ACUTE FLACID PARALYSIS

Dr. Muhammad Sajjad Sabir MBBS , DCH , MCPS, FCPSAssist Prof of Paediatrics

ACUTE- Rapid in onset

FLACCIDPARALYSIS

ACUTEFLACCID-PARALYSIS

Droopingwithout spasticity

ACUTEFLACCIDPARALYSIS-Loss of ability to

move a body part

What is AFP?a clinical syndrome characterized by

Rapid onset of weakness including (less frequently) weakness of the muscles of respiration & swallowing

Progressing to maximum severity within several days to weeks

Sudden onset of weakness or paralysis over a period of 15 days in a patient aged less than 15 years age

Flaccid paralysis evolving over hours or a few days

suggests involvement of the lower motor neuron complex

DEFINITION

Anterior horn cells AHC (spinal cord) acute poliomyelitisacute transverse myelitisPeripheral Nervesroots: GBS (post-infectious)toxins: Diphteria, porphyriaN-M junction:botulinum toxin , tick toxinMetabolic: Periodic paralysisMuscular: myositis (rare)A lesion compressing the spinal cord must be ruled out

Syndromes Presenting as AFP (DD)

Most common

Poliomyelitis Guillain-Barre SyndromeTransverse myelitis

Acute Flaccid Paralysis(AFP)Differential diagnosis

AFP in <15yrs age child is

notify-able disease to WHO

Polio surveillance officers—all districts

Poliomyelitis

Poliomyelitis

Polio= gray matter

Myelitis= inflammation of the spinal cord

Most affects children < the age of 5

Global eradication in near future

Etiology Enterovirus (RNA)

Three serotypes: 1, 2, 3

Clinical Classification of Poliomyelitis

Asymptomatic infection (Inapparent) (90- 95%)

Abortive poliomyelitis (5%)

Non- paralytic poliomyelitis (aseptic meningitis) (1- 4%)

Paralytic poliomyelitis (0.1-1%) Spinal form Bulbar form Bulbospinal form Encephalitic form

Poliovirus infections may follow one of several courses

Paralytic poliomyelitis

Prodromal period Preparalytic period Paralytic period Convalescent period Sequela period

Commonly known as PolioOnly 1/1,000 to 1/100 (0.1% to 1%) infected individuals develop paralytic disease

Preparalytic period

High fever Cutaneous hyperesthesia or paresthesia in the

extremities Muscular pain is common Muscles are tender even to gentle palpation Severe headache & vomiting Lethargy Signs of meningeal irritation

(neck stiffness, Kerning & Brudzinski signs positive)

Paralytic poliomyelitis

Weakness of one or more muscle groups (spinal or cranial)

Loose & Floppy Limbs, hypotonia-- Flaccid paralysis

Asymmetric paralysis

Paralysis is complete – fever normalizes

Weakness persists

Respiratory & vasomotor changes

Bladder & bowel dysfunction

Tendon reflexes are absent with paralysis.

Sensory defects do not occur in poliomyelitis

Paralytic poliomyelitis Paralytic period

Spinal type: most common

Paralysis of extremities (muscle groups ) leg > arm proximal > distal Asymmetric paralysis

Paralysis of diaphragmatic & intercostal

muscles affects respiratory movement

Paralysis of abdominal muscle -- stubborn constipation

Paralytic poliomyelitis

Sequela Poliomyelitis may lead to severe asymmetrical

persistent paralysismuscular atrophies deformities of limbs

Paralytic poliomyelitis

Diagnosis

WHO recommends diagnosis of poliomyelitis be confirmed by isolation and identification of poliovirus in the stool, with specific identification of wild-type and vaccine type strains

Polioviruses may be isolated from 80 to 90% of acutely ill patients

whereas less than 20% may yield virus within 3-4 wk after onset of paralysis

Identification of poliovirus in stool

Stool examination

Two samples 24 hr apart

Within 14 days of onset of paralysis

8-10 grams or thumb size

Collected in a clean wide mouth bottle – (plastic or glass) with screw cap

Sample stored below 8°C

No dessication or leakage till received at WHO Accredited Lab

Collection of sample

Laboratory FindingsCerebrospinal fluid

aseptic menigitis pleocytosis: 50~500×109/L protein: normal or slightly increase glucose and chloride; normal albuminocytologic dissociation

