• Male predominance: M:F ratio ≈ 2:1 ^[1]
• Mean age of diagnosis: ~55 years old, typically discovered during endoscopic examination of middle-aged and older adults ^[1]
• Prevalence in patients undergoing endoscopy for GERD symptoms: approximately 5–15%
• General population prevalence (from autopsy and screening studies): estimated at 1–2%, suggesting many cases are undiagnosed
• In Hong Kong, squamous cell carcinoma (SCC) remains the most common esophageal cancer subtype (~90% of cases) ^[4], unlike Western countries where adenocarcinoma has overtaken SCC. However, with increasing Westernization of diet, rising obesity rates, and increasing GERD prevalence in Asia, the incidence of Barrett's esophagus and esophageal adenocarcinoma is rising in Hong Kong and other Asian populations.
• The annual risk of progression from Barrett's esophagus to adenocarcinoma is approximately 0.5% per year (or ~1 in 200 patient-years) ^[3]. While this sounds low, over decades of surveillance, it becomes clinically significant.

Protective factor — an interesting one:

• H. pylori infection is considered a protective factor against Barrett's esophagus ^[3]. Why? H. pylori-associated atrophic gastritis leads to parietal cell atrophy → reduced gastric acid secretion → less acid available to reflux into the esophagus. The eradication of H. pylori in developed nations may paradoxically have contributed to the rise of GERD and Barrett's esophagus. This is the so-called "H. pylori paradox" — eradicating it reduces peptic ulcer and gastric cancer risk but may increase GERD-related disease.

Barrett's esophagus develops as a consequence of chronic, usually long-standing GERD ^[1][2]. In Hong Kong, the prevalence of GERD has been increasing, with current estimates of ~6–9% of the population experiencing weekly reflux symptoms. This mirrors global trends driven by:

• Increasing obesity rates (especially visceral/central obesity)
• Adoption of Western dietary patterns (high-fat, processed foods)
• Ageing population (reduced esophageal motility, increased hiatus hernia prevalence)
• Widespread use of medications that relax the LES (calcium channel blockers, anticholinergics, benzodiazepines)

As described above, when multiple anti-reflux mechanisms fail:

Key mechanisms of LES dysfunction ^[2]:

• ↓ LES tone: The intrinsic smooth muscle becomes hypotonic → less effective barrier. Factors: fatty foods, alcohol, chocolate, caffeine, smoking, drugs (CCBs, nitrates, anticholinergics)
• Transient LES relaxations (TLESRs): These are the most common mechanism of reflux — inappropriate, non-swallowing-related relaxations mediated by a vagal reflex triggered by gastric distension. They are more frequent and prolonged in GERD patients.
• Hiatus hernia: Anatomically, the LES sits within the diaphragmatic hiatus. When the GEJ herniates into the thorax (sliding hiatus hernia — Type I), the crural diaphragm no longer reinforces the LES. Additionally, the intra-abdominal esophageal segment is shortened or lost, and the angle of His becomes obtuse ^[2][5]. This creates a "two-sphincter" problem — the LES and crural diaphragm are now separated.

• Normal esophageal pH is ~7 (neutral). In GERD, the distal esophageal pH drops to < 4 for prolonged periods.
• Acid (HCl) and pepsin cause direct epithelial damage (pepsin is activated at low pH and causes proteolytic destruction).
• Bile salts (duodenogastroesophageal reflux) are particularly important in Barrett's pathogenesis — bile salts at neutral or slightly acidic pH are toxic to squamous epithelium and promote intestinal metaplasia via activation of CDX2, a key intestinal transcription factor.
• Inflammatory mediators (IL-1β, IL-6, IL-8, TNF-α) are released in response to mucosal injury → inflammatory infiltrate → further tissue damage.

