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Benign oesophageal disease

Andre Sevette 9th June 2004 NSW AST training program


(With The panel of experts present: Dr Garrett Smith & Prof David Hunt)

10-30%

of patients with suspected angina don't have coronary disease. these 50% will have oesophageal disorders.

From

Anatomy
- Muscular tube - Conduit from the pharynx to the stomach - C6 (Cricoid cartilage) to below the diaphragm - From the incisor 40-45 cm (actual 2025cm) - Passes behind aortic arch and left main bronchus. - Enters abdomen through oesophageal hiatus 2-4 cm below the diaphragm

Anatomy
- Held in position by: . Reflection of the peritoneum onto the stomach . Phreno-oesophageal ligament to the oesophagus .

Anatomy
Three area of narrowing - Cricopharangeus - Behind the aortic arch - LOS (thickening of the circular muscles ~ 4cm) The muscles upper 1/3 of oesophagus is striated, remainder is smooth muscle peristalsis wave 4-6cm/s (reflex regulated in the medulla)

Arterial supply:
Upper inferior thyroid artery Middle Bronchial arteries and oesophageal branches directly from aorta Lower L inferior phrenic and gastric

Venous drainage:
Upper oesophageal venous plexus to azygos vein Lower oesophageal branches of the coronary vein, a tributary of the portal vein

Histology:
- Stratified columnar epithelium with scattered mucus glands - No serosa hence does not heal as well as the rest of GIT - Lower Oesophageal Sphincter (LOS) Contraction: -adrenergic & cholinergic Gastrin Relax: -adrenergic,VIP and NO CCK & glucagon

Symptoms:
- Dysphagia: difficulty swallowing - Odynophagia: pain on or painful swallowing - Globus: lump in the throat - Heart burn: Stomach/Substernal burning sensation radiating up to the neck and relieved acutely (but transiently) by antacids

Oesophageal Motility Disorders(1)


(i) Achalasia

(ii) Others
Diffuse oesophageal Spasm Nutcracker Oesophagus Hypertensive LOS Scleroderma & other collagenvascular disorders (eg CREST)
(The panels comments were: Although they do see few Achalasias a year, they rarely see any of the other disorders )

Diffuse oesophageal Spasm


- 3-5% of motility disorders - Normal peristalsis + Spontaneous contraction + increase in LOS pressure - Aetiology is unknown, ? defect in neural inhibition normally mediated by NO - Hypersensitive oesophagus - Dx on Manometry - Endoscopy is unremarkable & Ba Swallow is N or disorganised (Corckscrew)

Diffuse oesophageal Spasm

Nutcracker Oesophagus
- High amplitude peristaltic waves (>180mmHg) prolonged (>6s) - Endoscopy unremarkable but Endo US shows thickening of muscularis propria - Higher incidence of psychiatric disorders

Hypertensive LOS
- Elevated LOS pressure (>45mmHg) with normal peristalsis - LOS relaxation is normal

Treatment
- Medical Rx effective in 80% - Agents acting on Smooth Muscle (eg Nitrates, Ca channel blockers), - Psychoactive agents (eg Benzodiazepines, Tricyclics) (?more effective) - Botox injection - Surgical Rx, reserved for Px with dysphagia and poor oesophageal emptying Myotomy (Lap / Thoracoscopic)

Ineffective motility
- Scleroderma (80% of Px), other Collagen Vascular disorders (SLE, RA, MCTD), Amyloidosis, Alcoholism, MS, myxoedema etc - Affect the myenteric plexus + fibrosis and vascular obliteration (Predominantly distal SM) - or absent peristalsis and LOS pressure

Achalasia
- Uncommon (0.5-1 in 100,000), M=F, 20-50s - Ineffective relaxation of the LOS combined with loss of oesophageal peristalsis impaired oesophageal emptying and gradual dilatation - or loss of inhibitory myenteric ganglion cells & progressive neural fibrosis - Also decreased production of NO & VIP - Slight increase risk of SCC

Achalasia - Presentation
- Dysphagia - delayed and progressive presentation (mean 2 years) - Stress or cold fluid exacerbates symptoms - Spontaneous or forced regurgitation of undigested food - 10% will have pulmonary complication - Can have heartburn (not GORD) - Chest pain ( heartburn) - 30-50% resolves with Myotomy

Achalasia - Diagnosis
- Air fluid levels on plain Xray - Ba swallow: dilated oesophagus with Bird's beak tapering - Manometry is gold standard . Resting LOS pressure is usually normal (may be elevated) . Complete absence of peristalsis - Endoscopy: dilated oesophagus with tightly closed LOS gentle pressure will admit the scope with a "pop.

