Management of acute spinal cord injury.

Review Article

Management of Acute Spinal Cord Injury Deborah M. Stein, MD, MPH, FACS, FCCM; Kevin N. Sheth, MD, FAHA, FCCM, FNCS ABSTRACT Purpose of Review: This article provides an overview of acute spinal cord injury with an emphasis on practical issues regarding initial evaluation and management. Spinal cord injury continues to be a devastating neurologic injury and a significant public health burden, both in terms of patient morbidity as well as societal costs. Optimal management is highly dependent on a strong multidisciplinary and interprofessional collaborative approach. Recent Findings: In contrast to prior experience, current guidelines strongly suggest avoidance of steroids in patients with spinal cord injury. Additionally, early evaluation with MRI and decompressive surgery can be important for achieving good outcomes. Summary: Effective management of acute spinal cord injury requires a team skilled in the approach to short- and long-term respiratory management as well as vigilance for common secondary complications including systemic thrombosis, infection, and pain syndromes.

Address correspondence to Dr Deborah M. Stein, R Adams Cowley Shock Trauma Center, 22 South Greene St, Baltimore, MD 21201, [email protected]. Relationship Disclosure: Dr Stein reports no disclosure. Dr Sheth serves on the editorial boards of Neurocritical Care, Neurosurgery, and Stroke. Unlabeled Use of Products/Investigational Use Disclosure: Drs Stein and Sheth report no disclosures. * 2015, American Academy of Neurology.

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EPIDEMIOLOGY Acute spinal cord injury is a particularly devastating consequence of traumatic injury. Approximately 40 cases per million population occur in the United States, equalling approximately 12,000 new cases in the United States each year.1 Worldwide rates range from 12 cases per million to nearly 60 cases per million population in different countries.2,3 Currently, between 238,000 and 332,000 people in the United States live with spinal cord injury.1 More than 80% of patients with spinal cord injury are male. Although classically considered a disease of young adults, the average age at the time of traumatic spinal cord injury has been increasing from approximately 29 years of age in the 1970s to more than 40 years of age in 2010.1 In some centers, the number of newly injured geriatric patients with spinal cord injury has increased fivefold over the past 3 decades,4 which Continuum (Minneap Minn) 2015;21(1):159–187

is largely thought to be due to the overall aging of the population and increased activity level of older adults. The most frequent injuries are incomplete quadriplegia (41%) followed by incomplete paraplegia (19%), complete paraplegia (18%), and complete quadriplegia (12%). Average yearly expenses for a patient with spinal cord injury range from more than $1 million in the first year for a high quadriplegic to more than $40,000 in subsequent years for a person with an incomplete spinal cord injury at any level. Estimated lifetime costs range from $1.1 million to more than $4.6 million depending on the degree of neurologic disability and age at injury.1 MECHANISM OF INJURY Injuries to the spinal cord typically occur at two peaks of age: young adults ages 15 to 29 and patients older than age 65. The most common cause www.ContinuumJournal.com

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

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Acute Spinal Cord Injury KEY POINTS

h Spinal cord injury is expected to become even more common in the elderly population because of overall aging of the population and the increased activity level of older adults.

h Injuries to the spinal cord typically occur at two peaks of age: young adults ages 15 to 29 and patients older than age 65.

of traumatic spinal cord injury is motor vehicle crashes.1 Falls are a common cause of spinal cord injury in older patients and the second leading cause of spinal cord injury overall. Spinal cord injuries in younger patients are also frequently caused by intentional violence, most typically gunshot wounds or sports-related injuries. Injuries to the spine tend to occur at areas of maximal mobility. Most typically, injuries occur when significant forces to the spinal column cause fractures, ligamentous disruption, or combined injuries that result in direct compression and injury to the spinal cord. Injuries to the spinal column are

commonly classified by location of injury (craniocervical, subaxial cervical, or thoracolumbar) and mechanism of injury (flexion, extension, or axial load) (Figure 10-1). The ‘‘three column’’ concept of thoracolumbar spine injuries (Figure 10-25) was described by Denis in 1984 and dictates that, generally, at least two of the three columns of the spine need to be disrupted to be considered unstable and subject the spinal cord to risk of injury.6 The major exception to this occurs in patients with underlying disorders such as spinal spondylosis or ankylosing spondylitis, which predisposes the spinal cord to injury without significant dis-

Examples of types of cervical fractures by mechanism. A, Flexion injury. First panel with subluxation of C5 on C6 vertebrae (arrow). Second panel with wedge fracture of C4 vertebral body (arrow). Third panel with locked facet (arrow) indicating facet dislocation. B, Extension injury. First panel with posterior spinous process fracture (arrow). Second panel demonstrates a hangman’s fracture of C2 (arrow). C, Axial load injury. First panel demonstrates burst fracture (arrow). Second panel demonstrates a compression fracture with loss of vertebral height at C5 (arrow).

FIGURE 10-1

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traction of bony elements. Cervical spinal cord injuries account for more than 50% of traumatic spinal cord injuries and are associated with much higher short- and long-term morbidity than injuries affecting the cord at the thoracic or lumbar levels.7 Spinal cord injury should always be suspected and ruled out in any patient sustaining a significant mechanism of trauma. Spinal precautions (eg, long board for transport, flat positioning, and log-roll turning) and immobilization with cervical collars are indicated for all major trauma patients until the spine can be adequately assessed. PATHOPHYSIOLOGY Injury to the spinal cord typically occurs in two phases (Figure 10-38). The first phase is the primary injury that occurs at the time of trauma and is directly related to a primary mechanical force applied to the spinal cord. Dumont and colleagues described the four characteristic mechanisms of primary injury.9 The most common mechanism is impact plus persistent compression,10 and the others are impact with transient compression, distraction, and laceration or transection. Impact with transient compression most commonly occurs with hyperextension injuries in underlying conditions such as cervical spondylosis. Distraction injuries, where the vertebral elements are pulled apart, can cause shear or stretching of the spinal cord and may be responsible for some pediatric injuries in which fractures are less common and in spinal cord injury without radiographic abnormality (SCIWORA).11 Lacerations and transections occur frequently with penetrating mechanism of injury and in the setting of blunt trauma with extreme displacement of the spinal column or bone fragments. The primary injury to the spinal cord tissue from this mechanism generally occurs as a result of mechanical forces at the moment of impact of the trauma and is currently irreversible. Continuum (Minneap Minn) 2015;21(1):159–187

The three columns of the spine. The anterior column includes the anterior longitudinal ligament, the anterior two-thirds of the vertebral bodies, the annulus fibrosus, and the intervertebral disks. The middle column includes the posterior longitudinal ligament, the posterior one-third of the vertebral bodies, the annulus, and intervertebral disks. The posterior column includes all of the bony elements formed by the pedicles, transverse processes, articulating facets, laminae, and spinous processes.

FIGURE 10-2

Reprinted with permission from Highsmith JM, Spine Universe.5 B www.SpineUniverse.com. www.spineuniverse.com/conditions/ spinal-fractures/types-spinal-fractures.

The second phase of injury to the spinal cord is mediated by a number of microvascular, biochemical, and cellular processes (Figure 10-49). These secondary insults are the targets of almost all management strategies for patients with spinal cord injury. The magnitude of the secondary insults are determined by the energy transferred to the spinal cord at the moment of injury and the subsequent development of additional systemic factors such as hypotension and hypoxia. Local factors also contribute, such as hemorrhage, ischemia-reperfusion injury, glutamate release, alterations in intracellular calcium concentrations, electrolyte and fluid disturbances, edema, apoptosis, and inflammation.9 Many of these mechanisms of additional injury have been elucidated in animal

KEY POINTS

h Generally, at least two of the three columns of the spine need to be disrupted to be considered unstable and subject the spinal cord to risk of injury.

h Spinal cord injury should be considered in every patient who sustains a significant trauma, especially those with traumatic brain injury or an acute confusional state.



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h The primary injury to the spinal cord tissue from the penetrating mechanism of injury generally occurs as a result of mechanical forces at the moment of impact of the trauma and is currently irreversible.

h The second phase of injury to the spinal cord is mediated by a number of microvascular, biochemical, and cellular processes. The secondary insults are the targets of almost all management strategies for patients with spinal cord injury.

