CURRENT ESSENTIALS PEDIATRICS - part 7 pptx

It is a fibrous formation within the muscle, not tumor trans-• Hip dysplasia associated in 20% of cases • Diagnosis is by physical examination, but magnetic resonanceimaging MRI may be ne

• Causes—diseases of the cervical spine, injury to the domastoid during delivery, or intrauterine pressure

sternoclei-• Sternocleidomastoid mass is often palpable It is a fibrous formation within the muscle, not tumor

trans-• Hip dysplasia associated in 20% of cases

• Diagnosis is by physical examination, but magnetic resonanceimaging (MRI) may be needed to completely evaluate

• Rheumatoid arthritis—older children

• Trauma and mild respiratory illness may precede onset

• Unilateral flattened occiput from intrauterine pressure or backsleeping causes apparent torticollis when infant is supine

• Motor weakness, cerebral palsy, dystonia, spasticity producetorticollis

■ Treatment

• Passive stretching is usually effective <1 year

• Surgical release after 1 year is effective in uncomplicated cases

• Excision of the fibrous “tumor” is unnecessary

Arthrogryposis Multiplex Congenita

■ Essentials of Diagnosis

• Congenital fibrous ankylosis of many joints—shoulders adducted,elbows extended, wrists flexed, fingers stiff, dislocated hips, kneesextended, club feet, scoliosis

• Usually bilateral involvement

• Infants usually have normal mental and sensory development butsevere physical disability

• Variable inheritance—may be associated with other somaticabnormalities

• Diagnosable by intrauterine ultrasound

(amy-• Intrauterine bands may cause contractures

■ Treatment

• Passive mobilization early

• Prolonged casting is contraindicated because of further stiffness

• Surgical joint release, tendon transplant, capsulotomies, osteotomiessometimes needed

■ Pearl

Fetal akinesia (lack of muscle movement) can also produce dramnios, pulmonary hypoplasia, micrognathia, hypertelorism, short- ened umbilical cord depending on severity of the akinesia.

polyhy-18

• Ocular abnormalities include subluxation of the lens, cataract,coloboma, megalocornea, strabismus, myopia, and nystagmus

• Defect is in genes coding for fibrillin One-third of cases are radic mutations, two-thirds are familial Sex distribution equal

spo-• Diagnosis is usually clinical but testing shows ↓serum teins,↑urinary hydroxyproline excretion Genetic testing available

mucopro-• Diagnosis is much more obvious as children grow Tall stature isthe most common reason for investigation

■ Differential Diagnosis

• Homocystinuria—patients look marfanoid but urinary tine is elevated in homocystinuria

homocys-• Familial tall stature

• Ehlers-Danlos syndrome shares some findings

■ Treatment

• Regular ophthalmologic evaluation and care

• Regular orthopedic evaluation and care, especially to preventscoliosis

• Regular cardiac evaluation with serial echocardiograms β-blockersmay reduce the progression of aortic root dilation

■ Pearl

The rate of mutation of the fibrillin gene appears to be related to nal age The older the father, the higher the mutation rate.

pater-18

ver-• Short stiff neck, low hairline, low-set ears, deafness, web neck,high scapula

• Structural and functional renal abnormalities

• Gene inversion on long arm of chromosome 8 Increased risk ininfants with fetal alcohol syndrome

■ Differential Diagnosis

• VACTERL syndrome has many of the same characteristics

• Sprengel deformity of the scapula causes similar short neck

■ Treatment

• Many patients have no symptoms

• Fusion of the cervical vertebrae causes neurologic symptoms withgrowth—tingling, numbness, paralysis of upper extremities

• All patients require hearing evaluation

• Renal, orthopedic, neurology, and sometimes cardiology cialists should follow these children

spe-■ Pearl

Minor trauma may cause serious injury to the spinal cord in patients with Klippel-Feil syndrome Spinal fusion can reduce this risk.

