Figure 1. Free intraperitoneal air is present below the diaphragm. Evidence of respiratory distress syndrome and early bronchopulmonary dysplasia is seen in the lungs.
Figure 2. Pneumoperitoneum without bowel wall pneumatosis or portal vein gas is observed.
Figure 3. Extravasation of oral contrast material into the peritoneal cavity is present. The Penrose drain in the right lower quadrant is outlined.
Surgical placement of a percutaneous abdominal Penrose drain was performed. Intestinal contents were not recovered, nor were there signs of peritonitis or bleeding. A radiograph after introduction of diluted water-soluble contrast material through a feeding tube is shown (Figure 3). Peritoneal cultures later grew Staphylococcus coagulase-negative species. The gastrointestinal (GI) leak spontaneously resolved.
Multiple causes of isolated neonatal gastric perforation include (1) spontaneous and mechanical disruptions1,2; (2) traumatic, secondary to feeding-tube placement or vigorous respiratory resuscitation2; (3) drug associated, eg, with dexamethasone for neonatal chronic lung disease3- 5 or after indomethacine for treatment of PDA6,7; (4) focal GI perforation or necrotizing enterocolitis (NEC)8; (5) isolated gastric ischemia secondary to hypoxia9; and (6) congenital absence of bowel wall muscle.10
Spontaneous gastric perforations usually occur within week 1 of life and are typically in full-term or large premature infants. Overdistention of the stomach with consequent rupture has been demonstrated in infants with gastric outlet obstruction. Other conditions associated with mechanical obstruction from functional gastric obstruction include pyloric atresia, duodenal obstruction with atresia or volvulus, tracheoesophageal fistula, left diaphragmatic eventration, and negative pressure ventilation.1 Reports of perforation associated with esophageal intubation, mechanical ventilation, or direct perforation with feeding tubes are reported with premature and very ill infants.11,12
Corticosteroids3,4 and nonsteroidal anti-inflammatory drugs6,13 have a known ulcerogenic potential. Nonsteroidal anti-inflammatory drugs may induce erosive gastritis, linear ulcerations, and gross or occult hemorrhage due to inhibition of prostaglandin synthase and local impairment of ion transport. Corticosteroids are ulcerogenic by decreasing mucosal resistance to peptic digestion. Inhibition of surrounding inflammation may mask the symptoms of ulceration leading to a "silent" perforation.
This infant had never been fed and was receiving an H2-receptor antagonist at the time of the perforation. Use of these agents has been proposed to prevent the complication of steroid-associated ulcers from increased acid secretion.4,14
Focal GI perforations unassociated with NEC occurring in very low-birth weight neonates have been increasingly reported and may involve the stomach. Expected signs or symptoms of NEC or evidence of gastroesophageal bleeding are usually absent. Isolated gastric ischemia leading to perforation is not a likely explanation because of the stomach's ample blood supply. Absence of gastric muscle, advanced as a cause of gastric perforation resulting from microscopic gaps in the muscularis and surrounding normal mucosa and submucosa, may be a normal variant.
The exact origin of this gastric perforation remains unknown; multiple contributory factors were functional gastric obstruction, use of dexamethasone and indomethacin, a feeding tube, extremely low birth weight, and needed ventilatory support.
Although temporary gastric sealing was documented, 2 subsequent perforations developed. The latest perforation, 26th day of life, was associated with a large PDA, respiratory and metabolic acidosis, and hemodynamic instability after which support was ended. Autopsy permission was denied.
Accepted for publication December 24, 1996.
Reprints: Daniel B. Sobel, MD, Division of Neonatology, Department of Pediatrics, Maine Medical Center, 22 Bramhall St, Portland, ME 04102.
Radiological Case of the Month. Arch Pediatr Adolesc Med. 1998;152(6):600. doi:
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