TOXICOLOGY Poisoning May Be
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Drug-Induced Angle-Closure Glaucoma
10.5005/jp-journals-10008-1100 ArujREVIEW K Khurana ARTICLE et al Drug-induced Angle-Closure Glaucoma Aruj K Khurana, Bhawna Khurana, Ashok K Khurana Regional Institute of Ophthalmology, Post Graduate Institute of Medical Sciences, Rohtak, Haryana, India Correspondence: Ashok K Khurana, Senior Professor, Regional Institute of Ophthalmology, Post Graduate Institute of Medical Sciences, Rohtak, Haryana, India ABSTRACT Drug-induced angle-closure glaucoma is an important entity for the ophthalmologist as well as the general physician as it represents a preventable cause of potential blindness. This brief review highlights the fact that a high index of suspicion, in a susceptible individual followed by confirmation on appropriate imaging modality (UBM, ultrasound or anterior segment OCT) can alleviate the threat to sight and also help to institute appropriate therapy. Keywords: Acute angle closure, Drug-induced glaucoma. INTRODUCTION factors exist for this syndrome.9 Other sulfa-based drugs known Drug-induced angle-closure glaucoma is an important entity to be associated with AACG: Acetazolamide, hydrochloro- 10 for the ophthalmologist as well as the general physician as it thiazide and cotrimoxazole. represents a preventable cause of potential blindness.1 Acute Anticholinergic drugs implicated in the causation of AACG angle-closure glaucoma can develop in a susceptible individual include atropine, homatropine, cyclopentolate and ipratropium by various classes of drugs.2 Practitioners using any of these bromide.10,11 Atropine is often used to treat bradycardia, drugs should be aware of their potential to cause acute angle especially related to general anesthesia. Postoperative AACG closure, such that a patient presenting with signs or symptoms has been reported in patients after general anesthesia for of acute angle closure should be immediately referred to an abdominal, orthopedic, facial and endoscopic surgery.12 3 ophthalmologist. -
Methamphetamine Presentations to an Emergency Department: Management and Complications
Isoardi Katherine (Orcid ID: 0000-0002-1176-7923) Abstract Objective: There is little recent published data characterising methamphetamine intoxication. This study aims to describe the clinical effects, management, complications and disposition of patients with methamphetamine exposure. Methods: This is a retrospective review of patients presenting with methamphetamine intoxication to an Emergency Department in 2016. All presentations were extracted from a relational database and each medical record reviewed. Demographics, clinical features, complications and disposition were extracted. Results: There were 378 presentations of 329 patients (234 males [71%]), median age 31 years (range 16-68 years). The commonest clinical effect was acute behavioural disturbance, occurring in 295 (78%) presentations. This was successfully managed with oral sedation alone in 180 (61%) patients with the remainder receiving parenteral sedation. Other effects included tachycardia in 212 (56%), hypertension in 160 (42%) and hyperthermia in 17 (4%) presentations. No antihypertensives were given. One patient was actively cooled. Complications included 21 (30%) presentations with rhabdomyolysis and 43 (11%) presentations with acute kidney injury. There were two seizures, three intracranial bleeds and one myocardial infarction. The majority of This is the author manuscript accepted for publication and has undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/1742-6723.13219 This article is protected by copyright. All rights reserved. patients (310 [82%]) were managed solely within the emergency department. The median length of stay was 14 hours. There were 41(11%) mental health admissions. -
Unintentional Fentanyl Overdoses Among Persons Who Thought They
