Hypotension in the Emergency Department and Contrast Extravasation on Computerized Tomography Predict Blood Transfusion in Low-Energy Pelvic Fractures.

INTRODUCTION: Although low-energy pelvic fractures seldom present with significant hemorrhage, early recognition of at-risk patients is essential. We aimed to identify predictors of transfusion requirements in this cohort. METHODS: A 7-y retrospective chart review was performed. Low-energy mechanism was defined as falls of ≤5 feet. Fracture pattern was classified using the Orthopedic Trauma Association/Arbeitsgemeinschaft für Osteosynthesefragen system as A, B, or C. Primary outcome was transfusion of ≥2 units of packed red blood cells in the first 48 h. Univariable analysis and logistic regression analysis were performed. A P value ≤0.05 was considered significant. RESULTS: Five hundred forty six patients were included with median (interquartile range) age of 86 (79-91) and median (interquartile range) Injury Severity Score of 5 (4-8). Five hundred forty one (99%) had type A fractures. Twenty six (5%) had the primary outcome and 17 (3%) died. Logistic regression found that systolic blood pressure <100 mmHg at any time in the Emergency Department, Injury Severity Score, and pelvic angiography were predictors of the primary outcome. Seventeen percent of those who had the primary outcome died compared with 2% who did not (P = 0.0004). Three hundred sixty four (67%) received intravenous contrast for computerized tomography scans and of these, 44 (12%) had contrast extravasation (CE). CE was associated with the primary outcome but not mortality. CONCLUSIONS: Hypotension at any time in the Emergency Department and CE on computerized tomography predicted transfusion of ≥2 units packed red blood cells in the first 48 h in patients with low-energy pelvic fractures.

Protective and aggressive bacterial subsets and metabolites modify hepatobiliary inflammation and fibrosis in a murine model of PSC.

OBJECTIVE: Conflicting microbiota data exist for primary sclerosing cholangitis (PSC) and experimental models. GOAL: define the function of complex resident microbes and their association relevant to PSC patients by studying germ-free (GF) and antibiotic-treated specific pathogen-free (SPF) multidrug-resistant 2 deficient (mdr2-/- ) mice and microbial profiles in PSC patient cohorts. DESIGN: We measured weights, liver enzymes, RNA expression, histological, immunohistochemical and fibrotic biochemical parameters, faecal 16S rRNA gene profiling and metabolomic endpoints in gnotobiotic and antibiotic-treated SPF mdr2-/- mice and targeted metagenomic analysis in PSC patients. RESULTS: GF mdr2-/- mice had 100% mortality by 8 weeks with increasing hepatic bile acid (BA) accumulation and cholestasis. Early SPF autologous stool transplantation rescued liver-related mortality. Inhibition of ileal BA transport attenuated antibiotic-accelerated liver disease and decreased total serum and hepatic BAs. Depletion of vancomycin-sensitive microbiota exaggerated hepatobiliary disease. Vancomycin selectively decreased Lachnospiraceae and short-chain fatty acids (SCFAs) but expanded Enterococcus and Enterobacteriaceae. Antibiotics increased Enterococcus faecalis and Escherichia coli liver translocation. Colonisation of GF mdr2-/- mice with translocated E. faecalis and E. coli strains accelerated hepatobiliary inflammation and mortality. Lachnospiraceae colonisation of antibiotic pretreated mdr2-/- mice reduced liver fibrosis, inflammation and translocation of pathobionts, and SCFA-producing Lachnospiraceae and purified SCFA decreased fibrosis. Faecal Lachnospiraceae negatively associated, and E. faecalis/ Enterobacteriaceae positively associated, with PSC patients' clinical severity by Mayo risk scores. CONCLUSIONS: We identified novel functionally protective and detrimental resident bacterial species in mdr2-/- mice and PSC patients with associated clinical risk score. These insights may guide personalised targeted therapeutic interventions in PSC patients.