DOCSLIB.ORG

Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical Practice Guideline

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical Practice Guideline Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical Practice Guideline Note: Active Table of Contents – Click each header below to jump to the section of interest Table of Contents INTRODUCTION .................................................................................................................................. 6 DEFINITIONS ....................................................................................................................................... 6 RECOMMENDATIONS ........................................................................................................................ 7 1. POTASSIUM (K+) ............................................................................................................................. 7 3- 2. PHOSPHATE (PO4 ) ........................................................................................................................ 9 3. MAGNESIUM (MG2+) ...................................................................................................................... 10 4. CALCIUM (CA2+) ............................................................................................................................ 12 5. SLIDING SCALE ELECTROLYTES ............................................................................................... 14 METHODOLOGY ............................................................................................................................... 15 COLLATERAL TOOLS & RESOURCES ........................................................................................... 17 1 Copyright © 2017 University of Wisconsin Hospitals and Clinics Authority Contact: [email protected] Vermeulen, [email protected] Last Revised: 12/2017 Content Expert: Name: Philip Trapskin, PharmD, BCPS – Department of Pharmacy Phone Number: (608) 263-1328 Email Address: [email protected] Contact for Changes: Name: Philip Trapskin, PharmD, BCPS – Department of Pharmacy Phone Number: (608) 263-1328 Email Address: [email protected] Guideline Authors: Emily Jackson, PharmD Sara Shull, PharmD, BCPS Joshua Vanderloo, PharmD, BCPS Original authors: Lindsey Goldsmith, PharmD; Gordon Sacks, PharmD Reviewers: Pierre Kory, MD – Critical Care Kenneth Kudsk, MD – General Surgery Edward Lalik, MD – Hospitalist Joshua Medow, MD – Neurological Surgery Anne O’Connor, MD – Cardiovascular Medicine David Yang, MD – Medical Director of UW Health Clinical Laboratories Theodore Berei, PharmD, BCPS – Cardiovascular Medicine Caitlin Curtis, PharmD, BCNSP – Nutrition Support Jeff Fish, PharmD, BCPS – Critical Care Marie Pietruszka, PharmD, BCPS – General Medicine Committee Approvals: Pharmacy and Therapeutics Committee – December 2017 2 Copyright © 2017 University of Wisconsin Hospitals and Clinics Authority Contact: [email protected] Vermeulen, [email protected] Last Revised: 12/2017 Table 1. UW Health Guidelines for the Use of Oral, Enteral, and Intravenous Electrolytes in Adults1-34 Gastric (NG/OG/PEG) For patients with A Standard Adult IV High-risk Adult IV Electrolyte Concentration Oral enteral access in small Notes dose dose bowel, IV preferred due to adverse GI effects 20 mEq potassium 20 mEq potassium chloride powder packets Use oral/enteral 3.6-3.9 mmol/L chloride 20 mEq (see note 4) (dilute in ~100 mL per supplementation caps/tabs/powder packet, see note 3) 40 mEq potassium 40 mEq potassium Consider oral/enteral 1. If CrCl < 30 mL/min, reduce dose by 50% chloride chloride powder packets 3.1-3.5 mmol/L repletion; 40 mEq 40 mEq (see note 4) 2. For oral doses >20 mEq, divide into Potassium caps/tabs/powder (dilute in ~100 mL per (see note 4) increments of 20 mEq given every 2 hours (see note 2) packet, see note 3) Normal 3. If patient is fluid restricted, dilute oral powder If asymptomatic: may consider combination of enteral reference: in 50 mL and IV repletion with 20 mEq oral potassium chloride 3.5-5.1 4. Intravenous infusion rate: caps/tabs/powder and 40 mEq IV (see note 4) mmol/L 2.5-3.0 mmol/L 60 mEq (see note 4) 60 mEq (see note 4) Peripheral line: max 10 mEq/hour If symptomatic: IV repletion recommended (see IV Central line: max 20 mEq/hour dose columns) < 2.5 mmol/L IV repletion recommended (see IV dose columns) 80 mEq (see note 4) 80 mEq (see note 4) Consider no replacement, except in patients admitted on cardiac units, who