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PAEDIATRIC GASTROENTEROLOGY José M Moreno-Villares • Isabel Polanco CLINICAL PUBLISHING An Atlas of Investigation and Management

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Page 1: PAEDIATRIC - Clinical Publishing ebook Chp 1.pdfPAEDIATRIC GASTROENTEROLOGY ... London, UK Iñaki Eizaguirre, MD, PhD Paediatric Surgery Department ... Associated Professor of Paediatrics

PAEDIATRIC GASTROENTEROLOGY

José M Moreno-Villares • Isabel Polanco

CLINICAL PUBLISHING

An Atlas of Investigation and Management

Moreno-V

illares • Polanco

CL

INIC

AL

PU

BL

ISHIN

G

An Atlas of Investigation and Management

PAEDIATRICGASTROENTEROLOGYWritten by practising clinicians, this comprehensive full-colouratlas provides essential reading for all those who managepaediatric disorders. All the major disorders of paediatricgastroenterology are covered in this volume: diarrhoea andvomiting, coeliac disease, cow’s milk allergy, inflammatorydisorders, short bowel syndrome, appendicitis, gastrointestinalbleeding, liver disease, and abdominal masses. More unusual andchallenging aspects such as congenital gastrointestinalmalformations, diagnosing abdominal pain, failure to thrive, andpaediatric clinical dietetics are also addressed. There is a wealthof valuable information on how to make accurate diagnoses andeffectively manage children with gastrointestinal disorders,presented in a logical clear way, taking the reader throughclinical presentation, differential diagnosis, prognosis andtreatment options.

Concisely written and with numerous illustrations, PaediatricGastroenterology: an Atlas of Investigation and Managementprovides an easy and accessible format to quickly read andreview material. Readers will find this an invaluable aid toidentify disorders correctly through visual memory, createinvestigative strategies for diagnosis and determine appropriatemanagement.

Related titles:

Esophageal Diseases: an Atlas of Investigation and ManagementMF VaeziISBN 978 1 904392 55 2

Inflammatory Bowel Disease: an Atlas of Investigation and ManagementTR Orchard, R Goldin, P TekkisISBN 978 1 84692 013 4

Website: www.clinicalpublishing.co.uk

ISBN: 978 1 84692 009 7

9 781846 920097

ISBN 978-1-84692-009-7PA

ED

IAT

RIC

GA

STR

OE

NT

ER

OL

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Page 2: PAEDIATRIC - Clinical Publishing ebook Chp 1.pdfPAEDIATRIC GASTROENTEROLOGY ... London, UK Iñaki Eizaguirre, MD, PhD Paediatric Surgery Department ... Associated Professor of Paediatrics

CLINICAL PUBLISHINGOXFORD

An Atlas of Investigation and Management

PAEDIATRICGASTROENTEROLOGY

José M Moreno-Villares, MDNutrition Unit

Department of PaediatricsHospital Universitario 12 de Octubre

Madrid, Spain

Isabel Polanco, MD, PhDProfessor of Paediatrics

Head of Department of Paediatric Gastroenterology and NutritionHospital Infantil Univeritario La Paz

Facultad de Medicina, Universidad AutónomaMadrid, Spain

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Clinical Publishingan imprint of Atlas Medical Publishing LtdOxford Centre for InnovationMill Street, Oxford OX2 0JX, UK

Tel: +44 1865 811116Fax: +44 1865 251550Email: [email protected]: www.clinicalpublishing.co.uk

Distributed in USA and Canada by:Clinical Publishing30 Amberwood ParkwayAshland OH 44805 USA

Tel: 800-247-6553 (toll free within U.S. and Canada)Fax: 419-281-6883Email: [email protected]

Distributed in UK and Rest of World by:Marston Book Services LtdPO Box 269AbingdonOxon OX14 4YN UK

Tel: +44 1235 465500Fax: +44 1235 465555Email: [email protected]

© Atlas Medical Publishing Ltd 2009

First published 2009

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted,in any form or by any means, without the prior permission in writing of Clinical Publishing or Atlas MedicalPublishing Ltd.

Although every effort has been made to ensure that all owners of copyright material have been acknowledgedin this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions broughtto our attention.

A catalogue record of this book is available from the British Library

ISBN-13 978 1 84692 009 7ISBN e-book 978 1 84692 604 4

The publisher makes no representation, express or implied, that the dosages in this book are correct.Readers must therefore always check the product information and clinical procedures with the mostup-to-date published product information and data sheets provided by the manufacturers and the mostrecent codes of conduct and safety regulations. The authors and the publisher do not accept anyliability for any errors in the text or for the misuse or misapplication of material in this work.

