post polio residual paralysis ppt

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Page 1: Post polio residual paralysis PPT

POST POLIO RESIDUAL PARALYSIS

Presented by: Moderator Dr. M. Sai krishna Dr.M.Pardhasaradhi MS(ortho)

ANDHRA MEDICAL COLLEGE , VSKP

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• Etymology• Historical aspects• Pathology• Course of disease• Pattern of deformities• Principles of management• Deformities of individual joints• POST POLIO SYNDROME

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Etymology

• The term derives from the Ancient Greek poliós meaning "grey", myelós, referring to the grey matter of the spinal cord, and the suffix -itis, which denotes inflammation., i.e., inflammation of the spinal cord’s grey matter.

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HISTORICAL ASPECTS

• The first description of paralytic poliomyelitis was given by Underwood 1789.

• Causative org was found to be polio virus identified by Karl Landsteinar in 1908.

• The first polio vaccine was developed in the 1950s by Jonas Salk.

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• World Polio Day (24 October) was established by Rotary International to commemorate the birth of Jonas Salk.

• Albert Sabin developed live attenuated, oral polio vaccine (OPV).

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Introduction

• Polio is caused by poliovirus, that initially invade the gastrointestinal tract and subsequently spread to the central nervous system (CNS).

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Pathology

• Poliovirus multiplies in the intestinal wall and then is disseminated throughout the body through blood circulation.

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• Poliovirus has a specific affinity for the anterior horn cells. This causes lower motor neuron type of flaccid paralysis and normal sensation. The cells undergo necrosis.

• Cell recovery depends on the extent of damage.

• With minimal damage, the cells recover completely.

• Necrotic bodies are subsequently replaced by scar tissue.

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Introduction

Infectious disease characterized by

Asymmetric flaccid motor paralysis• Clinical manifestations: 1. asymptomatic infection (90-95%) 2. abortive poliomyelitis 3. non paralytic polio myelitis 4. paralytic polio myelitis (1%)

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The course of the disease• The course of the disease is subdivided into the

following stages.• 1. The acute phase (lasting from 5 to 10 days) is

the period of acute illness when paralysis may occur

• 2. The convalescent phase or recovery phase encompasses the period following the acute phase, during this time a varying degree of spontaneous recovery in muscle power takes

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• 3. The chronic or residual phase is the final phase. The residual paralysis is permanent. It encompasses the rest of the patient’s life-span.

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

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• This is explained by the fact that some muscles have a short column of cells in the spinal cord and others have long columns.

• Those with short columns develop complete paralysis.

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• Inaccessibility to medical care to majority of childrens have led to large number of people with moderate to severe deformalities.

Progressive deformities in residual phase.

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CAUSES OF PROGRESSIVE DEFORMITY

• MUSCLE IMBALANCE• UNRELIEVED MUSCLE SPASM• GROWTH• GRAVITY AND POSTURE• BONY DEFORMITIES

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CAUSES OF PROGRESSIVE DEFORMITY

MUSCLE IMBALANCE – • Flaccid paralysis is the main cause of

functional loss and muscle imbalance .• when a muscle or a group of muscle is

paralysed,the opponent strong muscle pull the joints to their side.

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UNRELIEVED MUSCLE SPASM• Muscle spasm,” a principal manifestation of

poliomyelitis in its early stages, is characterized by protective contraction of the muscles to prevent a potentially painful movement

• This can be prevented by passive stretching and splinting.

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GROWTH• Bony growth depends upon the stimulus by

active healthy stretching around the growth plate , which is lacking in case of polio affected childrens causing limb length inequality , attenuation of blood vessels and reduced blood supply leading to reduced growth of the bone.

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GRAVITY AND POSTURE• Gravity plays an important role in maintaining

the posture and deformity.• Paralysed group of muscles are not in a

position to maintain posture.

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• Bony Deformities

• Apart from deformities due to soft tissue stretching and contracture, bony deformities duly occur in polio patients over a period of time.

• eg:, genu valgus due to persistent iliotibial band contracture which subsequently lead to subluxation at the knee.

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HOW TO RECOGNIZE PARALYSIS CAUSED BY POLIO

• Paralysis (muscle weakness):– usually begins when the child is small, often during an

illness like a bad cold with fever and sometimes diarrhea– Intact sensory system asymmetrical paralysis of the

muscles depending upon the segment of the spinal cord involved.

– Paralysis is of the ‘floppy’ type (not stiff). Some muscles may be only partly weakened, others limp or floppy

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• In time the affected limb may not be able to straighten all the way, due to shortening, or ‘contractures’, of certain muscles.

• The muscles and bones of the affected limb become thinner than the other limb. The affected limb does not grow as fast, and so is shorter.

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• Unaffected arms or legs often become extra strong to make up for parts that are weak.

• Knee jerks and other tendon reflexes in the affected limb are reduced or absent

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DEFORMITIES

• Vary according to degree of muscle imbalance, or if patient presented in early phase or late phase.

• Early stage– Child is febrile with rigidity of neck and tender

muscles.– Asymmetric involvement

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• Most Severely Paralysed Muscle - Tibialis Anterior

• Most common muscle Paralysed - Quadriceps

femoris• Most commonly involved muscles in Upper Limb - Deltoid and Opponens

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• Late stage:– Paralysis may result into wasting weakness.– The common deformity at hip is flexion-abduction-

external rotation.– The common deformity at knee is flexion, in severe

cases triple deformity comprising of flexion, posterior sublaxation and external rotation.

– At foot equino varus is commonest others may be equino valgus calcaneo valgus and calcaneo varus.

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OTHER COMMON DEFORMITIES

• Weight bearing (supporting the body’s weight) on weak joints can cause deformities.

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Clinical Examination of a Polio Patient

• The clinical assessment of a polio affected patient is most important for phasing the course of management taking into consideration the residual muscle power, age of the patient, severity of the deformities, ambulatory status, socioeconomic background.

