- Acute spinal cord injury (SCI) is often associated with systemic hemodynamic and pulmonary derangements, and inadequate perfusion or oxygenation of the spinal cord has the potential to worsen neurological injury.
- Hypotension after acute SCI is common. SCI often occurs in the setting of other significant injuries, and the first consideration is to confirm or rule out systemic injuries that result in blood loss, such as lacerations, vascular injuries, injuries to the abdominal contents, and long bone or pelvic fractures, as the cause of the hypotension. Isolated SCI can also result in hypotension, inasmuch as the sympathetic signals from the spinal cord that increase the heart rate and the resistance in the systemic arterioles exit in the thoracic segments T1 to T4. With lesions above this level, bradycardia and hypotension can result. The administration of intravenous fluid is the first step to correct this, but because of lack of resistance in the vascular system, blood may pool within the vascular system, and pharmacologic methods become necessary to maintain hemodynamic support. Phenylephrine, whose almost exclusively α-adrenergic activity increases the tone in the vascular system, is an option, but its administration may result in reflex bradycardia because of the lack of β-adrenergic input. Norepinephrine, which has both α- and β-adrenergic activity, is often a preferable agent in this setting.
- The target for blood pressure needs to be individualized. The first consideration is to ensure that perfusion is sufficient to normalize systemic markers of tissue perfusion, such as urine output, serum lactate level, and arterial pH. Placement of a central venous catheter to help assess intravascular volume and provide access for vasoactive medications can aid in the process of resuscitation. There are, however, no measurable indices of the adequacy of spinal cord perfusion and no practical way to determine perfusion pressure of the spinal cord. Arbitrary systemic MAP goals have therefore been postulated as surrogate markers of adequate spinal cord blood flow. In uncontrolled small case series of patients with acute SCI who have been managed with MAP targets between 85 and 90mm Hg, improved neurological outcome has been claimed. The American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) guidelines for the management acute SCI considers this level III evidence and recommends that MAP be kept between 85 and 90mm Hg for the first 7 days after the injury. The dose of vasoactive medication needed to produce this level of pressure in some patients may produce arrhythmias or excessive vasoconstriction, especially in patients with preexisting medical comorbid conditions, and the risks and benefits of this strategy must be weighed on an individual basis. If this regimen is selected, the patient must be monitored carefully in an intensive care unit.
- The pulmonary consequences of SCI are reflected by the level of the spinal injury. The diaphragm is innervated by the roots of C3 to C5 roots, and so complete lesions above C3 usually result in the need for urgent intubation and mechanical ventilation. In lesions below C5, diaphragmatic function is preserved, but in the acute phase there is flaccid paralysis of the intercostal and abdominal muscles. In this setting, the chest wall collapses with diaphragmatic contraction, markedly reducing the efficiency of respiration. This results in shallow respirations that are compensated by an increase in respiratory rate, and the loss of the abdominal muscles decreases the ability to cough and clear secretions. This promotes a cycle of increasingly rapid shallow breaths, progressive atelectasis, and subsequent fatigue. During the acute phase of SCI, respiratory function must be carefully monitored, and vigorous suctioning and promotion of pulmonary toilet are crucial. Signs of progressive fatigue, such as a persistently rising respiratory rate or an increase in partial pressure of carbon dioxide, should prompt intubation. Respiratory failure occurs in about one third of patients with cervical SCI at an average of 5 days after injury.
- The mean length of time for mechanical ventilation for patients with acute cervical SCI is about 5 weeks. This is largely because the ability to wean from mechanical ventilation is dependent on the transition from flaccid to spastic paralysis of the intercostal muscles. As this occurs, the chest wall regains much of its rigidity, and inspiratory function approaches preinjury levels. This means that most patients with injury below C3 are eventually able to be weaned from mechanical ventilation, but tracheostomy may need to be considered for many of these patients. Expiratory function and ability to cough, however, remain markedly diminished, and affected patients will continue to need aggressive pulmonary toilet.
- Pharmacologic agents aimed at limiting secondary injury after SCI, such as methylprednisolone and GM1 ganglioside, have been studied in human trials. Unfortunately, the results of these trials have been disappointing. In the case of GM1 ganglioside, an initial pilot study had promising results, but a subsequent larger multicenter, randomized, controlled study showed no benefit at 1 year in comparison with placebo. Methylprednisolone, evaluated in the Second National Acute Spinal Cord Injury Study (NASCIS II), purportly did show a benefit. However, there have been concerns about the design and conclusions of this study, and the AANS/CNS graded the results as level III evidence. The use of methylprednisolone does appear to be associated with increased risk of serious complications with level I evidence. The guidelines thus recommend that neither methylprednisolone nor GM1 ganglioside be used in the treatment of acute SCI.
- The use of hypothermia to limit secondary neurological injury has significant potential and has been shown to be beneficial in improved cerebral function after cardiac arrest. The value of hypothermia in acute SCI is unclear. The use of modest hypothermia (32°C to 34°C) in acute SCI has been reported to yield acceptable complication rates and improved neurological outcomes. The AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves classified these findings as level IV evidence and stated that the evidence is insufficient to recommend or discourage this treatment.