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Prospective study of a prosthetic H-graft portacaval shunt
Prospective Alexander S. Rosemurgy,
Study of a Prosthetic Portacaval Shunt MD,
Earl W. McAllister,
This study was undertaken to prospectively evaluate the 8-mm Gore-Tex@ interposition H-graft portacaval shunt. Thirty-six high-risk patients at the University of South Florida-affiliated hospitals received small-diameter shunts because of bleeding esophagogastric varices over a recent 2-year period. Portal vein and portal vein-inferior vena cava gradients were significantly reduced after shunting. These pressure changes were manifested clinically by the absence of variceal rebleeding and improvement of ascites; in addition, the incidence of encephalopathy was low. The 8-mm graft maintained hepatopedal flow in 67% of the patients, but reversal of flow did not result in complications commonly associated with poor portal perfusion. Graft thrombosis occurred in four ( 11%) patients. All grafts were successfully revised, three by operative revision and one by an interventional radiologist. Operative mortality was low ( 11%) , and morbidity was unusual. The small-diameter H-graft portacaval shunt is a safe and effective method of treatment for bleeding esophagogastric varices.
ptimal treatment for variceal bleeding secondary to portal hypertension continues to be one of the most 0 controversial subjects in general surgery. Methods of treatment previously thought to be panaceas have undergone continual technical revisions to improve operative results [I ,2]. Nonetheless, the goals of operative therapy for bleeding secondary to portal hypertension continue to be control of variceal hemorrhage and avoidance of progressive hepatic failure and encephalopathy through the maintenance of hepatopedal flow. From the Department of Surgery, University of South Florida, Tampa, Florida. Requests for reprints should be addressed to Alexander S. Rosemurgy, MD, 730 Harbourside Medical Towers, 4 Columbia Drive, Tampa, Florida 33606. Presented at the 3 1st Annual Meeting of the Society for Surgery of the Alimentary Tract, May 15-16,199O.
MD,
H-Graft
Robert E. Kearney,
MD, Tampa, Florida
Portacaval shunts have been most successful at controlling variceal hemorrhage, but, with diversion of portal flow, they carry a relatively high risk of subsequent hepatic failure and encephalopathy [3-51. Beginning in 1967, selective shunting, popularized by the late Dr. Dean Warren, offered hope for selective decompression of esophageal varices while maintaining portal hypertension and prograde portal blood flow [6]. Early results were encouraging; however, other controlled studies demonstrated that only a minority of selectively shunted patients maintained portal perfusion 3 to 5 years after surgery [ 71. Documentation of recollateralization of esophagogastric varices in these patients has led to modifications of the original shunt, adding to the complexity of an already difficult operation [2]. In addition, the development of postoperative ascites in these patients has further reduced our enthusiasm for selective shunting. In 1980, Rypins and Sarfeh reintroduced the concept of partial portal decompression and systematically studied the ability of progressively narrower polytetrafluoroethylene (PTFE) portacaval grafts to control variceal hemorrhage and maintain prograde portal blood flow [8,9]. These studies showed that small-diameter portacaval shunts could control variceal hemorrhage while generally maintaining prograde portal flow, with a distinct survival advantage demonstrated for those patients who did maintain prograde flow [IO]. Furthermore, their operative design was simple and their operative mortality was low. Johansen [I I] studied partial portal decompression by constructing small stoma side-to-side shunts in 50 alcoholic cirrhotic patients with acceptable operative mortality and shunt patency. In contrast to Sarfeh’s work, the lo- to 12-mm calibrated anastomosis of his study resulted in stagnation or reversal of portal blood flow in all of the patients studied postoperatively with duplex ultrasonography. We were initially attracted to the small-diameter H-graft shunt because of its perceived technical simplicity and our institutional dissatisfaction with conventional selective shunting. We undertook this prospective trial of 8-mm H-graft portacaval shunts to test the ability of a small-diameter portacaval shunt to control variceal hemorrhage and simultaneously maintain portal perfusion. PATIENTS
AND METHODS
From November 1987 through March 1990, 36 patients at the University of South Florida underwent portacaval shunting using an 8-mm externally reinforced Gore-Tex@ (W.L. Gore, Flagstaff, AZ) interposition graft. There were 24 men and 12 women, ranging in age from 38 to 8 1 years, with a mean age of 56 years. Reasons for surgical intervention were bleeding esophageal varices after failed sclerotherapy in 23 (64%) patients, bleeding gastric varices in 12 (33%) patients, and bleeding intesti-
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TABLE I Preshunt and Postshunt Measurements (mean f SEM)
Portal vein pressure (mm Hg) Inferior vena cava pressure (mm Hg) Portal vein-inferior vena cava gradient
Preshunt
Postshunt
31 f 1.0 12 f 0.8 20 f 0.7
20 f 0.9’ 14 f 0.9 7 f 0.6”
(mm Hg) * p CO.01 for differences between preshunt and postshunt values by paired student’s t test.
nonabsorbable suture. Shunt patency was assessed radiologically on the fifth postoperative day via transfemoral cannulation of the shunt. Direction of portal blood flow and shunt gradients were assessed; large collateral varices were embolized if present and easily accessible. Eight (22%) of the 36 patients underwent repeat radiologic study 4 to 18 months after shunting. Clinical follow-up was obtained in all patients. Differences in preshunt and postshunt manometrics were compared using the paired Student’s t test. Crude and actuarial survival statistics were computed.
