CLUBFOOT

POLIDAKTILI
SPINA BIFIDA

ORTHOPEDIC’S CONGENITAL
ABNORMALITIES
Maksimus Bisa Ladopurab
CLUBFOOT
(Talipes Equinovarus)
• The most important congenital
abnormalty of the foot
• Easy to diagnose but difficult to
correct completely
• Incidence 1-2 per thousands live
birth, boys are affected twice as
often as the girl, and the condition is
bilateral in one third of cases.
ETIOLOGY
• Remains unknown
• Studies of Handelsman
→neuromuscular cause.
• Exist from the early stages of
embryonic development so is
obvious at birth.
• Genetic factor responsible in about
10%, the rest appears to be cause by
an initial mutation of the family tree.
• One parent and one child have
clubfeet, the chances of a
subsequent child being so afflicted
is one in four.
• Exist from the early stages of
embryonic development so is
obvious at birth.
• Genetic factor responsible in
about 10%, the rest appears to
be cause by an initial mutation
of the family tree.
• One parent and one child have
clubfeet, the chances of a
subsequent child being so
afflicted is one in four.
CLINICAL FEATURES
• the foot is both turned and twisted
inwards so the sole faces posteromedially.
• the ankle is in equinus,
• the heel is inverted, unusually small and
high
• the forefoot is adducted and supinated,
• sometimes the foot also has a medial arch
(cavus) and the talus may protrude on the
dorsolateral surface of the foot.
• In some cases the calf is abnormally thin.
• the foot cannot be dorsiflexed
and everted until the toes
touch the front of the leg, this
manouvere meets varying
degrees of resistance or the
deformity is fixed
PATHOLOGICAL
ANATOMY
• The neck of the talus points downwards
and deviates medially. The body is rotated
slightly outwards in relation to both the
calcaneum and the ankle mortise.
• The posterios part of calcaneum is held
close to the fibula by a tight calcaneo-
fibular ligament and is tilted into equines
and varus, and also medially rotated
beneath the ankle.
• The naviculare and the entire forefoot are
shifted medially and rotated into
supination.
TREATMENT
• General principles of treatment are
- begin early- at least within the first few
days of eye.
- The treatment consists: repeated
manipulation and adhesive strapping
which maintains correction, maintenance
of correction for long period and
supervision of the child the end of growth.
• The aim of the treatments to produce and
maintain a plantigrade, supple foot that
will function will.
• The aim of the treatments: to
produce and maintain a
plantigrade, supple foot that
will function well.
CONSERVATIVE
TREATMENT
The three main components of the
deformity are always corrected in the
following order:
1. The forefoot must be brought into
rotational alignment with the hind
foot.
2. Both hind foot and forefoot are
together gradually brought out of
varus and supination.
3. Equinus is corrected by bringing the
hell down and dorsiflexing the ankle.
• 40% of Congenital clubfeet will
have responded satisfactory
within the first 3 to 4 month
treatment.
• Resistant cases will usually
notice after 8 to 12 weeks of
serial manipulation and
strapping.
• Early operation shown no to be
better than those of late
surgery.
OPERATIVE
TREATMENT
The objectives of clubfoot surgery are
• The complete release of joint
‘’tethers’’(capsular and ligamentous
contractures and fibronic bands.
• Lengthening of tendons so that the
foot can be positioned normally
without undue tension.
Acces to the involved structures
is through
• An extended postero medial incision(
Turco)
• A posterior curved transverse
incision extended anteriorly on both
medial and lateral sides( Cincinatti-
Crawford).
• A posterolateral incision combined
with a separate cutved medial
incision( Caroll)
• The foot, in its corrected position is
immobilized in plaster cast.
• Kirschner wires are sometimes
inserted across the talonavicular
and subtalar jonts to augment the
hold.
• The wire and cast are removed at 6-
8 weeks after which hobble boots
(Dennis browne) or a custom ankle
foot orthosis is used.
Denis Browne Splint
