NURSING 1310 - PEDS MODULES EXAM 4.

PEDS MODULES EXAM 4 UNIT 11: GI DISORDERS REVIEW OF ANATOMY & PHYSIOLOGY • Upper GI Tract o Mouth o esophagus • Lower GI Tract o Stomach o Duodenum o Jejunum o Ileum o Cecum o Appendix o Ascending colon o Transverse colon o Descending colon o Sigmoid colon o Rectum o Anal canal o Anus • Accessory structures o ??? PEDIATRIC DIFFERENCES • Peristalsis more rapid than in adults = diarrhea • Fever increases peristalsis CONGENITAL MALFORMATIONS • Present at birth • PARENTS’ REACTIONS o Disintegration ▪ They’re torn apart ▪ Also in denial – it’ a protective mechanism until they can accept the situation o Adjustment ▪ Acceptance of the situation o Reintegration ▪ Total acceptance ▪ Working to move on with their lives INFLUENCES ON PARENTS’ REACTIONS • Sex of child, expectations o Thought their kid was going to be a doctor or a lawyer • Socioeconomic status o Enough money to have the problem repaired? • Religion o The condition is the work of God • Strength of marriage o They blame the other for the bad genes • Do they have an adequate support system? • Source of maladaptation o Can the problem be fixed? CLEFT LIP/PALATE • Congenital malformations of lip/palate • Occur during embryonic development • Cleft palate is a midline fissure of the palate that results from failure of the two palatal processes to fuse INCIDENCE OF CLEFT LIP/PALATE • Variable based on ethnicity o More common in Asians & American Indians • Boys more often get cleft lip and palate • Girls get just cleft palate more frequently • Tend to occur together o She’s never seen cleft palate alone – always with cleft lip ETIOLOGY OF CLEFT LIP/PALATE • Genetics: Chromosomal problems o Trisomy 13 o Pierre Robin Syndrome ▪ A condition in which an infant has a smaller than normal lower jaw, a tongue that falls back in the throat, and difficulty breathing. It is present at birth. • Environmental: o Tobacco o ETOH ▪ Some patients insist a little alcohol will settle their stomach o Dilantin o Steroids o Folic acid deficiency o Anticonvulsants o Retinoids ▪ The retinoids comprise a class of chemical compounds that are vitamers of vitamin A or are chemically related to it. Retinoids have found use in medicine where they regulate epithelial cell growth PATHOPHYSIOLOGY OF CLEFT LIP/PALATE • Structural failure in fusion of maxillary processes between 4–10 weeks gestation → abnormal opening in lip/palate → failure to maintain an effective suction during feeding  aspiration and respiratory difficulties. ASSESSMENT OF CLEFT LIP/PALATAE • Unilateral/bilateral cleft • Nasal distortion • Nasal sounds with crying and speaking • Feeding/swallowing difficulties o Infant unable to create suction in the oral cavity that is necessary for feeding o Ability to swallow is usually normal DIAGNOSIS OF CLEFT LIP/PALATE • US (ultrasound) prenatally at 13–14 weeks o Referral to surgeon if positive result • PE (physical examination) at birth THERAPEUTIC MANAGEMENT OF CLEFT LIP/PALATE • Collaborative approach: o Pediatrician o Surgeon o Nurses o ENT (ear, nose, throat specialist) o Social worker o Orthodontist • Modification of feeding: o Adaptive nipples ▪ Cross-cut ▪ Lambs nipple • Looks like the teat of a cow ▪ Other feeders o Asepto syringe ▪ A syringe designed to fit directly into large lumen tubing; also used for intr aoperative irrigation ▪ Has a bulb on the end ▪ Only good for 24 hours when use with feeding then must be change out due to bacterial growth o Breck feeder ▪ This is a syringe with a feeding tube extension. ▪ The bottle part has a very large base to the nipple – easier for the malformed mouth to suck ▪ Nipple is larger with wider opening to create seal o Haberman Feeder ▪ The feeder's design enables the feeder to be activated by tongue and gum pressure, imitating the mechanics involved in breastfeeding, rather than by sucking. A one-way valve separates the nipple from the bottle. Before starting the feeding, air is squeezed out of the nipple and is automatically replaced by breastmilk or formula through the valve. Milk cannot flow back into the bottle and is replenished continuously as the baby feeds. A slit valve opening near the tip of the nipple shuts between jaw compressions, preventing the baby from being overwhelmed with milk ▪ Nipple is larger with wider opening to create seal ▪ Only this one has a large nipple chamber that allows the feeder to provide extra assistance by squeezing the chamber if needed ▪ Also only this one has a slit cut, allowing the feeder to control the flow of liquid by positioning the slit vertically or horizontally within the mouth • Can reduce choking and gagging o Pigeon Bottle o See above – it’s basically the same thing with the one way valve o Has a bulbous tip that fits naturally into the oral cavity with a Y cut nipple that increases the flow of liquid • Infants with clefts tend to allow excessive air during feedings, so it’s important to pause during feedings and burp the infant SURGICAL REPAIR OF CLEFT LIP AND PALATE • REPAIR OF LIP o Done prior to palate repair o At 2–3 months based on: ▪ Rule of 10: age 10 weeks, 10 pounds, Hemoglobin 10 ▪ Naso-aveolar molding • Done before surgery to bring the cleft segments closer together before definitive cleft lip repair, reducing the need for cleft lip revision o Tennison-Randall flap/Z-plasty: ▪ Crosses philtral mid-line o Millard rotational advancement technique: ▪ Does not cross mid-line ▪ Advances a triangle of tissue in the upper third of the lip o Additional revisions may be needed at a later age • REPAIR OF PALATE o At 6–12 months o There is concern that early CP repair interferes with skeletal growth of the midface o Postpoining palate closure beyond the child’s first words may result in increased speech disorders ▪ Veau-Wardill-Kiner procedure or ▪ Furlow Z-Plasty PRE-OPERATIVE CARE FOR CLEFT LIP/PALATE • Assessment of child & family o Can child take food o Is the baby crying because he is hungry? • Nutrition teach ESSR method, use of adaptive feeders o Enlarge nipple with cross cut o Stimulate them by rubbing nipple on lip o Swallowing (allow them time to swallow) o Rest • Use of adaptive feeders o Haberman feeder o Pigeon bottle o Mead-Johnson Cleft Palate nurser • Position infant in upright position with head supported by the caregiver’s hand or cradled in the arm o Allows gravity to assist with the flow of liquid so it is swallowed instead of being lost through the nose • Breast feeding poses less problems because the breast tissue is able to conform to cleft • Explain post-op interventions • Education: address parents’ concerns o How will the baby look? o Is the baby in pain? POST-OPERATIVE CARE OF CLEFT LIP/PALATE • Airway management, bleeding, pain... • Cheiloplasty (lip surgery): supine, elbow restraints o Keep them from pulling at lips o remove one elbow restraint at a time for ROM o No lips on sheet o Apply petroleum jelly to operative sight for the first few days o Keep tongue depressors, thermometers, pacifiers, spoons, straws and other objects out of mouth • Palatoplasty: prone, bilateral elbow/jacket restraints o Jacket needed because they’re older and can flip over • Make sure head of bed is elevated • Clear suction??? • Blenderized diet – no hard items NURSING MANAGEMENT OF CLEFT LIP/PALATE • Pre-op: Assessment, nutrition: teach ESSR • Post-op: Cheiloplasty-supine, elbow restraints • Palatoplasty–prone, elbow/jacket restraints • Assess airway • Assess how parents are coping o May not want to look at the child • Positioning – no lips on the sheet • Protect operative site • Feeding o NPO at first o Then nothing harder than mashed potatoes o Feed from cup w/out spouts DISCHARGE INSTRUCTIONS FOR CLEFT LIP/PALATE • No straws