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Peritoneovenous shunt for intractable ascites of hepatic, nephrogenic, and malignant causes
Peritoneovenous Shunt for Intractable Ascites of Hepatic, Nephrogenic, and Malignant Causes Albert0 Holm,
MD,
Norman B. Halpern,
A retrospective analysis of 54 patients with a peritoneovenous shunt inserted to control massive ascites refractory to conventional medical treatment is presented. The cause of ascites was hepatic in 29 patients (Group 1,54 percent), malignant in 13 (Group 2,24 percent), and nephrogenic in 12 (Group 3,22 percent). The peritoneovenous shunt failed in 11 patients (20 percent) : 6 in Croup 1,3 in Croup 2, and 2 in Group 3. Shunt outflow ohstruction (thrombosis) was the principal cause. Systemic sepsis in five patients and variceal hemorrhage in three were the factors responsible for most of the deaths (22 percent). Of the 42 patients who survived operation, the peritoneovenons shunt was effective in controlling the massive ascites in 37 (86 percent). Eight patients ( 15 percent), four with hepatic and four with nephrogenic ascites, survived 3 years or more without ascites. Removal of at least 50 to 70 percent of ascitic fluid at the time of shunt insertion was considered an important factor in decreasing morbidity and mortality. A peritoneovenous shunt can be effective for a long-term period in controlling massive ascites with an hepatic or nephrogenic cause in a selected group of patients; however, in patients with malignant ascites, although the benefit was substantial in half, the survival period did not exceed 6 months.
From the Department of Surgery, University of Alabama School of Medicine, Birmingham, Alabama. Requests for reprints should be addressed to Joaquin S. Aldrete, MD, Department of Surgery, UAB, University Station, Birmingham, Alabama 35294.
162
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MD,
Joaquin S. Aldrete,
MD, Birmingham, Alabama
he effectiveness of a peritoneovenous shunt to relieve T massive ascites refractory to conventional medical treatment is well established. However, the evaluation of long-term results, morbidity, and mortality has varied from enthusiastic support to reluctant acceptance [Z-q. The most common indication for peritoneovenous shunt insertion is ascites caused by hepatic disease. The same device has been used in a smaller number of patients with ascites of malignant or nephrogenic origin; the indications in these two groups are even more uncertain because of the scarcity of objective data [7-101. This retrospective review attempted to objectively evaluate the long-term effectiveness, the morbidity, and the mortality incurred by inserting peritoneovenous shunt in patients with massive refractory ascites of hepatic, nephrogenic, and malignant tumor origin. MATERIAL AND METHODS
All the records of patients who underwent insertion of a peritoneovenous shunt for massive refractory ascites from 1975 to 1984 at the hospital of the University of Alabama in Birmingham were located and reviewed. To define the population of patients to be studied, the following criteria were used: hepatic ascites in patients with cirrhosis documented by liver biopsy (Group 1); malignant ascites in patients with abdominal carcinomatosis proven by biopsy (Group 2); nephrogenic ascites in patients with end-stage renal disease and without evidence of another cause of ascites (Group 3). Massive ascites were defined as markedly distending the abdomen and producing persistent discomfort, dyspnea, and early satiety, in most cases rendering the patient unable to perform routine activities. Ascites of he patic and malignant origin were considered intractable when they remained present despite appropriate conventional medical treatment properly carried out for a minimum of 3 consecutive weeks, which included restriction of both oral fluid intake to less than 1,000 ml/day and sodium to less than 500 mg/24 hours, and diuretics (usually spironolactone 400 mg/day and furosemide 80 mg/ day). An increase of the serum creatinine level above 2.5 mg/dl during the period of treatment was also considered a reason for intractability, since diuretics could no longer be used. Nephrogenic ascites was considered intractable when it persisted despite three or more sessions per week of hemodialysis using high ultrafiltration flow for at least 4 consecutive weeks. The presence of massive, intractable disabling ascites was the indication for operation in all patients. If the patient was thought to be able to survive the operation in the opinion of the consultant surgeon, the patient underwent insertion of peritoneovenous shunt. The following were considered contraindications for this operation: peritonitis, systemic sepsis, primary congestive heart failure,
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failure of more than two systems of organs, loculated or thick ascites, uncorrectable coagulopathy, and active hepatic disease (encephalopathy and presence of variceal hemorrhage). In all cases, a Le.Veen peritoneovenous shunt was utilized. Prior to operation, prophylactic antibiotics were given, and electrolyte and coagulation abnormalities were corrected. In Groups 1 and 2, the body weight and 24hour urine volume were measured and recorded; in Group 3 patients, the body weight and abdominal girth were the parameters used. The peritoneovenous shunt was inserted using the original technique described by LeVeen et al [II,I2]. The shunt was considered effective when all of the following improvements occurred and persisted for a period of at least 2 months after its insertion: decrease of abdominal girth, a substantial weight loss, increase of effective diuresis (except in Group 3), improvement of respiratory function, nutritional intake, and capacity for physical activity. RESULTS There were 54 patients who met the criteria previously described. Thirty-six patients were men (67 percent) and 18 were women (33 percent). Their ages ranged from 30 to 70 years (mean 47 f 1.5 years). The duration of ascites prior to peritoneovenous shunt insertion ranged from 2 to 84 months (mean 20.6 f 2.6 months). The cause of the ascites was as follows: Group 1, hepatic in 29 patients (54 percent): 26 with alcoholic cirrhosis, 2 with sclerosing cholangitis with cirrhosis, and 1 with thrombosis of the hepatic veins; Group 2, abdominal carcinomatosis in 13 patients (24 percent): 11 with primary tumor in the abdomen including the colon in 5, diffuse lymphoma in 3, the pancreas in 2, and the ovary in 1, and 2 with breast cancer; Group 3, nephrogenic in 12 patients (22 percent): chronic renal failure caused by diabetes mellitus in 4, hypertensive nephrosclerosis in 3, pyelonephritis in 3, polycystic kidney disease in 1, and systemic amyloidosis in 1. There were no operative or anesthetic complications during the insertion of the peritoneovenous shunt. The amount of ascites drained at operation ranged from 3,000 to 12,000 ml (mean 5,350 f 758 ml). The appearance of ascitic fluid was recorded in 34 patients; it was described as straw-colored in 27 patients in Groups 1 and 3 and blood-tinged or turbid in 5 and 2 patients, respectively, in Group 2. In patients with nephrogenic or malignant ascites, the total content of proteins in the ascitic fluid ranged from 2.7 to 5.2 g/d1 (mean 3.5 f 0.6 g/dl). In 37 patients (69 percent), a substantial weight loss of 3 kg or more was recorded by the time they left the hospital: 21 patients in Group 1 (72 percent), 6 in Group 2 (46 percent), and 10 in Group 3 (83 percent). The weight loss ranged from 3.4 to 18.2 kg (mean 8.3 f 1.5 kg). Temporary weight loss with reaccumulation of ascites postoperatively was recorded in 12 patients (22 percent), whereas no weight loss was observed in 5 (9 percent). In Group 1, the recorded weight loss was more than 10 kg in 12 patients (57 percent), whereas in Groups 2
TABLE I Postoperative Compllcatlons No. of Patients
causes Recurrence of ascites Coagulopathy Progressive liver failure Upper gastrointestinal bleeding systemic sepsis Persistent fever Renal failure’ Respiratory distress syndrome Edema in upper extremities Wound infection
11 6 6 5 5 5 4 3 2 2
* In Groups 1 and 2.
