| Article Access Statistics|
| Viewed||9379 |
| Printed||192 |
| Emailed||10 |
| PDF Downloaded||128 |
| Comments ||[Add] |
| Cited by others ||2 |
Click on image for details.
|Year : 1990 | Volume
| Issue : 4 | Page : 181-4
Pneumatic dilatation in achalasia cardia results and follow-up.
Supe AN, Samsi AB, Bapat RD, Mathur SK, Ramakantan RR
Department of Surgery, Seth G.S. Medical College, Parel, Bombay, Maharashtra.
Department of Surgery, Seth G.S. Medical College, Parel, Bombay, Maharashtra.
Pneumatic dilatation is one of the more recent methods in the management of achalasia cardia. Fifty dilatations were done in 42 patients with achalasia cardia over 5 years. There was a significant decrease in the maximum diameter of the oesophagus and a significant increase in diameter in the narrowed lower oesophageal segment in all the patients. Of the patients studied, 95.23% were relieved of their symptoms after only one to two sessions. There were no immediate complications. Out of the 38 patients on long term follow up, 8 (21.05%) had recurrence of symptoms. On repeat dilatations, 4 (50%) of them had good response. Late complication like reflux oesophagitis was observed in only 1 patient over a median follow up period of 22 months. It was thus concluded that pneumatic dilatation is a safe, simple and effective procedure in managing patients with achalasia cardia.
|How to cite this article:|
Supe A N, Samsi A B, Bapat R D, Mathur S K, Ramakantan R. Pneumatic dilatation in achalasia cardia results and follow-up. J Postgrad Med 1990;36:181
|How to cite this URL:|
Supe A N, Samsi A B, Bapat R D, Mathur S K, Ramakantan R. Pneumatic dilatation in achalasia cardia results and follow-up. J Postgrad Med [serial online] 1990 [cited 2019 Dec 6];36:181. Available from: http://www.jpgmonline.com/text.asp?1990/36/4/181/832
Achalasia cardia is characterised by the disordered motility of the oesophagus and defective relaxation of hypertensive lower oesophageal sphincter. As it is impossible to normalize the disordered motility of the oesophagus, management of achalasia cardia is directed towards lowering the oesophageal sphincter pressure. There are two modalities, which are commonly practised world over. Partial destruction of the gastro- oesophageal sphincter is achieved either surgically by cardiomyotomy,, or by brisk stretching of the, sphincter muscles with balloon dilatation,,. Drugs like calcium antagonists and smooth muscle relaxants have been tried with satisfactory results, but their long-term usefulness is not yet proved. We present here our results and follow up of pneumatic dilatation in patients with achalasia.
Forty-two patients (15 males and 27 females; age ranging from 21 to 62 yr, mean 37.4 yr) with achalasia cardia were treated with pneumatic dilatation, as an outdoor procedure over a period of 5 years. Predilatation barium swallow of all these patients showed oesophageal dilatation and disordered peristalsis proximal to beaked terminal oesophageal segment. Patients having sigmoid oesophagus were excluded. Endoscopy was performed in all patients to eliminate a benign stricture or malignant obstruction as a cause of the radiographic abnormality.
No sedation was given. Topical pharyngeal anaesthesia with 4% lignocaine solution was used. After an overnight fast, a Rusch latex balloon dilator (9 mm tube) was passed under fluoroscopic control, so that the balloon could be extended across the area of lower esophageal sphincter keeping its midpoint at the sphincter (See [Figure - 1]). In seven cases, dilator could not be advanced across the constriction; hence, an endoscope (GIFIT10 or XP) was passed into the oesophagus. A guide wire was then passed through the biopsy channel, well past the, gastroesophageal junction and endoscope was removed. A sialastic (pneumatic) dilator was then threaded over guide wire under fluoroscopic control and lower oesophageal sphincter was dilated. Later Rusch dilator was introduced and dilation was carried out. Balloon was inflated to a pressure of 250-300 mm Hg for one minute. The balloon was then deflated and withdrawn. No food or medication was given to patients orally for 2-3 hours following dilatation and were later advised to take liquids only for 24 hours. The dilatation session was repeated on 3rd and 5th day. At the end of week a post-dilatation barium-swallow was done. Patients were asked to follow up every six monthly or earlier if they had recurrence of symptoms.
