Increase In Portal Flow Research Articles

SerpinB3 as hepatic marker of post-resective shear stress

Post-resective liver failure is a frequent complication of liver surgery and it is due to portal hyperperfusion of the remnant liver and to arterial vasoconstriction, as buffer response of the hepatic artery. In this context, splenectomy allows a reduction of portal flow and increases the survival chance in preclinical models. SerpinB3 is over-expressed in the liver in oxidative stress conditions, as a mechanism of cell defense to provide survival by apoptosis inhibition and cell proliferation. In this study, the expression of SerpinB3 was assessed as predictor of liver damage in in vivo models of major hepatic resection with or without splenectomy. Wistar male rats were divided into 4 groups: group A received 30% hepatic resection, group B > 60% resection, group C > 60% resection with splenectomy and group D sham-operated. Before and after surgery liver function tests, echo Doppler ultrasound and gene expression were assessed. Transaminase values and ammonium were significantly higher in groups that underwent major hepatic resection. Echo Doppler ultrasound showed the highest portal flow and resistance of the hepatic artery in the group with > 60% hepatectomy without splenectomy, while the association of splenectomy determined no increase in portal flow and hepatic artery resistance. Only the group of rats without splenectomy showed higher shear-stress conditions, reflected by higher levels of HO-1, Nox1 and of Serpinb3, the latter associated with an increase of IL-6. In conclusion, splenectomy controls inflammation and oxidative damage, preventing the expression of Serpinb3. Therefore, SerpinB3 can be considered as a marker of post-resective shear stress.

Can pretransplant TIPS be harmful in liver transplantation? A propensity score matching analysis

BackgroundTransjugular intrahepatic portosystemic shunt has been established as an effective treatment for complicated portal hypertension. This retrospective study investigated the effect of pretransplant transjugular intrahepatic portosystemic shunt placement on intraoperative graft hemodynamics and surgical outcomes after liver transplantation. MethodsOf 1,081 patients who underwent liver transplantation between January 2007 and June 2017 at Cleveland Clinic (OH, USA), 130 patients had transjugular intrahepatic portosystemic shunt placement before liver transplant. We performed a 1:2 propensity score matching to compare intraoperative graft hemodynamics and surgical outcomes between the transjugular intrahepatic portosystemic shunt group (n = 130) and the no-transjugular intrahepatic portosystemic shunt group (n = 260). ResultsThe transjugular intrahepatic portosystemic shunt did not increase operative time, the volume of blood transfusion, duration of hospital stay, or complication rates. Graft and patient survivals were similar between the groups. Mean intraoperative cardiac output and graft portal flow in the transjugular intrahepatic portosystemic shunt group were greater than in the no-transjugular intrahepatic portosystemic shunt group (P = .03 and P = .003, respectively). In multivariate analysis, male sex, younger age, low platelet count, absence of portal vein thrombosis, and pretransplant transjugular intrahepatic portosystemic shunt placement were independently associated with increased portal flow volume (P < or = 0.03 each). Transjugular intrahepatic portosystemic shunt malposition was observed in 17 patients (13.1%). The 1-year patient survival was 70.6% with transjugular intrahepatic portosystemic shunt malposition and 92.0% without transjugular intrahepatic portosystemic shunt malposition (P = .01). ConclusionOur findings suggest that pretransplant transjugular intrahepatic portosystemic shunt placement increases graft portal flow but does not compromise surgical outcomes after liver transplantation. Transjugular intrahepatic portosystemic shunt malposition, however, is not uncommon and may increase the complexity of transplantation.

Somatostatin and the “Small-For-Size” Liver

“Small-for-size” livers arising in the context of liver resection and transplantation are vulnerable to the effects of increased portal flow in the immediate postoperative period. Increased portal flow is an essential stimulus for liver regeneration. If the rise in flow and stimulus for regeneration are excessive; however, liver failure and patient death may result. Somatostatin is an endogenous peptide hormone that may be administered exogenously to not only reduce portal blood flow but also offer direct protection to different cells in the liver. In this review article, we describe key changes that transpire in the liver following a relative size reduction occurring in the context of resection and transplantation and the largely beneficial effects that peri-operative somatostatin therapy may help achieve in this setting.

