REVIEWS OF INFECTIOUS DISEASES • VOL. 12, NUMBER 5 • SEPTEMBER-OCmBER 1990 © 1990 by The University of Chicago. All rights reserved. 0162-0886/90/1205-0019$02.00

REVIEW ARTICLES

Emphysematous Gastritis: Case Report and Review

Ali R. Moosvi, Louis D. Saravolatz, Dominic H. Wong, and Stuart M. Simms*

From the Divisions of Infectious Diseases and Gastroenterology and the Department of Radiology, Henry Ford Hospital, Detroit, Michigan

Emphysematous gastritis is a condition involving gastric wall inflammation, radiologic or intraoperative evidence of intramural gas, and systemic toxicity. A recent case of emphysematous gastritis in a 57-year-old diabetic man is reported, and 27 cases published since 1889 are reviewed. Predisposing factors include ingestion of corrosive substances (37070) and alcohol abuse (22070). Diagnosis of emphysematous gastritis is based on the clinical presentation of an acute abdomen with systemictoxicity and on radiographs demonstrating gas bubbles within the stomach wall. For the case reported herein, computed tomography was useful both in establishing the diagnosis and in following the resolution of emphysematous gastritis. Organisms most commonly involved were Escherichia coli (six cases), Streptococcus species (six cases), Enterobacter species (five cases), and Pseudomonas aeruginosa (three cases). The mortality was 61070 (17 of 28 patients), and morbidity with gastric contractures occurred in 21070 of cases (6 of 28). Optimal therapy has not been defined; however, antimicrobial chemotherapy and surgery, when appropriate, may improve survival rates.

Case Report

Emphysematous gastritis is a rare, lethal infection of the gastric wall caused by gas-producing organisms. Since Fraenkel's description of this entity in 1889 [1], 27 cases have been reported in the Englishlanguage literature [2-26]. Fraenkel reported a young man who died after severalattacks of severeabdominal pain, blood vomitus, and diarrhea. At autopsy, rod-like organisms and multiple gas vesicles were found in the stomach wall. From the time of Fraenkel's report until the present, there has been some confusion about the definition of emphysematous gastritis. In this article, we report a case and suggest a new definition. In addition, we review the literature and compare this condition with others that involve gas collections in the stomach wall.

A 57-year-old obese man with a history of alcohol abuse, hypertension, diabetes mellitus, and Charcot's joints was admitted to the hospital with complaints of fever, chills, painless swelling,and redness of both ankle joints. His temperature was 39.1°C; abdominal examination was unremarkable, and rectal examination revealed guaiac-negative brown stool. Both ankles were swollen and red, and the overlying skin was ulcerated with a foul-smelling, purulent discharge. The white blood cell count was 6,900/mm 3 (290/0 polymorphonuclear leukocytes, 43 0J0 band forms), and the hemoglobin level was 11.8 g/dL. Purulent material was aspirated from both ankle joints. Cultures of the joint aspirates and blood yielded f3-lactam-sensitive Staphylococcus aureus. The patient's condition worsened despite the administration of nafcillin (12 g/d) and cefoxitin (12 g/d). He became lethargic and developed bilateral wheezing and a respiratory rate of 38. An arterial blood gas determination disclosed the following values: Pao; 69 mm Hg; Pacoj, 37 mm Hg; and pH, 7.35. The lactic acid level in the blood was 2.7 mM. A below-the-knee amputation was performed on the right side on day 2 and on the left side on day 4. Postoperatively, the patient was ventilator-dependent for 7 days.

Received for publication 10 March 1989 and in revised form 5 January 1990. The authors thank Dr. Wilmer Rutt (Internal Medicine), Dr. Gary Talpos (General Surgery), and Dr. Michael Alpern (Radiology) for their improvement in the management of our patient. Weare also indebted to Ms. Linda Jasina and Ms. Elaine Graybar for their expert secretarial help. • Deceased. Please address requests for reprints to Dr. Louis Saravolatz, Division of Infectious Diseases, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202. 848

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Figure 2. Abdominal CT performed on day 15 reveals gas in the stomach wall and a large soft-tissue mass with the appearance of an abscess (arrows). Figure 1. An abdominal radiograph reveals a large collection of air (arrows) lining the proximal gastric wall; however, smaller air bubbles (mottled areas) are also evident.

