The trusted source for
healthcare information and
Sports-Related Injuries in Children and Adolescents
Author: Linton Yee, MD, FAAP, Associate Professor, Duke University School of Medicine, Department of Pediatrics, Division of Emergency Medicine, Durham, NC.
Peer reviewer: Carl Menckhoff, MD, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Medical College of Georgia, Augusta.
Virtually all children and adolescents participate in athletics or physical activity, whether it be on a highly competitive level or playground or backyard play. There are many well established benefits to athletic participation, among them being improved health, a sense of team and individual accomplishment, the promotion of self esteem, and the improvement and refinement of fine and gross motor skills.1,2 Despite the tremendous benefits of athletic participation, there are inherent risks to any athletic endeavor, whether the activity is organized or spontaneous. Additionally, because there are more children and adolescents participating in sports, there are, due to sheer numbers, more injuries. With the growing interest in extreme sports (such as skateboarding and motocross) and non-traditional sports (e.g., rock climbing), there are even higher risks involved than before. Because they are still growing and acquiring motor and cognitive skills, pediatric and adolescent athletes are at higher risk for injury than adult athletes. This article will focus on some of the more common and acute issues affecting the pediatric and adolescent athlete. This will include closed head trauma (specifically concussions), spinal cord injuries, and injuries to the axial and appendicular skeleton (shoulder, hip, knee, hand).
— The Editor
Sports have been divided into different groups based on the amount of contact involved or probability of contact.3 Collision sports such as football, ice hockey, rugby, martial arts, boxing, and rodeo involve a purposeful and forceful collision with another player or object (such as the ground). Sports like basketball and soccer are thought to involve less contact and force when there is a collision than that seen in football or ice hockey. At times it can be difficult to distinguish what is truly a contact or collision sport because of the amount of physical play involved.
There are estimates that in 2005-06 at least 7.2 million high school students participated in athletics, up from 4 million in the 1971-72 school year.4 High school athletes have been reported to account for around 2 million injuries, 500,000 physician visits, and 30,000 hospital admissions annually.5
In the 0-9 age group, bicycle and playground injuries, along with scooter and trampoline injuries, are common. In the 10-19 age group, football, basketball, and bicycle riding contribute to the majority of injuries in males, while basketball injuries are predominant in females. Males ages 10-14 have the highest rates of injury overall.6
It is thought that more than 3.5 million children age 14 and younger seek medical treatment for sports-related injuries each year.7 Most injuries occur during unorganized and informal activities, and result from a fall, collision, overexertion, or impact with an object. Death from sports-related activities are rare and is generally associated with brain injury. Sports in which a helmet is strongly recommended (bicycle riding, skating, and skateboarding) contribute to the majority of sports and recreational related head injuries.
In addition to the well known association of contact sports (such as football) with severe head trauma, baseball and softball were found to have a relatively high fatality rate, primarily as a consequence of head trauma.8
All traumatic sports-related injuries have the potential for significant morbidity. Therefore, primary attention must be directed to the establishment and maintenance of the airway, spinal immobilization, and evaluation of the cardiovascular system. Adherence to ATLS (Advanced Trauma Life Support), PALS ( Pediatric Advanced Life Support), and ACLS (Advanced Cardiac Life Support) protocols takes precedence before the assessment of any secondary injury. The player should be on supplemental oxygen; an airway should be established if necessary; intravenous access should be obtained; and, based on the mechanism, the player should be put in cervical spine immobilization with a collar and long backboard.
It has been estimated that in the United States pediatric and adolescent athlete population there are at least 300,000 head injuries each year,9,10 and approximately 20% of all reported pediatric head injuries are thought to be attributed to sports-related activities.11,12 The ultimate goal in the management of the head injured pediatric or adolescent athlete is to correctly assess and manage the patient. To do this, pertinent elements of the history and physical exam must be ascertained.
Sports such as football, rugby, ice hockey, soccer, baseball, softball, volleyball, boxing, martial arts, wrestling, surfing, skateboarding, and equestrian events have inherently higher risks of head injury. In the United States, organized sports such as football and ice hockey are well known to have a significantly higher incidence of head injury than other sports. Game conditions, as opposed to practice conditions, contribute to higher incidences of concussion, with the exception of volleyball or cheerleading.13
Head injuries can be the result of a direct blow to the head or a combination of rotational and translational acceleration.14
Acute trauma to the brain will result in either a focal injury (such as an epidural hematoma, a subdural hematoma, intraparenchymal hemorrhage, subarachnoid hemorrhage, or cerebral contusion) or diffuse damage (such as a concussion or diffuse axonal injury). Focal lesions require emergent care and intervention. The subdural hematoma is the most common focal brain injury and cause of sports-related fatalities; 87% of all football-related fatalities occur as a result of a subdural hematoma.13,14
Epidural hematomas, with their brief loss of consciousness followed by a lucid phase and subsequent decompensation, also are of significant concern. Diffuse axonal injury results from the shearing of white matter tracts from the cortex to brain stem.15,16
Concussion is the most common type of head injury in the pediatric and adolescent athlete. There are many definitions, with the American Academy of Neurology stating that a concussion is a trauma-induced alteration in mental status that may or may not involve a loss of consciousness.17 A concussion also has been described as a mild traumatic brain injury that is caused by an impact or jolt to the head or as an immediate and transient impairment of neural function due to mechanical force.18-20
Athletes may present with confusion, memory loss (anterograde and/or retrograde), alteration in mental status, decreased level of consciousness, headache, inability to process information, decreased attention span, and lack of coordination.
Common findings in a concussion include both somatic and behavioral changes. Headache, dizziness or balance problems, nausea and vomiting, a foggy or dazed sensation, visual or hearing difficulty, emotional lability, and fatigue often are seen.
Confusion and amnesia have been established as the most prominent and consistent features of a concussion and can be immediate or delayed in onset. The athlete will have an inability to maintain a cogent stream of thought or to carry out a sequence of tasks. He/she will not be able to readily concentrate on items and is easily distracted.
