Shunt Operations for Esophageal Varices

SHUNT OPERATIONS FOR ESOPHAGEAL VARICES ORMAND C. JULIAN,

M.D., F.A.C.S. * AND

CHARLES

E.

FILDES,

M.D. t

ETIOLOGY OF PORTAL SYSTEM BLOCK

Obstruction to the free return of blood from the splanchnic bed through the liver to the systemic system by disease within the liver or in the extrahepatic venous channels stimulates the formation of large venous collaterals wherever they are anatomically possible. The relationshif between the obstruction and collateral vein formation is a direct one. However, it is somewhat less easily understood why the increased, pressure behind the obstruction should not be relieved by adequate collateral formation. The possibility of formation of a real arteriovenous shunt, within the diseased liver, between the hepatic artery and portal vein radicals at some point in their course to form the common hepatic vein drainage of the liver has been entertained. It is of interest to note in this connection that ligation of the portal vein in dogs, when it is done in two stages, produces a mass of collateral veins, but fails to produce a lasting portal vein hypertension. The venous collaterals formed in the dog in response to portal vein ligation may be more efficient, perhaps due to a shorter course and less friction, than they are in man. It is also possible that in some cases of portal hypertension there is an additional presently undiscovered factor which comes into play and maintains the portal vein pressure at an elevated level in spite of large collaterals. It is both convenient and probably accurate to divide the causes of portal flow obstruction into those which are intrahepatic and those which involve veins outside of the liver (Table 1). Portal hypertension of varying degrees develops some time during the course of the common types of cirrhosis of the liver. Gastrointestinal hemorrhage arising from esophageal varices occurs in a large proportion of such patients, and massive bleeding is the cause of death in a significant number. The Laennec form of cirrhosis has long been considered the typical form for the production of esophageal varices and hemorrhage. The fibrosis which From the Department of Surgery, University of Illinois College of Medicine, Chicago, and Vascular Service, Veterans Administration Hospital, Hines, Illinois. Published with the permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expressed and the conclusions drawn by the authors. * Assistant Professor of Surgery, University of Illinois College of Medicine; Attending Surgeon, Veterans Administration Hospital, Hines, Illinois. t Attending Surgeon, Veterans Administration Hospital, Hines, Illinois. Now at Veterans Administration Hospital, Poplar Bluff, Missouri. 229

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occurs during a long-continued incomplete or intermittent biliary obstruction will similarly produce portal hypertension and varices. The incidence of portal hypertension in the large number of persons who had infectious hepatitis during World War II has been low, but a few such Cases have been observed. Other intrahepatic diseases may be expected to produce the ,syndrome of portal hypertension. One such unusual case was that of schistosomiasis reported by Blakemore in which portal hypertension was present and was relieved by a portacaval shunt. TABLE 1 . ~.f". ( '1

ETIOLOGY OF PORTAL SYSTE'M'BLOCK

I. Intrahepatic " ,: A. Portal cirrhosis (Laennec) B. Cirrhosis secondary to biliary tract disease with chronic or intermittent bile flow obstruction .. C. Fibrosis of healed hepatitis. D. Schistosomiasis II. Extrahepatic A. Portal vein thrombosis 1. Trauma 2. Infection 3. Stasis due to intrahepatic obstruction (combined intrahepatic and, extrahepatic block) 4. Spontaneous B. Congenital obliteration of portal vein C. Cavernomatous degeneration of portal vein (possibly representing last stage of organization of portal vein thrombosis)

Conditions which result in partial or complete obliteration of the portal vein may be listed as extrahepatic causes of portal hypertension. Some are congenital, such as the extension into the portal vein of the obliterative process which destroys the umbilical vein, and some are acquired, such as a thrombosis of the portal vein secondary to infection or trauma. We believe that the true pathologic processes responsible for obstruction to the portal vein have not been investigated adequately. Surgical exploration of the hepatoduodenal ligament is certainly not sufficient for study of a pathologic entity, and autopsy information on this point is deficient. Evidences of portal hypertensIon are certainly rare in patients younger than 6 years of age. If congenital absence or atresia or abnormal obliteration of the portal vein is the cause of the syndrome in these patients, some explanation is needed as to why the signs do not appear earlier. Obstruction secondary to portal vein thrombosis is better established as a clinical entity. Before the application of early surgery in appendicitis and the introduction of chemotherapy, the occurrence of a phlebitis of the portal vein was a dreti.ded complication. Lesser degrees

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of inflammation in the presence of thrombosis of the vein would produce a relatively silent thrombosis and later lead to the syndrome of portal hypertension. Clarification of the processes which produce such a thrombosis will probably lead to the recognition of portal vein thrombosis secondary to infection, to trauma, and to the stasis of cirrhosis of the liver. Certain cases of portal vein thrombosis are spontaneous without any recognizable predisposing cause. The cavemomatous changes within the portal vein which are often ascribed to congenital causes or considered a neoplastic process are indistinguishable from the changes which would be expected when a thrombosed portal vein becomes incompletely and inefficiently recanalized. Thrombosis of the hepatic vein (Giares syndrome) leads to portal hypertension when recovery occurs. Blakemore has reported one such case which he successfully treated with a portacaval anastomosis. Thrombosis of the splenic vein, when it occurs distal to the coronary vein, will produce an elevated tension only within the portion of the portal system represented by the splenic vein, the coronary vein, and the vasa breva. This hypertension is moderate, but would result in dilatation of the esophageal veins, since they must carry the venous blood from the splenic area. In such a case there would be no elevation of pressure within the superior mesenteric or' portal veins. Linton and others have suggested that such a splenic vein thrombosis will be recognizable by the fact that, although the pressure within the splenic vein is high, mesenteric radical pressures will not be elevated. We have sought to recognize this condition by estimating, either manually or by manometer readings, the pressure within the splenic vein before and after the splenic artery is interrupted. In splenic thrombosis the splenic vein pressure distal to the obstruction falls to normal or below when the splenic artery is no longer bringing blood into the spleen. This evidence would not be valid if the inferior mesenteric vein enters the splenic vein on the spleen side of the occlusion. In this circumstance the surgeon will not be misled, because a splenorenal anastomosis would still be necessary. The continued elevated pressure in the splenic vein, after artery occlusion, would indicate this necessity. SURGICAL MANAGEMENT

Whatever the cause of the portal obstruction, the most distressing complication of the resulting hypertension is the formation and subsequent rupture of esophageal varices. This problem has been approached surgically in several ways. An indirect method of increasing collateral channels is the Talma operation of implantation of omentum into the abdominal wall. The portal radicles of the omentum tend to form con-

