BACKGROUND: Studies suggest disparities in outcomes in minoritized children after severe traumatic brain injury. We aimed to evaluate for disparities in intracranial pressure-directed therapies and outcomes after pediatric severe traumatic brain injury.
METHODS: We conducted a secondary analysis of the Approaches and Decisions for Acute Pediatric TBI (ADAPT) Trial, which enrolled pediatric severe traumatic brain injury patients (Glasgow Coma Scale score  ≤8) with an intracranial pressure monitor from 2014 to 2018. Patients admitted outside of the United States were excluded. Patients were categorized by race and ethnicity (Hispanic, non-Hispanic Black, non-Hispanic White, and \"Other\"). We evaluated outcomes by assessing mortality and 3-month Glasgow Outcome Score-Extended for Pediatrics. Our analysis involved parametric and nonparametric testing.
RESULTS: A total of 671 children were analyzed. Significant associations included older age in non-Hispanic White patients (P < .001), more surgical evacuations in \"Other\" (P < .001), and differences in discharge location (P = .040). The \"other\" cohort received hyperventilation less frequently (P = .046), although clinical status during Paco2 measurement was not known. There were no other significant differences in intracranial pressure-directed therapies. Hispanic ethnicity was associated with lower mortality (P = .004) but did not differ in unfavorable outcome (P = .810). Glasgow Outcome Score-Extended for Pediatrics was less likely to be collected for non-Hispanic Black patients (69%; P = .011).
CONCLUSIONS: Our analysis suggests a general lack of disparities in intracranial pressure-directed therapies and outcomes in children after severe traumatic brain injury. Lower mortality in Hispanic patients without a concurrent decrease in unfavorable outcomes, and lower availability of Glasgow Outcome Score-Extended for Pediatrics score for non-Hispanic Black patients merit further investigation.

BACKGROUND: Facial bone fractures triggered by low-height falls are rare in toddlers, while severe intracranial injuries resulting from minor trauma are extremely rare.
METHODS: Herein, we report the case of a 2-year-old girl who fell from a baby chair, striking her chin, who rapidly developed impaired consciousness 3 h later. The patient subsequently presented with a mandibular fracture and acute obstructive hydrocephalus due to a traumatic isolated subarachnoid hemorrhage in the posterior cranial fossa. She was successfully treated with ventricular drainage, which achieved a favorable outcome.
CONCLUSIONS: Maxillofacial trauma and head injuries are closely associated. Even in minor cases of maxillofacial trauma, vigilant monitoring and prompt intervention are crucial to prevent fatal outcomes in toddlers.

The prevalence of bacterial infections significantly increases among patients with severe traumatic brain injury (STBI), leading to a notable rise in mortality rates. While immune dysfunctions are linked to the incidence of pneumonia, our observations indicate that endogenous pathogens manifest in the lungs post-STBI due to the migration of gut commensal bacteria. This translocation involves gut-innervating nociceptor sensory neurons, which are crucial for host defense. Following STBI, the expression of transient receptor potential vanilloid 1 (TRPV1) in dorsal root ganglion (DRG) neurons significantly decreases, despite an initial brief increase. The timing of TRPV1 defects coincides with the occurrence of pulmonary infections post-STBI. This alteration in TRPV1+ neurons diminishes their ability to signal bacterial injuries, weakens defense mechanisms against intestinal bacteria, and increases susceptibility to pulmonary infections via bacterial translocation. Experimental evidence demonstrates that pulmonary infections can be successfully replicated through the chemical ablation and gene interference of TRPV1+ nociceptors, and that these infections can be mitigated by TRPV1 activation, thereby confirming the crucial role of nociceptor neurons in controlling intestinal bacterial migration. Furthermore, TRPV1+ nociceptors regulate the immune response of microfold cells by releasing calcitonin gene-related peptide (CGRP), thereby influencing the translocation of gut bacteria to the lungs. Our study elucidates how changes in nociceptive neurons post-STBI impact intestinal pathogen defense. This new understanding of endogenous risk factors within STBI pathology offers novel insights for preventing and treating pulmonary infections.

