25/06/2014

Objectives

The Gastrointestinal System

(Part 2)

At the end of this session students should be able to:

1. Describe the common gastrointestinal system health
conditions in the child.
2. Perform health assessment of the
gastrointestinal system on the child
according to age.

Prepared by: M. Cole

MSN, BSN, RN

Objectives

Objectives

contd

3. Describe the pathophysiology, incidence,

clinical manifestation and prognosis of
each disease process.

contd

6. Use the nursing process to provide age

appropriate nursing care for the child with
a gastrointestinal system condition.

4. Explain diagnostic tests for each condition

identified.

7. Describe health promotion strategies used

to restore health for the child with a
gastrointestinal system condition.

5. Describe treatment modalities for the

different conditions.
3

Dental caries

Dental caries

Is a progressive and destructive process causing

decalcification of the tooth enamel, destruction of dentin
and cavitation of the teeth.
It can spread into the tooth pulp and may cause
inflammation and abscess.
fluorideandfluorosis.com

25/06/2014

Etiology

Pathophysiology

Many organisms may cause dental caries.

Streptococci is such organism, the main cariogenic

agent.

Streptococci produces a extra cellular polysaccharide

and forms a plague over the teeth.
Gradual tooth decay begins following demineralization
of the enamel.

Pathophysiology

Risk factors

contd

Destruction of dentin occurs with cavity formation

occurring causing inflammation and abscess formation.

Biting and contact surface are the most common sites.

Carbohydrate rich foods especially chocolate which stick to

teeth
Poor oral hygiene with inadequate dental care
Sleeping with feeding bottle in mouth
Sweetening agents like honey
Fluoride deficiency/excess

10

Clinical manifestations

Treatment

Pits and fissures in biting and contact surfaces commonly

in molars as initial features.

Cavity formation involving pulp, dental abscess

Sepsis

11

Analgesics to relieve pain

Extraction
Antibiotics

12

25/06/2014

Preventative measures

Preventative measures contd

Dietary modification by avoiding carbohydrate rich food

and avoiding oral retaining.
Use of fluoride tooth paste
Avoidance of chewing gum, chocolates, bottle feeding

Good oral and dental hygiene with correct brushing

technique.
Mechanical movement of plaque and debris.
Dental sealant to pits and fissures.
Regular dental check-up

13

14

Oesophageal stricture

Oesophageal stricture

Narrowing of the oesaphagus.

Acquired oesaphageal stricture in childhood are most
likely a result of reflux oesophagitis, corrosive injury or
anastomotic scaring.

aurorahealthcare.org

15

Clinical manifestations

nejm.org

16

Diagnostic test

Drooling
Inability to swallow saliva and fluids
Difficulty feeding - ability to take liquids but not solids
Regurgitation of undigested food

17

Oesaphagoscopy - to evaluate the length, character,

ability to dilate the defect and the condition of the mucus
membrane.

18

25/06/2014

Gastro-oesophageal reflux

Treatment

(Infant)

Sedation and dilation (using rubber balloon, dilator)

Resection with end to end anastomosis

Regurgitation of stomach secretions into the esophagus

through the gastroesophageal (cardiac) valve.
Occurs mainly in infants and adolescent

19

20

Pathophysiology

Gastro-oesophageal reflux contd

Occurs from a neuromuscular disturbance in which the

gastroesophageal (cardiac) sphincter.
The lower portion of the esophagus spasm and allow easy
regurgitation of gastric contents into the esophagus.

drbrandonfox.com

21

22

Clinical manifestations

Gastro-oesophageal reflux contd

Regurgitation occurs almost immediately after feeding or

when the infant is laid down after a feeding.

If the amount of the reflux is large or constant, an infant

does not retain sufficient calories and will fail to thrive.

Vomiting
Irritability and apnea may be evident

Diagnostic test

Fiberoptic endoscopy or
Oesophagography (barium swallow) will
show the involved sphincter and the reflux
of stomach contents into the esophagus.