Physical exam may reflect an impaired level of consciousness with an altered Glasgow Coma Score, lack of balance or coordination, a history of post traumatic seizure, unsteady gait, sluggish response to questions or commands, slurred speech, poor concentration, a glassy stare, personality changes, and a decreased ability to play at the usual level.
The neurologic examination, with a focus on the mental status, is the key to assessing orientation, attention, concentration, and memory.10 Orientation includes time, place, questions about opponents, plays, teammates, and the circumstances of the injury. Concentration can be assessed by the patient's ability to recite numbers in reverse order. Memory can be tested by apprising the patient's ability to recall past opponents, what plays were called, or major news events or prominent people.
There are a number of classification schemes for concussions. Some focus on duration of confusion and post traumatic amnesia, while others emphasize a loss of consciousness.17,21,22 All grading scales agree that the hallmarks of a concussion are confusion and amnesia.
Loss of consciousness may be fairly simple to establish if there are multiple witnesses to the event. There is more difficulty in recognizing head injury in cases in which there is no loss of consciousness but rather a change in the level of alertness. The vast majority of head injuries, and therefore concussions, fall into this less defined category; 90% of concussions have no documented loss of consciousness but rather a transient period of post traumatic amnesia or loss of mental alertness.23
The common classification systems are presented in Table 1: Cantu classification system, Colorado Medical Society classification system, and the American Academy of Neurology classification system.
A more recent classification scheme has been proposed in which concussions would be categorized into simple or complex.24 Grading scales would not be used. The focus would be on combined measures of recovery to determine injury severity (and/or prognosis). (See Table 2.) In a simple concussion, the athlete would have suffered an injury that resolved without complication over a 7- to 10-day period. No further intervention would be required and the athlete could resume normal activities without consequence and would not require subspecialty follow-up. The key with simple concussions would be rest until all symptoms have resolved and then a graded program of exertion before a return to the sport. In a complex concussion, the athlete will have persistent symptoms (including symptom recurrence with exertion), specific injury (such as loss of consciousness over one minute), or prolonged cognitive impairment. This complex concussion group also includes those with multiple concussions or those who have repeated concussions with less force. More extensive testing is required in this group, along with subspecialty consultation.
Post Concussive Syndrome. With post concussive syndrome, there is a vast array of symptoms with a normal neurologic exam.
Athletes may have headaches, dizziness, visual complaints, fatigue, and difficulty sleeping, along with disrupted memory and concentration abilities. Further neuropsychologic evaluation should be undertaken, which may include imaging.
Second Impact Syndrome. The second impact syndrome is a rare condition in which an athlete sustains a second concussion before recovering completely from the first. This can lead to fatal brain swelling or permanent brain injury and can occur after apparently minor head trauma or, in some cases, no known history of trauma.25,26
It is thought that cerebral autoregulation is altered by the first injury, allowing cerebral edema to develop rapidly after a second relatively mild injury. Disruption of brain metabolism, with increased glucose demands and decreased cerebral blood flow, causes injury to some neurons and leaves others vulnerable to further injury.10
There are no nationally accepted guidelines regarding the management of sports-related concussions. No widely accepted standardized criteria exist for grading concussions, and difficulty in determining whether a player has sustained a concussion also has been an issue. There is great debate as to how many concussions are too many, and return-to-play parameters vary according to the classification system used to grade the concussion. (See Table 3.)
Spinal Cord Injuries
In all collision or contact sports there is a risk of spinal cord injury. In pediatrics, sports injuries are thought to be the second most frequent cause of spinal injuries, after motor vehicle accidents.27,28 By age 8, the pediatric athlete is very similar in proportion to an adult; therefore, spinal injuries become more common.29
A complete spinal cord lesion involves all of the tracts of the spinal cord with bilateral and equal neurologic deficits. Injuries with unequal deficits are known as incomplete spinal cord lesions. The incomplete lesions usually can be grouped into anterior cord, central cord, and Brown-Séquard syndromes.
The central cord syndrome is the most common incomplete spinal cord lesion; it results from a forced hyperextension injury. A concussion or contusion to the central region of the spinal cord is sustained when the ligamentum flavum is pushed into the spinal cord. The hallmark of this injury is weakness that is greater in the upper extremities than the lower extremities, with variable sensory loss.
The anterior cord syndrome is seen when there is damage to the anterior portion of the spinal cord from either a mechanical or vascular injury. Herniation of a disc, extension of bony fragments, and contusion to the cord, as well as injury to the anterior spinal artery all can cause damage to the anterior spinal cord.
Deficits include distal motor paralysis, loss of distal pinprick, pain, and temperature perception but preservation of vibration, pressure, light touch, and proprioception.
Brown-Séquard syndrome is a hemi-section of the spinal cord, usually from a penetrating lesion. The deficits include ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.
Spinal Cord Injury Without Radiographic Abnormality (SCIWORA). In SCIWORA, there are neurologic deficits with no radiographic abnormalities. It is thought that the mechanism of injury is due to the elastic nature of the juvenile spine, which allows for self reducing but significant intersegmental displacements when forced in flexion, extension, and distraction. Even though the vertebral column is not disrupted, the spinal cord is susceptible to injury; the injury pattern is seen in a much higher frequency in those younger than age 8.30,31 The initial clinical presentation predicts the eventual neurologic outcome. A significant injury will result in a poor prognosis, while moderate or minor injuries will have a good prognosis.
"Stinger" or "Burner"
Trauma to the neck or shoulder from a fall or collision can result in a stinger or burner. The injury causes stretching or compression of the upper trunk of the fifth and sixth brachial plexus nerve roots in the neck and shoulder. The hallmark is burning pain that radiates down an upper extremity, with associated numbness, tingling, and/or weakness.
Stingers are considered common injuries but there is no accurate data on the true incidence of the injury because many players don't report the injury to the training staff or physician.32-34 Stingers typically are seen in collision sports, especially in football, as the result of tackling another player. Injuries also are seen with other sports such as hockey, gymnastics, wrestling, and surfing, although not with the same frequency.
