PONSETI TECHNIQUE IN THE MANAGEMENT OF

CLUBFOOT DEFORMITY- A STUDY

By

DR. MD NAYEEM ALI

Dissertation Submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfillment

of the requirements for the degree of

MASTER OF SURGERY

IN

ORTHOPAEDICS

Under the guidance of

DR. M.S. PATIL

M.S. (Ortho)

DEPARTMENT OF ORTHOPAEDICS

AL-AMEEN MEDICAL COLLEGE

BIJAPUR

2013

I

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “PONSETI TECHNIQUE IN

THE MANAGEMENT OF CLUBFOOT DEFORMITY- A STUDY”

is a bonafide and genuine research work carried out by me under the guidance of

DR. M.S. PATIL, Professor, Department of Orthopaedics, Al-Ameen Medical

College, Bijapur, for the award of M.S. Degree (Orthopaedics), examination to be

conducted by the Rajiv Gandhi University of Health Sciences, Bangalore. This work

is original and has not been submitted by me for any other Degree or Diploma of this

or any University.

Place: Bijapur Signature of the Candidate

Date: DR. MD NAYEEM ALI

I

CERTIFICATE BY THE GUIDE & CO GUIDE

This is to certify that the dissertation entitled “PONSETI TECHNIQUE

IN THE MANAGEMENT OF CLUBFOOT DEFORMITY- A

STUDY” is a bonafide research work done by DR. MD NAYEEM ALI under my

supervision and guidance, in partial fulfillment of the requirement for the degree of

M. S. (Orthopaedics).

Signature of Guide

DR. M.S. PATIL

M.S. (Ortho)

Professor

Department of Orthopaedics

Place: Bijapur Al Ameen Medical College

Date: BIJAPUR

II

ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE

INSTITUTION

This is to certify that the dissertation entitled “PONSETI TECHNIQUE

IN THE MANAGEMENT OF CLUBFOOT DEFORMITY- A

STUDY” is a bonafide research work done by DR. MD NAYEEM ALI under the

guidance of DR. M.S. PATIL, Professor, Department of Orthopaedics, Al-Ameen

Medical College, Bijapur, in partial fulfillment of the requirement for the degree of

M. S. (Orthopaedics).

Signature and Seal of the HOD Signature and Seal of the Principal

DR. ASHOK H. SASNUR DR. B.S. PATIL

M.S. (Ortho), D. Ortho M.D. (Med)

Professor and Head Dean

Department of Orthopaedics Al Ameen Medical College

Al Ameen Medical College BIJAPUR

BIJAPUR

Place: Bijapur

Date:

III

COPYRIGHT

Declaration by the Candidate

I hereby declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall have the rights to preserve, use and disseminate this

dissertation / thesis in print or electronic format for academic / research

purpose.

Place: Bijapur Signature of the Candidate

Date: DR. MD NAYEEM ALI

© Rajiv Gandhi University of Health Sciences, Karnataka

IV

ACKNOWLEDGEMENT

First of all I am thankful to my parents and my elder brother for their support in every

aspect and stage of my life, and to become the doctor and the person I am today.

As I complete this humble contribution to scientific pursuit, it gives me immense

pleasure to acknowledge all those who helped me in this endeavour.

It is my proud privilege to express my esteemed regards and sincere thanks to my

Guide Dr. M.S. PATIL, Professor, Department of Orthopaedics, Al Ameen Medical

College, Bijapur, for his guidance, concepts relatred studies, constant encouragement,

and enthusiasm, which he rendered during the pursuit of my post-graduate studies and

in the preparation of this dissertation.

With proud privilege and deep sense of respect I would like to express my gratitude

and indebtedness to Dr. A. H. Sasnur, Professor and Head, Department of

Orthopaedics, Al Ameen Medical College, Bijapur, for his constant inspiration,

extensive encouragement and support, which he rendered during pursuit of my post-

graduate studies and in preparation of this dissertation.

I am grateful to Dr. V.V. Mundewadi, Professor, Department of Orthopaedics, Al

Ameen Medical College, Bijapur, for his guidance throughout my studies and

preparation of this dessertation.

I am grateful to Dr. Prakash A. Sasnur, Associate Professor, Department of

Orthopaedics, Al Ameen Medical College, Bijapur, for his guidance, throughout the

study, and encouragement.

I express my sincere gratitude to Dr. Ismail Hathiwale , Assistant Professor, Dr.

Ramangouda Biradar, Assistant professor, Dr. S.S. Taradi, Senior resident, Dr. A.

A. Magi, Senior resident, and Dr. Ravi Biradar, Senior resident, for their valuable

suggestions and support during my study.

V

I am grateful to Dr. B. S. Patil, Dean, Al Ameen Medical College, Bijapur, for

permitting me to utilize the resources in completion of my work.

I am thankful to my colleagues Dr. Danish, Dr. Shamikh, Dr. Ahmed Jilani, Dr.

Pavan, Dr. Chidanand, Dr. Jagirdar, Dr. Umesh, Dr. Azhar for their help and support.

A very special thanks to Dr. Ajay, Dr. Kiran and for helping me prepare this thesis.

I am thankful to Mr. Riyaz, Mr. Hazrat, Mrs jabeen for their help and support.

I thank the O.T. Staff, Anaesthesiology Staff, Radiology Staff, Records Section Staff,

Library Staff and all Hospital Staff for their support and co-operation in my study.

Place: Bijapur Signature of the Candidate

Date: DR. MD NAYEEM ALI

VI

LIST OF ABBREVIATIONS USED

(In alphabetical order)

# Number CLB Curvature of lateral border of footCorr. CorrectionCTEV Congenital talipes equnovarusEH Empty heelEq. Equinus ICFSG International clubfoot study groupLHT Lateral part of head of talusMC Medial crease of the sole of the footN No PC Posterior crease of anklePMR/PMSTR Posteromedial soft tissue releasePSS Pirani severity scoreRE Rigid equinusS.D. Standard deviationS.E.M Standard error of meanvs VersusY Yes

VII

ABSTRACT

BACKGROUND:

Clubfoot deformity is among the commonest congenital anomaly. Its incidence is 2

per 1000 live births per year. Its incidence is more in developing nations. Male to

female ratio is about 2:1. It has been treated since many years by conservative and

surgical methods. Investigators did research and has better understanding of CTEV, in

regards of anatomy, pathoanatomy and biokinematics which led to better conservative

management.

AIMS AND OBJECTIVES:

To evaluate the effectiveness of Ponseti technique, by Pirani severity scoring, this

study was done to reproduce the clinical results, in terms of mobility, flexibility,

cosmetically acceptable and plantigrade foot, and the technique.

MATERIAL AND METHOD:

This prospective study was conducted during September 2010 to September 2012 in

Al Ameen medical college, Bijapur, and the cases were selected on OPD basis. Total

29 patients with 38 clubfoot entered in study. Our study was completed by 34 foot.

There were 3 foot (2 patients) dropout, and 1 foot was reffered for posteromedial soft

tissue release. Our treatment was by Ponseti technique, and severity asscssment was

done by Pirani severity scoring. Equinus correction was done by cast application or by

percutaneous tenotomy.

RESULTS:

Average number of cast applied was 7.97, and before tenotomy it was 6.41. Average

number of cast increases with increase in age and Pirani severity score. 80.00% of

patient had no residual deformity at the time of follow up. The p-value (<0.0005)

showed high significance of treatment. 17.41% had statistically insignificant residual

deformity. The failure was 2.86%.

CONCLUSION:

Ponseti technique of treatment for clubfoot deformity is very effective, and produces

painless, mobile, flexible, plantigrade and cosmetically acceptable foot without need

of any major surgical intervention.

KEY WORDS:

Clubfoot, CTEV, Ponseti technique, Pirani severity score, Percutaneous tenotomy.

VIII

TABLE OF CONTENTS

SERIAL NO. CONTENTS PAGE NO.1. INTRODUCTION 12. AIMS AND OBJECTIVES 53. REVIEW OF LITRATURE

a. Historical review b. Normal anatomy of foot c. Etiology d. Pathoanatomy e. Bio-Kinematicsf. Diagnosis and clinical features g. Classification and severity scoringh. Radiographi. Treatment

781320242932334646

4. METHODOLOGY 575. RESULTS 676. DISCUSSION 857. CONCLUSION 918. SUMMARY 939. BIBLOGRAPHY 9610. ANNEXURE

a. Sample Consent Formb. Case Proformac. Key to Master Chartd. Master chart

105105108109110

IX

LIST OF TABLES

TABLE NO.

CONTENTS PAGENO.

1 The system of Ponseti and Pmoley for the classification ofcongenital talipes equinovarus

35

2 Summary of the system of Harrold and Walker for theclassification of congenital talipes equinovarus

35

3 Catterall’s system for classification of congenital talipesequinovarus

37

4 The system of Dimeglio et al. For the classification ofcongenital talipes equinovarus

37

5 Dimeglio classification scoring system 386 Morphology scores according to the ICFSG scoring system 397 Functional evaluation scores according to the ICFSG scoring

system40

8 Radiological parameter scores according to the ICFSGscoring system

41

9 Pirani severity scores 4310 Pirani’s hindfoot and forefoot scores according to severity 4411 Details of age of patients in months 6812 Frequency of distribution of age of patient at presentation 6813 Distribution of sex of patient 6914 Correlation between age of presentation and sex 6915 Side (Laterality) of involvement of patients 7116 Corelation between laterality and sex for patients 7117 Number of total cast in tenotomised foot 7418 Number of total cast in non tenotomised foot 7419 Correlation b/w no. Of casts and PSS before eq. Correction 7520 Correlation between age and no. Of cast before eq.

Correction75

21 Method of equinus correction in foot 7722 Distribution of sex among cast applied and tenotomised foot,

for Eq. Corr.77

23 Comparison of correction of equinus in the same age group 7924 Pirani severity score distribution 7925 Correlation between pirani severity score and method

equinus correction81

26 Percent of Posteromedial soft tissue release 8127 Details of Pirani score- paired samples 8328 Paire sample test for three pairs 8429 Complications related to cast 8830 Key to master chart 109

X

LIST OF FIGURES

FIGURE NO.

CONTENTS PAGENO.

1 Diméglio’s parameters 382 Diméglio’s parameters 393 Pirani severity score 454 Showing cavus deformity 615 Showing plaster of paris and soft cotton rolls 616 Steps of cast application 617 First cast, showing cavus and pronated forefoot correction 618 Adductus deformity 619 Varus deformity 6210 Correcting adductus 6211 Second cast 6212 Third cast 6213 Fourth cast 6214 Fifth cast 6215 Equinus deformity 6516 Abducted foot in 5 degrees of dorsiflexion 6517 Manipulation to correct the equinus by cast application 6518 Percutaneous Tenotomy done. Entry of blade close to

tendo achillis. 20 Degrees of dorsiflexion achieved66

19 Last cast 6620 After treatment (after last cast) 6621 Denis browne splint 8922 Pressure sore over lateral aspect of talus 8923 Eczema 8924 Bruise over thigh 8925 Loose and broken cast 8926 Blanching 89

XI

LIST OF CHARTS

CHART NO.

CONTENTS PAGENO.

1 Distribution of sex 702 Frequency of distribution of age at presentation and sex 703 Side (Laterality) of involvement of patients 724 Laterality and percentage of patients 725 Male (no. of patients) 736 Female (no. of patients) 737 Correlation between side sex (no. of patients) 738 PSS vs average no. of casts 769 Correlation between age and no. of cast before eq. correction 7610 Method of equinus correction in foot 7811 Distribution of sex among cast applied and tenotomised foot for

eq. corr.78

12 Correction of equinus in the same age group 8013 Pirani severity score distribution 8014 PSS vs method of equinus correction 8215 Percentage of PMR 82

XII

Introduction

1

INTRODUCTION

Clubfoot, also called as “Congenital talipes equinovarus” or “CTEV”. It is idiopathic

and one of the commonest congenital condition. It is a severe anomaly of foot, needs to

be corrected. Nicolas Andry (1743), described the term “Pedis Equinal” in his

“Orthopaedicia” which means foot of the horse. The term “Talipes Equinovarus” is

derived from latin language, Talus means ankle, Pes means foot and equinus means

horse like (plantar flexed) and varus means adducted and inverted.

Clubfoot was first depicted in ancient Egyptian tomb paintings, and in India, the

treatment of the same was described around 1000 B.C. The written description of the

condition was first described by Hippocrates in 400 B.C. He also mentioned that it can

be treated with serial manipulation and strapping and the condition should be treated as

early as possible, before the deformities get established 1.

The incidence of congenital talipes equinovarus is 1-2 per thousand live birth totaling

around 100000 baby is born with this deformity every year, among which 80% are born

in developing nations 2,3. There are studies mentioning that the incidence of clubfoot is

increasing 4, making it a challenge for us to treat it with more specific and accurate

methods. Gartland’s famous observation of clubfoot in 1964 was “We are still crippling

with a problem the cause of which is not known, the pathological anatomy of which is

uncertain, the behavior of which is uncertain and the treatment of which remains

controversial” 5. This stands good even today.

There are few theories describing the etiology of congenital talipes eqinovarus which

are most acceptable till now, eg.- mechanical factors in utero, neuromuscular defect,

primary germ plasma defect, arrested fetal development, hereditary, etc.

All the theories explains certain anatomical changes in foot, which gives it a deformity

to be called as CTEV. The changes are mainly in position and shape of talus,

2

calcaneun, navicular and cuboid. The tendon sheath fascia are fibrosed and contracted

primarily or secondary to the changes in the normal anatomical position and shape of

bones. The deformities are equinus of ankle, calcaneum is in inverted and in equinus

below the talus, talar head prominence over the dorsolateral of foot, medial and plantar

subluxation of navicular to the talus, cuboid is in front of calcaneum with medial

subluxation, medial tilt of anterior part of talus, shortened talar neck, narrow posterior

ankle mortise, talar tilt out of ankle mortise 6,7.

The treatment of CTEV started in the ancient times which has been conservative

management in form of manipulation with strapping, casting etc 1,6.

Since years it has been treated by different conservative and surgical methods. But it has

high tendency to relapse, need for repeat surgeries, extensive soft tissue handling,

scarring, which ultimately gives non flexible painful foot with disabilities 3.

The purpose of the treatment of CTEV is to reduce the deformities with painless

functional plantigrage foot with good mobility without any modified shoes and within

cosmetically acceptable limits.

The recent trend for clubfoot treatment includes series manipulation, streching,

immobilization, and for the relapse and resistant cases management includes soft tissue

releases osteotomy immobilization.

The methods described by J.H. Kite, Ignacio V. Ponseti and French are conservative.

Amongst these, the technique described by Ignacio V. Ponseti which includes gradual

and sequential correction of all deformities by manipulation and immobilization with

cast at about weekly interval gained maximum popularity.

Ignacio V. Ponseti gave different understanding as from others in that he described

about the interdependent movements of tarsal bones and considered, the view that tarsal

joints move on a fixed axis of motion, to be incorrect. He described the Kite’s method

of correction in which the abduction of calcaneus under the talus was prevented by

3

applying counter pressure over the calcaneocuboid joint as “Kite’s error”. This is very

essential in correction of heel varus as the calcaneus cannot be everted unless it is fully

abducted under the talus 8. French functional method of physiotherapy has less

reduction of operative procedure compared to Ponseti technique 9.

So the study of correction of clubfoot deformity by Ponseti techique is done to analyze

its effectiveness and functional outcome in children below two years of age and without

any prior treatment for the same.

4

Aims and Objectives

5

AIMS AND OBJECTIVES

1. To evaluate the effectiveness of Ponseti technique in management of Clubfoot.

2. Functional outcome.

3. To study the drawbacks of Ponseti technique.

6

Review of litrature

7

REVIEW OF LITRATURE

HISTORICAL REVIEW

The history of clubfoot comes from as early as Egyptian times. There are pictorial

depiction of clubfoot in the Egyptian tomb paintings, and the treatment was described in

India as early as 1000 B.C 1.

