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Return to Medscape coverage of: 8th United European Gastroenterology Week

Management of Achalasia
Disclosures

Peter N. Meier, MD
Introduction
Achalasia is a denervation disorder primarily affecting the lower esophageal sphincter (LES) and involving
the esophageal smooth muscle. The etiology of this disorder is unclear. Gangliocytes are diminished or
absent in the region of the smooth muscle layer of the esophageal sphincter and are replaced by
lymphocytes and hypertrophic nerve fibers. This leads to dilatation of the esophageal body with subsequent
narrowing of the esophago-gastric junction. Mainly involved are inhibitory nerve fibers; the transmitters
affected are nitric oxide (NO) and vasoactive intestinal peptide, (VIP) and their involvement leads to loss of
peristalsis and a lack of sphincter relaxation. This disorder is irreversible.
In 1672, Sir Thomas Willis, in what is assumed to be the first report on treatment of achalasia, described
the successful dilatation of the sphincter with the use of a whale bone. Today there are 4 therapeutic
options for the treatment of achalasia. However, treatment is strictly palliative and is aimed at reducing LES
tone to facilitate clearance, improve symptoms, and prevent complications. In the long term, untreated
achalasia can lead to profound dysphagia, weight loss, and chronic aspiration. Achalasia is also considered
a premalignant condition. In a Turkish study it was concluded that DNA aneuploidy, p53 positivity, and
higher cellular proliferation index may have important roles in the pathogenesis of esophageal cancer in
primary achalasia.[1]

Botulinum toxin injection as well as systemic medication to relax the smooth musculature are available as
noninvasive therapies. Invasive measures include pneumatic dilatation and surgical interventions.

Drug Therapy
Established smooth muscle relaxants for decreasing LES tone include calcium antagonists (ie, nifedipine),
which can be applied effectively in patients suffering from achalasia. Calcium channel blockers improve the
symptoms. However, even in the median term, outcome is very disappointing, and these agents are not
suitable for long-term treatment. In a new study, sildenafil at a dose of 50 mg decreased the LES tone
because of its prolonged inhibitory effect on smooth muscle cells, but the effect was only moderate.[2]
Botulinum toxin injection is a simple technique that can be used to inhibit the release of acetylcholine; this
leads to a prolonged NO effect, with very few acute side effects. This treatment provides fast and effective
improvement in clinical symptoms. However, one third of patients experience recurrence of symptoms
approximately 3 months after the first injection, and approximately two thirds have recurrence after 1 year.
Patient age and type of achalasia appear to be key predictors of response.[3] A second injection of
botulinum toxin can improve the already satisfactory result.

Invasive Procedures
Pneumatic dilatation, with the aim of rupturing the muscle fibers, is the most common and effective method
for treating achalasia.
A prospective study on single dilatation revealed a long-term effect maintained after 5 years in 30% to 40%
of patients.[4] When this group of patients was stratified by age, the clinical results for those over 40 were
clearly better than those for the younger patients. Therefore, this therapy is not recommended for children
and juveniles. However, there are no data on the prevention of complications, and therapeutic efficacy can
only be assessed by symptomatic or functional improvement.

An analysis of pneumatic dilatation found that a postdilation LES pressure greater than 10 mm Hg was the
best predictor of prolonged remission; patients with values greater than 20 mm Hg had little benefit.
Effective dilatation therapy shows a 5% risk factor for perforation and other life-threatening events.
However, the risk of complications depends largely on the experience of the center, because the frequency
of complications decreases with increasing number of interventions performed. It is therefore
recommended that pneumatic dilatations be performed in centers experienced in this method. Other
complications include chest pain, intramural hematoma, and traumatic epiphrenic diverticula, which
probably represent expression of incomplete perforations.

In comparison to pneumatic dilatation, the aim of surgical myotomy is the total disruption of function under
distinctly advantageous conditions. Disadvantages to this approach include surgical requirements, such as
anesthesia and laparotomy, as well as the frequent occurrence of postoperative reflux.

Discussion
All of this raises the question of which therapy should be the preferred approach and thus recommended to
the patient. Only a few comparative, randomized, prospective studies addressing this question have been
performed.
Data comparing the surgical method with pneumatic dilatation are available from only 1 prospective,
randomized study, which showed that surgical treatment was more effective than endoscopic treatment.[5]
Even if one argues that surgical treatment was performed by very experienced surgeons and that the
endoscopic treatment was less effective, the results may be considered valid. Given the fact that
laparoscopy provides access to the LES, it appears that especially in younger patients laparoscopic
myotomy should be the preferred treatment. Data from a randomized study showed that for pneumatic
dilatation the cumulative remission rate was higher, and at 1 year it was more effective than botulinum
toxin.[6] A recent prospective study comparing botulinum toxin with pneumatic dilatation showed a 1-year
remission rate in the dilatation group of 59% and in the botulinum toxin group of 21% (P = .0002).[7]

Previous pneumatic dilatation does not affect the results of myotomy. In patients who did not respond to
botulinum toxin, the myotomy was technically straightforward and the result was excellent. Contrary to this,
in patients who responded to botulinum toxin, the LES muscle had become fibrotic. The induction of
inflammation and fibrosis seems to be an important side effect that will distinctly hamper subsequent
laparoscopic measures.[8]

Conclusion
When comparing all therapeutic methods and prioritizing them by preference, one would first recommend
laparoscopic myotomy for the following reasons:
Surgical therapy shows the best long-term results, particularly in young patients, and this laparoscopic
procedure is considered to be minimally invasive. Pneumatic dilatation should be seen as the second-line
therapeutic option. This method also shows good long-term results, but has a higher complication rate.
Botulinum toxin injection should only be considered for selected patients. Botulinum toxin injection can be
offered as primary therapy in elderly patients, in patients with severe comorbidity, and in patients in whom
surgery would present a high risk. Drug therapy should be seen only as a short-term and interim strategy.

In summary, definitive treatments for achalasia that have the potential of meeting satisfactory long-term
management objectives are pneumatic dilatation or surgical myotomy.

References
1. Bektas A, Yasa MH, Kusu I, et al. Flow cytometric DNA analysis, and immunohistochemical p53,
PCNA and histopathologic study in primary achalasia: preliminary results. Gut. 2000;47(suppl
III):A66-67.
2. Bortolotti M, Mari C, Lopilato C, et al. Effects of sildenafil on esophageal motility of patients with
idiopathic achalasia. Gastroenterology. 2000;118:253-257.
3. Pasricha PJ, Rai R, Ravich WJ, et al. Botulinum toxin for achalasia: long-term outcome and
predictors of response. Gastroenterology. 1996;110:1410-1415.
4. Eckardt VF, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by
pneumatic dilation. Gastroenterology. 1992;103:1732-1738.
5. Csendes A, Braghetto I, Henriquez A, Cortes C. Late results of a prospective randomised study
comparing forceful dilatation and oesophagomyotomy in patients with achalasia. Gut.
1989;30:299-304.
6. Vaezi MF, Richter JE, Wilcox CM, et al. Botulinum toxin versus pneumatic dilatation in the
treatment of achalasia: a randomised trial. Gut. 1999;44:231-239.
7. Bruley des Varannes S, Galmiche J-P. Botulinum toxin: reassessment in the treatment of
achalasia. Endoscopy. 2000;32(suppl 1):E17 [Abstract 48/03E ].
8. Patti MG, Feo CV, Arcerito M, et al. Effects of previous treatment on results of laparoscopic Heller
myotomy for achalasia. Dig Dis Sci. 1999;44:2270-2276.

Copyright © 2001 Medscape Portals, Inc.

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