|Year : 2019 | Volume
| Issue : 4 | Page : 335-339
Ultrasound in acute viral hepatitis: Does it have any role?
Vinay Maurya, R Ravikumar, Manoj Gopinath, Birma Ram
Department of Radiology, Command Hospital, Kolkata, West Bengal, India
|Date of Submission||06-Dec-2018|
|Date of Acceptance||27-Feb-2019|
|Date of Web Publication||8-Jul-2019|
Department of Radiology, Command Hospital, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
Background: The role of ultrasound in acute viral hepatitis (AVH) is limited to exclude the surgical causes of jaundice. However, there are certain ultrasound features which can help us to suspect AVH in the initial few days before the onset of clinical jaundice. Therefore, the aim of the present study was to detect the changes in the hepatobiliary system on ultrasound in the cases of AVH and to find the significance of these ultrasound findings by comparing them with controls. Materials and Methods: All serologically proven cases of enterically transmitted cases of AVH formed the study group and all healthy patients with clinical diagnosis of lower urinary tract symptoms who had no hepatobiliary disease were taken as controls. Results: Out of 120 cases, 102 cases were male and 18 cases were female. Maximum number of cases 54 (45%) were seen in 21–30 followed by 24 cases (20%) in the age group of 31–40 years. Hepatomegaly was seen in 104 (86.6%) of cases and 38 (25.3%) of controls (P < 0.01). Gall bladder (GB) wall thickening was seen in 91 (75.8%) of cases and 22 (14.6%) controls Contracted GB was seen in 75 (62.5%) cases of AVH and 16 (10.6%) of controls (P < 0.01). Porta nodes were seen in 72 (60%) cases and 15 (10%) controls (P < 0.01). Splenomegaly was seen in 33 (27.5%) of cases and 24 (16%) of controls. Periportal cuffing was seen in 28 (23.3%) of cases and 24 (16%) of controls. Conclusion: The ultrasound findings of hepatomegaly, enlarged porta hepatis nodes, contracted gallbladder and GB wall thickening are significant suggesting a role of ultrasound in the early diagnosis of acute viral hepatitis.
Keywords: Acute viral hepatitis, role, ultrasound
|How to cite this article:|
Maurya V, Ravikumar R, Gopinath M, Ram B. Ultrasound in acute viral hepatitis: Does it have any role?. Med J DY Patil Vidyapeeth 2019;12:335-9
|How to cite this URL:|
Maurya V, Ravikumar R, Gopinath M, Ram B. Ultrasound in acute viral hepatitis: Does it have any role?. Med J DY Patil Vidyapeeth [serial online] 2019 [cited 2020 Jan 21];12:335-9. Available from: http://www.mjdrdypv.org/text.asp?2019/12/4/335/262236
| Introduction|| |
Acute viral hepatitis (AVH) is an inflammation of the liver due to viral infection. Almost all cases of viral hepatitis are caused by one of five viral agents: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), the HBV-associated delta agent or hepatitis D virus, and hepatitis E virus  (HEV). The clinical presentation and laboratory tests are sufficient to clinch the diagnosis of acute viral hepatitis. The use of diagnostic ultrasound has been limited to exclude the surgical causes of jaundice in patients who present with a cholestatic picture, suggesting extrahepatic biliary obstruction. The aim of this study was to detect the changes in the hepatobiliary system in cases of AVH and to find the significance of these ultrasound findings by comparing them with controls.
| Materials and Methods|| |
The study was conducted in the Department of Radiology at a tertiary care hospital.
This was prospective case–control study.
Patients presenting clinically with jaundice underwent detailed clinical examination and based on clinical diagnosis were worked up for viral hepatitis and subjected to relevant serological and liver function tests and ultrasound examination prospectively. All serologically proven cases of enterically transmitted viral hepatitis, i.e., HAV and HEV from August 3, 2016 to August 5, 2018 were included as cases in the study.
Patients reporting for ultrasound examination with the complaints of dysuria, burning or frequency of micturition, and symptoms of urinary tract infection who had no hepatobiliary disease were taken as controls during the same period.
- Patients detected to have HBV and HCV infection were excluded from the study as they are not enterically transmitted and also cause chronic hepatitis
- Patients with gall stone disease were also excluded from the study.