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nections with the systemic vein of the abdominal wall. Not many cases have responded well to this form of treatment. Resection of the varicose vein-bearing area of the esophagus and stomach has produced good results. It has been used in one case in our series. Splenectomy has long been used in cases of portal hypertension having esophageal varices, splenomegaly and anemia. The results in preventing hemorrhage have been disappointing; Blakemore, Cole and others have recently pointed out that splenectomy is not a logical operation in these circumstances. There is a diminished tendency to bleed for a limited period because the actual amount of portal flow is reduced by that portion which enters the portal system through the splenic artery. The "blood picture in Banti's syndrome is improved in so far as hypersplEmism is present. The authors agree with Linton that splenectomy should not be applied in Banti's syndrome even in the very early cases, because it diminishes the possibilities when later on some form of portacaval shunt may be needed in the patient. Great care should be used to rule out the presence of portal hypertension in patients presenting the syndrome of splenomegaly and pancytopenia before a splenectomy alone is done. Venous Shunt Operations. Since 1877, when Von Eck first produced a functional fistula between the portal vein and the vena cava in the e:x:perimental animal, a number of attempts have been made to make sur~ical collateral shunts between the portal system and the vena cava. : The application of improved methods of vascular anastombsis by Blakemore, Blalock, Linton and others has made successful production of such shunts possible. Sites. A variety of methods and sites of direct venous shunt between the portal ~ystem and the vena cava have been explore~. Two sites offer most promise of an efficient shunt: (1) between the portal vein and the vena cava, and (2) between the splenic vein, aftet splenectomy, and the side of the renal vein with preservation of the k i d n e y . ' Indications. The indication for venous shunt operation is portal hypertension, usually as evidenced by esophageal varices with or without bleeding. There is some clinical evidence to support the view that ascites in the presence of portal hypertension is in part a reflection of the increased portal pressure. Linton and Blakemore have both reported patients in whom the production of a satisfactory· venous shunt has resulted in the diminution of the tendency to form ascitic fluid. Experimental evidence, however, indicates that ascites is due both to increased portal pressure and to the protein metabolic defect, and may develop in the absence of any portal hypertension. Therefore, at this time, ascites is not to be considered a primary indication for a portacaval shunt, but rather ascitic patients should be operated upon when other evidence of portal hypertension exists. Modem medical treatment of

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Laennec's cirrhosis has resulted in many successes in the treatment of ascites. With improvement of liver function, especially in respect to a rise in blood albumin, failure to relieve ascites by a prolonged medical course is usually due to failure to regain liver compensation, because the liver was too severely damaged, or to the continued presence of an excessive portal hypertension. The latter reason for failure may be suspected in patients in whom the blood albumin level is in excess of 3 per cent and in whom the x-ray demonstrates the presence of esophageal varices. In these circumstances a portacaval shunt is recommended because the demonstration of the varices is proof of the existence of portal hypertension, which in itself constitutes a primary indication. If this group of medical treatment failures is allowed to go on indefinitely with repeated paracenteses, they eventually die of wasting ascites. Choice of Operation. The choice of the type of shunt between the portal '. and systemic circulations in individual cases is not yet based on any definite rules. It has been generally stated that the splenorenal anastomosis is preferable in those caseS having an extrahepatic block, while an anastomosis between the portal vein and the vena cava is more desirable when the block is intrahepatic. This statement has been based upon the assumption that patients with an extrahepatic block frequently will not have a portal vein of normal consistency and that a portal-vena cava operation will be impossible. The anastomosis between the portal vein and the vena cava theoretically would seem to allow for the most direct and friction-free flow between the two systems and therefore would be more efficient in reducing the portal system pressure. The development of methods for the production of a lateral anastomosis between the portal vein and vena cava has removed some of the earlier objections that this shunt permanently deprived the liver of any portal vein flow and that the operative technic required a dangerous period of complete portal vein obstruction during which mesenteric thrombosis might be encouraged. The objection that the splenorenal anastomosis, by its indirectness, interposes a greater amount of friction in the flow from the portal system to the renal vein is somewhat minimized by the large size of the splenic vein in these pathologic cases. The anastomotic opening is certainly as large in a splenorenal anastomosis as it can be made in any portal veinvena cava shunt. The production of a splenorenal anastomosis does not necessitate invasion of such an area as the hepatoduodenal ligament which contains vital structures, the common duct, and the hepatic artery, in circumstances in which they are obscured to some degree at least by the many collateral veins in the field. Accidents to such structures are entirely avoided in splenorenal anastomosis. Preoperative Preparation. The preoperative preparation of patients

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who are to be subjected to portacaval anastomosis is of greatest importance in cases having intrahepatic obstruction. These will show varying degrees of liver dysfunction, and every medical facility must be brought to bear to improve liver function before surgery is undertaken. In the most severe forms of liver disease it will be questionable whether the portal hypertension and resulting esophageal varices actually represent the primary danger as compared to the imminence of liver failure. Such patients with seriously damaged livers will certainly be operated upon infrequently, and then only when evidences of improved function occur during the course of good medical management. We have attempted the anastomosis between the portal vein and vena cava six times, principally in patients who previously had had splenectomy. The splenorenal type of anastomosis has been attempted in fourteen patients. Some of these cases will be presented in detail; others are included in Table 2. NONOBSTRUCTIVE LATERAL.ANASTOMOSIS BETWEEN PORTAL VEIN AND VENA CAVA CASE I. W. S., a 40 year old white man, was first seen by the Vascular Surgical Service of the Veterans Administration Hospital, Hines, Illinois, in 1948. Since 1940 the patient had had attacks of weakness associated with tarry stools and hematemesis. These occurred with increasing frequency and duration. There was no history of jaundice or ascites, and the patient had been well between attacks. In 1946 a splenectomy had been done. The spleen was said to have been much enlarged. Six months after splenectomy the esophageal bleeding recurred. Laboratory examination on admission demonstrated a severe anemia, a normal prothrombin time, normal excretion of bromsulfalein sodium, normal protein concentration and distribution, and negative cephalin flocculation test. The patient was given suitable blood transfusions, and an attempt was made to sclerose the large esophageal varices which were seen at esophagoscopy. This procedure served only to cause a recurrence of the bleeding. The patient was operated upon September 16, 1948. Through a transverse subcostal incision the duodenum was reflect.ed medially, exposing the hepatoduodenal ligament and the vena cava. The portal vein was surrounded by a network of thin-walled veins which made its exposure difficult. A 1 cm. anastomosis was accomplished with Use of the Freeman clamp (Fig. 78). The initial portal vein pressure, measured with a water manometer, was 510 rom. of water. Mter the anastomosis the tension was 400 rom. of water. The patient recovered rapidly from his operation and was allowed early ambulation. The stools became negative for blood on the third postoperative day. There was a weight gain of 20 pounds in eight weeks following

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operation. During the ninth week there was a single tarry stool each day for three consecutive days without other symptoms. He had been discharged from the hospital and did not report for examination at that time. Five months postoperatively his weight gain continued, blood counts were normal, and there had been no further evidence of bleeding. In June 1949, nine months postoperatively, the patient was readmitted to the hospital after a period of about six days of melena without hematemesis. He complained of weakness and dizziness. It was found that

A

InfeT'toT' vena bava

Fig. 78. Lateral portacaval anastomosis. Construction of a side-to-side portal vein-vena cSva anastomosis with use of the Freemen clamp (shown at the left). A ,Holding suture to mark the site of the anastomosis; B, clamp in place and incisions made; C, placement of simple continuous suture.

this attack had begun at a time when the patient had attempted suicide with barbiturates. The anemia was corrected with transfusions and the patient was discharged. He has since been lost sight of. Comment. The clinical picture presented by this patient strongly suggested that he represented an extrahepatic portal vein block. The tests of liver function were all normal. However, a biopsy specimen of the liver, taken at the time of the portacaval anastomosis, showed increased fibrous tissue and extensive regeneration of liver lobules. The fact that the portal vein was normal except for increased pressure, together with this biopsy evidence, indicates that this patient's portal

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block was intrahepatic. The resumption of bleeding, seven months postoperatively, must be considered as evidence that the portacaval anastomosis was closed, even though there seems to have been an unusual predisposing cause for the attack of bleeding observed. CASE II. S. M., 24 year old white man, was referred to the Vascular Surgical Service of the Veterans Administration Hospital, Hines, Illinois, in September 1948. Since 1946 the patient had suffered seven attacks of hematemesis, four of which required hospitalization and transfusions. A splenectomy was performed in February 1948. This was followed in May and July by additional attacks of hemorrhage, both requiring transfusions. At the time of transfer to the Vascular Service, there was evidence of continued bleeding in small amounts in that the daily stools were strongly positive for blood. The liver function tests were entirely normal. The patient's prothrombin time was normal. Esophageal varices were demonstrated by x-ray and by esophagoscopy. A portal vein to vena cava anastomosis was indicated in this patient because of the splenectomy, and this was attempted in October 1948. At operation the liver in. this patient appeared to be entirely normal, and a biopsy confirmed this impression. The portal vein was easily exposed in the hepatoduodenal ligament and its tension measured 450 mm. of water. As the freeing of the portal vein was carried out, it was noticed that the vessel was extremely thick-walled and fibrous. It was 6 mm. in diameter, In order to investigate the possibility of making an anastomosis with such a thick-walled vessel, it was isolated between bulldog clamps and opened. The rigid lumen was found to be less than 2 mm. in diameter, not suitable for any operative procedure. The operation was therefore terminated, and the patient made a good immediate postoperative recovery, but resumed esophageal bleeding one month postoperatively. Attacks continued until June 1949, when an esophagogastrectomy (Dr. Charles B. Puestow) was done. There has been no bleeding since the resection.

