History:
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?
7.55
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.
Hyponatraemia.
Profound hypochloraemia.
Formulation:
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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