Portal hypertension

Endoscopy plays a major role in the management of gastrointestinal varices in portal hypertension. It is used for the prophylaxis of the fi rst bleeding episode, therapy of active bleeding and prophylaxis of recurrent bleeding. Today not only nonselective betablockers, but also endoscopic band ligation is an option in the primary prophylaxis of the fi rst bleeding episode in patients with large esophageal varices. Acutely bleeding varices should be treated by ligation, pharmacological and antibiotic therapy. Prophylaxis of recurrent bleeding despite endoscopic and pharmacologic treatment is patient dependent: shunt surgery is an option in young patients in a good medical condition (Child-Pugh class A). In patients with refractory ascites and a bilirubin level below 3 mg/dl, TIPS is a good option. Nevertheless, the fi rst-line treatment in most patients in Germany is endoscopic band ligation. Bleeding from ectopic varices and due to hypertensive gastropathy should be treated individually either by endoscopy, TIPS or drug therapy.

We report two cases of children followed for many years with an original diagnosis of non-A/non-B hepatitis. One child developed serious cirrhosis with portal hypertension. Long-term observation of the course of their hepatic disease provided the diagnosis of cystic fibrosis. These cases demonstrate that cystic fibrosis though rarely presenting with initial hepatic signs, can manifest itself with only long-term hepatic symptoms. We therefore strongly recommend analysis of sweat chloride concentration in cases of hepatic disease of unknown origin.

Cirrhotic cardiomyopathy is a clinical syndrome in patients with liver cirrhosis characterized by an abnormal and blunted response to physiologic, pathologic, or pharmacologic stress but normal to increased cardiac output and contractility at rest. As many as 50% of cirrhotic patients undergoing liver transplantation show signs of cardiac dysfunction, and 7% to 21% of deaths after orthotopic liver transplantation result from overt heart failure. In this review, we critically evaluate the existing literature on the pathophysiology and clinical implications of cirrhotic cardiomyopathy. (J Am Coll Cardiol 2010;56:539-49)

Background & Aims: In healthy subjects, exercise pro-During exercise, an increase in cardiac output and a motes marked hemodynamic and humoral changes redistribution of blood flow from other territories (especharacterized by an increase in cardiac output, a rediscially the splanchnic area) through an adrenergic-meditribution of blood flow to muscular territories under acated vasoconstriction 6 are the main physiological changes tivity, and an increase in sympathoadrenergic activity.

Simvastatin improves liver generation of nitric oxide and hepatic endothelial dysfunction in patients with cirrhosis, so it could be an effective therapy for portal hypertension. This randomized controlled trial evaluated the effects of continuous simvastatin administration on the hepatic venous pressure gradient (HVPG) and its safety in patients with cirrhosis and portal hypertension. Methods: Fifty-nine patients with cirrhosis and portal hypertension (HVPG >12 mm Hg) were randomized to groups that were given simvastatin 20 mg/day for 1 month (increased to 40 mg/day at day 15) or placebo in a double-blind clinical trial. Randomization was stratified according to whether the patient was being treated with ␤-adrenergic blockers. We studied splanchnic and systemic hemodynamics and variables of liver function and safety before and after 1 month of treatment. Results: Simvastatin significantly decreased HVPG (؊8.3%) without deleterious effects in systemic hemodynamics. HVPG decreases were observed in patients who were receiving ␤-adrenergic blockers (؊11.0%; P ‫؍‬ .033) and in those who were not (؊5.9%; P ‫؍‬ .013). Simvastatin improved hepatic, fractional, and intrinsic clearance of indocyanine green, showing an improvement in effective liver perfusion and function. No significant changes in HVPG and liver function were observed in patients receiving placebo. The number of patients with adverse events did not differ significantly between groups. No patient was withdrawn from the study based on adverse events. Conclusions: Simvastatin decreased HVPG and improved liver perfusion in patients with cirrhosis. These effects were additive with those of ␤-adrenergic blockers. The beneficial effects of simvastatin should be confirmed in longterm clinical trials for portal hypertension.

