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TOPIC -POLIOMYELITIS PRESENTATION ..pptx
- 1. POLIOMYELITIS DR BIPUL BORTHAKUR PROFFESORAND HEAD DEPARTMENT OF ORTHOPAEDICS ASSAM MEDICAL COLLEGE DIBRUGARH , ASSAM
- 2. INTRODUCTION • In Greekpolios means grey ,myelos –medulla itis -inflammation • It is an acute viral infection • Caused by an RNA virus • There are three antigenic type :1 ,2 , 3 • Primarily an infection of alimentary tract • Infect the CNS in very small percentage of people • Localized in anterior horn cells and brain stem motor nuclei • Results in varying degrees of paralysis and possibly death
- 3. HISTORY • Pre vaccinationera was found in all countries • First case recorded in late 1700 with first epidemic in late 1800 • Two countries in which polio is endemic as of 2021 • All reported cases are of type 1 wild poliovirus • India is certified as polio free since 27th March 2014
- 4. Morphology of poliovirus •Virion is spherical in shape • about 27 nm in size • Has 60 subunits, having four viral proteins(VP1-VP4) • Arranged in icosahedral symmetry • VP1 carries the major antigenic site
- 5. PATHOGENICITY • Virus entersthe body through oropharyngeal route • Incubation period is 6 – 20 days • Multiplies in alimentary canal and passes to lymphatic tissue • Carried to the spinal cord and brain
- 6. • CNS virusmultiply in neurons and destroy them • Anterior horn damaged by viral multiplication, toxic byproducts • Lesion in anterior horn of spinal cord causes flaccid paralysis • Clinically weakness when more then 60% nerve cell damaged • Paralysis more common in lower limb muscles • clinical recovery occurs by 1st month and almost complete by 6th
- 7. CLINICAL COURSE • 95%people remain asymptomatic • 4 -8 % have mild symptoms fever and sore throat • Poliomyelitis develops in 0.5 – 2% patients • Course is divided into three phase • Acute stage • Convalescent • Chronic
- 8. ACUTE STAGE • stagegenerally lasts 7 to 10 days • Symptoms range from • mild malaise • generalized encephalomyelitis • widespread paralysis • Treatment in acute stage • Bed rest • Analgesics • Anatomic positioning • Passive range of movement exercise
- 9. CONVALESCENT STAGE • 2days after the temperature returns to normal and continues for 2 years • Muscle power improves during this stage in 1st four month • Strength should be assessed • Monthly for 6 month • And then every 3 month • In mild to moderate contracture • Passive stretching exercises • Wedging cast
- 10. • Contractures persistinglonger than 6 months • Surgical release of tight fascia and muscle aponeuroses • Lengthening of tendons • orthoses should be used until no further recovery is anticipated
- 11. CHRONIC STAGE • begins24 months after the acute illness • Orthopedist help the patient to achieve maximum functional activity • Goals of treatment • correcting any significant muscle imbalances • preventing or correcting soft-tissue or bony deformities
- 12. • Static jointinstability controlled by orthoses • Dynamic joint instability results in a fixed deformity • Young children are more prone to develop bony deformity • Soft tissue surgery to be done before fixed bony changes develop • Tendon transfers, should be done in young children before the development of any fixed bony changes
- 13. CLINICAL FEATURES • InapparentInfection • Inapparent infection happens in susceptible individual • Seroconversion happens • Abortive poliomyelitis or minor illness • Phase of primary viremia • Fever, headache sore throat malaise • Last for 1-5 days
- 14. • Paralytic poliomyelitisor major illness • Minor illness followed by major illness 3-4 days later • Biphasic fever , headache stiff neck • Flaccid paralysis Paralysis is classified as • Spinal • Bulbar • Bulbospinal Recovery happens over 4-8 weeks completed by 6 months • Non-paralytic poliomyelitis • Disease does not progress beyond aseptic meningitis
- 15. RESIDUAL PARALYSIS • Recoverybegins after acute phase of illness in paralyzed muscle • Recovery ranges from mild to severe residual paresis at 60 days • Maximum neurological recovery in 1st six month continues up to 2 years • After 2 years no more recovery is expected and is known as post polio residual paralysis • Persist for life