The first written description of clubfoot was given by Hippocrates in 400 B.C 10. He also

wrote the cause of the deformity to be mechanical factor during intrauterine life.

Malpositionaning leading to malalignment of the bones and secondarily soft tissue. He

also mentioned that the condition should be treated as soon as possible after birth,

before the deformities get well established. He also described repeated manipulation and

maintaining it by strong bandage application. He also emphasized on over correction of

deformity so that recurrence may be avoided. After correction of deformity , he allowed

special shoes to wear for maintenance of correction 1.

Ambroise Pare, the “father of modern surgery”, who first published his works in 1575,

made a perforated steel orthosis for ankle-foot orthosis to correct club foot, among

many other orthosis and prostheses. He also suggested manipulation and bandage/ splint

for treatment of clubfoot 10,11.

For many years the treatment of clubfoot remained in hands of barber-surgeons,

charlatans, and bonesetters, and minimal information is available concerning their

practice 1.

Next literature was given by Arcaeus in 1658. He wrote a small treatise "Decurandis

Vulneribus" about stretching technique and maintenance of correction by two

mechanical devices 12,13.

8

Nicolas Andry in 1743 gave a correction method, comparing deformed foot with bent

tree and correcting with iron plate and bandages.

In the 18th century, Cheselden, at St. Thomas' Hospital, treated clubfeet by repeated

stretching using tape to maintain the improved position. In the year 1803, Scarpa

published his historical Memoir on Congenital Club-foot of children, it did not gain

much popularity. He did forceful stretching and application of complicated mechanical

devices, which later known as Scarpa’s shoes. His method was never so successful so,

not widely accepted 1,13.

In 1806 T. Sheldrake published an essay “Distortions of the Legs and Feet of

Children”. He mentioned use of strapping bandages like Hippocrates, and claimed child

below age of 2 months will be cured of all deformity in every sense in three months. He

thought that half of the deformities are due to muscles and half due to ligaments 1,15,.

Delpech began performing percutaneous tenotomy in 1816 and published his work in

1823. He used it for correction of equinus deformity in clubfoot 16.

In 1829, Dr. Stromeyer in February, 1831, he made his first section of the Achilles

tendon 17. At the same time Stromeyer did several tenotomy without any immediate

complication. At the same time he did tenotomy of british surgeon W.J. Little, who

acquired equinovarus deformity due to polio 18. In 1839 W.J. Little described his

success in tenotomy,and he was the first surgeon to perform tenotomy in England 18,19.

In 1836 Mc Guerin was the first to use plaster of paris in the treatment of CTEV to

maintain manipulation 10,20.

Deformity of talar head and neck was stated by Adams in 1852 and 1855 in his article

for etiology of clubfoot. He also described its association with congenital anomalies 21,22.

9

In 1857 Solly was the first to introduce a bony procedure – partial cuboidectomy for

correction of the deformity 23.

Adams W. in 1866 said that primarily changes are in talus and the soft tissue

contractures are secondary to bony deformity. This was set back for Scarpa’s concept 13.

H.O. Thomas (1834-1891) who discovered Thomas splint and Thomas test, also

developed “Thomas Wrench” for manipulation of clubfoot. But his point of application

was not so defined and it was a forceful menupulation 1.

In 1894 Sir Robert Jones gave up surgical procedures and adopted conservative and

manipulative techniques. He said that there is no foot which cant be corrected if it is

started in first weeks of life and it will be corrected in 2 months. Full correction is

achieved till child starts walking. And tenotomy is very rarely required. Denis Browne

(1892-1967), father of pediatric surgery, who deviced Denis Browne rod, and we are

still using similar abduction orthosis with some modification 1.

Kite treated many case of clubfoot in mid and late 1900’s. Kite corrected components of

clubfoot separately, and not simultaneously. He corrected cavus to avoid foot pronation

but correcting heel varus took many serial casts. He recommended "getting all the

correction by abducting the foot at the midtarsal joint" with the thumb pressing "on the

lateral side of the foot near the calcaneocuboid joint." But correcting heel varus by

abduction of forefoot against pressure over calcaneocuboid itself prevented calcaneal

eversion and heel from varus correction 1.

Ponseti, who attempted to understan the pathophysiology of clubfoot from his

predecessors and developed his current method of treatment of clubfoot. His

understanding of anatomy of normal foot and clubfoot was greatly enhanced by the

book “Precis de Manual Operatoire” written by Farabeuf in 1872. Farabeuf described

how in the normal foot when the calcaneus rotates under the talus, it adducts, flexes, and

inverts. More precisely, as the foot goes into varus, the calcaneus adducts and inverts

under the talus while the cuboid and the navicular adduct and invert in front of the

10

calcaneus and the talar head, respectively. Farabeuf also explained that in the clubfoot

deformity the ossification center of the talus responds to the abnormal pressures placed

on it by the displaced navicular. He also observed that while bony deformities in the

infant with clubfoot were reversible and recurrences are high due to soft tissue

contractures. Previously, clubfoot patients were occasionally treated at an early age, so

surgery was usually necessary to correct the deformity. Ponseti also took some

guideline from the studies of Huson. Huson in 1961 gave idea about simultaneous

movement of tarsal joints about moving axis and not like hinges 1. An study was done

by Green A and Lloyd-Roberts GC. with a follow up of average 15 years for long term

follow of early surgical procedure for treatment of clubfoot, but the results were not

satisfactory 24.

In 1963 Ignacio V. Ponseti, and Eugene N. Smoley did a study with good results. The

results of treatment in sixty-seven patients with a total of ninety-four severe congenital

club feet were evaluated five to thirteen years after the initial treatment. The results in

71% of the feet were good; in 28 per cent a slight residual deformity persisted; and in

one foot a poor result was obtained 25,26.

A thirty year follow up sutdy was done for treatment of clubfoot by conservative

method of Ponseti by Cooper DM, Dietz FR. It was published in 1995 with seventy

patients and the excellent result were for 78% of foot 27.

RA Agrawal, MS Suresh and Rajat Agrawal published their study in 2005 mentionaning

that Ponseti technique is very effective in management of idiopathic clubfot and the full

correction was achieved by tenotomy in 58 feet out of 60 feet. He concluded that “The

Ponseti method is a safe and effective treatment for congenital idiopathic clubfoot and

radically decreases the need for extensive corrective surgery. Non compliance with

orthotics has been widely reported to be the main factor causing failure of the

technique” 28.

Atul Bhaskar and Shraddha Rasal did correction of clubfoot deformity by Ponseti

technique and the results were excellent for twenty-eight children correction, four had a

11

fair outcome and eight cases had relapse in their deformity. Poor splint compliance and

fitting along with incomplete correction of the deformity were identified as the chief

causes leading to a poor result 29.

Charles EJ Docker, Simon Lewthwaite and Nigel T Kiely found similar excellent results

with Ponseti technique and mentioned tendoachillis tenotomy to be part of it. In their

article they said “similar good results and low requirement for surgical interventions

other than Achilles tenotomy, which forms part of the Ponseti regimen, were found in

both cohorts” 30.

Ponseti method is well effective upto age of two years, but it is still effective in older

children with good results31.

Previously the trend to treat clubfoot was after the child has passed early infancy, and it

was single staged correction of all deformities. But now trend has changed to

manipulate and treat the deformity gradual and sequential. Ponseti method can be

followed surely in early age as well as older and children who are treated with other

manipulative methods.

12

NORMAL ANATOMY OF FOOT

For the correction of clubfoot deformity, it is necessary to understand the normal

anatomy of foot. The clubfoot deformity is exaggeration of normal equinovarus

position. The mechanism of movement of tibiotalar, subtalar and midtarsal (chopart’s

joint) are considered as one unit as their movement are interdependent. The osseus

component of foot may be divided into tarsus, metatarsus and phallanges. The soft

tissue components includes the muscles, tendons, ligaments and capsule. It will be

detailed below.

TARSAL BONES

There are seven tarsal bones of foot-

1. Talus

2. Calcaneus

3. Navicular

4. Cuniform- medial, midddle and lateral

5. Cuboid

These are arranged in two rows, proximal and distal rows. On the medial side there ia

one tarsal bone that is navicular connecting the two raws. The proximal raw contains

talus and navicular. The are not arranged side by side but the are arranged vertically

over each other. Talus lies above calcaneus by three articulations. Distal raw is formed

by three cuniform bones and a cuboid. Between talus and three cuniform bone, the

navicular bone lies on the medial side. The three cuniform and the cuboid bone are

arranged side by side to form the transverse arch which is convex dorsally. On the

lateral aspect calcaneus articulates directly to the cuboid.

13

TALUS

It is the 2nd largest bone among tarsus. Its an irregular bone. It is the only bone without

any muscle attachment, and is wholly covered by articular cartilage except for the

attachments of ligaments.

It has three parts – 1. Body 2. Neck 3. Head . the body has three articular surfaces. The

three articular surfaces together known as trochlea. The superior articular surface of

talus is wider anteriorly compared to posterior from side to side. Being broader

anteriorly , the shape is called as wedge shaped. On the posterior aspect of talus, there is

groove, that directs the tendon of flexor hallucis longus medially. Initially in the early

age , the groove is shallow , but later as the age advances the groove becomes more

deeper. The lateral tuberosity on the lateral aspect of the groove gives attachment to the

talfibular ligament. Sometimes there is separate ossification centre for the lateral

tubercle persists to be called as “os trigonum”. Inferior surface of talus has a groove

over similar groove of calcaneum. This is called tarsal canal and it contains talo

calcaneal interosseus ligament. The head, anteriorely have articular surface for navicular

and inferiorely it has three articular facets for calcaneum in two compartments.

THE CALCANEUS:

It is irregular bone and the largest of all tarsal bones. Calcaneum articulates with talus

and cuboid. It has three articular facets superiorly for talus. Forming three joints-

anterior middle and posterior talocalcaneal joints. Anterior and middle joint collectively

called as anterior talocalcaneal joint. The capsule of the anterior and posterior joint is

divided by the calcaneal sulcus, which makes sinus tarsi and contains ligament and

neurovascular structures.

On the medial border of calcaneus, there is a horizontal eminence protruding upwards,

is called suntentaculum tali. As the name suggests, it supports talar head and neck. It is

located under the middle articular facet of talus. It provides attachments to fibres of

tibialis posterior , deltoid ligament, spring ligament (calcaneo-navicular ligament) and

acts as pully for flexor hallucis longus. The long axis of calcaneus is directed forwards

upwards and laterally.

14

NAVICULAR:

It’s a boat shaped bone and is located between head of talus and three cuniform bones.

Its convex surface has three articular facets for three cuniform bones. It forms a ball and

socket type of joint with talus. Its medial tuberosity gives attachment to the tibialis

posterior tendon.

CUBOID:

It’s a cube shaped bone and has three articular surfaces for calcaneus , 4th and 5th

metatarsals and to the lateral cuniform. It is firmly placed between the bones by which it

articulates, and it movements are mainly with calcaneus.

CUNEIFORM BONES:

These are wedge shaped bones, arranged in the distal raws of tarsal bones. Proximally

the articulate with the navicular and distally they articualte with the first three

metatarsal bones.

JOINTS OF ANKLE AND FOOT

THE TIBIO TALAR JOINT:

The joint is formed by the tibia fibula and the talus. The trochlea of talus forms tenon

wedge in the ankle mortise formed by the lower end of tibia, medial and lateral

malleolus. The joint is stabilized by the tibiofibular interosseus ligament, medial and

lateral ligaments of the ankle joint. As there is no muscle attachment to the talus, its

movements are passive and secondary to the movements of calcaneus and navicular.

The movements of the subtalr joints are connected with the vertical motion of the ankle

joint. When the foot is in dorsiflexion only a part of the talus is in mortise and the

anterior part of trochlea is broader then the posterior. While in plantar flexion, the

narrow part is inside the mortise and the wider part of trochlea is out of the joint. In

prolonged plantar flexion , bony changes occures in the anterior part of the trochlea.

15

SUBTALAR JOINTS:

It refers to the three talocalcaneal joints. But the synovial cavity is devided into two

compartments by the talocalcaneal interosseus ligaments, which are anterior and

posterior talocxalcaneal joints. The anterior and middle talocalcaneal joint together

called as anterior talocalcaneal joint between the anterior and middle facet of calcaneum

with the head and neck of the talus.

CHOPART’S JOINT OR MIDTSRSAL JOINT:

The mid tarsal joints includes taloanvicular joint, calcaneo navicular joint and

calcaneocuboid joint. The talonavicular joint is the most mobile of all the intersal joints.

It’s a ball and socket type of joint. Compared to hip, acetabulum is formed by navicular,

spring ligament, talonavicular capsule and calcaneum. Calcaneo cuboid joint is ‘S’

shaped and cuboid is firmly wedged between the chopart and lisfrnc joint bridging these

two. Due to this tight arrangement, the mobility of the cuboid is restricted medially by

the navicular and cuniform, and its all movements are the accompanying of calcaneus,

and its own mobility is very less.

NAVICULO-CUNIFORM AND LISFRANC JOINTS:

The naviculocuniform joints have very less mobility. Similarly the tarsometasal joints

also have very little mobility. Little mobility is possible due to lax ligaments of first

tarso metasal joint. Other tarsometatarsal joints have very little mobility because thye

are bound with strong ligaments and interlocking joints.

TALOCALCANEONAVICULAR JOINT:

This joint is formed by head of talus, anterior end of calcaneous, navicular and spring

ligament. The joint, as it is of ball and socket variety, has been compared with the hip

joint. The acetabulum for head of talus is formed by the by the posterior concave

surfaces of the navicular, the middle and anterior facets of the anterior part of the

calcaneus and the spring ligament. Spring ligament bridges the interval between the

navicular and the sustentaculum tali. It has a fibrocartilagenous central part that

supports the medial portion of the talar head. The composite socket for the head of the

talus is completed by fibroelastic tissues than the bony elements. These structures are

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arranged as follows: dorsomedially are the talonavicular capsule, the deltoid ligament

and the tendon of the tibialis posterior, in subtalar the spring ligament, laterally the

calcaneonavicular portion of the bifurcated ligament (Y-ligament) and posteriorly the

talocalcaneal interoseous ligament.

MUSCLES:

EXTRINSIC MUSCLES:

Extrinsic muscles are two, the gastrocnemius and soleus, collectively called as triceps

surae. They are the chief plantar flexors of the foot. The insertion is by a common

tendon, the tendochillis. It is inserted on the posterior aspect of calcaneus on the

tuberosity, which is placed slightely medially. So these muscle contraction causes

plantar flexion as well as little inversion of foot.

FLEXOR HALLUCIS LONGUS:

This muscle originates from the lower 3rd of posterior surface of fibula and introsseus

membrane. It is inserted over proximal phallanx of great toe.

FLEXOR DIGITORUM LONGUS:

This originates from the posterior surface of tibia and passes behind the medial

malleolus behind the tendon of tibialis posterior in separate tunnel. Distally it is joined

by the quadratus plantar, and divides into four tendons which insert on the terminal

phallanges.

TIBIALIS POSTERIOR:

Tibialis posterior is the chief adductor , inverter and flexor of foot. It originates from the

posteromedial surface of the tibia, interosseus membrane and corresponding surface of

fibula. It passes posterior to medial malleolus and anterior to the tendon of flexor

hallucis longus, in separate tunnel. It has got insertion on tarsal and metatarsal bones.

But it is aminly inserted into the tuberosity of navicular bone, cuniform, metatarsal base,

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spring ligament and suntentaculum tali. It works by making medial malleolus as

fulcurum and it pulls the navicular medially and downwards.

