Thread by @jamiekwillows

1/
#medtwitter is fairly comfortable managing “normal” DKA right? But how about in the anuric dialysis patient? The cookbook protocol can be deadly.

Read this #tweetorial to learn about how their DKA pathophysiology is fascinatingly different.

#meded #nephpearls #endotwitter

2/
Quick recap of normal DKA pathophysiology;

🔑 insulin requirement > insulin supply

✅ “stress hormones” rise
✅ blood glucose rises & because glucose is an osmotic diuretic, there is a huge, inappropriate urine output
✅ body makes ketones as alternative fuel, so pH falls

3/
Recap of normal DKA;

✅ patient symptomatic,extracellularly dry, 6 litres down & counting
✅ whole body K low due to osmotic diuresis, but often ⬆️K at first due to hypertonicity/ low insulin/ acidosis
- serum K then rapidly falls as INsulin drives K & glucose INtracellularly

4/
Usual life-saving protocol involves treating any underlying precipitant, giving iv insulin (& usual subcut insulin) and aggressively repleting volume & electrolytes.

☠️ many protocols don’t mention that for dialysis patients this cookbook medicine can be lethal ☠️

5/
Patients with ⬇️GFR are actually relatively protected from DKA;
👍 decreased exogenous insulin metabolism by kidney proximal tubules = harder to be deficient
👍 in-centre haemodialysis patients seen 3 times a week = earlier illness recognition (despite being less symptomatic)

6/
But dialysis patients do sometimes go into DKA, & are at ⬆️risk of;
❗️severe hyperkalaemia (limited K excretion)
❗️serious underlying drivers (big two here are ischaemia & infection)
❗️rapid fall in glucose with treatment = higher risk of hypoglycaemia and large tonicity swing

7/
However the key difference in chronically anuric dialysis patient in DKA is...

🔴 no huge osmotic diuresis 🔴

Therefore;
✅ higher initial serum glucose level (as no glycosuria)
✅ removes need for large volume & electrolyte resuscitation

⚠️ hence not for ‘the protocol’ ⚠️

8/
Tzamaloukas 2008 proposed 3 anuric hyperglycaemia phenotypes to help frame managing volume status

1. Dry anuric patient
- due to ⬆️RR/fever/vomiting
- high tonicity, normal/high Na
👉 Mx includes 250ml boluses

2. Euvolaemia
- high tonicity, low Na
👉 Fixes with iv insulin

9/
Phenotype 3 (most interesting)

intracellular to extracellular water movement (>2L) due to ⬆️⬆️extracellular glucose & tonicity
+
huge THIRST due to same
+
zero osmotic diuresis

=

extracellularly HYPERvolaemic DKA
(with associated hypertension++ and pulmonary oedema)

10/
❗️This is a rather unusual type of pulmonary oedema - it is reversible with iv insulin alone ❗️

(when insulin drives glucose into cells water follows from interstitium = less extracellular water = resolution of pulmonary oedema)

11/
Its well reported that hyperglycaemia causes pulmonary oedema in dialysis patients via these mechanisms even in absence of pre-existing heart disease

This may be even more likely in DKA state due to;
☑️ altered pulmonary capillary permeability
☑️ acute myocardial dysfunction

12/
Other facts about the wet patient in phenotype 3;
👉 Normal initial tonicity provides (insensitive) indirect indication of high fluid consumption in anuric hyperglycaemia.
👉 severity increases with higher initial glucose levels & if volume state uncontrolled to begin with.

13/
Treatment recommendations for DKA in dialysis cohort are based on case reports;
✅ iv insulin
✅ critical care level monitoring of electrolytes, glucose & volume state
✅ be aware of ⬆️hypo risk (especially associated with insulin bolus in case series)
✅ say no to iv bicarb

14/
Treatment (cont)
✅ small fluid boluses with re-assessment if hypovolaemic
✅ if hypervolaemic, go with higher concentrations of iv glucose when the sugars fall
✅ caution with K replacement
✅ high index suspicion for infective / ischaemic precipitants

15/
Big obvious question is; given the anuric patient in DKA is often hyperkalaemic, volume overloaded & acidotic - doesn’t dialysis just fix all those things?

As you’d expect there’s no good evidence on potential harms, or whether early or late dialysis strategy best.

16/
Clearly if hyperK or volume overload is life-threatening then easier decision.

Potential downsides to early HD;
❌ doesn’t fix underlying pathophysiology of insulin deficiency (if anything dialyse out insulin)
❌ masks severity
❌ cerebral oedema risk from tonicity swing

17/
Key learning points aren’t anything about anuric DKA - you may never see this.

It’s that the rules are always different in dialysis patients. Treatments are less tried and tested. Evidence base = case reports. Familiar protocols can become dangerous. Call for help early.

Fin/
As ever, I’m a trainee so any disagreements / criticism / sharing experience much appreciated.

References;

sciencedirect.com/science/articl…

ncbi.nlm.nih.gov/m/pubmed/67652…

cambridge.org/core/services/…

ncbi.nlm.nih.gov/pmc/articles/P…

ncbi.nlm.nih.gov/pmc/articles/P…