Traumatic Brain Injury Patients Research Articles

Evaluation and Pharmacologic Management of Paroxysmal Sympathetic Hyperactivity in Traumatic Brain Injury.

Paroxysmal sympathetic hyperactivity (PSH) can occur in up to 10% of severe traumatic brain injury (TBI) patients and is associated with poorer outcomes. A consensus regarding management is lacking. We provide a practical guide on the multi-faceted clinical management of PSH, including pharmacological, procedural and non-pharmacological interventions. In addition to utilizing a standardized assessment tool, the use of medications to manage sympathetic and musculoskeletal manifestations (including pain) is highlighted. Recent studies investigating new approaches to clinical management are included in this review of pharmacologic treatment options. While studies regarding pharmacologic selection for PSH are limited, this paper suggests a clinical approach to interventions based on predominant symptom presentation (sympathetic hyperactivity, pain and/or muscle hypertonicity) and relevant medication side effects.

Experimental animal models in traumatic brain injury research: a comprehensive review of methods and outlook

Traumatic brain injury (TBI) remains a significant public health concern worldwide, necessitating effective research models to elucidate its pathophysiology and develop therapeutic interventions. Animal models play a crucial role in TBI research, offering valuable insights into injury mechanisms and potential treatments. However, selecting the appropriate model can be challenging due to diverse array of available options and their respective advantages and limitations. In this comprehensive review, we examine four commonly used animal models of TBI: the weight drop, fluid percussion, cortical impact, and blast injury models. Each model is characterized by distinct injury mechanisms, allowing researchers simulate various aspects of TBI pathology. We discuss the unique advantages and disadvantages of each model, providing insights into their applications and considerations for model selection based on research objectives and outcome measures. Furthermore, we highlight emerging directions in TBI modelling, emphasizing the importance of refining and innovating models to replicate the complexity of human TBI. By critically evaluating and understanding the subtlety of different TBI models, researchers can make informed decisions to enhance the translational potential of preclinical TBI research and ultimately improve clinical outcomes for TBI patients.

Machine learning models for predicting early hemorrhage progression in traumatic brain injury.

This study explores the progression of intracerebral hemorrhage (ICH) in patients with mild to moderate traumatic brain injury (TBI). It aims to predict the risk of ICH progression using initial CT scans and identify clinical factors associated with this progression. A retrospective analysis of TBI patients between January 2010 and December 2021 was performed, focusing on initial CT evaluations and demographic, comorbid, and medical history data. ICH was categorized into intraparenchymal hemorrhage (IPH), petechial hemorrhage (PH), and subarachnoid hemorrhage (SAH). Within our study cohort, we identified a 22.2% progression rate of ICH among 650 TBI patients. The Random Forest algorithm identified variables such as petechial hemorrhage (PH) and countercoup injury as significant predictors of ICH progression. The XGBoost algorithm, incorporating key variables identified through SHAP values, demonstrated robust performance, achieving an AUC of 0.9. Additionally, an individual risk assessment diagram, utilizing significant SHAP values, visually represented the impact of each variable on the risk of ICH progression, providing personalized risk profiles. This approach, highlighted by an AUC of 0.913, underscores the model's precision in predicting ICH progression, marking a significant step towards enhancing TBI patient management through early identification of ICH progression risks.

Guiding lights in the early postoperative computed tomography following cranial surgery for traumatic brain injury patients

