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NCC content Flashcards

1
Q

When does the primordial gut form?

A

during the 4th week of gestation

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2
Q

What 3 parts make up the primordial gut?

A
  • foregut
  • midgut
  • hindgut
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3
Q

What does the foregut become?

A
  • *the cranial part**
  • oral cavity, pharynx, tongue, tonsils, salivary glands
  • upper and lower respiratory system
  • esophagus
  • stomach
  • duodenum
  • liver and biliary apparatus, gallbladder, pancreas, spleen
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4
Q

What circulation supplies the foregut?

A

-celiac artery

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5
Q

What does the midgut become?

A
  • small intestine
  • ascending colon and large portion of transverse colon
  • cecum
  • appendix
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6
Q

What circulation supplies the midgut?

A

superior mesenteric artery

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7
Q

Describe the physiologic umbilical herniation of the midgut.

A
  • During the 6th week: rotation 90 degrees counterclockwise, goes around axis of superior mesenteric artery
  • Returns to abdomen by week 10: small intestine goes back in first and occupies central region; large intestine rotates 180 degrees counterclockwise and occupies the rest of the abdomen
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8
Q

What does the hindgut become?

A
  • distal third of the transverse colon
  • descending colon
  • sigmoid colon
  • rectum and upper part of anal canal
  • epithelium of the urinary bladder
  • urethra
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9
Q

What circulation supplies the hindgut?

A

inferior mesenteric artery

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10
Q

How is age of presentation of NEC related to gestational age at birth?

A

inversely

FT will present more quickly, PT 3 weeks or so

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11
Q

Pathogenesis of NEC for PRETERM

A

precise pathogenesis remains unknown
MULTIFACTORIAL
-intestinal immaturity (digestion, absorption, motility)
-abnormal microbial colonization
-immature intestinal epithelial barrier (preterm babies have wider junctions that allow bacteria to penetrate gut)
-feedings (aggressive feedings, formula feedings)
-inflammatory process

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12
Q

Pathogenesis for NEC for TERM

A

precise pathogenesis remains unknown
-hypoxia-ischemia (acute primary ischemic injury to bowel)
aka kids with cyanotic heart disease, low apgars, chorio, exchange transfusion for hyperbili

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13
Q

GI symptoms of NEC

A
  • abdominal distention in 70% (compromises GI blood flow)
  • feeding intolerance
  • emesis (bilious or not)
  • bloody stools
  • abdominal wall erythema or bluish discoloration
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14
Q

Systemic symptoms of NEC mimicking sepsis

A
  • apnea/bradycardia
  • poor perfusion
  • lethargy
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15
Q

What is diagnostic for NEC?

A

pneumatosis or portal venous gas

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16
Q

What lab abnormality if characteristic for NEC?

A

hyponatremia

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17
Q

What is pneumatosis?

A

intramural air

-accumulation of hydrogen gas in the bowel wall from fermentation of carbohydrates by gas-producing organisms

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18
Q

What X-rays should I get for NEC?

A
  • left lateral decub (really helps with determining pneumoperitoneum) aka liver side up
  • A/P
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19
Q

Radiographic findings for NEC

A
  • ileus
  • pneumatosis
  • dilated loops
  • thickened bowel wall
  • pneumoperitoneum
  • portal venous gas
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20
Q

What is the football sign?

A

appearance of the falciform ligament that should not usually be visible?

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21
Q

What is the staging system for NEC called?

A

Bell Staging Criteria

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22
Q

What is Stage I of Bell Criteria?

A

-Suspected NEC (temp instability, a/b, gastric residuals, mild abd. distention, bloody stool, normal or mild ileus on X-ray)

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23
Q

What is Stage II of Bell Criteria?

A

-Definite NEC (radiographic evidence that NEC is present)

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24
Q

Compare Stage IIA and Stage IIB of Bell Criteria.

