Gastroenterology
For the general pediatrician
OVERVIEW & PURPOSE
Understand what diagnoses the pediatrician should be familiar with treating in the
outpatient clinic, and when to send patients to the specialist.
DIAGNOSES THAT SHOULD HAVE A REFERRAL (according to the experts)
1. Inflammatory bowel disease (IBD)
2. Celiac Disease
3. Direct Hyperbilirubinemia
4. Acute Hepatitis
5. Upper GI Bleed
6. Hematochezia
7. Weight loss with abdominal pain
8. Parents in Crisis
THINGS TO KNOW and HOW TO START THE WORKUP
1. Inflammatory Bowel Disease (Glick, Sarah R., MD, Carvalho, Ryan S, MD. Inflammatory Bowel
Disease. Pediatrics in Review. Vol.32 No.1 January 2011.)
a. “multifactorial disease characterized by chronic inflammation in the intestinal
tract of a genetically predisposed host” (Glick, Peds in Rev, 2011)
1. Risks include family history, ethnicity, tobacco exposure
ii. Ulcerative Colitis (UC)
1. Symptoms: diarrhea, bleeding, pain, dyspepsia
a. Extraintestinal manifestations include: pyoderma
gangrenosum, primary sclerosing cholangitis
iii. Crohn's Disease (CD)
1. Triad of abdominal pain, diarrhea, weight loss
a. Can see perianal tags, fissures, abscesses, or mouth sores
b. Growth failure may be the only sign in young children
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i. Poor appetite, fever, iron deficiency
c. Extraintestinal manifestations include: arthralgias, arthritis,
erythema nodosum
iv. Work-up to consider:
1. Blood work: CBC, ESR, albumin
2. Stool studies to rule out infectious cause
a. Calprotectin can show gut-specific inflammation
3. Imaging
a. CT abdomen can show thickening, abscess, fistulas
b. MRI can show thickening, abscess, fistulas
c. Endoscopy
i. UC: continuous inflammation beginning in rectum
and extending proximally
1. Friable tissue
2. Erosions
3. Crypt abscesses
4. Mucosal layer only
ii. CD: skip lesions often showing cobblestoning
1. Rectum typically spared
2. Terminal ileum often involved
3. Non-caseating granulomas
4. Full thickness of the wall
v. Treatment:
1. Use of steroids, 5-ASA, immunomodulators, biologics, and
probiotics
2. Nutritional therapy and supplements
vi. Possible sequelae
1. Toxic megacolon
2. Perforation
3. Colorectal cancer risk increased
4. Decreased height velocity
5. Osteopenia
vii. Things to consider in the outpatient setting:
1. Avoid use of NSAIDS
2. Restrict live vaccines in those that are immunocompromised
3. Annual eye exams
4. Close monitoring of growth
2. Celiac Disease ( Tracy R. Ediger, MD, PhD, Ivor D. Hill, MB, CHB, MD. C eliac Disease. P ediatrics in Review.
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Vol 35, issue 10. October 2014.)
