JC: D-K-hoorAy! New Paeds DKA guidelines

On Monday, the British Society for Paediatric Endocrinology and Diabetes published interim guidelines on the management of diabetic ketoacidosis (DKA) in our younger patients (under the age of 18). NICE are planning to fully review and publish on this likely early next year, however on completing their revision, the BSPED DKA group felt an early publication was important.

You can find the new guidelines here, so please review them for yourselves as we won’t cover everything. We’ve put together a summary of the changes, along with some of the evidence behind them, and how it may affect our management of young patients presenting in DKA.

Please note that these guidelines refer to anyone under the age of 18. For the sake of brevity, I haven’t typed out “children and young people” in full each time. However, all of the guidelines on this page refer to this population.

Diagnostic Criteria

First off, how we diagnose DKA has changed. Previous guidelines required ketonaemia (blood beta-hydroxybutyrate above 3mmol/L) together with acidosis (pH <7.3 or bicarbonate <18). New guidelines have kept the ketone and pH, but now the serum bicarbonate level must be lower if this criteria is used.

Change 1: Bicarbonate <15mmol/L

This brings advice from BSPED in line with international guidelines.​1​

Don’t forget that while blood glucose levels are generally raised, high sugars are not required to make a diagnosis of DKA in children and young people.

Grading Severity

We can also grade the severity of DKA differently now, which then influences fluid management later down the line. The new criteria are:

Change 2: pH <7.3 or bicarb <15 = Mild DKA
pH <7.2 or bicarb <10 = Moderate DKA
pH <7.1 or bicarb <5 = Severe DKA

The difference here is that previously pH >7.1 were classified as “mild or moderate”. This is stratified further in the 2020 guidelines.

Who you gonna call?

There is a subtle change in wording in the new guidelines. Previously it was recommended to always discuss children with DKA with a more senior doctor, however now the guidelines state:

Change 3: Always consult with the consultant paediatrician on call any child with suspected DKA, even if you feel confident of your management

Managing this condition is difficult, so it’s important to get the most senior paediatrician involved early on.

Resuscitation Fluids

Change 4: Shocked patients get 20ml/kg over 15 mins

Children in shock (tachycardia, prolonged central capillary refill, poor peripheral pulses, or hypotension) should have 20ml/kg resuscitation fluids, then be reassessed. Up to two further amounts of 10ml/kg can be given (up to 40ml/kg). During this time a discussion with HDU should be had, as after 40ml/kg, inotropes should be considered.

Bolus Fluids

Giving fluids to children in DKA has long thought to be a problem area, with the risk of cerebral oedema at the top of everyone’s thoughts. Previous guidelines were clear that bolused IV fluids were never (or cautiously if shocked) to be used in this population.

Much of this concern comes from reasonably old studies largely of a retrospective nature. Simon has blogged on this before and you can read his review of one of the more recent randomised controlled trials here.​2,3​ Suffice it to say, newer, higher-evidence studies have been published which show that we still probably need to be cautious, but not that cautious. BSPED reflects these in their new guidelines.

Change 5: All non-shocked DKA patients should get a 10ml/kg bolus over 60 mins

Those children who are alert, not shocked or dehydrated, and not nauseated or vomiting, don’t always require IV fluids. Oral rehydration can be used instead but regular monitoring is needed to ensure their ketone levels are falling and they are improving.

If they need IVs though, give them a bolus. 10ml/kg of 0.9% saline, or Plasmalyte 148 depending on local policy. If you’re giving IVs, don’t give oral fluids as well.

Maintenance Fluids

Once the circulating volume has been restored with adequate resuscitation fluids, it’s time to think about maintenance fluids.

Fluid requirement = Maintenance + (Deficit – Bolus)

Change 6: Calculate maintenance fluid requirements in the traditional (non-reduced) way

Previously maintenance fluids in DKA were calculated using a reduced formula. BSPED now recommends the traditional Holliday-Segar formula.

Remember change 2 – grading severity? This helps us to calculate fluid deficit so calculators at the ready!

