California Poison Control System

San Diego, CA, United States

California Poison Control System

San Diego, CA, United States
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News Article | May 9, 2017

Expired EpiPens may still be usable more than four years after their expiry date. Findings of a new study that looked at the potency of auto-injectors after their expiry date suggest it may be worth using one that is past the expiration if it is all you have got. The new study shows that long after their supposed expiration dates, the injectors still have the concentration of epinephrine potent enough to prevent potentially deadly allergic reactions. Epinephrine, more commonly known as adrenaline, is an active ingredient used in auto-injectors to help relax muscles. The hormone can counteract the symptoms of anaphylaxis, a serious, life-threatening allergic reaction, by opening the airways to reduce breathing difficulties, and reducing the swelling of the blood vessels to address low blood pressure and ease faint feelings. EpiPen manufacturer Mylan advises patients to replace the device each year. EpiPens supposedly expire 18 months after the manufacturing date, but some pharmacists do not receive the devices until six months after these were manufactured, which means that patients only have less than a year left until the injector they purchased has to be replaced. Purchasing life-saving EpiPens can be financially burdensome for some families since the prices of the auto-injection devices have skyrocketed by 400 percent since 2007 and because more insurance providers no longer provide coverage of the EpiPen. Concerned over the costly prices of EpiPen, which makes the device prohibitive for many families, Lee Cantrell, from the California Poison Control System in San Diego, and colleagues conducted an analysis of expired EpiPens and EpiPen Juniors. Cantrell and colleagues found that while the auto-injectors lose their potency over time, the EpiPens still retained at least 90 percent of the stated concentration of epinephrine 29 months after the expiry date. The devices were likewise found to contain 84 percent of the concentrations of epinephrine 50 months, or more than four years, past the stamped expiration. Cantrell said that these concentrations are considered to be enough for preventing anaphylactic shock. "In every pen we tested there was enough to give what would be considered a therapeutic dose," Cantrell said, adding that if his child has a life-threatening reaction and he has no alternative, he will absolutely use these expired EpiPens without hesitation. "I don't think there's a physician in the world who would rebut that." Cantrell and colleagues reported their study in the Annals of Internal Medicine. In a statement, Mylan encouraged patients to refill their EpiPen auto-injector when they expire given the potentially fatal threats posed by anaphylaxis. The company said that the expiration date is the last day that the medication is considered as safe and effective. "All epinephrine products have expiration dating whether they come in an auto-injector or vial," Mylan said. "This is required by law. An expiration date is the final day, based on performed quality control tests, that a product has been determined to be safe and effective when stored under the conditions stated in the package insert." © 2017 Tech Times, All rights reserved. Do not reproduce without permission.

Cantrell F.L.,California Poison Control System | Cantrell F.L.,University of California at San Francisco | Ogera P.,County of San Diego Medical Examiners Office | Mallett P.,County of San Diego Medical Examiners Office | Mcintyre I.M.,County of San Diego Medical Examiners Office
Journal of Forensic Sciences | Year: 2014

Methylphenidate (MPD) is a widely prescribed stimulant used primarily for the treatment for attention-deficit/hyperactivity disorder (ADHD). Suicide attempts involving MPD ingestion have been well described; however, deaths attributed solely to MPD ingestion have not been reported. A 62-year-old woman was found dead on her floor. The only discrepancy in among her medication quantities was that >three hundred 10 mg MPD tablets were missing. Analysis utilizing gas chromatography-mass spectrometry revealed elevated postmortem MPD peripheral and central blood, liver and vitreous humor concentrations. Considering both the central blood to peripheral blood ratio (0.89) and the liver to peripheral blood ratio (3.3), MPD does not appear subject to significant postmortem redistribution. With no other identifiable cause of death, we report what appears to be the first isolated MPD ingestion associated with a fatality. © 2014 American Academy of Forensic Sciences.

Cantrell F.L.,California Poison Control System | Wardi G.,University of California at San Diego | O'Connell C.,University of California at San Diego
Pharmacotherapy | Year: 2016

Background: The use of propofol as treatment of toxin-induced seizures is unclear. The goal of this study was to characterize the use of propofol for toxin-related seizures as reported to a statewide poison system. Methods: This study was a retrospective review of the electronic records from a poison control system from 2009 to 2012. Inclusion criteria were patient age (≥ 18 yrs) and cases coded with “seizure” that contained the term “propofol.” The age, sex, reported toxin(s) involved, recurrence of seizure activity following/during propofol use, and mortality were extracted. Results: Records review identified 235 poisoning cases, all of which involved adjunctive therapy with propofol. The age range was 18–82 years (53% female). A total of 155 different toxins were identified. Recurrent seizures occurred in 15.7% (n=37) of cases following propofol administration. The mortality rate was 6.8% (n=16) in cases with known outcomes. Conclusions: Propofol is being used as an anticonvulsant in poisoned patients and appears to have some utility as an adjunct in terminating toxin-related seizures once airway control has been established. Less clear, however, is at what point propofol therapy should be initiated. Prospective controlled studies are warranted to identify the role of propofol in controlling toxin-induced seizures. © 2016 Pharmacotherapy Publications, Inc.