TIBIALIS ANTERIOR:

It originates from the anterolateral surface of the tibial and passes below the extensar

retinaculum and inserted into the base of first metatarsal and medial cuniform. It

dorsiflexes and inverts the foot.

PERONEUS MUSCLES:

Peroneus longus and brevis originates from the lateral surface of the fibula and its

tendon passes poterior to the lateral malleolus. Peroneus longus turns medially to get

inserted into the base of first metacarpal and the first cuniform. Peroneus brevis gets

inserted into the base of first metatarsal. These are the chief pronator of foot and plantar

flexes the foot.

THE INTRINSIC MUSCLES:

These are the chief muscles which cause the cavus deformity of foot in CTEV. The

abductor hallucis, flexor digitorum brevis, abductor digiti quinti and quadratus plantae

(flexor accessories) has a common mass of muscle that arises in several successive

layers from the medial and plantar surface of the tuberosity of the calcaneus and the

plantar aponeurosis.

ABDUCTOR HALLUCIS:

It originates from the medial process of calcaneal tuberosity. Its runs along the medial

border of foot to get insert in along with the tendon of flexor hallucis brevis, in the base

of proximal phallanx of great toe on medial aspect.

MOVEMENTS:

All the joints of the foot have some major movement plane of movement and the others

have different.

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The horizontal movement occurs at the talonavicular and anterior subtalar joints. These

two joint gives most of the mobility in the horizontal plane but not the posterior

talocalcaneal or calcaneaocuboid joints. The calcaneocuboid joint very less mobility,

and the cuboid has its movements with the calcaneum only. Restriction of any

movement affects the movement of other, these are interdependent. Horizontal mobility

will be affected either by the restriction of subtalar joint or talonavicular join. The

vertical motion is mainly at the ankle joint.

SUPINATION:

Supination is combination of two movements, adduction and inversion. Adduction

occures chiefly at lisfranc joint and inversion at subtalar joint. While adduction

navicular is pulled medially over the head of talus by the pull of tibialis posterior. Along

with the navicular , the calcaneum is also pulled medially, by the insertion of tibialis

posterior on the spring ligament and sustentaculum tali. Inversion of calcaneum occures

due to the action of same. By this action the distance between the navecular and

sustentaculum tali and spring ligament decreases, and the socket size for the head of

talus decreases, and sinus tarsi opens laterally. In case of clubfoot these soft tissue

components of so called acetabulum gets contracted.

PRONATION:

It’s the combination of two movements, abduction and eversion. The chief muscles

responsible for this is peronei. Eversion of calcaneus occures mainly at the subtalar

joint. Abduction occures mainly at lisfranc joint. The eversion of calcaneus occures

along with there is the leteral migration of acetabulum of talar head. Socket capacity is

more at this position. And the sinus tarsi is closed.

PLANTAR FLEXION:

It occures mainly ant tibiotalar joint but also at talocalcaneonavicular joint. As talus has

no muscle attechment of it own so it follows the movements of the fellow bones. It is

accompanied with the supination of foot.

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DORSIFLEXION:

It occure at the ankle joint along with talocalcaneonavicular joint. It is accompanied

with the pronation of the foot. In this movement calcaneal tuberosity goes down by

relaxation of triceps surae and calcaneum everts. The navicular moves laterally over the

head of talus.

ETIOLOGY

Several theories have been proposed for the etiopathgenesis of clubfoot but each and

every theory has some drawbacks. The theories of CTEV are still in controversies for

full acceptance. The good thing with our concept is that we are understand the

deforming forces. Following are the theories postulated:-

1. Mechanical pressure in utero:

This is the first theory given by Hippocrates. He believed during the development of

foot, abnormal pressure to the foot in abnormal position cause the deformity.

Oligohydroamnios prevents fetal movements and makes the foot vulnerable to external

pressure and deformity 1,6.

This was disputed because of the absence of increased incidence in an overcrowded

uterus (twinning, large babies, hydramnios and primiparous uterus) 7.

2. Neuromuscular defect:

Isaacs proposed that the decreased bulk of muscles in clubfoot is due to neuromuscular

defect. He believed that CTEV is a resistant form of Arthogryposis multiplex congenita.

The pattern of abnormality was similar in both muscle groups. Thus shortening of the

posteromedial muscles may result from a small increase of fibrosis due to minor

innervation changes occurring in intra-uterine life. There is evidence that

immobilisation, stretching or relaxation of muscles does not account for the anomalies

observed. This study of the extrinsic muscles in talipes equino-varus indicates a

dominant neurogenic factor in its causation. He believed that the fibrosis of soft tissue

in clubfoot is not a primary factor 32.

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But still there are controversies to the theory, as if it is a neuromuscular defect then it

should have some association with neurological congenital conditions or other

neurological defects. It is believed that there is some association of spina bifida with

clubfoot, but again it is not consistent. Deformities associated with neurological defects

are not producing consistent clubfoot deformities, and moreover neurologically

produced clubfoot is less rigid then the non idiopathic clubfoot. Studies done for

surgically creating equnovarus in animals, that produced bony defects. So the primary

soft tissue changes still holding good for the etiology.

Matthew E. Lovell and Jose A Morcuende published that the relapse of the

conservatively treated patient are due to some neuromuscular disease 33.

3. Arrested fetal development:

Intrauterine environment: In 1863, Heuter and Von Volkman first proposed that the

arrest of fetal development early in embryonic life was a cause of congenital clubfoot.

The theory of intrauterine fetal development was again supported by Bohm in 1929.

The theory was opposed by Mau and Bessel-Hagen. Mau wrote that the embryonic foot

does not show the distortion of bones about tarsal joints, which is found in CTEV 6,7.

Victoria Diaz said “embryonic foot position changes with movements of talus and

calcaneus due to growth spurt in distal tibia and fibula. In fibular phase, foot goes into

usual fetal position of equinovarus and in tibial phase it is pronated into usual fetal

position. Any arrest in the tibial phase without growth spurt results in persistent

equinovarus deformity 34.

Environmental influence: teratogenic agents influence the growth of fetus in utero.

Infection with rubell and effect of thialidomide is well known on fetus. Many authors

believe that there are various environmental factors responsible for the appearance of a

clubfoot, as there are various substances capable of producing a temporary growth

arrest. But controversy to this study is that no such study is mentioning the consistent

effect of the teratogenic agents in causation of clubfoot.

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Blastemal defect in development of tarsal bone:

Waisbord described a defect in the cartilage analogue of tarsal bones as cause of the

deformity 35. Ponseti did not found any defect in the cartilage analogue in specimen

dissected by him.

Irani and Sherman described a primary germ cell defect in head and neck of talus, but

were unable to explain germ cell defect in unilateral clubfoot and correction of

deformity by realigning the navicular and calcaneus on talus without any correction in

the talus 7,13.

There are controversies to the theory too. Similar to the defect in Primary germ plasm

defect theory others have described the same abnormality of the talus, but they attribute

it to secondary adaptive changes. It is not clear, a unilateral deformity resulting from a

genetic defect, and why only head of the talus is involved, and not the body.

Primary rectracting fibrisis:

Zimmy et al.- Fibroblasts resembling myofibroblasts and mast cells were found in the

lateral and medial side of clubfoot and proposed that the cause for the contracture are

these myofibroblasts and the histamine secreted by the mast cells 36. Fukuhara observed

myofibroblast like cells in the spring ligament and speculated fibromatosis in the medial

tarsal ligaments as the cause of CTEV 37. Ippolito and Ponseti I.V. similarly described

primary retracting fibrosis as primary cause of CTEV deformity 38.

Heredity and Environmental factors:

There are studies with confusing evidence of the multifactorial evidence of CTEV

including genetic and environmental factors 39. Pedigree studies have established that

the disease is certainly not inherited in a single autosomal dominant or autosomal

recessive mendelian fashion, although a Mendelian component of inheritance cannot be

fully excluded. A genetic predisposition operating on a polygenic or in some cases

autosomal dominant basis was thought to manifest as Idiopathic CTEV when a

threshold for expression is exceeded. When the genetic predisposition alone does not

exceed the threshold, environmental factors may act alone or synergistically to reduce

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the threshold for expression to the point at which Idiopathic CTEV is manifest 39.

Palmar (1964) and Wynne Davies (1972) meticulously worked and and they concluded

that, incidence of clubfoot is increased in relatives and in siblings. So they concluded

that heridity plays a role in causation but the manner and extent in which it acts is

unclear. Wynne Davis concluded that a decreasing incidence of CTEV disorder as the

relationship of the parents become remote could be indicative of dominant gene with

reduced penetrance or multifactorial inheritance system. However the manner in which

the occurrence rate decreases is suggestive of a multifactorial model 40. A

preponderance of the condition among those patient with first degree relative affected

increasing the frequency to 2.9 per 1000 live births is highly suggestive of a heritable

component. Chung provided strong corroboration of the polygenic model of inheritance

in his study of incidence of CTEV according to race, conducted in the population of

Hawaii. Syndromic CTEV has either Autosomal dominant i.e. Craniocarpotarsal

Dysplasia or Whistling face Syndrome, or Autosomal recessive pattern i.e. Diastrophic

Dwarfism. It is also associated with Larson syndrome and Smith- Lemli- Opitz

syndrome. Gorlin R.J. described clubfoot associated with X- linked recessive pattern.

He wrote on Pirre-Robin syndrome with congenital heart malformation and CTEV 39,40.

Congenital abnormalities:

Cytological abnormality produces syndromes that include CTEV with maternal

unbalanced 6:11 translocation as reported by Clark. Insley reported a case of association

of CTEV with a deficiency of a part of long arm of chromosome 18 40.

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PATHOANATOMY

The deformity in clubfoot mainly are equinus, varus, adduction and frequently

associated with cavus deformity.

Equinus is fixed plantar flexion of foot. Both ankle and talocalcaneonavicular joints are

involved. In varus, the whole the tarsal bones except talus are rotated inwards,

respective to the lower leg. At the same time the calcaneous is inverted and the forefoot

is in pronation with respect to the hind foot, and this contributes to the cavus deformity.

Adduction occurs at the lisfranc’s joint. Except for the first metarsal bone, rest of the

metatarsal bones from second to fourth , hardly slides medially. The first metatarsal

bone slides because of its lax ligamental attachments, and the rest of the metatarsals are

unable to do so because of tight ligaments, capsule and the tight interlocking joints.

The cavus deformity is mainly caused by, medial soft tissue contractures, and forefoot

pronation with reference to hindfoot in supination.

Tibial torsion is present in variable degree and form. It may in internal or external

torsion.

Antonio scrapa was the first to describe the vivid anatomy of clubfoot 41. The CTEV

foot has smaller tarsal bones compared to normal foot. There are several different

deformity explained by different researcher, briefed below.

Talus:

This is the bone which is maximally deformed. Trochlea is broader anteriorily and

narrow posteriorely. The anterior part is out of ankle mortise and the narrow posterior

part is inside it, which is devoid of articular cartilage. The anterior part being wide

doesn’t accommodate in the ankle mortise thus hindering dorsiflexion thus being one of

the main cause of equinus deformity. Normally the neck and the head of talus makes an

angle of 150○ to the body, but the angle in clubfoot deformity decreases to 115○ to 135○.

Moreover the head which is normally directed forwards, is deviated medially along

navicular in whole making the articular surface more on saggital plane. The articular

24

surface is flattened and wider as compared to normal talar head. The posterior concave

facet is relatively shallow. The medial border of talus is underdeveloped.

Calcaneum:

It is involved in all the three deformities of CTEV, the equinus, varus and adductus. The

calcaneal malposition is the main contributor of the deformity and it is not much

deformed in shape. Posterior tuberosity is diaplaced medially and wide. The posterior

trochlear surface is narrow and underdeveloped. The sustentaculum tali is displaced

medially and inverted below the head of the talus. Anterior and middle articular facets

are flat and indistinguishable. But the axis of talus and calcaneum is parallel.

Navicular:

It is relatively flat as compared to the curvature of normal bone. It is displaced medially

and is more on saggital plane. In case of sever deformity, sustentaculum tali, navicular

tuberosity and medial malleolus lies close to each other. The adduction, medial

subluxation and being close to medial malleolus , gives it a bean shape.

Cuboid:

It lies in front of calcaneum and it is displaced medially along with the calcaneus. It

bridges the chopart and lisfranc joint. It aids in the lateral convexity of the foot.

Cuniform and Metatarsals:

These are adducted and normal in shape. The first metatarsal shows maximum plantar

flexion.

Tibia:

The lower end of tibia articulates with the posterior part of trochlea. Previously it was

supposed that tibia is rotated medially but later Swann et al. in 1969 demonstrated that it

is lateral torsion and if persistant, then it is indication for corrective osteotomy 42.

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Soft tissue contractures:

The CTEV foot is shorter than the normal foot. The muscles are atrophied and more

apparent when child grows. The muscles tendons and ligaments have more fibrous

content than normal. The ligaments and tendons have abnormal insertions too. The

posterior and medial soft tissue are contracted. The neurovascular bundle posterior to

the tibialis posterior may be shortened. The contractures are usually more dense and

thickened in the cases who has not undergone any manipulation or stretching.

Posterior contracture:

This includes tendoachillis, ankle capsule, subtalar capsule, posterior talofibular

ligament and calcaneofibular ligament. These contractures prevents the correction of

equinus deformity.

The Achilles tendon is always contracted and short, which prevents downward extrusion

of posterior tuberosity of the calcaneus, which is necessary for dorsiflexion. Its

attachment to the calcaneum is broader and wider. Its insertion is more towards the

medial side of the calcaneal tuberosity as compared to normal foot, resulting in varus

position of the calcaneus. This medial attachment must be divided while performing

posterior release or posteromedial soft tissue release, to aid in the correction of heel

varus.

Posterior talofibular ligament and calcaneofibular ligaments becomes thickened and

shortened as per Law of Davis 7,43. This results in prevention of movements of the

fibula, which is very essential for normal dorsiflexion at the ankle joint. This must be

excised in posteromedial soft tissue release to obtain good correction 44. The

dorsiflexion of the talus is prevented by the contracted and shortened posterior capsule

of the ankle and tight achilles tendon and posterior talofibular ligament. These

structures prevent the downward exit of the back portion of the trochlea out of the ankle

mortise, which is a prerequisite for the dorsiflexion.

26

Medial plantar contracture:

These include contracture of tibialsi posterior, deltoid ligament, spring ligament and

talonavicular capsule. The structures are contracted and forms like an indistinguishable

scar in the medial plantar aspect of the foot. This scar obscures the mid tarsal and sub

tarsal joints. According to Brockman it forms a shortened fibroelastic component of

acetabulum of head of talus. The fibrosed scarry structure keeps the tuberosity of

navicular, sustentaculum tali and medial malleolus in close proximity. And while

correcting the clubfoot, this scar resists forward and lateral migration of navicular and

as well lateral movement and eversion of anterior end of calcaneum. The fibrous tissue

forms deep layer of deltoid ligament which is located between contiguous surface of

medial malleolus and medial articulate surface of talus.

Tibilais posterior muscle is shortened and the tendon loses its cylindrical shape while

passing behind the medial malleolus and its sheath is thickened. The insertion of tendon

of tibialis posterior is diffused and over the fibrous scar. It has abnormal attachments to

spring ligament, sustentaculum tali and navicular. It has very wide insertion on

navicular tuberosity. It also blends with common mass of scar tissue, which maintains

sustentaculum tali, medial malleolus and medial tuberosity of the navicular in close

proximity.

Flexor hallusis longus and flexor digitorum longus are short and contracted which

causes flexion contracture of the digits more of first digit. The crossing of the two

muscles, the master knot of Henry, restricts the mobility of the navicular by its

attachment to undersurface of the same at the crossing of the two muscles.