Severe Traumatic Brain Injury (TBI) is a significant health issue, with neurofeedback and Hyperbaric Oxygen Therapy (HBOT) as potentially effective treatments. Neurofeedback uses operant conditioning for real-time psychological and physiological awareness, and HBOT increases blood oxygen levels, potentially enhancing cognitive abilities and the body\'s innate healing processes and reducing symptoms. On July 30, 2018, a 33-year-old female runner was hit by a car going 40 mph and thrown 30 feet, resulting in a severe TBI and a seven-week coma. After seven months of intensive rehabilitation, she started HBOT and neurofeedback treatments in November 2021, as recommended by her neuropsychiatrist. These treatments led to noticeable improvements in her cognition, sleep, conversation skills, emotional control, and relationships by January 2022. By December 2023, after 195 neurofeedback and over 300 HBOT sessions, she reported further improvements in various cognitive and emotional aspects and daily activities like feeding, toileting, grooming, and communication. Post-treatment quantitative electroencephalogram (qEEG) results in June 2024 showed moderate to large effects on her brain\'s average frequency band parameters (g = .612) and small to moderate average effects on 19 scalp electrode placement sites outcomes (uV2 g=.339 and Hz g=.333). This indicates significant progress in her recovery journey over a 31-month treatment period. This patient\'s case demonstrated noteworthy improvements in cognitive variables, namely, feeding (p=0.046), toileting (p=0.046), grooming (p=0.046), and communication abilities (p=0.046) per the objective measures, Disability Rating Scale (DRS) and the Glasgow Outcome Scale Extended (GOSE). Based on the qEEG effect sizes, DRS, and GOSE results from the pretest (2021) and posttest (2024), the patient has made noteworthy gains in brain recovery and overall quality of life.

UNASSIGNED: ClinicalTrials.gov identifier: NCT01437683..

BACKGROUND: Healthcare inequities for patients with traumatic brain injury (TBI) represent a major priority area for trauma quality improvement. We hypothesized a relationship between health insurance status and timing of withdrawal of life sustaining treatment (WLST) for adults with severe TBI.
METHODS: This multicenter retrospective observational cohort study utilized data collected between 2017 and 2020. We identified adult (age ≥ 16) patients with isolated severe TBI admitted participating Trauma Quality Improvement Program centers. We determined the relationship between insurance status (public, private, and uninsured) and the timing of WLST using a competing risk survival analysis framework adjusting for baseline, clinical, injury and trauma center characteristics. Multivariable cause-specific Cox regressions were used to compute adjusted hazard ratios (HR) reflecting timing of WLST, accounting for mortality events. We also quantified the between-center residual variability in WLST using the median odds ratio (MOR) and measured insurance status association with access to rehabilitation at discharge.
RESULTS: We identified 42,111 adults with isolated severe TBI treated across 509 trauma centers across North America. There were 10,771 (25.6%) WLST events in the cohort and a higher unadjusted incidence of WLST events was evident in public insurance patients compared to private or uninsured groups. After adjustment, WLST occurred earlier for publicly insured (HR 1.07, 95% CI 1.02-1.12) and uninsured patients (HR 1.29, 95% CI 1.18-1.41) compared to privately insured patients. Access to rehabilitation was lower for both publicly insured and uninsured patients compared to patients with private insurance. Accounting for case-mix, the MOR was 1.49 (95% CI 1.43-1.55), reflecting significant residual between-center variation in WLST decision-making.
CONCLUSIONS: Our findings highlight the presence of disparate WLST practices independently associated with health insurance status. Additionally, these results emphasize between-center variability in WLST, persisting despite adjustments for measurable patient and trauma center characteristics.

