Biopsy showed gastric mucosal necrosis, and necrosis was found on areas of the mucosal muscularis, muscularis, and serosa layer, where extensive neutrophil infiltration was present. Abscess formations were also found in the said areas, and the stomach and the greater omentum were phlegmonous (Fig. 4). Tissue culture specimens were positive for hemolytic streptococcus.
Acute PG was originally described by Cruveilhier in the early 18th century, and an average of 1 case report per year has appeared over the last 60 years.[4–6] The disease affects all age groups and is highly common in adults in their 50s to 70s, and the male-to-female ratio is 2:1. Acute PG is rare clinically, especially since the use of antibiotics, but becomes urgent and develops quickly once it occurs. With the high mortality of this disease, early recognition and immediate action are crucial. With <500 cases reported in the literature, it requires the attention of medical staff.
At present, acute PG's cause is not entirely clear presumably due to fester bacterium invading the stomach. Hemolytic streptococcus is reportedly found in approximately 70% of cases, followed by Staphylococcus aureus, Pneumococcus, and Enterococcus. Bacterial invasion of the gastric wall can be caused by gastric ulcer, chronic gastritis, and the like, with the pathogenic bacteria of the pharynx directly infringing into the damaged mucosa; respiratory tract infection or other infection, with the pathogenic bacteria entering the gastric wall through blood flow; the pathogenic bacteria entering the gastric wall through the lymphatic system in the case of cholecystitis and peritonitis. Furthermore, drinking, malnutrition, and being elderly are often cited as causes of the disease. Considering this case, the patient had the predisposing factor long-term alcohol consumption and gastritis, and he has not fully recovered from his recent respiratory tract infection (one of main pathogenic bacteria was hemolytic streptococcus). Considering that hemolytic streptococcus was cultivated from the percolate, we presumed that the acute PG was caused by pulmonary pathogen invasion into the stomach in this patient.
The pathophysiological process is chiefly caused by the bacteria's invasion of the submucosa, propagating and diffusing into the mucosa and serous membrane, and is classified into diffuse and localized types according to the lesion range.[10,11] The diffuse type is more common clinically than the localized type, and it is characterized by dark red stomach wall and diffuse thickening; when the stomach wall is squeezed, pus outflow occurs from the gastric wall. This type can also cause gastric cavity expansion and gastric wall perforation under severe circumstances. The localized type features gastric mucosal hyperemia and erosion, ulceration, necrosis, or bleeding. The localized type is associated with a lower mortality rate than the diffuse type (10% vs 54%, respectively). In our patient, the stomach wall was obviously swollen, and necrosis was found in parts of the stomach. The postoperative section of the abscess accumulated in the stomach wall. Hence, this case belonged to the diffuse type.
An early diagnosis of PG is difficult due to the nonspecific nature of its clinical manifestations, including acute abdominal disease, sudden onset of abdominal pain, high fever, chills, nausea, and vomiting. Thus, differentiating PG from an acute abdomen (e.g., perforation peritonitis, acute cholecystitis, and acute pancreatitis) is necessary. With the development of the disease, body temperature can increase, peritoneal irritation signs become obvious, such as abdominal tenderness, rebound pain, and the vomitus can change to abscess fluid.[5,9,13] Abdominal CT typically reveals the following characteristic findings of PG: thickening of the gastric wall, low-intensity areas within the gastric wall (indicative of an abscess), and gas accumulation. The patient's clinical manifestation included abdominal pain, epigastric peritonitis, and the feature of CT. Considering that the purulent patient vomited, we made a diagnosis of acute PG, having distinguished it from other acute abdominal diseases.
Acute PG has an extremely high mortality rate, and the key to successful treatment is early diagnosis and treatment. Before the advent of antibiotics, the fatality rate was as high as 83% to 92%, and the mortality rate reduced to 48% even after antibiotics became available. In addition, nutritional support and rehydration are very important to the success of the treatment.[14–16] However, if conservative treatment effect is ineffective, surgery should be performed immediately to avoid aggravation of the state of the illness. The condition of the patient in our center aggravated after conservative treatment. Hence, emergency operation was performed, and postoperative support treatment was provided. Finally, the patient recovered.
Acute PG lacks specific clinical performance, and abdominal CT is helpful for both early diagnosis and detecting complications. Once acute PG is detected, antibiotic treatment is important, but if this treatment fails, surgery should be performed immediately to improve the prognosis. At present, given the use of antibiotics, the incidence rate is extremely low. However, once the disease occurs, it rapidly progresses and has an extremely high fatality rate. Thus, it requires serious attention by clinicians.
This study was approved by the ethics committee at the Affiliated Hospital of Guizhou Medical University in China. The patient provided informed consent.
Conceptualization: Qian Wang, Haibin Wang, Zhiqiang Yan,Hongxin Yang, Haitao Xie.
Data curation: Hongxin Yang, Jiaju Chen.
Investigation: Hongxin Yang.
Writing – original draft: Hongxin Yang.
Writing – review and editing: Hongxin Yang, Qian Wang, Haibin Wang, Zhiqiang Yan.
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Keywords:Copyright © 2018 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.
acute phlegmonous gastritis; clinical manifestation; pneumonia; prognosis; treatment