Transcript Neonatal Gastrointestinal System

Neonatal Gastrointestinal
System
Carmelita Rivero, RNC
Madigan Army Medical
Center
Embryology
3,4 – Esophagus, liver, stomach,
and intestine are distinct elements.
 Weeks
7 – Intestinal loops herniate into
the umbilical cord.
 Week
9,10 – Intestines re-enter
abdominal cavity. Intestines continue to
rotate.
 Week
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
 umbilical
- common in African-American,
Down’s, hypothyroid.
 inguinal - more common in males
 femoral - more common in females
 Muscular
Development
 abnormal
recti
- prune-belly syndrome, diastasis
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
 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
development fails
to continue
General Treatment of GI
Patients
– bowel rest
 IV Fluids
 Gastric suction on low
 Antibiotics
 Surgical correction
 NPO
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
 Avoid
treatment for GE Reflux
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
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
 Symptoms
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

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



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
 Bilious
Symptoms:
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, nonpathogenic 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
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
 Onset:
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.
Imperforate Anus
 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
impact on physiology – affect
mucosal immune responses
 Direct
 Affect
intestinal indigenous microflora
 Mucosal
barrier function
 Mucosal and systemic immune maturation
Breastmilk Components
 Immunoglobins
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
 Not
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, antiinflammatory 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
The End