Keywords

Introduction

In 1969, Frankel and colleagues first attempted to define spinal cord injuries [1]. In 1982, this was expanded by the American Spinal Injury Association (ASIA) with the addition of a 0–5 motor scale of 10 predefined motor groups, representing specific motor distributions. Today, the ASIA scale is the preferred method of choice utilized as a neurologic examination tool in the diagnosis of acute SCI [2] (Tables 2.1 and 2.2).

Table 2.1 ASIA impairment scale
Full size table
Table 2.2 Key muscle group tested in ASIA evaluation
Full size table

A catastrophic cervical spine injury occurs when there is a structural distortion of the cervical spinal column associated with actual or potential damage to the spinal cord [3]. In the cervical spine, sports-related injuries are grouped into three separate categories. This classification has the additional utility to aid decisions regarding the safe return to play for the athlete [4]. When a type 1 injury occurs, the athlete sustains a permanent SCI. A permanent SCI encompasses those with complete paralysis as well as incomplete SCI syndromes. In an athlete with normal radiographic studies, but deficits which completely resolve within minutes to hours, a type 2 injury is diagnosed. Finally, type 3 injuries include those with radiographic abnormalities without associated neurologic deficits.

Prehospital Immobilization and Transportation

It is critical that athletes with a SCI be assessed and managed in the immediate period of injury on the field as any standard trauma patient. This involves a systematic approach to rapidly assess the extent of injuries and begin life-preserving therapy established in the Advanced Trauma Life Support (ATLS) protocol , which emphasizes addressing airway, breathing, and circulation status. After initial stabilization by medical personal on the field, the athlete can be transported off the field while maintaining strict immobilization of the spine.

Neurologic deficits can develop after treatment has begun if proper immobilization is not utilized. In a 1983 publication, Podolsky and colleagues reported that up to 25% of spinal cord injuries had been caused by or worsened under medical care [5]. While this number may be an overestimate, it emphasizes the importance of safe transport and initial stabilization of the athlete with a possible SCI. On the field, the athlete is immobilized with a cervical collar and a spine backboard, and the head is secured. It is important to note that although a cervical collar can effectively stabilize most cervical injuries, with complete ligamentous disruption, the collar has minimal effect, emphasizing the importance of manual stabilization in these instances [6]. Patients with a SCI should be transferred immediately to a center that specializes in SCI, which has been linked to better neurologic outcomes, reduced length of stay, fewer complications, and reduced mortality [7, 8]. Upon arrival at the hospital, the helmet and shoulder pads should be removed, if they are still in place, before radiographic examination. Of note, logroll maneuvers should be avoided with employment of a lift-and-slide technique preferred, given that they create less motion of the injured segment [9]. After initial resuscitation and radiographic evaluation, decisions can be made regarding the management of the injury.

Unstable spine injuries should be initially reduced and temporarily stabilized with cervical traction (Gardner-Wells tongs or halo device ). In cases where relevant, early cervical traction for reduction of cervical fractures/dislocations is recommended to optimize alignment and minimize compression of the spinal cord [10, 11]. It is of critical importance to obtain a contrast-enhanced CT or MRI prior to reduction to ensure the absence of a herniated disc which can worsen a SCI upon attempted reduction in this setting.

Adjunct Treatment/Pathophysiology of Spinal Cord Injury

To understand the currently investigated adjunct treatment options, a basic understanding of the pathophysiology of SCI is essential. An acute SCI can be thought of as an initial traumatic primary injury with a secondary injury that follows as a result of the progressive cascade of events that results in tissue destruction and systemic autonomic consequences.

The primary injury results from a mechanical insult to the spinal cord most commonly a result of failure of the integrity of the spinal column, leading to compressive and often sustained forces on the spinal cord. The result is disruption of neuronal axons, blood vessels, and cell membranes [12, 13]. This triggers a cascade of processes that define the secondary injury phase.

