The liver is very sensitive to hypoxia due to arterial hypoperfusion, which has been demonstrated in graft complications after liver transplantation (e.g., hepatic artery thrombosis, aneurysm), and can lead to serious complications such as severe biliary ischemic damage, graft loss, and even death of the recipient. Splenic arterial steal syndrome (SASS) is one of the lesser-recognized arterial complications after liver transplantation.The essence of SASS is that the large splenic artery “steals” hepatic arterial blood flow, resulting in poor hepatic arterial perfusion; without timely intervention, SASS can lead to serious graft complications. Without timely intervention, SASS can lead to serious graft complications. At present, the concept of “cirrhotic SASS” has not yet been formed in clinical practice, and its harmful effects have not yet been recognized. Cirrhotic SASS is the result of chronic liver disease and exacerbates the pathological process of liver damage. It is clinically nonspecific, and most often manifests as underlying liver disease combined with splenomegaly and other abnormalities. We confirmed the prevalence of SASS in patients with decompensated cirrhosis by three-dimensional CT angiography and angiography, and demonstrated that correction of SASS significantly improved liver function indexes, Child-Pugh scores, and ratings, and reduced the risk of gastrointestinal bleeding in cirrhotic patients. Therefore, this paper presents the concept of cirrhotic SASS for the first time in the international arena and confirms that SASS is an effective therapeutic target for improving liver function in patients with decompensated cirrhosis, and can be used as a bridging therapeutic measure for patients awaiting liver transplantation. Quan-Da Liu, Department of Hepatobiliary Surgery, General Hospital of the Rocket Force, People’s Liberation Army, China The concept of splenic arterial steal syndrome (SASS) is not new and has been sporadically reported in case reports in the literature of liver transplantation for 20 years [1-8]. SASS after liver transplantation was first proposed by Langer in Germany in 1990, and was first reported by Quan-Da Liu in China in 2003 [5-7]. The patient was diagnosed with “chronic rejection” after liver transplantation due to intractable abnormalities of liver and biliary enzyme profiles and biliary sludge and was treated with three ineffective hormonal shocks within two months (Figure 1). SASS can lead to serious consequences such as irreversible ischemic damage to the biliary tract and graft failure, but the concept and clinical dangers of SASS are still poorly understood by clinicians. In recent years, we have confirmed that SASS is also prevalent in patients with cirrhosis (especially in the decompensated stage) with splenomegaly, and at the same time, we have confirmed that SASS can be an important therapeutic target in cirrhosis, thus obtaining the effect of improving liver function [9]. 1. Splenic artery steal syndrome after liver transplantation 1.1 Definition of SASS after liver transplantation The essence of SASS is that the thick splenic artery “competes” with the hepatic artery for blood flow, resulting in poor perfusion of the hepatic artery and hypoxia of the graft cells. The biliary epithelium is more sensitive to hypoxia because the transplanted liver lacks arterial collateral circulation and the biliary system receives a single blood supply from the hepatic artery. Therefore, in addition to abnormalities in the enzyme profile of the hepatobiliary system, SASS after liver transplantation is clinically more often characterized by persistent progressive cholestasis and irreversible ischemic damage of the biliary tract. The phenomenon of arterial steal is most commonly seen in the splenic artery and occasionally in the gastroduodenal artery and left gastric artery. The incidence of SASS after liver transplantation has been reported in the literature to be up to 3.1-5.9% [2-4,7], and it has been analyzed to be much higher than reported [4]. Firstly, the clinical awareness of SASS is low; secondly, we and the literature statistics have excluded HAT cases, which is one of the important causes of acute hepatic artery thrombosis (HAT). We have had two successful cases of acute HAT occurring on the basis of SASS [7]. 