My education plan below is designed for training of pediatric residents over a three year period.
Part I: Conditions
This curriculum was designed based on the American Board of Pediatrics (ABP) 2012 Content Outline to teach pediatric residents… topics of pediatric gastroenterology and nutrition required to pass the ABP exam and practice the field of Pediatrics after their graduation. This task is accomplished through the lectures, seminars and concise sessions, primarily didactic in format, that could be during their rotations in a gastroenterology clinic, or on the wards.
(Noe J, Treat R, Goday P. American board of pediatrics–based pediatric gastroenterology curriculum. MedEdPORTAL Publications. 2015;11:10243.http://dx.doi.org/10.15766/mep_2374-8265.10243)
My suggestion to each resident before his/her elective is to copy and paste this Curriculum on your personal pediatric GI elective page (or a note book). During their elective month each topic has to be "covered"and marked as "done" or "completed". It is also strongly advised to keep your Q&A next to each topic, and keep all notes done during your GI rotation well organized.
1. Growth charts
2. Understand Anthropometric measurements 3. Understand what a Bone Age is and how to interpret results
Failure to Thrive (FTT)
Know observational clues of failure to thrive, like interaction with parents, neglect, etc.
Most common causes
Other causes: Improper formula preparation & poor feeding technique
Long term effects of FTT that occurs in infancy
Recognize problems with early solid food introduction in infancy
Changes that occur in absorption / digestion of different substrates as infant ages
Common nutritional deficiencies in adolescents, as well as how sports activity in adolescents affects nutritional needs Dietary risk factors for infants that can / will result in nutritional deficiency
Micronutrients Recognize the signs and symptoms of iron deficiency anemia
Be able to know major differences in infant formulas, including the use of low iron versus iron-supplemented formulas
Problems with hypo- and hyperphosphatemia of premature infants
Understand why adequate vitamin D, calcium and phosphorus are needed in children & adolescents
Know absorption, storage & metabolism of fat soluble vitamins, including that breast milk is deficient in vitamin D. Know absorption and metabolism of water soluble vitamins (B complex & C)
Know caloric requirements of infants, children and adolescents
Know caloric and protein requirements of pre-term and full term infants
Know fat quality difference in pre-term and full term infant formulas
Know difference between pre-term vs full term infant ability to digest fat, as well as absorb fat soluble vitamins
Protein differences between human and cow’s milk, including IgA and protective antibodies in human milk helping protect against ingested pathogens
Low vitamin K in human milk can lead to hemorrhagic disease of newborn
Which (common / major) drugs are contraindicated in breast feeding, including sedatives
Difference between human milk and formula
Which disorders of the breast interfere with breast feeding
Know which formulas contain and do not contain lactose, and how lactose intolerance differs from milk protein allergy
Goat milk fed infants and folate deficiency anemia
Understand milk protein allergy and when to use soy and casein hydrolysate formulas
How to increase calories in formulas, and the risks of doing so
When to introduce solid foods, and risks of doing so too early
Rickets can come from low Ca or PO4. Signs of rickets and how to manage
Clinical signs, lab & radiologic signs of low Vitamin K, Vitamin D
Folate deficiency occurs with malabsorption
Know nutritional complications of a vegan diet Know the signs, symptoms and causes of the following vitamin / mineral deficiencies:
Marasmus and Kwashiorkor Know signs & symptoms of refeeding syndrome
Tube Feeding / Enteral Nutrition vs Parental nutrition
Complications of tube feeding
Complications of parenteral nutrition
Advantages of enteral over parenteral nutrition, and when to choose each route
When to use bolus vs drip feeds
Nutritional issues with specific diseases Gastroenteritis and secondary lactose intolerance
Why to reefed early with acute gastroenteritis
Nutritional risks of Crohn’s
What deficiencies occur with renal disease and their importance
Nutritional aspects of cholestasis
Nutritional problems with cystic fibrosis Why nutrition is important in malignant disease
Understand caloric needs (e.g. higher or lower) in neurologically impaired children
Nutritional risk in burn patients
Risks of food elimination in food allergy conditions
Risks and indications of “protein shakes” and “sport shakes”, as well as nutritional complications of athletes
What nutrients vegetarians and vegans need
Diagnosis of Obesity
Risk factors of obesity
Complications of obesity, e.g. Type 2 DM, Metabolic syndrome, Dyslipidemia
Risk factors of “fad” weight loss techniques.
