The epidemiology of pelvic ring fractures: a population-based study.

BACKGROUND: The severity of pelvic ring fractures (PRFs) can range from minor injury with low-energy mechanism to high-energy injury causing prehospital death. The purpose of this study was to prospectively describe the comprehensive pelvic fracture occurrence in an inclusive trauma system. METHODS: A 12-month prospective, population-based epidemiologic study was performed in the Hunter Region, New South Wales, Australia (population of 600,000, served by one Level I trauma center and 7 referring hospitals). Patient demographics, mechanism, injury severity, shock parameters, and outcomes were recorded prospectively. The database included all pelvic fractures from the region: high-energy pelvic fractures (HE-PRFs), low-energy pelvic fractures (LE-PRFs), and prehospital deaths (PD-PRFs). RESULTS: The incidence of PRF in the trauma system was 23 per 100,000 persons (138 fractures). The incidences of HE-PRF and LE-PRF were each 10 per 100,000 persons, whereas there were 3 PD-PRFs per 100,000. HE-PRF compared with LE-PRF occurred predominantly in men (64% vs. 20%, p < 0.05), younger persons (41 +/- 3 vs. 83 +/- 1 years, p < 0.05), those who had a higher Injury Severity Score (23 +/- 3 vs. 6 +/- 1, p < 0.05), and those with lower blood pressure (111 +/- 1 mm Hg vs. 153 +/- 1 mm Hg, p < 0.05), but the inhospital mortality rate was not statistically different (15% vs. 8%, p = NS). The overall mortality of the cohort was 23% (60% of those were from the PD-PRF group). The PRF-related mortality was 7% (HE-PRF: 7%; LE-PRF: 2%; PD-PRF: 33%), which was always attributable to bleeding. The incidence of demonstrated pelvic fracture-related arterial bleeding was 1.3 per 100,000 persons per year. CONCLUSIONS: LE-PRF and HE-PRF are equally frequent among hospital admissions. They represent two distinct demographic groups with similar mortality rate. Most PRF-related deaths occur prehospitally. Bleeding remains the primary cause of PRF-related mortality in all groups.

6-Chloro-3-alkylamino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide derivatives potently and selectively activate ATP sensitive potassium channels of pancreatic beta-cells.

6-Chloro-3-alkylamino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide derivatives were synthesized and characterized as activators of adenosine 5'-triphosphate (ATP) sensitive potassium (K(ATP)) channels in the beta-cells by measuring effects on membrane potential and insulin release in vitro. The effects on vascular tissue in vitro were measured on rat aorta and small mesenteric vessels. Selected compounds were characterized as competitive inhibitors of [(3)H]glibenclamide binding to membranes of HEK293 cells expressing human SUR1/Kir6.2 and as potent inhibitors of insulin release in isolated rat islets. 6-Chloro-3-(1-methylcyclobutyl)amino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide (54) was found to bind and activate the SUR1/Kir6.2 K(ATP) channels in the low nanomolar range and to be at least 1000 times more potent than the reference compound diazoxide with respect to inhibition of insulin release from rat islets. Several compounds, e.g., 3-propylamino- (30), 3-isopropylamino- (34), 3-(S)-sec-butylamino- (37), and 3-(1-methylcyclopropyl)amino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide (53), which were found to be potent and beta-cell selective activators of K(ATP) channels in vitro, were found to inhibit insulin secretion in rats with minimal effects on blood pressure and to exhibit good oral pharmacokinetic properties.

Mission to eliminate postinjury abdominal compartment syndrome.