or cups with spouts • Avoid nipple contact with palate suture line • Feeding from cup or spoon PROGNOSIS FOR CLEFT LIP/PALATE • May require multiple surgeries to achieve optimum aesthetic outcomes • Impaired facial growth • Dental anomalies: tooth alignment • Speech impairment – o Nasal sounds o Articulation errors • Self-esteem problems • Visible scar until refined in later procedures • Eustachian tube dysfunction o Improper drainage of middle ear o Middle ear infections/otitis media o Can cause hearing loss o Often have drain tubes put in CLEFT LIP/PALATE SURGERY VIDEOS • • GASTROSTOMY FEEDING FOR CLEFT LIP/PALATE • Indication – can’t orally ingest food for whatever reason • Feeding tube or Mushroom cath. (G-button) o G button replaces child’s PEG tube with a low-profile gastrostomy-button (or G- button). Like a PEG-tube, you can feed your child or give medicine through a G- button. o The button has a water-filled balloon on the inside that holds it in place. o G-buttons need to be replaced for different reasons (balloon leaks, your child grows, etc.) o It’s just a short tube with a balloon holding it in place inside the abdominal wall and a feeding port with a cap on the outside of the abdominal wall and also a port to inflate/deflate the balloon • Intermittent vs. continuous o Intermittent feeds by gravity ▪ Not pushed in ▪ She emphasized that the feeding syringe is an asepto syringe that must be replaced every 24 hours due to bacterial growth ▪ Extension tubing is apparently not changed every 24 hours. She bluffed her way through this though, so who knows? o Feed at room temperature – give time for the formula to warm up o Pacifier to satisfy sucking need o For continuous feeding know the amount in the bag and time frame of bag usage o NURSING MANAGEMENT FOR GT FEEDING • You can check for placement with the pop • If continuous feeding – no more than 4 hour’s-worth of food in the tubing o Bacterial growth PYLORIC STENOSIS • Hypertrophy & hyperplasia of pylorus muscle • Results in elongation and narrowing of the pyloric channel • Can result in partial or complete obstruction of path from stomach into intestine • INCIDENCE o Higher in: ▪ Full term males ▪ First-borns o Higher with PO erythromycin before the age of 2 weeks ▪ Symptomatic 2-5 weeks after birth • ETIOLOGY • Idiopathic (cause not known) • Genetic predisposition o First born children o Males o Caucasians • Related to hypergastrinemia o high blood levels of gastrin ▪ A peptide hormone that stimulates secretion of gastric acid by the parietal cells of the stomach and aids in gastric motility. It is released by G cells in the pyloric antrum of the stomach, duodenum, and the pancreas • Abnormal nerve/muscle cells • Associated with other GI disorders o Malrotation of Duodenum o Duodenum Atrasia (abnormal narrowing) PATHOPHYSIOLOGY OF PYLORIC STENOSIS • Increased pyloric muscle  stenosis of lumen between stomach and duodenum  partial/complete obstruction of stomach contents  vomiting. • With progression  dehydration and depletion of electrolytes  metabolic alkalosis (she also says slight metabolic acidosis but I don’t think so) ASSESSMENT OF PYLORIC STENOSIS • Initial: asymptomatic or slight non-bilious emesis 30-60 minutes after feeding • With progression: non-bilious projectile vomiting up to 3 feet o Usually consists of stale milk • Visible peristaltic waves across abdomen FROM LEFT TO RIGHT o Told a story about a doctor bringing in Pedialyte and giving it to baby and seeing the peristaltic waves • Palpable olive-shaped mass in right upper quadrant o Palpation done on empty stomach • Constipation • Don’t feed vomiting child CLINICAL MANIFESTATIONS OF HYPERTROPHIC PYLORIC STENOSIS • Projectile vomiting: o 3-4 feet from the child in side lying position o 1 foot or more when in a supine position o Usually occurs shortly after a feeding but may not occur for several hours o May occur after each feeding or appear intermittently o Non-bilious vomitus that may be blood-tinged • Infant hunger; eagerly accepts a second feeding after vomiting episode • No evidence of pain or discomfort except that of chronic hunger • Weight loss or failure to gain • Signs of dehydration • Distended upper abdomen • Olive shaped tumor in the epigastrium just to the right of the umbilicus • Visible gastric peristaltic waves that move from left to right across the epigastrium DIAGNOSTICS OF PYLORIC STENOSIS • Based on history o Example: history of vomiting • S & S: palpable olive-shaped mass • US (ultrasound) o Visualizes sausage shaped mass o Checks diameter/length of mass • UGI (upper GI) studies with contrast: o Helps to see a narrow lumen • Labs: o Chem 7 o CBC ▪ Common alterations: • Hypokalemia • Hyponatremia • Metabolic alkalosis THERAPEUTIC MANAGEMENT OF PYLORIC STENOSIS • Surgery o Fredet—Ramstedt procedure: involves opening in pyloric muscle ▪ A.K.A. Open pyloromyotomy • Periumbilically or small transverse upper abdominal incision • Laparoscopic: smaller incision • PRE-OP: o Hydration: IV fluids to correct fluid and electrolyte imbalances (metabolic alkalosis) o NGT (nasogastric tube) primarily for decompression • POST-OP: o Feedings resume 4-6 hours after surgery o Begin with small, frequent feedings o Dietary: ▪ Pedialyte post-op. ▪ Original notes say glucose and H2O ▪ Progress to formula/breast milk ▪ Full feeding schedule usually returns in about 48 hours NURSING MANAGEMENT OF PYLORIC STENOSIS • Pre-op: o NPO o NG tube o hydration via IV fluids with glucose and electrolyte replacement based on labs o vital signs (especially those that indicate electrolyte imbalances) ▪ prone to metabolic alkalosis from loss of hydrogen ions and to potassium, sodium, and chloride depletion o the skin, mucous membranes, and daily weight are assessed for alterations in hydration status and water gain or loss o if stomach decompression is used – ensuring patency of NG tube and recording type and amount of drainage • Post-op: • ABC’s (airway, breathing, circulation) • NG tube to LWS (low wall suction) • Most kids will exhibit some vomiting during the first 24 to 48 hours o Projectile vomiting alarming to parents and they may think the surgery was not successful o They may also think they did something wrong caring for child • IV fluids until child can take liquids • Monitor I & O, F & E (fluids and electrolytes) • Pain control/analgesics • Wound care • Assist with feedings 4-6 hours post-op o Start with clear liquids advancing to formula or breast milk as tolerated • Elevate HOB PROGNOSIS OF PYLORIC STENOSIS • Usually no recurrence • GER (gastro-esophageal reflux) INTUSSUSCEPTION (page 809) • Portion of intestine drawn into another • Part of intestine prolapses, invaginates, or telescopes into another portion • INCIDENCE • One of the most common causes of intestinal obstruction in children 3 months – 3 years • Common occurrences: o Boys o Cystic fibrosis (CF) o 60% of cases less than age 1 o More commonly occurs under age 3 o Most common location: ileocecal area ETIOLOGY OF INTUSSUSCEPTION • Idiopathic: 90% of cases • Related to viral infection • GI pathology o Polyps o Diverticulitis o Lymphoma PATHOPHYSIOLOGY OF INTUSSUSCEPTION • Portion of the intestine and mesentery telescopes into another pulling the mesentery with it → intestinal walls contacting each other, compression of mesentery (lympathic and venous obstruction) pressure continues growing until it reaches the arterial blood pressure, which is then also cut off → edema, increased pressure  ischemia, inflammation, leakage of blood and mucus (forms classic jelly-like stools)  obstruction of GI contents proximal to defect  increased ischemia, perforation, peritonitis and death • Ileocecal o Part of ileum goes into cecum