During the secondary injury phase , necrosis results from mechanical disruption of cellular membranes, with simultaneous upregulation of cytokines and release of glutamate, which may reach excitotoxic levels [14]. Ongoing hemorrhage with increasing edema continues with ischemia resulting from local effects (i.e., thrombosis, vasospasm, microvascular disruption) as well as from systemic autonomic effects on the cardiovascular system caused by the SCI itself. The resultant hypoxia leads to impaired neuronal homeostasis and further cell death [14]. The cellular inflammatory response, driven predominantly by macrophages, is thought of as the primary mediator of the progressive secondary injury. Through regulation of perfusion pressure and the potential addition of a neuroprotective agent/strategy, the early stages of the secondary injury are thought to be critical areas where medical intervention can benefit the patient.

Depending on the level of injury, SCI can be complicated by respiratory and cardiovascular dysfunction. Innervation to the muscles of inspiration and expiration may be compromised leading to decreased forced vital capacity and peak expiratory flow rate [15, 16]. This can lead to insufficient oxygen delivery to the spinal cord, which can be further worsened by systemic hypotension resulting from traumatic disruption of the descending vasomotor pathways of the spine. These carry supraspinal innervation to the preganglionic sympathetic neurons in the intermediolateral cell column between T1 and L2. Hypotension results from decreased sympathetic supply to the peripheral vascular system, and bradycardia may occur due to unopposed parasympathetic supply to the heart through the intact vagal nerve [17]. Lehmann and colleagues found that patients with severe cervical SCI are more likely to have bradycardia, hypotension, and cardiac dysrhythmias than patients with mild cervical SCI or thoracolumbar injury [18]. In addition to the aforementioned mechanisms of impaired ventilation , any pulmonary injury itself may be present and leads to poor gas exchange and decreased lung compliance. Furthermore, painful chest wall injuries may decrease ventilation.

It is recommended that hypotension be corrected as soon as possible with a goal mean arterial blood pressure maintained between 85 and 90 mmHg for the first 7 days following an acute SCI [19]. If a pressor is needed, norepinephrine is favored with dobutamine as second line when increased cardiac output is desired. Phenylephrine should be avoided in patients with a SCI level above T6 due to its proclivity to trigger reflex bradycardia as it is purely a peripheral vasoconstrictor.

Corticosteroid Administration

The 2013 American Association of Neurological Surgeons and the Congress of Neurological Surgeons (AANS/CNS) Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injury included the level 1 recommendation that the administration of methylprednisolone sodium succinate (MPSS) is not recommended [20]. MPSS has been the most extensively studied steroid in the medical management of acute SCI and is thought to work by its anti-inflammatory effects and halting peroxidation of neuronal membrane lipids [21,22,23]. The most frequently cited studies in the use of MPSS in acute SCI are the three National Acute Spinal Cord Injury Study (NASCIS) trials [24,25,26]. In all of the primary analyses, no significant difference was detected in motor, sensory, or functional recovery. However, post hoc analyses of NASCIS II data demonstrated that those receiving MPSS (30 mg/kg bolus at admission followed by 5.4 mg/kg/h for 23 h) within 8 h of injury improved significantly in both sensory and motor functions [26]. These differences remained significant 1 year post-injury. Additional post hoc analyses of NASCIS III data showed significantly greater motor recovery if a 48-h MPSS protocol (30 mg/kg bolus at admission followed by 5.4 mg/kg/h for 47 h) was used instead of a 24-h protocol, when treatment was started within 3–8 h [26]. The results from the third study also demonstrated no benefit to extending treatment past 24 h if MPSS was administered within the first 3 h after SCI. However, the 48-h MPSS protocol did show an increased incidence of severe pneumonia and severe sepsis (p = 0.02 and p = 0.07, respectively). High-dose MPSS has also been associated with increased prevalence of wound infections and death due to respiratory complications. Despite increased morbidity, there is no demonstration of increase in mortality with MPSS use [27].

Of note, there also appears to be a relationship between surgical timing and the safety of MPSS in acute SCI. In a multivariate analysis performed by Fehlings and colleagues, the primary data from STASCIS demonstrated that the 24-h MPSS protocol in combination with early surgery predicted significantly improved neurologic recovery at 6 months [28]. Particular consideration should also be given to the athlete with a cervical SCI. In this population, improvement in motor function is likely to have the greatest impact [29].

