Gastritis

Definition: Microscopic evidence of inflammation affecting the gastric mucosa (8)

Types

Infectious

Bacterial

H pylori - most common

1. Increased neutrophils
2. Chronic infection with increased lymphocyte and plasma cell infiltration

H Heilmannii - Cat vector

Chronic active gastritis
assoc w/ gastric carcinoma and MALT lymphoma

M Tuberculosis - Rare

granulomatous gastritis
endoscopy reveals gastric ulcers and mucosal hypertrophy

B cereus

acute necrotizing gastritis

Viral

Cytomegalovirus

Common in immunocompromised; possible in immunocompetent
Association with Menetrier's disease
Look for:

Hyperplastic gastric folds
Protein-losing enteropathy
Hypoalbuminemia

Infects the fundus and body leads to: wall thickening, ulceration, hemorrhage, perforation

Histological appearance:

acute and chronic inflammation (deeper mucosal inflammation than seen with HSV)
intranuclear cytoplasmic inclusions in endothelial and epithelial cells
cytomegalic cells

Viral Cx of mucosal Bx
immunohistochemical ddtection of CMV early antigen

can use Ganicyclovir, however; symptoms are self limited and resolve in 1-2mo

Other Less common viral causes:

HCV
EBV
HHV7
Measles
Varicella
Influenza
HSV

Parasitic

Giardia lamblia - can infect stomach and cause:

Reactive gastritis
Chronic atrophic gastritis
Chronic active gastritis

Fish Parasites that can cause eosinophilic gastritis:

Anisakia simplex (Sushi and Sashimi in Japan)
Eustrongylides wenrichi (fresh water fish)

Cryptosporidiosis (Rare) - PUD and erosive gastritis

Fungal

Systemic infection more likely with immunocompromised pts

Candida albicans - most common fungal cause of gastritis
Aspergillus - Focal invasive gastritis

more likely with:

neutropenia
mucositis
glucocorticoid use

Reactive

"Reactive" refers to changes in gastric mucosa that are a reaction to ischemia, chemical agents, or trauma

Endoscopy shows antral erythema, erosions, and ulcerations
Histology reveals foveolar hyperplasia, mucosal edema, minimal or insufficent inflammatory cells

STRESS gastropathy

occurs within 24hrs of physiologic stress with secondary hypoperfusion
multiple superficial and typically asymptomatic erosions usually in fundus and proximal body, followed by antrum
Low risk of perforation (unless patient is newborn with reactive gastropathy), but may present with upper GI bleeding
Risk Factors:

Shock
Hypoxemia
burns
Major Surgery
Multiple organ system failure
Head injury

NEONATAL gastropathy

Sepsis patients in NICU
s/p Prostaglandin E for maintaining PDA patency
Focal Foveolar Hyperplasia
Antral mucosal thickening may cause gastric outlet obstruction
Indomethacin
Dexamethasone
Traumatic suctioning of the GI tract
Fetal Distress
Hypergastrinemia w/ maternal stress or antacid use
Hyperpepsinogenemia
Cow Milk Allergy

Medication Induced Gastritis

NSAIDs

Mechanism: inhibition of COX-2-mediated production of prostaglandins

inhibition of prostaglandins leads to:

decreased gastric mucosal blood flow
decreased secretion of mucous
decreased secretion of bicarbonate

compromised mucosal integrity / protective barrier
increased platelet-activating factor inducing platelet dysfunction

Clinical Manifestation

antral erosions and acute hemorrhage within 15-30min after feeding
Younger Children will have ulceration at antrum and incisure
Older Children/Adults typically have reactive gastropathy with epithelial hyperplasia, mucin depletion, enlarged nuclei, smooth muscle hyperplasia, vascular ectasia and edema

Risk Factors for complications

NSAIDs with Aspirin or 2 NSAIDs or High Dose
Age >65
Anticoagulant use
H pylori infection

Tx (or prevention)

PPI or misoprostol (cytoprotectant)
Note: H2 receptor antagonists are not effective for prevention

Others

Valproic Acid
Dexamethasone
Chemotherapy
KCl
Iron
Long-term fluoride ingestion

EtOH gastropathy

Subepithelial hemorrhage with minimal inflammation

More severe with Aspirin or NSAIDs

Traumatic gastropathy

Subepithelial hemorrhage in fundus and proximal body secondary to forceful wretching and vomiting
Ulcerations on gastric wall near or opposite a PEG or standard gastrostomy tube
Mallory-Weiss tears immediately above and below the GE junction
Linear erosions in herniated gastric mucosa of large hiatal hernias
Long-term nasogastric tube use
Gastric prolapse through gastrostomy tract

