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Parenteral nutrition,bed sores,physiotherapy,nsaids for pain,prevent dvt
acute flaccid paralysis and surveillance
AFP AND SURVEILLANCE
A clinical syndrome characterized by
rapid onset of weakness of limbs
accompanied by weakness of respiratory
muscles and difficulty in swallowing
progressing to maximum severity within
1 to 10 days.
AFP is defined as sudden
onset of weakness of a limb or
paralysis over a period of 15
days in a child less than 15
GLOBAL POLIO ERADICATION INITIATIVE
Results from involvement at any point in the
Common causes include
neuritis,nonpolio enteroviral illnesses,post
Highly infectious enteroviral disease.
Virus transmitted through faeco-oral route
multiplies in the intestine invades the nervous
system causes paralysis.
Age at onset <5 years.
Presents as acute febrile viral meningitis syndrome
with meningeal signs,headache,malaise,GI symptoms.
Motor signs develop within 1 to 4 days
-start with severe myalgias.
-lumbar involvement > cervical.
-spinal cord involvement > brainstem.
-no sensory deficit.
-paralysis within 1 – 2 weeks.
-atrophy appears rapidly,
progresses over several weeks.
Diagnosis by isolation of pathogen from
CSF – neutrophilic pleocytosis
lymphocytes and monocytes
Protein content raises over time,becomes
normal by 6 weeks.
Electrophysiology studies to differentiate polio
from GBS (acute denervation,reduced compound
MRI shows increased T2 weighted signal in
anterior horns and cord swelling.
Polio like illness due to non polio
Non-polio entero viruses like coxsackie
A7,enterovirus 71,japanese B virus,westnile
virus,tick borne encephalitis cause damage to
anterior horn cells resulting in AFP.
Immune attack (IgM,IgG,macrophages,complement
activation) directed at schwann cells,myelin
Axonal injury is secondary to pathological events of
demyelination ( bystander injury )
Synonymous with acute inflammatory
demyelinating polyneuropathy ( AIDP )
Two patterns of axonal involvement
- Involving both sensory and motor neurons
(acute motor-sensory axonal neuropathy)
- Involving only motor neurons
(acute motor axonal neuropathy)
Age at presentation - >3years .
An antecedent infectious disease with
campylobacter jejuni diarrhoea,
vaccinations precede AIDP.
(3days – 6 weeks before the onset of symptoms)
Motor + sensory symptoms
Autonomic symptoms in 30%.
Present with pain in the back,thighs and legs
along with motor weakness starting in legs and
Maximal weakness within 2 weeks.
CSF shows albumino-cytological dissociation.
Electrophysiology shows demyelination of
Slow or block of Nerve conduction velocity.
MRI is normal.
Differentiation from spinal cord
Absence of sensory level
Lack of spinal tenderness
Normal bowel and bladder function
IVIG given (2g/kg/day over 2 days).
-As early as the diagnosis is made.
-A/E : mild flu like symptoms,nausea,headache,malaise.
Plasmapheresis is equally effective.
- 5 exchanges of 50 ml plasma/ kg on alternate days (10
-Cannot be done in patients with cardiovascular
Trial of immunosuppressives,corticosteroids.
Supportive treatment and treatment of complications.
• Regressive : 90 % of patients make a good
Recovery begins 2 to 4 weeks after
progression stops starting from the last
muscles affected till lower limb ( descending
• Chronic Relapsing: Less than 5% of patients.
• Mortality: 3% die from complications.
Caused by inflammation of the spinal cord.
In 60% unknown
In 40% , associated with autoimmune
disorders such as:
– multiple sclerosis
– neuromyelitis optica
– systemic lupus erythematous
– Sjogren’s syndrome
In children <3 years and between 5-14 years.
H/O vaccination with OPV,MMR,Hep
A,DPT,influenza,varicella,Jap B,HiB in the
Earliest symptom is sensory loss or pain in the
Sudden onset of progressive weakness of legs.
Ascends leading to flaccid quadriplegia.
Bowel bladder involvement in 70% .
Maximal weakness by 48hrs.
85% showed a sensory level.
Cranial nerves not involved.
MRI shows focal areas of >> T2 signals in the
Elevated wbc’s , high IgG index in CSF.
Methyl prednisolone (1g/1.73 sq m) iv daily
for a period of 3-5days
Oral prednisolone tapered over 2-3 weeks.
IVIG,immunosuppressants in non responders.
Residual disabilities of
gait,numbness,bladder dysfunction persist in
40-75% of the cases even after many years.
Better outcome if early time of diagnosis,
lower anatomic level,
involvement of only few spinal segments,
older age at onset,
lack of leucocytes in CSF.
• Inflammation of a nerve following an injury.
• Sciatic nerve injury leading to paralysis of the
foot and permanent sequelae following
intramuscular injection in the gluteal region is
POST DIPHTHERITIC POLYNEUROPATHY
Vaccine preventable illness caused by
exotoxin producing strains of
Initial symptoms of low grade fever,sore
throat,neck swelling,nasal twang,ipsilateral
Polyneuropathy occurs as a complication in
20% of patients.
Due to higher release of exotoxin.
The time between initial symptoms and onset
of polyneuropathy is termed as latency
Classic features include acute flaccid
Onset of paralysis is 4 – 6 weeks after the
onset of bulbar signs and symptoms.
Low fatality rate.
Paralysis resolves with time.
Early administration of antitoxin(im/iv)
neutralizes the exotoxin.
Poliomyelitis is targeted for eradication.
Highly sensitive surveillance including
immediate case investigation and specimen
collection are critical for the detection of wild
poliovirus circulation and for documenting the
absence of poliovirus circulation for polio-free
All patients with acute flaccid paralysis should be reported to
Surveillance Medical Officer of World Health Organization.
Every case of AFP within the last 6 months has to be reported.
Additionally, other conditions which need notification are:
• Isolated facial palsy
• Isolated bulbar palsy
• Unproved hypokalemia
• Neck flop
• Floppy baby
• Flaccid hemiplegia
• Postictal weakness (Todd’s paralysis)
• Postdiphretic polyneuritis.
Cases are investigated
within 48 hrs of
notification, by a trained
-Detailed medical history,
examination & investigations are
- Collection & transportation of
- Search for additional cases &
outbreak response in affected
- 60 days follow up examination
- Analysis of laboratory results
- Case classification
Stool Specimen Collection
For every cases of AFP,
2 stool specimens are collected (at least 24
Ideally within 14 days of onset of paralysis
(optimal time period for detection of polio virus)
Should also be collected in any late-reported AFP
case upto 60 days from the day of onset of
Voided stool sample is preferred.
Each specimen should be 8 g each.
Enema or purgatives are not recommended.
Collected in a clean, dry, screw-capped
Labelled and transported in the ‘cold chain’
2 types of cell lines are used:
– RD cell lines (derived from human rhabdomyosarcoma;
favour the growth of all enteroviruses)
– L20B cell lines (favour the growth of only poliovirus)
If cytopathic effects appears in L20B cell line,
the isolate then goes for neutralization test to
determine the serotype (type 1,2 or 3) of the
poliovirus by using appropriate antisera
Intratypic differentiation test is done to
determine whether the particular isolate is
wild poliovirus or vaccine poliovirus.
All wild poliovirus isolates undergo genetic
A case is classified as polio if wild poliovirus is
isolated from the stool specimen.
Others undergo additional investigations & are
classified as compatible with polio or
discarded as nonpolio AFP.