Anterior poliomyelitis

Dr. THOUSEEF FIRST YR PGMS ORTHO

Definition

• Poliomyelitis (polio) is a highly infectious viral disease

caused by any of three serotypes of human enteric

poliovirus, which mainly affects young children. The

virus is transmitted through contaminated food and

water, and multiplies in the intestine, from where it can

invade the nervous system.

Michael Underwood described poliomyelitis as a debility of the lower

extremities in the second edition of his book Treatise on the Diseases

of Children, 1789.

In 1840, Jacob von Heine described anterior acute poliomyelitis and

the differences with other types of paralysis.

Lesions in the spinal medula were demonstrated in 1870 by Jean-

Martin Charcot & Alex Joffroy.

When was it reported?Early cases

• Poliomyelitis was recorded in the late 1700’s with the first epidemic in the late 1800’s.

• The cases that were reported in 1979 where mild and self-limited and do not result in paralysis.

• The Bavarian neurologist Wilhelm Heinrich Erb coined the term “anterior acuta poliomielitis” for clinical adult cases

• In Greek, polios means grey and myelos medula. Of course, the ending –itis means inflammation of.

• Polio= gray matter

• Myelitis= inflammation of the spinal cord

Polio An EnterovirusPolio An Enterovirus• Poliovirus, the causative agent of

poliomyelitis

• A human enterovirus and member of

the family of Picornaviridae.

• Composed of a RNA genome and a

protein capsid. The genome is

single-stranded positive-sense RNA 7

Serotypes• Specificity to receptor restricts mutation rate; slow genetic drift

• Three serotypes with no cross immunity– Type 1 polio 90%

Weakest, only 1% causes neuroparalysis

– Type 2 polio 9% (Eliminated)

– Type 3 polio 1%Greater temperature stability

• Requires trivalent polio vaccine

• Polioviruses can also vary in phenotype of virulence, host cell lysis, and ability to raise host defense triggers

Polio Infection.

• Incubation 3 – 21 days

• On average 14 days

Predisposing factors. Severe muscular acitivity can lead to paralysis, as it increases the

blood flow

May produce paralysis in the limb or bulbar region

Injecting 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.

How is polio transmitted?

• Poliovirus is transmitted through both oral and fecal routes .

• Implantation and replication occurring in either the

orapgaryngeal and or in the intestine of mucosa.

• Most infected for 7-10 days before and after clinical

symptoms begin.

Pathogenesis and pathology.

• Enter through Mouth,

• Multiplies in Oropharynx tonsils and Intestines,

• Excreted in Stool.

• Enters the CNS from Blood.

• Spread along the Axons of peripheral nerves to CNS.

• Progress along the fibers of the lower motor neurons spinal

cord or brain.

Pathology and Pathogenesis.

• Destroy the Anterior horn cells of the Spinal Cord

• Do not Multiply in Muscles only muscles manifest with

weakness and flaccid paralysis result is secondary.

• Occasionally produce

Myocarditis,

Lymphatic hyperplasia.

It cause paralysis?

• Paralytic disease occurs 0.1% to 1% of those who become

infected with the polio virus.

• Paralysis of the respiratory muscles or from cardiac arrest if

the neurons in the medulla oblongata are destroyed.

• Patients have some or full recovery from paralysis usually

apparent with proximally 6 months.

Clinical features

• Often child around the age of 9months

• Gives history of mild pyrexia associated with diarrhoea

• Inability to move a part or whole of the limb.

• Paralysis of varying severity and assymmetrical

Types of poliomyelitis

• Spinal polio

• Bulbar polio

Spinal polio• Spinal polio is the most common

form of paralytic poliomyelitis;

• Results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column,

• Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia.

Bulbar polio• Making up about 2% of cases

of paralytic polio,

• Bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem.

• Nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis.

