The document discusses congenital talipes equinovarus, also known as clubfoot. It defines clubfoot and describes the bony and soft tissue abnormalities associated with it. The document discusses various theories for the cause of clubfoot, including mechanical, neuromuscular, genetic, and vascular factors. It also outlines the clinical features and types of clubfoot based on cause, treatment stage, and severity. The Pirani scoring system for assessing the severity of clubfoot deformities is introduced.

1. CONGENITAL TALIPES
EQUINOVARUS
PRESENTOR-DR VIRESH M
MODERATOR-DR MANIKYA R

2. Definition
• Developmental deformation
of foot
• Rotational subluxation of
talocalcaneonavicular joint
complex with talus in plantar
flexion & subtalar complex in
medial rotation & inversion
• Clinically characterized by
• Equinus & varus of heel
• Forefoot adduction
• Midfoot supination

3. CLUB FOOT
Definitions
Talipes: Talus = ankle
Pes = foot
Equinus: (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

4. CLUB FOOT
Planus: flatfoot
Cavus: highly arched foot
Varus: heel going towards
the midline
Valgus: heel going away
from the midline
Adduction: forefoot going
towards the midline
Abduction: forefoot going away
From the midline
Forefoot Hind foot

5. Epidemiology
• Commonest congenital orthopaedic abnormality
• 1.3:1000 live births
• Males>Females – 2:1
• 30-50% bilateral
• Much more common in Polynesian & Maori & lower in
Asians

6. ETIOLOGY
Theories :
• Mechanical factor in utero
• Neuromuscular defect
• Primary Germ Plasma defect
• Arrest of fetal development (otogenic theory)
• Heredity
• Heredity & environment
• Myogenic theory
• Drug induced
• Effect of eclipse
• Chromosomal theory

7. MECHANICAL FACTOR IN UTERO
Foetal theory (Browne 1933)
• Oldest theory
• Proposed by Hippocrates
• Believed that foot was held in equinovarus by
mechanical factors in utero.

8. Intrauterine factors
Pressure theories:
 Oligohydramnios
 Abnormal fetal positioning
 Overweight baby
 twins
Placental insufficiency
Constriction bands
Maternal illness ( anemia, thyroid disorders )
Infective pathogens (enteroviruses)

9. Neuromuscular imbalance theory
(Issac et al)
• Dominant neurogenic factor.
• Muscle imbalance may produce the deformity.
• Peroneal dysplasia, peroneal neuropathy and intrauterine
paralysis have been blamed to be the cause of clubfoot.
• Congenital fibre imbalance between type 1 & 2 muscle fibers
and atrophy of type 1 fiber found in peroneal and triceps surae
muscle in histopathological specimen.
• E.g.Cerebral palsy, spina bifida,poliomyelitis

10. • Martin et al demonstrated reduced motor unit counts in
the distribution of the common peroneal nerve as a
constant finding in CTEV.
• Sodre et al suggested the importance of accessory
muscles in producing equinovarus deformity depending
upon their insertion and dynamic action.

11. PRIMARY GERM PLASM
DEFECT
• Irani and Sherman (1963)
• Primary Germ Plasm defect
affecting the head and neck of
talus.
• Defect in cartilaginous talar
anlage producing dysmorphic
neck and navicular
subluxation.
• Occurs between conception
and 12 weeks

12. ARREST OF FETAL DEVELOPMENT
Bohm (1929) otogenic theory
•Normally the foot in 6 to 8 wk old
fetus has characteristics of Club foot
and becomes normal at 12 to 14 wks
•Arrest in physiological developmental
phase results into equinovarus
deformity. Temporary arrest at 7-8
weeks produces severe deformity
whereas arrest after 9th
week
produces mild to moderate deformity.