Comment. This patient was demonstrated to have a portal block in the portal vein itself. His liver function and liver biopsy were normal. The portal vein to vena cava anastomosis was rendered impossible by the pathologic process within the portal vein which represented the primary disease. The underlying cause of the portal vein change· cannot be determined. There is nothing in the patient's previous history to indicate trauma or intra-abdominal disease which may have been the etiology. The ·opportunity to have produced a favorable splenorenal vein anastomosis was lost in this patient by the previous splenectomy. CASE III. L. M., a 51 year old pharmacist, was admitted to the Surgical Service of the University of Illinois School of Medicine in

SHUNT OPERATION FOR ESOPHAGEAL VARICElS

August 1949. He apparently had been in good health until approximately six weeks before admission, when in the evening, after retiring, he became nauseated. There was,no pain. The patient went to the bathroom and vomited about l'pint of track, thick fluid, mixed with food. Shortly thereafter there was a diarrhea of a number of black, watery stools. This diarrhea lasted for about two days, and then the stools returned to normal consistency and color. The patient became jaundiced several days after the hemorrhage. The icterus lasted for a few days and then cleared. , X-ray examination of the stomach and esophagus disclosed varicosities of the lower esophagus. On admission the patient was found to have a normal temperature and normal blood pressu~e. He did not appear to be acutely ill. The liver could not be palpated, but the spleen was enlarged. Laboratory examination showed a prothrombin activity 30 per cent of normal, total proteins of 7.7 with an albumin-globulin ratio of 3.8:3.9. The nonprotein nitrogen was 48 mg. per 100 cc., the total cholesterol was 262 with 191 mg. per cent ester. Cephalin flocculation was 2-plus in twenty-four hours and 3-plus in forty-eight hours. Thymol turbidity was 36 units. There were 3.6 units of alkaline phosphatase per 100 cc. of serum. The icterus index was 13. The red blood cell count on admission was 3.09 million. This responded to preoperative transfusions, rising to 4.5 million just before surgery. The white blood cell count on admission was 4300. A diagnosis of intrahepatic portal vein block, on the basis of cirrhosis, was made, and on April 28, 1949, laparotomy was performed for the purpose of producing a portal vein-vena cava anastomosis. The abdomen was opened through a long right subcostal incision. A small amount of ascitic fluid was present, and the liver was small and showed extremely advanced cirrhosis with large and small lobulations. The portal vein and the vena cava were exposed without difficulty. The portal vein was found to be approximately normal in thickness, but to have a diameter of 12 mm.1t contained a pressure of 400 ffiffi. of water. An unusual anatomic anomaly was found to affect the hepatic artery, which extended between the inferior vena cava and portal vein from left to right, and then from right to left to cross nearly over the top of the portal vein. The gastro-duodenal artery arose from the hepatic artery to the right of the portal vein. At no point was it possible to bring the portal vein and vena cava together, because of the intervention of this hepatic artery. The apparent degree of liver damage was so great as to make it seem inadvisable to section the portal vein and do an end-to-side anastomosis to the vena cava. The operation was terminated therefore and the patient returned to his room in good condition. The patient was allowed early ambulation-on the second postoperative day. On May 12, two weeks postoperatively, the patient had an emesis of approximately 800 cc. of thick dark blood. The blood pres-

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sure dropped to 92/60. In spite of transfusions and supportive treatment, the patient deteriorated progressively and died on the twentieth postoperative day. At autopsy the cause of death was determined to be a portal vein thrombosis. The anatomical anomaly of the hepatic artery, found at operation, was confirmed. Comment. This patient was found at surgery to have a far more advanced degree of liver disease than had been suspected. The portal system block was certainly intrahepatic and of a high degree. At the present time such a patient, showing a splenomegaly, would be subjected to a splenorenal type of anastomosis rather than portal vein-vena cava.

CASE IV. P. M., 12 year old white boy, entered the Research and Educational Hospital of the University of Illinois on March 9, 1949, having the chief complaint of emesis of a large amount of bright red blood on February 8, 1949. He had been in excellent health until February 7, 1949, when he suddenly vomited a small amount of bloody material. The following morning, after eating breakfast with poor appetite, he vomited a large amount of red blood, partially clotted. Another emesis followed fifteen to twenty minutes later. The patient was hospitalized elsewhere and given blood transfusions. On a semiambulatory program and bland diet he had no further complaints. The patient was found to weigh 78 pounds and to have a blood pressure of 105/85. He did not appear ill. A blowing systolic murmur was heard in the second left interspace, but otherwise the heart sounds were normal. The abdomen was soft, the spleen was enlarged to the umbilicus; It was firm and nontender. The liver could not be palpated. There was no apparent distention of the abdomen, and the veins of the abdominal wall were not visible. A red blood cell count of 4.41 million, white blood cell count of 3000 with 44 per cent polymorphonuclear leukocytes, 41 per cent lymphocytes and 6 per cent eosinophils were found. The clotting time was nineteen minutes, bleeding time one minute. Platelets were 60,300; the reticulocyte count was 0.5 per cent. Clot retraction was complete in twenty-four hours; hematocrit was 39 per cent. Serum proteins totalled 8.2 gm., with an albumin-globulin ratio of 5.4:2.8. The icteric index was 8. Thymol turbidity was 13 units. The cephalin flocculation was negative in forty-eight hours. Prothrombin time was 66 per cent of normal. Chemical blood was found in the stools on three occasions on a meat-free diet. Bone marrow examination disclosed a cellular marrow which was normoblastic, having increased eosinophilia and increased megakaryocytes. X-ray examination of the esophagus showed numerous dilated varicosities involving its lower third. The upper half of the stomach also displayed a coarse pattern which might represent gastric varices.

