April 17 – 18, 2015 TABLE OF CONTENTS · Thank you to our dedicated faculty, CME reviewers, and...

April 17 – 18, 2015

TABLE OF CONTENTS

Welcome Letter ......................................................................................................................2

CME Information ...................................................................................................................3

Attendee List ..........................................................................................................................5

Program ..................................................................................................................................7

Cases

Case 1: Short Bowel Syndrome Patient .................................................................................9 Case summary/ Key points/Slides

Case 2: Kwashiorkor Patient ..................................................................................................21 Case summary/ Key points/Slides

Case 3: Cystic Fibrosis Patient ..............................................................................................34 Case summary/ Key points/Slides

Case 4: Critically Ill Obese Patient ........................................................................................50 Case summary/Key points/Slides

Case 5: Growth Failure, Micronutrients, Biliary Atresia Patient ...........................................62 Case summary/Key points/Slides

Case 6: Nutrient Deficiencies Patient ....................................................................................69 Case summary/Slides

Lunch Presentations Nutrition and EoE ......................................................................................................83 Enteral Nutrition Therapy in IBD ..............................................................................95

Test Questions ........................................................................................................................103

Evaluation Form ....................................................................................................................105

Welcome to the NASPGHAN and NASPGHAN Foundation’s Nutrition Course. We again congratulate all of our attendees for being selected. We hope the information presented in the course will be incorporated into clinical practice and that our attendees and faculty will as serve as ambassadors to share this information and new knowledge.

Thank you to our dedicated faculty, CME reviewers, and Nutrition Committee who developed the vision and the content for this program. Faculty will share the latest scientific information about pediatric nutrition as well as a series of case based clinical scenarios that are associated with your practice and our specialty.

And special recognition to Nutricia North America which provided support for this educational activity and gave us the first opportunity to offer such a unique course to our members.

The nutrition arena is exploding with new data, needs, products and possibilities. Coupled with our clinical need to provide quality nutrition care and best practice nutrition standards to all pediatric patients both with and without chronic disease, our timing is right.

Thank you,

Praveen Goday MBBS, CNSC Chair, NASPGHAN Nutrition University

John Barnard, MD President, The NASPGHAN Foundation for Children’s Digestive Health & Nutrition

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CHAIR: Praveen S. Goday, MBBS, CNSC Professor Medical College of Wisconsin Milwaukee, WI

FACULTY:Karin Ballard, MS, RD, LDNSenior Clinical Dietitian at Ann & Robert H Lurie Children’s Hospital of ChicagoChicago, Ill

Valeria Cohran, MD, MSMedical Director of Intestinal Rehabilitation and Transplant Assistant Professor of Pediatrics at Northwestern University Feinberg School of Medicine Ann & Robert H. Lurie Children’s Hospital of Chicago Chicago, IL

James E. Heubi, MDDirector, Clinical Translational Research Center Co-Director, Center for Clinical and Translational Science and Training Associate Dean, Clinical and Translational Research Professor, University of Cincinnati Department of Pediatrics Cincinnati, OH

Catherine Karls MS, RD, CD, CNSC Clinical Dietician SpecialistChildren’s Hospital of Wisconsin Miwaukee, WI

Rebecca Pipkorn, RD, CD, CNSD Clinical Dietitian SpecialistChildren’s Hospital of Wisconsin Milwaukee, WI

Ann Scheimann, MD, MBA Associate Professor of Pediatrics Johns Hopkins School of Medicine Baltimore, MD

Sally (Ritz) Schwartz, RD, CSP, LDN Senior GI NutritionistAnn & Robert H. Lurie Children’s Hospital of Chicago Chicago, IL

Robert J. Shulman, MD Professor of Pediatrics Baylor College of Medicine Children’s Nutrition Research Center Texas Children’s Hospital Houston, TX

Justine Turner, MBBS, FRACP, PhD Associate Professor, Department of Pediatrics Division of Gastroenterology, University of Alberta Edmonton, AB, CA

CME REVIEWER: Dinesh S. Pashankar, MDPediatric Gastroenterologist Associate Professor of Pediatrics Fellowship Program Director, Pediatric IBD Program Yale University School of Medicine New Haven, CT

INTRODUCTION:Nutritional disease is common. Thus nutritional status is an important characteristic that needs to be considered and assessed in all patient populations, especially children, as research demonstrates long-standing effects of nutritional status on future health. This course seeks to provide an update on nutritional assessment techniques and effective nutritional interventions to help learners implement optimal strategies into their clinical practice.

TARGET AUDIENCE:This activity is designed for senior pediatric gastro-enterology fellows and all practicing pediatric gastroenterologists.

LEARNING OBJECTIVES:After participating in this course, learners should better be able to:

1. Discuss the critical elements of pediatric nutrition usingcase-based format.

2. Implement appropriate nutritional assessment methodsin pediatric patients.

3. Optimize management of pediatric patients who have

specialized nutrition needs/requirements.

CME inForMation

Jointly sponsored by NASPGHAN and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition.

This educational activity is supported by an independent medical education grant from Nutricia North America.

A P R I L 1 7 - 1 8 , 2 0 1 5 R O S E M O N T , I L

Ritu Walia, MBBS, MDAssistant Professor Department of Pediatrics Section Chief Department of Pediatric Gastreoneterology West Virginia UniversityCharleston, WV

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AMA PRA STATEMENT:NASPGHAN designates this live activity for a maximum of9.5 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

STATEMENT OF DISCLOSURE:All faculty/speakers, planners, abstract reviewers, moderators, authors, coauthors, and administrative staff participating in the continuing medical education programs sponsored by NASPGHAN are expected to disclose to the program audience any/all relevant financial relationships related to the content of their presentation(s). Accordingly, the NASPGHAN staff have reported no financial relationships with any commercial interests related to the content of this educational activity.

Dr. Heubi, Dr.Goday, Dr. Pashankar, Dr. Scheimann, Dr. Shulman Dr. Turner and Dr. Walia have nothing to disclose

Dietitians Ballard, Karls, Pipkorn and Schwartz have nothing to disclose.

Dr. Cohran reported that she serves on the speakers bureau for Abbott Laboratories and Nutricia North America. Dr. Heubi disclosed he had an equity interest in Asklepion Pharma.

Conflict with Dr. Cohran and Dr. Heubi was resolved by restricting the presenters to best available evidence and the ACCME content validation statement.

In accordance with ACCME Standards for Commercial Support of CME, NASPGHAN and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition implemented mechanisms to identify and resolve conflicts of interest for all individuals in a position to control content of this CME activity. To resolve identified conflicts of interest, the educational content was peer-reviewed by the Faculty Chair who has nothing to disclose. The resulting certified activity was found to provide educational content that is current, evidence-based, and commercially balanced.

DISCLOSURE OF UNLABELED OR INVESTIGATIONAL DRUGS:This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the US Food and Drug Administration. The opinions expressed in the educational activity are those of the faculty. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings. Further, attendees/participants should appraise the information presented critically and are encouraged to consult appropriate resources for any product or device mentioned in this program.

PROVIDER CONTACT INFORMATION: Jointly sponsored by NASPGHAN and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition.For questions, please contact: NASPGHANPO Box 6, Flourtown, PA 19031 Phone: (215) 233-0808Fax: (215) 233-3918

HOW TO RECEIVE CME CREDIT: To receive CME credit for participating in this activity, participants must review the CME information (learning objectives, disclosures, etc.), attend the live course, and complete the activity posttest with a 60% minimum passing score and evaluation questions.

Complete the activity post-test and evaluation onsite or return via fax to Amy Manela at #215-233-3918.

Certificates will be provided immediately after completion of the posttest and evaluation. For any questions ... please email Amy Manela: [email protected]

DISCLAIMER:The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of NASPGHAN, The NASPGHAN Foundation for Children’s Digestive Health and Nutrition, or Nutricia North America. This material is prepared based upon a review of multiple sources of information, but it is not exhaustive of the subject matter. Therefore, health care professionals and other individuals should review and consider other publications and materials on the subject matter before relying solely upon the information contained within this educational activity.

POLICY ON PRIVACY/CONFIDENTIALITY: NASPGHAN and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition will make every effort to protect the privacy of every individual participant of this activity and will use information gathered only to maintain records as required by the American Medical Association (AMA) and ACCME. This activity does not require readers to “register” to review the material, with the exception of physicians and other health care providers who desire to receive CME credit for this accredited activity. If an individual completes a CME for this accredited activity, we are required by the AMA and ACCME to collect personal information on the individual, such as their name, address, and phone number, that will allow us to issue a CME certificate to them and to keep this information on file for up to 6 years.

Personal information gathered will not be released to any other company or organization for any purpose. This information remains totally confidential.

© Copyright 2015 NASPGHAN and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition.

PHYSICIANS:This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) and The NASPGHAN Foundation for Children’s Digestive Health and Nutrition. NASPGHAN is accredited by the ACCME to provide continuing medical education for physicians.

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N2U 2015 Attendees

Majdi Abu-Salih Community Health-Pediatric Digestive Care Fishers, IN Jose Andrade Hospital Central San Luis Potosi Mexico Nirav Desai Boston Children's Hospital Boston, MA Lauren Fiechtner Boston Children's Hospital Boston, MA Amanda Fifi Jackson Memorial Hospital Miami, FL Mary Pat Francisco Holston Med Group Kingsport, TN Mary Abigail Garcia University of CA, San Diego San Diego, CA Ahmad Ghazi-Askar University of Oklahoma Health Sci Ctr Oklahoma City, OK Guillermina Gomez Instituto Mexicano del Seguro Social Zapopan Mexico Maria Greene Lurie Children's Hospital of Chicago Chicago, IL Jay Hochman Children's Healthcare of Atlanta Atlanta, GA

Tatyana Hofmekler Emory University Atlanta, GA Punit Jhaveri Penn State Hershey, PA Rima Jibaly Michigan Peds GI Center/Genesys Hospital Flint, MI Sunpreet Kaur Ann & Robert H Lurie Children's Hospital Chicago, IL Benny Kerzner Children's National Medical Center Washington, DC Sivan Kinberg Columbia University Medical Center New York, NY Anjuli Kumar University of CA Irvine Long Beach, CA Maureen Leonard Mass General Hospital for Children Boston, MA Richard Lirio UMASS Memorial Children's Worcester, MA Valerie Marchand Sainte-Justine UHC Montreal, PQ Randolph McConnie Rush University Med Ctr Chicago, IL

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Caroline Meyer Washington University St. Louis, MO Gihan Naguib University of Maryland Baltimore, MD Stephen Nanton Avera Children's Hospital Sioux Falls, SD Nikhil Pai McMaster Children's Hospital Hamilton, Ontario, Canada Jennifer Panganiban UTSW Dallas, TX Minesh Patel University of Oklahoma Health Sci Ctr Oklahoma City, OK Rabindranath Persad University of Alberta Edmonton, AB Uma Phatak Yale University New Haven, CT James Rick Children's Medical Center of Dayton Dayton, OH Edgardo Rivera Rivera University of Chicago Chicago, IL Miguel Saps Nationwide Children's Hospitalital Columbus, OH Robert Simek University Medical Ctr Lubbock, TX

Vibha Sood Georgetown University Hospital Washington, DC Shilpa Sood NY Medical College Valhalla, NY Dana Steien University of Michigan Ann Arbor, MI Sana Syed Emory University Atlanta, GA Sofia Verstraete Universityof CA, San Francisco San Francisco Danielle Wendel Children's Hospital of Philadelphia Philadelphia, PA

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April 17 – 18, 2015

2015 Faculty: Praveen Goday, MBBS, CNSC – Chair Karin Ballard, MS, RD, LDN Valeria Cohran, MD, MS James Heubi, MD Catherine Karls, MS, RD, CD, CNSC Rebecca Pipkorn, RD, CD, CNSD Ann Scheimann, MD, MBA Sally Schwartz, RD, CSP, LDN Robert Shulman, MD Justine Turner, MBBS, FRACP, PhD Dinesh Pashankar, MD (CME Content Reviewer) Ritu Walia, MBBS, MD (CME Content Reviewer) Course Objectives: The goal of the course is to provide specialized nutrition education in critical areas associated with the practice of gastroenterology and nutrition with the goal to improve the existing nutritional knowledge base of postdoctoral fellows and recent graduates of pediatric gastroenterology training programs to improve the quality of care delivered.

