PH = 7.39, This is with in the normal range.
PCO2 = 32 mmHg, (<40). So, we have an element of respiratory alkalosis.
HCO3 = 18.8 mmol/L (less than 24). That can be either due to the presence of metabolic acidosis or as a compensatory mechanism for respiratory alkalosis.
To confirm that, we compare it to the expected results for acute respiratory alkalosis (We don’t have any evidence of chronic respiratory alkalosis for this patient).
For the compensation for acute respiratory alkalosis, we expect HCO3 to drop by 2 for every 10 PCO2 below 40. Accordingly, expected HCO3 is 22.4. Since the number here is less than that then we have additional metabolic acidosis.
Since we have metabolic acidosis, then we need to calculate the anion gap.
AG = Na – (C l+ HCO3) = 137 – (98 + 18.8) = 20.2, So we have HAGMA.
(We can also start the calculation with the low HCO3 then calculate the compensation using Winter’s formula, that is: expected pCO2 = 1.5 x HCO3 + 8 (+/- 2). It will be 34-38. This also confirm the presence of respiratory alkalosis.
Because we have HAGMA, then the next step is to calculate the Delta Ratio, That is: (AG – 12) / (24 – HCO3) = 1.57, So we have a pure HAGMA here.
Other abnormal findings:
Serum glucose = 25 mmol/L, very high.
In the presence of elevated glucose level, we get pseudo-hyponaetremia. The corrected Na level = measured Na + (Glucose – 5)/3 = approximately 144 mmol/L.
Ketones is 7 mmol/L, that is severe Ketosis. usual level is less than 0.4 mmol/L . This indicates massive insulin deficiency at cellular level.
Final conclusion is HAGMA + acute respiratory alkalosis.
The Cause of that what DKA + anxiety.
Due to the presence of lactate level more than 3 mmol/L. This patient should be treated as DKA (Not just hyperglycemia).
Follow the usual DKA guidelines/ protocols for the management of this patient.