Acute Poisoning in Shenyang, China: a Retrospective and Descriptive Study from 2012 to 2016
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Severe Organophosphate Poisoning with Delayed Cholinergic Crisis, Intermediate Syndrome and Organophosphate Induced Delayed Polyneuropathy on Succession
Organophosphate Poisoning… Aklilu A 203 CASE REPORT SEVERE ORGANOPHOSPHATE POISONING WITH DELAYED CHOLINERGIC CRISIS, INTERMEDIATE SYNDROME AND ORGANOPHOSPHATE INDUCED DELAYED POLYNEUROPATHY ON SUCCESSION Aklilu Azazh ABSTRACT Organophosphate compounds are the organic derivatives of Phosphorous containing acids and their effect on neuromuscular junction and Autonomic Synapses is clinically important. After exposure these agents cause acute and sub acute manifestations depending on the type and severity of the agents like Acute Cholinergic Manifestations, Intermediate Syndrome with Nicotinic features and Delayed Central Nervous System Complications. The patient reported here had severe Organophosphate Poisoning with various rare complications on a succession. This is the first report of Organophosphates Poisoning complicated by Intermediate Syndrome and Organophosphate Induced Delayed Polyneuropathy in Ethiopia and it is reported to increase awareness of health care workers on these rare complications of a common problem. INTRODUCTION phosphorylated by the Phosphate end of Organophosphates; then the net result is Organophosphate compounds are the organic accumulation of excessive Acetyl Chlorine with derivatives of Phosphorous containing acids and resultant effect on Muscarinic, Nicotinic and their effect on Neuromuscular Junction and central nervous system (Figure 2). Autonomic synapses is clinically important. In the Neuromuscular Junction Acetylcholine is released Following classical OP poisoning, three well when a nerve impulse reaches -
Fipronil Poisoning Presenting As Sinus Bradycardia - a Rare Case Report
Jemds.com Case Report Fipronil Poisoning Presenting as Sinus Bradycardia - A Rare Case Report Abhijit Wadekar1, Sreekarthik Pratapa2, Maharshi Patel3, Shilpa Gaidhane4, Nazli Khatib5, 1, 2, 3, 4 Department of Medicine, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. 5 Department of Physiology, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. INTRODUCTION Fipronil is an N-phenylpyrazole insecticide, a second-generation insecticide which is Corresponding Author: relatively new and now commonly used in cotton growing community of rural Central Dr. Shilpa Gaidhane, India. Farmer suicide and deliberate self-poisoning is menace to the Vidarbha region Department of Medicine, of rural Central India. There is paucity of research published on fipronil poisoning, Acharya Vinoba Bhave Rural Hospital, Sawangi, Wardha, Maharashtra, India. clinical features, complications and treatment data. It is scarcely documented E-mail: [email protected] worldwide. Agricultural insecticides are common household items in rural areas of DOI: 10.14260/jemds/2021/247 developing countries. Because of their easy availability, insecticides became a major source of deliberate self-poisoning. As per World Health Organization (WHO), around How to Cite This Article: 3 million poisoning cases with around 0.2 million deaths are noted annually in the Wadekar A, Pratapa S, Patel M, et al. world.1 About 99 % of these deaths occur in developing countries. Insecticide Fipronil poisoning presenting as sinus poisoning is an important public issue in India. Around 168,000 deaths occurred from bradycardia - a rare case report. J Evolution Med Dent Sci 2021;10(16):1166-1168, DOI: pesticide self-poisoning which totals to almost 19.7 % of the global suicides.2 The 10.14260/jemds/2021/247 most common cause of self-poisoning in Central India is ingestion of organophosphorus compounds (OPC). -
Neurology of Acute Organophosphate Poisoning
Indian Perspective Neurology of acute organophosphate poisoning Gagandeep Singh, Dheeraj Khurana1 Departments of Neurology, Dayanand Medical College, Ludhiana, and 1Postgraduate Institute of Medical Education and Research, Chandigarh, India Abstract Acute organophosphate (OP) poisoning is one of the most common poisonings in emergency medicine and toxicological practice in some of the less-developed nations in South Asia. Traditionally, OP poisoning comes under the domain of emergency physicians, internists, intensivists, and toxicologists. However, some of the complications following OP poisoning are neurological and involve neurologists. The pathophysiological basis for the clinical manifestations of OP poisoning is inactivation of the enzyme, acetylcholinesterase at the peripheral nicotinic and muscarinic and central nervous system (CNS) nerve terminals and junctions. Nicotinic manifestations occur in severe cases and late in the course; these comprise of fasciculations and neuromuscular paralysis. There is a good correlation between the electrophysiological abnormalities and the severity of the clinical