There is an acidaemia (pH < 7.31 on VBG).

In this example the pCO2 is in the normal range for a VBG, which doesn’t explain the acidaemia. However, the HCO3 is < 22, which fits with a metabolic acidosis contributing to the acidaemia.

The expected pCO2 would be 1.5x[HCO3^–] + 8 = 29; therefore, there is likely a respiratory acidosis, or inadequate compensation; however interpretation must be cautious from a VBG (rule applies for paCO2).

AG = Na – (Cl + HCO3)
Normal value = 12
This is a high anion-gap metabolic acidosis (HAGMA), with an AG of 122 – (87+14) = 21

This is done to determine if the acidosis is entirely due to the extra anions in the AG, or if there is also another cause contributing to the acidosis (i.e. a co-existing normal anion-gap metabolic acidosis – NAGMA)

Delta gap = (change in AG) – (change in HCO3)
where normal AG = 12, and normal HCO3 = 24
Delta gap < -6 implies there is a mixed HAGMA and NAGMA
Delta gap -6 to 6 implies there is only a HAGMA, with no co-existing NAGMA
Delta gap >6 implies there is a mixed HAGMA and a metabolic alkalosis

The delta gap is (21-12) – (24-14) = 9-10 = -1 suggesting only HAGMA

The delta ratio uses the same information, but is a ratio comparison

Delta ratio = (change in AG) / (change in HCO3)
<0.4 = NAGMA
0.4 – 0.8 = mixed HAGMA and NAGMA
0.8 – 2 = pure HAGMA
>2 = mixed HAGMA and a metabolic alkalosis

The delta ratio is 9/10 = 0.9 –> suggests pure HAGMA (see reference 3)

There is a lactic acidosis, with a raised lactate of 4.4.

NB: although a raised lactate is one of the causes of a high anion-gap, the lactate of 4.4 mmol/L does not explain the whole increase in the AG from 12 (normal) to 21. There are 9mmol/L of “extra anions” so something else must also be contributing.

There is also anaemia, hyponatremia, a significant hyperkalaemia and hyperglycaemia.

This question is a good example of how to work through an approach to metabolic acidosis on a blood gas.

A common mnemonic for HAGMA is “Left Total Knee Replacement” or LTKR

LTKR – Lactic acidosis, Toxins, Ketones and Renal failure

As you can see – all of the above could be contributing to this case.

There are many potential causes of a lactic acidosis, and several possible toxins include ethylene glycol, methanol and pyroglutamic acidosis.

Lactic acidosis – shock/sepsis related?
Ketones – DKA
Renal failure – known ESRF

Hyponatraemia – possibly hypervolaemic due to missed haemodialysis (HDx), pseudohyponatraemia due to hyperglycemia
Hyperkalaemia, hyperphosphataemia – in setting of missed HDx
Renal impairment – known ESRF
Mildly deranged LFTs with obstructive pattern – ?possible trigger for DKA, or just part of illness
Hyperglycaemia, ketosis – T1DM with poor control  DKA

HR approximately 60, sinus rhythm
Borderline right axis deviation
Increased PR interval (>0.2ms)
Mildly increased QRS duration (>0.12ms)
Widespread peaked T-waves, consistent with hyperkalaemia

Progress:

Received IV Ca2+ (membrane stabilisation), salbutamol, dextrose-insulin, NaHCO3 and antibiotics in ED as well as some 0.9% saline volume resuscitation. Transferred to ICU for urgent HDx and a DKA insulin protocol which saw correction of the biochemical and ECG abnormalities. Discharged to ward 2 days later for ongoing titration of subcutaneous insulin.

Great work!