Handbook of Common Poisonings in Children. INSTITUTION Food and Drug Administration (DREW), Washington, D.C
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Management of Poisoning
MOH CLINICAL PRACTICE GUIDELINES December/2011 Management of Poisoning Health Ministry of Sciences Chapter of Emergency College of College of Family Manpower Authority Physicians Physicians, Physicians Academy of Medicine, Singapore Singapore Singapore Singapore Medical Pharmaceutical Society Society for Emergency Toxicology Singapore Paediatric Association of Singapore Medicine in Singapore Society (Singapore) Society Executive summary of recommendations Details of recommendations can be found in the main text at the pages indicated. Principles of management of acute poisoning – resuscitating the poisoned patient GPP In a critically poisoned patient, measures beyond standard resuscitative protocol like those listed above need to be implemented and a specialist experienced in poisoning management should be consulted (pg 55). GPP D Prolonged resuscitation should be attempted in drug-induced cardiac arrest (pg 55). Grade D, Level 3 1 C Titrated doses of naloxone, together with bag-valve-mask ventilation, should be administered for suspected opioid-induced coma, prior to intubation for respiratory insuffi ciency (pg 56). Grade C, Level 2+ D In bradycardia due to calcium channel or beta-blocker toxicity that is refractory to conventional vasopressor therapy, intravenous calcium, glucagon or insulin should be used (pg 57). Grade D, Level 3 B Patients with actual or potential life threatening cardiac arrhythmia, hyperkalaemia or rapidly progressive toxicity from digoxin poisoning should be treated with digoxin-specifi c antibodies (pg 57). Grade B, Level 2++ B Titrated doses of benzodiazepine should be given in hyperadrenergic- induced tachycardia states resulting from poisoning (pg 57). Grade B, Level 1+ D Non-selective beta-blockers, like propranolol, should be avoided in stimulant toxicity as unopposed alpha agonism may worsen accompanying hypertension (pg 57). -
Murder by Poison in Scotland During the Nineteenth and Early Twentieth Centuries
Merry, Karen Jane (2010) Murder by poison in Scotland during the nineteenth and early twentieth centuries. PhD thesis. http://theses.gla.ac.uk/2225/ Copyright and moral rights for this thesis are retained by the author A copy can be downloaded for personal non-commercial research or study, without prior permission or charge This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the Author The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the Author When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given Glasgow Theses Service http://theses.gla.ac.uk/ [email protected] Murder by Poison in Scotland During the Nineteenth and Early Twentieth Centuries Karen Jane Merry Submitted for the Degree of Doctor of Philosophy School of Law Department of Forensic Medicine Faculty of Law, Business and Social Science Faculty of Medicine © Karen Jane Merry July 2010 ABSTRACT This thesis examines the history of murder by poison in Scotland during the nineteenth and early twentieth centuries, in the context of the development of the law in relation to the sale and regulation of poisons, and the growth of medical jurisprudence and chemical testing for poisons. The enquiry focuses on six commonly used poisons. Each chapter is followed by a table of cases and appendices on the relative scientific tests and post-mortem appearances. The various difficulties in testing for these poisons in murder and attempted murder cases during the period are discussed and the verdicts reached by juries in poisoning trials considered. -
Signs and Symptoms of Pesticide Poisoning
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Historical Materials from University of Nebraska-Lincoln Extension Extension 1997 EC97-2505 Signs and Symptoms of Pesticide Poisoning Larry D. Schulze University of Nebraska - Lincoln, [email protected] Clyde Ogg University of Nebraska - Lincoln, [email protected] Edward F. Vitzthum University of Nebraska - Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/extensionhist Part of the Agriculture Commons, and the Curriculum and Instruction Commons Schulze, Larry D.; Ogg, Clyde; and Vitzthum, Edward F., "EC97-2505 Signs and Symptoms of Pesticide Poisoning" (1997). Historical Materials from University of Nebraska-Lincoln Extension. 1225. https://digitalcommons.unl.edu/extensionhist/1225 This Article is brought to you for free and open access by the Extension at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Historical Materials from University of Nebraska-Lincoln Extension by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. University of Nebraska Cooperative Extension EC97-2505-A Signs and Symptoms of Pesticide Poisoning Larry D. Schulze, Extension Pesticide Coordinator Clyde L. Ogg, Extension Assistant, Pesticide Training Edward F. Vitzthum, Coordinator, Environmental Programs z Manage Your Risk z Signal Words z Read the pesticide Label z Routes of Exposure z Pesticide Toxicity z Recognizing Signs and Symptoms of Poisoning z Recognizing Common pesticide Poisonings { Organophosphate and Carbamate Insecticides { Organochlorine Insecticides { Synthetic Pyrethroid Insecticides { Plant-derived Insecticides { Inorganic Insecticides { Microbial Insecticides { DEET Repellent { Bipyridyl Herbicides { Chlorophenoxy Herbicides { Arsenical Herbicides { Wood Preservatives { Fumigants { Rodenticides { Fungicides z What To Do When Pesticide Poisoning Occurs z References z Pesticide Safety Telephone Numbers Accidental exposure or overexposure to pesticides can have serious implications. -
