No abstract

We report 15 children who developed transient liver dysfunction related to hepatic ischaemia. All patients had cardiocirculatory failure 24 h before the onset of liver injury (day 1). Peak serum values of transaminases occurred between day 1 and day 3: SGOT (mean: 759 IU/l, range: 150-4400); SGPT (418 IU/l, 95-2547). Transaminase values decreased rapidly and normalised from day 6 to day 10. Minimum values of prothrombin test (PT) occurred on day 1 (31%, 10-70) and 13/15 patients had a PT less than 50% (27%, 10-44). PT values normalized from day 3 to day 10. Hypoglycaemia was present in 8/15 patients on day 1. Liver dysfunction improved after correction of the circulatory failure. These results confirm that transient hepatic dysfunction, probably as a consequence of hepatic hypoperfusion, may occur frequently in children after acute circulatory failure. We conclude that the diagnosis of ischaemic liver injury or shock liver syndrome in children can be made on clinical and biochemical criteria, and that liver biopsy is unnecessary.

PONV never induced complications or delayed patient discharge and curative treatment was rapidly effective.

A one month old child inadvertently received an intravenous bolus injection of 50 mg of lidocaine instead of contrast iodine. The clinical picture comprised collapse, respiratory arrest, convulsions and coma. The calculated maximum level of lidocaine was 5.39 mg/l. The recovery was complete. The toxicity of lidocaine is discussed.