There are a number of ways in which a burner or stinger is sustained. Stretching of the brachial plexus will occur when the shoulder is depressed and the neck is laterally flexed away in the opposite direction. A percussive injury will be sustained when there is a direct blow to the supraclavicular fossa. Neck hyperextension and ipsilateral lateral flexion will cause nerve compression.35 The stretching mechanism tends to be seen more often in the younger athlete.
The key when evaluating this type of injury is to make sure that there is no cervical spine injury or more serious neurological injury. Stingers will involve only one upper extremity, while spinal cord injuries may involve multiple extremities. If there is cervical spine tenderness, bilateral extremity involvement, or lower extremity involvement, the player must be treated as if there is a possible cervical spine injury or spinal cord injury.
Examination may find the player favoring the affected extremity or shaking the extremity. There may be tenderness and spasm. Motor deficits can be seen in the muscles innervated by the C5 and C6 nerve roots (deltoid, supraspinatus, infraspinatus, biceps, pronator teres). Spurling's test involves passively hyperextending the neck and then laterally flexing the neck toward the involved side. If the axial load reproduces the symptoms, the test is considered positive.35
Imaging with plain films should be obtained in athletes when a fracture is suspected. MRI or CT scan can be done if the injury is thought to be more extensive.
The tingling, burning and loss of strength usually are transient, and, in most cases, will spontaneously resolve. Sometimes, however, complete resolution can take weeks or months. Rest, ice, nonsteroidal medications, and physical therapy may all be useful in the treatment of the stinger.
The shoulder consists of three bones: the clavicle, scapula, and humerus. In addition, there are a number of involved muscles, tendons, and ligaments. There are three joints in the shoulder: the glenohumeral joint, acromioclavicular (AC) joint, and sternoclavicular joint. Two of these, the glenohumeral and AC joints, enable movement. The shoulder has the most mobility of all the joints in the body, but this inherent mobility makes the shoulder highly susceptible to injury.
The glenohumeral joint is the focal point of the shoulder. This ball and socket joint is formed by the humerus and scapula. The rounded medial anterior humerus and the lateral dish shaped glenoid of the scapula are the points of articulation. The joint allows for circular movement of the arm and also allows the arm to hinge out, up and away from the body. The glenohumeral joint is encapsulated, with attachments to the scapula, humerus, and biceps head. Further reinforcement comes from the coracohumeral ligament and the glenohumeral ligaments.
The rotator cuff is comprised of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles and their associated tendons. The rotator cuff assists in keeping the humerus in the glenoid socket and reinforces strength and enhances mobility of the shoulder joint.
Examination of the shoulder involves visual inspection, palpation, and range-of-motion and neurovascular assessment. Both shoulders should be compared against each other for asymmetry. Tenderness on palpation of the AC joint suggests acromioclavicular injury. Range of motion in forward flexion, abduction, internal rotation, and external rotation must be evaluated.
Acromioclavicular Separation/Dislocation. Acromioclavicular separation/dislocation occurs when there is subluxation or dislocation of the AC joint.
This injury is usually the result of a fall onto an outstretched hand or direct trauma to the top of the shoulder or acromion, leading to misalignment of the distal clavicle with the acromion. Contact sports such as hockey, football, wrestling, and rugby have a high prevalence of these injuries.36-38 The pediatric and adolescent athlete will more likely fracture the clavicle rather than separate or dislocate the acromioclavicular joint.
The physical exam will be significant for tenderness with or without swelling over the AC joint. There also will be pain when lifting the arm. Elevation of the distal clavicle may be seen.
There are six grades for AC joint dislocation, based on the Rockwood classification. The first three types usually are considered nonoperative.37 The types are grouped according to ligament injury, joint capsule integrity, position of the clavicle, and damage to the trapezius and deltoid. In Type I injuries, the acromioclavicular ligaments are incompletely torn, the joint capsule is intact, and the coracoclavicular ligament and deltoid and trapezius remain intact. X-rays will be normal even with stress views. In Type II injuries, the acromioclavicular ligaments are torn; the joint capsule is injured, with slight detachment of the deltoid and trapezius; and the coracoclavicular ligament is sprained but still intact. Radiographs will show a misalignment of the inferior borders of the distal clavicle and the acromion process separated less than half of the diameter of the clavicle. Type III injuries involve tears of both the acromioclavicular and coracoclavicular ligaments, joint capsule damage, and detachment of the deltoid and trapezius, as well as dislocation of the AC joint and elevation of the clavicle. X-rays will show that the clavicle is separated by more than half of the diameter of the acromion process. When compared to the uninjured side, there will be widening of the AC and coracoclavicular (CC) joint spaces on AP (anteroposterior) views done with the patient standing, along with misalignment of the inferior border of the clavicle in relation to the inferior border of the acromion process.
Type IV, V, and VI involve larger ligament tears that can be associated with bayoneting or impalement through the trapezius, resulting in more instability of the clavicle.
Management of AC joint dislocations involves immobilizing the affected shoulder with a sling and referring Type II and III injuries for follow-up. Types IV, V, and VI often require surgical intervention.
Shoulder Dislocation. The shoulder is the most commonly dislocated major joint in the body. It usually occurs from direct trauma and can be seen with any sort of athletic activity ranging from football to surfing. The adolescent population has a higher frequency of dislocations when compared to the younger pediatric population, because the epiphyseal plates in the younger patient will fracture before dislocating.39
Anterior dislocations are by far the most common type of dislocation, representing approximately 95% of dislocations, with posterior dislocations representing 4%, and inferior dislocations (luxatio recta) 0.5%. Anterior dislocations are almost always the result of a traumatic injury, and are usually seen when there has been a fall on an externally rotated abducted arm or when there has been force in abduction, extension, and external rotation. There also may be a history of feeling the shoulder slipping out, followed by intense pain.40-44
In an anterior dislocation, the contour of the shoulder will appear squared off or flattened, with the acromion prominent and the humeral head palpable anteriorly. The arm will be in slight abduction and externally rotated, with the elbow flexed, and the forearm internally rotated. The humeral head will be palpable anteriorly. Abduction and internal rotation are extremely uncomfortable. Neurovascular assessment is essential with evaluation of the axillary nerve (as sensation over the deltoid may be affected) and evaluation of pulses.
