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GI

Terms in this set (86)

Duodenum
Location of digestion. Enzymes aid the digestion process.
Differences in anatomy of GI system for kids
-Smaller stomach capacity
-Increased peristalsis
-Enzymes not of sufficient quantity to aid digestion until 4-6 months
-Increased abdominal distention from gas
-Liver function immature at birth
-Digestive system intact by 2 years of age
Clinical manifestations of GI dysfunction
-FTT
-Spitting up, regurgitation
-N, V, D, Constipation
-Abd. pain, distention, GI bleeding
-Jaundice
-Dysphagia
-Hypoactive, hyperactive, or absent bowel sounds
-Fever
Cleft lip/palate
Failure of the maxillary processes to fuse between 5 and 12 weeks gestation. Failure of the tongue to move down at the correct time prevents the palatine processes from fusing. Multifactorial causes
Cleft lip/palate - Feeding
-Special bottles/nipples
-Palatal obturator
-Breastfeeding is the best if they can latch on
-Sippy cup
-NG feedings
Surgical correction of cleft lip
Closure of lip defect precedes correction of the palate
Lip closed usually between 2-3 months
Z-plasty to minimize retraction of scar
Protect suture line with logan bow or other methods
Cleansing of suture line, supine or side-lying- should not be prone, arm/elbow restraints for 2 weeks post-op.
Logan bow
Used after a cleft lip repair
Keeps traction to reduce scar tissue
Surgical correction of cleft palate
Typically 6-12 months
Effect on speech development
Increased incidence of OM, dentition issues, speech, and risk of aspiration.
Need follow up to ensure appropriate nutrition.
Sippy cups should be soft; no crackers; nothing hard in mouth.
Esophageal atresia/tracheoesophageal fistula
Foregut fails to lengthen, separate, and fuse into two parallel tubes (esophagus and trachea) at 4-5 weeks' gestation. Is associated with maternal polyhydramnios. Symptoms include excessive salivation and drooling, cyanosis, choking, coughing. Unable to pass an NG to the stomach. Should put a tube in to keep it decompressed. Is a surgical emergency.
First intervention - suction to clear airway
The 3 C's
Coughing
Cyanosis
Copious secretions
-Signs on EA/TEF-
Management of TEF
Maintenance of patent airway, prevention of pneumonia, gastric or blind pouch decompression, supportive therapy
Surgical interventions
Associated tracheomalacia
Tracheaomalasia
Trachea is not able to maintain support.
Hear expiratory stridor. See with children intubated for a long period of time.
Pyloric stensosis
Hypertrophy of the circular pylorus muscle. Stenosis occurs between stomach and duodenum. Olive like mass. Causes projectile vomiting (non-bilious, is the milk they just had); usually between 2-8 weeks. Is more common in males. Metabolic alkalosis (loss of hydrochloric acid), aspiration, imbalanced nutrition, volume deficit, risk for infection. Irritable (because they are hungry), failure to gain weight, peristaltic waves visible, hypoklemia. Van visually see reverse peristalsis.
Gestroesophageal reflux
Transfer of gastric contents into the esophagus. Three mechanisms allow reflux to occur: lower esophageal relaxations, incompetent lower esophageal sphincter, and anatomic disruption of esophagogastric junction.
GERD
Reflux acidity damages the esophageal mucosa. Present with h/o poor weight gain, recurrent vomiting, generalized irritability, and refusal to feed. Infants may have h/o arching and respiratory symptoms such as wheezing and apnea. Barium swallow and gastric emptying studies. Includes development of complications such as respiratory.
GERD Treatment
Smaller, thickened feedings; frequent burping; feeding upright; important to follow growth. Medications - Histimine H2 receptor agonists (Zantac, Pepcid) and proton pump inhibitors (Prevacid, Prilosec). Do not recommend rice cereal.
Nissen Fundoplication
Surgical treatment for GERD. Take the upper portion of the stomach and wrap it around the esophagus.
Gastroschisis
Abdominal contents located outside the abdominal wall. Usually occurs to the right of the umbilicus. Occurs in week 11 of gestation when abdominal contents fail to return to the abdomen. Keep defect moist and warm, cover with sterile saline; assess for other defects. Will loose heat and insensible water loss b/c gastric contents are not covered. Put contents in a silo, each day more will return to abdomen.
Omphalocele
Protrusion of abdominal contents through the umbilical cord. Usually occurs through the umbilical cord. Occurs in week 11 of gestation when abdominal contents fail to return to the abdomen, Keep defect moist and warm, covered, prevent infection; assess for other defects. Commonly see congenital heart defect too.
