0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Special Feature |

Radiological Case of the Month FREE

[+] Author Affiliations

Section Editor: Beverly P. Wood, MD

More Author Information
Arch Pediatr Adolesc Med. 1998;152(6):600. doi:.
Text Size: A A A
Published online

DENOUEMENT AND DISCUSSION: NEONATAL GASTRIC PERFORATION

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 disease35 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.

Holgersen  LO The etiology of spontaneous gastric perforation of the newborn: a reevaluation. J Pediatr Surg. 1981;16608- 613
Link to Article
Rosser  SBClark  CHElechi  EN Spontaneous neonatal gastric perforation. J Pediatr Surg. 1982;17390- 394
Link to Article
Ng  PCBrownlee  KGDear  PRF Gastroduodenal perforation in preterm babies treated with dexamethasone for bronchopulmonary dysplasia. Arch Dis Child. 1991;661164- 1166
Link to Article
O'Neil  EAChwals  WJO'Shea  MDTurner  CS Dexamethasone treatment during ventilator dependency: possible life-threatening gastrointestinal complications. Arch Dis Child. 1992;67 ((special issue)) 10- 11
Link to Article
St Vil  DLeBouthillier  GLuks  FLBensoussan  ALBlanchard  HYoussef  S Neonatal gastrointestinal perforations. J Pediatr Surg. 1992;271340- 1342
Link to Article
Grosfeld  JLChaet  MMolinari  F  et al.  Increased risk of necrotizing enterocolitis in premature infants with patent ductus arteriosus treated with indomethacin. Ann Surg. 1996;224350- 357
Link to Article
Gray  PHPemberton  PJ Gastric perforation associated with indomethacin therapy in a preterm infant. Aust Pediatr J. 1980;1665- 66
Mintz  ACApplebaum  H Focal gastrointestinal perforations not associated with necrotizing enterocolitis in very low-birth weight neonates. J Pediatr Surg. 1993;28857- 860
Link to Article
Lloyd  JR The etiology of gastrointestinal perforation in the newborn. J Pediatr Surg. 1969;477- 84
Link to Article
Herbur  PA Congenital defect in the musculature of the stomach with rupture in a newborn infant. Arch Pathol. 1943;3691- 94
Tan  CELKiely  EMAgrawal  MBrerton  RJSpitz  L Neonatal gastrointestinal perforation. J Pediatr Surg. 1989;24888- 892
Link to Article
Chen  JWWong  BWK Intestinal complications of nasojejunal feeding in low-birth weight infants. J Pediatr. 1974;85109
Link to Article
Lewis  JH Gastrointestinal injury due to medicinal agents. Am J Gastroenterol. 1986;81819- 834
Kelly  EJChatfield  SLBrownlee  KGNg  PCNewell  SJPrimrose  JN The effect of intravenous ranitidine on the intragastric pH of preterm infants receiving dexamethasone. Arch Dis Child. 1993;69 ((special issue)) 37- 39
Link to Article

Tables

References

Holgersen  LO The etiology of spontaneous gastric perforation of the newborn: a reevaluation. J Pediatr Surg. 1981;16608- 613
Link to Article
Rosser  SBClark  CHElechi  EN Spontaneous neonatal gastric perforation. J Pediatr Surg. 1982;17390- 394
Link to Article
Ng  PCBrownlee  KGDear  PRF Gastroduodenal perforation in preterm babies treated with dexamethasone for bronchopulmonary dysplasia. Arch Dis Child. 1991;661164- 1166
Link to Article
O'Neil  EAChwals  WJO'Shea  MDTurner  CS Dexamethasone treatment during ventilator dependency: possible life-threatening gastrointestinal complications. Arch Dis Child. 1992;67 ((special issue)) 10- 11
Link to Article
St Vil  DLeBouthillier  GLuks  FLBensoussan  ALBlanchard  HYoussef  S Neonatal gastrointestinal perforations. J Pediatr Surg. 1992;271340- 1342
Link to Article
Grosfeld  JLChaet  MMolinari  F  et al.  Increased risk of necrotizing enterocolitis in premature infants with patent ductus arteriosus treated with indomethacin. Ann Surg. 1996;224350- 357
Link to Article
Gray  PHPemberton  PJ Gastric perforation associated with indomethacin therapy in a preterm infant. Aust Pediatr J. 1980;1665- 66
Mintz  ACApplebaum  H Focal gastrointestinal perforations not associated with necrotizing enterocolitis in very low-birth weight neonates. J Pediatr Surg. 1993;28857- 860
Link to Article
Lloyd  JR The etiology of gastrointestinal perforation in the newborn. J Pediatr Surg. 1969;477- 84
Link to Article
Herbur  PA Congenital defect in the musculature of the stomach with rupture in a newborn infant. Arch Pathol. 1943;3691- 94
Tan  CELKiely  EMAgrawal  MBrerton  RJSpitz  L Neonatal gastrointestinal perforation. J Pediatr Surg. 1989;24888- 892
Link to Article
Chen  JWWong  BWK Intestinal complications of nasojejunal feeding in low-birth weight infants. J Pediatr. 1974;85109
Link to Article
Lewis  JH Gastrointestinal injury due to medicinal agents. Am J Gastroenterol. 1986;81819- 834
Kelly  EJChatfield  SLBrownlee  KGNg  PCNewell  SJPrimrose  JN The effect of intravenous ranitidine on the intragastric pH of preterm infants receiving dexamethasone. Arch Dis Child. 1993;69 ((special issue)) 37- 39
Link to Article

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections