THE BASIC TYPES OF PEDIATRIC FRACTURES

Introduction
The anatomy and biomechanics of pediatric bone differ from that of adult bone, leading
to unique pediatric fracture patterns, healing mechanisms, and management. In
comparison to adult bone, pediatric bone is significantly less dense, more porous and
penetrated throughout by capillary channels. Pediatric bone has a lower modulus of
elasticity, lower bending strength, and lower mineral content. The low bending strength
induces more strain in pediatric bone than for the same stress on adult bone and the low
modulus of elasticity allows for greater energy absorption before failure. The increased
porosity of pediatric bone prevents propagation of fractures, thereby decreasing the
incidence of comminuted fractures. The pediatric periosteum is extremely strong and
thick, functioning in reduction and maintenance of fracture alignment and healing.

Anatomy of Pediatric Bone

Pediatric long bones have three main regions: epiphysis, physis and metaphysis.
- Epiphysis: each end of a long bone with associated joint cartilage.
- Physis ( growth plate): cartilage cells that create solid bone with growth.
- Metaphysis : wide area below the physis, closest to the diaphysis/shaft.
- Another key component of bone is the periosteum, which is a thick, nutrient layer that
wraps circumferentially around bones. It serves a major role in healing the outer layer
of bone.

Pediatric Fracture Patterns

The mechanisms of fracture change as children age. Younger children are more likely to
sustain a fracture while playing and falling on an outstretched arm. Older children tend to
injure themselves while playing sports, riding bicycles, and in motor vehicle accidents.
Also, because a child’s ligaments are stronger than those of an adult, forces which would
tend to cause a sprain in an older individual will be transmitted to the bone and cause a
fracture in a child. Caution should therefore be exercised when assessing a young child
diagnosed with a sprain.

1. Plastic Deformation
- A force produces microscopic failure on the tensile/convex side of bone which does
not propagate to the concave side. The bone is angulated beyond its elastic limit, but
the energy is insufficient to produce a fracture.
- No fracture line is visible radiographically.
- Unique to children
- Most commonly seen in the ulna, occasionally in the fibula.
- Bend in the ulna of < 20° in a 4 year old child should correct with growth.
2. Buckle fracture
- Compression failure of bone that usually occurs at the junction of the metaphysis and
the diaphysis
- Commonly seen in distal radius.
- Inherently stable
- Heal in 3-4 weeks with simple immobilization.

3. Greenstick fracture
- Bone is bent and the tensile/convex side of the bone fails.
- Fracture line does not propagate to the concave side of the bone, therefore showing
evidence of plastic deformation.
- If the bone undergoes plastic deformation, it is necessary to break the bone on the
concave side to restore normal alignment, as the plastic deformation recoils the bone
back to the deformed position.

4. Complete fracture
- Fracture completely propagates through the bone.
- Classified as spiral, transverse, or oblique, depending on the direction of the fracture
line.
- Spiral fractures:
- Created by a rotational force.
- Low-velocity injuries
- An intact periosteal hinge enables the orthopedic surgeon to reduce the fracture by
reversing the rotational injury.
- Oblique fractures:
- Occur diagonally across the diaphyseal bone at 30° to the axis of the bone.
- Unstable, therefore alignment is necessary.
- Fracture reduction is attempted by immobilizing the extremity while applying
traction.
- Transverse fractures:
- Created by a 3-point bending force.
- Easily reduced by using the intact periosteum from the concave side of the fracture
force.

5. Physeal fractures
- Fractures to the growth plate can be caused by i) crushing, ii) vascular compromise of
the physis or iii) bone growth bridging from the metaphysis to the bony portion of the
epiphysis.
- Damage to growth plate may result in progressive angular deformity, limb-length
discrepancy or joint incongruity.
- The distal radial physis is the most frequently injured physis.
 - Most physeal injuries heal within 3 weeks. This rapid healing provides a limited
window for reduction of deformity.
- Physeal injuries are classified by the Salter-Harris (SH) classification system, based
on the radiographic appearance of the fracture.

