Selective Variceal Decompression After Splenectomy or Splenic Vein Thrombosis

With a Note on Splenopancreatic Disconnection.

W. DEAN WARREN, M.D., WILLIAM J. MILLIKAN, JR., M.D., J. MICHAEL HENDERSON, F.R.C.S., MOHAMMED E. RASHEED, M.D., ATEF A. SALAM, M.D.

Eight patients have had selective variceal decompression after a splenectomy or splenic vein thrombosis with successful control of bleeding. The principle veins utilized in these patients, either alone or in combination, were: (a) the splenic remnant, (b) the coronary, (c) the gastroepiploic, and (d) an inferior mesenteric that joined the splenic. High quality preoperative angiography is essential but operative exploration is often required to assess fully the possible shunt options. Simple splenectomy for thrombocytopenia in portal hypertension is rarely justifiable and creates far more problems than it solves. Complete splenopancreatic disconnection extends the selective shunt concept.

From the Emory University School of Medicine, Department of Surgery, Atlanta, Georgia

count of 50,000/cu mm or less; it is performed as either a specific procedure (usually in children with portal vein thrombosis) or combined with portal venous diversion via a central splenorenal shunt.7 The severe consequences of this approach have not been fully appreciated nor has

T HE BASIC CONCEPT of selective shunting ofesophagogastric varices while maintaining portal perfusion of the liver has now been well documented. 1-3 The patients with the greatest benefit from these procedures have been those with portal hypertension from conditions other than alcoholic liver disease, such as nonalcoholic cirrhosis, various types of hepatic fibrosis, and noncirrhotic portal vein thrombosis.4-6 Previous splenectomy or splenic vein thrombosis has been assumed to preclude use of selective procedures other than coronary-caval shunts. However, a serendipitous complication (Case 1) led us to reconsider alternative ways of achieving selective shunting following splenectomy or splenic vein occlusion. An important corollary issue, the role of splenectomy for the control of thrombocytopenia of portal hypertension, needs critical re-evaluation. Splenectomy is usually undertaken in patients with a large spleen and a platelet
Presented at the Ninety-Fifth Annual Meeting of the Southern Surgical Association, December 5-7, 1983, Hot Springs, Virginia. Supported in part by Public Health Service Research Grant AM 15736 and by General Clinical Research Center Public Health Service Research Grant 5MOlRR00039. Reprint requests: W. Dean Warren, M.D., Joseph B. Whitehead Professor and Chairman, Department of Surgery, 1364 Clifton Road, N.E., Atlanta, GA 30322. Submitted for publication: December 23, 1983.

its rationale been substantiated. An additional factor, called here the pancreatic siphon, was brought into focus in part by this study. It is the drainage of the entire pancreas to the decompressed splenic vein following a distal splenorenal shunt (DSRS). A new approach utilizing complete splenopancreatic disconnection is now being studied and will be discussed

briefly.
Case Reports The cases presented in this paper are a subset of a larger group in whom selective shunt might have been considered for variceal bleeding when there was splenic vein thrombosis or a prior splenectomy. To put this in perspective, the Emory group are referred seven to ten patients per year in this category. Thus, approximately 25 patients were referred over the time-span of the cases presented. Exploration with failure to find a suitable vein for selective decompression was undertaken in six further patients: these, plus the 12 patients who were not considered for surgery, have been managed by endoscopic sclerosis. Figure 1 illustrates potential venous pathways for selective gastroesophageal variceal decompression. A normal splenic vein is most easily and commonly used for transplenic decompression. When that option is not available the alternatives that should be sought are: (a)

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splenic vein remnant, (b) a coronary vein (left gastric), (c) a gastroepiploic vein, or (d) an inferior mesenteric that joins the splenic vein. We shall present a series of cases illustrating ways in which these natural tributaries can be used for selective decompression.
a

Case 1. This sentinel case suggested the feasibility of successful selective variceal decompression following splenectomy. A 58-year-old woman with posthepatitic cirrhosis and continuing gastroesophageal variceal bleeding was managed by urgent DSRS. In surgery there was difficulty in completing her shunt due to continuing variceal bleeding; huge splenogastric collaterals were occluded with a vascular clamp. A DSRS was completed under PitressinO cover. Profuse bleeding at the splenic hilus following removal of the clamp could not be controlled, leading to splenectomy as a life-saving maneuver. Surprisingly, the shunt showed good flow clinically at the end of her operation and her postoperative angiogram at 10 days showed shunt patency by direct catheterization. Follow-up angiography at 18 months showed unequivocal shunt patency

Portal

v.

