Carcinoma Oesophagus

Dr. S. Ranita Devi

Professor
Department of Surgery
RIMS
 Introduction – CA Oesophagus
• 6th most common cancer in the world
• 7% of all GI malignancies

• Common in China, South Africa, Asia

• In India, common in Karnataka, Orissa

• When patient presents with Dysphagia, often it is fairly advanced and

inoperable – only palliation is the possibility.
Fig. Gross outer look and cut-section of proliferative and indurated lesions of CA oesophagus
 Introduction (contd)
• Poor prognosis because of –
1. More lymph vessels are present in submucosa than capillaries –
hence, spread is fast
2. Lymph flow in submucosal plexus runs in a longitudinal direction –
hence primary tumour can extend for a considerable length both
superiorly and inferiorly
3. Aggressiveness
4. Difficult approach for surgery
5. Late presentation
6. Poor survival rate – only 5-10% of diagnosed will survive for 5 years
• Factors responsible for Early spread and Aggressive behaviour of CA
Oesophagus –
1. Lack of serosal layer

2. Proximity of vital structures

3. Extensive lymphatic drainage

4. Late presentation
 Etiology
A. Precancerous conditions
1. Achalasia Cardia – 30%

2. Corrosive strictures – 30%

3. GORD with Barrett’s Oesophagus

4. Plummer-Vinson’s syndrome – 15%

5. Tylosis (Hovels-Evans Syndrome)

 Etiology (contd)
B. Carcinogens
1. Tobacco, Smoking, Alcohol

2. HPV 16, 18

3. Nitrosamines

4. Fungal contamination of food

 Etiology (contd)
C. Others
1. Oesophageal web

2. Obesity

3. Low Socioeconomic status

• Helicobacter pylori infection – associated with reduced risk of CA

 Site

1. Upper third – 17%

2. Middle third – 50%

3. Lower third – 33%

 Pathology
1. Squamous cell carcinoma – most common type worldwide
• Affects upper and middle third
2. Adenocarcinoma – most common in western countries
• Affects lower third
• Incidence increasing

• Lower 3 cm of oesophagus is lined by columnar epithelium, so

Adenocarcinoma is common here
• Barrett’s columnar metaplasia also more prone for Adenocarcinoma
 Gross types

1. Fungating – 60%

2. Ulcerative – 20%

3. Annular – 15%

4. Polypoid

5. Varicoid (diffuse submucosal type)

 Spread
1. Local/Direct Spread
• Starts as mucosal ulceration – spreads to submucosa
• Then, spreads both transversely and longitudinally
• Lack of serosal layer in oesophagus – favours local extension
• After this, structures in vicinity are involved
• Tracheo-oesophageal fistula
• Broncho-oesophageal fistula
• Oesophago-aortic fistula – torrential bleeding, death

• These are contraindications for Surgery and Radiotherapy

 Spread (contd)
2. Lymphatic spread
• By both lymphatic permeation and lymphatic embolisation
• Palpable Left Supraclavicular Lymph Node – Troisier’s Sign
• Thorax – paraoesophageals, tracheobronchial, subdiaphragmatic nodes
• Abdomen – Coeliac nodes

3. Blood spread
• Secondaries in Liver, Lungs, Brain, Bones
 Clinical Features
1. Dysphagia - Recent onset, Progressive, more for solids

2. Regurgitation

3. Anorexia, loss of weight, cachexia

4. Pain – substernal, in the abdomen

5. Features of Broncho-oesophageal Fistula

6. Left Supraclavicular Lymphadenopathy

 Clinical Features (contd)

7. Liver secondaries, ascites

8. Bronchopneumonia, malaena

9. Hoarseness of voice – due to recurrent laryngeal nerve involvement

10. Hiccough – due to phrenic nerve involvement

11. Back pain – due to nodal spread (paraoesophageal/coeliac nodes)

 Dysphagia in CA Oesophagus
• Progressive
• Recent onset
• Mainly for solids
• Means 60% of lumen is involved
• Only when disease is fairly advanced
• Poor prognosis

• It is a late symptom – because of smooth muscle can dilate with ease

due to lack of serosal layer
 Investigations
1. Barium Swallow
• Irregular persistent intrinsic filling defect
• Shouldering – characteristic
• Can also detect abnormal axis and fistula
2. Oesophagoscopy
• To visualise growth and take biopsy
3. Biopsy
• Confirmation and histological type
4. CT Scan
• Assess local infiltration, involvement of vital structures, operability
Fig. Barium swallow showing irregular filling-defects and Shouldering sign in
middle 1/3rd oesophagus
Fig. Barium swallow showing irregular filling-defects
Fig. CA Oesophagus – Endoscopic view
Fig. Endoscopic views of CA oesophagus – at different levels and of different gross
types
 Investigations (contd)
5. Chest X-Ray
• To rule out aspiration pneumonia
6. Bronchoscopy
• To rule out involvement of bronchus
7. Ultrasound Abdomen
• To rule out liver secondaries, abdominal lymph node involvement
8. Endoscopy ultrasound
• To assess depth of wall involvement, mediastinal lymph nodes
 Investigations (contd)

