The latest medical research on Emergency Medicine

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about emergency medicine gathered by our medical AI research bot.

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Persistent Neuroinflammation and Brain Specific Immune Priming in A Novel Survival Model of Murine Pneumosepsis.

Shock

Pneumonia is the leading cause of sepsis and septic shock. Patients who survive pneumonia are vulnerable to long-term complications including incre...

Hot off the Press: Prospective Validation of a Checklist to Predict Short-term Death in Older Patients After Emergency Department Admission in Australia and Ireland.

Academic Emergency Medicine

This is a prospective observational study looking to validate the CriSTAL decision rule, designed to predict the short-term risk of death in an eld...

Clinical Gestalt for Early Prediction of Delayed Functional and Symptomatic Recovery from Mild Traumatic Brain Injury is Inadequate.

Academic Emergency Medicine

There are limited prognostic tools to guide clinicians in acute risk-stratification of adult mild TBI patients (mTBI). While the majority of mTBI p...

Diagnoses, damned diagnoses and statistics: Dealing with disparate diagnostic coding systems within the New South Wales Emergency Department Data Collection.

EMA - Emergency Medicine Australasia

The aims of the present study were to describe the distribution of Systematised Nomenclature of Medicine - Clinical Terms (SNOMED-CT) codes used in the current New South Wales Emergency Department Data Collection (NSW EDDC) and classify duplicate and redundant terms into clinically meaningful sub-groups for future analyses.

This was an analysis of ED diagnosis codes using a large state-wide administrative ED dataset between 2015 and 2018.

A total of 7.4 million (77%) of ED episode diagnoses were coded with SNOMED-CT. Of those coded with SNOMED-CT, 12 152 unique codes were identified. Around 1000 of the most frequently used codes accounted for 90% of the presentations coded with SNOMED-CT and 5000 codes accounted for 99.8% of these. Around 7000 codes were deemed to be redundant, and duplication in terms exists across all sub-groups.

The use of SNOMED-CT in the NSW EDDC has resulted in substantial use of non-specific, duplicate and redundant codes, limiting the capacity of the NSW EDDC to be used for effective data analysis.

Daily Changes in The Expression of Clock Genes in Sepsis and Their Relation with Sepsis Outcome and Urinary Excretion of 6-Sulfatoximelatonin.

Shock

Whereas the circadian system controls the daily production of melatonin and the daily activity of the immune system, increasing evidences support the association between circadian misalignment with the alterations in the immune response and melatonin rhythm during sepsis. The aim of this study was to analyze the daily changes in clock genes expression and the urinary excretion of 6-SM (6-sulfatoxymelatonin, the major melatonin metabolite), and their connection with the innate immune activity, oxidative status in blood, and clinical outcome during sepsis.

Healthy volunteers, non-septic ICU patients, and septic ICU patients, were evaluated. The expression of bmal1, per2, clock, and cry1 genes was determined by PCR in blood; 6-SM was assessed in urine by ELISA; plasma cytokines IL-1β, IL-6, IL-8, TNFα, and IL-10 were determined by a multiplex array method, and lipid peroxidation (LPO) and protein oxidation (AOPP) by spectrophotometry. Hematological and biochemical data, and clinical scores of the patients, were also recorded.

Clock gene rhythm was maintained in non-septic patients but blunted in septic ones, whereas the innate immune and the oxidative stress responses were significantly higher in the latter. 6-SM excretion was also more elevated in septic than in non-septic patients, and it correlated with the degree of the immune response and oxidative status. 6-SM also correlated with SOFA and procalcitonin in the patients. Proinflammatory cytokines, LPO, and AOPP were normalized in the patients once recovered from sepsis.

Our data suggest a relationship between clock genes rhythm disruption, the immune response and the oxidative status, with 6-SM acting as a compensatory response. ICU conditions are not a main clock disrupter because the significant differences found in the responses of septic versus non-septic patients under the same ICU environment.

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

Shock

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.

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.

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 hours after CLP demonstrated increased expression of SIRT1 mRNA and protein compared to sham controls. Administration of EX-527 18 hours after CLP reduced SIRT1 protein expression in cardiac tissue at 36 hours. Moreover, treatment with EX-527 improved cardiac performance with increased global longitudinal strain and longitudinal strain rate.

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.

The Greater Omentum - A Vibrant and Enigmatic Immunologic Organ Involved in Injury and Infection Resolution.

Shock

Once thought of as an inert fatty tissue present only to provide insulation for the peritoneal cavity, the omentum is currently recognized as a vib...

Pharmacokinetics of Tranexamic Acid Given as an Intramuscular Injection Compared to Intravenous Infusion in a Swine Model of Ongoing Hemorrhage.

Shock

Tranexamic acid (TXA) improves survival in traumatic hemorrhage, but difficulty obtaining intravenous (IV) access may limit its use in austere environments, given its incompatibility with blood products. The bioavailability of intramuscular (IM) TXA in a shock state is unknown. We hypothesized that IM and IV administration have similar pharmacokinetics and ability to reverse in vitro hyperfibrinolysis in a swine controlled-hemorrhage model.

Twelve Yorkshire cross swine were anesthetized, instrumented, and subjected to a 35% controlled hemorrhage, followed by resuscitation. During hemorrhage, they were randomized to receive a 1 g IV TXA infusion over 10 minutes, 1 g IM TXA in two 5 mL injections, or 10 mL normal saline IM injection as a placebo group to assess model adequacy. Serum TXA concentrations were determined using liquid chromatography-mass spectrometry, and plasma samples supplemented with tissue plasminogen activator (tPA) were analyzed by rotational thromboelastometry (ROTEM).

