ICU Cases · Acid–base
Ethylene glycol poisoning — the dual gap and the race to block metabolism
A long case on a classic, time-critical toxic ingestion — ethylene glycol poisoning. Tests the recognition of the dual anion-and-osmolar gap, the principle that the metabolites (not the parent alcohol) cause the harm, the immediate blockade of alcohol dehydrogenase with fomepizole, and the indications for haemodialysis.
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A 47-year-old man is brought to the emergency department by his partner, who found him ataxic and incoherent at home. He had appeared well earlier in the evening. On arrival he is confused and agitated, his respiratory rate is 30, his heart rate 110, his blood pressure 150/90, and his oxygen saturation 97 per cent on room air. He smells faintly of alcohol but is deteriorating faster than ethanol alone would explain, and he is now complaining of flank pain and has passed only small volumes of dark urine.
His initial blood gas shows a severe metabolic acidaemia: pH 7.10, PaCO2 18 mmHg, HCO3 6 mmol/L, base excess −22. His biochemistry shows sodium 142, chloride 98, potassium 5.8, creatinine 180, glucose 6.5. The anion gap is 38 mmol/L (corrected little, as his albumin is normal), and his osmolar gap is 35 mOsm/kg.
[3]References5ShowHide
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- [2]Lynd LD, Richardson KJ, Purssell RA, et al. An evaluation of the osmole gap as a screening test for toxic alcohol poisoning. BMC Emergency Medicine, 2008.PMID 18442409
- [3]Kraut JA, Madias NE. Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clinical Journal of the American Society of Nephrology, 2007.PMID 17699401
- [4]Bersten AD, Soni N (eds) Oh's Intensive Care Manual. 8th edition, Elsevier, 2018.
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