SEMINAR ON

Club foot

(Congenital Talipes Equinovarus ) Date 02.10.2016

Presenter :Dr Abhishek chaudhary Trainee in orthopaedic surgery SGITO

In this presentation

• Whats a club foot??• epidemiology• etiology• Pathoanatomy• Diagnosis and Differential diagnosis• Management and prognosis• summary

Whats a club foot… Fixation of the foot in adduction, in supination and in

varus and equinus. The calcaneus, navicular and cuboid bones are medially rotated in relation to talus, and are held in adduction and inversion by ligaments and tendons.

has 4 basic deformation:1. fore foot : adduction2. mid foot : cavus3. hind foot : inversion or varus4. hind foot : equinus

- 1 to 2 per 1000 births - male : female = 7:5 - 50% bilateral,25% family history, - 33 % identical twin prevalence - 20% cases are syndromic

Cases perRace thousand birth

Chinese 0.39 (minimum)Japanese 0.53Malay 0.68Filipino 0.76Caucasian 1.12Puerto Rican 1.36Indian 1.51South African black 3.50 (maximum)Polynesian 6.81

Epidemiology of club foot..

Etiology of club foot..

• Idiopathic ,Multifactorial .

• Theories • 1) fetal theory (packaging syndrome)• 2) foot devlopmental arrest theory• 3) retractile fibroblast and collagen• 4) primary germplasm theory(dysplasia of lowerlimb bud)• 5) genetic association -HOX (homeobox genes)• 6) muscular theory

Schematic illustration of the critical periods in human development. During the first two weeks development, of the embryo is usually not susceptible to teratogens. During these pre-embryonic stages, a teratogen either damages all or most of the cells, resulting in its death, or damages only a few cells, allowing the conceptus to recover and the embryo to develop without birth defects. Red denotes highly sensitive periods when major defects may be produced (e.g. amelia, absence of limbs). Yellow indicates stages that are less sensitive to teratogens when minor defects may be induced (e.g. hypoplastic thumbs)

Etiology

- chromosomal theory polygenic (multi factorial)- defect in unfertilized germ cell : - in family - race (palynesia-Maori)

WeekTERM30128 50

- Embryonic theory (0-12) weeks defect occurs during fertilized germ cell

Otogenic theory -- arrest theoryLower limb bud dysplasia Specification defect (Hoofnick)limb specification at 5 month (teratogen)- neuromuscular- vascular- bone

CTEV : post specification defect

primary muscleabnormality?

Intra uterine pressure(packing syndrome)

20

Ponseti : genetic, embryonic malformation, collagen over production in ligament, collagen fibres wavy arranged, dense, many cells

Pathoanatomy of clubfoot..• Herzenberg digital 3D assembly of clubfoot showed• Dysmorphic small talus poorly placed in ankle joint.• Talar neck body declination angle decreased to 90 degree• Talar neck internally rotated 45 degree in relation to ankle joint axis• Internal rotation of calcanium 22 degree• Body of talus externally rotates..

• Major deformity– Inward rotation of the whole foot on the talus

• Rotation primarily takes place in :– talocalcaneal joint– talonavicular joint– calcaneocuboid joint

Pathoanatomy

Talocrural (ankle ) joint :– Talus in equinus– Talus in mortise = external rotation (horizontal breach)– Posterior = capsule & ligament contracted

Pathoanatomy

Talus• Constriction encasement • Head & neck : medial & plantar deviation

Pathoanatomy

Talocalcaneal joint:Calcaneus :rotation in 3 dimensions :

– Sagittal– Coronal– Horizontal

Pathoanatomy

Talonavicular joint :• Navicular : displaced medial & plantarward

• Tib.posterior tendon• Tibio-navic. Ligament (deltoid lig.)• Calcaneo-navic.lig. (spring lig.)• Talo-navic. Ligament• Bifurcate ligament• Cubonavic. Oblique ligament• All navicular ligament

contracted

Pathoanatomy

Calcaneo-cuboid joint:• Cuboid displaced medially on calcaneus and under navicular &

cuneiform.

