Hemodynamic and ventilatory failures are common after SCI, especially following injuries of the cervicothoracic spine. In these cases, ischemia is the most common culprit for continued secondary neurologic insult . Therefore, in patients with acute SCI, cardiac, hemodynamic, and respiratory monitoring in an ICU setting are crucial to detect cardiopulmonary insufficiency [21••]. Within the spinal cord, direct injury to the microcirculation can lead to alterations in blood flow [7••]. At the systemic level, SCI is often accompanied by hemodynamic instability from the loss of sympathetic tone.
In the setting of hypotension, providers should first differentiate between hypovolemic systemic shock and neurogenic shock. Sympathetics supplying the heart exit the spinal cord in the ventral roots of T1–T5. Injury at or above these levels will disrupt sympathetic outflow leading to unopposed parasympathetic input. The end result of neurogenic shock is, therefore, peripheral vasodilation leading to warm extremities and hypotension with bradycardia [7••]. Hypotension should be treated with blood transfusions, volume replacement, and vasopressors as needed. Spinal shock, on the other hand, is a physiological dysfunction that results in decreased tone and hyporeflexia in the setting of an upper motor neuron lesion. The resolution of spinal shock is marked by the return of the bulbocavernous and deep tendon reflexes [7••]. In the end, hypotension with concomitant loss of local spinal cord autoregulation of the microcirculation will compromise spinal cord perfusion and worsen ischemic injury.
Needless to say, hypotension (SBP <90 mm Hg) must be corrected as soon as possible [21••] in order to prevent ischemic insult to the spinal cord and to potentially enhance neurologic outcomes . There is a level III recommendation to maintain mean arterial blood pressure of at least 85–90 mm Hg for the first 7 days following acute SCI [21••], a guideline, which we follow at our institution. First line treatment for hypotension is volume resuscitation with at least 1–2 L of crystalloids, followed by blood transfusions, depending on the presence of additional injuries and the hematocrit. However, if the increased blood volume and venous return is not matched by sufficient cardiac output, volume restoration alone will be inadequate to increase blood pressure, and vasopressors should be initiated. Given the loss of sympathetic tone, the agent of choice should have both α- and β-adrenergic properties, such as norepinephrine or dopamine [7••]. Phenylephrine can also be used, but caution should be used when doing so because its purely α-adrenergic effects will increase cardiac afterload and may worsen bradycardia .
Following recovery from neurogenic shock, patients with cervical and high thoracic SCI can still have resting hypotension because of sympathetic disruption. However, the majority of these individuals (50 %–90 %) will also have autonomic dysreflexia resulting in episodes of significant hypertension up to 300 mm Hg [7••]. These episodes of hypertension are trigged by nonpainful or painful sensory stimuli, such as a full bowel or bladder, below the level of the SCI. Autonomic dysreflexia can occur as early as 4 days after the injury and can result in a life-threatening crisis if not recognized [7••]. Most episodes can be managed by eliminating the stimulus (emptying the bladder, evacuating the bowel, or changing patient position) , but sometimes pharmacologic intervention is required. Conversely, orthostatic hypotension is quite common in the acute SCI phase, especially during changes in patient position (attempting to stand up, transferring to the wheelchair); however, 41 % of individuals with SCI who have orthostatic hypotension are asymptomatic . In those who have symptomatic orthostatic hypotension, maintaining adequate circulating volumes, positioning more slowly, and pharmacologic agents such as fludrocortisone, midodrine, pyridostigmine, caffeine, and epoetin can be helpful [7••].
Respiratory compromise and failure
Respiratory failure and compromise are common in SCI, especially with injury to the cervical cord . The decision to intubate is usually related to respiratory compromise from one or more of the following: loss of innervation of the diaphragm (C3–C5), fatigue of innervated respiratory muscles, hypoventilation (PaCO2 > 50 mm Hg, pH < 7.30), V/Q mismatch, secretion retention, as well as other associated injuries. Intubation may complicate the opportunity for a closed spine reduction, which is safer in an awake and communicative patient. However, it should be noted that, in the acute setting, cough function is abnormal with any injury above T11 [7••]. More specifically, with an injury at C1–C3 cough is absent, C4–T1 it is nonfunctional, T2–T4, it is weak, and T5–T10 it is poor [7••]. Only injuries at T11 and below will allow for normal cough function in the acute setting. Vital capacity in the acute phase will also be abnormal if the injury is above T11. More specifically, at C1–C3 it is normal only 0 %–5 % of the time, C4 it is normal 10 %–15 % of the time, C5–T1 it is 30 %–40 %, T2-T4 it is 40 %–50 %, T5–T10 it is 75 %–100 %, and at injuries below T11 it is typically normal [7••]. It is safe to assume that patients injured at C4 and above will fail to maintain a respiratory effort in the acute phase and have a significant chance of requiring a tracheostomy within the first week [7••]. Injuries at C5 may or may not require intubation in the acute setting and, therefore, need to be evaluated on a case-by-case basis as well as watched carefully for respiratory failure. As expected, patients with thoracic SCIs, especially in the lower thoracic region, have a lower rate of intubation compared with those with cervical injuries . However, a significant proportion (up to 50 %) still gets intubated because of additional injuries such as flail chest, pulmonary contusions, pneumothoraces, and hemothoraces .