1. Discuss the critical elements of pediatric nutrition using case-based format. 2. Implement appropriate nutritional assessment methods in pediatric patients. 3. Optimize management of pediatric patients who have specialized nutrition

needs/requirements.

Agenda Friday, April 17, 2015 6:00 – 6:20 p.m. Registration and pre-conference assessment O’Hare Foyer 6:20 – 6:30 p.m. Opening Remarks/Dinner: Praveen Goday, MBBS, CNSC O’Hare BC

6:30 – 8:00 p.m. Panel discussion: burning topics and cases submitted by attendees 8:00 - 8:45 p.m. Nutrition Jeopardy: Host: Praveen Goday, MBBS, CNSC

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8:45-10:00 p.m. Reception Directors

Saturday, April 18, 2015 7:00-7:25 a.m. Continental Breakfast and Introductory Comments O’Hare Foyer

7:30-8:20 a.m. 2015 Case based discussions Group 1: Short Bowel Syndrome Patient JFK

Group 2: Kwashiorkor Patient O’Hare A Group 3: Critically Ill Obese Patient Dulles

Group 4: FTT and Feeding Disorders Patient Directors 8:25-9:20 a.m. Group 1: Cystic Fibrosis Patient JFK Group 2: Growth Failure in Liver Disease Patient O’Hare A Group 3: Kwashiorkor Patient Dulles

Group 4: Short Bowel Syndrome Patient Directors 9:25 – 9:40 a.m. Break and Check Out

9:45 -10:40 a.m. Group 1: Kwashiorkor Patient JFK Group 2: Critically Ill Obese Patient O’Hare A Group 3: Cystic Fibrosis Patient Dulles Group 4: Growth Failure in Liver Disease Patient Directors

10:45 -11:40 a.m. Group 1: Critically Ill Obese Patient JFK Group 2: FTT and Feeding Disorders Patient O’Hare A Group 3: Growth Failure in Liver Disease Patient Dulles Group 4: Kwashiorkor Patient Directors 11:45 – 12:45 Short topic discussion and Box Lunch O’Hare BC EN/IBD Patient and EoE/Nutrition Patient 12:50 – 1:45 p.m. Group 1: Growth Failure in Liver Disease Patient JFK Group 2: Short Bowel Syndrome Patient O’Hare A Group 3: FTT and Feeding Disorders Patient Dulles

Group 4: Cystic Fibrosis Patient Directors 1:50 - 2:45 p.m. Group 1: FTT and Feeding Disorders Patient JFK Group 2: Cystic Fibrosis Patient O’Hare A Group 3: Short Bowel Syndrome Patient Dulles Group 4: Critically Ill Obese Patient Directors 2:50 – 3:10 p.m. Report Back O’Hare BC

Reconvene to discuss the 6 cases presented by each assigned group 3:10 – 3:30 p.m. Post-test/Evaluation and Departures of Course Registrants O’Hare BC

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Case Summary - Short Bowel Syndrome Patient

Background of Case:

• 3 ½-year-old AAF who presents for a second option. She is a former 26-week infant who had NEC. She has approximately 45 cm of residual bowel anastomosed to the transverse colon.

• TPN-dependent • Minimal oral intake • Diarrhea up to 60 ml/kg with Enfacare

Pertinent Physical Findings and Initial Findings

• 10th percentile weight and length • Mild scleral icterus • Hepatomegaly, but liver edge soft • Spleen tip palpable 2 cm below LCM • Labs

o Hemoglobin 7.9 with MCV 65 o ALT 200, AST 157, T Bili 5/D, Bili 3.0, INR 1.6 o GGT 150 /Alk Phos 350 o Serum Na 132 o Urine Na < 10

Recent Diet History

• She takes very little by mouth, and the family is not currently using the G tube • Her bilirubin levels have risen over the last 3 months

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Key Points for Case - Short Bowel Syndrome Patient

1. Additional Lab Data/Studies Requested?

a. Additional lab data - I

i. Albumin 3.1 ii. PT 14.5 sec

iii. INR 1.6 iv. Alk P 450/GGT 160 /Tbili 5.0 v. Hgb 7.9/MCV 65

vi. Plt 175 vii. Serum Na 132

viii. Urine sodium < 10

b. Additional lab data - II

i. Prealbumin 23 ii. Zinc 18 low

iii. Copper 45 low iv. Fe 35 low v. TIBC 660 high

vi. Selenium 25 low vii. 25OH Vit D 26

Upper GI with small bowel follow through demonstrates a loop of dilated small bowel > 5 cm

2. Initial Nutrition Assessment

3. What is in the TPN? Intralipid content

Association with higher intralipid content and cholestasis

4. What is not in the TPN? Do you need extra supplementation?

i. Copper deficiency

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ii. Copper is a cofactor for ferroxidase, aiding in the incorporation of iron into hemoglobin

iii. Ceruloplasmin has a copper-dependent oxidase activity that oxidizes iron and allows ferric iron to bind to transferrin for transport

iv. Copper levels return to normal in 1–2 months with supplementation v. Copper deficiency may also see pancytopenia, neutropenia, and thrombocytopenia

vi. Selenium deficiency vii. None in pediatric trace elements; may need separate supplementation

viii. Part of glutathione peroxidase, which protects cell components from oxidative damage due to peroxides produced in cellular metabolism

ix. Zinc deficiency a. Present in pediatric trace; 90% excretion in stools, so need extra in TPN b. Cofactor for > 70 different enzymes; facilitates wound healing, helps

maintain normal growth rates, normal skin hydration, sense of taste and smell

x. Urine sodium is low. Need more sodium supplementation

5. What nutritional supplement can we use via the G tube?

i. Amino acid-based formula a. Increased MCT for better absorption, especially in the setting of liver

disease. Some patients have milk protein allergy, enteritis. b. Andorsky et al.: breast feeding and amino acid-based formulas associated

with decreased TPN dependence ii. Choice of type and route of delivery for nutrition support

iii. Vomiting and diarrhea - GJ tube and continuous feedings given the emesis iv. Joly et al. Gastro 2009: adult patients who had increased caloric intake using

gastrostomy tube feedings instead of mainly the oral route

6. What is the optimal design of nutritional support to meet the patient’s needs (macronutrients, micronutrients, prebiotics/probiotics)?

i. Prebiotics a. Neither hydrolyzed nor absorbed by the GI tract b. Fermented selectively by gut flora c. Stimulates growth and activity of bifidobacteria/lactobacilli d. Broken into SCFA and help with water reabsorption

ii. Pectin/Benefiber dietary fibers that converted to short chain fatty acids that improve water reabsorption

iii. Some centers have used stage 2 green beans iv. Avoid probiotics in patients with central line, because of the risk of translocation

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7. Once nutritional support is initiated, how should the patient be monitored/adjusted throughout delivery of the regimen?

i. High likelihood multiple micronutrient deficiencies ii. Ubesie et al J Peds 2013: Iron, Vitamin D, zinc deficiencies are common during

transition and with full enteral nutrition

8. Dilated loops of bowel can be seen in intestinal adaptation.

This may lead to small bowel bacterial overgrowth.

Perhaps a candidate for a STEP procedure in setting of poor enteral tolerance, bacteremia.

9. She was a premature infant. The mean intestinal length for a 24-26 week infants is 70 cm + 6.3 cm.

Sturjis et al JPS 2009

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© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T Y


• 3 year old former 26 week infant who had NEC

• 45 cm of residual bowel anastomosed to transversecolon

• TPN dependent

• Minimal Oral intake and vomiting with feedings

• Has G-tube but doesn’t use since 60 ml/kg daily onminimal feedings of milk based formula

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YAdapted from AGA teaching deck.

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Adapted from AGA teaching deck.

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YStruijs et al. J Pediatr Surg.2009;44:933-938..

Norms for Intestinal Length


• Physical findings

• 10th percentile

– Small but proportionate

– Hepatomegaly but liver edge soft

– Spleen tip palpable 2 cm below LCM

• Labs-

– ALT 200, AST 157 T Bilirubin 5.0 Direct Bilirubin 3.0

– INR 1.6

– GGT 150 Alkaline Phosphatase 350

– Urine electrolytes Na < 10

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•Underlying diagnosis and remaining SI

•Nutrition

–Formula

–TPN

•Fiber– Prebiotics

– Pectin/Benefiber


• TPN

– Fluid volume

– Intralipid

– Electrolyte content

– Trace Elements

– Vitamins

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T Y9Wessel et al. Semin Perinatol. 2007;31(2):104-11.

Sodium(mEq/L)

Potassium(mEq/L)

Chloride(mEq/L)

Bicarbonate(mEq/L)

Gastric 140 15 155 -

Ileostomy 80-140 15 115 40

Colostomy 50-80 10-30 40 20-25

Secretory 60-120

Diarrhea 30-40 10-80 10-110 30

Normal Stool 5 10 10 0

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• 1100

• Na 4 meq/kg

• K 2 meq/kg

• Acetate 1.5 meq/kg

• Intralipid 3 mg/kg

• MVI 5 ml


Table 10. Parental Multi-Trace Element Products Available in North America

Product (Distributor)Neonatal and Pediatrics

Contentper mL

Zinc, mg(μmol)

Copper, mg (μmol)

Chromium,mcg (μmol)

Manganese,mg (μmol)

Selenium,amcg (μmol)

Multitrace-4 Neonatal(American Regent) 1 mL 1.5

(22.94)0.1

(1.57)0.85

(0.02)0.025

(0.0005)0

(0)

Multitrace-4 Pediatric(American Regent) 1 mL 1

(15.3)0.1

(1.57)1

(0.02)0.025

(0.0005)0

(0)

Trace Elements Injection 4,USP—Pediatric(American Regent)

1 mL 0.5(7.65)

0.1(1.57)

1 (0.02)

0.03(0.0006)

0 (0)

Vanek et al.Nutr Clin Prac. 2012:4:440-491.

Parental Multi-Trace Element Products in North America


Nutrition in Clinical Practice 2012:4:440-491

Table 6. Current Daily Parenteral Recommendations for Infants and Children38

Trace Elements Infants ChildrenCopper 20 mcg/kg/d (no max stated)b 20 mcg/kg/d (500 mcg/d maxc,d)b

Chromium 0.2 mcg/kg/d (max 5 mcg/d)e 0.2 mcg/kg/d (max 5 mcg/dc)e

Floride No recommendations No recommendations

Iodine 1 mcg/df 1 mcg/df

Iron Premature: 200 mcg/kg/df

Infant: 50-100 mcg/kg/df50-100 mcg/kg/df

Manganese 1 mcg/kg/d (max 50 mcg/dc) 1 mcg/kg/d (max 50 mcg/dc)

Molybdemun Premature: 1 mag/kg/dInfant: 0.25 mcg/kg/d(max 5 mcg/dc)

0.25 mcg/kg/d (max 5 mcg/dc)

Selenium Premature: 2-3 mag/kg/dInfant: 1-3 mcg/kg/d(no max stated)

1-3 mcg/kg/d(100 mcg/d maxc,d)

Zinc Premature: 450-500 mcg/kg/dInfants <3 mo: 250 mcg/kg/dInfants <3 mo: 50 mcg/kg/d(max 5000 mcg/d)

50 mcg/kg/d (max 5000 mcg/dc)

Vanek et al.Nutr Clin Prac. 2012:4:440-491.

Current Daily Parenteral Recommendations

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• Enteral

– Has g-tube

– Choice of formula

– Route of feedings

– Fluid intake


• Supplemental g tube feedings

• TPN content

• Supplemental g tube feedings

• TPN content

• Laboratory data?• Laboratory data?


