Gastrointestinal System Part 2

8/20/2019 Gastrointestinal System Part 2

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25/06/20

The Gastrointestinal System(Part 2)

Prepared by: M. Cole

MSN BSN RN

Objectives

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

1. Describe the common gastrointestinal system healthconditions in the child.

2. Perform health assessment of thegastrointestinal system on the childaccording to age.

2

Objectives cont’d

3. Describe the pathophysiology, incidence,clinical manifestation and prognosis ofeach disease process.

4. Explain diagnostic tests for each conditionidentified.

5. Describe treatment modalities for thedifferent conditions.

3

Objectives cont’d

6. Use the nursing process to provide ageappropriate nursing care for the child witha gastrointestinal system condition.

7. Describe health promotion strategies usedto restore health for the child with agastrointestinal system condition.

4

Dental caries

Is a progressive and destructive process causingdecalcification of the tooth enamel, destruction of dentinand cavitation of the teeth.

It can spread into the tooth pulp and may causeinflammation and abscess.

5

Dental caries

fluorideandfluorosis.com

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Etiology

Many organisms may cause dental caries.

Streptococci is such organism, the main cariogenicagent.

7

Pathophysiology

Streptococci produces a extra cellular polysaccharideand forms a plague over the teeth.

Gradual tooth decay begins following demineralizationof the enamel.

8

Destruction of dentin occurs with cavity formationoccurring causing inflammation and abscess formation.

Biting and contact surface are the most common sites.

Pathophysiology cont’d

9

Risk factors

Carbohydrate rich foods especially chocolate which stick toteeth

Poor oral hygiene with inadequate dental care

Sleeping with feeding bottle in mouth

Sweetening agents like honey

Fluoride deficiency/excess

10

Clinical manifestations

Pits and fissures in biting and contact surfaces commonlyin molars as initial features.

Cavity formation involving pulp, dental abscess

Sepsis

11

Treatment

Analgesics to relieve pain

Extraction

Antibiotics

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Preventative measures

Dietary modification by avoiding carbohydrate rich foodand avoiding oral retaining.

Use of fluoride tooth paste

Avoidance of chewing gum, chocolates, bottle feeding…

13

Preventative measures cont’d

Good oral and dental hygiene with correct brushingtechnique.

Mechanical movement of plaque and debris.

Dental sealant to pits and fissures.

Regular dental check-up

14

Oesophageal stricture

Narrowing of the oesaphagus.

Acquired oesaphageal stricture in childhood are mostlikely a result of reflux oesophagitis, corrosive injury oranastomotic scaring.

15

Oesophageal stricture

aurorahealthcare.org nejm.org16


Drooling

Inability to swallow saliva and fluids

Difficulty feeding - ability to take liquids but not solids

Regurgitation of undigested food

17

Diagnostic test

Oesaphagoscopy - to evaluate the length, character,ability to dilate the defect and the condition of the mucusmembrane.

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Treatment

Sedation and dilation (using rubber balloon, dilator)

Resection with end to end anastomosis

19

Gastro-oesophageal reflux(Infant)

Regurgitation of stomach secretions into the esophagusthrough the gastroesophageal (cardiac) valve.

Occurs mainly in infants and adolescent

20

Gastro-oesophageal reflux cont’d

drbrandonfox.com

21

Pathophysiology

Occurs from a neuromuscular disturbance in which thegastroesophageal (cardiac) sphincter.

The lower portion of the esophagus spasm and allow easyregurgitation of gastric contents into the esophagus.

22

Gastro-oesophageal reflux cont’d

Regurgitation occurs almost immediately after feeding orwhen the infant is laid down after a feeding.

If the amount of the reflux is large or constant, an infantdoes not retain sufficient calories and will fail to thrive.

In addition, aspiration pneumonia or esophageal stricturefrom the constant reflux of hydrochloric acid into theesophagus can occur.

23


Vomiting

Irritability and apnea may be evident

Diagnostic test Fiberoptic endoscopy or Oesophagography (barium swallow) will

show the involved sphincter and the refluxof stomach contents into the esophagus.

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Treatment

Traditional treatment:

Feed infants a formula thickened with rice cereal whileholding them in an upright position

Then keeping them upright in an infant chair for 1 hourafter feeding so gravity can help prevent reflux.

25

Treatment cont’d

H2 receptor antagonist Zantac (Ranitidine) or

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

26

Treatment cont’d

Gastroesophageal reflux is usually a self-limitingcondition.

As the oesophageal sphincter matures and the childbegins to eat solid food and is maintained in a moreupright position, the problem resolves.

