title: Effect of hypertonic saline dextran on acid-base balance in patients undergoing surgery of abdominal aortic aneurysm.
abstract: OBJECTIVE
  To evaluate the magnitude and cause of metabolic acidosis after infusion of 7.5% sodium chloride 6% dextran 70.
  
  
  METHODS
  Randomized, prospective clinical study.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Two groups of 14 patients each, undergoing repair of abdominal aortic aneurysm.
  
  
  METHODS
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.affiliation: Clinic of Anesthesiology, Ludwig-Maximilians-University Munich, Germany.
authors.forename: Dirk
authors.initials: D
authors.lastname: Bruegger
authors.forename: Andreas
authors.initials: A
authors.lastname: Bauer
authors.forename: Markus
authors.initials: M
authors.lastname: Rehm
authors.forename: Markus
authors.initials: M
authors.lastname: Niklas
authors.forename: Matthias
authors.initials: M
authors.lastname: Jacob
authors.forename: Michael
authors.initials: M
authors.lastname: Irlbeck
authors.forename: Bernhard F
authors.initials: BF
authors.lastname: Becker
authors.forename: Frank
authors.initials: F
authors.lastname: Christ
mesh_terms: D000136:Acid-Base Equilibrium / Q000187:drug effects*; D000138:Acidosis / Q000209:etiology; D000368:Aged; D000704:Analysis of Variance; D017544:Aortic Aneurysm, Abdominal / Q000601:surgery*; D003911:Dextrans / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D005440:Fluid Therapy / Q000009:adverse effects / Q000379:methods*; D006801:Humans; D008297:Male; D019990:Perioperative Care; D011446:Prospective Studies; D012462:Saline Solution, Hypertonic / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D012965:Sodium Chloride / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D003911:Dextrans; D012462:Saline Solution, Hypertonic; C104375:hypertonic saline-dextran solution; D012965:Sodium Chloride