Blood lactate levels have been shown to correlate with injury severity as well as the overall prognosis of the severely injured patient [20]. Kaplan et al.

were able to show among 282 patients with a major vascular injury, that initial emergency department acid-base variables (pH, base deficit, lactate, anion gap, apparent strong ion difference and strong ion gap) were able to discriminate survivors from non-survivors [21]. Sindert et al. published recently a large study with 489 trauma patients, where they were testing the diagnostic utility of Base Deficit (BD) measurements at triage and four hours later, in distinguishing learn more minor from major injury [22]. They wanted to test, if infusion of chloride-rich solution, such as normal saline (NS), confuses the results. Even infusion of more than 2000 ml of normal saline didn’t confound the prognostic value of GS-4997 BD. In this study, there were clear differences in BE and pH values between the two different fluid strategy groups. The reason for this difference remains unclear. Considering

BE and pH values as markers of adequate tissue oxygenation, conventional fluid therapy appears to be more effective than small volume resuscitation in compensating the hypovolaemia. Because 300 ml of hypertonic saline (NaCl 7.5%) contains 385 mmol of selleck compound Chloride ions (1283 mmol/l), it could cause hyperchloraemic acidosis. Chloride levels were not measured in this study. There was no statistically significant difference between the lactate levels, which would support some other cause for the HAS1 acidosis than lactataemia and compromised tissue oxygenation. The greater decrease of the haemoglobin level within the HS-group is presumably explained by a larger intravascular volume effect of the HS and haemodilution. There is evidence, that infusion of hypertonic saline dextran causes metabolic acidosis. Kreimeier and Messmer in their review article suggest, that acidosis after bolus infusion of hypertonic saline would be due to improvement

of nutritional blood flow and a wash-out of acidic substances and metabolites, rather than only hyperchloraemia [24]. There has been an extensive interest in hypertonic saline during the past few decades because of its ease of transport, logistical feasibility for military use, speed of administration and rapid correction of haemodynamics [25]. In fluid resuscitation the basic mechanism of action of hypertonic saline is rapid osmotic mobilisation of water from intercellular spaces, endothelial cells and red blood cells into intravascular space. Because cells become oedematous during shock, hypertonic saline has been shown to normalize cell volume rather than reduce it below normal. Infusion of hypertonic saline dilates arterioles and reduces peripheral and pulmonary vascular resistance by directly relaxing smooth muscle and decreasing blood viscosity.