LIVER TRANSPLANTATION 17:891-895, 2011

ORIGINAL ARTICLE

Hemodynamic Consequences of Spontaneous

Splenorenal Shunts in Deceased Donor Liver
Transplantation
Federico Castillo-Suescun, Gabriel C. Oniscu, and Ernest Hidalgo
Scottish Liver Transplant Unit, Royal Inrmary of Edinburgh, Edinburgh, United Kingdom

The presence of large spontaneous splenorenal shunts (SSRSs) is a risk factor for poor portal vein ow and liver dysfunction. The disconnection of splenorenal shunts by left renal vein (LRV) ligation has been suggested as a potential solution for
improving portal ow. We reviewed the hemodynamic consequences of splenorenal shunts in deceased donor liver transplantation and investigated the role of LRV ligation. In 10 patients who underwent liver transplantation at our institution
between January 2006 and April 2010, an SSRS was diagnosed preoperatively. Intraoperative portal and hepatic artery
ows were measured with a transit time owmeter. The shunt was disconnected in 6 patients for whom the portal ow after
reperfusion was less than or equal to 1200 mL/minute. LRV ligation resulted in signicant increases in the portal ow. There
were no differences in renal function for the patients who underwent renal vein ligation and the patients who did not
undergo ligation. In conclusion, LRV ligation disconnects splenorenal shunts and modulates the portal inow without any
detrimental effects on renal function. Liver Transpl 17:891-895, 2011. V 2011 AASLD.
C

Received August 18, 2010; accepted March 5, 2011.

Portal hypertension leads to the development of an

extensive network of portosystemic collateral vessels.
In 5% to 12% of patients, these collaterals include
spontaneous splenorenal shunts (SSRSs).1-4 In
advanced stages of chronic liver disease, the portal
vein (PV) ow may become hepatofugal, and this may
lead to a portal steal phenomenon with a dramatic
decrease in hepatic perfusion.3,5-9 Not infrequently,
this is associated with PV thrombosis.10-12
However, large portosystemic shunts such as SSRSs
may jeopardize the portal ow and lead to graft dysfunction due to portal hypoperfusion.13
The optimal surgical approach to SSRSs has not
been well dened.14 In order to determine when these
shunts should be closed to prevent portal
hypoperfusion, portal ow and portal pressure measurements should be obtained before and after reper-

fusion.15 Because of the buffer response, this should

be correlated with measurements of the hepatic artery
(HA) ow16 to provide a full assessment of the consequences of SSRS disconnection by left renal vein
(LRV) ligation.
We present a series of SSRS patients undergoing
orthotopic liver transplantation for whom intraoperative hemodynamic measurements were obtained.

PATIENTS AND METHODS

From January 2006 to April 2010, 263 adult liver
transplants were performed in our unit. Ten patients
(3.8%) were found to have an SSRS during the preoperative assessment. All patients who were assessed
for liver transplantation in our program underwent

Abbreviations: ALD, alcoholic liver disease; CT, computed tomography; DBD, donation after brain death; DCD, donation after cardiac death; HA, hepatic artery; HCV, hepatitis C virus; IVC, inferior vena cava; LRV, left renal vein; MELD, Model for End-Stage
Liver Disease; PBC, primary biliary cirrhosis; PV, portal vein; SSRS, spontaneous splenorenal shunt.
This article was presented at the 16th Annual International Congress of the International Liver Transplantation Society
(Hong Kong, 2010).
Address reprint requests to Ernest Hidalgo, M.D., Ph.D., FRCS Ed., Scottish Liver Transplant Unit, Royal Inrmary of Edinburgh, 51 Old
Dalkeith Road, Edinburgh, United Kingdom EH14 4SA. E-mail: ernest.hidalgo@luht.scot.nhs.uk
DOI 10.1002/lt.22304
View this article online at wileyonlinelibrary.com.
LIVER TRANSPLANTATION.DOI 10.1002/lt. Published on behalf of the American Association for the Study of Liver Diseases

C 2011 American Association for the Study of Liver Diseases.

