Iron Poisoning

Total Page:16

File Type:pdf, Size:1020Kb

Iron Poisoning ,11 Iron Poisoning Jeffrey S. Fine, MD D ron poisoning has always been of particular Iron is a group-VIII transition metal, with electrons interest to pediatricians: children are frequently distributed throughout five 3d orbitals. When iron forms exposed to iron-containing products, and they chemical compounds or complexes with large proteins experience the worst toxicity. The first well-described such as hemoglobin, these electrons shift between cases of iron poisoning were published in the 1940s higher and lower energy orbitals and achieve different and 1950s, the classic animal experiments were per- spin states. 2,4 With this variable electron distribution, formed in the 1950s and 1960s, and the use of the iron can exist in oxidation states between -2 and +6, chelator deferoxamine as an antidote for iron poison- either donate or receive electrons, and achieve variable ing was introduced in the 1960s. redox potentials during electrochemical reactions. Most of what we know about the clinical presentation, This makes iron an ideal mediator of diverse biologi- the pathology, and the pathophysiology of iron poison- cal redox reactions such as when electrons are trans- ing comes from this early work although research con- ferred down the mitochondrial cytochrome chain. tinues. What has changed most over the past 50 years is Table 1 lists some basic facts about the physical chem- the approach to management. As with many types of istry and biochemistry of iron. poisoning, there is now an emphasis on excellent sup- Physiologically, iron exists primarily in 2 stable oxi- portive care with an individualized approach to gastroin- dation states: ferrous iron (Fe +2 or Fe [II]) and ferric testinal decontamination and a selective use of antidotes. iron (Fe +3 or Fe [III]). In aqueous solution Fe +2 is oxi- With this strategy, the deaths related to iron poisoning dized to Fe +3, which often forms insoluble complexes have been reduced to only a small number each year. This at physiologic pH. Iron chelators such as transferrin or article reviews the epidemiologic, clinical, animal, and deferoxamine form soluble complexes with Fe +3. laboratory science related to iron poisoning and its man- A typical American diet contains approximately 15 agement and focuses on several areas of controversy. to 40 mg of iron per day most of which is in the ferric form, which is insoluble at physiologic pH and poorly absorbed. This Fe +3 is released from food proteins and Background reduced to the ferrous form by gastric acid. Iron is the fourth most abundant atomic element in Absorption of dietary iron takes place primarily in the the earth's crust and is found in the minerals hematite, duodenum and upper jejunum and is regulated accord- magnetite, and siderite.~ Biologically, iron is an essen- ing to the state of the body's iron stores. Heme iron is tial nutrient for most living organisms because it is a absorbed better than nonheme iron, and different food component or cofactor of many critical proteins and components may affect iron absorption. For instance, enzymes such as hemoglobin, myoglobin, catalase, ascorbate increases and phytates decrease absorption; xanthine oxidase, aconitase, reduced nicotinamide however the overall effect of food is to decrease iron adenine dinucleotide, ribonucleotide reductase, perox- absorption. The body efficiently recycles iron released idases, and cytochrome oxidase. 2,3 from senescent red blood cells, so the daily require- ment for iron is approximately 1 mg to cover losses of iron in stool, sweat, and urine. Menses accounts for an Jeffrey S. Fine, MD, is Assistant Director of Pediatric Emergency additional need of 1 mg/d for women. Thus approxi- Services at Bellevue Hospital and an assistant professor of Pediatrics mately 10% of dietary iron is absorbed. 1-3 at New York University School of Medicine, New York, New York. The intestinal mucosal cell has few barriers to iron Curr Probl Pediatr 2000;30:71-90. Copyright © 2000 by Mosby, inc. uptake, but once inside the cell the transfer of iron to 0045-9380/2000/$12.00 + .15 53/1,/104055 the plasma is highly regulated. The physiology of iron doi:10.1067/mps.2000.104055 absorption and metabolism is quite complex and out- Curr Probl Pediatr, March 2000 71 TABLE 1. Iron facts Epidemiology of Iron Poisoning Atomic no.: 26 The American Association of Poison Control Centers Atomic weight: 55.85 (AAPCC) is a consortium of 66 regional poison control Density: 7.784 g/cm 3 and information centers located throughout the United Normal serum level: 80-180 pg/dL (1¢32 #mol/L) States. Each year the AAPCC collects standardized epi- Ferrous = Fe+2 or Fe (11) demiologic data about poisonings reported to these cen- Ferric = Fe+3 or Fe (111) ters, and this information is published annually. For Required daily dose: I mg/kg per day (maximum 15 mg) 1997, the AAPCC reported 1.5 million poisoning expo- sures for children and adolescents younger than 20 years. 