Acute Abdominal Pain
Pattern of referred visceral pain Differential diagnosis, by age, and evaluation of common causes of acute abdominal pain NSAID and GI injury / symptoms Laboratory and a physical exam presentation of appendicitis
Cholelithiasis Signs, symptoms, laboratory work up for acute pancreatitis Differential diagnosis of chronic or recurrent pancreatitis
Understand presence of malrotation and / or volvulus
Understand presence of intussusception
Sites of injury for blunt abdominal trauma
Management of post-op obstruction
Chronic Abdominal Pain
Differential Diagnosis of functional abdominal pain in a pre-teen Clinical signs, evaluation & management of functional abdominal pain Recognize and manage irritable bowel syndrome
Recognize and manage functional dyspepsia
Role of lactose intolerance in functional abdominal pain
Recognize signs of abdominal migraines
Formulate age based differential diagnosis of abdominal masses
Common differential diagnosis of vomiting
Significance of bilious emesis, including newborns and toddlers
Evaluation and management of projectile vomiting in infant
Evaluation of cyclic vomiting
Difference between rumination and regurgitation
Understand that physiologic reflux in infants is normal Signs and symptoms of esophageal trauma, including that alkali burns can have no mouth injury
Symptoms and treatment of foreign bodies, including those that require urgent intervention
Complications (including respiratory) and symptoms of GERD (poor growth, pain, anemia, dystonic movements)
How to evaluate & treat GERD
Know common causes of infectious diarrhea:
E. Coli ,Campylobacter, Salmonella, Shigella
C. difficile. Giardia.
Mechanism and treatment of lactose intolerance
Incidence of lactase and sucrose-isomaltase in different ethnic groups
Symptoms, testing and treatment of milk protein intolerance, including breast fed infants
Differential diagnosis and a work-up of non-infectious intractable diarrhea of infancy
Toddler’s diarrhea (a.k.a. chronic non-specific diarrhea of early childhood) diagnosis & prognosis
Know that malnutrition, chronic infection, systemic disease, & immunodeficiency can lead to chronic diarrhea
Why adequate enteral nutrition is important in protracted diarrhea
Signs of fecal overflow incontinence
Differential diagnosis of constipation in young child
Mechanism of action of laxatives, softeners, and lubricants
Evaluation & treatment of unconjugated hyperbilirubinemia, including high likelihood of breast milk jaundice. Increased RBC turnover and decreased intracellular metabolism & excretion in infants with jaundice
Know sepsis, galactosemia, metabolic and endocrine disorders presented with a mixed and conjugated hyperbilirubinemia
Signs, symptoms, testing and management of biliary atresia
Presentation of cholecystitis
Presentation of choledochal cyst
Presentation & Management of obstructive jaundice
Chronic hepatitis infectious, autoimmune
Alpha-one antitrypsin deficiency
Evaluation of hepatomegaly
Know physical exam changes of liver that occur with age
How to evaluate a patient with “upper GI bleed
Differential diagnosis of vomiting bright red blood (including varices) and coffee ground emesis
Etiology of occult blood vs bright red blood per rectum
Evaluation of melena
Know signs, symptoms and management of a Meckel’s diverticulum
How to evaluate suspected ulcer disease & its risk factors
Mechanism & Indications for H2 blockers vs PPI
Know H. pylori gastritis and how to diagnose it
Cystic fibrosis, pancreatitis, pancreatic insufficiency
Inflammatory bowel disease
Clinical manifestations of Crohn’s vs ulcerative colitis
Part II : Required reading
The residents are expected to be familiar with the subject being presented at the lecture (see the list of lecture topics below).
