Critical care : the official journal of the Critical Care Forum
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Numerous lines of evidence support the premise that withholding and withdrawing life support measures in the intensive care unit are not the same. These include questionnaires, practical observations and an examination of national medical guidelines. It is important to distinguish between the two end of life options as their outcomes and management are significantly different. Appreciation of these differences allows the provision of accurate information, and facilitates decision making that is compassionate, caring and adherent to the needs of the patient and their family.
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The majority of deaths on the intensive care unit now occur following a decision to limit life-sustaining therapy, and end-of-life decision making is an accepted and important part of modern intensive care medical practice. Such decisions can essentially take one of two forms: withdrawing -- the removal of a therapy that has been started in an attempt to sustain life but is not, or is no longer, effective -- and withholding -- the decision not to make further therapeutic interventions. Despite wide agreement by Western ethicists that there is no ethical difference between these two approaches, these issues continue to generate considerable debate. In this article, I will provide arguments why, although the two actions are indeed ethically equivalent, withdrawing life-sustaining therapy may in fact be preferable to withholding.
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Comparative Study
Microvascular permeability during experimental human endotoxemia: an open intervention study.
Septic shock is associated with increased microvascular permeability. As a model for study of the pathophysiology of sepsis, endotoxin administration to humans has facilitated research into inflammation, coagulation and cardiovascular effects. The present study was undertaken to determine whether endotoxin administration to human volunteers can be used as a model to study the sepsis-associated increase in microvascular permeability. ⋯ Although experimental human endotoxaemia is frequently used as a model to study sepsis-associated pathophysiology, an endotoxin-induced increase in microvascular permeability in vivo could not be detected using three different methods. Endotoxin administration to human volunteers is not suitable as a model in which to study changes in microvascular permeability.
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Comparative Study
Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study.
Increased intramucosal-arterial carbon dioxide tension (PCO2) difference (DeltaPCO2) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in DeltaPCO2. ⋯ In this model of endotoxemia, intramucosal acidosis was corrected by increased blood flow and so might follow tissue hypoperfusion. In contrast, anion-gap metabolic acidosis was left uncorrected and even worsened with aggressive volume expansion. These results point to different mechanisms generating both alterations.
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Acute lung injury or acute respiratory distress syndrome (ALI/ARDS) in the course of sepsis is thought to result from increased pulmonary capillary permeability and resultant edema. However, when the edema is assessed at the bedside by measuring the extravascular thermal volume by transpulmonary dilution, some ALI/ARDS patients with sepsis may have normal extravascular lung water (EVLW). Conversely, a raised EVLW may be present even when criteria for ALI/ARDS are not met, according to GS Martin and colleagues in this issue of Critical Care. ⋯ Overhydration is particularly difficult to recognize. Additional diagnostics may be required to improve the delineation of pulmonary edema so as to redirect or redefine treatment and improve patient morbidity and, perhaps, mortality. Monitoring EVLW by single transpulmonary thermal dilution, for instance, might have a future role in this process.