The patient continued to be febrile. On day 11 his temperature rose to 39.8°C. He became stuporous and developed abdominal distention, epigastric tenderness, and hypoactive bowel sounds. The hemoglobin level dropped to 7.5 g/dL. The CSF obtained by lumbar puncture was normal. The patient developed respiratory insufficiency with arterial blood gas levels as follows: Pao., 48 mm Hg; Paco., 67 mm Hg; and pH, 7.20. He was intubated and transferred to the intensive care unit for the management of septic shock. Abdominal radiographs (figure I) showed an irregular collection of gas bubbles lining the proximal gastric wall, and a diagnosis of emphysematous gastritis was made. The antibiotic regimen was changed to vancomycin (2 g/d), rifampin (600 mg/d), and clindamycin (1.8 g/d), An upper-gastrointestinal series done with water-soluble contrast material confirmed the intramural nature of the gas. The gastric mucosa was irregular and scalloped. A IS-em mass was present along the posteroinferior aspect of the proximal end of the stomach. There was no extravasation of the contrast material. The chest radiograph showed no infiltrates. Computed tomography (CT) of the head demonstrated mild to moderate generalized atrophy. The patient developed a rash, and the antibiotic regimen was changed to tobramycin (660 mg/d) and imipenem-cilastatin (2 g/d), CT of the abdomen on day 15(figure 2) disclosed gas lining the stomach wall and a large soft-tissue mass containing a few gas bubbles. This finding was

consistent with the appearance of an abscess. The nasogastric aspirate contained Enterobacter aerogenes, Enterobacter cloacae, and Candidaalbicans. The patient was managed conservatively, as surgery was considered a high risk. On day 20 the gastric aspirate suddenly increased in amount and became purulent and hemorrhagic. The organisms on multiple aspirate cultures were E. aerogenes, E. cloacae, C. albicans, and, later, Escherichia coli and Pseudomonas aeruginosa. The patient started improving and became more alert; his temperature decreased to 38.2°C, bowel sounds reappeared, and abdominal tenderness decreased. CT of the abdomen on day 25 (figure 3) showed a decrease in the amount of intramural gas and dis-

Figure 3. Abdominal CT performed on day 25 reveals that the abscess wall is no longer present, thereby supporting the clinical impression that the abscess drained into the gastric lumen. However, gastric fluid (arrows) is seen within the stomach.

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appearance of the mass, thus supporting our suspicions that the abscess had spontaneously drained into the gastric lumen. Upper-gastrointestinal endoscopy on day 27 revealed a large area of whitish exudate, consistent with coagulation necrosis, along the greater gastric curvature. This area was sharply demarcated from the surrounding erythematous, cobblestone-like mucosa. The antrum was normal. A gastric biopsy was not performed because the risk of perforation was believed to be excessive.The patient continued to have low-grade fevers, and cultures of the nasogastric aspirate repeatedly yielded previouslyisolated organisms despite adequate antibiotic therapy. An indium scan was performed on day 35 in a search for other foci of infection. Increased activity was seen in the distal extremities and right lower quadrant of the abdomen but not in the stomach itself. CT of the abdomen on the same day demonstrated no intraabdominal abscess but showed persistence of the gastric air. On day 44 the patient had a laparotomy since it was believed that sequestered infection in the gastric wall could not be eradicated with antibiotic therapyalone. The proximal end of the stomach appeared inflamed and was adherent to the spleen. The gallbladder was enlarged and inflamed. Subtotal gastrectomy, splenectomy, and cholecystectomy were performed. The resected gastric tissue appeared necrotic, with pockets of gas and pus. The microscopic appearance was that of extensive mucosal necrosis with submucosal microabscesses and gramnegative rods, and many clear spaces presumably containing gas were noted in the necrotic mucosa and submucosa. A gastric swab culture yielded R aeruginosa, C albicans, nonhemolytic Streptococcus, and Corynebacterium, whereas culture of the gallbladder yielded C albicans and anaerobic streptococci. Amphotericin B was added to the antibiotic regimen, and a total dose of 2 g was administered over a period of 3 weeks. The patient gradually improved and was finally discharged on day 105. Methods

