Spinal Cord Injury Medicine. 2. Acute Care Management of Traumatic and Nontraumatic Injury

2.1 Clinical Activity: To discuss the acute care management of a 20-year-old man admitted to the trauma center with a C4 American Spinal Injury Association grade A spinal cord injury after a snowboarding accident 

PATIENTS WITH ACUTE TRAUMATIC spinal cord injury (SCI) should be managed at a trauma center with SCI experience, particularly patients with concomitant injuries. Level 1 trauma centers have been shown to have better outcomes in acute SCI than lower-level trauma centers or nondesignated hospitals, although the differences between level 1 and level 2 were small in isolated SCI.1 Transfer to such a center is advocated as soon as the patient is stable, with the suggestion that emergency medical services in urban areas should consider bypassing the nearest hospital to take SCI patients to level 1 trauma centers directly.2 Level 1 trauma centers are required to have in-house neurosurgical consultation and can therefore more rapidly assess patients and intervene. These centers also often have well-defined, evidence-based protocols for SCI care and staff well-trained in SCI because of a higher volume of an otherwise low-incidence injury.

Principles of spine stabilization are well established and have changed little in recent years. Timing of decompression of the neural elements, however, is controversial. Animal data have consistently suggested increased neuronal loss from prolonged compression.3, 4 Human studies have been conflicting, but comparisons are marred by differences in time points chosen, types of injuries included, and surgical procedures performed. It is likely that little difference exists in outcome between patients undergoing surgical decompression later than 48 hours and those treated even later than that.5 However, decompression within 24 hours may improve neurologic recovery, particularly in patients with incomplete injuries, but to date, data are inadequate to mandate such a standard.6 These studies agree that there is not an increased risk of neurologic deterioration from early surgery, as was previously thought. Further, early surgery is associated with fewer complications and shorter acute care lengths of stay.7, 8

Although adopted as a standard of care more than a decade ago,9, 10 the use of high-dose methylprednisolone as a neuroprotective agent in acute SCI has now been called into question, based on methodologic concerns of the primary studies.11 In light of the enrollment of a high number of patients with minimal deficit into the National Acute Spinal Cord Injury Study (NASCIS) trials, it is particularly difficult to determine the benefit of the protocol in people with complete SCI and in people who have incomplete SCI with a significant deficit. Both the neurosurgical guidelines12 and the Consortium for Spinal Cord Medicine clinical practice guideline2 consider the use of high-dose methylprednisolone to be a treatment option rather than a standard. Concerns have been expressed about the increased risk of infection and gastrointestinal bleeding associated with the 48-hour–long infusion. Steroid myopathy has been shown to be associated with both the 24-hour–long and the 48-hour–long infusions.13 The prevalence and functional implications of this myopathy are presently unknown. Despite these caveats, the use of the NASCIS protocol remains high in the United States.14

Spinal cord perfusion has been a recent area of exploration for neuroprotection. Hypotension has been recognized as a contributor to secondary neurologic injury and should be avoided.15 However, clear data on optimal blood pressure to ensure adequate perfusion, as well as any other intervention to improve spinal cord perfusion in traumatic SCI, are lacking. Routine use of a lumbar drain to reduce cerebrospinal fluid (CSF) pressure has reduced the prevalence of ischemic SCI associated with abdominal aortic aneurysm repair.16 The effect of this intervention in traumatic SCI is currently in clinical trial. Although human data are limited, the neurosurgical guideline has recommended that the mean arterial pressure be maintained at 85 to 90mmHg for the first 7 days after injury.17 However, a randomized controlled trial is needed to confirm the safety and efficacy of this intervention. Physiatrists may facilitate transfer of patients receiving this care out of the intensive care unit (ICU) by advocating for the use of abdominal binders, lower-limb compression, and oral vasopressors such as midodrine as other options to maintain adequate cord perfusion.

