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      Management of Calcium Channel Antagonist Overdose with Hyperinsulinemia-Euglycemia Therapy: Case Series and Review of the Literature

      case-report

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          Abstract

          Calcium channel antagonists (CCAs) are commonly involved in drug overdoses. Standard approaches to the management of CCA overdoses, including fluid resuscitation, gut decontamination, administration of calcium, glucagon, and atropine, as well as supportive care, are often ineffective. We report on two patients who improved after addition of hyperinsulinemia-euglycemia (HIE) therapy. We conclude with a literature review on hyperinsulinemia-euglycemia therapy with an exploration of the physiology behind its potential use.

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          2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System.

          Frank Rodgers, T Litovitz, Cherith N Reid … (2005)
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            Calcium-antagonist drugs.

            D Abernethy, Peter J. Schwartz (1999)
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              Beneficial myocardial metabolic effects of insulin during verapamil toxicity in the anesthetized canine.

              J Kline, E Leonova, John Raymond (1995)
              Myocardial depression from verapamil toxicity may result from alterations in carbohydrate metabolism as well as calcium-channel antagonism. We hypothesized that pharmacologic doses of insulin may be effective in reversing both of these deficits. Randomized, controlled, prospective study. Laboratory of an urban hospital. Thirty mongrel dogs. Thirty mongrel canines were anesthetized with alpha-chloralose. Toxicity was induced by the administration of 0.1 mg/kg/min iv of verapamil, until there was a 50% reduction in mean arterial pressure, for 30 mins (titration), followed by a continuous verapamil infusion of 1 mg/kg/hr. Animals (n = 6 per group) were randomized to the control group (saline only) or to one of four treatment protocols: a) calcium chloride (20 mg/kg), then 0.6 mg/kg/hr; b) hyperinsulinemia-euglycemia (4.0 U/min of recombinant insulin, with arterial glucose concentration clamped to +/- 10 mg/dL [+/- 0.5 mmol/L] of the basal value); c) epinephrine, with a starting rate of 1.0 microgram/kg/min, titrated to maintain left ventricular pressure at basal values; or d) glucagon, a 0.2-mg/kg bolus, followed by a 150-microgram/kg/hr infusion. Animals were monitored until death or 240 mins; infusate volumes were held constant for all groups. During verapamil titration, the myocardial respiratory quotient increased from 0.84 +/- 0.05 to 1.07 +/- 0.11 (p < .05, paired t-test) and myocardial glucose uptake doubled, despite a reduction in cardiac work (p < .05, paired t-test). Net myocardial lactate uptake also increased significantly, excluding myocardial ischemia. In controls, this trend continued, indicating preferential carbohydrate metabolism during untreated verapamil toxicity. Despite hyperglycemia, the plasma insulin concentration was not significantly different in controls (basal value 11 +/- 2 vs. 39 +/- 21 microU/mL at 30 mins). Hyperinsulinemia-euglycemia increased both myocardial glucose and lactate uptake five-fold, and significantly increased the ratio of myocardial oxygen delivery/work, along with superior improvements in maximal left ventricular elastance at end systole compared with other treatments (p < .05 vs. other treatments, contrast analysis). Verapamil toxicity renders the heart dependent on carbohydrate metabolism. Inasmuch as the positive inotropic effects of all treatments were coincident with increased indices of myocardial carbohydrate uptake, adequate treatment of verapamil toxicity appeared to require maximal myocardial carbohydrate utilization. Hyperinsulinemia-euglycemia allows larger increases in myocardial carbohydrate metabolism and myocardial contractility than calcium chloride, epinephrine, or glucagon, resulting in improved survival rates during severe verapamil toxicity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Case Rep Crit Care
                Journal ID (iso-abbrev): Case Rep Crit Care
                Journal ID (publisher-id): CRIM.CRITICAL.CARE
                Title: Case Reports in Critical Care
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-6420
                ISSN (Electronic): 2090-6439
                Publication date (Print): 2012
                Publication date (Electronic): 14 February 2012
                Volume: 2012
                Electronic Location Identifier: 927040
                Affiliations
                1Department of Internal Medicine and Pediatrics, University of Texas Medical Branch, 301 University Boulevard, Route 0354, Gaveston, TX 77555, USA
                2Department of Pulmonary, Allergy, and Critical Care, University of Texas Medical Branch, Gaveston, TX 77555, USA
                Author notes
                *Shiwan K. Shah: skshah@ 123456utmb.edu

                Academic Editors: P. Kopterides and K. Lenz

                Article
                DOI: 10.1155/2012/927040
                PMC ID: 4010055
                PubMed ID: 24826345
                SO-VID: a27fde29-6579-4bb2-a1e7-a021ac8631ae
                Copyright © Copyright © 2012 Shiwan K. Shah et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 November 2011
                Date accepted : 17 January 2012
                Categories
                Subject: Case Report

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