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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 42  |  Issue : 4  |  Page : 130-137

Hemodynamic analysis of portal hypertension in patients with liver cirrhosis


1 Department of Radiodiagnosis, Faculty of Medicine, Tanta University Hospital, Tanta, Egypt
2 Department of Internal Medicine, Faculty of Medicine, Tanta University Hospital, Tanta, Egypt

Date of Submission13-Jun-2014
Date of Acceptance10-Aug-2014
Date of Web Publication21-Nov-2014

Correspondence Address:
Aly A Elbarbary
Department of Radiodiagnosis, Faculty of Medicine, Tanta University Hospital, 31111 Tanta
Egypt
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DOI: 10.4103/1110-1415.145276

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  Abstract 

Objective
The aim of this study was to evaluate the role of duplex Doppler ultrasound in portal vein and upper gastrointestinal endoscopy in the assessment of signs of portal hypertension in patients with liver cirrhosis.
Patients and methods
This study included 50 patients and 20 apparently healthy individuals as controls. All of them were subjected to a thorough assessment of history, complete clinical examination, and some important laboratory investigations. Also, color duplex Doppler ultrasound was performed for all the participants and upper gastrointestinal endoscopy only for the patients.
Results
We found that portal vein diameter, congestion index, arterial pulsatility index, and arterial resistive index were significantly higher in the patients than in the controls, whereas portal vein flow velocity and the liver vascular index were significantly lower in the patients than in the controls.
Conclusion
Duplex Doppler ultrasonography remains the first step in the evaluation of patients with liver cirrhosis and portal hypertension. The best hemodynamic parameter in the assessment of portal hypertension is the congestion index, whereas arterial indices are less prone to variability and are more reproducible compared with venous indices. Upper gastrointestinal endoscopy is the gold standard in the treatment of esophageal varices and also effective in preventing recurrent variceal bleeding.

Keywords: duplex Doppler ultrasonography, liver cirrhosis, portal hypertension


How to cite this article:
Elbarbary AA, Elbedewy MM, Elbadry AM. Hemodynamic analysis of portal hypertension in patients with liver cirrhosis. Tanta Med J 2014;42:130-7

How to cite this URL:
Elbarbary AA, Elbedewy MM, Elbadry AM. Hemodynamic analysis of portal hypertension in patients with liver cirrhosis. Tanta Med J [serial online] 2014 [cited 2017 Dec 12];42:130-7. Available from: http://www.tdj.eg.net/text.asp?2014/42/4/130/145276


  Introduction Top


The portal vein (PV) is formed by the union of superior mesenteric and splenic veins posterior to the pancreas. It ascends to the porta hepatis posterior to the common bile duct and the hepatic artery, where it splits into right and left branches to supply corresponding lobes of the liver. The liver has a dual blood supply, about 70-80% contributed by the PV and the rest by the hepatic artery. Blood from these vessels mixes in the hepatic sinusoids, which are located between cords of hepatocytes and are lined by fenestrated endothelium. The blood from each hepatic lobule then drains through the hepatic veins and finally into the inferior vena cava [1].

Portal hypertension is an almost unavoidable complication of chronic liver disease, especially in cirrhosis, and it is responsible for the more lethal complications such as gastroesophageal varices and massive gastrointestinal bleeding, ascites, hepatorenal syndrome, and hepatic encephalopathy. The appearance of these complications represents the major cause of death. The prevalence of esophageal varices is very high: when cirrhosis is diagnosed, varices are present in about 40% of compensated patients and in 60% of those with ascites [2].

Duplex Doppler ultrasound is a noninvasive technique for the estimation of PV pressure as a direct measurement requires puncturing of the PV surgically or percutaneously and these are not easy in clinical practice and lead to many complications [1].

Duplex Doppler ultrasound has a limitation in the determination of the actual pressure gradient; thus, we measure the velocity at a particular point to provide the gradient at that point [3].

Endoscopy is useful in the diagnosis and treatment of complications of portal hypertension such as bleeding esophageal varices, gastric varices, and hypertensive gastropathy. Three endoscopic techniques are currently used: endoscopic band ligation, endoscopic sclerotherapy, and variceal obliteration with glue [4].