- 16. • 2nd and3rd lumbar and 5th and 6th cervical segmental show greatest involvement. • Lower limbs are affected twice as frequently as upper limbs. • Muscles with highest incidence of involvement • quadriceps, tibialis anterior, hip abductors, medial hamstrings in the lower limb • deltoid, triceps and pectoralis major in the upper limbs • complete paralysis seen in • tibialis anterior; tibialis posterior, long flexor and extensor muscles of toes in lower limbs • intrinsic muscles of hands, deltoid and triceps in upper
- 18. Laboratory diagnosis • Specimen •Throat swab ,rectal swab, blood, CSF • Viral isolation • Serodiagnosis • Molecular diagnosis • Reverse transcriptase PCR • sequencing
- 19. PREVENTION • Immunization isthe means of preventing poliomyelitis • Infants to be immunize by 6 months of age • Two type of vaccines • Inactivated (Salk ) polio vaccine(IPV) • Oral (Sabin) polio vaccine(OPV)
- 20. TREATMENT • Early andappropriate to the stage and degree of paralysis • Children Bulbospinal and respiratory paralysis require hospitalization • Children with isolated limb paralysis can be managed at home • After acute phase of illness recovery helped by physiotherapy ,ambulation • Orthosis for ambulation in some cases • Fixed deformities and contracture require orthopedic intervention
- 21. Prevention of deformity •Firm rubber mattress • Bed boards • Padded footboard • Alternating change of position • Padded rolls under knee • External rotation of thighs to be prevented. • Passive movements of the joints.
- 22. Principles of Managementof Polio Deformities 1. Strengthening of the unaffected muscles, stretching of the shortened muscles 2. Range of motion exercise of joints 3. Appropriate use of orthosis and splints, gait and walking aids 4. Early correction of deformities by soft tissue release procedures. 5. Restoring muscle balance by tendon transfers.
- 23. 6. Adequate compensationfor equalizing the leg length by modification in the footwear. 7. Limb length equalization 8. Correction of bony deformities at an early stage
- 24.
- 25. PHYSICAL THERAPY Chronic/residual stage: •Active hypertrophy exercises • Passive stretching exercise • Achieve maximal functional activity
- 26. Orthosis and otherapparatus • Used during convalescent stage and residual stage. Hip KAFO KAFO
- 27. Knee orthosis(KO) or Knee brace Anklefoot orthosis (AFO) Milwaukee brace or CTLSO
- 28. Cock up splint Opponenssplint Knuckle bender splint
- 29. RECONSTRUCTIVE SURGERY • Forcorrection of paralytic deformities and for the total physical rehabilitation. • These procedures may include – I. Release of contractures: a) Fasciotomies, b) Capsulotomies, II. Re-establishment of power: a) Tendon transfer, b) Muscle transplantation III. Stabilization of a relaxed or flail joint: a) Tenodesis, b) Fixation of ligaments
- 30. IV. Correction ofdeformities: a) Osteotomies, b) Arthrodesis V. Limb lengthening : Ilizarov techniques VI. Joint replacement surgery VII.Correction of pelvic obliquity, Spine deformity & stabilization
- 31. Tendon transfer • Indicatedwhen dynamic muscle imbalance results in a deformity • Surgery delayed until the maximal returns of muscle strength. Objectives : • To provide active motor power • To eliminate the deforming effect of a muscle • To improve stability by improving muscle balance.
- 32. Criteria for selectingthe tendon for transfer • Strength : Muscle to be transferred must be strong enough. • Efficiency : Transferred tendon attached as close as possible to the insertion of paralysed tendon. • Excursion : have a range of excursion similar too one is replacing or reinforcing • Neurovascular : The nerve and blood supply must not be impaired.
- 33. • Articular :Joint must be in satisfactory position. Contracture must be released before tendon transfer. • Tension : Transferred tendon must be securely attached to bone under tension slightly greater than normal. • Agonist muscles are preferable then antagonists.
