An evaluation of the "Obesity Paradox" in isolated blunt abdominal trauma in the United States.

BACKGROUND: The obesity paradox theorizes a survival benefit in trauma patients secondary to the cushioning effect of adiposity. We aim to evaluate the impact of body mass index (BMI) on abdominal injury severity, morbidity, and mortality in adults with isolated, blunt abdominal trauma in the United States. METHODS: We reviewed the National Trauma Data Bank (2013-2021) for adults sustaining isolated, blunt abdominal trauma stratified by BMI. We performed a doubly robust, augmented inverse-propensity weighted multivariable logistic regression to estimate the average treatment effect (ATE) of BMI on mortality and the presence of abdominal organ injury. RESULTS: 36,350 patients met the inclusion criteria. In our study, 41.4 % of patients were normal-weight (BMI 18.5-24.9), 20.6 % were obese (BMI 30-39.9), and 4.7 % were severely obese (BMI≥40). In these cohorts, the abdominal abbreviated injury scale (AIS) was 2 (2 -3). Obese and severely obese patients had significantly reduced presence of pancreas, spleen, liver, kidney, and small bowel injuries. The predicted probability of abdominal AIS severity decreased significantly with increasing BMI. Crude mortality was significantly higher in obese (1.3 %) and severely obese patients (1.3 %) compared to normal-weight patients (0.7 %). Obese and severely obese patients demonstrated non-statistically significant changes in the mortality of +26.4 % (ATE 0.264, 95 %CI -0.108-0.637, p = 0.164) and +55.5 % (ATE 0.555, 95 %CI -0.284-1.394, p = 0.195) respectively, compared to normal weight patients. CONCLUSION: BMI may protect against abdominal injury in adults with isolated, blunt abdominal trauma. Mortality did not decrease in association with increasing BMI, as this may be offset by the increase in co-morbidities in this population.

Who benefits from resuscitative thoracotomies following penetrating trauma: The patient or the learner?

BACKGROUND: Resuscitative thoracotomy (RT) is a salvage procedure following traumatic cardiac arrest. We aim to evaluate RT trends and outcomes in adults with cardiac arrest following penetrating trauma to determine the effect on mortality in this population. Further, we aim to estimate the effect of hospital teaching status on the performance of resuscitative thoracotomies and mortality. METHODS: We reviewed the National Trauma Data Bank (2017-2021) for adults (≥16 years old) with penetrating trauma and prehospital cardiac arrest, stratified by the performance of a RT. We performed multivariable logistic regressions to estimate the effect of RT on mortality and the effect of hospital teaching status on the performance of resuscitative thoracotomies and mortality. RESULTS: 13,115 patients met our inclusion criteria. RT occurred in 12.7% (n = 1,664) of patients. Rates of RT trended up over the study period. Crude mortality was similar in RT and Non-RT patients (95.6% vs. 94.5%, p = 0.07). There was no statistically significant difference in the adjusted odds of mortality based on RT status (OR 0.82, 95%CI 0.56-1.21). University-teaching hospitals had an adjusted odds ratio of 1.68 (95% CI 1.31-2.17) for performing a RT than non-teaching hospitals. There was no difference in the adjusted odds of mortality in patients that underwent RT based on hospital teaching status. CONCLUSION: Despite up-trending rates, a resuscitative thoracotomy may not improve mortality in adults with penetrating, traumatic cardiac arrest. University teaching hospitals are nearly twice as likely to perform a RT than non-teaching hospitals, with no subsequent improvement in mortality.

NUCLEAR FACTOR-ERYTHROID-2-RELATED FACTOR REGULATES SYSTEMIC AND PULMONARY BARRIER FUNCTION AND IMMUNE PROGRAMMING AFTER BURN AND INHALATION INJURY.

