Oesophageal Cancer

 Introduction and Epidemiology

Oesophageal cancer follows malignant transformation of oesophageal tissue. 

Transformation may affect the epithelium giving rise to the two main forms, squamous cell carcinoma and adenocarcinoma. 

Epidemiology

It is a common malignancy worldwide and main areas of high incidence span China, across to Caspian Sea and down the eastern coast of Africa to South Africa.

Eighty to eighty five percent of cases are found in the developing world.

Worldwide male to female ratio is 15:1.

The incidence according to the Nairobi Cancer Registry is 9.1/100,000.

Risk factors

Heredity factors, achalasia of the oesophagus, tobacco smoking, heavy alcohol consumption, gastroesophageal reflux disease (GERD) and associated obesity, Barrett’s oesophagus, as well as other sources of inflammation such as hot beverages, Plummer–Vinson syndrome e.t.c. Human papillomavirus (HPV) is also emerging as a major risk factor for oesophageal cancer.

Others are corrosive injury to the esophagus by swallowing strong alkalines (lye) or acids.

Particular dietary substances, such as nitrosamines that may contaminate stored foods are also associated with a high risk.

Radiotherapy to the chest also increases the risk of oesophageal carcinoma.

 Diagnosis

The main symptom is progressive dysphagia. Others are heart burn, and odynophagia. 

In advanced cases with trache-oesophageal fistula – coughing and choking on drinking fluids may be a feature.

Grading of Dysphagia

GRADE  FEATURE
0 Normal swallowing
1 Difficulty with solids
2 Difficulty with semi solids
3 Difficulty with liquids
4 Total dysphagia

 

  • Signs include wasting, dehydration, and anaemia.
  • Radiological evaluation should include barium swallow, chest radiograph, chest CT scan.
  • CT scan is also valuable for tumour staging. It detects evidence of distant tumour spread.
  • Endoscopy is also used in diagnosis and staging. Endoscopic biopsy is used in diagnosis and endoscopic ultrasound for determination of loco-regional spread.
  • Histology is the ultimate diagnostic procedure. Tissue is obtained at endoscopy, and iodine staining is useful in picking very early stages (T0 and Tis) or severe dysplasia.

Comparison of TNM and grading systems (Squamous cell carcinoma) of Oesophageal Cancer

Stage  TNM (G)  LEVEL
Stage 0: Tis, N0, M0, GX or G1;  any location
Stage IA:  T1, N0, M0, GX or G1;  any location
Stage IB:  T1, N0, M0, G2 or G3; any location
T2 or T3, N0, M0, GX or G1;  lower oesophagus
Stage IIA: T2 or T3, N0, M0, GX or G1;  Upper or middle
T2 or T3, N0, M0, G2 or G3;  lower oesophagus
Stage IIB:  T2 or T3, N0, M0, G2 or G3; upper or middle
T1 or T2, N1, M0, any G;  any location
Stage IIIA T1 or T2, N2, M0, any G; any location
T3, N1, M0, any G; any location
Stage IIIA:  T4a, N0, M0, any G; any location
 T3, N2, M0, any G; any location
T4a, N1 or N2, M0, any G;  any location
Stage IIIB: T4b, any N, M0, any G;  any location
Stage IIIC:  T4a, N1 or N2, M0, any G;  any location
T4b, any N, M0, any G;  any location
Any T, N3, M0, any G;  any location
Stage IV:  Any T, any N, M1, any G; any location

Staging and risk assessment

Staging is essential and has a bearing on the management options and prognosis.

Oesophageal carcinoma may be staged using the TNM classification or equivalent anatomic staging systems.

TNM classification is illustrated in tables below

 TNM staging for oesophageal cancer-Primary tumour (T)

TX: The primary tumour can’t be assessed.
T0: There is no evidence of a primary tumour.
Tis: Limited to epithelium. High-grade dysplasia. 
T1: Invaded the lamina propria, muscularis mucosa, or submucosa
T1a: Invaded the lamina propria or muscularis mucosa
T1b: Invaded into the submucosa
T2: Invaded thick muscle layer (muscularis propria).
T3: Invaded the adventitia.
T4: Invaded nearby structures.
T4a: Invaded pleura, pericardium, or diaphragm, but resectable surgically. 
T4b: Invaded trachea, aorta, or other crucial structure and surgically unresectable.