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CONTD

• Radiographic examinations of the joints are essential, both weight bearing and non-weight bearing to know the status of the joints in terms of subluxation/dislocation to ascertain the stability of the joints.

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• Ambulatory Status • Observation of Gait/Gait Analysis Abductor Lurch Extensor Lurch Hand to Knee Gait The Calcaneus Gait Foot Drop Gait Short Limb Gait

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ABDUCTOR LURCH

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FOOT DROP GAIT

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• Examination of the Joint• Muscle Charting

Grade 0 total paralysis (no contraction palpated)

Grade 1 evidence of slight contractility but no joint movement

Grade 2 complete range of motion with gravity eliminated

Grade 3 complete range of motion against gravity

Grade 4 complete range of motion against some resistance

Grade 5 complete range of motion against maximal resistance

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Differential diagnosis of post polio paralysis

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PrognosisPrognosis depends on two factors:• i. severity of initial paralysis, and• ii. diffuseness of its regional distribution.

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• If total paralysis persists beyond the second month, significant recovery is unlikely.

• If the initial paralysis is partial, prognosis is better.

• In general, the more extensive the paralysis in the first 10 days of illness the more severe the ultimate disability.

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Management

• Management starts with diagnosis & accurate muscle charting (assessing power & deformities)

• Discussion of expectations• Assessment resources • Family support

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Management in convalescent phase

ObjectivesAttainment of maximal recovery in individual

muscles.Restoration and maintainence of normal range

of joint motionPrevention of deformitiesAchievement of as good a physiological status

of the neuromusculoskeletal system

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Prevention of deformity

• firm rubber matress• bed boards to be placed beneath matress and

should be hinged to permit sitting in the later convalescent phase.

• Padded footboard to maintain ankles in neutral position.

• Alternating change of position for maintaience of good muscle tone of gluteus maximus and erector spinae.

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contd• Knees should be held in slight flexion with

padded rolls under knee and behind the ends of proximal tibia to prevent genu recurvatum and posterior subluxation of knee.

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• External rotation of thighs to be prevented.• All the joints of the limbs are carried passively

through the ROM to relieve muscle pain.

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MANAGEMENT OF MUSCLE SPASM• Muscle spasm is protective contraction of

muscle to prevent potentially painful movement.

• They are due to inflammatory changes in the posterior ganglia and meninges.

• Application of moist heat intermittently.

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General Principles—Principles of Management of Polio Deformities

1. Strengthening of the unaffected muscles, stretching of the shortened muscles.

2. Range of motion exercises of joints 3. Appropriate use of orthosis and splints, gait

and walking aids.

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contd

4. Early correction of deformities not amenable to conservative line of treatment by soft tissue release procedures.

5. Restoring muscle balance by tendon transfers.

6. Adequate compensation for equalizing the leg length by modification in the footwear.

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7. Stabilization of the joints by bony blocks/arthrodesis and soft tissue plications.

8. Limb length equalization by limb lengthening/ shortening.

9. Correction of bony deformities at an early stage.

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10. Special mention needs to be made regarding management of pelvic obliquity and scoliosis which are decompensating involving pelvis.

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• PHYSICAL THERAPY• SURGICAL TREATMENT

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PHYSICAL THERAPY

In the residual stage the physical therapy regimen is directed toward:

• Increasing motor strength of muscle by active hypertrophy excercises.

• Preventing or correcting deformity by passive stretching.

• Achieve maximum functional activity.

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Active hypertrophy excersices

• Progressive resistance exercises entail the use of activity graded in proportion to the strength of the involved muscles; they are recommended in the residual stage of poliomyelitis to increase the strength and improve the endurance of such individual muscles or groups of muscles as a “fair”.

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Passive Stretching Exercises

• When a limb is continuously maintained in one position, contracture and fixed deformity will develop as a result of the effects of gravity and dynamic imbalance of muscles.

• Passive stretching exercises should be performed gently.

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Functional Training

• The purpose of a functional training program is to enable the patient to overcome the handicaps imposed by the physical disability.

• At times the activity of stronger muscles is suppressed to prevent the development of deformity.

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ORTHOSES AND OTHER APPARATUS

• Use of an apparatus may be necessary during the asensitive period of the convalescent stage and the residual stage of poliomyelitis.

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• The primary objectives of the orthosis are :to (1) support the patient and enable the patient

to walk and increase functional activity, (2) protect a weak muscle from overstretching, (3) augment the action of weak muscles or

substitute for those completely lost, (4) prevent deformity and malposition, and (5) correct deformity by stretching certain groups

of muscles that have been contracted.

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General Principles of Orthosis

• Locomotion without an orthosis but with the support of crutches should be attempted in order to stimulate active muscular function through the exercise of walking.

• Use of an orthosis should not, however, be postponed if deformities appear likely to develop from the stress of weight bearing

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• In general, use of an orthosis should be as minimal as the condition permits.

• The patient should understand clearly that wearing the orthosis will help her in the early convalescent stage of the disease and that it may be discarded at a later date after training or reconstructive surgery.

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Specific Applications LOWER EXTREMITY

Paralysed muscle/group

Orthoses used

toe extensor and anterior tibial muscles dorsiflexion-assist spring orthosis

gastrocnemius and soleus muscles plantar flexion–assist spring below-knee orthosis with a dorsiflexion stop at neutral position

flail ankle and foot double-action ankle joint (both plantar flexion–assist and dorsiflexion-assist), a varus or valgus T-strap is added to the shoe

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Page 65: Post polio residual paralysis PPT

Paralysed muscle/group

Orthoses used

knee above-knee orthosis with a drop-lock knee joint is prescribed

genu recurvatum results from paralysis of the triceps surae in the presence of some strength of the quadriceps femoris

above-knee orthosis with a free knee joint constructed so that complete extension of the orthosis at the knee is prevented

flexion deformity of the knee is present as a result of dynamic imbalance between the hamstrings and quadriceps femoris muscles,

Engen extension knee orthosis

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UPPER EXTREMITY

Paralysed muscle/group Orthoses used

paralyzed shoulder muscles, particularly the deltoid

sling, which allows functional use of the forearm and hand. During the initial period of 6 to 8 weeks, an abduction shoulder splint may be worn at night and during part of the day to prevent overstretching of the deltoid muscle, particularly when there is associated paralytic subluxation or dislocation of the shoulder joint.

wrist extensors are paralyzed cock-up wrist splint

weakness of the opponens of the thumb. opponens splint

intrinsic muscles of the hand are paralyzed

, hyperextension of the metacarpophalangeal joints is prevented by a knuckle-bender dynamic splint.

