Traumatic Spinal Cord Injury

Abstract

Objective:

This article provides a review of the initial clinical and radiologic evaluation and treatment of patients with traumatic spinal cord injuries. It specifically highlights essential knowledge for neurologists who encounter patients with these complex injuries.

Latest Developments:

There has been improvement in the care of patients with traumatic spinal cord injuries, particularly in the prehospital evaluation, approach for immediate immobilization, standardized spinal clearance, efficient triage, and transportation of appropriate patients to traumatic spinal cord injury specialized centers. Advancements in spinal instrumentation have improved the surgical management of spinal fractures and the ability to manage patients with spinal mechanical instability. The clinical evidence favors performing early surgical decompression and spine stabilization within 24 hours of traumatic spinal cord injuries, regardless of the severity or location of the injury. There is no evidence that supports the use of neuroprotective treatments to improve outcomes in patients with traumatic spinal cord injuries. The administration of high-dose methylprednisolone, which is associated with significant systemic adverse effects, is strongly discouraged. Early and delayed mortality rates continue to be high in patients with traumatic spinal cord injuries, and survivors often confront substantial long-term physical and functional impairments. Whereas the exploration of neuroregenerative approaches, such as stem cell transplantation, is underway, these methods remain largely investigational. Further research is still necessary to advance the functional recovery of patients with traumatic spinal cord injuries.

Essential Points:

Traumatic spinal cord injury is a complex and devastating condition that leads to long-term neurologic deficits with profound physical, social, and vocational implications, resulting in a diminished quality of life, particularly for severely affected patients. The initial management of traumatic spinal cord injuries demands comprehensive interdisciplinary care to address the potentially catastrophic multisystem effects. Ongoing endeavors are focused on optimizing and customizing initial management approaches and developing effective therapies for neuroprotection and neuroregeneration to enhance long-term functional recovery.

INTRODUCTION

Traumatic spinal cord injury is a devastating and complex event, often resulting in severe and permanent disabilities. It affects a considerable number of people, with an estimated annual incidence of 54 per one million people. In the United States alone, more than 294,000 people are currently living with traumatic spinal cord injury-related disabilities, and approximately 17,000 new cases are reported each year.¹ Traumatic spinal cord injuries have exhibited a higher prevalence among young men and a disproportionate representation among non-Hispanic Black people.¹ The primary mechanism of injury remains motor vehicle accidents, followed by falls. [KP 1] Other causes include gunshot wounds, physical assault, and sports or recreational activities. Notably, the average age of individuals with traumatic spinal cord injuries has increased over the past few decades, increasing from an average age of 29 years in the 1970s to an average age of 43 years since 2015. It is anticipated that the incidence of traumatic spinal cord injuries will continue to increase, particularly in older adults with underlying spondylosis and spinal canal stenosis because of spinal cord injuries resulting from falls.^1,2 Traumatic spinal cord injuries may affect cervical, thoracic, and lumbar spinal regions (50%, 35%, and 11%, respectively).² [KP 2] Despite advances in acute care and surgical management, patients with traumatic spinal cord injuries have reduced overall life spans and higher mortality, especially in the first year after an injury, compared with the general population.³ [KP 3] Cervical spinal cord injuries, particularly above C5, are associated with quadriplegia, whereas injuries of the thoracic spinal cord can result in paraplegia. Cervical spinal cord injuries are commonly associated with higher rates of morbidity and mortality especially in older adults. In addition to a higher spinal injury (eg, cervical versus lumbar injury), increasing patient age, injury mechanism, and the presence of multisystem trauma increase the risk of mortality and affect life expectancy after traumatic spinal cord injuries.⁴ Traumatic spinal cord injuries have a substantial effect on health care costs, with annual medical treatment costs that range from $30,770 to $62,563 per year.⁵ The lifetime cost of care for young patients (25 years old) with traumatic spinal cord injuries is estimated between $1.1 and $4.6 million depending on the severity of their injury.^3,6 Therefore, understanding the cellular and molecular mechanisms of traumatic spinal cord injuries and developing new effective treatments is crucial to improving long-term patient outcomes.

KEY POINTS.

[KP 1] Motor vehicle accidents, followed by falls, are the most common causes of traumatic spinal cord injuries.

[KP 2] The cervical spine is the most commonly injured spinal cord region, accounting for 50% of traumatic spinal cord injuries, and is associated with higher rates of morbidity and mortality especially in older adults.

[KP 3] Patients with traumatic spinal cord injuries experience higher mortality rates compared with the general population.

[KP 4] Vertebral fracture and dislocation, direct impact resulting in spinal cord compression, and spinal cord laceration or transection are the primary mechanisms of traumatic injury to the spinal cord.

[KP 5] Early recognition of traumatic spinal cord injuries is crucial, and the main therapeutic focus in traumatic spinal cord injury is the avoidance or correction of secondary injuries, especially hypoxia and hypoperfusion.

[KP 6] When spinal injury is suspected, immediate spinal immobilization is important to maintain spinal stability and prevent secondary spinal cord injuries.

[KP 7] Neurologists can be crucial for refined neurologic assessment of the level of traumatic spinal cord injury and severity of motor and sensory deficits as well as for the management of acute and chronic complications.

[KP 8] The American Spinal Injury Association Impairment Scale is recommended as the preferred method for standardizing the neurologic examination of patients with traumatic spinal cord injuries and assessing the severity of the injuries.

[KP 9] The severity of neurologic impairment in traumatic spinal cord injuries can be exaggerated initially by a temporary spinal shock, cord swelling, and systemic complications.

[KP 10] The American Spinal Injury Association Impairment Scale grade holds significant prognostic implications for traumatic spinal cord injury outcomes.

[KP 11] There are specific spinal cord syndromes that can be seen in patients with incomplete traumatic spinal cord injuries such as central cord syndrome, Brown-Séquard syndrome, and anterior cord syndrome.

[KP 12] High-cervical traumatic spinal cord injury commonly presents with respiratory failure due to loss of diaphragmatic function.

