Clinics in chest medicine
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Clinics in chest medicine · Dec 2008
ReviewCorticosteroids and human recombinant activated protein C for septic shock.
This article summarizes the current knowledge on the benefit/risk profile from the use of low-dose corticosteroids and activated protein C in treating septic shock. Physicians should consider using low-dose corticosteroids and drotrecogin alpha activated in the treatment of patients who have vasopressor-dependent septic shock with persistent signs of hypoperfusion, organ dysfunction, or hypotension. The optimal timing for initiating these treatments is from 6 to 24 hours from onset of shock. When patients are receiving these drugs, physicians should systematically screen for superinfection and serious bleeding events.
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Prompt diagnosis, intervention, and risk assessment are critical in caring for septic patient but remain difficult with currently available methods. Biomarkers may become useful adjuncts to clinicians and ultimately serve as targets for future therapeutic trials in sepsis. The most relevant markers are reviewed in this article, including interleukin-6, C-reactive protein, procalcitonin, triggering receptor expressed on myeloid cells-1, and biomarker panels.
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Clinics in chest medicine · Dec 2008
ReviewThe heterogeneity of the microcirculation in critical illness.
Microcirculation, a complex and specialized facet of organ architecture, has characteristics that vary according to the function of the tissue it supplies. Bedside technology that can directly observe microcirculation in patients, such as orthogonal polarization spectral imaging and sidestream dark field imaging, has opened the way to investigating this network and its components, especially in critical illness and surgery. These investigations have underscored the central role of microcirculation in perioperative disease states. ⋯ This review focuses on studies conducted to date on the microcirculatory beds of critically ill patients. The functional anatomy of microcirculation networks and the role of these networks in the pathogenesis of critical illness are discussed. The morphology of microvascular beds that have been visualized during surgery and intensive care at the bedside are also described, including those of the brain, sublingual region, skin, intestine, and eyes.
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Severe sepsis, defined as inflammation and organ failure due to infection, continues to result in a mortality of approximately 30% despite advances in critical care. Current therapy includes timely administration of antibiotics, source control of infection, aggressive fluid resuscitation, support of failing organs, and use of activated protein C where clinically indicated. ⋯ Additional therapeutic strategies are aimed at restoring the natural anticoagulant levels, blocking deleterious effects of the complement cascade, reversing cytopathic hypoxia, and inhibiting excessive lymphocyte apoptosis. Molecules with pluripotent activity, such as interalpha inhibitor proteins and estrogen-receptor ligands, are also being investigated.
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Cellular dysfunction is a commonplace sequelum of sepsis and other systemic inflammatory conditions. Impaired energy production (related to mitochondrial inhibition, damage, and reduced protein turnover) appears to be a core mechanism underlying the development of organ dysfunction. The reduction in energy availability appears to trigger a metabolic shutdown that impairs normal functioning of the cell. This may well represent an adaptive mechanism analogous to hibernation that prevents a massive degree of cell death and thus enables eventual recovery in survivors.