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PEDS Unit 5 GI Gastrointestinal Dysfunction in the Pediatric Population The gastrointestinal (GI) tract anatomy includes the mouth, esophagus, stomach, small intestine, large intestine, and anus. Topics covered include the gut microbiome, functional GI disorders, disorders of motility, intestinal parasitic disease, inflammatory disorders, hepatic disorders, structural defects, obstructive disorders, and malabsorption syndromes. Gut Microbiome The gut microbiome is a complex community of trillions of microorganisms (bacteria, viruses, fungus, others) living primarily in the large intestine. These microorganisms play crucial roles in health and disease. Key Functions: o Digestion and Metabolism: Breaking down complex substances (carbohydrates, fibers) the body cannot digest, producing short-chain fatty acids for colon cell energy and anti- inflammatory effects. o Immune System Regulation: Supporting immune system development and function, interacting with immune cells, influencing responses to pathogens. o Protection against harmful bacteria: Maintaining balance between good and bad bacteria to prevent harmful overgrowth. o Vitamin Production: Producing essential vitamins like K, B12, and folate. o Barrier Protection: Maintaining gut lining integrity, preventing harmful substances from leaking into the bloodstream ("leaky gut"). o Mood and Brain Function: Communicating with the brain via the gut-brain axis, influencing mood/behavior (e.g., serotonin production). o Detoxifier: Helping break down and eliminate toxins and medications. o Assists with food digestion, absorption, and nutrient generation. Supports immune system, protects against nutrient deficiency and slow gut motility. The gut controls many body functions. Factors Influencing Microbiome Composition: o Diet: Rich in fibers, fruits, vegetables promotes health; high sugar, processed foods, antibiotics disrupt balance.
PEDS Unit 5 GI o Age: Evolves from infancy through adulthood, most changes in the first few years. o Environment: Stress, hygiene, sanitation exposure. o Medications: Especially antibiotics disrupt balance. Dysbiosis (imbalance) can contribute to: Inflammatory bowel disease (Crohn's, UC), obesity, metabolic disorders, autoimmune disorders, mental health disorders (anxiety, depression). Research suggests personalized medicine approaches like probiotics, prebiotics, and fecal microbiota transplants (FMT) to restore balance. Functional GI Disorders Children have persistent GI symptoms with no identifiable structural or biochemical abnormality. Related to problems with the gut-brain interaction affecting normal digestive system function. Common in children. Diagnosed based on specific criteria (e.g., Rome IV), symptom frequency/duration, and exclusion of other causes. Management involves dietary changes, psychosocial support, and sometimes symptom-based medications. Education is important as they are chronic but not life-threatening and symptoms are typically manageable. Examples: Infantile Colic, Functional Dyspepsia, Irritable Bowel Syndrome (IBS), Functional Abdominal Pain (FAP), Functional Constipation, Functional Diarrhea, Rumination Syndrome, Cyclic Vomiting Syndrome (CVS), Aerophagia. Disorders of Motility A category of pediatric GI dysfunction. Includes Diarrhea, Constipation, Hirschsprung Disease, Vomiting, and GERD. Diarrhea Definition: Three or more loose or liquid stools in 24 hours. Affects digestion, nutrient absorption, and can cause dehydration and severe illness. Acute Diarrhea: Caused by inflammation from infectious pathogens, decreased absorption, increased peristalsis. Usually self-resolving.
PEDS Unit 5 GI Complications: Fecal impaction, anal fissure, rectal prolapse, urinary infections, megacolon (chronic). Diagnosis: Stool tests (blood, parasites), lab work (anemia), imaging (X-ray, ultrasound, barium enema), motility studies. Screenings for celiac, allergies for chronic issues. Treatment: Dietary modifications, behavioral interventions, medications. o PEG solution (e.g., Miralax): Often first-line, dosed by weight, safe for long-term use. May need pediatric GI referral. Nursing Considerations: Avoid rectal exams if possible (emotional impact). Promote good toileting habits, hygiene. Educate on diet (fiber, water), activity, medication adherence. Advocate for balanced diet. Hirschsprung’s Disease Also known as Congenital Aganglionic Megacolon. A structural anomaly. Cause: Lack of ganglionic cells in colon segments, causing decreased motility and mechanical obstruction. Risk Factors: Family history. Symptoms: o Newborns: Failure to pass meconium within 24-48 hrs, refusal to eat, abdominal distension. o Infants: Failure to thrive, constipation, vomiting, diarrhea. o Older children: Anemia/undernourished appearance, abdominal distension, visible peristalsis, palpable fecal mass, constipation, very foul smelling ribbon-like stools. Diagnosis: Rectal biopsy confirms absence of ganglionic cells. Treatment: Surgical removal of the aganglionic section. Pre-surgery: high protein/calorie, low-fiber diet; sometimes TPN. Temporary colostomy is needed. Often two surgeries needed. Side Effect: Enterocolitis (bowel inflammation). Monitor for this. Nursing Considerations: Prepare for surgery, monitor for complications (enterocolitis, dehydration), ensure bowel sounds, facilitate referrals. Vomiting Definition: Forceful ejection of gastric contents through the mouth.