nal varices in 1 (3%) patient. Two (6%) patients were in Child’s class A, 20 (56%) patients were in Child’s class B, and 14 (39%) patients were in Child’s class C. Twentynine (8 1%) patients had poorly controlled or uncontrolled ascites prior to shunting. All patients had portal hypertension secondary to cirrhosis; cirrhosis was due to alcohol in 72%, chronic hepatitis in 14%, unknown causes in ll%, and methotrexate toxicity in 3%. Twelve (33%) patients underwent emergency portacaval shunting, 8 (22%) underwent urgent shunting, and 16 (45%) underwent elective shunting. Twenty-nine (8 1%) of the 36 patients underwent preoperative angiography with measurement of inferior vena cava pressures and calculation of corrected sinusoidal pressures. All operations were performed through a right upper quadrant oblique abdominal incision. Preshunt portal vein and inferior vena cava pressures were measured intraoperatively using a calibrated transducer and a 25-gauge needle. Eight-millimeter externally supported Gore-Tex@ grafts, as short as possible with bevels at the ends of the graft oriented at 90’ with respect to each other, were sewn into place with a running nonabsorbable suture. Following shunt placement, pressures were remeasured and a shunt gradient was calculated. The coronary vein and other portasystemic collaterals were ligated when possible, but no rigorous attempts were made to ligate collaterals. Fourteen patients had intraoperative color-flow Doppler (Acuson 128 with linear array 5MHz probe, Acuson Corp., Mountain View, CA) assessment of the portal vein and inferior vena cava prior to and after shunting. After the first few shunts, the grafts were marked with metal clips to aid in postoperative cannulation. The incisions were closed in two layers using running
RESULTS All 36 patients underwent placement of g-mm ring reinforced Gore-Tex@ grafts in the portacaval position. Estimated operative blood loss ranged from 100 mL to 3,000 mL, with an average estimated loss of 738 f 102 mL @EM). Operative blood loss associated with elective, urgent, and emergency operations were 756 f 124 mL, 725 f 253 mL, and 723 f 201 mL, respectively. Duration of operations ranged from 3 to 9 hours, with an average of 4.3 f 0.24 hours. Prolonged operative times occurred occasionally because of unacceptable intraoperative shunt gradients leading to shunt revisions, unanticipated anatomic variations, or difficulty in obtaining ultrasonographic equipment intraoperatively. Portal vein pressures and portal vein-inferior vena cava gradients significantly decreased (p <0.05) with shunting (Table I). Of the 14 patients assessed by color-flow Doppler, 10 had prograde portal flow and 4 had “mixed” or “stagnant” flow before shunting. Two patients with prograde flow and two with mixed flow prior to shunting showed reversal of flow by intraoperative Doppler assessment after shunting. The effect of shunting on portal blood flow is unknown in nine (25%) patients as they did not undergo sufficient study either before or after shunting. Reasons for this include the emergency nature of their shunt operation, the unavailability of intraoperative ultrasound at surgery, or death during the immediate postoperative period. Therefore, in 27 patients, the direction of flow in the portal vein was known both before and after shunting. Of the 24 patients with preshunt hepatopedal or mixed portal flow, 7 (29%) developed hepatofugal flow with Hgraft portacaval shunting (Table II); 3 patients were in Child’s class B and 4 were in Child’s class C at the time of shunting. Sixty-seven percent of patients with hepatopeda1 flow before shunting maintained hepatopedal flow after shunting. Portal vein and inferior vena cava pressures and portal vein-inferior vena cava gradients were not different in patients who did or did not experience reversal of flow with shunting (Table III). Venography through transfemoral cannulation of the shunt and portal vein done on postshunt day five demonstrated graft thrombosis in three patients. Thrombectomy was successfully performed by an interventional radiologist in one case, and two cases required reoperation. An additional patient had very slow flow and clot in the portal vein distal to the shunt. Ill-advised radiologic
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TABLE II Direction of Portal Vein Flow Before and After H-Graft Portacaval Shunt’
Hepatopedal flow Hepatofugal flow Mixed flow
Preshunt
Postshunt
21 (78%) 3 (11%) 3(11%)
14 (52%) 10 (37%) 3 (11%)
’ Excluding those patients in whom the direction of flow was not known both before and after shunting.
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thrombectomy was attempted and resulted in thrombosis of the shunt, which required reoperation. All three patients undergoing operative shunt revision had successful revision of their shunts with subsequent demonstration of shunt patency by postoperative transfemoral cannulation of the shunt (Table IV). Technical causes for shunt thrombosis could not be identified in any of the patients who underwent shunt revision. There was no postoperative rebleeding in the 36 patients who underwent shunting. Six patients had wound complications: one patient had an infection, three experienced temporary postoperative incisional ascitic leaks, and two developed wound hernias. No patient had ascites beyond the immediate postoperative period. Three patients had temporary encephalopathy and one had continuation of mild to moderate preoperative encephalopathy after shunting. All four patients with postoperative encephalopathy were classified as Child’s class C preoperatively. Two of the four patients developed reversal of prograde portal flow with shunting and two patients became temporarily encephalopathic despite maintenance of prograde flow. In patients with postshunt encephalopathy, the average postshunt portal vein-inferior vena cava gradient was 7 f 1.7 mm Hg and the average postshunt portal vein pressure was 21 f 3.0 mm Hg. Of the seven patients who experienced reversed portal flow with shunting, one patient was encephalopathic for several days after shunting, one patient died during the immediate postoperative period, and one patient experienced continuation of preoperative encephalopathy. This last patient died of unknown causes 3 months after shunting. Five (71%) of the seven patients in whom portal flow reversed with shunting are doing well. There were four (11%) postoperative deaths. One patient, a Child’s class C, died due to fulminant liver failure within 24 hours of surgery. He demonstrated mixed portal flow prior to shunting but hepatofugal flow after shunting. A second patient died on the fifth postoperative day due to a respiratory arrest brought on by excessive narcotic administration. A third perioperative death was due to toxic epidermal necrolysis in a patient who had been under treatment previously for the same condition. The last postoperative death was due to a gastric perforation just prior to discharge following ill-advised preoperative gastric sclerotherapy. Two additional patients died more than 30 days after shunting: one patient died of complications of a subdural hematoma, a result of a fall, and one patient was found dead at home after doing well for 3 months. The opportunity to document shunt patency just prior to death or at autopsy was available in five of the six patients and all shunts were patent. All survivors have been monitored for up to 29 months. During follow-up, three (10%) patients have rebled despite documented shunt patency: one from alcoholic gastritis, one from a prepyloric ulcer, and one from persistent gastric varices. The latter patient underwent splenic artery embolization and over the past 8 months has not rebled. Twenty-six (87%) patients are doing well with no rebleeding or clinical encephalopathy, while one THE AMERICAN
TABLE III Preshunt and Postshunt Pressure Measurements in Patlents Who Reversed Hepatopedal Portal Blood Flow with Shuntlng (Group 1) and In Patlents Who Malntalned Hepatopedal Flow wlth Shuntlng (Group 2) Preshunt (mm l-!g) Inferior Portal Vein Vena Cava Group 1 (n = 7) Group 2 (n = 14)
30 f 29 f
1.0 1.7
12 f 0.9 9 f 0.9
Postshunt (mm Hg) Inferior Portal Vein Vena Cava 21 f 19 f
1.2 1.7
14 f 0.09 12 f 1.1
TABLE IV Preshunt and Postshunt Measurements at the Time of Operative Shunt Revlslon In Three Patlents Preshunt
Portal vein pressure Inferior vena cava pressure Portal vein-Inferior vena cava gradient
Postshunt
(mm Hg)
(mm Hs)
25 f 3.6 7 f 3.5 18 f 4.4
19 f 8.1 11 f 6.8 af 1.7
(3%) patient is affected by encephalopathy, which existed in its present form prior to shunting. Eight patients have consented to follow-up radiologic evaluation of their shunts. All shunts are patent 4 to 18 months after portacaval shunting, with an average portal vein pressure for the eight patients of 16 f 1.6 mm Hg and an average portal vein-inferior vena cave gradient of 10 f 0.7 mm Hg. Reversal of portal flow to hepatofugal flow was not seen in any of the late follow-up radiologic shunt studies. COMMENTS
Until Warren [q introduced the concept of selective variceal decompression, the only definitive treatment of portal hypertension was total portal decompression. Unfortunately, selective splenorenal shunts have not proven to remain selective because of persisting hypertension in the portal system. Ideal therapy for variceal hemorrhage due to portal hypertension would involve portal decompression with maintenance of hepatopedal portal blood flow. This prospective study was undertaken to evaluate the ability of the &mm Gore-Tex@ interposition portacaval shunt to achieve these therapeutic goals. The patients in this study were generally an older group of male Child’s class B and C alcoholic cirrhotics who developed uncontrolled bleeding esophagogastric varices after sclerotherapy failed. The majority of patients had ascites before undergoing H-graft portacaval shunting, and most were operated on urgently or emergently. In most patients, attempts to defer surgery to an elective setting proved impossible despite aggressive intervention with vasopressin injection, variceal balloon tamponade, and endoscopic variceal sclerotherapy. Despite the general urgency with which the operations were undertaken, the patients experienced little morbidity and low mortality.
