Axial loading

The mechanism of injury to the cervical spine and associated anatomic risk factors that lead to serious neurologic injury have been the subject of active interest and debate within the sports medicine and spine surgery communities. Early research suggested that serious cervical spine injuries occurred from forced hyperflexion2–7,¹⁶ or hyperextension.^17–20 However, more recently axial loading has been defined as the most likely mechanism for catastrophic injury to the cervical spine during sports competition.

Axial loading occurs when a player strikes another player with the top of the head as the point of initial contact (so-called ‘spear tackling’). Axial loading places the cervical spine at a biomechanical disadvantage and makes it particularly susceptible to severe injury. Typically, most forces from a traumatic load to the cervical spine are dissipated through controlled spinal motion, the paravertebral muscles, and the intervertebral discs. When the top or crown of the helmet is used for initial contact, the neck is typically flexed approximately 30° and loses its normal cervical lordosis and ability to properly distribute force (Fig. 126.1). In this position the cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine (Fig. 126.2).²¹

Fig. 126.1 (A) In the normal upright anatomical position, the cervical spine is slightly extended with a natural cervical lordosis. (B) When the neck is flexed to approximately 30°, the cervical spine is straightened and loses its ability to properly distribute force.

Fig. 126.2 (A) Spear-tackler’s spine involves loss of the normal cervical lordosis and an axial load. (B) The straightened cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine, first compressing the intervertebral discs. When maximum compression is reached the spine flexes and fails (C) with potential fracture, subluxation, or dislocation (D,E).

In athletes with cervical spinal stenosis, axial loading followed by forced hyperextension or hyperflexion can cause transient or permanent sensory and motor changes. Penning¹⁹ described a ‘pincer mechanism’ with compression of the spinal cord between a vertebral body and the spinolaminar line of an adjacent vertebra. Compression of the spinal cord occurs in hyperextension when the distance between the posteroinferior margin of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the subjacent vertebra decreases (Fig. 126.3). With hyperflexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior margin of the inferior vertebra approximate. Eismont et al.²⁰ also noted that hyperextension causes narrowing of the anteroposterior diameter of the spinal canal and can compress the spinal cord. Torg et al.²² described an axial load input with subsequent hyperextension and indentation of the ligamentum flavum with compression of the spinal cord. In each of these mechanisms, the anteroposterior diameter of the spinal canal decreases, resulting in compression of the spinal cord. Transient or permanent cervical cord injury can occur and usually involves a contusion of the spinal cord with temporary restriction of blood flow and a focal area of ischemia.⁸

Fig. 126.3 Hyperextension ‘pincer mechanism’ as described by Penning.¹⁹ During hyperextension, the distance between the posteroinferior aspect of the superior vertebral body and the anterosuperior aspect of the spinal laminar line of the subjacent vertebra decreases, and the cord is pinched between the two vertebral bodies.

While advances in helmet materials and equipment used in American football lead to a decrease in head injuries, it also contributed to the development of dangerous playing techniques using the top of the helmet as the initial point of contact. Torg et al.²³ compared the total number of head and neck injuries in the National Football League between 1971 and 1975 with previous work done by Schneider²⁴ analyzing injuries between 1959 and 1963. The major difference between these time periods was the type and quality of helmet worn during competition. The study found a reduction in intracranial hemorrhages of 66% and deaths due to intracranial injury of 42%. However, the study also found a 204% increase in cervical spine fractures, subluxations, and dislocations and a 116% increase in the number of cases of permanent quadriplegia. The majority of cases of permanent quadriplegia that occurred were due to direct compression when a player struck another player with the top of his helmet.

Delineation of the axial load mechanism as the major cause of catastrophic cervical spine injury in American football resulted in rule changes that caused a sustained decrease in the rate of cervical spine injuries and quadriplegia. In 1976 the National Collegiate Athletic Association banned ‘spearing,’ defined as intentionally striking an opponent with the crown of the helmet, as well as other tackling techniques in which the helmet is used as the initial point of contact. In 1976, the rate of cervical spine fracture, subluxation, and dislocation was 7.72/100 000 and 30.66/100 000 in high school and college athletes, respectively. In 1987, this had decreased to 2.31/100 000 and 10.66/100 000 serious injuries to the cervical spine in high school and college athletes, respectively.²¹ Injuries resulting in permanent quadriplegia also significantly decreased as a result of the rule changes. In 1976, the rate of quadriplegia was 2.24/100 000 and 10.66/100 000 in high school and college athletes, respectively. In 1977, only 1 year after the rule changes, these rates decreased to 1.30/100 000 and 2.66/100 000 in high school and college athletes, respectively, and have continued to remain low.²¹

In 1990 Torg and colleagues²⁵ further confirmed axial loading as the mechanism in catastrophic cervical spine injury by review of actual game films and videotapes. Analysis of films allowed an accurate determination of the mechanism of injury in 85% of cases, and axial loading was found to be the mechanism in every case.