Case definition. Emphysematous gastritis was defined as a condition involving gastric wall inflammation, radiographic or intraoperative evidence of intramural gas, and systemic toxicity. We did not in-

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elude patients with phlegmonous gastritis, as they lack evidence of intramural gas. Data identification and selection. Our review method was based on the suggestions made by Mulrow [27]. We reviewed all English-language articles dealing with emphysematous gastritis, from the first case report in 1889to the present (table 1). Our main data base was compiled from a computer-assisted search of MEDLINE. We then cross-checked these data with the references in the articles and with data bases such as the Science Citation Index and the Excerpta Medica. Validity assessment. We assessed the validity of each diagnosis on the basis of our definition of emphysematous gastritis. We concluded that the case reported by Farfel and Eichhorn [25] might be better termed phlegmonous gastritis. Meyers and Parker [12], in their review in 1967, assessed the cases reported by Dassel [26] and by Roy and associates [28] as emphysematous gastritis. However, as Dassel and Roy et al. correctly reported, their cases involved gastric infarction and corrosive gastritis, respectively. On the other hand, what Morton and Stabins [2] called phlegmonous gastritis and Berry et al. [9] called corrosive gastritis could be better renamed emphysematous gastritis. There are certain limitations to a review that includes cases from as far back as 1889.Only one-third of the 28 cases of emphysematous gastritis occurred in an era in which modern microbiologic techniques were available. Gastric contents were not cultured in all cases. In fact, anaerobic cultures did not become commonplace until the 1960s [29]. Therefore, in the early reports, anaerobic organisms, though probably involved, were not identified. On the other hand, emphysematous gastritis could be diagnosed on the basis of clinical presentation and an abdominal roentgenogram. Unfortunately, information regarding culture techniques is mentioned in only one previous case report. In our patient, cultures for aerobic bacteria were performed with chocolate, blood, Columbia colistin-nalidixic acid, and MacConkey agar media. The aerobic culture plates wereincubated under ambient conditions. Specimens were collected with the use of an anaerobic transport device (Vacutainer; Becton-Dickinson, Cockeysville, Md.) and placed on plates with bacteroides-bile-esculin, reduced phenylethyl alcohol, and reduced and nonreduced enriched

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Table 1. Reported cases of emphysematous gastritis, 1889-1990. [Reference] Age*/sex year

Predisposing factor(s)

Isolated organism(s) (source)

Comments; outcome Died Died First use of abdominal radiograph, contracture; died First use of VGI

[1] 1889 [2] 1928 [3] 1946

351M 121M 371M

Gastroenteritis Surgery for perforated duodenal ulcer Hydrochloric acid ingestion, alcohol abuse

Rodlike organism Clostridium perfringens (St) Proteus mirabilis (Asp), E. aerogenes (BId), E. coli (Abs)

[4] 1947

151F

Gastroenteritis

[5] 1952 [6] 1963

I mo/M 61/M

Gastroenteritis Surgery for gastric ulcer, alcohol abuse

E. coli, nonhemolytic streptococci, S. aureus (Asp) E. coli (St) P. aeruginosa, E. aerogenes, nonhemolytic streptococci (Asp)

[6] 1963

44/M

[7] 1965 [8] 1966 [9] 1965 [10] 1966

44/F 63/F 44/F 44/F

Surgery for perforated gastric ulcer, alcohol abuse Hydrochloric acid ingestion Adenocarcinoma with ulceration Hydrochloric acid ingestion Hydrochloric acid ingestion

[11] 1967 [12] 1967

70/F 58/M

Surgery for intestinal obstruction Ammonia ingestion

[12] 1967

14/F

Hydrochloric acid ingestion

[12] 1967

59/F

Sodium hydroxide and sulfuric acid ingestion

[13] [14] [15] [16] [17] [18] [19] [20] [21]

