Portal Venous Flow Research Articles

Changes in hepatic hemodynamics due to primary liver tumours.

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls. The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change. The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01). On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

The relationship between portal venous and hepatic arterial blood flow. I. Experimental liver transplantation.

The relationship between the changes in portal venous and hepatic arterial blood flows, in the liver is a much disputed question, it has tremendous significance in the practice of transplantation, and an explanation has been available since 1981, when Lautt published the so-caled “adenosine washout theory”. According to our earlier observations the decrease of portal pressure or flow consistently led to an increase in hepatic artery flow. At the same time changes in hepatic artery flow or pressure seemed to produce only inconsistent effects on the portal circulation. In the present experiments liver transplantation (OLTX) was carried out on mongrel dogs by Starzl's method. Electromagnetic flow probes were placed on the hepatic artery and the portal vein before removal of recipient’s liver, and after completion of all vascular anastomoses to the newly inserted liver, during the recirculatory phase of OLTX. The flow probes were connected to a Hellige electromagnetic flowmeter, portal venous and systemic arterial pressures were also recorded. The control HAF was 241±23 ml/min, the average PVF was 517±47 ml/min before removal of the recipients's liver. In the recirculatory phase the HAF increased, by 71±12% (p < 0.001). The PVF decreased in most animals after OLTX. The decrease was in average –40.2±3.5% (p < 0.001). The THBF calculated by adding the HAF and PVF showed a small, but not significant decrease during recirculation. The systemic arterial pressure decreased slightly and portal vein pressure rose in most animals after OLTX. There was a substantial increase in portal inflow resistance and prehepatic arteriolar resistance and a decrease in hepatic artery resistance. The decrease of PVF after OLTX can be explained by progressive fluid accumulation in the liver parenchyma and increased sinusoidal and portal inflow resistance. The prolonged and continuous increase in hepatic artery flow during the recirculatory phase of OLTX may be due to the decrease of portal flow. The exact mechanism, by which a change in portal flow leads to arteriolar dilatation, can be most probably explained by the “adenosine washout theory” of Lautt.

Measurement of portal and splenic venous flow volume (PV and SV), congestion index (CI) and SV/PV% in various liver diseases using by Dopplar echo-sonography

Measurement of portal and splenic venous flow volume (PV and SV), congestion index (CI) and SV/PV% in various liver diseases using by Dopplar echo-sonography

Doppler ultrasound measurement of intestinal blood flow in inflammatory bowel disease.

Our aim was to assess the role of Doppler ultrasound (US) in detecting changes in the splanchnic hemodynamic variables measured in patients with active or quiescent inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) and healthy subjects. Sixty-five patients, 31 with Crohn's disease (CD), 24 with ulcerative colitis (UC), 10 with IBS, and 10 matched normal subjects were evaluated by means of Doppler US. The mean velocity of portal and mesenteric venous flow, the blood flow volume of portal and mesenteric veins, and the resistance index (RI) of the superior mesenteric artery (SMA) were studied in all patients. Patients with active IBD had a splanchnic venous flow that was significantly higher, and an RI of the SMA significantly lower, than the IBS patients and healthy controls; however, a higher portal and mesenteric blood flow and lower RI of the SMA was documented in patients with active UC but not in those in whom the disease was quiescent. Patients with quiescent CD had significantly higher portal and mesenteric blood flow and lower RI of the SMA than IBS and healthy controls. No significant differences were found between IBS patients, quiescent UC patients, and healthy controls. This study shows that Doppler US can demonstrate splanchnic hemodynamic changes in active IBD patients and, in particular, can be used to differentiate between active and quiescent UC. However, the assessment of CD activity by means of Doppler US requires further investigation.

Prolonged enteral fast with parenteral nutrition decreases PCO2 and flow volume in portal vein: its association with bile secretion.