Printed by Henry Ling Ltd, Dorchester, Dorset, UK

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Preface vi

Contributors vi

Abbreviations viii

1 Failure to thrive in infants and children 1JOSÉ M MORENO-VILLARES, MD, AND

ANTONIO MONICA GUERRA, MD

2 Vomiting 11JOSÉ M MORENO-VILLARES, MD, AND

MARÍA JOSÉ GALIANO SEGOVIA, MD

3 Diarrhoea 19Acute diarrhoea 19ENRIQUETA ROMÁN RIECHMANN, MD

Chronic diarrhoea 25ANGELES CALZADO AGRASOT, MD, BEGOÑA POLO MIQUEL, MD, AND

CARMEN RIBES-KONINCKX, MD, PHD

4 Constipation 34CAROLINA GUTIÉRREZ, MD, AND

JERÓNIMO GONZÁLVEZ, MD

5 Abdominal pain in childhood 46IÑAKI X. IRASTORZA TERRADILLOS, MD, AND

JUAN C. VITORIA CORMENZANA, MD, PHD

6 Gastrointestinal bleeding 56GEORGE GERSHMAN, MD, PHD

7 Cow’s milk allergy 65ANTONIO NIETO, MD, PHD, AND

ANGEL MAZÓN, MD

Contents

8 Abdominal masses 72JUAN A. TOVAR, MD, PhD

9 Liver disease 84Cholestasis 84PIOTR SOCHA, MD, JOANNA PAWŁOWSKA, MD, AND

ANIL DHAWAN, MD, FRCPCH

Hypertransaminasaemia in childhood 92LUÍS PEÑA-QUINTANA, MD, AND

DANIEL GONZÁLEZ-SANTANA, MD

10 Coeliac disease 99ISABEL POLANCO, MD, PHD

11 Ulcerative colitis 104CARLOS SIERRA SALINAS, MD, AND

JAVIER BLASCO ALONSO, MD

12 Crohn’s disease 110DAVID ZIRING, MD, AND

JORGE VARGAS, MD

13 Short bowel syndrome 117JAVIER BUENO, MD

14 Congenital gastrointestinal malformations 124

IÑAKI EIZAGUIRRE, MD, AND

AGUSTÍN NOGUÉS, MD

15 Paediatric appendicitis 134ADOLFO BAUTISTA CASASNOVAS, MD

16 Paediatric clinical dietetics 144AMAYA PEÑALVA ARIGITA, RD

Index 155

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ContributorsAdolfo Bautista Casasnovas, MD, PhDHead of Paediatric Surgery SectionUniversity Hospital of Santiago de

CompostelaSantiago de Compostela, Spain

Javier Blasco Alonso, MDGastroenterology, Hepatology and

Nutrition DivisionHospital Materno-InfantilMálaga, Spain.

Javier Bueno, MDPaediatric Liver Transplantation UnitPaediatric Surgery DepartmentHospital Valle de HebrónBarcelona, Spain

Mª Ángeles Calzado Agrasot, MDPaediatric Gastroenterology and

Hepatology Unit Hospital La FeValencia, Spain

Anil Dhawan, MD, FRCPCHPaediatric Liver CentreInstitute of Liver StudiesVariety Club Children’s HospitalKing’s College HospitalLondon, UK

Iñaki Eizaguirre, MD, PhD Paediatric Surgery DepartmentDonostia HospitalSan Sebastian, Spain

María José Galiano Segovia, MDCentro de Salud Maria MontessoriLeganésMadrid, Spain

George Gershman, MD, PhDAssociate Professor of Pediatrics David Geffen School of MedicineChief, Division of Pediatric

Gastroenterology and NutritionHarbor-UCLA Medical Center TorranceCalifornia, USA

Jerónimo Gonzálvez Piñera, MD, PhD Associated Professor of Paediatric

SurgeryDepartment of Paediatric SurgeryUniversity General HospitalAlbacete, Spain

provides concise and practical information for readers.Topics on the three main areas of the speciality –gastroenterology, hepatology, and nutrition – constitute thebody of this book. The authors were carefully selected toprovide a comprehensive and clear account of their assignedtopics. All of them have been willing to dedicate their time,knowledge, and effort in preparing their chapters. Our mostsincere thanks to them. It has been a pleasure to work withClinical Publishing’s production team who have helped toproduce a book of outstanding quality.

We hope and expect that this Atlas will be of benefit to allphysicians dealing with gastrointestinal problems inchildren.