27

Treatment cont’d

Laparoscopic or surgical myotomy procedure (narrowingof the esophageal sphincter)

Followed by temporary placement of a NGT.

28

Gastroesophageal reflux disease(Adolescent)

Affects about 20% of adults; symptoms frequently beginin adolescence.

Irritation to the esophagus occurs when stomachcontents, including hydrochloric acid, reflux through thelower esophageal sphincter and irritate the esophageallining.

29

Etiology

Reflux occurs because of an incompetent sphincterespecially when the adolescent lies supine or when intra-abdominal pressure is increased by a full stomach, liftingor bending, or tight clothing.

It is potentially dangerous because it can lead to erosion ofthe esophagus with perforation or stricture of theesophagus.

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Clinical manifestation

The typical symptom is heartburn that occurs 30-60minutes after a meal.

31

Diagnostic Test

Based on history (typical symptoms of heartburn) and, ifsymptoms are severe.

Endoscopy to reveal the irritated esophagus(oesophagitis).

32

Treatment

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

Antacids (relieve pain by decreasing the concentration ofthe stomach acid)

H2-receptor antagonists (Pepcid or Zantac) to preventheartburn symptoms.

Proton pump inhibitors such as omeprazole (Prilosec) tohalt the release of stomach acids

33

Treatment cont’d

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 spicyfoods.

34

Treatment cont’d

Avoiding foods that delay gastric emptying such as fattyfoods, chocolate, or alcohol and eating smaller portionsmay also be helpful.

Weight loss, avoiding bending after meals, and removingtight belts are also recommended steps.

35

Gastroenteritis

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 causemild to severe dehydration.

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Pathophysiology

Believed that the causative agent damages and destroysepithelial cells lining the intestine causing the followingclinical manifestations.

Diarrhea occurs when intestinal fluid output overwhelmsthe absorptive capacity of the gastrointestinal tract.

37

Pathophysiology

The decrease in total body water causes a reduction inintracellular and extracellular fluid but the clinicalmanifestations of dehydration are most closely related tointravascular volume depletion.

38

Pathophysiology

The 2 primary mechanisms responsible for acute gastroenteritis are:

damage to the villous brush border of the intestine, causingmalabsorption of intestinal contents and leading to an osmoticdiarrhea, and

the release of toxins that bind to specific enterocyte receptors andcause the release of chloride ions into the intestinal lumen, leading

to secretory diarrhea.

39


Nausea

Vomiting

Diarrhea

Fever

Dehydration

Electrolyte imbalance

40

Diagnostic test

Stool culture may be done

41

Treatment

IVF

Electrolytes

Antibiotics

Rehydration salts/fluids

Diet when vomiting and diarrhea subsides

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Nursing management

Administer and monitor IVF

Skin care

Administer medication as ordered

Offer rehydration fluids

43

Diarrhoeal diseases

Is the passage of loose, liquid or watery stool at leastthree times per day.

The recent change in consistency and the character of thestool rather than the number of stool is more important.

44

Diarrhoeal diseases

colon-cleanse-information.com

45

Acute Diarrhoea

Is an attack of loose motion with sudden onset whichusually last 3 – 7 days but may last up to 10 – 14 days.

Caused by infection of the large intestine but can also beassociated with infection of the gastric mucosa and thesmall intestine.

Acute GE is usually use to describe acute diarrhoea46

Chronic Diarrhoea

When loose motion is occurring for 3 weeks or more.

Usually related to underlying organic disease with orwithout malabsorption.

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Dysentery

Diarrhoea with watery stool and visible blood in the stool.

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Persistent Diarrhoea

Refers to the episode of acute diarrhoea that last for 2weeks or more and may be due to infective state.

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Etiology

A large number of organism are responsible for acutediarrhoea. 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, malariaetc.)

Fungi (Candida albicans)

50

Etiology cont’d

Other causes of diarrhoea are related to nutritional anddietary factors:

Overfeeding

Underfeeding/malnutrition

Food allergies

Food poisoning

Some drugs such as antibiotics cause diarrhoea51

Etiology cont’d

Malnutrition:

Children who die from diarrhoea often suffer fromunderlying malnutrition, which makes them morevulnerable to diarrhoea.

Each diarrhoeal episode, in turn, makes their malnutritioneven worse. Diarrhoea is a leading cause of malnutrition inchildren under five years old.

52

Etiology cont’d

Source: Water contaminated with human faeces, e.g. fromsewage, septic tanks and latrines, is of particular concern.

Animal faeces also contain microorganisms that can causediarrhoea.

