Professionalism of Admitting and Consulting Services and Trauma Patient Outcomes.

OBJECTIVE: To determine whether trauma patients managed by an admitting or consulting service with a high proportion of physicians exhibiting patterns of unprofessional behaviors are at greater risk of complications or death. SUMMARY BACKGROUND DATA: Trauma care requires high-functioning interdisciplinary teams where professionalism, particularly modeling respect and communicating effectively, is essential. METHODS: This retrospective cohort study used data from 9 level I trauma centers that participated in a national trauma registry linked with data from a national database of unsolicited patient complaints. The cohort included trauma patients admitted January 1, 2012 through December 31, 2017. The exposure of interest was care by 1 or more high-risk services, defined as teams with a greater proportion of physicians with high numbers of patient complaints. The study outcome was death or complications within 30 days. RESULTS: Among the 71,046 patients in the cohort, 9553 (13.4%) experienced the primary outcome of complications or death, including 1875 of 16,107 patients (11.6%) with 0 high-risk services, 3788 of 28,085 patients (13.5%) with 1 high-risk service, and 3890 of 26,854 patients (14.5%) with 2+ highrisk services (P < 0.001). In logistic regression models adjusting for relevant patient, injury, and site characteristics, patients who received care from 1 or more high-risk services were at 24.1% (95% confidence interval 17.2% to 31.3%; P < 0.001) greater risk of experiencing the primary study outcome. CONCLUSIONS: Trauma patients who received care from at least 1 service with a high proportion of physicians modeling unprofessional behavior were at an increased risk of death or complications.

Predicting risk of postoperative lung injury in high-risk surgical patients: a multicenter cohort study.

BACKGROUND: Acute respiratory distress syndrome (ARDS) remains a serious postoperative complication. Although ARDS prevention is a priority, the inability to identify patients at risk for ARDS remains a barrier to progress. The authors tested and refined the previously reported surgical lung injury prediction (SLIP) model in a multicenter cohort of at-risk surgical patients. METHODS: This is a secondary analysis of a multicenter, prospective cohort investigation evaluating high-risk patients undergoing surgery. Preoperative ARDS risk factors and risk modifiers were evaluated for inclusion in a parsimonious risk-prediction model. Multiple imputation and domain analysis were used to facilitate development of a refined model, designated SLIP-2. Area under the receiver operating characteristic curve and the Hosmer-Lemeshow goodness-of-fit test were used to assess model performance. RESULTS: Among 1,562 at-risk patients, ARDS developed in 117 (7.5%). Nine independent predictors of ARDS were identified: sepsis, high-risk aortic vascular surgery, high-risk cardiac surgery, emergency surgery, cirrhosis, admission location other than home, increased respiratory rate (20 to 29 and ≥30 breaths/min), FIO2 greater than 35%, and SpO2 less than 95%. The original SLIP score performed poorly in this heterogeneous cohort with baseline risk factors for ARDS (area under the receiver operating characteristic curve [95% CI], 0.56 [0.50 to 0.62]). In contrast, SLIP-2 score performed well (area under the receiver operating characteristic curve [95% CI], 0.84 [0.81 to 0.88]). Internal validation indicated similar discrimination, with an area under the receiver operating characteristic curve of 0.84. CONCLUSIONS: In this multicenter cohort of patients at risk for ARDS, the SLIP-2 score outperformed the original SLIP score. If validated in an independent sample, this tool may help identify surgical patients at high risk for ARDS.

The COST of liver disease: The Cirrhosis Outcomes Score in Trauma Study.