74/M 31 mo/M 39/F 45/M 82/F IO/F 16 mo/M 67/F 121M

1968 1968 1969 1973 1975 1976 1977 1977 1982

E. coli, P. mirabilis (PF) C. perfringens (Asp)

a-Hemolytic streptococci, E. coli, C. perfringens (St, PF, liver) Bacillus subtilis (PF) P. aeruginosa, S. aureus, Proteus vulgaris (PF) Streptococcus viridans (BId), P. vulgaris, Enterobacter species (GF, PF)

Necrotic cast; died Gas in portal vessels; died Contracture, gastric sinus tract; died Died

Died

E. coli (St)

Phytobezoar Potassium hydroxide ingestion Alcohol abuse

E. aerogenes (PF)

[22] 1984 [23] 1986 [24] 1987

4 mo/M 331M 41/M

Leukemia, sepsis, chemotherapy, steroids Zinc chloride ingestion Sodium hydroxide ingestion Lymphoma, chemotherapy, disseminated strongyloidiasis Gastroenteritis (?), malnutrition Darvocett overdose, alcohol abuse Acute hemorrhagic pancreatitis, sepsis

[PR] 1990

57/M

Diabetes mellitus, alcohol abuse

NOTE. St = stomach; Asp = aspirate; BId = blood; Abs GF = gastric fluid. * Ages are in years unless otherwise indicated. t Eli Lilly, Indianapolis.

Died Necrotic cast, contracture Necrotic cast, contracture

Strongyloides stercoralis

Clumps of gram-positive cocci (St) Klebsiella pneumoniae, Streptococcus faecalis, Bacteroides species E. aerogenes, E. cloacae, C. albicans, P. aeruginosa (St), nonhemolytic and anaerobic streptococci

= abscess;

blood agar media. Anaerobic culture plates were incubated at 35°C, and organisms were identified with the use of prereduced anaerobic sterile media and gas-liquid chromatographic methods devised by Virginia Polytechnic Institute (Blacksburg, Va.).

VOl

=

Gas in vessels; died Died Contracture Left gastric arteriogram Died Died Died Contracture Died Died First use of CT First gastroscopy; died Gastric abscess, gastroscopy, indium scan

upper-gastrointestinal series, PF

=

peritoneal fluid;

Discussion

Etiology and pathogenesis. The normal stomach, with its generous blood supply, acidity, and mucosal barrier, is well protected against infection.

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Under certain circumstances these barriers may be overwhelmed. Mucosal injuries and their possible causes include liquefaction necrosis produced by alkalis, coagulation necrosis produced by acids, and alteration in the mucosal barrier produced by alcohol [30, 31]. One can postulate that organisms first start growing within the gastric lumen and then enter the stomach wall through a mucosal erosion or ulceration. It is unclear whether hematogenous spread of infection to the gastric wall occurs. The organisms may then localize to any layer, proliferate, and produce gas. Specimens from the stomach wall itself have been cultured in only five cases of emphysematous gastritis [2, 5, 10, 14, 21]; usually only the nasogastric aspirate has been cultured. Most frequently isolated in the 28 cases reviewed herein were streptococci (six cases) and organisms of the family Enterobacteriaceae, namely, E. coli(sixcases)and Enterobacter species (five cases). Other organisms included R aeruginosa (three cases) and Clostridium perfringens (three cases). It is possible that ingestion of corrosive substances, antacids, or H2 antagonists, in addition to the normal aging process, may alter gastric acidity and predispose to bacterial colonization. In the current series, information regarding the use of antacids and H2 antagonists is lacking. Five (50070) [3, 7, 10, 12]of the 10patients with a history of corrosive substance ingestion and three (50070) [2, 11, 21] of the six patients over the age of 65 years had gastric contents colonized with bacteria. Predisposing factors. Age and sex are not predisposing factors of emphysematous gastritis. Ingestion of corrosive substances, the commonest predisposing factor, was reported in 10 cases (37070). Acid was ingested by six patients [3, 7, 9, 10, 12, 19],alkali by three [12, 15, 20], and both by one [12]. A history of alcohol abuse was noted in six cases (22070), including our own [3, 6, 16,23]. Recent abdominal surgery [2, 6, 11] and gastroenteritis [1, 4, 5, 22] were involved in four cases (15070) each. There were isolated reports of phytobezoar [14], adenocarcinoma of the stomach [8], leukemia [18], acute hemorrhagic pancreatitis [24], and disseminated strongyloidiasis (in a patient with lymphoma who was receiving chemotherapy) [21]. Our patient was the only one who had a history of diabetes mellitus. Clinicalfeatures. An acute abdomen usually develops 1 week after the initiating cause. However, the onset may vary from a few hours to as long as 6 weeks. Patients typically develop abdominal pain,

