|Year : 2022 | Volume
| Issue : 4 | Page : 216-222
Comparative ultrasonography evaluation of the portal vein congestion index in chronic hepatitis B virus infection and apparently healthy adults
Gbenga Jacob Aderibigbe1, Chukwuemeka Agi1, Ebbi Donald Robinson2, Enighe Wananyo Ugboma1
1 Department of Radiology, University of Port Harcourt Teaching Hospital, Port Harcourt, Rivers State, Nigeria
2 Department of Radiology, Faculty of Clinical Sciences, Rivers State University Teaching Hospital, Port Harcourt, Rivers State, Nigeria
|Date of Submission||02-Mar-2022|
|Date of Decision||26-May-2022|
|Date of Acceptance||26-May-2022|
|Date of Web Publication||04-Oct-2022|
Ebbi Donald Robinson
Lecturer, Consultant Radiologist, Department of Radiology, Faculty of Clinical Sciences, Rivers State University Teaching Hospital, Port Harcourt, Rivers State
Source of Support: None, Conflict of Interest: None
Background: Sonography is a useful tool in the study of the hepatic haemodynamic alterations that occur in chronic hepatitis B virus (HBV) infection using the portal vein congestion index (PVCI). The study was aimed at sonographically assessing the portal vein congestion index in adults with chronic HBV infection and at comparing the same with apparently healthy adults.
Methods: This was a comparative, cross-sectional study carried out amongst 124 subjects (62 chronic HBV patients and 62 uninfected, apparently healthy individuals). The participants underwent routine grey scale evaluation of the liver, Doppler ultrasonographic evaluation of the portal vein and the ratio of the portal vein cross-sectional area in centimetre square to the portal vein velocity in centimetre per second.
Results: In healthy controls, the mean PVCI was 0.048±0.010 cm, while the mean PVCI in chronic HBV patients was 0.077±0.028 cm (P < 0.001). The mean of duration of illness was 3.63 years with a range of 0.5–15. There was a weak negative correlation between PVCI and duration of illness (r = −0.130, P = 0.313).
Conclusions: The PVCI was significantly higher in chronic HBV patients compared to healthy subjects. However, there was a weak correlation between PVCI and duration of illness in patients with chronic HBV.
Keywords: Doppler ultrasound, hepatitis B virus, portal vein congestion index, portal vein cross-sectional area, portal vein velocity
|How to cite this article:|
Aderibigbe GJ, Agi C, Robinson ED, Ugboma EW. Comparative ultrasonography evaluation of the portal vein congestion index in chronic hepatitis B virus infection and apparently healthy adults. J Clin Sci Res 2022;11:216-22
|How to cite this URL:|
Aderibigbe GJ, Agi C, Robinson ED, Ugboma EW. Comparative ultrasonography evaluation of the portal vein congestion index in chronic hepatitis B virus infection and apparently healthy adults. J Clin Sci Res [serial online] 2022 [cited 2022 Dec 5];11:216-22. Available from: https://www.jcsr.co.in/text.asp?2022/11/4/216/357840
| Introduction|| |
Hepatitis B virus (HBV) is the prototype member of the Hepadnaviridae family that have a strong preference for infecting liver cells. The presence of hepatitis B surface antigen (HBsAg) in serum for at least 6 months establishes the chronicity of infection. The diagnosis of chronic HBV infection is made with serological assays that detect the presence of HBsAg for at least 6 months, or serological assays that detect the presence of Hepatitis B core antibody immunoglobulin G, in serum or plasma but also in capillary/venous whole blood and oral fluid.
Portal vein congestion index (PVCI) was originally described by Moriyasu et al. as a reliable indicator to differentiate various liver disorders including chronic viral hepatitis. It is defined as the ratio of ultrasound measured portal vein area in centimetre square to the portal vein velocity in centimetre per second (by doppler ultrasonography). Since then, the congestion index of the portal vein had been evaluated for many different clinical applications in diseases involving the liver.
The parameters used in the calculation of the portal vein congestion index take into account portal vein dilatation and decreased flow velocity, both of which are usually described as features of portal hypertension. It has also been reported that a congestion index value above 0.1 suggests the diagnosis of portal hypertension with a 95% sensitivity. The hepatic venous pressure gradient is the gold standard for assessing the severity of portal hypertension; however, it is not widely available and it is an invasive procedure, unlike ultrasonography.
Chronic HBV infection affects approximately 360 million people worldwide. Hepatocellular carcinoma will develop in approximately 55% of patients with chronic HBV infection. Africa is said to have over 75 million individuals living with chronic HBV infection with a seroprevalence of about 8.83%. In Nigeria, the prevalence of chronic HBV infection is 2%–20% across various states. A study done at the University of Port Harcourt Teaching Hospital (UPTH) amongst health workers in Port Harcourt, Rivers state Nigeria, found a prevalence of 4.2%. Another study from the same institution done in 1976, where blood donors were studied, found a prevalence of 4.6%.
