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Harvey Aiges, MD Joel Rosh, MD

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1 Harvey Aiges, MD Joel Rosh, MD
GI and Nutrition Harvey Aiges, MD Joel Rosh, MD

2 Compared to human milk, cow milk formula is more likely to contain which one of the following?
More essential fatty acids Higher protein concentration Increased lactose content Lower Calcium-phosphate ratio Lower iron concentration 5

3 Human Milk has: Low protein (very bio-available)
High lactose Low iron (very bio-available if taken alone) Low Calcium-Phosphate ratio Inadequate Vitamin K ? Adequate Vitamin D Immunoglobulins (including SIgA)

4 Riboflavin Protein Essential fatty acids Vitamin B12 Copper 5
A 4 mo old boy with “short gut” from extensive small bowel resection at 2 wks of life is receiving amino acids, hypertonic glucose and trace mineral by PN and is growing well. Last week drying and thickening of skin with desquamation began. The most likely cause of a deficiency is: Riboflavin Protein Essential fatty acids Vitamin B12 Copper 5

5 The most likely cause is a deficiency of: Riboflavin Protein
A 4 mo old boy with “short gut” from extensive small bowel resection at 2 wks of life is receiving amino acids, hypertonic glucose and trace mineral by PN and is growing well. Last week drying and thickening of skin with desquamation began. The most likely cause is a deficiency of: Riboflavin Protein Essential fatty acids Vitamin B12 Copper

6 Change feeds to soy-based formula Obtain stool cultures
A 4 wk old boy has diarrhea and intermittent vomiting for 2 wks. He is getting cow milk formula, 175 to 200 ml q3h (8 feeds/24 hrs). Birth wt = 3.2Kg. PE = afebrile, wt 5.0Kg (90th %ile). Abdomen is slightly protuberant. No tenderness and bowel sounds are hyperactive. Which is most appropriate at this time? Change feeds to soy-based formula Obtain stool cultures Determine stool pH Instruct parents to reduce volume of feeds Schedule rectal manometry 6

7 Improved school performance Flushing and sweating
A 7 yr old boy who has had school problems for the past 2 months received a megavitamin that supplies 50,000 u of Vitamin A, 100 mgs of thiamine, 100 mg of niacin, 1 g of ascorbic acid, 2000 u of Vit D, and 500 mg of Vit E . The most likely effect of this regimen will be: Improved school performance Flushing and sweating Increased thiamine level in CSF Increased intracranial pressure Less URIs than in his peers 4

8 Hypervitaminosis Vit A (>20,000 IU/d) – Inc ICP (pseudotumor), irritability, headaches, dry skin, Hepatosplenomegaly, cortical thickening of bones of hands and feet Vit D (>40,000IU/d)-Hypercalcemia, constipation, vomiting, nephrocalcinosis Vit E (100mg/kg/d) – NEC/hepatotoxicity - ?due to polysorbate 80 (solubilizer)

9 Folic acid Niacin Riboflavin Cobalamin Thiamine
An adolescent girl on a strict vegan diet is most likely to develop deficiency of which of the following water-soluble vitamins? Folic acid Niacin Riboflavin Cobalamin Thiamine 6

10 Vitamin Sources Thiamine – grains, cereals, legumes
Riboflavin – dairy, meat, poultry, leafy vegetables Pyridoxine – all foods Niacin – meats, poultry, fish, wheat Biotin – yeast, liver, kidneys, legumes, nuts Folic acid – leafy vegetables,fruits, grains B12 (Cobalamin) – eggs, dairy, meats (not in plants) Vit C – fresh fruits and vegetables

11 Vitamin Deficiencies (fat soluble)
A – night blindness, xerophthalmia, Bitot spots, keratomalacia D – rickets/osteomalacia, low Ca/Phosp E – neurologic deficit (ataxia, ocular palsy, decreased DTRs) K - coagulapathy

12 Vitamin Deficiencies(water-soluble)
Thiamine (B1) –beriberi, cardiac failure Riboflavin (B2) – seborrheic dermatitis, cheilosis, glossitis Pyridoxine (B6) – dermatitis, cheilosis, glossitis, peripheral neuritis, irritability Vit B12 – megaloblastic anemia, post spinal column changes

13 Vitamin Deficiencies(water-soluble)
Vit C – scurvy, poor wound healing, bleeds Folic acid – megaloblastic anemia, FTT Niacin – pellagra (diarrhea, dermatitis, dementia), glossitis, stomatitis Biotin – organic acidemia, alopecia, seizures

