Hypertrophic Gastritis (Ménétrier Disease)

Definition and Characteristics

• Ménétrier disease: Also known as hypoproteinemic hypertrophic gastropathy.
• Characterized by:
  • Massive gastric folds in the fundus and body of the stomach.
  • Mucosa exhibits a cobblestone or cerebriform appearance.
  • Antrum is typically spared.
• Histology:
  • Foveolar hyperplasia (expansion of surface mucus cells).
  • Decreased or absent parietal cells.

Clinical Features

• Associated with:
  • Protein loss from the stomach.
  • Excessive mucus production.
  • Hypochlorhydria or achlorhydria.
• Symptoms:
  • Epigastric pain, vomiting, weight loss.
  • Decreased appetite.
  • Peripheral edema due to protein loss.

Etiology

• Cause is unknown.
• Associated with:
  • Cytomegalovirus (CMV) infection in children.
  • H. pylori infection in adults.
• Increased levels of transforming growth factor-α (TGF-α) in the gastric mucosa:
  • Stimulates epithelial cell growth.
  • Inhibits gastric acid secretion.

Diagnosis

• Radiographic or endoscopic examination reveals characteristic mucosal changes.
• Biopsy: Essential for diagnosis and to rule out gastric carcinoma or lymphoma.

Treatment

• Medical treatment:
  • Acid suppression.
  • Octreotide.
  • Eradication of CMV or H. pylori.
• Surgical treatment:
  • Total gastrectomy: Indicated for patients with:
    • Continued massive protein loss despite optimal medical therapy and a high-protein diet.
    • Development of dysplasia or carcinoma.

Prognosis and Surveillance

• Increased risk of gastric neoplasms.
• Recommended endoscopic surveillance every 1 to 2 years.

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Mallory-Weiss Tear

Definition and Characteristics

• Mucosal lacerations at the gastroesophageal (GE) junction.
• Caused by forceful vomiting, retching, coughing, or straining.
• Occur high on the lesser curvature of the stomach.
• Account for 10%–15% of acute upper gastrointestinal (GI) hemorrhages.
• Rarely associated with massive bleeding.
• Mortality rate: Approximately 3%–5%.
• Higher risk of massive hemorrhage in alcoholic patients with portal hypertension.

Clinical Presentation

• Symptoms include:
  • Hematemesis (vomiting blood).
  • Possible melena (black, tarry stools).
  • Epigastric pain.

Diagnosis

• Endoscopy is the diagnostic tool of choice.
• Visualizes the mucosal tear and assesses bleeding.

Treatment

• Endoscopic management is effective for active bleeding:
  • Multipolar electrocoagulation.
  • Epinephrine injection.
  • Endoscopic band ligation.
  • Endoscopic hemoclipping.
• Angiographic transarterial embolization:
  • For patients with persistent or recurrent bleeding after endoscopy.
• Surgical intervention (rarely needed):
  • Anterior gastrotomy to access the lesion.
  • Oversewing the bleeding site with deep sutures to reapproximate mucosa.

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Dieulafoy Gastric Lesion

Definition and Characteristics

• Accounts for 0.3%–7% of non-variceal upper GI hemorrhages.
• Caused by an abnormally large (1–3 mm) tortuous submucosal artery without a primary ulcer.
• Erosion of overlying mucosa exposes the artery to gastric contents.
• Typically located near the GE junction along the lesser curvature.
• Mucosal defect: Small (2–5 mm), surrounded by normal mucosa.

Risk Factors

• More common in men (2:1 ratio).
• Associated with:
  • Cardiovascular disease.
  • Chronic kidney disease.
  • Diabetes mellitus.

Clinical Presentation

• Sudden onset of massive, painless hematemesis.
• Bleeding is often intermittent, making detection challenging.

Diagnosis

• Upper endoscopy:
  • Diagnostic modality of choice.
  • Correctly identifies the lesion in 80% of cases.
  • May require repeat procedures due to intermittent bleeding.
• Angiography:
  • Useful if endoscopy is inconclusive.
  • May reveal a tortuous artery with contrast extravasation.

Treatment

• Endoscopic therapies:
  • Bipolar electrocoagulation.
  • Heater probe thermocoagulation.
  • Injection sclerotherapy.
  • Endoscopic hemoclipping.
• Angiographic transarterial embolization:
  • For persistent bleeding after endoscopy.
• Surgical intervention (if other treatments fail):
  • Gastric wedge resection to remove the offending vessel.
  • Localization techniques:
    • Endoscopic tattooing.
    • Intraoperative endoscopic guidance.

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Gastric Varices

Definition and Classification

• Dilated submucosal veins in the stomach.
• Commonly associated with portal hypertension and cirrhosis.
• Account for 10%–30% of variceal hemorrhages.
• Classification:
  • Isolated gastric varices (IGV):
    • Type 1 (IGV1): Located in the fundus.
    • Type 2 (IGV2): Ectopic varices anywhere in the stomach.
  • Gastroesophageal varices (GOV).

Etiology

• Develop due to:
  • Portal hypertension (generalized).
  • Sinistral hypertension from splenic vein thrombosis.
• Portal hypertension pathway:
  • Increased pressure transmitted via the left gastric vein to esophageal varices.
  • Via short and posterior gastric veins to fundic varices.
• Splenic vein thrombosis:
  • Often secondary to pancreatitis.
  • Retrograde flow through short gastric veins causes varices.

