SPORTS MEDICINE



Ovid: Pediatrics

Editors: Tornetta, Paul; Einhorn, Thomas A.; Cramer, Kathryn E.; Scherl, Susan A.
Title: Pediatrics, 1st Edition
> Table of Contents > Section III: – Specialty Clinics > 24 – SPORTS MEDICINE

24
SPORTS MEDICINE
24.1 KNEE PAIN
LAWRENCE WELLS
Knee pain as the presenting symptom or complaint can
come from a variety of sources. The approach to diagnosis, and to
ultimately recommending a course of treatment, lies in four steps:
  • Have an appreciation of normal knee anatomy.
  • Obtain a thorough history, including onset and duration of symptoms, mechanism of injury, and precipitating causes of pain.
  • Perform a complete physical examination
    if necessary, taking into account surrounding areas (spine, hip, ankle)
    that may be sources of referred knee pain.
  • Order supplemental studies, such as
    radiographs, magnetic resonance imaging (MRI), bone scans, and special
    procedures (arthrocentesis, arthrometer testing, and examination under
    anesthesia) if they can aid in identifying the cause of knee pain.
The knee is a hinged joint with three major bony articulations surrounded by a complex array of ligaments and tendons (Figs. 24.1-1, 24.1-2 and 24.1-3 and Table 24.1-1).
The menisci are found between the medial and lateral femoral tibial
articulations. They provide increased surface area to dispense
weightbearing forces between the femur and tibia, as well as provide
supplemental stability for the knee (Fig. 24.1-4).
There are several bursae, which are fluid-filled sacs
that allow adjacent soft tissue envelopes to glide across one another
about the knee. The most commonly involved in injury are the
prepatellar bursa (Fig. 24.1-5), pes anserine
bursa, and infrapatellar tendon fat pad. When inflamed, they present as
tender, soft, boggy structures overlying the area of injury.
The knee also is surrounded by a complex array of
neurovascular structures—the popliteal artery and vein and the tibial,
common peroneal, and saphenous nerves.
Appreciating the anatomy of the knee helps one to
conduct specific examinations of each area previously listed and
identify areas of injury. Localizing the pain to a particular area is
the key to making the correct diagnosis. If the pain cannot be
localized on physical examination, one should consider a referred pain
from another area, such as the hip, spine, or ankle (Fig. 24.1-6).
Figure 24.1-1 Surface anatomy of the knee. A; Suprapatellar and infrapatellar depressions. B; Adductor tubercle. C; Patella. D; Joint line. E; Tibial tubercle.

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Figure 24.1-2 Normal knee anatomy.
Figure 24.1-3 Ligaments of the knee. A; Posterior cruciate ligament. B; Anterior cruciate ligament. C; Patellofemoral articulation.
TABLE 24.1-1 KNEE LIGAMENT AND TENDON ANATOMY

Structure

Origin

Insertion

Anterior cruciate

Posterior lateral intercondylar notch

Medial tibial spine

Posterior cruciate

Anterior medial femoral notch

Proximal posterior tibia

Lateral collateral ligament

Lateral femoral condyle

Fibular head

Medial collateral ligament

Medial femoral epicondyle

Medial tibial shaft

Quadriceps tendon

Rectus femoris and 3 vastus muscles

Superior patella

Patella tendon

Inferior patella

Tibial tubercle

Pes anserine tendons

Gracilis, semitendinosis, and semimembranosus muscles

Medial tibial shaft superficial to medial collateral ligament

Lateral hamstring

Long and short biceps femoris muscle

Fibular head and proximal tibia

Iliotibial band

Tensor fascia lata

Gerdy tubercle

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Figure 24.1-4 Axial view of knee menisci.
PATHOGENESIS
The most common causes of knee pain are from traumatic
injuries—acute versus repetitive microtrauma accumulated over time.
However, one needs to take a comprehensive approach in identifying the
cause of pain. The anagram VINDICATER is a useful tool as one begins to
formulate a differential diagnosis for knee pain (Box 24.1-1).
DIAGNOSIS
Patient History
The history can frequently provide many helpful clues to
identify the cause of knee pain. Obtaining a complete history can be
difficult in a young child. Therefore, in addition to the child, it is
important to interview the caretakers who are familiar with the child
and circumstances related to the child’s symptoms (Tables 24.1-2 and 24.1-3).
Figure 24.1-5 Prepatellar bursa.
Figure 24.1-6 Sources of referred pain.
Physical Examination
  • Begin with inspection of the knee alignment (Fig. 24.1-7), observation of the gait pattern, palpating pulses, and a neurologic exam (Table 24.1-4).
  • Follow with evaluation of joint motion, tests for ligament stability, and direct palpation to identify specific areas of injury.
    • □ Localized tenderness is an important finding to identify the source of pain (Fig. 24.1-8).
    • □ Meniscal injuries often present with
      joint line tenderness extending from the midportion of the knee in the
      coronal plane posteriorly behind the femoral condyle.
    • □ Tender crepitance along the joint line
      with flexion-rotation (McMurray test) or compressionrotation maneuvers
      (Appley test) suggest a meniscal tear.
    • □ Severely displaced menisci often found in buckethandle type tears can also limit full knee motion, especially extension.
  • The patellofemoral joint is assessed with the patient lying supine and sitting with the knee bent at 90 degrees (Fig. 24.1-9).
    • □ Attempts at translating the patella
      medially and laterally can elicit a sense of apprehension or resistance
      from the patient in the case of patellar subluxation or dislocation (Fig. 24.1-10).
    • □ Painful crepitance and tenderness along medial or lateral parapatellar retinaculum are also signs of patellofemoral injury.
    • □ Malalignment is determined by measuring
      the Q angle, which is formed by the intersection of a line drawn along
      the long axis of the thigh and a line drawn from the midpoint of the
      patella to the tibial tubercle.
      • □ The normal value of the Q angle is 10 degrees in men and 15 degrees in women.
      • □ Increased Q angles are thought to represent lateral tracking or misalignment of the patellofemoral joint.
    • □ Direct tenderness of the infrapatellar tendon can represent patellar tendonitis, commonly seen in repetitive jumping sports.
    • □ Sinding-Larsen-Johansson syndrome and
      Osgood-Schlatter disease are represented by tenderness over the
      inferior pole of the patella and tibial tubercle, respectively.
    • □ Tenderness over the lateral femoral
      epicondyle is often present with iliotibial band tendonitis, and
      tenderness over the pes anserine area can represent an inflamed bursa
      adjacent to medial hamstring insertions (Figs. 24.1-8B and 24.1-11, 24.1-12, 24.1-13, and 24.1-14; Table 24.1-5).
  • The knee ligament exam is conducted with both the patient sitting and supine.
    • □ Lying supine often helps the patient to
      relax, thus avoiding inadvertent hamstring contraction that can
      compromise the examination results (Table 24.1-6).

