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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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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Every patient who has sepsis and septic shock must be evaluated appropriately at presentation before the initiation of antibiotic therapy. However, in most situations, an abridged initial assessment focusing on critical diagnostic and management planning elements is sufficient. Intravenous antibiotics should be administered as early as possible, and always within the first hour of recognizing severe sepsis and septic shock. ⋯ The duration of antibiotic therapy typically is limited to 7 to 10 days. Longer duration is considered if response is slow, if there is inadequate surgical source control, or if immunologic deficiencies are evident. Antimicrobial therapy should be stopped if infection is not considered the etiologic factor for a shock state.
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Sepsis is often associated with systemic intravascular activation of coagulation, potentially leading to widespread microvascular deposits of fibrin, and thereby contributing to multiple organ dysfunction. A complex interaction exists between activation of inflammatory systems and the initiating and regulating pathways of coagulation. A diagnosis of sepsis-associated disseminated intravascular coagulation can be made by a combination of routinely available laboratory tests, for which simple diagnostic algorithms have become available. Strategies to inhibit coagulation activation may theoretically be justified and are being evaluated in clinical studies.
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Right ventricular dysfunction is common in sepsis and septic shock because of decreased myocardial contractility and elevated pulmonary vascular resistance despite a concomitant decrease in systemic vascular resistance. The mainstay of treatment for acute right heart failure includes treating the underlying cause of sepsis and reversing circulatory shock to maintain tissue perfusion and oxygen delivery. Decreasing pulmonary vascular resistance with selective pulmonary vasodilators is a reasonable approach to improving cardiac output in septic patients with right ventricular dysfunction. Treatment for right ventricular dysfunction in the setting of sepsis should concentrate on fluid repletion, monitoring for signs of RV overload, and correction of reversible causes of elevated pulmonary vascular resistance, such as hypoxia, acidosis, and lung hyperinflation.