a. “autoimmune small intestinal enteropathy caused by a permanent sensitivity to
gluten from wheat, rye, and barley in genetically susceptible individuals” (Ediger,
Peds in Rev, 2014)
b. Pathophysiology:
i. Genetic component and environmental triggers (possibly infectious)
ii. Inability to process gluten → inflammatory cascade with IL15, CD4-T cells,
and B cells → villus atrophy and crypt hyperplasia → antigliadin antibody
(AGA), tissue transglutaminase (tTG), and anti-endomysium antibody
(EMA)
c. Presentation:
i. Can occur at any age, most presenting between 6 months- 2 years
1. Symptoms: abdominal pain, diarrhea, nausea or vomiting, chronic
constipation not responding to usual treatment, growth failure,
weight loss, chronic fatigue, short stature, delayed puberty,
amenorrhea, recurrent aphthous stomatitis, dermatitis
herpetiformis, repetitive fractures, osteopenia, or osteoporosis
a. Celiac crisis is an emergency: presents with electrolyte
imbalance, hypoproteinemia, and vascular compromise
ii. May present as iron deficiency anemia that does not respond to iron
supplements
d. Work-up to consider:
i. Screening tests should occur after age 1, once gluten is introduced
ii. AAP recommends testing at age 3 for those that are:
1. Symptomatic
2. At high risk:
a. DM1
b. Autoimmune disease
c. First degree relative with diagnosis
iii. Request TTG IgA and IgA level
1. Can occur yearly if first degree relative
2. Testing for HLA-DQ2 or HLA-DQ8 not recommended
a. Consider if already on a gluten-free diet
b. If negative, likely not celiac disease
e. Treatment:
i. Strict adherence to gluten free diet for life
f. Prognosis:
i. If non-adherence, risk of bone demineralization, an increased risk for
intestinal malignant tumors, increased mortality
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3. Direct Hyperbilirubinemia ( Erlichman, J., & Loomes, K. (n.d.). Causes of cholestasis in neonates and
young infants (S. A., Ed.). Retrieved May 10, 2017, from https://www.uptodate.com)
a. Causes of cholestasis are due to obstruction, infection, metabolic errors, toxins, or
immunologic issues
b. Symptoms: hyperbilirubinemia, mostly direct
c. Tests to consider:
i. Liver function tests, liver ultrasound looking for choledochal cyst,
autoimmune workup, genetic testing
d. Differential:
i. Biliary atresia
1. Signs/Symptoms: Jaundiced infant with acholic stools, dark urine
a. Can be elevated direct or indirect bili
i. Obtain fractionated bilirubin if ongoing jaundice
ii. If direct, need to refer
iii. Breast milk jaundice is unconjugated bilirubin
2. Diagnosis: above tests, intra-op cholangiogram
3. Treatment: Kasai procedure
a. Done before 3 months of age for best outcomes
4. Prognosis:
a. Almost all patients require eventual transplant
i. Most common indication for liver transplant
b. At risk for ascending cholangitis
ii. Choledochal Cyst
1. Prevalence: highest in Asian females
2. Symptoms: abdominal pain, jaundice, and palpable RUQ mass,
fever, nausea, vomiting, pancreatitis
3. Workup to consider: ultrasound
a. shows intra and extrahepatic biliary tree dilatation
4. Treatment: removal of cyst
5. Future risks: malignancy - cholangiocarcinomas
a. Monitor periodically
iii. Alagille Syndrome
1. Syndrome with lack of interlobular bile ducts
2. Autosomal dominant: JAG1 mutation
3. Associated features include: pulmonary artery stenosis; tetralogy of
fallot; neonatal cholestasis, butterfly vertebrae; abnormal
radius/ulna; eye abnormalities; facies consistent with prominent
forehead, hypertelorism, pointed chin, straight nose
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4. Risks: Increased intracranial bleeding (despite liver function)
a. Do not do Kasai procedure
iv. Metabolic/Genetic causes
1. Consider work up for alpha-1 antitrypsin, primary sclerosing
cholangitis, galactosemia, tyrosinemia, disorders of lipid
metabolism or bile acid metabolism
v. Idiopathic neonatal hepatitis
1. Diagnosis of exclusion if all other testing negative
4. Acute Hepatitis ( MedStudy-section on acute hepatitis-NEED TO CITE CORRECTLY)
a. Differential Diagnosis
i. Viral hepatitis
1. Hepatitis A - RNA virus
a. Transmission:
i. fecal-orally, sexually, (NOT transplacental)
ii. 15-50 day incubation
b. Symptoms: often acute, self-limited with nonspecific
symptoms
c. Diagnosis:
i. High IgM HAV, anti HAV IgM
d. Prognosis:
i. No carrier or persistent states
ii. Prolonged cholestasis up to 4 months
e. Treatment:
i. Supportive care
ii. Monitor for fulminant hepatitis
f. Prevention:
i. Hepatitis A vaccine
g. Post exposure prophylaxis
i. Hepatitis A vaccine OR IG within 2 weeks of
exposure (IG if < 12 months)
1. Household contacts, Sexual partners, Needle
sharing partners, Daycare/nursing home in
close contact
2. Hepatitis B - DNA virus
a. Transmission:
i. Sexually, Contaminated fluids or needles
ii. Incubation: 1-6 months
b. Symptoms:
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i. Acute Symptoms: prodromal constitutional,
serum-sickness like with fever, urticaria, arthritis
ii. Chronic State
1. Asymptomatic, chronic persistent hepatitis
a. Can progress to cirrhosis or
hepatocellular cancer
c. Diagnosis:
i. HBsAg: anti-HBs IgG is positive with infection &
vaccine
1. If HBsAg and anti-HBsAg negative, consider
anti-HBc IgM during “the window”
ii. IgM HBcAg persists for life
iii. HBeAg indicates infectivity
d. Treatment:
i. HBIG and hepatitis B vaccine to Moms with +
serologies, and to those with exposures to acutely
infected patients with HBV
e. Prevention:
i. Hepatitis B vaccine
f. Sequelae:
i. Associated with polyarteritis nodosa
ii. Risk for hepatocellular carcinoma
3. Hepatitis C - RNA virus
a. Transmission:
i. Blood exposure, sexual transmission, IV drug use,
Tattoos/piercings
b. Diagnosis:
i. Positive anti-HCV antibody
1. Confirm with RIBA
ii. Positive HCV-RNA PCR is active virus
c. Treatment:
i. Interferons and ribavirin
d. Prognosis:
i. 70-80% become chronic disease
ii. Associated with small vessel vasculitis, neuropathy,
mixed cryoglobulinemia, and porphyria cutanea
tarda
iii. Risk of hepatocellular carcinoma
4. Hepatitis D - RNA virus
a. Transmission:
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i. Requires concomitant hepatitis virus, associated
with IV drug use
b. Diagnosis:
i. anti-HDV IgM
5. Hepatitis E - RNA virus
a. Transmission:
i. Fecal-oral
b. Prognosis:
i. No chronic form
ii. HIGH risk of fulminant hepatitis in pregnancy
ii. Epstein-Barr Virus - DNA virus
1. Causes infectious mononucleosis
2. Symptoms: HSM, elevated transaminases, jaundice
3. Diagnosis: serum EBV IgM
4. Treatment:
a. Self resolution, some recommend short courses of
prednisone
b. Refrain from contact sports for at least 4 weeks after
symptoms onset
iii. Cytomegalovirus (CMV)
1. Kids/adults, course similar to EBV, often self resolves
i. Can be acquired through breast milk
b. Diagnosis: confirm with CMV IgM or PCR
c. Treatment: supportive
2. Neonatal CMV
a. Symptoms: severe liver disease, cirrhosis, HSM
i. Central nervous system manifestations
1. Periventricular calcifications
2. Microcephaly
ii. Systemic: Petechial rash, chorioretinitis, IUGR
b. Late sequelae include:
i. Hearing loss, language delays
b. Work up to consider:
i. Viral hepatitis panel including: IgM HAV, HBsAg, IgM HBc, anti HCV
antibody, and other infectious titers
5. Upper GI Bleed ( A pproach to upper gastrointestinal bleeding in children. Villa, Xavier,
MD-NEED TO CITE THIS CORRECTLY)
a. Differential:
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i. Mallory-weiss syndrome
ii. Foreign body
iii. Esophagitis
iv. Gastritis/Peptic ulcers
v. H pylori
vi. Pill esophagitis
vii. Esophageal varices
viii. Non-accidental trauma
ix. Swallowed maternal blood (neonate)
x. Congenital hepatic fibrosis (with resultant esophageal varices)
1. Associated with AR-PKD
2. Portal HTN and hematemesis or melena from esophageal varices
3. Exam: hepatosplenomegaly, normal AST/ALT
a. Concern for cholangitis
i. Jaundice, fever, RUQ pain
4. If with congenital dilation of bile ducts, Caroli Syndrome
b. Tests to consider:
i. Lab work: CBC with diff, coags, LFTs, BMP, inflammatory markers
ii. Chest/abdominal xray
iii. Abdominal ultrasound
iv. Esophagogastroduodenoscopy (EGD)
v. Stool calprotectin or stool antigen testing
vi. Neonate: Apt Test
1. Fetal hemoglobin resists alkali denaturation, leading to a positive
test result in infants who have ingested maternal blood
c. Treatment to initiate:
i. Stop NSAID use
ii. Consider acid suppression
6. Hematochezia (Lower gastrointestinal bleeding in children: Causes and diagnostic approach. Patel)
a. Differential:
i. Necrotizing enterocolitis
ii. Swallowed maternal blood
iii. Malrotation
iv. Anal Fissure
v. Milk-protein colitis
vi. Meckel diverticulum
vii. Coagulopathy
viii. Intussusception
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ix. Infection
1. Salmonella, Shigella, Campylobacter, E coli O157:H7, Clostridium (C.
diff is normal flora in age <1)
x. Juvenile polyps
xi. Irritable bowel disease
xii. Vascular anomalies
b. Tests to consider:
i. Hemoccult to confirm
ii. Lab work: CBC with diff, coags, LFTs, BMP, inflammatory markers
iii. Stool studies - bacterial and viral cultures
iv. Abdominal x-ray and/or ultrasound, consider CT
v. Meckel scan
vi. Colonoscopy
c. Treatment to initiate:
i. Dependent on etiology
7. Weight loss with abdominal pain
a. Differential is broad
i. Consider work up for any of the above, including screening tests guided by
location of pain
8. Parents in crisis
a. Referral is appropriate when parents are in crisis and need additional help or
counseling
WHAT TO BE COMFORTABLE WITH TREATING IN CLINIC
Of course, if there are problems or concerns, a referral or phone call is always an option.
1. Constipation
2. Allergic Colitis
3. Functional Abdominal Pain
4. Gastroesophageal Reflux
5. Hyperbilirubinemia - especially indirect
6. Nausea/Vomiting
7. Diarrhea
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8. Anal Fissures
9. Failure to Thrive
10. Picky Eaters
MORE DETAILS
Break down of each diagnosis and recommendations for treatment
1. Constipation (Colombo, Jennifer M., Wassom, Matthew C., Rosen, John M. Constipation and Encopresis in
Childhood. Pediatrics in Review. Vol 36, Issue 9. September 2015.)
a. Definition: hard stools that are difficult to pass
i. Infants: normal to have 3-4 stools per day on average
ii. Toddlers: normal to have 2-3 stools per day on average
1. Expect bowel continence by age 4
iii. Children: normal bowel habits vary
b. Symptoms: Abdominal pain, decreased appetite, painful stooling
c. Differential:
i. Infantile dyschezia
1. Healthy infants < 6 month with straining to stool
a. Stool is soft, therefore not constipation
i. Process of learning to stool
ii. Functional Constipation
1. Hard or infrequent stools
a. Diet and water intake contributes to symptoms
iii. Delayed meconium
1. Differential: Hirschsprung's Disease, anal stenosis, Cystic Fibrosis,
strictures
iv. Hypothyroidism
1. Would expect other systemic symptoms
v. Celiac Disease
1. Consider in children that do not respond to appropriate laxatives
d. Diagnosis:
i. Rome III Criteria for kids > 4 yo with 2 of the following:
1. < 2 stools per week, one episode of fecal incontinence per week,
signs of retention (postures, leg crossing), history of painful bowel
movements, large stool output (often obstruct the toilet), fecal mass
in rectum
e. Workup to consider:
i. Imaging is often not necessary due to inaccurate standardized scales by
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radiology (no one reads the amount of stool the same)
ii. Consider imaging if not responding appropriately to therapy OR if concern
for other etiology
f. Treatment:
i. Diet modifications (Sood, UpToDate, 2016)
1. Increase fluid intake
2. Increased fiber intake
3. Consider sorbitol containing juices (apple, pear, prune)
a. 2-4 oz per day for infants > 4 months old
4. Dark corn syrup (Karo Syrup)
a. may or may not contain osmotically active particles, so it is
possible that it will not help
ii. Medications:
1. Osmotic Laxatives: increase osmotic load of stool
a. Polyethylene glycol ( Miralax): Clean out: 1-1.5 g/kg x3-6
days
i. Maintenance Therapy: months to years with goal of
one soft stool per day
ii. End therapy when consistent stooling for 1-2 months
b. Lactulose: 1-3 mL/kg/day in 2 divided doses
i. Allows for smaller volume for kids that cannot drink
miralax
c. Magnesium hydroxide: Dosing by age
