Acute Hyperkalemia and Hyponatremia Following
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Hyponatremia and Hypernatremia MICHAEL M
This is a corrected version of the article that appeared in print. Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia MICHAEL M. BRAUN, DO, Madigan Army Medical Center, Tacoma, Washington CRAIG H. BARSTOW, MD, Womack Army Medical Center, Fort Bragg, North Carolina NATASHA J. PYZOCHA, DO, Madigan Army Medical Center, Tacoma, Washington Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the patho- physiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit. Am( Fam Physician. 2015;91(5):299-307. Copy- right © 2015 American Academy of Family Physicians.) More online yponatremia is a common elec- a worse prognosis in patients with liver cir- at http://www. trolyte disorder defined as a rhosis, pulmonary hypertension, myocardial aafp.org/afp. serum sodium level of less than infarction, chronic kidney disease, hip frac- CME This clinical content 135 mEq per L.1-3 A Dutch sys- tures, and pulmonary embolism.1,8-10 conforms to AAFP criteria Htematic review of 53 studies showed that the for continuing medical Etiology and Pathophysiology education (CME). -
1 Fluid and Elect. Disorders of Serum Sodium Concentration
DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol. -
Study Guide Medical Terminology by Thea Liza Batan About the Author
Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails proficiencyincommunicatingwithhealthcareprofessionalssuchasphysicians,nurses, or dentists. -
Hyperkalemia Masked by Pseudo-Stemi Infarct Pattern and Cardiac Arrest Shareez Peerbhai1 , Luke Masha2, Adrian Dasilva-Deabreu1 and Abhijeet Dhoble1,2*
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 International Journal of DOI 10.1186/s12245-017-0132-0 Emergency Medicine CASEREPORT Open Access Hyperkalemia masked by pseudo-stemi infarct pattern and cardiac arrest Shareez Peerbhai1 , Luke Masha2, Adrian DaSilva-DeAbreu1 and Abhijeet Dhoble1,2* Abstract Background: Hyperkalemia is a common electrolyte abnormality and has well-recognized early electrocardiographic manifestations including PR prolongation and symmetric T wave peaking. With severe increase in serum potassium, dysrhythmias and atrioventricular and bundle branch blocks can be seen on electrocardiogram. Although cardiac arrest is a worrisome consequence of untreated hyperkalemia, rarely does hyperkalemia electrocardiographically manifest as acute ischemia. Case presentation: We present a case of acute renal failure complicated by malignant hyperkalemia and eventual ventricular fibrillation cardiac arrest. Recognition of this disorder was delayed secondary to an initial ECG pattern suggesting an acute ST segment elevation myocardial infarction (STEMI). Emergent coronary angiography performed showed no evidence of coronary artery disease. Conclusions: Pseudo-STEMI patterns are rarely seen in association with acute hyperkalemia and are most commonly described with patient without acute cardiac symptomatology. This is the first such case presenting concurrently with cardiac arrest. A brief review of this rare pseudo-infarct pattern is also given. Keywords: Cardiac arrest, Hyperkalemia, Myocardial infarction, STEMI, ECG Background Case presentation Hyperkalemia that manifests with electrocardiographic A 27-year-old Caucasian male with a past medical his- findings of an ST segment elevation myocardial infarc- tory of hypertension presented to the emergency room tion (STEMI) is very rare. -
Electrolyte and Acid-Base Disorders Triggered by Aminoglycoside Or Colistin Therapy: a Systematic Review
antibiotics Review Electrolyte and Acid-Base Disorders Triggered by Aminoglycoside or Colistin Therapy: A Systematic Review Martin Scoglio 1,* , Gabriel Bronz 1, Pietro O. Rinoldi 1,2, Pietro B. Faré 3,Céline Betti 1,2, Mario G. Bianchetti 1, Giacomo D. Simonetti 1,2, Viola Gennaro 1, Samuele Renzi 4, Sebastiano A. G. Lava 5 and Gregorio P. Milani 2,6,7 1 Faculty of Biomedicine, Università della Svizzera Italiana, 6900 Lugano, Switzerland; [email protected] (G.B.); [email protected] (P.O.R.); [email protected] (C.B.); [email protected] (M.G.B.); [email protected] (G.D.S.); [email protected] (V.G.) 2 Department of Pediatrics, Pediatric Institute of Southern Switzerland, Ospedale San Giovanni, Ente Ospedaliero Cantonale, 6500 Bellinzona, Switzerland; [email protected] 3 Department of Internal Medicine, Ospedale La Carità, Ente Ospedaliero Cantonale, 6600 Locarno, Switzerland; [email protected] 4 Division of Hematology and Oncology, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada; [email protected] 5 Pediatric Cardiology Unit, Department of Pediatrics, Centre Hospitalier Universitaire Vaudois, and University of Lausanne, 1011 Lausanne, Switzerland; [email protected] 6 Pediatric Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy 7 Department of Clinical Sciences and Community Health, Università degli Studi di Milano, 20122 Milan, Italy * Correspondence: [email protected] Citation: Scoglio, M.; Bronz, G.; Abstract: Aminoglycoside or colistin therapy may alter the renal tubular function without decreasing Rinoldi, P.O.; Faré, P.B.; Betti, C.; the glomerular filtration rate. This association has never been extensively investigated. -
Is There a Relationship Between COVID-19 and Hyponatremia?
