This patient clearly has a very severe DKA. There is a significant mortality associated with patients presenting with such a low pH and abnormal GCS. This particular patient presented many challenges which will be explored below.

1. Why did the acidosis not improve despite treatment with insulin and a falling glucose.
There are a number of factors to take into account here.
a) pH is a log scale so small changes at low pHs are actually large acid/base shifts.
b) DKA does not resolve that quickly and there is a great deal of ketoacidosis to clear here.
c) failure to resolve should always raise the possibility of a serious underlying cause (e.g. surgical abdomen) and these should be actively sought. This may require imaging as the patient is often unable to co-operate. None were found on this occasion.
d) There is evidence of an iatrogenic hyperchloraemic acidosis here. As bicarbonate is low, chloride replaces bicarbonate as an anion in the circulation and contributes to the acidaemia. This can be avoided by giving hartmans, or even low concentration bicarbonate as fluid replacement. This may be valuable in situations like this where a raise in the pH may significantly contribute to the patients recovery.

2. Why was the GCS low?
This was a combination of metabolic abnormality and impending cerebral oedema.

3. Would you have treated the patient differently (in retrospect)
Less Normal Saline. In preference Hartmans or Bicarbonate. Bicarbonate is frowned upon by many, but in situations like this where there is gross acidaemia it may be required in the ICU setting.

4. What should happen to the patient now that the management plan appears to be failing?
Intubation and ventilation for impending cerebral oedema and further management. Further invasive monitoring (cardiac output) on ICU.

By this point it is clear that the patient is not correcting spontaneously and extracorporeal correction of fluid and electrolyte abnormalities was performed with a haemofiltration system.