Management a/Variceal Hemorrhage
The Distal Splenorenal Shunt
]. Michael Henderson, FRCS*
The distal splenorenal shunt (DSRS) was introduced in the mid-1960s by Warren and his colleagues44 as a physiologic approach to the control of variceal bleeding. The following data provided the rationale for this new approach: (1) total portosystemic shunts controlled bleeding, but the associated loss of portal flow accelerated liver failure, and (2) devascularization procedures maintained portal flow and liver function, but had unacceptable rebleeding rates. In the original paper,44 the authors stated, "Ideally, an operation should allow continued perfusion of hepatic parenchyma by portal blood flow from the intestine and yet decompress the venous system in the gastroesophageal area." Although now we readily accept this concept of selective variceal decompression, it was novel in 1966. Animal studies documented the practicality of draining the gastric fundus under conditions of venous hypertension through the short gastric veins and spleen to the left renal vein. The initial clinical studies in six patients demonstrated the technical feasibility of achieving selective variceal decompression and maintaining portal flow. 44 Hundreds of papers from many countries have reported clinical, hemodynamic, and metabolic data on the DSRS. This article attempts to summarize the current state of knowledge of this physiologic operation that aims to control variceal bleeding while maintaining liver function in portal hypertension.
PATIENT EVALUATION Portal hypertension and variceal bleeding embrace numerous etiologies and disease states of varying severity that demand a complete evaluation of these patients. This evaluation includes determination of the etiology of portal hypertension, assessment of bleeding risk, and determination of the *Professor of Surgery and Associate Director of Clinical Research Facility, Department of Surgery, Emory University School of Medicine, Atlanta, Georgia
Surgical Clinics of North America-Vol. 70, No.2, April 1990
status of the liver. Such an evaluation is an essential step in selecting the correct therapy for any given patient. The majority of patients with variceal bleeding seen in the United States will have cirrhosis. The severity of their cirrhosis determines survival. However, it is important to identify early those patients with normal hepatic function and portal hypertension. This includes patients with extrahepatic portal vein thrombosis and schistosomiasis, whose survival is dependent on control of their variceal bleeding rather than on liver function. Endoscopic risk factors 5. 27 for variceal bleeding, such as size, tortuosity, red wales, and hematocystic spots, help identify patients at greatest risk of rebleeding. Angiographic evaluation31 makes an indirect measurement of portal pressure from hepatic vein study, defines venous anatomy, and shows variceal inflow patterns. The features of particular importance in assessing patients for DSRS are patency of the splenic vein, size and location of collaterals, and anatomy and position of the renal vein. Assessment of liver status is based on clinical evaluation, biochemical and hematologic measurements, liver biopsy, and quantitative tests. 20 The basic questions to be answered from this assessment are the following: Will the patient's liver tolerate DSRS and function adequately for good quality of life thereafter? Conversely, is the patient's liver disease so far advanced that the only realistic long-term therapy is liver transplant? There are no rigid criteria we can use to answer these questions, but a combination of the preceding methods offers the current state of the art. The ideal patient for DSRS has had Significant variceal bleeding, has suitable venous anatomy, and has a reasonable life expectancy related to the underlying liver disease.
As with any operation, the technique of DSRS has evolved in the 22 years since its introduction. The shunt component of DSRS remains unchanged, with selective transsplenic decompression of gastroesophageal varices achieved by anastomosis of the distal end of the splenic vein to the left renal vein (Fig. 1).45 In contrast, there have been significant changes in the disconnection component of the operation. The goals of maintaining portal hypertension in the splanchnic/hepatic axis of the portal system and keeping portal flow to the liver are achieved by preventing the development of siphoning varices to the shunt. The major paths for such siphoning have been defined through the pancreas, across the stomach, and in the mesocolon. 21 The operative steps that facilitate the achievement of these goals are (1) total disconnection of the splenic vein from the pancreas (splenopancreatic disconnection [SPD])25, 46; (2) meticulous dissection and interruption of the left gastric vein, the right gastric vein, and the gastroepiploic arcade 48 ; and (3) taking down of the splenic flexure of the colon by interrupting the splenocolic ligament. 48 This modified operation has been termed DSRS-
SPD. Assessment of the adequacy of the shunt and disconnection components
THE DISTAL SPLENORENAL SHUNT
Figure 1. Schematic of distal splenorenal shunt. Gastroesophageal varices are selectively decompressed by the short gastric veins, spleen, and splenic vein to the left renal vein. Portal hypertension and prograde portal How are maintained in the superior mesenteric and portal veins to the liver. (From Henderson JM, Warren WD: Portal hypertension. Curr Prohl Surg 25:3, 1988; with permission.)
of this operation requires angiography. Direct shunt catheterization (Fig. 2) should measure splenic, left renal vein, and inferior vena cava pressure. This can be done safely in the first postoperative week, and shunt patency should be documented prior to hospital discharge. Interruption of collaterals and maintenance of portal flow are. documented by superior mesenteric artery injection followed to the venous phase. Early study (1 week) will document if an adequate operative disconnection has been achieved (Fig. 3). Many patients, however, develop collaterals in the first year after DSRS, and their pattern and effect on portal flow can only be documented by angiography (Fig. 4).
