Critical care : the official journal of the Critical Care Forum
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Review Historical Article
Bench-to-bedside review: a brief history of clinical acid-base.
The history of assessing the acid-base equilibrium and associated disorders is intertwined with the evolution of the definition of an acid. In the 1950s clinical chemists combined the Henderson-Hasselbalch equation and the Bronsted-Lowry definition of an acid to produce the current bicarbonate ion-centred approach to metabolic acid-base disorders. ⋯ This approach, using the strong ion difference (particularly the sodium chloride difference) and the concentration of weak acids (particularly albumin), pushes bicarbonate into a minor role as an acid-base indicator rather than as an important mechanism. The Stewart approach may offer new insights into acid-base disorders and therapies.
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This review describes current knowledge on the mechanisms that underlie glucocorticoid insufficiency in sepsis and the molecular action of glucocorticoids. In patients with severe sepsis, numerous factors predispose to glucocorticoid insufficiency, including drugs, coagulation disorders and inflammatory mediators. These factors may compromise the hypothalamic-pituitary axis (i.e. secondary adrenal insufficiency) or the adrenal glands (i.e. primary adrenal failure), or may impair glucocorticoid access to target cells (i.e. peripheral tissue resistance). ⋯ The molecular action of glucocorticoids results in genomic and nongenomic effects. Direct and indirect transcriptional and post-transcriptional effects related to the cytosolic glucocorticoid receptor account for the genomic effects. Nongenomic effects are probably subsequent to cytosolic interaction between the glucocorticoid receptor and proteins, or to interaction between glucocorticoids and specific membrane binding sites.
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Comparative Study
Can generic paediatric mortality scores calculated 4 hours after admission be used as inclusion criteria for clinical trials?
Two generic paediatric mortality scoring systems have been validated in the paediatric intensive care unit (PICU). Paediatric RISk of Mortality (PRISM) requires an observation period of 24 hours, and PRISM III measures severity at two time points (at 12 hours and 24 hours) after admission, which represents a limitation for clinical trials that require earlier inclusion. The Paediatric Index of Mortality (PIM) is calculated 1 hour after admission but does not take into account the stabilization period following admission. To avoid these limitations, we chose to conduct assessments 4 hours after PICU admission. The aim of the present study was to validate PRISM, PRISM III and PIM at the time points for which they were developed, and to compare their accuracy in predicting mortality at those times with their accuracy at 4 hours. ⋯ Among the three scores calculated at 4 hours after admission, all had good discriminatory capacity but only the PIM score was well calibrated. Further studies are required before the PIM score at 4 hours can be used as an inclusion criterion in clinical trials.
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The recognition and management of acid-base disorders is a commonplace activity for intensivists. Despite the frequency with which non-bicarbonate-losing forms of metabolic acidosis such as lactic acidosis occurs in critically ill patients, treatment is controversial. This article describes the properties of several buffering agents and reviews the evidence for their clinical efficacy. The evidence supporting and refuting attempts to correct arterial pH through the administration of currently available buffers is presented.
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Comparative Study
Procalcitonin and C-reactive protein during systemic inflammatory response syndrome, sepsis and organ dysfunction.
Both C-reactive protein (CRP) and procalcitonin (PCT) are accepted sepsis markers. However, there is still some debate concerning the correlation between their serum concentrations and sepsis severity. We hypothesised that PCT and CRP concentrations are different in patients with infection or with no infection at a similar severity of organ dysfunction or of systemic inflammatory response. ⋯ PCT and CRP levels are related to the severity of organ dysfunction, but concentrations are still higher during infection. Different sensitivities and kinetics indicate a different clinical use for both parameters.