From the Research
Significance of Lactic Acidosis in APAP-Induced Liver Injury
- Lactic acidosis is a significant prognostic marker in acetaminophen-induced fulminant hepatic failure, as evidenced by higher arterial lactate levels in nonsurvivors compared to survivors 1.
- The presence of lactic acidosis in APAP-induced liver injury can be attributed to two different scenarios:
- Early in the course of poisoning, where the toxic metabolite of paracetamol inhibits electron transfer in the mitochondrial respiratory chain, leading to aerobic respiration inhibition 2.
- Later in the course of poisoning, as a consequence of established liver failure, where lactate is elevated primarily due to reduced hepatic clearance, and potentially due to peripheral anaerobic respiration in shocked patients 2.
- Lactic acidosis can also occur in the absence of hepatic injury, as seen in a case report where a patient developed anion gap metabolic acidosis due to 5-oxoproline after an acute acetaminophen overdose, without substantial hepatic damage 3.
- The development of type B lactic acidosis with hypoglycemia in acetaminophen toxicity may be caused by a deficit in gluconeogenesis secondary to severe hepatic failure and/or a toxic metabolite of acetaminophen 4.
- Post-resuscitation arterial lactate concentration has been shown to be a strong predictor of mortality in patients with paracetamol hepatotoxicity, and is included in the modified King's College criteria for consideration of liver transplantation 2.