Letters to the Editor Indian Pediatrics 1998; 35:1032-1033 |
Duodenal Perforation in a Neonate |
On the third day of hospitalization, the baby had massive fresh bleeding per rectum for which he was transfused twice. Another two days later, he was noted to develop progressively increasing abdominal distension. The clinical impression of pneumoperitoneum was confirmed with a roentgenogram. A pediatric surgery consultation was sought. By this time, the child weighed only 1.7 kg; he was moribund with evidence of septicemia and multiple organ failure. On surgical exploration, the baby was found to have hemopneumoperitoneum resulting from a 5 mm diameter perforation of the anterosuperior aspect of first part of the duodenum. Rest of the bowel and stomach were normal. The perforation was closed in a single layer with 4 0' silk interrupted sutures. The wound was closed in layers after a thorough peritoneal lavage and placement of a peritoneal tube drain. The baby had a stormy post operative period which included episodes of hypoglycemia, hypothermia and bradycardia. The peritoneal fluid was negative for any organism. He was administered cardiotonic drugs (dopamine 5 µg/kg/min) and H2 antagonists (Ranitidine 1 mg/kg/day) along with 10% dextrose normal saline and intravenous antibiotics. He was started on nasogastric feeds after a week of surgery and was discharged thriving on thirteenth post-operative day. He has been doing well after six months with no fresh complaints. Neonatal perforations of the gastro- intestinal tract are rarely seen in the duo-denum. A recent 10 year study of gastro- intestinal perforations in 124 neonates from a leading tertiary pediatric center of USA did not encompass a single case of neonatal duodenal perforation; however the same study included 30 cases of spontaneous perforations of ileum (NNEC) and 5 cases of spontaneous perforations of stomach(1). The mortality in these patients even in the best centres of the world has been as high as 40%(2). Duodenal ulcer in neonates can be primary or secondary, the latter being more prevalent in this age group. In majority of the reported cases, significant serious underlying illness was reported prior to perforation; diarrheal dehydration being the most common antecedent process(3). Others included central nervous system abnormalities, malnutrition, failure to thrive, sepsis, pneumonia, prematurity and corti-costeroid medication before perforation(3). In contrast to the stress ulceration in adults, infants appear to have a higher frequency of single ulcers, perforation and duodenal (rather than gastric) location(2). A triphasic occurrence of duodenal perforation has been reported in children(4). A relatively high acid secretion in neonates has been noted during the first week to 10 days of life probably because of high maternal gastrin level causing increased parietal cell main and the high acid secretion(2). Between 10 to 25 weeks of age, there is again an increase in the acid and pepsin secretion related to the stress conditions mentioned earlier(5). The third peak comprises of primary peptic ulcers that occur most frequently after the age of 6 years with the incidence increasing progressively into the ten years and the clinicopathological picture in this group is very similar to that in adults. To conclude, the attending pediatricians should be on guard for the silent abdominal distension that heralds a perforated stress ulcer in a sick infant. Prevention must be focused on earlier recognition and use of the receptor antagonists in stressed patients.
Y.K. Sarin, |
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