• Metaplasia is a reversible adaptive response in which one differentiated cell type is replaced by another that is better suited to the hostile environment.
• In Barrett's: stratified squamous epithelium → specialized intestinal columnar epithelium containing goblet cells (intestinal-type metaplasia).
• Why intestinal-type? The intestinal epithelium has evolved to handle acidic/enzymatic environments. Goblet cells produce protective mucus. Columnar cells have a much thicker glycocalyx and secrete bicarbonate.
• This switch is driven by alteration of stem cell differentiation at the basal layer. The progenitor cells in the squamous epithelium (or possibly from the GEJ cardiac glands, or possibly from circulating bone marrow-derived stem cells) are reprogrammed by:
  • Chronic inflammation
  • Activation of transcription factors: CDX1, CDX2 (caudal-type homeobox genes — master regulators of intestinal differentiation), SOX9, HNF4α
  • Epigenetic changes
  • Hedgehog and BMP signaling pathway activation

This is the dreaded progression and the whole reason we care about Barrett's:

• Intestinal metaplasia → Low-grade dysplasia (LGD): Cells show architectural distortion and nuclear abnormalities but confined to the lower portion of crypts
• LGD → High-grade dysplasia (HGD): More severe cytological and architectural abnormalities; nuclear changes extend to the surface epithelium; carcinoma in situ
• HGD → Invasive adenocarcinoma: Penetration through the basement membrane

Key molecular events along this progression:

• p53 mutations (most common — TP53 loss of function → loss of cell cycle checkpoint → uncontrolled proliferation)
• p16/CDKN2A inactivation (loss of cell cycle inhibition at G1/S checkpoint)
• Aneuploidy (chromosomal instability)
• ERBB2 (HER2) amplification (in some adenocarcinomas — targetable with trastuzumab)
• Telomerase activation, COX-2 overexpression

The risk of developing esophageal adenocarcinoma is 30–100× compared with the normal population ^[2].

This is the internationally standardized endoscopic classification system for Barrett's esophagus:

• C = Circumferential extent: the length of the circumferential (full 360°) segment of columnar mucosa above the GEJ
• M = Maximal extent: the length of the longest tongue/island of columnar mucosa above the GEJ (including non-circumferential extensions)

Example: "C3M5" means 3 cm of circumferential Barrett's and the longest tongue extends 5 cm above the GEJ.

Why does this matter? It standardizes reporting, allows comparison between endoscopies, and helps stratify cancer risk (longer segments = higher risk).

Specialized intestinal columnar metaplasia of Barrett's esophagus causes NO symptoms by itself ^[2].

Barrett's esophagus is clinically silent. It does not produce any symptoms on its own. What patients experience are the symptoms of the underlying GERD (and occasionally complications of Barrett's itself, like stricture or ulceration). This is why Barrett's is typically discovered incidentally during endoscopy performed for GERD symptoms, or during screening/surveillance.

• By far the most common cause of the symptoms that bring a Barrett's patient to medical attention ^[7]
• GERD is present in ~90% of Barrett's patients, but only ~10% of GERD patients develop Barrett's ^[3]
• Key distinction: GERD without Barrett's will show either normal mucosa (non-erosive reflux disease — NERD) or erosive esophagitis on endoscopy, but no columnar metaplasia above the GEJ
• Pathophysiology: Same as Barrett's — LES dysfunction, hiatus hernia, delayed clearance — but the mucosal response has not yet progressed to metaplasia ^[7][8]

• Causes: Candida albicans (most common), HSV, CMV (especially in immunocompromised — HIV/AIDS, transplant recipients, chemotherapy)
• Why it mimics Barrett's/GERD: Causes odynophagia, dysphagia, and retrosternal pain
• How to differentiate:
  • Endoscopically: Candida → white adherent plaques; HSV → shallow, well-circumscribed ulcers with raised yellow edges; CMV → deep, large, single ulcers
  • Clinical context: immunosuppression is the key clue
  • Biopsy: viral inclusions (CMV — owl-eye intranuclear inclusions; HSV — multinucleated giant cells with Cowdry type A inclusions), fungal hyphae (Candida)
• Pathophysiology: Direct pathogen invasion of esophageal mucosa. Candida causes superficial mucosal invasion; HSV and CMV cause epithelial cell lysis and ulceration

