Duplex Doppler measurements of portal venous flow in normal subjects : Inter- and intra-observer variability

We investigated the variability of quantitative duplex Doppler measurements of portal flow. Measurements were validated in vitro using a flow phantom. The measured flow Q (ml/min), is related to the actual phantom output P (ml/min) according to the following formula: Q = 1.08 (P + 44) (r = 0.998). To estimate inter- and intra-observer variance, 38 subjects without portal hypertension were examined in two groups. Two observers examined the first group of subjects (n = 19), from a routine daily ultrasound schedule. Significant differences were found in mean +/- S.D. portal flow (692 +/- 182 ml/min vs. 613 +/- 185 ml/min, p = 0.04) and mean +/- S.D. velocity (15.3 +/- 3.9 cm/s vs. 13.2 +/- 2.6 cm/s, p = 0.01). The combined inter- and intra-observer coefficient of variation (S.D.) was 24% (158 ml/min), 9% (0.92 mm) and 24% (3.4 cm/s) for portal flow, diameter and velocity respectively. Non-systematic components of variance were the largest. Patient characteristics, age, sex, height, weight and body surface area did not influence measurement variations. In the second group of healthy volunteers (n = 19), where variance in measurements over 3 consecutive days was comparable to the combined variance in the first group, the non-systematic variance component was also the largest. We conclude that quantitative duplex Doppler measurements of portal venous flow are mainly subject to non-systematic variability. A coefficient of variation of 24% can be expected in diagnostic measurements in a single patient. Examination by a single observer is advisable. The value of this technique lies in the analysis of pathophysiological mechanisms in portal flow changes in large groups of subjects.     

Doppler hemodynamic study in portal hypertension and hepatic encephalopathy

BACKGROUND/AIMS: The aim of our study was to evaluate and compare the differences in the parameters of portal hypertension in two groups of patients with liver cirrhosis, with and without hepatic encephalopathy (HE). METHODOLOGY: 30 patients with liver cirrhosis, 17 (56.7%) of them with HE, were investigated by clinical, neurological, laboratory, endoscopic methods and with color Doppler ultrasonography (CDU) at the Institute for Digestive Diseases, Clinical Center of Serbia, Beograde. RESULTS: Significant correlation was found between the diameters of the right liver lobe and the portal vein (p=0.01), and also between the diameters of the spleen and splenic vein (p=0.0002), in both groups of patients. Mean portal vein diameter significantly increases (p=0.01) in patients with HE (14.87 +/- 1.86mm), compared to those without HE (13.2 +/- 2.31mm), while mean splenic vein diameter was not significantly different in the two groups. In patients with ascites, CDU showed significantly lower (p=0.03) portal flow velocity (11.87 +/- 6.25cm/ sec), compared to those without ascites (14.33 +/- 4.41cm/sec). Splenic flow velocity was not significantly different (16.00 +/- 6.60cm/sec with ascites and 14.61 +/- 5.29cm/sec without ascites). In patients with HE, portal flow velocity was significantly lower (9.00 +/- 5.41cm/sec) compared to those without HE (14.0 +/- 7.03cm/sec) (p=0.04). Mean splenic flow velocity was significantly lower (p=0.03) in patients with HE (12.60 +/- 4.16cm/sec), compared to those without HE (17.77 +/- 5.91cm/sec). Portal flow velocity shows linear decrease, related to the increase of the liver damage (Child-Pugh score), while splenic velocity was not related to this parameter. CONCLUSIONS: Ultrasonographic parameters of portal hypertension show significant correlation between the diameters of liver/portal vein and spleen/splenic vein. Portal hemodynamic parameter (blood flow velocity) is significantly related to the stages of liver damage, presence of ascites and HE, while splenic hemodynamics is specific and not directly related to these parameters.     

Doppler study of hepatic vein in cirrhotic patients： Correlation with liver dysfunction and hepatic hemodynamics

INTRODUCTIONThere are many studies on inflow to the liver in liver cirrhosis (LC) in relation to hepatic dysfunction and portal hypertension. In LC, there are changes in liver parenchyma as well as alteration of hepatic vasculature, including morphologica…     

Effect of propranolol on portosystemic collateral circulation in patients with cirrhosis

