Transcript Child Health Nursing Partnering with Children & Families

Child Health
Nursing
Partnering with
Children & Families
Jane W. Ball
Ruth C. Bindler
Chapter 30
Alterations in
Gastrointestinal
Function
Let’s Review the GI tract
FIGURE 30–1
The internal anatomic structures of the
stomach, including the pancreatic, cystic, and hepatic ducts; the
pancreas; and the gallbladder.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Pediatric Differences in
Anatomy and Physiology
• Duodenum: digestion takes place
• Enzymes that aid in digestion:
– Amylase ( saliva; digests carbs)
– Lipase (enhances fat absorption)
– Trypsin (which breaks down protein into
polypeptides and some amino acids)
(Infants are deficient in these enzymes
until around 4-6 mos…therefore
abdominal distention from gas is
common)
Pediatric Differences in
Anatomy and Physiology
• GI sx immature at birth
– Process of absorption and secretion do
not take place until after birth
– Sucking primitive reflex
– Voluntary swallow (at 6 weeks)
– Newborn’s stomach capacity is small at
birth ??? Implications..
• (frequent feedings, freq bowel movements,
and intestinal motility is greater than in
older kids (peristalsis) therefore greater
emptying time)
Pediatric Differences in
Anatomy and Physiology
• Liver function immature at birth and next few
weeks
• During first year of life
–
–
–
–
–
Gluconeogenesis (formation of glycogen from noncarbs)
Plasma protein
Ketone formation
Vitamin storage
Deamination
• GI structures in second year of life more mature
– Enlarged stomach capacity (to 3m/day)
– Sphincter control (mylination of sc)
What would be some signs/
symptoms of GI disorders in
infants/ children?
• Vomiting/ regurgitation
• Irritability/ fussiness
• Abdominal pain/ distension
• FTT
• Weight loss
• Stool changes
• Abdominal pain
GI Assessment Techniques
• Subjective
– Lifestyle and family factors
• Including family hx
– Diet
• ? Gaining weight
• Thorough h/o feeding pattern, ? Any problems
• Allergies (lactose intolerant, celiac disease)
– Elimination patterns
• I/O’s
• Encorpresis/ constipation
GI Assessment Techniques
• Objective
– Observe
• Abdominal distension
• Symmetry, bumps, bulges or masses
• Umbilicus
• Peristaltic waves
– Visible rippling waves= bowel obstruction
GI Assessment Techniques
• Objective (con’t)
– Auscultation
• Hyper/hypo bowel sounds
– Percussion
• Tympany vs dullness
– Palpation
• Light vs deep
• Rebound tenderness…peritoneal
inflammation
• McBurney’s point
Disorders of the GI System
• Structural defects
• Disorders of motility
• Intestinal parasitic disorders
• Inflammatory disorders
• Disorders of malabsorption
• Hepatic disorders
• Injuries to the GI system
Structural Defects
• Cleft Lip and Cleft Palate
• Esophageal atresia and
tracheoesophageal fistula
• Pyloric Stenosis
• Insussusception
• Abdominal Wall Defects
• Anorectal malformations
• Umbilical hernia
Cleft Lip and Cleft Palate
• Congenital malformation (failure of
the maxillary processes to fuse)
occurring during weeks 6-12
gestation
• Each abnormality may appear by itself
or may be seen together
• Varying degrees of severity
• Most common craniofacial deformities
overall in US
• Multifactoral causes
Cleft Lip and Cleft Palate
• Complication Associated with Cleft
Lip or Cleft Palate (see Table 30-1)
– Feeding problems
– Speech development
– Otologic
– Dental and orthodontic
– Developmental
Cleft Lip
• Opening between the nose and lip
• Apparent at birth
• Should be documented during
newborn assessment
• Assess child’s ability to suck and
swallow
• Cleft lip repair is performed during
first month of life
• Special feeding techniques if surgery
is delayed
FIGURE 30–2
A, Unilateral cleft lip. B, Bilateral cleft
lip. Courtesy of Dr. Elizabeth Peterson, Spokane, WA.
A
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 30–3
A, Repaired unilateral cleft lip (see Figure 30–2A). B, Repaired bilateral cleft lip
(see Figure 30–2B). Courtesy of Dr. Elizabeth Peterson, Spokane, WA.
A
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 30–2 (continued)
A, Unilateral cleft lip.
B, Bilateral cleft lip. Courtesy of Dr. Elizabeth Peterson,
Spokane, WA.
B
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 30–3 (continued)
A, Repaired unilateral cleft lip (see Figure 30–2A). B, Repaired
bilateral cleft lip (see Figure 30–2B). Courtesy of Dr. Elizabeth Peterson, Spokane, WA.
