The 21st International Symposium on Intensive Care and Emergency Medicine was dominated by the results of recent clinical trials in sepsis and acute respiratory distress syndrome (ARDS). The promise of extracorporeal liver replacement therapy and noninvasive ventilation were other areas of interest. Ethical issues also received attention. Overall, the 'state of the art' lectures, pro/con debates, seminars and tutorials were of a high standard. The meeting was marked by a sense of renewed enthusiasm that positive progress is occurring in intensive care medicine.

The datasets include severe sepsis information on 1) the number of severe sepsis cases, percent of hospital-acquired and non-hospital-acquired severe sepsis cases, and the percent of in-hospital severe sepsis deaths; 2) the average length of stay for severe sepsis hospitalizations, the respective median charge per day, and the expected payer for severe sepsis hospitalizations; 3) the severe sepsis patients who were alive at discharge and died within 30 days of discharge; and 4) the hospital-acquired severe sepsis in different type of hospitals (hospital size, location, teaching, and ownership). ICD-9-CM codes were used for data before October 1, 2015, and ICD-10-CM codes were used for data on or after October 1, 2015.

Associations between cytokines assessed in EBC and the outcomes of Death, Pneumonia, and Sepsis. An odds ratio greater than 1 is indicative of a positive association between the cytokine and the outcome; an odds ratio equal to 1 indicates that the cytokine and the outcome are independent of one another; an odds ratio of less than 1 is indicative of a negative correlation between the cytokine and the outcome.

Severe sepsis continues to lead to critical illness. Few therapeutic options exist other than antibiotic therapy and general supportive care. Large numbers of patients continue to die as a consequence of overactivation of the host inflammatory response and the resultant coagulopathy and disregulation of the normal controls of vasoactive tone. It is now known that a critical part of this host response occurs at the level of innate defence, without the need for antigen processing or the clonal expansion of cells targeted against the invading pathogen. This commentary will discuss the therapeutic targets revealed by our new understanding of the Toll-like receptor. The potential clinical difficulties that may result from intervention at this pattern-recognition receptor will also be explored.