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Gastritis: An Update in 2020

• Stomach (P Malfertheiner, Section Editor)
• Open access
• Published: 26 August 2020
• Volume 18 , pages 488–503, ( 2020 )

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• Massimo Rugge MD 1 , 2 ,
• Kentaro Sugano 3 ,
• Diana Sacchi 1 ,
• Marta Sbaraglia 1 &
• Peter Malfertheiner 4  

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Purpose of review

The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. “inflammation-associated cancer”). This review illustrates the updated criteria applied in the taxonomy of gastritis (Kyoto classification), elucidates the biological rationale for endoscopy biopsy sampling (heterogeneity of gastric mucosa), and finally reports the results of long-term follow-up studies supporting the reliability of biopsy-based gastritis staging as predictor of gastritis-associated cancer risk.

Recent findings

By assuming gastric atrophy as the “cancerization field” where (non-syndromic) gastric cancer mostly develops, recent long-term follow-up studies consistently demonstrate the prognostic impact of the gastritis OLGA staging system.

Helicobacter pylori eradication is the leading strategy in the primary prevention of gastric cancer. In a multidisciplinary dimension of secondary cancer prevention, the OLGA staging system reliably ranks the patient-specific cancer risk, thus providing the clinical rationale for a tailored follow-up strategy.

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Introduction

The “gastritis” label is extensively (but inappropriately) applied to a spectrum of clinical symptoms relating to the upper abdomen, and the epigastrium in particular. The correct medical definition for this cluster of symptoms is dyspepsia. More strictly speaking, in the absence of organic disorders, the various combinations of upper digestive symptoms (e.g. bothersome postprandial fullness, early satiation, epigastric pain, and epigastric burning) should be defined as functional dyspepsia. There is an update on the (sub)types of functional dyspepsia at the Rome IV conference [ 1 , 2 ].

At endoscopy, gastritis is described as any reddening or edema of the gastric mucosa, but neither of these endoscopic features is specific or exclusive to mucosal inflammation. A Japanese study on the accuracy of standard endoscopic imaging for the detection of H. pylori infection reported accuracy of 89% for nodularity and 77% for mucosal swelling [ 3 ].

The endoscopic assessment of gastritis has advanced significantly in recent times thanks to the use of high-definition endoscopy and virtual chromoendoscopy (narrow-band imaging [NBI], blue light imaging [BLI], and linked color imaging [LCI]) [ 4 , 5 , 6 ]. An endoscopic classification of gastritis has been proposed in Japan, but important steps in the validation process are still needed before it can be more generally accepted outside Japan [ 7 ].

The endoscopic detection and interpretation of gastric atrophy poses the greatest challenge. Although the combined use of high-definition endoscopy and virtual chromoendoscopy has significantly improved the accuracy of endoscopic assessments, the consistent implementation of these new technologies entails a steep learning curve, and they are still operator-dependent [ 8 , 9 ].

In a recent study involving magnifying endoscopy combined with NBI, the authors reported that vascular architecture can detect premalignant gastric conditions accurately (88%), and better than the serum pepsinogen I/II ratio (74%) [ 10 ].

Gastritis: Classification criteria

From the clinical and pathological perspective, gastritis is defined as “acute” or “chronic.” These two terms are commonly intended as synonymous with self-limiting or non-self-limiting, respectively. The temporal parameter used to distinguish acute from chronic diseases is largely subjective, and many “chronic” asymptomatic diseases may occasionally develop “acute” symptoms.

Equally questionable is the distinction between acute and chronic gastritis based on cellular inflammatory infiltrate: lymphocytes (typically associated with chronic inflammation) may prevail in some acute (i.e. self-limiting) forms of gastritis (lymphocytic gastritis), and granulocytes (typically associated with acute inflammatory lesions) can be found in chronic (i.e. non-self-limiting) inflammatory gastric diseases (e.g. H. pylori gastritis) (Figs.  1a, b and 2 ).

a , b Lymphocytic gastritis: high-grade mononuclear lymphocytic infiltrate within the lamina propria, in a gastric biopsy sample obtained from antral mucosa; intra-epithelial lymphocytes are also shown. ( a : Hematoxylin-eosin, original magnification ×40). In the same biopsy sample, the CD3-immunostain clearly documents the high-grade intra-epithelial lymphocytic infiltrate. ( b : CD3 immunostain, original magnification ×40).

Helicobacter pylori gastritis: the picture shows the high-grade granulocytic infiltrate within the lamina propria and inside the gastric glans (so-called active inflammation). (Hematoxylin-eosin, original magnification ×40).

As recently acknowledged in the Kyoto global consensus report, the most valid gastritis classification relies on etiology. Leaving aside the (far from negligible) number of mucosal inflammations of unknown etiology, the agents involved in the etiology of gastritis can be gathered into two main groups: environmental agents (which may or may not be transmissible), and host-related, non-transmissible agents. The two etiopathogenic situations may overlap (Table 1 ). The etiological classification of gastritis (with minor adjustments to the Kyoto proposal) is shown in the table [ 11 ••, 12 , 13 , 14 ].

Excluding a false-negative H. pylori result remains a special challenge. For this purpose, marked reactive changes in both the antral and oxyntic mucosa need to be interpreted in the context of atrophy of other etiologies, or use of a proton pump inhibitor (PPI) [ 15 ]. El Zimaity et al. reported that H. pylori may only be found in parietal cells in patients on PPI. This is a rather exceptional situation and is not used as a criterion for assessing H. pylori -related gastritis. The differential diagnosis should include lymphocytic gastritis, vasculitis, granulomatous diseases, inflammatory bowel disease, viral infections, and other bacterial diseases. It is only after excluding all of these forms that the term “ H. pylori -negative gastritis” should be considered [ 15 , 16 , 17 , 18 , 19 , 20 •].

Gastritis: 2020 definition

By definition, a diagnosis of gastritis requires the histological detection of inflammatory cells within the lamina propria. Leukocytes may also penetrate the glandular lumen and/or spread down into the submucosa. The topography, severity, and cellularity of the inflammatory lesions might sometimes enable us to distinguish between different etiological variants of gastritis. Leaving aside the cellular profile of the “inflammatory population,” gastritis can be divided into two main forms, non-atrophic and atrophic. The need to distinguish between the two is crucially related to the different cancer risk associated with these two histological variants.

Non-atrophic gastritis exhibits mucosal damage that can even be extensive and/or severe, and may recover with trivial residual sequelae, or progress to atrophic phenotypes.

Atrophic gastritis is usually long-standing, and not self-limiting, and results from noxious agents that markedly alter the resident population of the gastric glands (i.e. oxyntic glands in the corpus/fundus, mucosecreting glands in the antral mucosa). In both these mucosal compartments, atrophy is defined as a “loss of native glandular units” [ 21 , 22 ].

