Clinical significance of serum lactate levels in acetaminophen toxicity

January 6, 2011, 10:51 pm


Understanding lactic acidosis in paracetamol (acetaminophen) poisoning. Shah AD et al.  Br J Clin Pharmacol 2011 Jan;71:20-8.


Acetaminophen (APAP) can cause lactic acidosis at two different stages of toxicity.  First, patients with massive acetaminophen overdose can present early after ingestion — before onset of hepatotoxicity — with coma and elevated serum lactate. This occurs because the toxic metabolites of APAP inhibit mitochondrial respiration.  These patients in general do well with supportive care and treatment with N-acetylcysteine (NAC).

Second, in later stages of APAP toxicity, hepatic failure decreases lactate clearance.  In addition, medical instability, hypotension, and decreased perfusion may increase lactate production.  In this case, significantly elevated lactate suggests a poor prognosis; lactate level has been incorporated into the Modified King’s College criteria for selecting patients with APAP-related acute liver failure for transplantation.

This article is a complete review of lactate and APAP toxicity, and well worth reading.  The authors make the following clinical points:

  1. Elevated lactate in a patient presenting within 8 hours of acute APAP ingestion suggests mitochondrial inhibition and a significant overdose.
  2. APAP poisoning should be considered in the differential diagnosis of metabolic acidosis.
  3. Significantly elevated lactate in a patient with APAP-induced acute liver failure suggests a poor prognosis, and is part of the modified King’s College Criteria for considering liver transplant.
  4. Any patient with APAP toxicity and decreased mental status or acute liver failure should have lactate level measured.
  5. Since venous lactate correlates fairly well with arterial lactate levels, a venous lactate level can be drawn initially and should be sufficient if it is very high or very low.  Intermediate levels may require confirmation on an arterial sample.

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