ACUTE FLACCID

PARALYSIS
ACUTE FLACCID PARALYSIS

AFP is a clinical syndrome characterised by rapid onset of weakness,

progressing to maximum severity within several days to weeks.

In the Global Polio Eradication Initiative, AFP is defined as any case of AFP in
children <15 year old or any paralytic illness at any age when polio is
suspected.
COMMON CAUSES OF AFP:

GUILLAIN-BARRE SYNDROME
TRANSVERSE MYELITIS
TRAUMATIC NEURITIS
POST DIPHTHERIC NEUROPATHY
NON POLIO ENTEROVIRAL ILLNESSES
 ACUTE FLACCID PARALYSIS SURVEILLANCE

● All patients with AFP within the last six months should be reported to the
Surveillance Medical Officer of the World Health Organisation.

● Conditions that require notification:-isolated facial palsy, isolated bulbar

palsy, unproven hypokalemia, neck flop, floppy baby, flaccid hemiplegia,
encephalitis, postictal weakness and post diphtheric polyneuritis
4 STEPS-

Finding and reporting children with AFP

Transporting stool samples for analysis
Isolating and identifying poliovirus in laboratory
Mapping the virus to determine its origin
• Cases are immediately investigated within 48hours of notification by a trained medical officer.

• After confirming the case as AFP, the investigator –

 takes medical history

 conducts examination
 collection and transportation of stool specimens for laboratory testing
 search for additional cases and outbreak investigation in the affected community
 60 days follow up examination
 analysis of laboratory results and case classification
• From every case of AFP, 2 stool specimens are collected,ideally within
14days of onset of paralysis and atleast 24hours apart.(voided stool
sample is preferred)

• While the optimal period of detection of poliovirus in the stool is within

14 days of onset of paralysis,specimens maybe collected from any late
reported case upto 60 days from onset of paralysis.
• In cases where voided stool sample is not possible, other methods are included such as
digital extraction(when child is constipated or dies), postmortem stool
collection(contents of large intestine) and use of rectal tube.

• Enema or purgatives are not recommended

• Each specimen should be 8g each(size of an adult thumb), collected in a clean dry,screw

capped container.

• Specimens are collected,labelled and then transported in the ‘cold chain’

OTHER CONDITIONS CAUSING FLACCID
PARALYSIS
 POLIOMYELITIS
It is one of the most common virus infecting children.

• Infectious agent- the poliovirus belongs to the

enterovirus group.
It is an RNA virus with three distinct serotype --type
1,2,3 .
Type 1 is most frequent and type 2 is least common.
Types 1 and 3 cause paralytic polio.

• Reservoir-human beings are the only reservoirs.

• Mode of transmission-person to person.

• Route of transmission- Faeco-oral / respiratory

droplet inhalation / conjunctival contact.
• Incubation period- 7-14 days,but may range from 4 days to 4 weeks.

• Communicability-the poliovirus is highly communicable. The cases are infective

1 week before and 2 weeks after the onset of paralysis.
 PATHOGENESIS
The virus multiplies in the intestine when the immunity in the gut declines.

After the infection the virus is intermittently excreted in stools for up to

2 months or more.

This excretion is maximum just before the paralysis and during the first 2 weeks
after the onset of paralysis.

From the intestines, the virus travels to the regional lymph nodes and then into the
circulation.

The virus infects the nervous system via nerves or blood stream.
CLASSIFICATION
CLASSIFICATION CLINICAL FEATURES

Phase 1 (No CNS

involvement)

Inapparent infection 90% Asymptomatic

Abortive Polio 4-8% ● Low grade fever

● Sore throat
● Nausea
● Vomiting
● Unlocalised abdominal pain
● malaise
Recovery will be complete
 Phase 2 (Frank cases with CNS involvement)

Non paralytic poliomyelitis(aseptic meningitis)

1-2%
● Non specific illness (similar to Intense headache,stiff neck,nuchal spinal
abortive ) signs,recovers within 2-10 days
● Pre paralytic polio Imminent paralysis (back stiffness,head
lag)but soon recovers back to normal.

Paralytic poliomyelitis 0.5-1% There is return of fever(second hump)

● Spinal followed by rapid onset of flaccid paralysis
● Bulbar which is complete within 72 hours.
● Bulbospinal
● Encephalitic forms
 INVESTIGATIONS
These are done if there is AFP to differentiate from other causes.
• Virus isolation - the virus is present in the throat and faeces. The virus can be isolated in the
stools from onset to 8 or more weeks after the paralysis. The rate of detection is more during
the first 2 weeks after the onset of paralysis. Virus isolation can also be done from CSF,
oropharynx and urine in the early stages.
• Serology- rise in titre of polio antibodies in paired sera.
• CSF examination- CSF shows a moderate increase in cells and protein. Sugar and chloride
levels are normal.
This is useful in differentiating polio from other causes of AFP.
TREATMENT
● Started once the diagnosis is suspected. One should not wait for confirmation of diagnosis from the laboratory.
● It varies with the stage of the disease and severity of paralysis.

