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161 Cards in this Set
- Front
- Back
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what is the DDx of pediatric upper GI bleeding?
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gastritis, esophagitis, gastric ulcer, duodenal ulcer, esophageal varices, foreign body, epistaxis, coagulopathy, vascular malformation, duplication cyst
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what is the DDx of pediatric lower GI bleeding?
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upper GI bleeding, anal fissures, NEC (premature infants), midgut volvulus (usually children <1yr), strangulated hernia, intussusception, meckel's diverticulum, infectious diarrhea, polyps, IBD, hemolytic uremic syndrome, henoch-schonlein purpura, vascular malformation, coagulopathy
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what is the DDx of neonatal bowel obstruction?
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malrotation w/volvulus, intestinal atresia, duodenal web, annular pancreas, imperforate anus, hirschsprung's disease, NEC, intussusception (rare), meckel's diverticulum, incarcerated hernia, meconium ileus, meconium plug, maternal narcotic abuse (ileus), maternal hypermagnesemia (ileus), sepsis (ileus)
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what is the DDx of infant constipation?
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hirschsprung's disease, CF, anterior displaced anus, polyps
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what is the most commonly performed procedure by US pediatric surgeons?
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indirect inguinal hernia
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what is the most common inguinal hernia in children? what is it?
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indirect --> hernia lateral to hesselbach's triangle into the internal inguinal ring and down the inguinal canal (think: through the abdominal wall indirectly into the internal ring and out through the external inguinal ring)
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what is hesselbach's triangle? what type of hernia goes through hesselbach's triangle?
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a triangle formed by epigastric vessels, inguinal ligament, lateral border of the rectus sheath. a direct hernia from a weak abdominal floor goes through hesselbach's triangle (rare in children --> 0.5% of all inguinal hernias)
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what is the incidence of indirect inguinal hernia in all children? premature infants? male:female ratio? what % have a family hx?
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all children: ~3%. premature: up to 30%. male:female: 6:1. family hx: ~10%
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what are the risk factors for an indirect inguinal hernia?
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male gender, ascites, V-P shunt, prematurity, family hx, meconium ileus, abdominal wall defect elsewhere, hypo/epispadias, connective tissue dz, bladder exstrophy, undescended testicles, CF
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which side is affected more commonly in indirect inguinal hernias? what % are bilateral?
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right (~60%). ~15% are bilateral
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what are the signs/sx of indirect inguinal hernia? what is the silk glove sign?
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goin bulge, scrotal mass, thickened cord, silk glove sign --> hernia sac rolls under finger like a silk glove
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why should an indirect inguinal hernia be repaired?
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risk of incarcerated/straungluated bowel or ovary; will not go away on its own
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how is a pediatric inguinal hernia repaired?
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high ligation of hernia sac (no repair of the abdominal wall floor, which is a big difference b/w procedure in children and adults). note: high refers to high position on the sac neck next to the peritoneal cavity
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which infants need overnight apnea monitoring/observation?
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premature infants; infants >3 mo.s
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what is the risk of recurrence after high ligation of an indirect pediatric hernia?
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~1%
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describe the steps in the repair of an indirect inguinal hernia from skin to skin
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cut skin, then fat, then scarpa's fascia, then external oblique fascia through the external infuinal ring; find hernia sac anteriomedially and bluntly separate from the other cord structures; ligate sac high at the neck at the internal inguinal ring; resect sac and allow sac stump to retract into the peritoneal cavity; close external oblique, close scarpa's fascia, close skin
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define cryptorchidism
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failure of the testicle to descend into the scrotum
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define hydrocele, communicating hydrocele, noncommunicating hydrocele
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hydrocele: fluid-filled sac (i.e., fluid in a patent processus vaginalis or in the tunica vaginalis around the testicle). communicating: hydrocele that communicates w/the peritoneal cavity and thus fills and drains peritoneal fluid or gets bigger, then smaller. noncommunicating: does not communicate w/the peritoneal cavity, stays about the same size
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can a hernia be ruled out if an inguinal mass transilluminates?
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no. baby bowel is very thin and will often transilluminate
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from what abdominal muscle layer is the cremaster muscle derived? from what abdominal layer is the inguinal ligament (poupart's ligament) derived?
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cremaster: internal oblique. inguinal ligament: external oblique
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what nerve travels with the spermatic cord? what is in the spermatic cord (5 structures)?
