ssion Topography DTRs Sensor y feature s Bladder & Bowel involve ment Fever at onset System ic feature s Etiological clues Viral myositis Hours to few days Hours to few days Symmetric, generalized, Normal or reduced - - + - Viral prodrome Hypokalemic periodic paralysis Hours or few days Hours to few days Symmetric, proximal > distal, early neck flexor, respiratory weakness - - - - Precipitated by post prandial state or exertion Critical illness polyneuropa hy Hours to few days Hours to few days Symmetric, generalized, early respiratory involvement - - - +- Underl ying sepsis, shock, cardior espirat ory failure
- 13. How to differentiate among Polio Guillain Barre syndrome Traumatic Neuritis Transverse myelitis
- 17. Management Definitive care: Intravenous immunoglobulin: (IvIg) 2gm/kg: indicated in GBS, myasthenic crisis. Pulse methyprednisolone therapy 30mg/kg/day: for transverse myelitis. Antisnake venom in case of suspected envenomation. Intravenous potassium for hypokalemia.
- 18. Management Supportive care: Prevention of bedsores Bladder & bowel care Nutrition Physical & occupational theraphy
- 19. AFP SURVEILLENCE AFP surveillance identifies new cases & detects importation of wild poliovirus. The four steps of surveillance are: 1. Finding & reporting children with AFP. 2. Transporting stool samples for analysis. 3. Isolating & identifying poliovirus in the laboratory. 4. Mapping the virus to determine the origin of the virus strain.
- 20. AFP SURVEILLENCE Finding & reporting children with AFP The first link are staff in all health facilities: from district health centres to large hospitals They must promptly report every case of AFP in any child < 15 years of age. The number of AFP cases reported each year is used as an indicator of country’s ability to detect polio even in countries where disease no longer occurs. A country’s surveillance system needs to be sensitive enough to detect at least one case of AFP for every 1,00,000 children < 15 years of age even in absence of polio.
- 21. AFP SURVEILLENCE Transporting stool samples for analysis: Two stool samples should be collected at an interval of 24-48 hours apart & within 14 days of onset of paralysis. However, when AFP cases are seen late(i.e. greater than 2 weeks after paralysis), stool specimen may be collected up to 60 days after onset of paralysis. At least “one thumb sized” 8 gm of stool is required.
- 22. AFP SURVEILLENCE Isolating poliovirus: If poliovirus is isolated the next step is to distinguish between wild & vaccine related. If wild poliovirus is isolated then identify which of the two surviving types of wild virus is involved.
- 23. AFP SURVEILLENCE Mapping of the virus: Once the wild poliovirus is identified, further tests are carried out to determine from where the strain may have originated. By determining the genetic makeup of virus, wild virus can be compared to others & classified into genetic families which cluster in defined geographic areas. When the poliovirus has been pinpointed to precise geographical area, it is possible to identify the source of importation of poliovirus- both long range & cross border.
- 24. Thank you