SHUNT OPERATION FOR ESOPHAGEAL VARICES

A diagnosis of extrahepatic portal bed block was made, and the patient was subjected to laparotomy on March 28, 1949, for the purpose of doing a lateral portal vein to vena cava anastomosis. The liver appeared to be normal, and a biopsy specimen, reported later, confirmed this impression. The gallbladder was enlarged, thick-walled and somewhat edematous. It appeared to be the site of a subacute inflammatory process. There were no stones palpated in the gallbladder. The portal vein and the vena cava were isolated without difficulty. The pressure within the portal vein was found to be 458 mm. of water. The lateral anastomosis of the two vessels was done by the use of the Smith Freeman clamp. The portal vein and vena cava crossed at an angle greater than had been previously encountered, and it was not possible to make an anastomosis of good size. The completed shunt appeared to be 0.5 cm. in diameter. After the anastomosis had been made, the pressure within the portal vein was found to be 424 mm. of water. Compression of the portal vein above the lateral anastomosis did not produce distention of the distal portion. Therefore it was assumed that the anastomosis was patent despite the small fall in portal vein pressure. The patient did well postoperatively and was discharged from the hospital April 14, 1949. Objective measurement of the spleen size, as far as it could be accomplished, demonstrated that the spleen diminished in size during the months following surgery. However, the patient continued to show a definite pancytopenia and was readmitted to the hospital on January 19, 1950, for a splenorenal anastomosis. At the time of this second admission the liver function was again demonstrated to be normal. An intravenous pyelogram showed that the patient had normal renal function and that the kidneys were in normal position. Therefore on February 10, 1950, the patient was subjected to a second operation. The spleen was exposed and removed through a thoraco-abdominalincision, preserving the splenic vein. An end-to-side anastomosis was made between the splenic vein and the renal vein. The splenic vein was found to be large in diameter and thin-walled. It was under high tension. The tension was not measured because of the fact that the vein was so thin-walled it was feared that the needle puncture hole would cause complications. The increased tension. within the splenic vein did not diminish palpably after the splenic artery was ligated. After its anastomosis to the left renal vein, however, the pressure within the splenic vein fell remarkably and rapid, somewhat turbulent, flow from splenic to renal vein could be seen through the walls of the anastomosed vessels. Postoperatively, the patient was allowed ambulation on the twelfth day. Anticoagulants were started on the third day and continu,ed through the twelfth day because of an elevation of the platelet count to 2.5 million. The postoperat.ive course was without complication, and the esophageal varices hare not been examined postoperatively. There has been no

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bleeding. A postoperative intravenous pyelogram, taken six weeks after surgery, showed normal function of the left kidney.

Comment. This patient represents extrahepatic portal vein block. The possible relatioI1Ship between the obviously inflamed gallbladder, as seen at the time of first operation, to a possible block of the portal vein immediately at its entrance into the liver is the subject of conjecture. A generous portion of the portal vein was exposed at the time of the first operation, and no changes other than the increased pressure could be noted. CASE V. C. R, 49 year old white man, was admitted to the Vascular Service of the Veterans Administration Hospital, Hines, Illinois, in January 1949. A history of alcoholism of about twenty years' duration was obtained. The consumption had been moderate, but daily. The patient had been overweight for about ten years, but during the past two years had noted a gradual enlargement of his abdomen. Eighteen months before admission, the patient had had the first of four attacks of hematemesis. In each of these attacks, transfusions had been given. In the last attack, three months before present admission, the patient had been hospitalized in shock. On examination it was found that the liver was enlarged 4 cm. below the costal border. The spleen was large and could be palpated even in the presence of the ascites. X-ray examination of the esophagus revealed large varices. The red blood cell count was 3.2 million and the white blood cell count 4500. Liver function tests disclosed a marked depression of liver function. Mter a period of medical management the total proteins were 5.8 with an albumin-globulin ratio of 2.8:3. There was a bromsulfalein retention of 24 per cent. The prothrombin activit.y was 40 per cent of normal. Bleeding continued despite management. Because of the continued blood loss from the esophageal varices, it was thought necessary to subject this patient to the risk of laparotomy. With a Levin tube in place in the stomach, for the purpose of keeping the stomach empty of blood, the abdomen was opened through t long right subcostal incision. A large amount of ascitic fluid was aspirated from the abdomen before the procedure continued. The peritoneal surfaces were everywhere edematous, particularly in the region of the duodenum and hepatoduodenalligament, where there was also a marked increase in fibrous tissue. The duodenum was identified with great difficulty, and then reflected to the midline. The fibrous and edematous peritoneal surfaces of the posterior abdominal wall bled profusely from livery small move in the dissection. It was evident from palpation of the stomach and from the drainage from the Levin tube that significant bleeding was occurring. An approximately normal .blood pressure was maintained by adequate replacements of the blood loss. As the large volume of citrated blood was given, the tendency

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to bleed from the operative site gradually increased. After persisting • with the dissection for a reasonable period of time, it was necessary to abandon the procedure because of the continued bleeding. Postoperatively, the patient continued to bleed from the esophagus and stomach for a period of ten days. During this time he was given transfusions almost continually through one or two, and sometimes three, vena punctures. The rapid hemorrhage finally was controlled with a Patton tube, but there continued to be evidence that the patient was still bleeding, though at a lesser rate. Therefore the patient was returned to the operating room on the twenty-first postoperative day for an attempt at splenectomy and splenorenal anastomosis. There was less difficulty in dissection, and the operation was continued to the point of splenectomy and isolation of a suitable length of of splenic vein. As the renal vein was being partially clamped for the production of an anastomosis, blood from the stomach began to well up in the patient's nasopharynx. This was not aspirated into the lungs because of the inflated cuff on the intratracheal tube. The stomach was observed to be enlarged, presumably with contained blood and clots. The tempo of the opemtive procedure was greatly increased with the thought that perhaps reduction of pressure, if a satisfactory anastomosis could be made, might result in a diminution in the rate of esophageal bleeding. This haste resulted in a large tear of the splenic vein. Repair was not possible, so the vein was ligated and the wound closed. Replacement of blood lost through continued bleeding after surgery failed to maintain the patient's blood pressure, and he died twelve hours postoperatively of continued esophageal bleeding.

Comment. Several points of importance are illustrated by this patient. In spite of the poor prognosis given by his liver function tests, he was subjected to operation because of the severe bleeding. Such application of surgical treatment in the face of bleeding will no doubt be commonly needed, but probably will be seldom accompanied by success. The worsening of the bleeding from the operative wound during the course of massive transfusion in patients. with portal hypertension has been remarked upon by Linton, who suggests that it is the effect of introduction of citrate into patients with a damaged liver. SPLENORENAL ANASTOMOSIS

CASE VI. C. 0., 46 year old white man, was admitted to St. Mary's Mercy Hospital, Gary, Indiana, July 13, 1949, with the principal complaint of epigastric distress and loss of appetite. About the middle of May the patient had had an onset of anorexia and a feeling of fullness in the epigastric region. These complaints were intermittent, but had persisted until two weeks before admission" when the patient began to show generalized weakness. He felt dizzy on sitting up and was unable

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to walk more than a few steps without tiring. The following day he vomited dark red and black fluid and semisolid material. On the same day he had several copious tarry stooll1. The stools returned to normal color in about three days. The patient was admitted to the hospital two weeks after the beginning of the acute episode. On examination the only positive physical finding was an enlarged spleen.

Fig. 79. Splenorenal anastomosis. I. Showing transpleural incision being developed through diaphragm to expose spleen. Position of patient and placing of incision over tenth rib are shown in inset. Admission red blood cell count was 2,290,000, the white blood cell count 3700, with a normal differential. The platelets were 160,000; there was 0.9 per cent reticulocytes. Urinalysis was negative. Repeated tran!3fusions over a period of two weeks resulted in an elevation of the red blood cell count to 5 million with 100 per cent hemoglobin. The total protein was 7.4 gm. with an albumin-globulin ratio of 3.83: 3.57. The phosphatase was 2.4 Bodansky units; cholesterol 211, with 84 per cent ester; the cephalin and cholesterol flocculations were reported as strongly positive. Nonprotein nitrogen was 50 mg.

