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ACUTE FLACCID PARALYSIS
Dr Shreedhar Paudel
May, 2009
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DEFINITION
Sudden onset of weakness or paralysis over a
period of 15 days in a patient less 15 years of age
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INVOLVEMENT
Anterior horn cells
Poliomyelitis
Acute transverse myelitis
Nerve fibres
Postinfectious polyneuropathy (GBS
syndrome)
Toxins----diphtheria, porphyria
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INVOLVEMENT
Neuromuscular junction
Tick toxin
Botulinum toxin
Metabolic causes
Periodic paralysis
Muscular disease
Myositis
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GUILLIAN BARRE SYNDROME
DEFINITION
It is an idiopathic, acquired, postinfectious
polyneuropathyEPIDEMIOLOGY
Annual incidence is 0.4 to 1.7/ 100000
Male > female
Any age however rare before one year
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PATHOPHYSIOLOGY
Inflammation causes leakage of proteins into the CSF
causing raised CSF proteins without pleocytosis
Can involve the peripheral nerves, cranial nerves, dorsal
roots, dorsal root ganglia & sympathetic chain
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EITIOLOGY
Mycoplasma
Hepatitis B
CMV
EBV Measles
Mumps
Echovirus
Cocksakie virus
Influenza virus
Campylobacter jejuni
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CLINICAL FEATURES
Appear within 2 wksafter onset of viral infections
C/O numbness or parasthesias in the hand and feet
followed by a heavy weak feeling in the legs
Followed by inability to walk The weakness is symmetricalbeginning in the legs
and ascending to involve the arms, trunk, throat and
face
Progression can occur rapidly in hours or days ormore slowly over weeks
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SIGNS
Marked flaccidity ---- hypotonia
Complete areflexia
Minimal signs of sensory loss
Progress to bulbar signs and respiratory insufficiency
Cranial nerve involvement
Autonomic dysfunction --- hypotension,hypertension, orthostatic hypotension, tachycardia,urinary retention or incontinence, stool retention,
episodes of abnormal sweating, flushing,vasoconstriction
Intact sensations
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CLINICAL VARIANTS
Polyneuritis cranialis
Cranial nerve involvement
Miller fisher syndrome Ophthalmoplegia, ataxia, areflexia
Chronic progressive GBS
Symptoms persisting more than 6 weeks
Chronic relapsing GBS
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DIAGNOSIS
Clinical
Nerve conduction studies
slowing of nerve conduction
Electromyogram
extensive fibrillation showing denervation
CSFincreased proteins with normal leukocytes during 2nd
week of illness
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MANAGEMENT
SUPPORTIVE
Close monitoring of vital signs
Nursing care Repeated spirometries
Bowel and bladder care
Tube feeding
Care for bed sores Ventilatory support if required
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MANAGEMENT
SPECIFIC
Steroids-----2mg/kg for 2 weeks
Plasmapheresis-----to remove antibodies I/V immunoglobulins-----400mg/kg for 5 days or
1gm/kg for 2 days
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PROGNOSIS
Mortality 3%
Recovery
1 to 6 months, may take 12 months Delayed recovery may be followed by permanenent
neurological sequelea
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D/D of acute flaccid paralysis
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GB Syndrome Spinal cord
syndrome
poliomyelitis
Eitiology Delayed
hypersesitivity.antibody mediated
Trasverse
myelitis,spinalcord abscess,TB
Poliovirus type
I,II,III
History GI or URTI, 5 to
14days precedingsymptoms
Rapid progression
of symptoms
Unimmunized,
URTI or GIinfection
Symptoms Symmetric weakness
in LL gradually
ascending with
parasthesias. normal
bowel & bladder
function
Back pain.
Sensory loss
below the level of
lesion, sphincter
problems
Fever,.
meningism,
muscle
tenderness,
asymmetric
weakness
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Signs Symmetric flaccid
weakness, sensations
intact, gradually
ascending
Symmetric
areflexia,sensory
loss below the
level of lesion.,pain, bowel and
bladder
dysfunction
Assymmetric
flaccid weakness,
sensations intact,
muscle wasting
CSF findings Normal cell count
with raised protiens
2nd week of illness
Pleocytosis with
raised protiens
Pleocytosis with
raised protiens
EMG/NCS Signs of denervation,
NCS shows delayed
conduction
Normal initially NCS normal,
EMG denervation
later
Course and
prognosis
Recovery in majority
within 12 months
Depends on
eitiology
Permanent
disability in 1%
cases