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| Figure 1. Free air under the right hemidiaphragm |
Figure 2. Intraoperative photograph of the stomach showing the perforation in the anterior pre-pyloric region |
Case Report
An 11 year-old otherwise healthy girl presented to the emergency department with the sudden onset of severe, sharp mid-epigastric pain approximately 20 hours earlier. She subsequently began having episodes of nausea and vomiting, especially after trying to eat or drink. She had no hematemesis, diarrhea, melena, or hematochezia. She reported taking ibuprofen three to four times per week for five months for muscle aches or menstrual cramps. She was occasionally given an 800-milligram dose by her mother. She had last taken ibuprofen the day before the pain began. She had never been on steroids, and there was no personal or family history of peptic ulcer disease or endocrine problems. She had no prior surgeries.
On physical exam, she had a temperature of 101.6°F, a pulse of 120 and a blood pressure of 130/74. She was sitting up in bed with her knees flexed, avoiding sudden movements. She had diminished bowel sounds. Her abdomen was notably soft, but with exquisite tenderness in the mid-epigastrium. She was also slightly tender in the right lower quadrant. She had negative Rovsing's and obturator signs but a positive heel drop. Rectal exam revealed light-brown, heme negative stool.
Laboratory studies revealed a white cell count of 23.31-thousand. Her hematocrit was 40.2, and her blood type was B-positive. Abdominal x-rays revealed air-fluid levels and free air under the right hemidiaphragm (Figure 1). A nasogastric tube was placed without return of bloody fluid.
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| Figure 1. Free air under the right hemidiaphragm |
Figure 2. Intraoperative photograph of the stomach showing the perforation in the anterior pre-pyloric region |
With the pre-operative diagnosis of perforated gastric ulcer, the patient was taken to the operating room. Laparo-scopy confirmed the diagnosis of perforated gastric ulcer. A midline incision was made and the epigastrium explored. As seen in Figure 2, there was a dime-sized perforation through the anterior portion of the pre-pyloric region of the stomach. No other ulcers or perforations were noted. There was no frank pus in the peritoneum, but some of the gastric contents had tracked down into the right lower quadrant. The perforation was repaired using a patch of omentum.
The post-operative course was uncomplicated. A serum gastrin level came back normal. She was discharged on hospital day seven and instructed to avoid all non-steroidal antiinflammatories. Follow-up gastroduodenoscopy two months later demonstrated healing of the mucosa with no signs of gastritis and a negative rapid urease test. Antral and fundal biopsies were consistent with normal mucosa. The duodenal bulb was also visualized and appeared normal.
Secondary ulcers generally present more acutely than primary ulcers (the majority of which are now known to be due to Helicobacter pylori). Secondary ulcers often do not present until a complication such as hemorrhage or perforation develops, as in this case. Hence, they have a higher need for surgery and a higher morbidity and mortality rate. Drumm, et al reported in their series that 50 percent required surgery and there was an 18 percent mortality rate.1
A patient with a perforated ulcer will present with a history of epigastric abdominal pain that suddenly became diffuse. There may be pain in the right lower quadrant as enteral contents track down the right gutter. This may mimic an appendicitis. On exam the patient is often febrile with tachycardia and hypotension, and lies still to avoid exacerbating the pain. The knees may be flexed. Bowel sounds are diminished to absent. The abdomen is very tender and is often described as boardlike, though not so in this case. Laboratory tests reveal an elevated white cell count, and an upright abdominal Roentgenogram may reveal free air under the diaphragm.2
The incidence of non-steroidal anti-inflammatory induced ulcers in children is unknown. Other causes of secondary ulcers (Table 1) include steroids, sickle cell disease, and Zollinger-Ellison Syndrome. Once the stressor is removed, secondary ulcers rarely recur.
| Table 1. Etiologies Of Secondary Ulcers |
| Medications NSAIDS Corticosteroids Stress Systemic Illness Hyperacidic Conditions |
Any patient given a nonsteroidal anti-inflammatory drug (NSAID) should be cautioned about the risk of gastritis and/or gastric ulceration. Parents given prescriptions for NSAIDs should be instructed not to give the medication to their children. A patient who is believed to have sustained a gastric ulcer secondary to NSAIDs should avoid any further use of them. If a patient must be on an NSAID, then the supplemental concurrent use of misoprostol should be considered.
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