Chapter 18 Orthopedics 315

Osteogenesis Imperfecta

■ Essentials of Diagnosis

• Genetic connective tissue disease with recurrent bone fractures

caused by mutations in COL IA1 and 2 genes encoding for type I

procollagen

• Fetal type has intrauterine and perinatal fractures, blue sclerae, thinskin, joint hypermobility, otosclerosis, hearing loss, hypoplasticteeth, wormian bones, normal intelligence

• Later presentation (tarda type) is less severe

• Other forms fatal due to severe skeletal deformities and tory insufficiency due to thoracic constriction

respira-• Intrauterine ultrasound or chorionic villus sampling allow tal diagnosis and evaluation of severity

• Avoidance of injury, regular physical therapy

• Biphosphonates may be helpful

• Bone marrow transplant, growth hormone, gene therapy are imental

exper-■ Pearl

Osteogenesis imperfecta is a rare disorder Multiple bone fractures in different stages of healing are a red flag for child abuse first and osteo- genesis imperfecta second.

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■ Essentials of Diagnosis

• The most common form of short-limbed dwarfism Autosomaldominant 80% are new mutations on chromosome 4

• Caused by delayed ossification of cartilage

• Short upper arms and thighs, waddling gait, bowed legs, jointlimitation, short fingers of equal length, frontal bossing, hydro-cephalus, depressed nasal bridge, lumbar lordosis

• Thoracic and skull deformities cause respiratory insufficiencyand recurrent otitis

• Intelligence normal

• Narrowed spinal canal and foramen magnum may lead to gressive spinal cord compression with sudden death in infancy orparaplegia in older individuals

pro-• Phenotypic features are nearly diagnostic, even at birth Prenataldiagnosis is available

■ Differential Diagnosis

• Other forms of dwarfism and nonsyndromatic short stature

■ Treatment

• No specific therapy

• Patients should be monitored for foramen magnum compression

• Growth hormone therapy and limb lengthening surgery have beenused with some success to increase final height

• Recurrent otitis should be treated aggressively to prevent sclerosis and hearing loss

oto-■ Pearl

Mutations in fibroblast growth factor receptor gene are involved in a number of syndromes with skeletal abnormalities The mechanism by which the abnormal growth factor receptor protein produces achon- droplasia is not yet known.

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• Congenital vertebral anomalies are the cause of scoliosis in 5–7%

• Curvature <20° usually requires no treatment

• Curvature 20°–40° treated by bracing

• Curvature >40° usually resistant to bracing and may require spinalfusion

• Curvature >60° causes poor adult pulmonary function

■ Pearl

Idiopathic scoliosis of girls is usually convex to the right and rarely causes pain The presence of pain or a left convex curvature should dictate careful investigation for other disorders such as bone or spinal cord tumor.

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Slipped Capital Femoral Epiphysis

• Limitation of internal rotation on physical examination

• Lateral hip radiographs show posterior and inferior slippage of theproximal epiphysis

■ Differential Diagnosis

• Renal osteodystrophy or other metabolic bone disease

• Lower spine or disc disease causing sciatic pain

• Bone tumor of the proximal femur may cause hip pain

Chapter 18 Orthopedics 319

Genu Varum/Genu Valgum

■ Essentials of Diagnosis

• Genu varum (bowleg) is normal up to 2 years

• Genu valgum (knock knee) is normal in children from 2 to 8 years

• Persistent bowleg, increasing bowleg, unilateral bowing beyondage 2 should be evaluated

• Knock knee associated with short stature should be evaluated

• Monitor bowleg by measuring the inter-knee distance at everywell-child visit

■ Differential Diagnosis

• Bowleg may be associated with internal tibial torsion, Blount ease (proximal tibial epiphysial dysplasia), metaphysical chon-drodysplasia, achondroplasia, nutritional or hypophosphatemicrickets, lead or fluoride intoxication

dis-• Knock knee >age 8 associated with obesity

• Asymmetric bone growth following trauma to the growth platemay resemble either knock knees or bowleg depending on site ofinjury

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• Femoral anteversion produces toeing in beyond age 2–3 years

• This condition shouldn’t be mistaken for club foot but sometimes is

■ Treatment

• Most tibial torsion requires no therapy

• Discourage belly sleeping with feet turned in

• Tibial torsion >15° after age 7–10 years may require tibialosteotomy

• Braces or splints to promote external rotation are sometimes used

■ Pearl

Neither putting a toddler’s shoes on backwards nor using the old Browne splint to keep the feet at a 45° angle outward are proven to be better than waiting for natural resolution in most infants.

