genereal polio

1. SRI SIDDHARTHA MEDICAL
COLLEGE,TUMKUR
Subject seminar
Poliomyelitis part- 1
CHAIRPERSON: PROF. & HOD Dr. Kiran Kalaiah
MODERATOR: PROF. & HOD Dr. Kiran Kalaiah
SPEAKER: Dr. G. ARUN SIVA RAM

2. An acute, highly infectious endemic disease caused by
polio virus namely BRUNHILDE,LANSING and LEON that
inflicts typical temporary or permanent destructive
changes in muscular system & results in paralysis and
deformities
• Infantile paralysis

3. In Greek
• ,polios -grey
• myelos- medulla,
• itis-inflammation
• • Poliomyelitis — Inflammation of grey matter of spinal
cord

6. EPIDEMIOLOGY
• Low socio economic
• Tropical, over crowding
• Infants & young children
• Summer & fall
• Tropica climate

7. • 1988- WHO resolved to eradicate globally
• 350,000 cases in 1988
• America declared free – 1994
• Western pacific-2000
• Europe – 2002
• Last case in india – nov 2011
• 332 cases in 2011
• 550 cases in 2013

8. Agent • Poliovirus—filterable virus
• Genus—enterovirus
• Family—picornaviridae
• Single stranded RNA, outer capsid protein
• Isolated – brain and spinal cord
• Found in nasopharyngeal secretions and stools

9. • Stable in acidic environment
• Survives in stools for months at 4c and years at -20c
• Susceptible to chlorination
• Resistant to glycerol
3 serotypes:
1. BRUNHILDE—outbreaks
2. LANSING—virulent
3. LEON--VAPP

10. SEROTYPES
• No cross immunity
• Requires trivalent polio vaccine
1. Type 1—90% ( but 1%--neuroparalysis)
2. Type 2—9% (eliminated)
3. Type3—1%

11. Transmission
• Host: natural infection
• Mode: Faeco-oral
• Infective material: stool or oropharyngeal secrertion
• Communicability:7 to 10 days
• Incubation period: 3 to 21 days

12. Host
• Age: 6 months to 3 yrs
• Sex: M:F 3:1
• Immunity: 1st 6 months—maternal antibody,
• acquired through infection
• immunisation

13. Predisposing factors
•Severe muscular activity
•IM Injection
•Injectable vaccines with adjuvant
•Pt underwent tonsillectomy
•Rarely OPV

14. Cell columns in Anterior grey horn
• Each of the columns of motor neurons in the anterior gray horn
supplies a group of muscles having similar functions
• Individual muscles are supplied from cell groups (nuclei) within
the columns
• Axial (trunk) muscles- supplied from medial columns,
-

15. proximal limb muscles- midregion,
-distal limb muscles- lateral columns,
-retrodorsolateral nucleus
- intrinsic muscles of the hand and foot,
- -central nucleus supplies the diaphragm.
• Columns supplying extensor muscles lie anterior to columns
supplying flexors

18. • α (alpha) motor neurons:
-Large multipolar ,innervate the extrafusal fibers of skeletal
muscles
Beta motor neurons :
- innervate intrafusal fibers of muscle spindles with collaterals to
extrafusal fibers
γ (gamma) motor neurons:
- -Smaller, supplying the intrafusal fibers of neuromuscular
spindles

20. Anterior horn cells
• Two principal types of α motor neurons are recognised:
• 1.Tonic and 2.phasic
Tonic α motor neurons:
• -innervate slow, oxidative–glycolytic muscle fibers, readily
depolarised,
• have slowly conducting axons with small spike amplitudes.
.

21. Phasic α motor neurons: -
• innervate squads of fast, oxidative and fast, oxidative–
glycolytic (muscle fiber,
• larger,
• have higher thresholds, and have rapidly conducting axons with
large spike amplitudes

22. Motor unit
• A motor unit is made up of a motor neuron and the skeletal
muscle fibers innervated by that motor neuron's axonal
terminals
• Groups of motor units work together to coordinate the
contractions of a single muscle

23. • All of the motor units within a muscle are considered a motor
pool
• All muscle fibres in a motor unit are of the same fibre type
• When a motor unit is activated, all of its fibres contract
• Force of a muscle contraction is proportional to number of
activated motor units

25. Corticospinal tract
• Major descending pathway controlling movements of limbs
• Motor pathway starting at the cerebral cortex that terminates on
lower motor neurons
• more than one million neurons in the tract
• 30% originate in the primary motor cortex,
• 30% in premotor cortex and supplementary motor areas,
• 40% in somatosensory cortex, parietal lobe & cingulate gyrus

