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.

Initial Physiatric Consultation and Early Rehabilitation Intervention

The chart should be thoroughly reviewed, including all associated injuries, comorbid conditions, and diagnostic studies. It is important to document social information, including premorbid vocational and educational status, as well as the family and home situation. Obtaining prehospital records documenting any loss of consciousness and Glasgow Coma Scale (GCS) prehospital and at admission will help determine the severity of brain injury. A GCS of 8 or less is considered severe, a GCS between 9 and 12 is considered moderate, and a GCS of 13–15 is a mild TBI (Table 1).

Table 1 Glasgow Coma Scale

A thorough neurological examination includes a mental status evaluation and assessment of neurological recovery using the Rancho Los Amigos Scale of Cognitive Functioning (Table 2). The Rancho Los Amigos Scale is used for patients with moderate to severe TBI and spans from Level 1 to Level 8. Level 1 indicates no response to any stimuli. Level 8 is when all activities are purposeful and appropriate.¹¹

Table 2 Rancho Los Amigos Scale of Cognitive Functioning

Medical Considerations and Complications in Traumatic Brain Injury

Several potential medical complications unique to moderate to severe TBI must be assessed with emphasis on preventing disability. Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone). The degree of spasticity usually correlates with the severity of brain injury. It is one feature of the upper motor neuron picture. Treatment is indicated to improve positioning, prevent contractures, and sometimes to reduce pain. Physical modalities such as ice, stretching, splinting, inhibitive casting, and appropriate positioning can be used. Attempts should be made to position the patient with hips and knees flexed rather than in a supine position.

Medications can be used, but they provide varied results. Dantrolene acts directly on skeletal muscle and reduces muscle contraction by a direct effect on the excitation-contraction coupling mechanism. Dantrolene is effective for cerebral spasticity. It should not be used for people with liver dysfunction, and all those on Dantrolene should be given liver function tests. Baclofen inhibits monosynaptic and polysynaptic spinal reflexes, and is more effective for spinal spasticity. Sedation is a common side effect, and the dosage should be increased slowly. Tizanidine binds to central alpha2adrenergic receptors, and therefore reduces spasticity by acting centrally. Tizanidine is more effective for spinal spasticity than cerebral spasticity. Hypotension and elevated liver function tests are common side effects. Diazepam and other benzodiazepines are also effective, but are sedating and usually should be avoided. Local injections using Botulinum toxin, phenol, or alcohol can be used for specific muscles. Intrathecal Baclofen may be considered if the previously cited measures do not work.

Central dysautonomia, sometimes referred to as storming, is problematic in patients with severe brain injury. There is an increase in circulating catecholamines, leading to tachycardia, diaphoresis, hypertension, hyperthermia, pupillary dilatation, and increased spasticity or posturing. Beta-blockers such as propranolol and clonidine, alpha2-adrenergic agonists, can be used to treat the cardiovascular symptoms of central dysautonomia. Opioids are used to reduce pain. Antispasticity drugs are effective in decreasing the dystonia; particularly tizanidine, which has the added benefit of being an alpha2-adrenergic agonist.

The risk of seizures is increased by brain injury severity, depressed skull fracture, intracranial hematoma, early seizure, penetrating injury, and prolonged unresponsiveness. According to practice guidelines of the American Academy of Physical Medicine and Rehabilitation, there is evidence for the use of antiepileptic drugs within the first week after TBI. However, there is no good evidence to support their use after the first week of injury.¹²

Patients with TBI are at high risk for DVT, and prophylaxis is needed. Early on, if there is concern about bleeding mechanical methods such as sequential compressive devices and thigh high compressive dressings should be used. Pharmacologic prophylaxis should be started, when it is deemed safe, usually within 1–2 weeks. If this needs to be delayed even further, insertion of an inferior vena cava (IVC) filter should be considered.

Heterotopic ossification (HO) may occur in patients with severe brain injury. HO is the formation of ectopic bone and most commonly occurs at the hips, shoulders, elbows, and knees. Early signs of contracture (a hard endpoint with range of motion, pain, and erythema) might suggest this diagnosis. Initially a plain x-ray will be normal, but a three-phase bone scan as well as elevated serum alkaline phosphatase levels can confirm the diagnosis of HO. Anti-inflammatory agents, diphosphonate, and localized irradiation have been used. However, sometimes surgical resection is needed. Prevention is best, by providing range of motion and proper positioning, reducing spasticity, and avoiding prolonged chemical paralysis.

