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Washington Hilton Washington, DC October 9—10, 2015 CPNP Annual Symposium Program Book 1 1 NOTES Table of Contents President’s Welcome 2 Support 3 Program at a Glance 4 The gut balance revolution Gerard Mullin, MD, The Johns Hopkins University School of Medicine 9 Childhood obesity: Fighting a battle of epic proportions Shikha Sundaram MD and Helen Seagle RD, Children’s Hospital of Colorado 23 “Nutrition ROCKs HCT”: Nutrition Research for Optimizing Care in Kids undergoing hematopoietic cell transplantation Lori Bechard PhD, Med, RD, LDN, Boston Children’s Hospital 29 Nutrition for the child with cystic fibrosis Tami Miller RD, Children’s Hospital of Wisconsin 41 Nutritional issues in cholestatic disease Binita Kamath MBBChir, MRCP, MTR, The Hospital for Sick Children 48 Iron deficiency and the developing brain Michael K. Georgieff, MD, University of Minnesota 57 Nutrition and diet in the management of inflammatory bowel disease Athos Bousvaros MD, MPH and Karen Warman RD, Boston Children’s Hospital 68 Case study breakouts 83 The Elimination Diet: Practical Tips and Assessing nutritional needs in the hypometabolic child Nutrition care for children undergoing hematopoietic cell transplantation Troubleshooting pancreatic enzyme therapy (PERT) in cystic fibrosis Nutritional Issues in Alagille Syndrome Inflammatory Bowel Disease 101 Blenderized Tube Feedings: Managing a New Frontier Margaret Girten RD, CSP, LDN and Julia Driggers RD, LDN, CNSC, Children’s Hospital of Philadelphia 1 President’s Welcome I would like to welcome you all to the third annual NASPGHAN/CPNP Nutrition Symposium. I believe this year’s program is our best ever. We listened to your feedback from last year and made some significant changes. We expanded the nutrition content available on Friday to allow participants to take full advantage of their included registration to the NASPGHAN annual meeting. We shortened most of the talks during our Saturday symposium to allow for a greater number and variety of speakers. We changed our breakout sessions to a roundtable format to allow for more interaction with the presenters and your peers. Let us know what you think about these changes so we can continue to provide a high quality experience. We have also experienced great growth in our Council for Pediatric Nutrition Professionals (CPNP) over this past year. I am delighted to share that we have 130 members as part of our council from throughout North America and we have made great strides towards our council goals. We launched the listserv, developed our website and obtained status as an official provider of continuing professional education (CPE) through the Commission of Dietetic Registration (CDR). We will once again have a brief council meeting during the lunch hour on Saturday. I encourage everyone to attend to learn about what we are currently doing and what we have planned next! We hope you enjoy this year’s symposium. Next year, in lieu of our regular annual meeting will be the World Congress in Montreal, Canada (October 4-10, 2016), including a full day of nutrition content with presenters from around the world. There will be many more details to come regarding this exciting event. We hope to see many of you there! Thank you so much for being here. Sincerely, Jenny Crouse, MS, RD, CD, CDE President, Council for Pediatric Nutrition Professionals 2 NASPGHAN Nutrition Symposium CPNP Founders Thanks to the following companies for their support of this event and the establishment of the Council of Pediatric Nutrition Professionals Abbott Nutrition Dr. Schar Mead Johnson Nutrition Nestlé Nutrition QOL Medical Support for this year’s symposium has been generously provided by: Abbott Nutrition Mead Johnson Nutrition Nestlé Nutrition 3 NASPGHAN/CPNP ANNUAL SYMPOSIUM Friday, October 9, 2015 7:00AM - 8:00AM Meet the professor breakfast (extra fee – ticket required) EoE and Elimination Diets Amir Kagalwalla MD and Sally Schwartz RD 8:15AM – 10:00AM Plenary Session I Fairchild West International Ballroom Center Basic Science Year in Review Nicola Jones MD, PhD, The Hospital for Sick Children Business Meeting Clinical Science Year in Review William Balistreri MD, Cincinnati Children’s Hospital Medical Center 10:30AM – 12:00PM Concurrent Session I Nutrition Moderators: Russell Merritt MD and Ala Shaikhkhalil MD Lincoln Room LONG TERM COMPLICATIONS OF TPN: NOW THAT MY INTESTINAL FAILURE PATIENTS ARE NOT DYING OF LIVER DISEASE, WHAT ELSE SHOULD I WORRY ABOUT? Jane Balint MD, Nationwide Children’s Hospital Learning objectives: 1. Identify potential complications of lipid minimization strategies 2. Describe an approach to micronutrient monitoring in long term parenteral nutrition 3. Discuss renal and bone complications of parenteral nutrition Oral Abstract Presentation COMBATING CLABSIS-PREVENTING CENTRAL LINE INFECTIONS AND OTHER CENTRAL LINE CHALLENGES John Kerner MD, Lucile Packard Children’s Hospital Learning objectives: 1. Identify evidence based practices for CLABSI prevention 2. Describe at least one modality for the prevention of catheter-related venous thrombosis 3. Discuss the approach to the patient with central line occlusion Oral Abstract Presentation 4 Malabsorption Moderators: Michelle Pietzak MD and Maria Mascarenhas MBBS Georgetown Room ADVANCES IN CF THERAPIES AND THEIR EFFECT ON GASTROINTESTINAL MANIFESTATIONS Daniel Gelfond MD, WNY Pediatric Gastroenterology Learning objectives: 1. Outline pathophysiology of CF and impact of CFTR on clinical manifestations 2. Recognize gastrointestinal manifestations of the Cystic fibrosis and discuss therapeutic interventions 3. Outline recent development and advances in CF therapy targeting specific genetic mutations 4. Discuss role of wireless motility capsule as gastrointestinal biomarker of CFTR activity Oral Abstract Presentation DISCORDANT SEROLOGIES AND BIOPSIES: WHAT TO DO? Dascha C. Weir MD, Boston Children's Hospital Learning objectives: 1. Recognize the potential complexities in the use of celiac serologic markers and small intestinal biopsies in clinical practice. 2. Discuss a clinical approach to the treatment and monitoring of patients with discordant serology and biopsies. Oral Abstract Presentation 2:30PM – 4:00PM Concurrent Session II Virtual NAFLD (No Fee Registration required - See ticket for room assignments) Moderators: Stephanie Abrams, Amal Aqul, Sarah Barlow, Molly Bozic, Nirav Desai, Rima Fawaz, Ariel Feldstein, Regy Gonzales-Peralta, Nitika Gupta, Evelyn Hsu, Rohit Kohli, Jean Molleston, Karen Murray, Nadia Ovchinsky, Emily Perito, Jeff Schwimmer, Dellys SolerRodriguez, and Shikha Sundaram Speaker: Miriam Vos MD, MSPH, FAHA, Emory School of Medicine Learning objectives: 1. To address when to biopsy and when to re-biopsy in pediatric NAFLD 2. To understand dyslipidemia in the setting of NAFLD– how to assess and when to start medications 3. To discuss treatment with Vitamin E (and other medications) 5 Nutrition Moderators: Ruba Abdelhadi MD and Timothy Sentongo MD Lincoln Room BACTERIAL OVERGROWTH IN PEDIATRIC SHORT BOWEL SYNDROME Conrad Cole MD, Cincinnati Children’s Hospital Medical Center Learning Objectives: 1. Learn risk factors for developing bacterial overgrowth 2. Discuss diagnostic challenges 3. Understand the differential diagnosis 4. Review therapeutic options Oral Abstract Presentation STATE OF THE ART RESEARCH LECTURE - CUTTING EDGE OR CRAZY: IS SURGERY THE MOST EFFECTIVE TREATMENT FOR NASH? Stavra Xanthakos MD, Cincinnati Children’s Hospital Medical Center Learning objectives: 1. Review the current guidelines for when to consider bariatric surgery in youth 2. Describe the types of bariatric surgeries performed in adolescents, including risks and benefits 3. Review the evidence and gaps in knowledge re: bariatric surgery as a specific treatment for NASH Oral Abstract Presentation 5:00PM - 7:00PM CPNP Reception Holmead Room, Lobby Level Saturday, October 10, 2015 All sessions will take place in the Georgetown Room on the Concourse Level 7:30AM – 8:00AM Breakfast 8:00AM - 8:05PM INTRODUCTIONS Praveen Goday MBBS, CNSC, Chair, NAPGHAN Nutrition Committee 8:05AM - 8:35AM THE GUT BALANCE REVOLUTION Gerard Mullin MD, The Johns Hopkins University School of Medicine 8:35AM – 9:15AM CHILDHOOD OBESITY: FIGHTING A BATTLE OF EPIC PROPORTIONS Shikha Sundaram MD and Helen Seagle RD, Children’s Hospital of Colorado 9:15AM - 9:45AM “NUTRITION ROCKS HCT”: NUTRITION RESEARCH FOR OPTIMIZING CARE IN KIDS UNDERGOING HEMATOPOIETIC CELL TRANSPLANTATION Lori Bechard PhD, Med, RD, LDN, Boston Children’s Hospital 9:45AM - 10:15AM NUTRITION FOR THE CHILD WITH CYSTIC FIBROSIS Tami Miller RD, Children’s Hospital of Wisconsin Concourse Foyer 6 10:15AM – 10:30AM Break 10:30AM - 11:00AM NUTRITIONAL ISSUES IN CHOLESTATIC DISEASE Binita Kamath MBBChir, MRCP, MTR, The Hospital for Sick Children 11:00AM - 11:30AM NUTRITIONAL CHALLENGES IN CHILDREN WITH AUTISM Cade Nylund MD, MS, FAAP, Walter Reed National Military Medical Center 11:30AM – 12:00PM IRON DEFICIENCY AND THE DEVELOPING BRAIN Michael K. Georgieff MD, University of Minnesota 12:00PM – 1:00PM Lunch/Poster Session 1:00PM - 1:35PM NUTRITION AND DIET IN THE MANAGEMENT OF INFLAMMATORY BOWEL DISEASE Athos Bousvaros MD, MPH and Karen Warman RD, Boston Children’s Hospital 1:40PM - 3:10PM Case study breakouts [3 consecutive sessions, 30 minutes each] Dupont, Embassy, Cardozo – Terrace Level Concourse Foyer THE ELIMINATION DIET: PRACTICAL TIPS AND PITFALLS - Wendy Elverson RD, LDN, Boston Children’s Hospital ASSESSING NUTRITIONAL NEEDS IN THE HYPOMETABOLIC CHILD- Monica Cicchini MS,RD, CSP, LD Georgetown University Hospital NUTRITION CARE FOR CHILDREN UNDERGOING HEMATOPOIETIC CELL TRANSPLANTATION, NOW AND LATER - Lori Bechard PhD, Med, RD, LDN, Boston Children’s Hospital TROUBLESHOOTING PANCREATIC ENZYME THERAPY (PERT) IN CYSTIC FIBROSIS– Tami Miller RD, CSP, CD, Children’s Hospital of Wisconsin NUTRITIONAL ISSUES IN ALAGILLE SYNDROME – Binita Kamath MBBChir, MRCP, MTR, The Hospital for Sick Children INFLAMMATORY BOWEL DISEASE – Karen Warman RD, Boston Children’s Hospital 3:15PM - 4:15PM BLENDERIZED TUBE FEEDINGS: MANAGING A NEW FRONTIER Margaret Girten RD, CSP, LDN and Julia Driggers RD, LDN, CNSC, Children’s Hospital of Philadelphia 7 3:45PM – 5:15PM Psychology II - Psychology and Gastroenterology: Keys to Effective Integration Monroe Room, Concourse Level Moderator: Anthony Alioto PhD, BCB ABDOMINAL PAIN: INTEGRATING PSYCHOLOGICAL TREATMENTS INTO MEDICAL CARE Miranda vanTilburg PhD, University of North Carolina, Center for Functional GI and Motility Disorders Learning objectives: 1. Describe the role of psychosocial factors in functional abdominal pain disorders 2. Identify evidence-based psychological/behavioral treatments for functional abdominal pain disorders and how to integrate with medical care 3. Identify patients most likely to benefit from integrated care CONSTIPATION AND SOILING: INTEGRATED MODELS OF CARE Rose Schroedl PhD, Nationwide Children’s Hospital Learning objectives: 1. Summarize integrated models of care for constipation and fecal incontinence 2. Discuss the evidence-base for integrated models of care 3. Describe an algorithm for treatment decision making INTERDISCIPLINARY INPATIENT APPROACHES TO WEANING TUBE DEPENDENT CHILDREN FROM ENTERAL FEEDING Alan Silverman PhD, Medical College of Wisconsin Learning objectives: 1. Describe existing interdisciplinary care models for weaning tube dependent children 2. Summarize the current state of empirical support for interdisciplinary treatment approaches to weaning tube dependent children from enteral feeding 3. List methods for medical oversight that can help to ensure the safety of patients undergoing treatment 8 TheGutBalanceRevolution GerardE.MullinMD AssociateProfessorofMedicine www.thefoodmd.com JohnsHopkinsUniversitySchoolofMedicine NASPGHANCPNPNutritionSymposium October10th,2015 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved LearningObjectives • Knowtheroleofthegutmicrobiotainhuman healthanddisease • Becomefamiliarwiththepathophysiologyof obesityandhowalterationsinthegut microfloraleadtoobesity • Tounderstandhowprebioticsandprobiotics canpromotealeanmetabolismbyfosteringa healthygutmicrobiome Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Introductiontothegut microbiome Wearecompositeofspecies:a‘supra‐organism’ Ourmicrobialcensusexceedsthetotalnumberofour ownhumancellsby~10fold Ourlargestcollectionofmicrobesresidesinthe intestine(~10‐100trillionorganisms) Theaggregategenomesof thesegutspecies(microbiome) maycontain>100foldmore genesthanour‘own’genome Themicrobiomeisanintegral partofourgeneticlandscape (‘humanmetagenome’)andof ourgeneticevolution Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 9 Techniquesusedtocharacterize thegutmicrobiome NIH HUMAN MICROBIOME PROJECT Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Oral Tolerance, NF-κB, IL-10, IL-17 Obesity Nutrition & Metabolis m Defense and Repair BioFilm & Permeability Structural Integrity Communication Assimilation Properly Functioning Gastrointestinal MicroBiome Mast Cell Degranulation Detoxification & Biotransformation Transport GI Motility Entero-Hepatic ReCirculaton n-Butyrate SCFA Production Energy Phase III Detoxification Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved EcosystemsandBiodiversity • • • Increasedspeciesdiversityincreasestheefficiency andproductivityofanecosystem Morediversecommunitiesarefunctionallyless susceptibletoexternalstressors Inrelativeterms,increasingstresshasastronger negativeeffectonlow‐diversecommunities Ecosystem Functioning Global Ecosystem Changes Natural Processes Biodiversity Ecosystem Services Human Wellbeing Stability Khanna S and Tosh PK. (2014).. Mayo Clin Proc. 89(1): 107‐114. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 10 J. Physiol Biochem DOI 10.1007/s13105-0390-3 In Press 2/2015. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Exposuresinearlylife,infantgut microbiota,&futurehealth www.cmaj.ca/lookup/doi/10.1503/cmaj.130147 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved J. Physiol Biochem DOI 10.1007/s13105-0390-3 In Press 2/2015. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 11 Disorders Associated with an Altered Gut Microbiome Gastrointestinal Gallstones,ColorectalCancer, HepaticEncephalopathy,*IBS,IBD,FMF,Gastriccancerand lymphoma,*RecurrentC.difficle infection Non‐GI Anxiety,Arthritis,Asthma,Autism,Autoimmunedisorders, Cardiovascular*,Chronicfatigue,Chronickidneydisease, Depression,Diabetes,Eczema,*FattyLiver,Fibromyalgia, Hypercholesterolemia,ITP,MetabolicSyndrome,Mood disorders,MultipleSclerosis,Myoclonusdystonia, *Obesity,OxalickidneyStones,Parkinson’sDisease,etc. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved GutMicrobes2012;3(4):366‐373. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Proposed causes of dysbiosis of the gut microbiota. NatureReviewsImmunologyVol 9,May2009|313 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 12 Introductiontothegut microbiomeandobesity Twophylaof(mainlyanaerobic)bacteria linkedtoobesity: – Firmicutes (positively) – Bacteroidetes (negatively) Impactonmetabolismresults fromanimbalance ofthese phyla. Causeorconsequence? Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Obese mice have altered gut flora transfer of gut flora induces weight gain Ley, et al. PNAS 102(31):11070, 2005 Turnbaugh, et al. Nature 444 (21/28):1027. 2006 2006 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Microbialcommunitytransplant experiments Measuretotalbodyfatcontentbeforeandafter14‐ daycolonization Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 13 Comparisonofenergyextraction betweenobeseandleanmice Turnbaugh,etal.Nature 444:1027,2006 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Functionalinteractionsbetween thegutmicrobiotaandhost metabolism Nature 489, 242–249 (13 September 2012) doi:10.1038/nature11552 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Host remodeling of the gut microbiome andmetabolic changes in pregnancy Cell, 150: 470‐480, 2012 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 14 Dietaryeffectonthegutmicrobiota Green=BacteroidetesRed=Firmicutes DeFilippo C et al. PNAS. 2010;107(33):14691-14696. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Howsweetitis! “WeidentifyNAS‐alteredmicrobialmetabolic pathwaysthatarelinkedtohostsusceptibilityto metabolicdisease,anddemonstratesimilarNAS‐ induceddysbiosisandglucose intoleranceinhealthyhumansubjects. Collectively,ourresultslinkNASconsumption, dysbiosisandmetabolicabnormalities, therebycallingforareassessmentofmassiveNAS usage”...” Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Useofantibioticsinagriculture >50yearsofantibiotic useforgrowth promotion Economicbenefits Low‐levelexposure (subtherapeutic)is sufficientforeffect Differentclasseswork 15 Repeatedexposuretobroad‐spectrumantibioticsat ages0‐23monthsisassociatedwithearlychildhood obesity.Becausecommonchildhood infectionswerethemostfrequentdiagnosesco‐ occurringwithbroad‐spectrumantibiotic prescription,narrowingantibioticselectionis potentiallyamodifiableriskfactorforchildhood obesity. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved DietCanInfluenceMicrobialPopulations Brownetal.(2012)Nutrients.4(8):1095–1119. Diet Carbohydrate‐reduced Calorie‐restricted Complexcarbohydrates Refinedsugars BacteriaAltered EffectonBacteria Bacteroidetes Clostridiumcoccoides, Lactobacillus spp.and Bifidobacteria spp. Mycobacteriumavium subspecies paratuberculosisand Enterobacteriaceae C.difficile andC. perfringens References Increased Walker etal.BMC Microbiol.2011;11:7.] Decreased(growth prevented) Obesity2009;17:1906– 1915. Decreased Walkeretal.BMC Microbiol.2011;11:7. Increased Bergetal.Inflamm. BowelDis.2012 High‐fat Bifidobacteria spp. Decreased(absent) Zhangetal.ISMEJ. 2010;4:232–241. Highn‐6PUFAfrom saffloweroil Bacteroidetes Decreased DelaSerre etal.Am.J. Physiol.2010;299: Increased Turnbaughetal.Sci. Transl.Med.2009;1 Clostridiuminnocuum, Catenibacterium High‐fatandhigh‐sugar mitsuokai and Enterococcus spp. Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Diet‐induceddysbiosis anddiseases. Chan Y et al. Clinical Consequences of Diet-Induced Dysbiosis Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 16 Mechanismslinkingthegut microbiotatoobesity Metabolism(SCFA,lipids) Endocrine(GLP‐1,GLP‐2,PYY,L‐cell,Grp41r) HostGenetics(TLR‐4,TLR‐5) Inflammation(cytokines,inflammasome) IntestinalPermeability(zonulin) Antibiotics(meat,C‐section,overuse) Diet(Western) Environment(BPA,??GMOs) Immunity(age) Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Strategies to modulate the microbiota (“no substitute for life‐style”) • • • • • • • Antibiotics Prebiotics Probiotics Synbiotics Genetically modified bacteria Bacterial components, products Microbiota transplantation Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved fertilizeandseed Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 17 EOPertof etalBenefMicrobes. 2013Mar1;4(1):53‐652013 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved PrebioticRichFoods Jerusalemartichokes Onions Chicory Garlic Leeks Bananas Fruit Soybeans Burdockroot Asparagus Sugarmaple Chinesechives Peas Legumes Eggplant Honey GreenTea Yogurt,cottage cheese,kefir Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved PROBIOTICS PREBIOTICS Delzenne, Neyrinck, Bäckhed , Cani Targeting gut microbiota in obesity: effects of prebiotics and probiotics Nature Reviews | Endocrinology Volume 7 | November 2011 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 18 World J Gastroenterol 2014;21;20 (43): 16079-16094 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Strategies to modulate the microbiota (“no substitute for life‐style”) • • • • • • • Antibiotics Prebiotics Probiotics Synbiotics Genetically modified bacteria Bacterial components, products Microbiota transplantation Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved ProbableMechanismsofActionof theAnti‐obesityEffectsof Probiotics Arora T, et al., Probiotics: Interaction with gut microbiome and antiobesity potential, Nutrition Volume 29, Issue 4, April 2013, Pages 591–596 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 19 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Anti‐obesityEffectsofBifidobacteriaProbiotic SupplementationofAnimalStudies Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved World J Gastroenterol 2014;21;20 (43): 16079-16094 Anti‐obesityEffectsofProbioticLactobacillus SupplementationofAnimalStudies World J Gastroenterol 2014;21;20 (43): 16079 16094 20 Anti‐obesityEffectsofProbiotic Supplementation:HumanStudies World J Gastroenterol 2014;21;20 (43): 16079-16094 Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Strategies to modulate the microbiota (“no substitute for life‐style”) • • • • • • • Antibiotics Probiotics Prebiotics Synbiotics Genetically modified bacteria Bacterial components, products Microbiota transplantation Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 21 Questions? Copyright © 2015 [Gerard E. Mullin MD]. All Rights Reserved 22 Childhood Obesity: Fighting a Battle of Epic Proportions Shikha S. Sundaram, MD MSCI Associate Professor of Pediatrics Children’s Hospital Colorado Helen Seagle, MS RDN Clinical Dietitian in Lifestyle Medicine Children’s Hospital Colorado Disclosures • We have no financial relationships with a commercial entity to disclose. Objectives • To understand the epidemiology of pediatric obesity in the United States • To understand the myriad of complications of pediatric obesity • To understand the complex pathogenesis of obesity • To understand the dietitian skillset necessary to combat childhood obesity 23 Definitions • Body mass index (BMI) is a measure used to determine childhood overweight and obesity. • Overweight is defined as a BMI at or above the 85th percentile and below the 95th percentile for children and teens of the same age and sex. • Obesity is defined as a BMI at or above the 95th percentile for children and teens of the same age and sex. Prevalence* of Self-Reported Obesity Among U.S. Adults by State and Territory, BRFSS, 2013 *Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should not be compared to prevalence estimates before 2011. WA MT OR ME ND ID MN VT SD WI MI WY IA NE NV PA IL UT CO CA AZ KS OK NM OH IN WV MO VA KY NH MA RI CT NJ DE MD DC NC TN AR SC MS TX AK NY AL GA LA FL HI GUAM 15%–<20% 20%–<25% 25%–<30% PR 30%–<35% ≥35% 24 Has childhood obesity plateaued? Certain populations are disproportionately affected by obesity Complications of Childhood Obesity 25 Childhood Obesity Increases Risk of Adult Obesity AJCN 70S:145S,1999 Is Obesity Really all about ENERGY BALANCE? Etiopathogenesis of obesity: Obesogenic environment 26 Appetite Regulation • Leptin: Mediator of long term energy balance, suppressing the urge to eat when caloric intake maintains ideal fat stores. • Ghrelin: a fast acting hormone that may play a role in meal initiation Fat Patterning in Obesity • Adipocytes from some locations (gluteal & femoral) efficiently capture excess nutrients from the blood‐stream for storage, while others accumulate TGs but readily release them for use by other tissues. Fat Cell Development: Number and Size • • • • During growth periods in childhood: fat cells increase in number During periods of excess intake: fat cells increase in size Fat cells reach maximum size: fat cell numbers increase again Fat loss: cell size may shrink but not the number 27 What can we do? Refining the RD role Self‐ awareness Health literacy Cultural‐ awareness Services Diet assessment Behavior change Document 28 Nutrition ROCKs HCT: Nutrition Research for Optimizing Care in Kids during hematopoietic cell transplantation Lori J. Bechard, PhD, MEd, RD, LDN Disclosures • Currently employed by Nestle Nutrition – No products or services produced by this company are relevant to my presentation. • Previously employed by Boston Children’s Hospital Outline • Changes over the course of HCT – Energy expenditure – Body composition – Bone health • Feeding modalities during HCT • Other nutrition interventions – Vitamin D – Lipids – Exercise 29 HCT – a unique nutritional situation • • • • • • History Inflammation Infection Treatment Toxicity Survivorship http://www.stanfordchildrens.org/content‐public/topic/images/22/125422.gif Metabolic impact of HCT • Changes in energy expenditure • Changes in body composition • Changes in bone health What are the energy requirements of children undergoing HCT? • Prospective cohort study of 37 children undergoing HCT enrolled in a supportive care regimen including PN provided at 100% of measured REE (as opposed to standard of care) • REE measured weekly by indirect calorimetry 30 Indirect Calorimetry Measured at bedside weekly while hospitalized Decreased (NS) Significantly decreased 31 Are we overfeeding children undergoing HCT? Study Aims – Compare body composition in children fed standard PN (140% estimated REE) vs. PN titrated to measured REE (“PNTREE”) – Measure serial changes in REE by indirect calorimetry over the course of HCT Dual Energy X-Ray Absorptiometry (DXA) Measured at baseline, day 30 , and day 100 after HCT Change in percentage body fat from transplant (baseline) through hospitalization (day 30) and follow‐up (day 100). Repeated‐measures ANOVA indicated no significant difference in time course between treatments (P = 0.39 for time ∙ treatment interaction) Sharma et al, AJCN 2012;95:342‐51 32 REE changes over time despite different energy intakes Bechard, et al. Bone Marrow Transplant 2012 47(10);1301‐6 PNTREE Discussion • Total % body fat increased significantly in the standard group by 1.2 +0.5 kg from baseline to 30 days; the increase persisted to 100 days, but was not statistically significant – Clinically significant?? • Lean body mass decreased dramatically in both groups, persisted to 100 days, not influenced by increased intake with standard regimen – Suggests need for alternative and adjunctive therapies aimed at preserving lean mass • Weight and BMI z-score decrease significantly in both groups over study period – Likely influenced by loss of lean body mass – Is standard regimen simply contributing to increase in body fat? Clinical outcomes of PNTREE participants Sharma et al, AJCN 2012;95:342‐51 33 Low arm muscle area associated with decreased event-free survival in children undergoing allogeneic HCT Hoffmeister et al, BBMT 2013;19:1081‐6 16 Bone health research questions • What is the prevalence of low BMD in children undergoing allogeneic HCT? • What are the changes in BMD and markers of bone turnover from baseline to day 100? 