A
  • Stage IIA: mild NEC (prominent abd. distention, absent BS, grossly blood stools, ileus or dilated bowel loops with focal pneumatosis on X-ray)
  • Stage IIB: moderate NEC (mild acidosis, thrombocytopenia, abd. wall edema, tenderness, extensive pneumatosis, possible portal venous gas, early ascites on X-ray)
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25
Q

What radiographic sign is required for Stage IIIB of Bell Criteria?

A

pneumoperitoneum (free air)

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26
Q

Compare Stage IIIA and Stage IIIB of Bell Criteria.

A

-Stage IIIA: advanced NEC (resp & metabolic acidosis, mechanical ventilation, hypotension, oliguria, DIC, worsening wall edema & erythema with induration, prominent ascites with persistent bowel loop but no free air on X-ray)
Stage IIIB: advanced NEC (vital sign & lab evidence of deterioration, shock, evidence of perf. and pneumoperitoneum on X-ray)

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27
Q

Medical management for NEC

A
  • NPO
  • decompression (to help maximize blood flow to intestines by decreasing dilatation)
  • blood culture and abx (anaerobic coverage with free air)
  • serial abdominal X-rays, especially in first 24 hrs
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28
Q

Surgical management for NEC

A
  • peritoneal drainage (many eventually require surgery anyway and there is no way to assess necrosis; more likely to form strictures)
  • exploratory lap (may be better with intestinal necrosis)
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29
Q

Absolute indication for surgery with NEC

A
  • pneumoperitoneum
  • clinical deterioration despite medical treatment
  • abdominal mass with persistent intestinal obstruction or sepsis
  • development of intestinal stricture
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30
Q

Spontaneous ileal perforation vs. NEC

A

SIP: focal perforation not associated with infection and inflammation; presents early in life, most commonly occurs in terminal ileum
NEC: perforation presents at 3 week mark or so and associated with all the bad things

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31
Q

Risk factors for SIP

A
  • postnatal steroids
  • indocin
  • vasopressor use
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32
Q

Pathogenesis/Presentation of SIP

A
  • intestinal mucosa is robust and viable, no inflammation
  • submucosa thins, smooth muscle starts to have necrosis which leads to fragility, and a hole develops
  • these babies are fine one day and suddenly sick the next; lack of infectious symptoms
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33
Q

Diagnosis of SIP

A

pneumoperitoneum on xray

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34
Q

Pathogenesis of umbilical hernia

A
  • protrusion of tissue or visor through the umbilical fascial ring
  • ring fails to close completely
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35
Q

Incidence of umbilical hernia

A
  • more commonly associated with preterm infants and LBW infants
  • associated with trisomy 21, congenital hypothyroidism, Beckwith-Wiedemann syndrome
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36
Q

Management of umbilical hernia

A
  • diagnosed by physical exam
  • majority spontaneously close if defect is small by 3 years of age
  • surgery recommended if hernia persists after 4 to 5 years of age
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37
Q

Gastroschisis appears on which side of the cord?

A

right side

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38
Q

Etiology of gastroschisis

A

unknown for the most part, current thinking is there was a vascular accident during embryogenesis

39
Q

What prenatal lab work suggests gastroschisis?

A

elevated maternal serum alpha-fetoprotein

40
Q

Gastroschisis preoperative management

A
  • avoid bag/mask ventilation
  • bowel bag
  • right side-lying position
  • NPO, decompression
  • increase total fluids
  • antibiotics
41
Q

Gastroschisis surgical management

A
  • primary closure (preferred)

- staged closure with prosthetic silo

42
Q

Omphalocele etiology

A

unknown, but theories:

  • incomplete return of bowel into abdomen
  • incomplete closure of anterior abdominal wall
43
Q

Omphalocele association with other anoamlies

A
  • 50-70% will have associated anomalies

- Beckwith-Wiedemann should be considered

44
Q

What prenatal lab suggests omphalocele?

