scholarly journals Indian College of Radiology and Imaging Evidence-Based Guidelines for Interventions in Portal Hypertension and Its Complications

2022 ◽  
Author(s):  
Amar Mukund ◽  
Shaleen Rana ◽  
Chander Mohan ◽  
Naveen Kalra ◽  
Sanjay Saran Baijal
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Early Stage ◽  
Venous Pressure ◽  
Response To Treatment ◽  
Evidence Based ◽  
Interventional Radiologist ◽  
Hypertension Diagnosis ◽  
Evidence Based Guidelines ◽  
Gradient Measurement

AbstractPortal hypertension is a complication of chronic liver disease. Various radiological interventions are being done to aid in the diagnosis of portal hypertension; further, an interventional radiologist can offer various treatments for the complications of portal hypertension. Diagnosis of portal hypertension in its early stage may require hepatic venous pressure gradient measurement. Measurement of gradient also guides in diagnosing the type of portal hypertension, measuring response to treatment and prognostication. This article attempts to provide evidence-based guidelines on the management of portal hypertension and treatment of its complications.

Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Circulation ◽  
Chronic Liver ◽  
Noninvasive Markers ◽  
Collateral Formation

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, ­pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.

scholarly journals A72 VARICEAL BLEED & PORTAL HYPERTENSIVE GASTROPATHY IN A NON-CIRRHOTIC PATIENT WITH ISOLATED SPLENOMEGALY

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 85-86
Author(s):  
S Hasan ◽  
M Dmitriew ◽  
J Leonard
Keyword(s):  
Intensive Care ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Cirrhotic Patient ◽  
Rare Case ◽  
Treatment Plan ◽  
Venous Pressure ◽  
Retinal Dystrophy ◽  
Ct Guided ◽  
Variceal Bleed

Abstract Background Portal hypertension caused by cirrhosis is the most common etiology of esophageal varices. However, abnormalities of the spleno-portal axis in the absence of liver disease may also cause portal hypertension resulting in varices. We report a rare case of esophageal variceal bleed in a non-cirrhotic patient with isolated splenomegaly secondary to chronic G-CSF therapy. Aims This report outlines the case of a patient with Cohen Syndrome (CS) who presented with an upper gastrointestinal (GI) bleed in the setting of previously documented splenomegaly and portal hypertension. We expand on the clinical investigations, diagnosis, treatment plan and hospital course of this patient. Methods Case report, review of literature. Results A 26-year old male with previously diagnosed CS presented with large volume hematemesis and pancytopenia. CS is a rare autosomal recessive disorder. In our patient this manifested with congenital neutropenia, microcephaly, retinal dystrophy and global developmental delay. He required long term G-CSF therapy to manage chronic neutropenia and subsequently developed splenomegaly, a known side effect. The most recent MRI identified stable splenomegaly with a craniocaudal length of 23 cm, normal liver size and no radiographic evidence of cirrhosis. The imaging was also significant for gastroesophageal and splenorenal varices but no ascites or recanalization of the umbilical vein. A recent liver biopsy had shown mild pericellular fibrosis with no active liver disease or cirrhosis. In the past, the patient had declined EGD, therapeutic splenectomy or assessment of hepatic venous pressure gradient through invasive venography. His liver enzymes, bilirubin and albumin had always been within normal limits. The patient had no history of GI bleeding. Previous investigations for hematologic malignancies or myelodysplastic syndrome had been negative. Upon admission, an urgent EGD revealed active variceal bleeding in the esophagus and portal gastropathy. Given the extent of his congenital orofacial abnormalities a variceal band ligator could not be passed for appropriate intervention. The patient was transferred to the Intensive Care Unit and managed with intravenous proton pump inhibitor, octreotide, as well as transfusions of packed red blood cells, platelets and fresh frozen plasma. Within the next 48 hours, the patient underwent successful transjugular intrahepatic portosystemic shunt and CT-guided coil placements for the bleeding varices. Conclusions This is a rare case of variceal bleed in a non-cirrhotic patient with portal hypertension from iatrogenic splenomegaly. While there are previous reports of spontaneous splenic rupture secondary to G-CSF therapy we are the first to report variceal bleed as a complication. This is a life-threatening consequence that requires urgent intervention and intensive care. Funding Agencies None

