Epidemiology of Traumatic Spinal Cord Injury in the United States

The incidence of SCI is estimated to be approximately 40 new cases per million population per year, or roughly 11,000. The estimated prevalence in the United States is 250 million persons.² SCI primarily affects young adults. The average age at the time of injury is 37.6 years. The percentage of persons older than 60 years at injury has increased from 4.7% in 1980 to 10.9% since 2000. Of the SCI reported to the national database, 79% has occurred among males. Since 2000, MVC have accounted for 47.5% of SCI cases reported. Falls are the next most common cause of SCI, followed by acts of violence and recreational activities. Since 2000, the most frequent neurological category is incomplete tetraplegia (34.5%), followed by complete paraplegia (23.1%), complete tetraplegia (18.4%), and incomplete paraplegia (17.5%).³

Neurological Classification

Determining the neurological level and completeness of injury is the most accurate way of prognosticating recovery and functional outcome. Using the International Standards of Neurological and Functional Classification of Spinal Cord Injury, the examiner determines the motor and sensory level on the right and left and ascertains whether the injury is complete or incomplete.⁴

Using standard dermatomes and myotomes defined by the American Spinal Injury Association (ASIA), motor level is defined as the most caudal segment to have a muscle grade of 3. Five muscle groups are tested in the upper extremities, and five muscle groups are tested in the lower extremities. Each muscle group is supplied by two root levels, and each muscle group is graded from 0 to 5. Therefore, if the muscle grade is at least 3 of 5 the proximal root is believed to be intact. The sensory level is defined as the most caudal dermatome to have normal sensation to pin prick and light touch. Specific testing points are defined by ASIA⁴ (Figure 2).

Figure 2 American Spinal Injury Association Impairment Scale.

(Adapted from American Spinal Injury Association: International Standards for Neurological Classification of Spinal Cord Injury, rev. 2006. Chicago, American Spinal Injury Association, 2006.)

In addition to defining the neurological level, the completeness of injury must be determined. See the ASIA impairment scale in Figure 2. A complete injury results in no motor or sensory function preserved in the sacral segments (ASIA A). There are four incomplete levels of ASIA: B, C, D, and E. Incomplete is defined as sparing of sensory and/or motor function below the neurological level that includes the sacral (S4-S5) segments.

There are a number of incomplete SCI syndromes, including central cord syndrome, Brown-Sequard syndrome, anterior cord syndrome, dorsal column syndrome, cauda equina syndrome, and conus medullaris syndrome. Central cord syndrome occurs in the cervical cord and produces greater weakness in the upper extremities than lower extremities. Brown-Sequard syndrome is a lesion that produces ipsilateral motor and proprioceptive loss and contralateral loss of pain and temperature perception. Anterior cord syndrome causes variable loss of motor function, pain, and temperature perception while sparing proprioception. This is usually seen with injury to the anterior spinal artery in the thoracic level. Dorsal column syndrome is rare and would produce abnormal proprioception but preserved motor function and pain and temperature sensation. In cauda equina syndrome, the lumbosacral roots are injured because the spinal cord ends at approximately the L1-L2 level. This causes lower motor neuron symptoms, such as areflexic bladder, bowel, and lower limbs. Conus medullaris syndrome involves injury to the end of the spinal cord. At this level, the lumbar and sacral roots are affected.

Acute Medical Management

All patients with acute traumatic SCI receive methylprednisolone. This is based on the National Acute Spinal Cord Injury Studies (NASCIS), the last being NASCIS 3. This study concluded that patients treated within 3 hours of injury should receive 24 hours of steroids, and those treated in 3–8 hours of injury should receive 48 hours of steroids.⁵

The degree of respiratory dysfunction after SCI is related to the neurological level and the completeness of injury. The level of pulmonary dysfunction increases concomitantly with the level of injury.

C1-C3 neurological levels will require ventilatory support. The phrenic nerve (supplied by C3-C5 nerve roots) will be intact in patients with a C5 neurological level and below. As the level descends from mid-cervical to lower cervical, and then to thoracic, there will be greater innervation to abdominal and intercostal muscles—thereby making the work of breathing easier. The primary objective in early pulmonary management in SCI is to minimize secondary complications, including preventing hypoxemia, preventing and treating atelectasis, reducing risk of aspiration, and providing aggressive pulmonary management to compensate for impaired clearing of secretions.⁶

During spinal shock (temporary loss of all or most spinal reflexic activity below the level of injury), sympathetic activity is reduced or absent. This leads to bradycardia and hypotension. After resuscitation, elastic stockings, abdominal binders, adequate hydration, and gradual upright positioning are used to reduce the effects of orthostatic hypotension.

Bladder management is usually accomplished with an indwelling catheter, as the bladder is often initially areflexic. The goals of team bladder management are to allow the bladder to empty, prevent urinary retention, minimize urinary tract infections, and determine which methods facilitate independent bladder management. Methods may include use of an indwelling Foley catheter or placement of a suprapubic tube. Intermittent catheterization is appropriate for patients with use of their upper extremities.

Male patients who have reflex voiding and detrusor hyperreflexia may require a sphincterotomy procedure or pharmacological agents to reduce outflow resistance and allow use of an external catheter. Some patients with incomplete spinal cord injuries will be incontinent. Urodynamic studies are useful at some point to help classify the neurogenic bladder, in order to select adequate bladder management methods.

A bowel program should be established. Initially, a paralytic ileus is common. Patients may be placed on a stool softener and a daily or every-other-day suppository, with digital stimulation. This routine should be established about the same time each day. The goal is to prevent or minimize incontinence between bowel programs.

Deep venous thromboembolism (DVT) prevention is extremely important, as DVT and pulmonary embolism are major causes of morbidity and mortality in the SCI population. Sequential compression devices should be used, with or without elastic stockings, to improve lower extremity venous return. Such methods are contraindicated in patients with severe arterial insufficiency. Pharmacologic prophylaxis should be initiated within the first 72 hours, when not contraindicated. Low-molecular-weight heparin is the current recommendation. Anticoagulation should be continued for 8 weeks in patients with uncomplicated complete motor impairments, and for 12 weeks in complete motor injuries with other risk factors (lower limb fractures, history of thrombosis, cancer, heart failure, obesity, and age over 70). Vena cava filter placement is indicated in SCI patients with a contraindication for pharmacologic prophylaxis.⁷

Epidemiology of Traumatic Brain Injury in the United States

There are 1.4 million people who sustain TBI in the United States annually. Approximately 50,000 will die, 235,000 are hospitalized, and 1.1 million are treated and released from the emergency department.⁸ Between 80,000 and 90,000 people experience long-term disability associated with TBI.⁹ According to the TBI Model System database, MVCs account for 48.3%—with the next most common cause of TBI being falls, followed by violence. The most common cause of death from MVCs is TBI. Approximately 5.3 million Americans (or about 2% of the population) currently live with disabilities caused by TBI.¹⁰

Pathophysiology of Traumatic Brain Injury

Primary injuries occur at the moment of impact and can be focal or diffuse. Focal injuries include skull fractures, contusions, or extraaxial hematomas. They may develop in the region of direct impact (coup) or at the opposite site of the skull (contrecoup), where the brain contacts the skull. In addition, there are acceleration-deceleration and rotational forces that produce diffuse axonal shearing at the white-gray borders. This is referred to as a diffuse axonal injury (DAI).

Secondary injuries are the biochemical and physiological result of the primary brain injury. These cause tissue hypoxia and cerebral ischemia. Attempts should be made to minimize hypoxemia, hypercarbia, hypotension, and acidosis. Development of intracranial hematomas and cerebral edema also causes secondary brain injury.