- 34. ARTHRODESIS • Most efficientmethod for permanent stabilization of a joint. • control of one or more joints of the foot and ankle is lost stabilization is required • upper extremity, reach, grasp, pinch, and release require more mobility than stability
- 35. When to operate •Wait for at least 1.5 years after paralytic attack. • Around ankle and foot after 10 years. • Extra articular arthrodesis 3-8 years. • Triple arthrodesis > 10-11 years. • Ankle arthrodesis > 18 years.
- 36. HIP DEFORMITIES • Paralysisof the muscles around the hip : - Flexion and abduction contractures of the hip. - Paralysis of the gluteus maximus and medius. - Paralytic hip dislocation.
- 37. Iliotibial band contracture •FAbER deformities of the hip & genu valgum Flexion deformity of knee. • Spasm of hamstrings, hip flexors, TFL and hip abductors. • Pt assumes the frog position. • After few weeks, secondary contractures occurs, permanent deformity develops.
- 38. Contracture of ITBcan contribute to the following deformity : FAbER contracture of the hip Genu valgum and flexion contracture of the knee Limb-length discrepancy External tibial torsion, with or without knee joint subluxation Secondary ankle and foot deformities Pelvic obliquity Increased lumber lordosis
- 39. Conservative treatment forITB contracture • Hips in neutral rotation, slight abduction, and no flexion • Passive movements of joints • Hips to be stretched in extension, adduction & IR • Knee roll to be used to prevent genu recurvatum.
- 40. SURGERY Indications for Surgery: Hip & knee contracture > 30 degree Ober-Yount procedure : For abduction and ER contractures, a complete release of the hip muscles. Iliopsoas tendon, sartorius, rectus femoris, TFL, gluteus medius & minimus released.
- 41. Campbel’s release : Complete release of TFL, G,maximus from iliac wing and transfer of crest of ilium
- 42. Paralysis of gluteusmaximus and medius • Unstable hip and an unsightly and fatiguing limp. • G. medius alone palsy – Trendelenburg gait. • G. maximus alone palsy – Backward lurch. TREATMENT : • Sharrads’ Posterior transfer of the iliopsoas for paralysis of G. medius and maximus
- 44. Paralytic dislocation ofhip Causes : • Contracture of limbs before 2 yrs, gluteal muscles paralyzed but the flexors and adductors of the hip don’t. • Fixed pelvic obliquity, in which C/L hip is held in marked abduction. TREATMENT : • Simple abduction, sometimes aided by open adductor tenotomy and traction. • In combination with primary femoral shortening, varus derotation osteotomy of the femur and appropriate acetabular reconstructions. • Hip arthrodesis • Total hip arthroplasty
- 45. KNEE DEFORMITIES • Causedby paralysis of muscles acting across the knee joint. • Deformities includes : - Flexion contracture of the knee - Quadriceps paralysis - Genu recurvatum - Flail knee
- 46. Flexion contracture ofthe knee (FFC) Cause: -Contracture of ITB. -Quads palsy with normal/partially paralysed hamstrings. TREATMENT: • <15-20 degree contracture : - Posterior hamstring lengthening and capsulotomy. • 20-70 degree contracture : - Supracondylar extension osteotomy of the femur. • > 70 degree contracture: - Division of ITB and hamstring tendons + posterior capsulotomy.
