Refeeding Syndrome and Other Related Issues in the Paediatric Intensive Care Unit
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Refeeding Syndrome Relevance for Critically Ill Patients
Central European Journal of Clinical Research Volume 2, Issue 1, Pages 48-50 DOI: 10.2478/cejcr-2019-0007 REVIEW Refeeding syndrome relevance for critically ill patients María Bermúdez López1 1 Servicio Anestesiología, Reanimación y Terapéutica del Dolor. Hospital Universitario Lucus Augusti. Lugo. 27003. España. Correspondence to: María Bermúdez López, Servicio Anestesiología, Reanimación y Terapéutica del Dolor. Hospital Universitario Lucus Augusti. E-mail:[email protected] Conflicts of interests Nothing to declare Acknowledgment None Funding: This research did not receive any specific grant from funding agencies in the public, commercial or not-for profit sectors. Keywords: refeeding syndrome, hypophosphatemia, thiamine, nutritional support, malnutrition. These authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation. Central Eur J Clin Res 2019;2(1):48-50 _____________________________________________________________________________ Received: 05.03.2019, Accepted: 30.03.2019, Published: 10.04.2019 Copyright © 2018 Central European Journal of Clinical Research. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. It is essential to know that the high morbidity and mortality can be reduced by ear- ABSTRACT ly diagnosis and taking appropriate measures. Therefore, to be aware of this metabolic con- Refeeding Syndrome (RFS) is a poten- dition in critically ill patients is necessary for its tial life-threatening complication of the nutrition- prevention, recognition, and treatment. Despite al therapy in the replenishment phase after peri- many pathophysiological aspects of RFS re- od of starvation. -
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. -
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. -
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. -
Guidelinesonparenteral Nutrition, Chapter 11
Special Issue OPEN ACCESS Review Article Complications and Monitoring – Guidelines on Parenteral Nutrition, Chapter 11 Komplikationen und Monitoring – Leitlinie Parenterale Ernährung, Kapitel 11 Abstract Compared to enteral or hypocaloric oral nutrition, the use of PN (par- W. H. Hartl1 enteral nutrition) is not associated with increased mortality, overall K. W. Jauch1 frequency of complications, or longer length of hospital stay (LOS). The 2 risk of PN complications (e.g. refeeding-syndrome, hyperglycaemia, K. Parhofer bone demineralisation, catheter infections) can be minimised by carefully P. Rittler1 monitoring patients and the use of nutrition support teams particularly Working group for during long-term PN. Occuring complications are e.g. the refeeding- syndrome in patients suffering from severe malnutrition with the initi- developing the ation of refeeding or metabolic, hypertriglyceridemia, hyperglycaemia, guidelines for osteomalacia and osteoporosis, and hepatic complications including parenteral nutrition of fatty liver, non-alcoholic fatty liver disease, cholestasis, cholecystitis, The German and cholelithiasis. Efficient monitoring in all types of PN can result in Association for reduced PN-associated complications and reduced costs. Water and electrolyte balance, blood sugar, and cardiovascular function should Nutritional Medicine regularly be monitored during PN. Regular checks of serum electrolytes and triglycerides as well as additional monitoring measures are neces- 1 Dept. Surgery Grosshadern, sary in patients with altered renal function, electrolyte-free substrate University Hospital, Munich, intake, lipid infusions, and in intensive care patients. The metabolic Germany monitoring of patients under long-term PN should be carried out accord- 2 Dept. Medicine II, University ing to standardised procedures. Monitoring metabolic determinants of of Munich, Germany bone metabolism is particularly important in patients receiving long- term PN. -
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). -
Refeeding Syndrome: to Feed Or Not to Feed? Mayumi Nakamura, MPH, RD, CNSC, CSP Lauren Okamura, RD, CNSC