BACKGROUND: Cirrhosis in trauma patients is an indicator of poor prognosis, but current trauma injury grading systems do not take into account liver dysfunction as a risk factor. Our objective was to construct a simple clinical mortality prediction model in cirrhotic trauma patients: Cirrhosis Outcomes Score in Trauma (COST). METHODS: Trauma patients with pre-existing cirrhosis or liver dysfunction who were admitted to our ACS Level I trauma center between 2013 and 2021 were reviewed. Patients with significant acute liver trauma (AAST Grade ≥ 3) or those that developed acute liver dysfunction while admitted were excluded. Demographics as well as ISS, MELD, complications, and mortality were evaluated. COST was defined as the sum of age, ISS, and MELD. Univariate and multivariable analysis was used to determine independent predictors of mortality. The area under the receiver operating curve (AUROC) was calculated to assess the ability of COST to predict mortality. RESULTS: A total of 318 patients were analyzed of which the majority were males 214 (67.3%) who suffered blunt trauma 305 (95.9%). Mortality at 30-days, 60-days, and 90-days was 20.4%, 23.6%, and 25.5%, respectively. COST was associated with inpatient, 30-day, and 90-day mortality on regression analyses and the AUROC for COST predicting mortality at these respective time points was 0.810, 0.801, and 0.813. CONCLUSION: Current trauma injury grading systems do not take into account liver dysfunction as a risk factor. COST is highly predictive of mortality in cirrhotic trauma patients. The simplicity of the score makes it useful in guiding clinical care and in optimizing goals of care discussions. Future studies to validate this prediction model are required prior to clinical use.

Type I interferon signaling regulates the composition of inflammatory infiltrates upon infection with Listeria monocytogenes.

Type I IFN is key to the immune response to viral pathogens, however its role in bacterial infections is less well understood. Mice lacking the type I IFN receptor (IFNAR-/-) demonstrate enhanced resistance to infection with Listeriamonocytogenes. We have now determined that following infection with Listeria, the composition of innate cells recruited to the peritoneal cavity of IFNAR-/- mice reflects an increase in the frequency of neutrophils and a decrease in monocyte frequency compared to WT controls. These differences in inflammatory infiltrates could not be attributed to distinct bone marrow composition prior to infection or to level of apoptosis. We also observed no differences in neutrophil oxidative burst. However, blocking CXCR2 prevented enhanced neutrophil influx and hampered bacterial clearance. Taken together, these studies highlight a novel mechanism by which type I interferon signaling regulates the immune response to Listeria, through negative regulation of chemokines driving neutrophil recruitment.

Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study.

RATIONALE: Accurate, early identification of patients at risk for developing acute lung injury (ALI) provides the opportunity to test and implement secondary prevention strategies. OBJECTIVES: To determine the frequency and outcome of ALI development in patients at risk and validate a lung injury prediction score (LIPS). METHODS: In this prospective multicenter observational cohort study, predisposing conditions and risk modifiers predictive of ALI development were identified from routine clinical data available during initial evaluation. The discrimination of the model was assessed with area under receiver operating curve (AUC). The risk of death from ALI was determined after adjustment for severity of illness and predisposing conditions. MEASUREMENTS AND MAIN RESULTS: Twenty-two hospitals enrolled 5,584 patients at risk. ALI developed a median of 2 (interquartile range 1-4) days after initial evaluation in 377 (6.8%; 148 ALI-only, 229 adult respiratory distress syndrome) patients. The frequency of ALI varied according to predisposing conditions (from 3% in pancreatitis to 26% after smoke inhalation). LIPS discriminated patients who developed ALI from those who did not with an AUC of 0.80 (95% confidence interval, 0.78-0.82). When adjusted for severity of illness and predisposing conditions, development of ALI increased the risk of in-hospital death (odds ratio, 4.1; 95% confidence interval, 2.9-5.7). CONCLUSIONS: ALI occurrence varies according to predisposing conditions and carries an independently poor prognosis. Using routinely available clinical data, LIPS identifies patients at high risk for ALI early in the course of their illness. This model will alert clinicians about the risk of ALI and facilitate testing and implementation of ALI prevention strategies. Clinical trial registered with www.clinicaltrials.gov (NCT00889772).

Duration of Antibiotic Therapy in Necrotizing Soft Tissue Infections: Shorter is Safe.