13. GENETIC THEORY (Chromosomal
theory)• In otherwise normal infants is the result of a multifactorial
system of inheritance.
• It has been reviewed Cowell and Wen (1980) that clubfoot
maybe a part of a syndrome.
• 32.5% concordance rate among monozygotic twins
as compared to 2.9% among dizygotic twins
• Major gene effect (inherited in recessive manner)
with additional polygenes and environmental factors

14. RETRACTILE FIBROSIS (Primary soft
tissue defect)
• Fried (1959) suggested abnormal tibialis posterior tendon
and contracted deltoid ligaments.
• Ippolito and Ponseti (1989) postulated a primary
genetically induced retractive fibrosis as the cause.
• Increased fibrous tissue in muscles and ligaments leads
to contracture of soft tissues and hence development of
deformity.

15. Myogenic theory
• This theory postulates that primary defect is in muscles to
which the deformities follow.

16. Vascular Theory
• Hootnick et al have proposed the possibilities of
diminution of anterior tibial artery and its derivatives as the
possible cause of CTEV since majority of the limbs have
this abnormal arterial pattern.
• Clinically children with CTEV have mostly hypoplastic
hypotrophic anterior tibial artery along with calf muscle
atrophy.

17. Chemical theory
• This theory suggests the possibilities of certain
drugs/chemicals producing the clubfoot deformitiy.
• Duraiswamy (1967) produced congenital malformations of
limb by injecting insulin in the chick embryo.
• Use of aminopterin for abortions has also known to cause
clubfoot deformity.
• Association of AMC and severe clubfoot with the use of d-
tubocuraraine in the 1st
trimester.

18. Heredity and Environmental theory
• The deformity probably results from a combination of
multifactorial genetic predisposition and some intrauterine
environmental factors.
• There is an increased incidence of clubfoot among
relatives of the affected, heredity plays some role in the
etiology but the exact manner is unclear.
• The theories have encompassed a broad spectrum of
modes of inheritance like autosomal recessive, sex linked,
autosomal dominant.

19. • Further support for this combination theory is provide by
Idelberger’s study, in which he reported that both twins of
an identical set were affected in 33% of cases.
• The combined hypothesis maintains that some
intrauterine factor in conjunction with hereditary
predisposition causes a disturbance in development at a
critical stage of embryonic development of the foot.

20. Cosmic theory
• Though no authentic work could be traced about the effect
of cosmic rays on early developing embryo, especially
during eclipse it has been blamed as the possible cause
for clubfoot.

21. Adaptive Changes
Wolff’s Law
“ Every change in the use of static function of
bone caused a change in the internal form or
architecture as well as alteration in its
external formation and function according to
mechanical law ”
Davis Law
“ When ligaments and soft tissue are in loose
or lax state; they gradually shorten ”

22. • The etiology of clubfoot is still unknown. However from our
present knowledge it would appear that no single theory can be
implicated in all cases.
• In conclusion no one theory can explain the etiology of all
congenital idiopathic clubfeet. Evidence has been presented
that different causative factors can produce the same
deformity.
• The possibility exists that CTEV represents a deformity that
can be caused by many etiological agents
• The answer regarding the etiology of clubfoot will depend on
new advances in our knowledge of genetics and development
of advanced histochemical and microscopic examinations.

23. Bony abnormalities
• Talus:
Head & neck deviated medially & plantarward
Body rotated externally in the ankle mortise
Body extruded anteriorly
• Smaller than normal
• Angle formed by head & neck.
• Normal 150-160 degree
• In ctev reduced to 115-135 degree.