[KP 13] Spinal shock is transient and typically associated with absent reflexes (including bulbocavernosus), urinary retention, and bladder distension.

[KP 14] As a consequence of cervical and upper thoracic traumatic spinal cord injuries, neurogenic shock may manifest with refractory hypotension and bradycardia that are challenging to manage.

[KP 15] Determining the need for radiological assessment of the spine after a traumatic event relies on factors such as the patient’s mental status, the presence of neck or back pain, and the capacity to conduct a reliable physical examination.

[KP 16] In patients who have had traumatic spinal cord injuries, high-quality CT is the preferred initial imaging modality to characterize vertebral fractures.

[KP 17] MRI can reliably show the extent of spinal cord compression and signs of compressive epidural and intramedullary hematomas and can also help exclude ligamentous injury within the first 48 hours after traumatic spinal cord injuries.

[KP 18] In patients who have had traumatic spinal cord injuries, the Memphis criteria are useful to identify those at high risk for blunt cerebrovascular injury, and the Biffl scale (also referred to as Denver scale) is helpful to classify the severity of blunt cerebrovascular injury and predict the risk of ischemic stroke.

[KP 19] When mechanical ventilation is deemed necessary after traumatic spinal cord injury, orotracheal intubation combined with standard in-line cervical or video or fiberoptic laryngoscopy should not be delayed.

[KP 20] In cervical traumatic spinal cord injuries, patients often require an extended duration of mechanical ventilation, but most patients can be successfully liberated from the ventilator.

[KP 21] In patients with persistent respiratory failure, early tracheostomy may reduce ventilator-associated pneumonia, shorten intensive care unit length of stay, and decrease laryngotracheal complications.

[KP 22] Hypotension is associated with poor neurologic outcomes in patients with traumatic spinal cord injuries, and augmenting mean arterial pressure in the initial phase after injuries can improve functional outcomes.

[KP 23] In patients with traumatic spinal cord injuries above T6, phenylephrine should be used with caution because of the potential risk of reflex bradycardia.

[KP 24] Patients with traumatic spinal cord injuries are at higher risk of developing venous thromboembolism in the first 8 weeks after injury, secondary to vasomotor tone loss, venous stasis, and limited mobility.

[KP 25] Administration of thromboprophylaxis using low-molecular-weight heparin within 72 h of a traumatic spinal cord injury is currently recommended by the Paralyzed Veterans of America to minimize the occurrence of venous thromboembolism once there is no evidence of bleeding.

[KP 26] Administration of high-dose steroids has been discouraged because of its associated adverse effects in patients with traumatic spinal cord injuries.

[KP 27] There is no evidence supporting the use of pharmacologic or nonpharmacologic interventions for neuroprotection in patients with traumatic spinal cord injuries.

[KP 28] Emergent operative intervention should be considered for patients with traumatic spinal cord injuries whose neurologic function declines in the presence of mass effect or mass lesion.

[KP 29] The optimal timing of surgery for traumatic spinal cord injuries has not been conclusively established; however, prospective cohort studies suggest early surgery (within 24 hours) to achieve definitive cord decompression and spine stabilization may be beneficial.

[KP 30] Neurologists play a crucial role in identifying and addressing various complications that occur after traumatic spinal cord injuries, including autonomic dysreflexia, difficulty swallowing, muscle stiffness, pain, problems controlling sphincter muscles, and mood disorders.

[KP 31] Rehabilitation efforts for patients with traumatic spinal cord injuries should start as soon as the patient is clinically stable and should be individualized to achieve the patient’s fullest physical, emotional, social, vocational, and functional recovery.

[KP 32] Early engagement with physical therapy specialists is recommended to improve muscle retention and minimize deconditioning. Physical therapy sessions should occur at least once per day and last for at least 20 minutes per session.

[KP 33] Patients with traumatic spinal cord injuries located at T6 or higher commonly experience autonomic dysreflexia, a delayed complication that can trigger episodes of sudden and severe hypertension.

[KP 34] Mortality is highest in the first 6 to 12 months after traumatic spinal cord injuries.

[KP 35] The primary factors for prognostic assessment of traumatic spinal cord injuries include the American Spinal Injury Association Impairment Scale grade of severity, the level of the injury, and the cord’s radiologic appearance on spinal MRI.

PATHOPHYSIOLOGY

Traumatic spinal cord injury results from a direct impact on the spine that fractures or dislocates vertebrae and disrupts the ligaments and intervertebral disks, generating mechanical forces that can lead to primary spinal cord injury and neurologic impairment.⁷ The primary injury causes contusion with persistent or transient compression or distraction injury. It can also cause cord laceration or transection, which are mostly not amenable to treatment. [KP 4] Persistent spinal cord compression secondary to fracture dislocation injury or burst fracture with bony fragments is the most common primary injury.⁸ Transient compression is a less frequent presentation, and it is likely secondary to hyperextension injuries, especially in patients with cervical spondylosis, and distraction stretch-and-tear injuries in which two vertebrae are pulled apart. Spinal cord laceration and transection, which are less commonly encountered in the civilian population, occur in penetrating injuries, resulting in severe dislocation, sharp bony fragments, or missile injuries. The primary injury often damages ascending and descending pathways in the spinal cord and disrupts blood vessels and cell membranes. Soon after the onset of the primary insult, there is a cascade of complex secondary biochemical and cellular responses and processes, including disruption of the blood-spinal cord barrier, vasomotor dysfunction, hypoperfusion and reperfusion, ionic imbalance, mitochondrial damage, and induction of acute neuroinflammatory response, resulting in worsening hypoxia, ischemia, and cell death promotion.^8,9 Dying neurons release free radicals and fail to reuptake glutamate neurotransmitters, resulting in oxidative damage and excitotoxicity and further neurologic damage.⁹ This acute secondary phase appears to be followed by progressive neuronal cell death and axonal degeneration, mediated by persistent neuroinflammation that is characterized by extensive microglial and astroglial activation. Therefore, early recognition of traumatic spinal cord injury is crucial, and the main therapeutic focus in traumatic spinal cord injury is the avoidance or correction of secondary injuries. [KP 5]

EVALUATION

For any patient suspected of experiencing an acute spinal injury, essential aspects of care involve prehospital assessment and triage, which includes immediate immobilization by first responders, and careful clinical assessment at the emergency department, including urgent spine imaging.

