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Copyright ©The Author(s) 2024.
World J Diabetes. Jun 15, 2024; 15(6): 1178-1186
Published online Jun 15, 2024. doi: 10.4239/wjd.v15.i6.1178
Table 1 Lactic acidosis due to inadequate tissue oxygenation versus mitochondrial dysfunction[35]
Clinically relevant considerations
Lactic acidosis due to inadequate tissue oxygen supply to meet demand (Type A lactic acidosis)
Lactic acidosis due to mitochondrial dysfunction (Type B lactic acidosis)
Selected causesHypovolemia/dehydrationMetformin toxicity
SepsisSepsis
Heart failureCyanide poisoning
Respiratory failure
Clinical and laboratory featuresCapillary refill time > 3 sCapillary refill time 0-3 s
ScvO2 < 70%ScvO2 ≥ 70% and CO2 gap < 6 mmHg
ScvO2 ≥ 70% and CO2 gap > 6 mmHg
TreatmentFluid challenge, followed by fluid loading if capillary refill time or blood pressure improvesStop further administration and consider extracorporeal removal of toxic agent (e.g., metformin)
Empirical broad-spectrum antimicrobials for suspected sepsisEmpirical broad-spectrum antimicrobials for suspected sepsis
Vasopressors/inotropes to maintain a mean arterial pressure ≥ 65 mmHg
Supplemental oxygen and mechanical ventilation to maintain an arterial oxygen saturation of 94%-98%
Correct severe anemia and maintain hemoglobin 7-9 g/dL
Table 2 Risk factors for metformin-associated lactic acidosis
Risk factors
Mechanism
Kidney failure (any cause)Reduced renal elimination of metformin[45]
CimetidineReduced renal elimination of metformin[51]
RibociclibReduced renal elimination of metformin[52]
Excessive alcohol consumptionEthanol oxidation consumes nicotinamide adenine dinucleotides that are also required for lactate metabolism[50]