Atrophy may result from a loss of native glands, replaced by fibrosis (non-metaplastic atrophy), or a focal or extensive replacement of the native gland population by metaplastic glands. Metaplastic atrophy may feature two phenotypes: intestinal metaplasia (IM), affecting the mucosecreting glands (Fig.  3 ), and pseudo-pyloric metaplasia, which is also known as pseudo-pyloric gland metaplasia (PGM) or spasmolytic peptide-expressing mucosa (SPEM), which only affects the oxyntic glands [ 23 , 24 ].

Gastric mucosa atrophy: metaplastic variant. The largest portion of the biopsy sample (about 65%; OLGA score: 3) is covered by atrophic-metaplastic glands; goblet cells are the key marker of mucosal intestinalization. (Hematoxylin-eosin, original magnification ×5)

The histogenesis of SPEM is still debated and needs to be further addressed. Seminal experiments supported the hypothesis that SPEM originates (independently of stem cells) from “transdifferentiation” or “dedifferentiation” [ 25 , 26 ]. Other putative sources [ 27 , 28 ] include the progenitor cells located at the glandular neck, or a population of Troy-positive cells located at the bottom of the oxyntic glands. The idea of a possible transformation of SPEM into intestinalized epithelia is supported by molecular profiling studies and histological evidence of SPEM preceding the histological detection of oxyntic intestinalization by years.

Both subtypes of metaplastic changes are included in the spectrum of gastric atrophy [ 29 , 30 ].

The inclusion of other (minor) variants of metaplastic transformation (e.g. pseudo-pancreatic metaplasia) in the spectrum of atrophy is irrelevant. Any subtype of gastric atrophy may give rise to functional changes (in acid secretion or pepsinogen serum levels, for instance) and/or a “remodeling” of the intragastric microenvironment. There is increasing evidence to suggest that the “atrophy-associated” microbiome may be involved in promoting a cancer-prone microenvironment. Such a picture reinforces the priority of assessing and quantifying gastric mucosal atrophy endoscopically and histologically, considering the whole spectrum of atrophy phenotypes, all of which might be involved in creating cancer-promoting biological conditions. Taking this new approach, we need to reconsider the “traditional” view concerning the specific responsibility of intestinal metaplasia in gastric carcinogenesis, and return to a holistic concept of atrophy as the “cancerization field” for gastric adenocarcinoma [ 24 , 31 , 32 , 33 , 34 , 35 , 36 ].

Gastritis: Biopsy sampling protocols and histological assessments

The rationale behind gastric biopsy sampling takes into account the physiopathological compartmentalization of the gastric mucosa. Already in embryo, the gastric sac consists of two (functional, histological) compartments, and they remain distinct after birth.

Gastric compartmentalization (from the embryo to the adult)

There is a paucity of (sometimes contradictory) information on the characterization of the embryonic stomach: canonical Wnt signaling pathway is assumed to be virtually restricted to the cranial gastric segment and absent from the presumptive antrum. The distinctive profile of the embryonic stomach is supported by two recent complementary observations [ 37 , 38 ]: the deletion of Ctnnb1 , a canonical WNT-effector, is associated with ectopic Pdx1 expression, which results in cranial stomach antralization; and the deletion of Bapx1 (a transcription factor expressed in the mesenchyme of the distal stomach) results in an “oxyntic transformation” of the antral stomach (Fig.  4 ).

1. WNT-mediated gastric patterning mechanisms: WNT/beta-catenin signaling promotes oxyntic specification. 2. Transcription factors such as Pdx1, Nkx6.3, and Bapx1 (as expressed in mesenchyme surrounding the distal stomach) are specifically involved in promoting the caudal specification (mucosecreting antral mucosa). Abbreviations A: anterior; P: posterior; V: ventral; D: dorsal [ 36 , 37 ]

At birth, there are two main, histologically distinct gastric mucosal compartments: the oxyntic (corpus) mucosa, and the mucosecreting (antral) mucosa. A third area covers a narrow portion of the junctional area between the terminal esophagus and the most cranial segment of the stomach. The phenotype of native cardia-mucosa is still controversial. Equally credited theories support a glandular population including both native mucosecreting (antral type) and native oxyntic glands, or a mucosa natively consisting only of native oxyntic glands, with any mucosecreting component considered a metaplastic transformation of the resident oxyntic glands.

Distally to the cardia, the largest portion of the gastric mucosa consists of oxyntic glands (including chief, parietal end enterochromaffin-like [ECL] cells). The so-called atrophic border, better defined as the pyloric-fundic gland border, is an irregular boundary between the oxyntic and the mucosecreting compartments. The latter compartment consists of coiled mucosecreting glands extending from approximately two-thirds of the length of the stomach hook to the pyloric sphincter. The normal morphology of these areas is well established and easily recognizable. All these anatomical landmarks have important implications in the endoscopic and histological assessment of gastritis.

Obtaining gastric mucosa biopsy samples: The biological rationale

The different embryonic “patterning” and the post-natal histology and function of the stomach lend further support to the view of this organ as “two functions in one sac.” This compartmentalization provides the rationale for obtaining gastric biopsy samples representative of both mucosal compartments. In routine endoscopic practice, however, this recommendation is frequently ignored, for two main reasons: the increasing costs of the diagnostic procedure associated with obtaining, handling, and assessing multiple biopsy samples; and a preference for using one (or even more!) biopsy samples for a rapid assessment of Helicobacter pylori status.

Different protocols for the endoscopic biopsy sampling of the gastric mucosa have been proposed, but they all recommend obtaining samples from both the oxyntic and the mucosecreting mucosa. The recommended number of specimens to collect varies, depending on the clinical indication, and the aims of the endoscopy/biopsy procedure. In general, more extensive biopsy protocols are recommended for research purposes, while a minimum set of gastric biopsies is suggested for clinical purposes. The most widely applied clinical protocol is the updated Sydney System, which includes a total of five biopsy specimens, i.e. two from the oxyntic mucosa (both submitted in the same vial), one from the incisura angularis, and two from the antral mucosa (all three submitted in the same vial). Any focal lesions should also be sampled and submitted separately [ 8 , 39 , 40 •, 41 ].

Gastritis: The clinical value of a “structured” histology report

Gastric mucosal atrophy is recognized as the cancerization field in which more than 90% of gastric epithelial malignancies will eventually develop. This well-established evidence provides the rationale for assessing patients’ “individual” gastric cancer risk from their histological atrophy score, which also takes its topography (corpus, antrum, or both) into account. Consistent with this approach, histological gastritis staging has proved a reliable predictor of gastric cancer risk.

In East Asian countries, the extent of atrophy and its associated cancer risk continues to be assessed endoscopically according to the Kimura-Takemoto classification [ 42 , 43 , 44 ]. In the Western world, a biopsy-based assessment is recommended (Maastricht V, MAPS guidelines). OLGA (Operative Link for Gastritis Assessment) is a validated staging system that considers both the atrophy score and the compartment (oxyntic versus mucosecreting) from which the biopsy samples were obtained (i.e. oxyntic and antral mucosa, according to the Sydney System protocol) [ 45 , 46 ]. The combined antral and oxyntic scores (see Table 2 for atrophy scoring and staging) result in a “gastritis stage” (from 0 to IV) indicating the risk of malignancy. An alternative staging system called OLGIM (Operative Link on Gastric Intestinal Metaplasia) is based only on a score for intestinal metaplasia [ 47 , 48 ], and this makes it likely to be less sensitive in assessing atrophy than the (more comprehensive) OLGA approach [ 48 ].