BackgroundComputed tomography (CT) can be a substantial source of guiding lights during the early postoperative hours in traumatic brain injury (TBI) patients. However, controversy still exists regarding: What is the appropriate time for the first postoperative CT? And what are the guiding lights that can be gained from an early follow-up CT? Therefore, our objective was to reach more clear answers for these questions and to design a simple algorithm for the follow-up of TBI patients during the first 24 h after cranial surgery.MethodsThis is a retrospective study included 164 TBI patients who were surgically treated for various traumatic cranial and/or intracranial lesions in our neurosurgery department from January 2022 to April 2023. Pre- and postoperative clinical and radiological data of these patients were collected and analyzed.ResultsThe mean age was (23.46 ± 15.126) years. The mean glasgow coma scale (GCS) on presentation was (11.62 ± 3.004). 51.2% of patients had their first follow-up CT done within the first postoperative hour (0–1 h). Postoperative remarkable CT findings were detected in 39 patients (23.8%), with 13 cases (33.3%) of them required re-surgery. 69.2% of the postoperative remarkable findings were recognized in the first hour CT (P = 0.025). Acute subdural hematoma was the only significant primary lesion associated with the need for re-surgery (P = 0.015). Postoperative development of remarkable CT findings was significantly (P < 0.001) associated with increased possibility of re-surgery, high mortality rate, prolonged hospital stay and poor outcome.ConclusionsImmediate (0–1 h) follow-up CT brain can be more lucrative in the early postoperative assessment for TBI patients. The first hour CT can provide distinct guiding lights of significant value for the subsequent postoperative management and prediction of patients' clinical course and discharge outcome.

Neuroimaging with Rotterdam Scoring System and long-term outcomes in severe traumatic brain injury patients.

The Rotterdam Scoring System (RSS) attempts to prognosticate early mortality and early functional outcome in patients with traumatic brain injury (TBI) based on non-contrast head computed tomography (CT) imaging findings. The purpose of this study was to identify the relationship between RSS scores and long-term outcomes in patients with severe TBI. Consecutively treated patients with severe TBI enrolled between 2008 and 2011, in the prospective, observational, Brain Trauma Research Center database were included. The Glasgow Outcome Scale (GOS) was used to measure long-term functional outcomes at three, six, 12, and 24 months. GOS scores were categorized into favorable (GOS = 4-5) and unfavorable (GOS = 1-3) outcomes. RSS scores were calculated at the time of image acquisition. Of the 89 patients included, 74 (83.4%) were male, 81 (91.0%) were Caucasian, and the mean age of the cohort was 41.9±18.5 years old. Patients with an RSS score of 3 and lower were more likely to have a favorable outcome with increased survival rates than patients with RSS scores greater than 3. The RSS score determined on the head CT scan acquired at admission in a cohort of patients with severe TBI correlated with long-term survival and functional outcomes up to two years following injury.

Incidence and predictors of posttraumatic epilepsy and cognitive impairment in patients with traumatic brain injury: A retrospective cohort study in Malaysia.

Posttraumatic epilepsy (PTE) significantly impacts morbidity and mortality, yet local PTE data remain scarce. In addition, there is a lack of evidence on cognitive comorbidity in individuals with PTE in the literature. We sought to identify potential PTE predictors and evaluate cognitive comorbidity in patients with PTE. A 2-year retrospective cohort study was employed, in which adults with a history of admission for traumatic brain injury (TBI) in 2019 and 2020 were contacted. Three hundred one individuals agreed to participate, with a median follow-up time of 30.75 months. The development of epilepsy was ascertained using a validated tool and confirmed by our neurologists during visits. Clinical psychologists assessed the patients' cognitive performance. The 2-year cumulative incidence of PTE was 9.3% (95% confidence interval [CI] 5.9-12.7). The significant predictors of PTE were identified as a previous history of brain injury [hazard ratio [HR] 4.025, p = .021], and intraparenchymal hemorrhage (HR: 2.291, p = .036), after adjusting for other confounders. TBI patients with PTE performed significantly worse on the total ACE-III cognitive test (73.5 vs 87.0, p = .018), CTMT (27.5 vs 33.0, p = .044), and PSI (74.0 vs 86.0, p = .006) than TBI patients without PTE. A significantly higher percentage of individuals in the PTE group had cognitive impairment, compared to the non-PTE group based on ACE-III (53.6% vs 46.4%, p = .001) and PSI (70% vs 31.7%, p = .005) scores at 2 years post-TBI follow-up. This study emphasizes the link between TBI and PTE and the chance of developing cognitive impairment in the future. Clinicians can target interventions to prevent PTE by identifying specific predictors, which helps them make care decisions and develop therapies to improve patients' quality of life.