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SURGICAL MANAGEMENT

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• A multitude of operative procedures can be performed both for the correction of paralytic deformities and for the total physical rehabilitation of a child with poliomyelitis. These procedures may include

fasciotomy, capsulotomy, tendon transfers, osteotomy, and arthrodesis.

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Tendon Transfers

• Tendon transfer entails shifting the insertion of a muscle from its normal attachment to another site to replace the active muscular action that was lost by paralysis and to restore dynamic muscle balance.

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Principles of Tendon Transfer

1. The muscle to be transferred must have adequate motor strength to carry out the new function. Ordinarily, one grade of motor power is lost after a muscle is transferred.

2. The range of motion of muscles must be similar to that of the muscles for which they are being substituted; furthermore, whenever muscles are transferred in combination, their range of contraction should not differ significantly.

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3. The joints on which the transferred muscle is to act should have functional range of motion. All contractural deformity should be corrected by wedging casts or soft tissue release before tendon transfer.

4. The neurovascular supply of the transferred muscle must not be damaged while transferring the tendon

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5. A smooth gliding channel with adequate space must be provided for excursion of the tendon in its new location. The paratenon and synovial sheath are preserved over the tendon surface during dissection. It is preferable to pass the tendon beneath the deep fascia through tissues that permit free gliding rather than subcutaneously

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6. In rerouting of the tendon, a straight line of contraction must be provided between the origin of the muscle and its new insertion. Angular courses and passages over pulley systems should be avoided

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7. The tendon should be reattached to its new site under sufficient tension so that the transferred muscle will have a maximal range of contraction. The transferred muscle should be tested during the operation to ensure that it will hold the part in optimal position.

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ARTHRODESIS• A relaxed or flail joint is stabilized by

restricting its range of motion. • The object of arthrodesis in patients with

poliomyelitis is to reduce the number of joints the weakened or paralyzed muscles must control.

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When to operate

Wait for atleast 1 ½ yrs after paralytic attack Tendon transfer done in skeletally immature Extra articular arthrodesis 3-8 yrs Tendon transfer around ankle & foot after 10

yrs of age can be supplemented by arthrodesis to correct the deformity.

Triple arthrodesis >10 yrs Ankle arthrodesis >18 yrs

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Postoperative Care and Training

• Support of the part in an overcorrected position should be continued until the muscle has assumed full function and there is no tendency for the deformity to recur.

• A bivalved cast or an orthosis will hold the transferred tendon in a relaxed position.

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• It is best to teach the patient preoperatively to localize active contraction in the muscle to be transferred.

• Active exercises are continued postoperatively as soon as the reaction to surgery and pain have subsided.

• When tendon transfer is combined with arthrodesis, muscle reeducation is delayed until adequate bony union has taken place.

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Hip deformities

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Pathomechanics:• When gluteus maximus is paralyzed the

patient is unable to rotate the pelvis backwards. The result is that in the supporting phase of the affected limb, the trunk has to be thrown backward at the hip joint, the anterior muscles of the hip and the iliofemoral ligaments act as a check.

Hip deformities

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GLUTEUS MAXIMUS LURCH

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• Paralysis of abductors which stabilize the pelvis during stance phase, in the frontal plane, fail to do so effectively, thereby causing drop of pelvis on the other side, which is popularly referred to as Trendelenburg test, and bilaterally affections typically lead to wadding gait.

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Hip Deformities may be as a result of:I. Maintenance of wrong posture during acute

and convalescent phase. The frog posture that the children tend to assume — abduction external rotation of the hip and knee in flexion

II. Muscle imbalance — contracture of abductors — Tensor fascia lata and anterior fibres of gluteus medius.

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• Paralysis of the muscles around the hip can cause severe impairment

– Flexion and abduction contractures of the hip.

– Paralysis of the gluteus maximus and medius muscles.

– Paralytic hip dislocation

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Iliotibial band contracture

• The iliotibial band contracture produces flexion deformities of the hip and knee on the same side.

The three-pronged attachment of the upper part of the iliotibial band to the iliac crest. There is a middle prong (A) through the aponeurosis over the gluteus medius, an anterior one (B) through the tensor fasciae latae, and a posterior one (C) through the gluteus maximus. Proximally, the location of the iliotibial tract is anterior and lateral to the axis of the hip, whereas inferiorly, in a normal knee, it inserts on the tibia well in front of the axis of the knee joint.

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• Straight-leg raising usually is limited.

• The patient assumes the frog position, with the knees and hips flexed and the extremities completely externally rotated. When this position is maintained for even a few weeks, secondary soft tissue contractures occur; a permanent deformity develops

Iliotibial band contracture

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• Flexion, abduction, and external rotation contracture of the hip.

• The iliotibial band lies lateral and anterior to the hip joint, and its contracture can cause flexion and abduction deformity. The hip is externally rotated for comfort and, if not corrected, the external rotators of the hip contract and contribute to a fixed deformity

Iliotibial band contracture

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• Genu valgum and flexion contracture of the knee:

– With growth, the contracted iliotibial band acts as a taut bowstring across the knee joint and gradually abducts and flexes the tibia

Iliotibial band contracture

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Iliotibial band contracture deformities

• Limb-length discrepancy:

– Although the exact mechanism has not been clearly defined and may be related more to the loss of neurological and muscle function, a contracted iliotibial band on one side may be associated with considerable shortening of that extremity after years of growth.

