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Please see the Editorial Comment by Domen Plut discussing this article. Background: Image-guided interventions for Budd-Chiari syndrome (BCS) reduce hepatic congestion, thereby reducing liver stiff...

Background: Hepatic congestion is a frequent finding in patients with heart failure (HF). Physical examination has limitations in quantifying systemic congestion and requires correlation with echocardiographic and laboratory data (usually B-type natriuretic peptide, BNP, or N-terminal pro-B type natriuretic peptide, NT-proBNP). Hepatic elastography evaluates liver stiffness using a transducer that transmits low-frequency vibrations (50 Hz), and the speed of shear waves propagating through the tissues is measured by ultrasound. The faster the vibrations propagate in the hepatic parenchyma, the stiffer the liver, which, in case of HF, can be correlated with hepatic congestion. Objective: In this systematic review, case-controls, cohort studies, and randomized clinical trials were searched in MEDLINE, LILACS and Cochrane Database of Systematic Review, to evaluate the use of elastography in the detection of hepatic congestion in patients with HF. Methods: From the 49 articles retrieved, seven were selected for review, according to the inclusion and exclusion criteria. The most used methods for the diagnosis and evaluation of HF were echocardiography combined with BNP and NT-proBNP measurements. Results: Elastography performed at bedside was able to establish a significant correlation between increased liver stiffness and increased venous capillary pressure. In addition, liver elastography performed at hospital discharge was able to predict rehospitalization and mortality. Conclusion: Liver elastography is a non-invasive method that can be useful in predicting prognosis and mortality of individuals with HF, contributing to the clinical management of these patients.

In laparoscopic proximal gastrectomy, the hepatic left lateral segment often obstructs the operative field of view, especially around the esophageal hiatus. Therefore, a safe retraction method is needed. The present study aimed to determine the effectiveness of inverting the hepatic left lateral segment in laparoscopic proximal gastrectomy. This was a retrospective review of 81 consecutive patients who underwent laparoscopic proximal gastrectomy. Patients were divided into two groups, i.e., the Nathanson liver retractor group (n = 41) and hepatic left lateral segment inverting group (n = 40). The unedited video recordings of the procedures and the patients’ medical records were reviewed and compared. The hepatic left lateral segment inverting method provided a more satisfactory view of the operative fields and a wider working space around the esophageal hiatus than the Nathanson liver retractor. No intraoperative hepatic congestion and significantly improved postoperative liver enzyme elevations were observed with hepatic left lateral segment inverting method compared with the Nathanson liver retractor method. In laparoscopic proximal gastrectomy, the hepatic left lateral segment inverting method appears to provide improvements in both the operative field of view and liver protection compared with the Nathanson liver retractor method.

Critically ill patients frequently present with the systemic inflammatory response syndrome, which is largely a reflection of the liver's response to injury. Underlying hepatic congestion is a major risk factor for hypoxic liver injury, the most common cause for hepatocellular injury. Cholestatic liver injury often occurs in critically ill patients due to inhibition of farnesoid X receptor (FXR), the main regulator of bile acid handling, particularly in the liver and intestines. Additional injury to the liver occurs due to alterations in the bile acid pool with increased cytotoxic forms and disturbance in the typical processing of xenobiotics in the liver.

A 14-year-old boy presented with several months of increasing abdominal girth and fatigue. Imaging confirmed massive ascites and hepatic congestion secondary to central hepatic venous obstruction. Several large intrahepatic collateral veins were seen draining via caudate and emissary veins. After an unsuccessful attempt at retrograde recanalization utilizing intravascular ultrasound, the right hepatic vein was recanalized in an antegrade fashion by way of a prominent caudate collateral vein, and subsequently stented. We herein discuss the established treatment options for Budd-Chiari syndrome and describe our experience employing a single-access liver floss technique.

The viscoelastic properties of the liver and spleen can be assessed with magnetic resonance elastography (MRE). Several actuators, MRI acquisition sequences and reconstruction algorithms have been proposed for this purpose. Reproducible results are obtained, especially when the examination is performed in standard conditions with the patient fasting. Accurate staging of liver fibrosis can be obtained by measuring liver stiffness or elasticity with MRE. Moreover, emerging evidence shows that assessing the tissue viscous parameters with MRE is useful for characterizing liver inflammation, non-alcoholic steatohepatitis, hepatic congestion, portal hypertension, and hepatic tumors. Further advances such as multifrequency acquisitions and compression-sensitive MRE may provide novel quantitative markers of hepatic and splenic mechanical properties that may improve the diagnosis of hepatic and splenic diseases.