Propranolol has been demonstrated to be effective in lowering portal pressure in cirrhotic patients. This effect is mediated by a reduction of splanchnic arterial inflow and a consequent decrease of portal vein and portocollateral blood flow. Although experimental studies suggest a direct effect of the drug on portocollateral circulation, little information exists about relative flow changes occurring in the portal vein and in collateral veins feeding esophageal varices. This study addressed the problem in 12 cirrhotic patients selected on the basis of feasibility of Doppler flowmetry in both the portal and left gastric veins. Caliber, flow velocity and flow volume in both vessels were measured by Doppler ultrasound before and at 60, 120 and 180 min after an oral dose of 40 mg propranolol, together with heart rate and mean arterial pressure. A significant decrease in heart rate (-17.6% +/- 1.1%, p less than 0.001) and mean arterial pressure (-10.6% +/- 0.9%, p less than 0.005) confirmed effective beta-blockade. Baseline flow velocity was significantly lower in the portal vein than in the left gastric vein (12.4 +/- 0.6 vs. 15.4 +/- 1.5 cm/sec, p less than 0.05). Maximal hemodynamic effect was reached at 120 min after administration of propranolol. The vessel caliber did not change significantly. Flow velocity fell from 12.4 +/- 0.6 to 10.4 +/- 0.7 cm/sec in the portal vein (p less than 0.05) and from 15.4 +/- 1.5 to 11.1 +/- 0.9 cm/sec in the left gastric vein (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Duplex Doppler ultrasound of the hepatic artery in patients with acute alcoholic hepatitis

BACKGROUND: Acute alcoholic hepatitis (AAH) is a clinical diagnosis associated with increased hepatic artery diameter and flow. Duplex Doppler ultrasound (DDU) has been shown to accurately measure arterial flow in both liver and kidney transplant patients. The authors conducted a blinded, controlled study to evaluate the accuracy of measuring hepatic artery parameters with DDU in diagnosing AAH. STUDY: Duplex Doppler ultrasound was performed by an investigator, blinded to group makeup, on 22 consecutive hospital inpatients with the clinical diagnosis of AAH. The diagnosis of AAH was based on specific criteria, including the following: recent alcohol abuse, hyperbilirubinemia, prolonged prothrombin time, leukocytosis, hepatomegaly, hepatic bruit, and marked redistribution of isotope on 99mTc-sulfur colloid liver-spleen scan. Controls were 12 cirrhotic patients without AAH and 17 healthy volunteers. Duplex Doppler ultrasound measurements were obtained most consistently from the proximal right hepatic artery. Measured parameters included the following: peak systolic velocity (PSV); resistive index = (PSV - end diastolic velocity [EDV])/PSV; pulsatility index = (PSV - EDV)/mean velocity; and hepatic artery diameter. RESULTS: The mean hepatic artery diameter was significantly larger in patients with AAH (3.55 +/- 0.72 mm) than in patients with cirrhosis (2.75 +/- 0.69 mm; p = 0.003) and healthy controls (2.68 +/- 0.69 mm; p = 0.001). The mean PSV was significantly higher in patients with AAH (187 +/- 52 cm/s) compared with cirrhotic (67 +/- 51 cm/s) and healthy (66 +/- 51 cm/s) controls (p = 0.0001). The mean resistive index was lower in AAH patients (0.60 +/- 0.11) compared with cirrhotic (0.69 +/- 0.10; p value was not significant) and healthy controls (0.72 +/- 0.11; p = 0.004). The mean pulsatility index was lower in AAH patients (1.04 +/- 0.47) compared with cirrhotic (1.36 +/- 0.45; p value was not significant) and healthy controls (1.53 +/- 0.45; p = 0.01). CONCLUSIONS: In the appropriate clinical setting, an elevated hepatic artery diameter or PSV measurement is suggestive of AAH. Duplex Doppler ultrasound offers a noninvasive test to assist in the diagnosis of AAH.     

Echo-Doppler evaluation of acute flow changes in portal hypertensive patients: flow velocity as a reliable parameter

In order to evaluate the behavior of the portal vein cross-sectional area during changes in portal flow, two groups of subjects were analyzed in two blinded cross-over studies using echo-Doppler flowmetry. The first group (I) consisted of 21 patients with cirrhosis and 16 controls. They received a standardized meal which is known to increase portal flow. The second group (II) consisted of 31 patients with cirrhosis who received a dose of propranolol which is known to decrease portal flow. In Group I, 30 min after the meal, the portal vein blood velocity increased by 35 +/- 6% (p less than 0.01) in cirrhotic patients and by 55 +/- 5% (p less than 0.01), in normal subjects. The portal vein cross-sectional area increased significantly in normal subjects (22 +/- 2%, p less than 0.01) but not in cirrhotic patients (4 +/- 2%, n.s.). In Group II, 2 h after propranolol, there was a significant decrease in portal blood velocity (-14 +/- 2%), whereas the portal vein cross-sectional area did not show any significant changes. These data demonstrate that, in portal hypersensitive patients, the portal area measured by echo-Doppler flowmetry can be assumed to be constant and hence its calculation to estimate changes in portal blood flow can be omitted. Therefore, the use of blood velocity alone is suggested to monitor acute changes in flow in portal hypertension using Doppler flowmetry. The elimination of the portal vein cross-sectional area measurement simplifies the quantitative calculation of portal hemodynamics and increases the reliability of the technique by avoiding a source of error.     

