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Partial Gastroesophagectomy for Esophageal Varices
PARTIAL GASTROESOPHAGECTOMY FOR ESOPHAGEAL VARICES GLENN E. SHELINE, M.D.,* DWIGHT E. CLARK, M.D., F.A.C.S.,t WILLIAM E. ADAMS, M.D., F.A.C.S.,t AND DALLAS B. PHEMISTER, M.D., F.A.C.S.§ PATHOGENESIS OF ESOPHAGEAL VARICES
Portal hypertension is an intermediate phase of a clinical syndrome which may be produced by anyone of a number of disease entities. It is probably never a primary disease. The causative factors have as a common denominator the ability to effect obstruction of the portal venous system. The primary block may occur within the portal vein or its tributaries, the liver, or the hepatic vein. The more distal the process, the more discrete is the clinical picture. Occlusion of the splenic vein may lead to congestion of the spleen. When the block is sufficient to cause splenomegaly, there may be secondary anemia, leukopenia, thrombocytopenia and a tendency toward repeated gastrointestinal hemorrhages, frequently associated with ruptured esophageal or gastric varices. 1 Components of this picture have been variously called Banti's syndrome, splenic anemia,2 hypersplenism3 and the syndrome of the portal bed block. 1 When the pathologic process is extrahepatic, involving only the portal vein or its tributaries, it may be classified in one of two groups.l In the first group obliterative scarring occurs in the vein, presumably as a result of the chronic phase of a thrombotic process, with little or no recanalization. In the second there is a reorganization of the portal vein and surrounding tissue into a mass of small vessels, termed "cavernomatous transformation of the portal vein." The etiology is unknown and is likely variable. When the process is intrahepatic, as in cirrhosis of the liver, the situation becomes more complex. The type of cirrhosis and efficacy of collateral vein formation determine to a considerable extent the development of portal hypertension and, secondarily, of Banti's syndrome. Rousselot4 described a group of cases of portal hypertension without From the Department of Surgery, University of Chicago School of Medicine. * Atomic Energy Commission Postdoctoral Fellow. t Associate Professor of Surgery, University of Chicago; Senior Attending Surgeon, Albert Merritt Billings Hospital, The University of Chicago Clinics. t Professor of Surgery, University of Chicago School of Medicine. § Professor Emeritus of Surgery, University of Chicago.
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visible obstruction and suggested that such increased pressure may occur as a primary disturbance of the portal system. It is possible that in these ca~es an obstructive factor was present but not found at surgery. One of the results of portal obstruction is congestion of all or a part of the portal system, depending on the site of obstruction, and, since the system is without valves, congestion of the tissues it drains. Associated with congestion is an increased venous pressure which may reach four or five times the normal levels.3 • 4 Presumably as a compensatory mechanism to decreased blood flow from the portal system through the liver, a group of collateral veins connecting directly with the general systemic circulation dilate and may ultimately carry a major portion of the portal blood flow. McIndoe 5 found in cirrhotic livers that 13 per cent or less of the fluid perfused through the portal vein was recovered from the hepatic vein. The collateral circulation is established chiefly by use of four previously existing but normally little used communications between the portal and caval systems. These vascular connections occur between the coronary vein and the intercostal veins, azygos system, and diaphragmatic veins; the superior and middle hemorrhoidal veins; the paraumbilical veins of the falciform ligament and the deep epigastric and internal mammary veins; branches of the portal system which supply organs that are either developmentally retroperitoneal or pathologically adherent to the abdominal wall and retroperitoneal branches of the inferior vena cava. The last group of communications is called the veins of Retzius. As a rule the collateral channels behave well. The exception arises from communications of the coronary vein. This route provides the shortest path, is not hindered by valves, and provides a relatively direct connection between the portal system and the lower esophageal veins. The submucosal veins of this portion of the esophagus are poorly supported by connective tissue2 and are unfortunately prone to dilatation and formation of varices which are in turn highly subject to rupture and hemorrhage. Gastric varices may also develop and bleeding result. Thus, Rivers and Wilbur, in a study of 668 patients with hematemesis, found that in 5 per cent bleeding was attributable to hepatic cirrhosis or splenic anemia. 6 TREATMENT
Therapy is administered according to the disease process in operation. In cirrhosis and other diseases of the liver, adequate medical management is essential. Surgical treatment in the cases of intrahepatic obstruction is directed at control of portal hypertension and one or more of the symptoms, such as esophagogastric hemorrhage, hypersplenism and ascites. Surgery is justified by the frequency with which components
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of this triad may lead to death in spite of the best care of the primary disease. In cases in which the pathology is limited to the extrahepatic veins, the surgeon may have the opportunity to sidetrack the primary obstruction. The present communication deals with the surgical approach and in particular with esophagogastric resection in the control of hemorrhage. A brief resume of previously described surgical procedures is presented. Splenectomy. It has been estimated that blood passing through the spleen contributes 20 to 40 per cent of the total portal flow. 2 • 3 Splenectomy removes this portion of the portal blood flow and thus tends to reduce the portal pressure. It also interrupts the vessels which feed into varices of the cardia, diaphragm and esophagus by way of the gastrolienal ligament. Rousselot4 in 1936 reported a series of thirty-one cases of Banti's syndrome treated by splenectomy. Seven of the eleven patients with esophageal hemorrhage prior to surgery eventually died of this complication, and the author states "that in this type of case, operation should be avoided." Barg and Dulin7 splenectomized twenty-two patients with Banti's syndrome and had six operative deaths. Of the remaining sixteen, four are symptom free; two have malaise and weakness; two had repeated esophageal hemorrhages, but were living at time of report; four are dead of gastroesophageal hemorrhage; one is dead following hemorrhage at paracentesis site; one is dead of unknown cause; and two are lost to follow-up. It was concluded that splenectomy for this syndrome has a favorable influence on ascites and in general is preferable to a nonoperative regimen but that it does not assure relief from gastroesophageal hemorrhage. According to Whipple, l splenectomy may afford relief until the hypertension rebuilds, but is permanent only when the obstruction lies within the splenic vein. Blakemore 8 states that splenectomy will cure only the small group of cases of splenic vein thrombosis in which the obstruction is distal to the entrance of the coronary vein. In the presence of ·esophageal varices, splenectomy for a splenic vein thrombosis which lies proximal to the entrance of the coronary vein should be done only when it is accompanied by a splenorenal anastomosis. 9 Ligation of the Coronary Vein. As a means of preventing hemorrhage from gastroesophageal varices, ligation of the coronary vein with and without splenectomy has been practiced. 2 Whipple 1 and Blalock 9 describe the results of this procedure as disappointing and discouraging. In an effort to accomplish the same end, Crafoord and Frenckner10 injected, through an esophagoscope, the esophageal varices of a patient who had repeated esophageal hemorrhage following splenectomy. Over a period of three years this patient had no further symptoms and no esophagoscopic evidence of recurrence, and only small defects in the
