Week 6 Pediatric Notes

Abdominal Assessment
Summary Checklist: Abdomen Examination
 Inspection
o Contour, symmetry, umbilicus, skin, pulsation or movement, hair
distribution, and demeanor
 Auscultation
o Bowel sounds; note any vascular sounds
 Percussion
o All four quadrants and borders of liver and spleen
 Palpation
o Light and deep palpation in all four quadrants, and palpate for
liver and spleen

Developmental Competence
 Newborn : abdomen - protuberant
o Umbilical cord -  two umbilical arteries and one vein
surrounded by mucoid connective tissue, called Wharton’s jelly.
Dries within a week, hardens, and falls off by 10 to 14 days; skin
covers area by 3 to 4 weeks.
o May note an umbilical hernia; appears at 2 to 3 weeks and
especially prominent when infant cries
o Abdomen shows respiratory movement.
 Child : Under age 4 years, abdomen looks protuberant when child is
both supine and standing.
 After age 4 years, potbelly remains when standing because of lumbar
lordosis, but abdomen looks flat when supine.
 School-age child has a slim abdominal shape as he or she loses
potbelly.

Inspection of the Abdomen

 Contour – Flat, Convex, Concave, Distended
o Determine profile from rib margin to pubic bone; contour
describes nutritional state and normally ranges from flat to
rounded. – Fat, Fluid, Flatus, Hernia , Ascites
 Symmetry
o Abdomen should be symmetric bilaterally.
 Umbilicus
o Normally it is midline and inverted, with no sign of discoloration,
inflammation, or hernia.
 Skin – Lesions, scars, striae, dilated veins, jaundice, cyanosis
o Surface smooth and even, with homogeneous color; assess skin
turgor
  Pulsation or movement – thin person - see pulsations from aorta
beneath skin in epigastric area,
 Peristalsis – wavelike movements visible in thin adults or in clients with
GI obstruction
 Hair distribution - Pattern of pubic hair growth normally has diamond
shape in adult males and an inverted triangle shape in adult females.
 Demeanor - A comfortable person is relaxed quietly on examining table
and has a benign facial expression and slow, even respirations.
 Fat – fat tissue along both sides and the skin does not look taut
 Fluid- flanks protrude, and protrusion moves to dependent sides
 Flatus – protrusion midline, no change in the flanks
 Liver Cirrhosis
 Hernias – protrusion through the abdominal muscles wall are visible

Contour

Auscultation of Bowel Sounds

 This is done BEFORE because percussion and palpation can increase
peristalsis, which would give a false interpretation of bowel sounds.
o Use diaphragm endpiece in all quadrants - bowel sounds are
relatively high pitched.
o Hold stethoscope lightly against skin; pushing too hard may
stimulate more bowel sounds.
o Begin in RLQ at ileocecal valve area because bowel sounds are
normally always present here.
o Expected: high pitched clicks and gurgles 5-35x/min, irregular.
Absent bowel sounds – NO heard sounds for 5 full minutes
o Hypoactive—decreased, can follow abdominal surgery or with
inflammation
o Hyperactive—loud, high-pitched signal increased motility
o Borborygmi – loud growling sounds, hyperactive indicate  GI
motility – diarrhea, anxiety, bowel inflammation, food reaction
Percussion and Tympany
 Percuss general tympany, liver, and splenic dullness.
o To assess relative density of abdominal contents, to locate
organs, and to screen for abnormal fluid or masses
o Yields highly variable results therefore not recommended
o General tympany
 First, percuss lightly in all four quadrants to determine
prevailing amount of tympany and dullness in clockwise
manner.

Palpation
 Perform palpation – palpate tender areas last
o Start light palpation – use finger pads on one hand to palpate a
depth of 0.5, expected: soft, no nodules, no guarding
o Then proceed to deep palpation – 2 handed : top hand
depresses the bottom hand 2.5-7.5 cm ( 1-3 in) in depth , stool
can be palpable at the descending colon
o Provide comfort, enhance muscle relaxation – bend knees
o Note location, size, consistency, and mobility of any palpable
organs and presence of any abnormal enlargement, tenderness,
or masses
o If you identify a mass, first distinguish it from a normally palpable
structure or an enlarged organ.
o Mild tenderness normally present when palpating sigmoid colon,
Any other tenderness should be investigated.
o Rebound tenderness (Blumberg’s sign) – apply firm pressure
with extended fingers for 4 seconds with the hand at 90° angle,
after releasing pressure observe pt’s response/pain -indicates
irritation or inflammation, use it at all quadrants