• Albumin 3.1

• PT 14.5 Sec

• INR 1.6

• Alk Phos350/ GGT 150

• Tbili 5.0/D Bili 3.0

• Hgb 7.9/MCV 65

• Plt 90

• Urine Na < 10

• Urine K > 150

• 25OH Vit D 26

• Prealbumin 23 (18-45 gm/dl)

• Zinc 18 (29-115 mcg/dl)

• Copper 45 (87-187 mcg/dl)

• Fe 35 (55-120 mcg/dL)

• TIBC 660 (230-430 mcg/dL)

• Selenium 25 (40-103 mcg/l)

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© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T Y16

42 patients treated vs 49 historical cohort

– Outcome serum D bili < 2 mg/dl

• Results:

Risk of death 9.5% vs 35% in fish oil vs. control patients

Fish oil cohort almost 9 times likely to reverse cholestasis as compared to control group

No side effects

– hypertriglyceridemia, coagulopathy, or essential fatty aciddeficiency

Effective in reducing cholestasis in patients receiving TPNAnnals of Surgery 2009:250:295-402


• 31 patients with short bowel syndrome

• Results:

Similar decline in bilirubin as in the Omegaven® studies

8/13 had mild essential fatty acid deficiency

– More of the low lipid group received bowel decontamination

Need randomized controlled trials

– What’s the minimum amount needed to prevent complications of essential fatty acid deficiency?

– What’s the effect on neurodevelopment?Cober et al J Pediatr 2012;160:421-7


Ubesie et al. J Pediatr. 2013;163:1692-1696.

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Ubesie et al. J Pediatr. 2013;163:1692-1696.


• TPN

– Electrolytes

– Vitamins

– Trace Elements

• Enteral Nutrition

– Type, route

• Prebiotics/Fiber

– Included with formula

– supplementsHurt et al. JPEN J Parenter Enteral Nutr. 2011 Sep;35(5 Suppl):60S-72S.


• TPN

– Electrolytes

– Vitamins

– Trace Elements

• Enteral Nutrition

– Type, route

• Prebiotics/Fiber

– Included with formula

– supplementsHurt et al. JPEN J Parenter Enteral Nutr. 2011 Sep;35(5 Suppl):60S-72S.

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• Short chain carbohydrates (oligosaccharides)

• Alter the balance of bacteria

– Increases in bifidobacteria and lactobacilli

• Serves as an energy source for colonic bacteria

– Short chain fatty acids: butyrate, propionate and acetate

• Increase epithelial cell proliferation

• Decrease epithelial cell apoptosis

• Excretion of pancreatic enzymes

Stoiodis et al. Nutrition Research Reviews. 2011:24:2130.


• Slows gastric emptying

• Enhances water and sodium re-absorption

– Pectin

– Benefiber®

• Butyrate

– Primary short chain fatty acid (SCFA)

– Energy source for colonocytes

– Regulates colonocyte proliferation

• Beneficial in the presence of a colon


Any Other Comments or Thoughts

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Case Summary – Kwashiorkor Patient

Background of Case (Pediatrics 2013;132:e229): • A 15-month-old female presented to the emergency department with a 3-month history of

progressive body swelling that was noted initially around the eyes and feet and then became generalized. Over the past few weeks she developed skin rashes.


• Irritability • Generalized swelling, more pronounced in the lower extremities • Reddish tint to hair • Scaly, hyperpigmented, desquamating rash on his thighs and arms • Erythematous desquamating rash over his perineum with lessor involvement of his legs

and trunk • Modest hepatomegaly

Labs

• Albumin 2.0 g/dL • Total protein 3.2 g/dL • Hgb 7.7 g/dL • Serum sodium 132 mEq/L • BUN and creatinine normal • Urinalysis normal • ALT 126 IU, AST 180 IU, alkaline phosphatase 25, total bilirubin 0.4 g/dL

Recent Diet History

• Intermittent spitting up and rash thought due to food allergy • Fed a diet of coconut and rice milks managed by pediatrician and chiropractor

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Key Points for Case - Kwashiorkor Patient

1. Additional lab data required

2. Nutritional support a. Route b. Composition

3. Feeding schedule

a. Determination b. Rationale

4. Prevention of refeeding syndrome

5. Use of antibiotics

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• 15-month-old female infant born at term (25th % forweight and height)

• Because of ‘intermittent spitting up and rash oncheeks’ thought to have food allergy so placed ondiet of coconut and rice milk

• Presented to the emergency department with 1-month history of progressive body swelling thatinitially began around the eyes and feet

• Over the past 3 months developed persistent skinrashes


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• Irritable infant with generalized swelling, morepronounced in the lower extremities

• Reddish tint to hair

• Scaly, hyperpigmented, desquamating rash on histhighs and arms

• Erythematous desquamating rash over hisperineum with lessor involvement of his legs andtrunk.

• Modest hepatomegaly

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T Yhttp://chaariahospital.blogspot.com/2010/08/kwashiorkor.html?vm=r


http://artistsforhope.blogspot.com/2010/03/kwashiorkor.html

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http://www.medscape.com/viewarticle/742325



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• From the Ga language spoken in a region ofGhana

• Describes the sickness a baby gets when thenew baby comes

• Child who gets displaced from breastfeedingas the result of a sibling being born

Williams CD. Lancet. 1935;226:1151–1152.

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© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YWilliams CD. Lancet. 1935;226:1151–1152.


• Protein deficiency

• Alterations in protein/energy ratio

• Protein quality – availability of indispensableamino acids

• Oxidative stress – perturbation of glutathionemetabolism

• Infection

Duggan MB. Paediatr Inter Child Health. 2012;32:190-203.


Tilg et al. Nature Rev. 2013;10:261-262.Smith et al. Science. 2013;339:548-554.

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© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YGarrett W. N Engl J Med. 2013; 368:1746-1747.

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YSmith et al. Science. 2013;339:548-554.


Hemoglobin 7.7 g/dL

Glucose 65 mg/dL

Albumin 2.0 g/dL

Total protein 3.2 g/dL

Serum sodium 132 mEq/L

ALT 126 IU/L

AST 180 IU/L

Total bilirubin 0.4 g/dL

Alkaline phosphatase 25 IU/L

BUN and creatinine normal

Urinalysis normal

28



• PT 16.3 sec

• Zinc 34 µg/dl (≥65 NL)

• Phosphorous 3.0 mg/dL

• Magnesium 1.5 mg/dL

• Free T4 0.7 ng/dL (≥0.76 NL)


• Enteral– Oral

– Nasogastric

– Nasoduodenal

– Nasojejunal

• Parenteral– Central

– Peripheral

29


• Protein– Whole

– Hydrolyzed

– Elemental

• Carbohydrate– Lactose

– Glucose polymers

• Fat– Long chain

– Combination long and medium chain



• PT 16.3 sec

• Zinc 34 µg/dl (≥65 NL)

• Phosphorous 3.0 mg/dL

• Magnesium 1.5 mg/dL

• Free T4 0.7 ng/dL (≥0.76 NL)

30

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YStanga et al. Eur J Clin Nutr. 2008;62:687-94.



Ashworth et al. Guidelines for the Inpatient Treatment of Severely Malnourished Children – WHO 2003.

31


• Days 1-7

– F75

– 100 mL•kg-1•d-1

• Days 7-onward

– F100

– 150-220 mL•kg-1•d-1

• Monitor heart and respiratory rate, weight gain

Contents per 100 mL F-75 F-100

Energy (kcal) 75 100Protein (g) 0.9 2.9Lactose (g) 1.3 4.2


• Additional potassium, magnesium, phosphorus

• Vitamin A (200,000 IU) once

• For ≥ 2 wk– Folic acid: 5 mg then 1 mg/d

– Zinc: 2 mg•kg-1•d-1

– Copper: 0.3 mg•kg-1•d-1

– Multivitamin

• Iron: 3 mg•kg-1•d-1 when gaining weight


32


• Addition of antibiotics (amoxicillin or cefdinirfor 7 d) to therapeutic regimens foruncomplicated severe acute malnutritionassociated with a significant improvement inrecovery and mortality rates.

Trehan et al. N Engl J Med. 2013;368:425-435.

33

Case Summary: Cystic Fibrosis Patient

Background of Case:

• KJ is a 10-year-old male with CF who has just transferred to your CF center due to parental job relocation. His parents state that he has had always had good lung function and his GI tract has always “been a problem.” He is on pancreatic enzyme replacement therapy (PERT). He has intermittent abdominal pain, does not like to eat, and gets full easily. He has a history of frequent “clean-outs” and did have an intestinal resection soon after birth. He does have increased gas and says that he has 2–3 stools/day. When asked what they look like, he says that he does not look before he flushes the toilet. He has worked with the RD at his previous CF center.

Pertinent Physical Findings and Initial findings

• BMI 10th percentile – Mild wasting – Abdominal distension – Mid-abdominal surgical scar – Increased BS

• Labs

– Glucose 128 – ALT 40, albumin 4 – Vitamin D 22,vitamin E 14, vitamin A 32, PIVKA II abnormal, zinc 60

Recent Diet History

• He usually has a bowl of cereal for breakfast and drinks a glass of orange juice. He eats lunch in school and buys whatever is on the menu and usually has a slice of pizza and fries. He has a small bag of chips or a couple of cookies when he comes home from school. Dinner is usually whatever the family has for dinner, but he does not finish his meal and eats less than his younger sister.

• He has tried Pediasure, Ensure, and calorie boosters (oil, butter, duocal, scandical) in the past, but will eat less food when he does so and so his mother stopped them

• Tube feeds have been suggested in the past, but his family does not want to try them

34

Key Points for Case - Cystic Fibrosis Patient

1. Additional Data/Studies Requested? i. Previous growth chart

ii. Surgical history iii. CBC iv. Essential fatty acid profile v. OGTT

vi. DXA

2. Nutrition Assessment i. Significance of nutritional assessment and BMI

ii. Monitoring frequency of nutritional status iii. PERT usage and vitamin supplements

3. Nutritional therapy: dietary interventions and timing of introduction of tube feeds

4. Choice of type of formula and PERT management

5. Monitoring/adjustment of nutritional plan

6. Significance of comorbid conditions

7. Impact of psychosocial factors

35


Case Presentation and Slides Provided by Maria Mascarenhas


• 10 year old male with CF & PI, good lung function with intermittent abdominal pain, decreased oral intake, gas & early satiety

• History of frequent “clean-outs” & intestinal resection soon after birth

• Stools: 2-3/day. When asked what they look like, he says that he does not look before he flushes the toilet

• Has worked with the RD at his previous CF center


Physical Findings

• BMI 10th percentile

– Mild wasting

– Abdominal distension, mid abdominal surgical scar, increased BS

• Labs

– Glucose 128, ALT normal, Albumin normal

– Vitamin D 22ng/L; Vitamin E 4.9 (5.5-9); Vitamin A: retinol 0.07 (0.2-0.5); PIVKA II 30.2 (<6.3); Zinc 60 (60-120)

36


• Breakfast: bowl of cereal & orange juice

• Lunch: slice of pizza and fries

• Snacks: small bag of chips or cookies

• Dinner: family meal; eats < than his younger sister, lots of 'battles' at meal times

• Tried oral supplements & calorie boosters, but ate less food and so they were stopped

• Refused tube feeds previously



• Previous growth chart

• Surgical history

• Pulmonary function

• CBC

• Essential fatty acid profile

• OGTT

• DXA

• Gastric emptying scan

37


• Poor appetite/Drugs/GI symptoms with eating• GERD/Malabsorption• Inflammation/infection/Energy expenditure

WEIGHT LOSS

LUNG DAMAGE

Increased work of breathing

Hyperinflation

Decreased ventilatory muscle mass

Loss of respiratory muscle strength


• Long term survival is linked to nutritional status

• Many studies looking at correlation of nutritional status & pulmonary function & survival

– early Boston vs Toronto experience

– wasting independent predictor of survival

– improved survival associated with changes in dietary management

– declining FEV1 is strongly associated with increased mortality

Zemel et al. J Pediatr. 2000; 137(3):374-380. Stallings et al. J Am Diet Assoc. 2008; 108(5):832-839. McPhail et al. J Pediatr. 2008; 153(6):752-757. Sharma et al. Thorax 2001; 56:746-750.


Cystic Fibrosis Foundation: Registry: Annual Data Report to the Center Directors. 2013; Bethesda, MD.

MalesFemales

Goal50th Percentile

<5 10 20 30 40 50 60 70 80 90

70

80

90

100

60

FEV 1

Perc

ent P

redi

cted

BMI PercentileFEV1 percent predicted is positively correlated with BMI percentile for

patients 6 to 20 years of age (p<0.0001).