9. Positron Emission Tomography (PET)

• To see response to therapy

10. Thoracoscopy and laparoscopy

11. Complete haemogram

 TNM Staging
A. Tumour
• T0 = No primary tumour

• Tis = Carcinoma in situ – high grade dysplasia

• T1a = Invasion into Lamina Propria, Muscularis Mucosae

• T1b = Invasion into Submucosa

• T2 = Invasion into Muscularis Propria

• T3 = Invasion into Para-oesophageal tissue without spread to adjacent structures

• T4a = Invades resectable adjacent structures (pleura, diaphragm, pericardium)

• T4b = Invades unresectable adjacent structure (aorta, trachea, vertebral body)

 TNM Staging (contd)
B. Nodal status
• Nx = Lymph nodes cannot be assessed

• N0 = No regional lymph node metastasis

• N1 = 1-2 positive regional lymph nodes

• N2 = 3-6 positive regional lymph nodes

• N3 = 7 or more positive regional lymph nodes

 TNM Staging (contd)
C. Metastasis
• M0 = No distant metastasis

• M1 = Distant metastasis
 Treatment

A. Curative (20%)
• Indications:
i. Early growth
ii. No involvement of adjacent peri-oesophageal structures or distant
organs

B. Palliative (80%)
 Curative treatment

• For Early growth confirmed with absence of nodal spread, curative

surgery is main approach – Radical Oesophagectomy

• Extent of resection:
• Proximal extent – 10 cm above macroscopic tumour
• Distal extent – 5cm below macroscopic tumour
• Proximal stomach has to be removed
 Curative treatment (contd)
• If nodes are present, multimodal approach
• Curative resection + radiotherapy and chemotherapy

• Neoadjuvant therapy prior to surgery

• Aggressive chemoradiation
• Upper 1/3rd growths
• Unfit for surgery
 Upper 1/3rd growth

1. Mainly by Radiotherapy

2. If early and operable case, McKeown 3-phase en bloc

Oesophagectomy and anastomosis in the neck is done

3. Split sternum approach oesophagectomy

 Middle 1/3rd growth

• Ivor-Lewis 2-phase Oesophagectomy

• Palliative radiotherapy
 Lower 1/3rd growth

1. Left abdominothoracic approach for lower oesophagus – Sweet

approach

2. Orringer’s Transhiatal Blind Total Oesophagectomy

3. Palliative surgery
 Surgical approaches for CA Oesophagus

1. Ivor-Lewis 2-phase oesophagectomy

2. McKeown’s 3-phase en bloc oesophagectomy

3. Left abdominothoracic approach for lower oesophagus – Sweet

approach

4. Orringer’s Transhiatal Blind Total Oesophagectomy

5. Thoracoscopic – Laparoscopic Oesophagectomy and

Lymphadenectomy
 Oesophageal substitutes
1. Stomach
• Preferred
• Complication: Post-prandial fullness with bile or acid regurgitation
2. Colon
• Better
• Less postprandial problems but needs 3 anastomoses
3. Jejunum

• Transposition is done through these routes - posterior mediastinum

(shortest), right pleural space, retrosternal, subcutaneous
 Complications of Oesophagectomy
1. Haemorrhage
2. Respiratory infection
3. Septicaemia
4. Chylothorax
5. Anastomotic leak – Thoracic leak is most dangerous
6. Hoarseness of voice
7. Stricture formation (40%)
8. Gastro-Oesophageal Reflux
9. Conduit necrosis
10. Colonic dysmotility
• Unlikely surgical cure, even in absence of systemic spread –

1. Loss of weight > 20%

2. Esophageal axis is abnormal on barium test
3. Nodes – multiple on CT Scan
4. Grade – invasive, poorly differentiated
5. Tumour length > 8 cm
6. Horner’s Syndrome

“LENGTH”
 Palliative treatment
• Done to –
• Relieve pain
• Relieve dysphagia
• Prevent aspiration and bleeding

• Indications –
i. Patient not fit for surgery
ii. There is blood spread
iii. There is adjacent organ spread
iv. There is peritoneal/liver spread
 Palliative treatment (contd)
1. Endoscopic therapy
i. Self-expanding metal stents (SEMS)
ii. Endoscopic laser
iii. Endoscopic bipolar diathermy
iv. Endoscopic photodynamic therapy
2. Intubation (eg: Mousseau-Barbin tube)
3. Palliative external radiotherapy
4. Intraluminal radiotherapy – Brachytherapy
5. Chemotherapy
6. Surgery
i. Orringer’s Transhiatal Blind Total Oesophagectomy
ii. Kirschner palliative gastric bypass
 Self-expanding metal stents (SEMS)
• Ideal method of palliation
• It is passed through endoscope under C-arm guidance
• Chances of perforation minimal
• Types –
a) Uncovered
b) Plastic covered
Fig. Self-expanding metal stents (SEMS)
 Terminal Events in CA Oesophagus
(causes of death)
1. Cancer cachexia
2. Sepsis
3. Mediastinitis
4. Immunosuppression
5. Malignant trachea-oesophageal fistula
6. Erosion into major blood vessel - haematemesis