B
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Cleft Lip
• Feeding a Child before Cleft Lip Repair
• Bottle with special nipple – longer and
narrower
• Hold infant in upright position
• Large cross-cut hole in nipple to allow the
child to get food into back of throat without
strong sucking
• Stimulate sucking by rubbing nipple on
infant’s lower lip
• Allow child to swallow and burp frequently
• ESSR method – Enlarge nipple, Stimulate
sucking, Swallow, Rest
Cleft Lip
• Surgery for Cleft Lip Repair
– Usually done early (first few days to
1st month of life) to improve
parental bonding and improve
feeding
– Plastic surgery with a staggered
suture line (often in shape of letter
“Z” to minimize scarring)
– After surgery Logan Bar over child’s
mouth to reduce tension on suture
line
Logan Bar
Cleft Lip Repair
• Pre-Op Care of the Child and
Parents
• Explain pre-op procedures to
parents
• Provide support and information
• Keep accurate record of child’s
growth and feeding schedule
• Infant:
– NPO X 4-6 hours pre-op
Cleft Lip Repair
• Nursing Diagnosis
– Pre-Op
• Imbalanced Nutrition: Less than body
requirements
• Risk for aspiration
• Altered parenting
Cleft Lip Repair
• Post-Op Care of Child and Family
• Encourage rooming-in
• Incision care: clean sutures with sterile
cotton swab and ½ strength H2O2 followed
by saline to prevent crusting (esp. after
feeding). May apply antibiotic ointment to
suture line
• DO NOT DISPLACE LOGAN BAR
• Special feeder – syringe with rubber tubing
into side of mouth, Breck feeder
• Diet advance from clear to diet for age over
48 hours
• Elbow restraints
Cleft Lip Repair
• Nursing Diagnosis
– Post-Op
• Risk of injury & Infection
• Pain
• Altered feeding patterns
Cleft Palate
• Repaired surgically between 6 months
to 2 years prior to talking
• Parents will care for child at home
until surgical repair
• Altered dentition and speech
dysfunction may also occur
• Frequent episodes of otitis media
– (due to opening into nasopharynx)
Cleft Palate
Cleft Palate Repair
• Post-op: sutures in child’s mouth
• Keep straws, pacifiers, spoons away
from child’s mouth for 7-10 days
post-op
• Elbow restraints and mittens
• Feeding – soft foods: baby food. Short
nipples may be used
• All feeding followed by rinsing mouth
with water to clean suture line
• No brushing teeth X 1-2 weeks
Cleft Palate Repair
• Nursing Diagnoses
– Pre-Op:
• Parental Knowledge Deficit
• Risk for Infection
• High Risk for Altered Family Processes
– Post-Op:
• Altered Skin Integrity
• Child: Pain
Success!!
Esophageal Atresia &
Tracheoesophageal Fistula
(TEF)
• Esophageal atresia and TEF
– a malformation that results from failure
of the esophagus to develop as a
continuous tube
– Foregut fails to lengthen, separate and
fuse into 2 parallel tubes (at 4-5 weeks
gestation)
– Associated with maternal
polyhydramnios
FIGURE 30–4
In the most common type of esophageal atresia
and tracheoesophageal fistula, the upper segment of the
esophagus ends in a blind pouch connected to the trachea; the
fistula connects the lower segment to the trachea.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
EA and TEF
• Signs/Sx:
• Apparent in immediate newborn period
–
–
–
–
–
Respiratory Distress
Difficulty feeding
Excessive drooling
Choking, coughing
Cyanosis
• Esophageal Atresia is a surgical
emergency!
• Tx: Surgical correction
EA and TEF
• Diagnosis
– Confirmed by attempting to pass an NG
Tube into stomach
• Usually a 5 or 8 French tube
• Nursing Care
– ID signs/symptoms of disease
– Careful Physical Assessment
EA and TEF
• Pre- and Post- Operative Care
• Pre-Op:
– NG tube to suction
– Prevent aspiration complication
• (increase HOB, NPO)
– Establish IV access: IVFs & IV abx
• Post-Op:
– Care of G-Tube
– Family teaching
FIGURE 30–5
Children with esophageal atresia
and other gastrointestinal disorders often require a
gastrostomy tube for feedings.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Pyloric Stenosis
• AKA Hypertrophic Pyloric Stenosis
• Etiology unknown, but often affects firstborn males
• Affects males 2-5 X more than females,
especially white males
• Present at birth
• Diagnosis by ultrasound
• Stenosis occurs b/t stomach and
duodenum
Pyloric Stenosis
• Pathophysiology:
– Obstruction of the pyloric sphincter by
hypertrophy of the circular muscle of the
pylorus
– With the enlarged muscle, there is severe
narrowing of the pyloric canal between the
stomach and duodenum
– With food, the muscle is irritated and becomes
further edematous thus causing the opening to
become narrower
– Usually there is a slow progression of edema
and narrowing of the opening into the
duodenum
Pyloric Stenosis
Pyloric Stenosis
• Clinical Manifestations:
– Initially, regurgitation after meals
– Within one week - projectile vomiting
– Vomiting occurs shortly after meals
– Vomiting is forceful and may spew 2-4
feet
– Infant constantly hungry
– Fails to gain weight or loses weight
– Stools decrease in number
– Dehydration results/ electrolyte
imbalances
Pyloric Stenosis
• Clinical Manifestations:
– Upper abdomen distended
– Olive-shaped mass palpable in RUQ
– Left-to-right peristaltic waves noticeable on
abdomen
– Best time to palpate mass is when infant is
relaxed during feeding
– S/Sx of dehydration – sunken anterior
fontanel, sunken eyes, decreased elasticity of
skin (tenting)
• Tx:
– Surgery – Pyloromyotomy
Pyloric Stenosis
• Nursing Care Pre- and Post-Op
– Fluid and electrolyte management
– IV
– NG Tube
– Analgesics
– Prevent Infection
– Support family
– Teaching
Intussusception
• Invagination (telescoping) of one
portion of intestine into another
– (like a sock).
• Multifactoral causes
• Commonly occurs in children b/t 3
months-6 years
• 3x more likely in boys than girls
• Common in children w/ CF, Celiac
Disease and gastroenteritis
Intussusception
• Mechanical Bowel Obstruction Occurs:
– Walls of the segments of the intestine press
against each other causing inflammation,
edema and decreased blood flow.
– As incarceration occurs, necrosis results with
hemorrhage, perforation and peritonitis.
• Classic Triad:
– Severe episodic pain
– “Currant jelly” stool
– Transverse tubular abdominal mass
Intussusception
Intussusception
Intussusception
• Clinical Manifestations:
– Sudden onset of abdominal pain in a
healthy child
– Child screams and draws knees up to
abdomen
– Pain is intermittent, child is relaxed
between pain intervals - paroxysmal
– Vomiting occurs and increases over time
– Stool changes from brown to bloodtinged and mucousy - “currant jelly” in
50% of cases
Intussusception
• Clinical Manifestations:
– Most patients (75%) will test + for
occult blood in stools
– Abdomen tender and distended
– Sausage-shaped mass in RLQ
(vertically-oriented)
– As obstruction progresses, child
becomes acutely ill with fever, and signs
of peritonitis
Intussusception
• Diagnosis:
– Often based on history and physical
examination alone
– Barium Enema is definitive (in 75% of
cases). It is therapeutic and curative in
most cases with less than 24-hour
duration.