Effect of metoclopramide on portal blood flow in patients with liver cirrhosis, measured by the pulsed Doppler system

The effect of metoclopramide on portal blood flow, the maximal diameter of the portal vein, and some cardiovascular haemodynamic variables was studied in 10 patients with cirrhosis of the liver and portal hypertension. Portal vein haemodynamics were studied by the pulsed Doppler system. Within 15 min of intravenous administration of 20 mg metoclopramide, portal blood velocity and portal blood flow decreased significantly, from 11.2 +/- 1.1 to 10.8 +/- 1.2 cm/sec and from 769.0 +/- 87.7 to 707.9 +/- 84.2 ml/min, respectively (p less than 0.001). Within about 30 min portal blood velocity and portal blood flow returned to basal values (p greater than 0.05). The maximal diameter of the portal vein, systolic and diastolic blood pressure, and heart rate remained unchanged. These results support the hypothesis that metoclopramide, which raises lower oesophageal sphincter pressure and reduces intravariceal blood flow, significantly decreases the portal blood flow in cirrhotic patients with portal hypertension.     

Reversed portal flow: Clinical influence on the long-term outcomes in cirrhosis

AIM: To elucidate the natural history and the longitudinal outcomes in cirrhotic patients with non-forward portal flow(NFPF).METHODS: The present retrospective study consisted of 222 cirrhotic patients(120 males and 102 females; age, 61.7 ± 11.1 years). The portal hemodynamics were evaluated at baseline and during the observation period using both pulsed and color Doppler ultrasonography. The diameter(mm), flow direction, mean flow velocity(cm/s), and mean flow volume(m L/min) were assessed at the portal trunk, the splenic vein, the superior mesenteric vein, and the collateral vessels. The average values from 2 to 4 measurements were used for the data analysis. The portal flow direction was defined as follows: forward portal flow(FPF) for continuous hepatopetal flow; bidirectional flow for to-and-fro flow; and reversed flow for continuous hepatofugal flow. The bidirectional flow and the reversed flow were classified as NFPF in this study. The clinical findings and prognosis were compared between the patients with FPF and those with NFPF. The median follow-up period was 40.9 mo(range, 0.3-156.5 mo).RESULTS: Twenty-four patients(10.8%) demonstrated NFPF, accompanied by lower albumin level, worse ChildPugh scores, and model for end-stage liver disease scores. The portal hemodynamic features in the patients with NFPF were smaller diameter of the portal trunk;presence of short gastric vein, splenorenal shunt, or inferior mesenteric vein; and advanced collateral vessels(diameter 8.7 mm, flow velocity 10.2 cm/s, and flow volume 310 m L/min). The cumulative incidence rates of NFPF were 6.5% at 1 year, 14.5% at 3 years, and 23.1% at 5 years. The collateral vessels characterized by flow velocity 9.5 cm/s and those located at the splenic hilum were significant predictive factors for developing NFPF. The cumulative survival rate was significantly lower in the patients with NFPF(72.2% at 1 year, 38.5% at 3 years, 38.5% at 5 years) than in those with forward portal flow(84.0% at 1 year, 67.8% at 3 years, 54.3% at 5 years, P = 0.0123) using the Child-Pugh B and C classifications.CONCLUSION: NFPF has a significant negative effect on the prognosis of patients with worse liver function reserve, suggesting the need for careful management.     

Hepatic arterial doppler sonography in patients with cirrhosis and controls: observer and equipment variability with use of the ultrasonic contrast agent SHU 508A

PURPOSE: The aims of this study on hepatic arterial Doppler sonography were to ascertain interobserver and interequipment variability, to investigate any potential artificial influence of the ultrasonic contrast agent on the Doppler measurements and to compare the results in healthy and cirrhotic subjects. METHODS: Doppler sonography of the left hepatic artery was performed in nine healthy and nine cirrhotic subjects by three independent observers using three different devices. Continuous infusion of the ultrasonic contrast agent SHU 508A and placebo were administered in a double blind fashion. Systolic, mean and end diastolic peak velocities as well as resistive and pulsatility indices were measured. RESULTS: Equipment associated variances (5.8 - 12.7 %) of the five Doppler parameters were greater than interobserver variances (0.3 - 3.6 %). No significant differences were observed between the velocities using ultrasonic contrast agent and placebo. Systolic (65.9 +/- 3.6 vs. 47.7 +/- 4.2 cm/s mean +/- SE, p = 0.02) and mean peak velocity (35.4 +/- 1.6 vs. 24.5 +/- 1.8 cm/s, p = 0.007) were significantly higher in cirrhotic than in healthy subjects whereas the resistive and pulsatility indices were not different. CONCLUSIONS: Doppler sonography of the left hepatic artery performed by various observers is reproducible as long as the same device is used. Under clinical conditions, velocities are correctly measured with the use of ultrasonic contrast agent and are elevated in patients with cirrhosis.     