The aim of this study was to evaluate the role of duplex Doppler ultrasound in PV and upper gastrointestinal endoscopy in the assessment of signs of portal hypertension in patients with liver cirrhosis.


  Patients and methods Top


Patients

Between June 2011 and July 2012, 50 patients with liver cirrhosis and 20 healthy individuals as controls were recruited from the internal medicine and radiodiagnosis departments in our institution. Written informed consent was obtained from all the patients after an explanation of the nature and purpose of our study was provided. The ethics committee of our hospital approved the study. Patients with other virus infections, malignancy, or mixed pathology were excluded from the study.

Methods

All the patients and the controls were subjected to the following:

(1) Thorough assessment of history.

(2) Complete clinical examination.

(3) Laboratory investigations, which included the following:

(a) Complete blood picture

(b) Alanine transferase (ALT), aspartate transferase (AST).

(c) Albumin, globulin ratio, blood urea, serum creatinine.

(d) Total bilirubin, direct bilirubin, indirect bilirubin.

(e) Alpha fetoprotein, viral markers (B&C).

(4) Duplex Doppler ultrasound of the portal venous system for assessment of portal venous system as a noninvasive and effective technique for estimation of PV pressure. All patients were kept in a fasting state overnight before the procedure at our institution. They were examined in the supine position in the right upper quadrant during quiet respiration [5]. The following main Doppler factors were always determined by the same equipment (with a 3.5-MHz convex transducer; B-K Medical, Cobenhagen, Denmark) and by the same operator.

Assessment of portal vein patency and blood flow

PV anatomy is evaluated using B-mode imaging. It is identified by following the splenic vein to the right until its junction with the superior mesenteric vein. This technique avoids confusing the PV with bile duct or the inferior vena cava. However, when the PV is difficult to observe in the supine position, the patient is examined in the left lateral decubitus position [6].

Estimation of portal hemodynamic parameters

Portal vein diameter and cross-sectional area

Perpendicular to the long axis of the vein, the cross-sectional area was calculated from the formula of an ellipse, (A × B)/4×∏, where A is the long axis of the vein and B is the short axis of the vein.

If they were equal, the cross-sectional area was calculated using the following formula: r2 × ∏, where r is half the diameter of the vein. The measurement of each vessel was performed from the inner wall to the inner wall at the site of the Doppler examination.

Portal vein flow velocity

The velocity of blood flow in the PV was calculated from the Doppler tracings. Normal velocity of the blood flow in the PV was15-20 cm/s. Portal hypertension was associated with an increase in blood flow and congestion, but with a decrease in blood velocity in the PV. Duplex Doppler ultrasound was used to show blood flow within both the PV with its main tributaries and abnormal collaterals of the portal venous system.

Measurement of the Vmax and the calculating Vmean : The sample volume was positioned in the center of the vessel and the gate was adjusted to eliminate the background. The velocity measured was the maximum velocity (Vmax ). The mean V was calculated using the software as follows: V peak obtained multiplied by a correction factor of 0.57 obtained from an experimental study on a circulation mode. Three measurements were obtained and the average was utilized.

Congestion index

The congestion index (CI) is the ratio between the cross-sectional area (cm 2 ) and the blood flow velocity (cm/s) of the PV. Doppler data were obtained while scanning the PV along its axis and with the sample volume in the middle of the PV trunk. Just after the Doppler signals were recorded, the PV cross-sectional area was measured from the B-mode image of the PV while scanning perpendicular to the long axis of the PV. The cross-sectional area was calculated using the formula for the cross-sectional area of an ellipse.

Arterial pulsatility index is calculated as follows:



Upper gastrointestinal endoscopy

All patients with positive data after duplex Doppler ultrasound underwent endoscopy for evaluation of the presence of portal hypertension. Upper gastrointestinal endoscopy was performed using a videoscope (CLV-240; Olympus Ltd, Tokyo Japan). Possible complications of endoscopic procedures were explained to the patients and their relatives and written informed consents were obtained before the endoscope.

Image analysis

Normal PV diameter is less than 10 mm, with a greater than 20-30% increase with food and respiration. In portal hypertension, the PV is dilated (>13 mm), with absent or less than 20% variation with respiration. The direction of portal blood flow can be determined by the color-flow pattern. The flow of blood within the vessel could be red or blue depending on whether the flow is toward or away from the transducer and above or below the baseline, respectively. Normal blood flow in the PV is toward the liver and is of low velocity, undulating with respiration. Endoscopic classification of esophageal varices is as follows:

Grade I: Small straight cords confined to the lower third of the esophagus.