FEV1 and BMI OutcomesThe data show that pulmonary function and nutritional status are highly correlated. Some centers are achieving the goals established in the CF Foundation Nutrition Guidelines.7

FEV1 Percent Predicted vs. BMI Percentile in Patients 6 to 20 YearsFigure 10

38


• International and US CF Foundation Nutritional Guidelines*

• Goals

– Normal growth and optimal nutritional status

– Ages 0-2 year: Weight for length >50th percentile

– Ages 2-20 year: BMI percentile at or above 50th percentile

– BMI for males:23

– BMI for females: 22*Borowitz et al. J Pediatr Gastroenterol Nutr. 2002; 35(3):246-259. *Stallings et at. J Am Diet Assoc.2008; 108(5):832-839. *Yankaskas. Chest. 2004;125(suppl):1S-39S.*Sinaasapppel et al. J Cyst Fibr. 2002;1(2):51-75. *www.cftrust.org.uk/aboutcf/publications/consensusdoc. *Stapleton.www.cysticfibrosis.org.au/books/nutritionbooks/PDF/CF.


Cystic Fibrosis Foundation: Registry: Annual Data Report to the Center Directors. 2013; Bethesda, MD.


• Different needs at different ages

• Greatest “at risk” period for malnutrition is the first 2 years of life, the first year after diagnosis and the peripubertal period into teenage year's

• Different needs to the general population focused on a low fat diet culture/education

• Start intervening when there is a deviation from CFF goals

• Consider other diagnoses and comorbidities

Ramsey et al. Am J Clin Nutr. 1992; 55(1) 108-116.Borowitz et al. Pediatr Gastroenterol Nutr. 2002; 35(3):246-259.Erskine et al. Nutr Clin Pract. 2007; 22(2):223-232.

39


• GI symptoms

• Growth history

• Diet history, vitamin supplements

• PERT use (lipase units/kg/meal, lipase units/kg/day)

• Anthropometry and growth chart

• Pubertal status

• Lab testing

• Determine energy, protein and micronutrient needs


• Nutritional assessment at every visit & review:

– Weight, length/height, weight for length, BMI, head circumference in infants

– Nutritional education & dietary counseling

– Review PERT

– Review need for micronutrient supplementation: fat soluble vitamins (A, D, E, K), Ca, Fe, Zn, Na (salt), essential fatty acids

• Nutritional education assess and update at every visit

Ramsey et al. Am J Clin Nutr. 1992; 55(1) 108-116.Borowitz et al. J Pediatr Gastroenterol Nutr .2002; 35(3):246-259.Erskine et al. Nutr Clin Pract. 2007; 22(2):223-232.Stapleton et al. J Am Diet Assoc. 2008;100:1497-1500.


• See Patients more frequently with RD: - Infants: every 2 - 4 weeks

- Children 2 years and older: every 4 - 6 weeks

• Include: medical, behavioral, & nutritional assessment, education, interventions

• Look: for active pulmonary disease, sinusitis, GER, CFRD, liver disease

• Evaluate: PERT and salt usage

• Aim: Achieve patient’s target weight for length or BMI percentile taking into account genetic height potential

Borowitz et al. J Pediatr Gastroenterol Nutr. 2002; 35(3):246-259.

40


• Behavioral evaluation: assess early, check for ineffective feeding behaviors & parenting strategies, look for eating disorders in adolescents, check for skipping enzymes

• Behavioral strategies: are effective

– Increase calories one meal at a time

– Teaching parents alternative ways to respond to children who eat slowly or negotiate what he/she eats

– Identify appropriate rewards for improved eating behavior

• If cannot increase oral intake: tube feedsOpipari-Arragan et al. Pediatr Pulm. 2010; 45:78-82.Stark et al. J Pediatr Gastroenterol Nutr.1996;22(3):240-253.Jetalian et al. J Pediatr .1998;132(3 pt1):486-492.Ramsey et al. Am J Clin Nutr.1992; 55(1)108-116.Borowitz et al. J Pediatr Gastroenterol Nutr . 2002;35(3):246-259.


• Work with oral diet first, high calorie food, fat 35-40%

• Child involved in choices

• Family involved in behavioral management interventions

• Ensure if adding supplements do not displace food intake**

• Tube Feeding if oral interventions fail

– No well designed randomized controlled trials

– Families often feel this means they have failed

**Smyth & Rayner Cochrane Database of Systematic Reviews. 2014, Issue 11.


• Breast milk for infants (often with fortification)

• Whole milk after one year

• Complimentary foods should be a good source of protein and fat (meat!)

• Polymeric formula well tolerated

• Semi-elemental can be considered if poor tolerance

• MCT can be supplemental, still requires enzymes andlimitations include diarrhea, less calories and not providing essential fatty acids

Colombo et al. Acta Paediatr. 2007; 96 (8):1228-1232.Erskine et al. J Pediatr. 1998; 132: 265-269.Borowitz et al. J Pediatr Gastroenterol Nutr. 2002;35(3):246-259.

41


• Infants 2000-4000 U lipase with 120ml breast milk or formula

– Mouth care for infants (and breast feeding mother)

• Children 500-2500 U lipase/kg per meal (≤10000 U/kg/day or ≤ 4000 U/g fat/day); half meal dose with snacks

• Ideally taken with meals and orally

• Microspheres preferred formulation

• Acid blockade (used to optimize enzyme activity)

• Gold standard to assess adequacy is 72h fecal fat collection

• Recognize the limitations of current PERTSchibli et al. Curr Opinion Pulm Med. 2002; 8:542-546. Borowitz et al J Pediatric. 1995; 127:681-684.Ng & Franchini .Cochrane Database of Systematic Reviews. 2014 Issue 7.


Vitamin ANight blindness, follicular hyperkeratosis, xerosis and xerophthalmia, anorexia, immunosuppression

Vitamin D Rickets, osteomalacia, hypocalcemia, hypophosphatemia, bone pain

Vitamin E Thrombosis, axonal neuropathy, tunnel vision, muscle weakness

Vitamin K Coagulopathy due to decreased clotting factors, decreased osteocalcin

Zinc Growth impairment, alopecia, diarrhea, skin rash, immunosuppression

Copper Hypochromic microcytic anemia, neutropenia, osteopenia

Sodium Growth impairment


Vitamin AHeadache, nausea, vomiting, anorexia, dermatitis, mouth sores, hepatomegaly, poor cognition/vision, increased risk hip fracture

Vitamin D Hypercalcemia and its symptoms, including nephrocalcinosis

Vitamin E(Rare) Liver damage, impair leucocyte function, diarrhea, can increase vitamin K requirements and lead to bleeding if taking po anticoagulants

Vitamin K (Rare) High doses may impair action of po anticoagulants

Zinc Epigastric abdominal pain, nausea, diarrhea, suppress immune function, cause hypochromic anemia due to interference with copper absorption

CopperEpigastric abdominal pain, nausea, diarrhea, renal failure, severe leg tingling / cramps, hepatic injury

Micronutrient ToxicitiesMicronutrient Toxicities

42


Vitamin A

(IU)

Vitamin E (IU)

Vitamin D (IU)

Vitamin K (IU)

0-12 mths 1500 40-50 400

0.3-0.5*1-3 yrs 5000 80-150

400-8004-8 yrs 5000-10000 100-200

> 8 yrs 10000 200-400

*Ideal doses not available in current products

*Borowitz et al. J Pediatr Gastroenterol Nutr. 2002; 35(3):246-259.


• Incidence osteopenia ~40%; osteoporosis ~10-20%

• Etiological factors:

– Vitamin D / calcium malabsorption / GI Ca+2 loss

– Liver disease

– Glucocorticoids

– Malnutrition (particularly lean body mass)

– Hypogonadism; failure to achieve peak bone mass

– Reduced exercise tolerance

– Inflammatory cytokines (severe pulmonary disease)

– Genetic factors; M>F


• Vitamin D target 75-150nM/L (30-60ng/L) or > 125nM/L (50ng/L)

• Deficiency common (60-90%)

• Current recommendations

– Screen 25-OHD annually

Supplement 400-800IU/day ergocalciferol (D2)

If refractory high dose supplementation to 100 000IU weekly

If refractory consider calcitriol (D3) / sunlight (natural or artificial)

• Can we achieve this recommendation?

*Tangpricha et al. J Clin Endocrinol Metab . 2012; 97:1082-109 *Sermet-Gaudelus et al. J Cyst Fibrosis. 2011;10(Suppl 2):S16-S23. Brodie et al. Arch Dis Child. 2012; 97:982-984.

43

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T Y*Boyle et al. Am J Respir Crit Care Med. 2005; 172(2):212-217.


• 7% adults with fractures; BMD higher in the fracture group

Mean BMD (g/cm2)

Fracture Group Non-Fracture Group

LS 1.266 1.112 (P<0.001)

FN 1.129 0.987

• BMD higher in Fracture group

• DEXA BMD may not predict fracture risk in CF

• Bone quality may be more important

Stephenson et al. Chest. 2006; 130(2):539-544.


• Meta analysis, young adults 18.5-32 years:

– Vertebral 14% (6-31%)

– Non-vertebral (most common rib): 20% (20-39%)

• Decline in bone mass on immune-suppression post lung transplantation may mean osteoporosis is a relative contraindication

– post lung transplantation (non CF) rate of fractures 37-42%

Paccou et al. Calcif Tissue Int. 2010; 86:1-7.

44



• Incidence of 5-15%

• Pancreatic insufficient; F > M

• Average age of onset 18-21 years (rare < 10 years)

• Pathophysiology

– Unknown

– Insulin deficiency

– Insulin resistance

During intercurrent infection, severe illness, glucocorticoid therapy, liver disease, pregnancy, nocturnal EN (malnutrition)

Wilson et al. Clin Nutr. 2000; 19(2):87-93.


• Worsens nutritional impairment

• Worsens pulmonary function

• Weight loss and pulmonary decline begin 2-4 years prior to diagnosis of CFRD

• Increases mortality 6 fold

• Microvascular complications do occur

• Insulin therapy reverses negative changes in weight and lung function

– Continuous pump infusions may be advantageous


45


• Fasting blood glucose levels

• Yearly random blood glucose

– Screen if random level ≥7mM

• OGTT most sensitive test to detect CFRD without fasting hyperglycemia

– Not routinely indicated

– Indicated for screening when potential symptoms


• 2h glucose >11mM during 75g OGTT

• Fasting glucose ≥7mM at least 2x

• Fasting glucose ≥7mM and random ≥11mM

• Random glucose ≥11mM at least 2x with symptoms

– Unexplained polyuria or polydipsia

– Growth failure despite nutritional intervention

– Unexplained chronic decline in pulmonary function


• Combines management of both CF and DM

• Attention to CHO counting and consistency in intake

• Do not restrict protein with mild-moderate nephropathy

• Regular blood glucose monitoring with home tube feeding 2-3h into feed, on two nights per week

• No evidence to alter formula choices in CFRD


46



• Improve nutrition and can improve lung function

– G tube: Wt 2%, FEV1

Controls: Wt 3%, FEV1 13%

– G tube: Wt , FEV1 Safe and well tolerated

Requisite for acceptance for transplantation

– G tube: FEV1 4%, correlated with LBM

Levy et al. J Pediatr. 1985; 107(2):225-230.Wililams et al. Gut. 1999; 44(1):87-90.Steinkamp & Von der Hardt J Pediatr. 1994; 124(2):244-249.


• Early decrease in lung function

• Survival post G tube insertion related to initial lung function and degree of malnutrition

Efrati et al. J Pediatr Gastroenterol Nutr. 2006; 42(2):244-249.Oliver et al. Pediatr Pulm. 2004; 37(4):324-329.

47

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YWalker & Gozal. J Pediatr Gastroenterol Nutr. 2006 1998; 27(1):53-56.


• GER impacts weight gain

– WAZ –0.32 symptomatic GER vs 0.03 asymptomatic year pre and post PEG

• Patient acceptability can be poor

– Concerns ‘embarrassing, look bad, hurt, limit sports’

– Lack knowledge concerning 61%

• What is the attitude of professional care givers?

Oliver et al. Pediatr Pulm. 2004; 37(4):324-329.Gunnell et al . J Pediatr Gastroenterol Nutr.v2006 2005; 40(3):334-338.


• Interventions tried

– Take PERT with meals rather than after meals

– Prescribed CF specific vitamins with additional vitamin K and D and Zinc supplements

– Monitoring blood sugars

• Initially had an improved appetite after getting prokinetic and zinc supplements, but then weight gain plateaued.