Other causes: Diarrhoeal disease can also spread fromperson-to-person, aggravated by poor personal hygiene. Foodis another major cause of diarrhoea when it is prepared orstored in unhygienic conditions. Water can contaminate foodduring irrigation. Fish and seafood from polluted water mayalso contribute to the disease. 53

Incidence

Every year there are about two billion cases of diarrhoeal diseaseworldwide.

Diarrhoeal disease is a leading cause of child mortality and morbidityin the world, and mostly results from contaminated food and watersources.

Diarrhoea due to infection is widespread throughout developingcountries.

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**Key facts**

Diarrhoeal disease is the second leading cause ofdeath in children under five years old. It is bothpreventable and treatable.

Kills 1.5 million children every year.

Globally, there are about two billion cases of diarrhoealdisease every year.

Mainly affects children under two years old.

Leading cause of malnutrition in children under five yearsold.

55

Degree of Dehydration

Rated on a scale of three. Early dehydration/Mild – may or may not have signs or

symptoms.

Moderate dehydration:

thirst

restless or irritable behaviour

decreased skin elasticity

sunken eyes56

Degree of Dehydration cont’d

Severe dehydration:

shock,

with diminished consciousness,

lack of urine output,

cool moist extremities,

a rapid and feeble pulse,

low or undetectable blood pressure,

and pale skin.

57

Diarrhoea

The most severe threat posed by diarrhoea isdehydration.

During a diarrhoeal episode, water and electrolytes(sodium, chloride, potassium and bicarbonate) are lostthrough liquid stools, vomit, sweat, urine and breathing.

Dehydration occurs when these losses are not replaced.

58

Diagnostic test

Stool culture

Blood culture

Serology (evaluating antibodies to identify microbes with whichyou have recently been infected)

59

Treatment

Rehydration with IVF in case of severe dehydration orshock, oral rehydration salts (ORS) solution formoderate or no dehydration.

Nutrient-rich foods

Antibiotics (if cause is bacterial agent)

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Prevention

access to safe drinking-water

improved sanitation

exclusive breastfeeding for the f irst six months of life

good personal and food hygiene

health education about how infections spread

rotavirus vaccination

61

Nursing management

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 asordered

62

Helminthiasis

Infestation of worms

Common types are:

Round worms ( Ascaris lubricoides )

Pinworm or threadworm (Enterobius vermicularis)

Hook worm ( Ancylostoma duodenale, Necatoramericanus )

Tape worm (Taenia saginata, Taenia solum )63

Helminthiasis

hon.ch

infection-research.de

64

Etiology

Helminthiasis in human are caused by three types:

Nematodes (roundworm, pinworm, hookworm)

Cestodes (tapeworm)

Trematodes (fishworm, flukes)

65

Roundworm(Ascariasis)

Most common helminthic infestation.

Lives in the lumen of the small intestine.

The adult female round worm measures 20-40 cm andthe male measure 12-30 cm in length.

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Pathophysiology

The female produces approximately 200,000 to 300,000eggs per day.

Eggs are excreted in faeces and external environment theybecome infective in favourable conditions.

Mature eggs when ingested hatches in the duodenum torelease larvae.

67


The larvae penetrates the intestine, and are carried toliver then lung in the blood stream.

They break through the alveolar wall while in the lungand migrates into the bronchioles, get coughed upthrough the trachea.

68


They get re-swallowed to reach the small intestine, wherethey become adult worms in 60 to 80 day. They have a lifespan of 1.5 to 2 years.

69

Worm cycle

70

Montresor & Diarra, n.d (WHO)

Transmission

Mode of transmission: Feco-oral route of ingestion ofinfective eggs with food or soil or drink or bycontaminated hands and fingers.

Communicable period: Continued until all fertile eggsare destroyed and stools are negative of roundwormeggs.

Incubation period: About 2 months71


Abdomen pain

Abdominal distention

Nausea

Cough

Loss of weight

Growth failure

Vitamin deficiency

Voracious appetite

Bruxism

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Associated problems

Pica Sleeplessness

Urticaria

Fever

Diarrhea

ayurdoc.blogspot.com

73

Complications

Intestinal obstruction

Gangrene

Perforation

Obstructive jaundice

Appendicitis

Pancreatitis

Ascaris encephalopathy

Liver abscess

Peritonitis

Ascaris pneumonia

Convulsion and featureslike retinoblastoma.

clinicianonnet.blogspot.com

74

Treatment

Antihelmintics - Mebendazole or Albendazole

Piperazin cirtate- ideal drug for eradication ofroundworm infection as it causes paralysis of the worms.

75

Prevention

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.

76

Other helminthic infestation

Truchuris tricuria (whip worm): contaminated food, drinksand hands or indirectly through flies and insects.

Stronglyoides stercoralis : through skin contact withcontaminated soil.

Dracunculus medinensis (Guinea worm): contaminatedwater that contain crustaceans.

Shistoma mansoni or S. hematobium (flatworm):penetration of intact skin

Trichinosis : ingestion of undercooked meat contaminatedwith infective larvae.

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Protein-energy malnutrition

Results from an insufficient intake of high qualityprotein of from conditions in which protein absorption isimpaired or a loss of protein increases.

Clinical manifestation may not be apparent until thecondition is well advanced.

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Kwashiorkor

Results from severedeficiency of protein withan adequate caloric intake.

It accounts for most of themalnutrition worldwide.

nzdl.org

79

Kwashiorkor

caribbean-icons.org cs.stedwards.edu

80

Pathophysiology

Hypoproteinemia results in edema, this occurs due to ashift of body fluid from intravascular compartment tointerstitial spaces causing ascites.

The edema tends to be dependent

81

Etiology

Tends to occur after weaning when the child changes frombreast milk to a diet consisting mainly of carbohydrates.

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

age.

Most common in underdeveloped countries.

82


Swollen abdomen

Edema

GI changes – diarrhoea

Iron deficiency anemia

Hair thin and dry with patchy alopecia

Child becomes apathetic and irritable

Retarded growth

Muscle wasting83

Treatment

High protein diet

Prognosis

In untreated clients mortality rates is 30% or higher.

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Marasmus

Deficiency of all food groups, basically starvation.

These children will basically suck at anything includingclothing or a finger.

Treatment is high nutrients diet

85

Child with Marasmus

newfoundations.org.uk

86


Similar to Kwashiorkor

Iron deficiency anemia

Irritability

Retarded growth

Muscle wasting

Diarrhoea

87

Obesity

The accumulation of excess body fat.

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

i.dailymail.co.uk topnews.in 88

Incidence

Higher in female and adolescents of lower socioeconomicstatus

**Research also indicates that adolescents of affluent familiesare more prone to obesity.

89

Influential factors

Food choices

Eating practice

Lack of exercise

Hormonal changes

Excessive television watching

Overprotective parenting

Emotional factors

Genetics90


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Low self esteem

Emotional problems resulting in isolation

Excessive appetite

Weight gain

**Individuals with truncal obesity are more prone tocardiovascular disease and diabetes.

91

Treatment

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 themeal)

92

Recommendations

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

93

Appendicitis

Inflammation of the vermiform appendix, a small sac atthe end of the cecum.

94

Appendix

internal-optimist.blogspot.com

k n o l . g o o g l e . c o m

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Pathophysiology

A blockage of the lumen of the appendix occurs orinflammation as a result of an upper respiratory or otherbody infection followed by infection, inflammation andedema.

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Leading to compression of blood vessels and cellularmalnutrition.

Necrosis and pain results.

If not discovered early rupture will occur and fecal matterwill be spilled in the abdomen


97

Etiology

May be caused by:

Mechanical obstruction (fecaliths, intestinal parasites)

Anatomic defect

May be related to decreased fibre intake in the diet

98

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 McBurney’s point (1/3 way between anteriorsuperior crest of iliac and the umbilicus)

Nausea and vomiting

Guarding of abdomen

Rebound tenderness

Decreased bowel sound Fever

100

Diagnostic test

WBC increased

Elevated acetone in urine

101

Treatment

Surgical removal of the appendix

Antibiotics

Antipyretics

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Nursing management

Prevent perforation: do not give enemas, cathartics oruse heating pad

Support child and parents

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Nursing management cont’d

Post-op

Monitor NG tube aspirate

Position in semi-fowlers

Administer medications asordered

Monitor op site for signs ofinfection

IVF

Advancing diet

Pain relief and measures

Discharge teaching

104

Ruptured Appendix

The potential for peritonitis increases greatly.

The white blood cell count rises to more than20,000/mm3.

105

Nursing management

Position the child in a semi-Fowler's position (if possible,so that infected drainage from the cecum drainsdownward into the pelvis rather than upward toward thelungs).

IV fluid for hydration.

Preoperative antibiotics will be begun or as soon as the

ruptured appendix is confirmed106

Nursing management cont’d

Assess for signs of peritonitis with dressing changes.

boardlike (rigid) abdomen,

generally shallow respirations (because deep breathingputs pressure on the abdomen and causes pain),

and increased temperature.