– Digital rectal exam reveals mucous,
blood and sometimes the
intussusception
– Laboratory tests – CBCD, Lytes
Intussusception
• Treatment:
– 10% will have spontaneous reduction of
bowel
– Barium or contrast enema
– Manual Reduction (if unsuccessful or
bowel is strangulated or s/sx of
peritonitis= surgery)
– Surgical intervention is a last resort and
must be done if there are signs of
perforation and peritonitis
Intussusception
• Assessment – subjective parental
history of child’s physical and
behavioral SxS
• Nursing Diagnoses
– Altered GI Tissue Perfusion
– Pain
– Fluid Volume Deficit
– Parental Knowledge Deficit
– Parental Anxiety
Intussusception
• Nursing Management:
– VS
– Pain
– Abdominal exam (distention,
tenderness, auscultate BS Q4H)
– I/O’s
• Fluids/ electrolytes
– Note: admission is indicated for all pts
b/c up to 10% of reduction cases recur
w/in 24 hrs
Abdominal Wall Defects:
Gastroschisis & Omphalocele
• A congenital defect of the ventral
abdominal wall, characterized by
herniation of abdominal visceral outside
the abdominal wall
– Gastroschisis= occurs to the side (usually
right) of the umbilicus
– Omphalocele= through the umbilical cord
• Occurs in week 11 of gestation
– When abd contents fail to return to the abd
• Multifactoral causes
FIGURE 30–9
In omphalocele, the size of the sack depends on the extent
of the protrusion of abdominal contents through the umbilical cord. From
Rudolph, A. M., Hoffman, J. I. E., & Rudolph, C. D. (Eds). (1991). Rudolph’s
pediatrics(19th ed., p. 1040). Stamford, CT: Appleton & Lange.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Anorectal Malformations:
Anal Stenosis & Anal Atresia
• Anal stenosis:
– A thickened and constricted anal wall
– s/sx=characteristic ribbon-like stools
• Anal Atresia, aka Imperorate Anus
– PE reveals absent anal opening
– Failure to pass meconium also
diagnostic
• Associated anomalies up to 70% of
the time
FIGURE 30–10
Imperforate anus, which is often obvious at birth, can
range from mild stenosis to a complex syndrome that includes associated
congenital anomalies.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Imperforate Anus
Anorectal Malformations:
Anal Stenosis & Anal Atresia
• Clinical Manifestations:
– Failure to pass meconium during the
first 24 hours
– Absence or stenosis of rectal canal
– Stool in urine due to fistula to perineum
– Stool in vagina due to fistula
Anorectal Malformations: Anal
Stenosis & Anal Atresia
• DX=
–
–
–
–
Digital Rectal Exam
Ultrasound
Abdominal X-Rays
CT Scans
• Treatment=
– For low lesions with just an anal membrane,
serial rectal digital dilations are effective
– For higher lesions – 2 stage surgical repair
• Temporary colostomy
• Abdominal pull-through
FIGURE 30–11
This infant has several gastrointestinal problems and requires ostomies both for
gastric feedings and for drainage of fecal material. Note the appearance of a healthy stoma.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Umbilical Hernia
• Hernia= protrusion or projection of an organ or a
part of an organ through the muscle wall of the
cavity that normally contains it.
• Results from imperfect closure of the umbilical
muscle ring
• Often associated with diastasis recti (lateral
separation of the abdominal muscles)
• Etiology unknown
• Around week 11 gestation and obliterated
umbilical vessels occupy the space in the
umbilical ring
Umbilical Hernia
• Clinical Manifestations:
– Herniated umbilicus protrudes with
coughing, crying or straining
– Hernia can be reduced by pushing
contents back into fibrous ring
– Most defects spontaneously resolve by
3-4 years of age as the muscular ring
closes
– Surgery indicated in cases of
strangulation, increased protrusion after
2 years of age or no improvement in
large defect after 4 years.
Disorders of Motility
• Vomitting/ diarrhea
• Gastroesophageal Reflux
• Constipation and encorpresis
• Hirschsprung disease
• Parasitic disorders
• Gastroenteritis
Gastroesophageal Reflux
• GER is the regurgitation of stomach
contents into the esophagus d/t an
incompetent lower esophageal sphincter.
• Three mechanisms allow reflux to
occur
– Lower esphageal relaxations
– Incompetent LES
– Anatomic disruption of esophagogastric
junction (aka hiatal hernia)
Gastroesophageal Reflux
• What's the difference between GER
and GERD?
• Gastroesophageal reflux (GER)
– is the backward flow of stomach contents up
into the esophagus or the mouth. It happens
to everyone. In babies, a small amount of GER
is normal and almost always goes away by the
time a child is 18 months old.
• Gastroesophageal reflux disease (GERD)
– occurs when complications from GER arise,
such as failure to gain weight, bleeding,
respiratory problems or esophagitis
How is GERD diagnosed?
• S/Sx include:
– presence of vomiting, pain associated with
regurgitation, arching back (Sandifer
syndrome) and feeding refusal.
– However, in very young infants, it may be
difficult to differentiate GERD from normal GER
or colic because some of the symptoms are
similar—constant or sudden crying, spitting up
or vomiting, hiccups, irritability or pain and
refusal to eat. Infants with GERD can also have
atypical symptoms, including respiratory
problems.
GERD
• A small degree of reflux is common in all
infants
• Incidence
– up18% of all infants
– up to 70% w/ co-existing medical conditions
• Anatomy
– Shorter intra-abdominal Esophagus
– Immature LES
– Swallow less while asleep
How is GERD diagnosed?
• Diagnoses: on hx alone (mild) or pH probe
or upper GI endoscopy
• Tests include:
– endoscopic studies or
– measuring the amount of reflux with pHprobes
– A trial of medications may also be a useful
diagnostic tool.