Achalasia - Diagnosis

Achalasia - Treatment
- Palliation of dysphagia relieve functional obstruction of distal oesophagus (neuromuscular defect is not corrected) o Medical (Nitrates and Ca channel blockers) . Poorly absorbed, inconsistent and short lived effect . SE.

Achalasia - Treatment
- Botox injection: bind to cholinergic nerves and irreversibly inhibit Acetyl Choline release - 60-85% of patient get relief but 50% get recurrent symptoms within 6 months. - Efficacy decreased with repeated injection - Expensive - Cause intense inflammatory reaction which will make subsequent surgery more difficult and increase risk of perforation.
(Prof Hunt thought this was a theoretical problem and in practice he did not find surgery more difficult)

Achalasia - Treatment
- Graded

pneumatic dilatation (under fluoroscopy) Tears the muscle (myotomy) 30mm for 1-3min (day procedure) Can have repeated dilatation 60-90% success rate Efficacy is decreased after second dilatation perforation rate ~ 2%

Achalasia Surgical treatment


- Originally performed by Ernest Heller in

1914 for Achalasia Two myotomies: anterior and posterior - Modified Heller: anterior only - Excellent results in 90-95% - Traditionally trans-thoracic or transabdominal - Now minimally invasive Laparoscopic / Thoracoscopic

Achalasia Surgical treatment


- Controversies Length of myotomy Proximal 5-7 cm above GOJ ? evidence(1) longer gastric myotomies (>3cm) better relief from dysphagia Need for antireflux procedure as well
(The panel thought everyone should do an antireflux procedure, but the length and proximal extension of the myotomy is not as important.)

Benign oesophageal tumours


- From any layer - Mucosal: . Papillomas (sessile or pedunculated) - Intramural: . Leiomyoma, Fibroma Lipoma . Congenital cysts or reduplication (lower)

Benign oesophageal tumours


- Asymptomatic or may be large enough to encroach the lumen - Peristalsis is normal with Leiomyoma, but spasm with cysts and reduplication - Intraluminal lesions Dx on Endoscopy (should Bx) - Intramural lesions Dx Radiologically (smoothly rounded) should not be Bx

Gastro-oesophageal reflux disease


- Reflux of gastric content is normal

- GORD is when affects patients well being . Symptoms . Physical complications - Common - (difficult to assess - Px self treat) - 75% of oesophageal disease in clinical practice In the US(2)40% monthly 14% weekly (15-20% Australia) 7% daily

Gastro-oesophageal reflux disease


Pathogenesis: - Excessive exposure and reduced clearance of gastric content - Competent LOS Resting pressure >6mmHg Abdominal location of LOS (>1cm) (diaphragmatic crura and intra abdominal pressure) Total length >2 cm - Recurrent / prolonged relaxation

Gastro-oesophageal reflux disease


- Normal gastric emptying - Adequate oesophageal clearance - Contributing Factors: Familial, Obesity, Diet (Fat, Chocolate, Caffeine), Smoking, Drugs - Hiatus hernia 85% of Px with reflux have a sliding hernia But most people with a sliding hernia dont have disabling symptoms

Gastro-oesophageal reflux disease


Symptoms Mild / Severe - Heartburn (also in PUD and 40% IBS Px) - Regurgitation of previously ingested food - Waterwash (saliva production) - Dysphagia (defective peristalsis / stricture) - Odynophagia (severe oesophagitis) - Haematemesis

Gastro-oesophageal reflux disease


Complication Oesophageal: Oesophagitis Barretts (10%) Strictures (Panel: very rare now) Adenocarcinoma 50% of Px with GORD get complications

Gastro-oesophageal reflux disease


Complication Extra-oesophageal: Laryngitis Pharyngitis Sinusitis Pulmonary Adult onset asthma NB Poor correlation between frequency and severity of symptoms and prevalence of complication

