Gastric dysplasia causing gastric outlet obstruction

Abstract

Gastric dysplasia signifies the presence of atypical cells in the gastric mucosa, which have not invaded beyond the lamina propria, and it rarely leads to tissue growth large enough to cause gastric outlet obstruction (GOO) to the gastric contents. However, GOO is commonly observed as a first clinical manifestation of advanced invasive gastric cancer in developing countries where patients seek medical care late. The present case highlights the treatment journey of a young woman who presented to us with features of GOO. Her endoscopic and radiological findings revealed a nodular gastric antral thickening causing GOO. An endoscopic biopsy showed features of dysplasia. She underwent distal gastrectomy following discussion in a multidisciplinary tumour board. Histopathological examination of the gastrectomy specimen confirmed dysplasia without any invasion beyond lamina. To the best of our knowledge, this is perhaps the first report of dysplasia of the stomach presenting as GOO.

Background

Gastric cancer is one of the most common causes of gastric outlet obstruction (GOO) and its presence is considered as one of the clinical indicators of advanced malignancy. Gastric dysplasia represents a relatively benign stage of disease with a tendency for malignant transformation when tumour cells invade beyond the lamina propria. A disease limited to epithelium only has never been discussed as a pathology leading to nodular gastric thickening large enough to cause luminal obstruction. We present this case of a young woman with GOO, where tumour was limited to epithelium without any invasion beyond lamina propria.

Case presentation

A 30-year-old woman was referred to us with recurrent non-bilious vomiting and upper abdominal distension of 3-month duration. She had also reported a significant loss of weight (almost 12% in 3 months). She did not have dyspepsia, dysphagia, haematemesis or melena. She denied any history of corrosive ingestion. Her medical and family history was unremarkable. Her physical examination revealed poor nutrition status with anaemia. Abdominal examination was unremarkable except upper abdominal fullness. Bowel sounds were normally heard.

Investigations

Her complete blood count and peripheral smear revealed nutritional anaemia (haemoglobin of 80 g/L, microcytic and hypochromic red blood cells). Kidney and liver function tests were normal. An oesophagogastroduodenoscopy suggested large food residue in the stomach; there were multiple nodular thickening, ulcerations and a polypoidal lesion in the pyloric canal (figure 1). Pylorus could not be negotiated to visualise duodenum. Contrast enhanced CT scan (CECT) of the abdomen revealed a smooth circumferential lumen compromising hypodense wall thickening (up to 6 cm) with a longitudinal extent of 5 cm at distal body of stomach extending up to antropylorus (figure 2). There was no perigastric lymphadenopathy or ascites; liver was normal. CECT of the chest was unremarkable. Multiple endoscopic biopsies from the nodular antral mucosa suggested dysplasia. Rapid urease test was negative. Serum carcinoembryonic antigen and carbohydrate associated antigen (CA) 19-9 levels were 3.5 ng/mL and 11.9 U/mL, respectively.

Figure 1.

Endoscopic image showing narrowed pyloric canal with nodular thickening, ulcerations and a polypoidal lesion.

Figure 2.

(A) Axial and (B) sagittal section of CT scan showing asymmetrical circumferential heterogeneously enhancing wall thickening at gastric antropyloric region resulting in significant luminal compromise with resultant gross dilatation of stomach.

Differential diagnosis

The patient was diagnosed to have GOO with severe anaemia. The common causes of GOO in a young woman in Southeast Asia include post-corrosive ingestion pyloric stenosis, extraluminal compression, gastric cancer, gastric tuberculosis, gastric bezoar, Crohn’s disease and rarely peptic ulcer disease. Though biopsy was suggestive of gastric dysplasia, there was a high suspicion of invasive gastric cancer in view of rapid clinical course, and endoscopic and radiological findings.

Treatment

The present case was discussed in a multidisciplinary tumour board. In view of the presence of symptomatic GOO and high-grade dysplasia (HGD), she was planned for surgical resection. She was initially optimised for surgery, and anaemia was corrected. Diagnostic laparoscopy revealed a hard mobile distal antral mass; there were no ascites or peritoneal/liver/omental metastatic nodules. Thereafter, a D2 distal radical gastrectomy and Roux-en-Y gastrojejunostomy were performed. Histopathological examination of the gastrectomy specimen showed low-grade dysplasia; all the margins were negative (figure 3).

Figure 3.

Photomicrographs showing (A) gastric mucosa showing erosion and dysplastic glands (10× magnification), (B) glands lined by dysplastic cells showing loss of polarity.

