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STUDY OBJECTIVE: To determine the pathogenesis and clinical course of lactic acidosis in adults receiving standard medical care. DESIGN: Placebo arm of a 5-year prospective, randomized, blinded study comparing placebo and dichloroacetate as specific lactate-lowering therapy. Each patient received intravenous saline placebo in addition to conventional therapy. SETTING: Intensive care units of 10 tertiary care hospitals in North America. PATIENTS: One hundred twenty-six patients with lactic acidosis, defined as arterial blood lactate greater than or equal to 5 mmol/L and either arterial pH of less than or equal to 7.35 or base deficit greater than 6 mmol/L. Patients were followed for up to 6 months. MEASUREMENTS AND MAIN RESULTS: Mean [+ or -] SD demographic entry data for 126 patients included: age 56 [+ or -] 17 years, lactate 10.4 [+ or -] 5.5 mmol/L, pH 7.24 [+ or -] 0.14, calculated base deficit 14.1 [+ or -] 5.4, arterial systolic blood pressure 103 29 mm Hg, Glasgow Coma score 7.9 [+ or -] 4.9, and APACHE II score 19.2 [+ or -] 8.1. Despite fluids and pressors, 32% of patients had systolic blood pressures of less than or equal to 90 mm Hg in association with sepsis (59%), cardiac failure (18%), or hemorrhage (18%). The most common causes of lactic acidosis in the absence of shock were sepsis (49%), liver disease (15%), and respiratory failure (12%). The median survival was 38.5 hours. Survival at 24 hours was 59%. Arterial pH predicted 24-hour survival better than base deficit or bicarbonate level. Percent survival was 41% at 3 days and 17% at 30 days. Only 21% of patients survived to leave the intensive care unit, and 17% were discharged from the hospital. In patients receiving sodium bicarbonate, neither acid-base nor hemodynamic status improved. CONCLUSIONS: In this first prospective study of the clinical course of acute lactic acidosis in adults, nearly all subjects had both hemodynamic and nonhemodynamic (metabolic) underlying causes, many of which independently predicted survival and most of which were refractory to standard care.

Immediate, accurate evaluation of blunt trauma hepatic injury (BTHI, traumatic injury to the liver) is essential for establishing a patient's prognosis. Initial physiologic and biochemical variables in 185 patients with BTHI were used to develop predictors of injury severity and death. The model, which uses an anatomic scoring system known as the Injury Severity Score (ISS), and physiologic and neurologic measurements taken upon hospital admission and during the next 72 hours, is explained and evaluated. Injuries were the result of automobile accidents (51 percent), motorcycle accidents (11 percent), pedestrian-automobile contact (8 percent), falls (16 percent), and crush (5 percent). The model was then tested on another group of 323 patients with multiple trauma injuries, including BTHI. Overall, the pattern of internal injuries and their consequences for volume loss (blood and fluid loss), including shock, and the degree of neurologic impairment were the most important predictors of death. Admission base excess (BEA, an indicator of the alkalinity of the blood and body fluids) and the Glasgow Coma Score (GCS, a measurement of neurologic function) were the best predictors of a patient's probability of death. Careful, in-depth analyses are provided of the importance of cardiorespiratory, metabolic, and hematologic (blood) and coagulation factors for outcome. The value of physiologic parameters measured on admission, such as the ISS and plasma lactate levels (an indicator of injury), is carefully assessed. Other models that predict mortality after BTHI are evaluated. Blunt multiple trauma is beginning to be recognized as an important cause of death, and patient evaluation should distinguish between this form of injury and penetrating injury. (Consumer Summary produced by Reliance Medical Information, Inc.)