Traumatic brain injury (TBI) is a leading cause of mortality and long-term disability worldwide. In the U.S., more than 200,000 people were hospitalized due to TBI in 2020, and nearly 70,000 inpatient deaths were attributable to TBI in 2021.
Because of the delicate and complex nature of the brain, TBI can lead to a cascade of complications. Trauma and emergency nurses must be able to identify these complications quickly in order to ensure the best patient outcomes.
1. Brain herniation syndromes
Head trauma can cause bleeding within the cranial vault, swelling of neural tissues or abnormal flow of cerebrospinal fluid (CSF), all of which increase the volume within the skull. Since the skull is rigid, any increase in volume will increase intracranial pressure (ICP).
Increased ICP will create a pressure gradient, meaning parts of the brain are under higher pressure than others. Eventually, this pressure gradient will cause brain tissue to shift from regions of high pressure to regions lower pressure. Any displacement of brain tissue into a different area of the skull is known as brain herniation.
- Early signs: Brain herniation syndromes often begin with changes in alertness. Patients can exhibit increased agitation and anxiety or somnolence and difficulty awakening.
- Rising ICP: As ICP rises, patients might also experience nausea, vomiting, visual disturbances, light sensitivity, headaches and impaired pupillary reactions to light.
- Late signs: Critical late indicators of brain herniation include irregular breathing patterns, bradycardia and systolic hypertension accompanied by widened pulse pressure. (This combination of symptoms is known as Cushing’s triad.)
In addition, brain herniation encompasses several specific conditions that can manifest unique symptoms:
- Subfalcine herniation typically results in unilateral weakness, often in the lower limb contralateral to the injury.
- Symptoms of transtentorial herniation include pathological yawning, a Cheyne-Stokes breathing pattern, sixth cranial nerve palsy leading to gaze abnormalities, and unilateral pupillary changes such as sluggish response to light and non-reactivity.
- Cerebellar or tonsillar herniation usually leads to profound hypotension and respiratory arrest.
2. Paroxysmal sympathetic hyperactivity
Paroxysmal sympathetic hyperactivity (PSH) caused by TBI is essentially overactivity of the sympathetic nervous system. This sympathetic overactivity leads to transient yet significant clinical manifestations, including episodes of:
- Hyperthermia
- Hypertension
- Tachycardia
- Diaphoresis
- Dystonic posturing (abnormal muscle tone and posture)
Heightened sympathetic nervous system activity not only contributes to physical discomfort of the patient and agitation but also stimulates a marked increase in metabolic rates. Increased metabolic demand can lead to complications like cardiovascular strain and potential organ dysfunction.
3. Diabetes insipidus (arginine vasopressin deficiency)
Arginine vasopressin deficiency (AVP-D) occurs when trauma to the brain impacts the normal functioning of the posterior pituitary gland.
This gland is crucial for synthesizing and secreting vasopressin. Without adequate vasopressin levels, the kidneys cannot properly reabsorb water. This can lead to excessive urination, which can result in severe dehydration and can lead to a dangerous electrolyte imbalance. Such imbalances may affect cardiovascular stability and neurological health.
- In mild cases, when the patient is awake and their thirst sensation is retained, they will report increased thirst and experience excessive urination.
- However, AVP-D after TBI is usually identified in critically ill patients who may be intubated and unable to communicate. Nurses should be vigilant for increased urine output and hypernatremia as complications often associated with this condition.
Certain therapies, such as sedatives and pain relief medications, may mask some signs and symptoms of AVP-D, making it harder to detect. These signs may include:
- Altered mental status, including confusion, seizures, lethargy, and coma
- Decreased skin turgor (elasticity) and tenting
- Dry mucus membranes
- Increased respiratory and heart rate
- Hyperreflexia
4. Post-traumatic hydrocephalus
Hydrocephalus is a condition characterized by an abnormal and excessive accumulation of CSF within the ventricles of the brain.
This condition can occur after a TBI that has caused damage to the structures that regulate the flow and reabsorption of CSF. It can also result from obstructions to CSF flow caused by debris (such as blood or inflammatory cells) or structural damage within the brain.
Symptoms of post-traumatic hydrocephalus resemble other signs of increased ICP:
- Low-pressure indicators may involve confusion, lethargy, urinary incontinence and difficulty walking.
- High-pressure symptoms can manifest as a reduced level of consciousness and pupillary changes.
These symptoms resemble those of almost all severe TBIs, which can hinder the timely identification of hydrocephalus as a distinct condition.
Learn more about caring for patients with brain injury: This article is based on Critical Care Management of Traumatic Brain Injuries, an interactive online course from the Board of Certification for Emergency Nursing (BCEN®). Developed by nursing experts, this CE-eligible course examines the management of severe TBI in the acute care phase and beyond. To access this course and other learning opportunities for trauma nurses, visit BCEN Learn.
Critical Care Management of Traumatic Brain Injuries supports the continuing education requirements of the Trauma Certified Registered Nurse (TCRN®) program. The TCRN credential is the only national board certification for trauma nursing, and it spans the body of knowledge for care of the injured patient. More than 8,000 nurses worldwide have earned the TCRN credential. For more information, click here.