24. Navicular:
Medially displaced
Close to medial malleolus
Articulates with medial surface of
head of talus
Calcaneus
Anterior portion lies beneath the head of
talus causing varus and equinus of heel
In equinus
Rotated medially
posterior tuberosity displaced upwards &
laterally.
anterior end displaced downwards &
medially.
Sustantaculum tali displaced medially to
under talar head, may be
underdeveloped

25. • Cuboid
Displaced medially on the
dysmorphic distal end of the
calcaneus
• Talonavicular joint
In inversion
• Cuneiform and metatarsal:
Minimal displacements

26. Ponseti’s dissection of 7month
fetus
Tibio-talar plantar flexion
Medially displaced navicular
Adducted and inverted
calcaneus
Medially displaced
cuboid

27. Kinematic Coupling
• It is the term given to the manner in which the movement
of one tarsal bone affects the movement of others in the
subtalar joint.
• Calcaneal adduction, inversion and plantar flexion occur
together.
• Calcaneal abduction, eversion and dorsiflexion occur
together.
• Foot abduction causes calcaneal abduction.
• Calcaneal abduction corrects heel varus and calcaneal
plantar flexion.

28. Soft tiSSue
changeS
Posterior structures
Tendo achilles
 Post. capsule of
ankle joint & subtalar
joint

29. • Medial :
Tibialis posterior
FHL,FDL, Master Knot
of Henry
 Spring ligament
Deltoid ligament
Interossseus talo
calcaneal ligaments

30. • Plantar wards :
Plantar fascia
Plantar ligaments
Flexor hallucis
longus & abductor
hallucis
Laterally
Calcaneofibular
ligament
Calcaneocuboid joint

31. cLinicaL
featuReS• Deformity C-A-V-E
Cavus
Forefoot adduction
Heel varus
Heel equinus
Midfoot supination

32. COMPONENTS OF THE DEFORMITY
Equinus
1. Ankle joint equinus
2. Inversion of talocalcaneonavicular complex
3. Plantar flexion of foot

33. Components of deformity
• Varus
• Hindfoot is rotated inwards ,
• occur primarily at Talocalcaneonavicular joint
• Adduction
• foot is deviated medially
• Occurs at talonavicular calcaneo-cuboid and subtalar joint
• Cavus
• Forefoot plantar flexion in relationship to hind foot causes cavus
deformity
• Occurs at midtarsal joint.

34. • Features
Curved lateral border of foot
Devil’s thumbprint over the lateral malleolus. Skin on
lateral side is thinned and stretched & atrophied
Medial & Lateral skin creases
Navicular is closer to medial malleolus
Calcaneum is closer to the lateral malleolus
Heel small & high
On passive dorsiflexion and eversion, taut TA and post.
Tibial tendon can be palpated
Deep cleft on the medial planter surface
Lateral malleolus is posterior to and more prominent than
the medial malleolus

35. General
Calf atrophy
Calf shortening
Restricted ankle motion
Painful callosities and bursa on lateral aspect
The size of the of the foot is also smaller in length and
breadth

36. PATHOGNOMONIC SIGN
• In normal newborn,on
passive dorsiflexion, the
dorsum of the foot will
usually touch or closely
approximate the anterior
end of the lower tibia
• In clubfoot , dorsiflexion is
impossible even when
strong pressure is applied

37. 1.Types of clubfoot according to the cause of the
deformity
Idiopathic clubfoot is diagnosed when the child is
otherwise normal on physical examination and has no
associated neuromuscular, spinal or other syndromic
problems apart from the clubfoot deformity.

38. Secondary Clubfoot is diagnosed when the deformity
forms part of another health condition.
•Neurogenic clubfoot – clubfoot that is associated with
neurological abnormalities or results from a neuromuscular
disease such as Spina Bifida.
•Syndromic clubfoot – clubfoot that forms part of a wider
musculoskeletal syndrome, such as arthrogryposis or
amniotic band syndrome or other congenital syndromes.

43. Postural/Positional clubfoot is diagnosed when the child
has a very flexible clubfoot deformity with close to full range
of motion at both the ankle and forefoot.
•The postural clubfoot can be corrected with only one or
two casts.
•May need only exercises or limited brace use to maintain
correction.
•Thought to result purely from posture in the womb late in
the pregnancy.

44. Metatarsus adductus is not a clubfoot, but is diagnosed
when the child has forefoot adduction but normal range of
motion at the ankle.
•In Pirani scoring, the HFCS is zero, and the MFCS is
higher than zero.
•Metatarsus adductus can be confused with a clubfoot
deformity.