o Most common site • Ileocolic o Part of ileum goes into cecum, and then further into colon o Usually at the hepatic or splenic flexures, or somewhere along the transverse colon • Ileoileal o Part of ileum goes into another part of ileum • Colocolic o Part of colon goes into another part of colon ASSESSMENT OF INTUSSUSCEPTION • Classic triad: o Abdominal pain o Abdominal mass o Melana (black "tarry" feces that are associated with upper gastrointestinal bleeding) • Vomiting • Diarrhea/constipation • Sausage shaped mass • Current jelly stools • Dance sign (emptiness in lower right quadrant) • Shock • Fever SLIDE SHOWING NORMAL BOWEL COMPARED WITH ILEOILEAL INTUSSUSCEPTION DIAGNOSTICS OF INTUSSUSCEPTION • based on history • abdominal X-ray • US (ultrasound) confirms diagnosis • Air enema: 90% reduction o It pushes against the far wall of the telescoped portion and pushes it out CLINICAL MANIFESTATIONS OF INTUSSUSCEPTION • Sudden, acute abdominal pain • Child screaming and drawing the knees onto the chest • Child appearing normal and comfortable between episodes of pain • Vomiting • Lethargy • Passage of red, currant jelly-like stools (stool mixed with blood and mucus) • Tender, distended abdomen • Palpable sausage-shaped mass in upper right quadrant • Empty lower right quadrant (Dance sign) • Eventual fever, prostration, and other signs of peritonitis THERAPEUTIC MANAGEMENT OF INTUSSUSCEPTION • Spontaneous reduction (may resolve itself) • Conservative: non-surgical reduction: o Radiologist-guided pneumoenema (air enema) with/without contrast o Ultrasound guided hydrostatic saline enema ▪ No ionizing radiation needed in this one o Recurrence after conservative treatment is uncommon • IV fluids • NG decompression • Antibiotic therapy • Laparoscopic surgical resection if non-surgical unsuccessful o Manually reducing the invagination o Resecting any nonviable intestine if necessary o Serious complications or death are uncommon NURSING INTERVENTIONS FOR INTUSSUSCEPTION • Observe for passage of normal stool pre-conservative management o Indicates the intussusception has reduced itself o Immediately report to the practitioner • Maintain NPO, NGT to LWS (low wall suction) • Explain diagnosis/management to family • Monitor NG drainage – surgical intervention? o Check color of drainage o Make sure the NGT is patent o Put a mark and time on NGT to evaluate how fast it’s draining ▪ If it’s draining stomach too fast – electrolyte drainage o Check every 8 hours ▪ Lower than 500 ml is acceptable – no more than that ▪ No more than 100-150 ml in children COMPLICATIONS FOR INTUSSUSCEPTION • Ischemia • Peritonitis • Shock • Death without treatment PROGNOSIS OF INTUSSUSCEPTION • Recurrence possible with hydrostatic reduction HIRSCHSPRUNGS DISEASE (PAGE 779) • AKA congenital aganglionic megacolon • Mechanical obstruction related to inadequate motility of intestine resulting from absence of ganglion INCIDENCE OF HIRSCHSPRUNGS DISEASE • 1 in 5000 live births • Four times more common in males • More common in children with Down Syndrome • More common if there’s a family history • Common areas of occurrence (80% of cases) o Internal sphincter o Rectum o A few centimeters of the Sigmoid colon o If only the above three are involved it’s SHORT SEGMENT DISEASE ETIOLOGY OF HIRSCHSPRUNGS DISEASE • Congenital o Absence of ganglion • Genetics o Related to RET proto-oncogene mutation PATHOPHYSIOLOGY OF HIRSCHSPRUNGS DISEASE • Aganglion → Absence of peristalsis  accumulation of GI stool → abdominal distention proximal to defect → megacolon, ischemia  enterocolitis & obstruction. In rectal area  failure in relaxation of internal sphincter muscle  absence of defecation. • Enterocolitis may occur • The absence of ganglion ells in the affected bowel result in a lack of enteric nervous system stimulation o Decreases the internal sphincter’s ability to relax o Unopposed sympathetic stimulation of the intestine results in increased intestinal tone • There is also a loss of the rectosphincteric reflex o Normally when a stool bolus enters the rectum, the internal sphincter relaxes and the stool is evacuated o In Hirschsprungs disease the internal sphincter does not relax MANIFESTATIONS OF HIRSCHSPRUNGS DISEASE • vary with age o Newborn: ▪ Failure in passing meconium → marked abdominal distention ▪ Bile-stained vomitus ▪ Anorexia o Infants: ▪ Failure to thrive ▪ Constipation ▪ Diarrhea ▪ Vomiting ▪ Distention • Complications: o Enterocolitis: explosive, watery diarrhea o Fever o Child: ▪ Ribbon-like foul-smelling stool ▪ Abdominal distention ▪ Visible peristalsis ▪ Anemia ▪ Palpable fecal mass DIAGNOSTICS OF HIRSCHSPRUNG’S DISEASE • Based on history: absence of meconium • Physical Exam • X-ray • Contrast enema (barium enema): o Check for abnormalities • Anorectal manometric exam o Measures the pressure of anal sphincter muscle • Rectal Biopsy confirms diagnosis THERAPEUTIC MANAGEMENT OF HIRSCHSPRUNGS DISEASE • MILD: modified diet o Decreased fiber o Increased kilocalories o Increased protein diet • IV fluids, enemas • Surgical removal of aganglionic area with or without ostomy o Two stages ▪ Anorectal myomectomy for short-segment involvement ▪ Soave endorectal pull-through procedure: With or without ostomy closure, mostly done • Consists of pulling the end of the normal bowel through the muscular sleeve of the rectum, from which the anganglionic mucosa has been removed • With earlier diagnosis, the proximal bowel may not be extremely distended, allowing for a one-stage procedure and eliminating the need for a temporary colostomy o Ostomy is usually temporary, unless so much bowel is involve that a permanent ileostomy must be performed o Amount of bowel involved is usually known in advance o After the pull through procedure, anal stricture and incontinence may occur and require further therapy, including dilations or bowel retraining o Constipation and fecal incontinence are chronic problems for many patients after surgical correction for HD • TPN administration in some cases NURSING MANAGEMENT OF HIRSCHSPRUNGS DISEASE • Based on age at diagnosis • Assess for normal stool pre-op (did condition resolve?) • Measure abdominal girth o At widest point – usually umbilicus o Point of measurement marked with pen to insure accuracy o To reduce stress, leave tape measure in place beneath the child rather than removing it each time • Vital signs o Look for signs of shock o Also looking for signs of bowel perforation ▪ Fever ▪ Increasing abdominal distention ▪ Vomiting ▪ Increased tenderness ▪ Irritability ▪ Dyspnea ▪ Cyanosis • NPO • NG tube • Enemas • DIET: o DECREASED FIBER o Increased kilocalories o Increased protein • Hyperalimentation pre-op o Artificial supply of nutrients, typically intravenously • Newborns: no prep. Pre-op o The bowels are still sterile • Older age group: o Bowel prep with saline enemas, colon irrigation (GoLYTELY) o Antibiotics PO or IV to reduce intestinal flora • Colostomy care • Monitor VS o 4 x Q 15 minutes o 2 x Q 30 minutes o 4 x Q 1 hour o Q 4 hours • Check for perforation and signs of shock • Post op, place diaper below ostomy site to avoid contamination/infection DISCHARGE PLANNING & PROGNOSIS OF HIRSCHSPRUNG DISEASE • POST-OP: o Anal stricture o Enterocolitis ▪ Inflammation of both the small intestine and the colon. • Chronic problems: o Constipation/incontinence • Colostomy care • Monitor for perforation: o Increased abdominal distention o Dyspnea o Fever o Vomiting • 95% cure rate GASTROESOPHAGEAL REFLUX DISEASE (PAGE 782) • GER: The transfer of gastric contents into the esophagus o Most frequent after meals and at night • GERD: represents symptoms of tissue damage that result from GER • About 50% of infants younger than 