Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Rangari, Manisha; Gupta, Ritu; Jain, Mayank; Malhotra, Veena; Sarin, Shiv Kumar

doi:10.1111/j.1478-3231.2003.00879.x

Cited by 107 publications

(87 citation statements)

References 14 publications

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“…Transient ascites is seen in one fifth of children following the episode of bleed. 69 About 10% of children present with isolated splenomegaly. 70 Splenomegaly is almost universal and may be symptomatic with left upper abdominal discomfort (due to massive splenomegaly) or as pain (due to splenic infarcts) or sometimes as symptomatic hypersplenism.…”

Section: Chronic Portal Vein Thrombosis (Extra Hepatic Portal Venous mentioning

confidence: 99%

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Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

149

147

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Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion. ( J CLIN EXP HEPATOL 2015;5:22-40)

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Section: Chronic Portal Vein Thrombosis (Extra Hepatic Portal Venous mentioning

confidence: 99%

“…[85][86][87] Liver function derangement may be seen in EHPVO in the form of ascites, prothrombin time prolongation and low serum albumin in patients with prolonged portal hypertension. 69 …”

Section: Liver Functionmentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

149

147

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“…4 On prolonged follow-up patients with EHPVO have been reported to develop ascites, hypoalbuminemia and coagulopathy suggestive of liver dysfunction. 11,63 This is postulated to be due to effects of chronic deprivation of portal blood flow to the liver leading to atrophy with a possible contribution from chronic cholestasis occurring due to PCC. Based upon these observations, the natural history of PCC can be divided into four stages (Table 4): 1.…”

Section: Natural Historymentioning

confidence: 99%

“…These patients may develop recurrent cholangitis 20,48,51 and, eventually, liver dysfunction either due to secondary biliary cirrhosis or due to chronically diminished portal inflow. 11,63 Attrition of hepatocellular function in these patients may reach the stage that they are candidates for liver transplantation. 48,[69][70][71] A detailed description of natural history and prognosis of PCC has been reviewed elsewhere in this issue.…”

Section: Prognosismentioning

confidence: 99%

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Dhiman

Saraswat

Valla

et al. 2014

Journal of Clinical and Experimental Hepatology

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Portal cavernoma cholangiopathy (PCC) is defined as abnormalities in the extrahepatic biliary system including the cystic duct and gallbladder with or without abnormalities in the 1st and 2nd generation biliary ducts in a patient with portal cavernoma. Presence of a portal cavernoma, typical cholangiographic changes on endoscopic or magnetic resonance cholangiography and the absence of other causes of these biliary changes like bile duct injury, primary sclerosing cholangitis, cholangiocarcinoma etc are mandatory to arrive a diagnosis. Compression by porto-portal collateral veins involving the paracholedochal and epicholedochal venous plexuses and cholecystic veins and ischemic insult due to deficient portal blood supply or prolonged compression by collaterals bring about biliary changes. While the former are reversible after porto-systemic shunt surgery, the latter are not. Majority of the patients with PCC are asymptomatic and approximately 21% are symptomatic. Symptoms in PCC could be in the form of long standing jaundice due to chronic cholestasis, or biliary pain with or without cholangitis due to biliary stones. Endoscopic retrograde cholangiography has no diagnostic role because it is invasive and is associated with risk of complications, hence it is reserved for therapeutic procedures. Magnetic resonance cholangiography and portovenography is a noninvasive and comprehensive imaging technique, and is the modality of choice for mapping of the biliary and vascular abnormalities in these patients. PCC is a progressive condition and symptoms develop late in the course of portal hypertension only in patients with severe or advanced changes of cholangiopathy. Asymptomatic patients with PCC do not require any treatment. Treatment of symptomatic PCC can be approached in a phased manner, coping first with biliary clearance by nasobiliary or biliary stent placement for acute cholangitis and endoscopic biliary sphincterotomy for biliary stone removal; second, with portal decompression by creating portosystemic shunt; and third, with persistent biliary obstruction by performing second-stage biliary drainage surgery such as hepaticojejunostomy or choledochoduodenostomy. Patients with symptomatic PCC have good prognosis after successful endoscopic biliary drainage and after successful shunt surgery. ( J CLIN EXP HEPATOL 2014;4:S2-S14)

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“…It accounts for up to 30% of all variceal bleeds and is only second to cirrhosis [1]. EHPVO is generally considered as a benign disease, but hepatic dysfunction in the form of ascites and deranged liver functions occasionally occurs especially in patients with prolonged portal hypertension [4].…”

Section: Introductionmentioning

confidence: 99%

Systemic and pulmonary hemodynamics in patients with extrahepatic portal vein obstruction is similar to compensated cirrhotic patients

et al. 2008

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Background Patients with cirrhosis and portal hypertension exhibit a hyperdynamic circulation manifesting as increased cardiac output, heart rate and plasma volume; and decreased arterial blood pressure, systemic vascular resistance, and pulmonary vascular resistance. It is believed that these changes are related to both hepatocellular dysfunction and portal hypertension. However, the role of portal hypertension per se in producing these changes in circulation has not been clear. Extrahepatic portal vein obstruction (EHPVO), a vascular disorder of the liver characterized by cavernomatous transformation of the main portal vein, is an excellent model to study the role of portal hypertension per se in producing these changes because there is no hepatic dysfunction in EHPVO. The main aim of our study was, therefore, to evaluate alterations of systemic and pulmonary vascular systems in patients with EHPVO and compare them with patients with compensated cirrhosis. Patients and methods Consecutive patients of EHPVO, 15 years or older, and past variceal bleeders were studied. For comparison, consecutive patients with compensated cirrhosis and history of variceal bleed, matched for variceal status, and body surface area were included. The hemodynamic studies included the measurements of cardiac index (by Fick's oxygen method), and systemic and pulmonary vascular resistance indices. Results Fifteen patients of EHPVO and same number of controls (compensated cirrhotics) were included in the study. The baseline parameters in the two groups were comparable. Both EHPVO patients and cirrhotics had similar values in all the measured systemic and pulmonary hemodynamic parameters. The median (range) cardiac index in EHPVO was 3.8 (2.3-7.7) l min -1 m -2 , whereas it was 4.4 (2.8-8.9) l min -1 m -2 in cirrhosis (P = 0.468). The median (range) systemic vascular resistance index in EHPVO was 1,835 (806-3400) dyne s cm -5 m -2 , which was similar to that in cirrhotic patients (1,800 [668-3022], P = 0.520). Similarly, the values of median (range) pulmonary vascular resistance index were comparable in the two groups (71 [42-332] vs. 79 , P = 0.885). A subgroup analysis was done for 8 patients of EHPVO and 8 age-matched compensated cirrhotic patients, which also revealed similar values of cardiac index, cardiac output, systemic vascular resistance index, systemic vascular resistance, pulmonary vascular resistance index, and pulmonary vascular resistance in the two groups. Conclusions EHPVO patients have hyperdynamic circulation manifested by high cardiac index and low systemic and pulmonary vascular resistance indices. These hemodynamic changes are comparable with compensated cirrhotic patients who have similar grade of portal hypertension. This suggests a predominant role of portal hypertension per se in the genesis of systemic and pulmonary hemodynamic alterations.

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Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Cited by 107 publications

References 14 publications

Portal Vein Thrombosis

Portal Vein Thrombosis

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Systemic and pulmonary hemodynamics in patients with extrahepatic portal vein obstruction is similar to compensated cirrhotic patients

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