DOCSLIB.ORG

A Heart Too Drunk to Drive; AV Block Following Acute Alcohol Intoxication

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
A Heart Too Drunk to Drive; AV Block Following Acute Alcohol Intoxication Chinese Journal of Physiology 59(1): 1-8, 2016 1 DOI: 10.4077/CJP.2016.BAE364 Review Article A Heart too Drunk to Drive; AV Block following Acute Alcohol Intoxication Arthur H. van Stigt1, #, Ruben J. Overduin1, #, Liza C. Staats1, #, Vera Loen1, #, and Marcel A.G. van der Heyden2 1Participant in the Honours Program CRU2006 Bachelor, University Medical Center Utrecht, Heidelberglaan 100, 3584 CM, Utrecht, and 2Department of Medical Physiology, Division of Heart & Lungs, University Medical Center Utrecht, Yalelaan 50, 3584 CM Utrecht, The Netherlands Abstract Acute excessive alcohol consumption is associated with heart rhythm disorders like atrial fibrilla- tion but also premature ventricular contractions, collectively known as the “holiday heart syndrome”. More rarely but clinically significant are reports of atrioventricular (AV) conduction disturbances in binge drinkers with no underlying heart disease or chronic alcohol consumption. To obtain better insights into common denominators and the potential underlying mechanisms we collected and com- pared individual case reports of AV block following acute alcohol intoxication in otherwise healthy people. By screening PubMed, Google Scholar, Scopus and JSTOR, fifteen cases were found of which eight were sufficiently documented for full analysis. Blood alcohol levels ranged from 90 to 958 mg/dl (19 to 205 mM). Second and third degree AV block was observed most (6/8) albeit that in two of these patients a vagal stimulus led to deterioration from first into higher order AV block. In all cases, patients reverted to normal sinus rhythm upon becoming sober again. Mildly lowered body temperature (35.9 ± 0.5°C) was observed but can be excluded as a major cause of conduction blockade. We hypothesize that ethanol induced partial inhibition of calcium and potentially also sodium currents in conductive tissue structures may be one of the mechanisms of conduction slowing and block that may become exaggerated upon increased vagal tone. An impairment of gap junction function cannot be excluded as a contributing factor. In conclusion, cases of documented alcohol induced AV block are very rare but events can occur at relatively low serum alcohol levels which should prompt to awareness of this phenomenon in alcohol intoxicated patients. Key Words: alcohol, AV block, conduction, ECG, heart, intoxication, ion channel Introduction junctions (allowing direct ion flow from cell to cell) and connective tissue strands (producing an optimal The atrioventricular (AV) conduction system is source-sink relationship) (29). All four components essential for an optimal cardiac performance in which are subjected to tight regulation by numerous signal- timing of atrial contraction is tuned to its ventricular ing pathways of which some can adapt very rapidly counterpart. The speed of impulse propagation is de- to encounter the ever changing physiological demands, pendent on the amounts of depolarizing currents (cal- e.g. the sympathetic and parasympathetic pathways. cium and sodium currents determining action potential Many environmental substances can influence the AV upstroke), repolarizing potassium currents (determining conduction pathway by addressing one or more of the action potential duration and refractory period), gap above mentioned players. For example, grayanotoxins Corresponding author: Dr. Marcel A.G. van der Heyden, Department of Medical Physiology, Division of Heart & Lungs, Yalelaan 50, 3584 CM Utrecht, The Netherlands. Tel: +31 30 2538901, Fax: +31 30 2539064, E-mail: [email protected] #These authors contributed equally. Received: March 13, 2015; Revised (Final Version): May 21, 2015; Accepted: June 2, 2015. 