– In infants less than 3 months, try changing the
formula, if allergy is suspected.
Nonpharmacological
Treatment
• Try smaller, more frequent feedings.
• Thickening the formula also helps. Adding rice
cereal makes the liquid less likely to slosh up out of
the stomach into the esophagus. Studies show that
even though the total amount of reflux may not
change, the symptoms improve after the formulas
are thickened.
• Keeping the baby upright before and after feedings
will also decrease the amount of reflux.
• Burp several X’s during feeding
• If bottle feeding, find a nipple that makes a good
seal to prevent air into mouth
• If child is overweight, consult PCP to set weigh loss
goals
Medications for GERD
• The two major pharmacotherapies are H2blockers and proton pump inhibitors
(PPIs), both of which are effective in
decreasing acid secretion and have been
used safely in children.
• Another group of drugs, prokinetics, can
be prescribed to increase motility.
– These are usually given with medications that
inhibit the acid. Examples are metaclopramide
(Reglan) and cisapride (Propulsid).
• Antacids may be tried first in children with
mild symptoms.
Medications for GERD
• H2 receptor blockers:
– help decrease the amount of acid the
stomach makes, which, in turn, will cut
down on the heartburn associated with
reflux.
• H2-blockers include:
– cimetidine (Tagamet)
– ranitidine (Zantac)
– famotidine (Pepcid)
– nizatidine (Axid).
Medications for GERD
• Proton-Pump inhibitors:
– Prevent excess acid secretion in the
stomach
• omeprazole (Prilosec)
• lansoprazole (Prevacid)
• pantoprazole (Protonix)
• rabeprazole (Aciphex).
Surgery
• Management of severe GERD:
– Nissen fundoplication—the fundus of the
stomach is wrapped around the distal
esophagus to increase LES pressure.
GERD
• Nursing Care
– Risk for Aspiration related to reflux
– Fluid Volume deficit related to reflux
– Imbalanced nutrition, less than body
requirements
• Teaching
– Feeding techniques
– Positioning
– Medication administration
Constipation
• Constipation is a common complaint
and accounts for 25% of GI referrals
• Affects 3% of preschool-age children
and 1-2% of school-age children
– (For Infants) Defined by criteria of
• Pebble-like hard stools for a majority of BM’s
X 2 weeks
• Firm stools more than twice/week x 2 weeks
Constipation
• Constipation…think hardness, not
frequency
• Constipation may result from defects
in filling, or more commonly
emptying, or the rectum.
• Please refer to Table 30-5 in text.
Constipation
• Constipation can be caused by
underlying disease, diet or
psychological factors
• Three types of constipation
– Normal-Transit constipation (functional
constipation)
– Defecation Disorders
– Slow-transit constipation
• Fewer than 1/week BM’s
Constipation
• Nursing Care
• Important Education
– Dietary
– Medications
– Fluids
Medical Management of
Constipation
• Usually involves 2 stages (for severe
constipation)
– Soften stool (Lactulose)
– Evacuate stool (laxative)
• Meds:
– Osmotic Laxatives= lactulose, sorbitol, MOM,
Polyethylene glycol (Miralax)
– Lubricants= Mineral Oil
– Stimulant Laxatives= Dulcolax, Senna
– Stool Softeners= Colace
Encorpresis
• Abnormal elimination pattern
characterized by the recurrent soiling or
passage of stool at inappropriate times.
• 1% of school-age children
• Primary vs Secondary encorpresis
• Retention of stool of lower bowel/ rectum,
leads to constipation, dilation of lower
bowel and incompetence of the inner
sphincter
Encorpresis
• Dx:
– made on hx and PE, may perform barium
enema to r/o organic causes
• Tx:
–
–
–
–
Behavior modification
Dietary changes
Clear out impacted stool
Bowel program
• Nursing care:
– Centered around educating the child and
parents about the disorder and its tx
– Reassurance/ emotional support
Hirschsprung’s Disease
• Congenital aganglionic megacolon
• Absence of ganglion cells in the colon
results in mechanical obstruction due
to inadequate motility
• Most common area affected is
rectosigmoid colon
Hirschspung’s Disease
• Etiology? Usually congenital, often a
familial defect.
– Also associated w/ Down’s Syndrome
– And anomalies of urinary tract
• As stool enters the affected area, it
remains there until additional stool
pushes it through. The affected part
of the colon dilates; a mechanical
obstruction may result
Hirschsprung’s Disease
Hirschsprung’s Disease
• Clinical Manifestations:
– Failure to pass meconium within 24
hours
– Constipation during first month of life
– Bile-stained emesis
– Abdominal distension
– Distended abdomen
– Reluctance to eat
– Failure to thrive
– V/D; stool w/ ribbon-like appearance
Hirschsprung’s Disease
• Diagnosis:
– Digital examination of rectum reveals
absence of stool followed by explosive
release of gas
– Barium enema
– Rectal biopsy makes definitive diagnosis
– absence of ganglion cells
Hirschsprung’s Disease
Treatment
• Surgery to remove aganglionic bowel
– Usually 2 stagesSurgery – (if complete obstruction)
– First stage – temporary colostomy (until infant weighs
8-10kg or 10mos-1yr)—to decompress the colon
– Second stage – Abdominal pull-through with excision of
aganlionic segment and reanastomosis
• NG tube is generally inserted preop
• Milder cases
– Dietary modification, stool softeners, and isotonic
irrigation to prevent impaction
Hirschsprung’s Disease
• Nursing Care
–
–
–
–
–
Monitor F/E balance
Maintain nutrition
Pre- and Post-Op care
Pain relief
Promote bowel program
–
–
–
–
–
Constipation related to aganglionic bowel
Post-op: Altered skin integrity
Post-op: Risk for Infection
Post-op: Pain
Post-op: Risk for Fluid volume deficit/altered
nutrition < body requirements
• Nursing Diagnoses
Gastroenteritis
• Gastroenteritis
– inflammation of the stomach and small and
large intestines. It is an infection caused by
viruses, bacteria or parasites.
