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 Table of Contents  
Year : 2020  |  Volume : 1  |  Issue : 1  |  Page : 43-47

Prevalence of portal vein thrombosis in patients with chronic liver disease using triphasic computed tomography scan as diagnostic modality: A study in Jos, North-Central, Nigeria

1 Department of Radiology, Faculty of Clinical Sciences, College of Health Sciences, University of Jos, Plateau State, Nigeria
2 Department of Radiology, Jos University Teaching Hospital, Gwagwalada, Abuja, FCT, Nigeria
3 Department of Radiology, University of Abuja, Gwagwalada, Abuja, FCT, Nigeria

Date of Submission19-Jun-2020
Date of Decision01-Jul-2020
Date of Acceptance14-Jul-2020
Date of Web Publication25-Sep-2020

Correspondence Address:
Dr. Samuel Moses Danjem
Department of Radiology, Faculty Clinical Medical, University of Jos, Plateau State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JRMT.JRMT_15_20

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Background: Portal vein thrombosis (PVT) is one of the complications of chronic liver disease (CLD), and the prevalence varies from country to country as well as the method utilized in determining the presence of the thrombosis. Objective: The present study was aimed at determining the prevalence of PVT in patients with CLD in our locality using triphasic computed tomography as a diagnostic modality. Materials and Methods: This was a retrospective study. The triphasic computed tomography scan of the abdomen of 121 patients from January 2019 to April 2020 was retrieved and reviewed for the presence of PVT. Results: The mean age for the study population was 54.4 ± 13.4 years with age range of 22–100 years. Out of the 121 patients, 46 patients had PVT constituting the prevalence of 38.0%. The PVT is more in males (80.4%) than females (19.6). The thrombosis is more in the age group of 41–50 years. Conclusion: There is a high prevalence of PVT in our locality possibly because patients present in the later stage of CLD. PVT is associated with ascites and multiple hepatic masses.

Keywords: Chronic liver disease, portal vein thrombosis, triphasic computed tomography

How to cite this article:
Danjem SM, Salaam A J, Iroha U, Gabkwet A E, Igoh E O, Taiwo Y F, Kolade-Yunusa H O. Prevalence of portal vein thrombosis in patients with chronic liver disease using triphasic computed tomography scan as diagnostic modality: A study in Jos, North-Central, Nigeria. J Radiat Med Trop 2020;1:43-7

How to cite this URL:
Danjem SM, Salaam A J, Iroha U, Gabkwet A E, Igoh E O, Taiwo Y F, Kolade-Yunusa H O. Prevalence of portal vein thrombosis in patients with chronic liver disease using triphasic computed tomography scan as diagnostic modality: A study in Jos, North-Central, Nigeria. J Radiat Med Trop [serial online] 2020 [cited 2023 Jun 3];1:43-7. Available from: http://www.jrmt.org/text.asp?2020/1/1/43/296109

  Introduction Top

Portal vein thrombosis (PVT) refers to the formation of clot within the trunk of the portal venous draining into the liver which is characterized by partial or complete halting of normal blood flow to the liver. It is vital to understand the anatomy of the portal vein to know where the thrombus is formed as well as where it is distributed. The portal vein is a valveless conduit which originates as confluence of the superior mesenteric and the splenic veins behind the pancreatic neck from where it course to the porta hepatis and divides into the right and the left main branches. The portal vein supplies 75% of blood flow to the liver.[1] Thrombus can form in any vein and as well as its tributaries and branches.

The prevalence of PVT varies from country to country as well as the methods utilized in determining the presence of the PVT and also depending on the disease entity under consideration. PVT is reported to be a relatively rare disease entity possibly because the reports were based on clinical suspicion, case reports, and autopsy when it is suspected. Kumar et al.[2] reported a prevalence of 1% in the general population by an autopsy-based study. However, due to the increase in the use of technically advanced noninvasive liver imaging modalities such as Doppler ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI), PVT has been increasingly identified in patients with cirrhosis and hepatocellular carcinoma (HCC), with the estimated current prevalence of PVT in patients with cirrhosis put at 0.6%–26%.[3],[4]

Studies based on ultrasonography results reported a prevalence of 10%–28% in cirrhotic patients, excluding those with HCC.[4] The prevalence of PVT in liver transplant candidates (recipient) is said to be similar to that in other cirrhotic patients with the same degree of liver disease, although model for end-stage liver disease and child-Pugh scores was higher in patients with PVT confirming the fact that PVT prevalence increases with the severity of liver cirrhosis. Thus, PVT prevalence was reported to be low (1%) in compensated liver cirrhosis and up to 28% in decompensated liver cirrhosis.[5],[6],[7] The association between liver cirrhosis and malignancies, such as HCC, may increase PVT prevalence up to 44%.[6]