17 Bone loss in children after HCT • HCT has significant effect on BMD in childhood leukemia survivors, compared to chemotherapy alone (p=.006 in multivariate analysis) • Lower BMD Z-score (mean -1.26) among patients with fractures LeMeignen et al. Blood. 2011;118(6):1481‐1489 • 20% of children have vertebral compression fractures after HCT – many asymptomatic Taskinen et al. Cancer. 2007;110:442‐51 18 34 Bone changes following HCT in children from Petryk et al J Clin Endocrinol Metab 2006;291: 899–905 Change in BMC & BMD Z-score during HCT Adjusted for age, sex, Tanner stage, lean mass, fat mass, REE, energy intake, insulin sensitivity, inpatient steroid intake, and serum phosphorus. *significant decline from baseline; time trend significant at p<0.0001 for BMD Z‐ score, p=0.007 for BMC Z‐score. Error bars = + 1 standard error Bechard et al, Ped Blood Cancer 2015;62(4):687‐92 20 Challenges to feeding children during HCT • Many children require PN – Mucositis – Enteritis • Enteral feeding – Access – Tolerance • Volume management 35 Enteral feeding in pediatric HCT • Retrospective analysis of 49 pts., autologous and allogeneic transplants • NG-tube placed during conditioning or within 1st week • 86% maintained exclusively on EN • No significant weight loss • Engraftment comparable to historical controls Langdana, Bone Marrow Transplant, 2001 Feasibility of enteral feeding (EN) in children during allogeneic HCT • 65 children prospectively enrolled • EN via nasogastric tube on day +1 • 50 pts. (77%) received EN only – Faster platelet recovery (23 vs. 29 days, p=0.01) – Shorter length of stay (29 vs. 40 days, p<0.001) • 15 pts. (23%) required PN • PN group - more frequent and severe acute GVHD • No difference in weight or BMI outcomes Azarnoush et al., Bone Marrow Transplant, 2012;47:1191-5 Vitamin D • Deficiency and insufficiency common in HCT patients (Duncan et al, BBMT 2011;17:749-53) 36 Serum vitamin D levels in patients and controls From Campos et al, Nutrition 2014; 30:654‐9 25 Change in vitamin D status during HCT Adjusted for age, sex, Tanner stage, lean mass, fat mass, REE, energy intake, insulin sensitivity, serum phosphorus, inpatient steroid intake, and vitamin D intake *significant decline from baseline; time trend significant, p=0.001 Bechard et al, Ped Blood Cancer 2015;62(4):687‐92 26 Baseline vitamin D sufficiency associated with improved outcomes From Hansson et al, BBMT 2014;20:1537‐43. 27 37 Physical exercise • Systematic review of RCTs (van Haren, Phys Ther 2013;93:514-28) – Endurance exercise – Resistance exercise – Other types • Positive impact – Quality of life – Fatigue • Link with body composition changes? 28 Lipids in HCT • Energy and essential fatty acids • Problems with parenteral lipids • Omega-3 benefits? 29 Alternatives to soybean lipids in pediatric HCT? • Olive oil – 28 children randomized to olive oil vs MCT based lipid emulsion – Favorable lipid biomarkers Hartman et al, Clin Nutr 2009;28:631-5 • Blend of oils – 14 children randomized to soybean based vs. MCT/soybean/fish lipid emulsion – Similar lipid biomarkers Baena-Gomez et al, Ann Nutr Metab 2013;63:103-110 • Fish oil – Exclusive fish oil used to treat EFAD in case report of HCT patient with soy allergy Gura et al, Clin Nutr 2005; 24:839-47 30 38 Conclusions • HCT is associated with… – Decline in lean body mass – Changes in energy expenditure – Bone loss – Low vitamin D status • PN is not required for all • Research gaps remain 31 Future directions • Bone health • Body composition – Physical activity – Energy balance • Modular nutrients – Vitamin D – Omega 3 fatty acids • Long term outcomes Acknowledgements Boston Children’s Hospital – – – – – – – Chris Duggan, MD, MPH Sharon Collier, MEd, RD, LDN Kathy Gura, PharmD, RPh Henry Feldman, PhD Catherine Gordon, MD, MS Christy Duncan, MD Clinical Dietitians - Tara McCarthy, MS, RD, Sarah Larson, MS, RD, Katie Galvin, MS, RD Dana Farber Cancer Institute – Eva Guinan, MD – Melissa O’Connor, MS, RN, PNP Patients of the Dana-Farber Boston Children’s Cancer and Blood Disorders Center Stem Cell Transplant Program 33 39 For a copy of slides, please email: [email protected] 34 40 I have no financial relationships with a commercial entity to disclose. 41 The Changing Face of CF Learning Objectives: • Apply current consensus guidelines and research findings for the care of infants with CF • Gain further knowledge to manage pancreatic insufficiency • Discuss co-morbid complications which significantly impact the nutrition status of children with CF Early Intervention Newborn Screening Comprehensive Care Visit Frequency: • Monthly ‐ 0‐6 months • Every other month – 6‐12 months • Weight checks with PMD prn Care Coordination: • Education • Genetic Counseling • Community Resources (WIC, SNAP, Enzyme rebate programs) Clinical Intervention: Sweat testing Lab Monitoring Chest x‐rays 42 CF Growth Standards Age 0‐12 Months 12‐24 Months 2‐20 Years Chart Weight/length WHO > 50% WHO > 75% CDC BMI > 50% for age Nutritional strategies • Optimize calorie intake • Salt • Fat-soluble vitamins • Pancreatic enzymes Increase Calorie Intake • Breast milk or milk based formula – Offer Lactation support • > 60% of infants need high calorie breast milk or formula • Choose high calorie foods • Fortify complementary foods with fat 43 Salt Supplementation 0‐6 Months 6‐12 Months >12 Months Eating table foods 1/8 teaspoon 1/4 teaspoon Salt foods liberally • Add to applesauce with enzymes • Divide into 3‐4 bottle feedings • Counsel for extreme • Add to complimentary conditions foods • Avoid water as beverage Fat-soluble Vitamins • Vitamin deficiencies at newborn screening • Monitor levels and adjust doses • Supplement vitamin D When to Start PERT • 2 CFTR mutations associated with Pancreatic Insufficiency (PI) • Fecal elastase – Unequivocal signs/symptoms of malabsorption pending lab results • Lack of weight gain since birth • Visibly greasy or oily stools 44 PERT Dosing Guidelines • 3,000‐5,000 total lipase units at each feeding initially • May exceed 10,000 units lipase/day in infancy • 1750-2000 units lipase/kg = optimal growth • Frequent adjustments during infancy Optimizing Enzyme Efficacy • Synchronize food and enzymes • Dose at beginning or middle of meal • Do not crush or dissolve enzymes taken orally • Give divided doses for extended meal times • PPIs do not increase enzyme effectiveness Enteral Nutrition and PERT • No universal strategy to dose enzymes with tube feedings – Intact enzymes • PO enzymes before, middle and end of feeding • Suspend beads in nectar and flush into tube – Mechanical and chemical dissolution • Dissolve beads in bicarbonate solution • Crush beads or non-enteric coated enzymes – Add to formula + time = predigested formula 45 Troubleshooting Enzymes and Enteral Nutrition • Anecdotal evidence to use formulas with more LCT (Two Cal HN™ vs Nutren 2.0™ ) • Dose enzymes based on fat content of formula – 2000 units lipase/gm fat • Closed tube feeding systems CF-Related Diabetes • Occurs in ~ 20% Teens with CF – Start screening with OGTT age 10 • Requires insulin and few diet restrictions with carb counting – Dose insulin with overnight tube feedings • Greatly worsens clinical outcomes Constipation • Very common in CF: Sticky intestinal mucous • Leads to poor appetite, abdominal pain, symptoms of malabsorption from overflow diarrhea • Polyethylene Glycol (PEG) is common treatment – Daily dosing – Purge clean-outs • Chronic treatment often required 46 47 THE HOSPITAL FOR SICK CHILDREN Nutritional Issues in Cholestatic Disease NASPGHAN-CPNP Joint Session Binita M. Kamath, MBBChir MRCP MTR Associate Professor Division of Gastroenterology, Hepatology and Nutrition The Hospital for Sick Children University of Toronto October 2015 I have no financial relationships with a commercial entity to disclose. OUTLINE • Overview of cholestatic diseases • Mechanisms of nutritional impairment in cholestasis • Impact of poor nutrition in cholestasis • Optimizing nutrition in cholestasis 48 Cholestatic Diseases Cholestatic Diseases • Cholestasis = interruption in bile flow • Bile: bilirubin, bile salts, cholesterol • Hallmark disease: biliary atresia (BA) • Other diseases – Alagille syndrome – Progressive familial intrahepatic cholestasis – Alpha-1-antitrypsin deficiency Mechanisms of Nutritional Impairment in Cholestasis 49 Mechanisms of Malnutrition in Cholestasis 1. Severe depletion of intraluminal bile acids and secondary fat malabsorption 2. Poor intake due to a. organomegaly and/or ascites (reduced gastric capacity) b. anorexia (toxins?) 3. Portal hypertension exacerbates malabsorption 4. Pruritus Mechanisms of Malnutrition in Cholestasis 5. Increased energy expenditure • Measured REE almost 30% higher than expected in BA • Normal infants retain 50% energy intake for growth, but only 35% in BA 6. Hepatic IGF-1 7. Recurrent infections Assessment of Malnutrition in Cholestasis 1. Weight – affected by ascites 2. Anthropometrics a. mid-arm circumference b. TSF c. Head circumference 50 Impact of Poor Nutrition in Cholestasis Outcomes of Malnutrition in Cholestasis • Growth failure is an important factor associated with death or moving to ICU in a multi-center cohort (mostly BA) – height or weight <2 s.d., associated with increased morbidity and mortality PELD • Growth failure was an independent risk factor for pretransplant mortality, post-transplant mortality, and even graft failure in 755 listed BA patients (SPLIT) McDiarmid et al, Transplantation 2002 & Utterson et al, J Ped 2005 Outcomes of Malnutrition in Cholestasis • BA Research Consortium • N=100 • Infants with BA who ultimately required LT or died had poorer growth after HPE compared to those who survived with their native liver at 24 months of age DeRusso et al, Hepatology 2007 51 Outcomes of Malnutrition in Cholestasis • Severity of malnutrition and poor growth in children with BA before LT is predictive of cognitive performance years after transplantation Wayman KI et al, J Ped 1997 Optimizing Nutrition in Cholestasis CHO &Energy ‐ 120‐150% ‐ 2/3 as CHO polymer Vitamin E Vitamin D Protein ‐ 2‐3g/kg/d Vitamin K ‐BCAA? Lipid ‐ MCTs carried in PV system ‐ 30‐50% of total lipids as MCT H2O & Electrolytes ‐rarely restrict H2O ‐restrict Na to 2‐ 3mmol/kg/d 52 MCTs: The Data? • Difficult to specify the ideal dietary fat content and ratio of MCT to LCT – Limited data point to better fat solubilization and growth of cholestatic infants fed with 30% or 70% MCT against a 50/50% mixture of MCT/LCT – Very high (>80%) MCT to total lipid risks of essential fatty