Radiographic features of gastritis using the biphasic contrast technique

Eduard E. de Lange, M.D., is currently Assistant Professor of Radiology and Director of Non-Neuro Magnetic Resonance Imaging of the Department of Radiology University of Virginia Medical Center, Charlottesville, Virginia. Dr. de Lange received his medical education at the University of Leiden, The Netherlands. He then pursued training in surgery, gynecology, obstetrics, and tropical medicine, afler which he went to Hwidiem, Ghana, where he was director and chief physician at the St. Elisabeth Hospital for 2 years. Dr. de Lange then received his radiology training at the University of Leiden Hospital, The Netherlands. He joined the faculty at the University of Virginia Department of Radiology in 1983. In addition to his interests in fluoroscopy, he maintains special interest in abdominal and musculoskeletal diseases, particularly as manifested by magnetic resonance imaging. Curr

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FMDIOGRAPHIC FEATURES OF GASTRITIS USING THE BIPHASIC CONTRAST TECHNIQUE

Gastritis is probably the most common of all diseases of the stomach, perhaps afflicting as many as 80% of all persons over 50 years of age.’ Moreover, some studies have shown that as many as 60% of asymptomatic subjects may suffer from some form of this disease.’ As a diagnostic entity, gastritis has been a cause of confusion and disagreement among clinicians, endoscopists, radiologists, and pathologists. The diagnostic problems relate largely to differences in classification and terminology. Clinical, pathologic, and endoscopic findings often disagree. Most visual interpretations of the gastric mucosa do not correlate well with the histologic changes”; superficial edema, congestion, and exudate, for example, have few or no histologic counterparts. Conversely, the gastroscopic appearance may be normal in 30% of the cases that show histologic evidence of severe chronic gastritis.4 There is also a great deal of confusion about the role of radiology in the detection of gastritis; its yield of useful information is generally considered low. However, in most studies that have dealt with this subject, only single-contrast or double-contrast technique was used to examine the upper gastrointestinal tract. Neither method alone permits optimal visualization of all features of gastriCurr

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tis; therefore, many cases go undiagnosed. It is the biphasic-contrast technique, currently regarded as the most accurate radiographic examination of the stomach and duodenum, that is required to demonstrate gastritis optimally.5-7 In this monograph, the clinical and pathologic findings associated with the various forms of gastritis are discussed. Radiographic features revealed by the biphasic-contrast examination are described. The technique, which requires the use of a medium-dense barium suspension and a hypotonic agent, is described in Appendices A and B.

NORMAL

STOMACH

The mucus membrane of the stomach lies in irregular sinuous folds known as the gastric rugae. The direction of these folds is variable. Coming from . the fundus, they tend to run diagonally across the stomach toward the greater curvature. More distally along the lesser curvature, however, in the region of the corpus and antrum, the longitudinal folds on either side run more or less parallel and form the so-called gastric “pathway” or “magenstrasse.“’ The folds have a tendency to converge at the pylorus.

FIG 1. Norr nal 901 negligible quantlty

are The gl of inflammatory

cells

:ed, ant 1lY In the lamina propria.

is a

Macroscopically, the mucosa undulates in a fairly regular manner and looks like cobblestones separated by intervening grooves. This fine reticular pattern is called the areae gastriceae. Microscopically, the gastric mucosa is lined by a single layer of columnar cells (Fig 1). A mass of gastric glands opening on the surface through gastric pits, or foveolae, makes the surface appear thick. The glands are simple tubular or branched tubular, and they extend deep into the muscularis mucosae. Each gastric pit contains the tubular openings of several glands. Cells lining the pits are identical to those of the epithelial surface. The

FIG 2. Acute gastl Ws. The glands are widely separated of edema n manifested by the more lightly staining

due to FI& area IS.

glandular tubules, on the other hand, contain two types of cells, the chief cells and the parietal cells, which secrete pepsinogen and hydrochloric acid respectively.g

TYPES

OF

GASTRITIS

The term gastritis implies gastric mucosa. Gastritis is acute and chronic forms.‘“, ” seen in the antrum, less often dus.“, l3

inflammation of the usually divided into It is most commonly in the body and fun-

ACUTE

(HEMORRH4GICI

GASTRITIS

Damage or loss of surface epithelial cells, erosions, hemorrhage, congestion, and edema are indications of acute gastritis. Inflammatory cells are generally absent. Acute gastritis is often focal in nature, with normal mucosa between the focal lesions (Fig 2). Acute injury of the gastric mucosa can be caused by a number of agents, alcohol probably being the most common (Table 1). The damaging effect of anti-inflammatory drugs is wellestablished. Acute bacterial infections of the stomach have been described in staphylococcal food poisoning14 and cholera.15 In acute phlegmonous gastritis, there is invasion of the gastric wall by microorganisms such as Streptococci, Escherichia cob, and Staphylococcus aureus. If there are also gas-forming organisms present, the disease may result in emphysematous gastritis. The effect of viruses on the gastric mucosa is a matter of controversy. Some as yet unidentified viruses may be responsible for some cases of acute gastritis.” The infectious gastritites are extremely rare and will therefore not be discussed further. Patients suffering from acute gastritis usually present with symptoms of epigastric discomfort and fullness that are not relieved by belching. The gastritis is accompanied by nausea and often by pain and vomiting, which may be hemorrhagic. The patient may become pale and sweat profusely; there may be fever and tachycardia. Complete re-

TABLE

I

Etiology

of Acute

Alcohol Anti-inflammatory Acetylsalicylic Corticostemids Phenylbutazone Indomethacin Nonstemidal

(Hemorrhagic1

Gastritis*

drugs

anti-inflammatory

drugs

INSAIIJ~I

GASTRITIS

This is the most common type of chronic gastritis. Inflammation is localized in a band in the outer third of the mucosa. The principal change in

TABLE

2.

