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Clubfoot Clubfoot, or talipes equinovarus, is one of the most common congenital deformities affecting the lower limbs in approximately 1–2 in 1,000 live births. The incidence is higher in Hispanics and lower in Asians. Although clubfoot is recognizable at birth, the severity of the deformity can vary from mild to an extremely rigid foot that is resistant to manipulation (Dobbs and Gurnett 2009). Synonyms and Related Disorders Talipes equinovarus Genetics/Basic Defects 1. Pathogenesis a. Genetic cause: suggested because it tends to run in families (Lochmiller et al. 1998) b. Oligohydramnios: suggested as a cause from early amniocentesis data (CEMAT Group 1998) c. Osseous deformities (Shapiro and Glimcher 1979), muscle abnormalities (Herceg et al. 2006), and arrested fetal development (Fukuhara et al. 1994): hypothesized to play a role in pathogenesis 2. Etiology (Dobbs and Gurnett 2009) a. Most commonly as an isolated birth defect and considered idiopathic (Wynne-Davies 1964): various theories on etiologies include: i. Vascular deficiencies (Hootnick et al. 1982) ii. Environmental factors a) Early amniocentesis (<13 weeks gestation): associated with an increased risk in talipes equinovarus (an uncommon risk factor), compared to midgestational amniocentesis or chorionic villus sam- pling (Philip et al. 2004) b) Partially associated with amniotic fluid leakage: suggesting that oligohydramnios occurring at a critical gestational period may be detrimental to foot development (Tredwell et al. 2001) c) Environmental exposure to cigarette smoke in utero: an independent risk factor (Honein et al. 2000) iii. In utero positioning (Dunn 1972) iv. Abnormal muscle insertions (Bonnell and Cruess 1969) b. Genetic factors suggested by: i. Thirty-three percent concordance of identical twins and the fact that nearly 25% of all cases are familial (Lochmiller et al. 1998) ii. Differences in clubfoot prevalence across ethnic populations with the lowest prevalence in Chinese (0.39 cases per 1,000 live births) and the highest in Hawaiians and Maoris (seven per 1,000) (Beals 1978; Chung et al. 1969) c. Multifactorial and possibly polygenic causation suggested (Lochmiller et al. 1998; Wynne- Davies 1972) d. Prevalence of additional congenital anomalies i. Chromosomal abnormalities (e.g., trisomy 18 syndrome) in patients with clubfoot (24–50%) (Bakalis et al. 2002; Gurnett et al. 2008) ii. Distal arthrogryposis iii. Myelomeningocele H. Chen, Atlas of Genetic Diagnosis and Counseling, DOI 10.1007/978-1-4614-1037-9_46, # Springer Science+Business Media, LLC 2012 401

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Clubfoot

Clubfoot, or talipes equinovarus, is one of the most

common congenital deformities affecting the lower

limbs in approximately 1–2 in 1,000 live births. The

incidence is higher in Hispanics and lower in Asians.

Although clubfoot is recognizable at birth, the severity

of the deformity can vary from mild to an extremely

rigid foot that is resistant to manipulation (Dobbs and

Gurnett 2009).

Synonyms and Related Disorders

Talipes equinovarus

Genetics/Basic Defects

1. Pathogenesis

a. Genetic cause: suggested because it tends to run

in families (Lochmiller et al. 1998)

b. Oligohydramnios: suggested as a cause from

early amniocentesis data (CEMAT Group 1998)

c. Osseous deformities (Shapiro and Glimcher

1979), muscle abnormalities (Herceg et al.