Thornton S.L.,University of Kansas | Pchelnikova J.L.,University of California at San Diego | Cantrell F.L.,California Poison Control System
Journal of Pediatrics | Year: 2016

Objective To characterize pediatric exposures to the antidementia drugs donepezil, memantine, rivastigmine, and galantamine by reviewing a poison control system's database. Study design A retrospective review of a statewide poison control system's database identified cases of pediatric (less than 19 years of age) exposures to antidementia drugs over an 11-year period. Data collected included age, sex, drug(s) involved, route of exposure, reason for exposure, symptoms, and interventions. Results There were 189 cases identified (53% male, median age: 2.3 years, 99% unintentional exposures). Donepezil was the most commonly reported exposure (106 cases), followed by memantine (57), galantamine (18), oral rivastigmine (16), and transdermal rivastigmine (3). Coingestants were reported in 68 (36%) cases. Symptoms were reported in 38 (20%) cases. Gastrointestinal symptoms were most common (n = 21) followed by central nervous system depression (n = 15). Oral rivastigmine was associated with higher rates of symptoms. No bradycardia, seizures, or fasciculations were reported. Eighty-nine cases (47%) were evaluated at a health care facility, and 13 (7%) were admitted to a hospital. Oral rivastigmine exposures were associated with increased rate of health care facility evaluation. Activated charcoal was administered in 28 cases. Atropine was given only once, for drooling. There were no serious outcomes or deaths in this series. Conclusions Reported pediatric exposures to antidementia drugs resulted in minimal morbidity and no mortality. Oral rivastigmine exposures were found to be associated with more symptoms and health care facility evaluations. © 2016 Elsevier Inc.

Cantrell F.L.,California Poison Control System | Cantrell F.L.,University of California at San Francisco
Journal of Community Health | Year: 2014

In 2007, a new source of nicotine exposure was introduced to the United States market, the electronic cigarette (ECIG) or "e-cigarette". Since then, the USA ECIG market has been doubling annually. Despite their widespread popularity, there is a paucity of existing data regarding ECIG toxicity. We report the experience of a statewide poison system. The database of a statewide poison system was queried for human ECIG exposures from 2010 (when Poisindex code first generated)through 2012. Year, age, manner and route of exposure, estimate exposure amount, product concentration, if evaluated at healthcare facility and symptoms were recorded. A total of 35 cases were identified - 4 in 2010, 12 in 2011, 19 in 2012. Age range 8 months-60 years. Reported symptoms were mild and transient. Five patient swere evaluated in an emergency department and none were admitted. Product concentrations ranged from 4 to 30 mg of nicotine per ml. Poison centers are likely to see an increase in exposures to ECIG given their growing popularity. Our modest results suggest that adverse effects and accidental exposures to ECIG cartridges are unlikely to result in serious toxicity. © 2013 Springer Science+Business Media New York.

Wu A.H.B.,University of California at San Francisco | Kearney T.,California Poison Control System
Journal of Forensic and Legal Medicine | Year: 2013

Background We examined forensic serum toxicology and pharmacogenomics data from a woman on codeine shortly before she caused a motor vehicle accident. Methods A woman driving erratically collided with a parked car of a highway seriously injuring 2 men working to repair the parked vehicle. The woman tested positive for codeine, acetaminophen and barbital. She had been taking these medications for 20 years due to migraine headache. Serum toxicology and genotype analysis for cytochrome P450, UDP glucuronosyltransferase, and other metabolizing enzymes were measured. Results The woman was tried and convicted of driving under the influence resulting in bodily harm and was sentenced to 6 years. Toxicology results on peripheral blood showed a total and free codeine of 840 and 348 μg/L, respectively, and total morphine of 20 μg/L (17, 3, and 0 μg/L for morphine-3-glucuronide, morphine-6-glucuronide, and free morphine, respectively). She was heterozygous for CYP 2D6*2/*4 (extensive/poor metabolism) and heterozygous for UGT 2B7*1/*2 (extensive/ultra-rapid metabolism). The woman was also taking fluoxetine and bupropion which are strong inhibitors of CYP 2D6. Conclusions Based on her genotype and phenotype and reports by the arresting officer, we suggest that the subject in question was not intoxicated by opiates at the time of her motor vehicle accident and may have been falsely incarcerated. © 2013 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

