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Michael E Mullins, Commentary, Clinical Chemistry, Volume 63, Issue 2, 1 February 2017, Pages 462–463, https://doi.org/10.1373/clinchem.2016.265447
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Symptomatic CCB toxicity remains a challenging entity to treat. It seems intuitive that calcium salts should overcome the competitive inhibition of the L-type calcium channels. Although calcium salts are usually the first treatment, they are seldom very effective as the primary treatment. Extreme hypercalcemia carries some risks. Monitoring calcium concentrations is important for patient safety when using repeated doses or constant infusions of calcium salts.
Calcium salts for intravenous use are available as calcium chloride and calcium gluconate. Calcium chloride has 3 times as much elemental calcium as calcium gluconate has. However, calcium gluconate may safely go into a peripheral IV line, but calcium chloride should go through a central venous catheter whenever possible.
The hyperglycemia in this case has 2 potential causes—the CCB overdose and diabetes mellitus. CCB overdoses characteristically produce hyperglycemia, while β-blockers generally do not. For both CCB and β-blocker poisoning, the insulin doses should be much higher than normally used for controlling blood glucose in diabetes or treating diabetic ketoacidosis (1). Instead of 0.1 U/kg/h, as for diabetic ketoacidosis, the dose should be 0.5–1 U/kg/h with hourly checks of finger stick blood glucose. This approach is “hyperinsulinemia with euglycemia.” Often the patient with CCB overdose may need little or no supplemental dextrose for hours, but patients with symptomatic β-blocker overdose more often will need dextrose to match the insulin.
