Gangrene of the Stomach: A Case of Acute Necrotizing Gastritis Richard J. Strauss, MD, New Hyde Park, New York Murry Friedman, MD, New Hyde Park, New York Norbert Platt, MD, New Hyde Park, New York Walter Gassner, MD, Miami, Florida Leslie Wise, MD, New Hyde Park, New York
Gangrene of the stomach is a rare and fulminating catastrophic event which is often fatal [l-4]. Its cause has been attributed to embolization of atherosclerotic plaques [4], thrombosis of major arterial supply [3], occlusion of gastric vessels by therapeutically injected foreign bodies (for example, Gelfoam@ and autogenous clots) [5-B], psychogenic polyphagia resulting in massive gastric dilatation [9], ingestion of caustic materials [10,11], intrathoracic herniation of the stomach [12], volvulus of the stomach [13], and necrotizing gastritis caused by organisms producing primary necrosis and gangrene of the stomach wall [1,2]. The patient presented herein had gangrene of the stomach which appeared to be caused by a severe necrotizing infection with no known portal of entry. Since most surgeons have little or no personal precedent for the management of patients with this condition, we present this case and several similar cases found in the literature to familiarize the surgeon with this entity. We will confine our discussion to patients with gastric necrosis from other than mechanical or caustic chemical causes.
110 per minute, temperature was 100.5” F, and respiratory rate was 20 per minute. Upright chest and abdominal x-ray films showed free air under both diaphragms. (Figure 1.) A diagnosis of generalized peritonitis was made. After hydration was complete and antibiotic therapy instituted (intravenous Keflina), the patient was taken to the operating room. Exploration revealed diffuse fibrinopurulent peritonitis with 250 cc of free pus in the peritoneal cavity. The stomach was edematous and inflamed, and the distal one-third along the greater curvature was paper-thin and dark green in color. Strong arterial pulsations were present in the left and right gastric arteries and in both epiploic arteries. The duodenum, gallbladder, pancreas, and small and large bowel all appeared normal. The stomach was divided and the proximal gastric pouch examined, and although the serosa appeared normal and the transected edges bled vigorously, the rugal folds were alternately bright green and bright red in color. Although free air was seen under both diaphragms in the preoperative chest x-ray film, no evidence of gross gastric perforation could be found. Subtotal gastrectomy and Billroth II anastomosis was performed, and the patient made an uneventful recovery. Gross examination of the resected distal stomach showed that the mucosa was grossly necrotic, except for a few residual islands which measured 1.0 to 1.5 cm in size.
Case Report A fifty-three year old white female who had previously been in good health presented at the emergency room of the Long Island Jewish-Hillside Medical Center for the first time with a three week history of mild abdominal discomfort with occasional nausea. The pain, however, had become progressively more intense and steady for approximately 36 hours prior to her admission. She complained of severe abdominal pain, and on examination dehydration, tenderness, rebound, distension, and guarding in all four quadrants of the abdomen were found. There was decreased liver dullness, and no bowel sounds were present. Blood pressure was 110/60 mm Hg, pulse was
From the Departrnants of Surgery, Pathology. and Microbiology, Long Island Jewish-Hillside Medical Center, New Hyde Park, and the Health Sciences Center, State University of New York at Stony Brook, Stony Brook, New York. Reprint requests should be addressed to Leslie Wise, MD, Department of Surgery, Long Island Jewist+Hillside Medical Center, New Hyde Park, New York i1040
Volume 135, February 1979
Figure 1. Upright chest x-ray film showing free air under both diaphragms.
253
Strauss et al
Figure 2. Low (A) and higher power (8) views of microscopic sections showing the destroyed mucosa, the inflamed, thickened, infiltrated submucosa, and the compiereiy necrofic muscuiaris. Also seen is an area dense/y infiitrafed wifh infiammatory ceils.
In several places the wall appeared paper-thin and was extremely friable. The duodenal mucosa was well preserved. Residual normal mucti and viable gastric wall was seen at the proximal margin. Cultures taken of the peritoneal fluid at the time of surgery grew streptococci and Escherichia coli. No yeast or fungus was found. Histologic study of sections of the specimen revealed destruction of the wall of the distal stomach by a diffuse necrobiotic process extending through all layers of the stomach except the serosa, which was found to be only focally involved. There was an extensive purulent process completely destroying the mucosa and invading the muscularis and especially the submucosa with massive accumulation of inflammatory cells and necrosis of the underlying muscularis. (Figure 2.) In other microscopic sections (Figure 3), areas of gastric wall demonstrating full thickness coagulative necrosis were seen, as
Figure 3. An area of gastric wail showing full thickness coagulative necrosis as evidenced by loss of nuclei and homogenization of the cytoplasm. Liquefaction of the inner muscuiaris is aiso demonstrated.
