Methanol Toxicity
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Alcohol Intoxication Withdrawal Adult
Provincial Clinical Knowledge Topic Alcohol Intoxication Withdrawal, Adult Emergency Department V 1.5 © 2018, Alberta Health Services. This work is licensed under the Creative Commons Attribution-Non-Commercial-No Derivatives 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. Disclaimer: This material is intended for use by clinicians only and is provided on an "as is", "where is" basis. Although reasonable efforts were made to confirm the accuracy of the information, Alberta Health Services does not make any representation or warranty, express, implied or statutory, as to the accuracy, reliability, completeness, applicability or fitness for a particular purpose of such information. This material is not a substitute for the advice of a qualified health professional. Alberta Health Services expressly disclaims all liability for the use of these materials, and for any claims, actions, demands or suits arising from such use. Document History Version Date Description of Revision Completed By / Revised By 1.1 July 2015 Completed document (2013) reformatted into Dr. Bullard / Carla new topic template Milligan 1.2 January Minor edits in the Rationale section and form 1 Dr. Bullard / Sarah 2016 info in general care section as well as addition Searle of CIWA-Ar Scoring Reference tool to appendix 1.3 May 2016 Minor edits made to working group Sarah Searle membership list 1.4 June Removed link to Center for Addiction and Dr. Bullard / Sarah 2017 Mental Health assessment and documentation Searle form on pg. 35. Documentation requirements will continue as per local practice at this time. -
Methanol Interim AEGL Document
INTERIM 1: 1/2003 INTERIM 2: 2/2005 INTERIM ACUTE EXPOSURE GUIDELINE LEVELS (AEGLs) METHANOL (CAS Reg. No. 67-56-1) For NAS/COT Subcommittee for AEGLs February 2005 METHANOL Interim 2: 2/2005 PREFACE Under the authority of the Federal Advisory Committee Act (FACA) P. L. 92-463 of 1972, the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances (NAC/AEGL Committee) has been established to identify, review and interpret relevant toxicologic and other scientific data and develop AEGLs for high priority, acutely toxic chemicals. AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 minutes to 8 hours. AEGL-2 and AEGL-3 levels, and AEGL-1 levels as appropriate, will be developed for each of five exposure periods (10 and 30 minutes, 1 hour, 4 hours, and 8 hours) and will be distinguished by varying degrees of severity of toxic effects. It is believed that the recommended exposure levels are applicable to the general population including infants and children, and other individuals who may be sensitive or susceptible. The three AEGLs have been defined as follows: AEGL-1 is the airborne concentration (expressed as ppm or mg/m;) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, non-sensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. AEGL-2 is the airborne concentration (expressed as ppm or mg/m;) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects, or an impaired ability to escape. -
The Effects of Ethanol on Ketone Body Metabolism of Fasted Rats Henry S
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1975 The effects of ethanol on ketone body metabolism of fasted rats Henry S. Cabin Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Cabin, Henry S., "The effects of ethanol on ketone body metabolism of fasted rats" (1975). Yale Medicine Thesis Digital Library. 2432. http://elischolar.library.yale.edu/ymtdl/2432 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. YALE MEDICAL LIBRARY YALE MEDICAL LIBRARY Digitized by the Internet Archive in 2017 with funding from The National Endowment for the Humanities and the Arcadia Fund https://archive.org/details/effectsofethanolOOcabi The Effects of Ethanol on Ketone Body Metabolism of Fasted Rats by Henry S, Cabin B.A. University of Pennsylvania, 1971 Presented in partial fulfillment of the requirements for the degree of Doctor of Medicine, Yale University School of Medicine -March, 1975- ACKNOWLEDGEMENTS To Dr. Felig- who.has guided me through this research project from its inception, and for whom I have the highest esteem as a teacher, physician and human being. To Rosa, Bill and Andrea- without whose support and assistance this project would never have come to fruition. -
Alcoholic Ketoacidosis
Alcoholic Ketoacidosis: Mind The Gap, Give Them What They Need Brendan Innes BS, Stephanie Carreiro MD University of Massachusetts Medical School, Department of Emergency Medicine Introduction Differential Diagnosis Case Discussion Pancreatitis, Alcohol induced gastritis, Alcohol withdrawal, Diagnostic Criteria for Alcoholic Ketoacidosis2,3 • Patients with alcohol use disorder commonly present to the ED Alcohol induced hepatitis, Acute Kidney Injury, Sepsis, Binge drinking ending in nausea, vomiting, and decreased intake critically ill due to a myriad of underlying pathologies. Metabolic abnormality (Alcoholic ketoacidosis), Acute coronary syndrome, Pulmonary embolism Wide anion gap metabolic acidosis without alternate explanation • Alcoholic ketoacidosis (AKA) should be considered in anyone Clinical Data Positive serum/urine ketones with prolonged and/or binge consumption of alcohol. Low, normal, or slightly elevated serum glucose Anion Gap 36 130 83 27 Urinalysis Core Emergency Medicine Principles • Diagnosis and proper treatment results in rapid correction of 167 Lactate 1.9 5 11 1.9 Protein 2+ • Treatment for AKA requires glucose administration, thiamine underlying metabolic derangements often followed by rapid Salicylate, ethylene glycol, Ketones 3+ supplementation, and volume repletion. methanol not detected Urobilinogen + • D5 NS IV until rehydrated, D5 1/2NS for maintenance. clinical improvement. 