Lactic acidosis update for critical care clinicians

Area of Science:

• Biochemistry
• Pathophysiology
• Internal Medicine

Background:

• Lactic acidosis is a metabolic acidosis characterized by elevated lactic acid.
• It stems from either overproduction or underutilization of lactic acid.
• Mechanisms include tissue hypoxia (Type A) and impaired lactate clearance.

Purpose of the Study:

• To review the mechanisms of lactic acid production and clearance.
• To discuss the role of various conditions and drugs in lactic acidosis.
• To evaluate current and potential treatment strategies.

Main Methods:

• Literature review of lactic acidosis mechanisms.
• Analysis of causes including hypoxia, malignancies, and drug effects (e.g., metformin).
• Evaluation of treatment options like sodium bicarbonate, carbicarb, dichloroacetate, and hemofiltration.

Main Results:

• Type A lactic acidosis (overproduction) is often linked to circulatory or respiratory issues.
• Underutilization causes include liver disease and enzyme deficiencies.
• Metformin's risk is low, mainly in patients with severe renal/cardiac dysfunction.
• Sodium bicarbonate can worsen lactic acidosis; carbicarb shows promise but lacks extensive trials.
• Dichloroacetate improves lab values but not survival; hemofiltration's efficacy is questionable.

Conclusions:

• The primary treatment for lactic acidosis is to address the underlying cause.
• Current therapeutic interventions have limitations, with no universally effective treatment for Type A lactic acidosis.
• Further research is needed for effective management strategies.