45. 2.Types of clubfoot according to treatment stage:
Untreated Clubfoot is classified when the affected child is
under two years of age and has had no (or very little)
treatment to date.

46. Treated Clubfoot is classified when the affected child’s
feet have corrected with the Ponseti method and they have
completed the casting phase of treatment.
•Treated clubfoot are braced full time for three months and
at night for three to four years.
•Regular reviews are essential to prevent recurrence.

47. Resistant clubfoot is classified when a child has a
previously untreated clubfoot that does not correct with
the Ponseti method.
• Hindfoot and/or Midfoot contractures persist.
• Resistant clubfeet are often seen as part of a syndrome
( e.g. arthrogryposis, spina bifida) and surgery can be
necessary to correct the deformity.

48. Recurrent Clubfoot is classified in children who show
signs of recurrence in previously ‘treated’ clubfeet.
• Typical signs of recurrence are supination of the entire
foot(resulting from an overactive tibialis anterior muscle)
or hindfoot equinus (resulting from an overactive Gastro-
soleus complex).

49. • Most recurrence occurs because of failure to
appropriately wear the foot abduction brace.
Recurrence is treated by a return to Ponseti
casting or tenotomy. In some cases of recurrence
the child may require surgery.

50. Neglected Clubfoot is classified as a clubfoot in a child
older than two years who has had little or no treatment. By
this time child is already walking and bone and joint
deformities begin to appear.
•Ponseti treatment can safely be tried in these children also
and there are encouraging reports of good results in many
of these. Even if surgery is required the magnitude of
surgery is reduced by preoperative Ponseti casting.

51. Complex Clubfoot is classified for any clubfoot that has
received any type of treatment other than Ponseti method
(such as Kite manipulations or surgery)
•These clubfeet may have added complexity because of
changes from the manipulative or operative intervention.
•Evaluation and treatment of the complex clubfoot must be
individualized.

52. Atypical Clubfoot
• Deep posterior crease
• Transverse crease
• Marked ‘across foot’ cavus
• Hyperextended great toe. Appear short.
• Short fat foot

53. The Pirani Score
• A reliable method for assessing the amount of deformity in
congenital clubfoot
• Easy to use
• Inter-observer reliable and valid
• Formulated by Dr Shafique Pirani
 The Royal Columbian Hospital Clubfoot Clinic
Departments of Orthopaedic Surgery & Radiology,
University of British Columbia, Vancouver, Canada

54. •A child’s total Score (TS) is
between 0 and 6
•6 ‘signs’ are assessed, and each is
scored 0,0.5, or 1, depending on
severity.
•A total score of 0 = no deformity, a
total score of 6 = severe deformity

55. • The total Score is comprised of :
 Hindfoot Contracture Score (HFCS) between 0 and 3
 3 signs each scored 0,0.5, or 1
 Midfoot Contracture Score (MFCS) between 0 and 3
 3 signs each scored 0,0.5, or 1

56. Hindfoot Contracture Score
Posterior Crease(PC):
•Assess the depth of the crease and the presence of other
creases.
•The presence of several fine crease is scored 0, two or
three moderate creases is scored 0.5 and a single, deep
crease is scored 1. you cannot see the depth of the crease
in a deep crease.

57. Posterior Crease

58. Empty Heel (EH) :
•Hold the foot in mild correction and palpate with a single
index finger.
•Ascertain how much flesh there is in the heel between
your finger and the calcaneous.
•If it easy to palpate the calcaneous, which is not far under
the skin, score 0. Score 0.5 for a palpate-able calcaneous
which is felt through a layer of flesh. If the calcaneous is
deep under a layer of tissue and very difficult to palpate,
score 1. A heel that feels soft like the heel of your palm is
score 1, when it feels firm like the tip of your nose it is a
score 0.5 and when it feels hard like pressing on your
forehead score 0.