Exercise-induced gastropathy or gastritis

Long distance running may casue temporary alteration of blood circulation and motility (during or after a run)

Symptoms, usually post-exercise: abdominal cramps or epigastric pain, nausea, GER, vomiting
Anemia from chronic blood loss
Endoscopy: erosive and nonerosive gastropathy in all parts of the stomach

Radiation gastropathy

The stomachs ability to tolerate specific levels of radiation is not known (no known "safe" level)
Erosions and ulcerations may progress to bleeding, perforation, fibrosis, and gastric outlet obstruction
Acid suppression does not prevent radiation injury

Corrosive gastropathy

Common Etiologic Agents:

Oral Iron
Zinc-containing foreign bodies and fluids
Lithium or Mercuric Oxide button batteries
Pine Oil Cleaner
Hydrogen Peroxide
Potassium permanganate

Severity depends on:

concentration
duration of exposure
volume
amount of food in stomach at the time

Acid ingestion mainly causes gastric injury; although, gastric injury is also possible with large-volume alkali ingestion

Acid pools in antrum because of acid-induced pylorospasm

Endoscopy (FU HEN)

Friability
Ulcers
Hemorrhage
Erythema
Necrosis

Complications: antral and pyloric strictures may follow healing

Duodenal reflux (Bile gastropathy)

Reflux of duodenal contents into the stomach - normally occurs about 72min a day or 5% of a 24hr period

Granulomatous Gastritis

Infectious

TB, Syphilis, histoplasmosis, parasites, foreign body granulomas

Non-Infectious

Inflammatory Bowel Disease (IBD)

Most common: Focal gastritis due to Crohn Disease

Chronic Granulomatous Disease (CGD)

genetically heterogeneous condition causing defects in phagocyte nicotinamide adenine dinucleaotide phosphate (NADPH) oxidase leading to recurrent life threatening bacterial & fungal infections and granuloma formation

6 proteins affected (gp91phox, p47phox, p22phox, p67phox, p40phox, and EROS)

more often in boys (most North American mutations are x-linked: gp91phox deficiency)
manifestations:

chronic active focal gastritis in antrum with granulomas or multinuclear giant cells

Endoscopic finding of lipochrome-pigmented histiocytes

Other: Sarcoidosis, lymphoma, wegener granulomatosis

Eosinophilic Gastritis

Diagnosis

Gastritis Sx (vomiting, abd pain, blood loss, gastric outlet obstruction)
Eosinonophilic gastric infiltrate
exclusion of other causes of gastric infiltrate

other causes of mucosal eosinophilia

Crohn disease, scleroderma, parasitic infection
Specific Allergen sometimes identified

Cow milk/soy protein, egg, wheat

Endoscopy (P Fees)

Pseudopolyps (Antral)
Friability
Erosions
Erythema
Swollen folds

Typically occurs with Eosinophilic gastroenteritis

Peripheral eosinophilia seen in 50% of adults

Treatment

hypoallergenic diets, steroids, antiallergic medications

Lymphocytic Gastritis

Etiologies

Celiac
Menetrier disease
CMV
Chronic varioliform gastritis
Crohn disease
Idiopathic

Hyperplastic

Menetrier disease

aka protein losing hypertrophic gastropathy
features:

Giant Gastric folds
increased mucuous secretion
decreased acid secretion
protein-losing gastropathy

can be seen in neonates but typical presentation in 4yo
self-limited in children, adults condition may be premalignant
assoc w/ CMV
DDx if Giant Gastric Folds noted:

Lymphoma
H pylori, CMV, anisakiasis
Granulomatous gastridites
Plasmocytoma
SLE

EGD reveals giant rugal folds and erythema
Histology reveals

elongated and tortuous foveolae
decreased parietal and chief cell glands
cystic dilations
edematous lamina propria
increased eosinophils and lymphocytes

Test for increased CMV IgM, Positive CMV PCR, positive tissue culture

PPI Gastropathy

Parietal Cell Hyperplasia caused by long term or high dose PPI
seen 10-48mo after starting PPI
No dysplasia
Histology reveals

sessile hyperplastic glandular dilation foveolar hyperplasia and mild inflammation
pedunculated fundic gland polyp with cystic glandular dilation

Resolves with cessation of therapy (PPI)

Portal Hypertensive

more common in cirrhotic portal hypertension (but can occur in non-cirrhotic)
no relation to severity of liver dz, size of varices, or hypersplenism
Dx:

