Is Sodium Acetate Dextran Superior to Sodium Chloride Dextran for Small Volume Resuscitation from Traumatic Hemorrhagic Shock?

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Abstract
Small volumes (4 mL/kg body weight (bw)) of hypertonic sodium chloride dextran effectively restore cardiac output and nutritional blood flow and increase arterial pressure in severe hemorrhagic shock. It has been suggested that the chloride anion be replaced with acetate to provide a solution that avoids the risk of hyperchloremia and has the advantage of supplying a buffering base to optimize hypertonic resuscitation. This study compares the effects of hypertonic sodium chloride dextran solution (7.2% NaCl/10% dextran 60 [NaCl-Dx]; n = 7) with sodium acetate dextran (10.4% Na-Ac/10% dextran 60 [NaAc-Dx]; n = 6) on hemodynamic, oxygen transport, and metabolic variables. Both solutions had the identical osmolality (2400 mOsmol/kg). Dogs (16.9 ± 1.9 kg) were anesthetized and mechanically ventilated. Shock was induced by exteriorization of intestine and blood withdrawal (50% of blood volume) to maintain mean arterial blood pressure (MAP) at 40 mm Hg for 75 min. Thereafter, resuscitation was performed either with NaCl-Dx (4 mL/kg over 2 min) or NaAc-Dx (4 mL/kg over 4 min). During hypertonic resuscitation, there was a short-lasting decrease in MAP, which was more pronounced in the NaAc-Dx group (ΔMAP −7.3 ± 2.5 mm Hg). Cardiac index and oxygen consumption were normalized within 5 min after resuscitation with both solutions. In NaAc-Dx-treated animals, MAP remained at lower values as compared to NaCl-Dx-treated dogs at 5 and 30 min after resuscitation (52 ± 3 vs 74 ± 6, and 61 ± 7 vs 79 ± 12 mm Hg; P < 0.05). Arterial pH (7.27 ± 0.02 vs 7.17 ± 0.06 at 5 min, 7.31 ± 0.04 vs 7.23 ± 0.07 at 30 min, and 7.32 ± 0.05 vs 7.26 ± 0.05 at 60 min; P < 0.05) and bicarbonate concentrations (24.4 ± 2.1 vs 16.7 ± 9.5 at 5 min, 26.6 ± 1.8 vs 18.0 ± 1.9 at 30 min, and 27.5 ± 2.1 vs 19.1 ±1.7 mmol/L at 60 min; P < 0.05) in the plasma were normalized shortly after NaAc-Dx infusion; however, hyperlactemia persisted after resuscitation with NaAc-Dx (7.10 ± 1.48 vs 3.82 ± 1.45 at 30 min, and 5.40 ± 1.73 vs 2.71 ± 0.89 mmol/L at 60 min; P < 0.05). We conclude that NaAc-Dx offers no conclusive advantages as compared to NaCl-Dx for resuscitation from traumatic, hemorrhagic shock in our model of controlled hemorrhage. Although NaAc-Dx improved acid base status, hyperlactacidemia persisted.

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