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TABLE 24.1-2 HISTORY OF KNEE INJURY

Question

Areas to Consider

Is the pain localized to a specific area? Ask patient to point to exact area.

Joint line, patella tendon, pes anserine bursa

Is there a sense of giving way or locking?

Meniscal tear, loose body, chronic muscle weakness

What is nature of pain? Activity-related, sharp, dull, burning, acute, or chronic?

Overuse syndrome, fracture, reflex sympathetic dystrophy

Is one awakened at night from pain? Is pain relieved by salicylates or nonsteroidal antiinflammatory medications?

Infection or tumor

Was a “pop” felt or heard preceding symptoms? Was patient able to continue activity?

Ligament injury

Did knee swell immediately?

Meniscal, ligament injury or fracture

Is the pain accentuated with going up or down stairs?

Patellofemoral joint irritation

TABLE 24.1-3 OUTCOMES ANALYSIS OF KNEE INJURY MECHANISM

Mechanism

Potential Outcomes

Twisting planted foot

Meniscal or ligament injury

Fall directly onto knee

Contusion extensor mechanism or PCL injury

Valgus or varus stress

MCL, MM or LCL, LM injury, respectively

Sense of “pop,” immediate swelling, inability to continue activity participation

ACL or fracture

Sense of “giving way” or locking

Meniscal tear or patellofemoral injury

Constant or nighttime pain, relief with nonsteroidal antiinflammatory medications

Infection or tumor

Pain with use of stairs or prolonged sitting/squatting

Patellofemoral injury

ACL,
anterior cruciate ligament; LCL, lateral collateral ligament; LM,
lateral meniscus; MCL, medial collateral ligament; MM, medial meniscus;
PCL, posterior cruciate ligament.

TABLE 24.1-4 PHYSICAL EXAMINATION FOR KNEE PAIN

Inspection

Varus/Valgus Alignment

Thigh and Calf Circumference

Foot Position

Swelling, Absence of Normal Parapatellar Concavities

Gait

Limp

Short leg

Kneeling

Jump—double/single leg

Joint motion

Extension: normal 0 degrees

Flexion: normal 145 degrees

Popliteal angle: normal <20 degrees

Neurovascular examination

Popliteal, dorsalis pedis, posterior tibial artery

Tibial, common peroneal, and saphenous nerves

Skin color, warmth

Figure 24.1-7 Knee alignment.

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Figure 24.1-8 Potential causes of knee pain and their respective anatomic locations.
Figure 24.1-9 Supine evaluation of patellofemoral joint.

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Figure 24.1-10 Lateral translation and palpation of lateral patellar facet.
Figure 24.1-11 Testing collateral ligaments of the knee.
Figure 24.1-12 Lachman test for anterior cruciate ligament deficiency.
Figure 24.1-13 (A) Posterior sag sign, indicating posterior cruciate injury. (B) Absence of posterior sag, indicating normal posterior cruciate ligament.

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Figure 24.1-14 Meniscal injuries.
TABLE 24.1-5 DIAGNOSIS OF KNEE PAINa

Localized Tenderness

Diagnostic Considerations

Joint line

Meniscal injury

Patellofemoral

Patellar subluxation/prepatellar bursitis

Inferior patella

Sinding-Larsen-Johansson syndrome

Infrapatella tendon

Patellar tendonitis/anterior fat pad

Tibial tubercle

Osgood-Schlatter disease

Gerdy tubercle/lateral femoral epicondyle

Iliotibial band syndrome, lateral collateral ligament injury

Pes anserine

Pes anserine bursitis

a See also Figure 24.1-8.

TABLE 24.1-6 LIGAMENT EXAMINATION

Ligament

Test

Treatment

Outcome

MCL

Valgus stress at 30 degrees of flexion (Fig. 24.1-11)

Brace/early ROM

4-6 wk recovery

LCL

Varus stress at 30 degrees of flexion (Fig. 24.1-11)

Brace/early ROM

Same as MCL

ACL

Lachman, anterior drawer, pivot shift (Fig. 24.1-12)

Acute: ROM, hamstring strengthening, avoid sudden deceleration sports; ACL reconstruction after full ROM restored

Excellent with ACL reconstruction and post-op rehabilitation; return to sports 6-12 mo

PCL

Posterior drawer, posterior sagittal (Fig. 24.1-13), quad active test

Rehabilitate quads

Generally good for grade 1 and 2 injuries

PCL/PLC

Same as PCL plus reverse pivot shift and increased external rotation at 30 and 90 degrees of flexion

Surgical reconstruction within 2 wk of injury

Expect mild residual but improved laxity

ACL,
anterior cruciate ligament; LCL, lateral collateral ligament; MCL,
medial collateral ligament; PCL, posterior cruciate ligament; PLC,
posterior lateral corner; ROM, range of motion.

Radiographic Features
  • Routine x-rays of the knee should be part of every “painful knee” evaluation.
    • □ A standard knee x-ray exam should
      include a weight-bearing posteroanterior (10 to 15 degrees flexed),
      lateral, Merchant or sunrise patella view, and an intercondylar notch
      view of the knee.
    • □ When the patient is unable to stand, an anteroposterior view of the knee should be obtained.
    • □ After a satisfactory film is obtained, systematic careful evaluation of the x-ray is performed.
    • □ Although seemingly evident, it is wise to confirm the name on the films with the name of the patient being examined.
    • □ Appropriate indicators of the side (right vs. left) being examined should also be noted (Table 24.1-7).
  • When knee x-rays are normal, evaluate the spine, hip, and ankle regions to rule out sources of referred pain.
  • Additional imaging studies such as MRI
    and bone scans can be useful in determining and localizing the extent
    of injury and in making treatment decisions, but they should not be
    used as primary screening studies.
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  • Special procedures for diagnosing knee pain are given in Table 24.1-8.
TABLE 24.1-7 RADIOGRAPH EVALUATION GUIDELINES

Areas to Study

Significant Findings

Soft tissue contours

Effusion, soft tissue mass

Cortical margin

Erosions, lytic changes

Marrow contents

Lucency, blastic changes, calcification

Air-fluid levels

Open knee joint, penetrating trauma

Cortical discontinuity

Fracture

TABLE 24.1-8 SPECIAL PROCEDURES

Procedure

Benefits

Arthrocentesis

Decreased symptoms, diagnostic information; acute hemarthrosis suggests meniscal or ACL injury

Stress radiographsa

Rule out underlying physeal injury

Arthrometer testing

Noninvasive tool for ACL/PCL laxity assessment

Examination under anesthesia

Preoperative injury confirmation, improved clinical examination

a Caution: avoid iatrogenic popliteal artery injury with overzealous stress.