acid deficiency – Recent study shows effectiveness of enteral MCT formula (140% DRI) as compared to ad lib oral intake of same formula Macias-Rosales, JPGN 2015 PUFA / EFA • Intraluminal bile salt depletion • Levels difficult to measure and interpret. • Most centres lack access to clinical measurement Branch chain amino acids (BCAA) – Randomized study in children with ESLD demonstrated improved nutritional status and body composition in those with BCAA-enriched formula – MCT-containing complete BCAA formulas are expensive and not readily available Chin SE et al, 1992 53 Water and Electrolytes • Typically normal fluid – rarely restricted • Sodium restricted to 1-2 mmol/kg/day – Do not correct the hyponatraemia of ESLD – Severe hyponatraemia may require fluid restriction • Potassium 2mmol/kg/day Nutritional Requirements in Cholestasis Nutritional element Daily Requirement Source Lipid 30‐50% of total energy 30‐70% MCT PUFA/LCP >10% of total energy rapeseed, walnut, fish, sunflower, soybean oils Whey protein Protein 3‐4g/kg BCAA 10% total AAs Energy 120‐150% requirement for age CHO 2/3 as CHO, 1/3 as lipid CHO polymer Na Minimum K 2‐3 mmol/kg Fat Soluble Vitamins Shneider, Pediatrics 2012 54 Parenteral Nutrition • Indications – diarrhea, vomiting* – repeated episodes of gastrointestinal hemorrhage • Risk of worsening decompensated liver disease with PN is low – mild biochemical deterioration • Can typically achieve mixed enteral and PN Parenteral Nutrition • 20 year retrospective review, single centre • BA listed for LTx, <36 months • PN=25, Non-PN=22 • From the start of PN administration to the clinical endpoint, mean TSF z‐score increased from ‐2.5 ± 0.2 to ‐1.8 ± 0.2 (p=0.003), and mean MAC z‐score increased from ‐2.2 ± 0.2 to ‐1.4 ± 0.2 (p<0.0001). • Of the 22 patients in the non‐PN group, 6 (27%) received NG feeds Sullivan J, Liver Transp 2012 Parenteral Nutrition 55 Gaps in Knowledge Summary 56 Iron Deficiency and the Developing Brain Michael K. Georgieff, M.D. Professor, Pediatrics and Child Development Head, Section of Neonatology Director Center for Neurobehavioral Development University of Minnesota Masonic Children’s Hospital University of Minnesota Minneapolis, MN I have received a research grant from Mead Johnson Nutritionals. I have no conflict of interest for this presentation Learning Objectives Define the common causes of iron deficiency in newborn infants and toddlers Identify the regions of the brain that are particularly vulnerable to early childhood iron deficiency Characterize the behaviors that are affected by early life iron deficiency 57 Overview Why worry about iron? Nutrient-brain interactions- why the brain needs iron Iron needs in infancy – Sequelae of iron deficiency Fetal and neonatal iron – Term and preterm infants – Sequelae of iron deficiency Why Worry About Iron Deficiency? 2 billion people world-wide are iron deficient (WHO) – 30-50% of pregnant women Every cell/organ system needs iron for proper development and subsequent function Iron deficiency anemia is associated with clinical symptoms – Due to tissue level ID – Symptoms occur prior to anemia Main reason to worry is the effect on the developing brain – Cognitive and motor effects – Some temporary (while ID), others long-term (after iron repletion) – The long-term effects are the real cost to society • Increased depression, anxiety, risk of schizophrenia, autism • Loss of job and educational potential Early Nutrition and Brain Development: General Principles Positive or negative nutrient effects on brain development Based on… Timing, Dose and Duration of Exposure Kretchmer, Beard, Carlson, 1996 58 Nutrient‐Brain‐Behavior Relationships Various brain regions/processes have different developmental trajectories The vulnerability of a brain region to a nutrient is based on – When nutrient deficit/overload is likely to occur – Brain’s requirement for that nutrient at that time Behavioral changes must map onto those brain structures altered by the nutrient effect Rapid Hippocampal Development Fetus Late Infancy/Toddler Pubertal From Nelson and Thompson, 2001 Iron: A Critical Nutrient for the Developing Brain Iron containing enzymes and hemo‐proteins are involved in important cellular processes in developing brain – Delta 9‐desaturase, glial cytochromes control oligodendrocyte production of myelin – Cytochromes mediate oxidative phosphorylation and determine neuronal and glial energy status – Tyrosine Hydroxylase involved in monoamine neurotransmitter and receptor synthesis (dopamine, serotonin, norepi) – ID affects genome while ID and long after ID is treated 59 The Differential Effect of Timing of ID on Brain Development Rapid Hippocampal Development Fetus Late Infancy/Toddler Iron Deficiency in the Infant or Toddler (6-24 months) Factors Determining Infant Iron Status Lozoff et al, Nutr Rev, 2006 Courtesy of B. Lozoff, MD 60 ID in Infancy: Who is at risk? Most postnatal ID is due to inadequate dietary intake ± low stores at birth ± blood loss – Low stores at birth – Inadequate dietary intake • Low iron formula • Breast milk • Early change to cow milk – Blood loss • Hemorrhage at birth (anemia) • Parasitic infection, food intolerance (GI loss) Brain Development Affected by ID in Infancy Rapid Hippocampal Development Fetus Late Infancy/Toddler Neurobehavioral Sequelae of Early Postnatal Iron Deficiency in Humans Over 50 studies demonstrate dietary ID between 6 and 24 months leads to: – Behavioral abnormalities (Lozoff et al, 2000) • Motor and cognitive delays while iron deficient • Cognitive delays 19-23 years after iron repletion – Arithmetic, writing, school progress, anxiety/depression, social problems and inattention (Lozoff et al, 2000) • Characteristic of monoamine and hippocampal dysfunction – Electrophysiologic abnormalities (delayed ABR latencies) • At 6 months while iron deficient (Roncagliolo et al, 1998) • At 2-4 years after iron repletion (Algarin et al, 2003) • Characteristic of impaired myelination 61 Effect of Iron Deficiency in Infancy on General Cognitive Performance 115 (B Lozoff et al) Good Iron Status * Cognitive Composite Score 110 105 100 95 90 *initial difference, t = 10.1, p < 0.001 85 Chronic Iron Deficiency ** 1 5 Age (years) 12 *slope = 7.03, p = 0.001 **initial difference, t = 3.7, p = 0.04 **slope NS 17 Effect of Iron Deficiency in Infancy on Affect and Engagement Courtesy of B. Lozoff Effect of Iron Deficiency in Infancy on Affect and Engagement Courtesy of B. Lozoff 62 Motor Coordination and Affect in Human Toddlers: a Dose Response Effect (Lozoff et al, 2008) Score 0.5 0.4 0.3 p=0.05 p < 0.05 40 39 38 37 0 IDA 0.2 NA ID IS Shyness (EAS) 2.7 0.1 2.5 Score Probability of performing with poor coordination Orientation/Engagement (BRS) 44 43 42 41 0 IDA NA ID I S p < 0.01 2.3 2.1 1.9 0 IDA NA ID IS Major Dopamine Pathways Mesocorticolimbic Pathway Nigrostriatal Pathway Tuberohypophyseal Pathway Courtesy of B. Lozoff Neurotransmitter Effects in the Rat Effects on monoamines, esp dopamine, known since late 1970’s (studies by Yehuda, Youdim, Beard) While ID: Decreased DAT, D1R, D2R and increased SERT – Regional differences- Large effects in striatum, ventral midbrain – Changes related to timing and severity (E Unger et al, 2012) 63 Slower Nerve Conduction Velocity: Evoked Potential Latencies 3 Years after Iron Rx 110 4.1 *** *** 4.0 100 3.9 90 80 3.8 ABR Central Conduction Time (Wave I-V Interval, ms) Former Iron Deficient Anemic Control VEP Wave P100 Latency (ms) *** p < 0.001 Algarin et al. (2003). Pediatric Research 53:217‐223 Myelin Effects in the Rat Altered fatty acid profile in myelin fraction Decreased myelin proteins, including myelin basic protein Decreased oligodendrocyte proliferation Transcripts for myelin basic protein affected – short term (while ID) – long term (at P180 after iron repletion) (Studies by Connor, Clardy, Rao) Brain Development Affected by Fetal/Neonatal ID Rapid Hippocampal Development Fetus Late Infancy/Toddler 64 Fetal Iron: Endowment and Distribution Fetuses have 75mg of elemental iron per kilogram body weight during 3rd trimester – Term infant: 250mg – 24 weeker (500g): 37.5 mg Majority is in the RBCs (55mg/kg) Liver storage pools are relatively large at term (12 mg/kg); serum ferritin >40 mcg/L Non-storage tissues, including brain, heart, skeletal muscle account for the rest (8 mg/kg) What Can Negatively Affect Neonatal Iron Status? Decreased maternal iron supply – Fetus with very iron deficient mother (Hgb<8.5) – Common (>30%) in developing countries – No studies of newborn brain iron status Decreased placental iron transfer during gestation – Prematurity • Iron accreted during third trimester • Generally negative iron balance during NICU stay – IUGR due to maternal hypertension during pregnancy • 50% affected • 75,000 infants per year in US • 32% decrease in brain iron concentration (Georgieff et al, 1995) – Early cord clamping Term Infants: What Can Negatively Affect Neonatal Iron Status? Diabetes Mellitus during pregnancy – Chronically hypoxic fetus (IDM)=> Increased erythropoeisis – 65% affected – 150,000 infants per year in US – 40% decrease in brain iron concentration (Petry et al, 1992) Basic principle: Iron prioritized to RBCs over brain & other organs when Fe demand> Fe supply 65 Factors that Determine Preterm Infant Iron Status in the NICU Negative Iron Balance • • • • • • Low Endowment (IUGR) Phlebotomy Losses Iron Rx at 2 months Iron Rx < 2mg/kg/d rhEpo Rx Rapid Postnatal Growth Positive Iron Balance • • • • • • • Older gestation & AGA RBC Transfusion Iron Rx at 2 weeks Iron Rx @ 2-4 mg/kg/d Iron Rx @ 6mg/kd/d c rhEpo Parenteral Iron Slow Postnatal Growth Rate Preterm infants have elevated ZnPP at 34 weeks PCA (Winzerling &Kling) Neurobehavioral Sequelae of Fetal and Neonatal ID Fewer studies than in postnatal ID – Decreased maternal iron status • increased risk of schizophrenia in offspring (Insel et al, 2008) • increased risk of autism in offspring (Schmidt et al, 2014) – Term infants with low neonatal iron stores have • impaired auditory recognition memory processing (Siddappa et al, 2004) • poorer school age neurodevelopment (Tamura et al, 2002) • worse immediate and delayed recall at 3.5 y (Riggins et al, 2009) – Preterm infants with now iron stores at 36 weeks PCA • more abnormal reflexes (Armany-Sivan, 2006) • longer conduction times on BAER (Amin et al, 2010) – Early iron supplementation in preterms => higher mental processing composite score at 5.3 years (Steinmacher et al, 2007) SUGGESTS SIGNIFICANT HIPPOCAMPAL AND MYELIN IMPAIRMENTS Hippocampal Effects: Rodent Models Short and long-term genomic changes (ES Carlson et al, 2007) – Dendritic structure, synaptic efficacy, oxidative metabolism Reduced energy status (M deUngria et al, 2000) Glutamate and GABA sequestration (R Rao et al, 2003) Altered dendritic morphology (ES Carlson et al, 2009)* Long-term suppression of BDNF and its receptor (P Tran et al, 2009) Reduced LTP (long-term potentiation) (Pisasnsky et al, 2013) Reduced learning and memory – Morris Water Maze (B Felt and B Lozoff, 1996) – Radial Arm Maze (AT Schmidt et al, 2007) 66 Summary • Iron plays a critical role in early neurodevelopment • Early iron deficiency without anemia affects brain function • ID brain/behavior alterations persist after resolution of ID • Early detection of at-risk infants is crucial for brain health • Need new tools to detect pre-anemic iron deficiency References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. Lozoff B, Beard J, Connor J, Felt B, Georgieff M, Schallert T. Long‐lasting nueral and behavioral effects of early iron deficiency in infancy. Nutr Rev 64:S34‐S43, 2006. Kretchmer, N., Beard, J.L., Carlson, S. (1996). The role of nutrition in the development of normal cognition. American Journal of Clinical Nutrition, 63, 997S‐1001S. Thompson RA & Nelson CA, (2001) Developmental science and the media. Early brain development. American Psychologist 56(1), 5‐15. Lozoff et al, 2008 Dose‐response relationships between iron deficiency with or without anemia and infant social‐emotional behavior. J Pediatr. 2008;152(5):696‐702. Roncagliolo M, Garrido M, Walter T, Peirano P, Lozoff B. Evidence of altered central nervous system development in infants with iron deficiency anemia at 6 mo: delayed maturation of auditory brainstem responses. Am J Clin Nutr. 1998;68(3):683‐90. Algarín C, Peirano P, Garrido M, Pizarro F, Lozoff B. (2003). Iron deficiency anemia in infancy: long‐lasting effects on auditory and visual system functioning. Pediatric Research. 