Bradykinin release following trauma and hemorrhagic shock causes pulmonary alveolar leak in a rodent model.

Background: Hemorrhage accounts for 40% of the preventable death following severe injury. Activation of systemic coagulation produces bradykinin (BK), which may cause leak from the plasma to the extravascular space and to the tissues, which is part of the complex pathophysiology of trauma-induced end-organ injury. We hypothesize that BK, released during activation of coagulation in severe injury, induces pulmonary alveolar leak.

A proposed clinical coagulation score for research in trauma-induced coagulopathy.

Background: Trauma-induced coagulopathy (TIC) has been the subject of intense study for greater than a century, and it is associated with high morbidity and mortality. The Trans-Agency Consortium for Trauma-Induced Coagulopathy, funded by the National Health Heart, Lung and Blood Institute, was tasked with developing a clinical TIC score, distinguishing between injury-induced bleeding from persistent bleeding due to TIC. We hypothesized that the Trans-Agency Consortium for Trauma-Induced Coagulopathy clinical TIC score would correlate with laboratory measures of coagulation, transfusion requirements, and mortality.

SHOCK INDUCES ENDOTHELIAL PERMEABILITY AFTER TRAUMA THROUGH INCREASED ACTIVATION OF RHOA GTPASE.

Introduction: Severely injured patients develop a dysregulated inflammatory state characterized by vascular endothelial permeability, which contributes to multiple organ failure. To date, however, the mediators of and mechanisms for this permeability are not well established. Endothelial permeability in other inflammatory states such as sepsis is driven primarily by overactivation of the RhoA GTPase.

A pilot study of the metabolic profiles of apheresis platelets modified by donor age and sex and in vitro short-term incubation with sex hormones.

Background: Platelets are part of innate immunity and comprise the cellular portion of hemostasis. Platelets express sex hormone receptors on their plasma membrane and sex hormones can alter their function in vitro. Little is known about how age and sex may affect platelet biology; thus, we hypothesized that platelets from males and females have different metabolomic profiles, which may be altered by age and in vitro treatment with sex hormones.

Hormones, age, and sex affect platelet responsiveness in vitro.

Background: Female sex confers a survival advantage following severe injury in the setting of trauma-induced coagulopathy, with female platelets having heightened responsiveness likely due to estrogen. The effects of testosterone on platelet biology are unknown, and platelets express both estradiol and androgen receptors on the plasma membrane. We hypothesize testosterone decreases platelet responses in vitro, and there are baseline differences in platelet function and metabolism stratified by sex/age.

The α-globin chain of hemoglobin potentiates tissue plasminogen activator induced hyperfibrinolysis in vitro.

Background: Severe injury predisposes patients to trauma-induced coagulopathy, which may be subdivided by the state of fibrinolysis. Systemic hyperfibrinolysis (HF) occurs in approximately 25% of these patients with mortality as high as 70%. Severe injury also causes the release of numerous intracellular proteins, which may affect coagulation, one of which is hemoglobin, and hemoglobin substitutes induce HF in vitro.

Strategies for successful implementation of resuscitative endovascular balloon occlusion of the aorta in an urban Level I trauma center.

Background: The rationale for resuscitative endovascular balloon occlusion of the aorta (REBOA) is to control life-threatening subdiaphragmatic bleeding and facilitate resuscitation; however, incorporating this into the resuscitative practices of a trauma service remains challenging. The objective of this study is to describe the process of successful implementation of REBOA use in an academic urban Level I trauma center. All REBOA procedures from April 2014 through December 2019 were evaluated; REBOA was implemented after surgical faculty attended a required and internally developed Advanced Endovascular Strategies for Trauma Surgeons course.

Atypical May-Thurner syndrome caused by endovascular aortic aneurysm repair.

May-Thurner syndrome is characterized by unilateral lower extremity venous hypertension and stasis due to compression of an iliac vein between an iliac artery and the lumbar spine. In almost all cases, the left common iliac vein is compressed by the right common iliac artery; however, other patterns have been described. Rarely, May-Thurner syndrome may be created iatrogenically as a result of iliac artery stenting.

Epidemiology of Wire-Bristle Grill Brush Injury in the United States, 2002-2014.

Objectives: The purpose of this study was to investigate the epidemiology of wire-bristle grill brush injury.

Study Design And Setting: Cross-sectional analysis of national databases; literature review.

Subjects And Methods: The Consumer Product Safety Commission's National Electronic Injury Surveillance System (NEISS) was used to derive a national weighted estimate of emergency department visits for wire bristle injury from 2002 to 2014.