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Emphysematous gastritis in a hemodialysis patient. (Case Report).

Abstract: Emphysematous gastritis is a condition characterized by gas within the wall of the stomach and associated systemic toxicity. We report a case of emphysematous gastritis in a 43-year-old diabetic patient receiving hemodialysis and review 41 cases published since 1889. The most common predisposing factors included ingestion of corrosive substances, alcohol abuse, abdominal surgery, diabetes, and immuno-suppression. Diagnosis is based on clinical presentation of acute abdomen with associated features of systemic toxicity. The most commonly involved organisms were streptococci (nine cases), Escherichia coli (nine cases), Enterobacter species (six cases), Clostridium welchii (four cases), and Staphylococcus aureus (four cases). Computed tomography (CT) is the diagnostic procedure of choice. The mortality rate was 61% (25 of 41 patients). Gastric contractures after recovery were noted in 10% (4 of 4l patients). Antimicrobial therapy with antibiotics covering gram-negative organisms and anaerobes, and surg ery in appropriate cases may enhance survival.

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Emphysematous gastritis is characterized by air in the wall of the stomach due to invasion by gas-forming microorganisms. This entity is rare, with only 41 cases reported so far in the English-language literature. Because emphysematous gastritis is a lethal condition, early diagnosis and early treatment with antibiotics and surgery are necessary to avoid adverse outcome. We report a case of emphysematous gastritis diagnosed by performing computed tomography (CT) in a patient who was receiving hemodialysis. Our case is unique because this condition has not previously been reported in a hemodialysis patient.

Case Report

A 42-year-old white woman who was receiving hemodialysis for chronic renal failure due to diabetic nephropathy was discharged to home after being treated for bacteremia caused by Staphylococcus aureus. Two days after discharge, the patient presented with upper abdominal pain and fever. She was slightly lethargic and denied any diarrhea, melena, hematochezia, nausea, vomiting, or hematemesis.

On physical examination, the patient was drowsy, with a temperature of 39 [degrees]C (102.2[degrees]F), heart rate of 92 beats/mm, and respiratory rate of 22/mm, but she was normotensive and in no acute distress. The cardiopulmonary examination was unremarkable. Abdominal examination revealed severe tenderness in the epigastrium and left upper quadrant, with no rebound, rigidity, or masses. Rectal examination showed no evidence of occult blood.

A complete blood count revealed a hematocrit value of 35% and white blood cell count of 31,400/[mm.sup.3] with 81% polymorphonuclear neutrophils and 10% band forms. The SMA-18 reflected chronic renal insufficiency, with elevated levels of aspartate aminotransferase (149 U/L), alanine aminotransferase (119 U/L), and alkaline phosphatase (197 U/L). Amylase, lipase, and bilirubin levels were normal, and the lactic acid value was 2.3 mmol/L, which was the upper limit of normal range (0.5-2.2). Ultrasonography of the abdomen was performed in the emergency room and was unremarkable except for small kidneys. Worsening abdominal pain and metabolic acidosis prompted CT, which showed a markedly abnormal stomach with thickening of the wall and air in the submucosa (Fig. 1). A diagnosis of emphysematous gastritis was suspected. Endoscopy revealed a necrotic posterior wall of the stomach from the cardia down to the antrum with a clear line of demarcation and a normal esophagus and duodenum. An immediate total gastrectomy was performed. Treatment with vancomycin and gentamicin had been started at admission. All blood cultures, including those performed at admission, were negative, except for one sample from the tesio (ie, hemodialysis catheter), which grew a Staplylococcus species postoperatively, possibly a contaminant. The stomach cultures grew multiple Candida glabrata and few Candida krusei. The patient did remarkably well after surgery despite her multiple medical problems. Unfortunately, on the third postoperative day, she had severe he matemesis and signs of peritonitis thought to be due to an anastomotic leak at the gastrectomy site. The patient refused any further intervention, and she died the next day. Autopsy was not permitted.