José M Moreno-Villares, MDIsabel Polanco MD, PhD

Paediatric gastroenterology emerged as a speciality in the1960s. Since then it has become an essential component ofmajor academic paediatric programmes throughout theworld. The introduction of new diagnostic techniques thatrequired special skills, as well as the development ofcomplex new therapies for children with gastrointestinaldisorders, were cornerstones in the development of thespeciality. The recognition that appropriate nurition duringinfancy and childhood is vital for health and the profoundimpact that many gastrointestinal diseases may have upongrowth also contributed to the discipline’s development.

Many excellent paediatric gastroenterology texts havebeen published since the first textbook on the subject waspublished in the early 1970s, but there are not so many basedon excellent figures and comprehensive tables. PaediatricGastroenterology, An Atlas of Investigation and Management,

vi

Preface

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viiContributors

Daniel González-Santana, MD Paediatric Gastroenterology DivisionLas Palmas de Gran Canaria

UniversityHospital Universitario Materno-Infantil

de CanariasSpain

Antonio Monica Guerra, MD, PhDNutrition UnitUniversity of PortoPorto, Portugal

Carolina Gutiérrez Junquera, MD, PhDAssociated Professor of PaediatricsDepartment of Pediatric

GastroenterologyUniversity General HospitalAlbacete, Spain

Iñaki X. Irastorza Terradillos, MDPaediatric Gastroenterology DivisionHospital de CrucesBilbao, Spain

Angel Mazón, MDPaediatric Allergy DivisionHospital Infantil La FeValencia, Spain

José M. Moreno-Villares, MDNutrition UnitDepartment of PaediatricsUniversity Hospital 12 de OctubreMadrid, Spain

Antonio Nieto, MD, PhDPaediatric Allergy DivisionHospital Infantil La FeValencia, Spain

Agustín Nogués, MD Paediatric Radiology DepartmentDonostia HospitalSan Sebastian, Spain

Joanna Pawłowska, MDDepartment of Gastroenterology,

Hepatology and ImmunologyThe Children’s Memorial Health

InstituteWarsaw, Poland

Luis Peña-Quintana, MDPaediatric Gastroenterology,

Hepatology and Nutrition DivisionUniversity HospitalUniversidad de Las Palmas de Gran

CanariaSpain

Amaya Peñalva Arigita, RDUniversity Hospital Valle de HebrónBarcelona, Spain

Isabel Polanco, MD, PhDProfessor of PaediatricsHead of Department of Paediatric

Gastroenterology and NutritionUniversity Hospital La PazUniversidad AutónomaMadrid, Spain

Begoña Polo Miquel, MDPaediatric Gastroenterology and

Hepatology DivisionHospital La FeValencia, Spain

Carmen Ribes-Koninckx, MD, PhDPaediatric Gastroenterology and

Hepatology DivisionHospital La FeValencia, Spain

Enriqueta Román Riechmann, MDDepartment of PaediatricsHospital de FuenlabradaMadrid, Spain

Carlos Sierra Salinas, MDGastroenterology, Hepatology and

Nutrition DivisionHospital Materno-InfantilMálaga, Spain

Piotr Socha, MDDepartment of Gastroenterology,

Hepatology and ImmunologyThe Children’s Memorial Health

InstituteWarsaw, Poland

Juan A. Tovar, MD, PhDProfessor and Chief, Department of

Paediatric SurgeryUniversity HospitalLa PazMadrid, Spain

Jorge Vargas, MDDivision of Gastroenterology and

NutritionDepartment of PaediatricsMattel Children’s Hospital at UCLALos Angeles, USA

Juan C. Vitoria Cormenzana, MD, PhDProfessor of PaediatricsBasque Country UniversityChief, Paediatric Gastroenterology

DivisionHospital de CrucesBilbao, Spain

David Ziring, MDDivision of Gastroenterology and

NutritionDepartment of PaediatricsMattel Children’s Hospital at UCLALos Angeles, USA

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Abbreviationsviii

α1-ATD alpha-1-antitrypsin deficiency

AAP American Academy of Pediatrics

AFP alpha-fetoprotein

AIH autoimmune hepatitis

ALT alanine aminotransferase

AMA antimitocondrial antibodies

ANA antinuclear antibodies

APC antigen-presenting cell

ASCA anti-Saccharomyces cerevisiae

antibodies

ASMA antismooth muscle

antibody

AST aspartate aminotransferase

BA biliary atresia

BMI body mass index

BRIC benign recurrent intrahepatic

cholestasis

Btl. bottle

BUN blood urea nitrogen

CD coeliac disease

CFU colony-forming units

CK creatine kinase

CM cow’s milk

CMA cow’s milk allergy

CMV cytomegalovirus

CNS central nervous system

CPM caloric–protein malnutrition

CrD Crohn’s disease

CT computed tomography

CTT colonic transit time

Da Dalton

DH dermatitis herpetiformis

DNA HBV hepatitis B virus DNA

EBV Epstein–Barr virus

EC endoscopic capsule

EF elemental formulas

EH extensively hydrolyzed (formula)

