List three causes for the following combination of findings observed on a serum sample:
Parameter |
Patient Value |
Normal Adult Range |
Measured osmolality |
340 mOsm/kg* |
280 – 290 |
Sodium |
138 mmol/L |
135 – 145 |
Potassium |
4.0 mmol/L |
3.5 – 5.0 |
Chloride |
98 mmol/L |
95 – 105 |
Bicarbonate |
15 mmol/L* |
22 – 32 |
Glucose |
6.0 mmol/L |
4.0 – 6.0 |
Urea |
8.0 mmol/L |
6.0 – 8.0 |
Raised osmolar gap with raised AG
Methanol
Ethylene glycol
Ethanol
(Lactic acidosis can lead to a raised OG and AG; however, the osmolar gap does not reach the levels seen here.)
Let us dissect these results systematically.
So, what could account for this? Where did the extra osmoles come from?
Fortunately, Jeffrey Kraut comes to the rescue once again with an article which seems tailored to answering this question. In brief, there are a few situations which could cause the simultaneous increase of both the anion gap and the osmolar gap. Kraut lists the following as well-recognised causes:
Toxicological causes
Endocrine and metabolic disturbances
Kraut also cautions us to respect the timeframe of toxic exposure. When one quaffs a facefull of methanol, one imbibes a substance which is not dissociated at physiological pH: methanol has a pKa of 15.5. There will be a raised osmolar gap, but the anion gap will not increase until the intoxicated patient has had some time to process all that methanol into its acidic metabolites. Then, for a period of time the biochemistry results will reveal the classical picture with an increase in both anion and osmolar gaps. Finally, at some hypothetical point (where the patient is blind and comatose but not yet completely dead) the osmolar gap may decrease to a virtually normal level, leaving only a high anion gap.
Kraut, Jeffrey A., and Shelly Xiaolei Xing. "Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis." American Journal of Kidney Diseases 58.3 (2011): 480-484.