Outcome and follow-up

The patient gradually regained weight and is currently doing well after 20 months of follow-up period at 3-month interval. A screening CECT and upper gastrointestinal endoscopy performed after 1 year of surgery were unremarkable. She continues to be on active surveillance.

Discussion

GOO is defined as constellation of clinical manifestations including recurrent episodes of post-prandial non-bilious vomiting, abdominal pain, upper abdominal distension, early satiety, weight loss, and dehydration and dyselectrolytemia, due to obstruction to the gastric emptying. Box 1 highlights the causes of GOO. The aetiology of the GOO varies in patients of different age and gender; it also depends on the geographical region. Common causes of GOO in young patients in Indian subcontinent are post-corrosive pyloric stenosis, gastric cancer, peptic ulcer disease, gastric tuberculosis and extra-gastric causes. It was at the end of the 20th century when an aetiological shift was observed from benign peptic ulcer disease causing luminal obstruction towards malignant causes like gastric and pancreatic cancers; this can be attributed to the development of effective acid suppressing drugs and changing natural history of the disease.^1–3

Box 1. Causes of gastric outlet obstruction.

1. Gastric causes

   • Post-corrosive ingestion pyloric stenosis.

   • Neoplastic (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumour, carcinoids).

   • Chronic granulomatous infection (tuberculosis).

   • Post peptic ulcer pyloric stenosis (including Helicobacter pylori associated).

   • Crohn’s disease.

   • Eosinophilic gastroenteritis.

   • Post-surgery (eg, gastrojejunostomy).

   • Gastric bezoars.

2. Extra-gastric causes

   • Pancreatic—acute and chronic pancreatitis, annular pancreas, pancreatic cancer.

   • Duodenal—carcinoma.

   • Gallbladder—Bouveret syndrome, gallbladder cancer, cholangiocarcinoma.

   • Vascular—Wilkie’s syndrome.

3. Motility disorder

   • Diabetes mellitus.

   • Medications.

   • Post-surgery vagus injury (eg, fundoplication, bariatric procedures).

   • Amyloidosis.

Gastric cancer is the fifth most common cause of cancer worldwide.^{4 5} Majority of the patients present in advanced stage—GOO is a common presentation of advanced distal gastric cancer. Though distal gastric adenocarcinoma is the common cause of GOO in Asian population, pancreatic adenocarcinoma with gastric or duodenal extension usually accounts for similar symptoms in western population. Management of malignant GOO depends on the degree of obstruction and aetiology and includes gastrectomy (distal or total), bypass procedure (open/minimally invasive gastrojejunostomy), or endoscopic duodenal stenting.⁶

Gastric dysplasia that is defined as the presence of unequivocal neoplastic epithelium in the gastrointestinal tract without invasion of lamina propria^{7 8} is either detected incidentally following endoscopic screening or causes dyspepsia in majority of the patients. To the best of our knowledge, gastric dysplasia causing GOO has not been reported so far in the English literature.

The WHO classifies gastric dysplasia into two types—low and high grade.⁸ The risk of malignant transformation in the dysplastic lesion varies with the histological grade—HGD can turn into an invasive lesion in as high as 60%–80% of patients over a median follow-up of 4–48 months.⁷ The management of the HGD includes either endoscopic resection or surgical resection,⁹ and depends on the size and depth of the lesion, clinical symptoms, age of the patients, presence of comorbidities and availability of expertise for endoscopic resections. We offered surgery to our patient in view of young age, presence of GOO, and high suspicion of invasive cancer based on endoscopic and radiological features. Even after the endoscopic or open resections, these patients should be under close surveillance for the development of metachronous lesions.¹⁰

Patient’s perspective.

I was a mother of a 3-year-old child and living happily when I developed recurrent episodes of vomiting. I used to puke up whatever I used to eat. I was losing weight and was terribly worried. I felt something was terribly wrong with my belly. We consulted the doctors and went through a battery of investigations. After endoscopy and CAT scan, doctors told me that my stomach was not draining well due to some mass at its outlet, and I needed surgery to fix it. I was very scared and was worried for my young son. However, doctors operated upon me and everything went well. This has been more than 18 months now after my surgery and I am doing good. I have gained weight as well. I am so happy that I can take care of my son.

Learning points.

• Majority of cases of gastric dysplasia are either incidentally detected (following screening) or present with dyspepsia.

• Gastric dysplasia of the gastric antrum resulting in gastric outlet obstruction has not been reported in English literature.

• Treatment of non-invasive gastric cancer is evolving and needs to be discussed in a multidisciplinary setting for better treatment outcomes.

Ethics statements

Patient consent for publication

Obtained.