ACL, anterior cruciate ligament; PCL, posterior cruciate ligament.

TABLE 24.1-9 VASCULAR CAUSES OF KNEE PAIN

Cause

History

Physical Examination

Treatment

Outcome

Sickle cell disease

Pain crisis, +HbSS electrophoresis

Joint effusion, pyoarthrosis

Arthrotomy, antibiotics

Arthritis, disability

Hemophilia

Male gender, factor VIII deficiency

Painful swollen joint

Factor replacement, RICE, joint motion, arthroscopic synovectomy

Good with attention to prevention, maintaining adequate factor level

HbSS, homozygosity for hemoglobin S; RICE, rest, ice, compression, elevation.

TABLE 24.1-10 INFECTIOUS CAUSES OF KNEE PAIN

Cause

History

Physical Examination

Laboratory Findings

Diagnostic Tests

Treatment

Outcome

Septic arthritis

Sexually active adolescent

Swollen, tender, limited motion

↑Synovial WBC, ↑ESR, CRP, +blood culture, bone scan

Aspiration, culture

Arthroscopic lavage, RICE, joint motion after acute symptoms resolved

Excellent if treated within a few days of onset; delayed treatment results in arthritis

Osteomyelitis

Low-grade fever, dull pain

Metaphyseal tenderness, limited motion

↑WBC, ESR

X-ray shows osteolytic changes; biopsy, culture routine, +AFB

Surgical débridement, antibiotics

Physeal injury; limb length inequality if extensive

AFB,
acid-fast bacillus; CRP, C-reactive protein; ESR, erythrocyte
sedimentation rate; RICE, rest, ice, compression, elevation; WBC, white
blood cell count.

Differential Diagnosis
  • Vascular causes of knee pain are listed in Table 24.1-9.
  • Infectious causes of knee pain are listed Table 24.1-10.
  • As a whole, primary bone tumors around the knee are rare.
    • The most common and the most dangerous neoplastic lesions are listed in Table 24.1-11. Recognizing

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      them is vital to delivering appropriate treatment without delay.

    • Degenerative conditions are typically not found in the pediatric age group.
    • Primary inflammatory conditions of the knee are rare.
      • □ Generally, juvenile rheumatoid arthritis presents in the 2- to 6-year-old age group as a swollen knee and a limp.
      • □ Workup to rule out trauma, infection, and tumor are normal.
      • □ Treatment is primarily medical, and patients should be referred to a rheumatologist.
      • □ Outcomes are generally good with appropriate medical management.
      • □ Other considerations for inflammatory causes of knee pain include Lyme disease and lupus erythematosus.
      • □ Extensor mechanism disorders typically fall under the scope of overuse syndromes (Box 24.1-2), which are considered more fully in section 24.2.
    • Congenital causes—conditions with
      generalized ligamentous laxity, such as Ehlers-Danlos syndrome, Down
      syndrome, and nail-patella syndrome—typically make children more prone
      to injury, particularly of the patellofemoral joint.

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      • □ Treatment protocols usually do not differ from those of children without congenital conditions.
    • Traumatic causes of knee pain are listed in Table 24.1-12.
    • In cases in which the physical
      examination is unremarkable, one needs to consider referred sources of
      knee pain, which are given in Box 24.1-3.
TABLE 24.1-11 NEOPLASTIC CAUSES OF KNEE PAIN

Cause

History

Physical Examination

Laboratory Findings

Radiographic Findings

Treatment

Outcome

Baker cyst

Painless mass popliteal fossa

Firm rubbery nodule, transilluminates light

None needed

Normal

Observation

Many resolve spontaneously

Meniscal cyst

Painful nodule at joint line

Lateral mass, aspiration yields yellow gelatinous fluid

Normal

Usually associated with meniscal tear on MRI

Aspiration and arthroscopic partial meniscectomy

Good; unlikely recurrence with treatment of meniscal tear

Osteogenic sarcoma

2nd decade, insidious pain day and night

Tender soft tissue mass

↑Alkaline phosphatase, ↑LDH

Lytic/blastic changes; may present as pathologic fracture

Chemotherapy, limb salvage, rotationplasty, or amputation

70% 5-yr survival without metastatic disease

Chondroblastoma

Ill-defined pain

Swelling; may have localized tenderness

Normal

Epiphyseal location

Excision and curettage

<25% recurrence

Osteochondroma

Painful snapping sensation, adolescent

Palpable nodule in metaphyseal area

Normal

Metaphyseal nodularity; may be multiple

Excise if enlarged or increased tenderness

Generally benign

Osteoid osteoma

2nd decade; boys/girls 2:1; dull achy pain increased at night; relief possible but not certain with NSAIDs

Occasionally area of point tenderness is found; thigh/calf atrophy

Normal

Radiolucent nidus surrounded by reactive bone; increased uptake on bone scan

NSAIDs provide temporary relief; excision for persistent symptoms; preoperative CT helpful for defining lesion

Excellent with complete excision

Myositis ossificans

Recurrent contusions, contact sports

Swelling commonly of the distal thigh; limited ROM

Normal

Organized zonal pattern of peripheral ossification

RICE, ROM; avoid contracture formation

Excellent, full recovery expected

CT,
computed tomography; LDH, lactate dehydrogenase; MRI, magnetic
resonance imaging; NSAIDs, nonsteroidal anti-inflammatory drugs; RICE,
rest, ice, compression, elevation; ROM, range of motion.

