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Phlegmonous gastritis
The patient was treated with intravenous antibiotics (amoxicillin/clavulanic acid 6.6 g/d) and a proton pump inhibitor (esomeprazole 80 mg/d). Within a few days, her clinical status improved and abdominal ultrasound examination documented regression of the gastric wall thickening. Laboratory screening for predisposing factors such as diabetes mellitus, infection with human immunodeficiency virus, or immunoglobulin deficiency were negative and there was no clinical evidence of Crohn’s disease. Antibiotic treatment was stopped after 2 weeks. Six months later, follow-up gastroscopy was performed confirming complete resolution of the inflammatory changes in the stomach.
Phlegmonous gastritis is a rare but potentially life-threatening bacterial infection of the gastric wall. Since its first description in 1862, about 500 cases have been reported worldwide. Whereas the original reports dating back to the preantibiotic area suggest very high mortality rates in the range of 90%, phlegmonous gastritis still represents a life-threatening condition.1,2 In about one-half of the cases, acquired immunodeficiency states such as diabetes mellitus, human immunodeficiency virus, or alcoholism are identified as predisposing factors. In addition, gastric biopsies may herald the development of phlegmonous gastritis. Streptococcus spp. account for the majority of the cases, which can be isolated in about 70% of patients.1 Other organisms such as Staphylococcus spp., Escherichia coli Haemophilus influenzae, and Proteus or Clostridium spp. have been described as pathogens associated with this uncommon condition. Affected patients typically present with nonspecific symptoms such as abdominal pain, fever, nausea, vomitus, hematemesis, or diarrhea. In light of the devastating natural course of phlegmonous gastritis, timely preemptive administration of broad spectrum antibiotic along with a high index of suspicion are paramount. A computed tomography scan and transabdominal ultrasound examination are useful as initial tests, whereas endoscopic ultrasound examination typically demonstrates a diffusely thickened, hypoechogenic submucosal wall layer that is not commonly found in patients with other submucosal lesions, such as carcinoid or leiomyoma. The diagnosis can be confirmed by endoscopic forceps biopsy provided that sufficient submucosal tissue is included.1 Surgery should only be considered for cases refractory to conservative treatment.
References
1. Kim G, Ward J, Henessey B, et al. Phlegmonous gastritis: case report and review. Gastrointest Endosc. 2005;61:168-74.
2. Starr A, Wilson J. Phlegmonous gastritis. Ann Surg. 1957;145:88-93.
Phlegmonous gastritis
The patient was treated with intravenous antibiotics (amoxicillin/clavulanic acid 6.6 g/d) and a proton pump inhibitor (esomeprazole 80 mg/d). Within a few days, her clinical status improved and abdominal ultrasound examination documented regression of the gastric wall thickening. Laboratory screening for predisposing factors such as diabetes mellitus, infection with human immunodeficiency virus, or immunoglobulin deficiency were negative and there was no clinical evidence of Crohn’s disease. Antibiotic treatment was stopped after 2 weeks. Six months later, follow-up gastroscopy was performed confirming complete resolution of the inflammatory changes in the stomach.
Phlegmonous gastritis is a rare but potentially life-threatening bacterial infection of the gastric wall. Since its first description in 1862, about 500 cases have been reported worldwide. Whereas the original reports dating back to the preantibiotic area suggest very high mortality rates in the range of 90%, phlegmonous gastritis still represents a life-threatening condition.1,2 In about one-half of the cases, acquired immunodeficiency states such as diabetes mellitus, human immunodeficiency virus, or alcoholism are identified as predisposing factors. In addition, gastric biopsies may herald the development of phlegmonous gastritis. Streptococcus spp. account for the majority of the cases, which can be isolated in about 70% of patients.1 Other organisms such as Staphylococcus spp., Escherichia coli Haemophilus influenzae, and Proteus or Clostridium spp. have been described as pathogens associated with this uncommon condition. Affected patients typically present with nonspecific symptoms such as abdominal pain, fever, nausea, vomitus, hematemesis, or diarrhea. In light of the devastating natural course of phlegmonous gastritis, timely preemptive administration of broad spectrum antibiotic along with a high index of suspicion are paramount. A computed tomography scan and transabdominal ultrasound examination are useful as initial tests, whereas endoscopic ultrasound examination typically demonstrates a diffusely thickened, hypoechogenic submucosal wall layer that is not commonly found in patients with other submucosal lesions, such as carcinoid or leiomyoma. The diagnosis can be confirmed by endoscopic forceps biopsy provided that sufficient submucosal tissue is included.1 Surgery should only be considered for cases refractory to conservative treatment.