Autonomic dysfunction is common in acute SCI and is particularly noticeable in cervical level injuries. Bradycardia and neurogenic shock18 are commonly seen in the acute care setting, but autonomic dysreflexia may also occur in this early period19 and will certainly be a concern in hospitalized chronic SCI patients. Spinal shock and neurogenic shock, although related, are separate entities. Spinal shock refers to the loss of reflex neurologic activity in the spinal cord, and is defined by loss of all spinal reflexes. Neurogenic shock is loss of adequate tissue perfusion associated with hypotension of neurologic origin. However, acute SCI patients may have multiple causes of shock. Sepsis, hypovolemia, and cardiogenic shock must all be considered in the early period of SCI.2 Volume resuscitation is an appropriate initial measure, but vasopressors are often necessary. Patients using antihypertensive medications before injury may be particularly difficult to control until the medication effects are inactive. Bradycardia occurs because of unopposed vagal tone, with a greater effect seen in higher levels of injury. Stimulation of vagally innervated tissue may further lower heart rate, as is seen commonly during deep tracheal suctioning. Although the bradycardia is often self-limited, atropine may be used either as treatment or as pretreatment in the case of identifiable triggers.18 External pacing may be of benefit as well. Autonomic dysreflexia requires intact spinal cord reflexes19 and so will not be seen until emergence from spinal shock. Although hypertensive emergencies are uncommon in the early period, the instability of blood pressure as low-level dysreflexia occurs and resolves can be confounding to the acute care team. The physiatrist can be helpful not only with management but in identifying the source of dysreflexia. Hyperthermia is not a component of autonomic dysreflexia but may indicate the source of dysreflexia. However, heat dispersion is impaired in SCI,20 such that fever from a typical source may result in higher temperatures and longer periods of fever compared with a neurologically intact population. Strictly speaking, environmental fevers are unlikely in the ICU setting, considering its constant environmental control. However, a fever in the early weeks after tetraplegia without any identified source, or “quad fever,” can occur.21 This is a diagnosis of exclusion and may be related to a heightened febrile response to atelectasis.

Preventing complications remains vital in acute SCI. Prophylaxis of venous thromboembolism should begin no later than 72 hours after the onset of SCI and should include anticoagulation for most injuries.2, 22 Low–molecular-weight heparin has been compared with unfractionated heparin, at 5000U 3 times daily, with similar rates of deep vein thrombosis but higher rates of pulmonary embolism (PE) and bleeding in the unfractionated heparin group found.23 In light of the high rate of PE, an inferior vena cava (IVC) filter should be used in SCI patients who have contraindications to anticoagulation.24 If the contraindication is temporary, a temporary filter can be placed until pharmacologic prophylaxis can be instituted. There is no evidence to support routine placement of IVC filters.25

SCI confers a substantially higher risk of stress ulceration than all other kinds of trauma.26 Those with cervical injuries appear to be at particularly high risk. Either H2-blockers or proton pump inhibitors are indicated, to be started at admission and continued for 4 weeks.2 The use of acid-reducing agents beyond 4 weeks is not indicated unless other risk factors for peptic ulceration are present, such as a bleeding disorder, mechanical ventilation, or history of ulcer disease. Ongoing use of acid reducing agents may increase the risk of Clostridium difficile bowel infection.27

2.2 Clinical Activity: To summarize the physiatric interventions (in acute care) for the prevention of complications in this young man with an acute SCI 

The physiatrist is an important member of the team caring for the person with SCI in the acute care setting, both during the period immediately after injury and during any subsequent hospitalization. Although prevention of complications common to SCI is a fundamental role, balancing the standard practices used in acute care with the unique physiology of SCI is equally important.

Interventions that may be considered routine in any rehabilitation setting must not be overlooked during an acute hospital stay. Range of motion (ROM) should be started as soon as there are no medical or orthopedic contraindications to do so. Loss of shoulder ROM in the early period has been associated with increased shoulder pain during the rehabilitation phase.28 There may be reluctance to provide full range out of concern for spine stability, but there is no evidence that shoulder ROM in a supine patient wearing a hard cervical collar alters spinal alignment (with the exception of patients with ankylosing spondylitis). The swimmer’s radiographic view, which provides full range of the shoulder, is used routinely in emergency departments to evaluate for cervical spine injury, without concern that it might induce neurologic deterioration, even in an intact patient. Depending on the likely length of stay, splinting and orthoses may also be appropriate to preserve joint ROM in the highly susceptible areas of the hands and feet.

Bowel and bladder management are also fundamental needs in the acute care setting. The initiation of a bowel program should begin soon after enteral feeding is initiated.2 After a new injury, patients must be assessed for the presence or absence of the bulbocavernosus reflex to ascertain whether an upper motoneuron or lower motoneuron bowel program is appropriate.29 Established guidelines for bowel management need minimal adaptation for the acute care setting, although training of personnel may be necessary. In those with chronic SCI, the physiatrist should assist the acute care team in implementing the patient’s usual program so far as feasible. See section activity 3.330 for further discussion. A bladder program may also be initiated during the acute period, although this does not have the same urgency as the bowel program. The removal of an indwelling urinary catheter and initiation of intermittent catheterization can be recommended as soon as the patient no longer requires intravenous fluids and the medical status does not require strict monitoring of urinary outputs.2 However, physiatrists should be aware of the diuresis of third spaced fluid associated with mobilizing the patient and warn against volumes higher than 500mL per catheterization. The routine use of prophylactic antibiotics to prevent urinary tract infections is not recommended.31

Pulmonary complications are the leading cause of mortality in the first year after SCI.32 Pulmonary complication rates during the acute hospitalization have been reported to be 84% for C1-4 levels of injury, 60% for C5-8, and 65% for thoracic levels, indicating that all neurologic levels of injury are at risk.33 The primary contributors to pulmonary dysfunction after SCI are difficulty handling secretions, atelectasis, and hypoventilation.

