Clinics in chest medicine
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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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Hyperglycemia is common during the course of critical illness and is associated with adverse clinical outcomes. Randomized controlled trials and large observational trials of insulin therapy titrated to achieve glucose values approximating the normal range (80 to 110 mg/dL) demonstrate improved morbidity and mortality in heterogeneous populations and have led to recommendations for improved glucose control. Patients who have septic shock, however, appear to be at higher risk for hypoglycemia, and a recent randomized trial focusing exclusively on patients who had severe sepsis did not show benefit. The recent Surviving Sepsis consensus statement recommends insulin therapy using validated protocols to lower glucose (less than 150 mg/dL) pending the results of adequately powered trials to determine if normalization (less than 110 mg/dL) of glucose is needed to optimize outcomes in patients who have severe sepsis.
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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.