Post-traumatic hyperoxia after pediatric TBI

ABSTRACT Objective Hyperoxia has been suggested as a mechanism for secondary injury following adult traumatic brain injury (TBI), but its effects have not been well described in pediatric patients. Methods Pediatric (≤18yo) TBI patients were identified in a prospective institutional registry from October 2008 to April 2022. The first, highest, and the Area Under the Curve (AUC) PaO2 in the first 24 hours were collected and calculated for each patient from arterial blood gas reports after admission to the ICU. Neurological outcome after 6 months was measured using dichotomized modified Rankin Scale (mRS) and Glasgow Outcome Scale – Extended (GOS-E). Multivariable logistic regression models were used to determine if the three measurements for hyperoxia predicted an unfavorable outcome after controlling for well-established clinical and imaging predictors of outcome. Results We identified 98 pediatric patients with severe accidental TBI during the study period. Hyperoxia (PaO2 > 300 mmHg) occurred in 33% of the patients. The presence of elevated PaO2 values, determined by all three evaluations of hyperoxia, was not associated with unfavorable outcome after 6 months. Conclusion Utilizing multiple methods to assess exposure, hyperoxia was present in a substantial number of patients with severe TBI but was not associated with an unfavorable outcome.

Effect of erythropoietin on SOFA score, Glasgow Coma Scale and mortality in traumatic brain injury patients: a randomized-double-blind controlled trial.

Recent studies suggest that erythropoietin has an anti-inflammatory effect on the central nervous system. The authors aimed to investigate the effect of erythropoietin on Glasgow Coma Scale (GCS), Sequential Organ Failure Assessment (SOFA) scores, and the mortality rate of traumatic brain injury (TBI) patients. Sixty-eight patients with available inclusion criteria were randomly allocated to the control or intervention groups. In the intervention group, erythropoietin (4000 units) was administrated on days 1, 3, and 5. In the control group, normal saline on the same days was used. The primary outcomes were the GCS and SOFA score changes during the intervention. The secondary outcomes were the ventilation period during the first 2 weeks and the 3-month mortality rate. Erythropoietin administration significantly affected SOFA score over time (P=0.008), but no significant effect on the GCS, and duration of ventilation between the two groups was observed. Finally, erythropoietin had no significant effect on the three-month mortality (23.5% vs. 38.2% in the erythropoietin and control group, respectively). However, the mortality rate in the intervention group was lower than in the control group. Our finding showed that erythropoietin administration in TBI may improve SOFA score. Therefore, erythropoietin may have beneficial effects on early morbidity and clinical improvement in TBI patients.

An injectable refrigerated hydrogel for inducing local hypothermia and neuroprotection against traumatic brain injury in mice

BackgroundHypothermia is a promising therapy for traumatic brain injury (TBI) in the clinic. However, the neuroprotective outcomes of hypothermia-treated TBI patients in clinical studies are inconsistent due to several severe side effects. Here, an injectable refrigerated hydrogel was designed to deliver 3-iodothyronamine (T1AM) to achieve a longer period of local hypothermia for TBI treatment. Hydrogel has four advantages: (1) It can be injected into injured sites after TBI, where it forms a hydrogel and avoids the side effects of whole-body cooling. (2) Hydrogels can biodegrade and be used for controlled drug release. (3) Released T1AM can induce hypothermia. (4) This hydrogel has increased medical value given its simple operation and ability to achieve timely treatment.MethodsPol/T hydrogels were prepared by a low-temperature mixing method and characterized. The effect of the Pol/T hydrogel on traumatic brain injury in mice was studied. The degradation of the hydrogel at the body level was observed with a small animal imager. Brain temperature and body temperature were measured by brain thermometer and body thermometer, respectively. The apoptosis of peripheral nerve cells was detected by immunohistochemical staining. The protective effect of the hydrogels on the blood–brain barrier (BBB) after TBI was evaluated by the Evans blue penetration test. The protective effect of hydrogel on brain edema after injury in mice was detected by Magnetic resonance (MR) in small animals. The enzyme linked immunosorbent assay (ELISA) method was used to measure the levels of inflammatory factors. The effects of behavioral tests on the learning ability and exercise ability of mice after injury were evaluated.ResultsThis hydrogel was able to cool the brain to hypothermia for 12 h while maintaining body temperature within the normal range after TBI in mice. More importantly, hypothermia induced by this hydrogel leads to the maintenance of BBB integrity, the prevention of cell death, the reduction of the inflammatory response and brain edema, and the promotion of functional recovery after TBI in mice. This cooling method could be developed as a new approach for hypothermia treatment in TBI patients.ConclusionOur study showed that injectable and biodegradable frozen Pol/T hydrogels to induce local hypothermia in TBI mice can be used for the treatment of traumatic brain injury.Graphical