CONTROL OF VARICEAL BLEEDING Distal splenorenal shunt decompresses the stomach, distal esophagus, and spleen and, in approximately 85% of patients, controls variceal bleeding. In the nine reported randomized trials of DSRS,12, 13, 15, 28, 30, 33, 38, 42, 47 the variceal rebleeding rate has ranged from 3 to 30%, with an overall variceal
Figure 2. Direct transvenous shunt catheterization with pressure measurements in the splenic vein (6 mm Hg), left renal vein (LRV) (6 mm Hg), and inferior vena cava (IVC) (2 mm Hg). Corrected sinusoidal pressure (CSP) measurements are in the left upper corner (see text).
bleeding control rate of 85%. From these and other reported series, certain features have emerged. There is a significant risk of early rebleeding in the first postoperative month. 9. 34 Several factors contribute to this. First, a technical failure, with shunt thrombosis, may lead to early rebleeding. The most common cause for a technical failure is an inadequate dissection of the splenic vein out of the pancreas; sufficient vein must be dissected to allow the splenic vein to come down to the left renal vein with no kinking. Investigation requires shunt catheterization; if this is not possible, it should be followed by splenic artery injection. Failure to visualize the shunt by these two techniques requires reoperation, and it may be possible to redo a thrombosed shunt at this time. The second major factor contributing to early rebleeding is renal vein hypertension. This may occur if the renal vein is anatomically abnormal, such as retro- or circumaortic, or if there is a very large spleen outflow that may exceed 1 L per minute. Shunt catheterization will show the splenorenal anastomosis to be patent with no gradient across it, but there will be a gradient from the left renal vein to the inferior vena cava.
THE DISTAL SPLENORENAL SHUNT
Figure 3. Venous-phase superior mesenteric artery injection at 1 week after DSRS. Good continuing portal How, with minimal collaterals to the left upper quadrant, indicates a technically satisfactory disconnection component to DSRS.
In the normal.ease after DSRS, this latter gradient will usually be less than 10 mm Hg at 1 week, but when it is more than 10 mm Hg, renal vein hypertension is present and the bleeding risk is increased. Resolution of operative edema and opening of lumbar and gonadal collaterals lead to reduction of such a gradient within 4 to 6 weeks in most patients. Rebleeding in these patients should be managed expectantly once shunt patency is demonstrated. Transfusion, pitressin, sclerotherapy, or tamponade may occasionally be required, but reoperation should be avoided. The abnormal renal vein identified prior to operation may suggest splenocaval anastomosis. 39 Documentation of shunt patency prior to hospital discharge should be done routinely. Shunt catheterization, injection of contrast to show the outflow pattern, and pressure measurement are the preferred methods and are justified to exclude or define the two problems mentioned previously.34 Late rebleeding is less common because the long-term patency of this vein-to-vein shunt is excellent if the preceding steps are followed. Late shunt thrombosis is rare. 50 Shunt stenosis appears to be a risk in patients who have a "post-phlebitic" or recanalized splenic vein at the time of their
Figure 4. The same patient as in Figure 3 at l-year follow-up. Development of portaprival transgastric and retroperitoneal collaterals (confirmed at later operation) has not diverted all portal flow.
DSRS,52 and can sometimes be managed by shunt dilation. 17 Late rebleeding secondary to high flow in gastric collateral varices coursing across the stomach from the high-pressure portal to low-pressure splenic vein has been shown in patients who have DSRS with splenopancreatic disconnection. ls Late rebleeding requires evaluation with endoscopy and angiography. The bleeding site should be defined and other pathology excluded. Angiography should include both shunt catheterization and venous phase superior mesenteric artery study. Therapy must address the underlying problem, and may require reoperation. Bleeding control with DSRS has been similar to that with total portal systemic shunts. 12, 13, 15,28, 30, 33 Recurrent variceal bleeding will occur in less than 20% of patients in most series. Interposition shunts with prosthetic material, such as mesocaval and mesorenal shunts, are a higher risk group for late thrombosis and rebleeding. 30, 41 Distal splenorenal shunt gives significantly better control of variceal bleeding than endoscopic variceal sclerosis. 38. 40, 42, 47 The four randomized studies comparing these therapies showed a 20 to 58% rebleeding after sclerotherapy compared with 3 to 19% rebleeding after DSRS. In the
THE DISTAL SPLENORENAL SHUNT
context of these two therapies, there are two major questions at this time: When should rebleeding through sclerosis be considered failure of therapy? What surgical salvage should be used in such patients? The influence of these factors on survival is discussed below.
