Insulin therapy

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The successive aims of insulin treatment in ketoacidosis are

• inhibition of lipolysis and hence ketogenesis

• suppression of hepatic glucose production

• enhanced disposal of glucose and ketone bodies by peripheral tissues.

Soluble (unmodified) insulin only has a plasma half-life of approximately 5 min, so intermittent i.v. injections lead to unpredictable and fluctuating plasma insulin concentrations. Maximal stimulation of potassium transport into cells occurs with pharmacological plasma insulin concentrations and the risk of hypokalaemia is therefore greater with large doses of insulin. With modern insulin regimens, complications of treatment such as hypokalaemia and late hypoglycaemia are less common than with the obsolete high-dose intermittent bolus regimens.

• Intravenous insulin. Soluble insulin is administered as a continuous intravenous infusion at a rate of 5-10 (usually 6) U/h. This produces steady plasma insulin concentrations in the high physiological (or pharmacological at the higher rates) range that adequately suppress lipolysis, ketogenesis and hepatic glucose production, even in the presence of elevated levels of catabolic hormones. Insulin is diluted to a convenient concentration (usually 1 U/mL) with isotonic saline in a 50 mL syringe and delivered by a syringe-driver infusion pump connected via a Y connector. The infusion apparatus should be flushed through before connection to the patient. Alternatively, insulin can be added to a 500 mL bag of isotonic saline and mixed gently; the insulin must be injected using a needle of sufficient length to clear the injection port of the bag.

• Monitoring response. Capillary blood glucose is checked at the bedside at hourly intervals and the infusion rate is reduced to 1-3 U/h, when blood glucose has fallen to <15 mmol/L. The infusion rate should be adjusted to maintain euglycaemia until the patient is eating again and subcutaneous insulin is recommenced (Table 1.6). The rate required at this stage will vary according to (1) the degree of insulin resistance (see above) and (2) the rate of dextrose infusion. Intravenous insulin at 6 U/h should produce a steady and predictable fall in plasma glucose concentrations, averaging 4-6 mmol/h in adults. The commonest causes of failure to respond are mechanical, i.e. problems such as the pump being inadvertently switched off or set at the wrong rate and blockage of the delivery line. It is sound practice to cross-check (and record on the flow-chart) the prescribed rate of insulin delivery against the volume infused each hour during treatment. During treatment of ketoacidosis there is conversion of 3-hydroxybutyrate to acetoacetate. Nitroprusside-based tests may therefore give the mistaken impression that ketosis is either not resolving or is worsening. A rising plasma bicarbonate will allay such fears.

• Transfer to subcutaneous insulin. The first subcutaneous injection should comprise or include a dose of short- or rapid-acting insulin. This should be administered 60 min before the i.v. insulin infusion is terminated to allow time for absorption of insulin from the subcutaneous depot.

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