The editors and current author would like to thank and acknowledge the significant contribution of the previous author of this chapter from the 2004 first edition, Brent K. Ogawa. This current third edition chapter is a revision and update of the original author’s work.

A 12-year old male soccer player comes into the office with a chief complaint of pain to both knees. He reports a gradual onset of knee pain in the front of both of his knees that started about one year ago. The pain seems to be in the same spots and is worse after a hard practice or game and with running up and down hills. He noticed lumps just below both of his knees recently that are tender if he falls or accidentally bangs them. The patient does not remember an initial history of trauma or injury. He is otherwise healthy with normal birth and development.

Exam: VS are normal. Examination is unremarkable except for his knees. He is comfortable, in no significant acute pain. His right and left knee findings are identical. A mild prominence over the tibial tuberosity is visible. No erythema, edema or effusions are noted. No patellar grind is noted. The patella is normally placed and there is no tenderness over the patella. He has localized tenderness over the tibial tuberosity. His knee range of motion is full, but he experiences pain over the tibial tuberosity when he is asked to extend his knee against force (such as against gravity, or against resistance from the examiner). Motor strength is otherwise normal. McMurray, anterior drawer, Lachman, posterior drawer, and varus/valgus stress tests are all negative.

Imaging: Radiographs demonstrate moderate prominence of the tibial tuberosities bilaterally. There is mild soft tissue swelling with no evidence of fracture.

Clinical course: He is diagnosed with Osgood-Schlatter disease. He is instructed to rest and apply ice to the area, focus on stretching his hamstrings, and to take acetaminophen when needed. He is permitted to ambulate normally and jog briefly, but he must modify activity when pain occurs. After 5 weeks, the pain subsides, and after about one year he is symptom-free. There remains mild, nontender prominences over both knees as he becomes older.

Osgood-Schlatter disease (OSD), also known as traction apophysitis of the tibial tuberosity, is a finding in the skeletally immature athlete. It was first described independently by both Osgood and Schlatter in 1903. As the ages of ossification differ between genders, OSD typically presents in girls ages 8 to 13 and in boys ages 10 to 16, with a male to female predominance of 3:2. While this disorder has historically been more common in boys, the proportion of affected females is increasing potentially due to growing athletic participation among girls. The earlier presentation in girls is likely due to the appearance of the secondary ossification center of the tibial tuberosity two years earlier. OSD is seen most frequently in adolescents who are active in sports requiring strenuous use of the quadriceps muscles such as basketball, volleyball, sprinting, and gymnastics. Jumping puts the most force on the quadriceps and the insertion of the patella tendon into the tibial tuberosity. OSD is also common in running sports such as soccer, baseball, and football. This finding is seen more often unilaterally and preferentially on the left side although 25% of patients have a bilateral presentation. (1-3)

Repetitive trauma is the most widely accepted etiology of OSD. Repeated traction causes inflammation of the cartilage adjacent to the patellar tendon, resulting in softening and partial avulsion of the apophyseal ossification center. Upon skeletal maturation, the tibial tubercle apophysis then fuses with the rest of the proximal tibia, leaving the residual usually painless prominence of the tibial tuberosity. (2,4)

Growth of the proximal tibia is unique because it involves two growth centers in close proximity: the proximal tibial physis and the tibial tuberosity apophysis. An apophysis is a growth center, which does not contribute to the length of the bone. It is common for a tendon to insert over an apophysis, such as in the tibial tuberosity (patellar tendon) or calcaneus (Achilles tendon). The cartilage growth plate of the apophysis is a relative weak spot susceptible to micro-separation with trauma or overuse resulting in repetitive traction. Anatomically, the tibial tuberosity forms at 12 to 15 weeks of fetal growth, although there isn't a recognizable tibial tuberosity growth center until after birth. Southwick and Ogden described the development of the tibial tuberosity in 7 stages; 3 prenatal and 4 postnatal. Stages 1-3 involve fibrovascular ingrowth and vascularization of the area with anterior outgrowth. Postnatal stages include a separate and distinct tibial tuberosity growth center (stage 4) that later joins with the tibial growth plate (stage 7). There is a distinct secondary ossification center in the distal portion of the tuberosity (stage 5). During maturation (stage 6) there is a coalescence of the proximal tibial epiphyseal ossification center with the tuberosity ossification center. In the final stage (stage 7), there is fusion to form a contiguous structure. The vascular anatomy of the tuberosity is plentiful even until ages 10 to 12. Therefore, the unique anatomy and vascular supply combined with excessive extensor mechanism forces causes stress on the secondary ossification center, ultimately leading to OSD. (5,6)

On examination, the pain is localized to the anterior aspect of the proximal tibia over the tibial tuberosity and distal portion of the patellar tendon. There is a local prominence and tenderness on exam. Although patients may complain of pain with full extension of the knee, especially against force, they generally have full range of motion. They usually describe a dull ache exacerbated by jumping or stair climbing. Walking on flat surfaces does not cause pain. Patients may often have symptoms for 6 to 12 months prior to seeking medical attention or may present with pain following direct trauma to the tibial tubercle, such as a fall on a flexed knee. Although the tibial prominence may be highly indicative of OSD in many cases, a full knee exam should be performed to rule out other intra-articular pathology. (1)