In an attempt to clarify metabolic events during an enteral fast with parenteral nutrition (PN), changes in blood gas distribution and blood flow in the portal vein, and in bile secretion and hepatic blood flow were investigated in dogs. Dogs were maintained on glucose 25 kcal/kg/day for 7 days. In group I, 8 dogs received orally 10 kcal/kg/day and parenterally 15 kcal/kg/day. In group II, 8 dogs had no oral intake and the total calories were provided by PN for the same interval. On the 7th day, the difference in PCO2 between abdominal aorta and portal vein (A-P DCO2) and the concentration of total bile acids in the bile (TBAC) decreased in group II. The values of A-P DCO2 and TBAC were -5.9 +/- 1.2 mm Hg, 35.4 +/- 9.6 mmol/l in group I and -1.2 +/- 1.0 mm Hg, 18.7 +/- 7.3 mmol/l in group II. These decreases in group II were statistically significant (p < 0.01). Portal venous blood flow significantly decreased in group II, as compared to the levels in group I; however, hepatic blood flow, as estimated by the indocyanine green clearance rate, showed no significant decrease. After the 7-day study in group II, saline containing CO2 at high pressure was administered into the mesenteric vein to achieve gradation of A-P DCO2. Gradation of A-P DCO2 from -1.3 to -5.9 mmHg resulted in an increase in the secretion in TBAC and bicarbonate in the bile from 14.0 to 30.0 mmol/l and from 10.3 to 19.5 mmol/l, respectively. We tentatively conclude that portal hypocapnea plays a role in decreasing bile secretion during the enteral fast with PN administration.

Effect of meal ingestion on azygos and portal venous blood flow in healthy subjects non-invasively measured with magnetic resonance

Effect of meal ingestion on azygos and portal venous blood flow in healthy subjects non-invasively measured with magnetic resonance

Postprandial reversal of the portal venous flow in a patient with liver cirrhosis

The case of a 61-year-old man with alcoholic liver cirrhosis and a hepatocellular carcinoma is presented. He was examined with duplex Doppler before and after a meal. In the fasting state a sluggish hepatopetal portal venous flow was found. After the meal a pendulating flow and then hepatofugal flow were found. The magnitude and direction of flow alternated synchronously with the action of the heart, suggesting a significant role for the hepatic artery in the postprandial reversal of portal venous flow. One year after this examination the patient died from the complications of decompensated cirrhosis and liver failure. At autopsy a large hepatocellular carcinoma was detected.

Differential effects of dobutamine, dopamine, and noradrenaline on splanchnic haemodynamics and oxygenation in the pig

Supranormal oxygen (O2) transport may benefit critically ill patients. Catecholamines are clinically employed for this purpose. However, their effects on splanchnic haemodynamics and oxygenation are now well defined. The effects of dobutamine (DOBU), dopamine (DOPA), and noradrenaline (NA) on splanchnic blood flows electromagnetic flow probes), O2 deliveries and uptakes (catheterisation of portal and hepatic veins) were studied in nine anaesthetised (ketamine/flunitrazepam), ventilated, paralysed, and laparotomised pigs. All three catecholamines (DOPA at 15 micrograms.kg-1.min-1, DOBU at 13 micrograms.kg-1.min-1, NA at 0.4 micrograms.kg-1.min-1) significantly (P < 0.05) increased cardiac output and systemic O2 delivery. Only DOPA increased small intestinal and total hepatic blood flows, and O2 deliveries, and decreased O2 extractions. The same parameters did not change during DOBU. During NA, total hepatic blood flow and O2 delivery decreased, and hepatic O2 extraction increased. During all three catecholamines, small intestinal and total hepatic O2 uptakes did not change significantly. Whereas hepatic arterial blood flow decreased during both DOPA and NE, portal venous flow increased during DOPA. These data suggest that in the experimental model used splanchnic O2 supply and O2 reserve capacity appear improved by DOPA, unaffected by DOBU, and impaired by NA.

Doppler US of helical flow in the portal vein.

