Current Diagnosis & Treatment in Sports Medicine, 1st Edition

9. The Youth Athlete

Jan S. Grudziak MD, PhD

Volker Musahl MD

Injuries among the skeletally immature athlete are to some extent unique and specific to this population. Because the biology and physiology of soft tissues and bone are different in the pediatric or adolescent patient, an injury seen in the adult population might require treatment different from one occurring in a growing child. A typical example is an anterior cruciate ligament (ACL) injury in a skeletally immature patient.

Usually, the child is able to heal faster and more predictably than the adult. The growing organism can compensate for and correct residual deformities that are commonly accepted by pediatric orthopedic surgeons familiar with the amazing, restorative powers of the growing organism. Unfortunately, the growing parts are also subject to trauma, damage to the growth plate, and subsequent abnormal development. Surgically caused damage to a growth plate can result in progressive deformity and alter the initially perfect result of otherwise properly executed treatment. In this respect, injuries in the pediatric and adolescent population might be quite challenging to manage, and their results unpredictable. Detailed knowledge of the physiology and pathology of the immature organism is crucial to avoid iatrogenic insult to the growing organism and to improve the end result of treatment.

There is no doubt that the intensity and frequency of sport competition have increased in recent years. More teenagers involved in sports results in fewer problems related to drugs, obesity, teenage pregnancy, and lackluster performance in school. The competition of sport creates a valuable groundwork for the demands of adult life. Being involved in a sport teaches the young athlete how to focus on goals and achieve the highest level of performance. Girls join the rush and since some injuries happen to them at a higher than average rate, they contribute to the overall frequency of sports-related injuries. Some sports, such as soccer, have attracted more young athletes over the past two decades than ever before.

College and professional scouts seemingly infiltrate the earliest levels of competition. At the high school level they offer enticing deals, usually featuring some monetary incentives, such as a “free ride” scholarship.

All these factors mean that competition has become fiercer, as the pressure from peers and parents has increased significantly. Today's young athlete is better prepared to compete, but also faces greater pressure to win. This creates a perfect environment for overuse and repetitive trauma injuries. The increased intensity of sports training and competition is visible, especially at the high school level; although sports-related injuries among students occur in all age groups, they peak in high school students.

Some sports carry a higher risk for specific injuries (Table 9-1). Advances in equipment and technique sometimes totally change the spectrum of sport-specific injuries. Skiing is a typical example; in the past, tibia fractures and ankle fractures were the most common injuries. As a result of technical advancement and changes in equipment (bindings, skis, helmets), the prevalence of skiing-related injuries has decreased in all age groups, and the spectrum of the injuries has shifted from fractures to soft tissue injuries.

Growth Plate

Anatomy & Physiology

The growing human organism shows a unique blend of the ability to repair and to remodel a deformity, and vulnerability to growth problems as a result of an injury (Figure 9-1). The growth plate is most commonly responsible for these problems. The maturing bone, with its adjacent joint cartilage, undergoes a fascinating process that eventually results in a fully mature skeleton and mature hyaline cartilage. The blood supply evolves as well. In some circumstances, a richer blood supply to the growing bone provides advantages over the mature bone: for example, healing is faster and regeneration occurs more quickly. Sometimes, however, the unique patterns of blood supply to the young bone are unfavorable to the function of the skeletal system, potentially causing serious problems (Figure 9-2). Typical examples include a higher risk of avascular necrosis (AVN) of the

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femoral head after a femoral neck fracture, especially a subcapital fracture, and limb length discrepancy as a result of the overgrowth of a femur following its fracture.

Table 9-1. Sport-specific injuries and their rate (per year) among high school athletes in the United States.

 

Boys

Girls

Football

1.97

 

Wrestling

1.82

 

Soccer

1.19

1.14

Basketball

0.93

0.80

Track

0.68

0.73

Cross country

0.66

0.65

Cheerleading

 

0.51

Gymnastics

 

0.44

Swimming

0.21

0.21

 

Risk

Injuries

Ballet dancers

Low

Ankle, metatarsal, spondylolysis

Baseball

Moderate

Little League elbow, ankle

Basketball

Moderate

Ankle, knee sprains, anterior cruciate ligament (ACL), finger fractures

Cycling

High

Closed head injuries, fractures: femur, forearm

Diving

High

Head, C-spine

Football

High

Head, C-spine, knee

Gymnastics

Moderate

Spondylolysis, wrist

Ice hockey

Moderate to high

Head, shoulder, laceration, clavicle fracture, ACL

Horseback riding

Moderate to high

Head, C-spine

Running

Low to moderate

Overuse, lower extremities, pelvis

Skateboarding

High

Head, C-spine, knee, forearm fracture

Skating inline

Low to moderate

Wrist, upper extremities

Skiing

Moderate to high

Tibial fracture, ACL, thumb, shoulder, head, spine

Snowboarding

Moderate to high

Upper extremities (wrist), ankle, calcaneus

Soccer

Moderate

ACL, meniscus, overuse fractures

Swimming

Low

Overuse: shoulder, knee, back

Tennis

Low

Overuse: elbow; Sprains: lower extremities

Trampoline

High

Head, C-spine, upper extremities fractures

Weight lifting

Low to moderate

Overuse, acromioclavicular joint

Wrestling

High

Upper extremities fracture and dislocation

Adapted, with permission, from Staheli LT: Fundamentals of Pediatric Orthopedics. Lippincott-Raven, 1998.

Bone growth starts at the seventh embryonic week and continues until growth is finished at skeletal maturity. There are two distinct forms of bone formation: the endochondral and the intramembranous.

 

Figure 9-1. Physiology of the growth plate.

 

Figure 9-2. Blood supply to the growth plate.

Endochondral bone formation occurs at the growth plate, and is also responsible for repair of a fracture. Osteoblasts initiate endochondral bone formation; their activity results in the development of an osteoid, and its subsequent maturation into fully differentiated bone tissue. Endochondral bone formation occurs through maturation of the osteoid in the growth plate. Maturation starts from the reserve zone and advances through the proliferative zone, the maturation zone, the degenerative zone, and into the zone of provisional calcification. Bone development from the primary to secondary spongiosa occurs in the metaphysis. As a result, the new bone is deposed at the metaphyseal face of the growth plate.

A different mechanism forms bone on the periosteal surface of the clavicle, pelvis, scapula, and skull (CPSS). This process is called intramembranous bone formation.

The production of a new bone from a growth plate is a highly complicated process. An excellent review by Ballock and O'Keefe discusses the most important elements of the biochemistry and physiology of the growth plate (Table 9-2). The role and function of chondrocytes have been studied extensively. A differentiating chondrocyte of the growth plate undergoes a complex morphologic and biochemical alteration, with precise signaling at the molecular level. The proliferation of chondrocytes, their maturation, and hypertrophy ultimately culminate in precisely programmed chondrocyte death, or apoptosis. The synthesis, secretion, and mineralization of the matrix with resultant osteoid formation are controlled by many factors. Finally, vascular invasion, necessary for the distribution of the local growth factors and hormones, orchestrates endochondral bone formation as well as closure of the growth plate at maturity (Table 9-3).

The blood supply to the growth plate varies with age. The epiphyseal arteries, the metaphyseal network created by the main nutritional artery, and the perichondrial arteries of the perichondrial ring of LaCroix supply blood to the growth plate and secondary center of ossification. The epiphyseal arteries and their terminal branches supply blood to the epiphyses. The main nutritional artery of a long bone enters the metaphysis via a network of terminal vessels, which supply blood to the primary and secondary spongiosa. This artery does not penetrate the hypertrophic zone; instead oxygen and nutrients are transported into the growth plate via diffusion from arcades of the terminal branches of the main nutritional artery. The perichondrial arteries of the perichondrial ring of LaCroix supply the periphery of the growth plate. There is no connection between the epiphyseal and metaphyseal system as long as the growth plate exists. As a result, the blood supply to the epiphysis is limited, and relies exclusively on the network of epiphyseal vessels; thus, the probability of disrupting this system is relatively high. In the absence of additional blood flow from the metaphysis, with torn or kinked epiphyseal vessels, the risk of AVN following fractures increases. AVN of a femoral head following femoral neck fracture in children and teenagers is a prime example of this problem. The differences between adult and skeletally immature bone blood supply also explain the higher rate of AVN of the femoral head in adolescents, associated with intramedullary nailing of a femur fracture with the starting point in the piriformis fossa.

In this chapter we focus on the unique aspects of sports-related injuries suffered by skeletally immature athletes. First we discuss injuries to the growth plate. Subsequently injuries to the lower extremities (hip, knee, and foot and ankle) and upper extremities are discussed.

Injuries

The Hueter–Volkmann law states that compressive forces inhibit, whereas tensile stresses promote, the growth of long bones. This law holds true to a certain extent. An equilibrium of tensile and compression forces across the growth plate is part of the normal kinetics of a growing organism, and is necessary for normal function of the growth plate and growth of the bone. The abnormally high tension or compression can cause growth arrest rather than normal growth, and excessive forces through the growth plate, either acute or chronic, may fracture or permanently injure the growth plate.

The growth plate is quite resistant to mechanical damage, however, in younger children it is often the weakest link in the muscle/tendon/bone or ligament/bone chain. Very frequently an injury that causes sprain or strain in adults results in fracture through the growth plate in the pediatric or adolescent population. The mechanical properties of the growth plate seem to approximate those of articular cartilage, however, the complex, layered anatomy of the growth plate limits the ability to generate exact numbers. Very few studies discuss this subject, and the mechanical properties of the growth plate cartilage and mode of failure are not entirely understood. There are limited data about the compression properties based on animal models: numerical data regarding the shear forces, tensile properties, or model of failure of the growth plate cartilage have not been published.

In clinical settings the hypertrophic zone of the growth plate seems to be its weakest part, since the fracture line usually goes through this zone. The high

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content of cells, with a relatively low matrix component is the probable reason for this relative weakness. As the bone and growth plate mature, the matrix content augments the cartilage, the growth plate becomes thinner and more irregular, rather then smooth and linear, and resistance to damaging forces increases, especially to shear injuries.

Table 9-2. Factors regulating the matrix production, life cycle of the chondrocytes, vascular invasion, and final closure of the growth plate.

Regulation of synthesis of the matrix
Transcription factor Sox 9: required for expression of collagen types II, IX, XI, and aggrecan; might control cell surface protein expression
Transcription factors L-Sox 5, Sox 6: together with Sox 9 activate gene transcription
Regulation of proliferation of the chondrocytes
Parathyroid hormone-related peptide (PTHrP): controls the pace of hypertrophy
Indian hedgehog (Ihh): increases production of PTHrP
Transforming growth factor-β(TGF-β): inhibits cell hypertrophy, inhibits type X collagen expression and alkaline phosphatase activity, acting through Smad 3
Insulin-like growth factor-I (IGF-I): increases rate of cellular division
Fibroblast growth factor (FGF): controls PTHrP feedback with Ihh
Cyclin-dependent kinases (CDKs): stimulates chondrocyte proliferation
CDKs inhibitors: play a role in the termination of chondrocyte differentiation
Maturation and hypertrophy of the chondrocytes
Type X collagen (unique to hypertrophy zone)
Alkaline phosphatase: calcification of the matrix, increases phosphate ions
Bone morphogenic proteins (BMPs): completion of maturation
Thyroxin: induces type X via activation of BMP-2
Retinoid acid: increases Smad 1 and Smad 5, inducing expression of BMP
Core binding factor-1 (CBF-1): induces terminal differentiation
Smad 1,5,8: enhance hypertrophy
Matrix mineralization
Ca2+
Annexin II, V, and VI: part of calcium channels
Collagen types II and X: adhere to vesicles with annexin V, stimulate annexin V calcium channels and deposition of Ca2+
Alkaline phosphatase: hydrolyze the pyrophosphate
Matrix metalloproteinases (MMPs): necessary for angiogenesis and calcification, cleavage of type II
MMP-13: activates TGF-β
MMP-9: angiogenesis
Vitamin D3: increases activity of MMP and alkaline phosphatase, Ca2+ resorption
Chondrocyte apoptosis:
Caspases: cleave proteins
bcl-2 protein: blocks caspases
BAX: stimulates caspases
Phosphate ions: stimulate apoptosis, release of cytochrome c
FGF-2: binds to FGFR-3 increasing apoptosis
PTHrP: inhibits apoptosis
Vascular invasion
Vascular endothelial growth factor (VEGF): stimulates capillary invasion into growth plate
Core binding factor-1 (CBFA-1): stimulates angiogenesis
Basic fibroblast growth factor (BFGF): stimulates angiogenesis
PTHrP: slows angiogenesis
Physeal closure
Estrogen: closure of the growth plate in both females and males

Based on Ballock RT, O'Keefe RJ: The biology of the growth Plate. J Bone Joint Surg Am 2003;85-A:715.

Table 9-3. Patterns of growth rate and fusion of different growth plates.

 

Epiphyses and Apophyses

 

Appearance

Fusion

Femoral head

3–8 months

14–20 years

Greater trochanter

5–7 years

13–22 years

Lesser trochanter

6–11 years

12–20 years

Iliac crest

12–15 years

13–20 years

 

Proportions of the Growth of the Long Bones

 

Proximal Growth Plate

Distal Growth Plate

Femur

30%

70%

Tibia

55%

45%

Humerus

80%

20%

Radius

25%

75%

Salter & Harris Classification

The classification system of growth plate fractures is based on the classic work of Salter and Harris. They categorized growth plate injuries into five types (Figure 9-3):

Type 1 is a shear injury through the hypertrophic zone, which separates the epiphysis from the metaphysis. A classic type 1 is visible on a radiograph as displacement of the epiphysis in respect to the remaining part of a long bone. Often, however, injury forces are not strong enough to displace the epiphysis, and radiographs of such an injury might show no abnormalities except for soft tissue swelling. In this situation, a diagnosis of nondisplaced Salter–Harris 1 fracture is based on the mechanism of injury, combined with clinically discovered tenderness exactly at the level of the involved growth plate.

 

Figure 9-3. Salter–Harris classification (1–5) of physeal injuries.

Type 2 fracture extends through the growth plate and exits into the metaphysis, creating a Thurston–Holland fragment. Type 2 is an extraarticular fracture and often happens at the distal radius and distal femur. It should be easily appreciated on routine radiographs.

Type 3 traverses the epiphysis. It extends into the joint surface and splits the articular cartilage. The displaced fragment separates from the metaphysis through the hypertrophic zone of the growth plate. Because type 3 is an intraarticular fracture, it needs to be anatomically reduced and stabilized, and often requires surgery.

Type 4 is intraarticular as well, splits the epiphysis, crosses the growth plate instead of curving into it, and extends into the metaphysis, creating a free epiphyseal/ metaphyseal fragment. This type bears a high risk for permanent growth plate damage. It requires anatomic reduction as often as type 3.

Type 5 is a compression type, often unrecognized at first, as radiographs usually fail to show an injury. It is commonly diagnosed retrospectively, when a growth arrest causes growth problems as a result of a preceding compression injury.

The original Salter–Harris classification includes types 1 through 5. Type 6, added by some authors, is an injury to the periphery of a growth plate, and carries a relatively high risk for growth problems.

The growth plate injury can cause a deformation or abnormal growth of a bone with shortening or angulation. Generally, type 1 carries a low risk for physeal damage, type 2 higher, etc. More violent trauma increases the possibility of developing permanent growth plate problems. Displaced fractures more commonly end up with physeal bar formation; however, Salter–Harris types 1 and 2 can be left slightly displaced. The intraarticular

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types (types 3 and 4) might predispose a joint to osteoarthritis. Those types need anatomic reduction and stabilization, with the major factor being a reduction of the articular surface, not a reduction of the fracture line at the growth plate. The final outcome of a growth plate injury depends on several factors: the magnitude of forces causing the injury, type of growth plate fracture, age at the time of the initial trauma, and location of a fracture. The most important prognostic factor is the location of the fracture. For example, a Salter–Harris 2 fracture of the distal femur bears a much higher risk of growth arrest than a type 2 fracture of the distal radius.

Alignment of the Lower Extremities

Mechanical alignment of the lower extremities changes as a child grows. Usually the newborn presents with varus of the lower extremities. This “bowlegged” period lasts up to 18 and sometimes 24 months of age, after which the mechanics of the lower extremities changes into valgus or “knock-knees” (Figure 9-4). An examination of the mechanical axis of the lower extremities is not complicated, although radiographs are sometimes required in case of asymmetry, progressive deformities, pain, or lack of regression. Changes in the angular alignment at adolescence may be caused by trauma to the growth plate, metabolic diseases, endocrinologic problems, or other conditions such as an adolescent form of Blount's disease. Deformities that result in serious deviation of the mechanical axis must be corrected. Currently, asymmetric stapling of the growing physis seems to be the logical choice for slow correction of excessive valgus/varus deformity. The surgery requires a relatively small incision. The staples are removed after a slight overcorrection is achieved. Theoretically, the possibility of permanent growth plate closure and overcorrection does exist, but this situation is not a problem in clinical practice. After growth has ceased, or if the remaining growth potential is low, an osteotomy to acutely correct a deformity would be a better choice.

Torsional alignment of the lower extremities rarely causes long lasting problems and rarely requires surgical correction. To evaluate the rotational alignment of a child it is helpful to follow a certain order to assess the rotational profile:

  • Internal/external rotation of the hip.
  • Thigh–foot angle.
  • Tibial torsion.
  • Foot morphology.
  • Foot progression angle as a dynamic assessment.

Femoral anteversion and tibial torsion vary greatly as a child grows. The initially elevated femoral anteversion reduces to the adult level of 8–20° by the early school years, and the very common decreased tibial torsion, or internal tibial torsion, resolves spontaneously without intervention in the vast majority of children. Although a variety of orthopedic shoes and braces had been used to “speed up” the remodeling process, current research does not support the use of any orthopedic devices to treat rotational and angular “deformities” as the majority resolve spontaneously.

 

Figure 9-4. Alignment of the lower extremity and rotational elements. (

Grudziak JS and Bosch P: Angular Deformities of the Lower Extremities. In: Tometta, P and Einhorn TA, ed. Orthopedic Surgery Essentials. LWW, 2004.

)

Final anatomic alignment of the lower extremities is established around the age of 7–9 years. Therefore correction of a rotational deformity should be postponed until this age. Sometimes, an isolated rotational deformity may need to be corrected at this age if it creates functional or cosmetic problems. There is a strong

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belief, especially in the German speaking world, that decreased femoral anteversion is associated with arthritis of the hip joint, however, according to most researchers, arthritis of the hips, knees, and ankle joints does not seem to be related to increased anteversion of the femur or internal or external tibial torsion. A combination of increased femoral anteversion and increased external tibial torsion is a known risk factor for patella maltracking and anterior knee pain.

Ballock RT, O'Keefe RJ: The biology of the growth plate. J Bone Joint Surg Am 2003;85-A(4):715.

Garrick JG, Requa RK: Sports and fitness activities: the negative consequences. J Am Acad Orthop Surg 2003;11(6):439.

Kocher MS, Newton PO: What's new in pediatric orthopaedics. J Bone Joint Surg Am 2005;87(5):1171.

Purvis JM, Burke RG: Recreational injuries in children: incidence and prevention. J Am Acad Orthop Surg 2001;9(6):365.

Hip & Pelvis

Pathogenesis

In the adult population the pelvic ring consists of two innominate bones, connected by the symphysis pubis. Posteriorly, the ring is closed via the sacroiliac joints and the body of the sacrum. The general shape of the pelvis resembles the adult type with typical gender differences. In growing children the innominate bone is a combination of three separate bones: the ilium, ischium, and pubis. The central connecting point for the bones is the triradiate cartilage, made up of anterior and posterior horizontal limbs and a vertical limb. A connection between the ilium and ischium posteriorly and the os pubis anteriorly builds up the horizontal limb of the triradiate cartilage. The vertical limb connects the ischium and pubis. Apophyses are located over the top ridge of the iliac wind, along the ischial tuberosity, adjacent to the symphysis pubis, around the acetabulum, and at the anterior inferior iliac spine (Figure 9-5).

The femoral head articulates with the acetabulum, creating the hip joint. Growth of the acetabulum occurs at the triradiate cartilage apophyses, with adjacent parts of those three bones creating the cavity of the acetabulum. Additional growth centers at the superior brim of the acetabulum contribute to its depth and breadth. The acetabulum is more plastic, enlarging as a result of appositional growth from the ilium, ischium, and pubis.

The proximal femur grows from the proximal femoral physis. The femoral head is a secondary center of ossification, separated from the neck by a growth plate. In addition to this main growth plate, the proximal femur has two apophyses: at the lesser and greater trochanters.

 

Figure 9-5. Growth zones of the pelvis and femur. A: Iliac apophysis. B: Anterior inferior iliac spine (AIIS). C: Symphysis pubis. D: Ischial tuberosity. E:Acetabulum. F: Greater trochanter. G: Lesser trochanter. H: Femoral head.

The hip joint is fully formed at the moment of birth; the acetabulum will develop as a child grows but the structure is essentially similar to the adult joint. Contact surfaces include the semilunate cartilage of the acetabulum and the cartilage of the femoral head. The transverse ligament connects the distal horns of the semilunate cartilage. The acetabular labrum increases the depth of the acetabulum. The ligamentum teres connects the femoral head to the cavity of the acetabulum and supplies blood to a limited part (less then 5%) of the femoral head.

