Restrictive Pulmonary Dysfunction May Increase Blood Loss During Liver Resection.

BACKGROUND: Restrictive pulmonary dysfunction (RPD) is a risk factor for perioperative complications during gastrointestinal surgery. We hypothesized that high airway pressure due to RPD results in increased intraoperative blood loss during liver surgery. Thus, we investigated the effects of RPD on perioperative outcomes for liver resection. METHODS: This study included 496 patients who underwent curative liver resection at our hospital between April 2009 and April 2020. Perioperative outcomes for the RPD and control groups were compared. Restrictive pulmonary dysfunction was defined as % vital capacity <80%. RESULTS: Forty-one patients (8.3%) had RPD. No significant differences were observed in intraoperative blood losses (440 mL vs 320 mL, P = .340), overall complication rates (29.3% vs 31.2%, P = .797), or pulmonary complication rates (4.9% vs 9.0%, P = .286) between the RPD and control groups. In the 256 patients who underwent anatomical liver resection, 18 patients (7.0%) had RPD. The intraoperative blood loss was significantly higher in the RPD group (925 mL vs 456 mL, P = .013), but no differences in the overall complication rates (44.4% vs 37.3%, P = .528) or pulmonary complication rates (11.1% vs 10.5%, P = .589) between the two groups were detected. A multivariate analysis showed that RPD was an independent risk factor for intraoperative blood loss ≥500 mL during anatomical liver resection (odds ratio 4.132; 95% confidence interval 1.135-15.045; P = .031). DISCUSSION: Restrictive pulmonary dysfunction may be a risk factor for intraoperative blood loss during anatomical liver resection, which requires exposure of the main hepatic vein.

Second-harmonic generation (SHG) microscopy and hepatic venous pressure gradient-based validation of a novel histological staging system for alcoholic hepatitis.

Alcoholic hepatitis (AH) lacks specific histological staging. A novel fibrosis staging that encompasses perisinusoidal fibrosis and cirrhosis sub-stages, substantiated by Hepatic venous pressure gradient (HVPG) and automated fibrosis quantification, is imperative. To correlate novel histological staging system of AH with second-harmonic generation microscopy (SHG)-based q-fibrosis, HVPG, and activated hepatic stellate cells (HSCs). Liver biopsies of AH (n = 175) were staged semi-quantitatively as F0, F1, F2, F3A and F3B and Laennec substages of cirrhosis 4A, 4B and 4C. Stages were correlated with SHG q-fibrosis parameters, HVPG and HSCs. Mean age 41.2 ± 9.4 years, 96.6% males, bilirubin 20.58 ± 8.0 mg/dl and Maddrey's discriminant function 78.9 ± 36.7 displayed advanced fibrosis in 98.6%. With increasing histological stages, an increase in q-fibrosis indices and mean HVPG (p < 0.0001) were recorded; stage 4C showed the most significant difference from other stages (p < 0.000). Stages 3A and 3B were comparable with the stages 4A and 4B, respectively, for q-fibrosis (p = 1) and HVPG (p = 1). HSCs (> 30%) were significantly higher in stage 3 (75%) compared with 4 (49%) and 2 (59%), p = 0.018. Overall agreement for histological staging was excellent for all stages (0.82). SHG quantified fibrosis and HVPG corroborates the novel histological staging of AH. Expansive PCF matches with collagen content and clinical severity to early sub-stages of cirrhosis. This highlights the need for an accurate quantification and inclusion of PCF as a separate stage. SHG-based quantification can be a useful adjunct to histological fibrosis staging systems.

Parietal Peritoneum as a Novel Substitute for Middle Hepatic Vein Reconstruction During Living Donor Liver Transplantation.

BACKGROUND: Although autologous, cryopreserved, or artificial vascular grafts can be used as interpositional vascular substitutes for middle hepatic vein (MHV) reconstruction during living donor liver transplantation (LDLT), they are not always available, are limited in size and length, and are associated with risks of infection. This study aimed to evaluate the parietal peritoneum as a novel substitute for MHV reconstruction during LDLT. METHODS: Prospectively collected data of 15 patients who underwent LDLT using the right liver with reconstruction of MHV using the recipients' own parietal peritoneum graft were retrospectively reviewed. RESULTS: The 1-, 2-, 3-, and 5-mo patency rates were 57.1%, 57.1%, 57.1%, and 28.6%, respectively. Among the 15 cases assessed, the most recent 6 cases showed patent graft flow until discharge with 1-, 2-, 3-, and 5-mo patency rates of 80.0%, 80.0%, 80.0%, and 20.0%, respectively. All patients survived with tolerable liver function tests. There were no significant congestion-related problems, except for 1 patient who experienced MHV thrombosis requiring aspiration thrombectomy and stent insertion. There were no infection-related complications. All patients survived to the final follow-up, with a minimum follow-up duration of 8 mo. When comparing the latter 6 cases of peritoneal grafts and the recent 28 cases of conventional polytetrafluorethylene graft, the overall patency rate of the polytetrafluorethylene group was higher (P = 0.002). There were no major differences other than long-term patency rate. CONCLUSIONS: Parietal peritoneum may be a novel autologous substitute for MHV reconstruction during LDLT.

Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy.

Here we provide a detailed protocol describing the clinical procedure of hepatic venous pressure gradient (HVPG) measurement in patients with advanced chronic liver disease followed by an instruction for transjugular biopsy. Under local anesthesia and ultrasound guidance, a catheter introducer sheath is placed in the right internal jugular vein. Using fluoroscopic guidance, a balloon catheter is advanced into the inferior vena cava (IVC) and inserted into a large hepatic vein. Correct and sufficient wedge position of the catheter is ensured by injecting contrast media while the balloon is blocking the outflow of the cannulated hepatic vein. After calibrating the external pressure transducer, continuous pressure recordings are obtained with triplicate recordings of the wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHVP). The difference between FHVP and WHVP is referred to as HVPG, with values ≥10 mm Hg indicating clinically significant portal hypertension (CSPH). Before removing the catheter, pressure readings obtained in the IVC at the same level, as well as the right atrial pressure are recorded. Finally, a transjugular liver biopsy can be obtained via the same vascular route. Different systems are available; however, core biopsy needles are preferred over aspiration needles, especially for cirrhotic livers. Again, under fluoroscopic guidance a biopsy needle introducer sheath is advanced into an hepatic vein. Next, the transjugular biopsy needle is gently advanced through the introducer sheath: (i) in case of aspiration biopsy, the needle is advanced into the liver parenchyma under aspiration and then removed quickly, or (ii) in case of a core biopsy, the cutting-mechanism is triggered inside the parenchyma. Several separate passages can be safely performed to obtain sufficient liver specimens via transjugular biopsy. In experienced hands, the combination of these procedures takes about 30-45 min.

Feasibility and safety of bisegmentectomy 7-8 while preserving hepatic venous outflow of the right liver - A retrospective cohort study.

BACKGROUND: When a hepatic tumor is deeply located in segments 7 and 8 around the right hepatic vein (RHV), right hemihepatectomy (RH) could be excessive owing to the resection of large tumor-free segments. This study aimed to evaluate the feasibility and safety of bisegmentectomy 7-8 (S7-8) and to compare its surgical outcomes with those of RH. MATERIALS AND METHODS: Consecutive patients who underwent S7-8 and RH were enrolled in this study. In the S7-8 group, 14 patients with an obvious inferior right hepatic vein (IRHV) (median: 6 mm; range: 3.6-8.8 mm) underwent S7-8 without hepatic vein reconstruction. RHV reconstruction was performed in six patients without an IRHV, involving direct anastomosis of the RHV in five patients and reconstruction using a cryo-preserved iliac vein in one patient. RESULTS: A total of 61 patients were included (20 in S7-8 group; 41 in RH group). No significant differences were observed other than higher a model of end-stage liver disease score in the RH group than in the S7-8 group (7 [6-20] vs. 6 [6-9], P = 0.003). Post-hepatectomy liver failure including severe grades was more frequent in the RH group (43.9% vs. 10%, P = 0.008). In the S7-8 group, two patients with direct RHV reconstruction had RHV anastomosis obstruction, and eventually required insertion of a metallic stent. However, computed tomography performed 4 weeks after the operation showed intact venous outflow of the right liver in the S7-8 group. CONCLUSION: S7-8 can be performed safely in selected patients with a thick IRHV. For patients with no obvious IRHV, RHV reconstruction could be a good surgical strategy to retain venous outflow of the right liver with feasible outcomes.

4D Flow MR Imaging to Improve Microwave Ablation Prediction Models: A Feasibility Study in an In Vivo Porcine Liver.