53, 217‐23 Unger EL, Hurst AR, Georgieff MK, Schallert T, Rao R, Connor JR, Kaciroti N, Lozoff B, Felt B. Behavior and monoamine deficits in pre‐ and peri‐natal iron deficiency are not corrected by early postnatal moderate or high iron diet in rats. J Nutrition. 142: 2040‐9, 2012. Clardy SL, Wang X, Zhao W, et al. Acute and chronic effects of developmental iron deficiency on mRNA expression patterns in the brain. J Neural Transm Suppl. 2006;71:173‐96. Petry CD, Eaton MA, Wobken JD, Mills MM, Johnson DE, Georgieff MK. Iron deficiency of liver, heart, and brain in newborn infants of diabetic mothers. J Pediatr 121:109‐114, 1992. Siddappa AM, Georgieff MK, Wewerka S, Worwa C, Nelson CA, deRegnier R‐A. Auditory recognition memory in iron‐deficient infants of diabetic mothers. Pediatric Research 55: 1034‐1041, 2004. Tamura T, Goldenberg RL, Hou J, et al: Cord serum ferritin concentrations and mental and psychomotor development of children at five years of age, J Pediatr 2002; 140:165. Amin SB, Orlando M, Eddins A, MacDonald M, Monczynski C, Wang H. J Pediatr 2010; 156:377‐81. Insel, B.J., Schaefer, C.A., McKeague, I.W., Susser, E.S., Brown, A.S. (2008) Maternal iron deficiency and the risk of schizophrenia in offspring. Archives of General Psychiatry, 65, 1136‐44. Riggins T, Miller NC, Bauer PB, Georgieff MK, Nelson CA. Consequences of Low Neonatal Iron Status due to Maternal Diabetes Mellitus on Explicit Memory Performance in Childhood. Developmental Neuropsychology, 34:762‐79, 2009. Carlson ES, Tkac I, Magid R, O’Connor MB, Andrews NC, Schallert T, Gunshin H, Georgieff MK, Petryk A. Iron is essential for neuron development and memory function in mouse hippocampus. J Nutrition,139(4):672‐9, 2009. Tran PV, Fretham SJB, Carlson ES, Georgieff MK. Long‐term reduction of hippocampal BDNF activity following fetal‐neonatal iron deficiency in adult rats. Pisansky MT, Wickham RJ, Su J, Fretham S, Yuan L‐L, Sun M, Gewirtz JC, Georgieff MK. Iron deficiency with or without anemia impairs prepulse inhibition of the startle reflex. Hippocampus. 23(10):952‐62; 2013. Fretham SJB, Carlson ES, Georgieff MK. The role of iron in learning and memory. Advances in Nutrition, 2: 1‐10, 2011. Conceptual Model of Neurodevelopmental Effects of Early Iron Deficiency Infant Iron Deficiency Poor feeding practices Brain Iron Neurochemistry ‐dopamine, striatum Maternal Iron Deficiency Disadvantaged Environment Neuroanatomy ‐myelin, dendrites Neurometabolism ‐hippocampus Cognitive, Language Maternal Depression Sensory, Motor Parenting Affective‐ Social Learning Experiences Functional Isolation Limited Support for Child Dev. Poorer Outcome Courtesy of B. Lozoff From Lozoff et al, 2006 67 Individualized Nutrition Plans for Patients with IBD Karen Warman, RD Athos Bousvaros, MD, MPH Inflammatory Bowel Disease Center CPNP, October 2015 Dr. Bousvaros has the following financial relationships to disclose: Prometheus – research support Dyax ‐ consultant Shire – data safety monitoring board Janssen – research support Takeda – consultant Peabody Arnold ‐ medicolegal No products or services produced by any of these companies are relevant to my presentation. Crohn’s disease vs. Ulcerative Colitis • Can involve any part of the intestine. • Transmural inflammation • Abscesses and fistulae • Recurs after surgery • Nutritional therapies are effective • High colon cancer risk • Colon only • Inner lining only • Abscesses very rare • Surgery “cures” • Nutritional therapies usually ineffective • High colon cancer risk 68 Ulcerative colitis – continuous Crohn’s colitis - discontinuous Theory of pathogenesis Exposure of a genetically predisposed host to an environmental trigger, resulting in immunologically mediated damage against the bowel. Variable phenotypes of enterocolitis in IL‐10 deficient mice (Kim and Sartor, Gastroenterology 2005;128:891‐906) Escherichia coli IL-10 knockout mouse Enterococcus faecalis Cecal (Crohn-like) inflammation Distal colitis (UC-like) 69 Inflammatory Bowel Disease Diagnostic Approach • Suspect the diagnosis – History, Exam, CBC, ESR, Albumin – Possible role for serologic testing • Exclude other etiologies – Stool culture, C. difficile, TB skin test • Classify disease as CD or UC • Determine disease location – Upper endoscopy, colonoscopy, UGI/SBFT • Identify extraintestinal manifestations – Liver function tests, Joint, Skin, Eye exams Crohn’s – Oral ulcers Crohn’s disease – Small Bowel Imaging • Options – Upper GI/SBFT – Abdominal CT – Abdominal MRI Ascending colon ileum 70 Normal colon Smooth and shiny Normal vascularity Tortuous Normal folds Perianal CD Ulcerative colitis Loss of vascular pattern Granularity Exudate Diffuse continuous disease No ileal involvement 71 IBD ‐ management • • • • • Medical Surgical Nutritional Supportive (psychosocial) Surveillance Crohn’s colitis Deep fissures Segmental distribution Rectal sparing Ileal involvement Granulomas on biopsy The “Balancing Act” 72 Treatment options for UC and Crohn’s disease Ulcerative colitis Aminosalicylates Corticosteroids Induction Infliximab Calcineurin inhibitors Aminosalicylates 6MP/azathioprine Infliximab Maintenance Crohn’s disease Enteral nutrition Corticosteroids Infliximab Adalimumab Aminosalicylates? Antibiotics? 6MP/azathioprine Methotrexate Anti-TNF agents Goals For Nutritional Intervention Meet Nutrient Needs Symptom Control Treat IBD Nutrition and Diet • Nutrition is what our body needs on a daily basis to stay healthy • Diet (food) is the choice of what we eat. • and overall wellness 73 Nutrients At Risk Protein Calories Vitamin D Iron Zinc Folic Acid B12 Magnesium Calcium • • • • • • • • • Meet Nutrient Needs 19 Dietary Components Targeted 1. 2. 3. 4. 5. 6. Animal Fat High sugar intake Gliadin Emulsifiers Maltodextrins Low Fiber Intake Ingredients Cream, Skim Milk, Sugar, Vanilla Extract, Guar Gum, Salt, Mono & Diglycerides, Dextrose, Polysorbate 80, Carrageenan, Cellulose Gum. 20 What do they hear? Avoid – Raw vegetables – Cruciferous vegetables – Citrus fruits – Red meat – Carbonated beverages – Coffee – Tea – Alcohol – Fatty and fried foods – Spicy Foods – Sugars – Seeds – Popcorn Clinical Gastroenterology and Hepatology 2014;12:1592‐1600 21 74 Dig Dis Sci. 2013 May;58(5):1322‐8 Diets Studied as Treatment for IBD • Enteral Nutrition • Specific Carbohydrate Diet • Anti‐Inflammatory IBD AID Treat IBD • Emerging (Low FODMAP) 23 Nutrition as Primary Therapy Treat IBD • There is long-standing evidence supporting the use of enteral nutrition in children with newonset Crohn's Disease • With enteral feeding, nutrition is improved, and growth and development can be promoted, while avoiding the systemic toxicity of corticosteroid therapy • 62% European MDs, 36% Canadians and 4% of Americans report frequent use J Pediatr Gastroenterol Nutr. 2011 Jan;52(1):38‐42 75 Enteral Nutrition Treat IBD • For a period of 6 to 8 weeks the diet is a beverage that will support nutrient needs • These beverages replace standard meals • No solid foods are included • Either take by mouth or given by tube Theories as to why it works Treat IBD • Providing calories and nutrients • Removal of dietary components which – Affect microbial composition – Decrease pro‐inflammatory responses – Promote restitution of the epithelial barrier 26 How well does exclusive enteral nutrition work? Treat IBD • Response rates: J Hum Nutr Diet.2013 27(suppl. 2) 28‐35, – In adults: 55% – In children: 50% to 75% • Effective for Crohn’s disease but not Ulcerative Colitis – May be more effective in small bowel Crohn’s • Elemental (hypoallergenic) and Polymeric (whole protein) formulas both seem to work • Probably not a good long term treatment • Partial enteral nutrition has shown a 50% reduction in relapse in CD compared to a regular diet. Inflamm Bowel Dis. 2013 Jun;19(7):1374‐8 Gut 2006:;55:356‐361 Aliment Pharmacol Ther 2006 24,1333‐1340 76 28 Specific Carbohydrate Diet • Includes Treat IBD – Meat, fish, eggs, vegetables, nuts, low‐sugar fruits • Avoids – Sugar – Diary, except homemade fermented yogurt and lactose reduced milk – All grains (no wheat, rye, barley, corn, millet, quinoa, rice • No pasta, bread, baked goods 29 Specific Carbohydrate Diet • JPGN 2014;58:87‐91 – – – – Retrospective 7 children with Crohn’s No Immunosuppressive meds On diet 5 to 30 months Symptoms ,Serum albumin, C‐reactive protein, hematocrit, stool calprotectin either normalized or improved by 3 months. • JPGN 2014;59:516‐521 – Prospective study of 9 children with Crohn’s – All saw clinical and mucosal improvement on 12 to 52 weeks of SCD • J Acad Nutr Diet 2015;115:1226‐1232 – – – – – – Descriptive study of 50 Patients on SCD (9 had UC) remainder CD 42 % were on no medication Quality of Life questionnaire average: 60.0 on a scale of 35 to 70 Mean time on diet 34 months 16 of the patients reported eating forbidden foods (7 on no drugs) Meal preparation estimation of 10‐11 hours a week 30 77 Reasons For Adopting Specific Carbohydrate Diet Cases % Fear of long‐term consequences of medications 41 82 64 Efficacy of SDC compared to medications 32 Medications not effective 32 64 Adverse reactions to medications 28 56 Recommendation from internet forum 22 44 Recommendation from family/friends 15 30 Breaking the Vicious Cycle Book 4 8 Cost of the medications 1 2 Seeking alternatives treatment to medication 1 2 Fear of need for surgery 2 4 Fear of colon Cancer 1 2 31 Anti‐Inflammatory IBD AID Treat IBD • Texture progression is built into recommendations • Promotes – Food sources of Pre and Probiotics – Lean protein and Healthy fats (beans, nuts, olive oil, ground flaxseed, fish and soy) – Soluble fiber (steel‐cut oats, ground flax and lentils) – Vegetables and fruits • Decreases pro‐inflammatory – – – – – Refined sugar and certain starches Grains (with the exception of oats) Lactose Processed foods Trans fats 32 The Anti‐Inflammatory Diet (IBD AID) • 40 adults were consecutively offered the IBD‐AID diet – 13 chose not to try the diet – 24 had either a good or very good response – 3 patients results were mixed • 11 underwent further medical record review – 8 with CD and 3 with UC – Followed the diet for 4 or more weeks – 100% discontinued at least one of their prior IBD Rx – All had symptom reduction Journal of Nutrition 2014, 13:5 78 Diets Targeting Symptom Control Symptom Control • Low Residue/Fiber • Low Lactose • Low FODMAP 34 Low Fiber/residue diet Symptom control • Indications – To prevent bowel obstructions in patients with Crohn’s disease and narrowed segments of intestine. • (Gut 1985:26: 989‐93) 71 patients following low fiber were randomized to reintroduce fiber, showing no difference in outcome – To reduce (not eliminate) the residue in the colon pre‐ and postoperatively. – Definition is usually < 10 grams fiber per day. The diet is intended for short‐term use. Nutrition in Clinical Practice 2015 30:462‐73 Why not continue on low fiber? • High red meat protein intake • High fat • Trend towards highly refined foods with food additives and preservatives with added soybean oil (sources of Omega‐6) • Fiber offers pro and prebiotics that change the balance of beneficial bacteria. • Lignans, flavonoids and anti‐oxidants from fruits and vegetables • Higher sodium intake especially problematic with use of steroids 79 Primary sources of FODMAPS Low FODMAP Symptom Control • 52 patient with Crohn’s • 20 patients with UC • Instructed on Low FODMAP 70% followed the diet • 50% responded favorable to the diet defined as • Improvement in 5 out of 10 of the following symptoms • Abdominal pain • Bloating • Passing gas (wind) • Diarrhea Journal of Crohn’s and Colitis:2009; 3, 8‐14 38 Emulsifiers • CMC or polysorbate ‐80 given in drinking water or chow • Significant increase in colitis • Amount consistent human consumption • Polysorbate 80 – Ice cream, whipped cream, mayonnaise, salad dressings, rotisserie chicken • Carboxymethylcellulose 2013:J Crohn’s and Colitis 7,338‐341 – CMC, cellulose gum or cellulose and sodium carboxymethyl cellulose – Ice cream, dressing, cheese, icing, toppings, cottage cheese, cream cheese spread 2015:Nature 7, 92‐96 39 80 Diet Restriction At Risk Nutrients Low‐Residue/Fiber < 10 gm fiber/day ; generally insoluble fiber such as raw fruits and vegetables and whole grains Folate, Vitamins A & C, Potassium High fat