OSD is largely a clinical diagnosis, thus radiographs of the knee are usually unnecessary unless other pathology is suspected. Typical radiographic findings in OSD include an elevated tibial tubercle, prominence or fragmentation of the tibial tuberosity, soft tissue swelling, or calcification in the distal patellar tendon. However, these findings may also be found in normal variants, thus clinical correlation is important. The differential diagnosis of proximal tibia or anterior knee pain includes acute stress fracture, contusion of the tibial tuberosity, prepatellar bursitis, patellar tendonitis, and more rarely malignancy, osteomyelitis, or infectious apophysitis. (1,2)

Despite the ominous-sounding name, OSD is ultimately benign and self-limited, thus alleviating patient and parental fear is important. Treatment is mainly symptomatic and involves activity modification when discomfort becomes more extreme. Activity modification includes reducing exercises that stress the quadriceps, playing less, resting more during games and practices, and reducing jumping drills. Most patients can continue sports participation if symptoms resolve with rest and do not interfere with sports-related movements. Ice and non-steroidal anti-inflammatory drugs (NSAIDs) may be used as needed. Corticosteroids are not used because subcutaneous atrophy and fat pad necrosis can occur. A recent systematic review on conservative treatment of OSD considers activity modification as the consensus treatment for OSD. Hamstring stretching and quadricep strengthening can be useful following resolution of acute symptoms but lack high-level evidence from randomized control trials. The use of knee pads to prevent reaggravation of contusions can be helpful. Surgery is rarely indicated for OSD except in persistent, disabling cases which fail prolonged conservative care. In these cases, surgical intervention generally consists of ossicle excision after skeletal maturity is reached. (1,2,7)

The prognosis for OSD is good with symptom resolution upon fusion of the apophysis. Although the symptoms may decrease with activity reduction, local tenderness may persist. In the adult, a usually painless local prominence of the tibial tuberosity may remain. (1,2)

A 13-year-old boy presents to the office with a chief complaint of right heel pain. The patient states he has gradually noticed this pain since the beginning of baseball season 2 weeks ago. The pain is a dull quality, 5/10 severity over his right heel that is worse with sprint practices to steal second base. He has tried ice, which provides only temporary relief until the next practice. He is not taking any pain medications. There is no history of trauma or known injury and he is otherwise healthy.

Exam: Vital signs are within normal limits for age. Examination is unremarkable except for his right lower extremity. He is comfortable and in no acute pain. There is no visible deformity, muscle atrophy, or erythema. There is minimal soft tissue swelling and moderate tenderness to palpation over the back of the right calcaneus. Ankle range of motion is normal. He ambulates normally and he is even able to jump up and down.

Imaging: Radiographs of his right heel are obtained, which demonstrate no specific abnormality. He does have an open growth center (apophysis) over the Achilles tendon insertion region, but this is noted to be within normal limits for his age.

Clinical course: He is diagnosed with Sever's disease. He is instructed to modify athletic activity for 4 weeks, but he is permitted to ambulate normally. He is also instructed to apply ice and take NSAIDs if the pain continues. A heel wedge or shock absorptive heel cups are placed in his shoes, which he later reports helps to alleviate the pain with activity. He focuses on stretching and strengthening exercises for his calves and hamstrings. He subsequently recovers and returns to his normal athletic function after 4 weeks.

Sever's disease, also known as calcaneal apophysitis, was first described in 1912 by JW Sever. This condition describes inflammation of the open calcaneal growth center via the Achilles tendon insertion) secondary to traction. Similarly to OSD, Sever’s disease is a common overuse condition of the skeletally immature athlete. This disease is seen in children 8 to 15 years old and is more prevalent in sprinters and runners, especially athletes in basketball, baseball, soccer, football, track, cross-country, and gymnastics. The mechanism of this injury is similar to OSD, with the major stress resulting from running and pushing off with the foot. Cleats and high grip shoes permit greater grip into the ground and turf that permits greater force transmitted to the calcaneal apophysis. In Sever's disease, tension is placed on the calcaneus by the strong shearing forces caused by the plantar fascia and triceps surae. Associated pathology thought to predispose to this disease includes internal tibial torsion, forefoot varus, and tight heel cords. (8-11)

Clinically, these patients present with heel pain over the posterior calcaneus near the Achilles tendon insertion. Soft tissue swelling and induration may be present, although less often. They may have an antalgic gait secondary to pain, but in most instances their gait is normal during medical evaluation. Most of their pain and discomfort is sustained during athletic activity. After a short interval of rest, symptoms commonly subside. Radiographs are generally not necessary as the diagnosis is clinical. If there is concern for other pathology of the calcaneus, three views may be included: AP, lateral, axial (Harris views). Radiographs may show a sclerotic and fragmented calcaneal apophysis. An open growth center is present in Sever's patients, and symptoms usually subside as the growth plate achieves fusion/closure. If the diagnosis remains uncertain, oblique views and CT may be necessary to identify occult fractures. The differential includes stress fracture, avulsion fracture of the calcaneus, Brodie’s abscess, osteoid osteoma, simple bone cyst, plantar fasciitis, or Achilles tendon rupture. (8,9,12)

Treatment for this disease is mainly symptomatic. This includes activity restriction, ice, and NSAIDs as needed. Most patients with mild Sever's disease can still play, but they should be told to rest when pain occurs. Shock-absorbing insoles, orthoses, or heel cups/wedges may also be used. Taping may be done for athletes who cannot wear orthotics during their activity, such as gymnasts, however there are also heel cups integrated into ankle wraps that can be utilized for barefoot sports. Injection therapy and surgical intervention are not indicated in the treatment of Sever’s disease. Once acute symptoms have resolved, athletic activity can be gradually resumed, and patients should begin stretching of the Achilles tendon and strengthening exercises of the hamstring and calf muscles. The exact time frame for resolution of symptoms varies. Recurrence may occur but full recovery is expected upon reaching skeletal maturity. If conservative treatment is unsuccessful after 6 to 8 weeks, consider radiographs, or other studies to check for more occult sources of pain. (8-10)