In addition, aspiration pneumonia or esophageal stricture

from the constant reflux of hydrochloric acid into the
esophagus can occur.
23

24

25/06/2014

Treatment

Treatment

Traditional treatment:
Feed infants a formula thickened with rice cereal while
holding them in an upright position
Then keeping them upright in an infant chair for 1 hour
after feeding so gravity can help prevent reflux.

contd

H2 receptor antagonist Zantac (Ranitidine) or

Proton pump inhibitor Omeprazole (Prilosec) to reduce
the possibility of the stomach acid contents irritating the
esophagus.

25

Treatment

26

Treatment

contd

Gastroesophageal reflux is usually a self-limiting

condition.

As the oesophageal sphincter matures and the child

begins to eat solid food and is maintained in a more
upright position, the problem resolves.

contd

Laparoscopic or surgical myotomy procedure (narrowing

of the esophageal sphincter)
Followed by temporary placement of a NGT.

27

28

Gastroesophageal reflux disease

Etiology

(Adolescent)

Affects about 20% of adults; symptoms frequently begin

in adolescence.

Irritation to the esophagus occurs when stomach

contents, including hydrochloric acid, reflux through the
lower esophageal sphincter and irritate the esophageal
lining.

29

Reflux occurs because of an incompetent sphincter

especially when the adolescent lies supine or when intraabdominal pressure is increased by a full stomach, lifting
or bending, or tight clothing.
It is potentially dangerous because it can lead to erosion of
the esophagus with perforation or stricture of the
esophagus.
30

25/06/2014

Clinical manifestation

Diagnostic Test

The typical symptom is heartburn that occurs 30-60

minutes after a meal.

Based on history (typical symptoms of heartburn) and, if

symptoms are severe.
Endoscopy to reveal the irritated esophagus
(oesophagitis).

31

32

Treatment

Treatment

Goal: To provide symptomatic relief and to heal any oesophagitis identified.

Antacids (relieve pain by decreasing the concentration of

the stomach acid)
H2-receptor antagonists (Pepcid or Zantac) to prevent
heartburn symptoms.
Proton pump inhibitors such as omeprazole (Prilosec) to
halt the release of stomach acids

contd

Avoid lying down until 3 hours after a meal

Sleep at night with upper body elevated on a foam wedge.

Avoid acidic foods: tomato products, citrus fruits, or spicy

foods.

33

Treatment

34

Gastroenteritis

contd

Inflammation of the lining of the stomach and intestines,

may be caused by:
Bacteria e.g. Escherichia coli, Salmonella
Virus Rotavirus
Toxins
Allergies
The illness may resolve without complications or cause
mild to severe dehydration.

Avoiding foods that delay gastric emptying such as fatty

foods, chocolate, or alcohol and eating smaller portions
may also be helpful.
Weight loss, avoiding bending after meals, and removing
tight belts are also recommended steps.

35

36

25/06/2014

Pathophysiology

Pathophysiology

Believed that the causative agent damages and destroys

epithelial cells lining the intestine causing the following
clinical manifestations.

The decrease in total body water causes a reduction in

intracellular and extracellular fluid but the clinical
manifestations of dehydration are most closely related to
intravascular volume depletion.

Diarrhea occurs when intestinal fluid output overwhelms

the absorptive capacity of the gastrointestinal tract.

37

38

Clinical manifestations

Pathophysiology
The 2 primary mechanisms responsible for acute gastroenteritis are:
damage to the villous brush border of the intestine, causing
malabsorption of intestinal contents and leading to an osmotic
diarrhea, and

the release of toxins that bind to specific enterocyte receptors and

cause the release of chloride ions into the intestinal lumen, leading
to secretory diarrhea.

Nausea
Vomiting
Diarrhea
Fever
Dehydration
Electrolyte imbalance

39

40

Diagnostic test

Treatment

Stool culture may be done

41

IVF
Electrolytes
Antibiotics
Rehydration salts/fluids
Diet when vomiting and diarrhea subsides

42

25/06/2014

Nursing management

Diarrhoeal diseases

Administer and monitor IVF

Skin care
Administer medication as ordered
Offer rehydration fluids

Is the passage of loose, liquid or watery stool at least

three times per day.
The recent change in consistency and the character of the
stool rather than the number of stool is more important.

43

44

Acute Diarrhoea

Diarrhoeal diseases

colon-cleanse-information.com

Caused by infection of the large intestine but can also be

associated with infection of the gastric mucosa and the
small intestine.
Acute GE is usually use to describe acute diarrhoea

45

46

Chronic Diarrhoea

Is an attack of loose motion with sudden onset which

usually last 3 7 days but may last up to 10 14 days.

Dysentery

When loose motion is occurring for 3 weeks or more.

Diarrhoea with watery stool and visible blood in the stool.

Usually related to underlying organic disease with or

without malabsorption.

47

48

25/06/2014

Persistent Diarrhoea

Etiology

Refers to the episode of acute diarrhoea that last for 2

weeks or more and may be due to infective state.

A large number of organism are responsible for acute

diarrhoea. The infectious agents are:
Viruses (Rotavirus, Adenovirus, Enterovirus, measles virus etc.)
Bacteria (Campylobacter jejuni, E. coli, Shigella, Salmonella,
Cholera vibrio, Vibrio parahemolyticus etc.)

Parasites (E. hystolytica, G. lambia, Cryptosporidium, malaria

etc.)

Fungi (Candida albicans)

49

Etiology

50

Etiology

contd

Other causes of diarrhoea are related to nutritional and

dietary factors:
Overfeeding
Underfeeding/malnutrition
Food allergies
Food poisoning
Some drugs such as antibiotics cause diarrhoea

contd

Malnutrition:
Children who die from diarrhoea often suffer from
underlying malnutrition, which makes them more
vulnerable to diarrhoea.
Each diarrhoeal episode, in turn, makes their malnutrition
even worse. Diarrhoea is a leading cause of malnutrition in
children under five years old.
51

Etiology

52

Incidence

contd

Source: Water contaminated with human faeces, e.g. from

sewage, septic tanks and latrines, is of particular concern.
Animal faeces also contain microorganisms that can cause
diarrhoea.
Other causes: Diarrhoeal disease can also spread from
person-to-person, aggravated by poor personal hygiene. Food
is another major cause of diarrhoea when it is prepared or
stored in unhygienic conditions. Water can contaminate food
during irrigation. Fish and seafood from polluted water may
also contribute to the disease.

53

Every year there are about two billion cases of diarrhoeal disease
worldwide.
Diarrhoeal disease is a leading cause of child mortality and morbidity
in the world, and mostly results from contaminated food and water
sources.
Diarrhoea due to infection is widespread throughout developing
countries.
54

25/06/2014

Degree of Dehydration

**Key facts**

Diarrhoeal disease is the second leading cause of

death in children under five years old. It is both
preventable and treatable.
Kills 1.5 million children every year.
Globally, there are about two billion cases of diarrhoeal
disease every year.
Mainly affects children under two years old.
Leading cause of malnutrition in children under five years
old.

Rated on a scale of three.

Early dehydration/Mild may or may not have signs or
symptoms.
Moderate dehydration:

55

56

Diarrhoea

Degree of Dehydration contd

Severe dehydration:

thirst
restless or irritable behaviour
decreased skin elasticity
sunken eyes

shock,
with diminished consciousness,
lack of urine output,
cool moist extremities,
a rapid and feeble pulse,
low or undetectable blood pressure,
and pale skin.