OBJECTIVES: To determine the current incidence of postinjury abdominal compartment syndrome (ACS), the effect of intra-abdominal hypertension (IAH) on trauma outcomes, and the independent predictors of postinjury IAH. DESIGN: Prospective cohort study. SETTING: University-affiliated level 1 trauma center. PATIENTS: Eighty-one consecutive shock/trauma patients admitted to the intensive care unit (mean [SD] values: age, 41 [2] years; 70% male; injury severity score, 29 [1]; base deficit, 6 [0.5] mmol/L; lactate level, 29.73 [4.5] mg/dL; transfusions of packed red blood cells, 5 [0.5] U in first 24 hours; mortality rate, 2.5%; and multiple organ failure [MOF], 6%) had second hourly intra-abdominal pressure (IAP) monitoring. MAIN OUTCOME MEASURES: Intensive care unit length of stay, ACS, IAH, MOF, mortality. RESULTS: The mean (SD) IAP was 14 (1) mm Hg. No patients developed ACS. Sixty-one patients (75%) had sustained IAH. Both patients with IAH and those without had similar demographics and injury severity. Patients with IAH had worse metabolic acidosis (P = .02), received more crystalloids (P = .03), and underwent laparotomy more frequently (P = .005). One patient with IAH and one without died. MOF occurred in 1 patient without IAH (5%) vs 4 with IAH (7%). The mean (SD) intensive care unit length of stay was 11 (3) days in patients without IAH vs 8 (1) days in those with IAH. Intra-abdominal hypertension was poorly predictive of MOF (odds ratio, 1.17; 95% confidence interval, 0.96-1.43; P = .13). Of the 30 variables in multiple logistic regression analysis, only base deficit, laparotomy, and emergency department crystalloids were identified as weak predictors of IAP greater than 12 mm Hg. No predictors were found for the clinically more relevant IAP greater than 15 mm Hg and IAP greater than 18 mm Hg. CONCLUSIONS: Most of the severe shock/trauma patients developed sustained IAH. Based on univariate and multivariate analyses, there was no difference in outcomes between the trauma patients with IAH and those without. Multiple logistic regression analysis failed to show IAH as a predictor of MOF. The attenuation of the deadly ACS to a less deleterious IAH could be considered a success of the last decade in trauma and critical care.

Epidemiology of post-injury multiple organ failure in an Australian trauma system.

BACKGROUND: The epidemiology of post-injury multiple organ failure (MOF) is reported internationally to have gone through changes over the last 15 years. The purpose of this study is to describe the epidemiology of post-injury MOF in Australia. METHODS: A 12-month prospective epidemiological study was performed at the John Hunter Hospital (Level-1 Trauma Centre). Demographics, injury severity (ISS), physiological parameters, MOF status and outcome data were prospectively collected on all trauma patients who met inclusion criteria (ICU admission; ISS > 15; age > 18, head Abbreviated Injury Scale (AIS) <3 and survival >48 h). MOF was prospectively defined by the Denver MOF score greater than 3 points. Data are presented as % or Mean +/- SEM. Univariate statistical comparison was performed (Student t-test, Chi2 test), P < 0.05 was considered significant. RESULTS: Twenty-nine patients met inclusion criteria (Age 40 +/- 4, ISS 29 +/- 3, Male 62%), five patients developed MOF. The incidence of MOF among trauma patients admitted to ICU was 2% (5/204) and 17% (5/29) in the high-risk cohort. The maximum average MOF score was 6.3 +/- 1, with the average duration of MOF 5 +/- 2 days. Two patients had respiratory and cardiac failure, two patients had failure of respiratory, cardiac and hepatic systems, while one patient had failure of respiratory, hepatic and renal systems. One MOF patient died, all non MOF patients survived. MOF patients had longer ICU stays (20 +/- 4 versus 7 +/- 0.8 P = 0.01), tended to be older (60 +/- 11 versus 35 +/- 4 p = 0.07). None of the previously described independent predictors (ISS, base deficit, lactate, transfusions) were different when the MOF patients were compared with the non-MOF patients. CONCLUSION: The incidence of MOF in Australia is consistent with the international data. In Australia MOF continues to cause significant late mortality and morbidity in trauma patients. MOF patients have longer ICU stay than high-risk non MOF patients, and use significant resources. Our preliminary data challenges the timeliness of the 10-year-old independent predictors of post-injury MOF. The epidemiology, the clinical presentation and the independent predictors of post-injury MOF require larger scale reassessment for the Australian context.