Prehospital Triage and Immobilization

The management of patients with traumatic spinal cord injuries starts in the field by implementing basic resuscitation principles from the American College of Surgeons’ Advanced Trauma and Life Support course,¹⁰ including airway, breathing, and circulation, to ensure adequate ventilation, oxygenation, and perfusion. If spinal cord injury is suspected, first responders must rapidly resuscitate patients and institute a traumatic spinal cord injury algorithm for spinal clearance and immobilization, which is a widely accepted approach and is supported by Class II and Class III studies.^11–13 There are a variety of spinal immobilization devices, but the Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries¹¹ and the American College of Surgeons’ Advanced Trauma Life Support course manual¹³ recommend a rigid cervical collar and long rigid spine board secured with tapes or straps to prevent spinal instability. These rigid mechanisms allow for safe transport from the field to a specialized trauma care center where clinical and radiologic evaluations can take place according to the recommendations outlined in Figure 2-1.¹⁴ When a patient is suspected of having a cervical traumatic spinal cord injury and requires airway stabilization with tracheal intubation, the primary responder should manually stabilize the patient’s neck in line during intubation to minimize the risk of displacement of cervical spinal elements. Although spinal immobilization is important to maintain spinal stability and prevent secondary spinal cord injuries, it is also associated with some risks, even when applied appropriately. [KP 6] These risks include delayed transfer, airway compromise, and pain. In addition, full spinal immobilization could result in an increased risk of respiratory difficulties, especially when large straps are applied across the chest, as well as aspiration and pressure sores from prolonged immobilization. It is also important to know that mortality is reported to be higher in patients with penetrating neck trauma who are immobilized compared with those who are not immobilized.¹⁵

Figure 2–1.

Decision algorithm for immobilization and imaging of patients who have experienced traumatic cervical spinal cord injury.

CT = computed tomography; MRI = magnetic resonance imaging.

Data from Walters BC, et al, Neurosurgery.¹⁴

Clinical Assessment

Early recognition of the primary injury patterns in the field and on arrival to the emergency department can help localize the location and type of injury and avoid additional spinal cord damage during transportation. A comprehensive physical examination to carefully rule out other concurrent systemic injuries is necessary at the initial presentation. Neurologic examination should include a detailed motor and sensory assessment as well as a careful assessment of sacral nerve root function by evaluating rectal tone and tactile sensation in S4-S5 dermatomes or sensation to deep anal pressure. Therefore, neurologists can be crucial for refined neurologic assessment of the level of traumatic spinal cord injury and the severity of motor and sensory nerve deficits as well as for the management of acute and chronic complications. [KP 7]

Traumatic spinal cord injuries can be graded using the American Spinal Injury Association (ASIA) Impairment Scale [AIS]), which is recommended as the preferred tool to standardize the neurologic examination, classify the severity of the injury, and provide information on improvement at follow-up.^16,17 [KP 8] The AIS classifies severity of injury from A (complete injury, with loss of both motor and sensory function) to E (normal motor and sensory examination).¹⁸ Incomplete injuries (AIS B to D) preserve voluntary anal contraction and often bulbocavernosus reflex and present with various degrees of motor function and sensation caudal to the level of injury. AIS is scored B when there is a complete loss of motor and preservation of some sensatory functions. AIS can be scored C or D if motor function is partially spared below the level of injury. AIS is scored D when the majority of the muscle groups below the level of injury exhibit a motor strength grade of 3 or higher. When performing the AIS assessment, it is important to keep in mind that the levels of motor and sensory function should be determined on each side of the body. Incomplete injury should be considered if some function is preserved below the level of injury and there is perianal sensation or voluntary rectal tone, as opposed to involuntary tone, which may be partially preserved in complete spinal cord injuries. The severity of the neurologic impairment in traumatic spinal cord injuries can be exaggerated initially by traumatic brain injury, diminished level of consciousness, intoxication, distracting injuries, or temporary spinal shock.¹⁹ The neurologic examination can also worsen after initial presentation because of spinal cord swelling or the development of new systemic complications such as respiratory or circulatory failure. [KP 9] Therefore, to achieve more accurate prognostication, it is advisable to perform follow-up AIS assessments at the end of the initial hospitalization or at the beginning of the rehabilitation phase. [KP 10] This component of neurologic examination should be documented on the AIS form, which can be freely accessed online and is included as a PDF in the online version of this issue (SDC APPENDIX).¹⁸ [WK: Please include the submitted PDF titled “SDC ASIA-ISCOS-Worksheet_10.2019” as supplemental digital content for this article.]

There are specific spinal cord syndromes that can be seen in patients with incomplete traumatic spinal cord injuries (AIS B to D), such as central cord syndrome, Brown-Séquard syndrome, and anterior cord syndrome.⁷ [KP 11] The classic mechanism of central cord syndrome is a hyperextension injury, which is exacerbated by preexisting cervical spondylosis and central canal stenosis. It is characterized by disproportionally greater motor impairment in the upper extremities (especially distal upper), because of the mesial somatotopy of the arms in the descending corticospinal tracts, and a variable degree of lower extremity weakness. It may also be associated with bladder dysfunction and a variable degree of cervicothoracic sensory loss. Brown-Séquard syndrome, which is also known as lateral hemisection or hemicord syndrome, most often occurs in patients who experience ballistic and penetrating traumatic spinal cord injuries, such as a bullet or knife wound. It results in ipsilateral loss of proprioception, vibration, and motor function as well as contralateral loss of pain and temperature sensation. Anterior cord syndrome is more common in anterior spinal artery infarction, but it can also occur from injuries associated with disk- or bone-fragment retropulsion. It results in motor paralysis below the level of injury and loss of pain and temperature sensation at and below the level of injury. Other spinal cord syndromes can also occur after trauma but much less frequently, such as posterior cord syndrome, which is more commonly caused by infectious, metabolic, vascular, or inflammatory etiologies, or compression or epidural mass. Conus medullaris or cauda equina syndromes are more commonly caused by compression or infections.