PURPOSE: To characterize the effect of hepatic vessel flow using 4-dimensional (4D) flow magnetic resonance (MR) imaging and correlate their effect on microwave ablation volumes in an in vivo non-cirrhotic porcine liver model. MATERIALS AND METHODS: Microwave ablation antennas were placed under ultrasound guidance in each liver lobe of swine (n = 3 in each animal) for a total of 9 ablations. Pre- and post-ablation 4D flow MR imaging was acquired to quantify flow changes in the hepatic vasculature. Flow measurements, along with encompassed vessel size and vessel-antenna spacing, were then correlated with final ablation volume from segmented MR images. RESULTS: The linear regression model demonstrated that the preablation measurement of encompassed hepatic vein size (ß = -0.80 ± 0.25, 95% confidence interval [CI] -1.15 to -0.22; P = .02) was significantly correlated to final ablation zone volume. The addition of hepatic vein flow rate found via 4D flow MRI (ß = -0.83 ± 0.65, 95% CI -2.50 to 0.84; P = .26), and distance from antenna to hepatic vein (ß = 0.26 ± 0.26, 95% CI -0.40 to 0.92; P = .36) improved the model accuracy but not significantly so (multivariate adjusted R2 = 0.70 vs univariate (vessel size) adjusted R2 = 0.63, P = .24). CONCLUSIONS: Hepatic vein size in an encompassed ablation zone was found to be significantly correlated with final ablation zone volume. Although the univariate 4D flow MR imaging-acquired measurements alone were not found to be statistically significant, its addition to hepatic vein size improved the accuracy of the ablation volume regression model. Pre-ablation 4D flow MR imaging of the liver may assist in prospectively optimizing thermal ablation treatment.

Portal hypertension evolving from sickled hepatopathy: Could hepatic venous Doppler ultrasound be beneficial in its evaluation?

PURPOSE: Sickle cell intrahepatic cholestasis involves sickling within hepatic sinusoids leading to vascular stasis and localized hypoxia resulting in ballooning of the hepatocytes causing a direct back pressure effect with resultant intracanalicular cholestasis. Vascular stasis may ultimately lead to portal hypertension. We proposed to document findings suggestive of portal hypertension evolving from hepatopathy in steady-state sickle cell disease (SCD) patients using hepatic venous Doppler ultrasound. METHODS: This is a prospective case series of 6 SCD subjects in steady-state (median age, 30 years; range, 19-43), comprising of 3 males and 3 females, who underwent a routine Doppler ultrasound evaluation of their hepatic veins and were discovered to have an abnormal biphasic waveform pattern. Venous blood was obtained from all subjects to evaluate for P-selectin, homocysteine, foetal haemoglobin, haematocrit levels, white cell and platelet counts. Doppler ultrasound was also carried out on all subjects to evaluate for the hepatic waveform, right renal artery RI and PI along with the hepatic artery velocities. RESULTS: All the 6 subjects had reduced haematocrit (median value of 21.5%; range, 18-25%) and some degree of renal dysfunction (plasma cystatin-C ranged from 1.6 to 12.2 mg/L). Elevated white cell count, hyperhomocysteinemia, reduced SpO2(<94.0%) and reduced estimated GFR (eGFR < 90 ml/min) was also noted in 4 subjects (66.7%). Similarly, 4 subjects (66.7%) had elevated RI in the right kidneys while 3 subjects (50.0%) had elevated PI in the right kidney. CONCLUSION: Doppler ultrasound Hepatic vein waveform analysis may be a useful examination in the evaluation of patients with SCD as it may elicit feature of portal hypertension. Further studies are suggested to confirm this in a larger population of SCD patients using the gold standard.

Non-invasive assessment of portal hypertension by multi-parametric magnetic resonance imaging of the spleen: A proof of concept study.

BACKGROUND AND AIMS: Non-invasive assessment of portal hypertension is an area of unmet need. This proof of concept study aimed to evaluate the diagnostic accuracy of a multi-parametric magnetic resonance technique in the assessment of portal hypertension. Comparison to other non-invasive technologies was a secondary aim. METHODS: T1 and T2* maps through the liver and spleen were acquired prior to trans-jugular liver biopsy and hepatic vein pressure gradient (HVPG) measurement. T1 measurements reflect changes in tissue water content, but this relationship is confounded by the presence of iron, which in turn can be quantified accurately from T2* maps. Data were analysed using LiverMultiScan (Perspectum Diagnostics, Oxford, UK) which applies an algorithm to remove the confounding effect of iron, yielding the "iron corrected T1" (cT1). Sensitivity, specificity, diagnostic values and area under the curve were derived for spleen cT1, liver cT1, transient elastography, and serum fibrosis scores. HVPG was the reference standard. RESULTS: Nineteen patients (15 men) with median age 57 years were included. Liver disease aetiologies included non-alcoholic fatty liver disease (n = 9; 47%) and viral hepatitis (n = 4; 21%). There was strong correlation between spleen cT1 and HVPG (r = 0.69; p = 0.001). Other non-invasive biomarkers did not correlate with HVPG. Spleen cT1 had excellent diagnostic accuracy for portal hypertension (HVPG >5 mmHg) and clinically significant portal hypertension (HVPG ≥10 mmHg) with an area under the receiver operating characteristic curve of 0.92 for both. CONCLUSION: Spleen cT1 is a promising biomarker of portal pressure that outperforms other non-invasive scores and should be explored further.

