Acute and chronic injuries of the spine can pose significant challenges to young athletes as well as their parents, coaches, trainers, and treating physicians. These injuries can affect participation, performance, and enjoyment of youth sports. Recent evidence has shown that the prevalence of back pain in older children and adolescents may be higher than previously recognized with rates as high as 24% to 36%.^1,2 It has been postulated that this increased prevalence is secondary to the rise in participation of organized youth sports. In 2014 to 2015, an estimated 35 million preadolescents and adolescents participated in organized sports in the United States (Minnesota Amateur Sports Commission, Athletic Footwear Association, USA Today Survey, Michigan State). Before more organized sports-specific training, overuse injuries in children were rarely encountered. However, these injuries are now major sources of morbidity in children and adolescents.

The manifestation of both acute and chronic spine injuries in children and adolescents is distinct from that in adults and these injuries can be overlooked by the clinician unaware of the common diagnoses in this subgroup of athletes. Within the general adolescent population, pediatric athletes are an at-risk population with a unique set of diagnoses. Whereas the etiology of back pain in inactive adolescents is often nonspecific,³ back pain in pediatric athletes is usually due to an identifiable cause.⁴ Through careful history and physical examination, supplemented with appropriate imaging, clinicians can often correctly identify the diagnosis in the young athlete, prevent further disability, and allow earlier return to sports.

Throughout development, the spinal column undergoes changes in both its structure and degree of flexibility, making it more or less susceptible to injury at various stages. The cancellous and cortical bone within the vertebral body also changes throughout development. During the adolescent growth spurt, bone mineralization is delayed, making it susceptible to fracture in part because of the changing bone density and its associated elastic modulus.^5,6 Additionally, because changes in muscle length lag behind longitudinal bone growth, the adolescent growth spurt can cause increased muscle–tendon tightness, thereby increasing the potential risk of injury.

The morphology of the growth plate and its surrounding tissue makes it vulnerable to injury because it is less resistant to deforming forces than either ligaments or bone.⁷ Within the developing axial skeleton, the vertebral body contains superior and inferior physes, each with a contiguous ring apophysis (i.e., apophyseal ring) that close at approximately 18 years of age.⁸ The cartilaginous epiphysis will subsequently develop into the vertebral endplates as the skeleton matures. The attachment of the apophyseal ring to the annulus fibrosis is through Sharpey’s fibers, which are stronger than the fibrocartilaginous junction of the vertebral body. Posteriorly, the apophysis is firmly attached to the posterior longitudinal ligament.

The posterior column consists of the neural arch, pars interarticularis, facet joints, and spinous process. There are three primary growth centers within the posterior arch, one in the spinous process and one located in each of the pedicles, with each closing by 8 years of age.⁸ Ossification of the vertebral body occurs in a posterior direction, and this moving transition zone of ossification predisposes the posterior elements to injury. Incomplete ossification of the superior aspect of the pars interarticularis predisposes this region to a stress fracture from the abutting inferior articular facet above.⁹

The morphology of the intervertebral disk also changes throughout development. Unlike the adult population in which degenerative changes of the annulus fibrosis are encountered, adolescent intervertebral disk pathology generally involves the ring apophysis. During axial compression, the forces of the immature spine are transmitted outward to the annulus fibrosis and, if large, can cause an apophyseal ring fracture or a limbus vertebra (herniated disk into the vertebral body). In contrast, the same compressive forces in the adult spine would tear the annulus fibrosis and cause herniation of the nucleus pulposus.

The cervical spine has a normal lordotic curvature, allowing it to dissipate a significant amount of energy in flexion, extension, rotation, and axial loading. In younger children, normal range of motion (ROM) of the cervical spine is increased at all levels, which subsequently decreases with age. Additionally, the point of maximal mobility is found at higher levels. Children younger than 8 years have their maximal mobility centered between the C1 to C3 vertebrae,¹⁰ predisposing this age group to a higher risk of upper cervical spine injuries.¹¹ This is also secondary to a child’s proportionately larger head, leading to a fulcrum of flexion at C2 to C3. With growth and development, the segment of maximum mobility moves caudally, reaching C5 to C6 by adolescence, where it remains throughout adulthood. Other cervical anatomic factors that differ from adults include horizontally aligned facet joints; underdeveloped uncinate processes of C3 to C7, leading to flatter articular surfaces; a synchondrosis at the junction of the odontoid and C2 vertebral body; and less developed cervical supporting musculature.¹²

