Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter XIX.8. Sports Injuries
Brent K. Ogawa, MD
May 2003

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Osgood-Schlatter Disease

This is a 12 year old male soccer player who 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 a "bump" on both of his knees recently that is 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.

Examination is unremarkable with the exception of 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 good, 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 good. Varus and valgus stress tests are negative. McMurray, anterior drawer, Lachman, and posterior drawer tests are all negative.

Radiographs demonstrate moderate prominence of the tibial tuberosities bilaterally. There is mild soft tissue swelling. No evidence of fracture.

He is instructed to rest and apply ice massages to the area, focus on stretching his hamstrings, and to take acetaminophen. He is permitted to ambulate normally and jog briefly, but he must stop if any 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.


Traction apophysitis of the tibial tuberosity was first described independently by both Osgood and Schlatter in 1903 (1). This disease is usually seen in adolescents or older children 11-15 years of age, with a male to female predominance of 3:2 (2). Girls present earlier because the secondary ossification center of the tibial tuberosity appears 2 years earlier. Osgood-Schlatter is seen in children/teens who are very active in sports requiring strenuous quadriceps muscles such as basketball and volleyball. Jumping puts the most force on the quadriceps and the insertion of the patella tendon into the tibial tuberosity. Osgood-Schlatter is also common in running sports such as soccer, baseball and football, but less so than with the jumping sports. This disease is seen more often on the left side and 25% of patients have a bilateral appearance.

The exact etiology remains controversial, although repetitive trauma is the most widely accepted theory. Other less likely theories include avascular necrosis of the tibial tuberosity (although blood supply is abundant), infection (although patients are afebrile and without leukocytosis), and degeneration of the patella with heterotopic ossification (although histological studies show no tendon necrosis and normal tendon insertion) (2,3).

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 plate, 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 (patella tendon), calcaneus (Achilles tendon), etc. The cartilage growth plate of the apophysis is a weak spot which is susceptible to microseparation with trauma or overuse (pulling, traction). Anatomy of the tibial tuberosity starts at 12-15 weeks of fetal growth; however, there isn't a recognizable tibial tuberosity growth plate 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 plate (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 age 10-12. Therefore, because of its unique anatomy and vascular supply, combined with excessive pulling forces of the extensor mechanism, there is a failure of the secondary ossification center, ultimately leading to the disease.

The pain is localized to the anterior aspect of the proximal tibia over the tibial tuberosity. 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 have full range of motion. They may describe a dull ache exacerbated by jumping or stair climbing. Walking on flat surfaces does not cause pain. Patients may often have symptoms for 6-12 months prior to seeking medical attention. Although the tibial prominence may be highly indicative of Osgood-Schlatter in many cases, a full knee exam should be performed to rule out other intra-articular pathology.

Unless other pathology is suspected, radiographs of the knee are usually unnecessary, since this is largely a clinical diagnosis. In more severe cases, lateral radiographs of the knee will often show a decrease in homogeneity of the infrapatellar fat pad, soft tissue swelling, and a prominence/fragmentation of the tibial tuberosity.

The differential diagnosis includes acute stress fracture, contusion of the tibial tuberosity, prepatellar bursitis, and patellar tendonitis. Some have termed Osgood-Schlatter as a "tendonitis" of the patellar tendon insertion. Some consider the two terms, tendonitis and apophysitis to often be interchangeable. Other pathology may also be considered including osteomyelitis or tumor.

Despite the ominous sounding name, the end result is often the same with or without treatment; therefore, alleviating parental fear is important (2). Treatment is mainly symptomatic and involves reducing forceful use of the quadriceps, which equates to playing less, resting more during games and practices, and less jumping. Hamstring stretching, ice, and NSAIDs may be useful as needed. Corticosteroids are not used because subcutaneous atrophy and fat pad necrosis may occur. If the pain is severe, a knee immobilizer may be used to allow for both decreased tension over the patellar tendon by limiting extension. A cylinder cast was used in the past; however, a knee immobilizer is better because it allows for removal to prevent atrophy and stiffness, and allows the patient to shower. Surgery is rarely indicated. Being skeletally immature, these patients are at risk for subluxation of the patella, patella alta (high riding patella), nonunion of the bony fragment of the tibia, and premature fusion of the anterior part of the epiphysis leading to genu recurvatum (hyperextension of the knee). If patients remain symptomatic, surgery may be performed (rarely), usually after reaching skeletal maturity.

