DKA, Hypoglycaemia, Hyperglycaemic Hyperosmolar State Flashcards
What is DKA? What 3 things is it characterised by?
DKA is a serious and potentially life-threatening complication of diabetes mellitus.
Characterised by:
1) hyperglycaemia
2) ketosis
3) metabolic acidosis
Is DKA more common in type 1 or type 2 diabetes?
T1DM
Cause of DKA?
1) An absolute or relative deficiency of insulin
2) This leads to increased hepatic glucose production
3) Decreased peripheral glucose utilisation and enhanced lipolysis
4) Subsequent ketone formation (ketones can cross BBB)
What are the most common precipitating factors of DKA?
Infection, missed insulin doses, and MI.
What 3 metabolic derangements are seen in insulin deficiency?
1) Hyperglycaemia
2) Ketosis
3) Metabolic acidosis
What causes hyperglycaemia in insulin deficiency?
Increased gluconeogenesis and glycogenolysis in the liver, combined with decreased glucose utilization in peripheral tissues, result in hyperglycemia.
What causes ketosis in insulin deficiency?
Insulin deficiency promotes lipolysis, releasing free fatty acids that are converted to ketone bodies (β-hydroxybutyrate and acetoacetate) in the liver.
High levels of ketone bodies lead to ketonemia and ketonuria.
What causes metabolic acidosis in insulin deficiency?
Accumulation of ketone bodies causes an increase in the anion gap metabolic acidosis.
What triad is seen in DKA?
1) Hyperglycaemia
2) Ketosis
3) Metabolic acidosis
Clinical features of DKA?
- Polyuria & polydipsia
- Blurred vision, headache, & lethargy
- Deep, rapid (Kussmaul) breathing
- Sweet/fruity/acetone smell on breath
- Dehydration: dry mucous membranes, tachycardia, hypotension, decreased skin turgor
- Electrolyte imbalances (particularly hypokalaemia): cardiac arrhythmias
- Neuro: altered mental status (ranging from lethargy to coma), focal or generalised seizures
- Abdo: abdo pain, N&V, can sometimes mimic acute abdomen (confuse diagnosis)
What is the typical blood glucose level in DKA?
> 11 mmol/L
How does hyperglycaemia lead to polyuria & polydipsia?
Osmotic diuresis
Symptoms of hyperglycaemia?
1) Polyuria & polydipsia
2) Blurred vision
3) Headache
4) Lethargy
What is cause of Kussmaul breathing in DKA?
as a compensatory mechanism to expel excess carbon dioxide
Cause of dehydration in DKA?
Osmotic diuresis results in significant fluid and electrolyte loss (mainly hypokalaemia)
Why may potassium levels appear normal at DKA presentation despite loss due to osmotic diuresis??
due to the extracellular shift of potassium (K+) from insulin deficiency and acidosis
What potential triggers to ask about in DKA?
1) infections
2) MI
3) stroke
4) pancreatitis
5) medication non-compliance
Key points for DKA diagnosis for:
a) glucose
b) pH
c) bicard
d) ketones
a) >11 mmol/l OR known diabetes
b) <7.3
c) <15 mmol/l
d) ketones >3 mmol/l OR urine ketones ++ on dipstick
What are the main principles of DKA management?
1) fluid replacement (typically isotonic saline)
2) insulin
3) correction of electrolyte disturbance
4) long-acting insulin should be continued, short-acting insulin should be stopped
Why is slower infusion indicated in younger adults (18-25) for fluid replacement in DKA?
As they are at greater risk of cerebral oedema
rate of insulin given in DKA?
An intravenous infusion should be started at 0.1 unit/kg/hour.
When should dextrose be added to infusion in DKA?
Once blood glucose is < 14 mmol/l, an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime.
I.e. after starting insulin
Management of potassium in DKA?
1) Serum potassium is often high on admission despite total body potassium being low (due to extracellular shift).
2) Insulin causes potassium to be quickly taken up by cells, resulting in hypokalaemia.
3) Potassium may need to be added to replacement fluids
How does insulin affect potassium?
Causes potassium to be quickly taken up by cells, resulting in hypokalaemia.
What rate of potassium infusion requires cardiac monitoring?
if the rate of potassium infusion is greater than 20 mmol/hour
What insulin should be continued/stopped in patients with DKA?
long-acting insulin should be continued, short-acting insulin should be stopped
DKA resolution levels for:
a) pH
b) blood ketones
c) bicarb
a) >7.3
b) <0.6 mmol/L
c) >15 mmol/L
How long should the ketonaemia and acidosis take to resolve in DKA?
Should be resolved within 24 hours - if this hasn’t happened the patient requires senior review from an endocrinologist.
If the criteria for the resolution of DKA has been met, what else is required for the patient to be switched to SC insulin?
The patient is eating and drinking.
Who should the patient be reviewed by prior to discharge following DKA?
diabetes specialist nurse
If patient has met criteria for resolution of DKA and is eating and drinking, what is next step?
Switch to SC insulin
Complications of DKA?
1) Gastric stasis
2) Thromboembolism
3) Arrhythmias: secondary to hyperkalaemia/iatrogenic hypokalaemia
4) Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
5) Acute respiratory distress syndrome
6) AKI
7) Cerebral oedema
Why does DKA increase the risk of VTE?
Due to dehydration, immobility, and a hypercoagulable state.
Management of increased VTE risk in DKA?
VTE prophylaxis with low molecular weight heparin or unfractionated heparin may be considered for high-risk patients.
Iatrogenic complications as a result of DKA?
Incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
Who is cerebral oedema (as a complication of DKA) more common in?
Children