A

elevated maternal serum alpha-fetoprotein

45
Q

Omphalocele management vs. gastroschisis

A
  • increased IVF, but not as much if sac hasn’t ruptured
  • screening echo
  • chromosomes
46
Q

omphalocele surgical management

A
  • primary closure

- staged closure

47
Q

Omphalocele postoperative management

A

-watch LFTs if liver was out; could suggest occlusion of hepatic or portal veins

48
Q

Polyhydramnios is more common with…

A

proximal obstructions

49
Q

Abdominal distention is more common with…

A

distal obstructions and TEF (lower type of obstruction)

50
Q

Bilious emesis is more when…

A

obstruction is distal to the ampulla of Vater

51
Q

Early onset vs. late onset bilious emesis

A 
early = higher obstruction
late = lower obstruction
52
Q

when should a baby pass meconium by?

A

94% by 24 hrs of age

99.8% by 48 hrs of age

53
Q

Hypertrophic pyloric stenosis

A

hypertrophy of pylorus resulting in stricture of the outlet from the stomach to the small intestine

54
Q

Pyloric stenosis etiology

A

unknown, hereditary component

55
Q

pyloric stenosis incidence

A
  • first born more often affected
  • 4:1 male to female predominance
  • more common amount caucasian infants
56
Q

Pyloric stenosis clinical presentation

A
  • nonbilious vomiting, usually around 2-6 weeks of age that become projectile with time
  • signs/symptoms of dehydration, poor weight gain
57
Q

pyloric stenosis diagnostic evaluation

A
  • upper GI or abdominal ultrasound
  • “olive-shaped” mass in RUQ below liver
  • “string sign” (barium lining elongated pyloric channel)
  • “double track” sign (contrast caught between mucosal folds of hypertrophied area)
58
Q

pyloric stenosis postoperative care

A
  • warn parents that emesis can still occur after surgery until function has returned
  • NEVER place NG tube and risk perforating surgical site
  • feedings start 6 to 8 hrs post-op
59
Q

Duodenal atresia incidence

A
  • most common type of small bowel atresia
  • females more commonly affected than males
  • high incidence of associated conditions; 30% infants associated with trisomy 21
60
Q

Pathogenesis of duodenal atresia

A
  • congenital obstruction of duodenum, usually distal to ampulla of Vater
  • etiology unknown; thought to be from failure of recanalization of the duodenum during 8th week of gestation
  • may be atresia, stenosis, web, Ladd’s bands wrapping around or annular pancreas wrapping around
61
Q

Duodenal atresia postoperative management

A
  • delayed gastric emptying across reanastomosis site is normal
  • the higher the lesion, the more likely there will be a delayed response in function
62
Q

Jejunal and ileal atresia

A
  • failure of the lumen of the bowel to form properly

- thought to be d/t mesenteric vascular insult with subsequent necrosis and reabsorption of the affected segments

63
Q

Jejunal/ileal atresia incidence

A

-usually presents as an isolated defect

64
Q

Jejunal and ileal atresia types

A
  • 5 different types
  • I and II have normal bowel length, III and IV have shorter length and thus more trouble feeding
  • Type IIIB: apple peel or christmas tree - usually a familial form
65
Q

jejunal and ileal atresia on xray

A
  • “triple bubble” in proximal jejunal atresia

- gas or fluid-filled dilated loops of bowel with scant amounts of gas distal to the obstruction

66
Q

Meconium ileus

A

mechanical obstruction of the distal lumen d/t meconium

67
Q

Meconium ileus etiology

A

unknown; theories:
-d/t to hypo secretion of pancreatic enzymes or abnormal viscous secretions from the mucous glands of the small intestine

68
Q

meconium ileus incidence

A

-majority of cases are associated with cystic fibrosis

69
Q

meconium ileus xray

A
  • may show peritoneal calcifications from earlier perfs
  • dilated proximally, microcolon distally, no air in rectum
  • “soap bubble” appearance
70
Q

Contrast enema for meconium ileus

A

can be diagnostic and therapeutic if it’s hyperosmolar

71
Q

Meconium ileus management

A
  • if prenatal/postnatal perforation is present or enemas are not effective in evacuating meconium, then surgery is indicated
  • repeat enemas increased the risk for intestinal perforations
72
Q