The Care Triangle: Determining the Gaps in the Management of Atopic Dermatitis

2013 ◽  
Vol 17 (4) ◽  
pp. 276-282 ◽  
Author(s):  
Ashley O'Toole ◽  
Bjorn Thomas ◽  
Richard Thomas
Keyword(s):  
Atopic Dermatitis ◽  
Response To Treatment ◽  
Care Process ◽  
Evidence Based ◽  
Previous Response ◽  
Children And Young Adults ◽  
The Individual ◽  
Evidence Based Guidelines ◽  
Based Medicine

Background: Atopic dermatitis (AD) is a chronic, relapsing, intensely pruritic dermatosis that usually affects infants, children, and young adults. The treatment of AD entails an individualized regimen that depends on the age of the patient, the stage and variety of lesions present, the sites and extent of involvement, the presence of infection, and the previous response to treatment. Objectives: To identify the evidence surrounding potential strategies for closing these gaps—ultimately improving the quality of care, the care process itself, and patient outcomes—and to encourage discussions that help develop tools to bridge the gap between suggested therapy and what is done by the patient. Methods: Review of the literature including searches on PubMed Central and Medline and in seminal dermatology texts. Results: There are several disconnections between the evidence-based guidelines in the management of AD, what the individual dermatologist recommends, and what the patient does. Conclusion: Applying the concept of the care triangle requires a balance of evidence-based medicine, the physician's experiences and the patient's needs and expectations in the decisions surrounding appropriate management of the disease.

Urotensin II modulates hepatic fibrosis and portal hemodynamic alterations in rats

2009 ◽  
Vol 297 (4) ◽  
pp. G762-G767 ◽  
Author(s):  
William Kemp ◽  
Andrew Kompa ◽  
Arintaya Phrommintikul ◽  
Chandana Herath ◽  
Jia Zhiyuan ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Growth Factor ◽  
Hepatic Fibrosis ◽  
Transforming Growth Factor ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatic Tissue ◽  
High Dose ◽  
Urotensin Ii

The influence of circulating urotensin II (UII) on liver disease and portal hypertension is unknown. We aimed to evaluate whether UII executes a pathogenetic role in the development of hepatic fibrosis and portal hypertension. UII was administered by continuous infusion over 4 wk in 20 healthy rats divided into three treatment groups, controls (saline, n = 7), low dose (UII, 1 nmol·kg−1·h−1, n = 8), and high dose (UII, 3 nmol·kg−1·h−1, n = 5). Hemodynamic parameters and morphometric quantification of fibrosis were assessed, and profibrotic cytokines and fibrosis markers were assayed in hepatic tissue. UII induced a significant dose-dependent increase in portal venous pressure (5.8 ± 0.4, 6.4 ± 0.3, and 7.6 ± 0.7, respectively, P = 0.03). High-dose UII infusion was associated with an increase in hepatic transcript for transforming growth factor-β ( P < 0.05) and platelet-derived growth factor-β ( P = 0.06). Liver tissue hydroxyproline was elevated in the high-dose group ( P < 0.05). No systemic hemodynamic alterations were noted. We concluded that UII infusion elevates portal pressure and induces hepatic fibrosis in normal rats. This response may be mediated via induction of fibrogenic cytokines. These findings have pathophysiological implications in human liver disease where increased plasma UII levels have been observed.