Gastro-oesophageal reflux disease


GESA recommendation for Mx: Mild symptoms - Antacids /over the counter H2 antagonists - Lifestyle changes: Diet (Fatty, Spicy, Coffee, Acidic) ETOH (moderation OK) Smoking Late/large meals & early recumbency Drugs Tight clothes

Gastro-oesophageal reflux disease


GESA recommendation for Mx: Moderate to severe symptoms - First line Rx: 2-4/52 of double dose PPI (Superior to endoscopy for Dx) - Symptomatic control equates to endoscopic healing (even LA Grade C&D)

Gastro-oesophageal reflux disease


GESA recommendation for Mx - Further Ix if: Unclear Dx Symptoms persist/progress on Rx Complicated Symptoms Suggestion of other pathology (Ca, PUD, infective/drug induced oesphagitis)

Gastro-oesophageal reflux disease


GESA recommendation for Mx - Further Ix: Endoscopy Negative in >50% of Px with GORD Ideal for: - Dx and grading of oesophagitis - Other mucosal lesions - Dx and Rx strictures - Dx of Barretts

Gastro-oesophageal reflux disease


GESA recommendation for Mx - Further Ix: 24/24 ambulatory oesophageal pH monitoring pH <4 for >1 hours

Gastro-oesophageal reflux disease


GESA recommendation for Mx Trial of withdrawal of therapy Majority will have symptom relapse Repeat course of the previous Rx Followed by on demand H2 antagonist / PPI antacids a small proportion will be symptom free Majority continuous treatment / Surgery

Gastro-oesophageal reflux disease


Few topics of interest
- Barretts oesophagus - Dysplasia - H Pylori -Non-Acid reflux

Gastro-oesophageal reflux disease


Barretts - Transformation of pseudostartified to columnar epithelium - If gastric or pancreatic (rarer) no risk of AdenoCa
(The panel thought it is important to emphasise on non-acid secreting gastric mucosa is in the cardia and can extend upwards without risk of adenoCa)

- Specialised intestinal metaplasia risk of AdenoCa (much less if length <3cm) - Second yearly surveillance endoscopy with Bx (4 quadrant @ 2cm intervals) (GESA)

Gastro-oesophageal reflux disease


Barretts - Once present no evidence that Acid suppression will reverse progression to dysplasia - Recent study showed in Px with Barretts there is progression after antireflux surgery(3). - Also increased evidence in the role if Bile salts in Barretts(4).

Gastro-oesophageal reflux disease


Non-Acid reflux(5) - Animal studies have shown: Acid alone requires high concentration to damage the oesophageal mucosa - Oesophagitis has been observed in achlorhydric patients - Duodenogastro-oesophageal reflux (DGOR) is the reflux of duodenal content (bile acids and pancreatic secretions) into the stomach (normal postprandially and nocturnally)

Gastro-oesophageal reflux disease


Non-Acid reflux(5) - Contains trypsin as well as bile acids and can occurs at neutral and acidic pH too - Conjugated Bile salts @ low pH, Unconjugated bile salts and trypsin @ high pH can damage mucosa - Clinical studies: There is evidence that mucosal damage increase with increased exposure to the duodenogastrooesophageal reflux.

Gastro-oesophageal reflux disease


Non-Acid reflux(5) - Investigations . Scintigraphy (injection ofTc99m @ 5 min interval Camera for 60/60 can show duodenal reflux . Bilitec 2000 is spectrophometry, measure the bilirubin concentration in the oesophagus. (can have ambulatory monitoring) Problem with very low pH, food & mucosal folds

Gastro-oesophageal reflux disease


Non-Acid reflux(5) - Intraluminal impedance . It measures the opposition of current flow between 2 electrodes. . Bolus movement in hollow organs. . Detects wall, air, saliva and food all vary. It is pH independent and can determine the type and height of the refluxate

Surgical Treatment of GORD


- Surgery attempts to return the gastroesophageal junction below the diaphragm and form a barrier to reflux. - NB acid suppression with PPI might not be enough to prevent symptoms (impaired oesophageal clearance / non-acid reflux). - The cost of 10 year PPI treatment is ten times that of laparoscopic Nissen, including preoperative evaluation and postoperative care(7).

Surgical Treatment of GORD


Hills posterior gastropexy
- Musculomucosal flap valve created by the angle of His against the lesser curve - an important barrier to reflux. - Anchoring the LOS within the abdomen and posteriorly fixing it to the median arcuate ligament and accentuating the angle of His. - Not popular difficulty identifying the arcuate ligament.