Morbidity and Mortality Weekly Report Notes from the Field Unintentional Fentanyl Overdoses Among emergency departments; 2) holding a multiagency press Persons Who Thought They Were Snorting conference; 3) conducting media interviews; 4) informing Cocaine — Fresno, California, January 7, 2019 law enforcement, prehospital providers, and the public about Patil Armenian, MD1; Jeffrey D. Whitman, MD2; Adina Badea, PhD2; naloxone distribution and use; 5) educating persons on Whitney Johnson, MD1; Chelsea Drake, MS1; Simranjit Singh Dhillon3; the proper disposal of old or new but unused medications Michelle Rivera3; Nicklaus Brandehoff, MD1; Kara L. Lynch, PhD2 through the Fresno County Department of Behavioral Health/ California Health Collaborative drop-off containers§; and On January 7, 2019, three patients arrived at the Community 6) publicizing the California Central Valley Opioid Safety Regional Medical Center emergency department in Fresno, Coalition webpage,¶ which provides information about California, after snorting (i.e., nasally insufflating) white pow- naloxone and substance use disorders. der they thought was cocaine. One (patient A) was in cardiac On January 12, 2019, a similar drug overdose incident was arrest, and two (patients B and C) had opioid toxidrome reported in Chico, California, in which postmortem toxicol- (miosis, respiratory depression, and depressed mental status) ogy testing for one person confirmed fentanyl (1). Fourteen (Table). After spontaneous circulation was reestablished in other persons at the same event were hospitalized with opioid patient A, he was admitted to the intensive care unit, where toxidrome and later released. They reported thinking they he was pronounced brain-dead 3 days later. Patients B and C were snorting cocaine,** but confirmatory toxicology results responded to naloxone, but repeated dosing was required to are unavailable. -
Non-Steroidal Drug-Induced Glaucoma MR Razeghinejad Et Al 972
Eye (2011) 25, 971–980 & 2011 Macmillan Publishers Limited All rights reserved 0950-222X/11 www.nature.com/eye 1,2 1 1 Non-steroidal drug- MR Razeghinejad , MJ Pro and LJ Katz REVIEW induced glaucoma Abstract vision. The majority of drugs listed as contraindicated in glaucoma are concerned with Numerous systemically used drugs are CAG. These medications may incite an attack in involved in drug-induced glaucoma. Most those individuals with narrow iridocorneal reported cases of non-steroidal drug-induced angle.3 At least one-third of acute closed-angle glaucoma are closed-angle glaucoma (CAG). glaucoma (ACAG) cases are related to an Indeed, many routinely used drugs that have over-the-counter or prescription drug.1 Prevalence sympathomimetic or parasympatholytic of narrow angles in whites from the Framingham properties can cause pupillary block CAG in study was 3.8%. Narrow angles are more individuals with narrow iridocorneal angle. The resulting acute glaucoma occurs much common in the Asian population. A study of a more commonly unilaterally and only rarely Vietnamese population estimated a prevalence 4 bilaterally. CAG secondary to sulfa drugs is a of occludable angles at 8.5%. The reported bilateral non-pupillary block type and is due prevalence of elevated IOP months to years to forward movement of iris–lens diaphragm, after controlling ACAG with laser iridotomy 5,6 which occurs in individuals with narrow or ranges from 24 to 72%. Additionally, a open iridocorneal angle. A few agents, significant decrease in retinal nerve fiber layer including antineoplastics, may induce thickness and an increase in the cup/disc ratio open-angle glaucoma. -
Approach to the Poisoned Patient
PED-1407 Chocolate to Crystal Methamphetamine to the Cinnamon Challenge - Emergency Approach to the Intoxicated Child BLS 08 / ALS 75 / 1.5 CEU Target Audience: All Pediatric and adolescent ingestions are common reasons for 911 dispatches and emergency department visits. With greater availability of medications and drugs, healthcare professionals need to stay sharp on current trends in medical toxicology. This lecture examines mind altering substances, initial prehospital approach to toxicology and stabilization for transport, poison control center resources, and ultimate emergency department and intensive care management. Pediatric Toxicology Dr. James Burhop Pediatric Emergency Medicine Children’s Hospital of the Kings Daughters Objectives • Epidemiology • History of Poisoning • Review initial assessment of the child with a possible ingestion • General management principles for toxic exposures • Case Based (12 common pediatric cases) • Emerging drugs of abuse • Cathinones, Synthetics, Salvia, Maxy/MCAT, 25I, Kratom Epidemiology • 55 Poison Centers serving 295 million people • 2.3 million exposures in 2011 – 39% are children younger than 3 years – 52% in children younger than 6 years • 1-800-222-1222 2011 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System Introduction • 95% decline in the number of pediatric poisoning deaths since 1960 – child resistant packaging – heightened parental awareness – more sophisticated interventions – poison control centers Epidemiology • Unintentional (1-2 -
