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TO THE EDITORS:

We read with interest the article entitled “Contrast-Enhanced Ultrasound Diagnosis of Splenic Artery Steal Syndrome After Orthotopic Liver Transplantation” by Zhu et al.,[1] which was published in the August 2012 issue of Liver Transplantation. The authors report the value of contrast-enhanced ultrasound in the diagnosis of splenic artery steal syndrome (SASS) in patients who have undergone orthotopic liver transplantation (LT). Two hundred thirty-six of 274 patients who underwent LT were studied. Eight patients (3.4%) with reduced arterial flow on color Doppler flow imaging underwent contrast-enhanced ultrasound and were shown to have delayed arterial contrast wash-in enhancement, which supports a diagnosis of SASS. The diagnosis was confirmed by arteriography, which showed rapid splenic artery (SA) and delayed hepatic artery (HA) perfusion. SA embolization resulted in increased HA flow and decreased portal vein flow. In our opinion, arterial abnormalities such as a celiac trunk arcuate ligament and SASS are significant risk factors for postoperative arterial complications and are probably underestimated in patients who are candidates for LT. Thus, we are in complete agreement with the authors that this is an interesting topic and that the diagnosis can be made with this new imaging modality. However, we feel that the diagnosis should be made or considered preoperatively or intraoperatively rather than postoperatively. SASS is observed in patients with hypersplenism or portal hyperperfusion with a weak HA flow (buffer effect). These abnormalities are routinely sought in our practice, and the diagnosis can be suspected or made simply with a computed tomography (CT) scan when the SA is larger than the HA[2] or on the basis of the volume of the spleen.[3] If SASS is suspected, we intraoperatively evaluate the HA flow with and without SA occlusion. If the arterial flow improves during occlusion of the SA, the SA is ligated, or an arterial anastomosis is performed directly on the SA, especially if the recipient's HA is small and atrophied with the risk of subsequent anastomotic stenosis. We performed LT 115 times in the past 13 months, and 9 patients (8%) had confirmed SASS. The difference between the diameters of the SA at its curve and the common HA (SA diameter − HA diameter) was studied in 97 patients who underwent preoperative CT scanning or magnetic resonance imaging. The mean difference in the diameters was 6 mm (4-10 mm) for patients with SASS and 1 mm (−7 to 5 mm) for patients without SASS. For the 9 patients with confirmed SASS, the diagnosis was made intraoperatively in 8 cases; an arterial anastomosis was performed directly on the SA in 4 patients and on the HA in 4 patients associated with SA ligation. In 1 patient, the diagnosis was made postoperatively on the basis of a weak flow in the HA and biliary complications leading to SA embolization. In the subgroup of patients with an intraoperative diagnosis (n = 8), for 1 patient had retransplantation for delayed HA thrombosis (2 years after LT) probably related to misdiagnosed SASS, and 1 patient developed an arterial anastomotic pseudoaneurysm treated by embolization, but none developed splenic infarction. In the other subgroup (n = 106), 5 patients (5%) underwent an arcuate ligament section, and 5 (5%) developed postoperative arterial complications represented by anastomotic stenosis (n = 2), HA thrombosis (n = 2), or anastomotic pseudoaneurysm (n = 1). These complications were probably related to a misdiagnosed arcuate ligament (n = 1) and led to retransplantation [n = 2 (1 with an arcuate ligament)], angioplasty (n = 2), and pseudoaneurysm embolization (n = 1) with secondary fatal rupture. This strategy is probably more effective than postoperative screening alone, in which certain cases may be misdiagnosed or present as arterial thrombosis or anastomotic stenosis of unknown causes. Although the authors of this series reported 3 perioperative deaths, there were no reports on postoperative mortality, morbidity, primary graft nonfunction, or arterial or biliary complications. It should be noted that SA ligation is very effective in preventing SASS in most cases with fewer morbidities (eg, splenic infarction) in comparison with SA embolization.[4] We recommend a good preoperative arterial evaluation with a CT scan to prevent or treat these arterial abnormalities during LT and decrease the rate of arterial complications, which is still very high after LT.

  • Safi Dokmak, M.D.

  • Béatrice Aussilhou, M.D.

  • Jacques Belghiti, M.D.

  • Hepatobiliary and Pancreatic Surgery and Liver TransplantationBeaujon HospitalClichy, France

REFERENCES

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  2. REFERENCES
  • 1
    Zhu XS, Gao YH, Wang SS, Cheng Q, Ling Y, Fan L, et al. Contrast-enhanced ultrasound diagnosis of splenic artery steal syndrome after orthotopic liver transplantation. Liver Transpl 2012;18:966-971.
  • 2
    Mogl MT, Nüssler NC, Presser SJ, Podrabsky P, Denecke T, Grieser C, et al. Evolving experience with prevention and treatment of splenic artery syndrome after orthotopic liver transplantation. Transpl Int 2010;23:831-841.
  • 3
    Kirbas I, Ulu EM, Ozturk A, Coskun M, Harman A, Ogus E, Haberal M. Multidetector computed tomographic angiography findings of splenic artery steal syndrome in liver transplantation. Transplant Proc 2007;39:1178-1180.
  • 4
    Grieser C, Denecke T, Steffen IG, Avgenaki M, Fröhling V, Mogl M, et al. Multidetector computed tomography for preoperative assessment of hepatic vasculature and prediction of splenic artery steal syndrome in patients with liver cirrhosis before transplantation. Eur Radiol 2010;20:108-117.