medicina Review Is There a Relationship between COVID-19 and Hyponatremia? Gina Gheorghe 1,2,†, Madalina Ilie 1,2, Simona Bungau 3,† , Anca Mihaela Pantea Stoian 4 , Nicolae Bacalbasa 5 and Camelia Cristina Diaconu 6,7,* 1 Department of Gastroenterology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; [email protected] (G.G.); [email protected] (M.I.) 2 Department of Gastroenterology, Clinical Emergency Hospital of Bucharest, 105402 Bucharest, Romania 3 Department of Pharmacy, Faculty of Medicine and Pharmacy, University of Oradea, 410028 Oradea, Romania; [email protected] 4 Department of Diabetes, Nutrition and Metabolic Diseases, “Carol Davila” University of Medicine and Pharmacy, 020475 Bucharest, Romania; [email protected] 5 Department of Visceral Surgery, Center of Excellence in Translational Medicine, Fundeni Clinical Institute, 022328 Bucharest, Romania; [email protected] 6 Department of Internal Medicine, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania 7 Department of Internal Medicine, Clinical Emergency Hospital of Bucharest, 105402 Bucharest, Romania * Correspondence: [email protected]; Tel.: +40-0726-377-300 † This author has equal contribution to the paper as the first author. Abstract: Nowadays, humanity faces one of the most serious health crises, the severe acute respi- ratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. The severity of coronavirus disease 2019 (COVID-19) pandemic is related to the high rate of interhuman transmission of the virus, variability of clinical presentation, and the absence of specific therapeutic methods. COVID-19 can manifest with non-specific symptoms and signs, especially among the elderly. In some cases, the clinical manifestations of hyponatremia may be the first to appear. -
Serum Sodium Concentration [Na+] Less Than 135 Meq/L. INCIDENCE
HYPONATREMIA DEFINITION: Serum sodium concentration [Na+] less than 135 mEq/L. INCIDENCE IN CRITICAL ILLNESS: 30%. (The most common electrolyte abnormality encountered in clinical medicine.) ETIOLOGY: Hypo-osmolar hyponatremia: Serum osmolality is low (< 280 mOsm/kg H2O). Hypovolemic: Total body water deficit + greater degree of total body sodium deficit. o Renal losses (urine [Na+] > 20 mmol/L): Diuretic excess; mineralocorticoid deficiency; cerebral salt wasting; bicarbonaturia (renal tubular acidosis and metabolic alkalosis); ketonuria; osmotic diuresis. o Extrarenal losses (urine [Na+] < 20 mmol/L): Vomiting; diarrhea; “third spacing” (burns, pancreatitis, trauma). Euvolemic: Total body water excess + normal total body sodium. o The most common subcategory of hyponatremia. o Includes dilutional hyponatremia. Excess of water relative to sodium; serum chloride concentration is usually normal. o Includes SIADH: Diagnosis of exclusion. Inclusion criteria are plasma osmolality < 270 mOsm/kg + H2O; urine osmolality > 100 mOsm/kg H2O; euvolemia; urine [Na ] elevated; adrenal, thyroid, pituitary, renal insufficiency absent; diuretic use absent. o Urine [Na+] is typically > 20 mmol/L. o Glucocorticoid deficiency; hypothyroidism; stress; medications (vasopressin analogs, drugs that enhance vasopressin release, drugs that potentiate renal action of vasopressin, haloperidol, amitriptyline, other psychotropic medications). Hypervolemic: Total body water excess >>> total body sodium excess. o Urine [Na+] > 20 mmol/L: Renal failure. o Urine -
The Prognostic Effects of Hyponatremia and Hyperchloremia on Postoperative NSCLC Patients