Background: Early debridement improves outcome in necrotizing soft tissue infection (NSTI), but there is no consensus on duration of antimicrobial therapy. We recently changed practice to discontinue antibiotic agents early with a goal of 48 hours after adequate source control. We hypothesized that discontinuing antibiotic agents after a short course is safe in the treatment of NSTI. Patients and Methods: This was a prospective study of patients with NSTI comparing short duration of antibiotic agents to a control population after a change in practice. In 2018 we began discontinuing antibiotic agents within 48 hours of source control (absence of cellulitis and no evidence of active infection). Previously, antibiotic duration was at the discretion of the attending surgeon (generally 7-10 days). Patients were excluded from analysis if they were initially debrided at a referring facility, immune compromised, or died prior to source control. Patient characteristics and outcomes were evaluated. The primary outcome was treatment failure requiring antibiotic agents to be restarted with or without further debridement of infected tissue. Secondary outcomes included the duration of antibiotic therapy after source control. Results: We evaluated 151 patients; 119 admitted between January 1, 2011 and January 31, 2018 (PRE) and 32 admitted after January 31, 2018 (POST). Patients were not statistically different regarding characteristics, admission physiologic variables, and comorbidities. The median duration of antibiotic agents after source control in the PRE group was 180.3 hours (interquartile range [IQR], 100.7-318.8) versus 48 hours (IQR, 32.3-100.8) in the POST group (p < 0.01). Patients in each group were treated as described above, and treatment failure occurred in seven (5.9%) PRE patients and two (6.3%) POST (99.3% post hoc power at non-inferiority limit 20%, significance p < 0.05). Thirty-day all-cause mortality was not different between groups (6.7% vs. 6.3%; p = 0.94). Conclusions: Short-duration (48 hours) antibiotic agents after NSTI source control is as safe and effective as a longer course.

Emergency department length of stay is an independent predictor of hospital mortality in trauma activation patients.

BACKGROUND: The early resuscitation occurs in the emergency department (ED) where intensive care unit protocols do not always extend and monitoring capabilities vary. Our hypothesis is that increased ED length of stay (LOS) leads to increased hospital mortality in patients not undergoing immediate surgical intervention. METHODS: We examined all trauma activation admissions from January 2002 to July 2009 admitted to the Trauma Service (n = 3,973). Exclusion criteria were as follows: patients taken to the operating room within the first 2 hours of ED arrival, nonsurvivable brain injury, and ED deaths. Patients spending >5 hours in the ED were not included in the analysis because of significantly lower acuity and mortality. RESULTS: Patients spent a mean of 3.2 hours ± 1 hour in the ED during their initial evaluation. Hospital mortality increases for each additional hour a patient spends in the ED, with 8.3% of the patients staying in the ED between 4 hours and 5 hours ultimately dying (p = 0.028). ED LOS measured in minutes is an independent predictor of mortality (odds ratio, 1.003; 95% confidence interval, 1.010-1.006; p = 0.014) when accounting for Injury Severity Score, Revised Trauma Score, and age. Linear regression showed that a longer ED LOS was associated with anatomic injury pattern rather than physiologic derangement. CONCLUSION: In this patient population, a longer ED LOS is associated with an increased hospital mortality even when controlling for physiologic, demographic, and anatomic factors. This highlights the importance of rapid progression of patients through the initial evaluation process to facilitate placement in a location that allows implementation of early goal directed trauma resuscitation.

SIRT1 Mediates Septic Cardiomyopathy in a Murine Model of Polymicrobial Sepsis.