Abdominal Signs
 Rebound tenderness (Blumberg’s sign)
 Rovsing’s sign – pain to RLQ with palpation of the LLQ – indicates
right sided local peritoneal irritation
 Inspiratory arrest (Murphy’s sign) – inspire deep, examiner palpates
gallbladder fossa, pt has discomfort catching his breath
 Other special tests for Appendicitis:
o McBurney’s point tenderness – 1/3 distance from anterior
superior iliac spine to the umbilicus
o Iliopsoas muscle test – RLQ pain with passive right hip
extension. Inflamed appendix may lie against right psoas muscle
 o Obturator test – flex right hip and knee, internal rotation of
right hip elicits RLQ pain
o The Alvarado score (MANTRELS score) evaluation of RLQ pain –
pain, anorexia, n/v, tenderness, fever, leukocytosis

Gastrointestinal Dysfunction
Water, Water Everywhere
 Water is the body’s primary fluid
o Premature infant’s weight is 90% water
o Term infants are 75-80% water
o Reaches adult percentage by age 3 and adult distribution by late
school age
 Why are children more susceptible to dehydration?
o Increased percentage of extracellular water
o Greater metabolic demand
o More insensible water losses
o Greater ratio of body surface: total body weight

Types of Dehydration
 Isotonic
o Equal loss of water and electrolytes
o Loss of fluid from extracellular fluid leads to reduced circulating
fluid volume
o Normal serum sodium
o Usually r/t vomiting and diarrhea or inadequate PO intake
 Hypotonic
o Electrolyte loss exceeds fluid loss
o Fluids shift from in extracellular to intracellular
o Hyponatremia
 Hypertonic
o Fluid loss exceeds electrolyte loss
o Fluid shifts from intracellular to extracellular
o Hypernatremia

Types of fluids
 Isotonic
o Increases extracellular fluid volume
 Corrects dehydration from blood loss, vomiting, diarrhea
 Used during resuscitation
o D5W, 0.9% NS; LR
 Hypotonic
o Treats hypertonic dehydration (intracellular dehydration)
 o Shifts fluid from extracellular to intracellular
o Treats hypernatremia
o Too fast of an infusion can cause cerebral edema
o DO NOT give to patients with increased ICP, cerebral edema,
burns
o 0.45% NS (½ NS); 0.22% NS (¼ NS); 0.33% NS
 Hypertonic
o Treats hypotonic dehydration
o Shifts fluid from intracellular to extracellular (intravascular)
o Treats hyponatremia; cerebral edema
o 3% NS; 5% NS; 10% D5W

Signs Of Dehydration
 Mild Dehydration
o Weight loss:
 Infants: 3-5%
 Children: 3-4%
o Symptoms:
 No physical symptoms
 Cap refill >2 seconds
 Slight thirst
 Urine output decreased
 Moderate Dehydration
o Weight loss:
 Infants: 6-9%
 Children: 6=8%
o Symptoms:
 Slight tachycardic
 mild tachypnea
 Cap refill 2-4 seconds
 Moderate thirst
 Dry mucous membranes
 Decreased tear production
 Change in skin turgor
 Normal or sunken fontanel
 Oliguria
 Severe Dehydration
o Weight loss:
 Infants: equal to or more than 10%
 Children: 10%
o Symptoms:
 Tachycardia
 Tachypnea
 Hypotension
 Cap refill >4 seconds
  Extreme thirst
 Very dry mucous membranes
 No tears
 Skin cool and mottled
 Sunken fontanel
 Oliguria or anuria

Dehydration Therapeutic Management

 Mild
o Managed at home
o Oral rehydration 50mL/Kg every 4-6 hr
o IV if they can not reach the volume
 Moderate
o May be managed at home
o Oral rehydration 100mL/kg every 4-6 hr
o IV if they can not reach the volume
 Severe
o Requires hospitalization
o IV fluids
 20 mL/kg bolus over 5-20 minutes
o Maintenance fluids

Dehydration Nursing Care

 Daily weights
 Strict I & O’s
 Assess VS every 15-30 minutes
 Assess capillary refill
 Assess skin and mucous membranes
 Monitor LOC
 Management of oral rehydration or IV fluids, IV site assessment and
care

