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CTEV : Pathoanatomy and management

Dr anurag varshney

Dr.rml hospital new delhi

Complex organ that is required to be

Stable: for supporting the body weight in standing

Resilient: for walking and running

Mobile: to accommodate variations of surface

Cosmetic

THE NORMAL FOOT

3 main sectionsHindfoot talus, calcaneusMidfoot navicular, cuboid, cuneiformsForefoot metatarsals and phalanges

CONGENITAL FOOT DEFORMITIES

CLUB FOOT

METATARSUS ADDUCTUS

SKEWFOOT

PES PLANUS

CONGEMITAL VERTICL TALUS

TALIPES CALCANEOVALGUS

TARSAL COALITION

CONGENITAL HALLUX VALGUS

CONGENITAL OVERRIDING FIFTH TOE

CURLY TOE

ACCESSORY NAVICULAR

12. CONGENITAL HALLUX VARUS

13. POLYDACTYLY AND POLYSYNDACTYLY

14. SYNDACTYLY

15. MACRODACTYLY

16. CLEFT FOOT (ECTRODACTYLY)

HALLUX RIGIDUS

HALLUX VALGUS INTERPHALANGEUS

HAMMER TOE

MALLET TOE

LONGITUDINAL EPIPHYSEAL BRACKET

SUBUNGUAL EXOSTOSIS

GLOMUS TUMOR

CLUB FOOTGross deformity of the foot that is giving it the stunted lumpy appearance

Significance to know about ctev Every 3 minutes a child with clubfoot is born.

CLUB FOOTDefinitionsit is a congenital dysplasia of all musculoskeletal tissues distal to knee in the form of deformity of the foot and ankle joint complex characterized by forfoot adduction,heel varus ,and ankle equines with or without tibial internal torsion

Talipes: Talus = ankle Pes = footEquinus: (Latin = horse) Foot that is in a position of planter flexion at the ankle, looks like that of the horse. Calcaneus: Full dorsiflexion at the ankle

CLUB FOOTPlanus: flatfoot

Cavus: highly arched foot

Varus: heel going towards the midlineValgus: heel going away from the midlineAdduction: forefoot going towards the midlineAbduction: forefoot going away From the midline

ForefootHind foot

CLUB FOOTTypes1.Postural :Calcaneo-Valgus Equino-VarusLook for CDH Minor and correctable

2.Acquired, Secondary to :SYNDROMES clubfoot : Arthrogryposis Streeter dysplasia (Constriction bands) Prune Belly Syndrome Tibial Hemimelia Mbius Syndrome Freeman-Sheldon Syndrome(whistling face) (AD) Diastrophic dwarfism (AR) Larsen Syndrome (AR) Opitz Syndrome (AR) Pierre Robin Syndrome (X linked recessive)3.Idiopathic (Unknown Etiology) : Congenital Talipes Equino-Varus CTEV

HISTORYHippocrates first described the clubfoot deformity around 300B.C.

Scarpa 1803 congenital dislocation of the astragalo calcaneo scaphoid complex (twisting of scaphoid os calcis and cuboid around the astragalus)

Lorenz 1782- subcutaneous tenotomy of the Achilles tendon

Adams 1866 - differentiated acquired talipes equinovarus from the congenital variety

Guerin 1838- first to report PoP in treatment of clubfoot

Phelps 1890- one stage medial plantar soft tissue release with lengthening of the tendons

HICAM KITE 1930- popularized nonoperative treatment with serial manipulation and cast immobilizationIdiopathic (Unknown Etiology) : Congenital Talipes Equino-Varus

Commonest congenital orthopaedic abnormality

1 to 2 in 1000 live births (0.6 per 1000 in Asian population)

Much more common in Polynesian & Maori & lower in Asians

Males: Females :: 2.5:1.0

DOMINANT INHERITANCE WITH REDUCED PENETRATION / MULTIFACTORIAL

Bilaterality 50%

right side slightly more affected then left (almost equal)

Bilateral deformity more resistant then unilateral

EPIDEMIOLOGY

Etio-pathogenesisStill Unknown at this stage

SOME ETIOLOGICAL THEORIES ARE :

Mechanical factors in utero Retractive fibrotic response Neuromuscular defectArrested embryonic development Primary germ plasma defect Heredity Environmental factors Combined heredity and environmental factors Vascular hypothesis