1.2 Pathogenesis of SASS after liver transplantation The mechanism of SASS is not well understood, but it is recognized to be closely related to the hyperdynamic circulatory state of visceral blood flow, especially in the spleen and portal vein [8]. The liver receives a dual blood supply from the portal vein and the hepatic artery, and when portal venous flow (PVF) increases, hepatic arterial blood flow decreases, and vice versa, when PVF decreases, hepatic arterial blood flow increases (hepatic artery buffer response, HABR). In cirrhotic recipients, the visceral hyperhemodynamic state, such as splenomegaly and portal hypertension, is often present before surgery, and the hepatic artery resistance index is significantly increased; the recipient’s PVF can account for more than 90% of the total hepatic blood flow. According to the HABR principle, then hepatic artery blood flow is significantly reduced. This is the pathological basis for the “passive” portal hypertension and portal hyperperfusion that occurs in small-for-size grafts after adult living liver transplantation and split-reduced-volume liver transplantation [10]. In addition, cirrhotic graft recipients have abnormalities such as significant thickening of the splenic artery, accelerated blood flow, and splenic artery resistance that is significantly lower than that of the hepatic artery, which is the pathologic basis for the “active” robbing of blood flow by the splenic artery. Adequate hepatic artery blood flow is essential to maintain graft function. If persistent low arterial perfusion is not corrected, severe hepatic and biliary ischemic damage can occur. Especially when combined with factors such as rejection, endothelial damage, and recurrent hepatitis, the risk of serious complications such as irreversible biliary tract damage and graft loss after transplantation is greatly increased [2-7]. 1.3 Clinical manifestations of SASS after liver transplantation The clinical manifestations of SASS after liver transplantation are variable and nonspecific, but relatively mild compared to HAT. Clinically, it manifests in the early stage with persistent progressive hepatic impairment and recalcitrant cholestasis (Figure 1), and in the middle and late stages with serious consequences such as irreversible ischemic changes in the biliary tract and destruction of the biliary system (e.g., diffuse non-anastomotic bile duct stenosis), graft dysfunction, and even death of the recipients [2-8].Nussler et al. [3] reported only a small proportion (3/44, 6.8%) of mild SASS with no obvious Nussler et al [3] reported that only a small proportion (3/44, 6.8%) of mild SASS had no obvious clinical symptoms, and acute graft failure occurred in severe cases (13.6%); most (79.5%) developed symptoms within 3 months of transplantation; ischemic biliary destruction occurred in as many as 77.8% (7/9) of those who were diagnosed with SASS more than 3 months after transplantation. 1.4 Diagnosis and differential diagnosis of SASS after liver transplantation It is difficult to clinically differentiate SASS from early post-transplant rejection, organ preservation injury, and hepatitis recurrence [1-7]. One of the important reasons for this is the lack of awareness of SASS and its serious consequences among clinicians. When liver transplant recipients present with liver function abnormalities, they should first be differentiated and diagnosed from common complications such as rejection, hepatitis recurrence, and HAT.The diagnostic tools for SASS are color Doppler flow examination (CDFI), enhanced CT, and abdominal arteriography.The sensitivity of CDFI for monitoring hepatic arterial complications is 91%, and the specificity can be up to 99% [1]. Post-transplantation dynamic CDFI can provide timely information on hepatic hemodynamics. When CDFI suggests the presence of significant splenomegaly, splenic artery coarctation, high portal flow velocity/flow (portal flow velocity >25 cm/s or >1000 ml/min), while suggesting a weak hepatic artery flow spectrum (<35 cm/s) and a high resistance hepatic artery waveform, and a usual hepatic artery resistance index (RI) >0.8 Abdominal arteriography is considered to be the “gold standard” for the diagnosis of SASS (Figure 2) and is characterized by [1-7]: patent hepatic arteries with thin, slow flow and delayed peripheral arterial filling; and a large amount of arterial flow rapidly entering the abnormally thickened splenic arteries, with rapid splenic parenchyma filling. With the improvement of CT, especially three-dimensional CT revascularization (CTA) technology, enhanced CT and CTA can basically obtain the same results as abdominal arteriography. Therefore, we have recently relied more on CT and CTA to diagnose SASS [9] (Figure 3). 1.5 Treatment of SASS after liver transplantation SASS should be treated early once diagnosed. Treatment options include splenectomy, splenic artery ligation, and splenic artery coil embolization [1-7]; interstitial vascularization for reanastomosis of the hepatic artery and abdominal aorta has also been suggested. For those with definite or suspected preoperative SASS (e.g., presence of megasplenism, thickening of the splenic artery), concomitant splenic artery trunk ligation or bundling during transplantation is preferred, which can avoid postoperative splenic embolization or secondary splenectomy. For post-transplantation SASS, steel coil embolization of the main trunk of the splenic artery via femoral artery puncture is preferred, which is minimally invasive, safe, and avoids embolization complications such as splenic infarction. Splenectomy and interstitial vascular anastomosis for correction of SASS have higher surgical risks and complications, and are not routinely chosen. 