Outcomes for the infant with gastroschisis are usually affected by a number of complications, including cholestasis secondary to long term TPN, malrotation, midgut volvulus, hypoperistalsis, gastroesophogeal reflux (GER), and aspiration pneumonia.[3,7,14,22] The most common complications resulting in increased morbidity and mortality include intestinal atresia/stenosis, sepsis, and necrotizing enterocolitis (NEC).[45,46,47,48,49]
Intestinal atresia is seen in approximately 5% to 25% of newborns with gastroschisis.[45,46] The development of intestinal atresia/stenosis occurs secondary to torsion and volvulus of the exteriorized bowel, causing a disruption of mesenteric vessels and blood flow to the affected intestine. The size of the defect may also cause strangulation of the bowel, increasing the risk for an atretic/stenotic area to arise. Intestinal atresia is difficult to diagnose before the time of closure because of the inflamed and matted appearance of the bowel. In the postoperative period, intestinal atresia/stenosis should be considered in all infants who present with poor feeding tolerance, abnormal stooling patterns, and/or abdominal distention with vomiting. Affected infants may need to be returned to the operating room for further evaluation and possible repair. Bowel resection and anastomosis are frequently required and this places the infant at risk for short bowel syndrome. Intestinal atresia is considered a poor prognostic factor in infants with gastroschisis, with mortality ranging from 40% to 66%.[45,46,47]
Infection is another complication associated with gastroschisis defects. Initially, the newborn is at risk for infection because of the breach in skin integrity from the exteriorized bowel. The risk is then increased postoperatively in infants with a staged repair because of delayed closure of the defect. Other factors contributing to the risk of sepsis include central venous access, prolonged TPN, and the immaturity or incompetence of the neonatal immune system. According to a recent retrospective study looking at delayed closure of abdominal wall defects, sepsis was responsible for 71% of all mortality.
Postoperative interventions to prevent and/or minimize the risk of infection include continuation of broad-spectrum antibiotic therapy for an additional 3 to 7 days and a high index of suspicion for infection on the part of health care providers. The infant must be assessed for signs and symptoms of infection at the site of the repair, the site of central vascular access, and systemically. Aseptic dressing changes and constant monitoring of the wound site are necessary measures to decrease the risk for opportunistic infections.
NEC is a common complication that occurs in approximately 20% of all infants with gastroschisis defects. The development of NEC is facilitated by the diminished mesenteric blood flow to the intestine. The presentation of NEC in postoperative infants with gastroschisis is milder than that seen in preterm infants with the disease and occurs independent of the type of repair. Despite this, NEC is considered an independent predictor for increased sepsis and mortality by some. The management of post-gastroschisis repair NEC is the same as nonsurgical related NEC. There is some data that expressed breast milk may decrease the risk for NEC in the infant who has undergone surgery for gastroschisis.
NAINR. 2003;3(2) © 2003 W.B. Saunders
Cite this: Management of the Infant With Gastroschisis: A Comprehensive Review of the Literature - Medscape - Jun 01, 2003.