The sinusoidal obstruction syndrome (SOS) is an uncommon form of portal hypertension that occurs in hematopoietic-cell transplant recipients who receive intense conditioning treatments. The diagnosis is clinical and it is usually delayed, because in these patients there are many causes that can damage the liver and can delay its detection. We present the case of a 47-year-old man, whose diagnosis was made with clinical and analytical data supported by ultrasound signs that showed hepatic congestion. After treatment with defibrotide the patient improved clinically and analytically. Hepatic vascularization and perfusion also improved. Therefore, abdominal doppler ultrasound is shown as a noninvasive exploration useful for the clinical management of SOS and as an early marker of good clinical evolution.

Budd-Chiari syndrome (BCS) is a rare disorder caused by the obstruction of hepatic venous outflow, leading to sinusoidal congestion, ischemic injury to liver cells and portal hypertension. Long-term survival largely depends on whether hepatocellular carcinoma occurs. A recently available liver-specific contrast medium, gadolinium-ethoxybenzyl-diethylenetriamine penta-acetic acid (Gd-EOB-DTPA), reportedly has high diagnostic capability for detection of malignant liver tumors. However, there has been no report of the sue of Gd-EOB-DTPA-enhanced magnetic resonance imaging (MRI) for BCS. We present a case of chronic BCS who underwent both gadopentetate dimeglumine (Gd-DTPA) and Gd-EOB-DTPA-enhanced MRI. Hepatic congestion and edema were seen as slightly hypointense areas on Gd-EOB-DTPA-enhanced hepatobiliary-phase images, although these areas were observed as slightly hyperintense on previously obtained Gd-DTPA-enhanced delayed-phase image. Reduced uptake of Gd-EOB-DTPA by hepatocytes in the region of congestion or edema may account for this difference, which should be recognized in image interpretations.

OBJECTIVE. The purpose of this article is to illustrate the radiologic findings of various uncommon conditions that cause hepatic congestion in patients after living donor liver transplantation.CONCLUSION. Radiologic findings of hepatic congestion may vary according to the cause and the level of outflow obstruction. It is important for radiologists to be aware of such variations in order to make an early diagnosis of hepatic congestion and to enable timely proper management in recipients after living donor liver transplantation.

A 29-year-old woman with acute iliofemorocaval thrombosis was discovered to have suprarenal caval agenesis with azygous continuation, hepatic congestion, and fibrosis as a result of chronic Budd–Chiari syndrome. Three staged procedures were performed: pharmacomechanical thrombolysis of acute thromboses, transfemoral liver biopsy and hemodynamic assessment, and percutaneous endovascular creation of a "neocava" lined with endografts. Symptomatic improvement and patency were maintained at 12-week follow-up.

AIM To evaluate safety and outcomes of a new technique for extreme hepatic resections with preservation of segment 4 only. METHODS The new method of extreme liver resection consists of a two-stage hepatectomy. The first stage involves a right hepatectomy with middle hepatic vein preservation and induction of left lobe congestion; the second stage involves a left lobectomy. Thus, the remnant liver is represented by the segment 4 only (with or without segment 1, ± S1). Five patients underwent the new two-stage hepatectomy (congestion group). Data from volumetric assessment made before the second stage was compared with that of 10 matched patients (comparison group) that underwent a single-stage right hepatectomy with middle hepatic vein preservation. RESULTS The two stages of the procedure were successfully carried out on all 5 patients. For the congestion group, the overall volume of the left hemiliver had increased 103% (mean increase from 438 mL to 890 mL) at 4 wk after the first stage of the procedure. Hypertrophy of the future liver remnant (i.e., segment 4 ± S1) was higher than that of segments 2 and 3 (144% vs 54%, respectively, P < 0.05). The median remnant liver volume-to-body weight ratio was 0.3 (range, 0.28-0.40) before the first stage and 0.8 (range, 0.45-0.97) before the second stage. For the comparison group, the rate of hypertrophy of the left liver after right hepatectomy with middle hepatic vein preservation was 116% ± 34%. Hypertrophy rates of segments 2 and 3 (123% ± 47%) and of segment 4 (108% ± 60%, P > 0.05) were proportional. The mean preoperative volume of segments 2 and 3 was 256 ± 64 cc and increased to 572 ± 257 cc after right hepatectomy. Mean preoperative volume of segment 4 increased from 211 ± 75 cc to 439 ± 180 cc after surgery. CONCLUSION The proposed method for extreme hepatectomy with preservation of segment 4 only represents a technique that could allow complete resection of multiple bilateral liver metastases.

