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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTAwOTk4Ny1vdmVydmlldw==\nDrugs & Diseases > Emergency Medicine\nSalicylate Toxicity\nAuthor: Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA; Chief Editor: Timothy E Corden, MD more...\nSections Salicylate Toxicity\nToxicity Versus Serum Level\nBedside Ferric Chloride Testing\nTriage Care\nEmergency Department Management\nAntidotes, Other\nLaxatives, Osmotic\nUrinary Alkalinizing Agents\nSalicylates are ubiquitous agents found in hundreds of over-the-counter (OTC) medications and in numerous prescription drugs, making salicylate toxicity an important cause of morbidity and mortality. [1, 2, 3, 4]\nSalicylates are used as analgesic agents for the treatment of mild to moderate pain. Aspirin is used as an antipyretic and as an anti-inflammatory agent for the treatment of soft tissue and joint inflammation and vasculitides such as acute rheumatic fever and Kawasaki disease. Aspirin is also used to treat acute coronary syndrome. Low-dose aspirin helps to prevent thrombosis.\nAcetylsalicylic acid is colorless or white in crystalline, powder, or granular form. The chemical is odorless and is soluble in water. Salicylate is available for ingestion as tablets, capsules, and liquids. Salicylate is also available for topical application, in creams or lotions.\nSalicylate ingestion continues to be a common cause of poisoning in children and adolescents. The prevalence of aspirin-containing analgesic products makes these agents, found in virtually every household, common sources of unintentional and suicidal ingestion.\nHowever, the incidence of salicylate poisoning in children has declined because of reliance on alternative analgesics and the use of child-resistant containers. Repackaging has decreased children's accessibility to lethal amounts, and salicylate's association with Reye syndrome has significantly decreased its use.\nStill, more than 10,000 tons of aspirin are consumed in the United States each year. Aspirin or aspirin-equivalent preparations (in milligrams) include children's aspirin (80-mg tablets with 36 tablets per bottle), adult aspirin (325-mg tablets), methyl salicylate (eg, oil of wintergreen; 98% salicylate), and Pepto-Bismol (236 mg of non-aspirin salicylate per 15 mL).\nIngestion of topical products containing salicylates (eg, Ben-Gay, salicylic acid [keratolytic], oil of wintergreen or methyl salicylate), can cause severe salicylate toxicity. According to published sources, one teaspoon of 98% methyl salicylate contains as much as 7000 mg of salicylate, the equivalent of nearly 90 baby aspirins and more than 4 times the potentially toxic dose for a child who weighs 10 kg. [5, 6]\nSalicylate toxicity has been reported with the topical use of salicylate-containing teething gels in infants. [7] On the basis of a literature review, Greene et al estimated the allowable daily intake of methyl salicylate to be 11 mg/kg/d. [8]\nIngestion of topical products containing salicylates, such as Ben-Gay, salicylic acid (keratolytic), and oil of wintergreen or methyl salicylate, can cause severe salicylate toxicity. One teaspoon of 98% methyl salicylate contains 7000 mg of salicylate, the equivalent of nearly 90 baby aspirins and more than 4 times the potentially toxic dose for a child who weighs 10 kg. Salicylate toxicity has been reported with the topical use of salicylate-containing teething gels in infants. [7] On the basis of a literature review, Greene et al estimated the allowable daily intake of methyl salicylate to be 11 mg/kg/d. [8]\nA comprehensive review of the existing medical literature on methyl salicylate poisoning has determined that it is a relatively common source of pediatric exposures. [9] In younger children, most of these exposures are accidental. Intentional ingestions are much more common in adolescents.\nThe prevalence of alternative medicines and the popularity of herbs and traditional medicine formulae are increasing in North America. Many of these medicines may contain salicylate. Therefore, consider salicylate poisoning when topical herbal medicinal oil is involved.\nPercy Medicine contains bismuth subsalicylate as the active ingredient and is used as a constipation reliever. A case of neonatal salicylate poisoning due to administration of this medicine as a colic reliever has been reported. [10] Percy Medicine is available OTC, and parents should be educated that salicylate-containing products are not routinely recommended for children aged 1 year or younger.