Chronic liver disease such as chronic viral hepatitis B is characterised by progressive hepatic fibrosis and changes in hepatic vascular haemodynamics. Liver blood flow undergoes complex changes with the progression of chronic liver disease. Normally, the portal vein contributes 70%–75% of the hepatic blood flow, while the hepatic artery contributes the remaining 25%–30%. As chronic liver disease progresses, there is a growing obstruction to portal venous flow at the level of the sinusoids. This reduction in portal venous flow is counterbalanced by a reciprocal increase in hepatic arterial flow; consequently, the ratio of hepatic arterial to total hepatic blood flow is elevated in advanced liver disease. As the portal vein flow becomes obstructed, it initially compensates and maintains its blood flow by becoming increasingly dilated, while its flow velocity decreases. The ratio between portal vein area and velocity, called the PVCI, is thus increased in chronic liver disease.,
The burden of chronic HBV infection is enormous both for the individuals and healthcare resources as a result of its chronicity, possible complications and high cost of treatment. Unfortunately, most patients with chronic HBV infection in Nigeria present late with severe impairment of hepatic function, underlying advanced liver cirrhosis or hepatocellular carcinoma. The natural history of chronic HBV infection is variable and persons with chronic HBV infection need lifelong monitoring to determine if and when intervention is needed and to observe for serious sequelae. Consequently, early detection is important, and use of the PVCI in routine abdominal ultrasonography can potentially aid to identify patients with chronic liver disease. The study was aimed at comparing the Doppler sonographic findings of the portal vein congestion index in adults with chronic HBV infection, with those of apparently healthy adults.
| Material and Methods|| |
This was a hospital-based cross-sectional prospective study. It involved participants between the ages of 18 and 75 years with chronic HBV infection and apparently healthy volunteers as controls. This study was carried out at the Ultrasound Unit in the Radiology Department of UPTH over a duration of 6 months (July 2020 to December 2020). Approval was granted by the Ethical Committee of the UPTH, before commencement of the study. Participation was voluntary. The study was performed after the benefit and safety of the study had been explained to the patient, and an informed consent was obtained.
Subjects were recruited from UPTH and Rivers State University Teaching Hospital (RSUTH), both in Port Harcourt, Rivers State Nigeria. UPTH is an 800-bed multispecialist teaching hospital in the south–south geopolitical region of Nigeria. RSUTH is a 375-bed specialist health institution. The catchment area of these hospitals extends beyond Rivers State, to include much of the Niger delta region with a vast population.,
The study included subjects with known chronic viral hepatitis B (patients seropositive to HBsAg for duration of 6 months), aged between 18 and 75 years (study subjects). Patients aged below 18 or above 75 years of age; those with chronic liver disease, patients receiving vaso-active drugs such as beta blockers; those with co-existing HDV, HCV or HIV infection, patients with idiopathic portal hypertension, portal vein thrombosis, right heart failure, pregnancy were excluded from the study.
Subjects seronegative for HBsAg, aged between 18 and 75 years were included as control subjects. Patients aged below 18 or above 75 years of age, those with chronic liver disease, subjects on vaso-active drugs such as beta blockers, HDV, HCV or HIV infection, idiopathic portal hypertension, portal vein thrombosis, right heart failure, pregnancy were excluded.
The sample population was calculated using the Leslie Fisher's formula. Sixty two subjects with chronic HBV infection were studied. A control group of 62 healthy subjects were simultaneously scanned, giving a total of 124.
Systematic probability sampling was employed in the selection of subjects in the study. Under the supervision of a consultant gastroenterologist, a sampling frame drawn from the register of chronically infected HBV patients in the gastroenterology outpatient clinic of the internal medicine department of UPTH and RSUTH was used. The patients were numbered, and patients with even numbers were selected. The clinical diagnosis of chronic HBV infection was made after patients presenting at the clinic with a positive HBsAg test, test seropositive to HBsAg after 6 months of the initial positive test. The date of the first positive test was recorded and the test was repeated after 6 months and patients who were seropositive to HBsAg again after 6 months were recruited. Three patients were sampled per clinic day for the case group, over the data collection period.
The control group was drawn from eligible, apparently healthy members of staff, medical students and patients on routine medical checkup referred from the general outpatient clinics, which were seronegative for HBsAg. Serum HBsAg tests were carried out using LAB ACON test kits. Subjects were scanned using Canon medical system Xario 200 (2014) ultrasound scan machine with a 3–5 MHz multivariable curvilinear transducer with Doppler capability.
