The Effect of the Distal Splenorenal Shunt on Hypersplenism DUANE G. HUTSON, M.D., ROBERT ZEPPA, M.D., JOE U. LEVI, M.D., EUGENE R. SCHIFF, M.D., ALAN S. LIVINGSTONE, M.D., PATRICIA FINK, R.N.

Twenty-four patients with leukopenia and/or thrombocytopenia improved these deficiencies after distal splenorenal shunts. The average white blood cell count for 23 neutropenic patients increased by an average 1000 celLs/cu.mm p < .01. The average platelet count for 13 thrombocytopenic patients increased by more than 40,000, p < .02. Analysis of the data showed that patients older than 50 years, with a history of alcoholic liver disease and sinusoidal hyptetension greater than 15mm Hg were most likely to correct leukocyte and platelet defects after distal splenorenal shunts.

EMATOLOGIC DISORDERS are well documented

in association with cirrhosis of the liver and portal hypertension. Anemia, thrombocytopenia and leukopenia are the most frequently encountered. The association of these abnormalities with splenomegaly is considered to be due to sequestration of the formed elements within the enlarged spleen and questionable destruction by immune mechanisms. Support for this hypothesis is found in the almost uniform improvement in thrombocytopenia and leukopenia which follows splenectomy, although the anemia associated with cirrhosis and portal hypertension appears to be multifactorial in origin and in general does not respond to this therapy.4'5'8 Splenic venous hypertension due to portal block is thought to cause the splenomegaly which results in the sequestration and destruction of the leukocytes and thrombocytes. Since the initiating factor seems to be splenic venous hypertension, then therapeutic procedures which lower splenic venous pressure might be expected to improve these hematologic abnormalities. The distal splenorenal shunt effectively reduces splenic venous pressure to nearly that of the left renal vein thus a reduction in splenomegaly and hypersplenism following this procedure might be expected. With this hypothesis in mind, the effects of the distal splenorenal shunt on preexisting leukopenia and thrombocytopenia in 24 Presented at the Annual Meeting of the Southern Surgical Association, December 5-8, 1976, Palm Beach, Florida.

605

From the Department of Surgery, University of Miami School of Medicine, Miami, Florida

patients with cirrhosis of the liver and portal hypertension were analyzed.

Patient Selection During the past five years 66 patients were treated by distal splenorenal shunts for portal hypertension and bleeding gastroesophageal varices. Twenty-four of these patients (Table 1) demonstrated evidence of hypersplenism as indicated by 1) leukocyte counts of less than 5 x 103 and/or 2) platelet counts of less than 100 x 103. Hemoglobin and hematocrit determinations were of no value since all but one of these patients experienced repeated episodes of variceal hemorrhage requiring multiple transfusions. Nineteen males and five females comprised the group whose average age was 52 years (range 19-70 years) at the time of operation. Ten patients were alcoholics and one of the 14 patients with postnecrotic cirrhosis also suffered from Felty's Syndrome of many years duration. Corrected hepatic sinusoidal pressures were measured in 17 of the patients prior to surgery (X= 16mm mercury, SEM = 2mm mercury). Preoperative splenic size was recorded only as spleen palpable or nonpalpable. Intraoperatively, splenic size was estimated variously as minimally, moderately, or markedly enlarged. Repetitive physical examinations and complete blood counts were obtained at various times after operation ranging from 6 to 48 months (X = 21 months). Results The description of the sample under study (Table 1) shows that the increase in leuykocyte counts following

Ann. Surg.

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o

May 1977

TABLE 1.

Pt. No.

