MARINDUQUE STATE COLLEGE

CLUBFOOT

Mariel Anne M. Arao Lorna C. Gamis, RN, MAN

BSN 4B Watson (Group AM)
Overview clubfoot is a foot deformity diagnosed in newborns
the most severe form and most commonly known
as congenital talipes equinovarus.

it is a deformity that occurs in utero in approximately 1 of

every 1,000 births.
in children who have not had effective treatment, the most
severe form of this condition resembles a "club".
boys are twice as likely to be affected as girls.
if a family has one child with a clubfoot, the chances of
having another affected child increase markedly.
Definition
clubfoot is a complex deformity of
the ankle and foot that includes
forefoot adduction, midfoot
supination, hindfoot varus, and
ankle equinus.
deformities of the foot and ankle
are described according to the
position of the ankle and foot.
Cavus Adductus The underlying deformity of clubfoot can
be divided into four components
1. Cavus - in the midfoot is the first part of the
deformity of clubfoot
2. Adductus - is movement towards the
midline; is the second part of the clubfoot
Varus Equinus
deformity
3. Varus - means movement towards the
midline; varus of the hindfoot is the third part
of the deformity of clubfoot
4. Equinus - means an increase in the
plantartflexion of the foot; fourth part of the
clubfoot deformity
Definition
the more common positions involve
the following variations:
1. Talipes varus - an inversion, or bending
inward
2. Talipes valgus - an eversion, or
bending outward
3. Talipes equinus - plantar flexion, in
which the toes are lower than the heel
4. Talipes calcaneus - dorsiflexion, in
which the toes are higher than the heel
5. Talipes equinovarus - toes lower than
the heel and facing inward
Classification
1. Positional Clubfoot - refers to a flexible
foot that was held over time in an abnormal
position in utero.
2. Idiopathic Clubfoot - there is no known
cause for the deformity.
Untreated Clubfoot - all clubfeet from
birth up to 2 years of age that have had
very little or no treatment can be
considered as untreated clubfeet.
Treated Clubfoot - are usually braced
full-time for 3 months and at night up to
age 4 or 5 years.
Classification
2. Idiopathic Clubfoot - there is no known
cause for the deformity.
Recurrent Clubfoot - this is a clubfoot
which has achieved a good result with
Ponseti treatment, but the deformity has
recurred.
Neglected Clubfoot - is a clubfoot in a
child older than 2 years, where little or
no treatment has been performed .
Classification
2. Idiopathic Clubfoot - there is no known
cause for the deformity.
Complex Clubfoot - any foot with
deformity that has received any type of
treatment other than the Ponseti
method have added complexity
because of additional pathology or
scarring from surgery.
Resistant Clubfoot - this is a clubfoot
where Ponseti treatment has been
correctly performed but there has been
no significant improvement.
Classification
2. Idiopathic Clubfoot - there is no known
cause for the deformity.
"Atypical" Clubfoot - it involves a foot
that is often swollen, has a plantarflexed
first metatarsal and an extended big toe.
It can occur spontaneously but most
often occurs after slippage of a cast.
3. Secondary Clubfoot - occurs when there
is another disease or condition that is
causing or linked to the development of
clubfoot.

Causes
the precise cause of clubfoot is
UNKNOWN.
it can be associated with other
abnormalities of the skeleton that
are present at birth (congenital),
such as spina bifida, cerebral palsy,
and arthrogryposis
causes may include genetic
component, environmental factors,
seasonal variation, and in utero
positioning but have not been
consistently demonstrated
Several theories have been proposed to
explain the origin of clubfoot, considering
both intrinsic and extrinsic causes,
including:
intrauterine position of the foetus,
mechanical compression or increased
hydraulic pressure,
interruption in foetal development,
viral infections,
vascular deficiencies,
muscular alterations,
neurological alterations,
defect in the development of the
bones structures and genetic defects
Risk factors
1. Sex - more common in males
2. Family history - if either one of the parents or their other children
have had clubfoot, the baby is more likely to have it as well.
3. Smoking during pregnancy - if a woman with a family history of
clubfoot smokes during pregnancy, her baby's risk of condition
may be 20 times greater than average.
4. Not enough amniotic fluid during pregnancy
5. Getting an infection or using illicit drugs during pregnancy
Symptomatology
Foot abnormality - the ankle is in equinus, and the foot is supinated
(varus) and adducted
Bone displacement - the navicular is displaced medially, as is the
cuboid
Contractures - contractures of the medial plantar soft tissues are
present
Empty heel - the heel is small and empty; the heel feels soft to touch
 Pathophysiology Non-Modifiable Risk factors
Sex
Modifiable Risk factors Family history
Smoking mother during pregnancy Congenital conditions such as
Use of illicit drugs during pregnancy Amniotic Band Syndrome
Not enough amniotic fluid during
pregnancy or oligohydramnios