scholarly journals Nonalcoholic fatty liver disease and portal hypertension

2020 ◽  
Vol 1 (3) ◽  
pp. 149-169 ◽  
Author(s):  
Marvin Ryou ◽  
Nicholas Stylopoulos ◽  
Gyorgy Baffy
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Pressure Gradient ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Invasive Technique ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a substantial and growing problem worldwide and has become the second most common indication for liver transplantation as it may progress to cirrhosis and develop complications from portal hypertension primarily caused by advanced fibrosis and erratic tissue remodeling. However, elevated portal venous pressure has also been detected in experimental models of fatty liver and in human NAFLD when fibrosis is far less advanced and cirrhosis is absent. Early increases in intrahepatic vascular resistance may contribute to the progression of liver disease. Specific pathophenotypes linked to the development of portal hypertension in NAFLD include hepatocellular lipid accumulation and ballooning injury, capillarization of liver sinusoidal endothelial cells, enhanced contractility of hepatic stellate cells, activation of Kupffer cells and pro-inflammatory pathways, adhesion and entrapment of recruited leukocytes, microthrombosis, angiogenesis and perisinusoidal fibrosis. These pathological events are amplified in NAFLD by concomitant visceral obesity, insulin resistance, type 2 diabetes and dysbiosis, promoting aberrant interactions with adipose tissue, skeletal muscle and gut microbiota. Measurement of the hepatic venous pressure gradient by retrograde insertion of a balloon-tipped central vein catheter is the current reference method for predicting outcomes of cirrhosis associated with clinically significant portal hypertension and guiding interventions. This invasive technique is rarely considered in the absence of cirrhosis where currently available clinical, imaging and laboratory correlates of portal hypertension may not reflect early changes in liver hemodynamics. Availability of less invasive but sufficiently sensitive methods for the assessment of portal venous pressure in NAFLD remains therefore an unmet need. Recent efforts to develop new biomarkers and endoscopy-based approaches such as endoscopic ultrasound-guided measurement of portal pressure gradient may help achieve this goal. In addition, cellular and molecular targets are being identified to guide emerging therapies in the prevention and management of portal hypertension.

Transjugular Intrahepatic Portosystemic Shunt in Patients with Portal Hypertension: Patency Depends on Coverage and Interventionalist’s Experience

2018 ◽  
Vol 36 (3) ◽  
pp. 218-227 ◽  
Author(s):  
Matthias Buechter ◽  
Paul Manka ◽  
Guido Gerken ◽  
Ali Canbay ◽  
Sandra Blomeyer ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Venous Pressure ◽  
Portosystemic Shunt ◽  
Refractory Ascites ◽  
Control Group ◽  
Covered Stents ◽  
Group I ◽  
Intrahepatic Portosystemic Shunt

Background and Aims: Transjugular intrahepatic portosystemic shunt (TIPS) is the treatment of choice in decompensated portal hypertension. TIPS revision due to thrombosis or stenosis increases morbidity and mortality. Our aim was to investigate patient- and procedure-associated risk factors for TIPS-revision. Patients and Methods: We retrospectively evaluated 189 patients who underwent the TIPS procedure. Only patients who required TIPS revision within 1 year (Group I, 34 patients) and patients who did not require re-intervention within the first year (Group II [control group], 54 patients) were included. Results: Out of 88 patients, the majority were male (69.3%) and mean age was 56 ± 11 years. Indications for TIPS were refractory ascites (68%), bleeding (24%), and Budd-Chiari syndrome (8%). The most frequent liver disease was alcohol-induced cirrhosis (60%). Forty-three patients (49%) received bare and 45 patients (51%) covered stents, thus resulting in reduction of hepatic venous pressure gradient (HVPG) from 19.0 to 9.0 mm Hg. When comparing patient- and procedure-related factors, the type of stent (p < 0.01) and interventionalist’s experience (number of performed TIPS implantations per year; p < 0.05) were the only factors affecting the risk of re-intervention due to stent dysfunction, while age, gender, indication, Child-Pugh, and model of end-stage liver disease score, platelet count, pre- and post-HVPG, additional variceal embolization, stent diameter, and number of stents did not significantly differ. Conclusion: Patients undergoing TIPS procedure should be surveilled closely for shunt dysfunction while covered stents and high-level experience are associated with increased ­patency.

