Reflux esophagitis

ESOPHAGITIDES,

STRICTURES

ReAux HARRY

WEBS

Esophagitis

W. HALE, JR., M.D. AND THEODORE DRAPANAS, M.D.,Bufalo,

From the Department of Surgery, tbe Edward J. Meyer Memorial Hospital and the University of Bufalo, Buffalo, New York.

INCE 1884 when MacKenzie [I] defined “ oesophagitis” as “acute ideopathic inflammation of the mucous membrane of the esophagus giving rise to extreme odynophagia and often to aphagia,” considerable confusion has existed in the Iiterature as to the causes, cIassification and pathoIogy of infI ammatory conditions affecting the Iower esophagus. Peptic uIcer of the esophagus was described by Tileston in 1906 [I] and by others who reported discrete uIcers in the Iower esophagus apparently arising from ectopic gastric mucosa present in the Iower esophagus. In 1929 Jackson [2] described eighty-eight cases of ulceration in the Iower esophagus noted in 4,000 consecutive endoscopies, and discussed various possibIe etioIogic factors. WinkeIstein [?I, however, in 1934 proposed that diffuse esophagitis in some of these cases without discrete uIceration was possibIy a “peptic” esophagitis, i.e., an esophagitis resuIting from the irritant action on the mucosa of free hydrochIoric acid and pepsin. Rarrett in 1950 [I] differentiated between chronic peptic uIcer occurring in the esophagus which was Iined by a continuous sheet of gastric mucosa from “ refl ux ” esophagitis. The latter entity appeared to be the result of diffuse infIammatory erosion, ulceration and scarring produced by proIonged reffux of gastric juice in the presence of an incompetent cardioesophageat sphincter and frequently associated with hiatus hernia. Whether or not scattered islets of ectopic gastric mucosa in the esophagus Journal of Surgery.

Volume 93, February,

rpg7

New ITork

in contradistinction to a continuous sheet ever give rise to peptic esophagitis is debatabIe. It is apparent, moreover, that the term “ esophagitis” requires a cIarifying adjective and that the term “peptic esophagitis” is not an incIusive term, since refIux of aIkaIine juices into the esophagus after surgical procedures such as esophagojejunostomy can aIso cause an identical type of esophagitis. Furthermore, esophagitis can aIso be produced by protracted vomiting, nasogastric intubation and pyIoric obstruction without any pre-existing anatomic incompetence of the cardio-esophagea1 sphincter mechanism. It is betieved, therefore, that the term “reffux esophagitis” is the more appropriate designation for this group of cases. The folIowing factors may be active in the production of reffux and peptic esophagitis: (I) incompetence of cardio-esophageal mechanism with sliding hernia and after surgical (2) gastric hypersecretion and the operation; peptic ulcer diathesis; (3) protracted vomiting, nasogastric intubation and pyloric obstruction; (4) ectopic gastric mucosa, as “short esophagus” or scattered islets; and (3) individual SusceptibiIity.

S

American

AND

THE ROLE OF HIATUS HERNIA The mechanics of esophagea1 hiatus hernia and its roIe in the production of esophagitis have been eIucidated by AIIison [4], Sweet [r] and others. That there is some sort of sphincter mechanism between the esophagus and stomach is generaIIy agreed. The exact nature and mode of operation of this sphincter are stiI1 moot points. Probably there are severa components to this mechanism working together in the 228

Reff ux Esophagitis normal person to allow passage of food from the esophagus to the stomach and operating effectively to prevent regurgitation into the esophagus. Allison has compared the normally active diaphragmatic hiatus to a sling which aids tile sphincter action of the esophagogastric junction by accentuating the obliquity of the entrance of the esophagus into the stomach. The fibers of the right crus, through which the esophagus enters, pass anteriorly around the lolver end of the esophagus in a reinforced arch which pulls downward and backward on the esophagastric junction. In hiatus hernia ivhere the weakness lies posteriorly, the stomach is allowed to slide into the mediastinum allowing the junction to rise out of this sling. It has been stated that there are muscular fibers within the gastric wall which also act in a similar manner to that ascribed to the diaphragmatic sling [6], and that in addition there is a mucosal ffap valve lying over the esophageal orifice in the normal person [7]. These latter mechanisms, it is stated, are overcome by elevating the esophagus or depressing the fundus of the stomach to eliminate the normal oblique entry of the esophagus into the stomach with the fundus rising well above this point. Radiologic evidence tends to show what appears to be a physiologic sphincter at a point in-the lower esophagus above the diaphragm. However, the sphincter action is mediated; it does seem to exist. Even in the normal sufficient increase in the pressure person, gradient from abdomen to chest can cause regurgitation. In the patient with disturbance of relationship of the esophagogastric junction resulting from a sliding hiatus hernia, regurgitation may occur under the abdomen-chest pressure gradient normally found, especially when this is supported or enhanced by pyloric obstruction or spasm, constriction of a herniated stomach, increase in abdominal pressure associated with obesity or merely by the assumption of the reclining position. Further evidence of the importance of reflux as a factor in the causation of esophagitis is the high incidence of this condition folIowing operations which destroy.the norma esophagogastric relationship such as the Heyroosky-Grodahl bypassing operation, esophagojejunostomy and even after the Wendel and HeIIer types of cardioplasty. Paraesophageal hernias in which the esopha-