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lower esophagus were found with a contrast shadow roentgenogram. Injection treatment of esophageal varices has also been used at the Mayo Clinic. 2 Whipple! believes that this procedure is no better than the ligation method and that, at best, these procedures shut off one of the chief collaterals connecting the portal and systemic circuits, thus raising the portal hypertension. Modified Talma Operation. In an endeavor to promote the formation of additional collateral circulation, Talmal l and his associates described a procedure for attaching the omentum to the abdominal wall. In 1918, Mayo !2 introduced a modification in which the omentum is drawn into the incised rectus muscle and sutured there. Whipple1 and Blalock 9 both write discouragingly of this procedure. It has not gained wide acceptance. Portacaval Anastomosis. In 1877, Eck,13 while studying hepatic physiology, developed a procedure in dogs for the anastomosis of the portal vein to the inferior vena cava. He suggested its possible use in aiding venous return in cases with portal vein obstruction. The first such operation on a patient was claimed by Vidal in 1903,l4 This patient died of a septic endophlebitis after fourteen weeks. In 1912, Rosenstein!5 reported a case of cirrhosis and ascites in which he had made an Eck fistula. A five months' follow-up showed a marked decrease of ascites. Operative difficulties and a high mortality rate delayed adoption of this approach until Blakemore and Lord16 published their nonsuture method of blood vessel anastomosis. Originally they reported ten patients, five of whom had a splenorenal vein anastomosis accompanied by splenectomy and left nephrectomy. The second five had an end-to-side portal vein to inferior vena cava anastomosis. All survived surgery. The authors were much encouraged by the results and have, along with others, continued to study and apply the method. 8, 9,17,18,19 In 1948, Blakemore17 presented a discussion of the results of fiftyeight portacaval shunts, There were eleven postoperative deaths: three of cholemia; two with cerebral hemorrhage, one of cardiac failure, three cases of mesenteric thrombosis, one from intraperitoneal hemorrhage, and one from gastrointestinal hemorrhage. Of the thirty-five cases who gave a history of preoperative gastrointestinal bleeding, eleven had one or more attacks of hemorrhage after discharge from the hospital. Followup time ranged from a few months to three or more years, Five of these patients had had previous splenectomies. Four of the five had extrahepatic portal block which necessitated use of a vein other than the portal for the anastomosis. In patients with extrahepatic portal block and previous splenectomy, anastomosis was usually limited to the superior mesenteric vein or the inferior mesenteric vein, In cases with extrahepatic portal block and without previous surgery, the high incidence of portal vein involvement necessitated dependence primarily upon the
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splenic vein for establishment of an anastomosis. In the series of fiftyeight patients, a vena cava to portal vein anastomosis was employed only nine times with one postoperative death. Fear of thrombosis of the portal vein towards and into the liver was the chief reason the portal vein to vena cava shunt was not used more frequently. A single case of side-to-side vena cava to portal vein anastomosis was included. This new procedure offered these advantages: (1) portal flow to the liver, and (2) a lessened tendency to thrombosis extending toward the liver. More recently, Julian has presented a technic for the side-to-side portal vein vena cava anatomosis.1 8 Total Gastrectomy and Partial Gastroesophagectomy. In the two patients with Banti's syndrome, Phemister and Humphreys 20 did a total gastrectomy in one and an esophagogastric resection in the other. Each of these patients had multiple hemorrhages which began at an early age and persisted after splenectomy. A favorable response was obtained in each case. They point out that, like obliteration of the esophageal varices by ligation, resection of the bleeding segment imposes a greater load on the remaining collateral circulation. Thel'le collaterals, however, bleed infrequently. If patients with portal hypertension and extrahepatic block, especially the splenectomized ones, can be kept from bleeding to death, they may live in good health indefinitely. Resection therapy does not involve a nephrectomy or interruption of whatever portal circulation does reach the liver. It offers a possible control of gastroesophageal hemorrhage without dependence on the continued patency of a venous-venous anastomosis. Veins leading to or from the liver are not interfered with; hence the chance of a postoperative thrombus forming and extending into the liver is markedly diminished. On a physiological basis Gatch 23 reported "The tendency of esophageal varices to bleed is explained by their location where dilatation of them is favored by the negative pressure of the chest and not opposed by positive pressure of the abdomen. Relief from danger of death due to hemorrhage from these varices is the chief benefit which the victim of portal hypertension can expect from any operation. Gastroesophageal resection, I believe, is more likely to give him the relief, and with less danger, than portacaval shunt." Since the report of Phemister and Humphreys, two additional cases of Banti's syndrome with bleeding gastroesophageal varices have been treated in this clinic by partial esophagogastric resection with encouraging results. REPORT OF TWO CASES CASE
I
A 34 year old white man, was first seen at the University of Chicago Clinics in 1941 with a history of hematemesis and tarry stools occurring
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in episodes of several weeks' duration at the ages of 14, 28 and 31 years. Re presented himself for a check-up, although he had had no bleeding during the preceding three years. The initial hematemesis occurred while doing heavy work and was preceded by sudden and severe weakness. It was noted that an injury to the abdomen had been sustained at the age of 12 years. Physical Examirwtion. The spleen was enlarged, extending down to the umbilicus. The liver was not palpable. There was no ascites.
Fig. 71 (Case I). Roentgenogram of esophagus after the ingestion of barium showing marked esophageal varices in lower one-half of esophagus. No varicosities were demonstrable in the stomach. Fig. 72 (Case I). Roentgenogram of esophagus and proximal stomach following a barium meal, two and one-half weeks after surgery. No varices are seen nor were any demonstrated at fluoroscopy. A well-functioning esophagogastrostomy is shown.
Laboratory Studies. Blood studies showed a hemoglobin of 10.5 gm. and a red blood count of 4,500,000 cells per cubic millimeter. Repeated stool examinations were strongly positive for blood. Liver function studies were normal. Roentgenograms of the esophagus after the ingestion of barium revealed large varices of the lower half of the esophagus (Fig. 71). In view of the extensive varicosities and the repeated hemorrhages, surgery was recommended, but refused by the patient. In August 1948, after not being seen for five years, he was readmitted because of two large emeses of bright red blood during the preceding tw,elve hours.
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He was t.reated with transfusions, and t.he bleeding stopped. The patient was again advised to have surgery, but refused. His third admission on September 22, 1949, was preceded by three emeses of bright red blood which totaled approximately 1600 cc. The bleeding continued, and the next day he had an emesis of approximately 1100 cc. At, this time the patient was given per orem 1 ounce of a 7 per cent liquid gelatin every hour. This was continued for twent.y-four hours. No further bleeding was evident. After the patient.'s hemodynamics had been restored to normal, liver function studies were again performed and were within the normal range. On October 7, 1949, a transthoracic partial esophagogastrectomy and splenectomy were performed. In addition, the vessels to the proximal half of the stomach were ligated.