14 ALL Fanconi anemia Folate deficiency Iron deficiency
A previously healthy 15 mo appears pale. He has been fed goat milk exclusively since birth. Labs reveal: HgB=6.1, WBC=4800, plts=144K, MCV=109. Diff is 29%polys, 68%lymphs, 3%monos. Polys are hypersegmented. What is the most likely cause of these lab findings? ALL Fanconi anemia Folate deficiency Iron deficiency Vitamin B12 deficiency 6

15 An 8 mo old white infant is noted to have yellow skin
An 8 mo old white infant is noted to have yellow skin. The sclerae are normal in color. Of the following, which is the most useful diagnostic test? Measure serum bilirubin level Measure urine urobilinogen conc Measure serum Vitamin A level Evaluate dietary history Measure serum T4 level 6

16 Esophageal varices Esophagitis Gastric duplication Mallory-Weiss tear
A previously well 10 yr old has fever and persistent vomiting. Initially the emesis was clear, then bile-stained and now it contains bright red blood. Brother has AGE 1 wk ago. PE and CBC/SMA-7 are normal. The most likely cause of hematemesis is: Esophageal varices Esophagitis Gastric duplication Mallory-Weiss tear Peptic ulcer disease 6

17 Upper Presentation Hematemesis Coffee ground emesis Hematochezia
Rapid bleeding lesion Coffee ground emesis Slower bleed Hematochezia Melena

18 Upper GI Bleeding Esophagitis Gastritis Ulcer disease
H. pylori Mallory-Weiss Tear Caustic Ingestion/Foreign Body Esophageal varices Esophageal and gastric tumors Vascular anomalies Coagulapathy Epistaxis Tonsillitis/ENT Varices Duplication of gut IBD HSP Munchausen’s syndrome by proxy

19 Upper GI Bleeding (Infants)
Swallowed maternal blood Hemorrhagic disease of the newborn Coagulopathy Stress ulceration/gastritis Mallory-Weiss tear Allergy Esophagitis (GERD) Vascular anomaly Epistaxis Varices Duplication of gut Munchausen’s syndrome by proxy

20 Evaluation PE and VS Labs Stool guaiac Upper endoscopy with biopsy*
AXRay Tagged rbc study

21 Clostridium difficile toxin evaluation Stool for O & P
A 5 yr old girl was tx with amoxicillin for OM. One week later, she developed abd pain, and has been passing 6 stools daily that contain blood and mucus. PE has T of 101, abdominal distention and diffuse abd tenderness. Among the following, the most appropriate initial diagnostic study to perform is: Barium enema Colonoscopy Clostridium difficile toxin evaluation Stool for O & P Stool for rotavirus 6

22 Hemolytic-Uremic syndrome Henoch-Schonlein purpura Intussusception
For the past 6 wks, a 4 yr old has had painless, bright red rectal bleeding assoc with bowel movements. PE of abdomen and anus are normal. The rectal vault is empty and no blood is noted on gross inspection. The most likely cause of hematochezia is: Hemolytic-Uremic syndrome Henoch-Schonlein purpura Intussusception Juvenile Polyps Meckel’s diverticulum 6

23 Lower GI Bleed – 0 to 30 days Anorectal lesions
Swallowed maternal blood (APT test) Milk allergy NEC Midgut volvulus Hirschsprung’s disease

24 Remove milk and soy from the maternal diet GI referral for colonoscopy
A 4 week old is brought to you for streaks of bright red blood in the stool. Child is breast fed, thriving and content. Exam shows seborrhea, benign abdomen and perianal exam. Your next intervention: Remove milk and soy from the maternal diet GI referral for colonoscopy Call child welfare for possible abuse

25 Lower GI bleed – 30 days to 1 yr
Anorectal lesions Milk Allergy Intussusception Meckel’s diverticulum Infectious diarrhea Hirschsprung’s disease

26 Allergic Colitis Well appearing ± Irritable
Occurs with formula and breast milk Remove milk and soy from diet Protein hydrolysate Flex sig Reintroduce dairy at 1 year

27 Lower GI Bleed – 1-12 years COMMON: LESS COMMON: Anal fissure
Juvenile polyp Meckel’s diverticulum Infectious diarrhea IBD LESS COMMON: Henoch-Scholein purpura Hemolytic uremic syndrome Intestinal duplication Hemorrhoids