ABSTRACT: Major burn injury is associated with systemic hyperinflammatory and oxidative stresses that encompass the wound, vascular, and pulmonary systems that contribute to complications and poor outcomes. These stresses are exacerbated if there is a combined burn and inhalation (B+I) injury, which leads to increases in morbidity and mortality. Nuclear factor-erythroid-2-related factor (NRF2) is a transcription factor that functions to maintain homeostasis during stress, in part by modulating inflammation and oxidative injury. We hypothesized that the NRF2-mediated homeostasis after burn alone and combined B-I injury is insufficient, but that pharmacological activation of the NRF2 pathway has the potential to reduce/reverse acute hyper inflammatory responses. We found that, after burn and B+I injury, Nrf2 -/- mice have higher mortality and exhibit greater pulmonary edema, vascular permeability, and exacerbated pulmonary and systemic proinflammatory responses compared with injured wild-type (WT) controls. Transcriptome analysis of lung tissue revealed specific Nrf2 -dependent dysregulated immune pathways after injury. In WT mice, we observed that B+I injury induces cytosolic, but not nuclear, accumulation of NRF2 protein in the lung microenvironment compared with sham-injured controls. Bardoxolone methyl (CDDO-Me)-containing microparticles (CDDO-MPs) were developed that allow for dilution in saline and stable release of CDDO-Me. When delivered intraperitoneally into mice 1 hour after B+I injury, CDDO-MPs significantly reduced mortality and cytokine dysfunction compared with untreated B-I animals. These data implicate the role of NRF2 regulation of pulmonary and systemic immune dysfunction after burn and B+I injury, and also a deficiency in controlling immune dysregulation. Selectively activating the NRF2 pathway may improve clinical outcomes in burn and B+I patients.

Characterization of the Basal and mTOR-Dependent Acute Pulmonary and Systemic Immune Response in a Murine Model of Combined Burn and Inhalation Injury.

Severe burn injury leads to a cascade of local and systemic immune responses that trigger an extreme state of immune dysfunction, leaving the patient highly susceptible to acute and chronic infection. When combined with inhalation injury, burn patients have higher mortality and a greater chance of developing secondary respiratory complications including infection. No animal model of combined burn and inhalation injury (B+I) exists that accurately mirrors the human clinical picture, nor are there any effective immunotherapies or predictive models of the risk of immune dysfunction. Our earlier work showed that the mechanistic/mammalian target of rapamycin (mTOR) pathway is activated early after burn injury, and its chemical blockade at injury reduced subsequent chronic bacterial susceptibility. It is unclear if mTOR plays a role in the exacerbated immune dysfunction seen after B+I injury. We aimed to: (1) characterize a novel murine model of B+I injury, and (2) investigate the role of mTOR in the immune response after B+I injury. Pulmonary and systemic immune responses to B+I were characterized in the absence or presence of mTOR inhibition at the time of injury. Data describe a murine model of B+I with inhalation-specific immune phenotypes and implicate mTOR in the acute immune dysfunction observed.

Multiplexed Human Gene Expression Analysis Reveals a Central Role of the TLR/mTOR/PPARγ and NFkB Axes in Burn and Inhalation Injury-Induced Changes in Systemic Immunometabolism and Long-Term Patient Outcomes.

Burn patients are subject to significant acute immune and metabolic dysfunction. Concomitant inhalation injury increases mortality by 20%. In order to identify specific immune and metabolic signaling pathways in burn (B), inhalation (I), and combined burn-inhalation (BI) injury, unbiased nanoString multiplex technology was used to investigate gene expression within peripheral blood mononuclear cells (PBMCs) from burn patients, with and without inhalation injury. PBMCs were collected from 36 injured patients and 12 healthy, non-burned controls within 72 h of injury. mRNA was isolated and hybridized with probes for 1342 genes related to general immunology and cellular metabolism. From these specific gene patterns, specific cellular perturbations and signaling pathways were inferred using robust bioinformatic tools. In both B and BI injuries, elements of mTOR, PPARγ, TLR, and NF-kB signaling pathways were significantly altered within PBMC after injury compared to PBMC from the healthy control group. Using linear regression modeling, (1) DEPTOR, LAMTOR5, PPARγ, and RPTOR significantly correlated with patient BMI; (2) RPTOR significantly correlated with patient length of stay, and (3) MRC1 significantly correlated with the eventual risk of patient mortality. Identification of mediators of this immunometabolic response that can act as biomarkers and/or therapeutic targets could ultimately aid the management of burn patients.

Early expression of IL-10, IL-12, ARG1, and NOS2 genes in peripheral blood mononuclear cells synergistically correlate with patient outcome after burn injury.

