Clinical Nutrition E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: The Nutrition Society Textbook
- Sprache: Englisch
This second edition of Clinical Nutrition, in the acclaimed textbook series by the Nutrition Society, has been revised and updated in order to:
- Provide students with the required scientific basis in nutrition, in the context of a systems and health approach.
- Enable teachers and students to explore the core principles of nutrition and to apply these throughout their training to foster critical thinking at all times. Each chapter identifies the key areas of knowledge that must be understood and also the key points of critical thought that must accompany the acquisition of this knowledge.
- Are fully peer reviewed to ensure completeness and clarity of content, as well as to ensure that each book takes a global perspective and is applicable for use by nutritionists and on nutrition courses throughout the world.
Ground breaking in scope and approach, with an additional chapter on nutritional screening and a student companion website, this second edition is designed for use on nutrition courses throughout the world and is intended for those with an interest in nutrition in a clinical setting. Covering the scientific basis underlying nutritional support, medical ethics and nutritional counselling, it focuses solely on the sick and metabolically compromised patient, dealing with clinical nutrition on a system by system basis making the information more accessible to the students.
This is an essential purchase for students of nutrition and dietetics, and also for those students who major in other subjects that have a nutrition component, such as food science, medicine, pharmacy and nursing. Professionals in nutrition, dietetics, food sciences, medicine, health sciences and many related areas will also find this an important resource.
Libraries in universities, medical schools and establishments teaching and researching in the area of nutrition will find Clinical Nutrition a valuable addition to their shelves.
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Contents
Contributors
Series Foreword
Preface
First Edition Acknowledgements
1 Principles of Clinical Nutrition: Contrasting the Practice of Nutrition in Health and Disease
1.1 Introduction
1.2 The spectrum of nutritional problems
1.3 Nutritional requirements
1.4 Management pathways
1.5 Concluding remarks
2 Nutritional Screening and Assessment
2.1 Introduction
2.2 Nutritional screening
2.3 Nutritional assessment
2.4 Concluding remarks
3 Water and Electrolytes
3.1 Introduction
3.2 Fluid compartments of the body
3.3 Flux of fluid through the kidney and gastrointestinal tract
3.4 Body electrolyte content and concentration
3.5 Regulation of body water compartments
3.6 The metabolic response to starvation and injury
3.7 Body water compartments and electrolytes in starvation and injury
3.8 Effects of salt and water overload
3.9 Fluid therapy: practical aspects
3.10 Goal-directed fluid therapy
3.11 Implications of water and sodium metabolism in nutrition therapy for specific clinical conditions
3.12 Concluding remarks
4 Over-nutrition
4.1 Introduction
4.2 Aetiology
4.3 Clinical presentation
4.4 Clinical assessment
4.5 Treatment approaches
4.6 Prevention
4.7 Concluding remarks
Acknowledgements
5 Under-nutrition
5.1 Introduction
5.2 Pathophysiology of under-nutrition
5.3 Pathophysiology of under-nutrition complicated by stress
5.4 Chronic under-nutrition
5.5 Under-nutrition in the elderly
5.6 Severe acute malnutrition in children
5.7 Assessment of under-nutrition
5.8 Treatment
5.9 Potential problems with nutritional supplementation in under-nutrition
5.10 Prevention
5.11 Concluding remarks
6 Metabolic Disorders
6.1 Introduction
6.2 Energy intake, health and longevity
6.3 The metabolic syndrome
6.4 Pathophysiology of insulin resistance
6.5 Insulin resistance
6.6 The role of affluence in diabetes, dyslipidaemia, and essential hypertension
6.7 Alcohol
6.8 Concluding remarks
7 Eating Disorders
7.1 Introduction
7.2 Classification and features
7.3 History
7.4 Aetiology
7.5 Incidence and prevalence
7.6 Medical complications of eating disorders
7.7 Nutritional problems in eating disorders
7.8 Nutritional management of eating disorders
7.9 Concluding remarks
Acknowledgements
8 Adverse Reactions to Foods
8.1 Introduction
8.2 Food intolerance
8.3 Food allergy
8.4 Types of food allergy
8.5 Patterns of food-allergic responses
8.6 Diagnostic criteria for food allergy
8.7 Food-sensitive enteropathy
8.8 Specific food allergies
8.9 Multiple-food allergy
8.10 Scientific background: the basic mechanisms of immune response to dietary antigen
8.11 Concluding remarks
9 Nutritional Support
9.1 Introduction
9.2 Meeting nutritional needs
9.3 Oral feeding and oral nutritional supplements
9.4 Enteral tube feeding
9.5 Administration of drugs and enteral feeding
9.6 Parenteral nutrition
9.7 Special considerations with nutritional support
9.8 Concluding remarks
Acknowledgements
10 Ethics and Nutrition
10.1 Introduction
10.2 Brief history of medical ethics
10.3 Medical ethics: the four-principle approach
10.4 Definitions and ethical terms
10.5 Application of ethical principles to artificial nutritional support: clinical scenarios
10.6 Ethical conflict
10.7 Clinical guidelines in ethical care
10.8 Concluding remarks
11 The Gastrointestinal Tract
11.1 Introduction
11.2 Coeliac disease
11.3 Tropical enteropathy and tropical sprue
11.4 Inflammatory bowel disease
11.5 Irritable bowel syndrome and diverticular disease
11.6 Concluding remarks
12 Nutrition in Liver Disease
12.1 Introduction
12.2 Nutritional risk in liver-disease patients
12.3 Effect of nutritional state on liver disease
12.4 Effect of liver disease on nutritional state
12.5 Pathophysiology and nutrient requirement in liver disease
12.6 Disease-specific nutrition therapy
Acknowledgements
13 Nutrition and the Pancreas
13A DIABETES MELLITUS
13A.1 Introduction
13A.2 Presentation and diagnosis
13A.3 Principles of diabetic management and the role of diet
13A.4 Insulin/drugs
13A.5 Physical activity
13A.6 Diet
13A.7 Monitoring and follow-up
13A.8 Concluding remarks
13B PANCREATITIS
13B.1 Introduction
13B.2 Pathogenesis of acute pancreatitis
13B.3 Severity scores
13B.4 Metabolic consequences of acute pancreatitis
13B.5 Artificial nutrition
13B.6 Chronic pancreatitis
13B.7 Concluding remarks
14 The Kidney
14.1 Introduction
14.2 Assessment of nutritional status in kidney patients
14.3 Acute kidney injury