Neuromuscular defectImbalance between type I and type II muscle fibres and atrophy of type I fibres seen both in peroneal and triceps surae histologically CPN PALSY- weak peroneal muscles weak pronators and overacting of invertors

not all with spina bifida have clubfoot deformities associated with congenital neurologic defects dont have same constant characteristics of idiopathic clubfoot neurological deformed foot are flexible such clubfoot can be placed in dorsiflexion Plantar flexed talus and talipes calcaneovalgus are more common than TEV, in neurological problems

Retractive fibrotic response; Zimny et al identified myofibroblastic retractile tissues in medial ligaments Ponseti et al identified increase in collagen fibres in ligaments and tendonsDecreased density of nerve fibres in synovium of clubfeet. This lack of sensory input responsible for fibrosis and contractures.BUT, Clubfeet are associated with syndromes of inherent ligamentous laxity

.Arrested embryonic development Heuter and Volkmann ; BOHM6 8 week fetus has foot with many characteristics of congenital clubfoot, which become normal by 12 -14 weeks Victoria Diaz et al Fibula Phase calcaneus pushed and displaced into equinovarus tibial phase talus pushed and feet pronated tibial growth spurt

BUT, dysmorphic talar head and medial dislocation of navicular are never observed in fetal development .Primary germ plasma defect in cartilaginous talar anlagen produces dysmorphic talar neck and navicular subluxation which are not found in normal embryonic development Primary germ plasm defect in the talus: continued plantar flexion and inversion of this bone, with subsequent soft-tissue changes in the joints and musculotendinous complexes

Hypoplasia or absence of the anterior tibial artery in majority of CTEV patients**Absence of the dorsalis pedis pulse in the parents of children with clubfoot#Maternal smoking as a significant factor (Honein et al; Skelly et al)

.**Muir L et al. J Bone Joint Surg Br. 1995;77:114-6 # Milan B MD et al. Journal of Pediatric Orthopedics. 26(1):91-93, 2006.

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Wynne-Davies : polygenic inheritance, poligenic theory would explain why clubfoot vary in their degree of severity ,variance in rasistance and pathological antomy.Multifactorial inheritance established by genetic epidemiologic research by Idelberger32.5% concordance rate among monozygotic twins as compared to 2.9% among dizygotic twinsMajor gene effect (inherited in recessive manner) with additional polygenes and environmental factors Tachdjian Patient with CTEV that has one child affected then 25% chance of another affectedIf both parents are normal & have affected child then chance of another is 5% Idelberger K. et al 1939; 33:272276

.

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Intrauterine factors

Pressure theories: Oligohydramnios Abnormal fetal positioningPlacental insufficiencyConstriction bandsToxins ( Maternal alcoholism, smoking)Maternal illness ( anemia, thyroid disorders )Infective pathogens (enteroviruses)Drugs (abortifacients, salicylates, thalidomide, barbiturates)Electromagnetic radiation

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Adaptive Changes Wolffs Law Every change in the use of static function of bone causes a change in the internal form or architecture as well as alteration in its external formation and function according to mechanical law

PATHOLOGICAL ANATOMYCOMPONENTS OF DEFORMITY : EQUINUS fixed plantar flexed foot Ankle joint inversion of talocalcaneonavicular joint plantar flexion of forefoot

VARUS inward rotation of hindfoot talocalcaneonavicular joint (subtalar joint) calcaneus rotate through talocalcaneal joint in coronal and horizontal plane

ADDUCTION Talonavicular joint anterior subtalar joint Lisfranc region

CAVUS prominent transverse plantar crease midtarsal joint

pronation of the forefoot in relation to the hindfoot.

OSSEOUS DEFORMITIESTALUS : Body EXTERNALLY ROTATED (Herzenberg et al) - broader anterior portion of trochlea with flaring of facet articulating with fibula

Neck short ; decreased neck-body axis from normal 150 160 deg. To around 90-115 - internally rotated relative to ankle mortise

Head medially deviated ; talonavicular articulation in sagittal plane than normal coronal plane

Inferior surface anterior and middle facets of subtalar joint are noncongrant, shallow and lessdeveloped

Calcaneusinvolved in equenus varus adduction due to abnormal position but shape is almost maintainedAnterior portion lies beneath the head of talus causing varus and equinus of heelAnteriar end come downward andRotated medially while posterior end moves upward and lateraly