59. Empty Heel

60. Rigid Equinus(RE):
•Correct the plantar flexion as much as is comfortable for
the child (use the Ponseti method of manipulation).
•Assess the degree of dorsiflexion obtained: <90 = 0, 90 =⁰ ⁰
0.5, > 90 = 1⁰

61. Rigid Equinus

62. Midfoot Contracture Score
Medial Crease (MC) :
•Assess the depth of the crease and the presence of other
creases.
•The presence of several fine creases is scored 0, two or
three moderate creases is scored 0.5, and a single, deep
crease is scored 1.

63. Medial Crease

64. Lateral Head of Talus (LHT) :
•Palpate the head of the talus with the foot uncorrected
(may be easier to find if you move the foot into a more
deformed position).
•Keeping your finger/thumb on the Talus, correct the foot.
•If the talus completely sinks away under the navicular,
score 0. if it moves partially but doesn’t completely sink,
score 0.5, if it remains fixed and does not sink, score 1.

65. Lateral Head of Talus

66. Curved Lateral Border (CLB) :
•Do not hold in correction. Make sure the child’s foot is
relaxed.
•Observe from the plantar aspect, and use a pen held
against the edge of the foot.
•Assess the point on the lateral border of the foot at which it
deviates from a straight line.
•If the border of the foot (excluding the phalanges) is
straight and without deviation, score 0. if it deviates at the
level of the metatarsals, score 0.5. if it deviates at the
calcaneo-cuboid joint, score a 1.

67. Curved Lateral Border

68. Child has flexible foot with
near full range and low
Pirani Score.
Child scores in both hind
and mid foot categories
Child has mid- but no
hind- foot contracture
scores.
Child presents with an apparent clubfoot deformity.
The foot is assessed using the Pirani Score.
The child is given a general physical
assessment : parents asked if they’ve
noticed any other problems.
Some abnormalities
are noted during the
physical exam.
The physical assessment is
normal and no other
abnormalities are noted.
Secondary
Clubfoot
Idiopathic
Clubfoot
Neuropathic
clubfoot
Child has symptoms
indicative of a
syndromic condition
(e.g.arthogryposis)
Child has symptoms
indicative of a
neurological condition
(e.g. spina bifida)
Metatarsus
Adductus Postural
Clubfoot
Syndromic
clubfoot

69. Child presents with apparent clubfoot.
Parents are asked about the child’s treatment history
Child has had non-
Ponseti clubfoot
treatment
Treated
clubfoot
Resistant
Clubfoot
Foot has
corrected
Foot has not
corrected
Child has never had
clubfoot treatment
Clubfoot has had Ponseti
clubfoot treatment
Deformity
recurs
Neglecte
d
Clubfoot
Untreate
d
Clubfoot
Child is over
two years
Child is under
two years
Recurrent
Clubfoot
Complex
Clubfoot

70. PONSETI’S METHOD OF SERIAL
CASTING
Goal:
1. Plantigrade, pliable,pain free, normally shoe-
able foot in the shortest treatment time
2. Least disruption of child’s & family life.
3. Manipulation & serial casting followed by
Tendo achilles tenotomy
4. With long term application of foot abduction
brace

71. Serial casting
• Stood test of time
• Enjoyed periods of popularity (1930s, 1960s, 1990s)
• 2 major schools
• Kite (1930-1960)
• Ponseti (1960-2001)

72. Ponseti, 1960
• Simultaneous correction of all deformities
• 95% success rates,
• Stress on ABDUCTION as corrective force rather than
EVERSION
• Correct equinus last by percutaneous tenotomy in the
clinic

73. MANIPULATION AND LONG LEG CAST WITH KNEE IN 90*
FLEXION.
FIRST CAST : The cavus is first corrected by supinating the
forefoot and dorsiflexion of the first metatarsal.
The forefoot must never be pronated
Foot immobilized in a plaster cast for seven days.