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ilioinguinal nerve travels w/the spermatic cord. spermatic cord: 1. cremasteric muscle fibers, 2. vas deferens, 3. testicular artery, 4. testicular pampiniform venous plexus, 5. w/ or w/o hernia sac.
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what is the name of the fossa b/w the testicle and epididymis? what attaches the testicle to the scrotum? what is the hernia sac in an indirect inguinal hernia made of?
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fossa of geraldi. the gubernaculum. basicaly peritoneum or a patent processus vaginalis.
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how can the opposite side be assessed for a hernia intraoperatively
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many surgeons operatively explore the opposite side when they repair the affected side. a laparoscope is placed into the abdomen via the hernia sac and the opposite side internal inguinal ring is eamined.
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name the remnant of the processus vaginalis around the testicle
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tunica vaginalis
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what is a littre's inguinal hernia?
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hernia w/a meckel's diverticulum in the hernia sac
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what may a yellow/orange tissue that is not fat be on the spermatic cord/testicle?
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adrenal rest
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what is the most common organ in an inguinal hernia sac in boys? in girls? what lies in the inguinal canal in girls instead of the vas?
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boys: small intestine. girls: ovary/fallopian tube. in girls, round ligament lies in inguinal canal
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where in the inguinal canal does the hernia sac lie in relation to other structures? within the spermatic cord, do the vessels or the vas lie medially?
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hernia sac: anteromedially. the vas is medial to the testicular vessels
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what is a cord lipoma?
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preperitoneal fat on the cord structures (pushed in by the hernia sac); not a real lipoma. should be removed surgically, if feasible.
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what is a small outpouching of testicular tissue off of the testicle? what is a blue dot sign?
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testicular appendage (AKA appendix testes); should be removed w/electrocautery. blue dot on the scrotal skin from a twwisted testicular appendage.
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how is a transected vas treated? how do you treat a transected ilioinguinal nerve? what happens if you cut the ilioinguinal nerve?
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transected vas --> repair w/primary anastomosis. transected ilioinguinal nerve --> should not be repaired, many surgeons ligate it to inhibit neuroma formation. cut ilioinguinal nerve --> loss of sensation to medial aspect of inner thigh and scrotum/labia, loss of cremasteric reflex
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what is an umbilical hernia? what are the risk factors?
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fascial defect at the umbilical ring. risk factors: black or African American infant, premature infant
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what are the indications for surgical repair of an umbilical hernia?
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>1.5cm defect. bowel incarceration. >4 yrs of age.
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what is GERD? what are the signs/sx?
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gastroesophageal reflux disease. signs/sx: spitting up, emesis, URTI, pneumonia, laryngospasm from aspiration of gastric contents into the tracheobronchial tree, failure to thrive
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what are the causes of GERD?
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LES malfunction/malposition, hiatal hernia, gastric outlet obstruction, partial bowel obstruction, common in cerebral palsy
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how is the dx of GERD made? what cytologic aspirate finding on bronchoscopy can dx aspiration of gastric contents?
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24 hr Ph probe, bronchoscopy, UGI (manometry, EGD, U/S). lipid-laden macrophages can dx aspiration on bronchoscopy (from phagocytosis of fat)
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what is the medical/conservative treatment for GERD? surgical tx?
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medical/conservative tx: H2 blockers, small meals/rice cereal, elevation of head. surgical tx: Nissen 360 fundoplication, w/ or w/o G-tube
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what are the indications for surgery w/GERD?
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SAFE: stricture, aspiration (pneumonia/asthma), failure to thrive, esophagitis
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what is congenital pyloric stenosis?
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hypertrophy of smooth muscle of pylorus, resulting in obstruction of outflow
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what are the associated risks w/pyloric stenosis?
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family history, 1stborn males affected most commonly, decreased incidence in African American population
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what is the incidence of pyloric stenosis? average age at onset?
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1/750 births, male:female = 4:1. usually from 2 wks after birth to ~ 2 months.
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what are the symptoms and signs of pyloric stenosis?
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increasing frequency of regurgitation, leading to eventual nonbilious projectile vomiting. abdominal mass or olive in epigastric region (85%), hypokalemic hypochloremic metabolic alkalosis, icterus (10%), visible gastric peristalsis, paradoxic aciduria, hematemesis (<10%).
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why is the vomiting nonbilious in pyloric stenosis?