Age Years

1 2 3 4 5 6 7 8 9* 10 11 12 13 14 15 16 17

36 54

Sex

Alcoholic

49 63 42 49 62 62 38 19 67 42 50 53 51 51 52 59 57 56 63 46 70

M M M F M F M M F M M M F F M M M M M M M M M M

52

19M

No Yes Yes No No No No No No No No Yes No Yes Yes No Yes Yes No Yes Yes Yes No No 1OA

5F

14 NA

55

18 10 20 21 22 23 24 AUG

Corr Sinusoidal Pressure mm Hg

26 16 22 17 10 5 3 22 32 19 9 28 24 14 12 7 12 7 n= 18 X= 16 SEM = 2

Time of Follow up 24 9 22 36 41 12 7 46 6 18 18

9 12 21 10 36 6 12 15 48 12 18 9 48 21 months

Pre-op WBC x 103

Post-op WBC X 103

2 6 3 4 3 4 2 4 1 4 2 4 3 3 4 1 4 4 2 3 4 2 3 3 3.1 SEM=.24

4 6 6 4 4 5 3 4 1 5 3 4 3 6 5 3 4 5 3 3 3 4 4 6

4.1 SEM=.25 t = -3.12 p < .01

Pre-op Platelet Count X 103

Post-op Platelet Count X 103

86 138 111 103 230 54 89 130 38 94 60 260 53 150 138 63 150 109 90 140 180 87 100 87 114 SEM= 11 t= -.04 p >.9

52 42 121 73 82 108 40 69 120 114 92 260 57 96 216 60 206 66 40 136 216 170 162 66 111 SEM= 13

Splenic Enlargement Moderate Moderate Moderate Moderate Moderate Moderate Moderate Moderate Marked Moderate Moderate Moderate Moderate Marked Marked Moderate Moderate Minimal Moderate Moderate Moderate Moderate Moderate Moderate

* Felty's Syndrome with portal hypertension.

distal splenorenal shunt was significant, p < .01 for the entire group. The average platelet counts indicate that thrombocytopenia was not a general deficiency for this cohort. However, three subgroups were identified and analyzed. Leukocytes < 5 x 103, Platelets _ 100 x 103 There were 11 patients in this leukopenic subgroup including the patient with Felty's Syndrome. The average preoperative leukocyte count (exclusive of the patient with Felty's Syndrome) was X = 3.5 x 103, SEM = 0.2 x 103. This rose to X = 4.3 x 103, SEM = 0.3 x 103 postoperatively. The difference in leukocyte counts after, as compared to before therapy, is highly significant, p

103

6- t =-2.48 df = 28 p < .02

X 103, SEM = 0.3 x 103; Xplat = 87 X 103, SEM = 14 X 103, respectively. Splenorenal anastomoses had no discernable effect upon leukocytes or platelets in these patients (Fig. 1). The postoperative counts were on the average XWBC = 3.9 x 103, SEM = 0.3 X 103 for leukocytes and Xplat = 80 x 103, SEM = 7 X 103 for platelets. Only 25% of the patients at risk demonstrated a return of the leukocyte count to normal and platelet counts rose to greater or equal to 100 x 103 < 50 yrs.

n

=

8

| SEM

I

[ 2/8 PTS WBC 3 5000 ................. 25% 1/5 PTs $ PLATELETS 3 100,000.... 20%/ t

= -0.56

df = 14

xlo3

p>.S

ISEM

////,

4

PLATELET

0.62 df =28 t

=

COUNT x

p> .4

PRE-OP -

PRE - OP *

POST - OP

PLATELET COUNT x

103 100

t= Q46 df = 14 p

.5

7-75

2-

50

I1-

25

-0

FIG. 1. No significant difference between preoperative and postoperative counts in the under 50 age group.

125

-100

-

2-

1-

103 150

75

-50

-

Eight of the patients were younger than 50 years of age at the time of operation and their preoperative platelet and leukocyte counts averaged XWBC= 3.0

WBC

-

50 yrs. n= 15

* POST - OP

5

The Effect of Age

EFFECT OF AGE

607

25

-

-0 FIG. 2. Postoperative change in WBC is highly significant in over 50 year age group.

in one of five patients or 20Wo of the thrombocytopenic group. Fifteen patients were older than 50 years (Felty's patient exempted) and 14 presented with neutropenia, XWBC = 3.3 x 103, SEM = 0.3 x 103. The average postoperative leukocyte count was significantly increased to XWBC = 4.4 x 103, SEM = 0.3 X 103, p 50 yrs. n = 8 | SEM

n=5

>

-

.2

df = 14 p

-

< .01

I

60

40-

20-

Ann. Surg.