Mild: 2-5mm erythematous patches in mosaic pattern on endoscopy
Severe: cherry-red spots, confluent hemorrhagic appearance

Histology

Ectasia of mucosal capillaries and venules
submucosal venous dilation
no significant inflammatory infiltrate

Therapy

Nonselective beta blockers (propranolol, nadolol) to reduce portal venous pressure , may reduce blood loss
somatostatin analogues are used to control acute bleeding

Celiac Gastritis

Intraepithelial lymphocytic infiltrate in antrum
no gross endoscopic findings
resolves with gluten-free diet

Graft vs Host disease (GVHD)

Acute: occurs 21-100 days after transplant

anorexia, n/v, upper abd pain
variable endoscopic findings in stomach
Histology

early GVHD reveals crypt cell apoptosis and drop-out
advanced GVHD shows gastric ulceration, edema, fibrosis, perforation

Chronic: Rarely involves the stomach

Uremic

Acute renal failure or assoc physiologic stress
GI bleed assoc w/ ulcers or erosions
Gastric pH may increase in chronic renal failure secondary to increased urea in all tissues

Autoimmune

Henoch - Schonlein Purpura

Immune complex mediated small and medium size vessel vasculitis
most common in 4-6yo
Typically affecting the Skin, GI tract, kidneys, and joints
Findings:

colicky abd pain, n/v, GI bleed
less common:

intramural hematoma
intussusception
bowel infarction
bowel perforation
pancreatitis
appendicitis
cholecystitis

upper endodscopy NOT usually required for Dx, but; may show hemorrhagic, edematous mucosa with erosions in the stomach, duodenum, and jejunum

Histology

leukoclastic vasculitis (can be missed in shallow endoscopic Bx)

Pernicious Anemia

Achlorhydria, intrinsic factor deficiency, B12 deficiency
Endoscopy shows thin or absent rugae
Histology shows atrophic fundic gland gastritis, absence of parietal cells
Can by complicated by Gastric adenocarcinoma

Autoimmune thyroiditis and goitrous jevenille hypothyroidism associated with gastritis and mucosal atrophy

Vitiligo assoc w/ autoimmune atrophic gastritis
SLE assoc w/ hypertrophic gastropathy
Connective tissue disorders may have assoc mast cell or eosinophilic gastritis

Collagenous

Rare Gastritis presenting with epigastric pain and chronic Fe deficiency
Endoscopy non-specific
Bx reveal subepithelial collagen fibrosis with inflammatory infiltrate in the lamina propria
Tx: some improvement with acid suppression and Steroids

Cystinosis

damage caused by intralysosomal deposition of cystine
Cystamine lowers intracellular cysteine BUT causes hypergastrinemia and gastric hypersecretion after only one dose!

Hypersecretory States

Zolliger-Ellison syndrome
Systemic mastocytosis
Short bowel syndrome

gastric hypersectretion due to lack of negative feedback to inhibit gastrin secretion
may be transient (or persistent with PUD)
may inactivate pancreatic lipase and deconjugate bile salts - leading to worsening nutrition status

Hyperparathyroidism

hypercalcemia causes increased gastric acid secretion
typical leads to duodenal ulcer

References:

Kliegman, Robert. Nelson Textbook of Pediatrics. Edition 21. Philadelphia, PA: Elsevier, 2020.
Tortora, Gerard J. Principles of Anatomy and Physiology. 15th ed. Hoboken, NJ: J. Wiley, 2009. Print.
Moore, Keith L.,, Arthur F. Dalley, II, and Keith L Moore. Clinically Oriented Anatomy. Fifth edition. Baltimore: Wolters Kluwer Health, 2009. Print.
Kleinman RE, Goulet O, Mieli-Vergani G, et al, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis, and Management. 5th ed. Hamilton, Ontario: BC Decker; 2008.
The N A S P G H A N fellow concise reiew of peditric gastroeterolgy, hepatology, and nutrition. 1st edition (2011)
Wyllie, Robert & Hyams, J.S.. (2011). Pediatric Gastrointestinal and Liver Disease. 10.1016/C2009-0-53242-4. (Accessed online Feb 2020)
Coran, Arnold G, and N S. Adzick. Pediatric Surgery. Philadelphia, PA: Elsevier Mosby, 2012. Internet resource.
KLEINMAN, R. E., & WALKER, W. A. Walker's pediatric gastrointestinal disease: physiology, diagnosis, management. 6th Ed. Raleigh, NC: PMPH-USA, 2018. Print