FIGURE 10-3

Depiction of the primary and secondary spinal cord injuries. Reprinted with permission from Kwon, BK, et al, Spine J.8 B 2004 Elsevier Inc. www.sciencedirect.com/science/article/pii/S1529943003004935.

models of spinal cord injury, but, currently, no single pathway has been a successful target of pharmacologic intervention in humans. However, it is the mainstay of spinal cord injury treatment to attenuate, mitigate, and prevent these secondary processes through systemic treatment. INITIAL MANAGEMENT The initial management of a patient with spinal cord injury is the same as for any patient who has sustained a traumatic injury. As outlined in the American College of Surgeons’ advanced trauma life support (ATLS) course, the initial evaluation of any patient is dictated by the primary survey, which identifies immediately life-threatening injuries that

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require emergent intervention, and the secondary survey, during which a more detailed clinical examination is combined with imaging.12 The principle of the primary survey is a rapid and systematic evaluation that should be completed in the first few minutes of the patient’s arrival and follows the ABCDEs (airway, breathing, circulation, disability, and exposure) of resuscitation. The specific management of spinal cord injury can and should be deferred until other life-threatening injuries are evaluated and managed, as highlighted by Case 10-1. The physiologic consequence of the spinal cord injury, namely the risk of airway loss, inadequate oxygenation and ventilation, and



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KEY POINTS

h The airway of a patient with spinal cord injury should always be immediately secured by emergent endotracheal intubation in the following circumstances: complete spinal cord injury above the C5 level, respiratory distress, hypoxemia, and severe respiratory acidosis.

h Patients with injuries

FIGURE 10-4

above the C5 level often need urgent endotracheal intubation. Respiratory arrest is common in patients with injury above C3, and airway management and adequate oxygenation is critical in the initial minutes after injury for this group of patients.

Proposed pathways of secondary insults after spinal cord injury. DNA = deoxyribonucleic acid; ATP = adenosine triphosphate. Reprinted with permission from Dumont RJ, et al, Clin Neuropharmacol.9 B 2001 Lippincott Williams & Wilkins. journals.lww.com/clinicalneuropharm/Abstract/2001/09000/ Acute_Spinal_Cord_Injury,_Part_I__Pathophysiologic.2.aspx.

hypotension, require immediate attention during the primary survey. The airway of a patient with spinal cord injury should always be immediately secured by emergent endotracheal intubation in the following circumstances: complete spinal cord injury above the C5 level,13 respiratory distress, hypoxemia, and severe respiratory acidosis. Patients with cervical and high thoracic spinal cord injury are at high risk of airway loss due to several factors such as airway and neck edema or hematoma from direct neck trauma and local bleeding. In patients with high cervical spinal cord injury above the C5 level, loss of diaphragmatic innervation via injury to C3 to C5 levels, as well as loss of chest and abdominal wall strength, contributes significantly to a patient’s inability to maintain adequate oxygenaContinuum (Minneap Minn) 2015;21(1):159–187

h The chest wall and

tion and ventilation. Patients with complete injuries above the C3 level will invariably experience a respiratory arrest in the prehospital environment due to absence of diaphragmatic function. Inadequate oxygenation and ventilation occur frequently in patients with cervical and high thoracic spinal cord injury due to a number of factors.14 The chest wall and abdominal musculature that are so vital for effective ventilation are often severely compromised in the setting of spinal cord injury, resulting in hypoventilation and loss of ability to generate an effective cough and clear secretions. Aspiration, retention of secretions, and the development of atelectasis contribute to respiratory decompensation. Additionally, concomitant injuries such as pulmonary contusions and pneumothoraces may

abdominal musculature that are so vital for effective ventilation are often severely compromised in the setting of spinal cord injury, resulting in hypoventilation and loss of ability to generate an effective cough and clear secretions. Aspiration, retention of secretions, and the development of atelectasis contribute to respiratory decompensation.



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Case 10-1 A 32-year-old man presented to a trauma center after a high-speed rollover. He demonstrated agonal respirations in the field and was endotracheally intubated with cervical spine stabilization. His primary survey revealed blood in his airway with decreased breath sounds on the left and an oxygen saturation of 88%. A left tube thoracostomy was rapidly performed, resulting in improved oxygenation. His blood pressure was 72/40 mm Hg, his pulse rate was 82 beats/min, and his skin was cold and clammy. A focused assessment with sonography for trauma (FAST) was performed, revealing hemoperitoneum. He had sluggishly reactive but equal pupils and no spontaneous movement or motor response to painful stimulation. A massive transfusion protocol was initiated. He was emergently taken to the operating room after chest and pelvic radiographs were performed, revealing extensive pulmonary contusions. A splenectomy was performed. The patient’s head CT revealed diffuse axonal injury and diffuse subarachnoid blood. Cervical spine CT revealed a C4-C5 dislocation with a unilateral jumped/locked right facet, C3, C4, and C5 fractures with a 6-mm anterolisthesis of the major C4 vertebral body fragments and a narrowed canal across C4-C5 (Figure 10-5A and B). IV fluids were administered and norepinephrine was started for neurogenic

Imaging of the patient in Case 10-1. CT (A, B) shows C4-C5 dislocation (arrow, A) with a unilateral jumped/locked right facet (arrow, B) and 6 mm anterolisthesis of the major C4 vertebral body fragments across the posterior vertebral body fracture and disrupted intervertebral disk (arrows). Fractures also involve the C3 right lateral mass and transverse process, the C4 right lateral mass, transverse process and lamina, the C5 right lateral mass, and transverse process and anterior/superior vertebral body. The spinal canal appears mildly narrowed across C4-C5 (circle). MRI (C) of C4-C5 dislocation with unilateral jumped/locked right facet joint and disk disruption with intervertebral listhesis. Anterior longitudinal ligament and posterior longitudinal ligament are injured with disruption of the posterior ligament complex. The spinal canal remains mildly narrowed across C4-C5. Spinal cord injury is manifest as a subcentimeter focus of intramedullary hemorrhage at C4-C5 level (solid white arrow) with cord edema extending along a 9-cm segment from C2 to C6 (open white arrows).

FIGURE 10-5

shock. The patient was difficult to oxygenate and ventilate due to copious bloody secretions and high airway pressures consistent with his pulmonary contusions. He was maintained in a cervical collar in the intensive care unit (ICU) with strict bedrest and flat/log-roll precautions. MRI revealed a C4-C5 dislocation with unilateral jumped/locked right facet joint and disk disruption with intervertebral displacement. The anterior longitudinal ligament and posterior longitudinal ligament

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Continued from page 164 were injured with disruption of the posterior ligament complex, and there was a subcentimeter focus of intramedullary hemorrhage at the C4-C5 level with spinal cord edema extending along a 9-cm segment from C2 to C6 (Figure 10-5C). He remained on vasoactive medications with profound respiratory failure and underwent a tracheostomy on the ninth day of hospitalization. On the 12th day of hospitalization, the patient was following commands and a detailed neurologic examination was performed, revealing an American Spinal Injury Association (ASIA) 4B injury. He was ultimately weaned to tracheostomy collar/mask and discharged to a rehabilitation facility after 42 days of hospitalization. Comment. The competing priorities are quite typical of the multiply injured patient. As long as spinal stabilization is maintained, the patient’s other more life-threatening issues can be emergently addressed and specific management for the spinal cord injury can be deferred. This case also highlights how difficult the evaluation of the patient with spinal cord injury can be with other concomitant injuries.