2 months are reported to have GER • Physiologic GER usually resolves spontaneously age 1 year RISK FACTORS FOR GER • Neurologic impairment • Hiatal hernia • Repaired esophageal atresia o Atresia: (absence or abnormal narrowing of an opening or passage in the body) • Morbid obesity (increased pressure in gut) • Sandifer syndrome: an uncommon condition usually occurring in young children, characterized by repetitive stretching and arching of the head and neck that can be mistaken for a seizure o Likely represents a physiologic neuromuscular response attempting to prevent acid reflux from reaching the upper portion of the esophagus • Premature infants • Infants with bronchopulmonary dysplasia • Children who have had: o Tracheoesophageal or EA repairs o Extra corporeal membrane oxygenation (ECMO) o Neurologic disorders o Scoliosis o Asthma o Cystic fibrosis o Cerebral palsy CLINICAL MANIFESTATIONS AND COMPLICATIONS OF GER • INFANTS o Spitting up, regurgitation, vomiting (may be forceful) o Excessive crying, irritability o Arching of the back with neck extension or stiffening o May be “silent” (no clinical signs observed) o Weight loss o Growth failure (failure to thrive) o Respiratory problems ▪ Cough ▪ Wheeze ▪ Stridor ▪ Gagging ▪ Choking with feedings o Hematemesis o Apnea • CHILDREN o Heartburn o Abdominal pain o Non-cardiac chest pain o Chronic cough o Dysphagia o Nocturnal asthma o Recurrent pneumonia • COMPLICATIONS o Esophagitis o Esophageal stricture o Laryngitis o Recurrent pneumonia o Anemia o Barrett esophagus PATHOPHYSIOLOGY OF GASTOESOPHAGEAL REFLUX • inappropriate transient relaxation of the lower esophageal sphincter (LES) • Factors that increase abdominal pressure such as coughing and sneezing, scoliosis and overeating may contribute to GERD • Asthma (RAD) may result from stimulation of airway reflexes by the acid refluxate DIAGNOSTIC EVALUATION OF GER • History and physical exam usually sufficient • Upper GI series helpful in evaluating the presence of anatomic abnormalities o Pyloric stenosis o Malrotation o Annular pancreas o Hiatal hernia o Esophageal stricture • 24 hour intra-esophageal pH monitoring study is the gold standard in the diagnosis • Endoscopy with biopsy may be helpful to assess the presence and severity of esophagitis, strictures and Barrett esophagus and to exclude other disorders such as Crohn’s disease • Scintigraphy (gastroesophageal) detects radioactive substances in the esophagus after a feeding of the compound and assesses gastric emptying o Can differentiate between aspiration of gastric contents from reflux vs. aspiration from poor oropharyngeal muscle coordination • A modified barium swallow study with video fluoroscopy may also be used as a diagnostic tool for his condition THERAPEUTIC MANAGEMENT OF GASTROESOPHAGEAL REFLUX • No therapy needed for the infant who is thriving and has no respiratory complications • Avoid certain foods that exacerbate acid reflux o Caffeine o Citrus o Tomatoes o Alcohol o Peppermint o Spicy or fried foods • Lifestyle modifications in children: o Weight control o Small, more frequent meals o Smoking cessation (adults) o Thickened feedings o Upright positioning ▪ Elevate HOB or place infant in infant seat elevated 30 degrees after feedings • Hydrolyzed formula if cow milk protein sensitivity is suspected – occurs under medical supervision • PHARMOCOLOGICAL • H2 receptor antagonists o Cimetidine [Tagamet] o Ranitidine [Zantac] o Famotidine [Pepsid] • Proton pump inhibitors o Most effective when administered 30 minutes before breakfast ▪ Peak plasma concentrations occur with mealtime ▪ If given twice a day, second best time is 30 minutes before the evening meal o Takes several days of administration to achieve observable results o Esomeprazole [Nexium] o Lansoprazole [Prevacid] o Omeprazole [Prilosec] o Pantoprazole [Protonix] o Rabeprazole [Aciphex] • Both H2 receptor antagonists and PPIs reduce gastric hydrochloric acid secretion and may stimulate some increase in LES tone • Surgical management – reserved for children with severe complications or those who have failed to respond to medical therapy o Nissen fundoplication is most common surgical procedure o Performed laparoscopically o Involves passage of the gastric fundus behind the esophagus to encircle the distal esophagus o Complications from fundoplication ▪ Breakdown of the wrap ▪ Small bowel obstruction ▪ Gas-bloat syndrome ▪ Infection ▪ Retching ▪ Dumping syndrome NURSING MANAGEMENT OF GER • Reassure parents of the benign nature of the condition • Using bibs and protective clothes during feeding • Prone positioning when holding the infant after feeding o In the past, it was recommended that infants and older children were positioned upright during sleeping, but the task force on SIDS recommends supine position for sleeping o Do not place infants on their sides as alternative to fully supine sleeping • More frequent feeding times • If thickening formula with cereal, enlarge the nipple opening for easier sucking • Avoid feeding spicy foods, caffeine, chocolate, tobacco smoke, and alcohol ( for the child – I don’t know who gives the child tobacco and alcohol, but whatever) • Avoid vigorous play after feedings • Avoid feeding just before bedtime • NG tube or gastrostomy when regurgitation is severe and growth is restricted o Decreases the amount of emesis and provide constant buffering of gastric acid CELIAC DISEASE (PAGE 813) • AKA Gluten-sensitive/gluten-induced enteropathy or celiac sprue • Sensitivity to gluten, protein in wheat, barley, oats, rye o Leads to altered absorption • Child has permanent GI intolerance to dietary wheat and related proteins • Inability to digest gliadin component of gluten • Symptom complex disorder: o Steatorrhea (fatty, frothy, foul-smelling, bulky stools) o General malnutrition o Abdominal distention o Vitamin deficiencies ETIOLOGY OF CELIAC DISEASE • Genetics: chromosome 6 disorder • 1 in every 3000 – 4000 people • More frequent in Europe than the U.S. • More prevalent in women • Rarely reported in Asians or African Americans PATHOPHYSIOLOGY OF CELIAC DISEASE • Ingestion of gluten  atrophy of villi in small intestine and impairment in absorption • Failure to ingest gliadin  accumulation of toxic substance damage to mucosal cells  alteration in immunity  cytokines produced by CD4 T cells  atrophy small intestine villi  decreased absorption of essential nutrients: Fats, proteins, some carbohydrates, vitamin D, K, B12, folic acid ASSESSMENT OF CELIAC DISEASE • Manifestations usually insidious and chronic • Assessment based on age • Failure to thrive (first sign) • Diarrhea/constipation (first sign) • Abdominal pain • Steatorrhea stool • Iron deficiency anemia • Anorexia • Weight loss • Poor appetite • Distended abdomen • Pubertal delay • Muscle wasting with hypotonia (especially in legs and buttocks) • Lack of energy • Dental enamel defects • Alopecia • Abnormal LFT results • Irritability • Uncooperativeness • Apathy • CELIAC CRISIS o Acute severe episodes of profuse watery diarrhea and vomiting o May be precipitated by: ▪ Infections (especially gastrointestinal) ▪ Prolonged fluid and electrolyte depletion ▪ Emotional disturbance THREE HEADS OF CELIAC DISEASE • Leaky gut • Inflammation • Gut Dysbiosis (a microbial imbalance or maladaptation on or inside the body) DIAGNOSIS OF CELIAC DISEASE • Screening tests: o Antigliadin antibodies (IgA, IgG) = anti-food proteins antibodies o Antitissue transglutaminase antibody • 2 diagnostics needed to decrease change of false positive test • Biopsy of small intestine: abnormal mucosa (villous atrophy with hyperplasia of the crypts) while patient is eating adequate amounts of gluten and a full clinical remission