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obstruction is proximal to the ampulla of vater
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what is the DDx for pyloric stenosis?
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pylorospasm, milk allergy, increased ICP, hiatal hernia, GERD, adrenal insufficiency, uremia, malrotation, duodenal atresia, annular pancreas, duodenal web
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how is the Dx of pyloric stenosis made?
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usually by history and physical exam alone. U/S demonstrates elongated (>15mm) pyloric channel and thickened muscle wall (>3.5mm). if U/S is nondiagnostic, then barium swallow (shows string sign or double railroad track sign)
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what is the initial treatment of pyloric stenosis? what is the definitive treatment?
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initial tx: hydration and correction of alkalosis w/D10 NS + 20 mEq KCl (note: infant's liver glycogen stores are very small, therefore use D10, Cl- and hydration will correct the alkalosis). definitive tx: surgical, via fredet-ramstedt pyloromyotomy (division of circular muscle fibers w/o entering the lumen/mucosa).
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what are the postop complciations of pyloric stenosis? what is the appropriate postop feeding?
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unrecognized incision through the duodenal mucosa, bleeding, wound infection, aspiration pneumonia. b/w 6-12 hrs postop feeding w/pedialyte, advanced to full-strength formula over 24 hrs
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which vein crosses the pylorus?
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vein of mayo
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what is duodenal atresia? what is the anatomic location?
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complete obstruction or stenosis of duodenum caused by an ischemic insult during devt or failure of recanalization. 85% are distal to ampulla of vater, 15% are proximal (these present w/nonbilious vomiting)
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what are the signs of duodenal atresia? what is the DDx?
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bilious vomiting (if distal to the ampulla), epigastric distention. DDx: malrotation w/ladd's bands, annular pancreas.
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how is the dx of duodenal atresia made?
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plain abdominal film revealing double bubble, w/1 air bubble in the stomach and the other in the duodenum
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what is the tx of duodenal atresia?
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duodenoduodenostomy or duodenojejunostomy
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what are the associated abnormalities w/duodenal atresia?
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b/w 50% and 70% have cardiac, renal, or other GI defects; 30% have trisomy 21.
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what is meconium ileus? what is the incidence?
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intestinal obstruction from solid meconium concretions. occurs in ~15% of infants w/CF. >95% of patients w/meconium ileus have CF.
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what are the signs/sx of meconium ileus? what is neuhauser's sign?
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bilious vomiting, abdominal distention, failure to pass meconiums, neuhauser's sign, peritoneal calcification. neuhauser's sign: aka soap bubble sign --> groud glass appearance in RLQ on AXR from viscous meconium mixing w/air
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how is the dx of meconium ileus made?
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family history of CF, plain abdominal films showing significant dilation of similar-sized bowel loops but few (if any) air fluid levels, BE may demonstrate microcolon and inspissated meconium pellets in terminal ileum
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what is the treatment of meconium ileus?
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70% nonoperative clearance of meconium using gastrografin enema +/- acetylcysteine --> hypertonic, therefore draws fluid into lumen, separating meconium pellets from bowel wall (60% success rate). surgical treatment: if enema is unsuccessful, then enterotomy w/intraoperative catheter irrigation using acetylcysteine (mucomyst)
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what should you remove during all operative cases of meconium ileus?
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appendix
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what is the long-term medical treatment of meconium ileus?
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pancreatic enzyme replacement
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what is CF?
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inherited d/o of epithelial Cl- transport defect affecting sweat glands, airways, and GI tract (pancreas, intestine); dxed by sweat test (elevated levels of NaCl >60 mEq/L) and genetic testing
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what is DIOS?
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distal intestinal obstruction syndrome --> intestinal obstruction in older patients w/CF from inspissated luminal contents
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what is meconium plug syndrome? what is it also known as?
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colonic obstruction from unknown factors that dehydrate meconium, forming a plut. AKA neonatal small left colon syndrome
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what are the signs/sx of meconium plug syndrome? what is the major DDx? is meconium plut highly assoc w/CF?
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abdominal distention and failure to pass meconium w/in 1st 24 hrs of life, plain films demonstrate many loops of distended bowel and air-fluid levels. major DDx is hirschsprung's disease. not assoc w/CF (<5% have CF)
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what is the nonoperative treatment of meconium plug syndrome?
