The document discusses clubfoot, a congenital foot deformity. It describes the anatomy of the normal foot and characteristics of clubfoot including equinus, varus, adduction, and cavus deformities. It covers etiologies such as neuromuscular, fibrotic, and vascular theories. Treatment approaches include serial casting and surgery. The document provides details on the classification, presentation, and evaluation of clubfoot through history, examination, and radiography.

1. Dr anurag varshney
Dr.rml hospital new delhi

2. 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. •3 main sections
1.Hindfoot – talus,
calcaneus
2.Midfoot –
navicular, cuboid,
cuneiforms
3.Forefoot –
metatarsals and
phalanges

8. CONGENITAL FOOT DEFORMITIES

9. 1. CLUB FOOT
2. METATARSUS ADDUCTUS
3. SKEWFOOT
4. PES PLANUS
5. CONGEMITAL VERTICL TALUS
6. TALIPES CALCANEOVALGUS
7. TARSAL COALITION
8. CONGENITAL HALLUX VALGUS
9. CONGENITAL OVERRIDING FIFTH TOE
10. CURLY TOE
11. ACCESSORY NAVICULAR

10. 12. CONGENITAL HALLUX VARUS
13. POLYDACTYLY AND POLYSYNDACTYLY
14. SYNDACTYLY
15. MACRODACTYLY
16. CLEFT FOOT (ECTRODACTYLY)
17. HALLUX RIGIDUS
18. HALLUX VALGUS INTERPHALANGEUS
19. HAMMER TOE
20. MALLET TOE
21. LONGITUDINAL EPIPHYSEAL BRACKET
22. SUBUNGUAL EXOSTOSIS
23. GLOMUS TUMOR

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

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

13. CLUB FOOT
Definitions
it 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 = 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

14. 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

15. CLUB FOOT
Types
1.Postural :
Calcaneo-Valgus Equino-Varus
Look for CDH Minor and correctable

16. 2.Acquired, Secondary to :SYNDROMES clubfoot :
 Arthrogryposis
 Streeter dysplasia (Constriction bands)
 Prune Belly Syndrome
 Tibial Hemimelia
 Mӧbius 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

17. HISTORY
•Hippocrates 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 immobilization
Idiopathic (Unknown
Etiology) :
Congenital Talipes Equino-
Varus

18. 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

19. Etio-pathogenesis
Still Unknown at this stage
SOME ETIOLOGICAL THEORIES ARE :
Mechanical factors in utero
Retractive fibrotic response
Neuromuscular defect
Arrested embryonic development
Primary germ plasma defect
Heredity
Environmental factors
Combined heredity and environmental factors
Vascular hypothesis

20. Neuromuscular defect
• Imbalance 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 don’t 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
tendons
•Decreased 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

21. .Arrested embryonic development
• Heuter and Volkmann ; BOHM
• 6 – 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

22.  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.

23.  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
Idelberger
 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
 Tachdjian
 Patient with CTEV that has one child affected then 25% chance of another affected
 If both parents are normal & have affected child then chance of another is 5%
Idelberger K. et al 1939; 33:272–276
.

24. Intrauterine factors
 Pressure theories:
 Oligohydramnios
 Abnormal fetal positioning
 Placental insufficiency
 Constriction bands
 Toxins ( Maternal alcoholism, smoking)
 Maternal illness ( anemia, thyroid disorders )
 Infective pathogens (enteroviruses)
 Drugs (abortifacients, salicylates, thalidomide,
barbiturates)
 Electromagnetic radiation

25. Adaptive Changes
Wolff’s 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 ”

26. PATHOLOGICAL ANATOMY
COMPONENTS OF DEFORMITY :
1. EQUINUS – fixed plantar flexed foot
 Ankle joint
 inversion of talocalcaneonavicular joint
 plantar flexion of forefoot
2. VARUS – inward rotation of hindfoot
 talocalcaneonavicular joint (subtalar joint)
calcaneus rotate through talocalcaneal joint
in coronal and horizontal plane
3. ADDUCTION –
 Talonavicular joint
 anterior subtalar joint
 Lisfranc region
4. CAVUS – prominent transverse plantar crease
 midtarsal joint
pronation of the forefoot in
relation to the hindfoot.