28 Meckel Diverticulum Painless rectal bleeding < 4 years of age
Failure of omphalomesenteric duct to obliterate 2% of population Within 2 feet of ileocecal valve Meckel scan technetium 99m pertechnetate scan

29 amt Color Stool Pain Think Small Red Hard Yes fissure Sm-mod loose Varies (abd) IBD,HUS, inf nl, coated No Polyp Mod Red-T nl Yes-abd HSP Intuss HD????? Large MD

30 “breast milk” jaundice Choledochal cyst Hypothyroidism
A 3,200 gm newborn is noted to be jaundiced on postnatal day #10. Total Bili is 9.0 with a direct Bili of 0.8 mg/dl. Hct is 48%. Baby and mom are blood type O, Rh+. Baby is breast fed exclusively. The most likely explanation of high Bili is: Biliary atresia “breast milk” jaundice Choledochal cyst Hypothyroidism Neonatal hepatitis 6

31 Unconjugated Hyperbilirubinemia
Physiologic – exaggerated by hemolysis or hematoma Breast feeding Breast Milk (late onset) Crigler-Najjar syndrome I & II Hypothyroid Intestinal obstruction

32 Fructose aldolase deficiency Fructose 1,6 diphosphatase deficiency
A 3 wk old girl has fever and vomiting. PE include bulging fontanelle and hepatomegaly. The pt had jaundice and vomiting during the 1st wk after birth. She has been breast-fed. What is the most likely Dx? Fructose aldolase deficiency Fructose 1,6 diphosphatase deficiency Glycogen Storage Disease type 1 Neonatal adrenoleukodystrophy Galactosemia 6

33 Direct Hyperbilirubinemia
Extrahepatic 1.*** Extrahepatic Biliary Atresia 2. ***Choledochal Cyst 3. Choledocholithiasis 4. Extrinsic bile duct compression

34 Direct Hyperbilirubinemia
Intrahepatic Metabolic Familial intrahepatic cholestasis Infectious Anatomic – Paucity of intrahepatic bile ducts Misc – TPN, Neonatal Lupus

35 EHBA Direct Hyperbili Acholic stool Elevated transaminases and GGT
DISIDA scan (99mTc-disofenin) Liver biopsy Kasai portoenterostomy <8 weeks

36 Alagille syndrome Hereditary condition Bile duct paucity
Mutations JAGGED-1 gene Bile duct paucity Peripheral pulmonary artery stenosis Vertebral anomalies Posterior embroyotoxin Characteristic facies

37 Chronic active hepatitis Dubin-Johnson syndrome Gilbert syndrome
A 12 yr old girl has recurrent bouts of scleral icterus, often after viral illnesses. She is otherwise well and is taking no meds. Labs reveal: Total Bili of 3.4 mg/dl with direct Bili of 0.3 mg/dl. ALT/PT/APPT are all normal. The most likely cause of hyperbilirubinemia is: Chronic active hepatitis Dubin-Johnson syndrome Gilbert syndrome Hepatitis A Infectious Mononucleosis 6

38 Hepatitis Most common infectious cause viral
Mild-Asymptomatic transaminase elevation Hep A, EBV, CMV Clinical Hepatitis Fulminant Hepatic Failure Rare in HepA, Hep B

39 Hepatitis A Transmission oral/fecal RNA virus Incubation 2-6 weeks
Milder in young children Does not cause chronic infection Some patients may experience a relapsing course Hepatitis A vaccine to all children at 1 year

40 Severe RUQ pain, intense jaundice and dark urine in a 9 yr old girl w chronic mild jaundice from spherocytosis. Which diagnostic test is most likely to give correct diagnosis of her current state: Determine AST/ALT levels Determine presence of Hepatitis B surface Ag Radionuclide scan of liver Ultrasound of abdomen PAPIDA scan 6

41 School (first grade) avoidance Constipation
A 6 year old boy is brought to your office with a history of 36 hours of increasing anorexia and periumbilical pain. Last night he had his first episode of nocturnal enuresis in 3 years. He is afebrile and has a benign abdominal exam. Your diagnosis: Acute appendicitis Strep Pharyngitis School (first grade) avoidance Constipation 6