After acute symptoms resolve, gradual strengthening exercises of the extensor mechanism using isometric or short-arc terminal extension techniques should be performed. The use of knee pads to prevent reaggravation of contusions should be stressed to both patients and parents.

The prognosis for this disease is good with spontaneous healing usually occurring. As the disorganized ossification fuses with the beaklike portion of the epiphysis, symptoms diminish (4). Often patients decrease their activity voluntarily secondary to pain. Although the symptoms may decrease with activity reduction, local tenderness may persist. In the adult, a local prominence of the tibial tuberosity may remain; however, this is usually painless.


Sever's Disease

This is a 13 year old boy who 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 basketball season 2 weeks ago. The pain is a dull, 5/10 ache over his right heel that is worse with running, especially when running on the hardwood floor. 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. Birth and developmental history are unremarkable.

Examination is unremarkable except for his right lower extremity. He is comfortable 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.

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

He is diagnosed with Sever's disease. He is instructed to rest from 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 is placed in his right shoe, which he later reports helps to alleviate the pain. After 4 weeks, he focusses on stretching and strengthening exercises for his calves and hamstrings. He subsequently recovers and returns to his normal athletic function.


Sever's disease (calcaneal apophysitis), first described in 1912 by JW Sever, is inflammation of the open calcaneal growth plate (Achilles tendon insertion) secondary to traction on the apophysis of the os calcis by the Achilles tendon (5). This disease is commonly seen in children 8-13 years old and is more prevalent in runners, especially soccer and basketball players who play on hard or artificial surfaces, or football/baseball players who play with cleats which permit them to gain excess traction into the ground. The mechanics of this injury are similar to Osgood-Schlatter disease except that the major stress is running and pushing forward in Sever's, compared to jumping in Osgood-Schlatter's. 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 (6,7).

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 when stress on the Achilles tendon insertion is maximal. After a period of rest, symptoms commonly subside. Radiographs are not necessary, but if done, three views should be included: AP, lateral, axial (Harris views). Radiographs may show a sclerotic and fragmented calcaneal apophysis in severe cases, but most often, radiographs are normal. An open growth plate is present in Sever's patients, and symptoms usually subside as the growth plate achieves fusion/closure. Oblique views and CT may be necessary to identify occult fractures. Bone scanning may be useful to rule out a stress fracture (8).

The differential includes stress fracture, avulsion fracture of the calcaneus, Brodie's abscess, simple bone cyst, plantar fasciitis, or Achilles tendon rupture.

Treatment for this disease is mainly symptomatic. This includes rest from activity, 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. A posterior heel wedge 0.5 to 1.0 cm in height is recommended. By raising only the heel, tension is reduced on the Achilles tendon insertion site on the calcaneus. Shock absorbing insoles may also be used. Once acute symptoms have resolved, patients should begin stretching and strengthening exercises of the hamstring and calf muscles. Athletic activity can be gradually resumed. The exact time frame for resolution of symptoms varies. If conservative measurements fail after 6-8 weeks, a bone scan or other studies to seek more occult sources of pain should be considered.


Little League Elbow

This is a 13 year old right handed boy who 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 a lot during the week. He has complained of pain during practices, but has been told to continue practicing; "no pain, no gain." The pain is most severe over the medial aspect of his right elbow and does not radiate. He is able to do normal activities of daily living. His wrist and shoulder are unremarkable. His parents are concerned about him missing the All-Star game if he doesn't continue to perform at a high level.

Exam: His is exam is normal with the exception of his right elbow. No visible deformity, edema, or erythema. He is tender to palpation over the medial epicondyle. An elbow contracture of 15 degrees to full flexion is noted. He has full ROM about the shoulder and wrist. Sensation is intact. Upper extremity strength is good and sensation is intact. Perfusion, pulses and reflexes are all normal. Radiographs of his right elbow are obtained and show a minimally displaced right medial epicondyle fracture.

Despite initial apprehension, the patient and his parents decide to cease activity. Because there is minimally displacement (<2mm), a posterior splint is applied for 2 weeks. On return to the clinic, the patient reports improvement of his symptoms. The splint is removed and active range of motion exercises are taught. The patient continues these diligently. Six weeks later, after radiographic evidence of union, the patient is allowed to start a specific throwing program. He is back to pitch in the championships 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.


The term "Little League elbow" is used to describe a group of pathologic entities in and around the elbow joint in young throwers. The mechanism includes pitching, tennis serving, volleyball spiking/serving, football and javelin throwing. The syndrome is a result of a repetitive valgus stress during overhead throwing. This valgus stress results in lateral compression and medial traction on the elbow. The injury has expanded to include (9): 1) Medial epicondylar fragmentation and avulsion. 2) Delayed or accelerated apophyseal growth of the medial epicondyle. 3) Delayed closure of the medial epicondylar growth plate. 4) Osteochondrosis and osteochondritis of the capitellum. 5) Deformation and osteochondritis of the radial head. 6) Hypertrophy of the ulna. 7) Olecranon apophysitis with or without delayed closure of the olecranon apophysis.

The biomechanics of throwing are complex. The physical stresses associated with throwing produce exceptional forces in and about the elbow in the throwing athlete of any age. These forces include tension, compression, and shear localized to the medial, lateral, and posterior aspects of the elbow (10).
. . . . . 1. Tension overload of the medial elbow restraints: early and late cocking phases.
. . . . . 2. Compression overload on the lateral articular surface: early and late cocking phases.
. . . . . 3. Posterior medial shear forces on the posterior articular surface: late cocking and follow through phases.
. . . . . 4. Extension overload on the lateral restraints: acceleration phase.

A comprehensive history is important and should include age, handedness, activity level, sport played, and history of trauma. 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) (9).

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. Valgus stress of the elbow results 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 is fused and injuries tend to occur to muscular attachments and ligaments. The flexor muscles and ulnar collateral ligaments are often injured.

Examination should include both elbows looking for atrophy/hypertrophy, ROM, bony deformity, flexion contractures, and carrying angle. Also neurological and vascular exams with attention to the ulnar nerve should be performed.

Radiographs (AP, lateral, oblique) and comparison views are essential. Common findings include an immature elbow with elbow enlargement, fragmentation, and beaking or avulsion of the medial epicondyle. Lateral lesions usually involve the subchondral bone and manifest as osteochondrosis or osteochondritis dissecans (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. CT and MRI are also useful modalities.

The American Academy of Pediatrics and youth baseball organizations have made recommendations to reduce the risk of overuse elbow injuries in young athletes by providing leagues and coaches with guidelines limiting the number of pitches per day or per game, a young athlete can throw. It is far preferable to prevent these injuries, than it is to recover from these injuries. The onset of pain or swelling suggests the earliest onset of an injury. 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 elbow throwing stress for the remainder of the day once the onset of pain occurs.

Medial tension overload injuries are the most common and usually resolve within 4-6 weeks of rest, ice, and NSAIDs. After symptoms resolve, gradual return to throwing is allowed. If disability continues for an extended period of time, throwing should be disallowed until the next season.

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. In minimally displaced (<2mm) or non-displaced fractures, a single posterior splint for 1-2 weeks then progression to active ROM exercises is commonly used. When radiographic evidence of union is noted, a specific progressive throwing program is started. In moderately displaced fractures (>2mm) open reduction with internal fixation hardware is performed with early ROM exercises at 1-2 weeks to regain flexion and extension.

Medial ligament rupture to the ulnar collateral ligament 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. If the patient desires to continue throwing, surgical repair is needed. If the injury is detected early, conservative treatment including rest and alternating heat/ice is recommended.