Grade II: Moderate-sized clubbed varices with well-defined areas of normal mucosa between them forming several distinct vertical cords and confined to the lower half of the esophagus.

Grade III: Gross varices extending into the proximal half of the esophagus are so large and tortuous that normal mucosa may be not visible in between unless the esophagus is fully distended with air.

Grade IV: Varices like those of grade III, but with dilated capillaries on top or in between varices.

Statistical analysis

Statistical presentation and analysis of the present study were carried out using the mean value, SD, and χ2 -test by SPSSV. 16 (Minitab Inc., USA). A P-value less than 0.05 was considered significant.


  Results Top


From June 2011 to July 2012, 50 patients and 20 apparently healthy individuals as controls were included in this study; the patients presented with portal hypertension and were more susceptible to its complications such as esophageal varices.

Demographic data: The age of the 50 patients ranged from 45 to 65 years, mean age 51.560 ± 5.440 years. The age of the 20 control participants ranged from 44 to 54 years, mean age 49.600 ± 3.307 years. Comparison between all the patients and the controls in terms of the age showed no statistically significant difference (P > 0.05) as shown in [Table 1].
Table 1 Statistical analysis of age between patients and controls

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Comparison between all the patients and the controls in the PV diameter and velocity showed a statistically significant difference (P < 0.001) as shown in [Table 2] and [Figure 1] and [Figure 2].
Table 2 Statistical analysis of portal vein diameter between patients and controls

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Figure 1: (a) Doppler ultrasound of the portal vein with minimal pulsatile modulation of the portal fl ow in a healthy adult. (b) Doppler study of the portal vein showing a portal vein fl ow velocity of 25 cm/s.

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Figure 2: (a) Doppler study of the portal vein in a cirrhotic patient showing a portal vein fl ow velocity of 7.1 cm/s. (b) Doppler study of the hepatic artery showing a pusatility index of 1.64 and a resistive index of 0.78.

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Comparison between all the patients and the controls in the PV velocity showed a statistically significant difference (P < 0.001) as shown in [Table 3].
Table 3 Statistical analysis of portal vein fl ow velocity between patients and controls

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The CI ranged from 0.009 to 0.159 in patients, mean 0.104 ± 0.039, and from 0.050 to 0.090 in controls, mean 0.071 ± 0.014. There was a statistically significant difference (P < 0.05) as shown in [Table 4].
Table 4 Statistical analysis of the congestion index between patients and controls

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There were no esophageal varices in eight patients, 16%. Grade I esophageal varices were present in 12 patients, 24%. Grade II esophageal varices were present in eight patients, 16%. Grade III esophageal varices were present in eight patients, 16%. Grade IV esophageal varices were present in 14 patients, 28%, as shown in [Table 5] and [Figure 3], [Figure 4], [Figure 5].
Table 5 Grading of esophageal varices in the 50 patients

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Figure 3: (a) Grade I esophageal varices. (b) Grade II esophageal varices

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Figure 4: (a) Grade III esophageal varices. (b) Grade IV esophageal varices

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Figure 5: Positive correlation between grading of esophageal varices and portal vein diameter (mm); the portal vein diameter r was 0.887 and the P-value was less than 0.001.

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In eight patients, there were no esophageal varices as the CI ranged from 0.06 to 0.09, mean 0.07 ± 0.02.

In 12 patients, there were grade I esophageal varices as the CI ranged from 0.01 to 0.09, mean 0.06 ± 0.03. In eight patients, there were grade II esophageal varices as the CI ranged from 0.11 to 0.13, mean 0.11 ± 0.01. In eight patients, there were grade III esophageal varices as the CI ranged from 0.13 to 0.14, mean 0.13 ± 0.001. In 14 patients, there were grade IV esophageal varices as the CI ranged from 0.13 to 0.16, mean 0.14 ± 0.01. There was a high statistically significant increase in the CI in relation to esophageal varices in all patients (P < 0.001) as shown in [Table 6] and [Figure 6].
Figure 6: Positive correlation between grading of esophageal varices and the congestion index. Congestion index r was 0.900 and the P-value was less than 0.001.

