Objectives Trauma is an important non-obstetric cause of mortality in pregnant females. Methods The National Trauma Databank (NTDB) was queried between 2017 and 2018. Pregnant women >20 weeks gestation, who underwent trauma, were included. They were categorized into different age groups from 12-18, 18-35, and 36-50 years of age. The primary outcome measure was 30-day mortality. Results 1,058 pregnant trauma patients were included. Mean age was 26.7 ± 6 years. Of those 94.5% had blunt and 3.8% had penetrating injuries. Median GCS and ISS were 15 (15, 15) and 2 (1, 5), respectively. Penetrating trauma patients required more operative intervention (57.5%) than blunt trauma patients (24.6%). Univariate analysis comparing age groups 12-18, 19-35, and >36 years revealed differences. ( P < .05) in ED systolic blood pressure (110.9 ± 19.7 vs 117.3 ± 20.3 vs 129.1 ± 29.3 mmHg, P = .01) and diabetes mellitus (.0 vs 2.7% vs 6.6% P = .03). There was no difference in HLOS ( P = .72), complications ( P = .279), and mortality ( P = .32). Multivariate logistic regression analysis revealed that compared to patients 12-18 years old, patients 19 to 35 ( P = .27) or those >36 ( P = 1.0) did not show a significant difference in mortality. Patients with high ISS had higher complication rates (OR 1.09; 95% CI 1.04-1.15) and prolonged HLOS (OR 1.00; 95% CI 1.07-1.15). Conclusion On average pregnant women (>20 weeks gestation) who presented to trauma centers had minor injuries and maternal age or mechanism of injury did not affect mortality. Despite a low ISS, a significant number of these patients required operative procedures.

Background. Pulmonary arterial hypertension (PAH) is a complex pulmonary vasculature disease characterized by progressive obliteration of small pulmonary arteries and persistent increase in pulmonary vascular resistance, resulting in right heart failure and death if left untreated. Artemisinin (ARS) and its derivatives, which are common antimalarial drugs, have been found to possess a broad range of biological effects. Here, we sought to determine the therapeutic benefit and mechanism of ARS and its derivatives treatment in experimental pulmonary hypertension (PH) models. Methods. Isolated perfused/ventilated lung and isometric tension measurements in arteries were performed to test pulmonary vasoconstriction and relaxation. Monocrotaline (MCT) and hypoxia+Su5416 (SuHx) were administered to rats to induce severe PH. Evaluation methods of ARS treatment and its derivatives in animal models include echocardiography, hemodynamics measurement, and histological staining. In vitro, the effect of these drugs on proliferation, viability, and hypoxia-inducible factor 1α (HIF1α) was examined in human pulmonary arterial smooth muscle cells (hPASMCs). Results. ARS treatment attenuated pulmonary vasoconstriction induced by high K+ solution or alveolar hypoxia, decreased pulmonary artery (PA) basal vascular tension, improved acetylcholine- (ACh-) induced endothelial-dependent relaxation, increased endothelial nitric oxide (NO) synthase (eNOS) activity and NO levels, and decreased levels of NAD(P)H oxidase subunits (NOX2 and NOX4) expression, NAD(P)H oxidase activity, and reactive oxygen species (ROS) levels of pulmonary arteries (PAs) in MCT-PH rats. NOS inhibitor, L-NAME, abrogated the effects of ARS on PA constriction and relaxation. Furthermore, chronic application of both ARS and its derivative dihydroartemisinin (DHA) attenuated right ventricular systolic pressure (RVSP), Fulton index (right ventricular hypertrophy), and vascular remodeling of PAs in the two rat PH models. In addition, DHA inhibited proliferation and migration of hypoxia-induced PASMCs. Conclusions. In conclusion, these results indicate that treatment with ARS or DHA can inhibit PA vasoconstriction, PASMC proliferation and migration, and vascular remodeling, as well as improve PA endothelium-dependent relaxation, and eventually attenuate the development and progression of PH. These effects might be achieved by decreasing NAD(P)H oxidase generated ROS production and increasing eNOS activation to release NO in PAs. ARS and its derivatives might have the potential to be novel drugs for the treatment of PH.

Introduction Tracheostomies may be performed “early” or “late.” There is no agreement on the best timing for tracheostomy. This study compares tracheostomies and complications when performed within 48 hours with those performed from 48 hours to 21 days. Methods Patients who underwent tracheostomy in the 2017-2018 National Trauma Data Bank (NTDB) were categorized into 2 groups: early tracheostomy (≤48 hours) and late tracheostomy (>48 hours to 21 days). Primary outcome measured was mortality. Chi square models, Mann-Whitney U Test, and multivariate logistics were used for data analysis. Results 843 patients had tracheostomy performed, of which 16% underwent early tracheostomy. Majority were male in both early (84%) and late (74%) tracheostomy groups. Mortality was not statically significant in early (13%) or late (9%) ( P = .151). Total duration of ventilation in early tracheostomy group was less (5 days) compared to late tracheostomy group (16 days, P < .001). Patients with late tracheostomy had almost 18% cases of ventilator-associated pneumonia (VAP) when compared to early tracheostomy patients (7%, P < .001). Early tracheostomy patients also had shorter hospital length of stay (HLOS) (13 vs 27 days) and intensive care unit (ICU) length of stay (LOS) (7 vs 20 days) than late tracheostomy patients ( P<.001). Early tracheostomy patients also had shorter hospital length of stay (HLOS) (13 vs 27 days) and intensive care unit (ICU) length of stay (LOS) (7 vs 20 days) than late tracheostomy patients ( P < .001). Conclusion Tracheostomy performed as early as 48 hours is beneficial as it demonstrates a decrease time on ventilator, decreased HLOS, as well as lower VAP rates. Our data shows “hyper-early” tracheostomies might be more beneficial that the current national practice.