Neonatal GI Flashcards

1
Q

Gastrointestinal assessment

A

Look, listen feel.

  • maternal hx
  • look for distention and scaphoid appearance
  • bowel sounds present around 15-30m of life
  • liver margin should be right lower rib
  • umbilicious should be beige at birth
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2
Q

AXR characteristics

A

Should appear homogenous as gas across all four sections, with “mosaic” appearance

  • concerning if sections of bowel do not have any air, though the also shouldn’t be distended
  • upper obstructions present with minimal bowel gas
  • lower obstructions often present with copious bowel gas
  • air-fluid levels
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3
Q

Concerning features of neonatal vomit

A
  • change in vomiting pattern
  • blood or bilious vomit
  • other concerning clinical features in addition to the vomiting
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4
Q

What is bilious vomit

A
  • green vomit, produced by obstruction just distal to the bile duct
  • bile give the green colour, which would be mixed to a darker brown colour if the obstruction were further down the gut
  • green means go to OR ASAP
  • Volulus is the malrotation of the intestine. Bilious vomiting is a sign of volvulus and should be treated as volvulus until proven otherwise
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5
Q

Common causes of neonatal GI bleeding

A

anal fissures
cows milk protein allergy
swallowed maternal blood (cracked nipples)

NEC is the most common cause of bloody stool in preterm infants

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6
Q

Double bubble is a classic sign of

A

Duodenal atresia

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7
Q

Duodenal atresia mgmt

A

NPO, IV nutrition, NG to suction

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8
Q

Small bowel obstruction can present with

A

bilious emesis, within the first week of life. Usually generally well with feeding difficulties, so often irritable

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9
Q

small bowel obstruction mgmt

A

NPO
IV nutrution
NG suction
Surgery for resection

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10
Q

Meconium Ileus is

A

meconium is grossly thick and sticky, producing a small bowel obstruction that perforates before birth. the meconium in the peritoneum becomes calcified and presents as a density on AXR

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11
Q

Hirschsprungs disease is

A

Distal bowel ileus. the lower section of the bowel that is lacking ganglion cells will never function accordingly, meaning it must be removed to allow for peristalsis through the entirely of the bowel

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12
Q

Clinical presentation of Hirshsrpungs

A

may stool with rectal stimulation
delayed passage of meconium >24 hours. can present from birth to age 3.
associated with other chorosmal abnormalities

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13
Q

Hirshsprungs diese dx

A

AXR showing lack of distal bowel air comparative to the proximal bowel, secondary to reducing peristalsis causing a degree of bowel obstruction

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14
Q

Gastroschesis is

A

A defect in the anterior abdominal wall which allows peritoneal contents to protrude. Thought to be due to vascular disruption of blood supply to abdominal wall. Associated with maternal vasoactive drugs use and young maternal age

-presents to the right of umbilicus

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15
Q

Gastroschisis complications

A

Infection
fluid and sodium loss
heat loss
feeding issues after repair

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16
Q

Gastroschesis mgmt

A
  • sterile wrap (no dry gauze)
  • NPO NG to suction
  • IVF with increased TFI for insensible losses
  • Keep warm (plastic bag)
  • Abx
  • Place Baby on left side
  • intubation rather than CPAP to prevent bowel distention
  • silo placement with serial reduction, followed by surgical closure.
17
Q

When should neonates pass mex

A

within first 24 hours

18
Q

What is bilirubin

A

Bilirubin is the breakdown production of heme metabolism processed in the liver

19
Q

Physiologic heme is normal in term babies for what time frame

A

Day 3 - 7

20
Q

At extremely high levels, bilirubin can deposit in the basal ganglia and cause

A

Kernicterus

21
Q

treatments for hyperbilirubinemia

A
  1. phototherapy
  2. increase TFI by 20% due to insensible losses
  3. Exchange transfusion
  4. IVIG
22
Q

Hyperbilirubinemia definition

A

Unconjugated bili is a waste product of hemoglobin breakdown that is take up by the liver, where its converted into conjugated bilirubin

-conjugated bili is water-soluble and exerted into the bile to be cleared from the body

23
Q

Describe eBilirubin production

A

bilirubin is a product of heme catabolism.

approx 80-90% of bilirubin is produced during the breakdown of Hb

24
Q

why do we see it in neonates

A

neonates have more red cells which have a. shorter half life span than adults

25
Q

Whats BIND

A

bilirubin induced neurological dysfunction

  • occurs when bili crosses the BBB and binds to brain tissue resulting in brain injury if not treated rapidly
26
Q

Whats being neonatal hyperbili

A

Is a transient and normal increase in bili level occurring in almost all newborns, - physiologic jaundice

27
Q

Most common life-threatening GI disorder in the preterm neonate

A

necrotizing Entercolitis

28
Q

Risk factors for NEC

A

Prematurity, LBW

  • formula feeding
  • conditions that reduced BF to the gut (cardiac conditions, birth aphaxia, medications, growrth restrictions)
29
Q

Pathogensis of NEC

A

Involves bowel wall injury and inflammation leading to:

  • bacterial translocation into intestinal wall
  • gas accumulation in submucosal layer
  • necrosis
  • perforation
  • sepsis
  • death
30
Q

NEC mgmt

A

-NPO - bowel rest 7-14days
-IVF
-Abx
-surgical consultation
-In transport
(intubation, fluid, inotropic, blood support)