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Transcript
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