Nevertheless, suboptimal respiratory function leads to relative hypoxemia and worsening of spinal cord ischemia. We recommend that all patients with cervical spine injuries, in addition to those with lesions at C4 and above, be considered at a low threshold for intubation, as approximately one-third will eventually require ventilator support . In those patients who are not intubated, additional monitoring for signs of respiratory decompensation and subsequent respiratory failure, such as a vital capacity <1 L and a rising PCO2, is crucial. We recommend proceeding with intubation if clinicians are at all considering it, as proactive intubation under controlled settings is always preferable to emergency situations with potentially prolonged periods of hypoxemia. It goes without saying that in patients with known or presumed cervical spine injuries, intubation must be performed with manual in-line traction and/or with a cervical collar to prevent further neurologic injury. In this setting, an experienced team should be the ones to perform orotrachael intubation and a fiber-optic setup may additionally be required .
Over time, respiratory muscles become spastic and more rigid, actually allowing for improvement in respiratory function . Ventilatory weaning is related to the level of injury: on average 65 days for C1–C4, 22 days for C5–C8, and 12 days for thoracic injuries . To help prevent pneumonia and maintain secretions, patients are usually kept upright. However, tetraplegic patients maintain better ventilation in the supine position, and this must be weighed against the concern for secretions and potential aspiration . In these patients, flaccid abdominal musculature leads to overdistention of the diaphragm and decreased minute ventilation, which can be ameliorated with abdominal binders .
Other organ system general recommendations
Upon the patient’s arrival, a Foley catheter should be placed to avoid bladder distention from a neurogenic bladder, with a subsequent transition to intermittent catheterization to decrease the chance of infection. Neurogenic bowel is also common and an aggressive bowel regimen should be the standard of care. SCI patients are at high risk for stress ulcers, particularly if steroids have been given, and patients should, therefore, be maintained on gastrointestinal prophylaxis. Deep venous thrombus prophylaxis with either subcutaneous heparin or lovenox is paramount, though it should be noted that low-molecular weight heparin is associated with a statistically significant lower amount of deep vein thrombosis compared with unfractionated heparin . For patients who are bedbound or with limited mobility, an inferior vena cava (IVC) filter should be considered. IVC filters are known to be effective in preventing pulmonary emboli and have a low complication rate . SCI patients are also at high risk for pressure ulcers, and optimal medical management of underlying conditions such as diabetes and peripheral vascular disease must be maintained with a multidisciplinary approach to nursing, nutrition, and physical/occupational therapy. In any bedbound or limited mobility patient, pressure ulcers should be assumed to occur and, thus, must be monitored for daily.
Intraspinal pressure, spinal perfusion pressure, and blood flow
The benefit of placing lumbar drains to decrease intrathecal pressure (ITP) and subsequently improve spinal cord perfusion is unproven. A randomized trial of 22 patients demonstrated that drainage of cerebrospinal fluid, albeit a minimal amount, did not lead to a significant decrease in ITP nor did it cause any adverse events . Monitoring surprisingly showed an increase in ITP following decompression in both groups possibly related to an elimination of the pressure gradient across the level of injury . The pressure waveform was a useful measure of restoration of cerebrospinal fluid flow throughout the cord and intrathecal catheters may be useful for monitoring purposes. Although we do not routinely employ them at our institution, they have been used by the cardiothoracic surgery community following aortic aneurysm repair, in order to help prevent spinal cord ischemia, when spinal radiculomedullary arteries have been potentially compromised .
The National Acute Spinal Cord Injury Study (NASCIS) trials recommended that methylprednisolone be given in cases of blunt SCI less than 3 h old as a 30 mg/kg bolus followed by a 5.4 mg/kg/h infusion over 24 h, as well as for injuries 3–8 h-old as a bolus followed by a 24- to 48-h infusion [38, 39••]. For SCIs older than 8 h, NASCIS did not recommend giving steroids [38, 39••]. Based on new level 1 recommendations in 2013 by the AANS/CNS, methylprednisolone should not be given in the treatment of acute SCI because of associated harmful side effects including infections, sepsis, gastrointestinal bleeding, poor wound healing, psychiatric side effects, and even death [39••, 40••, 41, 42]. Therefore, the use of steroids have since started to fall out of favor among neurosurgeons over concern for potential complications . At our institution, across hospital services, we no longer use steroids in SCI patients. However, there still remains controversy regarding the new AANS/CNS guidelines, with some authorities stating that there is limited new evidence to justify this new recommendation [43••]. Those who disagree with the AANS/CNS guidelines acknowledge the concerns over the NASCIS trials, but point out that the trials support a small, but significant improvement in long-term motor function when methylprednisolone was initiated within 8 h of injury [43••]. These authors go on to state that there were only weak trends toward higher risks of infections and gastrointestinal complications and thus they believe that the use of steroids should be left to the discretion of the physician, in order to balance risk and benefit [43••]. They go on to advocate strongly for the consideration of methylprednisolone in patients with cervical SCI undergoing decompression based on a Cochrane meta-analysis demonstrating that these patients experience some benefit [43••, 44••].
GM-1 ganglioside (Sygen)
GM-1 mimics endogenous neurotrophic factors by stimulating nerve growth and repair, and reducing glutamate-mediated excitotoxicity [7••]. A phase 3 randomized controlled trial failed to show significant benefit, and the updated AANS/CNS guidelines state that the administration of GM-1 ganglioside for the treatment of acute SCI is not recommended [40••].