\nAlthough concentrations of salicylate persist following ingestion of aspirin tablets, it has been shown that the majority of salicylate concentrations declined following ingestion of salicylate as acetylsalicylic powder. In one study, salicylate concentrations increased or changed insignificantly in 50% of patients who ingested tablets, but following powder ingestions, concentrations declined in 94% of cases. [11]\nPhases and symptoms of salicylate toxicity\nThe acid-base, fluid, and electrolyte abnormalities seen with salicylate toxicity can be grouped into phases. (See Presentation and Workup.)\nPhase 1 of the toxicity is characterized by hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaluria. Potassium and sodium bicarbonate are excreted in the urine. This phase may last as long as 12 hours.\nIn phase 2, paradoxical aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys. This phase may begin within hours and may last 12-24 hours.\nPhase 3 includes dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4-6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.\nNausea, vomiting, diaphoresis, and tinnitus [12] are the earliest signs and symptoms of salicylate toxicity. Other early symptoms and signs are vertigo, hyperventilation, tachycardia, and hyperactivity. As toxicity progresses, agitation, delirium, hallucinations, convulsions, lethargy, and stupor may occur. Hyperthermia is an indication of severe toxicity, especially in young children.\nA high index of suspicion of salicylate toxicity is necessary, with prompt recognition of clinical signs and symptoms of salicylate poisoning, such as tinnitus, hyperventilation, tachycardia, and metabolic acidosis. [3] Early treatment can prevent organ damage and death. Treatments include stabilizing the ABCs as necessary, limiting absorption, enhancing elimination, correcting metabolic abnormalities, and providing supportive care. No specific antidote is available for salicylates.\nAfter ingestion, acetylsalicylic acid is rapidly converted to salicylic acid, its active moiety. Salicylic acid is readily absorbed in the stomach and small bowel. At therapeutic doses, salicylic acid is metabolized by the liver and eliminated in 2-3 hours. Salicylate poisoning is manifested clinically by disturbances of several organ systems, including the central nervous system (CNS) and the cardiovascular, pulmonary, hepatic, renal, and metabolic systems. Salicylates directly or indirectly affect most organ systems in the body by uncoupling oxidative phosphorylation, inhibiting Krebs cycle enzymes, and inhibiting amino acid synthesis.\nAcid-base status\nThe toxic effects of salicylates are complex. Respiratory centers are directly stimulated, causing a primary respiratory alkalosis. Salicylates also cause an inhibition of the citric acid cycle and an uncoupling of oxidative phosphorylation and may produce renal insufficiency that causes accumulation of phosphoric and sulfuric acids. The metabolism of fatty acids is likewise increased in patients with salicylate toxicity, generating ketone body formation. These processes all contribute to the development of an elevated anion-gap metabolic acidosis in patients with salicylate poisoning. This combination of a primary respiratory alkalosis and a primary metabolic acidosis is characteristic of salicylate poisoning, especially in adults, and should make the clinician suspect the diagnosis when it is present.\nCatabolism occurs secondary to the inhibition of adenosine triphosphate (ATP) ̶ dependent reactions with the following results:\nIncreased oxygen consumption\nIncreased carbon dioxide production\nAccelerated activity of the glycolytic and lipolytic pathways\nDepletion of hepatic glycogen\nHyperpyrexia\nAdult patients with acute poisoning usually present with a mixed respiratory alkalosis and metabolic acidosis. However, respiratory alkalosis may be transient in children such that metabolic acidosis may occur early in the course. Some patients with mixed acid-base disturbances have been found to have normal anion-gap metabolic acidosis; therefore, normal anion-gap acidosis does not exclude salicylate toxicity.\nRespiratory system effects\nSalicylates cause direct and indirect stimulation of respiration. A salicylate level of 35 mg/dL or higher causes increases in rate (tachypnea) and depth (hyperpnea) of respiration. Salicylate poisoning may rarely cause noncardiogenic pulmonary edema (NCPE) and acute lung injury in pediatric patients. It is more common in elderly patients with chronic salicylate toxicity. Although the exact etiology is not known, it causes severe hypoxia, necessitating treatment with high concentrations of oxygen. It also makes adequate hydration and sufficient administration of sodium bicarbonate difficult. Pulmonary edema has extremely high mortality in both children and adults; if present, hemodialysis should be considered as soon as possible.