The Stomach

Helicobacter pylori and Diseases of the Stomach

Helicobacter pylori is a gram-negative, flagellated, spiral bacterium that lives near the mucosal surface of the gastric mucosa. It is recognised as the strongest risk factor for the development of gastroduodenal ulcers. Studies have shown H. pylori infection in 60–80% of gastric ulcers and 95% of duodenal ulcers. Chronic active gastritis (superficial gastritis) is associated with H. pylori in close to 100% of cases. The organism was first isolated from gastric biopsies in the early 1980s by Marshall and Warren, and by the early 1990s H. pylori was firmly established as the causative agent for peptic ulcer disease (PUD). H. pylori is also considered by the World Health Organisation to be a dangerous carcinogen in the pathogenesis of gastric cancer and has been associated with MALT lymphoma (a low-grade B-cell lymphoma) of the stomach. In particular, MALT lymphoma has been associated with the H. pylori strains expressing the Cag-a protein.

Before the demonstration of H. pylori as the causative agent for PUD, the stomach was believed to be a sterile environment because of its acidity. H. pylori was found to produce the enzyme urease, and as a consequence it creates an alkaline ‘microenvironment’ for the organism in the gastric mucus, thus allowing it to survive in the stomach. Acute infection initially injures parietal cells, causing decreased gastric acid production. This is followed by the chronic stage of infestation, which is localised to the distal stomach and duodenum. Parietal cell function recovers, leading to abnormally high acid output. This causes antral gastritis and duodenitis, with approximately 1% of infected patients developing peptic ulcers every year. Many factors appear to determine whether or not a person infected with H. pylori will develop ulcers or other diseases; in reality most infected patients do not develop any associated problems. The precise mechanism of ulcer formation is not known; however, eradication of the organism by combined antibiotic and antisecretory therapy increases the healing rate of ulcers and lowers the recurrence rate.

H. pylori is found worldwide but is much more prevalent in developing countries. In developed countries the infection is more common in the lower socioeconomic groups, among ethnic and racial minorities, and in immigrants from less developed countries. It is more common in older patients from all the above groups. The precise mechanism of transmission is not known but it is likely to be oral–oral and/or faecal–oral.

There is about 90% prevalence of H. pylori in adenocarcinoma arising in the body or antrum of the stomach. The risk of developing polyps and gastric cancer is six times higher in patients with H. pylori infection and gastric cancer is much more prevalent in countries where the rate of H. pylori infection is high. A large meta-analysis conducted by Fuccio et al. demonstrated that the eradication of H. pylori in high-risk populations decreases the risk of gastric cancer. There is conflicting evidence regarding a possible association of H. pylori with non-ulcer dyspepsia ( Table 20.1 ).

Gastric Ulcer

Gastric ulcers penetrate the stomach wall through the mucosa into the submucosa and frequently the muscularis propria. Gastric ulcer is a common gastrointestinal disorder and is amenable to reliable radiographic detection. Almost all gastric ulcers (95%) are benign, with about 70% now shown to be caused by H. pylori infection and most of the remainder due to NSAIDs and alcohol abuse. Gastric ulcers are most prevalent in the distal stomach and along the lesser curvature. They are more common on the posterior wall of the stomach than the anterior wall and least common in the fundus. Benign greater curvature ulcers found in the distal half of the stomach are most often associated with NSAID use. NSAID- and alcohol-related ulcers are most often seen on the greater curvature of the antrum, due at least in part to a direct toxic effect of the ingested material. Benign ulcers are much less common in the fundus and along the proximal half of the greater curvature. These should always be considered suspicious for malignancy. Ulcers may be multiple, and in such cases each should be evaluated independently for criteria of benignancy.

In the elderly, ulcers are more evenly distributed throughout the stomach, particularly proximally along the lesser curvature. Steroid use, hereditary factors, emotional stress and smoking are other factors that may play a contributory role in the development of gastric ulcers.

Radiographic fluoroscopic signs of gastric ulcers are described as to whether they are seen in profile or en-face (straight on). The location and size of the ulcer in the stomach and position of the patient during barium studies will determine which of the features will be shown in any specific case. Based on the radiographic features of an ulcer, a determination should be made as to whether it demonstrates benign, indeterminate or malignant characteristics. Ulcers with clear-cut benign features can be treated medically and followed to complete radiographic healing. Ulcers with indeterminate or malignant features must be evaluated endoscopically and biopsied. Most benign gastric ulcers detected on double-contrast barium studies are 5–10 mm in size. ‘Giant’ ulcers (>3 cm) are almost always benign but have a higher rate of complications of bleeding or perforation.