gocardiac relationship is not altered usually accompanied by esophagitis. THE

ACID-PEPTIC

are not

PROBLEM

The importance of acid-peptic regurgitation as a causative factor of esophagitis, stenosis and stricture with or without evidence of hiatus hernia has been stressed by Winklestein [bl], Wangensteen [g] and others. Some confusion arises, however, as to whether the acid-peptic factor is important only when incompetence of the carclioesophageal sphincter mechanism exists or whether, in addition, a true ulcer diathesis with its associated hyperchlorhydric states, nervous tension and individual susceptibility may be present. We agree with the latter concept. The association of peptic duodenal ulceration has been high in our series (40 per cent) as well as in others. Frequently the symptoms of esophagitis may be identical to those present with duodenal ulcer. In many of our patients, impressively high free hydrochloric acid values were present. This appeared particularly significant in that esophagitis for the most part occurs in the older age groups in which decreased gastric acidity or anacidity is the common finding. MedicaI measures such as parasympathetic blocking agents, antacids and sedatives, al1 factors which diminish the acid factor, are usually effective in relieving the symptoms of esophagitis. Finally, symptoms of esophagitis occur in only a relatively small proportion of persons with hiatus hernia. The routine coincidenta1 demonstration of a hiatus hernia without dehnite symptoms is a rather frequent experience radiologically. CertainIy definite reflux and bathing of the Iower esophagus with gastric secretions occurs in this latter group, and the absence of esophagitis wouId tend to lend further strength to the importance of the acid-peptic factor as well as to the possibility of an individual susceptibility. MacLean and Wangensteen [g] have recently reported success in the treatment of early esophageal stricture in patients by subtota1 gastrectomy. Some of these patients did not have demonstrable hiatus hernias but many frad gastric and duodenal uIcers. Whatever the mechanism of esophagitis Ieading to stricture without demonstrabIe refIux was in these cases, it is significant that remova of the acid-bearing portion of the stomach and promotion of rapid 229

HaIe

and Drapanas

drainage caused a reversal of the progression of esophagitis. Abundant experimental evidence demonstrates the susceptibility of the esophageal mucosa to acid-peptic digestion. Selye [IO] was abIe to procluce hemorrhagic esophagitis in rats by pyloric ligation. Production of an esophagogastric anastomosis in dogs followed by histamine stimulation produces severe esophagitis, while removal of the acid-bearing portion of the stomach prior to anastomosis offers considerabIe protection against esophagitis [II]. Certainly, the hulk of clinica and experimental evidence indicates the great susceptibility of the esophagea1 mucosa to gastric juice. DIAGNOSTIC

ADJUNCTS

Refinements in diagnostic technics, particuIarIy radiologic and endoscopic, have done much to bring the problem of hiatus hernia ancl peptic esophagitis to the foreground. Together they constitute the most accurate means of making the diagnosis, for symptoms of hiatus hernia and esophagitis can mimic any disease, functiona and organic. Roentgenologists frequentIy observe hiatal hernias during an upper gastrointestinal examination as an incidental finding. In these cases, reflux is readiIy apparent with pressure on the barium-fiIIed stomach during fluoroscopy. Occasionally, however, a hiatus hernia may not he readily demonstrable roentgenographically in spite of a suspected cIinica1 diagnosis. FrequentIy in these cases, by placing the patient in the Trendelenburg position with pressure applied to the abdomen the herniated portion of the stomach fiIIed with barium may be demonstrated. The radiologic demonstration of esophagitis, however, presents a more diffIcuIt probIem. In advanced cases, stenosis and stricture formation with proximal diIatation may be shown in the lower esophagus, but if one waits for these signs, the surgical treatment is usualIy difficult. Close inspection in earIy cases may reveal fuzziness of the mucosal pattern with spasm, as evidenced by Iack of distensibiIity by a heavy barium mixture. Sometimes small areas of uIceration may be noted. The radioIogist frequently is unabIe to teII exactly where the cardio-esophageal junction Iies, the knowIedge of which becomes important to the surgeon contemplating repair. It is for these reasons that endoscopy should be an important part of the examination in 230

