Coceptos

Digestive Diseases and Sciences, Vol. 37, No. 11 (November 1992), pp. 1781-1784

CASE REPORT

Reversible Achalasia-Like Motor Pattern of Esophageal Body Secondary to Postoperative Stricture of Gastroesophageal Junction P. PARR1LLA, MD, PhD, J.L. AGUAYO, MD, PhD, L. MARTINEZ DE HARO, MD, PhD, A. ORTIZ, MD, PhD, D.A. MARTINEZ, MD, PhD, and G. MORALES, MD KEY WORDS: esophageal motor disorders; postsurgical stenosis of the cardia; pseudoachalasia.

Achalasia of the cardia is an esophageal motor disorder of unknown etiology characterized by an often hypertensive lower esophageal sphincter (LES), which does not relax after deglutition, and an aperistaltic esophageal body in which 100% of deglutitions provoke no response or the response consists of synchronic waves which, on occasions, are repetitive and reach a pressure equal or similar to normal (vigorous achalasia) (1). The term pseudoachalasia is used in cases where this motor pattern is secondary to known etiological circumstances; this has been described in Chagas' disease (2), gastric neoplasms due to myenteric plexi infiltration (3), distant neoplasms due to paraneoplastic neuropathy (4), pseudocysts of the pancreas with mediastinal involvement, probably due to compression (5), following surgical vagotomy (6), and in amyloidosis (7). The aim of this paper is to present two cases of benign stenosis of the cardia secondary to fibrosis following antireflux surgery, in which the patients developed a motor alteration in the esophageal body similar to that of achalasia of the cardia.

Manuscript received January 29, 1992; revised manuscript received April 27, 1992; accepted May 14, 1992. From the Department of Surgery, Virgen de la Arrixaca University Hospital, Murcia, Spain. Grant from the FISS (Fondo de Investigaciones Sanitarias de la Seguridad Social, Espafia). Address for reprint requests: Prof. P. Parrilla, Departamento de Cirugia, Hospital Universitario Virgen de la Arrixaca, 30120 E1 Palmar, Murcia, Spain.

CASE REPORT Case 1. A 31-year-old male had previously been operated on outside our unit for hiatus hernia and gastroesophageal reflux with pexia of the round ligament (8). Immediately after surgery, he presented with complete dysphagia, receiving parenteral nutrition until, two months after the operation, he was admitted to our hospital due to persistence of the dysphagia. Barium swallow showed dilatation of the esophageal body, reaching a maximum diameter of 5 cm, and a narrowing with complete closure at the level of the cardia. Esophagoscopy revealed a complete distal esophageal obstruction. In the manometric exploration, the LES could not be passed; in the esophageal body we observed a motor pattern characterized by the appearance of tertiary waves, often repetitive, in 100% of the deglutitions and a high percentage of spontaneous waves along the whole of the esophageal body (Figure 1). The patient underwent abdominal reoperation nine weeks after the first operation. An intense fibrosis of the abdominal esophagus was found, with complete closure of the cardia. A 2-cm resection was performed on the distal esophagus, including the fibrotic area. Reconstruction was carded out by means of an anastomosis from the end of the esophagus to the gastric fundus, after occlusion of the anatomic cardia. We added a 360~ fundoplication covering the area of the anastomosis. Pathological study of the resected segment revealed fibrosis without malignancy. There were no postoperative complications, and the patient was discharged on the tenth day. Barium swallow performed a month later showed a normal-sized esophagus. Likewise, manometry performed at the same time revealed vigorously normal motor behavior of the esophageal body (Figure 1). Between gastric and esophageal pressures, a high pressure zone of 8 mm Hg and 2.5 cm in length was identified, probably due to the antireflux surgery. No complete relaxation of this zone was ob-

Digestive Diseases and Sciences, Vol. 37, No. 11 (November 1992)

0163-2116/92/1100-1781506.50/09 1992PlenumPublishingCorporation

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Fig 1. Pre- (above) and postoperative (below) manometric tracings of patient 1.

served. Three years after operation the patient is asymptomatic. Case 2. A 77-year-old woman had been operated on 11 years previously outside our unit for hiatus hernia and gastroesophageal reflux, although details of the operation are unknown. She consulted us for dysphagia, which had progressed over the previous two years, and associated food regurgitations and sialorrhea during the last weeks. Barium swallow showed an esophageal dilatation of 6 cm diameter, associated with an epiphrenic diverticulum with a wide neck and of large dimensions (absent before the first operation) and with a narrowing of the cardioesophageal junction. Endoscopy revealed mild retention esophagitis, an epiphrenic diverticulum, a stricture of the cardia of 1.1 cm in diameter without the existence of mucosal lesions, and a normal stomach. Esophageal manometry showed a similar motor pattern to that observed in advanced cases of achalasia of the cardia (Figure 2). The lower esophageal sphincter could not be passed by the probe---not even with the aid of endoscopy---due to the presence of the diverticulum. A diagnosis of stenosis of the cardia, probably related to the previous operation and the epiphrenic diverticulum, indicated surgical treatment. At laparotomy we found intense fibrosis around some of the nonresorbable