9 These pediatric exposures accounted for 67% of side the scope of our discussion; the reader is referred all the reported poisoning exposures. Children younger to several recent reviews for more information. 1&5 A than 6 years accounted for 77% of the pediatric expo- typical adult has approximately 3 to 4 g of iron (30-40 sures and 50% of all reported exposures. mg/kg body weight); most of this iron is found in In 1997, there were 26,544 AAPCC-reported expo- hemoglobin or stored as ferritin. Only 3.5 mg (0.1%) sures for all types of iron-containing compounds by circulates in the plasma. 2 children and adolescents accounting for 1.7% of all Iron toxicity is related to the generation of free rad- reported pediatric poisoning exposures; 87% were in icals. 6,7 Both normal and pathologic cellular process- children younger than 6 years. Sixty-two percent of es produce superoxide (02-) and hydrogen peroxide these childhood exposures were to pediatric multivita- (H202) byproducts, whereas enzymes such as super- min tablets, which rarely lead to serious toxicity after oxide dismutase, glutathione peroxidase, and catalase ingestion. Thirty percent of these exposures were to normally metabolize and neutralize these free radicals. adult preparations such as iron pills or prenatal vita- One of the effects of 02 - is the release of stored iron mins with iron, which are responsible for almost all of from ferritin. The free iron reacts with O 2- and H202 the serious toxicity related to iron poisoning. to produce other more reactive and toxic-free radicals Iron-containing products are available in many house- such as the hydroxyl radical: 6,7 holds with young children. Iron pills are prescribed for most pregnant women, and many children are receiving 02- + Fe +3 --~ 02 + Fe +2 multivitamins with iron. Many of the prenatal vitamins are brightly colored, sugar coated, and resemble popu- Fe +2 + H202 --~ Fe +3 + HOo + OH- lar candies, such as M&M's or Good & Plenty (Fig 1). 1° Many children's multivitamins are associated with car- O2o- + H202 --~ O 2 + HOo + OH- toon characters like the Flintstones. In this regard, the The hydroxyl radical (HOo) formed through this comments of Spencer, u written in 1954, seem timely: reaction can depolymerize polysaccharides, cause Now it seems irrational that some things which children are DNA strand breaks, inactivate enzymes, and initiate expected to take, such as cod liver oil, remain unpalatable, lipid peroxidation, which is a self-amplifying process whereas ferrous sulphate tablets, which are intended main- that is particularly damaging to cellular and subcellular ly for adult use, are made both attractive and sweet. membranes. 6,7 For example, when lysosomal mem- The reasons that children ingest drugs are multifactor- branes are destroyed, proteolytic enzymes are released ial and include developmental level, inadequate parental inside the cell, causing further cell damage. If the dam- knowledge about the toxic potential of individual agents age is irreparable, it can also lead to cell death. 8 such as iron, access to medications, imitative behavior, The body protects itself from the toxicity of free iron lack of supervision, and intrafamilial conflict.12,13 by keeping it chelated during almost all phases of Almost all deaths from iron poisoning are in children absorption and distribution. From the enterocyte, iron is younger than 3 years and follow large exposures to adult accepted for transport through the plasma by transferrin, iron preparations (30-40 pills), although death after the a [31-glycoprotein with 2 high-affinity binding sites for ingestion of as few as 5 pills has been reported. 14,15 Fe+3. One third of the body's iron is stored as ferritin, a Early series reported mortality rates of 50% from iron macromolecule capable of binding up to 4500 iron poisoning, which undoubtedly reflected a reporting bias atoms. Sixty percent of this ferritin is in hepatocytes, and for very sick, hospitalized patients. 16 Despite the extra- 40% is in myocytes and reticuloendothelial cells. ordinary number of exposures to iron-containing prod- 72 Curr Probl Pediatr, March 2000 ucts, deaths rarely occur. For the past 10 years, there has been an average of only 3 to 4 deaths per year reported by the AAPCC, although there are sporadic increases; in 1992, 11 childhood deaths were reported.14,17 This num- ber of reported deaths may be an underestimation of the actual incidence, because some deaths are not reported to regional poison control centers. 18 Although mortality statistics are relatively well maintained, data about poisoning morbidity are diffi- cult to ascertain. The AAPCC reports a significant amount of epidemiologic information related to poi- soning, but the annual reports do not stratify all the data according to age.
