DEFORMITY AROUND KNEE

Presented by Dr Amitabh Das

DEFORMITY AROUND KNEE Genu valgum or ‘Knock knee’ Genu varum or ‘Bowleg’ Genu recurvatum or ‘hyperextented

knee’ Triple deformities Flexion deformity

HOW TO ASSESS GENU VARUM Patient sits at the edge of the couch with both legs

extended. In neutral position of the limb, hold the ankles from

behind. Try to approximate both malleoli so that they just

touch each other. Normally, they touch before the inner surfaces of

the knees come together, rather, there should be on an average 0.5 cm gap between the medial surface of the knees.

If the gap is more(In 10-16 age group <4 cm in female & <5 cm in male is regarded as normal) deformity is genu varum.

For unilateral varus, the distance between the centre of the medial surface of medial condyle & central plumb line of the body is measured.

HOW TO ASSESS GENU VALGUM

Patient sits at the edge of the couch with both legs extended.

In neutral position of the limb, hold the ankles from behind.

Try to approximate both knee so that they just touch each other.

Normally, both knee & malleoli should touch but in knock knee, there is a gap between both malleoli(In 10-16 age group, <8 cm in female & <4 cm in male is regarded as normal) & the gap is measured.

For unilateral valgus, the deviation medial malleolus from central plumb line of the body is measured.

HOW TO ASSESS GENU VALGUM If the medial surface of the two knees

touch each other before the medial malleoli can come together, the deformity is genu valgum.

For unilateral valgus, the deviation medial malleolus from central plumb line of the body is measured.

HOW TO ASSESS GENU VALGUM Q – angle:- This is an angle (normal-6 degrees)

between, -a line joining ASIS with centre

of the patella -the line of the patellar ligament

If there is knock knee this angle is increased

HOW TO ASSESS THE PATHOLOGY IN LOWER FEMUR OR UPPER TIBIA Ask the patient to

sit in squatting position. If deformity completely disappears, the total fault lies in the lower femur.

If it disappears partially or does not disappear, the fault will be in both components

Standing position showing genu varum

In squatting position genu varum partially disappeared

Definition:-

Genu varum or bow leg is a lateral curvature of the leg which involves either the tibia, the femur or both

A minor degree of deformity is very common & may be regarded as normal in a child of 3 years of age or less.

PHYSIOLOGIC GENU VARUM In vast majority of

cases genu varum corrects by itself with growth.

Mostly bilateral & symmetrical

Normal knee alignment 10-15 degrees of varus, which progresses to neutral alignment at about 18 months of age.

PHYSIOLOGIC GENU VARUM

The appearance of genu varum frequently is exacerbated or accentuated by concurrent internal tibial torsion.

An angle that measures <15 degrees is an indication of tibial torsion.

PHYSIOLOGIC GENU VARUM Most report that persistence of genu

varum beyond 2 yrs of age is abnormal, however, spontaneous correction of physiologic genu varum will occasionally be delayed until 30 months of age.

Even pronounced physiologic genu varum > 30 degrees can correct with continuing growth.

Over correction to excessive genu valgum is maximal at 4 yrs of age, & valgus angulation averages 8 degrees.

EVALUATION Observe the

alignment of the leg component to the thigh component.

Normally mid inguinal point, centre of patella & mid ankle joint are in one line, & if prolonged it should pass through second web.

Deviation of leg axis outwards is called valgus & inward is called varus

EVALUATION An excessive amount of bowing is often

more apparent than real from internal rotation of the legs as occurs with persistent fetal ante-version of the femoral necks or from obliquity of the tibial epiphysis.

TREATMENT Periodic observation, examination

& follow up.

Education & reassurance of the parents.

Corrects with growth after 3 years of age & required no treatment.

Definition:-

Genu valgum or knock knees,is the medial curvature, such that when the knees are touching, the ankles are separated.

A minor degree of deformity is very common & may be regarded as normal in a child of 3 years of age or less.

PHYSIOLOGIC GENU VALGUM Morley (1957) found that between the

age of 3-3 ½ years of children having knock knee of 5 cm or more as measured by the distance between medial malleoli with the extended knees just touching each other.

The laxity of medial collateral present in young children accentuates the deformity when the child is standing.

