Prognostic value of blood lactate, base deficit, and oxygen-derived variables in an LD50 model of penetrating trauma

Abstract

To determine whether blood lactate, base deficit, or oxygen-derived hemodynamic variables correlate with morbidity and mortality rates in a clinically-relevant LD50 model of penetrating trauma. Prospective, controlled study. University research laboratory. Anesthetized, mechanically-ventilated mongrel pigs (30 +/- 2 kg, n = 29). A captive bolt gun delivered a penetrating injury to the thigh, followed immediately by a 40% to 60% hemorrhage. After 1 hr, shed blood and supplemental crystalloid were administered for resuscitation. After penetrating injury, 50.7 +/- 0.3% hemorrhage (range 50% to 52.5%), and a 1-hr shock period, seven of 14 animals died, compared with six of six animals after 55% to 60% hemorrhage, and 0 of nine animals after <or=to47.5% hemorrhage. Only two of 13 deaths occurred during fluid resuscitation. At the LD50 hemorrhage, peak lactate concentration and base deficit were 11.2 +/- 0.8 mM and 9.3 +/- 1.5 mmol/L, respectively, and minimum mixed venous oxygen saturation, systemic oxygen delivery, and systemic oxygen consumption were 33 +/- 5%, 380 +/- 83 mL/min/kg, and 177 +/- 35 mL/min/kg, respectively. For comparison, baseline preinjury values were 1.6 +/- 0.1 mM, -6.7 +/- 0.6 mmol/L, 71 +/- 3%, 2189 +/- 198 mL/min/kg, and 628 +/- 102 mL/min/kg, respectively. Of all the variables, only lactate was significantly related to blood loss before and after fluid resuscitation in the 16 survivors. However, r2 values were relatively low (.20 to .50), which indicates that only a small fraction of the hyperlactacidemia was directly related to tissue hypoperfusion. In the whole population of survivors and nonsurvivors, both lactate and base deficit (but none of the oxygen-derived variables) correlated with blood loss. Arterial lactate is a stronger index of blood loss after penetrating trauma than base deficit or oxygen-derived hemodynamic variables. The reliability of arterial lactate depends on several factors, such as the time after injury, the proportion of survivors and nonsurvivors in the study population, and on factors other than tissue hypoxia. (Crit Care Med 1998; 26:154-161)