Pre-Hospital Use and Administration of Naloxone
Opioid Toxicity and Naloxone: Implications for the K-12 Population Elizabeth J. Scharman, Pharm.D., DABAT, FAACT, BCPS Director, West Virginia Poison Center Professor, WVU School of Pharmacy Outline • Definitions • Patterns of opioid exposure grades K-12 • Opioid Toxicology I. Opioid toxidrome II. Pharmacologic differences: effect on toxicity III. Designer opioids: what this means for WV • Naloxone I. Mechanism details II. Potential adverse effects III. Meaning of “response” to naloxone Definitions • Opioid – A drug that works by binding to the opioid receptors • Opioid receptors are where the body’s “natural” painkillers (endorphins for example) attach to decrease the perception of pain – Examples: morphine, hydrocodone, heroin, oxycodone • Naloxone – Opioid antidote • Competitively takes the place of the opioid on the opioid receptor 1 Young Opioid Abusers • Survey of 50 injection drug users 16-25 years – Hydrocodone/acetaminophen, oxycodone, oxycodone/acetaminophen most common initial opioid drugs misused • Average age first use = 14.5 years • Obtained from family member, their own Rx, friend/contact • Oral = 41, Sniffing/snorting = 8, Injecting = 1 – Followed initial use of alcohol (avg 12.8 years of age), marijuana (avg 12.5 years of age), Rx stimulants (avg 14.1 years of age) • Opioid misuse prior to heroin (n = 43) – Average age of first use = 16.1 years WV Poison Center Data 2014 2015 ≤ 5 years 6 – 19 years ≤ 5 years 6 – 19 years Heroin 1201 Single Opioid 59 30 64 21 Comb. Opioid 18 41 21 27 Acetaminophen 83 88 Non-steroidal 120 -
The Anticholinergic Toxidrome
Poison HOTLINE Partnership between Iowa Health System and University of Iowa Hospitals and Clinics July 2011 The Anticholinergic Toxidrome A toxidrome is a group of symptoms associated with poisoning by a particular class of agents. One example is the opiate toxidrome, the triad of CNS depression, respiratory depression, and pinpoint pupils, and which usually responds to naloxone. The anticholinergic toxidrome is most frequently associated with overdoses of diphenhydramine, a very common OTC medication. However, many drugs and plants can produce the anticholinergic toxidrome. A partial list includes: tricyclic antidepressants (amitriptyline), older antihistamines (chlorpheniramine), Did you know …… phenothiazines (promethazine) and plants containing the anticholinergic alkaloids atropine, hyoscyamine and scopolamine (Jimson Weed). Each summer, the ISPCC receives approximately 10-20 The mnemonic used to help remember the symptoms and signs of this snake bite calls, some being toxidrome are derived from the Alice in Wonderland story: from poisonous snakes (both Blind as a Bat (mydriasis and inability to focus on near objects) local and exotic). Red as a Beet (flushed skin color) Four poisonous snakes can be Hot as Hades (elevated temperature) found in Iowa: the prairie These patients can sometimes die of agitation-induced hyperthermia. rattlesnake, the massasauga, Dry as a Bone (dry mouth and dry skin) the copperhead, and the Mad as a Hatter (hallucinations and delirium) timber rattlesnake. Each Bowel and bladder lose their tone (urinary retention and constipation) snake has specific territories Heart races on alone (tachycardia) within the state. ISPCC A patient who has ingested only an anticholinergic substance and is not specialists have access to tachycardic argues against a serious anticholinergic overdose. -
Anticholinergic Drugs and Dementia