Discussion

Emphysematous gastritis is a rare condition of air within the stomach wall usually produced by gas-forming organisms. Fraenkel (1) first described this entity in 1889. He described a 35-year-old man who had debridement for a crush injury and subsequently died after several episodes of hematemesis, abdominal pain, and diarrhea. Autopsy revealed multiple gas vesicles in the gastric wall along with multiple rodlike organisms seen with microscopic visualization. Since then, 41 cases of emphysematous gastritis have been reported in association with multiple organisms (Tables 1 and 2). (2-37) However, specimens from the stomach wall have been cultured in only 11 cases. (1,2,5-7,12,13,15,24,28,37) Nasogastric aspirate has been cultured in most cases. In our case, cultures of the stomach wall grew C. glabrata and C. krusei. The gastric wall is usually well protected from severe inflammatory processes because the mucosal barrier, acidic pH, and excellent blood supply make the gastric tissue resistant to invasion. An antecedent injury to the gastric mucosa can, however, predispose the patient to invasion of the gastric wall and subsequent gas formation. Such injuries might have a wide variety of causes, but ingestion of corrosive substances was found to be the most common predisposing factor, accounting for 10 cases(acid in 6 cases, (19,26,28,30,31,36) alkali in 3 cases, (18,23,26) and both in 1 case (26) ). A history of alcohol abuse was noted in 9 cases, (3,7,10,13,15,22,32,36) and 4 patients, including ours, were diabetic. (6,10,33) Our patient was receiving hemodialysis and had an episode of staph ylococcal bacterernia, both of which could have been additional predisposing factors. Gastroenteritis was noted in 4 cases, (1,16,34,35) and previous abdominal surgery was reported in 7 cases. (2,13,27,32,37) Four patients were noted to be immunosuppressed, which might have predisposed them to emphysematous gastritis. The causes of immunosuppression included leukemia, (20) lymphoma, (17) chemotherapy, (17,20) steroids, (2,6,20) cyclophosphamide, (2) and cyclosporine. (6) Other isolated reports included emphysematous gastritis in patients with Wegener's granulomatosis, (2) gastric infarction, (9) Coca-Cola ingestion, (8) cocaine use, (3) pancreatitis, (14) phytobezoar, (24) gastric adenocarcinoma, (29) disseminated stongyloidiasis, (17) and thoracic empyema. (4)

Clinical features include a toxic clinical presentation with fever, chills, abdominal pain, and sometimes hematemesis. Rarely, vomiting of a necrotic cast of the stomach occurs and is due to dissection along the plane of muscularis mucosa by the invading organisms. Physical examination reveals epigastric tenderness, distention, and decreased bowel sounds in some cases. Severe leukocytosis and metabolic acidosis due to sepsis are the usual laboratory findings. The liver enzymes and alkaline phosphatase may show nonspecific elevation in some cases. Amylase may be elevated in some cases of antecedent gastric infarction.

Emphysematous gastritis can be diagnosed by radiographic findings of irregular mottled strips of gas within the gastric wall, but review by an experienced radiologist is necessary. An upper gastrointestinal series can confirm the presence of extraluminal gas when it shows a cobblestone appearance due to submucosal blebs. Computed tomography is the best imaging modality in establishing the diagnosis, and diagnostic findings include the presence of gas bubbles in the stomach wall, mainly along the greater curvature. The characteristic feature of these gas bubbles is that they are not affected by changes in the patient's position. Endoscopy can be helpful in the diagnosis and usually reveals bubbles of gas beneath the gastric mucosa. This was not seen in our case. Our patient had endoscopic findings suggestive of gastric necrosis, which might have predisposed her to emphysematous gastritis. These findings of gastric infarction were also confirmed by both gross and pathologic examination of the stomach after gast rectomy. Biopsic specimens obtained at endoscopy may also provide a clue to the diagnosis of ischemia. An (111) In scan was obtained in one case, without significant diagnostic benefit. (11)

The differential diagnosis of emphysematous gastritis is gastric emphysema. The latter condition involves accumulation of gas within the stomach wall without infection. Gastric emphysema has been reported to occur in cases of increased intraluminal pressure in the stomach due to outlet obstruction, volvulus, small bowel obstruction, forceful vomiting, and tumors. It has also been reported after instrumentation, nasogastric tube insertion, and ingestion of alcohol, acid, alkali, and nonsteroidal anti-inflammatory drugs. Gastric emphysema is usually self-resolving and can be differentiated from emphysematous gastritis by the benign clinical picture and CT. Emphysematous gastritis should also be differentiated from phlegmonous gastritis, which is characterized by inflammation of the gastric wall in the absence of intraluminal gas. A CT scan can be helpful in differentiating these two conditions.

Management involves initial stabilization of the septic condition by vigorous fluid resuscitation and early antibiotic support. Initial antibiotic therapy should cover gram-negative organisms and anaerobes. On the basis of the results of nasogastric aspirate culture and blood cultures, other antibiotics may be added to this regimen if appropriate. If the involved area is small and the patient's condition stabilizes with initial antibiotic therapy, surgery can be deferred. Indications for emergency surgery include deterioration despite optimal medical management, involvement of a large portion or the entire stomach, presence of peritoneal signs, or gastric infarction. Specimens of the resected stomach should be cultured. Emphysematous gastritis has a grave prognosis with a high immediate mortality. Of the 41 reported patients, 25 died. Of the 16 patients who recovered, 10 required surgery and 6 recovered with conservative management. Four of the 16 patients who recovered later had gastric contracture.

Summary

Emphysematous gastritis is a rare but lethal clinical entity. It is characterized by the presence of air in the stomach wall due to invasion by gas-forming organisms. Multiple predisposing factors that can cause damage to the gastric mucosal barrier have been implicated in the pathogenesis of this condition. Computed tomography is the diagnostic procedure of choice. Initial management should include conservative measures such as IV fluids and parenteral nutrition. Initial antibiotic therapy should cover gram-negative organisms and anaerobes. More specific antibiotic therapy should be given according to the results of nasogastric aspirate. Stomach wall specimens should be cultured in appropriate cases. Emphysematous gastritis has a high mortality. Awareness of emphysematous gastritis is important for clinicians, because early diagnosis and prompt management may improve survival in some patients.
Table 1

Isolated organisms in emphysematous gastritis

Organism isolated No. of patients

Streptococci 9
Escherichia coli 9
Enterobacter species 5
Clostridium welchii 4
Staphylococcus aureus 4
Pseudomonas aeruginosa 3
Klebsiella species 3
Proteus mirabilis 2
Proteus vulgaris 2
Candida glabrata 2
Candida krusei 1
Candida albicans 1
Yersiuia sp 1
Corynebacterium sp 1
Strongyloides stercoralis 1
Group D enterococci 1
Bacteroides fragilis 1
Citrobacter freundii 1

Table 2

Reported cases of emphysematous gastritis, 1889-2000 (a)

 Age (yr)/
Series (ref. no.) sex

Fraenkel, 1889 (1) 35/M
Morton and Stabins, 1928 (37) 72/M
Ween, 1946 (36) 37/M

Welch and Jones, 1947 (35) 15/F

Henry, 1952 (34) 1 mo/M

Farfel and Eichhorn, 1956 (33) 76/M
Gonzalez et al, 1963 (32) 44/M

 61/M


Han et al, 1965 (31) 44/F
Berry et al, 1965 (30) 44/F
Smith, 1966 (29) 63/F
Fink and Boyden, 1966 (28) 44/F


Sawyer et al, 1967 (27) 70/F
Meyers and Parker, 1967 (26) 59/F

 14/F


 58/M

Berens et al, 1968 (25) 74/M
Lagios and Suydam, 1968 (24) 31 mo/M
Clearfield et al, 1969 (23) 39/F

Kinkhabwala et al, 1973 (22) 45/F
Weston, 1975 (21) 82/F
Rowen et al, 1976 (20) 10/F

Jensen and Rodgers, 1977 (19) 16 mo/M
Bernardino and Lawson, 1977 (18) 67/F
Williford et al, 1982 (17) 72/M

Udassin et al, 1984 (16) 4 mo/M
de Lange et al, 1986 (15) 33/M
Bloodworth et al, 1987 (14) 41/M


