The Measurement of Serum Osmolality and Its Application to Clinical
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Hyperosmolar Hyperglycemic State (HHS) Erica Kretchman DO October 19 2018 Speaker for Valeritas, Medtronic, Astrazenica, Boehringer Ingelheim
Hyperosmolar Hyperglycemic State (HHS) Erica Kretchman DO October 19 2018 Speaker for Valeritas, Medtronic, AstraZenica, Boehringer Ingelheim. These do not influence this presentation Objective • Review and understand diagnosis of Hyperosmolar Hyperglycemic State (HHS) and differentiating from Diabetic Ketoacidosis • Treatment of HHS • Complications of HHS Question 1 • Which of the following is NOT a typical finding in HHS? 1. Blood PH <7.30 2. Dehydration 3. Mental Status Changes 4. Osmotic diuresis Question 2 • Hypertonic fluids, such as 3% saline, are the first line of treatment to correct dehydration in HHS 1. True 2. False Question 3 • Which of the following statements is INCORRECT about Hyperosmolar Hyperglycemic State? 1. HHS occurs mainly in type 2 diabetics. 2. This condition presents without ketones in the urine. 3. Metabolic alkalosis presents in severe HHS. 4. Intravenous Regular insulin is used to treat hyperglycemia. Hyperosmolar Hyperglycemic State (HHS) • HHS and DKA are of two of the most serious complications form Diabetes • Hospital admissions for HHS are lower than the rate for DKA and accounts for less than 1 percent of all primary diabetic admissions • Mortality rate for patients with HHS is between 10 and 20 percent, which is approximately 10 times higher than that for DKA • Declined between 1980 and 2009 • Typically from precipitating illness - rare from HHS itself PRECIPITATING FACTORS • The most common events are infection (often pneumonia or urinary tract infection) and discontinuation of or inadequate insulin -
Effect on Ca++. the Clinical Significance of This Observation Re- Suggest That Physiologic Jaundice Results from a Markedly In- Quires Further Evaluation
ABSTRACTS 413 effect on Ca++. The clinical significance of this observation re- suggest that physiologic jaundice results from a markedly in- quires further evaluation. creased load of bilirubin presented to the liver either from increased bilirubin synthesis or enhanced intestinal reabsorb- Controlled clinical trial of phenobarbital (PB) and light for tion and marked limitation in the capacity to conjugate. management of neonatal hyperbilirubinemia in a predomi- Studies performed at 4 hours of age in a monky born 2 weeks nant Negro population. O. S. VALDES, H. M. MAURER, C. N. post-maturely revealed that hepatic transport and conjugation SHUMWAY, D. DRAPER, and A. HOSSAINI. Med. Coll. of Virginia, of bilirubin was fully mature, indicating that maturation of Richmond, Va. (Intr. by W. E. Laupus). each of these functions may occur in utero. Low birth weight infants, less than 24 hrs of age, were randomly assigned to receive either oral PB, 5 mg/kg/day for 5 A controlled study of intravenous fibrin hydrolysate supple- days, blue light (200-300 footcandles) continuously for 4 days, a ment in prematures <1.3 kg. M. HEATHER BRYAN, PATRICK combination of PB and light, or no treatment. 90% or more of WEI, RICHARD HAMILTON, SANFORD H. JACKSON, INGEBORC C. the infants in each group were Negroes. Infants with a positive RADDE, GRAHAM W. CHANCE, and PAUL R. SWYER. Univ. of Coomb's test were excluded. Toronto and The Research Inst., The Hosp. for Sick Children, Toronto, Ont. Canada. We have compared the effect of early supplemental intra- Total serum bilirubin concentration, mg% (mean ± S.E.) venous 3.5% fibrin hydrolysate plus 10% dextrose to 10% No. -
Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder. -
Toxicology and Environmental Teaching Tue 1St Oct 2019