The en-face radiographic signs of gastric ulcers are best seen on double-contrast barium studies and to a lesser extent on compression views in the single-contrast examination. The primary sign of ulcer is a collection of barium in the ulcer crater along the dependent wall ( Fig. 20.4A ). Most benign ulcers are round or oval; some may have tear-drop or linear contour. If an ulcer is present on a non-dependent surface or is not filled with barium, it may be demonstrated as a ‘ring’ shadow, with barium coating the edge of the ulcer crater. If a ring shadow is seen with the patient in the supine position, and it is filled when the patient is turned prone, it is located on the anterior wall of the stomach. If the ulcer is on the posterior wall, it may be filled using the ‘flow’ technique—turning the patient with fluoroscopic guidance and observing while the barium bolus washes over the posterior wall.

En-face, a smooth mound of oedema is often seen surrounding the ulcer crater causing a circular filling defect. Radiating folds seen in healing ulcers should be smooth and symmetric and continue to the edge of the crater. The presence of normal areae gastricae extending to the ulcer crater is a sign of benignancy.

The classic description of a benign gastric ulcer refers to lesser curvature ulcers seen in profile. The ulcer, often referred to as the ‘ulcer niche’, projects beyond the lumen of the stomach. Sometimes a pencil-thin line of lucency, ‘Hampton line’, is present crossing the base of the ulcer (see Fig. 20.4B ). This is believed to represent preserved gastric mucosa with undermining of the more vulnerable submucosa. This sign is not common, but is virtually diagnostic of a benign ulcer. More often there is a thicker (2–4 mm) smooth rim of lucency at the base of the ulcer termed the ulcer collar. This is also a sign of benignancy. When there is more visible oedema associated with an ulcer, it forms an ulcer mound. The ulcer mound should be a symmetrical gently sloping mass ( Table 20.2 ).

Almost all (>95%) benign gastric ulcers heal in about 8 weeks when treated medically. Benign ulcers may heal completely without any radiographic residua. As benign ulcers heal, they may change shape from round or oval to linear crevices. There may be subtle retraction or stiffening of the affected wall (see Fig. 20.4C ). An easily recognisable radiographic sign of healed gastric ulcer is the presence of folds converging to the site of the healed ulcer. There may be a residual central pit or depression (see Fig. 20.4D ). The radiating folds should be uniform. Incomplete healing, irregularity of the folds, residual mass or loss of mucosal pattern all suggest the possibility of an underlying malignancy. The Carman meniscus sign is appreciated in the clinical setting of a large, flat ulcer with heaped-up edges. The edges of the ulcer trap a lenticular barium collection that is convex relative to the lumen when the edges are folded upon themselves during compression. These findings are indicative of a malignant gastric ulcer. Occasionally benign ulcers may heal with significant scarring. Severe retraction of the greater curvature from healed ulceration of the lesser curvature may cause narrowing of the mid-body of the stomach. Healing of antral ulcers may form prominent transverse folds or significant antral narrowing and deformity (see Fig. 20.4E ). Such scarring may lead to significant obstruction, an important complication of PUD.

The use of CT in the evaluation of gastric ulcers has been studied by several authors and found to be useful in the detection and characterisation of benign and malignant gastric ulcers. The differences between malignant and benign ulcers are important in treatment planning and follow-up of patients with gastric ulcers. Evaluation by VG and/or MPR has been studied and certain advantages and disadvantages have been elucidated.

The benefits of VG include the ability to evaluate for mucosal changes, which include morphological changes. This is similar to conventional gastroscopy. Another benefit is that as optical endoscopic criteria have been well established for benign and malignant ulcers, then similar criteria can be applied to VG. Characteristics of malignant ulcers on VG include ‘irregular or angulated shape; uneven base; asymmetric edge; bulbous enlargement and fusion or disruption of gastric folds reaching the crater edge’. Benign ulcer criteria by VG include: ‘smooth, regular, round or oval shape; even base; sharply demarcated or round edges; converging gastric folds with smooth tapering and radiation’.

The use of MPR images allows for better visualisation of ulcers in multiple planes, facilitating better detection and characterisation of the ulcers. MPR also provides mural and extramural information, including, but not limited to, enhancement patterns of the gastric wall, lymphadenopathy and evaluation of adjacent organs. Characteristics of malignant ulcers on MPR images include: ‘strong enhancement of the wall at the site of ulcer greater than adjacent wall; marked periulcer wall thickening with loss of normal wall stratification; perigastric fat infiltration, lymphadenopathy or metastatic disease’. Characteristics of benign ulcers include ‘no excessive enhancement when compared with the adjacent gastric wall and mild periulcer wall thickening with preservation of wall stratification’ ( Fig. 20.5A ). But some of the features for benign and malignant lesions may overlap and differentiation of benign from malignant ulcers may not be determined by CT alone. MDCT evaluation remains complementary to optical endoscopy (gastroscopy). Surgical complications such as penetration and perforation are easily identified on MDCT using water-soluble contrast medium (see Fig. 20.5B ).

