Portosystemic Collaterals Research Articles

Clinical and circulating biomarkers of survival and recurrence after radiofrequency ablation in patients with hepatocellular carcinoma.

Radiofrequency ablation (RFA) is an effective local treatment for curative intent in patients with cirrhosis of the liver and hepatocellular carcinoma (HCC) with diameter <3 cm. Several meta-analyses have shown that RFA and surgical resection are comparable in terms of their impact on overall survival. The only clinical data available on markers that are predictive of recurrence and survival after RFA treatment are based on retrospective observational studies. Prospective randomized trials are thus needed to further research in this area. In the present review we analyzed a number of clinical factors that are considered to predict recurrence or survival in HCC patients treated with RFA. We also discussed in detail the circulating biomarkers investigated to date, together with their potential to predict prognosis and recurrence after RFA therapy. Overall survival rates of patients with HCC are significantly affected by liver function, defined as Child-Pugh class, high baseline serum alpha-fetoprotein levels, and the presence of portosystemic collaterals. However, the development of local tumor progression does not significantly affect overall survival. This result is achieved by the effective therapies in patients who relapse after treatment with RFA. For this reason there is an urgent need to identify new circulating biomarkers.

Screening and Surveillance of Varices in Patients With Cirrhosis

Gastro-esophageal varices (GEV) and variceal hemorrhage (VH) are clinical milestones in the natural history of cirrhosis, as they are closely related to the severity of portal hypertension and define specific stages in disease progression. Variceal hemorrhage is a life-threatening complication of cirrhosis and is one of the clinical complications that defines cirrhosis decompensation. The goal of screening and surveillance of varices is to identify patients with GEV at a high risk of bleeding, so that prevention strategies can be implemented. There have been significant updates in the management of GEV over the last years, particularly in the use of non-invasive methods to assess the degree of portal hypertension and the likelihood of having GEV. This paper is focused on esophageal varices with or without extension along the lesser curvature (type 1 or GOV1), as special considerations are required for the management of cardiofundal varices (GOV2 - esophageal varices extending into the fundus, or IGV1 - isolated gastric varices in the fundus) or isolated gastric varices type 2 (IGV2 – gastric varices elsewhere in the stomach, not in the fundus).

Portal Hypertensive Vesiculopathy: A Rare Cause of Hematuria and a Unique Management Strategy

Portosystemic collaterals are common sequelae of portal hypertension. These often present as gastroesophageal varices. Ectopic varices can rarely be seen in duodenum, jejunum, rectum, and sites of surgical anastomoses. Bladder varices are extremely rare presenting with recurrent hematuria, with only a few reported cases. We report here a management of an unusual case of hematuria managed with blood transfusion, intravenous terlipressin, and endoscopic N-butyl cyanoacrylate glue injection.

Is serum apelin related to portal hemodynamics in patients with liver cirrhosis?