Arrested development of embryo in early stages Abnormal position and restricted movement in utero

Unilateral or bilateral deformity

of foot and ankle

Foot pointed downward and inward (plantar Foot pointed upward and outward (dorsiflexion
flexion and inversion) and eversion)

Talipes Talipes Talipes Talipes

Equinus Equinovalgus Equinovarus Calcaneous
Complications

Walking Post-treatment Psychological

difficulty/inability recurrence effects

Problems stemming from Arthritis Poor self-image

walking adjustments
Diagnostics and Laboratory tests
Foot imbalance due to clubfoot may be noticed during a
Fetal screening
fetal screening ultrasound as early as 12 weeks gestation,
ultrasound
but the diagnosis is confirmed by physical exam at birth.

Talocalcaneal parallelism is the radiographic feature of

clubfeet; the anteroposterior (AP) view is taken with the
Radiographs foot in 30 degrees of plantarflexion and the tube at 30
degrees from vertical. The lateral view is taken with the
foot in 30 degrees of plantarflexion.
Medical Management
The Pirani scoring system, devised by Shafiq Pirani, MD, of
Vancouver, BC, consists of six categories, three in the
The Pirani scoring
hindfoot and three in the midfoot; the Pirani scoring
system
system can be used to identify the severity of the clubfoot
and to monitor the correction.

With traditional nonoperative treatment, splintage begins

at 2-3 days after birth; merely bring the foot to the best
Traditional nonoperative position obtainable, and maintain this position either by
treatment strapping every few days or by changing casting weekly
until either full correction is obtained or correction is
halted by some irresistible force.
Medical Management
This method uses gentle stretching and casting to
gradually correct the deformity
Long-leg casts are applied after the feet are correctly
positioned
Treatment should ideally begin shortly after birth
Elements of the method include:
1. Manipulation and Casting - the baby's foot is gently
The Ponseti method
stretched and manipulated into a corrected position and held
in place with a long-leg cast (toes to thigh)
2. Achilles tenotomy - after the manipulation and casting
period, approximately 90% of babies will require a minor
procedure to release continued tightness in the Achilles
tendon (heel cord); new cast will be applied to the leg to
protect the tendon as it heals
Medical Management
Elements of the method include:
3. Bracing -to ensure that the foot will permanently stay in the
The Ponseti method correct position, your baby will need to wear a brace
(commonly called "boots and bar") for several years. The brace
keeps the foot at the proper angle to maintain the correction
Medical Management
Nonsurgical method to correct clubfoot uses stretching,
mobilization, and taping. The French method — also called
the functional or physical therapy method — is typically
directed by a physical therapist who has specialized
training and experience
The French method Begun soon after birth and requires family involvement
Each day, the baby's foot must be stretched and
manipulated, then taped to maintain the range of motion
gained by the manipulation. After taping, a plastic splint is
put on over the tape to maintain the improved range of
motion
Surgical Management
In the past, clubfoot surgery was performed in a way that
did not differentiate severity; the same procedure was
performed for all patients; Bensahel proposed a more
Surgical clubfoot release
individualized approach (ie, addressing only the structures
that are required are released); the surgery is tailored to
the deformity

An orthopedic surgeon makes an incision to access and

cut the anterior tibialis tendon, located along the inner arch
Tendon Transfer Surgery of the foot. This tendon is then moved to the other side of
the foot beneath the skin, where it is reattached to the
bones there using a small surgical button
 Nursing Intervention
Nursing Assist patient with muscle exercises as able or when

diagnosis allowed out of bed; execute abdominal-tightening

exercises and knee bends; hop on foot; stand on
toes.
Impaired physical Present a safe environment: bed rails up, bed in a
mobility related to down position, and important items close by.
musculoskeletal Execute passive or active assistive ROM exercises
impairment as to all extremities.
Let the patient accomplish tasks at his or her own
manifested by foot
pace. Do not hurry the patient. Encourage
deformity independent activity as able and safe.
Provide the patient with rest periods in between
activities. Consider energy-saving techniques.
Nursing Nursing Intervention
diagnosis Acknowledge and accept an expression of feelings
of frustration, dependency, anger, grief, and hostility.
Disturbed body Maintain a nonjudgmental attitude while giving care,
and help the client identify positive behaviors that
image related to
will aid in recovery.
permanent Assist the client in incorporating actual changes into
alteration in ADLs, social life, interpersonal relationships, and
structure and/or occupational activities.
function as Assist client for family interaction with each other
manifested by foot with the rehabilitation team.
abnormality Help the client to identify their strengths.
 Nursing Intervention
Nursing Monitor site of impaired tissue integrity at least