Lateral compression injuries, such as Panner's disease (osteochondrosis), is a malady of the growth degeneration or necrosis of the capitellum and is followed by regeneration and recalcification. 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. Panner's usually affects a younger population and onset is acute with fragmentation of the entire capitellar ossific nucleus. There are no loose bodies and no late sequelae unlike osteochondritis dissecans. These patients are also younger. 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 are rare.

Osteochondritis dissecans (OCD) is a focal lesion of the capitellum occurring in 13-16 year olds. They present with elbow pain and a flexion contracture of greater than or equal to 15 degrees. OCD of the capitellum is secondary to the compressive forces occurring between the radial head and capitellum during throwing. Again, these patients are older than Panner's disease. The etiology of OCD in the elbow is unclear. Theories include ischemia, trauma, and genetic factors. These patients present with poorly localized, dull pain with decreased range of motion during extension with "locking and catching," also unlike Panner's disease. CT and arthroscopy are beneficial in determining the extent and size of the lesion. OCD lesions can be divided into three types: Type I) Intact with no displacement or fracture of the articular cartilage. Treatment includes rest, splinting 3-4 weeks if the pain is severe, followed by ROM exercises. Type II) Shows evidence of fracture or fissure of the articular cartilage. Determining the size and stability of the fragment is important. If the fragment is small, arthroscopic removal may be performed. If the fragment is large, arthroscopic pinning is necessary. Type III) Complete detachment with the fragment lying freely. Treatment includes either trying to reattach the loose fragment or removal. Pain may be relieved; however, there may be little improvement in ROM. These patients should be seriously counseled about the dangers of continued throwing and are urged to abstain.

Posterior extension and shear injuries are uncommon in young throwers but the incidence increases with age. These types of injuries can be divided by age. 1) Childhood: Osteochondrosis of the olecranon. Treatment includes rest and gentle ROM exercises. Flexibility and strengthening are initiated once acute symptoms subside. 2) Adolescents: Avulsion fragments and lack of apophyseal fusion. For avulsion fragments, treatment usually requires arthroscopic removal. If there is lack of apophyseal fusion, rest and immobilization can produce good results. 3) Young adults: Partial avulsion of the olecranon and osteophyte formation at the tip of the medial border of the olecranon. Partial avulsion of the olecranon requires surgical reattachment of the olecranon and triceps. Osteophytes should be removed to decrease pain and increase ROM.

In summary, overuse injuries to the elbow of young throwing athletes occur often. 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, keeping an accurate pitching count, predetermining a stopping point based on number of pitches thrown, and recognizing early warning signs and stopping once the pain starts. Although many of these injuries have been blamed on throwing curve balls, some studies have shown that a properly thrown curve ball causes no more injuries than the traditional fastball (11,12,13).


Orbital fracture/Hyphema

This is a 10 year old boy who presents to the ED with a chief complaint of a "black eye". He was playing in a roller hockey game when a hockey stick was swung high and struck him in the face. Although he was wearing a helmet, he was not wearing protective eyewear. He complains of severe eye pain and tenderness around his right eye. He states he is able to see out of his left eye, but not his right eye. There was no loss of consciousness or other associated injuries. He is able to walk in to the ED with his parents.

Exam: He is alert and cooperative in moderate discomfort. He has his right eye closed during most of the examination. A large area of ecchymosis is noted over the right periorbital region. The skin is intact with no active bleeding. He has severe tenderness over the inferior orbital region. There is moderate soft tissue swelling of the eyelids. He opens his eye with difficulty and apprehension. It is still difficult to see his eye because of the periorbital swelling. A small amount of blood is visible in the anterior chamber. He is able to sense light from the right eye, but his vision is blurry. Visual acuity is 20/50 in the right eye and 20/20 in the left eye. His EOMs are probably conjugate, but it is difficult to be certain because of the periorbital swelling. He does complain of some eye pain with EOM. Pupils are equal and reactive to light. Normal sensation to light touch over his right cheek is noted. Fluorescein examination shows no evidence of corneal abrasion. His left eye exam is unremarkable. The remainder of his face and head are without signs of injury.

