DKA

Question 1

What is the triad of DKA

Answer 1

• Hyperglycaemia
• Ketonemia
• Metabolic acidosis

Question 2

Explain the pathophysiology of DKA

Answer 2

Decrease in the net effective concentration of circulating insulin + increase in counter regulatory hormones (GH, cortisol, adrenaline, glucagon)

Lack of insulin means we get hyperglycaemia, volume depletion (glucose drags water out of cells) and electrolyte imbalances.

Lack of insulin to inhibit NEFAS undergoing oxidation to ketones in the liver - this leads to ketogenesis and thus acidosis

Question 3

What triggers DKA

Answer 3

• Not enough insulin given
• Infection
• MI, pancreatitis - increase release of counter regulatory hormones

Question 4

How does DKA present

Answer 4

Increased thirst
Polyuria and dehydration
Weight loss
Excessive tiredness
N&V
Abdo pain
Reduced consciousness
Kussmaul respiration
Pear drop smelling breath

Question 5

How do we investigate DKA

Answer 5

VBG, blood ketones and CBG:
- Blood glucose ≥ 11
- Ketonemia > 3 or ketonuria (++ dipstick)
- Acidosis with raised anion gap or low HCO3

Question 6

What may U&Es show in DKA

Answer 6

• Hyponatremia - hyperosmolar state causing water to enter vascular space, creating dilution hyponatremia
• Insulin drives K into cells - therefore lack of insulin means K is increased in the blood causing hyperkalaemia

Question 7

How is DKA managed

Answer 7

FIGPICK
- Fluids: 1 litre IV saline 0.9% over 1 hour
- Insulin: FRII IV
- Glucose: dextrose infusion started when glucose < 14mmol/L
- Potassium: momitor, if correcting potassium, be wary as it can go to hypokalaemia quickly
- Infection: ABx if infective
- Charts: continue to monitor fluids - give sodium bicarbonate if pH < 6.9
- Ketones: continue monitoring - resolution when ketones <0.6mmol/L

Question 8

What can severe hyponatremia result in

Answer 8

Cerebral oedema - correct carefully as overcorrection leads to osmotic demyelination syndrome (can cause locked in syndrome)