A 13-year old right-handed boy presents to the clinic with a chief complaint of right elbow pain. The patient has noticed a gradual onset of pain over the past two months since baseball season started. He is the star pitcher for his little league team and pitches full games twice per week. He also practices most days of the week. He has complained of pain during practices but has been told to continue practicing. The pain is most severe over the medial aspect of his right elbow (ulnar side) and does not radiate. He can perform normal activities of daily living without pain. His parents are concerned about him missing the All-Star game if he doesn't continue to perform at a high level. There is no history of trauma or known injury and he is otherwise healthy.

Exam: VS are normal. His exam is normal except for his right elbow. There is no visible deformity, edema, or erythema. He is tender to palpation over the medial epicondyle of the distal humerus. An elbow contracture of 15 degrees to full flexion is noted. He has full range of motion (ROM) about the shoulder and wrist. Upper extremity strength is good, and sensation is intact. Perfusion, pulses, and reflexes are all normal.

Imaging: Radiographs of his right elbow are obtained and show a minimally displaced right medial epicondyle fracture.

Clinical course: Despite initial reluctance, the patient and his parents decide to cease activity. Because there is minimal displacement (< 2 mm), a posterior splint is applied for 2 weeks. On return to the clinic, the patient reports that his pain is now minimal. The splint is removed, and active range of motion exercises are advised. The patient continues these diligently. Six weeks later, after X-rays confirm bone union, the patient is allowed to start a graduated interval throwing program. He returns to pitch in the championship game the following season. The league commissioner decides that each team must keep an accurate pitching record of the number of pitches thrown per game. The community sports medicine physician is also asked to educate coaches and parents about the importance of identifying little league elbow early.

"Little League elbow" classically describes medial epicondyle apophysitis of the humerus, though colloquially it is used to describe a full group of elbow lesions also including medial epicondylar avulsion fractures, Panner disease, osteochondritis dissecans (OCD), and posterior shear injuries. Medial epicondyle apophysitis (MEA) describes an overuse injury prevalent in adolescent athletes in sports involving repetitive overhead arm motions, such as throwing. The syndrome is a result of a repetitive valgus stress resulting in lateral compression and medial traction on the elbow. The ulnar collateral ligament (UCL) is the main stabilizer to valgus stress and exerts traction on the medial epicondylar apophysis of the humerus. The open apophysis is the weakest point of the kinetic chain, and thus is primed to become inflamed and partially separated from the humerus. While baseball pitching is the most common mechanism, tennis serving, volleyball spiking/serving, football and javelin throwing can also cause MEA. Risk factors associated with MEA in baseball include a high volume of pitches per game, high pitch velocity, continued pitching despite arm fatigue, and playing on multiple teams simultaneously. (1,13,14)

A comprehensive history is important and should include age, handedness, activity level, sport and position played, type of overhead/overhand motion, and history of trauma. The typical history of MEA includes an insidious onset of medial elbow pain with overhead throwing and decreased throwing performance. In patients experiencing a medial epicondyle avulsion fracture, they may recall a pop at the time of injury. The age of the thrower can be helpful in the differential and is divided into three groups: 1) childhood (terminates with appearance of all secondary centers of ossification), 2) adolescence (terminates with fusion of all secondary centers of ossification to their respective long bones), and 3) young adulthood (terminates with completion of all bone growth and achievement of final muscular development). Because the age of the thrower corresponds to skeletal maturation, age narrows the differential of elbow injury type. During childhood, pain to the medial epicondyle secondary to microinjuries at the apophysis and ossification center is common. In adolescence, muscle strength, muscle mass, and throwing forces increase, thus valgus stress of the elbow can result in an avulsion fracture of the entire medial epicondyle. Some athletes develop enough chronic stresses to cause delayed union/malunion of the medial epicondyle. By young adulthood, the medial epicondyle fuses and injuries tend to occur to muscular attachments and ligaments. The flexor muscles and ulnar collateral ligaments are more often injured. (13,15)

Examination is likely to yield pain at the medial elbow and tenderness to medial flexor muscle palpation during and after throwing. Direct tenderness over the epicondyle can also be seen. Examination should also include both elbows assessing for atrophy/hypertrophy, range of motion, bony deformity, flexion contractures, valgus laxity, and carrying angle. Neurological and vascular exams with special attention to the ulnar nerve should be performed. (1,13)

Radiographs are essential for evaluating young athletes with chronic elbow pain. Unilateral radiographs may be sufficient for assessment but if the diagnosis remains elusive, some experts advocate for comparison imaging with bilateral anterior/posterior, oblique and lateral views with elbows flexed at 90 degrees that should be obtained. Valgus stress views should be obtained if there is concern for ligamentous integrity. Common findings include an immature elbow with medial epicondyle enlargement, fragmentation, and beaking or avulsion. Lateral lesions usually involve the subchondral bone and manifest as osteochondrosis or OCD of the capitellum or radial head. Posterior lesions present with hypertrophy of the ulna causing chronic impingements of the olecranon tip into the olecranon fossa. MRI may be useful in older athletes in which there is concern for UCL tear or for grading of OCD lesion. Ultrasound has also been demonstrated to have some utility in detecting unfused ossicles and bony fragmentation in medial epicondyle lesions. (13,16,17)

