Oesophageal Cancer and Barrett's Oesophagus Flashcards
Oesophageal Cancer
Until recent times oesophageal cancer was most commonly due to a squamous cell carcinoma but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.
The majority of tumours are in the middle third of the oesophagus.
Oesophageal Cancer - RFs
Risk factors smoking alcohol GORD Barrett's oesophagus achalasia Plummer-Vinson syndrome squamous cell carcinoma is also linked to diets rich in nitrosamines rare: coeliac disease, scleroderma
RF for Squamous:
- Alcohol
- Smoking
- Achalasia
- Plummer Vinson
RF for Adenocarcinoma:
- Alcohol
- Smoking
- Barrett’s Oesophagus
Oesophageal Cancer - Diagnosis
Diagnosis
Upper GI endoscopy is the first line test
Contrast swallow may be of benefit in classifying benign motility disorders but has no place in the assessment of tumours
Staging is initially undertaken with CT scanning of the chest, abdomen and pelvis. If overt metastatic disease is identified using this modality then further complex imaging is unnecessary
If CT does not show metastatic disease, then local stage may be more accurately assessed by use of endoscopic ultrasound.
Staging laparoscopy is performed to detect occult peritoneal disease. PET CT is performed in those with negative laparoscopy. Thoracoscopy is not routinely performed.
Oesophageal Cancer - Mx
Treatment
Operable disease is best managed by surgical resection.
The most standard procedure is an Ivor- Lewis type oesophagectomy. This procedure involves the mobilisation of the stomach and division of the oesophageal hiatus. The abdomen is closed and a right sided thoracotomy performed. The stomach is brought into the chest and the oesophagus mobilised further. An intrathoracic oesophagogastric anastomosis is constructed. Alternative surgical strategies include a transhiatal resection (for distal lesions), a left thoraco-abdominal resection (difficult access due to thoracic aorta) and a total oesophagectomy (McKeown) with a cervical oesophagogastric anastomosis.
The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis this will result in mediastinitis. With high mortality. The McKeown technique has an intrinsically lower systemic insult in the event of anastomotic leakage.
In addition to surgical resection many patients will be treated with adjuvant chemotherapy.
Oesophageal Ca Diagnosis: Example Question
A 70-year-old woman is investigated for heartburn. For the past 3 months she has experienced persistent heartburn after each meal. This was improved by a 4 week course of proton pump inhibitors but her symptoms returned shortly after stopping them. Clinical examination of her abdomen, hands and neck is unremarkable.
A full blood count shows the following:
Hb 12.6 g/dl
Platelets 331 * 109/l
WBC 6.8 * 109/l
A barium swallow is arranged:
SEE PASSMED BARIUM SWALLOW OESOPHAGEAL Ca
What is the most likely diagnosis?
Barrett's oesophagus Diffuse oesophageal spasm (corkscrew oesophagus) Achalasia Oesophageal web > Oesophageal cancer
The film shows narrowing and irregularity with hold-up of contrast noted in the mid thoracic oesophagus consistent with oesophageal cancer.
Barrett’s Oesophagus
Barrett’s refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold.
Histological features
the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
Management
endoscopic surveillance with biopsies
high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
Barrett’s Oesophagus - Example Question
A 75-year-old man is reviewed in gastroenterology clinic as part of on-going follow-up for Barrett’s oesophagus. The patient had been referred by his GP 2 months previously due to long-standing symptoms of gastro-oesophageal reflux: specifically, heartburn following eating and acid reflux upon lying flat in bed. No red-flag features of upper gastrointestinal tract malignancy had been identified.
An initial endoscopy was performed with results as documented below. Following discussion of the histology results, the patient elected to undergo endoscopic radiofrequency ablation. The procedure was uncomplicated aside from some mild chest pain in the first few days of recovery.
The patient was otherwise in good health, with other past medical history including only hypertension and osteoarthritis of both knees. Regular medications included paracetamol, omeprazole, ramipril and bendroflumethiazide. The patient reported a previous adverse reaction to penicillin but could not recall the details of this event.