The increasing cases of hepatitis in our environment with resultant cirrhosis as well as malignant transformation has led to more request for Triphasic CT to evaluate patients who presented with suspected case of HCC and liver cirrhosis. As mentioned earlier, Doppler ultrasound is a noninvasive imaging modality that is used for the evaluation of PVT; however, the tributaries such as the superior mesenteric and the splenic veins for thrombus may be difficult to assess by ultrasound due to distortion of the normal anatomy by the enlarged liver, overlying bowel gasses, and gross ascites. Contrast-enhanced CT and MRI are good modalities that provide better assessment of the venous system for thrombosis, but MRI is not readily available and its affordability is another major issue.

Few studies were carried out in Nigeria using radiological imaging to corroborate the incidence of PVT that was reported elsewhere. The aim of this study is to determine the prevalence of PVT in patients with chronic liver disease (CLD) (such as cirrhosis or HCC) using Triphasic CT scan and to compare our findings with those previously reported.

  Materials and Methods Top

This was a retrospective study of 121 patients referred to the radiology department with suspected CLD ranging from hepatic cystic lesions, chronic hepatitis infection to cirrhosis, and HCC who underwent triphasic CT examination of the abdomen between January 2019 and April 2020. The study was approved by the Research and Ethical Committee of the hospital.

Technique: All examinations were performed using a 16 slice CT machine (Brivo, general electric (GE), USA). For all three phases, section thickness, collimation, and reconstruction interval were adjusted as 5 mm (120Kvp, 180 mAs). We used 100–110 ml of nonionic iodinated contrast material containing 300 mg/ml of iodine was administered intravenously at a rate of 3.5 ml/s. Images were acquired in triphasic sequences; arterial at 28–35 s, Porto-venous phase at 60–70 s, and delayed phase at 5–10 min all in axial planes and were reformatted in coronal and sagittal planes.

Inclusion criteria were: patients over 18 years of age who had triphasic CT scan and those with hepatic pathologies.

All the 121 triphasic CT images were retrieved and retrospectively reviewed on a GE Advantage Windows 4.4 CT Workstation by a consultant radiologist with more than 5 years' experience. The information recorded from the CT images include the presence of hepatic mass which were grouped into nil, single, and multiple for those with hepatic mass; the presence of thrombus along the portal vein [Figure 1]. PVT was identified as a hypodense filling defect with Hounsfield unit (HU) higher than that of blood in the portal vein in all the contrast enhanced and the native phases of the study. Using the key findings of PVT on contrast enhanced CT as defined by Deleve et al.,[8] HU measurement aids to eliminate the pitfall of streaming effect arising from blood flow. Other information documented were the presence of ascites.
Figure 1: Triphasic computed tomography scan of a 52-year-old male patient showing a filling defect in the right main portal vein as a hypodense (hounsfield unit = 23) in precontrast phase; (a) In arterial phase (34 hounsfield unit); (b) portovenous phases (60 Hounsfield unit). (c) Ill-defined masses are seen elsewhere in the liver parenchyma (blue arrow). The patient has ascites

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Statistical analysis was performed using the SPSS version 21.0 software (SPSS Inc., Chicago, IL, USA). Quantitative data are described as the mean and standard deviation or median and range where appropriate. Qualitative data are described in percentages. The Chi-square test was used to compare the proportions, and t-Student tests were used to compare the means. Differences were considered to be statistically significant when the P < 0.05.

  Results Top

A total of 121 triphasic CT scans of patients were retrospectively reviewed with age ranging from 22 to 100 years, with a mean age of 54.4 ± 13.4 years. Thirty-five (28.9%) patients were in the age group of 51–60 years, whereas 5 (4.1%) patients were in the age <30 years who had triphasic CT scan for suspected liver pathologies. Eighty-eight (72.7%) of the patients were males, whereas 33 (27.3%) were females with a male-to-female ratio of 2.7:1 [Table 1].
Table 1: Demographic characteristics of patients who had triphasic computed tomography scan as well as the association between demographic characteristics of study population and portal vein thrombosis

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As shown on [Table 1] and [Figure 2], 46 (38.0%) patients had PTV, whereas 75 (62.0%) of patient had no PVT. Among the 46 patients with PVT, 9 (19.6%) were female and 37 (80.4%) were male [Table 1] and [Figure 2].
Figure 2: Pie chart showing the sex distribution of patients with portal vein thrombosis

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[Table 1] also shows the association between the age group distribution of the study population and PVT. There were more patients with thrombosis in the younger age groups from ≤30 years, 31–40 years, and the middle age groups 41–50 years than those without thrombosis in each of the age groups, respectively. While for the age groups 51–60 years, 61–70 years, and ≥71 years, there were more patients without thrombosis when compared to those with thrombosis. This was statistically significant (P = 0.041). The table also shows that age groups 41–50 years have the highest number of thrombosis.