42 Evaluation of Acute Abdominal Pain
History- Other sxs (Vomit, BM changes, Systemic) Physical Exam Skin, Lungs, Abdomen, Rectal exam (guaiac) Imaging Plain Films, Sonogram Lab CBC, lytes, Liver/albumin, Pancreas, Urine

43 Stool for guaiac CBC Urinalysis Abdominal sonogram
A 12 year girl comes to the office with 36 hours of abdominal pain, fever and anorexia. Pain is periumbilical and worse in the car than now. You think of appendicitis. Helpful lab tests could include all except Stool for guaiac CBC Urinalysis Abdominal sonogram 6

44 A 17 year old member of the track team comes in with epigastric discomfort and nausea. The big meet is tomorrow and he has been training hard for his last chance to win the medal in his event. He has no significant past medical history other than mild exercise induced asthma and uses an inhaler as he needs. He also uses ibuprofen for muscle pain when training. Your diagnosis:

45 Diagnosis Atypical asthma Performance anxiety Intestinal parasite
NSAID complication 6

46 GI referral for upper endoscopy Counseling for drug and alcohol abuse
An 18 year old who saw you to start birth control pills prior to going to college now comes in with recurrent, crampy post-prandial epigastric pain that sometimes travels below her right ribs. On exam you find that she has slight scleral icterus, vague epigastric tenderness and a belly button ring. Her urine pregnancy test is negative. Your next step: GI referral for upper endoscopy Counseling for drug and alcohol abuse Switch the form of birth control Order an abdominal sonogram 6

47 Further family and social history
A seven year old is seen for a bicycle accident. He is fine other than a few abrasions and an ecchymotic area on his abdomen where he hit the handlebars. 24 hours later, he has significant abdominal and back pain and recurrent non-bilious vomiting. You make the diagnosis with: Further family and social history Liver chemistries, amylase and lipase An upper GI series Stool for guaiac 6

48 Trauma Duodenal Hematoma Pancreatic pseudocyst Pancreatitis
Handlebar, seatbelts, abuse NGT relieves distention Pancreatic pseudocyst Pancreatitis

49 disimpaction dose of PEG (polyethelene glycol)
A 2 year old is brought to you for trouble stooling. Over the last 18 hours he has become “tired and miserable”. He now seems to vomit when straining to pass stool. On exam you notice that he appears lethargic and has a palpable mass in the mid-abdomen. Your next intervention is: disimpaction dose of PEG (polyethelene glycol) counseling on toilet training stat abdominal CT scan for appendicitis barium enema 6

50 Intussusception Most common cause of intestinal obstruction between 3 months – 6 years Sudden acute onset of severe, paroxysmal colicky pain that recurs at frequent intervals Well in between, can become weak and lethargic Current jelly stools 70-90% reduction

51 A 11 year girl comes to see you for recurrent periumbilical pain for the last 9 months. It is worse in the morning, especially on school days. There is no vomiting or weight loss but she does frequently have non-bloody diarrhea with resolution of the pain. Her exam is benign and stool is guaiac negative.

52 Your preferred working diagnosis:
school avoidance Crohn Disease irritable bowel syndrome ulcerative colitis 6

53 Her symptoms persist so you plan an evaluation that should include all of the following EXCEPT:
celiac serology lactose breath test abdominal CT scan stool for ova and parasites 6

54 Reasonable interventions for this patient would not include:
Cognitive behavioral therapy Dietary manipulation Trial of low dose Tri-cyclic antidepressants Empiric therapy for Helicobacter pylori Symptom-based therapy 6

55 RAP—Red Flag Symptoms Nocturnal awakening Persistent Vomiting
Dysphagia Bleeding Systemic Signs (Fever, Rash, Arthritis) Affected Growth/Development

56 Organic Causes of RAP Crohn’s Disease Celiac Disease Acid-Peptic/GERD
Carbohydrate malabsorption Infection (eg Giardia)

57 Symptom Based Diagnoses
Irritable Bowel Syndrome: Diarrhea Predominant Constipation Predominant Alternating Stool Pattern Nonulcer Dyspepsia Functional Abdominal Pain Abdominal Migraine Aerophagia

58 IBS Functional disorder Rome criteria
Abdominal discomfort or pain relieved with defecation an is associated with a change in frequency or consistency of stool No rectal bleeding Exclude other etiologies Infection, inflammatory, celiac