Etiology

of Chronic

Gastritis

Autoantibodies Aging

Viral Fungus stress Emotions

Chronic alcoholism Drinking of very hot Low socioeconomic Cigarette Chronic Irradiation

Trauma Major surgery Bums

Uiagn

GASTRITIS

Infiltration of the mucosa by inflammatory cells characterizes chronic gastritis. It is usually subdivided into three types: superficial gastritis, atrophic gastritis, and gastric atrophy.“, *I Although there is no direct confirmation, it is commonly assumed that repeated gastric mucosal injury or recurrent acute gastritis leads to chronic gastritis and that atrophic gastritis and gastric atrophy are likely to represent a common end result of repeated insults to the gastric mucosa.*G Chronic ga@itis has been attributed to a number of causes (Table 2).17-2o Intrinsic factor and gastric antibodies against parietal cells have been detected in patients with atrophic gastritis and gastric atrophy. Pernicious anemia is the most common condition in which chronic gastritis is associated with an immune reaction.21 There is good evidence that chronic gastritis and gastric atrophy become more common with advancing age, particularly after age 50; both are rare in childhood and adolescence? Chronic gastritis is also frequently seen in a number of dissociated conditions such as pancreatitis, cirrhosis, cholelithiasis, ankylostomiasis, tropical sprue, and infestation with Diphyllobothrium latum.23-26 In most patients, there is little relationship between chronic gastritis and symptoms, and many patients remain asymptomatic.’ There are indications that chronic gastric inflammation in some patients may produce discomfort or exacerbation of symptoms after meals, weight loss, heartburn, hemorrhage, and other symptoms.3 SUPERFICIAL

Caffeine Thermal Injury Irradiation Infection Bacterial

Probl

CHRONIC

Hadiol,

days after ab-

acid

Other drugs Antimetabolites Reserpine Histamine

Curr

covery usually ensues one to two staining from the offending agent.

smoking anti-inflammatory

Partial gastrectomy In association with Bile reflux November/December

19~7

liquids class

other

drug

abuw

diseases

281

tric rugae may either be enlarged or, in more advanced stages, thinned. The areae gastricae may be prominent and raised. The gland tubules show various degrees of atrophy, and some are absent; the number of parietal cells is decreased accordingly. The loss of glands may leave empty spaces in the lamina propria. The muscularis mucosae may be normal, but more often it is thickened and split in several places by the inflammatory exudate. The total thickness of the mucosa is, however, decreased (Fig 4). Intestinal metaplasia may vary from a few cells to large patches of typical intestinal epithelium. Irregular overgrowth (hyperplasia) of tubules and glands may occur, which may give a nodular appearance to the mucosal s&face, and eventually leads to the formation of hyperplastic polyps. FIG 3. Superficial gastritis. The lamina matory cells. This is manifested widely spaced from one another

propria is increased due to Inflamby the glands being much more than normal

appearance is infiltration of the lamina propria by lymphocytes, plasma cells, and occasional eosinophils. Leukocytes may be seen in the lamina propria, penetrating the surface epithelium. Occasionally, collections of neutrophils are seen in the dilated glandular openings (pits). The epithelium may slough, and erosions may form. The total thickness of the mucosa usually remains unchanged (Fig 3). True superficial gastritis is rare, and changes are often not strictly confined to the upper strata of the epithelium, but also involve the deeper portions of the mucosa. The rugal folds may be thickened. ATROPWC

GASTRITIS

Atrophic gastritis follows superficial gastritis, usually without any sharp dividing line.‘“z” The full thickness of the mucosa is involved. The gas-

GASTRIC

ATROPHY

The primary feature of gastric atrophy, which follows atrophic gastritis, is the irreversible disappearance of glands .‘O,I1 Active changes, such as infiltration by leukocytes, are absent. There is minimal inflammatory reaction in the lamina propria. The muscularis mucosae is usually quite thick; however, the total thickness of the mucosa is grossly reduced (Fig 5). Atrophic gastritis is always accompanied by metaplasia of the gastric gland cells, that resemble an intestinal type of epithe lium. Chronic

Erosive

Gastritis

Erosions are frequently present in gastritis, being found in 0.3% to 12.7% of all endoscopic examinations of the stomach.z7 A chronic form of erosive gastritis was described as early as 1933.2x Other names used for this entity are varioliform gastritis, verrucous gastritis, octopus-sucker gastritis, aphthous ulcers, dellen (imprint) gastritis,

FIG 4. Atrophic infiltrate

gastritis. of chronic

The mucosal Inflammatory

thickness cells widely

is normal. separating

There IS an the glands

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1987

evolution of the lesion, Although the erosions may heal completely, long-term follow-up shows that this is relatively rare, occurring in only 20% to 30% of cases3; in most patients, the lesions decrease or increase slowly. Sometimes the elevated rim of the erosions may undergo permanent fibrotic changes, or a chain of erosions may vanish, leaving instead a large, conspicuous fold with uniform mucosal bulging or polypoid structures.33-37 Healed chronic erosions may look like nodules, sessile polyps, or pancreatic heterotopias, especially if the central depression is very shallow or has disappeared. According to Japanese investigators, some of the erosions may develop into polyps, which may, in turn, develop into gastric carcinoma.“’ Indeed, one case of ca&noma associated with chronic erosive gastritis has been reported.3” FIG 5. Gastric atrophy. The overall thickness of the mucosa IS markedly diminished. The individual glands are decreased In number as evidenced by the increased intervening lamina proprla The number of inflammatory cells is normal.

smallpo)c-like gastritis, gastritis ulcerosa et erosiva, gastritis polyposa, complete erosions, and mature erosions.3 These terms describe the principal feature that is found in this disease: multiple mucosal elevations surrounding small, crater-like ulcerations. These erosions may affect the entire stomach but, more commonly, are confined to the antrum and the greater curvature. As the name of this condition implies, the erosions may persist for prolonged periods of time.2Y’ So Chronic erosive gastritis is common, having a world-wide distribution. Little is known about the etiology or pathogenesis of this entity. Allergic mechanisms have been suggested because eosinophils have been found in the inflammatory infiltrate.31 The disease is more commonly seen in men than in women. The prevalence of the disorder is greatest in the fifth and sixth decades. There is no evidence of gastric ulcer development at the site of erosions; however, a significant association with recurrent duodenal ulcers has been reported?‘, 33 The clinical picture includes hyperacidity and epigastric pain similar to the distress caused by ulcers. Some patients may develop anorexia and vomiting, and may experience severe weight loss. They experience pain that is exacerbated by eating, and their symptoms may mimic gastric cancer. Edema and hypoproteinemia may be occasionally observed as a result of gastric loss of proteins. Despite the presence of erosions, bleeding is not a common feature.” S-ymptoms may be prolonged, and ulceration may remain stable for many months. As often happens in gastric disorders, however, there is no clear correlation between clinical complaints and the appearance 01 Cut-r Bob/

Diagn

Radio!,

November/December

1987

An tral

Gastritis

In cases where inflammation is confined to the antrum, the term antral gastritis has been used as though it were a distinct entity. Although gastritis can occur in any region of the stomach, the annum is much more commonly affected than other regions. Studies have shown that, wherever else gastritis may occur in the stomach, the antrum is involved in as many as 90% of cases.” 3,13,‘10~4”,41 Multiple endoscopic biopsies have indicated that antral gastritis may spread proximally into the fundus4’, 43 and that, likewise, fundal gastritis tends to spread distally into the antrum.44 The result in both instances is diffuse inflammation of the entire gastric mucosa. It is generally true that gastritis in different locations in the stomach does not indicate different types of disease; however, a predominantly fundal involvement is more commonly seen with achlorhydria, pernicious anemia, and severe gastric secretory deficiency. Since antral gastritis describes only the location of the inflammatory changes and not a distinct entity, we prefer not to use this term. OTHER

FORMS

Hypertrophic

OF GASTRITIS Gastritis

The term hypertrophic gastritis or hypertrophic gastropathy is a descriptive term and refers to enlargement, either localized or diffuse, of the gastric folds. A great deal of controversy arose in the early 1960s concerning the histologic interpretation of this entity, and current views suggest that such a condition rarely, if ever, exists.3 Pathologically, the term is inappropriate because the conditions that cause it may not include the inflammation that the term gastritis implies. Moreover, the “hypertrophic” appearance of the mucosa may have several causes: transient edema or neuromuscular disturbances; glandular hyperplasia as seen in the 283

FIG 6. Acute erosion. The mucosal defect (right) does not extend beyond the muscularis mucose. The mucosa (left) is of normal thickness but shows early changes of necrosrs.