Value of portal hemodynamics and hypersplenism in cirrhosis staging

AIM: To determine the correlation between portal hemodynamics and spleen function among different grades of cirrhosis and verify its significance in cirrhosis staging. METHODS: The portal and splenic vein hemodynamics and spleen size were investigated by ultrasonography in consecutive 38 cirrhotic patients with cirrhosis (Child's grades A to C) and 20 normal controls. The differences were compared in portal vein diameter and flow velocity between patients with and without ascites and between patients with mild and severe esophageal varices. The correlation between peripheral blood cell counts and Child's grades was also determined. RESULTS: The portal flow velocity and volume were significantly lower in patients with Child's C (12.25±1.67 cm/s vs 788.59±234 mm/min, respectively) cirrhosis compared to controls (19.55±3.28 cm/s vs 1254.03±410 mm/min, respectively) and those with Child's A (18.5±3.02 cm/s vs 1358.48±384 mm/min, respectively) and Child's B (16.0±3.89 cm/s vs 1142.23±390 mm/min, respectively) cirrhosis. Patients with ascites had much lower portal flow velocity and volume (13.0±1.72 cm/s vs1078±533 mm/min) than those without ascites (18.6±2.60 cm/s vs1394±354 mm/min). There was no statistical difference between patients with mild and severe esophageal varices. The portal vein diameter was not significantly different among the above groups. There were significant differences in splenic vein diameter, flow velocity and white blood cell count, but not in spleen size, red blood cell and platelet counts among the various grades of cirrhosis. The spleen size was negatively correlated with red blood cell and platelet counts (r= -0.620 and r= -0.8.34, respectively). CONCLUSION: An optimal system that includes parameters representing the portal hemodynamics and spleen function should be proposed for cirrhosis staging.     

Gastric mucosal blood flow and hepatic perfusion index in patients with portal hypertensive gastropathy

Endoscopic laser Doppler velocimetry is a simple non-invasive method to measure gastric mucosal blood flow. The present study is an attempt to determine a correlation, if any, between gastric mucosal blood flow and the hepatic perfusion index in patients with portal hypertensive gastropathy and their relationship to the severity of liver disease. Thirty patients with portal hypertensive gastropathy due to cirrhosis of the liver (eight class A, 13 class B, nine class C, according to Child-Pugh Classification) and six normal subjects were recruited into the study. In all subjects, the gastric mucosal blood flow and venous vasomotor reflex response was measured at two sites: the lesser and greater curvature, using endosoopic laser Doppler velocimetry. The hepatic perfusion index was measured using dynamic liver scintigraphy. The hepatic perfusion index (ratio of arterial/portal venous perfusion) in normal subjects and patients with portal hypertensive gastropathy belonging to Child-Pugh class A, B and C were 0.36 ± 0.02, 0.53 ± 0.08, 0.62 ± 0.14 and 1.04 ± 0.28, respectively. The gastric mucosal blood flow was similar in Child's A, B and C cases, while the venous vasomotor reflex response was reduced according to the Child-Pugh score (Child's A 37.4 ± 5.4%, normal control 62.3 ± 10.9%, Child's B 38.3 ± 18.2%, Child's C 22.5 ± 15.2%) and was statistically significant. The gastric mucosal blood flow and hepatic perfusion index are inversely correlated. The hepatic perfusion index altered with grading of cirrhotic change. This study confirms that the severity of portal hypertensive gastropathy is correlated with Child-Pugh score.     

Patent paraumbilical vein: hemodynamic importance in Mansoni's hepatosplenic portal hypertension (Study with ultrasonography Doppler