The American Academy of Pediatrics (AAP) and youth baseball organizations have made recommendations to reduce the risk of overuse elbow injuries in young athletes. Pitch count restrictions depending on athlete age and planned offseason from overhead athletics are key preventative principles; ideally no more than 8 months in a single sport. It is advisable to coordinate pitching restrictions and expectations between coaches, parents, and players. It is certainly preferable to prevent these injuries than it is to recover from them and miss significant time in season. The initial focal elbow pain or swelling suggests impending pathology. Playing through such pain worsens the injury, so this practice should be discouraged. A basic strategy to reduce the risk of these injuries is to restrict further throwing for the remainder of the day once the onset of pain occurs. Medial tension overload injuries are the most common and usually resolve within 4 to 6 weeks of rest, ice, and NSAIDs. After symptoms resolve, gradual return to throwing is allowed and a defined graduated interval throwing program should be mandated before full clearance. If the recovery course continues for an extended period of time, many experts advocate for pitching to be postponed until the next season. (15,18,19)

There are other sports injuries that are often included in the group of injuries known as "Little League elbow". Medial epicondylar fractures occur with substantially more acute valgus stresses applied through violent muscle contraction causing an avulsion fracture of the medial epicondyle. This causes a painful elbow with tenderness over the medial epicondyle and elbow flexion contracture that may exceed 15 degrees. Patients often report a pop and sudden onset medial elbow pain. In minimally displaced (<2 mm) or non-displaced fractures, a single posterior splint for 1 to 2 weeks, then progression to active range of motion exercises (ROM) is commonly used. When radiographic evidence of union is noted, a specific progressive throwing program is started. In moderately displaced fractures (> 2 mm) open reduction with internal fixation hardware is performed with early ROM exercises at 1 to 2 weeks to regain flexion and extension. (1,20)

Medial ligament rupture to the UCL is not common in young athletes and is seen more in adults. Patients may have medial tenderness for months to years before the ligament is injured, usually in a sudden catastrophic event. MRI with joint arthrogram is the most common method to visualize the soft tissue of the elbow. If there is instability and the athlete desires to continue throwing at a high level, surgical repair is generally required; however new evidence has shown that conservative management can be initiated for those athletes that perform upper extremity weight bearing activity such as tumbling. Surgery may not be indicated for stable partial tears or for casual athletes, as most activities of daily living do not require an intact UCL and medial elbow stability. If the injury is detected early, conservative treatment including rest and alternating heat/ice may be adequate. (1,15)

Panner’s disease (osteochondrosis of the humeral capitellum), is a very rare condition characterized by degeneration or necrosis of the capitellum and is followed by regeneration and recalcification. It has been compared to osteochondrosis of the hip epiphysis, Legg-Calvé-Perthes disease. Panner’s is a focal, localized lesion of the subchondral capitellum and its articular cartilage. It is a self-limiting condition where the capitellum epiphysis essentially assumes a normal appearance as growth progresses. These patients typically present with pain and stiffness of the elbow. Panner’s usually affects younger boys (<10 years) and the onset is acute with fragmentation of the entire capitellar ossific nucleus. There are generally no loose bodies and no late sequelae unlike osteochondritis dissecans which is discussed below. Initial treatment of Panner’s includes rest, avoidance of throwing, and sometimes a posterior splint until acute symptoms resolve. Radiographic follow up is essential to ensure adequate healing. Late deformity and collapse of the articular surface of the capitellum is rare. (1,21)

Osteochondritis dissecans (OCD) of the elbow is a focal lesion of the capitellum with separation of articular cartilage from the subchondral bone occurring in adolescents in their second decade of life. OCD more commonly occurs in the knee and ankle. OCD of the capitellum is secondary to the compressive forces occurring between the radial head and capitellum classically sustained due to throwing. The etiology of OCD is unclear, though theories include ischemia, hyperinflammatory state, trauma, and genetic factors. These patients present with poorly localized, dull pain with decreased range of motion during extension with locking, clicking, and catching. Crepitus may be palpable on pronation and supination. It is important to distinguish these patients from those with Panner's disease, who are typically younger (<10 years), present instead with stiffness, and without loose bodies. MRI, CT, and arthroscopy are beneficial in determining the extent and size of the lesion. MRI grading of the lesion depends on the degree of cartilage separation, bony changes, and presence of loose bodies. Treatment depends on severity and size of cartilage separation. Stable, lower grade lesions generally respond well to conservative measures, while unstable lesions need surgical treatment. Nonoperative treatment consists of rest, activity restriction, NSAIDs, and sometimes a short period of immobilization. Surgical intervention generally consists of removal of loose bodies, abrasion chondroplasty, in situ fixation, osteochondral autograft transplantation system (OATS), or costal osteochondral transplantation (COT). These patients should be seriously counseled about the dangers of continued intense throwing and are urged to abstain. (22–24)

Posterior extension and shear injuries are uncommon in young throwers, but the incidence increases throughout adolescence. They are related to valgus, shear stress across the posterior olecranon leading to osteophytes, olecranon stress fractures, and loose body formation. Age and skeletal maturity influence injury pattern and therefore management. In childhood osteochondrosis of the olecranon is most common. Treatment includes rest and gentle ROM exercises. Flexibility and strengthening are initiated once acute symptoms subside. In adolescence, avulsion fragments and lack of apophyseal fusion require arthroscopic removal. If there is lack of apophyseal fusion, rest and immobilization can produce good results. Finally, in young adults, partial avulsion of the olecranon and osteophyte formation at the tip of the medial border of the olecranon is most likely. Partial avulsion of the olecranon requires surgical reattachment of the olecranon and triceps. Osteophytes should be removed to decrease pain and increase ROM. (24)

