Spinal Cord Injury

Spinal Cord Injury

Spinal cord injury (SCI) is a major health problem. Nearly200,000 people in the United States live each day with a dis-ability from SCI, with an estimated 11,000 new injuries occur-ring each year. SCI occurs almost four times more often in males than females. Young people aged 16 to 30 suffer more than half of the new SCIs each year. African Americans are at a higher risk than Caucasians, with the incidence rising in recent years. The most common cause of SCI is motor vehicle crashes, which ac-count for 35% of the injuries. Violence-related injures account for nearly as many SCIs (30%), with falls causing 19% and sports-related injuries causing 8% (CDC, 2001). There is a high frequency of associated injuries and medical complications.

The predominant risk factors for SCI include age, gender, and alcohol and drug use. The frequency with which these risk fac-tors are associated with SCI serves to emphasize the importance of primary prevention. The same interventions suggested earlier for head injury prevention will serve to decrease the incidence of SCI as well (see Chart 63-1) (CDC, 2001; Elovic & Kirschblum, 1999).

The vertebrae most frequently involved in SCI are the 5th, 6th, and 7th cervical (neck), the 12th thoracic, and the 1st lum-bar vertebrae. These vertebrae are the most susceptible because there is a greater range of mobility in the vertebral column in these areas (Dibsie, 1998).

Pathophysiology

Damage to the spinal cord ranges from transient concussion (from which the patient fully recovers) to contusion, laceration, and compression of the cord substance (either alone or in com-bination), to complete transection of the cord (which renders the patient paralyzed below the level of the injury).

SCIs can be separated into two categories: primary injuries and secondary injuries (Porth, 2002). Primary injuries are the re-sult of the initial insult or trauma and are usually permanent. Sec-ondary injuries are usually the result of a contusion or tear injury, in which the nerve fibers begin to swell and disintegrate. A sec-ondary chain of events produces ischemia, hypoxia, edema, and hemorrhagic lesions, which in turn result in destruction of myelin and axons (Hickey, 2003). These secondary reactions, believed to be the principal causes of spinal cord degeneration at the level of injury, are now thought to be reversible 4 to 6 hours after injury. Therefore, if the cord has not suffered irreparable damage, some method of early treatment is needed to prevent partial damage from developing into total and permanent damage.

Clinical Manifestations

Manifestations depend on the type and level of injury (Chart 63-7). The type of injury refers to the extent of injury to the spinal cord itself. Incomplete spinal cord lesions are classified according to the area of spinal cord damage: central, lateral, anterior, or periph-eral. The American Spinal Injury Association (ASIA) provides another standard classification of SCI according to the degree of sensory and motor function present after injury (Chart 63-8). “Neurologic level” refers to the lowest level at which sensory and motor functions are normal. Below the neurologic level, there is total sensory and motor paralysis, loss of bladder and bowel con-trol (usually with urinary retention and bladder distention), loss of sweating and vasomotor tone, and marked reduction of blood pressure from loss of peripheral vascular resistance. A completespinal cord lesion can result in paraplegia (paralysis of the lowerbody) or quadriplegia (paralysis of all four extremities).

If conscious, the patient usually complains of acute pain in the back or neck, which may radiate along the involved nerve. Ab-sence of pain, however, does not rule out spinal injury, and a care-ful assessment of the spine should be done in the face of any significant mechanism of injury. Often the patient speaks of fear that the neck or back is broken.

Respiratory dysfunction is related to the level of injury. The muscles contributing to respiration are the abdominals and in-tercostals (T1 to T11) and the diaphragm. In high cervical cord injury, acute respiratory failure is the leading cause of death.

Assessment and Diagnostic Findings

A detailed neurologic examination is performed. Diagnostic x-rays (lateral cervical spine x-rays) and CT scanning are usually per-formed initially. An MRI scan may be ordered as a further work-up if a ligamentous injury is suspected, since significant spinal cord damage may exist even in the absence of bony injury. A search is made for other injuries, because spinal trauma often is accompanied by concomitant injuries, commonly to the head and chest. Continuous electrocardiographic monitoring may be indicated if a cord injury is suspected since bradycardia (slow heart rate) and asystole (cardiac standstill) are common in acute spinal injuries.

