Splenic Steal Syndrome Research Articles

Initial experience in direct graft perfusion assessment following orthotopic liver transplant

Objective: classical methods of determining arterial blood supply of the graft following orthotopic liver transplantation (OLT) reflect the presence of blood flow in the trunk and large branches of the A. hepatica, without the characteristic of completeness of blood filling of peripheral sections, which is very important for objective evaluation of function. The aim of this study is to establish the diagnostic value of a direct perfusion study (IFlow) of the graft. Materials and methods. From 1998 to 2019, 245 OLTs were conducted. From 2015 to 2019, arterial changes were detected in 24 (23%) patients after 104 OLTs. A perfusion study was performed in 9 patients with suspected arterial graft failure. According to the IFlow study, liver hypoperfusion due to stenosis and/or splenic steal syndrome was detected in 8 cases and became an indication for therapeutic intervention. Results. Hepatic stenting and/or splenic artery embolization was performed to improve arterial blood supply to the liver. Endovascular procedures performed restored the perfusion index from 0.24 (0.01–0.89) to 0.61 (0.35–0.98). Conclusion. Absence of ultrasound and multispiral computed tomography signs of arterial complications does not rule out the need for perfusion angiography. Perfusion angiography allows to objectify the angiography data and perform corrective intervention in good time.

Current understanding and management of splenic steal syndrome after liver transplant: A systematic review.

Splenic steal syndrome (SSS) is a condition that can occur after orthotopic liver transplant (OLT). However, limited information is available about this condition. A systematic literature search of studies performed through May 2016 was conducted to identify reports of angiographically confirmed SSS and its variants. All of the factors relevant to this disorder were collected and analyzed. A total of 219 cases of SSS and its variants were identified. The condition occurred in 4.7% of patients after OLT, and 93.7% of cases were diagnosed within the first 2 months after OLT. Conventional arteriography demonstrated nonocclusive hepatic artery hypoperfusion in all affected patients. Abnormal liver function was the most common clinical presentation, reported in 71.9% of cases. Less common presentations included thrombocytopenia, acute graft failure, and persistent ascites. On Doppler ultrasound, a high resistance index of the hepatic artery was present in 84.1% of patients. Increased spleen volume (≥829 mL) before OLT was suggestive of a potential risk for SSS. Splenic artery embolization (SAE) was performed in 94.7% of cases; this procedure immediately reversed flow abnormalities on Doppler ultrasound and improved liver function tests in 96.3% of cases. The risk factors and potential etiologies of SSS remain largely unknown. Future studies should investigate the possible role of pre-OLT portal hypertension and portal hyperperfusion after OLT in the development of this syndrome. Collecting intraoperative hemodynamic data and performing Doppler ultrasound screening after OLT could potentially help clinicians to identify patients at high risk of arterial hypoperfusion and prevent potential complications from hepatic artery hypoperfusion.

Role of Doppler Sonography in Early Detection of Splenic Steal Syndrome.

To retrospectively investigate the role of Doppler sonography in the early detection of splenic steal syndrome. Fifty cases of splenic steal syndrome after orthotopic liver transplantation were identified. A control group was matched to the splenic steal syndrome group. Information was collected about the clinical presentation, liver enzyme levels, Doppler sonographic results, and follow-up after patients underwent splenic artery embolization. A persistent hepatic arterial diastolic reversal waveform was observed in 25 patients with splenic steal syndrome versus 0 control patients. The mean hepatic arterial resistive index (RI) values ± SD were 0.95 ± 0.09 in patients with splenic steal syndrome and 0.80 ± 0.10 in control patients (P < .0001). One week after orthotopic liver transplantation, the area under the receiver operating characteristic curve for the RI was 0.884 (95% confidence interval, 0.793-0.975; P = .001) for splenic steal syndrome diagnosis. After splenic artery embolization, there was normalization of the reversal waveform, with an average RI of 0.77 ± 0.11 (P < .0001). Dynamic changes in the hepatic arterial waveform and RI are keys to detecting splenic steal syndrome with Doppler sonography.