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diarrhea, nausea, vomiting, and occasionally hematemesis and melena. On examination the patients are febrile, toxic, and in some cases in profound shock. Abdominal examination reveals epigastric tenderness, distension, and decreased bowel sounds. A necrotic cast of the stomach mucosa was passed in three cases [6, 8]. In the first case, it was found attached to the gastrostomy tube when the latter was removed; in the second case, the patient vomited the cast; and in the third case, necrotic tissue appeared in the gastric aspirate. The hematologic profile usually reveals leukocytosis with a left shift. Diagnosis. Emphysematous gastritis is diagnosed on the basis of clinical features and the typical appearance on abdominal radiographs. These usually demonstrate tiny gas bubbles and mottled shadows conforming to the contour of the stomach wall, especially around the fundus and the greater curvature. Unlike intraluminal air or fluid, this gas remains constant with positional change. Six patients had gastric dilatation accompanying emphysematous gastritis [4, 13, 17, 19, 22, 23]. An upper-gastrointestinal series confirms the extraluminal collection of gas. The rugae are thickened, and the mucosa has a cobblestone appearance due to submucosal blebs. At times, the contrast material extravasates into the stomach wall where the gas is collected. Berens et al. [13] described a case in which radiographs obtained with Gastrografin contrast material (Squibb, Princeton, N.J.) revealed"several thin, branching lucent shadows representing intravascular air within the liver and possibly within small vessels in the gastric wall." This finding was confirmed at autopsy. Kinkhabwala et al. [16] performed a left gastric arteriogram that demonstrated a "hypertrophied left gastric artery with enlarged arterial tributaries during the arterial phase and intense capillary blush and enlarged draining veins during the venous phase." This increased vascularity is similar to that found in other inflammatory conditions such as tuberculosis but is not characteristic of adenocarcinomas, which are poorly vascularized. The first instance of the use of abdominal CT for emphysematous gastritis was reported by de Lange et al. [23]. They stated that CT may aid in diagnosing mild cases in which only a small amount of gas exists. Tomograms "may especially help in differentiating gastric emphysema from emphysematous gastritis, since they much better demonstrate gastric wall thickening, which is only seen in the latter [condition]," they noted. OUf patient's condition dictated