BackgroundApelin is the endogenous ligand of the angiotensin-like receptor. The expression of apelin–APJ (apelin receptor) signaling is associated with the development of portal hypertension (PH) and contributes toward the formation of Porto systemic collaterals and splanchnic neovascularization in PH.AimsWe aimed to study the relationship between apelin and portal hemodynamics in cirrhotic patients.Patients and methodsThus study included 60 cirrhotic patients from Menoufia University Hospitals (Egypt) and 20 healthy volunteers as a control group. Participants underwent a physical examination and laboratory investigations [complete blood count, urea, creatinine, alanine transaminase, aspartate transaminase (AST), serum albumin, bilirubin, international normalized ratio, hepatitis C virus antibody, hepatitis B virus antigen, hepatitis C virus PCR, alpha feto protein (AFP), and serum level of apelin]. Abdominal ultrasonographic studies of portal vein diameter, splenic size, and portal hemodynamics were carried out for all participants. Child–Pugh score, model for end-stage liver disease score, and AST/platelet (PLT) index were calculated for all participants.ResultsSerum apelin was highly significantly elevated in cirrhotics than in controls, with a P value of 0.001. Serum apelin was significantly correlated to some laboratory parameters in cirrhotics such as PLT count, alanine transaminase, AST, γ-glutamyl transferase, and bilirubin, with P value less than 0.05. There was a positive correlation between serum apelin level and the degree of liver fibrosis estimated by the AST/PLT index. Serum apelin was significantly correlated to portal vein diameter and portal flow velocity, with a P value less than 0.05, and highly significantly correlated to splenomegaly, with a P value of 0.001. The optimal cut-off point of serum apelin for the prediction of PH in cirrhotics is 2550 ng/dl, with a sensitivity of 89%, a specificity of 65%, and an accuracy of 81%.ConclusionSerum apelin is elevated in patients with cirrhosis and PH, and a positive correlation is found between serum apelin and the degree of hepatic fibrosis. Measurement of serum apelin represents a rapid, noninvasive method for the prediction of PH in cirrhotics and can assess the degree of hepatic fibrosis.

PREDICTORS OF VARICEAL BLEEDING AFTER ESOPHAGEAL VARICES BAND LIGATION IN EGYPTIAN CIRRHOTIC PATIENTS

ABSTRACT Background : Bleeding from oesophageal varices is a severe complication of portal hypertension. Endoscopic variceal ligation (EVL) is the treatment of choice for acute variceal bleeding. It is also performed for primary and secondary prophylaxis of bleeding from oesophageal varices. After Endoscopic Band Ligation (EBL), patients are at risk of post-interventional bleeding; the risk factors for this complication are poorly evaluated . The aim of this work : was to evaluate the risk factors for predicting variceal bleeding after elective endoscopic variceal ligation (EVL). Patients and Methods: This study will be carried out in Zagazig University Hospital and El-Galaa Family Military Hospital. The patients was subjected to different demographic, clinical, biochemical, ultrasonographic and endoscopic findings. Results : The incidence of bleeding after elective EVL was 6%. The results showed significant differences between the bleeders and non bleeders regards the severity of liver disease measured by Child-Pugh score , the platelets count, hemoglobin level, prothrombin time , the liver regards its ( size, echogenicity, irregularity of the surface, presence of HFL and Portosystemic collaterals ) , the size and extension of varices. Conclusion: For prediction of variceal bleeding after elective EVL; We can rely on many characteristics, such as age, gender, liver function, severity of varices, number of rubber bands, and so forth. But as demonstrated by the multivariate analysis, there were only four independent risk factors among these, namely moderate to excessive ascites, PT > 18, number of rubber bands placed, size and extent of varices. These four risk factors may therefore be more meaningful than the others for predicting the occurrence of bleeding following elective EVL.

Gallbladder Agenesis in 17 Dogs: 2006-2016.

BackgroundGallbladder agenesis (GBA) is extremely rare in dogs.Hypothesis/ObjectivesTo describe the history, clinical signs, diagnosis, treatment, and outcomes of dogs with GBA.AnimalsSeventeen client‐owned dogs with GBA.MethodsMedical records from 2006 through 2016 were retrospectively reviewed. Dogs were included when GBA was suspected on abdominal ultrasonography and confirmed by gross evaluation. Signalment, clinical signs, clinicopathological data, diagnostic imaging, histopathology, treatment, and outcome were recorded.ResultsDogs were of 6 different breeds, and Chihuahuas (10 of 17) were most common. Median age at presentation was 1.9 (range, 0.7–7.4) years. Clinical signs included vomiting (5 of 17), anorexia (2 of 17), ascites (2 of 17), diarrhea (1 of 17), lethargy (1 of 17), and seizures (1 of 17). All dogs had increased serum activity of at least 1 liver enzyme, most commonly alanine aminotransferase (15 of 17). Fifteen dogs underwent computed tomography (CT) cholangiography; common bile duct (CBD) dilatation was confirmed in 12, without evidence of bile duct obstruction. Gross evaluation confirmed malformation of the liver lobes in 14 of 17 dogs and acquired portosystemic collaterals in 5 of 17. Ductal plate malformation was confirmed histologically in 16 of 17 dogs. During follow‐up (range, 4–3,379 days), 16 of 17 dogs remained alive.Conclusions and Clinical ImportanceDogs with GBA exhibit clinicopathological signs of hepatobiliary injury and hepatic histopathological changes consistent with a ductal plate abnormality. Computed tomography cholangiography was superior to ultrasound examination in identifying accompanying nonobstructive CBD distention. Computed tomography cholangiography combined with laparoscopic liver biopsy is the preferable approach to characterize the full disease spectrum accompanying GBA in dogs.