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May 1977

might be related to the hematologic response to distal splenorenal shunt. As shown in Figure 6, the patients whose preoperative corrected sinusoidal pressures were greater than 15mm of mercury demonstrated a more than twofold greater response in normalization of the leukocytes and platelets than did those patients with pressures below 15mm of mercury. The time of followup seemed to be of no importance. The recovery rate was similar at all times of evaluation therefore it appears that a response will be noted on or before the sixth postoperative month or not at all. Splenomegaly seemed to improve after distal splenorenal shunt since nine of the 14 patients with preoperatively palpable spleens no longer presented with this physical finding (64%) in the postoperative period. One patient with a nonpalpable spleen preoperatively was found to have his spleen palpable in the postoperative evaluation.

0

FIG. 3. Age and initial low platelet count. In older patierits with preoperative thrombocytopenia the improvement in platelelt counts is striking. No significant change is demonstrated in the u nder 50 group.

counts below 5 x 103. Four of these were foLand to have increased their leukocyte counts to nonrnal or ten 44% of the group at risk. Only three of tU 'ieie ten patients (30W) were found to be thrombocytopen11%. aiiu all of these patients had normal platelet counts postoperatively (Fig. 4). All of the 13 patients in the non-alcoholic cohort (Felty's excluded) were neutropenic (Fig. 4). Only three patients increased their leukocyte cou nts to normal levels postoperatively (23%). There wass more than twice the incidence of thrombocytopenia in this subgroup, ten of 13 patients (77%) as connpared to the alcoholics (30%o). In addition, only three of these ten patients had normal platelet counts when studied after operation (30%o). One of these non-alcoholic responders was younger than 50 years whereas all of the thrombocytopenic patient: s who responded were age 50 years or older. Cor-rected sinusoidal pressures were not significantly diifferent between the alcoholic and non-alcoholic subg;roups. However, the two groups were significantly disrsimilar as to preoperative as well as postoperative p)latelet counts (Fig. 5).

The Effect of Sinusoidal Hypertension

Seventeen patients of the group were an alyzed with regard for corrected sinusoidal pressure as it

Discussion In a recent review on portasystemic venous shunts, Malt7 has written, "Hypersplenism in portal hypertension is relieved by a portacaval shunt in about 60%o of patients. Certain cure probably requires a splenectomy and shunt." Further, Child and Turcotte2 have stated, ". . . Experience has proved that a generous portacaval shunt that remains patent

ALCOHOLICS (n =10)

NON - ALCOHOLICS

*

4/9 PTS + WBC 35 000 ..... 44%

* 3/13 PTS A WBC .3 5000 ..... 23%

*

3/10 PTS PLATELETS 100,000 ..... 30%

* 10/13 PTS

3/3 PTS A PLATELETS 100,000 .... 100%

* 3/10 PTS A PLATELETS

*

(n =13)

PLATELETS

e100,000 ..... 77%

100,000 ..... 30%

FIG. 4. The difference in preoperative vs. postoperative WBC in both alcoholic and non-alcoholic patients is significant, p .05 3.30 ..... df = 21 ... p .1 tPLAT 2.59 ..... df =21 ... p < .02 FIG. 5. Pre and postoperative WBC in alcoholic vs. non-alcoholic patients were not significantly different. Platelet profiles indicated a significant difference between the two groups, non-alcoholics having the highest incidence of thrombocytopenia.

serves as a physiological splenectomy." Probably, these conclusions are based in part on personal experience and to some degree on the few reports which have addressed the problem of hypersplenism and portasystemic shunts specifically. For example Patton et al.1' concluded that portacaval shunt was as effective as splenectomy in relieving hypersplenism, without benefit of reported data. Morris and his colleagues9 suggested that the incidence of hypersplenism was about 30Wo in cirrhotics. They found 8 patients who were identified as presenting with "definite hypersplenism" and reported that all were relieved of this complication by side to side portacaval shunts, albeit only transiently in two patients. Rousselot'2 found that one third of his patients were cured of thrombocytopenia, one third evinced no change and the remaining one third were victims of progressive hypersplenism. More recently, Jackson and his coworkers3 indicated that nearly 15% of the patients in the V.A. Cooperative Study met the criteria for hypersplenism. In 17 patients with leukopenia who were treated by portacaval shunts, 8 showed improvement (47%), whereas 12 of the 14 leukopenic patients randomized to medical therapy continued with low white cell counts. Thrombocytopenia did not improve in the medically