suspected cases of esophagitis. The information obtained from this procedure is important from four aspects: (I) the cIegree of esophagitis, uIceration and stenosis can be evaluated, if (2) carcinoma may be ruIec1 out bs present; biopsy, if necessary; (3) the Ievel of the cardioesophageal junction can be accurately established; and (4) vaIuabIe information ma)- be gained concerning the amount of fixation of the lower esophagus to the mediastinal structures. In long-standing cases in which fibrosis of the muscular coats and the periesophageai tissues have occurred, the lower esophagus will appear fixed by esophagoscopy. It may then be anticipated that repair of the hernia may be extremely difficult, if not impossible. The endoscopic examination shows a characteristic set of changes. Toward the Iower third of the esophagus, the mucosa may appear to be hyperemic and reddened and n-ill frequentI>. bIeed easily on contact with the esophagoscope. The foIds may be prominent, which may slightly impede the passage of the instrument. FrequentIy, small uIcers may be noted which at times are covered with a yellowish membrane. The cardia in these cases is lax and patulous, and the instrument passes into the stomach without deviation. This lack of deviation is diagnostic of a patuIous diaphragmatic sling and is an important sign in the occasional case in which symptoms of esophagitis are present and the radiologic clemonstration of an actual hernia has been unsuccessful. OBJECTIVES

OF

THERAPY

In a previousIy reported study [12], a variety of surgical procedures carried out in an earlier period attested to our uncertainty in the management of reflux esophagitis but offered the opportunity of studying the effects of a number of different procedures. Further studies in these and subsequent patients have led us to plan a definite program of therapy which we believe at the present time yields the best resuIts. AI1 earIy cases of esophagitis and those of miId or moderate degree shouId be given a trial of medica therapy consisting essentiaIIy of an uIcer regimen inctuding antacids, antispasmedics, bIand diet and sedatives, if necessary. Along with this program, esophageal diIatation may be indicated for mild esophagea1 obstruction due to edema and spasm of the Iower esophagus. However, when destruction of the mucosa has occurred with progressive fibrotic

RetIux

Esophagitis

stenosis ancl particularly when control of symptoms by medical means has been inadequate, surgical measures are in order. Bleeding may be a serious Ixohlcm. Wllile sudden severe exsanguinating hemorrhage is infrequent, persistent debilitating blood loss is not uncommon ancl calls for surgical intervention if medical therapy does not bring prompt relief. Perforation is a dramatic event in the history of esophagi& and demands prompt surgery. IHowever, although this complication has been reported occ:ision:~II~- it apparently is quite rare, and 1x-ehave not seen it in our series. LVhilc, as stated, the indications for surgical intervention in esophagitis are similar to those in duodenal ulcer, the application of surgery sho~~ld be promptI\. made \vhen indicated as the price of procrastination is far higher in this disease than in the case of duodena1 uJcer Il’hcn marked intractable stenosis of the accompanied by mediasesophagus occurs, tinitis and librosis, the prohlern is far greater technicaII,v and the results poorer than in the LXSC of pyloric obstruction due to duodena1 ulcer Lvhich is treated so satisfactorily by any of several measures. Surgical treatment of retJus esophagitis has as its frrst objective prevention of refJux into the esophagus by restoring as nearly as possible the normal state such as f,> the repair of an existing hiatus hernia. In this procedure we favor the technic of Allison. Second, rapid tlrainage of the esophagus is sought by relieving any obstructing condition cl&a1 to the esophagus such as pyloric obstruction. A third ofljcctivc of the surgical therapy of esophagitis is the reduction of gastric acidity. Fourth, obstruction of the esophagus itself must be relieved, and in mild cases this may be accompJishetl I,> dilation after other surgery or by more direct surgical attack. A final aim of surgical therap) is the evaluation or treatment of other associated gastrointestinal disease.

esophagitis with peptic ulceration from birth. This case has been previousIS- reported [ 12). The symptoms in most cases were regu rgitntion of food, heartburn, retrosterna1 distrr.ss, tI>.sphagia and nervousness. Hemorrhage 11as :I prominent feature in eight patients. Se\ wc TABLE I

Gastric resection and hiatal hernix. fIiatn1 repair only.. Vagotomy, pyIoroplnsty xnd hintal repair. Vagotorny, gnstroenterostonl~ and hi:lt:ll repair. Gnstrectomy only.. Esophagoplasty for stricture.. Resection of esophaged stricture with: Proximd gnstrectorny, esophngog:lstrostonly and pyIoropIasty Totd gnstrcctorny and cs~)phagojejun~)sto~~~~. Total.

14 0 X 3 0 8 j hc,

obstructive symptoms \vere noted in t\\.cntJ one patients. Encloscopic examination rcvcalecl evidence of esophngitis in several cases \vith bizarre or minimal symptomatology. As mcntioncd previously, it was believed that esophagoscopy was an important diagnostic tool in these patients. Congenitally short esophagus was found in only two cases: one in :i ne\vborn with active peptic ulceration and the other in a forty-one year oJd woman with symptoms beginning in early chilcihootl. It \vas extremcl> cIiffIcuJt in other acivanced casts, ho\ve\,cr, to determine whether congenitalI) short esophagus was present or whether inflammation tl~re to esophagitis with resuJtant scarring and contractures caused the shortening encountered. Our findings of only two casts, ho\\cver, confirm the pre\,alent feeling that congenitaII,v short esophagus is coniparativcl~~ rare’, and that it occurs in relativeIy Foungcr patients usually associated \vith symptoms dating back to childhood. Nine patients under\vent repair of tile hiatus hernia as the sole procedure when minimal or earJy esophagitis was present. T\VO of these cases, hokvever, rcquirec1 further surgery, one requiring subtotal gastrectomy a year later for a bJeeding cIuodena1 ulcer. In the other case, progressive symptoms of esophagitis occurrecl and vagotomy with pyJoropJasty was added. Gastrectomy was the sole procedure performed in three patients, all of whom had persistent symptoms which demanded subsequent repair

The present series of cases consists of 102 pat,ients with reAux esophagitis treated in the past seven and a half J’ears. Table I shows the operative procedures employed in this period. A total of sixty operations were performed. A few patients underwent more than one procedure. The age mode appeared in the fifth and sixth decade of life. One patient, a newborn, had 23’

Hale and Drapanas of the hernia. Relief \vas promptly obtained after repair in t\vo patients while the third has continued to have mild to moderate dysphagia. We believe at the present time that repair of the hiatus hernia shouId be performed routinely, if present, in all cases in Lvhich gastric surgery is being considered for peptic disease. \Ve do not entireIy agree with N’angensteen, hohvever, that subtotal gastrectomy may be s&cient therapy in cases in which stricturing of the esophagus has occurred from reflux of gastric content. An attempt to repair the hiatus, if defective, shouId be made in a11 cases. This, of course, may not be possible in the congenitally short esophagus or in cases in which severe stenosis and shortening of the esophagus has occurred from progressive fibrosis. Treatment in the Iatter type of case at best is not entireIy satisfactory once stenosis and shortening with fixation of the hernia has occurred. DiIatation of the stricture in this stage usuaIIy yields only temporary benefit. EsophagopIasty was performed in six cases for reIief of stricture earIy in the series with extremeIy unsatisfactory resuIts, three cases requiring frequent diIatations postoperatively and the other three necessitating further surgery with excision of the stenosis and intrathoracic esophagogastrectomy. There is Iittle place for esophagopIasty alone, as we see it, owing to the depth and extent of the esophageai stenosis and the Iikelihood of recurrent disease. Under these circumstances, we agree with Sweet [r4] and others that the best result in these cases wiI1 be obtained by resection of the esophagea1 stricture along with the proxima1 two-thirds of the stomach followed by intrathoracic esophagogastric anastomosis and extramucosa1 pyIoropIasty. Roux-Y esophagojejunostomy, with or without gastrectomy in this series, was attendant with muItipIe digestive disturbances requiring further medica care, and in a sense paIIiation rather than cure resuIted. FinaIIy, the Iargest operative group of cases consisted of a direct attack on the acid-producing stomach aIong with the hiata1 repair. Earlier in the series we were interested in comparing the reIative merits of vagotomy and vagotomy and gastroenterospyIoropIasty, tomy, and subtota1 gastrectomy. AIthough our operative group is too smaI1 for statistica study, we now believe that repair of a sliding hiatus hernia, in cases of refIux esophagitis 232

