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Background Systemic infection is associated with long-term cognitive deficits and functional decline. In this study we hypothesized that severe systemic inflammation leads to a neuroinflammatory response that is characterized by microglial activation, and that these effects might be more pronounced in patients using medication with anticholinergic side-effects. Methods Based on the results of a pilot study in 8 patients, we assessed the number of MHC-II and CD-68 positive cells by immunohistochemistry and compared the number of microglia in specific brain regions of 16 well-characterized patients with septic shock and 15 controls. Results In the pilot study, patients with sepsis tended to have higher density of MHC-II and CD-68 positive microglia in the basal ganglia (putamen, caudate nucleus and globus pallidus) and of MHC-II positive microglia in the hippocampus. In the validation study, patients with sepsis had a significantly higher number of CD-68 positive cells in hippocampus (1.5 fold; p = 0.012), putamen (2.2 fold; p = 0.008) and cerebellum (2.5 fold; p = 0.011) than control patients. The density of MHC-II positive microglia was similar between sepsis and control groups. There was no consistent correlation between microglia counts and anti-cholinergic activity drugs score. Conclusion In patients who die during septic shock, severe systemic inflammation is accompanied by localized and strong upregulation of CD-68 positive microglia, but not of MHC-II positive microglia. We identified regional differences in the brain with increased microglial activation in putamen, hippocampus and cerebellum.

In 2014, there was still a shortage of available organs for transplantation, and 1044 patients were waiting for an organ in the Netherlands. Maximizing the pool of organ donors is part of the solution. In 2001, the Dutch Termination of Life on Request and Assisted Suicide Act was adopted, legalizing euthanasia under strict conditions. In 2010, 3136 reports were made of euthanasia and assisted suicide; in 2014, 5306 reports were made. Among them were patients with a desire to donate their organs after their deaths. Although a potential source of donor organs, only a few cases of organ donation after active euthanasia have been described. Since 2012, 16 combinations of these procedures have been performed in the Netherlands. The literature mentions 16 Belgian cases between 2005 and 2013. This limited number can be the result of lack of knowledge about this subject among healthcare professionals or because of practical, ethical, and/or legal considerations. Performing this combination has possible advantages, both in number as well as in transplantation outcomes. By describing a recent case in our center, we will try to outline the state of the art in the Netherlands and disseminate knowledge about the possibilities and limitations of organ donation after active euthanasia.

In recent years, emerging evidence has shown the potential risks of arterial hyperoxia, but observational studies failed to indisputably demonstrate its impact on clinical outcome of critically ill patients. Importantly, the lack of a clinical definition of hyperoxia and methodological limitations hamper the interpretation and clinical relevance of these studies.

Acute pancreatitis is an acute sterile inflammation of the pancreas. The diagnosis is made on the basis of a distinct clinical syndrome consisting of acute onset abdominal pain radiating to the back and frequently accompanied by nausea and/or vomiting, combined with a more than threefold increase of serum amylase or lipase above the upper limit of normal. In the western world the most common causes of acute pancreatitis are alcohol abuse and gallstones [1]. The disease is characterized by the premature activation of digestive enzymes in the pancreas, followed by a massive immunological response resulting in autodigestion of the gland, local, and subsequent systemic inflammation. The incidence of the disease varies between 5–20 per 100 000 persons per year, with 10–20% of patients developing severe pancreatitis of whom up to 30% may die as a result of the development of secondary complications such as pancreatitis-associated lung injury, infectious complications or multiple organ failure (MOF) [1]. This chapter will focus on recent developments in the understanding of the pathophysiology and immunopathology of acute pancreatitis and its complications and discuss the importance of early severity prediction including the merits of various prognostic markers.

The aim of this study was to compare self-reported beliefs with actual clinical practice of oxygen therapy in the ICU. Hyperoxia is frequently encountered in ventilated patients and prolonged exposure has repeatedly been shown to induce lung injury and (systemic) toxicity.

Mechanical ventilation and hyperoxia independently promote pulmonary injury and inflammation. However, the time course of the immune response following concurrent exposure is unclear. The aim of this preclinical study was to study both time-dependent and dose-dependent effects of supplemental oxygen during prolonged ventilatory support on pulmonary inflammation in a well-established murine model of ventilation comparing low and high tidal volumes.