Transcript GI Emergencies in the NICU - Calendar

GI Emergencies in the NICU
CHRISTY CUMMINGS, MD, CLC
N E O N A T O L OG Y
YALE NEW HAVEN HOSPITAL
Objectives
 Case-based learning
 Discussion of open abdominal wall defects and their
treatment
 Discussion of closed abdominal wall defects and
their treatment
 Q&A
Gastroschisis
 Full-thickness defect of abdominal wall exposing
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intestinal contents
Generally a small defect (3-6 cm) located right,
lateral to the umbilicus
1 : 40,000 births, Male> female
Infants are generally preterm or SGA
Malrotation affects all infants
Generally seen on U/S
Survival rate is higher than omphalocele, 95%
Gastroschisis - Treatment
 Gastric decompression
 Gut rest
 Antibiotics
 Silo suspension
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Sealed plastic device surgically attached to infant and suspended
above infant
Allows the bowel to return to normal size
Infants commonly have underdeveloped abdominal capacity, not
allowing for primary closure
Daily decompression allows for stretching of the abdominal tissue
and minimizes intestinal damage, respiratory decompensation
Primary closure generally for small defects or those term infants
with adequate abdominal tissue
Omphalocele
 Failure of the intestines to return from the umbilical
cord into the abd cavity resulting in a transparent
membrane that encapsulates intestinal tissue
 1 : 5,500 births, Male > female
 Frequently associated (50% - 77%) with other
syndromes such as trisomies, CHD, CDH
 Defects range from 2-15 cm on average
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Smaller defects may be overlooked
Larger defects may include spleen and liver also
 Most defects are clearly visible on U/S prenatally
 Survival rates are high (75% - 95%)
 But not as high as gastroschisis (higher incidence anomalies)
Omphalocele - Treatment
 Gastric decompression
 Antibiotics
 Gut rest and delayed feedings are important to allow
inflamed intestinal lumen to return to normal size
 Antibiotics
 Surgical repair is generally reserved for the most
severe cases and involves using gortex flaps to cover
the transparent sac.
 An unfortunate result of non-surgical closure is
malrotation
Duodenal Atresia
 Result of incomplete recanalization of the lumen
 1 : 6,000 - 10,000 births
 25% associated with Trisomy 21
 Other associated anomalies: TEF, malrotation, VACTERL and renal anomalies
 Polyhydramnios is the # 1 identifying risk factor
 70% of infants do not pass meconium
 Proximal atresias/obstruction generally results in vomiting within
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the first few hours of life
Distal atresias/obstruction results in emesis longer after delivery
Classic “double bubble” on xray; gasless pattern after the atresias
Survival rate 65%-84% with early intervention
Treatment: Gastric decompression, surgical removal of the atresia
area with a side to side anastomosis
Esophageal Atresia (EA)
 Failure of the trachea to differentiate from the esophagus
 Different types of disorder:
 85% have EA and a TE fistula
 8% have EA without any connection to the trachea
 1% have esophageal fistula and no connection to the stomach
 4% are an H type fistula
 1 : 4,500 births
 VATER and VACERL association is common
 20%-30% are preterm
 Clinical signs: excessive oral secretions, inability to pass
OG/NG, aspiration, chronic pneumonias
 survival rates 97% with intervention
 Mortality is associated with associative disorder
 Surgery depends on the type of disorder
Necrotizing Entercolitis (NEC)
 Necrosis of the mucosal/submucosal layer of intestinal
lining
 Any portion of the GI tract can be affected
 Etiology is still a debate…
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Selective bowel ischemia?
Delayed or lack of proper bacterial establishment? Infection?
The effects of feedings, medications, RBCs?
Osmolarity of certain formulas and the lack of feeding EBM play
large roles in increasing the risk of NEC
 Early EBM feeding decreases risk of NEC by 65% in
premies
 65%-92% of infants affected with NEC are preterm
infants
 Most commonly seen in infants 3-21 days post delivery
Necrotizing Entercolitis (NEC)
 Signs/symptoms:
 Abdominal distention, dusky abdomen, feeding intolerance,
increased emesis, bloody stools, VS instability
 Xray:
 Dilated loops, abnormal gas patter, thickened bowel wall
 Pneumatosis (tiny lucent soap bubbles)
 Treatment:
 Bowel rest
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Prevention of progressive injury
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NPO, Replogle to suction for 10-14 days
NPO, Fluid management, antibiotics
Serial KUBs to monitor status
Intestinal Perforation
 Spontaneous rupture of intestine/colon allowing
leakage of air into the abdominal cavity
(pneumoperitoneum)
 Most associated with NEC and ischemic bowel
 Most common risk factors:
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NEC, sepsis, mechanical ventilation, prematurity, long term
steroid usage, postoperative abdominal complications
 Survival is directly related to how quickly the staff is
able to identify clinical changes
Intestinal Perforation
 KUB: (A/P and left-lateral decubitus)
 Pneumoperitoneum, Football Sign, Rigler Sign, Ligament Sign
 Treatment involves:
 Surgery immediately
 Bowel rest—NPO for 10-14 days
 Gastric decompression
 Prevention of progressive injury
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NPO, Fluid management, antibiotics
Placement of abdominal drain +/-
Congenital Diaphragmatic Hernia (CDH)
 Herniation of intestinal contents into thoracic cavity
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Results in pulmonary hypoplasia leading to respiratory distress
 1 : 4,000 births
 Signs/symptoms:
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Cyanosis, respiratory distress, scaphoid abdomen
 Usually seen during routine prenatal U/S
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L:H ratio, presence of liver or other organs in chest
 Post delivery xray reveals intestinal loops in chest cavity
 Immediate intubation and gastric decompression is
essential to higher survival rates
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Intubation should be performed by most experienced team member
Congenital Diaphragmatic Hernia (CDH)