27. OSSEOUS DEFORMITIES
TALUS :
 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

28. Calcaneus
involved in equenus varus
adduction due to abnormal
position but shape is almost
maintained
Anterior portion lies beneath the
head of talus causing varus and
equinus of heel
Anteriar end come downward
andRotated medially while posterior
end moves upward and lateraly

29.  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

30. Tibio-talar plantar flexion
Medially displaced navicular
Adducted and inverted
calcaneus
Medially displaced
cuboid

31. Soft tissue changes
Tendo achilles
 Post. capsule of ankle
joint & subtalar joint
Post. talo fibular
Posterior structures :
Calcaneo-fibular
ligaments

32.  Medial :
Tibialis posterior
FHL,FDL, Master Knot
of Henry
 Talonavicular ligament
Calcaneo-navicular
ligament
Deltoid ligament
Interossseus talo
calcaneal ligaments
Capsules of naviculo
cuneiform & cuneiform
first metatarsal

33.  Plantar wards :
 Plantar fascia
 Plantar ligaments
 Flexor digitorum
brevis & abductor
hallucis
Laterally
 Calcaneofibular
ligament
 Bifurcated ligament
 Calcaneocuboid joint
capsule

34. • FLEXOR DIGITORUM ACCESSORIUS LONGUS – 7% of children requiring surgical correction
-Children 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

35. 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

36. Clinical test• Dorsi flexion test
– Screening 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 test
– To detect the tibial torsion

37. Radiology
 Plain radiograph: Can be assessed prior to treatment
with A-P &force dorsiflexed foot lateral veiw
 Foot 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 vertical
 Lat. View: Transmalleolar with the fibula overlapping the
posterior half of the tibia; in dorsiflexion foot

38. RADIOGRAPHIC FEATURES :
1. TURCO’S ANGLE – approaches parallelism
2. TALOCALCANEAL INDEX - < 40 degrees
3. KITE’S ANGLE - < 30 degrees
4. MEARY ANGLE – dorsal apex

39. Anteroposterior view
 Talocalcaneal angle; 30 –
55 degrees (KITE’S ANGLE)
 Calcaneal-second
metatarsal angle
 Talus –first metatarsal
angle: 5-15 degrees

40. 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

41. Dorsiflexed Lateral view
 Talocalcaneal view
25 – 50 degrees (TURCO’S)
 Calcaneal-first metatarsal view
 Tibiocalcaneal :
10-40 degrees
 Tibiotalar angle
 Talus-first metatarsal angle
 Talocalcaneal index (Kite's angles
from AP and Lateral views added)

43. 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

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

45. 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

46. Rigid : it’s 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: it’s 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.

47. Classification (Attenborough 1966)
Type
I(Extrinsic)
Non Rigid
Type
II(Intrinsic)
Rigid
Foot size Normal Smaller
Heel Normal size
Can be brought
down with ease
Minimal varus
Small , elevated
Cannot be brought
down with ease
Marked varus
Creases More or less normal Deep medial,
posterior and lateral
creases
Reduced creases
laterally

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

49. Reducibility(
degrees)
Score Additional
parameters
Score
90-45 4 Marked posterior
crease
1
45-20 3 Marked
mediotarsal crease
1
20-0 2 Cavus 1
0 t0 -20 1 Poor muscle
condition
1

51. Grade Type Score Reducibility
i Benign(20%) 1-4 >90% reducible
ii Moderate(30%) 5-9 >50%, soft-stiff,
reducible, partially
resistant
iii Severe(35%) 10-14 >50%, stiff-soft,
resistant, partially
reducible
iv Very severe(12%) 15-20 <10% stiff-
stiff,resistant

52. Pirani’s severity scoring
 Six parameters : 3 of midfoot and 3 of hindfoot
 Each parameter is given a value as follows:
0: normal
0.5: moderately abnormal
1: severely abnormal