BACKGROUND: No methods exist to rapidly and accurately quantify the immune insult created by burn injuries. The development of a rapid, noninvasive clinical biomarker assay that evaluates a burn patient's underlying immune dysfunction and predicts clinical outcomes could transform burn care. We aimed to determine a set of peripheral biomarkers that correlates with clinical outcomes of burn patients. METHODS: This prospective observational study enrolled two patient cohorts within a single burn center into an institutionally approved institutional review board study. Blood draws were performed <48 hours after injury. Initial unbiased immune gene expression analysis compared 23 burn patients and 6 healthy controls using multiplex immune gene expression analysis of RNA from peripheral blood mononuclear cells. We then performed confirmatory outcomes analysis in 109 burn patients and 19 healthy controls using a targeted rapid quantitative polymerase chain reaction. Findings were validated and modeled associations with clinical outcomes using a regression model. RESULTS: A total of 149 genes with a significant difference in expression from burn patients compared with controls were identified. Pathway analysis identified pathways related to interleukin (IL)-10 and inducible nitric oxide synthase signaling to have significant z scores. quantitative polymerase chain reaction analysis of IL-10, IL-12, arginase 1 (ARG1), and inducible nitric oxide synthase demonstrated that burn injury was associated with increased expression of ARG1 and IL-10, and decreased expression of nitric oxide synthase 2 (NOS2) and IL-12. Burn severity, acute lung injury, development of infection, failure of skin autograft, and mortality significantly correlated with expression of one or more of these genes. Ratios of IL-10/IL-12, ARG1/NOS2, and (ARG1-IL-10)/(NOS2-IL-12) transcript levels further improved the correlation with outcomes. Using a multivariate regression model, adjusting for patient confounders demonstrated that (ARG1-IL-10)/(NOS2-IL-12) significantly correlated with burn severity and development of acute lung injury. CONCLUSION: We present a means to predict patient outcomes early after burn injury using peripheral blood, allowing early identification of underlying immune dysfunction. LEVEL OF EVIDENCE: Prognostic/Epidemiological; Level II.

Peritraumatic Plasma Omega-3 Fatty Acid Concentration Predicts Chronic Pain Severity Following Thermal Burn Injury.

Chronic pain is a significant comorbidity of burn injury affecting up to 60% of survivors. Currently, no treatments are available to prevent chronic pain after burn injury. Accumulating evidence suggests that omega-3 fatty acids (O3FAs) improve symptoms across a range of painful conditions. In this study, we evaluated whether low peritraumatic levels of O3FA predict greater pain severity during the year after burn injury. Burn survivors undergoing skin autograft were recruited from three participating burn centers. Plasma O3FA (n = 77) levels were assessed in the early aftermath of burn injury using liquid chromatography/mass spectrometry, and pain severity was assessed via the 0 to 10 numeric rating scale for 1 year following burn injury. Repeated-measures linear regression analyses were used to evaluate the association between peritraumatic O3FA concentrations and pain severity during the year following burn injury. Peritraumatic O3FA concentration and chronic pain severity were inversely related; lower levels of peritraumatic O3FAs predicted worse pain outcomes (ß = -0.002, P = .020). Future studies are needed to evaluate biological mechanisms mediating this association and to assess the ability of O3FAs to prevent chronic pain following burn injury.

Plasma extracellular vesicles released after severe burn injury modulate macrophage phenotype and function.

Extracellular vesicles (EVs) have emerged as key regulators of immune function across multiple diseases. Severe burn injury is a devastating trauma with significant immune dysfunction that results in an ∼12% mortality rate due to sepsis-induced organ failure, pneumonia, and other infections. Severe burn causes a biphasic immune response: an early (0-72 h) hyper-inflammatory state, with release of damage-associated molecular pattern molecules, such as high-mobility group protein 1 (HMGB1), and proinflammatory cytokines (e.g., IL-1ß), followed by an immunosuppressive state (1-2+ wk post injury), associated with increased susceptibility to life-threatening infections. We have reported that early after severe burn injury HMGB1 and IL-1ß are enriched in plasma EVs. Here we tested the impact of EVs isolated after burn injury on phenotypic and functional consequences in vivo and in vitro using adoptive transfers of EV. EVs isolated early from mice that underwent a 20% total body surface area burn injury (burn EVs) caused similar hallmark cytokine responses in naïve mice to those seen in burned mice. Burn EVs transferred to RAW264.7 macrophages caused similar functional (i.e., cytokine secretion) and immune gene expression changes seen with their associated phase of post-burn immune dysfunction. Burn EVs isolated early (24 h) induced MCP-1, IL-12p70, and IFNγ, whereas EVs isolated later blunted RAW proinflammatory responses to bacterial endotoxin (LPS). We also describe significantly increased HMGB1 cargo in burn EVs purified days 1 to 7 after injury. Thus, burn EVs cause immune outcomes in naïve mice and macrophages similar to findings after severe burn injury, suggesting EVs promote post-burn immune dysfunction.

