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Some Recent Advances in Surgery of the Esophagus
Some Recent Advances in Surgery of the. Esophagus IVAN D. BARONOFSKY, M.D., PH.D., F.A.C.S.*
CARDIOSPASM CARDIOSPASM was
first described by Purden. 1 The disease is characterized by spasm of the lower esophagus and cardia, delayed passage and retention of food, and dilatation of the proximal esophagus. The most likely cause, as borne out by observation of the esophagus during roentgen examination, is a disordered neuromuscular mechanism. Roentgenologically the important point of obstruction is at the lower end of the esophagus. Whether the inferior constrictor, muscle or the vestibule of the esophagus is involved is not known, but a definite disorder of the peristaltic activity to the point of violence of the normal peristaltic waves is seen by the roentgenologist. Treatment for cardiospasm, therefore, should be aimed at the point of obstruction, the lower end of the esophagus. Whether the presence or absence of Auerbach's plexus is the cause of this disturbance has not yet been clearly defined. Biopsies of muscle layer have revealed Auerbach's plexus to be present in some patients with cardiospasm and absent in others. 2 Recent experimental evidence would suggest that cardiospasm may not only result from a destruction of the ganglion cells of Auerbach's plexus but also from 'a complete denervation of the narrowed segment. 3 Several decades ago Knight4 showed that some of the confusion that had resulted from previous experimentation in the production of cardiospasm in animals was a result of the type of experimental animal used. The cat, apparently, is the animal of choice. Diagnosis is often difficult. The Mecholyl test6 has been helpful. When a small dose of a cholinergic stimulant is administered subcutaneously (Mecholyl or Urecholine), severe retching or vomiting may result. Under the fluoroscope, deep phasic contractions are noted in the body of the From the Departm.ent of Surgery, The Mount Sinai H ospital, New York, N. Y. • Clinical Professor of Surgery, College of Physidans and S:p,rgeons, Columbia UnilJersity; Surgeon-in-Chief, The Mount Sinai Hospital.
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Fig. 292 Fig. 293 Fig. 292. Cardiospasm associated with hiatus hernia. Note arrow pointing to hernia. Also note waves in the esophagus. Fig. 293. Postoperative film following Heller procedure showing hernia reduced. There is still some element of spasm; however, barium moves through freely.
esophagus. This type of reaction usually does not occur in patients with obstruction of the lower end of the esophagus due to other causes. This abnormal response has been attributed to the denervation of the esophageal musculature in cardiospasm. A treatment that has been used in cases of cardiospasm in achalasia has been the-.divulsion'~of the muscle of the inferior constrictor of.,the , esophagus. This :.can be done by endoscopic dilatation by one of the many types of inflatable balloons presently on the market. Satisfactory results have been obtained in as high as 85 per cent of the cases. However, it is the feeling of many surgeons, because the procedure is blind, and because the result may not be lasting, that perhaps it is not the treatment of choice. A conservative approach may be attempted and if it is ineffective, surgical therapy can be instituted (Figs. 292-293). The most effective surgical approach is the simple myotomy of Heller. When the Heller operation is performed, however, emphasis should be given to the correction of the hiatus hernia which is inevitably present. The poor results following the Heller procedure, though few, are usually due to an esophagitis that probably has been caused by a hiatus hernia either pre-existing and unsuspected, or produced in the course of operative manipulation. This hernia must be repaired in order to insure a good result. It has been suggested that a Finney pyloroplasty be used after the Heller operation to prevent esophagitis. 6 W angensteen 7 has recently modified the performance of the Heller procedure by placing an inflatable balloon inside the esophagus through a gastrostomy opening. His present results, he finds, are improved over
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his earlier results. This approach seems logical since it does rupture all the small fibers of the cardioesophageal junction. REPLACEMENT OF THE ESOPHAGUS WITH VARIOUS PORTIONS OF THE BOWEL
In recognition of the fact that many symptoms can result from the presence of the stomach in the chest, and also that various complications can result from the loss of the sphincter of the lower end of the esophagus, various loops of bowel have been substituted for the esophagus or interposed between the esophagus and the stomach. Thus, as will be discussed later, segments of the right and transverse colon and of jejunum have been utilized. 8, 9, 10 These bowel segments, if carefully prepared, may be used to replace any form of diseased esophagus. PEPTIC ESOPHAGITIS
It has been estimated by various authors that about 20 per cent of people normally have regurgitation of gastric contents into the esophagus. This was determined by roentgen studies on patients admitted to a hospital for other diseases. It is entirely possible, therefore, for a peptic esophagitis to occur in people with normal anatomical relationships in the region of the cardioesophageal junction. In general, however, it is agreed that the sphincter mechanism at the lower end of the esophagus, whatever it be, is usually altered when esophagitis is present. If the mechanism is not altered, then acid must be secreted on the vulnerable esophageal mucosa in other ways. In 1935, Winkelstein described peptic esophagitis as a clinical entity associated with duodenal ulcer. Though he did not describe the common feature of an associated hiatus hernia, it is now recognized that hiatus hernia destroys the normal cardioesophageal sphincter mechanism and, therefore, allows for retention and regurgitation of peptic juice and, consequently, esophagitis. Thus, when esophagitis is present as a result of hiatus hernia, correction can be easily obtained by the repair of the hiatus hernia. Carver and Sealyll pointed out that in their series of 130 eases of peptic esophagitis, the following three factors were causative: (1) hiatus hernia (76 per cent); (2) surgical excision or destruction of the cardiac sphincter (13 per cent); (3) persistent vomiting (11 per cent). During the past few years, a more intimate knowledge of the pathology and physiology of esophagitis has been obtained. Because of the recent contributions of Barrett,12 Allison and Johnstone 13 and Wolf et a1.,14 a clearer picture of the classification of esophagitis has been obtained and a better therapeutic attack is now possible. Barrett recently described a cylindric type of epithelium present in the distal esophagus of certain people with esophagitis which resembles the epithelium of the cardiac region of the stomach, except that the glands are relatively atrophic and do not show parietal cells or secrete
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Fig. 294. Diagrammatic representation of types of peptic or reflux esophagitis. A, Severe extensive peptic esophagitis with marked narrowing of long segment proximal to a small hernial sac. There is usually a history of a duodenal ulcer, operation and/or intubation. A pre-existing hernial sac is not a prerequisite. The marked narrowing at the onset iR due to spasm and inflammatory exudate but may persist and become fibrotic. B, Diffuse peptic esophagitis of a moderate degree as seen with uncomplicated direct hernias and reflux. Lack of distensibility of minimal degree over a variable distance of distal esophagus. In some cases, superficial ulceration or mUltiple ulcerations are present in the terminal portion of the esophagus. C, Peptic esophagitis with superficial inflammatory changes with or without erosions or ulceration limited to a short segment of the terminal portion of the esophagus. The involved segment may be quite short and the evident inflammatory changes may not involve the entire circumference. D, In addition to a direct hiatus hernia, the distal esophagus over a distance of several centimeters is lined by cylindric or Barrett type of epithelium. This has been referred to as gastric-lined esophagus or heterotopic gastric mucosa. In this case, however, the inflammatory and ulcerative changes are indicated as being confined to the terminal portion of the squamous-lined part of the esophagus, that is, these changes are noted immediately proximal to the gastric-lined portion of the esophagus which itself shows no evident involvement. (Courtesy of The American Journal of Roentgenology.)
pepsin. This condition is "heterotopic gastric epithelium in the esophagus" or gastric-lined esophagus. He pointed out that the heterotopic epithelium was susceptible to ulceration under the influence of acid gastric juice and that chronic peptic ulcer of the esophagus showed, in addition to the ulceration, the presence of heterotopic epithelium by biopsy. Therefore he suggested the term "chronic peptic ulcer of the esophagus" for ulceration in heterotopic epithelium and a new term, "reflux esophagitis," for inflammation and ulceration of a normally squamous lined esophagus~in association with a hiatus hernia. In effect, from the foregoing, one might suggest that the peculiar entity of "congenitally short esophagus" would fall in the classification of Barrett's heterotopic gastric mucosa. Wolf et a1. l4 have recently described the roentgen findings in the entities previously mentioned (Figs. 294, 295). By describing these in conjunction with biopsies taken
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Fig. 295. Diagrammatic representation of types of peptic ulceration in association with gastric-lined esophagus or Barrett epithplium. A, Peptic ulceration within the gastric-lined segment. Moderate narrowing or limited distensibility is usually seen at the level of the ulceration. B, Peptic ulceration at the distal margin of the gastriclined segment with gastric rugae at its distal edge. C, Peptic ulceration at the proximal margin of the gastric-lined segment or within a region of mixed epithelium, that is, a combination of Barrett and squamous epithelium. An ulceration in this region may be referred to as marginal since squamous epithelium is present at its proximal edge. D, Peptic ulceration in the terminal portion of the esophagus which is lined by mixed epithelium or was the seat of minimal heterotopia or a very short gastric-lined segment of esophagus. This type of case creates difficulty in terminology since at different places about the ulceration there may be found normal gastric epit.helium, Barrett epithelium and squamous epithelium. The t.erm "marginal" has also been applied to this type of case. It is essentially similar to the situation diagrammed in C except there is no remarkable length of the distal esophagus that is lined by an atypical cylindric epithelium. It is evident that the roentgen findings corresponding to D may resemble those corresponding to B, as well as those corresponding to C in Figure 292. It is, therefore, often necessary to use the term peptic ulceration independent of the nature of the epithelium or until its nature is determined by microscopic examination. Moreover, more diffuse inflammatory changes are often present in the gastric or in the squamous-lined segments or in both which obscure the demarcations between individual segments. (Courtesy of the American Journal of Roentgenology.)
