This encompasses injury to the brain as a direct result from sudden damage. It excludes congenital and degenerative disease. Causes include:
- motor vehicle accident
- blunt trauma
- sporting accidents
Cerebral vascular accidents
Acquired TBI can be divided into two categories: primary and secondary
Primary brain trauma occurs due to the initial injury such as a fall or accident. Primary trauma includes concussion, contusions, lacerations, and haemorrhage.
Concussion: This is a transient mechanical head injury with disruption of neuronal activity and a change in the level of consciousnesses. It is considered a minor head injury.
Contusion: is the bruising of the brain tissue within a focal area. It develops an area of necrosis, infarction, necrosis and oedema. The injury coupe-contrecoupe is usually involved. Coupe- injury to the site of direct impact, contrecoupe- secondary injury caused on the opposite side of the direct impact caused by the to-fro movement of the brain inside the skull. This is a major head injury.
Lacerations: tearing of the brain tissue associated with fractures and penetrating injuries. Lacerations cannot be surgical repaired due to the texture of the brain. This is a major head injury.
Signs and symptoms can include:
- Decreased level of consciousness
- Nausea and vomiting
- Seizure (rare)
- Evaluate ABC
- Neurological assessments: GCS, AVPU, orientation to TPP
- Check for scalp lacerations
- Check ears and nose for leakage of CSF
- Educate on the warning signs of secondary brain injury
Primary injury can lead to severe disability or fatality but a large number of patients deteriorate due to secondary brain injury.
Secondary brain trauma is caused from processes and complications arising from primary trauma, it is an indirect result of the injury. Areas of the brain that were previously undamaged can be impacted by processes such as the inflammatory response, leading to oedema and complications of increased ICP. Furthermore, the disrupted metabolic processes of brain cells lead to free radicals causing more vascular damage and further increasing oedema and ICP.
Diffuse axonal injury: occurs after traumatic brain injury resulting in damage to the axons in the cerebral hemispheres, basal ganglia, thalamus and brain stem. Changes in the axons resulting from trauma, cause them to swell and disconnect. This takes between 12-14 hours to develop and can result in increased ICP
Here’s a playlist that discusses all aspects of traumatic brain injury and outlines primary and secondary TBI in great detail.
Cushing’s Triad is a set of three primary signs that often indicate an increase in intracranial pressure (ICP). These signs include the following:
1. A change in respirations, often irregular and deep, such as cheyne stokes
2. A widening pulse pressure (the difference between the Systolic and the Diastolic BP)
3. Bradycardia (slow heart rate).
Cushing’s Triad is an important, but late sign of raised intracranial pressure that doctors, paramedics and nurses must be on the look for with patients who have had a recent head injury, brain injury, neurosurgery, or anyone with a sudden altered level of consciousness.
Patients can only compensate for increased ICP for a limited time. Signs of decompensation, known as signs and symptoms of secondary brain injury can include:
- changes in the level of consciousness
- changes in vital signs: temperature, respiration rate, blood pressure
- ocular signs
- decreased motor functioning
The reticular activating system (RAS), located in the brain stem, is compressed due to the increased ICP. This decreases wakefulness by interrupting signalling to the RAS causing unconscious.
Frequent monitoring with the Glasgow coma scale and checking orientation to time, place, and person, will alert the nurse to deterioration. As well as the brain stem being compressed, the respiratory centre is also compressed with increased ICP. This causes respiratory alterations and Cheyne-strokes breathing may be present . Body temperature, blood pressure and Spo2 will also alter. Decreased motor functioning may cause the patients limbs to contort, decorticate or decerebrate positioning. The only motor response from the patient may result from using a painful stimulus Electroencephalogram, MRI, CT scans, and ICP monitoring can identify the presence of secondary brain injury.
Management of this patient requires a multidisciplinary approach.
Airway, breathing, circulation, and disability need frequent monitoring with a patient with increased ICP. Due to the altered level of consciousness, maintaining an airway may not be possible without intubation and mechanical ventilation. If intubation is not required, the head of the bed will be elevated to 30 degrees with the patient on their side to prevent aspiration and to maintain a patent airway. Secretions can accumulate in the airways which require careful suctioning as suctioning can decrease gas exchange, which increases ICP further. Drug therapy, such as diuretics and corticosteroids, can help to decrease the ICP by reducing oedema caused from inflammation and aid in returning adequate perfusion to brain tissues to minimise long term neuronal damage. Other pharmacological interventions can cause inaccurate neurological changes and therefore analgesia is given carefully. Non-opioids, such as propofol, help to decrease ICP and pain without negatively impacting cerebral blood flow.
Greve, M., & B, Zink. (2009). Pathophysiology of traumatic brain injury. Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine, 76(2), doi: 10.1002/msj.20104
Murthy, T., Bhatia, P., Sandhu, K., Prabhakar, T., & Gogna, R. (2005). Secondary brain injury: Prevention and intensive care management. Indian Journal of Neurotrauma, 2(1), 7-12. http://www.sciencedirect.com/
Nowak, T., & Handford, A. (2004). Pathophysiology: Concepts and applications for health professionals. New York, NY: McGraw-Hill.
Laskowski-Jones, L., & Baker, J. (2008). Nursing Management: Acute intercranial problems. In D. Browns & H. Edwards (Eds.), Lewis’s medical-surgical nursing: Assessment and management of clinical problems. (2nd ed., pp. 1570-1603). Sydney, Australia: Mosby Elsevier.