have had recent cardiac surgery, or who have cardiac disorders, including arrhythmias, prolonged QTc, and digitalis toxicity, or in 5. If CrCl < 30 mL/min, reduce dose by 50% patients with eclampsia or pre-eclampsia 6. If CrCl < 30 mL/min and using magnesium 1.5-1.8 mg/dL sulfate solution: In these patient populations, consider 0.05 g/kg IV Magnesium 1.5-1.8 mg/dL: Magnesium (see note 8, 9, 10) sulfate solution 2000 mg (dilute in ~50 mL) x 1 dose Magnesium sulfate Magnesium oxide Magnesium 1.1-1.4 mg/dL: Magnesium Magnesium solution 2000 mg (dilute 0.05 g/kg 0.1 g/kg 1.0-1.4 mg/dL elemental tablets 500 mg sulfate solution 2000 mg (dilute in ~50 in ~50 mL) every 4 hours (see note 8, 9, 10) (see note 8, 9, 10) BID x 2 doses mL) every 4 hours x 3 doses Normal x 5 doses 7. See Table 2 for alternative product contents reference: 8. For IV dosing, use actual body weight 1.6-2.6 unless actual is >130% ideal body weight; in mg/dL these cases, use ideal body weight 9. Maximum IV dose is 8g/day 0.1 g/kg 0.15 g/kg 10. Intravenous infusion rate < 1.0 mg/dL IV repletion recommended (see IV dose columns) (see note 8, 9, 10) (see note 8, 9, 10) Infuse doses of ≤ 0.05 g/kg over 12 hours or over 24 hours for supplements >0.05 g/kg Maximum infusion rate is 0.5 to 1 g/hr 3 Copyright © 2017 University of Wisconsin Hospitals and Clinics Authority Contact: [email protected] Vermeulen, [email protected] Last Revised: 12/2017 Gastric (NG/OG/PEG) For patients with A Standard Adult IV High-risk Adult IV Electrolyte Concentration Oral enteral access in small Notes dose dose bowel, IV preferred due to adverse GI effects Phosphate-potassium 11. Consider oral/enteral supplementation in Phosphate-potassium packet (PHOS-NAK Consider no 0.16 mmol/kg (see any asymptomatic patient, or combination of packet (PHOS-NAK C powder) 1 packet every replacement or use notes 15 to 18), oral/enteral and IV. 2.4-3.0 mg/dL powder) 1 packet every 4 hours while awake x 3 oral/enteral consider oral/enteral 12. If CrCl <30 mL/min, reduce IV dose by 50% 4 hours while awake x 3 B,C doses (dilute in ~75 supplementation supplementation 13. If CrCl <30 mL/min, use of phosphorus doses B,C mL) tablet (K-PHOS Neutral) preferred due to Phosphate-potassium lower potassium content: Phosphate-potassium packet (PHOS-NAK 0.16 mmol/kg (see 0.32 mmol/kg (see Phosphate 2.4-3.0 mg/dL: 1 tablet packet (PHOS-NAK powder) 2 (two) packets notes 15 to 18), notes 15 to 18), every 4 hours while awake x 2 doses 1.6-2.3 mg/dL powder) 2 (two) packets every 4 hours while consider oral/enteral consider oral/enteral every 4 hours while Phosphate 1.6-2.3 mg/dL: 1 tablet Phosphate B awake x 3 doses (dilute supplementation supplementation every 4 hours while awake x 3 doses awake x 3 doses B in ~75 mL) Phosphate 1.0-1.5 mg/dL: 1 tablet Normal Phosphorus TABLET (K- every 4 hours while awake x 4 doses reference: Phosphorus TABLET (K- 0.32 mmol/kg (see 15 mmol IV once over 14. See Table 2 for alternative product content PHOS Neutral) 2 (two) 2.3-4.7 PHOS Neutral) 2 (two) notes 15 to 18), 2 hours, then 0.32 15. For IV dosing, use actual body weight 1.0-1.5 mg/dL tablets every 4 hours mg/dL tablets every 4 hours consider oral/enteral mmol/kg (see notes unless actual is >130% ideal body weight; in B (crush & dilute in ~75 while awake x 4 doses B supplementation 15 to 18) mL) these cases, use ideal body weight 16. Maximum IV dose is 45 mmol; recheck phosphate level 6 to 12 hours after dose to determine if further supplementation is 15 mmol IV once over necessary 0.64 mmol/kg (see 2 hours, then 0.64 17. Administer IV dose over 2 to 3 hours for mild < 1.0 mg/dL IV repletion recommended (see IV dose columns) notes 15 to 18) mmol/kg (see notes or moderate hypophosphatemia and over 6 15 to 18) to 8 hours for severe hypophosphatemia 18. Round IV supplementation to the nearest 7.5 or 15 mmol increment 19. Ionized (unbound) calcium concentrations Ionized are preferred over total serum calcium Calcium concentrations for hypocalcemia monitoring 20. Use oral/enteral calcium for asymptomatic Normal Serum:≤4.59 Consider oral/enteral replacement if hypocalcemia ONLY reference: mg/dL Calcium carbonate chew Calcium carbonate D asymptomatic 21. Maximal oral calcium absorption occurs at Serum: 4.6- tabs 1000 mg every 4 suspension 1250 mg 2 g calcium gluconate or 1 g calcium elemental doses ≤500 mg and when given 5.2 mg/dL Whole blood: hours x 4 doses every 4 hours x 4 doses chloride (optimally infused over 2 hours) with a meal Whole ≤4.89 mg/dL 22. For IV administration, calcium gluconate blood: 4.9- preferred due to extravasation risk with 5.6 mg/dL calcium chloride 23. See Table 2 for alternative product contents A High-risk: clinically malnourished, active alcoholism, recent surgery, admitted for cardiac disease, graft-versus-host disease, diabetic ketoacidosis, or undergoing diuresis B Patients with hyperkalemia, impaired renal function, or that require larger doses of phosphate replacement should receive replacement using the phosphorus tablet (K-PHOS Neutral) as it contains less potassium than the phosphate-potassium packet (PHOS-NAK powder) C Replete if: active alcoholism, malnourished, liver cirrhosis,