2, Cirrhotic splenic artery steal syndrome 2.1 Pathogenesis of cirrhotic SASS The concept of cirrhotic SASS is rarely mentioned in the literature, much less confirmed in the literature. The pathophysiologic changes of cirrhotic SASS are exactly the same as those of SASS after liver transplantation, i.e., hypoxic damage to the liver parenchyma caused by low arterial perfusion of the liver.SASS is one of the major complications of decompensated cirrhosis. The abnormal features and manifestations of SASS, such as splenomegaly, thickening of the splenic artery, and hypersplenism (hypersplenism), are secondary to the long-term pathological changes of high intrahepatic vascular resistance, visceral hyperemia, and relatively low intra-splenic vascular resistance in cirrhotic patients. The cirrhotic liver is in fact in a significantly hypoxic pathological internal environment [11]: 1) 10-32% of patients with cirrhosis suffer from hepatopulmonary syndrome, which is characterized by diffuse intrapulmonary capillary dilatation resulting in an imbalance of ventilation-perfusion, thus leading to Systemic arterial hypoxemia; ② In addition, an important pathological change of cirrhosis, namely, endothelial capillarization of hepatic sinusoids (sinusoidal capillarization), which weakens the diffusion of oxygen from hepatic sinusoids to hepatocytes, leading to hepatic cell hypoxia, thus inhibiting the ability of hepatic cells to synthesize protein, energy metabolism, and regeneration, and so on. This is the basis of the “oxygen limitation theory” of cirrhosis; (3) The concept of cirrhotic SASS reveals that the highly dilated splenic artery “steals” blood flow originating from the celiac artery, which greatly reduces hepatic artery blood flow. that greatly reduces hepatic artery blood flow (Figure 3), thereby further exacerbating hepatic parenchymal hypoxia and hepatic impairment. Hepatocellular hypoxia is therefore an important pathologic alteration in the ongoing deterioration of liver function in cirrhotic patients. Recent studies of platelet function [12-14], suggest that thrombocytopenia in cirrhotic patients exacerbates hepatic fibrosis and impairs hepatic regenerative capacity. The concept of SASS, therefore, may partially explain a puzzle in clinical work: why cirrhosis and liver damage continue to progress slowly in patients with chronic viral liver disease after effective viral control [9]? 2.3 Diagnosis and management of cirrhotic SASS In cirrhotic patients, various “oxygenating” therapeutic measures can partially improve liver function [15].The concept of SASS provides a new therapeutic target for patients with decompensated cirrhosis, i.e., correction of SASS to achieve partial improvement of liver function. Our initial clinical results have confirmed the above concept [9]. For (decompensated) cirrhotic patients with combined splenomegaly and hypersplenism, we first used CTA to screen for cases consistent with the imaging features of SASS (Figure 3), and then chose abdominal arteriography to confirm the simultaneous implementation of splenic artery trunk coil embolization for correction of SASS (Figures 3,4). Since splenic artery embolization was not effective in correcting hypersplenism, we also jointly implemented splenic radiofrequency ablation to treat hypersplenism, except in patients with end-stage liver disease [9,15,16]. For patients at risk of bleeding from severe esophagogastric fundal varices, combined endoscopic sleeve/sclerotherapy was performed during hospitalization. The treatment results showed that, after the correction of SASS by blocking the main trunk of the splenic artery with microsteel rings, the caliber of the hepatic artery was significantly thickened, the blood flow was accelerated, and the hepatic perfusion in the arterial phase was significantly improved (Figs. 3,4); the various indexes of hepatic function, Child-Pugh scores, and ratings improved significantly [9]; the hypersplenism was also improved; the followup found improved regeneration of sclerotic livers, and an increase in the hepatic volume; and the same time, the significant reduced serious complications such as gastrointestinal bleeding associated with portal hypertension [15,16]. 3, Summary SASS is a relatively young and mysterious concept, yet a common and ignored phenomenon by hepatologists.SASS can lead to ischemic biliary damage in transplanted livers; SASS is also one of the causes of persistent liver function deterioration in cirrhotic patients. Therefore, increased awareness of SASS and early correction of SASS using appropriate means can avoid serious complications in transplanted livers; correction of SASS can also improve liver function in decompensated cirrhosis as a bridging therapeutic measure while waiting for liver transplantation [9,15,16].