Out of the 46 patients with PVT, 34 (73.9%) patients had ascites, whereas 12 (26.1%) patients had no ascites. There is association between PVT and ascites which was statistically significant (χ2 = 10.522, P = 0.001) [Table 2].
Table 2: Association between triphasic computed tomography findings and portal vein thrombosis

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The triphasic CT findings of patients with PVT showed that 1 (2.2%) patient had no mass (liver cirrhosis), 5 (10.9%) patients with PVT had single liver mass, whereas 40 (87.0%) patients with PVT had multiple hepatic masses. The association between multiple hepatic masses and PVT was statistically significant (χ2 = 60.043, P = 0.001) [Table 2].

  Discussion Top

Triphasic CT scan is one of the common investigations that are performed to evaluate suspected cases of CLD which results to cirrhosis and primary HCC because of its sensitivity in detecting thrombosis. Hence, triphasic CT was used in our study to determine the prevalence of patients who underwent the scan in the radiology department. The mean age for our study population was 54.4 ± 13.4 years. Similarly, Rajani et al.[9] also observed that PVT presented at the time of diagnosis in younger age with a mean age of 54 years in noncirrhotic patients when compared to those with cirrhosis. Hernandez-Conde et al.[10] also reported the mean age of 55 years in a similar study carried out in Madrid, Spain, to determine the prevalence and outcome of portal thrombosis in a cohort of cirrhotic patients undergoing liver transplantation. In consonant with our finding, Cruz-Ramón et al. in Mexico city, Mexico, reported a mean age of 57 years of patients who had PVT.[11]

In our study, there were more males who had triphasic CT scan than their female counterparts with the males constituting 80.4%, whereas the females constitute 19.6%. This could be that the males are exposed to hepatitis infections, and they are indulged in the consumption of alcohol which predisposes them to having CLD. The difference in sex distribution was also observed by Hernadez-Conde et al. who documented 75.4% of males and 24.6% of females in their study.[10]

The prevalence and incidence of PVT are said to vary among different studies because of the heterogeneity in the diagnosis methods (clinically, using imaging, during surgery for transplantation or at autopsy), different populations and variable follow-up time. The prevalence as reported by different authors range from 0.6% to 28%.[3],[12],[13]

In our study, the prevalence of PVT was 38.0% which is higher than the 11.2% and 10.7% prevalence documented by Amitrano et al.[3] and Nery et al.,[13] respectively, in ultrasonography-based studies. This is possibly because we used triphasic CT scan as a diagnostic imaging modality for making the diagnosis of PVT which is more sensitive in detecting PVT when compared with ultrasonography used by those authors.

PVT prevalence is said to increase with the severity of liver cirrhosis and presence of HCC. Thus, PVT prevalence was reported as low as 1% in compensated liver cirrhosis and up to 28% in decompensated liver cirrhosis.[5],[6],[7] In our locality, patients with liver disease present late, and they have to pay out of pocket for basic investigation in a country where there is extreme poverty, thus many of the patients in our study population have already undergone malignant transformation (HCC). This could also explain why the prevalence in our study is higher than those studies carried out elsewhere where the patients present much earlier and receive better health care. Similar to our study, Raja et al.[5] suggested that the association between liver cirrhosis and malignancies, especially HCC, may increase PVT prevalence up to 44%.

In a retrospective study of 150 patients with viral cirrhosis, the cumulative overall incidences of PVT were 12.8% at 1 year, 18.6% at 3 years, 20% at 5 years, and 38.7% at 8–10 years, respectively.[14] This explains the heterogeneity of PVT.

We observed that PVT is more common in men than in women with 37 (80.4%) males and 9 (19.6%) females with PVT out of the 46 patients with the thrombosis, which is consistent with data from Hernandez-Conde et al.[10] who also observed similar variation in the sex distribution of patients having PVT with males having 77.8% and females 22.2%. This could be explained by the fact that in the overall study population, there were more males who had The CT scan than the females.

We also found out that the younger age groups with liver cirrhosis and HCC are more prone to having PVT than the older patients. The preponderance for the younger patients could possibly be attributed to the fact that the younger patients are more likely to indulge in alcohol consumption more than the older patients, which further damages the liver resulting in defective platelet function which may predispose them to thrombus formation.

