GI Disorders during Newborn Period Factors causing esophageal manifestation
Dr. Roumilla Mendoza 1. duration of esophageal exposure
June 25, 2013
Group 4
Objectives:
1. To know the normal digestive tract phenomena
2. To differentiate the abnormal manifestations from the
normal
3. To know the management of the gastrointestinal
disorders during newborn period
Normal Digestive Phenomena
Regurgitation
- Effortless movement of stomach contents
into the stomach and mouth
- Developmental process
- Caused by immaturity of lower esophageal
sphincter (sphincter that prevents back up
of gastric contents)
- Very common especially during first few
months of life
GER (Gastroesophageal) Reflux
- Passage of gastric contents into the
esophagus with or without regurgitation
and vomiting
Pathophysiology
Anti-reflux barrier
- Crura of the diaphragm
- LES (Lower Esophageal Sphincter) tone
*LES- smooth muscle with sphincter-like
function
Reflux occurs when
- Insufficiency of LES tone
*can be brought by: infections, spicy and
fatty food, carbonated drinks, coffee, tea,
etc)
- Abnormal frequency LES relaxation
- Hiatal hernia
*Transient esophageal sphincter relaxation
GERD (Gastroesophageal Reflux Disease)
- Caused by increased intraabdominal
pressure (gastric distention from over
feeding, increased air swallowing.) [Hiatal
hernia ameliorate intraabdominal pressure.]
Pathophysiology
2. the causticity of the refluxate (Bile reflux is more
painful)
3. susceptibility of the esophagus to damage
Clinical manifestations (mostly caused by PAIN)
1. irritability
2. arching
3. choking
4. gagging
5. feeding aversion
6. failure to thrive
Diagnosis (NO GOLD STANDARD)
1. Esophageal pH monitoring
- monitors acid reflux only
- Insert probe via nose to the level of the
lower esophageal sphincter to document
esophageal events
2.Combined Multiple Intraluminal Impedance (MII) and
pH monitoring
- can document both acid and alkali reflux
3. Motility studies
4. Endoscopy and Biopsy (with neonatal scope)
5. Barium Contrast Radiography (rules out anatomical
problems)
6. Nuclear Scintigraphy
*High index of suspicion is important
Treatment (duration: 6-8 or 12 weeks)
1. Lifestyle change
- If breastfed, observe with normal diet of
mom then find out what the mom eats
that the baby’s allergic to.
- If baby is allergic to cow’s milk, there’s
50% chance he’s allergic to soy milk also.
- Don’t use hypoallergenic milk, it is only
preventive, not curative.
- Experiment on hydrolyzed milk
- Thicken milk to prevent GERD.
*Thicken milk with brown rice or cereal
- Prone position lessens GERD but
predisposes baby to SIDS (Sudden Infant
Death Syndrome)
2. Pharmacologic Therapies
- Histamine 2 Receptor Antagonists(H2RAs)