Splenic

v.

Superior mesentericv.

<

L. ~~~Gastroepiploic v.

with

increase in vein size (Fig. 2A). The SMA study showed develpancreatic collateral pathways from the portal vein to the DSRS, further increasing shunt flow and aiding patency, but demonstrating the pancreatic siphon effect (Fig. 2B). Her varices were decompressed and at 5 years she has had no recurrence of her variceal bleeding. Case 2. In this patient the coronary vein was used to achieve variceal decompression. A 60-year-old woman presented with recurrent, incapacitating hepatic encephalopathy secondary to a segmental mesocaval shunt done I year previously for recurrent variceal bleeding. The sequence of events in her previous course was: hypersplenism splenectomy
an

Inferior
mesenteric v.

opment of

'?8&0Yr7-fE '83
FIG. 1. Schematic of the potential venous drainage pathways that may be used for selective variceal decompression. Low pressure variceal drainage can be achieved by these singly or in combination, while high pressure mesenteric/portal venous flow is maintained to the liver.

variceal bleeding small mesocaval shunt hepatic encephalopathy. Ligation of her mesocaval shunt with restoration of portal venous per-

fusion dramatically reversed her encephalopathy

as

previously reported.'

To minimize her risk from recurrent gastroesophageal variceal bleeding on restoration of her portal hypertension, a coronary to left renal vein shunt was fashioned at the time of ligation of her mesocaval shunt. The path of the mobilized coronary vein was retropancreatic. Follow-up angiography at 1 year confirmed shunt patency by direct catheterization (Fig. 3). She has had no recurrent bleeding at 3 years, has no varices at endoscopy, and remains free of encephalopathy. Case 3. This patient had variceal decompression achieved using the coronary system via the splenic vein remnant and side-to-side splenorenal shunt. A 65-year-old man with cirrhosis secondary to hemachromatosis presented with six documented variceal bleeds. A splenectomy had been performed 7 years previously for hypersplenism. Full evaluation showed stable liver disease with moderate compromise. Angiography showed

stigmata of portal hypertension with variceal filling through his coronary vein. Transhepatic portography showed the coronary vein originated from his splenic vein remnant that remained patent (Fig. 4). At operation sufficient splenic vein was mobilized for a side-to-side splenorenal shunt: the selectivity of variceal decompression was achieved by ligation of the splenic vein between the coronary-splenic junction and the superior mesenteric vein. Postoperative shunt patency was documented by direct catheterization. The patient has had no further variceal bleeding.

also showing splenic vein thrombosis. At surgery, splenectomy and devascularization was performed. Following division of the splenic hilum, an appropriately sized splenic vein was found. Careful dissection proved the splenic vein to be patent from the tail of the pancreas to the inferior mesenteric vein. An inferior mesenteric to renal vein shunt was fashioned (Fig. 5), leaving the splenic vein remnant in situ. Follow-up shunt catheterization at 1 year documented variceal decompression by this shunt and superior mesenteric angiography shows continuing portal venous perfusion; there has been no further variceal bleeding. Case 5. The optimal use of the inferior mesenteric vein for variceal decompression is to use the superior portion as an extension of the splenic vein and ligate the inferior limb to prevent colonic venous effluent entering the shunt. A 40-year-old man presented with a history of two episodes of variceal bleeding controlled with conservative measures. His portal hypertension was documented to be secondary to alcoholic cirrhosis. He had undergone splenectomy for trauma 25 years previously. Angiographic evaluation showed good portal perfusion, a coronary vein filling his varices, and a splenic vein remnant in his pancreas. He had an end inferior mesenteric to side left renal vein shunt made, with ligation of the mesenteric end of his splenic vein to achieve selectivity. Angiography at 5 months showed enlargement of his shunt with variceal