at the various levels of the esophagitis, a clear picture of the disease entity was obtained. Thus, the Barrett ulcer is observed to have gastric mucosa at the line of the diseased area, while the more common reflux esophagitis has squamous epithelium. The treatment of esophagitis is related to its pathological nature and cause. Thus, esophagitis from reflux associated with the ulcer diathesis or gallbladder disease uniformly responds to treatment of the ulcer or removal of the gallbladder. Esophagitis (usually of the squamous-lined mucous membrane) due to esophageal hiatus hernia and loss of competence of the cardioesophageal sphincter is usually treated by repair of the esophageal hiatus hernia. Esophagitis due to a Barrett's ulcer must be approached a little
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differently. Because of the presence of heterotopic gastric mucosa above the diaphragm and an inability to replace this gastric mucoSa below the diaphragm, more radical treatments are in order. It is necessary to excise the gastric mucosa above the diaphragm and reanastomose the esophagus to the stomach in such a manner that the stomach lies below the diaphragm and the esophagus above. This can be accomplished by the interposition of segments of jejunum or colon (right or transverse). Wangensteen had previously suggested that gastric resection alone would suffice to alleviate the symptoms and signs of peptic esophagitis in many cases and recently reported excellent long-term results with this procedure. 16 The procedure, he claimed, was less formidable than any mentioned and excellent results had been achieved over a long period of time on observation. In those cases in which a severe stricture was present, a repeated dilatation had been necessary up to the time of gastric resection. Following gastric resection, few, if any, dilatations were necessary. Ellis16 has suggested a rather extensive procedure consisting of vagotomy and resection of the stricture and the distal stomach with esophagogastrostomy and gastroduodenostomy. HIATUS BERNIA
The problem of surgery for hiatus hernia resolves itself upon the attitude of the medical profession toward hiatus hernia. Too many physicians assume a rather casual attitude toward this potentially grave disease, probably stemming from the observation that hiatus hernia is a rather frequent finding on routine x-ray examination of the upper intestinal tract. However, there is a reported recurrence rate of anywhere between 10 and 30 per cent and a symptomatic recurrence rate as high. Baronofsky et al.17 have previously pointed out that the fate of hiatus hernias, as watched over a long period, is one of gradual enlargement in a high percentage of cases. This, coupled with the fact that hemorrhage, stricture and esophagitis are common accompaniments of hiatus hernia, should lead to earlier surgery on these cases. I believe that a hiatus hernia of moderate size should be treated surgically. In a similar study, Blades and Rall18 emphasize the fact that symptomatic hiatus hernia represents a serious lesion. In their series of 66 cases, 32 of the patients with asymptomatic hiatal hernia had dangerous complications including bleeding in 22, esophageal stricture in eight, carcinoma in one and perforation in one. It is to be emphasized that the main symptoms of hiatus hernia, common to all the types, are caused by esophagitis, and that a hiatus hernia is generally considered the most frequent cause of reflux esophagitis. Lindskog and Klein19 report that, of 41 patients with sliding hiatus hernia, 29 per cent had esophagitis. In our own early series, 61 per cent of the patients had esophagitis, if both esophagoscopic and roentgenologic evidence are included.
Some Recent Advances in Surgery of the Esophagus
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Fig. 297
Fig. 296. Preoperative x-ray showing large hernia above the diaphragm.
Fig. 297. Postoperative film showing repair with complete replacement of the stomach below the diaphragm.
More and more articles show the true percentage of symptoms associated with hiatus hernia. Thus, in a most recent series,20 as high as one-third of the patients seen had bleeding as a presenting symptom. Esophagoscopy was performed in all cases. Forty-three per cent of their cases had esophagitis, three with ulceration. Two had stricture and one had an associated ulceration and stricture. Of these 65 patients, onethird had peptic ulcer. Since the hiatus hernia allows regurgitation of acid peptic juice into the esophagus, those ulcer patients with high acid have more profound symptoms from the hiatus hernia. Considerable discussion has centered about the presence of the short esophageal type of hernia. Humphreys21 believes that a true congenitally short esophagus is characterized by the fact that the intrathoracic portion of the stomach derives its blood supply from the thoracic aorta and not from branches of the celiac artery. Other authors believe that a congenitally short esophagus, in reality, is a variation of Barrett's ulcer with heterotopic gastric mucosa. The treatment of hiatus hernia has received considerable attention in the literature (Figs. 296, 297). Knowledge of the anatomy of the area is most instrumental in obtaining good repairs. Allison22 has described a method of repair emphasizing the anatomical points of importance. The right and left diaphragmatic crura arise from the bodies of
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the first three or four lumbar vertebrae. The left fans out onto the diaphragm and does not contribute to the hiatus. The right crus forms the entire hiatus. It is the absence of the right crus that allows for diaphragmatic hernia. In the posterior mediastinum behind the esophagogastric junction there is a fat pad which is unsupported and unprotected. When this area is weakened, the herniated stomach passes upward and posteriorly, carrying with it the peritoneum and the endoabdominal fascia (comparable to the transversalis fascia in the lower abdominal wall). This fascia, in the area of the esophageal hiatus region, is called the phrenoesophageal ligament. It reflects onto the esophagus with the peritoneum, just as the peritoneum recurs to form the "sac" of the diaphragmatic hernia. Frequently this ligament is a tenuous, almost ethereal membrane of little value. After considerable experience with diaphragmatic hernia repair, I am of the opinion that either the abdominal or transthoracic approach can be used to perform a satisfactory operation. It must be mentioned that, with the abdominal approach, other diseases may be encountered and attacked at the same time. The transthoracic approach should be reserved for those cases where exposure may be a problem owing to obesity, the configuration of the thoracic cage, previous upper abdominal operations, etc. More important than the choice of approach is the attention to detail. The crural fibers must be carefully delineated for a considerable extent, and (in disagreement with a recent paper) the peritoneum should be entered by a radial incision made in the diaphragm just anterior to the spleen. A finger or a forceps is then inserted along the diaphragm until it reaches the sac of the diaphragmatic hernia. The sac can then be incised, using the intraperitoneal forceps as a guide. A Penrose drain is then placed around the esophagus from the thoracic side, and this is in turn brought through the hiatus to the intraperitoneal side, and tension exerted from below. When this tension is put on the esophagus, the crura are delineated by the forward pull of the drain. The crura are joined by interrupted silk mattress sutures behind the esophagus. Usually, tension on the first suture, which is the lowest or juxta-aortic one will outline the entire crural arch and only three or four more sutures will be required. Good, deep bites are taken and the crura approximated snugly, but not so tightly that the muscle is strangulated. The orifice immediately around the esophagus should admit a fingertip between the last suture and the esophageal wall. Sutures are then placed between the esophageal musculature or the remnant of the phrenoesophageal ligament and the diaphragm as it is formed by the crura. Thus the esophagus is fixed to the diaphragm much as one would fix an ileostomy as it comes through the abdominal wall. The rent in the diaphragm is then closed after hemostasis is observed. By using
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these simple maneuvers, excellent repair of the diaphragmatic hernia can be obtained with a low recurrence" rate. In those cases in which there is some shortening of the esophagus due to heterotopic gastric mucosa or a true congenital shortening of the esophagus, every effort should be made to bring the diaphragm above the cardioesophageal junction. This in itself will cure a percentage of cases. Effler and Groves23 recommend transplanting the esophagus anteriorly into a new hiatus and also the crushing of the phrenic nerve. Fisher and Johnson24 have recently reported on seven patients with short esophageal hiatus hernias which they treated by distal gastric resection. Wangensteen has proposed the use of distal gastric resection plus repair of the hiatus hernia in those cases where stricture is secondary to a hiatus hernia. He has reported singular success with this maneuver in cases in which repeated endoscopic' dilatation had to be used previously. When strictures result from the severe reflux esophagitis due to longstanding hiatus hernia, another very difficult problem is introduced. These strictures are a result of an esophagitis in a squamous-lined esophagus. Lindskog and Kline advise distal esophagectomy, combined with vagotomy, extensive proximal gastric resection and gastrojejunostomy for irreversible stricture formation. Others advocate resecting the involved area and interposing a jejunal or colonic segment between the esophagus and the stomach when stricture has occurred. Earlier treatment of hiatus hernias should obviate some of these difficulties. CAUSTIC STRICTURES OF THE ESOPHAGUS
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The pathological changes and treatment of lye burns of the esophagus have been well described by Burford. 25 • 26 In general, during the acute phase of the burn, it has been suggested that intravenous feedings, along with supportive therapy and antibiotics should be used. When the acute phase was over, oral feedings were allowed and, at about the third week, endoscopy with dilatation was attempted. On the basis of evidence presented, it would appear proper to give the esophagus complete rest in the early stages of a burn in order that early epithelization may take place. With epithelization, of course, comes complete healing. Lortat-Jacob27 administers corticosteroids immediately. He believes that even old strictures, when treated with cortisone, can regain a certain elasticity and that in some instances operation can be delayed or avoided. Though he immediately examines these patients endoscopically, evidence has shown that this is not particularly efficacious, as it does destroy the epithelium. Perhaps it would be wise to start cortisone therapy immedil1tely on these individuals and delay dilatation until later. Those strictures which do not respond promptly to dilatation should be operated upon without delay. Excellent results have ooen obtained recently with the interposition of a segment of right colon between the cervical esophagus and the stomach28 (Fig. 298).