How to calculate maintenance fluid requirements

Child’s weight in kg Multiply by Subtotal

1st 10 kg 100 A

11-20 kg 50 B

Any remaining kg over 20 C

20
TOTAL A+B+C= (divide by 24 for hourly rate)
 mL/day
Child’s weight in kg Multiply by Subtotal

1st 10 kg 4 A

11-20 kg 2 B

Any remaining kg 1 C
over 20
TOTAL A+B+C= 1
mL/hour

Expected Urinary Output

 Infant = 2 ml/kg/hr
 What would be the normal daily urine output for an infant weighing 6
kg?
 Children = 0.5 – 1 ml/kg/hr
 What would be the normal daily urine output for a child weighing 20
kg?
 *** REMEMBER THIS CALCULATES OUTPUT PER HOUR. FOR A
DAILY RATE, MULTIPLY BY 24 ***

Constipation
 Decrease in bowel movement frequency or trouble defecating for more
than 2 weeks
 Toddlers and preschoolers average 1-2 bowel movements per day
 Usually secondary to organic disorder or occur with systemic disorders
 May be due to the use of antacids, diuretics, antiepileptics,
antihistamines, opioids, an iron supplements.
 Newborns
o First meconium passed within 24-36 hours
o Early recognition of no stool would identify an underlying cause
 Infants:
o May be due to Hirschsprung disease, hypothyroidism, or
strictures
o Differentiate this form functional constipation, often related to
diet
o Less commonly seen in breastfed infants
 Children:
o Most due to environmental or normal development changes
o Onset of constipation at school-age may be due to stress or
changes in toileting
Constipation Management and Care
 Therapeutic Management
o Promote regular bowel movements
o Provide more fiber and fluids
o Eliminate constipating foods
o Daily fiber intake should be {age + 5 g}
o Stool-softeners
o Polyethylene glycol laxative
 Nursing Care
o Good history of bowel habits, diet, medications, change of life
events
o Education regarding dietary modifications
o Provide reassurance

Hirschsprung Disease
 AKA aganglionic megacolon
 Etiology:
o Believed to be familial, congenital defect
o Results from failure of the craniocaudal migration of ganglion
nerve cell precursors along the GI tract between 5- and 12-weeks
gestation
 Pathophysiology:
o Absence of parasympathetic ganglion cells in one segment of the
colon
o Without these nerves, the affected segment of the colon lacks
the ability to relax and move bowel contents along

Hirschsprung Disease Clinical Manifestations

 Neonate
o Failure to pass meconium
o Refusal to eat
o Bilious vomiting
o Abdominal distention
 Infants
o Failure to thrive
o Constipation
o Abdominal distention
o Vomiting
o Diarrhea may be explosive and watery
 Children:
o Chronic constipation
o Ribbonlike, foul-smelling stools
 o Abdominal distention
o Visible peristalsis
o Easily palpable fecal mass
o Look undernourished

Hirschsprung Disease Therapeutic Management

 Surgical removal of aganglionic portion of the bowel
o Relieves the obstruction
o Restores normal motility
o Preserves function of anal sphincter

Hirschsprung Disease Nursing Care

 Preop care
o Monitor for signs of enterocolitis, shock, bowel perforation
o Measure abdominal circumference
o Education regarding colostomy
 Postop care
o Promote hydration and nutrition
o No rectal temps
o Assess bowel sounds
o Ostomy care
o Educate family regarding ostomy care

Gastroesophageal Reflux (GER)

  Occurs during the day, most frequently after meals and at night
 Peak incidence is 4 months of age; typically resolves by end of first
year
o Considered GERD when FTT, respiratory problems, or dysphagia
develops
 Deemed pathologic when it persists into late infancy or is associated
with complications
 Common with EA/TEF repairs, prematurity, CP, neurologic disorders,
CF, asthma
 Pathophysiology
o Inappropriate relaxation or failure of lower esophageal sphincter
contraction leads to increased gastric or abdominal pressure and
results in reflux of gastric contents
o Delayed gastric emptying may be a contributing factor
o Repeated reflux of gastric contents can damage esophageal
mucosa

GER Clinical Manifestations

 Infants
o Forceful vomiting, excessive spitting up
o Irritability, arching of back
o Weight loss, FTT
o Aspiration and recurrent respiratory tract infections
o Respiratory symptoms (cough, wheeze, stridor, gagging,
chocking with feedings
o Hematemesis
o Apnea or ALTE
 Children
o Heartburn
o Abdominal pain
o Noncardiac chest pain
o Chronic cough
o Dysphagia
o Nocturnal asthma
o Recurrent pneumonia

GER Diagnostics
 Upper GI series
o reveals reflux and absence of gastric or duodenal obstruction
 24-hour intraesophageal pH monitoring (gold standard)
 Endoscopy with biopsy