Overuse injuries to the elbow of young throwing athletes are occurring with increasing frequency. They can be seen not just in baseball pitchers but also in quarterbacks, tennis players, volleyball players and javelin throwers. Because the biomechanics of throwing are complex, the physical stresses can cause a group of pathologic entities to include the medial, lateral, and posterior aspects of the elbow. Preventing these types of injuries involves teaching proper throwing mechanics, predetermining an age based stopping point based on number of pitches thrown (pitch counts), and recognizing early warning signs and stopping once the pain starts. Although many of these injuries have been blamed on learning to throw curveballs or breaking pitches, some studies have shown that at skeletal maturity a properly thrown curveball causes no more stress on the elbow than the traditional fastball. (25)

Clinical course: He is diagnosed with an orbital floor fracture and hyphema. Ophthalmology is consulted and further evaluation for the hyphema includes an intraocular pressure measurement, which is found to be normal. The patient and parents are advised to limit his activity for the first 72 hours without television or video games. His immunization records are current and the patient is sent home with acetaminophen for analgesia and follow-up in 3 days. He is specifically told to avoid NSAIDs since this will increase his bleeding risk. He recovers well with no diplopia or glaucoma complications. He is restricted from physical activity for 3-6 weeks and from blowing his nose for 4-6 weeks. The next season, he is sporting a new pair of safety goggles to every game and practice. The community league also implements a new rule requiring protective eyewear.

Orbital injuries are common injuries in athletes, especially those in high-risk sports with high-speed objects such as sticks, bats, balls, pucks, or aggressive body contact. In addition to sports, orbital injuries are most commonly seen in falls, motor vehicular accidents, and assault. Males aged 21 to 30 are at highest risk for orbital fractures because of their increased incidence of trauma. (26,27)

Anatomically, the orbit consists of 7 facial bones (26,28,29):

1. Frontal bone: superior orbital ridge and upper medial orbital ridge
2. Zygomatic bone: lateral orbital rim and inferior orbit
3. Maxilla: inferior and lower medial rims
4. Lacrimal: medial rim separating orbital from nares
5. Ethmoid: medial wall and part of posterior wall
6. Sphenoid: posterior orbit
7. Palatine: inferior orbit

Related anatomical structures that can be injured during an orbital fracture include the optic nerve, periorbital fat, extraocular muscles, and the inferior orbital nerve. Several types of orbital injuries can occur with blunt trauma to the eye. A blowout fracture is an isolated fracture of the orbital walls without involvement of the orbital rims. This often occurs when force against the eye without force against the rims increases intraorbital pressure, redirecting the pressure into the orbital walls. The orbital floor and medial orbital wall are the most common types of blowout fractures because they are the weakest parts of the orbit. The trauma may also be directed towards the orbital rim, leading to bending of the orbital walls and consequent fracturing. (26,29)

The principal morbidity associated with orbital fractures is eye injury. These injuries are multiple and can include corneal abrasion, lens dislocation, iris disruption, choroid tear, scleral tear, ciliary body tear, retinal detachment, hyphema, ocular muscle entrapment, and globe rupture. The history and physical are crucial in differentiating patients that require conservative or surgical treatment. The patient should be questioned regarding epistaxis or clear fluid from nares or ears, which suggests the possibility of a basilar skull fracture; loss of consciousness, which suggests the possibility of concussion or more serious brain injury; malocclusion, which suggests the possibility of facial, maxillary, or mandibular fracture; visual problems, hearing problems, and facial numbness or tingling. Other specific questions regarding the eye include the eye pain, presence of diplopia, painful eye motion (entrapment or periorbital edema), photophobia, flashes of light (retinal detachment), or blurred vision (hyphema, vitreous hemorrhage, retinal detachment). (26,29)

When an injury near the eye occurs, a thorough exam should be performed. This includes visual acuity, inspection for abrasions, laceration, foreign bodies, changes in pupillary dimension, or reactivity to light. Any change in visual acuity, blood in the anterior chamber, or change in the shape of the iris should warrant a consult with an ophthalmologist. The patient should also be inspected for asymmetry (proptosis or enophthalmos), corneal abrasions (fluorescein), nasal septum swelling/deviation, or clear rhinorrhea, which might be cerebrospinal fluid (CSF) that indicates a cribiform or basilar skull fracture. They should have their supraorbital ridge and frontal bone palpated for step-off fractures, and their hard palate and teeth palpated for stability. Evaluate the supraorbital, infraorbital, inferior alveolar, and mental nerve distributions for anesthesia. Finally, subcutaneous emphysema may indicate a rupture of the maxillary sinus. (26,29)

These patients may present with ecchymoses, enophthalmos of the globe (sunken eye), vertical dystopia (a change in vertical position of the pupil in relation to the unaffected side), or numbness in the area on the ipsilateral cheek supplied by the infraorbital nerve. Although a "black eye" was once felt to be a relatively benign injury for which medical attention was rarely sought, many instances of periorbital ecchymosis are due to orbit fractures.