BACKGROUND: The hemodynamical effect of the collateral portosystemic circulation upon the portal system has not yet been fully understood. The US-Doppler made possible the non-invasive study of the portal system by evaluating the parameters: flow direction, diameter and flow velocity in it's vessels. AIMS: To study the paraumbilical vein as a collateral portosystemic pathway and identify patterns for appraising its hemodynamic importance to the portal system. METHOD: US-Doppler study of the portal system of 24 patients with Mansoni's hepatosplenic schistosomic portal hypertension, previous esophagic variceal bleeding and patent paraumbilical vein with hepatofugal flow. The diameter and the mean flow velocity were measured in the paraumbilical vein and so were the mean flow velocity in the portal vein, right and left portal branches. The Pearson test (linear correlation) was applied to the portal vein's mean flow velocity and the paraumbilical vein's diameter and mean flow velocity. The patients were divided in four groups: D1-paraumbilical vein with diameter < 0.68 cm (n = 14), D2-paraumbilical vein with diameter > or = 0.68 cm (n = 10), V1-paraumbilical vein with mean flow velocity < 18.41 cm/seg (n = 13) and V2-paraumbilical vein with mean flow velocity > or = 18.41 cm/seg (n = 11). The mean flow velocity in the portal vein, right and left portal branches of the four groups were compared. RESULTS: The paraumbilical vein diameter was 0.68 +/- 0.33 cm (range: 0.15-1.30 cm) and the mean flow velocity was 18.41 +/- 11.51 cm/seg (range: 5.73-38.20 cm/seg). The linear correlation between the portal vein's mean flow velocity/paraumbilical vein diameter and the paraumbilical vein's mean flow velocity showed r = 0.504 and r = 0.735, respectively. In the group D2 there was an increase in the mean flow velocity in the portal vein (17.80 +/- 3.42/22.30 +/- 7.67 cm/seg) and in the left portal branch (16.00 +/- 4.73/22.40 +/- 7.90 cm/seg). In the group V2 there was an increase in the mean flow velocity in the portal vein (16.31 +/- 3.49/21.96 +/- 5.89 cm/seg) and in the left portal branch (14.22 +/- 4.41/21.94 +/- 7.20 cm/seg). There was no change in the right portal branch (13.67 +/- 5.74/15.43 +/- 3.43 cm/seg). CONCLUSIONS: In portal hypertension due to hepatosplenic schistosomiasis, the patent paraumbilical vein, with hepatofugal flow, diameter > or = 0.68 cm and mean flow velocity > or = 18.41 cm/seg causes an increase of the mean flow velocity in the portal vein and left portal branch. The best US-Doppler parameter to appraise the paraumbilical vein influence upon the portal system is the mean flow velocity. The correlation between the increase in portal vein's mean flow velocity is stronger with the paraumbilical vein's mean flow velocity than with its diameter. The increase in the portal vein's and left portal branch's mean flow velocity may be understood as the paraumbilical vein's hemodynamic influence upon the portal system. An active portosystemic collateral pathway increases the mean flow velocity in the vein's segment proximal to its point of origin.     

The effect of endoscopic injection sclerotherapy on portal blood flow and liver function

BACKGROUND/AIMS: It is still controversial whether endoscopic injection sclerotherapy can affect portal blood flow and liver function. To clarify this issue, we investigated the change in portal blood flow velocity and the relationship between liver function and portal blood flow after sclerotherapy. METHODOLOGY: Ten liver cirrhosis patients with F2 esophageal varices were enrolled in this study. All patients underwent sclerotherapy until all varices were eradicated. Portal blood flow velocity was measured using Doppler ultrasonography. The changes in laboratory parameters and the portal flow velocity were analyzed in each patient. RESULTS: Total mean portal blood flow velocity was changed from 7.5 +/- 5.3 cm/s to 10.3 +/- 3.5 cm/s by sclerotherapy. Six of ten cases had increase in portal blood flow velocity. Among them, 5 cases demonstrated improvement in serum albumin and total cholesterol level 3 months after sclerotherapy. CONCLUSIONS: Prophylactic endoscopic injection sclerotherapy among patients with early liver cirrhosis can improve liver function by increasing the portal blood flow.     

Hemodynamic analysis of esophageal varices in patients with liver cirrhosis using color Doppler ultrasound