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• Virus mainly localized in anterior horn cells and certain brain stem motor nuclei

Clinical manifestations: 1. Asymptomatic infection (90-95%) 2. Abortive poliomyelitis 3. Non paralytic polio myelitis 4. Paralytic polio myelitis (1%)Clinical course • Three stages - Acute stage - Convalescent stage - Chronic stage

Acute stage• 7-10 days• Superficial reflexes absent • Deep tendon reflexes disappear when the muscle group is

paralysed Treatment-

- Bed rest- Analgesics- Hot packs- Anatomical positioning of limbs to prevent flexion

contracture- Gentle passive ROM exercises

Distribution

• Lower limbs 92 %

• Trunk + LL 4 %

• LL + UL 1.33 %

• Bilateral UL 0.67 %

• Trunk + UL + LL 2 %

Convalescent stage

• Recovery phase

• Varying degree of spontaneous recovery in

muscle power takes place

• > 80% return of strength - recovered muscles

• < 30% of normal strength - paralysed muscle

Treatment:

• Vigorous passive stretching exercises

• Wedging casts for mild –mod contractures

• Surgical release of tight fascia & aponeurosis

• Lengthening of tendons may be necessary for

contractures persisting longer than 6months

• Orthoses used until further no recovery is anticipated

Chronic stage

•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

Causes of deformity in Polio

•1. Muscle imbalance

•2. Posture and gravity effect

•3. Dynamics of activity

•4. Dynamics of growth

Laboratory Diagnosis.

• Viral isolation from Throat swabs, Rectal swabs. Stool specimens,• Transported in frozen containers.• Produce cytopathic effect on Human and Monkey cells• Produce cytopathic effects.

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Viral Isolation• From feces - present in 80% of cases in 1st

week• In 50 % till 3rd week• In 25 % till several weeks• Collect the fecal sample at the earliest.• Primary monkey kidney is the ideal cell line for

isolation of virus• Viral isolation must be interpreted with

caution and clinical presentation

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Laboratory Diagnosis (Serology)

• Estimation of Antibodies Ig M

•A paired sample is essential.

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Goals of treatment

• To achieve maximal functional activity

• Correction of significant muscle imbalances

• Preventing or correcting of limb deformties

• Static joint instability can be controlled by orthoses

• Dynamic joint instability cannot be controlled by

orthoses, that results in fixed deformities

• Soft tissue surgeries such as tendon transfer should be

done before the developement of fixed bony changes

FOOT AND ANKLE

oRTHOSIS

Claw toes

Foot drop

equinovalgus

equinovarus

What surgeries are done in Polio?

Balancing of power

Stabilization procedures

Correction of deformities

Limb lengthening

TENDON TRANSFER• Tendon transfers are indicated when dynamic

muscle imbalance results in a deformity • Surgery should be delayed until the maximal

returns of the expected muscle strength has been achieved

• Objectives of tendon transfer• To provide active motor power • To eliminate the deforming effect of a muscle• To improve stability by improving muscle

balance

Criteria and selecting the tendon for transfer

• Muscle to be transferred must be strong enough

• Free end of transferred tendon should be attached as close as possible to the insertion of paralised tendon

• A transferred tendon should be retained in its own sheath or should inserted in the sheath of another tendon or it should be pass through the subcutaneous fat

• Nerve supply and blood supply of transferred muscle must not be impaired

• Joint must be in satisfactory position• Contracture must be released before tendon

transfer• Transferred tendon must be securely attached

to bone under tension slightly greater than normal

• Agonists muscles are preferable to antagonists

• Phasic muscle transfer is preferable to nonphasic transfer

• A nonphasic muscle should be trained by extensive physiotherapy before tranfer

• the ideal muscle for tendon transfer would the ideal muscle for tendon transfer would have the same phasic activity as the have the same phasic activity as the paralysed muscle , same size in cross section paralysed muscle , same size in cross section and of equal strength and could be placed in and of equal strength and could be placed in the proper relationship to the axis of the jointthe proper relationship to the axis of the joint

• Child with dynamic deformity an apropriate tendon transfer

ARTHRODESIS

• Most efficient method for permanent stabilization of a joint

• When the control of one or more joints • Bony procedures can be delayed until

skeletal growth is complete• When the tendon transfer and arthrodesis is

combined in the same operation the arthrodesis is performed first

• Most dependent parts of the body sujected to significant amount of deforming forces

