Gastritis, acuteK29.1

Gastritis was first described in autopsies in the 1800s (Kayacetin 2104).

Phlegmonous gastritis was first described by Fränkl in 1889 (Trum 2014).

The association between Helicobacter pylori colonization of the stomach and the development of gastritis was demonstrated in 1983 by a self-experiment of the first describer, Barry Marshall (Trede 1994 / Hahn 1999).

Omeprazole, a drug used for the prophylaxis and therapy of (acute) gastritis, has been one of the most frequently prescribed drugs worldwide since its development in 1979 (Lin 2021).

There is no generally accepted definition of acute gastritis, since gastritis itself is understood as a histological diagnosis and any form of "stomach upset" is usually referred to as gastritis (Sauerbruch 2021).

Acute gastritis is differentiated between:

- acute irritable gastritis

- erosive gastritis (Herold 2022)

Erosive gastritis is also called "stress gastritis". It results primarily from a dysregulation in the production of gastric acid (Megha 2022).

- Acute phlegmonous gastritis

This refers to a bacterial infection of the stomach. It is a rare but potentially life-threatening condition (Kasper 2015).

Everyone has probably been affected by acute gastritis at least once in their life (Zankl 2014). Due to the self-limited and variable course, no reliable prevalence figures exist (Messmann 2012).

The most common causative agent of chronic gastritis worldwide is Helicobacter pylori infection, which can result from untreated acute gastritis. However, these numbers have recently been declining with increasing prevalence of autoimmune gastritis (Azer 2022).

Phlegmonous gastritis:

This is extremely rare. To date, only 140 cases have been described worldwide (Trum 2014).

Most commonly, acute gastritis is caused by exogenous noxious agents (Messmann 2012).

Acute gastritis can be triggered by:

- Infections with

- H. pylori (infection occurs by the fecal-oral route [Azer 2022]).

- H. heilmannii

- Phlegmonous

- mycobacteria

- syphilis

- viral

- parasites

- mycoses (Kasper 2015)

- alcoholic excess

- alimentary excess

- Stress due to e.g. trauma, postoperative, shock, intracranial diseases

- Medications such as acetylsalicylic acid, NSAIDs, corticosteroids, cytostatics

- Food poisoning due to, e.g., toxin-producing streptococci, staphylococci, and others (Herold 2022)

- Phlegmonous gastritis (PG).

The cause of phlegmonous gastritis is as yet unknown (Trum 2014). It is common in extensive ulceration, gastric carcinoma and after gastric surgery (Siewert 2006) and is also seen (very rarely) after routine esophagogastroduodenoscopy biopsies (Jenssen 2014).

Pathogens are predominantly:

- Streptococci

- staphylococci

- E. coli

- Proteus

- Haemophilus species (Kasper 2015).

Phlegmonous gastritis particularly affects:

- elderly people

- alcoholics

- AIDS patients

- after mucosal injections with India ink

- in cases of polypectomy (Kasper 2015)

Acute gastritis results from inflammatory lesions of the gastrointestinal mucosa as soon as the integrity of the mucosa is disturbed by aggressive factors such as:

- infections

- bile reflux

- pepsin

- alcohol

- cigarettes

- various drugs such as acetylsalicylic acid, NSAIDs, corticosteroids, cytostatics (Lin 2021)

In acute gastritis triggered by H. pylori, there is initially excessive pepsin and acid secretion for 2 - 3 days, followed by a phase of hypochlorhydria lasting 2 - 3 weeks (Rösch 2005).

Acute gastritis can occur at any age.

The clinical symptoms are rather nonspecific and also highly variable. Some patients are asymptomatic (Messmann 2012).

Otherwise, the following symptoms may exist:

- epigastric pain

- nausea

- vomiting (Kasper 2015)

- loss of appetite

- unpleasant taste in the mouth (Herold 2022)

Phlegmonous gastritis:

Phlegmonous gastritis is clinically manifested by

- severe epigastric pain

- fever

- defensive tension of the abdomen (Siewert 2006)

For the diagnosis of gastritis itself, anamnestic data and gastroscopy are indicative. Ultimately, however, only histological examination is conclusive (Herold 2022). Since the acute form of the disease is usually only short and self-limited, in the vast majority of cases no further diagnosis is made, so that it is rather a purely tentative diagnosis (Sauerbruch 2021).