AIM: To study the portal hemodynamics and their relationship with the size of esophageal varices seen at endoscopy and to evaluate whether these Doppler ultrasound parameters might predict variceal bleeding in patients with liver cirrhosis and portal hypertension. METHODS: One hundred and twenty cirrhotic patients with esophageal varices but without any previous bleeding were enrolled in the prospective study. During a 2-year observation period, 52 patients who had at least one episode of acute esophageal variceal hemorrhage constituted the bleeding group, and the remaining 68 patients without any previous hemorrhage constituted the non-bleeding group. All patients underwent endoscopy before or after color Doppler-ultrasonic examination, and images were interpreted independently by two endoscopists. The control group consisted of 30 healthy subjects, matched to the patient group in age and gender. Measurements of diameter, flow direction and flow velocity in the left gastric vein (LGV) and the portal vein (PV) were done in all patients and controls using color Doppler unit. After baseline measurements, 30 min after oral administration of 75 g glucose in 225 mL, changes of the diameter, flow velocity and direction in the PV and LGV were examined in 60 patients with esophageal varices and 15 healthy controls. RESULTS: The PV and LGV were detected successfully in 115 (96%) and 105 (88%) of 120 cirrhotic patients, respectively, and in 27 (90%) and 21 (70%) of 30 healthy controls, respectively. Among the 120 cirrhotic patients, 37 had F1, 59 had F2, and 24 had F3 grade varices. Compared with the healthy controls, cirrhotic group had a significantly lower velocity in the PV, a significantly greater diameter of the PV and LGV, and a higher velocity in the LGV. In the cirrhotic group, no difference in portal flow velocity and diameter were observed between patients with or without esophageal variceal bleeding (EVB). However, the diameter and blood flow velocity of the LGV were significantly higher for EVB (+) group compared with EVB (-) group (P < 0.01). Diameter of the LGV increased with enlarged size of varices. There were differences between F1 and F2, F1 and F3 varices, but no differences between F2 and F3 varices (P = 0.125). However, variceal bleeding was more frequent in patients with a diameter of LGV >6 mm. The flow velocity in the LGV of healthy controls was 8.70+/-1.91 cm/s (n = 21). In patients with liver cirrhosis, it was 10.3+/-2.1 cm/s (n = 12) when the flow was hepatopetal and 13.5+/-2.3 cm/s (n = 87) when it was hepatofugal. As the size of varices enlarged, hepatofugal flow velocity increased (P < 0.01) and was significantly different between patients with F1 and F2 varices and between patients with F2 and F3 varices. Variceal bleeding was more frequent in patients with a hepatofugal flow velocity >15 cm/s (32 of 52 patients, 61.5%). Within the bleeding group, the mean LGV blood flow velocity was 16.6+/-2.62 cm/s. No correlation was observed between the portal blood flow velocity and EVB. In all healthy controls, the flow direction in the LGV was hepatopetal, toward the PV. In patients with F1 varices, flow direction was hepatopetal in 10 patients, to-and-fro state in 3 patients, and hepatofugal in the remaining 18. The flow was hepatofugal in 91% patients with F2 and all F3 varices. Changes in diameter of the PV and LGV were not significant before and after ingestion of glucose (PV: 1.41+/-1.5 cm before and 1.46+/-1.6 cm after; LGV: 0.57+/-1.7 cm before and 0.60+/-1.5 cm after). Flow direction in the LGV was hepatopetal and to-and-fro in 16 patients and hepatofugal in 44 patients before ingestion of glucose. Flow direction changed to hepatofugal in 9 of 16 patients with hepatopetal and to-and-fro blood flow after ingestion of glucose. In 44 patients with hepatofugal blood flow in the LGV, a significant increase in hepatofugal flow velocity was observed in 38 of 44 patients (86%) with esophageal varices. There was a relationship between the percentage changes in flow velocity and the size of varices. Patients who responded excessively to food ingestion might have a high risk for bleeding. The changes of blood flow velocity in the LGV were greater than those in the PV (LGV: 28.3+/-26.1%, PV: 7.2+/-13.2%, P < 0.01), whereas no significant changes in the LGV occurred before and after ingestion of glucose in the control subjects. CONCLUSION: Hemodynamics of the PV is unrelated to the degree of endoscopic abnormalities in patients with liver cirrhosis. The most important combinations are endoscopic findings followed by the LGV hemodynamics. Duplex-Doppler ultrasonography has no value in the identification of patients with cirrhosis at risk of variceal bleeding. Hemodynamics of the LGV appears to be superior to those of the PV in predicting bleeding.     

Increased blood flow through the portal system in cirrhotic rats

Portal venous pressure is the result of the interplay between portal venous blood flow and the vascular resistance offered to that flow. Whether portal hypertension is maintained only by an increased portal venous resistance or also by an increased blood flow within the portal venous system is still open to speculation. To resolve these differences, splanchnic and systemic hemodynamics were evaluated in cirrhotic rats, induced by CCl4. Blood flow and portal-systemic shunting were measured by radioactive microsphere techniques. All cirrhotic rats had portal hypertension (portal venous pressure 13.5 +/- 1.1 vs. 9.0 +/- 0.5 mmHg, in normal control rats; p less than 0.01), but portal-systemic shunting in cirrhosis (31% +/- 13% vs. 0.2% +/- 0.02%; p less than 0.05) was variable, ranging from 1% to 97%. Portal venous inflow, the total blood flow within the portal system, was increased in cirrhotic rats (5.75 +/- 0.04 vs. 4.52 +/- 0.36 ml/min per 100 g; p less than 0.05). Total splanchnic arterial resistance was reduced in cirrhotic rats (3.3 +/- 0.2 vs. 5.8 +/- 0.5 dyn X s X cm-5 X 10(5); p less than 0.01). Portal venous resistance, however, was not abnormally elevated in cirrhotic rats (4.6 +/- 0.5 vs. 4.7 +/- 0.5 dyn X s X cm-5 X 10(4), p = NS). Splanchnic hemodynamics in cirrhotic rats demonstrate that portal hypertension is maintained, at least in part, by a hyperdynamic portal venous inflow. The hemodynamic data in cirrhotic rats provided evidence that supports the role of an increased portal blood flow in portal hypertension and gives a quantitative definition of splanchnic hemodynamics in intrahepatic portal hypertension.     

