Module 6 – Notes
Gastrointestinal Disorders in Pediatric Patients
Cleft Lip and Cleft Palate:
Definitions / Etiology:
1. Cleft Lip -- A facial deformity involving a fissure or elongated
opening resulting from incomplete merging of embryonic
processes (during the 6th week of gestation) that normally
form the face or jaws. The defect may be either an
autosomal recessive or a conditioned dominant inheritance.
40% occurs with cleft palate.
2. Cleft Palate -- The cleft palate results from the failure of the
maxillary processes to fuse completely. The defect may be
inherited.
Assessment:
Assessment is made at birth or as part of the newborn
assessment and includes describing the location and extent of the
defect. Cleft lip can be a simple dimple in the vermilion border of
the lip or a complete separation extending to the floor of the nose.
Can be unilateral, bilateral, or midline.
Management and Nursing Care:
Treatment of cleft lip is complex involving many specialists including
plastic surgeons, nurses, ear, nose, and throat specialists,
orthodontists, audiologists, and speech therapists. Reconstruction
begins in infancy and can continue through adulthood.
Pre-op:
1. Maintain nutrition and preventing aspiration – infant has a
decreased ability to suck and lack of vaccum in mouth.
 May breast feed if has small cleft lip. More difficult to
breast feed with cleft palate.
 Bottle feeding -- Teach mother to feed with special
nipples or feeding devices such as a soft nipple with an
enlarged cross cut hole. Using specially made nipples for
feeding allows the infant to meet sucking needs and
muscle development for later development of speech.
 May use the ESSR system:
E = enlarge the opening
S = stimulate the suck reflex
S = swallow fluid appropriately
R = Rest when the infant signals
 Feed slowly and Bubble frequently – have a tendency to
swallow excessive amounts of air
 Hold in upright position during feeding
 Keep bulb syringe and suction equipment at bedside
 Position on side after feeding
2. Support to the family
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Assist parents in accepting a birth defect. May become
preoccupied by the baby’s appearance and experience
negative feelings toward the baby.
Help parents hold the infant and facilitate feeding process
Point out positive attributes of infant
Encourage parents to participate in caretaking activities
Explain surgical procedure - Introduce items before
surgery such as:
o Introduce cup, soup spoon prior to surgery
o Practice arm restraints on kid, teach parents
Post-op:
1. Prevent trauma to suture line
 Do not allow to suck
 Position on back or side with support on both sides to
prevent rolling
 Maintain lip protective device
 Maintain soft elbow restraints to prevent access to
operative site. Be sure to remove periodically to exercise
the arms and assess the skin. Do not leave unattended
when restraints are removed.
 Use jacket restraints on older kid
 Feed with syringe with rubber tubing
 Avoid hard objects in the oral cavity – thermometers,
tongue depressors, straws, forks until healing is complete.
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2. Reduce pain – which minimizes crying and stress on the
suture line.
3. Prevent infection
 Cleanse suture line after each feeding and prn with
normal saline or sterile water
 Give small amounts (5-15 ml) of water after feeding to
rinse away milk residue that could lead to bacterial
growth
 Keep suture line dry
 Call MD if increased swelling, excessive bruising, heat,
redness, drainage, fever, change in behavior, pain not
relieved by usual means, or any other concerns.
4. Follow –up and Referrals /Health Promotion and Maintenance:
 Teach parents how to bundle infant in blanket with arms
tucked inside to prevent infant from touching the sutures.
 Refer to Home Health nurse
 Social worker
 Crippled Services for financial aid
 Cleft Parent Support Group
 Speech therapy, Orthodontist, hearing loss may be due to
change in the Eustachian tubes
Esophageal Atresia
Etiology and Pathophysiology:
Esophageal atresia and tracheoesophageal fistula are congenital
defects of the esophagus An atresia is the absence or closure of a
normal body orifice or tubular passage.
In esophageal atresia there is failure of the esophagus to develop as
a continuous tube during the fourth and fifth weeks of gestation.
The gut fails to lengthen, separate, and fuse in to two parallel tubes,
the esophagus and the trachea. Instead the esophagus may end in
a blind pouch or develop as a pouch connected to the trachea by a
fistula called a tracheoesophageal fistula.
The types are esophageal atresia and tracheoesophageal fistula.
TEF is associated with other anomalies of the heart, GI, GU, and
musculoskeletal system.
Assessment:
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Excessive amounts of salivation / mucus, frothy bubbles in
the mouth and sometimes nose
Three “C’s” - Coughing, choking, and cyanosis when fed,
overflow may be aspirated
Food may be expelled through the nose immediately
following the feeding
Rattling respirations and frequent respiratory problems such
as aspiration pneumonia
Gastric distention, if fistula
History of polyhydramnios during pregnancy can suggest a
high gastrointestinal obstruction
Diagnosis:
Diagnosis is usually confirmed by attempting to pass a #8 ng tube
into the stomach and it meets resistance can only be advanced
minimally. Specific diagnosis is made by x-ray.