Prediction of Initial CRP/Albumin Ratio on In-Hospital Mortality in Isolated Traumatic Brain Injury Patients.

The CRP/albumin ratio (CAR) is a mortality predictor in intensive care unit (ICU) patients. The aim of the current study was to investigate the ability of CAR to predict in-hospital mortality (IHM) in patients with isolated traumatic brain injury (iTBI). We performed a retrospective analysis including 200 patients with iTBI admitted to our neurosurgical intensive care unit (NICU) between September 2014 and December 2016. Serum biomarkers, demographic and radiological data, several ICU scores, and cardiopulmonary parameters were analyzed. The rate of IHM was 27.5% (55/200) and significantly associated with a higher AIS head score (p < 0.0001), a lower albumin level (p < 0.0001), and the necessity of a higher level of inspiratory oxygen fraction (p = 0.002). Furthermore, advanced age (odds ratio [OR] = 0.953, 95% confidence interval [CI] = 0.927-0.981, p = 0.001), a lower GCS score (OR = 1.347, 95% CI = 1.203-1.509, p < 0.0001), a higher level of lactate (OR = 0.506, 95% CI = 0.353-0.725, p < 0.0001), a higher CAR (OR = 0.547, 95% CI = 0.316-0.945, p = 0.031) and a higher norepinephrine application rate (OR = 0.000, 95% CI 0.000-0.090, p = 0.016) were identified as independent predictors of IHM. ROC analysis showed an association between IHM and a CAR cut-off value of >0.38 (Youden index 0.073, sensitivity: 27.9, specificity: 64.8, p = 0.044). We could identify a CAR > 0.38 as a new independent predictor for IHM in patients with iTBI.

Recovery Potential in Patients Who Died After Withdrawal of Life-Sustaining Treatment: A TRACK-TBI Propensity Score Analysis.

Among patients with severe traumatic brain injury (TBI), there is high prognostic uncertainty but growing evidence that recovery of independence is possible. Nevertheless, families are often asked to make decisions about withdrawal of life-sustaining treatment (WLST) within days of injury. The range of potential outcomes for patients who died after WLST (WLST+) is unknown, posing a challenge for prognostic modeling and clinical counseling. We investigated the potential for survival and recovery of independence after acute TBI in patients who died after WLST. We used Transforming Research and Clinical Knowledge in TBI (TRACK-TBI) data and propensity score matching to pair participants with WLST+ to those with a similar probability of WLST (based on demographic and clinical characteristics), but for whom life-sustaining treatment was not withdrawn (WLST-). To optimize matching, we divided the WLST- cohort into tiers (Tier 1 = 0-11%, Tier 2 = 11-27%, Tier 3 = 27-70% WLST propensity). We estimated the level of recovery that could be expected in WLST+ participants by evaluating 3-, 6-, and 12-month Glasgow Outcome Scale-Extended (GOSE) and Disability Rating Scale outcomes in matched WLST- participants. Of 90 WLST+ participants (80% male, mean [standard deviation; SD] age = 59.2 [17.9] years, median [IQR] days to WLST = 5.4 [2.2, 11.7]), 80 could be matched to WLST- participants. Of 56 WLST- participants who were followed at 6 months, 31 (55%) died. Among survivors in the overall sample and survivors in Tiers 1 and 2, more than 30% recovered at least partial independence (GOSE ≥4). In Tier 3, recovery to GOSE ≥4 occurred at 12 months, but not 6 months, post-injury. These results suggest a substantial proportion of patients with TBI and WLST may have survived and achieved at least partial independence. However, death or severe disability is a common outcome when the probability of WLST is high. While further validation is needed, our findings support a more cautious clinical approach to WLST and more complete reporting on WLST in TBI studies.