There was no family history of Barrett’s oesophagus or oesophageal adenocarcinoma. The patient had never smoked and reported consuming 20 units of alcohol per week.
Report from initial endoscopy: minor hiatus hernia; 5 cm length of circumferential salmon-coloured epithelium extending above gastro-oesophageal junction; mild oesophagitis elsewhere; no mass lesion or ulceration in oesophagus or stomach; quadrant biopsies taken as per protocol.
Histology from endoscopic biopsies: all samples demonstrate flat intestinal metaplasia; mild dysplasia present in 4 of 8 samples; no high-grade dysplasia or adenocarcinoma.
Following successful endoscopic therapy, what is the appropriate schedule for follow-up surveillance endoscopy?
Every 6 months for 2 years, then every 1 year thereafter Every 3 months for 1 year, then every 6 months for 1 year, then every 1 year thereafter Every 1 year > Every 6 months for 1 year, then every 1 year thereafter Every 3 years
The patient has Barrett’s oesophagus associated with low-grade dysplasia, most likely secondary to his chronic gastro-oesophageal reflux and hiatus hernia. Endoscopic eradication therapy is indicated if any grade of dysplasia is present. Radiofrequency ablation is the preferred ablative therapy in patients with flat dysplasia or intra-mucosal carcinoma. This procedure is generally well tolerated aside from some short-lived chest pain. In the long-term, oesophageal strictures may occur. Radiofrequency ablation is effective, with 91 % of patients achieving complete eradication of dysplasia.
Following successful eradication of low-grade dysplasia, surveillance endoscopy should be performed every 6 months for the first year and then annually thereafter. After eradication of high-grade dysplasia or intra-mucosal carcinoma, surveillance should be more frequent: every 3 months for the first year, every 6 months for the second year and then annually thereafter.
Pophali P, Halland M. Barrett’s oesophagus: diagnosis and management. BMJ 2016;353:i2373.
Barrett’s Oesophagus - Surveillance: Example Question
A 72-year-old man attends gastroenterology clinic for follow-up after a recent upper gastrointestinal endoscopy. The patient had been referred by his GP for Barrett’s oesophagus screening due to long-standing and severe gastro-oesophageal reflux symptoms, associated with obesity and current smoker status.The patient reported suffering from severe heartburn after eating over the previous 10 years. He had been a regular user of over the counter anti-acid preparations, but had only sought medical advice in recent weeks after a close friend was diagnosed with gastric cancer.
The patient’s past medical history included obesity, hypertension, type 2 diabetes mellitus and gout. His regular medications were ramipril, allopurinol, metformin and gliclazide. The patient denied any drug allergies or intolerances. His father had undergone a partial gastrectomy for peptic ulcer disease, but there was no family history of Barrett’s oesophagus or oesophageal adenocarcinoma.
The patient was a retired school teacher who lived with his wife. He had smoked 10 cigarettes per day throughout his adult life and was abstinent from alcohol.
Following initial clinic assessment, an upper gastro-intestinal endoscopy was arranged (results given below). The patient had also been initiated on high-dose proton-pump inhibitor therapy, which had been associated with significant improvement in reflux symptoms.
Report from upper gastro-intestinal endoscopy: no evidence of hiatus hernia; 8 cm segment of circumferential salmon-coloured epithelium extending above gastro-oesophageal junction (quadrant biopsies taken as per protocol); no mass lesion or ulceration throughout oesophagus, stomach or first-part duodenum; mild-moderate oesophagitis and mild gastritis.
Histology from endoscopic biopsies: flat intestinal metaplasia present in 15 of 16 samples; no evidence of dysplasia or carcinoma.
In addition to continued proton-pump inhibitor treatment, what is appropriate management of this patient’s Barrett’s oesophagus?
Endoscopic mucosal resection > Surveillance endoscopy every 3 years Radiofrequency ablation Surveillance endoscopy every 1 year Risk factor modification advice only
Screening for Barrett’s oesophagus is recommended in individuals with chronic or severe gastro-oesophageal reflux disease symptoms, who also have three additional risk factors (out of: age > 50 years, male sex, white race, obesity, smoking), or who have a family history of Barrett’s oesophagus or oesophageal carcinoma.
