**1. Introduction**

148 Gastrointestinal Endoscopy

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Over the past four decades the incidence of oesophageal cancer has increased more rapidly than that of any other solid tumour in the Western World. This rise reflects the emergence of oesophageal adenocarcinoma as the most common pathological type. Despite this growing incidence, progress towards early detection and treatment has been slow and mortality figures have remained dismal – Cancer Research UK quotes overall one and five year survival rates of just 28% and 8% respectively.(CrUK, 2010) As a result, oesophageal cancer repreasents a real and growing public health problem and urgent action is required to improve detection and facilitate early intervention, ideally at a pre-malignant stage.

Most oesophageal adenocarcinoma develops following a well recognised series of cellular changes secondary to a multifactorial aetiology. In the classically described pathway there is initially a metaplastic change in the epithelial lining of the oesophagus (Barrett's oesophagus) which then progresses to 'low-grade' and then 'high-grade' dysplasia. As many as 30% of patients newly diagnosed with high-grade dysplasia may already have a coexistent invasive cancer, and between 5-60% of patients will develop cancer during surveillance over 1-7 years.

To date there is no early diagnostic test which can enable instantaneous accurate diagnosis of dysplasia. Clinicians are advised to take random biopsies from areas of Barrett's oesophagus in order to identify dysplasia, but even histological assessment of dysplasia is subjective and can be unreliable. As a result, significant dysplastic change (or even intramucosal cancer) may be missed. In addition, as dysplasia (the premalignant lesion) is difficult to identify, screening for early oesophageal cancer / high-grade dysplasia cannot currently be recommended, and as a consequence, oesophageal tumours present late and so have a poor prognosis.

The early recognition of high-grade dysplasia is paramount to enabling a successful treatment strategy. Surgery is one option for patients with confimred HGD, however the emergence of multiple endotherapies over the past 20 years have demonstrated the ability to cure focal high-grade dysplasia, thus preventing progression to invasive malignancy. In this chapter we will discuss the accuracy of endoscopic and histological diagnosis of dysplasia and will consider novel endoscopic adjuncts which may improve endoscopic sensitivity. We will then discuss the endoscopic therapeutic options that are available for management of dysplastic Barrett's oesophagus and will propose a endotherapy algorithm for use in specialist Barrett's surveillance centres.

Endoscopic Detection and Eradication of Dysplastic Barrett's Oesophagus 151

(Shaheen et al., 2000; Drewitz et al., 1997) (Jankowski et al., 2000; Spechler et al., 2010; Shaheen and Richter, 2009; Jankowski et al., 2002) This represents an increased risk of 30-100 fold compared to the general population. However, cancer rates in excess of 10% per year

Several studies have also noted regression of disease in patients treated with acid suppression, and even complete resolution has been described. Similarly there is some data suggesting that anti-reflux surgery can improve the histological appearance of Barrett's oesophagus, although it is not currently recommended for this purpose. (BSG Working

Endoscopic recognition of dysplasia within Barrett's oesophagus is difficult and unreliable, even for skilled endoscopists. A rigorous biopsy protocal such as that recommended by the British Society of Gastroenterologists (Box 1) is therefore necessary to identify any dysplastic change so that apropriate surveillance / endotherapy / surgery can be considered. Sites of biospy must be accurately recorded and when possible macroscopic lesions should be

Dysplasia is often macroscopically invisible. In patients with Barrett's oesophagus, endoscopists are therefore advised to follow a rigorous biopsy protocol. The British

**NB/** Even with strict adherence to this policy <5% of oesophageal mucosa is sampled.

have been described in patients with HGD. (Shaheen and Richter, 2009)

**4. Endoscopic recognition of dysplasia** 

classified using the Paris classification (Box 2).

Relative sampling volume = 0.05%

**Box 1. Biopsying Barrett's oesophagus**

Society of Gastroenterologists recommends the following:



Party, 2005).
