Head Abbreviated Injury Scale Score Research Articles

Critical traumatic brain injury is associated with worse coagulopathy.

As thromboelastography (TEG) becomes the standard of care in patients with hemorrhagic shock (HS), an association between concomitant traumatic brain injury (TBI) and coagulopathy by TEG parameters is not well understood and is thus investigated. Retrospective analysis of trauma registry data at a single level 1 trauma center of 772 patients admitted with head Abbreviated Injury Scale (AIS) score of 3 and TEG studies between 2014 and 2017. Patients were stratified to moderate-severe TBI by head AIS scores of 3 and 4 (435 patients) and critical TBI by head AIS score of 5 (328 patients). Hemorrhagic shock was defined by base deficit of 4 or shock index of 0.9. Statistical analysis with unpaired t tests compared patients with critical TBI with patients with moderate-severe TBI, and patients were grouped by presence or absence of HS. A comparison of TBI data with conventional coagulation studies was also evaluated. In the setting of HS, critical TBI versus moderate-severe TBI was associated with longer R time (p = 0.004), longer K time (p < 0.05), less acute angle (p = 0.001), and lower clot strength and stability (maximum amplitude [MA]) (p = 0.01). Worse TBI did not correlate with increased fibrinolysis by clot lysis measured by the percentage decrease in amplitude at 30 minutes after MA (p = 0.3). Prothrombin time and international normalized ratio failed to demonstrate more severe coagulopathy, while partial thromboplastin time was found to correlate with severity of TBI (p = 0.01). In patients with critical TBI, the presence of HS correlated with a statistically significant worsening of all parameters (p < 0.05) except for clot lysis measured by the percentage decrease in amplitude at 30 minutes after MA (LY-30). Thromboelastography demonstrates that, with and without hemorrhagic shock, critical TBI correlates with a significant worsening of traumatic coagulopathy in comparison with moderate/severe TBI. In HS, critical TBI correlates with impaired clot initiation, impaired clot kinetics, and impaired platelet-associated clot strength and stability versus parameters found in moderate-severe TBI. Hemorrhagic shock correlates with worse traumatic coagulopathy in all evaluated patient groups with TBI. Conventional coagulation studies underestimate TBI-associated coagulopathy. Traumatic brain injury-associated coagulopathy is not associated with fibrinolysis. Prognostic/epidemiological, level IV; prognostic/epidemiological, level III.

Isolated traumatic brain injury: Routine intubation for Glasgow Coma Scale 7 or 8 may be harmful!

Despite strong recommendations, there is no direct evidence supporting routine intubation of trauma patients with Glasgow Coma Scale (GCS) score of 7 or 8. We hypothesized that routine intubation may not be beneficial in isolated blunt head injury. A retrospective Trauma Quality Improvement Program study, including adult blunt trauma patients with GCS score of 7 or 8 and isolated head injury, was performed. Epidemiological and clinical characteristics, neurosurgical procedures, timing of intubation, and outcome variables were collected. The study population was stratified by the intubation procedure: immediate intubation (≤1 hour of admission), delayed intubation (>1 hour of admission), and no intubation. Multivariable regression analysis was used to determine risk factors for mortality and complications, as well as factors predictive of the decision to intubate. Of 2,727 patients with GCS score of 7 or 8 and isolated blunt head trauma, 1,866 patients (68.4%) were intubated within 1 hour of admission (immediate intubation), 223 (8.2%) had an intubation >1 hour of admission (delayed intubation), and 638 patients (23.4%) were not intubated at all. After correcting for age, sex, overall comorbidities, tachycardia, GCS, alcohol, illegal drug use, and head injury severity, immediate intubation was independently associated with higher mortality (odds ratio, 1.79; 95% confidence interval, 1.31-2.44; p < 0.001) and more overall complications (odds ratio, 2.46; 95% confidence interval, 1.62-3.73; p < 0.001). Increasing head Abbreviated Injury Scale (AIS) score, GCS score of 7, and tachycardia were identified as independent clinical factors associated with the decision to intubate. A policy of intubating all isolated blunt head injury patients 45 years or younger with head AIS score of 5 and GCS score of 7 would have improved intubation management, with seven immediate instead of delayed intubations and only three potentially unnecessary intubations. In patients with GCS score of 7 or 8 and isolated head injury, immediate intubation was associated with higher mortality and more overall complications. Intubation management could have been improved by intubating all patients younger than 45 years with head AIS score of 5 and a GCS score of 7 on admission. Therapeutic, level III.