2006), and arrested fetal development (Fukuhara

et al. 1994): hypothesized to play a role in

pathogenesis

2. Etiology (Dobbs and Gurnett 2009)

a. Most commonly as an isolated birth defect and

considered idiopathic (Wynne-Davies 1964):

various theories on etiologies include:

i. Vascular deficiencies (Hootnick et al. 1982)

ii. Environmental factors

a) Early amniocentesis (<13 weeks

gestation): associated with an increased

risk in talipes equinovarus (an uncommon

risk factor), compared to midgestational

amniocentesis or chorionic villus sam-

pling (Philip et al. 2004)

b) Partially associated with amniotic fluid

leakage: suggesting that oligohydramnios

occurring at a critical gestational period

may be detrimental to foot development

(Tredwell et al. 2001)

c) Environmental exposure to cigarette

smoke in utero: an independent risk factor

(Honein et al. 2000)

iii. In utero positioning (Dunn 1972)

iv. Abnormal muscle insertions (Bonnell and

Cruess 1969)

b. Genetic factors suggested by:

i. Thirty-three percent concordance of identical

twins and the fact that nearly 25% of all cases

are familial (Lochmiller et al. 1998)

ii. Differences in clubfoot prevalence across

ethnic populations with the lowest prevalence

in Chinese (0.39 cases per 1,000 live births)

and the highest in Hawaiians and Maoris

(seven per 1,000) (Beals 1978; Chung et al.

1969)

c. Multifactorial and possibly polygenic causation

suggested (Lochmiller et al. 1998; Wynne-

Davies 1972)

d. Prevalence of additional congenital anomalies

i. Chromosomal abnormalities (e.g., trisomy

18 syndrome) in patients with clubfoot

(24–50%) (Bakalis et al. 2002; Gurnett

et al. 2008)

ii. Distal arthrogryposis

iii. Myelomeningocele

H. Chen, Atlas of Genetic Diagnosis and Counseling, DOI 10.1007/978-1-4614-1037-9_46,# Springer Science+Business Media, LLC 2012

401

e. Recent identification of a rare mutation in the

transcription factor PITX1 in a large family with

idiopathic clubfoot: importance of genes

involved in early limb development (Gurnett

et al. 2008)

i. PITX1: the first gene implicated in clubfoot

that explains the specific involvement of the

foot, since PITX1 is expressed nearly exclu-

sively in the hindlimb and is responsible for

rapid evolutionary changes in pelvic mor-

phology in lower vertebrates (Shapiro et al.

2004).

ii. Specific involvement of the foot also appears

to exclude many of the skeletal muscle

contractile genes that are responsible for

distal arthrogryposis (Sung et al. 2003a, b;

Toydemir et al. 2006; Veugelers et al. 2004)

in the causation of idiopathic clubfoot, as

mutations in these genes cause both upper

and lower extremity involvement and were

not identified in idiopathic clubfoot patients

(Gurnett et al. 2009).

3. Multifactorial inheritance

a. Most infants with clubfoot (idiopathic congenital

clubfoot) have no identifiable genetic, cytoge-

netic, syndromal, or extrinsic cause. The idio-

pathic congenital clubfoot is primarily caused

by a multifactorial inheritance.

b. The observed percentages of talipes equinovarus

in relatives of an affected child are consistent

with a multifactorial mode of inheritance

(Wynne-Davies 1965, 1972)

i. Monozygotic twins with about 32.5% rate of

concordance (both twins affected with

clubfoot)

ii. First degree relatives (parents and siblings)

occurrence rate

a) 2.14%

b) About 17 times as high as the population

rate

iii. Second degree relatives (aunts and uncles)

occur

a) 0.61%

b) About six times as high as the population

rate

iv. Third degree relatives (cousins)

a) 0.2%

b) Near the incidence in the general

population

4. Part of a genetic syndrome

a. An autosomal recessive inheritance of clubfoot:

for example,

i. Diastrophic dwarfism

ii. Larsen syndrome

iii. Smith-Lemli-Opitz syndrome

b. An autosomal dominant inheritance of clubfoot:

for example,

i. Distal arthrogryposis type 2A (Whistling-

face syndrome)

ii. Distal arthrogryposis type 1

iii. Freeman-Sheldon syndrome

c. An X-linked recessive inheritance of clubfoot:

for example, Pierre-Robin syndrome

d. Other syndromic clubfoot: for example,

i. Meningomyelocele/spina bifida

ii. Sacral agenesis

iii. Constriction band syndrome

iv. Congenital myopathy

5. Part of a cytogenetic abnormality: Numerous cyto-

genetic abnormalities produce individuals with

multiple anomalies including clubfoot

6. Extrinsic causes

a. Teratogenic agents

i. Sodium aminopterin

ii. Position in utero at the time of d-tubocurarine

paralysis

b. Loss of amniotic fluid during gestation

c. Mechanical forces or positional influence

(restriction of fetal foot movement by the uterus)