and 3, weight loss over 10 kg was recorded in only one patient in each group (16 and 10 percent, respectively). The 24-hour urine volume increased from a mean of 932 ml i 18 recorded the day preceding the insertion of the shunt (range 795 to 1,045 ml) to a mean of 1,782 ml f 30 (range 1,525 to 1,975 ml) on the day prior to dismissal from the hospital in 21 Group 1 patients, and from 1,292 ml f 237 (range 650 to 2,000 ml) to 2,733 ml f 455 (range 800 to 3,500 ml) in 8 Group 2 patients. The preshunt to postshunt increments in the 24-hour urine output averaged a mean of 850 ml f 12 in Group 1 and 1,441 ml f 218 in Group 2. Postoperative complications occurred in 34 patients (63 percent); in 28 (82 percent), 2 or more complications were observed (Table I). The most common was recurrence of ascites due to peritoneovenous shunt failure in 11 patients (20 percent): 6 of 29 in Group 1 (20 percent), 3 of 13 in Group 2 (32 percent), and 2 of 21 in Group 3 (16 percent). The principal cause of shunt failure was thrombosis at the end of the venous limb placed in the superior vena cava in four patients; in all four, the precise cause of failure was documented by either peritoneal scanning with radionuclide (technetium-99m-labeled albumin), shuntogram, or cavagram. Of the other seven patients with shunt failure, in three the peritoneovenous shunt was removed because of infection, in two because of persistent leakage of ascitic fluid, and in two due to severe coagulopathy (Table II). Another significant complication was postshunt coagulopathy in six patients; in four cirrhotics it was corrected by transfusing fresh frozen plasma and platelet concentrates. As noted previously, fatal coagulopathy occurred in two patients with malignant ascites despite prompt ligation of the shunt. Progressive liver failure was observed in six cirrhotics; four of them had mild encephalopathy which responded to treatment, and the other two developed hepatorenal syndrome and subsequently died. The diagnosis of hepatorenal syndrome was established by the presence of progressive renal failure in a well-hydrated patient with a serum creatinine level of 3 mg/dl or greater and a urinary sodium level of less than 10 mEq/liter. Upper gastrointestinal bleeding occurred in five patients; the causes of hemorrhage were ruptured esophage-
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TABLE II Perltoneovenous Shunt That Required Removal or Revision Group
Cause of Failure shunt shunt shunt shunt
(blood) (blood) (blood) (proteinacaous)
Shunt Life
Second Shunt Placed
Survival From First Operation
Few h 20 d 4 mo 3d
Same operative d 6 d after removal
4 mo 30 d Lost to follow-up (5 mo) 3 mo
1 1 1 2
Clotted Clotted Clotted Clotted
3 1
1
Infected shunt Infected shunt Infected shunt
9d 20 d 26 d
3 1
Ascites leakage Ascites leakage
3 mo 12 d
2 2
Severe coagulopathy’ Severe coagulopathy’
Id ld
. Same d of removal
... ... ... 4 mo after removal 4 mo after revislon (on opposlte side)
.. .
11 d 26 d 29 d Alive 42 mo postop 5 mo 2d 3d
* Shunt ligation.