53. Mid foot score
 Curved lateral border [A]
 Medial crease [B]
 Talar head coverage [C]

54. Hind foot score
 Posterior crease [D]
 Rigid equinus [E]
 Empty heel [F]

55. Physical Examination Findings Score of 0 Score of 0.5 Score of 1
Curvature of lateral border of foot Straight Mild distal curve Curve at calcaneocuboid joint
Severity of medial crease (foot held in
maximal correction)
Multiple fine creases One or two deep creases Deep creases change contour of arch
Multiple fine creases One or two deep creases Deep creases change contour of arch
Medial malleolar–navicular interval (foot
held in maximal correction)
Definite depression felt Interval reduced Interval not palpable
Palpation of lateral part of head of talus
(forefoot fully abducted)
Navicular completely “reduces”;
lateral talar head cannot be felt
Navicular partially “reduces”;
lateral head less palpable
Navicular does not “reduce”; lateral
talar head easily felt
Emptiness of heel (foot and ankle in
maximal correction)
Tuberosity of calcaneus easily
palpable
Tuberosity of calcaneus more
difficult to palpate
Tuberosity of calcaneus not palpable
Fibula-Achilles interval (hip flexed, knee
extended, foot and ankle maximally
corrected)
Definite depression felt Interval reduced Interval not palpable
Rigidity of equinus (knee extended, ankle
maximally corrected)
Normal ankle dorsiflexion Ankle dorsiflexes beyond neutral,
but not fully
Cannot dorsiflex ankle to neutral
Rigidity of adductus (forefoot is fully
abducted)
Forefoot can be overcorrected
into abduction
Forefoot can be corrected beyond
neutral, but not fully
Forefoot cannot be corrected to
neutral
Long flexor contracture (foot and ankle
held in maximal correction)
MTP joints can be dorsiflexed to
90 degrees
MTP joints can be dorsiflexed
beyond neutral but not fully
MTP joints cannot be dorsiflexed to
neutral
Modified from Flynn JM, Donohoe M, Mackenzie WG: An independent assessment of two clubfoot-classification systems, J Pediatr Orthop 18:323, 1998.

56. Uses of Pirani’s score
 Assessment of progress by serial plotting of the score
 Predicting need for tenotomy (hs>1& ms<1)
 Estimation of probable no. of casts reqd*
 Very good interobserver reliability and reproducibility**

57. CLASSIFICATION [HAROLD AND WALKER]
Mild Varus and equinus deformity which can be manipulated beyond neutral
Moderate Varus and equinus within 20º short of neutral
Severe Varus and equinus cannot be reduced within 20º of Neutral

58. ICFSG(International club foot study group )
Classification System
 Bensahel et al , 2005
 Evaluating the outcome by calculating the global score of
summation of included three parameters :
 morphological (score 0 to 12),
 functional including-passive motion, muscular
strength, gait, and pain (score 0 to 36)
and radiological (score 0 to 12).
 Outcome best (0 score) to worst result (60 score).
Excellent 0 – 5
Good 6 – 15
Fair 16 – 30
Poor > 30

59. TREATMENT

62. NON OPERATIVE TREATMENT

63. The principles of treatment are based on following concepts :
1. Abnormal tarsal relationship maintained by pathological after soft tissues contractures
2. Soft tissues contractures must be stretched to restore normal tarsal relationships
3. After normal tarsal relationships, correction must be maintained until tarsal bones
remold stable articular surfaces
4. Recurrent deformity results from failure to either attain a complete correction or
maintain the correction

64. Ponseti management
According to ponseti Scientific Basis
of Management
 Clubfoot 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 deformation
 The forefoot is in some pronation,
causing the plantar arch to be more
concave (cavus).
 The clubfoot deformity occurs mostly
in the tarsus.

65.  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 bones
 correction 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 position
 Pronating 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

66.  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.

67. 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 management
 Most 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.

68.  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.

69. Ponseti cast application
 first step calming the child with a
bottle or breast feeding. When
possible have a trained assistant
 Exactly 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
malleolus
 While 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.

70.  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 arch—
neither 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.

71. 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

72. Cast application
Manipulation Padding

73. Plaster at toes Below knee pop

74. Molding Extension upto the thigh

75. Plantar support to toes Final appearance

76. 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.

77. 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 talus
 Abduction of approx.70
degrees in relationship to
the frontal plane of the
tibia possible

78. Percutaneous tenotomy under LA
Foot held in max dorsiflexion by an assistant
Tenotomy 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 weeks
Indicated to correct equinus when cavus, adductus, and varus fully
corrected but ankle dorsiflexion remains less than 10 degrees above neutral

79. 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 38.5°C/101.3°F or higher
without an explainable reason, such as a cold or virus

82. Foot Abduction braces
 Shoes 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

83. Bracing protocol
 Worn 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,
2007.487–493

85. • 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.