BACKGROUND: Cardiac dysfunction, a common complication from severe sepsis, is associated with increased morbidity and mortality. However, the molecular mechanisms of septic cardiac dysfunction are poorly understood. SIRT1, a member of the sirtuin family of NAD+-dependent protein deacetylases, is an important immunometabolic regulator of sepsis, and sustained SIRT1 elevation is associated with worse outcomes and organ dysfunction in severe sepsis. Herein, we explore the role of SIRT1 in septic cardiac dysfunction using a murine model of sepsis. METHODS: An in vitro model of inflammation in isolated H9c2 cardiomyocytes was used to confirm SIRT1 response to stimulation with lipopolysaccharide (LPS), followed by a murine model of cecal ligation and puncture (CLP) to investigate the molecular and echocardiographic response to sepsis. A selective SIRT1 inhibitor, EX-527, was employed to test for SIRT1 participation in septic cardiac dysfunction. RESULTS: SIRT1 mRNA and protein levels in cultured H9c2 cardiomyocytes were significantly elevated at later time points after stimulation with LPS. Similarly, cardiac tissue harvested from C57BL/6 mice 36 h after CLP demonstrated increased expression of SIRT1 mRNA and protein compared with sham controls. Administration of EX-527 18 h after CLP reduced SIRT1 protein expression in cardiac tissue at 36 h. Moreover, treatment with EX-527 improved cardiac performance with increased global longitudinal strain and longitudinal strain rate. CONCLUSIONS: Our findings reveal that SIRT1 expression increases in isolated cardiomyocytes and cardiac tissue after sepsis inflammation. Moreover, rebalancing SIRT1 excess in late sepsis improves cardiac performance, suggesting that SIRT1 may serve as a therapeutic target for septic cardiomyopathy.

Pulmonary contusion primes systemic innate immunity responses.

INTRODUCTION: Traumatic injury may result in an exaggerated response to subsequent immune stimuli such as nosocomial infection. This "second hit" phenomenon and molecular mechanism(s) of immune priming by traumatic lung injury, specifically, pulmonary contusion, remain unknown. We used an animal model of pulmonary contusion to determine whether the injury resulted in priming of the innate immune response and to test the hypothesis that resuscitation fluids could attenuate the primed response to a second hit. METHODS: Male, 8 to 9 weeks, C57/BL6 mice with a pulmonary contusion were challenged by a second hit of intratracheal administration of the Toll-like receptor 4 agonist, lipopolysaccharide (LPS, 50 microg) 24 hours after injury (injury + LPS). Other experimental groups were injury + vehicle or LPS alone. A separate group was injured and resuscitated by 4 cc/kg of hypertonic saline (HTS) or Lactated Ringer's (LR) resuscitation before LPS challenge. Mice were killed 4 hours after LPS challenge and blood, bronchoalveolar lavage, and tissue were isolated and analyzed. Data were analyzed using one-way analysis of variance with Bonferroni multiple comparison posttest for significant differences (*p < or = 0.05). RESULTS: Injury + LPS showed immune priming observed by lung injury histology and increased bronchoalveolar lavage neutrophilia, lung myeloperoxidase and serum IL-6, CXCL1, and MIP-2 levels when compared with injury + vehicle or LPS alone. After injury, resuscitation with HTS, but not Lactated Ringer's was more effective in attenuating the primed response to a second hit. CONCLUSION: Pulmonary contusion primes innate immunity for an exaggerated response to a second hit with the Toll-like receptor 4 agonist, LPS. We observed synergistic increases in inflammatory mediator expression in the blood and a more severe lung injury in injured animals challenged with LPS. This priming effect was reduced when HTS was used to resuscitate the animal after lung contusion.

Characterization of crash-induced thoracic loading resulting in pulmonary contusion.