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contrast enema is both diagnostic and therapeutic; it demonstrated microcolon to the point of dilated colon (usually in transverse colon) and reveals copious intraluminal material
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what are anorectal malformations? what is imperforate anus?
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malformations of the distal GI tract in the general categories of anal atresia, imperforate anus, and rectal atresia. imperforate anus is congenital absence of normal anus (complete absence or fistula)
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define high v. low imperforate anus. which is more common in women?
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high: rectum patent to level above puborectalis sling. low: rectum patent to below puborectalis sling. low is more common in girls.
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what are associated anomalies w/imperforate anus?
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VACTERL: vertebral abnormalities, anal abnormalities, cardiac, TE fistulas, esophageal atresia, radial/renal abnormalities, lumbar abnormalities
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what are the signs/sx of imperforate anus?
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no anus, fistula to anal skin or bladder, UTI, fistula to vagina or urethra, bowel obstruction, distended abdomen, hyperchloremic acidosis
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how is the dx of imperforate anus made?
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PE, the classic cross table invertogram plain x-ray to see level of rectal gas (not very accurate), perineal ultrasound
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what is the treatment of low imperforate anus w/anal fistula? high imperforate anus?
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low w/fistula: dilatation of anal fistula and subsequent anoplasty. high: diverting colostomy and mucous fistula, neoanus usually made at 1 yr of age
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what is hirschsprung's disease? what is it also known as?
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AKA aganglionic megacolon. neurogenic form of intestinal obstruction in which obstruction results from inadequate relaxation and peristalsis, absence of normal ganglion cells of the rectum and colon
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what are the associated risks w/hirschsprung's disease?
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family history, 5% chance of having 2nd child w/hirschsprung's
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what is the male:female ratio for hirschsprung's?
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4:01:00
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what is the anatomic location of hirschsprung's disease?
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aganglionosis begins at anorectal line and involves rectosigmoid in 80% of cases (10% have involvement to splenic flexure, 10% have involvement of entire colon)
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what is the classic history of hirschsprung's? what are the signs/sx?
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failure to pass meconium in 1st 24 hrs of life is classic hx. signs/sx: abdominal distention and bilious vomiting, >95% present w/failure to pass meconium in 1st 24 hrs, may also present later w/constipatoin, diarrhea, decreased growth.
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what is the DDx of hirschsprung's? what is needed for definitive diagnosis?
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meconium plug syndrome, meconium ileus, sepsis w/adynamic ileus, colonic neuronal dysplasia, hypothyroidism, maternal narcotic abuse, maternal hypermagnesemia (tocolysis). rectal biopsy needed for definitve dx, submucosal suction bx is adequate in 90% of cases; otherwise, full-thickness biopsy should be performed to evaluate auerbach's plexus
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what imaging studies should be ordered for hirschsprung's dx? what is the colonic transition zone?
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AXR: reveals dilated colon. unprepared barium enema: reveals constricted aganglionic segment w/dilated proximal segment, but this picture may not develop for 3-6 wks, BE will also demontstrate retention of barium for 24-48 hrs (normal evacuation = 10-18 hrs). colonic transition zone: transition (taper) from aganglionic small colon into the large dilated normal colon seen on BE
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what is the initial treatment of hirschsprung's?
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in neonates, a colostomy proximal to the transition zone prior to correction, to allow for pelvic growth and dilated bowel to return to normal size
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what is a leveling colostomy?
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colostomy performed for hirschsprung's dz at the level of normally innervated ganglion cells as ascertained on frozen section intraoperatively
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describe the following procedures: swenson, duhamel, soave
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swenson --> primary anastomosis b/w the anal canal and healthy bowel (rectum removed). duhamel: anterior, aganglionic region of the rectum is preserved and anastomosed to a posterior portion of healthy bowel; a functional rectal pouch is thereby created. soave: AKA endorectal pull-through, this procedure involves bringing proximal normal colon through the aganglionic rectum, which has been stripped of its mucosa but otherwise present
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what is the new trend in surgery for hirschsprung's disease?
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no colostomy; remove aganglionic colon (as confirmed on frozen section) and perform pull-through anastomosis at the same time (boley modification)
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what is the prognosis of hirschsprung's?
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overall survival rate >90%, >96% of patients continent, postop sx improve w/age
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what is malrotation and midgut volvulus? where is the cecum?
