Venous thromboembolism (VTE) is a frequent complication in critically ill patients and is associated with increased rates of morbidity and mortality. The use of thromboprophylaxis to reduce the risk of VTE in this patient population is the standard of care. This review will summarize the recommendations set forth in consensus guidelines for the prevention and treatment of VTE across subgroups within the critically ill patient population. In addition, the drug properties of the recommended pharmacologic agents for thromboprophylaxis will be highlighted including their pharmacokinetics, dosing and complications. The critical care practitioner may also encounter novel oral anticoagulants with increasing frequency. These agents will be briefly reviewed in terms of their approved and investigational indications and the clinical concerns related to their use will also be discussed.
Campylobacter jejuni is recognized as one of the most common agents of food-borne bacterial gastroenteritis in humans. Previous work has shown that C. jejuni isolates vary in their ability to invade and survive in laboratory grown cells. The correlation of these assays to actual lesion development in the hosts has not been determined. Therefore, this study aims to define the relationship between in vitro and in vivo assays for determining the virulence of C. jejuni isolates. Fifty-nine C. jejuni poultry isolates were analyzed in invasion and macrophage assays, and five isolates showing different invasion and survival abilities were examined for pathogenicity in the piglet model. All five isolates examined in the piglet model induced diarrhea without the presence of blood. Four of the five isolates produced microscopic lesions in piglets consisting of mucosal congestion, villous degeneration, and epithelial cell erosion. These studies imply that invasion or macrophage survival had little effect on the production of lesions typical of those noted in patients with campylobacteriosis. The most surprising finding was that isolates that produced a fluid exudate in piglets failed to invade epithelial cells. It is not known if the production of this fluid exudate is related to the production of a toxin(s) by C. jejuni. More work on the identification of the gene expressing this virulence factor is needed to confirm that this is indeed a putative toxin produced by C. jejuni.
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