NAVICULAR - medial and plantar displacement on head of talus - hypertrophy of medial tuberosity due to thick ligamentous structures tethering navicular to medial malleolus and calcaneus - false articulation with medial malleolus in sever e defomity

The navicular tuberosity is close to the medial malleolus

Tibio-talar plantar flexion

Medially displaced navicularAdducted and inverted calcaneusMedially displaced cuboid

Soft tissue changesTendo achilles Post. capsule of ankle joint & subtalar joint Post. talo fibular Posterior structures : Calcaneo-fibular ligaments

Medial : Tibialis posteriorFHL,FDL, Master Knot of Henry Talonavicular ligamentCalcaneo-navicular ligamentDeltoid ligamentInterossseus talo calcaneal ligaments Capsules of naviculo cuneiform & cuneiform first metatarsal

Plantar wards : Plantar fasciaPlantar ligamentsFlexor digitorum brevis & abductor hallucis LaterallyCalcaneofibular ligamentBifurcated ligamentCalcaneocuboid joint capsule

FLEXOR DIGITORUM ACCESSORIUS LONGUS 7% of children requiring surgical correctionChildren having first degree affected relatives are 7 times more likely to have this muscle than those without such pedigree

Deficient dorsalis pedis flow in 45% of clubfeet compared to 8% of controls (J Pediatr Orthop 2003)

Deficient posterior tibial artery also documented in severe clubfeet

ISCHEMIC NECROSIS of foot MISCELLANEOUS

SECONDARY CHANGES INTERNAL TIBIAL TORSION (?)

FOOT SIZE DECREASES TO 50%

MEDIAL BORDER CONCAVE & LAT.CONVEX

FOREFOOT PLANTAR FIXED

SKIN STRETCHED OVER DORSUM OF FOOT

CALLOSITIES OVER DORSUM

STUMBLING GAIT

NECROTISING FISTULA & TROPHIC ULCER

HYPOTROPHIC ANT. TIBIAL ART.

ATROPHY OF calf MUSCLES

Clinical testDorsi flexion testScreening text scratch test to detect muscle imbalance in an infant who can not follow commands - in a norml child when media sole scrached foot everts test for peroneals - if scratch lateral sole foot inverts tet for invertors Plumbline testTo detect the tibial torsion

RadiologyPlain radiograph: Can be assessed prior to treatment with A-P &force dorsiflexed foot lateral veiwFoot held in position of best correction, with weight-bearing, or simulated weight-bearing AP view: Taken with foot in 30 of plantar flexion and tube at 30 from verticalLat. View: Transmalleolar with the fibula overlapping the posterior half of the tibia; in dorsiflexion foot

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RADIOGRAPHIC FEATURES :

TURCOS ANGLE approaches parallelism

TALOCALCANEAL INDEX - < 40 degrees

KITES ANGLE - < 30 degrees

MEARY ANGLE dorsal apex

Anteroposterior viewTalocalcaneal angle; 30 55 degrees (KITES ANGLE)

Calcaneal-second metatarsal angle

Talus first metatarsal angle: 5-15 degrees

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AP radiograph: Talo-Calcaneal angle

Lines drawn through center of the long axis of talus (parallel to medial border) and through the long axis of calcaneum (parallel to lateral border), . Any angle less than 30 considered abnormal

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Dorsiflexed Lateral viewTalocalcaneal view 25 50 degrees (TURCOS)

Calcaneal-first metatarsal view

Tibiocalcaneal : 10-40 degrees

Tibiotalar angleTalus-first metatarsal angle

Talocalcaneal index (Kite's angles from AP and Lateral views added)

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ARE RADIOGRAPHS NEEDED ? In neonates NO,becouse small ossification center,no menifestation the shape and orientation of bone

During infancy helpful in assessing the correction. more accurate objective record for assesssment of correction

surgical planning

intraoperative assessment of correction

PODOGRAMS(a) Precorrection podograms showing reduced foot bimalleolar angles. (b) Postcorrection podograms showing improved foot bimalleolar angles achieved by ligamentotaxis.

