Question 1:
PH = 7.24, that is moderate acidaemia
HCO3 = 15.2 ( less than 24), that is low .So, we have metabolic acidosis.
Once we get metabolic acidosis, then we need to calculate the compensation and the anion gap.
We calculate the compensation using Winter’s formula, that is expected PCO2 = HCO3 x 1.5 + 8 (+/- 2). Accordingly, expected PCO2 should be between 28.8 and 32.8. So, we have additional respiratory acidosis.
Anion gap ={Na – (Cl + HCO3)} , in this case it will be 15.8, So we have HAGMA.
Because we have HAGMA, then we need to calculate the delta ratio, that is (AG – 12) / (24 – HCO3) = 0.43. Delta ratio between 0.4 – 0.8 means we have mixed HAGMA and NAGMA.
According to the above we have HAGMA + NAGMA + Respiratory acidosis.
Other calculations:
Na = 133 mmol/L, that is mild hyponatraemia. However, in the presence of hyperglycemia, Na level is usually falsely low. To correct Na level for glucose level, we use the following formula: Corrected Na = measured Na + {(Glucose – 5)/3} = 155.3, that is hypernatraemia..
K = 4.6, that is within normal range. However, K level usually is falsely elevated in the presence of acidosis. Serum K increases by 0.6mmol/L for every 0.1 decrease in PH below normal. Accordingly, corrected serum K should be around 4 mmol/L.
Serum glucose = 24 mmol/L, that is hyperglycemia
Lactate = 3.5, that is hyperlactataemia, sign of poor tissue perfusion
Ketones = 5.3, that is severe ketosis. This is usually causes by intracellular glucose deficiency.
This patient has HAGMA, Hyperglycemia, Hyperlactataemia and ketosis…So he was suffering from DKA at the time this test was performed.
Urea = 16.7 (high), Creatinine = 77 (normal).
We can calculate the urea-creatinine ratio to have an idea about the location of the pathology contributing to renal failure.
Urea-creatinine ratio = Urea x 1000/Creatinine = 216… level above 100 reflects pre-renal renal failure/ In patient with DKA is usually due to dehydration.
The final conclusion, this patient hasL
- HAGMA, could be caused by high lactate, ketone or urea. Most probably due to combination of them. This is caused by DKA.
- NAGMA caused by diarrhoea that leads to loss of HCO3 in stool
- Respiratory acidosis, this patient was drowsy and he was hypoventilating.
- Dehydration.
Question 2:
This patient is unwell, should be treated in resus bay with full monitoring.
Most important part of the management is rehydrating this patient with close monitoring of urine output. Be careful of administering insulin early. Many of those patients administer insulin subcutaneously but because they are very dehydrated, this insulin won’t get absorbed. When these patient gets rehydrated, the insulin in the subcutaneous tissue will get absorbed and this might results into fast correction of hyperglycemia and hypokalaemia. Rapid correction of hyperglycemia will lead to cerebral oedema.
My approach is to administer 1L on normal saline stat then check blood gas/ sugar level then start the sliding scale according to DKA protocol.
Adjust fluids level according to the changes in lactate and adjust the insulin level according to the changes in ketones levels.
Once we start insulin therapy, K level will drop, this will need replacement. Make sure the patient passes urine before starting K replacement therapy.
These patients need frequent checking of blood gases, preferably on hourly bases.
These patient need to be admitted to HDU or ICU.
Don’t forget to treat the precipitating cause and to cover the patient with prophylactic anti-coagulation.