Review article: a multidisciplinary approach to the diagnosis and management of Budd-Chiari syndrome.

BACKGROUND: Budd-Chiari syndrome (BCS) is a rare but fatal disease caused by obstruction in the hepatic venous outflow tract. AIM: To provide an update of the pathophysiology, aetiology, diagnosis, management and follow-up of BCS. METHODS: Analysis of recent literature by using Medline, PubMed and EMBASE databases. RESULTS: Primary BCS is usually caused by thrombosis and is further classified into "classical BCS" type where obstruction occurs within the hepatic vein and "hepatic vena cava BCS" which involves thrombosis of the intra/suprahepatic portion of the inferior vena cava (IVC). BCS patients often have a combination of prothrombotic risk factors. Aetiology and presentation differ between Western and certain Asian countries. Myeloproliferative neoplasms are present in 35%-50% of European patients and are usually associated with the JAK2-V617F mutation. Clinical presentation is diverse and BCS should be excluded in any patient with acute or chronic liver disease. Non-invasive imaging (Doppler ultrasound, computed tomography, or magnetic resonance imaging) usually provides the diagnosis. Liver biopsy should be obtained if small vessel BCS is suspected. Stepwise management strategy includes anticoagulation, treatment of identified prothrombotic risk factors, percutaneous revascularisation and transjugular intrahepatic portosystemic stent shunt to re-establish hepatic venous drainage, and liver transplantation in unresponsive patients. This strategy provides a 5-year survival rate of nearly 90%. Long-term outcome is influenced by any underlying haematological condition and development of hepatocellular carcinoma. CONCLUSIONS: With the advent of newer treatment strategies and improved understanding of BCS, outcomes in this rare disease have improved over the last three decades. An underlying haematological disorder can be the major determinant of outcome.

Patients With Signs of Advanced Liver Disease and Clinically Significant Portal Hypertension Do Not Necessarily Have Cirrhosis.

BACKGROUND & AIMS: Patients with hepatic venous pressure gradients (HVPGs) of 10 mm Hg or greater and chronic liver disease often are assumed to have cirrhosis. We investigated the association between HVPGs and cirrhosis, using histologic findings as the reference standard. We also assessed the prevalence and characteristics of patients with HVPGs of 10 mm Hg or greater without cirrhosis. METHODS: We performed a retrospective analysis of 157 consecutive patients, 89 with suspected cirrhosis and hepatic hemodynamic data collected from 2015 through 2017. Biopsy specimens collected had 10 or more portal tracts from each patient and were analyzed for features of cirrhosis. Biopsy specimens with histologic features of cirrhosis were excluded and the remaining biopsy specimens were re-reviewed by an expert pathologist. The fibrosis area was calculated digitally by image analysis. RESULTS: HVPG identified patients with cirrhosis with an area under the receiver operating characteristic curve of 0.879: 14 of 89 patients with HVPG of 10 mm Hg or greater (16%) had no histologic features of cirrhosis (METAVIR scores <4 and Ishak scores <6). The median HVPG was 11 mm Hg (range, 10-22 mm Hg). Based on METAVIR scores, 7 patients had fibrosis stage F3, 4 patients had fibrosis stage F2, and 3 patients had fibrosis stages F0 or F1. The mean area of fibrosis in livers was 16.2% ± 6.5%. All 14 patients had perisinusoidal fibrosis and 8 patients had hepatocyte ballooning. The most common diagnoses were nonalcoholic steatohepatitis (n = 5) and nodular regenerative hyperplasia (n = 4). An HVPG cut-off value of 12 mm Hg identified patients with cirrhosis with 92% specificity, misclassifying 5 patients with different etiologies of liver disease. CONCLUSIONS: In a retrospective analysis of 89 consecutive patients with chronic liver disease and an HVPG of 10 mm Hg or greater, 16% were not found to have cirrhosis upon biopsy analysis. Most of these patients had nonalcoholic steatohepatitis or nodular regenerative hyperplasia. Perisinusoidal fibrosis and hepatocyte ballooning might increase sinusoidal pressure. An HVPG cut-off value of 12 mm Hg or greater identified patients with cirrhosis with 92% specificity.