Hepatosplenic schistosomiasis portal hypertension: effect of esophagogastric devascularization with splenectomy on the diameter and mean flow velocity in the portal system (ultra-sonographic Doppler

BACKGROUND: Esophagogastric devascularization with splenectomy has been used for the treatment of upper digestive bleeding due to esophagic varices in hepatoportal mansoni's schistosomic portal hypertension. Nevertheless, early portal thrombosis has hampered this surgical technique (13.3% and 53.2%), compromising the good results on the hemorrhagic side. Supposing that portal circulatory changes, due to the surgical treatment, may play an important role in this kind of complication, our objective was to identify the hemodynamic facilitating factors. Portal hemodynamic aspects, identified by ultra-sonographic Doppler study, from two groups of patients: non-operated upon and splenectomized with esophagogastric devascularization in late post-operatory phase (in excess of 6 moths), with portal hypertension due to mansoni hepatoesplenic portal hypertension and in similar clinical conditions, were compared. METHOD: Fifty eight ambulatorial patients were studied, all had portal hypertension caused by mansoni's hepatosplenic schistosomiasis and previous bouts of digestive bleeding. They were divided in two groups: A--29 followed clinically/endoscopically, and group B--29 previously submitted to esophagogastric devascularization with splenectomy. In all was measured the diameter and mean flow velocity in the portal vein and its right and left branches by ultra-sonographic Doppler study. The results were submitted to statistical analysis for inter- and intra-group comparison. RESULTS: Group A (non-operated): the portal vein diameter was greater than the right and left branches (10.6 +/- 2.9, 8.0 +/- 1.8, 9.1 +/- 2.6 cm), the mean flow velocities in the portal vein and its branches were similar (15.62 +/- 6.17, 14.92 +/- 5.33, 16.12 +/- 4.18 cm/seg). Group B (operated): the diameter and mean flow velocity in all vessels were reduced (8.8 +/- 1.7, 5.2 +/- 1.2, 7.5 +/- 2.2 cm/12.53 +/- 2.60, 8.86 +/- 1.75, 9.69 +/- 3.75 cm/seg). CONCLUSIONS: After esophagogastric devascularization with splenectomy, there was a reduction of the diameter and mean flow velocity in the portal vein, its right and left branches.     

Adrenomedullin in cirrhotic and non-cirrhotic portal hypertension

AIM:Adrenomedullin (ADM) is a potent vasodilator peptide.ADM and nitric oxide (NO) are produced in vascular endothelial cells. Increased ADM level has been linked to hyperdynamic circulation and arterial vasodilatation in cirrhotic portal hypertension (CPH). The role of ADM in non-cirrhotic portal hypertension (NCPH) is unknown, plasma ADM levels were studied in patients with NCPH, compensated and decompensated cirrhosis in order to determine its contribution to portal hypertension (PH) in these groups.METHODS: There were 4 groups of subjects. Group 1consisted of 27 patients (F/M: 12/15) with NCPH due to portal and/or splenic vein thrombosis (mean age: 41±12years), group 2 consisted of 14 patients (F/M: 6/8) with compensated (Child-Pugh A) cirrhosis (mean age: 46±4),group 3 consisted of 16 patients (F/M: 6/10) with decompensated (Child-Pugh C) cirrhosis (mean age: 47±12).Fourteen healthy subjects (F/M: 6/8) (mean age: 44±8) were used as controls in Group 4. ADM level was measured by ELISA. NO was determined as nitrite/nitrate level by chemoluminescence.RESULTS: Adl level in Group 11 (236±61.4 pg/mL) was significantly higher than that in group 2 (108.4±28.3 pg/mL)and group 4 (84.1±31.5 pg/mL) (both P＜0.0001) but was lower than that in Group3 (324±93.7 pg/mL) (P=0.002). NO level in group 1 (27±1.4 μmol/L) was significantly higher than that in group 2 (19.8±2.8 μmol/L) and group 4 (16.9±1.6μmol/L) but was lower than that in Group 3 (39±3.6 μmol/L)(for all three P＜0.0001). A strong correlation was observed between ADM and NO levels (r=0.827, P＜0.0001).CONCLUSION: Adrenomedullin and NO levels were high in both non-cirrhotic and cirrhotic portal hypertension and were closely correlated, Adrenomedullin and NO levels increased proportionally with the severity of cirrhosis, and were significantly higher than those in patients with NCPH.Portal hypertension plays an important role in the increase of ADM and NO. Parenchymal damage in cirrhosis may contribute to the increase in these parameters.     

