Pediatric Primary Care: Practice Guidelines for Nurses, 2nd Ed.

CHAPTER 30

Musculoskeletal Disorders

Miki M. Patterson

I. INJURIES: SPRAIN, STRAIN, OVERUSE

Ankle sprain, 845

Ligament tear, 848.9

 

Dislocation, 839.8

Sprain, 848.9

 

Finger sprain, 842.1

Wrist sprain, 842

 

Fracture, 829

   

A. Etiology.

1. Damage or disruption to tendon (attaches muscle to bone), ligament (attaches bone to bone), from overstretching, exertion, repetitive application of excessive forces.

B. Occurrence.

1. Wrist, finger, ankle sprains are common among children.

C. Clinical manifestations.

1. Limp or pain with extremity or joint use.

2. Felt tearing or heard a “pop” during activity or with trauma.

D. Physical findings.

1. Pain, tenderness to palpation, swelling, discoloration (ecchymosis or erythema).

E. Diagnostic tests.

1. Radiograph in two planes to ensure no fracture and to assess bony relationships. May need views of unaffected side to compare ossification centers and normal alignment.

2. Physical exam: stress joints to varus, valgus, anterior, posterior. If a “give” is felt (e.g., at a knee or ankle joint “opening up”), refer patient to orthopedist. Palpation over physis should be pain free.

F. Differential diagnosis.

Dislocation, 839.8

  Ligament tear, 848.9

 

Fracture, 829

  Neurologic deficit, 781.99

 

1. Fracture, dislocation, ligament tears, neurologic deficit, vascular condition.

G. Treatment.

1. Protect, rest, ice, compression, elevation (PRICE) and medication for pain as needed:

a. Protect: with splint/brace or relief of weight bearing with crutches.

b. Rest: do not use extremity.

c. Ice: apply ice immediately for 10–20 minutes then every 3–4 hours for the first 24–48 hours.

d. Compression: with ACE wrap; do not pull tightly when wrapping; compression will decrease amount of blood allowed to seep from injured tissues and decrease range of motion at joint.

e. Elevation: above level of heart will decrease swelling accumulating from gravity.

f. Identify and alter factors that contributed to overuse.

g. May continue to do activities that do not cause pain.

h. Pain relievers such as ibuprofen or narcotic, if needed.

H. Follow up.

1. Return in 1 week to ensure resolution of majority of pain, swelling, and return of function.

2. Pain and swelling after 2 weeks requires further workup.

I. Complications.

Compartment syndrome, 958.8

 

Skin abrasion, 919

 

1. Missed fracture.

2. Caution: Salter fractures (through the growth plate) may not be visible on X-ray; if physis is tender, treat as fracture (Figure 30–1).

3. Compartment syndrome.

4. Skin breakdown (presents as burning sensation under brace or splint; results from ischemia of tissue; pressure should be relieved immediately).

J. Education.

1. Teach family to call immediately for any burning or worsening of pain, neurovascular changes such as paresthesias (numbness or tingling), pallor, paralysis, pulselessness, cyanosis–these 4 Ps are signs of compartment syndrome.

a. Considered a surgical emergency.

b. Most important: worsening pain and tightness.

c. Compartment syndrome is accumulation of pressure in tissues, not relieved with elevation.

d. Most common areas: calves, forearms, hands, feet.

Figure 30–1 Salter I fracture. Note the increased width compared to the distal tibial physis.

images

Source: Courtesy of Miki Patterson.

2. Range of motion, stretching should be pain free before beginning strengthening rehabilitation exercises then gradual return to regular activity.

II. INJURIES: FRACTURE, DISLOCATION

Dislocation, 839.8

  Fracture, 829

 

Ecchymosis, 459.89

  Point skin tenderness, 782

 

Erythema, 695.9

   

A. Etiology.

1. Damage/disruption to bone or joint, respectively, from trauma, exertion, overuse.

2. Most common causes: child abuse and neglect, sports, falls, motor vehicle or pedestrian/bicycle events.

B. Occurrence.

1. All age groups can be affected.

2. Fractures are most common presentation of child abuse; 70% of fractures in children younger than 6 months are inflicted.

3. Fractures suggestive of nonaccidental trauma in children: metaphyseal, rib (seen in 5–20% of abused children), scapular/distal clavicle/night stick (midshaft ulna), vertebral fracture or subluxation, fingers in nonambulating child, humerus (except supracondylar) in those younger than 3 years of age, bilateral/multiple fractures in different stages of healing as well as complex skull.

C. Clinical manifestations.

1. Felt tearing or heard “pop” or “crack.”

2. Most affect function.

3. Findings suspect for abuse:

a. Fracture in child younger than 1 year of age.

b. Unknown or unwitnessed injury.

c. Delay in seeking medical attention.

d. Changing story of how injury occurred.

e. Fracture does not fit mechanism described (e.g., twisting an extremity will result in spiral fracture, whereas direct blow produces transverse fracture).

D. Physical findings.

1. Pain, point tenderness, swelling, ecchymosis or erythema, loss of function, obvious deformity.

E. Diagnostic tests.

1. Radiographs in two planes: AP and lateral or both obliques.

2. May require computed tomography (CT) scan or MRI for complex injuries (i.e., pelvis or spine).

F. Differential diagnosis.

Sprain, 848.9

1. Sprain.

G. Treatment.

1. Protect with immobilization/splinting, compression, ice, elevation.

2. Do not use extremity.

3. Pain medication (typically narcotic) such as acetaminophen (Tylenol) with codeine at 1 mg/kg of body weight every 4–6 hours for small children or hydrocodone (Vicodin), oxycodone (Percocet), or morphine by weight for those > 100 pounds.

4. Dislocation and displaced fractures refer stat to orthopedist. Oral medication should not be used if surgical intervention is an imminent possibility.

