Limited resuscitation with hypertonic saline, hypertonic sodium acetate, and lactated ringer's solutions in a model of uncontrolled hemorrhage from a vascular injury

Background: Hypertonic sodium acetate-dextran solution (HAD) causes vasodilatation and buffers metabolic acidosis. In controlled hemorrhage models, HAD in small volumes increases cardiac output without increasing blood pressure, thus creating a 'high flow-low pressure' state. The objective of this study was to determine whether limited resuscitation of uncontrolled hemorrhage with HAD solution improves gut perfusion as measured by intestinal mucosal tonometry. Methods: Three groups of 10 swine were bled 25 mL/kg by means of a fernoral artery catheter to produce a mean blood pressure of 30 mm Hg. A 4-mm abdominal aortic laceration was then produced by pulling out a preimplanted wire loop. Groups were then randomly assigned to be resuscitated with either lactated Ringer's solution, a hypertonic saline-dextran solution or HAD solution sufficient to maintain a mean blood pressure of 45 mm Hg for 5 hours or until death. Outcomes were measured by survival, intraperitoneal blood loss, hemodynamic monitoring, and ileal mucosal tonometry. Results: HAD infusions caused transient worsening of hypotension and were associated with increased mortality (p = 0.038). Blood loss and volumes required for resuscitation were significantly increased in the lactated Ringer's solution group. HAD showed significant buffering effect against metabolic acidosis in arterial blood only, but intestinal ileal mucosal tonometry was not different among the groups. Conclusion: HAD did not improve gut perfusion despite buffering the systemic acidosis of shock and caused increased mortality. Limited resuscitation with any of these solutions is associated with significant mucosal acidosis.