74. PONSETI METHOD
• Steps:
Cavus is corrected by
supinating the forefoot and
dorsiflexing the 1st
metatarsal

75. PONSETI METHOD
To correct the varus and
adduction, the foot in
supination is abducted while
counter pressure is applied
over head of talus.

76. The calcaneus abducts by
rotating and sliding under
the talus and as the
calcaneus is abducted it
simultaneously extends and
everts and heel varus is
corrected.
5 –6 serial casts may be
required.
End point of casting is when
there is about 60 degree of
abduction

77. 1st Cast

78. 1st Cast

79. 1st Cast

83. IMMOBILIZATION IN CAST
• Above knee casts are given
• Plaster cast changed every week

84. • Cast Change Every 5 To 7 Days
• FROM 2nd
CAST ONWARDS ABDUCT THE FOREFOOT
WITH COUNTER PRESSURE ON HEAD OF TALUS
• Increase Abduction Gradually
• Never Pronate The Foot
• Never Touch The Heel.

85. First Cast is Critical as it corrects the supination and aligns the
forefoot with the hindfoot

87. Serial casting

88. • Percutaneous tenotomy of the Achilles tendon is often
required for complete correction of the equinus
• Tenotomy is indicated when HS>1,MS<1 & head of talus is
covered and abduction of foot is more than or equal to 60
degree.
• Post-tenotomy cast: Foot abducted to 60°. Cast removal
after 3 weeks.

89. PERCUTANEOUS TENDO
ACHIELLES TENOTOMY
• It is performed on OPD basis
• Under local or no anesthesia
• Parts are painted and assistant holds the foot in maximum
dorsiflexion
• The surgoen feels the taut TA tendon
• 11 no blade with BP handle is inserted vertically 2 cm
proximal to the insertion of tendo Achilles on medial side
to protect posterior tibial artery

90. • It is then turned horizontally, and moved towards the skin
till the assistant feels the sudden gain in dorsiflexion
• Atleast 15 degree of dorsiflexion has to be gained
• Wound is dressed with betadine gauze and final cast is
applied

92. ATYPICAL CLUBFOOT
• Carefully identify the Talar head laterally
• While manipulating the index finger should rest over the
posterior aspect of lateral malleolous while the thumb
exerts pressure over the talar head
• Do not abduct more than 30 degree
• After obtaining 30 degree of abduction emphasis is on
cavus correction
• All the metatarsal heads are lifted simultaneously for
cavus correction

93. • Always apply high groin cast in 110 degree flexion of knee
to prevent cast slippage
• After tenotomy atleast 10 degree of dorsiflexion should be
achived, if not then change cast every week in dorsiflexion
till sufficient dorsiflexion is achived

94. Kite, 1930
• Sequential correction in C-A-V-E order
• Serial wedging casts
• Achieved 60% success rates
• “What is gained without force, is achieved without
harm”

95. COMMON ERRORS IN CASTING
• Pronation or eversion of the foot- worsens the deformity
by increasing the cavus. Creates a new deformity of
eversion leading to a “bean shaped foot”
• Kite’s Error- thumb on the calcaneocuboid joint. The
calcaneus can evert only when it is abducted under the
talus.
• External rotation of the foot to correct adduction while
calcaneum remains in varus- this causes a posterior
displacement of the lateral malleolusby externally rotating
the talus in the ankle.

96. • Frequent manipulations without casting- the foot should
be immobilised with the contracted tissues at a maximum
stretch after manipulation.
• Applying a below knee cast- these do not hold the forefoot
abducted. Above knee casts also prevent slipage
• Attempt to correct equinus before heel varus and
supination- results in a rocker bottom foot
• Attempts to obtain a perfect anatomical correction- it is
wrong to assume that early aligment of the displased
skeletal elements results in a normal anatomy

97. END POINT TREATMENT
• No adduction / inversion deformity.
• Passive movement to calcaneovalgus position.
• Child is able to evert & dorsiflex foot voluntarly to about
90* .
• Talar head prominence over dorsum of foot is absent.