Load more

Recommended publications
  • Hypokalaemia in a Woman with Eating Disorder
    Grand Rounds Vol 11 pages 53–55 Specialities: Acute Medicine; Nephrology; Psychiatry Article Type: Case Report DOI: 10.1102/1470-5206.2011.0013 ß 2011 e-MED Ltd Hypokalaemia in a woman with eating disorder Zachary Z. Brenera, Boris Medvedovskya, James F. Winchestera and Michael Bergmanb aDivision of Nephrology, Department of Medicine, Beth Israel Medical Center, Albert Einstein School of Medicine of Yeshiva University, New York, USA; bDepartment of Medicine, Campus Golda, Rabin Medical Center, Petah-Tikva, Tel-Aviv University, Israel Corresponding address: Dr Zachary Z. Brener, 350 E. 17th St., Division of Nephrology, Beth Israel Medical Center, New York, NY 10003, USA. Email: [email protected] Date accepted for publication 13 April 2011 Abstract Chronic hypokalaemia often remains a diagnostic challenge, especially in young women without hypertension. A concealed diuretic abuse should be suspected, especially in young women with eating disorders. This case describes a woman with chronic hypokalaemia in whom a thorough medical history and proper laboratory tests were essential to early and accurate diagnosis. Keywords Hypokalaemia; eating disorders; diuretics. Introduction Chronic hypokalaemia often remains a diagnostic challenge, especially in young women without hypertension. After the exclusion of the most obvious causes, a concealed diuretic abuse associated with or without surreptitious vomiting and laxative abuse should be suspected, especially in young women concerned with their body image. A conclusive diagnosis may be difficult as such patients often vigorously deny diuretic intake[1]. Also, only a minority of patients with eating disorders (approximately 6%) abuse diuretics[2–4]. This case describes a woman with chronic hypokalaemia in whom a thorough medical history and proper laboratory tests were essential to an early and accurate diagnosis.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Magnesium: the Forgotten Electrolyte—A Review on Hypomagnesemia
    medical sciences Review Magnesium: The Forgotten Electrolyte—A Review on Hypomagnesemia Faheemuddin Ahmed 1,* and Abdul Mohammed 2 1 OSF Saint Anthony Medical Center, 5666 E State St, Rockford, IL 61108, USA 2 Advocate Illinois Masonic Medical Center, 833 W Wellington Ave, Chicago, IL 60657, USA; [email protected] * Correspondence: [email protected] Received: 20 February 2019; Accepted: 2 April 2019; Published: 4 April 2019 Abstract: Magnesium is the fourth most abundant cation in the body and the second most abundant intracellular cation. It plays an important role in different organ systems at the cellular and enzymatic levels. Despite its importance, it still has not received the needed attention either in the medical literature or in clinical practice in comparison to other electrolytes like sodium, potassium, and calcium. Hypomagnesemia can lead to many clinical manifestations with some being life-threatening. The reported incidence is less likely than expected in the general population. We present a comprehensive review of different aspects of magnesium physiology and hypomagnesemia which can help clinicians in understanding, identifying, and treating this disorder. Keywords: magnesium; proton pump inhibitors; diuretics; hypomagnesemia 1. Introduction Magnesium is one of the most abundant cation in the body as well as an abundant intracellular cation. It plays an important role in molecular, biochemical, physiological, and pharmacological functions in the body. The importance of magnesium is well known, but still it is the forgotten electrolyte. The reason for it not getting the needed attention is because of rare symptomatology until levels are really low and also because of a lack of proper understanding of magnesium physiology.