Whenever possible, histological staging should be complemented with etiological information, reference to clinical parameters, and other diagnostic details. Table 1 lists all the relevant etiological factors, and those most often resulting in atrophic mucosal changes.

From the histology report to the clinical patient’s management

In spite of the enormous progress made in endoscopic imaging technologies, with more to come, histology remains the gold standard for the diagnosis of gastritis. Advances in this area relate to an etiology-based diagnosis, already reflected in the new International Classification of Diseases (ICD-11), and to the clinical priority of gastritis staging in the long-term personalized management of gastritis patients. Relying on essential information about the etiology and staging of a case of gastritis, clinicians can safely proceed with the most appropriate therapy, and decide whether and what type of follow-up is required [ 49 , 50 ].

Having identified the cause of gastritis, the first step will be to eliminate the noxious agent whenever possible. In cases of H. pylori gastritis, eradication therapy is recommended in all international consensus and guideline reports [ 11 ••, 51 , 52 ].

In the absence of severe gastric disease and/or preneoplastic changes, the success of H. pylori eradication therapy can be tested with a noninvasive surrogate marker (urea breath test [UBT], fecal antigen test). A negative test result indicates the healing of H. pylori gastritis [ 53 ••]. Any specific infectious agent detected can be cured by appropriate antibiotic or antiviral treatments. No etiological therapy is available as yet for autoimmune gastritis, the clinical impact of which is constantly increasing all over the industrialized world. There is little evidence for glucocorticoid therapy to reverse the atrophy involved [ 54 ]. When pernicious anemia ensues, vitamin B12 supplementation is indicated. In the autoimmune setting, the (consistently recognized) risk of neuroendocrine neoplasia makes it important to adopt an appropriate staging system that includes IM-negative atrophic transformation (i.e. pseudo-pyloric metaplasia, or what is known as SPEM) [ 55 , 56 ]. SPEM is involved in hyperplastic/dysplastic ECL cell proliferation, and may theoretically be associated with a higher risk of gastric adenocarcinoma [ 25 , 57 , 58 ]. It is often more difficult to document the etiology of other forms of gastritis, but it may help to look for a systemic cause, as in Crohn’s disease (Fig.  5 ).

Epithelioid granuloma in Crohn-associated gastritis. Infectious etiology was excluded by both molecular biology testing and special stain for Koch’s bacilli. (Hematoxylin-eosin, original magnification ×40)

Leaving aside the etiology of gastritis, a histology report plainly expressing the “level of alarm” related to the severity of atrophic disease (and its associated cancer risk, in particular) could contribute to generating treatment and follow-up protocols tailored to individual patients’ clinical needs. This approach has been extensively applied in oncological practice and is the reasoning on which gastritis staging is based. In patients with “advanced” atrophic changes (high-risk OLGA/OLGIM stages III/IV), regular endoscopic follow-up serves the fundamental purpose of a reliable secondary gastric cancer prevention strategy [ 59 ].

Three different trials with a follow-up spanning several years produced significant evidence to support a high risk of gastric cancer developing in patients with OLGA stages III/IV (Table 3 ) [ 40 •, 60 , 61 ••]. Two of these three studies [ 40 •, 61 ••] were conducted in populations of consecutive dyspeptic patients undergoing endoscopy, with no histological evidence of neoplastic lesions (intraepithelial [IEN] or invasive gastric cancer [GC]). The studies had a similar patient distribution by stage, and the proportion of patients in stages III and IV never exceeded 3% (these patients were mainly males, and their median age was older than that of patients with stage 0/I/II disease). Such a low prevalence of patients “at risk” makes it feasible to implement dedicated programs of active surveillance. The two studies (involving 9191 patients in all) also consistently showed a dichotomous cancer risk, which was nil or negligible for stages 0/I/ II (low-risk stages) and high for OLGA stages III/IV (high-risk stages).

The third study [ 60 ] involved 93 patients who were followed up with paired endoscopies for more than 12 years (range: 144–204 months). It was conducted on a population living in a mountain valley previously identified as being at high risk of GC (with an incidence of gastric malignancy of 270/100,000/5 years, and an 80% prevalence of H. pylori ). As expected in this particular epidemiological context, the prevalence of high-risk stages was greater than in the two previously mentioned studies, but all the incident neoplastic lesions (detected by the end of the follow-up) were identified among patients enrolled with stage III/IV gastritis.

The high risk of cancer developing in such cases enables us to identify patients early enough in their progression to gastric malignancy for timely intervention, which involves endoscopic resection of crucial areas of the stomach showing signs of early gastric cancer. Further adjunctive evidence significantly links high-risk OLGA gastritis with H. pylori status, but eradication therapies may be ineffective in the more advanced stages of gastritis (particularly when it is already associated with intraepithelial neoplastic lesions, with male gender, or with advanced age) [ 41 , 62 , 63 ].

Histological staging should be combined with other information (family history, serology, endoscopy) to enable follow-up schedules to be tailored to a given patient’s clinical and pathological profile [ 64 ]. Even in patients with early gastric cancer, further progression can be stopped by adequate management of their gastritis, as shown in the Korean study by Choi [ 65 ].

As mentioned earlier, gastric (atrophic) intestinalization only accounts for one of the three “faces” of the atrophic transformation of the mucosa. Restricting the atrophy score to IM alone (as in the OLGIM approach) can have significant drawbacks in terms of a conclusive staging of gastritis, ultimately excluding patients who warrant a “dedicated” secondary prevention strategy from an appropriate follow-up program [ 13 ]. The updated endoscopic guidelines for managing gastritis fully embrace recent progress and the clinical relevance of proper gastritis staging for the purpose of cancer prevention [ 42 ].

Outlook into 2020

According to the Kyoto Global Consensus Conference, etiology is taken for reference in the classification of gastritis. The etiological picture of long-standing gastritis can include both environmental (e.g. H. pylori ) and host-related (e.g. Autoimmunity) agents, potentially resulting in the atrophic transformation of native gastric mucosa. Epidemiological evidence implicates the atrophic microenvironment in H. pylori gastritis as a major factor responsible for the etiopathogenesis of more than 90% of gastric malignancies.

The atrophic transformation of gastric mucosa gives rise to different histological phenotypes, all of which have been biologically profiled and can be histologically scored. They may also be associated with a range of functional changes, which can serve as (quantitative) serological markers of the atrophic process. It is easy to imagine the atrophy-remodeled gastric microbiota having a role as co-promoter in the atrophic cancer-prone microenvironment.