Cardiopulmonary complications are common in the acute phase of traumatic spinal cord injuries and are considered the most common cause of early death after injury.⁷ Respiratory failure can happen suddenly because of impaired diaphragmatic contraction caused by damage to cervical levels C3-C5 or loss of thoracic root innervation of the chest and abdominal accessory muscles. [KP 12] Hypotension can also occur in the setting of shock. It is important to distinguish between spinal shock and neurogenic shock. Spinal shock is a transient physiologic reflex depression of spinal cord function, which can occur immediately after damage to any region of the spinal cord and usually lasts for days or weeks after injury.²⁰ In addition, spinal shock is typically associated with absent reflexes (including bulbocavernosus reflexes), urinary retention, and bladder distension. [KP 13] Although the temporal course of spinal reflex recovery is a topic of debate, the recovery of reflexes is highly suggestive that a component of spinal shock existed at the time of presentation.²¹ Neurogenic shock is a subtype of distributive shock that usually occurs within the first hours after the injury and can last for days or even a few weeks after an injury and results from damage in the cervical and high thoracic (ie, above T6) spinal cord levels. It is associated with the loss of sympathetic outflow and unopposed vagal activity and results in a wide range of findings reflecting sympathetic dysfunction such as hypotension, bradycardia, and peripheral vasodilatation (eg, flushed skin and cold extremities).²⁰ [KP 14]

Radiologic Assessment

Coupled with the clinical examination, performing radiologic assessment soon after the trauma can guide decision making and lead to a timely clearance and appropriate decompression of the spinal cord. Congress of Neurological Surgeons Systematic Review and Evidence-based Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries²² provides clinicians with recommendations for cervical immobilization and radiologic assessment of the cervical spine after a traumatic spinal cord injury (Figure 2-1).¹⁴ Mental status check, assessment for neck pain or tenderness, and accurate and reliable neurologic examination are the main determinants of the need to image patients with traumatic spinal cord injury. [KP 15] Plain radiographs have been used traditionally as the initial screen to identify bony abnormalities such as fractures.²³ However, because of the poor sensitivity associated with plain radiography, more often it is replaced by CT without contrast, which can better characterize vertebral fractures but has very poor sensitivity for soft tissue injuries.¹⁴ [KP 16] For unconscious patients and those no obvious traumatic spinal fracture has occurred, conventional MRI, specifically, sagittal T1-weighted and sagittal and axial T2-weighted images are helpful to assess the degree of traumatic spinal cord compression, and extramedullary abnormalities (edema and hemorrhage) (Case 2–1).²⁴ MRI is also useful in evaluating the extent of spinal cord compression and disk herniation, and excellent in detecting compressive epidural and intramedullary hematomas, which can be crucial in guiding surgical decisions. MRI findings, such as the extent and location of spinal cord injury, can help clinicians predict functional outcomes and develop rehabilitation strategies.^24,25

Additionally, MRI, including short tau inversion recovery (STIR) sequences, within 48 hours of the trauma can help assess for the amount of occult ligamentous instability at the level of the injury, which has been associated with increased risk for subluxation, and guide the determination of when to discontinue use of the cervical collar. [KP 17] However, MRI is necessarily helpful in assessing spinal instability.

In the subacute and chronic phases after a traumatic spinal injuries injury, MRI can also be helpful in evaluating for a syrinx and progressive ascending myelomalacia.²⁶

Case 2–1

A 23-year-old man with a history of alcohol use disorder sustained multiple facial and rib fractures, left epidural and subdural intracranial hematomas, and C5-C7 fracture dislocation with spinal cord compression and a ligamentous injury at C5-C6 (Figure 2-2A, 2-2B, and 2-2C) after a high-speed motorcycle collision, during which he was not wearing a helmet. He was unconscious and apneic when paramedics found him. They intubated him with manual in-line neck stabilization. Then they transferred him to a specialized trauma center for further management. In the emergency department, he had persistent deficits consistent with American Spinal Injury Association Impairment Scale grade A at the C6 level. He was also severely hypotensive and was given a norepinephrine infusion to attain a target mean arterial pressure of 80 mm Hg to 90 mm Hg for the first 3 days. He was admitted to the neuroscience intensive care unit for further management. Within the first 24 hours, he underwent C6 corpectomy and spinal stabilization with C5-C7 fusion, placement of an intervertebral expandable biomechanical device, and placement of an anterior spinal plate at C5-C7 (Figure 2-2D). His course in the intensive care unit included acute respiratory failure, bilateral apical pneumothoraxes, lung contusion, worsening cerebral edema, neurogenic shock (treated with norepinephrine), and left jugular vein thrombosis, which required anticoagulation with low molecular-weight heparin, which was started 12 days after his injury. The intensive care unit team could not extubate him because of recurrent pneumonia and weak cough; therefore, the patient underwent a tracheostomy. Thirty-five days after the accident, he was transferred to the acute rehabilitation unit. During his rehabilitation stay, he started to experience sudden episodes of uncontrolled hypertension and facial flushing, which was suspected to be secondary to central nervous system storming and was managed with propranolol and avoidance of triggers such as a rapid change in bed position, fevers, bladder, or abdominal distension.

Figure 2–2.

Imaging of the patient in Case 2–1. Sagittal reformatted CT (A) shows a C6 fracture with severe dislocation compromising the spinal canal. Sagittal T2-weighted MRI (B) and short tau inversion recovery (STIR) (C) show C6 flexion-type injury with burst fracture, approximately 25% vertebral body height loss, posterior cortex fragment retropulsion, and resulting spinal cord compression associated with spinal cord edema and expansion. It also shows epidural hematoma with the largest component at C7-T1 causing moderate dural sac narrowing and rupture of the anterior longitudinal ligament at C5-C6, the posterior longitudinal ligament at C6, and of the ligamentum flavum at C5 and C6 (better visualized on the STIR image [C]). Sagittal reformatted CT (D) shows postoperative changes after C6 corpectomy and spinal stabilization with C5–7 fusion.