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Iliotibial band contracture deformities

• External tibial torsion, with or without knee joint subluxation:

– Because of its lateral attachment distally, the iliotibial band gradually rotates the tibia and fibula externally on the femur; this rotation may be increased if the short head of the biceps is strong. When the deformity becomes extreme, the lateral tibial condyle subluxates on the lateral femoral condyle and the head of the fibula lies in the popliteal space.

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Iliotibial band contracture deformities

• Secondary ankle and foot deformities:

– With external torsion of the tibia, the axes of the ankle and knee joints are malaligned, causing structural changes that may require surgical correction.

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Iliotibial band contracture deformities

• Pelvic obliquity:– When the iliotibial band is contracted, and the patient is

supine with the hip in abduction and flexion, the pelvis may remain at a right angle to the long axis of the spine

– When the patient stands , the affected extremity is brought into the weight-bearing position (parallel to the vertical axis of the trunk), the pelvis assumes an oblique position The iliac crest is low on the contracted side and high on the opposite side.

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• The trunk muscles on the affected side lengthen, and the muscles on the opposite side contract. An associated lumbar scoliosis can develop. If not corrected, the two contralateral contractures (the band on the affected side and the trunk muscles on the unaffected side) hold the pelvis in this oblique position until skeletal changes fix the deformity

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Iliotibial band contracture deformities

• Increased lumbar lordosis:

– Bilateral flexion contractures of the hip pull the proximal part of the pelvis anteriorly; for the trunk to assume an upright position, a compensatory increase in lumbar lordosis must develop.

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Positional Pes Varus.• Positional pes varus results from an ill-fitted orthosis

that fails to compensate for the external tibial torsion. • The axes of the knee and ankle joints do not occupy the

same horizontal plane in external torsion of the tibia.• When an above-knee orthosis manufactured with

these joints in the same horizontal plane is fitted to a limb with external tibial torsion, the appliance will force the foot into varus position so that the ankle is in line with the knee joint

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• Bivalved Casts. • Passive Stretching Exercises.

Conservative Treatment

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Surgery

• For abduction and external rotation contractures, a complete release of the hip muscles (Ober-Yount procedure) is indicated

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Ober-Yount procedure• Iliopsoas tendon, sartorius, rectus femorus, tensor fasciae

latae, gluteus medius and minimus

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COMPLETE RELEASE OF MUSCLESFROM ILIAC WING AND TRANSFER

OF CREST OF ILIUM

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BRADFORD FRAME

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PARALYSIS OF THE GLUTEUS MAXIMUS AND MEDIUS

• Paralysis result in unstable hip and an unsightly and fatiguing limp.

• During weight bearing on the affected side when the gluteus medius alone is paralyzed, the trunk sways toward the affected side and the pelvis elevates on the opposite side (the “compensated” Trendelenburg gait).

• When the gluteus maximus alone is paralyzed, the body lurches backward

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Treatment

• POSTERIOR TRANSFER OF THE ILIOPSOAS FOR PARALYSIS OF THE GLUTEUS MEDIUS AND MAXIMUS MUSCLES

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• Lowmans’s procedureExt oblique abdominal muscle to greater

trochanter

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PARALYTIC DISLOCATION OF THE HIP

• If a child contracts limbs in poliomyelitis before age of 2 years, and the gluteal muscles become paralyzed but the flexors and adductors of the hip do not, the child may develop a paralytic dislocation of hip.

• Muscle imbalance , coxa valga, laxity of capsule.

• Dislocation also can develop because of fixed pelvic obliquity,in which the contralateral hip is held in marked abduction, usually by a tight iliotibial band or a structural scoliosis

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Treatment • Reduction of the hip in young children often can be achieved

by simple abduction, sometimes aided by open adductor tenotomy and traction

• If the hip cannot be reduced by traction, open reduction and adductor tenotomy may be required,

• In combination with primary femoral shortening, varus derotation osteotomy of the femur, and appropriate acetabular reconstructions

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SURGICAL TREATMENT • Dynamic balance about the hip is restored by

appropriate muscle transfers.Age of onset of paralysis

<2 years Iliosoas transfer at the age 4-5 yrs. If the coxa valga deformity is greater than 150 degrees, it is best to correct the deformity and obtain a femoral neck–shaft angle of 110 degrees before iliopsoas transfer.

>2years iliopsoas transfer may be postponed and the stability of the hip monitored periodically. When the coxa valga exceeds 160 degrees and the femoral head starts to subluxate laterally, varization osteotomy is performed. In patients younger than 6 years, the femoral neck–shaft angle is reduced to 105 degrees; in older patients the angle is corrected to 125 degrees.

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Lloyd roberts technique of IT oblique osteotomy

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ARTHRODESIS OF THE HIP • Fusion of the hip in poliomyelitis may increase

the ability to walk and eliminate the need for orthotic support.

• A stiff hip burdens the spine and knee with abnormal stress and strain.

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• Ligamentous instability of the knee, progressive lumbosacral scoliosis, and trunk instability secondary to extensive paralysis of the abdominal muscles are absolute contraindications to hip fusion in poliomyelitis.

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ARTHRODESIS OF THE HIP

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Deformities of Knee

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Knee deformities

• The disabilities caused by paralysis of the muscles acting across the knee joint

– Flexion contracture of the knee– Quadriceps paralysis.– Genu recurvatum– Flail knee

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Flexion contracture of the knee Genu recurvatum

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Quadriceps Femoris Paralysis • The quadriceps is commonly affected by

poliomyelitis.• When there is slight genu recurvatum with

adequate strength of the triceps surae and hamstring muscles, the knee is stabilized by locking it in hyperextension .

• Patients so treated are able to walk satisfactorily.

