Gastrointestinal · Year 2 · from Gastrointestinal

Case 1: Gastroesophageal Reflux Disease with Barrett's Esophagus

Patient Presentation

Demographics: 62-year-old male

Chief Complaint: Chronic heartburn for 20 years with recent worsening dysphagia

History of Present Illness: The patient has experienced heartburn and regurgitation for over two decades, managed with intermittent over-the-counter antacids and PPIs. Over the past 6 months, he has noticed solid foods "sticking" in his lower chest, requiring multiple sips of water to pass. He has lost 8 pounds unintentionally. He denies odynophagia or hematemesis.

Past Medical History: Obesity (BMI 32), hypertension, hyperlipidemia

Social History: 25 pack-year smoking history (quit 10 years ago), occasional alcohol use

Physical Examination

  • Vital Signs: BP 142/88 mmHg, HR 76 bpm
  • General: Obese male in no acute distress
  • Abdomen: Soft, obese, non-tender
  • Cardiac/Pulmonary: Unremarkable

Workup and Results

  • Upper Endoscopy: Long-segment Barrett's esophagus (8 cm) with a nodular area; distal esophageal stricture at 36 cm
  • Histopathology: Intestinal metaplasia with goblet cells; nodular area shows high-grade dysplasia
  • CT Chest/Abdomen: No lymphadenopathy or metastatic disease

Endoscopic image showing Barrett's esophagus with salmon-colored columnar mucosa extending above the gastroesophageal junction. The irregular nodular area (arrow) was found to harbor high-grade dysplasia on biopsy.

Image Source: Wikimedia Commons, CC BY-SA 4.0

Diagnosis

Barrett's Esophagus with High-Grade Dysplasia and Peptic Stricture

Clinical Correlation

Barrett's esophagus represents intestinal metaplasia in response to chronic acid exposure. The progression from non-dysplastic Barrett's to low-grade dysplasia, high-grade dysplasia, and invasive adenocarcinoma follows a predictable sequence. High-grade dysplasia carries 5-10% annual progression risk to cancer and requires treatment. The peptic stricture developed from chronic inflammation and fibrosis, explaining the dysphagia to solids.

Treatment

  • Endoscopic eradication therapy: radiofrequency ablation (RFA) for flat dysplasia combined with endoscopic mucosal resection (EMR) for the nodular component
  • Stricture dilation at time of endoscopy
  • Continued high-dose PPI therapy indefinitely
  • Surveillance endoscopy every 3 months after treatment until eradication confirmed

All cases for this lecture as Markdown