86. Mitchell brace Dobbs dynamic brace

87. Dennis brown Romanus

88. CTEV Splint
 Straight inner border to prevent
forefoot adduction
 Outer shoe raise to prevent fooot
inversion
 No heel to prevent equinus
 Slight(1/8”) lateral sole raise
 Inner iron bar
 Outer t trap
 Walking age to 5 yrs of age

90. Follow up protocol
 2 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

91. Common errors(Kite errors)
 Pronation/eversion of 1st
metatarsal
 Premature dorsiflexion
of heel
 Counterpressure at
calcaneocuboid joint
 External rotation
 Below knee casts
 Short splints

92. 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.

93. Rocker bottom deformity
 Dorsiflexion via midfoot
before correction of
hindfoot varus
 Dorsal dislocation of
navicular on talus
 calcaneus Fixed in equinus
 hypermobility of
tarsometatarsal level

94. 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.

95. Equinus relapse
The tibia seems to grow faster then the gastrosoleus tendon unit. The muscle is
atrophic and the tendon appears long and fibrotic.
If 10 degree dorsiflexion is not achieved in 4–5 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 relapse
more 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.

96. EXTRINSIC/NON-
RIGID (TYPE I)
INTRINSIC/RIGID
(TYPE II)
FOOT Normal size smaller
Mild varus Marked varus
HEEL Normal size smaller
Can be brought down Can not
Minimal varus Marked varus
CREASES More or less N Deep posterior, medial
and plantar creases
Reduced creases laterally
(Kawashima and Uhtoff, 1990)

97. OPERATIVE TREATMENT

98. INDICATIONS :
1. FAILURE OF NONOPERATIVE TREATMENT IN AN INFANT
2. SYNDROMIC CLUBFOOT
3. DIMEGLIO GRADES 3 AND 4
4. RESIDUAL DEFORMITIES’ CORRECTION
5. NEGLECTED CLUBFOOT

99.  SOFT TISSUE RELEASES
 TENDON TRANSFERS
 BONY PROCEDURES

100. General Principles
 Goal: address all pathoantomic structures
 Decision regarding timing, extent
 “A la carte" approach [Bensahel]
 Turco’s ‘one size fits all’ approach
 Posteromedial-plantar-lateral release: when all deformities
present
 Posterior release: straight lateral border, flexible forefoot
and hindfoot, and palpable gap between medial malleolus
and navicular tuberosity

101. Turco(hockey stick
posteromedial incision)
One stage POSTEROMEDIAL SOFT TISSUE RELEASE (TURCO)
Indications : resistant
recurrent deformity

103. POSTERIOR RELEASE :
TAL – Z TECHNIQUE; medial half
Capsulotomy of ankle joint (tibiotalar) first
Capsulotomy of talocalcaneal joint
Transection of talofibular and calcaneofibular
ligament
Transection of posterior portion of deltoid
ligament on calcaneus

104. POSTERIOR RELEASE :
TAL – Z TECHNIQUE; medial half
Capsulotomy of ankle joint (tibiotalar) first
Capsulotomy of talocalcaneal joint
Transection of talofibular and calcaneofibular
ligament
Transection of posterior portion of deltoid
ligament on calcaneus

105. 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
talonavicular
Capsule
Incision of spring ligament anterior to
sustentaculum tali
and 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

106. 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

107. 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 sx
Dorsal structures,medial neurovescular bundle
deep deltoid ligament
Talocalcaneos introsseous ligament

108. INDICATIONS :
1. Obvious clubfoot deformity with RIGID foot
2. Walking on lateral border of foot with heel varus
3. posterior position of fibular or angle less than 76 degrees in relationship
of longitudinal plane of foot to bimalleolar plane.
4. Intoward rotated gait following clubfoot correction with abnormal subtalar
complex rotation
5. Parallelism of talocalcaneal angle
McKAY’S EXTENSILE SOFT TISSUE RELEASE

109. 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

110. Plantar: plantar fascia, Abd Hallucis and FDB, long and short
plantar ligs
medial: identify med structures, release tendon sheaths
talonavicular 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 sheaths
calcaneocuboid release, completion of talonavicular and subtalar
release
foot is maintained in corrected position by K-wiring the talonavic
jt and also the subtalar jt

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

114. 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)

115. COMPLETE SUBTALAR RELEASE (SIMMONS)
Differences with McKay procedure :
1. release of interosseous ligament
2. incision of sheath of FHL and FDL
3. retaining sheath of Tibialis Posterior
4. plane of incision for Z-plasty of tendoachilles
wedge calcaneocuboid osteotomy