Spring ligamnet (calcaneo navicular ligament): this ligament is migrated medially and is

always contracted and inelastic because of equino varus deformity. The navicular lies

close to sustentaculum tali and spring ligament, gets contracted (as per law of davis) and

this prevents forward and lateral movement of the navicular bone. The talonavicular

joint capsule also contracts, which is in a lax state due to the equinovarus position.

27

Plantar contracture:

Plantar contracture is the main reason for the cavus deformity in the club foot. The

structures involved are abductor hallucis, intrinsic toe flexors, quadratus plantae and

plantar aponeurosis. The contractures of the tissue are more prominent in older children.

In severe form of cavus deformity, abductor hallucis has an abnormal accessory origin

at the tendon sheath of tibialis posterior. The sheath of two flexor tendons and the

navicular tuberosity. As a result of adaptation to varus and adduction deformity the

flexors are shortened and contracted. Abductor hallucis has broad insertion over the first

metatarsal distal to the anterior tibialis tendon.

Peroneal tendons are weak. Intrinsic toe flexors are shortened. Calf muscles and

intrinsic toe flexors are also shortened. The ligaments on medial and posterior aspect of

the ankle joint are pulled into the joint by severe plantar flexion and varus displacement

of talus. There is marked thickening and shortening of the tibionavicular and plantar

calcaneonavicular ligament.

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BIO- KINEMATICS:

It is important to know the bio kinematics of different joints and bones for proper

correction of club foot. The correction of the severe displacements of the tarsal bones in

CTEV requires a clear understanding of the functional anatomy of tarsus.

The clubfoot deformity mainly occurs in tarsal bone. The tarsal bones which are mainly

cartilaginous in early life and are in their deformed shape and displaced position,

according to the severity of deformity 45.

Talus is in plantar flexion with its neck and head displaced and angulated medially with

a wedge shaped anterior articular surface. The navicular is displaced medially and

articulates almost to the medial part of head of talus and medial surface of it. It is very

close to the medial malleolus. The calcaneous is inverted and adducted below the of

talus. The cuniforms are less displaced medially as compared to navicular, and the

cuboid moves along with navicular, so the cuboid lies below the cuniforms. The tendons

of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus are

medially displaced 45.

There are controversies regarding axis of motion of subtalar joints. According to

Farabuef, Virchow H, Huson and Siegler, there is no fixed axis of motion of subtalar

joint. This is in contrast to the concept by Hicks, Elfnan and Inman which emphasis that

subtalar joint moves around a fixed axis 35. A good understanding of the tarsal

mechanics in the normal foot was given by Huson in his thesis “A functional and

anatomical study of tarsus”. He demonstrated that tarsal joints do not move as a single

hinge but rotate about a moving axis as in the case of the knee. Each joint has its own

specific motion pattern. These are described by means of discrete arcs, representing the

successive portion of a particular moving axis. This successive position is followed by a

fixed pattern which is characteristic for the joint concerned. He described “Constrained

Mechanism” in which motion of the tarsal joints occur simultaneously. If one of the

joint movements is blocked the other joint movements also get blocked. The ligaments

play an important role as “Kinematic Constraints” of joints apart from their share in

29

forced transmission to support the elastic vault structure of the foot 46. The concept of

passage of axis of rotation from anteromedial to posterolateral was given by Inman 47,48.

The movements of the joints of foot are not like mitered hinge in one axis but the

movements are interdependent and simultanuous like one axis moving around another

moving axis 45.

Siegler S, Chen J, Schneck CD described “Kinematic Coupling”. They observed the

range of motion of the foot-shank complex in any direction (dorsiflexion/plantarflexion,

inversion/eversion and internal rotation/external rotation) is larger than that of either the

ankle joint or the subtalar joint. Neither the ankle joint nor the subtalar joint are acting

as ideal hinge joints with a fixed axis of rotation. Motion of the foot-shank complex in

any direction is the result of rotations at both the ankle and the subtalar joints. However,

the contribution of the ankle joint to dorsiflexion/plantarflexion of the foot-shank

complex is larger than that of the subtalar joint and the contribution of the subtalar joint

to inversion/eversion is larger than that of the ankle joint 49.

The movements of the joints are affected by the curvature of the joint surfaces and

ligaments. Therefore the correction of extreme medial deviation and inversion of the

tarsal bone in the clubfoot requires simultaneous gradual shift of the navicular cuboid

and calcaneous before they can be everted into the neutral position. These

displacements are possible due the lax stretchable ligaments of the baby. There are still

some believers, thinking, simple pronation of foot on a fixed axis of chopart joint will

correct deformity, the varus and foot supination. But it is not so. In clubfoot, the anterior

2/3rd of the calcaneus lies beneath tha talus. Pronating the clubfoot on this imaginary

axis tilts the fore foot in more pronation and exaggerates the cavus and presses the

adducted calcaneus against the talus, leaving the hind foot uncorrected. It causes

persistence of equinus and varus deformity of heel. The abduction (lateral displacement)

of the calcaneus to its normal relationship with the talus will correct the heel varus

deformity of the clubfoot deformity. Correction of clubfoot is accomplished by

adducting the foot in supination while counterpressure is applied over the lateral aspect

of the head of the talus to prevent the rotation at the talus in ankle mortise. Cast is

30

applied to maintain the correction of manipulated foot and changed after five days. In

this five days, ligaments become lax and stretchable again and the tarsus remodels 45.

31

DIAGNOSIS AND CLINICAL FEATURES:

The diagnosis is purely based on the clinical features, tthe obvious deformities, the

cavus, varus, adductus and equinus. The clinical features may in its severity. It may be

looking like mild exageration of normal equinovarus position of foot or the medial

border of foot may be touching the tibia. Usually the deformity which are corrected by

just some initial manipulation are more towards positional deformity 45.

Equinus deformity of the foot is , along with inversion of heel, adduction and varus of

fore foot. The medial border is concave. The fore foot is in pronation with respect to the

hind foot, which itself is in supination. There is adduction deformity of the forefoot.

Head of navicular is palpable anterior to the lateral malleolus over the dorsum of foot.

The first metatarsal is more plantarflexed compared to rest of the metatarsals. The heel

may be soft due to total medial displacement and equinus of calcaneus or may be

palpated showing milder form. The tuberosity of navicular may be touching the medial

malleolus according to the severity. There are posterior and medial heel creases, and the

depth of the same depends on the degree of deformity of clubfoot. There is absence of

normal crease over the insertion of tendoachillis. There is lateral convexity of the lateral

border of foot. Ashish , Anand and Debra 3, due to lateral convexity, medial concavity

and relative pronation of forefoot compared to hind foot, has said it as bean shaped.

In neglected and older child who has started walking, may show keratinisation of lateral

border of foot, and these foot are very stiff. The stiffness of the foot increases with age,

and in foots devoid of any manipulation. Wasting of the leg muscles may be present and

it more pronounced along the advancing age. Early infancy doesn’t usually show

wasting. The knee 3 may be flexed but in walking older child it may be in an attitude of

hyperextention. Some other associated conditions and syndromes like Larsen syndrome,

arthrogryposis multiplex congenita, metatarsus adductus and association of anal/

oesophageal atresia should be ruled out to diagnose it as Idiopathic clubfoot.

Antenatal diagnosis of clubfoot can be made at 18-20 weeks of gestation.

Amniocentesis is adviced to ruleout some other condition like Larsen syndrome 3,38. The

32

clubfoot can be associated with some other conditions like, Down’s syndrome,

Arthrogryposis Multiples Congenita, Diastrophic dysplasia, Freemans sheldon

syndrome, Fetal alcohol syndrome.

The pathognomonic sign of clubfoot: In the normal newborn the foot is very pliable and

hypermobile. In passive dorsiflexion the dorsum of foot almost touches the anterior part

of lower leg. In clubfoot , even in more than normal pressure, the foot remains in

equinus. Normal foot has skin creases at the insertion of tendoachillis, but the clubfoot

doesn’t have it and usually the skin is smooth.

CLASSIFICATION AND SEVERITY SCORING:

According to Ponseti, the classification of a clubfoot may change with time depending

on management are as follows 45.

Typical clubfoot:

This is the classic clubfoot and is found in otherwise normal infants. It generally

corrects in five casts, and with Ponseti management the long-term outcome is usually

good or excellent.

Positional clubfoot: Rarely the deformity is very flexible and is thought to be due to

intrauterine crowding. Correction is often achieved with one or two castings.

Delayed treated clubfoot beyond 6 months of age.

Recurrent typical clubfoot may occur whether the original treatment was by Ponseti

management or other methods. Relapse is much less frequent after Ponseti management

and is usually due to a premature discontinuation of bracing. The recurrence is most

often supination and equinus that is first dynamic but may become fixed with time.

33

Alternatively treated typical clubfoot includes feet treated by surgery or non-Ponseti

casting.

Atypical clubfoot:

This category of clubfoot is usually associated with other problems. Start with Ponseti

management. Correction usually is more difficult.

Rigid or resistant atypical clubfoot may be thin or fat. The fat feet are more difficult

to treat. They are stiff, short, chubby, with a deep crease in the sole of the foot and

behind the ankle, and have shortening of the first metatarsal with hyperextension of the

metatarsal phalangeal joint. This deformity occurs in the otherwise normal infant.

Syndromic clubfoot: Other congenital abnormalities are present. The clubfoot is part

of a syndrome. The final outcome may depend more on the underlying condition than

the clubfoot. Is associated with Down’s syndrome ,Larsen’s syndrome, Arthrogyposis

multiplex, Diastrophic dysplasia, Mobius ’or Freeman Sheldon syndrome, Fetal alcohol

syndrome.

Teratologic clubfoot – such as congenital tarsal synchondrosis.

Neurogenic clubfoot – associated with a neurological disorder such as

meningomyelocele.

Acquired clubfoot – Such as in Streeter Dysplasia.

There are classification systems given by Ponseti and Smoley, Harrold and Walker,

Catterall, Diméglio et al., Pirani and International Clubfoot Study Group (ICFSG)

classification system. Three classification systems that are most accepted worldwide are

the Dimeglio et al. classification system, Pirani and International Clubfoot Study Group

(ICFSG) classification system 3,50.

34

Ponseti and Smoley reported the results of treatment of congenital talipes equinovarus

according to their classification system. Their classification system was based on ankle

dorsiflexion, heel varus, forefoot supination and tibial torsion. Feet were classified on

the basis of these measurements as either good, acceptable or poor (Table 1) 50.

Table 1The system of Ponseti and Smoley for the classification of congenital

talipes equinovarus.Ankle dorsiflexion

Heel Varus

Adduction of the fore part of the foot

Tibial torsion

Result

> 10○ 0○ 0○ - 10○ 0○ Good 0○ - 10○ 0○ - 10○ 10○ - 20○ Moderate Acceptable 0○ > 10○ > 20○ Severe Poor

Harrold and Walker considered the ability to correct the deformity. The grade of

deformity was determined by whether the foot could be held at or beyond the neutral

position (grade 1), or whether there was fixed equinus or varus of <20° (grade 2) or

>20° (grade 3) (Table 2) 50.

Table 2Summary of the system of Harrold and Walker for the classification of

congenital talipes equinovarus.Grade Severity Residual deformity with correction1 Mild Neutral or beyond2 Moderate < 20○

3 Severe > 20○

Catterall described four patterns depending on the evolution of the deformity which

was classified as resolving, caused by tendon or joint contracture, or secondary to a

false correction. Several clinical features are used for this classification (Table 3) 50.

The system of Diméglio et al. is derived from a detailed scoring system based on the

measurement of four parameters:

35

1. Equinus in the sagittal plane.

2. Varus deviation in the frontal plane.

3. ‘Derotation’ around the talus of the calcaneoforefoot block, and

4. Adduction of the forefoot on the hindfoot in the horizontal plane.

The above four are shown in diagrams ( Fig 1) .

The scale includes four additional points for the presence of Medial creases, a Posterior

crease, Cavus and poor Calf musculature. From the score, which has a maximum of 20

points, the deformity can be graded as benign, moderate, severe or very severe

(Table 4) 50.

Diméglio et al. also elaborated it to severity score (Table 5, Fig 1 and 2) as points for

difrerent deformities 50,51. The Dimeglio classification consists of 8 items. Scorings for 4

items range from 0–4 (best to worst). Four items only score zero or one. Total score

ranges between 20-0 (very severe: 16–20, severe 11–15, moderate 6–10, and postural

(0–5) 52.

In International Clubfoot Study Group (ICFSG), feet were scored on Morphology

(12 points); Passive joint motion (6 points); Muscle function (16 points); Dynamic

function (11 points); Pain (3 points) and X ray evaluation (12 points) for a total score of

60 points. Results were classified as Excellent (0 – 5 points); Good (6 – 15 points); Fair

(16 – 30 points) or Poor (>30 points). Scoring and assessments given below (Table

6,7,8) 53.

The Pirani clubfoot scoring system is commonly used and it documents the severity of

the deformity and also sequential scores which are an excellent way to monitor

progress. Pirani Clubfoot Score uses six clinical signs to quantify severity of each

component of the deformity. Each component is scored as shown 54 in Table 9,10 Fig 3.

Table 3

36

Catterall’s system for the classification of congenital talipes

equinovarusFoot Resolving

pattern

Tendon

contracture

Joint

contracture

False

correctionHindfoot Lateral

malleolus

Mobile Posterior Posterior Posterior

Equinus No Yes Yes Yes Creases medial No No Yes No Creases

posterior

No Yes Yes Yes

Crease anterior Yes No No Yes Forefoot Lateral border Straight Straight Curved StraightMobile Yes Yes No Yes Cavus ± ± ± No Supination No No Yes No

Table 4The system of Diméglio et al. for the classification of congenital talipes

equinovarusClassificationgrade

Type Score Reducibility

I Benign < 5 > 90% soft-soft, resolvingII Moderate 5 to < 10 > 50% soft-stiff, reducible, partly

resistantIII Severe 10 to < 15 < 50% stiff-soft, resistant, partly

reducibleIV Very severe 15 to < 20 < 10% stiff-stiff, resistant

Table 5Dimeglio classification scoring system

Rating 4 3 2 1 01.Equinus 45°–90°pltf 20°–45°pltf 20°pltf – 0° 0°–20°dorsx >+20°dorsx2.Varus 45°–90°var 20°–45°var 20°var-0° 0°–20°vlg >20°vlg3.Supination 45°–90°sup 20°–45°sup 20°sup-0° 0°–20°pron >20°pron4.Adductus 45°–90°add 20°–45°add 20°add – 0° 0°-<20○ abd >20°abd

37

5.Posteriorcrease

Yes No

6.Medialcrease

Yes No

7.Cavus Yes No 8.Deviantmusclefunction

Yes No

pltf = plantarflexion, dorsx = dorsalflexion, var = varus, vlg = valgus, sup = supination,pron = pronation, add = adduction, abd = abduction.