Patients with CLD and PVT may have complication such as ascites. The presence of ascites is an important factor that contributes to mortality and determines the choice of treatment modality such as transarterial chemoembolization and other modes of treatment such as ablation. Previous studies have reported that ascites is a common complication of portal hypertension.[15],[16] From our study, PVT was associated with ascites in most of the patients. Our finding is in consistent with Spaander et al.[17] who found ascites in approximately a quarter of all the patients at the time of diagnosis.

From our study, there was significant association between PVT and the number of hepatic masses. The association of tumor burden with PVT is also corroborated in other studies.[3],[12],[13]

The sample size is small in our study which is a limitation. We recommend that a larger multicenter study should be carried out to corroborate our findings and to also serve as reference.

  Conclusion Top

We found the prevalence of PVT to be 38.0%. We also reported that PVT is associated with ascites and tumor burden.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Manzano-Robleda Mdel C, Barranco-Fragoso B, Uribe M, Méndez-Sánchez N. Portal vein thrombosis: What is new? Ann Hepatol 2015;14:20-7.  Back to cited text no. 1
Kumar A, Sharma P, Arora A. Review article: Portal vein obstruction – Epidemiology, pathogenesis, natural history, prognosis and treatment. Aliment Pharmacol Ther 2015;41:276-92.  Back to cited text no. 2
Amitrano L, Guardascione MA, Brancaccio V, Margaglione M, Manguso F, Iannaccone L, et al. Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis. J Hepatol 2004;40:736-41.  Back to cited text no. 3
Tsochatzis EA, Senzolo M, Germani G, Gatt A, Burroughs AK. Systematic review: Portal vein thrombosis in cirrhosis. Aliment Pharmacol Ther 2010;31:366-74.  Back to cited text no. 4
Raja K, Jacob M, Asthana S. Portal vein thrombosis in cirrhosis. J Clin Exp Hepatol 2014;4:320-31.  Back to cited text no. 5
Francoz C, Valla D, Durand F. Portal vein thrombosis, cirrhosis, and liver transplantation. J Hepatol 2012;57:203-12.  Back to cited text no. 6
Kinjo N, Kawanaka H, Akahoshi T, Matsumoto Y, Kamori M, Nagao Y, et al. Portal vein thrombosis in liver cirrhosis. World J Hepatol 2014;6:64-71.  Back to cited text no. 7
DeLeve LD, Valla DC, Garcia-Tsao G. Vascular disorders of the liver. Hepatology 2009;49:1729-64.  Back to cited text no. 8
Rajani R, Björnsson E, Bergquist A, Danielsson A, Gustavsson A, Grip O, et al. The epidemiology and clinical features of portal vein thrombosis: A multicentre study. Aliment Pharmacol Ther 2010;32:1154-62.  Back to cited text no. 9
Hernandez-Conde M, Elba L, Juan R, Fernando P, Natalia FP, José LM, et al. Prevalence and outcome of portal thrombosis in cirrhotic patients undergoing liver transplant. Rev Esp Enferm Dig 2016;108:716-20.  Back to cited text no. 10
Cruz-Ramón V, Chinchilla-López P, Ramírez-Pérez O, Aguilar-Olivos NE, Alva-López LF, Fajardo-Ordoñez E, et al. Thrombosis of the portal venous system in cirrhotic vs. non-cirrhotic patients. Ann Hepatol 2018;17:476-81.  Back to cited text no. 11
Blachier M, Leleu H, Peck-Radosavljevic M, Valla DC, Roudot-Thoraval F. The burden of liver disease in Europe: A review of available epidemiological data. J Hepatol 2013;58:593-608.  Back to cited text no. 12
Nery F, Chevret S, Condat B, de Raucourt E, Boudaoud L, Rautou PE, et al. Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: Results of a longitudinal study. Hepatology 2015;61:660-7.  Back to cited text no. 13
Maruyama H, Okugawa H, Takahashi M, Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: Predictive factors and long-term outcomes. Am J Gastroenterol 2013;108:568-74.  Back to cited text no. 14
Runyon BA; Practice Guidelines Committee; American Association for the Study of Liver Diseases (AASLD). Management of adult patients with ascites due to cirrhosis. Hepatology 2004;39:841-56.  Back to cited text no. 15
Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology 2001;120:726-48.  Back to cited text no. 16
Spaander MC, van Buuren HR, Hansen BE, Janssen HL. Ascites in patients with noncirrhotic nonmalignant extrahepatic portal vein thrombosis. Aliment Pharmacol Ther 2010;32:529-34.  Back to cited text no. 17


  [Figure 1], [Figure 2]

  [Table 1], [Table 2]


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