Denis-18

↑risk of Pseudomonas after nail punctures through the shoe

• Infection penetrates across the growth plate in children <1 yearcausing septic arthritis and long-term growth problems

• Infection spreads via the periosteum in older children with fusedgrowth plates Joints are less often involved

• Symptoms—fever, irritability, pseudoparalysis, local redness,pain, tenderness

• High erythrocyte sedimentation rate (ESR) and white blood cellcount (WBC); positive blood or bone culture

• X-ray cannot detect early osteomyelitis or small infections Bonescan and MRI are more sensitive

■ Differential Diagnosis

• Clinical findings may suggest fracture, bone cyst, bone tumor

• Other serious infections, inflammatory and autoimmune tions may initially have the same nonspecific fever and systemicsymptoms of osteomyelitis

condi-■ Treatment

• Antibiotic therapy depending on culture and sensitivity for at least

3 weeks

• Splinting the limb minimizes pain and decreases lymphatic spread

• Aspiration of the affected bone is the best way to culture and toprovide surgical drainage if needed

■ Pearl

If acute symptoms and signs of osteomyelitis are not resolving within

3 days of initiation of therapy, consider surgical exploration for drainage and debridement.

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Pyogenic Arthritis

■ Essentials of Diagnosis

• Arises from adjacent osteomyelitis in infants (S aureus)

• In older children arises during systemic infections with organisms

having a predilection for joints (S aureus, Streptococcus species, Neisseria gonorrhea, Kingella kingae, tuberculosis, Salmonella

species)

• Risk increased in immunodeficiency, intravenous (IV) drug use,and sickle cell disease

• Symptoms—fever, malaise, emesis, restricted movement

• Joint aspiration for drainage and culture is key to diagnosis andtherapy

• Joint fluid WBC >100,000/µL, ESR >50

• Joint x-rays are insensitive WBC or gallium scan localizes infection

■ Differential Diagnosis

• Fever of unknown origin

• Noninfectious arthritis—inflammatory bowel disease, toid arthritis, Reiter syndrome, Lyme disease, rheumatic fever,systemic lupus, leukemia, drug reactions, autoimmune hepatitis

rheuma-• Hemarthrosis with bleeding disorders

• Associated with viral infection, mild trauma, or possibly allergy

• Limitation of motion of hip, especially internal rotation

• ESR, WBC normal Fever usually absent

• Hip joint aspirate yields sterile serous fluid with few WBC

■ Differential Diagnosis

• Pyogenic arthritis

• Other noninfectious arthritis—inflammatory bowel disease,rheumatoid arthritis, Reiter syndrome, Lyme disease, rheumaticfever, systemic lupus, leukemia, drug reactions, autoimmune hep-atitis

• Slipped capital femoral epiphysis

• Fracture

■ Treatment

• Rest and gentle traction

• Pain control with nonsteroidal anti-inflammatory agents

• Usually self-limited but may recur

• Monitor by x-ray for slipped capital femoral epiphysis

■ Pearl

Aseptic necrosis of the femoral head occurs in 1–2% of patients with transient tenosynovitis of the hip Coxa magna (asymptomatic enlarge- ment of the femoral head and broadening of the femoral neck) occurs

in 32.1% and may be a precursor of aseptic necrosis or long-term arthritis in the hip

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Avascular Necrosis (AVN) of the Proximal Femur

(Legg-Calvé-Perthes Disease)

■ Essentials of Diagnosis

• Highest incidence in 4–8-year-old males

• Persistent pain, limp, limitation of movement

• Joint aspirate normal Laboratory studies normal Systemic toms absent

symp-• X-ray shows joint effusion early Later findings are patchydecreased bone density around the joint

• Very late complications—necrotic ossification, collapse of femoralhead, fragmentation of the epiphysis, variegated bone density,involvement of metaphysis

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• Necrotic fragments that remain in place may be resorbed

• Local swelling and pain, sensation of joint “locking” or “givingway”

• X-ray of affected joint may show area of necrosis MRI helpful

in finding joint fragments

■ Differential Diagnosis

• Other arthritides

• AVN of the femoral head

• Sprains, strains, and fractures

■ Treatment

• Rest for 6–8 weeks

• Joint mice may be removed arthroscopically

• Attached necrotic fragments may be surgically drilled to promotemore rapid neovascularization and resorption

