Continuing Education Activity

Spinal shock is a result of severe spinal cord injury. It usually requires high-impact, direct trauma that leads to severe spinal cord injury and spinal shock. The initial encounter with a patient with spinal shock is usually under a trauma scenario. Ischemia of the spinal cord can also produce spinal shock; for example, a hypotensive patient in the medical intensive care unit (ICU) or a post-angiography patient with thrombotic occlusion of arteries that supply the cervical spine can develop this disease. Treatment of ischemic spinal shock is different from traumatic spinal shock. This activity reviews the evaluation and management of spinal shock and explains the role of the interprofessional team in managing patients affected by this condition.

Objectives:

• Describe the etiology and pathophysiology of spinal shock.
• Outline the recommended evaluation and examination for patients presenting with suspected spinal shock.
• Summarize the appropriate management of spinal shock.
• Explain the significance of collaboration and communication among the interprofessional team when diagnosing and treating patients with spinal shock.

Introduction

Spinal cord injury (SCI) is a common injury occurring in the United States with an incidence of approximately 54 per million persons per year.[1] According to the National Spinal Cord Injury Statistical Center, approximately 280,000 living survivors of traumatic SCI were reported in the United States in 2017. The prevalence of nontraumatic SCI is unknown, but it is thought to be three to four times greater.[2] Causes of spinal cord injury are diverse. Although trauma is the most common cause, other etiologies include myelopathies induced by autoimmune, infectious, neoplastic, vascular, and hereditary-degenerative diseases.[3]

The term "spinal shock" was first used by Hall in 1840.[4] Sherrington further defined this as a transient extinction of reflexes below the level of spinal cord injury.[5] Spinal shock is the sudden loss of reflexes and muscle tone below the level of injury that occurs after an acute onset of spinal cord injury.[6]

Acute traumatic SCI requires high-impact, direct trauma that leads to spinal cord injury and spinal shock. The initial encounter with a patient with spinal shock is usually under a trauma scenario. Ischemia of the spinal cord can also produce a spinal shock; for example, a hypotensive patient in the medical intensive care unit (ICU) or a post-angiography patient with thrombotic occlusion of arteries that supply the cervical spine can have a similar presentation. Treatment of ischemic spinal shock is different, and outcome expectations are also different. Cord injury is often associated with fracture-dislocation, tearing of ligaments, rotational distraction, as well as tearing of the disc space. If the spinal shock is not associated with significant injury of the spinal column itself, then the prognosis for these patients is more favorable than when a fracture is present. The overall treatment of patients with significant spinal shock and injury is a challenge, but aggressive medical management can reduce its effect on the overall functionality of the patient.[7] 

However, despite optimal care, deficits after a spinal shock may be permanent. Moreover, there are several definitions in the literature for spinal shock, which alters care received by the patient and consequently the clinical outcomes. Spinal shock has been defined as the absence of reflexes below the level of the lesion, with or without hypotension, while some definitions require the presence of hypotension. This activity reviews the evaluation and management of spinal shock and explains the role of the interprofessional team in managing patients affected by this condition.

Etiology

Traffic accidents involving motor vehicles, bicycles, or pedestrians account for approximately 50% of all SCIs.[3] In patients older than 65 years of age, domestic accidents such as falls are the most common cause of SCIs. Primary spinal cord injury may be due to transection of the cord, mechanical injury, abscess formation, or metastatic disease. Secondary spinal cord injuries may be due to occlusion or disruption of arterial blood supply to the spinal cord with resultant hypoperfusion and anoxic damage to the spinal cord.[3] 

Cervical spondylosis is the most common risk factor for SCI. It has a reported prevalence of 10% in patients with SCI.[3] Other risk factors for SCI after trauma or metastatic disease include congenital abnormalities of the spine, such as atlantoaxial instability, congenital fusions, or tethered cord. Transient spinal shock has been reported following the use of intrathecal iodinated contrast.[8]

Epidemiology

The worldwide annual incidence of spinal cord injury is reported to be around 15 to 40 cases per million.[9] The majority of these cases are young men and have SCI secondary to trauma. Approximately 55% of acute SCIs occur in the cervical region. Cervical spine SCI has a worse prognosis compared to SCI of other spinal levels, which is reflected in the decreased prevalence of cervical SCI in epidemiologic data.[3] In the United States, the National Spinal Cord Injury Statistical Center reported an incidence of 54 cases per one million people, equivalent to around 17,900 new SCI cases each year.[10]