Comment

This case illustrates the typical course of a young patient with a severe cervical traumatic spinal cord injury that caused severe neurologic deficits, respiratory failure, and neurogenic shock. Prehospital and emergency department medical care focused on ensuring adequate oxygenation and perfusion. The patient’s cord compression was appropriately treated with manual in-line neck stabilization in the field, followed by C6 corpectomy and spinal stabilization with C5–7 fusion within 24 hours of injury. The patient’s hospital stay was complicated by neurogenic shock, which was treated with vasopressors. His rehabilitation course was complicated by autonomic dysreflexia, which was managed with propranolol and the avoidance of triggers.

In addition to conventional MRI, new MRI modalities to assess spinal functional plasticity are currently being investigated. Some of these promising techniques include diffusion tensor imaging, which may be useful in quantifying the extent of axonal loss and predicting long-term functional outcomes after blunt traumatic spinal cord injury;²⁷ functional MRI (fMRI), which may be useful in measuring the anatomic functional and metabolic correlates of sensory-motor activities in patients with traumatic spinal cord injuries;²⁸ and magnetic resonance spectroscopy, which can measure the biochemical characteristics of the brain and spinal cord leading to ischemic, gliosis or cell death after a traumatic spinal cord injury.²⁹ The utility of these new emerging imaging modalities still requires validation in large clinical studies.

In clinical practice, patients with traumatic spinal cord injuries (mostly cervical) are at high risk of blunt cerebrovascular injury of their extracranial carotid and vertebral arteries, which is associated with an increased risk of morbidity and mortality.³⁰ The mechanisms of blunt cerebrovascular injury include impingement of vessel against bone, shearing and stretching of the vessel, or laceration of the vessel by bone fragments, leading to an intimal tear. Patients with atlanto-occipital or atlantoaxial dissociation injuries, cervical spine fractures that extend through the transverse foramen, or rotational injuries such as those resulting in unilateral or bilateral jumped or perched facets are at high risk of vascular injuries. Memphis criteria (and modified Memphis criteria)^31,32 have been developed to identify patients at high risk of blunt cerebrovascular injury (Table 2-1). If the anatomic relationships, mechanism of injury, and presenting symptoms indicate possible head or neck vascular injury, head and neck angiography should be considered. The Biffl scale (also referred to as the Denver scale)³³ classifies the severity of blunt cerebrovascular injury detected on neuroimaging, and it ranges from grades I to V (Table 2-2). [KP 18] The higher grades are usually associated with increased stroke risk.³⁰ Grade I represents a luminal irregularity or dissection with less than 25% luminal narrowing; grade II is a dissection with a raised intimal flap or vessel thrombosis, resulting in luminal narrowing greater than 25%; grade III is a dissecting aneurysm or a pseudoaneurysm, grade IV represents complete vessel occlusion or thrombosis, and grade V represents vessel transection with active extravasation or hemodynamically significant arteriovenous fistula (Table 2-2).³⁰

Table 2-1.

Memphis Screening Criteria^a

The presence of one or more of the following criteria indicates the need for CT angiography (CTA) or digital subtraction arteriography to exclude blunt cerebrovascular injury:

▶ Basilar skull fracture with involvement of the carotid canal

▶ Basilar skull fracture with involvement of petrous bone

▶ Cervical spine fracture

▶ Neurologic examination findings not explained by brain imaging

▶ Horner syndrome

▶ LeFort II or III fracture pattern

▶ Soft tissue injury of the neck (seatbelt sign or hanging or hematoma)

^aData from Miller PR, et al, Ann Surg.³²

Table 2-2.

Biffl Scale for Grading Blunt Cerebrovascular Injury^a

Injury grade	Angiographic characteristics
I	Luminal irregularity or dissection with <25% luminal narrowing
II	Dissection or intramural hematoma with ≥25% luminal narrowing
III	Pseudoaneurysm
IV	Occlusion
V	Transection with free extravasation

^aData from Biffl WL, et al, J Trauma.³³

CRITICAL CARE MANAGEMENT

Acute traumatic spinal cord injury is accompanied by intricate and potentially life-threatening respiratory and cardiovascular dysfunction, necessitating timely medical intervention to prevent neurologic compromise and mitigate morbidity.

Respiratory Management

Respiratory failure can stem from injuries to the brain, cervical spinal cord, or chest that result in airway obstruction, aspiration, and impairment of diaphragmatic contraction (which receives innervation from C3 to C5) or impairment of the thoracic accessory muscles (innervated by the thoracic roots T1 through T11). Thus, catastrophic airway loss and traumatic spinal cord injuries with a higher AIS grade and higher anatomic levels of injury, such as complete injuries above C3, inevitably cause acute ventilatory failure in the field (Case 2–1).³⁴ Patients with partial high-cervical cord injury or mid-cervical injury (C3 through C5), ventilation can sometimes be maintained by accessory inspiratory muscles. However, these patients remain at risk of respiratory failure, and they should be closely assessed and monitored.³⁵ The development of respiratory failure exacerbates the severity of traumatic spinal cord injuries assessed by the AIS. In addition, during the acute course of traumatic spinal cord injuries, patients may develop profound respiratory complications within hours to days after their injuries. These complications can be caused by worsening atelectasis, aspiration pneumonia, tissue and pulmonary edema, and accumulation of secretions and mucus plugging because of a weak cough.³⁶ The respiratory failure may be hypoxemic, hypercapnic, or, most commonly, mixed, depending on the underlying causes. In clinical practice, noninvasive ventilation has a very limited role in the initial care of patients with traumatic spinal cord injuries. Therefore, when mechanical ventilation is deemed necessary, orotracheal intubation combined with standard in-line cervical or video or fiberoptic laryngoscopy should not be delayed. [KP 19]