UNASSIGNED: Intracranial pressure (ICP)--guided therapy is the standard of care in the management of severe traumatic brain injury (TBI). Ideal ICP monitoring technique is not yet available, based on its risks associated with bleeding, infection, or its unavailability at major centers. Authors propose that ICP can be gauged based on measuring pressures of other anatomical cavities, for example, the abdominal cavity. Researchers explored the possibility of monitoring intra-abdominal pressure (IAP) to predict ICP in severe TBI patients.
UNASSIGNED: We measured ICP and IAP in severe TBI patients. ICP was measured using standard right frontal external ventricular drain (EVD) insertion and connecting it to the transducer. IAP was measured using a well-established technique of vesical pressure measurement through a manometer.
UNASSIGNED: A total of 28 patients (n = 28) with an age range of 18-65 years (mean of 32.36 years ± 13.52 years [Standard deviation]) and the median age of 28.00 years with an interquartile range (21.00-42.00 years) were recruited in this prospective study. About 57.1% (n = 16) of these patients were in the age range of 18-30 years. About 92.9% (n = 26) of the patients were male. The most common mode of injury (78.6%) was road traffic accidents (n = 22) and the mean Glasgow Coma Scale at presentation was 4.04 (range 3-9). The mean ICP measured at the presentation of this patient cohort was 20.04 mmHg. This mean ICP (mmHg) decreased from a maximum of 20.04 at the 0 h\' time point (at the time of insertion of EVD) to a minimum of 12.09 at the 96 hr time point. This change in mean ICP (from 0 h to 96 h) was found to be statistically significant (Friedman Test: χ2 = 87.6, P ≤ 0.001). The mean IAP (cmH2O) decreased from a maximum of 16.71 at the 0 h\' time point to a minimum of 9.68 at the 96 h\' time point. This change was statistically significant (Friedman Test: χ2 = 71.8, P ≤ 0.001). The per unit percentage change in IAP on per unit percentage change in ICP we observed was correlated to each other. The correlation coefficient between these variables varied from 0.71 to 0.89 at different time frames. It followed a trend in a directly proportional manner and was found to be statistically significant (P < 0.001) in each time frame of the study. The rise in one parameter followed the rise in another parameter and vice versa.
UNASSIGNED: In this study, we established that the ICP of severe TBI patients correlates well with IAP at presentation. This correlation was strong and constant, irrespective of the timeframe during the treatment and monitoring. This study also established that draining cerebrospinal fluid to decrease ICP in severe TBI patients is reflected in IAP. The study validates that IAP is a strong proxy of ICP in severe TBI patients.

UNASSIGNED: Intracranial pressure (ICP) monitoring is essential in severe traumatic brain injury (sTBI) cases; yet, the frequency of high ICP occurrences remains debated. This study presents a 9-year analysis of ICP monitoring using intraventricular catheters among sTBI patients.
UNASSIGNED: A retrospective review of 1760 sTBI patients (Glasgow Coma Score <9) admitted between January 2011 and December 2019 was conducted. Of these, 280 patients meeting monitoring criteria were included based on Brain Trauma Foundation (BTF) Guidelines. ICP was monitored using intraventricular catheters through right frontal burr holes. Initial ICP readings were recorded intraoperatively, followed by continuous monitoring. Patients with ICP >20 mmHg for 10-15 min during 72 h were categorized with high ICP. Data collected included demographics, computed tomography (CT) findings, intra- and post-operative ICP, and complications.
UNASSIGNED: Of 273 patients, 228 were male and 45 females, aged 18-80 (71.30% aged 18-45). Traffic accidents were the primary cause (90.48%). Fifty-two-point seventy-five percent experienced high ICP, correlating significantly with subdural hematoma (P < 0.001), intraventricular hemorrhage (P < 0.013), and compressed basal cisterns (P = 0.046) on initial CT. Twenty patients (7.3%) developed meningitis. Lower mortality rates and improved outcomes were observed in the low ICP group across discharge 3-and 6-month follow-ups.
UNASSIGNED: Adherence to BTF guidelines yielded a 52.75% high ICP rate. Significant correlations were found between high ICP and specific CT abnormalities. This study underscores the benefits of ICP monitoring in selected sTBI cases, suggesting a need to review criteria for initiating monitoring protocols.