2016 by The Chinese Physiological Society and Airiti Press Inc. ISSN : 0304-4920. http://www.cps.org.tw 2 van Stigt, Overduin, Staats, Loen and van der Heyden present in honey produced from the flowers of several marize the common denominators in individual cases family members of Ericaceae plants have strong vagal of alcohol induced acute AV block in otherwise healthy effects resulting in severe cases of conduction block individuals to gain better insights into the clinical course (26). Perturbation of AV conduction is classified in and etiology of this potentially dangerous condition. several categories. Whereas normal human PR intervals on the electrocardiography (ECG) are between 120 and Materials and Methods 200 ms, first-degree AV block is characterized by sinus rhythm with lengthening of PR times beyond 200 ms. PubMed, Google Scholar, Scopus and JSTOR Second-degree block shows both conducted and non- were screened for case reports published until No- conducted impulses in three different constitutions vember 2014, using combinations of the following (Mobitz type I and II, and 2:1/3:1 block). Third-degree search terms: ‘AV block’, ‘atrioventricular block’, AV block occurs when none of the atrial electrical ‘alcohol’, ‘ethanol’, ‘intoxication’, ‘PR prolongation’ activity is conducted to the ventricles (8). and ‘holiday heart syndrome’. French and German Alcohol is a well-known environmental factor equivalents of these search terms were also used to affecting heart function, structure and electrophysi- screen the above mentioned databases. References in ology. Chronic alcohol consumption (at least > 90 primary case-reports were used to retrieve additional g/day for five years or more) can result in alcoholic cases. A Chinese native speaker screened Chinese cardiomyopathy that is characterized by cardiac dys- literature bases with similar search terms. function, left ventricular dilation, normal or reduced left ventricular wall thickness, increased left ventricu- Results lar mass and normal ejection fraction to the point of severe alcoholic cardiomyopathy (14, 31). Atrial fibril- Cases of Acute AV Block following Alcohol Intake lation is one of the most common arrhythmias asso- ciated with severe chronic alcohol intake (14), whereas We found ten articles presenting a total of 15 ventricular arrhythmias and sudden cardiac death are cases. Upon further scrutiny three articles were less frequently observed (45). Furthermore, cardiac excluded from further analysis for the following conduction disturbances and even complete AV block reasons. In two articles (6 cases) the ECG param- have also been observed in heavy drinkers (32). In eters and clinical symptoms of the multiplex of 1978, Ettinger was the first to describe the relation- cases were described too briefly and with too little ship between acute excessive alcohol consumption and clinical details to allow any comparison with other cardiac (particularly supraventricular tachy-) ar- cases (23, 33). The third excluded article (1 case) rhythmias in allegedly healthy subjects under the was considered a semi-acute alcohol intoxication in name ‘holiday heart syndrome’ (18). The incidence which consumption of large quantities of whiskey of binge drinking (more than 5 alcoholic beverages had taken place since several weeks prior to AV block in one occasion) in adolescent and young adults re- (21). The remaining seven case reports describing mains at a high level in the last decade.1 The most 8 individual cases on non-chronic alcohol intake commonly seen arrhythmia after binge drinking in followed by an AV block in humans were used in the Ettinger study is atrial fibrillation, followed by our analysis. A short description of the individual atrial flutter, isolated ventricular premature beats, cases is presented and additional numerical data isolated atrial premature complexes and paroxysmal and key information are presented in Table 1. atrial tachycardia. Most of the included patients were Abdelazis et al. (2) (case 1): a 14-year-old boy however heavy periodical drinkers and the holiday was admitted with acute alcohol ingestion. On admis- heart syndrome was therefore initially considered sion, bradycardia (53 bpm) was noted. Saline infusion to be linked to chronic alcohol consumption. In ad- was given in view of hypotension. ECG showed second- dition to a case described by Ettinger, several other degree AV block (Mobitz type I with Wenkebach phe- studies showed cardiac arrhythmias after binge nomenon). Urine did not show any trace of other drugs drinking in non-alcoholic healthy subjects (17, 41), besides alcohol. The next day a repeated ECG was hinting at a true relationship between acute alcohol normal, as well as a twenty-four hours ambulatory intake and cardiac arrhythmias. Moreover, cases of ECG and an echocardiography. incidental excessive alcohol intake leading to acute Abdelazis et al. (2) (case 2): a 15-year-old girl was AV block have been reported as well, but this phe- admitted with acute alcohol ingestion. ECG showed nomenon is rather rare and data are scattered. It