TREATMENT
In general, most sources of knee pain in children are
from minor contusions, muscle strains, or tendonitis related to minor
trauma or overactivity. Most are resolved with conservative measures,
which include rest, application of ice to reduce swelling, compressive wraps, temporary bracing or splinting, and elevation
to prevent edema. This is known as the RICE program, which also
includes activity modification or restriction until symptoms have
resolved. Occasionally, a course of physical therapy is needed to aid
in restoring joint range of motion and muscle strength.
TABLE 24.1-12 TRAUMATIC CAUSES OF KNEE PAIN

Cause

History/Mechanism

Physical Examination

Treatment

Outcome

Contusion

Fall, blunt trauma

Localized tenderness

RICE

Self-limited recovery

Patellar subluxation, dislocation, or malalignment

Blunt trauma

Twisting injury

Parapatellar tenderness

Apprehension

↑Q angle

RICE, ROM, quadriceps strengthening

Typically resolves with nonoperative treatment

Proximal or distal realignment procedures for recurrent cases

Meniscal injuries (Fig. 24.1-14)

Twisting injury “Locked knee”

Effusion

Joint line tenderness

RICE, ROM

Arthroscopy for persistent mechanical symptoms

Prognosis good with preservation of as much meniscus as possible

Ligament injuries

Planted foot ± contact with sudden deceleration or valgus/varus stress

Point tenderness, instability on exam

RICE, restore ROM

Ligament reconstruction for persistent instability or multiple ligament injuries

Prognosis
generally good for isolated single ligament injuries; combined injuries
have longer rehab. and more guarded chance of full recovery

Osteochondritis desiccans

Diffuse pain, limp in adolescents

Effusion, occasional point tenderness

RICE, activity modification, arthroscopy for persistent or mechanical symptoms

Prognosis agedependent; spontaneous healing can occur in those <13 yr old

Bipartite patella

Adolescent, parapatellar pain

Usually discovered after blunt injury

Tenderness corresponds to superior lateral defect in patella ossification (75%)

RICE, activity modification

Surgical excision and reattachment of extensor mechanism for recalcitrant cases

Most respond to conservative treatment with resolution of symptoms

Knee dislocation

Older adolescent

High-impact injury, obvious deformity

Obvious deformity, generalized tenderness, may have associated neurovascular injury

Correct
deformity emergently, careful neurovascular exam and repair for
sustained vascular injury. Ligament reconstruction 7-10 days after
injury

Good for discovered and repaired vascular injuries. Residual instability (PCL) expected but minimal symptoms if repaired

Reflex sympathetic dystrophy

Disproportionate burning pain relative to injury

Marked tenderness to light touch, skin discoloration, atrophy, stiffness

Sympathetic block, TENS, physical therapy

Variable; advanced cases have poorer prognosis for recovery

LDH,
lactate dehydrogenase; PCL, posterior cruciate ligament; RICE, rest,
ice, compression, elevation; ROM, range of motion; TENS, transcutaneous
electrical nerve stimulation.

Referral should be made when the patient is not
responding to conservative measures, or if there is suspicion of
infection, vascular injury, obvious deformity, or fracture.

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Acknowledgment
I thank Kathrin Halpern for her assistance in the preparation of this manuscript.
SUGGESTED READING
Bruns DM, Maffuci N. Lower limb injuries in children in sports. Clin Sports Med 2000;19:4:637-662.
DeVellis
JP, Andrish JT. Knee ligament injuries in the skeletally immature
athlete. In: Orthopaedic knowledge update: sports medicine 2. Rosemont,
IL: American Academy of Orthopaedic Surgeons, 1999:355-364.
Gebhardt
MC, Hornicek FJ. Osteosarcoma. In: Orthopaedic knowledge update:
musculoskeletal tumors. Rosemont, IL: American Academy of Orthopaedic
Surgeons, 2002:175-186.
Gebhardt MC, Ready JE, Mankin HJ. Tumors about the knee in children. Clin Orthop 1990;255:86-110.
Iobst CA, Stanitski CL. Acute knee injuries. Clin Sports Med 2000; 19:621-635.
Smith
A, Scoles PV. The knee. In: Pediatric orthopaedics in clinical
practice, 2nd ed. Chicago: Yearbook Medical Publishers, 1988: 122-139.
Stanitski CL. Anterior knee pain syndromes in the adolescent. Instruct Course Lect 1994:211-220.
Stanitski
CL. Knee disorders. In: Orthopaedic knowledge update: pediatrics.
Rosemont, IL: American Academy of Orthopaedic Surgeons, 2002:191-201.
Stanitski CL, DeLee JC, Drez D. Pediatric and adolescent sports medicine. Vol 3. Philadelphia: WB Saunders, 1994.
Swenson TM, Harner CD. Knee ligament and meniscal injuries. Orthop Clin North Am 1995;26:529-545.
24.2 OVERUSE INJURIES
MICHAEL BUSCH ▪ DAVID L. MARSHALL ▪ KEITH H. MAY
An increasing number of young athletes are participating
in organized sports programs. Sports programs and recreational,
seasonal participation in a variety of sports are being replaced by
year-round competition in a single sport or activity. This trend toward
early specialization in a single activity has increased the number of
sports-related injuries in young athletes. In addition, there has been
a change in the pattern of injuries observed with the microtraumatic or
overuse injury predominating over the acute, or macrotraumatic injury.
PATHOPHYSIOLOGY
Overuse injuries are defined as those that occur when
repetitive submaximal stresses are applied to otherwise normal tissues.
If there is adequate time for the tissue to repair itself, the tissue
adapts to the demand and is able to undergo further loading without
injury. Without adequate recovery, the normal reparative processes are
overwhelmed; tissue failure (due to microtrauma) develops and
stimulates the body’s inflammatory response, leading to clinical injury.
Overuse injuries can occur in a variety of tissues such as bone, tendons, or growth cartilage (Box 24.2-1).
Growth cartilage is found in three locations in the child: the physes,
the epiphyseal surfaces, and the apophyses, all of which are
susceptible to overuse injuries.
DIAGNOSIS
Patient History
As in any aspect of physical diagnosis, the history is
important in diagnosing and treating overuse injuries. One must
remember that the period of abusive training may have occurred weeks to
months before the onset of clinical pain. Predisposing factors leading
up to the onset of pain must be sought.
Predisposing factors for overuse injuries can be grouped into two broad categories: intrinsic factors and extrinsic factors (Box 24.2-2).
Intrinsic factors such as limb alignment and resulting biomechanics are
innate to the athlete. Extrinsic factors are determined by the athlete,
and these include training regiments, shoes, and running surfaces.
OVERUSE SYNDROMES OF BONE
Stress injuries of bone can occur in any part of the
bone. Much like repetitive bending of a paperclip, repetitive loading
of virtually any element of the musculoskeletal system can lead to
structural fatigue. Ideally, this leads to remodeling and strengthening
that allows more activity as time

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goes on. If fatigue occurs faster than remodeling, the tissue fails resulting in clinical injury.

