Approach to a Limping Child

• Comprehensive history– Prenatal, perinatal and postnatal– developmental milestones for posture,

locomotion, dexterity, social activities, and speech previous procedures and significant medical conditions

– pain or other symptoms – family history may give clues to possible genetic

disorders such as congenital syndromes, muscular dystrophy, skeletal dysplasias, and other disorders affecting the musculoskeletal system

Characterization of Pain

Physical examination

• Examination of the musculoskeletal system as well as a comprehensive neurologic examination.

• Inspection, palpation, and evaluation of motion, stability, and gait.

• Basic neurologic examination including sensory examination, motor function, and reflex evaluation

Inspection

Palpation

• Contractures– loss of mobility of a joint – periarticular soft-tissue fibrosis or involvement of muscles crossing the

joint• Spasticity

– abnormal increase in tone associated with hyperreflexia and is common in cerebral palsy.

• Deformity – abnormal fixed shape or position – +/- associated muscle spasm, local tenderness, or pain on motion. – it an be defined as varus (away from midline) or valgus (apex toward

midline/coronal plane), or recurvatum or flexion deformity (sagittal plane).

– In the axial skeleton, especially the spine, deformity can be defined as scoliosis, kyphosis, hyperlordosis, and kyphoscoliosis

Range of Motion• Abduction: Away from the midline• Adduction: Toward the midline• Flexion: Movement of bending from the starting position• Extension: Movement from bending to the starting position• Supination: Rotating the forearm to face the palm upward• Pronation: Rotating the forearm to face the palm

downward• Inversion: Turning the hindfoot inward• Eversion: Turning the hindfoot outward• Internal rotation: Turning inward toward the axis of the

body• External rotation: Turning outward away from the axis of

the body.

Gait Assessment

• Cadence: The number of steps taken per minute

• Step length: The distance covered during one step

• Step period: The time measured from an event in one foot to the same event in the opposite foot

• Stride period: The time from heel strike of one foot to the next heel strike of the same foot

• Stride length: The total distance covered from one heel strike to the same-foot heel strike.

LIMPING

Back Pain

• Most frequent causes of back pain in children are trauma, spondylolysis, spondylolisthesis, and infection

• Tumor and tumor-like lesions that cause back pain in children are likely to be missed unless a thorough clinical assessment and adequate work-up are performed when required.

• Nonorthopedic causes of back pain include urinary tract infections, nephrolithiasis, and pneumonia.

Neurologic Evaluation

• Grade 0: No muscular contraction detected. • Grade 1: Trace contraction, barely detectable

clinically. • Grade 2: Active movement with gravity

eliminated. • Grade 3: Active movement against gravity. • Grade 4: Active movement against gravity and

some resistance. • Grade 5: Active movement against full

resistance.

ASSESSMENT• RADIOGRAPHIC ASSESSMENT.

– Plain radiographs– Advanced imaging includes special procedures such as nuclear

bone scans, ultrasonography, CT, MRI, and positron emission tomography (PET).

• PLAIN RADIOGRAPHS. – Anteroposterior and lateral views of the involved area with one

joint above and below. • NUCLEAR MEDICINE IMAGING.

– Bone scan - physiologic information rather than pure anatomy – emission of energy from the nucleotide injected into the

patient. – Total body radionuclide scan (technetium-99) - identify bony

lesions and may also help in evaluation of biologic activity of the primary bone lesion

ASSESSMENT• ULTRASONOGRAPHY.

– No ionizing radiation, no contrast material to be administered, and no biologically harmful effects and can be repeated as often as necessary.

– Disadvantages: Bone is not penetrated, static images are difficult to interpret, and the results are operator dependent.

• MAGNETIC RESONANCE IMAGING. – imaging modality of choice for further defining the exact

anatomic extent of most musculoskeletal lesions. • MAGNETIC RESONANCE ANGIOGRAPHY (MRA).

– good visualization of peripheral vascular branches and tumor neovascularity in patients with primary bone tumors. MRA is helpful in demonstrating encroachment onto and encasement of major vessels by the tumor mass

ASSESSMENT• COMPUTED TOMOGRAPHY.

– Allows visualization of the detailed bone anatomy and the relationship of bones to contiguous structures.

– Superior to MRI for assessment of bone involvement and cortical destruction (even subtle changes), including calcification or ossification and fracture.