H. Follow up.

1. Should be per orthopedist.

2. Many will not allow use of extremity for a period of time while healing.

3. Muscles will spasm around fracture to try to pull bone ends together for healing.

4. Fractures without fixation move for 10–14 days after injury while granulation occurs (even in casts).

5. Frequent X-rays may be needed to ensure alignment of fractures.

6. In 2–6 weeks: callus develops, bone ends become “sticky,” pain is reduced.

7. Consolidation begins at 3 weeks in infants, may take 3–6 months in older children, adults.

8. Weight bearing, casting, splinting, bracing, or full use are all related to fracture configuration, healing, patient specifics.

9. Remodeling of bone that occurs in children younger than 8 years of age allows acceptance of angulated fractures.

10. Increased circulation to fractured bone causes some overgrowth (basis for 1-cm overlap of fractured femurs in young children).

I. Complications.

Compartment syndrome, 958.8

 

Loss of alignment, 781.2

 

Skin abrasion, 919

 

1. Compartment syndrome.

2. Loss of alignment.

3. Shortening, angulation, delayed or nonunion of fracture.

4. Skin breakdown.

5. Neurovascular problems.

6. Infection.

7. Missed abuse.

J. Education.

1. Same as for sprains.

2. Family should seek medical attention for neurovascular changes or pain inside cast/splint/brace.

III. BACK PAIN

Scoliosis, 737.3

 

Back pain, 724.5

 

A. Etiology.

1. See Differential Diagnosis (below).

B. Occurrence.

1. Most common in preadolescent and adolescent.

C. Clinical manifestations.

1. Complaint of back pain, sometimes night pain (red flag), with/without numbness or tingling.

D. Physical findings.

1. May or may not have:

a. Deformity of spine.

b. Pain with motion.

c. Positive straight leg raise sign.

d. Tight hamstrings (unable to sit upright with legs extended straight out in front).

e. Neurologic changes or skin lesions.

E. Diagnostic tests.

1. Radiographs: AP and lateral thoracolumbar and/or lumbosacral spine.

2. Other testing as exam or history indicates (e.g., bone scan, MRI, labs: complete blood count (CBC) with differential, erythrocyte sedimentation rate [ESR], antinuclear antibodies [ANA], rheumatoid factor, or human leukocyte antigen B27 [HLA-B27]).

F. Differential diagnosis.

Ankylosis spondylitis, 720

Psoriatic arthritis, 696

 

Degenerative disk disease, 722.6

Reiter syndrome, 099.3

 

Discitis, 722.9

Scheuermann's kyphosis, 737.1

 

Inflammatory bowel disease, 569.9

Scoliosis, 737.3

 

Fracture, back, 805.8

Sickle cell crisis, 282.6

 

Kidney infection, 590.9

Spondylolisthesis, 756.12

 

Menstrual cramping, 625.3

Spondylolysis, 756.11

 

Osteoma, 213.9

   

1. Overuse (heavy backpacks).

Figure 30–2 (a) Spondylolisthesis (slipped forward) L-5 on S-1 with (b) spondylolysis (fractured).

images

Source: Courtesy of Miki Patterson.

2. Fracture, spondylolysis (defect or separation of pars interarticularis), and spondylolisthesis (anterior slippage of vertebral body) typically occur at L-5 (Figure 30–2).

3. Scheuermann's kyphosis (anterior wedging > 5° of 3 or more adjacent vertebrae).

4. Scoliosis (see later discussion).

5. Degenerative disk disease, infection, discitis.

6. Inflammatory conditions, such as ankylosis spondylitis, psoriatic arthritis, inflammatory bowel disease, Reiter's syndrome (morning stiffness is hallmark sign).

7. Neoplastic such as osteoid osteoma (hallmark sign: night pain or constant pain independent of motion).

8. Other: sickle cell crisis, functional illness, referred pain such as kidney infection or menstrual cramping.

G. Treatment.

1. Depends on diagnosis: rest, nonsteroidal anti-inflammatory drugs (NSAIDs), stretching, abdominal strengthening, proper posture and backpack use, or referral to orthopedist.

H. Follow up.

1. Symptoms should improve in 2 weeks for overuse or strains.

I. Complications.

1. Missed diagnosis (see Differential Diagnosis).

J. Education.

1. Demonstrate exercises to help ensure that they are done correctly.

2. Work with family on medication schedule.

3. If symptoms persist or new symptoms occur, call healthcare provider.

IV. SCOLIOSIS

Embryonic malformation, 759.9

A. Abnormal lateral curvature of spine, typically with vertebral rotation.

B. Etiology.

1. Idiopathic: 90% (most common), unknown etiology, familiar pattern has been noted.

C. Occurrence.

1. Idiopathic: 3–5% in adolescents screened; males = females.

2. 0.6% require treatment; however, females are treated more often (1%) than males (0.1%).

D. Clinical manifestations.

1. Does not typically cause back pain.

E. Physical findings.

1. Difficulty with fitting clothes.

2. S- or C-shape curve of spine.

3. Prominent: scapular, ribcage, paraspinal musculature (especially on forward bend test) or breast.

4. Asymmetric waistline or shoulder level.

5. Plumb line dropped from C-7 does not correlate with gluteal crease.

F. Diagnostic tests.

1. Inspection with minimal clothing.

2. Radiographs: scoliosis series, which is standing postero-anterior (PA) and lateral views of entire spine on one cassette.