was, a first-degree AV block. Except for a slow heart rate therefore, the purpose of this short review to sum- (60 bpm), cardiorespiratory observations showed no 1Substance Abuse and Mental Health Services Administration, Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings, NSDUH Series H-48, HHS Publication No. (SMA) 14-4863. Rockville, MD: Substance Abuse and Mental Health Services Administration, 2014. Table 1. Overview of acute ethanol intoxication cases with occurrence of any type of AV block Age Sex Origin of Serum Alcohol Type AV Block Clinical Signs Body Core Treatment Outcome Reference (y) Case Report Ethanol Level Source Temperature (mg/dl) (°C) 14 M United Unknown Unknown 2dAVB (Mobitz I Bradycardia (HR
Load more

Recommended publications
  • Alcohol Intoxication & Intervention Scale
    Alcohol Intoxication & Intervention Scale Alcohol affects each individual differently. The effect of alcohol on a person will vary according to the person's mood, the time of day, Standard Drink amount of food in the stomach, the mixer used, how fast the person One standard drink of beer drinks, and what and why they are drinking. There are a variety of One 12 oz bottle of beer positive and negative consequences related to drinking. One 12 oz can of beer One 8 oz glass of malt liquor (i.e. Blood Alcohol Level Old English, Mickey's) Once you know the definition of one standard drink (see chart to the One standard drink of wine right), you can estimate your Blood Alcohol Level (BAL). BAL levels One 4 oz glass of wine (pictured) represent the percent of your blood that is concentrated with alcohol. A One 3 ‐ 3.5 oz of fortified wine (i.e. BAL of .10 means that .1% of your bloodstream is composed of alcohol. port, sherry) One bottle of table wine is about 5 Some key factors that affect BAL: standard drinks How many standard drinks you drink One standard drink of hard alcohol Remember different drinks have different strengths either One 1.25 oz shot of hard liquor because of differences in proofs of hard liquor or because some (pictured) drinks contain more than one shot One mixed drink containing one 1.25 oz shot of hard liquor Food eaten along with drinking alcohol will result in a lower, One 750ml bottle of hard liquor ("a delayed BAL because the alcohol enters the bloodstream at a fifth") is about 17 standard drinks lower rate Intoxication and Intervention Scale Know the visible signs of intoxication.
    [Show full text]
  • 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.
    [Show full text]
  • Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum
    International Journal of Environmental Research and Public Health Review Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum Hiroshi Mitoma 1,* , Mario Manto 2,3 and Aasef G. Shaikh 4 1 Medical Education Promotion Center, Tokyo Medical University, Tokyo 160-0023, Japan 2 Unité des Ataxies Cérébelleuses, Service de Neurologie, CHU-Charleroi, 6000 Charleroi, Belgium; [email protected] 3 Service des Neurosciences, University of Mons, 7000 Mons, Belgium 4 Louis Stokes Cleveland VA Medical Center, University Hospitals Cleveland Medical Center, Cleveland, OH 44022, USA; [email protected] * Correspondence: [email protected] Abstract: Ethanol consumption remains a major concern at a world scale in terms of transient or irreversible neurological consequences, with motor, cognitive, or social consequences. Cerebellum is particularly vulnerable to ethanol, both during development and at the adult stage. In adults, chronic alcoholism elicits, in particular, cerebellar vermis atrophy, the anterior lobe of the cerebellum being highly vulnerable. Alcohol-dependent patients develop gait ataxia and lower limb postural tremor. Prenatal exposure to ethanol causes fetal alcohol spectrum disorder (FASD), characterized by permanent congenital disabilities in both motor and cognitive domains, including deficits in general intelligence, attention, executive function, language, memory, visual perception, and commu- nication/social skills. Children with FASD show volume deficits in the anterior lobules related to sensorimotor functions (Lobules I, II, IV, V, and VI), and lobules related to cognitive functions (Crus II and Lobule VIIB). Various mechanisms underlie ethanol-induced cell death, with oxidative stress and Citation: Mitoma, H.; Manto, M.; Shaikh, A.G. Mechanisms of endoplasmic reticulum (ER) stress being the main pro-apoptotic mechanisms in alcohol abuse and Ethanol-Induced Cerebellar Ataxia: FASD.