The beneficial effects of curcumin in cirrhotic rats with portal hypertension.

In liver cirrhosis with portal hypertension, the uneven distribution of vasoactive substances leads to increased intrahepatic vascular resistance and splanchnic vasodilatation. Angiogenesis also induces increased portal inflow and portosystemic collaterals. The collaterals may induce lethal complications such as gastroesophageal variceal hemorrhage, but the therapeutic effect of vasoconstrictors is still suboptimal due to poor collateral vasoresponsivenss. Curcumin has aroused much attention for its antifibrosis, vasoactive, and anti-angiogenesis actions. However, whether it affects the aforementioned aspects is unknown. Liver cirrhosis was induced by common bile duct ligation (CBDL) in Sprague–Dawley rats. Sham-operated rats were controls. CBDL and sham rats were randomly allocated to receive curcumin (600 mg/kg per day) or vehicle since the 15th day after BDL. On the 29th day, portal hypertension related parameters were surveyed. Portosystemic collateral in situ perfusion was performed to evaluate vascular activity. Chronic curcumin treatment decreased portal pressure (PP), cardiac index (CI) and increased systemic vascular resistance (SVR) in cirrhotic rats. In splanchnic system, curcumin decreased superior mesenteric artery (SMA) flow and increased SMA resistance. Mesenteric angiogenesis was attenuated by curcumin. Acute administration of curcumin significantly induced splanchnic vasoconstriction. The mesenteric protein expressions of p-endothelial nitric oxide synthase (eNOS), cyclooxygenase (COX) 2 (COX2), vascular endothelial growth factor (VEGF), p-VEGF receptor 2 (VEGFR2), and p-Erk were down-regulated. In collateral system, curcumin decreased portosystemic shunting and induced vasoconstriction. In conclusion, chronic curcumin administration in cirrhotic rats ameliorated portal hypertension related hemodynamic derangements and portosystemic collaterals. Curcumin also attenuated splanchnic hyperdynamic circulation by inducing vasoconstriction through inhibition of eNOS activation and by decreasing mesenteric angiogenesis via VEGF pathway blockade.

The Significance of Doppler Ultrasound in the Causes of Varicose Veins

Varicose veins could be clinically diagnosed with visual inspection but the use of Doppler ultrasound (US) in varicose veins is to identify the cause of varicose veins. Need for an extensive systematic review is therefore felt to itemize different causes of varicose veins. Relevant literature was searched and systematic analysis was performed with the aim to show the significance of US in the diagnosis of various causes of varicose veins. Various causes can be diagnosed with color and spectral Doppler US which can be usual causes and unusual causes as well including neovascularization, chronic venous ulceration, obesity, incompetency of the perforating veins, deep vein thrombosis, saphenofemoral junction incompetence, recurrence of the varicose veins after surgical treatment, vulvoperineal varicosities, intraosceous perforating vein incompetence, round ligament varicosity, persistent sciatic vein incompetence, congenital venous malformation and Klippel– Trenaunay syndrome, portosystemic collateral–related varicose veins, and pelvic congestion syndrome. It is concluded that duplex ultrasonography plays an important role in the diagnosis of the various causes of varicose veins.

