Normal Portal Pressure Research Articles

A Unique Presentation of Familial Idiopathic Colonic Varices

ABSTRACT Colonic varices typically occur in the setting of portal hypertension, and patients may present with rectal bleeding or occult anemia. Idiopathic colonic varices occur infrequently in the absence of cirrhosis and can involve the entire colon. We present a case of a 54-year-old Eastern European woman who had undergone diagnostic colonoscopy for newly diagnosed sigmoid adenocarcinoma and was incidentally found to have colonic varices with normal portal pressure gradients. Her 38-year-old daughter was found to have similar varices, raising concerns for hereditary etiology.

Surgical Shunt Procedures in Childhood Portal Hypertension: A Review Article

Normal portal pressure is between 0 and 10 mmHg and the pressure in the portal vein is slightly higher than that of the pressure in the inferior vena cava [1]. Portal Hypertension (PH) is usually defined as either a hepatice venous pressure gradient greater than 5mmHg or hepatic venous wedge pressure greater than 10mmHg [2]. It is usually encountered as a complication arising from chronic liver disease and cirrhosis. Common presentation of PH in children include catastrophic variceal hemorrhage usually from esophagus. Other common clinical features of PH include splenomegaly, hypersplenism, ascites, encephalopathy, and hepatopulmonary syndrome and portopulmonary hypertension. It has been reported that up to 15% of children with PH ultimately require shunt surgery [2]. Traditionally shunt surgery was a treatment option for children in whom control of variceal bleeding failed however; it was associated with relatively high rate of anastomotic stricture or thrombosis [1]. Nowadays it has also been reported that as the experience in vascular and transplant surgery together with microsurgical techniques have improved good success rates can be achieved even in small children [1]. In this review article, it is aimed to review the surgical treatment options in children with PH with special regard to shunt procedures under the light of relevant literature.

Splenic vein stenting for recurrent chylous ascites in sinistral portal hypertension: a case report

BackgroundSinistral portal hypertension results from obstruction or stenosis of the splenic vein and is characterized by normal portal vein pressures and liver function tests. Gastrointestinal bleeding is the most common presentation and indication for treatment. Although sinistral portal hypertension-related chylous ascites is rare, several cases have described successful treatment with portal venous, rather than splenic venous, recanalization. Splenectomy is effective in the treatment of sinistral portal hypertension-related bleeding, although recent studies have evaluated splenic vein stenting and splenic arterial embolization as minimally-invasive treatment alternatives. Splenic vein stenting may be a viable option for other presentations of sinistral portal hypertension.Case presentationA 59-year-old gentleman with a history of necrotizing gallstone pancreatitis was referred to interventional radiology for management of recurrent chylous ascites. Analysis of ascites demonstrated a triglyceride level of 1294 mg/dL. Computed tomography revealed splenic and superior mesenteric venous stricture. The patient elected to undergo minimally invasive transhepatic portal venography, which confirmed the presence of splenic vein and superior mesenteric vein stenosis. Venography of the splenic vein showed reversal of portal venous flow, multiple collaterals, and a pressure gradient of 14 mmHg. Two 10 mm × 40 mm Cordis stents were placed, which decreased the pressure gradient to 7 mmHg and resolved the portosystemic collaterals. At 6 months follow-up, the patient had no recurrent episodes of ascites.ConclusionThe current case highlights the successful treatment of sinistral portal hypertension-related intractable chylous ascites treated with transhepatic splenic vein stenting. Splenic venous stent patency rates of 92.9% at 12 months have been reported. Rebleeding rates of 7.1% for splenic vein stenting, 16% for splenectomy, and 47.8% for splenic arterial embolization have been reported in the treatment of sinistral portal hypertension-related gastrointestinal bleeding. The literature regarding splenic vein stenting for sinistral portal hypertension-related ascites is less robust. Technical and clinical success in the current case suggests that splenic vein recanalization may be a safe and viable option in other sinistral portal hypertension-related symptomatology.Level of Evidence: Level 4, Case Report.

Ligation of patent ductus venosus in a child with pulmonary arterial hypertension and hypersplenism

Introduction:Patent ductus venosus (PDV) is a rare and critical disease, and the majority of patients present with pulmonary arterial hypertension (PAH) or hepatopulmonary syndrome due to congenital portosystemic shunt. We reported that both PAH and hypersplenism were major complications of PDV in this case. This case report can assist the treatment and recovery of the patients with similar symptoms.Patient concerns:A 4-year-old male patient presented to our institution with a history of recurrent respiratory infections accompanied by leukocytopenia, thrombocytopenia and presented with tachypnoea. upon mild exertion.Diagnosis:A wide communication, 10 mm in diameter, between the portal vein and inferior vena cava was identified in the subcostal echocardiogram and computed tomography images. Echocardiography showed an estimated systolic pulmonary artery pressure of 106 mm Hg. Right-sided cardiac catheterization indicated a mean pulmonary arterial pressure of 30 mm Hg and a pulmonary vascular resistance of 3 Wood units. Chest X-ray revealed cardiomegaly with a prominent pulmonary segment.Interventions:The patient was treated with combination pharmacotherapy of bosentan and tadalafil and PDV ligation.Outcomes:A year later, the boy showed normal exercise tolerance and weight gain. Liver and spleen parameters, liver function, blood cells and the general condition of the boy improved.Conclusion:Initial combination therapy of bosentan and tadalafil is safe and effective in children with PAH associated with PDV. When PDV banding test shows normal portal pressure, PDV ligation is considered acceptable in children with PAH and hypersplenism associated with PDV.

PULMONARY HYPERTENSION AND LIVER TRANSPLANTATION IN PRIMARY BILIARY CIRRHOSIS: IS IT ALWAYS PORTO PULMONARY HYPERTENSION?

SESSION TITLE: Global Case Report Posters SESSION TYPE: Global Case Reports PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Pulmonary hypertension (PHTN), both arterial and venous, has been reported in up to 20% of patients at the time of liver transplantation (LTx). This is mostly attributed to Portopulmonary Hypertension (POPH), and generally improves after transplantation. We present a case of post-transplant worsening of PHTN in a patient with primary biliary cirrhosis (PBC) and discuss likely reasons. CASE PRESENTATION: A 61-yearold Egyptian lady, nonsmoker and non-alcohol consumer with PBC complicated by esophageal varices and ascites underwent routine pre LTx pulmonary evaluation. No pulmonary symptoms or abnormal exam findings. Spirometry and lung volumes were normal but diffusion capacity (DLCO) was low at 33ml/min/mmHg (32% predicted). Arterial blood gases were normal and no orhtodeoxia was detected.Contrast transthoracic echocardiogram (TTE) showed normal ejection fraction with grade 2 diastolic dysfunction and estimated right ventricle systolic pressure (RVSP) of 35 mmHg with no right to left shunt. Right heart catheterization showed Pulmonary artery 42/24 mmHg with mean pressures (MPAP) of 31 mm Hg, Pulmonary capillary wedge pressure (PCWP) 17mmHg, Trans pulmonary pressure gradient of 7, Cardiac output (CO) of 4.45 L/min and Pulmonary vascular resistance (PVR) of 3.1 WU. This was consistent with pulmonary venous hypertension from diastolic dysfunction. She was deemed low risk from pulmonary standpoint for liver transplantation and underwent uneventful transplant. Six months post-transplant she experienced significant fatigue and progressively worsening exertional dyspnea. Hemoglobin, kidney and liver function were normal. TTE revealed normal left sided chambers with RVSP 78mmHg. Repeat right heart catheterization showed mPAP 56 mmHg, PCWP 12 mmHg, CO 3.26 L/min, and PVR 13.2 WU, with significant vasoresponsiveness after inhaled nitic oxide (mPAP 39, PVR11.5). Repeat DLCO was 26 ml/min/mmHg with normal total lung capacity. No evidence of interstitial lung disease on high resolution chest scan was noted. Ventilation –perfusion lung scan did not reveal any changes of thromboembolic disease or significant right to left shunt. Doppler studies showed normal portal pressure. On the basis telangiectasia and positive anticentromere antibody (1:1280), she was diagnosed as incomplete crest syndrome. She was diagnosed as Group 1 PHTN secondary to Connective tissue disease and started on sildenafil and amlodipine. In view of progressive PHTN with functional class 3-4, she has also been started on iloprost inhaler. DISCUSSION: Severe PHTN is a relatively contraindication for LTx. The therapeutic potential of LTx in POPH has been reported by Bozbas, et al. with significant reductions in mPAPs after LTx. [1] However there are reports of new or worsening PHTN after LTx. The onset varied greatly from 1 month to 11 years post LTx, and mortality was high (69%). [2] In the immediate posttransplant period, systemic vascular resistance increases and this is associated with a proportional decrease in cardiac output. However hyperdynamic state may persist after LTx with increased hepatic blood flow. Despite normal portal pressure, portalsystemic collateral blood flow remains elevated after orthotopic liver transplantation, possibly because of persistent collateral circulation, which may keep portal tributary blood flow elevated.Our patient had mild initial PHTN with severe PHTN post LTx, likely due to increased pulmonary blood flow after improved portal hypertension. Incomplete CREST syndrome and PBC could be the cause for her worsening PHTN. The incidence of PHTN in PBC is 11.8%, mostly POPH but 30% do not have evidence of POPH. [3] Early DLCO and TTE follow-up may have alerted us to the worsening of PHTN, with potential improved prognosis with early start of specific pulmonary vasodilator therapy. CONCLUSIONS: In patients with autoimmune causes for liver cirrhosis and pulmonary hypertension, it’s important to consider alternative etiology for PHTN and not attribute it solely to POPH. Also, these patients may benefit form early follow up DLCO and TTE post LTx to assess progression or improvement Reference #1: Savas BS, Eroglu S, Oner EF, Moray G, Haberal M. Pulmonary hypertension improves after Orthotopic liver transplant in patients with chronic liver disease. Exp Clin Transplant. 2015;13(Suppl 3):115–9. Reference #2: Koch DG, Caplan M, Reuben A. Pulmonary hypertension after liver transplantation: Case presentation and review of the literature. Liver transplantation 2009;15(4)407 -12 Reference #3: Wallwork J, Williams R, Calne RY.Transplantation of liver, heart, and lungs for primary biliary cirrhosis and primary pulmonary hypertension. Lancet. 1987 Jul 25; 2(8552):182-5. DISCLOSURES: No relevant relationships by Maha Hamza, source=Web Response No relevant relationships by Tasleem Raza, source=Web Response No relevant relationships by Merlin Thomas, source=Web Response

Effects of terlipressin infusion on blood loss and transfusion needs during liver resection: A randomised trial.

Blood loss and perioperative blood transfusion requirements affect the long-term survival after liver resection for malignant tumours. Terlipressin is a synthetic vasopressin analogue with relative specificity for the splanchnic circulation where it causes vasoconstriction with subsequent reduction of blood loss during abdominal surgeries. We tried to examine the impact of terlipressin on blood loss and blood transfusion needs during liver resection. In this randomised, double-blind placebo-controlled trial 84 patients scheduled for major liver resections were randomly assigned to receive either terlipressin at the onset of surgery as an initial bolus dose of (1 mg over 30 minutes) followed by a continuous infusion of 2 μg/kg/h throughout the procedure (Terlipressin group) or the same volume and rate of 0.9% saline (Placebo group).The primary outcome was the amount of intra-operative blood loss. The mean (SD) of the amount of intra-operative blood loss was 1351 (887) in the terlipressin group versus 1892 (889) mL in the placebo group (P = 0.006). Thirteen (30%) patients received blood transfusion in the terlipressin group compared with t27 (64.2%) in the placebo group (P = 0.002) with a statistically significant difference in the median (range) number of the transfused units of packed RBCs [0 (0-5) units and 1 (0-6) units in the two groups respectively; P = 0.001]. Terlipressin infusion during major liver resection was associated with less bleeding compared to placebo. More studies are required to confirm our results especially in patients with normal portal pressure.