Procedure. Endotracheal anesthesia was employed. With the patient on his right side, the chest was opened through the bed of the left eighth rib. This afforded an excellent exposure. The phrenic nerve was crushed just above the diaphragm. Enormously dilated venins were present around the lower third of the esophagus, the largest of these being approximately 3 cm. in diameter. The inferior pulmonary ligament was divided, allowing retraction of the lung. A radial incision was made in the diaphragm, extending from the costal arch through the esophageal hiatus. This provided good exposure to the stomach and spleen. Greatly dilated short gastric vessels were observed. The esophagus and its accompanying dilated veins were carefully dissected from the posterior mediastinum by means of blunt and sharp dissection. At the level of the inferior pulmonary vein several of the large varices seemed to unite and form a large varix about 3 cm. in diameter. From this varix there was a large vein which went directly across the mediastinum and emptied into the inferior vena cava. This was divided and ligated. The enlarged spleen was removed, and the greater omentum was divided close to the stomach nearly to the pylorus. The vessels to the proximal third of the lesser curvature of the stomach were divided. The large dilated periesophageal veins were ligated 10 cm. above the cardia. Next, the stomach was divided just below the cardioesophageal junction, and the distal end closed. The lower 8 cm. of the esophagus was resected. The vagus nerves were divided, and an esophagogastrostomy was performed between the open esophagus and the fundus of the stomach. The liver, which showed mild cirrhotic changes, was biopsied. The diaphragm was closed around the midportion of the stomach with a continuous suture of 0 chromic catgut reinforced with interrupted mattress sutures of cotton. The lung was completely expanded and the chest closed. A No. 28 Pezzer catheter was brought out through the ninth interspace for drainage. The patient withstood the
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operative procedure well and received 4500 cc. of blood on the day of surgery. Postoperative Course. The patient's recovery was uneventful. Liquids by mouth were started on the seventh postoperative day, and by the tenth postoperative day he was taking soft food. An x-ray of the esophagus and stomach following the ingestion of barium was taken two and a half weeks after surgery. No varices were demonstrable, and the esophagogastrostomy was functioning satisfactorily (Fig. 72). There has been no recurrence of the bleeding to date (December 1950). Pathology. The spleen weighed 770 gm. The microscopic picture was quite characteristic of that seen in Banti's syndrome. The "fibroadenie" of Banti were striking. The specimen of esophagus and stomach was about 5 cm. in length and was attached to a mass consisting chiefly of large dilated veins (Fig. 73). Microscopic study revealed large veins in all coats of the esophagus. The largest were in the submucosa. Huge varicose veins were present in the periesophageal tissue (Fig. 74). The liver showed early portal fibrosis. CASE
II
M. D., a 56 year old white woman, was first admitted to the University of Chicago Clinics on September 19, 1944, because of diarrhea and malaise for a period of five years. She had lost 47 pounds during the preceding three years. In addition, she had periods of dizziness, nausea, vomiting, vague abdominal pain and cramping pains in the calf muscles. Darkening of the skin was noted six to eight months before and had been slowly progressive. The patient had been told three years before that she had mild diabetes. She tE)sted her urine frequently and obtained positive values intermittently. She did not take any insulin. Family history revealed that her mother and a sister had diabet~. Physical Examination. The skin showed a generalized brown color which was most accentuated on the face, arms, legs and in the body folds. The liver and spleen were markedly enlarged. There was no ascites. Laboratory Studies. There was a mild anemia. Fasting blood sugar was 180 mg. per 100 cc. Liver function studies were within normal range. Roentgenogram of the esophagus after the ingestion of barium was normal. A diagnosis of hemochromatosis was made. Clinical Course. The patient continued in fairly good condition with littl~ change in her symptoms or physical findings until October 1947, when she had an episode of vaginal bleeding. Examination at this time revealed extensive vaginal varices. Six months later she had her first episode of hematemesis. On December 30, 1948, she was readmitted to the hospital because of a second episode of gastroesophageal bleeding. At this time her skin was a bronze color. The spleen and liver were about the same size. The stools were strongly positive for blood. Liver
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-ESOPHAGUS
Fig. 73 (Case I ). Photograph of removed specimen. The large mas of dilated veins which lay on the urface of the esopha~us is shown.
Fig. 74. Photomicrograph of cross section of specimen. It shows a large vein in submucosa and two large veins in the periesophageal tissue.
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function studies showed definite evidence of impaired hepatic function. Roentgenogram of the esophagus after the ingestion of barium at this time demonstrated spectacular varices of the esophagus below the level of the aortic arch. Gastric varices were also seen around the cardia
•
Fig. 75 (Case II). Roentgenogram of stomach and lower esophagus after the ingestion of barium before surgery and four weeks postoperatively. The top two x-rays show extensive varicosities in the lower esophagus and proximal stomach. The bottom two x-rays show a well functioning gastroesophagostomy. No varices are demonstrable.
(Fig. 75). Esophagoscopy confirmed the presence of large varices beginning at the level of the junction between the upper and middle thirds of the esophagus. An unsuccessful attempt was made to inject the varicosities with a sclerosing agent. Moderate bleeding continued, and, because of the probability of a massive hemorrhage, surgery was advised.
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On March 4, 1049, a transthoracic partial esophagogastrectomy was performed along with a splenectomy.
Procedure. The chest was opened through the left eighth interspace. Large tortuous varices were present on the external surface of the esophagus. The diaphragm was opened and a markedly enlarged spleen removed. The left gastric vein was prominent and tortuous. The proximal three-fourths of the stomach was removed along with the distal 3 cm. of the esophagus. The vagus nerves were divided and an esophagogastrostomy performed between the open esophagus and the anterior wall of the remaining portion of the stomach. The liver was large, firm and nodular; a biopsy was made. The diaphragm and chest were closed in a fashion similar to that described for Case 1. Postoperative Course. The patient made a slow recovery following operation. Roentgenogram of the esophagus taken four weeks after surgery showed a well-functioning gastroesophagostomy. No definite varices were demonstrable (Fig. 75). There has been no evidence of further bleeding (December 1950). Pathology. The gross specimen consisted of approximately threefourths of the proximal stomach and distal 3 em. of the esophagus along with" a markedly enlarged spleen which weighed 550 gm. (Fig. 76). Microscopic examination revealed large dilated veins, particularly in the submucosa, of the stomach and esophagus (Fig. 77). The liver showed a moderately advanced cirrhosis. The spleen showed chronic passive congest.ion and moderate fibrosis of the lymphoid nodules. DISCUSSION
Bleeding from gastric and/or esophageal varices associated with portal hypertension presents one of the most serious and difficult problems which the clinician may encounter. Such bleeding, while common in patients with hepatic cirrhosis," may occur with little demonstrable liver damage or with extrahepatic obstruction and no liver disease. It has been estimated that 20 per cent of patients with cirrhosis die from gastrointestinal hemorrhage. In the two cases discussed each had repeated hemorrhages from large gastroesophageal varices. Although both had liver damage, in one it was minimal and in the other advanced. Neither patient has had postsurgical bleeding. Case 1 has returned to work and appears in excellent health. The second case, with the advanced liver disease, has continued to lose weight and strength. In the two cases presented the extent of the resection was varied. In Case I the lower 8 cm. of the esophagus and a small rim of stomach were removed. In Case II, because of the large gastric varices, the proximal three-fourths of the stomach was resected along with the lower 3 cm. of the esophagus. According to the preoperative roentgenograms, at least the lower half of the esophagus in both cases had large
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submucosal varices. In both cases varices remained above the resection However, there has been no bleeding since surgery, and no varices have been demonstrated by x-ray. Partial esophagogastrectomy apparently separates the esophagus from the high venous pressure of the portal circulation.
