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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 -
Use of Chlorofluorocarbons in Hydrology : a Guidebook
USE OF CHLOROFLUOROCARBONS IN HYDROLOGY A Guidebook USE OF CHLOROFLUOROCARBONS IN HYDROLOGY A GUIDEBOOK 2005 Edition The following States are Members of the International Atomic Energy Agency: AFGHANISTAN GREECE PANAMA ALBANIA GUATEMALA PARAGUAY ALGERIA HAITI PERU ANGOLA HOLY SEE PHILIPPINES ARGENTINA HONDURAS POLAND ARMENIA HUNGARY PORTUGAL AUSTRALIA ICELAND QATAR AUSTRIA INDIA REPUBLIC OF MOLDOVA AZERBAIJAN INDONESIA ROMANIA BANGLADESH IRAN, ISLAMIC REPUBLIC OF RUSSIAN FEDERATION BELARUS IRAQ SAUDI ARABIA BELGIUM IRELAND SENEGAL BENIN ISRAEL SERBIA AND MONTENEGRO BOLIVIA ITALY SEYCHELLES BOSNIA AND HERZEGOVINA JAMAICA SIERRA LEONE BOTSWANA JAPAN BRAZIL JORDAN SINGAPORE BULGARIA KAZAKHSTAN SLOVAKIA BURKINA FASO KENYA SLOVENIA CAMEROON KOREA, REPUBLIC OF SOUTH AFRICA CANADA KUWAIT SPAIN CENTRAL AFRICAN KYRGYZSTAN SRI LANKA REPUBLIC LATVIA SUDAN CHAD LEBANON SWEDEN CHILE LIBERIA SWITZERLAND CHINA LIBYAN ARAB JAMAHIRIYA SYRIAN ARAB REPUBLIC COLOMBIA LIECHTENSTEIN TAJIKISTAN COSTA RICA LITHUANIA THAILAND CÔTE D’IVOIRE LUXEMBOURG THE FORMER YUGOSLAV CROATIA MADAGASCAR REPUBLIC OF MACEDONIA CUBA MALAYSIA TUNISIA CYPRUS MALI TURKEY CZECH REPUBLIC MALTA UGANDA DEMOCRATIC REPUBLIC MARSHALL ISLANDS UKRAINE OF THE CONGO MAURITANIA UNITED ARAB EMIRATES DENMARK MAURITIUS UNITED KINGDOM OF DOMINICAN REPUBLIC MEXICO GREAT BRITAIN AND ECUADOR MONACO NORTHERN IRELAND EGYPT MONGOLIA UNITED REPUBLIC EL SALVADOR MOROCCO ERITREA MYANMAR OF TANZANIA ESTONIA NAMIBIA UNITED STATES OF AMERICA ETHIOPIA NETHERLANDS URUGUAY FINLAND NEW ZEALAND UZBEKISTAN FRANCE NICARAGUA VENEZUELA GABON NIGER VIETNAM GEORGIA NIGERIA YEMEN GERMANY NORWAY ZAMBIA GHANA PAKISTAN ZIMBABWE The Agency’s Statute was approved on 23 October 1956 by the Conference on the Statute of the IAEA held at United Nations Headquarters, New York; it entered into force on 29 July 1957. The Headquarters of the Agency are situated in Vienna. -
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. -
Warning: the Following Lecture Contains Graphic Images
What the новичок (Novichok)? Why Chemical Warfare Agents Are More Relevant Than Ever Matt Sztajnkrycer, MD PHD Professor of Emergency Medicine, Mayo Clinic Medical Toxicologist, Minnesota Poison Control System Medical Director, RFD Chemical Assessment Team @NoobieMatt #ITLS2018 Disclosures In accordance with the Accreditation Council for Continuing Medical Education (ACCME) Standards, the American Nurses Credentialing Center’s Commission (ANCC) and the Commission on Accreditation for Pre-Hospital Continuing Education (CAPCE), states presenters must disclose the existence of significant financial interests in or relationships with manufacturers or commercial products that may have a direct interest in the subject matter of the presentation, and relationships with the commercial supporter of this CME activity. The presenter does not consider that it will influence their presentation. Dr. Sztajnkrycer does not have a significant financial relationship to report. Dr. Sztajnkrycer is on the Editorial Board of International Trauma Life Support. Specific CW Agents Classes of Chemical Agents: The Big 5 The “A” List Pulmonary Agents Phosgene Oxime, Chlorine Vesicants Mustard, Phosgene Blood Agents CN Nerve Agents G, V, Novel, T Incapacitating Agents Thinking Outside the Box - An Abbreviated List Ammonia Fluorine Chlorine Acrylonitrile Hydrogen Sulfide Phosphine Methyl Isocyanate Dibotane Hydrogen Selenide Allyl Alcohol Sulfur Dioxide TDI Acrolein Nitric Acid Arsine Hydrazine Compound 1080/1081 Nitrogen Dioxide Tetramine (TETS) Ethylene Oxide Chlorine Leaks Phosphine Chlorine Common Toxic Industrial Chemical (“TIC”). Why use it in war/terror? Chlorine Density of 3.21 g/L. Heavier than air (1.28 g/L) sinks. Concentrates in low-lying areas. Like basements and underground bunkers. Reacts with water: Hypochlorous acid (HClO) Hydrochloric acid (HCl). -