Burn Injury Induces Proinflammatory Plasma Extracellular Vesicles That Associate with Length of Hospital Stay in Women: CRP and SAA1 as Potential Prognostic Indicators.

Severe burn injury is a devastating form of trauma that results in persistent immune dysfunction with associated morbidity and mortality. The underlying drivers of this immune dysfunction remain elusive, and there are no prognostic markers to identify at-risk patients. Extracellular vesicles (EVs) are emerging as drivers of immune dysfunction as well as biomarkers. We investigated if EVs after burn injury promote macrophage activation and assessed if EV contents can predict length of hospital stay. EVs isolated early from mice that received a 20% total body surface area (TBSA) burn promoted proinflammatory responses in cultured splenic macrophages. Unbiased LC-MS/MS proteomic analysis of early EVs (<72 h post-injury) from mice and humans showed some similarities including enrichment of acute phase response proteins such as CRP and SAA1. Semi-unbiased assessment of early human burn patient EVs found alterations consistent with increased proinflammatory signaling and loss of inhibition of CRP expression. In a sample of 50 patients with large burn injury, EV SAA1 and CRP were correlated with TBSA injury in both sexes and were correlated with length of hospital stay in women. These findings suggest that EVs are drivers of immune responses after burn injury and their content may predict hospital course.

Peritraumatic 17ß-estradiol levels influence chronic posttraumatic pain outcomes.

ABSTRACT: Biologic factors that predict risk for and mediate the development of common outcomes of trauma exposure such as chronic posttraumatic pain (CPTP) are poorly understood. In the current study, we examined whether peritraumatic circulating 17ß-estradiol (E2) levels influence CPTP trajectories. 17ß-estradiol levels were measured in plasma samples (n = 254) collected in the immediate aftermath of trauma exposure from 3 multiethnic longitudinal cohorts of men and women trauma survivors. Chronic posttraumatic pain severity was evaluated 6 weeks, 6 months, and 1 year after traumatic stress exposure. Repeated measures mixed models were used to test the relationship between peritraumatic E2 levels and prospective CPTP. Secondary analyses in a nested cohort assessed the influence of participant body mass index on the E2-CPTP relationship. In women, a statistically significant inverse relationship between peritraumatic E2 and CPTP was observed (ß = -0.280, P = 0.043) such that higher E2 levels predicted lower CPTP severity over time. Secondary analyses identified an E2 * body mass index interaction in men from the motor vehicle collision cohort such that obese men with higher E2 levels were at greater risk of developing CPTP. In nonobese men from the motor vehicle collision cohort and in men from the major thermal burn injury cohort, no statistically significant relationship was identified. In conclusion, peritraumatic circulating E2 levels predict CPTP vulnerability in women trauma survivors. In addition, these data suggest that peritraumatic administration of E2 might improve CPTP outcomes for women; further research is needed to test this possibility.

Peritraumatic Vitamin D Levels Predict Chronic Pain Severity and Contribute to Racial Differences in Pain Outcomes Following Major Thermal Burn Injury.

Major thermal burn injuries result in approximately 40,000 hospitalizations in the United States each year. Chronic pain affects up to 60% of burn survivors, and Black Americans have worse chronic pain outcomes than White Americans. Mechanisms of chronic pain pathogenesis after burn injury, and accounting for these racial differences, remain poorly understood. Due to socioeconomic disadvantage and differences in skin absorption, Black Americans have an increased prevalence of Vitamin D deficiency. We hypothesized that peritraumatic Vitamin D levels predict chronic pain outcomes after burn injury and contribute to racial differences in pain outcomes. Among burn survivors (n = 77, 52% White, 48% Black, 77% male), peritraumatic Vitamin D levels were more likely to be deficient in Blacks vs Whites (27/37 [73%] vs 14/40 [35%], P < .001). Peritraumatic Vitamin D levels were inversely associated with chronic post-burn pain outcomes across all burn injury survivors, including those who were and were not Vitamin D deficient, and accounted for approximately one-third of racial differences in post-burn pain outcome. Future studies are needed to evaluate potential mechanisms mediating the effect of Vitamin D on post-burn pain outcomes and the potential efficacy of Vitamin D in improving pain outcomes and reducing racial differences.