    [Show full text]
  • Novel Mutations Associated with Inherited Human Calcium-Sensing
    1 180 A García-Castaño, Novel mutations in the calcium 180:1 59–70 Clinical Study L Madariaga and others receptor gene Novel mutations associated with inherited human calcium-sensing receptor disorders: A clinical genetic study Alejandro García-Castaño1,*, Leire Madariaga1,2,*, Gustavo Pérez de Nanclares1,2, Gema Ariceta3, Sonia Gaztambide1,2 and Luis Castaño1,2 on behalf of Spanish Endocrinology Group and Renal Tube Group Correspondence should be addressed 1Biocruces Bizkaia Health Research Institute, CIBERDEM, CIBERER, Barakaldo, Spain, 2Hospital Universitario Cruces, to L Castaño UPV/EHU, Barakaldo, Spain, and 3Hospital Universitario Materno-Infantil Vall d’Hebron, Autonomous University of Email Barcelona, Barcelona, Spain LUISANTONIO. *(A García-Castaño and L Madariaga contributed equally to this work) CASTANOGONZALEZ@ osakidetza.eus Abstract Objective: Molecular diagnosis is a useful diagnostic tool in calcium metabolism disorders. The calcium-sensing receptor (CaSR) is known to play a central role in the regulation of extracellular calcium homeostasis. We performed clinical, biochemical and genetic characterization of sequence anomalies in this receptor in a cohort of 130 individuals from 82 families with suspected alterations in the CASR gene, one of the largest series described. Methods: The CASR gene was screened for mutations by polymerase chain reaction followed by direct Sanger sequencing. Results: Presumed CaSR-inactivating mutations were found in 65 patients from 26 families. These patients had hypercalcemia (median: 11.3 mg/dL) but normal or abnormally high parathyroid hormone (PTH) levels (median: 52 pg/ mL). On the other hand, presumed CaSR-activating mutations were detected in 17 patients from eight families. These patients had a median serum calcium level of 7.4 mg/dL and hypoparathyroidism (median: PTH 13 pg/mL).
    [Show full text]
  • 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.
    [Show full text]
  • VI.2 Elements for a Public Summary VI.2.1 Overview of Disease Epidemiology Vitamin B12 Deficiency Can Have a Number of Possible
    VI.2 Elements for a public summary VI.2.1 Overview of disease epidemiology Vitamin B12 deficiency can have a number of possible causes. Typically it occurs in people whose digestive systems do not adequately absorb the vitamin from the foods they eat. This can be caused by: Pernicious anemia, a condition in where there is a lack of a protein called intrinsic factor. The protein, which is made in the stomach, is necessary for vitamin B12 absorption. Other causes can be gastritis, surgery in which part of the stomach and/or small intestine is removed or conditions affecting the small intestine. Vitamin B12 deficiency can also occur in pregnancy and with long- term use of acid-reducing drugs. VI.2.2 Summary of treatment benefits A deficiency of vitamin B12 (cobalamin) is manifested by fatigue, weakness, mood fluctuations, memory loss, limb weakness, difficulty walking, tingling, and paralysis. Drug treatment involves the administration of vitamin B12 by injection. If the deficiency of vitamin B12 (cobalamin) depends on the underlying disease being resolved, the vitamin supplementation continues until normal levels of vitamin B12 are achieved. If the deficiency state cannot be resolved (e.g. inadequate secretion of intrinsic factor, genetic abnormalities related to the site absorption, etc.) therapy should be continued for life. VI.2.3 Unknowns relating to treatment benefits None. VI.2.4 Summary of safety concerns Risk What is known Preventability Damage to the optic nerve Optic nerve atrophy/blindness The product should be used (atrophy)/blindness in is a risk associated with with caution. patients with Leber´s disease treatment with (a disease that affects the hydroxocobalamin in patients optic nerve and often causes with Leber´s disease.
