Definition, Etiology, Classification, Poliomyelitis, Guillain- Barrie syndrome, Transverse myelitis ,Approach to a case of AFP, who afp surviallance

1. A
F
P
By - Dr. Vinaykumar S Appannavar

2. • Definition
• Etiology
• Classification
• Poliomyelitis
• Guillain- Barrie syndrome
• Transverse myelitis
• Approach to a case of AFP
2 VSA

3. 3
• Sudden onset of weakness or paralysis in a previously normal limb over a
period of 15 days in a patient
AFP syndrome is characterized by rapid onset of weakness of an
individual’s extremities, often including weakness of the muscles of respiration
and swallowing, progression to maximum severity within 1-10days.
• Acute - Sudden onset, Rapid progression
• Flaccid - Floppy or Soft and yielding to passive stretching at anytime during the illness.
• Paralysis - is loss of strength of muscles
VSA

4. 4
1. Poliovirus
2. Non-Polio Enterovirus
3. Neuroviruses – Herpes Viruses, WNV,
Rabies virus
4. Clostridium botulinum
5. Cornybacterium diptheriae
1. Guillain - Barre Syndrome
2. Transverse Myelitis
3. Traumatic Neuritis
4. Muscle disorder
5. Disorder of neuromuscular
transmission
VSA

5. 5 VSA
Poliovirus
Guillain - Barre Syndrome
Transverse Myelitis
Traumatic Neuritis
Non-Polio Enterovirus
Neuroviruses – Herpes Viruses,
WNV, Rabies virus
Clostridium botulinum
Cornybacterium diptheriae
Poliovirus

6. 6 VSA
Acute transverse
myelitis
Poliomyelitis,
Enterovirus
Myelin :AIDP

7. 7
Grey matter; inflammation of the spinal cord
VSA

8. 8
• CAPSID – 60 subunits each
of four proteins VP1- VP4
• Icosahedral symmetry
• C & D antigens
• Stable at acidic pH(3-5)
• Stabilized by MgCl2 against
thermal inactivation
• Inactivated by chlorine and
oxidizing agenst
VSA

9. 9
• 3 serotypes of poliovirus (genus
Enterovirus).
• Type 1 most frequently
associated with epidemics.
• Types 2 and 3 usually
associated with vaccine
associated paralytic polio (VAPP).
• Polioviruses spread from the
intestinal tract to the central
nervous system, where they
cause aseptic meningitis and
poliomyelitis.
VSA
ENTEROVIRUSESS
POLIO
VIRUSES
COXSAKIE A VIRUS
ECHO VIRUSES
COXSAKIE B VIRUS
OTHER [68,69,70, 71]
• Type 1
• Type 2
• Type 3

10. ADD A FOOTER 10
• Humans are the only known reservoir
• Spread is by Feco-oral route

11. 11
• Incubation period of 7 to 14 days.
• Poliovirus receptor – CD155
• The RNA is translated to produce proteins responsible for
replication of the RNA, shutoff of host cell protein synthesis,
and synthesis of structural elements that compose the
capsid
• In the contact host, wild-type and vaccine strains of
polioviruses gain host entry via the gastrointestinal tract.
• Vaccine strains of polioviruses do not replicate in the CNS,
a feature that accounts for the safety of the live-attenuated
vaccine
• The poliovirus primarily infects motor neuron cells in the
spinal cord (the anterior horn cells ) and the medulla
oblongata (the cranial nerve nuclei) VSA

12. 12
• 3 months-16 years
• Improved sanitation led to many less infants being exposed to poliovirus.
• When exposure occurred later and the individuals were not protected by maternal antibodies, there
were polio epidemics.
Now rare; present in:
a) Endemic settings.
b) Small outbreaks in areas.
c) Rarely as vaccine-associated paralytic polio (VAPP) cases
Endemic countries: Afghanistan, India, Nigeria and Pakistan VSA

13. 13
• Age
• Poor sanitation and hygiene
• Poverty
• Unimmunized status
• Pregnancy
• Tonsillectomy: a risk factor for bulbar paralysis
• Intramuscular injections or trauma
VSA

14. 14
• Poliovirus infections with wild-type virus may follow 1 of several courses: inapparent
infection, which occurs in 90–95% of cases and causes no disease and no sequelae;
abortive poliomyelitis; nonparalytic poliomyelitis; or paralytic poliomyelitis.
VSA
POLIO
VIRUS
Inapparent infection
Abortive poliomyelitis
Nonparalytic poliomyelitis
Paralytic poliomyelitis
(1) Spinal paralytic
poliomyelitis
(2) Bulbar poliomyelitis
(3) Polio encephalitis