The effect of neighborhood Area Deprivation Index on residential burn injury severity.

INTRODUCTION: Residential fires account for the majority of burn-related injuries and fatalities. Established risk factors for burn injury include male gender, racial minority, children and elderly individuals, poverty, and substandard housing characteristics. In North Carolina, the rate of residential fire injuries and deaths is higher than the national average. Therefore, we sought to describe residential fire hospitalizations at a large regional burn center and describe the neighborhoods in which they live. We hypothesized that patients living in areas with higher Area Deprivation Index (ADI) are more likely to have major residential burns. METHODS: We conducted a retrospective analysis of burn admissions from January 2002 to December 2015. We dichotomized patients into two cohorts: residential and non-residential burns and performed a bivariate analysis. Multivariate Poisson regression models were utilized to determine if ADI was associated with inhalation injury and ≥20% total body surface area burn. RESULTS: Of the 10,506 patients presented during the study period. Of these, 10,016 (95.3%) patients resided in North Carolina, and 7894 (78.8%) had a residential burn. Of the overall cohort, 6.0% (n=458) of patients had ≥20% TBSA burns and 6.4% (n=506) had inhalation injury. The majority of patients were in the highest (most disadvantaged) ADI quartile (n=3050, 39.5%), and only 6.8% of patients (n=525) were in the lowest (least disadvantaged) ADI quartile. In the Poisson multivariate regressions to determine if the ADI was associated with severe burns, patients in the highest ADI quartile had an increased relative risk of ≥20% TBSA burn (RR 1.31, 95% CI 1.02-1.68) and inhalation injury (RR 1.39, 95% CI 1.09-1.76) when compared to patients in the second-lowest ADI quartile when controlled for pertinent covariates. CONCLUSION: Residential structure fires represent the major source of burns and fatalities. People who reside in the highest ADI quartile are more like to present with higher burn injury severity in terms of burn size and the presence of inhalation injury. The use of the ADI to target neighborhoods for burn prevention is imperative.

The effect of burn mechanism on pediatric mortality in Malawi: A propensity weighted analysis.

INTRODUCTION: The burden of global trauma disproportionately affects low- and middle-income countries, with a high incidence in children. Thermal injury represents one of the most severe forms of trauma and is associated with remarkable morbidity and mortality. The predictors of burn mortality have been well described (age, % total body surface area burn [TBSA], and presence of inhalation injury). However, the contribution of the burn mechanism as a predictor of burn mortality is not well delineated. METHODS: This is a retrospective analysis of prospectively collected data, utilizing the Kamuzu Central Hospital (KCH) Burn Surveillance Registry from May 2011 to August 2019. Pediatric patients (≤12 years) with flame and scald burns were included in the study. Basic demographic variables including sex, age, time to presentation, %TBSA, surgical intervention, burn mechanism, and in-hospital mortality outcome was collected. Bivariate analysis comparing demographic, burn characteristics, surgical intervention, and patient outcomes were performed. Standardized estimates were adjusted using inverse-probability of treatment weights (IPTW) to account for confounding. Following weighting, logistic regression modeling was performed to determine the odds of in-hospital mortality based on burn mechanism. RESULTS: During the study period, 2364 patients presented to KCH for burns and included in the database with 1794 (75.9%) pediatric patients. Of these, 488 (27.6%) and 1280 (72.4%) were injured by flame and scald burns, respectively. Males were 47.2% (n = 230) and 59.2% (n = 755) of the flame and scald burn cohorts, respectively (p < 0.001.) Patients presenting with flame burns compared to scald burns were older (4. 7 ± 3.1 vs. 2.7 ± 2.3 years, p < 0.001) with greater %TBSA burns (17.8 [IQR 10-28] vs 12 [IQR 7-20], p < 0.001). Surgery was performed for 42.2% (n = 206) and 19.9% (n = 140) of the flame and scald burn cohorts, respectively (p < 0.001.) Flame burns had a 2.6x greater odds of in-hospital mortality compared to scald burns (p < 0.001) after controlling for sex, %TBSA, age, time to presentation, and surgical status. CONCLUSION: In this propensity-weighted analysis, we show that burn mechanism, specifically flame burns, resulted in a nearly 3-fold increase in odds of in-hospital mortality compared to scald burns. Our results emphasize flame and scald burns have major differences in the inflammatory response, metabolic profile over time, and outcomes. We may further utilize these differences to develop specialized treatments for each burn mechanism to potentially prevent metabolic dysfunction and improve clinical outcomes.