V

The ow measurements are shown in Table 2. The PV

ow increased signicantly from a mean of 203 mL/
minute (range 50-525 mL/minute) in the native PV
(data not shown) to a mean of 1173 mL/minute (range
300-1670 mL/minute) after graft reperfusion. When
the LRV was occluded, the PV ow increased further
in all cases but one; the mean ow was 2077 mL/minute (range 1245-3460 mL/minute).
Initially, the decision to ligate the LRV was made
shortly after portal reperfusion and before the arterial

No
HCV
18
Complete
ALD
16
No
PBC
29
No
ALD
12
No
ALD
13
No
ALD
14
No
ALD
23
Complete
Cryptogenic
9
No
ALD
10

Partial
Autoimmune
19

65
DCD
Whole
45
DBD
Whole
65
DBD
Whole
66
DBD
Whole
61
DBD
Whole
51
DBD
Whole
57
DBD
Whole
55
DBD
Split
67
DBD
Whole

Patient 6
Patient 5
Patient 4
Patient 3
Patient 2

55
DBD
Whole

RESULTS

Patient 1

routine Doppler ultrasound and triple-phase abdominal computed tomography (CT) examinations. CT
scanning was performed with a Toshiba Aquilion 16
CT scanner (a 1-mm slice thickness was used for
reconstruction of the arterial and venous phases). The
contrast agent Omnipaque (300 mL) was used. The
degree of collateralization and the presence of SSRSs
were determined during the portal venous phase of
the scan (60 seconds after the contrast injection;
Fig. 1); an SSRS was dened as a communication
with a diameter greater than 1 cm. The main
demographic data are shown in Table 1. The latest
follow-up data were recorded by August 1, 2010.
Institutional Review Board approval is not required.
Nine patients received a full graft, and 1 patient
received a split graft [an extended right lobe with segments I and IV-VIII, the main PV, the right HA, and the
entire inferior vena cava (IVC), including the middle and
right hepatic veins, with a graft-to-recipient weight ratio
of 1.6]. One graft was from a donation after cardiac
death (DCD) donor. We measured native and postreperfusion ows in the HA, PV, and portocaval shunt with a
transit time owmeter (MediStim, Oslo, Norway). PV
and HA measurements were obtained and recorded for
a non-SSRS cohort of 100 adult liver transplant recipients. The mean PV ow before the abdomen was closed
was 1740 mL/minute, with only 10% of the cases having a ow less than or equal to 1200 mL/minute. The
mean HA ow in these patients was 262 mL/minute.
On the basis of these data and presumptive physiological data,17-19 the LRV was ligated when the PV ow after
reperfusion was less than or equal to 1200 mL/minute.

Patient 7

CT image of an SSRS.

TABLE 1. Preoperative Demographics

Figure 1.

Patient 8

Patient 9

Patient 10

LIVER TRANSPLANTATION, August 2011

Recipient
age (years)
Type of donor
Type of graft
Pretransplant
PV thrombosis
Indication
MELD score
Hepatopulmonary
syndrome
Encephalopathy

892 CASTILLO-SUESCUN, ONISCU, AND HIDALGO

*LRV ligation.
Not obtained.

HA ow after reperfusion (mL/minute)

HA ow after reperfusion with LRV
clamping (mL/minute)

2000
Yes

2500
Yes

1990
No

1670

Partial

Patient 3

2331
Yes

1024

No

Patient 4

3460
No

1560

No

Patient 5

2110
No

1370

No

Patient 6

1245
Yes

837

No

Patient 7

254
160

98

Patient 5

480

Patient 4*

120

Patient 3

120

180

Patient 6

175

440

Patient 7*

120

Patient 9

1390
No

1400

Complete

314

255

Patient 9

1400
Yes

1200

No

Patient 8

Patient 8*

TABLE 3. Changes in the HA Flow in Response to LRV Clamping

300

Patient 2
Complete

No

Patient 1

*LRV ligation before PV reperfusion.

Pretransplant PV thrombosis
PV ow after
reperfusion (mL/minute)
PV ow after reperfusion with
LRV clamping (mL/minute)
LRV ligation

TABLE 2. Flow Measurements

243

300

Patient 10*

2350
Yes

1200

No

Patient 10

175

289

Mean

2077
6/10

1173

Mean

LIVER TRANSPLANTATION, Vol. 17, No. 8, 2011

CASTILLO-SUESCUN, ONISCU, AND HIDALGO 893

894 CASTILLO-SUESCUN, ONISCU, AND HIDALGO

Figure 2. Comparison of the mean serum creatinine levels of

patients with shunt ligation and patients without shunt ligation.