• Caused by direct chemical injury from medications lodging in the esophagus
• Common culprits: NSAIDs, bisphosphonates (alendronate), tetracyclines (doxycycline), potassium chloride, iron supplements
• Why it mimics Barrett's/GERD: Retrosternal pain, odynophagia, dysphagia
• How to differentiate: History of taking pills without adequate water, often in patients with motility problems or who take medications at bedtime. Endoscopy shows discrete ulceration at known "sticking points" (aortic arch, left atrium compression, above the LES) rather than the diffuse columnar change of Barrett's
• Pathophysiology: The tablet dissolves locally, creating a high-concentration acid or alkali environment → focal chemical burn → ulceration

• A chronic, immune-mediated/antigen-driven esophageal disease characterized by eosinophilic infiltration of the esophageal mucosa ( ≥ 15 eosinophils per high-power field on biopsy)
• Why it mimics Barrett's/GERD: Presents with dysphagia (especially for solids), heartburn that may not respond to PPI, food impaction
• How to differentiate:
  • Epidemiology: Younger patients (20s–40s), often with atopic history (asthma, eczema, food allergies)
  • Endoscopy: Characteristic rings ("trachealization" / ringed esophagus / "feline esophagus"), linear furrows, white exudates/plaques, mucosal edema — very different from the salmon-pink tongues of Barrett's
  • Biopsy: Dense eosinophilic infiltrate — no goblet cells or intestinal metaplasia
  • Fails to respond to standard PPI therapy (unlike GERD/Barrett's)
• Pathophysiology: Food or aeroallergens trigger a Th2-mediated immune response → eotaxin-3 release → eosinophil recruitment to esophageal mucosa → inflammation → fibrosis → stricture

These can present with dysphagia, regurgitation, and chest pain — mimicking GERD/Barrett's symptoms:

• Gastric or duodenal ulcers can produce epigastric pain that overlaps with GERD symptoms
• How to differentiate: Duodenal ulcer pain classically improves with eating (buffered by food) and worsens 2–3 hours later ("hunger pain"); gastric ulcer pain may worsen with eating. Neither typically causes regurgitation. OGD is diagnostic.
• Risk factors: H. pylori, NSAIDs, stress, excess gastric acid ^[11]

• Chronic epigastric pain/discomfort without an identifiable structural or biochemical cause
• Diagnosis of exclusion after OGD, H. pylori testing, and other workup are negative
• Rome IV criteria: bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning without structural explanation

• This is the critical one you must never miss. Esophageal pain and cardiac pain share the same spinal afferent pathways (T1–T5 dermatomes), making them clinically indistinguishable by symptom description alone.
• Cardiac chest pain must be excluded first in any patient presenting with retrosternal pain, especially if the patient has cardiovascular risk factors.
• How to differentiate: ECG, cardiac biomarkers (troponin), exercise stress testing. GERD-related chest pain is more likely to be postprandial, related to body position, relieved by antacids, and associated with other reflux symptoms. Anginal pain is more likely exertional, relieved by rest/nitrates, and associated with dyspnea.
• That said, nitrates relax both coronary arteries AND the LES — so relief with nitroglycerin does NOT reliably distinguish cardiac from esophageal pain.

Barrett's esophagus is fundamentally a histopathological diagnosis made in an endoscopic context. You cannot diagnose it by symptoms alone (it's asymptomatic), by blood tests, or by imaging. You need an endoscope AND a microscope.

Two criteria must be fulfilled by endoscopic examination to diagnose Barrett's esophagus ^[4]:

1. The endoscopist must document that columnar epithelium lines the distal esophagus
2. Histological examination of biopsy specimen from that columnar epithelium must reveal specialized intestinal metaplasia (characterized by goblet cells)

Let's unpack why both are needed and what each means from first principles.