Zollinger-Ellison syndrome; or foveolar hyperplasia of the type observed in Menetrier’s disease.45,46 Since hypertrophic gastritis does not represent true gastritis, we will not discuss this entity further, nor will we discuss the Zollinger-Ellison syndrome or Menetrier’s disease. OTHER

INFLAMMATORY

CONDITIONS

A number of other inflammatory conditions rarely occur in the stomach. These include bacterial or fungal infestations such as anthrax and moniliasis; granulomatous lesions such as Crohn’s disease, sarcoid, syphilis, and tuberculosis; eosinophilic gastritis; gastric inflammation associated with irradiation or freezing; and vascular abnor-

FIG 7. A, erosions they

284

become

are not well demonstrated clearly visible (arrows).

when the antrum IS collapsed, Note that the erosrons are lined

malities, such as periarteritis nodosa. Because of their rare occurrence, we will not further discuss these entities. RADIOGRAPHIC

FEATURES

OF GASTRITIS

As previously discussed, gastritis can involve a number of macroscopically visible mucosal changes. These changes include erosions, nodules, polyps, enlarged gastric rugae, thinning or absence of folds, and coarse areae gastricae. Other lesions, which are frequently seen radiographically, but lack endoscopically or pathologically demonstrable counterparts, are transverse folds, crenulation, antral spasm, and narrowing. Some features are better visualized by double-contrast (DC) tech-

however, during drug-induced along the gastric fold.

Curr

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Radial,

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same

November/December

case

(B),

1987

nique and compression

others by single-contrast (SCGC) technique.

graded-

EROSIONS

An erosion is a mucosal defect that does not extend beyond the muscularis mucosae. Two forms of gastric erosions can be distinguished: acute or incomplete erosions and chronic or complete erosions (Fig 6).47 Acute erosions are flat epithelial defects lacking any surrounding reactive mounds of edema. Animal experiments and prospective clinical studies have established the pathogenesis of the lesions. Fear, stress, certain medications, alcohol, bile reflux, or decreased capillary perfusion may lead to necrosis of small areas of surface epithelium that become desquamated and then produce acute erosions.48 The acute lesions are frequently associated with bleeding. In most cases they evolve and regress rapidly and usually heal completely within a short time. Chronic erosions are characterized by a central epithelial defect surrounded by a mound of elevated mucosa. The mucosal elevation may be edema, in cases of immature chronic erosion, or fibrosis, with the mature erosion.4g The elevated border of chronic erosions can also be caused by a circular contraction of the

muscularis mucosae around the defect.:j5 Erosions, chiefly the chronic type, are found during 8% to 15% of routine endoscopic examinations.50 Acute erosions may be solitary or multiple. They may be limited to the antrum and/or corpus or may involve the stomach diffusely. Chronic erosions are more commonly multiple and are usually limited to the antrum and/or corpu~.~~ Radiographically, the chronic or complete erosion is depicted as a small target lesion. It consists of a central collection of barium, corresponding to the mucosal defect, and a radiolucent halo, which corresponds to the surrounding mound of edema or inflammation. The central collection of barium is most commonly pinpoint and round; however, the shape may also be linear or irregular. The lesions are almost always multiple and may be grouped in clusters. The erosions tend to develop along the gastric rugae, producing localized thickening or scalloping of the affected folds. Complete erosions are usually seen on DC radiographs, especially with drug-induced hypotonia, and are less commonly found with SCGC technique (Figs 7 and 8). Sometimes, however, a slightly collapsed stomach permits better demonstration of the lesions on DC radiographs than does full gastric distention (Fig 9). The erosions of chronic erosive gastritis can persist, being found on consecutive examinations

FIG 8. A, erosions are faintly erosions (arrows).

CurrPmblDiagn

lladiol,

wible

on double-contrast

November/Uecember

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1987

B, single-contrast

graded-compression

films

of same

case

reveal

multiple

antral

285

FIG 9. A, double-contrast collapsed,

multiple

radiograph during drug-Induced antral erosions (arrows) become

hypotonia visible.

does

(Fig 10). Acute or incomplete erosions are seen as dots or streaks of barium without an associated radiolucent halo. These erosions are much more difficult to detect radiographically and are usually seen only on DC radiographs during drug-induced hypotonia (Fig ll)."l Incomplete erosions are not generally aligned along the mucosal folds, and thickening of folds is frequently absent. Linear erosions are frequently seen in patients who have ingested aspirin (Fig 12).52 Other lesions in the stomach may resemble chronic, or complete, erosions. These are submucosal masses with central ulcerations that are most commonly caused by metastatic disease, lymphoma, or pancreatic heterotopia. These lesions are usually larger than typical erosions, and their margins are much more sharply defined. The erosions seen in Crohn’s disease, syphilis, and infections caused by herpes simplex and cytomegalovirus are indistinguishable from the erosions caused by gastritis. Barium precipitations that present as very dense, punctate barium collections without a surrounding halo can be mistaken for erosions. These precipitations are usually seen when a high-density barium suspension is used L (Fig 13). NODULES As mentioned chronic gastritis

266

earlier, nodularity may occur in when there is hiyperplasia of tu-

not

reveal

significant

abnormality

6, when

the antrum

is slightly

bules and glands. Also, when the base of a complete erosion is elevated by circular contraction of the muscularis mucosae around the defect, the erosion may invaginate and assume the shape of a nodule. Finally, nodules may form when complete erosions heal and the thick mucosal mound is replaced by fibrosis.34-36 Since complete erosions and nodules are both expressions of the same disease, the lesions are frequently seen together in patients suffering from chronic gastritis. Studies have shown that, in cases where the presence of erosions has been verified, the nodules appear over time.53 As with complete erosions, nodules tend to be aligned in clusters along the mucosal rugae. There may be associated diffuse thickening and scalloping of the gastric rugae. In cases where radiographs show distinct changes, nodularity may be difficult to detect endoscopically, even in cases where radiographs show distinct changes.‘16 Radiographically, the nodules are seen as small filling defects measuring less than 0.5 cm. They are usually aligned along mucosal folds; scalloping of the involved folds is a characteristic finding. Both DC and SCGC techniques demonstrate these findings, however, SCGC is much clearer (Fig 14). In some instances, there may be considerable knobby thickening of the mucosal folds. Erosions are commonly associated with the nodules. It is necessary to distinguish between the nodular defects of chronic gastritis and a variety of other conditions. Usually larger than a nodule, the