116. “
. 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)

117. Residual deformities
 Residual hindfoot equinus : Achilles tendon
lengthening and posterior capsulotomy of ankle and
subtalar joints
 Dynamic metatarsus adductus : Transfer of anterior
tibial tendon, either as split transfer or entire tendon

118. Resistant clubfoot
 Metatarsus adductus : >5 yrs metatarsal osteototomy
 Hindfoor varus : <2-3 yrs modified Mckay procedure
3- 10 yrs
Dwyer osteotomy ( isolated heel varus)
Dilwyn Evans procedure (short medial column)
Lichtblau procedure( long lateral column)
10-12 yrs triple arthrodesis
 Equinus : Achilles tendon lengthening and posterior
capsulotomy of subtalar joint, ankle joint / Lambrinudi procedure
 All three deformities >10 yrs triple arthrodesis

119. Neglected clubfoot
 No / incomplete initial treatment till the age of 1 years
 Moderately flexible, moderately stiff, and rigid
 Modified Ponseti*: manipulation for 5-10 mins, two weekly
cast change, correction of foot to 30-40° abduction, and
AFO for 1 year
 Extensive soft tissue release upto 4 yrs
 Dilwyn-Evans, Lichtblau procedure
 Triple arthrodesis
 Ilizarov/ JESS
 Lourenco et al . Correction of neglected club foot by ponseti method. JBJS Br. 2007

120. Bony procedures
Dwyer osteotomy
 Osteotomy of calcaneus
 Opening wedge medial
osteotomy to increase the
length and height of
calcaneus
 For isolated heel varus
 Modified method uses
lateral incisions

122. Litchblau procedure
 Medial soft tissue release
 Lateral closing wedge
osteotomy of calcaneus
 Prevents long term
stiffness of hindfoot
 Shortens the lateral
column

123. 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

124. Salvage procedures
Triple arthrodesis
 Salvage 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 12
 Lateral closing wedge osteotomy through subtalar and
midtarsal joints

126. Triple arthrodesis
Dunn arthrodesis Hoke and kite

128. TALECTOMY
• severe, untreated clubfoot
•for previously treated clubfoot
uncorrectable by any other surgical
procedures
• neuromuscular clubfoot

129. TENDON TRANSFERS
• peronei are weak
• correction of foot achieved late
• laxity in peronei
relapse
Transfer 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 and
has a second relapse. Indications include persistent heel varus and
forefoot supination during walking; the sole shows thickening of
the lateral plantar skin.
1. Tibialis Anterior – to base of 3rd or 4th metatarsal (if tibialis posterior is
cut)
- to base of 5th metatarsal (if tibialis posterior is
preserved)
2. Split Tibialis Anterior Transfer
3. Tibialis posterior

134. EXTERNAL FIXATORS
INDICATIONS :
1. > 3 years, adolescents adults
2. relapsed, resistant or neglected clubfeet
3. arthrogryphotic foot
4. children treated with extensive open surgery
5. scarred or infected skin from previous surgery

135. 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

136. PRINCIPLES :
1. DISTRACTION HISTOGENESIS - below 8 years
2. WOLFF’S LAW
3. DIFFERENTIAL DISTRACTION on both sides to prevent articular
damage on convex side
(Convex side distraction is half the rate of concave side)

137. Ilizarov
 Correction slow enough
to protect soft tissue
 Correction at the focus
of deformity
 Simultaneous three-
dimensional, multilevel
correction
 Deformity correction
without shortening the
foot

138. CONTROLLED DIFFERENTIAL FRACTIONAL DISTRACTION USING
JESS
2 to 4 transfixing wires in prox tibia Metatarsal Transfixing wire
through
MTs
2 transfixing and 1 axial wire through calcaneum

139. JESS
 Fractional, 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

140. Results with JESS
 Good 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): 194–201

141. Complications of surgery
 Neurovascular injury
 Loss of foot (10% have atrophic dorsalis pedis artery bundle)
 Skin dehiscence
 Wound infection
 AVN talus
 Dislocation of the navicular
 Flattening and breaking of the talar head
 Undercorrection/ Overcorrection (esp with Cincinatti)
 Forefoot adductus
 Hindfoot varus
 Severe scarring
 Stiff joints
 Weakness of the plantar flexors of the ankle

142. Thank you
for your attention