Salter-Harris (SH) Physeal Injury Classification

Type Characteristics
I Separation through the physis, usually through areas of hypertrophic and
degenerating cartilage cell columns.
II
Fracture through a portion of the physis that extends through the metaphyses.

III Fracture through a portion of the physis that extends through the epiphysis
and into the joint.
IV Fracture across the metaphysis, physis and epiphysis.
V Crush injury to the physis.

SH
Classification from I - V
Image Source: Kliegman RM et Al. Nelson Essentials of Pediatrics. Saunders; 2007, p
2838

Differences between Pediatric and Adult Fracture Healing

1. Fracture Remodeling
- Process that occurs over time as a child’s bone reshapes itself to an anatomic
position.
- The amount of remaining bone growth provides the basis for remodeling. Thus, the
younger the child, the greater remodeling potential, and the less important reduction
accuracy is.
- Occurs over several months following injury.
- Factors affecting amount of remodeling:
- Age: younger children have greater remodeling potential.
 - Location: fractures adjacent to a physis undergo greatest amount of remodeling.
- Degree of deformity
- Plane of deformity with respect to adjacent joint: remodeling occurs more readily in
the plane of a joint than with deformity not in the plane of the joint.
2. Overgrowth
- Caused by physeal stimulation from the hyperemia associated with fracture healing.
- Prominent in long bones (ex. femur).
- Growth acceleration is usually present for 6 months to 1 year following injury.
- Does not present a continued progressive overgrowth unless complicated by a rare
arteriovenous malformation.
- > 10 years of age, overgrowth is less of a problem and anatomic alignment is
recommended.

3. Progressive Deformity
- Injuries to the physis can be complicated by progressive deformities with growth.
- The most common cause is complete or partial closure of growth plates.
- Deformities can include angular deformity, shortening of bone, or both.
- The magnitude of deformity depends on the physis involved and the amount of
growth remaining.

4. Rapid Healing
- Pediatric fractures heal more quickly than adult fractures due to children’s growth
potential and a thicker, more active periosteum.
→ the periosteum contributes the largest part of new bone formation around a
fracture.
- As children reach their growth potential, in adolescence and early adulthood, the
rate of healing slows to that of an adult.
- There is one downside to rapid healing, however; refractures.

Assessment
As with most problems in medicine, the initial approach to fractures includes a thorough
history and physical exam.

Practitioners must keep in mind that a young child may not be able to describe bony pain
or the circumstances of injury. Hence, toddlers and non-verbal children may simply
present with the refusal to weight bear or move the injured area, irritability, or due to a
caregiver’s observation of a new deformity.

Questions to include in the history of a child presenting with a suspected fracture include:
- Characterization of the Pain and Presenting Symptom:
- Location: is the pain localized to a particular region or does it involve a larger area?
 - Intensity: use a pain scale from 1-10.
- Quality of pain
- Onset of pain
- Duration of pain
- Progress of pain: is it static, increasing or decreasing?
- Is the pain radiating?
- Any aggravating or alleviating factors?
- Other considerations :
- Indicators of compromised neurovascular status (e.g.: change in or loss of
sensation, cold, pale, paralyzed limb)
- Mechanism of injury
- Possibility of non-accidental injury or child abuse, particularly in a child with
limited physical mobility, with an injury out of proportion to the mechanism, with
multiple injuries, or with a suspicious mechanism of injury (e.g.: a 2 month old
baby who developmentally cannot roll, but who “rolled off the changing table”)
- Rare possibility of underlying bone abnormality (family history of fractures, bone
or collagen disorders, prior fractures, mechanism out of proportion to injury).