PHYSIOLOGIC GENU VALGUM In determining the true angles

of the weight bearing knee joint it is necessary to take a frontal radiograph of both complete lower extremities standing so that the continuation of the tibial axis can be followed up to & through the centre of

femoral head. Unilateral genu valgum or severe bilateral

genu valgum, where inter-malleolar distance exceeds 10cm, should be examined radio logically to determine whether there is any disturbance of epiphyseal growth

TREATMENT Periodic observation, examination &

follow up. Education & reassurance of the parents. Physiologic genu valgum resolves

spontaneously by the age of 7-8 years without treatment.

In rare cases of uncorrected physiologic genu valgum > 20 degrees or more than 10 cm separation between malleoli, epiphysiodesis & osteotomy may be indicated.

Supra-condylar osteotomy of femur or merely tibial osteotomy is done depending upon maximum deformity.

BLOUNT`S DISEASE Tibia vara is most frequent non-

physiologic cause of genu varum in children & adolescents.

It is considered to be a developmental condition, which affects posteromedial aspect of the proximal medial tibial physis, resulting in a progressive varus deformity.

Afro-Caribbean with h/o early walking are usually affected.

TYPES

Early onset :- - It is difficult to

diagnose in its early form until 2 yrs of age, when x-ray changes shows epiphysis is sloping & may be fragmented on the medial side, & is accompanied by a characteristic beak like curving of medial metaphysis.

TYPES Late onset :- -Complete

metaphyseal arrest, can occur by the age of 6.

-Angular deformity & tibial shortening is seen.

PATHOLOGY Biopsy of the lesions reveals

disorganized physeal cartilage with abnormally large group of capillaries, densely packed hypertrophic chondrocytes, & island of almost acellular fibrous tissue.

Both fibrovascular & cartilagenous reparative tissue can be found at the physeal-metaphyseal junction .

RADIOLOGY Langenskjold (1975) divided radiographic

changes into various age group:- -Up to 3 years, there is irregularity of

metaphyseal edge. -Up to 6 years epiphyseal plate is

widened & fragmented. -Up to 10 years medial plate is growing

inwards & downwards into metaphysis. -At the age of 12 years medial tongue of

cartilage divides off & finally unites with tibia metaphysis on medial side, leaving lateral component still open.

TREATMENT Brace is useful in correcting mild deformity in

patients younger than 3 yrs. Early valgus osteotomy before 4 yr with mono

lateral plate or circular external fixation is done. Lateral epiphysiodesis for adolescent with

significant growth remaining. Interposing an inert material such as fat has

been described by Langenskjold. However, osteotomy is frequently indicated to

prevent a secondary pressure phenomenon on the joint cartilage & balancing of the knee with growth & in severe cases repeated osteotomy may be necessary.

SKELETAL FLOUROSIS Consumption of high intake of endemic

fluoride in the drinking water from birth can cause genu varum or genu valgum.

The toxic-effects of fluoride were severe and more complex and the incidence of metabolic bone disease (rickets,osteoporosis) & bony leg deformities (genu valgum, genu varum,bowing, rotational & wind-swept) was greater (>90%) in children with calcium deficiency as compared to <25% in children with adequate calcium who largely had the osteosclerotic form of skeletal fluorosis with minimal secondary hyperparathyroidism.

SKELETAL FLOUROSIS Drinking water supply with fluoride

<0.5 ppm and improvement of calcium nutrition provide protection against the toxic effects of fluoride and are recommended as the cost effective and practical public health measures for the prevention and control of endemic fluorosis

RICKETS Definition:- It is a metabolic disease

of childhood & is characterized by defective mineralization of bone matrix at growth plates.

The organic matrix of bone, fails to mineralize due to interference with calcification mechanism.

PATHOPHYSIOLOGY Defective vitamin D metabolism leads to

lowering of serum1,2-dihydroxyvitamin D (OH)2 D (calcitrol), which in turn causes intestinal malabsorption of calcium.

The normal calcium homoeostatic mechanisms initially defined the serum level of calcium so that urinary excretion is reduced.

The serum calcium falls despite the reduction in excretion & this stimulates the parathyroid glands to produce parathyroid hormone (PTH) which tends to normalize serum calcium at the expense of reducing serum phosphate.Therefore hypophosphataemia may be marked.