Recommended publications
  • Pharmacology/Therapeutics Ii Block 1 Handouts – 2015-16
    PHARMACOLOGY/THERAPEUTICS II BLOCK 1 HANDOUTS – 2015‐16 55. H2 Blockers, PPls – Moorman 56. Palliation of Contipation & Nausea/Vomiting – Kristopaitis 57. On‐Line Only – Principles of Clinical Toxicology – Kennedy 58. Anti‐Parasitic Agents – Johnson Histamine Antagonists and PPIs January 6, 2016 Debra Hoppensteadt Moorman, Ph.D. Histamine Antagonists and PPIs Debra Hoppensteadt Moorman, Ph.D. Office # 64625 Email: [email protected] KEY CONCEPTS AND LEARNING OBJECTIVES . 1 To understand the clinical uses of H2 receptor antagonists. 2 To describe the drug interactions associated with the use of H2 receptor antagonists. 3 To understand the mechanism of action of PPIs 4 To describe the adverse effects and drugs interactions with PPIs 5 To understand when the histamine antagonists and the PPIs are to be used for treatment 6 To describe the drugs used to treat H. pylori infection Drug List: See Summary Table. Histamine Antagonists and PPIs January 6, 2016 Debra Hoppensteadt Moorman, Ph.D. Histamine Antagonists and PPIs I. H2 Receptor Antagonists These drugs reduce gastric acid secretion, and are used to treat peptic ulcer disease and gastric acid hypersecretion. These are remarkably safe drugs, and are now available over the counter. The H2 antagonists are available OTC: 1. Cimetidine (Tagamet®) 2. Famotidine (Pepcid®) 3. Nizatidine (Axid®) 4. Ranitidine (Zantac®) All of these have different structures and, therefore, different side-effects. The H2 antagonists are rapidly and well absorbed after oral administration (bioavailability 50-90%). Peak plasma concentrations are reached in 1-3 hours, and the drugs have a t1/2 of 1-3 hours. H2 antagonists also inhibit stimulated (due to feeding, gastrin, hypoglycemia, vagal) acid secretion and are useful in controlling nocturnal acidity – useful when added to proton pump therapy to control “nocturnal acid breakthrough”.
    [Show full text]
  • Skin As a Mirror of Gastrointestinal Diseases
    Review article Skin as a mirror of gastrointestinal diseases Sunil Kumar Gupta1, Amanjot Kaur Arora1, Jasveen Kaur1, Veenu Gupta2, Deepinder Kaur2 Department of Dermatology, Venerology and Leprology1, Department of Microbiology2, Dayanand Medical College and Hospital, Ludhiana, Punjab, India ABSTRACT The closely related origins of the skin and the gastrointestinal system make for a fascinating grouping of diseases with concomitant involvement of these two important organ systems. The dermatologic manifestations may precede clinically evident gastrointestinal disease and help in early diagnosis, saving unnecessary wastage of time and resources. In this overview, we review the cutaneous manifestations of various hereditary, neoplastic and inflammatory gastrointestinal diseases including the various polyposis syndromes, hereditary colorectal cancers, inflammatory bowel diseases, etc. Dermatologic manifestations of acute and chronic hepatic and pancreatic diseases have also been discussed. This review underscores the importance of collaboration between dermatologists and gastroenterologists for better and efficient management of the affected patients. Keywords: Gastrointestinal diseases, Genodermatoses, Hepatitis, Inflammatory bowel disease, Pancreatic diseases, Polyposis syndromes INTRODUCTION diseases with skin and GIT involvement, genodermatoses, and the various hereditary Skin is the largest organ of the body. With a wide surface gastrointestinal cancers. area and being the outermost covering of the human body, skin has proven to be of good diagnostic help or atleast II.Cutaneous manifestations of liver diseases raise the index of suspicion that something inside the covering is wrong. Like many other systemic diseases, III.Cutaneous manifestations of pancreatic diseases. ,gastrointestinal tract (GIT) diseases may present with I. CUTANEOUS MANIFESTATIONS OF cutaneous symptoms, either primarily or secondarily as a GASTROINTESTINAL DISEASES sequalae to gut pathology, embryologic development being responsible for such clinically important associations.
