nursing care of children with altered gastrointestinal function- nursing-lectures.com

Nursing care of children with altered gastrointestinal function

Assessment

(1) Health history and physical function

Prenatal history (gestational age and birth wt) Neonatal and infancy GI problems (whether the problem associated with a change of

food or water intake. Life-style and family factors (family history and if the same problem with siblings) Socioeconomic status and living condition, hygiene and health practices. Well-being within a family. Changes in a child’s life e.g starting school, new sibling death. Assess digestive function in a 24hr Nutritional history.

(2) Physical Exam

Mouth: cleft, dental problems, infection. S&S of dehydration: dry mucous. skin color (pale jaundice). Liver. Peristalsis (visible in pyloric stenosis) Bowel sounds (increased with diarrhea). Tender abdomen (appendicits). Displaced heart (diaphragmatic hernia). Distended abdomen ( Hirschsprug’s disease). Hair: loss of pigment or brittle (decreased protein intake). Wt below 10th percentile. Abdominal and rectal assessment

(3) Clinical manifestation of GI problems.

1- Regurgitation (spitting up): normal until a round 8 months of age.

2- Vomiting (assess for onset, frequency, severity, quantity, degree of forcefulness &

presence of bile):

1) Mechanical: secondary to obstructive lesions.

2) Reflexive: due to GIT stimuli (infection or allergy).

3) Central: either CNS involvement (meningitis) or others such as sepsis, abnormal

metabolites.

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3- Abdominal distention due to accumulation of fluid or gases or both in the abdomen, or

as a result of congenital malformations, constipation, hernia, GIT perforation, or

cirrhosis.

4- Abdominal pain.

5- Diarrhea: an increase in the frequency and fluidity of the bowel movement and it may

be (1) acute due to infection, stress or reaction to drug, (2) chronic due to chronic

infection, obstructive inflammatory bowel disease or malabsorption.

(4) Laboratory and Diagnostic studies

4) CBC: infection, anemia, hemorrhage

5) ESR: inflammation.

6) Serum Na, Cl , K: electrolyte balance.

7) Liver enzymes: (1) ALT (Alanine aminotransferase) & AST (Aspartate

aminotransferase) assess liver cells integrity, (2) Alkaline phosphate: hepatic obstruction,

(3) Bilirubin: increased with hemolysis or liver damage, (4) Serum ammonia: impaired

hepatic detoxification of protein, (5) serum amylase: pancreatic enzyme

8) Absorption tests

9) Stool tests:

1. Stool pH: stool turns acid with malabsorption of sugars.

2. Stool fat, trypsin.

3. Stool culture, ova & parasites, occult blood.

Nursing Care

A. Monitoring and measurement:

v Caloric count.

v Intake & output.

v Daily weight.

v USG.

v Abdominal girth.









































v Stool chart.

B. Providing altered means for nutrition and elimination (NG tube, enema).

Impact of GI Alteration on the Child and the Family

A- Chronic alteration needs a lifetime of adjustment.

B- Family will experience negative feeding experiences leading to disturbance in

family’s feeling and achievement.

C- GI problems interferes with infant’s/child’s oral gratification and availability of

energy for mobility.

D- Family adaptation can be encouraged by early involvement in the child’s care.

GI Alterations

I- Anomalies and Obstructions.

Cleft lip & Cleft palate Pyloric stenosis Intussusception Hirschsprung’s disease

II- Alterations associated with an inflammatory bowel disease

Inflammatory bowel diseases: Ulcerative colitis and Crohn disease.

III- Malabsorption Alterations

Celiac disease.

IV- Gastroesophegeal Reflux (Chalasia)

Anomalies and Obstructions of the Digestive Tract

1) Cleft lip (CL) and cleft palate (CP)

- Most common of all facial anomalies

-Incidence rate of cleft lip is 1:7800.

- Incidence rate of cleft palate alone is 1:2000









































- CL with or without CP is more common in males, and CP alone is more common in

females

- Genetic basis is present and the role of non-hereditary factors is not clear

(1) Cleft lip results from incomplete fusion of the embryonic structures surrounding the

primitive oral cavity. The cleft may be unilateral or bilateral and is often associated with

abnormal development of the external nose, nasal cartilages, nasal septum, and maxillary

alveolar ridges. It may or may not be associated with CP. Cleft lip can be slightly

indentation (incomplete) or a widely opened (complete).