The gradient between wedged and free hepatic venous pressures was measured in 10 unselected adult patients suffering from fulminant viral hepatitis. The gradient was increased in all the studied patients, ranging from 0.9 to 2. 1 kPa; this finding indicates that portal hypertension was present in all these cases. Ascites was present in all the five patients having a gradient above 1.5 kPa and affected only two of the five patients having a gradient below 1.5 kPa; this observation suggests that portal hypertension plays a role in the mechanism of ascites in fulminant viral hepatitis. Portal hypertension in fulminant viral hepatitis is likely to be the consequence of an intrahepatic block due to massive necrosis of the liver cells.

Aplastic anemia, an unusual hematologic disease, is the paradigm of the human bone marrow failure syndromes. Almost universally fatal just a few decades ago, aplastic anemia can now be cured or ameliorated by stem-cell transplantation or immunosuppressive drug therapy. The pathophysiology is immune mediated in most cases, with activated type 1 cytotoxic T cells implicated. The molecular basis of the aberrant immune response and deficiencies in hematopoietic cells is now being defined genetically; examples are telomere repair gene mutations in the target cells and dysregulated T-cell activation pathways. Immunosuppression with antithymocyte globulins and cyclosporine is effective at restoring blood-cell production in the majority of patients, but relapse and especially evolution of clonal hematologic diseases remain problematic. Allogeneic stem-cell transplant from histocompatible sibling donors is curative in the great majority of young patients with severe aplastic anemia; the major challenges are extending the ben-efits of transplantation to patients who are older or who lack family donors. Recent results with alternative sources of stem cells and a variety of conditioning regimens to achieve their engraftment have been promising, with survival in small pediatric case series rivaling conventional transplantation results. (Blood.

Prehepatic portal hypertension (PHPH), related to thrombosis and the cavernomatous transformation of the portal vein (PVC), is the single most common cause of portal hypertension in children. Although it can be secondary to the direct damage that relates to neonatal catheterization of the umbilical vein, the latter condition represents <25% of cases, 1-7 and no cause is found in most cases (idiopathic PHPH). Even less commonly, it relates to regional trauma (or surgery, eg, after liver transplantation), tumors, or infection (eg, peritonitis, abscess). Although in the adult age group there is a clear correlation between pre-existing thrombophilia and PVC, coagulation abnormalities are not found to be primarily related to PVC in children, in fact, only minor disorder types have been reported in a small proportion of patients, and most coagulation profile abnormalities observed are acquired and secondary. Anatomically speaking, the initial thrombotic process seems to mainly involve the portal vein trunk, to which it is eventually limited in the typical disease condition; a variable extension, either downstream into the intrahepatic radicals, or upstream into the splanchnic system, or both, can be observed. Remarkably, in children who have had catheterization of the umbilical vein, the processes more than likely start in an inverse manner, with the thrombus initiating within the liver as a consequence of the direct (chemical, physical, or infection) damage of the intrahepatic veins and, more precisely, the left portal system. 2,7,12 A diffuse splanchnic venous thrombosis is exceptional in children (although it is relatively common in adults with thrombophilia). Although part of the portal system is not reachable for decompressive surgery (as the portal trunk and sometimes other veins are thrombosed), various types of portosystemic shunt have been performed with success; the type of shunt depends on the venous anatomy of each patient and the team's preferences (mesocaval and various splenorenal types of shunt). 14-20

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Patients with end-stage liver disease (ESLD) frequently have diverse abnormalities of carbohydrate, lipid, and protein metabolism that cause progressive deterioration of their clinical condition and lead to malnutrition. Malnutrition is almost universally present in patients with ESLD undergoing liver transplantation and has been associated with increased morbidity and mortality. It is essential to identify and correct nutritional deficiencies in this population and provide an adequate nutritional support during all phases of liver transplantation. In conclusion, this article reviews the etiologic factors, prevalence, assessment and management guidelines of nutritional disorders seen in patients with ESLD undergoing liver transplantation.

