Dear Paul,
I particularly like your last sentence "Food for thought".
It seems more complex than the sort of Tom-Whitehead approach to acid base I
was weaned on, but I'm open minded whether or not this SID / Stewart stuff
adds value eg in the care of the critically ill.
I may be wrong but I suspect this stuff has got far more into vogue in
Canada & USA than in Europe as a direct corollary to the greater acceptance
& use over here of "base excess" & "standard bicarbonate".
Best wishes,
Les
> From: Paul Holloway <[log in to unmask]>
> Reply-To: Paul Holloway <[log in to unmask]>
> Date: Wed, 16 Jun 2004 11:21:41 +0100
> To: [log in to unmask]
> Subject: Re: A metabolic pickle etc - but why the anion gap?
>
> 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
>>>
>>>
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