Chloride and Lactate are essential components (together with Na, K,
Ca(i) [+/- Mg(i)]) for the calculation of the apparent strong ion
difference (SID), a mechanism of assessing the influence of
electroneutrality on acid-base of particular interest in critical care
where the influence of low albumin on acid-base is ignored. It's utility
and influence on clinical outcomes is still being evaluated. Food for
thought.
Paul Holloway
ICU, JRH, Oxford
>>> Les Culank <[log in to unmask]> 06/16/04 10:46 AM >>>
Increasingly blood acid-base is measured nearer the patient, and blood
lactate is measured nearer the ICU patient; while not all labs include
chloride in their routine serum "U&E" profile. In this context, for
years
anion gap has been losing both availability & usefulness.
At its best it is not a directly measured analyte, and physiologically
it
was an artificial idea. Shouldn't we consider abandoning it
altogether?
Yours iconoclastically,
Les
From: Mohammad Al-Jubouri <[log in to unmask]>
Reply-To: Mohammad Al-Jubouri <[log in to unmask]>
Date: Wed, 16 Jun 2004 10:08:57 +0100
To: [log in to unmask]
Subject: Re: A metabolic pickle/little addition
Jonathan
What you are saying is of course true for a single acid-base
disturbance. In
mixed acid base disturbance, the anion gap will vary, for e.g: a case of
diabetic ketoacidosis + hypokalaemic alkalosis will have lower
calculated
anion gap than a case of diabetic ketoacidosis + hypochloraemic
alkalosis
(due to gastric stasis, not uncommon in DKA). If the acid producing
process
is overwhelming, then any bicarbonate generation by the alkalotic
process
will be mopped up, resulting in little if any rise in serum bicarbonate,
leaving serum chloride level as the main determinant of the anion gap
calculation.
regards
Mohammad
Jonathan Kay <[log in to unmask]> wrote:
What I meant to say was that I don't find the classification of
acidosis and alkalosis into "hypochloraemic" or "hyperchloraemic" to be
useful any more, and I don't mention those terms when teaching medical
students. The classification of metabolic acidosis into "normal anion
gap" and "high anion gap" is the concept I teach... do others use the
same approach?
I wouldn't expect the anion gap to be raised in metabolic alkalosis due
to vomiting until hypovolaemia occurs... does anyone have evidence to
support this?
Jonathan
PS: That's two emails I've had to correct this evening. I'll go and
take the thiamine..
On 15 Jun 2004, at 22:36, Jonathan Kay wrote:
> "The hypochloraemia due to vomiting has exaggerated the
> calculated anion gap."
>
> I don't think of it that way: they are the! same process...
>
> Jonathan
>
>
> On 15 Jun 2004, at 16:06, Mohammad Al-Jubouri wrote:
>
>> Sorry, just forget to say that thiamine deficiency in alcoholic
>> patients is the cause of raised pyruvate and lactate, as suggested
>> Tim Reynolds.
>> thanks
>>
>> Mohammad
>>
>> Mohammad Al-Jubouri wrote:
>> 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 potas! sium, 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
>>
>>
>> Mohammad Al-Jubouri wrote:
>> Dear All
>>
>> A 62-year-old lady presented with short history of vomiting and
>> breathlessness. Physical examination was unremarkable!!, CXR nor!
mal.
>> A biochemical profile showed:
>>
>> U/E: Na 143 mmol/L, K 4.6 mmol/L, urea 8.3 mmol/L, creatinine 150
>> umol/L, chloride 87 mmol/L, bicarbonate 8.0 mmol/L.
>> LFTs: Bilirubin 12 umol/L, ALP 102 IU/L, ALT 39 IU/L, AST 67 IU/L,
>> GGT 42 IU/L, albumin 46 g/L.
>> Others: glucose 11.2 mmol/L, CK 67 IU/L, adjusted calcium 2.24
>> mmol/L, phosphate 3.44 mmol/L, osmolality 361 mOsm/kg, CRP < 5 mg/L,
>> INR 1.0
>>
>> Acid base status: pH 7.13 kPa, PCO2 2.7 kPa, PO2 11.2 kPa
>> Anion gap 54 mmol/L
>> Osmolal gap > 50 mmol/L
>> Lactate 15 mmol/L
>> Beta-hydroxybutyrate 15 mmol/L
>> Serum alcohol 136 mg/dL
>> Toxic alcohols screen: to follow.
>>
>> Drug history: None.
>> Alcohol drinking: ++++
>>
>> Impression: Profound combined lactic/ ketoacdosis.
>>
>> Question: can all this be due to alcohol only? have you had any
>> experience with a similar case, would be grateful for your comments.
>>
>> regards
>>
>> Mohammad
>>
>>
>>
>>
>>
>> Dr. M A Al-Jubouri
>> Consultant Chemical Pathologist
>>
>>
>> ALL-NEW Yahoo! Messenger - sooooo many all-new ways to express
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>>
>> Dr. M A Al-Jubouri
>> Consultant Chemical Pathologist
>>
>>
>> ALL-NEW Yahoo! Messenger - sooooo many all-new ways to express
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>>
>> Dr. M A Al-Jubouri
>> Consultant Chemical Pathologist
>>
>> ALL-NEW Yahoo! Messenger - sooooo many all-new ways to express
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>> Instructions (How to leave etc.) http://www.jiscmail.ac.uk/
------ACB discussion List Information--------
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biochemistry. Please note, archived messages are public and can be
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via the internet. Views expressed are those of the individual and
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