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Fig. 298. A, X-ray of stricture of the esophagus due to ingestion of lye. B, Lateral view of the chest. Barium swallow in right colon which has been anastomosed to the upper esophaguB and the stomach. Arrow points to the stomach anastomosis. C, Posteroanterior view of the chest showing the right colon as it courses from the esophagus to the stomach.
It would appear that this is the procedure of choice if conservatism fails. The fate of the remaining burned esophagus, when it is by-passed, is one which has received some attention. It has been stated that carcinoma not infrequently arises in all burns of the esophagus and, therefore, excision at the time of reconstruction of the esophagus should be considered. ESOPHAGEAL RINGS
Schatzki and Gary29 and Ingelfinger and Kramer80 have described a. localized ringlike narrowing of the lower end of the esophagus. These authors have pointed out that the caliber of this ring might be reduced to a point where the swallowing of a large bolus of food might cause
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Fig. 299. Localized ring narrowing at the lower end of the esophagus. Though this is static in character it has given no symptoms.
obstruction. The ring is actually a thickening of a muscle area of the esophagus. Motion picture studies by Wolf of a patient with such a ring confirm the observations of Schatzki that this ring is static in character rather than contractile and that it is unchanging in location in relation to the esophagus. However, its relationship to the level of the diaphragm may change with filling and emptying of that region (Fig. 299). When it becomes incompletely distensible and replaces a normally distensible ring, it may become a surgical problem. 31 Sectioning of the muscle fibers was performed as one would in a pyloromyotomy. Continued study of the esophagus will probably reveal more pathological conditions resulting from changes in the neuromuscular structure of this organ. ESOPHAGEAL VARICES
Bleeding esophageal varices have a poor prognosis. It would appear from the literature that more than 50 per cent of patients with portal hypertension and varices die within a year or two from liver disease or hemorrhage or both. Baronofsky and Wangensteen32 have shown that not only is the varix itself important in the bleeding of esophageal varice!!! but also the acid peptic factor. It was noted that gastrectomy might prevent bleeding when other measures had failed. The close association between the bleeding due to gastric and esophageal varices and gastroduodenal ulcer was also noted. Recently, Enquist and Glied-
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man 33 reviewed autopsy data of 476 patients with cirrhosis and 1000 controls who had essentially normal livers. Spleen size seemed to be a good indication of the degree of portal hypertension that existed during life, whereas liver size was not. Upper gastrointestinal lesions which commonly served as sources of hemorrhage were found more often at autopsy in patients with cirrhosis than in those with normal livers. Thirty-four per cent of the patients with cirrhosis who succumbed to hemorrhage had some extravariceal source of bleeding; in 21 per cent, a lesion was present that could as well have been the source of hemorrhage as the varices; and in only 45 per cent of these patients did the bleeding originate in esophageal varices. The most common source of extravariceal bleeding in cirrhotic patients was the stomach. It would appear from this study that when the source of uncontrolled intestinal bleeding in a patient with cirrhosis has not been determined an abdominal approach should be used when surgery is indicated. This would permit the effective treatment of upper gastrointestinal hemorrhage regardless of the site of bleeding, since even if bleeding esophageal varices were found to be the cause, transgastric ligation could be employed. If it is definitely established that bleeding is due to esophageal varices, and if other means such as a Sengstaken balloon are ineffective, a transthoracic approach can be used. C. Stuart Welch34 prefers the transabdominal approach. George Crile, Jr.,35 in discussing transesophagealligation, noted that in patients with good liver reserve the mortality and morbidity were low. Thus, in six of nine patients with extrahepatic blocks where this procedure was used, bleeding was controlled for from four to nine years. It would also appear that, in patients with extrahepatic blocks who are bleeding massively, transesophagealligation may, ina certain percentage, protect them without any other future treatment. Those patients with extrahepatic block who continue to bleed following varix ligation may be subjected to an interposition operation using a segment of jejunum or colon, thus removing acid initiation from the varix. Transesophagealligation as a permanent treatment in patients with intrahepatic block has resulted in a high mortality rate and frequent recurrence of bleeding in the survivors. Bleeding due to intrahepatic block can usually be controlled with the Sengstaken-Blakemore balloon. A portacaval shunt can then be accomplished as an elective procedure. O'Sullivan and Payne36 have subjected patients to emergency portacaval shunts following the temporary control of hemorrhage by the use of a balloon, but the mortality was high. The condition of the liver is most important in selecting patients for portacaval shunts. If the patient is not jaundiced, and has a serum albumin above 3 grams per 100 ce., he should prove a fairly good surgical risk. Ascites, if present, increases the severity of the risk but should not be a deterrent to operation if the patient's general condition is otherwise satisfactory. Neurologic symptoms related to ammonia intoxication have been
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discussed by various authors. Hallenbeck and Shocket37 noted that in their series neurologic symptoms did not develop after splenorenal anastomosis but that neurologic symptoms of varying severity did develop subsequently in six out of 23 patients who survived end-to-side portacaval anastomosis. None of the six had any recognizable neurologic symptoms before surgery. These neurologic symptoms are related to increased blood ammonia levels following the ingestion or the breakdown of nitrogenous products in the intestine. In the presence of an open portasystemic shunt, no further breakdown of the ammonia into urea occurs, because the liver which normally performs this function is by-passed. The blood ammonia level increases, resulting in neurologic symptoms. 38 Nachlas,39 in reviewing portacaval shunts done for bleeding esophageal varices, questions the efficacy of this procedure because of the high rate of recurrent bleeding. Koop and Roddy 40 have utilized the colon as a replacement for the distal esophagus and proximal stomach in the management of bleeding varices in children, and other authors have used the jejunum to separate the acid factor from the varix. Arterialization of the liver has long been suggested as a method of regeneration of the cirrhotic liver, but experimental results do not support. this theory and in fact demonstrate progression of the cirrhosis. CARCINOMA OF THE ESOPHAGUS
The results of treatment in carcinoma of the esophagus have not improved much in the past few years. Mustard41 reported a series of 381 patients with only a 3 pel' cent five year survival rate, including operated and unoperated patients. Of 87 untreated patients, only two lived two years; none survived two and a half years. Of 125 patients treated with high voltage irradiation, only one survived five years, and this patient had a squamous cell carcinoma of the posterior wall of the hypopharynx. Mustard feels that cobalt therapy may prove as efficacious as surgery for carcinoma of the esophagus as one gains more experience with this modality. The five-year survival rate for patients who had complete excision and reconstruction of the esophagus was 19.4 per cent and this rate is higher for lesions of the lower third. Wider resections of the esophagus may be necessary because of submucosal spread. In order to approach more radically the lesions of the superior mediastinal and cervical segments of the esophagus, Waddell and Scanne1l42 describe an anterior approach which utilizes a sternal splitting incision. Provided that operability is determined, the stomach is brought up into the anterior mediastinum and anastomosed to the esophagus in the neck. The advantage of this surgical approach is that it allows easy and direct exposure of the esophagus from the aortic arch to the pharynx and that gross extensions of the tumor to lymph nodes and cervical and upper mediastinal areas can be removed readily with a
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primary tumor. A logical modification has been proposed by Scanlon43 as a two stage operation and has been accomplished by Watson44 and his group. This modification which Scanlon suggests as a two stage procedure is a total esophagectomy through a right thoracic approach combined with proximal gastrectomy and splenectomy. The proximal esophagus is brought out as a fistula in the neck, and a gastrostomy is performed for feeding purposes. Six months later, after irradiation, continuity is established by performing esophagocologastrostomy using the right colon as a transplant through the substernal tunnel. Watson, Neville 4fi and others have used the right colon for this purpose. A combination of surgery and extensive x-ray therapy may offer a new hope for the cure of carcinoma of the esophagus. TRACHEOESOPHAGEAL FISTULA
Much has been accomplished in the field of tracheoesophageal fistula in the last decade. Cameron Haight recently published his observations in over 200 patients with atresia of the esophagus46 and recommends primary anastomosis of the two segments of the esophagus whenever possible. For esophageal reconstruction he suggests using the right colon or the right half of the transverse colon via a substernal tunnel. The ages of his seven patients varied from two to seven year~. Excision of the distal segment of the esophagus is advisable. Mahoney and his group have also utilized this procedure in reconstructing the esophagus initially when an end-to-end anastomosis could not be done or in those instances where late reconstruction was necessary. The approach that has been suggested by both Haight and Potts47 is a right transpleural approach, whereas the original approach was extrapleural. REFERENCES 1. Purden, T.: Extraordinary Case of Dilatation of Esophagns Forming a Sac, Extending from Two Inches Below the Pharynx to Cardiac Orifice of Stomach. London M. & Physiol. J. 46: 540, 1821. 2. Hawthorne, H. R., Frobese, A. F. and Nemir, P. Jr.: Surgical Management of Achalasia of Esophagus. Ann. Surg. 144: 653, 1956. 3. Deloyers, L., Cordier, R. and Duprez, A.: New Approach to Physiology of 80Called Cardiospasm: Experimental Production of Cardiospasm in Cats After Destruction of Auerbach's Plexus. Ann. Surg. 146: 167, 1957. 4. Knight, G. C. : Relation of Extrinsic Nerves to Functional Activity of Esophagus. Brit. J. Surg. 22: 155, 1934. 5. Kramer, P. and Ingelfinger, F. J.: Esophageal Sensitivity to Mecholyl in Cardiospasm. Gastroenterolgy 19: 242, 1951. 6. Herron, P. W., Thomas, G. 1. and Merendino, K. A.: Experimental Approach to Cardiospasm: Appraisal of Finney Pyloroplasty in Prevention of Esophagitis Following Heller Myotomy. J. Thoracic Surg. 34: 609, 1957. 7. Wangensteen, O. H.: Technique of Achieving an Adequate Extramucosal Myotomy in Mega-esophagus (Achalasia, Cardiospasm, Dystonia). Surg. Gynec. & Obst. 105: 3, 339, 1957. 8. Sherman, C. D. Jr., Mahoney, E. D., Dale, W. A. and Stabins, S. J.: Intrathoracic Transplantation of Right Colon for Esophageal Reconstruction. Cancer 8: 1198,' 1955.