In view of the substantial, at times conflicting, literature on conversion to open surgery during laparoscopic cholecystectomy (LC), we have considered it timely to review the subject to identify the risk factors for conversion and its consequences. The review is based on a complete literature search covering the period 1990 to 2005. The search identified 109 publications on the subject: 68 retrospective series, 16 prospective nonrandomized studies, 8 prospective randomized clinical trials, 5 prospective case-controlled studies, 5 reviews and 7 others (3 observational, 2 population-based studies, 1 national survey, and 1 editorial). As the majority of reported studies are retrospective, firm conclusions cannot be reached. Single factors that appear to be important include male gender, extreme old age, morbid obesity, cirrhosis, previous upper abdominal surgery, severe/advanced acute and chronic disease, and emergency LC. The combination of patient-and disease-related risk factors increases the conversion risk. In the training of residents, the number of cases needed for reaching proficiency exceeds 200 cases. The value of predictive scoring systems is important in the selection of cases for resident training. Conversion exerts adverse effects on operating time, postoperative morbidity, and hospital costs, especially when it is enforced. There appears to be no absolute contraindication to LC that is agreed upon by all. There is consensus on certain individual risk factors and their additive effect on the likelihood of conversion. Predictive systems based on these factors appear to be useful in selection of cases for resident training.

Ultrasound (US) is essential in both assessment of the potentially cirrhotic liver and surveillance of selected patients with chronic hepatitis as liver biopsy can be misleading or inaccurate in up to 25% of cases. Various techniques are already in routine use, such as grey-scale imaging, Doppler US, and contrast-enhanced US (CEUS), while newer techniques such as elastography and hepatic vein transit time (HVTT) have the potential to exclude patients without significant fibrosis or cirrhosis; however, they are operator dependent and require specific software. Grey-scale imaging may demonstrate changes, such as volume redistribution, capsule nodularity, parenchymal nodularity, and echotexture changes. The Doppler findings in the hepatic and portal veins, hepatic artery, and varices allow assessment of liver cirrhosis. However, the operator needs to be aware of limitations of these techniques. Low mechanical index CEUS plays an important role in the assessment of complications of cirrhosis, such as hepatocellular carcinoma and portal vein thrombus. Optimized US technique is crucial for accurate diagnosis of the cirrhotic liver and its complications.

Clinical-A 45-year-old female was admitted to the hospital with three episodes of haematemesis. She was a diagnosed case of cirrhosis with portal hypertension since 3 years earlier. Examination revealed pallor, vitiligo, splenomegaly, and markedly dilated and tortuous veins on her abdominal wall, especially below the umbilicus . She had noted them become gradually prominent for the past 2 years. On auscultation a venous hum was heard over these dilated veins. Figure 1. Tortuous veins on the abdominal wall

portal pressure is the product of portal blood flow and resistance; an increase in either leads to increased portal pressure. cirrhosis is the underlying cause in most cases, but portal hypertension can develop due to pre-, intra-and post-hepatic obstruction to the flow, secondary to variety of causes. Diagnosis can be established by a combination of non-invasive imaging of portal vasculature and clinical or serological markers for the cause underlying cirrhosis. Development of gastro-oesophageal varices and ascites are the most important clinical manifestation of portal hypertension. non-selective beta-blockers and endoscopic band ligation are effective in primary and secondary prevention of variceal bleeding. active variceal haemorrhage is managed using a combination of vasoactive drugs (e.g. terlipressin) and endoscopic band ligation. if these measures fail, transjugular intrahepatic portosystemic stent (tipS) insertion achieves haemostasis. Diuretic therapy with spironolactone and furosemide are the mainstays of management of ascites. if ascites becomes refractory, repeat large-volume paracentesis and tipS in selected cases help to control symptoms. Development of ascites is an important landmark in the natural history of cirrhosis and liver transplantation should be considered definitive treatment.

Résumé La survenue d'une grossesse chez une patiente avec une hypertension portale est une situation inhabituelle pour le clinicien. Bien que la majoration de l'hypertension portale au cours de la grossesse ne soit pas parfaitement démontrée, il existe une surmorbidité indéniable, principalement en cas de cirrhose qui justifie la notion de grossesse à risque et impose une prise en charge multidisciplinaire. Les moyens de prévention ou de lutte contre l'hémorragie sont peu différents de ceux disponibles en dehors de la grossesse. La recherche et la prise en charge de l'hypertension portale, avant ou au début de la grossesse, peuvent réduire les risques de fausses couches, de naissance prématurée, de retard de croissance intra-utérin et la mortalité maternelle. Ces complications sont étroitement liées à la survenue d'hémorragie digestive. Les risques liés à la maladie sous-jacente doivent également être pris en compte, qu'il s'agisse d'une insuffisance hépatocellulaire en cas de cirrhose ou du risque thromboembolique pour les maladies vasculaires hépatiques associées à une thrombophilie. De manière générale, l'accouchement par voie basse, sous analgésie débutée précocement et assistée d'une extraction instrumentale, doit être préféré à la césarienne dont les indications doivent rester d'ordre obstétrical.