Work-Related Burn Injuries in a Tertiary Care Burn Center, 2013 to 2018.

The features of work-related burn (WRB) injuries are not well defined in the literature and they vary depending on geographical location. We wanted to describe these characteristics among patients treated in the UNC Burn Center to evaluate the potential impact of commonly accepted prevention efforts. Adults of working age, admitted between January 1, 2013, and December 31, 2018, were identified using our Burn Center Registry. Demographic data, characteristics of injury, course of treatment, and patients' outcomes were described. Differences between work-related and non-work-related injuries were evaluated using the Chi-square test and Student t-test where appropriate. Three thousand five hundred and forty-five patients were included. WRB cases constituted 18% of the study population, and this proportion remained relatively stable during the study timeframe. Young white males were the majority of this group. When compared with non-WRB patients, they were characterized by fewer co-morbidities, decreased TBSA burns, decreased risk of inhalation injury, shorter time of intensive care treatment, shorter lengths of hospital stay, and lower treatment cost. In contrast to non-WRB, among which flame injuries were the main reason for admission, work-related patients most often suffered scald burns. They also had a dramatically increased proportion of chemical and electrical burns, making the latter the most common cause of death in that group. WRB are characterized by a characteristic patient profile, burn etiologies, and outcomes. Learning specific patterns at this group may contribute to optimize work safety regulations and medical interventions.

The epidemiologic characteristics and outcomes following intentional burn injury at a regional burn center.

INTRODUCTION: Intentional burn injury outcomes are usually more severe, have a high mortality and are seen more often in low and middle-income countries. This study will examine the epidemiological characteristics of intentional burn injury patients and mortality outcomes at a regional Burn Center. METHODS: This is a retrospective study of 11,977 patients admitted to a regional Burn center from 2002 to 2015.Variables analyzed were basic demographics (sex, age, and race), total body surface area of burn (%TBSA), presence of inhalation injury, Charlson comorbidity index, intent of injury, mortality, and hospital and ICU length of stay (LOS). Chi-square tests, bivariate analysis and logistic regression models were utilized to determine the effect of burn intent on outcomes. RESULTS: Eleven thousand eight hundred and twenty-three (n = 11,823) adult and pediatric patients from 2002 to 2015 were included in the study. Three hundred and forty-eight (n = 348, 2.9%) patients had intentional burn injuries (IBI). Patients with IBI were younger, 26.5 ± 20 years compared to the non-intentional burn injury (NIBI) group (32 ± 22 years, p < 0.001). Mean %TBSA was significantly higher in the IBI vs. NIBI group at 14.6 ± 20 vs. 6.4 ± 10%, p < 0.001, respectively. Overall, Non-whites (n = 230, 66%) were more likely to have IBI, p < 0.001. Inhalation injury and mortality were statistically significant in the IBI group compared to the NIBI group, (n = 54,16%) vs. (n = 30, 9%) and (n = 649,6%) vs. (n = 329,2.9%), p < 0.001, respectively. Multivariate logistic regression did not show any significant increase in odds of mortality based on burn intent. In subgroup analysis of self-inflicted (SIB) vs. assault burns, SIB patients were significantly older, 38 years (±14.7) vs. 22.4 years (±20.5), p < 0.001 and had a higher %TBSA, 26.5 (±29.6) vs. 10.3 (±13.6), p < 0.001. Seventy three percent (n = 187, 73%) of assault burn patients were Nonwhite and Whites were more likely to incur self-inflicted burns, (n = 53% p < 0.001). CONCLUSION: We show that patients with intentional burn injuries have an associated increased %TBSA and inhalation injury without increased adjusted odds for mortality. Intentional burns increase health care expenditures. Violence prevention initiatives and access to mental health providers may be beneficial in reducing intentional burn injury burden.