after gluten is withdrawn SEROLOGIC TESTS FOR CELIAC DISEASE (EXTRA DIAGRAM SLIDE) • Tissue tansglutaminase antibodies, IgA and IgG o IgA and IgG isotypes o Enzyme immunoassay • Deamidated gliadin antibodies, IgA and IgG o IgA and IgG isotypes o Enzyme immunoassay • Endomysial antibodies, IgA o IgA isotype only o Immunofluorescence assay • For all of the above, antibody levels decrease with gluten free diet THERAPEUTIC MANAGEMENT OF CELIAC DISEASE • Dietary grain substitutes with corn & rice • Supplements: o iron, folic acid, fat soluble vitamins • lactose-free, gluten-free diet • ↑ calories, ↑ protein, ↓ fat diet • Avoid high fiber foods because the bowel is inflamed – can resume when inflammation has subsided NURSING MANAGEMENT OF CELIAC DISEASE • Dietary history (24 hour recall) • Assess nutritional status, G&D (growth and development) • Assess for S&S of infection o Temp o Runny nose • Dietary adherence • Follow-up care after discharge • Family support and education • Refer to support group: Celiac Sprue Association COMPLICATIONS OF CELIAC DISEASE • Anal stricture (passage becomes too narrow) • Constipation/fecal incontinence • Enterocolitis • Lymphoma of small intestine • CELIAC CRISIS o Anorexia o Severe episodes of profuse watery diarrhea o Vomiting o Weight loss o Untreated: lactose intolerance, vitamin deficiency GASTROENTERITIS • Acute diarrhea o Inflammation of stomach and intestine o Acute diarrhea defined as a sudden increase in frequency and a change in consistency of stools, often caused by an infectious agent in the GI tract o May be associated with upper respiratory or urinary tract infections, antibiotic therapy or laxative use o Acute diarrhea is usually self-limited (14 days duration) and subsides without specific treatment if dehydration does not occur • Chronic diarrhea o Defined as an increase in stool frequency and increased water content with a duration of more than 14 days o Often caused by chronic conditions such as: ▪ Malabsorption syndromes ▪ Inflammatory bowel disease (IBD) ▪ Immunodeficiency ▪ Food allergy ▪ Lactose intolerance • Chronic nonspecific diarrhea as a result of inadequate management of acute diarrhea o Intractable diarrhea of infancy ▪ Syndrome that occurs in the first few months of life ▪ Persists for longer than 2 weeks with no recognized pathogens ▪ Refractory to treatment ▪ Most common cause is acute infectious diarrhea that was not managed adequately • Chronic non-specific diarrhea (CNSD) o Also known as irritable colon of childhood and toddlers’ diarrhea o Common cause of chronic diarrhea in children 6 months to 54 months (about 4 ½ years) o Loose stools, often with undigested food particles o Lasts longer than 2 weeks’ duration o These children grow normally and have no evidence of malnutrition, no blood in their stool, and no enteric infection o Excessive intake of juices and artificial sweeteners such as sorbitol may be a factor • INCIDENCE OF ACUTE GASTROENTERITIS o Most common cause = virus: Rota and Norwalk ▪ Rotavirus more common in winter • Ages: infants/young children o Most severe at 3-24 months of age o Children younger than 3 months have some protection from maternally acquired antibodies • Incubation period: 48 hours • Diagnosis: ELISA • Two preventive vaccines available • Affects villus epithelial cells of small intestine • SYMPTOMS: o Mild to moderate fever o Vomiting followed by onset of foul-smelling watery stools o Fever and vomiting generally abate in 2 days, but diarrhea persists 5-7 days ▪ Norwalk more common in summer • Also called caliciviruses • Ages: older children • Incubation: 12-48 hours • Diagnosis: ELISA • Affects villus epithelial cells of small intestine • SYMPTOMS: o Abdominal cramps o Nausea o Vomiting o Malaise o Low grade fever watery diarrhea without blood • Duration 2-3 days • Tends to resemble so-called food poisoning symptoms with nausea predominating ETIOLOGY OF GASTROENTERITIS • Bacteria, viruses, parasites • Most common bacterial pathogens are Salmonella, Shigella, and Campylobacter • Rota and Norwalk viruses → most common causes • Most pathogens that cause diarrhea are spread by the fecal-oral route through contaminated food or water • Also spread person to person where there is close contact (e.g., daycare centers) PATHOPHYSIOLOGY OF GASTROENTERITIS • Damage/destruction of mucosal cells  ↓absorption of fluid and electrolytes from bowels • TRANSMISSION o Fecal/oral route ASSESSMENT OF GASTROENTERITIS • Depends on involved organism • Anorexia, Diarrhea/Nausea/Vomiting, liquid to watery stools • Abdominal Pain • Cramps • Dehydration • ROTA VIRUS o Fever o Vomiting o Watery stools o Abdominal pain • NORWALK VIRUS o Nausea o Vomiting o Diarrhea DIAGNOSIS OF GASTROENTERITIS • Check stool for: o O&P (ova and parasites) o Fatty substances o Viruses o Infectious organisms o Undigested sugars • UA (urinalasys) • Chem-7 o Especially sodium and potassium THERAPEUTIC MANAGEMENT OF GASTROENTERITIS • Contact precautions • Rehydration: IV fluids • Oral rehydration therapy: Pedialyte, Ricelyte, Lytren o More effective, safer, less painful, and less costly than IV rehydration o Enhances and promotes reabsorption of sodium and water o Greatly reduces vomiting, volume loss from diarrhea and the duration of illness ▪ Vomiting is NOT a contraindication unless it is severe– give in small amounts at frequent intervals o Commercially prepared or home recipes ▪ Use alone or in combination with breast milk and formula ▪ Diarrhea losses replaced 1:1 ▪ Orally or via NG tube o Sports drinks, tea, juices, or carbonated beverages are not appropriate for oral replacement therapy in small children • MODEL FOR REHYDRATION o Rehydration solution should consist of 75 to 90 mEq/L of sodium o Give 40 to 50 ml/kg of rehydration solution over 4 hours o Replacement and maintenance solution should consist of 40 to 60 mEq/L of sodium o Reevaluate the need for further rehydration; initiate maintenance therapy using maintenance formulations, with daily volumes not to exceed 150 ml/kg/day o In children with diarrhea without significant dehydration, the maintenance phase may be initiated without the need for rehydration solution o If additional fluids are needed, use low-salt fluids such as breast milk or water • Prevention: improve hygiene, clean water, education o Two rotavirus vaccinations now available o Early reintroduction of nutrients is desirable and gaining more widespread acceptance ▪ Continued feeding or early reintroduction of a normal diet has no adverse effects and actually lessens the severity and duration of the illness and improves weight gain compared with the gradual reintroduction of foods • Not the BRAT diet – has little nutritional value (low in energy and protein), is high in carbohydrates, and is low in electrolytes o Use of antibiotics is controversial ▪ May shorten the course of some diarrheal illness (e.g., those caused by Shigella) ▪ However most bacterial diarrheas are self-limiting, and often resolve before causative organism is determined ▪ They may also prolong the carrier period for bacteria such as Salmonella spp. o Anti-motility drugs such as loperamide are not recommended in children o Antiemetic drugs such as the phenothiazines are not recommended because of their side effects ▪ Vomiting tends to improve when dehydration is corrected ▪ However ondansetron has few side effects and may be administered if vomiting persists and interferes with Oral replacement therapy • Breast-feeding  passive immunity in newborns/infants o For the first three months NURSING MANAGEMENT OF GASTROENTERITIS • Maintain contact precaution • Assess frequently for S&S dehydration • Daily weight • Perianal skin care • Don’t take temperature