Spinal Shock

Etiology

Spinal shock is a transient physiologic condition caused by an acute SCI. Generally, SCIs are categorized as primary and secondary etiologies. Blunt force trauma, such as traffic collisions involving motor vehicles, bicycles, or pedestrians, accounts for approximately 50% of all SCIs.[3] In patients older than 65, falls are the most common cause of SCIs. Penetrating trauma (eg, gunshot and stabbing injuries) can also cause primary SCIs. Other primary etiologies include transection of the spinal cord, mechanical damage, abscess formation, and metastatic disease. Secondary SCIs are primarily due to ischemia from occlusion or disruption of the arterial blood supply to the spinal cord with resultant hypoperfusion and anoxic damage to the spinal cord.[3][9]

Cervical spondylosis is the most common risk factor for SCI, with 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 spinal cord. Transient spinal shock has been reported following the use of intrathecal iodinated contrast.[10]

Epidemiology

The worldwide annual incidence of SCI is reported to be around 15 to 40 cases per million.[11] 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 approximately 17,900 new SCI cases every year.[12]

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 (eg, fracture-dislocation, burst fractures, and acutely ruptured discs). Additionally,  primary injury can occur without pre-existing cord compression, including severe ligamentous injuries leading to transient spinal column dislocation or spinal cord laceration from sharp bone or metal.[3] Secondary injury mechanisms 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 due to necrosis or apoptosis.[3]

The underlying molecular mechanisms for spinal shock remain largely unknown. Animal models have been used to study the pathophysiology of spinal shock, which elucidates 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 3 to 6 days after the initial injury and can be visualized on magnetic resonance imaging (MRI) for up to 2 weeks. The slow process of central cord necrosis and vacuolization subsequently occurs, continuing for about 2 months. The characteristically thin rim of white matter surrounding the central core of necrosis remains intact throughout this process. Often, patients with SCIs begin losing neurologic function above the level of the lesion several days after the initial insult, primarily due to spinal cord pathway rearrangement. Once this process abates, normal function above the injury returns, although the exact time needed for this process has not been defined and may last from weeks to months. If a patient survives the initial injury but remains immobile, the area fills with gliotic tissue.[13] 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:[14]

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

History and Physical

Initial Assessment

As with any trauma patient, evaluation for SCIs should be performed after primary assessment with the ABCDE (ie, Airway, Breathing, Circulation, Disability, Exposure) protocol while ensuring spine immobilization during evaluation and transportation to minimize secondary injury.[4][5][6] Restricting spinal movement with a rigid cervical collar and supportive blocks on a backboard with straps is recommended. The patient transfer should be performed using the log-roll technique.[15] Frequently, this is initially done by emergency medical personnel while in the field. 

Patients with SCIs above the C5 vertebrae typically have respiratory drive loss, while injuries at the C5 vertebral level or below have ventilatory impairment, requiring ventilatory support. However, below the T5 vertebrae, SCIs usually do not cause respiratory failure. 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.[4][5][6]

Secondary Assessment

Following the initial stabilization of a patient, a more detailed examination can be performed by hospital clinicians. When evaluating patients with suspected spinal shock, clinicians should obtain relevant past medical history, if possible, from available family members or responsive patients as conditions (eg, osteoporosis and cervical spondylosis) are risk factors for SCI or may affect the neurologic exam (eg, dementia or alcoholism).[7][3][16][17] Additional history should be obtained, including the mechanism of injury (eg, a rollover motor vehicle collision, ejection from the vehicle, or restraint via seatbelt) and other potential traumatic injuries to help determine the severity and type of SCI and assess for differential diagnoses.[7][3][16][17] 

Clinicians should be familiar with the definitions of spinal shock and neurogenic shock. Although they are distinct entities, they can coincide within the same disease process, usually traumatic, in patients with SCI. Spinal shock is a temporary physiologic condition that occurs after an acute spinal cord injury (SCI) in which there is a sudden loss or impairment of spinal cord function below the level of injury, including the motor, sensory, reflex, and autonomic neural systems. Flaccid paralysis, absent bowel and bladder control, and loss of sensory and reflex activity are characteristic presentations of spinal shock.[4][5][6] Neurogenic shock is a component of spinal shock that refers to the hemodynamic instability commonly seen in these patients. Neurogenic shock is characterized by hypotension, bradycardia, and hypothermia secondary to sympathetic-parasympathetic dysfunction or imbalance.[18]