The most severe threat posed by diarrhoea is

dehydration.
During a diarrhoeal episode, water and electrolytes
(sodium, chloride, potassium and bicarbonate) are lost
through liquid stools, vomit, sweat, urine and breathing.
Dehydration occurs when these losses are not replaced.

57

58

Diagnostic test

Treatment

Stool culture
Blood culture
Serology (evaluating antibodies to identify microbes with which
you have recently been infected)

59

Rehydration with IVF in case of severe dehydration or

shock, oral rehydration salts (ORS) solution for
moderate or no dehydration.
Nutrient-rich foods
Antibiotics (if cause is bacterial agent)

60

10

25/06/2014

Prevention

Nursing management

access to safe drinking-water

improved sanitation
exclusive breastfeeding for the first six months of life
good personal and food hygiene
health education about how infections spread
rotavirus vaccination

Assess stools for frequency, amount, color, consistency

Assess S&S of dehydration; po fluid intake
Assess perianal skin breakdown and provide skin care
Obtain stool specimen
Administer antibiotics, antidiarrheals, IVF & electrolytes as
ordered

61

62

Helminthiasis

Helminthiasis
Infestation of worms
Common types are:
Round worms (Ascaris lubricoides)
Pinworm or threadworm (Enterobius vermicularis)
Hook worm (Ancylostoma duodenale, Necator
americanus)
Tape worm (Taenia saginata, Taenia solum)

infection-research.de

hon.ch

63

Roundworm

Etiology

(Ascariasis)

Helminthiasis in human are caused by three types:

Most common helminthic infestation.

Nematodes (roundworm, pinworm, hookworm)

Cestodes (tapeworm)
Trematodes (fishworm, flukes)

Lives in the lumen of the small intestine.

64

65

The adult female round worm measures 20-40 cm and

the male measure 12-30 cm in length.

66

11

25/06/2014

Pathophysiology

Pathophysiology contd

The female produces approximately 200,000 to 300,000

eggs per day.
Eggs are excreted in faeces and external environment they
become infective in favourable conditions.
Mature eggs when ingested hatches in the duodenum to
release larvae.

The larvae penetrates the intestine, and are carried to

liver then lung in the blood stream.
They break through the alveolar wall while in the lung
and migrates into the bronchioles, get coughed up
through the trachea.

67

68

Pathophysiology contd

Worm cycle

They get re-swallowed to reach the small intestine, where

they become adult worms in 60 to 80 day. They have a life
span of 1.5 to 2 years.

Montresor & Diarra, n.d (WHO)

69

70

Transmission

Clinical manifestations

Mode of transmission: Feco-oral route of ingestion of

infective eggs with food or soil or drink or by
contaminated hands and fingers.

Communicable period: Continued until all fertile eggs

are destroyed and stools are negative of roundworm
eggs.
Incubation period: About 2 months

71

Abdomen pain
Abdominal distention
Nausea
Cough
Loss of weight

Growth failure
Vitamin deficiency
Voracious appetite
Bruxism

72

12

25/06/2014

clinicianonnet.blogspot.com

Associated problems

Complications

Pica
Sleeplessness
Urticaria
Fever
Diarrhea

ayurdoc.blogspot.com

Intestinal obstruction
Gangrene
Perforation
Obstructive jaundice
Appendicitis
Pancreatitis
Ascaris encephalopathy

Liver abscess
Peritonitis
Ascaris pneumonia
Convulsion and features
like retinoblastoma.

73

74

Treatment

Prevention

Antihelmintics - Mebendazole or Albendazole

Piperazin cirtate- ideal drug for eradication of

roundworm infection as it causes paralysis of the worms.

Sanitary disposal of human excreta

Reduction of fecal contamination in soil
Provision of safe drinking water
Food hygiene
Good personal hygiene
Wash hands before and after defecation
Avoidance of open field defecation
Special attention for foods such as salads and vegetables
wash carefully.