• POSITRON EMISSION TOMOGRAPHY. – Provides complementary metabolic information in many oncology

applications. • LABORATORY STUDIES.

– May include a complete blood cell count; erythrocyte sedimentation rate; C-reactive protein assay; Lyme titers; and blood, wound, joint, periosteum, or bone cultures

– Rheumatoid factor, antinuclear antibodies, and human leukocyte antigen B27

– Creatine kinase, aldolase, aspartate aminotransferase, and dystrophin testing

COMMON CONDITIONS THAT CAN CAUSE LIMPING IN A CHILD

Painful (Antalgic) Gait Painless (Trendelenburg) Gait

Stance phase is shortened Stance phase is equalTrauma, infection, or pathologic fracture

Underlying proximal muscle weakness or hip instability

Child leans toward the unaffected side

Child leans toward the involved extremity

Common Causes of Limping

Age Antalgic Trendelenburg Leg Length Discrepancy

Toddler(1-3)

Infection (Septic arthritis, Osteomyelitis,

Diskitis)Toddlers fracture

Neoplasia

Hip dislocationNeuromuscular disease

Cerebral PalsyPoliomyelitis

(-)

Childhood(4-10)

Infection (Septic arthritis, Osteomyelitis,

Diskitis, Transient Synovitis)Legg-Calve-Perthes

Tarsal coalitionJRA

TraumaNeoplasia

Hip dislocationNeuromuscular disease

Cerebral PalsyPoliomyelitis

(+)

Adolescent(>10)

Slipped capital femoral epiphysis

JRATrauma

Tarsal coalitionNeoplasia

(+)

Coronal Plane Deformities

• Genu Varum– Bowleg– Usually secondary to normal in-utero positioning– Common during the 2nd year– May be secondary to metabolic bone disease,

asymmetric growth arrest, bone dysplasia and congenital neuromuscular disorder

• Genu Valgum– Knock-knees– Common during 3-4yrs– May be secondary to metabolic bone disease, skeletal

dysplasia, post-traumatic physical arrest, tumors and infection

Osgood-Schlatter Disease

• Pain over the tibial tubercle in a growing child• Traction apophysitis on the tibial tubercle

growth plate and the adjacent patellar tendon• More common in males, athletes, 10-15 years

old• Self-limited, resolves with skeletal maturity• (+) fragmentary ossification of the tibial

tubercle, patella alta• Tx: rest, restriction of activities, knee

immobilizer

Developmental Dysplasia of the Hip

• Hip subluxation– partial contact between the femoral head and

acetabulum,• Hip dislocation – hip with no contact between the articulating

surfaces of the hip• Two major groups– Typical DDH occurs in otherwise normal individuals

or those without defined syndromes or genetic conditions

– Teratologic hip dislocations usually have identifiable causes and occur before birth

• ETIOLOGY, INCIDENCE, AND RISK FACTORS – Actual dislocated or dislocatable hips are much less frequent,

being found in 1–1.5 of 1000 live births– Etiology is multifactorial

• genetic and intrauterine environmental factors• environmental factors, such as child-rearing practices

• RISK FACTORS FOR DDH – positive family history – more common among female patients

• greater susceptibility of females to maternal hormones such as relaxin, which increases ligamentous laxity.

– tighter intrauterine space and, consequently, less room for normal fetal motion • oligohydramnios, large birth weight, and first pregnancy• Left hip is the most commonly affected hip; in the most common fetal

position, this is the hip that is usually forced into adduction against the mother's sacrum

• PATHOANATOMY – If the hip is not dislocated at birth, all the specific

components of the hip joint, except for the ligamentum teres and the hip capsule, usually appear relatively normal.

– Teratologic dislocations frequently are accompanied by a small, shallow acetabulum and a stiff hip joint at birth.

– If untreated, deformity may occur• hypertrophy of the lateral cartilage of the acetabulum

(neolimbus formation), hypertrophy of the ligamentum teres, capsular laxity, hourglass constriction of the hip capsule and hypertrophy of the transverse acetabular ligament, and excess femoral anteversion.