59 IBS--Treatment Education and reassurance
Proper nutrition/food avoidance Some studies up to 50% improve with fiber Counseling/Cognitive-Behavior Medications: Antispasmodic Anti-diarrheal Probiotics Tricyclic antidepressants Serotonin receptor agents

60 A metabolic evaluation Stat head CT scan
A concerned 22 year old first time mom brings in her 6 week old “vomiter”. After every feed her son “vomits the whole thing”. You note the child is slightly above birth weight and the mother states he seems to be urinating less. You make the diagnosis with: A metabolic evaluation Stat head CT scan Upper endoscopy by your local Pediatric GI Abdominal sonography 6

61 Pyloric Stenosis Projectile, non-bilious emesis
Most common cause of gastric outlet obstruction in neonates, M>F “olive” pyloric sonogram Hypochloremic metabolic alkalosis Surgery

62 Get samples of a low allergy formula Order a pyloric sonogram
Your previous patient is now 2 and accompanies his mother with his 6 week old brother who has “vomiting”. This has increased over the last 24 hours. The mother is tired, overwhelmed and complains of her increased dry cleaning expenses as she shows you her vomit stained white blouse that now has green and yellow stains. As your nurse provides her a sympathetic ear, you Get samples of a low allergy formula Order a pyloric sonogram Call the ED to alert them of a neonatal bowel obstruction patient Send in your junior partner “to deal with it” 6

63 Once in the emergency room, proper management of this infant would include:
Intravenous fluid resuscitation Stat pediatric surgical consultation Contrast imaging of the bowel Nasogastric decompression All of the above 6

64 Volvulus Abnormal fixation of bowel mesentery during fetal development
Most occur in utero or early infancy Sudden onset of abdominal pain and bilious emesis Ischemia and necrosis UGI series

65 Vulnerable child syndrome Celiac disease Milk protein allergy
The previous mother is grateful and sends her own 45 year old post-partum mother to see you with her Trisomy 21 infant who was just sent home from the hospital “vomiting”. The child is just at birth weight. You send her to the ED and a series of radiographs do not show an obstructive pattern. Rather, there are only two pockets of air in the epigastric region. You are again the star as you diagnose: Vulnerable child syndrome Celiac disease Milk protein allergy Duodenal atresia 6

66 Duodenal Atresia Double-bubble sign 1:4,500 newborns 2-5% Trisomy 21
Assoc with obstructive processes i.e. annular pancreas Also found in fetal alcohol syndrome

67 Differentiating GER and GERD
Gastroesophageal Reflux. Passage of gastric contents into the esophagus Regurgitation Passage of refluxed gastric contents into oral pharynx Vomiting Expulsion of refluxed gastric contents from mouth GERD Gastroesophageal Reflux Disease. Symptoms or complications that occur when gastric contents reflux into esophagus or oropharynx In order to understand the pathophysiology and epidemiology of gastroesophageal reflux disease, or GERD, some basic definitions are needed. The literature has numerous studies which define GERD in a number of ways; in many, what is being described may in fact be normal physiological reflux. This slide highlights how to differentiate gastroesophageal reflux (GER) from GERD. Gastroesophageal reflux is actually normal and it is physiologic--simple passage of gastric contents into the esophagus. Regurgitation, which is a normal physiologic action and can also be pathologic depending upon its frequency, is passage of reflux gastric contents into the oral pharynx. Vomiting, expulsion of reflux gastric contents from the mouth, can be a component of GERD or other diseases, and is also physiologic. GERD are the symptoms and/or complications that occur with gastric content reflux into the esophagus or into the oral pharynx. GERD is the pathophysiologic or pathologic state.

68 Prevalence of Regurgitation in Healthy Infants
100 n = 948 ≥ 1 time a day ≥ 4 times a day Infants (%) 50 Regurgitation is the most common manifestation of gastroesophageal reflux (GER) in childhood. A cross-sectional survey completed by 948 parents showed that the prevalence rate of regurgitation (at least 1 episode daily) was 50% in 0 to 3-month-old infants, reached a peak of 67% at 4 months, and dropped dramatically to 5% in 10- to 12-month-old infants. A similar pattern was reported for regurgitation of at least 4 episodes daily. Many subjects in this survey “outgrew” GER by 7 months and most by 1 year. At 1-year follow-up, infants with previously reported daily regurgitation no longer were symptomatic – not one of their parents described spitting up as a current problem. These findings support the concept that GER in most infants and children is a physiologic and self-limiting condition. 0-3 4-6 7-9 10-12 Age (months) Nelson et al. Arch Pediatr Adolesc Med. 1997;151:569