anastomosis. For this reason, HA ows (Table 3) after

LRV clamping are missing for patients 1 and 2.
Patient 2 had almost complete PV thrombosis, and
after hepatectomy and thrombectomy, the LRV was
disconnected before liver implantation to ensure an
optimal ow at the time of reperfusion. In those
patients for whom the arterial anastomosis had been
completed before the occlusion of the LRV, the arterial
ow decreased in response to the clamping from
289 (open LRV) to 175 mL/minute (clamped LRV;
Table 3).
Overall, 6 of the 10 patients underwent LRV ligation. Patient 2 underwent retransplantation for HA
thrombosis. This was related not to the LRV ligation
but instead to an on-table thrombosis due to a hilar
injury during organ procurement that was not amenable to reconstruction.
Currently, 9 of the 10 patients are alive with no evidence of further PV complications. LRV ligation had
no impact on renal function; the postoperative serum
creatinine levels of the patients with LRV ligation and
the patients without LRV ligation were comparable, as
shown in Fig. 2.

DISCUSSION
Patients with chronic liver disease develop portal
hypertension, which opens portocaval communications such as SSRSs. The incidence of radiologically
diagnosed SRSSs in our group was 3.8%, although a
much higher incidence has been reported in patients
with cirrhosis.20
In this series, the presence of an SSRS was almost
invariably associated with a reduction in the PV ow.
Furthermore, 3 of the 10 patients had PV thrombosis
(which was complete for 2 patients).
An almost 2-fold increase was noted when the
shunt was occluded by LRV clamping. This effect was
reversible. When HA measurements were carried out,
the increase in the PV ow was followed by a reduc-

LIVER TRANSPLANTATION, August 2011

tion in the HA ow. The presence and degree of the

arterial buffer response16 are important considerations when one is deciding whether an SRSS needs to
be disconnected. A signicant reduction in the HA
ow may lead to an increased risk of biliary complications,21 although meaningful conclusions cannot be
drawn from this small series.
Although there is not strong evidence to suggest
that these shunts should be routinely closed after
reperfusion, it seems reasonable to assume that the
PV ow should be at least 1000 mL/minute.22-24 We
decided to occlude the LRV when the ow was less
than or equal to 1200 mL/minute. Only 2 studies
using a transit time owmeter (MediStim) and
addressing the same topic in whole liver transplantation have been reported previously.8,22 The authors
reported an increase in the PV ow after the disconnection of the portosystemic shunts, and this was
consistent with our observations.

ACKNOWLEDGMENTS
We acknowledge that this is a small, uncontrolled case
series and that a further evaluation of LRV ligation,
ideally in a randomized study, should be undertaken.
This study does suggest, however, that LRV ligation is
safe and produces an increase in the PV ow. We were
able to restore physiological PV ows and avoid potential complications due to poor portal ows (particularly
PV thrombosis). Although this does not translate into a
different transplant outcome, further studies of hemodynamics in deceased liver transplantation and the
implications for long-term outcomes are warranted.

REFERENCES
1. Bosch J, Pizcueta P, Feu F, Fernandez M, Garcia-Pagan
JC. Pathophysiology of portal hypertension. Gastroenterol Clin North Am 1992;21:1-13.
2. Bosch J, Navasa M, Garcia-Pagan JC, DeLacy AM, Rodes
J. Portal hypertension. Med Clin North Am 1989;73:
931-953.
3. De Carlis L, Del Favero E, Rondinara G, Belli LS, Sansalone CV, Zani B, et al. The role of spontaneous portosystemic shunts in the course of orthotopic liver
transplantation. Transpl Int 1992;5:9-14.
4. Rousselot LM, Moreno AH, Panke WF. Studies on portal
hypertension. IV. The clinical and physiopathologic signicance of self-established (nonsurgical) portal systemic
venous shunts. Ann Surg 1959;150:384-412.
5. Kita Y, Harihara Y, Sano K, Hirata M, Kubota K,
Takayama T, et al. Reversible hepatofugal portal ow after liver transplantation using a small-for-size graft from
a living donor. Transpl Int 2001;14:217-222.
6. Sekido H, Matsuo K, Takeda K, Morioka D, Kubota T,
Tanaka K, et al. Severe fatty change of the graft liver
caused by a portosystemic shunt of mesenteric varices.
Transpl Int 2002;15:259-262.
7. Fujimoto M, Moriyasu F, Nada T, Suginoshita Y, Ito Y,
Nishikawa K, et al. Inuence of spontaneous portosystemic collateral pathways on portal hemodynamics in living-related liver transplantation in children. Doppler
ultrasonographic study. Transplantation 1995;60:41-45.
8. Margarit C, Lazaro JL, Charco R, Hidalgo E, Revhaug A,
Murio E. Liver transplantation in patients with

LIVER TRANSPLANTATION, Vol. 17, No. 8, 2011

9.