Classification

Cummin classified CTEV as Supple: foot can be brought to normal position , alljoints are mobile Relapsed: deformities are corrected initially but appears again in later years partially or totally Recurrent : type of relapse , the cause being muscle imbalance which was overlooked initially

Rigid : its a type in which forefoot deformity is corrected but the hindfoot deformities remain uncorrected after conservative treatment Neglected : patient has not received any treatment for one year.

Resistant: its a type of clubfoot where there is no correction after conservative treatment Atypical clubfoot: short, chubby, stiff feet with a deep crease in the sole of the foot and behind the ankle, and shortening first metatarsal with hyperextension of the MTP joint.

Classification (Attenborough 1966)Type I(Extrinsic)Non RigidType II(Intrinsic)RigidFoot sizeNormal Smaller Heel Normal sizeCan be brought down with easeMinimal varusSmall , elevatedCannot be brought down with easeMarked varusCreases More or less normalDeep medial, posterior and lateral creasesReduced creases laterally

CLASSIFICATION SYSTEMS : DIMEGLIO---Based on Classification of clubfoot severity by A.Equinus deviation B. Varus deviation C. Derotation D. Adduction.

Reducibility( degrees)ScoreAdditional parametersScore90-454Marked posterior crease145-203Marked mediotarsal crease120-02Cavus10 t0 -201Poor muscle condition1

GradeTypeScoreReducibilityiBenign(20%)1-4>90% reducibleiiModerate(30%)5-9>50%, soft-stiff, reducible, partially resistantiiiSevere(35%)10-14>50%, stiff-soft, resistant, partially reducibleivVery severe(12%)15-201& ms 30

TREATMENT

NON OPERATIVE TREATMENT

The principles of treatment are based on following concepts :

Abnormal tarsal relationship maintained by pathological after soft tissues contractures

Soft tissues contractures must be stretched to restore normal tarsal relationships

After normal tarsal relationships, correction must be maintained until tarsal bones remold stable articular surfaces

Recurrent deformity results from failure to either attain a complete correction or maintain the correction

Ponseti managementAccording to ponseti Scientific Basis of ManagementClubfoot is not an embryonic malformation. A normally developing foot turns into a clubfoot during the second trimester of pregnancy. Clubfoot is rarely detected with ultrasonography before the 16th week of gestation. Therefore, like developmental hip dysplasia and idiopathic scoliosis, clubfoot is a developmental deformationThe forefoot is in some pronation, causing the plantar arch to be more concave (cavus).The clubfoot deformity occurs mostly in the tarsus.

No single axis of motion (like a mitered hinge) exists on which to rotate the tarsus,whether in a normal or a clubfoot. The tarsal joints are functionally interdependent. The movement of each tarsal bone involves simultaneous shifts in the adjacent bonescorrection of the extreme medial displacement and inversion of the tarsal bones in the clubfoot necessitates a simultaneous gradual lateral shift of the navicular, cuboid, and calcaneus before they can be everted into a neutral positionPronating the clubfoot on this imaginary fixed axis tilts the forefoot into further pronation, thereby increasing the cavus and pressing the adducted calcaneus against the talus. The result is a breach in the hindfoot, leaving the heel varus uncorrected

the anterior portion of the calcaneus lies beneath the head of the talus. This position causes varus and equinus deformity of the heel. Attempts to push the calcaneus into eversion without abducting it will press the calcaneus against the talus and will not correct the heel varus. Lateral displacement (abduction) of the calcaneus to its normal relationship with the talus will correct the heel varus deformity of the clubfoot.The bones and joints remodel with each cast change because of the inherent properties of young connective tissue, cartilage, and bone, which respond to the changes in the direction of mechanical stimuli.

Current ponseti management The Ponseti technique corrects the deformity by graduallyrotating the foot around the head of the talus (red circle) over a period of weeks during cast correction.When possible, start soon after birth (7 to 10 days). However, most clubfoot deformities can be corrected throughout childhood using this managementMost clubfoot deformities can be corrected in approximately 6 weeks by weekly manipulations followed by plaster cast applications. If the deformity is not corrected after six or seven plaster cast changes, the treatment is most likely faulty.

Surgery Vs casting : Surgery improves the initial appearance of the foot but does not prevent recurrence. Adult foot and ankle surgeons report that these surgically treated feet become weak, stiff, and often painful in adult life.Ponseti management is appropriate for use in children with arthrogryposis, myelomeningocele, Larsen syndrome and other syndromes. Treatment is more difficult as correction takes longer and special care must be given in infants with sensory problems as in myelodysplasia to prevent skin ulcers.