Strychnine Poisoning
0++- Poison HOTLINE Partnership between UnityPoint Health and University of Iowa Hospitals and Clinics November 2013 Strychnine Poisoning Strychnine is a chemical naturally found in the seeds of the tree Strychnos nux- vomica. It is mainly used as a pesticide to control rats, moles, gophers, and coyotes. Commercial baits are pelleted and often dyed red or green. Strychnine has on rare occasions been found to be mixed with street drugs such as LSD, heroin, and cocaine. Strychnine is a white, odorless, bitter tasting crystalline powder that can be taken by mouth, inhaled or given intravenously. Strychnine is highly toxic and Did you know …… only a small amount is needed to produce severe health effects in people. As little as 30 mg may cause death in an adult. Vaporizing alcohol and “smoking” the vapors (inhaling Strychnine blocks the action of the neurotransmitter glycine which controls how is a more accurate term) is a nerve signals are sent to muscles. Glycine is an inhibitory neurotransmitter and new method for alcohol works like an “off switch” for muscles. When this “off switch” is not working consumption. The alcohol is because it is being blocked by strychnine, muscles throughout the body have poured into a vaporizing severe, painful spasms. While these spasms may look like the patient is having machine or over dry ice and a seizure, it is not a true seizure and there is no post-ictal phase. Repetitive inhaled. The alcohol enters muscle spasms caused by strychnine will lead to fever, muscle break down the lungs where it is rapidly (rhabdomyolysis), severe metabolic acidosis and respiratory failure. -
Acute Poisoning: Understanding 90% of Cases in a Nutshell S L Greene, P I Dargan, a L Jones
204 REVIEW Postgrad Med J: first published as 10.1136/pgmj.2004.027813 on 5 April 2005. Downloaded from Acute poisoning: understanding 90% of cases in a nutshell S L Greene, P I Dargan, A L Jones ............................................................................................................................... Postgrad Med J 2005;81:204–216. doi: 10.1136/pgmj.2004.024794 The acutely poisoned patient remains a common problem Paracetamol remains the most common drug taken in overdose in the UK (50% of intentional facing doctors working in acute medicine in the United self poisoning presentations).19 Non-steroidal Kingdom and worldwide. This review examines the initial anti-inflammatory drugs (NSAIDs), benzodiaze- management of the acutely poisoned patient. Aspects of pines/zopiclone, aspirin, compound analgesics, drugs of misuse including opioids, tricyclic general management are reviewed including immediate antidepressants (TCAs), and selective serotonin interventions, investigations, gastrointestinal reuptake inhibitors (SSRIs) comprise most of the decontamination techniques, use of antidotes, methods to remaining 50% (box 1). Reductions in the price of drugs of misuse have led to increased cocaine, increase poison elimination, and psychological MDMA (ecstasy), and c-hydroxybutyrate (GHB) assessment. More common and serious poisonings caused toxicity related ED attendances.10 Clinicians by paracetamol, salicylates, opioids, tricyclic should also be aware that severe toxicity can result from exposure to non-licensed pharmaco- -
Dermal Exposure to Strychnine
Journal of Analytical Toxicology, Vol. 25, July/August 2001 [CaseReport Dermal Exposureto Strychnine Richard Greene 1 and Robert MeatheralP,* 1Emergency Department, Grace General Hospital and 2Laboratory Medicine, St. Boniface General Hospital, Winnipeg, Manitoba, Canada Downloaded from https://academic.oup.com/jat/article/25/5/344/778260 by guest on 24 September 2021 t Abstract ] tents into the toilet. She accidently spilled about 1 cupful on the floor, which she wiped up with a cloth soaked in a diluted Javex A non-fatal case of strychnine poisoning through dermal exposure is solution (sodium hypochlorite). Her dermal exposure was limited described. About 24 b after cleaning up a strychnine spill, a 50-year- to her left palm; she washed her hands about 30 rain after old woman presented to the emergency department with classical cleaning up the spill. During the prodromal time period, she signs of strychnine poisoning, consisting of marked pain in the experienced no irritation or dermatitis to the left hand. Except for muscles of her lower limbs, dermal sensitivity, and stiffness in her a tingling sensation in her left hand, she was asymptomatic until jaw. Her treatment was intravenous fluid replacement and about 22:00 h when her arms and legs began to shake, pro- alkalinization in anticipation of potential renal failure due to gressing to spasms. Over the course of the night, the frequency rhabdomyolysis. Her plasma creatine kinase was elevated to 677 and duration of these muscle contractions increased. By U/L with no rise in the heart specific MB fraction. Serum myoglobin morning, the pain was more severe in the muscles of her lower level obtained retrospectively was 195 pg/L. -
Question of the Day Archives: Monday, December 5, 2016 Question: Calcium Oxalate Is a Widespread Toxin Found in Many Species of Plants
Question Of the Day Archives: Monday, December 5, 2016 Question: Calcium oxalate is a widespread toxin found in many species of plants. What is the needle shaped crystal containing calcium oxalate called and what is the compilation of these structures known as? Answer: The needle shaped plant-based crystals containing calcium oxalate are known as raphides. A compilation of raphides forms the structure known as an idioblast. (Lim CS et al. Atlas of select poisonous plants and mushrooms. 2016 Disease-a-Month 62(3):37-66) Friday, December 2, 2016 Question: Which oral chelating agent has been reported to cause transient increases in plasma ALT activity in some patients as well as rare instances of mucocutaneous skin reactions? Answer: Orally administered dimercaptosuccinic acid (DMSA) has been reported to cause transient increases in ALT activity as well as rare instances of mucocutaneous skin reactions. (Bradberry S et al. Use of oral dimercaptosuccinic acid (succimer) in adult patients with inorganic lead poisoning. 2009 Q J Med 102:721-732) Thursday, December 1, 2016 Question: What is Clioquinol and why was it withdrawn from the market during the 1970s? Answer: According to the cited reference, “Between the 1950s and 1970s Clioquinol was used to treat and prevent intestinal parasitic disease [intestinal amebiasis].” “In the early 1970s Clioquinol was withdrawn from the market as an oral agent due to an association with sub-acute myelo-optic neuropathy (SMON) in Japanese patients. SMON is a syndrome that involves sensory and motor disturbances in the lower limbs as well as visual changes that are due to symmetrical demyelination of the lateral and posterior funiculi of the spinal cord, optic nerve, and peripheral nerves. -
Survival After Deliberate Strychnine Self-Poisoning, with Toxicokinetic Data
University of Wollongong Research Online Faculty of Science, Medicine and Health - Papers: part A Faculty of Science, Medicine and Health 2002 Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data David Michael Wood Guy’s and St. Thomas’ Hospital Emma Webster Royal Oldham Hospital Daniel Martinez Guy’s and St. Thomas’ Hospital Paul Ivor Dargan Guy’s and St. Thomas’ Hospital Alison L. Jones University of Wollongong, [email protected] Follow this and additional works at: https://ro.uow.edu.au/smhpapers Part of the Medicine and Health Sciences Commons, and the Social and Behavioral Sciences Commons Recommended Citation Wood, David Michael; Webster, Emma; Martinez, Daniel; Dargan, Paul Ivor; and Jones, Alison L., "Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data" (2002). Faculty of Science, Medicine and Health - Papers: part A. 1903. https://ro.uow.edu.au/smhpapers/1903 Research Online is the open access institutional repository for the University of Wollongong. For further information contact the UOW Library: [email protected] Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data Abstract Introduction Strychnine poisoning is uncommon, and in most severe cases, the patient dies before reaching hospital. The management of strychnine poisoning is well documented, although there are few data on the kinetics of elimination of strychnine after overdose. Case report A 42-year-old man presented shortly after ingestion of an unknown quantity of strychnine powder. After a respiratory arrest, with intensive supportive management requiring admission to an intensive care unit, he survived. Eight serum samples were taken over the first 5 days and analysed subsequently for strychnine concentrations. -
Small Dose... Big Poison
Traps for the unwary George Braitberg Ed Oakley Small dose... Big poison All substances are poisons; Background There is none which is not a poison. It is not possible to identify all toxic substances in a single The right dose differentiates a poison from a remedy. journal article. However, there are some exposures that in Paracelsus (1493–1541)1 small doses are potentially fatal. Many of these exposures are particularly toxic to children. Using data from poison control centres, it is possible to recognise this group of Poisoning is a frequent occurrence with a low fatality rate. exposures. In 2008, almost 2.5 million human exposures were reported to the National Poison Data System (NPDS) in the United Objective States, of which only 1315 were thought to contribute This article provides information to assist the general to fatality.2 The most common poisons associated with practitioner to identify potential toxic substance exposures in children. fatalities are shown in Figure 1. Polypharmacy (the ingestion of more than one drug) is far more common. Discussion In this article the authors report the signs and symptoms Substances most frequently involved in human exposure are shown of toxic exposures and identify the time of onset. Where in Figure 2. In paediatric exposures there is an over-representation clear recommendations on the period of observation and of personal care products, cleaning solutions and other household known fatal dose are available, these are provided. We do not discuss management or disposition, and advise readers products, with ingestions peaking in the toddler age group. This to contact the Poison Information Service or a toxicologist reflects the acquisition of developmental milestones and subsequent for this advice. -
Doxepin Hydrochloride Capsule Mylan Pharmaceuticals Inc.
