DKA Case Report | Surgo

DKA Case Report

by Jaspal Sandhu, Specialty Doctor in Emergency Medicine

During your time as a medical student, you will be expected to remember many lists and formulas, and sometimes these may seem pointless exercises. However, those lists will help you in clinical practice, when you just don’t know what is going on.

During a shift in the Emergency Department a standby was received for a male in his 50s with GCS <8 heart rate of 150 and BP 70/30, never a good start!

When the patient arrived to the resus room he was mottled from head to toe and looked peri-arrest. We had very little information at this stage other than the patient had been a bit unwell over past week and today the partner could not awaken the patient, so called 999. Patient had background of type 2 diabetes and hypertension, but was normally fit and active.

Physical examination of the patient was carried out with chest sounding clear, heart sounds normal, patient had prolonged capillary refill centrally, with severe mottling of skin, and GCS 8. Blood sugar was 10 with ketones present.

A venous gas showed Hydrogen ions 114, Base Excess(BE) -24, Bicarbonate 3, Glucose 10, and potassium 2, sodium 144, chloride 115 and lactate 2. Now lets take a moment to look at those figures;

  • With the H+ of 114, that’s a severe acidosis.
  • With the BE of minus 24, that would make it a severe metabolic acidosis. (normal range is -2 to +2, and BE of minus double figures is very bad and usually needs ITU, so needless to say -24 is very bad!)
  • Surprisingly the lactate was normal! Or should I say confusingly the lactate was normal!

The reality is that most people in this state would have had a very high lactate, so this was very unusual. Remember those formulae I spoke of earlier, well one formula is for working out an anion gap. Which is: Na – (Cl + HCO3) and should normally be 8-16. If you run the numbers this patient has an anion gap of 26, so it is massively high! This means that the acidosis is secondary to unmeasured anions.

This is where we can use a list, a mnemonic for causes of high anion gap acidosis is MUDPILES. 

Out of all those, only Urea/ DKA/ Lactate are not ingested toxins. I spoke with the family, and there was no history of having taken any overdose and no history of depression nor low mood. With the urea and lactate being normal on blood test, this only left DKA on that list. So with that, we started treating the patient as a DKA case.

I say we, because whilst I had been pondering anion gap acidosis, other doctors had been putting in central and arterial lines, nursing staff had been commencing fluid resuscitation and preparing drugs, and we had been speaking with the family to update them of their critically unwell loved one.

The patient went to ITU intubated and had scans carried out to make sure there was not another cause of this severe acidosis. Whilst talking to ITU team, it turned out that a similar case had presented to ITU with DKA related to SGLT 2 inhibitor use (drugs ending in –gliflozin). Now if you look those up in the BNF, it even gives an alert, that these can cause severe or life-threatening DKA with normal Glucose levels.

A few learning points here; firstly learn those tedious lists as they are handy- especially in stressful situations. Secondly no one expects you to remember everything, so talk to your colleagues and learn from them. Thirdly as soon-to-be junior doctors, you may be the only ones who still look things up in the BNF- it is useful!

Details of case changed to ensure confidentiality

Causes of High Anion Gap Metabolic Acidosis


M – methanol

U – urea


P – Paraldehyde/paraquat/paracetamol

I – Iron/Isoniazid

L – Lactate

E – Ethanol/Ethylene Glycol

S – Salicylates

Normal anion gap acidosis can also occur but it is far less common

SGLT2 Inhibitors (Gliflozins)

Mechanism of action

  • Inhibit the reabsorption of glucose in the proximal tubules of the kidney.
  • The sodium-glucose co-transporter 2 is the site of action for the drug.  It leads to an increase in glucose in the urine and a decrease in serum glucose.


  • Type II Diabetes Mellitus

Adverse effects

  • renal impairment
  • symptomatic osmotic effects i.e. polyuria
  • UTIs and genital infections due to the increased sugar content of the urine

Examples – empagliflozin, canagliflozin, dapagliflozin