Ponseti cast application first step calming the child with a bottle or breast feeding. When possible have a trained assistantExactly locate the head of the talus you can feel the prominent lateral part of the talar head barely covered by the skin in front of the lateral malleolusWhile moving the forefoot laterally in supination, you will be able to feel the navicular move ever so slightly in front of the head of the talus as the calcaneus moves laterally under the talar head.

All components of clubfoot deformity, except for the ankle equinus, are corrected simultaneously. To gain this correction, head of the talus, which is the fulcrum for correction reduce the cavus first :The cavus, which is the high medial arch is due to the pronation of the forefoot in relation to the hindfoot, The forefoot is supinated to the extent that visual inspection of the plantar surface of the foot reveals a normal appearing archneither too high nor too flat, Alignment of the forefoot with the hindfoot to produce a normal arch is necessary for effective abduction of the foot to correct the adductus and varus.

CORRECTION OF ADDUCTION AND HEEL VARUS

The whole foot abducted under the talus Thumb on head of the talus, not the calcaneus. The navicular moves away from the medial malleolus The foot should never be everted manipulation and casting are continous for next 2-3 weeks to abduct the foot gradually

Cast application Manipulation Padding

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Plaster at toes Below knee pop

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Molding Extension upto the thigh

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Plantar support to toes Final appearance

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EQUINUS CORRECTION; The equinus deformity gradually improves with correction of adduction and varus.

This is part of the correction because the calcaneus dorsiflexes as it abducts under the talus.

No direct attempt at equinus correction is made until the heel varus is corrected Final cast applied in maximally abduction and dorsiflexion,

in most children percutaneous tenotomy is done to prevent rochker bottam foot deformity

Residual equinus- manipulation and casting +/- percutaneous tenotomy Make certain that abduction is adequate for performing the tenotomy.

Casts and foot Adequate abduction

Best sign of sufficient abduction: ability to palpate the anterior process of the calcaneus as it abducts out from beneath talusAbduction of approx.70 degrees in relationship to the frontal plane of the tibia possible

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Percutaneous tenotomy under LAFoot held in max dorsiflexion by an assistantTenotomy done 1.5 cm above calcaneal insertion Additional 25-30 deg dorsiflexion obtained Cast with the foot abducted 60 to 70 degrees with respect to the frontal plane of the ankle, and 15 degrees dorsiflexion for 3 weeksIndicated to correct equinus when cavus, adductus, and varus fully corrected but ankle dorsiflexion remains less than 10 degrees above neutral

Precaution Notify your doctor or the clinic nurse if you notice any of the following Any foul-smelling odor or drainage coming from inside the cast. Red, sore, or irritated skin at the edges of the cast. Poor circulation in the toes (see #1 above). Cast slipping off. Child running a fever of 38.5C/101.3F or higher without an explainable reason, such as a cold or virus

Foot Abduction bracesShoes mounted to bar in position of 70 of ER and 15 of dorsiflexion in B/L cases and incase of U/L cases 30 to 40 of ER in normal side, distance between shoes set at about 1 wider than width of shoulders

Knees left free, so the child can kick them straight to stretch gastrosoleus tendon

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Bracing protocolWorn 24 hours each day for first 3 months then at night and at nap time, up to the age of four years.Haft et al: noncompliance with bracing protocol the most common cause of recurrence in children on Ponseti regimen#Without a diligent follow-up bracing program, relapse occurs in more than 80% of cases.relapse rate of only 6% in compliant families (Morcuende et al.).

#Haft, Geoffrey F. MD; Walker, Cameron G. PhD; Crawford,Haemish A. FRACS.J Bone Joint Surg Am, Volume 89-A(3).March 1, 2007.487493

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knee-ankle-foot braces, such as the Wheaton brace, maintain the foot abducted and externally rotated.

However, the knee-ankle-foot braces keep the knee bent in 90 degrees of flexion. This position causes the gastrocnemius muscle and Achilles tendon to atrophy and shorten, leading to relapse of the equinus deformity.

This is particularly a problem if a knee-ankle-foot brace is used during the initial 3 months of bracing, when the braces are worn full time.

Mitchell brace Dobbs dynamic brace

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Dennis brownRomanus

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CTEV SplintStraight inner border to prevent forefoot adductionOuter shoe raise to prevent fooot inversionNo heel to prevent equinusSlight(1/8) lateral sole raiseInner iron barOuter t trapWalking age to 5 yrs of age

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Follow up protocol2 weeks: to troubleshoot compliance issues

3 months: to graduate to the nights and naps protocol

Every 4 months: until age 3 years to monitor compliance and check for relapses Every 6 months: until age 4 years.

Every 1 to 2 years: until skeletal maturity

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Common errors(Kite errors)

Pronation/eversion of 1st metatarsalPremature dorsiflexion of heelCounterpressure at calcaneocuboid jointExternal rotationBelow knee castsShort splints

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The French method Bensahel/Dimeglio regime Daily manipulations by a skilled physiotherapist and temporary immobilisation with elastic and non-elastic adhesive taping Successful in 51% of cases ( of which 9% req TA tenotomy) ; 49% Reqd extensive soft tissue release -29% post release and 20% comprehensive posteromedial release**.

** Richards BS, Johnston CE, Wilson H. Nonoperative clubfoot treatment using the French physical therapy method. J Pediatr Orthop 2005;25:98-102.

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Rocker bottom deformityDorsiflexion via midfoot before correction of hindfoot varusDorsal dislocation of navicular on taluscalcaneus Fixed in equinus hypermobility of tarsometatarsal level

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Reasons for relapses

noncompliance of the bracing program.

If relapse occurs in infants who are braced, the cause is an underlying muscle imbalance of the foot that can lead to stiffness and relapse.

Early relapses loss of foot abduction and/or of dorsiflexion correction with recurrence of adductus and cavus.

Equinus relapseThe tibia seems to grow faster then the gastrosoleus tendon unit. The muscle isatrophic and the tendon appears long and fibrotic.

If 10 degree dorsiflexion is not achieved in 45 casts in children under 4 years of age repeat the percutaneous heel-cord tenotomy. Once the equinus is corrected, resume the nighttime bracing program.

Varus relapsemore common than equinus relapses.

treated by re-casting in the child between age 12 and 24 months, followed by resuming of a strict bracing program.

EXTRINSIC/NON-RIGID (TYPE I)INTRINSIC/RIGID (TYPE II)FOOTNormal sizesmallerMild varusMarked varusHEELNormal sizesmallerCan be brought downCan notMinimal varusMarked varusCREASESMore or less NDeep posterior, medial and plantar creasesReduced creases laterally

(Kawashima and Uhtoff, 1990)

OPERATIVE TREATMENT

INDICATIONS :

FAILURE OF NONOPERATIVE TREATMENT IN AN INFANT

SYNDROMIC CLUBFOOT

DIMEGLIO GRADES 3 AND 4

RESIDUAL DEFORMITIES CORRECTION

NEGLECTED CLUBFOOT

SOFT TISSUE RELEASES

TENDON TRANSFERS

BONY PROCEDURES

General PrinciplesGoal: address all pathoantomic structuresDecision regarding timing, extentA la carte" approach [Bensahel]Turcos one size fits all approachPosteromedial-plantar-lateral release: when all deformities presentPosterior release: straight lateral border, flexible forefoot and hindfoot, and palpable gap between medial malleolus and navicular tuberosity

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Turco(hockey stick posteromedial incision)

One stage POSTEROMEDIAL SOFT TISSUE RELEASE (TURCO)Indications : resistant recurrent deformity

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POSTERIOR RELEASE :

TAL Z TECHNIQUE; medial half

Capsulotomy of ankle joint (tibiotalar) first

Capsulotomy of talocalcaneal joint

Transection of talofibular and calcaneofibular ligamentTransection of posterior portion of deltoid ligament on calcaneus

POSTERIOR RELEASE :

TAL Z TECHNIQUE; medial half

Capsulotomy of ankle joint (tibiotalar) first

Capsulotomy of talocalcaneal joint

Transection of talofibular and calcaneofibular ligamentTransection of posterior portion of deltoid ligament on calcaneus

MEDIAL PLANTAR RELEASE:

Mobilization of navicular and anterior calcaneus (scar tissue and MASTER KNOT OF HENRY )RELEASE OR LENGTHENING OF TIBIALIS POSTERIOR

Release of superficial deltoid ligament and talonavicularCapsuleIncision of spring ligament anterior to sustentaculum taliand under head of talus

SUBTALAR RELEASE :

Release of posterior and medial joint capsule and bifurcated y ligaments

Naviculo-cuneiform capsulotomy medial displacement of cuneiform on navicular

INTERNAL FIXATION Ensure the relationship of the talus to the calcaneus and navicular is correct and stabilise the foot with 'K' wires with the first wire being passed from the dorsum of the foot across the first metatarsal shaft, the medial cuneiform, the navicular and into the talus second wire fixes the subtalar joint and this should maintain the foot in the corrected position.