Serological TestsNeutralizing antibodies (IgG) Antibodies to C antigen (IgM) Anti-D antibodies

Management

Isolation

Rest in bed

Neutral positioning of the limbs

Good nursing

No I.M Injection or surgery

Relief of pain and spasm of muscles

Physiotherapy

Treatment symptomatic and supportive

Prevention

control of source of infection: isolation: 40 days after the onset of illness

protection of susceptible population- vaccination : attenuated live vaccine by

Oral -- OPV

killed virus vaccine Injectable -- IPV

Guillain-Barre Syndrome (GBS)

Guillain-Barre Syndrome (GBS)

Post-infectious

acute, rapidly progressing

ascending

potentially fatal form of polyneuritis

involving mainly motor but sometimes also sensory and autonomic nervesalso known as: Acute inflammatory demyelinating polyneuropathy (AIDP)

Transverse MylitisA neurological condition in which the spinal cord is inflamed.

The inflammation damages nerve fibers, and causes them to lose their myelin coating leading to decreased electrical conductivity in the central nervous system.

2nd most common cause of symmetric AFP

Segmental dysfunction of spinal cord without evidence of spinal cord compression

Cause is either:a direct viral infection

or an autoimmune disease

Transverse Mylitis

Transverse MylitisParalysis usually affect only Lower Limbs (Paraplegia)

Rare above C-5→quadriplegia

Initially flaccid but gradual change to spasticity over few weeks

Sensory loss (with sensory level on the trunk) and

Autonomic disturbance (urinary retention and stool incontinence) usually present

MRI spine

Treatment Intravenous SteroidsHigh-dose I.V methyl-prednisolone for 3-5 days

Plasma Electrophoresis

Prolonged course

Complete recovery in 60% of cases

Botulism

BotulismIt’s a toxic neuromuscular blockade caused by Clostridium botulinum (anaerobic gram positive)

According to the type of infection, there are 3 types Infant B. due to exposure to soil , honeyFood-borne B. due to ingestion improperly

home preserved foods containing the toxinsWound B. due to wound contamination with

the organism

All three types of botulism result in

symmetric

descending

Flaccid paralysis of motor and autonomic nerves always beginning with cranial nerves

These symptoms preceded by constipation (infant botulism)

If untreated - paralysis of respiratory → death

Botulism

Pseudoparalysis

PseudoparalysisNot a true paralysis

May follow Unrecognized traumaFractureSprainToxic synovitis of hip or knee Acute osteomylitis

Careful exam show focal tenderness

Usually painful limping gait

Neurological exam → normal

Acute spinal cord compression

Trauma to the backSpinal epidural abscessVascular anomalies of the cordSpinal cord tumors

Clinically difficult to differentiate from Transverse Mylitis

CT scan/ MRI spine: Sensitive Can show nature of obstruction

Acute spinal cord compression

Prognosis & complications of AFPAccording to cause

Poliomyelitis

Respiratory

death

Limb atrophy

GBS

Respiratory

autonomic crises

residual weakness

death

Acute transverse myelitis

Residual deficits --bowel and bladder

dysfunction & weakness - lower Limbs

Poliomyelitis Guillain-Barre Syndrome

Transverse myelitis

Symmetry of

paralysis

asymmetrical symmetrical symmetrical

Type involves muscle groups

ascending paralysis

symmetrical hypotonia of lower limbs

sensation sensations intact

loss of sensation

"sensory level" below which sensation to pain or light touch is impaired

Poliomyelitis Guillain-Barre

Syndrome

Transverse myelitis

Cause Polio virusAnterior horn cells

Acute inflamatoryPoly-radiculopathy

a direct viral infection

or an autoimmune disease

Paralysis

Asymmetric symmetrical symmetrical

Proximal >distal

ascending Hypotonic lower limbs

Progression 24-48hrs Days-4weeks Hrs to days

Sensory changes No Yes Yes(Sensory level)

Muscle tenderness yes No No

CSF Cells ↑Proteins ↑

Cells = normal

Proteins ↑Cells ↑

Residual paralysis yes + yes