Levetiracetam Dosing Based on Glasgow Coma Scale Scores in Pediatric Traumatic Brain Injury Patients.

Severe traumatic brain injury (TBI) increases the risk of early posttraumatic seizures (EPTS). Guidelines suggest the use of prophylactic antiseizure agents, including levetiracetam. This study aims to evaluate the feasibility of using levetiracetam dosing based on Glasgow Comas Scale (GCS) scores with higher doses used for more severe TBI. Patients 6 months to 18 years old admitted to Penn State Hershey Children's Hospital (PSHCH) with a TBI who received levetiracetam for EPTS prophylaxis with at least one documented GCS score were included. Patients were divided into two cohorts: before and after implementation of the pediatric TBI Cerner PowerPlan at PSHCH which standardized levetiracetam dosing based on GCS scores. Primary outcome was appropriate dosing of levetiracetam based on GCS. Secondary outcomes included seizure occurrence and adverse effects. Eighty-five patients were included: 42 in the pre-PowerPlan group and 43 in the post-PowerPlan group. Overall, 46 (54%) patients received the appropriate levetiracetam dose based on GCS (pre-PowerPlan, n = 19 [45%] vs. post-PowerPlan n = 27 [63%], p = 0.104). Sixty-four percent of severe TBI patients received appropriate levetiracetam dosing after implantation of the PowerPlan compared with 28% prior to the PowerPlan (p = 0.039). Three patients in each group experienced a seizure while on levetiracetam. Two patients experienced agitation and somnolence attributed to levetiracetam. Levetiracetam dosing based on GCS scores in pediatric TBI patients is a novel approach, and dosing accuracy may be increased with use of a PowerPlan. Additional large-scale studies are needed to evaluate efficacy and safety of this approach prior to widespread implementation.

Using machine learning to discover traumatic brain injury patient phenotypes: national concussion surveillance system Pilot

ABSTRACT Objective The objective is to determine whether unsupervised machine learning identifies traumatic brain injury (TBI) phenotypes with unique clinical profiles. Methods Pilot self-reported survey data of over 10,000 adults were collected from the Centers for Disease Control and Prevention (CDC)’s National Concussion Surveillance System (NCSS). Respondents who self-reported a head injury in the past 12 months (n = 1,364) were retained and queried for injury, outcome, and clinical characteristics. An unsupervised machine learning algorithm, partitioning around medoids (PAM), that employed Gower’s dissimilarity matrix, was used to conduct a cluster analysis. Results PAM grouped respondents into five TBI clusters (phenotypes A-E). Phenotype C represented more clinically severe TBIs with a higher prevalence of symptoms and association with worse outcomes. When compared to individuals in Phenotype A, a group with few TBI-related symptoms, individuals in Phenotype C were more likely to undergo medical evaluation (odds ratio [OR] = 9.8, 95% confidence interval[CI] = 5.8–16.6), have symptoms that were not currently resolved or resolved in 8+ days (OR = 10.6, 95%CI = 6.2–18.1), and more likely to report at least moderate impact on social (OR = 54.7, 95%CI = 22.4–133.4) and work (OR = 25.4, 95%CI = 11.2–57.2) functioning. Conclusion Machine learning can be used to classify patients into unique TBI phenotypes. Further research might examine the utility of such classifications in supporting clinical diagnosis and patient recovery for this complex health condition.

Hospital-acquired infections as a risk factor for post-traumatic epilepsy: A registry-based cohort study.