al varices in three cirrhotics who died, and gastric mucosal ulcerations complicated by systemic sepsis in one cirrhotic and one renal patient. Five patients, four with cirrhosis and one with renal failure, died postoperatively from systemic sepsis; in three an infected shunt was found and removed, and in the other two, pneumonitis was the source of the sepsis. Of the 54 patients, 12 (22 percent) died within 1 to 30 days after operation. The operative mortality by groups was 9 of 29 patients in Group 1 (31 percent), 2 of 13 in Group 2 (15 percent), and I of 12 in Group 3 (8 percent). Of the 42 patients (78 percent) who left the hospital alive, 25 (60 percent) subsequently died within 3 to 60 months (mean 19 f 3.2 months). The majority of late deaths were attributed to the progression of their primary disease. In three patients the ascites recurred due to obstruction of the shunt in two and persistent ascites leakage in one. The ascites was controlled by the peritoneovenous shunt in 36 of the 42 surviving patients (86 percent); the other 6 (14 percent) required supplemental diuretics to control the ascites. Thus, these 36 patients who comprised 67 percent of the total number of patients studied can be considered as having good results; the overall survival period for these patients ranged from 3 to 108 months (mean 23.7 f 3.7 months) (Table III). None of the patients with abdominal carcinomatosis in Group 2 survived more than 6 months after insertion of the peritoneovenous shunt. The survival rates in Group 1 were 16 of 29 patients (55 percent) 6 months postoperatively, 12 (41 percent) 1 year postoperatively, 9 (3 1 percent) 2 years postoperatively, and 4 (14 percent) 3 or more years postoperatively. In Group 3,9 of 12 patients (75 percent) were alive 6 months postoperatively, 7 (58 percent) 1 year postoperatively, 5 (41 percent) 2 years postoperatively, and 4 (33 percent) 3 or more years postoperatively. COMMENTS Most patients with ascites respond favorably to conventional medical treatment. However, in 5 to 10 percent 164
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of these patients, the massive ascites persists despite appropriate medical treatment; for such patients, the insertion of a peritoneovenous shunt is indicated to attempt to decrease the refractory ascites [2,3]. It must be recognized that although the amount of ascites may be markedly decreased by inserting a peritoneovenous shunt, this change does not alter the natural course of cirrhosis [2,3,13,14]. Thus, only a palliative effect can be granted to peritoneovenous shunt in the overall management of cirrhosis. In patients with endstage renal disease maintained by hemodialysis, the development of intractable ascites has a worse prognosis; many therapeutic modalities have been tried, but the overall results have been unsatisfactory [IS-Z7]. Previous reports have suggested these patients may benefit from insertion of a peritoneovenous shunt [Z&19]. Ascites has been observed to occur in 15 to 50 percent of patients with extensive abdominal carcinomatosis; most of them die within 6 months from the onset of massive ascites [Z,20]. Some studies have reported that insertion of a peritoneovenous shunt provides significant palliation from the disabling ascites for the limited period of survival that these patients have [8,2Z]. The results observed in the present study are in accordance with those reported by other groups [Z3,13,14,22]. The effectiveness of peritoneovenous shunt in reducing the ascites, as assessed by weight loss, was higher in patients with cirrhosis. This is probably due to the physical characteristics of their ascitic fluid (transudate) which facilitates its removal by the shunt, compared with the lower weight loss observed in patients with nephrogenic or malignant ascites (exudate) which usually contain a high percentage of protein (more than 2.5 mg/dl), suspended particles, and cells. The observed high morbidity and mortality associated with peritoneovenous shunt insertion are due to the severity of the usually preterminal or terminal primary disease responsible for ascites, and to a lesser extent, to the complications caused by the shunt itself [ 1,5,8,22,23]. In the present study, shunt outflow obstruction was the principal cause of early peritoneovenous shunt failure and was
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I
PER1mNwvENous sBuNT FOR AsclTlIS
frequently seen in patients with cirrhosis; this is probably related to the common thrombogenicity of the ascitic fluid or due to thrombosis induced by the catheter itself. Occlusion of the venous tubing by proteinaceous or cellular products was seen in only one patient with carcinomatosis. The high viscosity of thii exudative ascites is likely to lead to the obstruction of the tubing. Postshunt coagulopathy has received extensive attention in the literature [I ,3,20,24,25]. Mild coagulopathies have been described as occurring frequently, but they usually respond to medical therapy. The reported incidence of severe coagulopathy ranges from 4 to 20 percent, and occurs more frequently in patients with end-stage liver disease and abdominal carcinomatosis. The presence of some anticoagulant products contained in the ascitic fluid appears to be activated when they are shunted into the venous circulation, resulting in severe coagulopathy. Infusion of clotting factors, epsilon-aminocaproic acid, and prompt ligation of the shunt venous tubing are the recommended therapy for this coagulopathy. The relatively low incidence of fatal coagulopathy observed in our series (4 percent) was thought to be related to the decrease of thromboplastic elements into the blood stream, due to the practice of removing a large amount of ascites at the time of peritoneovenous shunt insertion. In the present study, the postshunt rate of variceal hemorrhage in patients with cirrhosis (10 percent) parallels other studies [3,22]. It could be speculated that this low incidence is due to the decrease of the expanded plasma volume by removal of a substantial amount of ascites during the peritoneovenous shunt insertion, which theoretically results in a decrease of pressure in the splanchnic bed. The incidence of systemic sepsis (9 percent) was somewhat lower than that reported in similar series [23,26,27]. However, a distressing observation was that despite aggressive antibiotic therapy and prompt removal of the shunt when indicated, the mortality remained high, as in all patients with sepsis and peritoneovenous shunt. In patients with tense ascites, the abdominal wall is usually thin, and leakage of ascites around the site of insertion of the shunt abdominal limb is an ever-present threat. This complication occurred in 4 percent of the patients studied [3,I 31. Meticulous closure of the abdominal wound is essential to prevent this problem. Failure to prevent or promptly correct the leakage of ascitic fluid almost always leads to local infection, which eventually will require removal of the shunt. Although some studies claim resolution of the hepatorenal syndrome with peritoneovenous shunt, in a collective review, Epstein [20] concluded that the majority of those successes occurred in patients in whom the presence of the syndrome was not clearly documented [1,28-301. In the present series, a lower incidence of hepatorenal syndrome (two patients) was noted, but despite the peritoneovenous shunt, both died. The present study suggests that the insertion of a peritonecvenous shunt effectively relieves massive ascites not only of hepatic disease origin, but also for ascites resulting from renal and malignant disease. The acknowl-
TABLE III Results Per Group’f
Operative mortality Survived operation (>2 mo) Subseqently died Alive 36 or more mo Lost to follow-up (>4 mo)
&ovpl (n = 29)
Group 2 (n = 13)
(n = 12)
9 (31) 20 (69)
2 (19) 11 (85)
1 (8) 11 (92)
10 4
6
8 0 3
Group 3
7 4 0
* Values in parentheses are percentages. + Ascites was caused by clrhosis in Group 1 patients and abdominal carcinomatosis in Group 2 patients, and was of nephrogenic origin in Group 3 patients.