Vasopressin and nitroglycerin decrease portal and hepatic venous pressure and hepato-splanchnic blood flow.

Various methods are used to reduce venous blood pressure in the hepato-splanchnic circulation, and hence minimise blood loss during liver surgery. Previous studies show that combination of vasopressin and nitroglycerin reduces portal pressure and flow in patients with portal hypertension, and in this study we investigated this combination in patients with normal portal pressure. In all, 13 patients were studied. Measurements were made twice to confirm baseline (C1 and BL), during vasopressin infusion 4.8 U/h (V), and during vasopressin infusion combined with nitroglycerin infusion (V + N). Portal venous pressure (PVP), hepatic venous pressure (HVP), central haemodynamics and arterial and venous blood gases were obtained at each measuring point, and portal (splanchnic) and hepato-splanchnic blood flow changes were calculated. Vasopressin alone did not affect PVP, whereas HVP increased slightly. In combination with nitroglycerin, PVP decreased from 10.1 ± 1.6 to 8.9 ± 1.3 mmHg (P < 0.0001), and HVP decreased from 7.9 ± 1.9 to 6.2 ± 1.3 mmHg (P = 0.001). Vasopressin reduced portal blood flow by 47 ± 19% and hepatic venous flow by 11 ± 18%, respectively. Addition of nitroglycerin further reduced portal- and hepatic flow by 55 ± 13% and 30 ± 13%, respectively. Vasopressin alone had minor effects on central haemodynamics, whereas addition of nitroglycerin reduced cardiac index (3.2 ± 0.7 to 2.7 ± 0.5; P < 0.0001). The arterial-portal vein lactate gradient was unaffected. The combination of vasopressin and nitroglycerin decreases portal pressure and hepato-splanchnic blood flow, and could be a potential treatment to reduce bleeding in liver resection surgery.

Is there a standard for surgical therapy of hepatocellular carcinoma in healthy and cirrhotic liver? A comparison of eight guidelines

Background and aimsLiver resection (LR) and transplantation are the most reliable treatments for hepatocellular carcinoma (HCC). Aim was to compare different guidelines regarding indication for resection and transplantation because of...

The Curious Case of a Swollen Belly: Myxedema Ascites

Introduction: Less than 4% of patients with hypothyroidism develop ascites. Ascites as the only presenting feature of hypothyroidism is uncommon, hence diagnosis is often delayed. Once it is diagnosed, treatment of hypothyroidism leads to quick clinical improvement in ascites. We report a case of ascites secondary to severe hypothyroidism.Figure 1Case: A 56 year old female with long standing history of Hashimoto's thyroiditis and non-compliance to thyroid supplementation presented with a four week history of progressive painless abdominal distension. She had recently undergone extensive work-up at a regional hospital. Review of records revealed high ascitic fluid protein content (3.9 g/dl) and serum-ascites-albumin gradient (SAAG) of 1. Ultrasound and computed tomography of the abdomen and pelvis showed massive ascites. Morphology of liver and spleen was unremarkable without any evidence of increased portal pressure. Viral hepatitis serology was negative and tumor markers (CA19-9, CA125) were within normal limits. Hepatic Doppler ultrasound showed normal portal pressure without evidence of portal or hepatic vein thrombosis. We ordered thyroid stimulating hormone level that resulted as >100 units/ml, with low free T4 (0.2 ng/dl). Further evaluation revealed dyslipidemia and mildly elevated alanine and aspartate transaminases and creatine kinase, consistent with thyroid myopathy. The diagnosis of myxedema ascites was made on this diagnostic work-up and the patient was started on thyroid replacement. On a follow-up visit at 4 weeks, there was no clinical evidence of ascites and TSH decreased to 56 units/ml. Discussion: Severe uncontrolled hypothyroidism is a rare but reversible cause of ascites. Various theories have been hypothesized to explain the pathophysiology. These include: 1) an increase in capillary permeability leading to the extravasation of plasma proteins into the extravascular compartment; 2) direct hygroscopic effect caused by hyaluronic acid accumulating in the skin and producing edema; 3) diminished free water clearance due to excess ADH production. Myxedema ascites responds well to thyroid replacement therapy and is completely reversible. Conclusion: Our case illustrates that the diagnosis of myxedema ascites should be borne in mind in a patient with uncontrolled hypothyroidism who presents with ascites. It also signifies the need for testing TSH level as part of the workup for ascites of unknown etiology.

