Little League Shoulder

Also called proximal humeral epiphysiolysis, Little League shoulder was first described by Dotter in 1953.⁶ It is a stress fracture of the proximal humeral epiphyseal plate, which usually affects overhead throwers between the ages of 12 and 15 years, although it is now being seen in younger athletes. The exact etiology of this condition is not known, but repetitive overload on the epiphyseal plate is thought to be the common underlying cause.⁷

Signs and Symptoms

The patient usually presents with gradual onset of increasing shoulder pain, sometimes associated with a recent exacerbation as a result of a specific throw or pitch. Pain is generally localized to the upper arm.

Physical examination is usually consistent with that seen in impingement syndrome in the older population, including pain with full elevation and at extremes of internal and external rotation of the shoulder. Generalized weakness and limited active range of motion, especially in abduction and internal–external rotation, may also be present.8,9 The positive Neer’s impingement sign (Figure 17-5, A) and the alternative Hawkins’ impingement test (Figure 17-5, B) generally reproduce pain, although probably from rotational forces on the proximal humerus as opposed to impingement of the rotator cuff. Pain is usually localized to the proximal lateral humerus.

Referral and Diagnostic Tests

Comparison radiographs often show widening of the proximal humeral epiphyseal plate and sometimes show fragmentation (Figure 17-6). Magnetic resonance imaging (MRI) is usually not necessary but will rule out rotator cuff pathology and may demonstrate edema at the epiphysis.

Little League Elbow

Medial humeral epicondyle apophysitis, or Little League elbow, is often caused by repeated tensile stresses on the medial epicondyle.¹² The apophysis of the medial epicondyle is typically the weak link in adolescents when compared with the ulnar collateral ligament (UCL) or the flexor pronator mass. The specific etiology of medial humeral epicondyle apophysitis is still unclear; however, the traction forces of the UCL on the apophysis are the prime suspect. The highest levels of stress are created during the late cocking and early acceleration phases of throwing and may be significantly higher in the side-arm thrower.^13,14

Referral and Diagnostic Tests

Radiographs may reveal a widening or fragmentation of the epiphyseal plate of the medial humeral epicondyle when compared with the contralateral elbow (Figure 17-7).

Osgood-Schlatter Disease

Osgood-Schlatter disease is one of the most common causes of anterior knee pain in the adolescent patient. Other common terms for this condition include epiphyseal aseptic necrosis of the tibial tubercle, osteochondritis of the tibial tuberosity, or patellar tendinitis. This condition was first described by American orthopedist Robert B. Osgood and Swiss physician Carl B. Schlatter.³ It typically affects adolescents 10 to 15 years of age, with the onset of symptoms usually associated with active periods of growth and/or rapid changes in activity levels.^16–23 Explosive and eccentric activities are particularly aggravating to Osgood-Schlatter disease. It is often bilateral and may occur at an earlier age in girls than in boys. Osgood-Schlatter disease may occur once and resolve with appropriate measures or may present as recurring episodes associated with growth spurts throughout adolesence.^3,15 Once the condition is resolved, the patient may have a more prominent tibial tubercle.

Referral and Diagnostic Tests

Diagnosis is usually determined by history and physical examination. A radiograph is often normal but may show fragmentation and separation of the apophysis (Figure 17-8).

Treatment

The treatment of Osgood-Schlatter disease consists of limitation of aggravating activities to diminish symptoms along with cross-training to maintain conditioning. The condition is often self-limiting. Casting or immobilization is used only in severe cases that have not responded to conservative treatment or in cases in which the apophysis has separated from the tibia.

Treatment should focus on improving flexibility and the gradual return to conditioning exercises as the symptoms allow. Ice may be used to control pain and swelling. NSAIDs may be helpful in alleviating symptoms in the acute phases of the condition. Orthoses such as counterforce braces or neoprene knee sleeves have some limited benefit in controlling symptoms in some patients. A simple knee pad may provide protection from pain caused by bumping the hypersensitive area around the tibial tubercle.

Surgery is rarely indicated in acute cases unless complete avulsion of the apophysis has occurred (Figure 17-9). In some cases, individuals may have anterior pain localized to the tubercle that does not resolve and may be a result of bony ossicles that have not completely fused (Figure 17-10). Surgery is sometimes indicated in these individuals if conservative treatment is not successful in decreasing their symptoms.