15. 15
• In approximately 5% of patients, a nonspecific influenza-like syndrome occurs 1-2 wk
after infection.
• Fever, malaise, anorexia, and headache are prominent features, and there may be sore
throat and abdominal or muscular pain.
• Vomiting occurs irregularly. The illness is lasting up to 2-3 days.
• The physical examination may be normal or may reveal nonspecific pharyngitis,
abdominal or muscular tenderness, and weakness.
• Recovery is complete, and no neurologic signs or sequelae develop.
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16. 16
• 1% of patients infected with wild-type poliovirus,
• Signs of abortive poliomyelitis + more intense headache, nausea, and vomiting, as well
as soreness and stiffness of the posterior muscles of the neck, trunk, and limbs.
• Nuchal rigidity is the basis for the diagnosis of nonparalytic poliomyelitis
• The superficial reflexes, the cremasteric and abdominal reflexes, and the reflexes of the
spinal and gluteal muscles are usually the first to diminish.
VSA

17. 17
• 0.1% of persons
• 3 clinically recognizable syndromes
(1)spinal paralytic poliomyelitis
(2)Bulbar poliomyelitis,
(3) Polio encephalitis.
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18. 18
• A clinical entity without apparent involvement of the spinal cord
• The clinical findings seen with bulbar poliomyelitis with respiratory difficulty (other than paralysis of extraocular,
facial, and masticatory muscles) include
(1) nasal twang to the voice or cry caused by palatal and pharyngeal weakness
(2) inability to swallow smoothly, resulting in accumulation of saliva in the pharynx, indicating partial immobility
(3) accumulated pharyngeal secretions, which may cause irregular
(4) absence of effective coughing
(5) nasal regurgitation of saliva and fluids as a result of palatal paralysis
(6) deviation of the palate, uvula, or tongue
(7) involvement of vital centers in the medulla
(8) paralysis of 1 or both vocal cords, causing hoarseness, aphonia
(9) the rope sign, an acute angulation between the chin and larynx caused by weakness of the
hyoid muscles (the hyoid bone is pulled posteriorly, narrowing the hypopharyngeal inlet).
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19. 19
• The clinical findings associated with involvement of the respiratory muscles include
(1) Anxious expression
(2) Inability to speak without frequent pauses, resulting in short, jerky, breathless sentences
(3) Increased respiratory rate
(4) Movement of the ala nasi and of the accessory muscles of respiration
(5) Inability to cough or sniff with full depth
(6) Paradoxical abdominal movements caused by diaphragmatic immobility caused by spasm or
weakness of 1 or both leaves
(7) Relative immobility of the intercostal spaces, which may be segmental, unilateral, or bilateral.
When the arms are weak, and especially when deltoid paralysis occurs, there may be impending
respiratory paralysis because the phrenic nerve nuclei are in adjacent areas of the spinal cord
VSA

20. 20
• Based on the clinical presentation
Signs of LMN palsy
• Paralysis or paresis :
• Symmetrical/asymmetrical
• Proximal/distal
• Hypotonia
• Reduced muscle power
• DTR : absent or sluggish
• Plantar reflex: flexor (extensor response normal upto 2yrs.)
• Atrophy & wasting of muscles
VSA

21. • Spasticity : most apparent in flexors of UL & extensors of LL
• Exaggerated deep tendon reflexes
• Ankle clonus
• In initial stages there may be hypotonia with normal or brisk reflexes
• Plantar reflex : extensor
VSA

22. • History
• Clinical Examination
• Investigation
• Electro – Physiological studies
• Management
• Follow-up
VSA

23. Neurological examinationGeneral examination Systemic examination
General
observation
Posture
and gait
Sensory
system
Cerebellar
systemReflexes
Motor
system
Cranial
nerves
Appearance,
activity,
interaction with
parents
Consciousness,
Response to
stimuli ,
Looking around
while walking/
crawling
1.Circumduction
2.Hyperextension
of knee
3.Ataxic gait
4.Waddling gait
5.Slapping foot
drop
6.Toe walking
7.Dragging of the
limb while crawling
8.Varus / valgus
deformity of foot
1.Oculomotor
nerve
2.Trigeminal
nerve
3. Facial
nerve{LMN}
I4.X & X:
Muscles of
pharynx,
larynx & palate
1.Touch
2.Pain
3.Pressure
1.Finger nose test
2.Heel Knee test
3.Ataxia
4.Disdiadochokine
sis
5.Nystagmus
1.Superficial
reflexes
2. Deep
reflexes
1.Bulk
2.Tone
3.Muscle
power