MAINTENANCE OF PORTAL PERFUSION Distal splenorenal shunt aims to maintain portal hypertension in the splanchnic/hepatic axis and, hence, maintain prograde portal flow through the cirrhotic liver. 44 This is considered important in maintaining hepatocyte function in the damaged liver. How well is this hemodynamic goal achieved? Angiography has been the standard method for assessing portal perfusion, with a semiquantitative grading based on the number of intrahepatic portal vein radicles visualized on the venous phase of superior mesenteric artery injection31 : Grade 1. Good portal flow. Quaternary branches are seen to the periphery of the liver. Grade 2. Fair portal flow. Tertiary portal vein branches are seen. Grade 3. Poor portal flow. Only the portal vein and its bifurcation are visualized. Grade 4. No prograde portal flow. Portal vein thrombosis can be distinguished by wedged hepatic vein injection of contrast.
Angiography also· demonstrates collateral pathways that may develop in portal hypertension. 4, 29, 53 These also can be semiquantitated. 21 Most available data have come from such studies, but cineradiography33, 53 and Doppler ultrasound 3 have also been used to quantitate· portal hemodynamics after DSRS, Early postshunt studies show good continuing prograde portal flow in over 90% of patients, 21,29,38,50 Complete portal vein thrombosis occurs in 2 to 4% of patients, and nonoccluding thrombus in the portal vein occurs in 10 to 20%,19 The latter usually resolves spontaneously. Loss of portal flow after DSRS occurs more commonly in patients with alcoholic cirrhosis than with other etiologies of portal hypertension. 21,22 The following features have been noted in our own studies: (1) both alcoholic and nonalcoholic patients develop the same collateral pathways from the high-pressure portal to lowpressure splenic vein after DSRS 2\ (2) the patterns of collateral formation and portal perfusion changes are set in the first year after DSRS, with no change thereafter21 ; (3) the pancreatic collateral pathway is the primary detrimental path leading to loss of portal flow in 50 to 75% of alcoholic patients 21 , 22; (4) interruption of the pancreatic siphon leads to better maintenance of portal perfusion in alcoholic patients after DSRS,18 Other studies have shown "loss of selectivity" after DSRS 4 , 29, 53 and the development of collateral pathways as described previously. On reviewing these studies, it is of note that many of the illustrative angiograms do show maintenance of some portal flow even when such portaprival collaterals develop, A major question, which remains unanswered, is how much portal flow needs to be maintained to sustain adequate hepatocyte function,
Autopsy study late after DSRS has demonstrated the "honeycomb" pancreatic collaterals to the shunt that divert portal flow. 26 These portaprival collaterals do not lower portal pressure, as by corrected sinusoidal pressure (CSP, or wedge minus free hepatic pressure) (Fig. 2). In our experience, patients studied 1 year after with and without loss of portal perfusion showed persistence of CSP in both groups,23 although other data have shown a significant in CSP after DSRS. 38 In summary, achievement of the second goal of DSRS, to portal perfusion, is achieved in 90% of nonalcoholic cirrhotic patients. standard DSRS, 50 to 75% of alcoholic cirrhotic patients lose perfusion, but the modified DSRS with splenopancreatic disconnection improve maintenance of portal perfusion in alcoholics to 84%. Patients extrahepatic portal vein thrombosis and schistosomiasis maintain portal after DSRS.
SURVIVAL Data on survival after any procedure for variceal bleeding can be in the literature to support virtually any stance! Many variables, such patient population, disease severity, timing of therapy relative to the variceal bleed, patient compliance, and physician expertise, can outcome. Some of these issues have been addressed in editorials. 16. 35 are the data for DSRS? Six prospective randomized clinical trials have compared DSRS to portal systemic shunts in patients with cirrhosis (Table 1).12. 13. 15, 28, 30, These trials have entered patients with cirrhosis that is either or predominantly alcoholic. None of the trials have shown different rates of survival between total and selective shunt with from 2 to 10 years. The survival curve from the Emory randomized that compared DSRS to the interposition shunt is shown in Figure 5. is typical of the survival pattern in most of the trials; DSRS offers a but not significant, survival advantage. The data from these studies be extrapolated to all patients with portal hypertension and variceal ing; they are true only for the patient populations entered. Survival after DSRS in patients with nonalcoholic cirrhosis has significantly better than in patients with alcoholic disease. This was observed by Zeppa et al,54, 55 and subsequently it was confirmed in our experience. 50 Figure 6 shows the significant difference in survival in Emory experience, This series of nonalcoholic patients included a number with chronic active hepatitis. Other studies have failed to this difference in survival between alcoholics and nonalcoholics, but this probably due to smaller numbers and differences in disease severity. I, 7, No randomized study has compared total shunt with selective shunt in nonalcoholic patients. Patients with alcoholic cirrhosis do not maintain portal flow as as patients with nonalcoholic disease after DSRS. Data suggest that failure to maintain portal perfusion may be associated with
Table 1. Outcome of Randomized Trials of Distal Splenorenal Shunt Versus Total POriosystemic Shunts for Prevention of Recurrent Variceal Bleeding DSRS: NUMBERS (%)
TOTAL SHUNT: NUMBER (%)
No. of Patients
No. of Patients
Millikan et al"" Langer et al2B Fischer et al" Reichle et al33 Grace et al'3 Harley et allS
11 5.5 2 3 3.5 2.5
26 38 23 12 43 26
3(12) 5(13) 1(4) 1(8) 4(9) 3(12)
2(8) 1(3) 1(4) 0 7(18) 7(30)
7(27) 8(24) 1(4)
15(58) 20(56) 5(22) 4(33) 20(46) 14(54)
29 40 19 14 38 27
3(10) 0 0 1(7) 5(13) 2(7)
4(14) 0 1(4) 0 4(12) 1(4)
22(75) 16(41) 2(8)
21(72) 19(44) 0 4(30) 26(68) 18(67)
Abbreviations: DSRS = distal splenorenal shunt. OM = operative mortality.