occur. Up to 65% of patients with cervical spinal cord injury will have evidence of respiratory dysfunction on admission to the intensive care unit (ICU).15 Hypoxemia must be aggressively treated with supplemental oxygen as it is known to be detrimental to patients with neurologic injury. In addition, hypoxemia can result in severe bradycardia and even asystole in patients with high cervical spinal cord injuries due to unopposed vagal stimulation.16,17 Patients with cervical and high thoracic spinal cord injury experiencing impending respiratory failure will often describe heaviness in the chest or an inability to catch their breath, as demonstrated in Case 10-2. Often,

these patients will appear breathless while speaking and develop the very stereotypical breathing pattern (referred to as quad breathing) in which the chest goes in with inspiration and the abdomen goes out sharply with diaphragmatic contraction due to loss of chest wall and abdominal muscle innervation. Treatment of respiratory insufficiency following spinal cord injury begins with aggressive use of endotracheal intubation. In one study, all patients with complete injuries at the C5 level and above required a definitive airway, and nearly 80% of patients with complete injuries at the C6 level and below required intubation during their hospitalization.13 In another study, three

Case 10-2 A 21-year-old man presented to a trauma center following a diving incident into shallow water. The patient experienced a transient loss of consciousness with the impact. Upon presentation, his primary survey was significant for a blood pressure of 82/48 mm Hg with a pulse rate of 52 beats/min. He was breathing comfortably but reported some shortness of breath. On secondary survey, he was awake and alert and had 5/5 muscle strength in his biceps bilaterally, 5/5 strength in his wrist extensors on the right, 4/5 strength in his wrist extensors on the left, and 4/5 triceps muscle strength bilaterally. He had no sensation below the nipple line and no rectal tone or push (American Spinal Injury Association [ASIA] 27A). A CT scan revealed bilateral interfacet dislocation at C6-C7 with associated anterolisthesis, interspinous process widening, and severe canal narrowing. Fractures of the C7 superior endplate anteriorly, the right C7 superior articular process, and C6 spinous process were also noted (Figure 10-6A and B). The patient was placed in cervical traction, but his facet dislocation

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Imaging of the patient in Case 10-2. CT scan (A, B) shows bilateral interfacetal dislocation at C6-C7 (arrow) with associated anterolisthesis, interspinous process widening, and severe canal narrowing (circle). Fractures of the C7 superior endplate anteriorly, the right C7 superior articular process, and C6 spinous process are noted. T2-weighted MRI sequence (C) demonstrating traumatic spinal cord injury centered at C6-C7 with cord signal abnormality extending from C5 through T1 levels. C6-C7 anterior and middle column diskoligamentous injuries with ligamentum flavum partial tear (arrow) are also seen.

FIGURE 10-6

could not be reduced under fluoroscopic guidance. He developed worsening respiratory function with the development of ‘‘quad breathing,’’ in which the chest wall retracts and the abdominal wall protrudes with inspiration, and was intubated and taken to the operating room for open reduction and posterior spinal fusion. Postoperatively, an MRI revealed a traumatic spinal cord injury centered at C6-C7 with cord signal abnormality extending from the C5 through T1 levels and C6-C7 anterior and middle column diskoligamentous injuries with a partial tear of the ligamentum flavum (Figure 10-6C). The patient was transferred to the intensive care unit (ICU) and a mean arterial blood pressure of greater than 85 mm Hg was continued by using norepinephrine. He was kept intubated and underwent an anterior cervical diskectomy and fusion on his second day of hospitalization. Reevaluation by physical therapy revealed an ASIA of 22A. Postoperatively, the patient’s hospital course was complicated by persistent hypotension and bradycardia, which was treated with vasoactive infusions and enteral albuterol and midodrine. He developed severe acute respiratory failure, atelectasis, and ventilator-associated pneumonia. He received aggressive secretion clearance and underwent tracheostomy on the 10th day of hospitalization and was ultimately weaned to tracheostomy collar/mask on the 22nd day of hospitalization. The patient was discharged to an acute rehabilitation center 28 days after being admitted to the hospital. Comment. This case highlights the typical presentation and hospital course of a patient with a cervical spinal cord injury. The early onset of neurogenic shock and the progression of respiratory insufficiency necessitating intubation are frequently seen in patients with complete injuries. His neurologic worsening from his initial status on presentation was associated with ascension of his injury from edema and ischemia of the spinal cord. His hospital course and lack of significant recovery is also quite typical of a patient with a complete cervical spinal cord injury.

independent risk factors for the need of intubation were identified: an Injury Severity Score (a measure of overall traumatic injury burden based on the three most severely injured body regions) of greater than 16, spinal cord

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injury level above the C5 level, and completeness of injury.14 Table 10-118 lists some of the indications for urgent intubation in patients with traumatic cervical spine injury. All patients with cervical and high thoracic spinal cord



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KEY POINTS

TABLE 10-1

Indications for Intubation of the Patient With Traumatic Cervical Spine Injurya

b Absolute Indications Complete spinal cord injury above C5 level Respiratory distress Hypoxemia despite attempts at oxygenation Severe respiratory acidosis b Relative Indications Report of shortness of breath Development of quad breathingb Vital capacity of G10 mL/kg or decreasing vital capacity Need to travel remote from emergency department (eg, MRI, transfer to another facility)

b

Reprinted with permission from Stein DM, et al, Neurocrit Care.18 B 2012 Neurocritical Care Society. link.springer.com/article/10.1007%2Fs12028-012-9759-0. Quad breathing refers to the stereotypical breathing pattern in patients with cervical and upper thoracic spinal cord injury in which the chest wall retracts and the abdominal wall protrudes with inspiration.

injury should be carefully observed even if they have no immediate indication for intubation as the progression of injury due to edema and ischemia may result in worsening of respiratory function over minutes, hours, or days following injury. The ‘‘C’’ (circulation) portion of the primary survey following traumatic injury mandates evaluation and emergent treatment of hypotension and active hemorrhage. Although polytrauma patients will most likely be hypotensive as a result of hemorrhagic shock, neurogenic shock can play a significant role in patients with spinal cord injury at the T6 level and above due to the sympathectomy that occurs in the setting of spinal cord injury, causing the loss of supraspinal control of the sympathetic nervous system (Figure 10-719).17,20 This results in unopposed parasympathetic activity and stimulation of the vagus nerve, which leads to profound bradycardia and atrioventricular nodal block in addition to hypotension.20 In the patient with spinal cord injury, hypotension and subsequent hypoperfusion to the spinal cord worsen Continuum (Minneap Minn) 2015;21(1):159–187

and high thoracic spinal cord injury should be carefully observed even if they have no immediate indication for intubation as the progression of injury due to edema and ischemia may result in worsening of respiratory function over minutes, hours, or days following injury.

h Neurogenic shock is a

b Consideration Should Be Given

a

h All patients with cervical

secondary insults and are associated with poorer outcomes. Therefore, neurogenic shock should be aggressively treated. Neurogenic shock is a form of distributive shock (characterized by excessive vasodilatation such as in sepsis) with the characteristic finding of bradycardia. Patients with neurogenic shock are generally hypotensive with warm, dry skin due to vasodilatation, as opposed to patients with shock from other causes. As a general rule, the higher and more complete the injury, the more severe and refractory the neurogenic shock.21 Neurogenic shock following spinal cord injury typically lasts for 1 to 3 weeks and may not manifest on admission but develops over hours to days due to ascension of the injury from secondary insults. Due to the profound peripheral vasodilatation that occurs in neurogenic shock, the first-line therapy is fluid resuscitation to maintain euvolemia and treat the effective increase in circulating blood volume. Once euvolemia is achieved, second-line treatment of neurogenic shock is the use of pressors, inotropes,

form of distributive shock with the characteristic finding of bradycardia. Patients with neurogenic shock are generally hypotensive with warm, dry skin due to vasodilatation, as opposed to patients with shock from other causes. In general, the higher and more complete the injury, the more severe and refractory the neurogenic shock.



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h The first-line therapy in patients with shock is a goal of euvolemia. Pressors and inotropes can be used as a second-line therapy, and systemic causes of hypotension such as ongoing bleeding and cardiogenic shock should always be considered.

h As long as the spine is protected with cervical collars, in-line stabilization, flat positioning, and log-roll turning, specific management of a spinal cord injury is deferred until other life-threatening injuries are addressed.

The parasympathetic and sympathetic innervation of the heart will, respectively, reduce and increase the heart rate. Sympathetic neurons in the upper thoracic part of the spinal cord innervate the cardiovascular system of the upper thorax. The sinus node receives sympathetic innervation from T3-T4 and parasympathetic innervation from the vagus nerve. Parasympathetic afferent nerves from baroreceptors in the aortic arch and carotid sinus go to the medulla oblongata via the glossopharyngeal and vagus nerves.