AETIOLOGY Poor vitamin D & calcium intake. Lack of exposure to sunlight. Impaired renal function e.g.

glomerular failure or renal osteodystrophy.

Defective vitamin D absorption such as in coeliac diseaese or biliary obstruction.

PATHOLOGY The bone of the skeleton are soft &

porotic, & bend from the body weight or other external cause.

Epiphyseal line of the long bones forms a wide irregular band & metaphysis is broad & irregular from excessive proliferation of the cells of epiphyseal line.

The cartilage in the proliferating zone is hyperplastic, but instead of the normal palisade arrangement of the cells, the proliferating cells are arranged more haphazardly. Extent of zone is increased.

PATHOLOGY In the zone of calcified cartilage the deposit

of calcium salts in the intercellular matrix is greatly deficient or even absent.

In zone of ossification the bone deposited by the osteogenic cells from the diaphysis is poor in quality, deficient in calcium & of patchy distribution. Bone resorption may be increased & replaced by fibrous tissue.

In the metaphysis the bony trabeculae are weakened by lack of calcium, the continued strain stimulates connective tissue hyperplasia so that the extremity of bone appears mis-shapen & unmodelled

DEFORMITIES Enlargement of long

bones give rise to swelling at the bone ends, prominent at the costochondral junctions, & at the lower end of tibia.

The tibia gets bowed, assuming the knee a valgus attitude or both valgus or varus attitude (wind sweep deformity).

CLINICAL FEATURES Bone pain, so marked that patient awake at

night Proximal muscle weakness Pigeon chest Large head with broadened forehead, open

frontanelles & craniotabes. Harrison’s sulci Rickety rosary Pectus excavatum Protrubent abdomen Delayed dentition Wind sweep defomity

RADIOLOGICAL APPEARANCES Epiphysis:- -Delayed

appearance of epiphysis and widening of epiphseal plate, it lacks a bony cortical margin & appears indistinct.

-There may be epiphyseal separation

RADIOLOGICAL APPEARANCES Metaphysis:- -Splayed out giving

Champagne glass appearance ( widening and cupping of the distal ends of long bones) also called as trumpeting.

-Zone of calcification instead of forming a well defined area, is irregular & of low density.

-Its end appears arranged in longitudinal rows (fraying or streaking)

RADIOLOGICAL APPEARANCES Diaphysis:- -There is generalized

decalcification of bones resulting in increased radioluency between the diaphysis & epiphysis

-Space between diaphysis and epiphysis is increased.

- Deformity and bowing of the ends of long bones.

- Decreased density of cortex ( rarefraction trabecular pattern is course)

LABORATOY FINDINGS calcium level is normal or deceased (due

to compensatory hyperparathyroidism)

serum phosphorous is low.  Alkaline phosphates is normal.

Urinary calcium is low  Serum 25 – hydroxycholecalciferol is

decreased

TREATMENTPrevention:- -Adequate exposure of sunlight &

consumption of food rich in vitamin D like milk,cheese etc.

-Daily requirement of vitamin D is10 mcg

(400 I.U.) Active treatment :- -oral or parental administration of vitamin D

In active stage 15,000 mcg (60,0000 I.U) In milder cases 50-150 mcg (2000-6000 I. U)Adequate intake of calcium is ensured

It takes 2 -4 weeks for x- ray healing

DEFORMITY CORRECTION Correction by splinting: This method is used where

deformity is slight & disease still active. Correction by osteotomy: Before surgery, management of

metabolic defect with vitamin D, phosphorus & calcium should be carried out for several month.

TRAUMATIC DEFORMITY OF KNEE

Distal femoral physeal fracture

Proximal tibial physeal fracture

DISTAL FEMORAL PHYSEAL INJURIES It account for 6-9 % of all physeal

injuries (SALTER-HARRIS TYPE).

Angular deformity following distal femoral physeal injury accounts 18% - 51%

ANGULAR DEFORMITY IN DISTAL FEMORAL PHYSEAL INJURY Progressive

angulation after of distal femoral epiphysis is usually caused by

-asymmetric growth from either trauma to the physis at the initial injury, (Salter-Harris Type I or II)

-physeal offset with bony bar formation after healing, (Salter-Harris Type III or IV)

ANGULAR DEFORMITY IN PHYSEAL INJURY Risk of angular

disturbance is highest in patient with significant growth remaining.