Radiographically, routine facial views include Waters, Caldwell, and lateral projections. The Waters view is used for identifying inferior orbital rims, nasoethmoidal bones, and maxillary sinuses. The Caldwell projection provides the best view of the lateral rim and ethmoid bone. Lateral views may show air-fluid levels in the posterior maxillary sinus if the patient is lying supine. C-spine films are indicated if the patient complains of neck pain or if a suspected cervical injury cannot be ruled out. CT has replaced most conventional radiographs and is now the imaging tool of choice in patients with suspected blowout fractures. A CT scan with coronal views (done by tilting the patient's head in the CT ring or angling the CT ring) is the most useful for evaluating inferior and medial walls of the orbit to diagnose a blowout fracture. In patients without ocular injury or entrapment, a CT scan is not necessary, however it is still more useful and diagnostically superior to plain film radiographs. CT can also identify herniation of orbital fat or inferior rectus muscle into the maxillary sinus, foreign bodies, direct optic nerve involvement and the presence of retroocular edema or hematoma compressing the nerve. (26)

A forced duction test can determine if limitation of ocular movements is due to entrapped soft tissues or edema or contusion of a motor nerve or muscle. This is performed by anesthetizing the affected eye with topical anesthesia, grasping the sclera with a fine-toothed forceps at the level of the inferior rectus muscle and moving the eye in a superior/inferior direction. If the globe moves easily, entrapment is unlikely. In clinical practice, this test is only rarely performed since it is more convenient to merely wait to see if diplopia subsides with time. If the EOM normalizes, then management is non-surgical (EOM dysfunction is likely due to edema), while persistence of EOM dysfunction indicates the presence of muscle entrapment requiring surgical release. (30)

Depending on the extent of injury, consultation with ophthalmology, ENT, oromaxillofacial surgery, or plastic surgery may be warranted. Acetaminophen or narcotic analgesics can be used for pain. NSAIDs (non-steroidal anti-inflammatory drugs) are sometimes used, but these may cause bleeding, so it is preferable to avoid these especially if a hyphema is present. The consensus indications for early surgery (within 24 hours) include nerve incarceration, acute enophthalmos or hypoglobus (globe is displaced inferiorly), or extraocular muscle entrapment. In most other cases, surgeons wait 24-72 hours for reduction of edema but less than 14 days to avoid fibrosis. Blowout fractures without associated injuries do not require hospitalization. Even patients with signs of entrapment may be discharged home because most entrapment resolves as the swelling goes down. They should return if there is a change in visual acuity, increased pain, or flashing lights (suggests retinal injury). If entrapment continues for 2 weeks, surgical intervention may be needed. (26, 30)

A hyphema is a collection of red blood cells in the anterior chamber of the eye. This compartment is bounded by the cornea anteriorly, angle laterally, and lens and iris posteriorly. It normally contains and drains aqueous humor through the canal of Schlemm. Trauma is the most common cause of hyphema, often seen in baseball or hockey athletes where a blunt compressive force hits the globe causing tears in the vessels of the ciliary body, iris, and other structures in the anterior segment. Atraumatic causes of hyphema include microvascular disease such as diabetes causing retinal ischemia, carotid stenosis, iatrogenic (post-intraocular surgery), pupillary microhemangiomas, iritis, or intraocular tumors. Conditions that increase risk for developing a hyphema include neovascularization, leukemia, hemophilia, von Willebrand disease, sickle cell disease, and use of anticoagulants. The most common estimates of hyphema incidence are between 12 to 17 per 100 000, with the majority occurring in males. The majority of hyphemas occur in children and young adults. (31,32)

Hyphemas can be characterized as microhyphemas (RBCs detectable only under magnification) or macrohyphemas (visible even without the aid of a slit lamp). Corneal bloodstaining typically occurs after a prolonged hyphema and results from blood being forced into corneal endothelial cells. This is an serious sign and signifies the need for surgical evacuation of the hyphema. Increased intraocular pressure and secondary closed-angle glaucoma occurs secondary to RBCs and their blood products clogging the trabecular outflow meshwork. This occurs when the clot completely occludes the pupil/lens interface, blocking the flow of aqueous. (31,33)

Important historical information includes the mechanism of injury, type of assaulting object, whether protective eyewear was used, and past ocular history. The ocular examination should be certain to rule out a coexisting ruptured globe. A slit lamp examination should be performed to assess the presence of corneal abrasion. Visual acuity, pupillary reaction, extraocular movement, signs of corneal staining, and intraocular pressure are also important aspects of the examination. An exophthalmometer can be used to look for exophthalmos related to ocular trauma. CT should also be used in cases suspicious of open globe, foreign body, or orbital fracture. Ultrasound may be used after an open globe has been ruled out, as pressure from the probe may cause dangerous further extrusion of vitreous humor. (31)

Treatment includes both nonoperative and operative measures. Hyphemas are usually self-limited and resolve within one week. These cases can be managed by bedrest, elevation of the head at least 30 degrees to keep RBCs out of the visual field and trabecular outflow tract, and wearing eye shields. Bedrest in the first 2 to 5 days is crucial since rebleeding is a common complication during this period. Therefore, it is especially important to limit activities in infants and children who watch television or play video games. Watching television from a distance greater than 10 feet limits the amount of extraocular movement. In hyperactive children, bilateral patching may be required to minimize activity level. Anticoagulants and antiplatelet NSAIDs should be avoided to reduce the risk of rebleeding. Surgical intervention is indicated in cases unresponsive to medication, persistent high-grade hyphema, corneal bloodstaining, persistently elevated IOP, and uncontrolled glaucoma. (33)

