Esophageal & Gastric Disorders

Esophageal & Gastric Disorders: Diagnosis, Surveillance, and Eradication Protocols

Gastroesophageal Reflux Disease (GERD) and Barrett Esophagus

Gastroesophageal reflux disease (GERD) is primarily a clinical diagnosis, characterized by heartburn and acid regurgitation. For typical, mild symptoms, an empiric trial of daily proton pump inhibitors (PPIs) for 4 to 8 weeks is both diagnostic and therapeutic. However, Step 3 examinations focus heavily on when to deviate from empiric therapy and perform upper endoscopy (esophagogastroduodenoscopy or EGD). Diagnostic EGD is indicated for patients presenting with "alarm symptoms"—including progressive dysphagia, odynophagia, unexplained weight loss, iron deficiency anemia, persistent vomiting, or gastrointestinal bleeding—as well as those who are over 50 years of age with long-standing (>5 years) symptoms and multiple risk factors (e.g., male sex, white race, central obesity, history of smoking) to screen for Barrett esophagus and esophageal adenocarcinoma.

Long-term PPI use is highly effective but carries clinical risks that are frequently tested. Chronic acid suppression is associated with decreased absorption of calcium and magnesium, potentially leading to osteoporosis, increased fracture risk, and hypomagnesemia. It also increases susceptibility to Clostridioides difficile-associated diarrhea and community-acquired pneumonia, and can cause vitamin B12 malabsorption and acute interstitial nephritis. Therefore, clinicians must routinely review the indication for PPIs and attempt to taper patients to the lowest effective dose.

Barrett esophagus represents intestinal metaplasia, where normal stratified squamous epithelium is replaced by columnar epithelium containing goblet cells. Once diagnosed, management is strictly guided by the degree of dysplasia on histopathology:

• No dysplasia: Repeat EGD with biopsies in 3 to 5 years.
• Indefinite for dysplasia: Optimize PPI therapy for 3 to 6 months to reduce active inflammatory changes that mimic dysplasia, and repeat the EGD.
• Low-grade dysplasia: Preferred approach is endoscopic eradication therapy (such as radiofrequency ablation), though endoscopic surveillance every 12 months is an acceptable alternative.
• High-grade dysplasia: Endoscopic eradication therapy (RFA or endoscopic mucosal resection) is the standard of care, as the risk of progression to adenocarcinoma is high.

Peptic Ulcer Disease (PUD) and H. pylori Eradication

Peptic ulcer disease (PUD) most commonly results from Helicobacter pylori infection or the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Less common causes, such as gastrinoma (Zollinger-Ellison syndrome), should be suspected in cases of refractory, recurrent, or multiple ulcers located distal to the duodenal bulb, associated with severe diarrhea. Gastrinomas are diagnosed with fasting serum gastrin levels, followed by a secretin stimulation test if gastrin levels are equivocal. For NSAID-induced ulcers, the offending agent must be discontinued; if NSAID use is mandatory (e.g., severe inflammatory arthritis), co-prescription of a PPI or misoprostol (a prostaglandin E1 analog) is required to reduce recurrence risk.

Diagnostic testing for H. pylori must be carefully managed. Non-invasive options include the urea breath test and stool antigen assay. Invasive testing is performed via gastric biopsy during EGD (rapid urease test, histology, or culture). Crucially, PPIs, bismuth, and antibiotics can cause false-negative results. PPIs must be discontinued for at least 2 weeks, and antibiotics/bismuth for at least 4 weeks, prior to any H. pylori diagnostic test.

Eradication therapy has shifted due to rising clarithromycin resistance:

• Bismuth Quadruple Therapy: Now preferred as first-line in most regions. It consists of a PPI, bismuth subsalicylate, metronidazole, and tetracycline taken for 10 to 14 days.
• Clarithromycin Triple Therapy: Consisting of a PPI, clarithromycin, and amoxicillin (or metronidazole if penicillin-allergic) for 14 days. This regimen should only be used in areas where local clarithromycin resistance rates are documented to be low (<15%) and the patient has no prior macrolide exposure.
• Concomitant Therapy: PPI, clarithromycin, amoxicillin, and metronidazole for 10 to 14 days is another non-bismuth option.

Successful eradication must always be confirmed. This is done using either the stool antigen test or urea breath test, performed at least 4 weeks after completing eradication therapy and at least 2 weeks after stopping PPIs. If eradication fails, salvage therapy using a different regimen (e.g., levofloxacin-based triple therapy) is indicated.

Acute Upper Gastrointestinal Bleeding (UGIB)

Acute upper GI bleeding (bleeding proximal to the ligament of Treitz) is a medical emergency requiring rapid risk stratification and standardized stabilization. The initial assessment must focus on airway, breathing, and circulation.

• Resuscitation: Place two large-bore peripheral intravenous lines (14- or 16-gauge). Infuse isotonic crystalloids to restore hemodynamic stability.
• Transfusion Thresholds: Transfuse packed red blood cells (PRBCs) to maintain a hemoglobin level above 7 g/dL in most patients. For patients with active cardiovascular disease, unstable coronary disease, or massive ongoing bleeding, maintain a higher threshold of 8 to 9 g/dL. Over-transfusion must be avoided, especially in patients with portal hypertension, as it increases portal pressures and risk of rebleeding.
• Airway Protection: Intubate patients with altered mental status, massive ongoing hematemesis, or respiratory distress to prevent aspiration before endoscopy.
• Medical Adjuncts: Initiate an intravenous PPI infusion (e.g., pantoprazole 80 mg bolus followed by 8 mg/hour, or 40 mg IV twice daily) to promote clot stability by raising gastric pH above 6.0. In patients with suspected variceal hemorrhage (e.g., signs of cirrhosis), administer IV octreotide (a somatostatin analog that causes splanchnic vasoconstriction) and prophylactic IV ceftriaxone (to reduce bacterial translocation, infection, and mortality).
• Endoscopy Timing: Perform EGD within 24 hours of presentation after hemodynamics are stabilized. Endoscopy provides both diagnostic visualization and therapeutic intervention (e.g., band ligation for varices; epinephrine injection, thermal coagulation, or clip application for non-variceal bleeding).
• Prognostic Scores: Use the Glasgow-Blatchford Score at presentation to identify low-risk patients who can be safely managed as outpatients (score of 0 or 1), while the Rockall Score is used post-endoscopy to estimate rebleeding and mortality risk.