If the separationis a Salter-Harris Type II injury, the physis distal to the triangular metaphyseal fragment usually is spared.

The localized area of growth inhibition occurs in that portion of the physis not protected by the physeal fragment

TREATMENT If a localised area of premature arrest

constitutes < 25% - 50% of the total area of the physis & if at least 2 year of growth remain, excision of the bony bridge recommended.

-Kasser recommends that simultaneous corrective osteotomy should be performed when angular deformity exceeds 20 degrees.

Physeal resection about the distal femur has a high rate of failure, & one should consider epiphysiodesis in adolescents.

TREATMENT Hemiepiphysiodesis may be

considered in maturing adolescents with progressive varus or valgus angulation associated with a central bony bridge with some remaining growth medially or laterally.

If patient is approaching skeletal maturity, corrective osteotomy (open wedge) is preferred treatment.

ANGULAR DEFORMITIES IN PROXIMAL TIBIAL PHYSEAL INJURY In contrast to distal femoral physeal

injury proximal tibial physeal injury is rare, as it has got a intrinsic anatomic stability.

On lateral aspect, it is butressed by u/e of fibula.

Anteriorly, the tubercle projects down from the epiphysis to overhang the adjacent metaphysis.

ANGULAR DEFORMITIES IN PROXIMAL TIBIAL PHYSEAL INJURY Similar to distal femoral

physeal injury, injuries to proximal tibial epiphysis may cause shortening or angulation from subsequent growth inhibition.

-This can occur in all four types of Salter-Harris injuries.

-The amount of angulation depends on the proximity of the area of growth arrest to the periphery of the physis & the year left for growth after injury

TREATMENT If the area of growth arrest is localized to

less than a third of the total area of the physis & at least two years of growth remain, resection of the bony bridge may be attemted.

Alternatively, epiphysiodesis or stapling of the side of the physis opposite a peripheral bar may stop progression of the deformity.

Existing deformity at the time of surgery may require proximal tibial osteotomy.

If there is significant valgus deformity an open - wedge osteotomy can be done.

DEFORMITY OF KNEE IN OSTEOARTHRITIS

Osteoarthritis (OA) is characterized by degenerative changes in the articular margin of diarthrodial joints & subsequent new bone formation at the articular margins.

AETIOLOGY Age:- loss of mechanical resistance of

ageing cartilage, due to a defect in stabilizing components of the matrix.

Sex:- Female are more affected than male. Occupation:- manual labourer, factory

workers are more affected due to continueing using their joints even after muscular exhaustion.

Obesity:- failure of subchondral bone to deform with an impact load, leading to increased load, leading to increase cartilage damage.

AETIOLOGY Metabolic factors:- Diabetes &

hyperuricaemia has been found associated with OA.

Mechanical factors:- mechanical stress, such as single impact stress, gross anatomical damage, subtle mechanical dearrangement, joint hypermobility etc found to be associated with OA.

Development factors:- CDH, Perthes’s disease, SCFE found to be associated with OA.

AETIOLOGY Genetic influences:-OA often affects

multiple members of the same family, suggesting that there is hereditary susceptibility to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially identical twins, indicating a hereditary basis.

PATHOLOGY The primary lesion consists of degeneration

of hyaline cartilage. The cartilage easily & rapidly eroded until

the bone matrix is exposed. First areas of bone are exposed in a patchy

fashion. The perichondrium & the cartilage round

the periphery of the joint are stimulated into activity, & as a result, the non articular areas of bones are elevated above the remainder of the substance known as ‘lipping’.

In addition, irregular outgrowth appears in this area, at first cartiliginous but eventually ossified to form osteophytes.

PATHOLOGY There is synovitis with fibrosis involving the

capsule & sub synovial connective tissue. Synovial membrane & capsule are

involved in later stages, & are the site of inflammation & adhesions.

The synovial tags or polypi are insinuated into the joint, & when very exuberant insinuated into the joint, & when very exuberant the process is called “lipoma arborescens”.