■ Pearl

Arthritis often develops in a joint with mice Protect the joint from ther trauma to reduce the risk of late arthritis.

fur-18

Fibrous Dysplasia

■ Essentials of Diagnosis

• Idiopathic disorder Proliferation of fibrous tissue arising fromthe medullary canal causes uneven bone growth, pain, fractures,bony deformity (shepherd’s crook deformity of the femur is classic)

• Asymmetric distribution of bony involvement

• May be monostotic or polyostotic

• Polyostotic disease with endocrine disturbance (McCune-Albrightsyndrome) occurs in girls with precocious puberty, café au laitspots, hyperpituitarism, hyperthyroidism, hyperadrenalism

• Pain is rare, usually associated with fractures

• No treatment needed for small lesions

• Large lesions may provoke fractures and may require curettageand bone grafting

■ Pearl

If a young girl with bone pain or fractures has café au lait spots, she probably has McCune-Albright syndrome Ask about symptoms of pre- cocious puberty.

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• Familial cases are reported

• Major symptoms—fussiness, fever, tender swellings of multiplebone shafts (clavicle and mandible most common) without softtissue involvement

• Increased WBC, ESR, and alkaline phosphatase with mild anemia

• Cortical hyperostosis seen on x-ray

• Ewing sarcoma, metastatic neuroblastoma

• Prostaglandin E1or E2administration causes hyperostotic swelling

■ Treatment

• Resolves spontaneously in weeks or months

• Steroidal and nonsteroidal medications for symptom relief

• Occasionally there are long-term abnormalities of bone growthand deformity requiring surgical correction

■ Pearl

For unknown reasons, the frequency of sporadic cases is decreasing Familial cases are now relatively more likely.

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■ Essentials of Diagnosis

• Injury to the pars interarticularis of the spine 85% occur at L5

• Cause is repetitive stress Common problem of gymnasts, dancers,and football players

• Most common symptom is back pain worse on extension Painradiates to buttock or thigh

• Oblique x-rays of the spine reveal the posterior “Scottie dog sign”

• Stretching of the hamstrings

• Spine stabilization exercises

• Lumbosacral bracing or in severe cases surgical stabilization

■ Pearl

Sports with the highest incidence of back pain and injury are golf, nastics, football, dance, wrestling, and weight lifting Spondylolysis occurs more frequently in patients with spina bifida occulta.

gym-18

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Sports Medicine and Rehabilitation

Concussion 331

Radiculopathy (Burners and Stingers) 332

Rotator Cuff Injury 333

Anterior Knee Pain 334

Anterior Cruciate Ligament (ACL) Injury 335

Posterior Cruciate Ligament (PCL) Injury 336

Medial and Lateral Collateral Ligament Injuries 337

Elbow Pain 338

Hip Pain 339

Foot Pain 340

329

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Chapter 19 Sports Medicine and Rehabilitation 331

Concussion

■ Essentials of Diagnosis

• Temporary and immediate impairment of neurologic functionwith/without loss of consciousness (LOC) after head trauma

• Grade 1—no LOC Post-traumatic amnesia (PTA) or

confu-sion lasts <15 minutes

• Grade 2—no LOC PTA or confusion lasts >15 minutes

• Greater health risks after second concussion due to “second impactsyndrome” with loss of vascular auto regulation and cerebraledema

■ Differential Diagnosis

• Symptoms appearing after minor head trauma may be a response

to underlying brain tumor

• Consider cardiac arrhythmia, seizure, stroke, or migraine for anyLOC occurring during sports

• Drug abuse

■ Treatment

• Return-to-competition guidelines following concussion

• Grade 1—return to play in 15 minutes if examination normal

• Grade 2—return to play in 1 week if symptom free Hospital

evaluation if symptomatic >60 minutes Computed phy (CT) or magnetic resonance imaging (MRI) if symptomspersist for >1 week

tomogra-• Grade 3—return to play in 1 week if LOC <60 seconds and

if symptom free Return to play in 2 weeks if LOC >60 secondsand if symptom free Hospital evaluation as in Grade 2 forpersistent symptoms

• For a second injury restrictions are greater—Grade 1: no play for

1 week, Grade 2: no play for 2 weeks, and Grade 3: no play for

at least 1 month

■ Pearl

The “Standardized Assessment of Concussion (SAC)” is a 5-minute clinical screening instrument that can be used by trained nonmedical sports supervisors to assess the level of injury of a participant An SAC kit includes a training manual and can be obtained online.