    [Show full text]
  • Wound Classification
    Wound Classification Presented by Dr. Karen Zulkowski, D.N.S., RN Montana State University Welcome! Thank you for joining this webinar about how to assess and measure a wound. 2 A Little About Myself… • Associate professor at Montana State University • Executive editor of the Journal of the World Council of Enterstomal Therapists (JWCET) and WCET International Ostomy Guidelines (2014) • Editorial board member of Ostomy Wound Management and Advances in Skin and Wound Care • Legal consultant • Former NPUAP board member 3 Today We Will Talk About • How to assess a wound • How to measure a wound Please make a note of your questions. Your Quality Improvement (QI) Specialists will follow up with you after this webinar to address them. 4 Assessing and Measuring Wounds • You completed a skin assessment and found a wound. • Now you need to determine what type of wound you found. • If it is a pressure ulcer, you need to determine the stage. 5 Assessing and Measuring Wounds This is important because— • Each type of wound has a different etiology. • Treatment may be very different. However— • Not all wounds are clear cut. • The cause may be multifactoral. 6 Types of Wounds • Vascular (arterial, venous, and mixed) • Neuropathic (diabetic) • Moisture-associated dermatitis • Skin tear • Pressure ulcer 7 Mixed Etiologies Many wounds have mixed etiologies. • There may be both venous and arterial insufficiency. • There may be diabetes and pressure characteristics. 8 Moisture-Associated Skin Damage • Also called perineal dermatitis, diaper rash, incontinence-associated dermatitis (often confused with pressure ulcers) • An inflammation of the skin in the perineal area, on and between the buttocks, into the skin folds, and down the inner thighs • Scaling of the skin with papule and vesicle formation: – These may open, with “weeping” of the skin, which exacerbates skin damage.
    [Show full text]
  • Pressure Ulcer Staging Cards and Skin Inspection Opportunities.Indd
    Pressure Ulcer Staging Pressure Ulcer Staging Suspected Deep Tissue Injury (sDTI): Purple or maroon localized area of discolored Suspected Deep Tissue Injury (sDTI): Purple or maroon localized area of discolored intact skin or blood-fi lled blister due to damage of underlying soft tissue from pressure intact skin or blood-fi lled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, fi rm, mushy, boggy, and/or shear. The area may be preceded by tissue that is painful, fi rm, mushy, boggy, warmer or cooler as compared to adjacent tissue. warmer or cooler as compared to adjacent tissue. Stage 1: Intact skin with non- Stage 1: Intact skin with non- blanchable redness of a localized blanchable redness of a localized area usually over a bony prominence. area usually over a bony prominence. Darkly pigmented skin may not have Darkly pigmented skin may not have visible blanching; its color may differ visible blanching; its color may differ from surrounding area. from surrounding area. Stage 2: Partial thickness loss of Stage 2: Partial thickness loss of dermis presenting as a shallow open dermis presenting as a shallow open ulcer with a red pink wound bed, ulcer with a red pink wound bed, without slough. May also present as without slough. May also present as an intact or open/ruptured serum- an intact or open/ruptured serum- fi lled blister. fi lled blister. Stage 3: Full thickness tissue loss. Stage 3: Full thickness tissue loss. Subcutaneous fat may be visible but Subcutaneous fat may be visible but bone, tendon or muscle are not exposed.