PEDS Unit 5 GI Numerous causes (GI disorders, infections, allergies, obstructions, medications). Common in kids, usually self-limiting. Age, pattern, duration, associated symptoms help determine cause. Mechanism: Muscle contractions and sphincter relaxation/opening. Vomiting center in medulla. Risk Factors: Family history, psychological factors, head injury, migraines, blood sugar issues, pregnancy/substance use (adolescents), poor hygiene/food prep. Leading cause in young kids: Gastroenteritis. Presentation: Note appearance (food, bile, mucus, blood). Differentiate vomit vs. spit up vs. projectile vomit. Bilious vomit suggests obstruction. Non-bilious may suggest poor gastric emptying/high obstruction. Forceful vomit may suggest pyloric stenosis. Vomiting blood is a serious sign. Nursing Considerations: Assess appearance, behavior, distress, weight, vital signs, hydration, abdomen. Get history (illness, exposure, meds, diet, output, allergies). Inquire frequency, duration, associated symptoms. Prioritize: Treat dehydration first. Prepare for rapid intervention in severe cases. Diagnosis: Lab (CBC, BMP, urinalysis, pregnancy), imaging (ultrasound, CT, upper GI, brain scan). Treatment: Treat underlying cause, prevent dehydration. Oral rehydration or IV fluids. Antiemetics for severe cases. Avoid high sugar foods, reintroduce bland diet. Chronic vomiting can cause: Nutritional deficiencies, developmental delays, sleep/concentration issues. Monitor infants/young children closely for dehydration. Educate parents on signs needing emergent care. GER vs. GERD Due to underdeveloped or weak lower esophageal sphincter (LES) in infants/children. Gastroesophageal Reflux (GER): o Normal reflux of stomach contents into esophagus. Common in infants ("spit up"). Mild, usually not painful, self-limiting, resolves by 12-24 months. Doesn't affect growth. Managed with lifestyle changes (positioning, smaller feeds). Gastroesophageal Reflux Disease (GERD):
PEDS Unit 5 GI Includes Pinworms and Giardiasis. Pinworms (Enterobius vermicularis) Small white parasitic worms in intestines, common in kids. Spread fecal-oral via egg ingestion from contaminated surfaces/hands. Eggs survive 2-3 weeks. Females lay eggs around anus, causing perianal itching (especially at night). Also enuresis, restlessness, sleeplessness. Diagnosis: Tape Test (adhesive tape on perianal region collects eggs). Treatment: Antiparasitic meds (mebendazole >6 yrs, albendazole). Single dose, repeat in 2 wks if needed. Contagious, keep child home during incubation. Giardiasis (Giardia lamblia) Caused by Giardia lamblia. Transmitted person-to-person, food, animals, contaminated water/surfaces (poor sanitation areas). Common waterborne illness globally. Incubation: 1-3 weeks. Diagnosis: Stool testing. Treatment: Antifungals. Symptoms vary by age: Under 5: diarrhea, vomiting, anorexia. Over 5: abdominal cramps, intermittent loose, very smelly, pale, greasy stools (hallmark). Chronic cases: bloating, fatigue, weight loss. Inflammatory Disorders Includes Appendicitis, Inflammatory Bowel Disease (IBD), Peptic Ulcer Disease, Meckel Diverticulum. Appendicitis Definition: Inflammation of the appendix. Blockage (fecalith, lymphoid hyperplasia, foreign body) leads to infection/inflammation. A surgical emergency ; risk of rupture if untreated. Can progress to necrosis, perforation, peritonitis, death. Increased risk in older kids (10-19), males. Risk factors: prior abdominal surgery, family history, cystic fibrosis. Common (250k US cases/yr). Symptoms: Abdominal pain starting near umbilicus, migrating to lower right quadrant (McBurney's point). Pain intensifies with