26. • Neurons originate in layer V pyramidal cells of the neocortex—>
posterior limb of the internal capsule—> cerebral crus at the
base of the midbrain—> pons—> medulla
• About 80% of the total neurons cross over in the medulla
(lateral corticospinal tract)

27. PATHOGENESIS
• EXTRANEURAL RES-hyperplasia & congestion of spleen
& LN
• INTRANEURAL- motor neurons--congestion, edema,
haemorrhage
• Direct multiplication / cytotoxic substance / inflammation

35. ANTERIOR HORN CELLS
• Most affected
-swelling of cell
-enlargement of nucleus
-disappearance of Nissl bodies
-nucleus  chromatolytic degeneration & basophilic granules
fill cytoplasm
• All changes are reversible

36. • Interstitial chnages:
-edema
-perivascular mononuclear infiltration
-glial invasionfibrosis
• Meningeal changes:
-congestion, - diffuse cellular infiltration
• Nerve root neuritic pain

37. • Intermediate/ internuncial neurons
-dorsal to ant horn cells
-impulses from higher centre relay
-results in spasm of all muscles
• HIGHER CENTRES:
-Basal ganglia incordination, asynergic muscle
contraction
- Changes are reversible

38. • Wallerian degeneration -> within 3 days
• Involvement spotty & asymmetrical
• Innervated muscles  atrophied & fibrotic
• Each muscle  innervated by column of cells
• Shoreter column– tibialis anterior—permanent paralysis
• Weakness propotional to number of lost motor units

39. • Bones slender & rarefied
• Longitudinal growth reduced
• Fasciae thickened & contracted
• Subluxation & dislocations
• scoliosis

40. • Virus cultured from blood ( 3-5 days after infection)
• Oropharynx upto 3 wks, GIT upto 12 wks
• IgM persists < 6m
• Antibodies target– capsid protein VP1
• Humoral immunity doesn’t prevent shedding

41. Clinical features
• Asymptomatic (90-95%)
• Abortive polio
• Non paralytic
• Paralytic
• Polio encephalitis (rare)

42. • Child around 9 months age
• H/o mild pyrexia with diarrhoea
• Inability to move a part of whole limb
• Paralysis of varying severity and asymmetrical

43. stages
ACUTE STAGE-- systemic stage
( 7- 10 days) --> stage of meningeal irritation( pre paralytic)
--- >paralytic stage
CONVALESCENT STAGE
CHRONIC STAGE

44. SYSTEMIC STAGE
• Prodromal illness
• Fever, malaise , cervical lymphadenopathy
• No CSF changes

45. STAGE OF MENINGEAL IRRITATION
• CNS involvement
• High fever, prostration, headache
• Irritable, sensitive to touch
• Painful spasm ( mc quadriceps)
• Coarse tremors, sweating, neck rigidity
• Head drop sign, kernig & Brudzinski sign +ve

47. Meningeal irritation cont..
• Superficial refexes disappear  deep refexes
• CSF. - ground glass appearance
- cell counts > 250/ cu.mm
- albumin, globulin elevated
- glucose N/ elevated
• Recovery without paralysis

48. Paralytic stage
• Spinal polio 79%
• Bulbar polio 2 %
• Bulbo spinal 19%

49. Spinal polio
• MC form of paralytic poliomyelitis
• Results from viral invasion of the motor neurons of the
anterior horn cells
• Constitutional symptoms & meningeal signs continue +
flaccid muscle weakness & paralysis with reduced DTR

50. Paralysis
• Weakness is clinically detectable only when> 60% of the nerve
cells are destroyed
• Spotty & asymmetrical
• Proximal > distal
• lower extremity muscles > upper extremity muscles

51. • Muscles of back, abdomen, extremities, respiration
• Quadriceps, glutei, anterior tibial, hamstrings, and hip
flexors
• Deltoid, triceps, and pectoralis major are most often
affected
• Opposing muscles often in spasm—> contractures

52. Distribution
• Lower limb  92%
• Trunk + LL 4%
• LL+UL  1.33%
• Bilateral UL  0.67%
• Trunk + UL + LL  2%

54. Bulbar polio
• 2% of cases of paralytic polio
• Occurs when poliovirus invades and destroys nerves within the
bulbar region of the brain stem
• Paralysis of muscles supplied by the cranial nerves, produces
symptoms