X-RAY’S
• X-ray’s are used mainly to assess progress
after treatment.
• The anteroposterior film is taken with the
foot 30o plantarflexed and the tube
likewise angled 30o to the perpendicular.
• Lines can be through the long axis of the
talus parallel to its medial border and
through that of the calcaneum parallel to
its lateral border, in clubfoot this two lines
may be almost parallel
• The anteroposterior film is taken
with the foot 30o plantarflexed and
the tube likewise angled 30o to the
perpendicular.
• Lines can be through the long axis of
the talus parallel to its medial border
and through that of the calcaneum
parallel to its lateral border, in
clubfoot this two lines may be
almost parallel
• The lateral film is taken with
the foot in forced dorsiflexion.
In clubfoot lines drawn through
the mid-longitudinal axis of the
talus and the lower border of
the calcaneum meet at an angle
less than 20oproducing the so-
called rocker-bottom deformity
POLYDACTYLY
(EXTRA DIGITS)
• Is a common abnormality
• An extra little finger is usually
inherited and other variations maybe
present.
• An extra thumb is usually sporadic.
• An extra central digit, the rarest of
duplications, is often associated
with syndactyly and disorganization
of the skeleton.
SPINA BIFIDA
• Is a congenital disorder in which the
two halves of the posterior vertebral
arch (or several arches) have failed
to fuse.
• Occurs within the first 6 weeks of
gestation
• Often associated with
maldevelopment of the neural tube
and the overlying skin. The
combination of faults is called
dysraphism.
SPINA BIFIDA
• The most frequent site is the
lumbosacral region
• Incidence : 2 per 1000 births but if
one child is affected the risk for the
next child is ten times greater
• Not the bony defect itself but rather
it’s associated to the neurological
development of the spinal cord there
may be paralysis and loss of
sensation and sphincter control.
ETIOLOGIC FACTORS
• Alpha-fetoprotein
neural tube defects are associated
with high levels of alpha–feto
protein in the amniotic fluid and
serum. This offers an effective
method of antenatal screening
during the 15th to 18th weeks of
pregnancy. A positive test is an
indication for the fetal anatomy,
which can detect 95 % of cases of
spina bifida. folic acid
• Folic Acid
400 ug daily before conception and
continuing through the first 12
weeks of pregnancy has been shown
to reduce the risk of neural tube
defects in the foetus. Fortification of
food staples with folic acid for all
women of childbearing age prevent
up to 75 % of open spina bifida cases
before conception
PATHOLOGY
• The most significant ascpect of this
abnormality is not the bony defect itself
but rather the frequently associated
neurogical deficit that result from the
defective development of the spinal cord
(myelodisplasia)
• must always considered as a possible
cause of neurogenic deformities and
trophic ulcers in lower limbs as well as of
bladder and bowel incontinence.
PATHOLOGY
• Spina Bifida Occulta
The mildest degree of spine
bifida which is truly hiden
(occult)and being dectectable
only by radiographic
examination
Manifestation : dimple, hairy
patch, pigmented area or
hemangioma.
Spina Bifida Cystica

• Spina Bifida with Meningocele

The meninges extrude through a
larger defect in the neural
arches  forming a
meningocele covered by normal
skin and containing CSF and
nerve roots
• Spina Bifida with
Meningomyocele
The meningomyocele is covered
by the arachnoid and dura.
It is always associated with a
serious neurological deficit
which often includes bladder
and bowel incontinence,
sensory, and motor loss in the
lower limbs
• Spina Bifida with Myelocele
The most severe degree of
spina bifida
The skin and dura have failed
to close over the neural tube
so that the spinal cord and
nere roots lie completely
exposed
TREATMENT
Spina Bifida with Neurogical Deficit :
• Neurological treatment :
 removal of the sac
 VP-Shunt
• Orthopaedic treatment :
- flacid paralysis same with
polomyelitis
-spastic type  same with cerebral
palsy