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      The Effect of Bicarbonate Administration via Continuous Venovenous Hemofiltration on Acid-Base Parameters in Ventilated Patients

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          Abstract

          Background. Acute kidney injury (AKI) and metabolic acidosis are common in the intensive care unit. The effect of bicarbonate administration on acid-base parameters is unclear in those receiving continuous venovenous hemofiltration (CVVH) and mechanical ventilatory support. Methods. Metabolic and ventilatory parameters were prospectively examined in 19 ventilated subjects for up to 96 hours following CVVH initiation for AKI at an academic tertiary care center. Mixed linear regression modeling was performed to measure changes in pH, partial pressure of carbon dioxide ( pCO 2), serum bicarbonate, and base excess over time. Results. During the 96-hour study period, pCO 2 levels remained stable overall (initial pCO 2 42.0 ± 14.6 versus end-study pCO 2 43.8 ± 16.1 mmHg; P = 0.13 for interaction with time), for those with initial pCO 2 ≤40 mmHg (31.3 ± 5.7 versus 35.0 ± 4.8; P = 0.06) and for those with initial pCO 2 >40 mmHg (52.7 ± 12.8 versus 53.4 ± 19.2; P = 0.57). pCO 2 decreased during the immediate hours following CVVH initiation (42.0 ± 14.6 versus 37.3 ± 12.6 mmHg), though this change was nonsignificant ( P = 0.052). Conclusions. We did not detect a significant increase in pCO 2 in response to the administration of bicarbonate via CVVH in a ventilated population. Additional studies of larger populations are needed to confirm this finding.

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          Serial evaluation of the SOFA score to predict outcome in critically ill patients.

          Evaluation of trends in organ dysfunction in critically ill patients may help predict outcome. To determine the usefulness of repeated measurement the Sequential Organ Failure Assessment (SOFA) score for prediction of mortality in intensive care unit (ICU) patients. Prospective, observational cohort study conducted from April 1 to July 31, 1999. A 31-bed medicosurgical ICU at a university hospital in Belgium. Three hundred fifty-two consecutive patients (mean age, 59 years) admitted to the ICU for more than 24 hours for whom the SOFA score was calculated on admission and every 48 hours until discharge. Initial SOFA score (0-24), Delta-SOFA scores (differences between subsequent scores), and the highest and mean SOFA scores obtained during the ICU stay and their correlations with mortality. The initial, highest, and mean SOFA scores correlated well with mortality. Initial and highest scores of more than 11 or mean scores of more than 5 corresponded to mortality of more than 80%. The predictive value of the mean score was independent of the length of ICU stay. In univariate analysis, mean and highest SOFA scores had the strongest correlation with mortality, followed by Delta-SOFA and initial SOFA scores. The area under the receiver operating characteristic curve was largest for highest scores (0.90; SE, 0.02; P 90%), a decreasing score during the first 48 hours was associated with a mortality rate of less than 6%, while an unchanged or increasing score was associated with a mortality rate of 37% when the initial score was 2 to 7 and 60% when the initial score was 8 to 11. Sequential assessment of organ dysfunction during the first few days of ICU admission is a good indicator of prognosis. Both the mean and highest SOFA scores are particularly useful predictors of outcome. Independent of the initial score, an increase in SOFA score during the first 48 hours in the ICU predicts a mortality rate of at least 50%.
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            Continuous renal-replacement therapy for acute kidney injury.

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              Occurrence and adverse effect on outcome of hyperlactatemia in the critically ill

              Introduction Hyperlactatemia is frequent in critically ill patients and is often used as a marker of adverse outcome. However, studies to date have focused on selected intensive care unit (ICU) populations. We sought to determine the occurrence and relation of hyperlactatemia with ICU mortality in all patients admitted to four ICUs in a large regional critical care system. Methods All adults ([greater than or equal to] 18 years) admitted to ICUs in the Calgary Health Region (population 1.2 million) during 2003 to 2006 were included retrospectively. Lactate determinations were at the discretion of the attending service and hyperlactatemia was defined by a lactate level > 2 mmol/L. Results A total of 13,932 ICU admissions occurred among 11,581 patients. The median age was 63 years (37% female), the mean APACHE II score was 25 ± 9 (n = 13,922). At presentation (within first day of admission), 12,246 patients had at least one lactate determination and the median peak lactate was 1.8 (IQR 1.2 to 2.9) mmol/L. The cumulative incidence of at least one documented episode of hyperlactatemia was 5578/13,932 (40%); 5058 (36%) patients had hyperlactatemia at presentation, and a further 520 (4%) developed hyperlactatemia subsequently. The incidence of hyperlactatemia varied significantly by major admitting diagnostic category (P < 0.001) and was highest among neuro/trauma patients 1053/2328 (45%), followed by medical 2047/4935 (41%), other surgical 900/2274 (40%), and cardiac surgical 1578/4395 (36%). Among a cohort of 9107 first admissions with ICU stay of at least one day, both hyperlactatemia at presentation (712/3634 (20%) vs. 289/5473 (5%); P < 0.001) and its later development (101/379 (27%) vs. 188/5094 (4%); P < 0.001) were associated with significantly increased case fatality rates as compared with patients without elevated lactate. After controlling for confounding effects in multivariable logistic regression analysis, hyperlactatemia was an independent risk factor for death. Conclusions Hyperlactatemia is common among the critically ill and predicts risk for death.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi Publishing Corporation
                2314-6133
                2314-6141
                2015
                8 January 2015
                : 2015
                : 901590
                Affiliations
                1Division of Nephrology, Department of Medicine, Massachusetts General Hospital, 7 Whittier Place, Suite 106, Boston, MA 02114, USA
                2Division of Nephrology and Hypertension, Department of Medicine and Genetics, UNC School of Medicine, UNC Kidney Center, 7024 Burnett-Womack, CB No. 7155, Chapel Hill, NC 27599-7155, USA
                3Renal Division, Department of Medicine, Brigham and Women's Hospital, 75 Francis Street, MRB4, Boston, MA 02115, USA
                Author notes
                *Andrew S. Allegretti: aallegretti@ 123456partners.org

                Academic Editor: Boris Jung

                Article
                10.1155/2015/901590
                4306401
                0b09626b-82a1-4a72-9601-8e6541a13159
                Copyright © 2015 Andrew S. Allegretti et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 2 October 2014
                : 8 December 2014
                : 22 December 2014
                Categories
                Research Article

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