(2) Cleft palate occurs when the primary and secondary palatine plates fail to fuse during

embryonic development. CPs may involve only the uvula (incomplete) or extend to both

the soft palate and hard palate (complete cleft). Wide central palatal clefts may be

accompanied by partial or complete absence of nasal septal development, resulting in

communication between the nasal and oral cavities.

(3) Cleft palate associated with cleft lip

Selected Nsg Dx

1- Altered nutrition: less than body requirements RT physical defect, or difficulty eating

following surgical procedure.

2- Risk for trauma of the surgical site RT surgical procedure, dysfunctional swallowing.

3- Pain RT surgical procedure.

4- Altered family processes.

5- Potential for aspiration

3- Potential for infection (otitis media).

4- Potential for impaired verbal communication

Complications

• Due to the irregular shape of the palate it can cause speech difficulties. Sounds can be

hard to hear with inner ear problems creating speech problems.









































• Can affect the development of teeth and jaws.

• Can affect the bite of a patient.

• Can lead to orthodontics, oral surgeries, or Prosthodontics in patients with Clefts.

• The ear and soft palate are connected with the eustachian tube. If food or bacteria gets

into this area it can create infection. Thus children with Cleft tend to have more frequent

ear problems.

• Cleft reduces pressure buildup in the mouth making sucking weaker.

• Increase in chance of Infection

Therapeutic Management

(1) Surgical repair for cleft lip during the first weeks of life (Z-plasty).

(2) Initial surgical repair for cleft palate done during the 4-6 months of age.

• Surgical correction:cleft lip (1 to 2 months). cleft palate (6 to 18 months)

Preoperative Nursing Care

- Encourage parents to hold and touch the baby in the earliest hours or days

- Financial concerns must be discussed with parents

- Providing adequate nutrition and preventing aspiration: use large, soft nipple with large

holes, or long, soft nipples & upright position during feeding.

- Protected from otitis media

- feed upright; assess resp. status during feedings; feed slowly; burp frequently.

Postoperative Nursing Care

1- Preventing the disturbance of the surgical site after the operation: restrains may be

used. No straws, pacifiers, etc.; no tooth brushing; monitor site; remove restraints every

two hours.

2- Preventing aspiration

3- Preventing infection









































4- Providing optimal comfort

Follow-Up

1- Plot height and weight to assess adequacy of nutritional intake

2- Discuss with parent any feeding concerns

3-Assess respiratory status for evidence of infection related to aspiration of milk or

secretions

4- Assess the middle ear

5- Assess speech and teeth

2) Hypertrophic Pyloric Stenosis (HPS)

- An overgrowth of the circular muscle of the pylorus, results in obstruction/ partially /

narrowing of the pyloric sphincter.

- Cause is unknown, however there is a hereditary component.

- This condition usually develops in the first few weeks of life, causing projectile

vomiting, dehydration, metabolic alkalosis, and failure to thrive.

- The stomach contractions increase in frequency and force to empty the stomach content.

CM:

1- Regurgitate small amounts of milk immediately after feeding

2- Vomiting become projectile









































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3- Vomiting may occur during feeding or shortly after feeding or even after hours of

feeding

4- Vomitus contain no bile

5-Gastritis may occur due to prolonged stay of stomach content

6- Wt lose, FTT.

7- Signs of dehydration

Dx assessment

1- in 90% of the infants with pyloric stenosis, the mass can be palpated in the right

epigastrium under the edge of the liver (olivelike mass)

2- peristaltic waves can be noted after feeding moving from left to right

3- Radiograph and ultrasonography

Tx Management: surgery (pyloromyotomy: longitudinal incision through the circular

muscle fibers of the pylorus down to submucosa)

Nursing Care

1- Rehydration the infant and supporting the parents

2- Prevent postoperative fluid volume deficit

3- Providing optimal comfort: using pharmacological and non-pharmacological strategies

4- Teaching to facilitate care at home

Follow-up

1- plot wt and Ht

2- infants' Temp and inspect the surgical site

3- ask the parent about fluid intake/ episodes of vomiting

4- encourage parent to express their concerns

3) Intussusception









































Is an invagination of part of the intestine into an adjacent distal portion of the intestine. It

occurs in healthy, male infants around 6 -months of age and rarely occur before 3-months

or after 3-years of age. The cause is unknown. The most common type is near the

ileocecal valve pushing into the cecum and onto the colon. The involved intestine become

inflamed and edematous with bleeding from the mucosa. Untreated intussusception can

lead to intestinal gangrene, peritonitis and death

• The mesentery is compressed and angled, resulting in lymphatic and venous

obstruction.

