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