A 55 year old insulin dependent diabetic woman was brought to Casualty by ambulance. She was semi-comatose and had been ill for several days. Past history of left ventricular failure. Current medication was digoxin and a thiazide diuretic.
Results include: K+ 2.7, glucose 67, anion gap 34 (all in mmol/l)
Arterial Blood Gases
pCO2 32 mmHg
pO2 82 mmHg
HCO3 19 mmol/l
This lady is a known diabetic and she presents with mental obtundation and severe hyperglycaemia. The clinical diagnosis suggested by the history is diabetic ketoacidosis (DKA) or hyperosmolar non-ketotic coma (NKHC). There are several other points to always be aware of in diabetic patients:
A patient with an "obvious diabetic ketoacidosis" should always be approached with these considerations in mind.
This lady has a severe diabetic ketoacidosis complicating a pre-existing metabolic alkalosis (due to thiazide use). Further investigations are necessary to exclude a lactic acidosis. Results of urinalysis, lactate and electrolytes are urgently required.
This is certainly an "interesting case". The first thing to notice here is that a quick scan of the acid-base results suggests only a minor acid base problem Disorders with compensating effects on the pH are present so pH is normal. The initial suggestion of a mild metabolic acidosis balancing a mild respiratory alkalosis turned out to be wrong. The big clue to understanding this acid-base problem was the large anion gap - a gap of this size always suggests a severe metabolic acidosis. So if a severe metabolic acidosis is present why is the bicarbonate not low. Conclusion: the compensating alkalosis must be a metabolic one (which primarily affects the bicarbonate) and not a respiratory one (which primarily affects the pCO2). Additionally, as it is balancing a severe acidosis, the metabolic alkalosis itself must be a significant one.
The high delta ratio (4.4) also suggests a coexistent metabolic alkalosis or a previous compensated respiratory acidosis. There is no evidence of severe respiratory disease. Also as the pCO2 is less than 40, this provides further support that a second primary disorder is raising the [HCO3], that is, a metabolic alkalosis is present. The history suggests that this would have been caused by the thiazide diuretic therapy. Inadequate chloride intake is usually necessary for diuretic use to result in a metabolic alkalosis.
The overall picture suggested is a woman with a pre-existing metabolic alkalosis (due to thiazides) who has developed an acute metabolic acidosis (diabetic ketoacidosis and/or lactic acidosis).
Assuming the normal anion gap is 12 mmols/l, then the increase in the anion gap is 22 mmol/l and should be approximately matched by the decrement in the [HCO3] as the average delta ratio found in DKA is typically about 1.0. This predicts that a [HCO3] of up to 41 mmols/l was present before the onset of the acute ketoacidosis (as 41 - 22 = 19 which is the measured [HCO3]). Vomiting was not mentioned in the history but is common in DKA and may have contributed to the alkalosis and K+ loss.
As both primary disorders are metabolic ones, we can also use the [HCO3] to see if the pCO2 value is an appropriate one. The only caveat here would be the usual one that sufficient time (12-24 hours) had passed for the maximal respiratory response to occur. More than this amount of time has passed since onset, so this is not a problem. The predicted pCO2 of 36mmHg is close to the measured value of 32 so respiratory compensation is appropriate and there is little evidence of the presence of a primary respiratory acid-base disorder.
Do you think you could have diagnosed this acid-base problem merely by inspecting the blood gas results? Perhaps you might have considered a mild metabolic acidosis and a slight hyperventilation due to anxiety from the arterial puncture. Remember also if the acid-base disorder or hyperosmolality seems too small to explain the degree of obtundation, other causes of coma should always be considered in a diabetic patient (eg trauma, epilepsy, drug overdose in the younger adult, stroke in the older patient). The potential mistake here is to diagnose only a minor acid-base disorder. If the blood glucose or urine tests (glucose and ketones) were not checked, this patient could have been admitted to a medical ward as ‘?CVA’ without appropriate management. If an elderly patient presents with mental obtundation and marked hyperglycaemia but without evidence of ketoacidosis, then the diagnosis is hyperosmolar non-ketotic coma rather then diabetic ketoacidosis. In this case the elevated anion gap has indicated the presence of a severe acidosis.
Two situations giving rise to a mixed metabolic acidosis and alkalosis are: