Summary of Key Points
- •
Acute spinal cord injury consists of a traumatic primary injury followed by secondary injury resulting from a progressive cascade of local pathophysiologic processes. This happens alongside a myriad of systemic respiratory, cardiovascular, and immunologic consequences.
- •
The aim of medical management of the spinal cord–injured patient in the acute setting is to mitigate the expansion of the region of neural tissue destruction produced by the secondary injury. In the subacute and chronic setting, the aim is to prevent and manage complications that arise from dysfunction of the sensory, motor, and autonomic pathways.
- •
An unobstructed airway and adequate oxygenation and ventilation are of the utmost importance to the spinal cord–injured patient, as appropriate blood oxygenation is need to ensure adequate oxygen delivery to mitigate local ischemic effects on the injured spinal cord. Establishment of a definitive airway should be considered early for patients who are at risk for airway compromise or respiratory failure.
- •
Hypotension and bradycardia may result from traumatic disruption of the descending vasomotor pathways of the spine and unopposed vagal parasympathetic supply to the heart, but it is imperative that other potential causes of hemodynamic instability be investigated and managed appropriately.
- •
Patients with an acute spinal cord injury should have hypotension corrected as soon as possible and mean arterial blood pressure should be maintained between 85 and 90 mm Hg for the first 7 days following the injury to ensure adequate perfusion to the injured tissue.
- •
Numerous promising developments have been made in the search for a pharmacologic agent that improves recovery from a spinal cord injury by protecting against cell death or facilitating regeneration; however, none has yet demonstrated efficacy in the primary analysis of a phase III clinical trial.
- •
The intravenous administration of corticosteroids should not be considered standard of care but may be considered as a neuroprotective option for patients with cervical spinal cord injury if administered within 8 hours of the spinal cord injury. If given, 24-hour administration minimizes the adverse events that have been observed with 48-hour administration.
- •
Venous thromboembolic complications are common in patients with spinal cord injuries and prophylaxis should be considered within 72 hours of injury, as long as there is evidence of cessation of any active hemorrhage. This can be continued for 8 to 12 weeks or possibly longer as necessary.
- •
Patients with spinal cord injury are at high risk for gastrointestinal bleeding. For this reason, prophylaxis with a histamine H2-receptor agonist or proton pump inhibitor can be started as soon as possible and continued for 4 weeks following the injury or possibly longer as necessary.
- •
Autonomic dysreflexia is caused by an unbalanced reflex sympathetic output leading to hypertension precipitated by a sensory stimulus below the level of the lesion. Prompt recognition and management is critical, as deaths and life-threatening complications have been reported as a result of this consequence.
Individuals affected by acute spinal cord injury (SCI) are disproportionately young and healthy. The physical and emotional impact of such an injury can be devastating and the impact from costs to society as a whole is substantial. This has driven a compelling search by clinicians and basic scientists to find strategies to optimize the medical management of patients with these life-changing injuries.
This chapter reviews the pathophysiologic mechanisms of injury to the spinal cord imparted by the traumatic event and examines the essential considerations in acute critical care management of these patients, where prompt medical intervention can mitigate the deleterious effects of the injury. The discussion then explores developments made in the emerging field of neuroprotectant and neuroregenerative pharmacologic agents, which hold promise to minimize neural tissue destruction and to enhance the potential for recovery. The chapter concludes with a discussion of the medical management of subacute and chronic issues commonly encountered by patients with injuries to the spinal cord.
Pathophysiology
Acute SCI consists of a traumatic primary injury followed by secondary injury from a progressive cascade of tissue destruction and a myriad of systemic autonomic consequences. This section focuses on the pathophysiologic basis of neuronal destruction by these mechanisms and establishes a foundation for further discussion of the role for medical management in mitigating the injury and improving neurologic recovery.
Primary Injury
The primary injury results from a mechanical insult to the spinal cord. The most common mechanism is traumatic failure of the integrity of the spinal column, leading to compressive and often sustained forces on the spinal cord. Other mechanisms include laceration, distraction, shearing from sudden acceleration-deceleration, and indirect transmission of kinetic energy from ballistic injuries. Regardless of the mechanism, the result is a disruption of neuronal axons, blood vessels, and cell membranes; however, the anatomic continuity of the spinal cord is nearly always maintained, as complete transection is rare.
Secondary Injury
The primary injury triggers a cascade of pathophysiologic processes that collectively constitute the secondary injury phase. The mechanisms of the secondary injury begin within seconds and are often subclassified into the immediate (≤ 2 hours), early acute (≤ 48 hours), subacute (≤ 2 weeks), intermediate (2 weeks to 6 months), and chronic (> 6 months) phases ( Fig. 137-1 ).
