Orthopedic and Musculoskeletal Disorders in Childhood

I. LEARNING OBJECTIVES
a. Identify the normal findings for children on physical assessment of the
musculoskeletal system at various developmental stages.
b. Examine the signs and symptoms of selected orthopedic and musculoskeletal
disorders in the pediatric population.
c. Recognize the impact that genomics has on orthopedic disorders in infants and
children.
d. Formulate nursing diagnoses, nursing interventions, goals, and outcomes for
children with the selected disorders.
e. Incorporate findings of appropriate research articles in the plan of nursing care
for children with the above disorders.
f. Discuss primary preventions to decrease musculoskeletal trauma.
II. NORMAL DEVELOPMENT
a. Fetal development
i. Embryonic connective tissues -> cartilage -> calcifies to bone
b. Long bones increase in diameter by the apposition of new bone tissue around
the bone shaft
c. Long bones increase in length due to epiphyses
d. Smaller bones see ossification centers form in the calcified cartilage
e. Ligaments are stronger than bone until adolescence
f. Tanner Stage III sees increased bone rigidity and strength due to epiphyses
g. Bone growth completed around age 20; peak bone mass around age 35
III. PHYSICAL ASSESSMENT
a. Infants
i. General movement
1. Muscle strength
2. Use of extremities and joints
ii. Observe for head lag: weak neck muscle/floppy neck
iii. Check for torticollis: twisting of neck and head going off to one side
iv. Assessment of hips and legs
1. Good ROM
2. No restriction of abduction
3. Equal in length (use Galeazzi Test)
4. Equal thigh and gluteal folds
5. Firm femoral head in acetabulum – should
not be able to move femoral head out!
b. Toddler/Children
i. Toddler gait
1. Bow leggedness decreases, walking develops, muscles develop in
lower back and legs
2. Flat feet – arch to develop after walking for a few years
ii. Knock-knees normal until age 7
iii. Posture improves and becomes more graceful and balanced
iv. Evaluate muscle strength and joint mobility
v. Monitor spine for curvature
1. Thoracic spine has some kyphosis
2. Lumbar spine has some lordosis
c. Adolescent
i. Slumping shoulders and poor posture
ii. Check for scoliosis
IV. CHILDREN VS ADULT BONES
a. The child’s skeleton is still growing!
b. Bones are rapid healing when broken
c. Periosteum is thicker and more vascular – aids in more rapid bone growth and
repair
d. Stiffness is unusual
e. Bones are more porous -> absorbs more energy prior to breaking -> bending,
bowing of bone aka plastic deformation
V. DEVLOPMENTAL HIP DYSPLASIA

General • Affects females to males at a ratio of 8:1

• Most often occurs in first born
• ¼ cases have both hips involved
• Acetabular dysplasia or preluxation – formal head remains in the
acetabulum but the acetabulum is shallow and oblique
• Subluxation – femoral head remains in contact with the acetabulum,
but a stretched capsule and ligamentous tears cause the head of
femur to be partially displaced; largest %
• Dislocation – femoral head loses contact with acetabulum and is
displaced posteriorly and superiorly over the fibrocartilaginous rim
Pathophysiology • Maternal hormone secretion
o Increased maternal hormone = increased pelvic laxity
• Intrauterine position
o Breech position = increased incidence
• Genetics/heredity
• Cultural factors
Clinical • Restricted abduction • Delay in walking; limp or
Manifestations • Galeazzi Test – unequal knee waddling gait
height • Affected hip has shorter leg
• Asymmetric skin folds • Child may feel femur moving
• Wide perineum up and down in buttocks
• + Barlow and Ortolani signs • Prominent trochanter
• May not be apparent until child • Lordosis
begins to bear weight • Trendelenburg's sign
Diagnostic • 4 months and younger – ultrasound
Evaluation • After 4 months – x-ray
Management • Infants less than 1 year: full abduction in harness
• Toddler: gradual reduction by traction followed by plaster casting
• Older child: operative reduction is last resort
VI. CONGENITAL CLUB FOOT

General • May be unilateral or bilateral

• Males more frequently affected than females with a ration of 2:1
• Incidence 1-2:1000
• Increased incidence in families who already have one child with a
clubfoot
Management Non-Invasive Therapy
• Usually begin immediately, serial casting weekly, foot is manipulated
with each cast change
• Need to maintain correction with use of bi-valved casts, Denis
Browne shoes, or exercises
Surgical Therapy
• May be needed for most cases that do not respond to casting
• Correct bony deformity
• Lengthen or transplant tendons
• Release tight ligaments
VII. METATARUS ADDUCTUS