Strains and sprains

Soft tissue injuries to the cervical spine, such as muscle or tendon strains and ligament sprains, are probably the most common sports-related neck injuries. These injuries are typically mild and self-limiting and present with minor neck pain and without any neurologic symptoms. Indicators of a more significant spine injury include significant cervical muscle spasm, tentative active range of motion, and severe pain. Evaluation of the athlete includes active cervical spine range of motion and strength testing of the neck and upper extremities. Manual compression and axial load to the cervical spine (Spurling’s maneuver) should not cause pain or radicular symptoms and is helpful in ruling out more significant injury. The athlete can return to play when full pain-free range of motion and normal strength of the cervical spine are restored. It is important that no symptomatic athlete returns to competition. Occasionally, more significant ligamentous injury may go unrecognized but should be suspected if persistent muscle spasm and limited range of motion lasts days or weeks following the injury. In this case, flexion and extension radiographs of the cervical spine should be taken to rule out instability.

Stingers

‘Stingers’ or ‘burners’ are descriptive terms used to characterize transient unilateral upper extremity pain and paresthesias following a blow to the neck or shoulders. Because of confusion with a potentially more serious central cord injury called ‘burning hands syndrome,’²⁶ use of the term ‘stinger’ rather than ‘burner’ is encouraged. Stingers are very common and are reported in up to 50–65% of college football players.^27,28

Stingers are peripheral nerve injuries, not spinal cord injuries, and are considered a transient neurapraxia of the cervical nerve roots or upper trunk of the brachial plexus, usually involving the C5 and/or C6 distribution. Because the dorsal root ganglion is positioned within the neural foramen, symptoms may be purely sensory and in a dermatomal distribution. Stingers are characterized by burning dysesthesias that typically begin in the shoulder region and radiate unilaterally into the arm and hand. Weakness, numbness, or both are sometimes associated with the burning pain. Initially, there can be a great deal of posterior cervical tenderness because the posterior primary ramus of the nerve innervates the skin in that area and comes directly off the dorsal root ganglion.

Stingers usually result from one of two mechanisms: tensile overload or compression overload.²⁹ While either mechanism is possible in any athlete, the mechanism of injury is more likely depending on the age of the athlete. In most high school athletes, the mechanism involves a tensile or stretch injury when the involved arm and neck are stretched in opposite directions. This occurs as the neck is forcibly stretched away while the ipsilateral shoulder is depressed (Fig. 126.4). In the older college or professional athlete with a higher likelihood of degenerative changes of the cervical spine, a compressive mechanism is more likely. This involves a compression or ‘pinch’ of the cervical nerve root within the neural foramen as the neck is forcibly flexed in a posterolateral direction towards the symptomatic upper extremity (see Fig. 126.4).³⁰

Fig. 126.4 ‘Stingers’ result from either a tensile or compression load. A blow to the neck producing lateral neck flexion with ipsilateral shoulder depression causes a traction or tensile load to the cervical nerve roots and upper trunk of the brachial plexus. Forceful flexion of the neck in a posterolateral direction causes compression of the nerve roots within the neural foramen.

Stingers must be differentiated from spinal cord injuries. The key distinguishing feature is that stingers result in unilateral upper extremity impairment. Spinal cord injury results in multiple limb involvement, i.e. bilateral upper extremities or both upper and lower extremities. Stingers typically resolve in minutes. Sideline evaluation of an athlete with a stinger involves a complete neck and upper extremity neurologic examination. As the symptoms improve, the athlete will demonstrate improved cervical spine range of motion. Athletes with transient stingers are safe to return to play when symptoms have fully resolved, the athlete can demonstrate normal cervical neck range of motion, Spurling’s maneuver is negative, and neurologic and strength examinations are normal.