Other potential medical consequences of TBI include neuroendocrine disorders. There is a syndrome of inappropriate antidiuretic hormone (SIADH), which leads to hyponatremia. Diabetes insipidus causes excessive water secretion due to diminished ADH (vasopressin) secretion. This leads to dilute urine and causes hypernatremia, polydipsia, polyuria, and possibly hypotension due to decreased intravascular volume.

Epidemiology of Peripheral Nerve Injuries

The estimated incidence of peripheral nerve injuries in patients admitted to a Level I trauma center, including plexus and root injuries, is about 5%.¹³ The radial nerve is the most frequently injured nerve in the upper extremity due to mid-shaft humerus fractures, as the radial nerve travels around the spiral groove. Ulnar nerve injuries are associated with elbow fractures, with or without dislocations. The median nerve may also be injured at the level of the elbow or with supracondylar distal humerus fractures. Rarely, there may be peripheral nerve injuries due to forearm fractures—particularly in the rare case of compartment syndrome in the forearm.

In the lower extremity, the sciatic nerve is frequently injured. This is most often seen with acetabular fractures or femoral head dislocation because the sciatic nerve is directly posterior to the hip joint. When the sciatic nerve is injured, the common peroneal nerve is more prone to injury than the tibial nerve (these nerves are separate nerves, but are contiguous with each other as the sciatic nerve until they separate at the popliteal fossa). The common peroneal nerve lies more laterally, and there is less epineurium (connective tissue) protecting the common peroneal nerve than the tibial nerve. The peroneal nerve can be injured in the area of the fibula head, where it lies superficially. Compartment syndrome in the lower leg can also lead to tibial or peroneal nerve injuries, depending on the compartment affected.

Brachial plexus injuries occur largely as the result of MVCs or motorcycle crashes. They may be seen in patients with TBI, and there are signs upon examination in the unresponsive or minimally responsive patient. The absence of reflexes, flaccid tone, and poor movement compared to the other extremities suggests a brachial plexus injury. This is particularly true when there is no weakness of the ipsilateral lower extremity, and therefore a central etiology is less likely. Many times there will be an associated clavicle or scapular fracture on the same side as the brachial plexus injury, but fractures do not have to exist for brachial plexus injuries to be present. A careful neurological exam in the awake patient will usually differentiate a brachial plexus injury versus a central nervous system injury, such as a cervical SCI or effects of TBI.

Electrodiagnostic Testing and Classification of Peripheral Nerve Injury

A commonly used classification of peripheral nerve injury is the Seddon classification.¹⁴ Neurapraxia is the most mild because there is no axonal degeneration (Wallerian degeneration). There is focal demyelination or ischemia causing partial or complete conduction block at the site of injury. The nerve distal to the injured segment functions normally. Recovery is usually good and takes weeks to months, but may be only hours or days if mild and localized. Axonotmesis occurs when there is Wallerian degeneration. For recovery to occur, there must be regeneration of the nerve. Both the axon and the myelin are disrupted. The extent of recovery will depend on the extent of disruption, including the surrounding connective tissue (endoneurium and perineurium) as well as the distance between the site of injury and the muscles it supplies. Neurotmesis is diagnosed when the axon and all connective tissue, including the most external (the epineurium), are disrupted. There will be no spontaneous recovery and only surgery may be helpful.

Many times, electrodiagnostic studies (electromyography [EMG], plus nerve conduction studies) are used to confirm and prognosticate the recovery of a nerve injury. Wallerian (axonal) degeneration takes up to 9 days for motor fibers, and 11 days for sensory fibers, postinjury.¹⁵ This information is relevant in performing nerve conduction studies.

It may take up to 3 weeks to see axonal degeneration on needle EMG. When possible, waiting at least 3 weeks to perform EMG/nerve conduction studies will provide more valuable diagnostic information.

Rehabilitation of Nerve Injuries

The focus of early rehabilitation intervention is to improve function, control edema, decrease pain, and maintain range of motion. Elevation of the affected extremity, use of elastic sleeves or stockings, and providing massage are all helpful in decreasing and preventing swelling. Desensitization of the involved extremity, appropriate pain medications, and splints to maintain optimal positioning are all important.

