Gastric perforation

Several specific underlying causes of neonatal gastric perforation have been reported including intestinal atresias, perinatal stress, trauma, and exposure to cortico-steroids and nonsteroidal anti-inflammatory agents (Box 42.1). A variety of theories on the etiology of spontaneous perforations have been suggested but no single theory is universally accepted. The theories include congenital absence of gastric muscle, forces exerted during vaginal delivery, and pneumatic distention. Studies in dogs and human neonatal cadavers suggest that rupture is caused by overdistention and is in keeping with the law of Laplace. With gastric distention the greatest wall tension is exerted on the fundus, the site of most spontaneous perforations. Gastric distention can also produce ischemic changes, a finding present in 41% of cases in one series. A recent theory suggests that idiopathic gastric perforations result from a deficiency of C-KIT+, a receptor tyrosine kinase crucial for normal development of mast cells 21.