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sutures, which narrowed the diaphragmatic hiatus in front of the esophagus. Dissection of the fibrosis and removal of the sutures liberated the abdominal esophagus without identifying vagal trunks. This liberation was continued several centimeters above the diaphragm. We added a loose Nissen fundoplication constructed over a 44-caliber bougie, but no maneuver was associated over the diverticulum. Pathological study of the resected tissue showed fibrosis without malignancy. There were no postoperative complications and the patient was discharged after eight days. The postoperative barium study showed a reduction in the caliber of the esophagus and a good passage to the stomach; the epiphrenic diverticulum had reduced in size. Esophageal manometry revealed a recuperation of the normal motor phenomena of the esophageal body, with the appearance of peristaltic waves in over 70% of deglutitions (Figure 2). Two years after surgery the patient is asymptomatic. DISCUSSION The motility o f the esophageal body m a y be altered in the presence o f a distal esophageal stricture due to uncertain mechanisms (9-12). A notable Digestive Diseases and Sciences, Vol. 37, No. 11 (November 1992)

REVERSIBLE ESOPHAGEAL MOTOR DISORDERS

Fig 2. Pre- (above) and postoperative (below) manometric tracings of patient 2.

increase has been described in the percentage of simultaneous contractions that frequently occur in over 30% of deglutitions, although normal peristalsis is maintained, similar to the motor pattern of a diffuse spasm. The cases we describe present, as a novelty, complete disappearance of esophageal peristalsis, with 100% tertiary waves, similar to the motor pattern of achalasia of the cardia; we do not know whether this motor alteration is conditioned exclusively by mechanical compression or by the damage it may produce in the vagal trunks and myenteric plexus, although the reappearance of normal esophageal motor activity after surgical repair suggests that mechanical compression is the single etiologic factor. This means that postoperative strictures of the esophagogastric junction can be added to the list of the etiological circumstances of pseudoachalasia. As far as the production mechanism is concerned, the appreciable dilatation of the esophagus together with complete recuperation of the peristalsis, present in both cases, point towards the "comDigestive Diseases and Sciences, Vol. 37, No. 11 (November 1992)

mon camera" phenomenon. In case 1, the simultaneous contractions are vigorous in nature, because the esophageal muscle maintains its contraction capacity due to the short evolution of the process (two months). However, in case 2, with several years of evolution, the esophageal muscle has lost its capacity for generating contractions of a normal amplitude. This clinical observation again calls into question the pathogenesis of achalasia of the cardia in its idiopathic form. It is not known whether aperistalsis of the esophageal body is primary or secondary to the barrier effect that results from the lower esophageal sphincter not relaxing sufficiently. The reappearance of peristalsis following Heller's myotomy in some cases of achalasia (13, 14) and also following removal of the distal stenosis in our two patients is an argument in favor of aperistalsis of the achalasia possibly being secondary to sphincter dysfunction. Future studies will be necessary to clarify this controversy.

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SUMMARY

Two cases are presented of benign stenosis of the cardia secondary to fibrosis following antireflux surgery in which the patients developed a motor alteration in the esophageal body similar to that of achalasia of the cardia. There was a complete absence of contractions in one patient, which had developed over a long period of time, and a vigorous pattern in the other patient, which had evolved over a short period. In both cases, after surgical treatment of the stenosis, normal motility in the esophageal body returned. REFERENCES 1. Sanderson DR, Ellis FH Jr, Schlegel JF, Olsen AM: Syndrome of vigorous achalasia. Clinical and physiologic observation. Dis Chest 52:508-517, 1967 2. Earlam ILl: Gastrointestinal aspect of Chagas' disease. Am J Dig Dis 17:559-572, 1972 3. Tucker HJ, Snape WJ, Cohen S: Achalasia secondary to carcinoma: Manometric and clinical features. Ann Intern Med 89:315-318, 1978 4. Feczko PJ, Halpert RD: Achalasia secondary to nonintestinal malignancies. Gastrointest Radiol 10:273-276, 1985 5. Woods CA, Foutch PG, Waring JP, Sanowski RA: Pancreatic pseudocyst as a cause for secondary achalasia. Gastro-

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enterology 96:235-239, 1989 6. Greatorex RA, Thorpe JAC: Achalasia like disturbances of esophageal motility following truncal vagotomy and antrectomy. Postgrad Med J 59:100-103, 1983 7. Lefkowitz JP, Brand DL, Schuttler MD, Brugge WR: Amyloidosis mimics achalasia's effect on lower esophageal sphincter. Dig Dis Sci 34:630-635, 1989 8. Narbona-Arnau B: The sling approach to the treatment of reflux peptic esophagitis. In Hernia, 3rd ed. LM Nyhus, RE Condon (eds). Philadelphia, JB Lippincott, 1989, pp 668-682 9. Shulze KS, Goresky CA, Jabbari M, Lough JO: Esophageal achalasia associated with gastric carcinoma: Lack of evidence for widespread plexus destruction. Can Med Assoc J 112:847-864, 1975 10. Herrera AF, Colon J, Valdes-Dapena A, Roth JLA: Achalasia or carcinoma? The significance of the Mecholyl test. Dis Dis 15:1071-1073, 1970 11. Little AG, Correnti FS, Calleja JJ, Montag AG, Chow Y-CH, Ferguson MK, Skinner DB: Effect of incomplete obstruction on feline esophageal function with a clinical correlation. Surgery 100:430-436, 1986 12. Kaye MD: Anomalies of peristalsis in idiopathic diffuse oesophageal spasm. Gut 22:217-222, 1981 13. Ponce J, Miralbes M, Garrignes V, Berenguer J: Return of esophageal peristalsis after Heller's myotomy for idiopathic achalasia. Dig Dis Sci 31:345-347, 1986 14. Bianco A, Cagnssi M, Scrimieri D, Greco AV: Appearance of esophageal peristalsis in treated idiopathic achalasia. Dig Dis Sci 31:40-48, 1986

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