Trombosis y cavernomatosis portal: las claves para el éxito de un TIPS

Lombardo, S.; Espejo, J.J.; Pérez-Montilla, M.E.; Zurera, L.J.; González-Galilea, Ángel

doi:10.1016/j.rx.2017.08.006

Cited by 2 publications

(2 citation statements)

References 32 publications

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“…PVT can develop in the trunk of the PV, including its right and left intrahepatic branches, or it can originate everywhere in the portal system and may even extend to the splenic or superior mesenteric veins or towards the liver involving the intrahepatic PV branches[29]. PVT leads to portal hypertension and cavernous transformation of the PV, which causes difficulty with TIPS creation[30].…”

Section: Discussionmentioning

confidence: 99%

Incidence of portal vein thrombosis after splenectomy and its influence on transjugular intrahepatic portosystemic shunt stent patency

Dong¹,

Luo²,

Zheng³

et al. 2019

WJCC

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BACKGROUNDTransjugular intrahepatic portosystemic shunt (TIPS) is widely accepted as an alternative to surgery for management of complications of portal hypertension. TIPS has been used to treat portal vein thrombosis (PVT) in many centers since the 1990s. Although TIPS has good therapeutic effects on the formation of PVT, the effect of PVT on TIPS stenting has rarely been reported. Patients with splenectomy and pericardial devascu-larization have a high incidence of PVT, which can markedly affect TIPS stent patency and increase the risk of recurrent symptoms associated with shunt stenosis or occlusion.AIMTo investigate the incidence of PVT after splenectomy and its influence on the patency rate of TIPS in patients with cirrhosis and portal hypertension.METHODSFour hundred and eighty-six patients with portal hypertension for refractory ascites and/or variceal bleeding who required TIPS placement between January 2010 and January 2016 were included in this retrospective analysis. Patients without prior splenectomy were defined as group A (n = 289) and those with prior splenectomy as group B (n = 197). The incidence of PVT before TIPS was compared between the two groups. After TIPS placement, primary patency rate was compared using Kaplan–Meier analysis at 3, 6, 9 and 12 mo, and 2 and 3 years. The clinical outcomes were analyzed.RESULTSBefore TIPS procedure, the incidence of PVT in group A was lower than in group B (P = 0.003), and TIPS technical success rate in group A was higher than in group B (P = 0.016). The primary patency rate in group A tended to be higher than in group B at 3, 6, 9 and 12 mo, 2 years and 3 years (P = 0.006, P = 0.011, P = 0.023, P = 0.032, P = 0.037 and P = 0.028, respectively). Recurrence of bleeding and ascites rate in group A was lower than in group B at 3 mo (P ≤ 0.001 and P = 0.001), 6 mo (P = 0.003 and P = 0.005), 9 mo (P = 0.005 and P = 0.012), 12 mo (P = 0.008 and P = 0.024), 2 years (P = 0.011 and P = 0.018) and 3 years (P = 0.016 and P = 0.017), respectively. During 3-years follow-up, the 1-, 2- and 3-year survival rate in group A were higher than in group B (P = 0.008, P = 0.021, P = 0.018, respectively), but there was no difference of the incidence of hepatic encephalopathy (P = 0.527).CONCLUSIONPatients with prior splenectomy have a high incidence of PVT, which potentially increases the risk of recurrent symptoms associated with shunt stenosis or occlusion.

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Section: Discussionmentioning

confidence: 99%

Incidence of portal vein thrombosis after splenectomy and its influence on transjugular intrahepatic portosystemic shunt stent patency

Dong¹,

Luo²,

Zheng³

et al. 2019

WJCC

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“…Treatment may depend on the cause of CTPV but is usually to decrease portal pressure and relieve the symptoms of portal hypertension. Anti-coagulants are less likely to be employed for the management of CTPV due to an increased susceptibility of the patient to bleed secondary to portal hypertension and hence, TIPS can be opted instead [17]. The cause of portal hypertension is mainly due to thrombosis and cavernous transformation of extrahepatic portion of the portal vein.…”

Section: Discussionmentioning

confidence: 99%

Cavernous Transformation of Portal Vein in the Setting of Protein C and Anti-thrombin III Deficiency

Nasim

Majid

Tahir

et al. 2019

Cureus

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Cavernous transformation of the portal vein (CTPV), also known as portal cavernoma, is a sequelae of thrombosis in the portal vein causing its occlusion and portal hypertension. The etiology, however, remains unknown. Gastroesophageal variceal bleeding, splenomegaly, portosystemic collaterals, and ultimate hematologic abnormalities are among the prominent clinical features. Among the causes, predisposing an individual to CTPV is natural anticoagulant protein C and antithrombin III deficiencies. Determination of the etiology of CTPV may also give a direction toward the management plan to not only relieve the patient of the already developed complications but also to treat the primary cause of the pathology We discuss a case of a nine-year-old male child diagnosed as CTPV secondary to protein C and antithrombin III deficiency who was treated symptomatically for anemia and varices and was referred for transjugular intrahepatic portosystemic shunt (TIPS).

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Trombosis y cavernomatosis portal: las claves para el éxito de un TIPS

Cited by 2 publications

References 32 publications

Incidence of portal vein thrombosis after splenectomy and its influence on transjugular intrahepatic portosystemic shunt stent patency

Incidence of portal vein thrombosis after splenectomy and its influence on transjugular intrahepatic portosystemic shunt stent patency

Cavernous Transformation of Portal Vein in the Setting of Protein C and Anti-thrombin III Deficiency

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