Occasionally, cartilage formation occurs in this tags & they are then liable to be broken off into the joint, forming loose bodies.

PATHOLOGY The exposed bone ends of the articular

surface are subjected to considerable friction; in consequences the bone trabeculae in the immediate neighborhood fracture & repair & the marrow spaces are obliterated.

The change involves only a thin layer abutting the joint, & when the surface of this layer gradually becomes more & more smooth & polished due to continue rubbing, the process is known as eburnation.

CLINICAL FEATURES Low grade aching & stiffness experienced

after rest, due to inflammation of synovial membrane, resulting joint effusion & dissappear after some movements.

Pain due to reflex muscle spasm occurs to protect the joint from unnecessary movement.

As the disease progress, there is hyperaemia & venous stasis in the bony surface, producing continuous pain & is not relieved by rest or exercises, crepitus may be felt.

With muscle spasm & capsular contracture angular deformities become established result in varus or valgus deformities of knee.

RADIOLOGIC CLASSIFICATION OF OSTEOARTHRITIS Weight bearing x-rays are taken,

GRADE DESCRIPTION

KNEES

0 Normal

1 Doubtful narrowing of joint space & possible osteophytic lipping

2 Definite osteophytes & possible narrowing of joint space

3 Moderate osteophytes, definite narrowing of joint space, sclerosis &

possible deformity of bone ends

4 Large osteophytes, marked narrowing of joint space, severe sclerosis

& definite deformity of bone ends. Sub chondral cysts may be present

TREATMENT CONSERVATIVE:- -NSAID’s -Regular exercises -Weight control

OPERATIVE:- -Arthrodesis~giving pain relief &

stability but no mobility. -Osteotomy~giving pain relief,

stability & maintaining mobility. -Arthroplasty~TKR giving pain relief,

stability & mobility. -Joint debridement & drilling. -Joint surface allografting.

GENU RECURVATUM Congenital deformity of knee or genu

recurvatum is a rare condition since the time of its first description by Chatelain & is characterized by hyperextension of the knee.

TYPES There are three types:- -Traumatic developmental type:- most common & is due to malposition

in utero, legs may be caught by the chin or axilla with the knees extended & uterine compression may prevent them from assuming the usual flexed position.

-A primary embryonic defect:- usually accompanied by other

defects, such as hare lip, cardiac defect, spina bifida, CDH etc.

-Contracture:- of the quadriceps extensors muscle

dragging the knee into a deformed position.

CLINICAL FEATURES Knee fixed in hyperextension with

varying degree of subluxation or dislocation forwards of the tibia on femoral condyles.

Skin over the anterior aspect of of joint shows several transverse creases.

Patella is small or absent. On posterior aspect both femoral

condyles & hamstrings (as tense cords) are palpable.

There may be wind sweep deformity.

TREATMENT Proximal tibia related to distal femur,

but knee is markedly hyperextended:- -In this type treatment starts at birth

or thereafter. -Plaster cast is applied, flexing the

knee as much correction as possible. -Repeated at 2-3 days intervals until

flexion beyond 90 degrees is obtained. -Thereafter a bivalved cast is used

for flexion & extension exercises twice a day at 30 minutes interval for 3 months.

TREATMENT Proximal tibia dislocated forwards in

relation to distal femur:- -Manipulation & casting is done,

but if redution is not accomplised, then surgical intervention is indicated e.g.

-Osteotomy -Triple tenodesis

TRIPLE DEFORMITY OF KNEE Is described as in

flexed position of the knee, the tibia subluxates posteriorly & laterally & also rotates laterally over the femoral condyle. Gradually leg also goes in valgus.

Thus though it has been identified as triple subluxation, actually it is a “quadruple deformity complex.

PATHO DYNAMICS

The flexed attitude of the knee joint is a protective position & position of rest.

Therefore in any painful condition there is early tendency of spasm of the hamstrings.

This position allows enough of posterior space in knee joint for collection of blood or exudates.

The posterior capsule starts contracting with this flexed attitude.

This allow further mechanical benefit to hamstrings, specially the biceps & iliotibial band, which now became the main flexors of joint.

