|Year : 2014 | Volume
| Issue : 1 | Page : 38-40
Gastric gangrene due to acute necrotizing gastritis
Hari Charan Perigela, Murali Krishna Vasamsetty, Vara Prasad Bangi, Sivaraj Nagabhushigari
Department of General Surgery, Kurnool Medical College and Government General Hospital, Kurnool, Andhra Pradesh, India
|Date of Web Publication||10-Mar-2014|
Hari Charan Perigela
Associate Professor of Surgery, Kurnool Medical College and Government General Hospital, Kurnool, Andhra Pradesh - 518 001
Source of Support: None, Conflict of Interest: None
Gangrene of the stomach is a rare, often fatal disease which may be due to vascular, chemical, mechanical, or infectious etiologies. We report a case of gastric gangrene due to acute necrotizing gastritis in a 60-year-old male. 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 debridement by gastrectomy must be performed in those patients with transmural, diffusely infected, and nonviable gastric tissue.
Keywords: Acute necrotizing gastritis, gastric gangrene, subtotal gastrectomy
|How to cite this article:|
Perigela HC, Vasamsetty MK, Bangi VP, Nagabhushigari S. Gastric gangrene due to acute necrotizing gastritis. J NTR Univ Health Sci 2014;3:38-40
|How to cite this URL:|
Perigela HC, Vasamsetty MK, Bangi VP, Nagabhushigari S. Gastric gangrene due to acute necrotizing gastritis. J NTR Univ Health Sci [serial online] 2014 [cited 2020 Apr 7];3:38-40. Available from: http://www.jdrntruhs.org/text.asp?2014/3/1/38/128429
| Introduction|| |
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 a necrobiotic infection.  In literature, cases of acute necrotizing gastritis have been linked to peptic ulcer disease, gastric outlet obstruction, and vagotomy. . We present a case of gastric gangrene due to acute necrotizing gastritis in a patient in whom no apparent predisposing cause could be found.
| Case Report|| |
A 60-year-old male came to casualty with chief complaint of pain in the upper abdomen for the past 24 h. The pain was severe, continuous, and associated with nausea. There was no history of hematemesis or vomiting. On examination, he was in agonizing pain. His temperature was 101°F, pulse rate: 110/min, BP: 100/70 mm Hg. Abdomen was diffusely tender with rigidity on palpation. Bowel sounds were absent. The Ryle's tube showed necrotic foul smelling aspirate. Chest x-ray in erect posture showed no free gas under the diaphragm. Routine hemogram showed leucocytosis. Blood sugar, blood urea, and serum creatinine levels were within normal limits. Ultrasound abdomen showed evidence of free fluid.
After initial resuscitation, emergency laparotomy was planned. On exploration, fluid in the peritoneal cavity was sucked out. There was gangrene of the middle third of the stomach with intact extrinsic blood supply. On opening the stomach, it was filled with foul smelling necrotic material [Figure 1]. The contents of the stomach were suctioned [Figure 2]. The extent of the gangrene has been assessed [Figure 3] and [Figure 4]. There was normal pulsation of the gastric vessels. The esophagus, small intestine, colon, and rectum were pink and viable. Middle third of the gangrenous stomach was excised and end-to-end anastomosis was done with 2-0 black silk sutures [Figure 5]. The abdomen was closed in layers.
|Figure 1: Intraoperative photograph showing gangrenous portion of the stomach|
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|Figure 2: Intraoperative photograph showing suction of the stomach contents|
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|Figure 3: Intraoperative photograph showing nasogastric tube in the gangrenous stomach|
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|Figure 4: Intraoperative photograph showing junction of normal stomach and gangreous stomach|
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|Figure 5: Intraoperative photograph showing suturing the cut ends of the stomach after subtotal gastrectomy|
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Microscopic examination of the stomach showed destruction of the wall by a diffuse necrotic process extending through all layers. An extensive purulent process had completely destroyed the mucosa and had invaded the submucosa, with massive accumulation of inflammatory cells and necrosis of the underlying muscularis. Culture of the peritoneal fluid taken at the time of surgery grew Proteus mirabilis that was sensitive to cefuroxime.
Patient was put on cefuroxime, gentamicin, and metronidazole injections. The postoperative period was uneventful. Patient was discharged on 12 th postoperative day after suture removal.
| Discussion|| |
The abundant and anastomotic nature of the stomach's vascular supply makes gangrene very rare. Harvey et al.,  reported a case of multifocal gastric infarction secondary to atheromatous emboli, originating in a thoracic aortic aneurysm. In another report, 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. 
In our case, the finding of gangrene of the stomach was an operative surprise. Pulsatile gastric arteries made vascular accident unlikely. Both the domes of the diaphragm were normal, which ruled out a diaphragmatic hernia content strangulation as the cause of the gastric gangrene. No twisting of the stomach was noted and so volvulus was ruled out. There was no history or evidence of swallowing any corrosive substance.
The peritoneal cavity fluid grew proteus mirabilis. Transmigration of organisms into the peritoneal cavity across the gangrenous stomach was considered but, normally, the contents of the stomach are sterile. Therefore, we suspect that the stomach wall was involved as a result of some necrotizing infection. Abscess or spreading cellulitis of the stomach wall caused by microorganisms, known as phlegmonous gastritis, is a rare condition, with only about 500 cases having been reported in the world literature. The pathogenesis is unclear, although predisposing factors include chronic gastritis, increased age, alcoholism, hypoacidity, protein-energy malnutrition, and immunosuppression. ,
Acute necrotizing gastritis is a variant of phlegmonous gastritis, with organisms producing necrosis and gangrene of the stomach wall rather than just an intramural abscess. Etiologically, Streptococci, fusiform, and spirochetal organisms (commonly found in the mouth), or combinations of various organisms like Escherichia coli, Haemophilus influenza, Proteus, and Clostridia have been reported.  It occurs by hematogenous route and may involve a portion of the stomach (localized type) or the entire stomach (diffuse type).
Diagnosis may be delayed due to the lack of typical signs and this, combined with the rapid progression to peritonitis, often results in a fatal outcome. Surgical intervention with gastrectomy is thought to be the most effective form of treatment. At laparotomy, the stomach is usually found to have intact extrinsic blood supply. The submucosa is the layer most characteristically involved by contiguity but necrosis is rare and, if it occurs, is usually focal.
Diagnosis of acute necrotizing or gangrenous gastritis is usually made at laparotomy, although endoscopy, endosonography, and endoscopic snare biopsy have also been used to reach a diagnosis. However, in a patient with frank signs of peritonitis, as in the present case, these are not feasible.
Overall, the mortality rate is 17% for patients with a medically treated localized disease and 60% for the diffuse disease. Depending on the clinical situation, patients with the localized disease may respond to prompt and aggressive treatment. The mortality rate of patients treated by surgical resection is far lower than for those treated by medical therapy alone (20% vs. 50%). 
| Conclusion|| |
Gastric gangrene due to necrotizing gastritis is usually diagnosed at laparotomy. Treatment consists of resection of the gangrenous portion, followed by intravenous antibiotics. Increased awareness of this rare entity may lead to more prompt diagnosis and an increased chance for patient survival.
| References|| |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]