Key result
Early lactate surge on epinephrine is linked to ~38% lower 28-day mortality.
Why the study?
The prognostic value of an early increase in arterial lactate concentration induced by epinephrine infusion during shock was unclear.
Does an early increase in arterial lactate concentration under epinephrine infusion prognosticate 28-day mortality in patients with shock?
Cohort (n=100)
No
Does an early increase in arterial lactate concentration under epinephrine infusion prognosticate 28-day mortality in patients with shock?
Odds Ratio: 0.99 (95% CI 0.99–0.99)
Absolute Event Rate: 52.4% vs 84.7%
p-value: p=0.03
An early increase in arterial lactate concentration following epinephrine administration is associated with a better prognosis and lower 28-day mortality in patients with shock.
Early lactate rise may aid prognostic stratification in epinephrine-treated shock; hypothesis-generating and requires prospective validation before guiding care.
To determine whether an epinephrine-induced early increase in arterial lactate concentration can prognosticate the outcome during shock state, we conducted a retrospective study in a 16-bed medical intensive care unit of a teaching hospital in France. One hundred consecutive patients admitted because of a shock state irrespective of etiology and treated with epinephrine were included. Patients were not enrolled if they received epinephrine administration before intensive care unit admission. Sequential arterial lactate measurements were performed at the time of epinephrine infusion (H0) and 4 h later (H4) in which Deltalactate was defined as (100 x [arterial lactate(H4)-arterial lactate(H0)]/arterial lactate(H0)) and expressed as a percentage. Etiology of shock was septic (82%), cardiogenic (10%), or hemorrhagic (8%). Twenty-eight-day mortality rate was 72%. At admission, arterial lactate concentration was elevated (4.96 +/- 3.8 mmol/L) and was further increased upon epinephrine administration, reaching a peak at H4 (8.22 +/- 3.66). When patients were stratified according to their outcome, nonsurvivors displayed the same pattern as survivors, although with a significant upward shift in values (ANOVA, P = 0.0003). The Sequential Organ Failure Assessment score and Deltalactate were the only variables associated with the 28-day risk of death, with an odds ratio of 1.32 (95% confidence interval [CI], 1.06-1.65; P = 0.01) and 0.99 (95% CI, 0.99-0.99; P = 0.03), respectively, in multivariate analysis. At a value of 100%, Deltalactate predicted death, with a 71% sensitivity (95% CI, 51%-87%) and a 67% specificity (95% CI, 43%-85%). Kaplan-Meier survival analysis confirmed this finding, with a 52.4% death rate among patients with Deltalactate greater than 100 comparatively to 84.7% when Deltalactate was less than 100 (log-rank test, P = 0.0002). An adapted response (lactate production) to a pharmacological trigger (epinephrine) is associated with better prognosis during shock of various etiologies.
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Wutrich et al. (2010) conducted a cohort in Shock (n=100). Deltalactate >100% (early increase in arterial lactate under epinephrine) vs. Deltalactate <100% was evaluated on 28-day mortality (OR 0.99, 95% CI 0.99-0.99, p=0.03). An early increase in arterial lactate (Deltalactate >100%) under epinephrine infusion was associated with lower 28-day mortality compared to an increase <100% (52.4% vs 84.7%; P=0.0002).
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