Radiographs of the shoulder typically are anterior posterior views and lateral views in internal and external rotation and either an axillary or scapular Y-view. In an anterior dislocation the humeral head most often is in the subcoracoid position. The scapular Y view will demonstrate the humeral head anterior to the Y, and the axillary view will show it displaced anteriorly off of the glenoid. AP views may show a Hill-Sachs lesion, which results when the edge of the glenoid causes an impaction fracture to the posterolateral aspect of the humeral head. MRI can show a Bankart lesion, which may cause shoulder instability because of an anterior labral tear.
Reduction of Shoulder Dislocations. To reduce a shoulder dislocation, pain management and relaxation are essential. Conscious sedation with various agents can help to relax the patient and improve the chances of a successful procedure.
Stimson's Method. The patient is prone with the dislocated arm hanging over the side of the bed. Traction is applied above the wrist or above the elbow by another person or freely suspended weights can be attached to the wrist. As the muscles of the shoulder relax, reduction will take place.
Traction — Countertraction. The patient is supine and axial traction is applied to the arm with a sheet wrapped around the forearm and the elbow bent at 90 degrees. Another person applies countertraction using a sheet wrapped under the arm and across the chest while the shoulder is gently rotated internally and externally to disengage the humeral head from the glenoid.
External Rotation. With the patient supine or upright, stabilize the elbow against the trunk. Adduct the arm, and with the elbow flexed at 90 degrees, gradually rotate the arm externally.
Scapular Rotation. With the patient prone, use manual traction or place hanging weights on the wrist. Rotate the inferior tip of the scapula medially and the superior aspect laterally.
Management. Following successful reduction, arrangements for orthopedic follow-up should be done within 1 week. The patient should remain in a shoulder immobilizer or with a sling and swathe until orthopedic follow-up, and be cautioned not to remain immobilized for longer due to the risk of adhesive capsulitis. The patient should avoid abduction and external rotation of the arm.
A hip pointer is the result of blunt trauma from either a fall or direct blow to the iliac crest. There can be a contusion to the iliac crest, the greater trochanter of the femur, or to the surrounding soft tissue, virtually always with a history of acute injury. A hip pointer can occur in almost any sport in which blunt trauma to the hip can be sustained. It is seen with greater frequency in collision sports, such as football and ice hockey, but also can occur in basketball, volleyball, soccer, and gymnastics, among others.45-47
As with any injury to the pelvic region, assessment for blunt abdominal trauma must be a priority. Edema or ecchymosis can be present in the affected area. Tenderness over the iliac crest or greater trochanter can be elicited, and range of motion can be limited as a result of pain and discomfort. Sensation will be intact, although examination of motor strength and gait may be limited due to pain.
X-rays of the hip and pelvis can be obtained if there is a suspicion of fracture. Additionally CT imaging of the abdomen and pelvis can be performed if associated intraabdominal injuries are suspected.
Treatment involves rest, ice, anti-inflammatory and pain medications, as well as crutches and weight bearing as tolerated.
Knee injuries are some of the most common sports-related injuries presenting to the emergency department. Damage can occur to the bony structures comprising the knee, as well as the ligaments, muscles, tendons, or menisci.
The knee joint is the largest joint in the body and is one of the most susceptible to injury. Significant force vectors and stressors are placed on this joining point of the tibia and femur where there is minimal bony protection. Movement can be in extension, flexion, and slight rotation.
The tibiofemoral articulation and the patellofemoral coupling form the joints of the knee. The primary articulation points of the knee are the femoral and tibial condyles, with opposing condyles of the femur and tibia supporting weight bearing forces. The lateral meniscus and a smaller and more fixed medial meniscus are located between the tibia and femur. They form the largest synovial joint in the body and the menisci serve to enhance the articulation areas and assist in lubrication and cushioning of the joint.48-53
The medial collateral ligament (MCL) and the lateral collateral ligament (LCL) provide stability to the sides of the knee joint. These ligaments are extra capsular, with the MCL preventing extreme abduction and valgus forces and the LCL limiting adductive and varus stresses. Stabilization of the front of the knee is provided by the anterior cruciate ligament (ACL), by limiting anterior movement of the tibia on the femur The posterior cruciate ligament (PCL) provides posterior stability and prevents the tibia from shifting posteriorly on the femur.
The extensor apparatus is formed by the quadriceps muscles and it envelopes and stabilizes the patella. Distally, the quadriceps consolidates into the patellar ligament and then inserts into the tibial tubercle.
The prepatellar, superficial, and deep infrapatellar and pes anserinus bursae envelop the knee and permit friction-free movement between structures.
Physical Examination. Exam of the knee includes assessing the general appearance and evaluating for tenderness and range of motion. Visual inspection must include looking for ecchymosis, erythema, edema, and loss of landmarks, as well as the presentation of the knee in a resting position. Palpation of the bony structures and soft tissues is then performed. Tenderness should be assessed along the joint line, patella, femur, and tibia, as well as along the quadriceps and patellar tendons. Range of motion also must be evaluated. Normal flexion is 125-135 degrees and normal extension is 0 to 5-15 degrees above the horizontal plain. Neurovascular status also must be evaluated.
Evaluation of the Anterior Cruciate Ligament (ACL).ACL tears are the most severe of the knee injuries.54-56 An ACL tear can occur alone or in conjunction with a meniscal injury or a MCL tear. There is immediate and severe pain and the patient is not able to ambulate. The usual mechanism is twisting on a hyperextended knee. Female athletes have been noted to have an increased risk of sustaining ACL injuries.57
The three tests used to evaluate the ACL are the Lachman test, anterior drawer test, and MacIntosh test (pivot shift test).