Clinical profile and comparison of SAAG with ascites fluid total protein (AFTP) in cases of ascites at a tertiary referral hospital in Maharashtra

Aims: This observational prospective study was carried out with aims of 1) study various presentations and clinical features in ascites cases, 2) assess different etiological factors, 3) compare serum ascitic albumin gradient (SAAG) and ascitic fluid total protein (AFTP) in differentiating portal hypertension related causes of ascites from others, 4) study in hospital outcome in cases of ascites . Material and Methods : 100 consecutive ascites cases admitted in wards with clinical diagnosis and sonographic confirmation were recruited in the study. After history and detailed clinical examination cases were subjected to ultrasonography and portal vein Doppler to diagnose portal hypertension which was followed by paracentesis. Serum Albumin & total protein, ascitic fluid albumin and total protein, AFTP and SAAG was determined. Results : Mean age of diagnosis of ascites was 42.41 ±7.72 years and maximum cases in 30-49 years age group. 68% of cases of ascites had cirrhosis of liver, 16% peritoneal (abdominal) tuberculosis, 10% chronic heart failure (CHF), 4% nephrotic syndrome and 2% had ovarian malignancy. Mean AFTP and Mean SAAG was 1.77±0.73gm% and 2.05±0.52 gm% in 78 cases of portal hypertension related ascites respectively. In normal portal pressure cases (n=22) of ascites it was 3.01±0.37 gm% and 0.72±0.19 gm% respectively. Sensitivity of AFTP and SAAG in differentiating portal hypertension related etiology from other causes was 70.51% and 92.31% respectively .Though sensitivity was less, specificity was equal ( 95.45%). Eight cases had variceal bleeding, 9 had hepatorenal syndrome and 15 had hepatic encephalopathy. Total 16 cases of liver cirrhosis with ascites died in hospital commonest cause was hepatic encephalopathy and hepatorenal syndrome.

Percutaneous device closure of abernethy malformation—A treatable cause of hepatopulmonary syndrome

An eight-year-old girl was evaluated for unexplained cyanosis. A contrast echo was suggestive of pulmonary arteriovenous fistula. Further evaluation revealed Abernethy malformation (type 2) leading to hepatopulmonary syndrome. Percutaneous device closure of Abernethy malformation was done after anatomical and physiological evaluation of the portal circulation. Prior to closure, it is important to ensure adequate portal radicals into the liver and normal portal pressure after test balloon occlusion. Subcostal echocardiography can diagnose and guide device closure of Abernethy malformation, a treatable cause of hepatopulmonary syndrome.

Percutaneous device closure of persistent ductus venosus presenting with hemoptysis

An eight-year-old boy was evaluated for unexplained hemoptysis and cyanosis. A contrast echocardiogram was suggestive of pulmonary arteriovenous fistula. Further evaluation revealed persistent ductus venosus (PDV) and aortopulmonary collaterals. Both the PDV and aortopulmonary collaterals were closed percutaneously. PDV is amenable for device closure after detailed anatomical evaluation. Prior to closure, it is important to ensure adequate portal vein arborization into the liver and normal portal pressure after test balloon occlusion.

