poliomyelitis general aspects

1. Poliomyelitis- Part I
Presenter : Dr. Y. Shravan kumar, II Yr PG
Moderator: Dr. M. Anil Reddy sir
Chaired by: Dr. V. Abhilash Rao sir
Professor & HOD: Dr. J.Mothilal sir
Dept of Orthopaedic Surgery, PIMS
23 July 2019

2. Definition
• An acute, highly infectious disease caused by polio virus that
inflicts typical temporary or permanent destructive changes in
CNS & results in paralysis and deformities
• Infantile paralysis
• In Greek, polios -grey and myelos- medulla, itis-inflammation
• Poliomyelitis — Inflammation of grey matter of spinal cord
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3. 3
Type to enter a caption.
History

4. 4
History

5. History
• In 1789, Michael Underwood described poliomyelitis as a
debility of the lower extremities in the second edition of his book
‘Treatise on the Diseases of Children’
• In 1840, Jacob von Heine described anterior acute poliomyelitis
and the differences with other types of paralysis.
• Lesions in the spinal medulla were demonstrated in 1870 by
Jean- Martin Charcot & Alex Joffroy
• The Bavarian neurologist Wilhelm Heinrich Erb coined the
term “anterior acuta poliomielitis” for clinical adult cases
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6. Epidemiology
• Low socio-economic conditions
• Tropical, over crowding, poor hygiene
• Most common in infants & young children
• Serious illness- first few days of life
• Temperate climate - summer & fall
• Tropical climate - no seasonal variation
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7. Epidemiology
• 1988- WHO resolved to eradicate globally
• 350,000 cases in 1988
• America declared free- 1994
• Western pacific- 2000
• Europe - 2002
• Since 2009 Pakistan, Afghanistan, India, Nigeria-endemic
• Last case in India in nov 2011, not endemic now
• 332 cases in 2011
• 550 cases in 2013 globally
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8. Poliomyelitis in 2019 ??
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9. Case report
• 45 yr old female patient, M. Anjamma, R/O Jagityal with
chief complaints of pain in rt thigh with H/O fall from
bike
• k/c/o poliomyelitis in her childhood
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10. Pre-op radiographs
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11. Post-op radiographs
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12. Agent
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• Poliovirus- filterable virus
• Genus: enterovirus, Family- Picornaviridae
• Single stranded RNA , outer capsid protein
• Isolated in brain & spinal cord
• Found in nasopharyngeal secretions and stool
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13. PolioVirus
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• Stable in acidic environment
• Survives in stool for months at 40 C & years at -200 C
• Susceptible to chlorination, heat
• Resistant to glycerol, most disinfectants.
3 serotypes :
• Type 1 (Brunhilde) - most outbreaks
• Type 2(Lansing) - most virulent
• Type 3(Leon) - VAPP
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14. Serotypes
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• Specificity to receptor restricts mutation rate; slow genetic
drift
• No cross immunity
 Requires trivalent polio vaccine
Type 1 90%
Weakest, only 1% causes neuroparalysis
Type 2 9% (Eliminated)
Type 3 1%

15. How is polio transmitted?
15
• Host : natural infection occurs only in humans
• Mode of transmission : Faeco-oral
• Infective material : Stool or oropharyngeal secretions
• Period of communicability: shortly before & after onset of symptomatic
disease (7-10 days)
• Incubation period : 3 – 21 days, on average 14 days

16. Host
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• Age : most vulnerable - 6 months to 3 yrs
• Sex: M:F ratio 3:1
• Immunity: -first 6 months - maternal antibody
-Acquired through infection with wild polio virus
-Immunisation

17. Polio Infection
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Predisposing factors
• Severe muscular activity can lead to paralysis
• Intramuscular injections
• Injectable vaccines with adjuvant can predispose to paralysis
• Patients who underwent tonsillectomy have higher incidence as Ig G
secretion is reduced
• Rarely oral Polio vaccine produces poliomyelitis.