The orientation of the acetabulum, measured by inclination and anteversion, seems to change little, if at all, as a child grows. The acetabulum becomes more horizontal during development, thus covering more of the femoral head. The neck-shaft angle is usually around 120–135°. Femoral anteversion measures 35–45° at birth, gradually reducing to the adult value of 8–20°.

Clinical Findings

Pain in the groin or around the pelvis is usually the main reason to seek medical attention (Figure 9-6). A careful history will greatly aid the physician in establishing a proper diagnosis. A history of trauma or lack thereof, the presence of fever, malaise, or mechanical symptoms, and participation in sports with a higher incidence of pelvic and hip injuries should be ascertained. Acute onset of discomfort will be typical for an avulsion fracture, acute slipped capital femoris epiphysis, torn

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labrum, or fracture of the bony structure of the pelvis or femur. The inability to bear weight is also common. A dysplastic acetabulum, as a result of developmental dysplasia of the hip, may manifest with slowly progressing pain. Pain slowly increasing with activity will be common for stress fractures, overuse syndromes, and hip dysplasia. Fever and pain without previous injury might indicate septic arthritis (gonococcal arthritis in adolescents). Self-limiting pain lasting a few days, especially with a preceding upper respiratory infection, is characteristic of transient synovitis. Snapping and clicking around the hip or groin might point toward intraarticular pathology or coxa saltans. Bursitis usually presents as a localized pain. A malignant process might manifest as a diffuse discomfort, with prolonged duration. Radiation of pain into the groin could be the result of disk herniation. Retroperitoneal pathologic processes have been reported to cause radiating pain at the hip and knee region. Any knee pain might indicate hip pathology.

 

Figure 9-6. Seven-year-old soccer player with prolonged vague right hip pain and limp. A: Perthes disease of the right hip: Herring type B. B: Varus subtrochanteric osteotomy has increased the coverage of the femoral head.

Special Tests

FABER or Patrick's: Flexion, abduction, and external rotation: pain of the sacroiliac joint.

Whitman: Flexion of the hip causes simultaneous external rotation: slipped capital femoral epiphysis.

Trendelenburg: Insufficiency of the gluteus medius/ minimus muscles causing a drop of the contralateral pelvis while standing on the involved leg. It is caused by weakness due to paralysis, myelomeningocele, muscular dysplasia, or disc herniation; incorrect resting length due to hip dislocation, epiphyseal dysplasia (Fairbank), coxa vara, or slipped capital femoral epiphysis; and pain due to fracture, idiopathic chondrolysis, or AVN.

Duchenne: Lateral tilt of the trunk toward the involved side while testing the Trendelenburg. The causes are similar to Trendelenburg.

Thomas: Flexion of the nontested hip until the lumbar spine touches a hand placed under it. Flexion of the contralateral (tested) hip equals flexion contracture. It is also used to test for a labral tear: a snap with extension of the uninvolved hip.

Staheli: Prone over the edge of a table and extension of the involved hip: elevation of the pelvis equals flexion contraction.

Pace's sign: With the hip extended, forced internal rotation causes pain of the piriformis (piriformis syndrome).

Ober: In the side decubitus position, with the contralateral leg resting against the table, the tested leg is held abducted, with the knee flexed 90° and the hip slightly flexed. Holding the hip in abduction, the examiner extends the hip and then adducts the hip. With no iliotibial (ITB) contracture the leg could be adducted 20–30°.

Slipped Capital Femoral Epiphysis, Hip Dysplasia, & Legg–Calve–Perthes Disease

General Considerations

The classic triad of hip problems includes slipped capital femoral epiphysis (SCFE), developmental hip dysplasia (DDH), and Legg–Calve–Perthes (LCP) disease. Age at presentation, symptoms, classification, differential diagnosis, treatment, and return to sport guidance are shown in Table 9-4.

Clinical Findings

The age of onset of DDH varies: an early diagnosis provides the best chance to end up with an essentially normal hip. Late discovered DDH carries a less favorable prognosis. DDH is not a very common cause of hip/groin pain in adolescent patients, but should be kept on the differential diagnosis list (Figure 9-7).

SCFE, a disease that manifests from the preteen age to maturity, requires urgent surgical stabilization. Bilateral involvement might be as high as 60–70%. Early onset, short body stature, and delayed bony age raise suspicion of underlying endocrinologic disorders such as hypothyroidism and renal osteodystrophy. It is possible to attain an almost normal looking hip joint as a result of early treatment of early discovered, mild SCFE. However, asymptomatic SCFEs are a common cause of arthritis, with 30% of “idiopathic arthritis” showing typical changes of preexisting slippage (Figure 9-8)

 

Figure 9-7. Nineteen-year-old female with a 2-year history of groin pain. Bilateral dysplasia of the hip. Extreme reorientation of the acatabulum using Ganz osteotomy has addressed the dysplasia of the right hip. The patient is awaiting a similar procedure to improve the coverage of the femoral head and orientation of the acetabulum.

 

Figure 9-8. A 12-year-old male with 5 days history of right knee pain. A: Mild slipped capital femoral epiphysis of the right hip. B: Lateral radiograph shows the slipped capital femoral epiphysis (SCFE) much better then the anteroposterior view. C: SCFE treated with single screw fixation.

Table 9-4. Characteristics of DDH, SCFE, and LCP.1

 

DDH

SCFE

LCP

 

0–adulthood

7–8 to 14–15 years old

4–8 years old

Symptoms

Early: limited abduction, sonograph, X-ray
Walking age: none or limp
Late (teenage): pain, limp

Chronic or acute pain, groin or knee
Limp
Inability to bear weight
External rotation of the leg
Whitman
Trendelenburg
Slight shortening

Mild pain, discomfort
Limp
Decreased ROM
Trendelenburg

Classification

Dysplasia
Subluxation
Dislocation

Stable/unstable
Chronic/acute or acute on chronic
Mild, moderate, severe

Lateral pillar (Herring)
Types: A B C

Differential diagnosis

Usually radiographs are enough to establish diagnosis

Arthritis
DDH
Septic hip
Labral pathology
Neurogenic problems
Malignancy
Fracture
Knee problems

Septic hip
Transient synovitis
Dysplasias
Renal causes
Thyroid related
Trauma

Laboratory tests

Not necessary

Renal
Endocrine
Thyroid

None; if necessary renal, thyroid

Treatment

Age dependent

Urgent stabilization of the femoral head (usually single screw)
Osteotomy for persistent deformity

Very controversial
Benign neglect
Petrie cast
Femoral or pelvic osteotomy or combined

Complications

OA, pain

Persistent abnormal ROM
AVN
Reslip
OA
Chondrolysis
Progressive slippage

OA
Decreased ROM
Slight shortening

Return to sport/limitation

In cases treated early, with normal X-ray: no limits

Limited activities with no high impact activities until fusion of the physis

In active phases modification of activities Long term: avoid high impact activities

1DDH, developmental dysplasia of the hip; SCFE, slipped capital femoral epiphysis; LCP, Legg–Calve–Perthes disease; ROM, range of motion; OA, osteoarthritis; AVN, avascular necrosis.

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LCP is a disease of the femoral head, occurring as early as 2 years of age and up to 12 years of age. Current classification in based on Hering's work, with the denominator being a flattening of the lateral pillar as seen on anteroposterior (AP) radiographs:

  • IType A: minimal.
  • Type B: up to 50%.
  • Type C: more then 50%.

Treatment

Nonoperative treatment has consisted of bracing, range of motion (ROM) exercises, casting, and prolonged non-weight bearing. Currently treatment includes modification of activity and sometimes a limited period of Petrie's cast for synovitis. Indications for surgical treatment vary. Children who are 8 years of age or older at the onset of LCP with type C and B/C hips might achieve a better outcome with surgical treatment. Patients younger than 8 years of age with type A and B hips do well regardless of the treatment. Patients with type C hips do poorly with or without treatment in all age groups. Girls have a poorer prognosis.

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Rehabilitation & Return to Play

SCFE, DDH, and LCP influence the growth and anatomy of one of the most important joints in the lower extremities. A patient with early detected and successfully treated DDH will form a normal hip joint and should be allowed to participate in all activities. Patients with suboptimal results of DDH treatment and patients with LCP and SCFE should be advised to concentrate on low-impact activities. A significant percentage of theses patients will require total hip arthroplasty. Daily exercises, proper nutrition to maintain low body weight, diet, and selection of appropriate sports will be very important.

Avulsion Fractures

Pathogenesis

In growing individuals most avulsion fractures involve the muscles originating from the pelvis. The connection between the pelvis and the muscles usually occurs through an apophysis. Because this is commonly the weakest link of the working unit of bone, apophysis, tendon, and muscle, the fragment usually separates from the pelvis through the apophysis.

Clinical Findings

  1. Symptoms and Signs

Symptoms include pain and limitation of active motion of the injured muscle, especially with resistance. The patient might not recall any sudden onset of pain, but many young athletes report a painful “pop” and shot of pain with sudden acceleration or deceleration. The most common avulsion fracture sites include the following:

  • Anterior superior iliac spine (ASIS): origin of the sartorius.
  • Anterior inferior iliac spine (AIIS): origin of the straight head of the rectus.
  • Lesser trochanter: iliopsoas muscle.
  • Ischial tuberosity: hamstrings.
  • Posterior/superior brim of the acetabulum: origin of the reflected head of the rectus femoris.
  • Greater trochanter: gluteus medius and minimus.

Imaging Studies

Radiographs are taken to recognize the displaced and unstable avulsion fractures. The majority of the avulsion fractures are stable and minimally displaced.

Differential Diagnosis

  • Fractures, especially the hip/pelvis.
  • Stress fractures.
  • Any problem listed in Table 9-5 (groin pains).
  • SCFE.

Treatment

In rare occasions a severely displaced and unstable fracture might need an open reduction with internal fixation (ORIF) of the avulsed fragment, but the majority of avulsion fractures will be minimally displaced and stable. Those fractures may require an initial short period of immobilization, with the RICE (rest, ice, compression, and elevation) protocol employed.

Rehabilitation & Return to Play

As soon as symptoms are under control and the fracture remains undisplaced, walking with touchdown weight bearing is permitted. Gentle, active assisted and passive

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ROM exercise will be the next step, and once the patient is able to walk without pain, active ROM with increasing resistance might begin. Stretching should follow. Because the total time required to recover from an avulsion fracture might easily exceed 3 months, the parents and the patient should be informed about the prolonged recovery time as soon as diagnosis is established.

Table 9-5. Differential diagnosis of hip/pelvis problems.

Slipped capital femoral epiphysis
Legg–Calve–Perthes disease
Osteoarthritis
Septic arthritis
Transient synovitis
Gonococcal arthritis
Stress fractures
Overuse syndromes
Avulsion fractures
Lyme disease
Intraarticular pathology
Sacroiliac joint problems
Osteitis pubis
Snapping hip
Tumor
Pathologic fracture (through a cyst)
Osteoid osteoma
Osteomyelitis
Abdominal strain
Hernia
Radicular symptoms

Snapping Hip

Pathogenesis

Traditionally, the term “snapping hip” referred to symptoms of external and internal snapping hip. The traditional term, “internal snapping hip,” is very imprecise, as the symptoms could be caused by many factors. This term should therefore be abandoned, given that hip arthroscopy and magnetic resonance imaging (MRI) arthrographs have broadened our knowledge of the intraarticular pathology. The entire spectrum of the “internal snapping hip” will be discussed in the section on groin pain. This section will focus on the “external snapping hip” (ESH).

Clinical Findings

  1. Classification
  • Classic coxa saltans: tight iliotibial band.
  • Greater trochanteric bursitis.
  • Fibrosis of the gluteus maximus muscle.
  1. Symptoms and Signs
  • Painful snapping.
  • Pain at the greater trochanter.
  • Sudden snap and jerk with internal/external rotation.
  • Snap while getting up from squatting.
  • Tightness of the ITB as detected by the Ober test.

ESH often results in a quite frustrating experience. The tight ITB snaps over the greater trochanter with a hard jerk, possibly interfering with physical activities or even with activities of daily life. Usually the patient will easily demonstrate the snapping. Symptoms occur in early teenage years and are more frequent among girls. Runners and cyclists suffer ESH very frequently.

  1. Imaging Studies

Diagnosis of ESH is made based on clinical symptoms, but radiographs help to rule out other causes of hip pain. In cases when differentiation from internal snapping is necessary, MRI, computed tomography (CT) scan, bone scan, or bursography should be considered.

Differential Diagnosis

Differential diagnosis includes internal snapping, alignment problems of the lower extremity, and referred pain from the lumbar region.

Treatment

  1. Nonsurgical

Patients with symptoms of the classic coxa saltans might benefit from an extended ITB stretching program. Initially, the mechanical hard snap, characteristic of coxa saltans, may be the only reason why patients seek medical attention. However, with prolonged symptoms, the bursa between the lateral aspect of the greater trochanter and ITB becomes inflamed, causing pain with snapping. In this phase oral nonsteroidal antiinflammatory drugs (NSAIDs) and injection of long-acting steroids directly into the bursa may help reduce inflammation.

In the rare occasions when snapping is caused be a fibrotic gluteus maximus, proper stretching of the muscle should help in controlling the pain.

  1. Surgical

Surgical treatment of coxa saltans is occasionally necessary. Partial resection or Z-lengthening has been employed with overall good results. Surgery can be combined with stabilization of the ITB into the greater trochanter, using heavy stitches or suture anchors. Excision of the inflamed bursa is optional. Osteotomy of the greater trochanter or proximal femur has been tried; however, this should not be utilized as a primary surgical treatment. It might appear excessive to an adolescent patient to be placed in a half-spica cast, but some type of immobilization will increase the chance of eliminating the pain. A half-spica cast should be seriously considered for revision surgery, with a hip, knee, ankle, and foot orthosis (HKAFO) possibly serving the same purpose.

Return to Play

After surgery, with or without immobilization, the tissues will need time to heal. Stretching should begin 3–4 weeks later, but the return to sport requires restoration of muscle strength through physical therapy. Therapy should focus on strengthening the gluteus medius as well as other muscles around the hip joint.

Byrd JW, Jones KS: Hip arthroscopy in the presence of dysplasia. Arthroscopy 2003;19(10):1055.

Dobbs MB et al: Surgical correction of the snapping iliopsoas tendon in adolescents. J Bone Joint Surg Am 2002;84-A(3):420.

Herring JA et al: Legg-Calve-Perthes disease. Part II: Prospective multicenter study of the effect of treatment on outcome. J Bone Joint Surg Am 2004;86-A(10):2121.

Kuklo TR et al: Hip arthroscopy in Legg-Calve-Perthes disease. Arthroscopy 1999;15(1):88.

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Groin Pain

Pathogenesis

Various extraarticular or intraarticular factors can trigger groin pain (Table 9-5). Pain related to intraarticular pathology might be caused by loose intraarticular bodies, a labral tear, a torn ligamentum teres, an osteochondral fracture, Perthes disease, an SCFE, hip dysplasia, AVN, septic arthritis, hemophiliac arthropathy, Lyme disease, or a rare pathology such as synovial chondromatosis (Figure 9-9). Extraarticular causes include stress fracture, overuse, osteoid osteoma, avulsion fracture, apophysitis, iliopectineal bursitis, iliopsoas strain, piriformis syndrome, hamstring syndrome, adductor strain, athletic pubalgia, osteitis or osteomyelitis of the os pubis, cysts such as an aneurismal bone cyst of the os pubis, ilioinguinal nerve entrapment, abdominal hernia, and abdominal muscle strain. Some of these pathologies might present as snapping hip, which usually accompanies the intraarticular problems or inflammation of the iliopsoas muscle or iliopectineal bursa. In the last case, hip snapping occurs when the hip moves from flexion and external rotation into extension and internal rotation. This maneuver helps to determine the source of groin pain.

 

Figure 9-9. Seventeen-year-old male complaining of groin pain while walking. No history of trauma. A: Radiograph showing a lytic, round defect of the right femoral head. The lesion was removed. The defect was filled with a single-cylinder 10-mm osteochondral autograft, harvested from a non-weight-bearing part of the ipsilateral knee lateral femoral condyle, using the Osteochondral Autograft Transfer System (OATS) (Arthrex, Naples, FL). Pathology examination showed a chondroblastoma. B–D: One year after the lesion was removed. The follow-up CT scan shows very firm healing of the graft into the femoral head. There are no signs of recurrence of the tumor. The patient has been asymptomatic and has resumed full activity.

Clinical Findings

  1. Symptoms and Signs

The groin pain could be referred from the lumbar spine or retroperitoneal structures.

  1. Labral tear injuries
  2. Etiology—
  • Traumatic.
  • Degenerative.
  • Idiopathic.
  • Congenital.
  1. Morphology—
  • Radial flap.
  • Radial fibrillated.
  • Longitudinal peripheral.
  • Unstable.
  • Bucket handle.

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  1. Ligamentum teres injuries
  • Complete rupture.
  • Partial tear
  • Degenerative tear
  1. Imaging Studies

Radiographs of both hips in two projections are mandatory. Special views such as Judett's, inlet, outlet, or false profile might be necessary for particular patients, depending on the working diagnosis. A bone scan might facilitate diagnosis of stress fractures, inflammation, or infection. An ultrasound of the hip joint might show an accumulation of fluid, but will not narrow down the differential diagnosis. When a fluid distends the hip joint, aspiration of the joint under an image intensifier can provide more specific information about the inflammatory process. A fine cut CT scan with possible three-dimensional reconstruction permits a better understanding of the geometry and morphology of the hip. The intraarticular loose body may show up better on CT images than on MRI because the time needed to generate CT images is shorter. A CT also shows the detailed anatomy of a dysplastic hip.

MRI and MRI arthrography have improved and widened the understanding of hip pathology, especially if caused by intraarticular factors. Detailed images of the labrum, ligamentum teres, transverse ligament, and cartilage are useful, and will also aid in the differential diagnosis of benign and malignant processes, infection, and stress fracture (Figure 9-10).

 

Figure 9-10. Sixteen-year-old female cross-country runner with right groin pain and no obvious trauma. A: Radiograph showing fuzzy, narrow joint space. B–D: A CT scan shows a type 3 tear of ligamentum teres. The patient underwent arthroscopic resection of the fragment.

Differential Diagnosis

  • Genitourinary problems.
  • Thrombosis.
  • Phlebitis.
  • Femoral neuropathy.
  • Endometriosis and other gynecologic issues.
  • Pain related to previous hernia surgery.
  • Pain referred from the lumbar region.

Treatment

The varieties of problems that manifest as groin pain deserve thorough analysis (Figure 9-11). The final diagnosis guides the treatment. Modification of activity, a strengthening program, physical therapy, changing the posture and biomechanics of the gait, changing

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sport-specific techniques, NSAIDs, ice, stretching and massage, or surgery will be employed depending on the diagnosis. Hip arthroscopy emerges as a valuable diagnostic and therapeutic tool. In the pediatric population, hip arthroscopy is an excellent technique to treat the loose intraarticular body, problems related to Legg–Calve–Perthes disease, hip dysplasia and SCFE, ligamentum teres injuries, labral tears, and other rare illnesses.

 

Figure 9-11. Hemophiliac arthropathy, left hip. A, B: A CT with three-dimensional reconstruction shows a semiloose fragment of the femoral head. C, D:The fragment visualized during arthroscopy, measuring 2.5% 2.0 cm. E: The fragment is partially removed. F: Parts of the loose body.

Rehabilitation & Return to Play

Advances in diagnosis and treatment have made return to sports possible for greater numbers of patients. A properly guided rehabilitation program of the young patient should result in full recovery. In the rare cases of severe Perthes disease, AVN, arthropathy, and rheumatoid diseases, long-lasting limitation may be advocated.

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Septic Arthritis & Transientsynovitis

General Considerations

There are two very common causes of an acute hip/groin pain, which commonly are very challenging to diagnose: septic arthritis and transient synovitis.

Clinical Findings

  1. Symptoms and Signs

Septic arthritis and transient synovitis are completely unrelated, although both might manifest with refusal to walk or bear weight, pain of the groin, restricted ROM of the hip, limp, and joint effusion. Differentiating between these two syndromes is vital, because potential damage to hip cartilage and serious sequelae are very likely for untreated septic hip arthritis.

Treatment for septic arthritis and for transient synovitis is entirely different, and a decision about treatment must be made within a short period of time. Within the past 5 years three excellent papers have been published that help differentiate between benign, transient synovitis and the potentially dangerous septic arthritis. In the two studies by Kocher et al a history of fever, together with non-weight bearing, an erythrocyte sedimentation rate (ESR) higher then 40 mm, and a serum white blood cell (WBC) count higher then 12,000 cells/mm3 all pointed clearly toward septic arthritis. The probability of having septic arthritis with all four predictors was 99.6%. However, in a study by Luhmann et al the probability was only 59% with all four predictors. They found that a history of fever, a WBC >12,000, and a previous health care visit yielded a 71% probability of septic arthritis.