Refeeding Syndrome: To Feed or Not To Feed? Mayumi Nakamura, MPH, RD, CNSC, CSP Lauren Okamura, RD, CNSC 1 Objectives • Define refeeding syndrome and identify patients at risk • Identify risk factors, signs and symptoms and lab alterations that characterize refeeding syndrome • Implement safe feeding advancement practices for pediatric patients with or at risk for refeeding syndrome 2 Refeeding Syndrome Definition • Potential life-threatening metabolic condition in which there are severe shifts in electrolytes and fluid in malnourished patients who are undergoing aggressive refeeding whether orally, enterally or parenterally. • The hallmark biochemical feature is hypophosphatemia. • Refeeding syndrome also commonly causes hypomagnesemia and hypokalemia, thiamine deficiency, sodium and fluid imbalances and alteration in glucose. 3 Refeeding Syndrome Metabolism • During starvation, the body switches from carbohydrates to fat and protein as the main source of energy. Intracellular minerals become depleted yet serum concentrations may remain normal. This happens because the intracellular compartment contracts during starvation. • Once fed, during anabolism, the body switches back to carbohydrates as the main source of energy and there is a surge of insulin when glucose enters the blood. Insulin stimulates the absorption of phosphorus, potassium, magnesium and water into the cell. This process decreases serum levels of these minerals which are already depleted. Sodium and water retention can occur due to decreased renal excretion and cause extracellular fluid overload. Edema can also occur due to low serum albumin levels decreasing oncotic pressure. 4 Symptoms of Refeeding 5 Refeeding Syndrome Who’s at risk? • >10% wt loss in 1-2 months • Underfeeding or fasting for 7-14 days • Protein calorie malnutrition • Medical neglect/Social issues • Diagnoses at higher risk – FTT – Anorexia Nervosa – Oncology – Malabsorptive syndromes and GI diseases – Uncontrolled DM 6 Beginning Nutrition Support • Identify who is at risk for refeeding syndrome. -
An Infant with Chronic Hypernatremia
European Journal of Endocrinology (2006) 155 S141–S144 ISSN 0804-4643 An infant with chronic hypernatremia M L Marcovecchio Department of Paediatrics, University of Chieti, Via dei Vestini 5, 66100 Chieti, Italy (Correspondence should be addressed to M L Marcovecchio; Email: [email protected]) Abstract A 4-month-old boy was presented with failure to thrive, refusal to feed, delayed motor development, truncal hypotonia, and head lag. His plasma osmolality and sodium were significantly high, while his urine osmolality was inappropriately low and did not increase after desmopressin administration. Despite his hyperosmolality, he presented with a lack of thirst and became clearly polyuric and polydipsic only at the age of 2 years. Initial treatment with indomethacin was ineffective, while the combination of hydrochlorothiazide and amiloride was effective and well tolerated. European Journal of Endocrinology 155 S141–S144 Introduction (61 ml/kg) respectively. Other investigations including thyroid and adrenal function were normal. He was Chronic hypernatremia in young patients is generally refusing oral fluids despite being hypernatremic. the result of alterations in the mechanisms controlling A cranial magnetic resonance imaging scan excluded fluid balance (1). Excessive water loss, as in diabetes structural abnormalities in the hypophysis, hypo- insipidus, or an inadequate fluid intake, as in adipsic thalamus and surrounding area. There was no response hypernatremia, may be the underlying cause. The to 0.3 mg 1-desamino-8-D-arginine-vasopressin (DDAVP) differential diagnosis between these conditions is given intravenously (osmolality pre- 374 mosmol/kg; important in order to choose the appropriate treatment. post- 371 mosmol/kg). This suggested a tubular defect However, pitfalls in the diagnosis are often related to an causing nephrogenic diabetes insipidus (NDI). -
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. -
Prevalence and Risk Factors of Hypophosphatemia in Pediatric Intensive Care Unit
Journal of Anesthesia & Critical Care: Open Access Prevalence and Risk Factors of Hypophosphatemia in Pediatric Intensive Care Unit Abstract Research Article Background: Hypophosphatemia is often unrecognized in critically ill patients despite its potential serious complications. Volume 1 Issue 6 - 2014 Objectives: To estimate the prevalence of hypophosphatemia and to identify risk 1 factors and outcome associated with this disturbance in children admitted to PICU. Hanaa Ibrahim Rady * and Khalil Abdel Khalek Mohamed2 Subjects and Methods: In a prospective cohort study, 72 children admitted 1 consecutively to a pediatric intensive care unit (PICU) were monitored regarding their Department of Pediatrics, Cairo University, Egypt 2Pediatrics and Neonatal Intensivist, Egypt at admission, malnutrition, clinical severity score at admission (pediatric index of *Corresponding author: Hanaa I Rady, Assistant mortalityphosphorus or PIM),serum sepsis levels (C-reactive during the protein first 7 days and cultures),of admission. use ofAge, dopamine, gender, diagnosisdiuretics, Professor of Pediatrics, Gameat el Doual Al Arabia antacids and steroids, starvation period, length of stay and outcome were analyzed as Street, Mohandessin, Egypt, Tel: +201001482444; Fax: independent variables for hypophosphatemia. 