    [Show full text]
  • Angina Bullosa Haemorrhagica (Oral Blood Blister) (PDF)
    Patient Information Maxillo-facial Angina Bullosa Haemorrhagica (Oral Blood Blister) What is Angina Bullosa Haemorrhagica? Angina Bullosa Hemorrhagica (ABH) is a condition where an often painful, but benign blood-filled blister suddenly develops in the mouth. The blisters are generally not due to a blood clotting disorder or any other medical disorder. It is a fairly common, sudden onset and benign blood blistering oral (mouth) disorder. It mainly affects people over 45 years and both males and females are equally affected. Usually there is no family history of the condition. It may be associated with Type 2 Diabetes, a family history of diabetes or Hyperglycaemia. What are the signs and symptoms of ABH? The first indication is a stinging pain or burning sensation just before the appearance of a blood blister The blisters last only a few minutes and then spontaneously rupture (burst), leaving a shallow ulcer that heals without scarring, discomfort or pain They can reach an average size of one to three centimetres in diameter The Soft Palate (back of the mouth) is the most affected site If they occur on the palate and are relatively big, they may need to be de-roofed (cut and drained) to ease the sensation of choking Patient Information Occasionally blisters can occur in the buccal mucosa (cheek) and tongue Approximately one third of the patients have blood blisters in more than one location. What are the causes of ABH? More than 50% of cases are related to minor trauma caused by: hot foods, restorative dentistry (fillings, crowns etc) or Periodontal Therapy (treatment of gum disease).
    [Show full text]
  • Poisoning in Children
    ARTICLE IN PRESS Current Paediatrics (2005) 15, 563–568 www.elsevier.com/locate/cupe Poisoning in children Fiona JepsenÃ, Mary Ryan Emergency Medicine, Royal Liverpool Children’s NHS Trust, Alder Hey, Liverpool L12 2AP, UK KEYWORDS Summary Poisoning accounts for about 7% of all accidents in children under 5 Poisoning; years and is implicated in about 2% of all childhood deaths in the developed world, Child; and over 5% in the developing world (National Poisons Information Service). In Accidents; considering this topic, however, it is important to differentiate accidental overdose Home (common in the younger age groups) and deliberate overdose (more common in young adults). Although initial assessment and treatment of these groups may not differ significantly, the social issues and ongoing follow-up of these children will be totally different and the treating physician must remain aware of this difference. The initial identification and treatment of these children remains the mainstay of management, and many ingested substances do not have a specific antidote. Supportive treatment must be planned and the potential for delayed or long-term effects noted. The specific presentation and treatment of some of the commonly ingested substances will be addressed in this article, and guidance given on when to contact expert help. & 2005 Elsevier Ltd. All rights reserved. Introduction such as bleaches, detergents and turpentine sub- stitutes. More than 100 000 individuals are admitted to Toxic compounds may be ingested or inhaled hospital in England and Wales annually due to either accidentally or deliberately. Accidental poisoning, accounting for 10% of all acute admis- poisoning can occur at any age, but is much more 1 sions.1 However, the true incidence of acute common in children.
    [Show full text]
  • 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.
    [Show full text]
  • Critical Care Nursing of Infants and Children Martha A