• As the edema from the obstruction increases, pressure within the area of intussusception

increases.

• When the pressure equals the arterial pressure, arterial blood flow stops, resulting in

ischemia and the pouring of mucus into the intestine

• Venous engorgement also leads to leaking of blood and mucus into the intestinal lumen

forming the classic currant-jelly stools

A barium enema confirms the Dx ( initially an abdominal radiograph is obtained to detect

intraperitoneal air from a bowel perforation, which contraindicate a barium enema)

Clinical Manifestations:









































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¬ Early symptoms

– Crampy abdominal pain and a drawing up of the knees to the chest

– Separated by periods of apathy

– Poor feeding and vomiting

¬ Late symptoms

– Worsening vomiting, becoming bilious

– Abdominal distension/ Palpable abd. Mass (sausage-shaped)

– Heme positive stools

– Followed by “currant jelly” stools

– Dehydration (progressive)

– If untreated, necrosis and perforation are possible

Treatment:

¬ Supportive therapy

– Initiate IV access

– Nasogastric tube placement and drainage

– Antibiotics if ischemic bowel suspected

¬ Radiographic

– Hydrostatic (barium, water soluble contrast)

¬ Operative

– Manual

– Resection and reanastamosis









































Nursing Interventions

¬ Care of child with abdominal surgery. Preop and postop teaching of child and family.

¬ Passage of a normal brown stool is a sign that the bowel has reduced

4) Hirschsprung Disease (congenital aganglionosis or aganglionic megacolon)

A congenital anomaly resulting from an absence of ganglion cells in the colon, Absence

of ganglion cells results in loss of the rectosphincteric reflex (lack of enteric nervous

system stimulation) which cause a mechanical obstruction caused by a reduced motility

in colon. Hirschsprung disease is more common in males and children with Down’s

syndrome, it can be an acute, life threatening condition or a chronic disorder. In

Hirschsprung disease peristalsis cannot occur. Genetic factors have associated with 3-5%

of the cases, 80% of cases are due to autosomal dominant genetic mutations.

Clinical Manifestations:

¬ Newborn Period

– Failure to pass meconium within 24-48 hours after birth

– Spitting up

– Poor feeding

– Visible bowel loops

– Bile-stained vomitus

– Abdominal distention

¬ Infancy

– Failure to thrive

– Constipation


– Diarrhea and vomiting

– Explosive watery stools









































– Fever

¬ Childhood

– Symptoms more chronic

– Constipation

– Ribbonlike & foul smelling stools


– Palpable fecal masses

– Poorly nourished

– Anorexia, nausea, lethargy

Treatment:

¬ Treated by surgical removal of non-motile part of intestine

¬ Child may have a colostomy (usually only temporary)

¬ Pre and postoperative nursing care for abdominal surgery considerations

¬ Discharge planning and teaching

Nsg Care

¬ Pre-op

– Monitor sign of dehydration

– Improving nutritional status

• Low fiber, high calorie, high protein

• TPN

• Enemas

– Sterilizing colon









































• Saline enemas with antibiotic solutions

• Oral antibiotics

– Psychological preparation for possible colostomy Parent and child

• Stress colostomy is temporary

¬ Post-op

– Stoma Care

– Diaper pinned below dressing to prevent contamination ( Foley catheter may be used)

– Monitor vs, abdominal girth, surgical site

– Skin and stoma care

– NPO until bowel sounds return (NGT)

– Assess pain

¬ Discharge teaching

– Colostomy care

– High fiber diet

Nsg Care (after removing colostomy)

NG tube

When infant pass stool remove the NG

Diet is gradually introduced

After 10th day of surgery the Dr will perform rectal exam

The child will have difficulty or slow toilet train (training advised to be after 2 years of

age)

For follow-up visit S&S of enterocolitis may be after the surgery or after 6-8 years later

B) Alteration associated with an inflammatory process:









































Inflammatory Bowel Diseases IBD:

May occur at any age. Some result from known infectious diseases and some are not

associated with any recognized infection. Includes 2 separate but closely related

conditions: ulcerative colitis and Crohn’s disease; both have similar geographic

distribution and genetic component

Etiology is unknown but runs in families; may be related to infectious agent and altered

immune responses. Peak incidence occurs between the ages of 15 – 35; second peak 60 –

80

Both diseases are chronic diseases with recurrent exacerbations.









































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Diagnostic Tests









































¬ Colonoscopy, sigmoidoscopy: determine area and pattern of involvement, tissue

biopsies; small risk of perforation

¬ Upper GI series with small bowel follow-through, barium enema

¬ Stool examination and stool cultures to rule out infections

¬ CBC: shows anemia, leukocytosis from inflammation and abscess formation

¬ Serum albumin, folic acid: lower due to malabsorption

1) Ulcerative Colitis

¬ Inflammatory process usually confined to rectum and sigmoid colon

¬ Inflammation usually is limited to the mucosa and submucosa and involve continuous

segments with varying degrees of ulceration

¬ Inflammation leads to mucosal hemorrhages and abscess formation, which leads to

necrosis and sloughing of bowel mucosa

¬ Mucosa becomes red, friable, and ulcerated; bleeding is common

¬ Chronic inflammation leads to atrophy, narrowing, and shortening of colon

Manifestations

¬ Diarrhea with stool containing blood and mucus; 10 – 20 bloody stools per day leading

to anemia, hypovolemia, malnutrition

¬ Fecal urgency, tenesmus, LLQ cramping

¬ Fatigue, anorexia, weakness

Crohn’s Disease

¬ Can affect any portion of GI tract, but terminal ileum and ascending colon are more

commonly involved









































¬ CD involves all layers of the bowel wall (transmural) in a discontinuous fashion (skip

lesions)

¬ Fibrotic changes occur leading to local obstruction, abscess formation and fistula

formation

¬ Fistulas develop between loops of bowel (enteroenteric fistulas); bowel and bladder

(enterovesical fistulas); bowel and skin (enterocutaneous fistulas)

¬ Absorption problem develops leading to protein loss and anemia

Manifestations:

¬ Often continuous or episodic diarrhea; liquid or semi-formed; abdominal pain and

tenderness in RLQ relieved by defecation

¬ Fever, fatigue, malaise, weight loss, anemia

¬ Fissures, fistulas, abscesses

Complications of IBD

¬ Hemorrhage: can be massive with severe attacks

¬ Toxic megacolon: usually involves transverse colon which dilates and lacks peristalsis

(manifestations: fever, tachycardia, hypotension, dehydration, change in stools,

abdominal cramping)

¬ Colon perforation: rare but leads to peritonitis and 15% mortality rate

¬ Increased risk for colorectal cancer (20 – 30 times); need yearly colonoscopies

¬ Abscess, fistula formation

¬ Bowel obstruction

¬ Extraintestinal complications

¬ Arthritis

¬ Ocular disorders

¬ Cholelithiasis









































Treatment for IBD

v Sulfasalazine (Azulfidine): salicylate compound that inhibits prostaglandin production

to reduce inflammation

Nursing implications

(1) Warn the parents that the urine will turn to orange-red and soft contact lenses yellow

(2) Teach the child/parent to take the medication with or just after the meals to avoid GI

irritation

(3) Ensure adequate fluid intake

(4) Administer folic acid

(5) Using sunscreens and protective clothing while outside

v Corticosteroids: reduce inflammation and induce remission; with ulcerative colitis

may be given as enema; intravenous steroids are given with severe exacerbations

v Immunosuppressive agents (azathioprine (Imuran), cyclosporine): for clients who

do not respond to steroid therapy alone. Used in combination with steroid treatment and

may help decrease the amount of steroid use

v New therapies including immune response modifiers, anti-inflammatory

cyctokines

v Metronidazole (Flagyl) or Ciprofloxacin (Cipro): For the fistulas that develop

v Anti-diarrheal medications

v Diet therapy

– Correction of nutrient deficits









































– Provide adequate nutrient, protein and energy for normal growth & healing

– Prevent hyperactive bowel activity

– Severe symptoms

• NPO

• TPN

Surgical Treatment

– 25% of patients require a colectomy (in case of toxic megacolon)

– Total proctocolectomy with a permanent ileostomy

• Colon, rectum, anus removed

• Closure of anus

• Stoma in right lower quadrant

Nsg Care

¬ Teaching to control symptoms, adequate nutrition, if client has ostomy: stoma

care.

¬ Controlling diarrhea

¬ Optimal comfort and assessing for complications

¬ Providing essential nutrients

¬ Monitoring physical activity

¬ Preserving skin integrity

¬ Supporting adjustment of the child and family to IBD









































Malabsorptive Alterations:

¬ Disorders associated with some degree of impaired digestion and/or absorption.