254
evidenced by loss of nuclei and homogenization of the cytoplasm. In the submucosa, vascular thrombosis occurred, giving the specimen an infarcted appearance. The duodenal mucosa was well preserved and residual normal mucosa and viable gastric wall was seen at the proximal margin. On gram-stained microscopic sections, the entire thickness of the involved stomach was also found to be massively infiltrated with gram-positive rods. (Figures 4 and 5.) Comments
the abundant and anastoWhen one considers motic nature of the vascular supply to the stomach, it is not surprising that gangrene occurs so infrequently. Babkin, Armour, and Webster [14] in 1943 found that tying all the gastric arteries (leaving the esophageal arteries intact) did not cause gastric infarction in the dog. The lack of infarction was explained by the presence of multiple anastomoses between the left gastric artery and branches of the phrenic and esophageal arteries. Somervall [15] in 1945 ligated the four main gastric vessels in fourteen patients to relieve hyperacidity and prevent ulceration after gastroenterostomy. He was careful not to interfere with the venous return from the stomach, and no patient developed gangrene of the stomach. However, when Babkin, Armour, and Webster [14] ligated both the gastric arteries and gastric veins in dogs, necrosis of the stomach was produced in each case. Bauman, in 1909, reported the first case of gastric infarction of any major degree. This finding was made incidentally during autopsy of a ninety year old woman. Gastric infarction is a rare lesion, and in a
The American
Journalof Surgery
Necrotizing Gastritis
Figure 4. High power microscopic views of an area of destruction in the muscuiarb ptvpria showing numerous gram-positive and gram-negative rods and gram-positive cocci. Numerous acute poiymorphonuciear ceils are also present (A).
Figure 5. Microscopic section showing severe necrotizing infection with bacteria s~?~~nding a small fragment of destroyed muscle tissue. study by Cohen [3] only four cases were identified after more than 23,000 autopsies were done at the Los Angeles County General Hospital over a twelve year period. These four patients all demonstrated both arterial obstruction and impediment to venous flow. The venous impediment was caused by the presence of congestive heart failure, and failure of the right heart was tantamount to ligation of the entire venous return of the stomach, including any anastomotic venous channels that may have existed. Another study indicating the importance of venous occlusion as an etiologic factor in gastric infarction [9] was of an eighteen year old girl with psychogenic polyphagia who was operated on for increasing ab-
Volume 135, February 1975
dominal pain, tenderness, and distension. At operation, the entire stomach was necrotic and contained an enormous amount of undigested food, with a total volume of more than 15 liters. The necrosis was explained by vascular insufficiency initiated by the increased intraluminal pressure; distension of the stomach at a pressure of 20 cm of water resulted in a profound reduction of blood flow to the mucosa [IS]. The occlusion of the venous drainage of the stomach, as a result of high intramural tension with increased intramural venous pressure, appeared to be a highly significant factor in this case. Although venous impediment appeared to be important in several of the preceding patients, addi-
255
Strauss et al
tional reports have appeared indicating arterial vascular compromise as the sole cause of gastric infarction without venous occlusion. In one report by Harvey, Doberneck, and Black [4], a sixty-four year old woman was found to have multifocal gastric infarcts secondary to atheromatous emboli originating in a thoracic aortic aneurysm. In another report [5], a patient was described with extensive gastric necrosis after therapeutic transcatheter embolization of the left gastric artery with fragments of gelatin sponge for recurrent massive upper gastrointestinal hemorrhage. Phlegmonous gastritis [17,18] has been shown to produce either an abscess or spreading cellulitis of the stomach wall. Hemolytic streptococcus is the most common infecting organism, but many other bacterial strains have been implicated, particularly fecal organisms. The diagnosis is usually made at laparotomy and the stomach is found to have an intact extrinsic blood supply, with thrombosis of the microscopic intrinsic vascular plexus producing the appearance of extensive infarction. There is dark discoloration of the wall and sloughing of the mucosa. The submucosa is the layer most characteristically involved by contiguity. In this entity necrosis is rare, and if it occurs, it is usually focal. The syndrome of acute necrotizing gastritis appears to be a variant of phlegmonous suppurative gastritis, with organisms producing primary necrosis and gangrene of the stomach wall rather than only intramural abscesses [1,2]. Etiologically, the bacteria involved in this condition have been reported to be fusiform and spirochetal organisms (commonly found in the mouth), streptococci, or combinations of various organisms. Only two studies specifically dealing with patients having severe acute necrotizing gastritis were found. In 1943 Rosenthal and Tobias [1] described a patient with a history and findings similar to ours. She was admitted with abdominal pain and vomiting. The abdomen was moderately distended, and there was marked epigastric tenderness with rebound. An abdominal x-ray film revealed pneumoperitoneum and marked elevation of the right diaphragm. At operation there was a considerable quantity of reddishbrown fluid in the peritoneal cavity. The stomach was dilated, and there were two large areas (6 cm) of frank necrosis. The necrotizing process was so violent that the integrity of the gastric wall was sufficiently compromised to permit the escape of gastric contents without any evidence of gross perforation. At the periphery of the involved area, the mucosa appeared generally normal. Microscopically, a purulent process appeared to extend through the entire stomach, with