Current Problems in Cancer 43 (2019) 402–410 Contents lists available at ScienceDirect Current Problems in Cancer journal homepage: www.elsevier.com/locate/cpcancer The prognostic effects of hyponatremia and hyperchloremia on postoperative NSCLC patients Wei Li a,b,1, Xiaowei Chen a,1, Liguang Wang a,c, Yu Wang a, ∗ Cuicui Huang a, Guanghui Wang a,d, Jiajun Du a,d, a Institute of Oncology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, PR China b Department of Thoracic Surgery, Shandong Juxian People’s Hospital, Rizhao, PR China c Department of Oncology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, PR China d Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, PR China a b s t r a c t Electrolytic disorders are common in lung cancer patients. But the association between serum electrolytes levels and survival in patients undergoing lung cancer resections for non–small-cell lung cancer (NSCLC) has been poorly inves- tigated. A retrospective study was conducted on consecutive postoperative NSCLC patients. Pearson’s test was used to determine the association between serum sodium and chlorine levels and clinical characteristics, and cox regression and Kaplan-Meier model were applied to analyze risk factors on overall survival. We found that hyponatremia was an independent prognostic factor associated with poor prognosis in NSCLC patients undergoing complete resection (log-rank test, P = 0.004). In addition, we found that hyperchloremia predicted a poor clinical outcome in patients with non-anion-gap (log-rank test, P = 0.011), whereas it predicted a favorable clinical outcome in patients with high- anion-gap (log-rank test, P = 0.002). -
Electrolyte Disorders and Arrhythmogenesis
Cardiology Journal 2011, Vol. 18, No. 3, pp. 233–245 Copyright © 2011 Via Medica REVIEW ARTICLE ISSN 1897–5593 Electrolyte disorders and arrhythmogenesis Nabil El-Sherif1, Gioia Turitto2 1State University of NY, Downstate Medical Center and NY Harbor VA Healthcare System, Brooklyn, NY, USA 2Methodist University Hospital, Brooklyn, NY, USA Abstract Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mecha- nisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of elec- trolyte disorders. Potassium (K+) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most signifcant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and + non cardiac drugs are known to suppress the HERG K channel and hence the IK, and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricu- lar tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia de- pends on serum K+ level. At 5.5–7.0 mmol/L K+, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K+, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca++) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathy- roidism, results in shortening of both intervals. -
Hypercalcemia and Hyponatremia
Hypercalcemia and Hyponatremia Santosh Reddy MD FACP Assistant Professor Scott & White/Texas A&M Etiology of Hypercalcemia Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. Sources of calcium are most commonly the bone or the gastrointestinal tract Etiology Hypercalcemia is a relatively common clinical problem. Elevation in the physiologically important ionized (or free) calcium concentration. However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin; , increased protein binding causes elevation in the serum total calcium. Increased bone resorption Primary and secondary hyperparathyroidism Malignancy Hyperthyroidism Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid Increased intestinal calcium absorption Increased calcium intake Renal failure (often with vitamin D supplementation) Milk-alkali syndrome Hypervitaminosis D Enhanced intake of vitamin D or metabolites Chronic granulomatous diseases (eg, sarcoidosis) Malignant lymphoma Acromegaly Pseudocalcemia Hyperalbuminemia 1) severe dehydration 2) multiple myeloma who have a calcium- binding paraprotein. This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia) Other causes Familial hypocalciuric hypercalcemia Chronic lithium intake Thiazide diuretics Pheochromocytoma Adrenal insufficiency Rhabdomyolysis and acute renal failure Theophylline toxicity Immobilization -
