Hyperlactatemia caused by intra-venous administration of glycerol: A case study
A 53-year-old woman with a medical history of the craniotomy for meningioma removal 10 years ago, was again scheduled the operation for her regrown tumor removal. She also had hypothyroidism for the past 10 years, which was treated with oral prednisolone at 20 mg/day and levothyroxine sodium at 50 μg/day.\nshows the results of blood chemistry tests performed at the time of admission to the hospital.\nThe patient was admitted to our ICU after the initial attempt of tumor removal, which resulted in failure because of severe hemorrhage prior to tumor handling. Surgery was then performed 3 months after ICU discharge, and the patient was once again admitted to the ICU after surgery. During both stays in the ICU the patient was administered 200 mL of Glyceol® over a period of 30 minutes, every 6 hours from 0:00 am. Despite her stable general condition, routine arterial blood gas analysis (Diagnostics 860, Chiron, CA, US) at around 6:30 every morning indicated reappeared hyperlactatemia. The fact that repeated measurements of her lactate levels were normal at other time points, made us to consider Glyceol® administration as the cause of her transient hyperlactatemia.\nTo exclude the possibility of impaired tissue perfusion caused by rapid infusion of hypertonic solutions as another cause of this transient hyperlactatemia, the patient was alternately administered Glyceol® and 20% mannitol solutions. The lactate levels increased gradually and peaked 45 minutes after Glyceol® administration, while no significant change was observed in case of mannitol. Blood glucose level increased slightly after Glyceol® administration but the increase was not significant []. This transient hyperlactatemia was reproducible by administration of Glyceol®.\nMetabolic abnormality was also considered another possible cause of her transient hyperlactatemia; however her amino acid analysis, urinary organic acid analysis and serum acyl carnitine analysis all showed normal results, and hyperammonemia, hypoglycemia, or ketonuria were not observed. In addition, impaired perfusion, infection and convulsive seizure were not observed during patient admission. Liver diseases including hepatitis, congenital metabolic diseases, glycerol metabolism abnormality, any diseases similar to Reye's syndrome, mitochondrial disorders and other conditions were all considered as differential diagnoses but were all unlikely because of her laboratory finfings. Moreover, Glyceol® administration produced hyperlactatemia even after correcting her hemoglobin concentrations in order to improve oxygen transport, while increased urinary excretion of lactic and pyruvic acids was found [].\nSince mannitol and Glyceol® administration resulted in different levels of lactate concentration, transient hyperlactatemia was unlikely to be triggered by impaired tissue perfusion caused by rapid infusion of hypertonic solutions.\nWe then performed a retrospective chart review and found other nine patients admitted to Jichi Medical University Hospital ICU after intracranial surgery and administered Glyceol® during the past year. All nine cases were confirmed to be without notable dehydration, infection or convulsive seizure before or after the administration of Glyceol®. We found that their lactate levels increased in general, peaked approximately 45 minutes after Glyceol® administration and returned to preadministration levels around 3 hours after []. No significant change in blood glucose was seen during Glyceol® administration.