Physical examination should include assessment of the joint in question and, whenever
non-accidental injury may be a possibility, a screening exam of the entire skeleton,
fundoscopy, as well as an abdominal and cutaneous appraisal for other signs of trauma.
One should always examine a joint above and below the symptomatic one. Important
features to include in the examination of all fractures are:
- Inspection
- Patient movement
- Discrepancy in limb length
- Palpation
- Assessment of local temperature, warmth, tenderness
- Existence of swelling or mass
- Tightness, spasticity, contracture
- Bone or joint deformity
- Evaluate anatomic axis of limb
- Range of Motion
- Assess and record the active and passive range of motion of the joint
- Neurovascular assessment of the injured area
- Inspect the color of the limb
- Palpate for pulses, and to elicit appropriate sensation to touch, temperature
- If possible, elicit strength in neighboring muscle groups
Finally, plain radiographs are the first step in evaluating most musculoskeletal disorders.
When indicated, advanced imaging may include nuclear bone sans, ultrasonography, CT,
MRI and PET scans.

Common Causes of Pediatric Fractures

Cause Pathology Presentation Investigation
Child abuse - 30-50% of children seen by - Femur - Diagnosis requires
orthopedic surgeons are the - Distal femoral multiple factors:
victims of non-accidental metaphyseal history, clinical
corner presentation,
injury behavioural and
- Posterior rib
- Scapular spinous physical observation.
process
- Proximal
humeral
Cause Pathology Presentation Investigation
Birth Injury - Potential complication of - Clavicular - X Ray
forceps delivery fractures - Cephalohematoma
- Complication of - Humeral fractures at the site of injury
cephalopelvic disproportion - Femoral fractures and calcification
and shoulder dystocias around fracture
will help indicate
if fracture
occurred during
birth or after.
Rickets - Lack of vitamin D and - No specific - Measure 25-
metabolite disturbances → fracture pattern hydroxyvitamin D
defective mineralization of - May present with levels
bone matrix bowed limbs,
- Similar to osteomalacia in “rickety rosary”,
adulthood craniotabes
 Osteomyelitis - Acute or chronic infection of - Long bones - Upon suspicion,
bone → lesions of the immediate referral
metaphyses to orthopedic
surgeon for body
fluid tests,
aspiration of bone
and imaging
Copper - Copper deficiency → - No specific - Slit-lamp
deficiency impaired bone calcification fracture pattern examination for
Kayser-Fleischer
rings
- Serum
ceruloplasmin and
24-h urinary copper
excretion
- Liver biopsy

Management
Although primary prevention of fractures is ideal, fractures remain a common
presentation in pediatrics. Due to their immature, growing bones, care providers must
remain vigilant regarding potential fractures, as they may present with subtle signs and
symptoms. A high index of suspicion and appropriate treatment of orthopedic injuries can
prevent the long-
Definition

Osteopenia, a condition characterised by a reduction in bone mineral content, is a

common disease of preterm babies between the tenth and sixteenth week of life.
Prematurely born infants are deprived of the intrauterine supply of minerals affecting
bone mineralization.

Causes of MBD

The aetiology is multifactorial:

Fetal:

The strongest predictor for the development of biochemical and radiological MBD
is premature or low birth weight delivery

Infant:

Decreased mineral intake:

Preterm delivery <32 weeks gestation,

Very low birth weight osteopenia incidence up to 30% in infants <1500g (75% in

infants <800g),

Prolonged total parenteral nutrition,

Delayed enteral nutrition,

Failure to provide multicomponent of mineral fortification of human milk feeds,

Bronchopulmonary dysplasia.

Increased mineral excretion

 Frusemide increases urinary calcium excretion,

Clinical manifestations

Most premature infants born before 30 weeks have some degree of osteopenia, but will not have any
physical symptoms.

Infants with severe osteopenia may have decreased movement or swelling of an arm or leg due to an
unknown fracture.
Screening, monitoring and diagnosing

 Biochemical tests of osteopenia of prematurity are not definitive.

 Serum phosphate: suspicious if < 1.5, likely if < 1.1 mmol/L.

 The alkaline phosphatase (ALP) is more elevated than usual for preterm babies.
Levels above 600 or 800 IU/L are quoted. However, the ALP only rises high if
there is bone turnover. If the condition is very severe the ALP may not be very
high.