  1. Imaging Studies

Radiographs are taken in two standard views. They might show distention of the joint or another reason for the hip pain. An MRI will help to distinguish between osteomyelitis, iliopsoas abscess, pathology of the sacroiliac (SI) point, or other soft tissue problems.

Differential Diagnosis

  • Septic arthritis versus transient synovitis.
  • Gonococcal arthritis.
  • Iliopsoas abscess.
  • Osteomyelitis of the pelvis.
  • Avulsion fractures.
  • Apophysitis.
  • SI joint problems.

Treatment

Treatment is based on differentiation between septic arthritis and transient synovitis. Hip aspiration is mandatory in questionable cases. Unfortunately, because about 50% of culture from the fluid joint will be negative, even in the presence of a septic joint, the decision-making process will still depend on clinical symptoms and results of additional studies.

In cases in which the clinical level of suspicion for septic arthritis is high, a formal debridement of the hip joint will be necessary with 6 weeks of intravenous antibiotics. Transient synovitis does not need treatment.

Rehabilitation & Return to Play

In cases of transient synovitis patients will be able to return to sport as soon as the symptoms subside, with no limitations. Proper treatment of septic arthritis diagnosed within 72 hours of the onset of symptoms should yield excellent results with full recovery and return to full activity. In contrast, the results of neglected septic arthritis can be catastrophic. Total destruction of the femoral head, stiffness of the hip, chronic pain, limb length discrepancy, limping, and fast deterioration of the joint are the rule. These patients need either an osteotomy of the femur/pelvis with unpredictable results, fusion of the joint, or early arthroplasty.

Kocher MS et al: A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. J Bone Joint Surg Am 2003;85-A(6):994.

Kocher MS, et al: Hip arthroscopy in children and adolescents. J Pediatr Orthop 2005;25(5):680.

Kocher MS et al: Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am 2004;86-A(8):1629.

Luhmann SJ et al: Differentiation between septic arthritis and transient synovitis of the hip in children with clinical prediction algorithms. J Bone Joint Surg Am 2004;86-A(5):956.

Santori N, Villar RN: Acetabular labral tears: result of arthroscopic partial limbectomy. Arthroscopy 2000;16(1):11.

Knee

Anatomy

The knee of a growing athlete is a changing complex driven by growth of the epiphyses, ligaments, muscles, and cartilage. The overall mechanics and function are similar to those of the adult knee; one of the major differences is the presence of growth plates. The distal femoral growth plate looks like two reversed, shallow parachutes, which span each femoral condyle, and connect at the center of the femur. The periphery is slightly more proximal then the “tips” of each parachute. The central “tip” creates the most distal point of the physis. The connection between the lateral and medial part of the growth plate occurs at the roof of the intercondylar

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notch, and extends through the entire width of the distal femur in the AP direction. The growth plate is about 2–3 mm thick. The ACL originates at the medial aspect of the lateral condyle epiphysis, with its origin adjacent to the physis of the lateral condyle, especially posteriorly.

The growth plate of the tibia more closely resembles a flat disk. It is neither concave nor convex. The center of this growth plate lies at the same level as its periphery. In younger individuals, the anterior part confluences into the growth plate, or apophysis, of the tibial tubercle. Later in skeletal maturity, the tibial growth plate creates a separated layer across the proximal tibia, as the tibial tubercle apophysis separates from it.

The ligaments, menisci, and articular cartilage of the condyles, tibial plateau, and patella are similar to those of the matured knee. In an immature knee the footplate of the ACL insertion is entirely within the articular aspect of the epiphysis. The connection with the tibia is via the epiphysis and physis of the upper tibia.

Clinical Findings

  1. Symptoms and Signs

A detailed history is the most important element in the decision-making process. The history should include the circumstances of the injury, direction and magnitude of injury forces, position of the leg at the time of injury, and description of the offending factors. A history of noncontact injury is characteristic of the ACL tear, especially with a “pop” felt at the time of injury. A “pop” might also be associated with patella dislocation. Contact injury with a “pop” more likely points toward a meniscal injury, a collateral ligament tear, or a fracture rather than an ACL tear (Figure 9-12). ACL injury, meniscal tear, and osteochondral fracture typically present with an acute swelling. Locking and catching will be most common with a meniscal injury and a loose intraarticular body. A “giving way” sensation correlates with a ligamentous injury, including ACL, and with patellar instability; a grinding sensation from the knee points to patellofemoral pathology or loose body versus a meniscal injury.

Inspection allows assessment of the color, appearance, and defects of the skin, the amount and distribution of swelling, position of the knee (flexion contraction), fullness/puffiness of the joint line, effusion, appearance of the tibial tuberosity, atrophy of the quadriceps, position of the patella (alta, baja), and camelback sign of the skin (prominent fat pad with patella subluxation). The overall mechanical alignment of the lower extremity should be noted as well. During palpation, it is important to look for warmth of the skin, for grinding, especially from the patellofemoral joint, for the point of maximum tenderness, and for details of an effusion, if present. A dynamic examination will include testing of ROM, stability, and dynamic anatomy of the knee as well as an evaluation of quadriceps and hamstrings strength. ROM of the knee should be unrestricted and there should be no catching or locking. Patella tracking should be undistorted and the Q angle should be less than 10. The J sign is positive when the patella subluxes laterally with the knee approaching its full extension. The apprehension test indicates patellar tracking problems as well as possible previous patella dislocation. The patella relocation test is similar to the relocation test for a shoulder: with a positive apprehension test the patient feels much more comfortable when direct pressure is exerted to stabilize the patella within the femoral groove. Pain of the middle facet of the

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patella as well as pain over the medial retinaculum and crepitation are closely associated with dislocation of the patella. Other causes of knee pain and locking are medial plica and displaced meniscal tear. Clinical symptoms of medial plica consist of a hard snapping usually over the medial condyle. The plica might be palpated over the medial condyle as a fold of fibrous tissue, and while inflamed and irritated, might cause pain with direct pressure over it. The majority of plicas are clinically silent.

 

Figure 9-12. Fifteen-year-old soccer player, after being tackled down, with acute onset of right knee pain. A: Salter 2 fracture of the distal femur. B: The fracture is anatomically reduced and secured with two titanium 7.3-mm screws. Titanium screws will allow an MRI of the knee to be obtained to assess for possible ligamentous injury to the joint.

  1. Imaging Studies

After the clinical part of the examination is completed, four radiographs of the knee should be obtained. The AP, lateral, Merchant, and tunnel views are the most critical radiographs in the adolescent population. They may show pathognomonic findings, making proper diagnosis easy or obvious (fractures, dislocation of the patella, tumor, osteochondroma) (Figure 9-13). A bone scan, CT scan, or MRI will help to further narrow down the diagnosis.

  1. Special Tests

Direct palpation of the patella and femoral condyles or the Wilson test can be used when testing for cartilage injuries. The Wilson test indicates a typical osteochondritis dissecans (OCD) of the medial part of the lateral condyle. For this test the knee is internally rotated, flexed, and extended. With internal rotation the tibial spine engages into the OCD defect thus creating pain. External rotation relieves the pain. A positive Wilson test in 30° of flexion, resulting in pain, is highly correlated with an OCD. Direct palpation of femoral condyles localizes a cartilage defect, as the patella does not cover a significant portion of the femoral condyles. Meticulous palpation shows very precisely the location of an OCD or osteochondral fracture (OCF). Pain with direct palpation may be positive in the presence of a cartilage/bone bruise as well. Anterior knee pain with active hyperextension and direct pressure at the patella signifies the possibility of patellofemoral arthritis or osteochondral changes, whereas tenderness of the distal pole of the patella is characteristic of Sinding–Larsen–Johansson syndrome. Pain at the midsubstance of the patellar ligament might indicate a jumper's knee. Pain and enlargement of the tibial tuberosity is are pathognomonic for Osgood–Schlatter disease.

 

Figure 9-13. A 9–year-old female with a severely comminuted femoral shaft fracture as a result of a skiing accident. The fracture could not be treated with a flexible intramedullary nail because of comminution. A: The fracture is stabilized by a complex External Fixateur and temporary half-spica cast B:Full recovery after 8 months.

The McMurray test and Apley test are commonly used to assess a knee for potential meniscal problems. The McMurray test involves extending the knee from full flexion while rotating the foot internally or externally. The Apley test (grinding test) requires a prone position. The knee is flexed 90° and the tibia is compressed against the femur. The tibia is rotated externally and then internally. Pain with both tests as well as joint line tenderness indicate meniscal pathology.

To test medial collateral ligament (MCL) and lateral collateral ligament (LCL) instability the examiner should exert valgus/varus stress forces on a knee that is flexed 30°. Laxity might indicate an MCL or LCL tear or physeal fracture. A positive valgus/varus test in full extension is indicative of a cruciate ligament or growth plate injury.

The anterior drawer, Lachman, and posterior drawer tests check the stability of the knee in the sagittal plane. The anterior drawer and Lachman tests can be graded from 0 to 3, with either a soft or solid end point. Comparison with the contralateral side improves the precision of the examination, especially while testing patients

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with generalized laxity. Pivot shift starts with the knee held in internal rotation and flexed: as the knee straightens into full extension, the tibia subluxates anteriorly; with flexion, the tibia reduces with an audible clunk.

Sagittal, valgus/varus instability and laxity while testing for a posterolateral corner might be observed in patients with Down, Marfan, or Morquio syndromes, osteogenesis imperfecta type 1, and pseudochondrodysplasia. Various symptoms, relatively common in syndromic patients, might be related to the underlying disease rather than to orthopedic problems. For example, anterior knee pain is very common in congenital patella dislocation and nail-patella syndrome (hypoplasia/splitting of the nail, hypoplasia or an absent patella with a hypoplastic lateral condyle and hypoplastic fibular head, iliac spurs, flexion contracture of the elbow with a small capitellum and radial head). Patients with Marfan syndrome show increased laxity as well. Knee hyperextension with laxity and patella and hip dislocation are common in trisomy 21. Diminished ROM with “dimpling” and occasional striae in arthrogryposis are pathognomonic features of the disease. Sometimes, fixed hyperextension of the knee is visible in spina bifida patients and congenital dislocation of the knee. Genu valgum is common in Morquio and Ellis van Creveld syndrome. Rickets usually results in genu varum; however genu valgum could also be seen in this condition.

Faraj AA et al: Arthroscopic findings in the knees of preadolescent children: report of 23 cases. Arthroscopy 2000;16(8):793.

Post WR: Clinical evaluation of patients with patellofemoral disorders. Arthroscopy 1999;15(8):841.

Anterior Cruciate Ligament Tear

Skeletally immature athletes are experiencing more ACL injuries than ever before. The injury is occurring in an increasingly larger number of very young children, with the average age of occurrence declining. The majority of these injuries (about 70%) are the result of a noncontact activity. Usually, the injured knee is close to full extension just prior to a sudden change of direction, during sudden deceleration, or at the time of landing. At the moment of injury, the athlete's center of gravity is low and behind the knee, and the foot is planted flat or in pronation. The contact mode of ACL injuries usually involves flexion and valgus-producing impact. Sports in which there is a high risk of incurring an ACL injury are football, soccer, basketball, volleyball, lacrosse, and skiing.

Prevention

Guided prevention may help to lower the prevalence of ACL injuries. Because the injury is now more common, athletic trainers and coaches should offer specifically designed ACL prevention programs to all students involved in competitive sports. The University of Pittsburgh Sport Medicine Center Program is an excellent example of an ACL prevention curriculum. A significant reduction in ACL injuries could be achieved, especially among girls. Specifically designed training can help to improve reaction time, muscle preparedness, muscle mobilization, proprioception, and general conditioning. It will also teach proper sport-specific techniques. The program should include weight lifting, proprioception, and plyometric and balance training. The Internet offers a good source of information on this topic. Sites such as http://www.girlscanjump.com provide an excellent overview and links to other pages related to ACL prevention problems.

Clinical Findings

  1. Symptoms and Signs
  • Sudden “pop.”
  • Effusion.
  • History of giving way.
  • Anterior drawer.
  • Lachman test.
  • Finacetto: severe subluxation of the tibia.
  • Anterior drawer with external or internal rotation of the foot.
  • Restricted ROM with an impinging tear.
  • Pivot shift.
  • Pivot jerk.

The last two tests should be performed with the patient under anesthesia as they can result in significant discomfort.

Clinical symptoms of an ACL tear in the pediatric population seem to be identical to those in adults. A typical mechanism of injury, subsequent swelling and effusion, and a subjective sensation of instability are the hallmarks of this injury. With a chronic injury, patients frequently report the knee giving way and collapsing. Pain is not a part of an ACL injury; however, very often it is reported as one of the symptoms. This could be related to a meniscal tear or a bony bruise of the lateral compartment. Pain can also indicate a growth plate injury of the distal femur and proximal tibia. Careful palpation and radiographic assessment help to establish the proper diagnosis. Stress radiographs may be necessary as well.

  1. Imaging Studies
  • Radiographs: mainly to rule out skeletal injuries.
  • MRI: the gold standard for an ACL tear; the classification system is similar to adults (Figure 9-14)
 

Figure 9-14. A: A 14-year-old female basketball player with an anterior cruciate ligament (ACL) tear. B, C: An 8-year-old male with a torn ACL.

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Differential Diagnosis

  • Physeal fracture.
  • Tibial spine fracture.
  • Meniscal injury.
  • Tear of other ligaments.
  • Osteochondral injury.
  • Patella dislocation.

Treatment

Several options are available when caring for an immature athlete. The first is to reconstruct the ACL surgically as described for the adult athlete with an ACL rupture (see Chapter 3, this volume) or to use physeal sparing techniques. The second option is to wait until the child reaches skeletal maturity and then reconstruct the ACL. The next option is to allow the child to play sports after a decision has been made as to whether to brace or not to brace the knee, hoping to protect it from further damage. The last option is to allow some activities while limiting others.

  1. Nonoperative

Nonoperative treatments with bracing, a proprioception program, and strengthening exercises do not prevent a child from incurring subsequent, additional injuries. Braces do not guard against additional trauma. Unlimited activity, with or without a brace, will increase the risk for further injuries and should be discouraged. Sports such as rowing, light weight training, bicycling, or running on an elliptical training track carry a relatively low risk for additional injuries. Swimming is safe as well, except for the breaststroke.

  1. Operative

Theoretically, all children with an ACL injury not willing to change their level of activity should have the ACL reconstructed. On the other hand, results of ACL reconstruction in skeletally immature children are still not as good as in the adult population, and the failure rate and subsequent revision rate are higher.

The consensus now is to either reconstruct the ACL or to limit activity, eliminating all possible movements that may increase the risk of added injury to the ACL-deficient knee. If a family wants a child to continue playing sports requiring cutting, pivoting, changing direction, twisting, and a stop-and-go type of activity, it is advisable to have the torn ACL reconstructed. Prior to the surgery, a thorough discussion with the family about the pros and cons of the procedure is mandatory.

In addition to the usual surgical risks, reconstructing a torn ACL in a skeletally immature patient increases

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the possibility of growth disturbances such as shortening or angulation, failure of the graft, and persistent symptoms if a nonisometric reconstruction is performed.

  1. The Growth Plate

The development of problems following reconstruction of an ACL in a skeletally immature athlete is related to factors such as drilling tunnels across the growth plate, choices of graft, method of fixation, tension across the growth plate, and placement of the tunnels through the periphery or center of the growth plate. Just drilling a tunnel across a growth plate might itself result in growth arrest and physeal bridge formation. In an experimental study drilling a hole through a physis up to 10% of the growth plate diameter seems to be safe. Reaming the tunnel through a periphery of the growth plate carries a higher risk for physeal bony bridge formation than reaming it through the center part of the physis. Therefore the risk of significant growth problems caused by the femoral tunnel is greater than the risk caused by the tibial tunnel. Passing a soft tissue graft is safer than crossing a growth plate with a bony block. Adding an interference screw across a physis may result in growth arrest. Even tensioning a graft passed just adjacent to the periphery of a growth plate might slow down the growth of the physis. In one study a tensioned graft placed outside a physis caused an angular deformity of the extremity, without physeal bone bridge formation. Another study reported on genu valgum formation with over-the-top passage of the graft and extraphyseal graft placement. All the potential problems should be discussed with the patients and the family prior to the surgery.

Table 9-6. Tanner's staging for boys and girls.

Stage for Girls

Pubic Hair

Breast

1

None

Preadolescent

2

Scarce, light, straight

Elevated by small amount

3

More hair, darker, starting to curl

Breast and areola bigger

4

Coarse, curly, still less than the adult

Areola, papilla form secondary mound

5

Adult triangle, spreads to thighs

Mature. Nipple projects, areola part of breast contour

Stage for Boys

Pubic Hair

Penis

Testes

1

None

Preadolescent

Preadolescent

2

Scanty, long, light

Slight enlargement

Larger, pink, texture changed

3

Darker, curling

Longer

Larger

4

Adult type but less

Glans and breath increase

Larger, scrotum dark

5

Adult, spread to thighs

Adult size

Adult size

Adapted, with permission, from Tanner JM: Growth at Adolescence, 2nd ed. Blackwell Scientific Publications, 1962.

Once the decision to go ahead with surgery is made, the type of ACL reconstruction should be carefully selected to diminish the risks of graft failure and growth problems. The graft should be placed in a biomechanically optimal position. Any given procedure should be individually tailored to each child or adolescent to minimize the risks and provide the patient with the best possible reconstruction of the ACL. Biological age, maturity, and growth plate function are the most important factors to consider. Each child develops at an individual pace. To determine a particular child's stage of development, it is necessary to consider age, gender, height, Tanner stage, onset of menarche, height of parents and older siblings, bony age, late versus early boomers in the family, and general distribution of height in the family (Table 9-6). Wide-open physes signify that considerable growth remains. The appearance of the proximal tibial and distal femoral physes is very important. The morphology of the proximal tibial physis is quite unique and the shape of the physis provides additional information about the maturity process. Initially, the physis blends with the tibial tuberosity growth plate, smoothly sloping anteriorly and distally. As a child matures, the proximal tibial physis becomes more horizontal and separates from the tibial tubercle. The tibial tubercle growth plate separates from the main proximal tibial growth plate usually 1–2 years prior to skeletal maturity, and fuses earlier than the tibial growth plate.

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The magnitude of potential permanent growth problems associated with an ACL reconstruction is proportional to the growth remaining. Generally 1–2 cm of remaining growth should not pose a danger of creating a significant deformity. The Green and Anderson graft, the Moseley straight-line graph method, or the Multiplier Method by Paley and colleagues will help calculate the exact remaining growth of each individual patient. In a clinical setting, the most practical way to predict the remaining growth is the method of Menelaus and Westh. It is based on a few facts:

  • IThe proximal tibia grows 6 mm/year.
  • The distal femur grows 10 mm/year.
  • Girls stop growing at age 14 years.
  • Boys stop growing at age 16 years.

For example, an average 13-year-old boy will grow about 3 cm from the distal femur and 1.8 cm from the proximal tibia.

  1. Tunnel Placement

The adult, transphyseal type of ACL reconstruction requires drilling of tunnels across the distal femoral and proximal tibial metaphysis and physis. This method can be used in older adolescents, but in individuals with significant growth remaining, this type of reconstruction poses a high risk of injury to the growth plates. The graft should not interfere with the development of the physis. Extraarticular reconstruction, extraphyseal methods, or total or partial transepiphyseal graft placement all offer “physis-friendly” routes for the graft.

Extraarticular methods have been largely abandoned, as they do not allow isometric placement of the ACL graft. In addition, the extraarticular positioning of the graft can still result in growth disturbances without the benefit of isometric reconstruction. Extraphyseal and partial or total transepiphyseal methods of reconstruction offer better biomechanics and appear to be safe for the growing extremity. In Tanner's stage 1 and 2, with significant growth remaining and a high risk for shortening of the limb or/and an angular deformity, extraphyseal or transepiphyseal reconstructions seem to lower the risk (Figure 9-15). During extraphyseal ACL reconstruction, a graft is passed into the joint usually through a shallow groove under the intermeniscal ligament and is then stabilized in an over-the-top position at the femoral side. This method is relatively safe but is not entirely isometric, and the position of the graft is not very secure, especially over the brim of the tibia.

A total transepiphyseal reconstruction requires drilling the tibial tunnel within the tibial tubercle epiphysis and through the epiphysis of the lateral femoral condyle (Figure 9-16). This is currently the method of choice if both the distal femoral and proximal tibial growth plates are wide open and there is significant growth remaining. This method is technically very demanding. The tunnels should be drilled under the guidance of an image intensifier. The femoral tunnel starts laterally at the center of the lateral condyle and exits as close to the ten thirty or eleven o'clock position for the right knee and one to one thirty position for the left knee. The tunnel must enter the joint just distal to the femoral physis. The tibial tunnel starts between the joint line and the distal extension of the growth plate of the tibial tubercle. It exits about 5 mm at the front of the anterior margin of the posterior cruciate ligament (PCL). The size of the tunnel may limit the diameter of

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the graft, since the tibial tubercle epiphysis is quite narrow and thin. Especially in younger children, drilling a tunnel larger then 6–7 mm might violate the growth plate of the tubercle, thus increasing the risk for genu recurvatum. On the femoral side, the epiphysis can accommodate essentially any tunnel, even up to 12 mm. The transepiphyseal technique places the graft into an isometric position. The reconstructed knee regains excellent stability, and safety appears to be satisfactory based on early results. There have been no reports of growth problems using this method, but the lack of long-term studies is a potential drawback.