SHUNT OPERATION FOR ESOPHAGEAL VARICES

per 100 cc. Red cell fragility was normal; the bromsulfalein retention was 48 per cent in five minutes and 12 per cent in thirty minutes. The prothrombin time showed 65 per cent activity on admission, but rapidly rose to 100 per cent on a few days of administration of vitamin K. Esophagoscopy demonstrated the presence of large varicosities of the esophagus. On August 4, 1949, splenectomy and splenorenal vein anastomosis were performed through a thoracoabdominal incision. The pressure within the splenic vein was observed to be high, but was not measured because of the thinness of the distended vein wall. The patient withstood the procedure well. The spleen weighed 1310 gm. Microscopic examination of the spleen showed a diffuse fibrocellular granulomatous disease with typical tubercles throughout. The postoperative course of the patient was febrile, due to the development of a diffuse, spotty atalectasis of the left lung. The present follow-up period in this patient is nine months. During this time there has been no evidence of gastrointestinal bleeding. The patient considers himself to be entirely well and is working normally. Intravenous pyelogram shows normal functioning of both kidneys. CASE VII. M. M., 49 year old housewife, was admitted to The Chicago Memorial Hospital on November 18, 1949, having had repeated episodes of hematemesis since September 3, 1949. She had been in apparent good health until the spring of that year, when, while teaching school, she became weak and nearly fainted. A red blood count taken by her doctor on the same day disclosed a low count, said to be a little over 3 million. The following two days the patient had several tarry stools each day and was hospitalized. An x-ray diagnosis of duodenal ulcer was made, and the patient was placed on ulcer management. She adhered to this regimen for several months, losing weight and not feeling well. During the last week. of August another episode of melena occurred, and on September 3 she had an emesis of red blood. The patient was rehospitalized with a diagnosis of bleeding duodenal ulcer, and a laparotomy was performed. No ulcer was found. At the time of this operation the liver was found to be enlarged and nodular. Splenomegaly was demonstrated. She remained in the hospital five weeks, receiving a number of transfusions, and then was discharged. She returned to the hospital on November 9, 1949, and experienced two attacks of hematemesis during the early days of this admission. At the time of transfer to The Chicago Memorial Hospital, the patient was febrile and complained of a steady ache in the area of the left upper abdominal quadrant. The skin showed a mild icteric tinge, and the patient stated that she felt that she was still bleeding. The past history was negative for any alcohol consumption. The patient had had, a cholecystectomy in 1931, which had not been followed by jaundice. There had been two normal deliveries at term.

243

244

ORMAND C. JULIAN, CHARLES E. FILDES

Admission physical examination showed the patient to be thin and pale, but mentally bright. The pulse was 78, the blood pressure 94/62. The liver was palpable, but nontender. The spleen was tender and enlarged, extending down to the left iliac crest. There did not appear to be any ascites. The subcutaneous abdominal' veins were not distended.

Fig. SO. Splenorenal anastomosis. II. The diaphragmatic incision has been completed and continued through peritoneum to the left rectus border. The spleen is enlarged as in most of the cases. Laboratory findings on admission were a red blood cell count of 3.88 million; hemoglobin 11.9 gm.; white blood cell count 7400 with normal differential; hematocrit 36; urinalysis negative; prothrombin time 37 per cent of normal; 20 per cent bromsulfalein retention in one hour. The nonprotein nitrogen was 33; the icteric index 53; thymol turbidity was 10 units; cephalin flocculation 4-plus; total protein 6.2 gm. with an albumin-globulin ratio of 3:3.2; the platelet count. was 198,000. Bleeding continued, as was evidenc~d by repeated tarry stools, and on November 26 the red blood cell count had dropped to 2.89 million and the hemoglobin to 8.5 gm. The patient was difficult to

SHUNT OPERATION FOR ESOPHAGEAL VARICES

245

transfuse because she repeatedly had febrile reaction to the infusion. There continued to be icterus, but the. index dropped to 23. The patient was operated upon on December 5; 1949, in spite of the continued bleeding, in the hope that a successful shunt operation would stop the bleeding and give the patient an opportunity to improve the liver function. A.spleen weighing 1200 gm. was removed through a thoracoabdominal incision, preserving the splenic vein. The vein was 12 mm. in diameter, thin-walled and under a markedly increased pressure. This pressure did not palpably diminish following ligation of the splenic artery, but aflter production of the end-to-sideanastomosis with the renal vein it obviously dropped precipitously. Through the wall of the vein, blood could be seen to flow rapidly from the splenic to the renal vein through the large opening that had been made. The postoperative course was mal'redby repeated blood transfusion reactions and the development of a purulent left pleural space infection which required tapping in the early postoperative period and open drainage five months postoperatively. In spite of this infection, pain, and repeated bouts of fever which accompanied it, the patient's postoperative condition steadily improved. Blood was no longer detected in the stool by chemical means after the fourth postoperative day.

Comment. This case resembles Case V of this report in that the operation was done while the patient was still actively' bleeding and would encourage us to apply surgical treatment in such circumstances when it appears that the continued bleeding and repeated transfusions constitute a great danger to the patient. From, a theoretical standpoint, the reduction in portal pressure prodllced by the shunt is the best method for stopping esophageal hemorrhage. CASE VIII. G. DeC., a 42 year old white man, was admItted for the fifth time to the Veterans Administration Hospital, Hines, Illinois, on October 28, 1949. The complaints on these admissions had been edema of the legs, abdominal swelling, recurrent abdominal pains, and attacks of nausea with emesis of small amounts of blood. A history of chronic alcoholism was obtained. On previous admissions moderate depression of liver function had been found. The liver and spleen were enlarged, and esophageal varices had been seen on fluoroscopy and esophagoscopy. On this admission the patient showed ascites, mild icterus, hepatomegaly and splenomegaly. Evidences of lowered liver function were bromsulfalein retention of 37 per cent; thymol turbidity of 23 units; total protein of 6.3, with albumin-globulin ratio of 2.8:3.5; cephalin flocculation of 4-plus in twenty-four hours. The patient's general strength improved on hospital management, and the leg edema disappeared. No significant change was noted in the liver function or ascites.

246

ORMAND C. JULIAN, CHARL1!lS E. F'lLD1!lS

A splenorenal anastomosis was done on December 1, 1949. At operation the splenic vein was found to be under tension of 390 mm. of water after ligation of the splenic artery. A large anastomosis was made, after which the splenic vein was observed to diminish in size and obviously contain only a fraction of its previous pressure. Compression of the splenic vein at this time caused a rapid dilatation and turgidity which receded again imm~diately when compression was relieved. The spleen weighed 1200 gm. The liver was enlarged, pale and granular.

Renal' a.and v. Fig. 81. Splenorenal anastomosis. III. The spleen has been removed, preserving a good length of splenic vein which is shown held in a bulldog clamp. The renal vein is exposed through an incision in the posterior parietal peritoneum.

There were no local postoperative complications, but the patient became temporarily psychotic from the fifth postoperative day. Recovery occurred gradually, and the patient was discharged March 24, 1950. The patient was readmitted four months postoperatively for study. At this time there was no ascites and the liver was not palpable. Edema of the legs had not recurred. Protein studies and liver function tests were essentially as before. Alcohol consumpt.ion had been continued, and the patient had not returned. to work. CASE IX. H. B., a 50 year old white man, has been under treatment at the University of Illinois Departments of Medicine and Surgery inter-

SHUNT OPERATION FOR ESOPHAGEAL VARICES

247

mittently since July 1946. In 1944 the patient had had several attacks of colicky, right upper quadrant abdominal pain with jaundice. Cholecystectomy had been performed elsewhere in February 1946. Jaundice recurred without pain in July 1946. The jaundice'fluctuated from July until December 1946, when an exploration of the common duct area was done. The common duct was represented by a'fibrous strand which

A

B Fig. 82. Splenorenal anastomosis. IV. A, The end of the splenic vein anastomosed to the renal vein using clamp devised by Dr. Harry Southwick to partially occlude the latter. B shows the round form usually taken by the anastomosis after release of the clamps. ~as

followed up into the liver until bile could be aspirated by needle.

