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Achalasia of the Esophagus: a Surgical Disease

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Achalasia of the Esophagus: a Surgical Disease Achalasia of the Esophagus: A Surgical Disease Valerie A Williams, MD, Jeffrey H Peters, MD, FACS Achalasia is a primary esophageal motility disorder of un- signaling as it relates to the distal esophagus and LES in clear etiology. As treatment has evolved during the past 10 achalasia has been a subject of growing investigation. Nitric to 15 years, it has become primarily a surgical disease. It is oxide is thought to be the major inhibitory neurotransmit- uncommon, but not rare, affecting approximately 1 in ter controlling relaxation of esophageal smooth muscle.9,10 100,000 individuals per year.1 Occurring equally in men It has been suggested that nitronergic inhibitory neurons and women, it is an acquired condition usually diagnosed are lost in greater proportion than cholinergic neurons dur- between 20 and 50 years of age, but can occur at any age. In ing the achalasia disease process.11 1672, Sir Thomas William first described the disease as Supporting this thesis, studies in knockout mice lacking “cardiospasm” and treated the problem with dilation using nitric oxide synthase (NOS) have found high LES resting a whale sponge attached to a whale bone. It was not until pressures and absent LES relaxation.12 In humans, speci- 1927, whenAFHurst determined that the problem was mens from achalasia patients have shown complete loss of the result of an inability of the lower esophageal sphincter NOS enteric neurons and NOS activity as compared with (LES) to relax, and named the disease achalasia, a Greek nonachalasia specimens.13 Bruley des Varannes and col- term meaning failure to relax.2 Normal individuals have a leagues14 recently reported a study suggesting a serum- lower esophageal high-pressure zone, which completely re- borne substance, supporting an immunologic mechanism. laxes with initiation of a swallow. In achalasia, residual Gastric fundic muscle from normal humans was cultured pressures in the LES remain well above normal after swal- with serum from achalasia patients, gastroesophageal reflux lowing, resulting in a functional outflow obstruction at the disease patients, or normal subjects. The normal fundus gastroesophageal junction. In addition, the LES can be incubated with serum from achalasia patients had a de- hypertensive, resulting in higher than normal resting pres- crease in NOS neurons as compared with controls. In ad- sures, and the esophageal body is aperistaltic, all leading to dition, relaxation of electrically stimulated circular muscle failure of bolus transport.3 When untreated, intraesopha- contractions was substantially decreased after incubation geal pressures rise and the esophagus slowly dilates, often to with serum from patients with achalasia. the point of gross deformity.4 The most common secondary cause of achalasia is Cha- gas’ disease15,16 a systemic disease caused by infestation by the protozoan Trypanosoma cruzi. Chagas is transmitted to ETIOLOGY humans by the reduviid or “kissing bug” and infects intra- Achalasia can be primary (idiopathic) or secondary. Pri- mural neurons, causing autonomic dysfunction. Chagas’ mary achalasia is thought to result from a complete loss or disease is common in South and Central America, and relative absence of inhibitory ganglion cells in the myen- worldwide is considered to be the most common cause of teric (Auerbach’s) plexus of the esophagus. This loss creates achalasia.15,16 Pseudoachalasia occurs through infiltration an imbalance between excitatory and inhibitory neurons of the LES by cancer or by iatrogenic condition, such as a 5 causing failure of the LES to relax. Several studies have tight fundoplication or external appliance, such as a documented diminished numbers of myenteric ganglion in band.17,18 diseased esophageal specimens and demonstrated the pres- ence of lymphocytic infiltrate and collagen deposition PRESENTATION AND DIAGNOSIS 6-8 within ganglion. Given these findings, an infectious Achalasia is a slowly progressive disease. As a consequence, agent, such as a virus, and its subsequent immune response, patients often present late in the course of this disease, is thought to be the cause of the ganglion loss, but the exact when their symptoms and anatomic abnormalities have etiology remains unknown. Neurotransmission and cell become prominent. Diagnosis earlier in the disease process is possible, given conscientious attention to patients’ Disclosure Information: Nothing to disclose. esophageal reports and a high degree of suspicion. Clinical Received March 31, 2008; Revised July 14, 2008; Accepted August 13, 2008. symptoms include slowly progressive dysphagia for solids From the Department of Surgery, University of Rochester Medical Center, and