The subject of the lecture will be announced on this site a week in advance. All residents are expected to read on this subject before the lecture (see below), and a short (8-12) multiple choice quiz will be given before the lecture to assess baseline knowledge.
A resident on her/his required month long Pediatric GI/Nutrition rotation is expected to read and be well familiar with the whole set of updates on every subject in the field of Pediatric GI/ Nutrition. During this month each resident will be offered a 100 multiple choice question test, and all errors made by a resident will be discussed and analyzed with a pediatric GI attending during this rotation.
All residents are strongly encouraged to give their feedback, offer any subjects of their interest for discussions, etc. I will offer my personal e-mail address for communication: firstname.lastname@example.org
EoE: http://www.espghan.org/fileadmin/user_upload/guidelines_pdf/ Guidelines_2404/Management_Guidelines_of_Eosinophilic_Esophagitis.27.pdf
Food allergy: Current Opinion in Pediatrics, 201`2, 24950: 615-620.
GER and GERD: http://www.naspghan.org/files/documents/pdfs/position-papers/FINAL%20-%20JPGN%20GERD%20guideline.pdf
Current Opinion in Pediatrics 2013, 25(5): 597-603.
Liver function tests: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3915727/
Current Opinion in Pediatrics, 2015, 27: 625-633.
by Isabel Rojas, MD Norberto Rodriguez-Baez, MD
Serum aminotransferases are chemistry tests used to assess for a liver injury. These enzymes are found in several different tissues. Increased levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) can assist in the identification of the liver injury and direct additional evaluation. AST (aspartate aminotransferase) and ALT (alanine aminotransferase) are released from damaged hepatocytes, indicating liver injury.
AST is found in high concentrations in liver, heart muscle, skeletal muscle, kidney, brain, pancreas, lung, leukocytes and red blood cells.
ALT is more specific for liver disease, due to its presence in low concentrations in other tissues.
Elevation itself is not diagnostic of any disease, however, evaluated in conjunction with patient’s history and physical exam; it can suggest a particular diagnosis and direct the evaluation. Differential diagnosis of marked elevated aminotransferases (>1,000 U/L) include: viral hepatitis (A to E), toxic or drug-induced liver injury, ischemic hepatitis and, less commonly, autoimmune hepatitis, Wilson’s disease and acute obstruction of the biliary tract. A disproportionately isolated increase in AST suggests: hemolysis, acute rhabdomyolysis secondary to a viral illness, myopathy process, myocardial disease and recent vigorous physical activity. Although the value of the AST: ALT ratio is not well-documented in children, a ratio >4 in the appropriate clinical setting is highly suggestive of fulminant Wilson’s disease.
Increased aminotransferases may be the only manifestation of celiac disease. Nonalcoholic fatty liver disease may present with isolated increase in ALT. Differential diagnosis of elevated transaminases in a transplanted patient include: acute or chronic cellular rejection, de novo autoimmune hepatitis, infection, and biliary or vascular complications. There is poor correlation between degree of elevation of aminotransferases and extent of liver cell damage. A rapid decline in aminotransferases with increasing bilirubin and coagulopathy reflect massive liver damage and poor prognosis in a child with acute liver failure.
Chronic, mild elevation: ALT>AST (<150 U/L or <5X normal): 1. Hepatic origin: a. α1-antitrypsin deficiency b. Autoimmune hepatitis c. Chronic viral hepatitis (B, C and D) d. Hemochromatosis e. Medications and toxins f. Steatosis and steatohepatitis g. Wilson’s disease. 2.Nonhepatic origin: a. Celiac disease b. Hyperthyroidism
Severe, acute elevation: ALT>AST (>1,000 U/L or >20–25 X normal) Acute bile ducts obstruction; Acute Budd-Chiari syndrome; Acute viral hepatitis; Autoimmune hepatitis; Hepatic artery ligation; Ischemic hepatitis; Medications/toxins; Wilson’s diseases.