Fig. 76 (Case II). Photograph of removed specimen. Spleen, proximal threequarters of stomach and distal! inch of esophagus are shown.
Both cases had a complete vagotomy which greatly reduced the acidpeptic digestive factor. Wangensteen21 advocates that this factor is an important cause of bleeding from the mucosa in the presence of portal hypertension. That the ideal method of therapy for bleeding gastroesophageal varices has not been devised is indicated by the failures observed in all procedures. Too few cases of partial esophagogastrectomy have
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been performed, and the follow-up period has been too short to evaluate this method fully. One of the patients, reported by Phemister and Humphreys, upon whom a total gastrectomy was performed in August 1944, had hemorrhages during the first three years after operation. But during the subse-
'Fig. 77 (Case II). Photomicrograph of removed stomach. It shows extensive dilated vessels in the submucosa. No ulceration of the mucosa was observed.
quent three and a third years, aside from a two months' period of moderate anemia, he has remained in as good health as the average patient after gastrectomy performed for other conditions. He is working full time as a salesman. The second patient who· had a partial esophagogastrectomy in December 1946 has been well and free of any bleeding to date (December, 1950). <\.t the University of Iowa22 partial esophagogastrectomy and splenec-
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tomy has been performed on five patients who had massive esophageal hemorrhage as a result of portal cirrhosis. The results were gratifying. Schafer and Kittle24 have recently reported six cases with esophagogastric varices treated by partial esophagogastrectomy. Only one of tht' six patients had a recurrence of bleeding after resection. The cases had been followed for too short a time to warrant any final conclusion, but the early results were very gratifying .. It has been pointed out20 that partial gastroesophagectomy might increase the load on other collateral channels. If such is true, the possibility of a massive hemorrhage is probably remote, since they are not subjected to trauma or the acid-peptic factor, as are the esophageal varices. Case II had some bleeding from vaginal varices which was easily controlled. Gastroesophageal resection is a procedure of considerable magnitude, but in experienced hands the mortality and morbidity are not prohibitive. The experiences to date are sufficiently encouraging to warrant further trial, particularly in cases in which the hemorrhage has not been controlled by splenectomy or a shunt. SUMMARY
A brief review of the literature pertaining to the surgical treatment of bleeding gastroesophageal varices associated with portal hypertension is presented. Two cases with hemorrhage from gastroesophageal varices treated by partial gastroesophagectomy, splenectomy and vagotomy are discussed. The two cases reported by Phemister and Humphreys, one treated by esophagogastrectomy and the other by total gastrectomy, are brought up to date. The operative technic is described. REFERENCES 1. Whipple, A. 0.: The Problem of Portal Hypertension in Relation to the Hepatosplenopathies. Ann. Surg. 122:449, 1945. 2. Walter, W., Moersch, H. J. and McKinnon, D. A.: Bleeding Esophageal Varices. An Evaluation of Methods Directed toward Their Control, Especially by Direct Injection of a Sclerosing Solution. Arch. Surg. 41 :1101, 1940. 3. Womack, N. E.: The Surgery of Portal Hypertension, in Cole's Operative Technic, General Surgery. New York, Appleton-Century-Crofts, Inc., 1949. 4. Rousselot, L. M.: The Role of Congestion (Portal Hypertension) in So-Called Banti's Syndrome. J.A.M.A. 107:1788, 1936. 5. McIndoe, A. H.: Vascular Lesions of Portal Cirrhosis. Arch. Path. 5:23, 1928. 6. Rivers, A. B. and Wilbur, D. L.: The Diagnostic Significance of Hematemesis. J.A.M.A. 98:1629, 1932.
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7. Barg, E. H., and Dulin, J. W.: Splenectomy in the Treatment of Banti's Syndrome. Arch. Surg. 41:91,1940. 8. Blakemore, A. H.: Indications for Portacaval Anastomosis-Analysis of Cases. Surg., G\ynec. & Obst. 84:645, 1947. 9. Blalock, A.: The Use of Shunt or By-Pass Operations in the Treatment of Certain Circulatory Disorders, Including Portal Hypertension and Pulmonic Stenosis. Ann. Surg. 125:129, 1947. 10. Crafoord, C. and Frenckner, P.: New Treatment of Varicose Veins of the Esophagus. Acta Otolaryngologica. 27:422, 1939. 11. Vander Veer, E. A.: Talma Operation for Cirrhosis of the Liver. Surg., Gynec. & Obst. 15:278, 1912. 12. Mayo, W. J.: The Surgical Treatment of the Cirrhoses of the Liver and Their Complications. Papers Mayo Clinic. 10:143, 1918. 13. Eck, N. V.: The Ligature of the Portal Vein. Voyeno Med. J., 1877. 14. Vidal, M. E.: Discussion of de Martel's Case. Rev. de Chirurgie. 42:1181,1910. 15. Rosenstein, P.: Vber die Behandlung der Leber Cirrhose durch Aulegung einer Eck'schen FisteI. Arch. f. klin. Chirurgie. 98:1082, 1912. 16. Blakemore, A. H. and Lord, J. W.: The Technic of Using Vitallium Tubes in Establishing Portacaval Shunts for Portal Hypertension. Ann. Surg. 122:476, 1945. 17. Blakemore, A. H.: The Portacaval Shunt in the Surgical Treatment of Portal Hypertension. Ann. Surg. 128:825, 1948. 18. Julian, O. C. and Metcalf, W.: Non-obstructive Lateral Portal Vein-Vena Cava Anastomosis. Arch. Surg. 59:433, 1949. 19. Blakemore, A. H.: Portacaval Anastomosis. Surg., Gynec. & Obst. 87:277, 1948. 20. Phemister, D. B. and Humphreys, E. M.: Gastro-Esophageal Resection and Total Gastrectomy in the Treatment of Bleeding Varicose Veins in Banti's Syndrome. Ann. Surg. 126:17, 1947. 21. Baronofsky, 1. 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. 22. Womack, N. A.: Personal communication. 23. Gatch, W. D.: Mechanism of Blood Flow in Veins of Abdomen and Lower Extremities. Arch.Surg. 61: 34, 1950. 24. Schafer, P. W. ~nd Kittle, C. F.: Partial Esophagogastrectomy in the Treatment of Esophagogastric Varices. Arch. Surg. 61: 235, 1950.