rectally o Stimulates the bowel increasing the passage of stool • Assess stools o Color and consistency • I&O o Accurate measurement of output is essential to determine whether renal blood flow is sufficient to permit the addition of potassium to the IV fluids • VS DEHYDRATION • Output exceeds intake • Can result from impaired oral intake, but is often a result of abnormal losses such as vomiting or diarrhea, when oral intake only partially compensates for the • Other significant causes: o Diabetic ketoacidosis o Burns • TYPES • Dehydration is classified into three categories on the basis of osmolality and depends primarily on the serum sodium concentration: o Isotonic ▪ Water and electrolytes loss in equal proportions ▪ Primary form of dehydration in children ▪ There is no osmotic force between the ICF and the ECF, so the major loss is sustained from the ECF compartment • Significantly reduces the plasma volume and the circulating blood volume o Affects the skin, muscles and kidneys ▪ Shock is the greatest threat to life ▪ Children with isotonic dehydration display symptom characteristics of hypovolemic shock ▪ Plasma sodium remains within normal limits, between 130 and 150 mEq/L (we learned 135-145 mEq/L) o Hypotonic (hyposmotic or hyponatremic) ▪ Electrolytes loss is greater than water loss leaving the serum hypotonic ▪ Because ICF is more concentrated than ECF, water moves from the ECF to the ICF ▪ This further increases the ECF volume loss and shock is a frequent finding ▪ Because there is a greater proportional loss of ECF in hypotonic dehydration, the physical signs tend to be more severe with smaller fluid loss than with isotonic or hypertonic dehydration ▪ Serum sodium concentration is less than 130 mEq/L o Hypertonic (hyperosmotic or hypernatremic) ▪ Water loss exceeds electrolyte loss ▪ Usually caused by a proportionately larger loss of water or a larger intake of electrolytes ▪ This type of dehydration is the most dangerous and requires more specific fluid therapy ▪ Hypertonic diarrhea may occur in infants who are given fluids by mouth that contain large amounts of solute, or in children who receive high- protein NG tube feedings that place an excessive solute load on the kidneys ▪ In hypertonic dehydration, fluid shifts from the lesser concentration of the ICF to the ECF ▪ Plasma sodium concentration is greater than 150 mEq/L ▪ Because the ECF volume is proportionately larger, hypertonic dehydration consists of a greater degree of water loss for the same intensity of physical signs ▪ Shock is less apparent ▪ However CNS disturbances, including alterations in consciousness, poor ability to focus attention, lethargy, increased muscle tone with hyperreflexia, and hyperirritability to stimuli are more likely to occur ▪ CNS changes are serious and may result in permanent damage • Sodium is the chief solute in ECF and is the primary determinant of ECF volume • Na is considered a unique electrolyte in that water balance determines sodium concentration • When water is lost and sodium concentration becomes elevated, compensatory mechanisms in the kidney stop ADH secretion so water is retained ??? • The thirst mechanism (not fully functional in infants) is also stimulated so water is replaced, thus increasing the total body water content and returning sodium to a normal level • Potassium is primarily found inside the cell (ICF) but small amounts are also found in the ECF • Sodium depletion in diarrhea occurs in two ways: out of the body in stool and into the ICF compartment to replace potassium to maintain electrical equilibrium ASSESSMENT/MANAGEMENT OF DEHYDRATION • Poor skin turgor • ↓ output • Earliest detectable sign is usually tachycardia • Followed by dry skin and mucous membranes o Sunken fontanels o Signs of circulatory failure (coolness and mottling of extremities) o Loss of skin elasticity o Prolonged capillary filling time • From the book: respiratory rate normal slight tachypnea (rapid) hyperpnea (deep and rapid) blood pressure normal normal to orthostatic ( 10 mm Hg change) orthostatic to shock behavior normal irritable, more thirsty hyperirritable to lethargic thirst slight moderate intense mucous membranes normal dry parched tears present decreased absent, sunken eyes anterior fontanel normal normal to sunken sunken external jugular vein visible when supine not visible except with supraclavicular pressure not visible even with supraclavicular pressure skin capillary refill 2 seconds slowed capillary refill (2-4 seconds [decreased turgor]) very delayed capillary refill (4 seconds) and tenting; skin cool, acrocyanotic or mottled urine decreased oliguria oliguria or anuria THERAPEUTIC MANAGEMENT OF DEHYDRATION • Fluid replacement therapy • Mild dehydration rate: 50 mL/kg/day (or 48 hours) • Severe dehydration rate: 100 mL/kg/day (or 48 hours) • Mild REHYDRATION: 50 ml/kg of oral rehydration solution • Moderate REHYDRATION: 100 mL/kg of oral rehydration solution • Parenteral re-hydration o Started whenever the child is unable to ingest sufficient amounts of fluids and electrolytes o Patients who usually require IV fluids are: ▪ Those with severe dehydration ▪ Those with uncontrollable vomiting ▪ Those who are unable to drink for any reason ▪ Those with severe gastric distention o IV administration of fluid begins immediately, although the exact nature of the dehydration and the serum electrolyte values may not initially be known ▪ Solution selected is based on what is known regarding the probable type and cause of the dehydration ▪ Usually involves an isotonic solution such as 0.9% sodium chloride or lactated Ringers • Both are close to the body’s serum osmolality of 285 to 300 mOsm/kg • Do not contain dextrose, which is contraindicated in the early treatment stages of diabetic ketoacidosis • Parenteral rehydration therapy has three phases: o 1. Expand ECF volume quickly and to improve circulatory and renal function ▪ During initial therapy, an isotonic solution is used at a rate of 20 ml/kg, given as an IV bolus over 20 minutes, and repeated as necessary after assessment of child’s response o 2. Subsequent therapy is used to replace deficits, meet maintenance water and electrolyte requirements and catch up with ongoing losses ▪ Water and sodium requirements for the deficit, maintenance, and ongoing losses are calculated at 8 hour intervals, taking into consideration the mount of fluids given with the initial boluses and the amount administered during the first 24 hour period o 3. Final phase of therapy allows the patient to return to normal and begin oral feedings, with a gradual correction of total body deficits ▪ The potassium loss in ICF is replaced slowly by way of the ECF • Although the initial phase of fluid replacement is rapid in both isotonic and hypotonic dehydration, it is contraindicated in hypertonic dehydration because of the risk of water intoxication, especially in the brain cells, specifically the central pontine cells • Central pontine myelinolysis may occur with an over correction of fluid deficit and an overly rapid correction of serum sodium concentration • Where there is an apparent lag time for sodium to reach a steady state when diffusing in and out of brain cells, water diffuses almost instantaneously • Consequently, rapid administration of fluid causes equally rapid diffusion of water into the dehydrated brain cells, causing marked cerebral edema • Because ECF volume is maintained relatively well in hypertonic as opposed to the other types of dehydration, shock is not a usual manifestation DAILY MAINTENANCE FLUID REQUIREMENTS • Child’s weight in kilograms • 100 mL/kg for first 20 kg of body weight • 50 mL/kg for second 10 kg of body weight • 20 mL/kg for