During the immediate phase of secondary injury, petechial white matter hemorrhages occur from disruption of the microvasculature. Necrosis results from mechanical disruption of cellular membranes, and there is a concomitant up-regulation of cytokines and release of glutamate, which may reach excitotoxic levels. This is followed by the early acute phase, which is marked by ongoing hemorrhage and increasing edema. Ischemia is the fundamental factor characterizing this stage, and it results from both local effects, such as vascular disruption, vasospasm, and thrombosis, as well as from systemic autonomic effects on the cardiovascular system caused by the SCI. The resultant hypoxia leads to impaired neuronal homeostasis and further cell death. These early stages of the secondary injury phase are where medical intervention through regulation of tissue perfusion and potential administration of a neuroprotectant agent is thought to hold the greatest promise for altering neurologic and functional outcomes. During the subacute phase, astrocytes at the periphery of the lesion proliferate and begin to form the gliotic scar, a physical and chemical barrier to axonal regeneration. Following these first three phases are the intermediate and chronic phases. The intermediate phase marks glial scar maturation and regenerative axonal sprouting. Scar formation continues and leads to the formation of cysts, and often a syrinx, in the chronic phase. There is hope that cell-based regenerative strategies may hold promise in these later phases.
Systemic Consequences of Spinal Cord Injury
The local effects of the acute SCI are often further exacerbated by respiratory and cardiovascular dysfunction in the acute postinjury period. Depending on the level of injury, innervation to the muscles of inspiration and expiration may be compromised. Dysfunction of the diaphragm (C3 to 5), scalene muscles (C4 to C8), sternocleidomastoid (C1 to C4), and intercostal muscles (T1 to 11) leads to decreased forced vital capacity and peak expiratory flow rate. Inadequate ventilation and oxygenation 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 because of unopposed parasympathetic supply to the heart via the intact vagal nerve ( Fig. 137-2 ). The classic clinical picture of bradycardia and hypotension that characterizes neurogenic shock is more likely to occur if the level of injury is above T6 because the sympathetic innervation to the heart arises from T1 to T6. This is borne out in clinical studies, such as that of Guly and associates where it was found that a significantly greater portion of patients with cervical SCI presented with neurogenic shock than those with thoracic or lumbar SCI. The severity of the injury also contributes to the likelihood of neurogenic shock. Lehmann and colleagues found that patients with severe cervical SCI are more likely to have bradycardia, hypotension, and cardiac dysrhythmias than are patients with mild cervical SCI or thoracolumbar injury.
If left untreated, the systemic hypoxemic and hypotensive effects attributable to the SCI will further exacerbate the local pathophysiologic effects on the spinal cord and lead to further neural tissue damage during the secondary injury phase. Support of the respiratory and cardiovascular system is often needed in spinal cord–injured patients, and the specifics relating to medical management are outlined in the following section.
Acute Medical Management
Spinal cord–injured patients should be assessed and managed in the immediate period, as any trauma patient would, with a systematic approach to rapid assessment of injuries and institution of life-preserving therapy established in the Advanced Trauma Life Support Guidelines. It is essential to recognize and appropriately manage the injuries that often occur concomitantly with a traumatic SCI. This section reviews the specific considerations for medical management of a patient with an acute SCI in the immediate postinjury period.
Airway Protection and Ventilation
An unobstructed airway and adequate oxygenation and ventilation are of the utmost importance in spinal cord–injured patients. Appropriate arterial blood oxygenation is needed to ensure adequate oxygen delivery to the spinal cord to mitigate the local ischemic effects resulting from secondary injury mechanisms.
Any patient with diminished upper airway reflexes that may compromise airway protection should have a definitive airway established. Clinicians must be mindful of these considerations because patients with SCI often present with associated factors that may compromise airway protection including diminished level of consciousness from traumatic brain injury or intoxication. Establishment of a definitive airway should also be considered early in the management of any patient with signs of impending airway compromise such as abnormal breath sounds, dysphonia, or high-risk injuries such as maxillofacial trauma or injury to the soft tissues of the neck with evidence of hematoma.
In addition to airway compromise, patients with an acute SCI, particularly those with high cervical spine injuries, are at high risk for respiratory failure. Dysfunction of the muscles of inspiration and expiration caused by the injury to the spinal cord may be further exacerbated by pulmonary injury, which leads to poor gas exchange and decreased lung compliance. Furthermore, painful chest wall injuries may decrease ventilation. Vigilance for signs of impending respiratory failure such as agitation, tachypnea, decreased capillary oxygen saturation or hypercarbia is imperative. In these cases, definitive airway with positive pressure ventilation should be strongly considered to avoid hypoxemia.
Intubation
During the intubation of a patient with a SCI, maintaining alignment of the potentially unstable spine is of the utmost importance, particularly in patients with cervical SCI. If airway protection is required in an urgent manner, rapid-sequence induction with manual in-line spinal immobilization is generally considered the standard of care. In patients without an emergent need for airway protection, fiberoptic tracheal intubation is safest.