69 Pathophysiology of GERD
Delayed gastric emptying time Transient lower esophageal sphincter relaxation; decreased LES pressure Impaired esophageal clearance On the schematic in this slide, the pathophysiology of GERD is shown. There have been a number of well designed case-control studies which compared series of children with GERD to normal controls. Using a technique called esophageal manometry showed that transient lower esophageal sphincter relaxation was consistently more common in children with GERD. This was also associated with inhibition of lower esophageal body peristalsis. Other mechanisms contributing to GERD are overall decreased tone or pressure of the LES, as well as impaired esophageal clearance. These tend to occur more frequently in older children and adults than in infants. Orlando et al, eds. Textbook of Gastroenterology: JB Lippincott Co;1995:1214. Fennerty et al. Arch Intern Med. 1996;156:477. Kawahara et al. Gastroenterology 1997;113:399.

70 Presenting Symptoms and Signs of GERD
Infants Feeding refusal Recurrent vomiting Poor weight gain Irritability Sleep disturbance Apnea or Apparent Life-Threatening Event (ALTE) Older child/adolescent Recurrent vomiting Heartburn Dysphagia Asthma Recurrent pneumonia Upper airway symptoms (chronic cough, hoarse voice) The specific symptoms and signs of GERD in infants (on the left) are compared in this slide to older children and adolescents (on the right). First, whether the infant group or the older child group, GERD-related symptoms are different than you see in an adult. It’s not until they reach pre-adolescence and adolescence that you start to see the typical symptoms, such as heartburn or dysphasia. In the infant GERD symptoms such as feeding refusal, recurrent vomiting, poor weight gain are described. A syndrome called Sandifer’s syndrome can be seen in infants (i.e., arching or head tilting) and is more commonly described in children 18 months to three years of age. In this GERD-related syndrome, the child will turn their head to the side in order to increase LES pressure and lengthen the esophagus and decrease exposure of the esophagus to acids. In the older child and adolescent recurrent vomiting can occur, as well as asthma, recurrent pneumonia. These latter two symptoms are what are called extra- or supra-esophageal manifestations of GERD. Rudolph et al. J Pediatr Gastroenterol Nutr. 2001;32:S1.

71 Diagnosis of GERD Barium swallow/Upper gastrointestinal series (anatomy) Ambulatory single or dual-channel pH monitoring Impedance Endoscopy and biopsy Radionuclide scanning Supra-esophageal GERD is diagnosed in similar ways as esophageal GERD, and at present, there is not one gold standard for diagnosis. Comprehensive history and physical exam and initiation of empiric therapy are common practice and appear to be effective. Diagnostic tests like barium swallow, endoscopy and biopsy and ambulatory dual channel pH probe have all been used or considered and may be indicated based on the presenting symptoms of the patient, but none are the definitively accurate test.

72 Rudolph et al. J Pediatr Gastroenterol Nutr. 2001;32:S1.
Complications of GERD Erosive esophagitis Peptic stricture Barrett’s esophagus Adenocarcinoma What are some of the complications of GERD? Four of the most serious GERD-related complications are shown in this slide: erosive esophagitis, peptic stricture, Barrett’s esophagus and adenocarcinoma. Erosive esophagitis used to be an entity that was felt to be relatively rare in the pediatric population. However a recent study performed by the Pediatric Endoscopy Database System Clinical Outcomes Research Initiative Registry (PEDS-CORI) led by Mark Gilger at Texas Children’s, demonstrated a high percentage of children with erosive esophagitis who underwent diagnostic upper endoscopy. In a cohort of over 8,000 pediatric patients, erosive esophagitis was observed in 13%; a much higher prevalence rate than expected or previously believed. Peptic stricture, also occurs in childhood, and now Barrett’s esophagus and adenocarcinoma, which previously had been felt to be adult diseases, have been described in the pediatric population. Rudolph et al. J Pediatr Gastroenterol Nutr. 2001;32:S1.