\nIncreased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, although the serum glucose levels may sometimes be within the normal range. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose and symptoms of CNS hypoglycemia (eg, altered mental status) may occur even when blood glucose levels are within the reference range.\nFluid and electrolyte effects\nSalicylate poisoning may result in dehydration because of increased gastrointestinal (GI) tract losses (vomiting) and insensible fluid losses (hyperpnea and hyperthermia). All patients with serious poisoning are more than 5-10% dehydrated. Renal clearance of salicylate is decreased by dehydration. Hypokalemia and hypocalcemia can occur as a result of primary respiratory alkalosis.\nCNS effects\nSalicylates are neurotoxic; this initially manifests as tinnitus. Significant ingestion can lead to hearing loss at serum levels of 30-45 mg/dL or higher. CNS toxicity is related to the amount of drug bound to CNS tissue. It is more common with chronic than acute toxicity. Acidosis worsens CNS toxicity by increasing the amount of salicylate that crosses the blood-brain barrier and increases CNS tissue levels. Other signs and symptoms of CNS toxicity include nausea, vomiting, hyperpnea, and lethargy. Severe toxicity can progress to disorientation, seizures, cerebral edema, hyperthermia, coma, cardiorespiratory depression, and, eventually, death.\nIn one case report of fatal acute acetylsalicylate toxicity in a 34-year-old oligophrenic woman, brain histopathology revealed acute white matter damage, with myelin disintegration and caspase-3 activation in glial cells. Only sparse changes in grey matter were noted. [13]\nGI tract effects\nNausea and vomiting are the most common toxic effects. This can be caused by CNS toxicity or by direct damage to the gastric mucosa. Salicylates can disrupt the mucosal barrier and occasionally cause GI bleeding. Pylorospasm, decreased GI tract motility, and bezoar formation can occur with large doses. These slow elimination and cause greater amounts of salicylates to be absorbed from the GI tract.\nHepatic effects\nHepatitis can occur in children ingesting doses at or above 30.9 mg/dL. [14] Reye syndrome is another form of pediatric salicylate-induced hepatic disease. It is characterized by nausea, vomiting, hypoglycemia, elevated levels of liver enzymes and ammonia, fatty infiltration of the liver, increased intracranial pressure, and coma.\nHypoprothrombinemia and platelet dysfunction are the most common effects. Bleeding may also be promoted either by inhibition of vitamin K–dependent enzymes or by the formation of thromboxane A2.\nMusculoskeletal effects\nRhabdomyolysis can occur because of dissipation of heat and energy, resulting from oxidative phosphorylation uncoupling.\nOccurrence in the United States\nAccording to the American Association of Poison Control Centers' National Poison Data System, 10, single exposures to acetylsalicylic acid, alone or in combination with other drugs, were reported in 2017, along with 5875 single exposures to methyl salicylate. About 4500 of these exposures were intentional. Over 200 exposures resulted in major outcomes, and 23 fatal cases were noted. [1]\nAge-related demographics\nGenerally, the degree of the toxicity is more severe in elderly individuals and infants, as well as in persons with coexisting morbidity or chronic intoxication.\nAcid-base disturbances vary with age and severity of the intoxication. Infants rarely present with pure respiratory alkalosis. Respiratory alkalosis may not develop in an infant or it may be short-lived. The most common presentation for a child is metabolic acidosis.\nFactors contributing to a decline in the incidence of pediatric salicylate intoxication include increased acetaminophen and ibuprofen use and child-resistant packaging.\nA 16% morbidity rate and a 1% mortality rate are associated with patients presenting with an acute salicylate overdose. The incidence of morbidity and mortality for a patient with chronic intoxication is 30% and 25%, respectively.\nAccording to the Toxic Exposures Survey from the American Association of Poison Control Centers, 24% of analgesic-related deaths are due to aspirin alone or aspirin in combination with other drugs. Early identification of salicylate poisoning and the expeditious institution of appropriate treatment can be lifesaving.