SEMINAR ON CLUBFOOT BANGALORE OTHOPAEDIC SOCIETY TEACHING PROGRAMME

1. SEMINAR ON
Club foot
(Congenital Talipes Equinovarus )
Date 02.10.2016
Presenter :Dr Abhishek chaudhary
Trainee in orthopaedic surgery SGITO

2. In this presentation
• Whats a club foot??
• epidemiology
• etiology
• Pathoanatomy
• Diagnosis and Differential diagnosis
• Management and prognosis
• summary

3. 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 : adduction
2. mid foot : cavus
3. hind foot : inversion or varus
4. hind foot : equinus

4. - 1 to 2 per 1000 births
- male : female = 7:5
- 50% bilateral,25% family history,
- 33 % identical twin prevalence
- 20% cases are syndromic
Cases per
Race thousand birth
Chinese 0.39 (minimum)
Japanese 0.53
Malay 0.68
Filipino 0.76
Caucasian 1.12
Puerto Rican 1.36
Indian 1.51
South African black 3.50 (maximum)
Polynesian 6.81
Epidemiology of club foot..

5. 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

6. 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)

7. Etiology
- chromosomal theory
polygenic (multi factorial)
- defect in unfertilized
germ cell :
- in family
- race (palynesia-Maori)
Week
TERM3012850
- Embryonic theory
(0-12) weeks
defect occurs during
fertilized germ cell
Otogenic theory -- arrest theory
Lower limb bud dysplasia
Specification defect (Hoofnick)
limb specification at 5 month
(teratogen)
- neuromuscular
- vascular
- bone
CTEV : post
specification defect
primary muscle
abnormality?
Intra uterine pressure
(packing syndrome)
20
Ponseti : genetic, embryonic malformation, collagen
over production in ligament, collagen
fibres wavy arranged, dense, many cells

8. 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

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

12. Pathoanatomy
Talus
• Constriction encasement
• Head & neck :
medial & plantar deviation

13. Pathoanatomy
Talocalcaneal joint:
Calcaneus :
rotation in 3 dimensions :
– Sagittal
– Coronal
– Horizontal

15. 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

16. 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

18. 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

19. 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

20. Examination
• History-deatailed family history
neuromuscular disorders.
• Physical examination-
supine,prone,pliabilty of foot,spine exam,
• Radiologic examination

24. Radiology : age more than (4-5) months
AP : talo-calcaneal angle :
(200-400), CTEV < 200
Lat : talo-calcaneal angle :
(350-500), CTEV<350

25. Diagnosis..
1. Non rigid type (packing syndrome)
2. Rigid type :
– Moderate
– Severe
3. Resistance rigid type :
– AMC Arthrogrypsosis multiplex congenita
– Myelomeningocele
– Constriction band

26. Differential diagnosis
1. Constriction bands (Streeter disease)
2. Arthrogrypsosis multiplex congenita
3. Myelomeningocele
4. Sacral agenesis
5. Tibial agenesis
6. Charcot-Marie disease

27. Amniotic band syndrome

28. Arthrogrypsosis multiplex congenita

29. Spina bifida

30. Caudal regression syndrome

31. Tibial agenesis

32. Charcot-Mary disease

33. 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

34. 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

35. 20th century treatment
Hugh Owen Thomas (1834 -1891) Wrench

36. 21 st century…
1. Conservative
2. Operative

37. Conservative treatment..
Golden period:
– 1st week
– laxity :estrogen
Methods :-
Serial plastering
Stretching  Dennis Brown splint
Adhesive strapping
Physiotherapy

38. Ponseti :
Concept biomechanical
understanding
SURGERY is the wrong approach for the treatment of the clubfoot.
Ponseti

39. 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 abduction
Equinus correction :
– mostly close tenotomy
– tendo achilles non stretchable collagen, thick and stiff

40. 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 abduction
d. maximal abduction of forefoot
e. 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

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

42. Ponseti
club foot
correction

43. Ponseti

44. 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%

45. Tenotomy …

46. Methods of measuring progress of
correction
• Dimeglio classifiction
• Pirani score

48. 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 padding
10. Improper moulding

49. Plaster correction complication..
1. Neuromuscular
2. Pressure necrosis

50. Plaster correction complication
3. Rocker bottom foot
5. Increase cavus deformity
6. Longitudinal breach
7. Stiff joint
8. flat top talus

51. Ready! Set! Brace! Foot abduction brace
Followup :
every 3 weeks till 2 years
Then every 6 months till 5 years

52. Static ankle foot orthosis (AFO) for daytime

53. 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

54. 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.

55. 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 firm
3.Rigid
Treatment options:
Ponseti
PMR +osteotomy
JESS,ILIZAROV
Talectomy
Triple arthodesis

56. Operative treatment..
Indication
1. Conservative Tx—fail Ponseti + 5%
2. Neglegcted clubfoot.
3. Relapsed ,resistant clubfoot

57. 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.

59. 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..

63. Ilizarove external fixator

64. Joshi external fixator –differential distraction osteosynthesis

65. Triple arthrodesis (adult)

68. Surgical complications..
1. Infection
2. Bad scar
3. Stiff joint
4. Over/under correction
5. Navicular dislocation
6. Flattening or beaking talar head
7. Talar necrosis
8. Weakening of the muscles
9. Skew foot (severe valgus of the heel and adduction of
the fore foot)
10. Main artery injury  foot necrosis

70. • 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

71. • 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

72. • Thank you ..