Natural history and course of acquired lactic acidosis in adults

https://doi.org/10.1016/0002-9343(94)90047-7Get rights and content

Abstract

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 6mmol/L. Patients were followed for up to 6 months.

measurements and main results: Mean ± SD demographic entry data for 126 patients included: age 56 ± 17 years, lactate 10.4 ± 5.5 mmol/L, pH 7.24 ± 0.14, calculated base deficit 14.1 ± 5.4, arterial systolic blood pressure 103 ± 29 mm Hg, Glasgow Coma score 7.9 ± 4.9, and APACHE II score 19.2 ± 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.

References (43)

  • TJ Iberti et al.

    Low sensitivity of the anion gap as a screen to detect hyperlactatemia in critically ill patients

    Crit Care Med

    (1990)
  • PW Stacpoole et al.

    Treatment of lactic acidosis with dichloroacetate

    NEJM

    (1983)
  • PW Stacpoole et al.

    Dichloroacetate in the treatment of lactic acidosis

    Ann Intern Med

    (1986)
  • DJ Cooper et al.

    Bicarbonate does not improve hemodynamics in cricitally ill patients who have lactic acidosis

    Ann Intern Med

    (1990)
  • PW Stacpoole et al.

    A controlled clinical trial of dichloroacetate treatment in patients with lactic acidosis

    NEJM

    (1992)
  • G Teasdale et al.

    Assessment of coma and impaired consciousness

  • WA Knaus et al.

    An evaluation of outcome from intensive care in major medical centers

    Ann Intern Med

    (1986)
  • SAS Institute, Inc

    SAS User's Guide: Basics and SAS User's Guide: Statistics, Version 5 Edition

    (1985)
  • GW Snedecor et al.

    Statistical Methods

    (1980)
  • EL Kaplan et al.

    Nonparametric estimation from incomplete observations

    J Am Statist Assoc

    (1958)
  • JD Kalbfleish et al.

    The Statistical Analysis of Failure Time Data

    (1980)
  • Cited by (151)

    • Metabolic Acidosis: Differentiating the Causes in the Poisoned Patient

      2022, Emergency Medicine Clinics of North America
      Citation Excerpt :

      Many clinicians may be inclined to treat toxin-induced metabolic acidosis with a buffer such as sodium bicarbonate to increase serum pH. This practice should be discouraged. The administration of sodium bicarbonate has never been shown to improve outcomes in patients with metabolic acidosis and can be detrimental in some.65 Paradoxic intracellular acidosis can occur due to increased production of carbon dioxide.66

    • Lactic Acidosis: Current Treatments and Future Directions

      2016, American Journal of Kidney Diseases
      Citation Excerpt :

      Limited data suggest that at a given blood lactate level, acidemia is associated with worse clinical outcomes8,9; however, further work is required on this important issue. Sustained hyperlactatemia in sepsis or low-flow states carries mortality ≥ 60%.1,10 Next, we first provide a brief description of the current therapy of lactic acidosis and then suggest potential future therapies that derive from advances in our understanding of the pathophysiology of the disorder.

    View all citing articles on Scopus

    This work was supported by DK 35448 and RR 00082 from the National institutes of Health.

    View full text