Zvosec D.L.,Hennepin County Medical Center | Zvosec D.L.,Minneapolis Medical Research Foundation | Smith S.W.,Hennepin County Medical Center | Smith S.W.,University of Minnesota | And 4 more authors.
American Journal of Emergency Medicine | Year: 2011

γ-Hydroxybutyrate (GHB) and its prodrugs are drugs of abuse that were also sold as "dietary supplements." Users present to emergency departments with overdose, impaired driving, withdrawal, and associated trauma. We compiled a series of GHB-associated deaths to elucidate lethal risks, GHB concentrations, cointoxicants, products, uses, and medical interventions. Death records were reviewed for toxicology, autopsy findings, and history. Inclusion cutoffs were as follows: 5/10 mg/L of GHB (antemortem blood/urine) and 50/20/7 mg/L of GHB (postmortem blood/urine/vitreous). Of 226 deaths included, 213 had cardiorespiratory arrest and 13 had fatal accidents. Seventy-eight deaths (35%) had no cointoxicants. Sixteen deaths involved "supplements" and 1 involved pharmaceutical GHB (Xyrem, Jazz Pharmaceuticals, Palo Alto, CA). Postmortem blood GHB was 18 to 4400 mg/L (median, 347 mg/L) in deaths negative for cointoxicants. Cardiorespiratory arrest occurred prehospital in 100% of 184 cases with available history. Of 72 cases with antemortem adverse effects reported, medical assistance was delayed or absent in 66; of these, acute GHB ingestion was known in 51, including 40 left to "sleep off" adverse effects. Thirty others were left "sleeping" and found dead. γ-Hydroxybutyrate is lethal even without cointoxicants, directly and through fatal accidents. Medical interventions were frequently delayed or absent despite known GHB ingestion, and witnessed adverse events and cardiorespiratory arrest occurred prehospital. Education is needed about the lethality of GHB and the necessity for prompt medical intervention. © 2011 Elsevier Inc. All rights reserved.

Vohra R.,View Medical | Seefeld A.,View Medical | Cantrell F.L.,California Poison Control System | Clark R.F.,University of California at San Diego
Journal of Emergency Medicine | Year: 2011

Background: Salvia divinorum, a hallucinogenic herb, has in recent years become popular among teenagers and young adults. Salvia is presently marketed as a "legal" alternative to other drugs of abuse, but little is known about the clinical toxicity of this substance. Objectives: The purpose of this study is to describe the clinical and demographic features of this emerging substance of recreational abuse using data obtained from the records of a poison control center. Methods: We performed retrospective review of exposures to the herbal hallucinogen Salvia divinorum as reported to the California Poison Control System (CPCS) over the last 10 years. Demographic and clinical data were collected and compiled from the computerized records of the CPCS for the search terms "salvia" and "sage." Results: There were 37 exposures to S. divinorum and 96 exposures to non-hallucinogenic Salvia species. Eighteen (49%) of the exposures were to S. divinorum alone. Intentional Salvia exposures resulted in a variety of neurologic, cardiovascular, and gastrointestinal effects. Notably, the use of concomitant substances of abuse was associated with a high rate of complications and psychomotor disturbances. Conclusions: Intentional use of S. divinorum, whether alone or in combination with alcoholic beverages and other drugs, causes neurologic, cardiovascular, and gastrointestinal effects. This poison-center-based review helps to characterize the clinical toxicity of S. divinorum, but more clinical and pharmacologic research is warranted for this rapidly emerging substance of abuse. © 2011 Elsevier Inc.

Cantrell F.L.,California Poison Control System | Cantrell F.L.,University of California at San Francisco | Mena O.,County of San Diego Medical Examiner's Office | Gary R.D.,County of San Diego Medical Examiner's Office | McIntyre I.M.,County of San Diego Medical Examiner's Office
International Journal of Legal Medicine | Year: 2015

Gabapentin (GBP) (Neurontin®, Horizant®, Gralise®) is a widely prescribed medication used primarily for the treatment of epilepsy and neuropathic pain. GBP has a favorable adverse effect profile in therapeutic dosing with the most common reported effects being dizziness, fatigue, drowsiness, weight gain, and peripheral edema. Even with intentional GBP self-poisonings, serious effects are rare. A 47-year-old female was found dead at work with her daughter’s bottle of GBP 600 mg. There were 26 tablets missing and the decedent’s only known medication was hydrocodone/acetaminophen. Following initial detection by an alkaline drug screen (GC-MS), analysis utilizing specific liquid chromatography–mass spectrometry revealed an elevated postmortem GBP peripheral blood concentration of 37 mg/L, central blood 32 mg/L, liver 26 mg/kg, vitreous 32 mg/L, and gastric contents 6 mg. Screening for volatiles, drugs of abuse, alkaline compounds, and acid/neutral compounds was negative with the exception of ibuprofen (<2 mg/L) detected in peripheral blood. This report presents a fatality that appears to be associated with an isolated and acute GBP ingestion. © 2015, Springer-Verlag Berlin Heidelberg.