Portal hypertension is an intermediate phase of a clinical syndrome which may be produced by anyone of a number of disease entities. It is probably never a primary disease. The causative factors have as a common denominator the ability to effect obstruction of the portal venous system. The primary block may occur within the portal vein or its tributaries, the liver, or the hepatic vein. The more distal the process, the more discrete is the clinical picture. Occlusion of the splenic vein may lead to congestion of the spleen. When the block is sufficient to cause splenomegaly, there may be secondary anemia, leukopenia, thrombocytopenia and a tendency toward repeated gastrointestinal hemorrhages, frequently associated with ruptured esophageal or gastric varices. 1 Components of this picture have been variously called Banti's syndrome, splenic anemia,2 hypersplenism3 and the syndrome of the portal bed block. 1 When the pathologic process is extrahepatic, involving only the portal vein or its tributaries, it may be classified in one of two groups.l In the first group obliterative scarring occurs in the vein, presumably as a result of the chronic phase of a thrombotic process, with little or no recanalization. In the second there is a reorganization of the portal vein and surrounding tissue into a mass of small vessels, termed "cavernomatous transformation of the portal vein." The etiology is unknown and is likely variable. When the process is intrahepatic, as in cirrhosis of the liver, the situation becomes more complex. The type of cirrhosis and efficacy of collateral vein formation determine to a considerable extent the development of portal hypertension and, secondarily, of Banti's syndrome. Rousselot4 described a group of cases of portal hypertension without From the Department of Surgery, University of Chicago School of Medicine. * Atomic Energy Commission Postdoctoral Fellow. t Associate Professor of Surgery, University of Chicago; Senior Attending Surgeon, Albert Merritt Billings Hospital, The University of Chicago Clinics. t Professor of Surgery, University of Chicago School of Medicine. § Professor Emeritus of Surgery, University of Chicago.
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visible obstruction and suggested that such increased pressure may occur as a primary disturbance of the portal system. It is possible that in these ca~es an obstructive factor was present but not found at surgery. One of the results of portal obstruction is congestion of all or a part of the portal system, depending on the site of obstruction, and, since the system is without valves, congestion of the tissues it drains. Associated with congestion is an increased venous pressure which may reach four or five times the normal levels.3 • 4 Presumably as a compensatory mechanism to decreased blood flow from the portal system through the liver, a group of collateral veins connecting directly with the general systemic circulation dilate and may ultimately carry a major portion of the portal blood flow. McIndoe 5 found in cirrhotic livers that 13 per cent or less of the fluid perfused through the portal vein was recovered from the hepatic vein. The collateral circulation is established chiefly by use of four previously existing but normally little used communications between the portal and caval systems. These vascular connections occur between the coronary vein and the intercostal veins, azygos system, and diaphragmatic veins; the superior and middle hemorrhoidal veins; the paraumbilical veins of the falciform ligament and the deep epigastric and internal mammary veins; branches of the portal system which supply organs that are either developmentally retroperitoneal or pathologically adherent to the abdominal wall and retroperitoneal branches of the inferior vena cava. The last group of communications is called the veins of Retzius. As a rule the collateral channels behave well. The exception arises from communications of the coronary vein. This route provides the shortest path, is not hindered by valves, and provides a relatively direct connection between the portal system and the lower esophageal veins. The submucosal veins of this portion of the esophagus are poorly supported by connective tissue2 and are unfortunately prone to dilatation and formation of varices which are in turn highly subject to rupture and hemorrhage. Gastric varices may also develop and bleeding result. Thus, Rivers and Wilbur, in a study of 668 patients with hematemesis, found that in 5 per cent bleeding was attributable to hepatic cirrhosis or splenic anemia. 6 TREATMENT
Therapy is administered according to the disease process in operation. In cirrhosis and other diseases of the liver, adequate medical management is essential. Surgical treatment in the cases of intrahepatic obstruction is directed at control of portal hypertension and one or more of the symptoms, such as esophagogastric hemorrhage, hypersplenism and ascites. Surgery is justified by the frequency with which components
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of this triad may lead to death in spite of the best care of the primary disease. In cases in which the pathology is limited to the extrahepatic veins, the surgeon may have the opportunity to sidetrack the primary obstruction. The present communication deals with the surgical approach and in particular with esophagogastric resection in the control of hemorrhage. A brief resume of previously described surgical procedures is presented. Splenectomy. It has been estimated that blood passing through the spleen contributes 20 to 40 per cent of the total portal flow. 2 • 3 Splenectomy removes this portion of the portal blood flow and thus tends to reduce the portal pressure. It also interrupts the vessels which feed into varices of the cardia, diaphragm and esophagus by way of the gastrolienal ligament. Rousselot4 in 1936 reported a series of thirty-one cases of Banti's syndrome treated by splenectomy. Seven of the eleven patients with esophageal hemorrhage prior to surgery eventually died of this complication, and the author states "that in this type of case, operation should be avoided." Barg and Dulin7 splenectomized twenty-two patients with Banti's syndrome and had six operative deaths. Of the remaining sixteen, four are symptom free; two have malaise and weakness; two had repeated esophageal hemorrhages, but were living at time of report; four are dead of gastroesophageal hemorrhage; one is dead following hemorrhage at paracentesis site; one is dead of unknown cause; and two are lost to follow-up. It was concluded that splenectomy for this syndrome has a favorable influence on ascites and in general is preferable to a nonoperative regimen but that it does not assure relief from gastroesophageal hemorrhage. According to Whipple, l splenectomy may afford relief until the hypertension rebuilds, but is permanent only when the obstruction lies within the splenic vein. Blakemore 8 states that splenectomy will cure only the small group of cases of splenic vein thrombosis in which the obstruction is distal to the entrance of the coronary vein. In the presence of ·esophageal varices, splenectomy for a splenic vein thrombosis which lies proximal to the entrance of the coronary vein should be done only when it is accompanied by a splenorenal anastomosis. 9 Ligation of the Coronary Vein. As a means of preventing hemorrhage from gastroesophageal varices, ligation of the coronary vein with and without splenectomy has been practiced. 2 Whipple 1 and Blalock 9 describe the results of this procedure as disappointing and discouraging. In an effort to accomplish the same end, Crafoord and Frenckner10 injected, through an esophagoscope, the esophageal varices of a patient who had repeated esophageal hemorrhage following splenectomy. Over a period of three years this patient had no further symptoms and no esophagoscopic evidence of recurrence, and only small defects in the