TOXICOLOGY AND ENVIRONMENTAL TEACHING TUE 1ST OCT 2019 CASE ONE The ambulance bring in a 50 year old woman who has been found confused at her home by friends. There is no history available, but she was last seen well around dinner yesterday. She has no known past history and her medications are unknown. Initial Obs: - GCS M 5, E4, V4 pupils large and reactive - SBP 110 - HR 120 - Sats 99% o/a - Afebrile - BSL 8 1. She is confused and denies any ingestion or overdose. She dose state she only took some sleeping medication. What investigations would you do and how would you manage her presentation? Look up NHI: prior hx, community dispensing etc Investigations: Bloods, VBG, ECG Consider differential diagnoses : sepsis, trauma, metabolic 2. You note a community dispensing for 60 x 20mg amitriptyline tablets a few days ago. Her ECG and VBG are shown, please describe and discuss the findings: Potential toxic dose > 10mg/kg onset, toxicity usually rapid onset in 1- 2hrs VBG pH 7.35 PCO2 4.0 HCO3 15 Na 143 K 4.2 Lactate 3.5 - Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2). - Broad QRS complexes. - Positive R’ wave in aVR. ECG Features of Sodium-Channel Blockade Interventricular conduction delay — QRS > 100 ms in lead II Right axis deviation of the terminal QRS: o Terminal R wave > 3 mm in aVR o R/S ratio > 0.7 in aVR Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1) receptor blockade. -
Interpretation of Canine and Feline Urinalysis
$50. 00 Interpretation of Canine and Feline Urinalysis Dennis J. Chew, DVM Stephen P. DiBartola, DVM Clinical Handbook Series Interpretation of Canine and Feline Urinalysis Dennis J. Chew, DVM Stephen P. DiBartola, DVM Clinical Handbook Series Preface Urine is that golden body fluid that has the potential to reveal the answers to many of the body’s mysteries. As Thomas McCrae (1870-1935) said, “More is missed by not looking than not knowing.” And so, the authors would like to dedicate this handbook to three pioneers of veterinary nephrology and urology who emphasized the importance of “looking,” that is, the importance of conducting routine urinalysis in the diagnosis and treatment of diseases of dogs and cats. To Dr. Carl A. Osborne , for his tireless campaign to convince veterinarians of the importance of routine urinalysis; to Dr. Richard C. Scott , for his emphasis on evaluation of fresh urine sediments; and to Dr. Gerald V. Ling for his advancement of the technique of cystocentesis. Published by The Gloyd Group, Inc. Wilmington, Delaware © 2004 by Nestlé Purina PetCare Company. All rights reserved. Printed in the United States of America. Nestlé Purina PetCare Company: Checkerboard Square, Saint Louis, Missouri, 63188 First printing, 1998. Laboratory slides reproduced by permission of Dennis J. Chew, DVM and Stephen P. DiBartola, DVM. This book is protected by copyright. ISBN 0-9678005-2-8 Table of Contents Introduction ............................................1 Part I Chapter 1 Sample Collection ...............................................5 -
Acute Kidney Injury and Chronic Kidney Disease: Classifications and Interventions for Children and Adults Teresa V
Acute Kidney Injury and Chronic Kidney Disease: Classifications and Interventions for Children and Adults Teresa V. Lewis, PharmD, BCPS Assistant Professor of Pharmacy Practice University of Oklahoma College of Pharmacy Adjunct Assistant Professor of Pediatrics University of Oklahoma College of Medicine 1 Disclosures • Teresa V. Lewis, Pharm.D., BCPS • Nothing to disclose Objectives 1. When given specific patient details, identify those with increased Identify which adult or pediatric patients are at risk for development of acute kidney injury (AKI) and recommend appropriate preventive interventions. 2. Design an evidence-based plan to manage AKI for a given patient. 3. Compare and contrast the RIFLE, pRIFLE, and Kidney Disease Improving Global Outcomes (KDIGO) classification systems for AKI. 4. List risk factors for development of chronic kidney disease (CKD). 5. Compare and contrast the Kidney Disease Outcomes Quality Initiative (KDOQI) staging of CKD with the Kidney Disease Improving Global Outcomes (KDIGO) CKD staging criteria. 