In Cases 4, 5, and 6 an inferior mesenteric vein (which joined the splenic vein) was anastomosed to the left renal
vein.
Case 4. In this instance the inferior mesenteric vein was used but followed splenectomy at the same operation. This patient also illustrates that preoperative angiography, including splenoportography, may not tell the whole story. A 15-year-old boy was referred following a 4-unit UGI bleed, documented to be from gastroesophageal varices. Evaluation confirmed portal hypertension secondary to portal vein thrombosis; preoperative angiography, with splenoportography, was interpreted as

decompression and continuing good prograde portal venous flow. Case 6. A 25-year-old man presented with recurrent gastric variceal bleeding 8 years following splenectomy and gastric devascularization and 4 years after a makeshift mesocaval shunt. The etiology of his portal hypertension was portal vein thrombosis. Radiological evaluation showed large gastric varices, but also filling of his inferior mesenteric vein which communicated with his splenic vein remnant and pancreatic collateral varices. At operation the inferior mesenteric vein was mobilized, confirmed to enter the splenic vein, and used to make a side-to-side shunt to the left renal vein. The inferior ramus of the inferior mesenteric vein was not ligated as the increased volume of flow was thought to be necessary to maintain shunt patency. Angiography by shunt catheterization at I week showed the anastomosis to be patent, with communication via pancreatic collaterals to his gastric varices (Fig. 6). We

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FIGS. 2A and B. A. Case 1: direct shunt catheterization at 18 months shows enlarged splenic vein remnant and shunt patency. B. Venous phase of superior mesenteric angiogram at 18 months shows grade I portal venous flow, but in addition there is development of pancreatic collateral veins from the portal vein to the shunt-the pancreatic siphon. anticipate this shunt will enlarge with time and, to date, this has controlled his bleeding. Later angiographic dilation ofthe anastomosis with occlusion of the caudad limb of the inferior mesenteric vein is planned. Case 7. This case illustrates clearly the need to inspect the splenic vein in surgery even when it is not shown by conventional angiography or splenoportography. A 26-year-old woman was referred with one major documented variceal bleed following caesarian section, and portal vein thrombosis was documented as the etiology of her portal hypertension. Both on splenic arterial injection and splenoportography approximately 3 cm of splenic vein was visualized and a diagnosis made of splenic vein thrombosis (Figs. 7A and B). At operation, dissection behind the pancreas showed a patent splenic vein considerably larger than that seen at angiography of sufficient length to perform a conventional DSRS. A very large varix off the superior border of the splenic vein (4 cm from the hilus) accounted for the deceptive angiographic appearance leading to the erroneous preoperative diagnosis. Her postoperative course was uncomplicated, shunt patency and continuing portal venous flow combining to control bleeding and maintain quantitatively measured hepatic function.
Case 8. This final case illustrates that in the situation of complete portal and splenic vein thrombosis, the gastroepiploic vein may act as the primary splenic outflow track and be a suitable vessel for selective transplenic variceal decompression. A 23-year-old woman was referred following three variceal bleeds secondary to portal vein thrombosis. Angiographic evaluation confirmed the diagnosis with good portal venous perfusion of the liver through cavernous transformation (Fig. 8): no splenic vein could be visualized either on venous phase splenic artery study or at splenoportography. However, a large gastroepiploic vein was seen as the main splenic outflow track (Fig. 8). At operation this was mobilized and used to make a gastroepiploic renal shunt. Early postoperative patency was documented by splenic angiography at 1 week (Figs. 9A and B). Continued patency of the shunt with enlargement of the gastroepiploic vein was shown by splenic artery injection at 5 months (Fig. 10). The superior mesenteric artery injection revealed no pancreatic siphon pattern (occluded splenic vein). This finding emphasized the crucial nature of pancreatic branches joining a patent decompressed splenic vein in the development of this phenomenon. There has been no recurrence of bleeding.

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Coronary v.
MaW. :.
1

varices

Gastroesophageal

r'3%
zmach

..~....

Short

gastric vv.

Inferior mesenteric v.
L. Kidney

ii,2
Wo1i#
FIG. 5. An inferior mesenteric-renal shunt (end-to-side) utilizes pancreatic collaterals, the coronary system, and splenic vein remnant to decompress
vein.
FIG. 3. Case 2: shunt catheterization at I year demonstrates patency of this patient's coronary-renal shunt.

varices. Selectivity is achieved by ligation of the central end of the splenic

Discussion Long-term studies of the selective distal splenorenal shunt have confirmed the early achievement of the phys-

FIG. 4. Case 3: transhepatic portography prior to shunt shows the coronary vein (tt) communicating with the splenic vein remnant (4-): this demonstrates the feasibility of selective variceal decompression along this combined pathway, with occlusion of the superior mesenteric end of the splenic vein.

FIG. 6. An inferior mesenteric-renal shunt (side-to-side) decompressed gastric varices in Case 6 via pancreatic collaterals. To achieve selectivity, both the central end of the splenic vein and caudad end of the inferior

mesenteric vein must be occluded.