Orthoses (splints) are also used to assist with function. In the upper extremities, the most common type of splint treats weakness or loss of finger and wrist extension due to radial nerve injuries. A static wrist cock-up splint retains some wrist extension, promoting more effective hand grip and finger flexion. A dynamic wrist and digit extension splint can also be used to encourage functional hand grip, while keeping the fingers and wrist extended. In the lower extremity, a resting foot drop splint is used when a patient has a sciatic nerve injury or a peroneal nerve injury causing weakness or absence of ankle dorsiflexion. For ambulation, a custom molded ankle foot orthosis (MAFO) is prescribed to allow toe clearance and ankle protection. If the patient is non weight bearing on the extremity due to an orthopedic injury, waiting to prescribe a custom MAFO is appropriate. An MAFO is not necessary while the patient is non weight bearing on the affected extremity, and the nerve may recover by the time weight bearing is allowed. It is important to maintain range of motion, so that if the nerve does recover the affected limb will have the best functional outcome.

Many medications have been used for neuropathic pain. They include tricyclic antidepressants, anticonvulsants, and topical agents. Anticonvulsant drugs, particularly Gabapentin, pregabalin, and carbamazepine, are commonly used. Topical agents such as transdermal lidocaine patches are also effective.

Acute Hospital Care

Following initial resuscitation and/or resuscitative surgery, most polytrauma patients can be expected to experience a significant ICU stay. Although care must first be directed to the diagnosis and treatment of life-threatening injuries, fixation of orthopedic injuries should occur without unnecessary delay. If attention must be paid to nonorthopedic injuries such as intracranial, thoracic, or intraabdominal injuries—or if a patient remains in a nonresuscitated state for several hours—simple splinting of extremity fractures, traction for long bone fractures, and/or the use of pelvic compression devices may be required as temporizing maneuvers. Time permitting, external fixation devices may be employed to better stabilize fractures in the more stable but still critical patient.

A careful and thorough head-to-toe tertiary survey to include a complete neurological exam should be performed by an experienced examiner as soon as practical to rule out potentially significant missed injuries and possible associated spinal cord injuries. All of these tasks are made more difficult in the intubated and unresponsive patient.

Once the polytrauma patient is resuscitated and all injuries have been properly addressed, early consultation with a physiatrist experienced in the care of trauma patients should occur. Although it may seem counterintuitive that significant rehabilitation can occur in an acute ICU setting, there are simple and effective rehabilitative modalities that can and should be initiated in the ICU. Passive range of motion exercises performed by experienced physical therapists may benefit patients by reducing complications such as joint contracture and muscle atrophy. Likewise, the use of pressure pads, functional bracing, and compressive dressings at amputation sites may promote healing and avoid long-term complications.

Proper wound care, especially at open fracture and amputation sites, and decubitus prevention will avoid unnecessary morbidity and shorten ICU stays. Because polytrauma patients are often significantly hypercatabolic, adequate nutritional support should be instituted early and markers of protein synthesis measured frequently to facilitate rapid wound healing. Although not traditionally considered as such, nutritional support is a vital part of acute rehabilitative care. Timely and proper application of these modalities may very well have a significant impact on rehabilitation potential and outcome.

Once the patient is transferred out of the ICU, rehabilitation should be continued with a goal of maximizing functional recovery. Early involvement of a physiatrist and a team of physical and occupational therapists is critical for the seamless transition of rehabilitation care from the ICU to the floor. A unified rehabilitation plan, designed by a well-trained physiatrist and carried out regularly and without interruption, is in the patient’s best interest. The specific rehabilitative regimen for a particular patient is extremely variable, based not only on the pattern of orthopedic injuries present and the method of their repair but the presence or absence of significant associated injuries (especially TBI).

Generally, in-hospital rehabilitation will follow a logical progression from immobilization (occasionally with casts or braces) to passive range of motion exercises. If the patient is cooperative, this is followed by conditioning exercises—especially if the patient experienced significant deconditioning or muscle atrophy. Finally, varying degrees of weight bearing will be allowed—often aided by the use of crutches or walkers. The provision of adequate analgesia is absolutely critical during this early rehabilitative phase. Narcotics or nonsteroidal drugs must be timed properly to have maximum effect during periods of increased activity, yet not be dosed in a fashion to produce lethargy or foster dependency. For patients with low pain tolerances or previous drug dependency, early involvement of a pain management consultant may facilitate and shorten rehabilitation. Lack of appropriate participation in rehabilitation by a patient may be a sign of depression, and if so should trigger involvement of a psychologist or psychiatrist. Patients with significant TBI are particularly challenging because they may not be able to adequately participate in any meaningful active rehabilitation regimens.

As noted previously, polytrauma patients account for approximately 10% of all inpatient rehabilitation admissions. Because many insurance carriers will not certify an inpatient rehabilitation admission unless a patient can engage in a set amount of meaningful rehabilitation therapy activities daily, many polytrauma patients may need to be transferred first to a skilled nursing facility once inpatient acute care is complete.