PATHO DYNAMICS While lying down patient tries to keep

the hip in external rotation, till the outer part of the knee rest on a support or couch.

In this position gravity assisted contraction of the IT-band helps in outer subluxation of the tibiofibular component.

Taking further advantages, the IT-band & bicep femoris contracts further & therefore fibulotibial component rotates laterally.

Above deforming forces pull the leg outwards, i.e. in valgus.

CAUSES Main causes are:-

Tuberculosis

Rheumatoid arthritis

Postural contracture

TRIPLE DEFORMITY IN TUBERCULOSIS Tuberculosis of knee is second in

frequency of hip joint. Two anatomical points to be noted

are large extent of synovial membrane, & the marked vascularity due to late junction of the femoral & tibial epiphyses. Much growth of the leg takes place in this region.

PATHOLOGICAL ANATOMY The disease may begin

either in bone, usually in the femoral or tibial epiphysis or in the patella or synovial membrane, later being the most frequent site.

-The synovial membrane is thickened, grey & translucent, & in places gelatinous or even caseous.

-Fluid is present in varying amount, & adhesions form so that the outlying synovial pockets become loculated.

PATHOLOGICAL ANATOMY -Granulations spread

under & over the cartilage, which, being eroded by pressure & friction, may become detached, leaving the bone exposed.

-At the same time, softening & stretching of the ligaments tend to produce subluxation of the tibia, which slips backwards & rotates laterally(triple deformity).

-Inflammation takes place leading to thickeing of the joint, so called spindle-shaped tumor, known as ‘white swelling’ is formed

CLINICAL FEATURES Pain associated with night cries. Swelling of the joint due to

synovial thickening & presence of fluid.

Limping Muscular atrophy & spasm Shortening in early stage cause

lengthening by stimulating growth locally, but in more destructive lesion shortening is the rule.

TREATMENT Conservative treatment:- -skin traction -Thomas splint with knee flexion

piece applied, which allows the pull to be made in the line of deformity, & as treatment progresses, it can be adjusted daily until full extension is obtained.

-Care must be taken to avoid backward rotational displacement of tibia & is achieved by reverse dynamic sling.

-AKT should be started

TREATMENT Operative treatment:- -Extra-articular abscess should be

drain out -Synovectomy, in those whose

knees remain warm & swollen after conservative treatment.

-Arthrodesis,where there is marked destruction of joint.

TRIPLE DEFORMITY IN RHEUMATOID ARTHRITIS

DEFINATION:-

It is a systemic disease of young and middle

aged adults characterized by proliferation and

destructive changes in synovial membrane,

periarticular structure, skeletal muscle &

perineural sheaths. Eventually the joint are

fused and ankylosed . It is widespread

vasculitis of small arterioles.

 

PATHOLOGYThe earliest changes is swelling and congestion of

synovial membrane & the underlying connective

tissue, which becomes infiltrated with lymphocytes,

plasma cells & macrophages.

Effusion of the synovial fluid into joint space takes

place during active phase of the disease.

Hypertrophy of synovial membrane occurs with

formation of lymphoid follicles.

Inflammatory granulation tissue (pannus) is formed

spreading over and under the articular cartilage which

is progressively eroded and destroyed .

PATHOLOGYLater fibrous adhesion takes place between the layers

of pannus across the joint space and fibrous ankylosis

may occur.

Microscopically the subcutaneous nodules shows

central area of fibrinoid necrosis consisting of swollen

& fragmented collagen fibers fibrinous exudates &

cellular debris , surrounded by palisade of radially,

arranged proliferating mononuclear cells.

Nodules have loose capsule of fibrous tisuue.

CLINICAL FEATURES Multiple joints pain Morning stiffness Knee joint is tender & swollen As disease progress there is limitation of

joint movement. Flexion deformity accommodate the

swollen & proliferating tissues with reduction in pain.

With further progress there is more loss of cartilage & subchondral bone with subluxation of joints.