 

Figure 9-15. Different types of anterior cruciate ligament reconstruction. A: Extraphyseal. B: Transepiphyseal. C: Partial transepiphyseal. D:Transphyseal.

 

Figure 9-16. Intraoperative, image intensifier radiographs, showing the position of the transepiphyseal tunnels. A: The guide pin is positioned using the Femoral Retrograde Marking Hook (Arthrex, Naples, FL). B: Position of the femoral guide pin. C: Tibial guide pin traversing the apophysis of the tibia. D:Anteroposterior radiographs showing both guide pins in place. The pins avoid violating the growth plates.

In older adolescents, with still open growth plates and 1–2 cm of remaining growth, the partial transepiphyseal method may be an excellent option. In this method the tibial tunnel is placed transphyseally. Because the tibial tunnel is more vertical and goes through the center of the physis, the transphyseal tibial tunnel carries less risk for the development of significant growth disturbances. Proximally, the graft is routed either over the top or using the transepiphyseal method.

For girls 14 years and older and boys 16 years and older, in Tanner's stage 4, with minimal growth remaining, it is generally safe to proceed with the transphyseal type of reconstruction. The surgeon, however, should be aware of the skeletal maturity of the patient, family history, Tanner's staging, and height patterns in the family. This will help in the decision-making process.

  1. Grafts and Fixation

Currently, most of the transepiphyseal, extraphyseal, and partial transepiphyseal reconstructions of the ACL in growing patients are accomplished using soft tissue grafts (Figure 9-17). Most surgeons performing ACL reconstruction in skeletally immature patients use hamstring autografts. Double or quadruple grafts have been

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used, and the hamstrings are usually used as a free graft. However, for an extraphyseal repair, the distal attachment of the hamstrings to the tibia can be left intact, and the free proximal end of the tendon rerouted into the joint. In younger children, however, the tendinous portion of the hamstrings might be quite tenuous. In this situation other sources of grafts may need to be considered. The bone patella tendon bone grafts can be used safely only if the bone plugs do not contact the growth plate. The routine, adult-type placement of the bony plugs will result in a premature closure of the physis. In the skeletally immature patient the tibial plug is usually partially cartilaginous, thus potentially leading to poor fixation.

 

Figure 9-17. An 8-year-old female soccer player. Reconstruction of the torn anterior cruciate ligament using hamstring autografts. Proximal fixation is achieved using a Drummond button. Distal over-the-post fixation with a large fragment AO screw.

ITB autografts can also be considered and used safely. In cases of insufficient quality of an autograft, to diminish graft-related morbidity, or if cosmetics is an important issue, posterior or anterior tibial tendon allografts or Achilles tendon allografts might be considered. Fixation devices should not violate the growth plates. Femoral fixation can be accomplished by a staple over the post, by a transfixion pin, or by using EndoButton with or without a washer. Intraarticular staples for ACL graft fixation have not been recommended.

The tibial end of the graft can be secured over the post or over a staple(s) or can be sown into the periosteum, or the distal attachment of the hamstrings to the tibia can be preserved. Interference screws, routinely employed for both tunnels in adults, can be used safely in older adolescents for fixation of the tibial end of the graft when a partial transepiphyseal method is chosen. Except for one case report there are no reports to date about using interference screws for femoral fixation in growing children.

  1. Partial Anterior Cruciate Ligament Tear

A partially torn ACL can be left alone, with the nonreconstructive approach being suitable, if the knee is stable. However, the family should be informed that there is a 30% risk of a subsequent total ACL tear. The torn portion of the ACL sometimes blocks ROM and might need to be excised. Augmentation of AM (anteromedial) or PL (posterolateral) bundle might be considered.

Rehabilitation & Return to Play

After ACL surgery the patient undergoes 5–9 months of rehabilitation. A specially designed postoperative protocol should facilitate the communication with a physical therapist. Generally, during the first days, the patient is allowed to perform heel slides, straight leg rises, and isometric exercises of the quadriceps muscles. Weight bearing can start as soon as tolerated by the patient. With a simultaneous meniscal repair, non-weight bearing is recommended for about 6 weeks. Cutting, pivoting, changing direction, and sudden stop-and-go movements begin about 4 months after surgery. At this time the physical therapist can start sport-specific exercises. After successful treatment the patient is usually released to full activity within 5–9 months. To date, except for the generally accepted belief in a higher failure rate after ACL reconstruction, the exact rate of reinjury among skeletally immature patients is not known.

Meniscal injuries discovered during surgery should be treated concurrently. They will be discussed later in this chapter.

Fracture of the Tibialspine/Eminence

Pathogenesis

The same forces that cause an ACL tear might result in a tibial spine/eminence fracture; the pain, however, is usually more pronounced. This fracture extends through the epiphysis of the proximal tibia. A large part of the tibial plateau is avulsed from the tibia and might be elevated, displaced, or comminuted. Very often it does extend into the physis. A large, sanguinous effusion with fatty droplets is typical of this fracture.

The tibial eminence fracture is a typical avulsion fracture. The ACL is prestretched before avulsing the tibial

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spine. For this reason even an anatomically reduced fracture might result in persistent laxity of the knee. This, however, does not seem to cause significant problems.

Clinicial Findings

  1. Symptoms and Signs
  • Pain.
  • Inability to bear weight.
  • Effusion.
  • Laxity.
  • ACL-specific tests are positive.
  1. Classification
  • Type 1: nondisplaced.
  • Type 2: hinged, open trap door.
  • Type 3A: displaced.
  • Type 3B: comminuted or rotated.
  1. Imaging Studies

Lateral and AP radiographs are essential in recognizing the fracture and its displacement (Figure 9-18). They also help in monitoring the position of the eminence following a closed reduction by hyperextension. In cases of irreducible, displaced tibial spine fractures additional studies such as CT scan and MRI might be necessary. In cases of displaced or comminuted fractures, the exact extent of the injury is appreciated only during arthroscopy.

Differential Diagnosis

This is the same as for an ACL injury.

 

Figure 9-18. Type 3 tibial spine fracture of a 14-year-old basketball player. A: The anteroposterior view: this view certainly underestimates the amount of displacement. B: Lateral radiograph showing the exact displacement of the tibial eminence.

Complications

Late laxity is very common following tibial eminence fractures but rarely causes clinical problems. Abnormal function of the growth plate is rare. Sometimes it takes a long time to recover full ROM, and the patient may require a prolonged course of physical therapy.

Treatment

A cylinder cast applied in hyperextension can reduce and stabilize a tibial spine fracture. If the radiographs show a satisfactory position of the avulsed fragment, the cast is kept on for 6–8 weeks. An arthroscopically assisted reduction and internal fixation are a better option for nonreducible type 2 and type 3 fractures. Visualization can be difficult secondary to a large hematoma in the joint. Additional problems may arise: comminution of the fragment, entrapment of the medial or lateral meniscus with or without a tear, and abutment of the avulsed fragment against the intermeniscal ligament, which might render the accurate reduction of the fragment quite difficult. Fixation accomplished by a metal or bioabsorbable screw will be most appropriate for a solid one-piece fragment.

Heavy stitch, lasso stitch, and wires are a good option for a noncomminuted fracture as well. Fixation of a comminuted fracture is done by weaving a heavy stitch or wire through the distal end of the ACL and through the footprint of the ACL. A lasso technique might be used as well. The stitches or wires used for fixation are passed through very small tunnels in the tibia, and secured over a bony bridge between the tunnels.

Whether a nonoperative or surgical treatment was chosen, a period of non-weight bearing for 6 weeks is

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mandatory. The cast is then removed and the leg protected in a long, postoperative, hinged knee brace. The brace should permit a gradual increase of the ROM of the knee. A drop lock will lock the brace in full extension for walking and overnight.

Rehabilitation & Return to Play

As soon as the brace is applied, the patient can start gentle exercises of the quadriceps and hamstrings. ROM should be increased gradually, for example, 10–15° every 5 days. Weight bearing increases gradually as well. Before discharge from the office, the patient must demonstrate full strength of the hamstrings and quadriceps, as well as full ROM. Total recovery usually takes 3–4 months.

Anderson AF: Transepiphyseal replacement of the anterior cruciate ligament in skeletally immature patients. A preliminary report. J Bone Joint Surg Am 2003;85-A(7):1255.

Anderson AF: Transepiphyseal replacement of the anterior cruciate ligament using quadruple hamstring grafts in skeletally immature patients. J Bone Joint Surg Am 2004;86-A(suppl 1, pt 2):201

Andrish JT: Anterior cruciate ligament injuries in the skeletally immature patient. Am J Orthop 2001;30(2):103.

Barber FA: Anterior cruciate ligament reconstruction in the skeletally immature high-performance athlete: what to do and when to do it? Arthroscopy 2000;16(4):391.

Edwards TB et al: The effect of placing a tensioned graft across open growth plates. A gross and histologic analysis. J Bone Joint Surg Am 2001;83-A(5):725.

Fuchs R et al: Intra-articular anterior cruciate ligament reconstruction using patellar tendon allograft in the skeletally immature patient. Arthroscopy 2002;18(8):824.

Guzzanti V et al: Physeal-sparing intraarticular anterior cruciate ligament reconstruction in preadolescents. Am J Sports Med 2003;31(6):949.

Johnson DH: Complex issues in anterior cruciate ligament surgery: open physes, graft selection, and revision surgery. Arthroscopy 2002;18(9 suppl 2):26.

Kocher MS et al: Management and complications of anterior cruciate ligament injuries in skeletally immature patients: survey of the Herodicus Society and The ACL Study Group. J Pediatr Orthop 2002;22(4):452.

Kocher MS, et al: Physeal sparing reconstruction of the anterior cruciate ligament in skeletally immature prepubescent children and adolescents. J Bone Joint Surg Am 2005;87(11):2371.

Millett PJ et al: Associated injuries in pediatric and adolescent anterior cruciate ligament tears: does a delay in treatment increase the risk of meniscal tear? Arthroscopy 2002;18(9):955.

Senekovic V, Veselko M: Anterograde arthroscopic fixation of avulsion fractures of the tibial eminence with a cannulated screw: five-year results. Arthroscopy 2003;19(1):54.

Meniscal Injuries

Pathogenesis

The crescent-shaped fibrocartilaginous menisci transform forces between femoral condyles and the tibial plateau. The medial meniscus is more C-shaped; the lateral one is more rounded and more mobile. In the pediatric population the proportion of menisci to knee is essentially the same as in the adult population. The blood supply comes from the periphery, and in early childhood as much as 60% of the peripheral meniscus is supplied by the arteries. This proportion changes as a child grows, and ultimately only the peripheral 30% of the menisci receives a blood supply. The menisci, especially the medial meniscus, serve as a secondary restraint to anterior translation of the tibia. The majority of meniscal tears result from an indirect, twisting injury of the knee with simultaneous flexion. Sometimes the patient recalls a “snap” or “pop,” and a sudden onset of pain. Usually there is a well-defined moment of trauma. Pain after injury and swelling with effusion are typical, and the patient may experience difficulties with weight bearing.

Clinical Findings

  1. Symptoms and Signs
  • Effusion.
  • Swelling.
  • Decreased ROM.
  • Lack of full extension.
  • Hard block of motion with a displaced meniscal tear.
  • Joint line tenderness.
  • McMurray: the knee is passively extended from a fully flexed position with external and internal rotation.
  • Apley (grinding): prone, 90° of flexion, compression against the femur with internal and external rotation.
  • Quadriceps atrophy with chronic injury.

A diagnosis of a meniscal injury in the pediatric population can be difficult for several reasons: the classic McMurray and Apley test results commonly might not be present, and an examination in an acute setting could be quite unreliable. Joint line tenderness and pain seem to be the most common clinical symptoms in this age group. The tenderness is more sensitive and specific for a lateral meniscus injury and less so for a medial meniscus injury.

Meniscal tears in adolescent patients usually result from abnormal forces applied to normal meniscal tissue; in other words, the degenerative tears, very common among adults, are quite rare. Very commonly, the meniscal tears in this age group occur at the periphery of the meniscus. The classification of meniscal injuries is described in Chapter 3 of this volume (Figure 9-19).

 

Figure 9-19. A–D: Types of meniscal tears. I–IV: MRI classification of meniscal images.

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  1. Imaging Studies

Radiographs in four views help establish a diagnosis of simultaneous bony injuries. The MRI has become the gold standard in the evaluation of the menisci, PCL, medial collateral ligament (MCL), lateral collateral ligament (LCL), and ACL, with an accuracy in assessing meniscal injuries among adults close to 95%. In the pediatric population, however, MRI is not as accurate.

A meniscal tear can be divided into four grades, with only type III pathognomonic for a tear. Typically, a type III injury is seen as a high signal density across the entire meniscus. In the pediatric population the MRI is commonly overread, and interpretation of type I and II tears might be very difficult. The different blood supply in the pediatric population is one of the sources of mistakes. Because the positive and negative predictive values are lower for the pediatric population than for adults, the MRI reading should be used exclusively as an additional study. The final diagnosis should be based on a detailed history, a physical examination, and additional tests, not exclusively on MRI images.

Differential Diagnosis

  • Patella dislocation.
  • Intraarticular loose body.
  • Osteochondral fracture.
  • Osteochondrosis dissecans.
  • Ligament or capsular strain.
  • Unusual pathology (pigmented villonodular synovitis, osteochondroma, foreign body).

Treatment

A patient going into the operating room usually carries an established diagnosis. Sometimes, however, even after an extensive work-up, arthroscopy is the only way to confirm the diagnosis. This is particularly true in the pediatric or adolescent population. In this age group, the probability of finding some unexpected injuries, or not finding the expected damage, is significant.

In cases in which a diagnosis of a meniscal tear is established, a surgeon can leave the tear alone, repair it, or remove part of or the whole meniscus. In young patients a majority of meniscal injuries are reparable, and preservation is the key. Debridement of the meniscus might be necessary in some cases, but even then, it should be very conservative. Treatment of meniscal injuries is described in Chapter 3 of this volume. In no patient is it more important, if possible, to save or repair the meniscus than in the pediatric athlete.

Rehabilitation & Return to Play

After meniscal repair the patient is not allowed to bear weight for about 6 weeks. ROM can be started as soon as the patient's pain is under control. Formal physical therapy typically starts 2–3 weeks after surgery and includes active, passive, and active assisted ROM and strengthening exercises. Patients return to full activities 3 months after surgery

Bloome DM et al: Meniscal repair in very young children. Arthroscopy 2000;16(5):545.

Klimkiewicz JJ, Shaffer B: Meniscal surgery 2002 update: indications and techniques for resection, repair, regeneration, and replacement. Arthroscopy 2002;18(9 Suppl 2):14.

Discoid Meniscus

Pathogenesis

A majority of discoid menisci (DM) occur in the lateral compartment. The prevalence among Asians is much higher (up to 17%) than in whites (5%).

The lateral DM have been divided into three types: complete, incomplete, and the Wrisberg type. A complete DM obliterates the entire lateral compartment of the knee. It is thicker than the normal meniscus, which could be up to 14 mm thick. The middle zone of the meniscus is the thickest one, and the peripheral zone is usually of normal height. The partial DM is enlarged and thicker compared to normal size. Its shape resembles a sausage (Figure 9-20)

 

Figure 9-20. Partial, lateral discoid meniscus in a 6- year-old male. A–C: An MRI showing the abnormal size of the lateral meniscus. D: Intraoperative view of the lateral compartment.

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The Wrisberg type is missing the meniscotibial coronary ligaments of the posterior horn and is by definition unstable. Currently the most popular theory concerning the formation of the DM points to an abnormal motion of the initially unstable meniscus as an impulse preventing the meniscus from maintaining its normal shape. The abnormal motion propels enlargement of the meniscus into its abnormal shape and size. The previous theory about lack of involution from a discoid form into a normal crescent shape has not been supported by anatomical studies.

Clinical Findings

  1. Symptoms and Signs
  • Snapping knee.
  • Pain.
  • Locking.
  • Lack of extension.
  • Bulging of the lateral joint line.

Clinical symptoms include locking, catching, snapping of the knee, and an audible clunk. Other symptoms include pain, which might be a late symptom, usually associated with a tear, or the appearance of a “cyst” at the lateral joint line. Sometimes the enlarged meniscus might cause the knee to lock up. Initial symptoms usually occur at school age, however, 2- or 3-year-old children might already be diagnosed with a DM. A high level of suspicion is necessary to make a proper diagnosis.

Many findings have been linked to DM: cupping of the lateral tibial plateau, high riding fibular head, hypoplasia of the lateral femoral condyle and lateral tibial spine, abnormal shape of the lateral malleolus, widening of the lateral joint space, and hypoplasia of the peroneal muscles. An abnormally high position of the fibular head and widening of the joint space are the only features significantly associated with the DM.

  1. Imaging Studies

The most accurate imaging for DM is an MRI, which has a high positive predictive value of 92% (Figure 9-21). The diagnosis of DM is established if three or more, 5-mm-wide, contiguous sagittal sections show an uninterrupted meniscus from the anterior to the posterior tibial plateau. Two cuts showing equal height of the midsubstance of the meniscus indicate a high probability of DM. The “bow tie” sign helps establish the diagnosis. Diagnosis of the Wrisberg type could be difficult, as the meniscus may not be enlarged.

 

Figure 9-21. Partial, medial discoid meniscus, right knee. A–D: MRI images showing the abnormal size of the medial meniscus. E: Direct view of the meniscus: the meniscus was unstable and was repaired by the inside-out method.

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Treatment

The move toward saving and stabilizing a DM is similar to the trend in meniscal surgery. The total meniscectomy commonly used in the past to “treat” DM should be abandoned, as removal of the entire meniscus can speed up development of osteoarthritis of the knee. An OCD of the femoral condyle following total excision of the DM has been reported.

The goal of surgical treatment is to preserve the meniscus, stabilize it, and reshape it to as close to its normal contour as possible. Saucerization of the meniscus and repair of the instability are probably the best option. Reshaping of the DM is not easy, and requires a lot of time and patience. The abnormal structure of the DM, especially of a complete one, creates problems with visualization during surgery. The cartilage of the DM is also more sturdy and difficult to reshape.

Return to Play

Recovery from DM surgery usually takes 3 months and is similar to recovery from repair of a “normal” meniscus. The patient resumes normal activity after physical therapy.

Ahn JH et al: Discoid lateral meniscus in children: clinical manifestations and morphology. J Pediatr Orthop 2001;21(6):812.

Kim SJ et al: Radiographic knee dimensions in discoid lateral meniscus: comparison with normal control. Arthroscopy 2000;16(5):511.

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Klingele KE et al: Discoid lateral meniscus: prevalence of peripheral rim instability. J Pediatr Orthop 2004;24(1):79.

Osteochondrosis Dissecans (OCD) and Osteochondral Fractures (OCF)

Pathogenesis

OCD is a disease of the cartilage and the subchondral bone that results in isolation and sometimes sequestration of an osteochondral fragment without significant trauma. The “classic” OCD typically involves the lateral aspect of the medial condyle (51–85% of all OCDs). An OCD can involve the weight-bearing surface of the medial condyle, the lateral condyle, and the patella (Figure 9-22).

The juvenile form of OCD occurs in younger teenagers with wide-open physes; the adolescent form is seen when a patient nears skeletal maturity. The lesion happens more commonly in boys (about twice as often as among girls). Bilateral involvement is observed in about 25% of cases, which usually show different patterns and different times of onset.

The etiology of OCD is still uncertain. Initially it was thought to be an inflammatory process of the osteochondral layer of the cartilage. For this reason, the suffix “itis” has been used. The inflammatory theory has never been proven. At present all of the possible etiologies include the following:

  • Microtrauma: repetitive injury to the lateral aspect of the medial condyle by contact with the tibial eminence.
  • Engagement of the odd facet of the patella against the femoral condyle in full flexion.
  • Diminished blood supply to the subchondral bone.
  • Localized epiphyseal dysplasia.

Hereditary influence is slight, although several members of one family have been reported to have OCD problems. The OCF is related to acute trauma. It can involve the medial and lateral condyle as well as the patella. OCF of the lateral femoral condyle is correlated with patella dislocation.

Clinical Findings

  1. Symptoms and Signs
  • No history of trauma.
  • Usually vague symptoms, activity-related.
  • Pain.
  • Swelling.
  • Locking.
  • Loose body symptoms.
  • Tenderness of the femoral condyle.
  • Wilson test.
  1. Classification
  • Grade 1: depressed osteochondral fracture.
  • Grade 2: osteochondral fragment attached by an osseous bridge (trap door).
  • Grade 3: detached nondisplaced fragment.
  • Grade 4: displaced fragment (loose body).
  1. Imaging Studies

Radiographs may show the exact extension of the OCD or OCF. For a typical OCD of the knee, the best and most sensitive radiograph is the tunnel view. AP, lateral, and Merchant views can help to visualize the defect and the position of loose fragments.