Acuity Is Seasonal in a Tertiary Care Burn Center.

Supply and demand dictate resource allocation in large academic institutions. Classic teaching is that burns is a seasonal specialty with winter being the "busiest" time of year. Resident allocation during the winter and summer months, however, is traditionally low due to the holidays and travel peaks. Our objective was to evaluate our acuity-defined as patient complexity-based on seasons, in order to petition for appropriate mid-level provider allocation. We performed a retrospective review of all admissions to an accredited, large academic burn center. All patients admitted between January 1, 2009 and December 31, 2018 were eligible for inclusion. Demographics, length of stay, injury characteristics, and mortality were evaluated. Thirteen thousand four hundred fifty-eight patients were admitted during this study period. Most patients were admitted during the summer. Patients admitted to the intensive care unit were more likely to be admitted in the winter, although this was not statistically significant. Winter admissions had the longest lengths of stay, and the highest incidence of inhalation injury. Female and elderly patients were more likely admitted during the winter. There was a significant difference in mortality between summer and winter seasons. Acuity is seasonal in our large academic burn center and resource allocation should align with the needs of the patients. This data may help large centers petition their institutions for more consistent experienced mid-level providers, specifically during critical seasons.

Sex-Based Differences in Inpatient Burn Mortality.

BACKGROUND: Among burn patients, research is conflicted, but may suggest that females are at increased risk of mortality, despite the opposite being true in non-burn trauma. Our objective was to determine whether sex-based differences in burn mortality exist, and assess whether patient demographics, comorbid conditions, and injury characteristics explain said differences. METHODS: Adult patients admitted with burn injury-including inhalation injury only-between 2004 and 2013 were included. Inverse probability of treatment weights (IPTW) and inverse probability of censor weights (IPCW) were calculated using admit year, patient demographics, comorbid conditions, and injury characteristics to adjust for potential confounding and informative censoring. Standardized Kaplan-Meier survival curves, weighted by both IPTW and IPCW, were used to estimate the 30-day and 60-day risk of inpatient mortality across sex. RESULTS: Females were older (median age 44 vs. 41 years old, p < 0.0001) and more likely to be Black (32% vs. 25%, p < 0.0001), have diabetes (14% vs. 10%, p < 0.0001), pulmonary disease (14% vs. 7%, p < 0.0001), heart failure (4% vs. 2%, p = 0.001), scald burns (45% vs. 26%, p < 0.0001), and inhalational injuries (10% vs. 8%, p = 0.04). Even after weighting, females were still over twice as likely to die after 60 days (RR 2.87, 95% CI 1.09, 7.51). CONCLUSION: Female burn patients have a significantly higher risk of 60-day mortality, even after accounting for demographics, comorbid conditions, burn size, and inhalational injury. Future research efforts and treatments to attenuate mortality should account for these sex-based differences. The project was supported by the National Institutes of Health, Grant Number UL1TR001111.

The Effect of Pre-existing Seizure Disorders on Mortality and Hospital Length of Stay Following Burn Injury.

Patients with a seizure disorder have a higher incidence of burn injury; however, there are limited studies that examine the association between pre-existing seizure disorders (PSD) and burn outcomes. This is a retrospective study of admitted burn patients. Variables analyzed include patient demographics, clinical characteristics, associated PSD, hospital length of stay (LOS), and mortality. Multivariate logistic regression was performed to analyze the impact of PSD on burn mortality and LOS. Seven thousand six hundred and forty patients met the inclusion criteria and 1.31% (n = 100) patients had a PSD. There was no difference in mortality rate between patients with or without PSD (odds ratio [OR] = 2.28, 95% confidence interval [CI] = 0.87 to 5.93). Multivariate logistic regression showed that patients with PSD had significantly increased odds of longer hospital LOS (OR = 2.85, 95% CI = 1.73 to 4.67). Seizure disorder management is mandatory in reducing burn injury and decreasing the costs associated with increased hospital LOS.