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Welcome back to the tasty morsels of critical care podcast.
DKA is bread and butter for critical care providers. In fact the combination of bread and butter in the absence of insulin is a core part of the pathophysiology of the disease.
An exam worthy summary of the pathophys might go as follows.
- lack of insulin stimulates lipase which leads to the production of free fatty acids from lipid stores peripherally
- FFAs are converted to ketone bodies in the liver in the presence of excess glucagon
- ketones dissociate significantly at physiological pH, this sucks up the supply of base buffer in the body and eventually overwhelms it with unbuffered acid and acidaemia developing. Beta hydroxybutarate is a name of a ketone that you might want to mention if pressed to name one.
- both the high sugar and high ketones lead to osmotic diuresis which results in water, sodium and other electrolyte loss.
It’s probably worth contrasting this with the pathophysiology of Hyperglycaemic Hyperosmolar State which used to rejoice in the onomatopoeic glory of HONK. In fact comparing and contrasting DKA and HHS seems to be a favourite exam question.
HHS is characterised physiologically by
- just enough insulin to prevent ketone generation but not enough to allow peripheral uptake
- slower onset and hyperosmolarity as a key feature
- HHS has impaired thirst mechanisms in context of hyperosmolarity
- hyperglycaemia itself is proinflammatory (and the higher degree of it in HHS suggests the higher rise in VTE)
What criteria might we use to diagnose DKA.
- Ketone>3
- GLucose>11
- HCO3<15 +/- pH<7.3
The one niche novelty version of DKA is the much discussed and not particularly frequently seen euglycaemic DKA. This seems to be a feature of the SGLT2 inhibitors which is secondary in difficult pronounciation only to their actual generic names of the glifozins. These meds are going to become a much more common med given that the EMPEROROR and DAPA-HF trials have declared these drugs mortality reducers in heart failure even in those with out diabetes.
Management here is pretty much as expected if you’ve been doctor for longer than 2 years. I would refer you to your hospital’s or a national guideline for the details. Some points for style include.
- given some insulin (though not too much)
- give some fluid (though the evil abnormal saline can cause its own issues)
- ketones are probably a better treatment target than the glucose level.
- look for some precipitants (even though the answer is always non compliance and even in those with pumps it’s non compliance as the tubing kinked somewhere and no one noticed)
- be careful with the K as this is probably the best way to kill them. a pH of 7.1 with a K of 3 is a real danger zone as both insulin and correction of acidosis will cause the K to drop fairly precipitously.
- finally on a logistic point it’s fairly common for these guys in Ireland to end up getting an art line for the frequent sampling but as one of my very grey and wise ICU bosses pointed out – a CVC would be infinitely more use than an art line in this scenario given that it gives access for bloods, multiple lumens for infusions and allows concentrated potassium correction.
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