Only in the case of complications such as hemorrhages is an instrumental diagnosis immediately indicated (Messmann 2012).

Gastroscopy

Multiple sharply circumscribed superficial erosions are seen - especially proximally - usually < 2 mm in size (Kayacetin 2014).

- Erosive Gastritis:

If the epithelial defects are larger, they are also referred to as "erosive gastritis" (Herold 2022).

- Helicobacter- pylori gastritis:

In this case, an antrum-dominant gastritis with typical erosions is seen. Sometimes there is also corpus-dominant gastritis without erosions, but with erythema and edema (Braun 2022).

Serological tests

Serologic testing can detect antibodies to detect H. pylori infection. However, it is not possible to differentiate between an acute or chronic form of gastritis (Azer 2022).

Acute gastritis histologically shows a marked infiltrate of neutrophils, hyperemia, and edematous swelling in the area of the lamina propria (Kasper 2015 / Kayacetin 2014). The mucosa may be necrotically altered with low neutrophil infiltration (Kayacetin 2014).

- Acute phase of H. pylori gastritis:

Here, granulocytic infiltration and excessive pepsin and acid secretion with subsequent hyperchlorhydria are found (Sauerbruch 2021).

- Erosive gastritis:

In the erosive course, the substance defect is limited to the lamina propria, in contrast to the substance defect in ulcer, which always involves the muscularis mucosa (Braun 2022).

- Phlegmonous gastritis:

In this case, there are histologically distinct acute inflammatory infiltrates of the entire gastric wall (especially the submucosa [Siewert 2006]). Sometimes necrosis is also detectable (Kasper 2015).

In addition to other diseases of the stomach, duodenum, pancreas or gallbladder (Herold 2022), differential diagnosis should also exclude:

- chronic active gastritis caused by Helicobacter pylori.

In this case there is a lymphoplasmocytic inflammation and a neutrophilic cryptitis.

- Dysplasias

These are manifested by nuclear stratification, hyperchromasia, increased mitotic rate, etc.

- chemical gastropathy

In this case, stretching of the mucosa, smooth muscle hyperplasia and regenerative changes are found

- Trauma after biopsy (Kayacetin 2014).

- Chronic gastritis (Azer 2022)

- Ulcers

Gastritis may result in the development of a stress ulcer and/or gastric hemorrhage (especially in erosive gastritis) (Herold 2022).

In acute gastritis, general measures are indicated in the first instance:

- elimination of noxious substances

- temporary abstinence from food with avoidance of solid food (Herold 2022).

Drug therapy is usually not necessary (Messmann 2012).

If the symptoms are more severe, the following can be used if necessary:

- Proton pump inhibitors (PPI) such as omeprazole.

- For nausea/vomiting, an antiemetic such as Vomex A (Herold 2022).

- Water and electrolyte supplementation for vomiting (Sauerbruch 2021).

Acute gastritis caused by Helicobacter pylori:

In Helicobacter pylori gastritis, complete eradication with triple drug therapy - consisting of proton pump inhibitor plus 2 antibiotics(clarithromycin plus amoxicillin or clarithromycin plus metronidazole) - for 7 - 14 days is required. If necessary, bismuth may also be prescribed as quadruple therapy for 10 days (Lehmeyer 2022).

Erosive gastritis:

Proton pump inhibitors such as omeprazole (Lin 2021).

Dosage recommendation: 40 mg / d (Weihrauch 2022).

Phlegmonous gastritis:

In this case, therapy with antibiotics is initially indicated. If there is no improvement under this, gastrectomy may be necessary (Kasper 2015).

Acute gastritis usually heals spontaneously (Herold 2022). The only exception is acute gastritis caused by infection with Helicobacter pylori, which progresses to a chronic form if left untreated (Sauerbruch 2021).

Phlegmonous gastritis

This is lethal in up to 70 %, as it is a systemic toxicity (Trum 2014).

Erosive gastritis can often be prevented in polytrauma patients, major surgery, myocardial infarction, etc. by early use of proton pump inhibitors such as omeprazole. The reduction in disease with early therapy is between 30-55% (Megha 2022).

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