Hi,
The lactate and B-OH butyrate should be mostly ionized at pH 7.1 and
therefore need a counterion, ie sodium , which is accounted for in the
osmolal gap. Therefore, they can't contribute to the osmolal gap; there has
to be another neutral molecule - acetone ? Is that being measured as part
of the alcohols ?
Wolfgang
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Wolfgang Schneider
Division of Medical Biochemistry, Montreal General Hospital
1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada
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Mohammad Al-Jubouri <[log in to unmask]>@JISCMAIL.AC.UK> on 2004-06-15
10:46:47 AM
Please respond to Mohammad Al-Jubouri <[log in to unmask]>
Sent by: Clinical biochemistry discussion list
<[log in to unmask]>
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Subject: Re: A metabolic pickle
Thanks to all replies
Most of you agree that this represents a case of alcoholic ketoacidosis but
find the accompanying lactic acidosis atypical. There are at least 3
further samples showing less severe metabolic derangement during her
therapy with saline infusion, 10% dextrose/insulin infusion and pabrinex.
This is therefore a genuine metabolic derangement and citrate contamination
is not to blame. She needed potassium, magnesium and phosphate supplements
as you might expect with treated metabolic acidosis. Her biochemical
parameters quickly recovered back to normal within 24 hours. The
hypochloraemia due to vomiting has exaggerated the calculated anion gap.
The osmolal gap can probably be expalined by ethanol (30 mmol) + lactate
(15 mmol) and B-OH-Butyrate (15 mmol), but I am still waiting for toxic
alcohols screen.
Learning point: Profound hyperlactataemia can accompany alcoholic
ketoacidosis.
Regards
Mohammad
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