Spinal cord injury

Spinal cord injury

TRAUMA sensory level is the lowest dermatome with normal pinprick and light touch sensation. Neurological deficit – in general, injuries are describe...

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TRAUMA

sensory level is the lowest dermatome with normal pinprick and light touch sensation. Neurological deficit – in general, injuries are described as complete or incomplete. Complete injuries result in absence of motor or sensory function below the level of the lesion. Incomplete injury is defined by partial preservation of neurological function more than one level below the level of spinal cord injury. Incomplete injuries can result in various patterns of remaining sensory and motor function (e.g. sacral-sparing, anterior cord, Brown-Séquard and cauda equina syndrome).

Spinal cord injury Bob Winter Dave Knight

Management Airway: manipulating and securing the airway is often difficult. The choice of technique depends on the situation and the clinician’s experience, but must ensure non-displacement of the cervical spine. If intubation is required, a difficult airway should be anticipated because: • immobilization of the cervical spine leads to suboptimal positioning • cricoid pressure and rapid-sequence induction are required • there may be associated maxillofacial trauma • pre-vertebral swelling occurs due to haematoma. The difficult nature of the airway has led many clinicians to recommend the use of awake fibre-optic intubation. This technique allows preservation of muscle tone, and spinal integrity can be monitored throughout the intubation. The disadvantage is that it requires skill and specialized equipment, which are often unavailable in the acute situation.

The annual incidence of acute spinal cord injury is 15–40 cases/1,000,000. Over 50% of cases are the result of road traffic accidents, with falls, industrial accidents, sports or violence making up most of the remainder. The typical patient is young (peak incidence is at 20–40 years of age) and male (male to female ratio is 4:1). Mechanisms of injury: acute spinal cord injury can be initiated by a number of distinct mechanical forces. Distraction occurs when the bony spine is hyperextended, as in rapid acceleration and deceleration injuries. Compression results from axial loading compromising the spinal cord due to encroachment of vertebral body fragments or intravertebral discs. Torsional injuries result from high-impact collisions, which twist and tear spinal cord tissue. Penetrating trauma can directly damage the spinal cord. Penetrating trauma can affect the cord at any level, but blunt trauma tends to affect the regions of the cord that are flexible or at the junctions of flexible and inflexible segments. The lower cervical or upper lumbar regions (above and below the thorax, respectively) are vulnerable to this type of injury. The true incidence of acute spinal cord injuries in the upper cervical spine is probably high, but because they are often fatal, accurate figures are difficult to ascertain.

Breathing: the diaphragm is supplied by C3–5 segments of the spinal cord. Injury above C3 results in apnoea and is usually fatal unless controlled ventilation is initiated immediately. Many patients with injuries below C5 have normal diaphragmatic function but proceed to respiratory failure in the early stages of acute spinal cord injury. The reasons for this are a combination of underlying associated pulmonary injury (e.g. contusion, pneumonia), loss of abdominal muscle tone and absent intercostal muscle function. The initially flaccid intercostal muscles cause the chest wall to contract rather than expand during inspiration, which results in a 70% reduction in forced vital capacity. Respiratory wean is later aided by the spasticity that develops in these intercostal muscles and maximal inspiratory force can eventually return to almost 60% of pre-injury level. Many spinal injuries do not occur in isolation and patients may develop respiratory failure because of the multisystem effects of polytrauma. Direct detrimental effects on pulmonary function include rib fractures, pulmonary contusions, pneumothorax, haemothorax and pneumonia. Indirect effects include head injury, abdominal injury and increased capillary leak (secondary to massive transfusion, systemic inflammatory response) leading to acute lung injury. It is not uncommon to find a patient in respiratory failure despite minimal neurological deficit; and a high index of suspicion needs to be maintained at all times. Weaning from mechanical ventilation is often slow and requires meticulous attention to fluid management, nutrition, early protective lung ventilation and measures to reduce ventilator-associated pneumonia. An early tracheostomy is often desirable but its impact on operative cervical spinal fixation needs to be considered. The contractility of the diaphragm is maximal in the supine position.

Classification of injury Level – the level of spinal cord injury determines the extent of neurological deficit. There may be a heterogeneous pattern of sensory and motor deficit. The motor level is defined as the lowest myotome level with power 3/5 (weak movement against gravity). Motor function is classified according to the Medical Research Council (MRC) grading for power. This system grades power between 5/5 (normal power) and 0/5 (no movement). The

Bob Winter is Consultant at Queen’s Medical Centre, Nottingham, UK. He has an interest in the immediate management of trauma. Dave Knight is Specialist Registrar in Anaesthetics at Queen’s Medical Centre, Nottingham, UK. He qualified from Leeds University and has trained in Yorkshire, New Zealand, and Nottingham. He is currently undergoing advanced level ICU training at Queen’s Medical Centre and aims to pursue a career in critical care. His interests include sepsis and immunonutrition.

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TRAUMA

Patients with cervical cord lesions who have lost intercostal function and are dependent on diaphragmatic breathing wean optimally when managed supine.