The use of angiotensin II antagonists in the treatment of portal hypertension remains controversial. Our aims were to assess the effect of Irbesartan on portal pressure and to evaluate its safety in cirrhotic patients with portal hypertension. Twenty-five cirrhotic patients were treated in a pilot study with Irbesartan 300 mg orally once daily for 60 days. Hemodynamic evaluations and biochemical tests were performed before therapy and after two months of treatment. Three patients (12%) discontinued treatment for symptomatic arterial hypotension (mean arterial pressure -26.% +/- 3.1 versus basal). In the 18 responders, the hepatic venous pressure gradient diminished by a mean of 18.1% +/- 10.5 from baseline (p = 0.02); the gradient decreased by 20% or more in only 5 patients (23%). The mean arterial pressure decreased significantly during therapy (92 +/- 7 vs 109 +/- 25 mm Hg, P &lt; 0.001). In conclusions, Irbesartan induced a marginal reduction in portal pressure and its safety was...

In the Western world, cirrhosis related to chronic hepatitis C and B and alcoholic cirrhosis are the most common causes for portal hypertension. Noncirrhotic portal hypertension represents a relatively infrequent group of conditions that causes portal hypertension in the absence of cirrhosis. As with cirrhotic portal hypertension, most cases of noncirrhotic portal hypertension are caused by increased portal venous outflow resistance, although, rarely, an increased flow in the portal circulation may be responsible. Ultimately, even in the cases in which there is a chronically increased flow (e.g., in arteriovenous fistulae), intravascular changes evolve, leading to increased resistance. Pathophysiologically, the causes for portal hypertension can be categorized into three groups based on whether the block to portal flow is at the portal venous level, in. the sinusoidal bed, or at the hepatic veins. Further, presinusoidal resistance to portal flow can occur either at an intra-hepatic site or at the extra-hepatic level; similarly, the postsinusoidal hepatic venous outflow blockage could be intra-hepatic or extra-hepatic . Although development of varices and subsequent bleeding from them are the main manifestations of portal hypertension from all causes, there are unique features related to noncirrhotic portal hypertension that are worthy of mention. The clinical manifestations of pre-sinusoidal portal hypertension characteristically are devoid of ascites and encephalopathy, whereas ascites is a cardinal feature of post-sinusoidal obstruction. The prognosis of portal hypertension caused by presinusoidal conditions is relatively better than that of any cause of portal hypertension.

Ectopic varices (EcV) comprise large portosystemic venous collaterals located anywhere other than the gastro-oesophageal region. No large series or randomized-controlled trials address this subject, and therefore its management is based on available expertise and facilities, and may require a multidisciplinary team approach. EcV are common findings during endoscopy in portal hypertensive patients and their bleeding accounts for only 1-5% of all variceal bleeding. EcV develop secondary to portal hypertension (PHT), surgical procedures, anomalies in venous outflow, or abdominal vascular thrombosis and may be familial in origin. Bleeding EcV may present with anaemia, shock, haematemesis, melaena or haematochezia and should be considered in patients with PHT and gastrointestinal bleeding or anaemia of obscure origin. EcV may be discovered during panendoscopy, enteroscopy, endoscopic ultrasound, wireless capsule endoscopy, diagnostic angiography, multislice helical computed tomography, m...

Splenomegaly is a frequent ®nding in patients with liver disease. It is usually asymptomatic but may cause hypersplenism. Thrombocytopenia is the most frequent manifestation of hypersplenism and may contribute to portal hypertension related bleeding. A number of therapies are available for treating thrombocytopenia due to hypersplenism including splenectomy, partial splenectomy, partial splenic embolization, TIPS etc. None is entirely satisfactory. Hypersplenism usually improves following liver transplantation. Therapy with cytokines such as thrombopoietin may oer hope for the future. Patients with liver disease also have abnormalities in coagulation. This is not surprising as all coagulation proteins (except for von willebrand factor vWF) and most inhibitors of coagulation are synthesized in the liver. Genetic or acquired abnormalities of coagulation may predispose to thrombosis of the hepatic or portal veins with signi®cant clinical sequelae. An understanding of the mechanisms involved in coagulation and thrombosis is valuable in choosing from the increasing treatment options available. These include clotting factors, haemeostatic drugs and newer therapies such as recombinant factor VIIa. Splenic artery aneurysms are the most common visceral artery aneurysms in man. Rupture is frequently catastrophic. These aneurysms are being increasingly recognized in liver transplant patients and require treatment before or during transplant surgery.