News Article | October 26, 2016

Veterinarians know this opioid as a powerful elephant sedative. Security hawks know it too, thanks to its apparent use by the Russian government to put down a hostage crisis in 2002 (yes, really). But in the past year more U.S. doctors and paramedics are getting first-hand knowledge about the deadly effects of carfentanil from users who have overdosed on it. The drug is 10,000 times more potent than morphine and 100 times more powerful than fentanyl, the drug that pop star Prince overdosed on earlier this year. When carfentanil is used to cut other opioids such as heroin it can offer users a longer or more intense high—if they survive it. A recent wave of overdoses in states including Ohio and Kentucky has taught law enforcement officers and first responders that the medication used to reverse opioid overdoses—a powerful chemical called Narcan, or naxolone—often fails to rouse patients who have taken too much carfentanil. This is because the drug binds so tightly to the brain’s opioid receptors that naloxone, at currently common doses, is unable to dislodge that bond and reverse its sedating effects to get patients breathing again, says Michael Lynch, the medical director of the Pittsburgh Poison Center. As a result, hard-fought state efforts to make naloxone available over-the-counter to drug users or their friends or families—to quickly address overdoses and save lives—could be rendered useless in cases when heroin is cut with carfentanil. At standard doses of one or two milligrams, naloxone may not be powerful enough to counteract the drug. “It just takes micrograms of this stuff [carfentanil] to potentially cause an overdose,” Lynch says. Drug users who unwittingly use the substance (thinking they are consuming only heroin) may overdose and die before paramedics can arrive. “Too often drug users who overdose may be headed straight to the morgue, not the hospital,” agrees Hallam Gugelmann, an attending physician at California Pacific Medical Center–St. Luke’s Hospital Emergency Department in San Francisco. For now, even hard estimates about the scale of carfentanil use remain elusive: There are no standard, hospital-level lab tests that can quickly identify the drug. Pricey private lab testing remains out of reach for most patients and hospitals. So for now most clinicians proceed with their best guesses about when a patient has used carfentanil versus other opioids. Gugelmann says he recently treated a woman in her 80s who had quickly used all her prescription morphine for her leg pain and had resorted to taking a drug a family member had illegally purchased for her. The family thought it was morphine because it looked like her prescription medication, but minutes after she took the drug they knew something was wrong. It was likely laced with carfentanil, Gugelmann says, adding that the woman quickly stopped breathing and remained unresponsive after emergency responders applied their standard dose of naloxone. Even a second dose only barely—and temporarily—got her breathing again with help from an air mask. At the hospital she had to receive more naloxone intravenously, and the incident led to a 10-day hospital stay. The doctor says he sees at least 20 similar cases each month, roughly two patients per shift. Yet he cannot even be sure they had used carfentanil. He assumes that they were exposed to it, or to a different fentanyl-related drug, because they were not revived by naloxone. The U.S. Drug Enforcement Administration also lacks national or state tallies on carfentanil use and deaths, the agency told Scientific American. So far, however, limited data from medical examiner's and coroner’s offices indicate that Ohio is the hardest-hit state. Others are also bracing for carfentanil problems, according to the DEA. Several states—West Virginia, Georgia, Rhode Island, Florida and Michigan among them—have recently asked the DEA for carfentanil samples for comparison testing to confirm other suspected cases, the agency said. Last month the DEA issued a nationwide warning to the public and law enforcement agencies about the opioid. Medical personnel may have to administer multiple doses of naloxone if someone has used carfentanil, the agency instructed. “Continue to administer a dose of naloxone every 2-3 minutes until the individual is breathing on his/her own for at least 15 minutes or until EMS arrives,” it said. That means a single patient might get five or seven doses of the life-saving chemical—and that is before the patient gets to the hospital and likely receives even more. Heavy naloxone use could quickly take a toll on local and national supplies—and prices—says Gugelmann, who is also the assistant medical director for the San Francisco Division of the California Poison Control System. At his hospital, he says, staff have had some close calls in the middle of the night when they ran out of the substance and had to call in emergency shipments from a different hospital. “Obviously,” he says, “this carfentanil situation is extremely concerning.”

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