General • Very common

• Often related to intrauterine position
• Medial adduction of toes + forefoot
• Frequently associated with inversion and convexity of the lateral
border of the foot
• Often causes pigeon toed gait
Management • Surgical Therapy
• May be needed for most cases that do not respond to casting
• Correct bony deformity
• Lengthen or transplant tendons
• Release tight ligaments

VIII. DUCHENNE MUSCULAR DYSTROPHY

General • One of nine types of MD
• Characterized by
progressive muscle
weakness and wasting of
symmetrical groups of
skeletal muscles
• Symptom onset is early in
childhood
• Affects 1 in 3,500 males –
typically X-linked; rare in
females, usually a
mutation
• Dystrophin - a protein
product in skeletal muscle
- is absent

Clinical • Early onset – start seeing symptoms 3-5 years

Manifestations • Delay in walking and motor development
o Progresses to abnormal gait on a level surface
o Difficulty running, riding a bike, climbing stairs
• Frequent falls
• Lordosis
• Gower’s sign
• Muscles become enlarged from fatty infiltration and feel unusually
firm or woody on palpation
• Ultimately involves all voluntary muscles
• Loss of independent ambulation usually by 9-12 years
• Slowly progressive weakness during teen years
• Relentless progression until death from respiratory or cardiac failure
usually between 15-25 yrs old
Diagnostic Elevated creatinine phosphokinase (CPK) levels; muscle biopsy;
Evaluation electromyography; prenatal testing
Management • Community resources for housing
• Mobility – wheelchairs, vans
• PT, OT – educating parents
• Social aspect – school is important for this child
• Social aspect – respite care for parents
• Assistance with independence – modifying clothes
• Genetic counseling
Complications Contracture deformities
• Passive ROM, brace torso, frequent rest periods
 Atrophy of disuse
• Occurs quickly from inactivity
• PT even if limited for a few days
• 3 hours of ambulation a day to maintain muscle strength
Respiratory infections
• Prompt and vigorous antibiotic treatment
• PD&C, turning every 2 hours or as needed
Obesity
• Contributes to premature loss of ambulation
• Restricted physical activity can lead to boredom and eating
• Diversified recreational program
Cardiac manifestations
• Can lead to cardiac failure
• Medications may be helpful in early stages
• Digoxin, diuretics
When these patients are hospitalized, us nurses must prevent #1,2,3
complications. Prioritizing is important in this case.

IX. OSTEOGENESIS IMPERFECTA

General • = frequency across gender, race, and ethnicity

• About 35% of children born have no family history
• Often due to a new mutation and nothing parents did
• Eight types of OI (very mild-very severe)
Pathophysiology Majority of cases caused by a dominant mutation to type 1 collagen
genesis.
Clinical • Fragile bones that break easily
Manifestations • Muscle weakness, hearing loss, fatigue
• Joint laxity, curved bones, scoliosis, blue sclera, short stature
Management • Blood or skin biopsy to check amount of type 1 collagen
• Surgical insertion of rods to strengthen bones
• Meds to strengthen bones: biphosphate therapy
• Minimize fractures, maximize mobility and independence, promote
general health
Nursing • Safe exercise
• Adequate wheelchair/walker/braces
• Safe handling and protective positioning
• Do not change diapers by holding onto ankles
• Skin care
• Nutrition and healthy eating
• No smoking
X. LEGG-CALVE-PERTHES DISEASE

General • Unknown etiology

 • Affects males and females with a ratio of 4:1
• Most often occurs in children age 2-12 years with most cases
occurring between 4-8
Pathophysiology Aseptic necrosis of the femoral head because of insufficient blood
supply. This is a self-limiting disease but has the potential for structural
abnormality of the hip.
Clinical • Limping on affected side
Manifestations • Pain is increased with activity, decreased with rest
• Joint dysfunction-limited abduction and internal rotation of hip
• Hx of pain, limb and joint dysfunction – suspect dx
Diagnostic X-ray, bone scans, CT and MRI
Evaluation
Management • Prognosis best when younger child/early onset
o Earlier treatment, less invasive treatment
• Initial therapy: rest/activity restrictions
• Use of casts, braces: keeps femoral head abducted in acetabulum
• Surgery if conservative methods don’t work or to shorten duration
of immobilization
Nursing Family teaching
• Care and management of casts, braces, and post-op needs
Pre-operative
• CMS checks
• non weight bearing and bed rest
Post-operative
• CMS checks
• Observe dressing/surgical site
• Teaching and reinforcing post-surgical limitations

