Diabetic Keto-Acidosis & HHS

Question 1

What causes DKA?

Answer 1

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies.

Question 2

What are the most common precipitating factors of DKA?

Answer 2

Infection, missed insulin doses, myocardial infarction

Question 3

What are the clinical features of DKA?

Answer 3

Abdominal pain

Polyuria, polydipsia, dehydration

Kussmaul respiration (deep hyperventilation)

Acetone breath (‘pear drops’ smell)

Question 4

What are the key diagnostic criteria for DKA?

Answer 4

Glucose >11 mmol/L or known diabetic

pH <7.3

Bicarbonate <15 mmol/L

Ketones >3 mmol/L (serum) or urine ketones ++

Question 5

How is DKA managed?

Answer 5

Fluid resuscitation: most patients with DKA are deplete ~5 - 8 litres.

Insulin: an IV infusion should be started at 0.1 unit/kg/hour. Once blood glucose is <15 mmol/L, an infusion of 5% dextrose should be started.

Correct any hypokalaemia

Continue long-acting insulin, stop short-acting insulin

Question 6

What are the complications of DKA and it’s treatment?

Answer 6

Gastric stasis

Thromboembolism

Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia

iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia

Acute respiratory distress syndrome

Acute kidney injury

Question 7

True or false: DKA has a higher mortality than HHS?

Answer 7

False. HHS has a higher mortality than DKA and may be complicated by vascular complications such as myocardial infarction, stroke or peripheral arterial thrombosis.

Question 8

Why is it important to differentiate between HHS and DKA?

Answer 8

It is extremely important to differentiate HHS from diabetic ketoacidosis (DKA) as the management is different, and treatment of HHS with insulin (e.g. as part of a DKA protocol) can result in adverse outcomes.

Question 9

What is the pathophysiology of Hyperosmolar hyperglycaemic state (HHS)?

Answer 9

Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium.

Severe volume depletion results in significant raised serum osmolarity and hyper-viscous blood. (Serum osmolarity >320 mosmol/kg)

Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume. (i.e. there is fluid in the veins but not in the tissues)

Question 10

What are the clinical features of HHS?

Answer 10

Fatigue, lethargy, nausea and vomiting.

Decreased consciousness, confusion.

Associated with MI, stroke and peripheral arterial thrombosis due to hyperviscosity of blood.

Dehydration, hypotension (late), tachycardia.

Question 11

How might you recognise HHS based on investigations?

Answer 11

Hypovolaemia

Marked hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis

Significantly raised serum osmolality (>320 mosmol/kg)

Question 12

How is HHS managed?

Answer 12

1. Normalise osmolality (gradually)
   - Done by giving fluids WITHOUT insulin. This will lower blood glucose, reducing osmolality.
   - Insulin may be required in a mixed HHS/DKA picture where ketones are raised.
2. Replace fluids and electrolytes
3. Normalise blood glucose (gradually)

Question 13

What ‘sick day’ advice should be given to all patients with diabetes?

Answer 13

The following are key messages that should be given to all patients with diabetes if they become unwell:

• Increase frequency of blood glucose monitoring to four hourly or more frequently
• Continue regular medications (with exception of metformin if renal function is at risk)
• Encourage fluid intake aiming for at least 3 litres in 24hrs
• If struggling to eat may need sugary drinks to maintain carbohydrate intake
• It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell