Only recently it has been recognized that vitamin D, which in reality is a steroid prohormone, may be of great interest to various aspects of critical illness not only because of its classic function in the regulation of calcium homeostasis but of its suspected pleiotropic effects. Since 2011, several observational studies have demonstrated a strong association between vitamin D deficiency and adverse outcomes, specifically higher mortality in this vulnerable population. The major current vitamin D and nutrition guidelines do not specifically address vitamin D requirements of critically ill patients, and typical nutrition formulas and supplements contain only modest amounts that are likely insufficient to correct vitamin D deficiency or unable to cover even daily requirements of severely ill individuals. In this chapter, the current knowledge on vitamin D is summarized and an overview on data that are specifically relevant to a number of disease states in critically ill patients is given. Readers are also referred to the general aspects of vitamin D as it pertains to acute illness in the chapter by Dr Youssef et al.

Vitamin D has receptors in a vast majority of cells, and thus a normal vitamin D state is preferable to ensure an adequate function and appropriate response of the different receptors to a multitude of changes, namely, in critical illness. Vitamin D has many sources and exists in two different forms. Vitamin D state is divided into sufficient, insufficient, and deficient, and the variety in levels depends on plenty of factors, including the role of vitamin D-binding protein and possible influences from testing assays. Other possibilities that may take place in case of acute illness are also taken into consideration and discussed here. This chapter deals with the general aspects of vitamin D role in acute illness and how a replete state may affect the outcomes. The prevalence of vitamin D deficiency in critical illness and the frequency of testing and correction in case of deficiency are all considered here. ▶Chapter 67, “Specific Considerations Relevant to Critical Illness” by Dr. Amrein et al., discusses specific considerations of critical illness where vitamin D may have a role.

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We present two variant cases of spontaneous rectus sheath hematoma (SRSH). A 71-year-old woman presented with ST elevation myocardial infarction and was found to have multivessel coronary artery disease. She was treated with aspirin, clopidogrel, eptifibatide, and heparin. Heparin was continued while preoperative workup for coronary artery bypass grafting was done. She developed a large 20x10 cm actively bleeding SRSH while on heparin. It was surgically evacuated. The second case represents an atypical cause of SRSH. A 64-year-old woman with Wegener's Granulomatosis presented with anemia and abdominal pain. Abdominal CT showed a large 22 cm SRSH without active bleeding that was treated conservatively. Both patients did well on follow-up. The incidence of SRSH is likely to increase in the coming years with the increasing use of antithrombotic agents for many disease processes. Clinicians should be aware of typical and atypical presentations of SRSH and its variant management options.

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The control of IL-10 production in Toll-like receptor (TLR) signals remains to be elucidated. Here, we report that β-arrestin 2 positively regulates TLR-triggered IL-10 production in a p38 mitogen-activated protein kinase (MAPK)-dependent mechanism. In vitro studies with cells including peritoneal macrophages and HEK293/TLR4 cells have demonstrated that β-arrestin 2 forms complexes with p38 and facilitates p38 activation after lipopolysaccharide (LPS) stimulation. Deficiency of β-arrestin 2 and inhibition of p38 MAPK activity both ameliorate TLR4-stimulated IL-10 response. Additionally, in vivo experiments show that mice lacking β-arrestin 2 produce less amount of IL-10, and are more susceptible to LPS-induced septic shock which is further enhanced by blocking IL-10 signal. These results reveal a novel mechanism by which β-arrestin 2 negatively regulates TLR4-mediated inflammatory reactions.