Diabetic Ketoacidosis- Glucagon is the Problem!

Another common topic and also a frequent presentation to the ED is DKA. On the whole I think of this as straight forward ie bang up some fluids and insulin and it'll sort itself out! That being said when you actually read about it things are a little bit more complicated.

Your hospital will have it's own policy and approach, but a nice little guide has been produced by the Joint British Diabetes Societies Inpatient Care Group:

http://www.bsped.org.uk/clinical/docs/DKAManagementOfDKAinAdultsMarch20101.pdf

Let's start with some background to put things in perspective:

• It is potentially life threatening, although mortality rates have fallen in the last 20 years from 7.96% to 0.67%!
• Cerebral oedema especially in children and adolescents is the most serious complication.
• The typical fluid deficit in DKA may be 100 ml/kg!
• It is now possible to measure blood ketones at the bedside.
• The treatment of DKA has developed and will continue to develop as our understanding increases.

The rest of this post is about adults, there are key differences in the management of children/ adolescents.

Definition:

1. Blood glucose >11
2. Ketones > 3 (or 2+ on urine)
3. pH <7.3 or bicarb <15

Pathophysiology:

Its a lack of insulin, right? Well yes and no.

Type one diabetics have impaired insulin production and therefore cannot bring their sugars down, but Insulin also acts to oppose other hormones (glucagon). It is this lack of opposition that causes the metabolism of fatty acids which in turn produces the ketones. So it is good to think of it as unopposed gluconeogenesis: the production of ketones lowers the pH and therefore gives us the acidosis ie. not a sugar problem.

Bang up some fluids and give insulin:

Treatment is aimed at correct the abnormalities and these patients are certainly dry and in need of lowering their blood sugars, but actually we need to think of treatment goals as switching off the gluconeogenesis and ketone production.

1. Fluid resuscitation - the link at the top contains a bit of debate as to the fluid to give, but essentially 0.9% Chloride is the answer because you can add potassium when it is needed.
2. Insulin- fixed rate infusion based on weight (0.1 units/kg/hr) - this corrects the sugars but also suppresses ketogenesis!
3. Monitor K+ and add it to fluids given - remember insulin will push it into intracellular space.
• hypokalaemia is a complication of treatment.
4. Give glucose when blood glucose is <14 - DKA is not a sugar problem but the production of ketones driven by glucagon, what we don't want is the sugar to fall and the gluconeogenesis to begin again!!!

What should I be worried about?

Things to worry about are the complications mentioned above: cerebral oedema and hypokalaemia.

Other things that warrant a higher level of care (HDU/ ITU) include:

• pH <7.1
• bicarb <5
• cardiovascular compromise
• Blood ketones >6
• Hypokalaemia on admission
• Anion gap >16
• Reduced GCS

Question:

A 36 year old lady who frequently attends the department with diabetic problems presents with a three day history of abdo pain and vommiting. She ways 65kg. Her observations are as follows: HR 117, Bp 109/76, RR 30, Sats 99% (21%). The results of her blood gas are as follows:

• pH: 7.23,
• Pa O2: 10
• Pa CO2: 1.4
• HCO3: 11.2
• Glucose: 36

a) What are the diagnostic criteria for Diabetic Ketoacidosis (DKA)? (3)

b) Write an appropriate prescription for an insulin regime in this patient. (2)

c) Give three features that should trigger discussion with critical care? (3)

d) What would be an appropriate fluid regime for this patient? (2)

Clever Marks:

Another question could quite easily ask you to calculate the anion gap - I have left this out of the gas information as I intend to do another medical maths entry on this topic.