Why isn't endoscopic appearance alone sufficient? Because:

1. Columnar epithelium in the distal esophagus could be gastric cardia-type (no goblet cells) — this does NOT carry the same cancer risk
2. Visual assessment alone has limited specificity — inflammation, hiatus hernia, and normal variants can confuse the picture
3. Goblet cells are the histological hallmark that defines the "intestinal" nature of the metaplasia and confirms the cancer-predisposing phenotype

What Are Goblet Cells?

Goblet cells are mucus-secreting cells with a characteristic "goblet" (wine glass) shape. They are normally found in the intestine but NOT in the esophagus or gastric cardia. Their presence in the esophageal epithelium proves that the metaplasia is of the specialized intestinal type — the type associated with cancer progression via the metaplasia–dysplasia–carcinoma sequence.

On histology, goblet cells are identified by:

• Distended, mucin-filled cytoplasm (stains blue with Alcian blue at pH 2.5)
• Nucleus pushed to the base of the cell
• Interspersed among columnar absorptive-type cells

Simply seeing Barrett's mucosa and taking one random biopsy is not enough. Dysplasia can be patchy and invisible — a single biopsy can easily miss it. Therefore, a systematic biopsy protocol is essential.

The "Seattle protocol": biopsy every 1–2 cm in 4 quadrants ^[3]

This means:

• Endoscopic 4-quadrant biopsy should be performed and obtained at 1-cm intervals ^[2] (or 2-cm intervals for surveillance of non-dysplastic Barrett's)
• Biopsies are taken at the 12, 3, 6, and 9 o'clock positions at each level throughout the entire Barrett's segment
• Any mucosal irregularities in the segment should be removed with endoscopic resection with pathological evaluation ^[2] — visible lesions (nodules, ulcers, raised areas) are biopsied or resected separately because they have the highest yield for dysplasia/carcinoma

Why 4-quadrant? Dysplasia is often focal and not uniformly distributed across the Barrett's segment. The more biopsies you take, the higher the detection rate. The Seattle protocol maximizes sampling coverage of the entire metaplastic segment.

Why 1–2 cm intervals? Modeling studies show that intervals wider than 2 cm significantly reduce the sensitivity for detecting dysplasia. At 1-cm intervals, the detection rate for HGD approaches 95%.

Biopsies are processed and examined by a GI pathologist. The critical questions on the pathology report:

Grading Dysplasia — What the Pathologist Looks For

While OGD + biopsy diagnoses Barrett's, you may also need to assess the underlying GERD for management purposes (especially if considering anti-reflux surgery) ^[14]:

If biopsies from the Barrett's segment reveal HGD or intramucosal carcinoma, further staging investigations are needed to determine if there is invasive cancer or nodal involvement:

These are not diagnostic for Barrett's but are part of the overall assessment:

ALL patients with Barrett's esophagus should receive PPI whether they are symptomatic or not ^[2]

This is a critical exam point. Let's understand why:

Mechanism of PPIs: PPIs ("proton pump inhibitors") — the name tells you what they do. They irreversibly inhibit the H⁺/K⁺-ATPase (the "proton pump") on the apical surface of gastric parietal cells. This is the final common pathway for acid secretion, regardless of the stimulus (histamine, acetylcholine, gastrin). By blocking this pump, PPIs reduce gastric acid output by ~90–95%.

Why lifelong PPI in Barrett's?

1. Reduce ongoing acid injury: Even though metaplasia is already established, continued acid + bile exposure drives the inflammatory milieu that promotes the metaplasia → dysplasia → carcinoma sequence. PPIs markedly reduce acid exposure.
2. May promote partial regression: Some studies show that with sustained acid suppression, small islands of squamous epithelium can re-grow within the Barrett's segment ("squamous re-epithelialization"). Complete regression is rare, but any reduction in metaplastic area theoretically reduces cancer risk.
3. May slow dysplastic progression: Observational data suggest PPI use is associated with ~50% reduction in the risk of progression to HGD/adenocarcinoma. The mechanism: reduced acid-driven DNA damage, reduced cell proliferation rate, reduced inflammatory cytokine milieu.