256
formation of a purulent exudate on the serosa. In the central area of gangrene, all cellular architecture had disappeared. The violent necrobiotic process in this case resembled infarction. However, a careful search of all the major vessels in the vicinity failed to disclose thrombosis or occlusion. The diagnosis was made at laparotomy; the patient was treated by suture inversion of the necrotized areas but died on the fourth postoperative day of respiratory failure. It should be noted that this was in the period before effective broad spectrum antibiotics were available. The pathogenesis of the lesion was not clear but the authors stated that a possible explanation was acute peptic digestion. Whether this process was initiated by some form of chronic inflammation in the mucosa or by another factor is unknown; however, once begun it extended through the submucosa and continued to cause a gangrenous process of the gastric wall. Many similarities can be seen between this case and our case, and perhaps the same underlying causes were at work in its pathogenesis. In the report by Behrand, Katz, and Robertson [2], a case of acute necrotizing gastritis in which the major arteries were again not occluded was described. They concluded that the cause was a necrotizing infection spreading to the stomach and originating in an overwhelming periodontal infection. The cultures taken at operation and at autopsy grew the same types of organisms as were cultured from the mouth, base of the teeth, gastric mucosa, and peritoneal fluid (that is, fusobacteria, Escherichia coli, and grampositive and gram-negative cocci and bacilli). The authors commented that both their patient and that of Rosenthal and Tobias [I] had what were examples of necrotizing infection. In these two patients as well as in ours, an interesting finding was the sharp line of demarcation between necrotic and healthy tissue at the pylorus. It does not seem likely that the difference between the normal pH of the stomach and the duodenum could alone limit the extension of an infection which involved all layers of the stomach. Due to the relatively nonspecific clinical picture, phlegmonous or necrotizing gastritis is often misdiagnosed preoperatively as acute appendicitis, hemorrhagic pancreatitis, mesenteric artery occlusion, gangrenous cholecystitis, or most commonly, perforated gastric or duodenal ulcer. In the majority of patients laparotomy is performed and the appearance of the stomach is diagnostic. Because of the submucosal vascular thrombosis, the pathologic changes may resemble extensive infarction, The submucosa is characteristically thickened and contains purulent exudate, and the serosa may be involved by contiguity in which intense fibrinopurulent
The American Journal of Surgery
Necrotlzing Gastritis
deposits cover the external surface of the stomach. In our patient, the presence of numerous clumps of gram-positive cocci strongly suggests that streptococci and staphylococci were at least partly responsible for the necrosis, although the mode of entry of the organisms is unknown. Hematogenous dissemination of bacteria has been suggested as has direct invasion of the gastric mucosa through an ulcer. Because of the limited number of patients with phlegmonous or necrotizing gastritis seen by any one physician, a rational basis for therapy has not been established. The multiplicity of treatments recommended for phlegmonous gastritis or its more destructive variant, acute necrotizing gastritis, is evidence that none is completely satisfactory. There is also the diagnostic problem as to whether the bacterial infection is secondary to infarction or to a primary infection. Starr and Wilson [17] reported on twenty-five patients with phlegmonous gastritis with a mortality of 48 per cent. These patients were treated variously by subtotal gastrectomy, gastrotomy, antibiotics alone, or diagnostic exploratory laparotomy followed by antibiotics. They reported that six of eight patients treated by subtotal gastrectomy survived and concluded that subtotal gastrectomy was a relatively safe and effective means of treating phlegmonous gastritis. Of four patients whose disease was diagnosed at exploratory laparotomy and who were then treated by penicillin, three died. There were eight additional patients treated by antibiotics alone, and in this group there was a 50 per cent mortality. The report by Starr and Wilson [I 71 analyzed only cases reported after 1945 when antibiotics were available. They found a reduction of mortality to 48 per cent as compared with mortalities of 84 per cent in 1938 [19] and 90 per cent in 1919 [20]. The presence of survivors in all groups implies that the problem of treating phlegmonous gastritis is more than one of medical versus surgical management. The common factors in all of the survivors were the early recognition of acute phlegmonous gastritis by laparotomy or gastroscopy and the prompt institution of intensive supportive measures and antibiotics. In patients with acute severe necrotizing transmural infection producing gangrenous nonviable gastric tissue, fundamental surgical principles should be followed and debridement by gastrectomy must be performed. It is not unlikely that the pathologic process of the patient described in the present report began as a case of pblegmonous gastritis and progressed over a short period of time to acute necrotizing gastritis.