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lower esophagus were found with a contrast shadow roentgenogram. Injection treatment of esophageal varices has also been used at the Mayo Clinic. 2 Whipple! believes that this procedure is no better than the ligation method and that, at best, these procedures shut off one of the chief collaterals connecting the portal and systemic circuits, thus raising the portal hypertension. Modified Talma Operation. In an endeavor to promote the formation of additional collateral circulation, Talmal l and his associates described a procedure for attaching the omentum to the abdominal wall. In 1918, Mayo !2 introduced a modification in which the omentum is drawn into the incised rectus muscle and sutured there. Whipple1 and Blalock 9 both write discouragingly of this procedure. It has not gained wide acceptance. Portacaval Anastomosis. In 1877, Eck,13 while studying hepatic physiology, developed a procedure in dogs for the anastomosis of the portal vein to the inferior vena cava. He suggested its possible use in aiding venous return in cases with portal vein obstruction. The first such operation on a patient was claimed by Vidal in 1903,l4 This patient died of a septic endophlebitis after fourteen weeks. In 1912, Rosenstein!5 reported a case of cirrhosis and ascites in which he had made an Eck fistula. A five months' follow-up showed a marked decrease of ascites. Operative difficulties and a high mortality rate delayed adoption of this approach until Blakemore and Lord16 published their nonsuture method of blood vessel anastomosis. Originally they reported ten patients, five of whom had a splenorenal vein anastomosis accompanied by splenectomy and left nephrectomy. The second five had an end-to-side portal vein to inferior vena cava anastomosis. All survived surgery. The authors were much encouraged by the results and have, along with others, continued to study and apply the method. 8, 9,17,18,19 In 1948, Blakemore17 presented a discussion of the results of fiftyeight portacaval shunts, There were eleven postoperative deaths: three of cholemia; two with cerebral hemorrhage, one of cardiac failure, three cases of mesenteric thrombosis, one from intraperitoneal hemorrhage, and one from gastrointestinal hemorrhage. Of the thirty-five cases who gave a history of preoperative gastrointestinal bleeding, eleven had one or more attacks of hemorrhage after discharge from the hospital. Followup time ranged from a few months to three or more years, Five of these patients had had previous splenectomies. Four of the five had extrahepatic portal block which necessitated use of a vein other than the portal for the anastomosis. In patients with extrahepatic portal block and previous splenectomy, anastomosis was usually limited to the superior mesenteric vein or the inferior mesenteric vein, In cases with extrahepatic portal block and without previous surgery, the high incidence of portal vein involvement necessitated dependence primarily upon the
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splenic vein for establishment of an anastomosis. In the series of fiftyeight patients, a vena cava to portal vein anastomosis was employed only nine times with one postoperative death. Fear of thrombosis of the portal vein towards and into the liver was the chief reason the portal vein to vena cava shunt was not used more frequently. A single case of side-to-side vena cava to portal vein anastomosis was included. This new procedure offered these advantages: (1) portal flow to the liver, and (2) a lessened tendency to thrombosis extending toward the liver. More recently, Julian has presented a technic for the side-to-side portal vein vena cava anatomosis.1 8 Total Gastrectomy and Partial Gastroesophagectomy. In the two patients with Banti's syndrome, Phemister and Humphreys 20 did a total gastrectomy in one and an esophagogastric resection in the other. Each of these patients had multiple hemorrhages which began at an early age and persisted after splenectomy. A favorable response was obtained in each case. They point out that, like obliteration of the esophageal varices by ligation, resection of the bleeding segment imposes a greater load on the remaining collateral circulation. Thel'le collaterals, however, bleed infrequently. If patients with portal hypertension and extrahepatic block, especially the splenectomized ones, can be kept from bleeding to death, they may live in good health indefinitely. Resection therapy does not involve a nephrectomy or interruption of whatever portal circulation does reach the liver. It offers a possible control of gastroesophageal hemorrhage without dependence on the continued patency of a venous-venous anastomosis. Veins leading to or from the liver are not interfered with; hence the chance of a postoperative thrombus forming and extending into the liver is markedly diminished. On a physiological basis Gatch 23 reported "The tendency of esophageal varices to bleed is explained by their location where dilatation of them is favored by the negative pressure of the chest and not opposed by positive pressure of the abdomen. Relief from danger of death due to hemorrhage from these varices is the chief benefit which the victim of portal hypertension can expect from any operation. Gastroesophageal resection, I believe, is more likely to give him the relief, and with less danger, than portacaval shunt." Since the report of Phemister and Humphreys, two additional cases of Banti's syndrome with bleeding gastroesophageal varices have been treated in this clinic by partial esophagogastric resection with encouraging results. REPORT OF TWO CASES CASE
I
A 34 year old white man, was first seen at the University of Chicago Clinics in 1941 with a history of hematemesis and tarry stools occurring
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in episodes of several weeks' duration at the ages of 14, 28 and 31 years. Re presented himself for a check-up, although he had had no bleeding during the preceding three years. The initial hematemesis occurred while doing heavy work and was preceded by sudden and severe weakness. It was noted that an injury to the abdomen had been sustained at the age of 12 years. Physical Examirwtion. The spleen was enlarged, extending down to the umbilicus. The liver was not palpable. There was no ascites.
Fig. 71 (Case I). Roentgenogram of esophagus after the ingestion of barium showing marked esophageal varices in lower one-half of esophagus. No varicosities were demonstrable in the stomach. Fig. 72 (Case I). Roentgenogram of esophagus and proximal stomach following a barium meal, two and one-half weeks after surgery. No varices are seen nor were any demonstrated at fluoroscopy. A well-functioning esophagogastrostomy is shown.
Laboratory Studies. Blood studies showed a hemoglobin of 10.5 gm. and a red blood count of 4,500,000 cells per cubic millimeter. Repeated stool examinations were strongly positive for blood. Liver function studies were normal. Roentgenograms of the esophagus after the ingestion of barium revealed large varices of the lower half of the esophagus (Fig. 71). In view of the extensive varicosities and the repeated hemorrhages, surgery was recommended, but refused by the patient. In August 1948, after not being seen for five years, he was readmitted because of two large emeses of bright red blood during the preceding tw,elve hours.
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He was t.reated with transfusions, and t.he bleeding stopped. The patient was again advised to have surgery, but refused. His third admission on September 22, 1949, was preceded by three emeses of bright red blood which totaled approximately 1600 cc. The bleeding continued, and the next day he had an emesis of approximately 1100 cc. At, this time the patient was given per orem 1 ounce of a 7 per cent liquid gelatin every hour. This was continued for twent.y-four hours. No further bleeding was evident. After the patient.'s hemodynamics had been restored to normal, liver function studies were again performed and were within the normal range. On October 7, 1949, a transthoracic partial esophagogastrectomy and splenectomy were performed. In addition, the vessels to the proximal half of the stomach were ligated.