Practical prescribing ^[15]:

• Examples: Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole ^[15]
• Dose: High-dose (e.g., omeprazole 20 mg BD or esomeprazole 40 mg daily) — aim to fully suppress acid
• Timing: ALL PPIs except dexlansoprazole should be administered 30 min–1 hour before meals (before parietal cells are stimulated to secrete acid) to ensure maximal efficacy ^[15]. Why? PPIs bind to actively secreting proton pumps. If taken on an empty stomach without subsequent eating, fewer pumps are active → drug is wasted. Taking the PPI before breakfast activates the pumps as food arrives, and the drug catches them in their active state.

These target the underlying GERD and are adjunctive to PPIs ^[15]:

• Mechanism: Block histamine H2 receptors on parietal cells → reduce acid secretion (but only one of three stimulatory pathways, so less potent than PPIs)
• Examples: Cimetidine, Famotidine ^[15]
• Role in Barrett's: Sometimes added at bedtime for nocturnal acid breakthrough (acid secretion that occurs during sleep despite daytime PPI). However, regular use of H2RA will lead to tolerance and loss of therapeutic effects → should be used intermittently only ^[15]
• Not a substitute for PPI in Barrett's

• There is growing evidence that low-dose aspirin may reduce the risk of progression from Barrett's to adenocarcinoma by ~50% (via COX-2 inhibition → reduced prostaglandin-mediated cell proliferation and angiogenesis)
• The AspECT trial (2018) showed that high-dose PPI + aspirin together provided the greatest reduction in progression
• Current guidelines: Aspirin chemoprevention is NOT routinely recommended for all Barrett's patients, but may be considered in those already taking aspirin for cardiovascular indications. The decision should weigh bleeding risk vs cancer prevention benefit.

• Methods of surveillance ^[13]:
  • Chromoendoscopy
  • High-resolution white light endoscopy
  • Narrow band imaging (NBI)
• Seattle protocol biopsies (4-quadrant, every 1–2 cm) + targeted biopsy/EMR of any visible mucosal abnormality
• Expert GI pathologist review mandatory for any dysplasia diagnosis

Consider discontinuing surveillance when:

• Patient's life expectancy is < 5 years (comorbidities, advanced age)
• Patient declines continued surveillance
• Patient has had complete eradication of intestinal metaplasia (CEIM) confirmed on 2 consecutive endoscopies after treatment — but even then, surveillance continues at reduced frequency (every 1–3 years) because of risk of recurrence / buried Barrett's

A "stricture" (Latin: strictura = narrowing, from stringere = to draw tight) is a fibrous narrowing of the esophageal lumen.

Here's the sequence:

1. Chronic acid/bile reflux → ongoing mucosal inflammation in the Barrett's segment
2. Repeated cycles of injury and repair → fibroblast activation → collagen deposition in the submucosa and muscularis
3. Progressive fibrosis → circumferential scar tissue contracts → lumen narrows
4. The result is a peptic stricture — a fibrotic narrowing typically occurring at or near the squamocolumnar junction

This is essentially the same process as scar contracture anywhere in the body — chronic inflammation leads to fibrosis, and fibrosis leads to contraction and narrowing. The esophagus happens to be a tube, so contraction of scar tissue shrinks the tube's diameter.

• Progressive mechanical dysphagia — solids before liquids (because the lumen narrows gradually)
  • Why solids first? A partially narrowed lumen can still pass liquids (which conform to any shape) but cannot pass solid food boluses that exceed the luminal diameter. Symptoms typically appear when the lumen narrows to < 13 mm (normal ~20 mm). Complete obstruction (dysphagia for liquids too) occurs when the lumen reaches < 9 mm.
• Food impaction — a food bolus gets stuck at the stricture site → acute presentation requiring emergency endoscopic removal
• Patients often modify their diet unconsciously — eating slower, chewing more, avoiding certain solid foods — and may not report dysphagia until the stricture is quite advanced

• OGD: Visible narrowing of the lumen; fibrotic, pale, smooth appearance (benign stricture) vs irregular, friable, nodular (malignant stricture). Biopsies must always be taken from any stricture to exclude malignancy — a Barrett's-associated stricture could harbour adenocarcinoma within its walls.
• Barium swallow: Smooth, tapered narrowing with proximal dilation in benign stricture; irregular "apple-core" or shouldered narrowing in malignant stricture.