609

treated patients whereas five of 9 in the surgically treated group were improved (56%). On the other hand, MacPherson and Innes6 in an earlier study, provided data which suggested that portacaval shunt therapy had no discernable effect on hypersplenism secondary to portal hypertension. Conversely they were able to show that in 46 patients, splenectomy led to a uniform increase in white cells as well as platelets in the peripheral blood. Data derived from yet another propsective randomized trial by Conn and his co-workers'0 supports the contention that portacaval shunt therapy provides no help to hypersplenism in cirrhotics. In fact, these authors have shown that, whereas only 3% of their patients were leukopenic preoperatively, 11% were found to have this deficiency after surgery. Similarly an 8% incidence of thrombocytopenia prior to shunt surgery was found to escalate to 17% postoperatively. The results of this study shed no light on the controversy concerning the efficacy of portacaval shunt therapy in relieving hypersplenism. The data indicate, however, that the distal splenorenal shunt does have a profound effect on leukopenia associated with portal hypertension. Ninety-nine percent of the time an improvement in the peripheral white blood cell counts may be expected. However, in only 27% of instances does the white cell count return to "normal." Under the conditions of leukopenia
1S mm Hg CORRECTED

(n = 8)

(n =9)

PRE - OP

WBC*

.......

* PLATELETS .......

POST - OP * WBC

.......

* PLATELETS .......

*

3.0

* WBC

129

* PLATELETS .........

3.4 114

4.0

. WBC .........

4.4

109

* PLATELETS ......... 120

2/8 A WBC

3 5000 * 1/4

....

25%

+ PLATELETS

3

100,000 ....... 25%

. 4/9 A WBC .3 5000 ..... 44% * 3/5

.

A

PLATELETS

100,000 ...6 0%

FIG. 6. Normalization of peripheral counts occurs more frequently in patients whose preoperative corrected sinusoidal pressures are greater than 15mm Hg.

HUTSON AND OTHERS

61(

in the absence of thrombocytopenia, 40%o of patients returned their white cell counts to normal. Thirteen patients demonstrating thrombocytopenia were improved to one degree or another and 6 of these patients (46%) were found to have normal platelet counts when examined postoperatively. This is in striking contradiction to the statement by Bengmark1 writing on "the Warren shunt, . . . its influence on the platelet count is negligible. Thus it is not suitable in hypersplenism." Examination of the population of white cell and platelet counts before and after surgery from leukopenic and/or thrombocytopenic patients, clearly shows that the distal splenorenal shunt has a positive effect. Statistical analyses indicate significant improvements. Consideration of other factors has shown that older patients (greater than 50 years) are more apt to show improvement and that young, non-alcoholics benefit least. We have been able to confirm Jackson's finding that higher initial portal pressures are more likely to be associated with improvement in the peripheral counts after surgery.

References 1. Bengmark, S.: Surgical Management of Portal Hypertension. Clinic. Gastroenterol. 4:395, 1975.

DiSCUSSION

DR. PAUL T. DECAMP (New Orleans, Louisiana): Like so many of you, we have watched with interest the careful way in which Dr. Warren and the Miami group have followed the effects of this procedure, and it's interesting to hear these figures, which perhaps in their multiplicity are confusing us at the moment, but I'm sure will be crystal-clear when we have time to read the paper. We have had a series of 12 cases in which we have done the Warren procedure. Seven of these were moderately hypersplenic, and our results roughly parallel those of the authors. Two of five with low platelet count responded, and none of three with a low white count responded. None of these patients had a major hypersplenic clinical problem, either before or after their surgery, and I would like to ask Dr. Zeppa if any of his patients did. Frankly, in such a case we would be a little hesitant to leave the spleen behind. I rise principally to endorse the still relatively unpopular Warren procedure. We waited until they proved it worked and it wasn't too hazardous; but empirically it certainly has a lot going for it. Segmental variceal decompression with minimal portal venous diversion has much to recommend it. And certainly, if it will control the hemorrhage, it should be better, and certainly couldn't be worse, than procedures which directly permit or encourage portal venous diversion. So there remains only the technical fears that have apparently discouraged a number of us. This is an operation which does require a degree of technical competence, and only each individual surgeon in his own conscience can decide whether he has that competence or not.

