CHRISTY CUMMINGS, MD, CLC

NEONATOLOGYYALE NEW HAVEN HOSPITAL

GI Emergencies in the NICU

Objectives

Case-based learningDiscussion of open abdominal wall defects

and their treatmentDiscussion of closed abdominal wall defects

and their treatment Q&A

Gastroschisis

Full-thickness defect of abdominal wall exposing intestinal contents

Generally a small defect (3-6 cm) located right, lateral to the umbilicus

1 : 40,000 births, Male> femaleInfants are generally preterm or SGAMalrotation affects all infantsGenerally seen on U/S Survival rate is higher than omphalocele,

95%

                                           

            

Gastroschisis - Treatment

Gastric decompressionGut restAntibioticsSilo suspension

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 > femaleFrequently associated (50% - 77%) with other

syndromes such as trisomies, CHD, CDHDefects range from 2-15 cm on average

Smaller defects may be overlooked Larger defects may include spleen and liver also

Most defects are clearly visible on U/S prenatallySurvival rates are high (75% - 95%)

But not as high as gastroschisis (higher incidence anomalies)

                                                

Omphalocele - Treatment

Gastric decompressionAntibioticsGut rest and delayed feedings are important

to allow inflamed intestinal lumen to return to normal size

AntibioticsSurgical 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 lumen1 : 6,000 - 10,000 births25% associated with Trisomy 21

Other associated anomalies: TEF, malrotation, VACTERL and renal anomalies

Polyhydramnios is the # 1 identifying risk factor70% of infants do not pass meconiumProximal atresias/obstruction generally results in vomiting

within the first few hours of lifeDistal atresias/obstruction results in emesis longer after

deliveryClassic “double bubble” on xray; gasless pattern after the

atresiasSurvival rate 65%-84% with early interventionTreatment: 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 birthsVATER and VACERL association is common20%-30% are pretermClinical signs: excessive oral secretions, inability to

pass OG/NG, aspiration, chronic pneumoniassurvival rates 97% with interventionMortality is associated with associative disorderSurgery 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 affectedEtiology is still a debate…

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 NECEarly EBM feeding decreases risk of NEC by 65%

in premies65%-92% of infants affected with NEC are

preterm infantsMost 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

NPO, Replogle to suction for 10-14 days Prevention of progressive injury

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: 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

NPO, Fluid management, antibiotics Placement of abdominal drain +/-

Congenital Diaphragmatic Hernia (CDH)

Herniation of intestinal contents into thoracic cavity Results in pulmonary hypoplasia leading to respiratory distress

1 : 4,000 birthsSigns/symptoms:

Cyanosis, respiratory distress, scaphoid abdomen

Usually seen during routine prenatal U/S 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 Intubation should be performed by most experienced team

member

Congenital Diaphragmatic Hernia (CDH)