High postoperative portal venous flow pulsatility indicates right ventricular dysfunction and predicts complications in cardiac surgery patients

BackgroundRight ventricular failure after cardiac surgery is associated with morbidity and mortality. Right ventricular dysfunction results in hepatic venous congestion, which impacts the portal circulation. We aimed to determine whether an increased portal flow pulsatility fraction was associated with right ventricular dysfunction in cardiac surgery patients. We also aimed to describe the haemodynamic factors and postoperative complications associated with an increased portal pulsatility in this setting. MethodsWe conducted a prospective single-centre cohort study, recruiting adults undergoing cardiac surgery. Portal flow was assessed before, during, and after surgery by Doppler ultrasound. A detailed haemodynamic and echocardiographic assessment was performed at the same time points. ResultsA total of 115 patients were included. Both systolic and diastolic right ventricular dysfunction were associated with a higher portal pulsatility fraction (P=0.008 and <0.001, respectively). A positive association was present between portal pulsatility fraction and measurements representative of venous pressure (central venous pressure, inferior vena cava diameter). A post-procedural portal pulsatility fraction ≥50% measured in the operating room was present in 21 (18.3%) patients and was associated with an increased risk of major complications (odds ratio=5.83, confidence interval, 2.04–16.68, P=0.001). The addition of portal flow assessment to a predictive model including EuroSCORE II and systolic right ventricular dysfunction improved prediction of postoperative complications. ConclusionsHigh portal flow pulsatility fraction is associated with right ventricular dysfunction, signs of venous congestion and decreased perfusion, and an increased risk of major complications. Portal vein Doppler ultrasound appears to be promising for risk assessment in the perioperative period. Clinical trials registrationNCT02658006.

Establishing a porcine model of “Small for Flow Syndrome”

Introduction The concept of "Small for Flow Syndrome” (SFFS) arises from the observation that the determining factor of the appearance of the “Small For Size Syndrome” (SFSS) and the posthepatectomy liver failure is the increase of portal inflow against a reduced hepatic mass. The criteria that define the SFFS are intraoperative and determined by: a portal pressure >20mmHg or a portal flow >250mL/min/100g. They indicate that we must take measures to prevent the development of the SFSS, as a consequence of the structural alterations caused by this inflow. Materials and Methods An experimental study (10 minipigs) of 24-hour survival was carried out. An hyperextended hepatectomy (90%) was performed. It consists on resecting the lateral and medial left lobes, and lateral and medial right lobes. Blood tests, hepatic and systemic hemodynamics, hepatic function (PDR), histology, and volumetry were assessed before and after the surgery. Intracranial pressure (ICP) and hepatocyte proliferation were evaluated. Results In all of the swines the surgery was completed with success and hemodynamic stability to start the postoperative observation period. The percentage of hepatic volume remaining after surgery was 8.85±2.59% (volumetry by CT). Hemodynamic data were measured at the beginning, after the hepatectomy, and 24 hours after. There was an increase in portal pressure after surgery, 20.90±4.50mmHg. Portal flow varies from 68'38±23’54ml/min/100g to 245’02±115’62ml/min/100g. This increase in portal flow through a reduced sinusoidal volume is reflected in the increase in the portosystemic pressure gradient, going from 1.11±1.90 to 13.20±7.16mmHg. PDR values went from?? 12.30±5.47 to 4.54±1.82 and R15 from 17.53±10’86 to 52’12±13'00 after surgery. There are significant histological damages, oscillating the score from 0.75±1.16 to 5.62±2.55. After surgery 75% of the animals had a Ki-67<2%. The ICP was monitored, observing a gradual increase in it. Discussion After the resection there is a deterioration in the liver function (decreases the PDR and increases the INR), similars to hepatic transplant models with reduced grafts. The histological disorders are compatible with those described in the literature in relation to the SFSS. Above 20 mmHg of portal pressure all animals showed histological damage. Since the aim of establishment of an animal model of SFFS is a better understanding of this clinical syndrome as well as studying the possible preventive and curative methods, we strongly believe that, in a porcine model with normal parenchyma, 90% liver resection can be considered as ideal model. Following 90% hepatectomy, we can render the hemodynamic, histological, and biochemical changes of the SFFS. Conclusion Hyperextended hepatectomy in porcine model is a feasible, reproducible and appropriate model to study the pathophysiology, prediction, prevention, diagnosis and management of SFFS.