G. Differential diagnosis.

Cerebral palsy, 343.9

Neurofi bromatosis, 237.7

 

Emotional disturbance, 313.9

Polio, 045.1

 

Muscular dystrophy, 359.1

Spina bifi da, 741.9

 

Myopathies, 359.9

Vertebra fracture, 805.8

 

1. Congenital: embryonic malformation.

2. Paralytic: polio, muscular dystrophy, cerebral palsy, spina bifida, myopathies, neurofibromatosis.

3. Traumatic: fracture of vertebrae.

4. Hysterical: rare, nonstructural, result of emotional disturbance.

H. Treatment.

1. Orthopedic referral all curves > 10°.

2. Orthopedic treatment for curves 10–20° observation.

3. Curves 20–40°: bracing (controversial) to prevent further curvature.

4. Curves > 40°: surgical intervention, posterior spinal fusion with segmental instrumentation occasionally requires anterior release.

I. Follow up.

1. Per orthopedics: until skeletal maturity (about 1 year after menstruation for girls).

J. Complications.

Lumbar back pain, 724.2

1. Progressive untreated scoliosis may result in significant deformity, cardiopulmonary compromise, debilitating lumbar back pain.

K. Education.

1. If braces and/or exercises ordered, ensure compliance.

2. Bracing helps delay progression of curve.

3. Frequent skin inspection necessary with brace use.

4. Continue usual activities if pain free in brace.

V. HIP PAIN

Hip pain, 719.45

A. Differential diagnosis.

1. Infection: septic arthritis, osteomyelitis, Lyme disease, psoas abscess, appendicitis.

2. Inflammatory: transient synovitis, systemic arthritis, juvenile rheumatoid arthritis (JRA), Kawasaki disease, idiopathic chondrolysis.

3. Orthopedic conditions: Legg-Calvé-Perthes disease, avascular necrosis (AVN), slipped capital femoral epiphysis (SCFE), stress fracture, apophyseal injuries, trochanteric bursitis, muscular strain.

4. Neoplastic: osteoid osteoma, leukemia, solid tumor primary, pigmented villonodular synovitis (PVNS), or sickle cell crisis pain.

VI. SEPTIC HIP/SEPTIC ARTHRITIS

Appendicitis, 541

Psoas abscess, 015

 

Avascular necrosis, 733.4

Septic arthritis, 711

 

Chondrolysis, 733.99

Sickle cell crisis, 282.6

 

Juvenile rheumatoid arthritis, 714.3

Slipped capitol femoral

 

Kawasaki disease, 446.1

  epiphysis, 732.2

 

Legg-Calvé-Perthes disease, 732.1

Systemic arthritis, 716.9

 

Leukemia, 208.9

Transient synovitis, 727

 

Lyme disease, 088.81

Trochanteric bursitis, 726.5

 

Muscular strain, 848.9

Fever, 780.6

 

Osteoma, 213.9

Hip pain, 719.45

 

Osteomyelitis, 730.2

Septic arthritis hip, 711.08

 

Pigmented villonodular synovitis (PVNS), 719.2

   

A. Infection in joint; hip joint is infected often, second only to knee in children.

B. Etiology.

1. Bacterial infection spread hematogenously or from osteomyelitis of the femoral head.

2. Most common organisms are Staphylococcus and Streptococcus.

C. Occurrence.

1. Males = females; infancy to 6 years.

D. Clinical manifestations.

1. Hip pain.

2. Refusal to bear weight.

3. Fever.

4. Ill-appearing child with extreme pain and resistance to hip motion. Infection builds up pressure in hip capsule and can impede blood flow.

E. Physical findings.

1. Fever > 37°C, typically lie with hip flexed and externally rotated.

2. Infants may be irritable with pseudoparalysis of lower extremity.

F. Diagnostic tests.

1. Elevate white blood cells (WBC) and ESR.

2. Ultrasound or radiographs demonstrate widening of joint space.

3. Diagnosis confirmed with CT or ultrasound-guided aspiration.

G. Differential diagnosis.

Septic sacroiliac joint, 711.08

1. Septic sacroiliac joint.

H. Treatment.

1. Emergent referral to hospital for surgical drainage of hip joint.

2. Intravenous antibiotics tailored to culture results.

3. Make sure child receives nothing by mouth (NPO).

I. Follow up.

1. Per orthopedics, usually 1–2 weeks postop and 3–6 months to follow hip maturity.

J. Complications.

Joint destruction, 718.9

 

Osteomyelitis, 730.2

 

Septicemia, 038.9

 

1. Septicemia, osteomyelitis, joint destruction.

K. Education.

1. Prepare family for child's hospitalization and treatment with IV antibiotics.

VII. DEVELOPMENTALLY DISLOCATED HIP

Breech birth, 763

 

Dislocated hip, 835

 

Hip dysplasia, 755.63

 

A. Broad spectrum of hip dysplasia regarding dislocated or dislocatable or subluxing femoral head in relation to acetabulum at birth or early development.

B. Etiology.

1. Genetic, intrauterine position, postnatal positioning.

C. Occurrence.

1. Most common hip disorder in children.

2. 1 in 100 infants have hip instability at birth and true dislocation is seen in 1 of 1000 births.

Figure 30–3 Barlow maneuver: knees flexed and brought to midline with gentle downward pressure to see if hip “clunks” out posteriorly.

images

Source: Courtesy of Miki Patterson.

3. Ratio: 6 female: 1 male.

4. Left hip > right.

5. Higher frequency in firstborn children.

D. Clinical manifestations.

1. Breech birth commonly associated with this condition.

2. Difficulty diapering (abducting leg).

3. Older children may have awkward Trendelenburg gait, leg length discrepancy, pain with ambulation.

E. Physical findings.

1. Difficult in infants due to variety of levels of hip dysplasia.

2. Unequal thigh skin creases/gluteal folds.

3. Limited abduction.

4. Positive Barlow maneuver (to see if dislocatable with femur flexed and midline: adduct 10° gentle pressure posterior feel click with telescoping; Figure 30–3).

5. Positive Ortolani maneuver (abducting hip, feel it clunk back into place; Figure 30–4).

6. Galeazzi test (prone with knees flexed and heels at buttock): positive when knee heights are different (Figure 30–5).

Figure 30–4 Ortolani maneuver: Abduct hip while pushing up posteriorly with fingers trying to pop hip into the socket. A click is a positive finding.

images

Source: Courtesy of Miki Patterson.

Figure 30–5 Positive Galeazzi test. Note knee height difference.

images

Source: Courtesy of Miki Patterson.

F. Diagnostic tests.

Arthrogryposis, 728.3

 

Congenital anomalies, 759.9

 

Leg length discrepancy, 736.81

 

Septic hip, 711.08

 

1. Ultrasound of hips. Radiographs less helpful because femoral heads have not ossified.

G. Differential diagnosis.

1. Congenital anomalies, arthrogryposis, septic hip, leg length discrepancy.

H. Treatment.

1. Refer to orthopedist.

2. Treatment goal: Reduce femoral head to anatomic position.

3. May need Pavlik harness, hip spica cast, or surgical intervention.

I. Follow up.

1. Reexamine hips each visit.

J. Complications.

Degenerated changes, 721.9

  Scoliosis, 737.3

 

Dysplasia, 755.63

  Unstable gait, 781.2

 

Low back pain, 724.2

   

1. Delayed treatment affects normal growth of hip joint.

2. If untreated: residual dysplasia, limited range of motion, unstable gait, pain, functional scoliosis, low back pain, early degenerated changes.

K. Education.

1. Report any range-of-motion or neurovascular changes.

2. Important to hold and cuddle baby even in braces and casts.

VIII. TRANSIENT SYNOVITIS

Fever, low-grade, 780.6

 

Transient synovitis, 727

 

Urinary tract infection, 599

 

A. Etiology.

1. Unknown theory of post-traumatic or allergic cause.

2. Infection frequently assumed because 32–50% follow upper respiratory tract infection.

B. Occurrence.

1. 0.2–3% of children 3–8 years of age; 6:1 male-to-female ratio.

C. Clinical manifestations.

1. Pain and limp.

D. Physical findings.

1. Symptoms present.

2. Fever absent or low grade. Do not appear severely ill.

E. Diagnostic tests.

1. Negative CBC and ESR.

2. Ultrasound positive: effusion.

F. Differential diagnosis.

Legg-Calvé-Perthes disease, 732.1

 

Osteomyelitis, 730.2

 

Septic arthritis, 711

 

1. Septic arthritis must be ruled out. Osteomyelitis, Legg-Calvé-Perthes disease.

G. Treatment.

1. Conservative.

2. NSAIDs, rest, return to activity as tolerated.

H. Follow up.

1. If concerned, follow up in 1–2 days to be sure symptoms are resolving.

I. Complications.

Legg-Calvé-Perthes disease, 732.1

 

Septic arthritis, 711

 

1. Missed septic arthritis (rare).

2. 1–2% may develop Legg-Calvé-Perthes disease.

J. Education.

1. Any fever > 38.4°C or ill appearance of child should prompt reexamination.

IX. HIP PAIN: LEGG-CALVÉ-PERTHES DISEASE

Hip pain, 719.45

 

Legg-Calvé-Perthes disease, 732.1

 

Transient synovitis, 727

 

A. Idiopathic AVN of femoral head in children.

B. Etiology.

1. Unknown cause of avascularity; however, multiple theories include trauma, transient synovitis, systemic abnormalities, vascular disturbances from intraosseous venous hypertension and venous obstruction.

C. Occurrence.

1. 1 in 1200 in general population.

2. 4:1 male-to-female ratio.

3. Typically 4–8 years of age.

4. Bilateral in only 15%; reported to be associated with attention-deficit/ hyperactivity disorder (ADHD).

D. Clinical manifestations.

1. Pain of groin, medial thigh, or knee.

E. Physical findings.

1. Pain with weight bearing.

2. Limited internal rotation or abduction of hip.

3. Muscle spasm may have atrophy of thigh, calf, or buttock from disuse.

4. Leg length inequality.

F. Diagnostic tests.

1. Radiographs: AP pelvis and frog lateral hips.

2. Initial X-rays may be normal; may need CT to see early changes.

3. Four stages:

a. Initial: interruption of blood supply, “crescent sign” areas of hyperand hypodense appearance of femoral head.

b. Fragmentation: epiphysis appears fragmented.

c. Reossification: normal bone density returns, deformity becomes apparent.

d. Healed: healing complete, residual deformity common.

G. Differential diagnosis.

Knee fracture, 822

  Slipped capital femoral epiphysis (SCFE), 732.2

 

Septic hip, 711.08

  Transient synovitis, 727

 

1. Knee problem, fracture.

2. Transient synovitis.

3. Septic hip, SCFE.

4. Neuromuscular condition.

H. Treatment.

1. Refer to orthopedist.

2. Goal: prevent femoral head deformity, alter growth disturbances.

3. Generally try to unload femoral head while allowing motion.

4. Abduction brace and bed rest, home traction with progressive abduction of legs.

5. Surgical adductor release or derotational femoral or pelvic osteotomies and spica body cast occasionally needed.

I. Follow up.

1. Per orthopedics.

2. Patients will be followed long term, bed rest with traction, bracing, and surgery performed as indicated.

J. Complications.

Degenerated changes, 721.9

 

Unstable gait, 781.2

 

1. May not show on initial films.

2. Delayed treatment affects normal growth of hip joint.

3. Residual deformities (coax magna), limited range of motion, unstable gait, pain, early degenerated changes seen with treated and untreated.

K. Education.

1. Progressive until body replaces “dead” femoral head with new bone; younger it occurs, longer body has to replace collapsing bone and remodel femoral head.

2. No pressure should be put on rebuilding bone, but should be able to move in joint for shaping.

X. HIP PAIN: SLIPPED CAPITAL FEMORAL EPIPHYSIS

Slipped capital femoral epiphysis, 732.2

A. Femoral neck “slips” (displaces anteriorly) at physis (growth plate), leaving femoral head behind in acetabulum (Figure 30–6).

