Neonatal Gastrointestinal System

Carmelita Rivero, RNC

Madigan Army Medical Center

EmbryologyWeeks 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 herniaasymmetric - mass, organomegaly,

intestinal obstruction

AssessmentHernias

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

AssessmentUmbilicus - abnormal

green/dark yellow staining - in utero meconium passage

wet, foul smelling, or red - infectionpersistent, clear, drainage - patent

urachusThick, gelatinous - LGAThin, small - IUGR2 vessel cord - possible congenital

anomalies

AssessmentBowel sounds

Audible within 15-30 minutes after birth Hyper/hypoactive is not necessarily

pathologic.Hyperactive - malrotation, Hirschprungs,

diarrheaHypoactive - ileus

Palpation Masses Organ Enlargement - liver 1-2 cm below

right costal margin, mid clavicular line.

Risk FactorsGI disease in familyGenetic syndromesFetal ultrasound - view of dilation or

obstructionMaternal polyhydramniosFailure to pass meconium within 24-48

hoursAbdominal distentionBilious vomiting

How does

it happen?Normal

develop-ment fails

to continue

General Treatment of GI Patients

NPO – bowel rest IV FluidsGastric suction on lowAntibioticsSurgical correction

The Esophagus

Tracheoesophageal Fistula (TEF)

Incidence : 1 in 4000 live births50-70% 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 anomalyHistory of polyhydramnios Inability to swallow saliva leads to

droolingGavage tube cannot be passedCoughing, choking or cyanosis with

feedingsAbdominal distentionRecurrent 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 RefluxCan result in:

Failure to thriveAspirationAnemiaEsophagitisApneaReflex bronchospasmSIDS-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 : PhysiologyAnatomic and functional immaturity of

the GI tract – Term Infants Immaturity of the lower esophageal

sphincter (LES) Positioning of the LESAlterations in gastric and esophageal

motilityDelayed gastric emptyingair swallowingFrequent prone positioning

GE Reflux : TreatmentTreatment 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 birthsMales are affected 4:1First 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 vomitingDehydrationVisible peristaltic waves in epigastriumPalpable pyloric “olive”Failure to thrive

Abdominal CavityDuodenal 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 distentionMay pass meconium in the first 24

hours, then bowel movements cease.Jaundice

Duodenal Atresia

Diagnosis:History of polyhydramniosPrenatal diagnosisPresence of bilious vomitingCXR 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.

MalrotationThe 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.

MalrotationAcute Symptoms:

Bilious vomitingAbdominal distention and painRectal bleedingSigns of shock and sepsis

“Less Acute Cases”:Failure to thrive Intermittent bilious vomitingAbdominal tenderness

OmphaloceleThe 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 anomaliesgenitourinary anomaliesskeletal anomalieschromosomal 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.

GastroschisisGastroschisis 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 EnterocolitisAn 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 FactorsMost important risk factor – prematurity

Necrotizing EnterocolitisUnknown 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 EnterocolitisOnset: Day 3 – 10 of life, preterm

infants may present later in life.Early Symptoms:

Abdominal distention – earliest signGastric residualsbilious vomitingBloody stoolsLethargyTemperature instabilityVisible loops of bowel

Necrotizing EnterocolitisLate 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 hypotensionSepsis, shock, DIC

Meconium IleusMechanical 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 IleusSymptoms:

Abdominal distentionBilious vomitingFailure to pass meconium within 12-24

hoursPalpable, 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 birthsEtiology: Failure of differentiation of the

urogenital sinus and cloaca during embryological development.

Imperforate Anus20-75% 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.

Imperforate AnusHigh Imperforate Anus:

More common and more complexMore frequent in malesRectourinary and rectovagival fistulas

are common associationsCan be associated with lack of

innervation, causing bowel/bladder incontinence

Diagnosed by x-ray,contrast x-ray, and ultrasound.

Imperforate AnusLow Imperforate Anus:

Male:female ratio closer to 1:1Perineal fistula is a common associationDiagnosed 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 FeedingsFrom 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 FeedingsThe 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 FeedingsConsiderations

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 FeedingsMinimal 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 AcidsCasein, lacotalbumin, lactoferrin,

haptocorrinAmino acids for building blocksHave antimicrobial activityImprove absorption of nutrients

Breastmilk ComponentsMaturation

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 PermeabilityColostrum 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 FortifierFortifier is a powdered cow’s milk productPowdered fortifier cannot be made sterileFortifier 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

BreastmilkDonor milk vs Formula

Affects immune components Decreased antibacterial properties Less NEC vs formula

The End