Enteral Only formula used None, complete nutrition Specific Carbohydrate Diet All grains, lactose, processed meats and legumes Folate, thamin, B6, riboflavin, niacin, calcium and Vitamin D Low‐FODMAP Fermentable Oligo‐, Di and Mono Saccharides and Polyols No wheat, barley and rye, Defines vegetables and fruits No sugar alcohols Folate, thiamin, B6 , riboflavin, niacin, calcium and Vitamin D, Vitamins A and C without guidance Anti‐Inflammatory IBD AID All grains except Oatmeal Lactose, processed meats, trans fats. Folate, thiamin, B6 , riboflavin, niacin, calcium and Vitamin D, 40 Meet Nutrient Needs Treat IBD Symptom Control Summary • Enteral nutrition is the only diet approach to induction at this time • 80% enteral nutrition is the 2nd best option • Maintenance is likely to be a hybrid of the diets based on – Functional symptoms – Ability to follow a restrictive diet – Degree of motivation from both the family and the child – Nutritional status 42 81 Meet Nutrient Needs Discourage With functional Pain Fruits and Vegetables Added HFCS and large amounts of Juice Low FODMAP guidelines Grain Additives Wheat, Barley and Rye in large amounts Low FODMAP guidelines Lean meat and Legumes Processed meats and limit high fat meats Low FODMAP guidelines for Legumes Dairy Additives Low FODMAP guidelines Fats Encourage Omega‐3’s Multivitamin meeting DRI Polysorbate 60/80 and Carboxymethullose Consider: Decrease caraggean and high fructose • Probiotics and Omega 3 from corn syrup Natural sources 43 44 82 CPNP Symposium, Saturday 10/9/15 Case Study Breakout: The Elimination Diet: Practical Tips and Pitfalls Wendy Elverson, RD, LDN, Boston Children’s Hospital, Center for Nutrition CASE: Baby Girl Jane with FPIES (Food Protein Induced Enterocolitis Syndrome) History: Full term, breast fed, @ 2 weeks fussiness, abdominal distension, mucous in stool Milk free/soy free diet for mother and Ranitidine followed by Omeprazole Rx for baby. 2 months ↑ Omeprazole. 3 months nursing refused, EBM (expressed breast milk) via bottle refused→ Nutramigen vomiting, diarrhea, irritability→ Alimentum vomiting, diarrhea, irritability→ Elecare infant (per mother “Like a New Baby”). 6 months oat cereal introduced,? fussiness solids stopped. 6 ½ months retry oat and sweet potato introduced around the same time→ Day 9 classic FPIES symptoms (2‐3 hours after ingestion repetitive vomiting, pallor, retching) presumably to oat. 6 ½‐11 months symptoms with multiple other foods. Not classic FPIES symptoms. Symptoms included diarrhea, mucous in stool, irritability, night waking, single episode vomiting. Foods causing one or more symptoms mentioned above: apple, pear, carrot, cauliflower, Neocate Nutra (contains corn syrup solids and rice starch), white potato, egg and watermelon). 11 months lamb introduction day 3 resulted in FPIES symptoms. Dietitian Visit One: Age 12 months Foods tolerating: Banana, avocado, Elecare infant (intake of 65 calories per Kg per day) Growth: Weigh: 49th%ile, Length: 71st%ile. Growth history looks good. Recommendations: o Avoid: milk, soy, oat, rice, lamb, carrot, sweet potato, cauliflower o Foods to trial: Quinoa, flounder or tilapia or sole, white potato, canola oil, blueberry, peach, plum, prune, broccoli, spinach, pea, corn o Recommendations: Continue Elecare infant. Solids 3 times per day. Separate all feeding by 2‐3 hours. Food before formula at meal time. Try sippy cup, Finger food ideas given. Dietitian Visit Two: Age 17 months Foods tolerating: Banana, avocado, tilapia, quinoa (flakes and puffs), potato (pieces and Cheecha puffs), corn (cereal and quinoa corn pasta), Elecare infant 20‐24 fl. Oz. per day Foods questioned: Baked egg Growth and Nutrition: Weight: 41st %ile, Length: 65th%ile. Food processor nutrient analysis of a typical day meeting greater than 80% DV for vitamins and minerals except vitamin D (290 IU). Adequate protein intake. Calorie intake 85 calories per Kg per day. 83 Recommendations: o Avoid: Milk, soy, oat, rice, lamb, carrot, sweet potato, cauliflower o Foods to trial: Canned coconut milk in cooking and cereal, homemade potato pancakes (quinoa or corn flour and corn oil), canola oil, chicken, beef or turkey, red or orange fruit or vegetable such as tomato or clementine), ground flaxseed, legumes other than soy, peanut (Bamba or peanut flour as skin test negative) o Other recommendations: Continue Elecare infant (20‐24 fl. Oz. per day). Introduce one new food every 3‐5 days. 3 meals and 2 snacks per day separated by 2‐3 hours. Solids before formula at meal and snack time. Start 400 IU vitamin D daily. Dietitian Visit Three: Age 21 months Foods Tolerating: Banana, avocado, tilapia, quinoa (flakes and puffs), potato (pieces and Cheecha puffs), corn (cereal and quinoa corn pasta), canola oil, grapes, pollock, chicken, garlic, shredded coconut, peanut butter, wheat, cucumber, watermelon, cinnamon, lemon, Elecare infant 18‐20 fl. Oz. per day. Food Questioned: Baked egg (not tried since visit two), Strawberry day 3 of introduction (few bites) → 2 hours post ingestion vomited 3 times, lethargic and pale. Growth and Nutrition: Weight 41st%le, Length 70th%ile. Recommendations: o Avoid: milk (fresh), soy, oat, rice, lamb, carrot, sweet potato, cauliflower, strawberry o Foods to trial: Kidney bean turkey or pork, retry baked egg, baked milk, calcium fortified coconut milk as a beverage once a day. o Other recommendations: Continue Elecare infant ~20 fl. Oz. per day until age 2 years (then transition to whole milk or coconut milk depending on tolerance to dairy), continue vitamin D 400 IU per day. Discussion Points: 1. FPIES: What is it? 2. What are the most common foods that trigger FPIES? 3. Which food group should be introduced first? 4. At what pace should new foods be introduced? 5. Should volume of food on first few days of introduction be limited? 6. What are your favorite FPIES friendly finger foods? 7. How do you advance texture for the infant with FPIES who is only taking a few foods? 8. If a baby with FPIES is breast feeding and refusing all formula what nutrients should you be concerned about after 6 months of age? 84 CPNP Symposium, Saturday 10/9/15 Case Study Breakout: Nutrition for the Hypometabolic Child Monica Cicchini, MS, RD, CSP, LD, MedStar Georgetown University Hospital Case Presentation: Past medical history significant for: Down Syndrome, severely neurologically impaired due to Hypoxic Ischemic Encephalopathy. He has seizures, hydrocephalus, dysphagia, global developmental delays, and diabnois of cerebral palsy. Fed Solely through G‐J tube. Currently on Elecare because of history of "vomiting." Vomiting may be secondary to congestion/respiratory status. No change in vomiting when transitioned from Similac Advance to Elecare at 6 months of age. Dietitian Visit One: 22 months old Anthropometrics: 10.8 kg (10%ile, wt/age z‐score ‐1.28), 75 cm (0%ile, length/age z‐score ‐3.15), wt/length 92%ile, z‐score 1.39) Diet: 24 ounces Elecare 20 kcal/oz daily. 45 kcal/kg, 1.3 gm/kg, 67 mL/kg Labs: CBC/CMP Normal Supplement: poly‐vi‐sol Recommendations: o Decrease to 22 ounces/day Elecare (decrease by 10% total kcal) o Increase water to 100 mL/kg/day Dietitian Visit Two: 28 months old Anthropometrics: 11.25 kg (6%ile, wt/age z‐score ‐1.52), 78 cm (0%ile, length/age z‐score ‐3.77), wt/length 91%ile, z‐score 1.33) Diet: 22 ounces Elecare 20 kcal/oz daily plus 4.5 ounces water. (39 kcal/kg, 1.1y gm/kg, 89 mL/kg) Labs: CBC/CMP Normal Supplement: poly‐vi‐sol Recommendations: o Change to Complete Pediatric Reduced Calorie 660 mL/day (35 kcal/kg, 1.76 gm/kg) o Add 400 mL free water o Add Centrum Complete (crushed) o Check Vitamin D levels and replace if low o Add Morton Lite Salt with a goal of 1‐3 mEq/day Na and K o Evaluate meds for any additional kcal 85 Dietitian Visit Two: 36 months old Anthropometrics: 14 kg (42%ile, wt/age z‐score ‐.2), 81 cm (0%ile, length/age z‐score 4.36), wt/length 100%ile, z‐score 2.84) Diet: Complete Pediatric Reduced Calorie 660 mL/day plus 400 mL free water (28 kcal/kg, 1.41 gm/kg) Labs: CBC/CMP Normal Supplement: Centrum Complete Recommendations: o Decrease to to Complete Pediatric Reduced Calorie 600 mL/day (26 kcal/kg, 1.28 gm/kg) o Add 600 mL free water o Continue Centrum Complete (crushed) o May benefit from calcium supplement o Check Vitamin D levels and replace if low o Continue Morton Lite Salt with a goal of 1‐3 mEq/day Na and K o Evaluate meds for any additional kcal Discussion Points: 1. What are nutritional areas to consider in an initial visit with a hypometabolic child? 2. What are appropriate minimum calorie and protein goals? If protein is low are their modulars that you can use? 3. What are some formulas you can use if you are managing a hypometabolic child? Can you use a blenderized diet? If so, how would it be managed? 4. What are some supplements you can use to meet micronutrient needs? 5. When giving large fluid flushes should distilled (electrolyte free) water be used or can that lead to hyponatremia and possible seizure activity? 6. What are the pros and cons for using morton lite salt versus pedialyte to achieve sodium/potassium goals 7. How would your recommendations change if the patient was a po feeder but required thickened feedings 8. What lab values and testing would you consider besides CBC, CMP and Vitamin D level? 9. What would you manage from 3 years to beyond? What are your growth expectations and based on which growth chart 86 Nutrition care for children undergoing hematopoietic cell transplantation - now and later Lori J. Bechard, PhD, RD, LDN Case presentation • 17 yo female with CML, presents for HCT from unrelated donor • Well nourished at presentation • High dose cyclophosphamide & TBI for conditioning --> Anorexia, nausea, emesis • • • • Inpatient course PN initiated to provide 140% estimated requirements Minimal oral intake for 3 weeks Engraftment at 24 days post transplant Slow resumption of oral intake • • • • Outpatient course Discharged from hospital Oral intake continues to improve with resolution of mucositis Readmitted 2 weeks later with abdominal pain, diarrhea, anorexia Colonoscopy and biopsy revealed graft-versus-host disease • • • • Acute GI GVHD Treated with prednisone, mycophenylate, cyclosporine Kept NPO for large amounts of bloody stool Diet SLOWLY liberalized with decreasing stool output Poor oral intake persists with accompanying weight loss • • • • Enteral feedings initiated G tube placed Supplemental feedings with polymeric formula Oral intake somewhat improved Discharged with overnight G tube feedings • • • • Case update Oral intake up and down Uses G tube for medications, occasional feedings Weight gain remains problematic Persistent chronic oral GVHD; at risk for osteoporosis with long term steroids Questions for discussion 1. How should energy needs be assessed in children undergoing HCT? 2. What is the best route for feeding children undergoing HCT? 3. How do complications of HCT impact nutritional status, both short term and long term? 87 Nutrition challenges in a medically and socially complex child with Cystic Fibrosis Tami Miller, RD, CSP, CD Initial Presentation: 4 yr old male with CF (F508del/621+1G‐‐>T) and pancreatic insufficiency arrived in ER with respiratory distress, worsening cough, poor weight gain and growth. He previously received care out of state and moved to Wisconsin 9 months earlier; interim care was managed by his PMD. Child received G‐tube feedings beginning at age two, but the move resulted in a lapse of supplies, formula and medication refills. The child lived in a chaotic household which resulted in foster placement within a few months of receiving care at our institution. Growth Height (z‐score) Weight (z‐score) BMI (z‐score) July, 2013 91.4 cm (‐3.5) 11.5 kg (‐ 4.4) 4% (‐1.8) Physical assessment: Extremity wasting, thin hair, barrel chest, clubbing, distended abdomen. He appeared 1‐2 years younger than reported age. Lung function (FEV1) was 50% of predicted value. Nutrition Prescription: Estimated energy needs based on DRI: 1500+ calories (130 Cal/kg); 26+ grams protein (2.2 gm/kg); Nutrition Intervention: High calorie oral diet; peptide based 1 cal/ml formula: 3 cans over night; 1 can in AM & PM (1200 cals / 38 gm pro = 80% enteral support). Zenpep 10,000 3/meal & before daytime tube feedings; 2/snack; 3 crushed in overnight tube feeding. CF vitamins + vit. D Interval History: In the next year of care