 The calcium level may be normal, elevated or even low.

 A bone x-ray will show very poor mineralisation and as the infants grow can
show changes of rickets or fractures.

 An abnormal calcium to phosphate (Ca++ : PO4 ratio in the urine. In normal

infants it is less than 1.0 (both measured in mmol/L))

Prevention and treatment

Optimizing enteral intake of calcium and phosphorus by adding powdered fortifier to

breast milk or using a formula made for premature infants.

Switching from Lasix to an anticalciuric diuretic, such as Chlorothiazide IV or PO as

soon as medically possible.

Limiting the use of Aminophylline and Dexamethazone therapy by switching to

Albuterol and weaning steroids as soon as medically possible.

Maintaining vitamin D intake of 400-IU per day.

Physical therapy (i.e., range-of-motion exercises of the upper and lower extremities)
to enhance bone mineralization and bone mineral content in VLBW infants in stable
condition.

Cautious handling in infants with nutritional rickets to avoid bone fractures.

Early minimal enteric feeds with human milk may increase bone mineral content in
preterm infants , although clinical benefits are not conclusive
Provision of early calcium and phosphate content

OSTEOMYELITIS
Introduction
The term osteomyelitis encompasses a broad group of infectious diseases characterized by
infection of the bone and/or bone marrow. The pathogenesis of these diseases can follow
acute, subacute or chronic courses and involves a range of contributory host and pathogen
factors.

Definition

Osteomyelitis is an inflammatory bone disorder caused by infection, leading to necrosis and

destruction of bone.

CLASSIFICATION

Acute osteomyelitis is an infection characterized by edema, locally decreased blood supply

and pus formation. The term is often used interchangeably with hematogenous osteomyelitis
and refers to osteomyelitis before osteonecrosis has occurred

Acute osteomyelitis can develop after bacteremia, mostly in prepubertal children and in
elderly patients.

Untreated or due to treatment failure, the infection can progress to a more chronic phase.

Chronic osteomyelitis is defined as bone infection in the presence of osteonecrosis. It is

associated with formation of a large area of devascularized dead bone, a sequestrum
AETIOLOGY
Staph. Pyogenes
Salmonella
Escherichia coli .
PREDISPOSING FACTORS
It occurs mainly in children.
Poor living conditions predispose to it, and there may be an obvious primary focus of
infection, such as a boil, sore throat.
There is often a history of preceding injury and some patients may develop infection in a
subperiosteal haematoma.
Pathology
The infection usually starts in the vascular metaphysis of a long bone or in the centre of a
short bone.
Common sites are the lower end of the femur and upper end of the tibia, either end of the
humerus, radius and ulna, and the vertebral bodies. Because of the confi ned space and
tension, tissue necrosis occurs readily and an abscess may form within the bone. The pus
usually breaks out under the periosteum, stripping it and eventually penetrating to a point on
the surface.
Large areas of bone may become necrotic, making penetration by antibiotics diffi cult and
forming ‘ sequestra ’ or hidden areas of dead and infected bone. These may act as foreign
bodies.

Clinical features of acute osteomyelitis.

● Fever — acute onset with malaise
● Pain — localized to metaphysis classically
● Swelling — often associated with joint stiffness
● Tenderness — localized
● Oedema and pus (late sign) — pus may break through the periosteum, causing a
fluctuant mass maintaining the sepsis in chronic form.
● If the centre of the shaft becomes infected, the nutrient artery may thrombose, leading
to sequestration of the whole shaft. In this case, if the patient survives, the sequestrated
shaft may become surrounded by a shell of new bone, with holes through which pus may
 continue to fi nd its way to the surface, forming persistent sinuses. This shell is called an
involucrum. With improved management this complication is now rarely seen.
● Swelling of nearby joints is usually due to a ‘ sympathetic ’ effusion. Occasionally,
especially if the metaphysis is intracapsular, the joint itself may become infected.
Diagnosis
1. Blood culture
2. Xray
3. Proper physical examination
4. erythrocyte sedimentation
Management
Urgent treatment is required if the condition is suspected and includes:
Broad - spectrum antibiotics
Initially these are often given parenterally.
The antibiotics usually control the septicaemia and fever quite quickly.
If pus is suspected, surgical drainage is necessary. Pus may break through the periosteum or
this may need to be incised.
Following drainage, antibiotics can be continued or changed according to the culture result
(broad - spectrum agents can be switched to a more narrow - spectrum agent). If the
condition then settles, a total of 6 weeks ’ antibiotic therapy is usually recommended.