Surgical Treatment of GORD


Hills posterior gastropexy
- Modified Hills uses the preaortic fascia and the condensation of the crus as the anchor for the repair. - Good to excellent result, ? less side effect than fundoplication.

Surgical Treatment of GORD


Fundoplication
- Mobilise the lower oesophagus and wrap the fundus of the stomach around it either totally or partially

Surgical Treatment of GORD


Total Fundoplication:
- Originally described by Nissen in 1956 - 360 fundal wrap around the distal oesophagus with division of the short gastric vessels (floppy).
(Dr Smith thought everyone would do a floppy wrap these days)

- Modified (Rosetti & others) not dividing the short gastrics and using a lower part of the fundus/greater curve for the wrap (no evidence for dysphagia and some evidence flatulence)(8)

Surgical Treatment of GORD


Nissen Fundoplication:
- The fold should be approximately 2 cm wider (too generous) can cause dysphagia

Surgical Treatment of GORD


Partial Fundoplication(<360):
- Nissen cause an over competent GOJ responsible for the post-op dysphagia and gas-bloat. - Belsey a 240 vertical fundoplication via a left thoracotomy - Toupet (posterior fundoplication) . Recent review(8) no long-term difference in reflux control . Less wind related S/E . ? Less short term dysphagia

Surgical Treatment of GORD


Anterior fundoplication . Flinders group first prospective randomised study of Anterior vs Nissen (180 anterior wrap anchored to the right hiatal pillar and oesophagus) Less dysphagia & Flatulence Trade-off less effective reflux control

Surgical treatment failure


- Primary symptoms unchanged or worse - Minimal improvement in the Primary Symptoms - New Symptoms (complication) eg dysphagia, diarrhea, Gas-Bloat syndrome - Presence of oesophagitis or incorrect position of the fundoplication on endoscopy surgery not controlling GORD

Surgical treatment failure


1 - Dysphagia: ~50% of patients experience dysphagia immed iately post-op. (oedema & inflammation) resolves spontaneously in 2-3/12

3-25% persist beyond 3/12 and need Rx

Surgical treatment failure


1 - Dysphagia: Causes: - Peptic Stricture (+ Recurrent oesophagitis). - Wrap too tight of too long - Achalasia (missed / new) - Slipped fundoplication - Paraoesophageal hernia

Surgical treatment failure


1 - Dysphagia: - Slipped fundoplication . Correctly fashioned but later a portion of the stomach herniates . Incorrectly mistaking the proximal stomach for distal oesophagus wrap around the stomach

Surgical treatment failure


1 - Dysphagia: - Slipped fundoplication

Surgical treatment failure


1 - Dysphagia: - Using body instead of fundus

Surgical treatment failure


1 - Dysphagia: - Paraoesophageal hernia is usually from the fundoplication itself, and may results from an attempt to construct a floppy wrap. - Patient with ineffective preoperative oesophageal motility Traditionally ? loose wrap / Toupet to avoid postoperative dysphagia - Recent study comparing the two found at 3/12 more dysphagia and gas-bloat syndrome with Nissen but by 12 months these differences disappeared(9).

Surgical treatment failure


1 - Dysphagia: - Achalasia has been reported to develop after and presumably as a consequence of antireflux surgery - Early or later - Mechanism not known - Functional LOS dysfunction.

Surgical treatment failure


1 - Dysphagia: Treatment . Dilate Strictures and obstructions successful in up to 50% . Hernias re-operation - more challenging - Success lower (70-85%)

Surgical treatment failure


2 - Gas-Bloat Syndrome: -Ill-defined and variable (early satiety,
abdominal distension, nausea, pain, flatulence, inability to belch. Causes . Inability of the GOJ to relax in response to gastric dilatation . Aerophagia (frequent habit of GORD Px) . Inability of the stomach to relax and accommodate food . Surgical injury to the vagus nerve

Surgical treatment failure


2 - Gas-Bloat Syndrome:
Treatment . Most resolve in 6/12 Avoid gas producing foods Frequent small volume meals Gas reducing drugs (simethicone) Pro-kinetic agents (Metochlopromide, Erythromycin) Advice to stop aerophagia
(The panel thought there was poor evidence of any treatment efficacy)

