Blood Gas #25


A 45yr alcoholic female with epilepsy, previous traumatic head injury and T2DM presented to ED following a syncopal episode and a fall onto her face.

PMH: depression, PTSD and agoraphobia.  On sertraline and carbamazepine.

pH 7.55 Na 130 mmol/L
pCO2 58 mmHg K 2.5 mmol/L
pO2 35 mmHg Cl 58 mmol/L
HCO3 51 mmol/L Glucose 6.1 mmol/L
Lactate 1.0 mmol/L Creatinine 101 mmol/L
GGT 394 mmol/L (Creat 58 mmol/L 3 weeks ago)
Urea 8.3 mmol/L Serum osmolality 276 mmol/Kg
Urine osmolality 475 mmol/Kg Urine sodium 61 mmol/L

[expand title=”Interpretation”]

What is the pH?


What is the primary process?

Metabolic alkalosis.

Is there compensation?

Expected pCO2 = (0.7 x bicarb) + 20 +/- 5

35.7 + 20 (+/- 5) = 55.7 therefore maximally compensated.

Are there other clues to diagnosis?

Anion gap = Na – (HCO3 + Cl): 

130 – (58 + 51) = 21


Electrolyte clues:

Marked hypokalaemia.


Profound hypochloraemia.




45 year old female with marked metabolic alkalosis and profound electrolyte disturbance in the context of alcoholism and a known previous head injury.  She should be investigated for SIADH : serum and urinary osmolalities and electrolytes should be requested, as should her serum cortisol.  Her renal, adrenal, thyroid and hepatic function should be assessed.

Causes of metabolic alkalosis : CLEVERRR

(Contraction, Licorice, Endocrine, Vomiting, Excess alkalis, Refeeding alkalosis, Renal Retention of bicarb).

Case Resolution:

The patient was admitted under the medical team.  Renal function improved post IV fluids.  eGFR was 37 on arrival, which improved to >90 on day 2.  TSH was elevated.  She was investigated for ? SIADH.

Serum osmolality was 276.  Urine osmolality was 475. Urine sodium was 61.

Sertraline was ceased as it was thought to be contributing to her hyponatraemia.



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