Impact of Functional Hepatic Venous Outflow Obstruction on Perioperative Outcome After Living-Donor Liver Transplant.

OBJECTIVES: An optimal initial graft function after living-donor liver transplant depends on optimal graft hemodynamics. Nonmechanical impediments to free hepatic venous outflow, due to elevated central venous pressure, may obstruct the "functional" hepatic venous outflow. Here, we evaluated whether central venous pressure affected early graft function and outcomes in adult living-donor liver transplant recipients. MATERIALS AND METHODS: This prospective observational study included 61 living-donor liver transplant recipients without technical complications who received transplants from August 2013 to November 2014. Hemodynamic variables were measured preoperatively, at anhepatic phase, 30 minutes postreperfusion, at end of surgery, and during postoperative days 1-5. RESULTS: Patients with high central venous pressure showed functional hepatic venous outflow obstruction, which caused delayed recovery of graft function. Although postoperative central venous pressure was the only identified independent risk factor for mortality, all 5 deaths in our study group occurred in those who had high central venous pressure at the anhepatic, postreperfusion, end of surgery, and postoperative phases. A postoperative central venous pressure value of ~11 mm Hg was determined to be the cutoff for high-risk mortality, with area under the curve of 0.859 (sensitivity of 80%, specificity of 68%). Increased central venous pressure was associated with increased portal venous pressure (increase of 45%, range, 28%-89%; P = .001). Central venous pressure at end of surgery (r = 0.45, P ≤ .001) and at posttransplant time points (r = 0.29, P = .02) correlated well with portal venous pressure at end of surgery. Other risk factors for early allograft dysfunction were Model for End-Stage Liver Disease and cardiac output posttransplant. CONCLUSIONS: High central venous pressure, modulating portal venous pressure, can result in functional hepatic venous outflow obstruction, causing delayed graft function recovery and increased risk of mortality. Maintaining a central venous pressure below 11 mm Hg is beneficial.

Radical surgical treatment of Budd-Chiari syndrome through entire exposure of hepatic inferior vena cava.

OBJECTIVE: Therapies for Budd-Chiari syndrome (BCS) can be divided into three main categories: medical, endovascular, and surgical. Surgery is applicable to the disease when other therapeutic options have failed. We introduce a surgical method of recanalization through exposure of the entire hepatic inferior vena cava (IVC) and hepatic vein (HV) outflow tract for BCS and investigate the long-term outcomes. METHODS: From July 2002 to December 2015 in our center, 83 consecutive symptomatic BCS patients with failure of endovascular therapy were treated by radical surgical recanalization. IVC recanalization was the first goal for all patients, and recanalization of at least one HV was the second goal for selected patients at the same surgical operation. Patients were followed up, and data on technical and clinical success, survival, and patency of target vessels were analyzed. RESULTS: Technical success of surgical recanalization was achieved in 80 patients (96.4%), with relief of clinical symptoms and improvement of liver function. During a mean follow-up of 84 ± 25.9 months, the cumulative 1-, 3-, and 5-year primary patency rates of the HV were 96.7%, 90.0%, and 83.3%, respectively. The cumulative 1-, 3-, and 5-year primary patency of the IVC was 86.7%, 71.7%, and 68.3%, respectively. No factor demonstrated significant association with recurrence of obstruction. During follow-up, 10 patients died, 8 of end-stage hepatic disease and 2 of unknown causes. The cumulative 1-, 3-, and 5-year all-cause survival rates were 91%, 90%, and 87%, respectively. Female sex, encephalopathy, severe ascites, and hypersplenism had an impact on survival in univariate analysis. With Cox regression, encephalopathy was the only independent determining factor for surgical survival. CONCLUSIONS: Surgical recanalization through exposure of the entire hepatic IVC for BCS is suitable for most primary BCS patients after failure of endovascular therapies.

Explant portal vein for reconstructing middle hepatic vein in right lobe living donor liver transplantation-outcome analysis.