• M.c deformities includes- - equinus - equino varus

- equino valgus - calcaneous

- cavovarus - claw toes

- dorsal bunion

PPRP OF FOOT AND ANKLE

PEABODY’S CLASSIFCATION

1. limited extensor invertor insufficiency

2. gross extensor invertor insufficiency

3. evertor insufficiency

4. triceps surae insufficiency

1. LIMITED EXTENSOR INVERTOR INSUFFICIENCY

- tibialis anterior paralysis

- equinus and cavus

- plano valgus

•Transfer of EHL to base od 1st MT

•If valgus deformity is fixed talonavicular arthrodesis is combined

2. GROSS EXTENSOR INVERTOR INSUFFICIENCY

TYPE A

-paralysis of extensors of toes and tibialis anterior

-equinus

-equino valgus

•Transfer of peroneus longus to dorsum of 1st cunieform bone

•Talonavicular arthrodesis is combined if deformity is fixed

• TYPE B

– paralysis of both tibialis anterior & tibialis posterior and toe extensors

• Transfer of both peroneals to dorsum of foot

• Hoke arthrodesis is combined in severe deformity

3.EVERTOR INSUFFICIENCY

paralysis of peroneal muscles

- varus foot

•Slight-mod impairement:

EHL to base of 5th MT

•Severe:-tibialis anterior to cuboid

EHL to base of 5th MT

• 4.TRICEPS SURAE INSUFFICIENCY

• Calcaneovarus deformity- tibialis posterior,FHL

• calcaneovalgus deformity- both peroneals attached to calcaneum

• calcaneocavus - transfer of peroneals,tibialis posterior

when to operate

1. wait for atleast 1 1/2 years after paralytic attack

2. tendon transfers done in skeletally immature

3. extra articular arthrodesis 3-8 years

4. tendon transfer around ankle and foot after 10yr of age can be supplimented by arthrodesis to correct the deformity

4. triple arthrodesis >10-11 years

5. ankle arthrodesis >18 years

CLAW TOE• Hyperextension of MTP and flexion of IP• Seen when long toe extensors are used to substitute dorsiflexion of ankleTreatment:For lateral toesdivision of extensor tendon by z-plasty

incision,dorsal capsulotomy of MTP

For great toeFHL transferred to prox.phalanx,IP joint arthrodesis (or)

division of EHL ,proximal slip attached to neck of 1st MT,distal slip to soft tissues+ IP arthrodesis

Dorsal bunion

• Shaft of 1st MT is dorsiflexed and graet toe is plantar flexed

• Seen in muscle imbalance, between anterior tibial and peroneus longus muscle

Lapidus operation

• remove abnormal bone from MT head• If anterior tibial is overactive- detach its

tendon And transfer it to 2nd or 3rd cuneiform bone

• remove the inferior wedge of bone from 1st metatarso cuneiform joint

• bring the end of the FHL through the tunnel in 1st MT and anchor to the capsule over dorsum of MTP joint

• .

EQUINUS FOOT• Anterior tibial muscle• Peroneal and long toe extensor muscles• Treatment:• Serial stretching and cast• Achilles tendon lengthening• Posterior capsule release• • Posterior bone block of cambell• Lambrinudi operation• Pantalar arthrodesis

EQUINOVARUS DEFORMITY

• Tibialis anterior• Long toe extensors and peroneal muscle

• Treatment:• Young children4-8 yrs:• 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)

• Children >8yrs:• Triple arthrodesis• Anterior transfer of tibialis posterior• Modified jones procedure

EQUINO VALGUS DEFORMITY

• Anterior and posterior muscle weakness with strong peroneals and gastroconemius-soleus muscle

• Treatment:• Skeletally immature:• 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

CAVOVARUS DEFORMITY• Seen due to imbalance of extrinsic muscles or by

unopposed short toe flexors and other intrinsic muscle• • 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

• Extensor hallucis longus is transferred to the neck ofneck of 1st MT

CALCANEUS DEFORMITY

• Gastroconemius-soleus muscle

Keeping in slight equinus position during acute stage of poliomyelitis•Plantar fasciotomy ,intrinsic muscle release before tendon transfer•Depends on residual strength of GS muscle•Transfer of peroneus brevis and tibialis posterior to the heel•Both peroneals trasfered for calcaneo valgus deformity•Posterior tibial and FHL can be transfered for cavovarus deformity •Anterior tibial tendon can be transferred posteriorly-DRENNAN TECHNIQUE

• For mild deformity –braces used • Tenodesis of achilles tendon to fibula• There is progressive equinous deformity with

subsequent growth in pt with achilles tenodesis

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

plantar flexion and• cavoequinus deformity because – intrinsic

muscle may retain some function• Radical plantar release • tenodesis• In older pt mid foot wedge resection may be

required• ANKLE ARTHRODESIS

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