vohmo 135, Fobruary 1978
Summary
Of the several causes of gastric necrosis, the rarest is acute necrotizing gastritis which appears to be a variant of phlegmonous gastritis. In acute necrotizing gastritis all four major gastric vessels are patent, but gastric gangrene occurs secondary to an overwhelming necrobiotic infection. The case presented herein is of unusual interest because it appears to be only the third reported case of acute necrotizing gastritis with overt gangrene of the stomach. Review of the literature on suppurative gastritis emphasizes the rarity and high morbidity of acute necrotizing gastritis; the patient reported on in this study, however, survived after subtotal gastrectomy and antibiotic therapy. It is our opinion that debtidement by gastrectomy must be performed in those patients with transmural, diffusely infected, nonviable gastric tissue. References 1. Rosenthal J, Tobias MJ: Acute phlegmonous gastritis with multiple perforations. Am J Surg 59: 117, 1943. 2. Behrand A. Katz AB, Robertson JW: Acute necrotiting gastritis. Arch Surg 69: 16, 1954. 3. Cohen EB: Infarction of the stomach. Am J Med 5: 645, 1951. 4. Harvey RL, Doberneck RC, Black WC: Infarction of the stomach following atheromatous embolization. Gasfroenferology 62: 469, 1972. 5. Bradley E, Goldman ML: Gastric infarction after therapeutic embolization. Surgery 79: 421, 1976. 6. Bookstein JJ, Chlosta LM, Foley D. et al: Transcatheter hemostasis of gastrointestinal bleeding using modified autogenous clot. Radiology 113: 277, 1974. 7. Tadaverthy SM. Knight L, Ovitt TW, et al: Therapeutic transcatheter arterial embolization. Radiology 112: 13, 1974. 6. Reuter SR. Chuana. VP: Control of abdominal bleeding with -auiogenbus embolized material. Radiology 14: 66, 1974. 9. Kerstein MD, Goldberg B, Panter B, et al: Gastric Infarction. Gastroenterology 67: 1236, 1974. 10. Berry WB, Hall RA, Jordan GL: Necrosis of the entire stomach secondary to ingestion of a corrosive acid. Am J Surg 109: 652, 1965. 11. Gryboski W, Page R, Rush B: Management of total gastric necrosis followina lye ingestion. Ann Surg 161: 469, 1965. 12. Gibbons WD: Gaig&noui intrathoracic stomach. Mad J Aust 1: 451, 1966. 13. Sellers TH, Papp C: Strangulated diaphragmatic hernia with torsion of the stomach. Br J Surg 43: 289, 1955. 14. Babkin BP, Armour JA, Webster DR: Restoration of the functional capacity of the stomach when deprived of its main arterial blood supply. Can Med Assoc J 48: 1, 1943. 15. Somervell TH: Physiological gastrectomy. Br J Surg 33: 146, 1945. 16. Edlich RF, Borner JW, Kuphal J, et al: Gastric blood flow. Am J Surg 120: 35, 1970. 17. Starr A, Wilson JM: Phlegmonous gastritis. Ann Surg 145: 68. 1957. 16. Gonzalez-Crussi F, Hackett RL: Phlegmonous gastritis. Arch Surg 93: 990, 1966. 19. El&on E. Wright M: Phlegmonous gastritis. Swg C/in North Am 18: lj53, i938. 20. Sundberg H: Phlegmonous gastrltls. JAMA 73: 602, 1919.