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failure of the normal bowel rotation w/resultant abnormal intestinal attachments and anatomic positions. w/malrotatoin, the cecum usually ends up in the RUQ.
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what are ladd's bands?
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fibrous bands that extenf rom the abnormally placed cecum in the RUQ, often crossing over the duodenum and causing obstruction
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what is the usual age at onset of malrotation/midgut volvulus? what is the usual presentation?
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33% present by 1 wk, 75% by 1 mo., 90% by 1 yr. usual presentation: sudden onset of bilious vomiting (BILIOUS VOMITING IN AN INFANT IS MALROTATION UNTIL PROVEN OTHERWISE). vomiting is bilious b/c twist is distal to ampulla of vater.
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how is the dx of malrotation/volvulus made?
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upper GI contrast study showing cutoff in duodenum, BE showing abnormal position of cecum in upper abdomen
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what are the possible complications of malrotation/volvulus?
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volvulus w/midgut infarction, leading to death or necessitating massive enterectomy. rapid diagnosis is essential!
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what is the tx for malrotation and midgut volvulus?
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IV antibiotics and fluid resuscitation w/LR, followed by emergent laparotomy w/ladd's procedure, 2nd look laparotomy if bowel is severely ischemic in 24 hrs to determine if remaining bowel is viable.
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what is the ladd's procedure? in what direction is the volvulus reduced? where is the cecum after reduction?
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ladd's: 1. COUNTERCLOCKWISE reduction of midgut volvulus 2. splitting of ladd's bands 3. division of peritoneal attachments to the cecum, ascending colon 4. appendectomy. cecum is in LLQ after reduction
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what is the cause of bilious vomiting in an infant until proven otherwise?
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malrotation w/midgut volvulus
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what is omphalocele? how is the dx made?
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defect of abdominal wall at umbilical ring; sac COVERS extruded viscera. diagnosed on prenatal u/s. may be seen on fetal u/s after 13 wks gestation w/elevated maternal AFP.
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what comprises the sac in omphalocele? what organ is often found protruding from an omphalocele but is almost never found w/a gastroschisis?
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sac: peritoneum and amnion. the liver can protrude w/omphalocele
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what are the possible complications of omphalocele? what are associated abnormalities?
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malrotation of the gut, anomalies. 50% of cases occur w/abnormalities of the GI tract, cardiovascular system, GU tract, musculoskeletal system, CNS, and chromosomes.
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what is the treatment of omphalocele?
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1. NG tube (decompression) 2. IV fluids 3. prophylactic antibiotics 4. surgical repair of defect
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what is the treatment of omphalocele: small (<2cm) v medium v large (>10cm) defect
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small: closure of abdominal wall. 2-10cm: removal of outer membrane and placement of silicone patch to form a silo, temporarily housing abdominal contents, silo is then slowly decreased in size over 4-7 days as abdomen accomodates the viscera, defect then closed. large: skin flaps or treatment w/betadine spray, mercurochrome, or silver sulfadiazine over defect, allows an eschar to form that epithelializes over time allowing opportunity for future repair months-yrs later.
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what is the pentalogy of cantrell?
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D COPS: diaphragmatic defect (hernia), cardiac abnormality, omphalocele, pericardium malformation/absence, sternal cleft
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what is gastroschisis? where is the defect?
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defect of abdominal wall; sac does not cover extruded viscera. defect is lateral to umblicus. umbilicus is most commonly to R of defect
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how is gastroschisis dx'ed prenatally? what is the usual size of the defect?
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possible at fetal ultrasound after 13 wks gestation, elevated maternal AFP. usually 2-4cm.
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what are the possible complications of gastroschisis?
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thick edematous peritoneum from exposure to amnionic fluid, malrotation of the gut. other complications include hypothermia, hypovolemia from 3rd spacing, sepsis, metabolic acidosis from hypovolemia and poor perfusion, NEC, prolonged ileus
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what is the treatment of gastroschisis? what is a silo?
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primary: NG tube deompcression, IV fluids (D10 LR), IV antibiotics. definitive: surgical reduction of viscera and abdominal closure, may require staged closure w/silo. a silastic silo is a temporary housing for external abdominal contents, silo is slowly tightened over time
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what is the prognosis of gastroschisis?
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>90% survival rate
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what are the associated anomalies w/gastroschisis?