Procedure. Endotracheal anesthesia was employed. With the patient on his right side, the chest was opened through the bed of the left eighth rib. This afforded an excellent exposure. The phrenic nerve was crushed just above the diaphragm. Enormously dilated venins were present around the lower third of the esophagus, the largest of these being approximately 3 cm. in diameter. The inferior pulmonary ligament was divided, allowing retraction of the lung. A radial incision was made in the diaphragm, extending from the costal arch through the esophageal hiatus. This provided good exposure to the stomach and spleen. Greatly dilated short gastric vessels were observed. The esophagus and its accompanying dilated veins were carefully dissected from the posterior mediastinum by means of blunt and sharp dissection. At the level of the inferior pulmonary vein several of the large varices seemed to unite and form a large varix about 3 cm. in diameter. From this varix there was a large vein which went directly across the mediastinum and emptied into the inferior vena cava. This was divided and ligated. The enlarged spleen was removed, and the greater omentum was divided close to the stomach nearly to the pylorus. The vessels to the proximal third of the lesser curvature of the stomach were divided. The large dilated periesophageal veins were ligated 10 cm. above the cardia. Next, the stomach was divided just below the cardioesophageal junction, and the distal end closed. The lower 8 cm. of the esophagus was resected. The vagus nerves were divided, and an esophagogastrostomy was performed between the open esophagus and the fundus of the stomach. The liver, which showed mild cirrhotic changes, was biopsied. The diaphragm was closed around the midportion of the stomach with a continuous suture of 0 chromic catgut reinforced with interrupted mattress sutures of cotton. The lung was completely expanded and the chest closed. A No. 28 Pezzer catheter was brought out through the ninth interspace for drainage. The patient withstood the
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operative procedure well and received 4500 cc. of blood on the day of surgery. Postoperative Course. The patient's recovery was uneventful. Liquids by mouth were started on the seventh postoperative day, and by the tenth postoperative day he was taking soft food. An x-ray of the esophagus and stomach following the ingestion of barium was taken two and a half weeks after surgery. No varices were demonstrable, and the esophagogastrostomy was functioning satisfactorily (Fig. 72). There has been no recurrence of the bleeding to date (December 1950). Pathology. The spleen weighed 770 gm. The microscopic picture was quite characteristic of that seen in Banti's syndrome. The "fibroadenie" of Banti were striking. The specimen of esophagus and stomach was about 5 cm. in length and was attached to a mass consisting chiefly of large dilated veins (Fig. 73). Microscopic study revealed large veins in all coats of the esophagus. The largest were in the submucosa. Huge varicose veins were present in the periesophageal tissue (Fig. 74). The liver showed early portal fibrosis. CASE
II
M. D., a 56 year old white woman, was first admitted to the University of Chicago Clinics on September 19, 1944, because of diarrhea and malaise for a period of five years. She had lost 47 pounds during the preceding three years. In addition, she had periods of dizziness, nausea, vomiting, vague abdominal pain and cramping pains in the calf muscles. Darkening of the skin was noted six to eight months before and had been slowly progressive. The patient had been told three years before that she had mild diabetes. She tE)sted her urine frequently and obtained positive values intermittently. She did not take any insulin. Family history revealed that her mother and a sister had diabet~. Physical Examination. The skin showed a generalized brown color which was most accentuated on the face, arms, legs and in the body folds. The liver and spleen were markedly enlarged. There was no ascites. Laboratory Studies. There was a mild anemia. Fasting blood sugar was 180 mg. per 100 cc. Liver function studies were within normal range. Roentgenogram of the esophagus after the ingestion of barium was normal. A diagnosis of hemochromatosis was made. Clinical Course. The patient continued in fairly good condition with littl~ change in her symptoms or physical findings until October 1947, when she had an episode of vaginal bleeding. Examination at this time revealed extensive vaginal varices. Six months later she had her first episode of hematemesis. On December 30, 1948, she was readmitted to the hospital because of a second episode of gastroesophageal bleeding. At this time her skin was a bronze color. The spleen and liver were about the same size. The stools were strongly positive for blood. Liver
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-ESOPHAGUS
Fig. 73 (Case I ). Photograph of removed specimen. The large mas of dilated veins which lay on the urface of the esopha~us is shown.
Fig. 74. Photomicrograph of cross section of specimen. It shows a large vein in submucosa and two large veins in the periesophageal tissue.
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function studies showed definite evidence of impaired hepatic function. Roentgenogram of the esophagus after the ingestion of barium at this time demonstrated spectacular varices of the esophagus below the level of the aortic arch. Gastric varices were also seen around the cardia
•
Fig. 75 (Case II). Roentgenogram of stomach and lower esophagus after the ingestion of barium before surgery and four weeks postoperatively. The top two x-rays show extensive varicosities in the lower esophagus and proximal stomach. The bottom two x-rays show a well functioning gastroesophagostomy. No varices are demonstrable.
(Fig. 75). Esophagoscopy confirmed the presence of large varices beginning at the level of the junction between the upper and middle thirds of the esophagus. An unsuccessful attempt was made to inject the varicosities with a sclerosing agent. Moderate bleeding continued, and, because of the probability of a massive hemorrhage, surgery was advised.
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On March 4, 1049, a transthoracic partial esophagogastrectomy was performed along with a splenectomy.
Procedure. The chest was opened through the left eighth interspace. Large tortuous varices were present on the external surface of the esophagus. The diaphragm was opened and a markedly enlarged spleen removed. The left gastric vein was prominent and tortuous. The proximal three-fourths of the stomach was removed along with the distal 3 cm. of the esophagus. The vagus nerves were divided and an esophagogastrostomy performed between the open esophagus and the anterior wall of the remaining portion of the stomach. The liver was large, firm and nodular; a biopsy was made. The diaphragm and chest were closed in a fashion similar to that described for Case 1. Postoperative Course. The patient made a slow recovery following operation. Roentgenogram of the esophagus taken four weeks after surgery showed a well-functioning gastroesophagostomy. No definite varices were demonstrable (Fig. 75). There has been no evidence of further bleeding (December 1950). Pathology. The gross specimen consisted of approximately threefourths of the proximal stomach and distal 3 em. of the esophagus along with" a markedly enlarged spleen which weighed 550 gm. (Fig. 76). Microscopic examination revealed large dilated veins, particularly in the submucosa, of the stomach and esophagus (Fig. 77). The liver showed a moderately advanced cirrhosis. The spleen showed chronic passive congest.ion and moderate fibrosis of the lymphoid nodules. DISCUSSION
Bleeding from gastric and/or esophageal varices associated with portal hypertension presents one of the most serious and difficult problems which the clinician may encounter. Such bleeding, while common in patients with hepatic cirrhosis," may occur with little demonstrable liver damage or with extrahepatic obstruction and no liver disease. It has been estimated that 20 per cent of patients with cirrhosis die from gastrointestinal hemorrhage. In the two cases discussed each had repeated hemorrhages from large gastroesophageal varices. Although both had liver damage, in one it was minimal and in the other advanced. Neither patient has had postsurgical bleeding. Case 1 has returned to work and appears in excellent health. The second case, with the advanced liver disease, has continued to lose weight and strength. In the two cases presented the extent of the resection was varied. In Case I the lower 8 cm. of the esophagus and a small rim of stomach were removed. In Case II, because of the large gastric varices, the proximal three-fourths of the stomach was resected along with the lower 3 cm. of the esophagus. According to the preoperative roentgenograms, at least the lower half of the esophagus in both cases had large
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submucosal varices. In both cases varices remained above the resection However, there has been no bleeding since surgery, and no varices have been demonstrated by x-ray. Partial esophagogastrectomy apparently separates the esophagus from the high venous pressure of the portal circulation.