Phase Treatment

Abortive Polio Analgesics, sedatives, bed-rest

Exertion avoided for 2 weeks

Non-paralytic and paralytic polio Symptomatically treated for 2-3 weeks

- Strict bed rest
- Sedatives
 - Pain relief (massage)
- Hydration and diet to be maintained
- Bowel and Bladder care - laxatives to
relieve constipation
- Antibiotics (IM injections avoided)
- Respiratory support

Treatment after acute phase is over - Physiotherapy

- Surgical management - after 2 years
- Rehabilitation - callipers and crutches
provided
 GUILLAIN-BARRÉ SYNDROME

It is a rapidly progressive, predominantly motor , symmetric polyradiculoneuropathy that leads to

bulbar and respiratory compromise.
There are 4 subtypes:

Acute inflammatory demyelinating polyneuropathy (AIDP)

Acute motor axonal polyneuropathy (AMAN)

Acute motor and sensory axonal neuropathy (AMSN)

Miller Fisher Syndrome (MFS)

It occurs usually as a post infectious phenomenon
About two-thirds patients have an antecedent upper respiratory or gastrointestinal infection
1-6 weeks prior to onset of symptoms.
PREDISPOSING FACTORS

1. Infections :
● Viral infections-EBV(infectious mononucleosis), measles, mumps, rubella,
varicella, cytomegalovirus, influenza, hepatitis B, hepatitis A, HIV
● Bacterial infections-Campylobacter jejuni, brucellosis
2. Systemic lupus erythematosus
3. Hodgkins disease
4. Sarcoidosis
5. Immunosuppression
6. Rabies vaccine
 PATHOGENESIS
● Immunological reaction due to hypersensitivity. It is directed against the
myelin sheath of the peripheral nerves.

● Microscopically, there is endoneural perivascular mononuclear cell

infiltration along with multifocal demyelination involving the peripheral
nerves.

● The demyelination proceeds from root to distal intramuscular nerve

ending.
 CLINICAL FEATURES
● Motor weakness : ascending symmetric paralysis (Landry’s paralysis)
Begins in the lower limbs and progressively involves the trunk, upper limbs,diaphragm,
respiratory,pharyngeal and laryngeal muscles.
1. In the limbs proximal group of muscles is affected more than the distal group.
2. The paralysis progresses gradually over a period of few days to 10 days( max 4 weeks).
Maximum intensity : 2 to 4 weeks
3. Tendon reflexes are absent or diminished.
4. Pain in the muscles is an early feature and may be severe enough to mimic encephalopathy in
children

● Higher functions- consciousness is normal

● Cranial nerve- Bilateral cranial nerve involvement. Facial nerve is frequently involved.
● Other nerves involved are III-VI and IX-XII
 ● No objective sensory symptoms present
● Autonomic nervous system- Dysautonomia : tachycardia, arrhythmia, ileus, bladder
dysfunction, labile blood pressure and impaired thermoregulation.
● The extraocular muscles are spared.
Other rare manifestations include-
❖ Hyponatremia
❖ Decreased higher mental functions
❖ Irritable child
❖ Urinary retention
 DIAGNOSIS
Features required for diagnosis:

• Progressive weakness in more than 1 limb (usually starts in legs)

• Areflexia in weak limbs

Features that strongly support diagnosis:

• Progression of symptoms over days to 4 weeks

• Relative symmetry of symptoms
• Mild sensory symptoms
• Autonomic dysfunction
• Cranial nerve involvement- b/l weakness of facial muscles
• Absence of fever at the onset of neurological symptom
 INVESTIGATIONS
1. CSF ANALYSIS
a. Normal pressure
b. Xanthochromic appearance due to elevated proteins (rise in proteins begins
in late first week and maximises by 2-3 weeks)
c. Cytoalbuminological dissociation- Diagnostic of GBS
d. Glucose normal
e. Culture sterile

2.Nerve conduction velocity studies - axonal or demyelinating neuropathy

3. Serum creatinine kinase - normal or elevated minimally
4. Sural nerve biopsy may show segmental demyelination,focal inflammation,wallerian
degeneration.
5. Serology- serum for EBV and CMV antibodies .
 TREATMENT
1.Supportive Care 2.Immunosuppressive 3.Intravenous 4.Plasmapheresis 5.Prevention
Drugs immunoglobulin of secondary
● Cardiorespiratory ● iv high dose pulse therapy 200-250 mL/kg/body infections
care methylprednisolon weight of plasma is
● Physical therapy e therapy IVIG is the DOC removed on alternate
● Nutrional -iv high dose IG within days in 4-6 sittings
management 3-4 days of onset of within a total period
● Management of weakness. of 8-12 days
neuropathic pain -Dose- 2g/kg over 2-5
● Prevention of days
DVT
● Bowel and
bladder care
HOW TO DIFFERENTIATE AMONG
1. POLIO
2. GUILLAIN BARRE SYNDROME
3. TRAUMATIC NEURITIS
4. TRANSVERSE MYELITIS
THANK
YOU