    [Show full text]
  • Court Intervention: Pre-Sentence Investigation
    If you have issues viewing or accessing this file contact us at NCJRS.gov. ------~--- ---- .. National Criminal Justice Reference Service COURT INTERVENTION: PRE-SENTENCE This microfiche was 'produced from documents received for inclusion in the NCJRS data base. Since NCJRS cannot exercise control over the physical condition of the documents submitted, INVESTIGATION the individual frame quality will vary. The resolution chart on this frame may be used to evaluate the document quality. TECHNIQUES FOR DRINKING/DRIVING OFFENSES 2 8 1.0 :; 11111 . 111111:~ W IIp·2 .2 W I.r.: I~ w: J:,i 14.0 ..,.I.::. u. - 1.1 tIl&.:.u - , == I 111111.25 11111·1.4 111111.6 I ! I MICROCOPY RESOLUTION TEST CHART NATIONAL BUREAU OF STANDARDS-1963-A .. ' ~ ...,.. '~'''';'''' ..' .. ~" - q P ARTI'CIPANT'S Microfil~ing proced~;~~~sed to create this fiche comply with & the standards set forth i1141CFR lOl-11.SD4. MANUAL Points of view or opinions stated in this document are those of the author(s) and do not represent the official U.S. Department of Transportation DATE FILMED ~ National Highway Traffic Safety Administration position or policies of the U. S. Department of Justice. Washington, D.C. 20590 '-, . ~ , .... ~ 1. _ .I. ' 1 9/04/81' " National Institute of Justice -;: .J.____ .... United States Department of Justice Washington, D. C. 2053<1 • , --~---.~--~. --- ~ I ! CONTENTS SEMINAR AGENDA iii ; - l AGENDA PRE-SENTENCE INVESTIGATION SEMINAR Day One 0900-1200 1. Introduction and Overview UNITS 1. Introduction and Overview 1 i: This unit covers: (a) introduction and administrative infor­ 2. The Problem Drinking Drive 9 mation, (b) information on DOT/NHTSA standards, (c) the genesis of the project, and (d) explanation of the ASAP 3.
    [Show full text]
  • Background Paper 6.14 Harmful Use of Alcohol Alcohol Use Disorders and Alcoholic Liver Diseases
    Priority Medicines for Europe and the World "A Public Health Approach to Innovation" Update on 2004 Background Paper Written by Warren Kaplan, Ph.D, JD, MPH Background Paper 6.14 Harmful use of Alcohol Alcohol Use Disorders and Alcoholic Liver Diseases By Rene Soria Saucedo (MD, MPH, PhDc) January 2013 Update on 2004 Background Paper, BP 6.14 Alcohol Use Disorders Table of Contents Abbreviations: ..................................................................................................................................................... 5 Executive Summary ............................................................................................................................................ 6 Burden of Disease ............................................................................................................................................ 6 Treatment Options ........................................................................................................................................... 7 1. Introduction ................................................................................................................................................. 8 1.1 Alcohol Consumption (ACo) and its relationship with Alcohol Use Disorders (AUD) ........... 8 1.2 Alcohol Use Disorders (AUD) .......................................................................................................... 9 1.3 Alcoholic Liver Diseases (ALD) .....................................................................................................
