International Journal of Surgery 12 (2014) 1228e1234
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Splenic artery syndrome after orthotopic liver transplantation: A review Soniya Pinto a, Shilpa N. Reddy b, *, Mindy M. Horrow b, Jorge Ortiz c a
University of Illinois Chicago, Metropolitan Group Hospitals, Department of Surgery, 836 W. Wellington Ave, Room 4807, Chicago, IL 60657, USA Einstein Medical Center, Department of Radiology, 5501 Old York Road, Philadelphia, PA 19141, USA c University of Toledo, Department of Surgery and Transplant, 2801 W B Bancroft St., Toledo, OH 43606, USA b
h i g h l i g h t s We We We We
summarize the pathophysiology and epidemiology of Splenic Artery Syndrome (SAS). discuss the clinical, laboratory, and diagnostic features commonly seen in SAS. review treatment options for SAS that have been performed to date. summarize current data regarding the utility of prophylaxis for SAS.
a r t i c l e i n f o
a b s t r a c t
Article history: Received 7 March 2014 Received in revised form 16 September 2014 Accepted 29 September 2014 Available online 12 October 2014
Splenic Artery Syndrome (SAS) has emerged as a controversial cause for graft ischemia in orthotopic liver transplant (OLTx) recipients. A complex combination of factors including hepatic artery hypoperfusion and portal hyperperfusion can result in SAS. Clinical and laboratory ﬁndings suggest graft ischemia but are generally non-speciﬁc. Conventional angiography ﬁndings of hepatic artery hypoperfusion with early and rapid ﬁlling of the splenic artery are suggestive of the diagnosis in the appropriate clinical setting. Treatment involves proximal splenic artery embolization, surgical splenic artery ligation, or in extreme cases, splenectomy. Most patients with SAS improve clinically following treatment. However, no randomized control trials are available to compare treatment options. Identiﬁcation of at risk patients with pre-operative CT scans and intra-operative ultrasound has been proposed by some and may allow for prophylactic treatment of SAS. © 2014 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
Keywords: Transplant Liver Steal Splenic Hypoperfusion
1. Introduction Vascular complications, especially those related to the hepatic artery, are well-recognized causes of graft failure in the early postoperative period following OLTx. Hepatic Artery Thrombosis (HAT) [1e3] and Hepatic Artery Stenosis (HAS) [4,5] may warrant revascularization or in certain cases, re-transplantation [6,7]. Over the past couple decades, Splenic Artery Syndrome (SAS) has emerged as a controversial cause of hepatic artery hypoperfusion leading to graft ischemia [8e10]. SAS describes a decrease in hepatic artery blood ﬂow in the absence of HAS and HAT, and is commonly associated with increased blood ﬂow through an enlarged splenic
Abbreviations: SAS, Splenic Artery Syndrome; OLTx, Orthotopic Liver Transplant; CT, Computed Tomography; DUS, Doppler Ultrasound. * Corresponding author. E-mail addresses: [email protected]
, [email protected]
(S.N. Reddy). http://dx.doi.org/10.1016/j.ijsu.2014.09.012 1743-9191/© 2014 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
artery . Consequences of SAS include early graft dysfunction and biliary ischemia occasionally leading to re-transplantation [8e10]. Several studies have reported successful treatment of SAS and functional restoration of the graft with splenic artery embolization [11,12]. Other studies have stressed the importance of pretransplant evaluation and intervention to prevent SAS in an attempt to reduce post-transplant complications and irreversible graft dysfunction [13,14]. Our review summarizes the pathophysiology, epidemiology, diagnosis and available treatment options, and possible prevention strategies of SAS. 2. Pathophysiology SAS is a poorly understood and controversial cause of nonocclusive hepatic arterial hypoperfusion in OLTx recipients. The entity was initially described by Manner et al., in 1991 as a true arterial ‘steal’ resulting in preferential diversion of blood ﬂow away from the hepatic artery and towards the splenic artery . These
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initial observations were predominantly supported by conventional angiography demonstrating rapid and preferential ﬁlling of either the splenic artery, or less commonly the gastroduodenal artery (GDA), at the expense of the hepatic artery [8,15]. However, in 2008, Quintini et al. proposed that portal venous hyperperfusion, and not splenic artery steal, was primarily responsible for SAS . Through the use of DUS, Quintini's group not only interrogated dynamic changes in systemic blood supply to the liver but also assessed changes in portal venous ﬂow. Their work suggested that portal hyperperfusion caused sinusoidal injury in liver transplants through two main mechanisms: 1) direct damaging effect of elevated portal venous pressures and 2) hepatic arterial hypoperfusion caused by the hepatic artery buffer response (HABR) . HABR refers to physiologic auto-regulation of the systemic and splanchnic circulations of the liver with respect to maintaining adequate hepatic blood ﬂow . Adenosine, a strong vasodilator, has generally been accepted as the key in this auto-regulatory pathway . It is hypothesized that adenosine is constantly released into spaces surrounding hepatic arterioles and portal venules. When portal ﬂow decreases, there is decreased washout of