Biliary ductal changes are a common radiological finding in patients with portal hypertension, however only a small percentage of patients (5%-30%) develop symptomatic bile duct obstruction. The exact pathogenesis is not clear, but an involvement of factors such as bile duct compression by venous collaterals, ischemia, and infection is accepted by most authors. Although endoscopic retrograde cholangiopancreatography was used to define and diagnose this condition, magnetic resonance cholangiopancreatography is currently the investigation of choice for diagnosing this condition. Treatment is indicated only for symptomatic cases. Portosystemic shunts are the treatment of choice for symptomatic portal biliopathy. In the majority of patients, the changes caused by biliopathy resolve after shunt surgery, however, 15%-20% patients require a subsequent bilio-enteric bypass or endoscopic management for persistent biliopathy. There is a role for endoscopic therapy in patients with bile duct stones, cholangitis or when portosystemic shunt surgery is not feasible.

Identity control theory (ICT), like selfdiscrepancy theories generally, assumes that people are motivated to verify their identities by seeking feedback from others which is not discrepant from their own self-views . When the dimension of meaning that is relevant to the identity is one of evaluation, people want others to evaluate them at the same level as they evaluate themselves. Evaluations by others that are more negative than self-evaluations disconfirm their identity and lead to negative self-feelings, as do evaluations that are more positive than self-evaluations .

We report an unusual case of 71-year-old man with liver cirrhosis who present- ed recurred bleedings from the stoma of ileo conduit after radical cystoprosta- tectomy. The haemorrhagic episodes could not be treated by local mesure, and a trans-jugular intra hepatic porto-caval shunt was performed, displacing an en- doprothesis and a self expandable stent. We highlight the role of TIPS

The efficacy and complications of esophageal tamponade as the first procedure in the routine management of acute variceal hemorrage were evaluated in 151 consecutive bleeding episodes treated at a specialized unit. The Sengstaken-Blakemore tube was employed in the 118 cases in which emergency endoscopy demonstrated bleeding esophageal varices, and the Linton-Nachlas balloon in the 33 cases with bleeding from gastric varices. Hemostasis lasting at least 24 hr was obtained in 91.5% of cases treated with the Sengstaken- Blakemore balloon and in 88% of those treated with the Linton-Nachlas balloon. Permanent hemostasis was obtained in 47.7% of all cases. The only severe complication noted in these 151 episodes of bleeding treated by tamponade was pulmonary aspiration, which was detected in 10% of cases. This complication was related to the presence and degree of encephalopathy (P<0.001 and was prevented by orotracheal intubation prior to tamponade. These results indicate that balloon tamponade continues to be a reliable and valuable method to arrest bleeding from esophagogastric varices.

and outcome were evaluated. An acute-overt bleeding was defined as hematemesis, rectal blood loss and/or melena. Results: In the period 2005-2008 in 22 patients had BAE for acute-overt GI bleeding: 12 males, mean age 65 (35-87) years. All patients had negative upper-en ileocolonoscopy. Clinical presentation was rectal blood loss in 11 (50%), melena and blood cloths in 7 (32%) and hematemesis and melena in 4 (18%) patients. In 18 (82%) transfusion was necessary; 11 (50%) patients presented with hemodynamic instability. Mean hemoglobin at presentation was 7.0 (5.3-10.1) g/dL (mean MCV 88). In 11 (50%) patients use of NSAID's, steroids and/or oral anticoagulation was reported. The enteroscopes used were diagnostic DBE in 12, therapeutic DBE in 7, and SBE in 3 patients. Mean insertion depth was proximal 247 (130-400) cm and distal 96 (30-150) cm. During BAE a likely cause of bleeding was found in 10 (45%) patients: in 4 (40%) tumoreus laesions (2 GIST and 2 adenocardinoma), in 4 (40%) vascular abnormalities (3 angiodysplasia and 1 jejunal varices), and 2 Dieulafoy-like-lesions were found. The pathologic findings were all located in the jejunum: 5 proximal and 5 in the mid-distal jejunum. Endoscopic therapy was applied in 6 (60%) patients, 4 patients had surgery. Two patients died due to other causes, all other patients were symptom free at mean follow-up of 23 (3-38) months. In 5 (23%) patients, wireless capsule endoscopy (WCE) was performed before BAE: in 1 case WCE was true positive, WCE was false negative in 3 cases (1 angiodysplasia and 2 tumors) and in 1 case false positive. Conclusion: BAE found the source of GI bleeding in nearly half of patients presenting with an acuteovert GI bleeding, with an initial negative upper-and lower endoscopy. Cause of bleeding could be treated endoscopically in majority of patients. The sensitivity for detection of acute small bowel bleeding seems higher for BAE as compared to WCE.