Nodes (N)

NX: Nearby lymph nodes can’t be assessed.
N0: The cancer has not spread to lymph nodes immediately surrounding 
 oesophagus
N1: Cancer has spread to 1 or 2 nearby lymph nodes.
N2: Cancer has spread to 3 to 6 nearby lymph nodes
N3: Cancer has spread to 7 or more nearby lymph nodes.
M0: Not metastasised to distant nodes, organs or tissues
M1:  Has metastasised to distant nodes, organs or tissues

It is important to also look at the histological grading of tumours when evaluating the stage of oesophageal cancer. Poorly differentiated tumours tend to grow as well as spread faster.

Histological grading (G) of Oesophgeal Cancer

GX: Not possible to assess
G1: Well differentiated
G2:  Moderately differentiated
G3:  Poorly differentiated
G4:  Undifferentiated

 Management

Multidisciplinary approach to patient management is essential. All patients should be staged prior to multidisciplinary consultations. Supportive treatment consists of:

  • Fluid management; ensuring daily fluid and electrolyte needs are met.
  • Nutritional management; ensuring daily nutritional needs met,
  • Counselling and other supportive services.
  • For advanced disease palliative care services should be enlisted.

Definitive treatment options vary between surgery, radiotherapy and chemotherapy. Choice of treatment modality is dependent on tumour stage and general fitness of the patient. The role of curative resection in oesophageal cancer is only considered in cases of early disease. Curative surgery is applied to stages 0, I, and II oesophageal cancers. For Stage III, surgery is applied as palliative care

Surgical Options

Resection: Sub-endothelial for high grade dysplasia Oesophagectomy: Preoperative radiotherapy is recommended for stages II and III to shrink tumour and render it amenable to resection. Preoperative chemotherapy may also confer some benefit.For patients not fit for surgery, chemoradiotherapy (Cisplatin, 5FU-based) is recommended and Chemoradiotherapy for upper third tumours.Late squamous cell carcinoma:
Surgical resection has little influence on survival. If considered, it must have clear indications outweighing the lack of improved survival. Stenting/intubation: These are preferably carried out endoscopically when and where possible. In most cases, stents are inserted for restoration of swallowing and also to relieve symptoms in presence of tracheo-oesophageal fistulae.Percutaneous endoscopic gastrostomy or other form of gastrostomy may be performed.

Follow-up

All patients require regular follow up to assess recurrence or development of signs of distant disease. Regular clinic visits should be scheduled (every 3-6 months during which time radiological (chest radiographs, CT scans repeat barium swallow), weight, and other investigations should be performed. Ideally, visits should be as close as possible to the patient’s home.

 Pharmacological management

5-fluorouracil, cisplatin, vinblastine, epirubicin, interferon alpha-2a, paclitaxel, docetaxel, irinotecan, vinorelbine.

The standard regimen is a combination of 5FU and cisplatin with or without radiotherapy. 

Where resources are available, a platinum compound and a taxane can be used.

Always refer to manufacturers' information on dosing. Dosing should also be individualized.

 Prognosis

The occasional patient who presents with early disease can be cured by surgery.

But in our setting, where most patients present with late disease, the prognosis is poor.

References

  1. Cook MB, et al. Cigarette smoking and adenocarcinoma of the oesophagus and oesophagogastric junction: a pooled analysis from the international BEACON consortium. J Natl Cancer Inst 2010;102: 1344-1353.
  2. Allum WH, et al. Long-term results of a randomized trial of surgery with or without preoperative chemotherapy in oesophageal cancer. J Clin Oncol 2009;27: 5062-5067
  3. Atsumi K, et al. Chemoradiation for small cell oesophageal carcinoma. Report of 11 cases from multi-institution experience. J Radiat Res. (Tokyo) 2010; 51:15-20

 

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