The initial physical examination must include an evaluation with the Glasgow Coma Scale (GCS) and the American Spinal Injury Association (ASIA) scale.[5][7] The ASIA scale is an international communication tool for researchers and clinicians to quantify the neurological impairment resulting from an SCI.[19] (For additional information, see StatPearl's companion topic, "Spinal Cord Injuries").[20] A complete spinal cord injury (ie, ASIA grade A), or spinal shock, is characterized by absent reflexes and a rostral zone of spared sensory levels, reduced sensation in the next caudal level, and no sensation in the levels caudal to the injury. Additional findings include reduced muscle power at the vertebral level immediately below the injury, followed by complete paralysis in more caudal myotomes.[6] Autonomic dysfunction with bowel and bladder incontinence is also present. In male patients, priapism may develop. Furthermore, autonomic dysregulation may result in hypothermia, bradycardia, and hypotension with SCIs in the cervical or upper thoracic region; therefore, vital sign monitoring is essential. Neurologic examination should also include an assessment of the cranial nerves as they may be independently affected secondary to trauma.[4][5][6] 

Clinicians should visually inspect and palpate the spine for hematomas, bruising, bony injuries, midline deviation, and pain. This often can be performed while transferring patients with the log rolling technique.[17] If hypotension is determined to be secondary to neurogenic shock as opposed to volume depletion from hemorrhage due to other injuries, repetitive fluid boluses, which may lead to pulmonary edema, are not recommended. Instead, 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.[4][5][6]

Duration of Clinical Features

In spinal shock that occurs after cord transection, there is a sequential rostrocaudal depression of reflex activities. The recovery of reflexes occurs in a caudorostral pattern. The duration of spinal shock depends on the recovery of reflexes, which can range from approximately 1 hour for superficial reflexes to several weeks or months for deep tendon or autonomic reflexes. Previously, experts believed that the bulbocavernosus reflex is the first reflex to return after a cord transection. However, recent studies have shown that the pattern of regaining reflexes commonly follows the following order: delayed plantar reflex, bulbocavernosus reflex, cremasteric reflex, ankle jerk, Babinski sign, and knee jerk.[21][14] One review by Ditunno et al suggested 4 phases of reflex recovery comprised of the following progression:[22]

• Phase 1: Between 0 and 24 hours, this phase 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: From day 1 to day 3, this phase is driven by denervation supersensitivity and receptor upregulation. Cutaneous reflexes are more prominent in this phase, while deep tendon reflexes remain absent.
• Phase 3: Between 4 days and 1 month, this phase is driven by synaptic and short axon growth. Deep tendon reflexes usually return in most patients, and the Babinski sign may appear.
• Phase 4: The duration of this phase ranges from 1 to 12 months and 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 also appear in this stage.

Evaluation

Diagnostic Imaging Studies

Radiographic imaging is the next most crucial step in managing a patient with suspected SCI once hemodynamic stability is established. Indications for diagnostic imaging for SCIs include trauma patients with any spinal pain, positive neurological exam findings, or who are unconscious. Computed tomography (CT) of the brain and cervical spine without contrast, as well as the chest, abdomen, and pelvis with and without contrast, should be performed.[4] Visualization of the entire spine is recommended, as 20% of trauma patients have multiple spinal injuries.[5] High-quality 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.[23] A spinal surgeon should be consulted if a fracture is identified on initial spine imaging in trauma patients. If an SCI is suspected, but no fracture is apparent on imaging studies, a neurology consultation may assist with further evaluation and management. A CT angiogram is indicated if a cerebrovascular injury is suspected.[4]

Magnetic resonance imaging (MRI) is superior to other diagnostic imaging studies when identifying spinal pathology. However, MRI is technically challenging and time-consuming for an unstable patient. MRI is indicated in patients with a negative CT scan suspected of having SCI due to increased sensitivity compared to CT imaging. A recent study reviewed 1550 patients with negative CT imaging following blunt trauma and found that MRI successfully detected spinal abnormalities in 182 patients. The study concluded that CT alone is insufficient to rule out SCI, especially in patients with ongoing neurological deficits who are obtunded or who are unexaminable.[24] Therefore, MRI is recommended in all patients with SCI for further evaluation, surgical planning, and determination of a prognosis. However, emergent surgery should not be delayed to perform an MRI.[4]

Treatment / Management

Spinal shock is a transient physiologic condition, typically improving within a few days to weeks. Therefore, management is not necessarily treating spinal shock but rather mitigating spinal cord damage and preempting secondary complications. This primarily consists of hemodynamic and respiratory stability to prevent further neurogenic injury and supportive therapy. In some patients, surgical decompression may be considered.