The choice of induction agent varies, but generally the agent should produce minimal hypotension and no harmful effects on the central nervous system. Propofol and thiopental are usually avoided because of their potential to exacerbate hypotension. Ketamine may, in fact, induce hypertension; however, its use in patients with injury to the central nervous system is controversial because of concerns regarding its effect of raising neuraxial pressure. Etomidate has minimal effect on hemodynamics and, despite some concerns regarding its safety in critically ill patients, it remains a reasonable option. Short-acting opioids are a good option for analgesia to avoid prolonged apnea in cases of difficult intubation. Neuromuscular blockade with succinylcholine is safe within 48-hours of injury but should be avoided after that because of the potential for a lethal hyperkalemic response. Nondepolarizing neuromuscular blocking agents such as rocuronium should be used beyond the 48-hour time window.
Hypotension and bradycardia should be anticipated during induction and endotracheal intubation of a patient with a high cervical SCI and positive pressure ventilation can cause hypotension secondary to raised intrathoracic pressure in the setting of low systemic vascular resistance. With vigilance, these can be managed in a timely manner with fluids, vasoactive agents, and atropine, all discussed further in the following section.
Circulatory Support
The injured spinal cord is particularly susceptible to the deleterious effects of systemic hypoperfusion. This is supported by considerable preclinical evidence suggesting that prompt hemodynamic resuscitation improves recovery after acute SCI. Obvious ethical considerations preclude prospective evaluation of the effects that hypotension can have on SCI in humans, but numerous retrospective studies report that volume resuscitation and controlled blood pressure augmentation improve neurologic outcomes. Based on data of this nature, it is recommended that hypotension (systolic blood pressure < 90 mm Hg) be corrected as soon as possible and mean arterial blood pressure be maintained between 85 and 90 mm Hg for the first 7 days following an acute SCI.
Hypotension may be a result of neurogenic shock, but it is imperative that the other potential causes of hemodynamic instability such as hemorrhage, tension pneumothorax, cardiac tamponade, and sepsis be considered and managed appropriately if present. Adequate fluid resuscitation is essential but can be particularly challenging in patients with an SCI. Fluid overload needs to be avoided, as these patients are at high risk for pulmonary edema. Initial base deficit or lactate level can be used as a marker of the severity of shock and guide further resuscitation. Isotonic crystalloids are considered as the first line for management of hypotension, as albumin administration may increase mortality in trauma patients. An optimal algorithm to guide fluid resuscitation in a spinal cord–injured patient is unknown and further research in this area is greatly needed.
Vasoactive agents should be considered early in the setting of hypotension that is not appropriately responsive to fluid resuscitation. There are numerous agents ( Table 137-1 ), and the optimal choice remains a matter of debate. The level of the lesion may be used to guide selection of an appropriate agent. Patients with injuries above T6 should have a vasoactive agent with both inotropic and chronotropic effects to counter the disruption of cardiac sympathetic innervation as well as vasoconstrictive properties because of the vasoplegic effects of the disruption of the thoracolumbar sympathetic outflow. Norepinephrine is frequently used in this instance, and dobutamine can be considered particularly when increased cardiac output is needed. Lesions below T6 leave the sympathetic innervation to the heart uninterrupted so inotropic and chronotropic effects are of lesser importance than peripheral vasoconstriction. In such cases, phenylephrine may be considered, as it is specific for α 1 receptors. Phenylephrine should not be administered to patients with a SCI above T6 because of its propensity to trigger reflex bradycardia as a response to peripheral vasoconstriction. Epinephrine has been associated with increased rates of arrhythmias and should be used with caution. Dopamine has been shown to be associated with higher risk of death in cardiogenic and septic shock when compared with norepinephrine and should be used with caution for management of neurogenic shock. Vasopressin should generally be avoided in the spinal–cord injured patient because its antidiuretic effects may lead to hyponatremia and exacerbate spinal cord edema.