¬ Includes digestive defects (digestive enzymes are low or are missing), absorptive

defects (intestinal mucosal transport system is impaired), and anatomic defects (extensive

surgical resection of the bowel or removal of some of the bowel).

Gluten-Sensitive Enteropathy ( Celiac Disease) GSE

Its the second cause of malabsorption after Cystic fibrosis

GSE may have genetic basis

GSE controlled by strict adherence to the dietary regimen

Pathophysiology and Etiology

Mucosa of the small bowel damaged by gluten-containing food ( wheat, barley, rye,

oats). The toxicity of gluten more severe from wheat. Glutine protein contain glutenin

and gliadin ( gliadin is causative agent). Inflammation causes damage to mucosal tissue

of the small intestine, especially the villi that absorb nutrients, which results in

malabsoption of food. Celiac disease symptoms may start in childhood or adulthood, with

onset and severity influenced by the amount of gluten that is eaten

How gluten damage the mucosa there are two explanations

a. Enzymatic insufficiency ( peptidose) cause accumulation of toxic gluten peptide

b. Gluten toxicity results from alteration in immunologic response.

This causes symptoms associated with malnutrition and malabsorption, such as: diarrhea,

weakness, weight loss, abdominal pain, abdominal distention, fatigue, oral ulceration,

bleeding tendency, bone and joint pain, and anemia. Decreased absorption of nutrients

(malabsorption) can cause vitamin deficiencies that deprive the brain, peripheral nervous

system, bones, liver and other organs of vital nourishment, which can lead to other

illnesses

CM and Dx assessment

1- problem started after the introduction of solid food 6-12.

1- Steatorrhea









































2- Stool is bulky foul smelling

3- Absorption of protein, Carbohydrate, Ca, Vit: D , k , B12, B6 and Iron is impaired.

4- Abd distention

5- Child appear malnourished

6- poor Wt gain, failure to grow may be with no S&S of GI disturbances

7- behavioral changes: irritability, lack of cooperative, apathy

8- Failure to thrive pot belly muscle wasting

Assessment

1- family history.

2- child’s dietary history (introduction of new food)

3- on PE abd distention, foul smelling fatty stool

Dx Test

1- Malabsorption screening test ( D-xylose absorption test, that reveal bowel surface area

and later look for fatty stool).

2- CBC

3- Biopsy of jejunal: atrophy of villi

4- Serum protein and immunoglobulin dec.

5- With the positive response to the withdrawal of gluten free diet will confirm the

diagnosis of GSE.

Management

· Dietary management.

· Children in crisis may need:

1- Replacement therapy IV.

2- Vit administration









































3- Corticosteroid to decrease inflammation for the bowel

4- N/G to decrease the distention

5- Before discharge the parents should know the cause of GSE and be knowledgeable

about diet.

Gastroesophageal Reflux (GER)

It is the transfer (backward flow) of gastric contents into the esophagus.

Gastroesophageal Reflux Disease (GERD) includes symptoms of tissue damage that

result from GER. GER becomes the disease (GERD) when complications such as FTT,

bleeding, or dysphagia develop. GERD has also been associated with respiratory

conditions such as apnea, bronchospasm, laryngospasm, and pneumonia

Normally the peristalsis in esophagus and bicarbonate in salivary secretions neutralize

any gastric juices (acidic) that contact the esophagus; during sleep and with

gastroesophageal reflux esophageal mucosa is damaged and inflamed; prolonged

exposure causes ulceration, friable mucosa, and bleeding; if untreated there is scarring

and stricture

Causes of GER are related to dysfunction of the lower esophageal sphincter (LES), delay

in gastric emptying, poor clearance of esophageal acid and the susceptibility of the

esophageal mucosa to acid injury.