FIGURE 10-7

Reprinted from Hagen EM, et al, Tidsskr Nor Laegeforen.19 tidsskriftet.no/article/2265051. Printed with permission from B Kari C. Toverud, MS, CMI.

or a combination. No established recommendations currently exist for a specific agent of choice.21,22 Table 10-218 lists some of the potential benefits and risks of the commonly used agents. EVALUATION Most significant spinal cord injuries should be readily apparent during the ‘‘D’’ (disability) portion of the primary survey with rapid recognition of major motor deficits. As long as the spine is protected with cervical collars, cervical spine manual stabilization, flat posi-

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tioning, and log-roll turning, specific management of a spinal cord injury is deferred until other life-threatening injuries are addressed. As part of the secondary survey, a very careful and detailed evaluation should be performed to precisely identify the degree of both motor and sensory deficits. Over hours to days following injury, neurologic deficits will almost invariably worsen. An accurate assessment of the degree of neurologic dysfunction as close to the injury as feasible is important as it has significant prognostic value and



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Vasoactive Agents Used to Treat Neurogenic Shocka

TABLE 10-2 Agent

Alpha Activity Beta Activity Considerations

Norepinephrine

+++

++

Probably the preferred agent

Phenylephrine

++

None

May worsen bradycardia

Dopamine Low dose (3Y10 mcg/kg/min) + High dose (10Y20 mcg/kg/min) ++

++ +++

May lead to inadvertent diuresis at low dose

Epinephrine

+++

++

Rarely needed

Dobutamine

None

+++

May cause hypotension if not euvolemic

+ = small effect; ++ = moderate effect; +++ = large effect. a Reprinted with permission from Stein DM, et al, Neurocrit Care.18 B 2012 Neurocritical Care Society. link.springer.com/article/ 10.1007%2Fs12028-012-9759-0.

predicts the risk of development of subsequent complications.15 The full examination described by ASIA includes a detailed motor and sensory examination and is the preferred evaluation tool (Figure 10-823).24 The neurologic examination in this setting focuses on motor, sensory, rectal tone, and rectal sensation findings. ASIA uses the Medical Research Council (MRC) 0 to 5 scale for assessment of motor strength of 10 muscle groups on each side of the body. The scores for all 20 muscle groups are added, providing the total ASIA motor score. Sensation is evaluated as absent (0 points), altered (1 point), normal (2 points), or untestable. ASIA also defines a five-element scale, the ASIA impairment scale, which classifies a patient’s lesion as complete or incomplete. The combination of the ASIA impairment scale with the ASIA motor score comprises the best description of a patient’s neurologic status following spinal cord injury. Of note, the presence of spinal shock, in which a loss of spinal reflexes occurs below the anatomic level of injury, may confound the ability to obtain an accurate initial evaluation due to loss of apparent function unrelated to neuronal injury. Spinal shock typically develops in the hours after injury and may last from several days up to 4 to 6 weeks. Continuum (Minneap Minn) 2015;21(1):159–187

Specific Syndromes In addition to complete and incomplete injuries as defined by the ASIA impairment scale, a number of discrete incomplete neurologic syndromes have been described (Figure 10-9). The most common of these following injury is the central cord syndrome. As Case 10-3 highlights, this injury is common in older patients with underlying cervical spondylosis. Central cord syndrome is typically due to a hyperextension injury and is typically not associated with bony injury, but rather is caused by a buckling of the ligamentum flavum which contuses the cord, resulting in central injury. The loss of cervical motor function with relative sparing of lower extremity strength is characteristic, due to the somatotopic organization of the upper extremity motor fibers as the most medial of the corticospinal tracts. Brown-Se´quard syndrome is a less common spinal cord injury syndrome in which hemiplegia occurs with ipsilateral loss of light touch and proprioception with contralateral loss of pain and temperature sensation. This syndrome is typically due to traumatic hemisection of the spinal cord most typically from penetrating spinal cord injury, often from missiles or knife wounds, or a lateral mass fracture of the spine. Anterior cord syndrome is also relatively rare following trauma and is more

KEY POINT

h The American Spinal Injury Association scale is the most widely used tool to evaluate and follow neurologic deficits after spinal cord injury.



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FIGURE 10-8

Reprinted with permission from the American Spinal Injury Association (ASIA) International Standards Committee; Kirshblum S, et al.23 B 2014 American Spinal Injury Association. www.asia-spinalinjury.org/elearning/ISNCSCI.php.

American Spinal Injury Association International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) examination worksheet.


FIGURE 10-9

Schematic depiction of the four major cord syndromes. A, region of the spinal cord affected in central cord syndrome; B, region of the spinal cord affected in Brown-Se´quard syndrome; C, region of the spinal cord affected in anterior cord syndrome; D, region of the spinal cord affected in posterior cord syndrome. Created by Polarlys and Mikael Ha¨ggstro¨m, MD. Released under the Attribution-Share Alike 3.0 Unported license.

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Case 10-3 A 76-year-old man was walking his dog when he was suddenly pulled forward, falling and striking his forehead on the ground. No loss of consciousness was noted. He immediately experienced tingling and weakness in his hands. Upon presenting to a trauma center for evaluation, his primary survey was unremarkable. He was hemodynamically stable with normal oxygenation and nonlabored respirations. His secondary survey revealed bilateral upper extremity weakness predominantly in his hands and relatively normal motor strength throughout his lower extremities. Sensation was slightly diminished to light touch in the left leg. He had intact rectal tone and sensation (Figure 10-10).

FIGURE 10-10

American Spinal Injury Association evaluation of the patient in Case 10-3 with central cord syndrome.

A CT scan of the cervical spine revealed chronic cervical spondylosis and no cervical spine fracture (Figure 10-11A). Cervical spine MRI demonstrated a spinal cord contusion at the level of C4 with multilevel degenerative changes of the cervical spine, resulting in moderate to severe spinal stenosis from C3-C4 through C6-C7 (Figure 10-11B). On the second day of hospitalization, he underwent a laminectomy and posterior spinal fusion. Postoperatively, the patient remained in the intensive care unit (ICU) on low dose vasoactive medications for 7 days following the injury to maintain a mean arterial blood pressure of greater than 85 mm Hg. The patient was extubated on the fifth day of hospitalization, but developed secretion retention and required high-flow nasal cannula and aggressive secretion clearance. He ultimately did well and was transferred to an acute spinal cord rehabilitation facility on the 12th day of hospitalization. At his 6-month follow-up, he was living at home with only slight bilateral triceps and hand grip weakness.

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FIGURE 10-11

Imaging of the patient in Case 10-3. A, CT demonstrates no evidence of cervical spine fracture. B, MRI demonstrates spinal cord contusion (arrow) at the level of C4 with multilevel degenerative changes of the cervical spine resulting in moderate to severe spinal stenosis from C3-C4 through C6-C7.