24. Measurements : Midarm,
midthigh, forearm, midcalf
Bulk
Inspection :
• Look for obvious
atrophy/hypertrophy
• Compare with other
side
• Look for small muscles
wasting of hand, tremor,
fasciculation
• Look for deformity/
contracture.
Tone
• Tone is a state of partial
contraction of a muscle
• Assessed by passive movement
at joints
• Look for position & posture of
limb
Hypotonic leg : abducted,
flexed, externally rotated at hip,
flexed at knee with foot in
plantar flexion
• Palpation : feel for flabby,
rubbery, stiffness
• Note the resistance to passive
movement
Muscle power
0 = no detectable contraction
1 = flicker of movement
2 = active movement eliminating gravity
3 = active movements against gravity
4 = active movement against some
resistance
5 = active movement against good
resistance
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25. 25
Grades
Reflexes are recorded as :
• Absent = absent or 0
• Diminished =  or +
• Normal = N or ++
• Brisk =  or +++
• Exaggerated =  or ++++ with clonus
Reflex Site of
Stimulation
Normal response CNS
segment
Biceps Biceps tendon Contraction of biceps C5-6
Triceps Triceps tendon Extension of elbow C6-8
Brachio-
radialis
Styloid process Flexion of elbow &
pronation of forearm
C5-6
Knee Patellar tendon Extension of knee L2-4
Ankle Achilles tendon Plantar flexion of ankle L5,S1
Reflex Normal response CNS segment
Upper
abdominal
Umbilicus moves up &
towards the area
stroked + contraction
of abd. wall
T7-9
Lower
abdominal
Umbilicus moves
down
T11-12
Cremastric Scrotum elevates T12L1
Plantar Flexion big toe S1
VSA

26. 26
• Virus recovery from stool, throat washing, blood.
• Polymerase chain reaction amplification of poliovirus RNA from CSF or serologically, by comparing
viral titers in acute and convalescent sera.
• Electrodiagnostic investigations reveal normal sensory nerve studies.
• Motor nerve studies: show normal to mildly slowed conduction velocities and low to normal
amplitudes.
• MRI may be helpful to evaluate involvement of anterior horn of the spinal cord or other findings.
VSA

27. 27
• The management is supportive and aimed at limiting progression of disease
• Patients with the nonparalytic and mildly paralytic forms of poliomyelitis may be treated at home.
• All intramuscular injections and surgical procedures are contraindicated during the acute phase of
the illness, especially in the 1st wk of illness, because they might result in progression of disease.
• Mainly supportive: pain relief and physical therapy for muscle spasms.
• Patients with bulbar involvement require close monitoring of cardiovascular status and autonomic
dysfunction.
• Mechanical ventilation: Respiratory failure.
• Treatment of complications.
VSA

28. 28
• Acute gastric dilation
• Melena severe enough to require transfusion may result from single or multiple superficial intestinal
erosions
• Mild hypertension for days or weeks is common.
• In the later stages, because of immobilization, hypertension may occur along with hypercalcemia,
nephrocalcinosis, and vascular lesions.
• Dimness of vision, headache, and a lightheaded feeling
• Myocarditis
• Acute pulmonary edema occurs occasionally, particularly in patients with arterial hypertension.
• Hypercalcemia occurs because of skeletal decalcification that begins soon after immobilization
and results in hypercalciuria.
VSA