Recurrent stingers are more common in the presence of cervical degenerative disc disease. Levitz et al.³⁰ studied 55 athletes with recurrent stingers. The mechanism of injury was extension combined with ipsilateral compression in 83% of patients, and 70% had a positive Spurling’s sign. Eighty-seven percent of patients had evidence of disc disease by magnetic resonance imagimg (MRI), and 93% had disc disease or narrowing of the intervertebral foramina. The authors concluded that nerve root compression in the intervertebral foramina secondary to degenerative disc disease was the likely cause of recurrent or chronic stinger syndromes in collegiate and professional athletes. Athletes with more than one stinger can be placed in a protective neck collar that limits lateral neck flexion and hyperextension.

Rarely, more significant nerve injury and axonotmesis occurs causing chronic symptoms. Patients usually demonstrate persistent weakness in the distribution of the upper trunk of the brachial plexus, and muscle atrophy may be present in severe cases. Electromyography will assess the distribution and degree of injury and should be performed if symptoms have lasted more than 3 weeks. Most cases of axonotmesis have a high likelihood of recovering within 1 year.²⁷

Cervical cord neurapraxia and transient quadriplegia

Injury to the spinal cord can be complete or be neurapraxic – a reversible injury with motor and sensory function returning within 24–48 hours. Neurapraxia of the cervical spinal cord is characterized by an acute, transient sensory and/or motor change to more than one extremity. Symptoms include burning pain, numbness, tingling and loss of sensation with or without motor changes of paresis or complete paralysis.³¹ Several other terms have been used to describe cervical cord neurapraxia and have been used interchangeably, including ‘transient quadriplegia,’³¹ ‘central cervical spinal cord syndrome,’³² and ‘spinal cord concussion.’³³

The most typical pattern of incomplete spinal cord injury is the central cord syndrome. This involves weakness of the upper extremities in excess of lower extremity findings secondary to the lamination of the corticospinal tracts and selective damage to fibers serving arm and hand function. ‘Burning hands syndrome’ described by Maroon²⁶ is characterized by burning dysesthesias of the hands and associated weakness of the upper extremities and is a variant of central cord syndrome. Transient quadriplegia is a temporary paralysis characterized by loss of motor function, with or without sensory disturbances.³¹

Episodes of cervical cord neurapraxia are transient by definition and complete recovery usually occurs in 10–15 minutes, although in some patients gradual resolution occurs over 1–2 days. Except for burning paresthesia, the athlete does not experience neck pain, and there is complete return of motor function and full, pain-free range of motion of the cervical spine. Torg et al.³⁴ studied 110 patients with transient cervical cord neurapraxia and found that 40% presented with plegia (complete motor weakness), 25% with paresis (incomplete motor weakness), and 35% with only paresthesia and sensory symptoms. The neurapraxia resolved in 74% of patients within 15 minutes and lasted more than 24 hours in 11% of patients. Eighty percent of patients had symptoms in all 4 extremities, 15% in the upper extremities only, 2% in lower extremities only, and 3% with symptoms in the ipsilateral upper and lower extremities. Of 110 patients, 109 had a complete neurologic recovery, with one patient having a residual hemiplegia following operative intervention. For those athletes who did return to football, the recurrence rate for transient cervical cord neurapraxia was 56% with no athlete experiencing permanent neurologic injury, although the follow-up period was only 3 years and some athletes chose to retire from collision sports.

Cervical spinal stenosis

Cervical spinal stenosis is an important factor in the occurrence of cervical cord neurapraxia and the severity of neurologic injury following cervical spine trauma. Cervical spinal stenosis is a congenital or developmental narrowing of the cervical spinal canal defined by the midsagittal diameter or cross-sectional area. A diminished anteroposterior diameter of the spinal canal can be caused by congenital narrowing of the spinal canal, developmental spinal stenosis from degenerative changes, cervical instability, or intervertebral disc protrusion.