BACKGROUND: The aim of the study was to study the four week patency rates of the reconstructed neo middle hepatic vein specifically using the explant portal vein (PV) in right hemiliver live donor liver transplantation (LDLT). We hypothesized that short term patency of the neo-MHV should result in good graft and patient outcomes. METHODS: Pre, intra and post operative variables were prospectively collected for 88 consecutive patients undergoing right hemiliver LDLT from January 2014 to October 2015. RESULTS: Explant PV was used to reconstruct neo-MHV in 76 (86.4%, 76/88) patients. Neo MHV patency rate at 28 days with explant PV was 89.4% (59/66) and with other conduit (PTFE) was 90.9% (10/11). All occlusions were detected after 7 days. There was no impact of the patency of the neo-MHV on the incidence of early allograft dysfunction, sepsis, rejection, morbidity or mortality, despite the contribution of the anterior sector to the graft volume being more than 50% in close to two-thirds of patients. CONCLUSION: The reconstructed neo-MHV has excellent short term patency rates at 4 weeks. Perhaps due to the absence of early occlusions, there was no impact on graft or patient outcomes in the study population.

Modified total cavopulmonary shunt as a staged Fontan operation.

The left superior vena cava became occluded in an infant with hypoplastic left heart syndrome. After a bidirectional Glenn procedure, he presented with severe oxygen desaturation and right ventricular dysfunction; the left superior vena cava drained into the inferior vena cava through collateral veins. As salvage therapy, we created a modified total cavopulmonary shunt using only autologous tissue in which the right hepatic vein and inferior vena cava drained into the pulmonary artery via a lateral tunnel in the right atrium. Immediately after surgery, his oxygen saturation increased and right ventricular function improved.

The portal hypertension syndrome: etiology, classification, relevance, and animal models.

BACKGROUND: Portal hypertension is a key complication of portal hypertension, which is responsible for the development of varices, ascites, bleeding, and hepatic encephalopathy, which, in turn, cause a high mortality and requirement for liver transplantation. AIM: This review deals with the present day state-of-the-art preventative treatments of portal hypertension in cirrhosis according to disease stage. Two main disease stages are considered, compensated and decompensated cirrhosis, the first having good prognosis and being mostly asymptomatic, and the second being heralded by the appearance of bleeding or non-bleeding complications of portal hypertension. RESULTS: The aim of treatment in compensated cirrhosis is preventing clinical decompensation, the more frequent event being ascites, followed by variceal bleeding and hepatic encephalopathy. Complications are mainly driven by an increase of hepatic vein pressure gradient (HVPG) to values ≥10 mmHg (defining the presence of Clinically Significant Portal Hypertension, CSPH). Before CSPH, the treatment is limited to etiologic treatment of cirrhosis and healthy life style (abstain from alcohol, avoid/correct obesity…). When CSPH is present, association of a non-selective beta-blocker (NSBB), including carvedilol should be considered. NSBBs are mandatory if moderate/large varices are present. Patients should also enter a screening program for hepatocellular carcinoma. In decompensated patients, the goal is to prevent further bleeding if the only manifestation of decompensation was a bleeding episode, but to prevent liver transplantation and death in the common scenario where patients have manifested first non-bleeding complications. Treatment is based on the same principles (healthy life style..) associated with administration of NSBBs in combination if possible with endoscopic band ligation if there has been variceal bleeding, and complemented with simvastatin administration (20-40 mg per day in Child-Pugh A/B, 10-20 mg in Child C). Recurrence shall be treated with TIPS. TIPS might be indicated earlier in patients with: 1) Difficult/refractory ascites, who are not the best candidates for NSBBs, 2) patients having bleed under NSBBs or showing no HVPG response (decrease in HVPG of at least 20% of baseline or to values equal or below 12 mmHg). Decompensated patients shall all be considered as potential candidates for liver transplantation. CONCLUSION: Treatment of portal hypertension has markedly improved in recent years. The present day therapy is based on accurate risk stratification according to disease stage.

Congestive hepatopathy.

Passive hepatic congestion may result from a variety of distinct cardiovascular conditions. Injury to the liver caused by congestion is often asymptomatic and may not be recognized clinically. Diagnosis of congestive hepatopathy is important as it has the potential to cause complications including hepatic fibrosis and development of benign and malignant liver masses. This review will summarize the pathophysiologic mechanisms of congestive hepatopathy and provide both description and examples of its multimodality imaging findings. Examples of alternative disease which may have a similar imaging appearance will be provided. Knowledge regarding the characteristic imaging findings of congestive hepatopathy will allow for its accurate identification. Reviewing both the benefits and limitations of imaging performed to evaluate congestive hepatopathy and its complications will help to avoid pitfalls and enable recommendation of appropriate next steps in diagnostic evaluation.