This case demonstrates how misdiagnosis, including inappropriate laparotomy and delayed ethylene-glycol therapy, could occur. She admitted to deliberate ingestion of ethylene glycol. The patient was discharged after 2 weeks with residual renal failure requiring intermittent hemodialysis. The patient's abdominal CT scan was judged normal no surgery was performed. Laboratory readings for plasma lactate never exceeded 3.6 mmol/L ( Table 1). Dialysis rapidly decreased the ethylene glycol level, the anion-gap metabolic acidosis, and the lactate measured with the Radiometer point-of-care analyzer. ![]() Repeated analysis confirmed high point-of-care readings for lactate and comparatively low plasma-lactate results. Resuscitation continued, but now included high-flux dialysis and an intravenous infusion of ethanol to counter ethylene glycol. An urgent ethylene glycol test showed a plasma concentration of 15 mmol/L. Urine analysis found calcium oxalate crystals. Two hours later, full laboratory investigations showed an increased serum osmolarity (353 mmol/L) and an osmolar gap of 33 mmol/L. Unexpectedly, the plasma lactate concentration was only 1.5 mmol/L. Blood work at admission included a laboratory plasma-lactate measurement, for which a sample was drawn minutes after the arterial blood-gas sample. Although family consent was obtained for immediate laparotomy, we delayed to obtain an abdominal CT scan and to improve her hemodynamics and reduce her acidosis. Use of sedatives and neuromuscular blocking medications precluded an adequate abdominal examination. A general surgeon was consulted in case the lactate elevation represented severe mesenteric ischemia requiring urgent laparotomy. She was transferred to the hospital's intensive care unit. This can expedite diagnosis and treatment by hours, compared with waiting for laboratory results for plasma ethylene glycol. ![]() ![]() By comparing lactate results from the iSTAT or Bayer devices with that from the Radiometer, ethylene-glycol ingestion can be diagnosed at the point of care. We also showed that lactate gap can be exploited to expedite treatment, diagnose late ethylene-glycol ingestion and terminate dialysis. Interpretation: We demonstrated how inappropriate laparotomy or delayed therapy might occur if clinicians are unaware of this phenomenon or have access to only a single analyzer. Lactate gap was determined by comparing the Radiometer result with the corresponding result from any of the other analyzers. The i-STAT and Bayer point-of-care analyzers and the Beckman and Vitros laboratory analyzers reported minimal lactate elevations. Another major ethylene glycol metabolite, glyoxylate (but not oxalate or formate), caused similar elevations. Results: With the Radiometer 700 point-of-care analyzer, glycolate addition resulted in an artifactual, massive lactate elevation, even at low glycolate concentrations. Methods: We phlebotomized blood, added various concentrations of metabolites of ethylene glycol, and tested the resulting samples with the 5 most common lactate analyzers. We therefore wished to determine why discrepancies in lactate measurements occur and whether this “lactate gap” could be clinically useful. Ethylene glycol ingestion was subsequently diagnosed. Mesenteric ischemia was suspected, with a potential need for laparotomy however, plasma lactate measurements were below 4 mmol/L. ![]() Background: A patient presented with severe acidosis and a point-of-care lactate measurement of 42 mmol/L.
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