YS Liu, KH Tam, KN Yuen, CS Ho

Abstract

We report a case of spontaneous rupture of stomach in a preterm Chinese baby. This rare condition is potentially lethal and requires early recognition and combined expert neonatal and surgical care to ensure a successful clinical outcome. The risk factors that can be identified in this patient were prematurity, hypoxia and sepsis.

Abstract We report a case of spontaneous rupture of stomach in a preterm Chinese baby. This rare condition is potentially lethal and requires early recognition and combined expert neonatal and surgical care to ensure a successful clinical outcome. The risk factors that can be identified in this patient were prematurity, hypoxia and sepsis.

Keywords Outcomes; Pathogenesis; Rupture of stomach

A Chinese 35-gestational weeks male baby developed grunting and respiratory distress at 8 hours of life. He was initially treated as having sepsis with Penicillin and Netromycin. Subsequently, all the cultures results were negative.

He was given oxygen supplement for one day. This was taken off on the next day because of clinical improvement.

Oral feeding was started on day-two. However, he developed abdominal distention and poor oral feeding on day-five of life. No vomiting was noticed all along. The clinical diagnosis was necrotizing enterocolitis and Metronidazole was introduced.

Despite antibiotic treatment, he developed shock and disseminated intravascular coagulation four hours after the onset of abdominal distension. Investigations also revealed metabolic acidosis and hyponatremia. The abdominal X-ray film (fig. 1 and fig. 2) showed free peritoneal gas and the tip of the orogastric tube was located in left lower quadrant of abdomen outside the stomach, but there was no radiological evidence of necrotizing enterocolitis.

Fig. 1 Abdominal X Ray film showing the tip of orogastic tube located at left lower quadrant.	Fig. 2 Abdominal X Ray showing pneumoneritoneum.

In view of the clinical evidence of peritonitis, urgent laparotomy repair was done in the same day. The operative findings were: pus in the lesser sac and a ragged edge perforation along the greater curvature from mid-fundus to antrum with the orogastric tube protruding out. Gastric repair was undertaken. Peritoneal swab was sent for culture and grew Escherichia Coli and Coagulase negative staphylococcus.

Post-operatively, his condition remained poor disseminated intravascular coagulation and shock persisted. Therefore, Dopamine, platelet concentrate and plasma were given. Respiratory-wise, he was put on artificial ventilation and failed to be weaned off ventilator. Abdominal examination showed increased distention and increased gastric aspirate. Hence, antibiotics were changed to Amikacin and Netromycin was stopped. An urgent upper gastrointestinal study with water soluble contrast showed leakage of contrast from the stomach.

He had another laparotomy done for the repair of the perforation in the upper part of the greater curvature. The peritoneal abscess was drained. Peritoneal swab grew acinetobacter and Escherichia Coli. Post-operatively, initial contrast studies showed radiological leakage from repair site which was sealed off with conservative management.

He was put on total perenteral nutrition and antibiotics. Then feeding was introduced progressively and was well tolerated.

The remaining problems are failure to thrive secondary to small-stomach syndrome, and cholestatic jaundice.

Discussion

Spontaneous rupture of stomach is extremely rare in neonates.¹ There are only few cases reported in the literatures. But it is important to look for it, as it carries a high mortality and morbidity^1,3 especially when the diagnosis and treatment is delayed.^1,4

The pathogenesis can be due to ischaemia, infection of stomach or increased pressure secondary to mechanical obstruction.⁵ Most of the time, the aetiology is multifactorial. Some pathologists consider it as a form of necrotizing enterocolitis. The usual site of rupture is the great curvature of the stomach.¹ It is proposed that better resuscitation of neonates and premature infants to prevent hypoxia can prevent the problem of gastric perforation.³

The poor prognostic indicators included: male sex, metabolic acidosis, hyponatremia and delayed operation.¹

For the clinical features, it usually presents as poor oral feeding and abdominal distention. Vomiting is not a usual complaint. Therefore it can mimic sepsis and mislead our management. Most of the time it will deteriorate with conservative treatment and surgery is still the mainstay of management. But there is a case report of an infant treated successfully with conservative management.²

The early complications are breakdown of anastomosis, peritonitis, respiratory atelectasis and pneumonia.

The late complication is usually the "failure to thrive" secondary to residual small stomach volume. Also the patients may suffer from cholestasis as a result of prolonged perenteral nutrition.

References

1. Chung MT, Kuo CY, Wang JW, Hsieh WS, Huang CB, Lin JN. Gastric perforation in the neonate: Clinical analysis of 12 cases. Acta Paediatr Sin 1994(Sep-Oct);35(5):460-5.

2. Umeda T, Sugito T, Hashimoto R, Nakashima C, Ieda K, Mizuno 5, Suzuki C. A case report of an infant with perforated gastric ulcer treated with conservative therapy. Acta Neonatol JPN 1995(31/3):480-3.

3. Bruce J, Bianchi A, Doig CM, Gough DCS, Dickson AP. Gastric perforation in the neonate. Pediatr Sura mt 1993(811):17-9.

4. Prabhakar G, Agarwal LD, Shulcla A, et al. Spontaneous gastrointestinal perforation in the neonate. Indian Pediatr 1991(Nov);28(11):1277-80.

5. Tam PKH. Stomach and Gastric Outlet Surgery of the Newborn. 1 st edition Edi: Frecman NV, Burge DM, Griffiths DM, Malone PSJ, Churshill Livingstone, Edinburgh 1994;85-106.