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Portal vein and inferior vena cava pressures were documented in all patients before and after shunting. Although the &mm interposition shunt does not lower portal vein pressure to normal or the portal vein-inferior vena cava gradient to zero, it does significantly lower both. These pressure changes were manifested clinically by the absence of variceal rebleeding and improvement in ascites yet with a low incidence of postoperative encephalopathy. Portal vein flow was assessed in most patients before and after shunting. The 8-mm interposition shunt allows most patients to maintain hepatopedal flow, even in the absence of rigorous attempts to obliterate collaterals. But, unlike Sarfeh and co-workers’ experience [8], even in those patients who experienced continuation of preshunt hepatofugal flow or postshunt reversal of hepatopedal portal flow, complications commonly associated with poor portal perfusion were unusual. Maintenance of hepatopedal flow may not be the issue [II]. It may be that the critical factor determining clinical outcome is not the direction of portal blood flow but instead the ability to maintain portal and mesenteric hypertension below an unestablished critical threshold that limits variceal rebleeding and above an unestablished threshold that limits hepatic encephalopathy. It has been suggested [I21 that the maintenance of such mesenteric venous hypertension may limit the intestinal absorption of nitrogenous compounds and the consequent formation of false neurotransmitters that lead to clinical encephalopathy. Although more than one third of the patients in this series had hepatofugal portal flow after shunting, only one significant complication occurred in those patients: one postoperative death due to apparent fulminant liver failure. Interestingly, this patient had an accessory right hepatic artery. Postoperative alterations in hepatic arterial inflow not apparent at re-exploration for deterioration hours after shunting could have contributed to his rapid postop erative deterioration. As a group, the patients underwent partial portal decompression with minimal complications. Although the patients in this study were “high-risk” and the operations were usually undertaken with urgency, the operative mortality was low when compared with that of most reports [13,24]. Furthermore, most postoperative deaths were preventable. Judicious use of analgesics would have prevented one death. Avoidance of aggressive gastric sclerotherapy could have avoided another death due to a postshunt gastric perforation. Control of quiescent chronic toxic epidermal necrolysis postoperatively could have prevented a third patient’s death. Ascites was uniformly improved by partial portal decompression and no patient experienced variceal rebleeding, with the exception of one patient with presumed persistent hypertensive gastropathy who was treated by splenic artery embolization. Despite the poor general health of the patients, deaths following discharge have been very unusual. Furthermore, one of the two late deaths was preventable. Better attention to one patient’s needs would have prevented an in-hospital fall on the day of discharge. This patient began to manifest a chronic subdural hematoma weeks
later, presumably as a result of the fall, and died despite aggressive operative intervention. Similarly, deterioration of liver function or late liver failure has not been seen during follow-up. The maintenance of portal perfusion demonstrated in the postoperative venographic shunt studies has persisted in all of the late follow-up radiologic shunt studies with no recollateralization demonstrated. What are the drawbacks associated with this method of portal decompression? The operative technique is not as simple as it would first appear. Partial removal of the caudate lobe of the liver is almost always necessary to obtain proper graft positioning and placement. The graft can be easily tailored and each anastomosis can be easily completed, but the graft must lie perfectly between the portal vein and vena cava. Occasionally, technical inadequacies are not apparent until postshunt portal vein pressures and shunt gradients are calculated. A drop of less than 10 mm Hg in the portal pressure with shunting, coupled with a drop of less than 10 mm Hg in the portal vein-inferior vena cava gradient with shunting, warrants documentation of shunt patency. Although we found intraoperative ultrasound occasionally helpful in determining shunt patency, documenting shunt patency generally involved opening the graft or one of the anastomoses, adding to the operative time and undoubtedly to the operative complications. Only when the operating surgeon is convinced of graft patency can the operative procedure be completed. Even then, the patient is not immune to graft thrombosis, which occurred in nearly 11% of patients. Moreover, it is imperative that the shunt be studied within the first week postoperatively and prior to discharge so that if thrombosis is indeed present, thrombectomy can be performed by an interventional radiologist or early operative revision can be done. Unfortunately, operative revision was required in 8% of our patients, unlike the experience of Sarfeh and Rypins [ 151. In this small number of patients, a new interposition shunt was placed with only moderate difficulty. Reshunting decreased portal hypertension and reduced portal vein-inferior vena cava gradients by a degree similar to the initial shunting procedure in the patients as a group. Patients can sucessfully undergo reshunting after perioperative graft thrombosis. It is of concern that when perioperative graft occlusion occurred, no apparent technical causes could be identified at the time of revision. It is our belief, however, that graft occlusion is most likely in patients with “stagnant flow” in the portal vein distal to the interposition shunt. Patients have done well after discharge, and no graft thrombosis has been documented during the follow-up period. Similarly, operative blood loss was not trivial, although it seemed to relate less to the operative design or urgency under which shunting was done than to the presence of vascularized adhesions from previous abdominal operations. The small diameter H-graft interposition portacaval shunt is a safe and effective method for the treatment of bleeding esophagogastric varices secondary to hepatic cirrhosis. It decompresses the portal system and promotes maintenance of hepatopedal portal flow, even if collateral venous pathways are not completely obliterated. It may
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be considered as an alternative to conventional portacaval shunting and to the selective distal splenorenal shunt. Its use and applications warrant further investigation.
REFERENCES 1. Lillemce KD, Cameron JL. The interposition mesocaval shunt. Surg Clin North Am 1990; 70: 378-94. 2. Warren WD, Millikan WJ Jr, Henderson JM, et al. Splenopancreatic disconnection: improved selectivity of distal splenorenal shunt. Ann Surg 1986; 204: 346-53. 3. Spina GP, Galeotti F, Opocher E, et al. Selective distal splenorenal shunt versus side to side portacaval shunt: clinical results of a prospective, controlled study. Am J Surg 1988; 155: 564-71. 4. Harley HAJ, Morgan T, Redker AG, et al. Results of a randomized trial of end-to-side portacaval shunt and distal splenorenal shunt in alcoholic liver disease and variceal bleeding. Gastroenterology 1986; 91: 802-9. 5. Langer B, Taylor BR, Mackenzie DR, et al. Further report of a prospective randomized trial comparing distal splenorenal shunt with end-to-side portocaval shunt-an analysis of encephalopathy, survival and quality of life. Gastroenterology 1985; 88: 424-9. 6. Warren WD, Zeppa R, Foman J. Selective transplenic decompression of gastro-esophageal varices by distal splenorenal shunt. Ann Surg 1967; 166: 437-55. 7. Rikkers LF, Rudman D, Galambos JT, et al. A randomized, controlled trial of the distal splenorenal shunt. Ann Surg 1978; 188: 271-82. 8. Sarfeh IJ, Rypins EB, Conroy RM, et al. Portacaval H-graft: relationships of shunt diameter, portal flow patterns and encephalopathy. Ann Surg 1983; 197: 422-6. 9. Sarfeh IJ, Rypins EB, Mason GR. A systematic appraisal of portacaval H-graft diameters. Ann Surg 1985; 204: 356-62. 10. Rypins EB, Sarfeh IJ. Influence of portal hemodynamics on long-term survival of alcoholic cirrhotic patients after small-diameter portacaval H-grafts. Am J Surg 1988; 155: 152-7. 11. Johansen K. Partial portal decompression for variceal hemorrhage. Am J Surg 1989; 157: 479-82. 12. Rikkers LF. Portal hemodynamics, intestinal absorption, and postshunt encephalopathy. Surgery 1983; 94: 126-33. 13. Soutter DI, Langer B, Taylor BR, et al. Emergency portosystemic shunting in cirrhosis with bleeding varices: a comparison of portacaval and mesocaval shunts. HPB Surg 1989; 1: 107-18. 14. Cello JP, Grendell JH, Crass RA, et al. Endoscopic sclerotherapy versus portacaval shunt in patients with severe cirrhosis and acute variceal hemorrhage. N Engl J Med 1987; 316: 11-5. 15. Sarfeh IJ, Rypins EB. Partial shunting for portal hypertension: surgical technique. Contemp Surg 1988; 32: 11-6.
