1. Neonatal Gastrointestinal System
Carmelita Rivero, RNC
Madigan Army Medical Center

2. Embryology
Weeks 3,4 – Esophagus, liver, stomach, and intestine are distinct elements.
Week 7 – Intestinal loops herniate into the umbilical cord.
Week 9,10 – Intestines re-enter abdominal cavity. Intestines continue to rotate.

4. Embryology, cont…
Week 16 – Meconium appears and swallowing is observed.
Week 26 – Random peristalsis begins.
Week 34 – Suck/swallow become coordinated.
Week 36/38 – The GI system is mature.

5. Assessment Size and Shape
normal - slightly rounded, soft, and symmetric
abnormal -
distended - intestinal obstruction, infection
scaphoid - diaphragmatic hernia
asymmetric - mass, organomegaly, intestinal obstruction

7. Assessment Hernias Muscular Development
umbilical - common in African-American, Down’s, hypothyroid.
inguinal - more common in males
femoral - more common in females
Muscular Development
abnormal - prune-belly syndrome, diastasis recti

9. Assessment Umbilicus - abnormal
green/dark yellow staining - in utero meconium passage
wet, foul smelling, or red - infection
persistent, clear, drainage - patent urachus
Thick, gelatinous - LGA
Thin, small - IUGR
2 vessel cord - possible congenital anomalies

10. Assessment Bowel sounds Palpation
Audible within minutes after birth
Hyper/hypoactive is not necessarily pathologic.
Hyperactive - malrotation, Hirschprungs, diarrhea
Hypoactive - ileus
Palpation
Masses
Organ Enlargement - liver 1-2 cm below right costal margin, mid clavicular line.

11. Risk Factors GI disease in family Genetic syndromes
Fetal ultrasound - view of dilation or obstruction
Maternal polyhydramnios
Failure to pass meconium within hours
Abdominal distention
Bilious vomiting

12. How does
it happen?
Normal develop-ment fails
to continue

13. General Treatment of GI Patients
NPO – bowel rest
IV Fluids
Gastric suction on low
Antibiotics
Surgical correction

14. Tracheoesophageal Fistula (TEF)
The Esophagus
Tracheoesophageal Fistula (TEF)
Incidence : 1 in 4000 live births
50-70% of affected infants have associated anomalies.

15. 4 Types of TE Fistulas
The most common type is the esophageal atresia with tracheoesophageal fistula (85%)

16. TE Fistula - Presentation
Dependent upon type of anomaly
History of polyhydramnios
Inability to swallow saliva leads to drooling
Gavage tube cannot be passed
Coughing, choking or cyanosis with feedings
Abdominal distention
Recurrent pneumonia

18. TE Fistula - Treatment Elevate the head 30-45 degrees
Low suction to remove secretions from the esophageal pouch
Comfort measures
Assess for associated anomalies
Cardiac defects – 30%
GI anomalies – 12%
VATER/VACTERL – 15%

19. Gastroesophageal Reflux
GER - an effortless retrograde movement of gastric contents into the esophagus.
Regurgitation - movement of gastric contents into the mouth.
Physiologic reflux is a normal occurrence in infants, children, and adults.
Physiologic reflux can become a pathologic problem at any point.

20. Gastroesophageal Reflux
Infants with GER usually become symptomatic at 2-4 months of age, with a peak in symptoms seen at 4-5 months of age. Most resolve by 8-12 months.
This is probably due to the maturation of the GI system and the increase consumption of solid foods.