In helical portal venous blood flow, the usual laminar flow in the portal vein is replaced by a spiral. This changes the color Doppler ultrasound (US) appearance to one of alternating or parallel red and blue bands. Duplex US may appear to show hepatopetal, hepatofugal, or simultaneous bidirectional flow depending on placement of the cursor within the helix. Helical portal venous flow is unusual in normal individuals (2.2% of 135 patients). Its presence should prompt further scrutiny for signs of liver disease, particularly portosystemic shunts, as in 20% of 41 patients who subsequently underwent liver transplantation. It is a normal finding immediately after liver transplantation (43% of 35 patients) and transjugular intrahepatic portosystemic shunt (TIPS) creation (28% of 36 patients). In both liver transplant and TIPS recipients, helical flow is usually transient. Its persistence long after transplantation in association with a prolonged increase in portal venous velocity is a useful sign of portal vein stenosis. Helical flow may also occur in cases of neoplastic invasion or displacement of the portal vein.

Induction of anaesthesia by propofol and hepatic blood flow in the rabbit.

Effects of propofol (12.5 mg kg-1, i.v. bolus injection) or 0.9% sodium chloride on arterial blood pressure, arterial blood gases and hepatic circulation (radio-labelled microsphere technique) were studied in 15 conscious and unpremedicated rabbits. No significant changes were observed after sodium chloride. Propofol resulted in anaesthesia, respiratory depression (-49 +/- 14% decrease in PaO2; mean +/- SD) and hypotension (-49 +/- 13% decrease in mean arterial pressure; mean +/- SD) but no changes in hepatic arterial and portal venous blood flows. We conclude that propofol does not affect the liver circulation despite marked depression of mean arterial pressure and respiration.

Effects of PEEP on liver arterial and venous blood flows.

Total venous return decreases with positive end-expiratory pressure (PEEP). It is likely that the liver plays an important role in this response, either through the development of an increase in venous resistance or through an increase in the venous backpressure at the outflow end of the liver. In addition, hepatic arterial flow is reported to be selectively decreased by the application of PEEP. Therefore, to clarify the effects of PEEP on liver hemodynamics, we generated pressure-flow (P-Q) relationships in both liver vascular beds of anesthetized, mechanically ventilated pigs at PEEP of 0, 5, 10, and 15 cm H2O to obtain values of backpressure (Pback, mm Hg) from linear extrapolation of the P-Q relationships and resistance (mm Hg/ml/min/kg) from its slope. PEEP decreased portal vein flow (Qpv) and caused an increase in the liver venous resistance (from 0.08 +/- 0.01 to 0.16 +/- 0.02 mm Hg/ml/min/kg; p < 0.05). Ppvback and right atrial pressure (Pra) increased equally (from 5.1 +/- 0.3 to 9.9 +/- 0.4 mm Hg, p < 0.05, and from 4.0 +/- 0.2 to 8.6 +/- 0.5 mm Hg, p < 0.05, respectively, at PEEP 15). The reduction in portal venous flow was related to an increase in the backpressure to flow (as a result of an increase in Pra) and to an increase in liver venous resistances that may cause blood pooling in the splanchnic compartment and decrease venous return through the liver. PEEP increased Phaback (from 11.2 +/- 0.9 to 14.5 +/- 0.7 mm Hg at PEEP 15, p < 0.05) but did not change hepatic arterial resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatic circulation during nonpulsatile cardiopulmonary bypass.

