Management of Diabetic emergencies Flashcards
What is the pathophysiology behind DKA?
There is not enough insulin to cause glucose to move into the cells. This causes the cells to use fatty acid metabolism instead causing acidic ketones to be produced.
What are the blood glucose values for hypo and hyperglycaemia?
Hypo <4 and hyper >11
What are the management steps of DKA?
A-E
Confirm diagnosis - glucose >11, pH<7.3 and cap ketones >3mmol/L
IV fluids - dehydration more lethal than hyperglycaemia
Fixed rate insulin infusion - 0.1unit/kg/hour rapid ating insulin in saline
Investigate to find cause
What is the fluid resusciation regime for DKA?
1L of saline over first hour Add patassium chloride to subsequent fluids depending on VBG results 1L over 2 hours 1L over 2 hours 1L over 4 hours
What is the amount of potassium chloride you add to fluids depending on the VBG results?
k<4.5mmol/L = 40mmol KCL
k 4.5-5.5 = 20mmol KCL
k>5.5 = nil
What insulin should be given for DKA?
Fixed rate insulin infusion of 0.1unit/kg/hour of fast acting insulin e.g. actarapid in 50mls 0.9% saline
When cap glucose falls to <14mmol/L give 10% IV glucose at 125ml/hour in addition to saline - this drives more glucose into cells to reduce ketosis
Wen should intensive care be considered in DKA?
If ketones >6 HCO3 <5/pH<7.1 GCS<12 SBP<90 sats<92% HR >100
How should the patients long acting insulin be managed during DKA?
Continue long acting insulins and consider starting one if it is a new presentation
What are the targets on VGA for treating DKA?
Aim to reduce glucose by 3mmol/hour and reduce ketones by 0.5mmol/L/hour
What should you do with a patients insulin regime once you have treated their DKA?
When they are no longer acidotic and they are eating and drinking you should restart their normal insulin regime at a mealtime
What other considerations are there once a patient has been treated for DKA?
If they are not eating and drinking they require a variable rate insulin infusion
VTE prophylaxis
Consider NG tube, aspiration is a common cause of death
Education and medication review
How does hyperosmolar hyperglycaemic state differ to DKA?
Illness or infection slowly causes hyperosmolarity to develop. There is no acidosis/ketosis as there is enough insulin to cause glucose uptake. The dehydration and a prothrombotic state are the dangers
How can you confirm hyperosmolar hyperglycaemic state?
Marked hyperglycaemia >30mmol/L without ketosis
Serum osmolality >330mmol/L
Hypovolaemia
What is the management of hyperosmolar hyperglycaemic state?
Rehydrate at the same rate as in DKA (1L in first hour)
VTE prophylaxis (high risk of VTE)
If this is not correcting hyperglycaemia start insulin at 0.05units/kg/hour
Look for cause
Hold metformin for 2 days as it causes metabolic acidosis
How do you treat hyperglycaemia without DKA?
Rehydrate if nessesary
Stat dose of rapid acting (Novorapid) or short acting (Actarapid):
-In type 1 - 1 unit decreases blood glucose by 3mmol/L (aim glucose <12mmol/L)
-In type 2 (more insulin resistant) 0.1unit/kg
Identify and correct cause