B. Etiology.

1. Unknown; however, suspect multifactorial cause, biomechanical, obesity, endocrine, metabolic, trauma, genetics, and other causes (e.g., kidney disorders or radiation).

C. Occurrence.

1. Most common hip disorder of adolescents, 3 of 100,000 are 8–17 years of age.

2. Males (10–17 years of age) affected 2–3 times more often than females (8–15 years of age).

3. Left hip most often affected; bilateral 25–70%.

D. Clinical manifestations.

1. Hip, groin, medial thigh, knee pain; sometimes for months.

2. May be brought on by very minor trauma (chronic/acute or acute on chronic).

3. Antalgic gait (limp to keep weight off painful extremity) or inability to bear weight.

Figure 30–6 Slipped capital femoral epiphysis. Note the appearance of ice cream falling off the cone.

images

Source: Courtesy of Miki Patterson.

E. Physical findings.

1. Range of motion may be limited depending on severity of slip, may have limited internal rotation and abduction of the hip.

F. Diagnostic tests.

1. Radiographs AP pelvis and true lateral (not frog lateral because may cause more femoral head displacement).

G. Differential diagnosis.

Appendicitis, 541

 

Hip pain, 719.45

 

Testicular torsion, 608.2

 

1. Knee problem.

2. Infection.

3. Inflammation.

4. Referred pain such as appendicitis, testicular torsion.

5. Other orthopedic conditions or malignancy.

H. Treatment.

1. Immediate referral to orthopedist.

2. Do not allow further weight bearing because femoral head can “slip” further.

3. Surgical intervention with “pinning” by screw(s) to fuse physis between femoral head and neck.

I. Follow up.

1. Orthopedics typically allow partial weight bearing with crutches for 6–8 weeks.

2. Return in 2 weeks for wound check, staple removal.

3. Follow healing clinically and radiographically for several months/years.

J. Complications.

Avascular necrosis, 733.4

 

Chondrolysis, 733.99

 

Degenerative changes, 721.9

 

Malunion, 733.81

 

1. Missed on X-ray 25% of time.

2. Avascular necrosis.

3. Chondrolysis (acute hylan cartilage necrosis).

4. Loss of range of motion.

5. Limb shortening.

6. Early degenerative changes.

7. Malunion.

K. Education.

1. High incidence of recurrence of other hip.

2. Parents or child should report any similar findings and be seen immediately.

XI. KNEE PAIN: OSGOOD-SCHLATTER DISEASE

Knee pain, 719.46

 

Osgood-Schlatter disease, 732.4

 

A. Painful swelling of tibial tubercle, caused by traction and resulting in apophysitis.

B. Etiology.

1. Overuse by chronic repetitive knee flexion.

C. Occurrence.

1. 11–14 years of age during rapid growth.

2. Males > females, but ratio changing with increased female participation in sports.

3. Frequently bilateral.

D. Clinical manifestations.

1. Pain with running, jumping, kneeling. Resolves/fades with rest.

E. Physical findings.

1. Pain in anterior knee; warmth, swelling, and tenderness over tibial tubercle, especially with resistive knee extension (kicking motion) or squatting.

F. Diagnostic tests.

1. Radiographs of knee: AP and lateral and 10° obliques to rule out tumor or fracture.

2. Classic prominent tibial tubercle above physis (Figure 30–7).

Figure 30–7 Osgood-Schlatter disease: apophysitis of the tibial tubercle.

images

Source: Courtesy of Miki Patterson.

G. Differential diagnosis.

Knee fracture, 822

 

Sinding-Larsen-Johansson syndrome, 732.4

 

1. Tumor.

2. Fracture.

3. Sinding-Larsen-Johansson syndrome (apophysitis of distal pole of patella).

H. Treatment.

1. Limit activities, especially sports; ice after activity.

2. Hamstring and quadriceps stretching and strengthening.

3. Knee immobilizer or cylinder casting for brief periods to manage severe pain.

4. Ibuprofen.

I. Follow up.

1. Teach patients, families to decrease activity; wear knee immobilizer when painful.

2. Follow up until skeletal maturity seen in closure of physis or growth plate.

J. Complications.

Apophysis deformity, 738.9

 

Enlargement of tibial tubercle, 718.86

 

Tibia fracture, 823.8

 

1. Enlargement of tibial tubercle (bony prominence).

2. Pain may continue into adulthood.

3. Fracture of tibial tubercle.

4. Premature closure of apophysis causing recurvatum deformity.

K. Education.

1. “Bump” made because body thinks there is injury to bone which is being pulled apart at growth plate by patella; tendon bump will not go away.

2. Continued use while painful typically increases size of “bump”; this is cosmetically unappealing for most and may interfere with kneeling. Condition ceases to exacerbate on skeletal maturity.

XII. PHYSIOLOGIC GENU VARUM (BOW LEGS)

Genu varum, 736.42

A. Etiology.

1. Physiologic genu varum or bowing is part of normal development.

B. Occurrence.

1. Most common cause of bow legs in toddlers.

2. Varum is greatest at 6 months of age, may progress to neutral by 18–24 months of age.

3. Adult physiologic valgus (knock knee): about 8°, typically reached by 5–6 years of age.

C. Clinical manifestations.

1. Pain-free bowing appearance to legs of toddler.

D. Physical findings.

1. Gentle curve to entire leg.

2. Normal knee flexion, extension without pain.

3. Normal progression: 15° genu varum at birth (Figure 30–8); 0° (straight) 18–24 months; 10–12° genu valgum (knock knees) at 30 months to 4 years; 0° (straight) to 4–6° genu valgum normal at 4–6 years.