257
Gangrene of the stomach is a rare and fulminating catastrophic event which is often fatal [l-4]. Its cause has been attributed to embolization of atherosclerotic plaques [4], thrombosis of major arterial supply [3], occlusion of gastric vessels by therapeutically injected foreign bodies (for example, Gelfoam@ and autogenous clots) [5-B], psychogenic polyphagia resulting in massive gastric dilatation [9], ingestion of caustic materials [10,11], intrathoracic herniation of the stomach [12], volvulus of the stomach [13], and necrotizing gastritis caused by organisms producing primary necrosis and gangrene of the stomach wall [1,2]. The patient presented herein had gangrene of the stomach which appeared to be caused by a severe necrotizing infection with no known portal of entry. Since most surgeons have little or no personal precedent for the management of patients with this condition, we present this case and several similar cases found in the literature to familiarize the surgeon with this entity. We will confine our discussion to patients with gastric necrosis from other than mechanical or caustic chemical causes.
110 per minute, temperature was 100.5” F, and respiratory rate was 20 per minute. Upright chest and abdominal x-ray films showed free air under both diaphragms. (Figure 1.) A diagnosis of generalized peritonitis was made. After hydration was complete and antibiotic therapy instituted (intravenous Keflina), the patient was taken to the operating room. Exploration revealed diffuse fibrinopurulent peritonitis with 250 cc of free pus in the peritoneal cavity. The stomach was edematous and inflamed, and the distal one-third along the greater curvature was paper-thin and dark green in color. Strong arterial pulsations were present in the left and right gastric arteries and in both epiploic arteries. The duodenum, gallbladder, pancreas, and small and large bowel all appeared normal. The stomach was divided and the proximal gastric pouch examined, and although the serosa appeared normal and the transected edges bled vigorously, the rugal folds were alternately bright green and bright red in color. Although free air was seen under both diaphragms in the preoperative chest x-ray film, no evidence of gross gastric perforation could be found. Subtotal gastrectomy and Billroth II anastomosis was performed, and the patient made an uneventful recovery. Gross examination of the resected distal stomach showed that the mucosa was grossly necrotic, except for a few residual islands which measured 1.0 to 1.5 cm in size.
Case Report A fifty-three year old white female who had previously been in good health presented at the emergency room of the Long Island Jewish-Hillside Medical Center for the first time with a three week history of mild abdominal discomfort with occasional nausea. The pain, however, had become progressively more intense and steady for approximately 36 hours prior to her admission. She complained of severe abdominal pain, and on examination dehydration, tenderness, rebound, distension, and guarding in all four quadrants of the abdomen were found. There was decreased liver dullness, and no bowel sounds were present. Blood pressure was 110/60 mm Hg, pulse was
From the Departrnants of Surgery, Pathology. and Microbiology, Long Island Jewish-Hillside Medical Center, New Hyde Park, and the Health Sciences Center, State University of New York at Stony Brook, Stony Brook, New York. Reprint requests should be addressed to Leslie Wise, MD, Department of Surgery, Long Island Jewist+Hillside Medical Center, New Hyde Park, New York i1040
Volume 135, February 1979
Figure 1. Upright chest x-ray film showing free air under both diaphragms.
253
Strauss et al
Figure 2. Low (A) and higher power (8) views of microscopic sections showing the destroyed mucosa, the inflamed, thickened, infiltrated submucosa, and the compiereiy necrofic muscuiaris. Also seen is an area dense/y infiitrafed wifh infiammatory ceils.
In several places the wall appeared paper-thin and was extremely friable. The duodenal mucosa was well preserved. Residual normal mucti and viable gastric wall was seen at the proximal margin. Cultures taken of the peritoneal fluid at the time of surgery grew streptococci and Escherichia coli. No yeast or fungus was found. Histologic study of sections of the specimen revealed destruction of the wall of the distal stomach by a diffuse necrobiotic process extending through all layers of the stomach except the serosa, which was found to be only focally involved. There was an extensive purulent process completely destroying the mucosa and invading the muscularis and especially the submucosa with massive accumulation of inflammatory cells and necrosis of the underlying muscularis. (Figure 2.) In other microscopic sections (Figure 3), areas of gastric wall demonstrating full thickness coagulative necrosis were seen, as
Figure 3. An area of gastric wail showing full thickness coagulative necrosis as evidenced by loss of nuclei and homogenization of the cytoplasm. Liquefaction of the inner muscuiaris is aiso demonstrated.