When ventilation is necessary for patients with traumatic spinal cord injuries, duration depends on several factors, including the location of the injury, the severity and evolution of neurologic impairment, and the occurrence of other respiratory complications. Ventilation typically is prolonged in patients with cervical injuries. Although liberation from ventilation is possible and has been reported in many patients,³⁷ tracheostomies may be required for patients with poor AIS motor scores, persistent respiratory compromise, and the inability to manage secretions.³⁸ [KP 20] Daily intensive care unit (ICU) interventions including respiratory recruitment maneuvers, deep suctioning, aggressive pulmonary hygiene, and chest physiotherapy are beneficial in promoting airway compliance and clearance. In patients with persistent respiratory failure, early tracheostomy may reduce the risk of ventilator-associated pneumonia, shorten ICU length of stay, and decrease laryngotracheal complications.^39,40 [KP 21] This recommendation is not supported by high-quality evidence, and the optimal timing of tracheostomy is not well defined. Early diaphragmatic pacing has been shown to provide some benefits in helping liberate patients with acute cervical traumatic spinal cord injuries from ventilation, improving their spontaneous respiration, and reducing their hospital costs.^41,42 However, more large studies of early diaphragmatic pacing are required before any concrete recommendations can be made.

Cardiovascular Management

In the initial phase after traumatic spinal cord injuries, cardiovascular collapse can occur because of neurogenic shock and volume loss. Cardiovascular collapse may result in inadequate spinal cord perfusion and ischemia and contribute to secondary neurologic damage. Consequently, timely medical intervention is necessary to avert neurologic compromise and reduce morbidity.

Blood pressure augmentation.

Hypotension is associated with poor neurologic outcomes in patients with traumatic spinal cord injuries, and augmenting mean arterial pressure (MAP) in the initial phase after injuries can improve functional outcomes. [KP 22] However, there are no high-quality data regarding optimal blood pressure goals in the management of acute spinal cord injuries.⁴³ Maintaining MAP between 85 mm Hg and 90 mm Hg during the first week after the injury was recommended by the Congress of Neurological Surgeons.^14,44 Studies have evaluated shorter durations of 5 days and showed that augmenting MAP greater than 85 mm Hg correlates with better neurologic recovery in the first 72 hours and much weaker correlation during the remainder of the 7-day window.⁴⁵ Achievement of the recommended MAP goal often requires volume resuscitation and vasopressors. The use of vasopressors should be carefully considered on a case-by-case basis while taking into consideration bradycardia that accompanies hypotension from neurogenic shock (eg, consider agents with α1-adrenergic receptor and β1-adrenergic receptor agonistic effects), underlying comorbidities, and other potential multisystem complications that can occur after the injury. There is no unanimous agreement on the optimal pharmacologic agent for the treatment of neurogenic shock. Dopamine, norepinephrine, and epinephrine are vasopressors frequently used to address this condition.^46,47 In patients with traumatic spinal cord injuries above T6, phenylephrine should be used with caution because of the potential induction of reflex bradycardia. [KP 23] In these cases, patients may not be able to mount an appropriate sympathetic response to counteract bradycardia. However, for patients with lower thoracic injuries in whom vasodilation pathology is present, phenylephrine could be a consideration.⁴³

Management of Blunt Cerebrovascular Injury

The treatment strategy for blunt cerebrovascular injury depends on the mechanism, sites of injury, grade of injury, stroke burden, other associated injuries, and local expertise. Neurologists contribute to the recognition of blunt cerebrovascular injury and are often consulted to guide the treatment and follow-up plans. There have been no randomized trials comparing antiplatelet therapy with anticoagulation therapy (ie, unfractionated versus low-molecular-weight heparin) for the treatment of blunt cerebrovascular injury. When deciding the safest time to begin antithrombotic therapy, consideration should be given to the risk of new or worsening hemorrhage in the setting of existing stroke and other systemic injury burden, and it should be balanced with the risks of new stroke in the setting of thrombus propagation. In clinical practice, low-grade (Biffl grade I and II) blunt cerebrovascular injuries (Table 2-1) are often treated with antiplatelet or anticoagulation therapy.³⁰ Updated vessel imaging should be considered if the patient develops new or worsening neurologic deficits. The duration of therapy for blunt cerebrovascular injuries is also debated. The common approach is to continue therapy for 3 to 6 months, followed by repeated vessel imaging in the outpatient setting to determine the degree of vessel healing to guide further medical decisions. Medical treatment has a limited role in vascular injuries with Biffl grades of III and higher, and endovascular therapy or open surgical repair may be considered.

Venous Thromboembolism Prevention

Patients with traumatic spinal cord injuries are at higher risk of developing venous thromboembolism (VTE) in the first 8 weeks after injury, secondary to reduced vasomotor tone, venous stasis, and limited mobility.⁴⁸ [KP 24] There have been no randomized trials that assess the optimal prevention protocol, safest time to start thromboprophylaxis, or duration of treatment in patients with traumatic spinal cord injuries. Administration of thromboprophylaxis using low-molecular-weight heparin within 72 hours of traumatic spinal cord injury is currently recommended by the Paralyzed Veterans of America to minimize the occurrence of VTEs once there is no evidence of bleeding (strong recommendation, low-quality evidence, grade 1C).^49–51 [KP 25] Low-dose subcutaneous heparin alone has been shown to have little to no protection against VTE in patients with spinal cord injuries.⁵² However, low-dose heparin in combination with pneumatic compression stockings or electrical stimulation is recommended as a prophylactic treatment strategy.⁵¹ In terms of duration of thromboprophylaxis, the Spinal Cord Consortium and Congress of Neurological Surgeons recommend at least 8 weeks of pharmacologic treatment after acute spinal cord injuries because of the increased risk for VTE during that period.^50,51 Studies that evaluated the role of inferior vena cava filter placement did not find a reduction in overall or pulmonary embolism-specific mortality; therefore, it has not been recommended except in specific patients for whom there are contraindications for anticoagulation or for whom thromboprophylaxis has failed.^14,51

NEUROPROTECTION

Neuroprotection in spinal cord injury refers to strategies aimed at preserving and protecting the integrity and function of the spinal cord after an injury. These approaches aim to limit the extent of secondary damage, reduce inflammation, promote tissue repair, and enhance neural and functional recovery. Neuroprotective interventions may include pharmacologic agents, cellular therapies, gene therapies, antioxidants, anti-inflammatory agents, and other strategies designed to mitigate the cascade of events that leads to further injury and neurologic impairment.