29. 29
• About two-thirds of patients with acute flaccid paralysis do not regain full strength.
• The more severe the acute weakness, the greater the chance of residual deficits,
Bulbar squeals are rare.
• The mortality was 5 to 10% in the era of epidemics, and approached 50% for those
with bulbar involvement because of cardiovascular and respiratory complications.
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30. 30
• Jonas Salk created the inactivated poliovirus vaccine (IPV), using killed virus in 1952.
• The Sabin oral poliovirus vaccine (OPV), live attenuated virus, proved successful in 1960.
• Enhanced IPV, and the live-attenuated OPV, Induce production of antibodies against the
3 strains of poliovirus.
• IPV elicits higher serum IgG antibody titers, but the OPV also induces significantly greater
mucosal IgA immunity in the oropharynx and gastrointestinal tract, which limits replication
of the wild poliovirus at these sites.
• Live vaccine may undergo reversion to neurovirulence -The overall risk for recipients
varies from 1 case per 750,000 immunized infants in the United States to 1 in 143,000
immunized infants in India.
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31. 31
• As of January 2000, the IPV-only schedule is recommended for routine polio vaccination in
the United States. All children should receive 4 doses of IPV, at 2 mo, 4 mo, 6-18 mo, and
4-6 yr of age.
• To achieve this goal, the WHO used 4 basic strategies:
Routine immunization,
National Immunization Days,
Acute flaccid paralysis surveillance, and
Mop-up immunization.
This strategy has resulted in a >99% decline in poliomyelitis cases; in early 2002, there were only 10
countries in the world endemic for poliomyelitis. In 2012 there were the fewest cases of poliomyelitis
ever, and the virus was endemic in only 3 countries (Afghanistan, Pakistan, and Nigeria)
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32. 32
• This plan included the withdrawal of trivalent OPV (tOPV) with bivalent OPV (bOPV) in
all countries by 2016 and the introduction of initially 1 dose of IPV followed by the
replacement of bOPV with IPV in all countries of the world by 2019.
• As long as the OPV is being used, there is the potential that vaccine-derived poliovirus
(VDPV) will acquire the neurovirulent phenotype and transmission characteristics of the
wild-type polioviruses
• VDPV emerges from the OPV because of continuous replication in immunodeficient
persons (iVDPV) or by circulation in populations with low vaccine coverage (cVDPVs).
• The risk was highest with the type 2 strain. Between 2000 and 2012, 90% of the 750
paralytic cases of cVDPV and 40% of VAPP were caused by type 2 strains.
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33. 33
A postinfectious polyneuropathy
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34. 34
• GBS is the most common cause of acute flaccid paralysis in healthy infants and children
• It has an annual incidence of 0.6 to 2.4 cases per 100,000 population and occurs at all
ages and in both sexes.
• Occurs rarely in children younger than two years of age, but can occur in infants.
• Males are affected approximately 1.5 times more often than females in all age groups.
VSA

35. 35

36. 36
• The onset of weakness usually follows a nonspecific gastrointestinal or respiratory
infection by approximately 10 days
• Initial symptoms include numbness and paresthesia, followed by weakness
• Radicular back pain and myalgia are common in the initial stages; affected children can
be very irritable.
• Weakness usually begins in the lower extremities and progressively involves the trunk,
the upper limbs, and finally the bulbar muscles, but weakness is sometimes proximally
prominent
• Extraocular muscle involvement is rare, but many patients develop facial weakness
• Approximately 60% of children lose the ability to walk at some point in their illness; a
small proportion progress to flaccid tetraplegia.
The maximal severity of weakness is reached by 4 week after onset
VSA