38

Table 6Morphology scores according to the ICFSG scoring system

Range Score Hindfoot Varus ≤ 10° 1

Equinus > 10° 2Midfoot Supination/ pronation ≤ 10° 1

> 10° 2Adduction/ abduction ≤ 10° 1

> 10° 2Global alignment Rotation ≤ 10° 1

> 10° 2Pes cavus or flat foot ≤ 10° 1

> 10° 2

Table 7Functional evaluation scores according to the ICFSG scoring system

A. Passive motion Scores 0 1 2Ankle dorsiflexion Normal 10° NegativeAnkle plantarflexion Normal 10° 0° or Negative

Subtalar varus-valgus Flexible Stiff

39

Midtarsal pro/supination Flexible Stiff B. Muscle function Jones classification score 5,4 3 2,1,0

Triceps surae Normal Modera

te

Severe

Toe flexors Normal Modera

te

Severe

Extensors Normal Modera

te

Severe

Anterior tibial tendon Normal Modera

te

Severe

Extensor hallucis longus Normal Modera

te

Severe

Posterior tibial tendon Normal Modera

te

Severe

Peroneal tendon Normal Modera

te

Severe

Flexor hallucis longus Normal Modera

te

Severe

C. Dynamic function Score 0 1 2Intoeing None 10° > 10°Calcaneus None 10° > 10°Equinus None 10° > 10°Dynamic supination None 10° > 10°Limping None PositiveAbility to run None PositiveAbility to jump None PositiveShoe wear Normal Abnormal

Heel or toe walking Yes NoD. Pain Level 0 1 2 3

No pain Pain with activity Pain with sports constant

Table 8Radiological parameter scores according to the ICFSG scoring system

Standing AP views ScoreTalocalcaneal angle 0 1Cuboid-calcaneo alignment Normal AbnormalCubo-M5 axis Normal AbnormalTalo-M1 angle Normal AbnormalTalo-navicular Position Normal Abnormal

Standing lateral viewsTalo-calcaneal angle Normal Abnormal

40

Tibio-calcaneal angle Normal AbnormalTalo-navicular position Normal AbnormalTalo-M1 axis Normal AbnormalCalcaneo-M5 axis Normal AbnormalFlat top talus Normal Abnormal

Ankle AP standingMalleoli alignment Normal Abnormal

Each foot can receive a hindfoot score between 0 and 3, a midfoot score between 0 and

3 and a total score between 0 and 6. When assessed for inter-observer reliability, the

kappa score showed this to be almost perfect and much better than any of previous

scoring system. It is simple and reliable. A foot can be assessed in less than a minute

and no technical equipment is required 55. The score also helps in deciding when to

perform a heel-cord lengthening 56.

Pirani scoring signs is detailed below 57:-

Posterior Crease of the ankle (PC): It is the measure of the posterior contracture.

Score 0: When multiple fine creases are visible, that do not change the contour of the

heel. These creases allow the skin to adjust and stretch as the ankle dorsiflexes.

Score 0.5: When one or two deep creases are visible, that do not appreciably change the

contour of the heel.

Score 1: When one or two deep creases are visible that appreciably change the contour

of the heel.

Empty Heel (EH): It is the measure of the posterior contracture.

Score 0: The Calcaneus is immediately palpable (comparable with the feeling of gentle

pressure on the temple).

Score 0.5: The heel pad feels soft, but the Calcaneus is palpable deep within the heel

pad (comparable with the feeling of gentle pressure on the tip of the nose).

41

Score 1: The heel pad feels empty. No bony prominences can be felt (comparable with

the feeling of gentle pressure on the ball of thumb).

Rigid Equinus (RE): It is a measure of the posterior contracture. View the leg and foot

from the lateral side and measure the movement from the neutral position (0°- line).

Score 0: Clear Dorsiflexion - more than about 5° Dorsiflexion.

Score 0.5: Around neutral position can be achieved. Range: about 5° Plantar flexion to

5° Dorsiflexion.

Score 1: Clearly no neutral position can be achieved - more than about 5° Plantar

flexion.

Medial Crease of the sole of the foot (MC): It is a measure of the medial contracture.

Score 0: Multiple fine creases are seen which do not change the contour of the arch.

Score 0.5: One or two deep creases are seen which don't appreciably change the contour

of the arch.

Score 1: One or two deep creases are seen which appreciably change the contour of the

arch.

Lateral part of the Head of the Talus (LHT): The LHT is a measurement of how far

the Navicular reduces onto the head of the Talus.

Score 0: Loss of the ability to palpate the lateral edge of the head of the Talus (because

of the complete reduction of the Navicular onto the head of the Talus).

Score 0.5: Reduction of the ability to palpate the lateral edge of the head of the Talus

(because of partial reduction of the Navicular onto the head of the Talus).

Score 1: Still easily palpable head of the Talus even with the forefoot in as much

correction as is allowed by the deformity (because of fixed medial subluxation of the

Navicular).

42

Curvature of the Lateral Border of the foot (CLB): It is a measure of the medial

contracture.

Score 0: The lateral border of the foot is straight from the heel to head of the 5th

Metatarsal.

Score 0.5: The lateral border of the foot is mildly curved. The curvature appears to be in

the distal part of the foot in the area of the Metatarsals.

Score 1: A pronounced curvature of the lateral border of the foot is seen. The curvature

appears to be at the level of the Calcaneo-cuboid joint.

Table 9Pirani severity scores

Score Severity0 Normal

0.5 Mildly abnormal1 Severely abnormal

Table 10Pirani’s hindfoot and forefoot scores according to severity

Forefoot Scores 0 0.5 1Curved

lateral

border

Straight Mildly curved

distal part,area

of the

Metatarsals

Pronounced

curvature, appears

at the Calcaneo-

cuboid jointMedial

crease

Multiple fine

creases

One or two

deep creases

One or two deep

creases, change

the contour of the

arch.Lateral part

of the Head

of the Talus

Unability to palpate Reduction of

the ability to

palpate

Unability to

palpate even after

reductionHindfoot Scores 0 0.5 1

Posterior Multiple fine One or two One or two deep

43

crease of

ankle

creases deep creases creases. Change

the contour of the

heel.Rigid

equinus

> 5° Dorsiflexion Range:5°

Plantar flexion

to 5°

Dorsiflexion

> 5° Plantar

flexion

Empty heel Calcaneus is

immediately

palpable

Calcaneus is

palpable deep

within the heel

pad

Heel pad feels

empty.

44

RADIOGRAPH

45

Harwell first proposed the radiography as a technique to assist in evaluation and

treatment of clubfeet.

X-rays are not routinely ordered at birth as few bones in the foot are ossified. The two

views utilized are Anteroposterior and Lateral in stress dorsiflexion. The angles that are

measured on the Anteroposterior and on lateral view are Talocalcaneal angle, Talo-first

metatarsal angle, Talocalcaneal angle and Tibiocalcaneal angle. In the clubfoot, all of

these angles are decreased 3.

The measurement of angles are 27,36,58-60 :

Ap view:

Talocalcaneal (Kite's) angle: 20-40° is normal; <20° is clubfoot. Lines drawn throught

the long axis of the talus and os calcis.

Talus-1st metatarsal angle: 0°-20° is normal, <0° is clubfoot. Lines drawn through the

long axis of the talus and the 1st metatarsal.

Lateral view:

Talocalcaneal angle: Normal <25°. Lines drawn through the long axis of the talus and

inferior margin of the calcaneous.

Dorsiflexion lateral (Turco's) view: measure the talocalcaneal angle >35° is normal.

<35° with flat talar head is clubfoot.

TREATMENT

The spectrum of treatment options for clubfoot is large .It ranges from non-operative

methods including manipulation, strapping, repeated stretching and POP casting on one

side to operative methods like soft tissue surgery and bony procedure.

Repeated gentle manual correction:

46

The concept of serial repeated manipulation is from the time of Hippocrates.

Hippocretes did gentle manipulation and immobilization with strong bandages. The

serial gentle manipulation is done by others too e.g. Cheselden 61. He used strehching

tape for manipulation and to hold. Sofield used elastic traction for repeated streching 62.

Mechanical device for gradual correction :

In 1646, Fabricius treated clubfoot by a apparatus, boot fitted with a plate on the lateral

side hinged at the ankle connected with a turn-buckle for gradual correction. Ambrose

Pare also suggested similar metal splint in 1665. He used shoe like apparatus. Scarpa in

1803 used the method of gentle correction by stretching the contractures with the help

of his specially made shoe with springs 63.

Splint and wrench for forcible correction :

Bruckner (1796) was among first to use mechanical devices to produce forcible

correction. Hugh Owen Thomas Thomas (1886) initially used splint, but he rejected it

because the deformity was corrected by prolonged pressure on the soft parts of the foot.

He then deviced wrench for forcible correction by holding the correction with a

splint 63. Gibney and Ridlon from New York also used similar wrench for forcible

correction of clubfoot 64.

Use of Denis Browne splint after forcible correction :

Denis Browne disfavoured the use of Thomas wrench. He introduced his metal splint

in 1934 used with adhesive strapping for the maintenance of correction achieved

through forcible manipulation. The splint held the deformed forefoot in an over

corrected position of abduction and eversion with plantigrade position at the ankle. In

unilateral affection, the normal foot was also fastened with the splint by strapping. Both

the feet with the splints were connected with an aluminium bar 63.

Application of adhesive strapping and repeated manipulation :

47

In 1896 Whitman first opined the use of adhesive strapping for the correction of

clubfoot. Jones and Lovett in 1929 and Brockman in 1930 used strapping and repeated

manipulation for clubfoot treatment 63.

Manipulation and use of plaster of Paris cast for immobilisation:

Guerin was the first to use plaster of Paris cast for maintaining correction of clubfoot

after manipulation in 1838 10. Whitman in 1910 and Elmslie in 1920 emphasized the

use of plaster of Paris cast for the correction of clubfoot. Kite in 1930 treated clubfoot

by wedge plastering. Later on he changed to repeated manipulation and plastering 41,63.

Forefoot abduction device, devices used with plaster cast , osteotomies and external

fixators are other modalities of treatment adopted.

Mainly three conservative method for treatment of clubfoot became most accepted,

Kite’s method French functional method, and Ponseti method.

KITE’S METHOD:

He devised his method of treatment of clubfoot in 1930’s. In this method serial

manipulations are done and immobilised by cast. He did stepwise correction of

deformity. Initially he used to make wedge in cast for next corrections, but later he used

to change the cast repeatedly 22,59.

In this method gradual correction of abduction, heel varus and and equinus is done. It

can be explained by three point pressure concept. The calcaneocuboid joint acts as

fulcrum. Holding forefoot it distracted while the other hand holds the heel. The

manipulation, for correction of abduction, by counterpressure over calcaneocuboid

junction itself blocked the lateralisation of calcaneum. It is called as “ Kite’s error” by

Ponseti. After every 7-10 days, cast was changed. As the adduction is corrected, hee is

everted. Afterwards heel is given dorsiflexion after correction of adductus and varus.

The average number of cast applied was 20.4. After series of correction, the foot is put

into Denis Browne Bar. When patient starts walking, the splints were used at night only.

48

By day, shoes with an open toe box, straight medial border, lateral flaring of the sole,

and reverse Thomas heels were used until the age of 4 to 5 years 3,41,65.

FRENCH FUNCTIONAL METHOD:

The functional method was developed and implemented during the early 1970s. also

known as “French functional method” or “Bensahel’s functional method” 66.

In this method, consists of daily gentle manipulations for 30 minutes, of newborn’s

clubfoot, streching of the contracted tissue, stimulation and strengthning of the muscles

acting on the foot. The muscle stimulated mainly was peroneals. Reduction achieved by

manipulation is mantained by temporary immobilization of the foot with nonelastic

adhesive strappings and splinting. These done by trained physical therapist. The daily

treatments was continued for approximately two months and then reduced to three

sessions per week for an additional six months. Taping was continued until the patient

was ambulatory. After ambulation was achieved, a nighttime splint was introduced and

used for an additional two to three years. The surgery that was required was only a

posterior release 3,9,67.

PONSETI TECHNIQUE:

Ponseti first published his studies in 1963. It was not very popular at that time. His

technique become popular after 30 year follow up study of treatment of clubfoot in

1995 mentioning good to excellent results by Cooper DM and Deitz FR. by Ponseti

method of treatment 27,45.

His treatment is based on repeated manipulation to correct the deformity to an extent

and if needed to perform a percutaneous tenotomy. After tenotomy, a cast is applied for

three weeks in abduction and dorsiflexion. Removal of cast is followed by use of foot

abduction brace which is initially applied 24 hours a day and later just 3 to 4 hours a day

till the age of 3 to 4 years.

It is the most effective and least expensive treatment of club foot. It can be started

within 7 to 10 days after birth. The deformities are corrected in 6 weeks after 6 to 7

49

casts change. It can be started at the late childhood 45,68. There are studies supporting

Ponseti method of treatment effective till the age of 9 years and the results are

satisfactory 69. If started in time the success rate is more than 95% 45.

Setup:

Before casting we should make the environment comfortable to the child. The child

should be allowed to bottle fed or breast fed and keeping close to mother.

Manipulation and casting:

It can be started at the age of 7 to 10 days. Counseling of parents should be done and

the baby should be allowed to feed and the manipulation should be started.

Localisation of head of talus:

First palpate the lateral malleolus with thumb. The first bony prominence anterior to the

lateral malleolus is head of talus. It is covered with skin. Our fulcrum is lateral aspect of

head of talus, to abduct the adducted navicular bone, and fore foot. While thumb presses

over the head of talus, index and middle finger of same hand, at the same time holds

medial malleolus to stabilise the ankle mortise.

Anterior part of calcaneus is felt below the talar head. While abducting the supinated

fore foot, navicular moves laterally and the calcaneum moves laterally below talus.

Supination to reduce cavus:

Cavus is high medial plantar arch and it is due to the contracture of medio-plantar soft

tissue. Cavus is due to the relative pronation of forefoot relative to supinated hind foot.

It is corrected by elevation of first ray of foot and is always done before abduction. The

first ray is not elevated too much or too less. It is observational correction that it should

be like longitudinal medial arch. The cavus is corrected by two methods:

One hand method: Index finger is kept over the head of talus and thumb of same hand

is kept below the head of first metatarsal and is lifted.

50

Two hand method: Thumb of one hand kept over the head of talus and head of first

metatarsal is lifted by holding it with thumb (dorsally) and index finger (ventrally).

Correction of adduction and varus:

It is done by abducting the forefoot by using the talus as fulcrum, holding the forefoot

with index finger and thumb of other hand. Abduction should be gentle, not to put the

child in discomfort. Abduction is done, with forefoot supinated to 60○ to 70○ gradually.

All the deformities are corrected simultaneously and gradually except for the equinus.

Steps in cast application:

Ponseti recommends plaster material for casting because it is cheap and more moldable

than fibre glass. Before each casting foot is manipulated for 1 to 2 minute.

Applying the padding:

Cotton soft rolls 2 to 4 inches in width are applied, supporting the foot in head of first

metatarsal and talus. The cotton roll is applied snugly over foot and ankle and loosely

over cast and thigh. Half of the width of cotton is overlapped every time while wrapping

the limb. It is applied from toe towards thigh.

Applying cast:

2 to 4 inch wide plaster bandage is taken and is first applied below knee. It is done with

the help of an assistant holding the toe. The cast is rolled 3 to 4 times initially over the

toe of child covering the finger of assistant and then proximated towards the thigh.

While molding, the finger of assistant is taken out making space for the toes of baby,

preventing overcrowding.

Molding:

Now the cast is molded according to the manipulation and anatomic precision. It is

molded gently putting pressure over lateral aspect of head of talus lifting and abducting

the forefoot in supination. Molding is done mainly for medial arch, malleoli, heel and

head of talus, holding the foot in corrected position, the heel should never rest on the

51

hand of surgeon and the molding fingers of surgeons should be moving and should not

be static at one site to avoid pressure sore. Molding is done till plaster sets.

Extending cast to thigh:

Now holding the knee in 90○, the cast is applied upto thigh. Good padding is used over

thigh to avoid skin irritation. Plaster is applied back and forth over the anterior aspect of

knee to avoid more plaster in popliteal region, making cast removal easier.

Trim the cast:

Cast should be trimmed to free the distal aspect of foot, the metatarso-phalangeal joint,

leaving the cast in plantar aspect. It allows extension at metatarso-phalangeal joint.

First cast:

First cast is applied to correct the cavus deformity. Cast is applied by putting the

forefoot in supination by putting pressure over the plantar aspect of head of first

metatarsal and counter pressure over head of talus.