0.9 0.8 0.7 0.6 0.5 0.4
Total Dead Alive Median
o Selective • Non-select Alive
~ ~V V>6' Vc9 6'0 ~ c9V .96' /0c9 ~O /V>~ /VV /0'6'
Months Figure 5. Kaplan-Meier survival curve for patients randomized to DSRS (0) or portosystemic shunt (e) in the Emory trial. No significant difference in survival is shown any time point to 10 years (From Millikan WI, Warren WD, Henderson JM, et al: The prospective randomized trial: Selective versus nonselective shunt to control variceal bleeding. Ten-year follow-up. Ann Surg 201:715, 1985; with permission.)
survival. 22. 36 When portal perfusion is better maintained in the alcoholic patients by modified DSRS-SPD, survival is improved. 18 Four randomized trials 38 . 40. 42. 47 have compared DSRS to endoscopic sclerotherapy in management of variceal bleeding in patients with cirrhosis (Table 2). In three of these studies,38. 40, 42 there is no significant difference in survival between these therapies at short-term (1 to 2 years) follow-up, La 0.9
O. B 0.7
0.. 0.3 TOTAL DEAD ALIVE "EDIAN
Figure 6. Significant (F < survival advantage is shown in nonalcoholic patients (e) with alcoholic (0) patients DSRS in the Emory with standard DSRS. (From Warren WD, Millikan WJ, JM, et al: Ten years of portal hypertensive surgery at Emory: Results and new perspectives. Surg 195:534, 1982; with permission.)
Table 2. Outcome of Randomized Trials of Endoscopic Sclerotherapy Versus Distal Splenorenal Shunt in Prevention of Recurrent Variceal Bleeding REFERENCE
Henderson et al"' Rikkers et al38 Teres et al42
EVS: NUMBER (%)
DSRS: NUMBER (%)
Abbreviations: EVS = endoscopic sclerotherapy, DSRS = distal splenorenal shunt.
despite the significantly higher rebleeding rate in the sclerotherapy groups. Rebleeding was a significant cause of death in the sclerotherapy groups, but this was countered by a higher rate of death due to liver failure in the DSRS groups. The fourth study23,47 showed a Significant survival advantage to the group randomized to initial sclerotherapy (Fig. 7). In this study, however, 35% of the sclerotherapy patients failed this treatment owing to recurrent bleeding and were successfully rescued by surgical therapy. This latter study perhaps reflects the current goal of clinical practice, which should aim at initial control of variceal bleeding by sclerotherapy but should not hesitate to go to surgical salvage in patients whose bleeding is not readily stopped by injection therapy. Debate should center on the choice of surgical rescue: total shunt, partial shunt, selective shunt, or transplant?
EFFECT ON HEPATIC FUNCTION Hepatocyte function is the critical variable in determining survival in cirrhosis. When considering therapies to control variceal bleeding, a key factor is the anticipated effect of the selected treatment on liver function. Clinicians tend to "lump" together all patients with cirrhosis, which they consider a "bad" or "terminal" disease. These concepts are incorrect because cirrhosis includes a spectrum of diseases that differ in etiology, activity disease, functional reserve, and complications. Improvement in our ability 1.0 0.9 0.8
,.. .. * ,..
6 0.6 i=
00.5 0.. 0 0.4
0.3 TOTAL DEAD
MONTHS Figure 7. Kaplan-Meier survival curves for patients randomized to DSRS (e) or endoscopic variceal sclerosis (0) at median 61-month follow-up. The significantly improved survival of the sclerotherapy group was achieved with surgical rescue of the 35% of patients who failed sclerotherapy. The asterisk (*) indicates patients who required surgery and are still alive (i).