Gastric Erosions

Gastric erosions or aphthous ulcers are superficial ulcerations that do not penetrate the muscularis mucosa. They usually appear as small, shallow collections of barium 1 to 2 mm in diameter surrounded by a radiolucent rim of oedema. These are called ‘complete’ or ‘varioliform’ erosions ( Fig. 20.6 ). When the halo of oedema is lacking, the erosions are called ‘incomplete’. These appear as short linear or serpentine lines or dots of barium. Gastric erosions are most easily detected radiographically when they are multiple and complete. They are most often detected on double-contrast barium studies but may also be seen with compression technique. Single or incomplete erosions are commonly detected endoscopically but are infrequently identified radiographically. Erosions heal without scarring. Gastric erosions are most often causally related to H. pylori infection. Other causes include alcohol, NSAID ingestion and Crohn disease. They may also be seen as a response to stress: for example, in patients with severe trauma.

Gastritis

Gastritis is a descriptive term with sometimes conflicting pathological, endoscopic and radiographic definitions. It is now better understood that many causes of gastritis, including H. pylori , alcohol and NSAID gastritis, lead to similar morphological changes. The most common findings are thick (>5 mm) folds with or without nodularity ( Fig. 20.7A ). Erosions, while less commonly seen, are a frequent sign of H. pylori gastritis. Other signs of gastritis include antral narrowing, inflammatory polyps and prominent areae gastricae. The radiological findings are similar to endoscopic findings.

There is considerable overlap of findings between patients who are biopsy-positive or -negative for H. pylori . Therefore it is often not possible at this time to distinguish between ulcers and gastritis caused by H. pylori or those caused by chemical irritants (alcohol, NSAIDs and other causes of gastritis). Owing to the prevalence of H. pylori , its association with many gastric diseases and effective treatment options, it is important for the radiologist to recognise findings that suggest the presence of the infection. It has been shown that thickened gastric folds, although nonspecific, are still the single most useful radiographic sign for the diagnosis of H. pylori gastritis and that the combination of thick folds and enlarged areae gastricae may be the most specific findings.

Atrophic Gastritis

Atrophic gastritis is a combination of atrophy of the gastric glands with histological inflammatory changes. Atrophic gastritis is found in more than 90% of patients with pernicious anaemia and is characterised by loss of parietal and chief cells, leading to achlorhydria, and atrophy of the mucosa and mucosal glands. Atrophic gastritis causes a decrease in the production of intrinsic factor, which in turn causes malabsorption of vitamin B ₁₂ .

Radiographic findings of atrophic gastritis include loss of rugal folds and a tubular, featureless narrowed stomach (see Fig. 20.7B ). Areae gastricae may be absent. The radiographic features are non-specific, but because of the important prognostic implications of atrophic gastritis, an appearance suggesting this diagnosis should trigger an appropriate clinical work-up.

Atrophic gastritis may be associated with gastric polyps, carcinoma and ulcers, both benign and malignant. Intestinal metaplasia, which may be seen histologically in atrophic gastritis, is considered a premalignant condition. The diagnosis of intestinal metaplasia may be suggested by areas of focal enlargement of the areae gastricae.

Infectious Gastritis

H. pylori gastritis is by far the most common infection affecting the stomach. Tuberculosis, histoplasmosis and syphilis are usually lumped together with other granulomatous processes causing gastritis. Ulceration, thick folds and mucosal nodularity are common features, with antral narrowing being a late feature of these diseases. Monilia (Candida) may involve the stomach. This almost always occurs in the presence of severe oesophageal disease. Prominent aphthous ulceration may be seen in such cases.

In immunocompromised patients, cytomegalovirus, crytosporidiosis and toxoplasmosis may occur. Radiographic findings are non-specific but there are some suggestive signs. Deep ulceration, and even fistulisation to adjacent structures may be seen with cytomegalovirus. Cryptosporidium primarily affects the small bowel, causing severe diarrhoea and thick, small bowel folds. It rarely involves the stomach but has been shown to cause deep ulcers, antral narrowing and rigidity. Strongyloides is a parasitic infection with a worldwide distribution affecting the stomach, duodenum and proximal small bowel evidenced by thickened, effaced folds and narrowing. In advanced cases, the stomach may be narrowed and have thickened folds.