• A trial of oral supplements lasted 2 weeks and then he agreed to tube feeds with a standard intact 1 kcal/ml formula with sustained weight gain and linear growth

• Social work support was very helpful

48


• Nutrition plays an important role in the care of the patient with CF

• Growth assessment should be done at every visit. Goal is BMI > 50th percentile for children aged 2-20 years or weight for length > 50th percentile for children 0-2 years

• Annual monitoring should be part of management

• PERT should be reviewed at every visit (total daily dose) & when the patient is not growing optimally

• The CF center dietitian should evaluate the patient quarterly or more often if there is growth failure

49

Case Summary - Critically Ill Obese Patient

Background of Case:

• RC is a 14 ½-year-old AAF who admitted to the PICU with history of acute onset of progressive respiratory distress, fever, myalgias accompanied by chest pain, and worsening abdominal pain and lower extremity pain

– History of epigastric pain, vomiting for 3 months with 30 lb weight loss – Declining school performance –A C/D student


• BMI 50.9 – Lungs with diffuse crackles – Hepatomegaly,marked epigastric pain – Acanthosis nigricans

• Labs – ALT 595, amylase 843, lipase 3435 – Triglycerides 200, LDL 130, HDL 38, cholesterol 185, glucose 120, BUN 8,

creatinine 0.9 – Insulin 22.5

Recent Diet History

• Due to epigastric pain/vomiting over past 3 months has limited diet to french fries, Ritz crackers, small amount of tuna, juice, sweet tea, and rarely pancakes with eggs or meatloaf

– Diet recall: No breakfast except on weekends. At school, has water with french fries or Ritz crackers for lunch. At home, has chips, water with chicken or potatoes with water, and sweet tea or juice for dinner.

50

Key Points for Case - Critically Ill Obese Patient

1. Additional Lab Data/Studies Requested? a. Additional lab data - I

i. Albumin 3.3 ii. PT 14.5 sec

iii. INR 1.2 iv. Alk P 131/GGT 350/Tbili 1.0 v. Hgb 11.4/MCV 82

vi. Plt 140 b. Additional lab data - II

i. 25OH Vit D 11 ii. Prealbumin 10

iii. Zinc 60 iv. Vit B12 699 v. RBC folate 280 (260–800)

vi. Homocysteine 10.1 vii. Vit B1 67 (nl 87–280)

2. Initial Nutrition Assessment

a. Pitfalls of energy requirement determination i. Initial Nutritional Assessment

ii. Assessment of Energy Requirements 1. Equations for estimation of energy expenditure

a. Hamwi, Weir equation, Harris–Benedict, Penn State Harris Benedict, Ireton–Jones, American College of Physicians

2. Other techniques a. Indirect calorimetry

3. Timing for introduction of nutrition support? 4. Choice of type and route of delivery for nutrition support? 5. What is the optimal design of nutritional support to meet the patient’s needs

(macronutrients, micronutrients, prebiotics/probiotics)? 6. Once nutritional support is initiated, how should the patient be

monitored/adjusted throughout delivery of the regimen? 7. Any considerations in special populations?

51



• RC is a 14 year old African-American female admittedto the PICU with acute onset of progressiverespiratory distress, fever, myalgias accompanied bychest pain and worsening abdominal pain and lowerextremity pain

– History of epigastric pain, vomiting for 3 months with 30 lb weight loss

– Declining school performance –A C/D student



• BMI 50.9

– Lungs with diffuse crackles

– Hepatomegaly, marked epigastric pain

– Acanthosis nigricans

52


• Labs-

– ALT 595, Amylase 843, Lipase 3435

– Triglycerides 200, LDL 130, HDL 38, Cholesterol 185 Glucose 120, BUN 8, Creatinine 0.9

– Insulin 22.5


Is She Malnourished?Is She Malnourished?


• History

– Appropriateness of height for age

– Appropriateness of weight for age

– Unintentional changes in body weight

– Adequacy of dietary intake

– Presence of GI symptoms

– Functional capacity

– Level of metabolic stress

53


• Physical Exam

– Loss of subcutaneous fat

– Muscle wasting

– Edema


• Due to epigastric pain/vomiting over past 3 months haslimited diet to french fries, Ritz crackers, small amountof tuna, juice, sweet tea, and rarely pancakes witheggs or meatloaf

– Diet Recall: No breakfast except on weekends. At school has water with french fries or Ritz crackers for lunch. At home has chips, water with chicken or potatoes with water, sweet tea or juice for dinner


54


• Albumin 3.3

• PT 14.5 Sec

• INR 1.2

• Alk P 131/ GGT 350/Tbili 1.0

• Hgb 11.4/MCV 82

• Plt 140

• 25OH Vit D 11

• Prealbumin 10

• Zinc 60

• Vit B12 699

• RBC folate 280(260-800

• Homocysteine 10.1

• Vit B1 67 (nl 87-280)


• Assessment of Energy Requirements

– Equations for estimation of energy expenditure

• Schofield, WHO

• Hamwi, Weir equation, Harris-Benedict, Penn State Harris Benedict, Ireton-Jones, American College of Physicians

– Other techniques

• Indirect calorimetry

Port et al. Curr Opin Clin Nutr Metab Care. 2010;13:184-191.McClave et al. JPEN J Parenter Enteral Nutr . 2011: 35: 88s.


55


• Malnourished patient expected to be unable to eat > 5– 7 days

• Normally nourished patient expected to be unable toeat > 7 – 9 days


• Macronutrients

– Protein

– Fat

– Carbohydrates

• Micronutrients

– Electrolytes

– Vitamins

– Trace Elements

• Prebiotics/ProbioticsHurt et al. JPEN J Parenter Enteral Nutr . 2011;35: 60S.


56



• Burning feet

• Numbness and tingling starting in the feet and occasionally progressing to hands

• RadioculoneuropathyMimicking Guillan-Barre Syndrome

• RED FLAG: persistent emesis

• Diabetes: increase thiamin needs 5-fold


Visual abnormalities

OpthalmoplegiaNystagmus

PtosisDiplopia

AtaxiaPeripheral neuropathy

Altered mental status

DisorientationApathy

Memory loss

57


• Give B1 with intravenous (IV) dextrose if suspect

• B1 with B-complex, Mg for maximum absorption and neurologic function

• Early symptoms resolve with oral B1 until symptoms disappear

• 50-100 mg daily IV or intramuscularly for advanced neuropathy or protracted vomiting



58


Stomach Duodenum

Adapted from Shikora et al. Nutr Clin Pract.2007;22:29-40.

Jejunum Ileum

WaterCopperIodine

FlourideIntrinsic factor

ETOH

CalciumIronPO4

MgCopper

SeleniumThiamin

RiboflavinNiacinBiotinFolateADEK

Thiamin CaRiboflavin PO4

Niacin MgPantothenate FeBiotin ZnFolate Cr B6 MnADEKVitamin CPeptides

Vitamin CFolate

B12

DK

MgBile acids


Iron Microcytic anemia

Vitamin B12 Macrocytic anemia

Folate Macrocytic anemia

Copper Microcytic anemia and neutropenia; can cause pancytopenia

Pyridoxine Sideroblastic anemia


59


Thiamine

Peripheral neuropathy, ophthalmoplegia and nystagmus, ataxia, and encephalopathy, and may lead to permanent impairment of recent memory (Wernicke encephalopathy) The diagnostic criteria for Wernicke encephalopathy require 2 of the following 4features: (1) dietary deficiency, (2) oculomotor abnormality, (3) cerebellar dysfunction, and (4) confusion or mild memory impairment

Vitamin B12

Subacute combined degeneration, in which the peripheral nerves and posterior columns of the spinal cord are chiefly affectedNumerous neurologic symptoms and signs have been associated with vitamin B12 deficiency, including paresthesias, loss of cutaneous sensation, weakness, decreased reflexes, spasticity, ataxia, incontinence, loss of vision, dementia, psychoses, and altered mood.

Niacin hallucinations, and encephalopathy

Copper Can be indistinguishable from vitamin B12 deficiency

Pyridoxine Burning feet syndrome

Vitamin ESigns and symptoms of hyporeflexia that progress to ataxia, including limitations in upward gaze; profound muscle weakness and visual-field constriction; severe, prolonged vitamin E deficiency = complete blindness, cardiac arrhythmia, and dementia


• Numbness and tingling of extremities

• Macrocytic anemia

• Pernicious anemia (late stage)

• 1/2 of patients with symptoms of deficiency have normal B12 levels

• Methylmalonic acid more accurate for screening

Treatment: 700-2000 mcg weekly for several weeks


• Etiology of deficiency

– Inadequate intake

Stores deplete in a few months postoperation

– Noncompliance with supplements

– Malabsorption

– Medications

• Symptoms

– Early: fatigue, weakness,headaches, palpitations,diarrhea, and red painfultongue

– Chronic: smooth, shiny tongue

• Assessment

– Homocysteine with red blood cell folate most sensitive indicator of status

• Treatment– 1 mg daily folic acid

Charney et al. ADA Pocket Guide to Nutrition Assessment. 2004.Brolin et al. Int J Obese. 1991;15:661-7.

60


• Myelopathy

– Spastic ataxic gait with brisk lower extremity reflexes

• Sensory Ataxia

– Loss of vibratory perception in ankles

• Anemia

– Due to decreased activity of Cu dependent enzymes with impaired iron absorption and transport

– Ring sideroblast formation due to inadequate conversion of ferric to ferrous iron for incorporation into the protophyrin molecule

• Neutropenia

– Attributed to impaired maturation and increased destruction of myeloid precusors from marrow, and increased clearance from the circulation


• Peripheral neuropathy; loss of deep tendon reflexes

• Diminished perception of vibration and position

• Ptosis

• Opthalmoplegia

• Myopathy

• Dysarthria

• Treated with 400 IU vit E daily

61

Case Summary – Growth Failure, Micronutrients, and Biliary Atresia Patient

Background of Case:

• AK is a 5-month-old Hispanic male with biliary atresia s/p hepatoportoenterostomy at age 6 weeks who was seen in clinic with a 2 month history of poor nutritional intake.

– History of frequent loose stools, poor appetite, and recently vomiting medications

– Increasing abdominal girth


• Generally thin-appearing infant with decreased muscle mass and protuberant abdomen – Weight 5.9 kg (3rd percentile, –2 z score – Length 63 cm (25td percentile, –0.64 z score) – Weight/length (15th percentile, –1 z score) – Scleral icterus – Hepatosplenomegaly

• Labs

– Total bilirubin 7 mg/dL, direct bilirubin 5.5 mg/dL – ALT 240 U/L, GGT 1580 U/L – WBC 8,000, Hgb 10 gm%, platelets 80K –

Recent Diet History

• With increasing abdominal girth over the past month, formula intake has declined, along with baby food and now vomiting medications

– Diet recall: Drinks pregestimil but not finishing usual number of bottles; takes small amounts of jar baby food

– Takes fat-soluble vitamins 2 ml AquaADEK q day, vitamin K 2.5 mg q day

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Key Points for Case: Growth Failure , Micronutrients, and Biliary Atresia Patient

1. Additional Lab Data /Studies Requested? a. Additional lab data 1

i. Albumin 3.0 gm/dl ii. PT 14.5 Sec

iii. INR 1.2 iv. Hgb 10.5 /MCV 101 v. Plt 80,000

vi. Sodium 136, Bicarb 25, BUN 12

b. Additional lab data 2 i. 25OH Vit D 14 ng/ml

ii. Prealbumin 9 mg/dl iii. Vitamin A 25 mcg/dl iv. Vitamin A/RBP 0.9 v. Vitamin E 3 mcg/ml

vi. E/lipid ratio 0.6

2. Initial Nutrition Assessment a. Growth failure and outcomes

i. Predictors of liver transplantation or early death b. Fat-soluble vitamin supplementation

i. Challenges and monitoring

3. Timing for introduction of nutrition support?

4. Choice of type and route of delivery for nutrition support?

5. What is the optimal design of nutritional support to meet the patient’s needs (macronutrients, micronutrients, prebiotics/probiotics)?

6. Once nutritional support is initiated, how should the patient be monitored/adjusted throughout delivery of the regimen?