Diagnosis
Initial Investigations
• FBC
• CRP (+/-ESR)
• Blood culture
• X-ray (mandatory to exclude fracture, remember x-ray changes are a late sign).

OSTEOGENESIS IMPERFECTA
Definition/Description
Osteogenesis imperfecta (OI) is a rare genetic disorder of the synthesis of collagen that
affects bone and connective tissue that can also be referred to as brittle bone disease.
OI can occur by both inheritance and spontaneous genetic mutation and has been linked
to over 150 genetic mutations that all take effect on the genes COL1A1 and COL1A2. These are
the genes that make up type I collagen.
The mutation can either cause collagen production that is too low, or cause abnormal
polypeptide chains that are unable to properly form type I collagen.

Aetiology
Osteogenesis imperfecta is a genetic disorder that can be caused by inheritance from a parent
with OI, or a random genetic mutation.
The genetic disorder in most cases is passed from one of the parents to the child through
autosomal dominant inheritance.
This means that one copy of the mutated gene in each cell is enough to cause the osteogenesis
imperfecta.
This type of inheritance is usually the cause for most people with type I or type IV OI. Random
mutation of the COL1A1 or COL1A2 gene may also occur.
These children have no family history of OI and tend to have either type II or type III
osteogenesis imperfecta, which are more serious. The least common way that osteogenesis
imperfecta is caused by autosomal recessive inheritance. This is when each cell has two copies
of the mutated gene. This cause occurs by two people that are carriers of the mutated gene
passing one copy each to a child. This cause usually results in a child with type III OI.

Types

There are four primary types of osteogenesis imperfecta that are described by the Sillence
Classification of Osteogenesis Imperfecta.
"Sillence Classification of Osteogenesis Imperfecta

Type I (most common form)

 Mildest form of OI
 Mild to moderate fragility without deformity
 Most fractures occur before puberty
 Associated with blue sclerae, triangular face, hearing loss (beginning in twenties or
thirties), easy bruising

Type II
 Most severe form of OI (perinatal lethal)
 Stillbirth or death during infancy or early childhood
 Extreme fragility of connective tissue
 Multiple in utero fractures
 Usually intrauterine growth retardation
 Severe bone deformity
 Soft, large cranium
 Micromelia: long bones crumpled and bowed; ribs beaded 
Type III
 Moderately Severe                                                    
 Progressive deformities
  Scoliosis
 Triangular face, large skull
 Severe osteoporosis
 Severe fragility of bones; usually in utero fractures
 Factures heal with deformity and bowing
 Associated with tinted sclerae (blue, purple, or grey)
 Extremely short stature
 Usually wheelchair bound by teenage years

Type IV
 Variable but usually milder course; normal or near-normal lifespan
 Mild to moderate skeletal fragility and osteoporosis (more severe than type I)
 Associated with bowing of long bones
 Barrel-shaped rib cage
 Bones fracture easily before puberty; some children improve at puberty
 Light or normal sclerae; may or may not have moderately short stature and joint
hyperextensibility.

CHARACTERISTICS/CLINICAL PRESENTATION
Due to the different classifications, a patient with osteogenesis imperfecta can present anywhere
from appearing normal with fractures that occur occasionally, to someone very small in stature
with deformities to both the spine and long bones throughout the body. The clinical presentation
of patients with OI is easier to picture when broken down into the four primary classifications.
Type I
  Due to only 50% of the collagen being produced, the patient's bones are predisposed to
fracture. Most fractures in this classification occur before the child reaches puberty.
 Lax Joints
 Low muscle tone
 Tinted sclerae that may appear to be slightly blue, grey, or purple
 Possible scoliosis
 Stature should not be affected much, if at all
 Possible hearing loss that usually occurs in the third or fourth decade of life
 Triangular shaped face
 Very mild to no bony deformities
 Teeth may be brittle and easily broken.