Beyond the Cholinergic Crisis Galle Medical Association Oration 2015
Reviews Beyond the cholinergic crisis Galle Medical Association Oration 2015 Jayasinghe S S Department of Pharmacology, Faculty of Medicine, University of Ruhuna, Galle, Sri Lanka. South Asian Clinical Toxicology Research Collaboration, Department of Medicine, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. Correspondence: Dr. Sudheera S Jayasinghe e-mail: [email protected] ABSTRACT Introduction: Organophosphates (OP) are the most frequently involved pesticides in acute poisoning. In Sri Lanka it has been ranked as the sixth or seventh leading cause of hospital deaths for many years. Neurotoxic effects of acute OP have been hitherto under-explored. The aims of the studies were to assess the effects of acute OP poisoning on somatic, autonomic nerves, neuro- muscular junction (NMJ), brain stem and cognitive function. Methods: Patients following self-ingestion of OP were recruited to cohort studies to evaluated the function of somatic, autonomic nerves, NMJ, brain stem and cognition. Motor and sensory nerve function was tested with nerve conduction studies. Cardiovascular reflexes based autonomic function tests and sympathetic skin response (SSR) was used to evaluate autonomic function. NMJ function was assessed with slow repetitive supramaximal stimulation of the median nerve of the dominant upper limb. Brain stem function and cognitive function were assessed with Brain Stem Evoked Response Audiometry (BERA) and Mini Mental State Examination (MMSE) respectively. The data of the patients were compared with age, gender and occupation matched controls. Results: There were 60-70 patients and equal number of controls in each study. Motor nerve conduction velocity, amplitude and area of compound muscle action potential on distal stimulation, sensory nerve conduction velocity and F-wave occurrence were significantly reduced. -
ENLON-PLUS (Edrophonium Chloride, USP and Atropine Sulfate, USP) Injection
NDA 19-677/S-005 NDA 19-678/S-005 Page 3 ENLON-PLUS (edrophonium chloride, USP and atropine sulfate, USP) Injection Rx only DESCRIPTION ENLON-PLUS (edrophonium chloride, USP and atropine sulfate, USP) Injection, for intravenous use, is a sterile, nonpyrogenic, nondepolarizing neuromuscular relaxant antagonist. ENLON-PLUS is a combination drug containing a rapid acting acetylcholinesterase inhibitor, edrophonium chloride, and an anticholinergic, atropine sulfate. Chemically, edrophonium chloride is ethyl (m-hydroxyphenyl) dimethylammonium chloride; its structural formula is: Molecular Formula: C10H16ClNO Molecular Weight: 201.70 Chemically, atropine sulfate is: endo-(±)-alpha-(hydroxymethyl)-8-methyl-8-azabicyclo [3.2.1]oct-3-yl benzeneacetate sulfate (2:1) monohydrate. Its structural formula is: Molecular Formula: (C17H23NO3)2·H2SO4·H2O NDA 19-677/S-005 NDA 19-678/S-005 Page 4 Molecular Weight: 694.84 ENLON-PLUS contains in each mL of sterile solution: 5 mL Ampuls: 10 mg edrophonium chloride and 0.14 mg atropine sulfate compounded with 2.0 mg sodium sulfite as a preservative and buffered with sodium citrate and citric acid. The pH range is 4.0- 5.0. 15 mL Multidose Vials: 10 mg edrophonium chloride and 0.14 mg atropine sulfate compounded with 2.0 mg sodium sulfite and 4.5 mg phenol as a preservative and buffered with sodium citrate and citric acid. The pH range is 4.0-5.0. CLINICAL PHARMACOLOGY Pharmacodynamics ENLON-PLUS (edrophonium chloride, USP and atropine sulfate, USP) Injection is a combination of an anticholinesterase agent, which antagonizes the action of nondepolarizing neuromuscular blocking drugs, and a parasympatholytic (anticholinergic) drug, which prevents the muscarinic effects caused by inhibition of acetylcholine breakdown by the anticholinesterase. -