An MRI is especially helpful in distinguishing between stable and unstable lesions. The value of MRI at follow-up is limited. Signs of instability based on a T2 image include the following:

  • High signal beneath the OCD.
  • High signal line traversing the subchondral bone into the lesion.
  • Focal osteochondral defect of the articular cartilage >5 mm.
  • 5-mm fluid-filled cyst beneath the lesion (Figure 9-23)

Differential Diagnosis

  • Osteochondrosis dissecans versus osteochondral fracture.
  • Accessory centers of ossification.
  • Osteonecrosis.
  • Epiphyseal dysplasia.

Treatment

  1. Nonsurgical

Treatment of OCD is as controversial as its etiology. A consistent, universally accepted treatment protocol does not exist. Elimination of high-impact activities seems to be logical, and protected weight bearing forms the foundation of nonoperative treatment. Non-weight bearing usually lasts several weeks until the symptoms subside; however, the real question is how long the patient should avoid high-impact activities. Moving the knee is recommended. A brace or even a brief period of casting may be necessary for very active students, but the period of immobilization should be limited.

The length of nonoperative treatment and restriction of activities varies, depending on the treating physician's preferences and experience. About 50% of OCD will heal spontaneously following a nonoperative protocol, a fact commonly cited in the literature. In one study, however, 10 OCDs, which were assessed arthroscopically, were reported to be stable. During a second look arthroscopy, at an average of 7.5 years later, 7 of 10 were unstable.

 

Figure 9-22. Avascular necrosis of the femoral condyle in a 13-year-old female following steroid therapy for dermatomyositis. A: Two years ago. B: One year ago. C: Current radiographs. Osteochondral defect of the tibia plateau after resection of an adamantinoma, at age 10, 6 years ago. D, E: MRI images of the tibia. F: Arthroscopic pictures of the lateral tibial plateau. The crater-like defect occupies about 50% of the lateral plateau.

 

Figure 9-23. Fourteen-year-old male who fell while skateboarding. A: Free, osteochondral fragment next to the lateral femoral condyle, in the lateral gutter of the knee. B: The fragment is reattached via open reduction with internal fixation, using microscrews from a maxillofacial set and osteochondral darts (Arthrex, Naples, FL). C, D: Postoperative radiographs in anteroposterior and lateral views: despite being countersunk, the screws look very prominent on the lateral radiograph. E: The screws are removed: part of a broken microdrill bit is left in place. Repair of the retinaculum was accomplished using suture anchors.

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Risk factors for failure of nonoperative treatment of the OCD include:

  • Older age.
  • Larger lesions (determined by medial–lateral diameter, not anteroposterior).
  • Lesions of the weight-bearing area (Cahill Zone 2 on an AP radiograph).
  • Lesions between 30 and 60°: between Blumensat's line and the posterior femoral line (Cahill Zone B on a lateral radiograph).
  1. Surgical

Indications for surgical treatment include the following:

  • A juvenile OCD that is symptomatic despite 6–12 months of nonoperative treatment.
  • Detachment of the previously stable OCD.
  • Symptomatic loose body.
  • Predicted growth plate closure within 12 months.
  • Symptomatic nonunion confirmed by bone scan or MRI.

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Surgical options include the following:

  • Simple excision or removal of the loose body (not recommended except for a very small lesion of the non-weight-bearing surface).
  • “Refreshment” and drilling of the crater.
  • Microfracture.
  • Reattachment with metal pins (weak); screws (countersunk microscrews from maxillofacial set, cannulated 3.5-mm or 2.4-mm screws, Herbert screw); bioabsorbable OCD darts, arrows, and screws; bone pegs.
  • Subchondral, retrograde bone grafting.
  • Osteochondral transport (mosaicplasty).
  • Osteochondral allografts.
  • Autologous chondrocyte transplantation (Figure 9-24)
  1. Sleeve Fractures

Sleeve fractures are unique to the patella and involve the proximal or distal pole of the patella or its midsubstance. They can occur at the attachment of the patella tendon into the tibia; in this case, a sort of a slide of the sleeve of soft tissue overlying the patella occurs, rather than a classic bony fracture.

Clinically these fractures manifest with weakness of the quadriceps mechanism, a history of hyperflexion trauma, and minimal abnormalities on radiographs. Sometimes a deficit is palpable at the fracture side, and an MRI usually shows fracture patterns and the anatomy of the patella tendon.

 

Figure 9-24. Atypical, bilateral osteochondritis dissecans (OCDs) in a 14-year-old female baseball player. A: Left knee, atypical OCD dissecting the entire posterior part of the lateral femoral condyle. B, C: Displaced OCD of the contralateral knee, lateral condyle.

Treatment of patients with an intact extension mechanism consists of immobilization in a cylinder cast in extension for about 6 weeks, followed by a hinged, long knee brace with gradually increasing ROM and weight bearing.

For patients with a deficit of extension, an open reduction with internal fixation will be necessary to restore full function of the knee. Because the majority of fractures involve soft tissue, heavy sutures passed trough bony tunnels drilled in the patella, or suture anchors, will help restore the continuity of the extensor mechanism.

Rehabilitation & Return to Play

Return to play is a decision very difficult to categorize. Generally, because OCF occurs through “normal” bone, the patient should have no problem returning to full activities 3–4 months after surgery.

The decision regarding patients after OCD surgery, however, is much more complex. The fact that OCD occurs in a clearly pathologic environment worsens the prognosis. The detached OCD, reattached into the “crater” of a potentially abnormal bone, might not heal. A lesion that has been “silent” and stable until skeletal maturity might break off from the femur after skeletal maturity is reached. Presently we lack a reliable tool to follow the OCD and provide predictable information

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about healing. For all these reasons, there is no universal consensus as to whether and when high-impact activities should be allowed. Return to sports after symptoms subside, or 4–6 months after surgery, can be considered. It has been proposed that high-impact activities be limited until the patient reaches skeletal maturity.

After surgery for sleeve fractures, casting and rehabilitation are similar to the nonoperative approach. Patients return to sports at an average of 4 months following the injury.

Aglietti P et al: Results of arthroscopic excision of the fragment in the treatment of osteochondritis dissecans of the knee. Arthroscopy 2001;17(7):741.

Brittberg M, Winalski CS: Evaluation of cartilage injuries and repair. J Bone Joint Surg Am 2003;85-A(suppl 2):58.

Mizuta H et al: Osteochondritis dissecans of the lateral femoral condyle following total resection of the discoid lateral meniscus. Arthroscopy 2001;17(6):608.

Pill SG et al: Role of magnetic resonance imaging and clinical criteria in predicting successful nonoperative treatment of osteochondritis dissecans in children. J Pediatr Orthop 2003;23(1):102.

Osgood–Schlatter Disease

Pathogenesis

Osgood–Schlatter disease (OSD) is a painful swelling of the growing tibial tuberosity, categorized as a traction apophysitis. Pain occurs at the growth plate of the tibial tuberosity. The patellar tendon connects to the tibial tuberosity via a growth plate, and similar to other locations, this type of anatomic setup commonly results in pain in growing children. Typically, OSD occurs among active girls and boys; however, even a classic couch potato might suffer from this condition.

Clinical Findings

  1. Symptoms and Signs

Symptoms occur during a growth spurt, and sometimes last up to 2 years. Bilateral prevalence is not uncommon.

  1. Imaging Studies

Radiographs help to rule out all other causes of pain of the proximal tibia. A diagnosis of OSD is strictly based on history and clinical symptoms. The commonly observed fragmentation of the apophysis of the tibial tuberosity is not a sign of OSD.

Treatment

OSD is a self-limiting condition. Treatment, which targets the symptoms and aims to alleviate the severity of pain, consists of icing, ice massage, and stretching of quadriceps, hamstrings, and calf muscles. NSAIDs help to alleviate the pain; modification of activity might be necessary. A cylinder cast applied for 2–3 weeks is sometimes necessary to reduce the inflammation and to decrease the pain. Strengthening of the hamstrings and quadriceps is a valuable addition to the treatment plan. In sports necessitating frequent contact of the knee with hard objects (volleyball), kneepads will protect the tibial tuberosity from direct injuries.

Prognosis

OSD is not a recognized risk factor for osteoarthritis. Fractures through the tibial tubercle in patients with preexisting OSD have been reported; however, no statistical correlation between OSD and subsequent fracture of the tibial tuberosity has been confirmed. The risk of fracture does not increase with OSD, and there is no reason to limit the level of activity because of OSD.

In very rare cases, the fragmentation of the tibial tuberosity does not unite, and a small ossicle within the patella tendon causes constant irritation of the tendon. In these circumstances excision of the offending ossicle may be recommended.

Return to Play

Pain will be the only factor limiting the patient's activities. OSD, as a self-limiting condition, should not prevent students from participating in sports. Continuous participation in sports despite suffering from OSD has not been linked to detrimental long-term effects.

Sinding–Larsen–Johansson Syndrome & Jumper's Knee

Pathogenesis

Sinding–Larsen–Johansson syndrome is similar to Osgood—Schlatter disease. It affects the distal pole of the patella instead of the tibial tuberosity.

Jumper's knee manifests as a pain at the midsubstance of the patellar tendon and is considered a form of overuse tendinitis.

Clinical Findings

  1. Symptoms and Signs
  • Pain at the distal pole of the patella or midsubstance of the patellar tendon.
  • Pain related to activity.
  1. Imaging Studies

The reported fragmentation of the distal pole of the patella represents a normal variation of the radiographic appearance of the patella.

Differential Diagnosis

  • Type 1 of the symptomatic bipartite patella.
  • Sleeve fracture.

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  • Osgood–Schlatter symptoms.
  • Tibial tuberosity fracture.

Treatment, Rehabilitation, & Return to Play

Treatment, prognosis, and physical therapy programs are identical to the Osgood–Schlatter protocol.

Congenital Dislocationof the Patella

Pathogenesis

The likelihood that a patient with congenital dislocation of the patella will become involved in sports is rather low. Usually, the condition is recognized and treated in early childhood.

Clinical Findings

  1. Symptoms and Signs

Typically, the patella is palpated lying against the lateral femoral condyle. Flexion contraction of the knee, which is normal at an early age, persists beyond the age of walking, and valgus alignment develops as a child grows.

 

Figure 9-25. A–C: Congenital dislocation of the patella in a 7-year-old female with trisomy 21. C: Proximal and distal realignments were performed. Distal derotation of the femur was necessary to correct the abnormal torsion of the femur. D: Fulkerson osteotomy and proximal realignment, performed in a different patient for habitual subluxation of the patella.

  1. Imaging Studies

Radiographs fail to show the nonossified patella and its position. MRI is the best modality to show the entire joint and the patella. It might show dysplasia of the lateral femoral condyle as well. Ultrasonography does not require anesthesia, and may visualize the patella well enough to confirm the diagnosis.

Treatment

Early treatment is the rule. Results are much better with early intervention and restoration of proper alignment and position of the patella. Several surgical options have been discussed in the literature, and generally proximal and distal realignment is required to stabilize the patella. A medial transfer of the lateral part of the patella tendon can augment extensile lateral release with medial plication and transfers of the vastus medialis obliquus (VMO). With early treatment results have been excellent (Figure 9-25).

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Patella Instability & Dislocation in Adolescents

Pathogenesis

Patella dislocation among teenagers is an entirely different problem, occurring more frequently in girls than in boys. The first occurrence usually results from violent trauma. In girls this is typically a twisting-valgus injury to the knee. Boys are more likely to sustain a direct blow to the patella, which causes the patella to dislocate. The acutely dislocated patella reduces spontaneously in the majority of cases.

Clinical Findings

  1. Symptoms and Signs
  • Direct or indirect injury to the knee.
  • Knee “going out.”
  • “Pop” at the time of injury.
  • Effusion.
  • Apprehension and relocation tests are positive.

Risk factors include the following:

  • Patella alta.
  • Abnormal femoral and tibial torsion.
  • Excessive genus valgum.
  • Hypoplasia of the lateral condyle.
  • VMO hypoplasia.
  • Vastus lateralis contracture.
  • Hypoplasia of the femoral sulcus.
  • Generalized laxity.

Imaging Studies

Regular radiographs in four positions are necessary, and sometimes reveal an obvious fracture or loose body. A CT scan will further localize a potential loose body. MRI is more specific in revealing osteochondral defects and position of the patella in extension of the knee.

Differential Diagnosis

  • Meniscal injury.
  • ACL tear.
  • Physeal fractures.
  • Fractures of the patella.

Treatment

  1. Nonsurgical

Initial studies should rule out any concomitant fracture or osteochondral fractures. The treatment of first time dislocators without associated osteochondral injury consists of 2–3 weeks of immobilization with protected weight bearing. Prolonged VMO and quadriceps strengthening are necessary to change the dynamic vector of the extensor mechanism. Patella tracking orthosis (PTO) can be a valuable addition to the treatment, and can initially be used for sports activities as well.

Nonoperative treatment has been effective in 80–85% of cases. The remaining patients will experience recurrent dislocations. The greater the number of risk factors present, the more likely the patient will experience two or more episodes of dislocation.

  1. Surgical

Indications for surgery include the presence of an osteochondral fracture requiring ORIF, recurrent dislocation, and patella fracture. In an acute setting surgery is targeted toward repairing the fractures. Acute rupture of the medial retinaculum is a relative indication.

In a chronic setting, lateral release, proximal and distal soft tissue realignment, and tibial tubercle osteotomy should be considered.

Rehabilitation & Return to Play

After the first traumatic dislocation, return to sport could take as long as 3–4 months, especially if a surgical procedure was necessary to repair a bony or osteochondral defect. Two to three months of nonoperative treatment, consisting of immobilization and physical therapy, is usually enough to allow the patient to return safely to full activity. Chronic dislocators may need more time before returning to sports.

Symptomatic Plica

Pathogenesis

An asymptomatic plica may be discovered in about 50% of the population; symptomatic plicas have of the knee joint have probably been overdiagnosed. Patients report a history of popping, snapping, and giving way. The mediopatellar plica is most commonly discovered during a physical examination. Other problems of the knee have symptoms that mimic the painful plica and vice versa: plica might imitate meniscal injuries, osteochondral problems, and patella symptoms (Figure 9-26).

Clinical Findings

  1. Symptoms and Signs

The inflammation of a previously silent plica might be triggered by a direct injury or by repetitive trauma. Once inflamed or irritated it will begin to cause activity-related knee pain.

  1. Classification
  • Suprapatellar.
  • Mediopatellar.
  • Infrapatellar (ligamentum mucosum).
  • Lateral patellar.
 

Figure 9-26. An 8-year-old male with pain and swelling following a fall on the left knee while biking. A: A bone scan shows a mild increase in uptake around the left knee. B–F: MRI showing hypertrophic synovium. Final diagnosis: pigmented villonodular synovitis.

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  1. Imaging Studies

MRI is the only modality that might show a plica.

Treatment

  1. Nonsurgical

Initial treatment is always focused on stretching, icing, modification of activity, rest, and a patellofemoral program. It sometimes takes several months to relieve pain related to symptomatic plica.

  1. Surgical

Arthroscopic excision of recalcitrant symptomatic plica is a relatively simple procedure, with a success rate between 70 and 90%. A significant percentage of plicas will regrow and become symptomatic again; scar tissue

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created during surgery may contribute to recurring symptoms as well.

Rehabilitation & Return to Play

Recovery from surgical treatment is relatively short, and should not last more than 4–6 weeks. Patients should continue the stretching and strengthening program.

Bipartite Patella

Pathogenesis

The bipartite patella represents a failure to unite two or more centers of ossification into one bone. Because the bipartite patella is generally asymptomatic, it is most frequently discovered on radiographs taken for other reasons. Sometimes, however, the fibrocartilagenous connection between the fragments is disrupted as a result of trauma or repetitive trauma, and the previously nonproblematic patella becomes painful.

Classification (Saupe)

  • Type 1: inferior pole of the patella (5%).
  • Type 2: lateral patellar margin (20%).
  • Type 3: superior-lateral quadrant of the patella (75%)

Treatment

Symptomatic bipartite patella requires immobilization in a cylinder cast for 4–6 weeks, with physical therapy to start soon after. If pain persists, several surgical options are available. A symptomatic, small bipartite patella can be excised. “Refreshment” of the connection between the two parts of the patella, with fixation using screws or wires and supplementary bone grafting, will be a better option for large, painful fragments.

Rehabilitation & Return to Play

Return to sport after 2–3 months of treatment is a realistic expectation. The student will enjoy unrestricted activities after recovery is completed.

Medial Collateral Ligamentsyndrome: Breaststroke Knee

About 50% of sports-related complaints are associated with problems of overuse, and a typical example is the breaststroke knee (BK). Its repetitive microtrauma to medial structures of the knee causes prolonged pain and discomfort over the medial knee. The MCL appears to be the most affected structure, but the inferomedial margin of the patella may be painful as well.

Poor technique, especially during the initial phase of the rearward throughst and the whip kick, will intensify the symptoms. The amount of hip abduction at initiation of the kick should ideally be between 35 and 45°, and changes in this angle increase the likelihood of developing BK. Athletes with general laxity are at higher risk of suffering BK.

Pain and inflammation over the medial knee may last for a long time, and can mimic medial meniscus symptoms. Pain increases with activity.

Acute symptoms need to be treated by icing, modification of activity, NSAIDs, and stretching. Prevention relies on proper conditioning, general strengthening, and developing a mechanically sound technique.

Proximal Tibiofibular Jointsubluxation

A patient with lateral joint pain and catching could be suffering from symptoms originating at the proximal tibiofibular joint. The joint might be acutely dislocated, with rupture of the posterior tibiofibular ligament, LCL, and biceps femoris. An acute dislocation might occur after a twisting and landing injury (snowboarding) or with fracture of the tibia.

Chronic instability has been seen among teenagers with increased general laxity or as a part of Marfan syndrome.

The differential diagnosis includes a torn lateral meniscus, an LCL sprain, a joint cyst, and posterolateral corner injury.

Treatment consists of strengthening and stretching. The athlete could try to use an elastic knee sleeve. In resistant cases, surgical reconstruction of the joint capsule, arthrodesis of the joint, or resection of the fibular head may be necessary.

Canizares GH, Selesnick FH: Bipartite patella fracture. Arthroscopy 2003;19(2):215.

Grelsamer RP: Patellar malalignment. J Bone Joint Surg Am 2000;82-A(11):1639.

Rodeo SA: Knee pain in competitive swimming. Clinics Sports Med 1999;18(2):379.

Foot & Ankle

Lateral Ankle Sprain & Salter-Type Fractures of the Distal Fibula

Pathogenesis

A typical inversion injury that causes a tear of the lateral ankle ligaments very often disrupts the open growth plate of the distal fibula. Caution should be exercised and it is necessary to be aware of the possibility of an

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injury to the physis to establish the proper diagnosis. Radiographs are useful in cases in which the epiphysis of the fibula has been displaced. Unfortunately, this is seldom the case, and the majority of Salter 1 injuries to the distal fibula present with negative radiographic findings except for soft tissue swelling. In this situation an appropriate diagnosis can be established based on the location of the point of maximum tenderness. Tenderness over the distal growth plate of the fibula and a history of inversion trauma to the ankle are enough to diagnose a Salter 1 fracture of the distal fibula, despite negative findings on radiographs.

Tenderness indicative of injury to the lateral ankle ligaments [anterior talofibular (ATF) and calcaneofibular (CF)] is anterior and slightly distal compared to the tenderness of the growth plate. As an adolescent approaches skeletal maturity, the rate of Salter type injuries declines, and the probability of a classic lateral ankle sprain increases. Just before the physis of the distal fibula closes, it is possible to observe a concomitant Salter 1 fracture together with a tear of the lateral ankle ligaments.

Clinical Findings

  1. Symptoms and Signs
  • Inversion injury to the ankle.
  • Inability to bear weight.
  • Point of maximum tenderness.
  • Delay in seeking medical attention (especially true with Salter 1 injuries: “They called me from the ED and said there is no fracture visible on the X-ray.”).
  1. Imaging Studies

With all the limitations discussed above, radiographs are mandatory, as additional injuries may be discovered, such as OCD of the talus. A CT scan may be necessary to evaluate for a possible Tillaux or triplane fracture of the distal tibia. An MRI is recommended for long-lasting problems or for symptoms indicative of osteochondral injury.

Differential Diagnosis

  • Salter 1 fracture versus ankle sprain.
  • Other fractures of the distal fibula.
  • Fractures of the distal tibia.
  • Osteochondral fracture or OCD.
  • Syndesmotic injury.

Treatment

Treatment of a Salter 1 fracture of the fibula consists of 4–6 weeks of a short leg cast. The patient is asked not to bear weight for about 2 weeks, after which weight bearing can be gradually increased. A persistent pain when trying to bear weight will increase the non-weight-bearing time. After the cast is removed, a solid or hinged brace-boot might be used for added protection. The patient returns to full activities usually after 2–3 months.

A Salter 1 fracture of the distal fibula can reoccur several times in the same ankle. Fortunately, this physis is very resistant to potential growth arrest, and very rarely causes abnormal growth, even after multiple episodes.

