Newsletters

POSTED: June 19th, 2026
POSTED IN: 2026 EM Pulse Q2, EM Pulse - The Official Newsletter of MOCEP, forum, Forum Topic,

Written by: Jennifer Cooper-Lewis, DO, FACEP

Traumatic Brain Injury (TBI) is sustained by an estimated 1.7 million people in the United States annually. The highest rates of TBI are seen in a trimodal distribution, children less than 5 years, adolescents 15 to 19 years and adults over 75 years. The most common cause of TBIs in all age groups is due to falls. The symptoms of TBI are broad and range from mild to moderate to severe TBI. Severity is determined most commonly using the Glasgow Coma Scale (GCS), duration of loss of consciousness and post injury amnesia. Forty-three percent of patients hospitalized for TBI report a residual disability one year after their initial injury. There are over 55,000 deaths annually attributed to a TBI in the United States.

There are two distinct phases of TBI, primary and secondary injury. Primary injury is during the initial injury and is due to direct mechanical damage. It includes skull fractures, intracranial bleeding, and diffuse axonal injury. Secondary injury begins after the initial injury and can last weeks to months. Secondary injury involves molecular and cellular events that can lead to long-term morbidity. Excessive glutamate release after primary injury leads to intracellular calcium overload, resulting in mitochondrial dysfunction, oxidative stress, and apoptosis. There is also a release of proinflammatory mediators resulting in cerebral edema and elevated intracranial hypertension.

Non-contrast head Computed Tomography (CT) is the standard imaging modality for diagnosing lesions that require urgent surgical intervention. Imaging also reveals signs of midline shift, asymmetry from one hemisphere exerting mass effect on the other hemisphere. A shift of over 5 mm can result in subfalcine herniation and death, which is treated by surgical intervention as well. Any change in the patient’s mental status, change in pupil size, or seizure-like activity warrants an immediate repeat CT. Currently, there are no biomarkers available to test for TBI, although a large amount of research is underway. Neuron-specific enolase (NSE), ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), S100 calcium-binding protein B (S100B), and tau protein are being extensively studied for future use.

Management of TBI focuses on initial stabilization of the patient and prevention of the secondary injury.  Hypoxia and hypotension should be avoided in patients with a TBI to mitigate the increased morbidity and mortality associated with PaO2 less than 60 mm HG and systolic blood pressure less than 90 mm HG. Hyperventilation is not recommended as prolonged hypocapnia can cause intracranial infarction. If elevated intracranial pressure (ICP) is suspected, hypertonic saline or mannitol is recommended. Normothermia and normoglycemia are important to maintain to avoid increasing cerebral metabolic demand. Any coagulopathies present must be addressed as coagulopathy is associated with a 9-fold increased risk of mortality. Prophylaxis for posttraumatic seizures is recommended for patients with a moderate or severe TBI and an abnormal CT, recommended for the first week after injury. Patients with severe TBI are at an increased risk of intracranial hypertension. If the ICP rises to greater than 22 mm HG, immediate treatment is advised. Moderate and severe TBI patients warrant early surgical consultation and admission for monitoring.

Patients with moderate TBI will make a complete recovery in 60% of cases, however 25% of patients will have a residual disability. Patients with a severe TBI will only have a favorable recovery 25% to 33% of cases. Early recognition and treatment of TBI complications are important to help decrease morbidity and mortality.

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