PEDS Unit 5 GI movement. Decreased bowel sounds, rigid abdomen, nausea, vomiting, fever. Diagnosis: Physical exam, increased WBC count, ultrasound/CT/MRI. Treatment: Appendectomy (surgery). Antibiotics pre/post-op. Pain control important. Inflammatory Bowel Disease (IBD) Chronic inflammation of the GI tract. Includes Crohn’s Disease (CD), Ulcerative Colitis (UC), IBD unspecified (IBDU). Goal is to induce/maintain remission. Increased colorectal cancer risk. Often confused with IBS. IBD has inflammation, IBS does not. Etiology is multifactorial (genetic susceptibility, environmental triggers, altered immune response/microbiome). Risk factors: family history, smoking, diet, activity, medications. Incidence increasing, especially Crohn's. More aggressive if childhood onset. Characterized by exacerbations and remissions. UC: Affects mucosal layers of rectum and colon. Causes bloody diarrhea, pain, urgency. CD: Affects anywhere in GI tract. Involves all layers, discontinuous ("skip lesions"). Causes inflammation, ulcerations, strictures, adhesions, fistulas. Causes abdominal pain, diarrhea, weight loss. Higher risk for anal fissures. Both can have extraintestinal manifestations (joint pain, rashes). Diagnosis: Symptoms, blood tests (inflammation, liver), stool tests, endoscopy with biopsy. Treatment: Medications (steroids for induction, immunosuppressants, biologics), nutritional therapy (enteral/exclusion diets), lifestyle (exercise, stress management, no smoking). Surgery for non- responsive cases. UC surgery can be curative; CD surgery is not curative. FMT is potential treatment. Irritable Bowel Syndrome (IBS) Functional GI disorder with altered gut-brain axis communication. Chronic, no inflammation. Affects large intestine. More frequent in adolescents (22-35%) than children (6-14%). Etiology unclear, likely genetic/environmental/stress/microbiome factors. Risk factors: family history, diet (high fat, low fiber), food intolerances, GI infections, Vitamin D deficiency.
PEDS Unit 5 GI Diagnosis: Meckel’s Scan (nuclear imaging) detects gastric tissue. Other imaging for obstruction/inflammation. Treatment: Surgical removal if symptomatic (bleeding, obstruction). Nursing: Monitor for bleeding (bright red, dark/sticky stool). Post-op: pain, infection, return of bowel function. Educate families on complications/when to seek care. Hepatic Disorders Includes Biliary Atresia, End Stage Liver Disease, Hepatitis. End Stage Liver Disease and Hepatitis covered in AH1. Biliary Atresia Rare, serious condition in infants. Bile ducts are blocked or absent , causing bile to back up in the liver. Leads to liver damage and cirrhosis. Cause unknown, congenital. Symptoms (first weeks-months): Jaundice, dark urine, pale/clay colored stools , enlarged liver, difficulty gaining weight. Diagnosis: Blood tests (liver function), ultrasound, liver biopsy, duct X- ray with dye. Treatment: Kasai procedure (damaged ducts removed, intestine attached to liver for drainage) is main treatment. Most effective if done early (2-3 months). If Kasai fails or damage continues, liver transplant may be needed. Poor prognosis if untreated. Nursing: Monitor for liver failure signs (jaundice, swelling, poor growth). Post-op: site infection, pain. Nutritional support is crucial (special formulas/supplements, fat-soluble vitamins A, D, E, K). Educate parents on care, follow-up, transplant possibility. Structural Defects Includes Cleft Lip/Palate, Hernia, Esophageal Atresia, Tracheoesophageal Fistula. Cleft Lip and Cleft Palate Facial malformations from incomplete fusion during embryonic development. Can occur together or separately. Cause: Failure of facial tissues to fuse. Etiology: genetic and environmental (BMP4 gene, family history, maternal
