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Acidosis as a presenting feature of chloramphenicol toxicity
Insights
Metabolic acidosis can be an early sign of chloramphenicol (CAP) toxicity in critically ill children. Reduced CAP doses are recommended for these patients to prevent severe adverse effects.
Area of Science:
- Pediatric Pharmacology
- Toxicology
- Critical Care Medicine
Background:
- Metabolic acidosis is a known complication of Gray Baby Syndrome.
- However, it has not been previously identified as a presenting feature of chloramphenicol toxicity.
Purpose of the Study:
- To investigate metabolic acidosis as a presenting feature of chloramphenicol toxicity in seriously ill children.
- To determine the relationship between serum chloramphenicol concentrations and the development of metabolic acidosis.
Main Methods:
- Case series of four seriously ill children (4 months to 11 years) who received intravenous chloramphenicol.
- Monitoring of serum chloramphenicol concentrations and clinical signs, including metabolic acidosis, hypotension, hypothermia, and abdominal distension.
Main Results:
- Unexplained metabolic acidosis developed 40-81 hours after initiating chloramphenicol therapy in all four patients.
- Serum chloramphenicol concentrations ranged from 30 to 84 micrograms/ml when acidosis was detected.
- Hypotension, hypothermia, and abdominal distension occurred approximately 23 hours after the onset of acidosis.
- Acidosis and Gray Baby Syndrome signs resolved upon reduction of serum chloramphenicol levels.
Conclusions:
- Metabolic acidosis should be recognized as an early indicator of chloramphenicol toxicity.
- Reduced chloramphenicol dosages are advised for severely ill pediatric patients, particularly those with impaired liver function, to mitigate toxicity risks.
Abstract:
Metabolic acidosis has previously been described in the gray baby syndrome, but has not been documented as a presenting feature. Four seriously ill children (bronchiolitis, hypoaldosteronism, dysautonomia, Reye syndrome), ages 4 months to 11 years, received chloramphenicol (CAP) intravenously. After initial stabilization, unexplained metabolic acidosis occurred 40 to 81 hours after beginning CAP. Serum CAP concentrations were 84, 62, 80, and 30 micrograms/ml, respectively, when acidosis was recognized. Hypotension, hypothermia, and abdominal distension occurred a mean of 23 hours after the onset of acidosis. Acidosis resolved and signs of the gray baby syndrome cleared with the decrease in serum CAP concentrations. Metabolic acidosis should be considered an early sign of CAP toxicity, and CAP should be used in reduced doses in severely ill patients, especially those with liver dysfunction.