Racial disparities in mortality after severe traumatic brain injury in childhood: mediators identified by Oaxaca-Blinder decomposition of trauma registry data

BackgroundIn the United States social disparities in health outcomes are found wherever they are sought, and they have been documented extensively in trauma care. Because social factors cannot cause a trauma outcome directly, there must exist mediating causal factors related to the nature and severity of the injury, the robustness of the victim, access to care, or processes of care. An understanding these mediators is the point of departure for addressing inequities in outcomes.FindingsData were extracted from the registry of the Trauma Quality Improvement Program of the American College of Surgeons for 2007 through 2010. Inclusion criteria were age less than 19 years and head Abbreviated Injury Scale score of 4, 5, or 6. An Oaxaca-Blinder decomposition was undertaken to analyze the relative contributions of a large set of covariates to the difference in mortality rates between Black and White children. Covariates were aggregated into the following categories: “Severity,” “Structure and Process,” “Mechanism,” “Demographics,” and “Insurance.” Eligible for analysis were 7273 White children and 2320 Black children. There were 1661 deaths (17.3%) The raw mortality rates were 15.6 and 22.8% for White and Black children, respectively. Factors categorized as “Severity” accounted for 95% of the mortality difference, “Mechanism” accounted for 13%, “Insurance” accounted for 5%, and “Demographics” accounted for 2%. The contribution of “Structure and Process” did not attain statistical significance.ConclusionsSeverity of injury accounts for most of the disparity between Black and White children in traumatic brain injury mortality rates. Mechanism, insurance status, and gender make a small contributions. Because insurance status like other social factors cannot directly affect trauma survival, what mediates its contribution requires further study.

Traumatic brain injury induced temperature dysregulation: What is the role of β blockers?

Traumatic brain injury (TBI) is associated with sympathetic discharge that leads to posttraumatic hyperthermia (PTH). Beta blockers (ββ) are known to counteract overactive sympathetic discharge. The aim of our study was to evaluate the effect of ββ on PTH in critically-ill TBI patients. We performed retrospective cohort analysis of the Medical Information Mart for Intensive Care database. We included all critically ill TBI patients with head Abbreviated Injury Scale (AIS) score of 3 or greater and other body region AIS score less than 2 who developed PTH (at least one febrile episode [T > 38.3°C] with negative microbiological cultures (blood, urine, and bronchoalveolar lavage). Patients on preinjury ββ were excluded. Patients were stratified into (ββ+) and (ββ-) groups. Propensity score matching was performed (1:1 ratio) controlling for patient demographics, injury parameters and other medications that influence temperature. Outcomes were the number of febrile episodes, maximum temperature, and the time interval between febrile episodes. Multivariate linear regression was performed. We analyzed 4,286 critically ill TBI patients. A matched cohort of 1,544 patients was obtained: 772 ββ + (metoprolol, 60%; propranolol, 25%; and atenolol, 15%) and 772 ββ-. Mean age was 63.4 ± 15.4 years, median head AIS score of 3 (3-4), and median Injury Severity Score of 10 (9-16). Patients in the ββ+ group had a lower number of febrile episodes (8 episodes vs. 12 episodes; p = 0.003), lower median maximum temperature (38.0°C vs. 38.5°C; p = 0.025), and a longer median time between febrile episodes (3 hours vs. 1 hour; p = 0.013). On linear regression, propranolol was found to be superior in terms of reducing the number of febrile episodes and the maximum temperature. However, there was no significant difference between the three ββ in terms of reducing the time interval between febrile episodes (p = 0.582). Beta blockers attenuate PTH by decreasing the frequency of febrile episodes, increasing the time interval between febrile episodes, and reducing the maximum rise in temperature. ββ may be a potential therapeutic modality in PTH. Therapeutic, level IV.

Mediators of racial disparities in mortality rates after traumatic brain injury in childhood: data from the Trauma Quality Improvement Program.

Social disparities in healthcare outcomes are almost ubiquitous, and trauma care is no exception. Because social factors cannot cause a trauma outcome directly, there must exist mediating causal factors related to the nature and severity of the injury, the robustness of the victim, access to care, or processes of care. Identification of these causal factors is the first step in the movement toward health equity. A noninferiority analysis was undertaken to compare mortality rates between Black children and White children after traumatic brain injury (TBI). Data were derived from the Trauma Quality Improvement Program (TQIP) registries for the years 2014 through 2017. Inclusion criteria were age younger than 19 years and head Abbreviated Injury Scale scores of 4, 5, or 6. A noninferiority margin of 10% was preselected. A logistic regression propensity score model was developed to distinguish Black and White children based on all available covariates associated with race at p < 0.10. Stabilized inverse probability weighting and a one-tailed 95% CI were used to test the noninferiority hypothesis. There were 7273 observations of White children and 2320 observations of Black children. The raw mortality rates were 15.6% and 22.8% for White and Black children, respectively. The final propensity score model included 31 covariates. It had good fit (Hosmer-Lemeshow χ2 = 7.1604, df = 8; p = 0.5194) and good discrimination (c-statistic = 0.752). The adjusted mortality rates were 17.82% and 17.79% for White and Black children, respectively. The relative risk was 0.9986, with a confidence interval upper limit of 1.0865. The relative risk corresponding to the noninferiority margin was 1.1. The hypothesis of noninferiority was supported. Data captured in the TQIP registries are sufficient to explain the observed racial disparities in mortality after TBI in childhood. Speculations about genetic or epigenetic factors are not supported by this analysis. Discriminatory care may still be a factor in TBI mortality disparities, but it is not occult. If it exists, evidence for it can be sought among the data included in the TQIP registries.

