DR A.

I AIYEGBUSI

PROLONGED
STRETCHING TO
CORRECT
DEFORMITIES
 INTRODUCTION
Limitations of mobility can be caused by a variety of changes in
connective tissue such as:
 Tightening of connective tissue fasciae e.g following trauma,
surgery, radiation damage or burns

 Oedema in and around joints due to acute trauma and

infection, and an increase in connective tissue in chronic
conditions

 Changes in joint structure resulting from fracture

 Separation of the 'mus articularis' i.e. cartilage and/or bone

from the joint surface
 Disc damage; rupture, protrusion and/ or prolapsed discs
 Flexibility is considered to be an important factor
affecting physical health
 Range of movement (ROM) is a fundamental
part of normal function of the musculoskeletal
system
 A certain amount of flexibility is necessary for
the success of all physical movements
 Individual differences in physical condition and
range of joint movement can largely be due to
innate, hereditary factors
 Flexibility can, however, be significantly
increased with intensive training of the elastic
connective tissues, even in 'naturally stiff'
persons.
 A decrease in mobility may cause changes in
function, which puts abnormal loading on the
muscle-tendon system and joint structure.

 Thus, stretching is commonly included in the

warm-up process in both training and
competition situations.

 Furthermore, stretching is important in recovery
following intense training and competition.
 Prolonged immobility may, however, lead to
structural changes as elastic fibres are replaced
by tougher fibrous tissue to such an extent that
stretching treatments are no longer effective and
such tissue must be manipulated while the
patient is anaesthetized

 Disease, injury and surgery will cause changes

in the tissue mobility. Changes will also arise
following intense stretching and as a result of
prolonged immobilization
 Position can affect restrictions in mobility.
Movement is easiest in a neutral position when
ligaments are most loose.

 Ligaments will begin to tighten and joint

surfaces press against each other as joints are
taken to their furthest limits of ROM.

 Movement in other directions will decrease or

disappear completely.
 WHAT IS A
DEFORMITY?
A deformity, dysmorphism, or dysmorphic
feature:
 major difference in the shape of body part or
organ compared to the average shape of that
part.
 Any deviation from the normal anatomy of a
bone or joint
 Cause could be genetic or environmental,
Congenital or Acquired
 Could be due to disorders of the bone, joint or
soft tissues.
 CONGENITAL DEFORMITIES
 Due to faulty development and are present
at birth, though they may not be recognized
until later.
 They vary from severe malformations to
minor abnormalities of structure

 Incidence varies in different countries and

among different races
 Only about half of these affect the
musculoskeletal system.
 ACQUIRED DEFORMITY
Deformity may be said to exist at a joint when
the joint cannot be placed voluntarily in the
neutral anatomical position.

2 Types:
 Arising at a joint

 Arising from a bone

 Causes of Joint deformities
 Dislocation or subluxation
 Muscle imbalance
 Tethering or contracture of muscles or
tendons.
 Contracture of soft tissues .
 Arthritis
 Posture
 Unknown causes.
Seven causes of deformity arising at a joint.- 1.
Dislocation. 2. Muscle imbalance. 3. Tethering of muscle or
tendon. 4. Soft-tissue contracture. 5. Arthritis. 6. Posture.
7. Idiopathic (cause unknown).
1-Dislocation or subluxation.
 Usually caused by injury
 May be due to congenital deformity,
 May follow disease of the joint (pathological
dislocation).

2-Muscle imbalance.
 Unbalanced action of muscles upon a joint may hold
it continuously in a particular arc of its range.

 In time, secondary contractures occur in the

dominant muscles or in the soft tissues, preventing
the joint from returning to the neutral position
The two fundamental causes of muscle imbalance
are:
 Weakness or paralysis of muscles
 Spasticity of muscles.
 Thus equinus deformity at the ankle may follow
paralysis of the dorsiflexor muscles (for
instance, in poliomyelitis)

 A similar deformity may be caused by spasticity

of the calf muscles, which overpower their
antagonists. This occurs commonly in cerebral
palsy.
 3-Tethering or contracture of muscles or tendons.
 Issues with the normal to-and-fro gliding of muscles
and tendons, or their elongation and retraction may
cause the joint to be held in a position of deformity.