    [Show full text]
  • Reducing the Negative Consequences of Drinking and Alcohol Intoxication
    European status report on alcohol and health 2014 Reducing the negative consequences of drinking and alcohol intoxication Reducing the negative consequences of drinking and alcohol intoxication Background The pattern of drinking is just as important for alcohol-related harm as the volume of alcohol consumed. Most alcohol is consumed in heavy drinking occasions, which is the most risky pattern of drinking and one that can cause harm not only to the drinkers themselves but also to others. Taking action in drinking environments is one important strategy for reducing the frequency and size of heavy drinking patterns.1 Pubs, bars and nightclubs are key locations for the consumption of alcohol, particularly among young people. These drinking venues can be both a hub of social and recreational activity and a source of revenue for local economies. However, the congregation of large numbers of drinkers in drinking environments means they are often associated with high levels of intoxication and alcohol-related harm, including violence, road traffic crashes, public disorder and unintentional injury. Factors that have been associated with problematic venues include a permissive atmosphere, crowding, low levels of comfort, poorly trained staff and cheap drinks promotions.2 Interventions in drinking environments can reduce alcohol-related harm by targeting both the way in which alcohol is served and the conditions in which it is consumed, resulting in wide- ranging benefits that include averting problems that often harm people who are not drinking,
    [Show full text]
  • Acute Alcohol Intoxication May Cause Delay in Stroke Treatment
    Arokszallasi et al. BMC Neurology (2019) 19:14 https://doi.org/10.1186/s12883-019-1241-6 CASEREPORT Open Access Acute alcohol intoxication may cause delay in stroke treatment – case reports Tamas Arokszallasi1*, Eszter Balogh1, Laszlo Csiba1,2, Istvan Fekete1, Klara Fekete1 and Laszlo Olah1 Abstract Background: The signs and symptoms of acute alcohol intoxication resemble those of vertebrobasilar stroke. Due to their shared symptoms including double vision, nystagmus, dysarthria, and ataxia, the differential diagnosis of alcohol intoxication and vertebrobasilar stroke may pose a challenge. Moreover, if alcohol intoxication and stroke occur simultaneously, the signs and symptoms of stroke may be attributed to the effects of alcohol, leading to delayed stroke diagnosis and failure to perform reperfusion therapy. Case presentations: Three cases of alcohol intoxication and stroke are presented. The first patient (female, 50 years old) had dysarthria, nystagmus and trunk ataxia on admission. Her blood alcohol level was 2.3‰. The symptoms improved after forced diuresis, but 5.5 h later progression was observed, and the patient developed diplopia and dysphagia in addition to her initial symptoms. Angiography showed occlusion of the basilar artery. Intraarterial thrombolysis was performed. The second patient (male, 62 years old) developed diplopia, dysarthria and trunk ataxia after consuming 4-units of alcohol, and his symptoms were attributed to alcohol intoxication. Two hours later, neurological examination revealed dysphagia and mild right-sided hemiparesis, which questioned the causal relationship between the symptoms and alcohol consumption. Cerebral CT was negative, and intravenous thrombolysis was administered. The third patient (male, 55 years old) consumed 10 units of alcohol before falling asleep.