Clearance of secretions is primarily achieved by abdominal muscle contraction producing a forced expiration or cough. Weak or paralyzed abdominal muscles preclude an effective cough. Techniques of manually assisted cough have been shown to be more effective in clearing secretions than standard suctioning, which is limited to effective clearance of only the right mainstem bronchus.34 This is significant because pneumonia is most common in SCI in the left lower lobe.35 In addition, larger and firmer mucus plugs can be mobilized that cannot be accommodated by the suction catheter. The “quad cough,” or abdominal thrust, and the tussive squeeze or costophrenic technique, in which the hands are placed over the lower rib cage instead of the epigastrium, are both easily applied in the acute care setting.36 Contraindications to the abdominal thrust are abdominal injuries or recent surgery. A recently placed IVC filter is a relative contraindication because of potential migration of the filter. Contraindications to the tussive squeeze include lower-rib fractures and thoracic injury or surgery. Neither should be performed within 1 hour of a meal. The mechanical insufflator–exsufflator (M-IE) is extremely effective and can be administered via tracheostomy or mouth piece. Contraindications to use of the M-IE include a history of pneumothorax, barotrauma, or emphysema. There is also risk, as with traditional suctioning, of excessive vagal stimulation and bradycardia in those with tetraplegia.

After SCI, a restrictive ventilatory deficit occurs and there is a resultant decrease in all lung volumes. Vital capacity (VC) declines in tetraplegia and high paraplegia from respiratory muscle weakness. Prompt mechanical assistance (either intubation or noninvasive means) should be performed in people with severe respiratory distress or in patients whose VC is below 15mL/kg.37 Atelectasis has been estimated to be present in 60% of SCI patients on admission to rehabilitation facilities.38 The Consortium for Spinal Cord Medicine clinical guidelines for Respiratory Management Following Spinal Cord Injury37 supports the use of higher tidal volumes than those usually used in intensive care settings in patients requiring mechanical ventilatory assistance. The tidal volume is titrated upward while monitoring the airway pressure, until the atelectasis resolves on chest radiograph and the patient is afebrile.37 In a retrospective review, this protocol was shown to speed resolution of atelectasis and decrease ventilator weaning time.38 However, it is well established that low-volume ventilation improves outcomes in the general trauma setting, primarily because of the high frequency of acute lung injury and adult respiratory distress syndrome in this population. Therefore, these 2 disorders should be resolved or ruled out before initiation of a high-volume weaning protocol.2

Dysphagia is also a contributor to respiratory deterioration after SCI. Although up to 30% of patients with tetraplegia have dysphagia at admission to inpatient rehabilitation,39 up to two thirds of patients undergoing elective cervical spine surgery have postoperative dysphagia, which has been shown in both anterior and posterior cervical spine approaches.40 It is likely, then, that the rate of dysphagia in acute SCI is higher than that documented later in the course in the rehabilitation setting. People with cervical spine surgery, tracheostomy, prolonged orotracheal intubation, halo stabilization, and concomitant brain injury should be evaluated for dysphagia.2 A dysphagia evaluation in this early phase should be considered in all people with cervical SCI. Older age is also associated with increased risk of dysphagia in both the acute and rehabilitation settings. In the presence of a rigid cervical orthosis or halo, it is difficult to compensate for dysphagia using a typical chin-tuck position. Use of nasogastric access for short-term enteral feeding can be used until the risk of aspiration diminishes.

An understanding of acute SCI physiology is needed to optimize early nutrition as well. Nutrition is a key parameter in outcomes of trauma patients. However, estimates of nutritional needs after SCI are difficult. Nitrogen loss is obligatory after SCI and cannot be prevented by increased protein feeding. Therefore, measuring urine urea nitrogen is an unreliable way to estimate nutritional needs. Even commonly used caloric estimates for people with SCI have been shown to cause overfeeding in the acute period. Whenever possible, a metabolic cart should be used to determine actual needs.41 Although it is now common practice to initiate nutritional support within 72 hours in all trauma patients, 1 study has suggested that early feeding of people with acute traumatic SCI confers no benefit and may increase risk of pneumonia.42 Further data are needed in this area.