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FIGS. 7A and B. The venous phase of splenic artery injection (A) and splenoportography (B) in Case 7 show 3 cm of splenic vein, then wider dispersal of contrast into varices. At exploration the main splenic vein (not visualized on either of these studies) was suitable for conventional DSRS.

iologic goals envisioned in its development. 1-3 Control of bleeding from gastroesophageal varices has been excellent. Portal perfusion of the liver in the early postoperative period is maintained in over 90% of patients, drops to 60% at 1 year, and is maintained near that level thereafter.

The major beneficiaries of these physiologic achievements the nonalcoholics in whom late hepatic portal perfusion continues in a higher proportion (78%), hepatocyte function is preserved,3 and survival is markedly improved in both duration and quality of life when compared to those patients with alcoholic liver disease.44 Consequently, every effort is made to achieve a selective shunt in the nonalcoholic with bleeding varices. The problem presented in this paper, postsplenectomy variceal bleeding, however, needs special scrutiny and understanding.
are

Hypersplenism and Splenectomy

A particularly disheartening group of patients are those in whom prior splenectomy and diffuse thrombosis of the portal system have precluded the use of a selective shunt. Three of the eight patients presented had undergone splenectomy for hypersplenism-is splenectomy indicated in the patient with portal hypertension and thrombocytopenia? We have recently reviewed our experience with patients whose platelet counts were less than 50,000/cu mm prior to shunt surgery. We shall present some of the data in those 33 patients which is pertinent to this paper. This degree of hypersplenism is seen in eight to ten per cent of our referral population with variceal bleeding. In contradistinction to our overall referral pattern (64% alcoholic, 36% nonalcoholic), this group was 79% nonalcoholic. Intraoperative bleeding (3%) and operative mortality (6%) were not different to our overall experience.

FIG. 8. Venous phase splenic angiography in Case 8 shows splenic vein thrombosis, good portal perfusion (Tt), and a large gastroepiploic vein (dotted) as the main splenic outflow track.

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FIGS. 9A and B. A. The schematic shows the anatomy of the gastroepiploic shunt in Case 8. B. The immediate post-shunt splenic artery study shows a patent shunt with visualization of the gastroepiploic - left renal vein and inferior vena cava (dotted).

The mean (SD) preoperative platelet count of 36,300 9,400/cu mm rose significantly (p < 0.001) to 81,100 48,000 at 7 to 10 days. The continuing benefit of splenic decompression in correcting thrombocytopenia is seen with the significant (p < 0.01) platelet rise maintained at
1 year (100,300 80,000) and agrees with the earlier data from Miami.8 In no patient with hypersplenism, portal hypertension, and variceal bleeding have we considered splenectomy indicated simply to correct the hematological abnormality, and in no postshunt patient has the hypersplenism been a problem. On the contrary, we have seen many patients referred with recurrent bleeding following an earlier splenectomy who have thus been deprived of the optimal management of selective decompression of varices.

illustrated by Patients 2, 4, 5, and 8 in whom a small shunt with a relatively smaller flow has remained patent, enlarged with time, and decompressed varices. It is our

Anatomic and Technical Features Consideration of the normal venous pathways intercommunicating in the gastropancreatic-splenic system reveals several pathways by which esophagogastric varices may be selectively decompressed. The veins of the portal system are valveless, thus facilitating the numerous combinations that can be utilized for variceal drainage. A point of great importance is the greater technical success and long-term patency of the shunt when normal veins are anastomosed, rather than either a dilated variceal collateral or an interposed fabric prosthesis. This is well

~~

FIG. 10. Splenic angiography in Case 8 at 5 months shw signifint enlargement of the shunt and variceal decompression.

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Portal

v.

mesenteric v.

Ivcjv.

lnf. mesenteric ligated

FiG. 11. The pancreatic siphon with a conventional DSRS. Pancreatic veins connect the high pressure portal venous system to the low pressure intrapancreatic splenic vein. Enlargement of these pathways occurs over time, as illustrated in Figure 2B, with drainage of pancreatic hormones to the systemic circulation.