manifestations. Neurophysiological abnormalities characteristic of nicotinic junctions (mainly neuromuscular junction) dysfunction include: (1) single, supramaximal electrical-stimulus-induced repetitive response/s, (2) decrement–increment response to high frequency (30 Hz) repetitive nerve stimulation (RNS), and (3) decremental response to high frequency (30 Hz) RNS. Atropine ameliorates muscarinic manifestations. Therapeutic Address for correspondence: Dr. Gagandeep Singh, agents that can ameliorate nicotinic manifestations, mainly neuromuscular, are oximes. Department of Neurology, However, the evidence for this effect is inconclusive. This may be due to the fact that Dayanand Medical College, there are several factors that determine the therapeutic effect of oximes. These factors Ludhiana - 141 001, include: The OP compound responsible for poisoning, duration of poisoning, severity of Punjab, India. -
Nerve Agent - Lntellipedia Page 1 Of9 Doc ID : 6637155 (U) Nerve Agent
This document is made available through the declassification efforts and research of John Greenewald, Jr., creator of: The Black Vault The Black Vault is the largest online Freedom of Information Act (FOIA) document clearinghouse in the world. The research efforts here are responsible for the declassification of MILLIONS of pages released by the U.S. Government & Military. Discover the Truth at: http://www.theblackvault.com Nerve Agent - lntellipedia Page 1 of9 Doc ID : 6637155 (U) Nerve Agent UNCLASSIFIED From lntellipedia Nerve Agents (also known as nerve gases, though these chemicals are liquid at room temperature) are a class of phosphorus-containing organic chemicals (organophosphates) that disrupt the mechanism by which nerves transfer messages to organs. The disruption is caused by blocking acetylcholinesterase, an enzyme that normally relaxes the activity of acetylcholine, a neurotransmitter. ...--------- --- -·---- - --- -·-- --- --- Contents • 1 Overview • 2 Biological Effects • 2.1 Mechanism of Action • 2.2 Antidotes • 3 Classes • 3.1 G-Series • 3.2 V-Series • 3.3 Novichok Agents • 3.4 Insecticides • 4 History • 4.1 The Discovery ofNerve Agents • 4.2 The Nazi Mass Production ofTabun • 4.3 Nerve Agents in Nazi Germany • 4.4 The Secret Gets Out • 4.5 Since World War II • 4.6 Ocean Disposal of Chemical Weapons • 5 Popular Culture • 6 References and External Links --------------- ----·-- - Overview As chemical weapons, they are classified as weapons of mass destruction by the United Nations according to UN Resolution 687, and their production and stockpiling was outlawed by the Chemical Weapons Convention of 1993; the Chemical Weapons Convention officially took effect on April 291997. Poisoning by a nerve agent leads to contraction of pupils, profuse salivation, convulsions, involuntary urination and defecation, and eventual death by asphyxiation as control is lost over respiratory muscles. -
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. -
Sound Management of Pesticides and Diagnosis and Treatment Of
* Revision of the“IPCS - Multilevel Course on the Safe Use of Pesticides and on the Diagnosis and Treatment of Presticide Poisoning, 1994” © World Health Organization 2006 All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either expressed or implied. The responsibility for the interpretation and use of the material lies with the reader. In no event shall the World Health Organization be liable for damages arising from its use. CONTENTS Preface Acknowledgement Part I. Overview 1. Introduction 1.1 Background 1.2 Objectives 2. Overview of the resource tool 2.1 Moduledescription 2.2 Training levels 2.3 Visual aids 2.4 Informationsources 3. Using the resource tool 3.1 Introduction 3.2 Training trainers 3.2.1 Organizational aspects 3.2.2 Coordinator’s preparation 3.2.3 Selection of participants 3.2.4 Before training trainers 3.2.5 Specimen module 3.3 Trainers 3.3.1 Trainer preparation 3.3.2 Selection of participants 3.3.3 Organizational aspects 3.3.4 Before a course 4. -
Role of Muscarinic Acetylcholine Receptors in Adult Neurogenesis and Cholinergic Seizures
Role of Muscarinic Acetylcholine Receptors in Adult Neurogenesis and Cholinergic Seizures Rebecca L. Kow A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2014 Reding Committee: Neil Nathanson, Chair Sandra Bajjalieh Joseph Beavo Program Authorized to Offer Degree: Pharmacology ©Copyright 2014 Rebecca L. Kow University of Washington Abstract Role of Muscarinic Acetylcholine Receptors in Adult Neurogenesis and Cholinergic Seizures Rebecca L. Kow Chair of the Supervisory Committee: Professor Neil M. Nathanson Department of Pharmacology Muscarinic acetylcholine receptors (mAChRs) are G protein-coupled receptors (GPCRs) that mediate important functions in the periphery and in the central nervous systems. In the brain these receptors modulate many processes including learning, locomotion, pain, and reward behaviors. In this work we investigated the role of mAChRs in adult neurogenesis and