Etiologies (Gastroschisis/NEC/Atresia/Volvulus)

Gastroschisis and intestinal atresia frequently coexist, with atresia incidence between 5–10% [e821-c16, e959-c18]. Two distinct patterns emerge: early-onset atresia with dilated but non-thickened bowel, and late atresia from progressive constriction causing ischemia and necrosis—termed "vanishing gastroschisis" when the defect constricts severely [e821-c17, e821-c18, e959-c19, e959-c20]. Management remains controversial; options include immediate repair at closure, stoma creation, or delayed exploration at 4–6 weeks [e821-c20, e9616-c17]. No high-quality evidence guides choice [e821-c20, e959-c22]. Necrotizing enterocolitis (NEC) shares overlapping pathophysiology with these ischemic insults. Volvulus—whether midgut or gastric—demands urgent intervention . In malrotation with heterotaxy, right atrial isomerism confers higher volvulus risk than left [e879-c2, e879-c3]. Hirschsprung disease rarely presents as a true emergency if irrigations are performed correctly: large-bore tube (≥20F), small aliquots, active mixing [e311-c1, e311-c2]. Stasis precipitates bacterial translocation and sepsis . For total colonic aganglionosis, timing of pull-through hinges on ileostomy output consistency—not age or weight—because liquid effluent predicts poor anastomotic healing [e645-c16, e645-c17, e1052-c17, e1052-c18]. Sodium loss from high-output ileostomy arrests growth even when serum sodium remains normal; measure effluent and urinary sodium [e645-c24, e645-c25, e645-c27, e1052-c23, e1052-c24, e1052-c26].