Williamson et al, 1989 (13) 28/F
 491M
Monteferrante and Shimkin, 1989 69/F
 (12)
Caruana et al, 1990 (11) 54/F
Moosvi et al, 1990 (10) 57/M







Binmoeller and Benner, 1992 (9) 72/F
Hadas-Halpren et al, 1993 (8) 16/M
McKelvie and Fink, 1994 (7) 76/M
Van Allan et al, 1995 (6) 42/M

Lin et al, 1995 (5) 58/M



Sud et al, 1996 (4) 42/M
Bashour et al, 1998 (3) 77/M

Chemey et al, 1999 (2) 69/M


Yalamanchili and Cady, 2003 42/M
 (present study)


Series (ref. no.) Predisposing factors

Fraenkel, 1889 (1) Gastroenteritis
Morton and Stabins, 1928 (37) Sx for perforated duodenal ulcer
Ween, 1946 (36) Hydrochloric acid ingestion,
 alcohol abuse
Welch and Jones, 1947 (35) Gastroenteritis

Henry, 1952 (34) Gastroenteritis

Farfel and Eichhorn, 1956 (33) Diabetes mellitus
Gonzalez et al, 1963 (32) Gastric ulcer Sx, alcoholism

 Alcohol abuse, Sx for perforated
 gastric ulcer

Han et al, 1965 (31) Hydrochloric acid ingestion
Berry et al, 1965 (30) Hydrochloric acid ingestion
Smith, 1966 (29) Ulcerated adenocarcinoma
Fink and Boyden, 1966 (28) Hydrochloric acid ingestion


Sawyer et al, 1967 (27) Sx for intestinal obstruction
Meyers and Parker, 1967 (26) Sodium hydroxide ingestion,
 sulfuric acid ingestion
 Hydrochloric acid


 Ammonia ingestion

Berens et al, 1968 (25) --
Lagios and Suydam, 1968 (24) Phytobezoar
Clearfield et al, 1969 (23) Potassium hydroxide

Kinkhabwala et al, 1973 (22) Alcohol abuse
Weston, 1975 (21) --
Rowen et al, 1976 (20) Leukemia, chemotherapy, steroids,
 sepsis
Jensen and Rodgers, 1977 (19) Zinc chloride ingestion
Bernardino and Lawson, 1977 (18) Sodium hydroxide ingestion
Williford et al, 1982 (17) Lymphoma, chemotherapy,
 disseminated strongyloidiasis
Udassin et al, 1984 (16) Malnutrition, gastroenteritis
de Lange et al, 1986 (15) Alcohol
Bloodworth et al, 1987 (14) Hemorrhagic pancreatitis, sepsis


Williamson et al, 1989 (13) Sx for necrotic colon
 Alcohol, peritonitis (Sx)
Monteferrante and Shimkin, 1989 --
 (12)
Caruana et al, 1990 (11) Gastropancreatic fistula, PD
Moosvi et al, 1990 (10) Diabetes, alcoholism







Binmoeller and Benner, 1992 (9) Gastric infarction
Hadas-Halpren et al, 1993 (8) Vomiting, cola ingestion
McKelvie and Fink, 1994 (7) Alcohol, NSAID use
Van Allan et al, 1995 (6) Diabetes, immunosuppression with
 prednisone, cyclosporine
Lin et al, 1995 (5) Acute gastric dilation



Sud et al, 1996 (4) Thoracic empyema
Bashour et al, 1998 (3) Cocaine and alcohol abuse

Chemey et al, 1999 (2) Wegener's granulomatosis,
 steroids, Sx for bleeding
 duodenal unlcer, cyclophosphamide
Yalamanchili and Cady, 2003 Diabetes, hemodialysis
 (present study)


Series (ref. no.) Isolated organisms

Fraenkel, 1889 (1) Rodlike organism (S)
Morton and Stabins, 1928 (37) Clostridium perfringens (S)
Ween, 1946 (36) E. coli (Abs), P. mirabilis (Asp)
 Enterobacter aerogenes (B)
Welch and Jones, 1947 (35) S. aureus. E. coli, nonhemolytic
 streptococci (Asp)
Henry, 1952 (34) E. coli (S), coagulase-negative
 staphylococci (B)
Farfel and Eichhorn, 1956 (33) --
Gonzalez et al, 1963 (32) --