98. CONCLUSION
• Proper understanding of the patho anatomy is a must
• Ponseti’s method is now the standard and the best mode
of treating clubfoot
• Indications for surgery is limited in clubfoot but well
defined

99. Foot abduction brace
 It’s a orthotic used to maintain correction
of deformity obtained by Ponseti’s
technique.
 Consists of two straight last open toe
shoes and a connecting bar.
 Shoes are mounted onto bar in position
of 70 degree of external rotation and 15
degree dorsiflexion in bilateral cases

100.  In unilateral cases,40 degree ER in normal side and 70
degree in affected side
 Distance between shoes should be 1 inch wider than
shoulder width
 Knees are left free so that child can kick them,which
leads to stretching of gastrosoleus tendon
 The onus of maintaining correction using FAB should be
given to parents under regular follow up.

101. At the end of casting, the foot is
abducted to an exaggerated
amount, which should measure 60
to 70 degrees (thigh-foot axis).
After the tenotomy, the final cast
is left in place for 3 weeks.
Ponseti’s protocol then calls for a
brace to maintain the foot in
abduction and dorsiflexion.
This degree of foot abduction is
required to maintain the abduction
of the calcaneus and forefoot and
prevent relapse.
INTRODUCTION

102.  The medial soft tissues remain
stretched out only if the brace is used
after the casting.
 The abduction of the feet in the
brace, combined with the slight bend
(convexity away from the child),
causes the feet to dorsiflex

103. Foot abduction brace

104. How to measure for the correct SFAB.
In general the real length of the foot sole of the baby in
centimeters corresponds with the size of the SFAB needed
Do not add a centimeter as an allowance for growth.

105. Three weeks after the tenotomy, the cast is removed
and a brace is applied immediately.
The brace consists of open-toe high top straight-last
shoes attached to a bar .
For unilateral cases, the brace is set at 60 to 70 degrees
of external rotation on the clubfoot side and 30 to 40
degrees of external rotation on the normal side .
 In bilateral cases, it is set at 70 degrees of external
rotation on each side. The bar should be of sufficient
length so that the heels of the shoes are at shoulder
width .
BRACING PROTOCOL

106.  The bar should be bent 5 to 10 degrees with the
convexity away from the child, to hold the feet in
dorsiflexion.
The brace should be worn full time (day and night)
for the first 3 months after the last cast is
removed.
After that, the child should wear the brace for 12
hours at night and 2 to 4 hours in the middle of
the day, for a total of 14 to 16 hours during each
24-hour period.

107. This protocol continues until the child is 3 to
4 years of age.
Occasionally, a child will develop excessive
heel valgus and external tibial torsion while
using the brace.
In such instances,the physician should
reduce the external rotation of the shoes on
the bar from approximately 70 degrees to
40 degrees

108. Types of braces
New modifications to original Ponseti ‘s brace
makes the foot more secure in the brace,
more easily applied to the infant, and allow
the infant to move. This flexibility may
improve compliance.

109. 1. H.M. Steenbeek working
for the Christoffel Blinden
Mission in Katalemwa
Cheshire Home in
Kampala, Uganda.
2. Developed a brace that
can be made from simple,
easily available materials
3. Contains a inspection hole
near heel to observe for
proper position of foot in
brace.

110. 2. John Mitchell has designed a brace
under
Dr Ponseti’s direction.
This brace consists of shoes made of a
very soft leather and a plastic sole that is
molded to the shape of the child’s foot,
making this shoe
very comfortable and easy to use.

111. Dr. Matthew Dobbs of the Washington
University School of Medicine in St. Louis, USA
developed a new dynamic brace for clubfoot
that allows the foot to move while maintaining
the required rotation of the foot .
An ankle-foot orthoses are required as part
of this brace to prevent ankle plantar flexion.

