Effects of nonshunting operations on portal venous pressure and hepatic blood flow

Kawasaki, Seiji; Kidokoro, Akio; Sugiura, Mitsuo; Sanjo, Kensho; Idezuki, Yasuo

doi:10.1016/0002-9610(87)90607-6

Cited by 16 publications

(14 citation statements)

References 10 publications

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“…The contribution of splenic blood to the PV flow in patients with cirrhosis can be as high as 60% 20. Ligation of the splenic artery and splenectomy have been proposed for the treatment of portal hypertension in patients with cirrhosis and recurrent episodes of gastrointestinal bleeding 21‐27. In an elegant study, Luca et al9 demonstrated that in patients with cirrhosis and severe portal hypertension, the temporary occlusion of the splenic artery causes a significant and marked reduction in the PV pressure gradient; this supports the theory that splenic inflow helps to maintain portal hypertension in these patients.…”

Section: Discussionmentioning

confidence: 89%

Splenic artery embolization for the treatment of refractory ascites after liver transplantation

et al. 2011

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Refractory ascites (RA) is a challenging complication after orthotopic liver transplantation. Its treatment consists of the removal of the precipitating factors. When the etiology is unknown, supportive treatment can be attempted. In severe cases, transjugular intrahepatic portosystemic shunts, portocaval shunts, and liver retransplantation have been used with marginal results. Recently, splenic artery embolization (SAE) has been described as an effective procedure for reducing portal hyperperfusion in patients undergoing partial or whole liver transplantation. Here we describe our experience with SAE for the treatment of RA. Between June 2004 and June 2010, 6 patients underwent proximal SAE for RA. Intraoperative flow measurements, graft characteristics, embolization portal vein (PV) velocities before and after SAE, and spleen/liver volume ratios were collected and analyzed. The response to treatment was assessed with imaging (ultrasound/computed tomography) and on the basis of clinical outcomes (weight changes, diuretic requirements, and the time to ascites resolution). The PV velocity decreased significantly for each patient after the embolization (median = 66.5 cm/second before SAE and median = 27.5 cm/second after SAE, P < 0.01). All patients experienced a significant postprocedural weight loss (mean = 88.1 ± 28.4 kg before SAE and mean = 75.8 ± 28.4 kg after SAE, P < 0.01) and a dramatic decrease in their diuretic requirements. All but 1 of the patients experienced a complete resolution of ascites after a median time of 49.5 days (range = 12-295 days). No patient presented with postembolization complications. In conclusion, SAE was effective in reducing the PV velocity immediately after the procedure. Clinically, this translated into a dramatic weight loss, a reduction of diuretic use, and a resolution of ascites. SAE appears to be a safe and effective treatment for RA.

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Section: Discussionmentioning

confidence: 89%

Splenic artery embolization for the treatment of refractory ascites after liver transplantation

et al. 2011

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“…Based on these observations, ligation of the splenic artery and splenectomy were proposed for the treatment of portal hypertension in patients with cirrhosis and recurrent episodes of hemorrhage from esophageal varices 8–14. However, these nonshunting procedures caused only a mild reduction in portal pressure (PP)9, 10 which was suggested to be due to compensatory increases in mesenteric blood inflow 7…”

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confidence: 99%

Effects of splenic artery occlusion on portal pressure in patients with cirrhosis and portal hypertension

