Surgery for Esophageal Motor Disorders

Transcription

1 EDITORIAL Surgery for Esophageal Motor Disorders Tom R. DeMeester, M.D. Diffuse esophageal spasm is an esophageal motor disorder characterized clinically by substernal chest pain, dysphagia, or both. It differs from achalasia in that diffuse spasm produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient's general condition. True symptomatic diffuse esophageal spasm is uncommon; indeed, in the manometric laboratory, with strict adherence to diagnostic criteria, diffuse esophageal spasm is found five times less frequently than achalasia. Historically, surgery has been used to treat diffuse spasm if the patient's chest pain or dysphagia persists and does not improve with medical therapy. The usual surgical procedure is a smooth muscle myotomy of the body of the esophagus and the distal esophageal sphincter. Since the function of the latter is destroyed by the myotomy, some form of antireflux procedure is recommended to preserve the competency of the lower esophageal sphincter and to avoid marked gastroesophageal reflux after the operation. The Table catalogs the surgical experience with this disease from 1964 through the recent work of Drs. Henderson and Ryder, described starting on p 23 of this issue of The Annals of Thoracic Surgery Overall, there is a 77% incidence of success with surgical therapy, a result that falls considerably short of what one would like from an operation of this magnitude for benign disease. This assessment is underscored by another article in this issue by Drs. Orringer and Orringer entitled "Esophagectomy: Definitive Treatment for Esophageal Neuromotor Dysfunction," which appears on p 237. Why is this so? On reflection, I can think of at least four reasons. First is the difficulty of diagnosing esophageal motor abnormalities. Primary motor disorders of the esophagus are classically thought to consist of two clearly dis- From the Department of Surzerv, Universitv of Chicago Pritzker School of Medicine,-95 East 59th 'St, ChicaG, IL tinct entities, namely, achalasia and diffuse spasm-and esophageal manometry is proclaimed to be the method by which the two can be distinguished. Recently, however, there has been evidence to suggest that the differentiation of these two sharply defined disorders may not always be feasible 111. The manometric abnormalities seen in diffuse esophageal spasm affect mainly the distal one-third or two-thirds of the esophagus. The proximal segment is often normal, but as in achalasia, it too may be involved to a lesser degree. The response of the distal portion of the body of the esophagus to a single swallow is characterized by the occurrence of several nonsequential repetitive pressure peaks or giant waves of abnormally high amplitude and long duration. However, the esophagus usually retains some degree of peristaltic performance, which is not true of achalasia. A minority of patients can show impaired relaxation of the lower esophageal sphincter similar to that seen in achalasia with or without increased sphincter pressure. In most patients, the distal esophageal sphincter relaxes completely. Unfortunately, there is no general agreement as to how frequent or severe these manometric abnormalities must be to justify the manometric diagnosis of diffuse spasm, although a criterion of 3% or more repetitive or nonperistaltic responses to swallowing has been suggested [Ill. Some reports present criteria defining the actual magnitude of the abnormal contractions, but most reported tests have been performed using recording systems incapable of measuring the true magnitude of the esophageal waves. Furthermore, manometric abnormalities similar to diffuse esophageal spasm have been reported in patients with obstructing esophageal lesions, a variety of endocrine and neuromuscular disorders, chronic alcoholism, presbyesophagus, and chronic gastroesophageal reflux U21. Complicating things further is the frequent finding of spontaneous, nonperistaltic contractions in apparently normal by The Society of Thoracic Surgeons

2 226 The Annals of Thoracic Surgery Vol34 No 3 September 1982 Summary of Results of 199 Operations for Diffuse Esophageal Spasm ( ) Reference Ellis and colleagues (1964) [11 Craddock and colleagues (1966) [21 Nicks (1969) [3] Ferguson and colleagues (1969) [41 Henderson and colleagues (1974) P I Flye and Sealy (1975) [6] Leonardi and colleagues (1977) [71 Ferguson and colleagues (1977) 181 Henderson and Ryder (1982) PI Total Symptomatic Results No. of Patients Procedure Good Poor F11w-u~ Period Myotom y a Nissen short Nissen " sparing lower esophageal sphincter. 'I'ostmyotomy reflux patients requiring further operation. 31 (77%) 5 (1%) 6 (84%) 12 (92%) 12 (71%) 4 (1%) 11 (1%) 1 (91%) 13 (87%) 8 (4%) 6 (67%) 12 (63%) 13 (87%) 143 (77%) 9 (23%) l(l6%) 1(8%) 5 (29%) (2'7 1 (9%) 2 (13%) (2") 12 (6%) 3 (33%) 7 (37%) 2 (13%) 43 (23%) yr 3 mo-12 yr Not noted 6 mo-12 yr 3-48 mo Not noted 1-6 yr 4 yr (mean) 8-11 yr 7-1 yr 2-7 yr 1-3 yr individuals [13]. Therefore, it is difficult to make the diagnosis with any confidence, and the inclusion of such individuals in a surgical series of patients who have abnormalities other than diffuse spasm is not uncommon. One senses this difficulty in the current article by Drs. Henderson and Ryder as they struggle for a precise mechanism for making the preoperative diagnosis of the condition. They conclude that muscle hypertrophy is the most consistent finding, and document its presence in all the patients included in their report. But the presence of esophageal muscle hypertrophy is difficult to determine without doing a thoracotomy, and like Drs. Henderson and Ryder, we are left with the problem of making an accurate preoperative diagnosis. Since therapeutic success is based on the principle that accurate diagnosis precedes therapy, we can assume that the results of surgery for diffuse esophageal spasm will be less than satisfying until the diagnosis can be made with greater precision. The second reason for less than satisfactory surgical results is that the performance of esophageal surgery requires a change in the surgeon's thought process. He or she is no longer extirpating an organ, the function of which will be destroyed with its removal, but attempting to surgically improve the function of an organ to be left in the body. In the past, the success of esophageal surgery, like that of ulcer surgery, was based purely on the symptomatic improvement of patients, or on the information

3 227 Editorial: DeMeester: Esophageal Motor Disorders derived from a roentgenographic barium swallow. Today, we realize that a simple statement like the patient is symptomatically improved or the barium swallow is normal is not an adequate evaluation of an esophageal procedure. The postoperative presence of what appear to be esophageal symptoms may be due to another disease entity that has been misdiagnosed; likewise, the absence of symptoms may reflect a temporary placebo effect of the operation. The success of a procedure depends upon both relief from symptoms and verification that the deficiency in esophageal function has been corrected or improved by the operation. Surgeons find themselves in a somewhat difficult position here because they have shunned the development and use of diagnostic tools that can be used to assess esophageal procedures objectively. For example, the gastroenterologist now does most of the esophagoscopy and esophageal function testing. As a result, such procedures are no longer under the control of the surgeon. This situation has come about through a shift in the emphasis in surgical training from disease-oriented programs to procedure-oriented programs. Only a few programs emphasize the pathophysiology of disease and drill the trainee in all aspects of an abnormality, from diagnosis through medical and surgical management. Today, most programs direct their attention solely to surgical procedures, and graduates of such programs find it difficult to critically evaluate a procedure that is designed to improve function using existing technology. To make matters worse, the difficulty of documenting functional improvement after operation on the esophagus is compounded by other problems. Such documentation usually requires that the patient volunteer for postoperative testing. Ensuring volunteer cooperation can be difficult in today s mobile and informed-consent society. Similarly, the pattern of patient referrals can interfere with the attempt to analyze surgical results. Most surgeons find it necessary to send the patient back to the gastroenterologist who referred the patient initially. Thus, they are seldom involved in firsthand follow-up evaluation or, even more rarely, in postoperative esophageal function testing. All these factors apply pressure on surgeons that work against any energies they may wish to devote to serious evaluation of their own operative results. Given the difficulties involved, we can appreciate the effort expended by Drs. Henderson and Ryder in obtaining postoperative esophageal motility studies in 68% of their patients. The data show that their procedure reduced the distal esophageal sphincter pressure but increased the postoperative incidence of diffuse motility abnormalities from 8.1 to 96.4%. However, no statement was made concerning the manometric characteristics of this abnormal motility or its pertinence in relation to postoperative esophageal function symptoms. Consequently, an opportunity to further our understanding of the physiological effects of myotomy on the function of the body of the esophagus has been missed. The third reason for less than satisfactory results of surgery for esophageal motor disorders is the insatiable desire of surgeons to make their own modifications of technique without knowing the effects on organ function. Only recently have we begun to appreciate that when an operation is designed to improve function, surgical technique becomes paramount-and changes in technique can have a profound effect on postoperative esophageal function. No change in technique should be made indiscriminately; changes should be accepted and applied only after their effects on function have been carefully evaluated. In this area, the article by Drs. Henderson and Ryder makes an important contribution. A review of their experience indicated to them that a partial fundoplication ( antireflux procedure), either with or without a was not an acceptable means of protecting the patient against postoperative gastroesophageal reflux after a myotomy. In an attempt to correct this deficiency, total fundoplication (Nissen antireflux procedure) and gastroplasty were performed. Although these procedures corrected the reflux problem, they added resistance to the emptying of the esophagus, with resultant dysphagia. This situation led them to modify the Nissen fundoplication by making it a short gastric wrap (.5 cm), thus reducing the resistance of

4 228 The Annals of Thoracic Surgery Vol34 No 3 September 1982 the reconstructed cardia and the incidence of postoperative dysphagia. In their most recent patients, they have dropped the and have used only a short (.5 cm) Nissen fundoplication; this action has reduced the incidence of dysphagia even further without increasing the incidence of postoperative reflux. The experience of Drs. Henderson and Ryder nicely demonstrates how slight modifications in esophageal surgical technique can alter functional results. However, they would have been better clinical scientists had they been able to document these observations objectively, reporting the changes in sphincter pressure observed with each technical modification and using radioisotope esophageal clearance studies to measure the improvement in dysphagia. The fourth reason for obtaining less than satisfactory results from surgery for esophageal motor disorders is a philosophical one: the creation of a defect to correct a defect can never restore the function of an organ to normal. Therefore, a myotomy for diffuse spasm, as it is currently used, is merely palliative. It appears antithetical that we also have in this issue an article by Drs. Orringer and Orringer entitled Esophagectomy: Definitive Treatment for Esophageal Neuromuscular Dysfunction until we realize that this represents not the initial treatment but rather a salvage treatment for patients in whom previous operations designed to improve esophageal function have failed. That failures should occur is not unreasonable when one consid.ers the possibility of making an error in diagnosis, the change in thought process required to move from extirpative to functional surgery, the profound effect technique can have on postoperative function, and the application of a therapy based on the principle of making a defect to correct a defect. The pertinent question is: When should one revert to an esophagectomy as the solution instead of making another attempt at an esophageal procedure? Drs. Orringer and Orringer s response is that there is no absolute correct course of action in such patients; the decision must be based upon the surgeon s individual experience. My own experience has provided some helpful guidelines. 1. When the overriding complaint of a patient who has already undergone multiple esophageal procedures is dysphagia rather than regurgitation or heartburn, extirpation should be seriously considered. The presence of weak contractions in the body of the esophagus, or failure of the distal esophageal sphincter to relax following a primary peristaltic wave on the motility study, usually indicates extensive scarring of the distal esophagus-and a need for its replacement. The distention of a balloon in the distal esophagus initiates, through a local reflex arc, a contraction in the body of the esophagus above the balloon that can be felt manually, and a relaxation of the esophagus and distal sphincter below it. This mechanism is responsible for the so-called secondary peristaltic wave of the esophagus, which propels a bolus of food into the stomach that has failed to reach that destination with the primary peristaltic wave. The reflex is commonly damaged by performing multiple surgical procedures on the esophagus, and postoperatively these patients are required to swallow repetitively to induce a primary peristaltic wave in order to push the bolus of food into the stomach. If all three of these observations are present, I favor removal of the esophagus over attempting another esophageal procedure at the risk of another failure. Drs. Orringer and Orringer have shown that esophagectomy and replacement with an acceptable esophageal substitute can restore reasonable swallowing if properly performed by an experienced surgeon. It is wise, however, to counsel patients who undergo this procedure not to anticipate normal swallowing, lest they expect us to do what we are unable to do. The miracle is that despite surgical failures, the discipline of esophageal surgery moves forward. It is advanced by practitioners who are interested enough to take the time to report

5 229 Editorial: DeMeester: Esophageal Motor Disorders their experiences, by evaluating the validity of each reported experience, and determining where the findings fit into the whole of things through dialogue in our journals and at our society meetings. Surgeons who read or listen are continually encouraged to perform their craft more skillfully and to gather information about their own experience more scientifically. As members of one guild, we all eat from one basket, and the privilege of eating is coupled with the responsibility of returning to fill the basket with better-cultivated fruits from our own garden. So, Drs. Henderson and Ryder, and Drs. Orringer and Orringer-eat up. References Ellis FH, Olsen AM, Schlegel JF, et al: Surgical treatment of esophageal hypermotility disturbances. JAMA 188:862, 1964 Craddock DR, Logan A, Walbaum PR: Diffuse esophageal spasm. Thorax 21:511, 1966 Nicks R: The surgery of esophageal dysrhythmias. Aust NZ J Surg 39:167, 1969 Ferguson TB, Woodbury JD, Roper CL, Burford TH: Giant muscular hypertrophy of the esophagus. Ann Thorac Surg 8:29, Henderson RD, Ho CS, Davidson JW: Primary disordered motor activity of the esophagus (diffuse spasm). Ann Thorac Surg 18:327, Flye MW, Sealy WC: Diffuse spasm of the esophagus. Ann Thorac Surg 19:677, Leonardi HK, Shea JA, Crozier RE, Ellis FH Jr: Diffuse spasm of the esophagus: clinical, manometric, and surgical considerations. J Thorac Cardiovasc Surg 74:736, Ferguson TB: Discussion of Leonardi et a1 [6] 9. Henderson RD, Ryder DE: Reflux control following myotomy in diffuse esophageal spasm. Ann Thorac Surg 34:23, 1982 (this issue) 1. Kramer P, Harris LD, Donaldson RM Jr: Transition from symptomatic diffuse spasm to cardiospasm. Gut 8:115, Mellow M: Symptomatic diffuse esophageal spasm: manometric follow-up and response to cholinergic stimulation and choleresterose inhibition. Gastroenterology 73:237, Bennett JR, Hendrix TR: Diffuse esophageal spasm: a disorder with more than one cause. Gastroenterology 59273, Orlando RC, Bozymski EM, Blaylock NB: Tertiary contractions of the esophagus: a manometric study in healthy subjects. Gastroenterology 72:119, 1977