PG patients typically present with acute abdominal pain, vomiting and fever. But although this symptom triad is considered characteristic of PG [4], retrospective studies have shown that considerable shares of patients don't experience any complaints besides an acute abdomen. In detail, epigastric pain has been reported in 95% of cases, whereas nausea, vomiting and fever are described by two thirds of affected individuals only [1]. A certain relief of pain may be achieved by changing from a supine to a sitting position (Deininger's sign) [5], and fever may be accompanied by chills. Patients less commonly present hematemesis or coffee-ground emesis [6]. Moreover, purulent emesis has been reported and is considered pathognomonic for PG [7].
Upon perforation, patients deteriorate rapidly and develop signs of diffuse peritonitis, sepsis and multiple organ failure [8]. There is one case report describing the discharge of pus to liver and spleen, giving rise to multiple hepatic and splenic abscesses [9].
Laboratory analyses of blood samples should be conducted to assess the patient's general condition and typically yield the following results [5]:
Such results are non-specific, though, and it is necessary to perform diagnostic imaging in order to correlate the clinical picture with severe gastritis. Endoscopy is very helpful to this end, but computed tomography scans may also be carried out. During an endoscopic examination, multiple lesions of the gastric mucosa may be observed. In general, they are largely covered by mucopurulent exudate and are prone to bleed. Generalized edema and erythema are also seen. Endosonography may allow for a better examination of deeper layers of the gastric wall. In this context, hypoechoic lesions in the submucosal layer have been described [1]. Images obtained by means of computed tomography typically show marked thickening of the gastric wall and intramural hypodense regions [10].
Phlegmonous gastritis (PG), sometimes also referred to as suppurative gastritis, is a rare type of stomach infection and inflammation. It is provoked by pyogenic bacteria, most commonly by pathogens of the genus Streptococcus [1], and is associated with high mortality [2]. It has been speculated that patients with a medical history of recurrent gastritis, those suffering from chronic ulcer that may or may not be the result of drug abuse, as well as immunocompromised individuals are at higher risks of developing PG [3], but the disease' pathophysiology remains poorly understood. About half of PG patients have no medical history of stomach disease. PG may be restricted to determined parts of the stomach lining, or may affect the whole stomach. Accordingly, localized and diffuse PG may be distinguished. Successful treatment regimens comprise the administration of antibiotics and surgery. Because survival rates are similar in either case, most patients are initially prescribed antibiotics and surgical interventions are postponed for refractory cases and complications [2]. If necessary, partial or complete gastrectomy may be performed.