et al. 2006

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The specific contribution of splenic blood inflow to portal hypertension in patients with cirrhosis is still unclear. In this study, we investigated this contribution by assessing the hemodynamic effects of transient splenic artery occlusion. In 15 cirrhotic patients, portal pressure gradient (PPG) was measured just before inserting a transjugular intrahepatic portosystemic shunt (TIPS), in baseline conditions, for 15 minutes after splenic artery occlusion and 5 minutes after recovery. Splenic artery occlusion caused a significant decrease in PPG (range, Ϫ4% to Ϫ38%, median Ϫ20%, P Ͻ 0.001) which promptly returned to baseline values after recovery of the splenic inflow. The decrease in PPG showed a significant correlation with spleen volume (r ϭ 0.70, P Ͻ 0.005), liver volume (r ϭ Ϫ0.63; P Ͻ 0.01), and spleen/liver volume ratio (r ϭ 0.82, P Ͻ 0.001). Seven out of eight patients with a spleen/liver volume ratio greater than 0.5 had a marked decrease in PPG (Ͼ20%), whereas none of patients with a ratio lesser than 0.5 had a marked PPG response. In conclusion, in cirrhotic patients with portal hypertension, splenic artery occlusion causes a significant reduction in portal pressure (PPG). The drop in PPG is directly related to spleen volume and indirectly related to liver volume. The spleen/liver volume ratio accurately predicts the drop in PPG and may be used to identify patients who could obtain a significant advantage from surgical and nonsurgical procedures decreasing splenic inflow. See Editorial on Page 1186In patients with chronic liver disease, portal hypertension is induced by the hemodynamic interaction of abnormally high portal blood inflow and increased intrahepatic vascular resistance. 1 The splanchnic hyperemia is sustained mainly by splanchnic vasodilation, with increased mesenteric and splenic artery blood inflow. 2 Splenomegaly is a common finding in patients with cirrhosis and portal hypertension and is associated with increased splenic 3-5 and portal blood inflow. 6 The importance of the splenic blood inflow in the context of the splanchnic hyperemia is suggested by the observation that, in patients with cirrhosis, the contribution of splenic flow can increase portal blood flow by up to 60%. 7 Based on these observations, ligation of the splenic artery and splenectomy were proposed for the treatment of portal hypertension in patients with cirrhosis and recurrent episodes of hemorrhage from esophageal varices. [8][9][10][11][12][13][14] However, these nonshunting procedures caused only a mild reduction in portal pressure (PP) 9,10 which was suggested to be due to compensatory increases in mesenteric blood inflow. 7 After whole-organ liver transplantation, despite the normalization of intrahepatic resistance and PP, portal blood inflow remains elevated for months, which has Abbreviations: PPG, portal pressure gradient; PP, portal pressure; CT, computed tomography; NS, not significant. Address reprint requests to

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“…Moreover, the weight of the spleen varies from 150 g to 2 kg with an average of 723 g in 350 splenectomized patients in Japan [5]. The beneficial effect of splenectomy during esophagogastric devascularization in IPH was related with a significantly more pronounced reduction of portal pressure (-21 ± 4.1%) after operation compared with that in patients with liver cirrhosis (-8.9 ± 1.6%) [35]. On the other hand, Eguchi et al [16] found a significantly higher incidence of portal thrombosis after splenectomy in patients with IPH than in those with liver cirrhosis (25 vs 1.8%).…”

Section: Discussionmentioning

confidence: 93%

“…Unfortunately, in our case it was not possible to establish the exact etiological factors, but a high level of gamma globulin confirmed the potential role of a immunological mechanism in this disease. Investigations of splanchnic hemodynamics demonstrated that both increased splenic artery blood flow and presinusoidal portal vascular resistance might play a key role in the development of portal hypertension in IPH [33][34][35]. It is a well-documented fact that the diameters of the portal and splenic veins are significantly larger in patients with IPH than in those with liver cirrhosis [6,36].…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Portal Hypertension: Report of a Case

Mishin¹

2005

Visc Med

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Background: Idiopathic portal hypertension (IPH), the socalled Banti’s syndrome, is a condition clinically characterized by splenomegaly, hypersplenism, and increased portal pressure. IPH is uncommon in the Western world. In this article we report on a well-documented case of this rare form of disorder. Case Report: A 27-year-old woman was referred to our hospital with symptoms of severe pancytopenia, massive splenomegaly, and moderate esophageal varices with red color signs despite endoscopic variceal ligation. Upon admission, the hepatic functional reserve was satisfactory (Child-Pugh class A). The color-Doppler ultrasound showed an anatomically normal and non-thrombotic splenoportal venous axis. A complete gastroesophageal devascularization with splenectomy (Hassab-Paquet procedure) was performed. Intraoperatively the liver looked grossly normal while the microscopic examination revealed an inflammatory cell infiltration and fibrosis of the portal tract but no signs of liver cirrhosis. The final diagnosis of IPH was made based on the definitions adopted by the Japan IPH Study Committee. The patient has been asymptomatic for 12 months postoperatively, and hematological indices reached their normal values. The esophageal varices were eradicated. Conclusion: The literature on treatment strategies of esophageal varices due to IPH was reviewed with particular reference to the role of devascularization procedures and splenectomy in the management of this rare condition.

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Effects of nonshunting operations on portal venous pressure and hepatic blood flow

Cited by 16 publications

References 10 publications

Splenic artery embolization for the treatment of refractory ascites after liver transplantation

Splenic artery embolization for the treatment of refractory ascites after liver transplantation

Effects of splenic artery occlusion on portal pressure in patients with cirrhosis and portal hypertension

Idiopathic Portal Hypertension: Report of a Case

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