    [Show full text]
  • Mechanism of Hypokalemia in Magnesium Deficiency
    SCIENCE IN RENAL MEDICINE www.jasn.org Mechanism of Hypokalemia in Magnesium Deficiency Chou-Long Huang*† and Elizabeth Kuo* *Department of Medicine, †Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas ABSTRACT deficiency is likely associated with en- ϩ Magnesium deficiency is frequently associated with hypokalemia. Concomitant hanced renal K excretion. To support magnesium deficiency aggravates hypokalemia and renders it refractory to treat- this idea, Baehler et al.5 showed that ad- ment by potassium. Herein is reviewed literature suggesting that magnesium ministration of magnesium decreases ϩ deficiency exacerbates potassium wasting by increasing distal potassium secre- urinary K excretion and increases se- ϩ tion. A decrease in intracellular magnesium, caused by magnesium deficiency, rum K levels in a patient with Bartter releases the magnesium-mediated inhibition of ROMK channels and increases disease with combined hypomagnesemia potassium secretion. Magnesium deficiency alone, however, does not necessarily and hypokalemia. Similarly, magnesium ϩ cause hypokalemia. An increase in distal sodium delivery or elevated aldosterone replacement alone (without K ) in- ϩ levels may be required for exacerbating potassium wasting in magnesium creases serum K levels in individuals deficiency. who have hypokalemia and hypomag- nesemia and receive thiazide treatment.6 J Am Soc Nephrol 18: 2649–2652, 2007. doi: 10.1681/ASN.2007070792 Magnesium administration decreased urinary Kϩ excretion in these individuals (Dr. Charles Pak, personal communica- Hypokalemia is among the most fre- cin B, cisplatin, etc. Concomitant magne- tion, UT Southwestern Medical Center quently encountered fluid and electro- sium deficiency has long been appreci- at Dallas, July 13, 2007).
    [Show full text]
  • Magnesium Sulfate for Neuroprotection Practice Guideline
    [Type text] [Type text] Updated June 2013 Magnesium Sulfate for Neuroprotection Practice Guideline I. Background: Magnesium sulfate has been suggested to have neuro-protective effect in retrospective studies from 1987 and 1996. Since that time three randomized control trials have been performed to assess magnesium therapy for fetal neuroprotection. These studies have failed to demonstrate statistically significant decrease in combined outcome of cerebral palsy and death or improved overall neonatal survival. However, these results did demonstrate a significant decrease in cerebral palsy of any severity by 30%, particularly moderate-severe cerebral palsy (40-45%). The number needed to treat at less than 32 weeks gestation is 56. The presumptive mechanism of action for magnesium sulfate focuses on the N-methyl-D-aspartate receptor. Additional magnesium effects include calcium channel blockade resulting in cerebrovascular relaxation and magnesium mediated decreases in free radical production and reductions in the production of inflammatory cytokines. Magnesium sulfate should not be used as a tocolytic simply because of the potential for neuro-protective effects. In a recent committee opinion, ACOG states “the available evidence suggests that magnesium sulfate given before anticipated early preterm birth reduces the risk of cerebral palsy in surviving infants” but specific guidelines should be established. “The U.S. FDA has recently changed the classification of magnesium sulfate injection from Category A to Category D. However, this change was based on a small number of neonatal outcomes in cases in which the average duration of exposure was 9.6 weeks. The ACOG Committee on Obstetric Practice and the Society for Maternal-Fetal Medicine continue to support the use of magnesium sulfate in obstetric care for appropriate conditions and for appropriate, short term (usually less than 48 hours) durations of treatment.” II.