In Western countries, histology-based gastritis staging (with the OLGA system) has consistently proved reliable in predicting the cancer risk associated with atrophy. Any (complementary) endoscopy-based risk assessment (as suggested in authoritative literature) is also welcome. The reliability of endoscopic staging still needs to be supported by large-scale studies, however, and validated in terms of its clinical reproducibility.

Over the coming years, we will see how this multidisciplinary approach can be optimized for the purpose of designing global strategies for eradicating gastric cancer and implementing patient-tailored prevention strategies. The available evidence does suggest that combining primary and secondary prevention strategies can realistically succeed in cutting the epidemiological impact of gastric cancer – the world’s fourth leading cause of cancer-related death.

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Rugge, M., Sugano, K., Sacchi, D. et al. Gastritis: An Update in 2020. Curr Treat Options Gastro 18 , 488–503 (2020). https://doi.org/10.1007/s11938-020-00298-8

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• Volume 12, Issue 5
• Acute necrotising gastritis in a 14-year-old girl
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• Ayad Ahmad Mohammed
• Department of Surgery , College of Medicine, University of Duhok , Duhok City , Iraq
• Correspondence to Dr Ayad Ahmad Mohammed, ayadduhok{at}gmail.com , ayad.mohammed{at}uod.ac

A 14-year-old female patient presented with acute generalised abdominal pain and two attacks of non-bilious vomiting for 2 days. She visited the emergency department and at presentation she was pale, dyspnaeic and there was no jaundice. Abdominal examination showed moderate abdominal distension with generalised abdominal tenderness. The bowel sounds were negative on auscultation. Plain abdominal X-ray showed hugely distended stomach with no free air detected in the peritoneal cavity. During laparotomy there was huge distension and gangrene of the stomach involving the whole stomach up to the fundus. Total gastrectomy done with roux-en-y reconstruction of the gastrointestinal continuity. The histopathological study of the sample showed gastric necrosis.

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The stomach has rich blood supply and therefore resist ischaemia. Gastric gangrene is rare and associated with high mortality if untreated early with surgical intervention. This may be caused by a variety of causes like vascular causes, chemical substances, alcohol or infectious causes which may follow upper respiratory tract infection. 1 2

Necrotising gastritis is the rarest form of gastritis which is one of the types of phlegmonous gastritis. 3

In this type of gastritis, the four major blood vessels supplying the stomach are patent but the necrosis is mostly due to a transmural infectious necrotising cause. It may occur in immunocompetent or immunocompromised subjects like patients with leukaemia. 3 4

Case presentation

A 14-year-old female patient presented with acute generalised abdominal pain and two attacks of non-bilious vomiting for 2 days, the pain was poorly localised started gradually then the patient developed abdominal distension, dyspnoea and sweating. She visited the emergency department and at presentation she was pale, dyspnoeic and there was no jaundice.

Examination of the vital signs showed tachycardia; pulse rate: 120 beats/min, blood pressure: 90/55 mm Hg, SPO 2 : 90% with room air.

Abdominal examination showed moderate abdominal distension with generalised abdominal tenderness. The bowel sounds were negative on auscultation. Resuscitation done for the patient and then sent for investigations.

Investigations

The complete blood count showed low haemoglobin: 9 g/dL, and elevated white blood cells: 20 ×10 9 /L . Plain abdominal X-ray showed hugely distended stomach with no free air detected in the peritoneal cavity ( figure 1 ).

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Plain abdominal X-ray showing hugely distended stomach.

Endoscopy was not done because the patients was in shock state.

We first start with resuscitation of the patient, two intravenous lines put in the peripheral veins and the patient received intravenous fluid and broad spectrum antibiotics. Nasogastric tube put for gastric decompression and the aspirate was about 700 cc of brown coloured fluid mixed with food particles. Then the patient transferred to the operation theatre.

During exploratory laparotomy there was huge distension and gangrene of the stomach involving the whole stomach up to the fundus, the small and the large bowel were normal ( figures 2 and 3 ).

Intraoperative picture showing distended gangrenous stomach.

Intraoperative picture showing distended gangrenous stomach with normal distal part.

Total gastrectomy done with roux-en-y reconstruction of the gastrointestinal continuity, figure 4 .

Intraoperative picture showing the gangrenous stomach after being resected.

The histopathological study of the sample showed gastric necrosis.

Outcome and follow-up

The patient was admitted for 6 days with no postoperative complications and she is on regular follow-up.

Necrotising gastritis may be caused by a variety of causes like occlusion of all the arterial supply of the stomach, gastric volvulus, bulimia nervosa, ingestion of corrosive agents, iatrogenic after the injection of haemostatic agents and could be caused also by a number of micro-organisms like Bacillus cereus, Streptococcus pyogenes and Escherichia coli , or fungal infections which can be isolated from the stomach and blood cultures, in some other groups of patients no identifiable micro-organisms could be isolated. 4–7

The patient may present with signs of food poisoning like acute epigastric pain, coffee ground vomitus. Later on if the condition is not treated urgently the patient may develops shock state and signs of peritonitis and septicemic syndrome. 8 9

The necrosis may affect part of the stomach, the whole stomach, or may be so extensive that may extend to the oesophagus to a variable length, but the oesophagus and the duodenum are rarely involved. 10

Radiological examination by X-ray or CT scan may show or endoscopy may show marked gastric dilatation, purple coloured mucosa and areas of necrotic mucosa, if the patient has delayed presentation there may be gastric perforation. Histology of the specimen may show transmural necrosis, areas of haemorrhages and inflammatory changes. 11

The condition is treated initially with resuscitating the patient with intravenous fluids and parenteral broad spectrum antibiotics, gastric decompression using nasogastric tube. The surgical options may be total or subtotal gastrectomy with reconstruction of the gastrointestinal continuity. 6 8

Patient’s perspective

The pain that I felt was the worst pain in my life, I thought I am dying and I just wanted to reach the operation room to have anaesthesia. When I awaked from anaesthesia still there was pain but I felt better. I have been told that surgery was successful and I can go home in a matter of days.

Learning points

Patients with necrotising present to the emergency hospital in critical situation, the aim of treatment of such patients are:

Resuscitation should be the first step of treatment.

During surgery, the necrotic and gangrenous stomach should be removed which may be partial or total gastrectomy.

Long-term follow-up is needed because such patients are liable for vitamin B 12 deficiency and iron deficiency anaemia.

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Contributors AAM and SHA have contributed to the concept of reporting the case and the patient data recording. Drafting the work, design and revision done by AAM. SHA took the consent from the patient for publishing the case. Final approval of the work to be published was done by AAM.

Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests None declared.

Provenance and peer review Not commissioned; externally peer reviewed.

Patient consent for publication Obtained.

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The condition, lessons for the clinician, poster presentations:, section editor’s note, suggested readings, case 5: a 13-year-old boy with abdominal pain and diarrhea.

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Drs Sudhanthar, Okeafor, and Garg have disclosed no financial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.

