History of Hepatic Encephalopathy is Not a Contraindication to TIPS Placement for Refractory Ascites

2020 ◽  
Author(s):  
Sammy Saab ◽  
Matthew Zhao ◽  
Ishan Asokan ◽  
Jung Jun Yum ◽  
Edward Wolfgang Lee
Keyword(s):  
Hepatic Encephalopathy ◽  
Refractory Ascites ◽  
History Of

Refractory Ascites as the Only Presenting Symptom of Chronic Calcified Constrictive Pericarditis: A Diagnostic Challenge

2014 ◽  
Vol 17 (1) ◽  
pp. 42
Author(s):  
Shi-Min Yuan
Keyword(s):  
Computed Tomography ◽  
Liver Cirrhosis ◽  
Female Patient ◽  
Constrictive Pericarditis ◽  
Delayed Diagnosis ◽  
Young Female ◽  
Refractory Ascites ◽  
Diagnostic Challenge ◽  
Massive Ascites ◽  
History Of

Extracardiac manifestations of constrictive pericarditis, such as massive ascites and liver cirrhosis, often cover the true situation and lead to a delayed diagnosis. A young female patient was referred to this hospital due to a 4-year history of refractory ascites as the only presenting symptom. A diagnosis of chronic calcified constrictive pericarditis was eventually established based on echocardiography, ultrasonography, and computed tomography. Cardiac catheterization was not performed. Pericardiectomy led to relief of her ascites. Refractory ascites warrants thorough investigation for constrictive pericarditis.

Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration

2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatic Encephalopathy ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Refractory Ascites

Natural History of Patients Taking Rifaximin-α for Recurrent Hepatic Encephalopathy and Risk of Future Overt Episodes and Mortality: A Post-hoc Analysis of Clinical Trials Data

2016 ◽  
Vol 38 (5) ◽  
pp. 1081-1089.e4 ◽  
Author(s):  
Christian A. Bannister ◽  
James G. Orr ◽  
Alan V. Reynolds ◽  
Mark Hudson ◽  
Peter Conway ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Hepatic Encephalopathy ◽  
Natural History ◽  
Post Hoc Analysis ◽  
History Of ◽  
Post Hoc

History of Hepatic Encephalopathy Is Associated With Symptoms of Depression in Liver Transplant Candidates

2017 ◽  
Vol 112 ◽  
pp. S567
Author(s):  
Alex N. Zimmet ◽  
George Stukenborg ◽  
Blake Niccum ◽  
Gold Adkins ◽  
Jennifer Wang ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Transplant ◽  
Symptoms Of Depression ◽  
History Of ◽  
Transplant Candidates

History of Hepatic Encephalopathy

2020 ◽  
Vol 24 (2) ◽  
pp. xiii-xvii
Author(s):  
Vinod K. Rustgi
Keyword(s):  
Hepatic Encephalopathy ◽  
History Of

Burden of Cirrhosis and Minimal and Past History of Overt Hepatic Encephalopathy on Patients and Caregivers

2016 ◽  
Vol 6 ◽  
pp. S53-S54
Author(s):  
Deepa Shrestha ◽  
Radha K. Dhiman ◽  
Sandeep Grover ◽  
Sunil Taneja ◽  
Ajay Duseja ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Past History ◽  
Overt Hepatic Encephalopathy ◽  
History Of

Clinical Characteristics and Outcomes of Transjugular Intrahepatic Portosystemic Shunt Procedure for Portal Hypertension Secondary to Myeloproliferative Neoplasms

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1612-1612
Author(s):  
Christopher R Reilly ◽  
Daria V. Babushok ◽  
Ranjeeta Bahirwani ◽  
Jeffery Mondschein ◽  
Elizabeth O. Hexner
Keyword(s):  
Portal Hypertension ◽  
Hepatic Encephalopathy ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Variceal Bleeding ◽  
Clinical Characteristics ◽  
Myeloproliferative Neoplasms ◽  
Portosystemic Shunt ◽  
Refractory Ascites ◽  
Common Complication ◽  
Intrahepatic Portosystemic Shunt