Hospital-acquired infections are a common complication for patients with moderate or severe traumatic brain injury (TBI), contributing to morbidity and mortality. As infection-mediated immune responses can predispose towards epilepsy, we hypothesized that post-injury hospital-acquired infections increase the risk of post-traumatic epilepsy (PTE). A retrospective cohort study of adults with moderate to severe TBI was conducted using data from the Victorian State Trauma Registry in Australia. Infections were identified from the International Statistical Classification of Diseases and Related Health Problems 10th Revision-Australian Modification (ICD-10-AM) codes, and diagnosis of PTE was determined by the Glasgow Outcome Scale - Extended questionnaire regarding epileptic fits at 24 months follow-up. Of all TBI patients (n = 15 152), 24% had evidence of having had any type of infection, with the most common being pneumonia, urinary tract, and respiratory infections. Of those who responded to the PTE question at 24 months (n = 1361), 11% had developed PTE. Univariable analysis found that the incidence of PTE was higher in patients who had any type of infection compared to patients without an infection (p < 0.001). After adjustment for covariates associated with both development of PTE and risk of infection, multivariable analysis found a solid association between infection and PTE (adjusted RR = 1.59; 95% CI: 1.11-2.28; p = 0.011). Having any type of complicating infection acquired during admission was also associated with poor GOSE outcomes at subsequent follow-ups (adjusted OR = 0.20; 95% CI: 0.11-0.35, p < 0.001). These findings suggest that hospital-acquired infections contribute to PTE development after TBI. Future investigation into infections as a modifiable target to reduce poor outcomes after TBI is warranted. Hospital-acquired infections are common in patients with traumatic brain injuries. A database study of adults with moderate or severe brain injuries in Australia examined whether these infections are associated with the development of epilepsy after a brain injury. 24% of patients had infections, with pneumonia and urinary tract infections being the most common. Of those surveyed 2 years after the injury, 11% developed post-traumatic epilepsy. Patients with infections had a significantly higher risk of epilepsy, even when accounting for other known risk factors, and infections were also linked to poor outcomes more broadly. The study suggests that preventing hospital-acquired infections could be a crucial target for improving outcomes after traumatic brain injuries.

Ionized hypocalcemia as a prognostic factor of early mortality in traumatic brain injury

ABSTRACT Traumatic brain injury (TBI) is a common neurological condition. It can affect mental, physical, and cognitive functions and is a common cause of mortality. Electrolytes imbalance is common in those patients. Effective therapy of electrolytes abnormalities improves neurological outcome and reduces mortality. Therefore, we studied the predictive significance of ionized hypocalcemia for early mortality in TBI patients. Patients and method This observational study in the intensive care units of the Ain Shams University hospitals was done on sixty adult patients with TBI of both sexes, divided into two groups: group A (ionized hypocalcemic patients), and group B (normocalcemic patients). On admission, medical history, physical examination including neurological evaluation, and appropriate investigations were performed. Ionized calcium was measured at the start of the 28-day study and then every five days after that. Results There was no statistically significant difference between the two groups for demographic data, brain injury type, or the number of intubated patients (p > 0.05). There was a statistically significant difference for diffuse axonal damage, subdural hemorrhage, cerebral edema, GCS, and mean blood pressure (p < 0.001). Serum ionized calcium in group A was significantly lower than in group B on the day of admission and day five (p < 0.001). On the day of admission, there was a significant difference in serum sodium (p < 0.05). In both groups, there was a significant difference in the ICU stay as regards survivors (p < 0.001). There was a statistically significant difference in 28-day mortality between the two groups (p = 0.001). Conclusion In TBI patients, ionized hypocalcemia on admission and on day five, hypernatremia and disturbed conscious level are strongly linked to greater fatality rates.

Characteristics and Neural Mechanisms of Sleep-Wake Disturbances After Traumatic Brain Injury.