6. Design an evidence-based plan to prevent progression of CKD for a given patient. 3 Kidney Development and Maturation • Nephrogenesis • Begins around 9 weeks of gestation • Complete by 36 weeks of gestation • Immature renal function at birth • Lower renal blood flow • Immature glomeruli • Immature renal tubule function • Kidney function will be similar to adult values by age 2 years 4 Presentation Outline • Diagnostic Workup • Acute Kidney Injury • Drug Induced Nephrotoxicity • Chronic Kidney Disease 5 DIAGNOSTIC WORK-UP Blood Urea Nitrogen (BUN) • Normal: 8-20 mg/dL • Amino-acids metabolized to ammonia and converted in liver to urea • Urea is filtered and reabsorbed in proximal tubule (dependent on water reabsorption) • Normal BUN:Serum creatinine (Scr) ratio is 10-15:1 • Elevated BUN:Scr ratio suggests true or effective volume depletion 7 Serum Creatinine (Scr) • Freely filtered • Actively secreted • Scr lags behind glomerular filtration rate (GFR) by 1-2 days due to: 1. -
Severe Hyponatremia with Hypouricemia in a Patient with Medullary Hemorrhage: a Case Report
SUTIRTHA CHAKRABORTY, TAPAS K BANERJEE SEVERE HYPONATREMIA WITH HYPOURICEMIA IN A PATIENT WITH MEDULLARY HEMORRHAGE: A CASE REPORT The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine SEVERE HYPONATREMIA WITH HYPOURICEMIA IN A PATIENT WITH MEDULLARY HEMORRHAGE: A CASE REPORT Sutirtha Chakraborty1, Tapas K Banerjee2 1Consultant & Chief, Dept. of Biochemistry, Peerless Hospital & B K Roy Research Centre, Kolkata 700094, India 2Sr. Consultant & Head, Dept. of Neurology, National Neurosciences Centre, Peerless Hospital, Kolkata,India Corresponding Author: Dr Sutirtha Chakraborty, MD Consultant & Chief, Dept. of Biochemistry Peerless Hospital & B K Roy Research Centre, Kolkata 700094 , India e‐mail: [email protected] Mobile +91 9874787638 ABSTRACT Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and occurs due to various causes. Here we present a case of SIADH who was diagnosed using commonly available biochemical tests. This case report also discusses the interaction of the laboratory physician with the treating clinician and the approach needed to arrive at a correct diagnosis. It highlights the importance of serum uric acid and fractional excretion of urinary uric acid in the diagnosis of SIADH. It also discusses the approach needed to distinguish SIADH from Cerebral Salt wasting syndrome, where the presenting feature is also hyponatremia. KEY WORDS Hyponatremia, SIADH, Uric Acid. CASE REPORT A 68 year old gentleman was admitted to the Dept. of Neurology with a history of sudden onset uneasiness followed by slurring of speech and giddiness. Examination by the Consultant Neurologist showed that he was conscious and obeying commands with a Glasgow Coma Scale of 14/15.Power was grade 4/5 in all four limbs and DTRs preserved. -
Reporting Terminology and Codes Chemical Pathology (V3.0)
Standards for Pathology Informatics in Australia (SPIA) Reporting Terminology and Codes Chemical Pathology (v3.0) Superseding and incorporating the Australian Pathology Units and Terminology Standards and Guidelines (APUTS) ISBN: Pending State Health Publication Number (SHPN): Pending Online copyright © RCPA 2017 This work (Standards and Guidelines) is copyright. You may download, display, print and reproduce the Standards and Guidelines for your personal, non- commercial use or use within your organisation subject to the following terms and conditions: 1. The Standards and Guidelines may not be copied, reproduced, communicated or displayed, in whole or in part, for profit or commercial gain. 2. Any copy, reproduction or communication must include this RCPA copyright notice in full. 3. No changes may be made to the wording of the Standards and Guidelines including commentary, tables or diagrams. Excerpts from the Standards and Guidelines may be used. References and acknowledgments must be maintained in any reproduction or copy in full or part of the Standards