Toxicology

Hyperinsulinemic euglycemic therapy (HIET)

Mechanism of action:

Insulin increases the plasma concentrations of ionized calcium, improves the hyperglycemic

acidotic state, improves the myocardial use of carbohydrates, and exerts an independent

ii.

Dextrose prevents the development of hypoglycemia after insulin administration.

iii.

Potassium prevents the development of hypokalemia after insulin administration.

iv.

Onset of action is as soon as 5 minutes; however, it may take up to 30 minutes for full effects

to be seen.

Circulation 2023;148:e149-84):

If baseline glucose is less than 200 mg/dL, administer 50 mL of 50% dextrose in water before

insulin administration; may consider an infusion of 10%–20% dextrose to maintain a serum

glucose concentration greater than 100 mg/dL

ii.

Correct hypokalemia before initiating insulin therapy. Maintain normokalemia with potassium

replacement during insulin infusion and after withdrawal.

iii.

Bolus 1 unit/kg of regular insulin intravenously, followed by a continuous intravenous infusion

at 0.5–1 unit/kg/hour; increase rate every 10 minutes to a maximum of 10 units/kg/hour.

stability is obtained. Then, HIET should be tapered over several hours while monitoring

for hemodynamic deterioration. Dextrose therapy likely must be continued after

discontinuation of HIET to prevent hypoglycemia.

Adverse effects: Hypoglycemia, hypomagnesemia, and hypokalemia

Vital signs every 15–60 minutes with a goal mean arterial pressure greater than 65 mm Hg and

a HR greater than 50 beats/minute

ii.

Serum glucose every 15 minutes; then every 30–60 minutes once stable to target serum

concentrations greater than 100 mg/dL

iii.

Serum potassium every hour during the insulin infusion; then every 6 hours to maintain

concentrations above 2.8 mEq/L

iv.

Monitor for fluid overload and iatrogenic hyponatremia. Utilization of more concentrated

dextrose infusions (e.g., 50% dextrose) and more concentrated insulin infusions (e.g., 16 units/

mL) may be necessary.

Intravenous lipid emulsion (J Emerg Med 2015;48:387-97; J Med Toxicol 2017;13:124-5)

Mechanism of action is not well known; however, it is thought to be owing to a combination of

binding lipid-soluble agents and the provision of free fatty acids that increase cardiac energy and

intracellular calcium.

Improves HR and may reduce mortality as an individual treatment or in combination with other

therapies.

Evidence is limited to animal models and human case reports, and its role in therapy is controversial.

Bolus of 1.5 mL/kg of 20% lipid emulsion (such as Intralipid) over 2-3 minutes (typical dose

is usually 100 mL)

ii.

A repeat bolus may be considered if no response after initial bolus

iii.

The bolus may be followed immediately by an infusion of 20% lipid emulsion at a rate of 0.25

mL/kg/minute. After 3 minutes at this infusion rate, the infusion rate may be adjusted to 0.025

mL/kg/minute (i.e., 1/10 the initial rate) if there has been a significant response; total duration

is not to exceed 6 hours.