E. Diagnostic tests.

1. Radiographic bowing of entire limb, no acute angulation seen (Figure 30–8).

2. Medial proximal tibial physeal changes suggestive of pathology (Blount's disease), refer to orthopedist.

F. Differential diagnosis.

Achondroplasia, 756.4

Osteogenesis imperfecta, 756.51

 

Blount's, 732.4

Osteomyelitis, 730.2

 

Chondrodysplasia, 756.4

Renal failure, 593.9

 

Leg fracture, 827

Rickets, 268

 

1. Blount's, vitamin D-resistant rickets, renal failure, chondrodysplasia, achondroplasia, osteogenesis imperfecta, osteomyelitis, neoplasm, fracture.

G. Treatment.

1. Generally resolve spontaneously.

Figure 30–8 Physiologic genu varum. Normal “beaking” of distal femur and proximal tibial metaphysis.

images

Source: Courtesy of Miki Patterson.

2. Refer to orthopedics for obvious asymmetry, clear progressive deformity, or if associated with pain.

3. Osteotomy and correction of angulation may be performed using internal or external fixation devices.

H. Follow up.

1. Return visits every 3–6 months.

I. Complications.

Blount's, 732.4

 

Tibia vara, 732.4

 

1. Tibial vara or Blount's disease (abrupt deformity medial proximal tibia).

2. May be seen in younger than 5 years of age but more common in adolescents.

3. Females > males.

4. Bilateral 80% of time.

5. Higher incidence in obese and African American children.

6. Will not correct with age.

J. Education.

1. Reassurance of normal finding.

2. Encourage child not to sleep or sit with legs tucked underneath; position might delay spontaneous correction.

XIII. IN-TOEING: METATARSUS ADDUCTUS

Metatarsus abductus varus, 754.53

A. Etiology.

1. Unknown, theory of intrauterine position.

B. Occurrence.

1. Most common childhood foot problem.

2. 1 in 5000 births.

3. 1:20 in sibling.

4. Males, twins, preterm infants have higher incidence.

5. Seen first year of life; left > right, often bilateral.

C. Clinical manifestations.

1. Medial deviation of forefoot on hindfoot, in-toeing gait.

D. Physical findings.

1. C-shaped foot.

E. Diagnostic tests.

1. No radiographs needed for infants.

2. Children older than 4 years of age should have standing foot films, 3 views.

F. Differential diagnosis.

Spastic anterior tibialis, 781

 

Talipes equinovarus, 754.51

 

1. Spastic anterior tibialis.

2. Talipes equinovarus (clubbed foot).

G. Treatment.

1. Most will correct with normal use.

2. Severe deformity: Refer to orthopedist for stretching, serial casting of flexible conditions; surgical intervention is rare.

H. Follow up.

1. Per orthopedics until deformity is corrected.

2. Serial casting may be done weekly. Have parents remove semirigid cast night before appointment. Teach to stretch, then apply new cast with orthopedist holding position.

I. Complications.

1. Cast/skin complications.

2. Neurovascular problems.

3. Incorrect position, especially if cast slips and toes are no longer visible (common with infants).

J. Education.

1. Most resolve spontaneously.

2. Return to orthopedist if circulation problems, irritability (e.g., suspect cast is bothering child), or if child kicks cast off.

XIV. IN-TOEING: TIBIAL TORSION

Tibial torsion, 736.89

A. Etiology.

1. Normal development in utero, genetic influence.

B. Occurrence.

1. Birth 0–20° internal tibial rotation normal: 90% correct with growth, adults achieve 0–20° of external rotation.

C. Clinical manifestations.

1. Curved appearance to tibia or in-toeing or out-toeing gait.

2. If knees are pointing forward, feet may either point in (internal tibial torsion) or out (external tibial torsion); becomes less noticeable with running.

D. Physical findings.

1. Thigh-foot angle (Figure 30–9). Child prone with knee bent at 90° angle of imaginary line drawn down thigh and middle of foot. Normal 0–30° external.

2. Foot progression angle is angle of foot compared to line extended in front of ambulating child. Best observed from directly behind patient (Figure 30–10).

Figure 30–9 Thigh-foot angle. A line drawn along the axis of the femur bisects the foot.

images

Source: Courtesy of Miki Patterson.

E. Diagnostic tests.

1. None if younger than 8 years of age and symmetrical pain-free appearance.

2. If needed, standing leg length X-ray (scanogram) done on long cassette.

F. Differential diagnosis.

Hip dysplasia, 755.3

1. Developmental dysplasia of hip, neuromuscular conditions.

G. Treatment.

1. Observation.

2. None unless unilateral or severe or remains after age 8 years.

3. Tibial osteotomy rare but may be performed for severe cases.

H. Follow up.

1. If persists at 8 years of age, refer to orthopedist.

Figure 30–10 Foot progression angle: normal variations.

images

Source: Courtesy of Miki Patterson.

I. Complications.

1. Rare and related to surgical intervention.

J. Education.

1. Reassurance and handouts.

2. Despite grandparents' (or older relatives'/caregivers’) insistence, braces are not effective. Studies show same improvement or correction through normal growth without braces.

3. Many athletic children, adults have tibial torsion; does not result in any increased incidence of arthritis or interfere with activity.

XV. IN-TOEING: FEMORAL ANTEVERSION

Femoral anteversion, 755.63

A. Etiology.

1. Normal and appears when child begins walking, causing ligaments to get looser; thus hips are allowed more internal rotation, especially in children 2–6 years of age.