55. • Often associated with encephalitis
• Runs more fulminating course
• Constitutional & meningeal symptoms – severe
• somnolence, stupor, emesis common
• Cranial nerves- 9, 10, 11, 12 affected
• Nasal speech, nasal regurgitation of food, inability to swallow,
accumulation of secretions, aspiration, absent gag reflex,
medullary centres of respiration

56. Respiratory paralysis
Spinal type
• Intercostal muscles (T1-T12)
• Diaphragm (C3-C5)
Encephalo-bulbar type
• Medullary centers of respiration
• Arrhythmic respirations
• Intercostal diaphragm normal

57. Shortening of muscles
• Tight painful muscles
• Spasm —> shortening due to contractures
• If spastic muscle is antagonist to paralysed muscle—>
stretching & weakness—> deformities
• Muscles of back, hamstrings, calf mc affected

58. Convalescent stage
• Recovery phase
• Begins 2 days after the temperature returns to normal &
continues for 2 years
• Varying degree of spontaneous recovery in muscle power takes
place

59. • Maximum return occurs within 6 months
• Muscles with > 80% return of strength recover spontaneously,
muscle with < 30% of normal strength at 3 months should be
considered permanently paralyzed

60. Chronic stage (residual paralysis )
• Usually begins 24 months after the acute illness
• This is the time for orthopaedic intervention
• Most Severely Paralysed Muscle --Tibialis Anterior
• Most common muscle Paralysed --Quadriceps femoris
• Most commonly involved muscles in Upper Limb --Deltoid and
Opponens pollicis

61. Investigations

62. Laboratory Diagnosis.
Viral isolation from
• Throat swabs
• Rectal swabs
• Stool specimens
Serological

63. Viral Isolation
• From stool- present in 80%of casesin1stweek
• In 50% till 3rdweek
• In 25% till several weeks
• Collect the fecal sample at the earliest.
• Primary monkey kidney is the ideal cell line for isolation of virus

64. Stool examination
• Two samples 24 hr apart
• Within 14 days of onset of paralysis
• 8-10 grams / thumb size
• Collected in clean wide mouth bottle

65. Serological
• 3 types of antibodies:
• Neutralising Antibodies - IgG
• Antibodies to c- antigen - IgM
• Anti-D antibodies

66. Differential diagnosis
1. Suppurative meningitis
2. Viral encephalitis
3. Toxic encephalitis
4. Lymphocytic choriomeningitis
5. Tuberculous meningitis
6. Acute rheumatic fever causing pain
7. Trichinosis causing muscle pain

67. Conditions simulating paralytic
poliomyelitis
1. Ac rheumatic fever (psuedoparalysis)
2. Bone & joint inflammation
3. Scurvy
4. Infectious polyneuritis of GBS
5. Peripheral neuritis
6. Botulism
7. Ac encephalomyelitis

68. Complications
• Bronchopneumonia - bulbar type -aspiration
• Atelectasis
• Contractures & deformities about joints due to severe
muscle imbalance
• Prolonged inactivity—>mobilisation of calcium from
bone— >hypercalcemia—>hypercalciuria—>renal
calculi—>renal impairment

69. Prognosis
• Wide spread paralysis associated with CSF with high cell
counts
• Encephalo-bulbar associated with low cell counts
• High mortality- bulbar type (resp failure)
• Paralysis of muscles of deglutition lasts 1-2m
• Max return of muscle power occurs within 6m

70. Post-polio syndrome

71. • Newly occurring late manifestations of poliomyelitis that develop
in patients 30 to 40 years after the occurrence of the acute
illness
• 25–60% of the patients who had acute polio may experience
PPS

72. Causes:
• Chronic poliovirus infection,
• Death of the remaining motor neurons with ageing,
• Damage to the remaining motor neurons caused by increased
demands or secondary insults,
• Immune-mediated syndromes

73. • Characterised by neurological, musculoskeletal, and general
manifestations
Musculoskeletal manifestations include
• Slowly progressive muscle weakness in muscle groups already
involved
• muscle pain, joint pain, spondylosis, scoliosis, and secondary
root and peripheral nerve compression
• General manifestations include generalised fatigue and cold
intolerance.

74. Diagnostic criteria for post-polio
syndrome
1. A prior episode of paralytic poliomyelitis with residual motor
neuron loss
2. A period of neurological recovery followed by an interval (15
years or more) of neurological and functional stability.