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• During the stance phase of gait, quadriceps weakness is compensated for by tilting the trunk and center of gravity of the body forward.

• The only functional disabilities are difficulty climbing steps and running. In the presence of knee flexion deformity, however, the knee joint becomes unstable because it cannot be locked in hyperextension.

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MUSCLE TRANSFER to restore knee extension power, biceps femoris, semitendinosus, sartorius, tensor fasciae latae, and adductor longus.[

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Treatment• TRANSFER OF BICEPS FEMORIS AND SEMITENDINOSUS

TENDONS

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Flexion contracture of the knee

• Flexion contracture of the knee can be caused by a contracture of the iliotibial band.

• Iliotibial band also causes genu valgum and an external rotation deformity of the tibia on the femur.

• Flexion contracture also can be caused by paralysis of the quadriceps muscle when the hamstrings are normal or only partially paralyzed.

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Treatment • <15 – 20* contracture:

– Posterior hamstring lengthening and capsulotomy.• 20-70* contracture:

– supracondylar extension osteotomy of the femur

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• >70* knee flexion contracture:– Division of the iliotibial band and hamstring

tendons,combined with posterior capsulotomy.

– Skeletal traction after surgery is maintained through a pin in the distal tibia; a second pin in the proximal tibia pulls anteriorly to avoid posterior subluxation of the tibia.

– Long-term use of a long-leg brace may be required to allow the joint to remodel.

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GENU RECURVATUM

• In genu recurvatum the knee is hyperextended

• Genu recurvatum from poliomyelitis is of two types

– Lack of power in the quadriceps

– The hamstrings and the gastrocnemius-soleus muscles weakness.

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GENU RECURVATUM

• Lack of power in the quadriceps:– The quadriceps lacks the power to lock the knee in

extension; the hamstrings and gastrocnemiussoleus usually are normal

• The hamstrings and the gastrocnemius-soleus muscles weakness:– These muscle weakness causes hyperextension of the knee

often followed by stretching of the posterior capsular ligament.

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GENU RECURVATUM

• The pressures of weight bearing and gravity cause changes in the tibial condyles and in the proximal third of the tibial shaft.

• The condyles become elongated posteriorly

• Their anterior margins are depressed compared with their posterior margins

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GENU RECURVATUM

• The angle of their articular surfaces to the long axis of the tibia which is normally 90 degrees becomes more acute.

• The proximal third of the tibial shaft bows posteriorly

• Partial subluxation of the tibia may gradually occur.

• There is frequently calcaneus deformity of foot.

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Treatment

• Closing wedge osteotomy for genu recurvatum.

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• TRIPLE TENODESIS FOR GENU RECURVATUM

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• Other Surgical methods of correcting genu recurvatum.

• A . Irwin's technique. • B. Modified dome osteotomy. • C. Open-up wedge osteotomy.

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FLAIL KNEE

• The knee is unstable in all directions.• Muscle power sufficient to overcome this instability is

unavailable for tendon transfer.

Treatment :• Locking knee long leg knee brace.• Knee arthrodesis

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DEFORMITIES OF FOOT AND ANKLE

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• Foot and Ankle are the most dependent parts of the body subjected to significant amount of deforming forces

• M.c deformities includes- 1. Claw toes 2. Cavus deformity and claw toes 3. Dorsal bunion 4. Talipes Equinus 5. Talipes Equino Varus 6. Talipes Equino Valgus 7. Talipes Calcaneus

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PEABODY’S CLASSIFCATION

1. Limited extensor invertor insufficiency2. Gross extensor invertor insufficiency3. Evertor insufficiency4. Triceps surae insufficiency

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LIMITED EXTENSOR INVERTOR INSUFFICIENCY

Tibialis Anterior muscle paralysis produces slowly progressive deformity 1. Equinus 2. Cavus 3. Varying degree of plano valgus

Muscle power is redistributed by transferring the EHL tendon to base of 1st metatarsal + plantar fasciotomy.

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GROSS EXTENSOR INVERTOR INSUFFICIENCY

TYPE A-Paralysis of Extensors of toes and Tibialis Anterior in the presence

of relatively normal Tibialis Posterior muscle. Produces

-Equinus

-Equino Valgus • Transfer of Peroneus Longus to dorsum of 1st cunieform bone.

• Talo-navicular arthrodesis is combined if deformity is fixed.

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• TYPE B– Paralysis of both Tibialis Anterior & Tibialis Posterior

and toe extensors– Transfer of both Peroneals to dorsum of foot.

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EVERTOR INSUFFICIENCY

Paralysis of Peroneal muscles producing

- Varus foot

• Deformity produce Slight to moderate impairment:

Transfer of EHL to base of 5th MT.

• Severe:- Tibialis anterior to cuboid

EHL to base of 5th MT

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TRICEPS SURAE INSUFFICIENCY

• Calcaneo-Varus deformity- Tibialis posterior,FHL are transferred.

• Calcaneo-Valgus deformity- both peroneals attached to calcaneum

• Calcaneo-Cavus in which both invertors and evertors are strong. transfer of peroneals,tibialis posterior tendons to calcaneus.

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CLAW TOE• Hyperextension of

MTP and flexion of IP• Seen when long toe

extensors are used to substitute dorsiflexion of ankle

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Treatment: For lateral 4 toes :

Procedure 1: division of extensor tendon by z-plasty incision,dorsal capsulotomy of MTP joint.

Procedure 2:

Girdlestone- Taylor tendon transforDorsolateral incision. Divide the long flexor tendon and suture them to lateral side of proximal phalanx to extensor expansion.

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Dickson and Diveley procedure

For great toe-EHL tendon is divided proximal to IP joint.-Proximal end is attached to taut flexor tendons.-Distal part of extensor tendon sutured to soft tissues on dorsum of proximal phalanx to assist maintain opposition of raw surfaces of IP joint.-Arthrodesis of interphalangeal joint.