14.4 Chronic kidney disease and diabetic kidney disease
14.5 Kidney transplantation
14.6 Concluding remarks
Acknowledgements
15 Nutritional and Metabolic Support in Haematological Malignancies and Haematopoietic Stem-cell Transplantation
15.1 Introduction
15.2 Haematological malignancies
15.3 Rationale for nutritional intervention in haematological malignancies
15.4 Nutritional and metabolic support following HSCT
15.5 Concluding remarks
16 The Lung
16.1 Introduction
16.2 Prevalence and consequences of weight loss and muscle wasting
16.3 Causes of weight loss and muscle wasting
16.4 Outcomes of nutritional intervention
16.5 Acute lung injury
16.6 Concluding remarks
16.7 Acknowledgements
17 Nutrition and Immune and Inflammatory Systems
17.1 Introduction
17.2 The response of the immune system to activation
17.3 The effects of proinflammatory cytokines
17.4 Control systems for cytokines
17.5 Damaging and life-threatening effects of cytokines
17.6 Influence of malnutrition on key aspects of the cytokine response
17.7 Antioxidant defences and their impact on immune and inflammatory systems in patients
17.8 Immunomodulatory effects of lipids
17.9 Route and content of nutritional provision and immune function and patient outcome
17.10 Concluding remarks
18 The Heart and Blood Vessels
18.1 Introduction
18.2 Atherosclerosis
18.3 Dietary lipids and coronary heart disease
18.4 Plasma lipoproteins
18.5 Lipoprotein metabolism
18.6 Other dietary factors and coronary heart disease
18.7 Diet and hypertension
18.8 Diet and stroke
18.9 Diet and peripheral vascular disease
18.10 Diet and chronic heart failure
18.11 Micronutrients and cardiovascular disease
18.12 Concluding remarks
Acknowledgements
19 Nutritional Aspects of Disease Affecting the Skeleton
19.1 Introduction
19.2 Overview of bone metabolism and mineral-ion homeostasis
19.3 Age-appropriate biochemical reference ranges
19.4 Pharmaceutical agents commonly used in bone disease
19.5 Diagnostic imaging assessment of the skeleton
19.6 Rickets/osteomalacia (vitamin D deficiency)
19.7 Mineral-ion homeostasis in preterm infants
19.8 Corticosteroid-induced bone disease
19.9 Post-transplant bone disease
19.10 Osteoporosis associated with chronic disease
19.11 Anorexia nervosa
19.12 Senile osteoporosis
19.13 Concluding remarks
20 Nutrition in Surgery and Trauma
20.1 Introduction
20.2 The stress response to trauma and its effects on metabolism
20.3 Nutritional support in perioperative care
20.4 Feeding the severely traumatised patient
20.5 Concluding remarks
Acknowledgements
21 Infectious Diseases
21.1 Introduction
21.2 Human immunodeficiency virus infection
21.3 Tuberculosis
21.4 Malaria
21.5 Gastrointestinal infections
21.6 Concluding remarks
22 Nutritional Support in Patients with Cancer
22.1 Introduction
22.2 Cancer cachexia
22.3 Nutritional support in cancer
23 Paediatric Nutrition
23.1 Introduction
23.2 Growth
23.3 The impact of development on nutrition
23.4 Infant feeding
23.5 Preschool children
23.6 Schoolchildren and adolescents
23.7 Under-nutrition in children
23.8 Nutrition as treatment
23.9 Overweight in children: ‘fatness’ and ‘obesity’
23.10 Concluding remarks
24 Cystic Fibrosis
24.1 Introduction
24.2 Definition and pathology
24.3 Clinical features
24.4 Malnutrition
24.5 Other nutritional complications of CF
24.6 Nutritional management
24.7 Vitamin supplementation
24.8 Minerals
24.9 Infant feeding
24.10 Concluding remarks
Acknowledgements
25 Illustrative Cases
25.1 Introduction
25.2 Children
25.3 Anorexia of psychological origin and refeeding syndrome
25.4 Malnutrition in the older person
25.5 Bowel disease
25.6 Catabolic illness
25.7 Dysphagia
25.8 Obesity
Index
Access to Companion Site
The Nutrition Society Textbook Series
Introduction to Human Nutrition
Introduction to human nutrition: a global perspective on food and nutritionBody compositionEnergy metabolismNutrition and metabolism of proteins and amino acidsDigestion and metabolism of carbohydratesNutrition and metabolism of lipidsDietary reference standardsThe vitaminsMinerals and trace elementsMeasuring food intakeFood compositionFood and nutrition: policy and regulatory issuesNutrition research methodologyFood safety: a public health issue of growing importanceFood and nutrition-related diseases: the global challenge
Public Health Nutrition
An overview of public health nutritionNutrition epidemiologyFood choiceAssessment of nutritional status at individual and population levelAssessment of physical activityOvernutritionUndernutritionEating disorders, dieting and food fadsPHN strategies for nutrition: intervention at the level of individualsPHN strategies for nutrition: intervention at the ecological levelFood and nutrition guidelinesFetal programmingCardiovascular diseaseCancerOsteoporosisDiabetesVitamin A deficiencyIodine deficiencyIron deficiencyMaternal and child healthBreast feedingAdverse outcomes in pregnancy
Nutrition and Metabolism
Core concepts of nutritionMolecular aspects of nutritionIntegration of metabolism 1: EnergyIntegration of metabolism 2: MacronutrientsIntegration of metabolism 3: Protein and amino acidsPregnancy and lactationGrowth and agingNutrition and the brainThe sensory systems and food palatabilityThe gastrointestinal tractThe cardiovascular systemThe skeletal systemThe immune and inflammatory systemsPhytochemicalsThe control of food intakeOvernutritionUndernutritionExercise performance
Sport and Exercise Nutrition
Nutrient basicsExercise physiologyExercise biochemistryCarbohydrateProtein and amino acidsFat metabolismFluids and electrolytesMicronutrientsSupplements and ergogenic aidsNutrition for weight and resistance trainingNutrition for power and sprint trainingNutrition for middle-distance and speed-endurance trainingNutrition for endurance and ultra-endurance trainingNutrition for technical and skill-based trainingNutrition for disability athletesCompetition nutritionLosing, gaining and making weight for athletes Eating disorders and athletesBone healthNutrition and the gastrointestinal tract for athletesImmunityTravelPopulation groups: IPopulation groups: IITraining and competition environments
This edition first published 2013First edition published 2005© 2005, 2013 by The Nutrition Society
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Library of Congress Cataloging-in-Publication Data
Clinical nutrition / edited on behalf of the Nutrition Society by Marinos Elia . . . [et al.]. – 2nd ed. p. ; cm. Includes bibliographical references and index.