Association of Insurance Status With Treatment and Outcomes in Pediatric Patients With Severe Traumatic Brain Injury.

To determine whether a health insurance disparity exists among pediatric patients with severe traumatic brain injury using the National Trauma Data Bank. Retrospective cohort study. National Trauma Data Bank, a dataset containing more than 800 trauma centers in the United States. Pediatric patients (< 18 yr old) with a severe isolated traumatic brain injury were identified in the National Trauma Database (years 2007-2016). Isolated traumatic brain injury was defined as patients with a head Abbreviated Injury Scale score of 3+ and excluded those with another regional Abbreviated Injury Scale of 3+. None. Procedure codes were used to identify four primary treatment approaches combined into two classifications: craniotomy/craniectomy and external ventricular draining/intracranial pressure monitoring. Diagnostic criteria and procedure codes were used to identify condition at admission, including hypotension, Glasgow Coma Scale, mechanism and intent of injury, and Injury Severity Score. Children were propensity score matched using condition at admission and other characteristics to estimate multivariable logistic regression models to assess the associations among insurance status, treatment, and outcomes. Among the 12,449 identified patients, 91.0% (n = 11,326) had insurance and 9.0% (n = 1,123) were uninsured. Uninsured patients had worse condition at admission with higher rates of hypotension and higher Injury Severity Score, when compared with publicly and privately insured patients. After propensity score matching, having insurance was associated with a 32% (p = 0.001) and 54% (p < 0.001) increase in the odds of cranial procedures and monitor placement, respectively. Insurance coverage was associated with 25% lower odds of inpatient mortality (p < 0.001). Compared with insured pediatric patients with a traumatic brain injury, uninsured patients were in worse condition at admission and received fewer interventional procedures with a greater odds of inpatient mortality. Equalizing outcomes for uninsured children following traumatic brain injury requires a greater understanding of the factors that lead to worse condition at admission and policies to address treatment disparities if causality can be identified.

Troponin I as an early biomarker of cardiopulmonary parameters during the first 24 h of intensive care unit treatment in isolated traumatic brain injury patients

ObjectiveCardiopulmonary (CP) complications are well-known phenomena after an isolated traumatic brain injury (iTBI) and they may be associated with an elevated serum troponin I (TnI) value. However, the influence of an elevated TnI level on CP parameters within the first 24 h after an iTBI is still unknown. The current study was conducted to assess the associations between the initial TnI value on admission and CP parameters during the first 24 h of intensive care unit (ICU) treatment in iTBI patients. Patients and MethodsA total of 288 patients with iTBIs, who were admitted to our emergency department between January 2010 and November 2016 were retrospectively analyzed. Blood samples were taken on admission to determine TnI value. Each patient's demographic data, treatment regime, computed tomography results, and intra-hospital outcomes were evaluated, as well as several CP parameters, within the first 24 h of ICU treatment. The entire study population was stratified into patients with an initial TnI elevation (TnI positive) and without an initial TnI elevation (TnI negative). ResultsIncreased TnI values on admission were found in 59 (20.5%) patients. There were significant correlations between an initially elevated TnI value and a lower Glasgow Coma Scale score (p = 0.003), higher head Abbreviated Injury Scale score (p<0.0001), and higher Acute Physiology and Chronic Health Evaluation II score (p = 0.005) on admission, as well as a lower Glasgow Outcome Scale score (p = 0.0002) and higher modified Rankin Scale score (p = 0.0001) at discharge. In addition, a significantly higher norepinephrine application rate (NAR) (p<0.0001) and inspiratory oxygen fraction (FiO2) (p = 0.028) were needed in the TnI positive group. ConclusionPatients with elevated TnI values on admission require more circulation support (NAR and FiO2) within the first 24 h of ICU treatment after an iTBI. Therefore, the TnI may be a useful biomarker to improve ICU treatment of these patients.