PEDS Unit 5 GI smoking/substance use, folic acid deficiency). Detection prenatally or at birth. Complications: Feeding difficulties , speech issues, dental problems, increased ear infections/hearing loss (palate structure affects ear connection). Growth/development delays due to feeding issues. Diagnosis: Ultrasound/exam, feeding assessment, imaging. Treatment: Surgery (Cheiloplasty for lip, Palatoplasty for palate). Multidisciplinary team needed. Feeding: Position upright during feeding. Use specialized bottles/nipples. Avoid sucking on pacifiers/objects post-surgery. Post-op: Elbow restraints to prevent touching surgical site, loosen frequently. Early dental care needed. Parents need guidance on feeding/milestones. Hernias Definition: Weakness in abdominal wall allowing for protrusion. Risk of incarceration/strangulation (ischemia). Common: Inguinal (groin), Umbilical (umbilicus). Rare/Serious: Congenital Diaphragmatic Hernia (CDH). Usually asymptomatic (just notice bulge). Inguinal: bulge in groin/scrotum/labia. Umbilical: bulge around umbilicus. Diagnosis: Primarily physical exam. Ultrasound may be used. CDH often prenatal ultrasound. Etiology/Risk: Increased abdominal pressure, syndromes, family history, low birth weight, prematurity, chronic cough. Inguinal more common in males; Umbilical in premies/African-Americans. Treatment: Umbilical/ventral usually watchful waiting unless symptomatic. Inguinal usually surgical repair. CDH is emergency, needs stabilization then surgery. Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF) Anomalies of esophagus/trachea, often together, diagnosed soon after birth. EA: Esophagus fails to form a continuous passage , ends in blind pouch. Prevents food reaching stomach. Symptoms: Frothy saliva/drooling, choking, coughing, difficulty breathing when feeding. Cannot pass NG tube. Diagnosis: Inability to pass tube, X-ray. Treatment: Surgical connection of esophageal ends.
PEDS Unit 5 GI Causes: Majority idiopathic. Risk factors: recent infection, celiac, cystic fibrosis, surgery, polyps. Symptoms: Sudden, severe abdominal pain with intermittent crying. Green vomiting. Abdominal distension. Red jelly-like stools (blood and mucus). Palpable abdominal mass (sausage-shaped). Dance sign: Empty right lower quadrant on palpation. Diagnosis: X-ray, ultrasound. Contrast enema (diagnostic/therapeutic). Treatment: Hydrostatic reduction (enema). Surgery for recurrent cases or if shock/peritonitis/prolonged symptoms. Manual reduction or bowel resection may be needed. Malabsorption Syndromes Result in decreased nutrient absorption. Includes Celiac Disease, Short Bowel Syndrome. Celiac Disease Definition: Permanent intestinal intolerance to dietary gluten. Also called celiac sprue, etc.. Autoimmune condition triggered by gluten (gliadin protein). Immune response causes inflammation/atrophy of intestinal lining. Effects: Malabsorption, diarrhea, weight loss, anemia, nutrient deficiencies. Onset: Symptoms appear ages 1-5 , often after introducing gluten solids. Risk factors: Family history, genetic predisposition, other autoimmune disorders (Down syndrome, T1 diabetes), early protein introduction. Symptoms: Diarrhea/constipation, abdominal pain, fatigue, skin rashes. Non-classic: migraines, chronic fatigue, joint pain, allergy symptoms. Failure to thrive (infants). Diagnosis: Blood tests (tTG-IgA antibodies), genetic markers. Definitive: EGD biopsy. Do NOT exclude gluten before testing. Treatment: Lifelong gluten-free diet restores intestinal lining. Untreated can cause: Autoimmune/neurological disorders, malnutrition, intestinal cancers, growth/development delays, impaired bone health. Short Bowel Syndrome
PEDS Unit 5 GI Malabsorptive disorder due to decreased mucosal surface area from missing or surgically removed small intestine. Body struggles to absorb enough nutrients. Requires parenteral nutrition (PN) (nutrients directly into bloodstream). Causes: Surgery (Crohn's, cancer, trauma), congenital (born with shorter intestine), diseases causing damage/removal. Mortality rate in infants 27-37% in 5 years. Multidisciplinary approach needed. Symptoms: Frequent watery diarrhea , frequent dehydration , electrolyte imbalances. Inability to absorb calories leading to nutritional deficiencies, weight loss, fatigue. Complications: Vitamin deficiencies (B12, D, iron), kidney stones. Severe: intestinal failure. Management: Diet (small, frequent, high calorie/nutrient), PN is necessary. Meds (anti-diarrheals, antibiotics - short-term).