Hypothermia

The early induction of hypothermia has also been anecdotally reported to be beneficial in acute SCI. The mechanism for the neuroprotective benefit of systemic therapeutic hypothermia has yet to be elucidated [30]. It is hypothesized to result from reductions in cellular apoptosis [31], inflammation [32], glutamate excitotoxicity [33], edema, and other additional factors. In a phase I trial in patients with acute SCI, 14 patients were treated with 48 h of 33 °C intravascular hypothermia [34]. At the 1-year follow-up, 6/14 (42.9%) converted from complete SCI to incomplete. This is favorable considering the commonly reported value of 20% reported in the literature [35]. This underpowered study gathered enough data to garner support for further studies.

Medications

Vast research has been conducted on potential pharmacologic agents that aid in neuroprotection; unfortunately few therapeutic benefits have been realized from these studies. The three agents with the most current literature are GM-1 ganglioside, riluzole, and minocycline [36]. GM-1 ganglioside is an endogenous substance found in the mammal central nervous system and has shown to be anti-cytotoxic and anti-apoptotic. Preclinical animal trials demonstrated improvement in motor score at 3–5 days post-injury. Phase II trials in humans have shown to improve ASIA motor score at 1-year post-injury. However, phase III randomized control trial (RCT) showed no difference in motor scores at 52-week follow-up. Riluzole has been another highly investigated pharmacologic agent; it is a sodium channel blocker currently used in amyotrophic lateral sclerosis (ALS). Preclinical and phase I/II studies have shown improvement in ASIA motor score with its administration. It is currently undergoing a multicenter phase III RCT. Minocycline is a tetracycline antibiotic with anti-inflammatory properties. Preclinical and phase I studies have demonstrated improved motor scores, and phase II/III studies are currently underway. In addition to the above agents, newer neuroprotective and neuroregenerative therapies continue to be studied. As SCI research expands, providers will need to remain up to date with developing evidence-based standards.

Surgical Timing

Evidence exists that persistent compression of the spinal cord is a reversible form of secondary injury [37]. The Surgical Timing Acute Spinal Cord Injury Scale (STASCIS) was an international, multicenter prospective cohort study designed to determine whether early decompression (within 24 h) versus late (after 24 h) was more beneficial after traumatic cervical SCI. An improvement of two or more grades of the ASIA Impairment Scale (AID) was seen in 19.8% of early surgery patients compared to 8.8% in the late surgery patients [28]. This consensus for early decompression has been demonstrated beneficial in the thoracolumbar region [38] and cauda equina syndrome [39]. From these studies it can be concluded that when feasible, early decompression is desirable.

Expert Opinion

  • Acute SCI is an initial traumatic injury with a secondary injury due to a biochemical cascade. Since the initial injury has already occurred, most modalities of management focus on reducing the secondary injury cascade.

  • Initial care should concentrate on removing mechanical compression of the cord and maintaining spinal cord perfusion.

  • Mechanical compression on the cord can be removed via reduction techniques and/or surgery. There is evidence to support better outcomes with early surgical intervention.

  • Avoidance of spinal cord hypoperfusion is of the utmost importance and should be emphasized as soon as the SCI is diagnosed. Current recommendations would suggest maintaining a mean arterial pressure (MAP) greater than 85–90 mmHg for 7 days post-injury.

  • Although the NASCIS trials demonstrate complications with steroid administration, there is also evidence of neurologic improvement. Given that most athletic SCIs are likely to be isolated injuries, without the same comorbidities of the general trauma population, they may be a population ideally suited for high-dose steroid administration. Since the benefits outweigh the risks, we would recommend athletes with an isolated SCI receive IV steroids for acute SCI. This assumes administration of the steroids within 8 h of injury.

  • Pharmacologic agents focused on neuroprotection and regeneration remain in their infancy. Further research is warranted before these promising modalities can be utilized in standard practice.