at CF Center, child had intermittent CF exacerbations with 3 courses of IV antibiotics. FEV1 = 80% predicted. He was in foster care and received consistent respiratory and nutrition therapies. Foster parents note slow eating; refusal to sit at table; poor appetite; distracted at meals. Foster parents want G‐tube removed. Revised Nutrition Intervention: High calorie diet; peptide based 1.5 cal/ml formula: 3 cans overnight with 5 crushed Zenpep 10,000. Estimated energy needs increased to 1770 Calories/day (105 Cal/kg) to support increased weight, activity, lung function, growth. Enteral nutrition supplied 66% of energy needs. Cyproheptadine prescribed. Behavioral strategies implemented: Limit meals to 20 minutes, no grazing, positive behaviors rewarded; negative behaviors ignored. Growth Height (z‐score) Weight (z‐score) BMI (z‐score) July, 2013 91.4 cm (‐3.5) 11.5 kg (‐ 4.4) 4% (‐1.8) August, 2014 104 cm (‐ 2.1) 16.8 kg (‐1.6) 55% (0.12) Recent Updates: FEV1 improved to 85% predicted with one hospitalization in last year. Child attends school which requires “healthy” foods at snack and lunch, and limited time to eat. Poor appetite continues. Weight did not increase in 6 months. Updated Nutrition Interventions: PM tube feeding was restarted for additional support. Energy needs increased to 1700‐ 1940 Calories/day (90‐102 Cal/kg). Enteral nutrition now supplies 77‐88% of estimated needs. Growth Height (z‐score) Weight (z‐score) BMI (z‐score) July, 2013 91.4 cm (‐3.5) 11.5 kg (‐ 4.4) 4% (‐1.8) August, 2014 104 cm (‐ 2.1) 16.8 kg (‐1.6) 55% (0.12) June, 2015 111 cm (‐1.8) 19 kg (‐1.3) 50% (0) Discussion: What are some approaches to pancreatic enzyme therapy with tube feeding support? What approaches can be considered to work towards “normal” eating schedule by increasing the number of meals while balancing enteral feedings to meet the need for adequate nutrition? How much recovery of growth could be expected over time? 88 CPNP Symposium: Breakout Session October 2015 Binita M. Kamath, MBBChir Nutritional Issues in Alagille Syndrome 2 month old with cholestasis diagnosed with Alagille syndrome based on family history in the father and a positive mutation in JAGGED1. From birth taking regular infant formula by mouth and growing along the 3rd percentile. 6 months old – develops itching. No weight gain in the preceding 3 months. Infant formula concentrated to 0.8kcal/ml. 10 months old – spontaneous femur fracture. Weight now falling. Cessation of linear growth. Itching worsens. 12 months old – GT inserted. 14 months – weight gain improved. Gaining 21 g/day. Taking small amount of solids. Itching worsening. 23 months – biliary diversion. 34 months – listed for liver transplantation. Discussion Points: 1. What are the potential causes of growth impairment in Alagille syndrome? 2. What are the particular considerations of considering a G-tube in a child with Alagille syndrome? 3. What are the nutritional implications of a biliary diversion? 4. How does a liver transplant impact growth and nutrition in Alagille syndrome? 89 Andy is a 15 year old young man with Crohn’s disease January 27, 2012 (age 11 y 4 months) presented to GI in 2012 at the age of 11 years with h/o oral inflammation initially thought to be secondary to an orthodontic appliance RX: antibiotics as well as 2 courses of prednisolone, improving with therapy, but would return. No fevers, abdominal complaints, joint pains, rashes, redness of the eyes, blood in the stool or vomiting. Appetite: excellent Energy Level: Good, but not playing sports Physical Findings: Bowel movement 1 formed daily Multiple anal skin tags. April 03, 2012 (11 years 7 months) Endoscopy was reported as normal, but oral biopsies showed evidence of "squamous mucosa with reactive epithelial changes . The findings are reflective of a chronic inflammatory process. There was a single non necrotizing granuloma in the colon Some worsening of a mouth sore over the last several days; Medications: Ferrous sulfate 45 mg by mouth daily. Vitamin D supplement 50,000 IU 30 days Started: Flagyl (antibiotic) possible side effects metallic taste and risk of neurological symptoms for long term use Mesalamine (Asacol) (5 ASA) risk of reversible low sperm count, nausea and vomiting June 05, 2012 1 (11 years 9 months) Symptoms: resolution of oral ulcers and some improvement in anal tags No abdominal pain, nocturnal stools, fever, joint pain, rashes, redness of the eyes Appetite: Improved Energy level Improved Bowel Movements 3 -4 without blood or mucus Noted high Liver function tests MEDICATIONS: Flagyl ( metronidazole) 250 mg p.o. t.i.d. Asacol 1200 mg p.o. b.i.d. Iron sulfate 45 mg extended release once daily. Antibiotic Long-term use often limited by nerve damage, dose reduction may decrease risk 3-7% have increase in colitis 5 ASA Suppleme nt . July 17, 2012 11 years 10 months Family consulted a homeopathic practitioner who recommended started supplements instead of standard therapy. Family elected to keep therapy and start supplements Added Moducare 1 tablet PO BID Plant sterol Liver fraction iron supplement2 tablets pol daily 1300 mg Acetyl glutathione 200 mg po daily Lyop-spheric Vitamin C 1 packet daily Fish oil 1 teaspoon daily Lauricidin or monolauric acid (from coconut oil) 1.5 grams Po BID Symptoms: No abdominal pain, no new mouth sores. Bowel Movement 1-2 /day without blood or mucus Appetite: somewhat poor Energy: good 90 Stopped the Flagyl at this visit September 18, 2012 12 years Family expressed desire to avoid all medications if possible , very concerned about the elevated Liver enzymes Symptoms: Denies, however mother does most of the talking. Bowel Movements 1/day No nausea, abdominal pain Energy level: good Appetite: good Medications: None. MD discussed concern of no medical management in light of increase in inflammatory markers Started Pentasa Pentasa 1500 mg po q am and 2000 mg 5-ASA Headaches, diarrhea and 3-7% worsening of colitis nightly abdominal pain Difficulty swallowing tabs (requires 7 daily) Vitron-C 65 mg elemental 1 per day daily Lactobacillus GG 1 capsure February 19, 2013 12 years 5 months Appetite: good Energy level: good Bowel Movement 1/day Anemia worsened Increased Fe to 2 daily May 21, 2013 15:30 12 years 8 months Bowel movements one formed stool per day without blood or mucus. Appetite/Diet struggle with eating red meat and green leafy vegetables concerned about Iron intake August 20, 2013 No change , except significant concern with swallowing multiple capsules. Referred to psychology June 16, 2015 14 years 9 months Symptoms Abdominal pain as often as 5-6 times per week. His pain is often in the periumbilical region. The pain lasts typically 5-6 minutes and is described as a constant pain. Bowel movements: Increased, but no blood or mucus on stools No fevers, joint pains, rashes, mouth sores or inflammation of the oral or perianal area. Meds unchanged MD recommended nutritional supplements due to suboptimal weight gain July 07, 2015 (1st RD visit) REASON FOR VISIT : Inflammatory Bowel Disease, induction therapy with Enteral nutrition Mother asking about use of several supplements including Kids DHA, Rainbow Light D3 200 IU/day, Smarty Pants Multivitamin, Intesti Flor Probiotic and Digestive Aide, in addition to taking Vitamin C 125 mg and Iron 65 mg daily. He has tried Ensure in the past, reporting that it was not well tolerated, both in flavor and resulting in stomach ache. He reports bloating and urgency to move his bowels. 24 hour recall Bagel with cream cheese and 1 cup milk Sandwich with mozzarella cheese, tomato and basil Oatmeal Raisin Cookies Meat loaf with soup, yogurt and corn Grilled cheese Sandwich with sweet biscuits. Growth Chart (Based on CDC growth charts) 14yr 10m (178.0 Months), male 91 Value Imperial %ile Z Score 50%ile IBW (pounds) Weight (kg) 59.5 131 lb 2.8 oz 64 0.36 56 134 pounds 6.66 oz Height (cm) 174.6 68.74 in 75 0.68 169 BMI (kg/m) 19.52 54 -0.09 20 Genetic Growth Potential : 175.0 cm = 25-50%ile Expected linear growth based on CDC growth standard is 0.5 cm/month. IBW (kg) 60.97 kg Fluid Requirement : 2300 ml/day or 100 ml/hour Skin Fold Measurement Mid-Arm Muscle Area (MMA) Value 26.7 cm 14.0 mm 223 mm 3958 mm2 Mid-Arm Fat Area (MFA) 1715 mm2 Mid-Upper Arm Circumference (MUAC) Tricep Skinfold (TSF) Mid-Arm Muscle Circumference (MMC) 50-75 %ile 75%ile Comparative Standards : Based on Schofield equation @Input factor of 1.5 = estimated need of 2590 calories/day Nutrition Diagnosis: Altered GI function related to relapse in Inflammatory bowel disease evidenced by history. There is supporting literature to use enteral nutrition as a key component to treatment. (family not receptive to full enteral diet) Nutrition Intervention: Begin minimum of 4 Boost High Protein supplements (240 calories/ 240 cc bottle) 960 calories Minimum of 4 daily with Clean diet as the remainder of nutrients) Also reviewed the number of supplements that he is on. Advised to discontinue the digestive Enzyme as there is currently no evidenced that it is needed. July 29, 2015 14 years 10 months Symptoms : complaint of focal lower abdominal pain, early satiety and weight loss, had suggested further imaging to assess the status of his Crohn’s disease. An MRI of the abdomen completed on July 9 demonstrated “severe active inflammation of the long segment of distal small bowel, with prestenotic dilation and intraluminal stasis. Additional short segment of mild active inflammation in the left upper quadrant. Findings are in keeping with active Crohn’s flare.” In the several weeks since these findings he has been taking several cans of Ensure on a daily basis but is unable to be large volumes of food. He was suggested to follow a low residue diet given the severity of his stenosis. Fortunately, he has not had any suggestion of obstruction to this point. Pentasa 1500 mg po q am and 1500 mg nightly 5-ASA Headaches, diarrhea and abdominal pain Difficulty swallowing tabs (requires 6 daily) do not crush 3-7% worsening of colitis Culturelle Digestive Health, 1 cap, PO, daily Ferrum, which is 4 tablets p.o. t.i.d Nutrition supplementGerman nutraceutical Boost Plus Supplement VSL#3 oral powder for reconstitution August 11, 2015 92 8/15 Humira Biologic Anti-TNF Injection site reactions Increased risk of TB including immune suppression, the rare risk of hepatosplenic T-cell lymphoma, infection, hepatitis, psoriasis, infusion reactions in the more likely risk of possible response due to antibody formation. Has been taking Boost plus , adopting many gluten free grains (decreasing but not eliminating gluten) with focus on Clean diet. 24 hour recall 11 am 1 boost plus and Udi’s GF bagel with egg, cheese and ham 3 pm 1 Boost Plus 7 pm GF macaroni with two large meatballs made with GF breadcrumbs 8 pm 2 gf cookies and 1 boost Plus 10 pm 2 cookies (that contained wheat) By history this is approximately 2000 calories/day Growth Chart 14yr 11m (179.0 Months), male, (CDC growth chart) Value Imperial %ile Z Score Weight (kg) 59.7 131.0 lb 9.86 oz 63 0.34 Height (cm) 175.5 69.09 in 77 0.75 44 -0.16 BMI (kg/m2) 19.38 50%ile IBW (pounds) IBW (kg) 56.0 135 lb 12.89 oz 61.6 kg 170.0 20.0 Fluid Requirement : 2294.0 ml/day or 100.0 ml/hour Comparative Standards : Based on Schofield equation @Input factor of 1.5 = estimated need of 2590 calories/day Nutrition Diagnosis: Altered GI function related to Crohn’s disease evidenced by MRI. There are strictures that may require surgery. The only known nutrition based therapy to decrease inflammation is 100% enteral nutrition. Nutrition Intervention: Discussed what is known about use of nutrition as a primary treatment for Crohn’s disease. Encouraged the use of 5 to 6 Boost plus (or provide samples of Ensure plus , Pedisure Peptide or Peptamen (all 1.5 calories/cc) for the next 6 to 8 weeks as a primary therapy for Crohn’s . AM agreed to this therapy in hopes of avoiding surgery. It was made clear that this therapy will be part of a medical plan that should maximize the changes of avoiding surgery, but will not guarantee. August 31, 2015 15 years REASON FOR VISIT : Crohns disease, Using Enteral nutrition to assist with induction therapy. Currently taking Boost Plus (360 calories/8 fl. ounces bottle) seven daily ( 2500 calories) plus 1 tablespoon of applesauce with VSL #3 and 1 cup of clear juice daily. He reports that he feels well. His mother believes that his "color" has improved. They are not eating in front of him. They report that although it has been hard, they find that they are finding other activities to do as a family. His energy level is good, although he needed to rest a bit more than his 18 year old brother while on vacation. Mother was unsure of whether this was due to the heat and sun that he did not tolerate. His bowel movement are reported as normal, soft, without any abdominal pain. Mother questions whether to encourage him to go out for cross country while on the enteral formula He reports that the current amount of formula his keeping him satisfied, he would not like to drink more. He is currently drinking 8 fl. ounces every 2 to 3 hours of the waking day. They are concerned about whether he will need permission to do this at school. 