75

76

Other helminthic infestation

Protein-energy malnutrition

Truchuris tricuria (whip worm): contaminated food, drinks

and hands or indirectly through flies and insects.
Stronglyoides stercoralis: through skin contact with
contaminated soil.
Dracunculus medinensis (Guinea worm): contaminated
water that contain crustaceans.
Shistoma mansoni or S. hematobium (flatworm):
penetration of intact skin
Trichinosis: ingestion of undercooked meat contaminated
with infective larvae.

77

Results from an insufficient intake of high quality

protein of from conditions in which protein absorption is
impaired or a loss of protein increases.
Clinical manifestation may not be apparent until the
condition is well advanced.

78

13

25/06/2014

Kwashiorkor

Results from severe

deficiency of protein with
an adequate caloric intake.

Kwashiorkor
nzdl.org

It accounts for most of the

malnutrition worldwide.
caribbean-icons.org

cs.stedwards.edu

79

80

Pathophysiology

Etiology

Hypoproteinemia results in edema, this occurs due to a

shift of body fluid from intravascular compartment to
interstitial spaces causing ascites.

Tends to occur after weaning when the child changes from

breast milk to a diet consisting mainly of carbohydrates.

Incidence

The edema tends to be dependent

The highest incidence is in children 4 months to 5 years of

age.
Most common in underdeveloped countries.

81

82

Treatment

Clinical manifestations

Swollen abdomen
Edema
GI changes diarrhoea
Iron deficiency anemia
Hair thin and dry with patchy alopecia
Child becomes apathetic and irritable
Retarded growth
Muscle wasting

High protein diet

Prognosis

83

In untreated clients mortality rates is 30% or higher.

84

14

25/06/2014

Marasmus

Child with Marasmus

Deficiency of all food groups, basically starvation.

These children will basically suck at anything including
clothing or a finger.
Treatment is high nutrients diet
newfoundations.org.uk

85

86

Clinical manifestations

Obesity

Similar to Kwashiorkor
Iron deficiency anemia
Irritability
Retarded growth
Muscle wasting
Diarrhoea

87

i.dailymail.co.uk

Incidence

The accumulation of excess body fat.

Having Body Mass Index (BMI) of greater than 30 kg/m
square.

topnews.in

88

Influential factors

Higher in female and adolescents of lower socioeconomic

status

**Research also indicates that adolescents of affluent families

are more prone to obesity.

89

Food choices
Eating practice
Lack of exercise
Hormonal changes
Excessive television watching
Overprotective parenting
Emotional factors
Genetics
90

15

25/06/2014

Clinical manifestations

Treatment

Low self esteem

Emotional problems resulting in isolation
Excessive appetite
Weight gain

**Individuals with truncal obesity are more prone to

cardiovascular disease and diabetes.

Diet modification
Exercise
Behaviour modification (such as eating only at a table,
using smaller plates, eating only at specific times,
recording food intake and feelings at the time of the
meal)

91

92

Recommendations

Appendicitis

Proper nutrition and healthy food choice

Good eating habits
Decreased fast food intake
Exercising for 30 minutes at least four times per week
Decrease television and computer use
Parent/children exercising at home

Inflammation of the vermiform appendix, a small sac at

the end of the cecum.

93

94

Appendix

Pathophysiology

knol.google.com

A blockage of the lumen of the appendix occurs or

inflammation as a result of an upper respiratory or other
body infection followed by infection, inflammation and
edema.

internal-optimist.blogspot.com

95

96

16

25/06/2014

Pathophysiology

Etiology

contd

Leading to compression of blood vessels and cellular

malnutrition.
Necrosis and pain results.
If not discovered early rupture will occur and fecal matter
will be spilled in the abdomen

May be caused by:

Mechanical obstruction (fecaliths, intestinal parasites)

