Critical Care - Spinal Cord Injury

A spinal cord injury, or SCI for short, refers to damage to the spinal cord, which is a collection of nerve fibers that transmit information between the brain and the body.

Spinal cord injuries can result from a mechanical force that damages the neurological tissue, its blood supply, or both, which can result from traumatic events, such as motor vehicle crashes; falls; or injuries from recreational activities and sports. As the nurse, you’ll provide patient-centered care for critically ill patients with spinal cord injuries.

Spinal cord injuries involve both primary and secondary mechanisms. The primary injury is the damage that occurs from a sudden trauma to the spine. It’s characterized by contusion, or bruising; compression, or crushing under pressure; laceration, or tearing; transection, or severing of the spinal cord; and distraction, where a stretching force causes two adjacent vertebrae to be pulled apart.

Primary injuries involve several mechanisms, including hyperflexion, hyperextension, rotation, axial loading, and penetrating trauma. Hyperflexion injuries occur from a forward and downward head motion. In contrast, hyperextension injuries involve backward and downward head motion. Both of these injuries are common in the cervical area of the spine, which has the most mobility.

Rotation injuries are a twisting motion of the spine. Axial loading, or compression injuries, occur when a force is applied vertically to the spinal cord, causing compression fractures and burst fractures of the vertebrae which send bony fragments into the spinal cord. Lastly, penetrating trauma, like a wound that comes from a stabbing, gunshot, or shrapnel from an explosion, can also cause spinal cord injuries.

Now, after the primary injury occurs, the secondary injury begins and involves a series of events that result in further neurologic damage over weeks and months. The acute phase begins with depolarization of the neurons damaged by the trauma and an imbalance of ions like potassium and sodium, leading to a disruption in transmission of nerve signals and cellular edema. This is followed by an accumulation of glutamate, an excitatory neurotransmitter, that in turn contributes to an influx of intracellular calcium which leads to apoptosis, or cell death. This is also accompanied by free radical formation, continued release of inflammatory cytokines, and increasing edema.

After this comes the subacute phase, which involves scar formation by glial cells, and remodeling at the site of injury. Finally, the chronic phase begins as the glial scar matures.

Clinical manifestations of spinal cord injuries vary depending on the location of the injury and whether the injury is incomplete or complete. Incomplete injuries result in a mix of sensory and motor loss below the level of the injury; whereas complete injuries result in total loss of both sensory and motor function below the level of the injury.

For example, an injury between C1 and T1 leads to tetraplegia, also called quadriplegia, which may involve loss of function of the limbs and trunk, as well as loss of innervation to the diaphragm, requiring mechanical ventilation. On the other hand, an injury between T2 and L1 leads to paraplegia, where upper limb function remains intact, but there’s paralysis of both lower limbs. There can also be a loss of accessory respiratory muscle function, as well as bowel and bladder dysfunction.

Now, immediately after the injury, patients with spinal cord injuries can experience spinal shock, which involves flaccid paralysis, and a complete loss of sensory, motor, bowel, bladder, and reflexive activity below the injury.

With injuries at or above the level of T6, neurogenic shock can also develop resulting in interrupted sympathetic outflow and unopposed parasympathetic activity. This leads to bradycardia, massive peripheral vasodilation, hypotension, venous pooling, decreased venous return, and decreased cardiac output, leading to impaired organ perfusion and an increased risk of venous thromboembolism.

Patients with injuries at or above the level of T6 can also experience autonomic dysreflexia. This is a neurologic emergency that occurs when a noxious sensory stimulation, such as a distended bowel or bladder, tight clothing, or pain from a pressure injury, stimulates sympathetic neurons.