METAPHYSEAL/DIAPHYSEAL STRESS INJURIES
The simplest example of stress injury in bone is the
stress fracture. Among youths, these most commonly occur with distance
running. The athlete may experience gradual onset of symptoms and
eventually be unable to run because of pain. Acute failure can occur
through the weakened bone resulting in a complete fracture.
Pathogenesis
  • Virtually any bone can be affected
  • Most common metaphyseal and diaphyseal
    stress fractures in young athletes include the fibula, metatarsals,
    tibia, femur, and ulna.
  • Stress fractures of the metatarsals
    (typically the second or third) and the distal fibula rarely have
    complications other than pain and disability.
  • Fractures of the tibia, humerus, and forearm rarely displace but do represent potential risk for morbidity.
Epidemiology
  • Most occur in later adolescence, ages 16 to 19.
  • Boys and girl are equally affected.
Diagnosis
  • Initially, only about 10% of radiographs are abnormal.
  • Bone scan and magnetic resonance imaging (MRI) are much more sensitive.
  • Bones scans result in radiation exposure,
    but are useful if the exact area of involvement is in question.
    Findings must be correlated to the clinical symptoms. As many as 50% of
    adolescents with stress fractures will show multiple areas of stress
    response on bone scans that do not correlate to areas of symptoms.
  • MRI detects subtle marrow edema and early cortical failure.
Treatment
  • Rest treats most diaphyseal and metaphyseal stress fractures.
  • Crutches are often necessary. Occasionally, immobilization is needed.
  • Healing time can range from 4 to 12 weeks.
  • Alternative training, gradual resumption of sports, and monitoring for recurrent symptoms are necessary.
  • Some stress fractures require surgery.
    • □ Stress fractures of the hip are rare
      but have the highest potential for morbidity. Femoral neck fractures
      can displace, disrupt the blood supply to the femoral head, and lead to
      avascular necrosis.
    • □ Stress fractures of the fifth metatarsal tend to be recurrent and are often best managed with an intramedullary screw.

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SPONDYLOLYSIS
Pathogenesis
  • Fracture through the pars interarticularis of the lumbar vertebrae.
  • Commonly seen in athletes who are under
    the age of 20 and involved in a sport that requires repetitive
    extension of the lumbar spine, such as gymnastics, cheerleading,
    diving, football (linemen), and dance.
  • The most common location is L5-S1, followed by L4-L5.
Diagnosis
  • Pain with palpation is worse with single or dual leg hyperextension.
  • Flexion usually is painless.
  • Hamstrings frequently are tight.
  • Anteroposterior, lateral, and oblique x-rays of the lumbar spine may be negative.
  • Look for the fracture through the neck of the “Scotty dog” on the obliques.
  • If clinical suspicion is high, and x-rays
    negative, consider computed tomography (CT), single-photon emission
    computed tomography (SPECT), or MRI.
Treatment
  • Modify activities to avoid extension for 4 to 8 weeks.
  • Consider rigid lumbar support bracing for 4 to 8 weeks.
  • Physical therapy for truncal stabilization, and functional progression back to sport.
  • Can resume activities without the brace 8 to 12 weeks from diagnosis.
APOPHYSEAL CONDITIONS
OSGOOD-SCHLATTER DISEASE
Pathogenesis
  • A disorder of the proximal tibial
    apophysis that commonly affects young athletes, but may bother other
    active youngsters who are not involved in formal, organized sports.
  • The tubercle of the proximal tibia is the insertion site of the patellar tendon.
  • Because of the strength or the quadriceps, large tensile forces are transmitted through the patellar tendon insertion.
  • The normal transition from the ossified
    and unossified tubercle into the tendon undergoes fatigue failure and a
    healing response ensues.
Epidemiology
  • While activity plays a role, some
    individuals appear to be predisposed to this condition; 20% to 30% of
    youngsters will have siblings who have had the same problem.
  • Typically, the child is between 10 to 15 years of age at the onset.
  • Boys are more commonly affected than girls; however, female gymnasts seem to be particularly prone to this problem.
  • Approximately 15% of teenage boys and 10% of teenage girls are affected.
  • Incidence of bilaterality varies considerably.
Diagnosis
  • Typically significant pain and prominence on the presenting side and some degree of findings on the contralateral side.
  • Many patients have a prior history of heel pain compatible with Sever disease (calcaneal apophysitis).
  • Pain is usually well localized to the prominent tibial tubercle.
  • Pain is typically related to activities.
  • There should be no signs or symptoms of intraarticular problems of the knee joint itself.
  • The diagnosis can then be made clinically.
  • A lateral radiograph of the knee can be helpful to confirm the diagnosis by showing irregularity of the tibial tubercle.
  • The radiograph should also rule out any other osseous problems, such as tumor or infection.
Treatment
  • In most, it simply runs its course with time, with symptoms lasting 1 to 4 years.
  • In approximately 3% of patients a
    persistent ossicle forms, which can remain symptomatic and ultimately
    require surgical excision.
  • Associated tuberosity fractures are so rare that there appears to be no sound evidence that activity restriction is required.
  • Symptomatic measures include ice,
    nonsteroidal antiinflammatory drugs (NSAIDs), compressive sleeve or
    band, activity modifications as indicated by the symptoms, and
    hamstring stretching.
  • Casts/rigid braces are rarely used, except for severe acute exacerbation.
SINDING-LARSEN-JOHANSSON SYNDROME
Pathogenesis
  • Pathophysiology is similar to Osgood-Schlatter disease but the pain is located over the inferior pole of the patella.
  • Typically patient is between 8 to 13 years of age at onset.
  • Bilaterality varies considerably.