    [Show full text]
  • The Effect of Alcohol Consumption on Risk for Sepsis and ARDS
    The Effect of Alcohol Consumption on Risk for Sepsis and ARDS E. L. Burnham, M. Moss, and G. S. Martin I Introduction Alcohol is the most frequently abused drug throughout the world, and alcohol-re­ lated problems are a common occurrence among patients admitted to hospitals and intensive care units (ICUs). Alcohol affects all tissues of the body. Its effects on im­ mune function and the systemic inflammatory response syndrome (SIRS) remain topics of active investigation. In regard to immune function, alcohol consumption alters the response at several points along the inflammatory cascade. Due to these potent modulating effects on immune function, alcoholic patients have an increased incidence and severity of infection, particularly in the lung. This association be­ tween alcohol use and infection is especially evident in the post-operative setting. Among patients with sepsis, a prior history of chronic alcohol abuse confers a sig­ nificant increase in the likelihood of respiratory dysfunction and development of acute respiratory distress syndrome (ARDS). Chronic alcohol abuse similarly in­ creases the mortality from ARDS. One possible mechanism by which chronic alco­ hol abuse may increase susceptibility to acute lung injury (ALI} is through altera­ tions in pulmonary glutathione homeostasis. This chapter discusses the immuno­ modulatory effects of alcohol and the epidemiological and experimental evidence associating chronic alcohol abuse, sepsis, and the development of ARDS. I Background Alcohol is the most commonly abused drug in the world, with approximately half the US population consuming alcohol regularly. Fifteen to twenty million individuals meet the criteria for alcoholism [ 1]. The economic cost of alcohol in the USA is around $100 billion (USD), with > 10% of this cost directly attributable to medical services [2].
    [Show full text]
  • Diagnostic Codes Used for Data Extraction A) ICD Codes the Codes on the Following Sheet Will Be Used to Identify
    Appendix 1: Diagnostic codes used for data extraction A) ICD codes The codes on the following sheet will be used to identify people in the Admitted Patients Data Collection and Emergency Department Data Collection (cases). Codes were selected based on identification by NSW Health as reflective of an acute alcohol problem1 or, where indicated (*) from Turning Point Alcohol and Drug Centre guidance for calculating alcohol and other drug statistics 2. Where indicated (~), additional codes are included on the basis of discussion between investigators and specialists in the field. ICD-9-CM and ICD-10-AM codes were mapped using the Australian Consortium for Classification Development mapping tables, with backwards mapping from ICD-10- AM to ICD-9-CM3, and alcohol-specific code mapping developed by Chikritzhs et al.4. ICD-10-AM Conditions ICD-9-CM Conditions E24.4 *Alcohol-induced pseudo- No alcohol-specific code available Cushing's syndrome E51.2 ~Wernicke encephalopathy 291.1 Alcohol-induced persisting amnestic disorder F10 Mental and behavioural 291 Alcohol-induced mental disorders disorders due to use of alcohol 303 Alcohol dependence syndrome 305.0 Nondependent alcohol abuse G31.2 *Degeneration of nervous 303 Alcohol dependence syndrome system due to alcohol G62.1 *Alcoholic polyneuropathy 357.5 *Alcoholic polyneuropathy G72.1 *Alcoholic myopathy No alcohol-specific code available I42.6 *Alcoholic cardiomyopathy 425.5 *Alcoholic cardiomyopathy K29.2 *Alcoholic gastritis 535.3 *Alcoholic gastritis K70.0 Alcoholic fatty liver 571.0 *Alcoholic
    [Show full text]
  • Alcohol, Murder and Medical Jurisprudence In
    © 2014 Michele Rotunda ALL RIGHTS RESERVED “DRUNKENNESS IS NO EXCUSE FOR CRIME” – ALCOHOL, MURDER, AND MEDICAL JURISPRUDENCE IN NINETEENTH- CENTURY AMERICA by MICHELE ROTUNDA A Dissertation submitted to the Graduate School – New Brunswick Rutgers, The State University of New Jersey in partial fulfillment of the requirements for the degree of Doctor of Philosophy Graduate Program in History Written under the direction of Susan R. Schrepfer And approved by ___________________________________________ ___________________________________________ ___________________________________________ ___________________________________________ New Brunswick, New Jersey May 2014 ABSTRACT OF THE DISSERTATION “DRUNKENNESS IS NO EXCUSE FOR CRIME” – ALCOHOL, MURDER, AND MEDICAL JURISPRUDENCE IN NINETEENTH-CENTURY AMERICA BY MICHELE ROTUNDA Dissertation Director: Susan R. Schrepfer Using a variety of court cases as evidence, this study focuses on several competing, and often unresolved, models of responsibility for crimes related to intoxication that emerged in nineteenth century America. Drunkenness truly was “no excuse” for crime in the early years of the nineteenth century; however, changes in the fields of medicine, the law, and society created the circumstances under which such a defense became more viable, and certainly more prevalent, if only intermittently successful, by mid-century. American courts began, in the 1820s, to accord an expanded exculpatory value to intoxication due to several factors: 1. The medicalization of alcohol use from delirium tremens to dipsomania to inebriety created categories of mental illness from which to argue for limited or even absent responsibility under the law. 2. American law, beginning in 1794, allowed for a greater recognition of the issue of intent in crimes, in particular, creating statutory degrees of violent crimes that were dependent on establishing appropriate mens rea.