Role of Steroids in Medical Management

The potential neuroprotective effects of high-dose methylprednisolone to mitigate the inflammatory cascade and secondary injury following acute traumatic spinal cord injuries have been investigated in large randomized controlled studies (NASCIS I, II, and III [National Acute Spinal Cord Injury Studies]).^53–55 Overall, all these trials showed no significant benefits from using high-dose methylprednisolone, except for an association with modest improvement in motor outcome, which was only observed on a post hoc analysis (Class III evidence) restricted to patients treated within 8 hours of their injuries in the NASCIS II study.⁵⁴ These studies showed higher rates of wound infection, pneumonia, sepsis, acute respiratory distress syndrome, gastrointestinal hemorrhage, and death among patients treated with steroids.^53–55 Based on the literature, there is no compelling evidence that supports the use of steroids as a neuroprotective agent after traumatic spinal cord injuries, and there is a level 1 recommendation from the Congress of Neurological Surgeons against using high-dose methylprednisolone for the acute management of patients with traumatic spinal cord injuries.⁵⁶ [KP 26]

Role of Other Investigational Therapeutics

Several pharmacologic and nonpharmacologic interventions have been attempted to achieve neuroprotection and improve functional outcomes after traumatic spinal cord injuries. Local epidural cooling or systemic therapeutic hypothermia have shown some promising results,⁵⁷ but there is no strong evidence available to support its use in clinical practice. Systemic Hypothermia in Acute Cervical Spinal Cord Injury⁵⁸ is a multicenter randomized controlled trial with a planned size of 120 patients that is being conducted to evaluate the efficacy of modest therapeutic hypothermia (eg, 33°C [94.4°F]) for 48 hours in treating acute cervical spinal cord injuries. Other potential neuroprotection agents include riluzole to reduce neuronal apoptosis. Riluzole is a glutamate antagonist approved to treat amyotrophic lateral sclerosis. In a phase 1 clinical trial, riluzole was well tolerated with a 2-week treatment course at the dose approved for amyotrophic lateral sclerosis and exhibited potential efficacy in patients with traumatic spinal cord injuries.⁵⁹ The RISCIS trial (Riluzole in Acute Spinal Cord Injury Study) to determine the efficacy of riluzole in the acute treatment of spinal cord injuries⁶⁰ is an ongoing phase 2B/3 multicenter controlled trial with a planned size of 193 patients. Investigational studies of other neuroprotective strategies for patients with traumatic spinal cord injuries, such as electrical spinal cord stimulation, minocycline, and fibroblast growth factor are being conducted⁶¹; however, there is no available evidence to support the use of these strategies. [KP 27]

INDICATIONS AND TIMING OF SURGICAL MANAGEMENT

Although the primary injury to the spinal cord is currently irreversible, the goal of spine surgery is to eliminate the source of further secondary injuries and promote neurologic recovery with decompression, spinal canal deformity correction, vertebral fracture reduction, and fixation and fusion. Rapid closed reduction to restore spine alignment until patients are taken to surgery is recommended for fracture and dislocation injuries.¹⁴ If patients with traumatic spinal cord injuries experience a decline in neurologic function in the presence of mass effect or a mass lesion, emergent operative intervention is warranted.⁶² [KP 28] Optimal timing of surgery has not been decisively established; however, evidence favors performing surgical decompression within 24 hours (early intervention), regardless of the severity or location of injury.^63,64 [KP 29] The results of the largest prospective observational multicenter study, STASCIS (Surgical Timing in Acute Spinal Cord Injury Study), was published in 2012.⁶⁵ This study evaluated 313 patients with acute cervical spinal cord injuries who were randomized to early surgery (eg, less than 24 hours) or late surgery (eg, more than 24 hours) and found that at 6 months after injury, an improvement of 2 or more grades in AIS scores was seen in 19.8% of the early-surgery group as compared with 8.8% in the late-surgery group. There is emerging literature (based on small cohort studies) that suggests even earlier intervention (8–12 hours after traumatic spinal cord injuries) is associated with better outcomes.⁶⁶

However, a follow-up prospective observational study SCI-POEM (Surgical Treatment for Spinal Cord Injury study) evaluated 159 patients with traumatic spinal cord injuries who had early surgery (12 or fewer hours after injury) or late surgery (more than 12 hours and fewer than 14 days after injury) and found no significant or clinically meaningful neurologic improvements 12 months after injury.⁶⁷ In addition, a recent randomized controlled trial of 72 patients with preexisting cervical canal stenosis who sustained traumatic spinal cord injuries showed that early surgical treatment was associated with accelerated recovery within the first 6 months but produced similar motor regain at 1 year after injury compared with delayed surgical treatment.⁶⁸ The clinical evidence favors early surgical decompression (ie, earlier than 24 hours after injury), yet there is still no high-level evidence or standardized guidelines to guide the timing and optimal surgical interventions for acute traumatic spinal cord injuries, and additional large cohort prospective studies are warranted.

EARLY RECOVERY AND REHABILITATION

Traumatic spinal cord injuries not only limit independence and impair physical function, but they also cause many systemic complications, including contractures, spasticity, autonomic dysreflexia, poor nutrition, neurogenic bladder and bowel, urinary tract infections, pressure ulcers, orthostatic hypotension, deep vein thrombosis (DVT), and depressive disorders (Figure 2-3).⁷ Neurologists play an essential role in the management of patients with traumatic spinal cord injuries as well as associated traumatic brain injury and systemic complications. Neurologists can also contribute to the diagnosis and treatment of many complications such as autonomic alterations, dysphagia, spasticity, pain, sphincter dysfunction, and mood disorders. [KP 30] Early rehabilitation starts in the intensive care unit to prevent these complications, and efforts are individualized and based on the location and severity of the injury, the age of the patient, and the presence of underlying comorbidities. [KP 31] In addition, a multidisciplinary team of physical and occupational therapists, dietitians, psychologists, speech therapists, social workers, and patient families are all involved in the rehabilitation process and can assist in minimizing and managing these complications.

