Acute Gastritis

General Information

Description

• acute gastritis is characterized by alteration of gastric mucosa including hyperplasia, erosive changes, and inflammation (which may be minor)
• acute gastritis is generally grouped into 3 categories: infectious, ulcero-hemorrhagic, or secondary to drugs, oncologic protocol, or caustic agents (chemical/reactive)
• see Chronic Gastritis for information on other causes such as autoimmune, collagenous, eosinophilic, lymphocytic, or granulomatous gastritis among others

Definitions

• gastritis refers to irritation, injury, or inflammation of gastric mucosal lining, but definition is sometimes limited to gastric inflammation; and in clinical practice, gastritis has sometimes been used to refer to acute symptoms of nausea and vomiting prior to an underlying diagnosis
• gastropathy may be used to refer to gastric mucosal injury without inflammation

Also called

• gastropathy
• non-atrophic gastritis
• stress-related mucosal disease, a type of acute gastritis, is also known as
  • ulcero-hemorrhagic gastritis
  • stress ulcer/ulceration
  • stress erosions
  • stress gastritis
  • acute erosive gastritis
  • gastric erosion
  • acute hemorrhagic and erosive gastropathy
  • ulcers due to stress-related mucosal disease
    • referred to as Curling's ulcer in patients with burns
    • referred to as Cushing ulcers in patients with brain trauma or increased intracranial pressure
• caustic or chemical gastritis, a type of acute gastritis, is also known as
  • iatrogenic gastritis
  • drug and chemotherapy gastritis
  • reactive gastritis
• reactive gastropathy is also known as chemical gastropathy

History and Physical

Clinical presentation

• acute gastritis is usually asymptomatic, but may present with
  • nausea and vomiting (with or without diarrhea)
  • epigastric pain or dyspepsia
  • acute upper abdominal pain
  • fever
  • weight loss
  • upper gastrointestinal bleeding
• alarm symptoms in patients presenting with upper gastrointestinal (GI) concerns indicating prompt upper endoscopy include
  • weight loss
  • dysphagia
  • overt GI bleeding
  • abdominal mass
  • iron-deficient anemia

History

• ask about
  • all current medications
  • conditions associated with immunosuppression
  • surgical history
  • history of radiation therapy, chemotherapy, or malignancy
  • presence of immune-mediated chronic diseases such as inflammatory bowel disease or sarcoidosis (see also Chronic Gastritis)
• ask about ingestions that can cause gastritis, such as
  • alcohol
  • recent raw shellfish
  • corrosive chemicals

Physical

• tachycardia and/or hypotension may indicate gastrointestinal bleeding
• signs of infectious gastritis include
  • fever
  • enlarged lymph nodes (in Epstein-Barr virus infection)

Chemical or Reactive Acute Gastritis

Overview

• chemical-induced/reactive is the most common form of acute gastritis seen in general practice, and results from acute or prolonged irritation from noxious agent(s)
• most commonly involves antrum, but may also affect oxyntic mucosa (Virchows Arch. 2018 Nov;473(5):533-550)
• etiology of chemical gastritis may remain idiopathic, but causative agents include
  • bile reflux
    • usually predominately affects distal stomach, unlike drug-induced gastritis which typically affects distal and antral stomach equally
    • may be potentiated by gastroenterostomy or partial gastrectomy
  • alcohol
  • caustic agents (ingested accidentally or with self-harm/suicidal intent)
  • medications or medical procedures, including (not comprehensive)
    • nonsteroidal anti-inflammatory drugs (NSAIDs)
    • chemotherapeutic agents or radiation therapy
    • 5-aminosalycilic acid
    • biphosphonates
    • selective serotonin inhibitors
    • platelet aggregation inhibitors
    • iron
    • colchicine
    • doxycycline
• histological findings
  • may have signs of long-standing repeated injury including foveolar hyperplasia with corkscrew appearance, smooth muscle fiber hyperplasia, paucity of inflammatory cells, surface epithelium exfoliation, foveolar epithelium mucin depletion, nuclear enlargement, and hyperchromasia
  • mucosal congestion and edema (normal vs. pathological not well defined)