further clarified the regulation of muscarinic agonist-induced seizures. We first investigated the role of mAChRs in adult neurogenesis in the subventricular zone (SVZ) and the subgranular zone (SGZ). We were unable to detect any modulation of adult neurogenesis by mAChRs. Administration of muscarinic agonists or antagonists did not alter proliferation or viability of adult neural progenitor cells (aNPCs) in vitro. Similarly, muscarinic agonists did not alter proliferation or survival of new adult cells in vivo. Loss of the predominant mAChR subtype in the forebrain, the M1 receptor, also caused no alterations in adult neurogenesis in vitro or in vivo, indicating that the M1 receptor does not mediate the actions of endogenous acetylcholine on adult neurogenesis. We also investigated the interaction between mAChRs and cannabinoid receptor 1 (CB1) in muscarinic agonist pilocarpine-induced seizures. -
Aluminium Phosphide Poisoning: a Case Report
International Journal of Medical Toxicology and Forensic Medicine. 2014;4(4): 149-53. Aluminium Phosphide Poisoning: a Case Report 1 1 Vaghefi SS *, Emamhadi MA 1 Department of Forensic Medicine and Toxicology, Loghman Hakim Poison Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran A R T I C L E I N F O A B S T R A C T Article Type: Background: Aluminum phosphide as pesticide commonly Case Report used to protect crops from pests. Despite the limited number of cases of poisoning with this substance, it is Article History: important due to the high risk of being fatal. The major Received: 9 April 2014 cause of the poisoning is suicide attempt. Due to the lack of Revised: 14 April 2014 specific treatment in poisoning, taking more than 500 mg is Accepted: 9 May 2014 fatal. Case Report: The patient was a 16-year-old woman who Keywords: attempted suicide by consuming some 4.5gram aluminum Aluminum Phosphide phosphide tablets. Within half an hour after consumption Poisoning she had vomiting and nausea then smoking cigar, followed Hearing Loss closely by smoking in her mouth flames around his mouth is created which will burn (grade II). Subsequently she had argument with her husband and injured her right ear. During the admission she was alert, 2nd degree burn were observed on the upper lip and around the mouth and nose and ears areas. Physical examination was normal, when she arrived she had severe hypotension and her oxygen saturation was 69% with tachycardia. The patient was immediately intubated and received mechanical ventilation. -
Vol 3 No 2 Mar Apr 2003 Online.P65
School Pesticide Monitor A Bi-monthly Bulletin on Pesticides and Alternatives Vol. 3 No. 2 March/April 2003 Beyond Pesticides / National Coalition Against the Misuse of Pesticides 701 E Street, SE, Suite 200 Washington, DC 20003 202-543-5450 [email protected] www.beyondpesticides.org Three New Reports Reveal Children’s Chemical Exposure Evidence Continues to Mount for School Pesticide Reform U.S. EPA released their second edi-tion of tion letters to students and teachers. bicides, pest repellents and disinfectants. America’s Children and the Environment: The Environmental Working Group (EWG), Measures of Contaminants, Body Burdens, The Centers for Disease Control and Preven- in partnership with Mt. Sinai School of Com- and Illnesses (www.epa.gov/envirohealth/ tion (CDC) released the second National Re- munity Medicine and Commonweal, released children) in February. Included in the report port on Human Exposure to Environmental a similar study, Body Burden: The Pollution are the results of a Minnesota study of pes- Chemicals (www.cdc.gov/exposurereport), In People (www.ewg.org/reports/ ticides in schools, which found that some which measured blood and urine samples for bodyburden/index.php). Published in the pesticides have been detected at indoor con- 116 chemicals that found their way into the peer-reviewed journal Public Health Reports, centrations potentially hazardous to chil- human population through pollution or con- the study offers an up-close and personal dren weeks and months after application. sumer products. look at nine individuals whose bodies were tested for 210 chemicals. Subjects contained Forty percent of the responding custodians The report found positive results for 89 an average of 91 compounds, most of which reported that their schools provided no no- chemicals in the volunteers tested, including did not exist 75 years ago. -
A Review of Aluminium Phosphide Poisoning and a Flowchart to Treat It Arh Hig Rada Toksikol 2016;67:183-193 183