Assessment of Liver Perfusion by IntraVoxel Incoherent Motion (IVIM) Magnetic Resonance-Diffusion-Weighted Imaging: Correlation With Phase-Contrast Portal Venous Flow Measurements.

To prospectively verify, in vivo, Le Bihan's model of signal decay in magnetic resonance/diffusion-weighted imaging (intravoxel incoherent motion) in healthy liver parenchyma. Informed consent and institutional board approval were obtained. To measure both underfasting and postprandial conditions, apparent, slow, and fast diffusion (D*) coefficients and perfusion fraction of liver parenchyma, 40 healthy volunteers (19 women and 21 men) underwent a 3.0-T magnetic resonance imaging examination, including portal venous flow measurements by a 2-dimensional phase-contrast sequence, and multi-b diffusion-weighted imaging acquired before and 30 minutes after a 600-Kcal meal. Parameters were measured by fitting procedure with regions of interest drawn on the right liver lobe. Paired-sample t test was performed to search for any statistically significant difference between preprandial and postprandial values of each parameter and of portal flow. Pearson correlation coefficients were calculated to evaluate the relationship between portal flow increase and diffusion-weighted imaging parameter changes in postprandial conditions. Interobserver agreement for measurement of the intravoxel incoherent motion parameters was determined, both for preprandial and postprandial values. Mean increase in postprandial portal flow was 98% (P < 0.0009). The t test did not show any statistically significant difference between the preprandial and postprandial values for apparent, slow diffusion coefficients and perfusion fraction (P ≥ 0.05), whereas a statistically significant postprandial increase (P < 0.01) of D* was detected. Correlation with portal venous flow increase at Pearson test was statistically significant for D* (P = 0.04) and nonsignificant for the other parameters. All the parameters showed wide variability, with a higher percent coefficient of variation for D*. Interobserver agreement was always greater than 0.70. This study verifies Le Bihan's theory, confirming that in the liver, D* is influenced by perfusional changes related to portal venous flow.

Splanchnic net balance of oxygen and metabolites in response to a discontinuous mesenteric vein infusion of ammonium in sheep

To simulate daily episodes of high absorption associated with the intake of diets with high N content, four wethers (42 ± 3.4 kg body weight), fitted with permanent catheters in the femoral artery and splanchnic vessels, were infused with 340 μmol into the mesenteric vein for 3 h, during the morning meal, over seven consecutive days. On the 7th day, mass transfers of , urea, glucose, lactate, ß-OH-butyrate and O2 were measured across portal-drained viscera (PDV), liver and splanchnic tissues during the last 90 min of the infusion. Measurements were repeated on the following day, at the same time, without the infusion. Plasma concentration in the portal vein (+332 μm; p = 0.006), portal absorption (+424 μmol/min; p < 0.001), liver uptake (+375 μmol/min; p = 0.003) and urea N production (+338 μmol/min; p = 0.059) were higher during infusion. Mass transfers of urea, glucose, lactate, ß-OH-butyrate and O2 across the PDV, and glucose, lactate, ß-OH-butyrate and O2 across the liver, were not altered by the infusion. Results suggest that a daily, discontinuous increase in portal flow during a meal stimulates liver removal and urea N production but does not significantly affect liver glucose production and O2 consumption in sheep.