Therapeutic siRNA targeting endothelial KDR decreases portosystemic collateralization in portal hypertension

Development of portosystemic collateral vessels and gastroesophageal varices is responsible for the most serious clinical consequences of portal hypertension, but effective clinical therapies are limited. Here we developed and investigated the therapeutic potential of an innovative liposomally-formulated short-interfering RNA (siRNA) technology based on clinical stage components, capable to attenuate production of the endothelial kinase insert domain receptor (KDR), which controls portosystemic collateralization and contributes to disease progression and aggravation. These siRNAs were first validated in vitro, and then, their therapeutic potential on portosystemic collateralization and pathological angiogenesis was tested in vivo in mouse models of portal hypertension (portal vein-ligation). siRNAKDR-lipoplexes efficiently transported siRNAKDR to vascular endothelial cells in mesenteric microvenules and portal vein of portal hypertensive mice, where collaterogenesis and angiogenesis take place. This systemic treatment significantly downregulated pathological KDR overexpression, without causing complete KDR knockout, preserving homeostatic baseline KDR levels and thus limiting adverse effects. siRNAKDR-lipoplex-induced endothelial-specific KDR knockdown drastically reduced by 73% the portosystemic collateralization, and impaired the pathologic angiogenic potential of vascular endothelial cells at different levels (cell proliferation, sprouting and remodeling). Targeting endothelial KDR with therapeutic siRNAKDR-lipoplexes could be a promising and plausible treatment modality for attenuating the formation of portosystemic collaterals in a clinical setting.

Spectrum of Liver Disease in Common Variable Immunodeficiency

Introduction: Common variable immunodeficiency (CVID) is a primary immunodeficiency syndrome characterized by defective production of immunoglobulins, low serum Ig levels and most often manifests as recurrent bacterial sinopulmonary infections. The spectrum of liver disease associated with CVID, important to the clinician faced with a new case, has not been recently characterized. Most often reported is its association with nodular regenerative hyperplasia (NRH) and, occasionally, autoimmune hepatitis. We aim to determine the contemporary spectrum of chronic liver disease in CVID at a large tertiary care facility. Methods: This is a single center retrospective cross-sectional analysis of data from 1,458 patients with CVID, defined as serum immunoglobulins at least 2 standard deviations below the normal mean, within the files of the CVID Registry. Chronic liver disease (CLD) was defined by any of the following: 6 months or more of abnormal liver function tests (LFTs), serologic evidence of viral hepatitis by demonstration of viremia, hepatitis of other etiologies, histologic findings of chronicity (fibrosis, cirrhosis, inflammation, NRH), portal hypertension (esophageal varices, portosystemic collaterals, or splenomegaly) or imaging showing hepatic abnormalities consistent with cirrhosis. Results: 1,458 subjects with CVID were included. Average age at time of CVID diagnosis was 49.8±19 years, 65% were female, 91% Caucasian. A minority 53 (3.6%) had a liver biopsy. Table 1 presents a summary of demographic characteristics and comorbidities. Nine hundred twelve (17.6%, CI: 15.6, 19.5) had CLD (at least 6 months of abnormal liver tests). A specific diagnosis was assigned in 10.2%. (95% CI: 6.8, 9.6). NRH was the most common diagnosis (4.7%), a frequency similar to that described by Fuss. Surprisingly, there were 3 (0.89%) with PSC and only 16 (1.1%) had chronic viral hepatitis B or C.Table: Table. Demographics and ComorbiditiesConclusion: In CVID:1) Chronically abnormal liver tests are seen in nearly 20%;2) Non-specific liver test abnormalities without certain other diagnoses are most common;3) NRH is the most frequent assigned diagnosis, yet accounts for less than half of the cases;4) Fatty liver disease is common;Further investigation is necessary to determine the cause and clinical implications of those with undiagnosed chronic liver test abnormalities. Fuss, et al. J Clin Immunol. 2013;33:748-58.Figure