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Anjali Garg , Sathyan Sudhanthar , Chioma Okeafor; Case 5: A 13-year-old Boy with Abdominal Pain and Diarrhea. Pediatr Rev December 2017; 38 (12): 572. https://doi.org/10.1542/pir.2016-0223

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A 13-year-old boy presents to his primary care provider with a 5-day history of abdominal pain and a 2-day history of diarrhea and vomiting. He describes the quality of the abdominal pain as sharp, originating in the epigastric region and radiating to his back, and exacerbated by movement. Additionally, he has had several episodes of nonbloody, nonbilious vomiting and watery diarrhea. His mother discloses that several family members at the time also have episodes of vomiting and diarrhea.

He admits to decreased oral intake throughout the duration of his symptoms. He denies any episodes of fever, weight loss, fatigue, night sweats, or chills. He also denies any hematochezia or hematemesis. His medical history is significant for a ventricular septal defect that was repaired at a young age, but otherwise no other remarkable history.

During the physical examination, the adolescent is afebrile and assessed to be well hydrated. Examination of the abdomen reveals tenderness in the epigastric region and the right lower quadrant on light to deep palpation, with radiation to his back on palpation. There are no visible marks or lesions on his abdomen. Physical examination is negative for rebound tenderness, rovsing sign, or psoas sign. The remainder of the examination findings are negative.

Complete blood cell count, liver enzyme levels, pancreatic enzyme levels, and urinalysis results are all within normal limits.

Our patient was asked to observe his hydration status and pain at home and to report any changes. However, he arrived at the emergency department the next day due to increased severity of abdominal pain. The pain had localized into the right lower quadrant. Further imaging revealed the diagnosis.

The differential diagnosis for an adolescent who presents with abdominal pain is broad, including gastrointestinal causes such as gastroenteritis, appendicitis, or constipation and renal causes such as nephrolithiasis or urinary tract infections. With our patient, the more plausible answers were ruled out through laboratory studies and physical examination, and he was assumed to have gastroenteritis based on the history of similar symptoms in his family members. However, with the worsening of his abdominal pain, further diagnostic study became imperative and a computed tomographic (CT) scan of the abdomen was obtained to assess for appendicitis or nephrolithiasis.

The CT scan showed a cecum located midline; the large intestine was on the left side of the abdomen, and the small intestine was on the right ( Figs 1 and 2 ). The appendix was buried deep in the right pelvis, and there was no indication of appendicitis. These findings were consistent with intestinal malrotation. Intestinal malrotation is rare beyond the first year of life. Maintaining a higher index of suspicion in any patient with an acute presentation of severe abdominal pain is imperative because of the severity of potential complications such as bowel obstruction, volvulus, and eventual necrosis. Our patient’s pain is assumed to have been due to compressive effects of the peritoneal bands (Ladd bands), which were irritated by an initial gastroenteritis. He did not have the signs or symptoms of a more severe complication, such as bowel obstruction or volvulus.

Computed tomographic scan of the abdomen showing intestinal malrotation, specifically of the subtype nonrotation. The small bowel is present in the right hemi-abdomen and the large bowel in the left hemi-abdomen. The cecum is midline in the pelvis. Haustra are still present, excluding any sign of obstruction.

Swirling appearance of the mesentery is known as the whirl sign, which is also indicative of malrotation. This computed tomographic scan shows the superior mesenteric vein wrapped around the superior mesenteric artery.

Owing to the severity of the pain, our patient was taken for surgery, specifically, a Ladd procedure and a prophylactic appendectomy. Ladd bands were seen to extend from the cecum to above the duodenum. During the procedure, these bands were lysed, then the mesentery was spread out, and the bowels were rearranged. He tolerated the surgery well and was discharged 3 days after the operation.

His abdominal pain improved after surgery, and he has been doing well at his postoperative checks.

Intestinal malrotation is when the intestines fail to rotate properly in utero. From the fifth to 10th weeks of embryologic development, the small intestine lies in the right aspect of the abdomen, with the ileocecal junction midline, and the large intestine in the left hemi-abdomen. The segments are then pushed out of the abdomen into the umbilical cord. Both segments grow in the first stage of rotation. During the second stage of rotation, the small intestine rotates counterclockwise 270 degrees around the superior mesenteric artery. The remaining intestine is pulled into the abdomen, and the mesentery is fixed to the retroperitoneal space. The large intestine comes in last, with the final segment of the cecum lying anterior to the small intestine in the right lower quadrant.

Nonrotation is the most frequent cause of intestinal malrotation. Nonrotation occurs when the 270-degree rotation does not occur and, thus, the mesentery is not fixed to the retroperitoneal space. Derangements of the second stage of rotation are defined as having the small intestine in the right hemi-abdomen, with the cecum midline in the pelvis, and the large intestine in the left hemi-abdomen.

One percent of the population has intestinal rotation disorders. The incidence decreases with age. Approximately 90% of patients are diagnosed within the first year of their life, with 80% among them within the first month after birth. Due to a delay in diagnosis, the 10% of patients who present beyond that first year after birth can have severe complications.

Symptoms of malrotation are different in infants compared with adolescents. Neonates typically will have bilious emesis. In contrast, children and adults commonly exhibit acute abdominal pain. Some older patients have had chronic abdominal pain that goes unnoticed; others may be asymptomatic before diagnosis. The co-occurrence of intestinal malrotation with congenital cardiac anomalies is a common finding. Twenty-seven percent of intestinal malrotation patients were found to have a concurrent cardiovascular defect such as ventricular septal defect or another minor/major abnormality.

The diagnostic modality of choice is an upper gastrointestinal tract contrast study. This study modality shows any obstruction and depicts the malrotation through contrast media. Sometimes a contrast medium is not needed for diagnosis, as in the case of our patient, where CT scanning was enough to diagnose the malrotation.

Asymptomatic neonates and all symptomatic individuals, regardless of age, go through the Ladd procedure to correct the abnormality. However, the guidelines are not as clear for treatment of children older than 1 year who are asymptomatic. Currently, there is some consensus for performance of the procedure regardless of symptom status because of the severity of the complications or mortality that can occur due to malrotation. The narrow pedicle of the mesentery that forms in malrotation is prone to volvulus and ischemia, leading to complications at any point in an individual’s life. A diagnostic laparoscopy should be performed at the very least and can be therapeutic as well. Removal of the appendix has been suggested to prevent any diagnostic complications on future presentation. Additionally, the Ladd procedure can lyse Ladd bands, which are abnormal fibrous adhesions from the cecum that also arch over the duodenum. Removal of these bands is imperative because they can cause intestinal obstruction and ischemia as well.

Diagnosis of intestinal malrotation should be considered in a patient presenting acutely with severe abdominal pain, especially in a patient with known cardiac anomalies.

Often the symptoms of intestinal malrotation can be vague, and a patient can be asymptomatic for years before presentation.