Hashemi-Domeneh, et al. A review of aluminium phosphide poisoning and a flowchart to treat it Arh Hig Rada Toksikol 2016;67:183-193 183 Review DOI: 10.1515/aiht-2016-67-2784 A review of aluminium phosphide poisoning and a flowchart to treat it Behrooz Hashemi-Domeneh1,2, Nasim Zamani1,2, Hossein Hassanian-Moghaddam1,2, Mitra Rahimi1,2, Shahin Shadnia1,2, Peyman Erfantalab1,2, and Ali Ostadi1,2 Toxicological Research Center, Department of Clinical Toxicology, Loghman-Hakim Hospital, Shahid Beheshti University of Medical Sciences1, Excellence Center of Clinical Toxicology, Iranian Ministry of Health2, Tehran, Iran [Received in February 2016; CrossChecked in February 2016; Accepted in September 2016] The use of pesticides such as aluminium phosphide (AlP) has increased in the recent years and improved the quantity and quality of agricultural products in a number of developing countries. The downside is that AlP causes severe chronic and acute health effects that have reached major proportions in countries such as India, Iran, Bangladesh, and Jordan. Nearly 300,000 people die due to pesticide poisoning in the world every year. Poisoning with AlP accounts for many of these deaths. Unfortunately, at the same time, there is no standard treatment for it. The aim of this article is to give a brief review of AlP poisoning and propose a treatment flowchart based on the knowledge gained so far. For this purpose we reviewed all articles on the management of AlP poisoning published from 2000 till now. Using a modified Delphi design, we have designed a handy flowchart that could be used as a guide for AlP poisoning management of patients in emergency centres. -
Organophosphate and Carbamate Pesticides
ORGANOPHOSPHATE AND CARBAMATE PESTICIDES What are ORGANOPHOSPHATE and CARBAMATE PESTICIDES? Organophosphates are phosphoric acid esters or thiophosphoric acid esters. When developed in the 1930s and 1940s, their original compounds were highly toxic to mammals. Organophosphates manufactured since then are less toxic to mammals but toxic to target organisms, such as insects. Malathion, dibrom, chlorpyrifos, temephos, diazinon and terbufos are organophosphates. Carbamates are esters of N-methyl carbamic acid. Aldicarb, carbaryl, propoxur, oxamyl and terbucarb are carbamates. Although these pesticides differ chemically, they act similarly. When applied to crops or directly to the soil as systemic insecticides, organophosphates and carbamates generally persist from only a few hours to several months. However, they have been fatal to large numbers of birds on turf and in agriculture, and negatively impacted breeding success in birds. Many organophosphates are highly toxic to aquatic organisms. How can people be exposed to organophosphate and carbamate pesticides? People can be exposed to organophosphates and carbamates pesticides through accidental exposure during use. People can accidentally inhale the pesticides if they are in an area where they were recently applied. The chemicals can be ingested with food or drinks that are contaminated. How can these pesticides exhaust affect my health? Acetylcholinesterase is an enzyme found in the nervous system, red blood cells and blood plasma. These pesticides damage nerve function by acting as acetylcholinesterase inhibitors in the nervous system. Breathing - Short-term exposure can produce muscle twitching, headache, nausea, dizziness, loss of memory, weakness, tremor, diarrhea, sweating, salivation, tearing, constriction of pupils, and slowed heartbeat. Long-term exposure can produce delayed neurotoxicity, such as tingling and burning in the extremities. -
Managing Pesticide Poisoning Risk and Understanding the Signs and Symptoms Clyde L
EC2505 Revised June 2018 Managing Pesticide Poisoning Risk and Understanding the Signs and Symptoms Clyde L. Ogg, Extension Educator Jan R. Hygnstrom, Project Manager Cheryl A. Alberts, Project Coordinator Erin C. Bauer, Entomology Lecturer The potential for accidents with pesticides is real. Ac- cidental exposure or overexposure to pesticides can have seri- ous consequences. While most pesticides can be used with relatively little risk when label directions are followed, some are extremely toxic and require special precautions. The Poison Control Centers receive about 90,000 calls each year related to pesticide exposures. Pesticides are re- sponsible for about 3 percent of all accidental exposures to children 5 years and younger and about 4 percent for adults. In addition, pesticides are the cause of about 3 percent of children’s deaths reported to the Poison Control Centers. Routes of Exposure Pesticides can enter the human body three ways: 1) der- mal exposure, by absorption through the skin or eyes; 2) oral exposure, through the mouth; and 3) through inhalation or respiratory exposure, by inhaling into the lungs. Some classify exposure through the eyes as ocular exposure. Dermal exposure results in absorption immediately after Figure 1. Absorption rates of different a pesticide contacts the skin or eyes. Absorption will contin- parts of the body based on the absorption ue as long as the pesticide remains in contact with the skin or of parathion into the forearm over 24 eyes. The rate at which dermal absorption occurs is different hours. for each part of the body (Figure 1). Maiback and Feldman (1974) measured the amount of the pesticide parathion absorbed by different parts of the human body over 24 hours.