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9. Harrison, A. W.: Transthoracic SIlUIlI Bowel Substitution in High Strictures of Esophagus. J. Thoracic Surg. 18: 316, 1949. 10. Merendino, K. A. and Thomas, G. I.: Jejunal Interposition Operation for Substitution of Esophagogastric Sphincter. Surgery 44: 1112, 1958. 11. Carver, G. M. Jr. and Sealy, W. C.: Peptic Esophagitis. A.M.A. Arch. Surg. 68: 286, 1954. 12. Barrett, M. R.: Chronic Peptic Ulcer of Esophagus. Brit. J. Surg. 38: 175, 1950. 13. Allison, P. R. and Johnstone, A. S.: Esophagus Lined with Gastric Mucous Membrane. Thorax 8: 87, 1953. 14. Wolf, B. S., Marshak, R. H. and Som, M. L.: Peptic Esophagitis and Peptic Ulceration of Esophagus. Am. J. Roentgenol. 79: 5, 741, 1958. 15. MacLean, L. D.: Etiology and Treatment of Esophagitis. Minnesota Med. 783. 1958. 16. Ellis, F. H. Jr.: Physiologic Operation for Ulceration and Stricture of Terminal Esophagus. Proc. Staff Meet. Mayo Clin. 31: 615, 1956. 17. Baronofsky, I. D., Sprafka, J. L. and Azad, M.: Fate of Esophageal Hiatus Hernia: Clinical and Experimental Study. Surgery 36: 3, 519, 1954. 18. Blades. B. and Hall, E. R.: Consequences of Neglected Hiatal Hernias. Ann. Surg. 143:822, 1956. 19. Lindskog, G. E. and Kline, J. L.: Problem of Hiatus Hernia Complicated by Peptic Esophagitis. New England J. Med. 257: 3, 110, 1957. 20. Hoffman, R. F., Cruze, K. and Byron, F. X.: Symptomatic Hiatus Hernia. J.A.M.A. 169: 2, 1959. 21. Humphreys, G. H. II, Ferrer, J. M. Jr. and Wiedil, P. D.: Esophageal Hiatu! Hernia of Diaphragm; Analysis of Surgical Results. J. Thoracic Surg. 34: 6, 749,1957. 22. Allison, P. R.: Reflux Esophagitis, Sliding Hiatal Hernia and Anatomy of Repair. Surg. Gynec. & Obst. 92: 419, 1951. 23. Effler, D. B. and Groves, I,. K.: Short Esophagus; Mechanism of Pain and Surgical Therapy. A.M.A. Arch. Surg. 75: 4, 639,1957. 24. Fisher, H. C. and Johnson, M. E.: Esophageal Hiatus Hernia; Manifestation of Peptic Esophagitis; Treatment by Gastric Surgery. A.M.A. Arch. Surg, 75: 4, 660, 1957. 25. Burford, T. H., Webb, W. R. and Ackerman, L.: Caustic Burns of Esophagus and their Surgical Management: Clinico-Experimental Correlation. Ann. Surg. 138:453,1953. . 26. Lawrence, G. H. and Burford, T. H.: Caustic Burns of Esophagus. Postgrad. Med. 18: 159. 1955. 27. LortaWacob, J. L.: Cicatricial Stenosis of Esophagus. Lyon chir. 54: 1, 43, 1958. 28. Nardi, G. L.: Surgical Treatment of Lye Strictures of Esophagus by Mediastinal Colon Transplant without Resection. New England J. Med. 256: 777,1957. 29. Schatzki, R. and Gary, J. E.: Dysphagia Due to Diaphragm-Like Localized Narrowing in Lower Esophagus ("Lower Esophageal Ring"). Am. J. Roentgenol. 70: 911, 1953. . 30. Ingelfinger, F. J. and Kramer. P.: Dysphagia Produced by Contractile Ring in Lower Esophagus. Gastroenterology 23: 419, 1953. 31. Allison, P. R.: Observations on Conservative Approach to Non-Malignant Lesions at Cardia. J. Thoracic Surg. 32: 150, 1956. 32. Baronofsky, I. D. and Wangensteen, O. H.: Obstruction of Splenic Vein Increases Weight of Stomach and Predisposes to Erosion or Ulcer. Proc. Soc. Exper. BioI. & Med. 59: 234,1945. 33. Enquist, I. F. and Gliedman, M. L.: Sources of Upper Gastrointestinal Bleeding in Patients with Cirrhosis. Surg. Gynec. & Obst. 106: 153, 1958. 34. Welch, C. S.: Ligation of Esophageal Varices by Transabdominal Route. New England J. Med. 255: 677, 1956. 35. Crile, G. Jr.: Transosophageal Ligation of Bleeding Esophageal Varices. Surgery 42: 3, 583, 1957. . 36. O'Sullivan, W. D. and Payne, M. A.: Emergency Portacaval Shunt. Surg. Gynec & Obst. 102: 668, 1956.
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37. Hallenbeck, G. A. and Shocket, E.: Evaluation of Portacaval Shunts for Portal Hypertension. Surg. Gynec. & Obst. 105: 1, 49, 1957. 38. McDermott, W. V. Jr., Wareham, J. and Riddell, A. G.: Bleeding Esophageal Varices; Study of Cause of Associated "Hepatic Coma." Ann. Surg.144: 318, 1956. 39. Nachlas, M. M.: Critical Evaluation of Venous Shunts for Treatment of Cirrhotic Patients with Esophageal Varices. Ann. Surg. 148: 169, 1958. 40. Koop, C. E. and Roddy, S. R.: Management of Bleeding Varices in Children. Ann. Surg. 147: 17, 1958. 41. Mustard, R. A. and Ibberson, 0.: Carcinoma of Esophagus; Review of 381 CasEls Admitted to Toronto General Hospital 1937-1953 Inclusive. Ann.Surg. 144: 927, 1956. 42. Waddell, W. R. and Scannell, J. G. ~ Anterior Approach to Carcinoma of Superior Mediastinal and Cervical Segments of Esophagus. J. Thoracic Surg. 33: 663, 1957. 43. Scanlon, E. F.: Discussion of Mustard, R. A.: Selection of Therapy for Esophageal Cancer. A.M.A. Arch. Surg. 75: 674, 1957. 44. Watson, W. L. and others: Torek Esophagectomy; Case Against Segmental Resection for Esophageal Cancer. J. Thoracic Surg. 32: 347, 1956. 45. Neville, W. E. and Clowes, G. H.Jr.: Reconstruction of Esophagus with Segments of Colon. J. Thoracic Surg. 35:"2, 1958. 46. Haight, C.: Some Observations on Esophageal Atresias and Tracheo-esophageal Fistulas of Congenital Origin. J. Thoracic Surg. 34: 2,141, 1957. 47. De Boer, A. and Potts, W. J.: Congenital Atresia of Esophagus with Tracheoesophageal Fistula. Surg. Gynec. & Obst. 104: 475, 1957. The Mount Sinai Hospital, New York 29, N.Y.