Severe, acute elevation: AST>ALT (>1,000 U/L or >20–25 X normal)1. : a. Alcohol-related liver injury. Cirrhosis; Acute rhabdomyolysis; Myopathy; Strenuous exercise.
Mild chronic elevation: (AST>ALT (<150 U/L, <5 X normal)
Alcohol-related injury; Cirrhosis; Hypothyroidism; Macro-AST; Myopathy.
Suchy FJ, Sokol RJ, Balistreri WF. Liver Disease in Children. 3rd ed. New York, NY: Cambridge University Press; 2007. Feldman M, Friedman LS, Brandt LJ. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Pennsylvania, PA: Saunders; 2010.
Celiac disease: JPGN, Volume 54, Number 1, January 2012; Current opinion in Pediatrics, 2014, 26(5): 585-589.
Hirschsprung disease: Current Opinion in Pediatrics, 2013, 25(3): 368-374.
Foreign bodies of the GI tract: http://www.naspghan.org/files/documents/pdfs/cme/jpgn/ Management_of_Ingested_Foreign_Bodies_in_Children_.28.pdf
Esophageal Caustic Injury: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096249/
Up to date online. Ferry GD. Caustic esophageal injury in children. Available at: http://www.uptodate.com/con
Upper GI hemorrhage:
Upper GI Bleeding Tiffany Patton, MD Ruba Azzam, MD
Upper gastrointestinal (UGI) bleeding refers to bleeding from a site proximal to the ligament of Treitz. Presentation of UGI bleeding includes hematemesis, coffee ground emesis, and melena. The cause of bleeding varies with age. Upper GI bleeding is the indication for 5% of all childhood upper endoscopies. The incidence increases to 6%–25% in critically ill children, with only 0.4% caused by life-threatening bleeds.
1. Hematemesis—vomiting of bright red blood (usually an indication of a large-volume or rapidly bleeding lesion)
2. Coffee-ground emesis—refers to the appearance of blood denatured by contact with gastric acid
3. Melena—black, tarry stools caused by bacterial oxidation of blood from anywhere in the GI tract proximal to the colon (may occur with as little as 50–100 mL of UGI bleeding)
The cause of UGI bleed varies with age:
1. Neonates—swallowed maternal blood, hemorrhagic disease of the newborn, stress gastritis, peptic ulcer disease, vascular anomaly, coagulopathy, and milk protein sensitivity
2. Infants—stress gastritis, peptic ulcer disease, Mallory-Weiss tear, vascular anomaly, gastrointestinal duplications, esophageal/gastric varices, foreign body, and hereditary telangiectasia
3. Child/Adolescent—Mallory-Weiss tear, esophagitis/gastritis, peptic ulcer disease, varices, caustic ingestion, vasculitis (HSP), Crohn disease, foreign body, tumor and telangiectasia
History and physical examination are critical to determining the etiology of UGI bleeding. Clinical signs may be associated with specific diseases:
1.Hyperactive bowel sounds, borborygmi (UGI bleed)
2. Petechiae, purpura (coagulopathy, thrombocytopenia)
3.Hemangiomas, telangiectasia (vascular anomalies)
4.Caput medusae, spider angioma, jaundice (chronic liver disease)
5. Epistaxis (nose bleed)
1. First assess vital signs, cardiovascular stability, and level of consciousness. Assess physical signs and symptoms of pallor, diaphoresis, restlessness, lethargy, and abdominal pain. Orthostatic changes (increase in pulse by 20 beats/min or decrease in systolic blood pressure >10 mmHg when moving from supine to sitting) can be more ominous signs of rapid blood loss 2. Laboratory evaluations required in any undiagnosed, clinically significant upper GI bleed: complete blood count with platelets and differential, reticulocyte count, coagulation panel (PT, PTT, INR), chemistry panel, liver function tests, blood type and crossmatch 3. Nasogastric tube placement and irrigation. Aspiration of bright red blood or coffee grounds confirms that the bleeding point is proximal to the pylorus