Meconium ileus postoperative management

A
  • need pancreatic enzymes when beginning feeds
  • Genetic testing: DNA (80-90% sensitive) or sweat chloride
  • pulmonary toilet: CPT, aerosols, humidity
  • can develop volvulus, perforation with peritonitis, infection
73
Q

Meconium Plug syndrome

A

mechanical obstruction of the distal colon/rectum due to thick, inspissated meconium

  • lack of good colonic motility
  • etiology is unknown; associated with mag therapy, IDM, prematurity, hypothyroidism, hypotonia and sepsis
74
Q

Meconium plug diagnostic evaluation

A
  • xray: dilated loops of bowel and few air fluid levels
  • water soluble contrast enema can be diagnostic and therapeutic
  • can be difficult to differentiate from Hirschsprung’s and meconium ileus
75
Q

Meconium plug management

A
  • enemas
  • digital rectal exam
  • surgery if nothing is successful in passing meconium
76
Q

Malrotation/volvulus

A

abnormal rotation and fixation of intestines during 7th to 12th week of gestation

77
Q

Malrotation/volvulus etiology

A

unknown; occurs when intestines do not rotate and/or the mesentery does not fixate during embryologic development

78
Q

Malrotation/volvulus incidence

A

-associated with abdominal wall defects, intestinal atresia, imperforate anus, cardiac anomalies, and trisomy 21

79
Q

Malrotation/volvulus incidence

A
  • most cases present during 1st month
  • bilious emesis, abd. distention, tenderness, bloody emesis or stools
  • signs of shock and sepsis if necrotic
80
Q

Malrotation/volvulus surgical management

A
  • laparotomy (Ladd’s procedure)

- appendectomy commonly done to r/o appendix as the cause of abdominal pain later in life

81
Q

Hirschsprung’s disease etiology

aka congenital megacolon or aganglionic megacolon

A

-caused by failure of migration of neural crest neuroblasts to the distal portion of the colon

82
Q

Hirschsprung’s incidence

A
  • occurs predominantly in white males
  • 1/3 will have positive family history
  • associated anomalies not common
  • increased risk of hearing loss, ocular neuropathies, and decreased peripheral nerve function
83
Q

Hirschsprung’s diagnostic evaluation

A
  • x-ray nonspecific
  • barium enema: transition zone
  • anal manometry
  • rectal biopsy: definitive diagnosis
84
Q

Hirschsprung’s surgical management

A
  • staged repair: colostomy with later pull-through procedure

- complete pull-through repair: laparoscopic surgery

85
Q

Hirschsprung’s prognosis

A
  • dysmotility of colon: stooling abnormalities-constipation or incontinence
  • rectal stenosis
  • stricture formation
86
Q

Anorectal malformations

A

wide spectrum of abnormalities characterized by stenotic or atretic anal canal

87
Q

anorectal malformation etiology

A

-failure during embryonic development of differentiation of the urogenital sinus and cloaca

88
Q

anorectal malformation incidence

A
  • more common in males

- associated with GU, vertebral, CV, and esophageal atresia with TEF (THINK VATER/VACTERL)

89
Q

Anorectal malformation: high vs. low lesions

A

any lesion above pubococcygeal line is high, below is low

90
Q

low anorectal malformation

A
  • rectum has descended below the sphincter muscle complex

- rarely a fistula

91
Q

high anorectal malformation

A
  • located above the sphincter muscle

- usually has a fistula

92
Q

anorectal malformation diagnostic evaluation

A
  • xray of sacrum (Wangensteen-Rice technique: inverted lateral radiograph)
  • MRI/echo
  • VCUG
  • perineal and spinal ultrasounds
93
Q

anorectal malformation preoperative management

A
  • serial urinalysis to check for fistula

- observe closely for enterocolitis or possible perforation

94
Q

urinary incontinence with anorectal malformation

A

-higher likelihood if the lesion is high

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