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Ann Thorac Surg 1996;61:1110-1111
© 1996 The Society of Thoracic Surgeons
General Thoracic Surgery, Deaconess Hospital, 110 Francis St, Suite 2C, Boston, MA 02215.
This article from the Department of Surgery of The University of Bologna on the timing of delayed complications after esophagomyotomy for achalasia provides us with an excellent review of a timely topic, carefully researched and well presented. Although others have noted a gradual deterioration in the level of improvement of patients after esophagomyotomy with the passage of time [1, 2], none have so carefully documented the precise timing of the symptomatic deterioration. Di Simone and associates do not specifically state what type of a Heller myotomy was performed, but I assume their approach was similar to that of other European surgeons, namely a transabdominal approach with some type of an antireflux maneuver, probably a Dor partial wrap.
Of their 129 patients, only 40 were followed up for more than 10 years. In 23 of the 129 patients, 1 with a stricture, reflux esophagitis developed postoperatively; in 8 of these 23 a columnar-lined esophagus developed. In 1 of these 8, an intramucosal adenocarcinoma was diagnosed 8 years postoperatively. Complications of gastroesophageal reflux disease, therefore, predominated among the causes of postoperative symptomatic deterioration, being detected after a mean of 76.5 months. Dysphagia was the next most common postoperative sequela, occurring in 18 patients (insufficient myotomy, 11; periesophageal scarring, 7), whereas megaesophagus was the cause of persistent or recurrent symptoms in 9, in 2 of whom squamous cell carcinoma developed. The onset of symptoms in these patients occurred earlier postoperatively than was true of patients with gastroesophageal reflux disease: 1 year after an insufficient myotomy, 1
years later in patients with periesophageal scarring, and 1
years postoperatively for patients with megaesophagus. Thus 50 of the 129 patients (39%) showed evidence of severe symptomatic deterioration during a follow-up period extending to 20 years.
Our analysis of the clinical results in 68 patients indicated that 10 to 20 years after a transthoracic esophagomyotomy without an antireflux procedure only 13% had a poor result, which was more apt to follow a reoperation than a primary myotomy (27% versus 10%). The cause of a poor late result was different than that reported by Di Simone and associates in that clinically important gastroesophageal reflux disease occurred in only 4.4% of our patients during a median follow-up interval of 13.6 years. Only 1 patient was considered to have a poor result because of an inadequate myotomy, and this was apparent shortly after the operative procedure. One might question the diagnosis of an inadequate myotomy when symptoms of dysphagia recur as late as 30 months postoperatively. In our experience, such cases exhibit either persistent postoperative dysphagia or its recurrence very shortly after operation. Four patients with megaesophagus had persistent or recurrent dysphagia. None of the patients in our review were diagnosed as having periesophageal scarring. This is a finding seemingly limited to the European experience, for it has not been commented on in postmyotomy publications on this side of the Atlantic. Because the transthoracic approach predominates in the United States and the transabdominal approach in Europe, could the difference in approach have something to do with the occurrence of periesophageal scarring in the European experience? Late deterioration in the symptomatic results has also been reported by the Toronto group [2], whose patients routinely undergo a Belsey antireflux procedure at the time of myotomy. Their review consisted of 35 postmyotomy patients having a minimum follow-up of 10 years. Six of these patients, including those undergoing remyotomy, ultimately required esophagectomy and 1 a Roux-en-Y diversion and antrectomy due to disabling gastroesophageal reflux disease, the most common cause of late deterioration in their experience in spite of the performance of an antireflux procedure at the time of myotomy.
Both of these studies reinforce the findings from Bologna that late deterioration occurs after myotomy regardless of the approach employed and whether or not an antireflux procedure is done. Unfortunately, Di Simone and associates do not hypothesize on what leads to this late deterioration of results. We have postulated that even though myotomy corrects the obstruction at the distal esophagus, the underlying motor disorder in the body of the esophagus persists and may well deteriorate further with the passage of time, leading to increasing impairment of esophageal emptying, so that previously inconsequential acid reflux becomes more and more significant with the passage of time. However, we do not have objective data to substantiate this view.
Of further interest in the Italian report is the development of Barrett's esophagus in 8 patients with postoperative gastroesophageal reflux disease, presumably secondary to the myotomy, because esophagitis was not present preoperatively. Parenthetically, it should be pointed out that some untreated patients with achalasia may also have gastroesophageal reflux, which may have been present for many years before the performance of myotomy [3, 4]. In 1 of the 8 patients in the present report intramucosal adenocarcinoma developed. Including 2 such cases that we are reporting [5] and this case, there are now reports of 22 patients with achalasia and Barrett's esophagus in whom an adenocarcinoma developed up to 30 years after the diagnosis of achalasia. The risk is obviously not great, certainly not as great as the risk of squamous cell carcinoma, which we have found to be 14 times that of the normal population [6] and was true of 2 cases with megaesophagus in this report. It does, however, point out the importance of close continued surveillance of patients with achalasia. Whether or not the vigorous routine surveillance program proposed by Di Simone and associates is justified is another question, for presumably yearly endoscopy and biopsy would not be cost-effective, because the risk of squamous cell carcinoma and particularly adenocarcinoma in Barrett's esophagus is low. Obviously, patients with achalasia who are symptomatic postoperatively require special studies to determine the cause, and yearly endoscopy for those in whom Barrett's esophagus develops is clearly indicated. For the asymptomatic postoperative patient with achalasia, periodic brush biopsies may be a more cost-effective method of detecting the late development of cancer, and a case could be made for long-term surveillance beyond the 10-year limit proposed by Di Simone and associates.
The study being reported here, coupled with our findings and those of the Toronto group, support the prediction of Norman Barrett who, more than 30 years ago, wrote, ``As the esophagus of a patient who has achalasia cannot be restored to physiological normality, it is probable that the late results of this disease are less satisfactory than early postoperative assessments suggest'' [7].
References
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