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 co counter coup injury where the coo injury occurs directly at the point of impact and the counter coup 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 of penetrating trauma. In contrast, secondary brain injuries are caused by the bodys 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 CP, 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 over stimulate 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, the 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 l 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 BP 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.

A severe TBI may also lead to hypertension as the body attempts to perfuse the brain when the CPP is compromised. Patients with damage to certain parts of their brain are typically unconscious and can exhibit abnormal posturing such as decorticate and decerebrate posturing.

Finally, if the hypothalamus which regulates body temperature is damaged, the patient may experience fever which is referred to as a neurogenic fever.

When caring for your critically ill patient with a traumatic brain injury. Your goals of care include maintaining a normal ICP and reducing the effects of secondary brain injury.

Begin by assessing your patients airway breathing and circulation or abcs for any emergent life threating findings activate emergency protocols as needed.

Next check for increased ICP by frequently monitoring for any changes in neurologic status. You can assess your patient's L using a tool like the Glasgow coma scale or G CS for short, which evaluates verbal motor and eye opening responses.

Any decrease in the G CS indicates a deteriorating neurologic status and increasing ICP also look for other neurologic deficits such as unequal pupil dilation, poor pupil accommodation and reactivity to light and unequal strength in extremities.

Now, if your patient has an ICP monitor in place, be sure to keep a close eye on the ICP. To ensure it remains within the prescribed range.

You'll also need to maintain their BP at the targeted range by administering the prescribed IV fluids and vasopressors. This will maintain a mean arterial pressure or a map that can provide adequate CPP, which can be calculated by subtracting the ICP from the map.

Also keep in mind that carbon dioxide is a potent vasodilator that increases ICP and that hypoxia can lead to cerebral ischemia.

So be sure to monitor for hypercapnia and hypoxia by assessing pulse oximetry, obtaining serial arterial blood gasses or ABGS and monitoring end tidal carbon dioxide or ET CO2 values as ordered for intubated patients, adjust ventilator settings based on the ABG and pulse oximetry values per protocol.

Also take precautions to avoid increasing their ICP by stimulating their airway during suctioning to do this temporarily hyper oxygenate your patient prior to suctioning, refrain from suctioning longer than 10 seconds for each suctioning pass and limit each suctioning episode to two passes with the suction catheter.

In addition, remember that fever can increase cerebral oxygen consumption. So take steps to maintain a normal thermic body temperature by administering prescribed antipyretics or cooling blankets as needed.

Be sure to administer the prescribed anti seizure medications. Keeping in mind that seizures can also increase ICP lastly to facilitate venous drainage from the brain elevate your patient's head to 30 degrees as prescribed and maintain their head in a neutral midline position.

If your patients, ICP is above normal, youll need to act quickly to reduce it. Administer IV osmotic diuretics like Mannitol or hypertonic saline as prescribed to decrease cerebral edema.

Also administer the prescribed analgesics and anxiolytics as needed. Since untreated pain and anxiety can increase ICP for patients with an ICP monitor in place.

Follow your facility's protocol to drain excess CSF finally, be sure to notify the health care provider. If your assessment findings indicate your patient's condition is worsening.

All right. As a quick recap, a traumatic brain injury is any damage to the brain caused by blunt or penetrating trauma.

Clinical manifestations include an altered level of consciousness, headache, dizziness, nausea, vomiting and fatigue. When caring for your critically ill patient with a TBI.

Your goals of care include maintaining a normal ICP and reducing the effects of secondary brain injury