(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).
- 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.
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.
A. Monitoring and measurement:
v Caloric count.
v Intake & output.
v Daily weight.
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.
I- Anomalies and Obstructions.
- Cleft lip & Cleft palate
- Pyloric stenosis
- 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
• 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
(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
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.
1- Regurgitate small amounts of milk immediately after feeding
2- Vomiting become projectile
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
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)
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
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
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)
¬ 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
¬ Supportive therapy
– Initiate IV access
– Nasogastric tube placement and drainage
– Antibiotics if ischemic bowel suspected
– Hydrostatic (barium, water soluble contrast)
– Resection and reanastamosis
¬ 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.
¬ Newborn Period
– Failure to pass meconium within 24-48 hours after birth
– Spitting up
– Poor feeding
– Visible bowel loops
– Bile-stained vomitus
– Abdominal distention
– Failure to thrive
– Abdominal distention
– Diarrhea and vomiting
– Explosive watery stools
– Symptoms more chronic
– Ribbonlike & foul smelling stools
– Abdominal distention
– Palpable fecal masses
– Poorly nourished
– Anorexia, nausea, lethargy
¬ 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
– Monitor sign of dehydration
– Improving nutritional status
• Low fiber, high calorie, high protein
– Sterilizing colon
• Saline enemas with antibiotic solutions
• Oral antibiotics
– Psychological preparation for possible colostomy Parent and child
• Stress colostomy is temporary
– 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)
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.
¬ 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
¬ 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
¬ 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
¬ 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
¬ Ocular disorders
Treatment for IBD
v Sulfasalazine (Azulfidine): salicylate compound that inhibits prostaglandin production to reduce inflammation
(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
– 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
¬ 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
¬ 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.
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
1- family history.
2- child’s dietary history (introduction of new food)
3- on PE abd distention, foul smelling fatty stool
1- Malabsorption screening test ( D-xylose absorption test, that reveal bowel surface area and later look for fatty stool).
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.
· 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
¬ 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.
¬ Atypical chest pain (Esophagitis)
¬ Sore throat with hoarseness
¬ Bronchospasm and laryngospasm
¬ Barium swallow (evaluation of esophagus, stomach, small intestine)
¬ Upper endoscopy: direct visualization; biopsies may be done
¬ 24-hour ambulatory pH monitoring
¬ Diagnosis may be made from history of symptoms and risks
¬ Treatment includes
1. Life style changes
2. Diet modifications
¬ 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
¬ 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
¬ 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
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. 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 3 109 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
-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
-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
• NURSING INTERVENTIONS/RATIONALES
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
• NURSING INTERVENTIONS/RATIONALES
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
• EXPECTED OUTCOMES
Child remains free of symptoms of peritonitis
Signs of peritonitis are recognized early (specify)
See Postoperative Care in Nursing Care Plan: The Child Undergoing Surgery, Chapter 27
Nursing Diagnosis: Risk for infection related to presence of infective organisms in abdomen
Patient Goal 1: Will experience minimized risk of spread of infection
• NURSING INTERVENTIONS/RATIONALES
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
• EXPECTED OUTCOME
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
• NURSING INTERVENTIONS/RATIONALES
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
• EXPECTED OUTCOME
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
• NURSING INTERVENTIONS/RATIONALES
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
• EXPECTED OUTCOMES
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.