We describe a patient with a diagnosis of heterotaxia and independent drainage of the suprahepatic veins into the venous atrium who underwent total extracardiac cavopulmonary connection in which hepatic vein drainage remained directly into the atrium. In the immediate postoperative period she showed increasing cyanosis that suggested substantial right-to-left shunt. Surgical ligation of the suprahepatic veins resolved the complication effectively without signs of hepatic congestion or portal hypertension.

Chronic heart failure (CHF) in children occurs mostly as a result of systolic dysfunction of the systemic ventricle or of congenital defects leading to large left-to-right shunts and pulmonary overcirculation. The ensuing symptoms and signs are similar in both cases, and include respiratory distress, poor feeding and growth, and hepatic congestion. Grading the severity of the symptoms accurately and reproducibly is important for studying CHF and the response to therapy. The Ross classification for young children and the New York Heart Association classification for older children are frequently utilized for such grading. The standard therapy for CHF in children consists of diuretics, to reduce cardiac preload and improve symptoms, and the maximization of nutritional support. The role of digoxin in treating CHF in children is controversial, especially regarding those children with pulmonary overcirculation where the function of the systemic ventricle is usually well preserved. As the importance of neurohormonal changes in the pathogenesis of worsening CHF is elucidated, newer medications aimed at counteracting such changes are becoming more important in the medical therapy of CHF in children. ACE inhibitors improve function and survival in adults with CHF, and they probably do the same in children with systemic ventricular dysfunction. It is less clear how effective they are in pulmonary overcirculation, but patients with high flow and low pulmonary resistance are most likely to benefit. In infants receiving treatment with ACE inhibitors, it is necessary to monitor for renal insufficiency or renal failure. beta-Adrenoceptor blockade has also been established as an effective therapy for adults with CHF with beneficial effects on survival and left ventricular function. While data for the pediatric population are limited, early studies suggest that beta-adrenoceptor antagonists (beta-blockers) may work well in infants and children with CHF. Caution must be used by starting treatment with very low dosages of beta-blockers and gradually increasing to the desired goals with close monitoring of blood pressure and heart rate. It is clear that larger multicenter trials are crucial to our ability to provide the most appropriate treatment for children with CHF. The demand for effective medical treatment will increase as more patients with palliated single ventricles survive surgery and then develop CHF from dysfunction of a hypertrophic and dilated single ventricle.

INTRODUCTION: Scimitar syndrome is a congenital heart disease characterized by an abnormal drainage of the right lung into the inferior vena cava, the right atrium or a variety of venous connections from the anomalous pulmonary vein to a systemic vein. This left-to-right shunt induces pulmonary hypertension and is an indication for surgical repair in cases of a history of recurrent pneumonia or significant left-to-right shunting. A corrective approach, which consists of rerouting the anomalous pulmonary flow to the left atrium, is usually performed. Complications of scimitar repair are stenosis, thrombosis and occlusion of the scimitar vein and its deviation. CASE PRESENTATION: This case report describes a 53-year-old Caucasian woman with known scimitar syndrome, undergoing surgical repair due to invaliding symptoms of dyspnoea, and presenting with postoperative Budd-Chiari syndrome due to anomalous drainage of her right hepatic vein into the left atrium. It is an interesting cause of liver pathology caused by Budd-Chiari that never has been described before. CONCLUSIONS: This case report emphasizes the importance of a thorough preoperative evaluation, and the importance of antecedents in newly presenting pathology. It is an interesting cause of a known hepatic syndrome, the Budd-Chiari syndrome. This case report is of interest to many specialties, including Hepatology, Cardiology, Radiology and Cardiovascular Surgery. It exposes a new interesting anatomic variation of the scimitar syndrome with significant postoperative implications. ispartof: J Med Case Rep vol:8 issue:1 pages:273- ispartof: location:England status: Published online

The features of hepatic congestion on computed tomography, ultrasound and nuclear medicine sulphur colloid scans have been reviewed. Hepatic congestion may not be appreciated clinically, especially in the elderly, but the features described should be sufficiently characteristic to establish the diagnosis. The CT appearance may be confused with neoplastic infiltration, so that recognition of the condition may avoid further unnecessary investigations.