Second to fifth cast:

In these cast gradual correction of adductus and varus is done. Heel or calcaneum is

never tried for vulgus. Holding over the lateral and plantar aspect of first metatarsal

abduction is done in supinated position making lateral aspect of head of talus as the

fulcrum, supported by the thumb of other hand. Casts are applied at 5 to 7 days interval

till 60○ to 70○ of abduction is achieved. The varus deformity is gradually corrected as

calcaneus moves laterally and its anterior part comes out of talus.

Characteristics of adequate abduction:

Foot should be abducted to 60○ to 70○ in relation to frontal plane of tibia. The possible

dorsiflexion at this stage should be 0○ to 5○. The best sign of significant abduction is to

be able to palpate the anterior process of calcaneus as it abducts out of talus. The

oscalcis should be in neutral or right vulgus position.

52

Correction of equinus:

It is done after 60○ to 70○ of abduction, and correction of varus. If after 5 to 6 casts,

there is dorsiflexion of about 0○ to 5○, more 2 to 3 casts are applied to achieve 15○ to 20○

of dorsiflexion. The cast is applied by holding over the insertion of tendo achillis,

pulling it down and dorsiflexing the foot simultaneously by putting pressure over whole

sole with palm of the head of the surgeon’s hand. Whole of the sole should be lifted to

avoid rocker’s bottom foot.

If 15○ to 20○ of dorsiflexion is not achieved by cast application, then tendo achillis

tenotomy is indicated.

Cast removal:

Each cast is removed just before the new cast is applied. It is not removed day before or

hours before the clinical visit. The removal of cast is done by:-

Cast knife - cast is soaked in water for 20 minutes and then removed with knife.

Soaking and unwrapping - soaking is done for more time and then unwrapped by

holding the end of plaster bandage, which is left while putting the cast.

Tenotomy:

It is an outdoor procedure.

Indication–

If dorsiflexion is not beyond 10○ of dorsiflexion, tenotomy is indicated, provided that

the adductus and varus are fully corrected.

Preparation-

Prepare the family by explaining that it is an minor procedure and will be done under

local anaesthesia.

Eqipment-

Tenotomy blade should be #11 or #15 or opthalmic knife. Xylocaine 2% etc.

53

Skin preparation-

Skin preparation should be done with an antiseptic solution from mid calf to mid foot.

Anaesthesia-

Xylocaine 2% is infiltrated in the region of tenotomy. The quantity should not be too

much to hinder with proper palpation of tendon which looks bluish.

Setup for tenotomy-

Under all aseptic precautions, an assistant holds the foot in maximum possible

dorsiflexion, to make the tendoachillis taught. Local anaesthetic is infiltrated. Scalpel

blade is introduced 1.5 cm proximal to the insertion of tendo achillis, anterior and

parallel to the tendon, as close as possible to it , taking care of the medial neurovascular

structures passing. Now the blade is rotated to make the sharp border posterior, and the

tendon is cut. Succesful tenotomy is comfirmed by the “pop or snap” appriciation while

cutting. More 15○-20○ of dorsiflexion is acieved after successful tenotomy.

Post tenotomy cast:

This is the last cast applied immediately after tenotomy. The cast is applied in 60○-70○of

abduction and a 15○-20○ of dorsiflexion. This is kept for 3 weeks. Patient is sent home

same day after application of the cast.

Cast is removed after 3 weeks and the foot is ready for Bracing.

Bracing:

After the removal of final cast which was applied for 3 weeks a brace is applied to

maintain the foot in abduction and dorsiflexion. The bar attached to straight-last open-

toe shoes. The length of the bar should be of such length, so that the heels of the shoes

are at shoulder width. In unilateral cases, the brace is kept at 60○ to 70○ of external

rotation on the clubfoot side and 30○ to 40○ of external rotation on the normal side. In

bilateral cases, it is set at 70○ of external rotation on each side. This abduction is kept to

maintain the abduction of the calcaneus and forefoot and to prevent relapse. The medial

soft tissues remain stretched out only if the brace is used after the casting. The knees are

54

free in the brace, so that the child can kick them “straight” to stretch the gastrosoleus

tendon. The bar is bent 5○ to 10○ with the convexity away from the child. It holds the

feet in dorsiflexion. This helps to maintain the stretch on the gastrocnemius muscle and

heel-cord tendon.

Bracing protocol:

The brace should be worn 24 hours a day for the first 3 months after the removal of the

last cast. After that the brace should be worn 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. This 14

to 16 hours protocol continues until the child is 3 to 4 years of age.

The child is regularly followed for any evidence of relapse, and it should be treated

promptly.

Types of braces:

H.M. Steenbeek Brace- It is a brace that can be made from simple, easily available

materials. It is effective in maintaining correction, easy to use, fabricate and

inexpensive.

John Mitchell Brace- These shoes are made of a very soft leather and a plastic sole that

is molded to the shape of the child’s foot.

Dr. Matthew Dobbs Brace – This is a 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.

M.J. Markel Brace – In this we first place the shoes on the infant and then “click” each

shoe onto the bar.

Dr. Jeffrey Kessler Brace – It is a brace that is flexible and inexpensive. The bar is made

of thin polypropylene.

55

Dr. Romanus Brace – It is made of malleable plastic that is molded to the shape of the

child’s foot. Inside it is covered by smooth leather.

Relapse:

Regular follow up is done to find out the relapse in early stage. It should be done as:-

At 2 weeks- To check for compliance of full-time bracing.

At 3 months- To graduate to the nights-and-naps schedule.

After 3 month to 3 yaers- Every 4 months to monitor compliance and for relapses.

At age of 3 to 4 years- Every 6 months.

4 years till maturity- Every 1 to 2 years.

The relapses are treated by cast or braces. Equinus is corrected by casting and tenotomy

followed by bracing. Varus is treated by recasting and bracing. Dynamic supination is

corrected by tibialis anterior tendon transfer after age of 2.5 years.

56

Methodology

57

METHODOLOGY

SOURCE OF DATA:

This study was conducted in Al Ameen Medical College in Bijapur Karnataka. The

source of data is all confirmed cases of clubfoot in Al Amen Medical College. The

study was done from September 2010 to September 2012, and cases were selected on

OPD basis. The cases were confirmed to be idiopathic clubfoot, by ruling out any other

congenital anomalies example spinal abnormalities, Arthrogryposis multiplex congenita

or history of exposure to radiation or any teratogenic drug intake during pregnency.

INCLUSION CRITERIA:

All cases are selected on the basis of

1. Adduction, Supination, equinus and varus deformity of the foot with or without

wasting of calf muscles.

2. Age less than 2 years.

3. Virgin clubfoot.

EXCLUSION CRITERIA:

1. Postural, Syndromic, Neglected, Relapsed, club foot.

2. Patients above the age of 2 years.

3. Patients who are unfit and noncompliant to the described technique.

29 patients entered in the study with 38 idiopathic clubfoot, after explaining the

treatment. Patient were explained for about 6 to 10 casts at weekly interval, tenotomy

and wearing of foot abduction brace till 3 to 4 years of age, and then regular follow up

till maturity. Patients were also explained about other methods of treatment.

Radiographs were not taken except for few initial patients. The reason for not taking

radiograph was, that every time the foot cannot be put in the same position, bones are

not well ossified and Pirani scoring system, which is followed here, doesn’t need

radiographic evaluation.

58

Routine Blood investigations were done before tenotomy.

Scoring of the foot was done before first casting and then on every visit before applying

cast, and changes were scrutinised.

MANIPULATION AND APPLICATION OF CAST:

FIRST CAST:

Correction Of Cavus:

Baby was allowed to sleep or bottle fed or breast fed on the mother’s lap. Head of the

talus palpated in front of the lateral malleolus, lifting the head of first metatarsal by

holding it with thumb and index finger of one hand and pressing gently over the head of

talus (as fulcrum) with thumb of other hand, cavus was corrected. This corrects the

pronated forefoot, aligning it with already supinated hind foot (fig 4).

Cast Application:

After 1 to 2 minutes of gentle manipulation, cotton soft rolls of 3 inch width was

wrapped from toe towards the thigh, while assistant holds the head of first metatarsal

gently. Cotton soft rolls were applied covering half of its width in every rotation. It was

applied snugly over the foot and the ankle, and loosely over the calf and thigh. Thigh

was covered with extra cotton. Plaster bandage (3 inch width) applied from toe, while

assistant holding the toe, towards knee. Initially 3 to 4 rotations given over the toe

covering the assistant’s finger then gradually proximated towards knee. Plaster was

applied snugly over the foot and ankle and loosely over calf (Fig 5,6).

Molding of casts:

It was done according to the manipulation. Assistant leaves the foot and surgeon starts

molding by lifting head of first metatarsal using head of the talus as fulcrum, making

medial longitudinal arch normal. Molding was done over malleoli, talar head, medial

arch and heel.

59

Extending The Cast:

Cast was extended upto thigh keeping knee at 90○ of flexion, with more plaster over

anterior aspect of knee and less over popliteal fossa. First cast correcting the cavus and

forefoot pronation is shown in Fig 7.

After applying cast, toes were checked for capillary filling and overcrowding or any

excessive cry or leg banging of baby to rule out any abnormal pressure due to cast

application. Patients were asked to revisit after 7 days.

Cast Removal:

First cast and all the cast were removed by soaking the whole cast with water and

unrolling the so formed soft plaster bandage, by holding end of the plaster bandage

which was left for identification.

SECOND TO LAST CAST TO CORRECT ADDUCTION AND VARUS:

After all the preliminary requirement for baby’s comfort, manipulation was started

within hour of previous cast removal. The casting protocol is same.

Manipulation For Correction Of Adductus:

1 to 2 minutes of manipulation is done before cast application. It is done by holding the

head of first metatarsal by index finger on the plantar aspect and the thumb on the

medial aspect of one hand, and thumb of other hand over the lateral aspect of head of

talus. Making talus as fulcrum foot was abducted by the hand which is holding

metatarsal head. Lifting of metatarsal head is done at the same time to keep the caves

corrected and keeping foot in supination. Eversion of heel was never tried as it comes

gradually along with the correction of adduction (Fig 8,9,10).

Cast Application:

Cast applied (Fig 11,12,13,14) same way from toe to knee and then extended to the

thigh. Cast was molded in the same way as manipulation done, with same pressure

points with fingers continuously moving to avoid pressure sores.

60

61

62

CORRECTION OF EQUINUS:

After an average of 6.41 cast application, sufficient abduction of 40○-50○ was achieved.

If 0○ - 5○ degrees of dorsiflexion was possible and tendo achillis was strechable, then 2

to 3 more casts were applied to achieve a final dorsiflexion of 15○ to 20○ (Fig 15,16).

Cast application for equinus correction is done by holding posterior aspect of heel just

above the insertion of tendo achillis, pulling it down, and pushing the whole of the sole

dorsally at the same time with whole of the palm of another hand (Fig 17).

Tenotomy was done if, tendoachillis was not strechable, after about 5-9 cast, provided,

0○ to 5○ of dorsiflexion was achieved with an abduction of 40○-50○.

PERCUTANEOUS TENOTOMY:

Ponseti recommends it under local anaesthesia but it was not possible in our setup due

to non compliance of baby. So we use short acting general anaesthesia for tenotomy.

Parents were explained about the procedure, being a minor one, and basic investigations

were done. Limb of the patient is prepared by scrubbing with antiseptic solution in

operation theatre. Short acting general anaesthesia was given by anaesthetist.

Steps For percutaneous Tenotomy (Fig 18):

- Painting was done from mid of leg to mid foot.

- Draping was done keeping the ankle exposed.

- Assistant holds the foot in maximum dorsiflexion while the patient is in supine

position, foot rotated externally with knee flexed and thigh externally rotated.

- Tendoachillis was palpated and identified ( bluish in light skin ).

- Scalpel blade #11 or #15 was put from medial side of tendon. The point of

insertion of blade is 1.5 cm proximal to the attachment of tendo achillis on

calcaneum.

63

- Blade is kept parallel to the tendon. It is inserted just anterior and touching to the

tendon, to avoid the injury to the neurovascular bundle which is present antero

medial to it.

- Now the sharp edge of blade is rotated posteriorly to cut the tendon using its tip.

- A “POP or SNAP” is felt after successful tenotomy, which gives an additional

15○ to 20○ of dorsiflexion.

- Wound is dressed. No need of putting stiches most of the time.

- Single dose of injectable antibiotic given before procedure and started with oral

NSAID and antibiotic for 3 days.

LAST CAST APPLICATION:

It was applied after gaining 15○ to 20○ of dorsiflexion and 40○-50○ of abduction and

satisfactory varus correction. This cast was applied keeping the foot in 40○-50○ of

abduction and 15○ to 20○ of dorsiflexion for 3 weeks (Fig 19). After removal of cast, the

outcome is, a painless, plantigrade with good mobility and cosmetically acceptable foot

(Fig 20).

BRACING:

After the removal of last cast, the brace was applied. Here we used Denis Browne splint

keeping the heel at shoulder width apart with foot in abduction of 40○-50○ and

dorsiflexion of 15○-20○. Knees are kept free (Fig 21).

Brace was adviced to apply whole day and night for next 3 months. Then brace is

applied whole night and 2 to 4 hours in the midday till the age of 4 years. Regular

follow up were done after after application of Denis Browne splint at 14 th day, after 3

month and after every 4 month till the age of 4 years, to look for relapse and wear and

tear of splint. At the age of 4 years splint should be removed. Patients are counselled to

come every 6 month after the age of 4 years till maturity.

64

65

66

Results

67

RESULTS

Total 29 patients entered in our study group. 2 patients discontinued the treatment. 1

patient was referred for posteromedial soft tissue release, and is taken as failure. So the

management with Ponseti technique was completed with 26 patient with 34 affected

foot.

The mean age at presentation of all the patients were 5.1 month (153 days), with range

of 0.33-18 months (10-540 days) (table 11). Most frequent age at presentation was 3.0

months.

Table 11Details of age of patients in months

Total 29 PatientsRange 0.33-18Mean 5.0631Median 3.5Mod 3.0Standard Deviation 4.15307Minimum 0.33Maximum 18

The minimum age at presentation for starting treatment was 10 days. The most

common age at presentation was between 0-6 months, and the least common was

between age >18-24 months with no patient in our study (table 12).

Table 12Frequency of distribution of age of patient at presentation

Range (month) Frequency Percent0-6 18 62.07%

>6-12 9 31.03%>12-18 2 06.90%>18-24 0 00.00%Total 29 100.00%

68

There were total 19 male and 10 female patients, who entered in study and constituted

65.52% and 34.48% respectively (table 13, chart 1).

Table 13Distribution of sex of patient

Number Percentage Male 19 65.52%

Female 10 34.48%Total 29 100%

Presentation for both sexes individually is also maximum between 0-6 months (table 14,

chart 2). The male to female ratio is 1.9:1.0 (19/10).

Table 14Correlation between age of presentation and sex

Range

(month)

0-6 >6-12 >12-18 >18-24 Total

Male 11 7 1 0 19Percentage 37.93% 24.14% 3.45% 0 65.52%

Female 7 2 1 0 10Percentage 24.14% 6.89% 3.45% 0 34.48%

69

70

Side of involvement: There were 9 (31.03%) of bilateral and 20 (68.97%) unilateral

cases. Among the unilateral cases there were 12 (41.38%) right and 8 (27.59%) left

cases (table 15, chart 3,4).

Table 15Side (Laterality) of involvement of patients

Laterality Unilateral Bilateral TotalFrequency 20 9 29

R L12 8

Percentage 41.38% 27.59%68.97% 31.03% 100%

Laterality and sex: Among male, unilateral patient are 12 (63.16%) and bilateral are 7

(36.84%), the same among females are 8 (80%) and 2 (20%) respectively (table 16,

chart 5,6,7).

