Treating achalasia: from whalebone to laparoscope.
OBJECTIVE
To review the pathophysiology and management of achalasia.


METHODS
Peer-reviewed publications located via MEDLINE using the search term esophageal achalasia (subheadings: complications, drug therapy, epidemiology, etiology, physiopathology, surgery, and therapy) published in English from 1966 to December 1997.


METHODS
Of 2632 citations identified, 4.5% were selected for inclusion by authors' blinded review of the abstracts. New developments in the understanding of achalasia or reports of therapeutic efficacy in either controlled trials or uncontrolled consecutive series involving 10 patients or more observed for a year or longer were reviewed in detail.


METHODS
All 6 controlled therapeutic trials were included, and therapeutic efficacy in uncontrolled series was assessed by the authors extracting the patients with a good-to-excellent response from each study and calculating a pooled estimate of response rate with individual studies weighted proportionally to sample size.


RESULTS
Achalasia results from irreversible destruction of esophageal myenteric plexus neurons causing aperistalsis and failed lower sphincter relaxation. The only therapies that adequately compensate for this dysfunction for a sustained time are pneumatic dilation and Heller myotomy. The single controlled trial comparing these treatments found surgery superior to dilation (95% vs 51% nearly complete symptom resolution, P<.01). In uncontrolled trials pneumatic dilation (weighted mean [SD]) is 72% (26%) effective vs 84% (20%) for Heller myotomy. The limitation of dilation is a 3% risk of perforation; thoracotomy morbidity has been the major limitation of myotomy. Surgical morbidity has been sharply reduced by laparoscopic techniques.


CONCLUSIONS
Both pneumatic dilation and surgical myotomy are effective therapies for achalasia; laparoscopic Heller myotomy is emerging as the optimal surgical therapy.
Department of Medicine, Northwestern University Medical School, Chicago, Ill 60611-3053, USA.
A E
AE
Spiess
P J
PJ
Kahrilas
D001905:Botulinum Toxins / Q000627:therapeutic use; D018678:Cholinergic Agents / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D004106:Dilatation; D004931:Esophageal Achalasia / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery / Q000628:therapy*; D006801:Humans; D007548:Isosorbide Dinitrate / Q000627:therapeutic use; D010535:Laparoscopy; D009543:Nifedipine / Q000627:therapeutic use; D014665:Vasodilator Agents / Q000627:therapeutic use
D018678:Cholinergic Agents; D014665:Vasodilator Agents; D001905:Botulinum Toxins; D009543:Nifedipine; D007548:Isosorbide Dinitrate