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PA23.1-2 | Oral & Oesophageal Cancers — SDL Guide (Part 3)

Clinical Features and Prognosis of Oesophageal Carcinoma

Diagram showing progressive oesophageal carcinoma obstruction, dysphagia sequence, late presentation due to absent serosa, major clinical features, and stage-based prognosis. — **Panel A:** Vertical oesophageal cutaway and cross-sections showing oesophageal lumen, exophytic carcinoma, muscular wall, luminal narrowing >50-60%, and complete obstruction.. **Panel B:** Timeline comparing progressive mechanical dysphagia from solids to liquids with achalasia-type dysphagia for solids and liquids from the start.. **Panel C:** Transverse oesophageal wall showing absence of serosa, adventitia, T3 adventitial invasion, T4 adjacent structure invasion, and late dysphagia.. **Panel D:** Clinical feature map showing weight loss, odynophagia, regurgitation, recurrent laryngeal nerve-related hoarseness, tracheo-oesophageal fistula with aspiration pneumonia, haematemesis or malaena, mediastinal mass on CXR, and 5-year survival by stage..

The cardinal symptom is progressive dysphagia — beginning with difficulty swallowing solids, progressing over weeks-to-months to difficulty with semi-solids, then liquids, and ultimately complete obstruction. This progressive pattern (solids first, liquids last) distinguishes mechanical obstruction (carcinoma, stricture) from functional obstruction (achalasia — dysphagia for solids AND liquids from the start).

Why does presentation come so late?
The oesophagus has no serosa. It can accommodate luminal encroachment until >50–60 % of the circumference is involved before dysphagia becomes manifest. By the time the patient presents with dysphagia, the tumour is usually T3 or T4 — hence the characteristically late stage at presentation.

Other clinical features:
• Odynophagia (painful swallowing)
• Weight loss — profound, multifactorial (mechanical obstruction + anorexia + tumour catabolism)
• Regurgitation of undigested food
• Hoarseness — recurrent laryngeal nerve invasion
• Aspiration pneumonia — tracheo-oesophageal fistula
• Haematemesis/malaena — ulceration into blood vessels
• Mediastinal mass on CXR

Prognosis is poor:
• Overall 5-year survival: ~15–20 %
• Stage at presentation is the dominant determinant — T1/T2 (submucosal/muscularis propria) with negative nodes: ~50–60 % 5-year survival; T4/N+ distant: <5 %
• Oesophageal SCC: slightly better surgical resectability than adenocarcinoma in some series
• Adenocarcinoma: if caught in Barrett surveillance at high-grade dysplasia stage → endoscopic resection with excellent outcomes

CLINICAL PEARL

Dysphagia red flags in practice: Progressive dysphagia in any patient >40 years is oesophageal carcinoma until proven otherwise — mandate urgent upper GI endoscopy and biopsy. Do not reassure and send home. The distinction between SCC and adenocarcinoma has therapeutic implications: SCC is more radiosensitive (relevant when surgical resection is not feasible); adenocarcinoma responds to trastuzumab if HER2-positive. In India, oesophageal SCC predominantly affects the mid-oesophagus; in the West, adenocarcinoma of the lower third dominates. Knowing this shapes your index of suspicion by geography.

SELF-CHECK

A 55-year-old man presents with a 3-month history of progressive dysphagia — initially to solids, now to semi-solids — along with 8 kg weight loss. He is a bidi smoker and consumes alcohol daily. Barium swallow shows an irregular 'rat-tail' narrowing in the mid-oesophagus. The MOST likely histological diagnosis is:

A. Squamous cell carcinoma

B. Adenocarcinoma with Barrett oesophagus

C. Carcinoid tumour

D. Leiomyosarcoma

Reveal Answer

Answer: A. Squamous cell carcinoma

Mid-oesophageal location + tobacco/alcohol exposure + Indian demographic profile = oesophageal SCC. Adenocarcinoma arises in the lower third on a Barrett (GERD) background and is the dominant type in obese Western patients. Carcinoid and leiomyosarcoma are rare oesophageal tumours and do not cause the progressive 'rat-tail' narrowing pattern.

Comparing Oral SCC and Oesophageal Carcinoma — Integrative Perspective

A four-panel diagram compares oral squamous cell carcinoma, oesophageal squamous cell carcinoma, and oesophageal adenocarcinoma through shared carcinogen exposure, precursor lesions, Indian relevance, and dominant risk factors. — **Panel A:** Shared squamous mucosal field, oral cavity, oesophagus, tobacco, alcohol, areca nut/gutka, hot drinks, nutritional deficiency, dysplastic foci. **Panel B:** Normal oral squamous epithelium, leukoplakia, erythroplakia, oral submucous fibrosis, dysplasia, invasive oral squamous cell carcinoma, buccal mucosa, lateral tongue. **Panel C:** Normal oesophageal squamous mucosa, Plummer-Vinson syndrome, achalasia, dysplasia, invasive oesophageal squamous cell carcinoma, constricting mid-oesophageal mass. **Panel D:** Gastro-oesophageal junction, chronic GERD, Barrett oesophagus, columnar metaplasia, dysplasia, distal oesophageal adenocarcinoma.

Oral and oesophageal SCC share a common carcinogen pathway — tobacco, alcohol, and nutritional deficiency — and this is not coincidental. Both arise in squamous-lined mucosa, both may be caused by the same field of carcinogenesis (hence patients with oral SCC have higher rates of oesophageal SCC and vice versa), and both have premalignant counterparts.

Key comparisons:

Feature	Oral SCC	Oesophageal SCC	Oesophageal Adenocarcinoma
Precursor	Leukoplakia, erythroplakia, OSMF	No well-defined single precursor (Plummer-Vinson, achalasia)	Barrett oesophagus
India relevance	Highest worldwide incidence	Common	Less common
Dominant risk	Gutka, areca nut, tobacco	Tobacco, alcohol, hot drinks	GERD, obesity
Spread route	Cervical LN	Mediastinal LN; early intramural	Coeliac/gastric LN
Prognosis	Stage-dependent; early = good	Late presentation; ~15–20 % 5-yr	Better if caught at Barrett stage

Field cancerisation links all aerodigestive SCC — a patient with oral SCC requires endoscopic surveillance of the oesophagus. Conversely, a patient with oesophageal SCC should have the oral cavity and larynx examined.