and Guidelines. Apart from any use as permitted under the Copyright Act 1968 or as set out above, all other rights are reserved. Requests and inquiries concerning reproduction and rights should be addressed to RCPA, 207 Albion St, Surry Hills, NSW 2010, Australia. This material contains content from LOINC® (http://loinc.org). The LOINC table, LOINC codes, LOINC panels and forms file, LOINC linguistic variants file, LOINC/RSNA Radiology Playbook, and LOINC/IEEE Medical Device Code Mapping Table are copyright © 1995-2016, Regenstrief Institute, Inc. and the Logical Observation Identifiers Names and Codes (LOINC) Committee and is available at no cost under the license at http://loinc.org/terms-of-use.” This material includes SNOMED Clinical Terms® (SNOMED CT®) which is used by permission of the International Health Terminology Standards Development Organisation (IHTSDO®). -
Diagnostic Accuracy of Calculated Serum Osmolarity to Predict Dehydration in Older People: Adding Value to Pathology Laboratory Reports
Open Access Research BMJ Open: first published as 10.1136/bmjopen-2015-008846 on 21 October 2015. Downloaded from Diagnostic accuracy of calculated serum osmolarity to predict dehydration in older people: adding value to pathology laboratory reports Lee Hooper,1 Asmaa Abdelhamid,1 Adam Ali,1 Diane K Bunn,1 Amy Jennings,1 W Garry John,2 Susan Kerry,2 Gregor Lindner,3 Carmen A Pfortmueller,4 Fredrik Sjöstrand,5 Neil P Walsh,6 Susan J Fairweather-Tait,1 John F Potter,1,2 Paul R Hunter,1,2 Lee Shepstone1 To cite: Hooper L, ABSTRACT et al Strengths and limitations of this study Abdelhamid A, Ali A, . Objectives: To assess which osmolarity equation best Diagnostic accuracy of predicts directly measured serum/plasma osmolality ▪ – calculated serum osmolarity Dehydration has become a generic term we and whether its use could add value to routine blood to predict dehydration in have clearly described dehydration type (water- older people: adding value to test results through screening for dehydration in older loss dehydration) and used serum osmolality, pathology laboratory reports. people. the correct reference standard. BMJ Open 2015;5:e008846. Design: Diagnostic accuracy study. ▪ Assessment of equations in five different groups doi:10.1136/bmjopen-2015- Participants: Older people (≥65 years) in 5 cohorts: of older people including healthy free-living older 008846 Dietary Strategies for Healthy Ageing in Europe people, frailer people living in residential care, (NU-AGE, living in the community), Dehydration and older people visiting emergency care or ▸ Prepublication history and Recognition In our Elders (DRIE, living in residential staying in hospital, living in several European additional material is care), Fortes (admitted to acute medical care), countries, and including men and women, available. -
Using Osmolality to Diagnose and Treat Hyponatremia in Covid-19 Patients
SCIENTIFIC RESOURCE USING OSMOLALITY TO DIAGNOSE AND TREAT HYPONATREMIA IN COVID-19 PATIENTS ARTICLE SUMMARY Recent publications have shown that COVID-19 (coronavirus disease 2019), an infectious disease caused by a novel coronavirus known as severe acute respiratory syndrome coronavirus (SARS-CoV-2), is associated with electrolyte disorders including hyponatremia.1,2,3 Early diagnosis and etiologic determination are critical in any hyponatremic patient to ensure proper treatment and to avoid potential harm to the patient.4,5 Osmolality testing is quick, inexpensive and effective to help with early detection and diagnosis of hyponatremia.6 Osmolality testing can help ensure that appropriate treatment strategies are implemented early for hyponatremic patients which may be even more significant in patients hospitalized with COVID-19.5,7,8 As clinicians and researchers continue to expand their understanding of COVID-19, additional laboratory testing is important to consider to help better understand and diagnose a COVID-19 patient’s underlying conditions. OSMOLALITY TESTING CAN HELP WITH EARLY DIAGNOSIS AND ETIOLOGICAL DETERMINATION OF HYPONATREMIA, WHICH IS CRITICAL FOR THIS PATIENT POPULATION As association between COVID-19 of hyponatremia. The use of urine and respiratory failure. and hyponatremia has been shown in osmolality to establish a correct Understanding the the literature.1,2,3 Hyponatremia is an underlying diagnosis of hyponatremia is underlying causes electrolyte disorder that occurs when critical to avoid inappropriate treatment -