Flexion, combined with axial loading, is a common mechanism of injury implicated in cervical spine injuries in contact sports.^13,14,15 Cervical flexion decreases the normal lordotic alignment, thereby decreasing the cervical spine’s ability to dissipate axial compression. When the maximum energy dissipation is exceeded, the patient may sustain compression or burst fractures with the potential for spinal cord injury (Figure 7-1). The fracture pattern will depend on the degree of cervical flexion at the time of injury. In adolescents, flexion fractures generally occur at the C5 and C6 levels because it is the site of maximal mobility. Before the mid-1970s, flexion-type cervical spine injuries were frequently encountered in high school and collegiate football players secondary to spearing (helmet-first football tackles). However, rules banning this form of tackling have dramatically reduced the rate of these injures encountered on the football field.¹³ Axial cervical spine injuries can also occur in hockey, gymnastics, diving, and cheerleading.^16,17,18 Predisposing risk factors in these sports include mechanical increases in acceleration, elevation of the athlete above the playing surface, and violent collisions either with an opponent or an object.

Cervical hyperextension injuries are also encountered in pediatric sports and may result from falls, whiplash injuries, and blows to the anterior head.¹⁵ The anterior cervical soft tissues are less robust than the posterior ligamentous
structures and confer less resistance to forced hyperextension. Increased cervical instability can be encountered if the hyperextension mechanism of injury is combined with rotation, predisposing the patient to neurologic injury.¹⁹

Acute injuries to the thoracolumbar spine occur less commonly than cervical spine injuries in the pediatric population and represent fewer than 8% of spine fractures in those younger than 8 years of age.²⁰ Adolescents are more predisposed to these injures, and sports are the leading cause.²¹ When injured, compression fractures are the most common thoracolumbar fracture seen in this age group; however, burst fractures can also occur.^21,22 Axial loading and trunk hyperflexion or hyperextension, as seen in falls landing in a seated position, can predispose to thoracolumbar injury. Gymnastics, diving, snowboarding, and jumping sports have been associated with this mechanism of injury.^18,23

The majority of thoracolumbar injuries in the pediatric and adolescent population are stable fractures (e.g., spinous process, transverse process, compression fractures) that can be treated nonoperatively. These fractures heal uneventfully and are not associated with growth arrest. Bed rest and activity restriction followed by a thoracolumbosacral orthosis (TLSO) for 4 to 12 weeks is the mainstay of treatment.²⁴ Compliance can be difficult in this active patient population, and sports activity is restricted during this period of healing. The athlete can return to sports after undergoing a gradual rehabilitation program in conjunction with radiographic union and resolution of pain.²¹

Burst fractures are a small subset of thoracolumbar fractures in children; however, it is important to recognize these fractures in children because improper management can cause physeal arrest and progressive sagittal or coronal spinal deformity.^22,25 These injuries occur secondary to axial load mechanisms that push the nucleus pulposus, or ring apophysis, or both into the vertebral body, causing it to fracture.²⁶ Fracture fragments from the vertebral body can retropulse into the spinal canal and compromise neural function; however, in the immature spine, the percentage of canal compromise does not necessarily correlate with the risk of spinal cord injury as is seen with the adult (Figure 7-2). Rather, the level of injury in the thoracic spine has been found to be associated with neurologic compromise.^22,27 Absolute indications for surgical treatment of burst fractures are those that are associated with neurologic injury. There is controversy regarding management of neurologically intact patients. Classic surgical indications include those with 40% loss of height, 20 degrees kyphotic deformity, or 40% canal compromise from a retropulsed fragment.^22,28,29 Studies that have assessed operative and nonoperative
management of burst fractures have shown only minor improvements in the degree of kyphosis with surgical management and no differences in clinical outcomes.^22,25,30