Factors associated with posttraumatic meningitis among traumatic head injury patients: a nationwide study in Japan

PurposePosttraumatic meningitis is one of the severe complications that can result in increased mortality and longer hospital stay among trauma patients. Factors such as cerebrospinal fluid (CSF) fistula and basilar skull fracture are associated with posttraumatic meningitis. However, it remains unclear whether procedures such as burr hole surgery in the emergency department and decompressive craniectomy are associated with posttraumatic meningitis. The aim of this study was to assess factors associated with posttraumatic meningitis with a nationwide hospital-based trauma registry in Japan.MethodsThis was a retrospective observational study with a 12-year study period from January 2004 to December 2015. We included trauma patients registered in the Japanese Trauma Data Bank, whose head Abbreviated Injury Scale score was ≥ 3 in this study. The main endpoint was the occurrence of meningitis during hospitalization. Multivariable logistic regression analysis was used to assess independent parameters associated with posttraumatic meningitis such as CSF fistula, burr hole surgery in the emergency department, and decompressive craniectomy.ResultsAmong 60,390 head injury patients with head AIS score 3 or more, 284 (0.5%) patients had posttraumatic meningitis. Factors associated with posttraumatic meningitis were burr hole surgery in the emergency department (adjusted odds ratio [AOR] 2.158 [95% confidence interval (CI) 1.401–3.325]), decompressive craniectomy (AOR 2.123 [95% CI 1.506–2.993]), external ventricular drainage (AOR 1.843 [95% CI, 1.157–2.935]), CSF leakage (AOR 3.328 [95% CI 2.205–5.022]), and basilar skull fracture (AOR 1.651 [95% CI 1.178–2.314]).ConclusionsIn this population of trauma patients, burr hole surgery in the emergency department and decompressive craniectomy was associated with posttraumatic meningitis.

Racial disparities and the acute management of severe blunt traumatic brain injury

BackgroundTraumatic brain injury (TBI) is a significant source of morbidity and mortality. In patients with TBI, racial disparities have been shown to exist in patient outcomes. Identifying where disparities occur...

Association of Brain Atrophy and Masseter Sarcopenia With 1-Year Mortality in Older Trauma Patients

Older adults are disproportionately affected by trauma and accounted for 47% of trauma fatalities in 2016. In many populations and disease processes, described risk factors for poor clinical outcomes include sarcopenia and brain atrophy, but these remain to be fully characterized in older trauma patients. Sarcopenia and brain atrophy may be opportunistically evaluated via head computed tomography, which is often performed during the initial trauma evaluation. To investigate the association of masseter sarcopenia and brain atrophy with 1-year mortality among trauma patients older than 65 years by using opportunistic computed tomography imaging. This retrospective cohort study was conducted in a level 1 trauma center from January 1, 2011, to December 31, 2014, with a 1-year follow-up to assess mortality. Washington state residents 65 years or older who were admitted to the trauma intensive care unit with a head Abbreviated Injury Scale score of less than 3 were eligible. Patients with incomplete data and death within 1 day of admission were excluded. Data analysis was completed from June 2017 to October 2018. Masseter muscle cross-sectional area and brain atrophy index were measured using a standard clinical Picture Archiving and Communication System application to assess for sarcopenia and brain atrophy, respectively. Primary outcome was 1-year mortality. Secondary outcomes were discharge disposition and 30-day mortality. The study cohort included 327 patients; 72 (22.0%) had sarcopenia only, 71 (21.7%) had brain atrophy only, 92 (28.1%) had both, and 92 (28.1%) had neither. The mean (SD) age was 77.8 (8.6) years, and 159 patients (48.6%) were women. After adjustment for age, comorbidity, complications, and injury characteristics, masseter sarcopenia and brain atrophy were both independently and cumulatively associated with mortality (masseter muscle cross-sectional area per SD less than the mean: hazard ratio, 2.0 [95% CI, 1.2-3.1]; P = .005; brain atrophy index per SD greater than the mean: hazard ratio, 2.0 [95% CI, 1.1-3.5]; P = .02). Masseter muscle sarcopenia and brain atrophy were independently and cumulatively associated with 1-year mortality in older trauma patients after adjustment for other clinical factors. These radiologic indicators are easily measured opportunistically through standard imaging software. The results can potentially guide conversations regarding prognosis and interventions with patients and their families.