firm conviction that a successful selective shunt is superior

to available alternative techniques (total shunt, gastric

devascularization, or sclerotherapy) as a long-term management modality, and a determined effort to achieve such a shunt is indicated.9 From our experience with these patients, additional points of importance in the management ofthe operative
Tail of pancreas less distal segment of splenic vein

procedure have been clarified. First, the failure to visualize a splenic vein by angiographic studies does not preclude its usefulness. In Patients 4 and 7, a diagnosis of splenic vein obliteration was made, but at operation a useable vein was found. Therefore, we look for the vein behind the body of the pancreas as a first step in the operative assessment of our surgical options. A second point relates to the size of the vein utilized in the anastomosis. It has been well documented in our total experience that veins enlarge rapidly with increasing flow. Therefore, the anastomotic orifice should be made large enough to accommodate the ultimate venous dilation and increased flow, even with a very small vein. An additional measure utilized by our group is the interruption of the anterior row of sutures in the anastomosis. This not only ameliorates the immediate pursestring effect, but allows for later angiographic dilation if this is needed. The need to use one of the primary tributaries of the gastrosplenic venous system (splenic, coronary, gastroepiploic, or an inferior mesenteric joining the splenic) has been emphasized earlier. This is important to maintain long-term patency and to decompress specifically the variceal system when there is diffuse thrombosis within the portal system. It should be noted that the inferior mesenteric vein joins the superior mesenteric vein in a significant per cent of patients and is not used in these instances because of lack of selectivity.

The Pancreatic Siphon

A final point of importance has been clarified, in part due to the study of Patients 1 and 8. From a series of observations, including angiograms of postshunt collateral pathways, the effect of shunts on liver volume,3"10 and the specificity of variceal drainage when the total splenic vein was occluded (Case no. 8), the singular importance of the transpancreatic collaterals to the shunt became apparent. There are numerous data to indicate the importance of pancreatic hormones in hepatic regeneration and the prevention of hepatic atrophy.1 Figure 11 gives a good illustration of the problemlarge collaterals leave the portal vein into the head of the pancreas, drain through the body and tail of the pancreas via intrapancreatic branches that communicate directly with the shunt. We have generally referred to this specific collateralization as the pancreatic siphon. The interruption of this loss of flow from the portal vein could be important in the simple quantitative consideration of preserving portal perfusion of the liver, but the qualitative aspects are probably of more importance in stabilizing hepatic mass. If the pancreatic branches of the portal vein are converted into outflow tracts, then none ofthe pancreatic

Gonadal vein

Inferior mesenteric vein ligated

FMG. 12. Splenopancreatic disconnection. Complete separation of the splenic vein from the pancreas interrupts the pancreatic collateral pathways. This provides for greater selectivity of variceal decompression and maintenance of pancreatic venous drainage to the portal system.

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hormones reach the liver directly, a physiologic aberration thought to be of great significance. "I Thus, we believe the interruption of this pancreatic siphon to be an important component of the expanded concept of selectivity of the shunt. However, further study and a much longer period of time will be required to critically evaluate the clinical as well as physiologic results of this new procedure. In conclusion, we would einphasize the following four points: 1. Splenectomy for portal hypertensive thrombocytopenia is seldom justified, and rarely in children. 2. Selective shunts are often possible and highly desirable for postsplenectomy variceal bleeding. 3. Operative exploration is sometimes necessary to identify properly the appropriate venous anatomy. 4. Splenopancreatic disconnection could prove to be an important extension of the selective shunt concept (Fig. 12). References
1. Warren WD, Millikan WJ Jr, Henderson JM, et al. Ten years portal hypertensive surgery at Emory: results and new perspectives. Ann Surg 1982; 195:530-542.

2. Rikkers LF, Rudman D, Galambos J, et al. A randomized controlled trial of the distal splenorenal shunt. Ann Surg 1978; 188:271282. 3. Henderson JM, Millikan WJ Jr, Wright L, et al. Quantitative estimation of metabolic and hemodynamic hepatic function: the effects of shunt surgery. Surg Gastroenterol 1982; 1:77-85. 4. Zeppa R, Hensley GT, Levi JU, et al. The comparative survival of alcoholics versus nonalcoholics after distal splenorenal shunt. Ann Surg 1978; 187:510-514. 5. Warren WD, Millikan WJ Jr, Smith RB III, et al. Noncirrhotic portal vein thrombosis. Physiology before and after shunts. Ann Surg 1980; 192(3):341-349. 6. Henderson JM, Millikan WJ Jr, Wright-Bacon L, et al. Hemodynamic difference between alcoholic and nonalcoholic cirrhotics following distal splenorenal shunt-effect on survival? Ann Surg 1983; 198(4):325-334. 7. Soper NJ, Rikkers LF. Effect of operations for variceal hemorrhage on hypersplenism. Am J Surg 1982; 144:700-703. 8. Hutson DG, Zeppa R, Levi JU. The effect of the distal splenorenal shunt on hypersplenism. Ann Surg 1977; 185:605-612. 9. Warren WD. Control ofvariceal bleeding: reassessment ofrationale. Founder's Lecture SSAT. Am J Surg 1983; 148:8. 10. Henderson JM, Heymsfield SB, Horowitz J, Kutner M. Measurement of liver and spleen volume by computed tomography: assessment of reproducibility and changes found following a selective distal splenorenal shunt. Radiology 1981; 141(2):525-527. 11. Starzl TE, Porter KA, Francavilla JA, et al. A hundred years of the hepatotrophic controversy. In Hepatotrophic Factors-Ciba Foundation Symposium. Amsterdam: Elsevier/Excerpta Medica/ North Holland Publishing, 1978; 111-138.