2. Stool Softeners: decrease surface tension of stool
a. Docusate: 5mg/kg/day (max 400mg/day)
b. Mineral Oil: 1-3mL/kg/day divided in 2 doses
i. Not for children < 1 year old
3. Stimulant Laxatives: produces peristaltic activity in the colon, best
for rescue therapy
a. Senna (Ex-lax): Dosing by age, give at bedtime
b. Bisacodyl: Dosing by age
iii. Behavior modifications
1. Toilet Sitting Program
a. Practice after all meals for 5 minutes
b. Feet must be supported to stool
g. When to refer:
i. Worsening symptoms, failure to thrive, bloody stools, abdominal
distention, sacral dimple, lack of improvement, parent crisis
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2. Allergic Colitis (Clinical manifestations of food allergy; Diagnostic Approach and Management of Cow’s-Milk
Protein Allergy in Infants and Children)
a. Pathogenesis
i. Often occurs in first 3 months of life
ii. Can occur with breast milk, may occur with soy milk as well
iii. History of eczema or atopy common
b. IgE vs non-IgE Reaction
i. IgE are rapid in onset (minutes to 2 hours) from time of ingestion and can
include skin, respiratory, GI tract, and CV symptoms
1. Ex: anaphylaxis, angioedema
ii. Non-IgE mediated reactions are subacute or chronic in nature and are
limited to GI tract and skin manifestations
1. Ex: FPIES, cow’s milk allergy
c. Symptoms:
i. Frequent regurgitation, reflux, GI bleed, Failure to thrive, abdominal
distension
d. Treatment:
i. Breast-fed infants
1. Maternal elimination of milk and milk products
a. Continue for ~ 2 weeks for symptom resolution
b. Supplement mother with calcium
ii. Hypoallergenic formulas
1. Extensively hydrolyzed formulas
a. Similac Alimentum
2. Amino-acid based formulas
a. Enfamil Nutramigen (similar oil blend to standard
formulas)
b. Neocate (beneficial for malabsorptive disorders)
c. Elecare (beneficial for malabsorptive disorders)
3. Remember: There is an estimated “30-64% rate of cross-reaction to
soy protein” in infants with non-IgE cow’s milk allergy and a 8-14%
cross-reactivity in IgE mediated allergy (Martinez, Peds in Rev, 2011)
a. Soy may not be a good option
e. When to refer?
i. Ongoing FTT, non-resolving symptoms, parent crisis
3. Functional Abdominal Pain (M cFerron, Waseem. Peds in Rev, 2012)
a. Defined as long-lasting pain that is intermittent or constant
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i. High prevalence with estimated 2-4% of all general pediatrics office visits
b. Pathogenesis:
i. Combination of multiple systems - enteric nervous, CNS, visceral
hypersensitivity, psychological factors, abnormal response to pain
1. Possible association with early life events such as abdominal
surgery, or cow milk protein allergy
c. Symptoms: Alarming symptoms: weight loss, ulcers, fevers, FTT, unexplained
chronic symptoms
d. Diagnosis: Often difficult, need to outline expectations from the beginning;
judiciously order tests for those with “red flags”
e. Differential:
i. Broad, but also includes functional dyspepsia, irritable bowel syndrome,
abdominal migraine, and functional abdominal pain
1. Functional Dyspepsia: pain in upper abdomen > 2 months, bloating,
early satiety, nausea
2. Irritable Bowel Syndrome: abdominal discomfort or pain associated
with change in bowel, and improving with defecation
3. Abdominal migraine: paroxysmal episodes of intense, periumbilical
pain lasting 1 hour or more; healthy between. Also with pain,
nausea, vomiting, headache, etc. Family hx of migraine common
4. Functional: 2 months or longer of abdominal pain
f. Treatment:
i. Time-limited trial of acid suppression
a. Stop if no improvement
ii. Pain management
a. Dicyclomine, SSRIs, probiotics
iii. Psychologic Support
a. CBT
b. Good sleep habits
iv. Dietary Changes
a. Avoidance of ‘trigger’ foods
b. Small, frequent meals
c. Limit non-absorbed carbs (juices)
g. When to refer?