EIA enzyme immunoassay

ERCP endoscopic retrograde

cholangiopancreatography

ESPGHAN European Society of

Pediatric Gastroenterology,

Hepatology, and Nutrition

FGID functional gastrointestinal

disorders

FTT failure to thrive

GER gastro-oesophageal reflux

GERD gastro-oesophageal reflux disease

GFD gluten-free diet

GGT gamma glutamyl transpeptidase

GI gastrointestinal

GIST gastrointestinal stromal tumour

GN ganglioneuroma

Hb haemoglobin

HB hepatoblastoma

HC head circumference

Hct haematocrit

HD Hirschsprung’s disease

HIV human immunodeficiency virus

HP Helicobacter pylori

HPN home parenteral nutrition

HSP Henoch–Schönlein purpura

HUS haemolytic uraemic syndrome

IBD inflammatory bowel disease

IBS irritable bowel syndrome

IF infant formula

IDI intractable diarrhoea of infancy

IGF-1 intestinal growth factor

IL interleukin

INSS International Neuroblastoma

Staging System

IQ intelligence quotient

LA laparoscopic appendectomy

LDH lactate dehydrogenase

LF lactose-free (formula)

LKM liver/kidney microsomal

antibodies

MAC middle arm circumference

MCV mean cell volume

MIBG meta-iodine-benzyl-guanidine

MRI magnetic resonance imaging

NAFLD nonalcoholic fatty liver disease

NASH nonalcoholic steatohepatitis

NB neuroblastoma

NEC necrotizing enterocolitis

NK natural killer cells

NKT natural killer T cells

NPD negative predictive value

NSAID nonsteroidal anti-inflammatory

drug

OA open appendectomy

OCTN organic cation transporter gene

ORS oral rehydration solution

ORT oral rehydration therapy

pANCA anti-neutrophil cytoplasmic

antibody with perinuclear staining

pattern

PFIC progressive familial intrahepatic

cholestasis

PH partially hydrolyzed (formula)

Pi protease inhibitor

PN parenteral nutrition

PPV positive predictive value

RAST radioallergosorbent test

RDA recommended dietary allowances

RDW red blood cell differentiation width

RNA HCV hepatitis C virus RNA

SBS short bowel syndrome

Sc scoop

SE semi-elemental (formula)

SGOT serum glutamic oxalacetic

transaminase

SGPT serum glutamic pyruvic

transaminase

SIOP Societé Internationale d´Oncologie

Pédiatrique

STEP serial transverse enteroplasty

TPN total parenteral nutrition

TNF tumour necrosis factor

TS tricipital skinfold

TSH thyroid stimulating hormone

UC ulcerative colitis

UPDG galactose-1-phosphate-uridyl

transferase

US ultrasonography

WBC white blood count

WD Wilson´s disease

WI Waterloo index

WHO World Health Organization

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Failure to thrive in infants and childrenJosé M Moreno-Villares, MD, and Antonio Monica Guerra, MD

Chapter 1

Introduction

Evaluation of growth and development in the primary caresetting is a cornerstone of paediatric care. Usually headcircumference, weight, and length are measured at birth,and then on an intermittent basis throughout the rest ofchildhood. When a divergence from the standard growthcurve occurs, in either direction, a careful assessment isrequired to determine the aetiology.

Undernutrition or ‘failure to thrive’ (FTT) is a commonnutritional problem in the infant and toddler paediatricpopulation. The identification of patients with FTT is aroutine part of residency training in paediatrics.

Inappropriate nutrient intake and growth parameters

FTT is a clinical label frequently used to describe infantsand young children, generally under 3 years, who fail togrow as expected using established growth standards for ageand gender along a period of time (usually longer than 3months) (1.1).

