New horizons (Baltimore, Md.)
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Inflammation and tissue injury elicit profound changes in the concentrations of several plasma proteins. These proteins are predominantly synthesized in the liver and named acute-phase proteins. The regulatory mechanisms that control this response are highly complex and include the release of various mediators affecting specific subsets of acute-phase genes. ⋯ Although some acute-phase proteins have been shown to minimize tissue damage, as well as to participate in hemostasis, tissue repair, and regeneration in response to injury, the actual in vivo functions of several acute-phase reactants remain speculative. Measurements of acute-phase protein plasma concentrations can be of diagnostic or prognostic value under certain clinical conditions. Further characterization of the regulatory mechanisms that govern the acute-phase response in vivo could lead to the development of new therapeutic strategies aimed at improving the organism's integrated response to injury.
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Artificial ventilation using intermittent positive airway pressure is the mainstay support of patients in respiratory failure. By maintaining alveolar ventilation and alveolar stability, positive airway pressure can sustain respiratory gas exchange between the lungs and circulation, thereby supporting pulmonary homeostasis in patients who would otherwise be unable to maintain oxygen transfer and CO2 elimination. However, positive-pressure ventilation (PPV) also results in complex cardiovascular interactions. ⋯ However, when considered in this manner, such interactions can be understood more easily. In most patients it is usually clear which process is dominant, permitting adjustments in overall therapy in order to optimize care. This review identifies these interactions and demonstrates which are dominant in specific clinical scenarios.
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Multiple organ failure is the most common cause of death in critically ill patients in the United States. Acute respiratory failure is the most important single component of this clinical scenario, with a mortality risk > 50%. Key pathophysiologic events occur in the pulmonary microvasculature at the interface between circulating elements and the external environment. ⋯ We are now approaching the threshold for utilization of several new and specific approaches. While no single pharmacologic therapy is likely to be curative for this complex problem, it is probable that certain approaches will be of clinical benefit in the near future. This review is designed to provide a basis for understanding this evolution.
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Organ interactions are increasingly recognized as key determinants of the pathogenesis and potential for resolution of tissue injury during critical illness. A paradigm for a systems model that takes into account the modulatory effects of organ interactions and incorporates the expanding number of molecular and cellular pro-inflammatory networks is still lacking. Unifying hypotheses for multiple organ dysfunction during the systemic inflammatory response syndrome have been slow to emerge. ⋯ These regulatory elements include: a) control of systemic endotoxemia, bacteremia, and vasoactive by-products of sepsis and trauma by the gut-liver axis of inflammation, mononuclear phagocytic clearance, and Fc and complement receptor-mediated events; b) production and export of endogenous cytokine and eicosanoid mediators by Kupffer cells, especially in relation to changes in the prevailing hepatic oxygen supply; c) metabolic inactivation and detoxification of such mediators via cell-to-cell interactions at the Kupffer cell-hepatocyte interface; and d) cytokine-driven synthesis of acute-phase proteins that critically modulate metabolism and inflammation. Our goal is to summarize and integrate recent information that sheds light on mechanisms by which hepatic function modulates host defense homeostasis, thereby influencing pulmonary function in the adult respiratory distress syndrome. Liver-lung interactions are presented as a heuristic paradigm of organ interactions that dynamically modulate systemic immunophysiologic responses during critical illness.
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Pediatric critical care resource use in the United States is rapidly expanding despite low occupancy rates and organizational and leadership characteristics that suggest inefficient resource use in pediatric ICUs (PICUs). Studies confirm widespread inefficiencies. Use of PICU resources relates directly to severity of illness, and as a result mortality rates are directly related to efficiency rates. ⋯ Pediatric studies have focused more on efficiency evaluated on each day of ICU stay according to therapies used and severity of illness. If institutions are functioning in a very inefficient manner, a re-evaluation of admission and discharge criteria, as well as other hospital services, may be required to develop more efficient use of the PICU. The solution generally involves reducing the number of patients who are "too healthy to benefit." One intervention that has been successful in reducing resource use by these patients is a risk assessment program that contributes actual mortality risk information.(ABSTRACT TRUNCATED AT 250 WORDS)