Uncoventional Views on Certain Aspects of Toxin-Induced Metabolic Acidosis

This discussion will highlight the following 9 specific points that related to metabolic acidosis caused by various toxins. The current recommendation suggests that alcohol dehydrogenase inhibitor fomepizole is preferred to ethanol in treatment of methanol and ethylene glycol poisoning, but analysis of the enzyme kinetics indicates that ethanol is a better alternative. In the presence of a modest increase in serum osmolal gap (<30 mOsm/L), the starting dose of ethanol should be far less than the usual recommended dose. One can take advantage of the high vapor pressure of methanol in the treatment of methanol poisoning when hemodialysis is not readily available. Profuse sweating with increased water ingestion can be highly effective in reducing methanol levels. Impaired production of ammonia by the proximal tubule of the kidney plays a major role in the development of metabolic acidosis in pyroglutamic acidosis. Glycine, not oxalate, is the main final end product of ethylene glycol metabolism. Metabolism of ethylene glycol to oxalate, albeit important clinically, represents less than 1% of ethylene glycol disposal. Urine osmolal gap would be useful in the diagnosis of ethylene glycol poisoning, but not in methanol poisoning. Hemodialysis is important in the treatment of methanol poisoning and ethylene glycol poisoning with renal impairment, with or without fomepizole or ethanol treatment. Severe leucocytosis is a highly sensitive indicator of ethylene glycol poisoning. Uncoupling of oxidative phosphorylation by salicylate can explain most of the manifestations of salicylate poisoning.

Correlation of Urine Ammonium with Urine Osmolal Gap in High Anion Gap Matabolic Acidosis: Comparison to Urine Anion Gap / 대한내과학회지

OBJECTIVES: Urine anion gap(UAG) and urine osmolal gap(UOG) were proposed as indirect measures of urine ammonium(NF4+). While the former is known to have its usefulness limited to hyperchloremic metabolic acidosis, the latter is reported to have its correlation with urine NE4+ in ketoacidosis. This study was undertaken to evaluate the correlation of urine NH with IJOG in high anion gap metabolic acidosis(AGMA) and to compare it with UAG. METHODS: We measured urine NH' by enzymatic determination, UOG(=0.5 X [urine osmolality-{2 X (Na++K+)+urea+glucose)]), and UAG(=Na++K+-Cl-) in 18 patients(serum AG=24.4+/-1.6mmol/L ) with AGMA. RESULTS: When they were grouped into those with acute disorders(n=11) and those with chronic disorder(n=7), urine Nk4+ concentration was higher (p40mmol/d) had the UOG>40mmol/L. CONCLUSION: In contrast to the UAG, the UOG has a significant correlation with urine NH4+ in AGMA.