Management

• symptoms generally resolve rapidly after correction of underlying cause
• bile reflux gastritis does not have a universally accepted management strategy, but proton pump inhibitor (PPI) therapy may help improve symptoms
• medication-induced gastritis management
  • withdraw causative agent if possible
  • acid-suppression therapy with PPIs or misoprostol may be effective for treatment of nonsteroidal anti-inflammatory drug (NSAID)-induced gastritis
  • in patients who must continue taking NSAIDs, consider switching to COX-2 inhibitor, along with use of PPI
  • see also Prevention of NSAID-induced Gastrointestinal Toxicity

Infectious Acute Gastritis

Viral causes

• cytomegalovirus-associated gastritis
  • most often occurs in patients with immunocompromise such as those with malignancy, steroid-induced immunosuppression, post-transplant, or AIDS
  • presentation may include
    • epigastric pain, fever, and atypical lymphocytosis
    • endoscopic findings frequently consist of congested and edematous mucosa with multiple erosions and ulcerations
• herpes simplex or varicellar/zoster virus gastritis
  • rare, and most often occurs in patients with immunosuppression such as radiation therapy, chemotherapy, or malignancy
  • mucosa may have multiple small ulcers (may cause cobblestone appearance),
• Epstein-Barr virus (EBV) gastritis
  • rarely may occur in immunocompetent adults and may appear as marked lymphoid hyperplasia
  • endoscopic findings include granular, congested mucosa and mural thickening
  • presentation may mimic malignant lymphoma with enlarged lymph nodes, and histological findings of dense lymphocytic infiltrate
  • tests helpful for differentiation/diagnosis include appropriate immunohistochemical phenotyping, flow cytometric analysis, and diffuse detection of EBV RNA by in situ hybridization

Bacterial causes

• Helicobacter pylori Infection (most common cause of infectious gastritis)
• other common culprits include streptococci, E. coli, enterobacteria or other Gram-negative bacilli, and Staphylococus aureus
• emphysematous gastritis is caused by gas-forming organisms, and is associated with high mortality rate most often due to delayed diagnosis resulting in necrotizing gastritis
  • common causative organisms include Clostridium perfringens, E. coli, Streoptococcus, Enterobacter, and Pseudomonas aeruginosa
  • associated etiologic factors reported to include
    • large intake of alcohol
    • upper respiratory tract infection
    • AIDS or other immunocompromised states
    • infected peritoneal-jugular venous shunts
    • biopsies (rarely)
  • risk factors include history of
    • surgery
    • corrosive material ingestion
    • gastroenteritis
    • gastrointestinal infarction
  • clinical presentation
    • acute upper abdominal pain
    • peritonitis
    • fever
    • hypotension
    • intravascular thrombosis is reported to be common
  • diagnosis and testing
    • upper endoscopy shows edematous thick gastric wall lined with granular mucosa covered in exudate
    • histology shows edematous submucosa with polymorphonuclear infiltrates, and Gram positive and negative organisms
    • abdominal ultrasound or computed tomography may be helpful for diagnosis
    • if untreated, extensive mucosal and mural necrosis will be seen on imaging
  • management consists of gastric resection combined with broad spectrum antibiotic therapy
• mycobacteria gastritis
  • M. tuberculosis-gastritis occurs in endemic areas or in patients with severe immunocompromise
    • endoscopic findings may include bleeding ulcers/erosions and narrowed, deformed antrum due to thickened wall
    • histological findings may include ulcerated mucosa with necrotizing granulomas
    • may be diagnosed with detection of acid-fast bacilli on special stains, culture, or polymerase chain reaction which helps distinguish from Crohn disease
  • Mycobacterium avium complex-gastritis is rare, and may occur in patients with AIDS, presenting as a refractory chronic ulcer
    • histologically appears as expanded lamina propria by numerous foamy histiocytes forming granulomas without necrosis
    • abdominal computed tomography may show mesenteric lymphadenopathy
  • Actinomycosis-gastritis involves chronic, large, ill-defined ulcerated mass mimicking gastric cancer
    • histologic findings include neutrophil infiltrations and intramural sinus formation, and silver stain highlights sulfur granules and long thin rods
  • secondary or tertiary syphilis may lead to gastritis
    • endoscopy may show nodular rugal hypertrophy with mucosal erosions/ulcers or luminal obstruction
    • histologic findings include dense lymphoplasmacytic infiltrate with varying amounts of neutrophils and lymphocytes
    • other features that may be present include gland destruction, vasculitis, and ill formed granuloma
    • immunofluorescence studies and polymerase chain reaction is necessary for definitive diagnosis

