2006年7月
Acid-base balance during continuous veno-venous hemofiltration: The impact of severe hepatic failure
INTERNATIONAL JOURNAL OF ARTIFICIAL ORGANS
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- 巻
- 29
- 号
- 7
- 開始ページ
- 668
- 終了ページ
- 674
- 記述言語
- 英語
- 掲載種別
- 出版者・発行元
- WICHTIG EDITORE
Background: Continuous renal replacement therapy (CRRT) affects acid-base balance but the influence of severe hepatic failure (SHF) on this effect is unknown.
Aim: To assess the effect of SHF on acid-base balance in patients receiving CVVH.
Design: Retrospective laboratory investigation.
Subjects: Forty patients with SHF and acute renal failure (ARF) treated with CVVH and 42 critically ill patients with severe ARF but no liver disease also treated with CVVH (controls).
Intervention: Retrieval of clinical and laboratory data from prospective unit and laboratory databases.
Methods: Quantitative acid-base status assessment using the Stewart-Figge methodology. Comparison of findings between the two groups.
Results: Although CVVH had a major effect on acid base balance in both groups, patients with SHF had a higher mean lactate concentrations (4.8 vs. 3.1 mmol/L; p < 0.0005), a greater base deficit compared to controls (-1 vs. 4.1 mEq/L; p < 0.0001) and a lower PaCO2 tension (36.8 vs. 42.5 mmHg; p < 0.0001), despite the use of bicarbonate replacement fluid. The acidifying effect of hyperlactatemia was slightly worsened by an increased strong ion gap (9.3 vs. 4.9 mEq/L; p < 0.0001). It was, however, attenuated by an increased strong ion difference apparent (SIDa) (43.6 vs. 41.9 mEq/L; p < 0.05) secondary to hypochloremia (96 vs. 100 mmol/L; p < 0.0001) and by hypoalbuminemia, although hypoalbuminemia in SHF patients (26 vs. 23; p < 0.005) was less pronounced than in controls.
Conclusion: The use of CVVH does not fully correct the independent acidifying effect of liver failure on acid-base status. Increased lactate and strong ion gap values maintain a persistent base deficit despite the alkalinizing effects of hypoalbuminemia and hypochloremia. The correction of acidosis in SHF patients may require more intensive CVVH.
Aim: To assess the effect of SHF on acid-base balance in patients receiving CVVH.
Design: Retrospective laboratory investigation.
Subjects: Forty patients with SHF and acute renal failure (ARF) treated with CVVH and 42 critically ill patients with severe ARF but no liver disease also treated with CVVH (controls).
Intervention: Retrieval of clinical and laboratory data from prospective unit and laboratory databases.
Methods: Quantitative acid-base status assessment using the Stewart-Figge methodology. Comparison of findings between the two groups.
Results: Although CVVH had a major effect on acid base balance in both groups, patients with SHF had a higher mean lactate concentrations (4.8 vs. 3.1 mmol/L; p < 0.0005), a greater base deficit compared to controls (-1 vs. 4.1 mEq/L; p < 0.0001) and a lower PaCO2 tension (36.8 vs. 42.5 mmHg; p < 0.0001), despite the use of bicarbonate replacement fluid. The acidifying effect of hyperlactatemia was slightly worsened by an increased strong ion gap (9.3 vs. 4.9 mEq/L; p < 0.0001). It was, however, attenuated by an increased strong ion difference apparent (SIDa) (43.6 vs. 41.9 mEq/L; p < 0.05) secondary to hypochloremia (96 vs. 100 mmol/L; p < 0.0001) and by hypoalbuminemia, although hypoalbuminemia in SHF patients (26 vs. 23; p < 0.005) was less pronounced than in controls.
Conclusion: The use of CVVH does not fully correct the independent acidifying effect of liver failure on acid-base status. Increased lactate and strong ion gap values maintain a persistent base deficit despite the alkalinizing effects of hypoalbuminemia and hypochloremia. The correction of acidosis in SHF patients may require more intensive CVVH.
- リンク情報
- ID情報
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- ISSN : 0391-3988
- Web of Science ID : WOS:000239585300004