A 38 years old lady, smoker, with no significant medical or surgical history presented to our emergency department for epigastric pain associated with postprandial nausea and vomiting occurring for ten days. The patient declares that she had started losing weight forty-five days prior to presentation (around 10 Kgs). This was associated with a decreased appetite. Review of system otherwise was negative. On physical examination, her vital signs were within the normal range. Abdominal examination was unremarkable, and no abnormal findings were noted except for a yellow-white tongue.
An Esophagogastroduodenoscopy was done and showed a stenosing tumor of the antrum infiltrating the distal two-third of the stomach with a malignant appearance. Despite difficulty crossing the tumor, duodenal examination showed no abnormalities. Biopsies were taken and revealed helicobacter pylori gastritis with the absence of malignant cells. The patient was on started on antibiotics and proton pump inhibitors (PPIs) for helicobacter pylori.
Still suspecting malignancy, an enhanced abdominal and pelvic CT scan was done and showed gastric parietal thickening. No parietal pneumatosis, no infiltration of peri-gastric fat, and no pneumoperitoneum and intraperitoneal fluids were seen (Fig. 1). Purified protein derivative (PPD) skin test was done to rule out primary gastric tuberculosis and was negative. An oral contrast barium study was then ordered and it showed a fixed and constant narrowing on several radiographs at the level of antrum-pylorus, associated with rigidity of the gastric wall extending over the distal half. These findings raised suspicion of gastric malignancy, specifically Linitis Plastica (Fig. 2).
Supportive treatment was continued, with nasogastric tube decompression and parenteral feeding, however, the patient's condition failed to improve. Ten days after admission, and due to high suspicion of malignancy and absence of a definite diagnosis, surgical biopsy by laparotomy was planned. During surgery, the stenosis at the level of antrum was palpable and had circumferential rigidity infiltrating the lesser curvature upward till 3 cm distal to the cardia. No perigastric infiltrates, adhesions or invasion were noted. A biopsy was taken to rule out lymphoma and a feeding jejunostomy was created by the primary surgeon. The anatomopathological report was identical to the prior biopsies, showing chronic ulcerative changes associated with chronic gastritis lesions and no signs of malignancy.
Post-operative supportive treatment continued without any improvement in obstructive symptoms. Follow up oral contrast studies on postoperative days six and thirteen showed the same findings without any improvement in the stenosis (Fig. 3).
On the fourteenth postoperative day (24th day after admission), and due to failure of medical treatment and absence of a definite diagnosis, the final decision to perform distal gastrectomy was taken. Intraoperatively, an extemporaneous examination of the resection edges was exempt from malignant cells. Reestablishment of digestive continuity was done using a Billroth II anastomosis. The final pathology report was of a chronic antral peptic ulcer, associated with peri-ulcerous chronic gastritis. Foreign body granulomas were also seen in the specimen. Again no malignant cells were identified. The patient recovered quickly postoperatively and was discharged home a few days later without complications. The true etiology that caused her condition was never found during her hospital stay.
One month later, we received a phone call from the patient's spouse informing us that his wife was severely anxious and threatened that she will repeat what failed to kill her the first time. She subsequently confessed that she had attempted suicide by ingesting bleach right before she developed GOO. She had decided to keep the incidence a secret throughout her stay, even when invasive surgery was planned. This was the true etiology behind the presentation.