THE DISTAL SPLENORENAL SHUNT
to define where individual patients lie on this spectrum of cirrhosis can lead not only to a better selection of initial therapy for variceal bleeding but also to better understanding of the effect of each therapy on the liver disease. With the many viable therapies currently available to treat such patients, interest must focus on how to select the right therapy for the right patient at the right time. How does DSRS affect hepatic function? Data from our group have documented that liver function can be maintained after DSRS, as shown by measurement of maximal rate of urea synthesis, 51 ammonia tolerance, 51 and galactose elimination capacity.36 Rikkers et aP8 have documented unchanged liver function, as measured by galactose elimination capacity and indocyanine green clearance. The critical variable. in maintaining quantitative liver function appears to be maintenance of portal perfusion. 36 Liver volume can be quantitated by computed tomography (CT) scan. 20 Data before and longitudinally after DSRS have documented reduction in liver volume, 18, 20, 47 but the character of this anatomic volume loss appears to be more related to loss of nonfunctional tissue, such as fat, rather than loss of functional hepatocyte mass. Concurrent with this, measurement of spleen volume has shown that a significant reduction is achieved to approximately 50% of preshunt volume by DSRS. This reduction in spleen volume is associated with a Significant rise in the platelet count. 23 The best available "control" population against which to compare these function changes are patients managed by sclerotherapy. In our randomized study, 23, 47 galactose elimination capacity (GEe) showed Significantly different patterns between patients successfully managed by the two therapies (Fig. 8). The difference in the first year, with an increase in GEC in the sclerotherapy group and a decrease in the DSRS group, was significant (P < 0.05). The pattern after the first year was not different, with the slight decline in each group representing the natural history of the underlying disease. In this same study, liver volume showed a greater reduction in the DSRS group (n = 21:1730 ± 124 to 1429 ± 99 cc:P < 0.001) than in the sclerotherapy group at 1 year (n = 25: 1755 ± 117 to 1642 ± 110:P = 0.07). These data suggest that one pays a slightly greater cost in hepatic function for the better bleeding control of DSRS in the first year compared with sclerotherapy. 23, 47 In summary, hepatic function is maintained after DSRS, and maintained portal perfusion is the most critical variable. HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy is a complication of chronic liver disease that is often precipitated by bleeding, infection, electrolyte imbalance, sedatives or narcotics, and constipation. Severe "spontaneous" encephalopathy can occur, and is a harbinger of severe liver disease. Total portal venous diversion by total portosystemic shunts is a major precipitant of this type of encephalopathy. What are the incidence and type of encephalopathy after DSRS? Data are conflicting, with encephalopathy after DSRS in the random-
e" 250 p
Figure 8. Hepatocyte function, measured by galactose elimination capacity (GEC), is significantly better maintained in the first year of sclerotherapy compared to the first year after DSRS. Galactose elimination capacity falls in parallel thereafter in both groups.
ized trials varying from 5 to 47%. This complication is not only an important endpoint that should be evaluated in such clinical trials, but it can also be a major incapacity to the patient when it occurs. Langer et a1 28 provided an excellent analysis of objective assessments of encephalopathy and "quality of life." This study found both Significantly lower encephalopathy and significantly better quality of life after DSRS compared with portacaval shunt. Three of the other trials comparing DSRS with total shunts found significantly lower encephalopathy after DSRS,12, 30, 33 whereas the final two 13, 15 showed no significant difference between DSRS and total shunts, Hutson et a}24 pointed out that the occurrence of severe encephalopathy after DSRS warrants full investigation because a reversible precipitating cause may be found. This requires angiography with emphasis on the detection of large collateral varices that lead to portaprival flow. Occlusion or surgical interruption of such collaterals can reverse encephalopathy. It is difficult to determine whether encephalopathy may be solely due to the underlying cirrhosis or be contributed to by the DSRS. In the randomized trials comparing DSRS to sclerotherapy, two studies 39,47 showed no significant difference in encephalopathy between the therapies, suggesting that it is indeed the underlying liver disease rather than the DSRS that is the main contributor. In the third trial,42 encephalopathy was Significantly higher (P < 0.05) after DSRS (24%) than after sclerotherapy (8%), but the modified retroperitoneal DSRS used in that trial may have led to inadequate portal-shunt disconnection of portaprival collaterals. No postoperative angiographic data were presented to document the effectiveness of this component of the operation. In summary, the incidence of encephalopathy, particularly at an
THE DISTAL SPLENORENAL SHUNT
incapacitating level, appears to be less after DSRS than after total shunts, and probably is not significantly increased over the rate of encephalopathy due to advanced chronic liver disease.