Anatomic defect
May be related to decreased fibre intake in the diet

97

98

Clinical manifestations

Incidence

Most common in school age children and adolescents

Rarely occurs before 2 years of age

99

Diffuse pain, localizes to RLQ

Sharp pain at McBurneys point (1/3 way between anterior
superior crest of iliac and the umbilicus)
Nausea and vomiting
Guarding of abdomen
Rebound tenderness
Decreased bowel sound
Fever
100

Diagnostic test

Treatment

WBC increased
Elevated acetone in urine

101

Surgical removal of the appendix

Antibiotics
Antipyretics

102

17

25/06/2014

Nursing management

Nursing management contd

Post-op

Prevent perforation: do not give enemas, cathartics or

use heating pad
Support child and parents

Monitor NG tube aspirate

Position in semi-fowlers
Administer medications as
ordered

Monitor op site for signs of

infection
IVF
Advancing diet
Pain relief and measures
Discharge teaching

103

104

Ruptured Appendix

Nursing management

The potential for peritonitis increases greatly.

The white blood cell count rises to more than

20,000/mm3.

Position the child in a semi-Fowler's position (if possible,

so that infected drainage from the cecum drains
downward into the pelvis rather than upward toward the
lungs).
IV fluid for hydration.
Preoperative antibiotics will be begun or as soon as the
ruptured appendix is confirmed

105

Nursing management

106

Hepatitis

contd

Assess for signs of peritonitis with dressing changes.

boardlike (rigid) abdomen,
generally shallow respirations (because deep breathing
puts pressure on the abdomen and causes pain),
and increased temperature.

107

Inflammation and infection of the liver

Caused by invasion by hepatitis A, B, C, D, or E virus

108

18

25/06/2014

Common causes of Hepatitis

Organism

Mode of
transmission

Incubation

Clinical
manifestation

Available
immunization

Hep A

Fecal- oral route, person

to person, contaminated
water or food (shellfish)

4 weeks (10-50
days)

Acute onset (may be

less acute in young
children). Usually do
not become
jaundiced. Flu-like
symptoms

Immune serum
globulin
Hep A vacine

Blood and body fluids

1-6 months

Nausea, vomiting,
anorexia, fatigue,
upper RQ pain,
hepatomegaly

Hep B immune
globulin
Hep B vaccine

Hep B

Common causes of Hepatitis

contd

Organism

Mode of
transmission

Incubation

Clinical
manifestation

Available
immunization

Hep C

Blood and blood

products

6-7 weeks

Frequent episodes of
flu-like symptoms
without jaundice. Risk
of cancer

None

Hep D

Blood and blood

products. Found with
HBV

2-8 weeks

Same as HBV.

Hep B vaccine

Hep E

Fecal-oral route from

water

2-9 weeks

Severe flu-like
symptoms

None

109

110

Hepatitis A

Hepatitis A contd

Causative agent: A picornavirus, hepatitis A virus (HAV)

Incubation period: 25 days on average

Period of communicability: Highest during 2 weeks

preceding onset of symptoms

Mode of transmission:
In children, ingestion of fecally contaminated water or
shellfish
Day care center spread from contaminated changing tables
Type A occurs in children of all ages and accounts for
approximately 30% of instances.

111

112

Hepatitis A contd

Hepatitis B

Immunity:
Natural; one episode induces immunity for the specific
type of virus
Active artificial immunity: HAV vaccine (recommended for
all children 12 to 23 months of age and workers in day
care centers)
Passive artificial immunity: Immune globulin

Causative agent: A hepadnavirus; hepatitis B virus (HBV)

Incubation period: 120 days on average

113

Period of communicability: Later part of incubation period

and during the acute stage

114

19

25/06/2014

Hepatitis B contd

Hepatitis B contd

Mode of transmission:
Transfusion of contaminated blood and plasma or semen
Inoculation by a contaminated syringe or needle through IV
drug use
May be spread to fetus if mother has infection in third
trimester of pregnancy

Immunity:
Natural; one episode induces immunity for the specific
type of virus
Active artificial immunity: Vaccine for the HBV virus
recommended for routine immunization beginning at birth
and also to all health care providers
Passive artificial immunity: Specific hepatitis B immune
serum globulin

Tends to occur in newborns from placental-fetal transfer and

in adolescents after intimate contact or the use of
contaminated syringes for drug injection.
115

116

Hepatitis C

Hepatitis D

Hepatitis C is a single-strand RNA virus.