    [Show full text]
  • Rhabdomyolysis Following Acute Alcohol Intoxication 12,143-144 S
    Journal of CASE REPORT Accident and J Accid Emerg Med: first published as 10.1136/emj.12.2.143 on 1 June 1995. Downloaded from Emergency Medicine 1995 Rhabdomyolysis following acute alcohol intoxication 12,143-144 S. M. HEWITT1 & R.J. WINTER2 'Department of Accident and Emergency Medicine and 2Adult Intensive Therapy Unit, University Hospital, Nottingham, UK SUMMARY (148 mmol L-') levels. Serum creatinine kinase was grossly elevated at over 120 000 IU L-'. The case of a fit young man who developed Following aggressive intravenous fluid rhabdomyolysis after a short period of im- management including mannitol and bicarbonate, mobilization following acute alcohol intoxication low-dose dopamine (2.5 pg kg-' min-1)and surgical is described. Rhabdomyolysis should be decompression of the leg, the patient's renal considered in an intoxicated patient presenting function recovered. His recovery was complicated with muscle tenderness, particularly after by a pulmonary embolism which occurred whilst immobilization. he was awaiting skin grafting of the operated leg. Key words: alcohol, compartment syndrome, rhabdomyolysis DISCUSSION INTRODUCTION Rhabdomyolysis occurs following injury to skeletal muscle resulting in leakage of the intracellular Rhabdomyolysis has been previously described in contents into the circulation. It has been reported chronic alcoholics and also in binge drinkers in in association with a variety of seemingly unrelated association with other drugs,' 2 We report a case insults, and may be multifactorial.' A number of of rhabdomyolysis occumng in a previously healthy drugs and toxins have been implicated.3 Alcohol- male in whom the precipitating cause appears to related rhabdomyolysis has been attributed to a be acute alcohol intoxication and immobility.
    [Show full text]
  • UNIVERSITY of CALIFORNIA, IRVINE Absinthe's Influence On
    UNIVERSITY OF CALIFORNIA, IRVINE INTOXICATING WOMEN OF THE BELLE ÉPOQUE: Absinthe’s Influence on Painted Depictions of Women During the Bohemian Golden Age THESIS submitted in partial satisfaction of the requirements for the degree of MASTER OF ARTS in Art History by Skye Altamirano Thesis Committee: Professor James Herbert, Chair Associate Professor Roberta Wue Professor Sarah Farmer 2021 © 2021 Skye Tarrah Altamirano DEDICATION To the hopeful cynics, artists, and those who walk amongst the fringe. To Billy, the cats, and too much coffee. “What a delightful thing is the conversation of specialists! One understands absolutely nothing and it’s charming.” - Edgar Degas - ii TABLE OF CONTENTS Acknowledgements ..................................................................................................... iv Abstract of Thesis ......................................................................................................... v Introduction ................................................................................................................... 1 Under the Influence – The Mingling of Art, Women, and Leisure ................................. 4 The Spirit of an Era ..................................................................................................... 10 Absinthe and the Bohemian Woman .......................................................................... 10 Edgar Degas and The Absinthe Drinker (1875-76) .................................................... 14 Distilled Delirium ........................................................................................................
    [Show full text]