Liver metastases, a rare cause of portal hypertension and stoma bleeding. Brief review of literature

INTRODUCTIONPortal hypertension is an unusual complication of liver metastases, which is frequently occurring in malignant disease. Portal hypertension may cause oesophageal varices and also stoma varices (colostomy and ileostomy). Oesophageal varices and bleeding from these varices have been frequently reported in literature. Stomal varices have also been reported in literature mostly associated with liver cirrhosis. These stomal varices lead to the massive bleeding causing morbidity and mortality.Portal hypertension is a pathological increase in portal pressure gradient (the difference between pressure in the portal and inferior vena cava veins). It is either due to an increase in portal blood flow or an increase in vascular resistance or combination of both. In liver cirrhosis, the primary factor leading to portal hypertension is increase in portal blood flow resistance and later on development of increased portal blood flow. It has been postulated that in liver metastasis the increase in portal flow resistance occurs at any site within portal venous system as a consequence of mechanical architectural disturbance. PRESENTATION OF CASEWe report a case of a 64 year old gentleman who developed portal hypertension due to secondary metastases from colorectal cancer. He subsequently developed bleeding varices in his end colostomy. DISCUSSIONWe believe that the combination of extensive metastases and chemotherapy induced portal hypertension in our patient. CONCLUSIONOur case and other literature review highlight that the recurrent bleeding stoma associated with colorectal cancer should be investigated for portal hypertension.

The Impact of Resuscitated Fecal Peritonitis on the Expression of the Hepatic Bile Salt Transporters in a Porcine Model

Sepsis is often associated with cholestatic liver dysfunction caused by changes in the expression profile of hepatic bile salt transporters. However, in rodent endotoxin models, the role of ischemic hepatitis caused by liver hypoperfusion cannot be delineated. We hypothesized that hepatocytes change their expression pattern of bile salt transporters during early severe sepsis despite adequate resuscitation. Fifteen anesthetized and instrumented pigs were randomized to either fecal peritonitis (n = 8) or control (n = 7). Resuscitation was performed by hydroxyethyl starch and norepinephrine infusion. Hemodynamic parameters and markers of cholestatic and ischemic hepatic dysfunction were recorded. At baseline and after 21 h, messenger RNA (mRNA) and protein expression of bile salt transporters was determined by quantitative real-time polymerase chain reaction and immunohistochemistry, respectively, on in vivo liver biopsies. All resuscitated septic pigs developed a normotensive hyperdynamic circulation with increased portal flow. After 21 h of peritonitis, no signs of biochemical or histological cholestasis were present. Na-taurocholate cotransporting polypeptide and bile salt export pump mRNA were downregulated by 83% (P = 0.001) and 67% (P = 0.001), respectively, in comparison with controls, whereas multidrug resistance-associated protein 4 (MRP4) mRNA was upregulated by 85% (P = 0.02). Bile salt export pump and MRP2 staining were downregulated in septic pigs. During early porcine fluid-resuscitated sepsis, hepatic basolateral influx (Na-taurocholate cotransporting polypeptide) and canalicular efflux (bile salt export pump) of bile salts were downregulated without hemodynamic signs of hepatic hypoperfusion or biochemical signs of cholestasis. In parallel, the basolateral escape transport (MRP4) was markedly upregulated, possibly as an early adaptive response to counteract hepatocellular accumulation of toxic bile acids.

Favorable clinical outcome using a covered stent following transjugular intrahepatic portosystemic shunt in patients with portal hypertension

To compare retrospectively the clinical outcomes in patients treated with transjugular intrahepatic portosystemic shunt (TIPS) using the novel polytetrafluoroethylene-covered stents (Fluency) and bare stents. Sixty consecutive patients with portal hypertension treated with TIPS from April 2007 to April 2009 were included. TIPS creation was performed with Fluency stent grafts in 30 patients (group A) and with bare stents in 30 patients (group B). Liver function, TIPS patency and clinical outcomes were evaluated every 3 months after procedures. During hospitalization, there were no cases of hepatic encephalopathy (HE) and recurrence of variceal bleedings. Acute shunt occlusion was found in one patient in each group. Follow-ups were performed in group A with average time of 6.16 +/- 3.89 months and in group B with 8.34 +/- 4.42 months. The rates of recurrent bleeding, shunt occlusion, HE and mortality were 0.03, 0.0, 16.7 and 0% in group A, and 20.0, 30.0, 20.0 and 13.3% in group B, respectively. There was no difference of HE between group A and group B. The decrease of portal pressure and portosystemic pressure gradient, and the increase of portal flow were 34.1 and 23.3%, 60.0 and 52.8%, and 189.5 and 111.1% in group A and B, respectively. There were no differences of liver function between group A and B. The Fluency stent graft is relatively safe and effective in TIPS creation, with a high patency rate compared with bare stents.