Curr

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November/December

1987

FIG 10. Chro lnic erosive gastritis. A, multiple onstl .ates the lesions again, but they

Cur-r Probl

Diagn

Radio!,

large complete have become

November/December

198’i

erosions are seen in the antrum. B, radiograph of same patient smaller and some now have a more nodular appearance (arrows)

1 year

later

FIG 11. Small vature

incomplete erosions of the antrum

(arrows)

are seen

along

the greater

cur-

FIG 12. Double-contrast radiograph of patient who had icylic acid demonstrates multlple linear erosions rows).

ingested acetylsalin the antrum (ar-

1 FIG 13. Punctate (arrows). suspension

barium collections representing These artifacts may occur when IS used.

banum preclpitatlons a high-density barium

FIG 14. A, double-contrast onstrates multiple

radiograph of the antrum reveals no significant abnormality. B, single-contrast nodules (arrows) allgned alorlg the mucosal folds gtvlng a scalloped appearance

graded-compresslon to the Involved

technique folds

dem-

hyperplastic polyp is the extreme of the spectrum of nodular gastritis (see following section). The outline of a polyp is much sharper than that of a nodule, which has sloping edges. Furthermore, polyps are often pedunculated. Submucosal masses such as metastases, lymphoma, leiomyoma, or pancreatic rest are generally larger than nodules. Also, the outlines of these lesions are usually sharper than those of the nodules.

HY?‘ERPIASTIC

POLYPS

As discussed above, some mucosal nodules resent the healing phase of complete gastric

repero-

FIG 15. Hyperplastic polyps. A, on double-contrast radlograph the polyps appear as masses proJected tnto the gastric lumen when they are large and aligned along the edge of the stomach (straight arrow). When they are small and seen en face, a small semicircular radiodense line may be the only finding, one that can be easily overlooked (curved arrows). Note that there are antrai erosions and scalloping of folds. 6, single-contrast graded-compression technique clearly depicts the polyps as is demonstrated on this radiograph of the same patient (arrows).

.

290

sions. It is believed that an exuberance of the healing process that accompanies regenerative hyperplasia leads to the development of hyperplastic mucosal p01yps.~~ These lesions frequently accompany chronic atrophic gastritis and OCCUI most often in older patients.54,55 Although not true neoplasms, hyperplastic polyps constitute about 40% of all benign gastric tumors. They vary in size from less than 0.5 cm to as much as 3 cm in diameter, but are generally small, averaging 1.0 cm in diameter. Histologically, they are composed of superficial gastric epithelium. Inflammation and superficial ulceration may be seen near the surface. The polyps are frequently multiple and occur more often in the antrum than in other regions of

the stomach. Cellular at”ypia is uncommon. Malignancy is rare in hyperplastic polyps less than 2 cm in diameter, but malignancy may occur in larger growths, the reported incidence being 0.1% to 5% of cases.54,56 Adenomatous transformation probably occurs prior to malignant changes.“7 When patients are followed up over the years, hyperplastic polyps are found to increase in number and size. The lesions may regress or disappear..57 Although the development of malignancy in hyperplastic polyps is rare, the incidence of coexisting carcinoma in a stomach containing one or more hyperplastic polyps is high. These malignancies arise not in the polyps themselves, but elsewhere in the gastric mucosa.58 Polyps are readily visualized on SCGC films. The characteristic finding is a round or lobulated, welldefined filling defect that may be mobile if the lesion has a stalk. However, most polyps are sessile, particularly when small. The appearance of polyps on DC films varies. If seen en prof;le, they appear as a mass projecting into the gastric lumen; en face, only a radiodense circular or semicircular line may be seen if the lesion is small. More than one hyperplastic polyp is frequently found during an upper gastrointestinal series. The SCGC technique usually demonstrates a larger number of polyps than does DC technique (Fig 15). Hyperplastic polyps cannot easily be distinguished radiographically from other types of polyps, such as adenomatous polyps, small leiomyomas, or islands of ectopic pancreatic tissue. A large number of lesions tends to indicate hyperplastic polyps. If the lesion is single, endoscopic biopsy is necessary for confirmation.

ENLARGEMENT

OF GASTRIC

RIJGAE

In the normal stomach, the gastric rugae vary in size. The folds in the fundus and along the greater curvature are usually the most prominent, having a width of 0.5 to 1.0 cm. The folds in the antrum are smaller and measure 0.3 to 0.5 cm. Normal antral folds can easily be effaced when the stomach is distended, particularly during drug-induced hypotonia; however, this is not the case with the rugae along the greater curvature and fundus. Opinions differ as to when a fold must be regarded as abnormally coarse. Some authors believe that any fold thicker than 1.0 cm is abnormal; others use 0.5 to 0.8 cm as their limit.8’3’,5g-61 The DC and SCGC techniques are equally effective in demonstrating enlarged gastric folds. The folds often have irregular margins and are uneven in width and height. Abnormal folds cannot be easily flattened under external pressure and are not effaced when the stomach is distended (Figs 16 and 17). In rare cases of chronic gastritis, a single hypertrophied fold is found on the lesser curvature in the prepyloric region. On radiographs, this finding may superficially resemble a polyp. However, the lesion usually extends across a nondistorted pylorus into the base of the duodenal bulb, which is unusual for a polyp (Fig 181.“’ Although enlarged gastric folds are commonly seen in cases of gastritis, they may also be seen in many other conditions, such as Zollinger-Ellison syndrome, Menetrier’s disease, lymphoma, and eosinophilic gastritis. Large gastric folds may be associated with gastric or duodenal ulcer. Prominent antral folds are also seen in 10% of patients who

FIG 16. There rowed

C’urr

Probl

Diagn

Radio/,

Noveniber/Decernber

1987

are thickened

longitudinal

folds

In the antrum.

which

IS nar-

291

FIG 17. Thickened irregular folds (arrows). The

antral antrum

folds Erosions IS narrowed

are

present

on

SI

do not appear to have upper gastrointestinal tract pathology; this finding is especially common of the gastric among black patients.“” Enlargement rugae, therefore, is not a specific finding for gastritis. However, associated findings, such as erosions or nodules along the enlarged folds, make gastritis the likely diagnosis. THINNING

OR ABSENCE

OF FOLDS

In advanced atrophic gastritis, the mucosal thickness is decreased and, in gastric atrophy, it is

grossly reduced. The gastric folds show a corresponding decrease in height and width; in cases with severe atrophy, they are absent. These changes may be total or segmental. They are best demonstrated radiographically along the greater curvature and fundus of the stomach, where the gastric rugae are normally prominent (Fig 19). The DC and SCGC techniques demonstrate absence of folds equally well; however, thinned folds are more clearly depicted on DC films, especially during drug-induced hypotonia. Because contraction of the muscularis mucosae is capable of throwing

FIG 18. A, double-contrast film arrow). B, single-contrast

bulb

292

(curved

arrows).

reveals a polypoid lesion In the antrum (curved graded compression technique demonstrates This makes it more likely that the lesson represents

arrows). Note an erosion along the greater curvature (straight extension of the lesion across the pylorus into the base of the a thickened fold, a finding conftrmed by endoscopy Cur-r

Probl Diagn Radio!,

November/December

198;

FIG 19. A, lack of folds body, and is narrowed.

even a smooth mucous membrane into folds, even severe gastric atrophy may go undetected unless the stomach is completely relaxed. Atrophic gastritis and gastric atrophy cannot be distinguished from one another radiographically; histological confirmation is necessary. However, the absence of rugae on the greater curvature, together with distal tubular deformity and a bald fundus, strongly suggests a diagnosis of gastric atrophy.8,“” Curr

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Diagn

Radio&

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1987

COARSE

is noted along the greater curvature of the gastric there is thinning of folds In the fundus (B). The antrum Incidental note is made of a small hiatal hernia

AREAE

GASTRICAE

The areae gastricae represent the fine cobblestone pattern of the surface of the normal stomach. They are caused by the regular undulations of the gastric mucosa. This undulation is an intrinsic feature of the mucosa and does not depend on the state of contraction of the muscularis mucosae. It is unaltered by the degree of stretching or contrac293

FIG 20. Coarse areae gastricae. mucosal Iinits have ! an The lndlvldual irregular shape and are pron ounced. They measl Jre 5 to 6 mm in diameter. Note transverse folds and thlckened antral folds

tion of the stomach wall.“” Although areae gastricae are commonly present, their extent in the stomach varies, and they may be absent in normal individuals.5g’ 65 Areae gastricae are observed most frequently in the antrum and less commonly in the proximal body and fundus.“” The individual mucosal units normally measure 1 to 4 mm in diameter and have a regular shape.““, IX Ii7 Areae gastricae are considered coarse if they are irregular and measure greater than 4 mm.6x A coarse pattern is commonly associated with atrophic gastritis, but also occurs with hypersecretion and gastric or duodenal ulcer.65’ w 69 There is no correlation between the size of the areae gastricae and the severity or stage of disease.70 The areae gastricae are best visualized radiographically by DC technique (Fig 20).

TRANSVERSE FOLDS In normal individuals, the antral folds are oriented in a more or less longitudinal direction from the pylorus to the gastric body. In gastritis, transverse folds perpendicular to the lesser curvature are commonly encountered in the prepyloric region of the antrum. There may be a single fold OI multiple folds paralleling each other. The folds usually cover one half to two thirds of the antral circumference and do not extend to the greater curvature. Although the folds may be transient, they usually persist throughout the examination. Drug-induced hypotonia greatly facilitates their visualization, and they are readily identified on DC: films.6’7’ Once the hypotonia subsides, peristaltic waves of contraction often obscure the transverse folds, and they may become unrecognizable. Ero-

FIG 21. Multiple transverse antral folds perpendicular ture (arrows). Erosions are also present them are aligned along the folds

to the lesser curva(arrowheads); some 01

.

294

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1987

FIG 22. A singular transverse folds is seen in this case (arrow) erosion is seen at the end of the fold (curved arrow).

sions and/or nodules are frequently seen togethei with the abnormal folds (Figs 21 and 221.

CRENULATlON

Crenulation is a wrinkled or irregularly corrugated appearance of the antral wall frequently seen in gastritis. As with transverse folds, the finding involves the lesser curvature of the prepyloric region. However, the wrinkles are much smaller and thinner than the folds, and they usually involve no more than one third of the antral circumference. Crenulation can persist throughout the examination or may be transient .6.71 Drug-induced hypotonia is generally needed to demonstrate this finding, which is best visualized by DC technique. Erosions and/or nodules are also commonly seen with the wrinkles (Fig 23).

ANTRAL

SPASM

AND

NARROWING

The presence of an irregular, abruptly marginated, concentric narrowing of the antrum during drug-induced hypotonia strongly suggests gastritis.“, 71 This spasm may be transient or persistent, and the normal antral configuration with its symmetric, biconvex shoulders is not usually seen during the examination. Multiple nodular filling defects, erosions, and/or thickened folds are frequently present as well (Fig 241. The narrowing may also be smooth and involve flattening of both the lesser and greater curvatures, which gives the antrum a tapered appearance (Fig 251. Occasionally, an S-shaped deformity of the antrum is found (Fig 261.” These last two findings are more comChrr

Probl

Diagn

Radid,

November/December

1987

and a large

monly seen with atrophic gastritis. Although spasm and narrowing can be persistent, the deformed antral configuration is usually altered by peristaltic waves that return after the drug-induced hypotonia subsides; thus malignancy can generally be ruled out.” DISCUSSION

As demonstrated, gastritis may present with a number of radiographic features. In general, acute gastritis cannot be distinguished from chronic gastritis, nor can the various types of chronic gastritis be distinguished from one another. Erosions can be present in both conditions. Nodular@, polyps, irregular and coarse areae gastricae, thinning or absence of gastric rugae, transverse folds, crenulation, antral spasm, and a smoothly narrowed or Sshaped antrum are reliable indications of chronic gastritis.6J67 Thick folds are too nonspecific to permit the diagnosis of gastritis when they are the only abnormality, and additional evidence should TABLE

3.