Comment. This case illustrates a very typical mechanism, injury course, and recovery for an elderly patient with underlying cervical spinal stenosis. The hyperextension mechanism without bony fracture or ligamentous injury with the physical examination findings are classic for central cord syndrome. The patient’s good neurologic recovery is also quite typical of these incomplete injuries.

commonly described following an ischemic insult from disruption of flow in the anterior spinal artery, but can also result from trauma, in which axial compression and burst fractures cause retropulsion of the vertebral body and bone fragments into the anterior portion of the cord. The unusual deficit of this syndrome is due to the relative sparing of dorsal column sensory pathways with disruption of motor fibers in the corticospinal tracts and the pain/ temperature and light touch sensory fibers carried in the spinothalamic tracts. Prognosis for recovery following anterior cord syndrome is characteristically poor. Posterior cord syndrome is a syndrome in which the posterior aspect of

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the spinal cord is affected, resulting in loss of proprioception with preservation of motor function, pain/temperature sensation, and light touch due to the relative effect on the dorsal columns with sparing of the lateral and anterior tracts of the spinal cord. This syndrome most commonly is the result of a vascular compromise to the spinal cord or nonstructural diseases and is rarely the result of traumatic injury. Cauda equina syndrome in the setting of trauma is typically caused by retropulsion of fracture fragments in the lumbosacral region, resulting in lower spinal nerve root compression. The features of this syndrome are back and lower extremity pain, sensory loss, bowel and bladder dysfunction, and saddle



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anesthesia. Patients with this syndrome typically have reduced or absent perianal and perineal sensation, decreased rectal tone and contraction, and absent or decreased spinal reflexes such as the ‘‘anal wink’’ or bulbocavernosus reflex. For more information, refer to the article ‘‘Spinal Cord Functional Anatomy’’ by Tracey A. Cho, MD, in this issue . of In addition to the above welldescribed incomplete syndromes, spinal concussions have also been described.25 These can be either complete or incomplete, but are defined by a transient dysfunction that resolves and is not associated with radiographic abnormalities on imaging of the spinal cord. This syndrome is most commonly seen from sports injuries, particularly American football. Symptoms typically include numbness, tingling, and paresthesia. Spinal cord injury without radiographic abnormalities (SCIWORA) is a syndrome, commonly of the cervical or upper thoracic spine, most typically described in children.11 These injuries, as the name states, were classically characterized by an absence of radiographic findings. With the increasing use of MRI, however, findings of specific spinal cord abnormalities from complete transection, hemorrhage, and edema are increasingly seen. These injuries are likely related to the elasticity of the juvenile spine, which allows for displacement of the spinal cord without disruption of the ligamentous structures. SCIWORA has been reported in adults as well.26 There is some controversy whether patients with injury noted only on MRI actually constitute SCIWORA, but many clinicians still use this term to describe injuries with normal radiographs and abnormalities only noted on MRI.27 Prognosis following SCIWORA is primarily determined by the patient’s neurologic status on admission and degree of hemorrhage Continuum (Minneap Minn) 2015;21(1):159–187

noted in the spinal cord. Treatment is largely supportive and focuses on prevention of recurrent injury, although some patients with ligamentous disruption noted on MRI may benefit from surgical stabilization. IMAGING Although initial imaging of the spine following trauma historically was accomplished with plain radiographs, CT scan has almost entirely replaced plain radiographs as the initial imaging modality of choice.28 Imaging of the entire spine is indicated in the patient with spinal cord injury as up to 40% of patients will have a concomitant noncontiguous injury.21 CT scan is excellent for detection of bony injury and dislocations, but is limited in the evaluation of ligamentous and soft tissue injury (Figure 10-12). Therefore, MRI may detect occult injuries, particularly in the obtunded patient in whom symptoms referable to spinal cord injury may not be detected. In the symptomatic patient with spinal cord injury, MRI plays a pivotal role in establishing the diagnosis, planning operative therapy, and determining prognosis. Of particular interest is the sagittal T2-weighted sequence, which accurately assesses the degree of edema or hemorrhage in the spinal cord that is essential for prognostication.29

KEY POINTS

h Spinal cord injury without radiographic abnormalities (SCIWORA) commonly occurs in younger patients, and the degree of recovery often parallels the extent of initial neurologic deficits.

h In the symptomatic patient with spinal cord injury, MRI plays a pivotal role in establishing the diagnosis, planning operative therapy, and determining prognosis. Of particular interest is the sagittal T2-weighted sequence, which accurately assesses the degree of edema or hemorrhage in the spinal cord that is essential for prognostication.

ACUTE MANAGEMENT Anatomic Reduction and Surgical Management Anatomic reduction of the spinal column in the setting of spinal cord injury is indicated in the situation of any neurologic deterioration, facet dislocation, or bilateral locked facets. Closed anatomic reduction should be performed as soon as possible for the awake patient with fracture or dislocation injuries of the cervical spine.30 Most typically, anatomic reduction is accomplished with traction www.ContinuumJournal.com


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A 68-year-old man after a fall that resulted in interspinous and supraspinous ligament sprain of C6-C7 consistent with mild distraction injury. A, Sagittal and coronal reconstructions of CT demonstrating normal vertebral body alignment without anterior or posterior disk space widening. No facet displacement is shown. Fragmented osteophytes are noted anteriorly. The C6-C7 level is indicated by arrows. B, Sagittal views of short tau inversion recovery (STIR) MRI demonstrating disrupted ligamentum flavum (open white arrows) and interspinous ligament (stars). Posteriorly, the supraspinous ligament (black arrow) is stripped off the spinous processes. Abnormal signal is also seen in the posterior paraspinal musculature (white arrow).

FIGURE 10-12

Courtesy of David Dreizin, MD.

applied under fluoroscopic guidance. In patients who cannot be examined due to depressed level of consciousness or heavy sedation during closed reduction, MRI prior to reduction is recommended due to the high incidence

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of disrupted intervertebral disks or disk herniation that may be worsened with closed reduction.30 If closed reduction cannot be accomplished, emergent open reduction is usually recommended after additional imaging with MRI to better



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delineate anatomy and plan the operative approach.21 Goals of surgical management in the patient with spinal cord injury are to stabilize the spine, decompress the spinal canal, and prevent further neurologic injury. Although previous studies from the 1960s and 1970s failed to demonstrate improvement in neurologic outcome with emergent surgical decompression in patients with cervical spinal cord injury, additional studies in the 1990s began to demonstrate some benefit.31 Other studies, however, demonstrated no significant difference between early (less than 3 days) or late (greater than 5 days) decompression in patients with cervical spinal cord injury.32 The Surgical Timing in Acute Spinal Cord Injury Study (STASCIS), a multicenter, international, prospective cohort study of adults with cervical spinal cord injury, demonstrated that decompression within 24 hours of injury could be performed safely and was associated with improved neurologic outcome.33 Improvement in neurologic outcome was defined as at least a 2 grade ASIA impairment scale improvement at 6-month follow-up. Although some controversy still exists about the timing of spinal stabilization in patients who do not require spinal decompression, current recommendations include immobilization by either internal fixation or external immobilization of the cervical spine to accomplish early patient mobilization and rehabilitation.34 In thoracic and lumbar fractures, considerably less consensus exists on timing and necessity of surgical intervention. The Thoracolumbar Injury Classification and Severity Score (TLICS) was described in 2005 and defines injury based on three clinical characteristics: injury morphology, integrity of the posterior ligamentous complex, and neurologic status of Continuum (Minneap Minn) 2015;21(1):159–187

the patient.35 These factors can then be used to score injuries and determine the need and timing of surgical intervention. Several studies have documented superior non-neurologic outcomes such as complication rates, hospital length of stay, ventilator days, and overall resource utilization in patients treated with early surgical stabilization. Drug Therapies To date, no single pharmacologic therapy has been successful at mitigating the neurologic effects of spinal cord injury. Enthusiasm for the use of steroids for treatment of spinal cord injury, which was recommended as a standard of care therapy for decades based on the results of the National Acute Spinal Cord Injury (NASCIS) trials, has largely been abandoned.36 Despite a recent study by the Cochrane Database of Systematic Reviews suggesting efficacy if administered within 8 hours of injury,37 the use of methylprednisolone for the treatment of acute cervical spinal cord injury is no longer recommended according to the 2013 revision of Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries.38 They cite a lack of class I data as the beneficial effects published in the NASCIS trials were only found in post hoc subgroup analysis along with a demonstrable risk of detrimental side effects, including infections, gastrointestinal hemorrhage, hyperglycemia, and death. It should be noted, however, that considerable controversy still exists on the use of methylprednisolone for spinal cord injury and that it is still used in some centers. Similarly, despite some initial enthusiasm for GM1 ganglioside as a therapeutic agent for motor recovery following spinal cord injury,39 long-term follow-up in subsequent studies failed to demonstrate a durable effect40 leading

KEY POINTS

h The primary goals of surgical management are to stabilize the spine, provide adequate decompression, and prevent secondary injury. Closed reduction should be performed in a timely manner. The Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) suggested that surgery within 24 hours was associated with improved neurologic outcomes in patients with cervical spinal cord injury.

h Although some controversy still exists about the timing of spinal stabilization in patients who do not require spinal decompression, current recommendations include immobilization by either internal fixation or external immobilization of the cervical spine to accomplish early patient mobilization and rehabilitation.

h Based on the National Acute Spinal Cord Injury (NASCIS) trials and after several years of controversy, the American Association of Neurological Surgeons’ and Congress of Neurological Surgeons’ guidelines do not recommend steroids for acute cervical spinal cord injury.