The Lachman test is the most sensitive test for ACL rupture.49 The patient is placed supine, with the affected knee in 10 to 20 degrees of flexion. One hand stabilizes the distal femur. The other hand holds the posterior aspect of the proximal tibia just below the popliteal fossa, with the thumb over the anterolateral joint line. The proximal tibia is pulled anteriorly, with any laxity or displacement with anterior force being considered a positive test.
In the anterior drawer test, the patient is placed supine with the hips flexed at 45 degrees, the knee flexed at 90 degrees, and feet flat on the surface. With the affected leg's foot anchored in place, grasp the lower leg above the calf with both hands and pull firmly forward (anterior). Laxity in the anterior plane suggests a ruptured ACL. The pivot shift test or MacIntosh test also assesses ACL injury. In this test, the patient is placed in the supine position, with the injured knee extended and the affected tibia rotated internally. With valgus stress to the proximal tibia of the injured knee, the knee is then flexed. Any "clunk" felt at 30 degrees of flexion is considered a positive test.
Evaluation of the Posterior Cruciate Ligament (PCL). PCL tears usually are seen when there is direct trauma to the anterior region of the knee or if there is a fall onto a flexed knee. There are generally associated injuries to the knee. A significant valgus force will create the "terrible triad" consisting of a MCL tear, an ACL tear, and meniscus injuries.
In the posterior drawer test, with the patient supine and the hips flexed at 45 degrees, the injured knee is flexed 90 degrees. Posterior force is applied to the tibia. Any posterior translation indicates PCL injury.
The posterior sag sign also indicates PCL injury. The patient is placed supine with the hips flexed at 45 degrees and the knee at 90 degrees. The lateral view may show posterior translation of the tibia on the femur if there is a PCL injury and the tibial plateau may drift below the plane of the patella.
With the PCL sulcus test the patient will sit and have the knee at 90 degrees and hanging over the edge of the chair. There may be a widened space palpated between the tibial plateau and the femur if there is a PCL injury.
Evaluation of the Collateral Ligaments. Valgus stress tests will assess the integrity of the medial collateral ligaments (MCL), and varus stress tests will evaluate the lateral collateral ligaments (LCL). With the patient supine, the injured leg is allowed to hang over the table edge. The knee is then evaluated in full extension (0 degrees) and in 30 degrees of flexion. The lower thigh is stabilized with one hand and stress is then applied to the ankle or foot region in a gentle rocking motion. If there is laxity at 30 degrees with valgus force, then there is a MCL injury; if there is laxity at 0 degrees, there is a combined MCL and ACL/PCL injury. With varus or medial force, laxity at 30 degrees suggests LCL injury and at 0 degrees, a combined LCL and ACL/PCL injury.
Evaluation of the Meniscus.Meniscal injuries are the most common knee injuries. They will occur with twisting injuries in which there is rotation of the tibia with the knee in flexion or extension. There may be a history of an immediate painful sensation or there can be an intermittent or a locking sensation. An effusion with localized pain to the meniscus also can be present, as well as an associated ACL tear.
McMurray's test will evaluate for meniscal injury. With the patient supine, the hips are flexed to 45 degrees and the knee is flexed to 45 degrees. Holding the knee (along the medial joint line) and the ankle, varus or valgus force is applied to the flexed knee with internal or external rotation. The leg is then slowly extended. Valgus stress and external rotation will assess the medial meniscus. Varus stress and internal rotation will evaluate the lateral meniscus. A McMurray's test is considered positive if there is tenderness along the joint line or if a click is heard or palpated during the performance of the exam. The sensitivity of this test ranges from 26% to 58%, with the test specificity ranging from 59% to 94%.49
Apley's compression test also is used in the evaluation of meniscal injuries. The patient is placed prone with the affected knee flexed at 90 degrees. Pressure is then applied to the heel, compressing the tibia into the femur. The tibia is then rotated internally and externally. If pain is elicited or if there is a popping sensation, this is considered a positive test for meniscal injury.
The sports-related ankle injury is probably the most common injury overall, with ankle sprains comprising 20-30% of all sports-related musculoskeletal injuries.58-60 Ankle sprains, which usually involve the lateral or medial aspects, or tibiofibular syndesmosis, account for up to 85% of all ankle injuries.61 Inversion injuries comprise the 85% of ankle injuries, eversion injuries comprise 5% and combined injuries 10%.
In the pediatric population, the growth plates in the ankle, primarily the distal fibular physis, are more prone to injury than the ligaments.62 Pre-adolescents will sustain fractures more often than sprains because the growth plates are weaker than the ligaments. After the growth plates start to close in the adolescent and bones become stronger than ligaments, sprains become more common than fractures. Because the ankle is involved with an athlete's ability to pivot, jump, and run, sports such as basketball, volleyball, football, soccer, and gymnastics have a high incidence of injuries. In an older pediatric patient, landing on a plantar flexed and inverted foot is a common scenario for a lateral ankle sprain.
The ankle joint includes the talus, tibial plafond, medial malleolus, and the lateral malleolus. The mortise is made of the distal tibia and lateral malleolus. Movement planes include flexion, extension, internal rotation with plantar flexion, and external rotation with dorsiflexion.
There are five major ligaments in the ankle. The anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL) are located laterally. The superficial and deep deltoid ligaments are on the medial side and connect the distal tibia with the talus, calcaneous, and the navicular bones. The ATFL is the weakest ligament and the deltoid is the strongest, with the ATFL and CFL being the most frequently injured ligaments.
The physical exam consists of inspection, palpation, and assessment of range of motion. When comparing the injured ankle to the uninjured side, attention should be paid to skin color and temperature, as well as to bruising, swelling, and tenderness. A joint effusion can hide the soft tissue landmarks around the ankle joint, while soft tissue swelling without a joint effusion usually preserves the soft tissue landmarks.60 Deficits in range of motion as well as in the ability to bear weight and ambulate will exist. Neurovascular testing should include evaluation of sensation, motor weakness, capillary refill, and pulses.