DISCUSSION Barry Levine (San Antonio, TX): My congratulations on attaining very good results in a fairly debilitated group of patients that included 40% Child’s class C patients and a significant number of emergency operations. As you know, Dr. Sirinek and I believe that total sideto-side shunting is the procedure of choice for these patients. However, this is now the third series that has demonstrated good results using small-diameter shunts. Such an accumulation of data truly warrants our attention and, perhaps even more, our continued investigation. However, I do have a couple of questions. The first pertains to graft thrombosis. If only survivors are consid-
ered, you have a 14% thrombosis rate-including the one attributable to the radiologist. Furthermore, you do not have extended follow-up, so the long-term thrombosis rate is not known. Have you studied more patients since your manuscript was prepared and can you give us more complete data? The second point concerns the number of rebleeding episodes referable to gastritis. Another advocate of this procedure, Dr. Sarfeh, has told us that “gastritis” is a misnomer in this situation and that the defect is really a portal hypertensive gastropathy directly related to the level of portal venous pressure. A wide-diameter, totally decompressive shunt stops the rebleeding both from varices as well as from such “gastritis.” What is likely to be the outcome of your patients over the long term? Portal pressure has been only marginally decreased, and, therefore, you have have not eliminated postoperative bleeding from portal hypertensive gastropathy as a potential threat. Have you had any more occurrences of gastropathy bleeding? I. James Sarfeh (Irvine, CA): I would like to add my congratulations for your excellent results in a group of high-risk patients. You have surpassed our own results in Irvine. In comparing your experience in Tampa with ours in Irvine, there are remarkable similarities between the two series, but a few differences that deserve comment. First, our intraoperative pressure gradients with the 8mm diameter graft average about 5 cm of water higher than those obtained by you, which raises the question of collateral ligation. We previously showed that following the small-diameter portacaval H-graft, collateral ligation increases pressure gradients by 4 to 5 cm of water. We consider this an important part of the operation because by reducing the outflow tracts out of the portal system, more portal flow will be directed toward the liver and the shunt. Are you as aggressive in collateral obliteration as we are? The second difference between the series is that you reoperated on most of your patients with perioperative graft thrombosis, whereas we have successfully treated thromboses in our patients by standard interventional angiographic techniques. As you know, we perform portography within 5 days of operation, and any graft thromboses are treated with direct infusion of low-dose streptokinase into the graft. Why were these methods not effective in your patients? Finally, I am extremely gratified that by repeating our experiment and confirming the results, the concept of partial shunting has been independently validated. I would encourage you to now embark on prospective randomized studies. Michael Sarr (Rochester, MN): Several years ago while I was still at Hopkins, we reported Hopkins’ experience with the mesocaval C shunt, using a much larger bore total shunt. One of the problems we encountered was the occurrence of pseudointimal hyperplasia at the interface between autogenous tissue and the graft. Is this a concern of yours? How will you follow this problem?
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Layton Rikkers (Omaha, NE): *Dr. Rosemurgy, I would like to add my congratulations. Your results are most likely due to excellent preoperative and postoperative care and your surgical expertise. It is hard to say from these early data whether your results are due to the hemodynamic effects of the procedure. You had no problem with ascites in the postoperative period, which suggests more portal decompression than is desired. In addition, your early postoperative studies showed that most patients with preoperative hepatopedal flow in excess of 30% had lost their flow by the early postoperative interval. In contrast, only 10% to 15% of alcoholic cirrhotics undergoing the distal splenorenal shunt will lose portal flow by the time of their early postoperative studies, although nearly 50% are without hepatic portal perfusion after 1 year. Your hemodynamic results might be improved by more aggressive collateral ligation as suggested by Dr. Sarfeh. We all eagerly await the results of his randomized control trials to see whether the apparent hemodynamic benefits of this procedure over a total shunt equate to better clinical results. Alexander S. Rosemurgy (closing): Dr. Levine, the rate of occlusion of the shunts, including the one occluded by a radiologist, remains at around 11%. I believe occlusion to be an operative technical problem. I believe that what this shunt is able to do is to maintain the portal pressure above some critical threshold so that encephalopathy and liver failure don’t occur and yet below some critical threshold so that rebleeding is not a problem. I have not found gastritis or hypertensive gastropathy to be a problem in these patients. Although I did have the one patient who did bleed from discrete gastric varices, this patient underwent splenic artery embolization and has not had any further problems. I agree that follow-up beginning in November 1987 is not long follow-up. It will take a follow-up of 10 or more years, I think, before the final results on the shunt’s ability are in. I do not know what the long-term patency rates of the shunt are, but preliminary results are promising. I have studied all the patients who have had problems. I have studied some of the other patients randomly, but I now plan to document the patency of all of the patients’ grafts by transfemoral cannulation of the shunt. I think that is an integral aspect of their follow-up.
Dr. Sarfeh, we have not made vigorous attempts intraoperatively to ligate collaterals. If the coronary vein is patent and it is in front of us, we will ligate it. If the patient has had previous right upper quadrant surgery, I make virtually no attempt to ligate any collaterals. Similarly, at the time of follow-up radiologic studies (“shuntograms”) either early or late, we make minimal attempts to put coils into collaterals. I don’t think that it is sensible to presume that we are going to be able to maintain any separation between the portal and systemic systems; patients with portal hypertension are going to experience recollateralization. To me, the most important aspect of this is that we decrease the pressure below some apparent critical value that leads to recurrent hemorrhage. Insofar as reoperations are concerned for shunt occlusion, I have tried placing catheters across the shunts when they are occluded, leaving the tip of the catheter in the portal system and then infusing streptokinase. I have had no success with this technique. I have reoperated on three patients with graft occlusion and could not find a reason for the occlusion. The anastomoses were open and there was no defect with the shunt itself. The patients have undergone successful reshunting with adequate pressures. I admit that they do seem to have an apparent functional end-to-side portocaval shunt, as they have very stagnant flow in the distal portal system. Patients with a clot in their distal portal system beyond their shunt seem to be prone to thrombosis. Maybe it is propagation of the clot, but I can’t tell you for sure. Dr. Sarr, the patients are going to be monitored clinically. We intend to have these patients return in approximately 2 years to restudy them with transfemoral cannulation of the shunt. It is our hope that the flow velocity of these shunts is high enough so that late clotting will not be a problem. I do not expect to find a significant incidence of late shunt occlusion because of the shortness of the shunt. Dr. Rikkers, maybe it is not the direction of flow in the portal vein that is so much the factor, but as you have indicated, it may be the maintenance of some degree of portal hypertension that is more important. Residual portal hypertension impedes the absorption of certain substances, which may be responsible for encephalopathy, into the portal system.
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Study of a Prosthetic Portacaval Shunt MD,
Earl W. McAllister,
This study was undertaken to prospectively evaluate the 8-mm Gore-Tex@ interposition H-graft portacaval shunt. Thirty-six high-risk patients at the University of South Florida-affiliated hospitals received small-diameter shunts because of bleeding esophagogastric varices over a recent 2-year period. Portal vein and portal vein-inferior vena cava gradients were significantly reduced after shunting. These pressure changes were manifested clinically by the absence of variceal rebleeding and improvement of ascites; in addition, the incidence of encephalopathy was low. The 8-mm graft maintained hepatopedal flow in 67% of the patients, but reversal of flow did not result in complications commonly associated with poor portal perfusion. Graft thrombosis occurred in four ( 11%) patients. All grafts were successfully revised, three by operative revision and one by an interventional radiologist. Operative mortality was low ( 11%) , and morbidity was unusual. The small-diameter H-graft portacaval shunt is a safe and effective method of treatment for bleeding esophagogastric varices.
ptimal treatment for variceal bleeding secondary to portal hypertension continues to be one of the most 0 controversial subjects in general surgery. Methods of treatment previously thought to be panaceas have undergone continual technical revisions to improve operative results [I ,2]. Nonetheless, the goals of operative therapy for bleeding secondary to portal hypertension continue to be control of variceal hemorrhage and avoidance of progressive hepatic failure and encephalopathy through the maintenance of hepatopedal flow. From the Department of Surgery, University of South Florida, Tampa, Florida. Requests for reprints should be addressed to Alexander S. Rosemurgy, MD, 730 Harbourside Medical Towers, 4 Columbia Drive, Tampa, Florida 33606. Presented at the 3 1st Annual Meeting of the Society for Surgery of the Alimentary Tract, May 15-16,199O.
MD,
H-Graft
Robert E. Kearney,
MD, Tampa, Florida
Portacaval shunts have been most successful at controlling variceal hemorrhage, but, with diversion of portal flow, they carry a relatively high risk of subsequent hepatic failure and encephalopathy [3-51. Beginning in 1967, selective shunting, popularized by the late Dr. Dean Warren, offered hope for selective decompression of esophageal varices while maintaining portal hypertension and prograde portal blood flow [6]. Early results were encouraging; however, other controlled studies demonstrated that only a minority of selectively shunted patients maintained portal perfusion 3 to 5 years after surgery [ 71. Documentation of recollateralization of esophagogastric varices in these patients has led to modifications of the original shunt, adding to the complexity of an already difficult operation [2]. In addition, the development of postoperative ascites in these patients has further reduced our enthusiasm for selective shunting. In 1980, Rypins and Sarfeh reintroduced the concept of partial portal decompression and systematically studied the ability of progressively narrower polytetrafluoroethylene (PTFE) portacaval grafts to control variceal hemorrhage and maintain prograde portal blood flow [8,9]. These studies showed that small-diameter portacaval shunts could control variceal hemorrhage while generally maintaining prograde portal flow, with a distinct survival advantage demonstrated for those patients who did maintain prograde flow [IO]. Furthermore, their operative design was simple and their operative mortality was low. Johansen [I I] studied partial portal decompression by constructing small stoma side-to-side shunts in 50 alcoholic cirrhotic patients with acceptable operative mortality and shunt patency. In contrast to Sarfeh’s work, the lo- to 12-mm calibrated anastomosis of his study resulted in stagnation or reversal of portal blood flow in all of the patients studied postoperatively with duplex ultrasonography. We were initially attracted to the small-diameter H-graft shunt because of its perceived technical simplicity and our institutional dissatisfaction with conventional selective shunting. We undertook this prospective trial of 8-mm H-graft portacaval shunts to test the ability of a small-diameter portacaval shunt to control variceal hemorrhage and simultaneously maintain portal perfusion. PATIENTS
AND METHODS
From November 1987 through March 1990, 36 patients at the University of South Florida underwent portacaval shunting using an 8-mm externally reinforced Gore-Tex@ (W.L. Gore, Flagstaff, AZ) interposition graft. There were 24 men and 12 women, ranging in age from 38 to 8 1 years, with a mean age of 56 years. Reasons for surgical intervention were bleeding esophageal varices after failed sclerotherapy in 23 (64%) patients, bleeding gastric varices in 12 (33%) patients, and bleeding intesti-
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TABLE I Preshunt and Postshunt Measurements (mean f SEM)
Portal vein pressure (mm Hg) Inferior vena cava pressure (mm Hg) Portal vein-inferior vena cava gradient
Preshunt
Postshunt
31 f 1.0 12 f 0.8 20 f 0.7
20 f 0.9’ 14 f 0.9 7 f 0.6”
(mm Hg) * p CO.01 for differences between preshunt and postshunt values by paired student’s t test.
nonabsorbable suture. Shunt patency was assessed radiologically on the fifth postoperative day via transfemoral cannulation of the shunt. Direction of portal blood flow and shunt gradients were assessed; large collateral varices were embolized if present and easily accessible. Eight (22%) of the 36 patients underwent repeat radiologic study 4 to 18 months after shunting. Clinical follow-up was obtained in all patients. Differences in preshunt and postshunt manometrics were compared using the paired Student’s t test. Crude and actuarial survival statistics were computed.
