Diabetic Ketoacidosis Flashcards

1
Q

Which type of diabetes is DKA most common in?

A

Type I

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2
Q

Outline the underlying pathological process that leads to DKA and the associated dehydration

A

Insulin deficiency means that glucose cannot enter the cells
This therefore drives hyperglycemia but a low glucose state within the cells
Cells turn to alternative metabolic pathways leading to the production of ketone bodies
Ketone bodies are acidic in solution and this results in a ketoacidosis

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3
Q

What causes the severe dehydration in DKA?

A

Due to the insulin deficiency, glucose cannot enter the cells and serum glucose levels rise
Serum glucose levels exceed the renal threshold and glucose therefore enters the filtrate, this create an osmotic pressure which draws more water into the filtrate
Leading to polyuria and a dehydrated state

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4
Q

What are some precipitating factors to DKA?

A

Poor compliance to insulin therapy
Infection
Steroids
Other causes of stress on the body

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5
Q

How might someone with DKA present?

A
Abdominal pain
Features of dehydration- Lightheaded, Dizzy, Dry, Thirsty
Vomiting
SOB- Due to respiratory compensation
Sweet smelling breath

Remember that they may not have a formal diagnosis of Type I Diabetes. If there is known T1DM, ask about high glucose readings and ketone readings at home, they are taught to measure ketones when glucose is high at home

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6
Q

Why might a patient with DKA feel SOB?

A

This is due to the underlying respiratory compensation. Respiratory rate increases to decrease PCO2 in the aim of increasing pH (CO2 is acidic in solution)

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7
Q

Why do stresses on the body, such as infection, sometimes precipitate DKA?

A

Stress on the body causes increase in hormones that counteract the action of insulin, these include Adrenaline, Cortisol, Growth Hormone and Glucagon. These act to increase blood glucose levels as part of the stress response

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8
Q

What important differentials must be ruled out in DKA?

A

Must check for infection
Pregnancy- any female of childbearing age presenting with vomiting and abdominal pain should have a pregnancy test carried out.
Silent MI- Diabetes causes nerve damage and these patient can present with atypical pain pictures so an ECG should be done

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9
Q

What must be ruled out in a young female presenting with DKA like sx of vomiting and abdominal pain?

A

Pregnancy- check urine for Beta-HCG

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10
Q

Why should an ECG be done for potential DKA patients?

A

Patients can present with atypical pictures of an MI due to underlying neuropathy
Hyperkalaemia before treatment can lead to arrhythmia

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11
Q

What is an iatrogenic cause of DKA?

A

Steroids- act to increase glucose levels similar to stress response

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12
Q

What is the predominant ketone in DKA?

A

3-Beta-Hydroxybutyrate

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13
Q

What might the observations of a patient with DKA show?

A
Tachycardia
Tachypnoea
Hypotension
Dry mucous membrane
Low urine output
Sunken eyes
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14
Q

What type of shock can be caused by DKA?

A

Hypovolemic shock due to the huge fluid losses that occur via the kidneys

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15
Q

Outline the initial management of DKA?

A

It’s a medical emergency so requires and A-E approach
Fluid Resus comes first
Worry about insulin and electrolytes once haemodynamic stability is achieved

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16
Q

What is the biochemical triad of DKA?

A

Hyperglycaemia
Ketonaemia
Acidaemia

17
Q

What is the leading cause of mortality in DKA?

A

Cerebral oedema- particularly among young children and adolescents

Other causes of mortality in the adult population include severe hypokalaemia, ADRS and co-morbid states such as infection, MI and sepsis

18
Q

Why does the treatment for DKA precipitate hypokalaemia?

A

The treatment involves a fixed rate insulin pump (01.units/kg/hr) and insulin increases the activity of the sodium potassium ATPase, this drives potassium into the cells and can lead to hypokalaemia. Potassium replacement is an important part of the management.

19
Q

What is the key thing to focus on for the management of DKA?

A

The focus should be the blood ketone levels- targeting a drop of 0.5mmol/l/hr

The resolution of DKA depends upon the suppression of ketonaemia

20
Q

Who must always be involved in the management of patients with DKA?

A

The diabetic specialist team

21
Q

What factors must be measured for patients with DKA and used as treatment markers?

A

Blood ketone
Venous pH
Bicarbonate

22
Q

Should ABGs or VBGs be used to monitor DKA patients?

A

VBGs- these patients will need repeat VBGs every hour to check pH status. Repeat ABGs are painful and unnecessary

23
Q

What is the most important initial aspect of the management of DKA?

A

Fluid replacement- these patients are massively dehydrated with typical deficits of 100ml/kg

24
Q

What fluid should be used to replace deficits in DKA?

A

0.9% Saline- Depending on serum potassium levels 40 mmol of potassium should be added per litre. Pre-mixed bags of this are available.

25
Q

What is the target rate of reduction of blood ketones in DKA patients?

A

0.5mmol/l/hr

26
Q

What is the target rate of reduction of blood glucose in DKA?

A

3 mmol/L/hr

27
Q

What is the target rate of increase of bicarbonate in DKA?

A

Increase by 3 mmol/l/hr

28
Q

What is the target range for potassium for patients being managed for DKA?

A

Between 4 and 5

29
Q

What should be done to prevent hypoglycemia in patients being managed for DKA?

A

Once BMs fall below 14- 10% Dextrose should be added

This should be at the same time as fluid replacement with NaCl

30
Q

What is a sign patients should be started on 10% Dextrose?

A

Blood glucose fallen below 14- patients should not have their glucose stopped until they are eating and drinking normally

31
Q

How is the insulin therapy delivered in DKA patients?

A

A fixed rate insulin infusion at a rate of 0.1 units/kg

32
Q

Why should fluid be replaced cautiously in young DKA patients?

A

It can lead to cerebral oedema which is the leading cause of death in DKA

33
Q

Should patients baseline insulin therapy be continued when being treated for DKA? What are the names of the relevant insulins?

A

Long-acting insulin should be continued during the initial management of DKA. This includes insulin Levemir and Lantus.

Note- This avoids rebound hyperglycemia when IV insulin is stopped. This only applies to long acting insulin.

34
Q

Do priming doses of insulin need to be given in DKA?

A

No- the fixed rate insulin infusion is started at a rate of 0.1units/hr

35
Q

What are some serious complications of DKA, outline how they can be prevented/risk reduced?

A

Hypokalaemia and Hyperkalaemia- Careful cardiac monitoring and monitoring of serum potassium via VBGs. If Serum K+ is between 3.5 - 5.0 add in 40mmol KCL per 1L bag being used for fluid replacement

Hypoglycaemia- once glucose falls below 14 add 10% dextrose needs to be started

Cerebral Oedema- more common in children and careful fluid replacement should be undertaken in young adults with DKA.

36
Q

If someone is hypotensive what should be included in their fluid management?

A

Remember DKA is a medical emergency and so requires an A to E approach. As for any hypotensive patient a fluid challenge should be done- 500ml stat of NaCl 0.9%. Once the blood pressure is stabilised the normal fluid replacement can be done.