remaining kg of body weight CONSTIPATION • Alteration in frequency, consistency, or ease of passage of stool o A decrease in bowel movement frequency or trouble defecating for more than 2 weeks o Parents often define constipation as passing less than three stools per week o It may also be defined as painful bowel movements, which are often blood streaked or include the retention of stool with or without soiling, even with a stool frequency of more than three stools per week o The frequency of bowel movements, however is not considered a diagnostic criterion because it varies widely among children • OBSTIPATION: extremely long intervals between defecation • ENCOPRESIS: constipation with fecal soiling • May be secondary to other disorders o Strictures o Ectopic anus o Hirschsprungs disease o Hypothyroidism o Hypercalcemia resulting from hyperparathyroidism ▪ Maybe because the calcium excess fires the sphincter muscles? I don’t know o Vitamin D excess o Chronic lead poisoning o Drugs: ▪ Antacids ▪ Diuretics ▪ Antiepileptics ▪ Antihistamines ▪ Opioids ▪ Iron supplementation o Spinal cord lesions may be associated with loss of rectal tone and sensation ▪ Affected children are prone to chronic fecal retention and overflow incontinence • Idiopathic (functional) constipation = no known cause • Chronic constipation due to: o Environmental factors ▪ Not enough liquids ▪ Low fiber diet o Psychosocial factors ▪ Stress ETIOLOGY OF CONSTIPATION • Dietary: decreased sugar, bulk, fluid intake • Structural: stricture, stenosis • Disease process • Side effect of meds • Stress: psychological problem • More common in formula-fed infants STOOL PATTERN IN CHILDHOOD • Infants: o Pass first meconium stool within 24 to 36 hours after birth o MECONIUM PLUG: caused by meconium that has reduced water content ▪ Usually evacuated after digital examination o MECONIUM ILEUS: Luminal obstruction of the distal small intestine by abnormal meconium ▪ Initial manifestation of cystic fibrosis ▪ Treatment same for meconium plug ▪ Early surgical intervention may be needed • Breast fed: 1-7 stools/day or 1 Q 4-5 days?? (maybe hours) o Less common in breast-fed infants ▪ Have softer stools than bottle fed infants ▪ Also have decreased stools because of more complete digestion of breast milk with little residue • Formula fed: 1-2/day • From 1 year: 1-2 stools/day o Most constipation in early childhood is attributable to environmental changes, stresses, and changes in toileting patterns when a child begins to attain control over bodily functions ▪ School bathrooms lack privacy ▪ Rushing out the door after breakfast also impedes bathroom use o Constipation tends to be self-perpetuating ▪ A child who has experienced discomfort during bowel movement may deliberately try to withhold stool and the urge to defecate passes o Changing diet and/or adding fiber often corrects the problem ▪ “Age + 5g” of daily fiber intake is recommended for children age 3 and older o Stool softening agents such as docusate or lactulose may also be helpful ▪ Polyethylene glycol (PEG) 3350 without electrolytes (Miralax) is a chemically inert polymer that has been introduced as a new laxative in recent years • Tolerated well by children – can be mixed in beverage of choice MANAGEMENT OF CONSTIPATION • Dietary: increase fluids and fiber • Stool softeners o Colace, pericolace • Suppositories o Dulcolax • Enemas o Fleet NURSING MANAGEMENT OF CONSTIPATION • History taking: o Dietary habits o Precipitating factors • Infants: o Increased fluids o Increased sugar ▪ Add glucose to formula ▪ Increasing the carbohydrate (sucrose or corn syrup) in the infant’s formula • Children: o Increased fiber APPENDICITIS PAGE 785 • Inflammation of vermiform appendix • Blind sac at the end of the cecum • INCIDENCE o More common in ages 10 and older o Boys and girls affected equally • ETIOLOGY o Obstruction of the lumen of the appendix ▪ Kink in lumen ▪ Swollen lymphoid tissue frequently occurring after a viral infection ▪ Presence of parasites PATHOPHYSIOLOGY OF APPENDICITIS • Obstruction of mucous secretions  increased pressure on blood vessels  ischemia  necrosis  rupturing  fecal material in peritoneum  peritonitis  progressive peritoneal inflammation results in functional intestinal obstruction of the small bowel (ileus) SEQUENCE OF APPENDICITIS SYMPTOMS • Periumbilical pain  nausea  right lower quadrant pain  vomiting with fever • Perforation of appendix can occur within 48 hours of initial complaint of pain • Complications from perforated appendix: o Major abscess o Phlegmon ▪ An acute suppurative inflammation of subcutaneous connective tissue that spreads o Enterocutaneous fistula o Peritonitis o Partial bowel obstruction MANIFESTATIONS OF APPENDICITIS – CHECK THIS – RIGID ABDOMEN WAS ALWAYS PERITONITIS BEFORE Appendicitis: Peritonitis Dull periumbilical pain  right lower quadrant. Diffused, pain  severe with movement. Rigid, distended abdomen Chills Anorexia Nausea/Vomiting Decreased bowel sounds Increased Pulse ↑ temperature Increased BP Difficulty passing gas Dehydration Decreased bowel sounds Fever Anorexia Rebound tenderness Board-like abdomen Abdominal distention and rigidity DIAGNOSTICS OF APPENDICITIS • Based on: • History and physical o Pain is cardinal feature ▪ Initially generalized (usually periumbilical) ▪ Usually descends to the lower right quadrant ▪ Most intense site of pain may be at McBURNEY POINT (midway between the anterior superior iliac crest and the umbilicus ▪ Referred pain, elicited by light percussion around the perimeter of the abdomen, indicates peritoneal irritation ▪ Movement such as riding over bumps in an automobile or wheelchair, aggravates the pain o Fever o Change in behavior o Anorexia o Vomiting • Increased WBC o Elevated percentage of bands (shift to the left) indicates inflammatory process • C reactive protein (CRP) o Acute phase reactant that rises within 12 hours of the onset of infection • CT scan o The imaging technique of choice ▪ Considered positive in the presence of: • An enlarged appendiceal diameter • Appendiceal wall thickening • Periappendiceal inflammatory changes • Fat streaks • Phlegmon • Fluid collection THERAPEUTIC MANAGEMENT OF APPENDICITIS • Surgery: Laparoscopic Appendectomy vs. open o Open now rarely done • Antibiotic therapy: Meropenem (Merrem) • Nasogastric tube to Low Wall suction (also rarely seen now) • Pain medication NURSING MANAGEMENT OF APPENDICITIS • Pain assessment/management • One of the most reliable estimates is the degree of change in behavior o Children will assume a rigid, motionless, side-lying posture with the knees flexed on the abdomen ▪ Decreased range of motion of the right hip • No laxatives, enemas or heat to painful area o Stimulates bowel motility and risk of perforation • POST SURGERY: o NPO ▪ Minimizes vomiting and abdominal distention o IV fluids o Analgesics o TCDB (turn cough, deep breathing) o Monitor bowel sounds o Splinting ▪ May involve a Montgomery strap or wound binder o Progressive ambulation ▪ Early ambulation prevents buildup of flatus and promotes return of normal bowel function o Use of incentive spirometer ▪ Something about deep breaths into and out of it o Monitor I and O o Wound care/Dressing changes o NGT drainage/decompression until there is evidence of intestinal activity NECROTIZING ENTEROCOLITIS (NEC) PAGE 284 • Necrosis of large/small intestine • Acute inflammatory disease of bowel in preterm and high risk infants • INCIDENCE o LBW infants • ETIOLOGY o Idiopathic ▪ Appears to occur in infants whose gastrointestinal tracts have experienced vascular compromise ▪ Intestinal ischemia, immature gastrointestinal host defenses, bacterial proliferation and feeding substrate are now believed