Optimal Gastritis

Demonstration by Technique

of Lesions

in

LESION

DC

Erosions Nodules Hyperplastic pol.yps Enlarged gastric rugae Lack of folds Coarse areae gastricae Transverse folds Crenulation Antral spasm and narrowing

+

hCC.C’

t + + i-r iTV

+ + +

i29.5

FIG 23. A, the lesser antral

296

curvature circumference.

of the antrum shows an Irregularly corrugated B, spot film of the antrum reveals a small erosion

appearance. The wrinkles along a wrinkle (arrowhead).

involve

no nlore

than

one

tl iird

of the

FIG 24. Two cases the stomach.

of antral spasm, demonstratrng A, the antral folds are thick

the Irregular concentric antral narrowrng and there IS nodulanty. B, erosrons (arrows)

be sought. Such additional findings are frequently present, however, and make radiographic diagnosis of gastritis possible. Obviously, the more numerous the radiographic findings, the more contidently one can make the diagnosis. During upper gastrointestinal series, some features of gastritis are more clearly demonstrated with DC technique and others with SCGC technique (Table 3). Thus, the optimum procedure for showing all lesions is a combined study-the biphasic-contrast examination. This technique is considered highly accurate for the detection of small lesions, such as erosions and nodules, and is discussed in detail in Appendix A.” 7 It is neces-

that IS abruptly demarcated are also frequently seen.

from

the remainder

of

sary to employ this method to demonstrate consistently all features of this condition. The procedure requires the use of a medium-dense barium suspension (see Appendix B) to allow both good mucosal coating in the DC phase and sufficient transparency during the SCGC phase of the examination.“’ 73 Carefully controlled compression is used to visualize subtle lesions which can be missed when compression is applied either too firmly or not at all (Fig 271. The routine use of a hypotonic agent is also necessary, since this increases sensitivity in detecting superficial lesions.“’ Because gastritis usually involves the antrum, this region of the stomach should be examined with

FIG 25. There IS a smooth tapenng of the ant rum. Erc xion: s are four ld along a thickened antral fold f(cur ved arrol fls) and in the bc 1dy of the stomach (whirl 3 arrows).

Curr

Probl

Diagn

Radial,

November/December

1987

297

FIG 26. There is a smoothly narrowed S-shaped compresslon technique also demonstrates

particular care. quality films of them for small, nifying glass to mended as a racy.”

antrum A, nodules are seen a hyperplastic polyp (arrow)

The radiologist should obtain high the stomach and should scrutinize subtle lesions. The use of a magexamine the films is highly recommeans of achieving greater accu-

SUMMARY

Gastritis is a group of inflammatory disorders that can be diagnosed radiographically. The optimum radiographic examination of the stomach is the hiphasic-contrast technique, which includes the use of a medium-dense barium sulfate suspension and a h_vpotonic agent. Knowledge of the forms of gastritis, a careful application of biphasiccontrast technique, and a perceptive evaluation of information will help the radiologist to detect this entity with great frequency. APPENDIX

A

BIPhXSlC-COVTRAST EXAMINATION UPPER GISTROlNTES’lYN~4 L TRA(:T

OF TtiE

Background Information A number of individual radiographic techniques have been described for examining the stomach and duodenum.” These are tht: complete filling or single-contrast, the compression, the mucosal relief; and the double-contrast techniques. E&h technique has its limitations. ‘I’he complete ,fifZing technique provides a picture of thtt contours of the stomach and duodenum and, when the patient is turned, allows more contours to be examined. If the stomach were a cylinder \I iih its axis parallel 298

on the

double-contrast

radlograph

6, single-contrast

graded-

to the longitudinal axis of the body, it would always be possible to detect a lesion. However, since the stomach is not a simple cylinder, this method possesses only limited value. When compression is applied to a stomach that is completely filled with barium suspension, it is possible to add en @ce pictures to the contour diagnosis of the complete filling method. The use of a low-density barium suspension increases the transparency and, thus, the sensitivity of this method. However, compression is not always possible if the patient is obese. Moreover, the upper part of the stomach cannot be compressed because of its position beneath the thoracic cage. The mucosal relief study consists of the appli-cation of a small amount of barium suspension to the mucosa of an empty stomach, thereby outlining the surface of one gastric wall. This method yields very few useful results because there is no distention of the stomach, a necessary condition for detecting small lesions. The Japanese havr: popularized a double-contrast technique, which requires a small amount of high-density barium suspension and air or CO, gas. Double-contrasl technique provides a nearly ideal image of the in-. ner surface of the stomach, particularly of the posterior wall, when the patient is supine. However double-contrast images of the anterior wall cannot be easily obtained when the patient is prone because the corpus and antrum are then completel\r filled and the barium suspension obscures the anterior surface. Deep Trendelenburg position of the table, the injection of large quantities of gas into the stomach through a nasogastric tube, and other, complicated maneuvers are required to visualize this wall.

FIG 27. Single-contrast radlographs graded (B), and too much visible on B (arrows).

When used separately, none of these techniques can provide, in a simple way, complete visualization of the lining of the entire stomach without inconvenience both to the patient and the radiologist. Double-contrast technique, with the patient first supine and then erect, can precisely demonstrate the posterior wall of the antrum, corpus and total fundus; however, this technique does not readi!y demonstrate lesions on the anterior aspect of the stomach, particularly ones with sloping edges. Therefore, single-contrast graded-compression studies are necessary to ident@ anterior wall lesions consistently (Figs 28 and 2~31.The biphasiccontrast examination introduced ten years ago by Op den Orth is a standardized method that combines the best features of both techniques in one study, permitting the detection of small, superficial lesions in the entire stomach and duodenum.5,6 Also referred to as multiphasic technique,“’ this combined method is currently considered the

of same case (C) compresslon

with too Me (A), with Eroslons are only

most accurate radiographic examination for the upper gastrointestinal tract .7,” The biphasic-contrast procedure requires a barium suspension that provides excellent mucosal coating during gaseous distention of the stomach and duodenum in the DC phase of the study and also permits sufficient transparency of the barium during the SCGC phase. We have developed a medium-dense barium suspension that can be administered simultaneously with a gas-producing agent in the form of a cold, carbonated drink (“bubbly barium”) dispensed from a soda syphon. ‘Ilie formulation and preparation of the suspension are given in Appendix B. Glucagon is routinely used for gastric hypotonia and distention. During the examination, routine exposures are obtained with the patient in several positions. This results in a consistently high-quality study. The technique is easy to learn, and in experienced hands, requires only ten minutes for the complete 293

X-ray

beam +

radiog

FIG 28. Schematic dependent technique. radiograph the film. B, the barium the excavation

drawrng of stomach seen in cross section with excavation $ulcer wall. The lesions show different features that vary with the type of a thin layer of barium suspension (shaded) coats the dependent as a dense barium collection (black) and surrounds the protrusion with full-column single contrast technique, the stomach is completely pool C, when graded compression IS applred, the thickness of the as a densrty (black) and the protrusion as a filling defect (white).

examination including a fluoroscopy time of two to five minutes. In our department, residents are usually capable of performing the technique within this time after one to two months of fluoroscopy experience. The examination is best performed with a conventional radiographic/fluoroscopic unit so that the examiner can have his “hands on” the patient. The use of remote control equipment is not recommended. Careful review of

A

B

or diverticulum) radiographic wall and fills depicted as filled with barium pool

and protrusion P (nodule or polyp) on technique used. A, during double-contrast the excavation, which is depicted on the a filling defect with fading edges (white) on barium, and both lesions are obscured by is reduced and the lesions become visible,

the films obtained during the study is necessary, and the use of a magnifying lens to examine the radiographs is highly recommended. In addition, regular spot films are preferred over camera photo spots because the spatial resolution is better and subtle lesions are less likely to be missed. When photospots are made, the magnification format should be used when possible.