\nCategories of toxicity\nThe following 4 categories are helpful for assessing the potential severity and morbidity of an acute, single-event, non–enteric-coated salicylate ingestion:\nLess than 150 mg/kg ingested - Spectrum ranges from no toxicity to mild toxicity\nFrom 150-300 mg/kg ingested - Mild-to-moderate toxicity\nFrom 301-500 mg/kg ingested - Serious toxicity\nGreater than 500 mg/kg ingested - Potentially lethal toxicity\nAdvise patients and their families that use or overuse of seemingly benign OTC medications is sometimes dangerous. The ready availability of aspirin and aspirin-containing products does not establish the safety of aspirin.\nFor patient education information, see the First Aid and Injuries Center, as well as Aspirin Poisoning, Drug Overdose, Activated Charcoal, and Poison Proofing Your Home.\nGummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report. Clin Toxicol (Phila). 2018 Dec. 56 (12):1213-1415. [Medline]. [Full Text].\nMadan RK, Levitt J. A review of toxicity from topical salicylic acid preparations. J Am Acad Dermatol. 2014 Apr. 70 (4):788-92. [Medline].\nPearlman BL, Gambhir R. Salicylate intoxication: a clinical review. Postgrad Med. 2009 Jul. 121(4):162-8. [Medline].\nMund ME, Gyo C, Brüggmann D, Quarcoo D, Groneberg DA. Acetylsalicylic acid as a potential pediatric health hazard: legislative aspects concerning accidental intoxications in the European Union. J Occup Med Toxicol. 2016. 11:32. [Medline].\nTidy C. Salicylate Poisoning. Patient.info. Available at https://patient.info/doctor/salicylate-poisoning. 22 May 2014; Accessed: February 25, 2019.\nEllenhorn MJ, Barceloux DG. Medical Toxicology: Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc; 1988. 562.\nWilliams GD, Kirk EP, Wilson CJ, Meadows CA, Chan BS. Salicylate intoxication from teething gel in infancy. Med J Aust. 2011 Feb 7. 194(3):146-8. [Medline].\nGreene T, Rogers S, Franzen A, Gentry R. A critical review of the literature to conduct a toxicity assessment for oral exposure to methyl salicylate. Crit Rev Toxicol. 2016 Nov 11. 1-23. [Medline].\nDavis JE. Are one or two dangerous? Methyl salicylate exposure in toddlers. J Emerg Med. 2007 Jan. 32(1):63-9. [Medline].\nLewis TV, Badillo R, Schaeffer S, Hagemann TM, McGoodwin L. Salicylate toxicity associated with administration of Percy medicine in an infant. Pharmacotherapy. 2006 Mar. 26(3):403-9. [Medline].\nRose SR, Cumpston KL, Kim J, Difranco D, Wills BK. Absorption of salicylate powders versus tablets following overdose: a poison center observational study. Clin Toxicol (Phila). 2016 Jul 6. 1-5. [Medline].\nStolzberg D, Salvi RJ, Allman BL. Salicylate toxicity model of tinnitus. Front Syst Neurosci. 2012. 6:28. [Medline]. [Full Text].\nRauschka H, Aboul-Enein F, Bauer J, Nobis H, Lassmann H, Schmidbauer M. Acute cerebral white matter damage in lethal salicylate intoxication. Neurotoxicology. 2007 Jan. 28(1):33-7. [Medline].\nHamdan JA, Manasra K, Ahmed M. Salicylate-induced hepatitis in rheumatic fever. Am J Dis Child. 1985 May. 139(5):453-5. [Medline].\nChen GD, Stolzberg D, Lobarinas E, Sun W, Ding D, Salvi R. Salicylate-induced cochlear impairments, cortical hyperactivity and re-tuning, and tinnitus. Hear Res. 2013 Jan. 295:100-13. [Medline].\nWaasdorp Hurtado CE, Kramer RE. Salicylic acid ingestion leading to esophageal stricture. Pediatr Emerg Care. 2010 Feb. 26(2):146-8. [Medline].\nHaslinger V, Dietz W, Bartsch M, Simma B. Salicylate intoxication with symptoms of septicaemia in a 17-month-old girl. Klin Padiatr. 2011 Dec. 223(7):436-7. [Medline].\nRumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975 Jun. 55(6):871-6. [Medline].\nKuzak N, Brubacher JR, Kennedy JR. Reversal of salicylate-induced euglycemic delirium with dextrose. Clin Toxicol (Phila). 2007 Jun-Aug. 45(5):526-9. [Medline].\nBeauchamp GA, Hendrickson RG. Delayed Salicylate Toxicity in a 17-Year-Old Girl With Initially Undetectable Salicylate Concentration 3.9 Hours After Ingestion. Pediatr Emerg Care. 2016 Sep 30. [Medline].\n[Guideline] Chyka PA, Erdman AR, Christianson G, Wax PM, Booze LL, Manoguerra AS, et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007. 45(2):95-131. [Medline].\nMcCabe DJ, Lu JJ. The association of hemodialysis and survival in intubated salicylate-poisoned patients. Am J Emerg Med. 2017 Jun. 35 (6):899-903. [Medline].\nKirshenbaum LA, Mathews SC, Sitar DS, Tenenbein M. Does multiple-dose charcoal therapy enhance salicylate excretion?. Arch Intern Med. 1990 Jun. 150(6):1281-3. [Medline].\nKirshenbaum LA, Mathews SC, Sitar DS, Tenenbein M. Whole-bowel irrigation versus activated charcoal in sorbitol for the ingestion of modified-release pharmaceuticals. Clin Pharmacol Ther. 1989 Sep. 46(3):264-71. [Medline].