Medical Term Lay Term(S)
MEDICAL TERM LAY TERM(S) ABDOMINAL Pertaining to body cavity below diaphragm which contains stomach, intestines, liver, and other organs ABSORB Take up fluids, take in ACIDOSIS Condition when blood contains more acid than normal ACUITY Clearness, keenness, esp. of vision - airways ACUTE New, recent, sudden ADENOPATHY Swollen lymph nodes (glands) ADJUVANT Helpful, assisting, aiding ADJUVANT Added treatment TREATMENT ANTIBIOTIC Drug that kills bacteria and other germs ANTIMICROBIAL Drug that kills bacteria and other germs ANTIRETROVIRAL Drug that inhibits certain viruses ADVERSE EFFECT Negative side effect ALLERGIC REACTION Rash, trouble breathing AMBULATE Walk, able to walk -ATION -ORY ANAPHYLAXIS Serious, potentially life threatening allergic reaction ANEMIA Decreased red blood cells; low red blood cell count ANESTHETIC A drug or agent used to decrease the feeling of pain or eliminate the feeling of pain by general putting you to sleep ANESTHETIC A drug or agent used to decrease the feeling of pain or by numbing an area of your body, local without putting you to sleep ANGINA Pain resulting from insufficient blood to the heart (ANGINA PECTORIS) ANOREXIA Condition in which person will not eat; lack of appetite ANTECUBITAL Area inside the elbow ANTIBODY Protein made in the body in response to foreign substance; attacks foreign substance and protects against infection ANTICONVULSANT Drug used to prevent seizures ANTILIPIDEMIC A drug that decreases the level of fat(s) in the blood ANTITUSSIVE A drug used to relieve coughing ARRHYTHMIA Any change from the normal heartbeat (abnormal heartbeat) ASPIRATION Fluid entering lungs ASSAY Lab test ASSESS To learn about ASTHMA A lung disease associated with tightening of the air passages ASYMPTOMATIC Without symptoms AXILLA Armpit BENIGN Not malignant, usually without serious consequences, but with some exceptions e.g. -
Cerebral Salt Wasting: Truths, Fallacies, Theories, and Challenges
Journal Article Page 1 of 10 Use of this content is subject to the Terms and Conditions of the MD Consult web site. Critical Care Medicine Volume 30 • Number 11 • November 2002 Copyright © 2002 Lippincott Williams & Wilkins REVIEW ARTICLE Cerebral salt wasting: Truths, fallacies, theories, and challenges Sheila Singh, MD; Desmond Bohn, MB; Ana P. C. P. Carlotti; Michael Cusimano, MD; James T. Rutka; Mitchell L. Halperin, MD From the Departments of Pediatric Neurosurgery (SS, JTR) and Critical Care Medicine (DB), Hospital for Sick Children, Toronto, Canada; the Department of Anaesthesiology, University of Toronto, Toronto, Canada (DB); the Department of Pediatrics, Universidade de Sao Paulo, Ribeirao Preto, Brazil (APCPC); and the Department of Neurosurgery (MC) and Renal Division (MLH), St. Michael’s Hospital, University of Toronto, Toronto, Canada. Supported, in part, by a grant from Physicians Services Incorporated. Address requests for reprints to: Mitchell L. Halperin, MD, Division of Nephrology, St. Michael’s Hospital, Annex, 38 Shuter Street, Toronto, Ontario M5B 1A6, Canada. E-mail: [email protected] Cerebral salt wasting is a diagnosis of exclusion that requires a natriuresis in a patient with a contracted effective arterial blood volume and the absence of another cause for this excretion of Na+ . Background: The reported prevalence of cerebral salt wasting has increased in the past three decades. A cerebral lesion and a large natriuresis without a known stimulus to excrete so much sodium (Na+ ) constitute its essential two elements. Objectives: To review the topic of cerebral salt wasting. There is a diagnostic problem because it is difficult to confirm that a stimulus for the renal excretion of Na+ is absent.