ISBN 978-1-4051-6810-6 (pbk. : alk. paper) I. Elia, Marinos. II. Nutrition Society (Great Britain) [DNLM: 1. Nutrition Therapy. 2. Nutritional Physiological Phenomena. WB 400] 615.8′54–dc23
2012022785
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Cover image: courtesy of iStockphoto/skystardreamCover design by Sophie Ford (www.hisandhersdesign.co.uk)
Contributors
Dr Isabelle AeberliSt John’s Research Institute, IndiaETH Zurich, SwitzerlandProfessor Simon P AllisonFormerly University of Nottingham and Queen’s Medical CentreUKProfessor Bruce R BistrianBeth Israel Deaconess Medical CenterUSAProfessor Federico BozzettiUniversity of MilanItalyDr Eduard CabréHospital Universitari Germans Trias i PujolSpainDr Saveria CapriaLa Sapienza University of RomeItalyAbeed H ChowdhuryNottingham University Hospitals Queen’s Medical Centre, NottinghamUKPeter CollinsQueensland University of TechnologyAustraliaProfessor John A DodgeUniversity of SwanseaUKProfessor Marinos EliaUniversity of SouthamptonUKProfessor Filippo Rossi FanelliLa Sapienza University of RomeItalyProfessor Ken FearonUniversity of EdinburghUKProfessor Gema FrühbeckClinica Universidad de Navarra-CIBERobnSpainProfessor Miquel A GassullHospital Universitari Germans Trias i PujolSpainDr Kate GatenbyUniversity of LeedsUKProfessor Robert F GrimbleUniversity of SouthamptonUKProfessor Gianfranco GuarnieriUniversity of TriesteItalyDr Anna Paola IoriLa Sapienza University of RomeItalyCora F Jonkers-SchuitemaAcademic Medical Centre, AmsterdamThe NetherlandsProfessor Mark KearneyUniversity of LeedsUKProfessor Anura V KurpadSt John’s Research InstituteIndiaProfessor Olle LjungqvistÖrebro University Hospital and Karolinska InstitutetSwedenProfessor Dileep N LoboNottingham University Hospitals Queen’s Medical Centre, NottinghamUKProfessor John MacFieScarborough HospitalUKDrPaula McGurkUniversity Hospital Southampton NHS Foundation TrustUKDrClare McNaughtScarborough HospitalUKProfessor Simon H MurchWarwick Medical School, University of WarwickUKAssociate Professor Maurizio MuscaritoliLa Sapienza University of RomeItalyDr Nicholas I PatonNational University of SingaporeSingaporeProfessor Mathias PlauthStaedtisches Klinikum Dessau (Municipal Hospital Dessau)GermanyAssociate Professor Christine RoddaMonash UniversityAustraliaDr Tatjana SchützLeipzig University Medical CentreGermanyProfessor Jean-Marc SchwarzTouro University CaliforniaUSARoberta SitulinUniversity of TriesteItalyDr Rebecca J StrattonUniversity of SouthamptonUKProfessor Luc TappyUniversity of LausanneSwitzerlandDrMarian AE van Bokhorst-de van der SchuerenVU University Medical CentreThe NetherlandsEsther van den HogenMaastricht UMCThe NetherlandsDr Stephen WheatcroftUniversity of LeedsUKDr Anthony F WilliamsSt George’s, University of LondonUKKate WilliamsSouth London and Maudsley NHS Foundation TrustUKDr Jean-Fabien ZazzoHÔpital Antoine-Béclère (Assistance Publique-Hôpitaux de Paris)France
Series Foreword
The Nutrition Society was established in 1941 as a result of a group of leading physiologists, biochemists and medical scientists recognising that the emerging discipline of nutrition would benefit from its own Learned Society. The Nutrition Society’s mission was, and firmly remains, “to advance the scientific study of nutrition and its application to the maintenance of human and animal health”. It is the largest Learned Society for Nutrition in Europe and has over 2,700 members worldwide. For more details about the Society and how to become a member, visit the website at www.nutritionsociety.org.
Throughout its history, a primary objective of the Society has been to encourage nutrition research and to disseminate the results of such research. This is reflected in the several scientific meetings with the Nutrition Society, often in collaboration with sister Learned Societies in Europe, Africa, Asia and the USA, organised each year.
The Society’s first journal, The Proceedings of the Nutrition Society published in 1944, records the scientific presentations made to the Society. Shortly afterwards, in 1947, the British Journal of Nutrition was established to provide a medium for the publication of primary research on all aspects of human and animal nutrition by scientists from around the world. Recognising the needs of students and their teachers for authoritative reviews on topical issues in nutrition, the Society began publishing Nutrition Research Reviews in 1988. The journal Public Health Nutrition, the first international journal dedicated to this important and growing area, was subsequently launched in 1998. The Society is constantly evolving and has most recently launched the Journal of Nutritional Science in 2012. This is an international, peer-reviewed, online only, open access journal.
Just as in research, having the best possible tools is an enormous advantage in both teaching and learning. The Nutrition Society Textbook Series was established by Professor Michael Gibney (University College Dublin) in 1998. It is now under the direction of the second Editor-in-Chief, Professor Susan Lanham-New (University of Surrey), and continues to be an extraordinarily successful venture for the Society. This series of Human Nutrition textbooks is designed for use worldwide and this was achieved by translating the Series in multiple languages including Spanish, Greek, Portuguese and Indonesian. The sales of the textbook (>30,000 copies) are a tribute to the value placed on the textbooks both in the UK and worldwide as a core educational tool.
This Second Edition of Clinical Nutrition focuses on the metabolically compromised patient and provides a most thorough review of the importance of nutrition across the clinical spectrum. The textbook is aimed at those with an interest in nutrition in the clinical setting, including students, nutritionists, dietitians, medics, nursing staff or other allied health professionals.
In my capacity as the Chief Medical Officer (CMO) for England, and the UK Government’s Principal Medical Adviser, the professional lead for all Directors of Public Health and Chief Scientific Adviser for the Department of Health, it gives me great pleasure to write the Foreword for the Second Edition of Clinical Nutrition. I have been actively involved in NHS Research and Development from its establishment and I understand how important clinical nutrition is to the patient and the medical team. This textbook brings together science and clinical practice and is a valuable resource to all those working in the field.
Professor Dame Sally C. DaviesChief Medical OfficerChief Scientific Adviser
Preface
The Nutrition Society’s Textbook Series continues to go from strength to strength following its development over 10 years ago. The forward thinking focus that Professor Michael Gibney (University College Dublin) had at that time is to be especially noted. My task as the new Editor-in-Chief since 2009 is much easier than the visionary one that Professor Gibney had back in the late 1990s and it remains a tremendous honour for me to be following in his footsteps.
The first and second textbooks in the Series, Introduction to Human Nutrition (IHN) and Nutrition and Metabolism (N&M), are now out in Second Editions and sales continue apace. We are currently working on the Second Edition of the third textbook in the Series, Public Health Nutrition (PHN), and we are absolutely delighted now to present to the field of Nutritional Sciences, Elia et al.’s Clinical Nutrition Second Edition. This follows our publication last year of the fifth textbook in the Series, Sport and Exercise Nutrition First Edition (SEN1e). The sales of SEN1e have surpassed all expectations and we were most grateful to Dr Richard Budgett OBE, Chief Medical Officer for the London 2012 Olympic and Paralympic Games, for his enthusiasm, support and most generous Foreword.
Clinical Nutrition Second Edition (CN2e) is a great strength of the Textbook Series and the Nutrition Society is indebted to the Senior Editor, Professor Marinos Elia (University of Southampton), for his careful planning and editorial leadership of the book following the critical role he played with the development of the First Edition of Clinical Nutrition. Sincerest of thanks are also due to the Editors, Professor Olle Ljungqvist (Örebro University Hospital and Karolinska Institutet, Sweden) and Dr Rebecca Stratton (University of Southampton) for their immense work on this Second Edition.
This Second Edition is intended for those with an interest in nutrition in the clinical setting, whether they are dietitians or medics, nursing staff or other allied health professionals. The book starts by setting the scene in assessing nutritional status and discusses the clinical consequences and current management options with under-nutrition and over-nutrition, and eating disorders and metabolic disease. The subsequent later chapters deal with the different organ systems of the body, setting out the most up-to-date thinking on the role of nutrition, whether it involves nutritional support, nutritional education or a combination of both.