Emergency Management

The immediate management of the patient at the scene of the in-jury is critical, because improper handling can cause further dam-age and loss of neurologic function. Any patient involved in a motor vehicle or diving injury, a contact sports injury, a fall, or any direct trauma to the head and neck must be considered to have SCI until such an injury is ruled out. Initial care must in-clude a rapid assessment, immobilization, extrication, stabiliza-tion or control of life-threatening injuries, and transportation to the most appropriate medical facility.

At the scene of the injury, the patient must be immobilized on a spinal (back) board, with head and neck in a neutral position, to prevent an incomplete injury from becoming complete. One member of the team must assume control of the patient’s head to prevent flexion, rotation, or extension; this is done by placing the hands on both sides of the patient’s head at about the ear to limit movement and maintain alignment while a spinal board or cer-vical immobilizing device is applied. If possible, at least four peo-ple should slide the victim carefully onto a board for transfer to the hospital. Any twisting movement may irreversibly damage the spinal cord by causing a bony fragment of the vertebra to cut into, crush, or sever the cord completely.

The patient must be referred to a regional spinal injury or trauma center because of the multidisciplinary personnel and support services required to counteract the destructive changes that occur in the first few hours after injury. During treatment in the emergency and x-ray departments, the patient is kept on the transfer board. The patient must always be maintained in an ex-tended position. No part of the body should be twisted or turned, nor should the patient be allowed to sit up. Once the extent of the injury has been determined, the patient may be placed on a rotating bed (Fig. 63-7) or in a cervical collar (Fig. 63-8). Later, if SCI and bone instability have been ruled out, the patient can be moved to a conventional bed or the collar removed without harm. If a rotating bed is needed but not available, the patient should be placed in a cervical collar and on a firm mattress with a bedboard under it.

Management of Spinal Cord Injuries (Acute Phase)

The goals of management are to prevent further SCI and to ob-serve for symptoms of progressive neurologic deficits. The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are maintained. Many changes in the treatment of SCI have occurred during the past 20 years. Treatments such as hypo-thermia, corticosteroids, and naloxone were investigated and used during the 1980s; of these, high-dose corticosteroids have shown the most promise, but their use remains controversial (Short et al., 2000). Currently, regeneration therapy is being investigated; this involves transplanting fetal tissue into the injured spinal cord in hopes of regenerating the damaged tissue (Vacanti et al., 2001). SCI continues to be a devastating event, and new treatment methods are continually being investigated.

PHARMACOLOGIC THERAPY

In some studies, the administration of high-dose corticosteroids, specifically methylprednisolone, has been found to improve motor and sensory outcomes at 6 weeks, 6 months, and 1 year if given within 8 hours of injury (Hickey, 2003). In other studies, little improvement was found (Short et al., 2000). Use of high-dose methylprednisolone, a corticosteroid, is accepted as standard therapy in many countries and remains an established clinical practice in most institutions in the United States (Bracken, 2000; Hickey, 2003).

RESPIRATORY THERAPY

Oxygen is administered to maintain a high arterial PO₂ because hypoxemia can create or worsen a neurologic deficit of the spinal cord. If endotracheal intubation is necessary, extreme care is taken to avoid flexing or extending the patient’s neck, which can result in an extension of a cervical injury.

In high cervical spine injuries, spinal cord innervation to the phrenic nerve, which stimulates the diaphragm, is lost. Diaphragmatic pacing (electrical stimulation of the phrenic nerve) attempts to stimulate the diaphragm to help the patient breathe. Diaphragmatic pacing may be considered for the patient with a high cervical lesion but is usually carried out after the acute phase.

SKELETAL FRACTURE REDUCTION AND TRACTION

Management of SCI requires immobilization and reduction of dislocations (restoration of normal position) and stabilization of the vertebral column.

Cervical fractures are reduced and the cervical spine is aligned with some form of skeletal traction, such as skeletal tongs or calipers, or with use of the halo device. Early surgical stabilization has reduced the need for cervical traction in many patients with cervical spine injuries (Gaebler et al., 1999). A variety of skeletal tongs are available, all of which involve fixation in the skull in some manner (Fig. 63-9). The Gardner-Wells tongs require no predrilled holes in the skull. Crutchfield and Vinke tongs are in-serted through holes made in the skull with a special drill under local anesthesia.