DISTAL SPLENORENAL SHUNT IN PORTAL VEIN THROMBOSIS Patients with variceal bleeding secondary to extrahepatic portal vein thrombosis are an ideal group for DSRS. They have normal livers, so control of their variceal bleeding with a successful DSRS returns them to a normal life expectancy. They do, however, present some unique problems. First, for a clearer understanding of the pathophysiology of extrahepatic portal vein thrombosis, one should recall the lessons of Pavlov,14 who showed that good portal perfusion is maintained in extrahepatic portal vein occlusion through hepatopedal collaterals. The obstructed high-pressure splanchnic venous bed will collateralize to the normal low-pressure sinusoids, with the angiographic findings of cavernous transformation. 49 Second, long-term diversion of this portal flow away from the normal liver in these patients can lead to hepatic encephalopathy or neuropsychiatric abnormalities,43, 49 although data have been conflicting.2 Finally, approximately 80% of patients with this pathology will have a patent splenic vein suitable for DSRS. A recent review5 2 of 70 patients with portal vein thrombosis by our group has led to the following treatment strategy. Evaluation after stabilization from the acute bleed should concentrate on assessment of splenic vein patency by splenic arteriography and splenoportography if necessary. On occasion, the splenic vein, although patent, may not be visualized by these methods because of major collateral flow, so the final decision about the technical feasibility of DSRS depends on operative exploration. Splenectomy is not a good initial operation in these patients because the rebleeding rate is high, and such patients proved to be the most difficult subset in the above series. 52 Quantitative data on patients with portal vein thrombosis after DSRS show excellent stability of GEe, liver volume, portal perfusion, and liver blood flow. Reduction of spleen size by 50% is associated with a Significant (P < 0.05) rise in platelet count. One specific problem identified in this group was stenosis of the anastomosis of the DSRS in 25% of patients. 52 This was successfully managed by balloon dilation in the majority, but it mandates early restudy at 3 to 6 months. The mechanism of this stenosis probably relates to scarring in the splenic vein in a manner similar to the portal vein pathology. In summary, patients with portal vein thrombosis carry an excellent prognosis from variceal bleeding because they have normal liver function. However, their ability to tolerate bleeding episodes should not be an excuse to withhold treatment, which can definitively prevent rebleeding. Although sclerotherapy is an acceptable option in those with no shuntable veins, we believe that the best definitive therapy in this group is DSRS.
DISTAL SPLENORENAL SHUNT IN SCHISTOSOMIASIS
This issue is primarily targeted at the management of variceal bleeding in North America, so schistosomiasis as a cause of portal hypertension is rarely seen. On a worldwide basis, however, this remains a common cause of portal hypertension and variceal bleeding. Recent studies have supported the theoretical appeal of selective shunting in this population and will be addressed briefly. Historically, surgical therapies for variceal bleeding in schistosomiasis have paralleled therapies used in patients with cirrhosis. Review of 130 publications in 1984 by Raia et aP2 showed that splenectomy ± central splenorenal shunt, esophagogastric devascularization, and portacaval shunt had been used in 82% of patients. Recurrent bleeding was highest (54%) with splenectomy, and encephalopathy highest (60%) with portacaval shunt. Since the mid-1970s, groups in both South America8 and the Middle East6 • 10 have studied DSRS in this population. A prospective randomized trial comparing DSRS, central splenorenal shunt, and esophagogastric devascularization was started in 1977 in Sao Paulo. 8 A report in 1986 showed the superiority of DSRS over central splenorenal shunt, primarily with significantly lower encephalopathy, and no further total shunt patients were entered. 8 This study is ongoing, comparing DSRS and devascularization. In a carefully studied population from Egypt, Ezzat et apo have shown that DSRS can be safely and effectively applied to control variceal bleeding in patients with schistosomiasis. In a subsequent report with a minimum of 5-year follow-up,l1 their group of 45 patients with pure schistosomiasis showed (1) a 92% survival rate, (2) 95% shunt patency and bleeding control, (3) encephalopathy in 4.4%, and (4) continued portal perfusion (angiographic) in 94%. In summary, data are now appearing to support the use of DSRS in patients with schistosomiasis. In this population, control of variceal bleeding and maintenance of liver function with a low rate of encephalopathy can be achieved.
Distal splenorenal shunt (DSRS) provides selective decompression of gastroesophageal varices, with maintenance of portal hypertension and prograde portal flow to the cirrhotic liver. Accurate patient evaluation is essential to select appropriate patients for DSRS. Variceal bleeding control is greater than 85% and is as effective as total portosystemic shunts. Maintenance of prograde portal flow is >90% in nonalcoholic disease, but only 50% in alcoholic cirrhosis; the latter is improved by total splenopancreatic disconnection. Hepatic function is better maintained when portal flow is maintained. Encephalopathy is lower after DSRS than after total shunts. Survival is not significantly improved after DSRS in patients with alcoholic cirrhosis compared to outcome after total shunts. The survival in
THE DISTAL SPLENORENAL SHUNT
patients with nonalcoholic disease is significantly improved over that of alcoholics.