Should be chosen after consideration of the differential diagnostic list:
Plain films of the neck and chest may show the presence of foreign bodies or free air, suggesting a perforation
2. Upper GI contrast study can detect ulceration, radio-lucent foreign bodies, and duplication cysts
3. Abdominal ultrasound can assess portal blood flow when portal hypertension is suspected
4. Nuclear medicine (radiolabeled RBC scan) can detect actively bleeding sources with flow as low as 0.1 mL/min
5. Angiography can detect active bleeding at a rate of 0.5 mL/min or higher (therapeutic coiling/embolization of a bleeding vessel can be done simultaneously)
1. Is the currently preferred diagnostic and therapeutic modality, but is not required in hemodynamically stable patients without anemia
2. Identifies mucosal lesions and determines source of bleeding in ~90% of cases
3. Contraindicated if patient is unstable or has profound anemia
Fluid and blood resuscitation as needed to correct shock, fluid loss, and anemia
Correct any coagulopathy or metabolic/electrolyte abnormality. Endoscopic intervention (see Therapeutic Endoscopy)
Injection therapy (usually with 1:10,000 epinephrine in normal saline) can be injected into and near an oozing lesion
Contact thermal methods with heater probe; monopolar and bipolar probes provide hemostasis by local tamponade, coagulation, and blood vessel wall fusion
Endoscopic clip placement provides compression of bleeding vessel. Esophageal/gastric variceal management (see Therapeutic Endoscopy) a. Injection sclerotherapy
b. Band ligation
c. Sclerosing glue (N-butyl-2-cyanoacrylate) injected into varix solidifies on contact with blood, plugs the variceal lumen, and sloughs in 6 weeks to 6 months
d. Intraesophageal balloon tamponade (Sengstaken-Blakemore tube or Linton tube
1. Acid suppression with IV/PO proton pump inhibitors is helpful in acid peptic disease (most common cause of UGI bleeding in children)
2. Sulcralfate (40–80 mg/kg/day divided in 2–4 doses) binds directly to ulcer bases, facilitating healing in peptic ulcer disease
a. A synthetic octapeptide analogue octapeptide that reduces splanchnic and portal blood flow. May be used in variceal and non-variceal bleeds
b. Vasopressin causes peripheral vasoconstriction and may aggravate or produce renal failure
c. 1–2 mcg/kg IV bolus octreotide, followed by 1–4 mcg/kg/hour continuous infusion d. Dose of octreotide may be reduced by 50% over 12 hours when bleeding is controlled, and discontinued completely when reduced to 25% of original starting dose.
Part III: A core curriculum of lectures in Pediatric GI/Nutrition
1. Acute and chronic diarrhea
2. Gastrointestinal hemorrhage
3. Gastrointestinal manifestation of allergy: an allergic reaction to food and eosinophilic esophagitis.
4. GER and GERD
5. Acid-peptic disease (gastritis and PUD)
6. Celiac disease
7. Irritable Bowel Syndrome
8. Constipation, Hirschsprung’s disease, fecal incontinence
9. Intra-and extra-hepatic bile duct and gallbladder disorders
10. Liver functional tests and hepatitis
11. An acute and chronic pancreatic disorders
12. Chronic abdominal pain in children.
13. Foreign bodies and chemical ingestions.
14. Dietary analysis and a calorie counts in pediatric patients
15. Nutritional requirements in infancy, childhood, adolescence
16. Breast feeding
17. “Healthy choices”, modern concept of quality of food, definitions and discussion of such hot topics as …organic food, genetically modified food, “junk” food, nutritional supplements, etc.
18. Therapeutic diets (FODMAP, Paleo, Gluten-free, Fad, etc)
19. Dietary aspects of the therapy of Obesity