BackgroundTrauma is the leading cause of death and disability in patients aged 1–46 y. Severely injured patients experience considerable blood loss and hemorrhagic shock requiring treatment with massive transfusion of red blood cells (RBCs). Preclinical and retrospective human studies in trauma patients have suggested that poorer therapeutic efficacy, increased severity of organ injury, and increased bacterial infection are associated with transfusion of large volumes of stored RBCs, although the mechanisms are not fully understood.Methods and findingsWe developed a murine model of trauma hemorrhage (TH) followed by resuscitation with plasma and leukoreduced RBCs (in a 1:1 ratio) that were banked for 0 (fresh) or 14 (stored) days. Two days later, lungs were infected with Pseudomonas aeruginosa K-strain (PAK). Resuscitation with stored RBCs significantly increased the severity of lung injury caused by P. aeruginosa, as demonstrated by higher mortality (median survival 35 h for fresh RBC group and 8 h for stored RBC group; p < 0.001), increased pulmonary edema (mean [95% CI] 106.4 μl [88.5–124.3] for fresh RBCs and 192.5 μl [140.9–244.0] for stored RBCs; p = 0.003), and higher bacterial numbers in the lung (mean [95% CI] 1.2 × 107 [−1.0 × 107 to 2.5 × 107] for fresh RBCs and 3.6 × 107 [2.5 × 107 to 4.7 × 107] for stored RBCs; p = 0.014). The mechanism underlying this increased infection susceptibility and severity was free-heme-dependent, as recombinant hemopexin or pharmacological inhibition or genetic deletion of toll-like receptor 4 (TLR4) during TH and resuscitation completely prevented P. aeruginosa–induced mortality after stored RBC transfusion (p < 0.001 for all groups relative to stored RBC group). Evidence from studies transfusing fresh and stored RBCs mixed with stored and fresh RBC supernatants, respectively, indicated that heme arising both during storage and from RBC hemolysis post-resuscitation plays a role in increased mortality after PAK (p < 0.001). Heme also increased endothelial permeability and inhibited macrophage-dependent phagocytosis in cultured cells. Stored RBCs also increased circulating high mobility group box 1 (HMGB1; mean [95% CI] 15.4 ng/ml [6.7–24.0] for fresh RBCs and 50.3 ng/ml [12.3–88.2] for stored RBCs), and anti-HMGB1 blocking antibody protected against PAK-induced mortality in vivo (p = 0.001) and restored macrophage-dependent phagocytosis of P. aeruginosa in vitro. Finally, we showed that TH patients, admitted to the University of Alabama at Birmingham ER between 1 January 2015 and 30 April 2016 (n = 50), received high micromolar–millimolar levels of heme proportional to the number of units transfused, sufficient to overwhelm endogenous hemopexin levels early after TH and resuscitation. Limitations of the study include lack of assessment of temporal changes in different products of hemolysis after resuscitation and the small sample size precluding testing of associations between heme levels and adverse outcomes in resuscitated TH patients.ConclusionsWe provide evidence that ...

Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Even when patients survive the initial insult, there is significant morbidity and mortality secondary to subsequent pulmonary edema, acute lung injury (ALI), and nosocomial pneumonia. Whereas the relationship between TBI and secondary pulmonary complications is recognized, little is known about the mechanistic interplay of the two phenomena. Changes in mental status secondary to acute brain injury certainly impair airway- and lung-protective mechanisms. However, clinical and translational evidence suggests that more specific neuronal and cellular mechanisms contribute to impaired systemic and lung immunity that increases the risk of TBI-mediated lung injury and infection. To better understand the cellular mechanisms of that immune impairment, we review here the current clinical data that support TBI-induced impairment of systemic and lung immunity. Furthermore, we also review the animal models that attempt to reproduce human TBI. Additionally, we examine the possible role of damage-associated molecular patterns, the chlolinergic anti-inflammatory pathway, and sex dimorphism in post-TBI ALI. In the last part of the review, we discuss current treatments and future pharmacological therapies, including fever control, tracheostomy, and corticosteroids, aimed to prevent and treat pulmonary edema, ALI, and nosocomial pneumonia after TBI.

