Serial blood lactate levels can predict the development of multiple organ failure following septic shock

• Published in: The American journal of surgery Vol. 171; no. 2; pp. 221 - 226
• Main Authors: Bakker, Jan, Gris, Philippe, Coffernils, Michel, Kahn, Robert J., Vincent, Jean-Louis
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-02-1996; Elsevier; Elsevier Limited
• Subjects: Acidosis; Adult; Aged; Aged, 80 and over; Bacterial diseases; Bacterial sepsis; Biological and medical sciences; Blood; Blood pressure; Coagulation; Complications; Death; Failure; Female; Heart rate; Human bacterial diseases; Humans; Hyperlactatemia; Hypoxia; Infectious diseases; Lactates - blood; Lactic Acid; Lactic acidosis; Male; Mean; Medical sciences; Middle Aged; Mortality; Multiple Organ Failure - blood; Multiple Organ Failure - etiology; Multiple Organ Failure - mortality; Multiple regression analysis; Predictive Value of Tests; Sepsis; Septic shock; Shock, Septic - blood; Shock, Septic - complications; Shock, Septic - mortality; Statistical analysis; Survival; Survival Rate; Shock; Human; Infection; Lactates; Prognosis; Septicemia; Bacteriosis; Cardiovascular disease; Exploration; Survival; Blood
• ISSN: 0002-9610; 1879-1883
• DOI: 10.1016/S0002-9610(97)89552-9

Despite successful initial resuscitation, septic shock frequently evolves into multiple system organ failure (MSOF) and death. Since blood lactate levels can reflect the degree of cellular derangements, we examined the relation between serial blood lactate levels and the development of MSOF, or mortality, in patients with septic shock.
In 87 patients with a first episode of septic shock, we measured initial lactate (at onset of septic shock), final lactate (before recovery or death), “lactime” (time during which blood lactate was >2.0 mmol/L), and the area under the curve (AUC) for abnormal values (above 2.0 mmol/L). These measurements were correlated with survival and organ failure and scored for four systems (ie, respiratory, renal, hepatic, and coagulation), adding to a maximal score of 8.
Thirty-three (38%) patients survived. Of the 54 (62%) nonsurvivors, the 13 patients who died during the first 24 hours of septic shock had higher initial blood lactate levels than those who died later (mean ± standard deviation 9.6 ± 5.3 mmol/L versus 5.6 ± 3.7 mmol/L,
P <0.05).
The 74 patients who survived the first 24 hours of shock were studied in more detail. On presentation, survivors had a significantly higher mean arterial pressure (76 ± 12 mm Hg versus 63 ± 20 mm Hg,
P <0.001) and arterial pH (7.40 ± 0.07 versus 7.37 ± 0.09,
P <0.05) than nonsurvivors. Although the differences in initial blood lactate levels between survivors and nonsurvivors did not reach statistical significance (4.7 ± 2.5 mmol/L versus 5.6 ± 3.7 mmol/L), only the survivors had a significant decrease during the first 24 hours of septic shock. The survivors had a significantly lower lactime and AUC than the nonsurvivors. The duration of lactic acidosis was the best predictor of survival (multiple regression analysis,
R
2 = 0.266,
P <0.001), followed by age, heart rate, and mean arterial pressure. Patients with lower organ failure scores had lower initial blood lactate, lactime, and AUC. The duration of lactic acidosis was the only significant predictor of organ failure.
In patients with septic shock, serial determinations of blood lactate levels are good predictors of the development of MSOF and death. In this respect, the duration of lactic acidosis is more important than the initial lactate value. Although a number of factors may contribute to hyperlactatemia, these observations are compatible with a direct role of prolonged tissue hypoxia in the development of complications following septic shock.