Immobilization for 4 months and removal of K wires after 6 weeks

83.8% excellent or good results

OLDER CHILDREN WITH CAVUS DEFORMITY 3 5 yrs. Old

STEINDLER STRIPPING before PMSTR

excision of origin of plantar fascia

abductor hallucis, intrinsic toe flexors and abductor digiti quinti stripped subperiosteally from calcaneus

Structures preserved during sxDorsal structures,medial neurovescular bundle deep deltoid ligamentTalocalcaneos introsseous ligament

INDICATIONS :

Obvious clubfoot deformity with RIGID foot

Walking on lateral border of foot with heel varus

posterior position of fibular or angle less than 76 degrees in relationship of longitudinal plane of foot to bimalleolar plane.

Intoward rotated gait following clubfoot correction with abnormal subtalar complex rotation

5. Parallelism of talocalcaneal angle

McKAYS EXTENSILE SOFT TISSUE RELEASE

Position : prone

Cincinnati incision (Crawford)

Cincinnati incision. provides excellent exposure of the subtalar joint and is useful in patients with a severe internal rotational deformity of the calcaneus. One potential problem with this incision is tension on the suture line when attempting to place the foot in dorsiflexion to apply the postoperative cast. To avoid this, the foot can be placed in plantar flexion in the immediate postoperative cast and then in dorsiflexion to the corrected position at the first cast change when the wound has healed at 2 weeks. This cast change frequently requires sedation or outpatient general anesthesia.

Plantar: plantar fascia, Abd Hallucis and FDB, long and short plantar ligs

medial: identify med structures, release tendon sheathstalonavicular and subtalar release, lengthening tib post ( and also FHL, FDL)

Posterior: ankle and subtalar capsulotomy esp releasing post talofib and the calcaneofibular ligs

Lateral: identify lat structures, release peroneal sheathscalcaneocuboid release, completion of talonavicular and subtalar releasefoot is maintained in corrected position by K-wiring the talonavic jt and also the subtalar jt

STRUCTURES LEFT TO PREVENT ANKLE MOTION Posterior talofibular ligament deep deltoid ligament posterior tibiofibular ligament tibialfibular syndesmosis

CORRECTION OF ROTATION OF CALCANEUS

push calcaneocuboid joint ant. To ankle joint in lateral direction

push calcaneus post. To ankle joint in medial and plantar direction Talocalcaneal pin

OCCASIONALLY

Excision of medial portion of navicular and part of articular surface of calcaneus FHL transferred to peroneus longus (>2yr)

COMPLETE SUBTALAR RELEASE (SIMMONS)Differences with McKay procedure :

release of interosseous ligament

incision of sheath of FHL and FDL

retaining sheath of Tibialis Posterior

plane of incision for Z-plasty of tendoachilles

wedge calcaneocuboid osteotomy

. incomplete subtalar release does not allow the surgeon to correct the calcaneal rotation beneath the talus. The normalization of the talonavicular and calcaneocuboid joints requires a complete release of these joints. Otherwise, the forefoot adduction will persist.(Ghali, Smith, Clayden and Silk. The results of pantalar reduction in the management of clubfoot. J.B.J.S., 1983; 65-B, 1-7)

Residual deformitiesResidual hindfoot equinus : Achilles tendon lengthening and posterior capsulotomy of ankle and subtalar jointsDynamic metatarsus adductus : Transfer of anterior tibial tendon, either as split transfer or entire tendon

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Resistant clubfootMetatarsus adductus : >5 yrs metatarsal osteototomyHindfoor varus : 10 yrs triple arthrodesis