10.

11.

12.

13.

14.

15.

16.

17.

splenorenal shunts: intraoperative ow measurements to

indicate shunt occlusion. Liver Transpl Surg 1999;5:35-39.
Lee SG, Moon DB, Ahn CS, Kim KH, Hwang S, Park KM,
et al. Ligation of left renal vein for large spontaneous splenorenal shunt to prevent portal ow steal in adult living
donor liver transplantation. Transpl Int 2007;20:45-50.
Nonami T, Yokoyama I, Iwatsuki S, Starzl TE. The incidence of portal vein thrombosis at liver transplantation.
Hepatology 1992;16:1195-1198.
Chiu KC, Sheu BS, Chuang CH. Portal venous ow pattern as a useful tool for predicting esophageal varix bleeding in cirrhotic patients. Dig Dis Sci 2005;50:1170-1174.
Hidajat N, Stobbe H, Griesshaber V, Schroder RJ, Felix
R. Portal vein thrombosis: etiology, diagnostic strategy,
therapy and management. Vasa 2005;34:81-92.
Sadamori H, Yagi T, Matsukawa H, Matsuda H, Shinoura
S, Umeda Y, et al. The outcome of living donor liver
transplantation with prior spontaneous large portasystemic shunts. Transpl Int 2008;21:156-162.
Perkins JD. Techniques to ensure adequate portal ow
in the presence of splenorenal shunts. Liver Transpl
2007;13:767-768.
Rasmussen A, Hjortrup A, Kirkegaard P. Intraoperative
measurement of graft blood owa necessity in liver
transplantation. Transpl Int 1997;10:74-77.
Lautt WW, Legare DJ, Ezzat WR. Quantitation of the hepatic arterial buffer response to graded changes in portal
blood ow. Gastroenterology 1990;98:1024-1028.
Wynne HA, Cope LH, Mutch E, Rawlins MD, Woodhouse
KW, James OF. The effect of age upon liver volume and
apparent liver blood ow in healthy man. Hepatology
1989;9:297-301.

CASTILLO-SUESCUN, ONISCU, AND HIDALGO 895

18. Sainz-Barriga M, Reyntjens K, Costa MG, Scudeller L,

Rogiers X, Wouters P, et al. Prospective evaluation of
intraoperative hemodynamics in liver transplantation
with whole, partial and DCD grafts. Am J Transplant
2010;10:1850-1860.
19. Troisi R, Ricciardi S, Smeets P, Petrovic M, Van Maele G,
Colle I, et al. Effects of hemi-portocaval shunts for inow
modulation on the outcome of small-for-size grafts in living donor liver transplantation. Am J Transplant 2005;5:
1397-1404.
20. Tarantino G, Citro V, Conca P, Riccio A, Tarantino M,
Capone D, et al. What are the implications of the spontaneous spleno-renal shunts in liver cirrhosis? BMC Gastroenterol 2009;9:89.
21. Hashimoto K, Miller CM, Quintini C, Aucejo FN, Hirose
K, Uso TD, et al. Is impaired hepatic arterial buffer
response a risk factor for biliary anastomotic stricture in
liver transplant recipients? Surgery 2010;148:582-588.
22. Aucejo FN, Hashimoto K, Quintini C, Kelly D, Vogt D,
Winans C, et al. Triple-phase computed tomography and
intraoperative ow measurements improve the management of portosystemic shunts during liver transplantation. Liver Transpl 2008;14:96-99.
23. Henderson JM, Gilmore GT, Mackay GJ, Galloway JR,
Dodson TF, Kutner MH. Hemodynamics during liver
transplantation: the interactions between cardiac output
and portal venous and hepatic arterial ows. Hepatology
1992;16:715-718.
24. Paulsen AW, Klintmalm GB. Direct measurement of hepatic blood ow in native and transplanted organs, with
accompanying systemic hemodynamics. Hepatology
1992;16:100-111.