Figure 2–3.

Systemic complications after traumatic spinal cord injury.

The most common and important complication in the subacute and chronic phase of traumatic spinal cord injuries is the development of joint contractures and stiffness. Joint positioning is important to protect the articular structure and maintain the optimal muscle tone. Physical and occupational therapists will help in improving patients’ range of motion and strengthening exercises. Early engagement with physical therapy specialists is recommended to restore muscle retention and minimize deconditioning.⁶⁹ Physical therapy sessions should occur at least once per day and last for at least 20 minutes per session. [KP 32] If patients with chronic spinal cord injury experience extreme fatigue during physical therapy, electrical stimulation may be a useful alternative to strengthen the muscles and restore walking.^70,71 In addition, electric wheelchairs and brain-controlled neuro-prostheses are all additional tools to expedite functional recovery. Randomized clinical trials are needed to determine the effect of newer tools on the short- and long-term recovery of patients with traumatic spinal cord injuries.

Autonomic dysreflexia, which occurs after recovery from spinal shock and neurogenic shock as early as 4–5 days after injury and may reoccur at any time point through the course of recovery, is another problematic complication in the subacute and chronic phase of traumatic spinal cord injury (Case 2–1).⁷² Autonomic dysreflexia results from unopposed sympathetic activity triggered by cutaneous or visceral stimulation below the lesion, such as bladder distension, detrusor sphincter dyssynergia, fecal impaction, and pressure sores. It is more common and severe in patients with complete spinal cord injury and upper spinal cord (T6 or higher) lesions.^72,73 Signs and symptoms include tachycardia or reflex bradycardia, severe headache, and sudden paroxysmal hypertension. [KP 33] Above the lesion, patients with autonomic dysreflexia may experience flushing, perspiration, and increased secretions due to a compensatory increased parasympathetic response. Below the lesion, patients may experience piloerection and signs of vasoconstriction (eg, pale, cool limbs) due to excessive sympathetic nervous system activity. The most effective treatment interventions involve identifying and eliminating triggering factors. If medications are necessary, it is preferable to use short-acting direct vasodilators (eg, hydralazine). It is important to exercise caution when using vasoactive medications in patients with traumatic spinal cord injuries to prevent hypotension.⁷⁴

PROGNOSIS

The most common impairments experienced by patients with traumatic spinal cord injuries after being discharged from the hospital are incomplete quadriplegia (45%), incomplete paraplegia (22%), complete paraplegia (20%), and complete quadriplegia (13%)^75,76 There has been no improvement in the life expectancy of patients with traumatic spinal cord injuries over the past few decades.^43,77 Mortality is highest within the first 6 to 12 months after injury, especially in older patients and those with high cervical lesions and severe neurologic deficit.⁷⁸ [KP 34] Rehospitalizations because of urinary infections, pressure sores, and a variety of other conditions are very common in patients with traumatic spinal cord injuries (about 30% of patients in any given year).⁴³

Prognostication for patients with spinal cord injuries involves estimates of functional and neurologic recovery, and there are many disability scales with different characteristics and relative advantages that are now available.⁷⁹ The injury location, AIS grade, severity of injury, and appearance of the spinal cord on MRI are the main prognostic tools used to evaluate patients with traumatic spinal cord injuries.⁸⁰ [KP 35] The Spinal Cord Independence Measure is the most recommended tool to assess the functional abilities and impairment in the follow-up of patients with traumatic spinal cord injuries.¹⁷ This linear scale ranges from 0 to 100 and comprises sections on self-care activities, respiratory function, bladder and bowel management, and mobility.¹⁷ Recent clinical studies showed promising results for the use of MRI diffusion tensor imaging as a potential noninvasive prognostic tool in spinal cord injuries, but additional studies are needed.⁸¹

NEUROREGENERATION

The complex pathophysiology of traumatic spinal cord injuries and the lack of therapeutics to repair or regenerate damaged neurons necessitate new therapeutic approaches to mitigate poor outcomes after injury. Neuroregenerative therapies have emerged as the most exciting and active area of research to find new strategies to protect and regenerate the injured spinal cord and improve long-term functional outcomes. Transplantation of neural stem cells, embryonic stem cells, mesenchymal stem cells, induced pluripotent stem cells, oligodendrocyte precursor cells, Schwann cells, and olfactory ensheathing cells are a focus of active research.⁸² However, all of these novel therapies are strictly investigational and may be associated with adverse outcomes.⁸³

CONCLUSION

Traumatic spinal cord injuries remain a significant cause of morbidity and mortality, with limited effective treatments available. The most effective strategy to mitigate the effect of this devastating condition is through primary injury prevention, education, and the use of vehicle safety devices. In the event of an injury, prompt and effective management is crucial, starting with stabilizing patients at the prehospital stage and swiftly transporting them to a specialized traumatic spinal cord injury center. A comprehensive physical and neurologic examination, along with imaging evaluations, is necessary to determine the location and severity of the injury and guide decisions regarding surgical or conservative approaches. The advancement of spinal instrumentation has improved surgical management of spinal fractures and the ability to address spinal mechanical instability. Both surgical and nonsurgical approaches should be promptly implemented to stabilize patients with traumatic spinal cord injuries, with a focus on correcting hypoxia, reversing hypoperfusion, and preventing systemic complications, thus improving functional outcomes. The pathophysiologic processes following spinal cord injuries are highly complex, and our understanding of these processes requires further exploration. There are no proven strategies for neuroprotection, but research in neuroregenerative therapies holds promise in finding new methods to protect and regenerate the injured spinal cord, ultimately restoring functional capabilities.