37. ADD A FOOTER 37 VSA

38. ADD A FOOTER 38 VSA

39. 39
• Bulbar involvement occurs in about 50% of cases and can result in respiratory
insufficiency
• Dysphagia and facial weakness can be signs of impending respiratory failure, interfere
with saliva control and swallowing, and increase the risk of aspiration.
• Vocal cord paralysis may cause dyspnea or a hoarse voice. Severe bulbar and
respiratory muscle involvement can lead to death if GBS is not recognized and treated.
• The tendon reflexes are lost in GBS, usually early in the course, but are sometimes
preserved until later; areflexia is more common but hyporeflexia may be seen.
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40. 40
• CSF studies are helpful in diagnosing GBS.
• The CSF protein is usually elevated to more than twice the upper limit of normal, the
glucose level is normal, and there is no pleocytosis; there should be fewer than 10 white
blood cells/mm3 .
• Bacterial cultures are negative, whereas viral studies rarely isolate specific viruses.
• The dissociation between high CSF protein and a lack of cellular response
(cytoalbuminologic dissociation) in a patient with an acute or subacute polyneuropathy
is essentially diagnostic of GBS.
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41. 41
• On magnetic resonance imaging (MRI) of the spinal cord in
GBS, typical findings include thickening of the cauda equina
and intrathecal nerve roots with gadolinium enhancement
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42. 42
FEATURES NEEDED FOR DIAGNOSIS OF GUILLAIN-BARRÉ SYNDROME IN CLINICAL
PRACTICE
• Progressive weakness in legs and arms (sometimes initially only in legs).
• Areflexia (or decreased tendon reflexes) in weak limbs.
ADDITIONAL SYMPTOMS
• Progressive phase lasts days to 4 wk (often 2 wk).
• Relative symmetry.
• Mild sensory symptoms or signs (not present in acute motor axonal neuropathy).
• Cranial nerve involvement, especially bilateral weakness of facial muscles.
• Autonomic dysfunction.
• Pain (common)
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43. 43
• CSF: increased number of mononuclear cells or polymorphonuclear cells (>50 cells/µL).
• Severe pulmonary dysfunction with little or no limb weakness at onset.
• Severe sensory signs with little or no weakness at onset.
• Bladder or bowel dysfunction at onset.
• Fever at onset.
• Sharp spinal cord sensory level.
• Marked, persistent asymmetry of weakness.
• Persistent bladder or bowel dysfunction.
• Slow progression of weakness and without respiratory involvement (consider subacute
inflammatory demyelinating polyneuropathy or acute-onset chronic inflammatory
demyelinating polyneuropathy)
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44. 44
Critical care monitoring autonomic and
respiratory dysfunction.
• Children with the following should be
admitted to PICU:
a. Flaccid quadriparesis
b. Rapidly progressive weakness
c. Reduced vital capacity (≤20 mL/kg)
d. Bulbar palsy
e. Autonomic cardiovascular instability
N.B: Sedation and neuromuscular blockade
should be avoided in ventilated patients
because they obscure the course of the
illness

45. 45
Risk factors for respiratory failure in GBS:
Cranial nerve involvement.
Short time from preceding respiratory illness.
Rapid progression over less than 7 days.
Elevated CSF protein in the first week.
Severe weakness: unable to lift elbows above the bed unable to lift head above the bed
unable to stand.
20% of children with GBS require mechanical ventilation for respiratory failure.
VSA

46. 46
Immune modulatory therapy:
Intravenous Immunoglobulins Plasmapheresis
• IVIG is preferred to plasma exchange in children because of the relative safety and ease
of administration, although it has not been shown to have better results.
• Both therapies have been shown to shorten recovery time by as much 50%.
• Combining plasma exchange and IVIG neither improved outcomes nor shortened the
duration of illness.
• IVIG and plasma exchange are not recommended for ambulatory children with GBS who
have mild disease or for children whose symptoms have stabilized
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47. 47
• One regimen includes daily IVIG for 5 days at a dose of 0.4 gm/kg/day, which results in
an improvement within a mean of 2 to 3 days after the start of therapy.
• Other regimen includes use 2 gm/kg of IVIG given as a single dose or 1gm/kg/day for
2 days.
• Studies in children indicate that plasmapheresis may decrease the severity and shorten
the duration of GBS.
• It is most beneficial when started within 7 days of the onset of symptoms but is still
beneficial in patients treated up to 30 days after disease onset.
VSA

48. 48
• In general, the prognosis in affected children is better than adults.
• Recurrences are uncommon but can occur in children. Some may have a chronic
progressive course, whereas others may show recurrences or relapses.
• At long-term follow up, 93% were free of symptoms, and the remainder were able to walk
unaided.
• 50% are ambulatory by 6 mo, 70% walk within a year of onset of the disease.
• Mortality is approximately 3 to 4%, and usually is secondary to autonomic dysfunction
and respiratory failure.
VSA

49. 49 VSA

50. 50
• Transverse myelitis (TM) is a condition characterized by rapid development of both motor
and sensory deficits at any level of the spinal cord.
• TM presents acutely as either partial or complete cord involvement with bilateral signs
and in adults and older children with a clear sensory level
• TM has multiple causes and can be idiopathic or secondary to either an immune-
mediated condition (postinfectious or antibody driven) or as a result of direct infection
(infectious myelitis)
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51. 51
• TM is more common in adults but is estimated to affect around 2 per million children per
year.
• A bimodal age distribution is observed in those younger than 5 yr and older than 10 yr.
• Although they represent a small subset, children 5 yr of age and younger develop spinal
cord dysfunction over hours to a few days.
• The clinical loss of function is often severe and may seem complete. Although a slow
recovery (weeks to months) is common in these cases, it is likely to be incomplete.
• The likelihood of independent ambulation in young children is approximately 40%.
VSA