Patients with concurrent elevation in intraocular pressure (IOP) may require both topical and oral ocular hypotensive medications since persistently elevated IOP can cause optic nerve damage. In general, patients with an IOP higher than 30 mmHg (or 24 mmHg in sickle cell patients) should receive IOP lowering medication. Carbonic anhydrase inhibitors and topical beta blockers decrease aqueous production and IOP. Osmotic diuretics decrease IOP by reducing vitreous volume. Cycloplegics and topical steroids, which treat associated iritis may also be used. Cycloplegics are anticholinergic agents that block the response of the iris sphincter muscle and ciliary body to cholinergic stimulation, causing paralysis of accommodation (cycloplegia) and pupillary dilation (mydriasis). Antifibrinolytics promoting hemostasis such as tranexamic acid and aminocaproic acid may be used to prevent recurrent hyphemas, but these medications may cause serious adverse effects. (33)

Prognosis depends on the size of the hyphema. Patients with a small-sized hyphema can be treated with conservative management and have a good prognosis. Total hyphema is difficult to treat and visual outcome is poor (31). Promoting public awareness in parents regarding eye safety for their children is important but often difficult, especially in adolescents when image is important.

Prevention of orbital and ophthalmic injuries includes wearing safety glasses or goggles in those who participate in high-risk sports in which balls, bats, or pucks are used.

Questions

1. Osgood-Schlatter disease commonly presents in athletes of which sports?
2. Describe the age and gender demographics of Osgood-Schlatter disease.
3. How common is it common to have Osgood-Schlatter disease in both knees?
4.What is the location of traction injury in Sever’s disease?
5. Name 3 interventions for Sever’s disease in addition to ice, NSAIDs, and rest.
6. What is the most common type of little league elbow?
7. What types of athletes are subject to Little League elbow besides baseball pitchers?
8. What is the mechanism of an orbital blowout fracture?
9. What is the best imaging technique to identify an orbital blowout fracture?
10. What populations are especially at risk of developing a hyphema?
11. What medications are commonly used to reduce elevated intraocular pressure?
12. What is the most severe complication of a hyphema and how can you prevent this?

