Publications

Acute renal failure is still associated with a high mortality rate among intensive care patients, despite improvements in renal replacement therapies. The available intermittent and continuous renal replacement therapy techniques all have their own advantages and disadvantages. The best time to start renal replacement therapy and various other practical aspects of these techniques still need to be clarified. For these reasons, daily consultation between intensivists and nephrologists is necessary to select the best technique for the ICU patient with acute renal failure, based on the hemodynamic status, biological variables (uremia, coagulation, acid-base balance, electrolytes) and effects on other organ systems (cognitive state, pericarditis, myopathy). In the future, new markers of renal dysfunction may facilitate treatment choices.

<b>Rationale:</b> In August 2013, the Hospital Readmission Reduction Program announced financial penalties on hospitals with higher than expected risk-adjusted 30-day readmission rates for Medicare beneficiaries hospitalized for chronic obstructive pulmonary disease (COPD) exacerbation. In October 2014, penalties were imposed. We hypothesized that penalties would be associated with decreased readmissions after COPD hospitalizations. <b>Objectives:</b> To determine whether the announcement and enactment of financial penalties for COPD were associated with decreases in hospital readmissions for COPD. <b>Methods:</b> We used data from California's Office of Statewide Health Planning and Development to examine unplanned 30-day all-cause and COPD-related readmissions after COPD hospitalization. The preannouncement period was January 2010 to July 2013. The postannouncement period was August 2013 to September 2014. The postenactment period was October 2014 to December 2017. Using interrupted time series, we investigated the immediate change after the intervention (level change) and differences in the preintervention and postintervention trends (slope change). <b>Results:</b> We identified 333,429 index hospitalizations for COPD from 449 California hospitals. Overall, 69% of patients had Medicare insurance. For all-cause readmissions, the level change at announcement was 0.16% (95% confidence interval [CI], -1.07 to 1.38; <i>P</i> = 0.80); the change in slope between preannouncement and postannouncement periods was -0.01% (95% CI, -0.15 to 0.13; <i>P</i> = 0.92). The level change at enactment was 0.29% (95% CI, -1.11 to 1.69; <i>P</i> = 0.68); the change in slope between postannouncement and postenactment was 0.04% (95% CI, -0.10 to 0.18; <i>P</i> = 0.57). For patients with COPD-related readmissions, the level change at the time of the announcement was 0.09% (95% CI, -0.68 to 0.85; <i>P</i> = 0.83); the change in slope was 0.003% (95% CI, -0.08 to 0.09; <i>P</i> = 0.94). The level change at the time of the enactment was 0.22% (95% CI, -0.69 to 1.12; <i>P</i> = 0.64); the change in slope was -0.02% (95% CI, -0.10 to 0.07; <i>P</i> = 0.72). <b>Conclusions:</b> We did not detect decreases in either all-cause or COPD-related readmission rates at either time point. Although this would suggest that the Hospital Readmission Reduction Program penalty was ineffective for COPD, COPD readmissions had decreased at an earlier time point (October 2012) when penalties were announced for conditions other than COPD. Based on this, we believe early, broad interventions decreased readmissions, such that no difference was seen at this later time points despite institution of COPD-specific penalties.

The respiratory system is key to the management of patients with respiratory, as well as haemodynamic, compromise and should be monitored. The ventilator is more than just a machine that delivers gas; it is a true respiratory system monitoring device, allowing the measurement of airway pressures and intrinsic positive end-expiratory pressure and the plotting of pressure/volume curves. For effective and reliable monitoring, it is necessary to keep in mind the physiology, such as the alveolar gas equation, heart-lung interactions, the equation of movement, etc. Monitoring the respiratory system enables adaptation of not only respiratory management, but also haemodynamic management.

We hypothesized that cytokine production following delayed in vitro cell stimulation (to reproduce physiological cellular status at baseline) may be related to outcome in patients with septic shock. A total of 20 patients were included in a prospective clinical study, conducted in a medico-surgical intensive care unit in a university hospital. Blood samples were obtained at the onset of septic shock; these were treated to retain the cells, but to wash out autologous plasma (containing potential inflammatory stimuli such as cytokines, bacterial products and drugs) and replace it with foetal calf serum. Each treated sample was divided into two sets of four aliquots, to be stimulated either immediately or after an overnight period of resting incubation at 37 degrees C. The rest period was to allow recovery from potentially reversible endogenous or pharmacologically induced alterations in cellular response, in order to reproduce a near physiological state at baseline. In vitro cellular challenges used low-dose (0.2 ng/ml) or high-dose (1 ng/ml) CD14-dependent lipopolysaccharide and CD14-independent pokeweed mitogen to induce the production of tumour necrosis factor-alpha (TNF-alpha), and interleukins-1 beta and -10. Levels of TNF-alpha, interleukin-1 beta and interleukin-10 were significantly higher (P<0.05) when cell stimulation was delayed for 16 h, indicating a functional down-regulation of cells during septic shock. Moreover, TNF-alpha responses obtained with high-dose lipopolysaccharide were significantly greater in cells from patients who subsequently survived septic shock (n=13; median value 1392 pg/ml; range 592-2048 pg/ml) than in cells from non-survivors (n=7; median value 708 pg/ml; range 520-1344 pg/ml). These observations support the existence of individual differences in the inflammatory response that could influence patient outcome following septic shock.