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the repeated use of CT. These scans demonstrated irregularly thickened gastric walls containing gas bubbles. In our patient, CT revealed a large softtissue mass suggestive of an abscess arising from the gastric wall; this abscess later drained into the gastric lumen. An indium scan, a diagnostic tool not previously reported in cases of emphysematous gastritis, was done in our case. While the scan did not demonstrate increased uptake of indium in the stomach (even though there was active inflammation), it did show increased uptake in the right lower Quadrant, where the presence of an abscess was suspected. However, neither CT of the abdomen nor a laparotomy confirmed this suspicion. Therefore, the indium scan did not assist in confirming either the presence or the absence of emphysematous gastritis. This lack of utility could be explained by the fact that the proximal portion of the stomach overlies the spleen, which normally shows a nonspecific, increased uptake of indium-tagged red cells. Upper-gastrointestinal endoscopy was attempted in many previously reported cases, but corrosive damage to the esophagus prevented the stomach from being visualized during the acute phase of emphysematous gastritis. Bloodworth et al. [24]recently reported a case of emphysematous gastritis after acute pancreatitis in which gastroscopy was performed 4 days before the typical appearance of this condition on abdominal radiographs. The patient was found to have "multiple gastric erosions and a large clot adherent to the posterior wall of the gastric fundus." Endoscopy, including gastric visualization, was performed in the case reported herein. Initially, greenish-brown gastric fluid, debris, and necrotic tissue were aspirated. After lavage of the stomach, an area of whitish exudate - presumably from coagulation necrosis - could be seen near the greater curvature and the fundus. It was over the area of the suspected abscess, which was thought to have drained into the gastric lumen. This area of whitish exudate was clearlydemarcated from the surrounding mucosa, which appeared slightly erythematous and had a cobblestone appearance. Differentialdiagnosis. Emphysematous gastritis should be differentiated from other causes of gas collection within the gastric wall. There are two methods by which gas can collect within the stomach wall: by entering from the mucosal or serosal surfaces (gastric emphysema) or by being formed within (emphysematous gastritis).

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In gastric emphysema, air enters the stomach wall from the lumen, from the peritoneal surface, or from its connections with the esophagus and duodenum. This air is not produced by organisms within the gastric wall. There are three etiologic varieties of gastric emphysema: traumatic (tears), pulmonary (ruptured bleb), and obstructive (increased intragastric pressure). The prognosis is excellent in the first two conditions with nonsurgical management. In the obstructive variety, the cause and the duration of the obstruction determine the outcome. The clinical features of an acute abdomen in patients with emphysematous gastritis are usually absent in patients with gastric emphysema. The terms cysticpneumatosis and pneumatosisintestinalis refer to the presence of gas in the intestines. The stomach is the least common site of such gas. Kussin et al. [32] rightly suggested that "most, if not all, cases of cystic pneumatosis of the stomach can be better placed in the category of gastric emphysema (obstructive or pulmonary)." Another clinical entity to be distinguished from emphysematous gastritis is phlegmonous gastritis. This is a condition in which the gastric wall is inflamed in the absence of intramural gas. Prognosis. Mortality due to emphysematous gastritis is high. Seventeen (61 0J0) of the 28 patients died (table 1). One would expect that advances in antimicrobial therapy and aggressive supportive measures would have altered mortality in the recent past. However, the 55070 mortality due to emphysematous gastritis in the past two decades is not significantly different from the 65070 mortality observed before 1968(P> .05, Fisher's exact test). Six patients (21070) [3, 6, 12, 15, 19] developed contractures and strictures of the stomach, especially if a corrosive agent was ingested. Meyers and Parker [12] reported a case of gastric sinus-tract formation observed on uppergastrointestinal series. Management. The management of emphysematous gastritis has not been studied in a systematic manner; therefore, one cannot conclude that any specific approach is preferable to another. General principles governing the care of patients with acute intraabdominal infectious processes should be followed. The most important factor affecting outcome is probably the initial stabilization of the patient, which should be achieved by means of aggressive measures similar to those used in cases of septic shock. Intravenous fluids and nutritional support form the basis of therapy. Early institution of an-

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tibiotic therapy should help in limiting the extension of infection, and empiric therapy should include antimicrobial agents that are active against gramnegative and anaerobic bacteria. Specific therapy should be modified according to the results of the gastric fluid culture and sensitivity testing of the isolated organisms. Therapy directed against gramnegativeand anaerobic bacteria should continue even if these pathogens are not isolated, as they could be present intramurally without appearing in the gastric fluid. The patient's associated medical problems should be corrected if possible. During the acute phase of emphysematous gastritis, surgery should be delayed, as healing of the sutured stomach margins in the presence of active infection is poor. A major indication for emergency surgery is perforation. In those cases in which the disease is localized to a small area and the patient improves with medical therapy, surgery may be deferred until strictures actually develop. If laparotomy is performed, the stomach may appear grossly normal, inflamed, scarred, contracted, or adherent to the adjacent structures, depending on the stage of the disease. On palpation, the diseased stomach feels mushy or sounds crepitant. Microscopic evaluation in the early stages shows inflammation, mucosal erosions, and partial- or full-thickness necrosis. Collections of gas vesiclesmay appear in any or all layers of the gastric wall. In some cases pockets of pus or even an abscess may be present.

