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									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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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

                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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

                                                                                      © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                                                   Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                                             All rights reserved.
FIGURE 30–2 (continued)             A, Unilateral cleft lip.
B, Bilateral cleft lip. Courtesy of Dr. Elizabeth Peterson,
Spokane, WA.




                                                                  B

                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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

                                                                                      © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                                                   Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                                             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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      All rights reserved.
          Pyloric Stenosis
• AKA Hypertrophic Pyloric Stenosis
• Etiology unknown, but often affects first-
  born 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 blood-
    tinged 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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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.




                                                                                   © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                                                Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                                          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 pH-
    probes
  – 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 H2-
  blockers 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
• Nursing Diagnoses
  –   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
             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 life-
  threatening 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.
                     NEC
• Clinical Triad:
  – 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
                   NEC
• Nursing care:
  – 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    Bile salts,
• Due to shortened                f/e’s,
                                  absorption
  intestine after                 decrease
  surgical resection              cuasing
  of a portion of the             diarrhea,
                                  statorrhea,
  intestines                      decreased
• Sxs depend on                   absorption of
                                  fat soluble
  which area of the               vits
  bowel was resected    Colon     f/e mgmt is
                                  impaired

                        Jejunum   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 foul-
    odored)
  – Fluid retention
  – Weight loss and malnutrition
  – Fatigue
         Celiac Disease
• Also known as celiac sprue or gluten-
  sensitive 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.




                                                                                          © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                                                       Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                                                 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

                                                                                  © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                                               Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                                         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.




                                                                                           © 2006 by Pearson Education, Inc.
 Jane W. Ball and Ruth C. Bindler
                                                                                        Upper Saddle River, New Jersey 07458
 Child Health Nursing: Partnering with Children & Families                                                 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.




                                                               © 2006 by Pearson Education, Inc.
Jane W. Ball and Ruth C. Bindler
                                                            Upper Saddle River, New Jersey 07458
Child Health Nursing: Partnering with Children & Families                      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     • Behavioral effects
   – Developmental              – Aggression
     delay                      – Hyperactivity
   – Lower IQ                   – Impulsivity
   – Speech and                 – delinquency
     language problems          – Disinterest
   – Reading skills             – Withdrawal
     deficits
   – Learning disabilities
   – Lowered academic
     success
   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!!

								
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