 Famotidine, ranitidine, etc.
*if used for a month, it will cause
tachyphlaxis or rebound phenomenon
- Proton pump inhibitors
  Goes directly to cellular level  Meconium
 Given before meals (Omeprazole  darkly stained
1mg/kg/day)  should be passed in the first 48
- Prokinetic Therapy hours (if not passed out, there
 Improves motility could be an obstruction)
 Motilium, erythromycin  Transitional stool
* erythromycin acts on motilin  occurs 3rd -5th day of life; may occur
receptors and improve gastric earlier for breastfed infants
emptying  Exclusively Breastfed stool
 Slightly watery and sour smelling
3. Surgical  Milk Formula Stool
- Fundoplication (for neurologically impaired  Formed stools, less watery, more
patients, like cerebral palsy) smelly
 Meconium plug
Vomiting  Common in Western countries
- Highly coordinated reflex process  Common in pts. with cystic fibrosis
 Stools are very dry/dehydrated
Causes forming a plug = obstruction
1. Irritation of the gastric mucosa by material  Followed by watery stools
swallowed (i.e. maternal blood)
2. overfeeding (NB stomach capacity = 30ml) Infant Dyschezia
3. GIT obstruction - Occurs when the baby has not coordinated
4. Infection (UTI, sepsis) the increase in abdominal pressure with
5. Increased intracranial pressure pelvic floor relaxation
6. Cow’s milk allergy (some are coffee ground or - Self-limited constipation
blood stained) - Stools are soft with no blood
7. Metabolic disorders
Protuberant abdomen (normal ion NB)
Diagnosis Factors
1. History and Physical examination - Weak abdominal musculature
2. Diagnostics - Lordotic stance (spine has 3 curves)
Double bubble sign- seen in patient with high - Relatively large abdominal organs (e.g. liver
type of obstruction (e.g. duodenal atresia) is palpable, 1-2 cm in size)
 Radiography
 Contrast studies – upper GI Abdominal Mass
series to rule out malrotation Cystic abdominal mass
 Ultrasound – polyhydramnios - Hydronephrosis
signify obstruction in utero - Multicystic-dysplastic kidneys
Cow’s milk allergy - Adrenal hemorrhage
- Vomiting generally occurs 1-3 hrs after - Hydrometrocolpos
feeding - Intestinal duplication
- Other clinical manifestations: - Choledocal, ovarian, omental, or pancreatic
o Bloody diahrrea cysts
o Anemia
o Abdominal distention Solid masses
o Failure to thrive Neuroblastoma, congenital mesoblastic
- Treatment nephroma, hepatoblastoma, and teratoma.
o Extensively hydrolysed formula - Solid flank mass
o Breastfeeding Renal vein thrombosis
Hematuria hypertension,
thrombocytopenia
* Most common – renal mass
Stool Characteristics
*Mothers with DM and Hypertension… NB at risk for - Diagnosis: Ultrasound, MRC
abdominal masses - Treatment: surgical