The retrospective study of transjugular intrahepatic portosystemic shunt with covered or uncovered stents in patients with portal hypertension

To retrospectively compare the clinical outcome in patients with portal hypertension treated with transjugular intrahepatic portosystemic shunt (TIPS) using Fluency stent-graft (PTFE-covered stents) or bare stents. Approval of study and treatment protocol and waiver of informed consent for the retrospective study were obtained from institutional review board. Informed consent was obtained from each patient before procedure. Sixty consecutive patients with portal hypertension treated with TIPS from April 2007 to April 2009 were included. TIPS creation was performed with Fluency stent-graft in 30 patients (group A) and with bare stents in 30 patients (group B). Liver function, TIPS patency and clinical outcome were evaluated every 3 months. During hospitalization, there was no hepatic encephalopathy and recurrency of variceal bleeding.Acute shunt occlusion was observed in one patient with group A and another patient with group B.Follow-up was performed with average time of (6.2 +/- 3.9) months in group A and (8.3 +/- 4.4) months in group B. The rates of recurrent bleeding, acute shunt occlusion, hepatic encephalopathy and death were 3.3% and 20.0%, 0 and 30.0%, 16.7% and 20.0%, 0 and 13.3% in group A and B. The rates of recurrent bleeding, acute shunt occlusion and death in group A was lower than those in group B. There was no difference of hepatic encephalopathy between group A and B. The decrease of portal pressure and portosystemic pressure gradient, and the increase of portal flow and shunt flow in group A were higher than those in group B. There were no difference of liver function, ammonia and MELD between group A and B. Fluency stent-graft is safe and effective in TIPS creation, with high patency rate. Covered-stent can improve the clinical outcome of portal hypertension.

Combined use of propranolol and nifedipine offers better effects on portal vein nonuniform remodeling in carbon tetrachloride (CCl 4)-induced portal hypertensive rats

Portal hypertension is a hemodynamic syndrome due to pathological increase in portal flow and portal pressure. These pathological changes in external flow loads will inevitably cause vascular remodeling in the portal vein, which is usually measured by an opening angle. The present study showed that carbon tetrachloride (CCl 4)-induced portal hypertension fully developed at 8 weeks and the opening angle of portal vein increased progressively in the pathogenesis of intrahepatic portal hypertension which was significantly augmented at 10 weeks. Although portal pressure and portal flow were reduced, treatment with either propranolol or nifedipine alone for 3 weeks did not decrease the augmented opening angle of the portal vein, while combined treatment with propranolol and nifedipine markedly reduced the increased opening angle of the portal vein and endothelial nitric oxide synthase (eNOS) mRNA expression but not inducible nitric oxide synthase (iNOS) mRNA expression. The decreasing effect of propranolol plus nifedipine on the elevated opening angle was significantly weakened by L-arginine and markedly reinforced by N-nitro- l-arginine-mythel-ester (L-NAME). These results indicate that combined use of propranolol and nifedipine ameliorates portal vein remodeling in portal hypertension at least by the nitric oxide-dependent way.

