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|
What is the pH?
What is the primary process?
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
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).
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.