PH = 7.28, that is mild acidaemia
HCO3 = 17 mmol/L. So we have metabolic acidosis.
Next, we need to calculate the compensation and the anion gap.
For Compensation we use Winter’s formula, that is: Expected pCO2 = HCO3 x 1.5 + 8 (+/-2). Accordingly, the expected range is 31.5 – 35.5. So we have additional mild respiratory acidosis.
AG = Na – (Cl + HCO3) = 10, So we have NAGMA.
Other abnormal findings:
- K = 3.2 mmol, that is mild hypokalaemia
- Cl = 116, moderate hyperchloraemia
Final conclusion, Mild combined normal anion metabolic acidosis and respiratory acidosis with associated mild hypokalaemia and moderate hyperchloraemia.
Next we need to build a differential diagnosis for NAGMA, for that we use the mnemonic USED CRAP.
- U = Ureteroenterostomy
- S = Small bowel fistula
- E = Extra chloride
- D = Diarrhea
- C = Carbonic anhydrase inhibitors
- A = Adrenal insufficiency/ Addison’s disease
- R = Renal tubular acidosis
- P = Pancreatic fistula.
One of the medication that this patient used was Topiramate. Topiramate is a carbonic anhydrase inhibitor medication used to treat epilepsy and prevent migraines. It has also been used in alcohol dependence.
Carbonic anhydrase inhibitors block the carbonic anhydrase enzymes in the proximal convoluted tubule, inhibiting the reabsorption of Sodium bicarbonate (NaHCO3), which results in diuresis and metabolic acidosis.
Normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule. In patients receiving carbonic anhydrase inhibitors, proximal reabsorption of bicarbonate is decreased and distal delivery is increased. The distal tubule has only a limited capacity to reabsorb bicarbonate and when exceeded bicarbonate appears in the urine. This results in a hyperchloraemic metabolic acidosis. This can be considered as essentially a form of proximal renal tubular acidosis but is usually not classified as such.