It is decided not to order any plain film radiographs. A CT scan of the head with special views of the orbit is ordered, which shows a normal brain and skull. Coronal CT cuts show a fracture of the floor of the orbit with no muscle entrapment.

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 told 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 a narcotic analgesic and follow-up in 3 days. He recovers well with no diplopia or glaucoma complications. 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. Eye injuries can almost always be prevented with protective eyewear. Males are at higher risk for orbital fractures because of their increased incidence of trauma.

The aperture of the bony architecture surrounding the eye does not allow an object with a radius of greater than 5 cm to penetrate the globe (14). Fractures of the inferior rim are the most common. The thin orbital floor (maxilla) and the medial wall (ethmoid) are the weakest portions of the orbit. Internal wall fractures with or without bony rim fractures can occur. A direct blow to the bony rim may not cause a bony rim fracture, but can be enough to increase intraorbital pressures (as the globe is compressed) resulting in a "blowout fracture" of the weakest point of the orbital wall, which is usually the floor of the orbit.

Anatomically the orbit consists of 6 facial bones (14,15):
. . . . . 1. Frontal bone: superior orbital ridge and upper medial orbital ridge
. . . . . 2. Zygoma: lateral orbital rim
. . . . . 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

Related anatomical structures that can be injured during an orbital fracture include the optic nerve, periorbital fat, extraocular muscles, and the inferior orbital nerve.

The principle 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 patient should be questioned regarding epistaxis or clear fluid from nares or ears, loss of consciousness, visual problems, hearing problems, malocclusion, and facial numbness or tingling. Other specific questions regarding the eye include the presence of diplopia, painful eye motion (entrapment or periorbital edema), photophobia, flashes of light (retinal detachment), or blurred vision (hyphema, vitreous hemorrhage, retinal detachment) (14,16,17).

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 CSF. 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.

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 often not sought, many instances of periorbital ecchymoses are due to orbit fractures.

Radiographically, routine facial views include Waters, Caldwell, and lateral projections (14,15,16). 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.

Plain film radiographs have been largely replaced by CT scans. 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 may be helpful in identifying direct optic nerve involvement and the presence of retroocular edema or hematoma compressing the nerve.

A forced duction test can determine if limitation of ocular movements is due to entrapped soft tissues or to 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 (14). 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 function normalizes, then the EOM dysfunction is non-surgical (i.e., probably due to edema), while persistence of EOM dysfunction indicates the presence of muscle entrapment requiring surgical release.

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 are sometimes used, but these may cause bleeding, so it is preferable to avoid these especially if a hyphema is present. Tetanus prophylaxis may be indicated. 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; however, return if there is a change in visual acuity, increased pain, or flashing lights. If entrapment continues for 2 weeks, surgical intervention may be needed.

A hyphema is a collection of red blood cells in the anterior chamber of the eye. In the United States the incidence of hyphema occurs in 20/100,000 per year. Hyphema occurs more often in males (3:1) and is usually seen in a younger population, less than 30 years old (18). 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 ciliary body, iris, and other structures in the anterior segment. Other non-sports related causes of hyphema include microvascular disease such as diabetes causing neovascularization, retinal ischemia, carotid stenosis, or iatrogenic (post-intraocular surgery), sickle cell disease, pupillary microhemangiomas, iritis, or intraocular tumors.

Hyphemas can be divided into microhyphema (RBCs detectable by microscopy only) or macrohyphema (visible even without the aid of a slit lamp). Corneal bloodstaining results from blood being forced into corneal endothelial cells. It is an ominous sign and signifies the need for surgical evacuation of the hyphema. Intraocular pressure increases secondary to RBCs and their blood products clogging the trabecular outflow meshwork. Secondary angle-closure glaucoma resulting from pupillary block can occur. This occurs when the clot completely occludes the pupil/lens interface, blocking the flow of aqueous from the posterior to anterior chamber. People of African or Mediterranean descent are prone to sickle cell hemoglobinopathy and thus have a higher incidence of developing glaucoma due to the rigidity of RBCs causing slower passage through the trabecular meshwork and elevated intraocular pressure (18).