J-Pouch Ectopic Varices: A Rare Cause of Lower GI Bleed

Variceal bleeding is a life-threatening complication of portal hypertension in patients with cirrhosis. Varices are portosystemic venous shunts that arise as a result of portal hypertension, most commonly located in the gastroesophageal (GE) area. Ectopic varices (ECV) are enlarged portosystemic venous collaterals located anywhere outside of the GE region. ECV bleeds are uncommon but can lead to significant morbidity and mortality. We present a rare case of lower GI bleeding from a small bowel varix in a J-pouch. A 34-year-old female with a history of ulcerative colitis status post total proctocolectomy with ileal pouch-anal anastomosis (IPAA or J-pouch) and primary sclerosing cholangitis with compensated cirrhosis was transferred to our hospital for an overt, obscure GI bleed. She initially presented to an outside hospital (OSH) with hematochezia and syncope. EGD, push enteroscopy, pouchoscopy, and capsule endoscopy at the OSH all failed to find the source of bleeding. Due to continued overt bleeding requiring 14 U of packed RBCs over 10 days, she was transferred to our medical center. Repeat EGD found no blood and no gastroesophageal varices. Pouchoscopy revealed red blood and clots in the J-pouch, but normal underlying mucosa and no obvious source of bleeding. A tagged RBC scan was positive for bleeding localized to a loop of small bowel in the right lower quadrant. CT-angiogram demonstrated a large ectopic venous collateral adjacent to the IPAA (Fig. 1) which was supplied by the superior mesenteric vein and drained by the right gonadal vein (Fig. 2), consistent with a small bowel varix. This ECV was the most likely cause of her recurrent bleeding. She underwent TIPS with reduction of portosystemic gradient from 25 to 11 mmHg and significant decompression of the ECV, rendering selective embolization unnecessary. She was discharged 5 days later and had no further bleeding at a 2 month follow-up visit. ECV account for 1-5% of all variceal bleeding episodes. Small bowel varices are most commonly seen in patients with portal hypertension and prior abdominal surgery. A triad of portal hypertension, hematochezia without hematemesis, and previous abdominal surgery should prompt evaluation for small bowel varices via CT scan with both arterial and venous phases. This case illustrates that, although rare, small bowel varices can present as massive lower GI bleeding and require a multidisciplinary approach with therapy tailored based on institutional expertise.Figure: CTA venous phase showing large venous collateral adjacent to J-pouch consistent with small bowel varix.Figure: Venogram illustrating enlarged superior mesenteric vein (SMV) filling varix with outflow tract through the right gonadal vein (R Gonadal V.).

Multidetector Computed Tomography Findings of Splenic Artery Aneurysms Associated With Liver Involvement in Wilson's Disease

PurposeThe purposed of this study was to examine the incidence and multidetector computed tomography (MDCT) findings of splenic artery aneurysms (SAAs) in patients with liver involvement related to Wilson's disease. MethodsEighteen patients with clinically and/or pathologically proven Wilson's disease underwent triphasic MDCT. Arterial, portal, and equilibrium phase images were obtained. The analysis of the CT features included the presence and characteristics of the SAA, splenic artery (SA) diameter, the presence and size of the portosystemic collateral vessels, and spleen volume. ResultsSAAs were detected in 11 patients (61.1%). Eight (72.7%) patients had multiple aneurysms. In 6 (54.5%) patients, the SAAs were located in the distal third of the SA and the intraparenchymal part of the SA. In 3 (27.3%) patients, the SAAs were located only in the distal third of the SA. In 1 (9.1%) patient, the aneurysms were located in the intermediate, distal third, and intraparenchymal part of the SA; in another (9.1%) patient, the aneurysms were located only in the intraparenchymal part of the SA. There were significant differences between the patients with SAA and those without SAA with respect to SA diameter, portosystemic collateral vessel diameter, and spleen volume (P = .007, P < .001, and P = .006, respectively). ConclusionsThe incidence of SAAs seems to be higher in patients with liver involvement related to Wilson's disease compared with patients with other causes of cirrhosis and portal hypertension. Large portosystemic collaterals, increased SA diameter, and spleen volume were significant factors for the presence of SAAs.