Change 7: Mild DKA = 5% deficit
Moderate DKA = 7% deficit
Severe DKA = 10% deficit

This fluid deficit (minus the initial fluid bolus) is corrected over 48 hours. The guidelines go through example fluid calculations​4​ (pdf under the management section) so you can get your brains around this.

Remember though, if you have given resuscitation fluids, these are not subtracted from the maintenance calculation.

Change 8: In overweight/obese children use a maximum weight of 80kg or 97th centile for age (whichever is lower)

To avoid excessive fluid it’s important to consider ideal upper weight limits in overweight patients. Don’t forget the Third Rule of May​5​ – “if the dose you’ve calculated is more than you’d give an adult, it’s wrong”. BSPED have said they are creating an online calculator where this can all be printed and put in the notes for ease, however this won’t be available til March. We will update the blog with a link when it’s ready.

Potassium Maintenance

All fluids (except resuscitation/bolus fluids) should contain 40mmol/l potassium chloride.

Change 9: If the patient is hyperkalaemic at presentation, don’t give additional potassium until they’ve passed urine, or the potassium is back in normal range

It’s important to ensure the child isn’t anuric due to the risks of hyperkalaemia, so if they present with a high K, hold off on that potassium until it’s back to the upper limit of normal or they’ve had a wee!

Insulin

This is largely business as usual here. Don’t give boluses. Start an infusion 1-2 hours after starting fluid therapy. 0.05 units/kg/hr is likely to be sufficient, but go with local policy. Stop the patient’s own insulin pump if they are on one when you start IV insulin. Continue long-acting subcutaneous insulin in patients who already take it, or in patients that don’t:

Change 10: Consider starting a long-acting subcutaneous insulin alongside IV insulin

Additional Thoughts

Finally, the guidelines are clear to state that although they have been written with patients under 18 in mind, this could cause difficulties depending on where you work.

Change 11: Manage 16-17 year old patients according to the guidelines for the teams they are under

If your 16-17 year olds are managed by paediatrics – use these guidelines. If they’re managed by adult teams, use local adult guidelines. Use familiar protocols to avoid error or miscalculations.

As always in any guideline it’s important to note that these are guidelines and are there to support, not replace, clinical acumen. As such there may be some controversial parts…

In the emergency management section of the guidelines, we’re instructed to “give 100% oxygen by face-mask”. Regardless of the pedantic problems in actually achieving this FiO2 by face-mask only, it’s a bit surprising to see this written down in an era of avoiding hyperoxia. Titrate that oxygen down quickly to maintain appropriate saturations!

So there we go, a run down of changes to managing DKA in children and young adults. It would be great to hear your thoughts on these new guidelines, either in the comments section below, or on Twitter.

vb

Chris
@cgraydoc

Further reading.

For a wider overview of DKA management that incorporates the new guidelines have a look at Dani Hall’s post on DFTB.

References

  1. 1.
    Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. October 2018:155-177. doi:10.1111/pedi.12701
  2. 2.
    Kuppermann N, Ghetti S, Schunk J, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378(24):2275-2287. doi:10.1056/NEJMoa1716816
  3. 3.
    Carley S. Fluid Resuscitation in paediatric dka. St Emlyn’s. https://www.stemlynsblog.org/jc-fluid-resuscitation-in-paediatric-dka-st-emlyns/. Published 2018. Accessed 2020.
  4. 4.
    BSPED B. BSPED Interim Guideline for the Management of Children and Young People under the age of 18 years with Diabetic Ketoacidosis. BSPED. https://www.bsped.org.uk/media/1712/new-dka-guideline-v6-final.pdf. Published 2019. Accessed 2020.
  5. 5.
    May N. Apparent Life Threatening Events in Babies – Trouble BRUEing. St Emlyn’s. https://www.stemlynsblog.org/alte-brue/. Published 2016. Accessed 2020.