BACKGROUND: Pulmonary contusion (PC) is commonly sustained in motor vehicle crash. This study utilizes the Crash Injury Research and Engineering Network (CIREN) database and vehicle crash tests to characterize the occupants and loading characteristics associated with PC. A technique to match CIREN cases to vehicle crash tests is applied to quantify the thoracic loading associated with this injury. METHODS: The CIREN database and crash test data from the National Highway Traffic Safety Administration were used in this study. An analysis of CIREN data were conducted between three study cohorts: patients that sustained PC and any other chest injury (PC+ and chest+), patients with chest injury and an absence of PC (PC- and chest+), and a control group without chest injury and an absence of PC (PC- and chest-). Forty-one lateral impact crash tests were analyzed and thoracic loading data from onboard crash tests dummies were collected. RESULTS: The incidence of PC in CIREN data were 21.7%. Crashes resulting in PC demonstrated significantly greater mortality (23.9%) and Injury Severity Score (33.1 +/- 15.7) than the control group. The portion of lateral impacts increased from 27% to 48% between the control group and PC+ and chest+ cohort, prompting the use of lateral impact crash tests for the case-matching portion of the study. Crash tests were analyzed in two configurations; vehicle-to-vehicle tests and vehicle-to-pole tests. The average maximum chest compression and deflection velocity from the dummy occupants were found to be 25.3% +/- 2.6% and 4.6 m/s +/- 0.42 m/s for the vehicle-to-pole tests and 23.0% +/- 4.8% and 3.9 m/s +/- 1.1 m/s for the vehicle-to-vehicle tests. Chest deflection versus time followed a roughly symmetric and sinusoidal profile. Sixteen CIREN cases were identified that matched the vehicle crash tests. Of the 16 matched cases, 12 (75%) sustained chest injuries, with half of these patients presenting with PC. CONCLUSIONS: Quantified loading at the chest wall indicative of PC and chest injury in motor vehicle crash is valuable boundary condition data for bench-top studies or computer simulations focused on this injury. In addition, because PC often exhibits a delayed onset, knowing the population and crash modes highly associated with this injury may promote earlier detection and improved management of this injury.

Antioxidant treatment after injury suppresses second hit immune priming.

BACKGROUND: Pulmonary contusion (PC) is a common injury that often results in priming for exaggerated inflammatory responses to a second hit. Previous studies used a mouse model of pulmonary contusion and showed an early and sustained reduction of SIRT1 protein and activity in the lung and bronchoalveolar lavage (BAL) cells of injured mice. Sustained decrease in SIRT1 was associated with a primed phenotype in injured mice challenged with an inflammatory stimulus. This study tests the hypothesis that pulmonary contusion induces oxidant production that modifies and decreases SIRT1 and primes the lung for the second-hit response. METHODS: A mouse model of pulmonary contusion was used to investigate injury-induced oxidant changes in SIRT1. Second-hit responses were evaluated by infection (Streptococcus pneumoniae) and inflammatory challenge using bacterial lipopolysaccharide. BAL, lung tissue, and blood were collected and used to evaluate inflammatory responses and SIRT1 levels, oxidant modification, and activity. Levels of NO in the BAL from mice and patients with PC were also assessed. RESULTS: We found that oxidants produced as a result of pulmonary contusion resulted in modification of SIRT1. S-Nitrosylation was observed and correlated with increased inducible nitric oxide synthase expression after injury. Anti-oxidant treatment of injured mice preserved SIRT1 activity, decreased second hit responses and improved lung function. Elevated NO levels in the BAL of PC patients was associated with acute respiratory distress syndrome or diagnosis of pneumonia. CONCLUSIONS: We conclude that oxidative stress in the lung after injury induces redox modification of SIRT1 and contributes to priming of the lung for a second-hit response. Antioxidant treatment suggests that SIRT1 activity after injury may be beneficial in suppressing second-hit responses.

Toll-like receptor 2 participates in the response to lung injury in a murine model of pulmonary contusion.

Blunt chest trauma resulting in pulmonary contusion with an accompanying acute inflammatory response is a common but poorly understood injury. We report that Toll-like receptor (TLR) 2 participates in the inflammatory response to lung injury. To show this, we use a model of pulmonary contusion in the mouse that is similar to that observed clinically in humans based on histologic, morphologic, and biochemical criteria of acute lung injury. The inflammatory response to pulmonary contusion in our mouse model is characterized by pulmonary edema, neutrophil transepithelial migration, and increased expression of the innate immunity proinflammatory cytokines IL 1beta and IL 6, the adhesion intracellular adhesion molecule 1, and chemokine (CXC motif) ligand 1. Compared with wild-type animals, contused Tlr2(-/-) mice have significantly reduced pulmonary edema and neutrophilia. These findings are associated with decreased levels of circulating chemokine (CXC motif) ligand 1. In contrast, systemic IL 6 levels remain elevated in the TLR2-deficient phenotype. These results show that TLR2 has a primary role in the neutrophil response to acute lung injury. We suggest that an unidentified noninfectious ligand generated by pulmonary contusion acts via TLR2 to generate inflammatory responses.