scholarly journals 2261

2017 ◽  
Vol 1 (S1) ◽  
pp. 72-72
Author(s):  
Albert Liao ◽  
Grant W. Carlson ◽  
John William Eley ◽  
Theresa W. Gillespie
Keyword(s):  
Breast Cancer ◽  
Early Stage ◽  
Breast Conserving Surgery ◽  
The United States ◽  
Early Stage Breast Cancer ◽  
National Database ◽  
Evidence Based ◽  
Median Income ◽  
Study Results ◽  
Evidence Based Guidelines

OBJECTIVES/SPECIFIC AIMS: Evidence-based guideline-concordant care leads to better outcomes in patients with early stage breast cancer, including survival. However, previous studies of guideline compliance have been limited by small study sample sizes, localized geography, unknown causal factors, and lack of diverse population. We use a national database to assess socio-economic, clinical, and facility factors that impact treatment compliance with evidence-based guidelines from the American Society of Clinical Oncology (ASCO) and the National Comprehensive Cancer Network (NCCN). METHODS/STUDY POPULATION: This is a retrospective cohort study of the National Cancer Data Base Participant User File Breast 2014, which captures ~70%–80% of all newly diagnosed cancer cases in the United States. Female patients who were diagnosed with early stage breast adenocarcinoma (T0, T1, T1A, T1B, 2, 2A, or T2N1) from 2004 to 2014 were eligible for this study. RESULTS/ANTICIPATED RESULTS: A total of 807,314 patients were included in this study. Evidence-based guidelines examined with associated compliance rates include surgery completion (79.3% overall compliance), breast conserving surgery Versus mastectomy (88.05% vs. 11.95%, respectively), radiation after breast conserving surgery (77.5% overall compliance), HER2 testing (88.6% overall compliance), estrogen/progesterone receptor (ER/PR) testing (96.3% overall compliance), hormone treatment for positive ER/PR breast cancer (80.2% overall compliance), and sentinel lymph node biopsy completion (67.5% overall compliance). Univariate association between these guidelines and covariates such as facility type, facility location, age, race, insurance status, median income quartiles, achievement of high school degree, urban Versus rural, Charlson-Deyo score, year of diagnosis, and overall survival were assessed. Logistic regression analysis will be used to determine multivariate relationships between these characteristics and the probability that a patient will be compliant to guideline regimen. DISCUSSION/SIGNIFICANCE OF IMPACT: The results of this study will help identify socio-economic, clinical, and facility factors that influence guideline-concordant care and subsequent critical outcomes for patients with early stage breast cancer. Lack of guideline concordant care for specific stages of cancer or treatment modalities will point to a need for tailored interventions to enhance compliance. A prediction model will help identify the most important predictors of noncompliance in breast cancer treatment so noncompliance can be prevented in at-risk populations.

scholarly journals Vitamin A levels reflect disease severity and portal hypertension in patients with cirrhosis

2020 ◽  
Author(s):  
Benedikt Simbrunner ◽  
Georg Semmler ◽  
Alexander Stadlmann ◽  
Bernhard Scheiner ◽  
Philipp Schwabl ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Bile Acid ◽  
Hepatic Dysfunction ◽  
Venous Pressure ◽  
Serum Levels ◽  
Serum Bile Acid ◽  
Reflect Disease Severity ◽  
Registration Number ◽  
Ctp Score