254
evidenced by loss of nuclei and homogenization of the cytoplasm. In the submucosa, vascular thrombosis occurred, giving the specimen an infarcted appearance. The duodenal mucosa was well preserved and residual normal mucosa and viable gastric wall was seen at the proximal margin. On gram-stained microscopic sections, the entire thickness of the involved stomach was also found to be massively infiltrated with gram-positive rods. (Figures 4 and 5.) Comments
the abundant and anastoWhen one considers motic nature of the vascular supply to the stomach, it is not surprising that gangrene occurs so infrequently. Babkin, Armour, and Webster [14] in 1943 found that tying all the gastric arteries (leaving the esophageal arteries intact) did not cause gastric infarction in the dog. The lack of infarction was explained by the presence of multiple anastomoses between the left gastric artery and branches of the phrenic and esophageal arteries. Somervall [15] in 1945 ligated the four main gastric vessels in fourteen patients to relieve hyperacidity and prevent ulceration after gastroenterostomy. He was careful not to interfere with the venous return from the stomach, and no patient developed gangrene of the stomach. However, when Babkin, Armour, and Webster [14] ligated both the gastric arteries and gastric veins in dogs, necrosis of the stomach was produced in each case. Bauman, in 1909, reported the first case of gastric infarction of any major degree. This finding was made incidentally during autopsy of a ninety year old woman. Gastric infarction is a rare lesion, and in a
The American
Journalof Surgery
Necrotizing Gastritis
Figure 4. High power microscopic views of an area of destruction in the muscuiarb ptvpria showing numerous gram-positive and gram-negative rods and gram-positive cocci. Numerous acute poiymorphonuciear ceils are also present (A).
Figure 5. Microscopic section showing severe necrotizing infection with bacteria s~?~~nding a small fragment of destroyed muscle tissue. study by Cohen [3] only four cases were identified after more than 23,000 autopsies were done at the Los Angeles County General Hospital over a twelve year period. These four patients all demonstrated both arterial obstruction and impediment to venous flow. The venous impediment was caused by the presence of congestive heart failure, and failure of the right heart was tantamount to ligation of the entire venous return of the stomach, including any anastomotic venous channels that may have existed. Another study indicating the importance of venous occlusion as an etiologic factor in gastric infarction [9] was of an eighteen year old girl with psychogenic polyphagia who was operated on for increasing ab-
Volume 135, February 1975
dominal pain, tenderness, and distension. At operation, the entire stomach was necrotic and contained an enormous amount of undigested food, with a total volume of more than 15 liters. The necrosis was explained by vascular insufficiency initiated by the increased intraluminal pressure; distension of the stomach at a pressure of 20 cm of water resulted in a profound reduction of blood flow to the mucosa [IS]. The occlusion of the venous drainage of the stomach, as a result of high intramural tension with increased intramural venous pressure, appeared to be a highly significant factor in this case. Although venous impediment appeared to be important in several of the preceding patients, addi-
255
Strauss et al
tional reports have appeared indicating arterial vascular compromise as the sole cause of gastric infarction without venous occlusion. In one report by Harvey, Doberneck, and Black [4], a sixty-four year old woman was found to have multifocal gastric infarcts secondary to atheromatous emboli originating in a thoracic aortic aneurysm. In another report [5], a patient was described with extensive gastric necrosis after therapeutic transcatheter embolization of the left gastric artery with fragments of gelatin sponge for recurrent massive upper gastrointestinal hemorrhage. Phlegmonous gastritis [17,18] has been shown to produce either an abscess or spreading cellulitis of the stomach wall. Hemolytic streptococcus is the most common infecting organism, but many other bacterial strains have been implicated, particularly fecal organisms. The diagnosis is usually made at laparotomy and the stomach is found to have an intact extrinsic blood supply, with thrombosis of the microscopic intrinsic vascular plexus producing the appearance of extensive infarction. There is dark discoloration of the wall and sloughing of the mucosa. The submucosa is the layer most characteristically involved by contiguity. In this entity necrosis is rare, and if it occurs, it is usually focal. The syndrome of acute necrotizing gastritis appears to be a variant of phlegmonous suppurative gastritis, with organisms producing primary necrosis and gangrene of the stomach wall rather than only intramural abscesses [1,2]. Etiologically, the bacteria involved in this condition have been reported to be fusiform and spirochetal organisms (commonly found in the mouth), streptococci, or combinations of various organisms. Only two studies specifically dealing with patients having severe acute necrotizing gastritis were found. In 1943 Rosenthal and Tobias [1] described a patient with a history and findings similar to ours. She was admitted with abdominal pain and vomiting. The abdomen was moderately distended, and there was marked epigastric tenderness with rebound. An abdominal x-ray film revealed pneumoperitoneum and marked elevation of the right diaphragm. At operation there was a considerable quantity of reddishbrown fluid in the peritoneal cavity. The stomach was dilated, and there were two large areas (6 cm) of frank necrosis. The necrotizing process was so violent that the integrity of the gastric wall was sufficiently compromised to permit the escape of gastric contents without any evidence of gross perforation. At the periphery of the involved area, the mucosa appeared generally normal. Microscopically, a purulent process appeared to extend through the entire stomach, with