The arterial ketone body ratio, which reflects the hepatic mitochondrial redox potential (NAD+/NADH), decreases markedly during cardiopulmonary bypass (CPB). One of the reasons for arterial ketone body ratio reduction may be hepatic hypoperfusion during CPB. To evaluate the hepatic circulation under nonpulsatile CPB, the authors used color Doppler ultrasonography to measure the portal venous flow (PVF) in 24 adult patients before, during (aortic clamping and rewarming period), and after CPB. Nonpulsatile hypothermic CPB was performed at a flow rate of 2.4 L/min/m2. PVF was calculated from the product of mean flow velocity and cross-sectional area of the portal vein. PVF was maintained during CPB at 0.44 +/- 0.13 and at 0.54 +/- 0.18 L/min/m2. PVF (%) in relation to systemic blood flow was obtained by calculating PVF/CI or PVF/PI, where CI is the cardiac index and PI is the perfusion index. PVF (%) before, during, and after CPB was 18.3 +/- 9.3, 18.5 +/- 5.5, and 17.4 +/- 6.7%, respectively. In conclusion, PVF was maintained during nonpulsatile CPB at a flow rate of 2.4 L/min/m2 and depended upon systemic blood flow.

Nitric Oxide and the Treatment of Right Heart Failure with Atrial Fibrillation and Rapid Ventricular Response

Claire Gatecel, M.D., Instructor.Alexandre Mebazaa, M.D., Ph.D., Assistant Professor.Robert Kong, M.B., B.S., F.R.C.A., Instructor.Nathalie Guinard, M.D., Instructor.Nathalie Kermarrec, M.D., Resident.Joaquim Mateo, M.D., Instructor.Didier Payen, M.D., Ph.D., Professor, Department of Anesthesiology and Critical Care, Hopital Lariboisiere, 2, rue, Ambroise Pare, 75010 Paris, France.In Reply:--The authors thank Heinrich and Kao for clarifying the meaning of hepatic perfusion improvement after nitric oxide inhalation in the reported case. [1]We kept this point relatively ambiguous because of space constraints, although we agree this aspect must be clarified. Hepatic arterial flow is proportional to the pressure gradient between mean arterial and hepatic venous pressures, whereas portal venous flow is dependent on the pressure gradient between portal venous and hepatic venous pressures. Considering these mechanical determinants of liver perfusion, we agree with Heinrich and Kao that the patient benefitted from an increased perfusion pressure in the portal circulation. Accordingly, a Starling resistance have been described in the portal circulation, [2]and the high hepatic venous pressure observed before nitric oxide inhalation was much likely to be higher than the critical closing pressure described in the portal venous circulation for normal livers, leading to an impaired flow through this circuit.In light of the deleterious effects of a hepatic congestion for the portal circulation emphasized by Heinrich and Kao, manipulation of the hepatic arterial flow might be of more limited interest in the reported case. First, the arterial buffer response, [3]which has been confirmed to exist in humans, [4]might have led to a relatively high hepatic arterial flow in this patient with a presumably highly reduced portal venous flow. Second, trying to increase portal inflow to the liver would imply acting on mesenteric blood flow and thus on systemic blood flow, [5]which can be limited in the described clinical situation.Concerning the atrial fibrillation, we agree on the comment raising the necessity to control the ventricular rate. However, cardioversion was judged dangerous at the acute phase of the decompensation and was considered as a consequence rather than the cause of the right heart failure. Accordingly, normal sinus rhythm spontaneously recovered after the hemodynamic improvement, suggesting that the atrial fibrillation resulted from rather than in hemodynamic dysfunction. Two years after this acute episode, the patient is still in good hemodynamic condition and has been removed from the heart transplantation list.In conclusion, we believe that the observed beneficial effect of inhaled nitric oxide in this patient was the consequence of a significant decrease in hepatic venous pressure while mean arterial pressure was maintained. For the hospitals that "do not have the proper permission or setup for nitric oxide administration," we could advocate the use of a pharmacologic combination therapy to achieve these goals, although such a combination might be less effective or more difficult to use.Claire Gatecel, M.D., Instructor.Alexandre Mebazaa, M.D., Ph.D., Assistant Professor.Robert Kong, M.B., B.S., F.R.C.A., Instructor.Nathalie Guinard, M.D., Instructor.Nathalie Kermarrec, M.D., Resident.Joaquim Mateo, M.D., Instructor.Didier Payen, M.D., Ph.D., Professor, Department of Anesthesiology and Critical Care, Hopital Lariboisiere, 2, rue, Ambroise Pare, 75010 Paris, France.(Accepted for publication April 13, 1995.)