Forty-one of 42 patients with achalasia presented with dysphagia for solids or liquids with a feeling of stickiness in the retrosternal region. The duration ranged from 4 months to 12 yr (average 21.2 months). Only one patient had previously undergone cardiomyotomy. Regurgitation and vomiting was noted in 29 patients (69%), while weight loss of more than 5 Kg was observed in 8 patients (19%). History of nocturnal cough was present in 5 patients (11.9%). The maximum diameter of the oesophagus before treatment varied from 35 to 82 mm (mean 45.5 + 12.4 mm). The oesophagus was dilated more than 40 mm in 64.28% of patients. The mean diameter of the narrowed lower oesophageal segment was 2.35 + 1.6 mm before treatment.
Fifty dilatations were performed in 42 patients. All patients had relief of dysphagia and regurgitation within 24 hours of dilatation.
Barium swallow within a week of dilatation in 42 patients showed a decrease in the maximum diameter of the oesophagus from 45.5 + 12.4 ram to 30.5 + 11.5 mm, though it was not significant and increase in the diameter of the narrowed lower segment of the esophagus from 2.35 + 1.6 min to 10.2 + 2.3 mm (P < 0.01) (See [Figure:2]). None of the patients showed a hold up of the barium after dilatation. Thirty-seven patients (88%) complained of retrosternal pain during procedure but only in four patients (9.5%), it persisted for 24 hours. No perforations were encountered during the study. There was no mortality of the procedure.
The follow up period in our study ranged from 1 month to 4 years. The median follow up was 22 months. Four patients were lost to follow up. Out of remaining 38 patients, 8 patients developed recurrence of symptoms 36 months after their initial dilatation. Repeat dilatation did relieve symptoms in four patients. The remaining non-responsive four patients were subjected to surgery. There was no correlation between the response and the maximum diameter of oesophagus. Only one patient (2.63%) developed symptoms of reflux oesophagitis. None have developed stricture.
Pneumatic dilatation has been used as primary treatment of achalasia cardia and several authors have reported good results in 70-92.5% of cases,,,,,. The advantages of this method are rapidity of the procedure, no need of hospitalisation and avoidance of surgery, which has its own risks. Reflux oesophagitis is uncommon after pneumatic dilatation.
Other authors have favoured surgical treatment reporting good results in more than 80% of patients,,. The advantages of surgery is cutting of muscle fibres under direct vision, and therefore less chances of perforation and more complete section of muscle fibres. But reflux oesophagitis remains a major cause of late failures and is held responsible for 21-28% of the reinterventions,. Hence it has been suggested to use dilatations as the initial treatment and cardiomyotomy to be carried out in later stages.
All our patients showed subjective and objective improvement after pneumatic dilations and majority of them have been symptom-free over a mean follow-up period of 22.2 + 14.3 months. Thirty of the following 38 patients required only one dilatation for relief, while 8 patients (21.05%) required a second dilatation 4-6 months after the initial dilatations, of whom 4 patients had to be treated surgically again. Over all success rate was 89.47% (34 of 38). This compares very well with other series,.
Patients with a tortuous oesophagus are particularly difficult candidates for pneumatic dilatation. The technique of passing a guide wire is essential in such cases as it is difficult to pass the dilator directly into the achalasic segment. To overcome these problems, a dilator with a dilating bag on a flexible fibreoptic endoscope has been tried with good results.