Treatment of the ankle sprain depends on its severity. Initial RICE is mandatory. Details will be discussed in Chapter 4, this volume.

Tarsal Coalition

General Considerations

Multiple ankle sprains in a teenager should raise suspicions of the existence of a tarsal coalition. A tarsal coalition remains asymptomatic until the early teenage years. It is caused by a failure to differentiate the primitive mesenchymal tissue into separate hindfoot bones, which results in an abnormal connection between the bones. The coalition could be bony, cartilaginous, or fibrous.

Pathogenesis

Pain in patients with tarsal coalition is frequently at the level of the sinus tarsi or over the medial aspect of the subtalar joint. It is typically dull and aching and activity related; a limp is common after activities.

The most common coalitions are the calcaneonavicular and talocalcaneal. The incidence of coalition is estimated at about 1% of the population. Bilateral coalition occurs in about 50–80% of cases; many tarsal coalitions do not cause pain and go unrecognized, sometimes for life. Family occurrence has been reported.

There is an association between tarsal coalition and fibular hemimelia, syndactyly, Apert syndrome, Nievergelt syndrome, and carpal coalition. Tarsal coalition might be found during surgery for congenital clubfoot. In this case the coalition involves the subtalar joint.

Clinical Findings

  1. Symptoms and Signs
  • Multiple sprains.
  • Activity-related pain.
  • Pain at the sinus tarsi or ankle.
  • Limited or no subtalar motion.
  • Pain with inversion and eversion.
  • Peroneal spastic foot.

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Classification:

  • Bony.
  • Cartilaginous.
  • Fibrous.

Anatomic:

  • Subtalar: talocalcaneal.
  • Calcaneonavicular.
  • Other rare types: talonavicular, calcaneocuboid, cubonavicular, and naviculocuneiform.
  1. Imaging Studies

The classic radiographs in AP, lateral, oblique, and Harris heel views might show some common signs of tarsal coalition (Figure 9-27). The easiest coalition to see is the calcaneonavicular on the oblique view, seen as a bony connection between the anterior process of the calcaneus and the lateral horn of the navicular. On a lateral view, the anteater sign is pathognomonic for calcaneonavicular coalition. At the presence of the coalition, the anterior process of the calcaneus resembles the nose of an anteater. The C-sign on a lateral radiograph refers to a line drawn over the superior dome of the talus, down and posteriorly into the inferior outline of the sustentaculum tali. It is characteristic of subtalar coalition. A dorsal beaking of the anterior process of the talus suggests restricted ROM through the subtalar or Chopart joint. It might be found in tarsal coalition or as a result of clubfoot surgery with limited motion across those joints.

A Harris heel view may show abnormalities of the middle facet of the subtalar joint.

A fine cut CT scan is by far the most important examination confirming tarsal coalition, showing beautifully the location and extent of a coalition. The CT-based three-dimensional reconstruction better indicates the location of the bar, especially the subtalar bar and its relationship to the subtalar joint.

A nonbony coalition may not be directly visualized by CT images. Sometimes, an irregularity of the middle facet suggests its presence, and an MRI is necessary to reveal fibrous or cartilaginous coalition.

Differential Diagnosis

  • Fracture.
  • Infection.
  • Bone cyst.
  • Painful flatfoot.
  • Painful accessory navicular.
  • Complex regional pain syndrome.
  • Stress fracture.
  • Kohler disease.
 

Figure 9-27. Sixteen-year-old football player presenting with several months of dull ankle pain and a history of multiple sprains. Clinical examination reveals severely limited inversion and eversion and a flattening of the longitudinal arch of the foot. A: Lateral radiograph shows the classic C-sign: the imaginary C-line follows the dome of the talus, goes down over the posterior wall of the talus, and curves anteriorly under the sustentaculum tali. B–E:Four images of a CT scan with deformity of the medial facet and a bony bar between the talus and calcaneus.

Treatment

  1. Nonsurgical

Initially, cast treatment might be tried. A short leg cast worn for 4–6 weeks with protected weight bearing might alleviate the pain. Immobilization should be

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followed by physical therapy and a gradual return to activities. The success rate of nonoperative treatment is unpredictable, but is usually low.

  1. Surgical

When the cast does not work, an excision of the bar, with or without interposition of a biologically inert material, is the preferred treatment. Before surgery it is wise to carefully review all available studies looking for a possible second coalition in the same foot, as two tarsal coalitions in one foot can occur.

Excision of a calcaneonavicular coalition is done through a relatively small incision centered over the bar. Lambott osteotomes are the best tools to remove a tarsal bar. The entire coalition should be removed, leaving at least 1.0–1.5 cm of free space between the anterior process of the calcaneus and the navicular. The gap might be filled with an extensor digitorum brevis muscle.

An excision of the subtalar bar is more difficult, requiring a longer posteromedial incision. The flexor hallucis longus (FHL) is a hallmark of the sustentaculum tali; the FHL tendon crosses the ankle joint and curves anteriorly, coursing under the sustentaculum. This helps identify the middle facet. Before excision of the bar it is helpful to visualize the anterior and posterior subtalar facets. Following the orientation of the facets might further help to navigate into the middle facet, which is usually obscured by the coalition. The coalition is then excised using an osteotome, a high-speed bur, and Rongeur or Carsson incisors. The area of the excised middle facet may then be filled with surrounding soft tissues, such as a split flexor digitorum longus (FDL) tendon, or fat tissue, or it may be left alone. Bone wax can be applied to the area of excision, thus lowering the risk of forming a local hematoma, which might propagate bone formation.

Because feet with tarsal coalition are usually flat, other surgical procedures may be directed toward improving the mechanics of the foot; lateral column lengthening, medial closing wedge osteotomy of the calcaneus, or sliding osteotomy of the heel can improve stress distribution across the foot and ease the pain. Excision of the tarsal bar, however, is the preferred initial treatment.

After surgery a short leg cast is applied and worn for 4–6 weeks. ROM and strengthening exercises start as soon as the cast is removed.

Rehabilitation, Complications, & Return to Play

The calcaneonavicular coalition is an extraarticular structure, whereas the subtalar coalition is an intraarticular formation, taking away part of the normal cartilage of the subtalar joint. For this reason, the major prognostic factor for recovery and successful treatment is the location of the bar. The excision of the calcaneonavicular bar is usually easier, with a higher success rate and faster recovery. After surgery, the patient can return to sport within 2–3 months, assuming there are no symptoms.

Even after a careful excision of the subtalar coalition, the patient may still experience long-lasting pain of the foot, especially if more than 50% of the articular surface was occupied by the bar. In this situation the painful subtalar joint may need to be fused. The subtalar fusion might be done separately, or as part of a triple arthrodesis, especially if the Chopart joint is painful as well.

Sever Disease

Pathogenesis

The most common cause of heel pain in the pediatric or adolescent population is Sever disease, a self-limiting condition characterized by pain of the heel in growing individuals. The pain is activity related, is not the result of trauma, and is more intense the morning after strenuous physical activity. It usually occurs in active and sports-minded individuals, but can be observed among computer games players as well. The symptoms can last for a long time, sometimes even until growth of the foot is completed. Bilateral involvement is common.

Clinical Findings

  1. Symptoms and Signs
  • Pain at the posterior extent of the heel.
  • No swelling or effusion.
  • Pain frequently during intense exercise, or the morning after.
  • No night pain and no pain at rest.
  1. Imaging Studies

Radiographs are mandatory to rule out other causes of the heel pain rather than to confirm the diagnosis. An irregularity of the calcaneal apophysis is a normal finding and is not necessarily a sign of Sever disease.

Differential Diagnosis

  • Salter–Harris 1 fracture of the apophysis.
  • Achilles tendinitis.
  • Plantar fasciitis.
  • Stress fracture of the calcaneus.
  • Tarsal tunnel syndrome.
  • Subtalar coalition.
  • Osteomyelitis.
  • Bone cyst of the calcaneus.
  • Accessory navicular.
  • Tumor (Figure 9-28).
 

Figure 9-28. Calcaneal cyst barely visible on a lateral radiograph of the foot (A). The image was obtained after the patient sprained his ankle playing football. High frequency signal on an MRI (B–D), most likely consistent with a bony cyst. The cyst was subsequently curretaged and bone grafted (E). The final report shows lining of a unicameral bone cyst.

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Treatment

Treatment consists of modification of activity, rest as needed, ice, ice massage, and stretching of the gastrocnemius complex as well as the quadriceps and hamstrings. NSAIDs help to relieve symptoms. A gel heel pad can be used as well as arch supporting insets. If the symptoms do not resolve after a period of rest and stretching, cast immobilization for a brief period of time may be necessary.

Return to Play

Patients with symptoms of Sever disease do not need to stop playing sports. No study links Sever disease to arthritis or subsequent fracture of the heel. Playing through the pain is an acceptable option, as long as the patient and the parents are willing to accept it. However, the symptoms may be difficult to control and modification of activity may be necessary. Symptoms will fade when the apophysis closes up.

Iselin Disease

Pathogenesis

Iselin disease is an apophysitis of the growth plate of the base of the fifth metatarsal.

Clinical Findings

  1. Symptoms and Signs

Iselin disease manifests with activity-related pain localized at the base of the fifth metatarsal. Symptoms might last a long time, sometimes up to a year and a half. Patients complain of localized pain over the proximal part of the fifth metatarsal bone. They may try to avoid putting pressure over the fifth metatarsal and keep the involved foot in pronation or extreme supination.

  1. Imaging Studies

Similar to other “traction apophysitis,” radiographs may rule out other causes of lateral foot pain rather than confirm the diagnosis. The normal separation of the apophysis from the base of the fifth metatarsal should not be read as a fracture.

Differential Diagnosis

  • Salter-type fracture.
  • Jones fracture.
  • Osteomyelitis.
  • Tendinitis of the peroneus brevis.

Treatment

In an acute phase, the RICE treatment is usually most effective. In most cases, a few weeks of cast immobilization should alleviate the symptoms.

Rehabilitation & Return to Play

A careful and slow rehabilitation program offers patients the best chance to recover. Physical therapy with slowly advancing exercises of gradually increasing intensity will be the most important element in returning to sport. Very often, however, the treatment lasts for months, and prolonged pain with inactivity can be very discouraging to a young athlete.

Accessory Navicular

Pathogenesis

Multiple centers of ossification contribute to the formation of the navicular bone. The accessory navicular (AN), the most common accessory bone of the foot, is present in about 20–25% of the population. The unfused, accessory, medial part of the navicular bone forms a prominent bony mass, which sometimes becomes painful. Symptoms start in the preteen years.

Classification includes three types:

  • Type 1: a small ossicle within the tibialis posterior tendon, commonly termed the os tibiale externum.
  • Type 2: larger than type 1; connected to the navicular through a dense synchondrosis.
  • Type 3: enlarged navicular; the medial, prominent part of the navicular is the accessory ossicle fused to the navicular bone.

Clinical Findings

  1. Symptoms and Signs

A symptomatic AN causes redness, swelling, pain, and sometimes blisters and calluses over the most prominent part of the midfoot. Type 2 is the most commonly painful type. Pain is frequent in skiers, figure skaters, and hockey players, because direct pressure from tight footwear contributes to the discomfort. Commercially available shoes also cause symptoms, if the medial border of the shoe hits the level of the AN. Most likely, fracture through the dense, syndesmotic connection between the AN and the main navicular bone is responsible for the symptoms.

  1. Imaging Studies

The navicular bone becomes visible on radiographs after the first year of life, but sometimes does not appear until 5 years of age. Radiographs taken in AP, lateral, and oblique views confirm the diagnosis and help in differentiating the condition from other sources of pain.

Differential Diagnosis

  • Painful pes planus.
  • Tarsal coalition.
  • Koehler disease.

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Treatment

  1. Nonsurgical

The majority of AN patients will do fine with nonoperative treatment. Doughnut-type pads, which unload the most prominent part of the AN, will be sufficient to decrease pressure and to alleviate pain. A similar effect will be achieved by modification of the shoe or the boot, or by changing the brand of the shoes or boots worn. For example, skiers should be aware of various “last” in different ski boots. The boots vary in the “volume” of the heel, midfoot, and forefoot sections. Athletes should seek help in choosing optimal types of boots and customizing them with appropriate insets. Figure skating and hockey boots can be altered by punching out the part of the boot over the accessory bone.

  1. Surgical

Surgical excision is recommended after the nonoperative approach has failed. Simple excision of the offending bone is the standard of care. The previously popular Kidner procedure is rarely utilized today.

Rehabilitation & Return to Play

Usually 3–4 weeks of short leg cast after the surgery followed by another 3–4 weeks of physical therapy is sufficient. After completing treatment, the patient gradually returns to full activity.

Osteochondroses

  1. Koehler Disease

Pathogenesis

Koehler disease manifests with pain of the tarsal navicular and fragmentation of the bone, visible on radiographs. There is no history of trauma.

Clinical Findings

  1. Symptoms and Signs

Symptoms are more common in boys, typically under age 6 years. Pain occurs with activity and is relieved with rest. Weight bearing increases the pain. Point tenderness over the navicular is a pathognomonic finding.

  1. Imaging Studies

Radiographs will show fragmentation of the navicular and patchy increased density. As the symptoms subside, follow-up radiographs show reconstitution of the proper shape and structure of the bone.

Differential Diagnosis

  • Trauma.
  • Painful accessory navicular.
  • Infection.

Treatment

Koehler disease is a self-limiting condition, but a difference in duration of symptoms has been noted in children treated with a cast, as compared to no-cast treatment. Symptoms lasted less time in the casted group than in children without casting.

Other options such as arch-supporting insets may also be considered. Surgical treatment is unnecessary.

  1. Freiberg Infraction

Clinical Findings

  1. Symptoms and Signs

Freiberg disease is a painful infraction of the head of the second metatarsal that occurs predominantly among teenagers. Its etiology is unknown. A possible stress fracture or failure of proper development may cause this condition. The second metatarsal head may be fragile and therefore prone to develop microfractures during the second decade of life.

  1. Imaging Studies

Radiographs show infraction, fragmentation, and sometimes collapse of the metatarsal head. With a closed growth plate, the head might be enlarged and flattened.

Treatment

  1. Nonoperative

Treatment consists of nonoperative measures, with or without casting. Different insets to relieve the pressure from under the second metatarsal head might be used. Metatarsal pad or custom-molded, pressure-relieving insets should diminish the pain and discomfort.

  1. Operative

If a nonoperative approach fails to relieve the symptoms, a surgical approach should be considered. Exploration of the joint may be necessary, with cartilage shaving or resection of the head, and sometimes fusion of the second metatarsophalangeal joint. Arthroscopy of the joint, with articular cartilage reshaping and removal of possible loose bodies, has also been tried.

Return to Play

Return to sport should be guided by clinical symptoms.

Painful Os Trigonum, Fibulare, & Sessamoid

The foot is well known for its accessory ossicles. Accessory navicular, os fibulare, os trigonum, and bipartite sesamoid are the most common. The accessory bones represent a failure of fusion of separate centers of secondary

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ossification. They are very commonly discovered on radiographs taken for another reason. The bipartite or accessory bones may need treatment when causing pain or discomfort.

 

Figure 9-29. Symptomatic os fibulare.

The accessory navicular was discussed previously. Painful os trigonum is caused by an acute injury to the bone, the unfused posterior process of the talus, or repetitive trauma. Pain at the posterior ankle with plantar flexion, especially in ballet dancers, should raise suspicion for possible os trigonum. The diagnosis might be confirmed by a bone scan or local injection of an anesthetic agent. The injection is also a therapeutic measure. Treatment includes a brief period of immobilization, modification of activity, avoiding excessive plantar flexion, ice, and NSAIDs. In resistant cases, os trigonum needs to be excised.

Os fibulare appears on a radiograph as a separate center of ossification just distal to the lateral malleolus. It becomes irritated after an inversion injury. Treatment is similar to the treatment of an ankle sprain, and frequently requires a short period of wearing a non-weight-bearing cast. Painful os fibulare may be treated surgically after prolonged nonoperative treatment has failed. Options include simple excision or ORIF with bone grafting (Figure 9-29)

Bipartite sesamoids occur in approximately 10% of the population, with 25% presenting bilaterally. The tibial sesamoid is more likely to be bipartited; it is also more prone to fracture or trauma of the bipartite form.

Symptomatic bipartite or fractured sesamoid requires quite a prolonged period of protected weight bearing. Insets with a metatarsal bar, NSAIDs, modification of activity, and cast immobilization may increase the success rate of nonoperative treatment.

Surgical treatment of the resistant, painful bipartite sesamoid might include ORIF with bone grafting, partial excision of the sesamoid, or shaving. Excision of the entire sesamoid is the most radical and potentially problematic solution.

Letts M et al: Surgical management of chronic lateral ankle instability in adolescents. J Pediatr Orthop 2003;23(3):392.

Other Lower Extremity Problems

Chronic Exertional Compartment Syndrome

General Considerations

Chronic exertional compartment syndrome (CECS) is an overuse syndrome characterized by pain and sometimes dysesthesia or weakness of muscles embedded in a certain

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compartment. Symptoms are related to activity and subside at rest. CECS of the lower leg is well known; however, it frequently occurs in the forearm and thigh. Theoretically CECS can involve any muscle contained within a compartment. CECS of rare locations such as the gluteus muscles or muscles around the shoulder has been reported.

Pathogenesis

Muscles receive all necessary nutrients in the flow of blood, which occurs only during the relaxation phase of muscle contracture. During exercises, the muscles swell up, the arterial and venous blood flow slows down, and the intracompartmental pressure increases. Because the muscles are encased within very rigid compartments, there is no reserve space within them. As a result, blood flow is restricted, delivering an insufficient amount of oxygen and other vital elements. In addition, removal of potentially harmful products of metabolism is slower because of venous congestion. The organism reacts with pain.

The probable pathophysiology of the CECS is explainable based on present knowledge of physiology, anatomy, and physics. Why just limited numbers of athletes develop the symptoms is, however, unknown.

Clinical Findings

  1. Symptoms and Signs
  • Muscle pain during or after exercise.
  • Hypoesthesia or dysesthesia.
  • Tinnel sign.
  • Pedowitz criteria: resting pressure is >15 mm Hg, 1 minute after exercise it is >30 mm Hg, and5 minutes after exercise it is >20 mm Hg.
  1. Imaging Studies

Different imaging techniques have been employed to aid in diagnosing CECS. The different diagnostic tests are commonly more helpful in ruling out other causes of an extremity pain than in confirming the diagnosis of CECS. Radiographs help to diagnose fracture, tumor, or stress fracture. An MRI study facilitates the diagnosis of stress reaction versus stress fracture and may uncover other causes of pain. An MRI of the muscles involved in CECS may show a nonspecific, slightly increased signal on T2 images. T1 remains unchanged.

Near-infrared spectroscopy has been reported to be a valuable tool; however, its predictive value needs to be confirmed. A single-photon emission computed tomography (SPECT) bone scan with thallium-201 sometimes shows areas of ischemia, a rather late sign of CECS. A clinical history and measurement of intracompartmental pressure are still the gold standard of diagnosis.

Differential Diagnosis

  • Stress fracture.
  • Stress reaction.
  • Fracture.
  • Complex regional pain syndrome.
  • Tumor (osteoid osteoma).
  • Deep venous thrombosis.
  • Peripheral vascular disease.
  • Gastrocnemius strain.
  • Medial tibial stress syndrome (Figure 9-30).

Treatment

Treatment of CECS relies on stretching, icing, and rest. Nonoperative treatment, however, has had limited success. Surgical release of the involved compartments is usually necessary to relieve symptoms of an established and confirmed CECS. Prior to surgery, other possible causes of pain of the extremity must be excluded.

In the case of confirmed, lower leg CECS, the standard of care is an open, four compartment fasciotomy. The release of the “fifth compartment,” the tibialis posterior muscle compartment, may also be necessary. An endoscopically guided compartment release offers the advantage of a small incision and good visualization. Compartment release done through a very small incision (percutaneously), without endoscopic enhancement, seems to be the worst option, carrying the highest risk for nerve injury.

Return to Play

After successful surgery, return to sport depends exclusively on healing of the incisions, typically 6 weeks after the indexed surgery. On many occasions, the adolescent or pediatric patient resumes full activities much earlier, against official recommendations. This seems to have no detrimental effect on the final outcome of the treatment. With proper diagnosis and uncomplicated surgery, full recovery of function, return to sport, and relief of pain should be the expected outcome.

 

Figure 9-30. Stress fractures. Healed fracture of the distal tibia that happened 7 months ago. There is now pain over the proximal fibula of the ipsilateral leg. X-Ray shows periosteal reaction of the proximal fibula (A). MRI of the lower leg consistent with a stress fracture (B). Stress fracture of the right tibia in an 8-year-old baseball player (C). Bone scan shows increased uptake at the midshaft of the tibia (D).

Aoki Y et al: Magnetic resonance imaging in stress fractures and shin splints. Clin Orthop 2004;(421):260.

Fraipont MJ, Adamson GJ: Chronic exertional compartment syndrome. J Am Acad Orthop Surg 2003;11(4):268.

Hutchinson MR et al: Anatomic structures at risk during minimal-incision endoscopically assisted fascial compartment releases in the leg. Am J Sports Med 2003;31(5):764.