The method to best determine spinal stenosis in an athlete has been the subject of considerable debate. Early definitions used the absolute anteroposterior canal diameter to detect spinal stenosis – measured from the posterior aspect of the vertebral body to the most anterior point on the spinolaminar line. In general, a canal was considered normal if the diameter between C3 and C7 was >15 mm, and spinal stenosis was present if the diameter was <12 mm.³⁵

Torg et al.³¹ and Pavlov et al.³⁶ described a measurement to detect spinal stenosis using a spinal canal to vertebral body ratio (known as the ‘Torg ratio’). The ratio uses the anteroposterior diameter of the spinal canal and the anteroposterior width of the midpoint of the vertebral body (Fig. 126.5). The measurements are made at the level of the third through the sixth vertebral body on a routine lateral radiograph of the cervical spine. The ratio method eliminates error caused by magnification factors or differences in target-to-film distances. A spinal canal-vertebral body ratio of <0.8 indicates significant spinal stenosis. In Torg’s study,³¹ a ratio of <0.8 was recorded at one or more levels in 24 athletes with cervical cord neurapraxia, compared to a ratio of 1.0 or more in 49 age-matched controls with no neurologic complaints.

Fig. 126.5 The Torg ratio is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the spinolaminar line (a) divided by the anteroposterior width of the vertebral body (b).³¹

Eismont et al.²⁰ also observed that a smaller-diameter spinal canal measured by plain film significantly correlated with neurologic injury in 98 patients with cervical spine traumatic fracture-dislocations. Others studies have further documented the association of a small sagittal diameter of the spinal canal with the severity of neurologic injury following cervical spine trauma.^37,38

The Torg ratio has been the subject of considerable scrutiny, and its usefulness in sports and spine medicine questioned. Herzog et al.³⁹ found the ratio to have a high sensitivity (92%) but a low positive predictive value (12%) for detecting cervical spinal stenosis in a cohort of professional football players. In their study, 49% of professional football players had a Torg ratio <0.8 at one or more levels, but only 13% had true spinal stenosis documented on advanced imaging. Herzog et al. concluded that the Torg ratio was a poor predictor of true functional spinal stenosis and may yield many false-positive results, and the low positive predictive value of the ratio precludes its use as a screening tool for determining eligibility of an athlete for participation in contact sports.

Several problems exist which limit the usefulness of the Torg ratio in determining spinal stenosis. Most concerning is that the ratio does not account for the size of the spinal cord and define the anatomic relationship of the spinal cord within the spinal canal. In addition, the ratio does not identify soft tissue pathology that may be impinging on the spinal canal. Resnick⁴⁰ stated that roentgenography alone failed to assess the width of the cord and account for stenosis which results from ligamentous hypertrophy or disc protrusion. Cantu⁴¹ also argued that spinal stenosis cannot be defined by bony measurements alone and that normal canal size on a lateral radiograph does not rule out the possibility of ‘functional spinal stenosis.’ He defines ‘functional spinal stenosis’ as a loss of cerebrospinal fluid (CSF) around the cord or deformation of the spinal cord, as documented on computed tomography (CT), MRI, or myelography.⁴² The term ‘functional’ refers to the functional reserve or protective cushion of the CSF around the spinal cord.

While the Torg ratio has its limitations, Torg and colleagues^31,36 should be credited with their efforts to define a measure used to assess cervical spinal stenosis and the risk of cervical cord injury. In addition, it should be noted that the Torg ratio was created at a time when MRI was not widely available. In the setting of an athlete with a history of cervical cord neurapraxia or transient quadriplegia, an evaluation with MRI, myelogram, or contrast-positive CT should be performed. If the Torg ratio is measured early in the diagnostic evaluation, an abnormal ratio is a strong indicator to pursue advanced imaging.⁴¹

Whether congenital or acquired, the relationship of cervical spinal stenosis to serious neurologic injury is well established. The National Center for Catastrophic Injury Research has reported cases of quadriplegia in the absence of a spine fracture only when functional spinal stenosis is present, and conversely reported cases of complete neurologic recovery after spine fracture or dislocation only in the absence of functional spinal stenosis.⁴² In addition, the presence of cervical spinal stenosis places the athlete at higher risk to require surgery after a cervical disc herniation, for potential paralysis without a fracture-dislocation, and to develop paralysis and a greater degree of paralysis after fracture-dislocation.^20,42–46