C

FIG 29. Schemattc drawing of stomach In cross sectron wtth excavated and protruded lesions on the nondependent wall. A, durrng doublecontrast technique, the lessons are not visible on the radrograph because gravity prevents barium from poolrng on the nondependent wall. B, with full-column srngle-contrast technique, the lesions are obscured by the thick barium pool. C, when graded compression IS applied, the lesions become visible because the thickness of the barium pool is reduced. The excavatron IS depicted as a density and the protrusion as a filling defect. During graded-compression srngle-contrast technique, lesions on the nondependent wall appear rdentrcal to those on the dependent wall (see Fig 28,C) Lesions on the dependent and nondependent walls can be distinguished because of the difference in appearance during double-contrast examination (See also Fig 28,A). 300

Cur-r

Probl

Diagn

Radio&

November/December

1987

TECHNIQUE Materials

1. Soda syphon filled with 1 L of “bubbly barium.” Shake syphon vigorously before each time barium is dispensed. 2. Glucagon-02 mg in l-ml syringe. 3. Small compression paddle with hook (Holzknecht paddle) (Fig 30,AA). 4. Compression paddle with balloon (Fig 30,B). 5. Right-hand lead glove (to cover hand when using compressing paddle). 6. Film cassettes (sizes: 10” X 12” or 9.5” X 9.5”, and 14” x 17”). FIG 30. Holzknsht

Preliminary

1. Spot film technique: phototimed 90 kVp at beginning with DC filming; 120-125 kVp later with SCGC filming. 2. A biphasic-contrast exam should be tried on all patients. If it turns out that the patient is uncooperative or too debilitated, the study can be completed as a singlecontrast exam by skipping the DC part of the study. 3. Question the patient about relevant symptoms, previous abdominal surgery, having fasted after midnight, and possibility of pregnancy. 4. Explain procedure to the patient. Explain how to hold breath during spot filming (e.g., “Don’t take in a deep breath-just stop breathing”). Caution patient not to belch after drinking “bubbly barium.” 5. If the patient comes for barium swallow (BS) and UGI, start with the UGI and do BS at the end of the study. 6. Always apply just enough compression during single-contrast filming to “see through” the barium. Do not compress too firmly.

Curr

Pmbl

Diagn

Radio&

November/December

1987

pedal

(A) and compression

Method (Positions X-ray Table)

Described

pedal

are

with

balloon

in Relation

(6).

to

1. While the patient is lying supine on x-ray table, inject 0.2 mg of glucagon intravenously. 2. Raise the x-ray table to the upright position. The patient stands on footrest with his back against table top. (If patient cannot stand, tilt head of table up about 30”45”). Quickly scan abdomen with fluoroscope to check for contraindications to study: free air beneath diaphragm or residual barium from previous exam. 3. Wait until immediately before start of exam to shake chilled soda syphon and dispense “bubbly barium” into 10-0~ cup. Have patient hold cup of barium in left hand. (Have technician hold it if patient is disabled.)

301

4. Rotate patient

into left posterior oblique (LPO) position (to rotate spine away from esophagus). Ask patient to drink 1 cup of “bubbly barium” quickly and tell him not to belch. Scan the esophagus while the patient swallows. Obtain one (2-on-l) DC spotfilm (10” X 12” or 9.5” X 9.5”) at 90 kVp of lower esophagus and cardia during maximal gas distention after all gas bubbles have disappeared (Fig 31,A). Take one (2-on-l) DC spotfiZm in right posterior oblique (RPO) position while the patient drinks ‘/z cup of “bubbly barium” (Fig 31,B). Do not have the patient stop breathing or swallowing while making the exposures. 5. Take empty cup from patient. Turn x-ray table into horizontal position. Give patient a pillow on which to rest his head. 6. Ask patient to roll to his left three times (through three 360” rotations), stopping in the LPO position. (If patient cannot turn, roll him back and forth three times from one lateral position to the other.) This is to obtain good barium coating of the gastric mucosa at the same time as the CO, is dissociating from the barium suspension

FIG 31.

FIG 32. 7. Take four

(4-on-l) DC spotjlms (10” X 12” or 9.5” X 9.5”) in the following sequence from the distal to the proximal end of the stomach (9OkVp) : A. Antrum (patient LPOJ (Fig 32,AJ. B. Gastric body, inferior portion (patient supine) (Fig 32,Bl.

C. Gastric body, superior portion (patient between supine and RPOI IFig 32,C~. D. Fundus (patient RPOI (Fig 32,DJ. (Make each exposure with a fresh coating of barium by turning the patient from right lateral to required position.~

8. Take four (l-on-l) DC .spot$films of the entire stomach in the following sequence: A. LPO Wig 33) B. Anteroposterior supine (Fig 34) C. RPO (Fig 3.5) (First, turn patient to right lateral position to empty fundus and

FIG 34. Curr

I’robl

elevate head of table 15” before turning into RPO position). D. Right lateral (Fig 36) (Provided that the duodenum [C-loop] is sufficiently filled with barium. Otherwise, take this film at end of study [see step 131.1

FIG 36. Diagn

tiadiol,

November/December

1987

303

FIG 37.

9. Increase kVp to 120-125 for SCGC spot filming. Turn patient into right anterior oblique MO) position. Place compression paddle beneath patient and inflate balloon for graded compression of duodenal bulb. Take one (4-on-l) SCGC spot f;/m of duodenal bulb (Fig 37,A) and one spot$film of distended proximal duodenal loop (Fig 37,B). Turn x-ray table upright. Rotate patient to supine position. Use Holzknecht oaddle to obtain graded compression of bulb. Take two (4-on-l) SCGC spot Jilrns of: A. Duodenal bulb (patient LPO). Project

FIG 38. 304

the bulb slightly right and left from the spine (Fig 37,C and D). B. Use fluoroscope compression cone (or Holtzknecht paddle if patient is obese) and take four (4-on-l) SCGC spot jilms Of:

1. Antrum (patient LPO) (Fig 38,AJ 2. Gastric antrum-body (patient LPOAP) (Fig 38,B) 3. Gastric body (patient AP) (Fig 38,CJ 4. Gastric body-timdus (patient RPOi (Fig 38,D) ”

FIG 39.

distended lower esophagus (Fig 40,~~ and cardia while patient holds his breath and one spot Jilm during Valsalva maneuver to evaluate for sliding hiatal hernia (Fig 40,B).