nal varices in 1 (3%) patient. Two (6%) patients were in Child’s class A, 20 (56%) patients were in Child’s class B, and 14 (39%) patients were in Child’s class C. Twentynine (8 1%) patients had poorly controlled or uncontrolled ascites prior to shunting. All patients had portal hypertension secondary to cirrhosis; cirrhosis was due to alcohol in 72%, chronic hepatitis in 14%, unknown causes in ll%, and methotrexate toxicity in 3%. Twelve (33%) patients underwent emergency portacaval shunting, 8 (22%) underwent urgent shunting, and 16 (45%) underwent elective shunting. Twenty-nine (8 1%) of the 36 patients underwent preoperative angiography with measurement of inferior vena cava pressures and calculation of corrected sinusoidal pressures. All operations were performed through a right upper quadrant oblique abdominal incision. Preshunt portal vein and inferior vena cava pressures were measured intraoperatively using a calibrated transducer and a 25-gauge needle. Eight-millimeter externally supported Gore-Tex@ grafts, as short as possible with bevels at the ends of the graft oriented at 90’ with respect to each other, were sewn into place with a running nonabsorbable suture. Following shunt placement, pressures were remeasured and a shunt gradient was calculated. The coronary vein and other portasystemic collaterals were ligated when possible, but no rigorous attempts were made to ligate collaterals. Fourteen patients had intraoperative color-flow Doppler (Acuson 128 with linear array 5MHz probe, Acuson Corp., Mountain View, CA) assessment of the portal vein and inferior vena cava prior to and after shunting. After the first few shunts, the grafts were marked with metal clips to aid in postoperative cannulation. The incisions were closed in two layers using running
RESULTS All 36 patients underwent placement of g-mm ring reinforced Gore-Tex@ grafts in the portacaval position. Estimated operative blood loss ranged from 100 mL to 3,000 mL, with an average estimated loss of 738 f 102 mL @EM). Operative blood loss associated with elective, urgent, and emergency operations were 756 f 124 mL, 725 f 253 mL, and 723 f 201 mL, respectively. Duration of operations ranged from 3 to 9 hours, with an average of 4.3 f 0.24 hours. Prolonged operative times occurred occasionally because of unacceptable intraoperative shunt gradients leading to shunt revisions, unanticipated anatomic variations, or difficulty in obtaining ultrasonographic equipment intraoperatively. Portal vein pressures and portal vein-inferior vena cava gradients significantly decreased (p <0.05) with shunting (Table I). Of the 14 patients assessed by color-flow Doppler, 10 had prograde portal flow and 4 had “mixed” or “stagnant” flow before shunting. Two patients with prograde flow and two with mixed flow prior to shunting showed reversal of flow by intraoperative Doppler assessment after shunting. The effect of shunting on portal blood flow is unknown in nine (25%) patients as they did not undergo sufficient study either before or after shunting. Reasons for this include the emergency nature of their shunt operation, the unavailability of intraoperative ultrasound at surgery, or death during the immediate postoperative period. Therefore, in 27 patients, the direction of flow in the portal vein was known both before and after shunting. Of the 24 patients with preshunt hepatopedal or mixed portal flow, 7 (29%) developed hepatofugal flow with Hgraft portacaval shunting (Table II); 3 patients were in Child’s class B and 4 were in Child’s class C at the time of shunting. Sixty-seven percent of patients with hepatopeda1 flow before shunting maintained hepatopedal flow after shunting. Portal vein and inferior vena cava pressures and portal vein-inferior vena cava gradients were not different in patients who did or did not experience reversal of flow with shunting (Table III). Venography through transfemoral cannulation of the shunt and portal vein done on postshunt day five demonstrated graft thrombosis in three patients. Thrombectomy was successfully performed by an interventional radiologist in one case, and two cases required reoperation. An additional patient had very slow flow and clot in the portal vein distal to the shunt. Ill-advised radiologic
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TABLE II Direction of Portal Vein Flow Before and After H-Graft Portacaval Shunt’
Hepatopedal flow Hepatofugal flow Mixed flow
Preshunt
Postshunt
21 (78%) 3 (11%) 3(11%)
14 (52%) 10 (37%) 3 (11%)
’ Excluding those patients in whom the direction of flow was not known both before and after shunting.
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thrombectomy was attempted and resulted in thrombosis of the shunt, which required reoperation. All three patients undergoing operative shunt revision had successful revision of their shunts with subsequent demonstration of shunt patency by postoperative transfemoral cannulation of the shunt (Table IV). Technical causes for shunt thrombosis could not be identified in any of the patients who underwent shunt revision. There was no postoperative rebleeding in the 36 patients who underwent shunting. Six patients had wound complications: one patient had an infection, three experienced temporary postoperative incisional ascitic leaks, and two developed wound hernias. No patient had ascites beyond the immediate postoperative period. Three patients had temporary encephalopathy and one had continuation of mild to moderate preoperative encephalopathy after shunting. All four patients with postoperative encephalopathy were classified as Child’s class C preoperatively. Two of the four patients developed reversal of prograde portal flow with shunting and two patients became temporarily encephalopathic despite maintenance of prograde flow. In patients with postshunt encephalopathy, the average postshunt portal vein-inferior vena cava gradient was 7 f 1.7 mm Hg and the average postshunt portal vein pressure was 21 f 3.0 mm Hg. Of the seven patients who experienced reversed portal flow with shunting, one patient was encephalopathic for several days after shunting, one patient died during the immediate postoperative period, and one patient experienced continuation of preoperative encephalopathy. This last patient died of unknown causes 3 months after shunting. Five (71%) of the seven patients in whom portal flow reversed with shunting are doing well. There were four (11%) postoperative deaths. One patient, a Child’s class C, died due to fulminant liver failure within 24 hours of surgery. He demonstrated mixed portal flow prior to shunting but hepatofugal flow after shunting. A second patient died on the fifth postoperative day due to a respiratory arrest brought on by excessive narcotic administration. A third perioperative death was due to toxic epidermal necrolysis in a patient who had been under treatment previously for the same condition. The last postoperative death was due to a gastric perforation just prior to discharge following ill-advised preoperative gastric sclerotherapy. Two additional patients died more than 30 days after shunting: one patient died of complications of a subdural hematoma, a result of a fall, and one patient was found dead at home after doing well for 3 months. The opportunity to document shunt patency just prior to death or at autopsy was available in five of the six patients and all shunts were patent. All survivors have been monitored for up to 29 months. During follow-up, three (10%) patients have rebled despite documented shunt patency: one from alcoholic gastritis, one from a prepyloric ulcer, and one from persistent gastric varices. The latter patient underwent splenic artery embolization and over the past 8 months has not rebled. Twenty-six (87%) patients are doing well with no rebleeding or clinical encephalopathy, while one THE AMERICAN
TABLE III Preshunt and Postshunt Pressure Measurements in Patlents Who Reversed Hepatopedal Portal Blood Flow with Shuntlng (Group 1) and In Patlents Who Malntalned Hepatopedal Flow wlth Shuntlng (Group 2) Preshunt (mm l-!g) Inferior Portal Vein Vena Cava Group 1 (n = 7) Group 2 (n = 14)
30 f 29 f
1.0 1.7
12 f 0.9 9 f 0.9
Postshunt (mm Hg) Inferior Portal Vein Vena Cava 21 f 19 f
1.2 1.7
14 f 0.09 12 f 1.1
TABLE IV Preshunt and Postshunt Measurements at the Time of Operative Shunt Revlslon In Three Patlents Preshunt
Portal vein pressure Inferior vena cava pressure Portal vein-Inferior vena cava gradient
Postshunt
(mm Hg)
(mm Hs)
25 f 3.6 7 f 3.5 18 f 4.4
19 f 8.1 11 f 6.8 af 1.7
(3%) patient is affected by encephalopathy, which existed in its present form prior to shunting. Eight patients have consented to follow-up radiologic evaluation of their shunts. All shunts are patent 4 to 18 months after portacaval shunting, with an average portal vein pressure for the eight patients of 16 f 1.6 mm Hg and an average portal vein-inferior vena cave gradient of 10 f 0.7 mm Hg. Reversal of portal flow to hepatofugal flow was not seen in any of the late follow-up radiologic shunt studies. COMMENTS
Until Warren [q introduced the concept of selective variceal decompression, the only definitive treatment of portal hypertension was total portal decompression. Unfortunately, selective splenorenal shunts have not proven to remain selective because of persisting hypertension in the portal system. Ideal therapy for variceal hemorrhage due to portal hypertension would involve portal decompression with maintenance of hepatopedal portal blood flow. This prospective study was undertaken to evaluate the ability of the &mm Gore-Tex@ interposition portacaval shunt to achieve these therapeutic goals. The patients in this study were generally an older group of male Child’s class B and C alcoholic cirrhotics who developed uncontrolled bleeding esophagogastric varices after sclerotherapy failed. The majority of patients had ascites before undergoing H-graft portacaval shunting, and most were operated on urgently or emergently. In most patients, attempts to defer surgery to an elective setting proved impossible despite aggressive intervention with vasopressin injection, variceal balloon tamponade, and endoscopic variceal sclerotherapy. Despite the general urgency with which the operations were undertaken, the patients experienced little morbidity and low mortality.