REFERENCES 1. Adson MA, van Heernden JA, Ustrup DM: The distal splenorenal shunt. Arch Surg 119:609-614, 1984 2. Alagille D, Carlier JC, Chiva M, et al: Long-term neuropsychological outcome in children undergoing portal systemic shunts for portal vein obstruction without liver disease. J Pediatr Gastroentrol Nutr 5:861-866, 1986 3. Balondi L, Gaiani S, Mazziotti A, et al: Morphologic and hemodynamic changes in the portal venous system after distal splenorenal shunt: An ultrasound and pulsed Doppler study. Hepatology 8:652-657, 1988 4. Belghiti J, Grenier P, Noue! 0, et al: Long-term loss of Warren's shunt selectivity: Angiographic demonstration. Arch Surg 116:1121-1124, 1981 5. Beppu K, Inokuchi K, Koyanagi N, et al: Prediction of variceal hemorrhage by esophageal endoscopy. Gastrointest Endosc 27:213-218, 1981 6. Bessa SM, Helmy I, EI Sheikh SO, et al: The distal splenorenal shunt in patients with variceal bleeding due to schistosomal hepatic fibrosis. Surg Gynecol Obstet 165:143147, 1987 7. Brown SL, Busuttil RW: Survival of alcoholic vs nonalcoholic patients after portosystemic shunts. Arch Surg 119:1321-1324, 1984 8. DaSilva LC, Strauss E, Gayotto LCC, et al: A randomized trial for the study of the elective surgical treatment of portal hypertension in mansonic schistosomiasis. Ann Surg 204:148-153, 1986 9. Eckhauser FE, Pomerantz RA, Knol JA, et al: Early variceal rebleeding after successful distal splenorenal shunt. Arch Surg 121:547-552, 1986 10. Ezzat FA, Abu-Elmagd KM, Aly LY, et al: Distal splenorenal shunt for management of variceal bleeding in patients with schistosomal hepatic fibrosis. Ann Surg 204:566-573, 1986 11. Ezzat FA, Abu-Elmagd KM, Sultan AA, et al: Schistosomal versus nonschistosomal variceal bleeders-do they respond differently to selective shunt (DSRS)? Ann Surg 209:489-500, 1989 12. Fischer JE, Bower RH, Atamian S, et al: Comparison of distal and proximal splenorenal shunts: A randomized prospective trial. Ann Surg 194:531-544, 1981 13. Grace ND, Conn HO, Resnick RH, et al: Distal splenorenal vs portosystemic shunts after hemorrhage from varices: A randomized controlled trial. Hepatology 8:1475-1481, 1988 14. Hahn M, Massen 0, Nenki M, et al: De ecksche fistel zwischen der unteren hohlvene and der pfortaden und folgen fur den organismus. Arch Exp Pathol Pharmacol 32:162210, 1893 15. Harley HAJ, Morgan T, Redeker AG, et ·al: Results of a randomized trial of end-to-end portacaval shunt and distal splenorenal shunt in alcoholic liver disease and variceal bleeding. Gastroenterology 91:802-809, 1986 16. Henderson JM: Variceal bleeding: Which shunt? Gastroenterology 91:1021-1023, 1986 17. Henderson JM, EI Khishen MA, Millikan WJ, et al: Management of stenosis of distal splenorenal shunt by balloon dilation. Surg Gynecol Obstet 157:43-48, 1983 18. Henderson JM, Warren WD, Millikan WJ, et al: Distal splenorenal shunt with splenopancreatic disconnection: A four-year assessment. Ann Surg, in press 19. Henderson JM, Millikan WJ, Chipponi J, et al: The incidence and natural history of thrombus in the portal vein following distal splenorenal shunt. Ann Surg 196:1-7, 1982 20. Henderson JM, Warren WD: A method for measuring quantitative hepatic function and hemodynamics in cirrhosis: The changes following distal splenorenal shunt. Jpn J Surg 3:157-168, 1986 21. Henderson JM, Gong-Liang J, Galloway J, et al: Portaprival collaterals following distal splenorenal shunt: Incidence, magnitude, and associated portal perfusion changes. J Hepatol 1:649-661, 1985 22. Henderson JM, Millikan WJ, Wright-Bacon L, et al: Hemodynamic differences between
23. 24. 25. 26. 27. 28.
34. 35. 36. 37. 38.
44. 45. 46.