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Table 6 Statistical analysis of grade of esophageal varices in relation to the congestion index in 50 patients

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Comparison between all the patients and the controls in the arterial pulsatility index showed a statistically significant difference (P < 0.001) as shown in [Table 7] and [Figure 7] and [Figure 8].
Table 7 Statistical analysis of the arterial pulsatility index between patients and controls

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Figure 7: Positive correlation between grading of esophageal varices and the arterial pulsatility index. The arterial pulsatility index r was 0.814 and the P-value was less than 0.001.

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Figure 8: Positive correlation between grading of esophageal varices and the arterial resistive index. The arterial resistive index r was 0.236 and the P-value was less than 0.001.

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Comparison between all the patients and the controls in the arterial resistive index showed a statistically significant difference (P < 0.001) as shown in [Table 8] and [Figure 9].
Table 8 Statistical analysis of the arterial resistive index between patients and controls

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Figure 9: Negative correlation between grading of esophageal varices and portal vein flow velocity cm/s. The portal vein fl ow velocity r was −0.830 and the P-value was less than 0.001.

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Comparison between all the patients and the controls in the liver vascular index showed a statistically significant difference (P < 0.001) as shown in [Table 9] and [Figure 10].
Table 9 Statistical analysis of the liver vascular index between patients and controls

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Figure 10: Negative correlation between grading of esophageal varices and the liver vascular index. The liver vascular index r was −0.934 and the P-value was less than 0.001.

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  Discussion Top


Liver cirrhosis is a progressive chronic liver disease, and its clinical features are dependent on the duration of disease and the nature of the etiological factors [7]. Increased resistance to portal blood flow because of liver cirrhosis leads to portal hypertension [8]. In fact, portal hypertension results in the development of gastroesophageal and/or ectopic (colonic, enteric) varices as well as other mucosal lesions in the stomach, small intestine, and colon [9].

Clinically portal hypertension is diagnosed when portal bed stoppage has been found, with manifestations such as varices formed in the esophagus, fundus of the stomach, portal gastropathy, splenomegaly with secondary hypersplenism, ascites, and edema of the lower limbs; the symptoms may occur in various constellations [10-12].

We studied 50 patients with chronic liver disease and 20 apparently healthy individuals as controls; the mean age of the studied patients was 51.56 ± 5.44 years.

Doppler ultrasonography has enabled the noninvasive investigation of hepatic and portal hemodynamics [13,14].

Barakat [15] reported that with the availability of Doppler ultrasound, attempts have been made to study various blood flow characteristics in patients with liver cirrhosis and portal hypertension using simple and noninvasive techniques.

From this point of view, we studied the role of duplex Doppler ultrasound as a noninvasive technique for assessment of the portal venous system in patients with chronic liver disease. On the basis of the statistical findings of our study and depending on duplex Doppler ultrasound, we could assess portal hypertension by measuring hemodynamic parameters (PV diameter, PV flow velocity, CI, arterial pulsatility index, arterial resistive index, and liver vascular index).

In our study, there was a highly significant increase in the PV diameter (mm) in patients compared with the controls (P < 0.001); in the patient group, it ranged from 12.000 to 17.000 mm, mean 14.260 ± 1.690, whereas in the controls, it ranged from 10.000 to 13.000 mm, mean 11.000 ± 1.054.

In agreement with our study, Sarwar et al. [16] had shown that patients with PV diameter greater than 11 mm are more likely to have high-grade varices.

Also, Nicolau et al. [17] found an association between an increase in portal venous diameter with liver cirrhosis and portal hypertension.

Some other studies reported the same results as ours such as Hagen-Ansert [18], who reported that a measurement threshold of PV diameter greater than 13 mm is a predictor of portal hypertension in patients with cirrhosis.

In contrast, Jaheen [19]found that PV dilatation is a specific but insensitive indicator of portal hypertension; they noted that this sign may also occur in the absence of portal hypertension (e.g. in response to massive splenomegaly or acute PV thrombosis).

