Quintini Cristiano, Hirose Kenzo, Hashimoto Koji, Diago Teresa, Aucejo Federico, Eghtesad Bijan, Vogt David, Pierce Gregory, Baker Mark, Kelly Dympna, Miller Charles M
Department of General Surgery, Liver Transplant Center, Cleveland, OH 44195, USA.
Liver Transpl. 2008 Mar;14(3):374-9. doi: 10.1002/lt.21386.
Splenic artery embolization (SAE) improves hepatic artery (HA) flow in liver transplant (OLT) recipients with so-called splenic artery steal syndrome. We propose that SAE actually improves HA flow by reducing the HA buffer response (HABR). Patient 1: On postoperative day (POD) 1, Doppler ultrasonography (US) showed patent vasculature with HA resistive index (RI) of 0.8. On POD 4, aminotransferases rose dramatically; his RI was 1.0 with no diastolic flow. Octreotide was begun, but on POD 5 US showed reverse diastolic HA flow with no signal in distal HA branches. After SAE, US showed markedly improved flow, RI was 0.6, diastolic flow in the main artery, and complete visualization of all distal branches. By POD 6, liver function had normalized. RI in the main HA is 0.76 at 2 months postsurgery. Patient 2: On POD 1, RI was 1.0. US showed worsening intrahepatic signal, with no signal in the intrahepatic branches and reversed diastolic flow despite good graft function. On POD 7, SAE improved the intrahepatic waveform and RI (from 1.0 to 0.72). Patient 3: Intraoperative reverse diastolic arterial flow persisted on PODs 1, 2, and 3, with progressive loss of US signal in peripheral HA branches. SAE on POD 4 improved the RI (0.86) and peripheral arterial branch signals. Patient 4: US on POD 1 showed good HA flow with a normal RI (0.7). A sudden waveform change on POD 2 with increasing RI (0.83) prompted SAE, after which the wave form normalized, with reconstitution of a normal diastolic flow (RI 0.68). In conclusion, these reports confirm the usefulness of SAE for poor HA flow but suggest that inflow steal was not the problem. Rather than producing an increase in arterial inflow, SAE worked by reducing portal flow and HABR, thereby reducing end-organ outflow resistance. Evidence of this effect is the marked reduction of the RI after the SAE to 0.6, 0.72, 0.86, and 0.68, in patients 1-4, respectively. SAE reduces excessive portal vein flow and thereby ameliorates an overactive HABR that can cause graft dysfunction and ultimately HA thrombosis.
脾动脉栓塞术（SAE）可改善存在所谓脾动脉盗血综合征的肝移植（OLT）受者的肝动脉（HA）血流。我们提出，SAE实际上是通过降低肝动脉缓冲反应（HABR）来改善HA血流的。患者1：术后第1天（POD 1），多普勒超声（US）显示血管通畅，HA阻力指数（RI）为0.8。在POD 4时，转氨酶急剧升高；其RI为1.0，无舒张期血流。开始使用奥曲肽，但在POD 5时，US显示HA舒张期血流反向，HA远端分支无信号。SAE后，US显示血流明显改善，RI为0.6，主动脉有舒张期血流，所有远端分支均可清晰显示。到POD 6时，肝功能恢复正常。术后2个月时，主HA的RI为0.76。患者2：在POD 1时，RI为1.0。US显示肝内信号恶化，肝内分支无信号，尽管移植肝功能良好，但仍有舒张期血流反向。在POD 7时，SAE改善了肝内波形和RI（从1.0降至0.72）。患者3：在POD 1、2和3时，术中持续存在舒张期动脉血流反向，HA外周分支的US信号逐渐消失。在POD 4时进行SAE改善了RI（0.86）和外周动脉分支信号。患者4：在POD 1时，US显示HA血流良好，RI正常（0.7）。在POD 2时，波形突然改变，RI增加（0.83），促使进行SAE，此后波形恢复正常，舒张期血流重建（RI 0.68）。总之，这些报告证实了SAE对HA血流不佳的有效性，但表明流入道盗血并非问题所在。SAE并非增加动脉流入量，而是通过减少门静脉血流和HABR起作用，从而降低终末器官的流出阻力。这种效应的证据是，在患者1 - 4中，SAE后RI分别显著降低至0.6、0.72、0.86和0.68。SAE减少了过多的门静脉血流，从而改善了可能导致移植功能障碍并最终导致HA血栓形成的过度活跃的HABR。