– Commonly manifested as diarrhea
– Children under 5 years, 2 cases/year average
• Gastroenteritis caused by viruses may last
1-2 days.
– Viral Gastroenteritis accounts for 70-80% of
acute diarrhea in North America.
• Bacterial cases can last a week or more.
• Complications include: Dehydration,
electrolyte and acid base disturbance,
bacteremia and sepsis and malnutrition
Diarrhea
• What is it?
– Watery stool, increased frequency or both
• Acute vs Chronic Diarrhea
– Acute: lasting less than 2 weeks, which is
usually r/t bacterial or viral infections; most
common childhood reason for Diarrhea=
Rotavirus
– Chronic: lasting longer than 2 weeks, usually
r/t functional disorders, such as IBS, or
diseases such as UC or Crohn’s disease
Diarrhea
• What causes Diarrhea?
–
–
–
–
–
Bacterial, viral or parasitic infection
Food intolerances or allergies
Reaction to medications
Diseases such as Chron’s Disease or UC
Refer to Table 30-6 for Other causes of
Diarrhea in Children
• Meds used to tx Diarrhea
– Metronidazole (Flagyl)- anerobic bacteria,
some parasites and in combination for H pylori
– Imodium (an anti-diarrheal)
Parasitic Disorders
• Chart on page 1132 reviews major
parasites
Inflammatory Disorders
• Peptic Ulcer
• Appendicitis
• Necrotizing Enterocolitis
• Meckel’s Diverticulum
• Recurrent Abdominal Pain
• Inflammatory Bowel Disease
Peptic Ulcer
• Definition: peptic ulcer is erosion in the
lining of the stomach or duodenum (the
first part of the small intestine). The word
“peptic” refers to pepsin, a stomach
enzyme that breaks down proteins.
• Small ulcers may not cause any
symptoms. Large ulcers can cause serious
bleeding . Most ulcers occur in the first
layer of the inner lining. A hole that goes
all the way through is called a perforation
of the intestinal lining.
What causes Peptic Ulcers?
• Something damages the stomach lining.
• The most common cause of such damage is a
bacterium called Helicobacter pylori (H.pylori) .
• Most people with peptic ulcers have this organism
living in their gastrointestinal (GI) tract.
• Other factors can make it more likely for you to
get an ulcer , including:
– Using aspirin, ibuprofen, or naproxen
– Drinking alcohol excessively
– Smoking cigarettes and using tobacco
Peptic Ulcers
• Symptoms
• Abdominal pain is a common symptom
but it may not always be present.
• Other possible symptoms include:
–
–
–
–
–
–
–
Nausea , vomiting
Weight loss
Fatigue
Heartburn , indigestion , belching
Chest pain
Blood-tinged emesis
Bloody or dark tarry stools
Peptic Ulcers
• Dx: upper GI, or esophagogastroduodenoscopy,
and Guiac of stool and CBC w/ diff
• Tx: A combination of medications to kill the H
pylori, reduce acid levels, and protect the GI
tract.
• Medications include:
– Antibiotics to kill Helicobacter pylori
– Acid blockers (like cimetidine, ranitidine, or
famotidine)
– Proton pump inhibitors (such as omeprazole)
– Bismuth (may help protect the lining and kill the
bacteria)
Appendicitis
• Appendicitis= inflammation of the
appendix
• Occurs most often in adolescent males
(10-19yr)
• Caused when the opening from the
appendix into the cecum becomes
blocked.
– The blockage may be due to a build-up of thick
mucus within the appendix or to stool that
enters the appendix from the cecum.
– As edema continues, vascular supply is
compromised, bacteria followed by an immune
response…can lead to rupture.
Appendicitis
• Appendicitis should be suspected in any
child with pain in the RLQ
• Symptoms
• Two types of presentation: typical and atypical.
– The typical history includes pain starting centrally
(periumbilical) before localizing to the right iliac fossa
(the lower right side of the abdomen)
– Pain is usually associated with loss of appetite and fever
– Nausea or vomiting
– Lethargy
– Atypical symptoms may include pain beginning and
staying in the right iliac fossa, diarrhea and a more
prolonged, smoldering course.
Appendicitis
• Signs
– These include localized findings in the right iliac
fossa.
– Periumbilical tenderness
– Abdominal tenderness
– rebound tenderness
– digital rectal examination elicits tenderness
– Coughing causes point tenderness at
McBurney's point
– Guarding upon palpation, suspect Peritonitis
FIGURE 30–14
McBurney’s point is the common location of pain in children and
adolescents with appendicitis.
I
Appendicitis
• Other signs include:
– Rovsing's sign
• Deep palpation of the left iliac fossa may cause pain
in the right iliac fossa.
– Psoas sign
• Occasionally, an inflamed appendix lies on the psoas
muscle and the patient will lie with the right hip
flexed for pain relief.
– Obturator sign
• If an inflamed appendix is in contact with the
obturator internus, spasm of the muscle can be
demonstrated by flexing and internally rotating the
hip. This Maneuver will cause pain in the
hypogastrium.
Appendicitis
• Diagnosis is based on Hx and PE
• Abdominal CT or ultrasound
– For atypical presentation
• Labs: CBC w/ diff
– Also an elevation of neutrophilic white
blood cells.
– Pregnancy test to r/o ectopic pregnancy
Appendicitis
• Nursing Care
• Pre and Postoperative care
–
–
–
–
NPO, IVFs
Correction of fluid and electrolyte deficits
Surgical incision
Antibiotics
• Nursing Diagnosis
– Pain
– Risk for Infection
Necrotizing Enterocolitis
(NEC)
• A medical condition primarily seen in
premature infants, where portions of the
bowel undergo necrosis. Potentially lifethreatening inflammatory disease.