Indirect Acting Cholinergic Drugs
Editing File Indirect acting cholinergic drugs Objectives: ✓ Classification of indirect acting cholinomimetics ✓ Mechanism of action, kinetics, dynamics and uses of anticholinesterases ✓ Adverse effects & contraindications of anticholinesterases ✓ Symptoms and treatment of organophosphates toxicity. Important Notes Extra ❖ Also called Anticholinesterases Anticholinesterases prevent hydrolysis of Ach by inhibiting acetyl cholinesterase thus, increase Ach concentrations and actions at the cholinergic receptors (both nicotinic and muscarinic). Acetylcholine binds to acetylcholinesterase at M.O. two sites, anionic site and esteric site, then A the enzyme somehow breakdown the acetylcholine into acetic acid and choline. In order to inhibit this enzyme we need to create a substance that is similar to acetylcholine either in both sites or even one site. (Similar structure) Reversible anticholinesterases Irreversible anticholinesterases Durat Short Acting Intermediate Long Acting ion of actio acting n (Alcohols) (Carbamates (Phosphates esters) e.g. esters) e.g. e.g. insecticides, gas war e.g. Physostigmine, Drug edrophonium. Ecothiophate & Isoflurophate. s Neostigmine, Classi Using those drugs leads to death ficati Pyridostigmine. on Forms weak Binds to two sites used as insecticides(malathion) or hydrogen bond of cholinesterase nerve gases (sarin) . with enzyme. Form very stable covalent bond with All polar and cholinesterase . Feat acetylcholineste ures synthetic except All phosphates are lipid soluble except rase enzyme physostigmine. Ecothiophate -
Neonatal Medicine: Neostigmine
ID: NMedQ20.054-V1-R25 Queensland Health Clinical Excellence Queensland NEOSTIGMINE 1 • For reversal of non-depolarising neuromuscular blocker (e.g. vecuronium) Indication 1 2 • Neonatal transient or congenital myasthenia gravis when pyridostigmine is unsuitable Presentation • Ampoule: 2.5 mg in 1 mL • 0.05 mg/kg (50 microgram/kg)3 Dosage If further dose required, give 0.025 mg/kg (25 microgram/kg)3 (reversal agent) o 3 o Maximum total dose is 2.5 mg (2500 microgram) • Draw up 2.5 mg and make up to 5 mL total volume with 0.9% sodium chloride Preparation o Concentration now equal to 0.5 mg/mL • Draw up prescribed dose • Give atropine sulfate 0.02 mg/kg prior or concomitant with neostigmine3 (in Administration INTRAVENOUS separate syringe) 1 • IV injection over 1 minute Presentation • Ampoule: 2.5 mg in 1 mL Dosage (myasthenia • 0.05–0.25 mg (not mg/kg) every 2 to 4 hours1,4 gravis) • Draw up 2.5 mg and make up to 5 mL total volume with 0.9% sodium chloride IM Preparation o Concentration now equal to 0.5 mg/mL • Give 30 minutes before feed1 • Draw up prescribed dose Administration • Intramuscular injection into thickest part of the vastus lateralis in the anterolateral thigh (maximum 0.5 mL per site)5 Presentation • Ampoule: 2.5 mg in 1 mL Dosage (myasthenia • 0.05–0.25 mg (not mg/kg) every 2 to 4 hours1 gravis) • Draw up 2.5 mg and make up to 5 mL total volume with 0.9% sodium chloride Preparation o Concentration now equal to 0.5 mg/mL 1 SUBCUT • Give 30 minutes before feed Administration • Draw up prescribed dose • Subcutaneous injection -
Survey of Portable Analyzers for the Measurement of Gaseous Fugitive Emissions