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Neglected clubfootNo / incomplete initial treatment till the age of 1 yearsModerately flexible, moderately stiff, and rigidModified Ponseti*: manipulation for 5-10 mins, two weekly cast change, correction of foot to 30-40 abduction, and AFO for 1 yearExtensive soft tissue release upto 4 yrsDilwyn-Evans, Lichtblau procedureTriple arthrodesisIlizarov/ JESS

Lourenco et al . Correction of neglected club foot by ponseti method. JBJS Br. 2007

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Bony proceduresDwyer osteotomy

Osteotomy of calcaneusOpening wedge medial osteotomy to increase the length and height of calcaneusFor isolated heel varusModified method uses lateral incisions

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Litchblau procedureMedial soft tissue release Lateral closing wedge osteotomy of calcaneusPrevents long term stiffness of hindfootShortens the lateral column

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DILWYN EVANS PROCEDURE

4 8 years

medial incision lengthening of tibialis posterior lengthening of tendoachilles

lateral incision Wedge resection of clcaneocuboid joint calcaneocuboid fusion

DISADVANTAGES

Valgus deformity Restriction of subtalar and tarsal motion

Salvage proceduresTriple arthrodesisSalvage procedure for pain after previous surgical correction.Correction of large degrees of deformity in neglected clubfeet.Not performed before advanced skeletal maturity, at age 10 to 12Lateral closing wedge osteotomy through subtalar and midtarsal joints

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Triple arthrodesis Dunn arthrodesisHoke and kite

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TALECTOMY

severe, untreated clubfoot

for previously treated clubfoot uncorrectable by any other surgical procedures

neuromuscular clubfoot

TENDON TRANSFERS peronei are weak correction of foot achieved late laxity in peronei

relapseTransfer is indicated if the child is more than 30 months of age the ossific nucleus of the cuneiform is large enough to ensure the tendon can heal to the cuneiform and not damage the growth plate andhas a second relapse. Indications include persistent heel varus andforefoot supination during walking; the sole shows thickening ofthe lateral plantar skin. Tibialis Anterior to base of 3rd or 4th metatarsal (if tibialis posterior is cut) - to base of 5th metatarsal (if tibialis posterior is preserved)

Split Tibialis Anterior Transfer

Tibialis posterior

EXTERNAL FIXATORSINDICATIONS :

> 3 years, adolescents adults

relapsed, resistant or neglected clubfeet

arthrogryphotic foot

children treated with extensive open surgery

scarred or infected skin from previous surgery

ADVANTAGES :

can be done when conventional surgery is contraindicated : inadequate, scarred skin infected foot very short foot anesthetic clubfoot d/t myelomeningocele foot due to polio/ cerebral palsy

simultaneous correction of other deformities

softens the contractures/ tethers

less stiffness

PRINCIPLES :

DISTRACTION HISTOGENESIS - below 8 years

WOLFFS LAW

DIFFERENTIAL DISTRACTION on both sides to prevent articular damage on convex side(Convex side distraction is half the rate of concave side)

Ilizarov Correction slow enough to protect soft tissueCorrection at the focus of deformitySimultaneous three-dimensional, multilevel correctionDeformity correction without shortening the foot

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CONTROLLED DIFFERENTIAL FRACTIONAL DISTRACTION USING JESS

2 to 4 transfixing wires in prox tibia Metatarsal Transfixing wire throughMTs

2 transfixing and 1 axial wire through calcaneum

JESSFractional, differential distraction used to Sequentially correct deformities (Medial- 0.25 mm every 6 hours ,Lateral- 0.25 mm every 12 hours)

Distraction continued until approximately 20 degrees of dorsiflexion and overcorrection of the forefoot deformities was achieved Maintained in this overcorrected position for twice as long as the distraction phase by casts/braces

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Results with JESSGood or excellent results reported by Joshi in 84% of his patients Recommended in all who have not responded to serial plaster casting methods. Similar good results have been reported by other authors**

**Suresh et al,2003. Journal of Orthopaedic Surgery 2003: 11(2): 194201

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Complications of surgery Neurovascular injuryLoss of foot (10% have atrophic dorsalis pedis artery bundle)Skin dehiscenceWound infectionAVN talusDislocation of the navicularFlattening and breaking of the talar headUndercorrection/ Overcorrection (esp with Cincinatti)Forefoot adductusHindfoot varusSevere scarringStiff jointsWeakness of the plantar flexors of the ankle

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Thank you for your attention