Nonalcoholic fatty liver disease (NAFLD) is among the most common causes of chronic liver disease in the western world. It is now recognized that these patients have myriad of important co-morbidities (e.g., diabetes, hypothyroidism and metabolic syndrome). The workup of patients with suspected NAFLD should consist of excluding competing etiologies and systemic evaluation of metabolic comorbidities. NAFLD is histologically categorized into steatosis and steatohepatitis, two states with fairly dichotomous natural history. While significant progress has been made in terms of noninvasively predicting advanced fibrosis, insufficient progress has been made in predicting steatohepatitis. Currently, liver biopsy remains the gold standard for the histological stratification of NAFLD. While sustained weight loss can be effective to treat NASH, it is often difficult to achieve. Foregut bariatric surgery can be quite effective in improving hepatic histology in selected patients without liver failure or significant portal hypertension. Thiazolidinediones have shown promise and the results from the ongoing, large multicenter study should become available soon. Large multicenter studies of CB, receptor anatagonists are also underway but their results will not be available for several years. Several recent studies have highlighted that cardiovascular disease is the single most important cause of morbidity and mortality in this patient population. Conclusion: Health care providers should not only focus on liver disease but also concentrate on aggressively modifying and treating their cardiovascular risk factors. (HEPATOLOGY 2009;49:306-317.)

Background: Liver transplantation in presence of diffuse portal vein thrombosis is possible by using caval blood as portal inflow, through cavo-portal transposition. However, clinical results are heterogeneous and experimental studies are needed, but similar hemodynamic conditions are difficult to obtain, especially in small animals. Herein we describe a new simple model of cavo-portal transposition in rat.

Many imaging modalities can be used to evaluate various portosystemic collateral pathways seen in patients with portal hypertension. A knowledge of various typical and atypical pathways is essential for a proper understanding of the disease process. Transjugular transhepatic portographic appearance of such pathways are discussed in detail.

Portal hypertension has traditionally been viewed as a progressive process, involving ultrastructural changes including fibrosis, nodule formation, and vascular thrombosis, leading to increased intrahepatic resistance to flow. However, it is increasingly recognized that a significant component of this vascular resistance results from a dynamic process, regulated by complex interactions between the injured hepatocyte, the sinusoidal endothelial cell, the Kupffer cell and the hepatic stellate cell, which impact on sinusoidal calibre. Recent findings suggest these haemodynamic findings are most marked in patients with superimposed inflammation. The precise mechanisms for vascular dysfunction in cirrhosis with superimposed inflammation remain to be fully elucidated but several studies over the past decade have started to generate the hypothesis that inflammation may be a key mediator of the pathogenesis and severity of portal hypertension in this context. This review provides a comprehensive overview of the biological mechanisms for inflammation playing a key role in the severity of portal hypertension, and illustrates potential novel therapies that act by modifying these processes. Ó

Three young dogs were evaluated because of the sudden development of ascites. In each case ascites was referable to non-fibrosing hepatic disease associated with portal hypertension. Obstruction to portal flow was pre-sinusoidal in two cases and post sinusoidal in the other. In all cases ascites developed in the absence of severe hypoalbuminaemia. The ratio of the protein content of ascitic fluid in relation to the protein content of plasma proved useful in differentiating between pre-and post sinusoidal portal hypertension. All three animals died or were euthanased because of the sequelae of portal hypertension.