DCN No.: 92-275-065-09-12 Radian No.: 275-065-09 EPA No.: 68-01-0010 SURVEY OF PORTABLE ANALYZERS FOR THE MEASUREMENT OF GASEOUS FUGITIVE EMISSIONS Final Report Submitted To: Roosevelt Rollins (MD-77 A) Atmospheric Research and Exposure Assessment Laboratory Methods Research and Development Branch U.S. Environmental Protection Agency Research Triangle Park, NC 27711 Prepared By: Timothy Skelding Radian Corporation P.O. Box 13000 Research Triangle Park, NC 27709 April 20, 1992 275-065-09/cah.064op Final Report DISCLAIMER This material has been funded wholly by the Environmental Protection Agency under contract 68-D1-0010 to Radian Corporation. It has been subjected to the agency's review, and it has been approved for publication as an EPA document. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. 275-065-09/cah.064op Final Report ii TABLE OF CONTENTS Page UST OF TABLES . vi ABSmACT . vii 1.0 IN1RODUCTION . 1 1.1 Background . 1 1.2 Objectives ............................................... 2 1.3 EPA Reference Method 21 ...... '. 3 1.4 Instrument Requirements for the Survey . 5 2.0 THE ANALYZERS ............................................ 6 2.1 Flame Ionization Detectors . 6 2.1.1 Foxboro ........................................... 6 2.1.2 Heath . 9 2.1.3 MSA/Baseline . 11 2.1.4 Sensidyne . 11 2. 1.5 Thermo Environmental . 12 2.2 Photoionization Detectors . 12 2.2.1 HNu . 13 2.2.2 MSA/Baseline ..................................... 16 2.2.3 Mine Safety Appliance ............................... 17 2.2.4 Sentex . 17 2.2.5 Thermo Environmental . 18 2.2.6 Spectronics . 18 2.3 Infrared . -
Paraoxon: an Anticholinesterase That Triggers an Excitotoxic Cascade of Oxidative Stress, Adhesion Responses, and Synaptic Compromise
8th International Scientific Forum, ISF 2017, 7-8 September 2017, UNCP, USA, Proceedings Paraoxon: An Anticholinesterase That Triggers an Excitotoxic Cascade of Oxidative Stress, Adhesion Responses, and Synaptic Compromise Karen L.G. Farizatto Ben A. Bahr Biotechnology Research and Training Center, William C. Friday Laboratory, University of North Carolina - Pembroke, Pembroke, North Carolina, USA. Doi: 10.19044/esj.2017.c1p4 URL:http://dx.doi.org/10.19044/esj.2017.c1p4 Abstract The anticholinesterase paraoxon (Pxn) is an organophosphate (OP) and the active metabolite of the insecticide parathion. It potently inhibits the enzyme acetylcholinesterase and leads to enhanced glutamate release, diminished GABA uptake, oxidative damage, and neurodegeneration. The resulting increased levels of acetylcholine can trigger seizures and cause neuronal and excitotoxic damage in the brain. The brain susceptibility related to anticholinesterase toxins extends beyond potential brain damage and death from toxic levels of the agent. Asymptomatic low-level exposure to such toxins can also leave the brain vulnerable or even cause it to exhibit neurological problems later in life. The actions of Pxn and similar neurotoxins have been studied in order to examine the events associated with anticholinesterase toxicity in the brain. A recent study demonstrated that Pxn exposure initiates a pathogenic cascade involving seizure events and subsequent signs of damage including unique presynaptic vulnerability and associated behavioral deficits. In addition, Pxn-mediated synaptotoxicity is also associated with enhanced production of oxidative stress as well as integrin adhesion responses. These findings provide a better understanding of the molecular events involved in Pxn toxicity. Keywords: Paraoxon, neurotoxicity, excitotoxicity, anticholinesterase, synapse decline Paraoxon (Pxn), an anticholinesterase toxin, is in the organophosphate (OP) class of compounds that includes insecticides and military nerve agents (e.g. -
Today's Drugs