21. Gastroesophageal Reflux
Can result in:
Failure to thrive
Aspiration
Anemia
Esophagitis
Apnea
Reflex bronchospasm
SIDS-like events

22. GE Reflux : Symptoms Fussiness Irritability “Colic” Failure to thrive
Excessive regurgitation/vomiting
Refusal of feeding
Back arching with feeding
Gagging
Excess swallowing (about minutes after feeding)

23. GE Reflux : Symptoms
Fussiness is probably due to pain from exposure of the esophagus to acidic gastric contents.
Infants with reflux may first present with choking, gagging, apnea, wheezing, or recurrent pneumonia.
Infant apnea often occurs 1-2 hours after feeding.
Increased work of breathing can increase abdominal pressure, pushing gastric contents back up into the espohagus

24. GE Reflux : Physiology
Anatomic and functional immaturity of the GI tract – Term Infants
Immaturity of the lower esophageal sphincter (LES)
Positioning of the LES
Alterations in gastric and esophageal motility
Delayed gastric emptying
air swallowing
Frequent prone positioning

25. GE Reflux : Treatment Treatment for simple regurgitation
Frequent burping
Feeding slowly in a semi-upright position
Small frequent feedings
Conservative treatment for GE Reflux
Avoid supine position while awake
Avoid infant seats/swings that cause the infant to slouch.
Encourage an upright position such as an infant front pack.
Reduce smoke exposure

26. The Stomach Pyloric Stenosis: Stenosis of the pyloric musculature.
Incidence – 1 of every 500 births
Males are affected 4:1
First born more often affected, highest risk is the first born male of an affected mother. (hereditary component)

27. Pyloric Stenosis
Symptoms usually occur from 3-4th week of life up to the 5th month after birth.
Symptoms:
Non-bilious, projectile vomiting
Dehydration
Visible peristaltic waves in epigastrium
Palpable pyloric “olive”
Failure to thrive

28. Abdominal Cavity Duodenal Atresia:
Congenital obstruction of the duodenum. The atresia usually occurs distal to the ampulla of Vater.
Incidence – 1 in every 10,000 live births
Females more commonly affected than males
60-70% of cases have associated anomalies
Down’s Syndrome
Prematurity
Intestinal malrotation
Congenital heart disease
Anorectal anomalies
Tracheoesophageal abnormalities

29. Duodenal Atresia Presentation: Bilious Vomiting (85%)
Abdominal distention
May pass meconium in the first 24 hours, then bowel movements cease.
Jaundice

30. Duodenal Atresia Diagnosis: History of polyhydramnios
Prenatal diagnosis
Presence of bilious vomiting
CXR with “double bubble”

32. Malrotation
An assortment of intestinal anomalies of rotation and fixation.
Unknown incidence, occurs more often in males.
Associated with diaphragmatic hernia, intestinal atresia, omphalocele, and gastroschisis.

33. Malrotation
The intestine is subject to torsion around the superior mesenteric artery, occluding the blood supply.
The intestines may also twist on themselves (midgut volvulus) and occlude the intestinal lumen.
In both cases, ischemia and bowel necrosis then result.
Malrotation with volvulus is a surgical emergency. Goal is to release strangulation of the bowel.

34. Malrotation Acute Symptoms: Bilious vomiting
Abdominal distention and pain
Rectal bleeding
Signs of shock and sepsis
“Less Acute Cases”:
Failure to thrive
Intermittent bilious vomiting
Abdominal tenderness

36. Omphalocele
The herniation of abdominal viscera into the umbilical cord, usually covered by a pertoneal sac and with the umbilical arteries and veins inserting into the apex of the defect.
Believed to be caused by incomplete closure of the abdominal wall or incomplete return of the bowel into the abdominal cavity.

37. Omphalocele Incidence : 1 in 5,000 to 6,000 live births.
Large defects may also include the stomach, liver, and the spleen.
A rupture of the omphalocele can occur at any time, exposing the abdominal contents to amniotic fluid.
Mortality rate is related to severity of other defects; with associated heart disease is 80%, without heart disease is only 30%.

38. Omphalocele 30-50% have associated anomalies: prematurity (30%)
cardiac defects (19-25%)
neurological anomalies
genitourinary anomalies
skeletal anomalies
chromosomal anomalies (45-55%)
malrotation/atresia of the intestines

41. Gastroschisis Incidence : 1 in 30,000 to 50,000 live births.
The defect is usually smaller than an omphalocele and is usually placed to the right of the umbilicus.
Believed to be caused by failed closure of the lateral fold of the abdominal wall or an intrauterine vascular accident involving the omphalomesenteric artery with disruption of the umbilical ring causing herniation of the abdominal contents.

