OBJECTIVE: To evaluate the magnitude and cause of metabolic acidosis after infusion of 7.5% sodium chloride 6% dextran 70. DESIGN: Randomized, prospective clinical study. SETTING:University hospital. PATIENTS: Two groups of 14 patients each, undergoing repair of abdominal aortic aneurysm. INTERVENTIONS: Patients were randomly assigned to receive either 250 mL of hypertonic saline dextran (HSD) or a conventional fluid regimen with 250 mL of hydroxyethyl starch in normal saline solution (H-NS) during the period of aortic clamping. Additionally, normal saline was used in both groups to reach a target pulmonary artery occlusion pressure of 15-18 mmHg. pH, Paco2, and serum concentrations of sodium, potassium, magnesium, calcium, chloride, lactate, albumin, and phosphate were measured. Strong ion difference was calculated as (sodium + potassium + magnesium + calcium) - (chloride + lactate). The amount of weak plasma acid was calculated. MEASUREMENTS AND MAIN RESULTS: The infusion of HSD resulted in an immediate large increase in serum sodium (19 mmol/L) and chloride (22 mmol/L), whereas the infusion of H-NS led only to mild increases in serum sodium (3 mmol/L) and chloride (6 mmol/L). Both HSD and H-NS caused concomitant and equal decreases in the amount of weak plasma acid, strong ion difference, and pH (7.28-7.30). The reduction of bicarbonate was also identical and proportional to the extent of dilution due to infusion of HSD and H-NS. This induced metabolic acidosis was corrected spontaneously in both groups 24 hrs after surgery. CONCLUSION: Both the intravenous administration of 7.5% sodium chloride and the conventional fluid regimen with saline-based 6% hydroxyethyl starch solution resulted in a metabolic acidosis of equal extent. This suggests dilution of plasma buffers or a decrease in strong ion difference to be the primary cause of metabolic acidosis.
RCT Entities:
OBJECTIVE: To evaluate the magnitude and cause of metabolic acidosis after infusion of 7.5% sodium chloride 6% dextran 70. DESIGN: Randomized, prospective clinical study. SETTING: University hospital. PATIENTS: Two groups of 14 patients each, undergoing repair of abdominal aortic aneurysm. INTERVENTIONS:Patients were randomly assigned to receive either 250 mL of hypertonic saline dextran (HSD) or a conventional fluid regimen with 250 mL of hydroxyethyl starch in normal saline solution (H-NS) during the period of aortic clamping. Additionally, normal saline was used in both groups to reach a target pulmonary artery occlusion pressure of 15-18 mmHg. pH, Paco2, and serum concentrations of sodium, potassium, magnesium, calcium, chloride, lactate, albumin, and phosphate were measured. Strong ion difference was calculated as (sodium + potassium + magnesium + calcium) - (chloride + lactate). The amount of weak plasma acid was calculated. MEASUREMENTS AND MAIN RESULTS: The infusion of HSD resulted in an immediate large increase in serum sodium (19 mmol/L) and chloride (22 mmol/L), whereas the infusion of H-NS led only to mild increases in serum sodium (3 mmol/L) and chloride (6 mmol/L). Both HSD and H-NS caused concomitant and equal decreases in the amount of weak plasma acid, strong ion difference, and pH (7.28-7.30). The reduction of bicarbonate was also identical and proportional to the extent of dilution due to infusion of HSD and H-NS. This induced metabolic acidosis was corrected spontaneously in both groups 24 hrs after surgery. CONCLUSION: Both the intravenous administration of 7.5% sodium chloride and the conventional fluid regimen with saline-based 6% hydroxyethyl starch solution resulted in a metabolic acidosis of equal extent. This suggests dilution of plasma buffers or a decrease in strong ion difference to be the primary cause of metabolic acidosis.
Authors: Dirk Bruegger; Matthias Jacob; Stefan Scheingraber; Peter Conzen; Bernhard F Becker; Udilo Finsterer; Markus Rehm Journal: Intensive Care Med Date: 2005-07-06 Impact factor: 17.440
Authors: Dirk Bruegger; Gregor I Kemming; Matthias Jacob; Franz G Meisner; Christoph J Wojtczyk; Kristian B Packert; Peter E Keipert; N Simon Faithfull; Oliver P Habler; Bernhard F Becker; Markus Rehm Journal: Crit Care Date: 2007 Impact factor: 9.097
Authors: Matthias Jacob; Daniel Chappell; Peter Conzen; Mahlon M Wilkes; Bernhard F Becker; Markus Rehm Journal: Crit Care Date: 2008-03-04 Impact factor: 9.097