At the time of this procedure a reconstruction was not done because of bleeding from portal vein in the liver hilus. At a second operation on December 27, 1946, the intrahepatic bile duct was isolated and anastomosed to a Roux-Y intestinal loop (Dr. Warren Cole). From this operation to date, bile has constantly been present in the stools, but the pa.tient has had frequent attacks of chills, fever and jaundice. In April 1949 ascitic fluid began to form and rapidly attained alarming proportions. Repeated paracenteses were required. Omentopexy in the right~upper quadrant, on September 30,1949, did not change

248

ORMAND C. JULIAN,

C~RLES

E. FILDES

the rate of fluid formation. In November 1949 large esophageal varices were demonstrated on x-ray, but no esophageal bleeding has occurred during the course of illness. Liver function studies in January and February of 1950 indicated impairment. The proteins ranged from 5.4 to 6.5 with albumin-globulin ratio from 3.3:2.1 to 4.3:2.2, the latter values being obtained by concentrated medical therapy just before surgery. The cephalin flocculations were 4-plus in twenty-four hours and 4-plus in fortyeight hours in January 1950, and fell only slightly to time of surgery on March 20, 1950. The prothrombin activity ranged from 23 per cent to 57 per cent of normal, and the bromsulfalein excretion was 45 per cent during this period. Sixteen paracenteses were done from August 1949 to March 1950, yielding a total of 160,000 cc. of fluid. Splenorenal anastomosis was done March 20,1950. At operation the liver was found to be jaundiced, moderately enlarged, and granular: The spleen was large, and high pressure was present within the thin-walled splenic vein. The fall in pressure following anastomosis was striking. The postoperative course was not difficult, and in the short period of follow-up- eight monthsthere is little apparent tendency to form ascitic fluid.

Comment. The inciting factor in this case was the·damage to the common bile duct at the time of cholecystectomy. From this point there are two possible ways in which a portal hypertension may have' developed: (1) portal vein thrombosis secondary to the multiple operations, or portal vein compression by scar tissue from the same cause; or (2) intrahepatic portal obstruction due to the biliary cirrhosis. The latter etiology seems to be the most likely. The long-term response of the ascites will be watched with particular interest. CASE X. S. DeF., 17 year old white girl, had suffered at the age of 14 an illness characterized by fever, jaundice, loss of appetite, nausea and occasional vomiting, during which it had been noted that the spleen and liver were enlarged. After a period of several months the jaundice disappeared, but recurred at intervals since that time whenever the patient had an upper respiratory infection. In November 1949 hematemesis occurred, requiring hospitalization and transfusions, and on the night of March 10, 1950, the patient had a second hemorrhage. She was admitted to the Michael Reese Hospital, Chicago, on March 11, 1950, for a study of the continued anemia, hepatomegaly and splenomegaly. On admission the patient was found to be well nourished and did not appear acutely ill. The spleen was enlarged down to the umbilical level. The liver was palpable 4 cm. below the costal margin. There was no ascites and no icterus. The red ~tood cell count on admission was 0.96 million, with 8.4 gm. of hemoglobin, and white blood cell count of 10,400. The total protein

SHUNT OPERATION FOR ESOPHAGEAL VARICES

249

was 8.3 gm. with an albumin-globulin ration of 3.1 :5.2. The cholesterol was 96, with 68 per cent esters. There were 6.3 units of thymol turbidity, and the cephalin flocculation was 4-plus. The prothrombin time was normal. The platelet count was 180,000. X-ray of the esophagus and esophagoscopy failed to reveal esophageal varicose veins. In spite of these latter negative findings, a diagnosis of upper gastr·ointest.inal varicose veins, secondary to intrahepatic portal obstruction, was made, and the patient was operated upon on March 22, 1950. The spleen was found to be much enlarged and its capsule to be extensively scarred. The liver was enlarged and finely granular. The pressure within the splenic vein enlarged it to a diameter of 11 mm. It was thin-walled and under increased pressure, which did not diminish when the splenic artery was ligllted. A marked drop in pressure was noted when the endto-side splenorenal anastomosis was opened. This patient is of Mediterranean extraction, but American-born. A history was obtained that other members of the family were known to have enlarged spleens and anemia. The liver biopsy, taken at the time of operation, showed evidence of a healed hepatitis, and at this time it is assumed that the primary lesion in this patient was the hepatitis which occurred at the age of 14. CASE XI. O. F., 34 year old white man, was admitted to the Veterans Administration Hospital, Hines, Illinois, January 16, 1950, with a diagnosis of bleeding esophageal varices. He had previously been admitted, in January 1949, because of massive hematemesis and melena. At the time of the first admission esophageal varices could not be demonstrated by x-ray. During the first admission it was found that the spleen was enlarged, but that liver function tests, after replacement of blood loss through hemorrhage, were normal. He had been discharged from the hospital in gom! condition and placed on strict medical management. In the interval between January 1949 and January 1950 the patient had two further episodes of mild gastrointestinal bleeding. Four days prior to the present admission the patient had hematemesis, melena and severe weakness. Physical examination on admission revealed marked pallor. The spleen was palpable 2 cm. below the left costal margin, but the liver was not palpable. There was tarry stool in the rectum. The initial red blood cell count was 2.5 millions. The total protein and albumin-globulin ratio were within normal limits, as was the bromsulfalein test, prothrombin time, cephalin flocculation and alkaline phosphatase. Red cell fragility was normal; the urinalysis was normal. X-ray examination of the esophagus and stomach did not disclose varicosities, however, large esophageal varicosities were seen at endoscopy. It was thought that this patient had an extrahepatic portal obstruction, and on February 23,1950, a splenectomy and splenorenal anastomosis were performed. At operation the liver was finely granular, somewhat paler than normal, but had a sharp edge. The splenic vein was relatively thick-

250

ORMAND C. JULIAN, CHARLES E. FILDES

walled and under pressure of 390 mm. of water after ligation of the splenic artery. The anastomosis was accomplished without difficulty and the flow from splenic to renal vein observed. The great fall in pressure within the splenic vein after release of the clamps at the anastomosis was clearly demonstrated by palpation. During a part of the postoperative course the patient complained of epigastric pain which radiated up into the base of the neck. These symptoms finally subsided, but raised the question of whether thrombosis might be occurring in the esophageal varices. Stool examinations for blood have been negative in the eight-months follow-up period since surgery. CASE XII. M. L. K., a 42 year old white man, was admitted to the Veterans Administration Hospital, Hines, Illinois, on January 5, 1950, because of morning nausea and vomiting of three years' duration, increase in fatigue of six months' duration, and an attack of massive bloody vomiting in December 1949. The patient gave a history of heavy alcohol consumption for the past five years. Because of the morning nausea in recent months the patient had been taking about 2 ounces of whiskey in the morning when he got up and then continued to drink heavily throughout the day. There was a 70 pounds weight loss during the past year. Although he had vomited on numerous occasions before, it was in December 1949 that he first had hematemesis. At that time he was hospitalized elsewhere and was given three blood transfusions. Subsequently, x-ray examinations were said to be suspicious for duodenal ulcer, but he had not received treatment for it. In the past six or eight months tarry stools occurred frequently, and his weakness and fatigue increased. On admission to the hospital the patient· appeared to be well developed and moderately well nourished in spite of his history. The blood pressure was 160/90. The liver was palpable 3 cm. below the right costal margin and seemed to be irregular. The spleen was palpable to 3 cm. below the left costal margin. The skin was mildly icteric. Multiple spider nevi were present on the upper chest and neck. There was no apparent ascites, and the abdominal veins were not visible. Laboratory studies on admission revealed an icturus index of 25; prothrombin activity, 48 per cent of normal; thymol turbidity, 6 units; alkaline phosphatase, 6.7; the direct van den Bergh, 3.6-total, 6.6; red blood count 4.6 million with 13.5 gm. of hemoglobin; white blood cell and differential counts were normal. The bleeding time was one minute, with coagulation time three minutes, platelet count was 227,000; clot retraction was complete within twenty-four hours; tot.al protein 7.9, with an albumin-globulin ratio of 3.4:4.5; bromsulfalein retention, 40 per cent in thirty minutes; cephalin flocculation, 3-plus in twenty-four hours, 4-plus in forty-eight hours. X-ray examination of the esophagus showed varicosities at the lower end. There was a deformity of the duodenal bulb consistent with healed duodenal ulcer.