diagnosis once daily for color changes, redness, swelling,

warmth, pain, or other signs of infections.
Assist the patient to change position every 15 mins
Impaired skin and change chair-bound positions every hour.
integrity related to Use pillows or foam wedges to keep bony
cast application, prominences from direct contact with each other.
Keep pillows under the heels to raise off the bed.
traction or surgery
Check every two (2) hours for proper placement of
as manifested by footboards, restraints, traction, casts, or other
dryness of skin devices, and assess skin and tissue integrity.
Educate client about proper nutrition, hydration, and
methods to maintain tissue integrity.
 MARINDUQUE STATE COLLEGE

OSTEOGENESIS
IMPERFECTA
Mariel Anne M. Arao Lorna C. Gamis, RN, MAN
BSN 4B Watson (Group AM)
Overview It is very rare
It is the most common genetic disorder of the bone.
also known as It is a heterogeneous, autosomal dominant disorder
"brittle bone characterized by fractures and bone deformity.
disease" It occurs equally in all races and is equally prevalent
most
between males and females.
common
osteoporosis It is a biochemical defect that causes a decrease in the
syndrome in synthesis of collagen.
childhood It affects all connective tissue in the body.
Children may become disabled as a result of the severe
deformities.
Definition
osteogenesis imperfecta is a
group of autosomal dominant
diseases characterized by
excessive fragility of the bones
causing a high rate of fracture.
is an inherited (genetic) bone
disorder that is present at birth.
a child born with OI may have soft
bones that break (fracture) easily,
bones that are not formed normally,
and other problems.
Classification
A - Mild bone fragility; blue sclerae; normal teeth; hearing loss (occurs
between ages 20 and 30 years); autosomal dominant inheritance
Type I
B - Same as A except dentinogenesis imperfecta instead of normal teeth
C - Same as B but no bone fragility

Lethal; stillborn or die in early infancy; severe bone fragility, multiple

Type II
fracture at birth; 10% of cases of OI; autosomal recessive inheritance

Severe bone fragility leading to severe progressive deformities; normal

Type III sclerae; marked growth failure; most autosomal recessive inheritance; few
autosomal dominant inheritance
Classification
A - Mild to moderate bone fragility; normal sclerae; normal teeth; short
stature; variable deformity; autosomal dominant inheritance
Type IV
B - Same as A except dentinogenesis imperfecta instead of normal teeth;
approcximately 6% of cases of OI

Clinically similar to type IV; hyperplastic callus; collaem mutation is

Type V
negative

Sclerae and dentition normal; moderate to severe bone fragility; diagnosis

Type VI by bone biopsy because of similarities to other types; only identified in
eight persons to date
Classification
Type VII and
Clinically overlap types II and III but have white sclerae, rhizomelia, and
VIII
small to normal head circumference; severe osteochondroplasia and short
(recessive
stature in survivors
form)
Causes and Risk factors
it can be caused by mutations in one of several genes
such as mutations in the COL1A1 and COL1A2 genes Risk factors include:
wherein these genes provide instructions for making 1. Heredity - if one
proteins that are used to assemble type I collagen
parent has
in types I to V OI, the mode of inheritance is
osteogenesis
autosomal dominant and often involves a new
imperfecta, a child
dominant mutation
has a 50 percent
germ cell mosaicism may be the explanation for
chance of having a
cases occurring in families with healthy parents that
condition
have more than one child with OI
somatic mosaicism has been noted in brainstem
who have had multiple children with the same
dominant form
Symptomatology
Bluish to whitish sclera. The hues of the sclera may vary, but
the change in color can also occur in other diseases such as
progeria and Menkes syndrome.
Dentinogenesis imperfecta. The teeth break easily and erode
gradually.
Fractures. Over a lifetime numbers of fractures may reach a
hundred or even more.
High pain tolerance. People with osteogenesis imperfecta may
have a high tolerance for pain, as old fractures may be
discovered in infants only after a radiograph ordered for an
entirely different reason.
Height. Height is extremely variable with some patients having
near-normal height and others having significantly short stature.
 Pathophysiology
Non-Modifiable Risk factors
Modifiable Risk factors Heredity
Exposure to hazards Recessive gene mutation