Ota Y et al: Chronic compartment syndrome of the lower leg: a new diagnostic method using near-infrared spectroscopy and a new technique of endoscopic fasciotomy. Arthroscopy 1999;15(4):439.

Shah SN et al: Chronic exertional compartment syndrome. Am J Orthop 2004;33(7):335.

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Increased Femoral Anteversion with Increased External Tibial Torsion: Miserable Malrotation Syndrome

In clinical practice, a small subset of patients will manifest with so called miserable (malignant) malrotation syndrome (MMS). This syndrome, which can be diagnosed after the age of 9–10 years, consists of increased internal rotation of the hip with coincidental increased external tibial torsion. MMS is more commonly observed among girls, and is associated with patellar maltracking problems and knee pain. A patient with MMS walks with an internally rotated patellae, with a neutral foot progression angle. A patient who tries to correct the position of the patella routinely rotates the feet outward as a result of increased external tibial torsion.

Initial treatment consists of physical therapy and a patellofemoral program.

With persistent pain and with no sign of other intraarticular pathology surgical intervention might be warranted. It is wise to document the MMS by rotational CT assessment of the femoral anteversion and tibial torsion prior to surgical correction of MMS.

To correct the MMS it is necessary to address both levels of the deformity. Delgado et al perform the osteotomies as close to the knee joint as possible. The authors prefer a derotational femoral osteotomy over a

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trochanteric nail for correction of the femur. Correction of the tibial torsion is usually addressed by a supramalleolar osteotomy with cross pin fixation (Figure 9-31).

 

Figure 9-31. Three CT cuts necessary to evaluate the rotational profile: femoral neck orientation (A), position of the femoral condyles (B), and torsion of the tibia/lower leg (C). Miserable malalignment syndrome: derotational osteotomy using intramedulary fixation (D). Supramalleolar osteotomy of the tibia. Added osteotomy of the fibula allows for free derotation of the distal fragment. The osteotomy is stabilized by two smooth Steinman pins (E).

The results of the surgical treatment are usually good. In a series of 14 patients with 27 affected limbs all patients were very satisfied with the results.

A bilevel osteotomy for documented cases of MMS should provide lasting relief of pain.

Bruce WD, Stevens PM: Surgical correction of miserable malalignment syndrome. J Pediatr Orthop 2004;24(4):392.

Delgado ED et al: Treatment of severe torsional malalignment syndrome. J Pediatr Orthop 1996;16(4):484.

Tonnis D, Heinecke A: Acetabular and femoral anteversion: relationship with osteoarthritis of the hip. J Bone Joint Surg Am 1999;81(12):1747.

Contusions

Pathogenesis

Contusions are probably the most common injuries that occur around the pelvis and lower extremities. They are caused by direct blows to the most prominent parts of the pelvic girdle or to a muscle.

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Clinical Findings

  1. Symptoms and Signs

Contusions are common in football (tackle), baseball (sliding), and soccer (direct kick). The contused part of the body hurts. Redness, swelling, and the formation of a subcutaneous hematoma follow. The hematoma is sometimes quite large. Contusion of the quadriceps manifests with subcutaneous hematoma and deep pain with palpation and stretching; swelling accompanies a more serious contusion. In severe cases, the hemorrhage may depose a large quantity of blood within a compartment, creating the possibility of compartment syndrome (Figure 9-32).

 

Figure 9-32. Large hematoma of a quadriceps muscle after a direct blow to the right thigh while playing football.

The hip pointer refers to a contusion of the iliac wing or greater trochanter. It presents with localized pain after direct injury. Pain sometimes is pronounced, accentuated by rotation of the trunk.

  1. Imaging Studies

A radiograph may be considered after more violent injuries to rule out fractures. An MRI should be obtained in cases of large, nonresolving swelling and hematoma.

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Differential Diagnosis

  • Fracture.
  • Avulsion fracture.
  • Compartment syndrome.
  • Apophysitis.

Treatment

A classic RICE approach is the standard treatment for contusions. A patient with the hip pointer should be allowed to rest, with return to sport guided by symptoms. ROM exercises and stretching will aid in providing a gradual return to full activity.

Very extensive quadriceps contusions, especially if accompanied by a large hemorrhage, should be approached cautiously. Initially, the RICE approach is sufficient. Immobilization of the lower extremity, with the knee flexed, prevents the quadriceps from developing a flexion contracture. Monitoring for possible compartment syndrome might be necessary. Classic compartment symptoms such as pain, numbness, tingling, and weakness might occur several hours after the initial injury or even the next day. A large hematoma with numbness and tingling, increasing pain impossible to control by oral pain medication, and pain with stretching of the flexors or extensors of the knee joint will be an indication to release all compartments of the thigh.

The need to address an evolving compartment syndrome is obvious; evacuation of a large hematoma is controversial. Based on the current literature there is no reason to evacuate a hematoma unless there are neurologic symptoms.

Rehabilitation & Return to Play

If a patient does not develop significant problems, return to sport is guided by subjective symptoms. A rehabilitation program designed to recover full strength and function of the quadriceps and hamstring muscles will aid in returning to sport within a relatively brief period of time.

Diaz JA et al: Severe quadriceps muscle contusions in athletes. A report of three cases. Am J Sports Med 2003;31(2):289.

Upper Extremity Problems

Anatomy

  1. Shoulder

A shoulder girdle is composed of a scapula, a clavicle, and the proximal humerus. The glenohumeral joint is a spheroid joint between the glenoid of the scapula and the proximal humerus. A shoulder is not mature until age 25 years, when the clavicle fully ossifies. Other important ossification centers and their age at fusion are the body of the scapula (appears at 8 weeks fetal), acromion and coracoid (both at 15 years), clavicle (at 5 weeks fetal), body of the humerus (at 8 weeks fetal), head of the humerus (at 1 year), greater tuberosity (at 3 years), and lesser tuberosity (at 5 years). The scapular as well as the humeral ossification centers fuse at age 20 years. Until completely fused, the physeal cartilage of an apophysis is inherently weaker than the muscles and ligaments that attach to it. Therefore, excessive forces may lead to avulsion fractures rather then ligament ruptures in an immature athlete (Figure 9-33).

The glenohumeral joint is the most commonly dislocated large joint in the body. Recurrent dislocation rates in children can reach 100%. Static restraints (articular

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anatomy, labrum, joint capsule and ligaments, negative pressure) and dynamic restraints (shoulder muscles and scapulothoracic motion) all work together to prevent dislocation. The acromioclavicular (AC) joint is a gliding joint with very limited ROM. It consists of a capsule, an AC ligament (primary restraint to AP displacement of the distal clavicle), and a coracoclavicular (CC) ligament (primary restraint to superior displacement of the distal clavicle). The CC ligament is further divided into a trapezoid ligament and a stronger conoid ligament.

 

Figure 9-33. Schematic of the ossification centers of the clavicle (Cs, sternal border of the clavicle; Cm, medial clavicle; Cl, lateral clavicle), scapula (Sb, base of the scapula; Ia, inferior angle; Vb, vertical border; Cb, base of the coracoid; Ct, top of the coracoid; Ab, base of the acromion; At, top of the acromion), and proximal humerus (Hu, humerus head; Gt, greater tuberosity; Lt, lesser tuberosity).

Fifteen muscles move the shoulder. The rhomboideus major and minor, trapezius, latissimus, and levator scapulae connect the upper limb to the vertebral column. The pectoralis major and minor, subclavius, and serratus anterior connect the upper limb to the thoracic wall. The deltoid and teres major abduct and adduct the upper limb, respectively. Four muscles of the rotator cuff act to depress and stabilize the humeral head in the glenoid; supraspinatus, infraspinatus, and teres minor attach to the greater tuberosity of the humerus and externally rotate the upper limb; the subscapularis muscle attaches to the lesser tuberosity and internally rotates the upper limb. In contrast to degenerative muscle tears and tendinitis, which occur in the adult patient population, young athletes tend to develop avulsion fractures, since connection of a muscle to bone occurs usually via an apophysis.

The upper extremity muscles are innervated by the brachial plexus, formed by the ventral primary rami of C5–T1. The brachial plexus is protected underneath the clavicle and is organized into five levels: roots, trunks, divisions, cords, and branches. There are four preclavicular branches: the dorsal scapular nerve, long thoracic nerve, suprascapular nerve, and nerve to the subclavius. Preganglionic injuries to the brachial plexus can be differentiated from postganglionic injuries by the presence of scapular winging (injury to the long thoracic nerve) and Horner syndrome (injury to C8–T1, involving the stellate ganglion). Typical obstetric injuries to the brachial plexus result in Erb–Duchenne palsy at C5–C6, which involves the deltoid, rotator cuff, elbow flexors, as well as wrist and hand extensors, or Klumpke palsy at C8–T1, which involves Horner syndrome, wrist flexors, and hand intrinsics, and has a poorer prognosis.

 

Figure 9-34. Schematic of the throwing phases: (1) wind up; (2) cocking; (3) acceleration; (4) deceleration.

Little League Shoulder

General Considerations

Because Little League shoulder is a condition that affects mostly adolescent patients overusing their shoulder while pitching, preventive recommendations have been made by the USA Baseball Medical and Safety Advisory Committee. According to their guidelines a young pitcher should refrain from throwing more than 75 pitches per week (9–10 years old), 100 pitches per week (11–12 years old), or 125 pitches per week (13–14 years old). Athletes are at highest risk in their mid teens, when the growth spurt occurs and they develop more skillful and powerful pitching techniques (Figure 9-34).

Clinical Findings

  1. Symptoms and Signs

A typical patient with a Little League shoulder is an adolescent baseball pitcher who presents with a gradual onset of pain localized to the proximal humerus and exacerbated by vigorous throwing. Pain is not restricted to a certain phase of throwing. Sudden onset of pain and residual pain after throwing are rare. The average duration of symptoms is between 6 and 9 months.

A tenderness to palpation over the lateral proximal humeral physis is the most common clinical finding. This was found to be reliable in 70% of patients. Pain with passive ROM and resistance to external and internal rotations can be seen. Weakness with external rotation occurs in up to 25% of patients. Swelling is uncommon.

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  1. Imaging Studies

Bilateral AP radiographs in internal and external rotation allow both proximal humeri to be compared. Radiographic widening of the involved proximal humeral physis is found in almost all cases. In 50% of the patients, lateral metaphyseal fragmentation or demineralization may be found, which is indicative of chronic changes. However, contrary to a displaced Salter–Harris type I fracture, reossification of the epiphysis takes between 8 weeks and 12 months. Plain radiographs can show the proximal humeral physis and are usually sufficient to diagnose a Little League shoulder.

An MRI may be necessary in the diagnosis of a Little League shoulder. It can be helpful in diagnosing associated conditions, such as epiphyseal fractures, infections, osteomyelitis, bone bruises, cysts, or tumors.

Differential Diagnosis

  • Rotator cuff tendinitis.
  • Biceps tendinitis.
  • Multidirectional shoulder instability.
  • Traumatic anterior dislocation.
  • Traumatic posterior dislocation.
  • Clavicular epiphyseal injury.
  • SLAP lesion.

Treatment

Treatment of a patient with Little League shoulder starts with prevention and close supervision of young athletes, following the guidance of the USA Baseball Medical and Safety Advisory Committee. Treatment of Little League shoulder syndrome includes rest, ice, and NSAIDs.

Return to Play

An average recommended period of rest from throwing is about 3 months. A young athlete should be allowed to begin to throw again only after all symptoms have subsided. In the largest case series reported in the literature, 21 of 23 adolescent baseball players were able to return to asymptomatic pitching at the Little League level within 1–12 months (average 3 months) after being diagnosed with Little League shoulder symptoms.

Rotator Cuff Tendinitis

Rotator cuff tendinitis is very common in the adult athlete engaged in activity involving overhead motion. In adolescents, it is relatively frequent in athletes with increased joint laxity and instability. With prolonged overhead activity, excessive motions of the humeral head in the glenoid cause inflammation of the rotator cuff muscles, with pain in the shoulder and decreased strength. Typically, pain starts during warm-ups and shows no improvement as practice or the game progresses. Late cocking, with the shoulder in maximum external rotation, and deceleration phases produce the most prominent symptoms. Tenderness over the rotator cuff muscles is the leading symptom, but there is no bony tenderness.

Treatment consists of nonoperative measures; patients generally respond well, depending on their cooperation with the therapy. Conservative treatment consists of rest, physical therapy, with special attention to strengthening the rotator cuff muscles, and NSAIDs. In severe cases involving acute tears, rotator cuff repair is recommended.

Biceps Tendinitis

The short head of the biceps muscle originates from the coracoid process with the long head attached to the glenoid labrum. Biceps tendinitis is an inflammation that causes pain at the insertion of the short head to the coracoid process. It results from overuse of the arm and shoulder, commonly related to overhead activities. Adolescent athletes complain of pain while moving the arm and shoulder, especially with extension and elevation. On clinical examination there is a tenderness to touch of the anterior shoulder over the coracoid process, along the biceps tendon and muscle. In growing athletes an apothysitis of the coracoid process may cause point tenderness at the origin of the short head.

Treatment is usually nonoperative, unless an acute tear of the biceps is involved. Conservative treatment consists of ice, in conjunction with physical therapy. A brief period of immobilization in combination with NSAIDs usually provides sufficient pain relief.

The goal of physical therapy is to ensure a safe return to sport. Adolescent patients may safely return to sports after an injured shoulder has regained a pain-free full ROM and normal strength, as compared to the contralateral shoulder. Tendinitis can best be prevented by following proper warm-ups and stretching exercises for the arm and shoulder, and by following guidelines of the athletic associations.

Epiphyseal Fracture of the Distal Clavicle

AC injuries in the skeletally immature patient can be divided into five types. In contrast to AC injuries in the adult, the CC ligament never detaches from the periosteal sleeve of the distal clavicle. A type I injury is a contusion resulting from a direct force to the acromion, not violent enough to disrupt the AC or CC ligaments. In type II injuries the periosteal sleeve is partially torn with the CC ligament intact and AC ligaments disrupted.

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Therefore the distal clavicle is not displaced. Type III and IV injuries present with completely torn AC ligaments and a tear of the periosteal tube, leading to unstable superior displacement. In type III injuries the clavicle is displaced only in a superior direction, whereas in type IV injuries the clavicle is also displaced posteriorly. In type V injuries the AC ligament is not in continuity with CC ligaments attached to the periosteal sleeve, and the distal end of the clavicle is buried within the trapezius or deltoid muscle. Type III–V injuries involve displacement of the distal clavicle and display the typical “piano key sign.” A pseudodislocation of the distal clavicle due to unrecognized fractures has been described (Figure 9-35).

Type I, II, and III injuries can generally be treated nonoperatively with a shoulder sling or a figure-of-eight brace. Small bony prominences are generally accepted, as the risks of elective surgical repair outweigh the benefits of anatomic reconstruction. Interestingly, a new clavicle will remodel from the periosteal sleeve, and the displaced part of the broken clavicle will be reabsorbed over time. Open reduction and internal fixation may be considered for markedly displaced type IV and V injuries and for injuries involving neurovascular compromise during surgery. It is important to disengage the dislocated distal clavicle from underneath the trapezius and deltoid muscles, place it in the periosteal tube, and repair the periosteum. The deltoid–trapezius fascia imbrication over the clavicle will additionally stabilize the clavicle.

 

Figure 9-35. An anteroposterior radiograph of a 14-year-old soccer player showing a type III clavicular epiphyseal fracture.

Traumatic Shoulder Dislocation

General Considerations

Most acute, first-time shoulder dislocations are related to sports injuries, whereas recurrent dislocations usually are not. Episodes of recurrent dislocation are reported at 75–100% in adolescent athletes. Anterior dislocations are far more common than posterior dislocations, which are usually the result of epileptic seizures or electricity-related injuries. Because the glenohumeral joint has the largest ROM of any joint in the human body, it is relatively easy to dislocate.

Pathogenesis

Young athletes with glenohumeral joint dislocation usually report one of the following mechanisms of injury: an aggressive jerk during contact sports (football, wrestling) or a minor trauma (swimming, pitching). Glenohumeral joint dislocation need not involve trauma; it can occur when reaching overhead or putting a jacket on. Anterior instability commonly presents with pain or apprehension with abduction, external rotation, and extension. Posterior instability is suggested by pain or

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apprehension during a flexed, adducted, and internally rotated position. An initial traumatic dislocation is usually difficult to reduce without the assistance of a physician. A patient with recurrent dislocation and associated joint laxity can easily self-reduce the dislocation.

Clinical Findings

  1. Symptoms and Signs

Both shoulders should be examined to assess the difference between a noninvolved and an injured shoulder and to look for bilateral shoulder instability. Palpation of the shoulder reveals anterior tenderness in patients with anterior glenohumeral instability. ROM is full and the apprehension test with terminal external rotation, with the arm in the abducted position, is positive. Anterior and posterior drawer tests reveal laxity of the glenohumeral joint in the sagittal plane. The tests are performed at 0, 30, and 60° of abduction and at 0, 30, and 60° of external rotation. Laxity occurs in three grades. In grade I, the examiner can sublux the humeral head within the glenoid cavity. In grade II the humeral head can be subluxed onto the glenoid rim and in grade III it can be dislocated over the glenoid rim. During the anterior apprehension test, an anterior force is applied to the humeral head, with the arm held at 90° abduction and progressively externally rotated. A patient resists increasing external rotation secondary to discomfort and apprehension. With a relocation test, a patient feels more stable and experiences less apprehension as an examiner applies posteriorly directed pressure with a similar maneuver. A sulcus test is usually positive after traumatic dislocation of a shoulder, indicating inferior instability. For this test the arm is in neutral rotation, and a downward force is applied as the shoulder is relaxed.

  1. Imaging Studies

Standard shoulder radiographs include an AP and a lateral view of the shoulder, a scapula-Y view, and an axillary lateral view (Figure 9-36). An AP view in internal rotation can reveal a posterolateral impression fracture on the humeral head, a Hill–Sachs lesion. The axillary lateral view is more specific for glenoid fractures, deformity, or glenoid hypoplasia. Abnormalities of the glenoid, seen on plain radiographs, may be evaluated by a CT scan. A CT arthrogram provides valuable information about the labrum, capsule volume, and bony geometry of the humerus and the glenoid. For a CT and MRI arthrogram, radiopaque contrast dye is injected into the glenohumeral joint space under fluoroscopic guidance, prior to the imaging. A defect of the capsule can be detected by the presence of extravasation of the dye. An MRI can identify anterior labral pathology (Bankart lesion). MRI arthrograms show more detailed images of the labrum, insertion of the biceps into the labrum, rotator cuff, and capsular anatomy. Invasive tests can add valuable information to the diagnostic work-up, however, indications for these tests should be very specific (Figure 9-37).

 

Figure 9-36. Radiographs of a 17-year-old female field hockey player; a first time, acute, traumatic, anterior shoulder dislocation. A: An anteroposterior radiograph showing an inferior dislocation. B: An axial lateral radiograph showing anterior dislocation and posterolateral impingement of the humeral head (Hu) under the glenoid (Gl). C: An AP radiograph showing relocation of the shoulder.

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Sometimes examination under anesthesia (EUA) may be necessary for patients with guarding, pain, and discomfort during examination in the office, or who are extremely muscular. EUA will help in detecting the true magnitude and direction of instability, which may change the treatment plan. Diagnostic arthroscopy has been a wonderful tool, providing further information about the internal glenohumeral anatomy.

 

Figure 9-37. Coronal MR arthrogram of a right shoulder in a 17-year-old male soccer player showing an anterior labrum tear with extravasation of contrast inferiorly (arrow).

Treatment

  1. Nonoperative

Nonoperative treatment of traumatic anterior shoulder dislocation involves a closed reduction, preferably under conscious sedation, to prevent further damage during the reduction maneuver. The period of immobilization usually lasts 3–4 weeks. Restriction from sports activities for 6 weeks after the initial anterior shoulder dislocation may lower the recurrence rate. A physical therapy program designed to strengthen the rotator cuff and scapular muscles follows immobilization.

  1. Operative

Operative treatment involves surgical repair of torn structures, performed either arthroscopically or using open techniques. Techniques for repair of a skeletally immature shoulder injury are similar to those for the adult population.

Deitch J et al: Traumatic anterior shoulder dislocation in adolescents. Am J Sports Med 2003;31(5):758.

Postacchini F et al: Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg 2000;9(6):470.

Superior Labrum, Anterior, & Posterior Lesions

General Considerations

Injuries to the superior labrum in overhead-throwing athletes have been divided into superior labrum, anterior, and posterior (SLAP) lesions, and classified into four subtypes. The incidence of SLAP lesions, however, remains unclear, although reports in the literature indicate involvement of between 6 and 26% of patients complaining of shoulder pain. Recently more and more young patients are being diagnosed with SLAP. Type I, which occurs in 10% of all SLAPs, is characterized by fraying of the superior labrum. It is usually degenerative, and is associated with rotator cuff disease. In type II lesions (40%), the biceps anchor is detached from the superior labrum with simultaneous fraying of the SLAP complex. A type II lesion occurring in younger patients is more frequently associated with traumatic instability compared to types III and IV. Type III (35%), a bucket handle tear of the labrum with an intact biceps tendon, progresses to a more extensive type IV (15%), which is a bucket handle tear and extension of the tear into the biceps tendon. Types II, III, and IV are more common in younger patients.