liquids, regurgitation of bland undigested food, chest Rochester, NY. pain, and weight loss. Patients can also have a history sug- Correspondence address: Jeffrey H Peters, MD, Department of Surgery, Uni- versity of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY gestive of aspiration, including recurrent pneumonia or 14642. email: [email protected] chronic cough. © 2008 by the American College of Surgeons ISSN 1072-7515/09/$36.00 Published by Elsevier Inc. 151 doi:10.1016/j.jamcollsurg.2008.08.027 152 Williams and Peters Achalasia of the Esophagus J Am Coll Surg Abbreviations and Acronyms HRM ϭ high-resolution manometry LES ϭ lower esophageal sphincter NOS ϭ nitric oxide synthase Of important note, patients with achalasia can present with heartburn and, as such, mimic the presentation of gastroesophageal reflux disease. Reviewing the symptoms of 67 patients with achalasia, Spechler and colleagues19 found that 32 (48%) reported heartburn. This fact, cou- pled with diagnostic challenges in patients with early acha- lasia, including presence of a normal-caliber esophagus and artifactual LES relaxation on manometry (caused by rela- tive movement of the catheter and sphincter), likely leads to a small but real number of patients with achalasia erro- neously diagnosed with gastroesophageal reflux disease and undergoing Nissen fundoplication. In fact, it is not un- common for patients with achalasia to be treated with pro- ton pump inhibitors. The clinician should be aware of this possibility; a careful review of both the manometric study and video barium examination will almost always reveal the characteristics of achalasia. This occurs for several potential reasons. Physiologically, heartburn has been shown to be precipitated by esophageal distention.20 Different neural stimuli (luminal acid versus distention) can be interpreted by the brain as the same symptom. It has also been sug- gested that achalasia can develop in the setting of underly- ing gastroesophageal reflux disease. The retrospective symptom review referenced here showed that of those with ϭ Figure 1. Barium esophagogram in a patient with achalasia. Note heartburn, 47% (n 15) had heartburn before develop- the esophageal air-fluid level and characteristic “bird’s beak” nar- ment of dysphagia, which persisted once dysphagia devel- rowing created by a nonrelaxing lower esophageal sphincter. oped, and an additional 28% (n ϭ 9) had heartburn before development of dysphagia, which stopped after onset of particularly in early achalasia, with the radiologists’ focus dysphagia. Heartburn symptoms developed in the remain- on anatomic characteristics, such as dilation and empty- ing patients (25%) after onset of dysphagia. Interestingly, ing.21 Reviewing the symptoms and barium studies of 38 those patients reporting heartburn had considerably less patients with confirmed achalasia, Blam and colleagues21 LES resting pressures as compared with those without found a poor correlation between symptoms and barium heartburn symptoms. Both mechanisms are likely at play. study findings, which led to a diagnostic delay, particularly A simple chest radiograph can suggest the diagnosis in in patients who presented with atypical symptoms (ie, advanced cases by the absence of a gastric bubble and pres- heartburn, weight loss, cough, asthma). Atypical symp- ence of a dilated fluid-filled esophagus, generally seen as a toms were reported in 34% of patients and resulted in a right-sided posterior mediastinal shadow.4 Upper endos- median delay of 30 months before correct diagnosis, as copy should be performed in all patients to exclude ob- compared with 11 months in those who reported typical struction from tumor or stricture. Findings will commonly symptoms (dysphagia, chest pain, regurgitation). Careful include retention of saliva and undigested food associated examination of fluoroscopic or video images should be rou- with a dilated esophagus, but can be normal. A barium tinely done, which will almost always reveal a flaccid non- swallow is often diagnostic, showing a dilated aperistaltic peristaltic esophagus devoid of the usual “stripping” esophagus, presence of an air-fluid level, or a characteristic waves.22,23 “bird’s beak” appearance created by a nonrelaxing LES The gold standard for diagnosis of achalasia is esopha- (Fig. 1).4 Barium studies can be interpreted as “normal,” geal manometry, which is the most sensitive diagnostic test Vol. 208, No. 1, January 2009 Williams and Peters Achalasia of the Esophagus 153 Table 1. Manometric Characteristics of Achalasia Hypertensive lower esophageal sphincter resting pressure Incomplete or nonrelaxing lower esophageal sphincter Aperistalsis of the esophageal body Esophageal pressurization: elevated lower esophageal baseline pressure available.3,17 Manometry is especially helpful in establish-
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