Question 26.4

A 68-year-old Type 2 diabetic with a history of alcohol abuse is admitted with abdominal pain and the following results:

Parameter	Patient Value	Normal Adult Range
pH	6.87*	7.35 - 7.45
PaCO2	8 mmHg (1.1 kPa)*	35 - 45 (4.7-6.0 kPa)
PaO2	149 mmHg (20 kPa)
Bicarbonate	1.4 mmol/L*	22 – 26
Lactate	16 mmol/L*	< 2
Sodium	142 mmol/L	134 – 145
Potassium	4.7 mmol/L	3.5 – 5.1
Chloride	107 mmol/L*	95 – 105
Urea	14 mmol/L*	3.4 – 8.9
Creatinine	170 μmol/L*	60 – 110
Aspartate Aminotransferase	60 U/L*	< 40
Alanine Aminotransferase	70 U/L*	< 40
Lactate Dehydrogenase	1400 U/L*	50 - 150
Total bilirubin	20 μmol/L	< 20
Glucose	6.5 mmol/L*	3.0 – 5.4
Serum osmolality	314 mOsm/kg*	275 – 295

a) Give three likely diagnoses.

b) List two additional investigations that you would perform based on the above information.

College Answer

Let us dissect these results systematically.

The A-a gradient cannot be calculated, as no FiO₂ is supplied to us
There is acidaemia
The PaCO₂ is compensatory
The SBE is not supplied, but the bicarbonate is 1.4, suggesting a severe metabolic acidosis
The respiratory compensation is adequate and lurks around the natural limits of human respiratory compensation for metabolic acidosis- the expected PaCO₂(1.4 × 1.5) + 8 = 10.1mmHg
The anion gap is raised:
(142) - (107 + 1.) = 34, or 38.7 when calculated with potassium
The delta ratio, assuming a normal anion gap is 12 and a normal bicarbonate is 24, would therefore be (34 - 12) / (24 - 1.) = 0.95 (.e. mainly a high anion gap acidosis)
Urinary pH and electrolytes are not supplied, and are irrelevant.

So, what is making this diabetic drunk so acidotic?

Well, the lactate of 16 is probably contributing. But it does not account for the whole of the anion gap.

The college kindly gives us a measured osmolality, so we can calculate the osmolar gap:

314 - (142 × 2 + 14 + 6.5) = 9.5

Thus, toxic alcohol ingestion (eg. ethylene glycol or methanol) is less likely.

Three likely culprits of any of the below causes is all the college wanted, or any reasonable diagnosis.

Thus, investigations could include any two of the following:

Smeets, E. H. J., H. Muller, and J. De Wael. "A NADH-dependent transketolase assay in erythrocyte hemolysates." Clinica chimica acta 33.2 (1971): 379-386.

Lonsdale, Derrick, and Raymond J. Shamberger. "Red cell transketolase as an indicator of nutritional deficiency." The American journal of clinical nutrition 33.2 (1980): 205-211.

FENNELLY, JAMES, et al. "Red blood cell-transketolase activity in malnourished alcoholics with cirrhosis." The American journal of clinical nutrition 20.9 (1967): 946-949.