\nThanacoody R, Caravati EM, Troutman B, Höjer J, Benson B, Hoppu K, et al. Position paper update: whole bowel irrigation for gastrointestinal decontamination of overdose patients. Clin Toxicol (Phila). 2015 Jan. 53 (1):5-12. [Medline].\nProudfoot AT, Krenzelok EP, Brent J, Vale JA. Does urine alkalinization increase salicylate elimination? If so, why?. Toxicol Rev. 2003. 22(3):129-36. [Medline].\nOng GY. A simple modified bicarbonate regimen for urine alkalinization in moderate pediatric salicylate poisoning in the emergency department. Pediatr Emerg Care. 2011 Apr. 27(4):306-8. [Medline].\nJuurlink DN, Gosselin S, Kielstein JT, Ghannoum M, Lavergne V, Nolin TD, et al. Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup. Ann Emerg Med. 2015 Aug. 66 (2):165-81. [Medline].\nPapacostas MF, Hoge M, Baum M, Davila SZ. Use of continuous renal replacement therapy in salicylate toxicity: A case report and review of the literature. Heart Lung. 2016 Sep-Oct. 45 (5):460-3. [Medline].\nHerres J, Ryan D, Salzman M. Delayed salicylate toxicity with undetectable initial levels after large-dose aspirin ingestion. Am J Emerg Med. 2009 Nov. 27(9):1173.e1-3. [Medline].\nChyka PA, Erdman AR, Christianson G, et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007. 45(2):95-131. [Medline].\nMuhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA Professor of Emergency Medicine in Clinical Pediatrics, Weill Cornell Medical College; Attending Physician, Departments of Emergency Medicine and Pediatrics, Lincoln Medical and Mental Health Center; Adjunct Professor of Emergency Medicine, Adjunct Professor of Pediatrics, St George's University School of Medicine, Grenada\nMuhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Academy of Urgent Care Medicine, American College of Emergency Physicians, American Heart Association, American Medical Association, Association of Clinical Research Professionals, Public Responsibility in Medicine and Research, Society for Academic Emergency Medicine, Society for Simulation in Healthcare\nMuhammad Aslam, MD Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center\nMuhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics\nJoel R Gernsheimer, MD, FACEP Visiting Associate Professor, Department of Emergency Medicine, Attending Physician and Director of Geriatric Emergency Medicine, State University of New York Downstate Medical Center\nJoel R Gernsheimer, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Geriatrics Society\nTimothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin\nTimothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society\nFred Harchelroad, MD, FACMT, FAAEM, FACEP Chair, Department of Emergency Medicine, Director of Medical Toxicology, Allegheny General Hospital; Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine\nLance W Kreplick, MD, FAAEM, MMM Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC\nLance W Kreplick, MD, FAAEM, MMM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives\nMichael E Mullins, MD Assistant Professor, Division of Emergency Medicine, Washington University in St Louis School of Medicine; Attending Physician, Emergency Department, Barnes-Jewish Hospital\nMichael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians\nDisclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None\nMark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group\nMark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association\nAsim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital\nJeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center\nDisclosure: Merck Salary Employment\nJohn T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals\nJohn T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists\nencoded search term (Salicylate Toxicity) and Salicylate Toxicity\nSeafood Toxicity\nBotulinum Toxin in Pain Management\nBotulinum Toxin Injections in Plastic Surgery\nPathophysiology and Etiology of Lead Toxicity\nBotulinum Toxin for Laryngeal Dystonia\nLocal Anesthetic Toxicity\nDietary Supplement Causes Widespread Selenium Poisoning\nManagement of Tourette's Syndrome Reviewed\nAtopic Dermatitis: Five Promising Targeted Therapies\n'Tis the Season for Gout\nAccording to Pharmacist s\nTestosterone Replacement Therapy: Controversy and Recent Trends\nOTC Medication Use in Pregnancy and Breastfeeding\nProspective Health Professions Students' Misperceptions About Pharmacists\nPharmacy Education Needs to Address Diagnostic Safety\nFast Five Quiz: Generic Medications\nDiseases & Conditions Seafood Toxicity\nDiseases & Conditions Ethylene Glycol Toxicity\nProcedures Botulinum Toxin\nProcedures Botulinum Toxin in Pain Management"