 A muscle or tendon may be tethered to the

surrounding tissues in consequence of local infection
or injury
 An example is the anchoring of a flexor tendon of a
finger within its fibrous sheath as a result of
suppurative tenosynovitis, with consequent flexion
deformity at the interphalangeal joints.
 Or a muscle may lose its elasticity and
contractile power from impairment of its
blood supply.

 An important example is Volkmann's

ischemic contracture of the forearm flexor
muscles from occlusion of the brachial
artery or from increased intra-
compartmental pressure, with consequent
flexion deformity of the wrist and fingers.
4-Contracture of soft tissues.
 Contracture of soft tissues alone can account
for joint deformity.
 An example is Dupuytren's contracture: the
thickened and contracted palmar aponeurosis
pulls the MCP and PIP joints of one or more
fingers into flexion.

 Similarly, a flexion deformity of the knee or

elbow, or indeed of any joint, may occur from
contracture of the scarred skin after burns of the
flexor surface of the limb
5-Arthritis.
 Any type of arthritis may lead to joint
deformity.
 In some cases the joint is firmly fixed in a
deformed position by bony or fibrous
ankylosis.
 At times, the joint retains some movement but
is prevented from reaching the neutral
position. Thus flexion and adduction deformity
is common in osteoarthritis of the hip
 Ulnar deviation of the fingers is a well known
feature of rheumatoid arthritis of the
metacarpo-phalangeal joints.
6-Posture.
 Habitual adoption of a deformed position of a joint
often leads in time to permanent deformity.

 A common example is the lateral deviation of the

great toe at the MTP joint: hallux valgus. Common
in women who cramp their feet into narrow
pointed shoes

 Another postural deformity is fixed flexion of the

knees in a patient confined to bed for a long time
with the knees bent over a pillow.
Scoliosis Kyphosis
7- Idiopathic.
 Deformity occurs at a joint for no apparent
reason.
 Many children develop knock-knee deformity
between the ages of 3 and 5 years without
demonstrable cause which tends to correct itself
spontaneously.
 Another" common and more serious example is
the inversion deformity of the foot known as
talipes equino-varus or congenital club foot. A
more sinister deformity that is equally ill
explained is the idiopathic scoliosis of
adolescents.
 DEFORMITY ARISING IN A BONE
Causes.
There are three causes of deformity arising in
bone:
1. Fracture; This is by far the most common
cause. Unless a fracture is reduced so that the
fragments are perfectly aligned deformity will
result.

2. Bending;
3. Uneven epiphysial growth
1. FRACTURES
 S-shaped: Supracondylar # of humerus
 Cubitus valgus: Mal-united lat. Condyle of #
humerus

 Dinner Fork: Mal-united Colles #

 Mallet Finger: Avulsion of extensor tendon

 Genu Valgum/Genu Varum: # Tibial Condyle
 Ext. Rotation of Lower Limb: # neck of femur,
shaft, trochanters
 Dinner Fork: Mal-united Colles #
 Mallet Finger: Avulsion of extensor tendon
 2-Bending of softened bone.
 Many unrelated conditions can cause softening
of bone, with liability to bending and consequent
deformity.
 Are mostly generalized disorders in which
several or all of the bones are affected.
Examples are:
 Metabolic disorders: rickets, osteomalacia.
 Endocrine disturbances: parathyroid
osteodystrophy, Cushing's syndrome.
 Idiopathic: Paget's disease (osteitis deformans),
fibrous dysplasia of bone, senile osteoporosis.
 3-Uneven growth of bone.
 Disturbance of the epiphyseal cartilage (growth
plate) may lead to uneven growth and
consequent deformity.
 The usual effect of disturbance is that its growth
is retarded
 Occasionally it is accelerated

 Deformity occurs only if the growing cartilage is

affected more in one part than another

 or if the interference with growth affects only one

bone of a pair, as in the forearm or leg
frequent causes of retarded epiphyseal
growth are:
 Crushing fracture involving the epiphysial
growth plate

 Infection of the cartilage, usually from

adjacent osteomyelitis or joint infection;

 Enchondroma (a benign tumour) adjacent to

the cartilage, as in Ollier's disease (multiple
enchondromatosis.
In the relatively uncommon cases in which
epiphysial growth is accelerated the usual
cause is:
 local hyperemia induced by an adjacent
focus of infection

 or by a vascular tumors such as a,

haemangioma.
 Treatment of deformities
Many do not require treatment, or are not amenable
to it.

