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Carcinoma of the Oesophagus
Carcinoma of the oesophagus is a common, agressive tumour which is increasing in frequency.
Several histological types are seen, almost all of which are epithelial in origin. The vast majority of these tumours will be either squamous cell carcinoma (SCC) or adenocarcinoma (AC). In the last two decades there has been a particular rise in the amount of AC seen, to the extent that this has now overtaken SCC as the most common form of oesophageal tumour in some developed countries.
Incidence
- Carcinoma of the oesophagus represents the fifth most common malignant tumour in the developed world.
- In the UK the incidence is of the order 10 per 100,000 population.
- The number of new cases of AC in the UK is approximately 5 per 100,000 and the UK has the highest incidence of oesophageal AC of all countries from which figures are available.
- Males are more commonly affected by AC than females with a ratio of 7:1,1 and for all forms of oesophageal carcinoma with a M:F ratio of 2:1.
- The median age at presentation is 60 years.
The incidence of oesophageal carcinoma varies considerably with geographical location with high rates in China and Iran, where it has been directly linked to the preservation of food using nitrosamines. AC is seen more frequently in Caucasian populations whereas SCC is more frequent in people of African descent. In the last 30 years the incidence of AC has increased more than 350% in the West.
Risk factors
- The use of tobacco and alcohol are strong risk factors for both SCC and AC, and have a synergistic effect in this respect for squamous cell cancer and additive effect for AC. Cigarette smoking is associated with a 10 fold increase in risk for SCC, and a 2-3 fold increase in risk for AC.2
- The relative increase in risk caused by smoking remains high even after 30 years of giving up smoking for AC, but reduces within 10 years for SCC.3
- Obesity has been linked with increased risk for AC but reduced risk for SCC. It is thought that this may be due to the fact that obesity increases the risk of gastro-oesophageal reflux disease (GORD), in turn increasing the risk of Barrett's oesophagus, which is a precursor of AC. Chronic inflammation and stasis from any cause increase the risk of oesophageal SCC e.g. strictures due to caustic injury or achalasia.
- Tylosis and Plummer Vinson syndrome are also associated with an increased risk for SCC.
The classic RED FLAG symptoms are:
|
- Dysphagia
- Weight loss
- Loss of appetite
- Odynophagia
- Hoarseness
- Melaena
- Retrosternal pain
- Intractable hiccups
- Lymphadenopathy
These include:
- Oesophageal stricture from any cause
- Compression of the oesophagus from external sources e.g. enlarged lymph glands or bronchial carcinoma
- Intramural benign tumours e.g. leiyomyoma
- Metastatic tumours - most commonly from breast
The investigation of a patient with symptoms suggestive of oesophageal carcinoma may include:
- Full history - smoking, alcohol, previous GORD or stricture, weight loss, dysphagia, malaena
- Examination - anaemia, lymphadenopathy, evidence of metastases
- FBC
- Fine needle aspiration - of any palpable cervical lymph node
- CXR - looking for evidence of metastases
- Double contrast barium swallow
- CT/MRI scan of chest and upper abdomen - for staging purposes
- Endoscopic ultrasound - increases accuracy of staging
- Fluorodeoxyglucose (FDG)-PET scan - for accuracy of staging
- Endoscopy - with brushings and biopsy of any lesion seen
- ± bronchoscopy - in high oesophageal tumours or if hoarseness or haemoptysis present
| T Category | Depth of infiltration | N category | Regional lymph nodes |
| Tis | carcinoma in situ | NX | nodes cannot be assessed |
| T1 | invasion of lamina propria/submucosa | N0 | no node spread |
| T2 | invasion of muscularis propria | N1 | regional node metastases |
| T3 | invasion of adventitia | M0 | no distant spread |
| T4 | invasion of adjacent structures | M1 | distant metastases |
Primary treatment modalities include surgery alone or chemotherapy with radiation therapy.4,5
Non-drug
- Many patients will present late in the disease process with unresectable disease. For this group of patients the emphasis will be on palliation and symptom relief.
- Radiotherapy or laser ablation may be of use in reducing tumour bulk, and the use of stents may be useful in the short to mid term to help with swallowing.
- Nutritional status may be maintained by the use of liquid feeds, enteral nutrition or PEG tubes.
- Pain relief should be maintained at a level at which the patient experiences little, or no pain.
Surgery
- Oesophagectomy remains the treatment of choice for patients with resectable tumours, although there remains some controversy as to whether or not block dissection of the lymph nodes at the same time confers any added advantage.6 Operative mortality is of the order of 2-23%.
- Oesophagectomy may be thorascopically assisted.7 This is a minimally invasive procedure. The advantage is quicker recovery and fewer lung complications, but offset by a longer operating time and greater likelihood of incomplete resection.
- Photodynamic therapy (PDT) is an alternative to major surgery.8 A photosensitising agent is injected and then activated by exposing the tumour to light, usually a low power laser, via an endoscope. The agent absorbs energy from the light and produces high energy oxygen molecules that destroy tumour cells. This is an outpatient procedure, under sedation. One series 5 year disease specific survival was 76% in 56 treated with PDT as monotherapy.
- Preoperative adjuvant therapy with drugs and radiation is used in some centres, however a recent metanalysis has failed to show any advantage over surgery alone for resectable tumours.9
The patients pre-operative status and co-morbidity are strong predictors of outcome.
The prognosis for oesophageal carcinoma varies depending on the stage at presentation:
- The overall 5 year survival rate for resectable tumours ranges from 10-25%.
- 5 year survival rates for stage 1 oesophageal cancer range from 80-94%
- 5 year survival rates for stage 3 are between 10-14% 10
Document References
- Lagergren J; Adenocarcinoma of oesophagus: what exactly is the size of the problem and who is at risk?; Gut. 2005 Mar;54 Suppl 1:i1-5. [abstract]
- Devesa SS, Blot WJ, Fraumeni JF Jr; Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer. 1998 Nov 15;83(10):2049-53. [abstract]
- Heath EI, Limburg PJ, Hawk ET, et al; Adenocarcinoma of the esophagus: risk factors and prevention. Oncology (Williston Park). 2000 Apr;14(4):507-14; discussion 518-20, [abstract]
- British Society of Gastroenterology; Guidelines for the management of oesophageal and gastric cancer (2002)
- Scottish Intercollegiate Guidelines Network (SIGN); Management of oesophageal and gastric cancer; 2006.
- Koshy M, Esiashvilli N, Landry JC, et al; Multiple management modalities in esophageal cancer: epidemiology, presentation and progression, work-up, and surgical approaches. Oncologist. 2004;9(2):137-46. [abstract]
- NICE. Thoracoscopically assisted oesophagectomy - guidance; August 2006
- NICE. Photo-dynamic therapy for early oesophageal cancer: guidance; December 2006
- Malthaner RA, Wong RK, Rumble RB, et al; Neoadjuvant or adjuvant therapy for resectable esophageal cancer: a clinical practice guideline. BMC Cancer. 2004 Sep 24;4:67. [abstract]
- Visbal AL, Allen MS, Miller DL, et al; Ivor Lewis esophagogastrectomy for esophageal cancer. Ann Thorac Surg. 2001 Jun;71(6):1803-8. [abstract]
Internet and Further Reading Acknowledgements EMIS is grateful to Dr Hayley Willacy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2007.
DocID: 1906
Document Version: 20
DocRef: bgp266
Last Updated: 3 Apr 2007
Review Date: 2 Apr 2009
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