Thoracic trauma: when and how to intervene.

Trauma is the leading cause of death in patients younger than 40 years of age. Thoracic injuries are common and often can be managed by tube thoracostomy. In many patients, however, the thoracic injuries must be repaired surgically in one of three time periods: immediate, urgent, or delayed thoracotomy. In this article, we describe the general approach to effectively managing thoracic trauma patients. We review common injuries and scenarios that may be encountered by the surgeon and discuss the considerations and variables that enter into the decision-making process for operative intervention.

Colonic resection in the setting of damage control laparotomy: is delayed anastomosis safe?

Based on a large body of literature concerning the subject, trauma surgeons are becoming more comfortable with anastomosis rather than stoma creation in patients with destructive colon injuries requiring resection. This literature was largely generated before the widespread acceptance of the importance of damage control laparotomy (DCL). Thus, when such injuries occur in patients initially left in colonic discontinuity after DCL, the question of anastomosis versus stoma becomes more difficult, and there are no data to guide management decisions. The goal of this report is to describe the results of our early experience with delayed anastomosis (DA) after destructive colon injury in the setting of DCL. We reviewed the records of patients with destructive colon injuries at our Level I trauma center over a 5.5-year period for demographics, injury characteristics, and outcome. Studied outcomes included anastomotic leak, intra-abdominal abscess, and colon injury-related death. The decision to proceed with DA was based on individual surgeon opinion at the time of re-exploration. From January 1, 2000 to July 31, 2006, 92 patients sustained colon injury, 55 of which required resection (31 blunt mechanism and 24 penetrating). Twenty-two resections occurred in the setting of DCL. Six of these patients underwent stoma creation and 11 underwent DA. Three died before reoperation, and two had an anastomosis created during the initial DCL. The remaining 33 resections occurred during initial definitive operation, and 21 underwent anastomosis, whereas 12 had a stoma created. Comparing the 11 patients undergoing DA with the 21 undergoing immediate anastomosis, the anastomotic leak rate (0% vs 5%), abscess rate (36% vs 24%), and colon related-death rate (9% vs 0%; all P > 0.05) were similar. Six patients undergoing DA had a right hemicolectomy with ileocolonic anastomosis, four had a segmental left colon resection, and one had a near total abdominal colectomy with ileosigmoid anastomosis. Delayed anastomosis of colon injuries after DCL is safe in selected patients and has a similar complication rate as resection and anastomosis performed during initial definitive operation. DA avoids stoma creation in some patients who are not candidates for anastomosis during initial DCL. To our knowledge, this represents the first reported series of DA after DCL, an area in which further work is needed to carefully define indications for the safe application of this concept.

Increased insulin requirements are associated with pneumonia after severe injury.

BACKGROUND: Hyperglycemia after severe injury has been associated with an increased risk of infection and death. Strict glycemic control has been found to be valuable in select surgical populations. Varying amounts of insulin by infusion are required to maintain blood glucose levels within normal limits. Little is known about how insulin requirements are affected by the presence of infection, and therefore, the purpose of this study was to characterize this relationship. METHODS: Medical records of all intubated, injured patients admitted to the intensive care unit during a 16-month period were reviewed. Patients were included if they were managed with an insulin infusion, and they had a single bronchoalveolar lavage (BAL) culture performed for presumed pneumonia between 48 hours and 8 days. Mean hourly and 24-hour insulin requirements were analyzed before BAL was performed and then compared with values after cultures were obtained. This difference was then compared between patients with and without pneumonia. RESULTS: Eighty-two patients met inclusion criteria during the 16-month study period. The hourly and 24-hour insulin requirements significantly increased from before to after BAL was performed in patients with pneumonia (n = 54) and not in those without (n = 28) (p = 0.008). The 24-hour insulin requirement increased by 26.2 units from before to after BAL in the pneumonia group versus 7.6 units in the nonpneumonia group (p = 0.029). A mean hourly insulin requirement increase of 1.2 units more than the pre-BAL level demonstrated an 86% positive predictive value and 89% specificity for pneumonia. CONCLUSIONS: An increase in insulin requirements at the time of obtaining pulmonary cultures is associated with the presence of pneumonia and may represent a valuable tool for earlier recognition.

