Safety and efficacy of splenic artery embolization for portal hyperperfusion in liver transplant recipients: A 5‐year experience

Abstract

Severe portal hyperperfusion (PHP) after liver transplantation has been shown to cause intrahepatic arterial vasoconstriction secondary to increased adenosine washout (hepatic artery buffer response). Clinically, posttransplant PHP can cause severe cases of refractory ascites and hydrothorax. In the past, we reported our preliminary experience with the use of splenic artery embolization (SAE) as a way to reduce PHP. Here we present our 5-year experience with SAE in orthotopic liver transplantation (OLT). Between January 2007 and December 2011, 681 patients underwent OLT at our institution, and 54 of these patients underwent SAE for increased hepatic arterial resistance and PHP (n 5 42) or refractory ascites/hepatic hydrothorax (n 5 12). Patients undergoing SAE were compared to a control group matched by year of embolization, calculated Model for End-Stage Liver Disease score, and liver weight. SAE resulted in improvements in hepatic artery resistive indices (0.92 6 0.14 and 0.76 6 0.10 before and after SAE, respectively; P < 0.001) and improved hepatic arterial blood flow (HAF; 15.6 6 9.69 and 28.7 6 14.83, respectively; P < 0.001). Calculated splenic volumes and spleen/liver volume ratios were correlated with patients requiring SAE versus matched controls (P 5 0.002 and P 5 0.001, respectively). Among the 54 patients undergoing SAE, there was 1 case of postsplenectomy syndrome. No abscesses, significant infections, or bleeding was noted. We thus conclude that SAE is a safe and effective technique able to improve HAF parameters in patients with elevated portal venous flow and its sequelae. Liver Transpl 21:435-441, 2015. V C 2015 AASLD.

Safety and efficacy of splenic artery embolization for portal hyperperfusion in liver transplant recipients: A 5‐year experience

“…The 33% decrease in PV flow of our series resulted in the resolution of ascites and/or hydrothorax in all cases. Differently from the series by Presser et al, 1 we did not find a significant reduction of the hepatic artery RI (pre-and post-SAE, 0.68 6 0.09 versus 0.65 6 0.09, respectively; P 5 0.34) probably because of the fact that the indications for SAE in our experience were never related to an early increased hepatic arterial resistance as in most of their cases. Moreover, we did measure the pressure gradient at the level of the outflow anastomosis before SAE in all our patients to rule out a possible problem of outflow obstruction as the cause of persistent and refractory ascites, and none of our cases had a significant transanastomosis pressure gradient confirming that PHP was the main determinant of clinical signs of portal hypertension in our series.…”

“…Moreover, we did measure the pressure gradient at the level of the outflow anastomosis before SAE in all our patients to rule out a possible problem of outflow obstruction as the cause of persistent and refractory ascites, and none of our cases had a significant transanastomosis pressure gradient confirming that PHP was the main determinant of clinical signs of portal hypertension in our series. Finally, on the basis of our personal experience of 23 late SAEs after liver transplantation, we do agree with Presser et al 1 that SAE is a safe and effective technique to reduce PV flow and also WHVP in the case of PHP in order to treat persistent and refractory ascites or hydrothorax. …”

“…SAE was performed with proximal occlusion of the splenic artery as in the series reported by Presser et al, 1 and no cases of splenic abscess, infection, or bleeding were encountered. PV velocity was significantly reduced by SAE (57.31 6 24.34 versus 39.65 6 19.14 cm/second; P 5 0.01), and the diameter of the spleen showed a slightly significant reduction after SAE (15.25 6 1.91 versus 14.15 6 2.3 cm; P 5 0.047) confirming the data reported by Presser et al 1 In our series, we did also measure wedge hepatic venous pressure (WHVP) by cavography before and after SAE showing a significant reduction (22.54 6 6.93 versus 16.78 6 3.27 mm Hg; P 5 0.03). The 33% decrease in PV flow of our series resulted in the resolution of ascites and/or hydrothorax in all cases.…”

“…Our personal experience with refractory ascites and/or persistent hepatic hydrothorax due to PHP consisted of 23 patients who underwent SAE 110 6 61 days (range, 22-240 days) after liver transplantation. SAE was performed with proximal occlusion of the splenic artery as in the series reported by Presser et al, 1 and no cases of splenic abscess, infection, or bleeding were encountered. PV velocity was significantly reduced by SAE (57.31 6 24.34 versus 39.65 6 19.14 cm/second; P 5 0.01), and the diameter of the spleen showed a slightly significant reduction after SAE (15.25 6 1.91 versus 14.15 6 2.3 cm; P 5 0.047) confirming the data reported by Presser et al 1 In our series, we did also measure wedge hepatic venous pressure (WHVP) by cavography before and after SAE showing a significant reduction (22.54 6 6.93 versus 16.78 6 3.27 mm Hg; P 5 0.03).…”

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TO THE EDITOR:We read with interest the article by Presser et al 1 recently published in Liver Transplantation and reporting a single-center, 5-year experience of splenic artery embolization (SAE) for portal hyperperfusion (PHP) in whole liver transplant recipients. The authors describe a total of 54 patients who underwent SAE for PHP at different times after liver transplantation and compared this series with a control group matched by year of embolization, calculated Model for End-Stage Liver Disease score, and liver weight.

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