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Letters |
Dalhousie University Queen Elizabeth II Health Sciences Centre 1278 Tower Rd. Halifax, Nova Scotia B3H 2Y9 Canada Fax 902-473-7042 E-mail adfraser{at}is.dal.ca
To the Editor:
The case conference entitled "Ethylene glycol poisoning: toxicokinetics and analytical factors affecting laboratory diagnosis" (1) provided a thorough review of many toxicological aspects involved in the diagnosis and monitoring of ethylene glycol (EG) poisoning. The authors stated that "the most serious clinical features observed in EG poisoning are due not to the parent compound but to the metabolites". It was disappointing, therefore, that the authors did not include glycolic acid (GA) analysis in their investigations. Toxicologists first reported the importance of GA analysis in EG poisonings over 10 years ago (2)(3). The third case in this case conference was a diagnostic challenge to the authors because of repeated negative serum EG measurements. Based on our experience with GA analysis in many EG poisonings (4), the diagnosis of EG poisoning could have been made with serum GA analysis in case 3 without a renal biopsy. As stated in the conference, GA accounts for >90% of the anion gap in EG-poisoned patients (the anion gap in case 3 was 20 mmol/L).
It was also mentioned that initial serum EG concentrations in EG poisonings can be very high (127 mmol/L in case 2), whereas death has been reported with virtually undetectable serum EG concentrations. The authors consider this a discrepancy. In our experience, however, an alcoholic who drinks EG typically presents very late for medical attention after EG ingestion. Due to the rapid metabolism of EG to GA, one can anticipate having EG poisoning cases where the diagnosis can only be made by a renal biopsy or at autopsy (if GA analysis is unavailable). Our impetus to develop a serum GA method 8 years ago was based on a similar EG case (undetectable EG in serum) where the ingestion of EG was established by the presence of characteristic oxalate crystals in a renal biopsy several days later. We have had two cases since 1993 with negative EG measurements and GA concentrations >10 mmol/L on admission.
The authors of this conference noted that analysis of GA is unavailable at most medical centers and reference laboratories. In 1996, a report in this journal (5) described a robust gas chromatographic method for the simultaneous quantitation of EG and GA. Clinical laboratories with access to a gas chromatograph (equipped with a capillary column and a flame ionization detector) could easily develop a reliable method for GA quantitation in serum.
Further justification for GA analysis in the management in EG poisoning cases includes the following: Individuals (such as children) with low but measurable EG concentrations in the absence of GA may not require hemodialysis because toxic metabolite formation can be blocked efficiently by ethanol treatment. In addition, treatment of EG poisoning by hemodialysis in adults and children is still based on specific EG serum concentrations (6), not on the concentration of GA present. Because unmetabolized EG is relatively nontoxic (compared with GA), the availability of GA quantitation provides important laboratory support to clinicians treating EG poisoning cases. Continuing hemodialysis after all GA has been removed may not be required if the patient remains on ethanol treatment until the EG has lowered to <5 mmol/L.
Despite the low incidence of EG poisoning cases seen by most clinical toxicology laboratories, clinical chemists should provide analysis of GA and EG. In this laboratory, the presence of EG and GA are both screened for whenever a request for EG is received. The same rationale made for the availability of GA analysis in EG cases applies to methanol poisoning cases (7). Laboratories serving regional poison control centers should provide analysis of the toxic methanol metabolite (formate) in addition to GA analysis.
References
University of Pennsylvania, School of Medicine, Department of Pathology andLaboratory Medicine, 3620 Hamilton Walk, Philadelphia, PA 19104-6082
a Author for correspondence. E-mail wolfb{at}mail.med.upenn.edu.
To the Editor:
We appreciate Dr. Fraser's comments regarding the importance of glycolic acid measurements in the context of suspected ethylene glycol intoxication in the patient reported in Case 3 of our recent case conference (1). This particular patient was admitted to our hospital in December 1987, at which time only stat ethylene glycol testing was offered. Currently, there are several reported methods for glycolic acid measurement using either gas chromatography or HPLC (2)(3)(4)(5). It should be noted that very few laboratories routinely offer these measurements, and in most cases these highly specialized measurements will not be available on a stat basis. Nevertheless, it is important for clinical toxicology laboratories to be well prepared for these relatively infrequent cases of ethylene glycol poisoning. We believe that glycolic acid measurements can be useful as a supplement, but not as a substitute, to serum ethylene glycol determination, although in most cases the latter will be sufficient. Furthermore, serum ethylene glycol determined enzymatically should be confirmed by another method such as gas chromatography–mass spectrometry (6). However, in the acute setting of managing the intoxicated patient, the use of serum ethylene glycol (determined enzymatically on an automated analyzer (7)(8), anion and osmolar gaps coupled with arterial blood gases measurements will provide the greatest diagnostic yield at lowest cost. This approach is of particular utility in many medical centers that do not have access to a sophisticated reference toxicology laboratory. Thus, a recent survey of 95 teaching hospitals has shown that ethylene glycol determination was performed in only 25% of the polled hospitals (with a median turnaround time of 1.5 h), whereas if the test was sent out, the turnaround time was 42 h. (9).
References
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