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Portal vein and inferior vena cava pressures were documented in all patients before and after shunting. Although the &mm interposition shunt does not lower portal vein pressure to normal or the portal vein-inferior vena cava gradient to zero, it does significantly lower both. These pressure changes were manifested clinically by the absence of variceal rebleeding and improvement in ascites yet with a low incidence of postoperative encephalopathy. Portal vein flow was assessed in most patients before and after shunting. The 8-mm interposition shunt allows most patients to maintain hepatopedal flow, even in the absence of rigorous attempts to obliterate collaterals. But, unlike Sarfeh and co-workers’ experience [8], even in those patients who experienced continuation of preshunt hepatofugal flow or postshunt reversal of hepatopedal portal flow, complications commonly associated with poor portal perfusion were unusual. Maintenance of hepatopedal flow may not be the issue [II]. It may be that the critical factor determining clinical outcome is not the direction of portal blood flow but instead the ability to maintain portal and mesenteric hypertension below an unestablished critical threshold that limits variceal rebleeding and above an unestablished threshold that limits hepatic encephalopathy. It has been suggested [I21 that the maintenance of such mesenteric venous hypertension may limit the intestinal absorption of nitrogenous compounds and the consequent formation of false neurotransmitters that lead to clinical encephalopathy. Although more than one third of the patients in this series had hepatofugal portal flow after shunting, only one significant complication occurred in those patients: one postoperative death due to apparent fulminant liver failure. Interestingly, this patient had an accessory right hepatic artery. Postoperative alterations in hepatic arterial inflow not apparent at re-exploration for deterioration hours after shunting could have contributed to his rapid postop erative deterioration. As a group, the patients underwent partial portal decompression with minimal complications. Although the patients in this study were “high-risk” and the operations were usually undertaken with urgency, the operative mortality was low when compared with that of most reports [13,24]. Furthermore, most postoperative deaths were preventable. Judicious use of analgesics would have prevented one death. Avoidance of aggressive gastric sclerotherapy could have avoided another death due to a postshunt gastric perforation. Control of quiescent chronic toxic epidermal necrolysis postoperatively could have prevented a third patient’s death. Ascites was uniformly improved by partial portal decompression and no patient experienced variceal rebleeding, with the exception of one patient with presumed persistent hypertensive gastropathy who was treated by splenic artery embolization. Despite the poor general health of the patients, deaths following discharge have been very unusual. Furthermore, one of the two late deaths was preventable. Better attention to one patient’s needs would have prevented an in-hospital fall on the day of discharge. This patient began to manifest a chronic subdural hematoma weeks
later, presumably as a result of the fall, and died despite aggressive operative intervention. Similarly, deterioration of liver function or late liver failure has not been seen during follow-up. The maintenance of portal perfusion demonstrated in the postoperative venographic shunt studies has persisted in all of the late follow-up radiologic shunt studies with no recollateralization demonstrated. What are the drawbacks associated with this method of portal decompression? The operative technique is not as simple as it would first appear. Partial removal of the caudate lobe of the liver is almost always necessary to obtain proper graft positioning and placement. The graft can be easily tailored and each anastomosis can be easily completed, but the graft must lie perfectly between the portal vein and vena cava. Occasionally, technical inadequacies are not apparent until postshunt portal vein pressures and shunt gradients are calculated. A drop of less than 10 mm Hg in the portal pressure with shunting, coupled with a drop of less than 10 mm Hg in the portal vein-inferior vena cava gradient with shunting, warrants documentation of shunt patency. Although we found intraoperative ultrasound occasionally helpful in determining shunt patency, documenting shunt patency generally involved opening the graft or one of the anastomoses, adding to the operative time and undoubtedly to the operative complications. Only when the operating surgeon is convinced of graft patency can the operative procedure be completed. Even then, the patient is not immune to graft thrombosis, which occurred in nearly 11% of patients. Moreover, it is imperative that the shunt be studied within the first week postoperatively and prior to discharge so that if thrombosis is indeed present, thrombectomy can be performed by an interventional radiologist or early operative revision can be done. Unfortunately, operative revision was required in 8% of our patients, unlike the experience of Sarfeh and Rypins [ 151. In this small number of patients, a new interposition shunt was placed with only moderate difficulty. Reshunting decreased portal hypertension and reduced portal vein-inferior vena cava gradients by a degree similar to the initial shunting procedure in the patients as a group. Patients can sucessfully undergo reshunting after perioperative graft thrombosis. It is of concern that when perioperative graft occlusion occurred, no apparent technical causes could be identified at the time of revision. It is our belief, however, that graft occlusion is most likely in patients with “stagnant flow” in the portal vein distal to the interposition shunt. Patients have done well after discharge, and no graft thrombosis has been documented during the follow-up period. Similarly, operative blood loss was not trivial, although it seemed to relate less to the operative design or urgency under which shunting was done than to the presence of vascularized adhesions from previous abdominal operations. The small diameter H-graft interposition portacaval shunt is a safe and effective method for the treatment of bleeding esophagogastric varices secondary to hepatic cirrhosis. It decompresses the portal system and promotes maintenance of hepatopedal portal flow, even if collateral venous pathways are not completely obliterated. It may
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be considered as an alternative to conventional portacaval shunting and to the selective distal splenorenal shunt. Its use and applications warrant further investigation.
REFERENCES 1. Lillemce KD, Cameron JL. The interposition mesocaval shunt. Surg Clin North Am 1990; 70: 378-94. 2. Warren WD, Millikan WJ Jr, Henderson JM, et al. Splenopancreatic disconnection: improved selectivity of distal splenorenal shunt. Ann Surg 1986; 204: 346-53. 3. Spina GP, Galeotti F, Opocher E, et al. Selective distal splenorenal shunt versus side to side portacaval shunt: clinical results of a prospective, controlled study. Am J Surg 1988; 155: 564-71. 4. Harley HAJ, Morgan T, Redker AG, et al. Results of a randomized trial of end-to-side portacaval shunt and distal splenorenal shunt in alcoholic liver disease and variceal bleeding. Gastroenterology 1986; 91: 802-9. 5. Langer B, Taylor BR, Mackenzie DR, et al. Further report of a prospective randomized trial comparing distal splenorenal shunt with end-to-side portocaval shunt-an analysis of encephalopathy, survival and quality of life. Gastroenterology 1985; 88: 424-9. 6. Warren WD, Zeppa R, Foman J. Selective transplenic decompression of gastro-esophageal varices by distal splenorenal shunt. Ann Surg 1967; 166: 437-55. 7. Rikkers LF, Rudman D, Galambos JT, et al. A randomized, controlled trial of the distal splenorenal shunt. Ann Surg 1978; 188: 271-82. 8. Sarfeh IJ, Rypins EB, Conroy RM, et al. Portacaval H-graft: relationships of shunt diameter, portal flow patterns and encephalopathy. Ann Surg 1983; 197: 422-6. 9. Sarfeh IJ, Rypins EB, Mason GR. A systematic appraisal of portacaval H-graft diameters. Ann Surg 1985; 204: 356-62. 10. Rypins EB, Sarfeh IJ. Influence of portal hemodynamics on long-term survival of alcoholic cirrhotic patients after small-diameter portacaval H-grafts. Am J Surg 1988; 155: 152-7. 11. Johansen K. Partial portal decompression for variceal hemorrhage. Am J Surg 1989; 157: 479-82. 12. Rikkers LF. Portal hemodynamics, intestinal absorption, and postshunt encephalopathy. Surgery 1983; 94: 126-33. 13. Soutter DI, Langer B, Taylor BR, et al. Emergency portosystemic shunting in cirrhosis with bleeding varices: a comparison of portacaval and mesocaval shunts. HPB Surg 1989; 1: 107-18. 14. Cello JP, Grendell JH, Crass RA, et al. Endoscopic sclerotherapy versus portacaval shunt in patients with severe cirrhosis and acute variceal hemorrhage. N Engl J Med 1987; 316: 11-5. 15. Sarfeh IJ, Rypins EB. Partial shunting for portal hypertension: surgical technique. Contemp Surg 1988; 32: 11-6.
