DOI:10.2214/AJR.04.1189
AJR 2005; 185:1033-1035
© American Roentgen Ray Society
Unusual MDCT and Sonography Findings in Fulminant Hepatic Failure Resulting from Hepatitis A Infection
Banu Cakir1,
Mehmet Teksam1,
Nefise Cagla Tarhan1,
Iclal Isiklar1,
Nihal Uslu Tutar1,
Figen Ozcay2,
Mehmet Coskun1,
Banu Bilezikci3 and
Beyhan Demirhan3
1 Department of Radiology, Baskent University Faculty of Medicine, Fevzi Cakmak
Cad. 10. sok., No: 45 Bahcelievler, Ankara 06490, Turkey.
2 Department of Pediatric Gastroenterology, Baskent University Faculty of
Medicine, Ankara 06490, Turkey.
3 Department of Pathology, Baskent University Faculty of Medicine, Ankara 06490,
Turkey.
Received July 28, 2004;
accepted after revision October 15, 2004.
Address correspondence to B. Cakir.
Introduction
Fulminant hepatic failure is a severe liver injury that is associated with
encephalopathy and coagulopathy in persons without a history of liver disease.
Although hepatitis A virus infection tends to be self-limiting in childhood,
it has been shown to cause fulminant hepatic failure
[1]. CT and MRI findings have
been described in one study of three cases of fulminant hepatitis in the
radiology literature [2].
In this report, we describe the unusual sonography and MDCT findings in a
4-year-old boy with fulminant hepatitis A virus infection.
Case Report
A 4-year-old boy was transferred to our hospital from another hospital with
the diagnosis of fulminant hepatic failure resulting from a hepatitis A virus
infection of 3 weeks' duration. Before admission, he had been unconscious,
with involuntary tongue movements and abnormal flexion-extension of the legs.
On physical examination, icterus was identified, which had been present for 3
weeks. Liver function tests were all disturbed. The following values were
obtained: direct bilirubin level, 25.2 mg/dL (normal range, 0-0.25 mg/dL);
total bilirubin, 45 mg/dL (normal range, 0.2-1.2 mg/dL); aspartate
aminotransferase, 850 U/L (normal range, 0-40 U/L); alanine aminotransferase,
970 U/L (normal range, 0-40 U/L); alkaline phosphatase, 1,010 U/L (normal
range, 145-670 U/L); lactate dehydrogenase, 630 U/L (normal range, 180-430
U/L); and prothrombin time, 60.5 sec (normal range, 12-14 sec). Results of
serologic tests were positive for IgM anti-hepatitis A virus. Results of tests
for IgG anti-Epstein-Barr virus, IgG anti-cytomegalovirus, and hepatitis B
surface antibodies were positive. Results of tests for IgM anti-hepatitis B
core antigen and hepatitis B surface antigen were negative.
Sonography examination revealed heterogeneous liver parenchyma with hypo-
and hyperechoic areas mainly in the lateral segment of the left lobe
(Fig. 1A) and in the posterior
segment of the right lobe (Fig.
1B). These hyperechoic areas showed lobulated contours and were
located predominantly in the liver periphery.
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Fig. 1A —4-year-old boy with fulminant hepatitis A infection.
Transverse sonogram shows heterogeneous liver parenchyma and focal relatively
hyperechoic areas in lateral segment of left lobe peripherally.
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The hyperechoic areas seen on sonography were relatively hyperdense with
irregular contours on unenhanced MDCT images and were located within the
right, left, and caudate lobes. These lesions were localized mainly in the
periphery of the liver as seen on sonography
(Fig. 1C). After nonionic
contrast administration, these areas showed relatively low enhancement and
appeared as hypodense regions compared with the surrounding liver parenchyma
(Fig. 1D). The left and caudate
lobes were enlarged on both sonography and MDCT.
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Fig. 1C —4-year-old boy with fulminant hepatitis A infection.
Unenhanced abdominal CT image reveals multifocal relatively hypodense and
hyperdense areas. Hyperdense areas show lobulated contours within right, left,
and caudate lobes.
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Fig. 1D —4-year-old boy with fulminant hepatitis A infection.
Contrast-enhanced abdominal CT image illustrates relatively low-attenuation
areas consistent with regenerating parenchyma and relatively high-attenuation
areas consistent with necrosis.
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Percutaneous sonographically guided biopsy using a Tru-Cut needle from the
hyperechoic areas in the liver parenchyma was performed after MDCT and
sonography examinations. Hyperechoic areas were examined to rule out possible
malignancy. Histopathologic evaluation of the hyperechoic areas on sonography
and hyperdense areas on unenhanced MDCT revealed regenerating nodules in the
liver parenchyma. The remaining areas, which were relatively hypoechoic on
sonography and hyperdense relative to the regenerating parenchyma on enhanced
MDCT, were consistent with necrosis on pathologic examination. There were
destruction of reticulin structure, loss of hepatocytes, and inflammatory cell
infiltration in the necrotic areas on histopathologic examination
(Fig. 1E).
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Fig. 1E —4-year-old boy with fulminant hepatitis A infection.