52. 52
• Presumed autoimmune mediated
inflammation and demyelination of
the spinal cord.
• Postinfectious etiology largely
predominates in children
• An immunization history within the
few weeks preceding neurologic
difficulties.
VSA

53. ADD A FOOTER 53 VSA

54. 54
• TM is often preceded within the previous 1-3 wk by a mild nonspecific illness, minimal
trauma, or perhaps an immunization
• Depending on its severity, the condition progresses to numbness, anesthesia, ataxia,
areflexia, and motor weakness in the truncal and appendicular musculature at or distal to
the lesion
• Paralysis begins as flaccidity (paraparesis, tetraparesis), but over a few weeks, spasticity
develops and is evidenced by hyperreflexia and clonus
• Urinary retention is a common and early finding
VSA

55. 55
• Tenderness over the spine may point to trauma or infection.
• Increased tone, spastic weakness, legs more than arms
• Reflexes are usually brisk, with positive Babinski sign.
• Sensory ataxia, a sensory level.
• Sphincter dysfunction
VSA

56. ADD A FOOTER 56 VSA

57. 57
• Bilateral (not necessarily symmetric) sensorimotor
and autonomic spinal cord dysfunction
• Clearly defined sensory level.
• Progression of clinical deficits between 4 hours
and 21 days after symptom onset.
• Demonstration of spinal cord inflammation:
cerebrospinal fluid pleocytosis or elevated IgG index
or MRI revealing a gadolinium-enhancing cord
lesion.
• Exclusion of compressive, postradiation,
neoplastic, and vascular causes.
VSA

58. ADD A FOOTER 58 VSA

59. 59
• There are no standards for the treatment of TM
• Symptomatic management of bowel and bladder dysfunction.
• Management of respiratory, cardiovascular & autonomic dysfunction.
1. IV methylprednisolone 2. IV immunoglobulin (IVIG) or plasmapheresis.
• Cyclophosphamide has been reported to be useful in myelitis associated with systemic
inflammatory diseases
• Physical and occupational therapy may help promote functional recovery and prevent
contractures.
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60. 60
• Older children with acute TM have a better outcome than adults, with nearly 50% making
a good recovery by 2 yr.
• 40% recover incompletely.
• 10% don’t recover.
• The most common sequelae in the remaining 50% are sensory problems and bladder
dysfunction.
• Rapid progression, back pain, and spinal shock predict poor recovery.
• The treatment of acute flaccid myelitis has included steroids and IVIG; despite these
therapies, patients often have an incomplete recovery
VSA

61. 61 VSA

62. 62
• History
• Clinical Examination
• Investigation
• CSF Studies - If required
• Electro – Physiological studies
• Management
• Follow-up
VSA

63. Neurological examinationGeneral examination Systemic examination
General
observation
Posture
and gait
Sensory
system
Cerebellar
systemReflexes
Motor
system
Cranial
nerves
Appearance,
activity,
interaction with
parents
Consciousness,
Response to
stimuli ,
Looking around
while walking/
crawling
1.Circumduction
2.Hyperextension
of knee
3.Ataxic gait
4.Waddling gait
5.Slapping foot
drop
6.Toe walking
7.Dragging of the
limb while crawling
8.Varus / valgus
deformity of foot
1.Oculomotor
nerve
2.Trigeminal
nerve
3. Facial
nerve{LMN}
I4.X & X:
Muscles of
pharynx,
larynx & palate
1.Touch
2.Pain
3.Pressure
1.Finger nose test
2.Heel Knee test
3.Ataxia
4.Disdiadochokine
sis
5.Nystagmus
1.Superficial
reflexes
2. Deep
reflexes
1.Bulk
2.Tone
3.Muscle
power

64. ADD A FOOTER 64 VSA

65. 65
Hypotonic
postures
Trunk
Weakness

66. 66
Paralysis Right
Lower Limb
Neck Flop
VSA

67. 67
Paresis Both
Lower Limbs
VSA

68. 68
Continuous scrutiny of factors that determine the occurrence and distribution of disease
and other conditions of ill health.
 Surveillance includes data collection, analysis, interpretation and distribution of relevant
information for action
• To know when the disease occurs (Time)
• To know where the disease is (Place)
• To know who are affected (Person)
• To drive immunization activities
• To know when virus transmission is gone!
• Wild virus
• VDPV
• Vaccine virus
VSA

69. State
• State EPI Officer
District
• District Immunization Officer
Block/UA
• Senior Medical Officer
• Block Nodal Officer and MOIC
• Urban Zonal Nodal Officers
Supervision
Policy interventions
Supervision
Performance review
Field operations
VSA