Weight is a measure of the varying combination of height,body fat, and muscle bulk, which makes it a lessstraightforward measure of growth than height.Nevertheless, because of its widespread availability and easeof measurement, it is the most usual tool when growthmeasure is considered. What constitutes a normal rate ofweight gain (Table 1.1)? It is often assumed that normalgrowth constitutes tracking along the birth centile. However,weight at birth is a reflection of the intrauterine environmentand is of limited prognostic value. Many children deviatefrom their earlier centile position, and this divergence may

1

1.1 Eleven-month-old male, with growth faltering in thelast 4–5 months, more severe in the last 2 weeks.Reduction in >2 major percentiles for weight.

not become pathological. Although the most commonlyused definition of abnormality is that falling below apredetermined centile, usually the third (1.2), this wouldinclude a number of constitutionally small children. Analternative definition applies when a child has a weight curvethat has fallen more than two standard deviations or

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Failure to thrive in infants and children2

Normal weight gain

Birth to 5 months 15–30 g/day

6 to 12 months 15 g/day

12 months to 2 years 6–8 g/day

2 years to 6 years 38 g/month

Frequency of monitoring

Monthly for the first two months, every other month from 2 to 6 months; every 3rd month from 6 to 24 months, and yearly from 2 to 6 years old

Table 1.1 Normal weight gain and frequency ofmonitoring

1.2 An 18-week-old female, with irritability and poor weightgain since birth. Weight below 3rd percentile.

Definition of FTT

FTT describes an infant or child whose current weight orrate of weight gain is significantly below that expected ofsimilar children of the same age and sex. Most paedia tri ciansdiagnose FTT when a child’s weight for age falls below thefifth percentile of the standard growth charts or it crosses twomajor percentile lines (1.3). One problem arises from the useof different growth charts; misinter pretation may occur ifdifferent genetic back grounds are not considered. Thisproblem may be overcome if universal growth referencescould be used. The World Health Organization (WHO) hasrecently published charts resulting from the MulticenterGrowth Reference Study, and are intended to substitute forthe National Center for Health Stat istics/WHO(NCHS/WHO) growth reference, which has beenrecommended for international use since the late 1970s(www.who.int/childgrowth/standards/curvas_por_indicadores/en/index.html) (1.4, 1.5).

FTT is not a final diagnosis but a description of a physicalstate; therefore, a cause must always be sought. Because the description itself is vague it has been proposed to usegrowth failure or undernutrition as a diagnostic replacementfor FTT.

percentiles below a previously established rate of growth.However, up to 30% of healthy term infants cross onepercentile line and 23% cross two percentile lines (in eitherdirection) by the age of 2 years.

1.3 Four-month-old male. Loss of >2 major percentilessince birth.

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Until recently, the evaluation of a child with FTT focusedon factors related to external environment or to medicalcauses. Currently, the child’s feeding behaviour and theinteraction between the caregiver and the child has taken ongreater importance. Feeding is an interactive process thatdepends upon abilities and characteristics of both theparents and the child.

Aetiology

FTT has been historically dichotomized as organic versusnonorganic (1.6). Organic FTT results from a major organsystem illness or dysfunction, while nonorganic FTT isgenerally a diagnosis of exclusion. A third category has beenadded, mixed FTT, to recognize the fact that many organicFTT often have a psychological component. This approachis quite simplistic and inadequate for patient management.There is growing evidence that feeding difficulties are

Failure to thrive in infants and children 3

A

B

1.4 WHO growth curves. Height/length for age (boys).

A

B

1.5 WHO growth charts. Length/height for age (girls).

1.6 Aetiology of FTT.

Organiccauses

Nonorganiccauses

False failure to thrive

central to the development of the disorder. Family stressors,psychiatric disorders of parents, and disturbances in theinfant–parent relationship may interfere with thedevelopment of an adequate feeding relationship.

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Failure to thrive in infants and children4

It is important to note that an infant presenting withpresumed FTT may have a normal variant of growth1.Specific infant populations with growth variations also need

Genetic short Ex-premature Constitutional Catch down stature infant delay growth

Birth weight Low to normal Normal if corrected Low to normal Above expected for for gestation genetic background

Parental percentiles Low Normal Normal Normal

Progress along Low percentile but Low if corrected May be an initial Initial fall in 6–12 percentiles do not cross but follow fall in first 6 months months and then

percentiles percentile curves and then follow follow percentilespercentiles

Table 1.2 Normal variants of growth presenting as FTT

Inadequate caloric intake• Food not available– Type or volume of food not appropriate (e.g. too diluted

formula)– Poverty and food shortages– Neglect– Feeding technique, parent–infant interaction problems• Lack of appetite– Chronic illness– Psychosocial disorder• Mechanical feeding difficulties, e.g. oral-motor

dysfunction or malformation

Reduced absorption or digestion of nutrients• Pancreatic insufficiency: cystic fibrosis• Loss or damage to villous surface– Coeliac disease– Cow’s milk protein allergy– Vitamin or mineral deficiencies• Cholestasis