Clinical Presentation

• Bleeding incidence: 3%–30%.
• Higher risk with:
  • Splenic vein thrombosis.
  • Fundic varices.
  • Large varices.
  • Decompensated cirrhosis.

Diagnosis

• Endoscopy to visualize varices.
• Imaging studies:
  • To identify splenic vein thrombosis.
  • Assess variceal anatomy.

Treatment

• Splenic vein thrombosis with gastric varices:
  • Splenectomy is effective.
• Bleeding gastric varices in portal hypertension:
  • Volume resuscitation and correction of coagulopathy.
  • Temporary tamponade with a Sengstaken-Blakemore tube.
  • Endoscopic treatments:
    • Sclerotherapy.
    • Band ligation.
    • Glue (cyanoacrylate) or thrombin injection.
  • Rebleeding rates: 10%–35%.
  • EUS-guided therapies:
    • Cyanoacrylate-lipiodol injection.
    • Coil embolization of perforating veins.
  • Transjugular intrahepatic portosystemic shunt (TIPS):
    • Effective for uncontrolled bleeding.
    • Gastrorenal shunts may reduce TIPS efficacy.
  • Balloon-occluded retrograde transvenous obliteration (BRTO):
    • High success rate (75%–100%).
    • May aggravate esophageal varices due to increased portal pressure.

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Gastric Volvulus

Definition and Types

• Twisting of the stomach causing obstruction, ischemia, or necrosis.
• Types of Volvulus:
  • Organoaxial:
    • Rotation along the longitudinal (long) axis.
    • Accounts for ~66% of cases.
    • Often acute and associated with diaphragmatic defects.
  • Mesenteroaxial:
    • Rotation along the short vertical axis.
    • Accounts for ~33% of cases.
    • Usually partial (<180 degrees) and recurrent.
    • Not typically associated with diaphragmatic defects.
  • Combined rotations (rare).

Etiology

• Primary gastric volvulus:
  • Due to defects in gastric ligaments (e.g., gastrocolic, gastrohepatic ligaments).
• Secondary gastric volvulus:
  • Caused by anatomic abnormalities such as:
    • Paraesophageal hernia (most common in adults).
    • Congenital diaphragmatic defects (e.g., foramen of Bochdalek in children).

Clinical Presentation

• Acute symptoms:
  • Severe upper abdominal pain.
  • Abdominal distention.
  • Vomiting.
• Borchardt's triad:
  • Severe epigastric pain.
  • Intractable retching without vomiting.
  • Inability to pass a nasogastric (NG) tube.

Diagnosis

• Plain abdominal radiographs:
  • Show a spherical gas-filled stomach with air-fluid levels.
• Computed Tomography (CT) scan:
  • Confirms the diagnosis.
  • Visualizes the degree and axis of rotation.

Treatment

• Emergency management:
  • NG decompression to relieve pressure.
  • May lead to spontaneous detorsion.
• Surgical intervention:
  • Detorsion and reduction of the stomach.
  • Repair diaphragmatic defects if present.
  • Gastropexy to fix the stomach and prevent recurrence.
  • Fundoplication may be considered with paraesophageal hernia repair.
  • Resection of necrotic gastric tissue if ischemia occurred.
• High-risk patients:
  • Endoscopic detorsion.
  • Percutaneous endoscopic gastrostomy (PEG) tubes for fixation.

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Gastric Bezoars

Definition and Types

• Bezoars: Collections of indigestible material in the GI tract.
• Types:
  • Phytobezoar: Composed of vegetable fibers.
  • Trichobezoar: Composed of hair.
  • Pharmacobezoar: Composed of medications.
  • Other substances may also form bezoars.

Risk Factors

• Gastric dysmotility due to:
  • Previous gastric surgery (e.g., vagotomy, gastrectomy).
  • Gastroparesis.
  • Gastric outlet obstruction.
• Impaired grinding mechanism and migrating motor complexes dysfunction.

Clinical Presentation

• Often asymptomatic or with gradual symptom onset.
• Symptoms may include:
  • Early satiety.
  • Abdominal pain.
  • Nausea and vomiting.
  • Weight loss.
• Physical examination:
  • May reveal a palpable abdominal mass.

Diagnosis

• Imaging studies:
  • Abdominal radiographs or CT scans show a mass or filling defect.
• Upper endoscopy:
  • Confirms the presence of a bezoar.
  • Allows for direct visualization and potential treatment.

Treatment

• Chemical dissolution:
  • Enzymatic therapy:
    • Papain (caution due to hypernatremia risk).
    • Cellulase.
    • Acetylcysteine.
    • Soda (carbonated beverages).
  • Effectiveness varies based on bezoar composition.
• Endoscopic removal:
  • Fragmentation using:
    • Water jets.
    • Forceps.
    • Direct suction.
  • Fragments can be removed endoscopically or allowed to pass.
• Surgical removal:
  • Indicated when:
    • Conservative measures fail.
    • Complications arise (e.g., perforation, bleeding).
    • Bezoar composition contraindicates other treatments (e.g., trichobezoars).
• Preventive measures:
  • Address underlying gastric motility disorders.
  • Dietary modifications to avoid high-fiber, indigestible foods.

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