All patients in the study group underwent ELISA test for detection of IgG and IgM antibodies of HAV and HEV, respectively, and liver function tests which included serum bilirubin, serum alanine transaminase, aspartate transaminase, and alkaline phosphatase.
Both the study group and controls were instructed to report on an empty stomach after overnight fasting. All ultrasound examinations were done on GE Logiq P5 machine by two radiologists of >10 years' experience. The cases and controls were randomly assigned to both the radiologists who were blinded to each other's findings. All cases in the study group were recorded for age, sex, serology for the virus, and liver function test.
All cases and controls were scanned in supine and both lateral decubitus positions. Ultrasound findings were analyzed systematically for gall bladder (GB) distension and wall thickness, liver and splenic size, periportal cuffing, and lymph nodes at porta hepatis.
The liver was considered to be enlarged if the size was >15.5 cm in the midclavicular line. Spleen size >12 cm was considered as splenomegaly. Periportal cuffing was considered to be present when there were increased brightness and clear visualization of portal vein radicle walls. Lymph nodes at porta hepatis were evaluated for size, discrete or matted, and echogenicity. Partially distended or empty GB in the fasting state indicated the reduced volume of the GB. The gall bladder wall thickening which was diffuse and >3 mm was considered statistically significant.
Sonographic data were collected and tabulated in an Excel sheet was analyzed using IBM Statistical Packages for Social Sciences 22 (Armonk, New York, USA) to determine the means and proportions. Chi-squared test was used to compare the ultrasound findings in two groups. P < 0.01 were considered to indicate a statistically significant difference. Interobserver variability Kappa was calculated for different ultrasound findings.
Informed consent was obtained from the study group and controls and permission from the Institutional Ethical committee was obtained for the study (Command Hospital, Kolkata, letter number 2818/CHEC/IEC/RAD, dated 06 June 2016). The identity of patients was kept confidential.
| Results|| |
During the study period ranging from August 3, 2016 to August 5, 2018, 142 cases of suspected AVH underwent ultrasound examination of the abdomen but only 120 cases met our inclusion criteria. Out of 120 cases of AVH 102 cases were male and 18 cases were female with male-to-female ratio of 5.6:1. Out of 150 controls, 112 were male and 38 were female with M:F ratio of 2.9:1. Maximum numbers of cases 54 (45%) were seen in 21–30 followed by 24 (20%) of cases in 31-40 year age group [Table 1]. The youngest patient was 5-year-old boy, and the oldest patient was 64-year-old male. Hepatomegaly was seen in 104 (86.6%) of cases and 38 (25.3%) of controls with P = 0.000 and χ2 = 100. 5 [Table 2]. Gall bladder wall (GBW) thickening was seen in 91 (75.8%) of cases and 22 (14.6%) controls with P = 0.000 and χ2 = 102. 5 [Table 2]. Contracted GB was seen in 75 (62.5%) cases of AVH and 16 (10.6%) of controls with P = 0.000 and χ2 = 80. 1 [Table 2]. Porta nodes were seen in 72 (60%) cases and 15 (10%) controls with P = 0.000 and χ2 = 76. 3 [Table 2]. Splenomegaly was seen in 33 (27.5%) of cases and 24 (16%) of controls with P = 0.0214 and χ2 = 5.3 [Table 2]. Periportal cuffing was seen in 28 (23.3%) of cases and 24 (16%) of controls with P = 0.129 and χ2 = 2.3 [Table 2]. The interobserver variability kappa for hepatomegaly was κ = 0.838, GB wall thickening (κ = 0.879), contracted GB (κ = 0.890), porta nodes (κ = 0.875), splenomegaly (κ = 0.862), and periportal cuffing was κ = 0.849 [Table 2].
| Discussion|| |
The incidence of viral hepatitis in India is not well known. The national Integrated Disease Surveillance Programme which conducts surveillance across all Indian states for epidemic-prone diseases reported a total of 804,782 viral hepatitis cases  during 2011–2013. Sporadic cases and outbreaks of enteric borne AVH are very common in India, especially in monsoon season. HAV and HEV are transmitted by feco–oral route through contaminated food and water. In India, HEV is the most common cause of acute hepatitis. The incubation period of HAV and HEV is 14–28 days and 2–10 weeks, respectively, with an average incubation period of HAV being 28 days and 5–6 weeks for HEV. Once the patient becomes symptomatic, the presentation is so distinct that it poses no difficulty in diagnosing the case clinically. Liver function tests give a fair idea about the severity of hepatitis. However, the definitive diagnosis is based on detection of specific IgM antibodies to the virus present in patients' blood. The role of ultrasound in these patients is limited to ruling out surgical causes of jaundice.