Pathophysiology

Acute SCI is a two-step process involving primary and secondary mechanisms. Primary injury occurs as a combination of initial impact with underlying chronic cord compression. This can occur with fracture-dislocation, burst fractures, and acutely ruptured discs. In some cases, primary injury can occur without pre-existing cord compression. This is seen with severe ligamentous injuries leading to transient spinal column dislocation or spinal cord laceration from sharp bone/metal.[3] Mechanisms of secondary injury include inflammation, calcium-mediated mechanisms, sodium, glutamatergic pathways, vascular mechanisms, free radicals, and apoptosis. Histopathologically, hemorrhages develop in the central region of the spinal cord on injury (especially in the gray matter), likely secondary to trauma forces with direct mechanical disruption in the vasculature. In later injury, although the large arteries remain patent, local microcirculation remains disturbed, leading to ischemia. Cell death eventually occurs either via necrosis or apoptosis.[3]

Underlying molecular mechanisms for these injuries remain unknown for the most part. Animal models have been used to study the pathophysiology of spinal shock. These models elucidate the natural progression of injury in SCIs to some degree. After initial hemorrhagic foci in the gray matter, there appears to be significant protein accumulation in the gray matter of the spinal cord. Edema then ensues and peaks at three to six days post-injury. On magnetic resonance imaging (MRI), edema can be visualized for up to two weeks after the injury. The slow process of central cord necrosis and vacuolization then follows and continues for about two months. The characteristically thin rim of white matter surrounding the central core of necrosis remains intact throughout this process. Often it is observed that the patient starts losing neurologic function above the level of injury. Loss of function that happens several days post-injury above the level of the injury is primarily due to spinal cord pathway rearrangement. Once this process abates, the function above the injury returns to normal, although the exact time needed for this process is not precisely defined and could last from weeks to months. If a patient survives the initial injury but remains immobile, the area fills with gliotic tissue.[11]

The transection of the spinal cord results in spinal shock and transient extinction of reflexes below the level of injury. The main pathophysiological mechanisms include[6]:

1. Synaptic changes in cord segments below the level of injury (due to enhancement of presynaptic inhibition and high concentration of glycine)
2. Hyperpolarization of spinal motor neurons.
3. Sudden withdrawal of facilitatory inputs of the descending pathways disrupts the synaptic transmission and interneuronal conduction. 
4. A functional abnormality of the fusiform, gamma-efferent system that controls the sensitivity of the muscle stretch receptors
5. The loss of normal function of spinal cord interneurons and motoneurons in the corticospinal, rubrospinal, vestibulospinal, and reticulospinal pathways.

History and Physical

It is important to familiarize oneself with the definitions of spinal shock and neurogenic shock. Although they are distinct entities, they are seen as a spectrum of the same disease process in patients with SCI (usually traumatic).

Spinal shock is the altered physiologic state immediately after a spinal cord injury (SCI), which presents as loss of spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity.

Neurogenic shock is a component of the spinal shock syndrome and refers to the hemodynamic instability seen in these patients with hypotension, bradycardia, and hypothermia (secondary to sympathetic-parasympathetic dysfunction/imbalance).

When evaluating patients with suspected spinal shock, healthcare providers should obtain a detailed history of the accident. Often factors such as a rollover crash, ejection outside the car, or seat belt usage can give significant information on the severity and type of spinal cord injury that should be expected. The potential presence of intoxication is essential to obtain, as it will confuse the initial physical exam. It is important to understand that the energy necessary to produce spinal shock and spinal fracture during a traumatic event is very high, and patients should be thoroughly examined for other tissue and organ injury. While evaluating the patient, it must be assumed that their spine is unstable, and all the necessary precautions should be taken to keep it stable until final imaging is obtained and stability is established.

The initial physical examination must include the American Spinal Injury Association (ASIA) Scale, an international communication tool for researchers and clinicians to quantify the neurological impairment resulting from a spinal cord injury.[12] A complete cord injury (ASIA grade A), or spinal shock, is characterized by a rostral zone of spared sensory levels, reduced sensation in the next caudal level, and no sensation in levels below. It also exhibits reduced muscle power in the level immediately below the injury, followed by complete paralysis in more caudal myotomes. Reflexes are frequently absent, at least in the initial stage.[13] Autonomic dysfunction with bowel and bladder incontinence will be present. In male patients, priapism may develop. Autonomic dysregulation will result in bradycardia and hypotension.

In spinal shock that occurs after cord transection, there is a sequential rostrocaudal depression of reflex activities. The recovery of reflexes occurs in caudorostral pattern. The duration of spinal shock depends on the recovery of reflexes that can be around one hour in case of superficial reflexes and several weeks or months in case of deep tendon or autonomic reflexes.