Gastric Varices Secondary to Splenic Vein Occlusion due to Pancreatic Diseases

Gastric varices that arise secondary to splenic vein occlusion can result in hypersplenism or gastrointestinal hemorrhaging. This article review gastric varices secondary to splenic vein occlusion due to pancreatic diseases with regard to causes of the condition, as well as diagnostic and therapeutic approaches. Diagnosis of gastric varices is made following esophago-gastro-duodenoscopy, and splenic vein occlusions are diagnosed from enhanced computed tomographic scans in almost all cases. Specific findings of gastric varices secondary to splenic vein occlusion are based on endoscopic ultrasonographic color flow images of gastric variceal flow that clearly depicted round cardiac and fundal regions at the center, with varices expanding to the curvatura ventriculi major of the gastric body. Several treatment options for gastric variceal bleeding secondary to splenic vein occlusion have been proposed. Splenectomy, which decompresses the short gastric vein by cutting off inflow, has generally been considered the best treatment of choice in such condition. Endoscopic injection sclerotherapy using cyanoacrylate, is useful in the treatment of bleeding gastric varices due to splenic vein occlusion. As patients with splenic vein occlusion have normal portal pressure and normal hepatic function, portal systemic shunting is not indicated. Splenic arterial embolization, which reduces blood flow through the splenic parenchyma, is another effective method of controlling bleeding from gastric varices secondary to splenic vein occlusion. Treatment of gastric varices secondary to splenic vein occlusion is directed to the underlying pancreatic diseases.

Hepatic resection for hepatocellular carcinoma in patients with Child–Pugh's A cirrhosis: is clinical evidence of portal hypertension a contraindication?

BackgroundAccording to international guidelines [European Association for the Study of the Liver (EASL) and the American Association for the Study of Liver Diseases (AASLD)], portal hypertension (PHTN) is considered a contraindication for liver resection for hepatocellular carcinoma (HCC), and patients should be referred for other treatments. However, this statement remains controversial. The aim of this study was to elucidate surgical outcomes of minor hepatectomies in patients with PHTN (defined by the presence of esophageal varices or a platelet count of <100 000 in association with splenomegaly) and well‐compensated liver disease. MethodsBetween 1997 and 2012, a total of 223 cirrhotic patients [stage A according to the Barcelona Clinic Liver Cancer (BCLC) classification] were eligible for this analysis and were divided into two groups according to the presence (n = 63) or absence (n = 160) of PHTN. The demographic data were comparable in the two patient groups. ResultsOperative mortality was not different (only one patient died in the PHTN group). However, patients with PHTN had higher liver‐related morbidity (29% versus 14%; P = 0.009), without differences in hospital stay (8.8 versus 9.8 days, respectively). The PHTN group showed a worse survival rate only if biochemical signs of liver decompensation existed. Multivariate analysis identified albumin levels as an independent predictive factor for survival. ConclusionsPHTN should not be considered an absolute contraindication to a hepatectomy in cirrhotic patients. Patients with PHTN have short‐ and long‐term results similar to patients with normal portal pressure. A limited hepatic resection for early‐stage tumours is an option for Child–Pugh class A5 patients with PHTN.

