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Gastrointestinal Gastrointestinal Disorders Disorders in Childrenin Children
Dr. Nataliya Haliyash
Nursing Care of Children
Upon completion of this lecture, the students will be able to:
Describe the anatomy and physiology of the gastrointestinal (GI) system of the infant and child and how it differs from the adult GI system.
Describe the etiology, pathophysiology, clinical manifestations, diagnosis, and treatment of common GI alterations.
Explain how the pathophysiology is associated with the clinical manifestations of common GI alterations.
Discuss nursing management and interventions appropriate for children requiring abdominal surgery for specific disorders.
Identify the educational needs for families and describe appropriate content to be taught by the nurse.
Gastrointestinal Tract of a Child
Peculiarities of Gastrointestinal System of Neonate and Child Sucking and swallowing are automatic
reflexes initially, gradually coming under voluntary control as the nerves and muscles develop by 6 weeks of age.
The newborn's stomach capacity is only 10 to 20 ml
It expands rapidly to 200 ml by one month of age and reaches adult capacity of 2000-3000 ml by late adolescence.
Gastric emptying time:– 2 to 3 hours in the newborn – 3 to 6 hours by one to two months of age.
Peculiarities of Stomach of Neonate and Child The stomach lying horizontally, is round until
approximately 2 year of age. In horizontally lying of baby the gastric fundus is
lower as the antral part of the stomach. Lower esophageal sphincter has a poor development
of mucous membrane and muscular layer, its tone is decreased or relaxed.
Pyloric sphincter is developed well. The fundus of stomach is under the left dome of
diaphragm. Gastroesophageal reflux and regurgitation is frequent
in infants.
Peculiarities of Gastrointestinal System of Neonate and Child
Gastric acid secretionis deficient in several digestive enzymes that are usually not sufficient until 4-6 months of age.
Stomach pH is 5, comparing to 2 in adults. ↓ pancreatic enzyme activity:
– ↓ amylase, responsible for the initial digestion of carbohydrates, is insufficient resulting in an intolerance of starches.
– If cereals are given before 4-6 months, the infant may develop gas and diarrhea.
– lactase breaks down or hydrolyzes lactose. Lactase levels are low in the preterm infant, increase in infancy, and decline after early childhood.
– ↓ lactase level results in incomplete absorption of lactose, which can cause gas, abdominal distention, and diarrhea.
– ↓ lipase, responsible for digestion and absorption of fats. Fat in breast milk is absorbed more readily than in formula because human milk contains lipase.
Peculiarities of Gastrointestinal System of Neonate and Child
The infant's first stool is meconium– sticky and greenish black. – composed of intrauterine debris, such as bile pigments, epithelial
cells, fatty acids, mucus, blood, and amniotic fluid. – Passage of meconium should occur within the first 24 hours.
transitional stools:– appear by the third day after the initiation of feedings. – greenish brown to yellowish brown in color, less sticky than
meconium, and may contain some milk curds. typical milk stool:
– is passed by the fourth day. – In breast-fed infants the stools are yellow to golden in color and pasty
in consistency, with odor, similar to that of sour milk. – In infants fed cow's milk formula, the stools are pale yellow to light
brown, are firmer in consistency, and have a more offensive odor. Breast-fed infants usually have more stools than do bottle-fed
infants. The stool pattern can vary widely; six stools a day may be normal for one infant, whereas a stool every other day may be normal for another.
Peculiarities of Liver of Neonate and Child
The liver, from a gastrointestinal standpoint, is an exocrine gland that produces bile to digest fats.
The liver remains functionally immature until approximately 1 year of age
Physiologic or normal jaundice of neonate
During uterine life, more hemoglobin (HbF) is required to carry oxygen since the oxygen tension available to the fetus is decreased.
After delivery, the newborn no longer requires this extra hemoglobin and the excess cells are destroyed by the reticuloendothial system and not replaced.
When the erythrocytes are broken down, the end products of metabolism are formed, and hemoglobin becomes a protein, consisting of globin and heme.
Unconjugated (indirect) bilirubin is formed in the liver and spleen from these byproducts, and then binds to albumin in the plasma.
Since newborn albumin has limited binding capacity, a significant amount of unconjugated bilirubin accumulates and plasma concentrations may become elevated.
It results in visible jaundice
Physiologic or normal jaundice of neonate
should be investigated per hospital protocol, such as obtaining blood levels for the total and direct bilirubin.
shows a gradual rise in bilirubin of 8 mg/dL at 3-5 days after birth. The level falls to normal the second week of life.
Pathologic or abnormal jaundice – extreme elevation in bilirubin within the first 24 hours
of life.– the unconjugated level is >12 mg/dL when the baby
is formula-fed, – >14 mg/dL if the baby is breast-fed, – or if the jaundice is persistent past 2 weeks of age
further evaluation is warranted.
GI Disorders Categories
Structural Defects Inflammatory Disorders Disorders of Motility Disorders of Malabsorption
Structural Defects
Cleft lip and Palate 1:2000 births – varying degrees of severity 20-30% will have other congenital defects Incomplete fusion in first trimester Multidisciplinary management – speech, hearing
(prone to AOM), dentistry, plastic surgery, orthodontics Repair at 2-3 months (lip), at 18mos for palate,
restrain arms, minimize crying, upright (car seat to sleep), iced gauze, special long nipples for fdg, clean suture between fdg (water per bottle), antibiotic cream to sutures, no straws, metal utensils
Aspiration, family coping, altered nutrition, infection, ineffective breathing pattern, tissue integrity, (Parent) knowledge deficit
Cleft lip / palate can be unilateral and bilateral
Cleft lip and Palate
Cleft lip and palate surgery
Cleft lip repair. The edges of the cleft between the lip and nose are cut (A and B). The bottom of the nostril is formed with suture (C). The upper part of the lip tissue is closed (D), and the stitches are extended down to close the opening entirely (E).
Read more: http://www.healthofchildren.com/C/Cleft-Lip-and-Palate.html#ixzz0iKdghP7l
Teaching plan for caregivers related to
feeding an infant born with bilateral CL/CP. Anatomy and functioning of the palate Successful feeding techniques Breastfeeding can be accomplished If breastfeeding is unsuccessful, a breast pump may be used If breastfeeding, have mother place warm washcloth on breast to encourage let-down
prior to having infant latch on If bottle feeding, try regular nipple first Enlarging the nipple hole with a cross cut allows the infant to receive the formula in
the back of the throat, bypassing the sucking problem Stimulate sucking the lower lip by rubbing it with the nipple Place nipple in mouth and invert and infant will swallow Allow the infant to rest Facial expressions will change before choking and gagging by elevation of eyebrows
and wrinkling of forehead. Remove nipple slowly and gently from mouth Allow frequent rests Allow infant to consume 3–4 ounces Special nipples are available if needed An asepto syringe can be used if infant is unable to ingest adequate amounts with
nipple Caregivers also need to know who to call if help is needed
Infants with a cleft lip and palate or isolated cleft palate are usually not successful at breastfeeding directly from the breast. Using a breast pump and feeding breastmilk with a special bottle is encouraged.
If your baby is tiring easily and taking longer than 45 minutes to feed, then you should try the Mead-Johnson plastic squeeze bottle. It will probably take you and your infant a few tries to get the hang of using this so don't worry. It is important to relax and get to know your baby's feeding habits.
Here are a few tips that have helped other parents using the Mead-Johnson plastic squeeze bottle:
Before putting the nipple in the infant's mouth, gently squeeze the bottle so you can tell how much pressure is needed to get an even flow.
You may use different nipples with this bottle - premie nipples or Nuk orthodontic nipples also work well.
Don't wait until your baby is tired to begin squeezing the bottle - you should be applying pressure from the beginning of the feeding to prevent fatigue!
Do not squeeze formula into the mouth when the infant is resting. This could cause the baby to choke. It also disturbs the natural suck/swallow pattern.
If the baby falls asleep, you may want to unwrap the blanket, tickle the feet, or try another method that has worked in the past to awaken the baby.
Relax! Holding the baby in an upright position will prevent milk from coming through the nose during feeding. If this does happen, use the bulb syringe to gently clean the area.
Caring for families whose child has a cleft lip/palate
Help caregivers to understand this condition by explaining that:
1. Clefting occurs by the 35th day after conception, which is often before a woman knows she is pregnant.
2. The mother needs reassurance that she did nothing wrong during the pregnancy.
3. Many caregivers feel guilty about having a child with this disorder. Counsel caregivers appropriately.
4. Nothing is missing from their child's face.The pieces just need to be put together.
http://diapywipey.com/cleft-palate-bottles-buyers-guide
Esophageal Atresia & Tracheoesophageal Fistula Incomplete esophagus in 4-5th wk gestation 1:4000 births with 30% premature clinical manifestations:
– presents with copious, fine, frothy bubbles of mucus in the mouth and occasionally in the nose.
– secretions may clear with aggressive suctioning but will return. – ↑ salivation/drooling, – Rattling respirations and episodes of coughing, choking, and
cyanosis may occur and may be exaggerated with feeding, abdominal distension will also occur if a fistula is present between the esophagus and the trachea, pneumonia, air trapping in abdomen
Blind pouch, fistula with trachea or only fistula with trachea ↑ chance of associated anomalies Attempt NG placement, X-ray, echo, ultrasound – diagnostic tests Surgical emergency – Surgery in several stages (TPN then G-
tube) Very good prognosis
Esophageal Atresia &
Tracheoesophageal Fistula
Pyloric Stenosis Narrowing of pyloric sphincter (stomach to small
intestine) – obstruction– 2-8 weeks old, gradual onset and severity of
vomiting – projectile, BM/formula vomit without bile, easily re-fed, pyloric “olive” palpable below the liver edge, jaundice possible, wt loss, dehydration, gastric peristaltic waves, alkalosis
– Diagnose with an upper GI series– Make child NPO, monitor and replace needed fluid
& electrolytes IV, NG to suction, surgery– Begin small, freq. feedings 4-6 hours following
surgery (CL then ADAT)
Early signs of HPS
1. The infant is hungry and wants to be fed again, in spite of feeding and vomiting.
2. The infant does not act or look sick. 3. The vomiting becomes more and more
forceful, sometimes ejected several feet. This is the clue that it is structural in nature and not from other causes such as an infection.
Gastroesophageal Reflux
Normally caused by an incompetent/poorly developed lower esophageal (cardiac) sphincter – very common ~50% of all infants
Peak at 1-4 months Infants – reduce vol of fdgs, thickening formula fdgs
(rice cereal – doesn’t work with BM), keep infant upright after fdgs, smoke exposure elimination
Chn – sm, freq meals, limit contributing foods (acidic, caffeine, carbonated, peppermint, fatty/greasy foods), no food just before bed
Medications may be required intermittently or continuously
Differentiate between hypertrophic pyloric
stenosis and gastroesophageal reflux
In hypertrophic pyloric stenosis, the pyloric sphincter hypertrophies and increases to four times its normal width.
This results in a narrowed opening and gastric outlet obstruction, preventing the gastric contents from emptying into the duodenum.
This results in nonbilious vomiting, which increases in frequency and becomes projectile.
Gastroesophageal reflux refers to the regurgitation of gastric contents into the lower esophagus due to a decreased tone or relaxed esophageal sphincter, which is common in many healthy infants. It can result in respiratory disorders, esophagitis and its complications, as well as malnutrition if it is pathologic.
The American Academy of Pediatrics recommends
placing the infant with gastroesophageal reflux in the prone position. Although SIDS has been attributed to suffocation in the prone position, this was associated with puffy bedding materials. Eliminating these factors and placing the infant with reflux in the prone position is the safest position.
Gastroesophageal refluxdisorders GERD
1:300 infants Poor wt. gain (FTT), respiratory problems,
behavior problems, pain Diagnose with clinical history, Upper GI series
and endoscopy, pH probe, milk allergy testing Tx depends on severity
– Mild will tx like GER and resolve by 12-18 months– Severe may require medications and/or surgery
(Nissen fundoplication)
Omphalocele
Intraabdominal contents herniated though umbilical cord – 1:5000 births
Covered by sac (no sac is Gastroschisis 1:10,000 births)
Inc chance of other anomalies Protect sac (sterile, NS soaked gauze),
fluids, warmth, surgical repair (one to several stages of repair)
Prosthetic silo – 5-10 days prior to surgery
Omphalocele
Intussusception Intestine folds into itself like a telescope -
obstruction Fatal if not diagnosed and treated quickly
– Shock or sepsis within 12-24 hrs– Most common in boys, 3 mo - 6 yrs– N/V, acute, colicky, severe abd pain; child
screams and draws knees to chest, sausage-shaped mass, bloody, mucous “currant-jelly” stool, listlessness, lethargic, pale, weak, previous viral infection, constipation, parasites, foreign body ingestion
– Fluid & electrolytes, monitoring, NG to sux, pain meds, antibiotics, barium/air enema (diagnostic &/or corrective), X-ray, surgery
Intussusception
Intussusception
Nonsurgical treatment for intussusception is preferred.
This involves hydrostatic reduction using barium, a water soluble contrast agent, or air enema. The water soluble agent or air insufflation is considered safer with less risk of perforation of the bowel.
Hirschsprung’s Disease “Megacolon”, “Congenital Aganglionosis” –
Aganglionic cells in part(s) of the bowel– M>F, > with T-21 and congenital heart defects– At birth, fail to pass meconium, anorexia,
abdominal distension and emesis – Diagnosed: clinical hx, bowel patterns, lower GI
series, rectal biopsy– > birth (<5cm affected), ribbon-like, foul-smelling
stools; intestinal obstruction, abd discomfort/distension, bloating, distention, constipation, FTT, anemic (fever, GI bleeding & diarrhea = enterocolitis, life-threatening)
– Fluids & electrolytes, monitoring, NG to sux, pain meds, antibiotics, barium/air enema, rectal irrigation (bowel prep), surgery
Hernias Protrusion of organ (part of) through muscle wall
of cavity Diaphragmatic hernia
– Life-threatening – severe respiratory distress (50% survival rate)
– Must stabilize before surgery (Imaging, O2, NG to sux, Ventilator)
Umbilical hernia– Most common (1:6), F>M, LBW, T-21 and hypothyroidism– <2yo, prematurity, soft swelling at umbilical site, mass comes
and goes, easily reducible– Most resolve by 3-4 years of age– Discharge parents with s/sx of incarceration– Referral to surgeon – incarceration, inc after 2 yrs, little/no
improvement by 4yrs with large hernia
Hernias
Any incarcerated hernia may be life-threatening – Bowel trapped in inguinal canal,
strangulated– Tense, tender mass, fever, abd pain/rigidity,
shock– Reduction, fluid & elec replacement,
monitoring, NG, pain meds, antibiotics, surgery
Hernias
Inflammatory Disorders
Appendicitis Infected, inflamed appendix (teens – young
adults)– Abdominal pain, but this may be vague and poorly
localized in the periumbilical area. The pain gradually migrates to the RLQ.
– Anorexia and nausea with or without vomiting may occur but usually begin after the abdominal pain.
– Constipation or diarrhea may be present, and the child’s temperature may be normal or slightly elevated.
– Emesis, low-grade fever, inc WBC, rebound tenderness LR quad (McBurney’s point), rigid abd, dec/absent bowel sounds
Appendicitis
– Immediate bowel rest, then appendectomy (24-48 hrs of first symptoms)
– Rupture – fever rises sharply, peritonitis, sudden pain relief (diffuse pain), inc abd distention, tachycardia, shallow tachypnea
– IV antibiotics, fluids, electrolytes– Appendicitis is difficult in children because
the clinical manifestations are atypical. This increases the incidence of perforation.
Necrotizing Enterocolitis “Toxic megacolon” – inflammatory disease
(intestinal ischemia, bacterial/viral infection, gut immaturity)– Primarily with prematurity– Fever, explosive bloody diarrhea, emesis, abd
distention/tenderness, severe electrolyte imbalances, shock, sepsis, death
– Fast IV fluid and electrolyte replacement, antibiotics, NPO, OG to suction, TPN, immediate surgery resection
– BF has shown some protection
NEC
Meckel’s Diverticulum
Out-pouching of ileum that secretes acid – irritation and ulceration
1-3% of general population Symptoms appear by 2 yo, M>F Painless rectal bleeding, abdominal pain
rare, severe case will perforate &/or cause peritonitis (many may be asymptomatic)
Surgery – very good prognosis
Inflammatory Bowel Disease Crohn’s
– Chronic, inflammation of random segments of GI tract, and move around – through the wall involvement
– Often develop enteric fistulas between loops of bowel &/or nearby organs
– Often develops between 15-25 years of age– Subtle onset, crampy abd pain, diarrhea, fever,
anorexia, wt loss, malaise, joint pain, greatly inc rate of cancer
– Anemia common, inc ESR, hypoalbuminemia
Inflammatory Bowel Disease Ulcerative colitis
– Chronic, recurrent disease of colon & rectal mucosa– Inflammation, ulceration, hemorrhage, edema –
localized in a portion of the GI tract (may be removed)
– Peak onset at 12 years of age– Diarrhea, lower abd pain with passage of stool and
gas, blood & mucous in stool, anorexia, weight loss Treatment same for both Crohn’s and UC
– Antibiotics, anti-inflammatory, immunosuppressive, antidiarrheal, nutrition counseling (high protein/carb with low fiber diet), surgery
Peptic Ulcer
Erosion in lower end of esophagus, stomach or duodenum – M>F, rare in children
Abd pain (burning) with empty stomach, emesis & pain with meals, anemia, blood in stools, abd distention
Primary – healthy children Secondary – response to a preexisting
illness/injury, certain meds (aspirin, NSAIDs, steroids), Helicobacter pylori
Disorders of Motility
Constipation Formation of hard, dry stools, oozing of liquid stool
past impaction (often with an abnormal frequency) Disease, diet, psychological, ineffective peristalsis
(hypothyroidism, meds), obstruction (stricture, stenosis), Hirschsprung’s, lesions of spinal cord (muscle weakness)
Rare in infants, most common with toddlers – preschool age
Bananas, rice, cheese, milk – constipating foods Inc fluids and high-fiber foods (whole grain breads,
raw fruits and vegetables)
Disorders of Malabsorption
Celiac Disease
Genetic disorder – inability to digest gluten– 9-12 mo, diarrhea, abd distention, emesis,
anemia, malnutrition, steatorrhea, pale, watery and foul smelling stools; muscle wasting, edema, low serum albumin, wt loss, anorexia
– Fluids & electrolytes, monitoring, pain & antiemetic meds, D/C dietary instructions
– Gluten free diet – http://www.celiac.com/index.html
Teaching plan for child with celiac disease and the child’s family. Important to a teaching plan for the child with celiac
disease and the child’s family is to provide dietary education and adequate supervision of the dietary treatment. It is important for the nurse to explain the disease process, the signs and symptoms, and the rationale for the gluten-free diet. The family should meet with a dietician to assist in diet planning, nutrition education, and provide a resource person for assisting in dietary issues as they come up. The nurse should review the information provided by the nutritionist and teach the families to read all labels of commercially prepared foods. Teaching should also include referrals to community resources and support groups.
Lactose Intolerance
Inability to digest lactose (insufficiency of lactase)– >3 yo, watery diarrhea, bloating, flatulence,
crampy abdominal pain after ingestion of lactose
– Fluid/elec replacement, monitoring, pain meds, D/C dietary instructions
Biliary Atresia Pathologic closure/absence of bile ducts Jaundice at 2-3 w.o., abd distension,
hepatomegaly, splenomegaly Easy bruising, prolonged bleeding time,
itching, white/clay colored stools, tea colored urine, FTT, malnutrition
Fatal without tx –
– Early diagnosis – surgical correction of obstruction– Late diagnosis &/or surgical failure – liver
transplant (75-80% first yr survival rate)
Normal liver and gallbladder
Viral Hepatitis
Type A – common Type B – common Type C Type D Type E Immunization for A
& B
Inflammation of liver by viral infection
1/3 of all US cases are in children
Acute – anorexia, malaise, fatigue, RUQ pain, hepatosplenomegaly, fever, dark urine, light stools, jaundice (not all chn have jaundice) – complete recovery in 3-4 months
Chronic – Some chn will not completely recover and carry virus, transfer to others, develop serious liver disease several years later
Viral Hepatitis
HAV – most common acute, highly contagious– Fecal-oral route, person-person,
contaminated water, food (esp. shellfish)– Daycare, food handlers
HBV – Parenteral transmission – blood/body fluids exchange– Unprotected sexual activity, mother-fetus, IV
drug use– Chronic – may be very health and unaware
of disease
Viral Hepatitis HCV – blood and blood product
transmission– Low incidence in US, repeated transfusions, IV
drug use, multiple sexual partners
HDV – Defective virus, only infects with HBV– Diminishing liver fxn & mental status, inc jaundice
HEV – contaminated water– Rare in US, flood/rainy seasons in developing
countries
Cirrhosis
Degenerative disease of liver (fibrotic changes & fatty infiltration)
Any age as end stage of several disorders
Manifestations vary– Obstruction – similar to biliary atresia– Steatorrhea, rickets, hemorrhage, FTT, anemia,
pruritus,clubbing, cyanosis
Tx symptomatically, transplantation
Q & A?Q & A?