Factors that may cause LES pressure to vary:

– Increased gastric volume (post meals)

– Position pushing gastric contents close to gastroesophageal juncture (such as bending or

lying down)

– Increased gastric pressure (coughing, obesity or tight clothing)

– CNS disease

– Delayed gastric emptying

– Hiatal hernia

Children at risk

– Premature infants









































– Infants with bronchopulmonary dysplasia

– Children who have had tracheoesophageal or esophageal atresia repair, neurologic

disorders, scoliosis, asthma, cystic fibrosis, or cerebral palsy

Manifestations

¬ Heartburn after meals, while bending over, or recumbent

¬ May have regurgitation of sour materials in mouth, pain with swallowing

¬ Poor wt. gain, heme-positive emesis or stools, anemia, irritability, gagging or choking

after a feeding, apnea.









































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¬ Atypical chest pain (Esophagitis)

¬ Sore throat with hoarseness

¬ Bronchospasm and laryngospasm

Diagnostic Tests

¬ Barium swallow (evaluation of esophagus, stomach, small intestine)

¬ Upper endoscopy: direct visualization; biopsies may be done

¬ 24-hour ambulatory pH monitoring









































Collaborative Care

¬ Diagnosis may be made from history of symptoms and risks

¬ Treatment includes

1. Life style changes

2. Diet modifications

3. Medications









































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Medications

¬ Antacids for mild to moderate symptoms, e.g. Maalox, Mylanta, Gaviscon

¬ H2-receptor blockers: decrease acid production; e.g. cimetidine, ranitidine, famotidine,

nizatidine

¬ Proton-pump inhibitors: reduce gastric secretions, promote healing of esophageal

erosion and relieve symptoms, e.g. omeprazole (prilosec); lansoprazole (Prevacid)

initially for 8 weeks; or 3 to 6 months

¬ Promotility agent: enhances esophageal clearance and gastric emptying, e.g.

metoclopramide (reglan)

Dietary and Lifestyle Management

¬ Elimination of acid foods (tomatoes, spicy, citrus foods, coffee)

¬ Avoiding food which relax esophageal sphincter or delay gastric emptying (fatty foods,

chocolate, peppermint, alcohol)

¬ Maintain ideal body weight

¬ Eat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to

bed

¬ Elevate head of bed on 6 – 8² blocks to decrease reflux









































¬ No smoking

¬ Avoiding bending and wear loose fitting clothing

Surgery indicated for persons not improved by diet and life style changes

¬ Laparoscopic procedures to tighten lower esophageal sphincter

¬ Open surgical procedure: Nissen fundoplication

Nursing care

¬ Identify children with suggestive symptoms

¬ Teach parents regarding home care, feeding, positioning, and medications

¬ Provide care for child undergoing surgical repair

¬ Most infants and children outgrow GER, and simple conservative lifestyle changes are

all that is needed

Appendicitis

Acute appendicitis is the most common condition requiring emergentabdominal surgery

in childhood. Appendicitis occurs when the interior of the appendix becomes filled with

something that causes it to swell, such as mucus or stool. The appendix then becomes

irritated and inflamed. The blood supply to the appendix is cut off as the swelling and

irritation increase. Adequate blood flow is necessary for a body part to remain healthy.









































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When the blood flow is reduced, the appendix starts to die. Rupture (or perforation)

occurs as holes develop in the walls of the appendix, allowing stool, mucus, and other

substances to leak through and get inside the abdomen. An infection inside the abdomen

known as peritonitis occurs when the appendix perforates.

The clinical diagnosis of acuteappendicitis is often not straightforward because

approximatelyone-third of children with the condition have atypical clinicalfindings. The

delayed diagnosis of this condition has seriousconsequences, including appendiceal

perforation, abscess formation,peritonitis, sepsis, bowel obstruction, and death.

Physical findings more commonly associated with appendicitis include right lower

quadrant rebound tenderness and, to a lesser degree, percussion tenderness. The presence

of guarding and rigidity also increased the likelihood ratio of the diagnosis. Important

investigations include the diagnostic reliability of rising white blood cell (WBC) counts,

especially a count of over 15,000 per mm3 (15 3 10

9 per L) which increases the likelihood

ratio of appendicitis to 7.0. A low WBC count makes this diagnosis unlikely.

Ultrasonography appears to be useful in children with appropriate symptoms in whom the

diagnosis is uncertain. It does not appear useful in children with very weak or very strong

evidence of appendicitis because of the significant possibility of false-positive results.

Although computed tomographic (CT) scanning is accurate in predicting the presence or

absence of appendicitis, its added value in children with very strong evidence for or

against appendicitis is unclear.

In neonates, the clinical features of appendicitis are nonspecific and include irritability or

lethargy, abdominal distention, vomiting, a palpable abdominal mass and cellulitis of the

abdominal wall. In infants and children up to two years of age, symptoms include

vomiting, pain, diarrhea and fever. Diagnosis is more difficult in this age group because

the symptoms are nonspecific.