Intussusception
Intestine invaginate or telescopes into another. Mesentery becomes inflamed and obstruction can occur. Most common cause of intestinal obstruction in children between 3mo and 3yr. Onset usually abrupt - usually under 3yo. Acute abdominal pain with periods of comfort. Bilious emesis and palpable abdominal mass. Red currant-jelly stools b/c of blood and mucous. Classic triad of symptoms - abdominal pain, abdominal mass, bloody stools. Tx - hydrostatic reduction - barium enema or saline enema. Complications: perforation, peritonitis, sepsis and death.
Currant-jelly stool
Leaking of blood and mucous into intestinal lumen.
Volvulus
Occurs in the 7th - 12th week of gestation. 1 in 6,000live births. Malrotation of bowel interrupts blood flow and causes bowel necrosis. Bilious vomiting, abdominal distention, irritability d/t pain, bloody stools. Is a surgical emergency.
Hirschsprung disease
Congenital absence of ganglion cells in the rectum and colon causes an inadequate motility (decreased peristalsis) and mechanical obstruction of the intestine. Consider when no stool in 48 hours. Is genetically acquired and occurs when there is failure of the migration of neural crest cells in utero. Colon becomes a "megacolon". Clinical manifestations include the accumulation of stool with distention (stool can be pellet-like or ribbon-like), bilious vomiting, and abdominal distention. There is failure of the internal anal sphincter to relax and the infant may not have stool w/in first 24-48 hours. Enterocolits may occur.
Megacolon
Feces and gases distend colon. Failure to pass mecomium within 24-48 hours, abdominal distention, bilious vomiting. Can cause infection.
Diagnostic Evaluation of Hirschsprung Disease
-X-ray, barium enema
-Anorectal manometric examination
-Confirm diagnosis with rectal biopsy - gives a definitive diagnosis
Therapeutic Management of Hirschsprung Disease
Surgery: temporary ostomy and then a second stage "pull-though" procedure.
Anorectal malformations
Anal stenosis and anal atresia. Failure of growth of urorectal septum, lateral mesoderm structure, and ectodermal structures. Often are associated anomalies.
VACTERL
Condition of multiple complications Need three or more:
Vertebral defect
Anorectal malformation
Cardiac defects
Tracheoesophageal fistula
Esophageal atresia
Renal anomalies
Limb defects
Anorectal malformations operations
Anoplasty may be used to correct retroperitoneal defects (low defects). Higher defects may need 3 stage repair - temporary colostomy bowel decompression and protection of surgical site), reconstructive surgery (posterior sagital anorectoplasty) anywhere from 1-3 months or 3-6 months. Dilations start when operative site healed (2 weeks). When anal opening is at desired size (6-8 weeks after surgery), colostomy is closed.
Rectal prolapse
Most cases are self-limiting. In peds, should always be considered a presenting sign of an underlying condition and not a discrete disease entity. Found in 20% of CF patients - large bulky stools, coughing, paroxysms, and undernutrition. Most often < 6 years.
Congenital diaphragmatic hernia
Protrusion of abdominal contents into thoracic cavity. Occurs in 4th week of gestation. Failure of pleuroperitoneal musculature to close.
Appendicitis
Caused by an obstruction of the appendices lumen, causing edema. As edema continues, vascular supply is compromised and bacteria invade, which can lead to a ruptured appendix. Pain in R lower quadrant. Presence of fever and WBC above 10,000/mm3), rebound tenderness. Lie on R side with legs drawn up. Sudden relief of pain = rupture.
Umbilical hernia
Around 11th week of gestation, the obliterated umbilical vessels occupy the space in the umbilical ring. Inguinal hernias. Concern is for strangulation.
McBurney's point
Pain in right lower quadrant. Common location of pain in children with appendicitis.
Most common GI for Infants
Colic
Constipation
Volvulus
Intussusception
Most common GI for Older Children
Gastroenteritis
Appendicitis
Mesenteric lymphadenitis
Constipation
Approach to Appendectomy
1- w/ first hospitalization get controlled with WBC<12,000, ESR<40, Bands<5, tolerate oral intake, ambulating, controlling pain, afebrile
2- Come in later for Appy
Meckel's diverticulum
Omphalomesenteric duct fails to atrophy - it is a remnant of the connection from the yolk-sac to the small intestine present during embryonic development. out-pouching of the ileum remains and contains gastric contents, causing ulceration. Bowel obstruction, perforation, or peritonitis can occur. Diagnostic evaluation - bleeding most common, currant-jelly like stools. Tx - surgical removal.
Necrotizing enterocolitis (NEC)
Inflammatory disease producing vascular compromise of bowel mucosa. More common in premature infants. caused by intestinal ischemia, bacterial or viral infection, and immature gastrointestinal mucosa. Free air = perforation. Distended bowel, dilated bowel loops, and bowel wall thickening. Monitor stools and emesis for occult blood; abdominal girths. Blood cultures, anemia, leukopenia, leukocytosis, thrombocytopenia, electrolyte imbalance, metabolic or respiratory acidosis. Put NPO for 10 days. If perforate - surgical removal of dead gut and colostomy. Can re-anstomose after gained weight. Often supplemented with probiotics.