• All ligaments : contracted• Forefoot : supination and adduction• Calcaneo-cuboid joint corrected nicely if other 2 subtalar complex

are corrected except in resistant CTEV

Pathoanatomy

Muscles • Imbalance between agonist and antagonist• Muscles tonus determined by the amount of muscle

fibres type I & II• All muscle below knee in CTEV fibre Type I > II [similar

with L.M.N lesion : AMC(Arthrogrypsosis multiplex congenita), sacral agenesis, Charcot-Marie, post poliomyelitis]

• Some CTEV tendency to be recurrent

Pathoanatomy vascular

On color doppler • In normal population : a.dorsalis pedis 2.2.% absent

• In mild & moderate CTEV : a.dorsalis pedis = normal

• In severe CTEV : a.dorsalis pedis = 6.7% absent

Examination

• History-deatailed family history neuromuscular disorders.

• Physical examination-supine,prone,pliabilty of foot,spine exam,

• Radiologic examination

Radiology : age more than (4-5) months AP : talo-calcaneal angle :

(200-400), CTEV < 200

Lat : talo-calcaneal angle : (350-500), CTEV<350

Diagnosis..

1. Non rigid type (packing syndrome)2. Rigid type :

– Moderate– Severe

3. Resistance rigid type :– AMC Arthrogrypsosis multiplex congenita– Myelomeningocele– Constriction band

Differential diagnosis

1. Constriction bands (Streeter disease)2. Arthrogrypsosis multiplex congenita3. Myelomeningocele 4. Sacral agenesis5. Tibial agenesis6. Charcot-Marie disease

Amniotic band syndrome

Arthrogrypsosis multiplex congenita

Spina bifida

Caudal regression syndrome

Tibial agenesis

Charcot-Mary disease

Treatment of the clubfoot…

The goal of treatment :• Realignment the calcanium, navicular and cuboid

around the talus.

• Maintain the correction until stable normal function, no pain, plantigrade, good mobility, no callus formation, wearing normal shoe

regular Follow-ups to prevent relapse

History

• Egyptian : tomb painting• India (1.000 BC) : Tx• Hippocrates (400 BC) : manipulative Tx,

early Tx• Indian (Aztecs) Pre Columbian American

Tx : splint with cactus leaves

20th century treatment

Hugh Owen Thomas (1834 -1891) Wrench

21 st century…

1. Conservative2. Operative

Conservative treatment..

Golden period:– 1st week– laxity :estrogen

Methods :- Serial plastering Stretching Dennis Brown splint Adhesive strapping Physiotherapy

Ponseti :

Concept biomechanical understanding

SURGERY is the wrong approach for the treatment of the clubfoot. Ponseti

Ignacio Ponseti..

(3 June 1914 – 18 October 2009) was a Spanish physician..

Based on kinematic of the subtalar joint.

1st concept : the whole foot moves under the talus “calcaneo- pedis block”2nd concept : forefoot and hind foot are corrected simultaneously by abductionEquinus correction :

– mostly close tenotomy– tendo achilles non stretchable collagen, thick and stiff

Ponseti Clubfoot correction steps..

a. realign cavus : forefoot supinated using head of first metatarsal

b. fulcrum : head of the talus c. After forefoot in supination do abductiond. maximal abduction of forefoote. Dorso flexion of the ankle (+ tenotomy)

A,b,c,d steps are repeated in each plastering.Plaster cast above knee (groin), knee flexion 100 degree

if in last cast 70 degree of abduction achieved start equinus correction (e)

Ponseti club foot correction

Ponseti

Tenotomy …• 90 % of club foot correction requires tenotomy.• After achieving about 50 degree of abduction after

serial plaster and completely corrected cavus and varus.• LA/short GA• Successful tenotomy-sudden snap,palpable gap,more

then 10degreee of dorsiflexion.• Plaster 3 weeks • bracing for 3 months (24hours)• (2-4) hours day time, 12 hours at nigh• (3-4) years night splint• Ponseti success rates = 90%

Tenotomy …

Methods of measuring progress of correction

• Dimeglio classifiction• Pirani score

Tips tricks and pitfalls in ponseti technique..