Quantifying Increased Hepatic Arterial Flow With Test Balloon Occlusion of the Splenic Artery in Liver Transplant Recipients With Suspected Splenic Steal Syndrome

The purpose of this study is to quantify hepatic arterial flow (HAF) in liver transplants with splenic steal syndrome (SSS) pre- and post-test balloon occlusion of the splenic artery utilizing Doppler ultrasound (DUS) and quantitative digitally subtracted angiography (Q-DSA). A total of 193 liver transplants were evaluated retrospectively. Hepatic arterial velocity (HAV) and HAF were calculated utilizing DUS and Q-DSA (i-flow prototype, Siemens) pre- and post-splenic artery balloon occlusion. The rate of HAF increase, total HAF, and peak contrast density (PKD) by Q-DSA were compared with HAF by DUS. Of all, 4 suspected SSS cases underwent test-balloon occlusion with DUS and Q-DSA. Using DUS, HAV and HAF increased by 1.6- to 1.8-fold and 1.7- to 2.6-fold, respectively. Using Q-DSA, the HAF rate, total HAF, and PKD increased by 1.1 to 12.8, 1.5 to 7.6, and 1.3 to 5.3, respectively. Occlusion of the splenic artery in liver transplants with SSS doubles the HAF (+1.7- to 2.6-fold). The Q-DSA parameters correlate qualitatively but overestimate the resultant increased HAF.

Nonocclusive hepatic artery hypoperfusion syndrome (splenic steal syndrome) in liver transplant recipients.

There are numerous causes of reduced arterial inline flow to the liver transplant despite a patent hepatic artery. These include causes of increased peripheral resistance in the hepatic arterial bed, siphoning of the hepatic arterial flow by a dominant splenic artery (splenic steal syndrome), functional reduction of hepatic arterial flow in response to hyperdynamic portal inline flow, and small hepatic graft relative to normal portal inline flow (relative increase of portal flow). These causes are incompletely understood, and perhaps the most controversial of all is the splenic steal syndrome, which is possibly an underrecognized cause of graft ischemia in the United States. Splenic steal syndrome presents nonspecifically as graft dysfunction; if overlooked, it may lead to graft failure. Its incidence is reported to be 0.6 to 10.1% in liver transplant recipients, with some institutions performing prophylactic and/or posttransplant treatment procedures in up to a quarter of their transplant recipients. This wide disparity in the incidence of the diagnosis is probably because there are no objective diagnostic imaging criteria. This article presents a review of the literature that addresses the differential diagnostic considerations of hepatic artery hypoperfusion (splenic steal syndrome included) in the absence of an anatomical defect (hepatic artery stenosis, thrombosis, and/or kinks).

Abstract No. 333: Doppler diagnosis of splenic steal syndrome in liver transplant recipients with test balloon-occlusion of the splenic artery

Abstract No. 333: Doppler diagnosis of splenic steal syndrome in liver transplant recipients with test balloon-occlusion of the splenic artery

Arterial Steal Syndrome After Orthotopic Liver Transplantation

Arterial steal syndrome after orthotopic liver transplantation (OLT) is characterized by arterial hypoperfusion of the graft, which is caused by a shift in blood flow into the splenic or gastroduodenal arteries. In this report, we present mechanisms by which this syndrome caused ischemia in our patients. Steal was suspected by elevated levels of liver enzymes and the results of Doppler ultrasonography and computed tomographic angiography; it was confirmed by celiac angiography. Patients with established hepatic arterial thrombosis before angiography were excluded from this study. Steal was treated by embolization with a coil or by placement of an endoluminal narrowing stent. Ten patients at our institution (seven men and three women; mean age, 24.7 ± 11 years; range, 6 to 40 years) exhibited biochemical evidence of liver ischemia and graft failure at 1 to 170 days after having undergone orthotopic liver transplantation. Nine of those patients had splenic steal, and one had both splenic and left gastric artery steal syndrome. None of the patients had gastroduodenal artery steal syndrome. The eight patients with splenic steal syndrome and the patient with both splenic and left gastric steal syndrome were treated by transcatheter occlusion with a coil. The remaining patient with splenic steal syndrome was treated with an endoluminal narrowing stent placement. All patients improved clinically within 24 hours after treatment, exhibiting significant changes in their biochemical and radiological parameters. Follow-up ranged from 1 to 22 months (mean, 6.7 ± 6.6 months). One patient died from sepsis 1 month after having undergone coil embolization. He had no vascular anomalies at the time of death. We conclude that steal is a significant problem after OLT. Embolization and stenting are minimally invasive and successful treatments for steal, usually resulting early clinical improvement.