    [Show full text]
  • 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.
    [Show full text]
  • Calcium Gluconate
    CALCIUM GLUCONATE CLASSIFICATION Minerals and electrolytes TRADE NAME(S) Calcium Gluconate 10% (for IV use) Calcium Gluconate gel 2.5% (for topical use) DESIRED EFFECTS Lower potassium levels; pain relief and neutralizing fluoride ion MECHANISM OF ACTION Calcium is the primary component of skeletal tissue. Bone serves as a calcium depot and as a reservoir for electrolytes and buffers. INDICATIONS Suspected hyperkalemia in adult PEA/Asystole Antidote for calcium channel blocker overdose and magnesium sulfate toxicity Gel is used for hydrofluoric acid burns Suspected hyperkalemia with adult crush injury or peaked T-waves on EKG CONTRAINDICATIONS Should not be given to patients with digitalis toxicity Should be used with caution in patients with dehydration ADVERSE REACTIONS When given too rapidly or to someone on digitalis, can cause sudden death from ventricular fibrillation May cause mild to severe IV site irritation SPECIAL CONSIDERATIONS Must either use a different IV line or flush line with copious normal saline if being given with sodium bicarbonate. When used on hydroflouric acid burns, relief of pain is the only indication of treatment efficacy. Therefore, use of analgesic agents is not recommended. DOSING REGIMEN Suspected hyperkalemia in adult PEA/asystole or adult crush injury, or evidence of EKG changes (Ex. peaked T-waves) o Calcium gluconate 10% 15-30 ml IV/IO over 2-5 minutes KNOWN calcium channel blocker overdose - administer 3 grams IV/IO may repeat dose in 10 minutes if no effect. Hydrofluoric acid burns apply calcium gluconate gel 2.5% every 15 minutes to burned area and massage continuously until pain disappears.
    [Show full text]
  • Estonian Statistics on Medicines 2016 1/41
    Estonian Statistics on Medicines 2016 ATC code ATC group / Active substance (rout of admin.) Quantity sold Unit DDD Unit DDD/1000/ day A ALIMENTARY TRACT AND METABOLISM 167,8985 A01 STOMATOLOGICAL PREPARATIONS 0,0738 A01A STOMATOLOGICAL PREPARATIONS 0,0738 A01AB Antiinfectives and antiseptics for local oral treatment 0,0738 A01AB09 Miconazole (O) 7088 g 0,2 g 0,0738 A01AB12 Hexetidine (O) 1951200 ml A01AB81 Neomycin+ Benzocaine (dental) 30200 pieces A01AB82 Demeclocycline+ Triamcinolone (dental) 680 g A01AC Corticosteroids for local oral treatment A01AC81 Dexamethasone+ Thymol (dental) 3094 ml A01AD Other agents for local oral treatment A01AD80 Lidocaine+ Cetylpyridinium chloride (gingival) 227150 g A01AD81 Lidocaine+ Cetrimide (O) 30900 g A01AD82 Choline salicylate (O) 864720 pieces A01AD83 Lidocaine+ Chamomille extract (O) 370080 g A01AD90 Lidocaine+ Paraformaldehyde (dental) 405 g A02 DRUGS FOR ACID RELATED DISORDERS 47,1312 A02A ANTACIDS 1,0133 Combinations and complexes of aluminium, calcium and A02AD 1,0133 magnesium compounds A02AD81 Aluminium hydroxide+ Magnesium hydroxide (O) 811120 pieces 10 pieces 0,1689 A02AD81 Aluminium hydroxide+ Magnesium hydroxide (O) 3101974 ml 50 ml 0,1292 A02AD83 Calcium carbonate+ Magnesium carbonate (O) 3434232 pieces 10 pieces 0,7152 DRUGS FOR PEPTIC ULCER AND GASTRO- A02B 46,1179 OESOPHAGEAL REFLUX DISEASE (GORD) A02BA H2-receptor antagonists 2,3855 A02BA02 Ranitidine (O) 340327,5 g 0,3 g 2,3624 A02BA02 Ranitidine (P) 3318,25 g 0,3 g 0,0230 A02BC Proton pump inhibitors 43,7324 A02BC01 Omeprazole
    [Show full text]