ESOPHAGEAL GASTRIC MOTILITY DISORDER.pptx

Esophageal Motility disorder

1. A CASE SERIES ESOPHAGEAL MOTILITY DISORDER HOD: DR KRISHNAN CHIEF: DR RAMKUMAR ASST PROF: DR SHANTHI

2. CASE 1 A 29 yrs old female c/o difficulty in swallowing * 2 yrs initially to liquid; progressed to solid diet insidious onset gradual progression c/o vomiting *3 days H/o significant weight loss+ Past history: No H/O corrosive consumption Nil comorbidities

3. GC: FAIR VITALS : STABLE USG ABDOMEN: NORMAL STUDY UGI SCOPY OGJ 34cm Dilated Esophagus Peristalsis absent OGJ tight Stomach entered with a plop Stomach & Duodenum normal

4. CASE 2 A 47 yrs old male c/o difficulty in swallowing * 5yrs insidious onset, gradual progression solid > liquid h/o epigastric pain + on & off No H/o vomiting; Past history: nil comorbidities

5. GC: FAIR VITALS : STABLE USG ABDOMEN: NORMAL STUDY UGI SCOPY: OGJ – 39CM Lumen not dilated Reduced Persistalsis OGJ Tight, Stomach entered with a plop Stomach & Duodenum Normal

6. CASE 3 A 54 yrs old male was admitted with c/o difficulty in swallowing * 1yr on & off solid > liquid H/O feeling of constrictive sensation @ upper chest h/o abdominal pain + on & off No H/O loss of weight Past history: nil comorbidities

7. GC: FAIR VITALS : STABLE USG ABDOMEN: NORMAL STUDY UGI SCOPY OGJ 38cm Distal 2/3 rd of esophagus shows corkscrew type of peristalsis Lax LES + Stomach & Duodenum normal

8. BARIUM SWALLOW CASE 1 CASE 2 CASE 3

9. ACHALASIA CARDIA Is a smooth muscle motility disorder Pathogenesis - lower esophageal sphincter fails to relax &  absence of peristalsis Is a  functional obstruction at the gastroesophageal junction

10. ETIOLOGY The exact etiology of this degeneration is unclear though many theories have been proposed. These theories include autoimmune phenomenon, viral infection, genetic predisposition idiopathic S econdary achalasia may be seen in  Chagas disease caused by Trypanosoma cruzi , E sophageal infiltration by gastric carcinoma Eosinophilic gastroenteritis, lymphoma,  Certain viral infections Neurodegenerative disorders

11. CLINICAL PRESENTATION D ysphagia, initially with solids than to liquids though 70-97% of patients will have dysphagia to both solids and liquids at presentation. R egurgitation C hest pain, but an improvement of esophageal emptying rarely alleviates the pain. Regurgitation with possible aspiration, Nocturnal cough, Heartburn, Weight loss from difficulty eating. Hiccups Difficulty belching. Extra-esophageal symptoms includes structural or functional pulmonary abnormalities likely from recurrent aspiration or tracheal compression from the dilated esophagus. A "bullfrog neck" appearance can occur from severe dilatation and distortion of the cervical esophagus leading to tracheal obstruction and stridor. Physical examination may reveal an emaciated individual.

12. ECKARDT SYMPTOM SCORE It is used in the evaluation of symptoms, stages, and efficacy of achalasia treatment. It includes Weight loss C hest pain D ysphagia Regurgitation

13. DYSPHAGIA REGURGITATION RETROSTERNAL PAIN WEIGHT LOSS (KG) SCORE NONE NONE NONE NONE OCCASIONAL OCCASIONAL OCCASIONAL <5 1 DAILY DAILY DAILY 5-10 2 EACH MEAL EACH MEAL EACH MEAL >10 3 STAGE SCORE PROGNOSIS 1 0-1 REMISSION + 2 4-6 TREATMENT FAILURE 3 >6 TREATMENT FAILURE

14. INVESTIGATIONS Barium swallow UGI scopy mannometry

15. BARIUM SWALLOW  Best initial test to diagnose achalasia Classical finding - S mooth tapering of the lower esophagus to a   “bird’s beak" appearance. Timed Barium Swallow : A timed barium swallow is used to access esophageal emptying. This variant of the classic barium swallow is performed by having the patient drink 236 ml of barium in the upright position and taking radiographs at 1, 2 and 5 minutes after the last swallow.  The height of the barium column after five minutes, and the esophageal width are measured pre and post-treatment.

16. UGI SCOPY O GD has low accuracy in the diagnosis of achalasia It may be normal in the early stages of the disease. I n advanced cases include rosette appearance of the esophagogastric junction or an esophagus, which has become dilated, tortuous, and atonic often with retained food and saliva. The esophagus may be normal or show evidence of esophagitis due to chronic stasis. Pseudoachalasia A firm resistance of the scope passing through the esophagogastric junction, especially in an older patient or one with a short duration of symptoms and significant weight loss, should raise the concern for pseudoachalasia , especially malignancy.

17. MANOMETRY Is the most sensitive & gold standard test for the diagnosis of achalasia Manometry will reveal incomplete LES relaxation in response to swallowing, sometimes a lack of peristalsis in the lower esophagus, and an increase in pressure of the lower esophageal sphincter. Based on HRM, Achalasia is classified by the Chicago criteria (version 3.0) into three distinct categories,. The integrated relaxation pressure in type 1 is 10mmHg, type 2 achalasia 15 mmHg, and type 3 achalasia 17 mmHg

18. TREATMENT Current treatment modalities for primary idiopathic achalasia are nonsurgical or surgical. Nonsurgical pharmacotherapy, endoscopic botulinum toxin injection, pneumatic dilatation. Surgical L aparoscopic Heller myotomy (LHM) peroral endoscopic myotomy (POEM). 

19. PHARMACOTHERAPY  Nitrates C alcium channel blockers P hosphodiesterase-5 inhibitors Are less effective P rovide only short-term relief of symptoms

20. BOTULINUM TOXIN Endoscopic injection of botulinum toxin can be used in high-risk patients or those who relapse after myotomy. Botulinum toxin - Block the release of acetylcholine at the level of the lower esophageal sphincter U seful in patients who may not be candidates for surgery or dilatation or alternatively, as a bridge to more definitive therapy.  Limitations: short-lived (lasting about 6 to 12 months), repeated doses, cost

21. PNEUMATIC BALLOON DILATATION Is cost-effective non-surgical therapy for achalasia.  Pneumatic dilatation is the first treatment option for a patient in whom surgery fails Dilatation of the esophagus is achieved by disrupting the circular fibers of the LES with air pressure using a graded dilator approach.  Symptoms improve in 50%-93% of patients R ecurrence occurs in 30% at five years Complications : Usually minor, but severe complications like esophageal perforation could occur.

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