Having obtained clearance from the ethical committee of the institution, informed consent was obtained from the subjects. The study was explained to the subjects that met the inclusion criteria. The consent form was read out and explained (where necessary) and duly signed by participants and their witnesses. Questionnaires were then administered where the research participants' bio data and demographic data such as age, sex and duration of illness were recorded. Data obtained from ultrasonography, namely, portal vein velocity and portal vein cross-sectional area were then recorded on the datasheet. Then, the subject's weight and height were measured using a stadiometer and recorded on the data sheet.
All patients were studied in the morning following an overnight fast and at rest in supine position with the abdomen properly exposed and the head supported on a pillow. Ultrasound coupling gel was applied on the abdomen and the transducer was placed at the subcostal level in the midline to commence scanning. The portal vein was accessed either through a subcostal approach with the transducer directed posterio-caphalad or through the right intercostal approach with the transducer directed medially. All measurements were obtained during quiet respiration.
The portal vein can be identified by its hyperechoic walls on grey scale scan visible on grey scale ultrasound, its characteristic low velocity and typical waveform on Doppler interrogation compared to the anterior hepatic artery coursing next to it. It is formed by the union of the splenic and superior mesenteric vein posterior to the neck of the pancreas. On colour Doppler evaluation, the portal vein shows smooth fill in of colour at low gain. Furthermore, on pulsed Doppler, the portal vein shows continuous low-velocity waveform with respiratory variation, while hepatic artery shows a low resistance waveform with systolic and diastolic components. The Doppler angle was set between 55° and 60°, pulse repetition frequency at 4 kHz and wall filter at 100 Hz. The portal vein velocity measured was the time-averaged mean velocity, which is determined electronically with the software package of the ultrasound machine. Flow velocity data were obtained, while scanning the extra hepatic portal vein along its longitudinal axis at about the midpoint distal to the union of the splenic and superior mesenteric vein and proximal to its bifurcation at the porta hepatitis. The sample volume was set on the middle of the portal vein trunk [Figure 1].
|Figure 1: Measurement of the portal vein cross-sectional area: The portal vein cross-sectional area was measured on the B-mode grey scale image of the portal vein while scanning perpendicular to the long axis of the portal vein at a point which was about midway between the confluence of the splenic and superior mesenteric vein, and bifurcation of the portal vein during quiet inspiration|
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The portal vein cross sectional area was calculated using the formula Cross sectional area = (A × B) × 3.14159/4. Where A is the longitudinal axis of the portal vein, B is the axial axis of the portal vein and π= 3.14159. The portal vein congestion index (PVCI) was calculated as follows: Portal vein cross sectional area/Portal vein flow velocity [Figure 2].
|Figure 2: The portal vein cross-sectional area and flow velocity measured three consecutive times to minimise intra-observer variability and the mean value recorded. Wipes were used to wipe off the gel after the study. The portal vein cross-sectional area was calculated using the formula: Cross sectional area = (A × B) × 3.14159/4. Where A is the longitudinal axis of the portal vein, B is the axial axis of the portal vein and π= 3.14159. The portal vein congestion index was calculated using the formula: Congestion index = Portal vein cross sectional area/ Portal vein flow velocity|
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Continuous variables are summarised using mean or median, standard deviation and range. Ultrasonography parameters in patients with chronic HBV and apparently healthy controls were compared for significant differences using t-test. The correlation between portal vein congestion index and duration of illness was assessed using Pearson's correlation. The level of significance was set at P < 0.05. The data were analysed using the IBM Statistical Package for the Social Sciences (SPSS) Version 23.0 statistical software (SPSS) Inc, Chicago, Illionois, USA.
| Results|| |
A total of 124 persons were scanned during the study period. Sixty-two (50%) of these were chronic HBV patients and an equal number were healthy controls. The chronic HBV patients were aged 18–70 years with a mean age of 40.5±11.2 years, and healthy controls were aged 18–65 years with a mean age of 39.9±10.3 years. Forty-seven (75.8%) of the chronic HBV patients were male, while 46 (74.2%) of the healthy controls were male [Table 1].
There was no statistically significant difference of the portal vein congestion index between males and females in the control group P = 0.793. The mean body mass index (BMI) of chronic HBV patients was 24.71±3.10 and the mean BMI of healthy controls was 24.86±4.22 [Table 2].
PVCI in controls ranged from 0.03 to 0.07 cm, with a mean value of 0.048±0.010 cm, while the PVCI in patients with chronic HBV ranged from 0.03 to 0.17 cm, with a mean value of 0.077±0.028 cm (P < 0.001) [Table 3].
In controls, cross-sectional area of the portal vein ranged between 0.51 and 1.35 cm2, with a mean value of 0.88±0.18 cm2. However, in chronic HBV patients, the cross-sectional area of the portal vein ranged between 0.46 and 1.95 cm2, with a mean value of 1.05±0.28 cm2 (P < 0.001) [Table 3]. The mean of the portal vein mean flow velocity in controls was 18.37±2.04 cm/s and ranged between 14.50 and 24.20 cm/s, while the mean of the portal vein mean flow velocity was 14.51±3.17 cm/s in chronic HBV patients and ranged between 7.40 and 20.40 cm/Sec (P < 0.001) [Table 3].