CARDIOSPASM CARDIOSPASM was
first described by Purden. 1 The disease is characterized by spasm of the lower esophagus and cardia, delayed passage and retention of food, and dilatation of the proximal esophagus. The most likely cause, as borne out by observation of the esophagus during roentgen examination, is a disordered neuromuscular mechanism. Roentgenologically the important point of obstruction is at the lower end of the esophagus. Whether the inferior constrictor, muscle or the vestibule of the esophagus is involved is not known, but a definite disorder of the peristaltic activity to the point of violence of the normal peristaltic waves is seen by the roentgenologist. Treatment for cardiospasm, therefore, should be aimed at the point of obstruction, the lower end of the esophagus. Whether the presence or absence of Auerbach's plexus is the cause of this disturbance has not yet been clearly defined. Biopsies of muscle layer have revealed Auerbach's plexus to be present in some patients with cardiospasm and absent in others. 2 Recent experimental evidence would suggest that cardiospasm may not only result from a destruction of the ganglion cells of Auerbach's plexus but also from 'a complete denervation of the narrowed segment. 3 Several decades ago Knight4 showed that some of the confusion that had resulted from previous experimentation in the production of cardiospasm in animals was a result of the type of experimental animal used. The cat, apparently, is the animal of choice. Diagnosis is often difficult. The Mecholyl test6 has been helpful. When a small dose of a cholinergic stimulant is administered subcutaneously (Mecholyl or Urecholine), severe retching or vomiting may result. Under the fluoroscope, deep phasic contractions are noted in the body of the From the Departm.ent of Surgery, The Mount Sinai H ospital, New York, N. Y. • Clinical Professor of Surgery, College of Physidans and S:p,rgeons, Columbia UnilJersity; Surgeon-in-Chief, The Mount Sinai Hospital.
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. Ivan D. Baronofsky
Fig. 292 Fig. 293 Fig. 292. Cardiospasm associated with hiatus hernia. Note arrow pointing to hernia. Also note waves in the esophagus. Fig. 293. Postoperative film following Heller procedure showing hernia reduced. There is still some element of spasm; however, barium moves through freely.
esophagus. This type of reaction usually does not occur in patients with obstruction of the lower end of the esophagus due to other causes. This abnormal response has been attributed to the denervation of the esophageal musculature in cardiospasm. A treatment that has been used in cases of cardiospasm in achalasia has been the-.divulsion'~of the muscle of the inferior constrictor of.,the , esophagus. This :.can be done by endoscopic dilatation by one of the many types of inflatable balloons presently on the market. Satisfactory results have been obtained in as high as 85 per cent of the cases. However, it is the feeling of many surgeons, because the procedure is blind, and because the result may not be lasting, that perhaps it is not the treatment of choice. A conservative approach may be attempted and if it is ineffective, surgical therapy can be instituted (Figs. 292-293). The most effective surgical approach is the simple myotomy of Heller. When the Heller operation is performed, however, emphasis should be given to the correction of the hiatus hernia which is inevitably present. The poor results following the Heller procedure, though few, are usually due to an esophagitis that probably has been caused by a hiatus hernia either pre-existing and unsuspected, or produced in the course of operative manipulation. This hernia must be repaired in order to insure a good result. It has been suggested that a Finney pyloroplasty be used after the Heller operation to prevent esophagitis. 6 W angensteen 7 has recently modified the performance of the Heller procedure by placing an inflatable balloon inside the esophagus through a gastrostomy opening. His present results, he finds, are improved over
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his earlier results. This approach seems logical since it does rupture all the small fibers of the cardioesophageal junction. REPLACEMENT OF THE ESOPHAGUS WITH VARIOUS PORTIONS OF THE BOWEL
In recognition of the fact that many symptoms can result from the presence of the stomach in the chest, and also that various complications can result from the loss of the sphincter of the lower end of the esophagus, various loops of bowel have been substituted for the esophagus or interposed between the esophagus and the stomach. Thus, as will be discussed later, segments of the right and transverse colon and of jejunum have been utilized. 8, 9, 10 These bowel segments, if carefully prepared, may be used to replace any form of diseased esophagus. PEPTIC ESOPHAGITIS
It has been estimated by various authors that about 20 per cent of people normally have regurgitation of gastric contents into the esophagus. This was determined by roentgen studies on patients admitted to a hospital for other diseases. It is entirely possible, therefore, for a peptic esophagitis to occur in people with normal anatomical relationships in the region of the cardioesophageal junction. In general, however, it is agreed that the sphincter mechanism at the lower end of the esophagus, whatever it be, is usually altered when esophagitis is present. If the mechanism is not altered, then acid must be secreted on the vulnerable esophageal mucosa in other ways. In 1935, Winkelstein described peptic esophagitis as a clinical entity associated with duodenal ulcer. Though he did not describe the common feature of an associated hiatus hernia, it is now recognized that hiatus hernia destroys the normal cardioesophageal sphincter mechanism and, therefore, allows for retention and regurgitation of peptic juice and, consequently, esophagitis. Thus, when esophagitis is present as a result of hiatus hernia, correction can be easily obtained by the repair of the hiatus hernia. Carver and Sealyll pointed out that in their series of 130 eases of peptic esophagitis, the following three factors were causative: (1) hiatus hernia (76 per cent); (2) surgical excision or destruction of the cardiac sphincter (13 per cent); (3) persistent vomiting (11 per cent). During the past few years, a more intimate knowledge of the pathology and physiology of esophagitis has been obtained. Because of the recent contributions of Barrett,12 Allison and Johnstone 13 and Wolf et a1.,14 a clearer picture of the classification of esophagitis has been obtained and a better therapeutic attack is now possible. Barrett recently described a cylindric type of epithelium present in the distal esophagus of certain people with esophagitis which resembles the epithelium of the cardiac region of the stomach, except that the glands are relatively atrophic and do not show parietal cells or secrete
Ivan D. Baronojsky
1182 A
B
c
o
Fig. 294. Diagrammatic representation of types of peptic or reflux esophagitis. A, Severe extensive peptic esophagitis with marked narrowing of long segment proximal to a small hernial sac. There is usually a history of a duodenal ulcer, operation and/or intubation. A pre-existing hernial sac is not a prerequisite. The marked narrowing at the onset iR due to spasm and inflammatory exudate but may persist and become fibrotic. B, Diffuse peptic esophagitis of a moderate degree as seen with uncomplicated direct hernias and reflux. Lack of distensibility of minimal degree over a variable distance of distal esophagus. In some cases, superficial ulceration or mUltiple ulcerations are present in the terminal portion of the esophagus. C, Peptic esophagitis with superficial inflammatory changes with or without erosions or ulceration limited to a short segment of the terminal portion of the esophagus. The involved segment may be quite short and the evident inflammatory changes may not involve the entire circumference. D, In addition to a direct hiatus hernia, the distal esophagus over a distance of several centimeters is lined by cylindric or Barrett type of epithelium. This has been referred to as gastric-lined esophagus or heterotopic gastric mucosa. In this case, however, the inflammatory and ulcerative changes are indicated as being confined to the terminal portion of the squamous-lined part of the esophagus, that is, these changes are noted immediately proximal to the gastric-lined portion of the esophagus which itself shows no evident involvement. (Courtesy of The American Journal of Roentgenology.)
pepsin. This condition is "heterotopic gastric epithelium in the esophagus" or gastric-lined esophagus. He pointed out that the heterotopic epithelium was susceptible to ulceration under the influence of acid gastric juice and that chronic peptic ulcer of the esophagus showed, in addition to the ulceration, the presence of heterotopic epithelium by biopsy. Therefore he suggested the term "chronic peptic ulcer of the esophagus" for ulceration in heterotopic epithelium and a new term, "reflux esophagitis," for inflammation and ulceration of a normally squamous lined esophagus~in association with a hiatus hernia. In effect, from the foregoing, one might suggest that the peculiar entity of "congenitally short esophagus" would fall in the classification of Barrett's heterotopic gastric mucosa. Wolf et a1. l4 have recently described the roentgen findings in the entities previously mentioned (Figs. 294, 295). By describing these in conjunction with biopsies taken
Some Recenf Advances in Surgery of the Esophagus A
B
c
1183
o
Fig. 295. Diagrammatic representation of types of peptic ulceration in association with gastric-lined esophagus or Barrett epithplium. A, Peptic ulceration within the gastric-lined segment. Moderate narrowing or limited distensibility is usually seen at the level of the ulceration. B, Peptic ulceration at the distal margin of the gastriclined segment with gastric rugae at its distal edge. C, Peptic ulceration at the proximal margin of the gastric-lined segment or within a region of mixed epithelium, that is, a combination of Barrett and squamous epithelium. An ulceration in this region may be referred to as marginal since squamous epithelium is present at its proximal edge. D, Peptic ulceration in the terminal portion of the esophagus which is lined by mixed epithelium or was the seat of minimal heterotopia or a very short gastric-lined segment of esophagus. This type of case creates difficulty in terminology since at different places about the ulceration there may be found normal gastric epit.helium, Barrett epithelium and squamous epithelium. The t.erm "marginal" has also been applied to this type of case. It is essentially similar to the situation diagrammed in C except there is no remarkable length of the distal esophagus that is lined by an atypical cylindric epithelium. It is evident that the roentgen findings corresponding to D may resemble those corresponding to B, as well as those corresponding to C in Figure 292. It is, therefore, often necessary to use the term peptic ulceration independent of the nature of the epithelium or until its nature is determined by microscopic examination. Moreover, more diffuse inflammatory changes are often present in the gastric or in the squamous-lined segments or in both which obscure the demarcations between individual segments. (Courtesy of the American Journal of Roentgenology.)