Experimental atrophy/hypertrophy complex (AHC) of the liver: portal vein, but not bile duct obstruction, is the main driving force for the development of AHC in the rat

Backgroun/Aims: Patients with lobar or segmental impairment of bile flow or of portal venous blood flow frequently develop considerable atrophy of the area involved, followed by compensatory hypertrophy/hyperperlasia of the non-affected parts. This configuration is termed atrophy/hypertrophy complex of the liver. Methods: In order to analyze the relative contributions of bile duct and portal vein obstruction in the pathogenesis of atrophy/hypertrophy complex, we developed a rat model with selective bile duct and/or portal vein ligation of the anterior liver lobes, representing about two thirds of the liver mass. Evolution of total body weights and weights of the different liver lobes were determined, and morphometry and functional scintigraphy (hepatoiodida scanning) were performed immediately after ligation and at 30 h, 4, 8 and 28 days postoperatively. Results: The major findings were: 28 days after biliary and/or portal ligation there was no difference between the body weights of all animals, all ligated animals having compensated an initial body weight loss. Total liver weight remained constant during the whole observation period, while atrophy of the anterior and hypertrophy/hyperplasia of the posterior lobes occurred. A significant atrophy/hepertrophy complex developed only after selective portal ligation, but not after selective biliary ligation. Morphometrically analyzed histologic changes after selective biliary ligation were reversible, whereas in portally ligated liver lobes a progressive parenchymal destruction and involution with subsequent impairment of hepatic function of the concerned lobe were observed. Conclusions: The present findings indicate that impairment of portal venous flow is the major driving force for the development of lobar atrophy in the rat and that atrophy/hypertrophy complex can be produced in a rodent model.

Diagnosis of venoocclusive disease of the liver after bone marrow transplantation: value of duplex sonography.

The purpose of this study was to determine if duplex sonography of the hepatic vasculature can be used to detect venoocclusive disease in patients who have had bone marrow transplantation. Twenty-seven bone marrow transplant recipients were serially studied with hepatic duplex sonography before (n = 27) and biweekly after (n = 136) transplantation. Duplex waveforms were obtained from the hepatic artery and the portal and hepatic venous systems. Clinical records were reviewed to confirm the clinical diagnosis of venoocclusive disease (n = 5), including its time of onset and duration. Patients with venoocclusive disease were further split into two groups: those with clinically active disease and those with clinically inactive disease. The resistive index in the hepatic artery, the velocity in the portal vein, and the differences among bone marrow transplant values before and after transplantation were compared among the groups. On the basis of data obtained before transplantation, a resistive index greater than 0.76 and a change in resistive index greater than 0.10 after transplantation were considered abnormal. Similarly, velocity in the portal vein after transplantation was considered abnormal when the value was less than 4.3 cm/sec or more than 50.3 cm/sec. There was no statistically significant difference in the resistive index in the hepatic artery or velocity in the portal vein among patient groups. Hepatopetal portal venous flow was shown in 26 of 27 patients during the study. Portal venous flow was reversed in one patient with venoocclusive disease. Appropriately directed hepatic venous flow was demonstrated in all 27 patients. Our study shows that resistive index in the hepatic artery, velocity and flow direction in the portal vein, and flow direction in the hepatic vein as detected by duplex sonography are of no value in the diagnosis of venoocclusive disease after transplantation.