Type II
 Due to only 20% of the normal amount of collagen being produced due to malformation,
this is the most severe type of OI.
 Usually results in stillbirth or death occurring in the early years of childhood. There have
been a few people with type II OI that have survived into young adulthood.
 Respiratory problems that can lead to death

 Severe bone deformities.

 Multiple in utero fractures
 Soft, large cranium
 Micromelia: long bones that are crumpled and bowed; ribs beaded.
Type III
 Very short stature
 Triangular face
 Easily fractured bones
 Scoliosis
 Tinted sclerae that may appear to be slightly blue, grey, or purple
 Barrel-shaped chest
  Teeth may be brittle and easily broken
 Possibility of problems with respiration
 Possible hearing loss
 Increased joint laxity.
 "Severe osteoporosis
 Fractures heal with deformity and bowing
 Large skull
 Usually in utero fractures
 Usually wheelchair bound by teenage years
Type IV
 More severe than type I and less severe than type III
 Short stature that is not as extreme as type III
 Barrel shaped chest
 Scoliosis
 Sclera are normal
 Triangular shaped face
 Teeth may be brittle and fracture easily
 Skin may be thin and smooth
 Possible hearing loss
 Bruises easily
 High pitched voice
 May perspire excessively
 "Mild to moderate skeletal fragility and osteoporosis
 Associated bowing of long bones
 Bones fracture easily before puberty; some children improve at puberty
 Joint Hyperextensibility.

Systemic Involvement
Gastrointestinal
 Constipation that may be caused due to pelvic asymetry in more serious forms of OI.
 Difficulties swallowing solid foods in more serious forms of OI.

Cardiac
 Heart valve problems such as aortic valve insufficiency, aortic aneurysm, mitral valve
regurgitation, and mitral valve prolapse.

Respiratory
 Restrictive pulmonary disorder is common in people with severe forms of OI.
 Pulmonary complications due to rib fractures, weakness of the muscles in the chest wall,
chronic bronchitis, pneumonia, asthma and heart valve disorders.

Neurological
  Basilar invagination of the base of the skull may occur in OI patients in the adult years
and cause complications with the brain stem.

Renal
 Kidney stones have at times been associated with osteogenesis imperfecta. [7]

Integumentary
 Patients with OI may have thin skin.
 Excessive diaphoresis may be apparent.

Metabolic
 Elevated serum pyrophoshate
 Decreased platelet aggregation

Auditory
 Hearing loss/impairment is a common occurrence in patients with OI. This can occur
from deformity of the bony auditory structures. This can also be caused by a fracture of
the stapes bone.

Vision
 Sclera may be blue, purple, or grey tinted.
 Vision loss can occur.

Musculoskeletal
 Muscular atrophy
 Joint hypermobility
 Multiple fractures

MANAGEMENT

Medications
Current Pharmalogical Treatment
  Growth Hormone - This is used to improve bone metabolism and to improve growth for
statural purposes.
 Bisphosphonates - These are used to "promote bone mineral accretion while at the same
time reducing bone turnover.

Diagnostic Tests/Lab Tests/Lab Values

The diagnosis of osteogenesis imperfecta generally begins with the physician's findings during
an examination.
Physicians may find evidence of skeletal deformities accompanied by multiple past fractures
that have healed using x-rays or bone scans.
Wormian bodies, which are irregularly shaped islands of bone found in the wide sutures on
skull radiographs of patients with OI, may also be present.

Other ways to help confirm the diagnosis of OI include

 history of osteogenesis imperfecta in the family
 a skin biopsy
 DNA testing,
 ultrasound imaging before the child is born.