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unlike omphalocele, relatively uncommon except for intestinal atresia, which occurs in 10-15% of cases
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what are the major differences b/w gastroschisis and omphalocele
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in gastroschisis: no membrane coverings, uncommon associated abnormalities, lateral to umbilicus (not on umbilicus)
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what is appendicitis? what is its claim to fame?
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obstruction of the appendiceal lumen (fecalith, lymphoid hyperplasia), producing a closed loop w/resultant inflammation that can lead to necrosis and perforation. most common surgical disease requiring emergency surgery in children
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what is the affected age of appendicitis? what is the usual presentation? how is the dx made?
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very rare before 3 yrs. presentation: onset of referred or periumbilical pain followed by anorexia, nausea, and vomiting (note: unlike gastroenteritis, pain precedes vomiting, then migrates to RLQ where it intensifies from local peritoneal irritation). if patient is hungry and can eat, seriously question dx of appendicitis. dx is made by hx and PE.
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what are the signs/sx of appendicitis?
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signs of peritoneal irritation may be present: guarding, muscle spasm, rebound tenderness, obturator and psoas signs, low-grade fever rising to high grade if perofration occurs
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what is the DDx of appendicitis?
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intussusception, volvulus, meckel's diverticulum, crohn's disease, ovarian torsion, cyst, tumor, perforated ulcer, pancreatitis, PID, ruptured ectopic pregnancy, mesenteric lymphadenitis
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what is the common bacterial cause of mesenteric lymphadenitis?
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yersinia enterocolitica
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what are the associated lab findings w/appendicitis? what is the role of urinalysis?
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increased WBC (>10,000 per mm3 in >90% of cases, w/a L shift in most). u/a used to evaluate for possible pyelonephritis or renal calculus, but mild hematuria and pyuria are common in appendicits b/c of ureteral inflammation
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what is the hamburger sign?
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ask patients w/suspected appendicitis if they would like a hamburger or favorite food. if then can eat, seriously question the dx.
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what radiographic studies may be performed in appendicitis?
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often none, CXR to r/o RML or RLL pneumonia, abd films usually nonspecific but calcified fecalith is present in 5% of cases, u/s to evaluate for ovarian/gynecologic pathology
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what is the treatment of appendicitis?
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nonperforated: prompt appendectomy and cefoxitin to avoid perforation. perforated: triple antibiotics, fluid resuscitation, prompt appendectomy; all pus is drained and cultures obtained, w/postop antibiotics continued for 5-7 days +/- drain
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how long should antibiotics be administered in appendicitis if nonperforated? if perforated?
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24 hrs if nonperf'ed. if perf'ed usually 5-7 days or until WBCs are normal and patient is afebrile
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if a normal appendix is found upon exploration of appendicitis, what must be examined/ruled out?
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meckel's diverticulum, crohn's disease, intussusception, gynecologic disease
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what is the approximate risk of perforation in appendicitis?
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~25% after 24 hrs from onset of sx, ~50% by 36 hrs, ~75% by 48 hrs.
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what is the usual age at presentation of intussusception?
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disease of infancy; 60% present from 4-12 mo.s of age, 80% by 2 yrs.
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what is intussusception? what is its claim to fame?
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obstruction caused by bowel telescoping into the lumen of adjacent distal bowel; may result when peristalsis carries a leadpoint downstream. most common cause of SBO in toddlers (<2yrs old).
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what is the most common site of intussusception? what is the most common cause? what are the causes in older patients?
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terminal ileum involving ileocecal valve and extending into ascending colon. hypertrophic peyer's patches, which act as a lead point; many patients have prior viral illness. in older patients, caused by meckel's diverticulum, polyps, and tumors, all of which act as a lead point.
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what are the signs/sx of intussusception?
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alternating lethargy and irritability (colic), bilious vomiting, currant jelly stools, RLQ mass on plain abdominal film, empty RLQ on palpation (dance's sign)
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what is the intussuscipiens? what is the intussusceptum?
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intussuscipiens: recipient segment of bowel. intussusceptum: leading point or bowel that enters the intussuscipiens.
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what is the treatment of intussusception?
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AIR or barium enema; 85% reduce w/hydrostatic pressure (i.e., barium = meter elevation air = max of 120mmHg); if unsuccessful, then laparotomy and reduction by milking of the ileum from the colon should be performed
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what is meckel's diverticulum? what is the major DDx?