    University of Pennsylvania ScholarlyCommons Miscellaneous Papers Miscellaneous Papers 1-1-2001 Critical Care Nursing of Infants and Children Martha A. Q. Curley University of Pennsylvania, [email protected] Patricia A. Moloney-Harmon The Children's Hospital at Sinai Copyright by the author. Reprinted from Critical Care Nursing of Infants and Children, Martha A.Q. Curley and Patricia A. Moloney-Harmon (Editors), (Philadelphia: W.B. Saunders Co., 2001), 1,128 pages. NOTE: At the time of publication, the author, Martha Curley was affiliated with the Children's Hospital of Boston. Currently, she is a faculty member in the School of Nursing at the University of Pennsylvania. This paper is posted at ScholarlyCommons. http://repository.upenn.edu/miscellaneous_papers/4 For more information, please contact [email protected]. Please Note: The full version of this book and all of its chapters (below) can be found on ScholarlyCommons (from the University of Pennsylvania) at http://repository.upenn.edu/miscellaneous_papers/4/ Information page in ScholarlyCommons Full book front.pdf - Front Matter, Contributors, Forward, Preface, Acknowledgements, and Contents Chapter 1.pdf - The Essence of Pediatric Critical Care Nursing Chapter 2.pdf - Caring Practices: Providing Developmentally Supportive Care Chapter_3.pdf - Caring Practices: The Impact of the Critical Care Experience on the Family Chapter_4.pdf - Leadership in Pediatric Critical Care Chapter 5.pdf - Facilitation of Learning Chapter_6.pdf - Advocacy and Moral Agency: A Road Map for
    [Show full text]
  • Chelation Therapy
    Corporate Medical Policy Chelation Therapy File Name: chelation_therapy Origination: 12/1995 Last CAP Review: 2/2021 Next CAP Review: 2/2022 Last Review: 2/2021 Description of Procedure or Service Chelation therapy is an established treatment for the removal of metal toxins by converting them to a chemically inert form that can be excreted in the urine. Chelation therapy comprises intravenous or oral administration of chelating agents that remove metal ions such as lead, aluminum, mercury, arsenic, zinc, iron, copper, and calcium from the body. Specific chelating agents are used for particular heavy metal toxicities. For example, desferroxamine (not Food and Drug Administration [FDA] approved) is used for patients with iron toxicity, and calcium-ethylenediaminetetraacetic acid (EDTA) is used for patients with lead poisoning. Note that disodium-EDTA is not recommended for acute lead poisoning due to the increased risk of death from hypocalcemia. Another class of chelating agents, called metal protein attenuating compounds (MPACs), is under investigation for the treatment of Alzheimer’s disease, which is associated with the disequilibrium of cerebral metals. Unlike traditional systemic chelators that bind and remove metals from tissues systemically, MPACs have subtle effects on metal homeostasis and abnormal metal interactions. In animal models of Alzheimer’s disease, they promote the solubilization and clearance of β-amyloid protein by binding to its metal-ion complex and also inhibit redox reactions that generate neurotoxic free radicals. MPACs therefore interrupt two putative pathogenic processes of Alzheimer’s disease. However, no MPACs have received FDA approval for treating Alzheimer’s disease. Chelation therapy has also been investigated as a treatment for other indications including atherosclerosis and autism spectrum disorder.
    [Show full text]
  • Toxicology Review ◼ Organophosphates ◼ Cocaine ◼ ◼ Amphetamines Local Anesthetics ◼ Narcotics ◼ Mushrooms David Donaldson, D.O
    1/11/2019 Objectives ◼ Drugs of abuse ◼ Lithium ◼ Benzodiazepines ◼ Heavy metals ◼ Barbiturates ◼ Cyanide/Hydrogen sulfate ◼ Hallucinogens Toxicology Review ◼ Organophosphates ◼ Cocaine ◼ ◼ Amphetamines Local anesthetics ◼ Narcotics ◼ Mushrooms David Donaldson, D.O. ◼ Rave drugs ◼ Plants Emergency Medicine ◼ Isoniazid William Beaumont Hospital ◼ Hypoglycemics ◼ Inhalation toxins ◼ Biologic hazards 1 2 Benzodiazepines ◼ Stimulation of the benzodiazepine receptor ◼ Increases the sensitivity of the GABA receptor complex ◼ Leads to inhibitory effects ◼ Lipid soluble 3 4 Clinical Features Treatment ◼ CNS ◼ Activated charcoal ◼ Drowsiness ◼ Elimination enhancement ◼ Dizziness ◼ Not effective ◼ Slurred speech ◼ Respiratory support ◼ Confusion ◼ Ataxia ◼ Paradoxical reactions ◼ Respiratory depression 5 6 1 1/11/2019 Flumazenil ◼ Selective antagonist ◼ 0.2mg IV q minute (total of 3mg) ◼ Seizure Activity ◼ Co-ingestions ◼ Physically dependent on Benzodiazepines ◼ History of seizures 7 8 Barbiturates Barbiturates ◼ Lipid soluble ◼ Pharmacology ◼ Mimics ETOH intoxication ◼ Enhances the action of GABA receptors ◼ Lack of coordination ◼ Inhibits noradrenergic excitation at neuronal junctions ◼ Slurred speech ◼ Impaired thinking ◼ Skin bullae ◼ 6% 9 10 Barbiturates Treatment ◼ Mortality ◼ Airway ◼ Early ◼ Activated charcoal ◼ Cardiovascular ◼ Multi-dose ◼ Late ◼ Fluid support ◼ Pulmonary ◼ Alkalinization of urine ◼ Increases the excretion rate (5 to 10 fold) ◼ Hemodialysis ◼ 6 to 9 times more effective than alkalinization 11 12 2 1/11/2019 Hallucinogens