Sleep-wake disturbances (SWDs) are one of the most common complaints following traumatic brain injury (TBI). The high prevalence and socioeconomic burden of SWDs post-TBI have only been recognized in the past decade. Common SWDs induced by TBI include excessive daytime sleepiness (EDS), hypersomnia, insomnia, obstructive sleep apnea (OSA), and circadian rhythm sleep disorders. Sleep disturbances can significantly compromise quality of life, strain interpersonal relationships, diminish work productivity, exacerbate other clinical conditions, and impede the rehabilitation process of TBI patients. Consequently, the prompt regulation and enhancement of sleep homeostasis in TBI patients is of paramount importance. Although studies have shown that abnormal neural network function, neuroendocrine changes, disturbance of sleep-wake regulators, and immune inflammatory responses related to brain structural damage induced by TBI are involved in the development of SWDs, the exact neuropathological mechanisms are still poorly understood. Therefore, we systematically review the current clinical and experimental studies on the characteristics and possible neural mechanisms of post-TBI SWDs. Elucidating the neural underpinnings of post-TBI SWDs holds the potential to diversify and enhance therapeutic approaches for these conditions. Such advancements could hasten the recuperation of TBI patients and ameliorate their overall quality of life. It is our aspiration that departments specializing in neurosurgery, rehabilitation, and neuropsychiatry will be able to recognize and address these conditions promptly, thereby facilitating the healing journey of affected individuals.

Patient Factors Associated With Prolonged Length of Stay After Traumatic Brain Injury.

Background For traumatic brain injury (TBI) survivors, recovery can lead to significant time spent in the inpatient/rehabilitation settings. Hospital length of stay (LOS) after TBI is a crucial metric of resource utilization and treatment costs. Risk factors for prolonged LOS (PLOS) after TBI require further characterization. Methodology We conducted a retrospective analysis of patients with diagnosed TBI at an urban trauma center. PLOS was defined as the 95th percentile of the LOS of the cohort. Patients with and without PLOS were compared using clinical/injury factors. Analyses included descriptive statistics, non-parametric analyses, and multivariable logistic regression for PLOS status. Results The threshold for PLOS was >24 days. In the cohort of 1,343 patients, 77 had PLOS. PLOS was significantly associated with longer mean intensive care unit (ICU) stays (16.4 vs. 1.5 days), higher mean injury severity scores (18.6 vs. 13.8), lower mean Glasgow coma scale scores (11.3 vs. 13.7) and greater mean complication burden (0.7 vs. 0.1). PLOS patients were more likely to have moderate/severe TBI, Medicaid insurance, and were less likely to be discharged home.In the regression model, PLOS was associated with ICU stay, inpatient disposition, ventilator use, unplanned intubation, and inpatient alcohol withdrawal. Conclusions TBI patients with PLOS were more likely to have severe injuries, in-hospital complications, and Medicaid insurance. PLOS was predicted by ICU stay, intubation, alcohol withdrawal, and disposition to inpatient/post-acute care facilities. Efforts to reduce in-hospital complications and expedite discharge may reduce LOS and accompanying costs.Further validation of these results is needed from larger multicenter studies.

Extracellular vesicles in disorders of hemostasis following traumatic brain injury.

Traumatic brain injury (TBI) is a global health priority. In addition to being the leading cause of trauma related death, TBI can result in long-term disability and loss of health. Disorders of haemostasis are common despite the absence of some of the traditional risk factors for coagulopathy following trauma. Similar to trauma induced coagulopathy, this manifests with a biphasic response consisting of an early hypocoagulable phase and delayed hypercoagulable state. This coagulopathy is clinically significant and associated with increased rates of haemorrhagic expansion, disability and death. The pathophysiology of TBI-induced coagulopathy is complex but there is biologic plausibility and emerging evidence to suggest that extracellular vesicles (EVs) have a role to play. TBI and damage to the blood brain barrier result in release of brain-derived EVs that contain tissue factor and phosphatidylserine on their surface. This provides a platform on which coagulation can occur. Preclinical animal models have shown that an early rapid release of EVs results in overwhelming activation of coagulation resulting in a consumptive coagulopathy. This phenomenon can be attenuated with administration of substances to promote EV clearance and block their effects. Small clinical studies have demonstrated elevated levels of procoagulant EVs in patients with TBI correlating with clinical outcome. EVs represent a promising opportunity for use as minimally invasive biomarkers and potential therapeutic targets for TBI patients. However, additional research is necessary to bridge the gap between their potential and practical application in clinical settings.

Comparison of the efficacy of 0.9% normal saline with balanced crystalloid (Plasmalyte) in maintaining the metabolic profile in head injury patients undergoing evacuation of acute subdural haematoma - A randomised controlled trial.