to have a multifactorial role in the etiology of NEC ▪ Diminished blood supply causes large amount of death in mucosal cells lining the bowel • They stop secreting protective, lubricating mucus • The thin, unprotected bowel wall is attacked by proteolytic enzymes • Bowel wall continues to swell and break down • It is unable to synthesize protective IgM • The mucosa is permeable to macromolecules (e.g., exotoxins) which further hampers intestinal defenses • Gas forming bacteria invade the damaged areas to produce PNEUMATOSIS INTESTINALIS, the presence of gas in the submucosal or subserosal surfaces of the bowel o Early enteric feeding ▪ the delivery of a nutritionally complete food, containing protein, carbohydrate, fat, water, minerals and vitamins, directly into the stomach, duodenum or jejunum ▪ formula, hyperosmolar medications ▪ unclear whether this connection is a result of the formula imposing a stress on an ischemic bowel, serving as a substrate for bacterial growth, or both o Immature immune system o Hypoxia o Sepsis FACTORS IN DEVELOPMENT OF NEC • Prematurity • Intestinal ischemia • Colonization of pathogenic bacteria • Substrate in intestinal lumen o The surface or material on or from which an organism lives, grows, or obtains its nourishment PATHOPHYSIOLOGY OF NECROTIZING ENTERCOLITIS • Necrosis → ↓mucous secretion → ↓ activation of protective enzymes → edema & rupture → invasion of gas forming bacteria  septicemia & shock. MANIFESTATIONS OF NECROTIZING ENTERCOLITIS • SPECIFIC SIGNS o Gastric retention (undigested formula) o GI bleeding  blood in stools or gastric contents o Abdominal distention (often shiny) o Localized abdominal wall erythema or induration (hardening) o Bilious vomitus • NON-SPECIFIC SIGNS o Lethargy o Poor feeding o Hypotension o Vomiting o Apnea o Decreased urinary output o Unstable temperature o Jaundice DIAGNOSTICS OF NEC • X-ray: sausage-shaped mass o Progresses to marked distention and the characteristic pneumatosis intestinalis ▪ “soapsuds” or the bubbly appearance of thickened bowel wall and ultralumina o There may be air in the portal circulation or free air observed in the abdomen, indicating perforation • Guaiac and stool for OB (occult blood) • CBC: anemia, leukocytosis, leukopenia • Other labs: metabolic acidosis, electrolyte imbalance • BC (blood culture) o Bacteremia or septicemia may not be prominent early in the course of the disease THERAPEUTIC MANAGEMENT OF NECROTIZING ENTERCOLITIS • NPO 24-48 hours for birth asphyxia, ELBW, VLBW • Breast milk preferred for oral feeds o Confers some passive immunity (IgA), macrophages and lysozymes o Has been shown to decrease the risk of NEC • In infants: o Discontinuation of all oral feedings ▪ Time to reinstitute is usually at least 7-10 days after diagnosis and treatment ▪ Feeding usually reestablished using human milk o NGT placement for decompression o IV antibiotics, parenteral fluids, TPN ▪ Decreases the need for oxygen and circulation to the bowel o Correction of extravascular volume depletion, electrolyte abnormalities, acid- base imbalances and hypoxia • Bowel resection if perforation present o Surgical resection & anastomosis o Ostomy ▪ I assume to avoid the infected bowels o In some cases, intestinal transplantation has been successful • Sequelae in surviving infants includes: o Short bowel syndrome o Colonic stricture with obstruction o Fat malabsorption growth failure secondary to intestinal dysfunction NURSING MANAGEMENT OF NEC • No diaper (due to abdominal distention) o Could also place it very low on the child – not on abdomen! • Supine/side-lying position (not prone, because that would hurt (abdominal distention)) o Also easier to continuously observe the abdomen • Monitor vital signs for changes that might indicate bowel perforation, septicemia, or cardiovascular shock o Especially important to avoid rectal temperatures because of the increased danger of perforation • Measure abdominal girth Q 8 hours • Measure NGT output (residual?) Q 4 hours • Listen for bowel sounds • Colostomy care Q shift • Prevent possible transmission to other infants o Strict hand washing o Confirmed multiple cases are isolated o Persons with symptoms of GI disorder should not care for these or any other infants GIARDIASIS – INTESTINAL PARASITES • Common in young children related to developmental level • Transmission: Person to person, uncooked foods, H2O o Young children especially at risk because of typical hand-mouth activity and uncontrolled fecal activity • ^ incidence in daycare MANIFESTATIONS OF GIARDIASIS • INFANTS o Vomiting o Diarrhea o Weight loss (failure to thrive) o Anorexia • CHILDREN OLDER THAN 5 o Abdominal cramps o Intermittent loose stools o Stools that are: ▪ Malodorous (foul smelling) ▪ Watery ▪ Pale ▪ Greasy o Constipation • CHRONIC EPISODES: • Intermittent loose, foul-smelling stools/constipation • Possibility of abdominal bloating, flatulence, sulfur-tasting belches, epigastric pain, vomiting, headache, and weight loss DIAGNOSTICS OF GIARDIASIS • Because the Giardia organisms live in the upper intestine and are excreted in a highly variable patterns, repeated microscopic examination of stool specimens may be needed • Stool specimen: ELISA o Detects and measures antibodies in your blood. This test can be used to determine if you have antibodies related to certain infectious conditions ▪ Used most often • String test o Child swallows a gelatin capsule with a nylon string attached o Several hours later, the string is withdrawn and the contents are sent for lab analysis • biopsy MEDICAL MANAGEMENT OF GIARDIASIS • Anti-parasitics: metronidazole (Flagyl) – CHECK THIS o I did check – it is listed as an antiprotozoal as well as an anti-infective o Metallic taste o GI side effects including nausea and vomiting • Tinidazole (Tindamax): ^ cure rate o 80 – 100% cure rate after single dose o Also has metallic taste o GI side effects including nausea and vomiting • Albendazole (Albenza): decreased side effects • Nitazoxanide (Alinia) o No bitter taste o Should be taken with food to avoid gastrointestinal symptoms NURSING MANAGEMENT OF GIARDIASIS • Prevention & education: handwashing o Before meals, after bathroom, and when coming in from outside o Avoid placing finger in mouth and biting nails o Discourage children from scratching bare anal area o Use superabsorbent disposable diapers to prevent leakage o Change diapers as soon as soiled and dispose of diapers in close receptacle out of children’s reach o Don’t rinse cloth or disposable diapers in toilet o Disinfect toilet seats and diaper-changing areas ▪ Use dilute household bleach (10% solution) or ammonia (Lysol) and wipe clean with paper towels o Drink only treated water or bottled water, especially if camping o Wash all raw fruits and vegetables and food that has fallen on the floor o Avoid growing foods in soil fertilized with human or untreated animal excreta o Teach children to defecate only in a toilet, non on the ground o Keep dogs and cats away from playgrounds and sandboxes o Avoid swimming in in pools frequented by diapered children ▪ Swimming pool filters and interactive water fountains are sites of contamination o Wear shoes outside • Caution about side effects: o Metallic taste (Tindamax) o Nausea o Vomiting • No swimming in pools until cured • No swimming in lakes o In some cases, the medication must be repeated in 2 weeks to 1 month to kill organisms hatched since initial treatment HELMINTHIC INFESTATIONS - PIN WORMS (ENTEORBIASIS) • Hatched from eggs of nematode Enterobius vermicularis • Most common helminthic infection in the U.S. • Universally present in temperate climatic zones • May infect more than 30% of all children at any one time • Tr