Unlike the classical teaching that bulbocavernosus reflex is the first reflex to return after a cord transection, recent studies have shown that the pattern of regaining of reflexes follows the following order: delayed plantar reflex, bulbocavernosus reflex, cremasteric reflex, ankle jerk, Babinski sign, and knee jerk.[14][6]

Evaluation

The primary assessment of a patient with trauma and possible underlying spinal shock includes evaluation of airway, breathing, and circulation. Care should be taken to ensure movement of the spine does not occur to minimize secondary injury. The patient should be immobilized at the scene and during transport. A rigid cervical collar and supportive blocks on a backboard with straps are recommended.[15] The movement of the patient should be done using the log-roll technique. If mechanical ventilation is necessary on an emergent basis, rapid-sequence intubation with in-line spinal immobilization can be used; however, intubation over a flexible fiberoptic laryngoscope is the preferred method if the clinical situation allows. Profound hypotension is usually present, which should be treated immediately with a crystalloid fluid bolus. If hypotension is determined to be due to spinal shock (as opposed to volume depletion from hemorrhage due to other injuries), repetitive fluid boluses are not recommended, and the patient should be started on inotropes to maintain arterial blood pressure. Urinary retention should be assessed, and a urinary catheter should be placed as soon as possible. A thorough neurologic exam utilizing the ASIA score should then be completed. Neurologic examination should also include an assessment of the cranial nerves as they may be independently affected secondary to trauma.

Radiologic imaging is the next most important step in managing a patient with suspected SCI. Computed tomography (CT), especially spiral CT of the cervical spine, has a higher sensitivity for detecting spinal fractures when compared with a plain radiograph and should be employed first if available.[16] Magnetic resonance imaging (MRI) is not required in most cases and can be technically challenging in some patients. MRI is indicated, however, in patients with a negative CT scan suspected of having SCI. MRI is more sensitive than a CT scan and has been shown to reveal SCI in patients with negative CT scans. A recent study reviewed 1550 patients with negative CT scans after blunt trauma and found that MRI successfully detected spinal abnormalities in 182 patients. They concluded that CT scan alone is insufficient to rule out SCI, especially in patients with ongoing neurological deficits or those who are obtunded or unexaminable.[17] However, obtundation alone is not an indication for an MRI. In patients who are obtunded after blunt trauma but are noted to have preserved gross movement in all extremities with negative CT imaging, an MRI is not required.[18]

Treatment / Management

Patients with spinal shock will have hypotension and bradycardia due to autonomic dysregulation and imbalance. The sympathetic tone is lost, leading to decreased vascular resistance and hypotension. An unopposed parasympathetic tone leads to bradycardia. Maintaining adequate perfusion pressure to the spine is crucial in patients with spinal shock to prevent secondary ischemic injury. It is generally recommended to maintain mean arterial blood pressure at 85 to 90 mmHg for the first seven days after an acute SCI.[19] 

Judicious fluid management is necessary to avoid fluid overload and edema. Most patients will require inotropic therapy. Studies comparing various inotropic therapies in patients with SCI reported improved spinal cord perfusion with norepinephrine and better side-effect tolerance compared with dopamine or phenylephrine.[20] Midodrine and desmopressin have recently been shown to accelerate the liberation from intravenous noradrenaline in patients with spinal shock and effectively reduce the length of stay in the intensive care unit.[21] Profound bradycardia can be treated with atropine administration or temporary pacing and is usually seen in patients with higher cervical cord injuries (C1 thru C5.[22] Patients with spinal shock will usually develop paralytic ileus and require decompression. When this resolves, enteral nutrition should be started. Thermoregulation will also be altered in these patients with spinal shock, requiring external control to maintain body temperature. 

All patients require venous thromboembolism (VTE) prophylaxis, as untreated SCI patients can develop thromboembolism within 72 hours of admission.[23] Prevention of pressure ulcers with adequate prophylactic measures is essential in patients with spinal shock and SCI. To prevent this complication, turning and positioning with the appropriate log-roll techniques are required. Urinary catheterization is necessary due to urinary retention. However, intermittent catheterization is preferred over indwelling catheters to decrease the risk of catheter-association urinary tract infections.[24] All patients with SCI should receive gastric ulcer prophylaxis with proton-pump inhibitors for four weeks.[24]

No specific pharmacologic therapy is available to treat patients with SCI and spinal shock. Glucocorticoid treatment has been used; however, data supporting its efficacy is insufficient. The National Acute Spinal Cord Injury Study (NASCIS) I study compared the efficacy of low dose versus high dose methylprednisolone in acute spinal cord injury patients presenting within 48 hours. There was no difference in the improvements between high and low-dose groups. Since a true placebo group was absent, it remains ambiguous whether the improvement can be due to steroid use.