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Modified Jone’s procedure• Division of EHL proximal to IP joint• Proximal slip fixed to neck of 1st metatarsal • Distal slip fixed to soft tissues• Arthrodesis of IP joint by K wire fixation

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CAVUS AND CLAW FOOT• Primary deformity is forefoot Equinus resulting in clawing of

toes.• Clawing disappear if mild cavus of short duration is corrected.• In severe cavus large callosities or even ulcerations may

develop beneath the metatarsal heads.• Clawing may lead to dorsal dislocation of MTP joint • In severe cases all plantar stuctures may contract

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Conservative : metatarsal bar on the shoe, metatarsal pads.Surgical measures: Division PL tendon and imbricate to PB assuming that the

deformity is due to imbalance of Tibialis Anterior and PL. Arthrodesis of all IP joints assuming clawing is caused by

disturbance of function of intrinsic muscles of foot.

mild cavus with clawing

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moderate• young children : Steindler’s fasciotomy• older children : Dwyers calcaneal osteotomy. Japas V osteotomy

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Steindler’s fasciotomy • stripping of fat and muscles from both superficial and deep

surfaces.• Transverse division of fascia close to calcanea attachment.• Release of long plantar ligament extending from calcaneus

to cuboid.

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Cole’s Anterior wedge osteotomy• indicated in cavus without various or calcaneus or

gross muscle imbalance.• Advantage : preserves mid tarsal and sub-talar joints• Disadvantage: shortens the dorm of foot.• Osteotomy of the navicular and cuboid and defect is closed by

elevating the forefoot.

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Japas V osteotomy. • apex of v is proximal at highest point of cavus • lateral limb extends to cuboid• medial limb through intermediate cuneiform to medial border of foot.• no bone is excised• proximal border of distal fragment is pressed plantarwards, while

metatarsal heads are elevated correcting the deformity.

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Hibb’s operation• EDL tendons is divided and proximal end is inserted to 3rd

cuneiform.• EHL tendon is divided and fixed to neck of 1st metatarsal.• Interphalangeal joint arthrodesis.

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DORSAL BUNION• Shaft of 1st MT is

dorsiflexed and graet toe is plantar flexed resulting in prominent head of 1st metatarsal. If severe may result in subluxation of MTP joint.

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Pathogenesis : • Imbalance between TA and PL : normally TA raises the 1st

cuneiform and 1st MT and PL opposes this action. Unopposed action of TA causes this deformity. Thus before the transfer of PL, the effect of its loss on 1st MT must be considered. Every transfer of PL should be accompanied with midline transfer of TA to 3rd cuneform.

• Weakness of Anterior and lateral compartment muscles. unopposed action of posterior compartment muscles causes excessive plantar flexion of great toe.

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• Wedge of bone is removed from metatarso-cuneform and naviculo-cuneform joint.

• If TA is overactive, transfer it to 2nd or 3rd cuneiform.• FHL is detached and brought dorsally and attached to 1st

metatarsal, converting it into a plantar flexor of metatarsal rather than great toe.

• Subcutaneous plantar tenotomy• capsulotomy of 1st MTP joint.

lapidus technique

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• any deforming tendon except the FHL is divided and transferred to dorsum of foot to correct MT displacement. Fusion of joint.

Hammond technique

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• Commonest deformity

• Planter flexors are stronger than dorsiflexors and tight Tendo Achilles.

• If lateral imbalance is there Equinuovarus or Equinovalgus may result.

TALIPES EQUINUS

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MANAGEMENT :

1. No intervention : mild equinus

2. Conservative management: exercises, serial casting, orthosis and molded shoe wear.

3 .Surgical management:

a) soft tissue procedures

b) bony procedures

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Lengthening of Tendo-achillis1. Percutaneous Tenotomy 2. Z- plasty Tendon transfer 1. Anterior transfer of TP2. Anterior transfer of PL, PB

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Cambells Posterior bone block operation

• Usually combined with triple arthrodesis to correct lateral instability.

• A mechanical bone block is constituted on posterior aspect of talus and superior aspect of calcaneus in such a manner that it will impinge on posterior lip of distal tibia and prevent plantar flexion.

• Dorsiflexion is preserved.• Complications: Recurrence of deformity, degenerative

arthritis, flattening of talus, ankylosis of ankle

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Page 167: Post polio residual paralysis PPT

LAMBRINUDI PROCEDURE

• Talonavicular and Calcaneocuboid joint arthrodesis

• Wedge of bone removed from distal and plantar parts of talus, so that talus remains in equines but rest of foot is brought to corrected position.

Complications : recurrent of deformity

residual deformity

degenerative tarsal athritis

pseudoarthrosis of talonavicular joint

flattening of talus

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pantalar arthrodesis

• Surgical fusion of Tibio-talar, subtalar, talo-navicular,calcaneo-cuboid joints.

• Indications: • Calcaneous or Equinus deformity combined with lateral

instability of foot and whose leg muscles are strong enough to control the foot and ankle.

• Reccurance of deformity after post. bone block or lambrinudis• Foot deformity with unstable knee due to quadriceps palsy.

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Contraindications: • If full extension of knee is not possible• Insufficient hamstrings or triceps to prevent genu recurvatum

• When there is Equinus / Calcaneous deformity in addition to unstable knee, whether pantalar arthrodesis will effectively stabilize the knee may be determined before surgery by applying a short leg walking cast.

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Page 172: Post polio residual paralysis PPT

Talipes equino varus• Deformity: equinus at ankle,

inversion of heel at mid tarsal joint, adduction of forefoot. Cavus and clawing may develop in long standing cases.

• Weak peroneals • Weak Tibialis anterior• Normal triceps surae

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• Equinus thus produced increases mechanical advantage of TP which in turn encourages the fixation of hind foot inversion and forefoot adduction and supination.Cavus and clawing develop when toe extensors help to dorsiflex the ankle.