We are extremely honoured that the Foreword for the Second Edition has been written by Dame Sally Davies, Chief Medical Officer (CMO) for England, and the UK Government’s Principal Medical Adviser. It gives us great confidence in this Textbook to have such a seal of approval from someone so eminent in the clinical field. Our sincerest of thanks indeed for Dame Sally’s help and support.
The Society is most grateful to the textbook publishers Wiley-Blackwell for their continued help with the production of the textbook and in particular Nick Morgan, Sara Crowley-Vigneau and Marilyn Pierro, as well as Aravinthakumar Ranganathan, the project manager at SPi Publisher Services. In addition, many grateful thanks to Professor Lisa Roberts, Dean of the Faculty of Health and Medical Sciences, University of Surrey for her great encouragement of the Textbook Series production.
Finally, sincerest of thanks indeed to the Nutrition Society President, Professor Sean J.J. Strain (University of Ulster), for all his belief in the Textbook Series and to Professor David Bender, Honorary Publications Officer, for being such a great sounding board. The Series remains indebted to Sharon Hui (Assistant Editor, NS Textbook Series) and Jennifer Norton (NS Business Development Manager) for their huge contribution to the development of the Series and for making the textbooks such an enjoyable journey.
I do hope that you will find the textbook a great resource. Happy reading indeed!
With my warmest of wishes.
Professor Susan A. Lanham-NewHead, Department of Nutritional SciencesFaculty of Health and Medical Sciences University of Surreyand Editor-in-Chief, Nutrition Society Textbook Series
The Nutrition Society Textbook Series Editorial Team
Editor-in-ChiefSusan A Lanham-NewUniversity of Surrey, UKBusiness Development ManagerJennifer NortonThe Nutrition Society, UKAssistant EditorSharon S HuiThe Nutrition Society, UK
First Edition Acknowledgements
Editor-in-ChiefMichael J GibneyEditorsMarinos EliaOlle LjungqvistJulie Dowsett
Authors
Chapter 1: Principles of Clinical NutritionMarinos EliaChapter 2: Nutritional AssessmentKhursheed JeejeebhoyMary KeithChapter 3: OvernutritionGema FrühbeckChapter 4: UndernutritionAnura KurpadChapter 5: Metabolic DisordersLuc TappyJean-Marc SchwarzChapter 6: Eating DisordersJanet TreasureTara MurphyChapter 7: Adverse Reactions to FoodsSimon MurchChapter 8: Nutritional SupportKarin BarendregtPeter SoetersChapter 9: Ethics and NutritionJohn MacfieChapter 10: The Gastrointestinal TractMiguel A GassullEduard CabréChapter 11: Nutrition in Liver DiseaseMarietjie HerselmanDemetre LabadariosChristo Van RensburgAref HaffejeeChapter 12: Nutrition and the PancreasJean Fabien ZazzoChapter 13: The KidneyGianfranco GuarnieriRoberta SitulinGabriele ToigoChapter 14: Nutritional and Metabolic Support in Hematologic Malignancies and Hematopoietic Stem Cell TransplantationMaurizio MuscaritoliGabriella GriecoFilippo Rossi FanelliZaira AversaChapter 15: The LungAnnemie ScholsEmiel FM WoutersChapter 16: Nutrition and Immune and Inflammatory SystemsBruce BistrianBob GrimbleChapter 17: The Heart and Blood VesselsStephen WheatcroftBrian NoronhaMark KearneyChapter 18: Nutritional Aspects of Disease Affecting the SkeletonChristine RoddaChapter 19: Nutrition in Surgery and TraumaOlle LjungqvistKenneth FearonRoderick LittleChapter 20: Infectious DiseasesNicholas PatonMiguel A GassullEduard CabréChapter 21: Nutritional Support in Patients with CancerFederico BozzettiChapter 22: Pediatric NutritionAnthony F WilliamsChapter 23: Cystic FibrosisOlive TullyJulie DowsettChapter 24: Water and ElectrolytesMeritxell GirventGuzman FranchAntonio Stiges-SerraChapter 25: Illustrative CasesSimon Allison
1
Principles of Clinical Nutrition: Contrasting the Practice of Nutrition in Health and Disease
Marinos Elia
Institute of Human Nutrition,University of Southampton,Southampton, UK
1.1 Introduction
Clinical nutrition focuses on the nutritional management of individual patients or groups of patients with established disease, in contrast to public health nutrition, which focuses on health promotion and disease prevention in the general population. The two disciplines overlap, however, especially in older people, who are often affected by a range of disabilities or diseases. Working together, instead of independently, the two disciplines are more likely to facilitate successful implementation of local, national, and international policies on nutrition. To understand the overlap between them, it is necessary to consider not only some of the principles of nutrition that apply to health, but also special issues that apply to the field of clinical nutrition. These include altered nutritional requirements associated with disease, disease severity and malnutrition, and nonphysiological routes of feeding using unusual feeds and feeding schedules. This introductory chapter provides a short overview of these issues, partly because they delineate qualitative or quantitative differences between health and disease, and partly because they form a thread that links subsequent sections of this book, which is divided into discrete chapters addressing specific conditions.
It is now possible to feed all types of patients over extended periods of time, including those who are unconscious, unable to eat or swallow, or have little or no functional gastrointestinal tract. It is possible to target specific patient groups with special formulations, and even to change the formulation in the same patient as nutritional demands alter during the course of an illness. Since some of these formulations may be beneficial to some patient groups and detrimental to other groups or to healthy subjects, the distinction between physiology in health and pathophysiology in disease needs to be considered carefully. It is hoped that some of the principles outlined here will help to establish a conceptual framework for considering some of the apparently diverse conditions discussed in this textbook.
1.2 The spectrum of nutritional problems
Clinical nutrition aims to treat and prevent suffering from malnutrition. However, there is no universally accepted definition for ‘malnutrition’ (literally, ‘bad nutrition’). The following definition, which encompasses both under- and over-nutrition, is offered for the purposes of this chapter.
Malnutrition is a state of nutrition in which a deficiency or excess (or imbalance) of energy, protein, and other nutrients causes measurable adverse effects on tissue/body function (shape, size, and composition) and clinical outcome.
In this chapter and elsewhere, however, the term ‘malnutrition’ is mainly used to refer to under- rather than over-nutrition.
Both under- and over-nutrition have adverse physiological and clinical effects. Those relating to under-nutrition (Table 1.1) are diverse, which explains why malnourished patients may present to a wide range of medical disciplines. Several manifestations may occur simultaneously in the same individual, although some predominate. They may be caused by multiple deficiencies. Specific nutrient deficiencies may also have diverse effects, affecting multiple systems, but it is not entirely clear why the same deficiency can present in a certain way in one subject and a different way in another. For example, it is not clear why some patients with deficiency of vitamin B12 present to the haematologist with megaloblastic anaemia, others to the neurologist with neuropathy and other neurological manifestations (e.g. subacute combined degeneration of the cord), and still others to the geriatrician with cognitive impairment or dementia.
Table 1.1 Physical and psychosocial effects of under-nutrition.