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remnant of the omphalomesenteric duct/vitelline duct, which connects the yolk sac w/the primitive midgut in the embryo. major DDx is appendicitis.
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what is the usual location of meckel's diverticulum? is it a true diverticulum?
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b/w 45-90cm proximal to the ileocecal valve on the antimesenteric border of the bowel. yes it is a true diverticulum --> all layers of the intestine are found in the wall
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what is the incidence of meckel's diverticulum? what is the gender ratio? what is the usual age at onset of sx?
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2% of population at autopsy, but >90% are asymptomatic. 2-3x more common in males. most frequently presents in 1st 2 yrs of life, but can occur at any age
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what are the possible complications of meckel's diverticulum?
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intestinal hemorrhage (painless) - 50% (accounts for 50% of all lower GI bleeding in patients <2 yrs, bleeding results from ectopic gastric mucosa secreting acid --> ulcer --> bleeding). intestinal obstruction - 25% (most common complication in adults, includes volvulus and intussusception). inflammation (+/- perforation) - 20%.
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what % of meckel's diverticulum cases have heterotopic tissue? what is the most common ectopic tissue in a meckel's? what other pediatric disease entity can also present w/GI bleeding secondary to ectopic tissue?
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>50%; usually gastric mucosa (85%), but duodenal, pancreatic, and colonic mucosa have been described. enteric duplications can also present w/GI bleeding secondary to ectopic gastric mucosa.
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what is the most common cause of lower GI bleeding in children?
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meckel's diverticulum w/ectopic gastric mucosa
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what is the rule of 2s?
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meckel's diverticulum: 2% are SYMPTOMATIC, found ~ 2 feet from ileocecal valve, found in 2% of population, most sx occur before age 2, 1 of 2 will have ectopic tissue, most diverticula are ~2 inches long, male:female ratio = 2:1
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what is a meckel's scan?
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scan for ectopic gastric mucosa in meckel's diverticulum; uses technetium Tc99m pertechnetate IV, which is preferentially taken up by gastric mucosa
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what is NEC? what is its claim to fame?
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necrotizing enterocolitis - necrosis of intestinal mucosa, often w/bleeding, may progress to transmural intestinal necrosis, shock/sepsis, and death. most common cause of emergent laparotomy in the neonate.
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what are the predisposing conditions for NEC?
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PREMATURITY. stress: shock, hypoxia, RDS, apneic episodes, sepsis, exchange transfusions, PDA and cyanotic heart disease, hyperosmolar feedings, polycythenmia, indomethacin
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what is the pathophysiologic mechanism of NEC?
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probable splanchnic vasoconstriction w/decreased perfusion, mucosal injury, and probable bacterial invasion
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what are the signs/sx of NEC?
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abdominal distention, vomiting, heme+ or gross rectal bleeding, fever or hypothermia, jaundice, abdominal wall erythema (consistent w/perforation and abscess formation)
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NEC radiographic findings, lab findings
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fixed, dilated intestinal loops; pneumatosis intestinalis (air in the bowel wall); free air; portal vein air (sign of advanced disease). low hematocrit, glucose, platelets
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what is the treatment for NEC? what are the surgical indications?
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most are managed medically: 1. cessation of feedings 2. OG tube 3. IV fluids 4. IV antibiotics 5. ventilator support as needed. surgical indications: free air in abdomen revealing perf, positive peritoneal tap revealing transmural bowel necrosis
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what is the operation for NEC?
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1. resect 2. stoma
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what is an option for bowel perforation in <1000 gram NEC patients
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placement of percutaneous drain (w/o laporotomy!)
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is portal vein gas or pneumatosis intestinalis alone an indication for operation w/NEC? what are the indications for peritoneal tap?
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no. indications for tap: severe thrombocytopenia, distended abdomen, abdominal wall erythema, unexplained clinical downturn
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what are the possible complications of NEC? what is the prognosis?
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>90% overall survival rate. complications: bowel necrosis, gram-neg sepsis, DIC, wound infection, cholestasis, short bowel syndrome, strictures, SBO.
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what is physiologic jaundice? how is hyperbilirubinemia from physiologic jaundice treated?
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hyperbilirubinemia in 1st 2 wks of life from inadequate conjugation of bilirubin. tx: UV light
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what enzyme is responsible for conjugation of bilirubin? what is gilbert's syndrome? what is crigler-najjar syndrome?