References
1. Kim G, Ward J, Henessey B, et al. Phlegmonous gastritis: case report and review. Gastrointest Endosc. 2005;61:168-74.
2. Starr A, Wilson J. Phlegmonous gastritis. Ann Surg. 1957;145:88-93.
Phlegmonous gastritis
The patient was treated with intravenous antibiotics (amoxicillin/clavulanic acid 6.6 g/d) and a proton pump inhibitor (esomeprazole 80 mg/d). Within a few days, her clinical status improved and abdominal ultrasound examination documented regression of the gastric wall thickening. Laboratory screening for predisposing factors such as diabetes mellitus, infection with human immunodeficiency virus, or immunoglobulin deficiency were negative and there was no clinical evidence of Crohn’s disease. Antibiotic treatment was stopped after 2 weeks. Six months later, follow-up gastroscopy was performed confirming complete resolution of the inflammatory changes in the stomach.
Phlegmonous gastritis is a rare but potentially life-threatening bacterial infection of the gastric wall. Since its first description in 1862, about 500 cases have been reported worldwide. Whereas the original reports dating back to the preantibiotic area suggest very high mortality rates in the range of 90%, phlegmonous gastritis still represents a life-threatening condition.1,2 In about one-half of the cases, acquired immunodeficiency states such as diabetes mellitus, human immunodeficiency virus, or alcoholism are identified as predisposing factors. In addition, gastric biopsies may herald the development of phlegmonous gastritis. Streptococcus spp. account for the majority of the cases, which can be isolated in about 70% of patients.1 Other organisms such as Staphylococcus spp., Escherichia coli Haemophilus influenzae, and Proteus or Clostridium spp. have been described as pathogens associated with this uncommon condition. Affected patients typically present with nonspecific symptoms such as abdominal pain, fever, nausea, vomitus, hematemesis, or diarrhea. In light of the devastating natural course of phlegmonous gastritis, timely preemptive administration of broad spectrum antibiotic along with a high index of suspicion are paramount. A computed tomography scan and transabdominal ultrasound examination are useful as initial tests, whereas endoscopic ultrasound examination typically demonstrates a diffusely thickened, hypoechogenic submucosal wall layer that is not commonly found in patients with other submucosal lesions, such as carcinoid or leiomyoma. The diagnosis can be confirmed by endoscopic forceps biopsy provided that sufficient submucosal tissue is included.1 Surgery should only be considered for cases refractory to conservative treatment.
References
1. Kim G, Ward J, Henessey B, et al. Phlegmonous gastritis: case report and review. Gastrointest Endosc. 2005;61:168-74.
2. Starr A, Wilson J. Phlegmonous gastritis. Ann Surg. 1957;145:88-93.
A previously healthy 41-year-old woman presented with upper abdominal pain, nausea, vomiting, and fever for 4 days. On admission, the patient was febrile (40.1°C); her blood pressure, heart rate, and peripheral oxygen saturation were normal. Laboratory findings were notable for a C-reactive protein of 190 mg/L (reference range, less than 5 mg/L) along with a white cell count of 21,600/mm3 (reference range, 4,500-10,500/mm3). Liver enzymes, pancreatic lipase, and bilirubin were within normal limits. A computed tomography scan of the abdomen revealed wall thickening of the gastric antrum (Figure A).
Gastroscopy showed a heavily distorted gastric antrum with a fistula (Figure B, C). Consecutively, endoscopic ultrasound examination was performed, confirming circumferential thickening of the antral wall up to 20 mm with inhomogeneous hypoechogenic areas within the submucosa (Figure D). Deep endoscopic forceps biopsies were obtained. Histopathologic examination revealed extensive infiltration of the mucosa and submucosa by neutrophils (Figure E, F) and microbial cultures were positive for Streptococcus spp. (S. pyogenes, viridans group streptococci) and Rothia mucilaginosa.