To the Editor A corollary to the association of incident heart failure and an increase in serum gamma glutamyl transferase (GGT)1 is that fluctuations in the severity of heart failure might also have the potential to trigger fluctuations in the blood levels of this parameter. Fluctuations in serum GGT levels (including restoration to the normal range) also occur during the course of the natural history of …

Passive hepatic congestion is caused by stasis of blood within the liver parenchyma due to compromise of hepatic venous drainage. It is a common complication of congestive heart failure and constrictive pericarditis, wherein elevated central venous pressure is directly transmitted from the right atrium to the hepatic veins because of their close anatomic relationship (Fig. 1). The liver becomes tensely swollen as the hepatic sinusoids dilate and engorge to accommodate the backflow of blood. A variety of structural and functional hepatic derangements develop that have distinctive appearances on sonograms, CT scans, and MR images.

Cardiac ascites is a rare condition. Diagnosis is aided by liver histology, which characteristically shows diffuse hepatic congestion affecting the centrilobular region. In our case of refractory ascites due to constrictive pericarditis, diagnosis was delayed because centribular hepatic congestion was absent histologically. Contrary to numerous published reports, diffuse hepatic congestion is not uniformly present in cardiac ascites. Constrictive pericarditis is curable and should be considered in all cases of unexplained ascites, regardless of atypical hepatic histology.

Hepatic congestion resulting in hepatic rupture during pregnancy is a rare yet catastrophic event carrying a 60 to 70% maternal mortality rate. With preeclampsia and associated epigastric pain continuing to be a major problem confronting pregnant women, hepatic congestion may be more prevalent than believed. Current etiology, treatment, and characteristics of women who experience hepatic rupture are examined. A case report and nursing protocol are presented.

Summary A 65-year-old woman undergoing chronic haemodialysis for chronic nephritis had transiently elevated serum carcinoembryonic antigen levels, up to 26 ng/ml for nearly 3 months. This elevation was most probably due to cardiac failure with hepatic congestion and pulmonary oedema, because the antigen level returned to normal when the cardiac failure was properly treated, and comprehensive examinations revealed no other cause. During follow-up for 18 months, the carcinoembryonic antigen level has remained normal.

A patient with chronic calcific pericarditis, hepatic congestion, and fibrosis had massive ascites with a protein concentration of 5.1 g/100 ml. This fluid was in all likelihood largely derived from hepatic interstitial fluid. The ascites-serum concentration ratio for several protein species and molecular exclusion chromatography of these fluids suggested two processes may be involved in the transfer of protein from serum to ascites, namely bulk transfer of all species and molecular sieving.

High-resolution ultrasound has been recently introduced in the management of many conditions in which the fetus is at risk. In the detection of severe erythroblastosis fetalis, sonographic evaluation of fetal anatomic changes is being used in association with amniotic fluid spectral analysis to assess the degree of the hemolytic process. In 1981 it was reported that sonographically detected umbilical vein dilatation, resulting from hepatic congestion, could be used as a sign of impending fetal compromise. We analyzed data obtained from 47 patients in a total of 76 examinations, including sonographic measurement of umbilical vein diameter, associated ultrasound findings, results of amniotic fluid spectral analyses, and neonatal outcome. The collected data, divided in two groups according to the results of amniotic fluid spectral analyses (less than high zone II and greater than or equal to high zone II), showed that the sonographic measurement of umbilical vein diameter does not differ significantly between the two groups (p greater than 0.05). Therefore, the present and relatively large series demonstrates that dimensions of the umbilical vein cannot be used as a reliable predictor of worsening fetal disease.

Using bolus-enhanced CT, we encountered an unusual constellation of findings in seven patients with clinical evidence of right heart failure. These included retrograde hepatic venous opacification on the early bolus scans and a diffusely mottled pattern of hepatic enhancement seen only during the vascular phase of contrast administration. Ancillary CT findings include cardiomegaly, pleural effusions, ascites, and intrahepatic perivascular radiolucency. We believe that these CT abnormalities are caused by passive hepatic congestion. This pattern of abnormal hepatic enhancement represents a potential pitfall in the use of dynamic bolus-enhanced CT for the detection of focal hepatic masses. Recognition of passive hepatic congestion as a possible cause of mottled hepatic enhancement on CT may help explain clinical abnormalities of liver function in patients with heart failure and prevent confusion with other disease processes that produce abnormalities of hepatic attenuation.