DDH in a Neonate

• Barlow Provocative Maneuver – assesses the potential for dislocation of a

nondisplaced hip– Positive test• Hip will be felt to slide out of the acetabulum. • As the examiner relaxes the proximal push, the hip can

be felt to slip back into the acetabulum

• Ortolani Test– examiner attempts to reduce a dislocated hip – Positive• femoral head will slip into the socket with a delicate

“clunk” that is palpable but usually not audible

DDH in an Infant

• Signs of DDH usually appear on the 2nd-3rd month of life• Shortening of the thigh, the Galeazzi sign, is best

appreciated by placing both hips in 90 degrees of flexion and comparing the height of the knees, looking for asymmetry

• Asymmetry of thigh and gluteal skin folds is suggestive of DDH.

• Klisic test, in which the examiner places the 3rd finger over the greater trochanter and the index finger of the same hand on the anterior superior iliac spine. In the dislocated hip, the trochanter is elevated, and the line projects halfway between the umbilicus and the pubis.

DDH in a Walking Child

• limp, a waddling gait, or a leg-length discrepancy• affected side appears shorter than the normal

extremity, and the child will toe-walk on the affected side

• Trendelenburg sign is positive in these children, and a Trendelenburg gait is usually observed

• (+) limited abduction on the affected side and the knees are at different levels when the hips are flexed (the Galeazzi sign)

• Excessive lordosis, which develops secondary to altered hip mechanics, is common and is often the presenting complaint.

Radiographic Findings• UTZ

– provides dynamic assessment about the stability of the hip joint • RADIOGRAPHY.

– recommended for an infant once the proximal femoral epiphysis ossifies, usually by 4–6 mo.

– Hilgenreiner line - horizontal line drawn through the top of both triradiate cartilages

– Perkins line - vertical line through the most lateral ossified margin of the roof of the acetabulum, perpendicular to the Hilgenreiner line

– Shenton line - curved line drawn from the medial aspect of the femoral neck to the lower border of the superior pubic ramus

– Acetabular index - angle formed between the Hilgenreiner line and a line drawn from the depth of the acetabular socket to the most lateral ossified margin of the roof of the acetabulum.

– Center-edge angle is a useful measure of hip position– In children 6–13 yr old, an angle >19 degrees has been reported as normal,

while in children 14 yr and older, an angle >25 degrees is considered normal

Treatment

• NB to <6 months– Pavlik Harness

• 6 months – 2 years– Closed reduction– Open reduction (12 wks after closed reduction)– Traction

• >2 years– Open reduction– Concomita t acetabular procedure

DDH – Sequelae/Complications

• Avascular necrosis of the CFE• Redislocation• residual subluxation• acetabular dysplasia• postoperative complications– wound infections

Legg-Calve-Perthes• femoral head disorder of unknown etiology • temporary interruption of the blood supply to the bony

nucleus of the proximal femoral epiphysis• impairment of the epiphyseal growth and femoral head

deformity• Pathogenesis (4)

– growth disturbance in CFE and physis– the asymmetric repair process and the applied stresses on the

femoral head– superficial layers of articular cartilage continue to “overgrow” as

they are nourished by the synovial fluid. The deeper layers are, however, devitalized by the disease process, leading to epiphyseal trabecular collapse and deformity.

– iatrogenic - trying to contain, either nonsurgically or surgically, a noncontainable femoral head.

Legg-Calve-Perthes• CLINICAL PRESENTATION

– Limp of varying duration– Pain - activity related and may be localized in the groin or referred

to the anteromedial thigh or knee region• RADIOGRAPHIC FINDINGS

– Routine plain radiographs are the primary imaging tool for LCPD. Anteroposterior and Lauenstein (frog) lateral views are used to diagnose, stage, provide prognosis, follow the course of the disease, and assess results

– radionuclide bone scanning with technetium-99m may reveal the avascularity of the CFE

– MRI is sensitive in detecting infarction but cannot accurately portray the stages of healing.

– Arthrography may demonstrate any flattening of the femoral head and the hinge abduction phenomenon with abduction of the leg.