alcoholic and nonalcoholic cirrhotics following distal splenorenal shunt-effect on survival? Ann Surg 198:325-334. 1983 Henderson JM. Warren WD, Kutner MH, et al: Endoscopic variceal sclerosis compared with distal splenorenal shunt to prevent recurrent variceal bleeding in cirrhosis. Ann Intern Med, in press Hutson DG, Livingstone A, Levi JV, et al: Early hepatic failure or upper gastrointestinal bleeding following a distal splenorenal shunt. Surg Gynecol Obstet 155:46-48, 1982 Inokuchi K, Beppu K, Kayanagi N, et al: Exclusion of nonisolated splenic vein in distal splenorenal shunt for prevention of portal malcirculation. Ann Surg 200:711-717, 1984 Isomatsu T: Loss of selectivity of Warren shunt in long-term observation. Jpn J Surg 13:202-206, 1983 The Italian Liver Cirrhosis Project: Reliability of endoscopy in the assessment of variceal features. J Hepatol 4:93-98, 1987 Langer B, Taylor BR, Mackenzie DR, et al: Further report of a prospective randomized trial comparing distal splenorenal shunt with end-to-side portacaval shunt. Gastroenterology 88:424-429, 1985 Maillard IN, Flamant YM, Hay JM, et al: Selectivity of the distal splenorenal shunt. Surgery 86:663-671, 1979 Millikan WJ, Warren WD, Henderson JM, et al: The Emory prospective randomized trial: Selective versus nonselective shunt to control variceal bleeding. Ten-year followup. Ann Surg 201:712-722, 1985 Nordlinger BM, Nordlinger DF, Fulenwider JT, et al: Angiography in portal hypertension: Clinical significance in surgery. Am J Surg 139:132-141, 1980 Raia S, Mies S, Macedo AL: Surgical treatment of portal hypertension in schistosomiasis. World J Surg 8:738-752, 1984 Reichle FA, Fahmy WE, Golsorkhi M: Perspective comparative clinical trial with distal splenorenal and mesocaval shunts. Am J Surg 137:13-21, 1979 Richards WO, Pearson TC, Henderson JM, et al: Evaluation and treatment for early hemorrhage of the alimentary tract after selective shunt procedures. Surg Gynecol Obstet 164:6:530-536, 1987 Rikkers LF: Is the distal splenorenal shunt better? Hepatology 8:1705-1707, 1988 Rikkers LF, Rudman D, Galambos JT, et al: A randomized, controlled trial of the distal splenorenal shunt. Ann Surg 188:271-282, 1978 Rikkers LF, Soper NJ, Cormier RA: Selective operative approach for variceal hemorrhage. Am J Surg 147:89-96, 1984 Rikkers LF, Burnett DA, Volentine GD, et al: Shunt surgery versus endoscopic sclerotherapy for long-term treatment of variceal bleeding: Early results of a randomized trial. Ann Surg 206:261-271, 1987 Ross C, Potts JR: Early experience with the selective splenocaval shunt for variceal bleeding. Surg Gynecol Obstet 167:335-340, 1988 Santambrogia R, Spina GP, Opocher E, et al: Distal splenorenal shunt vs endoscopic sclerotherapy in the prevention of variceal bleeding: A randomized, controlled trial. J Hepatol 7:5173, 1988 Smith RB, Warren WD, Salam AA, et al: Dacron interposition shunts for portal hypertension: An analysis of morbidity correlates. Ann Surg 192:9-17,1980 Teres I. Bordas JM, Bravo D, et al: Sclerotherapy vs. distal splenorenal shunt in the elective treatment of variceal hemorrhage: A randomized controlled trial. Hepatology 7:430-436, 1987 Voorhees AB, Chaitman E, Schneider S, et al: Portal systemic encephalopathy in the noncirrhotic patient: Effect of portal systemic shunting. Arch Surg 107:659, 1973 Warren WD, Zeppa R, Foman JS: Selective transplenic decompression of gastroesophageal varices by distal splenorenal shunt. Ann Surg 166:437, 1967 Warren WD, Millikan WJ: Selective transplenic decompression procedure: Changes in technique after 300 cases. Contemp Surg 18:11-32, 1981 Warren WD, Millikan WJ, Henderson JM, et al: Selective variceal decompression after splenectomy or splenic vein thrombosis with a note on splenopancreatic disconnection. Ann Surg 199(6):694-702, 1984 Warren WD, Henderson JM, Millikan WI. et al: Distal splenorenal shunt versus endoscopic sclerotherapy for long-term management of variceal bleeding. Ann Surg 203:454-462, 1986
THE DISTAL SPLENORENAL SHUNT
48. Warren WD, Millikan WJ, Henderson JM, et al: Splenopancreatic disconnection: Improved selectivity of the distal splenorenal shunt. Ann Surg 204:346-355, 1986 49. Warren WD, Millikan WJ, Smith RB, et al: Noncirrhotic portal vein thrombosis: Physiology before and after shunts. Ann Surg 192:341-349, 1980 50. Warren WD, Millikan WJ, Henderson JM, et al: Ten years of portal hypertensive surgery at Emory: Results and new perspectives. Ann Surg 195:530--542, 1982 51. Warren WD, Rudman D, Millikan W, et al: The metabolic basis of portosystemic encephalopathy and the effect of selective vs. nonselective shunts. Ann Surg 180(4):573579, 1974 52. Warren WD, Henderson JM, Millikan WJ, et al: Management of variceal bleeding in patients with non-cirrhotic portal vein thrombosis. Ann Surg 207(5):623-634, 1988 53. Widrich WC, Robbins AH, Johnson WC, et al: Long-term follow-up of distal splenorenal shunts: Evaluation by arteriography, shuntography, transhepatic portal venography and cinefluorography. Radiology 134:341-345, 1980 54. Zeppa R, Hensley CT, Levy JV, et al: The comparative survival of alcoholics versus nonalcoholics after distal splenorenal shunt. Ann Surg 187:510-514, 1978 55. Zeppa R, Lee PA, Hutson DC, et al: Portal hypertension. A fifteen-year perspective. Am J Surg 155:6-9, 1988
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