Portal Vein/Aorta Ratio in Dogs with Acquired Portosystemic Collaterals.

BackgroundThe portal vein (PV) diameter increases in humans with portal hypertension (PH). However, there is no evidence of PV enlargement in dogs with PH.ObjectivesTo measure the PV‐to‐aorta (PV/Ao) ratio in dogs with PH (chronic hepatitis [CH], primary hypoplasia of the PV [PHPV]), in dogs with extrahepatic congenital portosystemic shunt (EH‐CPSS), and in healthy dogs, and to evaluate the relationship between PV/Ao ratio and splenic pulp pressure (SPP).AnimalsTwenty‐five dogs with acquired portosystemic collaterals (APSCs; 15 with CH, 10 with PHPV), 32 dogs with EH‐CPSS, and 20 healthy dogs.MethodsRetrospective study. The PV/Ao ratio was calculated with images obtained by computed tomography. SPP was measured at the time of liver biopsy in 45 dogs.ResultsMedian PV/Ao ratio was similar between dogs with CH (1.35, range 1.05–2.01) and healthy dogs (0.95, 0.80–1.15), but differed significantly between the CH group and both the PHPV (0.40, 0.24–0.67) and EH‐CPSS groups (0.30, 0.11–0.64) (P < .001). The PV/Ao ratio was significantly lower in the PHPV group than in healthy dogs (P < .05). It also correlated positively with SPP (r s = 0.71; P < .001). However, there was no intragroup correlation between SPP and the PV/Ao ratio in any group.Conclusions and Clinical ImportanceThe PV/Ao ratio can be evaluated in dogs with APSCs on computed tomography. Further studies are needed to examine the relationship between SPP and the PV/Ao ratio in larger groups of dogs with PH and to determine its clinical relevance.

Effects of Portal Hypertension on Gadoxetic Acid-Enhanced Liver Magnetic Resonance: Diagnostic and Prognostic Implications.

The aim of this study was to investigate the impact of portal hypertension (PH) on gadoxetic acid-enhanced liver magnetic resonance imaging (MRI) and assess diagnostic and prognostic implications in comparison to established imaging features of PH. Institutional review board-approved retrospective study of 178 patients (142 men; median age, 59.4 years) with chronic liver disease undergoing MRI and hepatic venous pressure gradient (HVPG) measurement between January 2008 and April 2015. Magnetic resonance imaging was assessed for established features of PH (splenic and portal vein diameters, portosystemic collaterals, ascites) and for features on 20 minutes delayed T1-weighted gadoxetic acid-enhanced MRI, that is, relative liver enhancement (RLE), biliary contrast excretion, or portal vein hyperintensity or isointensity (ie, portal vein hyperintensity sign, PVHS). Statistics encompassed linear regression, logistic regression, and survival analysis. There was an inverse correlation between HVPG and RLE (r = 0.18, P < 0.0001). On univariate analysis, clinically significant PH (ie, HVPG ≥ 10 mm Hg, n = 109) and severe PH (ie, HVPG ≥ 12 mm Hg, n = 99) were associated with delayed biliary contrast excretion (n = 33) and the PVHS (n = 74) (P < 0.01 for all). Multivariate analysis demonstrated significant associations between the PVHS and severe PH (odds ratio [OR], 3.33; P = 0.008), independently of spleen size (OR, 1.26; P = 0.002), portosystemic collaterals (n = 81; OR, 5.46; P = 0.0001), and ascites (n = 88; OR, 3.24; P = 0.006). Lower RLE and the PVHS were associated with lower 3-year, transplantation-free survival (hazards ratios, 0.98 and 3.99, respectively, P = 0.002 for all), independently of the Child-Pugh and Model for End-Stage Liver Disease scores. The presence of the PVHS on gadoxetic acid-enhanced MRI is an independent indicator of severe PH and may enable more accurate diagnosis. This feature and decreased hepatic contrast uptake may also comprise prognostic information.