However, there are definite sonographic features, which point toward the diagnosis of viral hepatitis even before the onset of clinical jaundice. These sonographic features are seen for a period of 7–10 days from the onset of the symptoms. These ultrasound features can strengthen the clinical diagnosis of AVH before the final confirmation by the laboratory. Sonographic features which are observed in AVH are hepatomegaly, GB wall thickening, contracted GB on fasting scans, porta hepatitis nodes, splenomegaly, and periportal cuffing.
Hepatomegaly or liver enlargement is not a specific finding of AVH, but it is the most common finding in cases of AVH since it is a systemic infection affecting the liver mainly. Pathological changes in all types of viral hepatitis are alike and comprise panlobular infiltration with mononuclear cells, hyperplasia of Kupffer cells, hepatic cell necrosis and variable degrees of cholestasis. Maximum liver enlargement recorded in this study was 20 cm in the midclavicular line. The incidence of hepatomegaly during icteric stage has been reported as 70% though Nandi et al. found hepatomegaly in all of their cases of HAV and HEV infection on clinical examination. In this study, hepatomegaly was seen in 104 (86.6%) cases with P < 0.001 which is significant as hepatomegaly was seen in only 38 (25.3%) of controls. Splenomegaly is seen in 10%–20% of cases of viral hepatitis, the incidence of splenomegaly in this study was 27.5%. The slightly higher incidence of splenomegaly could be because of the measurement of spleen on ultrasound, whereas other studies relied on clinical examination for diagnosing splenomegaly. This could be explained by the fact that splenic size was determined by ultrasound in this study, which has an objective criteria of diagnosing splenomegaly by measuring the craniocaudal extent in real-time mode. The finding is not significant as P = 0.0214 and cannot be taken as consistent finding in AVH. The cause of splenomegaly in viral hepatitis is probably immune complex-mediated and the spleen shows only mild enlargement. In this study the maximum splenic size recorded was 13.5 cm.
GB abnormalities in AVH have been described in the literature. These include thickening of the GBW, sludge in the lumen and change in the volume of GB or contracted gall bladder. In this study GBW thickening [Figure 1] was seen in 91 (75.8%) cases with P = 0.000 and χ2 = 102. 5. Sharma and Dasarathy  in their study of AVH cases found GBW thickening in 98.2% of the cases. There are many causes of GBW thickening which include acute cholecystitis, cirrhosis, Dengue fever, infectious mononucleosis, falciparum malaria, heart failure, severe malnutrition, ascites, and sepsis. Therefore, GBW is not specific to AVH, but it is very common in AVH and interpreted with other findings assumes importance in these cases. The mean GBW thickness was 6 mm with maximum thickness recorded as 11 mm. The thickened GBW showed multiple striations consisting of alternate hypoechogenic and hyperechogenic layers [Figure 1]. The GBW thickening in AVH is a fleeting finding seen within first 10 days of onset of symptoms and returns to normal as the patient recovers clinically.
|Figure 1: Ultrasound scan showing grossly thickened gallbladder wall with alternate hyper and hypoechogenic layers|
Click here to view
Contracted gallbladder in AVH is also a transient finding just like GBW thickening and has been well documented in various series. When a gallbladder is seen contracted with an apparently thickened wall in the fasting state, the diagnosis of parenchymal jaundice may be considered in appropriate clinical setting. This finding also lasts for a period of 7–10 days after the onset of symptoms and becomes normal as the patient recovers. The contracted GB was seen in 62.5% of cases and only in 10.6% of controls with P = 0.000 and χ2= 80. 1 [Figure 2]. The GBW thickening and lumen abnormalities are highly significant findings as they may be seen even before the appearance of clinical jaundice.
|Figure 2: High-resolution ultrasound scan showing contracted gallbladder with thickened wall|
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Enlarged porta hepatis lymph nodes have been reported as the most frequent ultrasound finding in acute viral hepatitis. The nodes are typically subcentimeter in size, discrete and oval in shape [Figure 3]. They are iso to hypoechoic and show preserved central echogenicity of fatty hilum. The porta hepatis lymph node enlargement was seen in 72 (60%) cases. The finding is significant (P < 0.001) as only 10% of normal controls showed enlarged nodes. Toppet et al. in their study of 58 children of acute Hepatitis A found enlarged porta hepatis nodes in all the cases. The plausible reason for detection of porta hepatis nodes is reactive enlargement secondary to inflammation in the liver.