DiSCUSSION DR. ROBERT ZEPPA (Miami, Florida): I rise to make three comments. The first is that I would agree entirely with Dr. Warren and his group about the splenectomy business. As we have shown in the past in a study of these patients early on, we demonstrated that thrombocytopenia and leukopenia is not an indication for splenectomy, and, in fact, is ameliorated by this shunt. The problem is, of course, as Dr. Warren has pointed out, that hematologists get a little frisky. In fact, in following many patients, the critical level thrombocyte count that we have found to be associated with spontaneous bleeding from gums or of the skin is at 10,000 or less; and as a matter of fact, 40% of our patients have platelet counts below 50,000 when we operate on them, and we never have seen a problem of hemorrhage there. (Slide) Second, I would like to corroborate the probability of survival in the nonalcoholic group. This group was studied up to 1981, and as you will note, they are substantially better than alcoholics. In fact, within this cohort of 91 patients that I mentioned previously, 22% of them were patients with chronic, aggressive hepatitis. Those patients did not contribute to the operative mortality, as I indicated a moment ago. However, 22% of this group was responsible for over 50% of the late deaths, suggesting that-and, in fact, we will have it drawn out shortly, as the computer gives us the information-this curve is being redrawn, this one is being split into the chronic aggressive patients, and those patients with stable cirrhosis. And we would anticipate that in the nonalcoholic with stable cirrhosis we would be somewhere well above eighttenths, or 80% probability of survival at 5 years. The third point I would like to make-and Dr. Warren's comments would be much appreciated. I have watched Inokuchi do this operation, and, of course, in the beginning he-he happens to be a devotee of the distal shunt in addition to his experience with the left gastric caval shunt-was doing it distally, and he did separate the pancreas from the splenic vein. However, he left a long segment of splenic vein attached to the portal vein, separate from where he had taken the splenic vein down, just as I think that diagram showed, Dean, that you showed here.

What he has shown in autopsy material is that the head vessels will not collateralize to the retroperitoneum, and he has shown large vessels developing in the remnant of splenic vein, ultimately connecting with the shunt. So what he does now-and it is an operation that I do not believe can be done in an alcoholic-is to take cautery and dislocate the spleen totally out of its bed, lift the pancreas up, dissect the whole thing out, and then plug it into the renal vein. In those patients-the Japanese patients-who are thin, and who have a relatively intact retroperitoneum, with nice areolar tissue, rather than the great, thick, horrendous mass that we see in the alcoholics, replete with collateral vessels as well as lymphatics, it works very well in his hands. And I must say I saw him do it, so I know he can. And I am anxious to see what happens to this series over a period of time. I wonder if Dr. Warren would comment about that possibility of linkage between the proximal pancreatic veins and the shunt through retroperitoneal collaterals.

DR. JAMES G. CHANDLER (Charlottesville, Virginia): Although not

so widely appreciated at the time, the benchmark paper by Drs. Warren,

Zeppa, Fomon, in 1967, describing the distal splenorenal shunt, was a tremendous contribution. Subsequently, it has been a particular pleasure for many of us to learn from Dr. Warren what he, himself, has learned about his own procedure. About 5 years ago, several authors, myself included, pointed out that it was likely that high-pressure and low-pressure venous systems residing in the same coelomic cavity would, in all probability, get together after a period of time. In fact, that does happen, but it is not as harmful as selective shunt detractors thought it might be, because the portal deprivation occurs slowly and is never as complete as it would be with a direct portacaval shunt. Unfortunately, this tendency to drain off splanchnic venous blood through a selective shunt consequent to collateralization is always going to be one step ahead of the surgeon. If Dr. Warren and his group have eliminated the pancreatic siphon, I suspect they will be able to return in a year or two to talk about conquering