 Nonhemolytic streptococci, P.
 aeruginosa, Enterobacter aerogenes
 (Asp)
Han et al, 1965 (31) Proteus mirabilis, E. coli (PF)
Berry et al, 1965 (30) --
Smith, 1966 (29) C. perfringens (Asp)
Fink and Boyden, 1966 (28) E. coli, C. perfringens, [alpha]-
 hemolytic streptocci (S, PF,
 liver)
Sawyer et al, 1967 (27) Bacillus subtilis (PF)
Meyers and Parker, 1967 (26) --

 Streptococcus viridans (B), Proteus
 vulgaris (PF), Klebsiella
 aerobact (GF, PF)
 Pseudomonas aeruginosa, P.
 vulgaris S. aureus (PF)
Berens et al, 1968 (25) --
Lagios and Suydam, 1968 (24) E. coli (S)
Clearfield et al, 1969 (23) --

Kinkhabwala et al, 1973 (22) Aerobacter aerogenes (PF)
Weston, 1975 (21) --
Rowen et al, 1976 (20) --

Jensen and Rodgers, 1977 (19) --
Bernardino and Lawson, 1977 (18) --
Williford et al, 1982 (17) Strongyloides stercoralis

Udassin et al, 1984 (16) --
de Lange et al, 1986 (15) Gram-positive cocci (S)
Bloodworth et al, 1987 (14) Bacteroides sp, Klebsiella
 pneumoniae, Streptococcus
 foecails (Asp)
Williamson et al, 1989 (13) Candida sp (S)
 --
Monteferrante and Shimkin, 1989 Group D enterococci, E. coli (S)
 (12)
Caruana et al, 1990 (11) Torulopsis glabrata (PF)
Moosvi et al, 1990 (10) S. aureus (B), Enterobacter
 cloacea, C. albicans, Enterobacter
 aerogenes, E. Coli, Pseudomonas
 aeruginosa (Asp), Corynebacterium,
 C albicans, nonhemolytic
 streptococci (gastric swab
 culture)

Binmoeller and Benner, 1992 (9) Clastridium welchii (B)
Hadas-Halpren et al, 1993 (8) -
McKelvie and Fink, 1994 (7) Staphylococcus aureus (S)
Van Allan et al, 1995 (6) Streptococcus viridans, yeast,
 gungi (S)
Lin et al, 1995 (5) E. coli, Klebsiella pneumoniae,
 Citobacter freundii, Bacteroides
 fragilis, Streptococcus viridans
 (Asp, S)
Sud et al, 1996 (4) E. coli (pleural fluid)
Bashour et al, 1998 (3) Clostridium perfringens (B), yeast
 (Asp), VRE baeteremia on day 46
Chemey et al, 1999 (2) Yersinia sp, Enterobacter sp,
 Enterococcus, Canadida krusei
 (Asp,S, PF)
Yalamanchili and Cady, 2003 Candida krusei (S)
 (present study)


Series (ref. no.) Outcome

Fraenkel, 1889 (1) Died
Morton and Stabins, 1928 (37) Died
Ween, 1946 (36) Died after Sx

Welch and Jones, 1947 (35) Recovered

Henry, 1952 (34) Died

Farfel and Eichhorn, 1956 (33) Recovered
Gonzalez et al, 1963 (32) Contracture after
 Sx
 Contracture after
 Sx

Han et al, 1965 (31) Recovered after Sx
Berry et al, 1965 (30) Recovered after Sx
Smith, 1966 (29) Died after Sx
Fink and Boyden, 1966 (28) Died after Sx


Sawyer et al, 1967 (27) Died after Sx
Meyers and Parker, 1967 (26) Died

 Died after Sx


 Died after Sx

Berens et al, 1968 (25) Died after Sx
Lagios and Suydam, 1968 (24) Died
Clearfield et al, 1969 (23) Recovered after Sx
 Sx; contracture
Kinkhabwala et al, 1973 (22) Recovered after Sx
Weston, 1975 (21) Died
Rowen et al, 1976 (20) Died