Surgical treatment failure


2 - Gas-Bloat Syndrome:
Treatment . If documented delayed gastric emptying gastric drainage procedure (Pyloroplasty or Gastro-enterostomy) or Botox injection into pyloric sphincter.
(The panel felt they would be very reluctant to dive into further surgery for this)

Surgical treatment failure


3 Diarrhoea
- Cause unknown suggested mechanism: Accelerated gastric emptying Vagal injury Post-operative dietary modification

Surgery for Para/oesophageal hernias


Types I (sliding)

Surgery for Para/oesophageal hernias


Types II (rolling or paraoesophageal)

Surgery for Para/oesophageal hernias


Types III (mixed)

Surgery for Para/oesophageal hernias


-

Type III associated with significant morbidity and mortality (incarceration of stomach or other viscera)

- Aims reduction of the hernia, complete excision of the sac, gastropexy, repair of the hiatus and antireflux procedure (fundoplication also help in anchoring)

Surgery for Para/oesophageal hernias


- Recent study with a 13 year follow-up showed high recurrence rate with laparoscopic (42%) compared to open (15%)(10) - NB most recurrence were asymptomatic and Dx on video Ba swallow - Also did not excise the sac contribute to recurrence 20% vs 0 % (6/12 follow up)(11)

Promising Endoscopic Procedures


- Endoscopic suturing - Endoscopic polymer injection - Endoscopic partial fundoplication - Stretta Procedure (RF energy delivered to the GOJ)
(With The panel felt there was no promising feature in any of these procedures!)

Bibliography
1. Woltman T.A., Oelschlager B.K., and Pellegrini C.A. Surgical Management of Esophageal Motility Disorders. Journal of Surgical Research 2004; 117: 34-43.
2. Kahrilas P.J. Gastroesophageal Reflux Disease. JAMA 25-91996; 276: 983-988. 3. Gurski R.R., Peters J.H., Hagen J.A., DeMeester S.R., Bremner C.G., Chandrasoma P.T., and DeMeester T.R. Barrett's esophagus can and does regress after antireflux surgery: a study of prevalence and predictive features. J.Am.Coll.Surg. 2003; 196: 706-712. 4. Liron R., Parrilla P., Martinez de Haro L.F., Ortiz A., Robles R., Lujan J.A., Fuente T., and Andres B. Quantification of duodenogastric reflux in Barrett's esophagus. Am.J.Gastroenterol. 1997; 92: 32-36.

Bibliography
5. Katz P.O. The role of non-acid reflux in gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2000; 14: 1539-1551.
6. Perkidis G., Lund R.J., Hinder R.A., McGinn T.R., Filipi C.J., Katada N., Cina R., Hinder P.R., and Lanspa S.J. Esophageal Manometry and 24-hour pH Testing in the Management of Gastroesophageal Reflux Patients. American Journal of Surgery 1997; 174: 634-638.

7. Isolauri J., Luostarinen M., Viljakka M., Isolauri E., Keyrilainen O., and Karvonen A.L. Long-term comparison of antireflux surgery versus conservative therapy for reflux esophagitis. Ann.Surg. 1997; 225: 295-299. 8. Watson D.I. Laparoscopic treatment of gastro-oesophageal reflux disease. Best.Pract.Res.Clin.Gastroenterol. 2004; 18: 1935.

Bibliography
9. Chrysos E., Tsiaoussis J., Zoras O.J., Athanasakis E., Mantides A., Katsamouris A., and Xynos E. Laparoscopic surgery for gastroesophageal reflux disease patients with impaired esophageal peristalsis: total or partial fundoplication? J.Am.Coll.Surg. 2003; 197: 8-15. 10. Hashemi M., Peters J.H., DeMeester T.R., Huprich J.E., Quek M., Hagen J.A., Crookes P.F., Theisen J., DeMeester S.R., Sillin L.F., and Bremner C.G. Laparoscopic repair of large type III hiatal hernia: objective followup reveals high recurrence rate. J.Am.Coll.Surg. 2000; 190: 553-560. 11. Edye M.B., Canin-Endres J., Gattorno F., and Salky B.A. Durability of laparoscopic repair of paraesophageal hernia. Ann.Surg. 1998; 228: 528-535.