112.  Dr. Jeffrey Kessler of the
Kaiser Hospital in Los
Angeles, USA developed a
brace that is flexible and
inexpensive.
 The bar is made of 1/8”
thick polypropylene and is
malleable.
 The brace allows child to
plantar flex during
kicking,returns to original
dorsiflexed position once

113.  Dr. Romanus developed this brace in Sweden.
 The shoes are made of malleable plastic that is
molded to the shape of the child’s foot.
 The inside is covered by very smooth leather,
which makes the construct very comfortable.
 The shoes are fixed to the bar with screws.

114. DENIS BROWNE SPLINT
First deviced by Denis
Browne(1892-1967) at
Ormond Street
hospital,London.
Consists of a curved bar
attached to soles of pair of
high topped shoes.
It is equipped with wing nuts
to allow individual abduction
of each foot.

115. Importance of bracing
The Ponseti manipulations combined with
the percutaneous tenotomy regularly
achieve an excellent result.
However, without a diligent follow-up
bracing program, relapse occurs in more
than 80% of cases.

116. Fitting a FAB
1.Fit the FAB immediately after cast removal
2.Fit most difficult foot first
3.Gently dorsiflex foot as much as possible.hold it
in that position and then push heel first in SFAB
4.Close the tongue of the shoe and check whether
heel is still in correct position by looking through
inspection hole.
5.Then lace the shoes
6.Fit the other foot in same way and inspect both
heels through inspection hole.

117. BRACE REVIEW SCHEDULE
Review 3 wks after the first brace is
issued,then after 5 weeks
Later review at 3 month interval upto 18
months,then every 6 months till 3 to 4 yrs
Assess Pirani score at every visit

118. EARLY RECURRENCE
• Almost always occurs due to failure of brace wear
• Loss of dorsiflexion is first sign
• Then heel varus and adductus may reappear
• Cavus rarely recurs
• TREATMENT
• 2 TO 3 repeat casts followed by tenotomy if needed.

119. LATE RECURRENCE
• Recognized as
• Swing phase dynamic supination
• Passively correctable
• Weight bearing on lateral border
• TREATMENT
• If dorsiflexion is 10 degree,tenotomy is needed else more
complex surgery is needed

120. INSTRUCTIONS FOR PARENTS
Watch them fit the brace and correct any
mistakes made
Advise them to return if deformity recurs
To continue bracing even though child is
uncomfortable for first few days,later child
gets used to it
Consistent use=compliant child,
inconsistent use=child who fights with
brace
Should help child learn to kick with both
feet simultaneously

121. The most compliant families are
those who understand Ponseti
management and the
importance of bracing.
Continued education
Take every opportunity to
educate the family about
Ponseti management.
Written material is very
helpful when available.
Often published material is
more convincing than
information given verbally .
INCREASING BRACE COMPLIANCE

122. Prepare family for bracing
Anticipate that failures are most likely due
to premature discontinuation of bracing.
Repeatedly emphasize the importance
of this phase of management.
 Make families aware that maintaining the
correction with bracing is equally important
to gaining the correction by casting and
tenotomy

123. Make certain the infant is comfortable in the
brace.
If the infant is uncomfortable, remove the brace
and examine the skin for evidence of irritation
with reddening of the skin .
Preparing the infant For the first few days,
suggest that the brace may be removed for brief
periods to improve tolerance.
Advise the parents to avoid removing the brace
if the infant cries. If the infant learns that by
crying the brace will be removed, the pattern
will be difficult to correct.
Encourage the family to make the bracing a part

124. Follow-up
Schedule a return visit in 10–14 days to
monitor the use of the brace.
If the bracing is going well, schedule the next
visit in about 3 months.
At that time, the bracing may be
discontinued during the day. The brace must
be applied for naps during the day and sleep
during the night.
Offer help Should the family experience
difficulty with bracing, encourage the family to
call or to return to clinic.