Abstract Background and Aims The liver plays a key role in the storage, metabolism and homeostasis of fat-soluble vitamins. We investigated the relation of Vitamin(Vit)A/D/E serum levels with severity of liver disease and portal hypertension (PHT). Methods VitA/D/E serum levels were assessed in 234 patients with advanced chronic liver disease (ACLD, i.e. hepatic venous pressure gradient [HVPG] ≥ 6 mmHg). Patients with hepatocellular carcinoma, pre-/post-hepatic PHT, TIPS or liver transplantation were excluded. Results Most patients were male (n = 153; 65%) with a median age of 57.6 (49.7–64.5) years. Thirty-two (14%) patients had HVPG 6–9 mmHg, 66 (28%) 10-15 mmHg, and 136 (58%) ≥ 16 mmHg, respectively. VitD deficiency (25-OH-vitamin-D <50 nmol/L) was found in 133 (57%) with higher prevalence in Child-Turcotte-Pugh (CTP)-C: 85% vs. B: 66% vs. A: 47% (p < 0.001). VitD levels displayed significant but weak correlations with hepatic dysfunction and PHT. VitE levels were normal in 227 (97%) patients and displayed no relevant association with hepatic dysfunction or PHT. Only 63 (27%) patients had normal (>1.05 µmol/L) VitA levels, while 58 (25%) had mild (0.70–1.04 µmol/L), 71 (30%) moderate (0.35–0.69 µmol/L), and 42(18%) severe(<0.35 µmol/L) VitA deficiency. VitA correlated with HVPG (Rho = −0.409), CTP score (Rho = −0.646), and serum bile acid levels (Rho = −0.531; all p < 0.001). The prevalence of decompensated ACLD (dACLD) continuously increased with severity of VitA deficiency (no: 40% vs. mild: 51% vs. moderate: 67% vs. severe: 91% had dACLD; p < 0.001). CTP score (per point; OR 2.46; 95%CI 1.80–3.37; p <0.001), age (per year; OR 0.95; 95%CI 0.92–0.98; p = 0.001) and elevated bile acid levels(>10 µmol/L; OR 3.62; 95%CI 1.61–8.14; p = 0.002) were independently associated with VitA deficiency. Conclusion VitA and VitD but not VitE deficiencies are highly prevalent in ACLD. VitA deficiency strongly correlates with hepatic dysfunction, PHT and bile acid levels and is associated with decompensated ACLD. Trial registration number NCT03267615.

scholarly journals Diagnosis of portal hypertension by transabdominal ultrasound

2015 ◽  
Vol 47 (1-2) ◽  
pp. 21-24
Author(s):  
Md Saad Ahamed ◽  
Shikha Kabir ◽  
AS Mohiuddin ◽  
Poritosh Kumar Chowdhury
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Superior Mesenteric Vein ◽  
Statistical Significance ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Deep Inspiration ◽  
Mesenteric Veins ◽  
Mesenteric Vein ◽  
Imaging Department

Portal hypertension is pathologic increase in portal venous pressure, with diversion of portal blood to the systemic circulation. The study was directed to measure as well as to compare the diameters of splenic, superior mesenteric and portal veins with their variation with respiration in normal subjects and in patients with portal hypertension. An analytic type of cross-sectional study was conducted at Radiology and Imaging Department of BIRDEM, Shahbag, Dhaka for one year (2011-12) among purposively selected 59 study subjects with chronic liver disease and portal hypertension, and 45 individuals without liver disease. Transabdominal ultrasonograpy of hepatobiliary system was carried out using computed sonography system with multiple probes having multiple frequency depending on physical built of the subjects. The diameters of selected veins were measured in the course of expiration and deep inspiration. In all control subjects, diameter variations of splenic vein and superior mesenteric vein were noted in the phases of respiration, the diameters increased during deep inspiration and decreased during deep expiration mean diameter and standard deviation of splenic vein and superior mesenteric vein were 6.95 ± 1.75 mm and 8.77 ± 2.06 mm respectively and during expiration they were 4.45 ± 1.24 mm and 5.66 ± 1.41 mm respectively. The difference in deep inspiratory and expiratory diameters had high statistical significance (p<0.0001). Patients with portal hypertension diameter variation with breathing at the level of splenic and superior mesenteric veins was observed only in 5 (9.47%) cases. Diminished response of splenic and superior mesenteric veins with respiration in transabdominal ultrasonography is an indicator of portal hypertension. DOI: http://dx.doi.org/10.3329/bmjk.v47i1-2.22558 Bang Med J (Khulna) 2014; 47 : 21-24

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