Legg-Calve-Perthes

• Classification

Legg-Calve-Perthes

• TREATMENT– NONOPERATIVE TREATMENT - mainstay of

treatment is nonoperative, specifically activity limitation and physical therapy to maintain hip range of motion

– OPERATIVE TREATMENT• Varus osteotomy - most common procedure. • Pelvic osteotomies - acetabular rotational

osteotomies, shelf procedures, and medial displacement or Chiari osteotomies

Osteomyelitis• Etiology

– Staphylococcus aureus is the most common infecting organism in all age groups, including newborns

– After 6 yr of age, most cases of osteomyelitis are caused by S. aureus, streptococcus, or Pseudomonas aeruginosa

– Salmonella species and S. aureus are the two most common causes of osteomyelitis in children with sickle cell anemia

• Fungal infections usually occur as part of multisystem disseminated disease

• Primary viral infection of bones is exceedingly rare.• A microbial etiology is confirmed in about 75% of cases of

osteomyelitis. Prior antibiotic therapy and the inhibitory effect of pus on microbial growth may explain the low bacterial yield.

Osteomyelitis

• PATHOGENESIS. • The unique anatomy and circulation of the ends

of long bones result in the predilection for localization of blood-borne bacteria

• Blood flow in this area is sluggish and provides an ideal environment for bacterial seeding.

• Phagocytes migrate to the site and produce an inflammatory exudate (metaphyseal abscess). The generation of proteolytic enzymes, toxic oxygen radicals, and cytokines results in decreased oxygen tension, decreased pH, osteolysis, and tissue destruction.

Osteomyelitis

• TREATMENT• Neonates– Anti-staphylococcal Penicillin• Nafcillin or Oxacillin• Cefotaxime

– Older Infants and Children• Cefazolin or Nafcillin

Osteomyelitis

• DIAGNOSIS– Blood culture– Aspiration for Gram stain and culture – No specific laboratory tests for osteomyelitis

• RADIOGRAPHIC EVALUATION– Within 72 hrs of onset of symptoms– Displacement of the deep muscle planes from the

adjacent metaphysis caused by deep-tissue edema– Lytic bone changes are not visible on radiographs until

30–50% of the bony matrix is destroyed. – Tubular long bones do not show lytic changes for 7–14

days after onset of infection. Flat and irregular bones can take longer.

Septic Arthritis

• May cause permanent disability• More frequent in infants and children• Most common: Staphylococcus aureus• May also be caused by Gonococcus in sexually

active adolescents• Usually hematogenous in origin• Neonates may present with subtle signs and

symptoms, while older infants and chidren usually manifest with pain, fever, limp or difficulty in ambulation

Septic Arthritis

• Diagnosis– Definitive Dx: Gram stain and culture– Blood culture– Radiographic findings• Widening of joint capsule• Soft tissue edema• Obliteration ofnormal fat lines

– UTZ is sensitive in detecting joint effusion– CT and MRI can confirm the presence of joint fluid

Septic Arthritis

• Treatment usually lasts for 10-14 days– Neonates: Nafcillin/Oxacillin + Cefotaxime– Children: Nafcillin or Cefazolin– MRSA : Clindamycin + Vancomycin– Immunocompromised: Vancomycin and

Ceftazidime or extended-spectrum penicillins and B-lactamase inhibitors, + aminoglycoside

– Dexamethasone for 4 days

Achondroplasia

• Autosomal dominant• At birth, nepnates present with short limbs, a

long and narrow trunk, large head with mid-facial hypoplasia and a prominent forehead

• Proximal segments of the limbs are usually short and fingers display a trident configuration

• Most joints are hyperextensible• Normal intelligence

Achondroplasia

• Diagnosis– Radiographic Findings• Large calvarial bones• Small cranial base and facial bones• Short vertebral pedicles, decrease interpedicular

distance, 1st to 5th lumbar vertebra• Fibula longer than tibia

• Treatment– Surgical correction may be done for severe spinal

canal stenosis

Osteogenesis Imperfecta

• Autosomal dominant• Triad– Fragile bones– Blue sclerae– Early deafness

• Most common genetic cause of osteoporosis• Connective tissue disorder• Defective type I collagen– Primary component of the ECM of bone and skin

Osteogenesis Imperfecta

• Diagnosis– Collagen biochemical studies or sequencing of cDNA– UTZ as early as 16wks AOG may detect sever OI

• Treatment– None– Supportive:• Severe nonlethal type: active physical rehabilitation while

the patient is young• Severely affected individuals: wheelchair ambulation• Orthopedic management: treatment of fractures and

correction of deformity

• Cause of death: Cardiopulmonary