The NASCIS II study found no difference in neurologic recovery after 1-year in patients who received methylprednisolone compared to placebo.[25] However, patients treated within 8 hours of injury had better motor function recovery if they received methylprednisolone (30 mg/kg bolus and 5.4 mg/kg/hr for 23 hours) compared to placebo. The authors reported similar complication and mortality rates among the groups and concluded that treatment with methylprednisolone is indicated for acute spinal cord trauma, but only if it can be started within 8 hours of injury.[25] These effects, however, are seen to be marginal with little impact on clinical recovery by experts in the field. In addition, the risk of complications, especially in patients with prolonged administration of glucocorticoids (48 hours or more), makes it a less favorable medical therapy for patients with SCI. NASCIS III study randomized acute (less than eight hours) SCI patients into three groups: 5.4 mg/kg/h dose of methylprednisolone (MP) for 24 hours, 5.4 mg/kg/h of methylprednisolone for 48 hours, or 2.5 mg/kg of tirilazad every six hourly for 48 hours. Results showed that 24 hours of MP therapy was sufficient for patients in whom it was initiated within three hours of injury. If the therapy was started between three and eight hours of injury, 48 hours of MP was associated with better neurologic outcomes. But this was associated with an increased risk of infection, including severe pneumonia and sepsis. In summary, all three NASCIS studies showed an increased risk of adverse events in populations who had been managed with steroids.[26]

The American Association of Neurological Surgeons and Congress of Neurological Surgeons do not recommend using glucocorticoids in acute spinal cord injury.[27] 

In the AO Spine guidelines, in patients without significant contraindications, methylprednisolone administration for 24 hours has been recommended within 8 hours of cervical injury. However, the evidence has been reported as weak.[28] Surgical decompression and reduction of the cervical spine are indicated with significant cord compression and neurologic deficits that are not amenable to closed reduction; however, the optimal timing of the surgery is not clear.[29]

Autonomic dysreflexia can also be seen in patients with SCI above the T6 level. Uninhibited sympathetic responses to noxious stimuli below the level of the injury cause vasoconstriction and hypertension in these patients. A compensatory parasympathetic response produces bradycardia and vasodilation above the level of the lesion. This is seen within the first year of injury but is unlikely to occur in the initial time period (first month of injury).[30] Management involves identifying the triggering factor, such as bowel or bladder distention, and treatment with antihypertensive agents. 

Orthostatic hypotension due to peripheral vasodilatation is common in the first few months of SCI. Patients with SCI also remain at high risk for pneumonia due to decreased cough reflex and poor secretion clearance. Chest physiotherapy and vaccination should be employed to decrease the risk of this complication. Bowel dysfunction is common after SCI and requires medical therapy to prevent complications. Rectal suppositories are the treatment of choice for managing chronic bowel dysfunction after SCI leading to constipation. Pressure ulcers are also common in patients with SCI and require vigilant pre-emptive skincare. Maintenance of adequate nutritional intake and weight is also crucial in preventing this complication. Pain, depression, and anxiety are common after SCI and should be treated accordingly. 

Functional recovery should be the primary goal after the spine has been stabilized. Range-of-motion and resistive exercises, upright positioning, and strengthening exercises should be employed as soon as possible.

Differential Diagnosis

• Cardiogenic shock
• Hypovolemic shock
• Sepsis
• Spinal abscess
• Vertebral fracture

Pertinent Studies and Ongoing Trials

Summary of current guidelines on managing spinal cord injury:

1. Immobilize the patient. A sandbag and tape are not sufficient. Spinal immobilization in patients with penetrating trauma is not recommended.
2. Perform imaging studies with CT scan.
3. The use of corticosteroids is not recommended.
4. Administration of GM-1 ganglioside is not recommended.[27]

Staging

Phases of reflex recovery[31]:

• Phase 1 (between 0 to 24 hours): This is driven by motor neuron hyperpolarization and is characterized by areflexia or hyporeflexia. The first pathological reflex during this period is the delayed plantar reflex followed by a bulbocavernosus, abdominal wall, and cremasteric reflexes. Sympathetic dysfunction can lead to bradyarrhythmias, atrioventricular conduction block, and hypotension.
• Phase 2 (day 1 to day 3): This is driven by denervation supersensitivity and receptor upregulation. Cutaneous reflexes are more prominent in this phase, while deep tendon reflexes remain absent.
• Phase 3 (4 days to 1 month): This is driven by synaptic and short axon growth. Deep tendon reflexes usually return in most patients, and the Babinski sign may appear.
• Phase 4 (1 to 12 months): This is driven by the growth of long axons and synapses. Cutaneous and deep tendon reflexes will be hyperactive even with minimal stimuli. Malignant hypertension and autonomic dysreflexia may appear in this stage.