Fig. 76 (Case II). Photograph of removed specimen. Spleen, proximal threequarters of stomach and distal! inch of esophagus are shown.
Both cases had a complete vagotomy which greatly reduced the acidpeptic digestive factor. Wangensteen21 advocates that this factor is an important cause of bleeding from the mucosa in the presence of portal hypertension. That the ideal method of therapy for bleeding gastroesophageal varices has not been devised is indicated by the failures observed in all procedures. Too few cases of partial esophagogastrectomy have
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been performed, and the follow-up period has been too short to evaluate this method fully. One of the patients, reported by Phemister and Humphreys, upon whom a total gastrectomy was performed in August 1944, had hemorrhages during the first three years after operation. But during the subse-
'Fig. 77 (Case II). Photomicrograph of removed stomach. It shows extensive dilated vessels in the submucosa. No ulceration of the mucosa was observed.
quent three and a third years, aside from a two months' period of moderate anemia, he has remained in as good health as the average patient after gastrectomy performed for other conditions. He is working full time as a salesman. The second patient who· had a partial esophagogastrectomy in December 1946 has been well and free of any bleeding to date (December, 1950). <\.t the University of Iowa22 partial esophagogastrectomy and splenec-
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tomy has been performed on five patients who had massive esophageal hemorrhage as a result of portal cirrhosis. The results were gratifying. Schafer and Kittle24 have recently reported six cases with esophagogastric varices treated by partial esophagogastrectomy. Only one of tht' six patients had a recurrence of bleeding after resection. The cases had been followed for too short a time to warrant any final conclusion, but the early results were very gratifying .. It has been pointed out20 that partial gastroesophagectomy might increase the load on other collateral channels. If such is true, the possibility of a massive hemorrhage is probably remote, since they are not subjected to trauma or the acid-peptic factor, as are the esophageal varices. Case II had some bleeding from vaginal varices which was easily controlled. Gastroesophageal resection is a procedure of considerable magnitude, but in experienced hands the mortality and morbidity are not prohibitive. The experiences to date are sufficiently encouraging to warrant further trial, particularly in cases in which the hemorrhage has not been controlled by splenectomy or a shunt. SUMMARY
A brief review of the literature pertaining to the surgical treatment of bleeding gastroesophageal varices associated with portal hypertension is presented. Two cases with hemorrhage from gastroesophageal varices treated by partial gastroesophagectomy, splenectomy and vagotomy are discussed. The two cases reported by Phemister and Humphreys, one treated by esophagogastrectomy and the other by total gastrectomy, are brought up to date. The operative technic is described. REFERENCES 1. Whipple, A. 0.: The Problem of Portal Hypertension in Relation to the Hepatosplenopathies. Ann. Surg. 122:449, 1945. 2. Walter, W., Moersch, H. J. and McKinnon, D. A.: Bleeding Esophageal Varices. An Evaluation of Methods Directed toward Their Control, Especially by Direct Injection of a Sclerosing Solution. Arch. Surg. 41 :1101, 1940. 3. Womack, N. E.: The Surgery of Portal Hypertension, in Cole's Operative Technic, General Surgery. New York, Appleton-Century-Crofts, Inc., 1949. 4. Rousselot, L. M.: The Role of Congestion (Portal Hypertension) in So-Called Banti's Syndrome. J.A.M.A. 107:1788, 1936. 5. McIndoe, A. H.: Vascular Lesions of Portal Cirrhosis. Arch. Path. 5:23, 1928. 6. Rivers, A. B. and Wilbur, D. L.: The Diagnostic Significance of Hematemesis. J.A.M.A. 98:1629, 1932.
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7. Barg, E. H., and Dulin, J. W.: Splenectomy in the Treatment of Banti's Syndrome. Arch. Surg. 41:91,1940. 8. Blakemore, A. H.: Indications for Portacaval Anastomosis-Analysis of Cases. Surg., G\ynec. & Obst. 84:645, 1947. 9. Blalock, A.: The Use of Shunt or By-Pass Operations in the Treatment of Certain Circulatory Disorders, Including Portal Hypertension and Pulmonic Stenosis. Ann. Surg. 125:129, 1947. 10. Crafoord, C. and Frenckner, P.: New Treatment of Varicose Veins of the Esophagus. Acta Otolaryngologica. 27:422, 1939. 11. Vander Veer, E. A.: Talma Operation for Cirrhosis of the Liver. Surg., Gynec. & Obst. 15:278, 1912. 12. Mayo, W. J.: The Surgical Treatment of the Cirrhoses of the Liver and Their Complications. Papers Mayo Clinic. 10:143, 1918. 13. Eck, N. V.: The Ligature of the Portal Vein. Voyeno Med. J., 1877. 14. Vidal, M. E.: Discussion of de Martel's Case. Rev. de Chirurgie. 42:1181,1910. 15. Rosenstein, P.: Vber die Behandlung der Leber Cirrhose durch Aulegung einer Eck'schen FisteI. Arch. f. klin. Chirurgie. 98:1082, 1912. 16. Blakemore, A. H. and Lord, J. W.: The Technic of Using Vitallium Tubes in Establishing Portacaval Shunts for Portal Hypertension. Ann. Surg. 122:476, 1945. 17. Blakemore, A. H.: The Portacaval Shunt in the Surgical Treatment of Portal Hypertension. Ann. Surg. 128:825, 1948. 18. Julian, O. C. and Metcalf, W.: Non-obstructive Lateral Portal Vein-Vena Cava Anastomosis. Arch. Surg. 59:433, 1949. 19. Blakemore, A. H.: Portacaval Anastomosis. Surg., Gynec. & Obst. 87:277, 1948. 20. Phemister, D. B. and Humphreys, E. M.: Gastro-Esophageal Resection and Total Gastrectomy in the Treatment of Bleeding Varicose Veins in Banti's Syndrome. Ann. Surg. 126:17, 1947. 21. Baronofsky, 1. 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. 22. Womack, N. A.: Personal communication. 23. Gatch, W. D.: Mechanism of Blood Flow in Veins of Abdomen and Lower Extremities. Arch.Surg. 61: 34, 1950. 24. Schafer, P. W. ~nd Kittle, C. F.: Partial Esophagogastrectomy in the Treatment of Esophagogastric Varices. Arch. Surg. 61: 235, 1950.