• Endoscopic balloon dilation or bougie dilation — physically stretches the stricture by passing progressively larger dilators through it. The "rule of three" applies: do not increase the dilator diameter by more than 3 mm (or 3 French sizes) in a single session, to minimize perforation risk.
• Intensify PPI therapy — reduce ongoing acid injury that drives fibrosis
• Repeat dilation as needed (strictures often recur — "refractory stricture")
• For refractory strictures: consider temporary self-expanding stent placement, intralesional steroid injection (triamcinolone — reduces fibrosis), or ultimately surgical resection if unmanageable endoscopically
• Always biopsy to exclude underlying malignancy

Barrett's ulcers develop within the metaplastic columnar epithelium of the Barrett's segment. The mechanism:

1. The metaplastic columnar epithelium is more acid-resistant than squamous epithelium, but it is not immune to acid-peptic injury
2. Areas of columnar epithelium exposed to particularly high concentrations of acid and/or bile (especially at the junction between Barrett's and squamous epithelium, where acid "pools") undergo focal necrosis
3. Necrosis extends through the mucosa → ulceration (breach of the epithelial surface extending at least into the muscularis mucosae)
4. Deep ulcers can penetrate into the submucosa or even the muscularis propria, risking hemorrhage from submucosal vessels or perforation

Barrett's ulcers are essentially the esophageal equivalent of peptic ulcers in the stomach/duodenum — same acid-driven mechanism, different location.

• Odynophagia (painful swallowing — the ulcer is directly irritated by the food bolus or acid contact)
• Retrosternal pain (continuous or exacerbated by eating/swallowing)
• Upper GI bleeding (hematemesis, coffee-ground vomiting, melena, or occult bleeding causing iron deficiency anemia) — if the ulcer erodes into a submucosal vessel
• An ulcer within a Barrett's segment should always raise the suspicion of underlying malignancy — adenocarcinoma can present as an ulcerated lesion

• OGD with biopsy: Visualize the ulcer; take multiple biopsies from the ulcer edges and base to exclude underlying dysplasia or adenocarcinoma
• Histology: Distinguish between a benign peptic ulcer (inflammatory debris, granulation tissue, regenerative epithelium) and a malignant ulcer (dysplastic/carcinomatous cells)

• High-dose PPI — eliminate the acid drive; promote ulcer healing
• Biopsy all ulcers to exclude malignancy
• Repeat OGD in 6–8 weeks to confirm healing and take follow-up biopsies — a non-healing ulcer is suspicious for malignancy
• Treat H. pylori if present (though H. pylori is less commonly implicated in Barrett's-related ulcers than in gastric/duodenal ulcers)
• Address risk factors: reduce NSAID use, smoking cessation

Bleeding in Barrett's esophagus can occur from several sources:

1. Barrett's ulceration — the most common mechanism. Deep ulcers erode into submucosal arterioles or venules → bleeding. This is analogous to a bleeding peptic ulcer in the stomach.
2. Erosive esophagitis — the surrounding squamous epithelium (not the Barrett's segment itself) may still have active reflux esophagitis with superficial erosions that ooze blood
3. Adenocarcinoma — tumour neovascularization produces fragile, abnormal blood vessels that bleed easily. Erosion of tumour into larger vessels (left gastric artery branches, aortic branches) can cause massive hemorrhage ^[19]

Presentation depends on the severity and rate of bleeding:

Coffee-ground vomiting occurs because hemoglobin is converted to hematin (dark brown) by gastric acid — this tells you the blood has been in contact with acid for some time (slower bleed) rather than brisk arterial hemorrhage (bright red hematemesis).

