Oesophageal carcinoma is relatively uncommon. It tends to present with increasing dysphagia, initially to solids and progressing to liquids as the tumour increases in size, obstructing the lumen of the oesophagus.
Oesophageal cancer is responsible for <1% of all cancers and 4-10% of all GI malignancies. There is recognised male preponderance with the squamous cell subtype, M:F 4:1. Blacks are more susceptible than caucasians, 2:1.
The incidence of the subtypes has regional variation. The squamous cell subtype has the greatest worldwide incidence (~90%), but the adenocarcinoma subtype is more common in many parts of North America and Europe. In addition, there are certain regions where individuals are at particularly high risk of developing oesophageal cancer, e.g. Iran, parts of Africa, Italy and China.
Predisposing factors include 8:
- alcohol and smoking: for squamous cell carcinoma and adenocarcinoma
- Barrett oesophagus: for adenocarcinoma
- coeliac disease
- ionising radiation
- caustic stricture/lye stricture
- Plummer-Vinson syndrome
- obesity: for adenocarcinoma
- history of oral or pharyngeal cancer
- human papilloma virus (HPV)
- tylosis (Howel–Evans syndrome): rare AD disease with hyperkeratosis of palm and sole with high incidence of oesophageal cancer
Patients present with progressive dysphagia, weight loss, chronic worsening gastroesophageal reflux and hoarseness, cough, vocal cord paralysis, or other signs and symptoms of mediastinal invasion.
- squamous cell carcinoma of oesophagus: 81-95% (worldwide)
- adenocarcinoma of oesophagus: 4-19% (worldwide)
- other types
* in western world adenocarcinoma is as common or even slightly more common than SCC
polypoid/fungating (most common)
- sessile/pedunculated tumour
- lobulated surface protruding
- irregular, polycyclic, overhanging, step-like "apple core" lesion
- ulcerating: large ulcer niche within bulging mass
- infiltrating: gradual narrowing with smooth transition
- superficial spreading carcinoma
See main article: oesophageal cancer staging.
- anterior jugular chain and supraclavicular nodes (primary in upper 1/3)
- para-oesophageal and subdiaphragmatic nodes (primary in middle 1/3)
- mediastinal and paracardial and coeliac trunk nodes (primary in lower 1/3)
- haematogenous: lung, liver, adrenal glands
Combination of CT scan, trans oesophageal ultrasound and PET/CT scan are used for staging of the disease. CT is the best initial modality for detection of the distant metastasis, gross direct invasion, and enlarged lymph nodes. Ultrasound is the most sensitive modality for assessment of the depth of invasion and regional enlarged lymph nodes. PET can be useful for re staging after the initial neoadjuvant therapy 7.
Many indirect signs can be sought on a chest radiograph and these include:
- widened azygo-oesophageal recess with convexity toward right lung (in 30% of distal and mid-oesophageal cancers)
- thickening of posterior tracheal stripe and right paratracheal stripe >4 mm (if tumour located in upper third of oesophagus)
- tracheal deviation or posterior tracheal indentation/mass
- retrocardiac or posterior mediastinal mass
- oesophageal air-fluid level
- lobulated mass extending into gastric air bubble (Kirklin sign)
- repeated aspiration pneumonia (with tracheo-oesophageal fistula)
- irregular stricture
- pre-stricture dilatation with 'hold up'
- shouldering of the stricture
- eccentric or circumferential wall thickening >5 mm
- peri-oesophageal soft tissue and fat stranding
- dilated fluid- and debris-filled oesophageal lumen is proximal to an obstructing lesion
- tracheobronchial invasion appears as displacement of the airway (usually the trachea or left mainstem bronchus) as a result of mass effect by the oesophageal tumour
- aortic invasion
- fistula formation to trachea (5-10%), bronchi or mediastinum: can be either due to direct tumour progression or iatrogenic effects (e.g. radiation therapy)
- oesophageal perforation
Treatment and prognosis
The 5 year mortality depends on the stage of the tumour. Unfortunately, most cases present with regional or distant metastatic disease (30% and 40%, respectively.
- localised disease: ~40% 5-year survival
- distant metastatic disease: ~5% 5-year survival
Endoscopic mucosal resection, without or with localised ablation is an option for localised (T1a) disease. These epithelial tumours are usually <2 cm, asymptomatic, and noncircumferential.
For T1b tumours and above, surgical options are mostly limited to oesophagectomy (including sometime with palliative colonic interposition (see case 19))
Imaging differential considerations include:
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