Intracranial pressure monitoring in adult patients with traumatic brain injury: challenges and innovations.

Intracranial pressure monitoring enables the detection and treatment of intracranial hypertension, a potentially lethal insult after traumatic brain injury. Despite its widespread use, robust evidence supporting intracranial pressure monitoring and treatment remains sparse. International studies have shown large variations between centres regarding the indications for intracranial pressure monitoring and treatment of intracranial hypertension. Experts have reviewed these two aspects and, by consensus, provided practical approaches for monitoring and treatment. Advances have occurred in methods for non-invasive estimation of intracranial pressure although, for now, a reliable way to non-invasively and continuously measure intracranial pressure remains aspirational. Analysis of the intracranial pressure signal can provide information on brain compliance (ie, the ability of the cranium to tolerate volume changes) and on cerebral autoregulation (ie, the ability of cerebral blood vessels to react to changes in blood pressure). The information derived from the intracranial pressure signal might allow for more individualised patient management. Machine learning and artificial intelligence approaches are being increasingly applied to intracranial pressure monitoring, but many obstacles need to be overcome before their use in clinical practice could be attempted. Robust clinical trials are needed to support indications for intracranial pressure monitoring and treatment. Progress in non-invasive assessment of intracranial pressure and in signal analysis (for targeted treatment) will also be crucial.

Early systemic insults following traumatic brain injury: association with biomarker profiles, therapy for intracranial hypertension, and neurological outcomes-an analysis of CENTER-TBI data.

PURPOSE: We analysed the impact of early systemic insults (hypoxemia and hypotension, SIs) on brain injury biomarker profiles, acute care requirements during intensive care unit (ICU) stay, and 6-month outcomes in patients with traumatic brain injury (TBI). METHODS: From patients recruited to the Collaborative European neurotrauma effectiveness research in TBI (CENTER-TBI) study, we documented the prevalence and risk factors for SIs and analysed their effect on the levels of brain injury biomarkers [S100 calcium-binding protein B (S100B), neuron-specific enolase (NSE), neurofilament light (NfL), glial fibrillary acidic protein (GFAP), ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), and protein Tau], critical care needs, and 6-month outcomes [Glasgow Outcome Scale Extended (GOSE)]. RESULTS: Among 1695 TBI patients, 24.5% had SIs: 16.1% had hypoxemia, 15.2% had hypotension, and 6.8% had both. Biomarkers differed by SI category, with higher S100B, Tau, UCH-L1, NSE and NfL values in patients with hypotension or both SIs. The ratio of neural to glial injury (quantified as UCH-L1/GFAP and Tau/GFAP ratios) was higher in patients with hypotension than in those with no SIs or hypoxia alone. At 6 months, 380 patients died (22%), and 759 (45%) had GOSE ≤ 4. Patients who experienced at least one SI had higher mortality than those who did not (31.8% vs. 19%, p < 0.001). CONCLUSION: Though less frequent than previously described, SIs in TBI patients are associated with higher release of neuronal than glial injury biomarkers and with increased requirements for ICU therapies aimed at reducing intracranial hypertension. Hypotension or combined SIs are significantly associated with adverse 6-month outcomes. Current criteria for hypotension may lead to higher biomarker levels and more negative outcomes than those for hypoxemia suggesting a need to revisit pressure targets in the prehospital settings.