Abstract Portal hypertension is a common complication of myeloproliferative neoplasms (MPN) and portends a poor prognosis. Arising in 7-18% of MPN patients, portal hypertension develops through several distinct mechanisms, including abdominal vein thrombosis, extramedullary hematopoiesis (EMH), and nodular regenerative hyperplasia (NRH). Similar to cirrhotic patients, MPN-associated portal hypertension presents with refractory ascites, gastrointestinal bleeding, hepatic encephalopathy, and susceptibility to infections. Transjugular intrahepatic portosystemic shunt (TIPS) procedure has been used empirically to treat refractory ascites and variceal bleeding in MPN-related portal hypertension; however, there is limited data in regards to TIPS effectiveness in MPN-associated portal hypertension. To assess the safety and efficacy of TIPS for treatment of portal hypertension in MPN, we performed a retrospective analysis of outcomes of TIPS procedure in patients with MPN in our institution. Using the University of Pennsylvania electronic medical record database, we identified nine patients with MPN who underwent TIPS procedure for treatment of refractory portal hypertension between 2005 and 2015. Patients with portal hypertension from causes other than MPN were excluded from the study. Clinical characteristics and long-term outcomes were analyzed. The mean age at time of TIPS was 47 years (range 30-67 years). Seven of nine patients were female (78%) and all seven carried a diagnosis of polycythemia vera (PV) or post-PV myelofibrosis (PV-MF); both male patients had a diagnosis of primary myelofibrosis (PMF) (Table 1). All nine patients were positive for JAK2V617F mutation, and one patient had a concurrent diagnosis of Philadelphia-chromosome positive CML. The most common etiology of portal hypertension was Budd-Chiari Syndrome (BCS) in six patients (67%), followed by NRH in five patients (56%), and EMH in two patients (22%); one patient had several distinct causes of MPN-related portal hypertension. Indications for TIPS included refractory ascites in five patients (63%), ascites and esophageal varices in three patients (33%), and ascites and hydrothorax in one patient. All patients demonstrated immediate normalization of portal pressures following TIPS without any reported periprocedural complications (Table 2). Additionally, all patients received indefinite anticoagulation (low molecular weight heparin, 3 patients; vitamin K antagonist, 2 patients; fondaparinux, 2 patients). TIPS intervention had 1-year patency rate of 89%. However, one third of patients required subsequent shunt revision at a median interval of 22.3 months (range 10-34 months) due to stent stenosis or thrombosis despite anticoagulation; one patient had radiographic evidence of TIPS dysfunction without clinical symptoms. Of note, all three patients who developed TIPS stenosis/thrombosis had BCS and NRH. The majority of patients (89%) experienced complete resolution of ascites, while the remaining patient had partial improvement in ascites but no longer required routine paracentesis. Grade 1 and 2 hepatic encephalopathy was the most common complication post-TIPS (67%), occurring in half of the patients with BCS and in all three patients with portal hypertension due to EMH. One patient had variceal bleeding in the setting of TIPS thrombosis. All patients were alive 2 years post-TIPS (excluding one patient with recent TIPS; range 2-5 years). Our study represents the first systematic analysis of outcomes of TIPS procedure for management of portal hypertension in MPN using data from a single-institution over a ten-year period. Our results suggest that TIPS procedure can be performed safely in this high-risk population, and can effectively mitigate the clinical consequences of portal hypertension in patients with MPN. However, the prevalence of TIPS complications, particularly of TIPS stenosis/thrombosis and hepatic encephalopathy, remains significant and must be balanced against the desired clinical benefits. Future studies with a larger number of patients are needed to delineate prognostic factors that identify MPN patients most likely to benefit from TIPS. Disclosures No relevant conflicts of interest to declare.

Burden of Cirrhosis and Minimal and Past History of Overt Hepatic Encephalopathy on Caregivers

2017 ◽  
Vol 7 ◽  
pp. S47 ◽  
Author(s):  
Deepa Shrestha ◽  
Sandeep Grover ◽  
Sahaj Rathi ◽  
Ajay Duseja ◽  
Yogesh Kumar Chawla ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Past History ◽  
Overt Hepatic Encephalopathy ◽  
History Of

scholarly journals Hepatic Encephalopathy in Two Goat Kids with Common Paternity

2008 ◽  
Vol 20 (6) ◽  
pp. 807-811 ◽  
Author(s):  
Gregory K. Wilkerson ◽  
Monali M. Bera ◽  
Timothy N. Holt ◽  
Robert J. Callan ◽  
Karamjeet Pandher
Keyword(s):  
Hepatic Encephalopathy ◽  
White Matter ◽  
Reference Interval ◽  
Laboratory Diagnostics ◽  
Cell Hyperplasia ◽  
Mental Deterioration ◽  
Mixed Breed ◽  
History Of ◽  
Portal Veins ◽  
The Brain

Two juvenile, intact, female mixed-breed goats from a common sire were presented for periodic neurologic deficits, seizures, and a generalized loss of body condition that occurred over a 4–6-week period. On physical examination, both goats were thin, obtunded, blind, and ataxic. Laboratory diagnostics revealed increased serum bile acids (95 μmol/l; reference interval: 0–50 μmol/l) in one of the goats. Both goats exhibited progressive physical and mental deterioration, and were eventually euthanized. Upon necropsy, no significant macroscopic lesions were noted. Microscopic examination, however, demonstrated hepatocellular atrophy and anomalies in the hepatic microvasculature, including duplication of hepatic arteries, small-to-indistinct portal veins, and oval cell hyperplasia. In addition, spongiform change was microscopically identified throughout the parenchyma of the brain, most notably within the white matter and along the junction of gray and white matter. The diagnosis of congenital portal vein hypoperfusion (suggestive of a portosystemic shunt) with resultant hepatic encephalopathy was proposed in each case based on the characteristic microscopic lesions in conjunction with the signalment and history of the goats. The observation that the affected kids were sired by the same buck suggests a hereditary basis for the condition in these animals as well.

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