42. Gastroschisis
Gastroschisis usually includes the small and large intestines and rarely, the liver.
The intestines are thick, edematous, and inflamed d/t exposure to amniotic fluid.
10% have intestinal malrotation and atresia,40% are either premature or SGA,but other anomalies are uncommon.
Mortality rate is 10-30%

44. Abdominal Wall Defects
Treatment:
Cover the bowel with a sterile plastic bag. Monitor the baby’s temperature, fluid and electrolytes closely.
Position the baby on his side and support the defect.
Handle bowel as little as possible, and, If necessary, use sterile gloves.

45. Necrotizing Enterocolitis
An acquired disease that affects the GI system, particularly of premature infants. It is characterized by areas of necrotic bowel, both large and small intestines.
Incidence: 70-90% occur in preterm infants.
Cases occur sporadically and in clusters
Mortality rate greatly exceeds all other GI surgical disorders.

46. NEC - Risk Factors
Most important risk factor – prematurity

47. Necrotizing Enterocolitis
Unknown etiology, a possible combination of the following five mechanisms:
Mucosal injury
Inflammatory mediators
GI immaturity
Infectious pathogens
Feedings

50. Necrotizing Enterocolitis
Breastmilk may provide some protective ingredients, but NEC can occur in infants who have received breastmilk.
Breastmilk has IgA, macrophages, non-pathogenic bacteria, and secretory molecules w/anti-bacterial properties.
The bacteria promote the growth of bacteria that excrete lactic acid and acetic acid which inhibit the growth of many pathogenic gram neg. bacteria.

51. Necrotizing Enterocolitis
Onset: Day 3 – 10 of life, preterm infants may present later in life.
Early Symptoms:
Abdominal distention – earliest sign
Gastric residuals
bilious vomiting
Bloody stools
Lethargy
Temperature instability
Visible loops of bowel

52. Necrotizing Enterocolitis
Late Symptoms:
Abdominal erythema – usually indicates peritonitis
Apnea and bradycardia – may become severe enough to require CPAP or intubation
Pneumatosis intestinalis, and/or free gas on KUB
Hypoperfusion and hypotension
Sepsis, shock, DIC

56. Meconium Ileus
Mechanical obstruction of the distal ileum d/t intraluminal accumulation of thick, inspissated meconium. It is considered a condition unique to cystic fibrosis. (Few patients w/o CF have it.)
Cystic Fibrosis – 1 in every 2,000 live births of white infants, 10-15% of cystic fibrosis children have meconium ileus.

57. Meconium Ileus Etiology: unknown, possible factors:
1. Hyposecretion of pancreatic enzymes
2. Abnormal, viscid secretions from the mucous glands of the small intestines.
Types:
Simple – an obstruction that presents in 48 hours. Treated with an enema (25-60%) Enema may need to be repeated.
Complicated – an obstruction with a volvulus, intestinal necrosis and perforation, or peritonitis with pseudocyst formation that presents in 24 hours.

58. Meconium Ileus Symptoms: Abdominal distention Bilious vomiting
Failure to pass meconium within hours
Palpable, rubbery loops of bowel. Small grapelike pellets of meconium may be palpable distally.
Complicated will present earlier. These infants will appear sicker, with signs of sepsis and respiratory distress.

59. Imperforate Anus
Several anorectal malformations characterized by a stenotic or atretic anal canal. A fistula between the rectum and the perineum, vagina, or urethra may also occur.
1 in every 5,000 live births
Etiology: Failure of differentiation of the urogenital sinus and cloaca during embryological development.

60. Imperforate Anus
20-75% of infants have associated anomalies, including: vertebral, genitourinary,cardivascular, and gastrointestinal malformations.
Classified as high or low, depending on the level of the defect. The dividing line is from the symphysis pubis to the coccyx.

62. High Imperforate Anus:
More common and more complex
More frequent in males
Rectourinary and rectovagival fistulas are common associations
Can be associated with lack of innervation, causing bowel/bladder incontinence
Diagnosed by x-ray,contrast x-ray, and ultrasound.

