DKA Flashcards

1
Q

How does DKA occur?

A
  • Excessive glucose with a lack of insulin
  • Therefore the glucose cannot enter the body cells to be metabolised, leading to a starvation like state
  • Lipolysis increases free serum fatty acids which converts to ketones
  • Ketone production is the only way to make energy, particularly in the presence of cortisol/glucagon/GH
  • The combination of severe hyperglycaemia and ketoacidosis is deadly
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2
Q

What are some triggers for DKA?

A
  • Infection eg UTI, surgery
  • MI
  • Pancreatitis
  • Chemotherapy
  • Antipsychotics
  • Wrong insulin dose / non-compliance
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3
Q

What patients get DKA?

A
  • Type 1 diabetics

- VERY OCCASIONALLY, type 2

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4
Q

What are the symptoms of DKA?

A
  • Gradual drowsiness
  • Vomiting
  • Dehydration
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5
Q

Who should you measure blood glucose in when they present?

A

ALL PATIENTS WITH UNEXPLAINED:

  • Abdominal pain
  • Vomiting
  • Polyuria, polydipsia
  • Lethargy
  • Anorexia
  • Ketotic breath
  • Dehydration
  • Coma
  • Deep breathing (Kussmaul hyperventilation)
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6
Q

What is the triad required for a DKA diagnosis?

A
  • Acidaemia (pH<7.3 or HCO3-<15mmol/L)
  • Hyperglycaemia (blood glucose >11mmol/L or known DM)
  • Ketonaemia (>3mmol/L or over 2+ on dipstick)
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7
Q

What investigations would you undertake?

A
  • ECG
  • CXR
  • Urine dipstick and MSU
    Bloods -
  • Capillary and lab glucose
  • Ketones
  • pH (only aBG if low GCS/hypoxia)
  • U+E’s
  • HCO3-
  • Osmolality
  • FBC
  • Blood cultures
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8
Q

What signs would you look for in DKA?

A
  • Abdominal tenderness
  • Dehydration
  • Hypotension
  • Kussmaul breathing
  • Ketotic breath
  • Reduced GCS
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9
Q

What signs suggest severe DKA?

A
  1. Blood ketones >6mmol/L
  2. Venous bicarbonate < 5mmol/L
  3. pH <7
  4. K+ < 3.5mmol/L on admission
  5. GCS <12
  6. O2 sats <92%
  7. Systolic BP <90mmHg
  8. Pulse >100bpm or <60bpm
  9. Anion gap above 16
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10
Q

What is euglycaemic DKA?

A
  • DKA with normal or near normal blood glucose
  • May occur in the presence of exhausted glycogen stores in the liver (vomiting, alcohol, malnourished)
  • SGLT-2 inhibitors can cause them
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11
Q

What are the three targets of treating DKA?

A
  1. Fluid resuscitation
  2. Insulin therapy
  3. Electrolyte monitoring
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12
Q

What is the insulin regimen in DKA?

A
  1. Give 10 units of soluble insulin either i/m or s/c if likely to be delay of 15 minutes in starting IV insulin
  2. Add 50 units soluble insulin (actrapid) to 50ml 0.9% saline. Fixed rate infusion at 0.1units/kg/hour
  3. Continue patients usual long acting insulin at usual doses and times, start if new T1DM
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13
Q

What is the fluid regimen in DKA?

A
  1. If systolic BP<90, give fluid bolus.
  2. Give 1 litre saline over 1hr.
  3. Two litres saline, each over 2 hours
  4. Two litres saline, each over 4 hours
  5. One litre saline, over 6 hours
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14
Q

Why do patients need potassium?

How do you give this in DKA?

A
IV insulin decreases plasma potassium levels
Don't add potassium to 1st bag 
If K+ >5.5 = Nil
If K+ 3.5-5.5 = 20mmol per 500ml fluid
If K+ <3.5 = Discuss with consultant ITU
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15
Q

How do you avoid hypoglycaemia in treatment of DKA?

A
  • When glucose <14mmol/L, start 10% glucose at 125ml/hr to run alongside saline
  • Slow down saline infusion to match fluid output
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16
Q

What should you monitor in a patient and how often?

A
  • Hourly monitoring
  • VBG, U+E’s, ketones, CBG, bicarbonate
  • Fluid input and output (consider catheter)
17
Q

When do you continue the fixed rate insulin until?

A
  • Until blood ketones <0.6mmol/L
  • Venous pH > 7.3
  • Venous bicarb >15mmol/L
18
Q

What are the metabolic treatment targets?

A
Aim for fall of - 
- 0.5mmol/L/hr of ketones
- 3mmol/L/hr of glucose
Aim for a rise of:
- 3mmol/L/hr of bicarbonate

Increase insulin infusion by 1unit/hr until target achieved.

19
Q

What are complications of DKA?

A
  • Cerebral oedema
  • Aspiration pneumonia
  • Hypokalaemia
  • Hypomagnesia
  • Hypophosphataemia
  • Hyponatraemia
  • Thromboembolism
20
Q

How can hyperkalaemia happen in DKA?

A
  • Severe dehydration leads to prerenal AKI, causing hyperkalaemia
  • Acidosis causes hyperkalaemia
  • When starting insulin, potassium dramatically falls so watch for hypokalaemia