Prognosis

The most common causes of death in patients with SCI are respiratory system diseases and cardiovascular events.[32] These include pneumonia, nonischemic heart disease, septicemia, pulmonary emboli, ischemic heart disease, suicide, and unintentional injuries.[3] The prognosis for spinal shock is poor and depends on underlying comorbidities, level of spinal cord injury, associated injuries, age, and type of injury.[3] Patients with C1 thru C3 injury have a 6.6 times higher mortality than the mortality rate for those with paraplegia.[3] Some studies have linked the recovery of reflexes in the initial phase of SCI as a prognostic indicator of functional recovery after spinal shock, although the evidence is limited.[31] 

A large multicenter retrospective study looking at trauma patients in Germany concluded that SCI complicates polytrauma presentation and can be found in every thirteenth patient.[33] Moreover, in polytrauma patients, more than 50% of the patients suffered complete cord lesions with spinal shock. They also noted that SCI only had a limited influence on mortality, although complications of multiorgan failure, sepsis, and extended hospital length of stay were more frequent in polytrauma patients with SCI.[33]

Complications

As discussed above, complications following an SCI with prolonged neurological deficits can have multiple systemic complications. They include pressure sores, VTE, sepsis, pneumonia, urinary complications, bowel complications, and cardiovascular events. Cardiovascular complications are the leading causes of morbidity and mortality in both acute and chronic stages of SCI.[34] Spinal shock occurs during the acute phase of SCI and neurogenic shock, with hemodynamic instability and autonomic dysfunction usually following. In the chronic phase of SCI-associated spinal shock, autonomic dysreflexia appears. Orthostatic hypotension can occur in both acute and chronic phases of injury.[34] Deep vein thrombosis, systemic atherosclerosis, and increased risk of cardiovascular disease have also been described as complications of SCI, which are present in this population in higher frequency when compared to age-matched controls.[34] In the acute phase of spinal shock, priapism has also been reported.[35]

Aside from systemic vascular complications of spinal shock, functional disability as a result of spinal injury is a major complication of spinal shock and is a primary determinant of morbidity and mortality in these patients. The data regarding motor axonal excitability is limited, and clear prognostic indicators of functional recovery have not been identified as yet. Some studies reported the existence of significant deterioration in peripheral motor axonal excitability and function in early spinal shock.[36] Mechanisms that eventually allow recovery and indicators that determine the degree of functional recovery remain unknown.

Deterrence and Patient Education

SCI and spinal shock are life-changing events for patients. Patient education regarding the disease process, potential complications, and prophylactic measures to prevent these complications should be essential for the treatment plan. Occupational and physical therapy focusing on strengthening exercises, mobility, and fall prevention must be incorporated to optimize clinical outcomes for these patients. Skincare, VTE prophylaxis, and maintaining the regular function of the urinary system and the bowels are essential to prevent the complications of urinary infections, bowel obstruction, and sepsis. Moreover, irregularities of these systems often trigger the dreaded autonomic dysreflexia, which may be a preventable condition if these noxious stimuli can be prevented.[30]

Enhancing Healthcare Team Outcomes

Spinal shock is associated with high morbidity and mortality and requires multifaceted comprehensive care to prevent devasting complications in patients who survive. These patients must be managed by an interprofessional team that includes a trauma surgeon, neurologist intensivist, neurosurgeon, ICU nurses, and the emergency department physician. These patients should be admitted to the ICU and closely monitored. The critical care nurse is pivotal in managing these patients, as they require support for all activities of daily living and vigilant monitoring for hemodynamic stability. These patients are at high risk of complications, including aspiration pneumonia, bacteremia, venous thromboembolism, and bowel and bladder dysfunction. The critical care nurse plays an important role in monitoring the patient for these potential complications, preventing their incidence, and communicating with the physicians to ensure early treatment if they occur.[37][38] 

The physical therapy and occupational therapy team is also a crucial part of the interprofessional team caring for these patients. Early therapy can maximize functional recovery and help improve clinical outcomes for these patients. A collaborative interprofessional team can maximize clinical recovery, prevent devastating complications, and improve outcomes for these patients. [Level 5]