SHUNT OPERATION FOR ESOPHAGEAL VARICES

The patient was kept on intensive therapy for his liver disease for a period of three months. The effect of this treatment was that the prothrombin time was raised to 100 per cent, the icterus disappeared, and the direct van den Bergh dropped to 1.8. A diagnosis of portal hypertension with esophageal varices was made, and splenorenal anastomosis was performed on April 13, 1950. At operation the liver was found to be firm and nodular. The spleen was much enlarged, but shrunk down to about half original size when the splenic artery was secured. Splenic vein pressure was 400 mm. of water after ligation of the artery. A satisfactory anastomosis was made in this case, and after removal of the clamps the collapse of the high splenic vein pressure was immediately and easily noted. This patient suffered a major postoperative complication with disruption of the suture line in the diaphragm, and protrusion of the stomach into the pleural space, where it perforated. Repair of the rent in the stomach was performed, after which the patient had a stormy course with recovery. CASE XIII. E. Q. B., a 31 year old white man, was first seen on the vascular service of the Veterans Administration Hospital, Hines, Illinois, on July 26, 1950. He had been well until October 1949, when he had an illness lasting three days, consisting of weakness associated with tarry stools and one episode of hematemesis. At that time he was put on ulcer management for a time and then was entirely well until May 1950, when he again had melena. Three days before the present admission he began to have tarry stools, large in volume, two or three a day, and became weak and pale. On admission he appeared acutely ill, pallor was noted, the blood pressure was 112/60 and the pulse 104. Examination of the abdomen was not remarkable. The spleen was not palpable. The red blood count was 1.69 million, the hemoglobin less than 7.5 gm., leukocytes 8,800, hematocrit 16 per cent, prothrombin time 18 seconds, cephalin flocculation 3 plus, thymol turbidity 2 units. The administration of suitable volumes of whole blood during the patient's course in the hospital succeeded in correcting the anemia but the prothrombin time could be elevated to only 15 seconds, or 48 per cent, and the blood proteins, not determined during the period of anemia, were 7.3 gm. total with 3.3 gm. of albumin and 4 gm. of globulin. The patient was taken to the operating room on the day of admission and an exploratory laparotomy performed. The expected duodenal ulcer was not found but rather the liver was found to be pale, fibrotic, and nodular. The veins about the cardia of the stomach were noticed to be enlarged and tense. N.o definitive surgical treatment was applied. Postoperatively repeated episodes of bleeding occurred. These were controlled by the Patton tube. It is of interest to note that the tube was left in the esophagus for a total of three weeks, at which time the bleeding had not entirely stopped as was evidenced by the continued

251

252

ORMAND C. JULIAN, CHARLES E. FILDES

presence of blood in the stool. On August 31,1950, the patient was again taken to the operating room and through the usual thoraco-abdominal incision an end-to-side splenorenal shunt was performed. The spleen was found to be enlarged and the splenic vein pressure to be well over 300 mm. of water. Owing to the dilation of the vein an unusually large anastomosis could be made. The remarkable enlargement of the veins about the cardia of the stomach was again observed. After opening of the shunt they collapsed. This was the first observation of this type to be made in this series. Several suture ligatures were taken through clumps of these deflated veins with the idea that more complete eradication of the bleeding varicosities might be accomplished. Postoperatively the stools became negative for blood on the second day.

Comment. The mistaken diagnosis of bleeding duodenal ulcer led to a laparotomy at which little could be accomplished. It is possible that a portacaval anastomosis could have been done, but neither the personnel nor the equipment had been prepared. Failing this procedure the work of Cole would suggest that a simple splenic artery ligation might have diminished or prevented the hemorrhage which had to be controlled before the second operation. The only really serious mistake that could have been made was splenectomy. This would have been an error in that it would have prevented the later accomplishment of the shunt and it would have an unusually bloody procedure due to the size and tension of the veins about the spleen. CASE XIV. J. J., a 56 year old white male steel plant employee, was admitted to the hospital on August 19, 1950. For one week prior to admission he had had gradually increasing weakness associated with abdominal discomfort and a diarrhea consisting of black stool. Four days prior to admission repeated emesis of blood had occurred. In the past history it was learned that the patient had been on ulcer management for the past two years. In 1948 he had had a smaller amount of hematemesis. The laboratory examination on admission showed a moderate anemia, 3.75 million red cells and 61 per cent hemoglobin. Transfusions were administered and the patient was taken to the operating room where laparotomy disclosed, instead of the expected ulcer, a contracted cirrhotic liver and an enlarged spleen. The surgeon closed the abdomen without doing any definitive procedure. Postoperatively the rate of bleeding from the upper intestinal tract increased and repeated transfusions were required. In spite of the continued bleeding or, alternatively, because of it, the patient was returned to the operating room for a splenorenal anastomosis eight days postoperatively. The patient withstood this operative procedure very well and it was noted that the emesis in the immediate postoperative period was free of blood for the first time since the admission to the hospital. An unusual finding was encountered at operation when the

I

J

SHUNT OPERATION FOR ESOPHAGEAL VARICES

253

enlarged spleen was mobilized and it was found that the splenic artery and vein were closely adherent, the adhesions being the result of an extensive sclerosis of the artery. A length of vein sufficient to do an endto-side anastomosis could not be obtained. The renal vein branch from the upper pole of the kidney ran a course of over 2 cm. before joining the other branches. This vein was therefore divided at the kidney surface and when swung upward provided just enough length to anastomose end-to-end to the splenic vein. The postoperative course was not unusual. The patient was discharged on the twenty-first post-operative day and bleeding has not recurred.

Comment. Except for the liver biopsy which shows moderate changes, laboratory work in this case is deficient. This patient, as in the case of the preceding one, was operated upon primarily with a diagnosis of bleeding ulcer. As has been noted in several cases, evidence of gastrointestinal hemorrhage disappeared immediately postoperatively. DISCUSSION

The series of patients reported is relatively small, but the experience gained in managing them has served as an increasingly valuable guide in subsequent cases. It is evident that the incidence of changes in the hepatoduodenal ligament and in the portal vein itself is high enough that failures to produce an anastomosis between the portal vein and the vena cava will be frequent. These have occurred in our experience both as a result of intrahepatic obstruction of cirrhosis and extrahepatic portal vein obstruction in which the limiting factor as to completion of a shunt was the primary pathologic process within the portal vein. Even though a large proportion of the patients in this series have had severe liver disease, only one of the two deaths has been due to liver failure, the other being due to continued esophageal bleeding following failure of the operation. On the other hand, it has been obvious that extensive liver disease is a factor in shunt operation, because its long-continued presence produces mechanical changes of fibrosis, edema, and great numbers of collateral veins which make the operations difficult or impossible. ~ The most important single point remains unclarified in this report and in others. This, of course, pertains to the ability of the shunts produced to remain patent. The rapid flow which can be seen to occur from the splenic to the renal veins after anastomosis gives the impression that such a shunt should remain open indefinitely, but direct evidence is lacking. It has not been demonstrated that the reduction of the portal pressure has either a good or a bad influence on the course of the hepatic disease. The patients we have seen have shown a general improvement in liver function after the successful completion of surgery; however, it must be remembered that they are kept on a favorable management

I\J

TABLE 2

~

SUMMARY OF EIGHTEEN CASES

1.

