In patients where symptoms are severe pneumatic d i l a t a t i o n may be considered. Blackwell & Castell (1984) have found that the patient with persistent and severe symptoms is uncom m o n and they have rarely had to resort to b a l loon di l atation or surgery. This probably reflects their pattern of referral as many of their patients seem to have noncardiac chest pain and not dysphagia, and severe d y sphagia seems to have been the usual indication for dilatation. Craddock et al (1966) treated 7 patients with diffuse oesophageal spasm with dilatation using boug i e n a g e and the Negus hydrostatic dilator with relief of symptoms. Winters et al (1984) report interesting results using oesophageal bougienage in patients with the nutcr a c k e r oesophagus in a prospective double blind controlled trial. There were no significant differences between the results of bougienage with a therapeutic dilator (54-F) or w i t h a p l a cebo dilator (30-F) with respect to chest pain, dysphagia, lower oesophageal sphincter p ressure or contraction amplitude. Chest pain scores at the end of the three month study period were significantly lower than baseline scores irrespective of the order in w h i c h the d ilators were used. No subjective or objective improvement could be demonstrated when therapeutive boug i e n a g e was compared with placebo bougienage. This was probably related to the small size (54-F) of the dilator used for their
di l atation as the usual dilator used in a c halasia is 90- 120F. They were therefore not using a therapeutic bougienage but two placebo g r o u p s . They thought that the improvement in symptoms at the completion of the study could be related to close physician-patient interaction. Goldin et al (1982), in a retrospective study of 24 patients with high amplitude p eristalsis treated with bougienage (50-60F), found that 83% reported symptomatic improvement following dilatation. 25% of a control group of untreated patients also reported improvement during the same period. The dura t i o n of remission in the treated group was very variable.
Rider et al (1969), using a flexible pneumatic d i l ator as a controlled expansion force (a Rider -Moeller Balloon), treated nine patients with diffuse oesophageal spasm p rimarily with chest pain but also with dysphagia. The smallest pneumatic dilator was distended to 300mm Hg and held in place for three minutes. The dumbbell shape of the dilator kept the lower section anchored in the stomach fundus and the upper part in the oesophagus with the central core at the cardia. None of these patients had any c omplications and they all achieved an excellent or good response. Rider, however, reports that the numb e r of dilatations necessary to achieve symptomatic relief varied from 1 to 22 over several years. No comment is made on the effect of dilatation on actual symptoms or m a n o m e t r y or on the duration of response. There was no placebo and no clinical results are given as to whether there was lower oesophageal sphincter dysfunction or g a s t ro-oesophageal reflux prior to dilatation. The d e s c ription of the
dilatation suggests that the lower oesophageal sphincter received the maximum dilatation although this usually functions normally in diffuse oesophageal spasm. Of the two case histories given only one patient had manometry performed prior to dilatation. Both these patients had dysphagia to solid foods and chest pain but were symptom free after dilatation for up to a year.
V a n trappen & Hellemans (1980) performed pneumatic dilatation in a series of 156 patients with severe dysphagia. A c cording to Vantrappen's criteria for diagnosis of oesophageal motility disorder 70% had true achalasia, 11% had diffuse oesophageal spasm and 17% had intermediate forms (17% pR and 2% P r ) . The results after dilatation were good or excellent in 80% of the achalasia patients. "Excellent" meant free of symptoms and "good" included short duration of pain or dysphagia less than once a week. 78% of the intermediate group experienced good or excellent results. The results in the patients with diffuse oesophageal spasm were less successful with only 45% being classed as excellent or good results. No reasons are given for the poorer results obtained in the group with diffuse oesophageal spasm but the d ilatations seem to have focused on the lower oesophageal sphincter which is not usually involved in diffuse oesophageal spasm.
Ebert et al (1983) reported the results of forceful pneumatic dilatation in nine patients with severe symptoms of diffuse oesophageal spasm and lower oesophageal sphincter d ysfunction who were unresponsive to medical therapy and bougienage. Under X-ray screening the balloon was positioned
to straddle the diaphragmatic hiatus and inflated to 8-12 Ib/sq in for 15 seconds. Manometry was repeated a mean of 14 m onths after dilatation. Pneumatic d i l atation in these patients produced clinical improvement in 89% of patients followed for an average of 37 months. The improvement in oesophageal symptoms was associated with a sustained decrease in lower oesophageal sphincter pressure in most cases. There was no change in the percentage of lower oesophageal sphincter relaxation with swallowing or in the pattern of baseline oesophageal motility following clinically successful pneumatic dilatation. Dysph a g i a and regurgitation were the symptoms most improved by dilat a t i o n which is probably related to the decrease in lower oesophageal sphincter pressure. In most studies of diffuse oesophageal spasm the lower oesophageal sphincter function is normal but all these patients had incomplete relax a t i o n with swallowing.
The deficiencies of the work so far published are:-
1. Some of the^/ patients with diffuse oesophageal spasm had