IBD (UC and Chron's)
Faulty regulation of the immune response of the intestinal mucosa. usually genetically triggered.
Chron's
Causes inflammation and ulcers anywhere throughout the GI tract. Increased chance of colon cancer later in life. Auto-immune disease. Sometimes have part of their intestines resected.
IBS
A functional disorder of the GI tract that is characterized as chronic and episodic. No structural cause, but triggered by events such as gastroenteritis or major life events/stressors.
UC
Aaffects large intestine and rectal mucosa. Much more pain and bloody diarrhea.
Peptic ulcer
Can be gastric or duodenal and primary (occurs in absence of pre-disposing factors; healthy children), or secondary (stress ulcers which occur in children with pre-exisisting disease or injury such as burns and children receiving medications such as salicylates, corticosteroids, and NSAIDS). Are usually caused by heliobacter pylori.
IBS/D - Treatment
Control inflammatory process to reduce or eliminate symptoms
Obtain long-term remission
Promote normal growth and development
Allow as normal a lifestyle as possible
Medications: 5-Aminosalicylates - mesalimine, olsalazine, and balsalazide (decrease inflammation by inhibiting prostaglandin synthesis)
Corticosteroids (inhibit production of adhesion molecules, cytokines, and leukotrienes).
Antibiotics (Flagyl and Cipro)
Immunomodulators
Surgery
Colorectal cancer is a long-term complication
Peptic Ulcers - Therapeutic Management
Antacids - neutralize gastric acid
Histamine (H2) receptor agonists - suppress gastric acid production (Tagamet, Zantec, Pepcid)
Proton pump inhibitors - inhibit hydrogen ion pump in parietal cells, inhibiting production of acid (Nexium, Protonix, Prevacid, Prilosec, and Aciphex)
Mucosal protective agents - protective barriers over ulcerated areas to protect against acid and pepsin (sucralfate, bismuth containing preparations)
Antibiotics (H. pylori)
Antacids
Neutralize gastric acid
Histamine (H2) receptor agonists
Suppress gastric acid production (Tagamet, Zantec, Pepcid)
Proton pump inhibitors
Inhibit hydrogen ion pump in parietal cells, inhibiting production of acid (Nexium, Protonix, Prevacid, Prilosec, and Aciphex)
Mucosal protective agents
Protective barriers over ulcerated areas to protect against acid and pepsin (sucralfate, bismuth containing preparations)
Gastroenteritis
Acute diarrhea. Leading cause of illness in kids <5. 20% of deaths in developing countries related to diarrhea and dehydration.
Prevention of diarrhea
Teach personal hygiene
Most diarrhea is spread by the fecal-oral route
Clean water supply, protect from contamination
Careful food preparation
Hand washing
Causes of diarrhea
Infection: rotavirus, food sensitivity, food intolerance, medications, emotional stress.
Types of constipation
Normal-transit constipation
Slow-transit constipation
Defecation disorders
Encopresis
Failure to control the bowels once the normal age for bowel control has been reached. Most common cause is constipation.
Primary ecopresis
Bowel control has never been acheived
Secondary encopresis
Child has had several months of bowel control and now no longer have control.
Constipation
Alteration in frequency, consistency, or ease of passage of stool. Can be caused by underlying disease, diet, or psychological factors. In NB period assess for: first stool passed within 24-36 hours, hirschsprung disease, hypothyroidism, meconium plug/ meconium ileus-(CF).
Normal-transit constipation
Most common form (95%). Stool traverses at a normal rate thru the colon and stool frequency is normal, but individual has difficult time passing stool or passes hard stools. Bloating and abdominal pain.
Slow-transit constipation
Most common in young females. GI time is longer and peristalsis is weaker.
Defecation disorders
Dysfunction of pelvic floor - ie anorectal malformations. Desire to avoid pain associated with passing large hard stools
Short Bowel Syndrome
Shortened intestine resulting from bowel resection. Extent of bowel loss determines severity of disorder. Location of bowel resection determines type of malabsorption.
Celiac Disease
Gluten-induced enteropathy and celiac sprue. Four characteristics: steatorrhea, general malnutrition, abdominal distention, and secondary vitamin deficiencies. Cannot have barley, rye, oats, wheat. Can have rice, corn, soy. No gluten!
Hyperbilirubinemia
Bilirubin is deposited in the tissue because the liver of the newborn can not process it. Starts from the head and works it's way down. Bilirubin can cross the blood brain barrier. Levels of 20 or higher are dangerous. Can cause kernicterus.