GER Therapeutic Management

 Thickened foods
  Histamine receptor antagonists and proton pump inhibitors reduce
gastric acid secretion and may stimulate some increase in LES tone (p.
1186)
 Proton pump block (Prilosec)
 Motility agents (metoclopramide, erythromycin)
 Nissen fundoplication

GER Nursing Care

 Identify children with symptoms suggesting GER
 Education
o Feeding
o Proper use of thickened formula
o Positioning
o Medications (when to administer PPIs)
o fundoplication

Appendicitis
 Inflammation and obstruction of the appendix
 Cause is due to obstruction by hardened fecal material
o Flow of mucous secretions is blocked, resulting in compression of
blood vessels. Leads to ischemia then necrosis then perforation
resulting in peritonitis
 Diagnosis:
o Based on presentation and history
o Elevated WBC and CRP
o CT scan

Appendicitis Clinical Presentation

 Pain is initially periumbilical; extends to RLQ
 o McBurney’s point
 Rebound tenderness
 Rigid abdomen
 Decreased or absent bowel sounds
 Vomiting
 Constipation or diarrhea may be present
 Fever
 Anorexia
 Tachycardia, Tachypnea
 Pallor
 Lethargy
 Irritability
 Guarded posture
 ** A sudden relief from pain is a sign of perforation

Appendicitis Management and Care

 Therapeutic Management
o Removal of appendix
o Antibiotic preop
 Nursing care
o Pain assessment and management
o Post op:
 Maintain IV fluids
 Assess bowel sounds
 NPO
 NGT on low continuous decompression until bowel sounds
return

Meckel Diverticulum
 a congenital (present at birth) outpouching or bulge in the lower part of
the small intestine A remnant of the omphalomesenteric duct that fails
to fuse during weeks 5-9 gestation; results in a fistula; Leads to
diverticulitis
 Diagnosis:
o Meckel scan (low radiation)
 Therapeutic Management:
o Surgical removal
 Presentation:
o Painless rectal bleeding
o Abdominal pain
o Umbilical tenderness
o Signs of intestinal obstruction
 Nursing care:
o Monitor VS (risk for bleeding)
 o Pain management
o Assess bowel sounds
o IV fluids
o NGT for decompression

Inflammatory Bowel Disease (IBD)

 Crohn Disease
o Autoimmune disorder
o Asymmetrical, patchy lesions
o Affects all layers of bowel wall
o Occurs at any point along GI track
o Therapeutic management:
 Corticosteroids
 Antibiotics
 Immunomodulators
 Methotrexate

 Ulcerative colitis
o Cause unknown
o Symmetrical GI ulcers
o Limited to mucosal layer
o Involves large intestine and rectum
o More blood loss
o Therapeutic Management
 5-aminosalicylates (mild to moderate
forms)
 Corticosteroids
 Immunomodulators
 Cyclosporine
 Tacrolimus

IBD Treatment and Care

 Nutritional support
o TPN
o Enteral feedings
 Surgical treatment
o Indicated for UC when medical and nutritional therapees fail to
prevent complications
o May be indicated for Crohn disease for same reasons

Structural Defects
Cleft Lip and Cleft Palate
 Etiology:
 o Multifactorial inheritance
o Exposure to teratogens
o Folate deficiency
 Pathophysiology:
o Lateral and medial tissues forming the upper lip fuse 7 weeks
gestation
o Palatal tissues forming the hard and soft palate fuse between 7-
10 weeks gestation

Preop Care
 Cleft Lip
o Encourage breastfeeding
o Wide-based nipple for bottle feeding
o Support cheeks
o Repair typically between 2-3 months of age
 Cleft Palate
o Maintain upright position for feedings
o Special nipples or syringe feeding
o Burp frequently
o Repair typically between 6-12 months of age
o May require staged surgery

Cleft Lip Repair & Cleft Palate Repair

 Cleft Lip Repair
o Cheiloplasty
o Position supine or side lying
 o Gentle oral aspiration (ATI)
o Keep suture line clean
 Apply antibacterial ointment if prescribed
 Cleft Palate
o Palatoplasty
o Position to promote drainage and a patent airway
o NPO for 4 hr postop; then liquids only for first 3-4 days before
progressing to soft diet
o NO SUCTION

Esophageal Atresia (EA)

 Atresia – termination of a passageway
o Usually refers to a pathologic closure or the absence of a normal
anatomic opening
 EA – the esophagus ends in a blind pouch and does not connect to the
stomach

Tracheoesophageal Fistula (TEF)

 Fistula – abnormal tube-like connection between two structures
 TEF – connection between trachea and esophagus
o Stomach acid irritates trachea