93 Interval between visits : 20 days Actual weight gain annualized : 20.0 grams/day or 7.3 kg/year Expected Weight Gain (based on CDC) : 5.3 kg/year Actual linear growth annualized : 0.0 cm/month or 0.0 cm/year. Expected Linear Growth (based on CDC) : 6 cm/year. Growth Chart 15yr (180.0 Months), male, (CDC growth chart) Value Imperial %ile Z Score 50%ile IBW (pounds) Weight (kg) 60.1 132.0 lb 8 oz 63 0.33 56.0 Height (cm) 175.5 69.09 in 76 0.7 170.0 BMI (kg/m2) 19.51 45 -0.13 20.0 IBW (kg) 135 lb 12.89 oz 61.6 kg Fluid Requirement : 2302.0 ml/day or 100.0 ml/hour Comparative Standards : Based on Schofield equation @Input factor of 1.5 = estimated need of 2599 calories/day Nutrition Diagnosis Altered GI function related to Crohns evidenced by history. He is doing well on the enteral formula, gaining weight well. Nutrition Intervention Continue enteral formula (exclusive) for the next 4 weeks, then we will discuss transition back to "clean diet" September 01, 2015 MD note: Improving on enteral nutrition and Humira. Re-evaluate for surgery after 3 months Medications Boost Nutritional Supplement (8 oz bottle), 6 refills Humira 40 mg/0.8 mL subcutaneous kit, 40 mg, Subcutaneous, Q14day, 11 refills Pentasa 500 mg oral capsule, extended release, 5 refills VSL#3 oral powder for reconstitution 94 95 96 97 98 99 100 BLENDERIZED TUBE FEEDINGS: MANAGING A NEW FRONTIER Julia Driggers RD, LDN, CNSC Mimi Girten, RD, CSP, LDN Children's Hospital of Philadelphia, Department of Gastroenterology and Nutrition Disclosures • Nothing to Disclose Introduction • Summarize history of enteral nutrition • Understand reasons for using blenderized tube feedings (BTF) instead of commercial formula • Identify & compare components of different blend types • Recognize traits of patients who might be suited for BTF 101 Introduction • Understand challenges for the dietitian. • Recognize how BTF works for the family. • Identify bumps in the road when using a BTF. • Recognize challenges moving forward So, what’s Blenderized Tube feeding? Designed By: Amy Dean In the Beginning… Designed By: Amy Dean 102 And back again… … … … Designed By: Amy Dean “Typical Diet” + Blender = Done? What’s in a Blend? Designed By: Amy Dean 103 Who’s a Good Fit? How‐To’s of Preparation & Administration of Blenderized Tube Feedings Pediatric Population 104 Types of Blend Thick vs. Thin Administration Creating a Recipe Preparation Equipment Food Safety Thick Formulas Administration – Thick Blends Use: Treatment of Gagging Refluxing Nissen Fundoplications Volume Intolerance 105 Administration – Thick Blends Description: Thick/Pasty Liquid High Caloric Density (> 30 kcal/oz) Minimal Free Water Administration – Thick Blends – Require a G-Tube (14-16 French) – Administered via Plunger Syringe only – Start 1 oz ‘Bolus’ pushed in slowly over 10 min. – Increase ‘Bolus’ to 2- 4 oz goal – Water flush (5-10 ml) proceeds TIME SAVER: Olive Oil or Oil Spray (PAM) can be used to lubricate the syringe and end of plunger for easier administration Administration – Thick Blends 106 Creating a Recipe – Thick Blends Recipe 1: w/ Commercial Formula Recipe 2: w/o Commercial Formula 8 oz Pediatric Formula 1.5 4 oz Strained sweet potato 4 oz Strained peaches 6 oz Plain yogurt 2 Tablespoon oil 6 Tablespoons sugar or cornstarch ½ Cup dry infant cereal 8 oz Whole milk 2.5 oz Strained chicken 4 oz Strained pears 4 oz Strained squash 6 oz Greek yogurt 1 Tablespoon oil 4 Tablespoons sugar or cornstarch ½ Cup dry infant cereal Estimated Caloric Content: Estimated Caloric Content: 1100‐ 1200 kcal 900‐1000 kcal 32% Fat, 55% CHO, 13% Pro 65% Free Water 30% Fat, 55% CHO, 15% Pro 64% Free Water 12‐15% Protein, 30‐35% Fat, 55‐60 % CHO 1) Choose a Protein Source • Liquid Protein (Milk/Formula) • 4 – 8 oz Needed Only • Thicker Protein (Meat/Yogurt) • 80-90 % Protein Needs from above Sources. Additional from Cereals 2) Choose a Carbohydrate Source • Use Stage II Fruits/Vegetables • Choose High Vit. A & Vit. C • Less than 8 – 12 oz (2-3 jars) 3) Thickening Agents/ CHO Source • Grains to add kcals/fiber/thicken • Need up to 8 TBSP Infant Cereal • Adding White Granulated Sugar or Cornstrach 4) Choose a Fat Source • Omega 3, Omega 6 Blend • 1-2 TBSP Thin Liquids Administration – Thin Blends Use: Natural / Holistic Option Formula Intolerance (**Volume Tolerant) Oral Aversions / Delayed Oro-motor skill Description: Medium/Thin Liquid Moderate Free Water 20-30 kcal/oz Formula 107 Administration – Thin Blends – Require a G-Tube (14-16 French) – Administered via Infinity® Pump Addendum to Directions for Use: “…DO NOT USE HOMEMADE BLENDERIZED OR LIQUIDIZED FOODS, OR OTHER NON-COMMERCIALLY AVAILABLE FEEDING SOLUTIONS…” – Thin formula required to flow through pump – Pump feeds to run < 2 hrs. for food safety – Possibly keep on ice (< 40 F) if hang time longer than 2 hrs. Use of Chill Bags Note: Fat can degrade pump tubing Administration – Thin Blends – • • • Administered via Plunger Syringe 60-90 ml syringe with plunger Push slowly Allows for varying degrees of thickness – • • • Administered via Gravity Syringe Syringe without plunger Elevated to gravity to flow through Formula required to be very thin Creating a Recipe– Thin Blends • Marsha Dunn Klein, MEd, OTR/L and • Suzanne Evans Morris, PhD, CCC‐SLP • Copyright © 2007 by Mealtime Notions, LLC • Charts may be reproduced for instructional use and educational purposes. They should not replace the advice of a physician 108 Protein 12‐15% Protein, 30‐35% Fat, 55‐60 % CHO Cows Milk 8 gm Pro/cup Hemp Milk 4‐5 gm Pro/cup Coconut Milk, canned 5 gm Pro/cup 2 slices Wheat Bread ½ cup Infant Cereal, cooked ½ cup Brown Rice, cooked 6 oz Carrots, BF Stage I 6 oz Green Beans, BF Stage III 140 7 80 4 100 2.5 90 0 90 3 4 oz Apple Sauce, pureed 2 oz Peaches, pureed 2 oz Prunes, BF Stage I 80 0 40 0 50 0 2 cups Soy Milk, original 220 16 1 Egg with Yolk, cooked 2.5 oz Chicken, BF Stage I 70 6 70 0 Mono‐ Olive Oil, Canola, Avocado, Nuts Omega 3‐ Flax, Canola, Walnut, Hemp, Fish 2 tsp Flaxseed Oil 2 tsp Canola Oil 80 0 80 0 1190 38.5 Molasses, Agave, Table Sugar, Corn Starch, Hemp Protein, Avocado 1 tsp 100 % Maple Syrup 20 0 1210 38.5 Getting Started with Blenderized Feeds Choose Appropriate • Thick Blend Type Blend • Thin Blend • Calorie, Protein, Fluid needs • 15‐20 % more Calories than formula Calculate Needs 50 % Calorie Needs from Formula • Start “Single Ingredient” Bolus (1‐2 oz) 1‐4 X day • Continue Formula ≥ 50% calorie need (Overnight or Bolus) Increase Blenderized Food and Variety • Add 1 New Ingredient per Blend • Note GI Reaction (Vomiting, Diarrhea, etc.) 109 Monitoring Tolerance of Blended Foods Pediasure 1.5 Puree Chicken Carrots Peas Pears Prunes √ Soft, light brown X X X Child with looser BM without straining Equipment Designed by Mimi Girten Equipment Designed by Mimi Girten 110 Tips and Timesavers • Whole foods blend easier when warm. • Use water from cooked vegetables as a source of liquids • Fruits should contain skin to add fiber Designed by Mimi Girten Tips for Preparing Whole Foods Difficult to Blend Foods Foods that Thicken Recipe • Corn • Pasta • Nuts • Wheat products • Fruits with small seeds • Bananas (Raspberries, Blackberries) • Flaxseeds, unground • Potatoes • Avocados TIME SAVER: VITAMIN TABLETS CAN BE CRUSHED IN A COFFEE GRINDER PRIOR TO ADDING TO RECIPE Blenderized Tube Feeding: Pediatric Outpatient Perspective 111 How it works…for the Dietitian • Nutrition assessment – Medical history – Nutritional history – Lab data – Growth parameters – Estimated needs – Medications – Bowel habits – Allergies Develop Parental Goals Feed real food Feel part of the family Less reflux and constipation Sit at the table Improve heath Improved tolerance (less gagging, retching, vomiting) Develop Nutritional Goals • Nutritional • Adequacy • Tolerance • Growth • Stable lab data • Less reflux and constipation • Improved volume tolerance • Reduction of gagging, retching and vomiting • Communication 112 • No right or wrong • Start slow and make changes based on tolerance. • Parent involvement is key. • Intolerance-return to the previous. Transition Plan Transition Plan Goal = 180 kcal/feeding Begin with 130 ml of current standard (1 kcal/ml) formula to 50 kcal BTF Feed # 1 Day 1 Day2 Day3 Day 4 Day 5 Day 6 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 110 ml & 70 kcal 130 ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130 ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130 ml & 50 kcal 130ml & 50 kcal 130ml & 50 kcal 130 ml & 50 kcal 130ml & 50 kcal Feed # 2 Feed # 3 Feed # 4 Feed # 5 Blenderized Tube Feeding (BTF) = 180 ml of current formula 50 calories 2oz brown rice ¾ c fresh apple 1 c most vegetables 2oz quinoa 1 c melon 2oz corn 1 c peaches ¾ c mixed vegetables 2oz bake potato ½ c applesauce ½ c corn or peas ~1/3cup hemp, oat milk 1oz fish, beef, pork, chicken 1 c almond milk 1 small cooked egg 1oz dry oats 2‐4oz coconut yogurt ½oz barley cereal 2oz almond yogurt 1 tsp walnut, flaxseed, sesame, etc. 113 Transition Plan 1 BTF, 4 CP ALL BTF 4 BTF, 1 CP 2 BTF, 3 CP 3 BTF, 2 CP Blenderized Tube Feeding (BTF) Commercial Product (CP) Food Allergies 114 Food Allergies Follow American Academy of Pediatrics (AAP) and American Academy of Asthma, Allergy and Immunology (AAAAI) Introduce 1 food at a time waiting 3-5 days to start a new food. Be sure to continuously check for nutritional adequacy. Begin transition as you would if child was eating orally. Hypoallergenic formula Fleischer DM, Spergel JM, Assa’ad AH, Pongracic JA. J Allergy Clin Immunol: In Practice 2013;1:29‐36 BTF and Food Allergies Fortified Soy milk: complete Fortified Rice milk: (low protein) Fortified Hemp, Oat, Almond (variable protein) Soy, Almond, Coconut Yogurt Meat Dairy Egg Other legumes Amaranth Arrowroot Barley Buckwheat Corn Oat Potato Quinoa Rice Rye Tapioca Recipe Analysis & Adjustments 115 KEYS TO SUCCESSFUL PREPARATION Be Organized Right Equipment Safe Food Practices Food Safety CLEAN: Wash hands and surfaces often SEPARATE: Don't cross-contaminate! COOK: Cook to proper temperature CHILL: Refrigerate promptly Partnership for Food Safety Education 2010 Communication and Follow Up is Essential RD Parent Medical Team 116 Initial Visit Assessment Develop Goals Plan & Transition Poor growth Constipation Volume limited Retching Growth Improve constipation All BTF Teaching Weekly Updates: phone & email Monthly Visits: Weight and re-assess Follow Up Visit Updates: 1 month follow up Visit: Plan: • Re-assess nutritional goals based on progress • Increase by 100 kcal every 2-3 days. • Reviewed excessive supplementation • Goal: 1800 kcal/day • Transitioned all feeds • 1.5 lb. weight gain over the month • Started on hypoallergenic MVI • Tolerated addition of blended food • Re-educated on food allergies • Every 6 week follow up till at goal kcal and catch up • Recipe analysis & adjustment at each visit How it works…for the family • Medical team • Insurance reimbursements • Supplies • Ingredient trials / transition • Recipe development • Prepare the blend • Time/Storage/Food Safety • Administration of feeds • Monitor & communicate 117 Bumps in the road… Inpatient admissions Insurance issues Reactions/Intolerance Emergencies Nutrient shortfalls Tube clogging/degradation Poor weight gain +/- growth Vacation and Travel Resources Supply List Support Groups Books & Websites Blogs Journals Food Safety Nutrient Analysis 118 BF ARE NOT a one size fits ALL Develop your own ideas & technique Every child and family is different Strategies for Success Develop your own resources & strategies Take it one step at a time Start with the basics 119 THANK YOU 120