Traction is applied to the tongs by weights, the amount de-pending on the size of the patient and the degree of fracture displacement. The traction force is exerted along the longitudinal axis of the vertebral bodies, with the patient’s neck in a neutral position. The traction is then gradually increased by adding more weights. As the amount of traction is increased, the spaces be-tween the intervertebral disks widen and the vertebrae may slip back into position. Reduction usually takes place after correct alignment has been restored. Once reduction is achieved, as ver-ified by cervical spine x-rays and neurologic examination, the weights are gradually removed until the amount of weight needed to maintain the alignment is identified. The weights should hang freely so as not to interfere with the traction. Traction is some-times supplemented with manual manipulation of the neck by a surgeon to help achieve realignment of the vertebral bodies.

A halo device may be used initially with traction or may be ap-plied after removal of the tongs. It consists of a stainless-steel halo ring that is fixed to the skull by four pins. The ring is attached to a removable halo vest, which suspends the weight of the unit cir-cumferentially around the chest. A metal frame connects the ring to the chest. Halo devices provide immobilization of the cervical spine while allowing early ambulation (Fig. 63-10).

Thoracic and lumbar injuries are usually treated with surgical intervention followed by immobilization with a fitted brace. Traction is not indicated either before or after surgery.

Surgical Management

Surgery is indicated in any of the following instances:

·      Compression of the cord is evident.

·      The injury results in a fragmented or unstable vertebral body.

·      The injury involves a wound that penetrates the cord.

·       There are bony fragments in the spinal canal.

·       The patient’s neurologic status is deteriorating.

Surgery is performed to reduce the spinal fracture or dislocation or to decompress the cord. A laminectomy (excision of the pos-terior arches and spinous processes of a vertebra) may be indi-cated in the presence of progressive neurologic deficit, suspected epidural hematoma, bony fragments, or penetrating injuries that require surgical débridement, or to permit direct visualization and exploration of the cord. Vertebral bodies may also be surgi-cally fused to create a stable spinal column.

Management of Complications of Spinal Cord Injury

SPINAL AND NEUROGENIC SHOCK

The spinal shock associated with SCI represents a sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury. The muscles innervated by the part of the spinal cord segment below the level of the lesion are without sensation,paralyzed, and flaccid, and the reflexes are absent. In particular,the reflexes that initiate bladder and bowel function are affected. Bowel distention and paralytic ileus can be caused by depression of the reflexes and are treated with intestinal decompression by insertion of a nasogastric tube (Hickey, 2003).Neurogenic shock develops due to the loss of autonomic nervous system function below the level of the lesion (Hickey, 2003). The vital organs are affected, causing the blood pressure and heart rate to fall. 

This loss of sympathetic innervation causes a variety of other clinical manifestations, including a decrease in cardiac output, venous pooling in the extremities, and peripheral vaso-dilation. In addition, the patient does not perspire on the para-lyzed portions of the body because sympathetic activity is blocked; therefore, close observation is required for early detection of an abrupt onset of fever.

With injuries to the cervical and upper thoracic spinal cord, innervation to the major accessory muscles of respiration is lost and respiratory problems develop. These include decreased vital capacity, retention of secretions, increased PaCO₂ levels and de-creased oxygen levels, respiratory failure, and pulmonary edema

DEEP VEIN THROMBOSIS

Deep vein thrombosis (DVT) is a potential complication of immobility and is common in patients with SCI. Patients who develop DVT are at risk for pulmonary embolism (PE), a life-threatening complication. One estimate from a meta-analysis of recent studies of the incidence of DVT and PE in SCI patients put the rate at 6.3% for PE and 17.4% for DVT (Velmahos et al., 2000). Manifestations of PE include pleuritic chest pain, anxiety, shortness of breath, and abnormal blood gas values (increased PaCO₂ and decreased PaO₂). Thigh and calf mea-surements are made daily. The patient is evaluated for the presence of DVT if there is a significant increase in the cir-cumference of one extremity. Low-dose anticoagulation ther-apy usually is initiated to prevent DVT and PE, along with thigh-high elastic compression stockings or pneumatic com-pression devices. In some cases, permanent indwelling filters may be placed in the vena cava to prevent dis-lodged clots (emboli) from migrating to the lungs and causing pulmonary emboli (Velmahos et al., 2000).

OTHER COMPLICATIONS

In addition to respiratory complications (respiratory failure, pneu-monia) and autonomic dysreflexia (characterized by pounding headache, profuse sweating, nasal congestion, piloerection [“goose bumps”], bradycardia, and hypertension), other complications that may occur include pressure ulcers and infection (urinary, respiratory, and local infection at the skeletal traction pin sites) (Sullivan, 1999).