edged high morbidity and mortality are due primarily to the advanced stage of the primary diseases requiring the operation. However, there are other determinant factors for the morbidity and mortality that are related to the shunt itself. The issue to address is: Are there any measures to take to decrease the well-documented high mortality (22 percent) and morbidity (63 percent) of ascites? Aside from the obvious precautions, such as meticulous operative technique, avoiding the established contraindications for the operation, and attention to details in the postoperative period, our study suggests that the incidence of some complications, such as pulmonary edema, variceal hemorrhage, and severe coagulopathy can be lowered by draining 50 to 70 percent of the total amount of ascites present at the time of insertion of the peritoneovenous shunt. It should be noted that extensive drainage of ascites resulted in immediate relief of the general discomfort and did not have any deleterious effect on the patient. The occurrence of late postoperative complications has been noted [I-3]. Shunt blockage and infection are the most commonly encountered, in the present study they occurred in 12 percent of the long-term survivors [4,22]. The mortality observed in the late postoperative period is caused by the progression of the usually advanced hepatic, renal, or malignant disease that determined the need for the peritoneovenous shunt [Z&2932]. It is not possible to objectively determine in the cirrhotic patients if the peritoneovenous shunt prolonged their survival. Nevertheless, it was clear that in 86 percent of the patients analyzed, the relief from the massive ascites greatly improved the quality of their lives. As expected, the patients with nephrogenic ascites survived longer, contrasting with the short survival noted in patients with carcinomatosis. 1. LeVeen HH, Brown T, d’Ovidio NG. Surgical treatment of ascites. In: Jordan GL, ed. Advances in surgery, vol. 14. Chicago: Year Book Medical, 1980: 107-50. 2. Greenlee HB, Stanley M, Reinhardt GF. Intractable ascites treated with peritoneovenous shunts (LeVeen): a 24 to 64 month follow-up of results in 52 alcoholic cirrhotics. Arch Surg 1981; 116: 518-24.
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3. Bernhoft RA, Pellegrini CA, Way LA. Peritoneovenous shunt for refractory ascites: operative complications and long-term results. Arch Surg 1982; 117: 631-S. 4. Stanley MM. Treatment of intractable ascites in patients with alcoholic cirrhosis by peritoneovenous shunts (LeVeen). Med Clin North Am 1979; 63: 523-35. 5. Hyde GL, Dillon M, Bivins BS. Peritoneal venous shunting for ascites: a 15-year perspective. Am Surg 1982; 48: 123-7. 6. Gleysteen JJ, Klamer Th W. Peritoneovenous shunts: predictive factors of early treatment failure. Am J Gastroenterol 1984; 79: 654-8. 7. Quazi R, Saxlov ED. Peritoneovenous shunt for palliation of malignant ascites. Cancer 1982; 49: 600-2. 8. Souter RG, Wells C, Tarin D, Kettlewell MW. Surgical and pathologic complications associated with peritoneovenous shunts in management of malignant ascites. Cancer 1985; 55: 1973-8. 9. Wolldridge TD, Bower JD, Holbert RD, Rubinsky MJ. LeVeen shunt (LS): long-term therapy for idiopathic ascites of chronic renal failure. Proceedings of the Dialysis Transplant Forum, Washington, DC, 1976. 10. Yen MC, Stewart EH. Peritoneovenous shunt for ascites associated with maintenance dialysis. Clin Nephrol 1977; 8: 446-8. 11. LeVeen HH, Christoudias G, Moon IP, et al. Peritoneovenous shunting for ascites. Ann Surg 1974; 180: 580-91. 12. LeVeen HH, Piccone VA. The LeVeen shunt for intractable ascites. In: Nyhus LM, Baker RJ, eds. Mastery of surgery. Vol. II. Boston: Little, Brown and Company, 1984: 873-80. 13. LeVeen HH, Wapnick S, Grosberg S, Kinney MJ. Further experience with peritoneovenous shunt for ascites. Ann Surg 1976; 184: 574-81. 14. Berkowitz HD, Mullen JL, Miller LD, Rosato EF. Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. Surgery 1978; 84: 120. 15. Arismendi GS, Izard MW, Hampton WR, Maher JF. The clinical spectrum of ascites associated with maintenance dialysis. Am J Med 1976; 60: 46-51. 16. Morgan AG, Terry SI. Impaired peritoneal fluid drainage in nephrogenic ascites. Clin Nephrol 198 1; 15: 61-5. 17. Popli S, Chen WT, Nakamoto S, et al. Hemodialysis ascites in anephric patients. Clin Nephrol 1981; 15: 203-5.
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18. Morgan AG, Sivapragasam S, Fletcher P, Terry SI. Hemodynamic improvement after peritoneovenous shunting in nephrogenic ascites. South Med J 1982; 75: 373-4. 19. Hobar PC, Turner WW, Valentine J. Successful use of the Denver peritoneovenous shunt in patients with nephrogenic ascites. Surgery 1987; 101: 161-3. 20. Epstein M. Peritoneovenous shunt in the management of ascites and the hepatorenal syndrome. Gastrcenterology 1982; 82: 7909. 21. Arnot RS, White H. Dissemination of tumor cells via LeVeen shunt. Lancet 1978; 1: 505-7. 22. Smadja C, France D. The LeVeen shunt in the elective treatment of intractable ascites in cirrhosis: a prospective study on 140 patients. Ann Surg 1985; 201: 488-93. 23. Greig PO, Langer B, Blendis LM, et al. Complications after peritoneovenous shunting for ascites. Am J Surg 1980; 139: 12531. 24. Schwartz ML, Swaim WR, Vogel SB. Coagulopathy following peritoneovenous shunting. Surgery 1979; 85: 671-6. 25. LeVeen HH, Moon IP, Ahmed N, et al. Coagulopathy post peritoneovenous shunt. Ann Surg 1987; 205: 305-11. 26. Prokesch RC, Rimland D. Infectious complications of the peritoneovenous shunt. Am J Gastroenterol 1983; 78: 235-40. 27. Wormser GP, Hubbard RC. Peritonitis in cirrhotic patients with LeVeen shunts. Am J Med 1981; 70: 358-62. 28. Fullen WD. Hepatorenal syndrome: reversal by peritoneovenous shunt. Surgery 1977; 82: 337-41. 29. Wapnick S, Grosberg S, Kinney M, et al. Renal failure in ascites secondary to hepatic, renal, and pancreatic disease: treatment with a LeVeen peritoneovenous shunt. Arch Surg 1978; 113: 581-5. 30. Schwartz ML, Vogel SB. Treatment of hepatorenal syndrome. Am J Surg 1980; 139: 370-3. 31. Appelquist P, Silvo J, Salmela L, Kostiainen S. On the treatment and prognosis of malignant ascites: is the survival time determined when the abdominal paracentesis is needed? J Surg Oncol 1982; 20: 238-42. 32. Capone RR, Buhac I, Kohberger RC, et al. Resistant ascites in alcoholic liver cirrhosis: course and prognosis. Dig Dis Sci 1977; 23: 867-71.