Excessive loss of nutrients• Vomiting– Gastro-oesophageal reflux– Other causes of vomiting: central nervous system

disorders, metabolic disease• Malabsorption/diarrhoea– Inflammatory bowel disease– Short bowel syndrome• Renal losses– Renal failure or tubular acidosis– Diabetes mellitus or diabetes insipidus

Defective utilization• Chromosomal or genetic abnormality• Metabolic disorder• Endocrine disorder• Congenital infections

Increased metabolism• Chronic infection or inflammation• Hypoxaemia (congenital heart disease, chronic lung

disease)• Hyperthyroidism• Malignancy

Table 1. 3. Classification of FTT by pathological causes

to be considered when making the diagnosis of FTT, forinstance, infants with intrauterine growth retardation orpremature infants.

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Within the group of normal variants of growth presentingas FTT, four main patterns occur (Table 1.2)2. There arealso growth curves available for syndromes with abnormalgrowth (e.g. Down syndrome, Noonan syndrome,Prader–Willi syndrome) (1.7, 1.8). There are many reasonswhy an infant does not take on adequate nutrition. A moreuseful classification of FTT is then based onpathophysiology, as shown in Table 1.3.

Evaluation

History and examinationThe history is essential in defining the underlying cause ofgrowth failure in children (1.9). The evaluation shouldinclude an assessment of the diet and eating behaviours, pastand current medical, social, and family history, and shouldinclude a complete physical examination (Table 1.4)3. A

Failure to thrive in infants and children 5

1.7 Patients with special conditions, e.g. Down syndrome,chromosomopathies and other genetic conditions, havetheir own growth rate and deserve specific growth curves.

1.8 Patient with a Silver–Russell syndrome.

1.9 Algorithm ofmanagement ofFTT in primarycare.

FFT is suspected

Basic laboratoryinvestigations

Treatment –primary care

Clinical history Physical examination

Assessment of intake

Further work up/treatment –hospital

Success

Lack of success

Follow upNutritional advice

Psychological support

Red flag signs

Nonorganic failure to thrive

Most likely normal variant of growth

Organic failure to thrive Anomalous results?

NoYes

Hospital

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Dietary history

• Amount of food and/or formula

• Is the formula prepared correctly?

• Food patterns: types of foods, especially beverageconsumption (milk, juices, sodas)

Feeding history

• When does the child eat? Where? With whom?

• Breastfed?

• Positioning of the child

• Feeding battles

• Snacking

Past and current medical history

• Obstetric history

• Birth history, including weight and height

• Neonatal period

• Recent acute illness especially upper airway infections,otitis, gastroenteritis

• Are they recurrent?

• Chronic medical conditions

• Past hospitalizations, injuries, accidents

• Vomiting?

Social history

• Who lives in the home?

• Who are the caregivers?

• Who helps to support the family?

• What is the child’s temperament?

• Any family problems?

Family history

• Medical conditions or FTT in siblings

• Growth pattern in other members of the family,especially parents and siblings

• Mental illness

Table 1.4 Evaluation of medical history in FTT

Normal Mild risk Moderate risk High risk

Weight for age (%) >90 75–89 60–74 <60%

Weight for height (%) >90 80–90 70–79 70%

Height for age (%) >95 95–90 89–85 <85%

Table 1.5 Classification of undernutrition in children15, 16

The severity of a child’s undernutrition can be classifiedmost easily using the Waterlow and Gomez criteria (Table1.5), as a percentage of the median for age. Further examina -tion beyond growth should include physical examination(1.10), including inspection of any physical sign of neglect orabuse, stigmas of underlying syndromes, dysmorphicfeatures, skin rashes, and observation of feeding if possible.

thorough psychosocial history is mandatory. An accurateassessment of growth requires the evaluation of current andpast parameters including height or length, weight, and headcircumference. Occasionally further assessments areperformed such as mid-upper arm circumference, variousskin fold thicknesses, body proportions and, if indicated,puberal assessment.

Failure to thrive in infants and children6

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1.10 Clinical signs of malnutrition in a patient with FTTwho was found to have coeliac disease.

Initial evaluation

• Full blood examination/erythrocyte sedimentation rateor C-reactive protein

• Chemistry panel: urea, creatinine, lytes

• Iron status: iron, ferritin, transferrin, % saturation

• Blood glucose

• Liver function tests: GGT, SGPT, SGOT, alkalinephospatase, bilirubin

• Urinalysis

• Urine culture

Second step

• Acid–base balance

• Immunoglobulins

• Coeliac screen

• Thyroid function test

• Bone age

• Stool microscopy and culture

Third step (if clinically indicated or abnormal data from the initial investigations)

• Metabolic screen (blood and urine for organic acidsand amino acids, ammonia, lactic/pyruvic acids, ketone bodies in urine)

• Karyotype

• Allergy investigations

• Sweat test

• pHmetry/endoscopy

Table 1.6 Investigations in failure to thrive

7Failure to thrive in infants and children

Observing or videotaping the interaction between aparent and a child, especially during a feeding session in theoffice, may provide valuable information about the aetiologyof FTT4.

