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Background: Paroxysmal sympathetic hyperactivity (PSH) occurs in a subset of patients with traumatic brain injury (TBI) and is associated with worse outcomes. Sepsis is also associated with worse outcomes after TBI and shares several physiologic features with PSH, potentially creating diagnostic confusion and suboptimal management of each. This is the first study to directly investigate the interaction between PSH and infection using robust diagnostic criteria. Methods: We performed a retrospective cohort study of patients with TBI admitted to a level I trauma center intensive care unit with hospital length of stay of at least 2 weeks. From January 2016 to July 2018, 77 patients diagnosed with PSH were 1:1 matched by age and Glasgow Coma Scale to 77 patients without PSH. Trauma infectious diseases subspecialists prospectively documented assessments corroborating diagnoses of infection. Extracted data including incidence, timing, classification, and anatomical source of infections were compared according to PSH diagnosis. We also evaluated daily PSH clinical feature severity scores and systemic inflammatory response syndrome (SIRS) criteria and compared values for patients with and without confirmed infection, stratified by PSH diagnosis. Results: During the first 2 weeks of hospitalization, there were no differences in rates of suspected (62%) nor confirmed (48%) infection between patients with PSH and controls. Specific treatments for PSH were initiated on median hospital day 7 and for confirmed infections on median hospital day 8. SIRS criteria could identify infection only in patients who were not diagnosed with PSH. Conclusions: In the presence of brain injury-induced autonomic nervous system dysregulation, the initiation and continuation of antimicrobial therapy is a challenging clinical decision, as standard physiologic markers of sepsis do not distinguish infected from noninfected patients with PSH, and these entities often present around the same time. Clinicians should be aware that PSH is a potential driver of SIRS, and familiarity with its diagnostic criteria as proposed by the PSH assessment measure is important. Management by a multidisciplinary team attentive to these issues may reduce rates of inappropriate antibiotic usage and misdiagnoses. [ABSTRACT FROM AUTHOR]

Traumatic brain injury is a leading cause of death and disability worldwide. Interventions that mitigate secondary brain injury have the potential to improve outcomes for patients and reduce the impact on communities and society. Increased circulating catecholamines are associated with worse outcomes and there are supportive animal data and indications in human studies of benefit from beta-blockade after severe traumatic brain injury. Here, we present the protocol for a dose-finding study using esmolol in adults commenced within 24 h of severe traumatic brain injury. Esmolol has practical advantages and theoretical benefits as a neuroprotective agent in this setting, but these must be balanced against the known risk of secondary injury from hypotension. The aim of this study is to determine a dose schedule for esmolol, using the continual reassessment method, that combines a clinically significant reduction in heart rate as a surrogate for catecholamine drive with maintenance of cerebral perfusion pressure. The maximum tolerated dosing schedule for esmolol can then be tested for patient benefit in subsequent randomized controlled trials. Trial registration ISRCTN, ISRCTN11038397, registered retrospectively 07/01/2021 https://www.isrctn.com/ISRCTN11038397 [ABSTRACT FROM AUTHOR]

Background: Electrographic seizures are frequent and associated with worse outcomes following traumatic brain injury (TBI). Despite this, the use of continuous electroencephalogram (cEEG) remains low. Our study describes cEEG usage and treatment dosing antiseizure medications (ASMs) in an international pediatric TBI population, hypothesizing that children monitored with cEEG have an increased rate of treatment ASMs because of electrographic seizure detection, compared with children who are not monitored with cEEG. Methods: This subanalysis of the TBI cohort of the international PANGEA study included children, 7 days to 17 years of age, with acute neurological insults admitted to pediatric intensive care units. We analyzed demographics, injury severity, and therapies including prophylactic or treatment ASMs. We evaluated the relationships between cEEG use, seizure frequency, and receipt of treatment ASMs. χ 2 or Fisher's exact test was used to analyze categorical variables, and the Kruskal–Wallis or Mann–Whitney U-test was used for continuous variables. Multivariable analysis for treatment ASM use was performed using logistic regression. Results: One hundred-twenty-three of 174 patients with TBI were included. Twenty-seven patients (21.9%) underwent cEEG at any point during pediatric intensive care unit admission. Preexisting seizure disorder (18.2% vs. 2.3%, p = 0.014) and neuromuscular blockade use (52.4% vs. 24.1%, p = 0.011) were more frequently observed in the group monitored on cEEG when compared with those that were not. Presenting median Glasgow Coma Scale score was worse in the cEEG group (7 vs. 9, p = 0.044). There was no significant difference in age, use of intracranial pressure monitoring, or hyperosmolar therapy between the cEEG monitored and nonmonitored groups. Patients who were monitored on cEEG were more likely to receive a treatment dose ASM than those without cEEG monitoring (66.7% vs. 28.1%, p = 0.0002). When compared with those without treatment ASM, the treatment ASM group had more electrographic seizures on their first electroencephalogram following injury (51.6% vs. 4%, p = 0.0001) and more clinical seizures (55.8% vs. 0%, p < 0.0001). Conclusions: Children monitored with cEEG after TBI have an increased prescription of treatment ASMs and clinical and electrographic seizures. The increased rate of treatment ASMs in the cEEG group may indicate increased recognition of electrographic seizures. [ABSTRACT FROM AUTHOR]

Background: Cerebral venous injury (CVI) includes injury to a dural venous sinus or major vein and leads to poorer outcomes for patients with blunt traumatic brain injury (TBI). We sought to identify the incidence, associated factors, and outcomes associated with CVI in a large national cohort. Methods: Adult patients with blunt TBI were identified from the National Trauma Databank (2013–2017). Outcomes included inpatient mortality, discharge disposition, stroke, length of stay (LOS), intensive care unit LOS, and duration of mechanical ventilation. Multivariate regression models were used to identify the association between exposure variables and CVI, as well as each outcome. Results: There were 619,659 patients with blunt TBI who met the inclusion criteria. CVI occurred in 1792 (0.3%) patients. Mixed intracranial injury type had the strongest association with CVI (odds ratio [OR] 2.89, 95% confidence interval [CI] 2.38–3.50), followed by isolated TBI (OR 1.76, 95% CI 1.54–2.02) and skull fracture (OR 1.72, 95% CI 1.55–1.91). CVI was associated with increased odds of mortality (OR 1.38, 95% CI 1.19–1.60), nonroutine discharge (OR 1.26, 95% CI 1.12–1.40), and stroke (OR 1.95, 95% CI 1.33–2.86). It was also associated with longer LOS (β 2.02, 95% CI 1.55–2.50) and intensive care unit LOS (β 0.14, 95% CI 0.13–0.16). Among locations of venous injury, superior sagittal sinus injury had significant associations with mortality (OR 2.93, 95% CI 1.62–5.30) and nonroutine discharge disposition (OR 1.94, 95% CI 1.12–3.35), whereas the others did not. Conclusions: We identified a 0.3% incidence of CVI in all-comers with blunt TBI as well as several injury-related variables that may be used to guide investigation for dural venous sinus injury. CVI was associated with poorer outcomes, with superior sagittal sinus injury having the strongest association. [ABSTRACT FROM AUTHOR]