Photomicrograph of histopathologic specimen shows regenerating nodules
(arrows), necrotic areas with destruction of reticulin structure,
loss of hepatocytes, and inflammatory cell infiltration (arrowheads).
(H and E)
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Discussion
Hepatitis A virus is an RNA virus that belongs to the Picornavirus family
and is the foremost cause of viral hepatitis. The fecal-oral route of
transmission has been hypothesized to cause epidemics in previously
unvaccinated populations [3].
Diagnosis of hepatitis A is established by detecting IgM anti-hepatitis A
virus antibodies in serum samples. Although enteric hepatitis A virus is a
mild, self-limiting infection that rarely causes fulminant hepatitis, in one
series researchers found that hepatitis A virus infection is the most common
cause of fulminant hepatic failure in Turkish children
[1]. Liver failure can be
classified as hyperacute (development of encephalopathy within 7 days of the
onset of jaundice), acute (1-4 weeks), or subacute (> 4 weeks)
[4]. In our case,
encephalopathy developed 3 weeks after the onset of jaundice, and liver
failure was classified as acute.
In fulminant hepatitis, massive necrosis of hepatocytes is present. The
necrotic areas contract in size, and hemorrhage, inflammatory cell
infiltration, proliferation of bile ducts, and bile staining without focal
fibrotic changes are seen within these areas. After several weeks, nodular
regeneration and fibrosis develop as irregular yellow-brown to green
surrounded by soft areas of necrosis
[5]. Sonography and MDCT are
used to evaluate liver parenchyma in fulminant hepatic failure. Previously
reported CT findings of fulminant hepatitis include decreased liver size
(massive necrosis), diffuse or localized (solitary or multiple) areas of
hypoattenuation in the liver, dilatation of the portal vein, narrow or
nondepicted hepatic veins, and focal or diffuse areas of hyperattenuation
(liver regeneration) during recovery
[6].
Itai et al. [7] have
identified postnecrotic scars showing low attenuation on unenhanced CT and
isoattenuation or hyperattenuation relative to the liver on enhanced CT.
Murakami et al. [2] have
reported imaging findings with pathologic correlations in three patients with
fulminant hepatitis. They showed areas of liver necrosis as low attenuation
before administration of contrast material and isoattenuation or
hyperattenuation compared with areas of liver regeneration on enhanced CT
images. Conversely, these authors showed areas of nodular liver regeneration
as hyperdense on unenhanced and hypodense on enhanced imaging. They also found
liver cell necrosis predominantly in the central region and nodular
regeneration in the periphery of the liver
[2].
In our case, sonography showed focal relatively hyperechoic areas in
heterogeneous liver parenchyma primarily in the periphery of the liver. MDCT
disclosed multifocal areas that appeared as relatively hyperdense on
unenhanced images, which showed mild enhancement after IV contrast injection.
These areas were identified as regenerating parenchyma on pathologic
examination. The remaining liver parenchyma was relatively hypoechoic on
sonography examination and showed high attenuation on enhanced MDCT relative
to the regenerating parenchyma. Necrosis was identified on histopathologic
evaluation of these areas. CT findings of our case appear similar with the
imaging findings reported by Murakami et al.
[2]. Sonography is primarily
the preferred imaging method in these conditions because it is a
cost-effective, fast, and noninvasive technique and lacks ionizing radiation.
Sonography also should be preferred in patients with hepatic failure and
encephalopathy because sonography can be easily performed bedside in ICUs.
Although necrosis is seen as low attenuation compared with normal liver
parenchyma after contrast administration, in our case and in the cases of
Murakami et al. [2], necrotic
areas appeared as high attenuation compared with regenerating parenchyma. The
mechanism of this enhancement may depend on inflammatory cell infiltration.
Itai et al. [7] found that the
combination of several findings—increased arterial supply, slow transit
rate of blood, an extensive interstitial space, and changes in the diffusion
rate between the interstitial space and the vascular space—results in
postnecrotic scar enhancement. The necrotic areas in our case may show similar
mechanisms of enhancement and are seen as relatively high-attenuation areas
compared with regenerating nodules on enhanced MDCT.
Only a few reports describe unusual imaging findings of nodular
regeneration and necrosis in patients with fulminant hepatitis
[2,
7]. Areas of focal regeneration
might be mistaken for malignant neoplasms on sonography and CT. Therefore, it
is important for radiologists and clinicians to be aware of these unusual
imaging findings in fulminant hepatitis so that further unnecessary studies
are avoided.
References
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experience with fulminant hepatic failure in Turkish children: etiology and
outcome. J Trop Pediatr 2003;49
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- Murakami T, Baron RL, Peterson MS. Liver necrosis and regeneration
after fulminant hepatitis: pathological correlation with CT and MR findings.
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- O'Grady JG, Schaim SW, Williams R. Acute liver failure: redefining
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- Robbins SL, Kumar V. The liver, the biliary tract, and the
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- Sekiyama K, Yoshiba M, Inoue K, Sugata F. Prognostic value of
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Sci 1994; 39:240
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Introduction
Case Report