B. Occurrence.

1. Normal in 2- to 4-year olds, usually corrects spontaneously by 8 years of age.

C. Clinical manifestations.

1. In-toeing gait.

2. Children tend to “W” sit pain free.

D. Physical findings.

1. Knees and toes point inward when standing.

2. Able to internally rotate hips up to 90°.

E. Diagnostic tests.

1. None.

F. Differential diagnosis.

Hip dysplasia, 755.63

 

Tibial torsion, 736.89

 

1. Tibial torsion, hip dysplasia.

G. Treatment.

1. Discourage “W” sitting.

2. Observation unless functional deformity after 8 years old.

3. Refer to orthopedist for unilateral, severe, or painful deformity.

4. Surgical intervention with femoral derotational osteotomy.

H. Follow up.

1. Yearly if not progressive.

I. Complications.

1. None unless surgical intervention.

J. Education.

1. Normal, child will grow out of it. Braces or shoe modification are ineffective.

XVI. FOOT PROBLEMS: TALIPES EQUINOVARUS (CLUBBED FOOT)

Clubbed foot, 754.51

 

Talipes equinovarus, 754.51

 

A. Rigid fixed foot deformity with inverted heel, forefoot adduction, and down-facing toes.

B. Etiology.

1. Unknown; possibly genetic, mechanical, chemical embryologic insults.

C. Occurrence.

1. Age: newborn.

2. 2:1 males to females.

3. 1.24 in 1000 live births.

4. Increased incidence in families where parents/siblings have same disorder.

D. Clinical manifestations.

1. Tight Achilles tendon, joint capsule, medial ligaments.

2. Short angulated talus, thin atrophic muscles.

E. Physical findings.

1. Small foot and calf, with rigid equinus deformed foot with heel in varus.

2. Prominent crease in arch of foot.

3. Adducted forefoot.

F. Diagnostic tests.

1. Clinical exam of newborn; radiographs are of little use.

G. Differential diagnosis.

Arthrogryposis, 728.3

 

Calcaneovalgus, 755.67

 

Spastic hemiplegia, 342.1

 

1. “Positional clubbed foot,” arthrogryposis, spastic hemiplegia, calcaneovalgus.

H. Treatment.

1. Refer to orthopedist. Serial casting and surgical intervention may be necessary.

I. Follow up.

1. Per orthopedist.

2. Treatment soon after birth: weekly visits for manipulation and casting by orthopedist experienced in this form of treatment.

3. If rigid deformity, surgical intervention may be necessary; may entail heel cord and joint capsule releases and casting typically at 6 months of age.

4. Casting or braces may be used for a period of time; follow up is ongoing because deformity may recur until about age 7 years.

J. Complications.

Leg length discrepancy, 736.81

1. Progressive deformity, leg length discrepancy, surgical complications.

K. Education.

1. Affected foot will always be smaller but may function near normal after correction.

XVII. PES PLANUS: FLAT FOOT

Pes planus flat foot, 734

A. Etiology.

1. Flexible normal (asymptomatic) genetic etiology or rigid (symptomatic) tarsal coalition (fusion of calcaneus with talus or navicular) common cause.

B. Occurrence.

1. Normal occurrence younger than 2 years of age due to medial fat pad. Rigid is rare.

C. Clinical manifestations.

1. Flat foot while standing; normal arch that returns while sitting and hanging over exam table is flexible pes planus.

2. Bilateral.

3. Hereditary expression.

4. May cause some discomfort for older children.

D. Physical findings.

1. Loss of normal plantar arch while standing.

2. Limited subtalar joint motion for rigid pes planus.

3. Look at parents' feet!

E. Diagnostic tests.

1. If rigid: radiographs, three standing views of both feet, CT or MRI looking for coalition.

F. Differential diagnosis.

Arthritis, 716.97

 

Arthrogryposis, 728.3

 

Foot fracture, 825.2

 

1. Overuse.

2. Arthrogryposis.

3. Neuromuscular condition.

4. Arthritis.

5. Infection.

6. Trauma/fracture.

G. Treatment.

1. Refer rigid pes planus to orthopedist, orthotics may decrease symptoms of older child with flexible pes planus.

2. Apply before sling.

H. Follow up.

1. May require further workup or referral if not pain free after 1 month.

I. Complications.

1. None known.

J. Education.

1. Proper shoe wear. Sneakers with built-in arch preferred.

XVIII. NURSEMAID'S ELBOW: RADIAL HEAD SUBLUXATION

Nursemaid's elbow, 832

A. Etiology.

1. Traction along axis of extended pronated arm resulting in radial head subluxation with annular ligament displacement.

2. Typically “pulling” child's hand/arm to prevent from falling or pulling away or swinging child by arms.

B. Occurrence.

1. Most common elbow injury of children age 1–4 years.

2. Female > males.

3. Left > right.

C. Clinical manifestations.

1. Will not use arm.

2. Holds arm close to body with elbow slightly flexed and pronated (palm down).

D. Physical findings.

1. Restricted supination of elbow.

2. Typically nontender or swollen; however, exhibits distress if tries moving elbow.

E. Diagnostic tests.

1. Radiographs AP and lateral of elbow if questionable success of reduction (note: many times these are reduced when arm is rotated to get lateral X-ray).

F. Differential diagnosis.

Elbow fracture, 813.01

1. Fracture.

G. Treatment.

1. Reduction maneuver.

a. Child in parent's lap.

b. Flex child's elbow to 90° with gentle pressure of thumb over radial head.

c. Fully or “hyper” pronate wrist then fully supínate wrist; typically click will be felt and child will stop resisting (Figure 30–11).

2. Sling and refer to orthopedist if child fails to use arm.

H. Follow up.

1. Call or visit to ensure child is using arm normally within 1 week.

I. Complications.

1. Unreduced radius.

J. Education.

1. Teach parents mechanism of injury to prevent reoccurrence (30–40%).

XIX. GROWING PAINS

Growing pains, 781.99

A. Etiology.

1. Unknown theory of periosteal irritation.

B. Occurrence.

1. Peak in 3–5 and 8–12-year olds.

Figure 30–11 Reduction maneuver for “nursemaid's elbow.” Flex elbow to 90°, fully pronate wrist (palm down), then with gentle pressure over radial head supínate the wrist (palm up).

images

Source: Courtesy of Miki Patterson.