• Urgent OGD — identifies the bleeding source, allows assessment of severity (Forrest classification for ulcer bleeding), and enables endoscopic hemostasis
• CBC: Assess Hb/Hct for anemia severity
• Iron studies: Confirm iron deficiency if chronic presentation
• Group and crossmatch: Prepare for possible transfusion

• Resuscitation: ABC approach, IV access, IV fluid resuscitation, blood transfusion if Hb < 7–8 g/dL (or earlier if hemodynamically unstable)
• IV PPI (e.g., omeprazole 80 mg bolus then 8 mg/hr infusion) — raises gastric pH to > 6, promoting platelet aggregation and clot stability (clots dissolve at pH < 5.4 due to pepsin activity)
• Endoscopic hemostasis: Injection therapy (dilute adrenaline 1:10,000), thermal coagulation (bipolar electrocoagulation, heater probe), mechanical (hemoclips), or combination
• Treat the underlying cause (optimize PPI, eradicate H. pylori, biopsy to exclude malignancy)
• If endoscopic hemostasis fails: interventional radiology (angiographic embolization) or surgery (very rare)

As covered extensively in previous sections, Barrett's esophagus predisposes to adenocarcinoma via a stepwise molecular progression:

• Risk of developing cancer is 30–100× compared with the normal population ^[13]
• Annual progression rate: ~0.5% per year (or ~1 in 200 patient-years) ^[3]
• ~7% of Barrett's patients develop adenocarcinoma over their lifetime ^[14]
• Adenocarcinoma affects the lower 1/3 of the esophagus (where Barrett's develops) and is not multicentric (unlike SCC) ^[19]
• Prognosis is poor if diagnosed late: > 50% metastasis at presentation, 5-year survival is just 5–10% ^[16] — this is precisely why surveillance exists: to catch it early when it IS curable

Not all Barrett's patients are equally likely to develop cancer. Higher-risk features include:

Once adenocarcinoma develops, it can spread via:

• Painless progressive dysphagia — the hallmark presentation; occurs when ≥ 75% of the lumen is occluded ^[16]
• Weight loss — combination of reduced intake (dysphagia, anorexia) and cancer cachexia (TNF-α, IL-6 mediated)
• Odynophagia — usually indicates extra-esophageal involvement ^[16]
• UGIB (hematemesis, melena, anemic symptoms) — from tumour surface ulceration or vessel erosion
• Regurgitation / aspiration pneumonia — from esophageal obstruction ^[16]
• Signs of locally advanced disease:
  • Hoarseness of voice — left recurrent laryngeal nerve palsy (the nerve loops under the aortic arch and ascends between the trachea and esophagus — vulnerable to invasion by distal esophageal tumours) ^[16]
  • Horner's syndrome — involvement of the sympathetic chain
  • Respiratory symptoms / stridor — tracheal invasion or tracheoesophageal fistula
  • Hypercalcemia — humoral hypercalcemia of malignancy (PTHrP secretion, ~10% of SCC; less common in adenocarcinoma)
  • Virchow's node (left supraclavicular lymphadenopathy) — distant metastasis via thoracic duct

• OGD + biopsy — confirmatory histological diagnosis ^[6]
• EUS — best for T and N staging ^[6]
• CT / PET-CT — for distant metastasis (M staging) ^[6]
• Diagnostic laparoscopy for OGJ tumours (detect peritoneal seeding) ^[6]

The management depends on staging (covered in detail in the management section):

The prognosis of esophageal adenocarcinoma is overall poor because most patients present at an advanced stage:

This enormous difference in survival between early and late detection is the entire justification for Barrett's surveillance programs. Catching adenocarcinoma at T1a (through surveillance biopsies) transforms a nearly lethal diagnosis into a curable one.

Already detailed in the management section but listed here for completeness:

• Gas bloat syndrome (90%, especially Nissen) ^[14]
• Dysphagia (50% early, 10% long-term) ^[14]
• Reflux recurrence (wrap too loose)
• Perforation → mediastinitis ^[14]
• Slipped Nissen ^[14]