Multimodal Analgesia and Opioid Use in Critically Ill Trauma Patients

Opioids are the mainstay of pain management in critically ill trauma patients. However, the risks of opioid use mandate a different approach. Multimodal analgesia employs a combination of opioid and nonopioid agents using different mechanisms that have synergistic effects in treating pain. This study examines the effects of multimodal analgesia on the opioid requirements of critically ill trauma patients. This was a pre-post cohort study of adult trauma ICU patients before and after implementation of a multimodal pain management order set. Patients were excluded if their hospital stay was less than 5 days, head Abbreviated Injury Scale score was greater than 1, or pre-injury medications included methadone or buprenorphine. The total oral morphine equivalent (OME) dose was calculated for each 24-hour period on days 2 through 5 of admission and the last 24 hours before discharge using standardized ratios. The primary endpoint was cumulative OME doses over the second through fifth days of admission. There were 65 patients in the pre-group and 62 in the post-group. Median cumulative OME dose was significantly lower in the post-group (125.6 mg, interquartile range [IQR] 45.0 to 415.0 mg) compared with the pre-group (481.5 mg, IQR 174.8 to 881.3 mg), p < 0.001. Patients who received 3 or more multimodal agents had a lower cumulative OME dose (116.3 mg, IQR 52.5 to 496.5 mg) compared with those who were on 1 to 2 multimodal agents (363 mg, IQR 115.5 to 743 mg) or 0 multimodal agents (479 mg, IQR 185 to 736.5 mg), p= 0.024. There were no differences between pre-group and post-group mean pain scores on hospital day 5 (4.48 ± 0.34 vs 3.50 ± 0.38, p= 0.058) or at hospital discharge (3.43 ± 0.34 vs 3.56 ± 0.32, p= 0.789). Implementation of a multimodal pain management strategy significantly reduced opioid use in critically ill trauma patients without compromising patient comfort.

Can trauma surgeons keep up? A prospective cohort study comparing outcomes between patients with traumatic brain injury cared for in a trauma versus neuroscience intensive care unit

BackgroundAlthough many patients with traumatic brain injury (TBI) are admitted to trauma intensive care units (ICUs), some question whether outcomes would improve if their care was provided in neurocritical care...

Association of time to craniectomy with survival in patients with severe combat-related brain injury

OBJECTIVEIn combat and austere environments, evacuation to a location with neurosurgery capability is challenging. A planning target in terms of time to neurosurgery is paramount to inform prepositioning of neurosurgical and transport resources to support a population at risk. This study sought to examine the association of wait time to craniectomy with mortality in patients with severe combat-related brain injury who received decompressive craniectomy.METHODSPatients with combat-related brain injury sustained between 2005 and 2015 who underwent craniectomy at deployed surgical facilities were identified from the Department of Defense Trauma Registry and Joint Trauma System Role 2 Registry. Eligible patients survived transport to a hospital capable of diagnosing the need for craniectomy and performing surgery. Statistical analyses included unadjusted comparisons of postoperative mortality by elapsed time from injury to start of craniectomy, and Cox proportional hazards modeling adjusting for potential confounders. Time from injury to craniectomy was divided into quintiles, and explored in Cox models as a binary variable comparing early versus delayed craniectomy with cutoffs determined by the maximum value of each quintile (quintile 1 vs 2-5, quintiles 1-2 vs 3-5, etc.). Covariates included location of the facility at which the craniectomy was performed (limited-resource role 2 facility vs neurosurgically capable role 3 facility), use of head CT scan, US military status, age, head Abbreviated Injury Scale score, Injury Severity Score, and injury year. To reduce immortal time bias, time from injury to hospital arrival was included as a covariate, entry into the survival analysis cohort was defined as hospital arrival time, and early versus delayed craniectomy was modeled as a time-dependent covariate. Follow-up for survival ended at death, hospital discharge, or hospital day 16, whichever occurred first.RESULTSOf 486 patients identified as having undergone craniectomy, 213 (44%) had complete date/time values. Unadjusted postoperative mortality was 23% for quintile 1 (n = 43, time from injury to start of craniectomy 30-152 minutes); 7% for quintile 2 (n = 42, 154-210 minutes); 7% for quintile 3 (n = 43, 212-320 minutes); 19% for quintile 4 (n = 42, 325-639 minutes); and 14% for quintile 5 (n = 43, 665-3885 minutes). In Cox models adjusted for potential confounders and immortal time bias, postoperative mortality was significantly lower when time to craniectomy was within 5.33 hours of injury (quintiles 1-3) relative to longer delays (quintiles 4-5), with an adjusted hazard ratio of 0.28, 95% CI 0.10-0.76 (p = 0.012).CONCLUSIONSPostoperative mortality was significantly lower when craniectomy was initiated within 5.33 hours of injury. Further research to optimize craniectomy timing and mitigate delays is needed. Functional outcomes should also be evaluated.

Severely injured trauma patients with admission hyperfibrinolysis: Is there a role of tranexamic acid? Findings from the PROPPR trial.