Adverse effect
Consequence
Physical
Impaired immune responses
Predisposes to infection
Reduced muscle strength and fatigue
Inactivity, inability to work effectively, and poor self-care. Abnormal muscle (or neuromuscular) function may also predispose to falls or other accidents
Reduced respiratory muscle strength
Poor cough pressure, predisposing to and delaying recovery from chest infection
Inactivity, especially in bed-bound patient
Predisposes to pressure, sores, and thromboembolism
Impaired thermoregulation
Hypothermia, especially in the elderly
Impaired wound-healing
Failure of fistulae to close, un-united fractures, increased risk of wound infection resulting in prolonged recovery from illness, increased length of hospital stay, and delayed return to work
Foetal and infant programming
Predisposes to common chronic diseases, such as cardiovascular disease, stroke, and diabetes in adult life
Growth failure
Stunting, delayed sexual development, and reduced muscle mass and strength
Psychosocial
Impaired psychosocial function
Even when uncomplicated by disease, undernutrition causes apathy, depression, self-neglect, hypochondriasis, loss of libido, and deterioration in social interactions. It also affects personality and impairs mother–child bonding
The spectrum of presentations is more diverse than this would indicate because protein–energy malnutrition frequently coexists with various nutrient deficiencies. For example, patients with gastrointestinal problems are frequently underweight and at the same time exhibit magnesium, sodium, potassium, and zinc deficiencies, due to excessive losses of these nutrients in diarrhoea or other gastrointestinal effluents. There may also be problems with absorption; for example, patients with Crohn’s disease affecting the terminal ileum, where vitamin B12 is absorbed, are at increased risk of developing B12 deficiency. Patients who have had surgical removal of their terminal ileum or stomach, which produces the intrinsic factor necessary for B12 absorption, fail to absorb vitamin B12. Isolated nutrient deficiencies may also occur, for example iron deficiency due to heavy periods in otherwise healthy women.
Another complexity is the interaction between nutrients, which may occur at the level of absorption, metabolism within the body, or excretion. One nutrient may facilitate the absorption of another; for example, glucose enhances the absorption of sodium (on the glucose–sodium co-transporter). This is the main reason why oral rehydration solutions used to correct salt deficiency due to diarrhoea (or fluid losses due to other gastrointestinal diseases) contain both salt and glucose. In contrast, other nutrients compete with each other for absorption. For example, because of competition between zinc and copper for intestinal absorption, administration of copper may precipitate zinc deficiency, especially in those with borderline zinc status. Other nutrients interact with each other during tissue deposition. Accretion of lean tissue requires multiple nutrients, and lack of one of them, such as potassium or phosphate, can limit its deposition, even when adequate amounts of protein and energy are available (Figure 1.1). This emphasises the need to provide all necessary nutrients in appropriate amounts and proportions.
Figure 1.1 Effect of omitting potassium (K) and phosphate (P) from a parenteral nutrition regimen on the nitrogen (N) balance of depleted patients receiving hypercaloric feeding. Data from Rudman et al. (1975).
1.3 Nutritional requirements
Effect of disease and nutritional status
Fluid and electrolytes
The principles of nutrient requirements in healthy individuals are described in Introduction to Human Nutrition (Gibney et al., 2009), an earlier volume in this textbook series. The average nutrient intake refers to the average intake necessary to maintain nutrient balance. The reference nutrient intake (RNI) refers to the intake necessary to satisfy the requirements of 97.5% of the healthy population (+2 standard deviations from the average nutrient intake). In patients with a variety of diseases, the requirements are more variable (Figure 1.2): for some groups of patients, they are higher than for those in health, while for other groups they are lower. For example, in patients with gastrointestinal fluid losses, the requirement for sodium may be double the RNI, while in patients with severe renal or liver disease who retain salt and water, the requirements may be well below the average nutrient requirement for healthy subjects ingesting an oral diet. The requirements for potassium and phosphate may also be well below the RNI for patients with severe renal disease in whom there is failure of excretion. Therefore, if recommendations for healthy individuals are applied to patients with certain types of disease, they may produce harm. A general guide to the requirements for sodium and potassium in patients with gastrointestinal fluid loss (above those for maintenance) is provided in Table 1.2, which shows the electrolyte content of various fluids. A person with a loss of 1.5 litres of small-intestinal fluid may require ~150 mmol of sodium above maintenance (the RNI for sodium is 70 mmol/day according to UK reference standards), whereas loss of the same volume of nasogastrically aspirated fluid requires only ~90 mmol extra sodium. Note that the requirements for potassium in patients losing gastrointestinal fluids are generally much lower than those for sodium (Table 1.2).
Figure 1.2 Frequency distribution of nutrient requirements in health and disease.
Excessive salt and fluid administration can be just as detrimental as inadequate intake, causing fluid retention and heart failure in some individuals. Fluid retention is often detected clinically by noting pitting oedema at the ankles or over the sacrum, but oedema can also affect internal tissues and organs, causing a variety of problems. Some of these problems are shown in Table 1.3. A recent study has questioned the routine clinical practice of administering large amounts of fluid in the early postoperative period in an attempt to reduce the risk of hypotension. In a randomised controlled trial carried out in Denmark, routine fluid administration was compared with a fluid-restricted regimen that aimed to approximately maintain body weight. In those receiving routine fluid therapy, not only did body weight increase significantly more than in the fluid-restricted group, but it significantly increased a variety of complications, including tissue-healing and cardiopulmonary complications. It also increased mortality, but this did not reach statistical significance, possibly because only a small number of subjects died during the course of the study. Acute accidental and elective surgical trauma is associated with a tendency to retain salt and water, at least partly because of increased secretion of mineralocorticoids and antidiuretic hormone. Therefore, administration of excess salt and water as in protein–energy malnutrition may lead to fluid retention that would not occur in normal subjects.
Table 1.2 Electrolyte contents of some body secretions (mmol/l).
Secretion/excretion
Na
K
Gastric
60
10
Pancreatic
140
5
Biliary
140
5
Small-intestinal
100
10
Diarrhoea
60
a
20
Faeces
25
55
Sweat
insensible
10
10
visible
60
10
a Variable (30–140 mmol/l)
Protein
Table 1.3 Some problems caused by oedema.
Site of oedema
Consequence
Liver
Abnormal liver-function tests
Gastrointestinal tract
Impaired gastric motility with subsequent delay in the time taken to tolerate oral food and recover from abdominal surgery; impaired absorption
Brain
Impaired consciousness in those with a head injury associated with some preexisting cerebral oedema
Wounds
Delayed healing
Figure 1.3 Effect of increasing protein (N) intake on N balance in depleted, healthy, and catabolic patients close to energy balance.
Figure 1.4 Effect of acute disease severity (expressed as multiples of normal BMR) on total energy expenditure (shaded area). The difference between total energy expenditure and BMR is due to physical activity (and some thermogenesis, which typically accounts for ~10% of energy intake). The increase in BMR is counteracted by a decrease in physical activity. (a) Infection, persistent fever (1 °C); (b) infection, persistent fever (2 °C); (c) burns 10% (first month), single fracture (first week), postoperative (first 4 days); (d) burns 10–25% (first month), multiple long-bone fractures (first week); (e) severe sepsis/multiple trauma (patient on respirator); (f) burns 25–95% (first month).