16.6 Digoxin: 0.3 ng/mL 17.2 241 RBCs 5/hpf • Thiamine 100 mg IV before glucose. • Failure to make the diagnosis can result in shock, hypokalemia, 49.3 PT/INR: >120/>11 Hyaline casts 21 • Supplement electrolytes PRN. VBG: pH 7.34, pCO2 25 • Continue treatment until anion gap closes, oral intake tolerated. 90% PMNs /hpf hypoglycemia, and acidosis. • Consider other causes of anion gap if gap does not close with Neutrophils 15.6x103/µL BNP: 66 pc/mL UTox: caffeine Trop: 0.1 ng/mL treatment Lipase: 13 U/L Case Description EKG: sinus tach • Consider sodium bicarbonate if despite treatment pH < 7.0. -
Diabetic Ketoacidosis
PRIMER Diabetic ketoacidosis Ketan K. Dhatariya1,2, Nicole S. Glaser3, Ethel Codner4 and Guillermo E. Umpierrez5 ✉ Abstract | Diabetic ketoacidosis (DKA) is the most common acute hyperglycaemic emergency in people with diabetes mellitus. A diagnosis of DKA is confirmed when all of the three criteria are present — ‘D’, either elevated blood glucose levels or a family history of diabetes mellitus; ‘K’, the presence of high urinary or blood ketoacids; and ‘A’, a high anion gap metabolic acidosis. Early diagnosis and management are paramount to improve patient outcomes. The mainstays of treatment include restoration of circulating volume, insulin therapy , electrolyte replacement and treatment of any underlying precipitating event. Without optimal treatment, DKA remains a condition with appreciable, although largely preventable, morbidity and mortality. In this Primer, we discuss the epidemiology , pathogenesis, risk factors and diagnosis of DKA and provide practical recommendations for the management of DKA in adults and children. Circulatory volume Diabetic ketoacidosis (DKA) is the most common acute acid decarboxylase and protein tyrosine phosphatase depletion hyperglycaemic emergency in people with diabetes mel- autoantibodies, as those who present with hyperosmo- A reduction in intravascular litus. DKA is the consequence of an absolute (that is, lar hyperglycaemic state (HHS), and their β-cell func- and/or extracellular fluid total absence of) or relative (that is, levels insufficient tion recovers with restoration of insulin secretion quickly volume, such that there may 2 be an inability to adequately to supress ketone production) lack of insulin and con- after treatment . Thus, individuals with ketosis-prone perfuse tissue. comitant elevation of counter-regulatory hormones, T2DM can often go back to oral glucose-lowering medi- usually resulting in the triad of hyperglycaemia, met- cation without the need for continuing insulin therapy. -
1 Effects of a Ketone-Caffeine Supplement on Cycling And
Effects of A Ketone-Caffeine Supplement On Cycling and Cognitive Performance in Chronic Keto-Adapted Participants THESIS Presented in Partial Fulfillment of the Requirements for the Degree Master of Science in the Graduate School of The Ohio State University By Madison Lee Bowling Graduate Program in Kinesiology The Ohio State University 2018 Thesis Committee Dr. Jeff Volek Dr. William Kraemer Dr. Carl Maresh 1 Copyrighted by Madison Lee Bowling 2018 2 Abstract As research begins to broaden our understanding of the effects of low carbohydrate, high fat ketogenic diets to different populations, it is crucial to utilize evidence associated with the metabolic and physiological adaptation of chronic implementation. Specific populations are finding that nutritional ketosis may prove advantageous to athletic or cognitive performance. Nutritional ketosis may be identified by an elevated plasma ketone concentration within the blood range 0.5 to 5 mmol/L that results from a chronic implementation of a ketogenic diet. Recently, science shows that ketones contribute to a vast range of therapeutic and performance benefits associated with nutritional ketosis, as a result, exogenous ketone supplements have become commercially available which have proven to induce acute nutritional ketosis without restriction of carbohydrate intake. We previously showed that a supplement containing ketone salts and caffeine significantly increased performance in a non-keto adapted population. To date, there are no reports of whether ketone supplements have an ergogenic effect in an already keto-adapted population. The primary purpose of this study was to determine the performance and metabolic effects of a supplement containing ketone salts and caffeine in a group of people habituated to a ketogenic diet. -
Methanol: Toxicological Overview