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Radiculopathy (Burners and Stingers)

Athletes of all levels get these common burners or stingers especially

in football Shoulder and neck conditioning to increase strength helps prevent injury Shoulder pads that ride high with air floatation devices

or extra padding also prevent injury

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Chapter 19 Sports Medicine and Rehabilitation 333

Rotator Cuff Injury

• Reduce inflammation—anti-inflammatory medication, ice, rest

• Gradually improve flexibility with stretching exercise

• Increase strength of scapular stabilizers and rotator cuff muscles

by isotonic or isokinetic exercise

• Biomechanic evaluation can assist in recovery by building specific skills and eliminating substitution patterns

sport-■ Pearl

The shoulder has the greatest range of motion of any joint in the body The muscles of the rotator cuff hold the humoral head in the socket They include the subscapularis, supraspinatus, infraspinatus, and teres minor. 19

Anterior Knee Pain

■ Essentials of Diagnosis

• Most common cause is “patellofemoral overuse” syndrome inrunners causing pain under patella and over medial surface.Swelling and crepitus of knee

• Plicae alares thickening or fibrosis occurs with repetitive trauma or macro trauma Pain on flexion and “popping” of theknee

micro-• Tendonitis of the patellar tendon

• Osgood-Schlatter disease—inflammation at the tibial tubercle inadolescent boys and girls causes joint pain

• Patellar chondromalacia—diagnosed by arthroscopy

■ Differential Diagnosis

• Hip pathology may refer to the knee

• Arthritis

• Neoplasm

• Tibial stress fracture

• Meniscus and ligament injuries

• Tight iliotibial band produces pain over the lateral femoral condyle

• Gastrocnemius-soleus injury produces posterior knee pain

■ Treatment

• Control inflammation with medication, ice, and rest

• Alignment problems should be treated with stretching andstrengthening

• Orthotics if there are foot deformities producing stress on thejoint

■ Pearl

There is no consensus on treatment of patellofemoral overuse syndrome Quadriceps strengthening and control of inflammation are the most common modalities suggested.

19

Chapter 19 Sports Medicine and Rehabilitation 335

Anterior Cruciate Ligament (ACL) Injury

• Lachman test—gentle traction on the tibia with knee bent 30°reveals increased movement (>4 mm)

• Anterior drawer test similar but with knee bent 90°

• X-ray and/or MRI needed in knee injuries

Posterior Cruciate Ligament (PCL) Injury

• Avulsion of the PCL is as common as a tear

• Bony fracture at the site of avulsion or elsewhere

Chapter 19 Sports Medicine and Rehabilitation 337

Medial and Lateral Collateral Ligament Injuries

• Pain reproduced by valgus stress in 20°–30° flexion

• Knee x-rays required to rule out other injury

• Initial therapy includes ice and elevation

• Bracing with full knee motion in brace after 7 days

• Strengthening exercises and weight bearing should begin in firstweek

• Brace should be used until there is pain-free full range of motion

■ Pearl

Functional bracing may be required even after the athlete returns to competition in order to permit complete ligament healing.

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Elbow Pain

■ Essentials of diagnosis

• Medial—medial epicondylitis secondary to overuse and valgus

stress, tendonitis, ulnar collateral ligament injury, ulnar neuritis,apophysitis, and fracture

• Lateral—chronic valgus stress causes focal injury of the

capitel-lum (5–12 year olds), osteochondritis dissecans of the capitelcapitel-lum(13–15 year olds), lateral epicondylitis (racquet sports)

• Posterior—dislocation, fracture, triceps avulsion, olecranon

bursitis

• X-rays needed especially to detect avascular necrosis of thecapitellum and Panner disease (fragmentation and sclerosis of thecapitellum)

• Prevention is the key to most of these athletic-related injuries

• Acute therapy includes ice, rest, and anti-inflammatory medications

• Evaluation of mechanics and physical therapy to strengthen armmusculature

• Orthopedic referral and possible surgery for osteochondritis secans

dis-■ Pearl

Little league pitchers are particularly prone to medial epicondylitis The 85 pitch rule was instituted in response to this problem.

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