IFCC Curriculum
The IFCC Curriculum AUTHORS: R. Greaves, J. M. Smith SECTION AUTHORS: R. Greaves, C Florkowski, L. Langman, J. Sheldon The IFCC Curriculum was developed as part of the IFCC eAcademy project by the Committee for Distance Learning. Authors: Janet M Smith [email protected] Ronda Greaves School of Health and Biomedical Sciences - RMIT University, PO Box 71, Bundoora, Victoria 3083 Australia [email protected] Section authors: Evidence Based Laboratory Medicine Section Chris Florkowski Clinical Biochemistry Unit, Canterbury Health Laboratories, PO Box 151, Christchurch, New Zealand [email protected] Immunology Section Jo Sheldon Protein Reference Unit, St. George's Hospital, Blackshaw Road, London SW17 0NH - UK [email protected] Mass Spectrometry Section Ronda Greaves School of Health and Biomedical Sciences - RMIT University, PO Box 71, Bundoora, Victoria 3083 Australia [email protected] Loralie Langman Department of Laboratory Medicine and Pathology Mayo Clinic 200 2nd Street SW Rochester, MN 55905 USA [email protected] Contacts: [email protected] _________________________________________ The IFCC Curriculum - Rev 0 - December 2017 (effective until further revision) 1 Contents INTRODUCTION .................................................................................................................................. 4 SECTION A: Laboratory Organisation and Management .......................................................... 9 Section A1: Laboratory Principles and Procedures: Learning Objectives ...................... -
Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits
MILESTONES IN NEPHROLOGY J Am Soc Nephrol 11: 1776–1788, 2000 Mark A. Knepper, Feature Editor Studies on Mechanisms of Cerebral Edema in Diabetic Comas EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS ALLEN I. ARIEFF AND CHARLES R. KLEEMAN WITH THE TECHNICAL ASSISTANCE OF ALICE KEUSHKERIAN AND HELEN BAGDOYAN From the Departments of Medicine, Wadsworth Veterans Administration Center and Cedars-Sinai Medical Center, and the Cedars-Sinai Medical Research Institute, and University of California Los Angeles Medical Center, Los Angeles, California 90048 with comments by ALLEN I. ARIEFF AND RICHARD STERNS Reprinted from J. Clin. Invest. 52:571–583, 1973 A BSTRACT To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were AUTHOR COMMENTARY evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose = 61 mM), both brain (cerebral cortex) and Allen I. Arieff muscle initially lost about 10% of water content. After 4 h of hyperglycemia, skeletal muscle water content remained low University of California, but that of brain was normal. Brain osmolality (Osm) (343 San Francisco mosmol/kg H2O) was similar to that of cerebrospinal fluid Sausalito, California (CSF) (340 mosmol/kg), but increases in the concentration of Na+, K+, Cl–, glucose, sorbitol, lactate, urea, myoinositol, and amino acids accounted for only about half of this increase. n 1936, Dillon, Riggs, and Dyer described a syndrome The unidentified solute was designated “idiogenic osmoles”. Iwhereby individuals who were being treated for diabetic When plasma glucose was rapidly lowered to normal with coma and apparently recovering suddenly deteriorated, with insulin, there was gross brain edema, increases in brain content worsening of coma, respiratory insufficiency, hypotension, of water, Na+, K+, Cl– and idiogenic osmoles, and a signifi tachycardia, high fever, and death (1).