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Published on: November 27, 2019
Evaluating lactate prognostic value in children suspected of acetaminophen-induced liver failure in Liberia
Mohamad K Haidar1,2, Nikola Morton3, Thomas Roederer4
1Epicentre, Paris, France. mohamad.haidar193@gmail.com.
Insights
Hyperlactatemia in young children with acetaminophen-induced liver injury indicates poor prognosis. A lactate level above 7.2 mmol/L suggests a high risk of mortality in these pediatric cases.
Area of Science:
- Pediatric Hepatology
- Toxicology
- Critical Care Medicine
Background:
- Acetaminophen (paracetamol) overdose is a common cause of acute liver injury in children.
- The prognostic value of hyperlactatemia in pediatric acetaminophen-induced liver injury (AILI) is not well-established.
- Early identification of high-risk pediatric patients is crucial for timely intervention.
Purpose of the Study:
- To investigate the prognostic significance of hyperlactatemia in young children with liver injury.
- To determine the optimal lactate threshold for predicting mortality in pediatric acetaminophen toxicity.
- To evaluate the utility of existing lactate thresholds in this specific population.
Main Methods:
- Retrospective medical chart review of children under 5 years old admitted with hepatocellular injury.
- Inclusion of patients with available blood lactate measurements on admission.
- Analysis of mortality rates, acetaminophen concentrations, and lactate levels.
Main Results:
- A total of 95 children were analyzed; 52% died during hospitalization.
- Children who died had significantly higher median lactate levels (10.7 mmol/L) compared to survivors (6.1 mmol/L).
- An optimal lactate threshold of 7.2 mmol/L predicted non-survival with 84% sensitivity and 70% specificity (AUC=0.80).
Conclusions:
- Hyperlactatemia is a significant predictor of mortality in pediatric acetaminophen-induced liver injury.
- A venous blood lactate concentration exceeding 7.2 mmol/L indicates a poor prognosis in young children with suspected acetaminophen toxicity.
- Established lactate thresholds (3.5-4 mmol/L) are insufficient for identifying non-survival in this pediatric cohort.
Background:
The prognostic significance of hyperlactatemia in young children with liver injury suspected to be attributed to repeated supratherapeutic doses of acetaminophen remain understudied.
Methods:
We conducted a retrospective medical chart review including children aged <5 years admitted with hepatocellular injury. The study was conducted in Bardnesville Junction Hospital operated by Médecins Sans Frontières in Monrovia, Liberia.
Results:
We analyzed 95 children with liver injury in whom a blood lactate measurement on admission was available. Eighty children (84%) were aged <2 years; 49 children (52%) died during hospitalization. The median acetaminophen concentration on admission was 20 mg/L with 60 (70%) children presenting concentrations exceeding 10 mg/L. Median lactate was significantly higher in children who died (10.7 mmol/L; interquartile range (IQR): 8.5-15.7) than those who survived (6.1 mmol/L; IQR: 4.1-8.5), P value < 0.001). The optimal threshold obtained was 7.2 mmol/L with a sensitivity of 84% and specificity 70% (area under curve = 0.80). The previously established thresholds of 3.5 and 4 mmol/L lactate had very low specificity identifying non-survival in children included in this study.
Conclusion:
In this setting, young children with ALF possibly attributed to acetaminophen toxicity were unlikely to survive if the venous blood lactate concentration exceeded 7.2 mmol/L.
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