Complications of cervical spine immobilization Airway • Delayed tracheostomy • Poor oral hygiene (causes bacteraemia and sepsis)

Circulation: many patients presenting with acute spinal cord injury are hypotensive. It is vital that hypovolaemic as well as cardiogenic and septic shock are considered and actively excluded before a diagnosis of spinal shock is considered. The absence of sensation below a complete spinal cord injury may make clinical diagnosis of accompanying injuries difficult. Liberal use of plain radiology and ultrasound are mandatory in the early assessment of hypotension. If the patient is stable, early CT of thorax and abdomen may improve the diagnostic yield. A complete cord lesion disrupts vertical transmission of impulses and this limits distal cord function. The resulting hypotension is due to loss of vasomotor tone and cardiac inotropy; this can also be described as spinal shock. Treatment is based mainly on a combination of judicious fluid management and vasopressors (e.g. norepinephrine). If the lesion is above the cardiac accelerator fibres (T1–T4), paradoxical bradycardia can accompany this hypotension. Problematic bradycardia usually responds to antimuscarinics or chronotropes. Transvenous pacing is seldom required. Hypovolaemic and spinal shock often co-exist and inappropriate fluid replacement or vasopressor therapy can result in further morbidity. The Swann–Ganz catheter has traditionally been used to guide therapy, but newer, less-invasive monitors (e.g. PiCCO, LiDCO or oesophageal Doppler) may be used as alternatives. Spinal shock can persist for 2–3 weeks and resolves as local reflexes begin to return local vasomotor tone. Autonomic hyperreflexia occurs in 85% of patients with complete injuries above T5 and is the result of excessive sympathetic response to stimulation below the level of injury, in the absence of the normal damping response of the descending cords. Relatively trivial problems, such as constipation or urinary retention, can trigger this potentially devastating problem and close cardiovascular monitoring needs to be maintained even in the post-ICU recovery phase.

Breathing • Increased risk of ventilator-associated pneumonia Circulation • Central venous catheter access difficult • Central venous catheter line care difficult • Increased risk of thromboembolism Neurological • Increased intracranial pressure Gut • Gastrostasis, reflux and aspiration more common • Delayed enteral nutrition Skin • Pressure sores (dependent areas and around collar) Staffing • Minimum of four staff required for log rolling, leading to crossinfection, limitation of barrier nursing and significant impact on staffing levels • Limited ability to perform physiotherapy 1

vein thrombosis initially (to reduce the risk of haemorrhage) and discontinue LMWH prophylaxis after 3 months (when the risk of thromboembolism is low).

Clearing the spine: the spine can be reliably cleared only if clinical examination is painless and the patient is alert, orientated and has no distracting injury. Many ICU patients never fulfil these criteria and a risk–benefit calculation needs to be made. The consequences of converting a neurologically intact undiagnosed, unstable injury into a complete cord lesion are colossal. The consequence of treating all unconscious blunt trauma patients with universal spinal precautions are subtler, but are probably responsible for considerably more morbidity and mortality (Figure 1). Clearance of the cervical spine using a single lateral film is known to miss over 15% of unstable injuries. At the other extreme, routine use of MRI is sensitive, but not specific, and is often impractical (expense, unsuitable for unstable patients). The current policy in the authors’ institution is outlined in Figure 2. With adequate CT and plain radiological views the incidence of missed unstable injuries is thought to be 0.1–0.5%.

Death: 85% of patients with acute spinal cord injury who survive the first 24 hours are alive 10 years later. The most common cause of death (not directly related to the initial injury) is pneumonia followed by non-ischaemic heart disease. The latter often occurs in young people who have no history of underlying heart disease and may be a result of occult autonomic dysfunction. The third most common cause of death is suicide; the lifelong impact of the injury on both patient and family should not be underestimated. Controversies Surgery: early spinal fixation allows patient mobilization and may reduce some of the morbidity associated with prolonged traction and enforced bed rest. Early fixation can precipitate neurological deterioration in an ischaemic acute spinal cord injury and indwelling metalwork may become infected. A recent trial has suggested that early fixation is associated with a shorter hospital stay, but no differences in mortality, intensive care stay or number of ventilator days were demonstrated.

Thromboprophylaxis: acute spinal cord injuries are at massive risk of thromboembolic phenomena and prophylaxis is mandatory. The most commonly used treatment is low molecular weight heparin (LMWH). Some spinal units use mechanical prophylaxis for deep

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Steroids: the use of high dose methylprednisolone in acute spinal cord injury is common in many hospitals. The evidence for this 316

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TRAUMA

Suggested protocol for radiological spine clearance in the unconscious patient • Plain three-view radiograph of cervical spine (anteroposterior, lateral and odontoid views) • High resolution CT (whole cervical spine down to T41) with 1.5–2 mm slices and sagittal reconstructions • Thoracolumbar anteroposterior and lateral plain radiographs • Reconstruction of thoracolumbar spine views if incidental thoracic or abdominal CT performed • Review of images by senior radiologist • Consideration of MRI if there is a radiological or focal neurological abnormality T1–T4 often poorly imaged by plain radiology

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treatment is based primarily on the second National Acute Spinal Cord Injury Study trial in which patients were randomized to methylprednisolone, naloxone or placebo within 12 hours of injury. The results suggested improvement in motor function at 1-year follow-up. Analysis of these results showed that benefit was demonstrated in a non-predetermined subgroup (treatment within 8 hours) and that the associated neurological improvement was relatively small. A recent Cochrane review of steroid treatment for acute spinal cord injury has not supported its routine use. 

FURTHER READING Bracken M B. Steroids for acute spinal cord injury. The Cochrane Database of Systematic Reviews 2002; 2: CD001046. Kerwin A J, Frykberg E R, Schinco M A. The effect of early spine fixation on non-neurologic outcome. J Trauma 2005; 58: 15–21. Morris C G T, McCoy E. Clearing the cervical spine in unconscious polytrauma victims, balancing risks and effective screening. Anaesthesia 2004; 59: 464–82.

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