• Most common GI emergency occurring
during the neonatal period
• Etiology is multifactorial:
– Intestinal ischemia
– Bacterial or viral infection
– Immaturity of the GI mucosa
NEC
NEC
• Clinical manifestations occur b/t 3-14 doa,
but can occur as early as the first day of
life and as late as 3 months of age.Initial
symptoms include:
– feeding intolerance (increased gastric
residuals, vomitting, irritability, and abdominal
distension)
– Bloody stools
– Decreased UO
– Bile-stained emesis
– Symptoms may progress rapidly to abdominal
discoloration with intestinal perforation and
peritonitis and systemic hypotension requiring
intensive medical support.
• Clinical Triad:
NEC
– Abdominal distension
– Bilious vomiting
– Bloody stools
• Dx:
– PE
– the presence of free peritoneal gas, and abd
wall changes on X-ray
– Heme + stool
– Labs: anemia, leukopenia, leukocytosis,
thrombocytopenia, electrolyte imbalances
NEC
• Nursing care:
NEC
– Observe for feeding intolerance
– Abdominal exam: Measure abdominal
circumference, and assess BS Q-8 Hrs
– Monitor VS and I/O’s
– Pre and Post Op care
• Nursing Dx
– Risk for Infection
– Ineffective Tissue Perfusion
– Imbalanced Nutrition
Meckel’s Diverticulum
• Meckel's diverticulum is one of the most common
congenital abnormalities.
• It occurs when the connection between the
intestine and the umbilical cord doesn't completely
close off during fetal development.
• This results in a small outpouching of the small
intestine.
• In some cases, the diverticula can become infected
(diverticulitis) cause an obstruction of the
instesitne, or cause bleeding from the intestine.
• The most common symptom of Meckel's
diverticulitis is painless bleeding from the rectum.
The stools may contain fresh blood or may look
black and tarry.
Meckel’s Diverticulum
• Omphalomesenteric duct fails to
atrophy
• Outpouching of the ileum remains
and contains gastric contents causing
ulceration
• Bowel obstruction, perforation or
peritonitis can occur
Meckel’s Diverticulum
Meckel’s Diverticulum
• Rule of 2’s
• Bowel obstruction is the most
common complication
• Dx: made on hx
• Tx: surgical incision
• Nursing Care:
– Pre and Postoperative care (similar to
other abdominal surgery)
Recurrent Abdominal Pain
• Frequent problem among young children
and adolescents, especially school-aged
girls
• Organic causes uncommon, but need to be
r/o.
• Pain is generally in periumbilical area and
occurs on a regular basis
• The hx should examine the pressure’s and
stresses in child’s life
• Nursing care: centered around supporting
child during assessment and dx tests
• ? Mental health referral
Inflammatory Bowel Disease
• Crohn’s Disease and Ulcerative Colitis
– Faulty regulation of the immune
response of the intestinal mucosa
– Usually genetically triggered
– Crohn’s disease can cause inflammation
and ulcers anywhere throughout the GI
tract
• Mouth to anus
– Ulcerative colitis effects large intestine
and rectal mucosa
Crohn’s Disease
• Clinical Manifestations:
–
–
–
–
–
–
–
–
Abdominal pain (esp RLQ)
Rectal bleeding
Diarrhea
Fever
Weight loss
Arthritis
Skin problems
Delayed growth
• Lesions are full-thickness, extend into bowel wall
• Affects anywhere in GI tract (illeum, colon and
rectum most common sites)
• More common in whites, age 15-25
Crohn’s Disease
• Complications:
– Intestinal Blockage:
• Thickening of the intestinal wall w/
swelling= freq diarrhea; also leads to scar
tissue
– Fistulas
• Tunnels through affected area to
surrounding tissues of bladder, vagina, skin
– Nutritional complications
• Deficiencies of proteins, calories, vitamins
Crohn’s Disease
• Treatment of Crohn’s Disease:
– may include drugs, nutrition
supplements, surgery, or a combination
of these options.
– The goals of treatment are to control
inflammation, correct nutritional
deficiencies, and relieve symptoms like
abdominal pain, diarrhea, and rectal
bleeding.
Ulcerative Colitis
• A form of colitis that causes inflammation
and ulcers in the lining of the rectum and
colon
• Surgery can cure the disease
– Illeostomy
– Illeoanal anastomosis “pull through”
• More common in Jewish descent
• Average onset b/f 20 yr; peak onset 12
yrs
• 5% of UC develop colon cancer
Ulcerative Colitis
• Clinical Manifestations:
– Cramping abdominal pain
– Rectal bleeding
– Diarrhea
– Fever
– Anorexia
– Growth failure
– Malaise
– Extraintestinal manifestations: joint pain
and swelling, skin lesions, arthritis,
uveitis
Ulcerative Colitis
picture of a colon of a patient with severe
UC
IBD
• Treatment:
– Includes pharmacologic interventions
(abx, antiinflammatory,
immunosuppressive and antidiarrheal
meds)
– Nutrition modification
– Surgery
– Pharmacologic Therapy: see Table on p
1142
IBD
• Nursing care:
– Help child/ family adjust to chronic disease
– Help family to find community support
– Educatate family/ child on
• s/sx of flare-ups
• Med teaching
• Monitor nutritional status
• Nursing Assessment:
– Assess for abdominal distension, tenderness
and pain
– Monitor BS, measure abdominal girth
Disorders of Malabsorption
• Malabsorption occurs when a child is
unable to digest or absorb nutrients
in the diet. Disorders of
malabsorption
– Short Bowel Syndrome
– Celiac Disease
– Lactose Intolerance
– (Cystic Fibrosis)
Short Bowel Syndrome
Illeum
• Due to shortened
intestine after
surgical resection
of a portion of the
intestines
• Sxs depend on
which area of the
bowel was resected Colon
Jejunum
Bile salts,
f/e’s,
absorption
decrease
cuasing
diarrhea,
statorrhea,
decreased
absorption of
fat soluble
vits
f/e mgmt is
impaired
Mostly
compensated
for by other
Short Bowel Syndrome
• The symptoms of short bowel
syndrome can include:
– Abdominal pain
– Diarrhea and steatorrhea (oily or sticky
stool, which can be particularly foulodored)
– Fluid retention
– Weight loss and malnutrition
– Fatigue
Celiac Disease
• Also known as celiac sprue or glutensensitive enteropathy
• A chronic malabsorption syndrome
more common in white Europeans
• Immunologic disorder characterized
by intolerance for gluten found in
wheat, barley, rye and oats. Affects
fat absorption
• ? Genetic factors
FIGURE 30–15
The child with celiac disease commonly demonstrates failure to grow and wasting of
extremities. The abdomen can appear large due to intestinal distension and malnutrition. From Zitelli, B.J., &
Davis, H. W. (Eds.). (1997). Atlas of pediatric physical diagnosis.St. Louis: Mosby. Used with permission from
Elsevier.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Celiac Disease
• Clinical manifestations:
– Diarrhea
– FTT
– Abdominal pain
– Large quantities of fat in stool
– Stools are greasy, foul smelling, frothy,
and excessive
– Eventually may develop protein
deficiency with wasted musculature, and
abd distension
Celiac Disease
• Diagnostic Tests
–
–
–
–
Fectal fat content
Duodenal biopsy
Trial of gluten free diet
Serum screening for IgA
• Tx
– Diet modification: Gluten-free diet
– Do not eat anything that contains the following grains:
wheat, rye, and barley.