Ascorbate lacks significant influence in rats with bile duct ligation-induced liver injury

BackgroundLiver inflammation may induce fibrogenesis, cirrhosis and portal hypertension. Liver cirrhosis is characterized by increased intrahepatic resistance and enhanced vasoconstrictive response. The splanchnic vasodilatation, angiogenesis and portosystemic collaterals formation further bring about lethal complications. Ascorbate is a potent antioxidant with anti-inflammation, anti-fibrosis, and anti-angiogenesis effects. However, the relevant influences in chronic liver injury have not been sufficiently explored. MethodsChronic liver injury was induced in Spraque-Dawley rats with common bile duct ligation (BDL). Ascorbate (250 mg/kg/day, oral gavage) or vehicle was administered starting on the 1st day after operation. On the 8th (hepatitis) and 29th (cirrhosis) day, serum biochemistry parameters, hepatic concentrations of lipid peroxidation-related substances, protein expressions of α-SMA, TGF-β, iNOS, eNOS, p-eNOS-Ser1177, p-eNOS-Thr496, VEGF, VEGFR2, p-VEGFR2, and liver histology were evaluated. In three series of paralleled groups, rats treated with 28-day ascorbate or vehicle received hemodynamic measurements, hepatic and collateral vasoresponsiveness perfusion experiments, mesenteric CD31 immunofluorescence staining, and Western blot analyses of mesenteric VEGF, VEGFR2, pVEGFR2, PDGF, PDGFβ, COX1, COX2, eNOS, p-eNOS-Thr495, p-eNOS-Ser1177 protein expressions. In another series, the severity of portosystemic shunting was evaluated. ResultsAscorbate did not influence hepatitis, oxidative stress, fibrosis, and hemodynamic parameters in BDL rats. The intrahepatic and collateral vasoresponsiveness were not affected, either from direct incubation or acute treatment with ascorbate. Furthermore, the mesenteric angiogenesis and severity of shunting were not influenced. ConclusionThe oxidative stress, fibrosis, hemodynamic derangements, angiogenesis and vascular functional changes in BDL-induced chronic liver injury may be too overwhelming to be modulated by ascorbate.

Extrahepatic Portal Venous Obstruction: What Should be the Mainstay of Treatment?

The two cornerstones of management for Extrahepatic portal vein obstruction (EHPVO) are endotherapy and surgery [Porto-systemic shunts (PSS)/Mesorex bypass (MRB)]. Endotherapy is the mainstay of treatment for acute variceal bleed control and has also been used extensively for secondary prophylaxis till variceal eradication is achieved. However, long-term follow-up beyond endoscopic eradication of esophageal varices (EEEV) indicates that there are numerous delayed bleed and non bleed sequelae of EHPVO, which merit surgery as a definitive procedure to decompress the hypertensive portal venous system. While endotherapy obliterates natural porto-systemic collaterals in the gastroesophageal region, persistently raised portal pressures manifest as an increase in secondary isolated gastric varices, ectopic varices, portal hypertensive vasculopathy, issues related to massive splenomegaly, portal biliopathy, growth retardation and hence impaired quality of life (QOL). An ideal management strategy should address both bleed and non-bleed consequences of EHPVO and translate into a near normal QOL. Further, MRB has opened up new dimensions to the management philosophy of EHPVO. This review article critically evaluates the role of surgery and endotherapy based on available literature and authors' own experience.Surgery and endotherapy are complementary. However, with increasing duration of follow-up post EEEV, it is evident that there is resurgence in the role of surgery (PSS/MRB) as a single one time definitive procedure for alleviating all bleed and delayed non bleed sequelae of EHPVO.Surgery for EHPVO (PSS/MRB) should not be allowed to become a dying art and future generations of surgeons should continue to receive training in this specialized area of surgery.