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MD,
Norman B. Halpern,
A retrospective analysis of 54 patients with a peritoneovenous shunt inserted to control massive ascites refractory to conventional medical treatment is presented. The cause of ascites was hepatic in 29 patients (Group 1,54 percent), malignant in 13 (Group 2,24 percent), and nephrogenic in 12 (Group 3,22 percent). The peritoneovenous shunt failed in 11 patients (20 percent) : 6 in Croup 1,3 in Croup 2, and 2 in Group 3. Shunt outflow ohstruction (thrombosis) was the principal cause. Systemic sepsis in five patients and variceal hemorrhage in three were the factors responsible for most of the deaths (22 percent). Of the 42 patients who survived operation, the peritoneovenons shunt was effective in controlling the massive ascites in 37 (86 percent). Eight patients ( 15 percent), four with hepatic and four with nephrogenic ascites, survived 3 years or more without ascites. Removal of at least 50 to 70 percent of ascitic fluid at the time of shunt insertion was considered an important factor in decreasing morbidity and mortality. A peritoneovenous shunt can be effective for a long-term period in controlling massive ascites with an hepatic or nephrogenic cause in a selected group of patients; however, in patients with malignant ascites, although the benefit was substantial in half, the survival period did not exceed 6 months.
From the Department of Surgery, University of Alabama School of Medicine, Birmingham, Alabama. Requests for reprints should be addressed to Joaquin S. Aldrete, MD, Department of Surgery, UAB, University Station, Birmingham, Alabama 35294.
162
THE AMERICAN JOURNAL OF SURGERY
MD,
Joaquin S. Aldrete,
MD, Birmingham, Alabama
he effectiveness of a peritoneovenous shunt to relieve T massive ascites refractory to conventional medical treatment is well established. However, the evaluation of long-term results, morbidity, and mortality has varied from enthusiastic support to reluctant acceptance [Z-q. The most common indication for peritoneovenous shunt insertion is ascites caused by hepatic disease. The same device has been used in a smaller number of patients with ascites of malignant or nephrogenic origin; the indications in these two groups are even more uncertain because of the scarcity of objective data [7-101. This retrospective review attempted to objectively evaluate the long-term effectiveness, the morbidity, and the mortality incurred by inserting peritoneovenous shunt in patients with massive refractory ascites of hepatic, nephrogenic, and malignant tumor origin. MATERIAL AND METHODS
All the records of patients who underwent insertion of a peritoneovenous shunt for massive refractory ascites from 1975 to 1984 at the hospital of the University of Alabama in Birmingham were located and reviewed. To define the population of patients to be studied, the following criteria were used: hepatic ascites in patients with cirrhosis documented by liver biopsy (Group 1); malignant ascites in patients with abdominal carcinomatosis proven by biopsy (Group 2); nephrogenic ascites in patients with end-stage renal disease and without evidence of another cause of ascites (Group 3). Massive ascites were defined as markedly distending the abdomen and producing persistent discomfort, dyspnea, and early satiety, in most cases rendering the patient unable to perform routine activities. Ascites of he patic and malignant origin were considered intractable when they remained present despite appropriate conventional medical treatment properly carried out for a minimum of 3 consecutive weeks, which included restriction of both oral fluid intake to less than 1,000 ml/day and sodium to less than 500 mg/24 hours, and diuretics (usually spironolactone 400 mg/day and furosemide 80 mg/ day). An increase of the serum creatinine level above 2.5 mg/dl during the period of treatment was also considered a reason for intractability, since diuretics could no longer be used. Nephrogenic ascites was considered intractable when it persisted despite three or more sessions per week of hemodialysis using high ultrafiltration flow for at least 4 consecutive weeks. The presence of massive, intractable disabling ascites was the indication for operation in all patients. If the patient was thought to be able to survive the operation in the opinion of the consultant surgeon, the patient underwent insertion of peritoneovenous shunt. The following were considered contraindications for this operation: peritonitis, systemic sepsis, primary congestive heart failure,
VOLUME 158 AUGUST 1989
failure of more than two systems of organs, loculated or thick ascites, uncorrectable coagulopathy, and active hepatic disease (encephalopathy and presence of variceal hemorrhage). In all cases, a Le.Veen peritoneovenous shunt was utilized. Prior to operation, prophylactic antibiotics were given, and electrolyte and coagulation abnormalities were corrected. In Groups 1 and 2, the body weight and 24hour urine volume were measured and recorded; in Group 3 patients, the body weight and abdominal girth were the parameters used. The peritoneovenous shunt was inserted using the original technique described by LeVeen et al [II,I2]. The shunt was considered effective when all of the following improvements occurred and persisted for a period of at least 2 months after its insertion: decrease of abdominal girth, a substantial weight loss, increase of effective diuresis (except in Group 3), improvement of respiratory function, nutritional intake, and capacity for physical activity. RESULTS There were 54 patients who met the criteria previously described. Thirty-six patients were men (67 percent) and 18 were women (33 percent). Their ages ranged from 30 to 70 years (mean 47 f 1.5 years). The duration of ascites prior to peritoneovenous shunt insertion ranged from 2 to 84 months (mean 20.6 f 2.6 months). The cause of the ascites was as follows: Group 1, hepatic in 29 patients (54 percent): 26 with alcoholic cirrhosis, 2 with sclerosing cholangitis with cirrhosis, and 1 with thrombosis of the hepatic veins; Group 2, abdominal carcinomatosis in 13 patients (24 percent): 11 with primary tumor in the abdomen including the colon in 5, diffuse lymphoma in 3, the pancreas in 2, and the ovary in 1, and 2 with breast cancer; Group 3, nephrogenic in 12 patients (22 percent): chronic renal failure caused by diabetes mellitus in 4, hypertensive nephrosclerosis in 3, pyelonephritis in 3, polycystic kidney disease in 1, and systemic amyloidosis in 1. There were no operative or anesthetic complications during the insertion of the peritoneovenous shunt. The amount of ascites drained at operation ranged from 3,000 to 12,000 ml (mean 5,350 f 758 ml). The appearance of ascitic fluid was recorded in 34 patients; it was described as straw-colored in 27 patients in Groups 1 and 3 and blood-tinged or turbid in 5 and 2 patients, respectively, in Group 2. In patients with nephrogenic or malignant ascites, the total content of proteins in the ascitic fluid ranged from 2.7 to 5.2 g/d1 (mean 3.5 f 0.6 g/dl). In 37 patients (69 percent), a substantial weight loss of 3 kg or more was recorded by the time they left the hospital: 21 patients in Group 1 (72 percent), 6 in Group 2 (46 percent), and 10 in Group 3 (83 percent). The weight loss ranged from 3.4 to 18.2 kg (mean 8.3 f 1.5 kg). Temporary weight loss with reaccumulation of ascites postoperatively was recorded in 12 patients (22 percent), whereas no weight loss was observed in 5 (9 percent). In Group 1, the recorded weight loss was more than 10 kg in 12 patients (57 percent), whereas in Groups 2
TABLE I Postoperative Compllcatlons No. of Patients
causes Recurrence of ascites Coagulopathy Progressive liver failure Upper gastrointestinal bleeding systemic sepsis Persistent fever Renal failure’ Respiratory distress syndrome Edema in upper extremities Wound infection
11 6 6 5 5 5 4 3 2 2
* In Groups 1 and 2.