Energy
In healthy subjects the energy requirements necessary to maintain energy stores are often calculated as multiples of basal metabolic rate (BMR). However, in many acute diseases (Figure 1.4) and a number of chronic diseases BMR has been found to be increased, which led to the view that the energy requirements in such states were also usually increased. This conclusion failed to take into account the decrease in physical activity that occurs as a result of many diseases and disabilities. This decrease counteracts or more than counteracts the increase in BMR, so that total energy expenditure in most disease states (and hence the energy intake necessary to maintain balance) is actually close to normal, or even decreased. As previously noted, there is also the need to consider changes in energy stores. In obese individuals it is desirable to reduce the energy stores by providing hypocaloric feeding, and in depleted patients to increase energy stores by providing hypercaloric feeding. In both cases, it is usually better to do this during the recovery phase of illness rather than the acute and more unstable phase of illness (see later in this chapter).
In estimating the energy requirements of a hospitalised patient, it is worth considering the energy contribution from nondietary sources, such as intravenous dextrose 5% (~200 kcal/l), dialysate, and fat-based drugs such as propofol (~1.1 kcal/ml) and drugs that may need to be administered with saline.
Metabolic blocks and nutritional requirements
Inborn errors of metabolism
When there is a block in a metabolic pathway that involves conversion of substance A to B, there is an accumulation of substance A, which may be toxic (either directly or via its products), and a depletion in substance B, which needs to be either formed within the body by alternative pathways or provided by the diet. An alternative strategy is to replace the enzyme responsible for the block, for example by organ transplantation, although this has only been used for a few metabolic disorders. One of the best known examples of a metabolic block occurs in phenylketonurea (PKU), due to deficiency of the enzyme phenylalanine hydroxylase, the gene of which is located on chromosome 12 (12q). In the absence of phenylalanine hydroxylase, the gene of which normally converts the amino acid phenylalanine to tyrosine in the liver, there is an accumulation of phenylalanine and its metabolites, which causes brain damage, mental retardation, and epilepsy. Tyrosine, which is distal to the block, is provided by the diet so the treatment for PKU is to ingest a low-phenylalanine diet (some phenylalanine is required for protein synthesis) (see later in this chapter for the duration of treatment). The diet, which is not found in nature, is specifically manufactured to restrict the intake of phenylalanine. Other metabolic blocks may require exclusion of other individual nutrients, for example restriction of galactose and lactose in children with galactosemia. Some diets may exclude whole proteins, which can cause food allergy or sensitivity. In the case of coeliac disease, which is responsible for a small-bowel enteropathy with malabsorption, this means avoiding gluten, which is found in wheat and wheat products (see Chapter 8). However, the problem here is not due to a block in a metabolic pathway, but to an abnormal reaction to food, which appears to be acquired.
Acquired metabolic blocks
Not all metabolic blocks are inherited as inborn errors of metabolism. For example, deficiency of phenylalanine hydroxylase can occur as a result of cirrhosis. Since in healthy subjects tyrosine can be formed from phenylalanine, some feed manufacturers have added little or no tyrosine to parenteral nutrition regimens, especially since tyrosine has a low solubility. However, a few patients with severe liver disease lose the ability to synthesise sufficent tyrosine, with the result that it becomes rate-limiting to protein synthesis, even in the presence of all other necessary amino acids (i.e. the enzymatic deficiency is ultimately responsible for the metabolic block in protein synthesis, which can be reversed by administering tyrosine). Other examples of acquired metabolic blocks due to amino acids involve histidine in some patients with renal disease, and cystine in liver disease. It is therefore essential that these amino acids (described as conditionally essential) are provided in the diet (oral or intravenous) of such patients, even though they are not essential for healthy subjects.
Acquired metabolic blocks may involve other types of nutrients. An interesting example concerns vitamin D, which is hydroxylated in the liver to produce 25-hydroxy vitamin D and further hydroxylated in the kidney to produce the active metabolite 1,25-dihydroxy vitamin D (Figure 1.5). Some patients with chronic renal failure are unable to produce sufficient amounts of 1,25-dihydroxy vitamin D, due to loss of activity of the enzyme 1 alpha hydroxylase in the kidney. Such patients may suffer from metabolic bone disease, which is at least partly due to deficiency of 1,25-dihydroxy vitamin D. This metabolic block can be bypassed by providing either synthetic 1,25-dihydroxy vitamin D or synthetic 1-hydroxy vitamin D, which is converted to 1,25-dihydroxy vitamin D in the liver (Figure 1.5). Such therapy differs from that used in the treatment of PKU in at least two ways: it involves administration of substance distal to the block (cf. restriction of phenylalanine, which is proximal to the block) and it is not found in the normal diet in any significant amounts. It is an example of nutritional pharmacology involving administration of a bioactive substance.
Figure 1.5 Metabolism of vitamin D in the liver and kidney. In renal failure, the formation of 1,25-dihydroxy vitamin D (1,25 (OH)2 D) in the kidney may be inadequate, in which case 1,25-dihydroxy vitamin D or 1-hydroxy vitamin D (25 (OH) D) can be prescribed.
Table 1.4 Some examples of nutritional pharmacology.
Type I (prenutrients)
Organic phosphates
The amount of calcium and phosphate that can be added to parenteral nutrition solutions is limited by the solubility of calcium phosphate, which can precipitate. Organic phosphates, such as glycerol-phosphate or glucose-phosphate, are soluble and do not precipitate in the presence of calcium. The organic phosphate is hydrolysed within the body to yield free phosphate
Dipeptides
Glutamine degrades during heat sterilisation and storage of parenteral amino acid solutions. It can be provided as a dipeptide (e.g. alanylglutamine), which is stable and can be stored for extended periods of time. Poorly soluble amino acids can be provided as soluble dipetides, such as glycyltyrosine or alanylcystine. The dipeptides are hydrolysed within the body to yield free amino acids
Type II (pharmacological doses)
Glycerol
Free glycerol is used as an emulsifying agent in intravenous fat solutions
Medium-chain triglycerides
Medium-chain triglycerides (up to 50% of total lipid) may be better absorbed and tolerated than long-chain triglyceride. In intravenous use, these may avoid infusional hyperlipidaemia
Glutamine
Glutamine may be given in large amounts (12–30 g), with the aim of improving clinical outcome (e.g. in intensive care units)
Oligofructose
Bifidobacteria or oligofructose, which is a fermentable bifidogenic substrate, can be given orally with the aim of changing intestinal microflora and reducing the growth of potentially pathogenic organisms
Type III (bioactive substances)
Erythropoietin
Increases utilisation of iron and Hb synthesis in anaemic patients with end-stage renal failure
1,25-dihydroxy and 1-hydroxy vitamin D
Used in renal failure when there is a block in 1α hydroxylation of 25-hydroxy vitamin D
Growth hormone
Aims to improve N balance
A variety of other bioactive substances have been used in clinical nutrition with the aim of improving outcome. Some products of metabolism require more than one class of substrate for their synthesis. For example, haemoglobin (Hb) comprises a variety of amino acids and iron, which forms part of the haem component. All the substrates may be available in adequate quantities, but a block in Hb synthesis can still occur as a result of a deficiency of erythropoietin, a bioactive substance produced by the kidney that stimulates Hb synthesis. Erythropoietin synthesis is upregulated during hypoxia, which explains the high Hb concentrations in people living at high altitudes. In contrast, lack of erythropoietin leads to anaemia. One of the features of end-stage renal failure is severe anaemia, which is at least partly due to the inability of the damaged kidney to produce enough erythropoietin. Traditionally, this anaemia was treated by repeated blood transfusions. Now that recombinant erythropoietin is available, it can be used to treat the anaemia and to eliminate or dramatically reduce the need for repeated blood transfusions, which carry the risk of transmitting infections, such as HIV and hepatitis, and which require admission of patients to special healthcare facilities. Importantly, injections of recombinant erythropoietin have also been shown to improve quality of life in patients with severe renal disease. Other examples of nutritional pharmacology, shown in Table 1.4, are divided into those involving administration of prenutrients, pharmacological doses of normal nutrients, and bioactive substances (see Table 1.4 for the rationale for specific types of nutritional pharmacology).