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h The mainstay of treatment of all patients with spinal cord injury is largely supportive, focusing on minimizing the secondary insults and preventing and aggressively treating complications that frequently occur. After surgical stabilization, patients with cervical and high thoracic spinal cord injury should be treated in a monitored setting such as an intensive care unit. These patients are at exceptionally high risk of organ dysfunction and failure and require high-level intensive support.

h Respiratory dysfunction occurs in more than 85% of patients with cervical spinal cord injuries, with more than 40% meeting criteria for respiratory failure by standardized organ dysfunction scales. The reasons for this are largely due to the intrinsic dysfunction from denervation of the muscles essential for adequate ventilation. Reduced vital and inspiratory capacity as well as reduced expiratory muscle force from diminished or absent diaphragm and chest wall musculature can lead to hypoxemia and hypercarbia.

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to a recommendation against its use.38 Other therapies such as thyrotropinreleasing hormone, nimodipine, and gacyclidine (GK-11) have also failed to demonstrate benefit in clinical trials. Studies into a number of other agents, such as an investigational Rho protein antagonist and riluzole (a benzothiazole which has demonstrated neuroprotective properties in animal models of traumatic spinal cord injury through sodium channel blockade and is US Food and Drug Administration (FDA)Yapproved for use in ALS), are currently ongoing. Other Therapies Other nonpharmacologic treatments of investigational interest in the acute treatment of spinal cord injury include stem cells and the use of therapeutic hypothermia. Animal models have demonstrated that treatment with allogeneic stem cells improves both motor and sensory function,41 but human data to date are limited and no large clinical trials of the use of stem cells in patients with spinal cord injury have been concluded. A trial was approved in 2010 but was later terminated by the company due to financial concerns. Similarly, a recent meta-analysis of animal studies on the use of systemic therapeutic hypothermia described the intervention as a ‘‘promising potential method of treating acute spinal cord injury.’’42 To date, no large study has been conducted, but noncontrolled studies have suggested the potential for benefit in patients with spinal cord injury.43 A large, randomized multicenter trial is being planned. INTENSIVE CARE UNIT MANAGEMENT Given that little can be done for the acute primary injury to the spinal cord, the mainstay of treatment of all patients with spinal cord injury is largely sup-

portive, focusing on minimizing the secondary insults and preventing and aggressively treating complications that frequently occur. After surgical stabilization, patients with cervical and high thoracic spinal cord injury should be treated in a monitored setting such as an ICU.21,44 These patients are at exceptionally high risk of organ dysfunction and failure and require high-level intensive support.15 Patients with lower thoracic and lumbar injuries are at much lower risk of cardiovascular and respiratory dysfunction, and much of the hospital course of these patients will be dictated by the sequelae of their concomitant injuries. Other than aggressive and early mobilization, patients with thoracic and lumbar level cord injuries will typically be managed much like any other injured patient with particular attention to skin breakdown and the potential for bladder and bowel dysfunction. Therefore, much of the subsequent discussion is referable specifically to patients with cervical or high thoracic spinal cord injuries. Respiratory Management Respiratory dysfunction occurs in more than 85% of patients with cervical spinal cord injuries, with more than 40% meeting criteria for respiratory failure by standardized organ dysfunction scales.15 The reasons for this are largely due to the intrinsic dysfunction from denervation of the muscles essential for adequate ventilation (Table 10-3). Reduced vital and inspiratory capacity as well as reduced expiratory muscle force from diminished or absent diaphragm and chest wall musculature can lead to hypoxemia and hypercarbia. Even in the presence of intact diaphragmatic function, the flaccid paralysis that occurs in the accessory muscles of ventilation innervated by the lower cervical and thoracic segments, such as the intercostal musculature, results in a



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KEY POINT

TABLE 10-3

h Respiratory management

Muscles of the Respiratory System

Muscle Group

Function

Innervation

Diaphragm

Major muscle of respiration

C3 to C5

is one of the most important aspects of the immediate critical care management of spinal cord injury and should employ rigorous chest physiotherapy, secretion clearance devices, bronchodilators, and assisted coughing devices.

During inhalation, the diaphragm contracts and moves downward During exhalation, the diaphragm relaxes, allowing for passive recoil Intercostal muscles

During inhalation, the external intercostal muscles contract and elevate the rib cage

T1 to T11

During exhalation, the internal intercostal muscles contract and pull the ribs down Abdominal muscles

Essential for an effective cough

T6 to L1

During exhalation, the abdominal muscles contract and compress the abdominal contents and push the diaphragm up Accessory muscles

Elevate the rib cage and assist in deep ventilation

C1 to C3

Inadequate alone for effective ventilation

decrease in efficacy of diaphragmatic movement by contraction of the chest wall with inspiration, which has been associated with a 70% decrease in maximal inspiratory force.45 Ineffective cough generation and overall increase in respiratory secretion production and increased bronchial tone from unopposed parasympathetic activity also contribute to respiratory dysfunction. Respiratory function is further compromised by concomitant injuries, such as pulmonary contusions and pneumothoraces or hemothoraces, as well as the development of complications, such as atelectasis, pneumonia, and pulmonary embolism. The development of respiratory dysfunction is directly related to the severity and completeness of the spinal cord injury as measured by ASIA and the ASIA impairment scale.15 Aggressive treatment of respiratory insufficiency is essential to minimize the risk of hypoxemia, which can exacerbate the ischemic insult to the spinal cord.44 The respiratory management of the patient with spinal cord injury should Continuum (Minneap Minn) 2015;21(1):159–187

ideally include a combination of chest physiotherapy, secretion clearance devices, bronchodilators, mucolytics, respiratory muscle training, assisted breathing, and assisted coughing devices and techniques.45 Weaning these patients from mechanical ventilation can be difficult and lengthy, and many patients with high complete injuries will require long-term mechanical ventilation.13 The transition of a flaccid paralysis of the accessory muscles of respiration to a spastic paralysis is coincident with the resolution of spinal shock, leading to overall improved ventilatory function due to the improved efficacy of diaphragm function against the rigid chest wall. Data suggest that aggressive pulmonary therapy initiated early after acute spinal cord injury is associated with improved survival, a reduced incidence of pulmonary complications, and a decreased need for long-term ventilatory support.45 Other studies have demonstrated the efficacy of dedicated weaning protocols in liberating patients from mechanical www.ContinuumJournal.com


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h Admission American Spinal Injury Association motor score has been shown to predict the need for tracheostomy, with 100% of patients with an admission American Spinal Injury Association score of less than 10 requiring tracheostomy.

h Current recommendations are to maintain mean arterial blood pressure between 85 and 90 mm Hg for the first 7 days following acute cervical spinal cord injury.

ventilation.21,46 Additionally, due to the high incidence of pneumonia in this patient population, a protocolized ventilator care ‘‘bundle’’ (a group of evidence-based practices that have been demonstrated to be of benefit to patient outcomes) should be utilized in mechanically ventilated patients with spinal cord injury.21 Although many patients with cervical spinal cord injury can be successfully extubated, some will ultimately require tracheostomy.47 Although the ideal timing of tracheostomy is not known, studies not limited to patients with spinal cord injury have demonstrated a reduction in ICU length of stay and duration of mechanical ventilation with the application of early tracheostomy.48 Other benefits of early tracheostomy in patients who will require prolonged mechanical ventilation include patient comfort, ease of secretion clearance, ability to perform safer weaning with tracheostomy collar/mask trials, and ability to communicate more effectively. Admission ASIA motor score has been shown to predict the need for tracheostomy, with 100% of patients with a score of less than 10 requiring tracheostomy.47 In patients with high cervical spinal cord injuries (C1 to C3), loss of diaphragmatic innervation leads to a universal need for mechanical ventilation. Recent application of new technologies such as a laparoscopically implanted diaphragm pacing system has allowed for many of these patients to be liberated from mechanical ventilation.49 Cardiovascular Management Cardiac dysfunction following cervical spinal cord injury is very common and is associated with severity of injury as measured by ASIA and the ASIA impairment scale. As many as 60% of patients with cervical spinal cord injury will meet criteria for cardiovascular failure and more than 90% of patients have cardio-