EA and TEF Clinical Manifestations

 Excessive oral secretions
 Abdominal distention
 Apnea
 Increased respiratory distress during feeding
 Three C’s
o Coughing
o Choking
o Cyanosis
EA and TEF Nursing Care
 Preop
o HOB elevated
o Gastric decompression tube
o NG tube to low suction for secretions
o NPO
o Maintain IV
o Monitor fluids/electrolytes, respiratory status, thermoregulation
 Postop
o Do not feed orally; feed by GT or IV
o GT or NGT to suction
o Advance feeds slowly
o Manage chest tube if inserted
o Discharge dependent on ability to take oral fluids

Hypertrophic Pyloric Stenosis

 Hypertrophy of the pylorus
 Narrowing of the pyloric sphincter at the outlet of the stomach
 Pathophysiology:
o Pylorus narrows due to progressive hypertrophy and hyperplasia
of the circular pyloric muscle
o Hypertrophy leads to obstruction of the pyloric sphincter,
resulting in gastric distention

Hypertrophic Pyloric Stenosis Clinical Manifestations

 Forceful vomiting, increases to projectile (usually begins by 3 weeks of
age)
 Emesis may be heme +
 NO bile in emesis
 Olive-shaped mass palpated below right costal margin (RUQ)
 Visible gastric peristaltic waves moving left to right
  Decreased frequency and volume of stools
 Signs of dehydration, FTT
 Infant is hungry = irritable

Hypertrophic Pyloric Stenosis Management and Nursing Care

 Therapeutic Management
o Pyloromyotomy
o Preop
 Rehydrated and correct metabolic alkalosis with IV fluids
and electrolytes
 stomach decompression
 NPO
 Nursing Care
o Nursing observation helps early diagnosis
o Correct dehydration and electrolyte imbalances
o Postop care:
 Increase feeds slowly 12-24 hr postop
 Monitor for infection
 Promote comfort
 Daily weights, I&O

Intussusception
 Telescoping of bowel segment into itself
o creates an obstruction resulting in
compromised blood supply
 If not treated can lead to intestinal
perforation and necrosis
 Affects children between 5 months and 3
years of age
o Cause is unknown
 Diagnostics is also the treatment:
o Air enema in IR
o Surgery if enema does not work

Intussusception Clinical Manifestations

 Sudden onset of abdominal colicky pain; intermittent
 Vomiting
 Currant jelly-like stools (stools are mixed with blood and mucous)
 Palpable sausage-shaped mass in RUQ
 Tender, distended abdomen
 Leads to lethargy, dehydration, shock

Volvulus
  Normal Development:
o Weeks 7-12 gestation, rapid growth of the small intestine
o Intestine rotates counterclockwise
 Instead:
o Intestine malrotates
o Blood flow is disrupted, leading to necrosis of bowel to short
bowel syndrome to death
 Clinical presentation:
o Bilious vomiting
o Firm, distended abdomen
 Nursing care:
o Prepare for surgical correction
o NPO
o IV fluids
o Ostomy care if applicable
o TPN, enteral feeds if short bowel results from surgical correction

Celiac Disease Pathophysiology

 AKA Gluten-induced enteropathy or gluten-sensitive enteropathy
 Villous atrophy in the small bowel in response to gluten
 Inability to digest gluten results in an accumulation of a toxic
substance that damages the mucosal cells which leads to villous
atrophy, hyperplasia of the crypts, and infiltration of the epithelial cells
with lymphocytes.
 Genetic predisposition

Celiac Disease Clinical Presentation

 Impaired fat absorption
o Steatorrhea
o Extremely foul-smelling stools
 Impaired nutrient absorption
o Malnutrition
o Anorexia
o Muscle wasting
o Anemia
o Abdominal distention
 Behavioral changes
o Irritability
o Uncooperative
o Apathy
 Celiac crisis
o Acute, severe episodes of profuse watery diarrhea and vomiting
o May preceded by:
 Infections
  Prolonged fluid and electrolyte depletion
 Emotional disturbance

Celiac Disease Diagnostics and Management

 Diagnostics
o Serum transglutaminase and antiendomysial antibodies in
children 18 months of age and up
o Biopsy of small intestine
o Appearance of small intestine demonstrates characteristic
changes of inflammation, hyperplasia, and atrophy
 Therapeutic Management
o Low gluten diet; eliminate wheat, rye, barley, and oats
o Replace grain foods with corn and rice
o If untreated, may have lactose intolerance
o Lactose intolerance will improve as mucosa heals with gluten
withdrawal
o Treat nutritional deficiencies