adenosine and increased adenosine concentration, leading to hepatic arterial vasodilation and increased hepatic arterial ﬂow. Conversely, in the setting of increased portal venous ﬂow, there is accelerated washout of adenosine, leading to hepatic artery vasoconstriction and decreased hepatic arterial ﬂow. The reason for portal venous hyperperfusion in post-transplant patients is not entirely clear. A discrepancy between the sizes of the transplant liver relative to the portal vein, as seen in undersized split grafts (also referred to as Small for Size Syndrome), has been implicated in portal venous hyperperfusion . Despite important observations made by Quintini's group, they failed to prove causality and the pathophysiology of SAS remains controversial. In 2012, Saad challenged the portal hyperperfusion theory, arguing that increased portal venous ﬂow may simply occur in response to primary hepatic arterial hypoperfusion . Saad pointed out that treating SAS with GDA coiling in cases of GDA ‘steal’ was effective even though it had little impact on portal venous perfusion . Saad concluded that while portal hyperperfusion and HABR are likely partly responsible for development of SAS, no study has established causality as of yet and the hemodynamics affecting liver transplant perfusion are complex and multifactorial . 3. Epidemiology The reported incidence of SAS in OLTx recipients ranges from 0.6% to 10.1% . This wide range is related in part to whether SAS is actually recognized as a post-transplant complication. Saad contends that SAS is “probably under-recognized in certain institutions (particularly in the United States and Japan), and it is probably over-diagnosed in others (particularly in Germany and Austria)” . Unfortunately, little data is available to determine if the risk of developing SAS depends on donor or recipient demographics, which may vary by region and country. 4. Clinical presentation SAS is a diagnosis of exclusion and should only be considered in the absence of cellular rejection, infection, and toxicity. Clinical features are non-speciﬁc ranging from a complete absence of symptoms to acute graft failure [11,12]. Of the 113 patients with SAS reported in the literature, 109 presented with transaminitis and decreased hepatic function with or without biliary ischemia and cholestasis (Table 1). Alanine/Aspartate Transaminases (AST/ALT) levels can be as high as 1520/1275 U/L and gammaglutamyl
transpeptidase levels are also often elevated [9,12,19]. Mild elevations in alkaline-phosphatase can be seen [11,12]. Nussler et al. reported the varying degrees of liver dysfunction including 6 of 44 patients presenting with acute graft failure . Occasionally, recurrent ascites may be the primary presentation of graft dysfunction. Patients usually have moderate to massive splenomegaly, which can further contribute to SAS [20,21]. Reports of leukopenia and thrombocytopenia in SAS patients are other signs of symptomatic hypersplenism [20,21]. If transplant biopsy is performed, histological analysis often reveals mild inﬂammation in SAS as opposed to the overt ﬁndings in acute rejection [22,23]. While SAS may develop any time from the immediate postoperative period to 5.5 years following transplantation (Table 1), the majority of patients are diagnosed within 2 months of transplantation . 5. Diagnostic imaging DUS is the initial test of choice for vascular and biliary complications in OLTx recipients given its availability, portability, and lack of ionizing radiation. Evaluation of hepatic artery velocity, waveforms, and particularly vascular resistance is helpful for determining the cause of hypoperfusion. The resistive index (RI), deﬁned by the formula; RI ¼ (Peak systolic velocity End diastolic velocity)/Peak systolic velocity helps differentiate SAS from HAS and HAT with collateralization. In HAS, very high velocities can be seen at the site of stenosis with a low resistance “parvus tardus” waveform distal to the site of stenosis [21,24,25]. In contrast, patients with SAS exhibit a high-resistance hepatic artery waveform with low diastolic ﬂow or reversal of diastolic ﬂow. The RI in the hepatic artery of patients with SAS is usually greater than 0.8 (Fig. 1a) and diastolic ﬂow may occasionally be reversed [9,11,26]. In addition, hepatic artery systolic velocities are unusually low ( 100 IU/L (27) Elevated GGTb > 200 IU/L (32) Bilirubin >2 mg/dL (27) Biliary tract destruction (12) No symptoms (3)
Unsuccessful treatment Post-intervention (successfully treated ptsa) Graft artery ﬂow on DUS 525 mL/min Transaminases back to baseline within 5 days Normalization of liver function; No objective data provided
Complications of treatment
None reported None reported None reported None reported Portal vein Graft failure thrombosis (3) (7 pts, all with distal splenic Sepsis artery coiling) requiring splenectomy (9) Sepsis with death (5) All of the above patients had distal splenic artery coiling None reported None reported
Elevated AST, ALT, and GGTb (no objective data provided) Elevated AST, ALT, bilirubin (no objective data provided)
Correction of elevated liver enzymes (no objective data provided) Improved liver function tests and liver enzymes (no objective data provided)