Return to play after cervical cord neurapraxia

Return to play after an episode of cervical cord neurapraxia is a frequently discussed and controversial area in sports medicine and spine surgery. Torg et al.⁴⁷ compared cohorts of asymptomatic college and professional football players with no history of transient neurapraxia, with a cohort of 45 high school, college, and professional athletes with an episode of transient neurapraxia, and 77 patients with permanent quadriplegia as a result of high school or college football. The Torg ratio was found to have a sensitivity of 93% for the detection of transient neurapraxia, but a low specificity and low positive predictive value. None of the 77 patients with permanent quadriplegia had an episode of transient neurapraxia before catastrophic injury to the spinal cord, and none of the 45 athletes with transient neurapraxia became quadriplegic. Developmental narrowing of the spinal canal in the quadriplegic group was also absent. The authors concluded that the occurrence of transient neurapraxia of the spinal cord and permanent quadriplegia were unrelated, and that developmental narrowing of the spinal canal in the absence of instability is not a predisposing factor for permanent neurologic injury. Therefore, congenital cervical spinal stenosis should not preclude an athlete from participation in contact sports.

Torg et al.³⁴ further characterized the relationship of the spinal cord to the spinal canal by analyzing MR images in 110 athletes with cervical cord neurapraxia. The disc-level canal diameter was measured as the shortest distance between the intervertebral disc and the osseous posterior elements and the transverse cord diameter determined. The MRI measurements were compared to the spinal canal–vertebral body ratio measured on lateral radiograph. The study found using both methods of measurement that the probability of recurrent cervical cord neurapraxia was inversely correlated with spinal canal size. Using logistic regression analysis, plots were generated to calculate the risk of recurrent neurapraxia that could be used in counseling athletes with a history of cervical cord neurapraxia about their individual risk of a recurrent episode. The authors concluded that: (1) cervical cord neurapraxia is a transient neurological phenomenon and individuals with uncomplicated neurapraxia may be permitted to return to their previous sport without an increased risk of permanent neurological injury; (2) congenital or degenerative narrowing of the sagittal diameter of the cervical canal is a causative factor; (3) the overall recurrence rate after return to play is 56%; and (4) the risk of recurrence is strongly and inversely correlated with sagittal canal diameter and is useful in the prediction of future episodes of cervical cord neurapraxia. Although controversial, Torg et al.²¹ do not believe that athletes who experience an episode of uncomplicated transient cervical cord are at risk of incurring permanent neurologic sequelae and should not be disqualified from participation in contact or collision sports.

Other experts strongly disagree. Cantu⁴¹ contends that cervical spinal stenosis increases the risk of permanent neurologic injury and asserts that a history of transient quadriplegia and functional spinal stenosis is an absolute contraindication to return to contact or collision sports. Table 126.1 contrasts return to play recommendations following cervical cord neurapraxia by Torg et al.²¹ and Cantu.⁴¹

Table 126.1 Guidelines for Return to Play After Transient Cervical Cord Neurapraxia

Initial assessment

The care of an injured athlete begins with observation of the event that leads to the potential injury. The medical team at sporting events should make every attempt to closely view all plays, as direct observation of the mechanism of injury is helpful in assessing the likelihood of significant injury.

The initial assessment of an injured athlete begins with a basic assessment of the ABCs – airway, breathing, and circulation – and level of consciousness. If any concerns regarding basic life support are present the EMS should be activated immediately. Any athlete suspected of having a spinal injury should not be moved and should be treated as if a spinal injury exists. Unconscious athletes are presumed to have unstable spine injuries until proven otherwise. All participants on the field including coaches, officials, and teammates must be aware of the dangers of moving a player with a suspected spinal injury before appropriate stabilization of the cervical spine.

If the athlete is not breathing, an adequate airway must be established. The jaw thrust maneuver allows opening of the airway while maintaining the cervical spine in a stable position. If spontaneous respiration does not resume, assisted ventilation may be necessary. In an unconscious athlete, an oral airway should be used to assist proper bag-valve-mask ventilation until endotracheal intubation can be performed in a controlled setting. High cervical spine injuries can cause apnea, ineffective breathing patterns, and paralysis of the phrenic nerve. Although rare, prolonged hypoxemia can lead to cardiac arrest.

Once adequate ventilation and circulation are established, the level of consciousness should be further assessed. The conscious athlete is questioned regarding person, place, situation, the presence of neck pain, and sensory or motor disturbances in any body part. A screening neurologic examination is performed to assess sensation and strength in all four extremities. In the unconscious athlete or athlete with altered mental status, the Glasgow Coma Scale may be a useful prognostic indicator of cerebral function (Table 126.2).¹⁰

Table 126.2 Glasgow Coma Scale

The Glasgow Coma Scale is scored between 3 and 15 (3 being the worst and 15 the best). A score of 13 or higher correlates with mild brain injury; a score of 9 to 12 correlates with moderate brain injury; and a score of 8 or less represents severe brain injury.