75. 3. A gradual or abrupt onset of new weakness or abnormal
muscle fatigue (decreased endurance), muscle atrophy, or
generalised fatigue.
4. Exclusion of medical, orthopaedic, and neurological conditions
that may be causing the symptoms

76. ACUTE FLACCID PARALYSIS
• Child <15 yrs
• Acute onset paralysis <4 wks
• Flaccid- floppy or limp paralysis
• 1 case AFP / year for every 1 lakh population

80. Management

81. PREVENTIVE MEASURES
LIVE OPV
Attenuated virus grown in monkey kidney tissue culture
Trivalent
Produces humoral and gut immunity
Immunity for life
3 adequately spaced doses of OPV

82. Acute stage
• Primary responsibility of paediatrician
• Earliest sign of CNS involvement- orthopaedic surgeon takes
active role
-Serial muscle evaluations
-Physiotherapeutic measures for relief of muscle pain and
spasm
-Positioning to prevent deformities of contracture and muscle
imbalance

83. Medical management
• Absolute bed rest in Isolation
• Adequate fluid intake
• Sedatives contraindicated
• Convalescent serum(60 ml +1ml/kg, repeated every 12 hrs)
• Paralysis of shoulder girdle- warning sign of respiratory
paralysis (C3C4C5 innervate diaphragm)

84. • Tracheostomy – Ventilator, -ve pressure of 12-18 cm H20
• O2 administration
• Frequent aspirations of mucus, mucolytics antibiotics
• Gradually weaned from ventilator
• Pt trained on movements of normal resp.

85. Orthopaedic management
• Acute phase – relief of muscle pain & spasm, prevention of
deformity
• Inventory of muscles initiated & repeated every 2-3 days
• -Required for identifying resp. paralysis
-areas of muscle imbalance
-development of contractures

86. • Paralysis develops 2-3 days after onset of fever, progression
ceases after patient becomes afebrile
• Positioning in a functional position to prevent deformity and to
secure functionally advantageous position
• Muscle imbalance requires relaxation of paralysed muscle and
stretching of spastic muscles

87. • Bed-firm boards under mattress
• Padded foot board –Neutral position of foot, prevents foot drop
• Standing reflex is stimulated—Tibialis anterior relaxed
• Foot- Right angle to leg
• Knee- Slight flexion –rolls beneath proximal tibia
• Thigh- Abduction, neutral rotation
• Arms- outwards-relaxes deltoid

88. • Warm salt bath-relieve muscle and nerve pain
• Hot, wet packs- relax ,relieve pain
• 20 min after heat application, joint should be put through full
ROM
• After febrile illness, patient is placed in Hubbard tank

89. Hubbard tank

90. SPLINTS AND BRACES
• They maintain muscles in relaxed state but prevents
physiological stretch necessary for reflex contraction which
maintains N muscle tone
• Stretched muscle becomes relatively ischemic and fibrotic
• Presently splints are avoided except when paralysis is
permanent and function must be aided

91. MASSAGE
• To encourage circulation
• Preceded by application of heat
• Strokes are directed centrally
EXERCISES
• Improve muscle strength
• Assistive
• Active
• eliminating gravity
• Against gravity
• Against resistance

92. Causes of deformity in Polio
1. Muscle imbalance
2. Posture and gravity effect
3. Dynamics of activity
4. Dynamics of growth

93. Deformities
• caused by intact, spastic/ contracted muscle, which is
antagonist of a paralysed muscle, soft tissue contractures,
skeletal changes
• Eg: Tight Hamstrings with paralysed Quadriceps flexion
deformity
• Contracture of fasciadeformity
Eg: Iliotibial band causes flexion of hip, pelvic obliquity, flexion,
genu valgum of the knee, ext. rotation of leg

94. • Improper positioning in a paralysed muscleContracture
Eg: Foot dorsiflexor paralysisfoot dropshortening of calf
muscle and contracted posterior capsule of the ankle

95. MOST COMMON DEFORMITIES
• Scoliosis
• Knee flexion
• Hip flexion
• Adduction, Int. rotation of shoulder
• Talipes Equino cavovarus
• Hyperextension of MCP

97. REFERENCES
• Turek’s orthopaedics, 7th edition
• Campbell’s operative orthopaedics, 13th & 11th edition
• Harrisons internal medicine
• Park text book of community medicine
• Tacdjian’s pediatric orthopaedics 3rd edition
• Kulkarni textbook of orthopaedics 3rd edition

98. THANK YOU
poliomyelitis part -2
(deformities and correction)