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Posted by Chris Gray

Dr Chris Gray BSc(Hons) MBBS MRCP(UK) MRCEM AICSM is an ST6 in Emergency Medicine and Intensive Care Medicine, training in Manchester and the North West. He is also an ALS, APLS, and ETC instructor and keen educator. He is @cgraydoc on twitter

  1. The question I want to post, is what to do with the uncompensated shock kid who is GCS 3, SBP in the 60’s, HR in the 180’s, super vasoconstricted, dry like a potato chip with a glucose of 66 mmol/L (~1200 mg/dl). His IVC was almost totally collapsed. This kid was the sickest DKA I’ve ever seen and he looked like was about to arrest. The consultant pediatrician jumped out of her skin when she saw I gave a 20 ml/kg bolus of NS. My priority was perfusion! This kid had no intravascular volume left, and even after the 20 cc/kg his vitals didn’t change. She called me incompetent and dangerous because of the “large volume of fluid” I had given.

    Besides getting my feelings hurt (not really), I was surprised she ordered pitiful amount of fluid infusion while this kid was in shock and remained in shock for many hours, despite pressors. Unfortunately, this kid didn’t do well, arrested the next morning and could not be resuscitated.

    I remember the mantra: Treat shock! The longer a shock state continues, multi organ disfunction gets closer and closer. This kid was not perfusing his brain, heart and kidneys, and he stayed like that for hours even in the hospital. He had no catecholamines left and all his functional reserve was gone. The team had such a fear of “causing” CE by volume expansion, that allowed this kid to die still hypovolemic

    There is some evidence showing that kids who “develop” CE, ALREADY HAVE CE when we start treatment. The hypothesis is that kids brains have higher oxygen demand and develop global ischemia from hypo perfusion a lot faster than adult brains. Also, the profound vasoconstriction with high catecholamines and acidosis, together with blood-brain barrier dysfunction lead to inflammatory changes causing CE. Here: https://www.nejm.org/doi/full/10.1056/NEJM200101253440404

    Another study (18 kids only) showed MRI was worse early in the severe DKA than after treatment: http://pediatrics.aappublications.org/content/131/1/e73?sso=1&sso_redirect_count=1&nfstatus=401&nftoken=00000000-0000-0000-0000-000000000000&nfstatusdescription=ERROR%3a+No+local+token

    And finally… Canadians (yes, great Canadians) found the highest features associated with CE were high BUN, low CO2, and bicarb treatment, suggesting that severe dehydration/hypovolemia and acidosis are important risk factors. https://www.jpeds.com/article/S0022-3476(04)01216-8/fulltext

    So… Going back to my question. What do I do for the profound shock, Glasgow of 3, severe DKA kid? Do I correct hypovolemia? In my simple way of thinking, delaying intravascular volume repletion to 36 hrs, is delaying brain perfusion for 36 hr. There is now enough evidence to suggest that its not the treatment, but the ischemia and blood-brain barrier dysfunction what causes CE and by delaying adequate brain perfusion we may be putting these kids at risk. I think a trial for rapid intravascular volume correction over shorter period of time vs 36 hrs with brain imaging in all kids early, is warranted.

    OK.. rant over.

    Reply

    1. I can’t comment on your specific case of course. I was not there and there may be many circumstances affecting the decision.

      Having said that I think there is a real shift in our understanding of CE in DKA in the way that you describe. In the latest guidance it’s clear that you treat shock if it’s present. That will require fluid boluses. In my opinion there are two reasons to do this.

      1. They are in shock (as you describe) and thus in a state of hypoperfusion. That needs rectifying and cannot wait. That is different to the dehydration seen in DKA which has taken hours/days to happen.
      2. This is arguably the most important point IMHO. This is that DKA may well be a manifestation of another pathology such as sepsis, which would not be easy to spot in the sort of patients you describe. Now, we are increasingly cautious with fluids in sepsis but in this circumstance the two pathologies interact into a world of badness. Give the bolus, reassess, search for the cause, and then reassess again and again and again……

      One of the more difficult human factors situations I found myseld in some years ago was not at all disimilar to the one you describe. It was tough, and I understand your concerns of a shared experience.

      vb and thanks for commenting.

      S

      Reply

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