73 Step-Up Therapy for GERD
FOR INFANTS Normalize feeding volume and frequency Consider thickened formula Positioning Consider trial of hypoallergenic formula FOR OLDER CHILDREN Avoid large meals Do not lie down immediately after eating Lose weight, if obese Avoid caffeine, chocolate, and spicy foods that provoke symptoms Eliminate exposure to cigarette smoke Step-up (i.e., start with the least invasive, most conservative approach first) or conservative therapy for GERD is shown in this slide. The left column depicts the approach for infant GERD; the right column the approach for older children with GERD. Shalaby et al. J. Ped. 2003;142:57.

74 Pharmacologic Management of Moderate-to-Severe GERD
Prokinetics Metoclopramide Many possible side effects which may include tardive dyskinesis (may be irreversible) Other agents include domperidone, bethanechol* and erythromycin H2RAs Available in tablet, elixir, or rapid dissolve form (must be dissolved in water, not on tongue) Pediatric safety, dosing data for ranitidine and famotidine PPIs Available in capsule, liquid suspension, or rapid dissolve form Pediatric safety, dosing data for lansoprazole and omeprazole There are three major classes of agents that are utilized to manage mild-to-moderate GERD; prokinetics, H2-receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). Both the H2RAs and the PPIs are available in liquid or suspension forms and are indicated for managing mild-to-moderate symptoms of GERD. There are pediatric safety dosing data available for ranitidine and famotidine, as well as for lansoprazole and omeprazole. Metoclopramide is a prokinetic that is utilized in a number of children, yet has shown efficacy in a moderate number. However, metoclopramide should be used with caution since it has many side effects and it crosses the blood-brain barrier. Bethanachol and domperidone (unavailable in the U.S.) are two additional prokinetics that have been used in children. Both have significant side effects and have only been shown to be marginally effective. With the removal of cisapride from the U.S. market, there is insufficient evidence that the other prokinetic agents are effective in the treatment of GERD in infants and children (Gibbons TE and Gold BD. The use of proton pump inhibitors in children: a comprehensive review. Paediatric Drugs, 2003; 5(1):25-40). Rudolph et al. J Pediatr Gastroenterol Nutr. 2001;32:S1. Gold. Paediatric Drugs 2002;4:673. Gibbons et al. Paediatric Drugs 2003;5:25. *Bethanechol not approved for pediatric GERD.

75 Ingestions Foreign bodies present with dysphagia and possibly poor handling of secretions Not all foreign bodies are seen on plain film—may need barium Endoscopic removal by 24 hours Alkali ingestions may burn esophagus and not the mouth

76 Diarrhea--Infectious
Viral—less than one week Rotavirus: most common cause of viral diarrheal disease in infants and toddlers Bacterial—sick, blood Salmonella, Shigella, Yersinia, Campylobacter, E Coli Parasitic—persistent **C. Difficile: After antibiotics/hospitalization Check for toxin A and B Colonization not pathogen in neonates

77 Diarrhea Leading cause of morbidity and mortality in developing countries Daycare centers important reservior In US 35-40 million episodes annually in kids <5 yrs 170,00 hospitalizations 300 deaths

78 Food Borne Fecal-oral Salmonella and Campylobacter
Poultry, unpasteurized milk Yersinia enterocolitica Pork Norwalk virus Raw seafood Water Giardia lamblia, Campylobacter, Cryptosporidium, Norwalk virus

79 E. Coli 0157:H7: associated Hemolytic Uremic Syndrome
Often presents with colitis (bloody diarrhea) Hemolysis, uremia develop Poly-- then oligouric renal failure Thrombocytopenia Severity varies Risk factors Uncooked meat, unpasteurized milk **associated with anti-diarrheal and antibiotic use***

80 Malabsorption Defect in intraluminal digestion Damage to intestine
Cholestasis Pancreatic insufficiency Damage to intestine Infection Viral, giardia Allergic enteropathy Celiac disease Short Bowel

81 Malabsorption Evaluation
Carbohydrate Check stool pH Check stool reducing substances Fat Qualitative vs. Quantitative (72 hour) measures Think CF—treated with enzyme replacement Protein

82 Dietary Diarrhea Clinically: Contributors: Well No blood, fever, etc.
Sorbitol, fruit juice, excessive fluids Lactose intolerance

83 Toddler’s Diarrhea Clinically well Stool Low fat
Good wt gain and growth Stool Frequent, undigested food Low fat - most commonly due to milk restriction High osmolarity fluids - juice, gatorade, powerade, ice tea, etc.