1. Red flags, persistence of symptoms > 2 months, parental crisis
4. Gastroesophageal Reflux (Sullivan, Peds in Rev, 2 012)
a. Definitions:
i. Gastroesophageal reflux (GER) = “passage of gastric contents into
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esophagus”, this is a normal physiologic occurrence
1. 67% of 4 month olds have one episode of reflex daily
2. At 12 months of age, that number drops to 5%
ii. Gastroesophageal reflux disease (GERD) = “passage of gastric contents into
the esophagus that results in troublesome symptoms” for the infant
b. Pathophysiology: Relaxation of lower esophageal sphincter combined with gastric
distension, and short esophagus
c. Symptoms:
i. Gastroesophageal reflux: Spitting up, ‘happy spitters’
ii. Gastroesophageal reflux disease: feeding difficulties, back arching,
irritability, FTT
1. Sandifer syndrome, brief resolved unexplained events
d. Diagnosis: by history and physical
e. Workup: often not needed
f. Treatment:
i. Lifestyle changes
1. Feeding support (positioning, feeding volume)
2. Can trial new formula (use for at least 2 weeks to evaluate
effectiveness)
a. Example: Enfamil AR which thickens in response to acid
b. Pre-made thickened formula maintains recommended
balance of nutrients instead of adding rice cereal at home
which is no longer recommended
3. Continue safe sleep practices
ii. Acid suppression
1. Four week trial of H2 blocker or PPI
a. Keep in mind, that use of acid suppressor along with
thickened formula for reflux counteract each other
i. Example: Enfamil AR (Children’s Health Partners, 2008)
iii. When to refer:
1. If symptoms persist >12-18 months of age
2. Bilious or projectile emesis, fever, HSM, lethargy, etc.
5. Indirect (Unconjugated) Hyperbilirubinemia ( Pashankar, J aundice in older children, 2001;
Maisels, N eonatal Jaundice, 2006.)
a. Yellow hue to the skin with total serum bili >1 mg/dL
b. Bilirubin Metabolism
i. Heme is catabolized to bilirubin→ released to circulation bound to
albumin→ transports to liver where it is conjugated by UGT-1→ excreted
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into the bile and gut
1. Enterohepatic circulation reabsorbes large amount of unconjugated
bilirubin in the infant due to lack of colonic bacteria
c. Differential:
i. Hemolytic Disease
1. ABO incompatibility: will often have positive DAT or Coombs test;
most symptoms occur within the first 24 hours; seen in a mother
with type O blood and infant with group A or B
2. G6PD deficiency: X-linked enzyme defect in the RBCs most common
in African Americans; increase in heme turnover
ii. Breastfeeding jaundice - First 2-4 days of life due to decreased calories
which is thought to stimulate enterohepatic circulation
iii. Breastmilk jaundice - Onset in 4-7 days of life
iv. Gilbert syndrome
1. Autosomal recessive disorder
2. UGT1 gene mutation
3. Jaundice with stress or illness
v. Crigler-Najjar syndrome, type 2
1. Absence of UDP-glucuronosyl transferase enzyme
2. Can treat with phenobarbital (induces enzyme activity)
vi. Sepsis
vii. Metabolic causes such as hypothyroidism or hypopituitarism
d. Workup to consider:
i. Labwork: Total serum bilirubin (especially if transcutaneous bilirubin is
elevated) with differential between direct and indirect, consider liver
function tests, CBC, retic count, coags, Coombs test, DAT, septic workup
ii. Red Flags: jaundice with a sleepy infant who is not nursing well
e. Treatment: phototherapy (converts bilirubin to products that can bypass the liver
and be excreted in the bile or urine), exchange transfusion
f. When to refer:
i. Signs of liver failure, rising bili with lowering AST/ALT, ascites
6. Nausea/Vomiting (Parashette, Kalyan Ray., Croffie, Joseph. Vomiting. Pediatrics in Review. 2013)
a. Vomiting center, located in the lateral medullary reticular formation of the
brainstem and is influenced by multiple different regions including: vagal afferent
system (GI tract, serotonin), vestibular system (motion sickness, muscarinic and