Fungal and parasitic causes

• Candida-associated gastritis
  • most common in patients with immunosuppression, but may also occur in patients with alcohol use disorder or those with corrosive chemical ingestion
  • mucosa appears with multiple, aphthous or linear ulcerations
  • periodic acid Schiff diastase stain or silver stain reveals yeast pseudohyphae in fibrinopurulent material
  • rule out gastric cancer if Candida colonization is found in large gastric ulcers
• phycomycosis gastritis is very rare and highly lethal, and is characterized by deeper invasion of gastric wall and blood vessels
• parasitic gastritis is rare
  • Cryptosporidosis gastritis has been reported in patients with AIDS
  • parasitic colonization of peptic ulcers and diffuse mucosal involvement have been reported in patients with immunosuppression
  • anisakiasis gastritis is acquired after ingestion of raw shellfish
    • presentation includes epigastric pain (caused by nematode larvae migrating into gastric wall)
    • management involves endoscopic removal of larval nematodes
    • granulomatous response to worm remnants with edema and marked eosinophilia may occur and involve a central abscess with granulation tissue

Management

• symptoms generally resolve rapidly after correction of underlying cause
• bacterial emphysematous gastritis is an urgent diagnosis, and management consists of gastric resection combined with broad spectrum antibiotic therapy
• for H. pylori gastritis, see Management content in Helicobacter pylori Infection
• for anisakiasis gastritis from raw shellfish ingestion, larval nematodes often removed endoscopically
• atropine plus omeprazole may increase effective treatment rates, reduce adverse reaction rates, and shorten duration of abdominal pain, diarrhea, and nausea and vomiting compared to anisodamine plus omeprazole in patients with acute gastritis

Ulcero-Hemorrhagic Gastritis

Presentation and Diagnosis

• ulcero-hemorrhagic gastritis most often occurs in patients in critical condition admitted to intensive care units, and is characterized by edematous and hyperemic mucosa with multiple petechiae
• mucosal changes often result from ischemia due to shock/hypotension or release of vasoconstrictive substances
  • typically located in body/fundus, but may be located in antrum if etiology is massive ingestion of gastrotoxic drugs or alcohol binge
  • histologically are erosive and edematous with congestion and hemorrhage of lamina propria, typically with little inflammation; regenerative atypia of gastric pits are common
• may be idiopathic

Management

• ulcero-hemorrhagic gastritis may be life-threatening due to uncontrolled hemorrhage
• initial management and assessment in adults
  • assess hemodynamic status and begin resuscitative measures as needed
    • prompt fluid replacement with crystalloid IV fluids
    • consider blood transfusion for hemoglobin < 7 g/dL
  • use a validated risk assessment scale, such as Rockall or Blatchford score to inform timing of endoscopy, time of discharge, and level of care
  • routine nasogastric or orogastric lavage not recommended
  • use proton pump inhibitor (PPI) before endoscopy to decrease likelihood of higher risk stigmata of hemorrhage at endoscopy, but do not delay endoscopy
  • for more information see Acute Nonvariceal Upper Gastrointestinal Bleeding
• atropine plus omeprazole may increase effective treatment rates, reduce adverse reaction rates, and shorten duration of abdominal pain, diarrhea, and nausea and vomiting compared to anisodamine plus omeprazole in patients with acute gastritis
• life-saving emergency gastrectomy may be required
• see also Acute Upper Gastrointestinal Bleeding in Children - Approach to the Patient