Jaundice Note: If obstruction is below Ampulla of Vater, vomit is

Physiologic bile stained
- Visible on the 2-3 days of life
- Decreasing in the 5-7 days of life Idiopathic Neonatal Hepatitis
- Result of increased bilirubin production - Sporadic/familial
after the breakdown of fetal red blood cells - Unknown cause
combined with transient limitation in the - Extension giant cell formation (biopsy)
conjugation of bilirubin by the liver - Prognosis: good

Pathologic jaundice Infectious:

- Could be direct or indirect - Bacterial – E. coli sepsis
- Within the first 24 hrs of life - Viral Cytomegalovirus- can be
- Jaundice after the first week of life documented by urine cultures
o TORCH
Establish the diagnosis o Hepatotropic viruses
- History o HIV
1. Feeding- breastfed? Bottle-fed? o Enteroviruses
(Differential diagnosis for breastmilk o Parvovirus B19
jaundice)
2. Color of stool (abnormal – grey, normal – *Cytomegalovirus – most common cause of
yellow to green) infectious hepatitis
3. Color of urine (Direct hyperbilirubinemia
if darkly stained) Metabolic
Galactosemia
- Physical examination - Deficiency of galactose-1-phosphate
uridyltransferase (GALT)
Cholestasis - Treatment: use of a lactose free formula
- Prolonged elevation of conjugated bilirubin
beyond 2 weeks of life Clinical Consequences of Neonatal Cholestasis
- Direct bilirubin is > 20% of total bilirubin Retention of
- Direct bilirubin is > 2mg/dl  Bile acid – pruritus, hepatotoxicity
 Bilirubin – jaundice
*Breastfeeding jaundice – indirect hyperbilirubinemia  Cholesterol – xanthoma, hypercholesterolemia
 Trace elements – copper
Algorithm on the Management of Cholestasis Progressive liver disease
(Please Refer to the last page)  Portal hypertension
 Hypersplenism
Biliary Atresia  Hemorrhage – varices
- progressive obliteration of the bile ducts  Liver Failure
- 1:5000 – 1:15,000
- Bile duct proliferation (biopsy) Reduced bile acid delivery to small intestine
- Treatment: Hepatoportoenterostomy (Kasai)
 Malabsorption
procedure
o Fat malnutrition – steatorrhea, growth
- MOST common cause of pediatric cirrhosis
retardation
←
o Fat soluble vitamins malabsorption
Choledochal Cyst
 Vit A- night blindness
- congenital dilatations of the common bile
 Vit D- Osteoporosis
ducts, intrahepatic and extrahepatic ducts
 Vit E- Macular Degeneration
- progressive biliary obstruction & cirrhosis
 Vit K- Hypoprothrombinemia
- most common : type 1
Management of cholestatic jaundice Modified Bell Staging for NEC
Stage Systemic signs Intestinal Radiographic
Nutritional signs signs
- Total caloric intake (125% RDA) I: Temp Elev Normal or mild
- Fat soluble vitamins Suspect instability, gastric ileus
- Medium chain triglyceride ed NEC apnea, residuals,
bradycardia mild abd
Therapeutic distentio
- Choloretics (to improve bile flow) n, occult
Ursodeoxycholic acid – 10-20 blood in
mg/kg/day stool
Phenobarbital – 3-10 mg/kg/day IIA: Mild Similar to I Abd Ileus, dilated
NEC distentio bowel loops w/
Necrotizing Enterocolitis (NEC) n± focal
tenderne pneumatosis
- Life threatening emergency of the GIT in the ss, (-)
newborn period bowel
- Various degrees of mucosal or transmural sounds,
necrosis of the intestine bloody
- Prematurity (greatest risk factor) stools
- Clinical manifestations may be sudden IIB: Mild acidocis Abd wall Extensive
catastrophic or insidious Modeat and edema pneumatosis,
e NEC trombocytope and early ascites ±
Pathogenesis nia tenderne PVG
Factors: ss ±
- Intestinal ischemia palpable
- Oral feedings (metabolic substrate) mass
- Pathogenic organisms IIIA: Resp and met Worsenin Prominent
o Bacterial – E. coli, Klebsiella, Advanc acidosis, g wall ascites,
Clostridium perfringens, ed NEC mech edema persistent bowel
Staphylococcus epidermidis ventilation, and loop, no free air
o Virus ( rotavirus) hypotension, erythem
oliguria, DIC a w/
Systemic Manifestations induratio
- Apnea/respiratory distress n
- Temperature instability IIIB: Vital signs Evidence pneumoperiton
- Lethargy Advanc and lab of eum
- Acidosis (metabolic and/or respiratory) ed NEC evidence of perforati
- Glucose instability deterioration, on
- Poor perfusion/shock shock
- Disseminated intravascular coagulopathy
- Positive results of blood cultures Management
- ABC’s
- Antimicrobials
- Bowel rest and decompression
- Surgical if with perforation
Algorithm on the Management of Cholestasis

Legend:
Condition

Jaundice infant
Question
2-8 weeks old

Action

Is the patient acutely

ill?
Require urgent care?
YES
o Manage the acute
illness
o Consider urinary tract or NO Normal
other infection Is there direct Indirect
o Metabolic disorders hyperbilirubinemi hyperbilirubinemia
o Hemolysis a
o Acute common duct
obstruction
Evaluate Further
Abnormal
Measure serum direct
bilirubin
duct obstruction

Cholestatic
Jaundice

Neonatal Cholestasis

Interahepatic disease
Extrahepatic
disease (bile
duct injury or
Hepatocyte Bile duct obstruction)
injury injury

Extrahepatic
biliary atresia
Metabolic Viral Idiopathic
disease disease Neonatal Intrahepatic
hepatitis bile duct
hypoplasia
or paucity