The anterior drawer test is used to evaluate the anterior talofibular ligament. The patient is seated with the knee flexed at 90 degrees and the ankle in slight plantar flexion. The anterior tibia is stabilized by one hand immediately above the ankle, while the other hand grasps the posterior heel. The foot is pulled in an anterior plane to assess the movement of the talus in an anterior direction. When compared to the unaffected side, the relative translation of the foot forward from 3 mm to 5 mm is consistent with a sprained ATFL.
In the inversion stress test or talar tilt test, the heel is held and the ankle is inverted. If there is increased laxity when compared to the unaffected side or if there is a palpable or audible "clunk," this is suggestive of injury to the ATFL (plantar flexion) or the CFL (dorsiflexion).
Ankle sprains are graded from I to III (the West Point Ankle Sprain Grading System). In a Grade I sprain, there is stretching of the ligament. Swelling and bruising are mild to moderate, loss of function is minimal, there is no instability, and weight bearing occurs with minimal difficulty. A Grade II sprain is consistent with a partial tear. There is moderate to severe swelling and bruising, moderate loss of function and mobility, moderate instability, and difficulty with weight bearing. A Grade III sprain results in a complete ligament tear, with severe swelling and bruising, near complete loss of function and range of motion, severe instability, and an inability to bear weight.
The Ottawa ankle rules are well accepted in the adult population. They provide almost 100% sensitivity, a high specificity, and reduce the number of unnecessary X-rays performed.63 While the Ottawa ankle rules were not designed for the pediatric population, there have been studies showing that the rules can be extrapolated to the pediatric population,64-66 with a tendency to image younger pediatric patients more often than older pediatric patients. The Ottawa rules require X-rays if there is pain in the malleolar zone along with bone tenderness at the posterior tip of the lateral malleolus or medial malleolus or if there is an inability to bear weight immediately after the injury or for four steps when the patient is initially evaluated.
Treatment of ankle sprains is fairly standard, and includes protection, rest, ice, compression, and elevation.
Splinting or casting will offer protection, with weight bearing as tolerated. Rest is essential to decrease the risk of further injury. For the first 24 hours, ice should be applied for 15-20 minutes every 2-3 hours. NSAIDs can be used for pain and help in decreasing inflammation. Compression can be done with an elastic wrap or with splinting. Elevation above the level of the heart will help decrease swelling.
Fractures should be splinted and referred to orthopedics.
Injuries to the fingers can result in damage to bone, tendons, or ligaments. Dislocations, which generally involve a dorsally displaced proximal interphalangeal (PIP) joint, can be reduced if there is no evidence of neurovascular compromise or marked angulation. Dislocations in a volar plane may require orthopedic consultation.67-69 Sprains (no evidence of fracture or dislocation) can be treated conservatively with splinting and follow-up.
Mallet Finger. A mallet finger is caused by an extensor tendon jamming injury at the distal interphalangeal (DIP) joint resulting in no active extension of the distal phalanx. This is the most common closed finger tendon injury.69 With the DIP in extension, forced flexion by an object, such as a baseball, basketball, or volleyball, will make the distal tip of a finger traumatically bend in flexion; this causes injury to the extensor tendon at the DIP joint. (See Figure 1.) The damage to the extensor tendon can range from a complete tear with avulsion fracture of the distal phalanx (approximately one-third of patients) to a partial tear or stretching. The middle finger is the most frequently injured digit.70
The patient will have tenderness and edema to the dorsal aspect of the DIP joint and will not be able to extend or straighten the finger at the DIP joint. Isolation of the DIP joint during the exam will confirm that the extensor tendon is involved.
Treatment will involve splinting the affected finger in a full-time extension splint across the DIP joint, and referring the patient for orthopedic consultation, especially if there is an associated avulsion fracture or if there is no passive extension at the DIP joint. If untreated, a swan neck deformity can develop.
Jersey Finger. Injury to the flexor digitorum profundus tendon resulting in no active extension at the DIP joint is known as a jersey finger. When the DIP joint is in active flexion, it is forced into extension This usually happens in sports in which tackling has a prominent role (football, rugby) and occurs when a finger gets caught in the jersey or clothing of another player. The ring finger is injured in about 75% of cases.71
Examination of the hand will be remarkable for tenderness and edema over the volar aspect of the DIP joint. The injured finger will be in extension. To assess the injured finger, evaluation of the flexor digitorum profundus and superficialis tendons must be completed. To evaluate the profundus tendon, hold the metacarpophalangeal (MCP) and PIP joints in extension and have the patient flex at the DIP joint. There will be no movement at the DIP joint if there is damage to the profundus tendon. To assess the superficialis tendon, the unaffected fingers should be held in extension and the patient should then attempt to flex the injured finger. If there is superficialis tendon injury, there will be no movement.68,72
This injury should be splinted in flexion and orthopedic or hand consultation should be obtained within seven days as all are considered surgical candidates and prognosis is compromised if there is a delay in treatment or if the tendon is retracted.
Boutonniere Deformity. A boutonniere deformity can result from damage to the central slip extensor tendon. The PIP joint is forcibly flexed or is the subject of an axial load when in active extension; this causes disruption of the central slip extensor tendon. Additionally, a laceration over the joint or a volar dislocation of the PIP can result in this injury.
The PIP joint often will be in flexion, with tenderness and edema to the PIP joint and dorsum of the middle phalanx. There is generally no active extension at the PIP joint and there is hyperextension at the DIP joint.
If no boutonniere deformity exists acutely, maximal tenderness over the central slip at the dorsal PIP may be the only clue to injury. The patient might still be able to extend the PIP acutely due to the lateral bands.
Management should include splinting of the PIP joint in extension with the DIP free, and orthopedic follow-up.
Skier's Thumb. Trauma to the ulnar collateral ligament of the thumb will result in instability to the MCP joint.