The patient in this question has Barrett’s oesophagus with intestinal metaplasia but without dysplasia or intra-mucosal carcinoma. The risk of progression of non-dysplastic Barrett’s oesophagus to oesophageal adenocarcinoma is 0.33 % annually, meaning that endoscopic surveillance is recommended over therapy. Recommended frequency for endoscopic surveillance is every 3-5 years.
In the presence of dysplasia, endoscopic therapy is required due to the much higher risk of progression to adenocarcinoma (10 % per annually in high-grade dysplasia). A tissue acquisitive technique such as endoscopic mucosal resection is required for nodular lesions, with ablative therapy such as radiofrequency ablation reserved for flat regions of dysplasia or intra-mucosal carcinoma.
Proton-pump inhibitor therapy is recommended in patients with Barrett’s oesophagus due to several cohort studies suggesting that it reduces the risk of progression to adenocarcinoma.
Pophali P, Halland M. Barrett’s oesophagus: diagnosis and management. BMJ 2016;353:i2373.
Barrett’s Oesophagus - Example Question
A 53-year-old businessman is referred to for an endoscopy by his GP after complaining of persistent dyspepsia which was not fully controlled with lansoprazole. His symptoms have been getting gradually worse for the past six months. He smokes around 20 cigarettes/day and drinks about 30 units of alcohol per week. There is no history of dysphagia or vomiting although he does describe some pain when swallowing foods such as meat. Clinical examination is unremarkable.
A photograph is taken of his lower oesophagus during endoscopy:
SEE PASSMED BARRETT’S
Biopsies are taken and are reported as follows:
Intestinal metaplasia with a villiform pattern noted. Multiple intermediate mucous cells and goblet cells noted. No dysplasia noted.
What is the most appropriate management?
Oral fluconazole Oesophagogastrectomy High dose proton pump inhibitor therapy Endoscopic ablation > High dose proton pump inhibitor therapy + endoscopic surveillance
This is Barrett’s oesophagus. The metaplastic mucosa needs to be monitored on a regular basis to check for any dysplastic or malignant changes. High dose proton pump inhibitor therapy is also recommended.
Barrett’s Oesophagus Screening and Surveillance
Screening for Barrett’s oesophagus is recommended in individuals with chronic or severe gastro-oesophageal reflux disease symptoms, who also have three additional risk factors (out of: age > 50 years, male sex, white race, obesity, smoking), or who have a family history of Barrett’s oesophagus or oesophageal carcinoma.
No dysplasia:Eg intestinal metaplasia but without dysplasia or intra-mucosal carcinoma. The risk of progression of non-dysplastic Barrett’s oesophagus to oesophageal adenocarcinoma is 0.33 % annually, meaning that endoscopic surveillance is recommended over therapy. Recommended frequency for endoscopic surveillance is every 3-5 years.
Dysplasia: Endoscopic eradication therapy is indicated if any grade of dysplasia is present. In the presence of dysplasia, endoscopic therapy is required due to the much higher risk of progression to adenocarcinoma (10 % per annually in high-grade dysplasia). A tissue acquisitive technique such as endoscopic mucosal resection is required for nodular lesions, with ablative therapy such as radiofrequency ablation reserved for flat regions of dysplasia or intra-mucosal carcinoma.
Radiofrequency ablation is the preferred ablative therapy in patients with flat dysplasia or intra-mucosal carcinoma. This procedure is generally well tolerated aside from some short-lived chest pain. In the long-term, oesophageal strictures may occur. Radiofrequency ablation is effective, with 91 % of patients achieving complete eradication of dysplasia.
Following successful eradication of low-grade dysplasia, surveillance endoscopy should be performed every 6 months for the first year and then annually thereafter.
After eradication of high-grade dysplasia or intra-mucosal carcinoma, surveillance should be more frequent: every 3 months for the first year, every 6 months for the second year and then annually thereafter.
