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Objectives Medical emergency teams were established to rescue patients experiencing clinical deterioration thus preventing cardiac arrest and unexpected hospital mortality. Although hospitals are encouraged to increase emergency calling rates to improve in-hospital mortality, there are increasing concerns about the impact these calls have on the workload of the teams and the skill levels on the general wards. We set out to examine the relationship between emergency calling rates and adjusted in-hospital mortality. Design Retrospective analysis of prospectively collected patient and emergency call data. Setting Tertiary, metropolitan, and regional hospitals in the State of Victoria, Australia. Patients Consecutive patients discharged from 1) St Vincent's Hospital Melbourne from January 2008 to June 2016 and 2) 15 Victorian hospitals from July 2010 to June 2015. Measurements and main results We studied 441,029 patients from St Vincent's Hospital Melbourne. Median age was 61.0 years (interquartile range, 45-74 yr), 57.2% were men, and 0.70% died; monthly emergency calling rates varied between 9.21 and 30.69 (median 18.4) per 1,000 discharges. In-hospital mortality adjusted for age, gender, emergency status, same day admission, year of discharge, and Charlson Comorbidity Index was not reduced by higher calling rates in the month of discharge (odds ratio, 1.019; 95% CI, 1.008-1.031). We then examined 3,339,789 discharges from 15 Victorian hospitals with median age 61 years (interquartile range, 43-74 yr), 51.4% men, and hospital mortality 0.83% where yearly emergency calling rates varied from 18.46 to 33.40 (median, 25.75) per 1,000 discharges. Again, adjusted mortality was not reduced by higher calling rates in the year of discharge (odds ratio, 1.003; 95% CI, 1.001-1.006). Conclusions With adjustment for patient factors, illness, and comorbidities, increased emergency calling rates were not associated with reduced in-hospital mortality. Efforts to increase calling rates do not seem warranted.

To determine factors independently associated with readmission to ICU and the independent association of readmission with subsequent mortality.Prospective multicenter observational study.Forty ICUs in Australia and New Zealand.Consecutive adult patients discharged alive from ICU to hospital wards between September 2009 and February 2010.Measurement of hospital mortality.We studied 10,210 patients and 674 readmissions. The median age was 63 years (interquartile range, 49-74), and 6,224 (61%) were male. The majority of readmissions were unplanned (84.1%) but only deemed preventable in a minority (8.9%) of cases. Time to first readmission was shorter for unplanned than planned readmission (3.2 vs 6.9 d; p0.001). Primary diagnosis changed between admission and readmission in the majority of patients (60.2%) irrespective of planned (58.2%) or unplanned (60.6%) status. Using recurrent event analysis incorporating patient frailty, we found no association between readmissions and hospital survival (hazard ratios: first readmission 0.88, second readmission 0.90, third readmission 0.44; p0.05). In contrast, age (hazard ratio, 1.03), a medical diagnosis (hazard ratio, 1.43), inotrope use (hazard ratio, 3.47), and treatment limitation order (hazard ratio, 17.8) were all independently associated with outcome.In this large prospective study, readmission to ICU was not an independent risk factor for mortality.

To determine the long-term impact of a medical emergency team on survival and to assess the utility of administrative data to monitor outcomes.Prospective study of cardiac arrests and survival. Retrospective study of administrative data.University affiliated tertiary referral hospital in Melbourne, Australia.All patients admitted to hospital in three 6-month periods between 2002-2007 (prospective) and 1993-2007 (retrospective).Implementation of a medical emergency team in November 2002.In the prospective analysis, rates of unexpected cardiac arrest and hospital mortality (referenced to 1000 patient-care days) were measured before (July-August 2002) and after (December 2002-May 2003, December 2004-May 2005, December 2006-May 2007) the introduction of the medical emergency team. Cardiac arrest rates decreased progressively from 0.78 per 1000 (95% confidence interval, 0.50-1.16) to 0.25 per 1000 (95% confidence interval, 0.15-0.39, p.001), and hospital mortality from 0.58 per 1000 (95% confidence interval, 0.35-0.92) to 0.30 per 1000 (95% confidence interval, 0.20-0.46, p.05); cardiac arrest rates achieved statistical significance at 2 yrs and hospital mortality at 4 yrs. Using administrative data adjusted for age, sex, case-mix, and comorbidity, hazard ratios for mortality for the three post implementation periods were statistically lower than for the 10 yrs pre implementation (0.85, 0.74, 0.65). The intensity of calling (calls/1000 patient-days) inversely correlated with cardiac arrest rate, unexpected mortality rate, and total hospital mortality rate.The introduction of a medical emergency team was associated with a progressive decline of unexpected cardiac arrests within 2 yrs, and of unexpected mortality within 4 yrs. This suggests that changes to organizational practice take time and benefits may not be immediately obvious. Such changes are reflected in total hospital mortality measured from administrative data and make monitoring simpler in the longer term. Finally, efforts to increase calling of emergency teams should reduce cardiac arrests and mortality.