Complications like perforation has been reported in 1.6 - 9.4% of patients,. There was no perforation in our series, confirming the safety of the long latex balloon. Complications such as reflux oesophagitis (10%) and peptic strictures (3.4%) have been reported. But in our series incidence was low. Though retrosternal pain was seen in 88% patients during procedure, it persisted in only 4 patients. Absence of mortality related to procedure again confirms the safety of the procedure. Thus the present study proves that pneumatic dilatation is safe, simple and effective procedure in managing patients with Achalasia Cardia.
We thank Dr GB Parulkar, Dean, Seth GS Medical College and King Edward Memorial Hospital for permitting us to utilise hospital records and publish this data and for his constant encouragement.
Agha FP, Lee HH. The esophagus after endoscopic pneumatic balloon dilatation for achalasia. Amer J Roentengenol 1986; 146:25-29. |
|2.||Bennett JR, Barzaga E, Hendrix TR, Siegel CF. Treatment of achalasia by pneumatic dilatation of the cardia. Gut 1968; 9:727. |
|3.||Bortolotti M, Lobo G. Clinical and manometric effects of nifedipine in patients with esophageal achalasia. Gastroenterology 1981; 80:39-44. |
|4.||Chawla YK, Dilawari JB, Reddy DN, Kataria S. Pneumatic dilatation in achalasia cardia. Ind J Gastroenterol 1987; 6:101-102. |
|5.||Cendes A, Larrain A, Strauszer T, Ayala M. Long-term clinical radiological and manometric follow-up period of patients with achalasia of the esophagus treated with esophagomyotomy. Digestion 1975; 13:27-32. |
|6.||Csendes A. and Strauszer, T.: Long term clinical, radiological and manometric follow-up of patients with achalasia treated with pneumatic dilatation. Digestion 1974; 11:128-134. |
|7.||Csendes A, Velasco N, Braghetto I, Henriquez A. A prospective randomised study comparing forceful dilatation and oesophagomyotomy in patients with achalasia of the oesophagus. Gastroenterology 1981; 80:789-795. |
|8.||Fellows IW, Ogilvie AL, Atkinson M. Pneumatic dilatation in achalasia. Gut 1983; 24:1020-1023. |
|9.||Gelfond M, Rozen P, Keren S, Gilat T. Effects of nitrates on LOS pressure in achalasia: a potential therapeutic aid. Gut 1981; 22:312-318. |
|10.||Jara FM, Toledo-Pereyra LH, Lewis JW, Magilligan DL. Long-term results of esophagomyotomy for achalasia of esophagus. Arch Surg 1979; 114:935-936. |
|11.||Kurlander DJ, Raskin HF, Kirsner JB, Palmer WL. Therapeutic value of the pneumatic dilatator in achalasia of the esophagus. Long term results in sixty-two living patients. Gastroenterology 1963; 45:604-613. |
|12.||Menzies Gow J, Gummer JWP, Edwards DAW. Results of Heller's operation for achalasia of the cardia. Brit J Surg 1978; 65:483-485. |
|13.||Olsen AM, Harrington SW, Moersch HJ, Andersen HA. The treatment of cardiospasm: analysis of a twelve-year experience. J Thoracic Surg 1951; 22:164-187. |
|14.||Patrick DL, Payne WS, Olsen AM, Ellis FH. Re-operation for achalasia of esophagus. Arch Surg 1971; 103:122-128. |
|15.||Rees JR, Thorbjarnarson B, Barnes Wm. H. Achalasia: results of operation in 84 patients. Ann Surg 1970; 171:195-201. |
|16.||Thorbjarnarson B. Causes of surgical failures in the treatment of achalasia. Bull Soc Int Chir 1975; 34:619-622. |
|17.||Vantrappen G, Hellemans J. Treatment of achalasia and related motor disorders. Gastroenterology 1980; 79:144-154. |
|18.||Vantrappen G, Hellmans J, Deloof W, Valembois P, Vandenbroucke J. Treatment of achalasia with pneumatic dilatations. Gut 1971; 12:268-275. |
|19.||Witzel L. Treatment of achalasia with a pneumatic dilator attached to a gastroscope. Endoscopy 1981; 13:176-177.