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Treatment

Young children4-8 yrs:• Double bar brace with ankle stop• Stretching of plantar fascia and posterior ankle structure with

wedging casting• TA lengthening• Posterior capsulotomy• Anterior transfer of tibialis posterior or • Split transfer of tibialis anterior to insertion of p.brevis (if

tibialis posterior is weak)• Anterior transfer of medial half of tendo-

calcaneous( Caldwell)

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Children >8yrs:• Steindlers fasciotomy• Triple arthrodesis• Anterior transfer of tibialis posterior• Modified jones procedure • When TP is weak TA is transferred laterally to

midline.

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Talipes equino valgus

• Tibialis anterior and Tibialis posterior are weak and Peroneal longus and brevis are strong and the triceps sure is strong and contracted. Triceps surae pulls the foot into equinus and the Peroneals into valgus.

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Treatment: skeletally immature• Double bar brace with ankle stop• Shoe with an arch support and medial heel wedge• Repeated stretching and wedging cast • TA lengthening• Anterior transfer of peroneals• Subtalar arthrodesis and anterior transfer of peroneals (Grice and green arthrodesis)

Skeletally mature :• TA lengthening• Triple arthrodesis followed by anterior transfer of

peroneals• Modified Jones

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TALIPES CAVOVARUS

Seen due to imbalance of extrinsic muscles or by unopposed short toe flexors and other intrinsic muscle

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• Plantar fasciotomy , Release of intrinsic muscles and resecting motor branch of medial and lateral plantar nerves before tendon surgery

• Peroneus longus is transferred to the base of the second MT

• EHL is transferred to the neck of neck of 1st MT

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TALIPES CALCANEUSDue to unopposed action of dorsiflexors

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• Plantar fasciotomy ,intrinsic muscle release before tendon transfer

• Transfer of TP and PL and FHL tendons to calcaneous. Green and Grice

• Posterior transfer of Tibialis Anterior ( Peabody )

• When EHL and EDL strength is good, both tibials and peroneials can be transferred posteriorly and EHL, EDL transferred proximally to act as dorsiflexors of ankle.

• If adequate muscles are not available, Tenodesis of Tendoachiles to fibula is done ( Westin )

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Page 183: Post polio residual paralysis PPT

Flail foot• All muscles paralysed distal to the knee• Equinus deformity results because

passive plantar flexion and• Cavoequinus deformity because – intrinsic

muscle may retain some function.Rx:• Radical plantar release • Tenodesis• In older pt mid foot wedge resection may be

required• ANKLE ARTHRODESIS

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DEFORMITIES OF SHOULDER

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• Biomechanical classification of the muscle around the shoulder joint (Saha 1967)

Prime Movers 1. Deltoi2. Pectoralis major

Bulky muscles working on a long lever. Exert major clavicular head force for lifting of arm during abduction

Superior Supraspinatus The streering group by virtue of their insertions close to the periphery of the humeral articular surface and very near the (part) junction of the neck-shaft axis, steer the head on the glenoid surface. They also exert a stabilising force, but their lifting force is minimal

Horizontal steerer—anterior

Subscapularis

Horizontal steerer—posterior

Infraspinatus , teres minor

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Intermediate group—depressors

1. Pectoralis major (sternal head)

2. Latissimus dorsi 3. . Teres major

They rotate humeral shaft during elevation and depress the head towards later part. They also exert a weak steering force on the head

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Pattern of the upper limb paralysis (Saha, 1967)Group Muscles involved Joint sobluxation

I Serratus anterior levator scapulae , Rhomboids Trapezius Deltoid Rotators

May or may not be present

II Deltoid-anterior and midpart Rotators, Girdle muscles-normal.

May or may not be present

III Same as group II + paralysis of elbow flexors and supinators

Often present

IV partial paralysis of trapezius, serratus, etc. geenohumerae muscles, muscles of elbow, wirst and fingers

Always present

V FLAIL UPPER LIMB present

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Treatment by Muscle and Tendon Transfer.

Muscle Requiring Replacement or Reinforcement

Action Choices of Muscles for Transfer

Supraspinatus Superior glider 1.Levator scapulae (first choice because of the direction and length of its fibers)

2.Sternocleidomastoid

3.Scalenus anterior

4.Scalenus medius

5.Scalenus capitis

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Infraspinatus Posterior glider (acting from behind)

1.Latissimus dorsi

2.Teres major

Subscapularis Posterior glider 1.Upper two digitations of the serratus anterior

2.Pectoralis minor

3.Pectoralis major (whole or part)

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 TENDON AND MUSCLE TRANSFERS FOR  PARALYSIS OF THE DELTOID

• The classic methods of transferring a single muscle to restore abduction of the shoulder do not consider the functions of the steering muscles.

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Bateman trapezius transfer for paralysis of deltoid.

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Arthrodesis of the Shoulder

• Arthrodesis of the shoulder is indicated when there is paralytic subluxation or dislocation of the shoulder and extensive paralysis of the scapulohumeral muscles.

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prerequisites • Because scapulothoracic motion will serve as a

substitute for glenohumeral joint motion, it is important that the motor strength of the trapezius and serratus anterior be normal.

• Normal function of the hand, however, is a primary requisite.

• It is best to delay shoulder arthrodesis until after epiphyseal closure has taken place.

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• The optimum position for shoulder fusion, as recommended by the Research Committee of the American Orthopedic Association, is 50 degrees of abduction, 20 degrees of flexion, and 25 degrees of internal rotation. This position is functional in that it allows the patient to reach the face and top of the head with the elbow flexed.

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• The shoulder should never be fused in external rotation because the limb will be positioned in an awkward and functionally poor position.

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• The lesser degree of abduction is functionally compensated for by fusing it in greater internal rotation.

• The most acceptable position of shoulder arthrodesis in females is 30 degrees of glenohumeral abduction, 5 to 10 degrees of flexion, and 45 degrees of internal rotation

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Methods of fusion: • 1. Intraarticular• 2. Extra-articular• 3. Combination of above two • 4. Compression arthrodesis.