Although OI is not always passed down from the parents, this would help the physician come to
a conclusion because if one of the parents have OI, they have a 50% chance of passing this
along to their child.
A skin biopsy is used to determine if there is enough type I collagen or if the collagen is
abnormal. DNA testing is accomplished by means of a blood test that is examined to locate the
genetic mutation.
Ultrasound imaging can be used to help diagnose OI before the child is born. The more severe
the type of OI, the earlier ultrasound imaging can detect the fractures and deformities. By 14-16
weeks, type II OI is usually possible to diagnose. Type III OI is possible to diagnose around 16-
18 weeks gestation. Types I and IV are generally not diagnosed with ultrasound.
Medical Management (current best evidence)
The current best evidence for the medical management of osteogenesis imperfecta can depend
on the form of OI and the severity its effect has been on the patient.

With multiple fractures to long bones causing deformity of the bones, it can be impossible in
some patients to achieve any weight bearing for ambulation.

To best help with the gross deformation of the structure of long bones there is a surgical
intervention that is called rodding. This procedure is most often performed in the femurs and
tibiae. Rodding consist of realigning the long bone and inserting an intermedullary metal rod.
This will promote the bone to hear to appear more like a normally shaped long bone and will
improve the chances of the child to be able to functionally bear weight and improve chances of
self ambulation.[5] Rodding does not help to improve the fragility of the long bones and further
medical treatment is still needed.

Bisphosphonates such as Pamidronate are used to decrease the amount of bone resorption.
Studies have found that children with OI that are given Pamidronate intravenously every one to
four months have shown decreases in bone pain, an increased sense of well being, and rise in
vertebral bone mass. It has been found that the child's vertebrae can regain a normal shape and
size.

With research continuing in the areas of allogenic bone marrow transplantation there has been
positive findings showing increased bone mineral content and new bone formation. There is
also research being done in the area of gene therapy.

Physical Therapy Management.

Physical therapy management for osteogenesis imperfecta can help prevent disuse atrophy of
muscle and disuse loss of bone mass. It has also been found that physical therapy can strengthen
muscles and even increase bone density in patients with OI.

Physical therapy may also help cardiovascular fitness, mental alertness, improved sleep,
and weight control, ability to fight infection, decrease the chance of certain cancers, and
improve activities of daily living.

Physical therapy should begin as soon as the child begins to show signs of muscular
weakness or motor skills are being accomplished later than other children of the same age.
Physical therapy intervention should include light resistance exercises to strengthen the hips and
the core. A combination of hip extension, hip abduction, spinal musculature strengthening, and
an aquatic exercise program twice a week has been found to increase the patient's ability to
achieve an upright position and ambulate.

Positioning is important in the care of children with OI. Neutral positioning of the head,
trunk, and extremities with the hips in extension is the correct positioning. In more severe cases
the prone position should be avoided.
 Physical therapy management may also include the selection and adaptation of
ambulation devices that are safe and beneficial to the patients. Adaptive equipment, even
powered wheelchairs, may be essential for the child to have as much independence as possible. 

Dietary Management
Many resources have stated the importance of nutrition for patients with osteogenesis
imperfecta. Patients with OI need to get adequate amounts of calcium, vitamin D, and vitamin
C.
Calcium is needed to develop peak bone mass and help prevent bone loss. Vitamin D is
responsible for helping the body to absorb calcium and may also be involved proper functioning
of the immune system.
Low levels of Vitamin D may also have a role in chronic pain. Vitamin C is involved in the
production of healthy connective tissues, and assists in the healing of wounds and fractures
which is very important for patients with OI.
Calcium is found in dairy products and other foods such as broccoli, kale, dried beans, nuts, and
soy products.
Vitamin D is mainly absorbed from sunlight through the skin but can also be found in
fortified foods and dietary supplements. Vitamin C is found in many fruits and Vegetables such
as citrus fruits, cantaloupe, strawberries, sweet potatoes, tomatoes, and bell peppers.