In the conscious athlete, it may be possible to clear the cervical spine on the field. The athlete must be alert, oriented, and without neck pain, neurologic symptoms, or distracting injury to the extremities. A brief four-extremity neurologic examination should be normal, and palpation of the cervical spine should be without tenderness. Active cervical spine range of motion should be pain free and without the development of neurologic symptoms and can be tested by asking the athlete to flex the chin to the chest and then rotate the head from side to side. If a cervical injury has been excluded, then the athlete can be assisted to the sitting position. If stable in the sitting position, the athlete can be helped to a stand, walked off the field, and further observed. If there is any suspicion for the presence of a cervical spine injury, it is better to err on the side of safety, and immobilize the cervical spine and transport the athlete for more definitive evaluation.

Equipment management

Protective equipment used in sports such as football and hockey can make the management of a spine-injured athlete more difficult. Each member of the medical team should be familiar and practiced in the operation of emergency equipment. Practice with the tools required for face mask removal of the catastrophically injured athlete is essential. The face mask should be removed as soon as possible before transportation and regardless of respiratory status, even if the athlete is conscious.⁴⁴ In football, the face mask is secured to the helmet with four or more plastic loop-straps that can be cut or removed. Several tools for removing the loop-straps have been described including screw drivers and various cutting tools such as knives, scissors, pruning shears, the Trainer’s Angel (Fig. 126.8), and the Face Mask Extractor.^51–53 Because moisture can rust the screws making screwdrivers unreliable, and injuries to other rescuers have been documented while using cutting instruments such as knives, scalpels, or box cutters, these tools are not recommended as the primary tool for loop-strap removal.⁵⁴

Fig. 126.8 The Trainer’s Angel. A tool specifically made for removing the loop-straps of the facemask from a football helmet.

The most widely used tool specifically made to remove loop-straps is the Trainer’s Angel. However, this tool may cause more head movement than other available devices. The face mask removal should be performed in the shortest time possible with the least amount of head and neck movement. The anvil pruner, commonly used for gardening, has been shown repeatedly to be the most efficient tool for removal of the loop-straps and is recommended by the Inter-Association Task Force.^44,54 Athletic trainers or another designated member of the responding medical team should have the appropriate removal equipment available and be familiar with its use before an emergency occurs.

Football helmets and chin straps should be left in place with few exceptions. If the athlete is wearing shoulder pads, football helmets hold the head in a position of neutral spinal alignment. If the helmet is removed from a down player wearing shoulder pads, the athlete’s head will hyperextend and may result in secondary injury to the cervical spine. The Inter-Association Task Force recommends removal of a helmet on the field under the following circumstances: (1) if the face mask cannot be removed in a reasonable period of time to gain access to the airway; (2) if after removal of the face mask the airway and ventilation cannot be adequately controlled; (3) if the helmet and chin straps do not hold the head securely such that immobilization of the helmet does not also immobilize the head; and (4) if the helmet prevents immobilization in an appropriate position.⁴⁴

If the helmet needs to be removed, spinal immobilization and alignment must be maintained. Removal of a football helmet in a suspected spine-injured athlete should be performed cautiously. Internal helmet padding should be removed or air padding deflated while an assistant manually stabilizes the chin and the back of the neck. A stiff flat-bladed object such as a tongue depressor can be used to pry the padding away from the helmet. Air padding can be deflated with a large-gauge hypodermic needle. The helmet should slide off the occiput with slight forward rotation or traction of the helmet. In contrast, motorcycle helmets are not as snugly fit to the head and are worn without shoulder pads. Removal of a motorcycle helmet before transportation achieves neutral spine alignment and allows better stabilization of the injured motorcyclist.