BRITISH MEDICAL JOURNAL 24 APRIL 1971 213 Gout Polyarteritis nodosa Neuropathic: Hydrallazine syndrome (procaine Haemochromatosis Takayasu's (pulseless) disease Carpal tunnel median nerve amide, oral contraceptives, etc.) Lipoidosis Wegener's granulomatosis compression Anticoagulant therapy Multicentric Reticulohistocytosis Charcot's joints, tabetic or Isoniazid shoulder-hand syndrome (Lipoid Dermatoarthritis) Neoplastic; Arthropathies associated syringomyelic Serum sickness Myositis ossificans with benign and malignant tumours: Diabetic arthropathy (neuropathic Br Med J: first published as 10.1136/bmj.2.5755.213 on 24 April 1971. Downloaded from Ochronosis Chondrosarcoma and infective) Miscellaneous: Osteomalacia Haemangioma Osborne's syndrome (ulnar nerve Acro-osteolysis syndrome Osteoporosis Left atrial myxoma compression and other compression Degos' syndrome Renal transplant syndrome Metastatic malignant disease neuropathies) Dupuytren's contracture Xanthomatosis (primary Multiple myelomatosis Paraplegia syndrome Knuckle pads (Hale White's syndrome) hypercholesterolaemia) Osteoid osteoma Shoulder-hand syndrome Paget's disease of bone Paget sarcoma Periostitis deformans (Soriano) Vascular: Pseudohypertrophic pulmonary Therapeutic: Septic focus syndrome Avascular necrosis (fat, caisson, etc.) osteoarthropathy Alcoholism Xyphoid syndrome Giant-cell arteritis Synovioma Corticosteroid arthropathy Today's Drugs With the help of expert contributors we print in this section notes on drugs in current use Treatment of Myasthenia-II Severe weakness leading to paralysis may result from either A myasthenic crisis can usually be corrected by administra- a deficiency (myasthenic crisis) or an excess (cholinergic tion of an anticholinesterase. A dose of 0 5 mg neostigmine crisis) of acetylcholine at the neuromuscular junction. The may be given by subcutaneous or intramuscular injection, differential diagnosis between these two conditions is often repeating this every 20 minutes with frequent edrophonium difficult, and the results of giving 10 mg edrophonium intra- tests. -
Phosphate Exposure Reviewer: Jessica Weiland, MD Author: L
Organophosphate Exposure Reviewer: Jessica Weiland, MD Author: L. Keith French, MD Target Audience: Emergency Medicine Residents, Medical Students Primary Learning Objectives: 1. Recognize signs and symptoms of organophosphate exposure 2. Describe safe and effective decontamination strategies for patients with organophosphate exposures 3. Describe the roles (including the indications, contraindications, and efficacy) of antidotes and other therapeutic interventions used in the care of patients with organophosphate exposure Secondary Learning Objectives: detailed technical/behavioral goals, didactic points 1. Describe the pathophysiology of organophosphates exposure 2. Compare organophosphate exposures with other toxicities that cause bradycardia, miosis, and hypotension, especially with regard to the differences and similarities in presentation, diagnosis, and management 3. Discuss the priorities for emergency stabilization of the patient with an organophosphate exposure Critical actions checklist: 1. Recognize the cholinergic toxidrome. 2. Administer atropine. 3. Administer pralidoxime. 4. Treat seizures with benzodiazepines. 5. Protect the airway. 6. Admit to the MICU. Environment: 1. Room Set Up – ED critical care area a. Manikin Set Up – Mid or high fidelity pediatric simulator, simulated sweat b. Props – Standard ED equipment For Examiner Only CASE SUMMARY SYNOPSIS OF CASE This is a case of a 27-year-old man who presents with vomiting, weakness, diaphoresis, and altered mental status. He is a depressed man who ingested a bottle of pesticide (parathion) he purchased over the Internet after researching ways to commit suicide. He will seize shortly after arriving to the emergency. He will also have signs of severe cholinergic poisoning. He will need large doses of atropine and benzodiazepines. He will need to be intubated and admitted to the ICU.