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Diagnosis
  • The pain is well localized over the inferior pole of the patella.
  • The pain is related to activities.
  • The diagnosis is clinical.
  • Lateral radiograph may show irregular ossification over the distal patella.
Treatment
  • Same as Osgood-Schlatter disease.
SEVER’S DISEASE (CALCANEAL APOPHYSITIS)
Pathogenesis
  • Heel pain is a common complaint of the young adolescent.
  • It is due to the very powerful but tight gastrocsoleus complex as it inserts on the back of the calcaneus.
Epidemiology
  • Seen more often in boys age 9 to 13.
  • More common in gymnastics, running, and sports in which cleats are worn (football, soccer).
  • Bilateral in 50% of cases.
Diagnosis
  • Pain localized to posterior aspect of calcaneus.
  • Pain with medial and lateral pressure on the heel (squeeze test).
  • Disease is associated with hyperpronation, femoral anteversion, tibial torsion.
  • Those affected usually have tight plantarflexors and weak dorsiflexors.
  • The diagnosis is made clinically. A
    lateral radiograph may show fragmentation and irregularity of the
    calcaneal apophysis, but this can be seen in asymptomatic heels.
Treatment
  • The condition is self-limited so
    treatment is conservative and aimed at symptomatic relief: ice, NSAIDs,
    modification of activities, ¼-inch silicone or Sorbothane heel cups,
    orthotics to correct any mechanical problem, physical therapy, and home
    exercises to stretch the plantarflexors and strengthen the dorsiflexors.
  • Casting for 2 to 3 weeks may be needed in extreme cases.
ISELIN’S DISEASE
Pathogenesis
  • This is an uncommon traction apophysitis at the base of the fifth metatarsal at the insertion of the peroneus brevis.
  • It occurs in skeletally immature athletes.
Diagnosis
  • Pain is located on the lateral side of the foot and exacerbated by running, jumping, and cutting.
  • Pain with resisted eversion.
  • Radiographs may show a widened and prominent apophysis at the base of the fifth metatarsal.
Treatment
  • Ice
  • NSAIDS
  • Activity modification to avoid pain.
  • Physical therapy to stretch the ankle evertors and strengthen the invertors.
APOPHYSITIS OF THE MEDIAL EPICONDYLE
Pathogenesis
  • Throwing produces a valgus moment at the
    elbow with compressive loads applied to the lateral side
    (radiocapitellar joint) and traction loads across the medial side.
  • In the late teen years and above,
    repetitive traction injuries involve the medial collateral ligament
    itself, and can lead to rupture of the ligament.
  • In the immature skeleton, the apophysis
    of the medial epicondyle can begin to fragment, which leads to a
    reparative process leading to pain and prominence.
Diagnosis
  • Point tenderness over the medial epicondyle.
  • Little or no loss of extension.
  • Radiographs usually show some degree of irregularity or fragmentation of the apophysis.
Treatment
  • Pain usually resolves with time and rest.
  • Avulsion of the medial epicondyle can
    occur with forceful throwing, so restriction of rigorous throwing, such
    as pitching, is prudent.
    • □ Batting is usually not troublesome, and many can play an infield position while this resolves.
    • □ Return to pitching in less than 6 months often results in recurrence.
APOPHYSITIS OF THE PELVIS
Pathogenesis
  • During periods of rapid growth, there is
    a strength-flexibility imbalance in the muscle tendon unit due to rapid
    growth of the bone relative to the muscle tendon.
  • Several apophyses in the pelvis are susceptible to traction injuries (Table 24.2-1).
  • These are most commonly seen in runners, sprinters, football players, and soccer players.

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TABLE 24.2-1 APOPHYSES IN THE PELVIS