Historical data important to illicit include the mechanism of injury, type of assaulting object, whether protective eye wear was used, ethnic origin, and past ocular history. The ocular examination should be certain to rule out a coexisting ruptured globe. 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.

Treatment includes both operative and nonoperative measures. In patients without an increase in intraocular pressure, behavioral modifications begin with limiting activities such as reading, which cause rapid shifts in the globe. Within the first 72 hours, rebleed is most common, therefore, this is the crucial time when children may have to be bedrested. 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. Patching of the affected eye only, is not beneficial because movement of the contralateral eye will cause movement of the affected eye (18). In general, patients should keep activity to a minimum for at least the first 5 days to prevent a rebleed.

Patients with concurrent elevation in intraocular pressure (IOP) may require both topical and oral ocular hypotensive medications. Persistent elevated IOP can cause optic nerve damage. Topical beta blockers decrease aqueous production and IOP. Osmotic diuretics decrease IOP by reducing vitreous volume. In general, patients with an IOP higher than 30mm Hg (or 24mm Hg in sickle cell patients) should receive IOP lowering medication. 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 such as aminocaproic acid may be used to prevent recurrent hyphemas, but this medication may cause serious adverse effects. Carbonic anhydrase inhibitors decrease aqueous production and IOP.

Supportive treatment including wearing a metal shield or glasses is recommended. Head elevation keeps the central cornea and pupillary aperture free of blood. Patients should also avoid aspirin to prevent further bleeding.

The most severe complication is a rebleed (usually seen in the first 72 hours). Hyphema resulting from a rebleed is usually more extensive than the initial trauma. Rebleeding may present as a total hyphema with blood filling the entire anterior chamber. This is called an "8-ball" hyphema (18). Such a significant hemorrhage leads to elevated IOPs and corneal blood staining. Hemosiderin collects in the stroma causing a yellow appearance in the cornea. This usually resolves spontaneously in a few years. Glaucoma may lead to optic nerve atrophy. This is especially seen in sickle cell patients.

Prognosis depends on the size of the hyphema. Patients with a small-sized hyphema can be treated with simple management and have a good prognosis. Total hyphema is difficult to treat and visual outcome is poor. Promoting public awareness in parents regarding eye safety for their children is important but often difficult, especially in adolescents when image is important. Just as wearing a helmet in football is mandatory, wearing goggles in high-risk sports should become obligatory.

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. What is the definition of Osgood-Schlatter's disease?

2. Who is Osgood Schlatter disease and Sever's disease commonly seen in?

3. Is it common to have Osgood-Schlatter disease in both knees?

4. What is the definition of Little League elbow?

5. What types of athletes are subject to Little League elbow besides baseball pitchers?

6. What is a blowout fracture of the orbit?

7. What is the best imaging technique to identify a blowout fracture?

8. How can you reduce elevated intraocular pressure?

9. What is the most severe complication of a hyphema and how can you prevent this?


References

1. Stanitski L. Osgood-Schlatter Disease. In: Stanitski L etal (eds). Pediatric and Adolescent Sports Medicine, volume 2. 1994, Philadelphia: WB Saunders, p. 1953.

2. McMahon P, etal. Sports Medicine. In: Skinner H (ed). Current Diagnosis and Treatment in Orthopedics, 2nd edition. 2000, New York: McGraw Hill, pp.152-153.

3. Turtel A, Minkoff J, Simonson B. The Patella: Its Afflictions in Relation to Athletics. In: Harries M, et al (eds). Oxford Textbook of Sports Medicine, 2nd edition. 1998, Oxford: Oxford University Press, pp. 457-459.

4. Graf K, Noordsis P, Reider B. Disorders of the Patella Tendon. Reider B (ed). Sports Medicine in the School Age Athlete, 2nd edition. 1996, Philadelphia: WB Saunders, pp. 389-394.