Management and Nursing Care:
Surgical correction usually done as soon as the infant is stable.
They ligate the fistula and anastomose the two ends of the
esophagus and close the fistula.
Pre-op:
1. Maintain patent airway and prevent aspiration pneumonia.
 Keep NPO and administer IV fluids
 Position with head elevated about 30 degrees
 Suction to prevent accumulation of oral secretions in the
blind pouch
 Insertion of gastrostomy tube for feedings
Post-op:
1. Maintain a patent airway
 Gentle suctioning
 Observe for respiratory distress or airway obstruction –
tachypnea, abnormal breath sounds
2. Maintain nutrition
 NPO – until bowel sounds return and no danger of
disturbing the surgical site.
 Adminster IV’s
 Total Parenteral Nutrition (TPN) and then Gastrostomy
tube feedings
3. Prevent trauma to anastomosis
4. Monitor weight and growth and developmental achievements
Pyloric Stenosis
Etiology / Pathophysiology:
The pylorus muscle which is at the distal end of the stomach
becomes thickened causing constriction of the pyloric canal between
the stomach and the duodenum and obstruction of the gastric outlet
of the stomach. Narrowing related to muscular hypertrophy,
spasms, and edema of the mucous membrane. Usually occurs in the
first weeks of life. Etiology unknown.
Assessment:
Clinical Manifestations:
1. Vomiting – progresses in frequency and the force is projectile of
3-4 feet.
2. Constant hunger and fussiness – infant wants to feed after
vomiting episode
3. Distended upper abdomen with visible gastric peristaltic waves
that move from left to right across the epigastrium especially
when feeding
4. Hypertrophied pylorus (olive shaped) seen in right epigastric
region
5. No pain
6. Weight loss
7. Dehydration and electrolyte imbalance
Diagnosis:
1. History and Physical examination
2. Ultrasound
3. Lab values – low Na and K+; metabolic alkalosis = decrease
in serum chloride levels and increase in pH and bicarbonate
Management and Nursing Care:
Surgical correction by a pyloromyotomy (Fred Ramstedt
procedure) or laproscopy
Pre-op:
1. Restore hydration and electrolyte balance
 NPO – stomach decompression and gastric lavage
 Careful monitoring of intake and output, urine specific
Gravity, vomiting, stools.
 Daily weighs
2. Support to parents – need to know it is a structural problem
and in no way a result of their parenting skills.
Post-op:
1. Monitoring of intake and output
2. Feeding begins with clear liquids containing glucose and
electrolytes. Regime example: 8 hours NPO, 10cc sterile
hater feed X 2. Increase to 15cc X 2, progressing to ½
strength formula, then full strength formula. Observe and
record the infant’s response to feeding.
3. Position with head slightly elevated
4. Assess surgical site and keep free from infection
5. Teach parent’s signs and symptoms of reoccurrence.
Gastroesophageal Reflux (GER)
Definition/ Pathophysiology:
The cardiac sphincter and lower portion of the esophagus are
weak allowing regurgitation of gastric contents back into the
esophagus. Due to a dysfunction / relaxation of the lower
gastroesophageal sphincter or delay in gastric emptying.
Assessment:
Clinical Manifestations:
Infants:
1. Regurgitation almost immediately after each feeding when
the infant is laid down
2. Excessive crying, irritability
3. Failure to thrive (FTH), weight loss
4. Reflux of the gastric contents predisposes the infant to
aspiration and the development of respiratory problems /
apnea.
Child:
1. Heartburn
2. Abdominal pain
3. Cough, recurrent pneumonia
4. Dysphagia
Management and Nursing Care:
1. Small frequent feedings of predigested formula of thicken the
formula
2. Frequent burping
3. Positioning --prone position- flat prone or head elevated
prone. Supine position is not used because it worsens the
GER. Avoid excessive handling after feedings.
4. Medications: Tagamet, Zantac, and Pepcid are used to
reduce gastric acidity. Reglan may be used to promote
gastric emptying.
5. If history of apnea, bradycardia r/t GER needs continuous
cardiac and apnea moinitoring. Arrange for CPR teaching for
the caregivers.
6. If infant doesn't respond to non-invasive therapy then a
Nissen fundoplication may be done to increase the
competence of the cardiac sphincter
Abdominal Wall Defects - Gastoschisis and
Omphalocele:
Gastroschisis – herniation of abdominal viscera outside the
abdominal cavity through a defect in the abdominal wall to the side
of the umbilicus. Not covered.
Omphalocele – herniation of abdominal contents through the
umbilical cord. Contents are covered by a translucent sac.
Diagnosis:
 Elevated Maternal serum alpha-fetoprotein.
 Routine Prenatal Ultrasound
 Direct observation after delivery
Nursing Care:
Pre-operatively – focus is on protection of the contents / sac. Cover
with warm, sterile, saline-soaked dressings over the defect. May
choose to replace the gut to the abdomen gradually over several
weeks. May place silo or silastic material over gut until it returns to
the abdomen. Surgery used to close defect. Provide for
thermoregulation and manage fluid volume.
Postoperatively – assess for ileus, maintain parenteral feedings, and
provide support to the parents.
Intussuception
Definition / Etiology:
Intussusception occurs when one segment of the bowel
telescopes into the lumen of an adjacent part of the intestine. It is
usually at the junction of the ileum with the colon. This leads to an
obstruction. The bowel becomes inflamed and edematous and
bleeding can occur. Can lead to necrosis and peforation.
Most commonly seen in infants 3-12 months.
Assessment:
Clinical Manifestations:
1. Colic – Intermittent abdominal pain at first and then constant
severe pain. Child frequently pulls knees to chest when pain
occurs.
2. Vomiting – sometimes can contain stool
3. Currant jelly-like stool – blood and mucus in the stool
4. Diarrhea
5. Dehydration
6. Ischemia, perforation, and shock are serious complications
Diagnosis:
1. X-ray of the abdomen revealing intraperitoneal air
2. Abdominal ultrasound
Management:
 Hydrostatic reduction -- Try non-surgical measures first. May
do an air enema (insufflation) blowing air in the bowel cavity
or barium enema. The force exerted by the air or flowing
barium is sufficient to push the telescoped portion of the
bowel into its original position
 Surgery – usually done if child is in shock or perforation of
bowel has occurred.
Nursing Care:
 NPO – NG tube inserted
 Assess bowel sounds
 Monitor for passage of barium or stool
 Gradual introduction of fluids and solids
Volvulus
Volvulus is a twisting of the bowel that leads to a bowel obstruction.
Signs and Symptoms:
vomiting of fecal material, abdominal distention and pain.
Treatment and Nursing care:
Resection of the portion of the bowel that is twisted or necrosed.
Child may have a temporary colostomy until the bowel heals.
Nursing care is similar for the child who had bowel surgery.
Hirschsprung's Disease
Etiology and Pathophysiology:
A disorder in which there is a congenital absence of parasympathetic
nerve ganglion cells in the large intestine / distal bowel. As a result,
this portion of the bowel is unable to transmit regular peristaltic
waves, which are coordinated with the proximal portion of the
bowel. When a stool reaches the affected bowel, it is not
transmitted on down the colon leading to accumulation of fecal
material and distention of the bowel proximal to the defect and then
bowel obstruction.
Thought to be a failure of embryonic migration of the hindgut
ganglion cells to the lower colon.
Assessment:
Clinical Manifestations:
1. Failure to pass meconium in first 24-48 hours in the newborn
2. Vomiting and reluctance to feed
3. Abdominal distention
4. Signs of intestinal obstruction
5. Foul odor of breath and stool
6. Older child – constipation, offensive and ribbon-like stools,
history of regular laxative use, palpable fecal mass
Diagnosis:
History and Physical
Barium enema
Rectal biopsy – absence of ganglionic cells in bowel mucosa
Management and Nursing Care:
1. Surgical Intervention
One type of repair is a colostomy, dissection of the nonfunctional bowel and anastomosis, later closure of temporary
colostomy.
Second type of repair is a one stage resection of the nonfunctional bowel and re-anastomosis. Laparoscopic-assisted
pull-through.
Nursing Care:
Pre-op:
1. Cleanse the bowel - Enemas until clear. Neomycin per rectum
2. NPO
Post-op:
1. NPO, NG tube, replace fluids with IV.
2. Monitor vital signs – NO rectal thermometers
3. Monitor for abdominal distention, bowel sounds
4. Assess incision for signs of infection
5. Administer pain medication
6. Assess colostomy site for bleeding and impaired skin
integrity. Teaching regarding colostomy care if this was done.
Appendicitis
Etiology and Pathophysiology:
Inflammation of the lumen of the appendix which becomes
quickly obstructed, yielding edema, necrosis and pain.
Assessment:
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Clinical Manifestations:
1. Abdominal pain – initially the pain may be vague and poorly
localized to the periumbilical area and gradually becomes
more intense and moves to the right lower quadrant.
2. Silent abdomen – no bowel sounds
3. Anorexia and nausea with or without vomiting
4. Diarrhea
5. Elevated temperature
6. If perforated – initially experience relief of pain. High fever
and dehydration/
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Diagnosis:
1. History and Physical - abdominal pain
2. Elevated WBC -- 15,000 – 20,000
3. Abdominal x-rays or abdominal ultrasound
Management and Nursing Care:
Surgery – appendectomy:
Pre-op
 NPO
 IV fluids to correct fluid and electrolyte imbalances
 Positions of comfort – try other methods beside giving
analgesics. Analgesics can mask the the signs of possible
rupture
 Antibiotics
 Cold application – no heat
 NO enemas or laxatives
Post – op
 NPO until intestinal peristalsis returns
 Antibiotics
 Pain medication
 D/c’d in several days if no complications. Teaching includes:
1. Care of incision
2. Decreased activity -- no contact sports, P.E., or heavy
lifting until permission from MD
3. Call MD if incision has increased redness, drainage,
opening, if pain increases and is not relieved by pain
medications, vomiting, decreased appetite, abdominal
swelling, increased temperature, change of behavior, or
any other concerns.
Diarrhea / Gastroenteritis – Severe
Etiology and Pathophysiology:
Diarrhea is seen when there is a disturbance of the intestinal tract
that alters motility and absorption and accelerates the excretion of
intestinal contents (3-30 stools per day).
Rapid emptying of the bowel results in loss of fluids and electrolytes
and impaired absorption of nutrients and water. This leads to
dehydration, electrolyte imbalances, and metabolic acidosis. Most
infectious diarrheas in this country are caused by a virus / Rotovirus.
Diarrhea can be separate disease, or it may be a symptom of
another disease, food, or dairy intolerance, or drug reaction.
Assessment:
 Clinical Manifestations:
1. Increased rate or peristalsis carrying intestinal contents (K+,
Na, Cl, H2O, bicarb) including base-bicarbonates along.
2. Large volume stools, loose to watery, blood, pus, or mucus in
stools, which are often green in color
3. Increase in frequency of stools (2-10 stools)
4. Cramps, nausea and vomiting
5. Urge to defecate with small stool present
6. Increased heart rate and repiratory rates, decreased tearing.
fever.
Dehydration:
1. Mucous membranes become dried and cracked
2. Skin dries and loses its normal elasticity, poor skin turgor
3. Fontanels are depressed and eyes appear sunken
4. Urine decreases greatly in amount and becomes dark in color
(concentrated)
Metabolic Acidosis:
1. Increased heart rate, decreased BP, increased Respirations,
arrhythmias
2. Cold, clammy skin
3. Changes in level of consciousness – stupor, lethargy
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Diagnosis:
o Stool culture – find causative organism
o Stool Test for O&P
o Diagnose Metabolic Acidosis – arterial blood gases reveal
decreased pH (under 7.35), a low HCO3 value (near or below
22 mEq/L)
Treatment and Nursing Care:
1. Restore fluid and electrolyte balance – oral rehydration
(Pedialyte), early reintroduction of foods
2. Weigh daily
3. Monitor intake and output – accurate recording of the number
and consistency, and odor of stools
4. Assess for signs of dehydraton
5. Isolate according to institution policy – infant should wear
disposable diapers and follow Standard Precautions.
6. Monitor electrolytes and for signs of metabolic acidosis.
7. Provide skin care to prevent excoriation.
Intestinal Parasitic Disorders
Intestinal parasitic disorders occur when there is lack of treated
water and food incorrectly prepared, or poor sanitation.
Most common is pinworms and roundworms. Others are hookworm.
Signs and symptoms:
Diarrhea, vomiting, anorexia, failure to thrive. Abdominal cramps.
Treatment:
Anthelmintics – mebandazole and pyrantel pamoate. Stools should
be examined 2 weeks after treatment and monthly for 3 months.
Complication:
Bowel obstruction with roundworms.
Failure to thrive
Celiac Disease
Celiac disease results from the inability to digest gliadin which is a
by-product of gluten breakdown. Inability to digest gliadin results in
the accumulation of the amino acid glutamine which is toxic to the
mucosal cells in the intestines. Damage to the villi impairs the
ability of the small intestines to absorb nutrients.
Signs and symptoms:
Diarrhea and failure to thrive are the most common. They may also
exhibit abdominal distention, vomiting, anemia, irritability, anorexia,
muscle wasting, edema.
Complications:
Hypocalcemia, osteomalacia, osteoporosis, depression.
Diagnosis:
measurement of fetal fat, duodenal biopsy, Serum screening for IgA
antibodies.
Nursing Care:
Lifetime dietary treatment – total exclusion of gluten from the diet –
barley, wheat, rye.
Care focuses on parent teaching and child teaching on ways to
eliminate gluten from the diet.