Alveolar interleukin-10 regulates neutrophil apoptosis in severely traumatized patients.

BACKGROUND: The lung produces a localized immunologic response to systemic trauma, characterized by an initial proinflammatory period with production of interleukin (IL)-8 and IL-18, followed by an anti-inflammatory phase with elevated levels of IL-10. Recent studies have shown a correlation between alveolar IL-10 and the rate of local neutrophil apoptosis. The aim of the present study was to further characterize the association of alveolar IL-8 and IL-10 after trauma with neutrophil activation, apoptosis, and phagocytic capacity. METHODS: Bronchoalveolar lavage fluid (BALF) was obtained from 17 trauma patients with an Injury Severity Score >/=16 who required mechanical ventilation. Neutrophils from venous blood of healthy volunteers were incubated in either (1) cell culture media (control), (2) culture media + BALF, (3) culture media + BALF + anti-IL-8 neutralizing antibody, or (4) culture media + BALF + anti-IL-10. Surface CD11b expression, ability to phagocytose fluorescent bacteria, and neutrophil apoptosis were determined by flow cytometry. RESULTS: Phagocytosis and CD11b expression were both augmented on postinjury day 1 when compared with controls. Neutralization of IL-10 or IL-8 produced no significant differences in phagocytosis or CD11b expression. However, neutralization of IL-10 significantly decreased the rate of apoptosis in samples from postinjury day 1. CONCLUSION: Phagocytosis and CD11b expression on neutrophils are IL-8 and IL-10 independent. However, our data indicate that alveolar neutrophil apoptosis is dependent on IL-10 at early time points after injury. Elucidation of this pathway may allow novel interventions to prevent posttraumatic pulmonary dysfunction.

Predicting Mortality and Independence at Discharge in the Aging Traumatic Brain Injury Population Using Data Available at Admission.

BACKGROUND: Aging worsens outcome in traumatic brain injury (TBI), but available studies may not provide accurate outcomes predictions due to confounding associated injuries. Our goal was to develop a predictive tool using variables available at admission to predict outcomes related to severity of brain injury in aging patients. STUDY DESIGN: Characteristics and outcomes of blunt trauma patients, aged 50 or older, with isolated TBI, in the National Trauma Data Bank (NTDB), were evaluated. Equations predicting survival and independence at discharge (IDC) were developed and validated using patients from our trauma registry, comparing predicted with actual outcomes. RESULTS: Logistic regression for survival and IDC was performed in 57,588 patients using age, sex, Glasgow Coma Scale score (GCS), and Revised Trauma Score (RTS). All variables were independent predictors of outcome. Two models were developed using these data. The first included age, sex, and GCS. The second substituted RTS for GCS. C statistics from the models for survival and IDC were 0.90 and 0.82 in the GCS model. In the RTS model, C statistics were 0.80 and 0.67. The use of GCS provided better discrimination and was chosen for further examination. Using a predictive equation derived from the logistic regression model, outcome probabilities were calculated for 894 similar patients from our trauma registry (January 2012 to March 2016). The survival and IDC models both showed excellent discrimination (p < 0.0001). Survival and IDC generally decreased by decade: age 50 to 59 (80% IDC, 6.5% mortality), 60 to 69 (82% IDC, 7.0% mortality), 70 to 79 (76% IDC, 8.9% mortality), and 80 to 89 (67% IDC, 13.4% mortality). CONCLUSIONS: These models can assist in predicting the probability of survival and IDC for aging patients with TBI. This provides important data for loved ones of these patients when addressing goals of care.