and 3, weight loss over 10 kg was recorded in only one patient in each group (16 and 10 percent, respectively). The 24-hour urine volume increased from a mean of 932 ml i 18 recorded the day preceding the insertion of the shunt (range 795 to 1,045 ml) to a mean of 1,782 ml f 30 (range 1,525 to 1,975 ml) on the day prior to dismissal from the hospital in 21 Group 1 patients, and from 1,292 ml f 237 (range 650 to 2,000 ml) to 2,733 ml f 455 (range 800 to 3,500 ml) in 8 Group 2 patients. The preshunt to postshunt increments in the 24-hour urine output averaged a mean of 850 ml f 12 in Group 1 and 1,441 ml f 218 in Group 2. Postoperative complications occurred in 34 patients (63 percent); in 28 (82 percent), 2 or more complications were observed (Table I). The most common was recurrence of ascites due to peritoneovenous shunt failure in 11 patients (20 percent): 6 of 29 in Group 1 (20 percent), 3 of 13 in Group 2 (32 percent), and 2 of 21 in Group 3 (16 percent). The principal cause of shunt failure was thrombosis at the end of the venous limb placed in the superior vena cava in four patients; in all four, the precise cause of failure was documented by either peritoneal scanning with radionuclide (technetium-99m-labeled albumin), shuntogram, or cavagram. Of the other seven patients with shunt failure, in three the peritoneovenous shunt was removed because of infection, in two because of persistent leakage of ascitic fluid, and in two due to severe coagulopathy (Table II). Another significant complication was postshunt coagulopathy in six patients; in four cirrhotics it was corrected by transfusing fresh frozen plasma and platelet concentrates. As noted previously, fatal coagulopathy occurred in two patients with malignant ascites despite prompt ligation of the shunt. Progressive liver failure was observed in six cirrhotics; four of them had mild encephalopathy which responded to treatment, and the other two developed hepatorenal syndrome and subsequently died. The diagnosis of hepatorenal syndrome was established by the presence of progressive renal failure in a well-hydrated patient with a serum creatinine level of 3 mg/dl or greater and a urinary sodium level of less than 10 mEq/liter. Upper gastrointestinal bleeding occurred in five patients; the causes of hemorrhage were ruptured esophage-
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TABLE II Perltoneovenous Shunt That Required Removal or Revision Group
Cause of Failure shunt shunt shunt shunt
(blood) (blood) (blood) (proteinacaous)
Shunt Life
Second Shunt Placed
Survival From First Operation
Few h 20 d 4 mo 3d
Same operative d 6 d after removal
4 mo 30 d Lost to follow-up (5 mo) 3 mo
1 1 1 2
Clotted Clotted Clotted Clotted
3 1
1
Infected shunt Infected shunt Infected shunt
9d 20 d 26 d
3 1
Ascites leakage Ascites leakage
3 mo 12 d
2 2
Severe coagulopathy’ Severe coagulopathy’
Id ld
. Same d of removal
... ... ... 4 mo after removal 4 mo after revislon (on opposlte side)
.. .
11 d 26 d 29 d Alive 42 mo postop 5 mo 2d 3d
* Shunt ligation.