Methanol Toxicological Overview Key Points Kinetics and metabolism readily absorbed by all routes and distributed in the body water undergoes extensive metabolism, but small quantities are excreted unchanged by the lungs and in the urine Health effects of acute exposure methanol is toxic following ingestion, inhalation or dermal exposure exposure may initially result in CNS depression, followed by an asymptomatic latent period metabolic acidosis and ocular toxicity, which may result in blindness, are subsequent manifestations of toxicity coma and death may occur following substantial exposures long-term effects may include blindness and, following more substantial exposures, permanent damage to the CNS Health effects of chronic exposure long-term inhalation exposure to methanol has resulted in headaches and eye irritation in workers methanol is considered not to be a mutagen or carcinogen in humans methanol is considered not to be a reproductive toxicant in humans PHE publications gateway number: 2014790 Published: August 2015 Compendium of Chemical Hazards: Methanol Summary of Health Effects Methanol may be acutely toxic following inhalation, oral or dermal exposure. Acute methanol toxicity often follows a characteristic series of features; initially central nervous system (CNS) depression and gastrointestinal tract (GI) irritation may be observed. This is typically followed by a latent period of varying duration from 12–24 hours and occasionally up to 48 hours. Subsequently, a severe metabolic acidosis develops with nausea, vomiting and headache. Ocular toxicity ranges from photophobia and misty or blurred vision to markedly reduced visual acuity and complete blindness following high levels of exposure. Ingestion of as little as 4–10 mL of methanol in adults may cause permanent damage. -
Alcohol Withdrawal
Alcohol withdrawal TERMINOLOGY CLINICAL CLARIFICATION • Alcohol withdrawal may occur after cessation or reduction of heavy and prolonged alcohol use; manifestations are characterized by autonomic hyperactivity and central nervous system excitation 1, 2 • Severe symptom manifestations (eg, seizures, delirium tremens) may develop in up to 5% of patients 3 CLASSIFICATION • Based on severity ○ Minor alcohol withdrawal syndrome 4, 5 – Manifestations occur early, within the first 48 hours after last drink or decrease in consumption 6 □ Manifestations develop about 6 hours after last drink or decrease in consumption and usually peak about 24 to 36 hours; resolution occurs in 2 to 7 days 7 if withdrawal does not progress to major alcohol withdrawal syndrome 4 – Characterized by mild autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia), mild tremor, anxiety, irritability, sleep disturbances (eg, insomnia, vivid dreams), gastrointestinal symptoms (eg, anorexia, nausea, vomiting), headache, and craving alcohol 4 ○ Major alcohol withdrawal syndrome 5, 4 – Progression and worsening of withdrawal manifestations, usually after about 24 hours from the onset of initial manifestations 4 □ Manifestations often peak around 50 hours before gradual resolution or may continue to progress to severe (complicated) withdrawal, particularly without treatment 4 – Characterized by moderate to severe autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia, fever); marked tremor; pronounced anxiety, insomnia, -
METHANOL 6 (CAS Reg
1 INTERIM 1: 1/2003 2 INTERIM 2: 2/2005 3 INTERIM ACUTE EXPOSURE GUIDELINE LEVELS 4 (AEGLs) 5 METHANOL 6 (CAS Reg. No. 67-56-1) 7 For 8 NAS/COT Subcommittee for AEGLs 9 February 2005 METHANOL Interim 2: 2/2005 10 PREFACE 11 Under the authority of the Federal Advisory Committee Act (FACA) P. L. 92-463 of 1972, the 12 National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances 13 (NAC/AEGL Committee) has been established to identify, review and interpret relevant toxicologic and 14 other scientific data and develop AEGLs for high priority, acutely toxic chemicals. 15 AEGLs represent threshold exposure limits for the general public and are applicable to emergency 16 exposure periods ranging from 10 minutes to 8 hours. AEGL-2 and AEGL-3 levels, and AEGL-1 levels as 17 appropriate, will be developed for each of five exposure periods (10 and 30 minutes, 1 hour, 4 hours, and 18 8 hours) and will be distinguished by varying degrees of severity of toxic effects. It is believed that the 19 recommended exposure levels are applicable to the general population including infants and children, and 20 other individuals who may be sensitive or susceptible. The three AEGLs have been defined as follows: 21 AEGL-1 is the airborne concentration (expressed as ppm or mg/m³) of a substance above which it 22 is predicted that the general population, including susceptible individuals, could experience notable 23 discomfort, irritation, or certain asymptomatic, non-sensory effects. However, the effects are not disabling 24 and are transient and reversible upon cessation of exposure. -
Evaluation of the Fate and Transport of Methanol in the Environment
