IntroductionDiagnosis of severe influenza pneumonia remains challenging because of a lack of correlation between the presence of influenza virus and clinical status. We conducted gene-expression profiling in the whole blood of critically ill patients to identify a gene signature that would allow clinicians to distinguish influenza infection from other causes of severe respiratory failure, such as bacterial pneumonia, and noninfective systemic inflammatory response syndrome.MethodsWhole-blood samples were collected from critically ill individuals and assayed on Illumina HT-12 gene-expression beadarrays. Differentially expressed genes were determined by linear mixed-model analysis and overrepresented biological pathways determined by using GeneGo MetaCore.ResultsThe gene-expression profile of H1N1 influenza A pneumonia was distinctly different from those of bacterial pneumonia and systemic inflammatory response syndrome. The influenza gene-expression profile is characterized by upregulation of genes from cell-cycle regulation, apoptosis, and DNA-damage-response pathways. In contrast, no distinctive gene-expression signature was found in patients with bacterial pneumonia or systemic inflammatory response syndrome. The gene-expression profile of influenza infection persisted through 5 days of follow-up. Furthermore, in patients with primary H1N1 influenza A infection in whom bacterial co-infection subsequently developed, the influenza gene-expression signature remained unaltered, despite the presence of a superimposed bacterial infection.ConclusionsThe whole-blood expression-profiling data indicate that the host response to influenza pneumonia is distinctly different from that caused by bacterial pathogens. This information may speed the identification of the cause of infection in patients presenting with severe respiratory failure, allowing appropriate patient care to be undertaken more rapidly.
Aims. Drug incompatibilities are relatively common in inpatients and this may result in increased morbidity/mortality as well as add to costs. The aim of this 12 month study was to identify real incidences of drug incompatibilities in intravenous lines in critically ill patients in two intensive care units (ICUs). Methods. A prospective cross sectional study of 82 patients in 2 ICUs, one medical and one surgical in a 1500-bed university hospital. One monitor carried out observations during busy hours with frequent drug administration. Patients included in both ICUs were those receiving at least two different intravenous drugs. Results. 6.82% and 2.16% of drug pairs were found to be incompatible in the two ICUs respectively. Among the most frequent incompatible drugs found were insulin, ranitidine and furosemide.
Conclusions:The study showed that a significant number of drug incompatibilities occur in both medical and surgical ICUs. It follows that the incidence of incompatibilities could be diminished by adhering to a few simple rules for medication administration, following by recommendations for multiple lumen catheter use. Future prospective studies should demonstrate the effect of applying these policies in practice.
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