RADIOLOGIC FINDINGS Juxta articular

osteoporosis Erosion of joint

margin Joint space is

decreased Subchondral

erosion & cyst formation

Fibrous & bony ankylosis in later stage

TREATMENT CONSERVATIVE:- -NSAID’S -DMARD’S -Splints & braces -Physical therapy OPERATIVE:- -Arthroscopic synovectomy -Open synovectomy -Proximal tibial osteotomy -Arthrodesis -Total joint arthroplasty

HEMOPHILIC ARTHRITIS

HEMOPHILIA:- -Definition:- It is characterized

by a bleeding diasthesis due to the defect in the clotting mechanism of blood

PATHOGENESIS Repeated hemorrhages into joint

produce synovial hyperplasia, haemosiderin deposition & fibrous scarring.

Increased intra-articular pressure due to haemarthrosis produce intra-articular adhesion result reduction of joint cavity & limitation of movements.

Restriction of motion will reduce the circulation of nutrients in articular cartilage & lead to progressive articular cartilage breakdown.

CLINICAL FEATURESThe common orthopedic manifestation are,

Hemorrhages into joint:- there is

sudden attack of haemarthosis in joint following minimal trauma, the bleeding occurs not only inside the synovial cavity of joint but also there is intra-osseous hemorrhages from subchondral bone.

Pain & gross deformity at knee Loss of movements

CLINICAL FEATURES Fixed flexion

contracture at knee Valgus & external

rotation deformities are seen

In late stages the deformity increases with posterior sub-luxation of tibia & lateral shift of tibia on the femur

RADIOLOGIC FINDINGS Early Stage:- - distended synovium - no para articular skeletal deformity. Intermediate stage:- -persistent boggy

swelling - osteoporosis -sub-chondral cyst -squaring of patella -inter-condylar notch is widened

RADIOLOGIC FINDINGS Late stage:- -Osteoporosis -Epiphyseal

overgrowth -Subchondral bone

collapse -Cyst formation

with marginal osteophyte

formation -posterior sub-

luxation of tibia & lateral shift of tibia on the femur

POLIOMYELITIS Poliomyelitis was recognized as a clinical

entity in the first half of the nineteenth century.

It is an acute infectious disease occurring sporadically or in epidemics & is caused by polio virus.

TREATMENTThis varies according to stages:- Acute Stage:- correcting factor

deficiency by -whole blood -FFP -Cryoprecipitate -joint aspiration & R-J Bandage -immobilization with splintLate Cases :- prolonged immobilization

with -caliper or splint -trial aspiration. -Reversed dynamic traction

Surgical Method:- -Fresh Frozen Plasma And Blood -Tranfusion -Synovectomy -Supracondylar osteotomy for severe flexion contracture -Arthrodesis -lengthening or release contractures -Joint replacement

PATHOGENESIS Poliovirus once established in the CNS,

has special affinity for the anterior horn cells of the spinal cord & for certain nuclei in the brain stem.

The early visible changes is chromatolysis of the Nissl substance in the cytoplasm of the nerve cell.

This is followed by inflammatory infiltrations of polymorphonuclear & mononuclear cells at first in the perivascular regions & then diffusely in the grey matter.

There is destruction of nerve cells in the anterior horn, peripheral nerve degenerates & muscle supplied by it atrophy.

PATHOGENESIS Tendons atrophy from disuse & lose

their normal glistening appearance. Considerable degree of osteoporosis is

found in bone. Joint capsules & ligaments when not

protected by healthy muscles become stretched, the joint became unduly mobile & may dislocate.

DEFORMITY OF KNEE JOINT In acute & early recovery stages of

poliomyelitis passive movement is limited by pain & muscle spasm, due to the contraction of hamstrings which limits SLR to 30 degrees.

The spasm can be aggravated by nerve tests, e.g. Lasegue & Kernig

Limitation of SLR Limitation increased by dorsiflexion of foot (Lasegue test)

DEFORMITY OF KNEE JOINT Due to limitation of movements at knee

due to pain there is gradually contracture of the muscles, commonest is iliotibial band & flexion deformity at knee persists.

It may also result from paralyzed quadriceps in the presence of stronger hamstrings.

Paralysed quadriceps also can cause genu valgum & genu recurvatum

TREATMENT

Flexion deformity:- Wedge plasters Rest of the limb in Thomas splint Reversed dynamic traction Division of IT Band Tendon lengthening Knock knee Osteotomy Genu recurvatum Proximal tibial osteotomy with transfer of

hamstrings to patella. Arthrodesis

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