BackgroundDamage control surgery has revolutionized trauma surgery. Use of damage control surgery allows for resuscitation and reversal of coagulopathy at the risk of loss of abdominal domain and intra-abdominal complications. Temporary abdominal closure is possible with multiple techniques, the choice of which may affect ability to achieve primary fascial closure and further complication.MethodsA retrospective analysis of all trauma patients requiring damage control laparotomy upon admission to an ACS-verified level one trauma center from 2011 to 2016 was performed. Demographic and clinical data including ability and time to attain primary fascial closure, as well as complication rates, were recorded. The primary outcome measure was ability to achieve primary fascial closure during initial hospitalization.ResultsTwo hundred and thirty-nine patients met criteria for inclusion. Primary skin closure (57.7%), ABThera™ VAC system (ABT) (15.1%), Bogota bag (BB) (25.1%), or a modified Barker’s vacuum-packing (BVP) (2.1%) were used in the initial laparotomy. Patients receiving skin-only closure had significantly higher rates of primary fascial closure and lower hospital mortality, but also significantly lower mean lactate, base deficit, and requirement for massive transfusion. Between ABT or BB, use of ABT was associated with increased rates of fascial closure. Multivariate regression revealed primary skin closure to be significantly associated with primary fascial closure while BB was associated with failure to achieve fascial closure.ConclusionsPrimary skin closure is a viable option in the initial management of the open abdomen, although these patients demonstrated less injury burden in our study. Use of vacuum-assisted dressings continues to be the preferred method for temporary abdominal closure in damage control surgery for trauma.

Background The use of blood products early in the resuscitation of bleeding trauma patients is widely accepted, but made difficult by limited supplies of D− red blood cell (RBC)‐containing products. Use of D+ RBC‐containing products would alleviate this issue, but could lead to alloimmunization. Risk associated with transfusing D+ RBC in emergency bleeding situations is being reconsidered. The level of concern surrounding emergency transfusion as it relates to future fetal harm was surveyed among surgeons and nurses. Methods Faculty and staff in the Departments of Surgery and Nursing were surveyed on the risks of receiving an emergency RBC transfusion and the subsequent potential for fetal harm. Answers were grouped as likely to accept (likely/very likely) or refuse transfusion (unlikely/very unlikely). Participants were compared by sex, and women by child‐bearing age, ([15–50 years] vs. [>50 years]). Results Ninety surveys were initiated with 76 fully completed. Male (n = 39) and female (n = 37) respondents were comparable. Most female respondents (30/37, 81%) were of childbearing age. Overall, both males (38/39, 95%) and females (33/37, 89%; p = .19) were likely to accept a transfusion in an emergency. There was no difference in transfusion acceptance if the risk of fetal harm was presented as 1% (p = .73) or 0.1% (p = .51). Most females (34/37, 92%) were not opposed to transfusion even if there was an unspecified risk of future fetal harm. Conclusion Most of the surgeons and nurses who responded would accept a transfusion in an emergency situation even if it might lead to harming a future fetus.

Sarcopenia is strongly associated with poor outcomes and mortality following injury among the geriatric population. Diagnosis using psoas area is most common but may be unavailable given limited radiographic evaluation following low-impact injuries. Masseter area has recently been identified as an available alternative and associated with 2-year mortality following injury. We sought to validate this measure and its association with early mortality following severe traumatic brain injury (sTBI) using a retrospective analysis of all geriatric trauma patients with sTBI admitted from 2011-2016 to our trauma center. Admission Glasgow Coma Scale (GCS) score ≤8 was used to identify sTBI. Bilateral masseter area was measured 2 cm below the zygomatic arch and the mean used for analysis. Sarcopenia was defined as mean masseter area one standard deviation or less from the sex-based mean. Multivariate models with logistic regression and Cox proportional hazards test followed univariate analysis. Kaplan-Meier survival curves were generated and evaluated by log rank. The primary outcome of interest was 30-day mortality. A total of 108 patients were identified for inclusion. Twenty-five patients, 16 male and nine female, had sarcopenia with mean masseter areas of 2.81 ± 0.45 cm and 2.24 ± 0.42 cm, respectively. Patients with sarcopenia had significantly increased rates of 30-day mortality (80.0% vs. 50.6%; p = 0.01). Sarcopenia (odds ratio [OR], 2.95; 95% confidence interval [CI] 1.03-8.49) and decreasing masseter area were significantly associated with 30-day mortality (OR, 0.66; 95% CI 0.46-0.95) in multivariate modeling. Masseter area is a readily available and objective measure to determine sarcopenia, which is significantly associated with in-creased 30-day mortality following sTBI.