Our study showed that there was a highly significant decrease in the PV flow velocity (cm/s) in patients compared with the controls (P < 0.001). In the patient group, it ranged from 12.000 to 20.250 cm/s, mean 14.038 ± 2.073, whereas in the controls, it ranged from 17.250 to 23.500 cm/s, mean 20.013 ± 1.742.

In agreement with our study, Jaheen [19] found that the portal venous flow velocity is significantly reduced in patients with cirrhosis and portal hypertension when compared with that of normal individuals.

Also, Liu et al. [20] reported that the decrease in the mean PV velocity correlated with the severity of portal hypertension and the risk of esophageal varix bleeding.

In our study, there was a significant increase in the CI in patients compared with the controls; in the patient group, it ranged from 0.009 to 0.159, mean 0.104. ± 0.039, and in the controls it ranged from 0.050 to 0.090, mean 0.071 ± 0.014.

There was a highly statistically significant increase in the CI in relation to esophageal varices in all patients (P < 0.001) and this was confirmed by Testa et al. [21], who found a significant relationship between the CI and the presence of esophageal varices.

Westra et al. [22] suggested that the CI reflects the pathophysiological hemodynamics of the portal venous system in portal hypertension.

Farias et al. [23] found that the PV CI was a sensitive marker of clinically significant portal hypertension (average 0.04 ± 0.02).

In agreement with our study, Jaheen found that the CI in the patients with cirrhosis was 2.5 times higher than that in the normal individuals (average of 0.07 ± 0.014 in normal and average of 0.104 ± 0.039 in cirrhosis) [19].

Nicolau et al. [17] reported that arterial indices are less prone to variability and are more reproducible compared with venous indices.

The arterial pulsatility index in our study was increased in the patients compared with the controls (P < 0.001); in the patient group, it ranged from 1.600 to 1.900, mean 1.75 ± 0.127, whereas in the controls, it ranged from 1.500 to 1.800, mean 1.567 ± 0.064, and this was confirmed by Zhang et al, [24] who found that the arterial pulsatility index in the patient group was higher than that in the healthy group (1.63 ± 0.48 vs. 1.17 ± 0.18, P < 0.001).

Our data showed that there was a significant increase in the arterial resistive index in patients compared with the controls (P < 0.001).

In agreement with this, Liu et al. [20] found that an increase in the hepatic arterial resistive index, a decrease in the PV velocity, and further increase in the portal pressure led to an increased risk of variceal bleeding.

Iwao and colleagues showed that the pulsatility index had the mean velocity in the denominator and reflected resistance in the distal capillary bed. In contrast, the resistive index had peak velocity in the denominator and reflected vascular compliance. Pulsatility was shown to be a better index than the resistive index in the estimation of portal hypertension [25].

The liver vascular index in our study showed a highly significant decrease in patients compared with the controls (P < 0.001).

Tarzamni et al. [26] found that the liver vascular index (P ≤ 0.0005) was significantly lower in patients with portal hypertensive gastropathy; also, it was correlated independently with portal hypertensive gastropathy (P = 0.018).

However, a few other studies have reported different findings compared with our results. Jeon et al. [27] and Richard et al. [28] reported that Doppler measurement was not useful in distinguishing the presence of varices. However, clinical tests including biochemistry and ultrasonography would be useful in selecting eligible patients for screening endoscopy.

Cales et al. [29] and Abdull and colleagues reported that endoscopic screening was the best technique for the detection of esophageal varices, and this was confirmed by De Franchis and Dib and colleagues, who found that there was no satisfactory nonendoscopic indicator to detect the presence of esophageal varices [30,31].


  Acknowledgements Top


 
  References Top

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Barakat M. Non-pulsatile hepatic and portal vein waveforms in patients with liver cirrhosis: concordant and discordant relationships. Br J Radiol 2004; 77:547-550.  Back to cited text no. 15
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Jaheen A. Prevalence of portal hypertensive gastropathy and its predictive factors. Gut Review 2003; 3:24-33.  Back to cited text no. 19
    
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Jeon SW, Cho CM, Tak WY, Ryeom HK, Kweon YO, et al. The value of Doppler ultrasonography and laboratory tests as non-invasive predictors of the presence of esophageal varices in patients with chronic liver disease. Korean J Gastroenterol 2006; 48:180-187.  Back to cited text no. 27
    
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

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