Apophysis

Muscle

Iliac crest

External obliques, gluteus medius, tensor fascia lata

Anterior superior iliac spine

Sartorius

Anterior inferior iliac spine

Rectus femoris

Ischial tuberosity

Hamstrings

Greater trochanter

Gluteus medius

Lesser trochanter

Iliopsoas

Treatment
  • Ice
  • NSAIDs
  • Modification of activities to maintain cardiovascular endurance
  • Stretching of the involved muscle-tendon unit once acute pain subsides
  • Gradual return to activities usually by
    the direction of a physical therapist (usually after 2 to 4 weeks; 4 to
    6 weeks if avulsion is present)
REPETITIVE PHYSEAL INJURIES
LITTLE LEAGUE SHOULDER
Pathogenesis
  • Repetitive stress to the shoulder can lead to widening and resorption around the proximal humeral physis.
  • This “physiolysis” has been termed “Little League shoulder” since it occurs primarily in Little League baseball players.
  • While typically affecting pitchers, other rigorous throwers, such as catchers, can develop this as well.
Diagnosis
  • Typically 12- to 15-year-old boys
  • Shoulder pain related to overhead throwing
  • Usually more painful in the deltoid region than the subacromial region
  • Differential diagnosis: rotator cuff tendonitis and impending pathologic fracture from a simple bone cyst to the upper humerus
  • Radiographic widening of the proximal humeral physis on the affected side confirms the diagnosis of Little League shoulder.
    • □ Need comparison with other shoulder.
Treatment
  • Primarily involves rest
  • Complications are uncommon, so if the symptoms are minimal, batting and playing infield positions are usually not painful.
  • Resolution can take up to 6 months.
  • Pitching is gradually resumed.
  • Monitor for resumption of symptoms.
GYMNAST’S WRIST
Pathogenesis
  • Gymnastic training often begins as early
    as age 4 or 5 and peaks in the early to mid-teens, during which the
    time spent in training may reach as high as 30 to 40 hours per week.
  • Because many maneuvers in gymnastics
    involve weight-bearing on the dorsiflexed wrist, often with a
    rotational component, the wrist is a common site of overuse injury.
  • The term gymnast’s wrist is a catchall term often used to describe any of a wide variety of wrist injuries in gymnasts.
  • The most common chronic injury seen is at the level of the distal radial physis.
Epidemiology
  • 80% to 90% of affected athletes are female.
  • Typically 12 to 14 years of age
  • Symptoms are bilateral in approximately one-third of patients.
  • Usually seen in gymnasts whose weekly training regimen exceeds 20 hours per week.
  • Vault and floor exercise are the events most likely to cause symptoms.
Diagnosis
  • Patients have pain with palpation over the distal radial physis.
  • There is pain at extremes of dorsiflexion.
  • This can be differentiated from dorsal impingement by the presence of pain on the volar and radial aspects of the physis.
  • Radiographs may be normal (stage 1), and the diagnosis is made clinically.
  • Radiographs may show widening of the
    distal radial physis, irregularity or cystic changes on the metaphyseal
    side of the growth plate, or breaking of the radial physis (stage 2).
  • With late presentations, the radiographs may show positive ulnar variance due to premature closure of the radial physis.
Treatment
  • Stage 1 (no radiographic changes)
    • □ Modified rest, which involves avoidance
      of axial compressive loads for a period of 2 to 4 weeks. During this
      time the athlete may continue to condition, maintain flexibility, and
      continue to train on the beam, practice aerial stunts, as well as
      footwork on the floor exercise.
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    • □ After the pain resolves, a gradual return to activity is allowed with close supervision.
  • Stage 2 (radiographic changes with no ulnar variance)
    • □ Avoidance of axial compressive loads for 6 to 12 weeks. Casting may be appropriate for the noncompliant athlete.
    • □ To improve compliance, it is important
      to inform the gymnast that absolute rest will provide the best chance
      of returning to a competitive level.
  • Stage 3 (positive ulnar variance)
    • □ Same as stage 2.
    • □ Consider MRI arthrography for
      triangular fibrocartilage complex (TFCC) tears. This should be
      suspected in any gymnast with wrist pain on the ulnar side.
    • □ Possible need for shortening osteotomy of the ulna.
Prevention
  • Educate athletes and coaches on the importance of wearing variance braces with workouts.
  • Recommend bi-annual routine wrist radiographs in all gymnasts training more than 16 hours per week.
  • Encourage strength and flexibility training of the wrists year-round.
  • Alternate compressive, axial-loading workouts (vault) with traction workouts (uneven bars).
  • Early stage diagnosis: encourage gymnasts at all ages to have wrist pain evaluated.
EPIPHYSEAL OVERUSE CONDITIONS
Perhaps the best example of a repetitive stress injury
of the epiphyses occurs at the capitellum—Panner disease and
osteochondritis of the capitellum. In these conditions, a segment of
epiphyseal bone becomes necrotic and can result in separation of the
bone segment and overlying articular cartilage. While technically
classified as an “osteochondrosis,” these have features of repetitive
stressinduced injuries, much like stress fractures.
PANNER’S DISEASE
  • Panner described a lesion of a young boy’s capitellum that he compared with Legg-Calvé-Perthes disease.
  • In patients under 10 years of age who develop irregularity of the capitellum, the course is usually quite benign.
  • An avascular segment of bone develops in the center of the capitellum, revascularizing in time.
  • Loose bodies do not typically form.
  • Sequelae are rare and treatment is simply rest.
OSTEOCHONDRITIS DISSECANS OF THE CAPITELLUM
Pathogenesis
  • While the term osteochondritis dissecans implies that there is an inflammatory process present, histologic studies have in fact failed to confirm this.
  • Appears to be a repetitive stress phenomenon
  • Most commonly occurs in baseball pitchers.
  • As the ball is accelerated during the pitching motion, a valgus moment is created at the elbow.
    • □ There is tension on the medial side of the elbow and compressive forces across the radial capitellar articulation.
  • The capitellum has an end arterial blood
    supply, which may explain its susceptibility to develop avascular
    necrosis from chronic repetitive compression loads.
Diagnosis
  • Side arm pitches, many curve ball
    techniques, and others can increase the compression loads across the
    lateral side of the elbow by bringing the ball further away from the
    midsagittal plane and accentuating the valgus moment.
  • Typically patients complain of an aching pain in the lateral side of the elbow.
  • Often they have flexion contractures.
  • Displaced fragments can result in a loose body sensation, a locked elbow, or significant synovitis and pain.
  • Plain radiographs typically show a sclerotic region or radiolucency. Tangential views may help.
  • Occasionally, CT scan or MRI are indicated.
Treatment
  • Osteochondritis of the capitellum can result in permanent arthrosis of the elbow joint.
  • Prevention through education is key.
    • □ Junior baseball programs should have
      rules limiting how much youngsters can pitch, typically three innings
      per game, up to six innings per week.
  • Occasionally, intact lesions heal with prolonged rest, but surgery is often necessary to remove unstable or displaced fragments.
  • Compared with simple arthroscopic débridement, there is no proven benefit to grafting, or other procedures.
TENDINOSES
ROTATOR CUFF TENDONITIS
Pathogenesis
  • Unlike in adults, tendon degeneration and rupture are rarely seen in youths.
  • P.287
  • The rotator cuff is a convergence of the tendons of the subscapularis, supraspinatus, infraspinatus, and teres minor.
    • □ These extend from the scapula out over the humeral head.
    • □ Together, they stabilize the humeral
      head against the glenoid fossa and they prevent the humeral head from
      rubbing beneath the arch of the acromion.
    • □ The supraspinatus muscle is the most important of these.