18. Basic concepts
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19. 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,
-proximal limb muscles- midregion, and
-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
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20. cell columns in anterior horn cell
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21. cell columns in anterior grey horn
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Cell column Muscles
Ventromedial (all segments) Erector spinae
Dorsomedial (T1–L2) Intercostals,
abdominals
Ventrolateral (C5–C8, L2–S2) Arm/thigh
Dorsolateral (C6–C8, L3–S3) Forearm/leg
Retrodorsolateral (C8, T1, S1–S2) Hand/foot
Central (C3–C5) Diaphragm

22. Anterior horn cells
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
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23. 23

24. 24

25. 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 (SOG) muscle fibers, readily
depolarised, have slowly conducting axons with small spike amplitudes.
Phasic α motor neurons:
- innervate squads of fast, oxidative (FO) and fast, oxidative–
glycolytic (FOG) muscle fiber, larger, have higher thresholds, and have
rapidly conducting axons with large spike amplitudes.
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26. 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
• 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.
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27. Motor unit
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28. 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
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29. Corticospinal tract
• 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)
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30. 30
Corticospinal tract

31. Pathogenesis
31

32. Pathogenesis
• Extraneural pathology —>RES —>Hyperplasia &
congestion of spleen & LN
• Intra neural pathology—>motor neurons —congestion,
edema, haemorrhage
• Directly multiplication or by cytotoxic substance or d/t
inflammation
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33. Pathogenesis

34. Pathogenesis

35. Pathogenesis

36. Pathogenesis

37. Pathogenesis

38. Pathogenesis

39. Pathogenesis

40. Anterior horn cells
• Anterior horn cells of cervical & lumbar enlargements most often affected
-Swelling of cell
- Enlargement of nucleus
-Disappearance of Nissl bodies
-nucleus undergoes chromatolytic degeneration & basophilic granules fill
cytoplasm
• All changes are reversible at this stage
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Pathogenesis

41. • Interstitial changes
-Edema
-Peri-vascular mononuclear infiltration (cuffing)
-Glial invasion—> fibrosis
• Meningeal changes
-congestion
-diffuse cellular infiltration
• Posterior ganglia & N. Roots—> peripheral neuritic pain
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Pathogenesis

42. Intermediate/ internuncial neurons
• Dorsal to ant horn cells
• Impulses from higher centres relay
• Results in SPASM of all muscles
Higher centres
-basal ganglia, pons, medulla, tegmentum
-perivascular cuffing, cellular infiltration
-changes are reversible & transitory
-basal ganglia—> Incordination, asynergic
contraction of muscles
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Pathogenesis

43. • Wallerian degeneration is evident within 3 days throughout the
length of nerve fibre
• Involvement is spotty & asymmetrical
• Innervated muscles—> atrophied & fibrotic
• Each muscle is innervated by column of cells
• Shorter column — tibialis anterior— permanent paralysis
• weakness is proportional to the number of lost motor units
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Pathogenesis

44. • Bones become slender & rarefied
• Longitudinal growth reduced
• Fasciae thickened & contracted
• Subluxation & dislocations
• Scoliosis
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Pathogenesis

45. • Virus can be cultured from blood 3-5days after infection
• Shed from oropharynx upto 3 wks, GIT upto 12 wks, in hypo
gammaglobulinemic patients upto 20 yrs
• Humoral & secretory immunity important
• IgM persists < 6m, IgG for life
• Target for antibodies- capsid protein VP1
• Humoral immunity doesn’t prevent shedding
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Pathogenesis

46. Clinical features
46

47. Clinical features
• Asymptomatic infection (90-95%)
• Abortive poliomyelitis(5%)
• Non paralytic polio myelitis(1%)
• Paralytic polio myelitis (0.1%)
• Polio encephalitis (rare)
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48. Clinical features
• Often child around the age of 9 months
• Gives history of mild pyrexia associated with diarrhoea
• Inability to move a part or whole of the limb.
• Paralysis of varying severity and asymmetrical
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49. Clinical features
• Acute stage -systemic stage
(7-10 days) -stage of meningeal irritation
(pre-paralytic stage)
-paralytic stage
• Convalescent stage
• Chronic stage
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50. Clinical features
Systemic stage
• Prodromal illness
• Fever, malaise, apprehension, cervical
lymphadenopathy
• No CSF changes
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51. Clinical features
Stage of meningeal irritation
• Involvement of CNS
• Sudden onset high fever, prostration, headache, pain in back &
neck
• Irritable, sensitive to touch,
• Painful spasms, MC quadriceps
• Coarse tremors, sweating, neck rigidity
• Head drop sign, kernig & Brudzinski sign +ve
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52. 52