10. Decrease kVp to 90. Turn patient into LPO position. Quickly scan the mediastinum to be sure that the esophagus is empty of barium. Turn the table into horizontal position and fluoro. Take two (4-on-11 DC spot films of duodenal bulb (Fig, 39,A and B) and n~o of the duodenal loop when they fill with air (Fig 39,C and D). gastroesophageal 11. Observe for spontaneous reflux as ,you turn patient into FM0 position. 12. Increase kVp to I -20-125. Observe esopha geal motility and look for lesions while p latient drinks sevet -al swallows of (noncarbonated) barium through a straw. Take one (2-on-l) SCGIC spot j2m of the bariun n-

.

FIG 40. Curr

Prohl

Diagn

Radial,

November/Decembet~

1987

305

13. Overhead films (120-125 kVp): Have the technician take one PA 14" X 17" of abdomen (Fig 41) and one right lateral 10” X 12” film of stomach, if necessary (see step 8, Fig 36).

APPENDLX

B

The recipe for a low-viscosity, medium-density (96.8% W/V, specific gravity 1.821 barium suspension designed for the biphasic-contrast technique is given in Table 4.73 A 1-L soda syphon* is filled with 1,000 ml of the mixture and refrigerated overnight (Fig 42). Refrigeration is essential because CO, gas will not dissolve into the suspension in sufficient quantities at room temperature. On the morning of the examination, the syphon is shaken vigorously for about ten minutes to resuspend its contents. The gas of one CO2 cartridge is then infused into the syphon to create bubbly barium, and the suspension is ready to use. The syphon must be shaken each time the bubbly barium is dispensed. When dispensed, bubbly barium dissociates in about 90 seconds and produces a volume that is approximately one third barium suspension and two thirds CO, gas (Fig 43). It is recommended that the soda syphon be in the fluoroscopy room when dispensing the carbonated barium suspension and that the patient drink the bubbly barium mixture as quickly as possible (see Fig 43). A 1-L syphon is sufficient for about six biphasic-contrast studies. If refrigerated between examinations or overnight, the bubbly barium will not dissociate in the syphon. The suspension is easy to prepare and, in our experience, is better tolerated by patients than an effervescent agent and a barium suspension given separately.

Kidde

*Soda King, Model Inc., 139 S. Third

100 Home Soda-Fountain Street, Mebane, NC.

FIG 41.

Syphon.

FIG 42. One

306

liter soda

syphon

Curr

with

Rob1

cartridges

Diagn

Radial,

for CO,

infusion

November/December

198i

3. Vilardell

Bockus

S: Gastritis,

in

Gastroenterology,

Berk ed

JE (edI: Gastroenterology. 4. Philadelphia, WI3 Saun-

ders Co, 1985, vol 2. 4. Taor RE, Fox B, Ware J, et al: Gastritis: Gastroscopic macroscopic. Endoscopy 1975; 7209. 5. Op den Orth JO, Ploem S: The standard biphasic-contrast gastric series. Radiology 1977; 122:530. 6. Op den Orth JO: The Standard Biphasic-Contrast

and

Ex:amination of the Stomach and Duodenum. Method, Results, and Radiological Atlas. The Hague, Martinus

FIG 43. Carbonated being given

barium is dispensed to the patient

TABLE Recipe

4. for Barium

from

Suspension

syphon

IOne

Baruspemt E-Z-H-I)+’ MC methylcellulose solution Mylicon drops (antiflatulent)’ Add water to

Immediately

before

Lancet 1956; 21543.

Liter)’ 18.

FC, Coghill NF: Aetiological factors in chronic gastritis. Br Med J 1966; 2:1409. 19. M, Varis K, Wiljasalo M: Studies of patients with gastritis: A lo-15 year follow-up. Stand J Gastroenterol 1966; 1:40. 20. Lees F, Granjean LC: The gastric and jejunal mucosa in healthy patients with partial gastrectomy. Arch Intern Med 1958; 101~943. 21. McFadyen IJ, Goldberg A, Dagg GH, et al: Incidence 01 gastric parietal cell antibody in families of patients with iron deficiency anemia. Br J Hematol 1966; 12:697.

740 pn

13% cups1 270 gmw3 cup1 100 ml ti ml 1,000 ml

‘From dr Lang EE, shtier HA: Barium suspension formulation for use with bubbly barium method. Radiolop 19R5: 154:8X Used by permission. tMallin&mdt, Inc., St. Louis, MO ++E-Z-EM Co.. Inc., W&bun/. NY. “Stuari Pharmaceuticals. Wilmington,

Nijhoff, 1979. 7. Maglinte DDT, Miller RE: Upper gastrointestinal radiology under threat. AJR 1984; 142:847. 8. Frik W. Magen, in Schinz HR, Baensch WE, Frommhold W, et al (edsl: Lehrbuch der Riintgendiagnostik. Stuttgart, West Germany, Georg Thieme Verlag, 1965, vol 5. 9. Leeson CR, Leeson TS, Paparo AA: Textbook of Histologv, ed 5. Philadelphia, WB Saunders Co, 1985. 10. Weinstein WM: The diagnosis and classification of gashitis and duodenitis. J Clin Gastroenteroi 1981; 3:7. 11. Whitehead R. Mucosal Biopsy of the Gastrointestinal Tract. Philadelphia, WB Saunders Co, 1979. 12. Heilman K: Gastritis: Ursache und ,,Bedeutung. Fortschritte der Medizin 1976; 94:1879. 13. MacDonald WC, Rubin CE: Gas& biopsy: A critical evaluation. Gastroenterology 1967; 53;143. 14. Palmer ED: The morphological consequences of acute gastroenteritis on the gasexogenous (Staphylococcus) tric mucosa. Gastroenterologv 1951; 19:462. 15. Pastore G, Schiraldi G, Tera G, et al: A bioptic study 01 gastrointestinal mucosa in cholera patients during an epidemic in southern Italy. An J Dig Dis 1976; 21:613. 16. Jones FA ted): Modern Trends in Gastroenterology. London, Butterworths, 1952, p 323. 17. Edwards FC, Edwards JH: Tea-drinking and gastritis.

Del

Edwards atrophic Siurala atrophic

22. Hradsky

M, Groh J, Langr F, et al: Histological

and his-

tochemical

Acknowledgments 23.

The author wishes to thank Dr. Hubert A Shaffer, Jr., for reviewing the manuscript; Dr. Robert E. Fechner for providing the histologic illustrations and reviewing the pathologic content; Dr. Carol Chowdhry for editorial assistance; Geneva Shifflett for preparing the manuscript; and Ursula Bunch for the photographs.

Ursache und Bedeuting. 1976; 94:1879. 2. Heinkel I(, Von Gaisberg U: Die chronische Gastritis der Sicht des Klinikers. Arh Soz Praelentive Med

schritte

K:

26.

Gastritis:

Fort-

disease: A study of patients troscopy. Ann Clin Res 1981;

der Medizin

9384. Cur-r Probl

25.

27.

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