Efficacy of Antiviral Therapy on Hepatitis C Recurrence After Liver Transplantation: A Randomized Controlled Study

Recurrence of hepatitis C virus (HCV) infection is a relevant problem of liver transplantation programs. We evaluated the effect of antiviral therapy on disease progression in 81 HCV-infected liver transplantation recipients. Patients with mild hepatitis C recurrence (fibrosis stage F0 to F2, n = 54) were randomized to no treatment (group A, n = 27) or peginterferon alfa-2b/ribavirin for 48 weeks (group B, n = 27). Patients with severe recurrence (F3 to F4, cholestatic hepatitis) were treated (group C, n = 27). All patients (n = 81) underwent a liver biopsy at baseline and after follow-up; paired hepatic venous pressure gradient (HVPG) measurements were available in 51 patients. Thirteen (48%) patients of group B and 5 (18.5%) of group C achieved sustained virological response. Liver fibrosis progressed > or =1 stage in 40 (49%) of 81 patients: 19 (70%) of group A versus 7 (26%) of group B (P = .001) and in 14 (54%) of group C. HVPG increased (6.5 to 13 mm Hg, P < .01) in patients in whom fibrosis worsened, whereas it decreased (5 to 3.5 mm Hg, P = .017) or remained unchanged in those with fibrosis improvement or stabilization, respectively. The only variable independently associated with fibrosis improvement/stabilization was treatment (odds ratio [OR] =3.7, 95% confidence interval [CI] 1.3 to 10, P = .009). Among treated patients, alanine aminotransferase (ALT) normalization and viral clearance were independently associated with histological or hemodynamic improvement/stabilization (OR 5.3, 95% CI 1.5 to 18, P < .01; OR 7.4, 95% CI 1.4 to 38, P = .01; respectively). Our data demonstrate that in liver transplantation recipients, antiviral therapy slows disease progression (particularly in sustained virological responders), as shown by its effects on liver histology and on HVPG.

Endoscopic Ultrasound–Guided Fine-Needle Aspiration of Ascites

The aim of this study is to report a large single-center experience with endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) of ascites. Consecutive patients at our institution in whom EUS-guided paracentesis was performed between January 1997 and July 2005 were identified retrospectively. All procedures were performed by or under the supervision of 1 of 5 experienced endosonographers with available on-site cytopathology. Sixty consecutive patients (33 men; mean age, 67 y) were identified. Previously attempted percutaneous paracentesis was unsuccessful in 3 of 6 patients. Ascites confirmed by EUS FNA was visible in 28 of 54 (52%) computerized tomography, 3 of 11 (27%) transabdominal ultrasound, and 4 of 8 (50%) magnetic resonance imaging examinations before EUS. Transgastric (n = 55) or transduodenal (n = 5) EUS-guided paracentesis (mean, 8.9; range, 1-40 mL) revealed malignancy in 16 (27%) from primary pancreatic (n = 9), gastric (n = 2), urothelial (n = 1), esophageal (n = 1), gallbladder (n = 1), bile duct (n = 1) cancer, and lymphoma (n = 1). The cytology from 2 patients was atypical (1 suspicious for malignancy and 1 considered reactive) and the remaining 42 were benign. Potential complications occurred in 2 of 60 (3%) patients with self-limited fever. Of the 8 of 60 (13%) patients who underwent subsequent surgery, 3 had metastatic pancreatic adenocarcinoma (n = 2) and metastatic small intestinal carcinoid (n = 1) to the peritoneum after negative EUS-FNA cytology. EUS frequently identifies ascites missed by other imaging studies. EUS-guided paracentesis may identify malignancy in a subset of patients. Negative ascitic fluid cytology from EUS FNA does not exclude possible peritoneal carcinomatosis.

A new cholestatic mouse model provides insights into renal reabsorption of sodium

A new cholestatic mouse model provides insights into renal reabsorption of sodium

Portal Hypertension: Contraindication to Liver Surgery?

In recent decades liver resection has become a safe procedure, mainly because of better patient selection. Despite this progress, however, outcomes of hepatectomy in cirrhotic patients with portal hypertension are still uncertain. The aim of this study was to elucidate early and long-term outcomes of liver resection in these patients. Between 1985 and 2003, a total of 245 cirrhotic patients underwent hepatectomy for HCC. Altogether, 217 patients were eligible for this analysis and were divided into two groups according to the presence of portal hypertension at the time of surgery: 99 patients with portal hypertension and 118 without it. Patients with portal hypertension had worse preoperative liver function (Child-Pugh A class patients: 66.7% vs. 94.9%; P<0.0001). No differences were encountered in terms of intraoperative and pathology data. Operative mortality was similar (11.1% vs. 5.1%; P=0.100), but patients with portal hypertension had higher morbidity (43.4% vs. 30.5%; P=0.049) and received a higher rate of blood and plasma transfusions (51.5% vs. 32.2%, P=0.004; 77.8% vs. 57.6%, P=0.0017). Considering only Child-Pugh A patients, short-term results were similar in the two groups in terms of mortality, morbidity, and transfusion rates. The 5-year survival rate was significantly higher in patients without portal hypertension (39.8% vs. 28.9%; P=0.020), although when considering only Child-Pugh A patients no difference of survival was encountered. Multivariate analysis identified Child-Pugh classification, tumor diameter, and vascular invasion as independent predicting factors for survival. Portal hypertension should not be considered an absolute contraindication to hepatectomy in cirrhotic patients. Child-Pugh A patients with portal hypertension have short- and long-term results similar to patients with normal portal pressure.

Abnormal Intrahepatic Portal Vasculature in Native and Allograft Liver Biopsies

Abnormal portal vessels in small portal tracts can be seen in association with various causes of portal hypertension, such as noncirrhotic portal hypertension (NCPH) and cirrhosis. Very little has been reported about the presence of abnormal portal vessels in livers with normal portal pressure. Little attention has also been given to the presence of abnormal vessels in liver allografts outside the setting of transplant vasculopathy/chronic rejection. This study reports on the portal vasculature abnormalities, many similar to those described in NCPH, encountered in routine native liver biopsies (n = 46) and allograft liver biopsies (n = 48). A classification scheme for the abnormal portal vasculature was adapted from the literature, and the portal vessels were divided into five groups (types 0-IV). Abnormal vessels were present in greater than 25% of the portal tracts in 88% of all the biopsies studied; there was no significant difference between the native and allograft biopsies. In the allograft biopsy group, there were correlations between vascular abnormalities and severity of a concurrent acute cellular rejection episode, the presence of prior rejection episodes, and length of time after transplant. Biopsies from patients with viral hepatitis C infection (HCV) showed more type IV lesions (absent or sclerosed portal vessels) with fragmentation when compared with biopsies obtained for other reasons. The number of portal tracts with abnormal portal veins and fragmented vessels correlated positively with increasing fibrosis. This is the first study to demonstrate the presence of abnormal portal vessels, some of the type seen in NCPH, in a significant number of both native and allograft liver biopsies in patients without evidence of portal hypertension. Abnormal portal vasculature tends to be associated with HCV and increased fibrosis, and, within the transplant group, with the severity of rejection, presence of prior rejection episodes, and increased time posttransplantation.

EUS-guided portal vein catheterization and pressure measurement in an animal model: a pilot study of feasibility

Background The extrahepatic portal vein is inaccessible to direct catheterization. Methods Because EUS can readily image the portal vein, the feasibility of EUS-guided portal vein catheterization by using a 22-gauge needle was studied in 7 normal pigs and 14 pigs in which portal hypertension was induced (7/14 anticoagulated). Results Catheterization was not possible by EUS or transhepatic methods in, respectively, 3 and 5 animals. One anticoagulated animal had a small amount of periduodenal bleeding as a result of EUS catheterization. The mean normal portal vein pressure (1 standard deviation) as determined by EUS and transhepatic methods was, respectively, 20.3 (4) mm Hg and 20.4 (2) mm Hg. Injection of polyvinyl alcohol particles increased the portal vein pressure by 10.2 (11.59) mm Hg. There was a close correlation under all conditions between the mean portal vein pressures obtained by EUS and transhepatic catheterization (r = 0.91). Conclusions EUS-guided portal vein catheterization appears to be feasible in an animal model and provides accurate pressure measurements.