256
formation of a purulent exudate on the serosa. In the central area of gangrene, all cellular architecture had disappeared. The violent necrobiotic process in this case resembled infarction. However, a careful search of all the major vessels in the vicinity failed to disclose thrombosis or occlusion. The diagnosis was made at laparotomy; the patient was treated by suture inversion of the necrotized areas but died on the fourth postoperative day of respiratory failure. It should be noted that this was in the period before effective broad spectrum antibiotics were available. The pathogenesis of the lesion was not clear but the authors stated that a possible explanation was acute peptic digestion. Whether this process was initiated by some form of chronic inflammation in the mucosa or by another factor is unknown; however, once begun it extended through the submucosa and continued to cause a gangrenous process of the gastric wall. Many similarities can be seen between this case and our case, and perhaps the same underlying causes were at work in its pathogenesis. In the report by Behrand, Katz, and Robertson [2], a case of acute necrotizing gastritis in which the major arteries were again not occluded was described. They concluded that the cause was a necrotizing infection spreading to the stomach and originating in an overwhelming periodontal infection. The cultures taken at operation and at autopsy grew the same types of organisms as were cultured from the mouth, base of the teeth, gastric mucosa, and peritoneal fluid (that is, fusobacteria, Escherichia coli, and grampositive and gram-negative cocci and bacilli). The authors commented that both their patient and that of Rosenthal and Tobias [I] had what were examples of necrotizing infection. In these two patients as well as in ours, an interesting finding was the sharp line of demarcation between necrotic and healthy tissue at the pylorus. It does not seem likely that the difference between the normal pH of the stomach and the duodenum could alone limit the extension of an infection which involved all layers of the stomach. Due to the relatively nonspecific clinical picture, phlegmonous or necrotizing gastritis is often misdiagnosed preoperatively as acute appendicitis, hemorrhagic pancreatitis, mesenteric artery occlusion, gangrenous cholecystitis, or most commonly, perforated gastric or duodenal ulcer. In the majority of patients laparotomy is performed and the appearance of the stomach is diagnostic. Because of the submucosal vascular thrombosis, the pathologic changes may resemble extensive infarction, The submucosa is characteristically thickened and contains purulent exudate, and the serosa may be involved by contiguity in which intense fibrinopurulent
The American Journal of Surgery
Necrotlzing Gastritis
deposits cover the external surface of the stomach. In our patient, the presence of numerous clumps of gram-positive cocci strongly suggests that streptococci and staphylococci were at least partly responsible for the necrosis, although the mode of entry of the organisms is unknown. Hematogenous dissemination of bacteria has been suggested as has direct invasion of the gastric mucosa through an ulcer. Because of the limited number of patients with phlegmonous or necrotizing gastritis seen by any one physician, a rational basis for therapy has not been established. The multiplicity of treatments recommended for phlegmonous gastritis or its more destructive variant, acute necrotizing gastritis, is evidence that none is completely satisfactory. There is also the diagnostic problem as to whether the bacterial infection is secondary to infarction or to a primary infection. Starr and Wilson [17] reported on twenty-five patients with phlegmonous gastritis with a mortality of 48 per cent. These patients were treated variously by subtotal gastrectomy, gastrotomy, antibiotics alone, or diagnostic exploratory laparotomy followed by antibiotics. They reported that six of eight patients treated by subtotal gastrectomy survived and concluded that subtotal gastrectomy was a relatively safe and effective means of treating phlegmonous gastritis. Of four patients whose disease was diagnosed at exploratory laparotomy and who were then treated by penicillin, three died. There were eight additional patients treated by antibiotics alone, and in this group there was a 50 per cent mortality. The report by Starr and Wilson [I 71 analyzed only cases reported after 1945 when antibiotics were available. They found a reduction of mortality to 48 per cent as compared with mortalities of 84 per cent in 1938 [19] and 90 per cent in 1919 [20]. The presence of survivors in all groups implies that the problem of treating phlegmonous gastritis is more than one of medical versus surgical management. The common factors in all of the survivors were the early recognition of acute phlegmonous gastritis by laparotomy or gastroscopy and the prompt institution of intensive supportive measures and antibiotics. In patients with acute severe necrotizing transmural infection producing gangrenous nonviable gastric tissue, fundamental surgical principles should be followed and debridement by gastrectomy must be performed. It is not unlikely that the pathologic process of the patient described in the present report began as a case of pblegmonous gastritis and progressed over a short period of time to acute necrotizing gastritis.