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Postpolio Paralysis of Elbow and Forearm

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• Most operations for paralysis of the muscles acting across the elbow are designed to restore active flexion or extension of the joint.

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MUSCLE AND TENDON TRANSFERS  TO RESTORE ELBOW FLEXION

:(1) flexorplasty (Steindler), (2) anterior transfer of the triceps tendon

(Bunnell and Carroll), (3) transfer of part of the pectoralis major

muscle (Clark),

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Bunnell modification of Steindler flexorplasty

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Bunnell anterior transfer of triceps for paralysis of biceps

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(4) transfer of the SCM muscle (Bunnell), (5) transfer of the pectoralis minor muscle

(Spira), (6) transfer of the pectoralis major tendon

(Brooks and Seddon), and (7) transfer of the latissimus dorsi muscle

(Hovnanian).

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Brooks-Seddon transfer of pectoralis major tendon for paralysis of elbow flexors

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MUSCLE TRANSFERS FOR PARALYSIS  OF THE TRICEPS

• A good triceps is essential, however, to crutch walking or to shifting the body weight to the hands during such activities as moving from a bed to a wheelchair.

• POSTERIOR DELTOID TRANSFER (MOBERG PROCEDURE)

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Affections of the Wrist and Hand in Poliomyelitis

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Common Patterns of Residual Polio Paralysispattern thumb fingers wrist

I Weak or paralyzed oppositions and abduction, normal long flexor and extensor muscle.

Weak intrinsics, normal long flexors and extensors.

normal flexors and extensors.

II Paralyzed intrinsics and weak long flexor and extensors

Paralyzed intrinsics, weak long flexors and extensors

Normal/weak extensors, normal flexors (at least the flexor carpi ulnaris-FCU

III Completely paralyzed except grade 1-2 power in the long flexor or extensor

Paralyzed intrinsics, partially functioning long flexors with grade 2-3 power in 1 or 2 fingers

WRIST DROP

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Thenar muscle paralysis with normal thumbextensor and flexor. Finger and wrist motors also functional

pattern I paralysis of polio hand

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Thenar muscle paralysis, weak thumb long flexors andextensor, paralyzed finger intrinsics, weak finger flexors, normal

wrist motors-pattern II paralysis of polio hand

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Deformities

• 1. Flexion and ulnar deviation of wrist with or without fixed contracture.

• 2. Volar subluxation of the midcarpal articulation contributing to or the cause of the above deformity.

• 3. Thumb web contracture • 4. Thrapeziometacarpal (or carpometacarpal) joint

contracture • 5. MCP joint extension contracture of 2 or more

fingers

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Reconstruction for Pattern I Paralysis

Opponensplasty:• Flexor digitorum sublimis of the ring finger

opponensplasty• Extensor carpi ulnaris (ECU) opponensplasty• Palmaris longus (PL) opponensplasty• Hypothenar muscle opponensplasty (Huber

1921): The abductor digiti minimi (ADM

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result of opponensplasty using thepalmaris longus transfer to the rerouted extensor polllcls brevisnote

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Reconstruction for Pattern II, Paralysis

For Paralyzed Thenar Muscles• Extensor indicis (El) opponensplasty is done if

the extensor indicis is at least grade 4 or the PL is transferred to the rerouted distal EPS tendon, alternatives as in pattern I.

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For Paralyzed Finger Intrinsics (Claw Fingers)• PL• ECRL• ECRB

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Reconstruction for Pattern III, Paralysis

1st Stage• For thenar muscle paralysis, the

trapeziometacarpal arthrodesis for intermetacarpal bone graft procedure isdone to maintain thumb in fixed palmar abduction.

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• For the weak finger intrinsics (claw), volar capsulodesis is done at the same stage.

• Followed by a 3 wks of plaster immobilization.

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2nd Stage (To improve flexion of the fingers and thumb)• The FDP tendon slips are side-stitched or

tenodesed to each other at the distal forearm so that whatever available flexion power there is can be evenly distributed for all fingers.

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3rd Stage (Drop Wrist)• When the pronator or a strong superficialis

tendon is available, the transfer of either of these to the ECRB tendon provides wrist extension.

• The available FCU or FCR can also be transferred to the EDC and EPL for finger and thumb extension

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Comprehensive Management of Poliomyelitis and Deformities of Foot and Ankle with the Ilizarov Technique

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• The aims of the treatment of poliomyelitis with the Ilizarov technique are .

• 1. To achieve comprehensive correction in minimum time

• 2. To minimize the energy expenditure of walking and improve gait

• 3. To discard the caliper or to minimize the extent of bracing.

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To this end the technique can be used to release contractures,

correct deformities, achieve joint stabilization and arthrodesis to perform limb lengthening. These procedures can be performed at various

levels simultaneously

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uses

• Flexion deformity of knee• Genu recurvatum• Shortening• Osteotomy correction• Foot deformity correction

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Page 225: Post polio residual paralysis PPT

• Ankle fusion• Hind foot lengthening• Calcaneus deformity• Triple arthrodesis

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WHO officially declares India ‘polio-free’ 27 /03/2014

• No polio cases were reported in India for the past three years.

• This is the fourth of six WHO Regions to be certified, marking an important step towards global polio eradication.

• With this step, 80 per cent of the world’s population now lives in certified polio-free regions.

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POST POLIO SYNDROME

• When new weakness appears in muscles previously affected by the polio and/or muscles thought to be unaffected originally, it may or may not be accompanied by other symptoms. This is a crucial point to recognize—a patient can have PPS even if new weakness is the only symptom

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REFERENCES

• TACHDJAN’s Paediatric orthopaedics• KULKARNI TEXT BOOK OF ORTHOPAEDICS• CAMPBELL’s OPERATIVE ORTHOPAEDICS• PARK TXT BOOK OF COMMUNITY MEDICINE• JOURNALS • INTERNET

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THANK YOU