Hemodynamic Management

Patients with spinal shock may have hypotension and bradycardia due to autonomic dysregulation and imbalance if neurogenic shock is also present. Typically, this occurs following cervical and upper thoracic spinal cord injuries above the T6 vertebrae because sympathetic tone is lost, leading to decreased vascular resistance and hypotension. Bradycardia results from the unopposed parasympathetic tone. Maintaining adequate perfusion pressure to the spine is crucial in patients with neurogenic shock to prevent secondary ischemic injury. A mean arterial blood pressure of >85 to 90 mmHg for the first 5 to 7 days following an acute SCI is generally recommended; discontinuation of pressors may be considered if no neurologic improvement is noted after 72 hours.[25][4]

Judicious fluid management is necessary to avoid fluid overload and edema. Most patients will require inotropic therapy. Studies comparing various inotropic treatments in patients with SCI reported improved spinal cord perfusion with norepinephrine with fewer adverse effects compared with dopamine or phenylephrine.[26] In adults, a dosage of norepinephrine 0.05 to 1 mcg/kg/min is commonly used.[27] Midodrine and desmopressin have recently been shown to accelerate the discontinuation of intravenous noradrenaline in patients with spinal shock, reducing the length of stay in the intensive care unit.[28] Profound bradycardia can be treated with atropine administration or temporary pacing.[29] (A1)

Respiratory Management

Patients with cervical and upper thoracic spinal cord injuries often require mechanical ventilation due to respiratory depression. Furthermore, trauma frequently leads to acute respiratory distress syndrome. Therefore, respiratory support is often necessary to stabilize the patient's condition. Additionally, patients with SCI also remain at high risk for pneumonia due to decreased cough reflex and poor secretion clearance. Chest physiotherapy, including percussion, incentive spirometry, and deep suctioning, should be employed to decrease the risk of this complication. Influenza and pneumococcus vaccinations are also recommended.[4][27]

Glucocorticoid Recommendations

No specific pharmacologic therapy is available to treat patients with SCI and spinal shock. Glucocorticoid treatment has previously been used to reduce inflammation and edema; however, data supporting its efficacy is insufficient. The National Acute Spinal Cord Injury Study (NASCIS) I compared the efficacy of low-dose versus high-dose methylprednisolone in acute spinal cord injury patients presenting within 48 hours of the initial injury. Although both groups demonstrated some improvement, no significant difference was identified. Since a true placebo group was absent, whether the improvement can be attributed to steroid use remains ambiguous.[27][4]

The NASCIS II study found no difference in neurologic recovery after 1 year in patients who received methylprednisolone compared to placebo.[30] However, patients treated within 8 hours of injury had improved motor function if they received a methylprednisolone dose of 30 mg/kg bolus followed by methylprednisolone 5.4 mg/kg/hr for 23 hours compared to placebo. The authors reported similar complication and mortality rates between the groups. They concluded that treatment with methylprednisolone is indicated for acute spinal cord trauma, but only if it can be started within 8 hours of injury.[30] These results, 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 the administration of glucocorticoids for >48 hours, makes steroid therapy for patients with SCI less favorable. The NASCIS III study randomized patients presenting within 3 to 8 hours of an SCI into three treatment groups: methylprednisolone (MP) 5.4 mg/kg/h for 24 hours, MP for 48 hours, and MP plus 2.5 mg/kg of tirilazad 4 times a day for 48 hours. Results showed that 24 hours of MP therapy was sufficient for patients in whom it was initiated within 3 hours of injury. If the treatment was started between 3 and 8 hours of injury, MP for 48 hours was associated with better neurologic outcomes; however, an increased risk of infection, including severe pneumonia and sepsis, was also noted with this dosage. In summary, all 3 NASCIS studies showed an increased risk of adverse effects in patients who had been managed with steroids.[31] Other studies have also demonstrated adverse effects with MP and minimal motor function improvement. Therefore, the American Association of Neurological Surgeons and Congress of Neurological Surgeons do not recommend using glucocorticoids in acute spinal cord injury.[32] Conversely, the AO Spine guidelines recommend methylprednisolone administration for 24 hours to treat SCIs in patients presenting in the first 8 hours without significant contraindications. However, some experts have stated the supporting evidence for this recommendation is weak.[33](A1)

Surgical Decompression

In some patients with spinal fractures, surgery within 24 hours of the injury may be performed to reduce spinal cord pressure and prevent secondary ischemic damage. Particularly for cervical spine injuries, studies have shown significantly improved neurologic outcomes in patients treated with surgical decompression. Potential benefits must be weighed against common surgical risks and the possibility of further vascular damage.[34] Additionally, the optimal timing of decompressive surgery is not clear as limited studies of surgical decompression before and after 24 hours of injury have been performed, and evidence of intervention within 12 hours of spinal injury has been ambiguous. A comparison of the neurological outcomes with surgical decompression within 12 hours versus after 12 hours from the time of injury has been completed by the Prospective, Observational European Multicenter (SCI-POEM) study[35][9][36](B2)

