- Insulin is a regulatory anabolic protein hormone that lowers blood glucose levels by binding to insulin receptors to increase glucose uptake, inhibit hepatic glucose output and promote glycogen production.
- An additional use for insulin is in combination with a dextrose infusion to help lower potassium levels in hyperkalaemia. Insulin causes an intracellular shift of potassium by stimulating sodium influx; exchanging intracellular sodium for extracellular potassium through activation of the Na+ - K+ -ATPase transporter. IV insulin is believed to cause a dose-dependent decrease in serum potassium, with 10 units estimated to lower serum potassium by 0.6 to 1.2 mEq/L. When administered intravenously, the potassium shifting effects of insulin occur within 15 min of administration1.
- High-dose insulin and glucose therapy is also an effective treatment for severe beta blocker and calcium channel-blocker poisoning, with studies showing greater efficacy in terms of haemodynamic stability than with conventional treatment2.
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycaemic syndrome (HSS)
In conjunction with glucose:
- Hyperkalaemia
- Severe beta-blocker and calcium channel-blocker toxicity
- Hypoglycaemia
- Rapid correction of hyperglycaemia may contribute to cerebral oedema and electrolyte imbalances
- Hypoglycaemia may occur if insulin dose is too high in relation to insulin requirement
- Hypoglycaemia may occur during treatment of hyperkalaemia and beta-blocker and calcium channel-blocker toxicity despite concurrent infusion of glucose, and blood glucose should be monitored regularly
| kg | ||
| Mode: | ||
| Weight: | ||
| Cefazolin for fractures/prophylaxis |
| Presentation: /mL |
| Calculated dose: in |
Note: Management of DKA / HSS requires I-STAT
Adult
| Blood Glucose Level (mmol/L) | Infusion dose (50 units in 50ml) |
|---|---|
| 5 or less | 0 units/hour (ml/hr) |
| 5.1 – 10 | 1 units/hour (ml/hr) |
| 10.1 – 15 | 2 units/hour (ml/hr) |
| 15.1 – 20 | 3 units/hour (ml/hr) |
| 20.1 – 25 | 4 units/hour (ml/hr) |
| Greater than 25 | 5 units/hour (ml/hr) |
- 10 units of Actrapid with 50ml of 50% glucose over 15 minutes
- Repeat as necessary to lower K+ to < 6.5 mEq/L
This antidote is only administered to critically ill patients with:
- Hypotension (SBP <90mmHg) despite fluid challenge and atropine administration
- Bradycardia < 60 unresponsive to atropine
- 2nd or 3rd degree Conduction blocks
- Commence therapy by administering 25g glucose (50ml of 50% solution)
- Administer Actrapid 1 unit/kg as an IV bolus
If required:
- Ongoing infusion of 25g glucose (50ml of 50% solution/hr) to maintain BSL 5.5-14mmol/L)
- Ongoing infusion of Actrapid 0.5units/kg/hr IV
Infusion table for ongoing treatment of beta-blocker/calcium channel-blocker toxicity
| Patient weight (kg) | Infusion rate (0.5units/kg/hr) (ml/h) |
|---|---|
| 50 | 25u/hr (12.5ml/hr) |
| 60 | 30u/hr (15ml/hr) |
| 70 | 35u/hr (17.5ml/hr) |
| 80 | 40u/hr (20ml/hr) |
| 90 | 45u/hr (22.5ml/hr) |
| 100 | 50u/hr (25ml/hr) |
- Monitor carefully for signs of hypoglycaemia every 20 minutes for the 1st hour in high-dose insulin therapy.
- Actrapid human insulin (rys) 1000IU in 10mL (100IU/mL) injection multidose vial
| Settings | |
|---|---|
| Current mode: | |
| Extended Care: | |
| Colour assist: | |
Moussavi K, Fitter S, Gabrielson SW et al. 2019. Management of hyperkalaemia with insulin and glucose: pearls for the emergency clinician. The Journal of emergency Medicine;57(1):36-42
Engebretsen KM, Kaczmarek KM, Morgan J & Holger JS. 2011. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clinical Toxicology:49:277-283
Queensland Ambulance Service DKA protocol.
Wyatt JP, Taylor RG, deWit K, Hotton EJ. 2020. Management of hyperkalaemia. In: Oxford Handbook of Emergency Medicine (5th ed). Oxford University Press.
Murray L, Little M, Pascu O, Hoggett K. 2015. high dose insulin therapy. In: Toxicology Handbook (3rd ed). Elsevier
Nickson CP, & Little M (2009). Early use of high-dose insulin euglycaemic therapy for verapamil toxicity. The Medical journal of Australia, 191 (6), 350-2
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