– The following can be eaten in any amount: corn,
potato, rice, soybeans, tapioca, arrowroot, carob,
buckwheat, millet, amaranth and quinoa.
Lactose Intolerance
• Inability to digest lactose d/t deficiency of
enzyme Lactase, which is produced by the
cells that line the small intestine
• Lactose is a disaccharide found in dairy
products
• Symptoms include:
– Explosive, watery diarrhea
– Abdominal pain, distension
– Excessive flatus
• Dx
– Hx
– Hydrogen breath test
– Stool acidity test (lactic acid buildup)
Lactose Intolerance
• Treatment and nursing care:
– Reduce/ eliminate lactose in diet
– Infants switch to soy-based formula
– Switch to soy-based formula
– Lactaid tablets for older children (aid in
digestion of lactose)
– Assure enough calcium in diet
– Nursing care: supportive tx
Hepatic Disorders
• Hyperbilirubinemia of the newborn
• Biliary atresia
• Viral hepatitis
• Cirrhosis
Hepatic Disorders
• Signs of Hepatic Disorders
– Jaundice
– Easy bruising, intense itching
– White or clay-colored stools
– Tea-colored urine
Hyperbilirubinemia of the
Newborn
• Bilirubin: a yellow pigment produced from
the breakdown of RBCs
• Newborns have more RBCs/kg than adults
• They produce more bilirubin than their
livers are capable of metabolizing
• Preterm infant more at risk for
hyperbilirub d/t an even shorter RBC
lifespan, and impaired bilirubin
conjugation d/t liver immaturity
Hyperbilirubinemia
• Majority of newborns experience
some degree of jaundice in the 1st
week of life
– Self-limiting
– Bilirubin levels peak b/t the 3-5th dol
– Hyperbilirubinemia: a level of bilirubin in
the blood that requires intervention to
prevent CNS damage
Hyperbilirubinemia
• Pathophysiology
• Neonatal physiologic jaundice results from
simultaneous occurrence of the following 2
phenomena:
– Bilirubin production is elevated because of
increased breakdown of fetal erythrocytes.
This is the result of the shortened lifespan of
fetal erythrocytes and the higher erythrocyte
mass in neonates.
– Hepatic excretory capacity is low both because
of low concentrations of the binding proteins
responsible for making bilirubin water soluble
(conjugation).
Hyperbilirubinemia
• Bottom line:
– Unbound, free and unconjugated
bilirubin is not water soluble…therefore
it can’t be excreted from circulation…it
moves to fatty tissue, leading to
jaundice.
– How is it removed from the system?
• Uncong. Bili. Attaches to albumin, then
moves to the liver, where it b/c “conjugated”
into direct bilirubin
• Direct bilirubin= water soluble, and excreted
into small intestine
Hyperbilirubinemia
• Clinical Manifestations of newborn
jaundice:
– 1st evident on the face, and progresses
downward to trunk etc.
• Symptoms of hyperbilirubinemia
– Visible jaundice heat to toe, including sclerae
– Lethargy or irritability
– Poor breastfeeding or bottle feeding
• Symptoms of acute bilirubin
encephalopathy:
– Lethargy
– Hypotonia
– Poor sucking ability
Hyperbilirubinemia
• Nursing care:
– ID newborn’s at risk/ observe s/sx of jaundice
– Promote successful BF/ refer for lactation
support
– Educate parents re: newborn jaundice
• Nursing assessment: refer to Table 30-5 in
text
• Tx:
–
–
–
–
–
Phototherapy
Hydration
IV y-Globulin
Exchange transfusion
Tin-mesoporphyrin (med)
FIGURE 30–16
A, Infant receiving phototherapy on a phototherapy blanket. B, Infant receiving
phototherapy in an incubator with overhead phototherapy lights.
A
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
FIGURE 30–17
This chart is recommended for use prior to infant discharge, to help assess the infant’s risk
of developing severe hyperbilirubinemia. For example, if a newborn is 48 hours old at discharge, and has a
TSB or TcB of 12 mg/dL, the infant is in the high intermediate risk zone for developing severe
hyperbilirubinemia. This assessment, in conjunction with other clinical factors, influences decisions regarding
continued hospital care, or timing of postdischarge follow-up. Redrawn from American Academy of Pediatrics.
(2004.) http://aappolicy.aappublications.org/cgi/content/full/pediatrics; 114/1/297.pdf, accessed 1/20/05.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Biliary Atresia
• The pathologic closure or absence of
hepatic or common bile ducts at any
point from the porta hepatic to the
duodenum
• The disorder leads to cholestasis,
fibrosis, and cirrhosis
• Most common pediatric liver disease
necessitating transplantation and the
most common cause of infant
jaundice
Biliary Atresia
• Etiology: unknown
• Blockage of bile flow from the liver to
duodenum causes inflammation and
fibrotic changes.