The diagnostic modality of choice is an upper gastrointestinal tract series, but other imaging, such as computed tomographic scan, can help diagnose the presence of malrotation in emergency situations.

A Ladd procedure should be conducted on a patient even if he/she does not have current symptoms of obstruction due to increased risk of obstruction or complications such as volvulus and gut necrosis with this disease.

This case is based on a presentation by Ms Anjali Garg and Drs Sathyan Sudhanthar and Chioma Okeafor at the 39th Annual Michigan Family Medicine Research Day Conference in Howell, MI, May 26, 2016.

Poster Session: Student and Resident Case Report Poster Presentation

Poster Number: 23

This case is based on a presentation by Ms Anjali Garg and Drs Sathyan Sudhanthar and Chioma Okeafor at the 2016 AAP National Conference and Exhibition in San Francisco, CA, October 22-25, 2016.

Poster Session: Section on Pediatric Trainees Clinical Case Competition

Abdominal Pain in Children: https://www.healthychildren.org/English/health-issues/conditions/abdominal/Pages/Abdominal-Pain-in-Children.aspx

Diarrhea: https://www.healthychildren.org/English/health-issues/conditions/abdominal/Pages/Diarrhea.aspx

For a comprehensive library of AAP parent handouts, please go to the Pediatric Patient Education site at http://patiented.aap.org .

This case was selected for publication from the finalists in the 2016 Clinical Case Presentation program for the Section on Pediatric Trainees of the American Academy of Pediatrics (AAP). Ms Anjali Garg, BS, was a medical student from Michigan State University College of Human Medicine, East Lansing, MI, when she wrote this case report, and she now is a medical resident at Rainbow Babies and Children's Hospital in Cleveland, OH. Choosing which case to publish involved consideration of not only the teaching value and excellence of writing but also the content needs of the journal. Other cases have been chosen from the finalists presented at the 2017 AAP National Conference and Exhibition and will be published in 2018.

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• Published: 06 September 2021

Phlegmonous gastritis: a case series

• Yoshikazu Yakami 1 ,
• Toshihiko Yagyu 1 &
• Tomoki Bando 1  

Journal of Medical Case Reports volume  15 , Article number:  445 ( 2021 ) Cite this article

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Phlegmonous gastritis is a rare and fatal infectious disease of the stomach, presenting varied and nonspecific endoscopic images, which are therefore difficult to diagnose. This report discusses three cases of phlegmonous gastritis, each with unique endoscopic images, and considers the differential diagnosis of this disease. These cases were initially suspected of scirrhous gastric cancer, gastric syphilis, and acute gastric mucosal lesion.

Case presentation

Case 1 A 32-year-old Asian man visited our hospital complaining of upper abdominal pain. Endoscopy raised suspicion of scirrhous gastric cancer. However, a histopathological examination showed no malignant cells, thus leading to the diagnosis of phlegmonous gastritis. The patient was started on antibiotic therapy, which was effective.

Case 2 A 33-year-old Asian man visited our hospital complaining of epigastralgia. Endoscopy raised suspicion of gastric syphilis. However, the serum test for syphilis was negative, and Streptococcus viridans was detected in the biopsy specimen culture, which led to the diagnosis of phlegmonous gastritis.

The patient was started on antibiotic therapy, resulting in significant improvement in the endoscopic image after 2 weeks.

Case 3 A 19-year-old Asian man visited our hospital complaining of epigastric pain. Endoscopy raised suspicion of acute gastric mucosal lesion. A gastric juice culture showed Pseudomonas aeruginosa and Streptococcus viridans , thus leading to the diagnosis of phlegmonous gastritis. The patient was started on antibiotic therapy, resulting in the disappearance of the gastric lesions.

In severe cases of phlegmonous gastritis, immediate surgical treatment is generally required. However, the endoscopic images are varied and nonspecific. These three cases suggest that clinicians need to consider the differential diagnosis of phlegmonous gastritis and make accurate diagnoses at an early stage.

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Phlegmonous gastritis is a rare and deadly infectious disease of the gastric wall, mainly occurring in the submucosa of the stomach. This disease is caused by suppurative bacterial infection and is conventionally managed by conservative treatment using antibiotics. In severe cases, such as perforation, urgent surgical treatment is required. Certainly, its mortality rate is not low. Therefore, this disease must be diagnosed correctly at an early stage. However, considering that the endoscopic images of phlegmonous gastritis are varied and nonspecific, making an early diagnosis is difficult. Herein, we report three cases of phlegmonous gastritis, each with unique endoscopic images, and consider a differential diagnosis. These cases were initially suspected of scirrhous gastric cancer, gastric syphilis, and acute gastric mucosal lesion. In severe cases, immediate surgical treatment is generally required. Therefore, accurate diagnoses and proper treatment need to be provided.

A 32-year-old Asian man visited our hospital, with complaints of epigastralgia, slight fever, and vomiting. He had a history of alcohol consumption (40 g/day) but had no medical history. His temperature was 37.4 °C. His white blood cell (WBC) count was 22,600/mm 3 , while his C-reactive protein level was 3.00 mg/dl. Abdominal computed tomography (CT) detected a thickened, edematous gastric wall.

Hence, the patient underwent esophagogastroduodenoscopy, which revealed a significant hyperplasia of the gastric folds with abundant mucopus, extensive redness and edema of the gastric mucosa, and poor distensibility of the gastric wall (Fig. 1 a). Considering this endoscopic image, scirrhous gastric cancer was suspected. On histopathological examination, mucosal necrosis and severe neutrophil infiltration were detected, with no malignant cells (Fig. 1 b).

a Endoscopic image of case 1. Significant hyperplasia of the gastric folds with abundant mucopus, and extensive redness and edema of the gastric mucosa were observed. b Histological image of case 1. Mucosal necrosis and neutrophil infiltration were detected, but no malignant cells were found

The clinical course (increased fever, epigastric pain, and elevated WBC count) as well as imaging (gastric wall thickness on CT and endoscopic findings) and histopathological findings led us to consider the serious infection and to diagnose the patient with phlegmonous gastritis, despite the biopsy specimen culture being negative.

Antibiotic therapy (levofloxacin, 500 mg/day × 7 days) was then provided, leading to the patient’s recovery.

A 33-year-old Asian man with epigastralgia visited our hospital. He had a history of excessive alcohol consumption (the exact amount was unknown), had no medical history, and was sexually active. The WBC count was 12,400/mm 3 . Abdominal CT detected localized thickening of the gastric wall, mainly in the antrum.

The endoscopic image revealed multiple shallow ulcers with slough fused into a map-like pattern in the same area (Fig. 2 a).

a Endoscopic image of case 2. Multiple shallow ulcers with slough fused into a map-like pattern were observed in the antrum. b Histological image of case 2. Immunostaining of the biopsy specimen was negative ( Treponema pallidum was not found)

Given the endoscopic findings, the patient was diagnosed with gastric syphilis. However, his serum test result for syphilis was negative, and the culture of biopsy specimen revealed the presence of Streptococcus viridans , resulting in the diagnosis of phlegmonous gastritis. In addition, immunostaining of the biopsy specimen was negative ( Treponema pallidum was not found) (Fig. 2 b). Thus, antibiotic therapy (amoxicillin, 750 mg/day × 14 days) was started. After 2 weeks, the endoscopic image revealed a remarkable improvement.