Hepatic blood flow during reduced liver grafting in pigs

Intraoperative changes in portal venous and hepatic arterial flow were compared in porcine recipients of reduced liver grafts with recipients of intact grafts and sham-operated controls. Control animals showed no significant changes in hepatic blood flow (measured with perivascular ultrasonic cuffs), heart rate, mean arterial pressure, cardiac output, acid/base balance, plasma sodium, potassium, glucose, or catecholamines. Recipients of intact or reduced grafts showed hypotension, reduced cardiac output, tachycardia, and increased systemic vascular resistance during the anhepatic phase, which lasted approximately 30 min. These changes returned to normal in recipients of intact grafts but in recipients of reduced grafts, levels returned only to 50-60% of baseline. After intact grafting, total liver blood flow and the portal and arterial components returned to baseline within 2 hr of revascularization, but after reduced grafting, hepatic arterial flow values remained depressed to 50-60% of baseline. Plasma epinephrine and norepinephrine were unaltered during control operation but increased 4- to 20-fold in recipients of all grafts. These returned towards baseline in all except recipients of reduced grafts, in which norepinephrine levels remained significantly elevated for the 4 hr of postoperative study. These data highlight persistent elevation of plasma norepinephrine after reduced liver grafting, which may have contributed to the diminished hepatic arterial flow. These results need to be confirmed in adult recipients of split liver grafts in whom grafts are comparatively small. In such patients receiving donor livers which have undergone prolonged storage, the effects of increased plasma norepinephrine levels upon donor agonal arterial spasm may be significant.

The Influence of Flow and Hematocrit on the Laser Doppler Flux Signal from the Surface of the Perfused Pig Liver

We tested the hypothesis that the measurement volume of the laser Doppler flowmeter (LDF) is too small to provide reliable quantitative estimates of total liver blood flow of large mammals, such as the pig. In a perfused pig liver, the influence of changing (i) hepatic arterial (HA) and portal venous flows individually (n = 9), (ii) HA flow at fixed portal venous flow (50%, 70%, and 100% expected total liver blood flow), and (iii) hematocrit (0-30%) at fixed total liver blood flow on LDF flux was tested (n = 8). Linearity of LDF with hepatic arterial flow and portal venous flow was confirmed; however, the slope of the regression lines was higher for hepatic artery [1.92 +/- 0.60 (SD)] than portal vein perfused livers (0.66 +/- 0.34; P < 0.001). With portal venous flow at 50% and 70% total liver blood flow, changing hepatic arterial flow produced linear LDF versus flow responses, but at 100% total liver blood flow, linearity was achieved in only 6/9 livers. The coefficient of variation for the slopes of regression lines was always > 30%. At constant total liver blood flow (100 ml/min per 100 g), LDF response decreased linearly by a factor of about 2 on changing the hematocrit from 30% to 5% and markedly fell as the hematocrit was further decreased to zero. These results suggest that (i) the LDF flux signal from the liver surface provides a poor measure of hepatic microcirculatory blood flow during changes in total liver blood flow as the LDF responds with about three times greater sensitivity to changes in hepatic arterial than in portal venous flow, and (ii) when hematocrit is falling, LDF may underestimate hepatic perfusion to a significant extent. In addition, due to high measurement variability, the LDF flux signal cannot be quantified in absolute perfusion units.

Auxiliary liver transplantation for acute liver failure.

