Neonatal Gastrointestinal System Carmelita Rivero, RNC Madigan Army Medical Center

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.

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.

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

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

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

Assessment Bowel sounds Palpation Audible within 15-30 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.

Risk Factors GI disease in family Genetic syndromes Fetal ultrasound - view of dilation or obstruction Maternal polyhydramnios Failure to pass meconium within 24-48 hours Abdominal distention Bilious vomiting

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

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

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

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

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

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%

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.

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.

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

GE Reflux : Symptoms Fussiness Irritability “Colic” Failure to thrive Excessive regurgitation/vomiting Refusal of feeding Back arching with feeding Gagging Excess swallowing (about 30-60 minutes after feeding)

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

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

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

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)

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

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

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

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

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.

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.

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

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.

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%.

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

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.

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%

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.

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.

NEC - Risk Factors Most important risk factor – prematurity

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

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.

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

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

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.

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.

Meconium Ileus Symptoms: Abdominal distention Bilious vomiting Failure to pass meconium within 12-24 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.

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.

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.

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.

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.

Types of Imperforate Anus

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.

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

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.

Initiating Feedings Minimal enteral nutrition = 5-25 cc/kg/day - trophic feeds to prime the gut Feeds are increased 10-20 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

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

Breastmilk Benefits of Breastfeeding VS Risks of Formula Feeding

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

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

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

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

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

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

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

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

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

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