107

Hepatitis

Inflammation and infection of the liver

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

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Common causes of HepatitisOrganism Mode of

transmissionIncubation Clinical

manifestation Availableimmunization

Hep A Fecal- oral route, person

to person, contaminatedwater or food (shellfish)

4 weeks (10-50

days)

Acute onset (may be

less acute in youngchildren). Usually donot become jaundiced. Flu-likesymptoms

Immune serum

globulinHep A vacine

Hep B Blood and body fluids 1-6 months Nausea, vomiting,anorexia, fatigue,upper RQ pain,hepatomegaly

Hep B immuneglobulinHep B vaccine

109

Common causes of Hepatitis cont’d

Organism Mode of

transmission

Incubation Clinical

manifestation

Available

immunizationHep C Blood and blood

products6-7 weeks Frequent episodes of

flu-like symptoms

without jaundice. Riskof cancer

None

Hep D Blood and blood

products. Found withHBV

2-8 weeks Same as HBV. Hep B vaccine

Hep E Fecal-oral route fromwater

2-9 weeks Severe flu-likesymptoms

None

110

Hepatitis A

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

Incubation period: 25 days on average

Period of communicability: Highest during 2 weekspreceding onset of symptoms

111

Hepatitis A cont’d

Mode of transmission:

In children, ingestion of fecally contaminated water orshellfish

Day care center spread from contaminated changing tables

Type A occurs in children of all ages and accounts for

approximately 30% of instances.112

Hepatitis A cont’d

Immunity:

Natural; one episode induces immunity for the specifictype of virus

Active artificial immunity: HAV vaccine (recommended forall children 12 to 23 months of age and workers in daycare centers)

Passive artificial immunity: Immune globulin

113

Hepatitis B

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

Incubation period: 120 days on average

Period of communicability: Later part of incubation periodand during the acute stage

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Hepatitis B cont’d 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

Tends to occur in newborns from placental-fetal transfer andin adolescents after intimate contact or the use ofcontaminated syringes for drug injection.

115

Hepatitis B cont’d

Immunity:

Natural; one episode induces immunity for the specifictype of virus

Active artificial immunity: Vaccine for the HBV virusrecommended for routine immunization beginning at birthand also to all health care providers

Passive artificial immunity: Specific hepatitis B immuneserum globulin

116

Hepatitis C

Hepatitis C is a single-strand RNA virus.

Transmission is primarily by blood or blood products, IVdrug use, or sexual contact.

The virus produces mild symptoms of disease, but there

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

Hepatitis D

Is similar to HBV in transmission, although it apparentlyrequires a coexisting HBV infection to be activated.

Disease symptoms are mild, but there is a high incidenceof fulminant hepatitis after the initial infection.

118

Hepatitis E

Enterically transmitted similarly to hepatitis A (fecallycontaminated water).

Disease symptoms from the E virus are usually mild,except in pregnant women, in whom they tend to besevere.

119

Hepatitis

Clinically, it is impossible to differentiate the type ofhepatitis from the signs that are present.

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Pathophysiology

The virus attacks the parenchymal cells, resulting in localdegeneration and necrosis of the tissue.

This stimulates the inflammatory process.

121


Swelling and accumulation of WBC blocks the liver tissue,resulting in an elevation in bilirubin and ALT and alkalinephosphatase in the blood.

The liver fails to produce enough albumin, resulting ingeneralized edema.

122

Diagnostic test

Laboratory studies - liver enzymes

Bilirubin (levels are increased in the urine)

Bile pigments (levels in the stool are decreased)

Serum bilirubin (levels are increased)

123

Treatment

Supportive measurement and bed rest

Hepatitis A is self limiting and does not result in chronicHepatitis

No treatment exist for Hepatitis B, antiviral is given for

chronic Hep. B.124

ReferencesBrowne, N.T., (2007). Nursing care of the pediatric surgical patient (2cd

ed.) Sudbury, MA: Jones and Bartlett Publishers.

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

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.

125

References

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.

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

Nursing. China: Wolters Kluwer Health, LippincottWilliams and Wilkins.

Stein, A.M. (2005). NCLEX-RN Review (5th ed.). New York: Thompson Delmar Learning.

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References

Towle, M., & Adams, E,D. (2008). Maternal-Child nursing care . Upper

Saddle River, New Jersey: Prentice Hall.

WHO (2009) Diarrhoeal Diseases. Retrieved fromhttp://www.who.int/mediacentre/factsheets/fs330/en/index.html

127

Scenario

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 yesterdaythe child stated she was not feeling well. “She wasn't eating, and she had pain inher stomach. Last night, the pain got worse and she started vomiting.” Pain nowlocalized in right lower quadrant. Legs drawn up against abdomen. Bowel soundssluggish. Rebound tenderness present. WBC count of 17,000/mm3.

What is the child’s diagnosis?

Create a post-operative care plan for this child.

128

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Gastrointestinal System Part 2

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