The uncritical use of bioactive substances can produce unpredictable serious side effects, including death. An example involves injections of pharmacological doses of growth hormone (GH) in critically ill patients. It was thought that GH might be beneficial in limiting the marked N loss that frequently occurs in such patients (equivalent to overcoming a metabolic block in net protein synthesis). GH is known to stimulate protein synthesis, and had previously been shown to improve N balance in a wide range of clinical conditions. However, in a large multicentre trial involving patients admitted to intensive care units, pharmacological doses of GH doubled mortality compared with the placebo group (from about 20 to 40%), sending a signal to the scientific and clinical community about the dangers of such interventions, especially when the mechanisms of action have not been previously evaluated.
The mechanism(s) responsible for the increased mortality with GH is still uncertain, but several suggestions have been made. One is that large doses of GH have detrimental effects on immune cells, which play a key role in host defence in critical illness. Another concerns the fluid-retaining properties of GH (see earlier for the detrimental effects of fluid overload). Yet another concerns the protein-stimulating properties of GH, which were, paradoxically, the main reason for using GH in the first place. Since muscle is thought to be a major site of action of GH, it is possible that stimulation of protein synthesis here may limit the availability of amino acids, including glutamine, to other tissues. These amino acids would normally be used for synthesis of proteins, for example the acute-phase proteins in the liver, which participate in the response to infection and inflammation. They are also normally used as fuel for a variety of cells, including immune cells (some preferentially utilising glutamine as a fuel), which play an important role in combating infection.
It has also been suggested that some of the detrimental effects of GH are due to cardiac arrhythmias from high concentrations of non-esterified fatty acids produced by the lipolytic effect of GH. Another suggestion is that the mortality is partly due to disturbances in glucose homeostasis, since GH produces significantly higher circulating glucose concentrations than the placebo. Hyperglycaemia in critically ill patients can have a range of detrimental effects, including predisposition to catheter-related sepsis in those receiving intravenous nutrition.
Effect of the route of feeding on nutrient requirements
In health, only the oral route is used to provide nutrients to the body; in clinical practice, other routes (or a combination) can be used. Before discussing their effect on nutrient requirements, it is necessary to briefly consider the type of nutritional support and feeding route. In general, food is the first line of treatment, but if this is inadequate to meet the needs of patients, oral supplements may be used, followed by enteral tube feeding and then intravenous feeding (parenteral nutrition). However, this linear sequence is inadequate in a number of situations. The first-line treatment for someone who has acutely developed short bowel syndrome is parenteral nutrition, not oral nutrition, oral supplements, or even enteral tube feeding. Similarly, tube feeding may be the first-line treatment for a patient with a swallowing problem – not oral food or supplements, which can cause detrimental effects. In some situations (e.g. cerebral palsy), oral feeding is possible, but this can take several hours per day and so it may be more practical to tube feed. In essence, the simplest, most physiological, and safest route to provide a patient’s nutritional requirements should be sought, while taking into account the practicalities of feeding. Occasional unusual and unsuspected routes deliver nutrients into the body (see below). The route of feeding can have major effects on nutrient requirements, particularly parenteral nutrition.
Parenteral nutrition
The use of the intravenous route for feeding raises a number of new issues, especially in relation to nutrients which are poorly absorbed by the gut. For some nutrients, such as sodium, potassium iodide, fluoride, and selenium, which are well absorbed, the intravenous requirements are similar to the oral requirements. For nutrients that are poorly absorbed, such as iron, calcium, and especially chromium and manganese, the intravenous requirements are considerably lower than the oral requirements, sometimes up to 10-fold lower (Figure 1.6). If the doses of some of these trace elements or minerals recommended for oral nutrition were to be used intravenously over prolonged periods of time, they would probably produce toxic effects.
Figure 1.6 Recommended doses of vitamins and trace elements for intravenous (IV) nutrition expressed as a percentage of the recommended nutrient intake (UK values). Those marked with an asterisk indicate nutrients for which there was inadequate information to establish a reference nutrient intake (RNI). For these nutrients, the midpoint of the estimated average oral intake is used for comparative purposes.
This consideration highlights the key role of the gut in regulating the amount of micronutrients absorbed in health. Sometimes the gut plays the only important role in controlling the status of nutrients within the body. For example, there is no effective physiological way of eliminating excess iron once it is within the body. In contrast to the recommended intakes of intravenous trace elements, those for intravenous vitamins are usually higher than the RNI for oral nutrition (Figure 1.6). There are several reasons why this is so. First, patients receiving parenteral (intravenous) nutrition usually have severe disease, which may increase the requirements for some vitamins. Second, patients are often affected by preexisting malnutrition and are in need of repletion. Third, the prescribed nutrients may not be delivered to the patient because they are lost during preparation or storage (e.g. vitamin C may be oxidised by oxygen present in the bag, a process catalysed by copper; vitamin A may be destroyed by sunlight; and some nutrients may be adsorbed on to the plastic bag containing the parenteral nutrition solution).
Gastric and jejunal feeding
Feed may be delivered directly into the stomach using a nasogastric tube, or a gastrostomy tube for long-term feeding in patients with swallowing difficulties. Jejunal feeding (e.g. jejunostomy or nasojejunal tube feeding) can be used in patients with poor gastric emptying, those at risk of regurgitation and aspiration pneumonia, and those with abnormal gastric anatomy and function. Nutrient requirements associated with these routes of feeding when the bowel is functioning normally are generally similar to those for oral feeding, although many patients on long-term tube feeding are physically inactive due to the underlying disease, and therefore their energy requirements may be less than in healthy subjects. An unusual complication of enteral tube feeding concerns the neurological control of eating. A few children who start tube feeding when young and continue receiving it for prolonged periods may ‘forget’ how to eat. They may have to relearn how to eat when tube feeding is terminated. In contrast, some patients with dementia appear to forget how to eat, have difficulty in relearning, and thus need to start tube feeding.