A 19-year-old Asian male college student visited our hospital, complaining of epigastralgia and vomiting. He had no history of drug and alcohol consumption and had no medical history. However, he had a fever (38.0 °C), with a WBC count of 15,900/mm 3 . Abdominal CT detected a thickened gastric wall, particularly in the antrum.

Endoscopic image showed large and shallow ulcers with reddish and edematous mucosa in the antrum, with some coagulation (Fig. 3 a). We initially suspected acute gastric mucosal lesion (AGML). However, the patient was eventually diagnosed with phlegmonous gastritis because Pseudomonas aeruginosa and S. viridans were found in the culture of gastric juice.

a Endoscopic image of case 3. Large and shallow ulcers with reddish and edematous mucosa were observed in the antrum, with some coagulation. b Histological image of case 3. Direct microscopy found no Helicobacter pylori

Meanwhile, the culture of gastric tissue was negative for Helicobacter pylori . Antibiotic therapy (tazobactam/piperacillin, 9.0 g/day × 10 days) was then started, and gastric lesions gradually disappeared.

H. pylori were not identified using direct microscopy in all cases (Fig. 3 b).

Phlegmonous gastritis is a rare inflammatory gastric disease caused by local or diffuse inflammation of the gastric wall [ 1 ]. The diffuse type is more common and has a higher mortality rate than the localized type. Case 1 was a diffuse type, whereas cases 2 and 3 showed a localized type. Imaging examinations are useful for diagnosing phlegmonous gastritis, which is suspected when gastric wall thickness is detected on abdominal ultrasonography or CT. Endoscopic ultrasonography for phlegmonous gastritis diagnosis is reportedly effective but is performed in few facilities [ 2 ].

By cause, phlegmonous gastritis is categorized into primary, secondary, and idiopathic types [ 3 , 4 ]. The most common is the primary type, which is caused by a mucosal injury such as peptic ulcer or gastric cancer. The secondary type is associated with the infection of other organs, such as biliary infection or hepatic abscess. It may also occur after endoscopic submucosal dissection and endoscopic ultrasound-guided fine-needle aspiration [ 5 , 6 ]. In the idiopathic type, as the name implies, the cause is unknown, and it mostly occurs in a compromised host. Moreover, cases 1 and 2 had a history of excessive alcohol consumption. Such a history is a causative factor of superficial gastritis, multiple small ulcers, and hemorrhagic erosions because alcohol can cause gastric mucosal injury, which induces phlegmonous gastritis [ 7 ]. Case 3 had no apparent background. However, he had an upcoming examination for promotion and felt extremely stressed. Mucosal injury such as AGML caused by mental stress could be the cause of phlegmonous gastritis [ 8 ]. Furthermore, temporary immunosuppression due to disruption in the rhythm of life might have triggered the onset of the disease in these three cases.

By clinical course, phlegmonous gastritis is categorized into acute, chronic, and subacute types [ 9 ]. All of our patients had a sudden onset of the disease, complaining of epigastralgia upon consultation. Therefore, they were categorized as the acute type.

The most common pathogenic cause of phlegmonous gastritis is Streptococcus (approximately 70%), which is resistant to gastric acid, followed by Enterococcus and Staphylococcus [ 10 ].

If the pathogen is found in the culture of gastric tissue or fluid, the diagnosis of phlegmonous gastritis could be made. However, pathogen is not always detected.

In case 1, although a pathogen was not identified, the patient was still diagnosed with phlegmonous gastritis because of other factors, such as the clinical course, symptoms, and imaging examinations.

Typically, the endoscopic image features of phlegmonous gastritis include reddish and edematous mucosa, swollen gastric folds, erosion, ulcer with slough, and mucopus adhesion. Considering that these features are nonspecific, various endoscopic images can be found in phlegmonous gastritis. Hence, we need to consider the differential diagnosis of phlegmonous gastritis.

Case 1 Scirrhous gastric cancer was suspected according to the following endoscopic image features: extensively reddish and edematous gastric mucosa, swollen gastric folds, abundant mucopus adhesion, and poor gastric wall distensibility.

Histopathologically, no malignancy was noted.

Obtaining a clinical history for several months is important because scirrhous gastric cancer takes a long time course.

Ultimately, imaging and histopathological examinations led to the diagnosis of phlegmonous gastritis.

Case 2 Gastric syphilis was suspected according to an endoscopic image feature, that is, multiple shallow ulcers with slough fused into a map-like pattern in the antrum. Furthermore, the patient was sexually active toward many unknown individuals. Regarding syphilis, the serum test and the immunostaining of the biopsy specimen were both negative ( Treponema pallidum was not found). However, S. viridans was detected in the culture; thus, the patient was diagnosed with phlegmonous gastritis.

When gastric syphilis is suspected, serum test and skin examination must be conducted.

Case 3 AGML was suspected because of the following endoscopic images: large and shallow ulcers with reddish and edematous mucosa and some signs of coagulation.

P. aeruginosa and S. viridans were found in the culture of gastric juice.

AGML is frequently caused by various factors, such as drugs (for example antibiotics, steroids, and nonsteroidal antiinflammatory agents), extreme mental or physical stress, and excessive alcohol consumption. Acute H. pylori infection must also be considered [ 11 ]. The patient had no history drug and alcohol intake and was negative for H. pylori infection. Considering that he had a history of mental stress, AGML caused by this stress was considered to be the cause of phlegmonous gastritis.

The treatment for phlegmonous gastritis is conservative treatment using antibiotics. However, surgical treatment is required in resistant or severe cases [ 12 ]. Given that fatal cases were occasionally reported, physicians need to make a correct diagnosis and start the appropriate treatment [ 13 ].

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There are no additional data available for this study.

Abbreviations

White blood cell

Computed tomography

• Acute gastric mucosal lesion

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Acknowledgements

We would like to thank Dr. Tomoaki Yamasaki of Osaka City General Hospital for correcting the English used in this manuscript.

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Yoshikazu Yakami, Toshihiko Yagyu & Tomoki Bando

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Yakami, Y., Yagyu, T. & Bando, T. Phlegmonous gastritis: a case series. J Med Case Reports 15 , 445 (2021). https://doi.org/10.1186/s13256-021-02999-9

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Differential Diagnosis II: Gastritis

There is very strong rationale for Gastritis as a differential diagnosis, as nearly all of symptoms the patient is presenting with match the clinical picture seen with inflammation of the gastrointestinal lining. Patients with Gastritis commonly present with previous H. Pylori exposure, use of NSAIDs, epigastric tenderness, alcohol use, anorexia due to a vague feeling of fullness with meals, and non-specific symptoms such as nausea and vomiting (McCance & Huether, 2019). All of these symptoms match the clinical picture of the 65 y.o. presenting female, making Gastritis a viable possibility as a diagnosis for her.