DEMENTIA Q&A 24 Anticholinergic drugs and dementia Anticholinergics are a class of drug used to treat a wide variety of medical conditions. As with any medication, anticholinergics can have many beneficial effects, but these need to be balanced against a number of potential risks. This sheet provides information about how these drugs work as well as the impact that they may have in respect to dementia risk and cognitive functioning. What are anticholinergics? in time.4 It has been estimated that in Australia, 33% of people over the age of 65 years take enough Anticholinergics are generally used to inhibit the medications with anticholinergic effects to potentially involuntary movements of muscles or balance the increase their risk of harm.5 The use of anticholinergics production of various chemicals within the body. They is more common in older people because these drugs have been used in treating a wide variety of medical are prescribed for the symptomatic management of conditions including symptoms of psychosis (which medical conditions that often occur in later life. can be caused by bipolar disorder and schizophrenia), depression, urinary incontinence (e.g. overactive How do anticholinergic drugs work? bladder), gastrointestinal spasms, allergies, respiratory Anticholinergics are a class of drug that block the conditions (such as asthma and chronic obstructive action of acetylcholine in the nervous system, a pulmonary disease), Parkinson’s disease, conditions chemical (neurotransmitter) that is used to control concerning muscles in the eye and pupil dilation, messages travelling from one cell to another. They do nausea, sleep disorders and cardiovascular complaints this by blocking the binding of acetylcholine to its (slow heart rhythms) (Table 1).1,2 Some cold and flu receptor in the nerve cells. -
Pharmacology of Ophthalmic Agents
Ophthalmic Pharmacology Richard Alan Lewis M.D., M.S., PHARMACOLOGY FOPS PHARMACOKINETICS OF Professor, Departments of Ophthalmology, • The study of the absorption, OPHTHALMIC Medicine, Pediatrics, and Molecular distribution, metabolism, AGENTS and Human Genetics and excretion of a drug or and the National School of Tropical agent Introduction and Review Medicine Houston, Texas PHARMACOKINETICS Factors Affecting Drug Penetration Factors Affecting Drug Penetration into Ocular Tissues • A drug can be delivered to ocular tissue: into Ocular Tissues – Locally: • Drug concentration and solubility: The higher the concentration the better the penetration, • Surfactants: The preservatives in ocular • Eye drop but limited by reflex tearing. preparations alter cell membrane in the cornea • Ointment and increase drug permeability, e.g., • Viscosity: Addition of methylcellulose and benzalkonium and thiomersal • Periocular injection polyvinyl alcohol increases drug penetration by • pH: The normal tear pH is 7.4; if the drug pH is • Intraocular injection increasing the contact time with the cornea and altering corneal epithelium. much different, it will cause reflex tearing. – Systemically: • Lipid solubility: Because of the lipid rich • Drug tonicity: When an alkaloid drug is put in • Orally environment of the epithelial cell membranes, relatively alkaloid medium, the proportion of the uncharged form will increase, thus more • IM the higher lipid solubility, the more the penetration. • IV penetration. FLUORESCEIN FLUORESCEIN Chemistry Dosage ● C20H1205, brown crystal ● Adults: 500-750 mg IV ● M.W. 322.3 e.g., 3 cc 25% solution ● Peak absorption 485-500 nm. 5 cc 10% solution ● Peak emission 520-530 nm. ● Children: 1.5-2.5 mg/kg IV Richard Alan Lewis, M.D., M.S. -
The Clinical Toxicology of Gamma-Hydroxybutyrate, Gamma-Butyrolactone and 1,4-Butanediol
Clinical Toxicology (2012), 50: 458–470 Copyright © 2012 Informa Healthcare USA, Inc. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.3109/15563650.2012.702218 REVIEW ARTICLE The clinical toxicology of gamma-hydroxybutyrate, gamma-butyrolactone and 1,4-butanediol LEO J SCHEP 1 , KAI KNUDSEN 2 , ROBIN J SLAUGHTER 1 , J ALLISTER VALE 3 , and BRUNO MÉGARBANE 4 1 National Poisons Centre, Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand 2 Department of Anesthesia and Intensive Care Medicine, Surgical Sciences, Blå Stråket 5, Sahlgrenska University Hospital, Gothenburg, Sweden 3 National Poisons Information Service (Birmingham Unit) and West Midlands Poisons Unit, City Hospital, Birmingham, UK; School of Biosciences and College of Medical and Dental Sciences, University of Birmingham, Birmingham,UK 4 Hôpital Lariboisière, Réanimation Médicale et Toxicologique, INSERM U705, Université Paris-Diderot, Paris, France Introduction. Gamma-hydroxybutyrate (GHB) and its precursors, gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-BD), are drugs of abuse which act primarily as central nervous system (CNS) depressants. In recent years, the rising recreational use of these drugs has led to an increasing burden upon health care providers. Understanding their toxicity is therefore essential for the successful management of intoxicated patients. We review the epidemiology, mechanisms of toxicity, toxicokinetics, clinical features, diagnosis, and management of poisoning due to GHB and its analogs and discuss the features and management of GHB withdrawal. Methods. OVID MEDLINE and ISI Web of Science databases were searched using the terms “ GHB, ” “ gamma-hydroxybutyrate, ” “ gamma-hydroxybutyric acid, ” “ 4-hydroxybutanoic acid, ” “ sodium oxybate, ” “ gamma-butyrolactone, ” “ GBL, ” “ 1,4-butanediol, ” and “ 1,4-BD ” alone and in combination with the keywords “ pharmacokinetics, ” “ kinetics, ” “ poisoning, ” “ poison, ” “ toxicity, ” “ ingestion, ” “ adverse effects, ” “ overdose, ” and “ intoxication. -
Additional Drug Coverage
Additional Drug Coverage Additional prescription drug coverage Your plan includes extra coverage for certain drugs and supplies as shown below. This is not a complete list of prescription drugs and supplies covered by our plan. For a complete list, please call Customer Service toll-free at (866) 868-0609 (TTY: 711), 7 a.m. – 7 p.m. CT, Monday – Friday and 7 a.m. – 3 p.m. CT, Saturday. Lower-cost Medicare prescription drugs and supplies Your plan covers some of your Medicare prescription drugs and supplies at a $0 copay. If you have questions, call us toll-free at (866) 868-0609 (TTY: 711), 7 a.m. – 7 p.m. CT, Monday – Friday and 7 a.m. – 3 p.m. CT, Saturday. These drugs and supplies are part of your Medicare prescription drug coverage.1 Breast cancer preventive medications PEG-3350/NaCl/Na Bicarbonate/KCl TriLyte Anastrozole Exemestane Certain diabetic supplies for the Raloxifene administration of insulin Tamoxifen Insulin Syringes & Pen Needles Certain cholesterol-lowering medications Shingles vaccine Atorvastatin 10mg & 20mg Tablet Shingrix Lovastatin 10mg, 20mg & 40mg Tablet Zostavax Simvastatin 5mg, 10mg, 20mg & 40mg Tablet Tobacco cessation medications Certain colon prep products Buproban 150mg GaviLyte-C Chantix GaviLyte-G Nicotrol Inhaler PEG-3350/Electrolytes Nicotrol Nasal Spray Y0066_200527_081500_C Lower-cost non-Medicare over-the-counter drugs These drugs are covered in addition to the drugs in your plan’s drug list (formulary).2 Your plan covers these over-the-counter drugs at a $0 copay. Certain colon preparation products Tobacco cessation medications Bisacodyl Tablets Nicotine Gum Magnesium Citrate Solution Nicotine Lozenges Polyethylene Glycol Powder Nicotine Patches 1Information about the appeals and grievance process for these prescription drugs and supplies can be found in your Evidence of Coverage. -
Toxidromes Toxi-What?
Toxidromes Toxi-what? • Toxidrome – Portmanteau of “toxic syndrome” – It is a constellation of commonly seen features and exam findings that are typical for certain types of poisonings Toxidrome Symptoms History & Signs Vital signs Labs & Imaging OMG! Toxidromes r my fav! • Interesting physical exam findings • A careful history & physical usually gives enough clues to get the answer • Don’t require labs, CTs, MRIs, or tricorders Poison versus Medicine • The dose is the difference…alcohol! • Nearly all medications are poisons that are sometimes helpful at a very low dose – Diphenhydramine (Benadryl) – anti-cholinergic – Aspirin – blocks the COX enzyme, poisons platelets Philip Theophrastus Bombast von Hohenheim aka PARACELSUS (1493-1541) “What is there that is not poison? All things are poison and nothing [is] without poison. It is only the dose determines whether something is or is not a poison.” Poison versus Venom Taipan Snake Goals • Overview of the most • Diagnostic pitfalls of common toxidromes toxidromes • Excited Delirium • Working as a team for patient care – History – Vitals – Treatment Anticholinergic Syndrome Cholinergic Syndrome Sympathomimetic Syndrome Opioid / Ethanol / Sedative Toxidrome First Case – Rave Gone Bad 20ish year old female brought in by ambulance from a party/rave. No eyewitnesses to events (they all fled). Patient is very confused and all of her muscles are rigid. PMH/PSH: Unknown Meds: Unknown Allergies: Unknown All other questions: Unknown Case 1: Physical Exam VS: T 41.4 HR 180 BP 196/130 HEENT: Pupils