All animals achieved class III shock. There was no difference in the concentration-time areas under the curve (AUC) between TXA given by either route. The absolute bioavailability of IM TXA was 97%. IV TXA resulted in a higher peak serum concentration during the infusion, with no subsequent differences. Both IV and IM TXA administration caused complete reversal of in vitro tPA-induced hyperfibrinolysis.

The pharmacokinetics of IM TXA were similar to IV TXA during hemorrhagic shock in our swine model. IV administration resulted in a higher serum concentration only during the infusion, but all levels were able to successfully correct in vitro hyperfibrinolysis. There was no difference in total body exposure to equal doses of TXA between the two routes of administration. IM TXA may prove beneficial in scenarios where difficulty establishing dedicated IV access could otherwise limit or delay its use.

Antithrombin III Contributes to the Protective Effects of Fresh Frozen Plasma Following Hemorrhagic Shock by Preventing Syndecan-1 Shedding and Endothelial Barrier Disruption.

Shock

Endothelial dysfunction during hemorrhagic shock (HS), is associated with loss of cell-associated syndecan-1 (Sdc1) and hyperpermeability. Fresh frozen plasma (FFP) preserves Sdc1 and reduces permeability following HS, although the key mediators remain unknown. Antithrombin III (ATIII) is a plasma protein with potent anti-inflammatory and endothelial protective activity. We hypothesized that the protective effects of FFP on endothelial Sdc1 and permeability are mediated, in part, through ATIII.

ATIII and Sdc1 were measured in severely injured patients upon admission (N = 125) and hospital day 3 (N = 90) for correlation analysis. In vitro effects of ATIII on human lung microvascular endothelial cells (HLMVECs) were determined by pre-treating cells with vehicle, FFP, ATIII-deficient FFP, or purified ATIII followed by TNFα stimulation. Sdc1 expression was measured by immunostaining and permeability by electrical impedance. To determine the role of ATIII in vivo, male mice were subjected to a fixed pressure exsanguination model of HS, followed by resuscitation with FFP, ATIII-deficient FFP, or ATIII-deficient FFP with ATIII repletion. Lung Sdc1 expression was assessed by immunostaining.

Pearson correlation analysis showed a significant negative correlation between plasma levels of Sdc1 and ATIII (R = -0.62; p < 0.0001) in injured patients on hospital day 3. Also, in vitro, FFP and ATIII prevented TNFα-induced permeability (p < 0.05 vs TNFα) in HLMVECs. ATIII-deficient FFP had no effect; however, ATIII restoration reestablished its protective effects in a dose-dependent manner. Similarly, FFP and ATIII prevented TNFα-induced Sdc1 shedding in HLMVECs, however ATIII-deficient FFP did not. In mice, Sdc1 expression was increased following FFP resuscitation (1.7 ± 0.5, p < 0.01) vs. HS alone (1.0 ± 0.3), however, no improvement was seen following ATIII-deficient FFP treatment (1.3 ± 0.4, p = 0.3). ATIII restoration improved Sdc1 expression (1.5 ± 0.9, p < 0.05) similar to that of FFP resuscitation.

ATIII plays a role in FFP-mediated protection of endothelial Sdc1 expression and barrier function, making it a potential therapeutic target to mitigate HS-induced endothelial dysfunction. Further studies are needed to elucidate the mechanisms by which ATIII protects the endothelium.

Risk Factors of Multidrug Resistant Pathogens Induced Infection in Severe Acute Pancreatitis.

Shock

A retrospective study was first performed to assess the multidrug resistant (MDR) pathogen in severe acute pancreatitis (SAP) patients who were treated using the step-up approach. We aim to assess the risk factors between MDR pathogen and potential covariates in SAP patients.

The clinical data of 51 SAP patients who were treated from June, 2013 to December, 2016 were retrospectively collected. A total of 23 patients in the MDR group and 28 patients in the non-MDR group were reviewed. The risk factors for MDR pathogen-induced infections in SAP patients were analyzed.

Hyperlipidemia was the leading cause of SAP in our study. The mean duration of hospital stay was significantly longer in the patients with MDR pathogen infections (P=0.0135). The hospitalization expenses of MDR group were much higher than those in non-MDR group. The mortality of MDR group (56.5%) was higher than that in non-MDR group (28.6%) (P=0.0436). Gram-negative isolates (63.8%) were commonly detected in SAP patients. Acinetobacter baumannii was the most common MDR pathogens. Systemic disease (P = 0.0136), initial use of carbapenem (P = 0.0438), and open necrosectomy (P = 0.0002) were the potential risk factors for MDR pathogen-induced infections in SAP. Furthermore, the logistic regression analysis revealed that open necrosectomy was the independent variable for MDR infections (OR: 15.6, 95% CI: 2.951-82.469, P = 0.0012).

MDR pathogen-induced infections were common in SAP patients and Acinetobacter baumannii was the main pathogen. Meanwhile, open necrosectomy was the independent risk factor for the infection of MDR pathogen.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0.

Providing Care or Caring.

Academic Emergency Medicine

"What do you want to do?" Matt asked. I looked up from the blue, gasping baby to the physician asking the question. "Well, back home I would have i...

Pain scores are not predictive of radiographically evident intraabdominal pathology in patients with abdominal pain.

Academic Emergency Medicine

Since 1989, when the term "oligoanalgesia" was coined, physicians have been encouraged to be more aggressive about treating pain (1). Although pain...