53. Clinical features
Stage of meningeal irritation cont..
• Superficial reflexes disappear—> deep reflexes
• CSF - ground glass appearance
-cell counts >250/cu.mm
-albumin , globulin elevated
-glucose N/ elevated
-sterile
• Recovery can occur without paralysis
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54. Clinical features
Paralytic stage
• Spinal polio 79%
• Bulbar polio 2%
• Bulbo spinal 19%
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55. 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
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56. Paralysis
• Weakness is clinically detectable only when> 60% of the nerve cells are
destroyed
• Spotty & asymmetrical
• Proximal > distal
• lower extremity muscles > upper extremity muscles
• 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
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57. Distribution
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92%
4 %
1.33 %
0.67 %
Lower limbs
Trunk + LL
LL + UL
Bilateral UL
Trunk + UL + LL 2 %

59. Bulbar polio
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• 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
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60. Bulbar polio
• 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
6017

61. Respiratory paralysis
Spinal type
-Intercostal muscles (T1-T12)
-Diaphragm (C3-C5)
Encephalo-bulbar type
-Medullary centers of respiration
-Arrhythmic respirations
-Intercostal diaphragm normal
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62. 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
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63. 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
• 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.
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64. 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
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65. Investigations
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66. Laboratory Diagnosis.
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Viral isolation from
Throat swabs
Rectal swabs
Stool specimens
Serological
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67. ViralIsolation
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• Fromstool- present in 80%of casesin1stweek
• In 50% till 3rdweek
• In 25% till severalweeks
• Collect the fecal sample at theearliest.
• Primary monkey kidney isthe ideal cell linefor isolation of virus
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68. 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
• Sample stored below 80C
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69. Serological
• 3 types of antibodies:
• Neutralising Antibodies - IgG
• Antibodies to c- antigen - IgM
• Anti-D antibodies

70. Differential diagnosis
• Conditions causing systemic symptoms
• Conditions causing meningeal irritation
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
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71. Differential diagnosis
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
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72. 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
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73. 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
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74. Post-polio syndrome
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75. Post-polio syndrome
•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
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
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76. Post-polio syndrome
•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.
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77. Post-polio syndrome
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.
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
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78. Acute flaccid paralysis
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79. Acute flaccid paralysis

83. Management
83

84. Treatment
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

85. 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

86. 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)

87. Medical management
• 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.
• Rocking/oscillatory bed alternate between Fowler
& Trendelenburg positions favour N breathing
rhythm.

88.  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
Orthopaedic management

89. Orthopaedic management
CHART OF INDIVIDUAL MUSCLES MAINTAINED
0= No contraction
1=Trace of contraction
2=Movement without gravity
3=Movement against gravity
4=Movement against gravity and slight resistance
5=Movement against gravity and strong resistance
6=Normal movement and strength

90. Orthopaedic management
 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

91. Orthopaedic management
 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

92. Orthopaedic management
 Warm salt bath-relieve muscle and nerve pain
Buoyancy reduces affects of gravity
 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

93. Hubbard tank

94. 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

95. Orthopaedic management
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

96. Causes of deformity in Polio
96
1. Muscle imbalance
2. Posture and gravity effect
3. Dynamics of activity
4. Dynamics of growth

97. 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
 Improper positioning in a paralysed muscleContracture
Eg: Foot dorsiflexor paralysisfoot dropshortening of calf muscle
and contracted posterior capsule of the ankle

98. MOST COMMON DEFORMITIES
MOST COMMON DEFORMITIES
 Scoliosis
 Knee flexion
 Hip flexion
 Adduction, Int. rotation of shoulder
 Talipes Equinocavovarus
 Hyperextension of MCP

99. REFERENCES
• Turek’s orthopaedics, 7th edition
• Campbell’s operative orthopaedics, 13th & 11th edition
• Harrisons internal medicine
• Park text book of community medicine
• Internet
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100. Thank You
100