InvestigationsLaboratory evaluation should be guided by history andphysical examination findings only. A well-targeted batteryof investigations may provide guidance. There are noroutine laboratory tests that should be performed on everychild, because the majority of children with FTT have nolaboratory abnormalities. In those requiring investigation, asimple initial sequence can be performed (Table 1.6).

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Treatment

Medical intervention is dictated by the disease diagnosed.Addressing identified issues of attachment and otherpsychosocial issues is crucial and often requires input froma multidisciplinary team. Most cases can be managed bynutrition intervention or feeding behaviour modification.Evaluation and treatment is generally accomplished inoutpatient settings rather than in the hospital.

Nutritional rehabilitation by means of increased caloricintake is often best supervised with the advice of anexperienced dietician, allowing exact caloric requirements tobe calculated. Asking the parent to write down the type offood and amounts a child eats over a 3-day period is one wayof quantifying caloric intake.

Failure to thrive in infants and children8

Dietary recommendationsChildren with FTT will need 150% of the recommendeddaily caloric intake, based on their expected, not actual,weight for height if tolerated5. As most of these children lackthe normal responses to internal hunger/satiation cues, highenergy snacks may improve their nutritional status6. Ininfants this increased caloric intake may be accomplished byconcentrating the infant formula or adding carbohydrates orlipids to the formula or the puréed foods (1.11). Toddlerscan receive more calories by adding cheese, butter, and soon to common toddler foods. In toddlers and older childrenwe can also use high-calorie milk drinks, that provide1.0–1.5 kcal/ml. Vitamin and mineral supplementation isalso sometimes required. If all these attempts fail it may benecessary to consider nasogastric tube feedings as a lastresort (1.12)7. The advantages are ensuring adequate caloricintake and decreasing or eliminating some of the emotionalstress and frustrations with feeding times. However, thereare also disadvantages, including the suppression of appetiteand sometimes the modification of feeding behaviour.

1.11 There are two ways to increase the caloric intake in an infant: to increase the strength of the regular formula or toadd caloric modules (carbohydrates or lipids or both) to the regular formula.

Infant formula 13% (68 kcal/100 ml)

Concentrate formula to 17%(89 kcal/100 ml)

Concentrate formula to 20%(105 kcal/100 ml)

Concentrate formula to 15%(78 kcal/100 ml)

Add maltodextrin 5 g/100 ml (20 kcal)

Add maltodextrin 5 g/100 ml (20 kcal)

Add MCT oil 2 ml/100 ml (16 kcal)

Add modulesConcentrateformula

(powder)

1 measure in 26 ml

1 measure in 23 ml

1 measure in 20 ml

88 kcal/100 ml

104 kcal/100 ml

124 kcal/100 ml

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Feeding or eating behavioursParental anxiety about a child’s FTT can be helped byreassurance. Paediatricians can intervene effectively in manyfeeding problems, providing useful guidance for parents(Table 1.7). Hospitalization is rarely required and may becounterproductive8. It may be necessary when the safety ofa child is a concern, outpatient management has failed, or ifthe FTT is severe.

Outcomes

It is ascertained that children with FTT are at risk of adverseoutcomes such as short stature, behaviour problems, anddevelopmental delay9–12. However, there are only a limitednumber of outcome studies on children with FTT, withdifferent definitions and designs, so it is difficult to make an

assessment on long-term results of FTT. Rudolph andLogan found only a small difference in intelligence quotient(IQ) (equivalent to 3 IQ points) in children with FTTcompared to their peers13. This small difference is ofquestionable clinical significance. The height and weightdifferences in their analysis were larger, but few childrenwere below the 3rd percentile at follow-up. In the light ofthese results, the aggressive approach to the identificationand management of FTT needs reassessing13.

In addition, it is often difficult to disentangle the effects ofFTT from those of the high-risk environments in whichFTT often occurs (poverty, family stress, and poor parentalcoping skills). Nevertheless, to decrease the risk of adverseeffects, it is important to recognize and treat FTT promptly.Sometimes this necessitates the intervention of community-based resources14.