Originally described as gamekeeper's thumb, this injury was the result of the repetitive motion of wringing the necks of game birds. The repetitive motion led to chronic stretching or tearing of the ulnar collateral ligament, with subsequent instability of the first MCP joint. Injuries are now more often the result of acute events, with skiers, football, basketball, hockey, and lacrosse players among those at risk.70
The prevalent mechanism of injury is the forceful radial deviation of the thumb. There can be a partial or complete tear of the ulnar collateral ligament depending on the forces involved. The history often will reflect a fall or a forced abduction of the thumb by a stick or ball. Patients also will have pain along the ulnar MCP joint and may complain of weakness or difficulty in generating pincer or grasp movements.
Physical exam may show edema, tenderness, and bruising to the MCP joint, primarily over the ulnar aspect. Significant bruising and swelling suggest severe ligament damage. Tears to the ligament usually occur distally, at the insertion of the ligament into the proximal phalanx, but also can occur proximally, at the origin at the metacarpal head.67-69 Assessments for strength involving pinching and grasping will show weakness.
Imaging studies always should include plain radiographs to evaluate for fracture or joint subluxation. An avulsion fracture of the volar base of the proximal phalanx is commonly associated with ulnar collateral ligament injuries.73 Incomplete lesions can be splinted, while complete lesions may require operative repair.
Athletic injuries in the pediatric and adolescent population are very common and can vary greatly. Many of the injuries are similar to those of the adult population; however, many have unique characteristics and more vigilant precautions should be taken with the pediatric and adolescent athlete because of their continued development and growth.
1. World Health Organization. Move for health: benefits of physical activity. Geneva, Switzerland: World Health Organization; 2006.
2. CDC. Guidelines for school and community programs to promote lifelong physical activity among young people. MMWR Morbid Mortal Wkly Rep 1997;46(RR-6);1-36.
3. Committee on Sports Medicine and Fitness. American Academy of Pediatrics: Medical conditions affecting sports participation. Pediatrics 2001;107:1205-1209.
4. National Federation of State High School Associations (NFHS). 2005-2006 High School Athletics Participation Survey. Indianapolis, IN: NHFS; 2006.
5. Comstock RD, Knox C, Yard E, Gilchrist J. Sports-related injuries among high school athletes—United States, 2005-06 school year. MMWR Morbid Mortal Wkly Rep 2006;55:1037-1040.
6. Gotsch K, Annest JL, et al. Nonfatal sports- and recreation-related injuries in treated in the emergency departments—United States, July 2000-June 2001. MMWR Morbid Mortal Wkly Rep 2002;51:736-740.
7. National SAFE KIDS Campaign (NSKC). Sports injury fact sheet. Washington, DC: NSKC; 2004.
8. Committee on Sports Medicine and Fitness. American Academy of Pediatrics: Risk of injury from baseball and softball in children. Pediatrics 2001;107:782-784.
9. Poirier MP, Wadsworth MR. Sports-related concussions. Pediatr Emerg Care 2000;16:278-283.
10. Perriello VA, Barth JT. Sports concussions: coming to the right conclusions. Contemp Pediatr 2000;2:132-139.
11. American Academy of Pediatrics, Section on Sports Medicine and Fitness. Guidelines for Pediatricians: Head injuries. Sports Shorts 2000;1:1.
12. The management of minor closed head injury in children. Committee on Quality Improvement, American Academy of Pediatrics. Commission on Clinical Policies and Research, American Academy of Family Physicians. Pediatrics 1999;104:1407-1415.
13. Schulz MR, Marshall SW, Mueller FO, et al. Incidence and risk factors for concussion in high school athletes, North Carolina, 1996-1999. Am J Epidemiol 2004;160:937-944.
14. Chorley JN. Sports-related head injuries. Curr Opin Pediatr 1998;10:350-355.
15. Penney DW, Perkin RM. Sports-related head injuries: learn the rules of this serious game. Pediatr Emerg Med Reports 2003;8:71-82.
16. Wojtys EM, Hovda D, Landry G, et al. Concussion in sports. Am J Sports Med 1999;27:676-687.
17. Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 1997;10:350-357.
18. Landry GL. Central nervous system trauma management of concussions in athletes. Pediatr Clin N Am 2002;49:723-741.
19. Warren WL Jr, Bailes JC. On the field evaluation of athletic head injuries. Clin Sports Med 1998;17:13-26.
20. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology 1997;48:575-580.
21. Cantu RC. Guidelines for return to contact sports after a cerebral concussion. Phys Sportsmed 1986;14:75-83.
22. Colorado Medical Society. Report of the Sports Medicine Committee: Guidelines for the Management of Concussion in Sports (revised). Denver: Colorado Medical Society; 1991:1.
23. Cantu RC. Second-impact syndrome. Clin Sports Med 1998;17:37-44.
24. McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med 2005;15:48-55.
25. Cantu RC, Voy R. Second impact syndrome. A risk in any contact sport. Phys Sportsmed 1995;23:27-36.
26. Proctor MR, Cantu RC. Head and neck injuries in young athletes. Clin Sports Med 2000;19:693-715.
27. Browne GJ, Lam LT. Concussive head injury in children and adolescents related to sports and other leisure physical activities. Br J Sports Med 2006;40:163-168.
28. Beattie LK, Choi J. Acute spinal injuries: assessment and management. Emerg Med Practice 2006;8:1-28.
29. Brown RL, Brunn MA, Garcia VF. Cervical spine injuries in children: a review of 103 patients treated consecutively at a level 1 pediatric trauma center. J Pediatr Surg 2001;35:1107-1114.
30. Viccellio P, Simon H, Pressman BD, et al. A prospective multicenter study of cervical spine injury in children. Pediatrics 2001;108:E20.
31. Pang D, Wilberger JE Jr. Spinal cord injury without radiographic abnormalities in children. J Neurosurg 1982;57:114-129.
32. Sallis RE, Jones K, Knopp W. Burners: offensive strategy for an underreported injury. Phys Sportsmed 1992;20:47-55.
33. Markey KL, Di Benedetto M, Curl WW. Upper trunk brachial plexopathy. The stinger syndrome. Am J Sports Med 1993;21:650-655
34. Hershman EB. Brachial plexus injuries. Clin Sports Med 1990;9:311-329.
35. Kuhlman GS, McKeag DB. The "burner": a common nerve injury in contact sports. Am Fam Physician 1999;60:2035-2042.
36. Clarke HD, McCann PD. Acromioclavicular joint injuries. Orthop Clin North Am 2000;31:177-187.
37. Dumonski M, Mazzocca AD, Rios, et.al. Evaluation and management of acromioclavicular joint injuries. Am J Orthop 2004;33:526-532.