Kernicterus
Irreversible brain damage caused by jaundice.
Pathologic Jaundice
Jaundice within the first 24 hours.
Physiologic Jaundice
Jaundice in the second day of life that is normal and resolves on it's own.
Kasai procedure
Removal of the blocked bile ducts and gallbladder and replacement with a segment of child's own small intestine. This segment of intestine is sewn to the liver and functions as a new extrahepatic bile duct system.
Biliary Atresia
Obliteration of bile ducts (fibrosis), progressive inflammatory process, immune mechanisms or viral injury. management includes Kasai procedure, liver transplant. They are Jaundice for 2-3 weeks after neonatal jaundice resolves. Dark yellow urine. Light-colored, pasty stools or white or tan. Blocked bile flow from liver to duodenum causes inflammation and fibrotic changes in liver. Lack of bile acids interferes with digestion of fat and absorption of fat-soluble vitamins A, D, E, & K. Steatorrhea and nutritional deficiencies. Abdominal pain, hepatomegaly, splenomegaly. Easy bruising, prolonged bleeding time, and intense itching d/t deposits of bilirubin. FTT and malnutrition. Liver biopsy. Hepatomegaly and abd distention. Poor fat metabolism - FTT, poor weight gain. Pruritis. Irritability
Abdominal trauma
Blunt or penetrating trauma to the abdomen. Common causes include falls, MVA, abuse, and GSW
Viral Hepatitis
Chronic inflammation of the liver. Causes include: viruses (EBV, CMV, HIV), chemical reactions, drug reactions, neoplasms, CHF, shock, idiopathic, autoimmune, or metabolic.
Signs of Hepatic Disorders
Jaundice
Easy bruising, intense itching
White or clay-colored stools
Tea-colored urine
Potential signs of GI Emergencies in Infants
Excessive salivation with cyanosis, coughing, and choking in newborn
Esophageal atresia and tracheoesophageal fistula
Abdominal viscera outside the abdominal cavity when born
Gastroschisis and omphalocele
Anorectal malformations
Abdominal pain
Changes in appearance of stool
Vomiting and/or anorexia
Changes in activity
Changes in level of consciousness
Preoperative care of child with cleft lip/palate
Facilitate feeding
Special feeding devices
Support for mothers who are breastfeeding
Provide psychosocial support
Prevent aspiration
Position upright for feedings
Suction equipment and bulb syringe
Feed slowly, use adaptive equipment as needed
Postoperative care of child with a cleft lip/palate
Assess vital signs
Measure intake and output
Position upright for feedings
After feedings, clean suture line
Maintain suture line
Antibiotic ointment, pain management
Soft elbow immobilizers for two weeks
Pre/Post-op care for Esophageal atresia and TE fistula
Suction important preoperatively
Care of the gastrostomy tube postoperatively
Infant (birth to 1 year) - GI specific
Congenital defects
Gastroesophageal reflux in infant vs. older child
Gastrointestinal disorders specific to this age group
Toddlers (1 Year to 3 Years) - GI specific
Meckel's diverticulum
Offer age-appropriate toys
Childproof the room
Use pictures for education of older toddler
Children (3-12 years) - GI Specific
Body image starts becoming important after 5 years old
Offer age-appropriate toys
Use pictures for education of younger child
Umbilical hernia repaired
Adolescents (13-17 years) - GI Specific
Appendicitis (10 to 19 years old)
Body image extremely important
Allow use of phone to satisfy peer needs
Give them handouts about peers with conditions and experiences
Intestinal parasitic Disorders
Occurence related to: untreated water, incorrect food preparation, and crowded conditions with poor sanitation. Young children most at risk in childcare settings and exposed to pets/wildlife. Prevent with good hygiene and take meds as ordered.
Abdominal Trauma
Blunt/Penetrating
Peds abdominal frame makes kids more exposed and vulnerable to injury.
Clinical manifestations of abdominal trauma
Pain
Abdominal distention
Guarding
Decreased or absent bowel sounds
Nausea and vomiting
Hypotension
Shock
Penetrating wounds, bruising, marks
Chelation
A reaction in which an organic compound containing carbonyl (CO) and hydroxyl (OH) groups interacts with a metal to form a compound the child can eliminate. Close monitoring essential and long-term follow-up essential.
Lead Poisoning
-5mcg/dL and below is safe
-Chelation therapy if 45mcg/dL or higher
-Causes of lead exposure: old homes, old blinds, toys/paints from china. To clean up; wet mop.
Poisoning
Keep potential poisons out of sight and out of reach.
Always reengage child-resistant closures immediately after using a pharmaceutical or consumer product.
Never transfer a substance from its original container to an alternate one.
Safely dispose of all unused medication and medication that is no longer needed.
Do not refer to medicines as candy.
Post the poison control center number near the telephone.
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