|Figure 3: Ultrasound scan right hypochondrium showing sub centimeter discrete lymph node at porta hepatis with preserved fatty hilum (arrow)|
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The increased brightness and clear visualization of portal vein radicle walls are described as periportal cuffing. This distinctive “bright liver” pattern, correlates with significant vacuolar hepatocellular degeneration. It is very often seen in patients with fever due to any other cause. Periportal cuffing was seen in 28 (23.3%) cases in this study with P = 0.1289. This finding is not significant (P > 0.01) as it was also seen in 16% of normal controls.
In India, enterically transmitted viral hepatitis cases show increased incidence during pre-monsoon and monsoon season. Moreover, it is around this same time the infectious diseases such as malaria and dengue fever also surge. In endemic areas, the condition that mimics viral hepatitis both clinically and sonologically is malarial hepatitis due to plasmodium falciparum. In hepatitis due to falciparum malaria serum bilirubin and serum aminotransferases are raised and hepatosplenomegaly is also very common. Sonologically, gallbladder shows wall thickening and contracted appearance similar to that seen in acute viral hepatitis. The diagnosis of malarial hepatitis should be suspected sonologically if the splenic size is >14 cm and there is the absence of enlarged nodes at porta hepatis. These findings should be correlated with clinical and laboratory findings to arrive at a correct diagnosis to avoid mortality due to falciparum malaria.
Though all cases which were serologically positive for HAV and HEV were included in the study; however, it is possible that study may have been confounded by false-positive cases as they may have been included in the study inadvertently.
| Conclusion|| |
Enterically transmitted AVH occurs sporadically and in outbreaks in India though the diagnosis of AVH is made clinically supported by laboratory investigations. However, there are certain ultrasound findings such as hepatomegaly, enlarged nodes at porta hepatis, GBW thickening, and appearance of the contracted gallbladder in fasting state which when seen in appropriate clinical setting strongly favor the diagnosis of acute viral hepatitis. Therefore, it should be carried out in all patients clinically suspected to have AVH not only to rule out surgical obstructive jaundice but also to reinforce the diagnosis sometimes even before the clinical onset of jaundice.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for 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.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Dienstag JL. Acute viral hepatitis. In: Harrison's Principle of Internal Medicine. 20th
ed., Ch. 332. New York: McGraw Hill; 2018
Kumar T, Shrivastava A, Kumar A. Viral Hepatitis Surveillance -India 2011-13. Vol. 64. Atlanta: Centers for Disease Control and Prevention. 2015. p. 758-62.
Giorgio A, Amoroso P, Fico P, Lettieri G, Finelli L, de Stefano G, et al.
Ultrasound evaluation of uncomplicated and complicated acute viral hepatitis. J Clin Ultrasound 1
Nandi B, Hadimani P, Arunachalam R, Ganjoo RK. Spectrum of acute viral hepatitis in Southern India. Med J Armed Forces India 2009;65:7-9.
Sharma MP, Dasarathy S. Gallbladder abnormalities in acute viral hepatitis: A prospective ultrasound evaluation. J Clin Gastroenterol 1991;13:697-700.
Maresca G, De Gaetano AM, Mirk P, Cauda R, Federico G, Colagrande C, et al.
Sonographic patterns of the gallbladder in acute viral hepatitis. J Clin Ultrasound 1984;12:141-6.
Nardi P, Biagi P, Bocchini S. Enlargement of the lymph nodes of the hilus hepatis: A further ultrasonographic sign of acute viral hepatitis. Radiol Med 1990;79:212-4.
Toppet V, Souayah H, Delplace O, Alard S, Moreau J, Levy J, et al.
Lymph node enlargement as a sign of acute hepatitis A in children. Pediatr Radiol 1990;20:249-52.
Mishra SK, Mohanty S, Das BS, Patnaik JK, Satpathy SK, Mohanty D, et al.
Hepatic changes in P. Falciparum
malaria. Indian J Malariol 1992;29:167-71.
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]