at the various levels of the esophagitis, a clear picture of the disease entity was obtained. Thus, the Barrett ulcer is observed to have gastric mucosa at the line of the diseased area, while the more common reflux esophagitis has squamous epithelium. The treatment of esophagitis is related to its pathological nature and cause. Thus, esophagitis from reflux associated with the ulcer diathesis or gallbladder disease uniformly responds to treatment of the ulcer or removal of the gallbladder. Esophagitis (usually of the squamous-lined mucous membrane) due to esophageal hiatus hernia and loss of competence of the cardioesophageal sphincter is usually treated by repair of the esophageal hiatus hernia. Esophagitis due to a Barrett's ulcer must be approached a little
.Ivan D. Baronofsky
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differently. Because of the presence of heterotopic gastric mucosa above the diaphragm and an inability to replace this gastric mucoSa below the diaphragm, more radical treatments are in order. It is necessary to excise the gastric mucosa above the diaphragm and reanastomose the esophagus to the stomach in such a manner that the stomach lies below the diaphragm and the esophagus above. This can be accomplished by the interposition of segments of jejunum or colon (right or transverse). Wangensteen had previously suggested that gastric resection alone would suffice to alleviate the symptoms and signs of peptic esophagitis in many cases and recently reported excellent long-term results with this procedure. 16 The procedure, he claimed, was less formidable than any mentioned and excellent results had been achieved over a long period of time on observation. In those cases in which a severe stricture was present, a repeated dilatation had been necessary up to the time of gastric resection. Following gastric resection, few, if any, dilatations were necessary. Ellis16 has suggested a rather extensive procedure consisting of vagotomy and resection of the stricture and the distal stomach with esophagogastrostomy and gastroduodenostomy. HIATUS BERNIA
The problem of surgery for hiatus hernia resolves itself upon the attitude of the medical profession toward hiatus hernia. Too many physicians assume a rather casual attitude toward this potentially grave disease, probably stemming from the observation that hiatus hernia is a rather frequent finding on routine x-ray examination of the upper intestinal tract. However, there is a reported recurrence rate of anywhere between 10 and 30 per cent and a symptomatic recurrence rate as high. Baronofsky et al.17 have previously pointed out that the fate of hiatus hernias, as watched over a long period, is one of gradual enlargement in a high percentage of cases. This, coupled with the fact that hemorrhage, stricture and esophagitis are common accompaniments of hiatus hernia, should lead to earlier surgery on these cases. I believe that a hiatus hernia of moderate size should be treated surgically. In a similar study, Blades and Rall18 emphasize the fact that symptomatic hiatus hernia represents a serious lesion. In their series of 66 cases, 32 of the patients with asymptomatic hiatal hernia had dangerous complications including bleeding in 22, esophageal stricture in eight, carcinoma in one and perforation in one. It is to be emphasized that the main symptoms of hiatus hernia, common to all the types, are caused by esophagitis, and that a hiatus hernia is generally considered the most frequent cause of reflux esophagitis. Lindskog and Klein19 report that, of 41 patients with sliding hiatus hernia, 29 per cent had esophagitis. In our own early series, 61 per cent of the patients had esophagitis, if both esophagoscopic and roentgenologic evidence are included.
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Fig. 296
1185
Fig. 297
Fig. 296. Preoperative x-ray showing large hernia above the diaphragm.
Fig. 297. Postoperative film showing repair with complete replacement of the stomach below the diaphragm.
More and more articles show the true percentage of symptoms associated with hiatus hernia. Thus, in a most recent series,20 as high as one-third of the patients seen had bleeding as a presenting symptom. Esophagoscopy was performed in all cases. Forty-three per cent of their cases had esophagitis, three with ulceration. Two had stricture and one had an associated ulceration and stricture. Of these 65 patients, onethird had peptic ulcer. Since the hiatus hernia allows regurgitation of acid peptic juice into the esophagus, those ulcer patients with high acid have more profound symptoms from the hiatus hernia. Considerable discussion has centered about the presence of the short esophageal type of hernia. Humphreys21 believes that a true congenitally short esophagus is characterized by the fact that the intrathoracic portion of the stomach derives its blood supply from the thoracic aorta and not from branches of the celiac artery. Other authors believe that a congenitally short esophagus, in reality, is a variation of Barrett's ulcer with heterotopic gastric mucosa. The treatment of hiatus hernia has received considerable attention in the literature (Figs. 296, 297). Knowledge of the anatomy of the area is most instrumental in obtaining good repairs. Allison22 has described a method of repair emphasizing the anatomical points of importance. The right and left diaphragmatic crura arise from the bodies of
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Ivan D. Baronofsky
the first three or four lumbar vertebrae. The left fans out onto the diaphragm and does not contribute to the hiatus. The right crus forms the entire hiatus. It is the absence of the right crus that allows for diaphragmatic hernia. In the posterior mediastinum behind the esophagogastric junction there is a fat pad which is unsupported and unprotected. When this area is weakened, the herniated stomach passes upward and posteriorly, carrying with it the peritoneum and the endoabdominal fascia (comparable to the transversalis fascia in the lower abdominal wall). This fascia, in the area of the esophageal hiatus region, is called the phrenoesophageal ligament. It reflects onto the esophagus with the peritoneum, just as the peritoneum recurs to form the "sac" of the diaphragmatic hernia. Frequently this ligament is a tenuous, almost ethereal membrane of little value. After considerable experience with diaphragmatic hernia repair, I am of the opinion that either the abdominal or transthoracic approach can be used to perform a satisfactory operation. It must be mentioned that, with the abdominal approach, other diseases may be encountered and attacked at the same time. The transthoracic approach should be reserved for those cases where exposure may be a problem owing to obesity, the configuration of the thoracic cage, previous upper abdominal operations, etc. More important than the choice of approach is the attention to detail. The crural fibers must be carefully delineated for a considerable extent, and (in disagreement with a recent paper) the peritoneum should be entered by a radial incision made in the diaphragm just anterior to the spleen. A finger or a forceps is then inserted along the diaphragm until it reaches the sac of the diaphragmatic hernia. The sac can then be incised, using the intraperitoneal forceps as a guide. A Penrose drain is then placed around the esophagus from the thoracic side, and this is in turn brought through the hiatus to the intraperitoneal side, and tension exerted from below. When this tension is put on the esophagus, the crura are delineated by the forward pull of the drain. The crura are joined by interrupted silk mattress sutures behind the esophagus. Usually, tension on the first suture, which is the lowest or juxta-aortic one will outline the entire crural arch and only three or four more sutures will be required. Good, deep bites are taken and the crura approximated snugly, but not so tightly that the muscle is strangulated. The orifice immediately around the esophagus should admit a fingertip between the last suture and the esophageal wall. Sutures are then placed between the esophageal musculature or the remnant of the phrenoesophageal ligament and the diaphragm as it is formed by the crura. Thus the esophagus is fixed to the diaphragm much as one would fix an ileostomy as it comes through the abdominal wall. The rent in the diaphragm is then closed after hemostasis is observed. By using
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these simple maneuvers, excellent repair of the diaphragmatic hernia can be obtained with a low recurrence" rate. In those cases in which there is some shortening of the esophagus due to heterotopic gastric mucosa or a true congenital shortening of the esophagus, every effort should be made to bring the diaphragm above the cardioesophageal junction. This in itself will cure a percentage of cases. Effler and Groves23 recommend transplanting the esophagus anteriorly into a new hiatus and also the crushing of the phrenic nerve. Fisher and Johnson24 have recently reported on seven patients with short esophageal hiatus hernias which they treated by distal gastric resection. Wangensteen has proposed the use of distal gastric resection plus repair of the hiatus hernia in those cases where stricture is secondary to a hiatus hernia. He has reported singular success with this maneuver in cases in which repeated endoscopic' dilatation had to be used previously. When strictures result from the severe reflux esophagitis due to longstanding hiatus hernia, another very difficult problem is introduced. These strictures are a result of an esophagitis in a squamous-lined esophagus. Lindskog and Kline advise distal esophagectomy, combined with vagotomy, extensive proximal gastric resection and gastrojejunostomy for irreversible stricture formation. Others advocate resecting the involved area and interposing a jejunal or colonic segment between the esophagus and the stomach when stricture has occurred. Earlier treatment of hiatus hernias should obviate some of these difficulties. CAUSTIC STRICTURES OF THE ESOPHAGUS
l
I
I
I ,J
The pathological changes and treatment of lye burns of the esophagus have been well described by Burford. 25 • 26 In general, during the acute phase of the burn, it has been suggested that intravenous feedings, along with supportive therapy and antibiotics should be used. When the acute phase was over, oral feedings were allowed and, at about the third week, endoscopy with dilatation was attempted. On the basis of evidence presented, it would appear proper to give the esophagus complete rest in the early stages of a burn in order that early epithelization may take place. With epithelization, of course, comes complete healing. Lortat-Jacob27 administers corticosteroids immediately. He believes that even old strictures, when treated with cortisone, can regain a certain elasticity and that in some instances operation can be delayed or avoided. Though he immediately examines these patients endoscopically, evidence has shown that this is not particularly efficacious, as it does destroy the epithelium. Perhaps it would be wise to start cortisone therapy immedil1tely on these individuals and delay dilatation until later. Those strictures which do not respond promptly to dilatation should be operated upon without delay. Excellent results have ooen obtained recently with the interposition of a segment of right colon between the cervical esophagus and the stomach28 (Fig. 298).