    [Show full text]
  • CLINICAL RESEARCH PROJECT Protocol #11-H-0134 Drug Name: Eltrombopag (Promacta®) IND Number: 104,877 IND Holder: NHLBI OCD Date: January 2, 2019
    CLINICAL RESEARCH PROJECT Protocol #11-H-0134 Drug Name: eltrombopag (Promacta®) IND number: 104,877 IND holder: NHLBI OCD Date: January 2, 2019 Title: A Pilot Study of a Thrombopoietin-receptor Agonist (TPO-R agonist), Eltrombopag, in Moderate Aplastic Anemia Patients Other Identifying Words: Hematopoiesis, autoimmunity, thrombocytopenia, neutropenia, anemia, stem cells, cytokine, Promacta® (eltrombopag) Protocol Principal Investigator: *Cynthia E. Dunbar, M.D., TSCBB, NHLBI (E) Medically and Scientifically Responsible Investigator: *Cynthia E. Dunbar, M.D., TSCBB, NHLBI (E) Associate Investigators: *Georg Aue, M.D., OCD, NHLBI (E) *Neal S. Young, M.D., Chief, HB, NHLBI (E) *André Larochelle, M.D., Ph.D., CMTB, NHLBI (E) David Young, M.D., TSCBB, NHLBI (E) Susan Soto, M.S.N., R.N., Research Nurse, OCD, NHLBI(E) Olga Rios, RN, Research Nurse, OCD, NHLBI (E) Evette Barranta, R.N, Research Nurse, OCD, NHLBI (E) Jennifer Jo Kyte, DNP, Research Nurse, OCD, NHLBI (E) Colin Wu, PhD, Biostatistician, OBR, NHLBI (E) Xin Tian, PhD, Biostatistician, OBR/NHLBI (E) *Janet Valdez, MS, PAC, OCD, NHLBI (E) *Jennifer Lotter, MSHS, PA-C., OCD, NHLBI (E) Qian Sun, Ph.D., DLM, CC (F) Xing Fan, M.D., HB, NHLBI (F) Non-NIH, Non-Enrolling Engaged Investigators: Thomas Winkler, M.D., NHLBI, HB (V)# # Covered under the NIH FWA Independent Medical Monitor: John Tisdale, MD, NHLBI, OSD 402-6497 Bldg. 10, 9N116 * asterisk denotes who can obtain informed consent on this protocol Subjects of Study: Number Sex Age-range 38 Either ≥ 2 years and weight >12 kg Project Involves Ionizing Radiation? No (only when medically indicated) Off-Site Project? No Multi center trial? No DSMB Involvement? Yes 11-H-0134 1 Cynthia E.
    [Show full text]
  • Study About the Efficacy of an Aerosol Plastic Dressing in Wound
    1.0 ANCC CE Contact Hours Study About the Effi cacy of an Aerosol Plastic Dressing in Wound Prevention After Compressive Adhesive Dressing Application in Plastic Surgery Procedures Enrique Salmerón-González , MD Elena García-Vilariño , MD Pilar Vilariño-López , MD Cristina García-Pons , MD Cristina Escalante-Ibáñez , MD Alfonso A. Valverde-Navarro , MD The use of compressive adhesive bandages is widely men placed over a layer of an aerosol plastic dressing and extended in the fi eld of plastic, aesthetic, and reconstruc- another bandage placed directly over the skin. A statisti- tive surgery, and the apparition of skin damage after its cally signifi cant decrease in skin damage incidence was removal is a relatively frequent complication. The aim observed in areas in which the aerosol plastic dressing of this study was to evaluate the capacity of an aerosol was applied as a layer between the adhesive dressing and plastic dressing for protecting the skin from the apparition the skin. Furthermore, a reduction in symptoms associ- of damage caused by adhesive dressings. A prospective, ated with the use of these adhesive dressings was found. randomized, simple-blind study was performed, evaluating The results of this study support the use of aerosol plastic skin damage incidence after removal of adhesive compres- dressings as a barrier for skin protection in patients in sive bandages in 80 subjects. The patients carried for whom an adhesive compressive dressing is applied to 48 hr an adhesive compressive dressing on their abdo- reduce the incidence of skin damage. he use of adhesive compressive dressings is established seromas ( Rogliani, Gentile, & Cervelli, 2008 ).
    [Show full text]