Liver histological, portal flow and plasmatic nitric oxide alterations caused by biliary obstruction and drainage in rats

To evaluate liver alterations caused by biliary obstruction and drainage. Thirty-nine male Wistar rats were randomly distributed in 4 groups: BO (n=18) bile duct ligation for 20 days, with a periodic evaluation of liver histological alterations, Doppler echography portal flow and measurements of NO and malondialdehyde (MDA); BO/DB (n=13) bile duct occlusion for 20 days followed by biliary drainage by choledochoduodenal anastomosis, 5 days follow-up, same BO group parameters evaluations; group CED (n=4) sham operation and portal flow evaluation trough 20 days; CHB (n=4) sham operation, with hepatic biopsy on 25th day and followed-up trough 25 days, by the same parameters of group BO, with exception of portal flow. Direct bilirubin (DB) and alkaline phosphatase (AP) were evaluated in the group BO, BO/DB and CHB. The bile duct ligation led to an increase of DB and AP, development of liver histological alterations, reduction of portal flow and increase of plasmatic NO and of MDA levels. The bile duct clearing resulted in a reduction of DB, AP, NO, MDA histological alterations and increase of portal flow. The biliary occlusion resulted in cholestasis and portal flow reduction, besides the increase of plasmatic NO and of hepatic MDA levels, and histological liver alterations, with a tendency of normalization after the bile duct clearing.

Changes in portal vein flow after adult living-donor liver transplantation: Does it influence postoperative liver function?

In adult living donor liver transplantation, using small grafts in cirrhotic patients with severe portal hypertension may have unpredictable consequences. The so-called small-for-size syndrome is present in most series worldwide. The goal of this study was to prospectively evaluate the influence of hemodynamic changes on postoperative liver function and on the percentage of liver volume increase, in the setting of living donor liver transplantation. Twenty-two consecutive adult living donor liver transplantations were performed at our institution in a 2-year period. We measured right portal flow and right hepatic arterial flow with an ultrasonic flow meter in the donor, and then in the recipient 1 hour after reperfusion. Postoperative liver function was measured by daily laboratory work. We also performed duplex ultrasounds on postoperative days 1, 2, and 7. Liver volume increase was estimated by magnetic resonance imaging graft volumetry at 2 months posttransplantation. We compared the blood flow results with the immediate liver function and its liver volume increase rate at 2 months. There was a significant increase in portal flow in the recipients compared with the donors (up to fourfold in some cases). Higher portal flow increase rates significantly correlated with faster prothrombin time normalization and faster liver volume increases. Median graft volume increase at 2 months was 44.9%. The increase in blood flow to the graft is well tolerated by the liver mass not affecting hepatocellular function as long as the graft-to body weight ratio is maintained (>0.8) and adequate outflow is provided. (Liver Transpl 2003;9:564-569.)

The induction of the immediate-early-genes Egr-1, PAI-1 and PRL-1 during liver regeneration in surgical models is related to increased portal flow

Background: The environmental triggers which control liver regeneration following partial hepatectomy (PH) are not clear. With respect to haemodynamic changes, the model of rat portal branch ligation (PBL) provides the unique opportunity to discriminate transcriptional events, which selectively result from increased portal flow. Aims: The potential role of portal over-flow on early expression of early growth response gene-1 (Egr-1), type-1 plasminogen activator inhibitor (PAI-1) and phosphatase of regenerating liver-1 (PRL-1) was analysed by a comparative experimental study using PBL and PH. Methods: Operative procedures were carried out in male Wistar rats. Growth kinetics were measured by liver weight indices. S-phase-specific mRNA-levels of H2B-histone protein (H2B), as well as expression analysis of Egr-1, PAI-1 and PRL-1 were examined by Northern blot experiments. Results: Growth patterns did not differ significantly between PBL and PH, whereas peak H2B expression occurred earlier after PH. Egr-1 and PAI-1 were specifically induced during the first few hours in the hyper-perfused lobes following PBL and PH. PRL-1-expression selectively peaked 3 h after PH and PBL in the hyper-perfused lobes. Conclusions: Increased portal flow after PBL and PH was associated with induction of Egr-1, PAI-1 and PRL-1. Thus, haemodynamic changes affect the molecular immediate-early response during liver regeneration.

Hepatic artery buffer response following left portal vein ligation: its role in liver tissue homeostasis.