THE ROLE OF LASER DOPPLER FLOWMETRY IN THE STUDY OF SKIN MICROCIRCULATION IN DIFFUSE LIVER DISEASES

Among the most important links in the pathogenesis of diffuse liver diseases (DLD) are macro- and microhemodynamic disorders that can develop in the liver and in the systemic circulation [2, 3, 7, 12]. Chronic hepatitis (CH) and especially liver cirrhosis (LC) are accompanied by disorders of the portal and systemic circulation, development of portal hypertension which leads to the emergence of portosystemic collaterals and hyperdynamic circulation [2, 3, 7, 12]. The resulting rheological changes in the blood, disorders of systemic hemodynamics run in parallel with the microcirculatory (MC) pathology. [8, 9, 12] In this condition, the inflammatory and reparative processes, maintainance of the adequate level of biochemical reactions in the tissues, cellular functions and changes in blood coagulation system are determined by the microcirculation (MC) status [2, 3, 12].

Portosystemic collaterals in living donor liver transplantation: What is all the fuss about?

Portosystemic collaterals are a common finding in patients with cirrhosis undergoing liver transplantation. Recently, there has been a renewed interest regarding their significance in the setting of living donor liver transplantation (LDLT) due to concerns of graft hypoperfusion or hyperperfusion and its impact on early posttransplant outcomes. Presence of these collaterals has greater significance in the LDLT setting when compared with the deceased donor liver transplantation setting as dictated by the difference in the physiology of partial liver grafts. We discuss current thinking of portal flow dynamics and the techniques for dealing with this clinical problem. Liver Transplantation 23 537-544 2017 AASLD.

N-butyl-2 cyanoacrylate (NBCA) embolus in the graft portal vein after portosystemic collateral embolization in liver transplantation recipient: what is the clinical significance?

Background An N-butyl-2 cyanoacrylate (NBCA) embolus in the graft portal vein was frequently observed after an intraoperative embolization of portosystemic collaterals performed to prevent portal steal in liver transplant (LT) recipients. The radiological and clinical features of NBCA emboli have not yet been described. Purpose To describe radiological and clinical features of NBCA embolus in graft portal vein after portosystemic collateral embolization in LT recipients. Material and Methods A total of 165 consecutive LT recipients who had undergone intraoperative NBCA embolization of varix were found in single institution's computerized databases of a clinical cohort of LT. Patients were evaluated for NBCA emboli (categorized into major and minor emboli according to location) on first postoperative computed tomography (CT). All electronic medical records and radiologic studies including follow-up was evaluated to determine any radiological and clinical abnormality associated with NBCA embolus. Results NBCA emboli were found in 24% (39/165) of recipients. Although most patients had minor emboli (77%, 30/39) without remarkable ultrasonography (US) abnormalities, seven (78%) of nine recipients with major emboli showed intraluminal echogenic lesions in graft portal vein on grayscale US, and five of them (71%) showed partial portal flow obstruction, although none exhibited any abnormality on contrast-enhanced US. Recipients with NBCA portal emboli showed no significant clinical abnormalities and were discharged safely. NBCA embolus eventually disappeared mostly within six months (82%, 32/39). Conclusion NBCA emboli are frequently observed after portosystemic collateral embolization in LT recipients and are not associated with poor clinical outcome. They may mimic ordinary thromboemboli on US.

Portal hypertension: Imaging of portosystemic collateral pathways and associated image-guided therapy.

Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases. This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen. A brief overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.