al varices in three cirrhotics who died, and gastric mucosal ulcerations complicated by systemic sepsis in one cirrhotic and one renal patient. Five patients, four with cirrhosis and one with renal failure, died postoperatively from systemic sepsis; in three an infected shunt was found and removed, and in the other two, pneumonitis was the source of the sepsis. Of the 54 patients, 12 (22 percent) died within 1 to 30 days after operation. The operative mortality by groups was 9 of 29 patients in Group 1 (31 percent), 2 of 13 in Group 2 (15 percent), and I of 12 in Group 3 (8 percent). Of the 42 patients (78 percent) who left the hospital alive, 25 (60 percent) subsequently died within 3 to 60 months (mean 19 f 3.2 months). The majority of late deaths were attributed to the progression of their primary disease. In three patients the ascites recurred due to obstruction of the shunt in two and persistent ascites leakage in one. The ascites was controlled by the peritoneovenous shunt in 36 of the 42 surviving patients (86 percent); the other 6 (14 percent) required supplemental diuretics to control the ascites. Thus, these 36 patients who comprised 67 percent of the total number of patients studied can be considered as having good results; the overall survival period for these patients ranged from 3 to 108 months (mean 23.7 f 3.7 months) (Table III). None of the patients with abdominal carcinomatosis in Group 2 survived more than 6 months after insertion of the peritoneovenous shunt. The survival rates in Group 1 were 16 of 29 patients (55 percent) 6 months postoperatively, 12 (41 percent) 1 year postoperatively, 9 (3 1 percent) 2 years postoperatively, and 4 (14 percent) 3 or more years postoperatively. In Group 3,9 of 12 patients (75 percent) were alive 6 months postoperatively, 7 (58 percent) 1 year postoperatively, 5 (41 percent) 2 years postoperatively, and 4 (33 percent) 3 or more years postoperatively. COMMENTS Most patients with ascites respond favorably to conventional medical treatment. However, in 5 to 10 percent 164
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of these patients, the massive ascites persists despite appropriate medical treatment; for such patients, the insertion of a peritoneovenous shunt is indicated to attempt to decrease the refractory ascites [2,3]. It must be recognized that although the amount of ascites may be markedly decreased by inserting a peritoneovenous shunt, this change does not alter the natural course of cirrhosis [2,3,13,14]. Thus, only a palliative effect can be granted to peritoneovenous shunt in the overall management of cirrhosis. In patients with endstage renal disease maintained by hemodialysis, the development of intractable ascites has a worse prognosis; many therapeutic modalities have been tried, but the overall results have been unsatisfactory [IS-Z7]. Previous reports have suggested these patients may benefit from insertion of a peritoneovenous shunt [Z&19]. Ascites has been observed to occur in 15 to 50 percent of patients with extensive abdominal carcinomatosis; most of them die within 6 months from the onset of massive ascites [Z,20]. Some studies have reported that insertion of a peritoneovenous shunt provides significant palliation from the disabling ascites for the limited period of survival that these patients have [8,2Z]. The results observed in the present study are in accordance with those reported by other groups [Z3,13,14,22]. The effectiveness of peritoneovenous shunt in reducing the ascites, as assessed by weight loss, was higher in patients with cirrhosis. This is probably due to the physical characteristics of their ascitic fluid (transudate) which facilitates its removal by the shunt, compared with the lower weight loss observed in patients with nephrogenic or malignant ascites (exudate) which usually contain a high percentage of protein (more than 2.5 mg/dl), suspended particles, and cells. The observed high morbidity and mortality associated with peritoneovenous shunt insertion are due to the severity of the usually preterminal or terminal primary disease responsible for ascites, and to a lesser extent, to the complications caused by the shunt itself [ 1,5,8,22,23]. In the present study, shunt outflow obstruction was the principal cause of early peritoneovenous shunt failure and was
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PER1mNwvENous sBuNT FOR AsclTlIS
frequently seen in patients with cirrhosis; this is probably related to the common thrombogenicity of the ascitic fluid or due to thrombosis induced by the catheter itself. Occlusion of the venous tubing by proteinaceous or cellular products was seen in only one patient with carcinomatosis. The high viscosity of thii exudative ascites is likely to lead to the obstruction of the tubing. Postshunt coagulopathy has received extensive attention in the literature [I ,3,20,24,25]. Mild coagulopathies have been described as occurring frequently, but they usually respond to medical therapy. The reported incidence of severe coagulopathy ranges from 4 to 20 percent, and occurs more frequently in patients with end-stage liver disease and abdominal carcinomatosis. The presence of some anticoagulant products contained in the ascitic fluid appears to be activated when they are shunted into the venous circulation, resulting in severe coagulopathy. Infusion of clotting factors, epsilon-aminocaproic acid, and prompt ligation of the shunt venous tubing are the recommended therapy for this coagulopathy. The relatively low incidence of fatal coagulopathy observed in our series (4 percent) was thought to be related to the decrease of thromboplastic elements into the blood stream, due to the practice of removing a large amount of ascites at the time of peritoneovenous shunt insertion. In the present study, the postshunt rate of variceal hemorrhage in patients with cirrhosis (10 percent) parallels other studies [3,22]. It could be speculated that this low incidence is due to the decrease of the expanded plasma volume by removal of a substantial amount of ascites during the peritoneovenous shunt insertion, which theoretically results in a decrease of pressure in the splanchnic bed. The incidence of systemic sepsis (9 percent) was somewhat lower than that reported in similar series [23,26,27]. However, a distressing observation was that despite aggressive antibiotic therapy and prompt removal of the shunt when indicated, the mortality remained high, as in all patients with sepsis and peritoneovenous shunt. In patients with tense ascites, the abdominal wall is usually thin, and leakage of ascites around the site of insertion of the shunt abdominal limb is an ever-present threat. This complication occurred in 4 percent of the patients studied [3,I 31. Meticulous closure of the abdominal wound is essential to prevent this problem. Failure to prevent or promptly correct the leakage of ascitic fluid almost always leads to local infection, which eventually will require removal of the shunt. Although some studies claim resolution of the hepatorenal syndrome with peritoneovenous shunt, in a collective review, Epstein [20] concluded that the majority of those successes occurred in patients in whom the presence of the syndrome was not clearly documented [1,28-301. In the present series, a lower incidence of hepatorenal syndrome (two patients) was noted, but despite the peritoneovenous shunt, both died. The present study suggests that the insertion of a peritonecvenous shunt effectively relieves massive ascites not only of hepatic disease origin, but also for ascites resulting from renal and malignant disease. The acknowl-
TABLE III Results Per Group’f
Operative mortality Survived operation (>2 mo) Subseqently died Alive 36 or more mo Lost to follow-up (>4 mo)
&ovpl (n = 29)
Group 2 (n = 13)
(n = 12)
9 (31) 20 (69)
2 (19) 11 (85)
1 (8) 11 (92)
10 4
6
8 0 3
Group 3
7 4 0
* Values in parentheses are percentages. + Ascites was caused by clrhosis in Group 1 patients and abdominal carcinomatosis in Group 2 patients, and was of nephrogenic origin in Group 3 patients.