Administration of tranexamic acid (TXA) in coagulopathy of trauma gained popularity after the CRASH-2 trial. The aim of our analysis was to analyze the role of TXA in severely injured trauma patients with admission hyperfibrinolysis. We reviewed the prospectively collected Pragmatic, Randomized Optimal Platelet and Plasma Ratios database. We included patients with admission hyperfibrinolysis (Ly30 >3%) on thromboelastography. Patients were stratified into two groups (TXA and No-TXA) and were matched in 1:2 ratio using propensity score matching for demographics, admission vitals, and injury severity. Primary outcome measures were 6-, 12-, and 24-hour and 30-day mortality; 24-hour transfusion requirements; time to achieve hemostasis; and rebleeding after hemostasis requiring intervention. Secondary outcome measures were thrombotic complications. We analyzed 680 patients. Of those, 118 had admission hyperfibrinolysis, and 93 patients (TXA: 31 patients; No-TXA: 62 patients) were matched. Matched groups were similar in age (p = 0.33), gender (p = 0.84), race (p = 0.81), emergency department (ED) Glasgow Coma Scale (p = 0.34), ED systolic blood pressure (p = 0.28), ED heart rate (p = 0.43), mechanism of injury (p = 0.45), head Abbreviated Injury Scale score (p = 0.68), injury severity score (p = 0.56), and blood products ratio (p = 0.44). Patients who received TXA had a lower 6-hour mortality rate (34% vs. 13%, p = 0.04) and higher 24-hour transfusion of plasma (15 vs. 10 units, p = 0.03) compared with the No-TXA group. However, there was no difference in 12-hour (p = 0.24), 24-hour (p = 0.25), and 30-day mortality (p = 0.82). Similarly, there was no difference in 24-hour transfusion of RBC (p = 0.11) or platelets (p = 0.13), time to achieve hemostasis (p = 0.65), rebleeding requiring intervention (p = 0.13), and thrombotic complications (p = 0.98). Tranexamic acid was associated with increased 6-hour survival but does not improve long-term outcomes in severely injured trauma patients with hemorrhage who develop hyperfibrinolysis. Moreover, TXA administration was not associated with thrombotic complications. Further randomized clinical trials will identify the subset of trauma patients who may benefit from TXA. Therapeutic study, level III.

Goal-directed platelet transfusions correct platelet dysfunction and may improve survival in patients with severe traumatic brain injury.

Platelet dysfunction, defined as adenosine diphosphate inhibition greater than 60% on thromboelastogram, is an independent predictor of increased mortality in patients with severe traumatic brain injury (TBI). We changed our practice to transfuse platelets for all patients with severe TBI and platelet dysfunction. We hypothesized that platelet transfusions would correct platelet dysfunction and improve mortality in patients with severe TBI. This retrospective review included adult trauma patients admitted to our Level I trauma center from July 2015 to October 2016 with severe TBI (head Abbreviated Injury Scale score ≥ 3) who presented with platelet dysfunction and subsequently received a platelet transfusion. Serial thromboelastograms were obtained to characterize the impact of platelet transfusion on clot strength. Subsequently, the platelet transfusion group was compared to a group of historical controls with severe TBI patients and platelet dysfunction who did not receive platelet transfusion. A total of 35 patients with severe TBI presented with platelet dysfunction. Following platelet transfusion clot strength improved as represented by decreased K time, increased α angle, maximum amplitude, and G-value, as well as correction of adenosine diphosphate inhibition. When comparing to 51 historic controls with severe TBI and platelet dysfunction, the 35 study patients who received a platelet transfusion had a lower mortality (9% vs. 35%; p = 0.005). In stepwise logistic regression, platelet transfusion was independently associated with decreased mortality (odds ratio, 0.23; 95% confidence interval, 0.06-0.92; p = 0.038). In patients with severe TBI and platelet dysfunction, platelet transfusions correct platelet inhibition and may be associated with decreased mortality. Therapeutic, level II.

Overresuscitation with plasma is associated with sustained fibrinolysis shutdown and death in pediatric traumatic brain injury.