Table 16Corelation between laterality and sex for patients

Male Percentage among

male

Female Percentage among

femaleBilateral 7 36.84% 2 20.00%Unilatera

l

Right 8 42.11% 5 50.00%Left 4 21.05% 3 30.00%

Total 19 100.00% 10 100.00%

71

72

73

BILATERAL, 36.84%

RIGHT, 42.11%

LEFT, 21.05%

Chart 5 -Male (No. of patients)

BILATERAL

RIGHT

LEFT

Total number of cast: Mean of total number of cast applied for 34 foot to completing

the study was 7.97. The average number of total cast requirement increased according

to age and Pirani severity scores (table 17,18).

Table 17Number of total cast in tenotomised footAge Average cast

>0-6 months 7.35>6-12 months 8.15>12-18 months 10>18-24 months ---

Table 18Number of total cast in non tenotomised foot

Pirani severity score Average cast≤1.5 7.35

2.0-3.0 8.153.5- 4.5 105.0- 6.0 ---

Cast and Pirani severity score: Total 35 foot were treated by Ponseti technique. But 1

foot was a failure case and reffered for posteromedial soft tissue release, and rest of the

34 foot were continued with Ponseti technique. Average number of casts applied before

equinus correction was 6.41 for the 34 foot. The average number of cast required in

different Pirani scoring group is shown below (table 19, chart 8 ). Number of

application of cast is more for greater scores. Then according to flexibility of tendo

achillis, equinus was corrected by application of cast or by tenotomy.

Table 19Correlation b/w no. of casts and PSS before eq. Correction

PSS Average no. Of cast≤1.5 ---

2.0-3.0 5.253.5- 4.5 6.305.0- 6.0 7.43

74

Age and number of cast: The mean age at presentation of patient was 5 month (or 150

days) and the average number of cast was 6.41. The average number of cast applied to

the age group ≤3 month was 5.69 and the same for >12 to 15 month group was

increased to 9 (table 20, chart 9).

Table 20Correlation between age and no. of cast before eq. correction

Age in month Average no. Of cast≤3 5.69

>3-6 6.5>6-9 7>9-12 8>12-15 9

75

76

Method of Equinus corredtion: Equinus was corrected by cast or tendo achillis

tenotomy. Out of 34 foot, tenotomy was done to 76.47% (26) foot, and cast correction

was done for 23.53% (8) foot (table 21, chart 10).

Table 21Method of equinus correction in foot

Frequency PercentTenotomy 26 76.47%

Cast 8 23.53%Total foot 34 100%

Sex and equinus correction: Among the tenotomised foot, 73.08% of foot were of

male and rest 26.92% were of female. Among cast applied foot the male constituded

75% and female 25% (table 22, chart 11).

Table 22Distribution of sex among cast applied and tenotomised foot, for Eq. corr.

Tenotomy CastFrequency Percent Frequency Percent

Male 19 73.08% 6 75%Female 7 26.92% 2 25%Total 26 100% 8 100%

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78

Correction of equinus in the same age group: The equinus of 0-6 month age group

was only corrected by both tenotomy and casting, and not in the higher age group (table

23, chart 12).

Table 23Comparison of correction of equinus in the same age group

By tenotomy By cast>0-6 months 14 8>6-12 months 11 0>12-18 months 1 0>18-24 months 0 0

Pirani severity score: Pirani severity score ranging 3.5-4.5 was the most common score

among foot counting 23 (table 24, chart 13).

Table 24Pirani severity score distribution

PSS No. of foot≤1.5 0

2.0-3.0 43.5- 4.5 235.0- 6.0 7

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80

Pirani severity score and method of Equinus correction: Both the methods of

equinus correction is equal in low scores but correction by cast decrease as score

increases (table 25, chart 14).

Table 25Correlation between Pirani severity score and method equinus

correctionPSS Eq. Correction method

Tenotomy Cast≤1.5 Frequency 0 0

Percent 0% 0%2.0-3.0 Frequency 2 2

Percent 50% 50%3.5- 4.5 Frequency 17 6

Percent 73.91% 26.09%5.0- 6.0 Frequency 7 0

Percent 100% 0

Posteromedial soft tissue release: One foot was a failure to Ponseti treatment, as it

needed posteromedial soft tissue release (table 26, chart15).

Table 26Percent of Posteromedial soft tissue release

PMR Frequency PercentNot done 34 97.14%

Done 1 2.86%

81

82

Significance of treatment: The mean initial Pirani score of the patients with 34 foot

before starting treatment was 4.147. The mean Pirani score after full correction, that is

after last cast is 0.147 and at the time of follow up at 6 month was 0.088. Three pairs

made, for paired T-test, refer Table 27.

The difference of Pirani score for Pair I (before treatment and after last cast) was 4.000.

The same for Pair II (before treatment and at follow up at 6 month) was 4.059. both of

them, considering mean standard deviations and Degree of freedom, have a significance

(2 tailed p- value) of <0.0005, and this is highly significant (table 28). For the third pair

the p-value is not significant.

Table 27Details of Pirani score- paired samples

No. Mean

PSS

Standard

deviation

Standard error

of mean

Range

Pair I Before

treatment

34 4.147 0.713 0.122 2.5

After last

cast

34 0.147 0.231 0.040 0.5

Pair II Before

treatment

34 4.147 0.713 0.122 2.5

At follow up 34 0.088 0.193 0.033 0.5Pair III After last

cast

34 0.147 0.231 0.040 0.5

At follow up 34 0.088 0.193 0.033 0.5

Table 28Paire sample test for three pairs

Paired DifferencesMean S.D S.E.M 99% T- Degree Significance

83

Pirani

score

Confidence

interval of

differences

value of

Freedom

(2-tailed)

Pair I 4.000 0.482 0.082 3.787 4.213 31.120 33 <0.0005*Pair II 4.059 0.520 0.089 32.042 33 <0.0005*Pair III 0.059 0.038 0.007 01.143 33 0.261

84

Discussion

85

DISCUSSION

In our study, the most common age range for presentation was 0-6 months. This

constitutes 62.07%. The ratio of male to female in our study was 1.9:1. This similar

male to female ratio was found in David A. Spiegel’s study 31,70. However the ratio on

different studies are different 2,26.

In our study, the average age of presentation was earlier in male than female. This may

be due to, that the patients coming here are more from villages and are of low

socioeconomic status and with less education (table 14).

Patients with isolated right side clubfoot(41.38%) were more common, more than the

bilaterally (31.03%) affected patients. Least common was isolated left sided clubfoot

(27.59%). In general, studies shows bilateral patients to be more common than ours, as

in R.A Agrwal et al’s 40% 28, Ankur G. et al’s 37.66% 2.

The total number of cast applied was 271 with average of 7.97 in our study (table

17 ,18). The average number of casts applied before equinus correction was 6.41 (table

19, chart 8).

The number of cast application increases as the Pirani severity score of foot increases.

The minimum number of cast in our study to correct adduction and varus was 5, and the

maximum was 9. Age and Pirani severity score for the patient who needed five cast in

the range of 0.5-8 month and 3 - 4.5 respectively. The same for 9 cast are 14 month and

4.5 respectively. So we can conclude that the number of cast depends on both age and

mean Pirani severity score at presentation (table 19,20 and chart 8,9). We can see a

ascending slope in the charts. Similar conclusion was given by RA Agrawal et al. 28.

The number of cast increases by the increase of Pirani severity score. The range for

86

number of cast applied was 5-9 in our study and the same for Ankur Gupta et al’s 2

study, whose range was 3-10 and in study of Ponseti IV and Smoley EN 25 , it is 5-10.

Our average number of cast application was 7.97, comparatively higher to Rebecca

Kampa et al’s 71 and Ankur et al’s 2 study.

We used, as usual, two methods for equinus correction

By cast application and

by Percutaneous tenotomy

We found, the earlier the age at presentation, lower the require the requirement of

number of cast application, provided Pirani score should not be towards higher side.

There was no apparent difference in proportion of tenotomy and cast application

seperately among male and female, for equinus correction (table 21,22). We can see, out

of 26 tenotomised foot, 19 (73.08%) are male and 7 (26.32%) are female. Among cast

applied patients , 6 (75%) are male and 2 (25%) are female for correction of equinus

(chart 10,11). The tenotomy required by Ankur et al. was 95%. Pirani did 90%

tenotomy, Laaveg et al. did 78% and Dobbs did it 91% 2. So requirement of tenotomy is

towards the lower side in our study.

For the correction of equinus maximum cast was applied in 0-6 months age group (table

23, chart 12).

Majoruty of the foot in our study were in the range of 3.5 - 4.5 according to Pirani

severity score (table 24).

We found that the frequency of tenotomy increases as the Pirani severity score of foot

increases (table 25, chart 14).

We had 1 foot with age 18 months and Pirani severity score of 5.5, who had a Pirani

severity score of 2 after application of 9 cast. It was a failure case and referred for

87

posteromedial soft tissue release. Failure percentage in our study was 2.86% (table 26,

chart 15).

70.58% of foot had no deformity after treatment and 82.35% (28 foot) at follow up had

no residual deformity and fully corrected. The Pirani score for the residual deformity

was mainly the adductus deformity with maximum of 0.5 in Pirani severity score. This

score of 0.5 in 6 foot is statistically insignificant. Ponseti management had good to

excellent result in 78% 25. Ankur et al.2 successful correction without any residual

deformity in 6 month of follow up. Successful initial correction in Ashish et al’s 3 study

was upto 95%. Recent study of Segev et al. 94% excellent results 3. Ponseti IV,Smoley

EN 26 had 71% good results.

The final outcome after the last cast was statistically highly significant. We did paired

sample T-test (table 27,28). The significance of treatment from presentation to last cast,

and presentation to follow up, the p-value of significance was less <0.0005. So there

was a significant reduction of Pirani severity score, showing high effectiveness of

Ponseti method of correction of clubfoot. The change in mean Pirani severity score after

treatment and at follow up was insignificant according to p-value.

Clinically the feet were painless, flexible, plantigrade, mobile and cosmetically

acceptable.

The complications in our study are mentioned in Table 29 (Fig 22-26).

Table 29Complications related to cast

1. Pressure sores 42. Skin blisters 13. Eczema 34. Bruise over thigh 45. Slippage of cast 36. Overcrowding of toes 47. Flat heel pad 18. Cast breakage 49. Blanching of toes 2

88

89

There were no major complication, like rocker bottom foot or flat foot. pressure sore, skin blisters were managed by keeping the foot without cast for 1 week or less. Bruise and eczema were managed coservatively only. For cast breakage , we re-enforced or reapplied the cast. For over crowding we did cast trimming.

The most common cast related complication was pressure sore usually grade 1, and cast

breakage.

At the time of follow up, 6 foot with 0.5 Pirani severity score were due were having the

adductus deformity only. We applied 2 more cast to correct it.

In our study, we found the baby uncooperative during cast application, because they

move their limbs. Tenotomy was done under short general anaesthesia. Tenotomy was

not possible with local anaesthesia because of babies don’t lie down still. We gave oral

antibiotic and analgesic after tenotomy. There was no any infection in any patient over

the surgical wound.

90

Conclusion

91

CONCLUSION

1. The incidence in males is twice as compared to females.

2. Right sided affection is most common.

3. Most commonly clubfoot presents with a Pirani severity score of 3.5-4.5.

4. The results are better if the treatment is started in younger age.

5. The number of cast applied in Ponseti method, increases with the increase in age

at presentation and Pirani severity score.

6. Correction of equinus is with cast is more effective in early age and low Pirani

severity score.

7. Compliance and regular visit to clinic was important.

8. Ponseti method of clubfoot treatment has excellent results, with low expenditure

and with minimum surgical intervention (percutaneous tenotomy).

9. Ponseti technique gives a painless, plantigrade, mobile and cosmetically

acceptable foot.

10. Ponseti tenchnique can be implemented in rural area after training plaster room

attenders also, with caution.

92

Summary

93

SUMMARY

The study was prospective time bound and on OPD basis, conducted from September

2010 to September 2012.

The study included 29 patients with 2 drop outs and 1 failure. The total number of foot

in the complete study was 34.

The mean age at presentation of the patients were 5.1 month (153 days). Male to

female ratio was 1.9:1. The right sided affection of foot was most common and left

sided affection was least in both the sexes.

3.5 to 4.5 was the most common Pirani score of feet. Average number of cast before

the equinus correction was 6.41, and the average of total number of casts applied was

7.97. The number of cast application was dependent on the age and severity of the

deformity. The number of cast to correct adduction and varus increased with age and

severity.

Out of the two methods of equinus correction, correction by cast application was more

common among lower age and low severity. 23.53% of patients were applied with cast

for correction of equinus. Percutaneous tenotomy was the method of equinus correction

in 76.47% of foot. Correction of equinus by cast, in younger foot, had better proportion

than in older foot with high Pirani severity score.

Failure of treatment was with 2.86% of foot, who was referred for posteromedial soft

tissue release. Excellent correction without any residual deformity was with 80.00% of

foot. The foot with with residual deformity (17.41%) were only with maximum of 0.5

Pirani severity score, which is statistically insignificant.

94

The result was concluded by paired T-test. The p-value was <0.0005 in the two groups

“before treatment-after treatment” and “before treatment at follow up”. The p-value

shows highly significant intervention.

So by the results of this study we can conclude the the Ponseti technique of clubfoot

deformity correction is very effective method providing the patient with painless,

plantigrade, mobile and cosmetically acceptable foot.

95

Biblography

96

BIBLOGRAPHY

1. Matthew B Dobbs, José A Morcuende, Christina A Gurnett, and Ignacio V

Ponseti: Treatment of Idiopathic Clubfoot- Iowa Orthop J. 2000; 20: 59–64.

2. Ankur Gupta, Saurabh Singh, Pankaj Patel, Jyotish Patel, and Manish Kumar

Varshney: Evaluation of the utility of the Ponseti method of correction of

clubfoot deformity in a developing nation. Int Orthop. 2008 February; 32(1):

75–79.

3. Ashish, Anand A, Sala DA, Clubfoot: Etiology and treatment. Indian J Orthop

[serial online] 2008 [cited 2010 Nov 13];42:22-8.

4. Charles Sorbie: Club Foot: Rising Incidence—Why? - foot and ankle

orthopedics; December 2008;31(12):1175.

5. John J. Gartland. posterior tibial transplant in surgical treatment of recurrent

clubfoot. JBJS. Vol 46-A, no 6, september 1964.

6. S. Nordin, M. Aidura, S. Razak, & WI. Faisham. Controversies in congenital

clubfoot : Literature review. Malaysian Journal of Medical Sciences, Vol. 9,

No. 1, January 2002 (34-40)

7. Turco V J: Clubfoot, Churchil – Livingstone, New York, 1981

8. Alok Sud & Akshay Tiwari & Deep Sharma & Sudhir Kapoor: Ponseti’s vs.

Kite’s method in the treatment of clubfoot- a prospective randomised study.

International Orthopaedics (SICOT) (2008) 32:409–413

9. B. Stephens Richards, Shawne Faulks, Karl E. Rathjen, Lori A. Karol, Charles

E. Johnston and Sarah A. Jones: A Comparison of Two Nonoperative Methods

97

of Idiopathic Clubfoot Correction: The Ponseti Method and the French

Functional (Physiotherapy) Method. J Bone Joint Surg Am. 2008;90:2313-21.

10. Steven L. Frick: Historical Overview of Clubfoot Treatment – Journey to the

Ponseti Method. Lovell and Winter’s Pediatric Orthopaedics 5th ed. Morrissy

and Weinstein eds., 2001.

11. Goyal PK, Williams AN. “To illustrate and increase Chyrurgerie”: Ambroise

Paré (1510-1590). Journal of Pediatric Surgery Volume 45, Issue 10 , Pages

2108-2114, October 2010.