ALERT!! SIGNS OF PERFORATION: in addition to fever include sudden relief from

pain after perforation, subsequent increase in pain (usually diffuse and accompanied by

rigid guarding of the abdomen) progressive abdominal distention, tachycardia, rapid-

shallow breathing, pallor chills and irritability

¬ Preop:

-semi-fowler’s or right side-lying

-avoid laxatives, enemas, heat applications. Nurse would not administer a laxative to

avoid increased bowel motility and risk of perforation

Treatment: surgery prior to rupture and peritonitis

-cold packs to abdomen









































-sudden relief of pain usually indicates a ruptured appendix

¬ Postop:

-monitor vs

-ambulate within 6 to 8 hours

-turn, cough, deep breathe

-monitor I & O, pain

-with rupture, slow recovery

NURSING CARE PLAN

The Child with Appendicitis

Nursing Diagnosis: Pain related to inflamed appendix

Patient Goal 1: Will experience no pain or reduction of pain to level acceptable to child

• NURSING INTERVENTIONS/RATIONALES

See Pain Assessment; Pain Management, Chapter 26

Allow position of comfort (usually with legs flexed) because it may vary among children

Provide small pillow for splinting of abdomen

Administer analgesia to provide pain relief

• EXPECTED OUTCOME

Child rests quietly, reports and/or exhibits no evidence of discomfort

Nursing Diagnosis: Risk for fluid volume deficit related to decreased intake and losses

secondary to loss of appetite, vomiting

Patient Goal 1: Will receive fluids for adequate hydration


Maintain NPO to minimize losses through vomiting and minimize abdominal distention

Maintain integrity of infusion site for IV fluids and electrolytes









































Administer IV fluids and electrolytes as prescribed

Monitor intake and output to assess hydration

• EXPECTED OUTCOMES

Child receives sufficient fluids to replace losses

Child exhibits signs of adequate hydration (specify)

Nursing Diagnosis: Risk for infection related to possibility of rupture

Patient Goal 1: Will experience minimized risk of infection


Closely monitor vital signs, especially for increased heart rate and temperature and rapid,

shallow breathing, to detect ruptured appendix

Observe for other signs of peritonitis (e.g., sudden relief of pain [sometimes] at time of

perforation, followed by increased, diffuse pain and rigid guarding of the abdomen,

abdominal distention, bloating, belching [from accumulation of air], pallor, chills, and

irritability) for appropriate treatment to be initiated

Avoid administering laxatives or enemas, because these measures stimulate bowel

motility and increase risk of perforation

Monitor WBC count as indicator of infection


Child remains free of symptoms of peritonitis

Signs of peritonitis are recognized early (specify)

POSTOPERATIVE CARE

See Postoperative Care in Nursing Care Plan: The Child Undergoing Surgery, Chapter 27

RUPTURED APPENDIX

Nursing Diagnosis: Risk for infection related to presence of infective organisms in

abdomen

Patient Goal 1: Will experience minimized risk of spread of infection










































Provide wound care and dressing changes as prescribed to prevent infection

Monitor vital signs and WBC count to assess presence of infection

Administer antibiotics as prescribed


Child demonstrates resolution of peritonitis as evidenced by lack of fever, clean wound,

normal WBC

Nursing Diagnosis: Risk for injury related to absence of bowel motility

Patient Goal 1: Will not experience abdominal distention, vomiting


Maintain NPO in early postoperative period to prevent abdominal distention and

vomiting

Maintain NG tube decompression until bowel motility returns

Assess abdomen for distention, tenderness, presence of bowel sounds to assess presence

of peristalsis

Monitor passage of flatus and stool as indicator of bowel motility


Child does not exhibit signs of discomfort; abdomen remains soft and nondistended; child

does not vomit

Nursing Diagnosis: Altered family processes related to illness and hospitalization of child

Patient (family) Goal 1: Will receive adequate support


Encourage expression of feelings and concerns to enhance coping

Encourage child to discuss hospital admission and treatments in order to clarify

misconceptions

See Nursing Care Plan: The Child in the Hospital, Chapter 26









































See Nursing Care Plan: The Family of the Child Who Is Ill or Hospitalized, Chapter 26


Child and family express feelings and concerns

Child and family demonstrate understanding of hospitalization and treatments

Data from Wong DL: Whaley & Wong's Nursing Care of Infants and Children, ed. 6, St.

Louis, 1999, Mosby, Inc.









































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