DOXEPIN HYDROCHLORIDE- doxepin hydrochloride capsule Mylan Pharmaceuticals Inc. ---------- Suicidality and Antidepressant Drugs Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders. Anyone considering the use of doxepin or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need. Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older. Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide. Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. Doxepin is not approved for use in pediatric patients. (See WARNINGS: Clinical Worsening and Suicide Risk, PRECAUTIONS: Information for Patients and PRECAUTIONS: Pediatric Use.) DESCRIPTION Doxepin hydrochloride is one of a class of psychotherapeutic agents known as dibenzoxepin tricyclic compounds. The molecular formula of the compound is C19H21NO • HCl having a molecular weight of 315.84. It is a white crystalline powder freely soluble in water, in ethanol (96%), and methylene chloride. It may be represented by the following structural formula: Chemically, doxepin hydrochloride is a dibenzoxepin derivative and is the first of a family of tricyclic psychotherapeutic agents. -
SINEQUAN® (Doxepin Hcl) CAPSULES ORAL CONCENTRATE
69-2135-00-1 SINEQUAN® (doxepin HCl) CAPSULES ORAL CONCENTRATE DESCRIPTION SINEQUAN® (doxepin hydrochloride) is one of a class of psychotherapeutic agents known as dibenzoxepin tricyclic compounds. The molecular formula of the compound is C19H21NO•HCl having a molecular weight of 316. It is a white crystalline solid readily soluble in water, lower alcohols and chloroform. Inert ingredients for the capsule formulations are: hard gelatin capsules (which may contain Blue 1, Red 3, Red 40, Yellow 10, and other inert ingredients); magnesium stearate; sodium lauryl sulfate; starch. Inert ingredients for the oral concentrate formulation are: glycerin; methylparaben; peppermint oil; propylparaben; water. CHEMISTRY SINEQUAN (doxepin HCl) is a dibenzoxepin derivative and is the first of a family of tricyclic psychotherapeutic agents. Specifically, it is an isomeric mixture of: 1-Propanamine, 3-dibenz[b,e]oxepin-11(6H)ylidene-N,N-dimethyl-, hydrochloride. 1 ACTIONS The mechanism of action of SINEQUAN (doxepin HCl) is not definitely known. It is not a central nervous system stimulant nor a monoamine oxidase inhibitor. The current hypothesis is that the clinical effects are due, at least in part, to influences on the adrenergic activity at the synapses so that deactivation of norepinephrine by reuptake into the nerve terminals is prevented. Animal studies suggest that doxepin HCl does not appreciably antagonize the antihypertensive action of guanethidine. In animal studies anticholinergic, antiserotonin and antihistamine effects on smooth muscle have been demonstrated. At higher than usual clinical doses, norepinephrine response was potentiated in animals. This effect was not demonstrated in humans. At clinical dosages up to 150 mg per day, SINEQUAN can be given to man concomitantly with guanethidine and related compounds without blocking the antihypertensive effect. -
Ingested Lethal Ageni's Strychnine
REVIEW OF CURRENT VERTEBRATE PESTICIDES D. Glen Crabtree Bureau of Sport Fisheries and Wildlife, Wildlife Research Center, B1dg. 45, Denver Federal Center, Denver 25, Colorado. For the purpose of this brief review, EmG>hasis will be placed on development, physical properties, physiological action, experience and limitations of vertebrate pesticides primarily of current opera- tional 1.m;portance in the control of field rodents and predatory animals. INGESTED LETHAL AGENI'S STRYCHNINE (C21H~202) 'Dlis al.kaloid was discovered by Pelletier and Cavento,}/in 1817 as a constituent in the seeds of Strychnos Nux-vomica or Strychnos !gnatii, which were used :for killing dogs, cats and birds in Europe at least as early as J.6ljo • Strychnine (probably the sulfate) appears to have been introduced as a pesticide in the United States about 1847 and became the g/ principal tool of the professional "wolfer" during the years 1800-1885. PHYSICAL PROPERTIES: ~e alkaJ.oid of commerce is a white or greyish white powder prepared from seeds grown in Southern Asia. It is quite stable, almost insoluble in water, but soluble in many organic solvents and to varying degrees in dilute acids With which it forms salts having limited solubility in water. Strychnine and its salts have an exceedingly bitter taste and are not absorbed through the normal intact skin. 327 Both the alkaloid and strychnine sul.fate are widely used today as vertebrate pesticides. In the case of the latter, allowance must be made in preparing l.ethal baits since it contains onl.y 78.04~ strychnine. PHYSIOLOGICAL ACTION: Ingested strychnine is proJJG>tly absorbed, mainly, from the intestinal tract.