It makes sense that Gastritis and Peptic Ulcer disease have almost identical clinical presentations, as they have a very similar etiology. Both involve damage to the mucosal barrier of the gastrointestinal lining that is typically preceded by an H. Pylori infection, and therefore both disease processes are commonly exacerbated by use of NSAIDS or caffeine and alleviated by antacids (McCance & Huether, 2019). Both can also be influenced by psychologic stress, which could be a big factor with this patient, as she raised two kids as a single parent. However, the two disease processes are ultimately different in that Peptic Ulcer disease involves significant erosion or break in the mucosal lining (sometimes extending as far as the vasculature and causing bleeding), while Gastritis is usually an inflammation of the lining without breakage (pictured in Figure 5). These differences are pictured in Figures 4 and 5 below:

Figure 4 . Peptic Ulcer (VS Hospitals, 2018)

Figure 5 . Endoscopy of normal gastrointestinal lumin compared with inflamed stomach wall (ePain Assist, 2019)

The patient’s history of Acute Pancreatitis, as well as her age being over 65, both indicate the possibility that her diagnosis is Peptic Ulcer disease over Gastritis. Additionally, Acute Gastritis often resolves spontaneously in a few days, and her abdominal discomfort has been going on for 2 months. Chronic gastritis often occurs with other autoimmune diseases such as rheumatoid arthritis, and patients sometimes start to see mucosal atrophy which can lead to pernicious anemia, as gut is atrophied and unable to absorb vitamin B12 (McCance & Huether, 2019). If she had Gastritis, she would likely present with more of these symptoms or maybe a history of autoimmune disease, which aren’t included in her clinical picture. This would be a consideration, but probably not definitive.

Given the similarities in presentation between Gastritis and Peptic Ulcer disease, it may be necessary for an endoscopy to be completed to confirm whether an ulcer has formed. The pictures below show endoscopies of an ulcer (Figure 6) and inflammation with no ulcer formation (Figure 7). Her provider may decide to order an endoscopy to confirm her diagnosis definitively.

Figure 6 . Endoscopy reveals ulceration of stomach lining (Meddiction, 2016)

Figure 7 . Endoscopy of normal antrum compared with endoscopy of inflamed stomach lining (Pathogenesis of Diseases of the Stomach, 2008)

Massage Guns the Likely Culprit in Two Cases of Acute Vertigo

— the relatively younger age of the two patients makes these cases particularly notable.

by Kate Kneisel , Contributing Writer, MedPage Today May 10, 2024

What caused acute vertigo in two healthy women? That's the diagnostic challenge described by David Elisha, BS, of Tel Aviv University School of Medicine in Israel, and Ronen Nazarian, MD, of Cedars-Sinai Medical Center in Los Angeles, in JAMA Otolaryngology-Head & Neck Surgery .

Based on findings from a complete physical examination, the clinicians determined that the first patient, age 31, had benign paroxysmal positional vertigo (BPPV) of the right side.

After treating the patient, they obtained a detailed history in an effort to identify the cause. In describing her recent activities, the patient described using a handheld percussive massage gun daily, most recently on her neck and shoulders 12 hours before her symptoms developed.

The second patient was a 48-year-old woman who had experienced repeated episodes of BPPV. She reported having undergone many standard treatments that initially had relieved her symptoms for short periods of time. However, the BPPV symptoms kept recurring.

On her fourth visit to the medical center, the patient had a complete re-evaluation, during which she described using a massage gun regularly around her upper neck and occiput. On the advice of the team, the patient stopped using the massage device, after which she had no more episodes of BPPV.

The two patients received the same diagnostic evaluations -- specifically, a comprehensive assessment of vestibular functions, including gait, Romberg, Fukuda, nystagmus, fistula, head-shaking, and finger-to-nose tests. In both cases, the clinicians performed the Dix-Hallpike maneuver, which elicited positive nystagmus, and confirmed the BPPV diagnosis.

Repositioning maneuvers provided significant relief of symptoms in both patients, and they were advised to stop using their massage guns. Their symptoms did not recur.

As the most common form of peripheral vertigo, BPPV has a prevalence of 3.2%. Most cases of BPPV occur due to displacement of otoconia within the semicircular canals of the inner ear, which in turn causes vertigo when moving the head, the authors explained.

Head trauma is well-known as a risk factor for BPPV; however, the authors suggested that cases of BPPV associated with less severe vibrational injuries are likely underreported. They cited data linking BPPV with exposure to vibration in association with a variety of activities and tools, "such as using electric toothbrushes , undergoing dental procedures, and engaging in intense exercise ."

"Associations between BPPV and handheld massage guns remain unexplored in existing literature," Elisha and Nazarian noted.

Handheld massage devices apply significantly more force than traditional devices, and their increasing availability has raised safety concerns about their use, the authors explained. Other case reports have linked these massage guns with cases of rhabdomyolysis and vertebral artery dissection .

To assess the impact of handheld massage guns on the user, accurate measurement in force per cm 2 is crucial. "Handheld massage guns are advertised to deliver 14 to 32 kgs of no-stall force with up to 5,000 strokes per minute and an amplitude of up to 16 mm, distinguishing these from other massage devices in both force delivery and design," the authors wrote. When used on the head and shoulders, this degree of force has the potential to dislodge otoliths within the inner ear, and lead to BPPV in susceptible individuals.

The risk of BPPV increases with age, likely as a result of age-related deterioration. However, the two patients' cases are notable since they are both relatively young, the authors noted, "challenging typical age-related expectations, and highlighting the potency of the powerful vibration inflicted by massage guns."

Clinicians who are assessing patients who have BPPV, especially when it is recurrent, should ask about the use of massage devices to identify potential associations. Furthermore, a comprehensive examination and history should include other lifestyle factors that may be potential causes of (particularly recurrent) BPPV.

"This observational report emphasizes the importance of considering the use of percussive massage guns during the evaluation of potential BPPV diagnoses," Elisha and Nazarian wrote, as the condition can have a significant effect on quality of life. Recurrences could be reduced through awareness, cautious use of percussive massage devices, and prompt recognition and treatment of BPPV.

"Although these findings are preliminary, they align with previous research indicating an association between vibrational exposure and BPPV. Given this context, manufacturers should issue generalized warnings on vertigo risks associated with these devices, especially when used near the head and upper neck," they concluded.

Kate Kneisel is a freelance medical journalist based in Belleville, Ontario.

Disclosures

The authors reported no conflicts of interest.

Primary Source

JAMA Otolaryngology-Head & Neck Surgery

Source Reference: Elisha D, Nazarian R "Benign paroxysmal positional vertigo after use of handheld massage gun" JAMA Otolaryngol Head Neck Surg 2024; DOI: 10.1001/jamaoto.2024.0543.