Dominant mutation in the COL1A1 or the COL1A2 genes

Production of abnormal Decrease in the production of

collagen I molecules normal collagen I molecules

> Mild bone > Severe bone > Severe bone > Mild to > Mild to moderate > Moderate to > Severe bone fragility
fragility fragility fragility to moderate bone bone fragility severe bone > Multiple fractures
> Blue sclerae > Multiple fractures severe fragility > Short stature fragility > Marked growth failure
> Hearing loss at birth progressive > Short stature > Variable deformity > Lethal
Type VI
> Dentinogenesis > Lethal deformities > Variable > Dentinogenesis > Stillborn or death in ealy infancy
imperfecta > Stillborn or death > Marked deformity imperfecta > Rhizomelia
in ealy infancy growth failure > Dentinogenesis > Hyperplastic callus > Small to normal head
Type I
imperfecta cirumference
Type II Type III Type V
> Severe osteochondroplasia
Type IV
> Short stature
Type VII & VIII
Complications
Respiratory infections. Repeated respiratory infections can be a
complication of severe osteogenesis imperfecta.
Basilar impression. Basilar impression can cause brainstem compression
and is a major neurologic complication in children with osteogenesis
imperfecta.
Hydrocephalus. Hydrocephalus can be communicating or non-
communicating and sometimes requires CSF shunting.
Cerebral hemorrhage. Cerebral hemorrhage caused by birth trauma is
another possible complication.
Diagnostics and Laboratory tests
Collagen synthesis is performed by culturing dermal fibroblasts obtained
analysis during skin biopsy

can be performed in pregnancies with the risk of

Prenatal DNA mutation
osteogenesis imperfecta to analyze uncultured chorionic
analysis
villus cells

as measured with dual-energy radiographic

Bone mineral density absorptiometry, is generally low in children and adults with
osteogenesis imperfecta
Diagnostics and Laboratory tests
images may reveal thinning of the long bones with thin
X-ray cortices or it may reveal beaded ribs, broad bones and
numerous fractures with deformities of the long bones

prenatal ultrasonography can be used to detect limb-

Ultrasonography
length abnormalities at 15 to 18 weeks gestation
Medical Management
Nutritional evaluation and condition are paramount to
Nutrition
ensure appropriate intake of calcium and vitamin D

In utero bone marrow In utero bone marrow transplantation of adult bone marrow
transplant has been shown to decrease perinatal lethality

A preclinical study demonstrated that RANKL inhibition

improves density and some geometric and biomechanical
RANKL inhibition
properties of oim/oim mouse bone but does not decrease
fracture incidence when compared with placebo.
Pharmacological Management
Cyclic administration of intravenous pamidronate reduces
the incidence of fracture and increases bone mineral
IV Pamidronate
density while reducing pain levels and increasing energy
levels

Oral bisphosphonates such as risedronate may have some

Risedronate effect in reducing fractures in patients with osteogenesis
imperfecta
Surgical Management
In patients with bowed long bones, intramedullary rod
Intramedullary rod replacement may improve weight bearing and, thus, enable
replacement the child to walk at an earlier stage than he or she might
otherwise

This procedure is reserved for cases with neurologic

Surgery for basilar
deficiencies, especially those caused by compression of
impression
brain stem
Nursing Nursing Intervention
diagnosis Present a safe environment: bed rails up, bed in a
down position, and important items close by.
Execute passive or active assistive ROM exercises
Impaired physical
to all extremities.
mobility related to Provide foam or flotation mattress, water or air
loss of integrity of mattress, or kinetic therapy bed, as necessary.
bone structures as Provide the patient with rest periods in between
manifested by activities. Consider energy-saving techniques.
limited range of Turn and position the patient every 2 hours or as
motion needed.
 Nursing Intervention
Nursing Provide a mouth care routine including
diagnosis toothbrushing at regular intervals with a soft-bristle
toothbrush and fluoride toothpaste.
Instruct the patient to rinse the mouth with warm
Impaired dentition
saline or an antiplaque mouth rinse.
related to genetic Assist the patient in performing oral hygiene every
predisposition as after a meal and as often as needed.
manifested by Advise avoiding high-sugar foods.
discoloration and Educate the patient about the importance of
breakage of teeth maintaining a healthy diet despite dentition
problems.
 Nursing Intervention
Nursing Consider the principles of proper body mechanics

diagnosis before any procedure, such as raising the head of

the bed and tucking elbows in.
Use assistive devices (pillows, gait belts, slider
Risk for injury boards) during transfer.
related to altered Validate the patient’s feelings and concerns related
mobility as to environmental risks.
manifested by Enhance safety through the use of medical alarm
systems
bone fragility
Coordinate with a physical therapist for
strengthening exercises and gait training to increase
mobility. Contact occupational therapists for
assistance with helping patients perform ADLs.
THANK YOU!