Occlusion of a lobar portal vein is known to induce atrophy of downstream liver lobes and hypertrophy of contralateral lobes. Changes in portal flow are known to be compensated by changes in hepatic arterial flow, thus defining the hepatic artery buffer response (HABR). To understand the role of liver flow in liver atrophy, we measured portal flow and hepatic artery flow after different degrees of left portal vein stenosis (LPVS). Surgery was performed to obtain 0, 43, 48, 59, 68, 72, 78, and 100% LPVS. Systemic and splanchnic blood flows were measured at 4 h or 7 days after surgery using radiolabeled microspheres. At 4 h, LPVS produced no changes in systemic hemodynamics. Increasing degrees of LPVS produced a significant decrease in left portal flow (P < 0.0001) and a fully compensatory increase in right portal flow (P < 0.0001) without significantly affecting total portal flow. Left hepatic artery flow increased by 210% (P = 0.002), and right hepatic artery flow decreased by 67% (P = 0.05) after full LPVS. There was a significant inverse correlation between portal and arterial flow changes induced by different degrees of LPVS in the left (r(2) = 0. 61) and right (r(2) = 0.41) lobes. Despite this HABR, we observed a reduction in left liver flow (-45%; P = 0.01) and an increase in right liver flow (+230%; P = 0.01) with 100% LPVS. At 7 days, a significant decrease in the weight of left liver lobes (-75%; P < 0. 0001) and a compensatory increase in the weight of the right lobes (+210%; P < 0.0001) were observed with 100% LPVS. Left and right liver flows were similar to results measured at 4 h, and HABR was still present. However, when expressed per gram of liver, liver flows were identical to results obtained with sham animals. Reduction in lobar portal flow is accompanied by an increase in ipsilateral hepatic artery flow and a compensatory increase in portal flow to the rest of the liver. In a given lobe, when compensatory HABR is overcome, liver weight changes occur so that at the end total liver flow per gram of liver tissue is restored. This suggests that in normal conditions liver flow is a major regulator of liver volume.

Azygos blood flow: Phase contrast quantitation in volunteers and patients with portal hypertension pre- and postintrahepatic shunt placement

Flow volume in the azygos venous system was quantitated with Cine-phase contrast (PC) velocity mapping in volunteers and compared with patients with known portal hypertension, who were referred for transjugular intrahepatic portosystemic shunt (TIPS) placement. Subsequently, the TIPS-induced hemodynamic effects on portal and azygos flow were analyzed. To assess intra- and intersubject variability, flow in the azygos veins was measured in each of 10 normal subjects at three different times. Subsequently, portal and azygos flow was quantitated in 20 patients with portal hypertension, before and after TIPS placement. All imaging was performed on a 1.5-tesla magnetic resonance imaging (MRI) system. Azygos flow was measured transaxially at the midthoracic level. Cine-PC flow measurements of the main portal vein followed morphological evaluation of the portal venous system with axial and coronal breath-held magnet resonance angiogram. Azygos flow in normal subjects was characterized by high inter- and low intrasubject variability. Azygos flow in patients with portal hypertension was significantly higher (P < .001). Following successful TIPS placement in 18 patients, Cine-PC revealed a mean decrease in azygos flow of 46.3% (P < .001) and a 134% (P < .001) increase of portal flow. Reflecting the complexity of portal hemodynamics, there was no correlation between the changes in the portal and azygos systems. In 2 patients with early occlusion of TIPS, documented invasively, portal and azygos flow values remained largely unchanged. Cine-PC enables the noninvasive, quantitative assessment of flow within the azygos venous system. Azygos flow was found to be markedly elevated in patients with portal hypertension. Combined portal and azygos PC flow measurements quantitate the therapeutic effect of TIPS placement. (Hepatology 1996 Nov;24(5):1109-15)

Azygos blood flow: phase contrast quantitation in volunteers and patients with portal hypertension pre- and postintrahepatic shunt placement.