7. Any considerations in special populations?

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• AK is a 5 month old Hispanic male born at 38 weeks gestation weighing 3.6 kg (50th %ile). Presented withconjugated hyperbilirubinemia, diagnosed with biliary atresia at 6 weeks and had hepatoportoenterostomy. Now presents in clinic with history of poor enteral intake over the last month

– History of frequent loose stools, poor appetite, and recently vomiting medications

– Increased abdominal girth



• Generally thin appearing infant with decreased muscle mass and protuberant abdomen

– Weight 5.9 kg (<3rd percentile, -2 z score)

– Length 63 cm (<25 th percentile, - 0.64 z score)

– Weight/Length (15th percentile, -1 z score)

– Scleral icterus

– Hepatosplenomegaly

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• Labs-

– Total bilirubin 7 mg/dL, Direct bilirubin 5.5 mg/dL

– ALT 240 U/L, GGT 1580 U/L

– Albumin 3.0 gm/dl, Protime 14.5 sec, INR 1.2

– WBC 8,000, Hgb 10 gm%, platelets 80K


• With increasing abdominal girth over the past month, formula intake has declined along with baby food and now vomiting medications

– Diet Recall: Drinks pregestimil but not finishing usual number of bottles.

– Takes fat soluble vitamins 2 ml AquaADEKS q day, vitamin K 2.5 mg q day


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• Hgb 10.5 /MCV 100

• Plt 80

• Sodium 135, Bicarb 28, BUN 19


• Albumin 3.3 gm/dl

• PT 14.5 Sec

• INR 1.2

• Hgb 10.5 /MCV 101

• Plt 80,000

• Sodium 136 mEq/l, Bicarb 25mEq/l, BUN 12 mg/dl

• 25OH Vit D 14 ng/ml

• Prealbumin 9 mg/dl

• Vitamin A 25 mcg/dl

• Vitamin A/RBP 0.9

• Vitamin E 3 mcg/ml

• E/Lipid ratio 0.6

• Vitamin B12 910 ng/L

• Folate 5 mcg/L


• Growth failure and outcomes

– Predictors of liver transplantation or early death

• Fat soluble vitamin supplementation

– Challenges and monitoring

DeRusso et al. Hepatology. 2007;46:1632-1638. Shneider et al. Pediatrics .2012;130;607.

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• Oral

• Enteral

– NG

– NJ

• Parenteral

– Central


• Macronutrients

– Protein

– Fat

– Carbohydrates

• Micronutrients

– Electrolytes

– Vitamins

– Trace Elements

• Prebiotics/Probiotics

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Key Points for Case – Failure to Thrive and Feeding Disorders Patient

1. Birth weight, parental size and prematurity should be factored in before making a diagnosis of FTT.

2. Lab studies are not usually necessary in children under 2 years of age but are probably important in older children with poor weight gain.

3. Most Feeding Disorders in developmentally normal children should be initially tackled by using hunger manipulation.

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• 2 month old male

• Birth weight =4.5 kg

• Taking only 80 kcal/kg per day

• Weight gain = 8 gm /day

• What do you want to do?


• LGA babies typically show a downtrend in weightpercentiles over the first 3 months of life

• LGA babies who do not show catch-down growth havehigher incidence of metabolic syndrome later in life

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• 14 month old male

• Birth weight = 2.2 kg; born at term

• Weight and length below the 3rd percentile but tracking

• Weight-for-length is at the 25th percentile

• What do you want to do?


• Ensure adequate calorie intake

• Ensure no GI symptoms

• Ensure normal physical exam

• Follow growth for a few months


Taal et al. Obesity. 2013;21:1261-8.

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• Patient was born at 36.5 weeks of gestation and wasSGA.

• Birth weight was 3 lb. 14 oz. lbs. and birth length was17 in.

• Growth was a consistent problem throughoutpregnancy

• Dysmorphic; genetic workup - negative



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• At this point

– 27 kcal/oz. formula; intake varies

– High-calorie baby food

– No grazing or juice

– No GI symptoms

– Screening labs negative

• What are your options?


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© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YMei et al. Clin Pediatr . 2011;50:402-7.

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YMei et al. Clin Pediatr . 2011;50:402-7.


• Premies under 32 weeks gestation

– May never catch up if growth during first months of life was poor

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• Weight-for-length < 2nd percentile (WHO growth chart) or BMI < 3rd percentile (CDC growth chart)

• Poor or no weight gain – Over a period of time that varies according to the age of the child

• Significant downtrend in weight percentiles– 30% of full-term infants cross one percentile and 23% cross two

percentiles between birth and 2 years

• These should be done along with– Assessment of parental size / growth

– Correction for prematurity (where applicable)



• 11 year old male

• Poor weight gain for several years

• BMI below the 3rd percentile

• Not SGA

What two parameters about his parents are important to consider?

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• Genetic short stature

– Short parents

– Low percentiles but do not cross percentiles


• To the average of the parents’ heights

– Add 2.5” if male

– Subtract 2.5” if female

• This is the median height expected for that child

– 8.5 cm on either side of the median will give

2 SD on either side


Mom’s height = 5’5”

Dad’s height = 5’ 8”

Midparental height =

5’ 6.5” + 2.5” = 5’ 9”Median target height

-2 SD

+2 SD

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• Constitutional delay

– Initial drop in percentiles, then follow their own line

– Family history +

– Bone age assessment


• 11 year old male

• Poor weight gain for several years

• BMI below the 3rd percentile

• Not SGA; will not attain target height; no hx of constitutional delay

• Picky eater; anxiety

Labs?


• Most older children should probably get screening labseither at the 1st or 2nd visit

– CBC, ESR

– Metabolic panel, electrolytes

– Anti-TTG IgA, serum IgA level

– Fecal elastase (?)

– Urinalysis

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• Decrease or eliminate juice intake

• Regular meals and snacks

– Feeding every 3 hours

– Meals limited to 20 minutes

– No feeding outside mealtimes except for water

• High-calorie beverages

• Cyproheptadine


• When do you consider/not consider a gastrostomytube?

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• 19 month female

• Weight and height just below the 3rd percentile

• Primary calorie source - breast milk

– Wants to breast feed all the time

– Breast feeds whenever she wants both day and night

– Able to eat all textures but eats very small amounts

• What do you do?


• Offer 3 meals and 2-3 snacks each day. Offer these at 3 hourly intervals (8 am, 11 am, 2 pm, 5 pm and 8 pm)

• Mom can breast feed after 2 pm and 8 pm feeds• Meals and snacks at the table in a high chair……. Offer her small

amounts of milk in an open cup with meals• Nothing but water between meals and snacks• Limit mealtimes to 30 minutes• No juice• Half of a Complete Chewable Pediatric Multivitamin daily• Mom can continue breastfeeding at night for now. Will consider

stopping it in 2 weeks

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• In two weeks

– Improved variety and amount of food being taken

– Increase in weight

– Mom decides to stop breast feeding at night too

– Discharged from clinic


• Overweight 10 month old female

• Breastfeeding all the time

• Has taken very small amounts of solids in the pastmonth

• No coughing, choking, gagging, or emesis


• Stop breast-feeding at night• Breast-feed her 3 times during the day• Stop breast-feeding to pacify her and to put her tosleep

• Place her in a high chair– offer solid foods before each breast-feed at least 3

times a day

• At least 3 hours in between breast-feedings• Offer her water in between from a cup

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• No improvement over 2 weeks

• Child eventually had a gastrostomy tube placed

• Went to the feeding team

• Eventually diagnosed with autism

• Was able to consume enough PO to get rid of G-tube


• 2 year old male• Eats only what he likes

– fries, crackers, Slim Jim; baked Lays; Chips Ahoy– Drink yogurt smoothies; juice; Chocolate milk: peach tea

mixed with water

• Until 18 months he was eating several different table foods • He has gradually increased the degree of restriction in his

diet to the point that he only eats the above foods • Growth is good• What do you do?


• For the next 2 days:

• No milk or juice or peach tea or the food that he normally eats

• Can give as much water as he wants but no water for 30 minutes prior to a meal or snack

• Place him in a high chair every 3 hours and offer him things that he used to eat but no longer eats

• Try to do this all day until 8 pm

• If it works, use this technique to gradually expand his diet

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• If this approach works

– Keep using it

• If the approach does not work

– Optimize his nutrition using high-calorie milk

– Continue to offer food and beverages in the high chair and every 3 hourly

– Need behavioral psychologist/ Feeding Team

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• Quick review of eosinophilic esophagitis, from the physician perspective

• Consider a real case, from the physician mothers perspective!

• Review nutrition support, with RD input!


Hawari and Pasricha. N Engl J Med .2007; 357:1446-1447.

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Normal Esophagus

GERD

EE

EE High Power


• Esophageal symptoms (and more related to esophageal dysfunction...)

• Eosinophil infiltration of the esophagus on histopathology (15 eosinophils per hpf)

• Non-responsive to PPI (not that simple...)

Papadopoulos et al. JPGN J Pediatr Gastroenterol Nutr. 2014;58:107–118.Liacouras et al. J Allergy Clin Immunol. 2011.Moawad et al. Aliment Pharmacol Therapeut. 2014;39(2):229-230.Vazquez-Elizondo et al. Aliment Pharmacol Therapeut. 2013;39(2):229-230.

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• Infants

– vomiting (reflux/GERD), feeding disorder, failure to thrive, colic

• School-age and older children

– Vomiting, regurgitation, abdominal pain, picky eating habits

• Older children and adolescents

– Dysphagia / swallowing difficulties

– Food impaction


Noel et al. N Engl J Med. 2004; 351:940-941.Furuta et al. Gastroenterology. 2007; 133(4):1342-63.

• History of atopy was present in greater than half of patients

– Rhinoconjunctivitis (57%)

– Wheezing (37%)

– Possible food allergy (46%)

– Family history of atopic disease (74%)

– Peripheral eosinophilia (60%)

– High IgE (73%)


• Tom, 5 years old, mum (adult GI doc) worried because he is small and picky, ? celiac disease (attg normal, DQ2 DQ2)

– anaphylaxis cashews, pistachios, shell fish

• Endoscopy mild linear furrowing; Histology basal cell hyperplasia, intraepithelial eosinophils: 16/hpf distal, 24/hpf proximal

• Growth 10th percentile height, crossed 50th to 10th percentile for weight at 4yo

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Arias et al. Gastroenterology. 2014: 146(7): 1639–1648.

Evidence base:

• No head to head comparisons

• Systematic review: "Efficacy of Dietary Interventions for Inducing Histologic Remission in Patients With EosinophilicEsophagitis: A Systematic Review and Meta-analysis"



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Diagnosis with EGIDS

MD discusses diagnosis/treatments

RD reviews dietary treatments & assess nutritional status of patient

Family decides on treatment & contacts EoEteam with start date


Assess patient nutritional status/family readiness for dietary therapy

Elimination Diet Elemental Diet

Directed Elemental EmpiricElimination Supplementation Elimination

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• Medical/family history

• Clinical data

– Symptoms, laboratory evaluation, meds

• Nutritional status:

– anthropometric data- height, weight, head circumference (<2yr), trends


• Nutritional history:o usual intake/diet history/food preferenceso supplementationo feeding environment

• Feeding history:o vomiting, gagging, aversion/refusal, dysphagia/food impaction with eatingo learned feeding difficulty: self selecting foods or textures, reducing

volume/variety of foods, drinking fluids between bites

• Social history/socioeconomic status:o family eating patternso access to food/supplemental feeding programs (WIC, food stamps)o lifestyle/activitieso readiness of child/family for diet therapy


1. Remission stage:(both elimination & elemental diet) Food antigen exclusion

2. Reintroduction stage: (elimination diet):Sequentially reintroducing the excluded foods back in the diet one food at a time followed by EGD every 6-8 weeks(elemental diet):adding in new foods with subsequent EGDs every 3 months

3. Maintenance stage: (both elimination & elemental diet): Excluding only trigger food(s) that resulted in recurrence of inflammation during the food reintroduction phase

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Greenhawt et al. J Allergy Clin Immunol. 2013;1(6):602-607.