Patient

Age

w.

40

S.

2. S.M.

3. L.M.

24

Liver Function

Normal

Normal

Pre-operative Bleeding

Type of Anastomosis

Result

Many attacks in 8 years (previous splenectomy without benefit)

Lateral portal vein to vena cava

Recurrence of bleeding in 9 months; diminished severity

Seven severe attacks in 4 1. Portal vein-vena cava No further bleeding failed due to obliteration years (previous splenecof portal vein tomy without benefit) 2. Esophageogastrectomy

51

Severely depressed; no ascites

One severe episode

Portal vein-vena cava failed due to anomaly of hepatic artery

Death 2 weeks postoperative; liver failure

12

Normal; marked pancytopenia

One severe episode

1. Lateral portal vein to .venacava

Some shrinking of spleen and continued anemia

2. Splenectomy and endto-side splenorenal

No bleeding, normal blood

1. Portal vein-vena cava failed due to edema, fibrosis and bleeding 2. Splenorenal failed due to rupture of splenic vein

Death due to continued severe esophageal bleeding

-----4. P.M.

5. C. R.

49

Severely depressed (ascites)

Admitted in 5th attack in 1l years; continuous bleeding during hospital course

o

~

~ p

~

i ~

~

l".! u.>

6. C. O.

46

Normal; marked pancytopenia

----,--,--------,

7.M.M.

49

Severely depressed (no ascites)

---'--1 8. G. DeC. 42 Severely depressed (long history of ascites) 50

Moderately depressed; biliary obstruction due to surgical injury of common bile duct (severe ascites)

No recurrence of bleeding; normal blood picture

1----------1

I

Continuous mild bleeding Splenectomy and end-tofOJ,l year with 2 severe side splenorenal exacerbations

1-------.-1---------Verymild,frequenthema- Splenectomy, spleno-retemesis nal anastomosis

--------,---,-------------1

9. H. B.

Splenectomy and end-toside splenorenal

One severe attack

No recurrence of bleeding; improvement in liver function noted

--------1

No bleeding

Regression in ascites formation; short follow-up

Splenectomy and end-toside splenorenal

17

Moderate depression; no ascites, hepatitis at age of 14

34

Normal

....~ o

'"l

o

;tt

Two attacks of hematemesis, 4 months

t'1

Splenectomy and end-to- I No bleeding side splenorenal

1---1-------------1-------------1------------1------------

11. O. F.

~ o

Z

------,---,------------ ,-------------1-------------1

10. S. DeF.

q

'tI t'1

1_____________ 1

Esophageal varices; no bleeding

rg

Four attacks in one year

Splenectomy and end-to- IN 0 bleeding side splenorenal

-------1---1-------------,-------------,---Continuous melena for 3 Splenectomy and end-to12. M. K. 42 Depressed

months; two attacks of hematemesis

I No bleeding

Ul

o

~

o t'1 > t"

~ ;tt ....

a

t'1

Ul

side splenorenal

--------1---1---------------1--------------13. E. Q. B.

31

Depressed

Two attacks of melena in I End-to-side splenorenal 8 mos. Severe. Bled to day of surgery

No bleeding t,;)

~

t-:l C1 ~

TABLE 2-Continued -

Patient

Age

--

--

-

-

-

----

Liver Function

Pre-operative Bleeding

Type of Anastomosis

Cirrhosis on biopsy; no reliable function tests

Continuous, moderate for 11 days

End-to-end splenorenal utilizing superior pole branch of renal vein

Result

--

14. J. J.

56

No bleeding

o

;
- - - - - - - - - -------------------------- ------------- - - - - - - - - - - 15. M.M.

------16. A. R.

39

-35

Portal cirrhosis on biopsy; function tests not disturbed

Two attacks: Nov. 1948 and May 1950

End-to-side spleno-renal shunt

No bleeding

~

------------- ------------- ------------- - - - - - - - - - - Moderate depression

Two severe attacks with hematemesis 1 mo. preop.

End-to-side splenorenal

No bleeding

mo. prior to surgery

39

Infectious hepatitis 1945; mild depressed function; Biopsy shows £ibrosis

o ~ po. ~

~

;
t"'

l"J

Ul

l"J

- - - - - - - - - ------------- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 18. T. W. S.

.... _Z

- - - - - - - - - ------------- ------------- - - - - - - - - - - - - - - - - - - - - - - Two severe attacks in 1 End-to-side splenorenal No bleeding 17. J. F. 55 Moderately depressed; portal cirrhosis on biopsy

~

t;

Three attacks of hematemesis in 2 yrs. p'rior to surgery

Side-to-side portacaval shunt employing a 1 cm. femoral vein graft

No bleeding

:5l ~ l"J

Ul

SHUNT OPERATION FOR ESOPHAGEAL" VARICES

257

and that the period of hospital rest preoperatively and postoperatively will have a favorable effect on liver function. The formation of ascitic fluid has been markedly diminYlhed in one patient in this series. This is in keeping with the results obtained by others and suggests that the abolition of the pressure factor in ascites has a favorable effect. Only indirect evidence has been sought as to the effect of the shunt operation on the varicose veins in the esophagus. Neither x-ray nor esophagoscopy is capable of accurately recording variations in the size of the esophageal varices. It is doubtful that the veins within the esophagus or cardia actually ever disappear after reduction of portal pressure. Some esophageal bleeding therefore may be expected to occur in these patients, although it should be much diminished in amount and frequency as compared to the patient's earlier course. Mild bleeding should not be taken as evidence that the anastomosis has closed or thrombosed. Postoperative bleeding has occurred in only one of the patients in this series where an anastomosis has been produced. With this factor in mind it is obvious that, to carry the indications for shunt operations to their logical conclusions, one would seek to operate on patients with portal hypertension before significant varicosities have developed and hope by shunting blood by a more direct route completely to prevent their formation. This aim will of course be unobtainable, because many of the patients first seek medical attention because of esophageal bleeding. At the Veterans Administration Hospital, Hines, Illinois, a step in the direction of such an early diagnosis of portal hypertension has been taken by establishing a joint medical and surgical board to investigate all patients with splenomegaly, cirrhosis, ascites and other related conditions for early signs of portal hypertension. The results of such a program will not be known for a long time. SUMMARY

1. Experiences with eighteen patients in whom a vascular shunt operation was done for portal hypertension are reported. 2. A splenorenal anastomosis was done in fourteen patients. In these patients there was one operative death which was due to continued bleeding from the varicose veins in the esophagus. In this patient the anastomosis failed. The remaining thirteen patients have had no recurrence of gastrointestinal bleeding in the present period of observation. 3. A portacaval anastomosis was attempted in six patients. Three failures to make the anastomosis were encountered. In one of the cases in which the anastomosis was completed the connection was made by the

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insertion of a 1 cm. long graft taken from the patient's femoral vein. In one of the three patients having the complete anastomosis, bleeding recurred nine montas postoperatively. • REFERENCES 1. Blakemore, A. H.: Surg., Gynec. & Obst. 84:645-653, 1947.

2. 3. 4. 5.

Blakemore, A. H.: Ann. Surg. 122:435, 1945. Blakemore, A. N.: Ann. Surg. 126:825, 1948. Blalock, A.: Ann. Surg. 125:129, 1947. Linton, R., Hardy, J. B. Jr., and Volwiler, W.: Surg., Gynec. and Obst. 87: 129,'1948. 6. Whipple, A. 0.: Ann. Surg. 122:449, 1945. 7. Southwick, H. W.: Arch. Surg. 60:372, 1950. 8. Julian, O. C. and Metcalf, W.: Arch. Surg. 59:433-436, 1949.