The choice of intravenous fluids is important in patients with traumatic brain injury (TBI), where large volumes may be required for resuscitation. Our study aimed to compare 0.9% normal saline (NS) with balanced crystalloid (Plasmalyte) in TBI patients in terms of metabolic and coagulation profile, brain relaxation score (BRS) and renal functions using serum urea, creatinine and urinary tissue inhibitor of metalloproteinases-2* insulin-like growth factor binding protein-7, [TIMP-2]*[IGFBP7], value to assess the risk of acute kidney injury. This randomised controlled trial on 90 TBI patients undergoing emergency craniotomy and subdural haematoma evacuation was conducted in a tertiary care institute. The patients were randomised to receive either NS (Group NS) or Plasmalyte (Group P) as the intraoperative maintenance fluid. The primary outcome measures included the potential of hydrogen (pH), base excess (BE) and chloride values from an arterial blood gas. The secondary outcomes were the coagulation profile, BRS and urinary [TIMP-2]*[IGFBP7]. The two groups' metabolic profile differences were analysed using two-way repeated analysis of variance. BRS was analysed using the Mann-Whitney U test. A P value < 0.05 was considered to be statistically significant. The pH and chloride values were significantly higher, and the BE values were significantly lower in Group P compared to Group NS (P < 0.001). Brain relaxation and coagulation profiles were comparable between the two groups. Serum creatinine (P = 0.002) and urinary [TIMP-2]*[IGFBP7] (P = 0.042) were significantly higher in the NS group. Plasmalyte maintains a more favourable metabolic profile than NS in TBI patients without affecting brain relaxation adversely.

Impact of anesthetic induction with etomidate, thiopentone, and propofol on regional cerebral oxygenation: An observational study in patients with traumatic brain injury

Abstract Background and Aims: Anesthetic induction plays a pivotal role in determining the operative course and the outcome in patients with acute traumatic brain injury (TBI). The present study compared the effect of anesthetic induction with etomidate, thiopentone, and propofol primarily on systemic hemodynamics and regional cerebral oxygenation (rScO2) and secondarily on the serum cortisol levels in TBI patients. Material and Methods: In this prospective observational study, eligible patients were recruited and divided into three groups as per the induction agent received. Data collected were hemodynamic parameters and rScO2 levels at baseline, following 3 min of preoxygenation, and over 10 min of induction. Serum cortisol levels were measured before and after 24 h of induction. The statistical analysis was done using R software. Results: A total of 115 patients were included: 32, 33, and 50 in thiopentone, propofol, and etomidate groups, respectively. A significant increase (P &lt; 0.001) in bilateral rScO2 was noted in all three groups following anesthetic induction. Intergroup comparison of the propofol and the etomidate groups revealed significantly lesser increase in contralateral rScO2 (P = 0.019) and a greater fall in mean arterial pressure (P = 0.003) on using propofol as an induction agent. Trend changes in bilateral rScO2 and hemodynamic parameters were comparable between thiopentone and etomidate groups. An insignificant fall in serum cortisol was observed in etomidate (P = 0.332) and thiopentone (P = 0.364) groups, but a significant increase was observed in the propofol group (P = 0.004). The Glasgow coma scale (GCS) score at discharge improved significantly in all the groups (P &lt; 0.001). Conclusions: In TBI patients, anesthetic induction with etomidate resulted in least hemodynamic changes compared to induction with thiopentone and propofol. The rScO2 increased in all three groups after induction, with the maximal increase observed with etomidate compared to propofol and thiopentone. Insignificant fall in serum cortisol was observed with etomidate and thiopentone, but not with propofol. Outcome at discharge, assessed with GCS, was comparable in all the groups. Key Messages: Anesthetic induction with etomidate produced least hemodynamic changes compared to induction with thiopentone and propofol in patients with traumatic brain injury. Consequently, maximal increase in cerebral oxygen saturation occurred with etomidate among the three induction agents. An insignificant decrease in serum cortisol was observed with etomidate and thiopentone, but not with propofol. Neurological outcome at discharge was similar with all drugs.