Flow volume in the azygos venous system was quantitated with Cine-phase contrast (PC) velocity mapping in volunteers and compared with patients with known portal hypertension, who were referred for transjugular intrahepatic portosystemic shunt (TIPS) placement. Subsequently, the TIPS-induced hemodynamic effects on portal and azygos flow were analyzed. To assess intra- and intersubject variability, flow in the azygos veins was measured in each of 10 normal subjects at three different times. Subsequently, portal and azygos flow was quantitated in 20 patients with portal hypertension, before and after TIPS placement. All imaging was performed on a 1.5-tesla magnetic resonance imaging (MRI) system. Azygos flow was measured transaxially at the midthoracic level. Cine-PC flow measurements of the main portal vein followed morphological evaluation of the portal venous system with axial and coronal breath-held magnet resonance angiogram. Azygos flow in normal subjects was characterized by high inter- and low intrasubject variability. Azygos flow in patients with portal hypertension was significantly higher (P < .001). Following successful TIPS placement in 18 patients, Cine-PC revealed a mean decrease in azygos flow of 46.3% (P < .001) and a 134% (P < .001) increase of portal flow. Reflecting the complexity of portal hemodynamics, there was no correlation between the changes in the portal and azygos systems. In 2 patients with early occlusion of TIPS, documented invasively, portal and azygos flow values remained largely unchanged. Cine-PC enables the noninvasive, quantitative assessment of flow within the azygos venous system. Azygos flow was found to be markedly elevated in patients with portal hypertension. Combined portal and azygos PC flow measurements quantitate the therapeutic effect of TIPS placement.

Portal hypertension in children.

Portal hypertension is an uncommon but serious complication in children. The etiology may be intrahepatic or from an extrahepatic vascular occlusion. The pathophysiology is unknown, but the development of increased vascular resistance and portal flow are believed to be the primary changes. Increased portal flow is created by a decrease in systemic vascular resistance regionalized to the splanchnic vascular bed. Abnormally reduced response to vasoactive substances may be responsible. Advances in ultrasonography and endoscopy may improve our ability to evaluate portal hypertensive vascular changes. However, pharmacologic management is still limited to controlling the hemodynamic disturbances after they have occurred. Nonsurgical shunt management is increasingly being used in children, limiting the need for surgical shunt placement. Liver transplantation is now a viable option for managing end-stage disease. Future management depends on understanding the role of vasoactive substances controlling portal flow velocity, subsequent development of targeted pharmacologic therapy, and application of nonsurgical shunt technology in children. Transjugular intrahepatic portosystemic shunt placement is the next technologic advance moving from the adult into the pediatric realm.

Outcome of portal-systemic shunt surgery for portal hypertension associated with intrahepatic obstruction in patients with agnogenic myeloid metaplasia.

Life-threatening portal hypertension (PHN) in patients with chronic myeloproliferative disorders may result from increased portal flow caused by marked splenomegaly or an increased resistance to portal flow from either a large vein thrombosis or an intrahepatic obstruction usually associated with agnogenic myeloid metaplasia (AMM). The former cause is correctable by splenectomy alone, whereas the latter requires portal-systemic shunt surgery. Few data exist regarding the outcome of portal-systemic shunt surgery in patients with AMM and intrahepatic obstruction. During the past 25 years, 13 patients with chronic myeloproliferative disorders underwent portal-systemic shunt surgery at our institution. The cause of PHN was intrahepatic obstruction in ten patients and hepatic vein thrombosis in three. Ten of the thirteen patients had AMM as initial diagnosis. Only one patient had intraoperative complications, and four patients had either sepsis or thrombosis during the postoperative period. Twelve patients survived the postoperative period and had a median postsurgical survival of 3 years (range, 0.25 to 19 years). The long-term complications of the operation were very few and included hepatic encephalopathy (one patient), portal vein thrombosis (one patient), and shunt occlusion (one patient). The procedure was successful in alleviating complications of PHN in all but one patient. Deterioration of hepatic function and subsequent hepatomegaly were unusual. Portal-systemic shunt surgery seems to be a useful option in patients with AMM and life-threatening PHN from intrahepatic obstruction.