To investigate the pathophysiology underlying raised lactate levels after cardiac surgery with cardiopulmonary bypass (CPB).Prospective observational study.Medical and surgical intensive care unit of a tertiary hospital.A total of 40 patients undergoing first-time coronary artery bypass grafting with CPB.The prothrombotic response to cardiac surgery with CPB was assessed by measuring plasma levels of prothrombin fragment 1 + 2 and plasminogen activator inhibitor (PAI) activity. The hemodynamic responses to cardiac surgery with CPB were also measured using standard techniques.After cardiac surgery, prothrombin fragment 1 + 2 levels increased 6-fold and PAI activity increase 2- to 3-fold (p.0001). Lactate levels were not associated with prothrombin fragment 1 + 2 and PAI activity levels after CPB. Lactate levels were associated with baseline PAI activity (p =.006), a history of hypertension (p =.02), raised baseline lactate levels (p =.02), an early increase in body temperature after CPB (p =.05), a late increase in oxygen consumption after CPB (p =.03), and a raised white cell count after CPB (p =.06). Lactate levels were inversely associated with the maximum activated clotting time level reached during CPB (p =.02). Multivariate linear regression demonstrated lactate levels were independently associated with baseline PAI activity.We found cardiac surgery with CPB was associated with a marked prothrombotic response. Lactate levels were associated with elevated baseline PAI activity and evidence of an amplified inflammatory response to cardiac surgery with CPB. Our findings implicate aspects of the inflammatory response, including microvascular thrombosis, in the development of raised lactate levels after cardiac surgery with CPB.

To compare the efficacy, safety, and cost of fixed-dose low-molecular-weight heparin (dalteparin) with adjusted-dose unfractionated heparin as anticoagulant for continuous hemofiltration.Prospective, randomized, controlled clinical trial.University-affiliated adult intensive care unitAll patients requiring continuous hemofiltration for acute renal failure or systemic inflammatory response syndrome (SIRS) were eligible. Fifty-seven patients were enrolled. Eleven were excluded, seven because of major protocol violations and four died before hemofiltration.Patients received continuous venovenous hemodialysis with filtration with prefilter replacement at 500 mL/hr and countercurrent dialysate at 1000 mL/hr. Filters were primed with normal saline containing anticoagulant. Dalteparin-treated patients received a commencement bolus of 20 units/kg and a maintenance infusion at 10 units/kg/hr. Heparin-treated patients received a commencement bolus of 2000-5000 units and a maintenance infusion at 10 units/kg/hr, titrated to achieve an activated partial thromboplastin time in the patient of 70-80 secs.The primary outcome measure--time to failure of the hemofilter--was compared using survival analysis. Twenty-two patients (13 with acute renal failure and nine with SIRS; total, 41 filters) were randomized to heparin. Twenty-five patients (16 with acute renal failure and nine with SIRS; total, 41 filters) were randomized to dalteparin. Mean (SE) activated partial thromboplastin time in the heparin group was 79 (4.3) secs. Mean (SE) anti-factor-Xa activity in the six patients given dalteparin who were assayed was 0.49 (0.07). Mean (SE) prehemofiltration platelet count was 225 (35.5) x 10(9) for heparin and 178 (18.1) x 10(9) for dalteparin (p = .24, unpaired Student's t-test). Mean (SE) prehemofiltration hemoglobin was 11.4 (0.61) g/dL for heparin and 10.6 (0.38) g/dL for dalteparin (p = .31, unpaired Student's t-test).There was no significant difference in the time to failure between the two groups (p = .75, log rank test). For dalteparin, Kaplan-Meier (K-M) mean (SE) time to failure of the hemofilter was 46.8 (5.03) hrs. For heparin, K-M mean (SE) time to failure was 51.7 (7.51) hrs. The 95% CI for difference in mean time to failure was -13 to 23 hrs. The power of this study to detect a 50% change in filter life was90%.Mean (SE) reduction in platelet count during hemofiltration was 63 (25.8) x 10(9) for heparin and 41.8 (26.6) x 10(9) for dalteparin (p = .57, unpaired Student's t-test). Eight patients given dalteparin and four patients given heparin had screening for heparin-induced thrombocytopenia; three of the dalteparin patients and one of the heparin patients were positive (p = 1.0, Fisher's exact test). There were three episodes of trivial bleeding and two episodes of significant bleeding for dalteparin, and there were three episodes of trivial bleeding and four episodes of significant bleeding for heparin (p = .53, chi-square test). The mean (SE) decrease in hemoglobin concentration during hemofiltration was 0.51 (0.54) g/dL for heparin and 0.28 (0.49) g/dL for dalteparin (p = .75, unpaired Student's t-test). The mean (SE) packed-cell transfusion volume during hemofiltration was 309 (128) mL for heparin and 290 (87) mL for dalteparin (p = .90, unpaired Student's t-test). Daily costs, including coagulation assays, of hemofiltration were approximately 10% higher using dalteparin than with heparin.Fixed-dose dalteparin provided identical filter life, comparable safety, but increased total daily cost compared with adjusted-dose heparin. Unfractionated heparin remains our anticoagulant of choice for continuous hemofiltration in intensive care.