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Dr Bernard Stacey Southampton General Hospital
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Incidence of adenocarcinoma of the oesophagus is fastest rising cancer in Western world Majority present late when only palliation possible Resection implies a major procedure and many have concurrent disease
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Blot WJ et al. JAMA 1991;265:1287-9
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1. Lower oesophageal sphincter 2. Crural diaphragm 3. Sling fibres of the stomach
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Longitudinal Circular Oesophageal wall histology distance in lower oesophagus
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How??
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Experimental oesophagitis Distal peristaltic contractions disappear LOS pressure by 60% Oesophagus 1-2cm shorter Oesophageal compliance by 30% Largely recovered by 4 weeks Zhang X et al. Am J Physiol Gastrointest Liver Physiol; 2005
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Attached to hypopharynx and diaphragm At lower end it blends with phreno-oesophageal ligament More muscle bulk than circular muscle Can shorten oesophagus by 5-6cm
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Mittal, R. K. et al. N Engl J Med 1997;336:924-932 Anatomy of the Esophagogastric Junction
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The phreno- oesophageal ligament: Origin - fascia transversalis Insertion: oesophageal wall Rich in collagen and elastic fibres
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The phreno-oesophageal ligament
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Fatty infiltration
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BMI and waist circumference correlates to in: intra-gastric pressure and G-O pressure gradient Also separation of LOS and crural diaphragm = perfect scenario for reflux
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Does weight loss help reflux? Remarkably little data! Yes: Derby 1999 23 pts BMI >23, GORD 6/12 - 80% lost wt and symptoms improved r = 0.548, p<0.001 No: Stockholm 1996 20 pts; pH study confirmed reflux - no significant improvement despite mean of 10kg wt loss Maybe: Amsterdam 2002 42 pts BMI 43 - wt loss, no gastric distension improved - with gastric distension continued reflux
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One extra oesophageal adenocarcinoma for every 5000 men over 60 treated
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?
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Lagergren J. NEJM 1999; 340: 825-31 OesCardia Recurrent symptoms7.72.0 ‘Long-standing’ reflux43.54.4
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Normaloesophagus MildOesophagitisSevereOesophagitisBarrett’sMetaplasia 100% of adults >30yrs Adenocarcinoma High Grade Dysplasia Low Grade Dysplasia months years 0.25% 2 - 5 years 0.08% 0 - 3 years 0.06% days - weeks 10% 3.5% 1.2% 95% don’t present Role of chemoprevention ?
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43% had Ca in resection specimen 24% progressed to Ca during 2-46 months follow up Ca incidence at 3 yrs 56% if diffuse 14% if focal HGD Veterans’ study – 7.3 yrs F/U: 4 / 79 Ca in 1 st year 12 / 75 Ca of whom 11 cured But: single pathologist
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~10% of population have reflux 10-15% of these have Barrett’s change (short > long segment) These get adenocarcinoma at 0.5%/year 40% of adenocarcinomas have no history of GORD <5% of adenocarcinomas are known to have Barrett’s on presenting with symptoms of their cancer
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Lagergren J. NEJM 1999; 340: 825-31 OesCardia Recurrent symptoms7.72.0 ‘Long-standing’ reflux43.54.4
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Dysphagia Weight loss Nausea and vomiting Pain uncommon (unless metastases)
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Stage TNM 1st seen5yr surv 1 T1 N0 M010%90% 2a T2/3 N0 M025%50% 2b T1/2 N1 M0 3 T3 N1 M045%15% Any T4 4 Any M120%0%
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T1
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T4
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Stenting Dilatation Alcohol injection Laser Brachytherapy
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Ultraflex Z-stent Wall stent Esophacoil Plastic stents
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Common Food bolus Tumour overgrowth “Knuckle” of stomach Reflux Rarer Stent migration Perforation Aspiration Airway compression
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Who will get the most problems?
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Weight loss Length of stricture (tumour volume) Not: Age, histology, BMI r=0.63 r=0.59
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1990 - 1996
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14 Median
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Poor Poor-mod Mod Mod-well Well
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1 2a 2b 3 4
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Stage:
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Nil Non-malignant Other malignancy Cardio-resp
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Never Ex Current
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Median = 14 months Mean = 41 months 1-year survival = 42.3% (58 / 137) 5-year survival = 12.4% (17 / 137 )
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