Ivan D. Baronofsky
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Fig. 298. A, X-ray of stricture of the esophagus due to ingestion of lye. B, Lateral view of the chest. Barium swallow in right colon which has been anastomosed to the upper esophaguB and the stomach. Arrow points to the stomach anastomosis. C, Posteroanterior view of the chest showing the right colon as it courses from the esophagus to the stomach.
It would appear that this is the procedure of choice if conservatism fails. The fate of the remaining burned esophagus, when it is by-passed, is one which has received some attention. It has been stated that carcinoma not infrequently arises in all burns of the esophagus and, therefore, excision at the time of reconstruction of the esophagus should be considered. ESOPHAGEAL RINGS
Schatzki and Gary29 and Ingelfinger and Kramer80 have described a. localized ringlike narrowing of the lower end of the esophagus. These authors have pointed out that the caliber of this ring might be reduced to a point where the swallowing of a large bolus of food might cause
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Fig. 299. Localized ring narrowing at the lower end of the esophagus. Though this is static in character it has given no symptoms.
obstruction. The ring is actually a thickening of a muscle area of the esophagus. Motion picture studies by Wolf of a patient with such a ring confirm the observations of Schatzki that this ring is static in character rather than contractile and that it is unchanging in location in relation to the esophagus. However, its relationship to the level of the diaphragm may change with filling and emptying of that region (Fig. 299). When it becomes incompletely distensible and replaces a normally distensible ring, it may become a surgical problem. 31 Sectioning of the muscle fibers was performed as one would in a pyloromyotomy. Continued study of the esophagus will probably reveal more pathological conditions resulting from changes in the neuromuscular structure of this organ. ESOPHAGEAL VARICES
Bleeding esophageal varices have a poor prognosis. It would appear from the literature that more than 50 per cent of patients with portal hypertension and varices die within a year or two from liver disease or hemorrhage or both. Baronofsky and Wangensteen32 have shown that not only is the varix itself important in the bleeding of esophageal varice!!! but also the acid peptic factor. It was noted that gastrectomy might prevent bleeding when other measures had failed. The close association between the bleeding due to gastric and esophageal varices and gastroduodenal ulcer was also noted. Recently, Enquist and Glied-
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Ivan D. Baronofsky
man 33 reviewed autopsy data of 476 patients with cirrhosis and 1000 controls who had essentially normal livers. Spleen size seemed to be a good indication of the degree of portal hypertension that existed during life, whereas liver size was not. Upper gastrointestinal lesions which commonly served as sources of hemorrhage were found more often at autopsy in patients with cirrhosis than in those with normal livers. Thirty-four per cent of the patients with cirrhosis who succumbed to hemorrhage had some extravariceal source of bleeding; in 21 per cent, a lesion was present that could as well have been the source of hemorrhage as the varices; and in only 45 per cent of these patients did the bleeding originate in esophageal varices. The most common source of extravariceal bleeding in cirrhotic patients was the stomach. It would appear from this study that when the source of uncontrolled intestinal bleeding in a patient with cirrhosis has not been determined an abdominal approach should be used when surgery is indicated. This would permit the effective treatment of upper gastrointestinal hemorrhage regardless of the site of bleeding, since even if bleeding esophageal varices were found to be the cause, transgastric ligation could be employed. If it is definitely established that bleeding is due to esophageal varices, and if other means such as a Sengstaken balloon are ineffective, a transthoracic approach can be used. C. Stuart Welch34 prefers the transabdominal approach. George Crile, Jr.,35 in discussing transesophagealligation, noted that in patients with good liver reserve the mortality and morbidity were low. Thus, in six of nine patients with extrahepatic blocks where this procedure was used, bleeding was controlled for from four to nine years. It would also appear that, in patients with extrahepatic blocks who are bleeding massively, transesophagealligation may, ina certain percentage, protect them without any other future treatment. Those patients with extrahepatic block who continue to bleed following varix ligation may be subjected to an interposition operation using a segment of jejunum or colon, thus removing acid initiation from the varix. Transesophagealligation as a permanent treatment in patients with intrahepatic block has resulted in a high mortality rate and frequent recurrence of bleeding in the survivors. Bleeding due to intrahepatic block can usually be controlled with the Sengstaken-Blakemore balloon. A portacaval shunt can then be accomplished as an elective procedure. O'Sullivan and Payne36 have subjected patients to emergency portacaval shunts following the temporary control of hemorrhage by the use of a balloon, but the mortality was high. The condition of the liver is most important in selecting patients for portacaval shunts. If the patient is not jaundiced, and has a serum albumin above 3 grams per 100 ce., he should prove a fairly good surgical risk. Ascites, if present, increases the severity of the risk but should not be a deterrent to operation if the patient's general condition is otherwise satisfactory. Neurologic symptoms related to ammonia intoxication have been
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discussed by various authors. Hallenbeck and Shocket37 noted that in their series neurologic symptoms did not develop after splenorenal anastomosis but that neurologic symptoms of varying severity did develop subsequently in six out of 23 patients who survived end-to-side portacaval anastomosis. None of the six had any recognizable neurologic symptoms before surgery. These neurologic symptoms are related to increased blood ammonia levels following the ingestion or the breakdown of nitrogenous products in the intestine. In the presence of an open portasystemic shunt, no further breakdown of the ammonia into urea occurs, because the liver which normally performs this function is by-passed. The blood ammonia level increases, resulting in neurologic symptoms. 38 Nachlas,39 in reviewing portacaval shunts done for bleeding esophageal varices, questions the efficacy of this procedure because of the high rate of recurrent bleeding. Koop and Roddy 40 have utilized the colon as a replacement for the distal esophagus and proximal stomach in the management of bleeding varices in children, and other authors have used the jejunum to separate the acid factor from the varix. Arterialization of the liver has long been suggested as a method of regeneration of the cirrhotic liver, but experimental results do not support. this theory and in fact demonstrate progression of the cirrhosis. CARCINOMA OF THE ESOPHAGUS
The results of treatment in carcinoma of the esophagus have not improved much in the past few years. Mustard41 reported a series of 381 patients with only a 3 pel' cent five year survival rate, including operated and unoperated patients. Of 87 untreated patients, only two lived two years; none survived two and a half years. Of 125 patients treated with high voltage irradiation, only one survived five years, and this patient had a squamous cell carcinoma of the posterior wall of the hypopharynx. Mustard feels that cobalt therapy may prove as efficacious as surgery for carcinoma of the esophagus as one gains more experience with this modality. The five-year survival rate for patients who had complete excision and reconstruction of the esophagus was 19.4 per cent and this rate is higher for lesions of the lower third. Wider resections of the esophagus may be necessary because of submucosal spread. In order to approach more radically the lesions of the superior mediastinal and cervical segments of the esophagus, Waddell and Scanne1l42 describe an anterior approach which utilizes a sternal splitting incision. Provided that operability is determined, the stomach is brought up into the anterior mediastinum and anastomosed to the esophagus in the neck. The advantage of this surgical approach is that it allows easy and direct exposure of the esophagus from the aortic arch to the pharynx and that gross extensions of the tumor to lymph nodes and cervical and upper mediastinal areas can be removed readily with a
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primary tumor. A logical modification has been proposed by Scanlon43 as a two stage operation and has been accomplished by Watson44 and his group. This modification which Scanlon suggests as a two stage procedure is a total esophagectomy through a right thoracic approach combined with proximal gastrectomy and splenectomy. The proximal esophagus is brought out as a fistula in the neck, and a gastrostomy is performed for feeding purposes. Six months later, after irradiation, continuity is established by performing esophagocologastrostomy using the right colon as a transplant through the substernal tunnel. Watson, Neville 4fi and others have used the right colon for this purpose. A combination of surgery and extensive x-ray therapy may offer a new hope for the cure of carcinoma of the esophagus. TRACHEOESOPHAGEAL FISTULA
Much has been accomplished in the field of tracheoesophageal fistula in the last decade. Cameron Haight recently published his observations in over 200 patients with atresia of the esophagus46 and recommends primary anastomosis of the two segments of the esophagus whenever possible. For esophageal reconstruction he suggests using the right colon or the right half of the transverse colon via a substernal tunnel. The ages of his seven patients varied from two to seven year~. Excision of the distal segment of the esophagus is advisable. Mahoney and his group have also utilized this procedure in reconstructing the esophagus initially when an end-to-end anastomosis could not be done or in those instances where late reconstruction was necessary. The approach that has been suggested by both Haight and Potts47 is a right transpleural approach, whereas the original approach was extrapleural. REFERENCES 1. Purden, T.: Extraordinary Case of Dilatation of Esophagns Forming a Sac, Extending from Two Inches Below the Pharynx to Cardiac Orifice of Stomach. London M. & Physiol. J. 46: 540, 1821. 2. Hawthorne, H. R., Frobese, A. F. and Nemir, P. Jr.: Surgical Management of Achalasia of Esophagus. Ann. Surg. 144: 653, 1956. 3. Deloyers, L., Cordier, R. and Duprez, A.: New Approach to Physiology of 80Called Cardiospasm: Experimental Production of Cardiospasm in Cats After Destruction of Auerbach's Plexus. Ann. Surg. 146: 167, 1957. 4. Knight, G. C. : Relation of Extrinsic Nerves to Functional Activity of Esophagus. Brit. J. Surg. 22: 155, 1934. 5. Kramer, P. and Ingelfinger, F. J.: Esophageal Sensitivity to Mecholyl in Cardiospasm. Gastroenterolgy 19: 242, 1951. 6. Herron, P. W., Thomas, G. 1. and Merendino, K. A.: Experimental Approach to Cardiospasm: Appraisal of Finney Pyloroplasty in Prevention of Esophagitis Following Heller Myotomy. J. Thoracic Surg. 34: 609, 1957. 7. Wangensteen, O. H.: Technique of Achieving an Adequate Extramucosal Myotomy in Mega-esophagus (Achalasia, Cardiospasm, Dystonia). Surg. Gynec. & Obst. 105: 3, 339, 1957. 8. Sherman, C. D. Jr., Mahoney, E. D., Dale, W. A. and Stabins, S. J.: Intrathoracic Transplantation of Right Colon for Esophageal Reconstruction. Cancer 8: 1198,' 1955.