| Agent | Dose (µ/kg/min) | α 1 | β 1 | Considerations in neurogenic shock |
|---|---|---|---|---|
| Norepinephrine | 0.1–2.0 µ/kg/min | ++ | + | Good first option as an inotrope and vasoconstrictor. |
| Dobutamine | 2.5–20 µ/kg/min | ++ | Good option if increased cardiac output needed. | |
| Phenylephrine | 10–100 µg/min | ++ | Should not be used in patients with spinal cord lesions above T6; vasoconstriction can precipitate reflex bradycardia. | |
| Epinephrine | 0.1–0.5 µ/kg/min | ++ | ++ | Associated with increased risk of arrhythmias ; usually not used as first line. |
| Dopamine | 2–10 µ/kg/min | ++ | Associated with increased risk of death in cardiogenic and septic shock ; use should be considered carefully in neurogenic shock. | |
| 10–20 µ/kg/min | ++ | + | ||
| Vasopressin | 0.0–0.04 U/min | Antidiuretic effects may exacerbate spinal cord edema; use should be considered carefully in neurogenic shock. | ||
| SCI—Spinal cord injury |
Bradycardia and Other Arrhythmias
Patients with high cervical SCIs have been shown to have a significantly greater requirement for cardiovascular interventions when compared to patients with lower cervical SCIs. These patients are at high risk for symptomatic bradycardia, which may lead to asystole, and vigilance is necessary with any noxious stimulation, such as endotracheal suctioning. Symptomatic bradycardia should be treated upfront with atropine to ensure adequate cardiac output. Bradycardia that is refractory to atropine may respond to aminophylline. Otherwise temporary pacing should be considered. Bradyarrhythmias will typically resolve within a short time period but pacemaker placement should be considered for patients with high cervical SCIs and ongoing symptomatic bradyarrhythmic events 2 weeks after the injury.
Transfer
Whenever possible, patients with acute SCI should be transferred to a center specialized in the management of these injuries. Improved neurologic outcomes and fewer complications have been reported with early transfer to specialized centers. Furthermore, evidence has now emerged that early surgical intervention improves neurologic outcomes and expeditious transport to a center capable of providing definitive care affords the opportunity for early investigations and surgical decision making. During transport, the limitation of spinal motion is of paramount importance to prevent further injury. The patient should be secured to a backboard with the cervical spine immobilized with a rigid cervical collar and supportive blocks. The aforementioned considerations regarding airway protection, adequate ventilation, and circulatory support are critical during the immediate period following the injury, and means of support should be available during transport.
Administration of Neuroprotective and Neuroregenerative Agents
There have been numerous promising developments in the search for a medication that improves recovery from SCI by protecting against cell death or facilitating regeneration. Five pharmacologic agents have been evaluated through phase III trials to determine their efficacy. Of these, four had no significant demonstrable impact on recovery ( Table 137-2 ) and have not been adopted. The fifth agent, methylprednisolone sodium succinate (MPSS), has been shown to have benefit in post hoc analyses in two phase III trials but never in a primary analysis, leaving its role as a neuroprotectant an ongoing source of controversy. This section discusses the evidence for MPSS in the medical management of acute SCI and reviews emerging neuroprotectant and neuroregenerative pharmacologic options.
| Agent | Comparison | Findings |
|---|---|---|
| GM-1 ganglioside + MPSS * | vs. MPSS * | No significant differences in neurologic recovery at 26 week follow-up |
| Naloxone | vs. placebo | No significant differences in NASCIS motor score † at 6-months |
| Nimodipine | vs. placebo | No significant differences in ASIA motor or sensory scores at 1-year |
| Tirilizad mesylate | vs. MPSS * | No significant differences in NASCIS motor score † at 6-months |
* 24-hour MPSS administration protocol from NASCIS II (30 mg/kg bolus of MPSS at admission followed by 5.4 mg/kg/hour for 23 hours)
† Motor function tested in 14 muscle segments bilaterally. Score between 0 (no contraction in any muscle) and 70 (all normal responses). Only scores from the right side of the body were used in the analysis.
Corticosteroid Administration
Little else in the field of neurotrauma has raised as much debate as the administration of corticosteroids for acute SCI. Of these, MPSS has been the most intensely studied. It is thought to act by multiple mechanisms, which include halting peroxidation of neuronal membrane lipids and anti-inflammatory effects.
Six randomized controlled trials investigating the safety or efficacy of MPSS have been published. The most notable and frequently cited are the three National Acute Spinal Cord Injury Study (NASCIS) trials ( Table 137-3 ). No significant difference in motor, sensory, or function recovery was found in any of the primary analyses. However, post hoc analysis of the NASCIS II data revealed that those receiving MPSS (30 mg/kg bolus at admission followed by 5.4 mg/kg/h for 23 hours) within 8 hours of injury had significant improvements in sensory and motor function. Post hoc analysis of the NASCIS III data demonstrated significantly greater motor recovery if the 48-hour MPSS protocol (30 mg/kg bolus at admission followed by 5.4 mg/kg/h for 47 hours) was used instead of the 24-hour protocol when treatment was started within 3 to 8 hours. Notably, the 48-hour MPSS protocol had a significantly higher incidence of severe pneumonia (P = 0.02) and a higher incidence of severe sepsis that approached significance (P = 0.07).
Related posts:
Anatomy of Nerve Root Compression, Nerve Root Tethering, and Spinal Instability
Ventral and Ventrolateral Subaxial Decompression
Diffuse Idiopathic Skeletal Hyperostosis
Spinal Dural and Extradural Vascular Malformations
Spinal Wound Closure
Explant Analysis of Wear, Degradation, and Fatigue in Motion Preserving Spinal Implants
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