histamine), higher cortical centers, chemoreceptor trigger zone (blood and CSF,
dopamine)
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b. Differential:
i. Infants
1. GERD: see below
2. Pyloric stenosis
a. 3-6 week old infant
b. Hypochloremic, hypokalemic contraction alkalosis and
aciduria
c. Use of erythromycin increases risk
d. Diagnosed with US
3. Intestinal Atresia
a. Bilious vomiting, abdominal distension, failure to pass
meconium
b. KUB shows double bubble sign
ii. Beyond Infancy
1. Acute gastroenteritis
a. Viral > bacterial > parasitic
b. Vomiting followed by diarrhea
2. Eosinophilic esophagitis
a. Can present at any age
b. Vomiting, pain, FTT, allergies
c. Endoscopy with biopsy to diagnose
d. Treat with elimination diet (milk, soy, egg, peanut, wheat,
fish), PPIs, swallowed fluticasone
3. Cyclic vomiting syndrome
a. Associated with migraine headaches
i. Many respond to migraine treatments
b. Acute onset in the AM hours, lasts for a few hours-days, and
patients are healthy in between
c. Triggers are infection and emotional changes
d. Treat with lifestyle modifications, TCAs
c. Antiemetics
i. Serotonin receptor antagonists
1. Ondansetron: can cause headache, constipation, dizziness, and
prolonged qtc
ii. Dopamine receptor antagonists
1. Prochlorperazine, haloperidol, metoclopramide
a. Adverse effects: extrapyramidal reactions, drowsiness
iii. H1 receptor antagonists
1. Promethazine, diphenhydramine
a. Adverse effects: sedation
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iv. Muscarinic receptor antagonist
1. Scopolamine
7. Diarrhea ( CaJacob. Update on Diarrhea. Peds in Rev.)
a. Worldwide, diarrheal illness is second leading cause of death in kids < 5 years old
b. Definition: looser than normal stools
i. Only red, black, tarry, or white stools should be alarming
c. Etiology
i. Viral Gastroenteritis
1. Nonbloody, loose, watery stools
i. Norovirus, rotavirus
2. Often associated with vomiting
3. Treatment: supportive care
ii. Bacterial Gastroenteritis
1. Associated with high fever, bloody stools, severe pain, and CNS
involvement
a. Salmonella, shigella, campylobacter
1. Shigella is the most common cause of bloody
stools
b. E. coli O 157:H7 also commonly causes bloody stool
1. 20% of patients may develop HUS
c. Clostridium difficile
iii. Noninfectious Causes
1. Broad differential: IBD, IBS, immunodeficiency syndromes, motility
syndromes, hyperthyroid, congenital diarrhea, drug-related,
milk-protein intolerance
d. Persistent diarrhea
i. Greater than 14 days
1. Consider chronic illness, G iardia, Cryptosporidium, C . diff,
postinfectious diarrhea, celiac disease, food allergy
e. Treatment:
i. Vaccinations
1. Rotavirus
ii. Rehydration
1. Oral rehydration treatment
2. Reintroduction of regular diet
iii. Consider antibiotics in at risk patients (those less than 3 months)
1. Ampicillin, bactrim, erythromycin (campylobacter)
a. Oral metronidazole for c. diff
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iv. Antiemetics
1. Not for children < 3 years old
v. Antimotility agents
1. Not indicated in children (risk of toxic megacolon, ileus, minimal
benefits have been shown)
vi. Probiotics
1. Oligosaccharides that help with stimulation of intestinal flora
a. Limited benefits found
f. Work Up to Consider
i. Stool culture, c. diff, celiac testing, fecal elastase, fecal calprotectin
ii. Trial of avoidance of lactose
g. When to refer?
i. Onset of diarrhea in infants < 30 days, refractory to treatment, persistent
diarrhea, weight loss, hematochezia
8. Anal Fissures ( Lower gastrointestinal bleeding in children: Causes and diagnostic approach. Patel)
a. Why it is important: Most common cause of rectal bleeding in kids < 1 year
b. History: often consistent with constipation
c. Symptoms:
i. Streaking of blood on the outside of stool, seen on physical exam
d. Treatment:
i. Treat the constipation
ii. Lubricants (vaseline)
iii. Keep perineum clean and dry
e. Common etiologies:
i. Introduction of solid foods or cow’s milk
ii. Toilet training
iii. Start of school
f. When to refer?