References

1. Herring JA. Tachdjian’s Pediatric Orthopaedics. Sixth Edition. Elsevier; 2022.
2. Smith JM, Varacallo M. Osgood Schlatter Disease. In: StatPearls. StatPearls Publishing; 2022. Accessed May 17, 2022. http://www.ncbi.nlm.nih.gov/books/NBK441995/
3. Indiran V, Jagannathan D. Osgood-Schlatter Disease. N Engl J Med. 2018;378(11):e15. doi:10.1056/NEJMicm1711831
4. Seyfettino?lu F, Köse Ö, O?ur HU, Tuhanio?lu Ü, Çiçek H, Acar B. Is There a Relationship between Patellofemoral Alignment and Osgood-Schlatter Disease? A Case-Control Study. J Knee Surg. 2020;33(1):67-72. doi:10.1055/s-0038-1676523
5. Ogden JA, Southwick WO. Osgood-Schlatter’s Disease and Tibial Tuberosity Development. Clinical Orthopaedics and Related Research®. 1976;116:180-189.
6. Ogden JA, Hempton RF, Southwick WO. Development of the tibial tuberosity. The Anatomical Record. 1975;182(4):431-445. doi:10.1002/ar.1091820404
7. Neuhaus C, Appenzeller-Herzog C, Faude O. A systematic review on conservative treatment options for OSGOOD-Schlatter disease. Phys Ther Sport. 2021;49:178-187. doi:10.1016/j.ptsp.2021.03.002
8. Smith JM, Varacallo M. Sever Disease. In: StatPearls. StatPearls Publishing; 2022. Accessed May 17, 2022. http://www.ncbi.nlm.nih.gov/books/NBK441928/
9. Ramponi DR, Baker C. Sever’s Disease (Calcaneal Apophysitis). Adv Emerg Nurs J. 2019;41(1):10-14. doi:10.1097/TME.0000000000000219
10. Fares MY, Salhab HA, Khachfe HH, Fares J, Haidar R, Musharrafieh U. Sever’s Disease of the Pediatric Population: Clinical, Pathologic, and Therapeutic Considerations. Clin Med Res. 2021;19(3):132-137. doi:10.3121/cmr.2021.1639
11. Achar S, Yamanaka J. Apophysitis and Osteochondrosis: Common Causes of Pain in Growing Bones. Am Fam Physician. 2019;99(10):610-618.
12. Davison MJ, David-West SK, Duncan R. Careful assessment the key to diagnosing adolescent heel pain. Practitioner. 2016;260(1793):30-32, 3.
13. Hodge C, Schroeder JD. Medial Epicondyle Apophysitis (Little League Elbow). In: StatPearls. StatPearls Publishing; 2022. Accessed May 18, 2022. http://www.ncbi.nlm.nih.gov/books/NBK570592/
14. Mine K, Milanese S, Jones MA, Saunders S, Onofrio B. Risk Factors of Shoulder and Elbow Injuries in Baseball: A Scoping Review of 3 Types of Evidence. Orthop J Sports Med. 2021;9(12):23259671211064644. doi:10.1177/23259671211064645
15. Daruwalla JH, Daly CA, Seiler JG. Medial Elbow Injuries in the Throwing Athlete. Hand Clin. 2017;33(1):47-62. doi:10.1016/j.hcl.2016.08.013
16. Lee YY, Yang TH, Huang CC, et al. Ultrasonography has high positive predictive value for medial epicondyle lesions among adolescent baseball players. Knee Surg Sports Traumatol Arthrosc. 2019;27(10):3261-3268. doi:10.1007/s00167-018-5178-x
17. Stratchko L, Rosas H. Imaging of Elbow Injuries. Clin Sports Med. 2021;40(4):601-623. doi:10.1016/j.csm.2021.05.002
18. Bakshi NK, Inclan PM, Kirsch JM, Bedi A, Agresta C, Freehill MT. Current Workload Recommendations in Baseball Pitchers: A Systematic Review. Am J Sports Med. 2020;48(1):229-241. doi:10.1177/0363546519831010
19. Zabawa L, Alland JA. Association Between Parental Understanding of Pitch Smart Guidelines and Youth Baseball Player Injuries. Orthop J Sports Med. 2019;7(5):2325967119846314. doi:10.1177/2325967119846314
20. Mollah R, Fallahi AKM. Medial Epicondylar Elbow Fractures. In: StatPearls. StatPearls Publishing; 2022. Accessed May 19, 2022. http://www.ncbi.nlm.nih.gov/books/NBK558947/
21. Claessen FMAP, Louwerens JKG, Doornberg JN, van Dijk CN, Eygendaal D, van den Bekerom MPJ. Panner’s disease: literature review and treatment recommendations. J Child Orthop. 2015;9(1):9-17. doi:10.1007/s11832-015-0635-2
22. van Bergen CJ, van den Ende KI, ten Brinke B, Eygendaal D. Osteochondritis dissecans of the capitellum in adolescents. World J Orthop. 2016;7(2):102-108. doi:10.5312/wjo.v7.i2.102
23. Churchill RW, Munoz J, Ahmad CS. Osteochondritis dissecans of the elbow. Curr Rev Musculoskelet Med. 2016;9(2):232-239. doi:10.1007/s12178-016-9342-y
24. Looney AM, Rigor PD, Bodendorfer BM. Evaluation and management of elbow injuries in the adolescent overhead athlete. SAGE Open Medicine. 2021;9:20503121211003360. doi:10.1177/20503121211003362
25. Tamate TM, Garber AC. Curveballs in Youth Pitchers: A Review of the Current Literature. Hawaii J Health Soc Welf. 2019;78(11 Suppl 2):16-20.
26. Koenen L, Waseem M. Orbital Floor Fracture. In: StatPearls. StatPearls Publishing; 2022. Accessed May 20, 2022. http://www.ncbi.nlm.nih.gov/books/NBK534825/
27. Iftikhar M, Canner JK, Hall L, Ahmad M, Srikumaran D, Woreta FA. Characteristics of Orbital Floor Fractures in the United States from 2006 to 2017. Ophthalmology. 2021;128(3):463-470. doi:10.1016/j.ophtha.2020.06.065
28. Shumway CL, Motlagh M, Wade M. Anatomy, Head and Neck, Orbit Bones. In: StatPearls. StatPearls Publishing; 2022. Accessed May 20, 2022. http://www.ncbi.nlm.nih.gov/books/NBK531490/
29. Kim HS, Jeong EC. Orbital Floor Fracture. Arch Craniofac Surg. 2016;17(3):111-118. doi:10.7181/acfs.2016.17.3.111
30. Homer N, Huggins A, Durairaj VD. Contemporary management of orbital blowout fractures. Curr Opin Otolaryngol Head Neck Surg. 2019;27(4):310-316. doi:10.1097/MOO.0000000000000550
31. Gragg J, Blair K, Baker MB. Hyphema. In: StatPearls. StatPearls Publishing; 2022. Accessed May 24, 2022. http://www.ncbi.nlm.nih.gov/books/NBK507802/
32. Iftikhar M, Mir T, Seidel N, et al. Epidemiology and outcomes of hyphema: a single tertiary centre experience of 180 cases. Acta Ophthalmologica. 2021;99(3):e394-e401. doi:10.1111/aos.14603
33. Chen EJ, Fasiuddin A. Management of Traumatic Hyphema and Prevention of Its Complications. Cureus. 2021;13(6):e15771. doi:10.7759/cureus.15771

Answers to questions

1. Basketball, volleyball, sprinting, and gymnastics are common examples. Other activities with repeated jumping or running may also predispose athletes to Osgood-Schlatter disease.
2. Osgood-Schlatter disease commonly presents in older children or adolescents with male: female of 3:2. Females generally present at an earlier age (8-13 versus 10-16) due to earlier appearance of the secondary ossification center.
3. It is more common on the left, however, about 25% have it bilaterally.
4. Sever’s disease is a traction injury of the Achilles tendon insertion site on the apophysis of the os calcis (calcaneus).
5. Common interventions for Sever’s disease include heel cups, taping, and foot orthotics.
6. The term "little league elbow" is used to describe a group of pathologic entities in and around the elbow joint in young throwers secondary to overhead/overhand throwing. The most common form is medial epicondylar apophysitis.
7. Tennis serving, football quarterbacks, javelin throwers, volleyball spikers.
8. A direct blow against the eye without force against the rims increases intraorbital pressure, redirecting the pressure into the orbital walls.
9. CT scan, with special coronal views.
10. Patients with diabetes (due to neovascularization), those with coagulopathies (von Willebrand disease, hemophilia), and those with sickle cell disease are at higher risk of hyphema.
11. Carbonic anhydrase inhibitors, topical beta blockers, cycloplegics, and osmotic diuretics.
12. The most severe complication is a rebleed. Limiting physical activity in children within the first 72 hours is important. This includes bedrest, no television or video games, and bilateral eye patching.