d. Drugs

Clinical Features

1. Bilateral in about 50% of cases

2. Three major components of talipes equinovarus

a. Equinus (limitation of extension) of the ankle

and subtalar joint

b. Hindfoot and midfoot varus

c. Forefoot adduction

3. Evaluation of the foot, ankle, and leg

a. “Down and in” appearance

b. Shorter and wider than the normal foot

c. Flexible, softer heel due to hypoplastic calcaneus

d. Concave medial border

e. Transverse plantar creases or clefts at the

midfoot and at the posterior part of the ankle

f. Highly convex lateral border

402 Clubfoot

g. Internally rotated heel making the soles of the

feet facing each other in cases of bilateral

deformities

h. Internal rotation of the leg

i. Variable rigidity of the foot

j. Calf and foot atrophy (more obvious in older

child than in infant)

k. Mild hypoplasia of the tibia, fibula, and bones

of the foot

l. Pronounced tightness of the Achilles tendon

with very little dorsiflexion

m. Range of motion of the joints

4. Idiopathic clubfoot

a. An isolated deformity of the foot and leg

i. Identifiable in utero

ii. Consists of four components

a) Equinus

b) Hindfoot varus

c) Forefoot adductus

d) Cavus

b. When untreated, children with clubfoot walk on

the sides and/or tops of their feet, resulting in

(Dobbs and Gurnett 2009):

i. Callus formation

ii. Potential skin and bone infections

iii. Inability to wear standard shoes

iv. Substantial limitations in mobility and

employment opportunities

c. By far the most common form

d. Occurring more common in males than in

females (2 � 2.5:1)

e. Normal upper limbs

f. Associated features

i. Joint laxity

ii. Congenital dislocation of the hip

iii. Tibial torsion

iv. Ray anomalies of the foot (oligodactyly)

v. Absence of some tarsal bones

vi. A history of other foot anomalies in the family

5. Various associated anomalies in syndromic talipes

equinovarus

Diagnostic Investigations

1. Plain radiography

a. Limitations

i. Risk of ionizing radiation

ii. Proper positioning difficult

iii. Lack of ossification in some involved bones

a) Only talus, calcaneus, and metatarsals are

ossified in neonates

b) Cuboid ossification at 6 months

c) Cuneiforms ossification at 1 year

d) Navicular ossification after 3 years

b. Assessment

i. Hindfoot equinus (plantar flexion of the

anterior calcaneus)

ii. Hindfoot varus (calcaneus rotated around

the talus into a varus, i.e., toward midline,

position)

iii. Forefoot varus (increased forefoot supina-

tion on dorsoplantar view)

c. Common measurements

i. Anteroposterior talocalcaneal angle (typi-

cally <20� in a clubfoot)

ii. Talar-first metatarsal angle

a) Up to about 30� of valgus in a normal foot

b) Mild-to-severe varus in a clubfoot

iii. Medial displacement of the cuboid ossifica-

tion center on the axis of the calcaneus

representing either of the following:

a) Angular deformity of the calcaneus

b) Medial subluxation of the cuboid on the

calcaneus

2. CT scan

a. Limitations

i. Risk of ionizing radiation

ii. Lack of ossification of the tarsal bones

iii. Susceptible to motion artifact

b. Advantage: better assessment of complex

3-dimensional deformity by 3-dimensional

reconstructions

3. MRI

a. Limitations

i. Need for patient sedation

ii. Loss of signal caused by ferromagnetic

effects of fixation devices

b. Advantages

i. Capability of multiplanar imaging

ii. Excellent depiction of following:

a) Ossific nuclei

b) Cartilaginous anlage

c) Surrounding soft-tissue structures

c. Findings

i. Plantar flexion

ii. Varus angular deformity of the talus, calca-

neus, and cuboid

Clubfoot 403

Genetic Counseling

1. Recurrence risk: depends on underline etiology

a. Patient’s sib

i. Multifactorial trait: approximately 2.1%

(first degree relatives)