38. Simon RR, Koenigsknecht SJ, eds. Emergency Orthopedics: The Extremities. 3rd ed. Norwalk, CT: Appleton and Lange; 1995:387-389.
39. The shoulder. In: Netter's Concise Atlas of Orthopaedic Anatomy. Thompson JC, ed. Philadelphia, PA: Elsevier; 2002:43-64.
40. Riebel GD, McCabe JB. Anterior shoulder dislocation: a review of reduction techniques. Am J Emerg Med 1991;9:180-188.
41. Westin CD, Gill EA, et al. Anterior shoulder dislocation: a simple and rapid method of reduction. Am J Sports Med 1995;23:369-371.
42. McNamara RM. Reduction of anterior shoulder dislocations by scapular manipulation. Ann Emerg Med 1993;22:1140-1144.
43. Kothari RU, Dronen SC. Prospective evaluation of the scapular manipulation technique in reducing anterior shoulder dislocations. Ann Emerg Med 1992;21:1349-1352.
44. Mattick A, Wyatt JP. From Hippocrates to the Eskimo—- a history of techniques used to reduce anterior dislocation of the shoulder. J R Coll Surg Edinb 2000;45:312-316.
45. Boyd KT, Peirce NS, Batt ME. Common hip injuries in sport. Sports Med 1997;24:273-288.
46. Kocher MS, Tucker R. Pediatric athlete hip disorders. Clin Sports Med 2006;25:241-253.
47. Mares SC. Hip, pelvic, and thigh injuries and disorders in the adolescent athlete. Adolesc Med 1998;9:551-568.
48. Silbey MB, Fu FH. Knee injuries. In: Fu FH, Stone DA, eds. Sports Injuries: Mechanisms, Prevention, Treatment. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:1102-1134.
49. Solomon DH, Simel DL, Bates DW, et al. The rational clinical examination. Does this patient have a torn meniscus or ligament of the knee? Value of the physical examination. JAMA 2001;286:1610-1620.
50. Malanga GA, Andrus S, Nadler SF, et al. Physical examination of the knee: a review of the original test description and scientific validity of common orthopedic tests. Arch Phys Med Rehabil 2003;84:592-603.
51. Davids JR. Pediatric knee. Clinical assessment and common disorders. Pediatr Clin North Am 1996;43:1067-1090.
52. O'Shea KJ, Murphy KP, Heekin RD, et al. The diagnostic accuracy of history, physical examination, and radiographs in the evaluation of traumatic knee disorders. Am J Sports Med 1996;24:164-167.
53. Perryman, JR, Hershman EB. The acute management of soft tissue injuries of the knee. Orthop Clin North Am 2002;33:575-585.
54. Rodenberg RE, Cayce K, Hall S. Your guide to a dreaded injury: the ACL tear. Contemp Pediatr 2006;23:26-39.
55. Rodenberg RE, Cayce K, Hall S. Your role in treating and preventing ACL injury (part 2). Contemp Pediatr 2006;23:39-53.
56. Dorizas JA, Stanitski CI. Anterior cruciate injury in the skeletally immature. Orthop Clin North Am 2003;34:355-363.
57. Ireland ML. The female ACL: why is it more prone to injury? Orthop Clin North Am 2002;33:637-651.
58. DiGiovanni BF, Partal G, Baumhauer JF. Acute ankle injury and chronic lateral instability in the athlete. Clin Sports Med 2004;23:1-19.
59. Donatto KC. Ankle fractures and syndesmosis injuries. Orthop Clin North Am 2001;32:79-90.
60. Patel DR, Janiski C. Ankle sprains in young athletes part 1: how to evaluate. Contemp Pediatr 2005;22:65-72.
61. Sullivan JA. Ligament injuries of the foot and ankle in pediatric athletes. In: DeLee JC, Drez D, Miller MD, eds. Orthopedic Sports Medicine. 2nd ed. Philadelphia, PA: WB Saunders; 2004:2376-2390.
62. Cassillas MM. Ligament injuries of the foot and ankle in adult athletes. In: DeLee JC, Drez D, Miller MD, eds. Orthopedic Sports Medicine. 2nd ed. Philadelphia, PA: WB Saunders; 2004:2323-2375.
63. Bachmann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to exclude fractures of the ankle and mid foot: systematic review. BMJ 2003;326:417.
64. Clark KD, Tanner S. Evaluation of the Ottawa ankle rules in children. Pediatr Emerg Care 2003;19:73-78.
65. Myers A, Canty K, et al. Are the Ottawa ankle rules helpful in ruling out the need for x ray examination in children? Arch Dis Child 2005;90:1309-1311.
66. Boutis K, Komar L, Jaramillo D, et.al. Sensitivity of a clinical examination to predict need for radiography in children with ankle injuries: a prospective study. Lancet 2001;358:2118-2121.
67. Leggit JC, Meko CJ. Acute finger injuries: part I. Tendons and ligaments. Am Fam Physician 2006;73:810-816.
68. Leggit JC, Meko CJ. Acute finger injuries: part II. Fractures, dislocations, and thumb injuries. Am Fam Physician 2006;73:827-834.
69. Lyn E, Antosia RE. The hand. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 6th ed. Philadelphia, PA: Mosby Elsevier; 2006:576-621.
70. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg [Am] 2001;26:908-915.
71. Hankin FM, Peel SM. Sports-related fractures and dislocations in the hand. Hand Clin 1990;6:429-453.
72. Harrison B, Holland P. Diagnosis and management of hand injuries in the ED. Emerg Med Pract 2005;7:1-28.
73. Southhall JC, Sanders SP. Adult hand trauma. Trauma Reports 2006;7:1-12.