UNASSIGNED: Glial fibrillary acidic protein serves as a biomarker indicative of astroglial injury, particularly following instances of severe traumatic brain injury. This study aims to evaluate variations in serum glial fibrillary acidic protein levels within the first 3 days and their correlation with outcomes in patients with severe traumatic brain injury.
UNASSIGNED: Thirty-nine patients with severe traumatic brain injury were enrolled in the study. Their blood samples were collected at six distinct time points: T0 (upon admission), T1, T2, T3, T4, and T5 (6-, 12-, 24-, 48-, and 72-h post-admission, respectively). The blood samples were run for the quantification of serum glial fibrillary acidic protein levels and other biochemical tests. All patients were closely watched and the outcomes at discharge were evaluated.
UNASSIGNED: Glial fibrillary acidic protein levels tend to increase gradually from the time of admission to 48 h post-admission and then decrease at 72 h post-admission. Glial fibrillary acidic protein T2 is correlated with Acute Physiology and Chronic Health Evaluation II score, lactate, Simplified Acute Physiology Score II score and outcome. Glial fibrillary acidic protein max correlated with lactate, Acute Physiology and Chronic Health Evaluation II score, Simplified Acute Physiology Score II score, and outcome. Glasgow Coma Score at admission and glial fibrillary acidic protein T2 (OR = 1.034; p = 0.025), T3 (OR = 1.029; p = 0.046), T4 (OR = 1.006; p = 0.032), T5 (OR = 1.012; p = 0.048) and glial fibrillary acidic protein max (OR = 1.005; p = 0.010) were independent factors that have significant prognostic value in mortality in patients with severe traumatic brain injury. The predictive model in predicting mortality had the highest area under the curve based on glial fibrillary acidic protein T2 and Glasgow Coma Score T0 with an area under the curve of 0.904 and p < 0.001. In the multivariable regression model, glial fibrillary acidic protein max was associated with Glasgow score (p < 0.001; VIF = 1.585), lactate T0 (p = 0.024; VIF = 1.163), Acute Physiology and Chronic Health Evaluation II score (p = 0.037; VIF = 1.360), and Rotterdam score (p = 0.044; VIF = 1.713).
UNASSIGNED: Glial fibrillary acidic protein levels tend to increase gradually from the time of admission to 48 h post-admission then decreases at 72 h post-admission. Glial fibrillary acidic protein T2, T3, T4, T5, and glial fibrillary acidic protein max were independent factors with significant prognostic mortality values in patients with severe traumatic brain injury.

BACKGROUND: Chemokine-like factor 1 (CKLF1) may be involved in the inflammatory response and secondary brain injury after severe traumatic brain injury (sTBI). We determined serum CKLF1 levels of sTBI patients to further investigate the correlation of CKLF1 levels with disease severity, functional prognosis, and 180-day mortality of sTBI.
METHODS: Serum CKLF1 levels were measured at admission in 119 sTBI patients and at entry into study in 119 healthy controls. Serum CKLF levels of 50 patients were also quantified at days 1-3, 5, and 7 after admission. Glasgow coma scale (GCS) scores and Rotterdam computerized tomography (CT) classification were utilized to assess disease severity. Extended Glasgow outcome scale (GOSE) scores were recorded to evaluate function prognosis at 180 days after sTBI. Relations of serum CKLF1 levels to 180-day poor prognosis (GOSE scores of 1-4) and 180-day mortality were analyzed using univariate analysis, followed by multivariate analysis. Receiver-operating characteristic (ROC) curve was built to investigate prognostic predictive capability.
RESULTS: Serum CKLF1 levels of sTBI patients increased at admission, peaked at day 2, and then gradually decreased; they were significantly higher during the 7 days after sTBI than in healthy controls. Differences of areas under ROC curve (areas under the curve [AUCs]) were not significant among the six time points. Multivariate analysis showed that serum CKLF1 levels were independently correlated with GCS scores, Rotterdam CT classification, and GOSE scores. Serum CKLF1 levels were significantly higher in non-survivors than in survivors and in poor prognosis patients than in good prognosis patients. Serum CKLF1 levels independently predicted 180-day poor prognosis and 180-day mortality, and had high 180-day prognosis and mortality predictive abilities, and their AUCs were similar to those of GCS scores and Rotterdam CT classification. Combination model containing serum CKLF1, GCS scores, and Rotterdam CT classification performed more efficiently than any of them alone in predicting mortality and poor prognosis. The models were visually described using nomograms, which were comparatively stable under calibration curve and were relatively of clinical benefit under decision curve.
CONCLUSIONS: Serum CKLF1 levels are significantly associated with disease severity, poor 180-day prognosis, and 180-day mortality in sTBI patients. Hence, complement CKLF1 may serve as a potential prognostic biomarker of sTBI.