Elevated International Normalized Ratio (INR) is a marker of poor outcome but not necessarily bleeding or clinical coagulopathy in injured children. Conversely, children with traumatic brain injury (TBI) tend to be hypercoagulable based on rapid thromboelastography (rTEG) parameters. Many clinicians continue to utilize INR as a treatment target. Prospective observational study of severely injured children age < 18 with rTEG on arrival and daily thereafter for up to 7 days. Standard rTEG definitions of hyperfibrinolysis (LY30 ≥ 3), fibrinolysis shutdown (SD) (LY30 ≤ 0.8), and normal (LY30 = 0.9-2.9) were applied. The first 24-hour blood product transfusion volumes were documented. Abbreviated Injury Scale score ≥ 3 defined severe TBI. Sustained SD was defined as two consecutive rTEG with SD and no subsequent normalization. Primary outcomes were death and functional disability, based on functional independence measure score assessed at discharge. One hundred one patients were included: median age, 8 years (interquartile range, 4-12 years); Injury Severity Score, 25 (16-30); 72% blunt mechanism; 47% severe TBI; 16% mortality; 45% discharge disability. Neither total volume nor any single product volume transfused (mL/kg; all p > 0.1) differed between TBI and non-TBI groups. On univariate analysis, transfusion of packed red blood cells (p = 0.016), plasma (p < 0.001), and platelets (p = 0.006) were associated with sustained SD; however, in a regression model that included all products (mL/kg) and controlled for severe TBI (head Abbreviated Injury Scale score ≥ 3), admission INR, polytrauma, and clinical bleeding, only plasma remained an independent predictor of sustained SD (odds ratio, 1.17; p = 0.031). Patients with both severe TBI and plasma transfusion had 100% sustained SD, 75% mortality, and 100% disability in survivors. Admission INR was elevated in TBI patients, but did not correlate with rTEG activated clotting time (p = NS) and was associated with sustained SD (p = 0.006). Plasma transfusion is independently associated with sustained fibrinolysis SD. Severe TBI is also associated with sustained SD; the combined effect of plasma transfusion and severe TBI is associated with extremely poor prognosis. Plasma transfusion should not be targeted to INR thresholds but rather to rTEG activated clotting time and clinical bleeding. Prognostic and epidemiological study, level III.

Isolated subdural hematomas in mild traumatic brain injury. Part 1: the association between radiographic characteristics and neurosurgical intervention.

Isolated subdural hematomas (iSDHs) are one of the most common intracranial hemorrhage (ICH) types in the population with mild traumatic brain injury (mTBI; Glasgow Coma Scale score 13-15), account for 66%-75% of all neurosurgical procedures, and have one of the highest neurosurgical intervention rates. The objective of this study was to examine how quantitative hemorrhage characteristics of iSDHs in patients with mTBI at admission are associated with subsequent neurosurgical intervention. This was a 3.5-year, retrospective observational cohort study at a Level I trauma center. All adult trauma patients with mTBI and iSDHs were included in the study. Maximum length and thickness (in mm) of acute SDHs, the presence of acute-on-chronic SDH, mass effect, and other hemorrhage-related variables were double-data entered; discrepant results were adjudicated after a maximum of 4 reviews. Patients with coagulopathy, skull fractures, no acute hemorrhage, a non-SDH ICH, or who did not undergo imaging on admission were excluded. The primary outcome was neurosurgical intervention (craniotomy, burr hole, catheter drainage of SDH, placement of intracranial pressure monitor, shunt, or ventriculostomy). Multivariate stepwise logistic regression was used to identify significant covariates and to assess interactions. A total of 176 patients were included in our study: 28 patients did and 148 patients did not receive a neurosurgical intervention. Increasing head Abbreviated Injury Scale score was significantly associated with neurosurgical interventions. There was a strong correlation between the first 3 reviews on maximum hemorrhage length (R2 = 0.82) and maximum hemorrhage thickness (R2 = 0.80). The neurosurgical intervention group had a mean maximum SDH length and thickness that were 61 mm longer and 13 mm thicker than those of the nonneurosurgical intervention group (p < 0.001 for both). After adjusting for the presence of an acute-on-chronic hemorrhage, for every 1-mm increase in the thickness of an iSDH, the odds of a neurosurgical intervention increase by 32% (95% CI 1.16-1.50). There were no interventions for any SDH with a maximum thickness ≤ 5 mm on initial presenting scan. This is the first study to quantify the odds of a neurosurgical intervention based on hemorrhage characteristics in patients with an iSDH and mTBI. Once validated in a second population, these data can be used to better inform patients and families of the risk of future neurosurgical intervention, and to evaluate the necessity of interhospital transfers.

Pre-Trauma Center Management of Intracranial Pressure in Severe Pediatric Traumatic Brain Injury.