unrelieved by non-surgical measures, should be accompanied by subtoLl gastric resection. The rationale for gastrectomy as previously mcntioned is convincing. Certainly this is the procedure of choice in those cases with coexistent duodenal or gastric ulcer. In the present series, 40 per cent of the patients operated upon had direct evidence of active or chronic duodenal ulcer. The frequency- of this association has been stressed b\- other investigators [8, rz,r3j. ,\Ioreover, gaIIbladcIer disease, pancreatitis and maIignancy are frequcntI\- associated with this age group and it becomes’imperative that these conditions be also diagnosed and dealt n.ith. To accomplish these surgica1 aims, therefore, \ze have found the most satisfactory approach to the upper abdomen and Iower mediastinum is through the Ieft thoracoabdominal incision. The patient is placed on the operating table with his left side elevated so that the plane of the back is at 43 to Go” with the plane of the tabIe. The left arm is abducted from the trunk at a right angle and suspended from the nnesthetist’s shield. The appropriate eighth or ninth rib is then excised in its anterior one-half and the incision is extended across the chondral border and carried forward across the left rectus muscIe. If better exposure of the duodenum is necessar?-, this incision can be further extended across the midIine. The outer portion of the Ieft hemidiaphragm is then incised as needed in the direction of its muscle fibers back to the tendinous portion. The Ieft triangular ligament of the liver is sectioned and the base of the Iower lobe is freed from the diaphragm if adherent. Postoperatively, the left pleural cavity is drained with a dependent tube under water seal and removed in twenty-four to forty-eight hours. Through this approach, most of the problems, foreseen and unforeseen, can most easiIy be dealt \\ith and thorough ahdomina1 expIoration is readilv accomplished. In those cases of esophagi& occurring in the absence of hiatus hernia and inadequateI\- controIIed by medical measures, the most feasible surgical procedure would seem to be subtotal gastrectomy. FinaIIy, it should he emphasized that reAux esophagitis is a serious problem attended I~> a high incidence of crippling sequeIae which demands assiduous study and carefully planned treatment in order to avoid the more serious complications. Even so, resistant cases remain which tax the ingenuity of the surgeon and

RefIux Esophagitis Ieave room management

for further improvement of this disease.

6. BARRETT, N. R. Hiatus hernia. A review of some controversial points. hit. J. Surg., 42: 231, 1954. sphincter 7. MARCHAND, P. The gastro-esophageal and the mechanism of regurgitation. Brit. J. SW., 42: 504, ‘955. 8. WINKLESTEIN, A., WOLF, B. S., Sohl, hl. L. and MARCHAK, R. H. Peptic esophagitis with duodena or gastric ulcer. J. A. M. A., I $4: 885, 1954. s). MACLEAN, L. D. and WAZJGEXSTEE~,0. 1-I. The surgical treatment of esophageal stricture. Surp., Gynec. ~“rObst., 103: 3, 1956. IO. &LYE, H. The experimental production of peptic hemorrhagic esophagitis. Canad. M. A. J., 39:

in the

SUMMARY

The etioIogy and cIinica1 picture of esophagitis have been discussed. Based on experience with 102 cases of reffux esophagitis and predicated on the etiologic factors as understood today, a program of management has been discussed.

447. 1938.

FERGUSON, D. J., SANCHEZ-PALOMERA,E., SAKO, Y., CLATWORTHY, W., TOON, K. W. and WANGENSTEEN.0. H. Studies on exDerimentaI esoohagitis. &r&y, 28: IOZZ, 1950. L 12. STEWART, J. D., CHARDACK, W. hl. and ALFANO, G. S. RefIux esophagitis. Ann. Surg., 141: 627, ‘955. 13. BLADES, B. and HALL, E. R. The consequences of negtected hiata1 hernias. Ann. Surg., 143: 822, II.

REFERENCES I. BARRETT, N. R. Chronic peptic uIcer of the esopha-

gus and esophagitis. Brit. J. Surg., 38: 175, 1950. 2. JACKSON, C. Peptic ulcer of the esophagus. J. A. M. A., 92: 369, 1929. 3. WINKELSTEIN, A. Peptic esophagitis: a new clinica entity. J. A. M. A., 104: 906, 1935. 4. ALLISON, P. R. Reflux esophagitis, &ding hernia, and the anatomy of repair. Surg., Gynec. u Obst., 92: 419, ‘95’. g. SWEET, R. H. EsophageaI hiatus hernia of the diaphragm. Ann. Surg., 135: I, 1952.

1956. 14. SWEET, R. H., ROBINS, C. L., GEPIIAKT, R. and WILKINS, E. W., JR. The surgica1 treatment of peptic uIceration and stricture of the Iowcr esophagus. Ann. Surg., 139: 258, 1954.

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