Acute Flaccid Paralysis Lecture MBBS

2. ACUTE FLACID PARALYSIS
Dr. Muhammad Sajjad Sabir
MBBS, DCH , MCPS, FCPS
Assist Prof of Paediatrics

3. ACUTE- Rapid in onset
FLACCID
PARALYSIS

4. ACUTE
FLACCID-
PARALYSIS
Drooping
without spasticity

5. ACUTE
FLACCID
PARALYSIS-Loss of ability to
move a body part

6. 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

7. 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

8. Anterior horn cells AHC (spinal cord)
 acute poliomyelitis
acute transverse myelitis
Peripheral Nerves
roots: GBS (post-infectious)
toxins: Diphteria, porphyria
N-M junction:
botulinum toxin , tick toxin
Metabolic: Periodic paralysis
Muscular: myositis (rare)
A lesion compressing the spinal cord must be ruled out
Syndromes Presenting as AFP (DD)

10. Most common
 Poliomyelitis
 Guillain-Barre Syndrome
Transverse myelitis
Acute Flaccid Paralysis(AFP)
Differential diagnosis

11. AFP in <15yrs age child is
notify-able disease to WHO
Polio surveillance officers—all
districts

12. Poliomyeliti
s

13. 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

14. 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

15. Paralytic poliomyelitis
 Prodromal period
 Preparalytic period
 Paralytic period
 Convalescent period
 Sequela period
Commonly known as Polio
Only 1/1,000 to 1/100 (0.1% to 1%) infected
individuals develop paralytic disease

16. 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

17. 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

18. 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

19. Sequela
Poliomyelitis may lead to severe asymmetrical
 persistent paralysis
muscular atrophies
deformities of limbs
Paralytic poliomyelitis

20. 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

21. 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

22. Laboratory Findings
Cerebrospinal fluid
aseptic menigitis
 pleocytosis: 50~500×109
/L
 protein: normal or slightly increase
 glucose and chloride; normal
 albuminocytologic dissociation
Serological Tests
Neutralizing antibodies (IgG)
Antibodies to C antigen (IgM)
 Anti-D antibodies

23. 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

24. 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

25. Guillain-Barre Syndrome
(GBS)

26. Guillain-Barre Syndrome
(GBS)
Post-infectious
acute, rapidly progressing
ascending
potentially fatal form of polyneuritis
involving mainly motor but sometimes also
sensory and autonomic nerves
also known as: Acute inflammatory demyelinating
polyneuropathy (AIDP)

31. Transverse Mylitis
A 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.

32. 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

33. Transverse Mylitis
Paralysis 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

34. MRI spine

35. Treatment
Intravenous Steroids
High-dose I.V methyl-prednisolone for 3-5 days
Plasma Electrophoresis
Prolonged course
Complete recovery in 60% of cases

36. Botulism

37. Botulism
It’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 , honey
Food-borne B. due to ingestion improperly
home preserved foods containing the toxins
Wound B. due to wound contamination with
the organism

38. 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

39. Pseudoparalysis

40. Pseudoparalysis
Not a true paralysis
May follow
Unrecognized trauma
Fracture
Sprain
Toxic synovitis of hip or knee
Acute osteomylitis
Careful exam show focal tenderness
Usually painful limping gait
Neurological exam → normal

41. Acute spinal cord
compression

42. Trauma to the back
Spinal epidural abscess
Vascular anomalies of the cord
Spinal cord tumors
Clinically difficult to differentiate from
Transverse Mylitis
CT scan/ MRI spine:
 Sensitive
 Can show nature of obstruction
Acute spinal cord compression

43. Prognosis & complications of AFP
According 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

44. 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

45. Poliomyelitis Guillain-
Barre
Syndrome
Transverse
myelitis
Cause Polio virus
Anterior horn
cells
Acute
inflamatory
Poly-
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