Jensen and Rodgers, 1977 (19) Recovered after Sx
Bernardino and Lawson, 1977 (18) Recovered
Williford et al, 1982 (17) Died

Udassin et al, 1984 (16) Recovered
de Lange et al, 1986 (15) Died
Bloodworth et al, 1987 (14) Died


Williamson et al, 1989 (13) Died after Sx
 Died
Monteferrante and Shimkin, 1989 Died
 (12)
Caruana et al, 1990 (11) Recovered
Moosvi et al, 1990 (10) Improved after
 subtotal
 gastrectomy





Binmoeller and Benner, 1992 (9) Died
Hadas-Halpren et al, 1993 (8) Recovered in 7 days
McKelvie and Fink, 1994 (7) Died
Van Allan et al, 1995 (6) Recovered after Sx

Lin et al, 1995 (5) Recovered after
 gastrectomy


Sud et al, 1996 (4) Died
Bashour et al, 1998 (3) Died
 Died after
Chemey et al, 1999 (2) gastrectomy


Yalamanchili and Cady, 2003 Died
 (present study)

(a) B, blood; S, stomach; Asp, aspirate; PF, peritoneal fluid; Sx,
surgery; Abs, abscess; PD, peritoneal dialysis; GF, gastric fluid;
NSAID, nonsteroidal anti- inflammatory drug; VRE, vancomycin-resistant
Enterococcus faecium


Accepted January 14, 2002.

References

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(2.) Cherney CL, Chutuape A, Fikrig MK. Fatal invasive gastric mucormycosis occurring with emphysematous gastritis: Case report and literature review. Am J Gastroenterol 1999;94:252-256.

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(18.) Bernardino ME, Lawson TL. Emphysematous gastritis and gastric perforation: An unusual manifestation of alkaline corrosive ingestion. Gastrointest Radiol 1977;2:107-108.

(19.) Jensen AR, Rodgers BM. Emphysematous gastritis secondary to acid ingestion in an infant. J Fla Med Assoc 1977;64:484-487.

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(28.) Fink DW, Boyden FM. Gas in the portal veins: A report of two cases due to ingestion of corrosive substances. Radiology 1966;87:741-743.

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(30.) Berry WB, Hall RA, Jordan GL Jr: Necrosis of the entire stomach secondary to ingestion of a corrosive acid: Report of a patient successfully treated by total gastrectomy. Am J Surg 1965;109:652-655.

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(32.) Gonzalez LL, Schowengerdt C, Skinner HH Jr, et al. Emphysematous gastritis. Surg Gynecol Obstet 1963;l16:79-87.

(33.) Farfel B, Eichhorn RD. Emphysematous gastritis. Am J Gastroenterol 1956;25:125-130.

(34.) Henry GW. Emphysematous gastritis. Am J Roentgenol Radium Ther Nucl Med 1952;68:15-18.

(35.) Welch CE, Jones CM. Emphysematous gastritis. N Engl J Med 1947;237:983-985.

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RELATED ARTICLE: Key Points

* Emphysematous gastritis is characterized by systemic toxicity and air in the wall of the stomach due to infectious etiology.

* Any condition that can cause damage to the gastric mucosa barrier can predispose to emphysematous gastritis.

* Computed tomography is the procedure of choice for diagnosis.

* Initial antibiotic therapy should cover gram-negative organisms and anaerobes. More specific antibiotic therapy should be administered on the basis of the results of nasogastric aspirate.

* Emphysematous gastritis is a fatal condition.

From the Department of Internal Medicine and the Division of Nephrology, Robert Packer Hospital, Sayre, PA.

Reprint requests to Madhuri Yalamanchili, MD, 105-09 Crowne Chase Drive, Winston-Salem, NC 27104. Email: madhuriyalamanchili@yahoo.com

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Title Annotation:a discussion of the diagnosis of emphysematous gastritis
Author:Cady, William
Publication:Southern Medical Journal
Date:Jan 1, 2003
Words:3869
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