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Medication Overdoses in the Emergency Department: Oral Hypoglycemic Agents, Atypical Antipsychotic Agents, Beta- Blockers, Calcium Channel Blockers, and Digoxin

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Medication Overdoses in the Emergency Department: Oral Hypoglycemic Agents, Atypical Antipsychotic Agents, Beta- Blockers, Calcium Channel Blockers, and Digoxin Pharmacy and Wellness Review Volume 5 Issue 2 Article 2 June 2014 Medication Overdoses in the Emergency Department: Oral Hypoglycemic Agents, Atypical Antipsychotic Agents, Beta- Blockers, Calcium Channel Blockers, and Digoxin Brooke Marlowe Ohio Northern University Tara Tokar Ohio Northern University Kayti Kintner Ohio Northern University Kelsey Fink Ohio Northern University Grant Walliser Ohio Northern University, [email protected] Follow this and additional works at: https://digitalcommons.onu.edu/paw_review Part of the Emergency Medicine Commons, Medical Toxicology Commons, and the Medicinal and Pharmaceutical Chemistry Commons This Article is brought to you for free and open access by the ONU Journals and Publications at DigitalCommons@ONU. It has been accepted for inclusion in Pharmacy and Wellness Review by an authorized editor of DigitalCommons@ONU. For more information, please contact [email protected]. Emergency Medicine Medication Overdoses in the Emergency Department: Oral Hypoglycemic Agents, Atypical Antipsychotic Agents, Beta-Blockers, Calcium Channel Blockers, and Digoxin Brooke Marlowe, fourth-year pharmacy student from Granville, Ohio; Tara Tokar, fifth-year pharmacy student from Dayton, Ohio; Kayti Kintner, fourth-year pharmacy student from Sunbury, Ohio; Kelsey Fink, fifth-year pharmacy student from Hudson, Ohio; Grant Walliser, PharmD '07, adjunct professor of pharmacy, emergency medicine clinical pharmacist at Grant Medical Center events and patient fatalities.6 Pharmacists, as drug experts, This knowledge-based activity is targeted for all phannacists should be aware of toxicity potential for all medications and and is acceptable for 1.0 hour (0.1 CEU) of continuing should be prepared with the knowledge for treatment. education credit. This course requires completion of the program evaluation and at least a 70 percent grade Oral Hypoglycemics on the program assessment questions. Epidemiology Type 2 diabetes mellitus (DM2) is a disease on the rise, af­ ACPE Universal Activity Number (UAN): 0048-0000-14-197-HO 1-P fecting over 190 million patients in 2006, with a projected population of over 325 million by 2025.3 In the attempt to Objectives treat DM2, the use of oral hypoglycemics has steadily risen After completion of this program, the reader should be able with the disease prevalence. A variety of medication classes to: are available including sulfonylureas, biguanides, megliti­ 1. Explain the pathophysiology behind oral hypoglyce­ nides, thiazolidinediones and alpha-glucosidase inhibitors. mic agents, atypical antipsychotic agents, beta­ While such therapy choices are appropriate for controlling blockers, calcium channel blockers, and digoxin. blood glucose levels in the insulin-resistant patient, several 2. Describe the presenting symptoms associated with the of these classes have been shown to reach toxic levels, aforementioned drug classes in an overdose. thereby causing severe adverse effects. Biguanides, for exam­ 3. Discuss recommended treatment options in cases of ple, accounted for 40 percent of the 10,000+ cases, as did toxicity. sulfonylureas; a majority of which were seen in children.2.3 4. Describe the pharmacist's role in treating toxicological emergencies. Mechanism As there are several classes of oral hypoglycemics, it is im­ Abstract portant to make distinctions by which their mechanisms The number of medication toxicities has been steadily in­ work so that toxic levels can be more readily identified and creasing with more patients presenting to the emergency treated. Sulfonylureas work by lowering potassium channel department for both intentional and unintentional over­ permeability in pancreatic beta cells, leading to release of doses. Oral hypoglycemics, atypical antipsychotics, beta­ intracellular calcium and release of insulin-containing gran­ blockers, calcium channel blockers and digoxin overdoses ules. The result is a lowered threshold at which insulin will are some of the more common medication toxicities health be secreted in the presence of glucose.7 It should be noted care professionals may see in practice. Toxic doses of oral that the second generation sulfonylureas, including gly­ hypoglycemic agents, beta-blockers, calcium channel block­ buride, glipizide, and glimepiride, have a shorter half-life ers and digoxin have more definitive options for treatment, (t1;2) and duration of action (DOA).2 Meglitinides work simi­ while atypical antipsychotic overdoses are managed with larly in lowering the potassium channel permeability allow­ supportive care. Pharmacists in particular play a pivotal role ing for intracellular calcium to depolarize pancreatic beta in identifying presenting symptoms and recommending ap­ cells.s By stimulating the Peroxisome Proliferator Activated propriate treatment options in toxicological emergencies. Receptor-gamma (PPAR-gamma) in adipose, skeletal muscle, and liver tissue, thiazolidinediones promote the expression Introduction of glucose controlling genes in the presence of insulin. 