1. NEVER DO pronation during correction of adduction to abduction.

2 ALWAYS USE head of talus as fulcrum.(surface anatomy)

3. DON’T PRESS Calcaneum lateral ward to correct varus

4. DON’T CORRECT Equinus before adduction and varus are corrected Rocker bottom foot

5. NEVER DO Plaster immobilisation below knee.

6. DON’T TRY IN Nervous infant

7 . DON’T PUT Excess pressure on talar head

8. ILL trained assistant 9. Too much padding10. Improper moulding

Plaster correction complication..

1. Neuromuscular2. Pressure necrosis

Plaster correction complication

3. Rocker bottom foot5. Increase cavus deformity6. Longitudinal breach7. Stiff joint8. flat top talus

Ready! Set! Brace! Foot abduction brace

Followup :every 3 weeks till 2 yearsThen every 6 months till 5 years

Static ankle foot orthosis (AFO) for daytime

Relapsed clubfoot• Any foot requiring further intervention following

successful correction with ponseti technique. usually happens in first 6 months of correction.

• Initially supple (muscle dissemblance) later if ignored become rigid .

• Recurrence is in reverse order of deformity correction.

• Causes : non compliant of braces,idiopathic

Treatment options for relapse clubfoot• Ponseti: do overcorrection ,successive plaster for 2

weeks each, tenotomy,continue FAB till 5 years of age.• If requires (<10 % cases ) lenghtning of tendoachilles (if

age is >2.5 years) and tibialis anterior tendon transfer.

Neglected clubfoot• Clubfoot without any treatment or partial treatment which has bones

and joints of the foot deform into fixed equines, adducts, cavus, and supination as the patient walk on the side or dorsum of the foot.

• Classification:1.partially flexible-2.Partially firm3.Rigid

Treatment options:PonsetiPMR +osteotomyJESS,ILIZAROVTalectomyTriple arthodesis

Operative treatment..

Indication1. Conservative Tx—fail Ponseti + 5%2. Neglegcted clubfoot.

3. Relapsed ,resistant clubfoot

Postero medial release (Turco)One stage procedure

Free the calcanium-subtalar posterior,medial and lateral release

Talonavicular joint reduced and pinned-casting x 3 months then 3 year splints.

Cincinati-circumferential release

incision 8 to 9 cm long extending from the base of 1st metatarsal to the tendo calcaneus, curving it slightly just inferior to the medial malleolus.

Start posterioly and release /lengthen the ligaments or tendons as required..

Ilizarove external fixator

Joshi external fixator –differential distraction osteosynthesis

Triple arthrodesis (adult)

Surgical complications..

1. Infection2. Bad scar3. Stiff joint4. Over/under correction5. Navicular dislocation6. Flattening or beaking talar head7. Talar necrosis8. Weakening of the muscles 9. Skew foot (severe valgus of the heel and adduction of

the fore foot)10. Main artery injury foot necrosis

• Most commen congenital musculoskeletal disorder characterized by CAVE deformity requires as early as possible conservative treatment ( ponseti method).

• With success rate of more then 90 % all over and

upto 98 % in india ponseti method is standard and should be first line method of treatment in all age group including neglected clubfoot in adolecents.

• Conservative treatment provide the best long term results.

Summary of clubfoot

• http://globalclubfoot.com/ponseti/pirani-scoring/

• Textbook of paediatric orthopaedics tachdjians.

• Pubmed central J Child Orthop. 2016 Jul 19.• J Pediatr Orthop. 2016 Jul 2.• Netters atlas.• Campbell orthopedic textbook

References

• Thank you ..