Mean AST 38.4 ± 28.8 IU/L Decrease in bilirubin P < 0.001 Recovery of platelets P < 0.017 Median peak systolic Median peak systolic velocity in hepatic artery: velocity in 65 cm/s (P < 0.05) hepatic artery: 47 cm/s Hepatic artery Hepatic artery diameter: 3.7 ± 0.5 mm diameter: 2.5 ± 0.3 mm Portal vein Portal vein velocity velocity 851 ± 78 cm/s 962 ± 47 cm/s Portal vein Portal vein volume volume 55 ± 8 cm/s 76 ± 6 cm/s Clinical measures Elevated AST/ALT, poor not reported graft function, unspeciﬁed
None reported None reported
Mean AST 233.7 ± 227.8 IU/L Mean bilirubin 3.1 ± 2.3 mg/dL
None reported None reported
None reported None reported
None reported None reported
None reported None reported
symptoms (Table 3). A few studies have investigated the utility of prophylactic SAS treatment. The most common procedures performed for prophylactic SAS treatment are intra-operative splenic artery ligation or banding, and pre-operative splenic artery embolization (Table 3). Other prophylactic treatment options include aortohepatic bypass grafting and arcuate ligament division  Only one randomized control trial has been reported, which found that preoperative proximal splenic artery embolization in patients with severe portal hypertension prevented post-transplant
hepatic hypoperfusion and led to decreased operative time and blood loss . Mogl et al. also reported a decreased risk of complications in patients who underwent SAS prophylaxis relative to patients who were treated for SAS post-operatively. They argued that even when SAS was recognized and treated promptly, outcomes were better with prophylactic treatment . Interestingly, Mogl's group reported 2 patients who developed SAS despite prophylactic splenic artery banding, suggesting that prophylactic measures are not 100% effective in preventing SAS . It should
S. Pinto et al. / International Journal of Surgery 12 (2014) 1228e1234
Table 3 Prophylactic treatment of SAS. Author (year published)
Ptsa selected to undergo prophylaxis
Criteria for prophylaxis
Post-treatment events (number of ptsa)
Clinical outcomes of prophylaxis relative to no prophylaxis
Nussler et al. (2002)
Hypersplenism and enlarged splenic artery
Splenic artery ligation (15) Splenic artery banding (82)
Splenectomy (1) Portal vein thrombosis (1) Death due to sepsis and multi-organ failure (2)
Mogl et al. (2010)
Hypersplenism, dominant splenic artery branch relative to other celiac branches
Splenic artery ligation (78) Splenic artery banding (20)
Umeda et al. (2011)
Splenic artery embolization 12e18 h before transplantation
SAS (2) Splenectomy (1) Re-operation for bleeding due to ligation (1) Biliary tract complications (3) Re-OTLTx (12) Graft failure due to small for size syndrome (1)
Splenic artery banding and ligation can prevent development of SAS; Splenic artery ligation was seen to have greater morbidity and mortality than banding Rate of complications related to prophylaxis is lower than that seen in patients following embolization treatment for SAS
Wojcicki et al. (2012)
Decreased hepatic artery mean arterial pressure compared to radial artery
Intraoperative splenic artery ligation (5) Arcuate ligament division (1) Aortohepatic bypass grafting (1)
Patients with prophylactic treatment had decreased blood loss, shorter operation time, signiﬁcantly less ascites post-op, and signiﬁcantly lower mortality rate compared to no prophylaxis group Normalization of arterial inﬂow pressure to graft (7)
also be noted that prophylactic treatments can have signiﬁcant complications including the need for splenectomy, sepsis and reoperation for hemorrhage related to arterial ligation (Table 3). If prophylactic treatment is performed, intra-operative treatment is generally preferred since pre-operative procedures increase morbidity . Selection of an appropriate intra-operative strategy depends on the status of the recipient common hepatic artery. If the common hepatic artery is atrophic, modiﬁed vascular anastomoses may help prevent SAS. Anastomosing the donor hepatic artery with the recipient aorta via an iliac artery or with the splenic artery can be effective in preventing SAS . However, these techniques are technically demanding and HAT is a potential complication . In addition, an adequate conduit may not be immediately available for the interposition graft. If the recipient hepatic artery is adequate, a traditional donor to recipient anastomosis may be performed and splenic artery banding or ligation may be considered for prophylaxis of SAS .
Ethical approval None required. Financial support None. Author contribution Soniya Pinto M.B, B.S. e Data collection and writing. Shilpa Reddy, MD e Data collection and writing. Mindy Horrow MD e Data and Image collection and writing. Jorge Ortiz, MD e Study Design. Conﬂicts of interest None.
8. Conclusion Splenic Artery Syndrome may cause hepatic arterial hypoperfusion leading to ischemic biliary lesions and ultimately graft failure if not detected and treated promptly. Clinical and laboratory features are non-speciﬁc. The diagnosis is most reliably established on conventional angiography, though ultimately is only conﬁrmed by successful treatment. CEUS is a potential non-invasive alternative diagnostic modality. Minimally invasive interventional techniques are preferred over surgical treatment because of fewer complications. Identiﬁcation of high-risk candidates with preoperative CT may allow preemptive operative strategies or heightened post-operative surveillance. Hopefully an increased awareness of Splenic Artery Syndrome will improve outcomes after orthotopic liver transplantation.
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