Pressure ulcers are a leading cause of failure to make progress in acute inpatient rehabilitation and so should be a primary concern for the physiatrist during the acute stage. Pressure ulcers are largely preventable, and prevention strategies should start as soon as possible after an injury and continue throughout hospitalization. During acute hospitalizations, when patients are most often supine, the sacrum, heels, and occiput are the most common sites of injury. Time on the backboard should be minimized, because this is a predictor of sacral breakdown. Rather, flat supine positioning should be used during the immediate diagnostic and resuscitative period.43 Once complete, concerns of spine stability may still produce reluctance among staff to appropriately turn the patient and offload pressure areas. Rotating beds designed for the unstable spine are indicated in this case. Patient positioning must be monitored, however, to ensure that the patient is not sliding laterally in the bed with each turn, creating sacral shear and increasing the risk of skin breakdown. Once the spine is stable, routine turning every 2 hours should be implemented.2

Although the choice of surgery and spine orthosis are primarily the purview of the surgeon, physiatrists are expert in the functional implications of these choices. Case discussions with surgical teams may facilitate optimal decisions for both short- and long-term rehabilitation goals. The physiatrist and therapeutic team also have a role in preparing the patient and his/her family for the rehabilitation process. Education about the injury, about the rehabilitation process in general, about specific aspects of the intended rehabilitation location, and about living with SCI may all be started during the acute period as the patient and the family begin to ask those questions.

2.3 Clinical Activity: To prognosticate the extent of neurologic recovery for this newly injured person with SCI discussed above 

It is important to be able to prognosticate neurologic recovery of people who have sustained an SCI to provide accurate information to patients and their families, to guide each patient’s rehabilitation, and to help determine if new treatment methods are effective. Prognosis for neurologic recovery after SCI is best predicted by the neurologic physical examination, using the International Standards for Neurological Classification of Spinal Cord Injury.44, 45 The examination at 72 hours postinjury is superior to that at 24 hours postinjury for predicting recovery.

The major factors in predicting recovery in the first year after traumatic SCI include the initial neurologic level of injury, the patient’s initial motor strength, and, most importantly, whether by examination the injury is classified as neurologically complete or incomplete.46

2.4 Clinical Activity: To describe the acute evaluation of a 30-year-old woman who presents with a profound and rapid onset incomplete tetraplegia categorized as a nontraumatic SCI 

The initial evaluation includes a comprehensive history and physical examination, electrodiagnostic studies, and radiologic evaluation. The importance of the history and physical examination cannot be underestimated. Classic examples illustrating this need include people with spinal stenosis with myelopathy, motoneuron disease, and presumed multiple sclerosis (MS). For people presenting with neck or back pain, symptoms or signs, including a history of bowel and bladder disturbances, gait disorder, weakness, clumsiness, sensory loss, and changes in reflexes, will lead one to suspect myelopathy. Specific findings will lead the clinician to the appropriate diagnostic investigation. To illustrate the importance of the examination, in 1 study57 performed at an academic center, the history and examination identified an alternative diagnosis for 70% of patients who presented with abnormal MRI findings and presumed MS.

MRI has revolutionized the anatomic evaluation of the spinal cord. MRI can identify cord changes associated with cervical and lumbar stenosis and is the study of choice in evaluating nontraumatic SCI. Contrast enhancement is essential for evaluating inflammatory and neoplastic lesions of the spinal cord. MRI with gadolinium enhancement and T2-weighted imaging in diagnosing MS is highly sensitive, yet the specificity is limited because other diseases can mimic it by MRI criteria.58 After a diagnosis of presumed MS, disease progression depends on the identification of new lesions. A characteristic finding in transverse myelitis is T2 hyperintensity centrally involving more than two thirds of the volume of the spinal cord.59 Intramedullary tumors are typically hyperintense on T1-weighted images.

Vascular abnormalities can be identified by MRI and magnetic resonance angiography.60 Spinal angiography is the criterion standard for the diagnosis of spinal cord arteriovenous malformations and their characterization for treatment. When extradural spinal lesions are suspected, computed tomography scan is most helpful to evaluate for primary bone metastases and bony metastases of the vertebral column.

CSF evaluation is important in diagnosing inflammatory disorders of the spinal cord. In MS, the common tests include myelin basic protein antibodies, oligoclonal bands, and a host of other immunologic assays. Despite the utility of CSF antibodies in the diagnosis and prognosis of MS, some contention remains that MS is a metabolically dependent degenerative disease rather than an autoimmune disorder.61 The presence and persistence of CSF oligoclonal bands almost universally allows the distinction between MS and Devic’s neuromyelitis optica.62, 63 Further CSF evaluation includes the evaluation of viral titers, especially in cases of suspected transverse myelitis.

Serum laboratory investigation is directed at diseases that cause spinal cord pathology. Serology tests for Lyme disease, syphilis, human immunodeficiency virus, and other viral agents should be ordered. Rheumatologic studies should be investigated for causes of spinal vasculitis that could mimic MS and transverse myelitis. Glucose tolerance testing and serum hemoglobin A1C should be ordered for evidence of diabetes mellitus. Antiphospholipid antibodies should be tested, although with up to 32% of MS patients being positive, antibodies to β2 glycoprotein I should be included in this investigation to make the diagnosis.64