Correlation between hemodynamic parameters of the portal circulation in cirrhotic patients

The aim was to study the relationships between portal hemodynamic parameters in cirrhotic patients. Portal hemodynamics was assessed by scintisplenoportography and sonography, and the measurement of portohepatic gradient. Gradient between wedged and free hepatic venous pressures was 2.71 +/- 0.90 kPa (SD), and extrahepatic shunting was 49 +/- 31 p. 100 (SD) in 27 cirrhotic patients. Intrahepatic shunting was present in 17 p. 100 out of 23 cirrhotics. Portal blood flow was 0.582 +/- 0.196 l/min (SD) and hepatic resistance to portal blood flow was 4.84 +/- 2.62 kPa/l/min (SD). Portal blood flow correlated neither with the pressure gradient, nor with portosystemic shunting. The pressure gradient was significantly correlated with portal systemic shunting (r = 0.64, p less than 0.001). Hepatic resistance to portal blood flow was significantly (p less than 0.05) correlated with portal systemic shunting, however the value of the correlation coefficient was low (r = 0.433). The pressure gradient and portosystemic shunting were higher in patients with large esophageal varices than in those with small ones (respectively t = 2.665, p less than 0.02 and t = 3.00, p less than 0.01). Hemodynamic pattern was not correlated with the degree of hepatocellular failure, as assessed by the Child-Pugh index. In conclusion this study provides further evidence for the forward theory of portal hypertension in human liver cirrhosis.     

Observer variability in echo-Doppler measurements of portal flow in cirrhotic patients and normal volunteers

The intraobserver and interobserver variability in measuring the portal vein flow by the echo-Doppler technique was evaluated in a blind controlled study. A total of 22 cirrhotic patients and 14 normal volunteers were examined by two skilled operators using duplex Doppler within a period of 1-3 mo (6 cirrhotics and 7 normal volunteers by both observers). Area, mean velocity, and flow were measured (4 measurements: A, B on day 1; C, D on day 2). The intraclass correlation coefficient was used to assess both the statistical and clinical significance of intraobserver and interobserver agreement for the measurements of these three parameters. The level of intraobserver agreement for each parameter on normal subjects and cirrhotics was obtained from the two measurements on the same day and from the two measurements at the same time on consecutive days. Overall agreement between the four measurements was also calculated. Levels of interobserver agreement were obtained by calculating separately the intraclass correlation coefficient from each of the four pairs by measurements made on the same subject by the two observers over the same period of 2 days. The coefficient of variation was also used to compare the variability in these measurements. Overall, intraobserver agreement on normal subjects varied from good to excellent for observer 1, and from fair to good for observer 2. On cirrhotic patients, observer 1 was excellent at all times for all parameters. Observer 2 had lower intraclass correlation coefficient values, especially for velocity on consecutive days. For the best of the two observers on the portal flow, the coefficient of variation in cirrhotic patients ranged from 2%-30% with a mean +/- SEM of 12% +/- 4%. No acceptable interobserver agreement was found between the two observers in either of the two samples of subjects. These results support the use of this technique mainly for the determination of rapid and large changes in portal hemodynamics within a short period of time. The technique seems to have low precision in monitoring chronic changes in portal hemodynamics.     

Propranolol reduces the response of serum bile acids to oral chenodeoxycholic acid, possibly as a reflex reaction to reduced portal blood flow in healthy and cirrhotic subjects

To evaluate if a drug that affects splanchnic and portal flow reduces intestinal bile acid absorption, we studied the effect of propranolol (40 mg oral dose) both on the response of total bile acids (SBA) to oral chenodeoxycholic acid (CDCA 250 mg) and on the estimated hepatic flow by indocyanine green kinetics in 10 healthy and 14 cirrhotic subjects. In 18 subjects who showed a reduction in resting heart rate of almost -5%, propranolol significantly reduced the SBA area under the curve after CDCA in both healthy (mumol/l/h m +/- SD from 181.7 x 144.9 to 56.5 +/- 36.4 p less than 0.02) and cirrhotic (from 1412.1 +/- 1044.8 to 1129.2 +/- 978.8 p less than 0.01) subjects. Variable but not significant modifications were observed in estimated hepatic flow. These results suggest that the propranolol-induced changes in SBA response to CDCA could be a reflex reaction to changes in splanchnic/portal flow.