12. Scarpa, Antonils: A Memoir on the Congenital Club Feet of Children, and on the

Mode of Correcting that Deformity. Translated from Italians by J. H. Wishart.

Edinburgh, A. Constable and Co., l8l8.

13. Roshen N. Irani, Mary S. Sherman: Pathological anatomy of club foot. JBJS, 45-

A 45;1963.

14. JOHN R. KIRKUP. The Journal of Bone and Joint Surgery. EDITORIALS.

Nicolas Andry and 250 years of orthopaedy. VOL. 73-B, No. 3, MAY 1991.

15. Sheldrake T. Distortions of the legs and feet in children. 1806.

16. Alfonso A Haro and Lawrence A. DiDomenico. Frontal plane guided

percutaneous tendo achillis lenthening. The Journal of Foot and Ankle Surgery.

Vol.46, No.1, Jan/Feb 2007.

17. A.B Judson: Subcutaneous tenotomy. Biographical notes. 1899.

jbjs.org/data/Journals/JBJS/982/238.pdf

18. A treatise on the nature of club-foot and analogous distortions including their

treatment both with and without surgical operation : illustrated by a series of

98

cases and numerous practical isntructions by W.J. Little. Published by W. Jeffs

in London 1839.

19. A. T. Fripp: the problem of the relapsed club foot. J Bone Joint Surg. Br

November 1961 43-B:626-627.

20. Kite J. H. : The Clubfoot. Grune & Straton, New York, 1.1964.

21. Adams, W. Double Talipes Varus, and Sina bifida in a fetus at birth; also, The

Bones of the foot from an Adult Affected with Congenital Talipes Varus. Trans.

Pathol. Soc. London, 3:455-64, 1852.

22. Adams, W. A Series of four Specimens Illustrating the Morbid Anatomy of

Congenital Club-foot (Talipes varus). Trans. Pathol. Soc. London, 6:348-57,

1855.

23. H.A. Wilson: Bone operations for the correction of club-foot.1894.

jbjs.org/data/Journals/JBJS/991/159.pdf

24. Green AD, Lloyd-Roberts GC.: The results of early posterior release in resistant

club feet. A long-term review. Bone Joint Surg Br. 1985 Aug;67(4):588-93.

25. Ponseti IV,Smoley EN.: Congenital clubfoot: the results of treatment. J Bone

Joint Surg 1963;45A:261-266.

26. Ponseti IV,Smoley EN.: The Classic: Congenital Club Foot: The Results of

Treatment. Clin Orthop Relat Res. 2009 May; 467(5): 1133–1145.

27. Cooper DM, Deitz FR.: Treatment of idiopathic clubfoot: A thirty -year follow

up note. J Bone Joint Surg Am. 1995 Oct;77(10):1477-89.

99

28. Agrawal RA, Suresh MS, Agrawal R. Treatment of congenital club foot with

Ponseti method. Indian J Orthop 2005;39:244-7.

29. Bhaskar A, Rasal S. Results of treatment of clubfoot by Ponseti's technique in 40

cases : Pitfalls and problems in the Indian scenario. Indian J Orthop

2006;40:196-9.

30. Charles EJ Docker, Simon Lewthwaite, and Nigel T Kiely. Ponseti Treatment in

the Management of Clubfoot Deformity – A Continuing Role for Paediatric

Orthopaedic Services in Secondary Care Centres. Ann R Coll Surg Engl. 2007

July; 89(5): 510–512.

31. David A. Spiegel, Om P. Shrestha, Prakash Sitoula, Tarun Rajbhandary, Binod

Bijukachhe, Ashok K. Banskota: Ponseti Method for Untreated Idiopathic

Clubfeet in Nepalese Patients From 1 to 6 Years of Age. Clinical Orthopaedics

and Related Research. May 2009, Volume 467, Issue 5, pp 1164-1170.

32. Isaacs H, Handelsman JE, Badenhorst M, Pickering A.: The muscles in club

foot--a histological histochemical and electron microscopic study. J Bone Joint

Surg Br. 1977 Nov;59-B(4):465-72.

33. Matthew E Lovell, Jose A Morcuende: Neuromuscular Disease as the Cause of

Late Clubfoot Relapses. Iowa Orthop J. 2007; 27: 82–84.

34. Victoria-Diaz A, Victoria-Diaz J.:Pathogenesis of idiopathic clubfoot. Clin

Orthop Relat Res. 1984 May;(185):14-24.

35. Hanan Waisbrod, Tiberias, Israel: Congential Clubfoot; An anatomical study.

Journal of Bone & Surgery, Vol.55-B, 796-801, 1973.

36. Ponseti I V: Congential Clubfoot. Fundamentals of Treatment, Oxford

University Press, London, 1996.

100

37. K. Fukuhara, G. Schollmeier, Hans K. Uhthoff. The pathogenesis of club foot: A

histomorphometric and immunohistochemical study of fetuses. JBJS. Vol. 76-b,

no. 3, May 1994.

38. Ippolito E. & Ponseti I V: Congential clubfoot in Human fetuses; A histological

study. Journal of Bone & Joint Surgery, Vol.62-A, 8-22, 1980.

39. A.H. Cardy, S Barker, D. Chesney, L. Sharp, N. Maffulli and Z.

Miedzybrodzka.: Pedigree analysis and epidemiological features of idiopathic

congenital talipes equinovarus in the United Kingdom: a case-control study.

BMC Musculoskeletal Disorders 2007, 8:62.

40. Henry R Cowell, Barry K Wein, Wilmington, Delaware – Genetic aspects of

clubfoot, Journal of Bone & Joint Surgery, Vol.62-A, Dec, 1381-1384, 1980.

41. Kite JH.: Principles involved in the treatment of congenital clubfoot. J Bone

Joint Surg. 1939;21:595-606.

42. Mercer’s Orthopedic surgery 9th edition – volume 1, Page 180, 203.

43. Keith Eric Grant and Art Riggs: Myofascial Release. Chapter-9, page 150.

www.deeptissuemassagemanual.com/Riggs_Grant.pdf

44. Scott WA, Hosking SW, Catterall A.: Club foot. Observations on the surgical

anatomy of dorsiflexion. J Bone Joint Surg Br. 1984 Jan;66(1):71-6.

45. Clubfoot: Ponseti Management, Third Edition. 2009. Global Help. Page 4,5.

46. A. Huson.: Biomechanics of the foot and ankle. Chapter-15. Functional anatomy

of the foot. Page.409-431.

101

47. Carol A Oatis: Biomechanics of the Foot and Ankle Under Static conditions.

Journal Of The American Physiotherapy Association. 1988; Vol.68:1815-1821.

48. Inman VT: The Joints of the Ankle. Baltimore, MD, Williams & Wilkins, 1976.

49. Siegler S, Chen J, Schneck CD: The three-dimensional kinematics and

flexibility characteristics of the human ankle and subtalar joints Part 1,

Kinematics. J Biomech Eng. 1988 Nov;110(4):364-73.

50. Andrew M. Wainwright, Tanya Auld, Michael K. Benson, Tim N. Theologis.

The classification of congenital talipes equinovarus. THE JOURNAL OF BONE

AND JOINT SURGERY. VOL. 84-B, NO. 7, SEPTEMBER 2002.

51. Diméglio A, Bensahel H, Souchet P, Mazeau P, Bonnet F. Classification of

clubfoot. J Pediatr Orthop B. 1995;4(2):129-36.

52. Hanneke Andriesse, Ewa M Roos, Gunnar Hägglund and Gun-Britt Jarnlo.

Validity and responsiveness of the Clubfoot Assessment Protocol (CAP). A

methodological study. BMC Musculoskeletal Disorders 2006, 7:28.

http://www.biomedcentral.com/14 71-2474/7/28

53. Said Saghieh, Abdo Bashoura, Ghina Berjawi, Nadim Afeiche and Rayan

Elkattah. The correction of the relapsed club foot by closed distraction. Strat

Traum Limb Recon (2010) 5:127–135.

54. Clubfoot: Ponseti Management, Third Edition. 2009. Global Help. Page 27.

55. P. J. Dyer, N. Davis. The role of the Pirani scoring system in the management of

club foot by the Ponseti method. J Bone Joint Surg [Br] 2006;88-B:1082-4.

56. Clubfoot: Ponseti Management, Second Edition. 2005. Global Help. Page 22.

102

57. Treatment Of Congenital Clubfoot Using The Ponseti Method: Workshop

Manual. 2nd Edition. Page15-17.

58. Ponseti IV, Zhivkov M, Davis N, Sinclair M, Dobbs MB, Morcuende JA.

Treatment of the complex idiopathic clubfoot. Clin Orthop Relat Res. 2006

Oct;451:171-6.

59. Kenneth J. Noonan and B. Stephens Richards. Nonsurgical Management of

Idiopathic Clubfoot. J Am Acad Orthop Surg November/December 2003;

11:392-402.

60. Clubfoot. ICD-9. http://eorif.com/Pediatrics/clubfoot.html

61. Exner GU, Tschanz HP, Jacob HA, Wetz HH. Clubfoot orthosis with integrated

dynamic cuff for retention and redressing. Orthopade. 2001 Apr;30(4):214-7.

62. Harold A. Sofield. Elastic traction assisting correction of club feet. J Bone Joint

Surg Am, 1931 Apr 01;13(2):283-286.

63. N De Mazumdar. Journal Of Indian Association Of Pediatric Surgeons. Vol. 7

(January - March 2002). Article 8.

64. V.P. Gibney. Treatment of clubfoot: Report on the treatment of clubfoot by

means of the Thomas Wrench. American Orthopaedic Association, Washington

1888. Page 74-84. jbjs.org/data/Journals/JBJS/986/74.pdf

65. AV Sanghvi, VK Mittal. Conservative management of idiopathic clubfoot: Kite

versus Ponseti method. Journal of Orthopaedic Surgery 2009;17(1):67-71.

66. Henri Bensahel, Bernard Bienayme and Pascal Jehanno. History of the

functional method for conservative treatment of clubfoot. J Child Orthop (2007)

1:175–176.

103

67. Shawne Faulks RN and B. Stephens Richards. Clubfoot Treatment: Ponseti and

French Functional Methods are Equally Effective. Clin Orthop Relat Res (2009)

467:1278–1282.

68. RA Agrawal and Sureshwar Pandey. Step by Step management of clubfoot by

Ponseti technique. Jaypee. Fifth Edition. 2007. Page 57-109.

69. Cristina Alves, Carolina Escalda, Pedro Fernandes, Delfin Tavares and M.

Cassiano Neves. Ponseti Method: Does Age at the Beginning of Treatment

Make a Difference? Clin Orthop Relat Res. 2009 May; 467(5): 1271–1277.

70. Rijal R, Shrestha BP, Singh GK, Singh M, Nepal P, Khanal GP, Rai P.

Comparison of Ponseti and Kite's method of treatment for idiopathic clubfoot.

Indian J Orthop 2010;44:202-7.

71. Rebecca Kampa, Katherine Binks, Mia Dunkley and Christopher Coates.

Multidisciplinary management of clubfeet using the Ponseti method in a district

general hospital setting. J Child Orthop (2008) 2:463–467.

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ANNEXURE

SAMPLE INFORMED CONSENT FORM

TITLE OF THE STUDY:-

“PONSETI TECHNIQUE IN THE MANAGEMENT OF CLUBFOOT

DEFORMITY- A STUDY”

PRINCIPAL INVESTIGATOR : DR. MD NAYEEM ALI

P.G. GUIDE’S NAME : DR.M.S.PATIL

PURPOSE OF STUDY

This study is for better understanding of “Ponseti technique in management of clubfoot

deformity”.

RISKS AND DISCOMFORTS

We understand that my child may experience some pain or discomfort during the

examination or during the treatment. This is mainly the result of his/her condition and

the procedure of the study is not expected to exaggerate these feelings which are

associated with the usual course of treatment. The risk and possible complications

surgically and anaesthetically have been explained to me.

BENEFITS

The benefits of technique have been conveyed to us.

105

ALTERNATIVES

The various alternative modes of treatment available to him/her in his/her disease with merits

and demerits have been explained to us.

CONFIDENTIALITY:

I understand medical information produced by this study will become part of our hospital record

and will be subject to the confidentiality and privacy regulations of the hospital.

If the data are used for publication in the medical literature for teaching purposes, no names will

be used, and other identifiers, such as photographs and audio or videotapes, will be used only

with my special written permission. I understand, I may see the photographs and videotapes and

hear the audio tapes before giving this permission. For this purpose every effort will be made

by publishing person to contact me in the address furnished by me through postal

communication. If no response is received within a reasonable time, all the identities will be

removed from the photographs and case report before being submitted for publication.

REQUEST FOR MORE INFORMATION:

We understand that, we may be asked more questions about the study at any time. Researcher is

available to answer our questions or concern in this research period. We understand that we

will be informed of any significant new findings discovered during the course of this study,

which might influence our continued participation.

REFUSAL OR WITHDRAWL OF PARTICIPATION:

We understand that his/her participation is voluntary and we may refuse to participate or

discontinue participation in the study at any time without prejudice to my present or future care

at this hospital. We also understand that researcher may terminate his/her participation in the

study at any time after we have been explained the reasons for doing so.

106

INJURY STATEMENT

We understand that in the unlikely event of injury to him/her resulting directly from his/her

participation in this study. If such injury were reported promptly, then medical treatment would

be available to him/her, but no further compensation would be provided. I understand that my

agreement to participate in the study I am not waiving any of our legal rights.

We have explained to _________________________________________

(Patient’s parent Name)

The purpose of research, the procedures required and the possible risk and benefits to the best of

my ability.

-----------------------------------

Investigator Date:

We have been explained clearly about the reason for doing this study, reason for selecting

him/her as a subject in the study. We also have been explained about the risks, benefits and

confidentiality of the study. Alternative procedures that might be used in the treatment of

his/her disease also explained to me. We are willing to attend any follow up requested to me at a

future date. Freedom is given to me for the participation in the study or discontinues

participation at any time without prejudice.

All the above explained in detail to me clearly in my own language. We are giving consentvoluntarily for inclusion of my child in the study as a subject.

-----------------------------------

Participant’s parent

Date:

-----------------------------------

Witness to signature

107

CASE PROFORMA

Name :Age :Sex :Address :Consanguinity of Marriage :Antenatal H/O :Natal and Post Natal H/O :Birth Order :Immunisation :Unilateral/Bilateral :Family H/O :Any previous treatment :Assessment of the deformity using Pirani severity scoring system:-Before Treatment :-After Treatment :-At 6 months follow up :Percutaneous Tenotomy done : Y/NSurgery (PMSTR) : Y/N

Side Casting Percutaneous tenotomy Posteromedial soft tissue release

Right

Left

Residual deformity at the end of treatment : Y/NFollow – upResidual deformity : Y/NSupple / Stiff foot : Y/NRocker Bottom Foot : Y/NPain : Y/NWasting of calf muscle : Y/NNon specific complaints : Y/N

108

KEY TO MASTER CHART

Table 30B/L Bilateral Corr. Correction D.O Drop offEq. Equinus F Female L Left m Month / MonthsM Male N NoNo. NumberPMR Posteromedial soft tissue releasePSS Pirani severity scoreR Right Ref. Reffered Rx Treatment S.N. Serial numberTA Tendo achillisY Yes

109

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AL-AMEEN MEDICAL COLLEGE, BIJAPUR

ETHICAL COMMITTEE

The following study entitled “Ponseti technique in the

management of clubfoot deformity- a study” by DR. MD.

NAYEEM ALI, P.G.- M.S. ORTHOPAEDICS, 2010-13 batch has

been cleared from the ethical committee of this institution for the

purpose of dissertation work.

Chairman

Date: Ethical Committee,

Al-Ameen Medical College,

Bijapur

111