70. Reporting
units
(RU)
Informer
units
(IU)
Reporting
Sites
(RS)
• Reporting Units:
Government/private hospitals that:
• Maintain documentation of all its patients
• Required to send weekly “zero report” even if there are no VPD
cases
• Informer Units:
Health facilities that:
• Usually do not maintain detailed documentation of its
patients
• Not required to send zero report
• Report only when they see a VPD case
Every reporting site is given a unique ID at district level VSA

71. • It is an ongoing activity in which a designated official usually external
to the health facility visits regularly and collects data from
individuals, registers, medical records or log books at a reporting
site to ensure that no VPD case is missed from reporting
• This is critical to maintain sensitivity !
VSA

72. 72
 RCH Officer
 District Surveillance Officer (DSO)
 Taluk Health Officer (THO)
 Nodal Medical Officer
 Medical offier
 should regularly visit the hospitals/Practitioners to ensure that all AFP and Suspected
Measles cases are reported, encourage reporting from the private practitioners
 Record your searches in the registers and D-003 form. Share with WHO-NPSP unit and
DD-Immunization on monthly basis
 If no records are available motivate them to have registers with proper diagnosis / clinical
summary.
 List all unreported cases. Find out case details to determine if they are AFP/ Suspected
Measles cases
VSA

73. All cases of acute flaccid paralysis should be
reported ‘irrespective of diagnosis’ within 6
months of paralysis onset
VSA

74. • Current flaccid paralysis
• History of flaccid paralysis in the current illness
• Borderline, ambiguous or doubtful.
VSA

75. • No flaccid paralysis at the time of examination
And
• No history of flaccid paralysis anytime during the course of
illness
Or
• Not acute in onset (e.g. since birth)
Or
• Date of onset of paralysis is more than 6 months prior to
notification
VSA

76. When in doubt, include as AFP
VSA

77. 77
Non-AFP cases
Polio cases
Typical AFP cases
Borderline/ambiguous AFP cases
Surveillance
sensitivity is
adequate to detect
90% polio cases VSA

78. 78
Non-AFP cases
Polio cases
Typical AFP cases
Borderline/ambiguous AFP cases
Surveillance
sensitivity is
not good
enough &
detects only
50% polio
cases
Sensitivity
increases
and leads to
100%
detection of
polio cases
If stool is
collected
from
borderline or
ambiguous
cases…
VSA

79. •Information to SMO (Immediate notification)
•Case investigation
•Arrange for Stool specimen collection
•Active case search in community including outbreak response immunization
•Sensitize health facilities that missed the case (if any)
VSA

80. • Required to clinically confirm a notified case
• Important to obtain accurate epidemiological and clinical
information of the cases
• Should be done within 48 hours of reporting
• Gives opportunity for early sample collection and timely intervention
• Early medical aid reduces morbidity and mortality
VSA

81. • Information should be collected on all relevant sections
• Efforts should be made to obtain accurate information on:
• Date of onset of disease
• Immunisation history
• Contact/travel history
• Health facility contact history
VSA

82. ADD A FOOTER 82

83. Weekly VPD H002- Reporting Form
VSA

84. As soon as possible – should not wait for case investigation
Up to 2 months of onset of paralysis
2 specimens at least 24 hrs apart
Maintain cold chain during storage/shipment of stool samples
VSA

85. 85
The properties of wild poliovirus type 1 (WPV1)
show the risks of exposing stool specimens to
prolonged high temperatures:
–– at 25 °C, highly stable for at least 28 days
–– at 35 °C, stable for 04 days but becoming
undetectable by 16 days
–– at 45 °C, undetectable at 04 days
Specimens should arrive at the laboratory
preferably within 72 hours of collection

86. 86
Cold chain
Samples
National
Lab

87. 87
• All cases of acute flaccid paralysis should be treated in terms of
poliomyelitis
• Motor system examination
• Polio Eradication and Endgame Strategic Plan 2013-2018
• All cases of acute flaccid paralysis should be reported ‘irrespective of
diagnosis’ within 6 months of paralysis onset
• When in doubt, include as AFP
• Early stool sample collection
VSA

88. 88
• NELSON 21ST EDITION TEXTBOOK OF PEDIATRICS
• WHO GUIDELINES - 2018
• www.polioeradication.org
VSA

89. 89 VSA