Summary Emphysematous gastritis is a clinical entity with various predisposing factors and pathologic organisms. It is characterized by the presentation of gas in the stomach wall with potentially serious consequences. This condition should be suspected in patients who have a history of ingestion of corrosive substances, develop an acute abdomen, and have evidence of gas on abdominal radiographs. CT with water-soluble contrast material should be performed to confirm the intramural nature of the gas..CT will also help in diagnosing the presence of an intraabdominal abscess, including that arising in the stomach due to emphysematous gastritis. If CT can be performed, no additional useful information will be obtained from an upper-gastrointestinal series. Patients should be managed with intravenous fluids and nutritional support. Antibiotics' effective against gram-negative and anaerobic organisms

should be used. More specific antibiotic therapy should be administered according to the results of the nasogastric aspirate culture. Once the patient has stabilized, surgery should be considered. If the stomach is resected, a specimen of the resected tissue should be cultured. On the basis of previously reported cases, mortality due to emphysematous gastritis is high (61070). Increased awareness of this entity would lead to early diagnosis, prompt antibiotic therapy, and appropriate surgical intervention after stabilization and might ultimately improve survival rates.

References

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18. Rowen M, Myers M, Williamson RA. Emphysematous gastritis in a leukemic child. Med Pediatr OncolI976;2:433-7 19. Jensen AR, Rodgers BM. Emphysematous gastric secondary to acid ingestion in an infant. J Fla Med Assoc 1977;64: 484-7 20. Bernardino ME, Lawson TL. Emphysematous gastritis and gastric perforation. An unusual manifestation of alkaline corrosive ingestion. Gastrointest Radiol 1977;2:107-8 21. Williford ME, Foster WL Jr, Halvorsen RA, Thompson WM. Emphysematous gastritis secondary to disseminated strongyloidiasis. Gastrointest Radiol 1982;7:123-6 22. Udassin R, Aviad I, Vinograd I, Nissan S. Isolated emphysematous gastritis in an infant. Gastrointest Radiol 1984;9:9-12 23. de Lange EE, Slutsky VS, Swanson S, Shaffer HA Jr. Computed tomography of emphysematous gastritis. J Com put Assist Tomogr 1986;10:139-41 24. Bloodworth LL, Stevens PE, Bury RF, Arm JP, Rainford DJ. Emphysematous gastritis after acute pancreatitis. Gut 1987;28:900-2 25. Farfel B, Eichhorn R. Emphysematous gastritis. Am J Gastroenterol 1955;25:125-30

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26. Dassel P. Roentgen demonstration of gangrene of the stomach and intestine: a late finding in infarction of the gastrointestinal tract. AJR 1964;91:819-25 27. Mulrow CD. The medical review article: state of the science. Ann Intern Med 1987;106:485-8 28. Roy M Jr, Calconje MA, Mouton R. Corrosive gastritis after formaldehyde ingestion. Report of a case. N Engl J Moo 1962;266:1248-50 29. Finegold SM. Anaerobic bacteria in human disease. NewYork: Academic Press, 1977:71 30. Loeb PM, Eisenstein AM. Caustic injury to the upper gastrointestinal tract. In: Sleisenger M, Fordtran J, eds. Gastrointestinal disease: pathophysiology, diagnosis, management. 3rd ed. Philadelphia: W.B. Saunders, 1983:148-9 31. Ivey K, Roth J. Drug and chemical-induced injuries of the stomach. In: Berk JE, ed. Bockus gastroenterology. 4th ed. Vol. 2. Philadelphia: W.B. Saunders, 1985;975-1003 32. Kussin SK, Henry C, Navarro C, Stenson W, Clain DJ. Gas within the wall of the stomach. Report of a case and review of the literature. Dig Dis Sci 1982;27:949-54