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vascular dysfunction.15 Hypotension is associated with secondary injury following spinal cord injury due to reduction in spinal cord perfusion and has been associated with worse neurologic outcomes in animal models.50 Injury severity is associated with the clinical severity of cardiovascular symptoms.20,22 In many patients, these severe hemodynamic abnormalities will ultimately resolve after the first 2 to 6 weeks postinjury, although many patients with spinal cord injury have life-long alterations in cardiovascular function.51 Aggressive management of hypotension is recommended21,44 and may be associated with improvements in neurologic outcome.52 Treatment of hypotension and neurogenic shock following spinal cord injury initially involves volume resuscitation, taking care to avoid volume overload, followed by vasopressors as needed.21 Although no consensus has been reached on the best vasoactive agent of choice, recommendations are for use of an agent with both !-adrenergic and "-adrenergic activity to treat both the hypotension and bradycardia associated with sympathetic denervation.21 Current recommendations are to maintain mean arterial blood pressure between 85 and 90 mm Hg for the first 7 days following acute cervical spinal cord injury.44 This is based on several studies of aggressive protocolized blood pressure management52 and at least one prospective case series that demonstrated improved neurologic outcome with this aggressive hemodynamic treatment management strategy.53 Although IV vasoactive medications are frequently utilized after spinal cord injury, oral !-receptor agonists such as pseudoephedrine and midodrine hydrochloride have also been employed with success, particularly in the more subacute stages following injury. Treatment of bradycardia following spinal cord injury is typically reserved for symptomatic patients. Some patients,



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however, will have recurrent and sustained bradycardia that can progress to asystole if left untreated.16,17,20 This vagally mediated alteration in chronotropy is particularly prone to occur in the setting of mild hypoxia as may occur during endotracheal suctioning. The proposed mechanisms as outlined by Mathias are a combination of absent sympathetic activity, airway receptor stimulation, hypoxia, and positive pressure ventilation, which results in a loss of normal compensatory mechanisms.54 Therefore, avoidance of hypoxia is exceptionally important in this patient population. The use of vasoactive medications with "-agonist activity is typically first-line treatment. Long-term use of "-agonist therapy with enteral albuterol may be helpful as well. Alternative agents that can be used include theophylline and scopolamine. Individual episodes are treated with atropine during acute hospitalization, but pacemaker placement may be indicated if patients have persistent symptomatic bradycardia. Other Considerations The leading cause of morbidity and mortality following acute spinal cord injury is the development of complications. Due to immobility and the need for aggressive and invasive treatments, patients with spinal cord injury are at exceptionally high risk of developing a number of specific, albeit not unique, complications such as infections, gastrointestinal hemorrhage, venous thromboembolic disease, and skin breakdown. Infections remain a leading cause of death following spinal cord injury,1 and aggressive screening and treatment of all infections is paramount. Early removal of indwelling central venous catheters and meticulous aseptic technique for line maintenance is essential. Early application of a ventilator bundle to minimize the risk of ventilator-associated condiContinuum (Minneap Minn) 2015;21(1):159–187

tions is recommended.21 Aggressive management of hyperglycemia and careful attention to nutritional needs are also paramount. Evidence-based guidelines recommend early administration of enteral nutrition within 72 hours of admission to all patients with cervical spinal cord injury due to the known hypermetabolism that occurs following these injuries.21,55 Stress ulcer prophylaxis is indicated for all patients with cervical spinal cord injury due to the well-demonstrated increased risk of gastrointestinal bleeding in this patient population. The development of venous thromboembolic disease is one of the dreaded complications following spinal cord injury. Patients with spinal cord injury at all levels are at an exceptionally high risk of developing venous thromboembolic disease due to a number of factors such as immobility, but other mechanisms, such as alterations in fibrinolysis and abnormal platelet function, have also been proposed. The incidence of venous thromboembolic disease is reported to be between 12% and 64% and still accounts for nearly 10% of deaths in the first year following injury.56 Mechanical compression should be implemented as soon as possible in all patients with spinal cord injury,21 although the treatment is inadequate as the only prophylactic measure.57 Current recommendations for prophylaxis against venous thromboembolic disease include the use of a combination of modalities such as low molecular weight heparins, rotating beds, and pneumatic compression stockings.58 There is considerable controversy about the timing of the initiation of chemical prophylaxis against venous thromboembolism, but generally, beginning treatment is acceptable after 72 hours of injury. 21 Prophylactic inferior vena caval (IVC) filters are currently recommended only if chemical or mechanical prophylaxis is

KEY POINT

h Bradycardia can be expected in patients with spinal cord injury for several weeks, but individual episodes need not be treated unless the patient manifests clinical symptoms.



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h Chemical prophylaxis to prevent deep vein thrombosis is appropriate after 72 hours. Routine placement of inferior vena cava filters is not recommended.

h Autonomic dysreflexia is a syndrome following spinal cord injury that may affect patients in the acute or chronic phase, specifically in patients with high thoracic or cervical spinal cord injuries. In this syndrome, a typically noxious stimulus (bladder distension or fecal impaction) occurs below the level of injury leading to a dangerous rise in systolic blood pressure due to hyperactive thoracic sympathetic reflex activity, a loss of supraspinal sympathetic control, and inadequate parasympathetic response.

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contraindicated.21,58 Treatment for 3 months following injury is the recommended duration of prophylaxis based on both expert consensus and data from the natural history of venous thromboembolic disease following spinal cord injury. Skin breakdown is of considerable concern in the patient with spinal cord injury and is one of the most common complications. Due to prolonged immobility, life-long attention must be paid to protection against pressure ulceration, beginning during the acute hospitalization. Development of chronic pressure ulcers is an independent risk factor for mortality.59 Areas at greatest risk are those bony prominences below the level of injury such as the sacrum. First-line therapy involves frequent turning and repositioning. Skin must be frequently assessed and pressure reduction mattresses and padding should be used. Consideration should be given to transferring a patient to a center with expertise in spinal cord injury management to prevent these morbid complications. Autonomic dysreflexia is a syndrome following spinal cord injury that may affect patients in the acute or chronic phase, specifically in patients with high thoracic or cervical spinal cord injuries. In this syndrome, a typically noxious stimulus (bladder distension or fecal impaction) occurs below the level of injury leading to a dangerous rise in systolic blood pressure due to hyperactive thoracic sympathetic reflex activity, a loss of supraspinal sympathetic control, and inadequate parasympathetic response. Autonomic dysreflexia is defined as a greater than 20% increase in systolic blood pressure with a change in heart rate and at least one sign (eg, sweating, piloerection, facial flushing) or symptom (eg, headache, blurred vision, stuffy nose).60 If left untreated, malignant hypertension can result in intracranial hemorrhage, retinal detachment, seizures, coma, myocardial

infarction, pulmonary edema, and death. Although prevention is ideal, once autonomic dysreflexia occurs, first-line therapy is to remove the stimuli. If hypertension persists, pharmacologic intervention should be instituted with calcium channel blockade or nitrates. REHABILITATION A full discussion of the goals and benefits of acute rehabilitation for the patient with traumatic spinal cord injury are beyond the scope of this article, but a few items are particularly worthy of note. All patients with neurologic function following injury should receive some form of rehabilitative services, which ideally should begin during the acute hospitalization and be directed by pathways, standing orders, and protocols. Aggressive and early mobilization is a mainstay of therapy both during the acute hospitalization and rehabilitation. Another focus of acute care of the patient with spinal cord injury is bowel training as soon as enteral feeding is established to prevent ileus, constipation, and poor intrathoracic compliance due to abdominal distention. Bladder training is another focus and should be initiated as soon as the initial resuscitation is complete and adequate intravascular fluid balance has been established. Indwelling urinary catheters can then be removed and a regimen established for bladder catheterization, which also minimizes the risk of catheter-associated urinary tract infections. The general goals of rehabilitation are range of motion and strengthening exercises, pulmonary care, assistive-device training, mobilization, edema management, splinting of extremities to minimize contractures, and education of the patient, family, and caregiver.21 PROGNOSIS Prognosis for neurologic recovery is invariably one of the first things about which a patient or family of a patient with spinal cord injury will inquire. The