i. When symptoms worsen, if prolapse occurs, or in parental crisis
9. Failure to Thrive (FTT) ( Jaffe, Arthur C. F ailure to Thrive. 2 011)
a. Definitions:
i. “...a physiologic sign that a child is receiving inadequate nutrition for
optimal growth and development” (Jaffe, Peds in Review, 2011)
ii. One of three possibilities:
1. Inadequate intake of nutrition
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2. Poor absorption
3. Increased metabolic demand
iii. Other things to keep in mind:
1. Use the correct growth chart (specialized charts for genetic
conditions)
2. Consider that growth rate shifts throughout childhood can be
normal
b. Sequelae of FTT:
i. Possible long term problems in cognition
ii. Possible loss of overall height and weight loss
iii. Psychosocial issues as a result of or a cause of
c. Diagnosis:
i. History of intake, diet, social issues, preparation, output, etc.
1. Consider food diary
ii. Family history
iii. Physical exam
1. Dysmorphology
2. Signs of dehydration or malnutrition
d. Workup to consider:
i. Limited evidence to support need for lab work up
1. May help family
2. Let history guide work up
a. Screening labs to consider: CBC (anemia), ferritin, TIBC (iron
deficiency), Vitamin D level, B12 and folate, lead, TSH, zinc,
celiac screening, stool studies, sweat chloride
ii. Be aware of refeeding syndrome
1. Patients may be asymptomatic, but watch for lab changes
2. Laboratory features may include: hypophosphatemia, hypokalemia,
hypomagnesemia, thiamine deficiency, hyperglycemia, fluid
overload
e. Treatment:
i. Determine proper intake and nutritional repletion
1. Frequent weight checks
2. Assess ability to eat
ii. Interdisciplinary team approach is often needed
1. Refer to a center that can provide this
f. When to refer: as needed for the problem discovered, or to GI if other
gastrointestinal symptoms occur with FTT
19
10. Picky Eaters ( Zucker, Peds, 2015.)
a. Why it is important:
i. “14%-20% of parents report that their preschooler (ages 2-5 years old) is
‘often’ or ‘always’ selective with food” ( Zucker, Peds, 2015)
ii. Often associated with anxiety, depression, hypersensitivity to food, or
family conflicts
b. Etiology: multiple hypotheses including environmental factors, maternal
exposures during pregnancy, and genetics
c. Diagnosis:
i. Consider avoidant/restrictive food intake disorder (eating disorder in DSM V)
ii. Often no significant effect on growth
1. If there is, additional work up is likely needed
d. Work Up to Consider: None, unless other symptoms present to suggest underlying
disorder
e. Treatment:
i. Promote food acceptance: repeated exposures with appropriate modeling,
without coercion
1. “Infants and toddlers needed as many as 8-15 exposures to a
particular food before they gained acceptance of that food” ( Lam,
Front in Peds, 2015)
2. Often children will continue to accept more foods as they get older
f. When to refer: if additional symptoms suggest underlying etiology, weight loss, or
if parental crisis
RESOURCES
● Children's Health Partners. "Gastro-esophageal Reflux (GERD) in Infants." Children's
Health Partners, 2008. Web. 23 May 2017.
<http://www.childrenshealthpartners.com/illness_info/gastro-esophageal-reflux-gerd-in-in
fants.html>.
● Koletzko, S. Niggemann, A. Arato, J.A. et al. D iagnostic Approach and Management of
Cow’s-Milk Protein Allergy in Infants and Children: ESPGHAN GI Committee Practical
Guidelines. Journal of Pediatric Gastroenterology and Nutrition. Volume 55, Number 2.
August 2012.
● Lam, Jason. Picky Eating in Children. F rontiers in Pediatrics. Vol 3, issue 41. May 2015.
● MedStudy
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● UpToDate:
○ Erlichman, J., & Loomes, K. C auses of cholestasis in neonates and young infants (S.
A., Ed.). March, 2017. https://www.uptodate.com
○ Wesley, Burks. Clinical manifestations of food allergy: An overview. October, 2015.
https://www.uptodate.com
○ Patel, Nishaben. Lower gastrointestinal bleeding in children: Causes and diagnostic
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