Insulin (IV Infusion — ICU Glucose Control)

How it works

Insulin binds the insulin receptor to promote cellular glucose uptake and inhibit hepatic gluconeogenesis and ketogenesis; given intravenously it has a very short half-life, so its effect is titratable and disappears rapidly when the infusion stops.

Prescribing in practice

• Hypoglycaemia is the principal hazard and can develop rapidly; the infusion requires concurrent glucose monitoring and usually a substrate (glucose-containing fluid) to allow safe titration, with a clear protocol for stopping or reducing the rate.
• Insulin shifts potassium intracellularly, so potassium must be monitored and replaced to avoid hypokalaemia, particularly in diabetic ketoacidosis management.
• Use a dedicated infusion pump and a locally approved variable-rate algorithm; abrupt cessation in a ketosis-prone patient risks rebound hyperglycaemia and ketoacidosis.

Monitoring

Monitor capillary or blood glucose at frequent protocol-defined intervals alongside serum potassium, ketones and fluid balance during the infusion.

Counselling the patient

• Glucose is being controlled by a drip that is adjusted frequently based on regular blood tests.
• Report any sweating, shakiness, confusion or palpitations immediately as these may signal a low blood sugar.
• Nursing staff should never stop the infusion without ensuring an alternative source of glucose and insulin cover where the patient is ketosis-prone.

Evidence & guidelines

Intravenous insulin infusion is the standard of care for diabetic ketoacidosis and inpatient hyperglycaemia, with UK practice guided by national diabetes inpatient and DKA care standards.