DISCUSSION Barry Levine (San Antonio, TX): My congratulations on attaining very good results in a fairly debilitated group of patients that included 40% Child’s class C patients and a significant number of emergency operations. As you know, Dr. Sirinek and I believe that total sideto-side shunting is the procedure of choice for these patients. However, this is now the third series that has demonstrated good results using small-diameter shunts. Such an accumulation of data truly warrants our attention and, perhaps even more, our continued investigation. However, I do have a couple of questions. The first pertains to graft thrombosis. If only survivors are consid-
ered, you have a 14% thrombosis rate-including the one attributable to the radiologist. Furthermore, you do not have extended follow-up, so the long-term thrombosis rate is not known. Have you studied more patients since your manuscript was prepared and can you give us more complete data? The second point concerns the number of rebleeding episodes referable to gastritis. Another advocate of this procedure, Dr. Sarfeh, has told us that “gastritis” is a misnomer in this situation and that the defect is really a portal hypertensive gastropathy directly related to the level of portal venous pressure. A wide-diameter, totally decompressive shunt stops the rebleeding both from varices as well as from such “gastritis.” What is likely to be the outcome of your patients over the long term? Portal pressure has been only marginally decreased, and, therefore, you have have not eliminated postoperative bleeding from portal hypertensive gastropathy as a potential threat. Have you had any more occurrences of gastropathy bleeding? I. James Sarfeh (Irvine, CA): I would like to add my congratulations for your excellent results in a group of high-risk patients. You have surpassed our own results in Irvine. In comparing your experience in Tampa with ours in Irvine, there are remarkable similarities between the two series, but a few differences that deserve comment. First, our intraoperative pressure gradients with the 8mm diameter graft average about 5 cm of water higher than those obtained by you, which raises the question of collateral ligation. We previously showed that following the small-diameter portacaval H-graft, collateral ligation increases pressure gradients by 4 to 5 cm of water. We consider this an important part of the operation because by reducing the outflow tracts out of the portal system, more portal flow will be directed toward the liver and the shunt. Are you as aggressive in collateral obliteration as we are? The second difference between the series is that you reoperated on most of your patients with perioperative graft thrombosis, whereas we have successfully treated thromboses in our patients by standard interventional angiographic techniques. As you know, we perform portography within 5 days of operation, and any graft thromboses are treated with direct infusion of low-dose streptokinase into the graft. Why were these methods not effective in your patients? Finally, I am extremely gratified that by repeating our experiment and confirming the results, the concept of partial shunting has been independently validated. I would encourage you to now embark on prospective randomized studies. Michael Sarr (Rochester, MN): Several years ago while I was still at Hopkins, we reported Hopkins’ experience with the mesocaval C shunt, using a much larger bore total shunt. One of the problems we encountered was the occurrence of pseudointimal hyperplasia at the interface between autogenous tissue and the graft. Is this a concern of yours? How will you follow this problem?
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Layton Rikkers (Omaha, NE): *Dr. Rosemurgy, I would like to add my congratulations. Your results are most likely due to excellent preoperative and postoperative care and your surgical expertise. It is hard to say from these early data whether your results are due to the hemodynamic effects of the procedure. You had no problem with ascites in the postoperative period, which suggests more portal decompression than is desired. In addition, your early postoperative studies showed that most patients with preoperative hepatopedal flow in excess of 30% had lost their flow by the early postoperative interval. In contrast, only 10% to 15% of alcoholic cirrhotics undergoing the distal splenorenal shunt will lose portal flow by the time of their early postoperative studies, although nearly 50% are without hepatic portal perfusion after 1 year. Your hemodynamic results might be improved by more aggressive collateral ligation as suggested by Dr. Sarfeh. We all eagerly await the results of his randomized control trials to see whether the apparent hemodynamic benefits of this procedure over a total shunt equate to better clinical results. Alexander S. Rosemurgy (closing): Dr. Levine, the rate of occlusion of the shunts, including the one occluded by a radiologist, remains at around 11%. I believe occlusion to be an operative technical problem. I believe that what this shunt is able to do is to maintain the portal pressure above some critical threshold so that encephalopathy and liver failure don’t occur and yet below some critical threshold so that rebleeding is not a problem. I have not found gastritis or hypertensive gastropathy to be a problem in these patients. Although I did have the one patient who did bleed from discrete gastric varices, this patient underwent splenic artery embolization and has not had any further problems. I agree that follow-up beginning in November 1987 is not long follow-up. It will take a follow-up of 10 or more years, I think, before the final results on the shunt’s ability are in. I do not know what the long-term patency rates of the shunt are, but preliminary results are promising. I have studied all the patients who have had problems. I have studied some of the other patients randomly, but I now plan to document the patency of all of the patients’ grafts by transfemoral cannulation of the shunt. I think that is an integral aspect of their follow-up.
Dr. Sarfeh, we have not made vigorous attempts intraoperatively to ligate collaterals. If the coronary vein is patent and it is in front of us, we will ligate it. If the patient has had previous right upper quadrant surgery, I make virtually no attempt to ligate any collaterals. Similarly, at the time of follow-up radiologic studies (“shuntograms”) either early or late, we make minimal attempts to put coils into collaterals. I don’t think that it is sensible to presume that we are going to be able to maintain any separation between the portal and systemic systems; patients with portal hypertension are going to experience recollateralization. To me, the most important aspect of this is that we decrease the pressure below some apparent critical value that leads to recurrent hemorrhage. Insofar as reoperations are concerned for shunt occlusion, I have tried placing catheters across the shunts when they are occluded, leaving the tip of the catheter in the portal system and then infusing streptokinase. I have had no success with this technique. I have reoperated on three patients with graft occlusion and could not find a reason for the occlusion. The anastomoses were open and there was no defect with the shunt itself. The patients have undergone successful reshunting with adequate pressures. I admit that they do seem to have an apparent functional end-to-side portocaval shunt, as they have very stagnant flow in the distal portal system. Patients with a clot in their distal portal system beyond their shunt seem to be prone to thrombosis. Maybe it is propagation of the clot, but I can’t tell you for sure. Dr. Sarr, the patients are going to be monitored clinically. We intend to have these patients return in approximately 2 years to restudy them with transfemoral cannulation of the shunt. It is our hope that the flow velocity of these shunts is high enough so that late clotting will not be a problem. I do not expect to find a significant incidence of late shunt occlusion because of the shortness of the shunt. Dr. Rikkers, maybe it is not the direction of flow in the portal vein that is so much the factor, but as you have indicated, it may be the maintenance of some degree of portal hypertension that is more important. Residual portal hypertension impedes the absorption of certain substances, which may be responsible for encephalopathy, into the portal system.
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