vohmo 135, Fobruary 1978
Summary
Of the several causes of gastric necrosis, the rarest is acute necrotizing gastritis which appears to be a variant of phlegmonous gastritis. In acute necrotizing gastritis all four major gastric vessels are patent, but gastric gangrene occurs secondary to an overwhelming necrobiotic infection. The case presented herein is of unusual interest because it appears to be only the third reported case of acute necrotizing gastritis with overt gangrene of the stomach. Review of the literature on suppurative gastritis emphasizes the rarity and high morbidity of acute necrotizing gastritis; the patient reported on in this study, however, survived after subtotal gastrectomy and antibiotic therapy. It is our opinion that debtidement by gastrectomy must be performed in those patients with transmural, diffusely infected, nonviable gastric tissue. References 1. Rosenthal J, Tobias MJ: Acute phlegmonous gastritis with multiple perforations. Am J Surg 59: 117, 1943. 2. Behrand A. Katz AB, Robertson JW: Acute necrotiting gastritis. Arch Surg 69: 16, 1954. 3. Cohen EB: Infarction of the stomach. Am J Med 5: 645, 1951. 4. Harvey RL, Doberneck RC, Black WC: Infarction of the stomach following atheromatous embolization. Gasfroenferology 62: 469, 1972. 5. Bradley E, Goldman ML: Gastric infarction after therapeutic embolization. Surgery 79: 421, 1976. 6. Bookstein JJ, Chlosta LM, Foley D. et al: Transcatheter hemostasis of gastrointestinal bleeding using modified autogenous clot. Radiology 113: 277, 1974. 7. Tadaverthy SM. Knight L, Ovitt TW, et al: Therapeutic transcatheter arterial embolization. Radiology 112: 13, 1974. 6. Reuter SR. Chuana. VP: Control of abdominal bleeding with -auiogenbus embolized material. Radiology 14: 66, 1974. 9. Kerstein MD, Goldberg B, Panter B, et al: Gastric Infarction. Gastroenterology 67: 1236, 1974. 10. Berry WB, Hall RA, Jordan GL: Necrosis of the entire stomach secondary to ingestion of a corrosive acid. Am J Surg 109: 652, 1965. 11. Gryboski W, Page R, Rush B: Management of total gastric necrosis followina lye ingestion. Ann Surg 161: 469, 1965. 12. Gibbons WD: Gaig&noui intrathoracic stomach. Mad J Aust 1: 451, 1966. 13. Sellers TH, Papp C: Strangulated diaphragmatic hernia with torsion of the stomach. Br J Surg 43: 289, 1955. 14. Babkin BP, Armour JA, Webster DR: Restoration of the functional capacity of the stomach when deprived of its main arterial blood supply. Can Med Assoc J 48: 1, 1943. 15. Somervell TH: Physiological gastrectomy. Br J Surg 33: 146, 1945. 16. Edlich RF, Borner JW, Kuphal J, et al: Gastric blood flow. Am J Surg 120: 35, 1970. 17. Starr A, Wilson JM: Phlegmonous gastritis. Ann Surg 145: 68. 1957. 16. Gonzalez-Crussi F, Hackett RL: Phlegmonous gastritis. Arch Surg 93: 990, 1966. 19. El&on E. Wright M: Phlegmonous gastritis. Swg C/in North Am 18: lj53, i938. 20. Sundberg H: Phlegmonous gastrltls. JAMA 73: 602, 1919.
257