- 47. Quadriceps paralysis • Issevere as knee is extremely unstable • Weak quads, knee stabilized with Hand Knee gait. • Genu recurvatum, stabilized by locking in hyperextension • Knee may be extremely unstable if there is even a mild FFD. • Severe disability of knee, difficulty in climbing steps and running. TREATMENT : In early stage – Bracing. In gross genu recurvatum - Surgery
- 48. Surgery for Quadricepsparalysis • Muscle transfer to restore knee extension power • Transfer of biceps tendon and semitendinosus tendon to patella. Muscle transfer : - biceps femoris - semitendinosus - sartorius - TF - adductor longus
- 49. Genu recurvatum withstructural changes • Knee is hyperextended • Proximal tibial shaft bows posteriorly • Partial subluxation of tibia. TREATMENT : • Closing wedge osteotomy • Triple tenodesis
- 50. A. Origin ofGastrocnemius & post capsule is release B. ST & Gracilis tendon devided and passed through tibial tunnel, then passed through femoral tunnel. - Post capsule flap is sutured. C. Cross straps made with BF & ITB
- 51. Flail knee • Theknee is unstable in all direction • Insufficient muscle power for tendon transfer to overcome this instability. Treatment : • Locking knee long knee brace • Knee arthrodesis
- 52. Deformities of footand ankle • Most dependent part of the body subjected to significant number of deforming forces. • most common include claw toes, cavovarus foot, dorsal bunion, talipes equinus, talipes equinovarus, talipes cavovarus, talipes equinovalgus, and talipes calcaneus • Arthrodesis to delayed until about age 10 to 12 years to
- 54. Equinus foot (Talipes equinus ) • Foot is in fixed plantar flexion • Planter flexors are stronger than dorsiflexors • Tight tendo achilles Treatment : • Serial stretching and casting • Achilles tendon lengthening • Posterior capsule release • Posterior bone block • Lambrinudi operation • Pantalar arthrodesis
- 56. Talipes equinovarus • Weaknessof peroneals and TA • Normal triceps surae. with normal or strong TP • Cavus & clawing develop when toe extensors help to dorsiflex the ankle.
- 57. TREATMENT Skeletally immature : Conservative •Passive stretching • Wedging casting surgical • Steindler’s fascial stripping • Posterior capsulotomy • Tendo calcaneus lengthening Skeletally Mature Foot: • Triple arthrodesis • Steindler’s fascial stripping • Anterior transfer of tibialis posterior • Tendo calcaneus lengthening.
- 59. Talipes equino valgus •TA & TP muscle weakness with strong peroneals and triceps surae. • Triceps surae – pulls foot in equinus • Peroneals - valgus
- 60. TREATMEENT Skeletally immature : •Repeated stretching and wedging cast • Tendo calcaneus lengthening • Anterior transfer of peroneals • Subtalar arthrodesis and anterior transfer of Peroneals ( Grice and green arthrodesis ) Skeletally mature : • Tendo calcaneus lengthening • Triple arthrodesis f/b anterior transfer of peroneals • Modified jones operation
- 62. Talipes cavovarus • Imbalanceof extrinsic muscles • Unopposed short toe flexors and other intrinsic muscles TREATMENT : Release of intrinsic muscles and medial and lateral plantar nerves.
- 63. Talipes calcaneus • Paralysisof triceps surae. • Dorsiflexors remain functional. TREATMENT : • Planter fasciotomy : intrinsic muscle release before tendon transfer • Transfer of TP and PL and FHL tendons to calcaneus (Green and Grice) • Posterior transfer of tibialis anterior
- 64. Claw toe • Hyperextensionof MTPJ and flexion of IPJ • Seen when long toe extensors are used to substitute dorsiflexion of ankle.
- 65. TREATMENT • For lateraltoes: Procedure 1 : division of extensor tendon by z-plasty incision, dorsal capsulotomy of MTPJ Procedure 2 : Girdlestone-Taylor tendon transfer. • For great toe : Dickson & Diveley procedure - FHL transferred to prox. phalanx, IP arthrodesis - division of EHL, proximal slip attached to neck of 1st MT, distal slip to soft tissues + IPJ arthrodesis.
- 66. Flail foot • Allmuscles paralysed distal to the knee. • Equinus – due to passive planter flexion • Cavoequinus – intrinsic muscle may retain some function Treatment : • Radical planter release • Older pt – mid footwedge resection for forefoot equinus
- 67. DORSAL BUNION • shaftof the first metatarsal is dorsiflexed, and the great toe is plantarflexed • most common imbalance is between the anterior tibial and peroneus longus muscle • TREATMENT • Transfer of the flexor hallucis longus to the neck of the first metatarsal, with plantar closing wedge osteotomy of the first metatarsal is done for correction
- 68.