Cutaneous (skin)
Essential fatty acid deficiency can be treated or prevented by topical skin application of corn oil or safflower oil, which allows sufficient uptake of essential fatty acids into the body. These observations are of more scientific/historical than practical clinical interest, since essential fatty acids can usually be delivered into the gut or directly into veins. Irradiation of the skin with ultraviolet light can also be used to prevent vitamin D deficiency in housebound patients not exposed to direct sunlight. Alternatively, vitamin D tablets can be prescribed, especially since the amount of vitamin in the normal diet is unlikely to be sufficient to meet the RNI (10 µg/day for subjects aged over 50 years, according to UK recommendations).
Subcutaneous
Subcutaneous infusions of saline/dextrose may be given to maintain comfort and hydration in some terminally ill patients requiring palliative care who cannot drink or eat and who have poor venous access.
Rectal
One of the physiological functions of the large bowel is to absorb salt and water, a property that can be utilised by a rectal infusion of saline in terminally ill patients who are unable to eat/drink and have poor venous access. In the past, rectal feeding was used to provide a range of other nutrients, including alcohol, which is relatively well absorbed from the large bowel. In 1881, American President James A. Garfield received rectal feeding, which included alcohol, during his terminal illness following a gunshot wound inflicted by an assassin.
Peritoneal
During peritoneal dialysis with solutions of hypertonic glucose, which can cross the peritoneal membrane, several hundred calories may enter the systemic circulation. This is a side effect of treatment that is often not appreciated.
It is useful to remember that tissues that are used to provide nutritional access to the body can also be sites of abnormal nutrient losses; for example, loss of protein, loss of trace elements from burned skin, loss of protein from the kidney of patients with nephrotic syndrome, and loss of a variety of nutrients from the gut in patients with inflammatory bowel disease or diarrhoea.
Effect of the phase of disease on nutritional requirements
One of the first steps in the management of patients with severe acute disease is to resuscitate them to establish adequate oxygenation and acid–base status, as well as cardiovascular and metabolic stability. This may involve correcting dehydration or overhydration, and treating any hypoglycaemia or hypothermia. Aggressive nutritional support before this stability is established can precipitate further problems with adverse clinical outcomes. For example, a common consequence of major abdominal surgery or systemic illness is ileus or slow gastric emptying. To facilitate oral feeding after surgery, several actions are useful. These include:
Using appropriate analgaesia, including local anaesthetics given via a continuous epidural catheter during the first few days after surgery (this minimises the need for opiates, which have inhibitory effects on gastrointestinal motility).
Avoiding overhydration, which predisposes to postoperative ileus.
Ensuring that the patient is fully informed that they should eat.
For some patients, there are risks with giving normal food or oral nutrition shortly after surgery. Aggressive feeding by mouth or by a nasogastric tube may still lead to gastric pooling, predisposing to nausea, vomiting, regurgitation, or aspiration pneumonia. This is more likely to happen in patients who have swallowing problems or preexisting reflux problems (e.g. in association with a hiatus hernia), or who are nursed in a horizontal position.
Aggressive intravenous nutrition with copious amounts of glucose in the early phase of an acute illness, when there is insulin resistance, can result in hyperglycaemia, hyperosmolarity, and exacerbation of existing metabolic instability. During the early phase of a severe acute illness, it may therefore sometimes be necessary to start with hypocaloric nutrition and increase this over a period of time. This is to ensure metabolic stability and tolerance to nutrients, while maintaining adequate tissue function and limiting excess N loss.
Figure 1.7 Time frame for the management of a child with severe malnutrition (the 10-step approach recommended by the WHO (2000)).
Tissue repletion is mainly recommended during the recovery phase of an acute illness. Similarly, in obese patients the focus on long-term weight loss usually occurs after the acute phase of illness.
The WHO has provided a 10-step guide to the nutritional management of malnourished children, which reemphasises the need to consider nutritional support according to the phase of disease. Again, this begins with the stabilisation phase, associated with resuscitation, which is followed by the rehabilitation phase, which can take several weeks, and finally the follow-up phase (Figure 1.7). It is notable that the guidelines suggest withholding iron supplementation during the early phase of illness. This is because of concern about the possible adverse effects of iron, which has prooxidant properties that facilitate formation of free radicals, which in turn produce cellular damage. The risk is considered to be greater during the early phase of disease, when oxidant stresses are high and antioxidant defences are frequently low as a result of preexisting malnutrition.
A particular complication of aggressive refeeding of malnourished individuals is the refeeding syndrome. Rapid refeeding of such individuals can precipitate respiratory, cardiovascular, and metabolic problems, which may result in sudden death. For example, sudden death was reported when victims of World War II concentration camps were rapidly refed, especially with high-carbohydrate diets. The metabolic abnormalities of the refeeding syndrome include low circulating concentrations of potassium, magnesium, and phosphate, which enter lean tissue cells during the process of repletion under the influence of insulin. The low circulating concentrations of these nutrients can precipitate cardiac arrhythmias and sudden death. Slow initial refeeding while monitoring the circulating concentration of these nutrients can reduce the risk of developing the refeeding syndrome. Precise feeding schedules vary from centre to centre, but they may begin with half or less than half of the requirements in severely depleted individuals.
Alterations in nutritional therapy during the course of an acute disease may occur because the underlying disease has produced new complications or because it has resolved. Similarly, in more chronic conditions there is a need to review the diet at regular intervals. A therapeutic diet lacking particular dietary components may no longer be needed if, for example, a specific food allergy or sensitivity has resolved. Another consideration is whether a vulnerable developmental period has passed. It used to be thought that cerebral damage due to PKU did not occur after the early developmental period and that it would thus be possible to replace the phenylalanine-poor diet with a more normal diet during later childhood, despite persistence of the underlying metabolic abnormality. Children who reverted to a normal diet, especially during early childhood, were however found to be particularly vulnerable to regression of the developmental quotient (IQ) and development of other neurological symptoms. Children who stopped the phenylalanine-poor diet at or after the age of 15 were generally not affected in this way, but few long-term follow-up studies (e.g. 20–30 years) have examined effects on IQ. Many centres therefore recommend some restriction of phenylalanine throughout life.
Feeding schedules
In healthy people, food is normally ingested during a small number of meals, usually two to three per day, although additional snacks may also be taken. Most patients with disease follow similar patterns of eating, but some may require different feeding schedules. For example, children with certain forms of glycogen storage disease need to ingest small, frequent meals rich in carbohydrate to prevent hypoglycaemia. In patients receiving artificial nutritional support (enteral tube feeding or parenteral nutrition), less physiological feeding schedules may be employed, out of either necessity or convenience. Continuous feeding over prolonged periods of time, up to 24 hours per day, is simple and convenient to carers managing bed-bound patients, including those who are unconscious. Continuous feeding over prolonged periods may also be necessary when only slow rates of feeding are tolerated. For example, patients with certain intestinal problems, such as the short bowel syndrome, may be able to tolerate and absorb sufficient nutrients to meet their needs only if the gut is infused slowly with nutrients over a prolonged period of time during the day and the night. Such an enteral feeding schedule may avoid the need for parenteral nutrition, which is less physiological, more costly, and often associated with a greater number of serious complications.
