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LECTURE ON ACHALASIA S. RAD With the cases from his own file

LECTURE ON ACHALASIA S. RAD With the cases from his own file Tabriz University of Medical Sciences Tabriz-Iran. TECHNIQUE OF EXAMINATION Apart from clinical manometer no imaging modality compares to fluoroscopic examination with spot-filming for diagnosis of Achalasia .

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LECTURE ON ACHALASIA S. RAD With the cases from his own file

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  1. LECTURE ON ACHALASIA S. RAD With the cases from his own file Tabriz University of Medical Sciences Tabriz-Iran SR

  2. TECHNIQUE OF EXAMINATION Apart from clinical manometer no imaging modality compares to fluoroscopic examination with spot-filmingfor diagnosis of Achalasia. In fact any functional disorder in gastro-intestinal tract needs to be evaluated studying its state of being in rest and moving modifications. Fluoroscopy, an appropriate means to study movements, can give functional data and is the only one to be implemented for diagnosis in these cases. SR

  3. MECHANISM OF PRODUCTION Achalasiaanegative version of chalasia ( wide open gastric cardia with facilitated gastro-esophageal reflux ) means non relaxation of the sphincteric mechanism in the lower esophagus. Absence of the anatomical sphincter in the lower esophagus is compensated with the synergic action of multiple elements to play this role: The acute angle of the entrance of the lower esophagus into the stomach (namely angle of His), hypertonic circular muscles of the lower esophagus by creating high pressure zone in this area, phrenico-esophageal membrane (Laimer’s) and freely to and fro moving of the esophageal vestibula in diaphragmatic hiatus surrounded by sling muscles of the diaphragmatic crura, All are collaborating to close the cardia in resting state with the added effect of thegastrincontent of the stomach or circulating one to produce tough closure of the cardia to prevent gastro-esophageal reflux. SR

  4. ETIOLOGY Cerebral cortex is the dominating commander of the esophageal function. This is done by psychogenic effect or by cranial neural impact on the esophagus, specially vague or pneumo-gastric one (No X) via the ambiguous nucleus of this nerve in the brain as the main factor. This nervous impulse is effectuated by myenteric plexus (Auerbach) of the esophagus itself to autonomic movement of the organ. According to the above-mentioned origins, achalasia may be due to : -Psychogenic disturbance -Vagal transmitting defect, such as seen in vagotomy orChagasdisease. -Lack of myenteric or autonomic nervous plexus of the esophagus itself. SR

  5. The very first sign of the achalasia is the apparition of retention of fluid in its lumen which normally takes no more than 5 or 6 second to empty, subsequently a fluid level in the esopghagus is not seen in standing position, where the gravity should accelerate the stripping function of the organ. To notice this phenomenon it is mandatory to start examination in erect or upright position. This is just the opposite of esophageal involvement in scleroderma ( progressive systemic sclerosis) which demands examination in lying down position to suppress the gravity action of the stagnating fluid to notice the peristalsis only. SR

  6. Air bubble of the stomach is produced by aerophagia or swallowed air. In the case of achalasia stagnation of the fluid inside esophagus prevents air to reach the stomach and so, lack of gastric air bubble or its diminution may be another important sign of the insult. SR

  7. Achalasia may be seen at the level of the crico-pharyngeus muscle, called superior achalasia or at the lower end, the ordinary lower achalasia. In any case it is produced by non-relaxation of the sphincters, upper one been a true or anatomical sphinter ( crico-pharyngeus muscle) and a sphincteric mechanism in lower end or sometimes anatomical caused by non-relaxation of the crura sling muscle. A special type of this disorder may also be seen and caused by secondary obtruding factors of the cardia in fact pseudo-achalasia,a justified nomenclature. SR

  8. Pharyngeal achalasia SR

  9. Cricopharyngeus or UES SR

  10. There are no stripping waves and inactive peristalsis is not able to evacuate esophagus . Tubular esophagus or Ring A is located where the muscular part transforms to the vestibular region and non-relaxation of the lower end of the organ affects this point . That is why the lower end of the esophagus in achalasia appears conical ( Bird’s beak) caused by contractile state of the circular muscles. SR

  11. Conical and concentric tapering of the lower esophagus stands just at the cardia. SR

  12. Persistent retention because of the inactive stripping waves despite their force in: Vigorous achalasia. SR

  13. Vigorous achalasia. SR

  14. With previous operation ( Heller type ) there is usually a diverticulum formation at the cardia. SR

  15. Deformity due to the previous operation. SR

  16. Before and after operation. Inefficient operation in advanced cases. SR

  17. Huge epiphrenicdiverticulum is the rule in achalasia. SR

  18. Food retention in epiphrenicdiverticulum. SR

  19. Double epiphrenicdiverticulum. Sorry for the patient’s fore-arm inadvertently overlapping the lower end of the esophagus! SR

  20. Huge epiphrenicdiverticulum simulating Heart filled up with food! SR

  21. Diverticulum in achalasia simulating lung tumor. SR

  22. Achalasia demonstrated in chest CT, only a morphological evaluation SR

  23. Fluid level in the esophagus. In CT and barium study. Bird’s beak sign may be shown only in reformatting coronal aspect with MDCT SR

  24. Achalasia with unusual diverticulum simulating neural tumor. SR

  25. CTs of the same patient SR

  26. Deviation of dilated esophagus to the right side: Men’s socks appearance SR

  27. Men’s socks appearance. SR

  28. No relevant chest x-ray. There are always exceptions for the rules! SR

  29. Paraffinoma due to the oil ingestion in achalasia to facilitate swallowing in some way. SR

  30. Esophageal wall seen on the top of the mediastinal widening is in favor of achalasia. SR

  31. Operated thoracic transferred stomach usually presents a thick wall and should not be confused with achalasia. SR

  32. Odd pattern of the filled up thoracic stomach caused by narrowing of the pylorus or tight hiatus not widened during operation. SR

  33. Lung abscess simulating cavitating malignancy due to perforate achalasia. Notice fluid level in the esophagus at the plain film, best sign for fluid stagnation. SR

  34. Lung or mediastinalabscess caused by perforated achalasia. SR

  35. Lung abscess caused by repeated aspiration in achalasia. Notice: esophageal wall in mediastinum and absence of gastric air bubble. SR

  36. Pseudo-achalasia due to tumor infiltration of the cardia. SR

  37. Different cases of pseudo-achalasia. SR

  38. Pseudo-achalasia diagnosed in plain abdominal film. SR

  39. Achalasia may occur in children as well: One-year-old child One and half-year-old SR

  40. Four-year-old Seven-year-old SR

  41. Twelve-year-old child having trouble since infancy. SR

  42. Onset of malignancy in long standing achalasia. Tumor occurrence is almost always above the cardia Ninety-year-old patient SR

  43. Malignancy is located almost always above the cardia. SR

  44. Conclusion Achalasia may be guessed by the absence of the gastric air bubble on the chest x-rays in clinically suspicious settings. There is no air-fluid level seen on the plain film of the normal esophagus and its apparition is in favor of achalasia in most of the cases with mediastinal widening. Conical and concentric tapering of the cardia with reservation of the normal mucosal pattern confirms the diagnosis of the achalasia. SR

  45. THE END SR

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