C. Clinical manifestations.

1. Muscular pain (not joint): thighs, calves, behind knee.

2. Typically late afternoon, early evening after physically active day.

3. Can wake child from sleep.

D. Physical findings.

1. None.

E. Diagnostic tests.

1. Only if suspicious, X-ray to exclude fracture/lesion.

F. Differential diagnosis.

1. Diagnosis of exclusion:

a. No fever.

b. Not in joint.

c. No swelling, erythema, warmth.

d. No trauma.

e. No weight loss, rashes, unusual fatigue or behavior.

G. Treatment.

1. Massage, heat, acetaminophen/ibuprofen.

H. Follow up.

1. Follow up if lasts > 24 hours at time.

2. Follow up if child does not respond to medications and massage.

I. Complications.

1. None.

J. Education.

1. Normal, may come and go, child is not “faking.”

XX. COSTROCHONDRITIS

Costochondritis, 733.6

A. Etiology.

1. Diagnosis of exclusion.

B. Occurrence.

1. Unknown.

C. Clinical manifestations.

1. Insidious and persistent lasting hours to days.

2. Worse with position change and deep breathing. May be diffuse or localized. Common after repetitive new activity of upper trunk and arms.

D. Physical findings.

1. Skin lesions, chest wall syndrome tests, “crowing rooster,” “horizontal arm flexion,” “hooking maneuver” diagnostic: if pain is reproduced, test is positive (Figure 30–12).

2. Chest expansion test (tape measure around chest at fourth intercostal level max)–exhale then inhale = 5 cm excursion;.

E. Treatment.

1. NSAIDs, rest.

F. Diagnostic tests.

1. Radiographs of chest to rule out fracture or tumor.

2. CT, bone scan (most sensitive to rule out arthropathies, tumors, infection).

Figure 30–12 “Crowing rooster.” Elbows are pulled back and up to expand chest. A positive test is when pain is reproduced with this maneuver.

images

Source: Courtesy of Miki Patterson.

3. ESR, ANA, rheumatoid factor purpose to rule out: cardiopulmonary, abdominal sources associated with rheumatologic condition or assess structure of chest wall.

G. Differential diagnosis.

Ankylosing spondylitis, 720

 

Fibromyalgia, 729.1

 

Sternoclavicular hyperostosis, 733.3

 

1. Cardiopulmonary.

2. Esophagus, head, neck, and interior chest wall.

3. Ankylosing spondylitis.

4. Sternoclavicular hyperostosis.

5. Infection.

6. Fibromyalgia.

H. Follow up.

1. Within 2 weeks to document resolution of symptoms.

I. Complications.

1. Missed diagnosis.

J. Education.

1. Call for changes in symptoms.

XXI. OSTEOPOROSIS

Osteoporosis, 733

A. Etiology.

1. Bony calcium deficit from various causes including lack of intake while prepubertal, absorption or metabolic origin.

B. Occurrence.

1. Disease of childhood with severe adulthood complications.

C. Clinical manifestations.

1. Majority (50–66%) of total body calcium is deposited to bone by end of puberty.

2. Earlier in females than males.

3. Highest velocity of increased bone mineral content within 9–12 months of menarche.

D. Physical findings.

1. Stress fractures, fractures with minimal trauma or no findings in childhood.

E. Diagnostic tests.

1. Lack of calcium in past 3-day diet history.

2. Poor dietary habits.

3. High suspicion in lactose-intolerant or anorectic children.

E. Differential diagnosis.

1. None.

G. Treatment.

1. Increase dietary calcium intake or supplementation.

H. Follow up.

1. Continue to assess calcium intake, stress importance to prepubertal/ pubescent children.

I. Complications.

Dowager's hump (kyphosis), 737.1

 

Degenerative joint changes, 721.9

 

Fractures, 829

 

1. Fractures.

2. Dowager's hump (kyphosis).

3. Early adulthood degenerative joint changes.

J. Education.

1. Three servings of milk, cheese, yogurt daily: 1200 mg of calcium.

BIBLIOGRAPHY

American Academy of Pediatrics. Clinical practice guideline: Early detection of developmental dysplasia of the hip. Pediatrics. 2000;105(4):896–905.

Clark MC. Approaches to child with a limp; 2003. Retrieved June 11, 2011, from: http://www.uptodate.com/contents/approach-to-the-child-with-a-limp.

Flynn JM, & Mehta S. An evidence-based approach to the evaluation and management of hip pain in children. Pediatric Case Review. 2002;2(1):26–32.

Gregory PL, Biswas AC, & Batt ME. Musculoskeletal problems of the chest wall in athletes. Sports Medicine. 2002;32(4):235–250.

Gunner KB, & Scott AC. Evaluation of a child with a limp. Journal of Pediatric Health Care. 2001;15(1):38–40.

Hawk D & Bailie S. Pediatric/congenital disorders. In: Core curriculum for orthopaedic nursing Boston: Pearson Custom Publishing; 2009:259–326.

Kleposki RW, & Sehgal K. Common pediatric hip diseases in primary care. Clinical Advisory. 2010;13(6): 21–26.

Lincoln TL, & Suen PW. Common rotational variations in children, J Am Acad Orthopaedic Surgeons. 2003;11(5):312–320.

Proulx AM, & Zryd TW. Costochondritis: diagnosis and treatment. Am Fam Physician. 2009;80(6):617–620.

Shelton YA, & Mortimer E. Orthopaedic problems in the pediatric patient. In G Steinberg, C Akins, & D Baran, eds. Orthopaedics in primary care. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999.

Staheli LT. Fundamentals ofpedicatric orthopaedics. 4th ed. India: Lippincott Williams & Wilkins; 2008.



If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!