• Lack of bile acids also interferes with
digestion of fat-soluble vits
(K,A,D,E), leading to steatorrhea and
nutritional deficits
• Without tx, disease is fatal
Biliary Atresia
Biliary Atresia
• Clinical Manifestations:
–
–
–
–
–
–
Newborn is initially asymptomatic
Jaundice around 2-3 weeks
Abdominal distension
Increase in bilirubin levels
Splenomegaly
Easy bruising, prolonged bleeding time and
intense itching
– Tea-colored urine
– Clay-colored stools
– Ftt/ malnutrition
Biliary Atresia
• Dx: hx, PE and labs
• Tx: surgery to correct obstruction
• Liver Transplantation
• Nursing care: pre and postoperative,
teach the family, and prepare for
organ transplant
Viral Hepatitis
• An inflammation of the liver caused
by a viral infection
– Can be acute or chronic disease
– Acute: rapid onset, can dev into chronic
– Hep A (HAV)
– Hep B (HBV)
– Hep C (HCV)
– Hep D (HDV)
– Hep E (HEV)
FIGURE 30–19
The hepatitis virus causes degeneration and necrosis
of the liver, which results in abnormal liver function and illness.
Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
© 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
Viral Hepatitis
• Nursing Care:
–
–
–
–
–
Prevent spread of disease
Provide fluid and nutritional support
Promote G&D
Reduce risk of complications
Support child and family
• Refer to Table 30-8 for Comparison of
major types Hepatitis Types
• Refer to Table 30-9 for transmission,
immunization and prophylaxis for hepatitis
Cirrhosis
• Degenerative disease process that
results in fibrotic changes and fatty
infiltration in the liver
• Clinical Manifestations of cirrhosis
vary
• End-stage liver failure
• Tx: liver transplant
Injuries to the
Gastrointestinal System
• Trauma
• Ingestion of foreign objects
• Lead poisoning
Abdominal Trauma
• May be caused by blunt or penetrating
trauma
• Type of injury determines extent of organ
damage
• Dx: Hx, PE, CTscan, FAST (focused abd
sonogram for trauma)
• Nursing care:
– Provide emotional support
– Follow care orders
– Prevention teaching once stabilized
Poisons Ingestion
• Poisonings are the 2nd leading cause
of unintentional home-injury
• Do not use ipecac
• Airway, hemodynamic stability,
remove toxin and support
• Education on prevention
• Most common poison????
• Refer to Table 30-8 for Emergency Management
of Poisoning
Lead Poisoning
• A medical condition caused by increased
levels of the metal lead in the blood.
• Lead may cause irreversible neurological
damage as well as renal disease,
cardiovascular effects, and reproductive
toxicity.
• Healthy People 2010 goal: eliminate
childhood lead poisoning as a public health
issue in the U.S.
Lead Poisoning
• Routes of exposure:
– Mostly through lead-based paint in older
homes
– Pain can chip and flake into dust which
settles on the floor
– Children explore through putting things
in their mouths.
Lead Poisoning
• Other sources of lead exposure:
– Water from lead pipes
– Lead solder on canned foods
– Lead ammunition
– Pool cue chalk
– Collectible toys
– Jewelry
Lead poisoning
Why are children at greater risk?
• Children are at greater risk of lead
poisoning because they absorb and retain
more lead in proportion to their weight
than adults do.
• Causes problems with normal cell
function:
– Nervous system—can cause irreversible
damage to developing brain
– Blood cells—displaces Iron, which decreases
Heme production
– Kidneys—excreted through kidneys
– Has an adverse affect on vitamin D and
calcium metabolism.
Lead Poisoning
• Toxicology/ Distribution
• At least 99% of absorbed lead is
bound to erythrocytes upon entry
into the bloodstreatm
– 70% is stored in the bone
• Accumulates throughout life, but can be
released during stress
• Can have a ½ life of as many as 20 years
– 30% moves to major soft tissue storage
sites
• Liver, kidney, bone marrow and BRAIN
!
Lead Poisoning
• Pathophysiology: Lead toxicity can affect
any soft tissue of the body including:
–
–
–
–
–
–
Hematological
Renal
GI
Skeletal
Endocrine
CNS*** (Neurotoxicity w/in the Pediatric CNS
is most detrimental pathology)
Lead poisoning
• Three routes for absorption of lead in
children’s body:
– GI, Inhalation and Transplacental
• Clinical Manifestations:
– Depend upon the degree of toxicity:
• Decreased IQ scores.
• Cognitive deficits.
• Loss of hearing.
• Growth delays.
Lead Poisoning
• S/Sx:
• Acute Lead Poisoning:
– N/V
– Anorexia
– Constipation
– Abdominal Pain
Chronic Lead Poisoning
• Neurocognitive effects
– Developmental
delay
– Lower IQ
– Speech and
language problems
– Reading skills
deficits
– Learning disabilities
– Lowered academic
success
• Behavioral effects
– Aggression
– Hyperactivity
– Impulsivity
– delinquency
– Disinterest
– Withdrawal
Lead Poisoning Treatment
• Primary Prevention
• Secondary Prevention
• Depending upon Lead levels:
– Recent studies suggest that adverse
health effects exist in children at blood
lead levels less than10 µg/dL (CDC)
– Pb-B 10 to 19 micrograms/dL – need to
remove identifiable sources
– Chelation tx is indicated if BLL greater
than 45ug/dl
• (Succimer, EDTA, and BAL)
Lead Poisoning
• Nursing Assesment:
• Obtain a complete medical history.
– Developmental progress.
– Problems with attention.
• Obtain Lead level results.
Foreign Object Ingestion
• Assessment important
• Prepare child and parents for x-rays
and possible removal
• Education on prevention
The End!!