63. Imperforate Anus Low Imperforate Anus: Male:female ratio closer to 1:1
Perineal fistula is a common association
Diagnosed by x-ray,contrast x-ray, and ultrasound.
If a fistula is present, may be at risk for hyperchloremic acidosis from colonic absorption of urine.

64. Types of Imperforate Anus

67. Initiating Feedings
From fetal life to adulthood, the gut will atrophy if not exposed to stimuli.
In utero, fetal swallowing of amniotic fluid influences development of the gut.
Starting feeds prevents postnatal atrophy, allows intestinal motility to mature, primes the gut, and stimulates normal hormonal and enzyme secretion.

68. Initiating Feedings
The benefits of enteral feeds over parenteral feeds are:
Decreased incidence of cholestasis
Lower levels of serum bilirubin and alk phos.
Maintenance of intestinal mucosal integrity
Improved early weight gain
Decreased infection
Shorter duration of hospital stay

69. Initiating Feedings Considerations
Any significant fetal distress that can compromise the gut postnatally
Blood pressure instability, clinically significant PDA, ventilatory requirements
Maternal or neonatal drugs
Umbilical lines do not prevent the starting of feeds.

70. Initiating Feedings
Minimal enteral nutrition = 5-25 cc/kg/day - trophic feeds to prime the gut
Feeds are increased cc/kg/day w/o increasing the risk of NEC
There is no documented advantage to hypocaloric feeds (diluted formula)
Hyperosmolar (>300 mOsm/kg) feeds are associated with NEC

71. Breastmilk
AAP Recommendations: Exclusive breastfeeding for 6 month followed by continued breastfeeding as complementary foods are introduced with continuation of breastfeeding for 1 year or longer
Breast milk has bioactive molecules – provide exogenous support during vulnerable time

72. Breastmilk
Benefits of Breastfeeding VS
Risks of Formula Feeding

73. Breastmilk Passive immune protection
Direct impact on physiology – affect mucosal immune responses
Affect intestinal indigenous microflora
Mucosal barrier function
Mucosal and systemic immune maturation

74. Breastmilk Components
Immunoglobins
Not digested in stomach – works in intestines
Highest amount in colostrum, least in mature milk, very high in colostrum of preterm mothers
Binds to pathogens – make less infective
Allows maternal bacteria to flourish
Binds to dietary antigens – reduce allergenicity

75. Breastmilk Components
Amino Acids
Casein, lacotalbumin, lactoferrin, haptocorrin
Amino acids for building blocks
Have antimicrobial activity
Improve absorption of nutrients

76. Breastmilk Components
Maturation
Bacteria stimulate development of immune system
Failure of maturation can lead to atopic disease
Oligosaccharides and peptides promote growth of good bacteria
Epidermal growth factor, sCD14, transforming growth factor

77. Breastmilk Components
Antibacterial Defenses
Lysozyme – destroy gram negative bacteria
Glycans – decoys for pathogenic microbes – binds to them, prevents attachment to intestinal wall
Anti inflammatory – antioxidants, anti-inflammatory cytokines

78. Intestinal Permeability
Colostrum has hormones and growth factors that stimulate the proliferation of the absorptive cells lining the gut
Thickening of the gut wall also occurs and tight junctions form between the absorptive cells
Any formula feed can delay this process

79. Human Milk Fortifier Fortifier is a powdered cow’s milk product
Powdered fortifier cannot be made sterile
Fortifier interferes with antibacterial properties of breast milk – decreased lysozyme and IgA, decreased epidermal growth factor and transforming growth factor

80. Breastmilk
Preterm milk has increased calories, protein, sodium, chloride and decreased amounts of lactose. These differences last for the first month.
Hindmilk is higher in fat than foremilk
But…
Fortifier provides needed protien, calcium and phosphorus

81. Breastmilk Donor milk vs Formula Affects immune components
Decreased antibacterial properties
Less NEC vs formula

82. The End