TABLE V. Comparison of food prick skin testing and atopy patch testing precision in patients with eosinophilic esophagitis

Approach Definition Pros Cons

Elemental Diet exclusively consisting of amino acid–based formula

• Hypoallergenic• Nutritionally comprehensive• Reduces symptoms and eosinophil

counts

• Taste (may require feeding tube)• Expense• Age appropriateness• Excludes all food• May have adverse impact on quality of

life

Empiric diet Diet that eliminates the major food allergens from the diet (typically milk, egg, wheat, soy, peanut/tree nut, and fish/shellfish, though variants exist)

• Allergy testing not required• Studied across all ages• Reduces symptoms and eosinophil

counts

• Some avoidance may be unnecessary• Only four foods may be necessary• Expense• May be nutritionally incomplete

Targeted diet Diet that eliminates foods on the basis of allergy skin testing (skin prick test and/oratopy patch test)

• Most specific therapy• Can preserve diet• Established sensitivity, specificity,

and NLR/PLR to assist with add-back

• Reduces symptoms and eosinophil counts

• Testing precision and technique is inconsistent across centers

• Milk testing precision very poor when negative

• Empiric milk elimination as an addition greatly improves response

• Some avoidance may be unnecessary(sensitization without clinical allergy)


• 100% free amino acid based formulas

– several infant & child formula (1-13yr) available

– unflavored, flavored, ready to feed, semisolid foods

– hydrolyzed formulas are NOT appropriate

• No 100% free amino acid formula for teens

– need to supplement with vitamin and mineral supplement to ensure 100% DRI’s for age

• Formula is used to provide 100% estimated nutrition needs

– many centers allow 1 low allergenicity food (apples/grapes for oral stimulation)


• Advantages:– significant response with short term therapy– complete source of nutrition for infants & children

• Disadvantages:– cost/availability– palatability– quality of life issues– potential for exacerbating feeding difficulties– nutrition support (naso-gastric/gastrostomy tubes)– arduous food reintroduction – additional vitamin/mineral supplementation

needed for teens

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• Rapid improvement = as soon as 4 weeks to clean egd

– may be on solely elemental therapy for longer based on nutrition/developmental/medical status

• Primary form of nutrition (providing >75% of nutritional needs)

– for minimum 9 months (varies per patient)

• Food reintroduction: varies center to center

– individualized, start with low allergenicity fruits/vegetables


• Advantages: – ability to offer foods– ease of transition vs. elemental diet– cost vs. elemental diet– quality of life

• Disadvantages:– high risk of nutritional deficiencies– poor adherence– unrecognized offending food remaining in diet– quality of life


• Initial diet ~ 6-8 weeks– foods eliminated are added back one at a time– monitoring symptoms, repeat endoscopies

• High risk of nutritional deficiencies with any elimination diet– assess for deficiencies– recommend elemental formula, multivitamins

• Education: Initial and ongoing:– label reading, appropriate substitutes, cross contamination– back to basics of healthy meals:

• 2-3 cups of fortified milk substitute ( <3yr as milk substitute)/elemental formula

• fortified whole grains• fruits/vegetables • lean proteins • healthy fats

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Diet pre-elimination Pre-elimination diet following SFED

SFED with appropriatesubstitutes

SFED + elemental formulas to supplement

cheerios 1cup2% milk 1/2 cupbanana 1orange juice 1 cup

peanut butter jelly sandwich (2tbsp pb)granola bar 1grapes 1 cuplemonade 8floz

pretzels 1oz, water

baked chicken 3oz w/rice (1/2c)green beans (1/2c)dinner roll 12% milk 1 cupstrawberries 1 cupvanilla ice cream ½ cup

chocolate chip cookies 2-32% milk 1 cup

cheerios 1 cup2% milk 1/2 cupbanana 1orange juice 1 cup

peanut butter jelly sandwichgranola bar (peanut butter)grapes 1 cuplemonade 8floz

pretzels, water

baked chicken w/ricegreen beansdinner roll 2% milk cupstrawberriesvanilla ice cream

chocolate chip cookies2% milk 1 cup

corn chex 1 cuprice milk 4 ozbanana 1 orange juice 1 cup(ca/vit D fortified)

ham sandwich (2oz ham)ener-g bread, mustard, lettuce,tomatoenjoy life bar 1grapes 1 cuplemonade 8 floz

potato chips/freeze-driedgreenbeans 1oz/ water

baked chicken w/ricegreen beansslice breadrice milk 1 cupstrawberrieshomemade banana ice cream

enjoy life foods cookies 2

corn chex 1 cuprice milk 4 ozbanana 1 elemental formula 1 cup30kcal/oz

ham sandwch (2 oz ham)ener-g bread, mustard, lettuce, tomatoenjoy life bar1 grapes 1 cuplemonade 8floz

potato chips/freeze-dried greenbeans 1oz, water

baked chicken w/ricegreen beansslice breadrice milk 1/2 cupstrawberrieshomemade banana ice cream

enjoy life foodscookies 2elemental formula 8floz

Calories: 2,326Protein: 88gmCalcium: 1,200mg

Calories: 1,061Protein: 29gmCalcium: 300mg

Calories: 1,980Protein: 65gmCalcium: 600mg

Calories: 2,284Protein: 76gmCalcium: 594-872mg


Food Nutrients Alternative food sources

Milk Protein, Calcium, Vitamin D, B12, A, Riboflavin, Phosphorus, Panthothenic Acid, Potassium

Meats, legumes, whole grains, nuts, fortified foods/beverages (i.e. enriched soy milk)

Soy Protein, Iron, Zinc, Magnesium, Thiamin, Riboflavin, Pyridoxine,Folate, Calcium, Phosphorus

Meats, allowed grains/ legumes, fortified foods/beverages

Wheat Iron, Thiamin, Riboflavin, Folate, Niacin, Fiber

Other enriched grains (i.e.oat,corn,rice, soy flour), fruits, vegetables, legumes

Egg Protein, Pantothenic Acid, Biotin, Choline, Selenium

Meats, legumes, whole grains,fish, seafood

Peanut/Tree Nut Vitamin E, Selenium, Zinc, Manganese, Magnesium, Folate, Vitamin B6, Phosphorus

Allowed legumes, whole grains, vegetable oils, fish, seafood

Fish/Shellfish Protein, Omega 3 fatty acids, Iron, Phosphorus, Zinc,Selenium, B12

Whole grains, milk, nuts, meats, oils, flax seed, soy

Mofidi. Pediatrics. 2003;111:1463-1651.


Mukkada, et al. Pediatrics. 2010:126:e672-676.Haas, Maune. Immuno Allergy Clin N. 2009: 65-75.

• Ongoing nutritional assessmentweights at visits/endoscopies, signs of feeding dysfunction

• Food Diaries- close follow up with RDpre/during diet assess adequate nutrition & diet adherence

• Realistic diet plan

– Elemental formulas for supplementation

– Vitamin/mineral supplementation

– Keep mealtime as normal as possible, structured meals times at consistent location

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Problem Potential Solution

Inadequate nutrition Elemental formulas, add extra kcals with allowed foods. Focus on balanced nutrition, structured meals. Supplementation with feeding tube.

Feeding dysfunction Keep mealtime as normal as possible: structured meals/snacks, avoid grazing. No force feeding.Consult feeding team for evaluation

Poor adherence Education : appropriate substitutions, label reading, cross-contamination.Resource identification, Parent Mentor Program, positive reinforcement.

Palatability of elemental formulas

Flavoring with allowed ingredients: blenderize fruits, flavor packets, crystal lite,coffee syrups. Serve chilled, use straw-based containers vs. open cups.

Cross- contamination Proper hand washing /cleaning surfaces & utensils.Prepare allowed foods first, then cover /wrapSeparate condiments (avoid double dipping)

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Problem Potential Solution

Unfamiliar foods Involve child w/ food prep, serve variety of safe foods, different preparations of familiar foods, structured meals, allergy free cookbooks, websites of speciality food companies, FARE

Dining Out Have a plan, call ahead, go off peak hours,talk with manager. bring own food if unable to meet needs

Traveling Bring own food staples, stay at hotels with kitchenette, research hotel,area restaurants regarding dietary restrictions

Holidays/special occasions Plan gatherings around non-meal times, have non- food related activities, “non-cake” cake

Other caregivers/school/relatives Provide written explanation of diet/diagnosis. Provide list of acceptable/unacceptable foods. Bring own snacks/meals


✓ appropriate substitutes for nutritional complete

diet-specialty food products/resource list

✓ label reading guidelines

✓ cross contamination

✓ samples of elemental formulas

✓ vitamin and mineral supplementation

✓ tips for eating out, social events, traveling

✓ troubleshooting


• Nutrition therapy has a role in EoE; nutrition support is critical regardless of treatment

• Therefore management of EoE requires collaboration with a dietitian

• Personal and family factors are critical in determining treatment choices

– understanding of the impact of treatment choices on QOL for pediatric patients is lacking

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1. Noel et al. N Eng J Med 2004;351:9401-1

2. Licouras,MD et al: Clin reviews in Allergy and Immunol 2011

3. Haas A,Maune,N: Immunol Allergy clin N Am 2009: 29:67-75

4. Mukkada, et al: Pediatrics 2010: 126:e672-676

5. Sampson HA. J Allergy Clin Immunol 2004:;113:805-810

6. Liacouras CA et al. J Allergy Clin Immunol 2011;128(1):3-20.e6. Epub 2011 Apr 7

7. Kagalwalla, et al; Clin Gastroenterol Hepatol 2006; 4:1097–1102

8. Amsden, K, Schwartz S, et al;. Effect of Four Food Elimination Diet on Clinical and Histological outcomes in EosinophilicEsophagitis. Poster session presented at FALK Symposium: Eosinophilic Esophagitis: A Novel Chronic Inflammatory Disease of the GI Tract ;2013 September 6-7; Graz,Austria

9. Kagalwalla et al: JPGN 2012; 55:711-716

10. Liacouras, et al; Clin Gastroenterol Hepatol 2005; 3:1198–1206.6

11. Spergel, et al; Ann Allergy Asthma Immunol 2005; 95:336–343

12. Mofidi,S. Pediatrics 2003;111:1463-1651

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• Complex, involving genetic and environmental factors

• Studies of identical twins estimate the maximumcontribution of genetic factors to be 10%-UC, 30-40%-CD, making environmental factors largest contributionto risk

• Diet and intestinal microbiota are the most likelyenvironmental factors to be modifiable


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•Growth Failure

•Delayed Puberty

•Osteopenia and Osteoporosis

•Anemia

•Micronutrient Deficiencies

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YMassironi et al.Clin Nutr. 2013; 904-910.


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Adapted from Lee et al. Gastroenterology. 2015;doi:10.1053/j.gastro.2015.01.007.

Microbes

Host Mucosal Immunity

DietMucin AMPsIgAEpithelial Barrier

Metabolites MAMPSDirect invasion

FavorableEENPlant-based SCFAsGlu, Arg, His Thr, TrpCalcium and Vit D n-3 PUFA

UnfavorableWhole foodRed meat and fat Ironn-6 PUFA


• Limited by:

– Inability to include placebo control

– Contamination of study groups

– Inclusion of patients receiving medical therapies

• Other challenges:

– Accuracy of dietary intake information

– Interactions between foods consumed

– Difference in food metabolism among individuals


• 4% of N American peds GI use regularly vs 62% ofEuropean practitioners

• Mucosal healing

– Seen regardless of type of formula

– Lack of mucosal healing seen with corticosteroids

• Positive effect on linear growth

• Improved body composition

Zachos et al, Cochrane Database Syst Rev 2007; CD000542. Critich et al. J Pediatr Gastroenterol Nutr. 2012;54: 298–305.

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• N= 222 pediatric Crohn’s patients enrolled at time ofdiagnosis

• PCDAI, CRP, fecal calprotectin at 8, 12, 52 weeks aftertreatment

• Primary Endpoint-12 steroid free remission

– defined by PCDAI and CRP < 0.5 mg/dl

• Mean age 12.9 + 3.2 years

Levin et al. Inflamm Bowel Dis. 2014;20:278-285.


• 5-ASA n=29 EEN n=42 Corticosteroids n=114

• Remission PCDAI and CRP < 0.05 mg/dl

• 73% were in clinical remission week 12

• EEN and Steroids were associated with normal CRPremission week 12

• EEN was superior in mild to moderate disease

• Normal CRP predicted 1 year sustained remission 86%vs 61% for elevated CRP

Levin et al. Inflamm Bowel Dis. 2014;20:278-285.