Sever’s Disease

Also known as calcaneal apophysitis, Sever’s disease occurs as a result of inflammation of the growth plate at the insertion of the Achilles tendon on the posterior calcaneus. Sever’s disease is usually a result of repetitive activities causing inappropriate stress on the growth center (similar to other apophysitis conditions) and typically occurs in children ages 8 to 14 years. On occasion it worsens as a result of specific trauma.3,24

Referral and Diagnostic Tests

Radiographs are often normal but may reveal fragmentation or widening of the apophysis (Figure 17-11) compared with the unaffected side.

Signs and Symptoms

Physical examination usually reveals a kyphotic (humpback) deformity of 20 to 25 degrees that does not change when the patient bends forward in a flexed position (Figure 17-12). The kyphosis is commonly accompanied by scoliosis and a decrease in flexibility because of the structural nature of the deformity. Patients will usually have tenderness to palpation around the kyphosis. As with lower spine conditions, hamstring tightness is common. Although neurological complications are rare, a thorough neurological examination is essential (see Chapter 11).

Referral and Diagnostic Tests

Radiographs and MRI scans are helpful to rule out other conditions. Radiographs may reveal decreased disk space anteriorly, irregularly shaped vertebral end plates, and the presence of Schmorl’s nodes (Figure 17-13).

Differential Diagnosis

Differential diagnosis includes scoliosis, congenital kyphosis, multiple compression fractures, tumor, infection, tuberculosis, skeletal dysplasia, ankylosing spondylitis, and herniated nucleus pulposus.

Treatment

Core-strengthening and trunk stabilization exercises remain controversial in individuals with Scheuermann’s disease. Some believe that because this condition is usually self-limiting, no treatment is necessary.25,26 Others recommend strengthening to prevent associated back pain and stiffness.^25,26 In more extreme cases, casting or bracing is appropriate (Figure 17-14). Orthotic management typically requires 12 to 24 months of treatment to show significant improvement and is done to prevent worsening of the condition as opposed to actually correcting the deformity.

NSAIDs are helpful for exacerbations, and activity restrictions to prevent hyperextension of the spine may be indicated. Surgery is rarely indicated and typically is for intractable pain or unacceptable cosmetic deformity.25,26

Prognosis and Return to Participation

Because Scheuermann’s disease usually occurs in the thoracic spine, which normally has limited motion, most individuals do well with conservative management. In skeletally mature patients, the kyphosis is usually not progressive. This differs from adolescent scoliosis, which can continue to progress into adulthood (if the deformity is more than 50 degrees). For adults, the treatment is usually observation, antiinflammatory drugs, or reconstructive surgery, depending on the severity of the symptoms. Common complications associated with Scheuermann’s disease include chronic back pain, progressive deformity, and neurological deficits. Patient education is essential to help improve posture and overall body mechanics with daily activities.

Signs and Symptoms

Patients typically present with gradually increasing joint pain that may be associated with loss of motion. Patients are often asymptomatic for a significant period before the process starts to affect joint mechanics. As the disease progresses, they begin to experience increasing joint pain with activity and eventually experience pain even at rest.

Physical examination will usually reveal pain with joint motion and restricted range of motion depending on the progression of the disease.

Referral and Diagnostic Tests

Radiographs are often normal when patients initially present but may show signs of early bone loss in aggressive cases (Figure 17-17). An MRI study is usually ordered for patients with suspected AVN because it is much more sensitive in detecting the disease in its early stages (Figure 17-18). The MRI is able to detect changes in the bone marrow and provides the physician with a better indication of the extent of the affected area. MRI has replaced the bone scan and computed tomography (CT) scan as the diagnostic study of choice for evaluating AVN.⁴

Treatment

Once diagnosed, treatment is designed to prevent or slow progression of the disease. Activity modifications are initiated to limit impact-loading activities. If possible, contributing factors such as steroids, alcohol, or smoking are eliminated. NSAIDs or narcotic analgesics are used for pain control as needed.

As the disease progresses and function begins to be compromised, surgical procedures are available to retard the progression of the disease or replace the damaged joint if necessary (Box 17-2).

Prognosis and Return to Participation

AVN can be a devastating disease with typical progression and eventual destruction of the joint. Activities usually need to be restricted on a permanent basis, depending on the extent of the progression and the patient’s symptoms. In some cases spontaneous remission occurs, after which the individual is allowed to return to activities as tolerated.

Prevention

Prevention of AVN is based on the elimination or limiting of risk factors (i.e., alcohol use, steroid use, cigarette smoking). Of course, many other risk factors including trauma and caisson disease are inherent in certain sports or activities, and these risks need to be assessed by each individual.