edged high morbidity and mortality are due primarily to the advanced stage of the primary diseases requiring the operation. However, there are other determinant factors for the morbidity and mortality that are related to the shunt itself. The issue to address is: Are there any measures to take to decrease the well-documented high mortality (22 percent) and morbidity (63 percent) of ascites? Aside from the obvious precautions, such as meticulous operative technique, avoiding the established contraindications for the operation, and attention to details in the postoperative period, our study suggests that the incidence of some complications, such as pulmonary edema, variceal hemorrhage, and severe coagulopathy can be lowered by draining 50 to 70 percent of the total amount of ascites present at the time of insertion of the peritoneovenous shunt. It should be noted that extensive drainage of ascites resulted in immediate relief of the general discomfort and did not have any deleterious effect on the patient. The occurrence of late postoperative complications has been noted [I-3]. Shunt blockage and infection are the most commonly encountered, in the present study they occurred in 12 percent of the long-term survivors [4,22]. The mortality observed in the late postoperative period is caused by the progression of the usually advanced hepatic, renal, or malignant disease that determined the need for the peritoneovenous shunt [Z&2932]. It is not possible to objectively determine in the cirrhotic patients if the peritoneovenous shunt prolonged their survival. Nevertheless, it was clear that in 86 percent of the patients analyzed, the relief from the massive ascites greatly improved the quality of their lives. As expected, the patients with nephrogenic ascites survived longer, contrasting with the short survival noted in patients with carcinomatosis. 1. LeVeen HH, Brown T, d’Ovidio NG. Surgical treatment of ascites. In: Jordan GL, ed. Advances in surgery, vol. 14. Chicago: Year Book Medical, 1980: 107-50. 2. Greenlee HB, Stanley M, Reinhardt GF. Intractable ascites treated with peritoneovenous shunts (LeVeen): a 24 to 64 month follow-up of results in 52 alcoholic cirrhotics. Arch Surg 1981; 116: 518-24.
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3. Bernhoft RA, Pellegrini CA, Way LA. Peritoneovenous shunt for refractory ascites: operative complications and long-term results. Arch Surg 1982; 117: 631-S. 4. Stanley MM. Treatment of intractable ascites in patients with alcoholic cirrhosis by peritoneovenous shunts (LeVeen). Med Clin North Am 1979; 63: 523-35. 5. Hyde GL, Dillon M, Bivins BS. Peritoneal venous shunting for ascites: a 15-year perspective. Am Surg 1982; 48: 123-7. 6. Gleysteen JJ, Klamer Th W. Peritoneovenous shunts: predictive factors of early treatment failure. Am J Gastroenterol 1984; 79: 654-8. 7. Quazi R, Saxlov ED. Peritoneovenous shunt for palliation of malignant ascites. Cancer 1982; 49: 600-2. 8. Souter RG, Wells C, Tarin D, Kettlewell MW. Surgical and pathologic complications associated with peritoneovenous shunts in management of malignant ascites. Cancer 1985; 55: 1973-8. 9. Wolldridge TD, Bower JD, Holbert RD, Rubinsky MJ. LeVeen shunt (LS): long-term therapy for idiopathic ascites of chronic renal failure. Proceedings of the Dialysis Transplant Forum, Washington, DC, 1976. 10. Yen MC, Stewart EH. Peritoneovenous shunt for ascites associated with maintenance dialysis. Clin Nephrol 1977; 8: 446-8. 11. LeVeen HH, Christoudias G, Moon IP, et al. Peritoneovenous shunting for ascites. Ann Surg 1974; 180: 580-91. 12. LeVeen HH, Piccone VA. The LeVeen shunt for intractable ascites. In: Nyhus LM, Baker RJ, eds. Mastery of surgery. Vol. II. Boston: Little, Brown and Company, 1984: 873-80. 13. LeVeen HH, Wapnick S, Grosberg S, Kinney MJ. Further experience with peritoneovenous shunt for ascites. Ann Surg 1976; 184: 574-81. 14. Berkowitz HD, Mullen JL, Miller LD, Rosato EF. Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. Surgery 1978; 84: 120. 15. Arismendi GS, Izard MW, Hampton WR, Maher JF. The clinical spectrum of ascites associated with maintenance dialysis. Am J Med 1976; 60: 46-51. 16. Morgan AG, Terry SI. Impaired peritoneal fluid drainage in nephrogenic ascites. Clin Nephrol 198 1; 15: 61-5. 17. Popli S, Chen WT, Nakamoto S, et al. Hemodialysis ascites in anephric patients. Clin Nephrol 1981; 15: 203-5.
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18. Morgan AG, Sivapragasam S, Fletcher P, Terry SI. Hemodynamic improvement after peritoneovenous shunting in nephrogenic ascites. South Med J 1982; 75: 373-4. 19. Hobar PC, Turner WW, Valentine J. Successful use of the Denver peritoneovenous shunt in patients with nephrogenic ascites. Surgery 1987; 101: 161-3. 20. Epstein M. Peritoneovenous shunt in the management of ascites and the hepatorenal syndrome. Gastrcenterology 1982; 82: 7909. 21. Arnot RS, White H. Dissemination of tumor cells via LeVeen shunt. Lancet 1978; 1: 505-7. 22. Smadja C, France D. The LeVeen shunt in the elective treatment of intractable ascites in cirrhosis: a prospective study on 140 patients. Ann Surg 1985; 201: 488-93. 23. Greig PO, Langer B, Blendis LM, et al. Complications after peritoneovenous shunting for ascites. Am J Surg 1980; 139: 12531. 24. Schwartz ML, Swaim WR, Vogel SB. Coagulopathy following peritoneovenous shunting. Surgery 1979; 85: 671-6. 25. LeVeen HH, Moon IP, Ahmed N, et al. Coagulopathy post peritoneovenous shunt. Ann Surg 1987; 205: 305-11. 26. Prokesch RC, Rimland D. Infectious complications of the peritoneovenous shunt. Am J Gastroenterol 1983; 78: 235-40. 27. Wormser GP, Hubbard RC. Peritonitis in cirrhotic patients with LeVeen shunts. Am J Med 1981; 70: 358-62. 28. Fullen WD. Hepatorenal syndrome: reversal by peritoneovenous shunt. Surgery 1977; 82: 337-41. 29. Wapnick S, Grosberg S, Kinney M, et al. Renal failure in ascites secondary to hepatic, renal, and pancreatic disease: treatment with a LeVeen peritoneovenous shunt. Arch Surg 1978; 113: 581-5. 30. Schwartz ML, Vogel SB. Treatment of hepatorenal syndrome. Am J Surg 1980; 139: 370-3. 31. Appelquist P, Silvo J, Salmela L, Kostiainen S. On the treatment and prognosis of malignant ascites: is the survival time determined when the abdominal paracentesis is needed? J Surg Oncol 1982; 20: 238-42. 32. Capone RR, Buhac I, Kohberger RC, et al. Resistant ascites in alcoholic liver cirrhosis: course and prognosis. Dig Dis Sci 1977; 23: 867-71.
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