Supportive Therapy

Medical therapy to prevent secondary sequelae of spinal shock is also recommended to reduce patient morbidity. In addition to other management considerations for spinal shock, supportive therapies include:

Venous thromboembolism (VTE) prophylaxis: Secondary to immobility and trauma, all patients require VTE prophylaxis commonly comprised of low-molecular-weight heparin and intermittent pneumatic compression devices, as patients with spinal shock can develop thromboembolism within 72 hours of admission. Treatment duration with heparin typically is recommended for 8 to 12 weeks. In patients with contraindications to heparin prophylaxis, inferior vena cava filters may be considered.[9][27][4][37](A1)

Bowel and bladder management: Depending on the level of injury, a combination of bowel and bladder retention or incontinence may occur. Clinicians should adjust bowel regimens, including rectal stimulation, bulk formers, stool softeners, suppositories, and enemas until patients have approximately 1 bowel movement every other day.[4] Urinary catheterization is necessary due to urinary retention. However, intermittent catheterization at scheduled intervals is preferred over indwelling catheters to decrease the risk of catheter-associated urinary tract infections. As bladder function returns, the frequency of scheduled catheterizations can be reduced.[4][38] Additionally, all patients with SCI should receive gastric ulcer prophylaxis with proton-pump inhibitors for 4 weeks.[38]

Pressure ulcer prevention: Due to decreased sensation and immobility, pressure ulcers are common in patients with SCI and require vigilant preemptive skincare and adequate prophylactic measures. To prevent this complication in supine patients, the standard of care is to turn and reposition with the appropriate log-roll technique every 2 hours. For patients who can maintain a seated position, more frequent repositioning every 30 minutes for at least 30 seconds is recommended.[27]

Nutrition management: Nutritional clinicians should be consulted to evaluate and treat patients with spinal shock due to their changing metabolic and dietary needs as spinal cord function returns. Maintaining adequate nutritional intake is crucial to promote healing, decrease mortality, and prevent weight gain.[4][34]

Pain management: Pain, depression, and anxiety are common after SCI and should be treated accordingly in collaboration with pain specialists. Acetaminophen and nonsteroidal anti-inflammatory medications are preferred to avoid respiratory depression in patients with neurogenic shock. Other agents, including opioids, selective serotonin reuptake inhibitors, tricyclic antidepressants, and lidocaine patches, may also be utilized.[34]

Physical therapy: 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. Physical therapy for a minimum of 20 minutes each day is recommended.[4]

Differential Diagnosis

Conditions that may present with clinical features similar to spinal shock include:[18][17]

• Cardiogenic shock
• Hypovolemic shock
• Septic shock
• Malignancy
• Spinal infection (eg, epidural abscess)
• Epidural hematoma
• Disk herniation
• Spinal stenosis

Prognosis

The most common causes of death in patients with SCI are respiratory system disease and cardiovascular events.[39] These include pneumonia, non-ischemic heart disease, septicemia, pulmonary emboli, ischemic heart disease, and unintentional injuries.[3] The prognosis for spinal shock is poor and depends upon underlying comorbidities, level of spinal cord injury, associated injuries, age, and type of injury.[3] Patients with C1 through C3 vertebral injury have a 6.6 times higher mortality rate than 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.[22] 

A large multicenter retrospective study investigating trauma patients in Germany concluded that SCI complicates polytrauma presentation and can be found in every 13th patient.[40] Moreover, in polytrauma patients, >50% of the patients suffered complete spinal cord lesions with spinal shock. They also noted that SCI only had a limited influence on mortality. However, complications of multiorgan failure, sepsis, and extended hospital length of stay were more frequent in polytrauma patients with SCI.[40]

Complications

Spinal shock can have multiple systemic complications secondary to neurologic deficits, including pressure sores, VTE, sepsis, pneumonia, urinary complications, bowel complications, and cardiovascular events. Refer to "Supportive Therapy" in the Treatment section for additional information). Cardiovascular complications are the leading causes of morbidity and mortality in both acute and chronic stages of SCI.[41] 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.[41] 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 at a higher frequency when compared to age-matched controls.[41] In the acute phase of spinal shock, priapism has also been reported in males.[42]

Aside from systemic vascular complications of spinal shock, functional disability as a result of spinal cord injury is a significant complication of spinal shock and is a primary determinant of morbidity and mortality in this patient population. The data regarding motor axonal excitability is limited, and clear prognostic indicators of functional recovery have not yet been identified. Some studies reported the existence of significant deterioration in peripheral motor axonal excitability and function in early spinal shock.[43] Mechanisms that eventually allow recovery and indicators that determine the degree of functional recovery remain unknown.