9 In While incidences of toxic exposure to medications may be order to increase insulin sensitivity, biguanides will increase intentional or unintentional, trends are indicative of a rise in the ability to metabolize glucose, and decrease glycogenoly­ medication overdoses.1 Emphasis on opioid and prescription sis, the breakdown of glycogen to form glucose.10 Alpha­ analgesic abuse remains a high priority. However, several glucosidase inhibitors will slow the enzymatic breakdown of other medication classes may be overlooked. In 2004, there carbohydrates, thereby lowering the rise in post-prandial were upwards of 10,000 cases of oral hypoglycemic overdose blood glucose levels. By this process, glycosylated hemoglo­ used in the treatment of diabetes.2-3 A significant number of bin will be decreased.11 ln recognizing the basic mechanisms atypical antipsychotic overdoses were reported from 2001 to for the varying classes of oral hypoglycemics, identifying ap­ 2005, some of which ended in fatality. 4 Beta-blockers and propriate treatment becomes more clear. calcium channel blockers show a combined incidence of over 30,000 overdoses, 57 of which were fataJ.S.19,20 The cardiac Presenting Symptoms of Toxicity glycoside digoxin has also been associated with severe toxic Upon over-ingestion of oral hypoglycemics, patients will tend 4 THE PHARMACY AND WELLNESS REVIEW June 2014 Volume 5, Issue 2 Medication Overdoses in the Emergency Department... ..................................................................................................................... Emergency.Medicine to have similar presentations, yet the specific drug class will somatostatin-2 receptors on pancreatic beta cells, it inhibits be distinguishable upon the presence of unique symptoms. G-protein coupled voltage gated calcium channels from being As could be expected, patient presentation is associated with opened. This inhibition of calcium influx will stop further a hyperinsulinemic/hypoglycemic state. In sulfonylurea tox­ insulin release by pancreatic beta cells.13 Octreotide is U.S. icity, for example, it is common to see neuroglycopenia Food and Drug Administration (FDA) approved for the treat­ (glucose deficiency in the brain), coma and seizures, all asso­ ment of various endocrine related disease states such as ac­ ciated with low glucose levels. Additionally, counter­ romegaly and pancreatic tumors; however, it has not been regulatory hormone effects in response to the low glucose FDA approved as an antidote for sulfonylurea toxicity.13,14 may induce diaphoresis and tachycardia.3,7 An acute state Subcutaneous and intravenous routes of administration have may occur in as little as one to eight hours, where a chronic equivalent bioavailability with peak effects occurring after toxicity may be delayed over several days.3 Meglitinides will 30 minutes. Adult dosing of octreotide ranges from SO to present similarly to sulfonylureas, however, they are associ­ 100 mcg subcutaneously every six to 12 hours, while pediat­ ated with a quicker onset of action (30 minutes versus one to ric dosing requires 1 to 2 mcg/kg up to SO mcg every six to eight hours) in an acute situation.3 12 hours.13 Glucagon may also be used for the treatment of sulfonylurea overdose, as it will promote the breakdown of Patients with increased levels of thiazolidinediones will glycogen and synthesis of glucose to combat low glucose lev­ show no acute symptoms of toxicity, as they are dependent els.13 Glucagon, however, may also influence the release of on the presence of insulin to exert their effects. In a chronic insulin.13 Studies were not found to provide evidence of glu­ overdose, there would be an elevation of transaminases as cagon or octreotide as effective treatment options in megliti­ well as alkaline phosphatase levels, indicating hepatic toxic­ nide overdose. Activated charcoal will bind to meglitinide ity. Also associated with thiazolidinediones is an increased entities and is most effective early on in treatment.3 prothrombin time (PT) and international normalized ratio (INR), in addition to the expected hypoglycemic sequelae In the instance of lactic acidosis with excess biguanide such as bradycardia, coma and hypotension.3 ingestion, the primary goal in treating the patient is acid­ base restoration, which can be achieved with the use of so­ Biguanides are unique in that they have the potential to dium bicarbonate (1-2 mEq/kg). Activated charcoal may be cause lactic acidosis. It is common for patients with over­
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