Transmission is primarily by blood or blood products, IV

drug use, or sexual contact.

Is similar to HBV in transmission, although it apparently

requires a coexisting HBV infection to be activated.
Disease symptoms are mild, but there is a high incidence
of fulminant hepatitis after the initial infection.

The virus produces mild symptoms of disease, but there

is a high incidence of chronic infection with the virus.
117

118

Hepatitis E

Hepatitis

Enterically transmitted similarly to hepatitis A (fecally

contaminated water).

Clinically, it is impossible to differentiate the type of

hepatitis from the signs that are present.

Disease symptoms from the E virus are usually mild,

except in pregnant women, in whom they tend to be
severe.

119

120

20

25/06/2014

Pathophysiology

Pathophysiology

The virus attacks the parenchymal cells, resulting in local

degeneration and necrosis of the tissue.

contd

Swelling and accumulation of WBC blocks the liver tissue,

resulting in an elevation in bilirubin and ALT and alkaline
phosphatase in the blood.

This stimulates the inflammatory process.

The liver fails to produce enough albumin, resulting in

generalized edema.

121

122

Diagnostic test

Treatment

Laboratory studies - liver enzymes

Bilirubin (levels are increased in the urine)

Bile pigments (levels in the stool are decreased)

Serum bilirubin (levels are increased)

Supportive measurement and bed rest

Hepatitis A is self limiting and does not result in chronic
Hepatitis
No treatment exist for Hepatitis B, antiviral is given for
chronic Hep. B.

123

References

124

References

Browne, N.T., (2007). Nursing care of the pediatric surgical patient (2cd
ed.) Sudbury, MA: Jones and Bartlett Publishers.

Pillitteri, A. (2010). Maternal and child health nursing:

Care of the childbearing and childbearing family

(6th ed.). Philadelphia: Wolters Kluwer Health,
Lippincott Williams and Wilkins.

Datta, P. (2007). Pediatric Nursing. India: Jaypee Brothers, Medical

Publishers
Hatfield, N. T. (2008). Broadribb's Introductory Pediatric Nursing (7 ed.).
China: Wolters Kluwer Health, Lippincott Williams and Wilkins.
Madara, B., Avery, C.T., & Pomarico-Denino, V. (2008). Obstetric and
pediatric pathophysiology. Sudbury, MA: Jones and Bartlett Publishers.

Ricci, S,S., & Kyle, T. (2009). Maternity and Pediatric

Nursing. China: Wolters Kluwer Health, Lippincott
Williams and Wilkins.
Stein, A.M. (2005). NCLEX-RN Review (5th ed.). New
York: Thompson Delmar Learning.

125

126

21

25/06/2014

References

Scenario

Towle, M., & Adams, E,D. (2008). Maternal-Child nursing care. Upper
Saddle River, New Jersey: Prentice Hall.

Well-nourished, 10-year-old female with a history of no major medical problems.

Temperature 101.2 F; pulse 100; respirations 24. Mother reports that yesterday
the child stated she was not feeling well. She wasn't eating, and she had pain in
her stomach. Last night, the pain got worse and she started vomiting. Pain now
localized in right lower quadrant. Legs drawn up against abdomen. Bowel sounds
sluggish. Rebound tenderness present. WBC count of 17,000/mm3.

WHO (2009) Diarrhoeal Diseases. Retrieved from

http://www.who.int/mediacentre/factsheets/fs330/en/index.html

What is the childs diagnosis?

Create a post-operative care plan for this child.

127

128

22