ii. Autosomal recessive: 25%

iii. Autosomal dominant: not increased unless

a parent is affected

iv. X-linked recessive: 50% of male sibs

affected if the mother is a carrier

v. Chromosomal: increased risk, especially

a parent is a translocation carrier

b. Patient’s offspring

i. Multifactorial: approximately 2.1%

ii. Autosomal recessive: not increased unless

the spouse is also a carrier

iii. Autosomal dominant: 50%

iv. X-linked recessive: All daughters of affected

males will be carriers. All sons of an affected

male will be normal.

v. Chromosomal: increased risk

2. Prenatal diagnosis

a. Ultrasonography: Wide variation in the accuracy

of ultrasonography

i. Isolated clubfoot

a) Better prognosis especially detected in the

3rd trimester of pregnancy

b) Poor correlation between the prenatal

appearance of the foot on ultrasound find-

ings and the severity of the talipes at birth

ii. Complex clubfoot: associated with syndromic,

neuromuscular, or chromosomal conditions

3. Management

a. Traditional nonoperative approach

i. Appropriate initial management for all

children with clubfoot

ii. Splintage begins at 2–3 days after birth

iii. Order of correction

a) Forefoot adduction

b) Forefoot supination

c) Gentle correction of equinus

iv. Two methods most widely performed and

with highest reported long-term success rates

a) Kite and Lovell method

b) Ponseti method

v. “Montpellier” method: remains popular in

France

b. Ponseti method: currently widely utilized with

high success rate in treating clubfoot

i. Goal

a) To reduce or eliminate deformity

(equinus, hindfoot varus, forefoot

adductus, and cavus)

b) To attain functional, pain-free, planti-

grade foot with good mobility and with-

out calluses, and without need to wear

modified shoes

ii. Techniques

a) Serial manipulation

b) A specific technique of cast application

c) Possible percutaneous Achilles tenotomy

iii. Significant risk factors for the recurrence of

clubfoot deformity after correction with the

Ponseti method

a) Noncompliance of the parents

b) Lower educational level of the parents

iv. Outcome

a) Appears to be effective

b) Requires only a reasonable amount of

time out of the lives of the patient and

his or her parents

c) Frequently include some minimal inva-

sive surgery

c. Kite and Lovell method

a) Starting with stretching of the foot through

longitudinal traction applied to the foot

b) Less often requires minimally invasive

surgery

c) More time-consuming

d. “Montpellier” method

i. Require fairly extensive physical therapy

ii. Demand substantial parental time and

attention

iii. Long-term results yet to be confirmed

e. Operative approach

i. Should be considered only after a suitable

trial of manipulating the foot and holding it

in a suitable cast or other device has failed

ii. Operative treatment

a) Incisions

b) Medial plantar release

c) Posterior release

d) Lateral release

e) Reduction and fixation

f) Intraoperative assessment

g) Wound closure

404 Clubfoot

h) Revision surgery

i) Postoperative evaluation

iii. Treatment of residual deformity

a) Residual forefoot adduction

b) Residual cavus

c) Angulation of the heel for residual varus

or valgus

d) Dynamic forefoot supination

e) Residual toeing-in

f) Dorsal bunion (a painful swelling of the

bursa of the first joint of the big toe)

g) Overcorrected foot

h) Skin problems

f. Complications of treatment

i. Failure to correct (undercorrection) resulting

from:

a) Selection of inappropriate procedure

b) Inadequate performance of an appropri-

ate procedure

ii. Overcorrection resulting from:

a) Selection of an inappropriate procedure

b) Overzealous release of appropriate

structures

c) Inappropriate release of normal

structures

iii. Recurrence of deformity

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406 Clubfoot

Fig. 1 Bilateral talipes equinovarus in an infant

Fig. 2 Bilateral talipes equinovarus in an infant with Smith-

Lemli-Opitz syndrome

Fig. 3 Bilateral talipes equinovarus in a fetus with trisomy 18

syndrome

Fig. 4 Radiograph of talipes equinovarus in another infant

Clubfoot 407