Etiology
  • Many factors contribute to rotator cuff tendonitis.
    • □ In young athletes, inherent laxity of the glenohumeral capsule is likely a significant factor.
    • □ Overhead throwing in baseball, swimming, serving motion in tennis, and gymnastics precipitate symptoms.
  • Pain produces inhibition of the rotator cuff muscles, which precipitates impingement of the humeral head beneath the acromion.
    • □ With time, a well-established bursitis and tendonitis develop.
Diagnosis
  • Typical complaints: pain with overhead activities, and sensation of the arm becoming heavy, tired or “dead.”
  • Thoroughly examine the neck and shoulder looking for restriction of motion, muscle atrophy, and focal tenderness.
    • □ There may be tenderness along the course of the biceps tendon, as well.
  • The supraspinatus strength should be tested.
    • □ Glenohumeral laxity is common.
  • Plain radiographs are useful to rule out other bony abnormalities.
  • MRI can be diagnostic for rotator cuff tendonitis; however the diagnosis can usually be made clinically.
    • □ Partial and full thickness rotator cuff tears are rarely seen before 18 years of age.
Treatment
  • The principles of treatment center on restoring strength and motion of the rotator cuff and scapular stabilizers.
  • NSAIDs.
  • Often overhead activities are curtailed
    while physical therapy is initiated. Rehabilitation of the entire
    scapular thoracic complex is key.
  • As pain diminishes and strength returns,
    overhead sporting activities are initiated, with careful monitoring for
    evidence of recurrent impingement.
  • In recalcitrant cases, a subacromial or intraarticular injection of steroids can hasten resolution of the inflammatory phase.
  • Occasionally, surgical stabilization is necessary, though subacromial decompression is rarely indicated for youths.
SHIN PAIN
Shin pain is a common complaint in young athletes. Much like the term headache,
the diagnosis of “shin splints” refers to a collection of maladies with
the common feature being activity-induced pain in the midportion of the
leg. Specific diagnoses include:
  • Periostitis
  • Chronic exertional compartment syndrome
  • Stress fracture
  • Muscle herniation
  • Superficial nerve entrapment
Shin pain in youths should be evaluated for a specific diagnosis. Other considerations in the differential diagnosis include:
  • Deep venous thrombosis
  • Tumor
  • Infection
  • Popliteal artery entrapment
PERIOSTITIS
Pathogenesis
  • This clinical entity is also termed medial tibial stress syndrome and soleus syndrome.
  • The soleus muscle and its investing fascia originate in this area and are also implicated in causing the syndrome.
  • Three-fourths of running athletes with shin pain have posteromedial tenderness, and half of them are bilateral.
  • Boys and girls are equally affected.
  • Predisposing factors include:
    • □ Muscle weakness
    • □ Running shoes with a lack of heel cushion, inadequate arch support
    • □ Hard training surfaces.
    • □ Training errors such as sudden increases in intensity or mileage
    • □ Abnormal lower limb biomechanics
Diagnosis
  • Activity-related pain
  • No associated numbness
  • Recent increase in the intensity of sports participation, training, and competition schedule
  • Recent change in regimen or shoes, and surface training conditions
  • Pain and tenderness along the distal
    third of the posteromedial tibia—extending longitudinally along several
    centimeters, and not across to the anterior tibia
  • Varus hindfoot alignment, excessive forefoot pronation, genu valgum, excessive femoral anteversion, and external tibial torsion
  • No muscle herniation
  • P.288
  • Negative Tinel test
  • Normal radiographs
  • If confirmation of the clinical diagnosis
    is needed, bone scan shows a longitudinal pattern of radionuclide
    concentration rather than a transverse pattern more typical of a stress
    fracture.
Treatment
  • NSAIDs
  • Ice
  • Strengthening and stretching
  • Ultrasound
  • Foot orthoses
  • Graduated running program
  • Surgery rarely indicated
CHRONIC EXERTIONAL COMPARTMENT SYNDROME
Pathogenesis
  • With repetitive exercise, the interstitial pressure within the osseofascial compartments of the leg can become elevated.
  • When compartment pressures exceed capillary filling pressure, the muscle becomes ischemic and produces pain.
  • This usually has an onset associated with activity and is relieved by rest.
  • Unlike acute compartment syndromes
    resulting from trauma or arterial insufficiency, the pressure and blood
    flow to the muscles normalizes in chronic compartment syndromes and
    rarely result in tissue necrosis or residual disability.
  • The anterior compartment is the most commonly involved, although any of the four compartments in the lower leg may be affected.
Diagnosis
  • Typical complaints: aching pain, tightness, or a squeezing sensation brought on by and interfering with athletics
  • Usually relieved promptly after exercise
  • Some experience transient foot-drop with paresthesias across the dorsum of the foot if the anterior compartment is involved.
  • Plantar paresthesias with chronic posterior compartment syndrome.
  • Fascial defects with muscle herniation may be present over the anterior and lateral compartments.
  • If clinically indicated or desired, dynamic measurement of compartment pressures during exercise can confirm the diagnosis.
    • □ In chronic compartment syndrome, resting pressures typically are not elevated.
    • □ With exercise, the pressures rise to 70 to 100 mm Hg, while normal compartments rise to less than 30 mm Hg
    • □ MRI done immediately after exercise may have a role as well.
Treatment
  • Initial treatment includes activity modification, foot orthoses, physical therapy, and time.
  • Recalcitrant cases may require a fasciotomy.
    • □ All involved compartments should be released.
    • □ This can be done through limited skin
      incisions rather than through the extensive releases suggested for
      adequate management of the acute traumatic compartment syndrome.
    • □ Care must be taken to protect the saphenous vein, saphenous nerve, and the superficial branch of the peroneal nerve.
  • All compartments should be assessed because symptoms may not be adequate to identify all involved compartments.
  • History of bilateral symptoms should be specifically sought.
    • □ After unilateral surgical release,
      patients frequently increase their activity levels, only to develop
      pain on the side that had been asymptomatic.
  • Failures result from failing to
    appreciate multiple compartment involvement; from inadequate
    decompression, especially of the deep posterior compartments; and from
    excessive scar tissue response.
SUGGESTED READING
Busch
MT. Sports medicine. In: Morrissey RT, Weinstein SL. Lovell &
Winter’s pediatric orthopaedics, 4th ed. Philadelphia: Lippincott
Williams and Wilkins, 2001.
Combs JA. Hip and pelvis avulsion fractures in adolescents. Physician Sports Med 1994; 22:41-49.
Detmer DE. Chronic shin splints. Classification and management of medial tibial stress syndrome. Sports Med 1986;3:436-446.
Detmer
DE, Sharpe K, Sufit RL, et al. Chronic compartment syndrome: diagnosis,
management, and outcomes. Am J Sports Med 1985;13:162-170.
DiFiori J. Overuse injuries in children and adolescents. Physician Sports Med 1999; 27:75-84.
Kocher MS, Waters PM, Micheli LJ. Upper extremity injuries in the paediatric athlete. Sports Med 2000;30:117-135.
Kujala UM, Kvist M, Heinonen O. Osgood-Schlatter’s disease in adolescent athletes. Am J Sports Med 1985;13:236-241.
Mandelbaum
BR, Nativ A. Gymnastics. In: Reider B, ed. Sports medicine, the school
age athlete, 2nd ed. Philadelphia: WB Saunders, 1996:459-462.
Outerbridge AR, Micheli LJ. Overuse injuries in the young athlete. Clin Sports Med 1995;14:503-516.
Schenck RC. Athletic training and sports medicine, 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2000.
Walker RN, Green NE, Spindler KP. Stress fractures in skeletally immature patients. J Pediatr Orthop 1996;16:578-584.
Zetaruk M. The young gymnast. Clin Sports Med 2000;19:758-780.

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