Amongst chronic HBV patients, 14 (23%) had previous treatment for chronic HBV, and 48 (77%) had no previous treatment for chronic HBV [Figure 3]. The mean portal vein congestion index in patients with chronic HBV who had treatment was 0.059±0.026, while the mean of the portal vein congestion index in patients with chronic HBV who had no treatment was 0.083±0.026 and P = 0.005. PVCI was significantly lower in patients that received treatment compared to those that did not receive any treatment (P = 0.005).
|Figure 3: Previous treatment amongst chronic HBV patients HBV = Hepatitis B virus|
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Patients with chronic HBV infection reported duration of illness ranging from 0.5 to 15 years, with a mean of 3.63 years [Figure 4]. There was a weak negative correlation between PVCI and duration of illness (r = −0.130 P = 0.313).
|Figure 4: Scatter plot of the portal vein congestion index and duration of illness|
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| Discussion|| |
There was no statistically significant difference in all the ultrasound parameters in male and female healthy subjects (P = 0.793). This is in contrast to the findings reported in a study. from Zaria northern Nigeria, which revealed significantly higher mean values of the portal vein cross-sectional area and congestion index in males compared to females amongst apparently healthy subjects (P < 0.001). This difference could be accounted for by the fact that unlike in this study with males making up about 74.2% and females 25.8%, there were more females (51.6%) than males (48.4%) in the study done in Zaria. On the other hand, the PVCI in male patients with chronic hepatitis were significantly higher compared to female patients with chronic HBV infection in the present study (P = 0.026).
The mean value of the normal PVCI in this study was found to be 0.048±0.010 cm with a range of 0.03–0.07 cm. In contrast, another study reported a normal PVCI ranging from 0.0587 to 0.0857 cm, with a mean value of 0.0722 cm (n = 186). Another study done in Japan reported a mean PVCI of 0.070±0.029 cms (n = 85). However, the median PVCI in normal population was 0.021 with 1st quartile of 0.015 and 4th quartile of 0.029. The difference in sample size, inter-observer variability and the different type of ultrasound machine used for measurements may have accounted for the difference in values. In a study on inter-observer and inter-equipment variability of echo Doppler examination of the portal vein, it was revealed that a significant systematic variability exists between Doppler measurements of the portal vein flow velocity with different equipment. Furthermore, it was observed that Doppler indices of the portal and splenic vein showed significant inter-equipment variability even when the same technique of measurement was used.
The mean PVCI in patients with chronic HBV infection was 0.077±0.028 cm with a range of 0.03–0.17 cm. Thus, the present study revealed statistically significant difference between portal vein congestion index in patients with chronic HBV infection and healthy controls (P < 0.05). This can be explained by the fact that as chronic liver disease such as chronic HBV infection progresses, there is a growing obstruction to portal venous flow at the level of the sinusoids, the portal vein flow obstruction is initially compensated for by increasing dilation of the portal vein, while its flow velocity decreases. The ratio between portal vein cross-sectional area and mean velocity, called the congestion index, is thus increased in chronic liver disease., Later, the portal vein diameter returns to normal or becomes small as progressive portosystemic collaterals develop.
A literature search at the time of carrying out this study revealed no reports exclusively comparing PVCI in adults with chronic viral hepatitis B to apparently healthy uninfected adults. However, a similar study comparing congestion index of the portal vein in adults with chronic viral hepatitis B or chronic viral hepatitis C infection to apparently healthy adults had been conducted. The study carried out in India reported a median congestion index of 0.050 cm with 1st quartile 0.030 cm and 4th quartile 0.070 cm for patients with either chronic hepatitis B or C. While a median congestion index of 0.021 cm with 1st quartile of 0.015 cm and 4th quartile of 0.029 cm was found in controls (P < 0.01). Thus illustrating a significant difference in the congestion index between the normal population studied, and the chronic viral hepatitis group. This implies that portal vein haemodynamics is significantly altered in patients with chronic viral hepatitis B and C. The difference observed between the two groups is in agreement with the present study.
In a study in which PVCI was determined and compared between normal subjects and patients with chronic active hepatitis amongst other groups, demonstrated statistically significant differences between the congestion indices obtained. The PVCI was shown to be higher in chronic active hepatitis (0.119±0.084 cm2) compared to normal subjects (0.070±0.029 cm2), r = 0.45 and P < 0.01. It is important to note that the descriptive term 'chronic active hepatitis' used in the study was a class of chronic hepatitis based on an outdated general classification of chronic hepatitis that is no longer in use, and it represented various causes of severe chronic hepatitis including viral and autoimmune causes.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]