84 Lactose Intolerance Primary vs Secondary Management Diagnosis:
Primary rare < 5 years Management Restriction v. supplement If restriction supplement calcium Diagnosis: Clinical Breath test Disaccharidase levels in tissue ??genetics

85 Celiac Disease Autoimmune Triggered by gluten
Associated with hi risk populations Type 1 DM Down syndrome Chronic lymphocytic thyroiditis (Hashimoto) IgA deficiency Family history

86 Gastrointestinal Manifestations (“Classic”)
Most common age of presentation: 6-24 months Chronic or recurrent diarrhea Abdominal distension Anorexia Failure to thrive or weight loss Rarely: Celiac crisis Abdominal pain Vomiting Constipation Irritability

87 Non-Gastrointestinal Manifestations
Most common age of presentation: older child to adult Dermatitis Herpetiformis Dental enamel hypoplasia of permanent teeth Osteopenia/Osteoporosis Short Stature Delayed Puberty Iron-deficient anemia resistant to oral Fe Hepatitis Arthritis Epilepsy with occipital calcifications Listed in descending order of strength of evidence

88 Serological Tests first generation (guinea pig protein)
Antigliadin antibodies (AGA) Antiendomysial antibodies (EMA) Anti tissue transglutaminase antibodies (TTG) first generation (guinea pig protein) second generation (human recombinant) HLA typing Commercially available tests for celiac disease include the antigliadin, anti endomysial and anti tissue-transglutaminase tests. Tissue transglutaminase has been identified as the auto-antigen in celiac disease against which endomysial antibodies are directed. Initial transglutaminase tests used guinea pig protein as the antigen. Cloning of the gene for human transglutaminase has allowed for tests using human recombinant protein. In addition to antibody tests, some commercial laboratories are offering tests to identify the HLA DQ2 and DQ8 genotypes that are known to be strongly associated with celiac disease.

89 Histological Features
Normal 0 Infiltrative 1 Hyperplastic 2 This slide illustrates the various histolopathological findings that occur in celiac disease. Partial atrophy 3a Subtotal atrophy 3b Total atrophy 3c Horvath K. Recent Advances in Pediatrics, 2002.

90 Treatment Only treatment for celiac disease is a gluten-free diet (GFD) Strict, lifelong diet Avoid: Wheat Rye Barley

91 Hirschsprung’s Disease
History of delayed passage of meconium Failure to thrive Abdominal distension Vomiting/obstructive picture Potential complications: Perforation esp. cecal Enterocolitis/sepsis death

92 Hirschsprung’s Disease: Diagnosis
CLINICAL SUSPICION Obstructive series radiographs Barium enema (older child) Suction rectal biopsy—gold standard

93 Fecal overflow incontinence
A six year old is brought to you for diarrhea. Child stools multiple times during the day—seems to be all day. Often there is stool in the underwear. Your exam is notable for a tympanitic abdomen and LLQ mass. Your diagnosis: Neuroblastoma Giardiasis Lactose intolerance Fecal overflow incontinence

94 Treatment of Constipation
Stimulant laxatives— Senna, bisacodyl Stool softeners/osmotics PEG Lactulose ducosate Lubricants Mineral oil

95 Rectal Prolapse CF till proven otherwise
Constipation more common cause

96 IBD GENETIC INFECTION? PSYCHOGENIC DIETARY SMOKING DRUGS?
ENVIRONMENTAL DIETARY SMOKING DRUGS?

97 Crohn Disease Autoimmune Inflammatory process Presentation
Mouth to the anus; TI Presentation Abdominal pain, diarrhea, rectal bleeding, growth failure Associated symptom—GI/systemic Extra-intestinal manifestations Peri-anal changes, Fever, Apthous stomatitis, Uveitis/iritis, Skin Manifestations, Joint, Ankylosing spondylitis, Clubbing

98 IBD Interaction between genetic predisposition and environment
Increased in Northern European and Jewish population Family History increased risk Typically presents in adolescence and young adulthood

99 Crohn’s and Growth Failure
Can be presenting symptom Multi-factorial Nutritional ie. Poor intake Malabsorption Direct cytokine/inflammatory effect on bone

100 Ulcerative Colitis Inflammatory “the bloody diarrhea” Limited to colon
Continuous disease Extra-intestinal manifestations

101 Refeeding Syndrome Malnourished patients Electrolyte abnormalities
Hypophosphatemia Fluid retention Careful monitoring and slow refeeding Edema, muscle weakness, arrhythmias


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