Clinical Findings

  1. Symptoms and Signs

Traction and compression injuries may cause a SLAP lesion. Traction injuries are typical in baseball throwing. They also happen with attempts to brace during falls or after sudden pulls. Compression injuries may result from a fall onto an outstretched hand.

Patients usually complain of vague shoulder pain, exacerbated by overhead activity with popping, locking, or snapping. Sometimes torn and unstable fragments (type II–IV) block ROM of an injured shoulder, as they may be trapped between the humeral head and glenoid. Instability is usually not a part of a SLAP, but may be present with simultaneous Bankart lesions (Figure 9-38)

  1. Imaging Studies

Radiographic examination includes standard views of the shoulder: AP, an axillary, and an outlet view. An MRI and MRI arthrograms help detect labral pathology, especially with an intraarticular injection of gadolinium, which increases the sensitivity and specificity of detecting labral lesions up to 90%.

 

Figure 9-38. Anatomical preparation of a shoulder showing a type III superior labrum, anterior, and posterior (SLAP) lesion. Gl, glenoid; La, labrum; Bi, biceps tendon; Ac, acromion; Ca, coracoacromial ligament; Co, coracoid process.

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  1. Physical Examination

Clinical testing is still relatively subjective and not extremely predictable. The Speed biceps tension test is reported to be the most reliable, and is performed with the patient resisting downward pressure in 90° of forward elevation with the elbow extended and the forearm supinated. Pain as a result of inflammation, or damage of the superior labrum, is considered a positive test. In the O'Brien test, the patient's shoulder is held in 90° of forward flexion, 30° of horizontal adduction, and maximal internal rotation. Patients with a SLAP lesion report pain in response to resisted horizontal adduction and forward flexion of the shoulder. In a compression–rotation test, the patient is positioned supine. The glenohumeral joint is compressed with the shoulder at 90° of abduction and the elbow flexed at 90°. This test can trap the injured labrum between the glenoid and humeral head, which results in an audible clunk.

Treatment

Treatment for SLAP lesions is surgical. Type I lesions require debridement of the torn labrum. Type II lesions can usually be repaired with sutures, tacks, or suture anchors. Type III and IV injuries require resection of the unstable displaced bucket handle labrum fragment, followed by reattachment of the biceps anchor. Physical therapy is done after immobilization. The average return to sport for the young athletes is 6–9 months after surgery.

Bencardino JT et al: Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology 2000;214(1):267.

Kim TK et al: Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. Superior labrum anterior posterior. J Bone Joint Surg Am 2003;85-A(1)66.

Anatomy

  1. Elbow

An elbow consists of a humerus, an ulna, and a radius. A humeroulnar joint between the trochlea and the trochlear notch, a humeroradial joint between the capitellum and the radial head, and a proximal radioulnar joint between the radial notch and the radial head connect these three bones. In a young athlete, a radiograph of the elbow shows unique, age-specific bony anatomy of the joint. It is therefore crucial to understand patterns of ossification of an elbow. An ossification center of the capitellum appears at 2 years, the radial head at 5 years, the medial epicondyle at 7 years, the trochlea at 9 years, the olecranon at 10 years, and the lateral epicondyle at 11 years. Distal humerus ossification centers fuse with the body of the humerus at age 16–18 years. The proximal radius fuses at 15–18 years and the olecranon fuses with the body of the ulna at 16 years (Figure 9-39).

The essential stabilizer on the lateral side is the lateral ulnar collateral ligament (LUCL). It inserts at the lateral epicondyle and the supinator crest of the ulna. Deficiency of the LUCL results in posterolateral rotatory instability of the elbow. The MCL consists of the anterior band, which is the strongest of the elbow ligaments and is tight in extension, the posterior band, tight in flexion, and the transverse band.

Medial Epicondylitis (Little League Elbow)

General Considerations

Young athletes involved in throwing activities, such as pitching in baseball, commonly complain of medial elbow pain. During the acceleration phase of the throwing motion, an elbow is subjected to substantial valgus stresses, which increase tensile loads on the medial side and compression loads on the lateral side. Repetitive tensile loads onto the medial elbow may cause injury to

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a physis of the medial epicondyle. A medial epicondylitis in children and adolescents refers to a true apophysitis, also termed Little League elbow, whereas in adults a medial epicondylitis consists of tendinitis of the flexor—pronator tendons. Athletes with this condition are usually between 8 and 12 years old, commonly pitchers in baseball, with a history of heavy throwing.

 

Figure 9-39. Schematic of the ossification centers of the elbow. Ca, capitellum; Rh, radial head; Me, medial epicondyle; Tr, trochlea; Le, lateral epicondyle.

Clinical Findings

  1. Symptoms and Signs

Symptoms include medial elbow pain with insidious onset, in combination with a normal ROM of the affected joint, without locking or catching.

  1. Imaging Studies

Positive radiographic findings are not necessary to establish the diagnosis. Three views of the injured elbow, with comparison views, are usually sufficient. Until age 15 years, ossification centers of an elbow are at different stages of fusion, and multiple physeal lines make judgment of elbow pathology in an immature athlete difficult. The medial epicondyle and physis of a little league athlete's elbow may appear normal or may show widening of the physeal line.

  1. Physical Examination

The diagnosis is usually made based on a clinical examination. Inspection of the elbow may reveal mild soft tissues swelling over the medial epicondyle. Palpation exposes tenderness over a medial epicondyle. A valgus stress applied to an elbow may reproduce the pain. A Tinnel test can be positive, with paresthesias in the ulnar nerve distribution, secondary to soft tissue swelling around the medial epicondyle, and its ulnar groove.

Differential Diagnosis

  • Osteochondritis dissecans of the capitellum.
  • Panner disease.
  • Olecranon avulsion fracture.
  • Supracondylar humerus fracture.
  • Medial epicondyle fracture.
  • Elbow dislocations.

Treatment

Prevention of Little League elbow is a multidisciplinary task, with parents, trainers, and coaches working together to protect young athletes. The USA Baseball Medical and Safety Advisory Committee recommends that pitching should be limited to six innings per week, and should include mandatory rest between sessions. Assessment of throwing technique is necessary to initiate appropriate, and gradually advancing, throwing programs.

Management of Little League elbow is usually nonoperative, with rest from throwing activities being crucial for the results of treatment. Application of ice to the elbow as well as antiinflammatory medications can help in the process. Research has shown that the number of pitches thrown during a certain time period is the strongest determinant of elbow pain. Therefore, patients with moderate to severe symptoms should refrain from throwing and pitching until symptoms have completely subsided; the athletes can then enter specific practice programs with progressive throwing. The number and velocity of pitching may slowly advance, not exceeding the recommended intensity.

Lyman S et al: Effect of pitch type, pitch count, and pitching mechanics on risk of elbow and shoulder pain in youth baseball pitchers. Am J Sports Med 2002;30(4):463.

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Panner Disease

The combination of repetitive trauma, caused by throwing activities in adolescent patients, together with the limited blood supply to the distal humerus in immature patients causes the typical symptoms of Panner disease, an avascular necrosis of the capitellum. During cocking and acceleration phases of throwing, the lateral elbow is subjected to compression loads.

The clinical presentation of Panner disease is very similar to an OCD, except for locking and catching, which usually are not present. The onset is insidious, with pain aggravated by activity, and there is usually a history of mild trauma or overuse. On physical examination, the extension of the involved elbow is limited to 20°. The primary difference between OCD of the capitellum and Panner disease is the age of presentation. Generally, patients 10 years and younger suffer from Panner disease. Intraarticular loose bodies are more commonly seen in older adolescents.

Radiographs reveal a flattened capitellum with areas of sclerosis, and a rough, or fragmented articular margin.

Management is similar to treatment for an OCD and requires complete rest from throwing, until revascularization of the capitellum is radiographically confirmed.

Osteochondritis Dissecans of the Capitellum

The etiology of OCD is not entirely understood, however, this injury is usually seen in elbows subjected to repetitive microtrauma. OCD is a pathologic condition of the capitellum, with abnormal subchondral bone in the body of the capitellum, and overlying cartilage. An osteochondral fragment may separate, and become a loose body, causing decreased ROM, or locking. Athletes are usually 12–16 years old and present with lateral elbow pain with associated locking, catching, and loss of full extension of the joint. Patients with acute OCD usually present with joint effusion. Tenderness to palpation over the radiocapitellar joint is common, but not pathognomonic.

Plain radiographs help to establish the diagnosis of OCD and to assess the severity of the disease. The capitellum usually reveals an area of radiolucency, or a radiolucent line demarcating an osteochondral fragment. Loose bodies can also be seen, and the articular contour of the capitellum may be irregular. In cases of suspected damage to the intraarticular cartilage, an MRI may further delineate the pathology.

Treatment of OCD of the capitellum depends on the severity of the disease and the integrity of the articular cartilage. With no clinical or radiographic evidence indicating cartilage pathology or absence of loose bodies, treatment may be nonoperative, with rest, immobilization, and NSAIDs. Rest is continued until full radiographic resolution of the defect is appreciated. In more advanced stages, surgical treatment may be indicated for removal of loose bodies, or to restore continuity of the cartilage. Cartilage damage represents a difficult problem that may lead to permanent loss of function and premature arthritis.

Kiyoshige Y et al: Closed-wedge osteotomy for osteochondritis dissecans of the capitellum. A 7- to 12-year follow-up. Am J Sports Med 2000;28(4):534.

Takeda H et al: A surgical treatment for unstable osteochondritis dissecans lesions of the humeral capitellum in adolescent baseball players. Am J Sports Med 2002;30(5):713.

Yadao MA et al: Osteochondritis dissecans of the elbow. Instr Course Lect 2004;53:599.

Fracture of the Medialepicondyle

Medial epicondyle avulsion fractures result from acute, excessive valgus forces to the elbow. They usually occur in adolescent athletes, as the medial epicondyle ossification center begins to fuse. Young athletes usually report a sudden “pop,” or even “giving way” of the elbow during cocking or during the acceleration phase of throwing. The physical examination correlates well with the history, and reveals isolated medial elbow pain with swelling and decreased ROM. The most specific clinical test for medial epicondylar avulsion fractures is a valgus stress test at 30° of flexion. The test is positive when it elicits medial elbow pain. An injury to the MCL may present with similar findings.

Nonoperative treatment is the treatment of choice if there is no associated MCL injury and for fractures with less than 5 mm displacement. The elbow will be immobilized in a posterior splint, or cast at 90° of flexion, for 4–6 weeks. Protected active and passive ROM exercises will help regain full ROM.

Surgical treatment is warranted for displaced fractures and MCL-deficient joints. Surgery consists of an anatomic reduction of the displaced fragment. The MCL can be either repaired end to end or reconstructed. If indicated, an autologous palmaris longus tendon graft can be used, however, a high incidence of damage to the ulnar nerve is reported with reconstruction of an MCL.

Gradual return to athletic activity may be considered after several months of rehabilitation, with ROM exercises and progressive muscle strengthening. Moderate throwing will be allowed after 6 months with progressively advancing physical therapy programs.

Supracondylar Humerusfracture

Supracondylar humerus fractures are the most common fracture of the elbow. At our institution more than 200 supracondylar fractures, types II and III, are treated every year. Children are usually 5–8 years old and break

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their elbow after a fall onto an outstretched upper extremity. More then 90% of these fractures present as an extension type.

Garland classified supracondylar humerus fractures into types I, II, and III. Nondisplaced fractures are type I, angulated fractures with an intact posterior cortex are type II, and displaced fractures are type III. Children with these fractures should be evaluated carefully for associated neurovascular injuries, which occur in 5–20% of fractures. An inability to pinch (median nerve, anterior interosseous branch), to extend the wrist and thumb (radial nerve, posterior interosseous branch), or metacarpophalangeal (MCP) flexion and crossing fingers (ulnar nerve) indicate an injury to respective motor nerves (Figure 9-40).

Type I requires cast immobilization. Type II and III fractures usually need closed, or rarely open, reduction, and percutaneous pin fixation. The reduction maneuver consists of longitudinal traction, correction of medial or lateral displacement, hyperflexion, and pronation with pressure on the olecranon. Crossed pins have classically been used, but similar clinical outcomes have been reported using lateral pins only, decreasing the risk of iatrogenic injury to the ulnar nerve.

 

Figure 9-40. A: Lateral radiograph of a 4-year-old toddler who was run over playing football showing a type III supracondylar humerus fracture (arrowhead) and ipsilateral distal radius and ulna fractures; a “floating elbow” injury. B: Lateral radiograph of the patient in a long arm cast after closed reduction and percutaneous pinning of the distal humerus and closed reduction of both bone forearm fractures.

Postoperative management consists of cast immobilization for 3–4 weeks. ROM is then encouraged. Patients return to full activity 4–6 weeks later. Complications include cubitus varus deformity in 5% and transient nerve palsies in 5–15% of patients. Compartment syndrome (Volkmann ischemic contracture) is a rare but devastating complication.

Olecranon Avulsion Fracture

Young athletes with avulsion of the olecranon complain of acute pain, swelling, and decreased ROM. The predominant physical findings are tenderness over the olecranon and pain with extension. Radiographs reveal widening, or fragmentation of the olecranon physis, compared to the uninvolved contralateral side. Minimally (less than 2 mm) displaced fractures require a well-padded, posterior splint or cast for approximately 6–8 weeks. Displaced fractures, with significant step off, need to be treated using open reduction and internal fixation. Using either tension band wiring or cannulated screws stabilizes the fracture, however, patients need a cast to further protect the repair. They may return to sports roughly 3 months after an injury.

Elbow Dislocation

Pathogenesis

Falls on an outstretched hand or forceful supination of a forearm may result in dislocation of an elbow. Dislocations usually affect humeroulnar and humeroradial joints. Typically, the ulna is displaced posteriorly in respect to the trochlea. Rupture of the ulnar collateral ligament and rupture of the anterior capsule are frequent, as are fractures of the medial epicondyle, coronoid process, and radial head. Associated fractures with elbow dislocations take place in 75% of patients. A Monteggia fracture is a fracture of the ulnar shaft, with dislocation of the proximal radioulnar joint (Figure 9-41)

Clinical Findings

  1. Symptoms and Signs

Inspection of a dislocated elbow usually demonstrates medial and posterior displacement of the proximal forearm. Injuries to the ulnar, radial, and median nerves are common, with a rate of occurrence of 6%, 3%, and 3%, respectively. Vascular injuries occur in 3% of elbow dislocations.

  1. Imaging Studies

Compromised blood supply, following reduction, may require an angiogram.

 

Figure 9-41. A: Lateral radiograph of a 7-year-old soccer player showing a displaced fracture of the proximal to middle one-third of the ulnar shaft (arrowhead) and dislocation of the proximal radioulnar joint (arrow); “Monteggia fracture.” B: Lateral radiograph in a long arm cast status post closed reduction and percutaneous pinning of the ulna and closed reduction of the radial head.

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Treatment

Reduction of the dislocated elbow on the field is controversial. From a practical standpoint, an athletic trainer or coach may try to reduce the joint on the field, using gentle traction. The elbow can be relatively easy to reduce, because swelling and muscle spasm develop later. It is advisable to explain to the parents that neurovascular injury can happen secondary to the reduction maneuver. Ideally, reduction of any dislocated joint should be done in a controlled environment, with conscious sedation and analgesia, and with the ability to manage possible airway problems. The reduction maneuver consists of supination of the forearm, a posteriorly directed pressure to the proximal forearm, with axial traction. The elbow is then gently flexed as axial traction is continued, until the elbow is reduced. An elbow will be immobilized in a 90° posterior splint. Nerve function is usually improved after reduction; however, in some instances nerve injuries can be inflicted by a reduction. The likelihood of ischemic injury to the extremity is directly proportional to the time the elbow was left unreduced.

Loss of extension occurs in up to 30% of dislocations. Early active motion is therefore the key factor in rehabilitation of patients treated for elbow dislocations. Other symptoms include prolonged posttraumatic pain and increased valgus laxity of the joint.

Garland JJ: Management of supracondylar fractures of the humerus in children. Surg Gynecol Obstet 1959;109(2):145.

Kumar A, Ahmed M: Closed reduction of posterior dislocation of the elbow: a simple technique. J Orthop Trauma 1999;13(1):58.

Rasool MN: Dislocations of the elbow in children. J Bone Joint Surg Br 2004;86(7):1050.

Skaggs DL et al: Lateral-entry pin fixation in the management of supracondylar fractures in children. J Bone Joint Surg Am 2004;86-A(4):702.

Gymnast Wrist

  1. Wrist

General Considerations

Gymnastics continuously gains popularity in the United States. With increasing numbers of competitors, the rate of gymnastics-related injuries is on the rise as well. A gymnast with wrist pain sometimes presents a true diagnostic and therapeutic challenge.

Clinical Findings

  1. Symptoms and Signs

Wrist pain affects about 75% of male and 50% of female gymnasts. The intensity and duration may vary, but most young gymnasts complain of wrist pain for 4 months or longer before seeking medical treatment. Axial loading combined with hyperextension, commonly seen in activities such as pommel horse, horizontal bar, vault, and floor exercises, place significant stress on the wrist. Most female athletes complain of an ulnar-sided wrist pain, whereas male athletes complain equally frequently of radial and ulnar-sided pain. Physical examination findings are usually unspecific; mild swelling and tenderness at the wrist may be present.

  1. Imaging Studies

In children and adolescents, three views of a painful wrist, with comparison views, should be obtained. Until age 18 years, 29 ossification centers at the wrist are at different stages of fusion, making a precise diagnosis difficult. Stress-related changes can be seen as widening of the distal radial physis, epiphyseal cystic changes, beaking of the distal radial epiphysis, or metaphyseal

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irregularities. Premature closure of the distal radial epiphysis happens, with resultant positive ulnar variance in severe cases. An MRI helps to differentiate the pathology of cortical and trabecular bone, the articular surface, wrist ligaments, and the triangular fibrocartilage complex.

Treatment

Prevention of acute and chronic injuries is an important issue. The use of protective gear is as important as the setup of the training room and backups by spotters. As with any sports activity, proper warm-ups need to be emphasized, and rapid increases in intensity of exercises should be avoided. Treatment for patients with gymnast wrist is generally nonoperative. Ligamentous injuries, which are unusual in children and adolescent athletes, can be treated with immobilization or with surgical repair if they continue to result in instability and pain. Bony injuries require immobilization in a volar splint or cast. Cartilage injuries with disruption of the articular surface can be treated with debridement or repair, using open or arthroscopic techniques.

Distal Forearm Fractures

General Considerations

The incidence of distal radius fractures, reported to be about 370 per 100,000 a year (2001), has been continuously increasing. The peak incidence corresponds to the peak velocity of growth, between 11.5 and 12.5 years of age in girls and between 13.5 and 14.5 years of age in boys. The mechanism of injury usually includes a fall on an extended hand.

 

Figure 9-42. Schematic drawing superimposed on a lateral radiograph of a distal radius fracture (arrowhead) showing the silver fork deformity (arrow).

Clinical Findings

  1. Symptoms and Signs

The physical examination shows tenderness to palpation of the distal forearm, swelling, ecchymosis, and the presence of deformity.

  1. Imaging Studies

Standard AP and lateral radiographs are usually sufficient to make the diagnosis. Additional oblique views help detect subtle, nondisplaced, buckle fractures. Displacement, the presence and amount of comminution, distal radius articular surface tilt, radial length, radial inclination, and intraarticular extension dictate treatment for these fractures. Nondisplaced, Salter 1 fractures can be difficult to diagnose, as they may present with no changes on a radiograph, or with a mild widening of the distal radial physis. A history of trauma, with the presence of local tenderness over the distal radius growth plate, is sufficient to establish the diagnosis of a Salter 1 fracture (Figure 9-42).

Treatment

Treatment of displaced fractures requires a closed or open reduction and cast immobilization. Hematoma blocks, conscious sedation, or general anesthesia will diminish pain and discomfort during reduction. Acceptable limits of displacement and angulation vary depending on an athlete's age, location of the fracture, direction of deformities, and proximity to a growth plate. A well-molded cast will secure proper healing of the fracture and prevent fracture displacement. Immobilization time depends on the location of the

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fracture. Distal radius fractures, with close proximity to the growth plate, usually require 4–6 weeks of immobilization, whereas mid-shaft fractures usually need a cast for a longer time (Figure 9-43). Progressive ROM exercises can follow immobilization with gradual return to sports. Open reduction and internal fixation, using pins, plates, or intramedullary flexible nails, may be required for severely displaced or unstable fractures. The probability that a patient will require surgery increases with age.

 

Figure 9-43. A: Lateral radiograph of a 14-year-old football player showing a Salter 2 distal radius fracture. B: Lateral radiograph in a short arm cast after closed reduction.

Footnote

The authors would like to thank Joanna Grudziak, BA, MA, for her help in preparing this manuscript.

Khosla S et al: Incidence of childhood distal forearm fractures over 30 years: a population-based study. JAMA 2003;290(11): 1479



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