peds GI Flashcards
Non-bilious projectile vomiting, dehydration, poor weight gain, afebrile – often looking ill with hypochloremic metabolic alkalosis and Exam may reveal “olive” (thick pylorus)
hypertrophic pyloric stenosis
hypertrophic pyloric stenosis
pyloric channel thickening that leads to gastric outlet obstruction. this causes vomiting and witht he loss of HCl leads to hypocholremic alkalosis with eventual hypokalemia
treatment of hypertrophic pyloric stenosis
srugical- pyloromyotomy to relieve tightening
- prognosis is excellent
intussusception
proximal segment of bowel telescopes into the distal portion bringing the mesentary with it causing venous and lymphatic congestion leading to edema, ischemia and perforation
difference between adults and children with intussusception
addults have a leading point
“Classic” case = male under 10 months old
- intermittent abdominal pain
vomiting
“currant jelly stool”-LATE finding!! - may reveal palpable mass in right mid-abdomen (“palpable sausage”)
intussusception
“doughnut” with hyperechoic mesenteric fat with vessels/nodes inside intussusception
intussusception
classic diagnosis for intussusception and treatment
therapeutic enema:
- Air (pneumatic) reduction = most popular, cleaner, less risk if perforates
- Water-soluble contrast (hydrostatic) reduction= better than barium
* Success 80-95% success with either
** surgery may be indicated
recurrence with intussusception
yepppp
constipation may be associated with hypothyroidism, celiac disease, electrolyte abnormalities, Hirschsprung’s disease, neurologic disease (cerebral palsy, spina bifida), others…
organic
common between 6 months and preschool
trigger may be dietary transition – breastmilk to formula, liquids to solids, new food – and possibly milk allergy (especially in infants)
Functional constipation is the most common reason – no evidence of any organic disorder
traumatic defecation, i do not want to poop
functional constipation
prognosis of functional constipation
typically problematic x years, relapses >50%
affected children may become adults with IBS
Aka: congenital aganglionic megacolon
Consistent with embryonic enteric neuronal plexus development…HD always involves the rectum and extends proximally to area
where cephalad caudad nerve development ends
Hirschsprung’s disease
hirschsprung’s disease
- arrest of
- affects both
- genetics
- Adults appearance
- delayed passage of
- treatment
- arrest of neural crest cell migration
- affects both meissner’s submucosal and auerbach’s myenteric plexuses
- half of familial cases and 15% sporadic related to mutation in RET proto-oncogene
- short-segment
- meconium
- surgical- removal of affected portion
hirschprung’s diease
affected colon loses ability to relax (NO and other por-relaxation peptides no effect) leading to narrowed, collapsed contracted distally but portion that is proximal is dilated normal
Outpouching results from incomplete obliteration of vitelline (omphalomesenteric) duct – connecting the midgut to the yolk sac
Meckel’s diverticulum
THE most common congenital abnormality of the GI tract
Meckel’s diverticulum layers
it is ocnsidered a true diverticulum containing all layers of the ileal wall
Meckel’s diverticulum symptoms formation
the ectopic gastric mucosa within the diverticulum affects the parietal cells which secrete HCl which injures the neighboring tissue causing bleeding, abdominal pain and obstruction
The Rule of Twos…
- Occurs in 2% of population
- M:F ratio of 2:1
- Within 2 feet of the ileocecal valve
- Can be 2 inches in length, 2cm wide
- Complications typically occur at < 2 years old
- Approx 2-4% develop complications
meckel’s diverticulum
how is meckel’s diverticulum diagnosed
technetium-99m pertechnetate scan
Omphalocele and Gastroschisis
congenital defects in the abdominal wall and both are usually identified prenetaly then surgical repair
large central defect that involves the intestines, liver, and other organs are outside the abdomen in a sac
omphalocele
smaller defect, NOT involving umbilicus, usually bit to the right, and NO sac, no liverassociated with intestinal atresia in 10%
gastroschisis
bubbles of air in intestinal wall
necrotizing enterocolitis
**“pneumotosis intestinalis” = air within bowel wall. air may track up into portal venous system
prevalence of necrotizing enterocolitis
common!!! 7% and has a mortality of 20-30%
Typically presents within first 2 weeks, with onset of enteral feeding – abdominal distension, vital sign changes
consider Necrotizing enterocolitis !!!!!
necrotizing enterocolitis factors
it may be involved with prematurity, microbial overgrowth, mucosal immaturity, vascular factors leading to infarction that causes transmural necrosis, hemorrhage, subserosal air increasing perforation risk
prevention of necrotizing enterocolitis
getting infant closer to term gestation
treatment of necrotizing enterocolitis
- bowel rest/antibiotics
- surgery
what occurs in 10-35% of all cases mostly colonic origin in necrotizing enterocolitis
strictures