EVALUATION OF THE FATE AND TRANSPORT OF METHANOL IN THE ENVIRONMENT Prepared For: American Methanol Institute 800 Connecticut Avenue, NW, Suite 620 Washington, DC 20006 Prepared By: Malcolm Pirnie, Inc. 180 Grand Avenue, Suite 1000 Oakland, California 94612 JANUARY 1999 3522-002 TABLE OF CONTENTS Page EXECUTIVE SUMMARY .............................................................................................ES-1 1.0 BACKGROUND .................................................................................................... 1 1.1 Purpose and Scope of Report........................................................................ 1 1.2 Introduction and History of Use ................................................................... 1 1.3 Methanol Production..................................................................................... 3 1.4 Chemical and Physical Properties................................................................. 4 1.5 Release Scenarios ......................................................................................... 5 1.6 Fate in the Environment ............................................................................... 7 2.0 PARTITIONING OF METHANOL IN THE ENVIRONMENT........................... 9 2.1 Methanol Partitioning Between Environmental Compartments .................. 9 2.2 Air/Water Partitioning.................................................................................. 9 2.3 Soil/Water Partitioning................................................................................ -
A Case of Intentional Methanol Ingestion Sarah Gilligan MD, MS, Devin Horton MD Department of Internal Medicine, University of Utah, Salt Lake City
A Case of Intentional Methanol Ingestion Sarah Gilligan MD, MS, Devin Horton MD Department of Internal Medicine, University of Utah, Salt Lake City To understand the complications and management of • Any methanol ingestion of more than 1 mg/kg may be • Ophtholmalogic manifestations can include methanol toxicity. lethal. mydriasis, retinal edema leading to retinal sheen, afferent pupillary defect, and, most commonly, toxic • Methanol itself is relatively non-toxic, causing only CNS optic neuropathy. depression; the more severe manifestations of methanol History of Present Illness toxicity are related to the breakdown product formic acid • Studies have shown the optimal treatment of toxic or formate. optic neuropathy is high dose solumedrol followed • 41 year old female with depression, seizure disorder, by a prednisone taper. alcohol abuse, and history of multiple suicide attempts • Metabolism of methanol: alcohol dehydrogenase oxidizes presented to the emergency department reporting that methanol to form formaldehyde which is then oxidized to • It is important to assess the mental health of she had ingested anti-freeze and alcohol and inhaled formic acid. Formic acid is oxidized to non-toxic carbon patients treated for methanol ingestion to gasoline in an attempt to commit suicide. dioxide and water by folate dependent reactions. determine intent and risk of additional self-harm. Physical Exam • Initial manifestations of methanol overdose can be mild • Successful treatment of methanol ingestion requires • Normal vital signs confusion and the appearance of intoxication. early recognition and aggressive multifactorial • Mild suprapubic tenderness medical management aimed at decreasing the levels • Laboratory testing classically shows significant metabolic • Slurred speech and inappropriate affect but alert and of methanol and its metabolites and preventing acidosis with extremely high anion gap and high osmolar answer questions long-term end organ damage. -
Process Design and Simulation of Propylene and Methanol Production Through Direct and Indirect Biomass Gasification by Bernardo
Process Design and Simulation of Propylene and Methanol Production through Direct and Indirect Biomass Gasification by Bernardo Rangel Lousada A dissertation submitted to the graduate faculty of Auburn University in partial fulfillment of the requirements for the degree of Master in Chemical Engineering Auburn, Alabama August 6, 2016 Keywords: Process Design, Gasification, Biomass, Propylene, Methanol, Aspen Plus, Simulation, Economic, Synthesis Copyright 2016 by Bernardo Lousada Approved by Mario R. Eden, Chair and McMillan Professor of Chemical Engineering Allan E. David, John W. Brown Assistant Professor Professor of Chemical Engineering Selen Cremaschi, B. Redd Associate Professor Professor of Chemical Engineering Abstract As a result of increasing environmental concerns and the depletion of petroleum resources, the search for renewable alternatives is an important global topic. Methanol produced from biomass could be an important intermediate for liquid transportation fuels and value-added chemicals. In this work, the production of methanol and propylene is investigated via process simulation in Aspen Plus. Two gasification routes, namely, direct gasification and indirect gasification, are used for syngas production. The tar produced in the process is converted via catalytic steam reforming. After cleanup and treatment, the syngas is converted to methanol which will be further converted to high value olefins such as ethylene, propylene and butene via the methanol to propylene (MTP) processes. For a given feedstock type and supply/availability, we compare the economics of different conversion routes. A discounted cash flow with 10% of internet rate of return along 20 years of operation is done to calculate the minimum selling price of propylene required which is used as the main indicator of which route is more economic attractive.