If removal of the helmet or shoulder pads is required, the helmet and shoulder pads should always be removed simultaneously or neutral spine alignment will be lost.^55,56 Football shoulder pads elevate the torso of a supine athlete to the same height as a helmeted head. The front of the shoulder pads can be opened to allow access to cardiopulmonary resuscitation and defibrillation if needed without actually removing the shoulder pads. Indications to remove the shoulder pads include: (1) the helmet is being removed; (2) injuries require full access to the shoulder area; and (3) ill-fitting shoulder pads preclude adequate spinal immobilization.⁴⁴ To remove football shoulder pads, cut the jersey and other shirts from neck to waist and from midline to the end of each sleeve, cut all straps used to secure the pads to the torso, and cut the laces or straps over the sternum. Cervical stabilization is maintained by placing one’s forearms on the athlete’s chest while holding the maxilla and occiput. With assistance on both sides, the patient is lifted and the shoulder pads removed by spreading apart the front panels and pulling them around the head.⁴⁴

Immobilization and transportation

The medical team should be prepared to immobilize and transport an injured athlete if indicated. Every situation should be evaluated on an individual basis. When uncertainty exists, it is better to err on the side of caution and immobilize the patient until further diagnostic work-up can be performed. In general, any athlete with significant neck or spine pain, diminished level of consciousness, or significant neurologic deficits should be prepared for transport to a predetermined medical facility capable of definitive diagnostic and therapeutic neurosurgical procedures.

Manual stabilization of the head, neck, and shoulders should be performed as the athlete is being assessed. If transport is indicated, the athlete will need to be immobilized to an appropriate immobilization device, usually a standard spine board. To transfer a supine athlete to a spine board, the Inter-Association Task Force recommends a six-plus-person lift technique of the athlete onto a rigid long spine board.⁴⁴ One person is responsible for stabilization of the head and neck and will lead the team through all commands to lift the athlete and then lower onto the backboard. The rescuer’s hands should be placed palm-up underneath the shoulder pads, with the athlete’s head resting between the rescuer’s forearms.

To transfer an athlete who is prone or face down, a log-rolling technique is recommended (Fig. 126.9). This is performed with a minimum of four persons with one designated to maintain stabilization of the head and neck. If the prone athlete is not breathing, the athlete should be log-rolled immediately. The athlete can later be lifted a second time onto the spine board for immobilization as described above. If the athlete is conscious, the log-roll should be delayed until the backboard is available.

Fig. 126.9 The log-rolling technique is used to transfer a prone athlete with a suspected cervical spine injury and requires a minimum of four persons. The lead rescuer stabilizes the head and cervical spine by using a cross-arm technique and applying slight traction (A). Three assistants are positioned at the shoulders, hips, and knees and roll the patient towards themselves supine onto a spine board (B).

To immobilize the patient, the head and spine should be maintained in a neutral position at all times. Again, in most cases, the helmet and shoulder pads are left in place, and the face mask removed prior to transport. After removal of the face mask and with the chin strap in place, the helmeted head is secured to the spine board by adhesive tape or straps. Standard straps secure the body, pelvis, arms, and legs. Filling any gaps with rolled towels or rigid foam will further stabilize the patient. The straps should be applied firmly so the athlete does not move if rolled onto his/her side in response to vomiting. Transport of a spine-injured athlete should be directed to a trauma center or facility with diagnostic and surgical capabilities for spine injury.

Prevention of secondary injury

The pathophysiology of irreversible spinal cord injury involves not only the primary injury but also a cascade of secondary injury including neuronal edema, hypoxia, and aberration of cell membrane potential. Spinal cord resuscitation in an attempt to prevent secondary injury is recommended and supported by the National Acute Spinal Cord Injury Study.^57,58 This includes respiratory and hemodynamic support to facilitate spinal cord perfusion, prompt relief of spinal cord deformation through controlled realignment and stabilization, and intravenous administration of corticosteroids.^57,58 Intravenous methylprednisolone is given with a loading dose of 30 mg/kg body weight over 1 hour and is recommended as soon as possible, preferably within the first 4 hours after injury. This is followed by a subsequent dose of 5.6mg/kg body weight administered over the next 23 hours.

Education

The major risk factor for permanent neurologic injury in athletics is the use of spear-tackling techniques where the head is used as the initial point of contact producing axial compression and subsequent failure of the cervical spine. Prevention of cervical spine injuries through the teaching of proper tackling technique is the key intervention to decrease catastrophic cervical spine injuries. Educational programs emphasizing a ‘see what you hit’ technique of blocking and tackling should be implemented on a regular basis. Changes in equipment, rules, strengthening, and conditioning may also be helpful.