XI. SLIPPED CAPITAL FEMORAL EPIPHYSIS

General • Often seen before/during accelerated growth and onset of puberty

o Ages 10-16; median boy age, 13; median girl age, 12
• More commonly seen in obese children and boys
• Most often idiopathic; has been associated with endocrine
disorders, growth hormone therapy, renal osteodystrophy, and
radiotherapy
• Occurs in 2-10/100,000 in US, with bilateral involvement in up to
60% of cases
Pathophysiology • Head of femur displaces from neck of femur
o Prior to displacement the epiphyseal plate widens then
weakens
Clinical • Constant or intermittent pain in hip or groin
Manifestations o Radiates to knee or thigh, limp, loss of hip motion
 • Onset may be acute, chronic, or acute –on-chronic
• Lower extremity is held in a flexed, abducted, and externally rotated
position because of pain
• Attempts to move the limb are met with resistance
Management • Immediate non-weight bearing (NWB), no sitting, may ambulate
with crutches
• Surgical stabilization and correction (pinning with screws)
o More severe
o 6 months or more for immobilization
Nursing • Pre-operative
o NWB, no sitting, immediate eval with ortho, quick surgery,
CMS checks
• Post-operative
o Pain control
o CMS checks
o NWB for a while, touch down weight bearing (TDWB)
afterwards.
o After 6 months, may return to all contact activities 
o Teach proper use of crutches and importance of avoiding any
weight bearing on affected hip 

XII. OSTEOMYELITIS

General • Most frequently in children less than 10 years

• 2x as common in boys than girls
• Infectious process in the bone which can occur at any age
• Etiology: many organisms can cause osteomyelitis—some
relationship between age and organisms exists
o Neonates: Group B streptococci
o Older child: S.Aureus
o Since advent of Haemophilus influenza type B immunization
(HIB) in the late 1980s, this has become a less common
causative pathogen
Pathophysiology • Infected emboli from a focus of infection travels to the small arteries
in the bone metaphysis where they set up infectious process.
Infectious process leads to local bone destruction and abscess
formation, and bone necrosis
• Infants-more likely to have infection invade joint as blood vessels
cross the growth into the epiphysis and joint space
• Children-infection usually contained by the growth plate
Diagnostic • Increased SED rate or ESR, increased WBC, positive blood cultures
Evaluation • X-ray – radiographic signs, except for soft tissue swelling, are
frequently only evident after 2-3 weeks of infection
 • Bone biopsy may be needed if blood cultures, and x-rays are not
consistent with osteomyelitis
Management • Position for comfort, pain medication, monitor VS
• Antibiotics (IV/PO), antibiotic irrigations
• Possible surgical drainage with wound care

XIII. OSGOOD SCHLATTERS DISEASE

General • Most common in males, ages 10-16: active in sports

Pathophysiology • Pain and inflammation where patellar tendon attach to tibia
• Avulsion fractures can occur at distal portion of patellar tendon,
partial separation of tibial tubercle
o Separation cause by sudden or continuous stress on patellar
tendon during periods of rapid growth
Clinical • Pain which increases with activities and subsides with rest
Manifestations • May see temporary or permanent swelling at the area of tibial
tuberosity
Management • Rest
• Analgesics
• Self-limiting
• Resolved with closure of the growth plate

XIV. SCOLIOSIS
General • Lateral curvature of the spine
• Eventually causes cosmetic and physiologic alterations of the spine,
chest, pelvis,
• Occurs at any age; usually adolescent females
Pathophysiology 70% idiopathic, may be genetic, or may occur spontaneously or with
other deformity
Clinical Lateral curvature of the spine
Manifestations
Diagnostic •
Evaluation
Management • Observation with regular clinical evaluation and X-Rays
• Orthotic intervention with bracing
• Bracing and Exercise
o Moderate curves (25-45 degrees) in the growing child
o Goal of bracing is to slow the progression of the curve
o Boston brace
o Wilmington brace
o Exercises in and out of the brace
Surgical Fusion • Surgical intervention may be required for correction of severe
curves (45 degrees or more)
Preoperative
• X-Rays
• Blood work
• Blood donation
• Urine
Post-operative care
• Assessments: surgical site, CMS, neuro, pain, vital signs
• Respiratory care: cough, deep breathing, incentive spirometer
• Pain control – PCA to PO meds
• Progression to ambulation
o Lay flat, log-rolling, up to chair, ambulation
• Advance diet after POD 0
• May have additional lines/drains
o IV, arterial line, foley, JP drains, chest tube, NG tube
Discharge Teaching
• Pain control
• Ambulation and limitations
• Surgical site skin care
• Brace use
• Follow up visits