5. Sever JW. Apophysitis of the Os Calcis. NewYork Med J 1912;95:1025-1029.

6. Bordelon R. Heel Pain. In: DeLee J, Drez D (eds). Orthopedic Sports Medicine. Principles and Practice, volume 2. 1994, Philadelphia: WB Saunders, p. 1953.

7. Brage M, Larkin J. Ankle, Hindfoot, and Midfoot Injuries. Reider B (ed). Sports Medicine in the School Age Athlete, 2nd edition. 1996, Philadelphia: WB Saunders, pp. 426-427.

8. Mann R, Mann J. Foot and Ankle Surgery. In: Skinner H (ed). Current Diagnosis and Treatment in Orthopedics, 2nd edition. 2000, New York: McGraw Hill, pp. 444-445.

9. Miller CD, Savoie FH. Valgus Extension Injuries of the Elbow in the Throwing Athlete. J Am Acad Ortho Surg 1994;2(5):261-266.

10. Guy J, Micheli L. Pediatric and Adolescent Athletics. In: Schenck R, et al (eds). Athletic Training and Sports Medicine, 3rd edition. 1999, Rosemont, IL: American Academy of Orthopedic Surgery, pp. 807-808.

11. McMahon P, et al. Sports Medicine. In: Skinner H (ed). Current Diagnosis and Treatment in Orthopedics, 2nd edition. 2000, New York: McGraw Hill, p. 172.

12. Thabit G. Elbow Injuries in the Young Athlete. Sports Med Arthoscopy Rev 1996;4:114.

13. Micheli LJ, Fehlandt AF. Overuse Tendon Injuries in Pediatric Sports Medicine. Sports Med Arthroscopy Rev 1996;4:190.

14. Widell T. Orbital Fractures. eMedicine Journal. June 1, 2001. Vol. 2, No. 6. http://prx.hml.org:2204/wc.dll?emedclass~displayTopic~&BookId=3&Topic=202&id=369&accttype=P

15. Brady S, et al. The Diagnosis and Management of Orbital Blowout Fractures: Update 2001. Am J Emerg Med 2001;19(2):147-154.

16. Brunette D. Ophthalmology. In: Marx J, et al (eds). Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th edition. 2002. St. Louis: Mosby, p. 909.

17. Dutton J. Orbit and Oculoplastics. In: Yanoff M, et al (etal). Ophthalmology, 1st edition. 1999, Philadelphia: Mosby, pp .2.2-2.4, 15.7-15.8.

18. Irak I, Pacuraru A. Glaucoma, Hyphema. eMedicine Journal. September 4, 2001. Vol. 2, No. 9. http://prx.hml.org:2204/wc.dll?emedclass~displayTopic~&BookId=8&Topic=142&id=369&accttype=P

19. Kuhn F, Mester V. Anterior Chamber Abnormalities and Cataract. Ophthalmol Clin North Am 2002;15(2):195.

20. Brunette D. Ophthalmology. In: Marx J, et al (eds). Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th edition. 2002, St. Louis: Mosby, pp. 912-913.

21. Berke S. Post Traumatic Glaucoma. In: Yanoff M, et al (eds). Ophthalmology. 1999, Philadelphia: Mosby, pp. 18.1-18.4.


Answers to questions

1. Traction apophysitis of the tibial tuberosity.

2. Osgood-Schlatter: Usually older children or adolescents with male: female of 3:2. Those who do forceful contraction of the quadriceps (jumping sports such as basketball and volleyball). Sever's: Athletes who play with cleats (excess grip in the ground) who push hard while running; also soccer and basketball players.

3. It is more common on the left, however, about 25% have it bilaterally.

4. 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 throwing. Valgus stress results in lateral compression and medial traction on the elbow leading to the many types of injuries described in the text.

5. Tennis serving, football quarterbacks, javelin throwers, volleyball spikers.

6. A direct blow to the bony rim causing enough of an increase in intraorbital pressures to fracture the thin interior bones (usually the orbital floor).

7. CT scan, with special coronal views.

8. Topical beta blockers, cycloplegics, osmotic diuretics, carbonic anhydrase inhibitors.

9. 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 videogames, and bilateral eye patching.


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