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ASIA impairment scale is prognostic of neurologic recovery in the sense that complete injuries (ASIA A) carry a far worse prognosis for functional recovery than incomplete injuries (ASIA B through D).61 This concept was elegantly illustrated in a systematic review of the role of MRI in acute spinal cord injury.29 Patients were stratified by ASIA impairment scale and by radiographic findings on T2-weighted images into normal cord, single-level edema, diffuse edema, and hemorrhage (Figure 10-13). Of patients with a spinal cord that appeared normal on MRI, irrespective of their initial grade, all patients had a complete neurologic recovery. For patients who demonstrated hemorrhage in the spinal cord on T2-weighted images, 95% of the patients with an ASIA A grade remained an ASIA A (Figure 10-14). This study lends further evidence to the significant value of MRI in prognostication for patients with spinal cord injury. The life expectancy for a patient with spinal cord injury remains lower than for those without spinal cord injury.1 In one systematic review, the crude standard mortality rate was three times higher for patients with spinal cord injury than the general population.62

Mortality rates are the highest in the first year following spinal cord injury for all ages and all severities of injury. Data from the Spinal Cord Model Systems1 indicate that for a person age 20 who survives the first 24 hours after injury, the mean life expectancy is 45 (paraplegic), 40 (low quadriplegic), 35 (high quadriplegic), and a patient who is ventilator dependent at any level has a life expectancy of 19 years. For patients age 20 at time of injury who survive the first year, those numbers are 45, 40, 37, and 25 years, respectively. For those patients injured at ages 40 and 60, those numbers, not surprisingly, are significantly lower. For patients injured at age 40 who survive the first 24 hours, the mean life expectancy is 27 (paraplegic), 23 (low quadriplegic), 20 (high quadriplegic), and 8 years (ventilator dependent at any level). For a patient injured at age 40 who survives the first year, life expectancy is 28 (paraplegic), 24 (low quadriplegic), 21 (high quadriplegic), and 12 years (ventilator dependent at any level). For patients injured at age 60 who survive the first 24 hours, the mean life expectancy is 13 (paraplegic), 10 (low quadriplegic), 8 (high quadriplegic), and 2 years (ventilator dependent

KEY POINT

h The American Spinal Injury Association impairment scale is prognostic of neurologic recovery in the sense that complete injuries (American Spinal Injury Association A) carry a far worse prognosis for functional recovery than incomplete injuries (B through D).

Four injury signal patterns using sagittal T2-weighted MRI. A, Burst fracture of C6 and retrolisthesis of C6 on C7 by 4 mm (arrow) with normal cord (pattern 1). B, Single-level edema with severe central stenosis at C5-C6 and C5 fracture (fracture not seen) (pattern 2). C, Multilevel edema C1 to C5 with C3-C4 disk herniation (arrow) (pattern 3). D, Hemorrhage and surrounding edema centered at C6 (pattern 4) in a patient with bilateral C5 lamina fractures, inferior facet fractures, and grade 1 anterolisthesis of C5 on C6.

FIGURE 10-13

Modified with permission from Bozzo A, et al, J Neurotrauma.29 B 2011 Mary Ann Liebert, Inc. online.liebertpub.com/toc/neu/28/8.




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Acute Spinal Cord Injury KEY POINT

h Prognosis after spinal cord injury is largely dependent on the severity of injury and initial clinical status; however, most deaths after spinal cord injury occur in the first year. Every effort should be made to liberate patients from ventilators when possible, and vigilant attention to potential medical complications is of utmost importance.

FIGURE 10-14

Depiction of chances of neurologic recovery based on sagittal T2-weighted MRI patterns stratified by the ASIA impairment scale. For each MRI finding, the number of patients in the study with each ASIA impairment scale injury on initial presentation (left) and on follow-up evaluation (right). Reprinted with permission from Bozzo A, et al, J Neurotrauma.29 B 2011 Mary Ann Liebert, Inc. online.liebertpub.com/toc/neu/28/8.

at any level). For a patient injured at age 60 who survives the first year, life expectancy is 13 (paraplegic), 10 (low quadriplegic), 8 (high quadriplegic), and 4 years (ventilator dependent at any level). In the past, the leading cause of death following spinal cord injury was renal failure. More recently, sepsis, pneumonia, and respiratory failure are the most common causes of death,1 highlighting the need to prevent these complications. In addition to age and level and severity of injury, low educational status and income have also been shown to be associated with mortality.63 CONCLUSION This article reviewed the clinical presentation and management for patients with acute spinal cord injury, with a focus on traumatic spinal cord injury. This condition can be devastating, with considerable morbidity and public health impact. While acute spinal cord injuries can affect both the young and elderly, the absolute number of injuries may increase with

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an aging population. A multidisciplinary approach, including emergency neurosurgical evaluation, is important. The focus of a broad therapeutic approach to optimize overall outcomes requires vigilance to aspects of both neurologic and systemic critical care, with an emphasis on respiratory management. Steroids are no longer considered the standard of care in this disease. Further investigation, especially regarding acute medical therapies, is urgently needed. REFERENCES 1. National Spinal Cord Injury Statistical Center. Spinal cord injury facts and figures at a glance. Birmingham, AL: University of Alabama at Birmingham, 2013. 2. van den Berg ME, Castellote JM, MahilloFernandez I, de Pedtro-Cuesta J. Incidence of spinal cord injury worldwide: a systematic review. Neuroepidemiology 2010;34(3): 184Y192. doi:10.1159/000279335. 3. Chiu WT, Lin HC, Lam C, et al. Review paper: epidemiology of traumatic spinal cord injury: comparisons between developed and developing countries. Asia Pac J Public Health 2010;22(1):9Y18. doi:10.1177/1010539509355470.



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4. Fassett DR, Harrop JS, Maltenfort M, et al. Mortality rates in geriatric patients with spinal cord injuries. J Neurosurg Spine 2007; 7(3):277Y281. doi:10.3171/SPI-07/09/277.

18. Stein DM, Roddy V, Weingart S, et al. Emergency neurological life support: traumatic spine injury. Neurocrit Care 2012;17(suppl 1): S102YS111. doi:10.1007/s12028-012-9759-0.

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Acute spinal-cord injury.

Acute management of traumatic cervical spinal cord injury.

Medical treatments of acute spinal cord injury.

Bowel management in spinal cord injury patients.

Suicide following acute traumatic spinal cord injury.

Acute hydrocephalus following cervical spinal cord injury.

Methylprednisolone for acute spinal cord injury.

Pharmacological therapy for acute spinal cord injury.

Cervical ankylosis with acute spinal cord injury.

NASCIS. National Acute Spinal Cord Injury Study.

Walking Index for Spinal Cord Injury version II in acute spinal cord injury: reliability and reproducibility.

Classification of the severity of acute spinal cord injury: implications for management.

The prehospital management of suspected spinal cord injury: an update.

Management of behavior on a spinal cord injury unit.

Management of Neuropathic Pain Associated with Spinal Cord Injury.

Urodynamic Management of Neurogenic Bladder in Spinal Cord Injury.

Surgical management of urolithiasis in spinal cord injury patients.

The syndrome of acute anterior lumbar spinal cord injury.

Spinal cord perfusion pressure predicts neurologic recovery in acute spinal cord injury.

Methylprednisolone for the treatment of acute spinal cord injury: counterpoint.

Methylprednisolone for the treatment of acute spinal cord injury: point.

Role of an acute spinal cord injury unit.

Pulmonary management of the acute cervical spinal cord injured patients.

Spinal cord injury rehabilitation.