Pre-trauma center care is a critical component in severe pediatric traumatic brain injury (TBI). For geographically large trauma catchment areas, optimizing increased intracranial pressure (ICP) management may potentially improve outcomes. This retrospective study examined ICP management in nontrauma centers and during interfacility transport to the trauma center. Charts from a pediatric level I trauma center were reviewed for admissions between 2008 and 2013. Patients with a Glasgow Coma Scale score of 8 or less, head Abbreviated Injury Scale score of 3 or higher, and requiring intubation at a nontrauma center were included. Exclusion criteria included head injury secondary to drowning, stroke, obstetrical complications, asphyxia, and afflicted head trauma (younger than 5 years). Trauma center charts contained coalesced data from first responders, nontrauma centers, and transport. Twenty-five patients (74%) had increased ICP upon admission at trauma center, 48% experienced ICPs greater than 20 cm H2O within 12 hours of admission, 12% required an urgent craniotomy, and 16% had herniation syndromes on neuroimaging. Pre-trauma center ICP management included osmotherapy and head-of-bed elevation. Sixty-four percent of patients with increased ICP at trauma center admission received pre-trauma center ICP management. Early increased ICP is a common presentation of severe pediatric TBI during pre-trauma center management. However, what constitutes optimal care remains unknown. Given the difficulties of diagnosing early increased ICP in this setting, prophylactic raising ICP-lowering strategies may be considered.

Impact of a statewide trauma system on the triage, transfer, and inpatient mortality of injured patients.

In 2009, Arkansas implemented a statewide trauma system to address the high rates of mortality and morbidity due to trauma. The principal objective of the Arkansas Trauma System is to transport patients to the appropriate facility based on the injuries of the patients. This study evaluated four metrics that were crucial to system health. These measures included: treatment location, scene triage, admission to nondesignated facilities, and inpatient mortality. Furthermore, the authors sought to quantify how the system is selective toward the severely injured regarding triage and treatment location. The authors hypothesized that system implementation should increase the proportion of patients, particularly the severely injured, treated at Level I/II facilities. The system should increase the proportion of patients, especially the severely injured, admitted to Level I/II facilities directly from the scene. The system should result in fewer patients admitted to nondesignated facilities. Lastly, system implementation should result in fewer inpatient deaths. A pre-post study design was used for this evaluation. Data from the Arkansas Hospital Discharge data set (2007 through 2012) identified patients who were admitted as a result of their injuries. The ICD-MAP software was used to categorize those with and without severe injuries based on an Injury Severity Score of 16 or greater or head Abbreviated Injury Scale score of 3 or greater. The results indicate that while there was an overall increase in odds of patients being admitted to Level I/II facilities, those with severe injuries were associated with an even greater odds of admission to Level I/II facilities (p < 0.0001). System implementation was also associated with more severely injured patients admitted to Level I/II facilities from the scene. There were also fewer patients admitted to nondesignated hospitals after system implementation (p < 0.0001). System implementation was associated with fewer inpatient deaths (p = 0.02). Two years after implementation, the trauma system showed significant progress. The measures evaluated in this study are believed to support the effectiveness of the trauma system. Therapeutic study, level IV.

Characterization of children hospitalized with traumatic brain injuries after building falls

BackgroundUnintentional falls cause a substantial proportion of pediatric traumatic brain injury (TBI), with building falls carrying particularly high risk for morbidity and mortality. The cohort of children sustaining building fall-related TBI has not been well-examined. We sought to characterize children hospitalized with building fall-related TBIs and evaluate if specific factors distinguished these children from children hospitalized with TBI due to other fall mechanisms. We secondarily assessed if TBI severity among children injured due to a building fall varied between children from urban versus non-urban areas.MethodsThis was a secondary analysis of the Pediatric Health Information System (PHIS), an administrative database from pediatric hospitals. We identified children < 15 years old, hospitalized between 2009 and 2014, with an associated TBI-related diagnosis due to a fall as determined by International Classification of Diseases, Clinical Modification, Ninth revision (ICD9-CM) diagnosis codes. Urban versus non-urban status was determined using PHIS-assigned Rural-Urban Commuting Area codes. Injury severity (i.e. Injury Severity Score (ISS) and head Abbreviated Injury Scale (AIS) score) were calculated. Head AIS scores were dichotomized into minor/moderate (1–2) and serious/severe (3–6) for analysis. Frequencies, descriptive statistics, Chi-square analysis, and Mann-Whitney U analysis characterized populations and determined group differences.ResultsThe study cohort included 23,813 children, of whom 933 (3.9%) fell from buildings. Within the building fall cohort, 707 (75.8%) resided in urban areas, 619 (66.3%) were male, 513 (55.0%) were white, and 528 (56.6%) had government insurance; the mean age was 3.8 years (SD 2.9). There was a larger proportion of children with serious/severe TBI among those injured from building falls relative to other falls (63.4% vs 53.9%, p < 0.01). Among children injured from building falls, those from non-urban areas were more likely to sustain a serious/severe TBI relative to urban children (58.9% vs 53.6%, p < 0.01).ConclusionsChildren hospitalized following buildings falls with TBI sustained more severe injuries relative to other fall types. Although a majority of children hospitalized with building fall related-TBIs were from urban areas, those from non-urban areas frequently sustained serious head injuries. Future research should target expanding prevention efforts to include non-urban areas.