• RCT n= 50 pediatric Crohn’s with PCDAI > 20

• Primary outcome: PCDAI < 10

• Secondary outcomes: changes in ESR, CRP, albumin, platelets

• TEN vs PEN Remission – 42% vs 15%, p=0.035

• TEN– Greater reduction in PCDAI p=0.005

– Reduction in diarrhea p=0.02

Johnson et al. Gut 2006;55:356-361.

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• 47 patients on restricted diet x 6 weeks + PEN

– Diet eliminated: all gluten, dairy, animal fat, processed meats, emulsifiers, canned goods, packaged products

– 50% calories from a polymeric formula

• 70% of children achieved remission, 69% of adults

Sigall-Boneh et al. Inflamm Bowel Dis. 2014;20:1353-1360.

© 2 0 1 5 N A S P G H A N N U T R I T I O N U N I V E R S I T YSigall-Boneh et al. Inflamm Bowel Dis. 2014;20:1353-1360.


• Patients who continued supplemental NG feedings + general diet after EEN induced remission maintained remission longer

• Hospital for Sick Children• At 1 month 47 patients (72% remission CD)

• 28 children NG overnight with regular diet during day

• 19 patients who discontinued drip feedings

• 43% vs 60% relapse rate at 1 year

• PEN can be given as overnight NG feedings + normal day PO or short bursts of NG every few months

• Optimizes nutrition and growth

Wilschanski et al. Gut 1996;38543–548.

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• EEN

– effective induction therapy in newly diagnosed, active CD

– improved adverse-effect profile over corticosteroids

– promotes mucosal healing and has beneficial effect on linear growth

– 8-12 weeks to induce remission

– may be beneficial in children with stunting or pubertal delay

Critich et al. J Pediatr Gastroenterol Nutr. 2012;54: 298–305.



• Schofield equation (BMR) + activity factor

• EER x 1.1-1.2

• Protein: RDA (minimum)

• Fluid: At least 1x maintenance

– Generally requires water in addition to the prescribedvolume of formula

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•Polymeric formulas–Least expensive

–More palatable

–Over the counter

•Standard 1.0 or 1.5 calorie/mL formula

•Can use generic version as formula is oftenpurchased out of pocket


• Formula can be taken orally or by NG tube

• EEN used as monotherapy or with medications

• As EEN nears completion, there needs to be atransition plan

• Patients will relapse once back to a regular diet


• After 8-12 weeks of EEN, normal diet can be resumed

• No defined approach for food reintroduction

• Reasonable method

– Introduce a meal every 2-3 days

– Subsequently decrease formula volume

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• Practitioner buy-in and resources– Corticosteroids result in quicker remission– NG versus oral– Access to a Registered Dietitian

• Patient adherence– Placement of the tube– Palatable taste– Unable to eat foods

• Cost– Insurance vs out of pocket


• Enteral therapy offers an alternative to steroids inpatients with CD

• Has potential to improve growth and IBD symptoms

• Avoids the side effects of steroids

• Need further research

– Unclear of the mechanism

– Unclear of the best protocol

– No standard protocol for reintroduction of food

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April 17 – 18, 2015

Chicago, Illinois

POST TEST To receive your proof of attendance, please complete the following post-test in its entirety. Upon completion you will receive a document validating your attendance at the educational activity.

1. Stress-induced hyperglycemia during critical illness results from the following: a. Increased counter-regulatory hormone production (glucagon, glucocorticoids,

catecholamines) b. Inflammatory cytokine release c. Peripheral insulin resistance d. All of the above

2. Micronutrient Deficiencies commonly seen among obese patients include all of the

following except : a. Vitamin D b. Vitamin B1 c. Folate d. Vitamin A e. Copper

3. When prescribing PERT, the following are important points to remember:

a. Do not exceed a total daily dose of 10,000 lipase units/kg/day b. PERT should be given just before a meal c. PERT does not need to be given before snacks that are predominantly

carbohydrate containing d. Do not exceed a dose of 2500 lipase units/kg/meal e. All of the above

4. Which of the following tests should be done annually in patients with CF:

a. Fat soluble vitamin levels b. Vitamin C c. Vitamin B 12 d. Copper and ceruloplasmin e. Magnesium especially if they are on chronic PPI therapy

5. Which of these B vitamins has a toxicity syndrome that causes a sensory neuropathy? a. Riboflavin b. Niacin c. Cobalamin d. Folate e. Pyridoxine

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6. All of these deficiencies can be associated with a skin rash EXCEPT:

a. Zinc b. Essential fatty acids c. Copper d. Biotin e. Niacin

7. The most common iatrogenic complication in treating significant malnutrition can be

prevented by adequate supplementation with: a. Phosphorus b. Glucose c. Protein d. Zinc

8. Patients with Kwashiorkor have excess total body:

a. Potassium b. Sodium c. Magnesium d. Calcium

9. Which of the following is true with regard to failure to thrive (FTT)?

a. All children who are below the 3rd percentile for weight should be considered FTT

b. All children who cross two major percentiles for weight should be considered FTT

c. Birth weight should be a historical element that should be reviewed in every child with FTT

d. Children with FTT should have a minimal work up that includes a CBC, serum electrolytes, BUN, creatinine and a urinalysis

10. Biochemical evidence of fat soluble vitamin insufficiency in biliary atresia:

a. Is common for vitamins A and E b. Is inversely correlated with serum total bilirubin concentrations c. More common in infants with total bilirubin > 2mg/dL d. Is common for vitamins D and K e. All of the above

11. Sodium concentration of gastric output is approximately equal to:

a. 140 meq/L b. 75 meq/L c. 50 meq/L d. 25 meq/L

12. Copper deficiency has been associated with what hematologic abnormality: f. Anemia g. Neutropenia h. Thrombocytopenia i. Pancytopenia j. All of the above

104

April17‐18,2015Chicago,Illinois

Youmustcompletetheevaluationinitsentiretytoobtainyourstatementofcredit.

Toreceiveyourproofofattendance,pleasecompletethefollowingevaluation.Uponcompletionyouwillreceiveadocumentvalidatingyourattendanceattheeducationalactivity.

QualityofContentDelivered(1=Poorand10=Excellent)

InviteSpeakerBack?

Freefromcommercial

bias?CaseOne:ShortBowelSyndromePatientValeriaCohran,MD,MS

YesNo YesNo

CaseTwo:KwashiorkorPatientRobertShulman,MD

YesNo YesNo

CaseThree:CysticFibrosisPatientJustineTurner,MBBS,FRACP,PhD

YesNo YesNo

CaseFour:CriticallyIllObesePatientAnnScheimann,MD,MBA

YesNo YesNo

CaseFive:GrowthFailureinLiverDiseasePatientJamesHeubi,MD

YesNo YesNo

CaseSix:FTTandFeedingDisordersPraveenGoday,MBBS,CNSC

YesNo YesNo

LunchPanel:EN/IBDSpeaker:ValeriaCohran,MD,MS

YesNo YesNo

LunchPanel:EN/IBDSpeaker:RebeccaPipkorn,RD,CD,CNSD

YesNo YesNo

LunchPanel:EoE/NutritionSpeaker:SallySchwartz,RD,CSP,LDN

YesNo YesNo

LunchPanel:EoE/NutritionSpeaker:JustineTurner,MBBS,FRACP,PhD

YesNo YesNo

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Pleaseratethefollowingbycirclingyourresponse:1. Theprogramwasrelevanttomywork

StronglyAgree Agree Idon’tknow Disagree StronglyDisagree2. Contentmatchedstatedobjectives

StronglyAgree Agree Idon’tknow Disagree StronglyDisagree3. Usefulnessofhandouts/AV

Excellent VeryGood Good, Fair Poor4. Qualityoffacilities

Excellent VeryGood Good, Fair Poor5.Howwelldidtheeducationalsessionsgiveabalancedviewoftherapeuticoptions,includingtheuseofgenericnames?

Excellent VeryGood Good, Fair Poor6. Ifyouansweredanyoftheabovequestionswithascoreof‘Fair,’‘Poor,’‘Disagree’or‘StronglyDisagree’pleaseexplainindetail(e.g.sessiontitle,speakername,andsituation):Objective1:Discussthecriticalelementsofpediatricnutritionusingcase‐basedformat.7. BymeetingtheaboveobjectivemyprofessionalcompetencewillincreasebecauseIhaveacquirednew

strategiestouseinmypractice.

StronglyAgree Agree Idon’tknow Disagree StronglyDisagree8.BymeetingtheaboveobjectivemyprofessionalperformancewillimprovebecauseIshouldbeableto

implementthenewstrategies.

StronglyAgree Agree Idon’tknow Disagree StronglyDisagree9.Bymeetingtheaboveobjectivemypatientoutcomesshouldimproveduetotheimplementationofnewly‐

learnedstrategies.

StronglyAgree Agree Idon’tknow Disagree StronglyDisagreeObjective2:Implementappropriatenutritionalassessmentmethodsinpediatricpatients.10.BymeetingtheaboveobjectivemyprofessionalcompetencewillincreasebecauseIhaveacquirednew

strategiestouseinmypractice.



StronglyAgree Agree Idon’tknow Disagree StronglyDisagree12.Bymeetingtheaboveobjectivemypatientoutcomesshouldimproveduetotheimplementationof

newly‐learnedstrategies.

StronglyAgree Agree Idon’tknow Disagree StronglyDisagree

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Objective3:Optimizemanagementofpediatricpatientswhohavespecializednutritionneeds/requirements.13. BymeetingtheaboveobjectivemyprofessionalcompetencewillincreasebecauseIhaveacquired

newstrategiestouseinmypractice.



StronglyAgree Agree Idon’tknow Disagree StronglyDisagree15.Bymeetingtheaboveobjectivemypatientoutcomesshouldimproveduetotheimplementationof

newly‐learnedstrategies.

StronglyAgree Agree Idon’tknow Disagree StronglyDisagreePleaseanswerthefollowingbycirclingyourresponse:16. Doyoubelievethisactivitywasappropriateforthescopeofyourprofessionalpracticeoractivities?Yes No17.Wastheeducationalcontentscientificallysound?

Yes No18.Wasthemodeofeducationeffectiveforlearning?

Yes No19. Ifyouanswered“No”toanyoftheabovequestions,pleaseexplain:20. Didyouperceiveanyproduct/service/company/commercialbiasinanyeducationalsessionyouattendedormaterialsyoureceived?

Yes No21. Ifyouanswered“Yes”totheabovequestion,pleasedetailthesituationbelow(e.g.sessiontitle,speakername):22.Wereyousolicitedbysalespersonnelinaneducationalroomwhileyouattendedthiseducationalactivity?

Yes No23. Ifyouanswered“Yes”totheabovequestion,pleaseexplainindetail(e.g.who,when,where):24. Howmuchdidyoulearnasaresultofthiseducationprogram?

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25.Whatspecificallydidyoulearnduringthisactivitythatyouintendtointegrateintoyourpractice? 26.Whatquestionshaveariseninyourpracticeforwhichyouneedanswers/strategiesthatyoucan

implement?27.Whatpatient/clientproblemsorpatient/clientchallengesdoyoufeelyouarenotabletoaddressappropriatelyortoyoursatisfaction?28.Whatproblemsareyourpatients/clientscommunicatingtoyouthatneedattentionorfollow‐up? 29. Areyouinterestedinbasic,intermediateoradvancedleveltrainings?

Basic Intermediate Advanced30.Whatbarriersmightyouhavethatwouldinterferewithimplementationofnewinformationlearned

fromthistraining? 31. Howcanthistraining(theoverallmeeting)beimprovedtobetterimpactcompetence,performanceand/orpatient/clientoutcomes? Additionalcomments: Step2.PleaseenteryourpersonalinformationFirstName_________________________________LastName______________________________Degree________EmailAddress___________________________________________________________________________________________Address___________________________________________________________________________________________________City__________________________________________State_____________Zip_____________________________________AgreementBycompletingthisform,IattestthatIhaveattendedthesessionsindicatedabove.Pleasesign:______________________________________________________________________________________________________________Thepersonalinformationcollectedonthisevaluationisusedonlyforourrecordsandis

notdistributedtoanyindividualsorcompanies.

Weneedyourhelp!Pleaselookforashortfollow‐upsurveyin4‐6weeks.Yourfeedbackfromthesurveywillassistusinremainingcompliantbymeasuringtheimpactofthiseducationalactivityonyourcompetence,performanceand/orpatientoutcomes.Thismeasurementwillhelpinfutureplanning.

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