Ann.

Surg. * May

1977

2. Child, C. G. III and Turcotte, J. G.: Surgery and portal hypertension, in "The Liver and Portal Hypertension," Child, C. G. III, ed. Philadelphia, W. B. Saunders, 1964, pp.1-85. 3. Felix, W. R., Myerson, R. M., Sigel, B. et al.: The Effect of Portacaval Shunt on Hypersplenism. Surg. Gynecol. Obstet. 139:899, 1974. 4. Jandl, J. H. and Aster, R. H.: Increased Splenic Pooling and the Pathogenesis of Hypersplenism. Am. J. Med. Sci. 253:383, 1967. 5. Leevy, C. M., Cherrick, G. R., and Davidson, C. S.: Portal Hypertension (concluded). New. Engl. J. Med. 262:451, 1960. 6. MacPherson, A. I. S. and Innes, J.: Peripheral Blood Picture after Operation for Portal Hypertension. Lancet 264:1120, 1953. 7. Malt, R. A.: Portasystemic Venous Shunts. New Engl. J. Med. 295:24, 1976. 8. Martini, G. A.: Exhepatic Manifestations of Cirrhosis. Clinic. Gastroenterol. 4:439, 1975. 9. Morris, P. W., Patton, T. B., Balent, J. A. et al.: Portal Hypertension, Congestive Splenomegaly and Portacaval Shunt. Gastroenterology 42:555, 1962. 10. Mutchnik, M. G., Lerner, E. and Conn, H. O.: Effect of Portacaval Anastomosis on Hypersplenism in Cirrhosis: A Prospective Controlled Evaluation. Gastroenterology 68: 1070, 1975. 11. Patton, T. B., Johnston, C. G., Lyons, C. et al.: Lateral Portacaval Anastomosis for Portal Hypertension. Am. J. Gastroenterol. 32:291, 1959. 12. Rousselot, L. M., Pantre, W. F., Bono, R. F. et al.: Experiences with Portacaval Anastomosis: Analysis of 104 Elective End to Side Shunts for the Prevention of Recurrent Hemorrhage from Esophagogastic Varices (1952-1961). Am. J. Med. 34:297, 1963.

In the last four years we have done the procedure 12 times. There have been no operative or postoperative deaths. There has been a moderate morbidity, and the results have been satisfactory. One of the cases has persistent varices, a large spleen, and a moderate late hemorrhage. Presumptively, his shunt has thrombosed. Two cases have developed encephalopathy, one following a late portal vein thrombosis, and he has died four years postoperatively. The remaining cases have done very well. The operation is technically demanding, but it can be done with relatively little blood loss. We had three cases with multiple vascularized abdominal adhesions, and they averaged blood replacement of four units apiece. The remaining 9 cases averaged less than two units of blood per patient. Some technical points may be worth emphasizing. We approach the splenic vein from below in the base of the transverse mesocolon. We clamp all retroperitoneal tissues before we divide them. We use magnification in the dissection of the splenic vein and the performance of the venovenous anastomosis. We take great care to ensure that we have a large opening. It's very easy to purse-string this anastomosis using a monofilament suture. We take pressures, and if there is any more than two or 3 mm pressure differential across the anastomosis, we take it down and do it again. It is our feeling that the Warren procedure is indicated in portal hypertension, with bleeding esophageal varices, unless there is a positive indication for decompressing the liver or for removing the spleen. We employ it in cases of portal venous occlusion; and it's interesting to see some reports coming out of late bad effects in children with this disorder in whom more standard types of

The effect of the distal splenorenal shunt on hypersplenism.

The Effect of the Distal Splenorenal Shunt on Hypersplenism DUANE G. HUTSON, M.D., ROBERT ZEPPA, M.D., JOE U. LEVI, M.D., EUGENE R. SCHIFF, M.D., ALAN...
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