0020233473960; Email: | Results: More than half of our patients (58%) had hypophosphatemia on admission and Received: September 08, 2014 Published: November only 5 patients developed hypophosphatemia during their PICU stay. Malnutrition was 22, 2014 present in 21% of patients, but it did not show association with the hypophosphatemia (p=0.1753). The number of starvation days, PIM, days on mechanical ventilation and survivalConclusion: to discharge Hypophosphatemia were significantly was associateda common with problem hypophosphatemia in our PICU (p<0.05).and was associated with the presence of respiratory complaints, higher PIM, and increased starvation days. -
Eating Disorders - Refeeding Pathway V3.0: Table of Contents
Eating Disorders - Refeeding Pathway v3.0: Table of Contents Inclusion Criteria · 5-17 years (if ≥18, call ADO Med and Psych re: consent issues that may preclude admission) · Concern for eating disorder (Anorexia nervosa, avoidant restrictive food intake Stop and disorder, eating disorder unspecified, Bulimia nervosa) Review Exclusion Criteria · Other diagnosis resulting in severe malnutrition that is NOT an eating disorder (e.g. cystic fibrosis, IBD) · ≥18 years with refusal to consent to refeeding & NG tube or ≥ 21 years old Eating Disorders - Refeeding Care ED Inpatient PBMU: Medical Service (MBB) PBMU: Psychiatry Service Appendix Version Changes Approval & Citation Evidence Ratings Bibliography For questions concerning this pathway, contact: Last Updated: January 2021 [email protected] Next Expected Review: April 2022 If you are a patient with questions contact your medical provider, Medical Disclaimer © 2021 Seattle Children’s Hospital, all rights reserved Eating Disorder- Refeeding Pathway v3.0: Emergency Department Inclusion Criteria · 5-17 years (if ≥18, call ADO Med and Psych re: consent issues that may preclude admission) Stop and · Concern for eating disorder (Anorexia nervosa, avoidant restrictive Review food intake disorder, eating disorder unspecified, Bulimia nervosa) Exclusion Criteria · Other diagnosis resulting in severe malnutrition that is NOT an eating disorder (e.g. cystic fibrosis, IBD) · ≥18 years with refusal to consent to refeeding & NG tube or ≥ 21 years old Psychiatry admission -
CASE REPORT Anesthesia for a Long-Term Anorexic Patient with End
337 CASE REPORT Anesthesia for a long-term anorexic patient with end-stage liver cirrhosis : A Case Report Kayo Hirose*, Makoto Ogura†, and Yoshitsugu Yamada‡ *Department of Anesthesiology, Tokyo University Graduate School of Medicine, Tokyo, Japan, Department of Anesthesiology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan, †Department of Anesthesiology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan, ‡Department of Anesthe- siology, Tokyo University Graduate School of Medicine, Tokyo, Japan Abstract : Recent advancements in intensive care have increased the number of severe anorexia nervosa pa- tients presenting for surgery. We provided anesthesia to a patient who had a 22-year history of anorexia with life-threatening cirrhosis. Although surgery should be avoided in patients with end-stage cirrhosis, she was in the best preoperative optimized condition compared to her condition over the past few years. Potential com- plications are heart failure easily caused by deterioration of cirrhosis, lethal arrhythmias related to electrolyte disturbances and increased myocardial sensitivity to drugs, and refeeding syndrome in the postoperative period. The several rare events that we experienced are worth reporting. J. Med. Invest. 66 : 337-339, August, 2019 Keywords : anorexia, end-stage liver cirrhosis, anesthesia INTRODUCTION above 15 should be considered for transplant. According to the Mayo Natural History Model for Primary Biliary Cirrhosis, With an increase in the prevalence of anorexia nervosa (AN), the estimated 1-year and 5-year survival probabilities without severe AN patients have been presenting for surgery since the treatment in such patients are 58% and 1%, respectively. Due 2000s. (1) Patients with a long history of severe AN show sev- to the cirrhosis, her prothrombin time-international normalized eral complications, such as acute liver injury, cardiovascular ratio was prolonged to 1.5 and blood platelet count was decreased complications, pancytopenia, etc.