 Manipulative correction and retention in a plaster

or splint: displaced fracture

 Gradual correction by prolonged traction: for

deformity in certain types of arthritis

 Division or excision of contracted or tethered soft

tissue: Dupuytren's contracture or scouring from
burns
 Surgical intervention e.g. Osteotomy:
deformity from rickets

 Arthrodesis: for scoliosis

 Selective retardation of epiphysial growth

(in children) (example for deformity from
uneven epiphysial growth).
 Excellent exercises for improving joint mobility
include active and passive stretching as well as
dynamic exercises involving broad ranges of
movement

 The purpose of stretching is to increase the

elasticity of muscles, tendons, fasciae, joint
ligaments and joint capsules.

 Furthermore, stretching exercises aim to relax the

neuromuscular system in general
 An increase in muscle tone will often lead to
pain caused by the irritation of nerve endings
or the increase in pressure in and between
muscles which causes slowing of the
metabolism.

 Symptoms of pain can be reduced with the

relaxation of muscles by stretching
exercises.
CASE STUDY:
CORRECTION OF
CONGENITAL TALIPES
EQUINOVARUS
 Features of CTEV
 Short Achilles tendon
 High and small heel

 No creases behind Heel

 Abnormal crease in middle of the foot

 Foot is smaller in unilateral affection

 Callosities at abnormal pressure areas

 Internal torsion of the leg

 Calf muscles wasting
 Deformities do not prevent walking
 Treatment Goal
The goal of treatment for clubfoot is to obtain
a plantigrade foot that is functional,
painless, and stable over time

A cosmetically pleasing appearance

is also an important goal sought by
the surgeon and the family
TREATMENT
Appropriate treatment administered in 3 stages:
1. Correcting the deformity

2. Maintaining the correction until the foot

regains normal muscle balance

3. Observing the foot closely for several years to

prevent the deformity from recurring.

In newborns, corrective treatment for true clubfoot

should begin at once.
 SEQUENTIAL CORRECTION
 Deformities usually corrected in sequential
order: forefoot adduction first, then varus (or
inversion), then equinus (or plantar flexion).
 Forefoot adduction: corrected by uncurling the
front of the foot away from the heel (forefoot
abduction)
 Varus deformity: corrected by turning the foot
so the sole faces outward (eversion)

 Equinus is corrected by casting the foot with

the toes pointing up (dorsiflexion).
 Foot gently manipulated into a partially
corrected position and held in a cast for several
days or weeks.

 After cast removal: foot is manipulated into an

even better position and casted again.

 After correction: proper foot alignment is

maintained through exercise, night splints, and
orthopedic shoes.
 With manipulation and casting, correction
usually takes about 3 months.
 THE PONSETI METHOD
• Described by Dr. Ignacio Ponseti in the 1950s
and re-popularized around 2000 by Dr. John
Herzenberg
• The method, if correctly done, is successful in
>95% of cases in correcting clubfoot using
non- or minimal-surgical techniques.

• Typical clubfoot cases usually require 5 casts

over 4 weeks. Atypical clubfeet and complex
clubfeet may require a larger number of casts.
 Ponseti Technique
1. Always use long leg casts, change weekly.

2. First manipulation raises the 1st metatarsal to

decrease the cavus

3. All subsequent manipulations include pure

abduction of forefoot with counter-pressure on
neck of talus.

4. Never pronate !

5. Never put counter pressure on calcaneus or

cuboid.
6. Cast until there is about 60 degrees of external
rotation (about 4-6 casts)

7. Percutaneous tendo Achilles tenotomy in cast room

under local anesthesia, followed by final cast (3
weeks)

8. After final cast removal, apply Normal shoes with

Denis Browne bar set at 70 degrees external rotation
(40 degrees on normal side)

9. Denis Browne splint full time for two months, then

night time only for two-four years.

10.35% need Anterior Tibialis tendon transfer at age 2-

3