Failure to thrive in infants and children 9

1.12 In some severe FTT cases, especially if an organiccondition is underlying, it is necessary to provide enteralnutrition through a nasogastric tube. This patient hasbiliary atresia and FTT.

1 Make mealtimes pleasant

2 Avoid battles over eating. Encourage your child.Food should be used as nourishment, not as areward or punishment

3 You are responsible for deciding what food your child is offered; your child decides how much to eat

4 Offer a variety of healthy and tasty foods

5 Establish a routine of meals and snacks and settimes

6 Recognize your child’s cues indicating hunger,satiety, and food preferences

7 Accept your child’s wish to feed him- or herself

8 Try to eat together as a family

9 Establish a maximum time to finish a meal (forinstance 30 minutes)

10 Limit possible distractions during meals

Table 1.7 Useful guidance for parents. Tips forpreventing food hassles

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10 Failure to thrive in infants and children

10 Corbett SS, Drewett RF. To what extent is failure tothrive in infancy associated with poorer cognitivedevelopment? A review and meta-analysis. J Child PsycholPsychiatr 2004;45:641–54.

11 Zenel JA. Failure to thrive: a general pediatrician’sperspective. Pediatr Rev 1997;18: 371–8.

12 Drewett RF, Corbett SS. Cognitive and educationalattainments at school age of children who failked to thrivein infancy: a population-based study. J Child PsycholPsychiatr 1999;4:551–61.

13 Rudolf MCJ, Logan S. What is the long-term outcomefor children who fail to thrive? A systematic review. ArchDis Child 2005;90:925–31.

14 Wright CM, Callum J, Birks E, Jarvis S. Effect ofcommunity based management in failure to thrive:randomized controlled trial. BMJ 1998;317:571–4.

15 Waterlow JC. Classification and definition of protein-calorie malnutrition. BMJ 1972;3:566–9.

16 Gomez F, Ramos-Galvan R, Frenk S, Cravioto JM,Chavez R, Vazquez J. Mortality in second and thirddegree malnutrition. J Trop Paediatr 1956;2:77–83.

General reading

Frank DA, Zeisel SH. Failure to thrive. Pediatr Clin NorthAm 1988;35:1187–1206.

Gahagan S, Holmes R. A Stepwise approach to evaluationof undernutrition and failure to thrive. Pediatr Clin NorthAm 1998;45:169–87.

Jolley CD. Failure to thrive. Curr Probl Pediatr Adolesc HealthCare 2003;33:183–205.

Kessler DB, Baker SS, Silverman LA. Growth assessmentand growth failure. Consensus in Paediatr 2004;1:1–28.

Conclusion

It is common to confuse the description of poor growth witha diagnosis. The term ‘failure to thrive’, although firmlyentrenched in the medical lexicon, adds little to ourunderstanding of this condition and does not guide ourapproach. Many have suggested it should be abandoned. Itrepresents a nonspecific description of symptoms ratherthan a specific condition. Paediatricians and otherhealthcare workers must come to a better understanding ofthe complex dynamics of feeding normal children. Whenfeeding and caloric issues have been ruled out, otherconsiderations should be taken into account. It is not aquestion of referring a child who is not growing well to thefeeding expert, the gastroenterologist, or theendocrinologist, but rather the recognition that a rational,sequential approach needs to be followed, to allow forinvestigation of all the possible explanations of why a childis not growing.

References

1 Krugman SD, Dubowitz H. Failure to thrive. Am FamPhys 2003;68:879–84, 886.

2 Bergman P, Graham J. An approach to ‘failure to thrive’.Aus Fam Phys 2005;34:725–9.

3 McCann JB, Stein A, Fairburn CG, Dunger DB. Eatinghabits and attitudes of mothers of children withnonorganic failure to thrive. Arch Dis Child 1994;70:34–6.

4 Satter E. The feeding relationship: problems andinterventions. J Pediatr 1990;117:S181–9.

5 Maggioni A, Lifshitz F. Nonorganic failure to thrive: anoutpatient approach. Pediatr Clin North Am1998;45:169–87.

6 Kasese-Hara M, Wright C, Drewett R. Energycompensation in young children who fail to thrive. J ChildPsychol Psychiatr 2002;43:449–56.

7 Tolia V. Very early onset nonorganic failure to thrive ininfants. J Pediatr Gastroenterol Nutr 1995;20:73–80.

8 Marcovitch H. Failure to thrive. BMJ 1994;308:35–8.9 Dahl M, Kristiansson B. Early feeding problems in an

affluent society. IV. Impact of growth up to two years ofage. Acta Paediatr Scand 1987;76:881–8.

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