In summary, the following principles are worth reiterating: 1. In the treatment of acute liver failure, protection of the native liver in anticipation that it will recover, but positioning of the allograft in a manner that optimizes its function for both the short and long term (in the event that the native liver does not recover) are important goals. Therefore, orthotopic positioning offers advantages over the heterotopic position in most cases. Development of better techniques for predicting native liver recovery might remove any of these advantages of the orthotopic position. 2. Other than the presence of fibrosis, the performance of a native liver biopsy does not appear to predict native liver recovery. The decision of whether to attempt auxiliary grafting must be based on an understanding of the natural history of the disease causing the acute liver failure. 3. The heterotopic position has the advantage of not requiring partial native hepatectomy in order to accommodate the allograft. However, except for the recent experience of Terpstra et al, this technique has carried a higher risk of venous outflow obstruction. It also requires additional space within the abdomen, usually mandating the use of prosthetic abdominal wall closures and the construction of venous conduits for portal venous inflow to the liver. There is the additional theoretical concern about competition for portal venous flow leading to eventual atrophy of the allograft liver. 4. Common events that follow liver transplantation result in changes in portal venous resistance within the liver, events that therefore alter the relative distribution of portal venous inflow between native and auxiliary livers. These events include reperfusion injury, allograft rejection, allograft viral infection (e.g., cytomegalovirus, Epstein-Barr virus, recurrent viral hepatitis), and native liver regeneration. Attempts to control portal venous flow to favor one liver over the other must account for the effect of these factors. 5. In general terms, auxiliary transplantation is not indicated for diseases in which the residual native liver either represents an ongoing threat to the recipient or is incapable of supporting life alone. This may be the case in both metabolic disorders and in cirrhosis. Most of the alleged difficulties of native hepatectomy are no longer relevant. Therefore, auxiliary transplantation is rarely if ever indicated for chronic liver disease and may not be of any additional benefit over total transplantation in the treatment of many metabolic disorders. 6. In the treatment of acute liver failure, the value of an auxiliary transplant over total transplant is obtained when the native liver recovers and the patient is withdrawn from immunosuppression. If further experience shows the effectiveness of this option, total liver transplantation with the requirement for life-long immunosuppression will no longer be appropriate for the treatment of patients with acute liver disease.

Short- and long-term hemodynamic effects of transjugular intrahepatic portosystemic shunts: a Doppler/manometric correlative study.

The purposes of this study were to evaluate the effect of a well-functioning transjugular intrahepatic portosystemic shunt (TIPS) on the splanchnic and intrahepatic circulation, to determine if sonographic measurements can predict shunt dysfunction before clinical manifestations of portal hypertension occur, and to compare Doppler sonographic findings with portocaval gradient measurements before and after shunt revision. Forty-four patients with cirrhosis (n = 43) and myelofibrosis (n = 1) who underwent successful TIPS insertion were included in this prospective study. Indications for TIPS placement were: refractory ascites (24 patients), bleeding esophageal varices (17 patients), portal hypertensive gastropathy (two patients), and bleeding colonic varices (one patient). The portal vein and the inferior vena cava were catheterized; and the portocaval gradient was recorded before TIPS placement, at 2 and 12 months after TIPS placement, and when clinical or Doppler findings suggested shunt dysfunction. Doppler studies were done within 1 week before TIPS placement, within 2 days after TIPS placement, every 2-3 months thereafter, and before and after a TIPS revision. The Doppler studies included flow volume measurements in the portal vein and in the stent, as well as determination of the direction of flow in the segmental branches of the portal vein, in the splanchnic veins, and in portosystemic collaterals. Changes in Doppler findings and in catheter pressure measurements were compared using Spearman's rank correlation test. Significance was set at the .05 level. A marked decrease (-51%) in portocaval gradient was observed after TIPS placement. At Doppler sonography, portal vein velocity and diameter were both higher after TIPS placement, resulting in a marked increase in portal venous flow (170%). Mean flow velocity in the shunt was 55.8 +/- 3.6 cm/sec, and flow volumes in the shunt and in the main portal vein were 1596 ml/min and 1731 ml/min, respectively (p = nonsignificant). Dysfunction of the stent occurred in 27% of the patients. Changes in stent blood flow volume were closely related to changes in the portocaval gradient (r = -0.67, p < .001). Reduction of blood flow volume in the stent or change of direction of flow in intrahepatic portal veins or in collateral veins signaled shunt dysfunction (84% sensitivity, 89% specificity). Marked hemodynamic changes in the portal venous system occur soon after a TIPS procedure. Monitoring of shunt function with periodic Doppler sonography, including calculation of shunt blood flow, is useful in detecting shunt dysfunction before clinical signs occur.

Direction of portal venous blood flow and sensory evoked potentials in cirrhotics with distal splenorenal shunt

Direction of portal venous blood flow and sensory evoked potentials in cirrhotics with distal splenorenal shunt