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glucuronyl transferase. gilbert's: partial deficiency of glucuronyl transferase, leading to intermittent asymptomatic jaundice in 2nd-3rd decade of life. crigler-najjar: rare genetic absence of glucuronyl transferase activity, causing unconjugated hyperbilirubinemia, jaundice, and death from kernicterus (usually w/in the 1st year)
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what is biliary atresia? what is the incidence?
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obliteration of extrahepatic biliary tree. 1/16,000 births.
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what are the signs/sx of biliary atresia? what is the DDx?
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persistent jaundice (normal physiologic jaundice resolves in <2wks), hepatomegaly, splenomegaly, ascites and other signs of portal HTN, acholic stools, biliuria. ddx: neonatal hepatitis (TORCH), biliary hypoplasia.
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what are the lab findings in biliary atresia?
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mixed jaundice is always present (both direct and indirect bilirubin increased), w/an elevated serum alk phos level
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what is the classic rule of 5s of indirect bilirubinemia?
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bizarre: w/progressive hyperbilirubinemia, jaundice progresses by levels of 5 from head to toes --> 5 mg/dL = jaundice of the head, 10 mg/dL = jaundice of trunk, 15 mg/dL = jaundice of leg/feet
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how is the dx of biliary atresia made?
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1. U/S to r/o choledochal cyst and to examine extrahepatic bile ducts and gallbladder. 2. HIDA scan - shows no excretion into the GI tract (w/phenobarbital preparation) 3. operative cholangiogram and liver biopsy
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what is the treatment for biliary atresia?
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early laparotomy by 2 months of age w/a modified form of the kasai hepatoportoenterostomy
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how does a kasai work? what do you do if the kasai fails?
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anastomosis of the porta hepatis and the small bowel allows drainage of bile via many microscopic bile ducts in the fibrous structure of the porta hepatis. if fails: revise or liver transplantation.
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what are the possible postop complications w/biliary atresia?
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cholangitis (manifested as decreased bile secretion, fever, leukocytosis, recurrence of jaundice), progressive cirrhosis (manifested as portal HTN w/bleeding varices, ascites, hypoalbuminemia, hypothrombinemia, and fat-soluble vit KADE deficiencies)
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what are associated anomalies w/biliary atresia?
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b/w 25-30% have other anomalies, including annular pancreas, duodenal atresia, malrotation, polysplenic syndrome, situs inversus, preduodenal portal vein; 15% have congenital heart defects
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what is a choledochal cyst? what are the possible complications?
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cystic enlargement of bile ducts; most commonly arises in extrahepatic ducts, but can also arise in intrahepatic ducts. complicatoins: cholelithiasis, cirrhosis, carcinoma, portal HTN.
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what is the usual presentation of choledochal cyst?
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50% present w/intermittent jaundice, RUQ mass, and abdominal pain; may also present w/pancreatitis
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what are the anatomic variants of choledochal cysts: I-IV
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I: fusiform dilation of common bile duct. II: diverticulum of common bile duct. III: choledochocele involving intraduodenal portion of common bile duct. IV: cystic involvement of intrahepatic bile ducts (caroli's disease)
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how is the dx of choledochal cyst made? what is the tx?
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dx: U/S. tx: operative cholangiogram to clarify the pathologic process and delineate the pancreatic duct, bollowed by complete resection of the cyst and a roux-en-y hepatojejunostomy
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what condition are choledochal cyst patients at increased risk of developing?
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cholangiocarcinoma often arises in the cyst --> treat by complete prophylactic resection of the cyst
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what is cholelithiasis? what are the common causes in children?
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formation of gallstones. etiology differs somewhat from that of adults; most common cause is cholesterol stones, but there is an increased % of pigmented stones from hemolytic d/os.
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what is the DDx of cholelithiasis?
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hereditary spherocytosis, thalassemia, pyruvate kinase deficiency, sickle-cell dz, CF, long-term parenteral nutrition, idiopathic
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what are the associated risks w/cholelithiasis?
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use of oral contraceptives, teenage, + family hx
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what is the tx for cholelithiasis?
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cholecystectomy is recommended for all children w/gallstones
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what is an annular pancreas? what are the sx?
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congenital pancreatic abnormality w/complete encirclement of duodenum by the pancreas. sx: duodenal obstruction
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what is the treatment of annular pancreas?
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duodenoduodenostomy bypass of obstruction (do not resect the pancreas!)
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