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9. Harrison, A. W.: Transthoracic SIlUIlI Bowel Substitution in High Strictures of Esophagus. J. Thoracic Surg. 18: 316, 1949. 10. Merendino, K. A. and Thomas, G. I.: Jejunal Interposition Operation for Substitution of Esophagogastric Sphincter. Surgery 44: 1112, 1958. 11. Carver, G. M. Jr. and Sealy, W. C.: Peptic Esophagitis. A.M.A. Arch. Surg. 68: 286, 1954. 12. Barrett, M. R.: Chronic Peptic Ulcer of Esophagus. Brit. J. Surg. 38: 175, 1950. 13. Allison, P. R. and Johnstone, A. S.: Esophagus Lined with Gastric Mucous Membrane. Thorax 8: 87, 1953. 14. Wolf, B. S., Marshak, R. H. and Som, M. L.: Peptic Esophagitis and Peptic Ulceration of Esophagus. Am. J. Roentgenol. 79: 5, 741, 1958. 15. MacLean, L. D.: Etiology and Treatment of Esophagitis. Minnesota Med. 783. 1958. 16. Ellis, F. H. Jr.: Physiologic Operation for Ulceration and Stricture of Terminal Esophagus. Proc. Staff Meet. Mayo Clin. 31: 615, 1956. 17. Baronofsky, I. D., Sprafka, J. L. and Azad, M.: Fate of Esophageal Hiatus Hernia: Clinical and Experimental Study. Surgery 36: 3, 519, 1954. 18. Blades. B. and Hall, E. R.: Consequences of Neglected Hiatal Hernias. Ann. Surg. 143:822, 1956. 19. Lindskog, G. E. and Kline, J. L.: Problem of Hiatus Hernia Complicated by Peptic Esophagitis. New England J. Med. 257: 3, 110, 1957. 20. Hoffman, R. F., Cruze, K. and Byron, F. X.: Symptomatic Hiatus Hernia. J.A.M.A. 169: 2, 1959. 21. Humphreys, G. H. II, Ferrer, J. M. Jr. and Wiedil, P. D.: Esophageal Hiatu! Hernia of Diaphragm; Analysis of Surgical Results. J. Thoracic Surg. 34: 6, 749,1957. 22. Allison, P. R.: Reflux Esophagitis, Sliding Hiatal Hernia and Anatomy of Repair. Surg. Gynec. & Obst. 92: 419, 1951. 23. Effler, D. B. and Groves, I,. K.: Short Esophagus; Mechanism of Pain and Surgical Therapy. A.M.A. Arch. Surg. 75: 4, 639,1957. 24. Fisher, H. C. and Johnson, M. E.: Esophageal Hiatus Hernia; Manifestation of Peptic Esophagitis; Treatment by Gastric Surgery. A.M.A. Arch. Surg, 75: 4, 660, 1957. 25. Burford, T. H., Webb, W. R. and Ackerman, L.: Caustic Burns of Esophagus and their Surgical Management: Clinico-Experimental Correlation. Ann. Surg. 138:453,1953. . 26. Lawrence, G. H. and Burford, T. H.: Caustic Burns of Esophagus. Postgrad. Med. 18: 159. 1955. 27. LortaWacob, J. L.: Cicatricial Stenosis of Esophagus. Lyon chir. 54: 1, 43, 1958. 28. Nardi, G. L.: Surgical Treatment of Lye Strictures of Esophagus by Mediastinal Colon Transplant without Resection. New England J. Med. 256: 777,1957. 29. Schatzki, R. and Gary, J. E.: Dysphagia Due to Diaphragm-Like Localized Narrowing in Lower Esophagus ("Lower Esophageal Ring"). Am. J. Roentgenol. 70: 911, 1953. . 30. Ingelfinger, F. J. and Kramer. P.: Dysphagia Produced by Contractile Ring in Lower Esophagus. Gastroenterology 23: 419, 1953. 31. Allison, P. R.: Observations on Conservative Approach to Non-Malignant Lesions at Cardia. J. Thoracic Surg. 32: 150, 1956. 32. Baronofsky, I. D. and Wangensteen, O. H.: Obstruction of Splenic Vein Increases Weight of Stomach and Predisposes to Erosion or Ulcer. Proc. Soc. Exper. BioI. & Med. 59: 234,1945. 33. Enquist, I. F. and Gliedman, M. L.: Sources of Upper Gastrointestinal Bleeding in Patients with Cirrhosis. Surg. Gynec. & Obst. 106: 153, 1958. 34. Welch, C. S.: Ligation of Esophageal Varices by Transabdominal Route. New England J. Med. 255: 677, 1956. 35. Crile, G. Jr.: Transosophageal Ligation of Bleeding Esophageal Varices. Surgery 42: 3, 583, 1957. . 36. O'Sullivan, W. D. and Payne, M. A.: Emergency Portacaval Shunt. Surg. Gynec & Obst. 102: 668, 1956.
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37. Hallenbeck, G. A. and Shocket, E.: Evaluation of Portacaval Shunts for Portal Hypertension. Surg. Gynec. & Obst. 105: 1, 49, 1957. 38. McDermott, W. V. Jr., Wareham, J. and Riddell, A. G.: Bleeding Esophageal Varices; Study of Cause of Associated "Hepatic Coma." Ann. Surg.144: 318, 1956. 39. Nachlas, M. M.: Critical Evaluation of Venous Shunts for Treatment of Cirrhotic Patients with Esophageal Varices. Ann. Surg. 148: 169, 1958. 40. Koop, C. E. and Roddy, S. R.: Management of Bleeding Varices in Children. Ann. Surg. 147: 17, 1958. 41. Mustard, R. A. and Ibberson, 0.: Carcinoma of Esophagus; Review of 381 CasEls Admitted to Toronto General Hospital 1937-1953 Inclusive. Ann.Surg. 144: 927, 1956. 42. Waddell, W. R. and Scannell, J. G. ~ Anterior Approach to Carcinoma of Superior Mediastinal and Cervical Segments of Esophagus. J. Thoracic Surg. 33: 663, 1957. 43. Scanlon, E. F.: Discussion of Mustard, R. A.: Selection of Therapy for Esophageal Cancer. A.M.A. Arch. Surg. 75: 674, 1957. 44. Watson, W. L. and others: Torek Esophagectomy; Case Against Segmental Resection for Esophageal Cancer. J. Thoracic Surg. 32: 347, 1956. 45. Neville, W. E. and Clowes, G. H.Jr.: Reconstruction of Esophagus with Segments of Colon. J. Thoracic Surg. 35:"2, 1958. 46. Haight, C.: Some Observations on Esophageal Atresias and Tracheo-esophageal Fistulas of Congenital Origin. J. Thoracic Surg. 34: 2,141, 1957. 47. De Boer, A. and Potts, W. J.: Congenital Atresia of Esophagus with Tracheoesophageal Fistula. Surg. Gynec. & Obst. 104: 475, 1957. The Mount Sinai Hospital, New York 29, N.Y.