Critical care - Traumatic brain injury: Nursing

A traumatic brain injury, or TBI, is any damage to the brain caused by an external force. This can be from blunt trauma, such as from falls, motor vehicle crashes, or exposure to a blast wave from an explosion; or from penetrating trauma, like from a gunshot or knife wound, or if bone fragments enter the brain tissue when the skull is fractured. As the nurse, you’ll provide patient-centered care for critically ill patients with traumatic brain injuries.

Now, TBIs involve primary and secondary injuries. Starting with primary injuries, these involve the initial, mechanical forces that cause direct damage to the brain tissue. Examples include concussions, contusions, hematomas, shearing injuries, and lacerations. A concussion occurs when there’s a bump or jolt to the head, causing the brain to shift within the skull. This leads to a temporary disruption to neural impulses that cause reversible and typically mild neurologic deficits.

On the other hand, a contusion is bruising composed of small, scattered areas of bleeding in the brain tissue. Contusions often occur with acceleration-deceleration injuries, like a coup-contrecoup injury, where the coup injury occurs directly at the point of impact, and the contrecoup injury occurs on the opposite side of the brain where it collides with the inside of the skull.

If the force of impact is strong enough, a hematoma can develop, which is a large collection of blood within the skull that can lead to significant pressure on the brain.

On top of that, as the brain moves around inside the skull, a shearing injury, also known as a diffuse axonal injury, can occur as nerve fibers throughout the brain are stretched and torn. Finally, lacerations of the brain tissue can be caused by any type penetrating trauma.

In contrast, secondary brain injuries are caused by the body’s response to the initial injury, which can cause further damage to the brain and complicate recovery. Inflammation causes cerebral edema, which leads to increased intracranial pressure, or ICP. Increased ICP compresses cerebral blood vessels, which then decreases cerebral perfusion pressure, or CPP, which is the force that moves blood into the brain. The autoregulation of cerebral blood flow is also impaired so it can’t compensate for the decreased CPP. This results in cerebral hypoxia, ischemia, and mitochondrial dysfunction, which then leads to reduced production of energy for the cells, and apoptosis, or cell death.

In addition, the physical trauma from the TBI also causes excessive release of excitatory neurotransmitters like glutamate, that can overstimulate neurons, leading to damage and apoptosis. It can also disrupt the cellular membranes of neurons, causing an unregulated influx of calcium ions and an excessive accumulation of intracellular calcium, which can also trigger apoptosis. Finally, physical trauma disrupts the tight junctions between the endothelial cells that form the protective blood-brain barrier, increasing its permeability. This allows harmful substances from the bloodstream to leak into the brain, causing additional damage.

Clinical manifestations of TBIs vary widely based on the areas of neurologic damage and the degree of the injury. General clinical manifestations include headache, dizziness, nausea, vomiting, and fatigue, as well as changes in level of consciousness, or LOC.

Compression of cerebral blood vessels from edema or an accumulation of blood within the skull stimulates the Cushing response, manifested as the Cushing triad, that includes respiratory depression, increased blood pressure, and bradycardia. Likewise, compression of the third cranial nerve, also called the oculomotor nerve, can result in pupillary changes like impaired reaction to light and vision changes.