Figure 1
Teaching Case
SectionAbdominal imaging
Case TypeClinical Cases
AuthorsBattaglia V, Signorini F, Bonechi C, Gherarducci G, Nardini L, Brunu M, Zingoni G, Bartolozzi C
Connected authors
75 years, female
A 75-year-old woman, with no relevant clinical history, came to our department complaining about abdominal pain in the right hypochondrium and high fever (39.5°C) lasting for 3 days.
Laboratory data showed the presence of neutrophilia (13.500/mm3).
Laboratory data showed the presence of neutrophilia (13.500/mm3).
Infected hepatocellular carcinoma
The patient underwent ultrasound (US) examination (both baseline and post contrast agent).
Baseline US revealed the presence of an inhomogeneous area within the hepatic segment V (Fig. 1). After contrast agent administration, this lesion appeared as a large (approximately 6 cm) mass with a central anechoic area, expanding from segment V to the caudal portion of segment VI, and was associated with a hyperechoic rim in arterial phase. The central portion of the mass did not enhance (Fig. 2). A hepatic abscess was suspected and the patient underwent a Magnetic Resonance (MR) examination. The MR study was performed without intravenous contrast agent administration because of allergic diathesis of the patient, and confirmed the presence of a large subcapsular lesion in the segments V and VI.
The central component of the lesion was hyperintense on T1w and T2w secondary to necrotic hemorrhage. The surrounding rim was hypointense on T1w and hyperintense on T2w, compatible with an infectious reaction (Fig. 3-5).
A cytologic examination of the subsequent fine needle aspiration showed the presence of Escherichia coli infection, associated to necrosis, fibrin-leukocytes exudate, and cellular atypia.
Although antibiotic therapy was initiated, the fever persisted.
The patient was then subjected to exploratory laparotomy and wedge resection of the lesion.
Histology stated the diagnosis of a poorly differentiated HCC with necrotic exudate fibrin-leukocyte and intense desmoplastic reaction.
Baseline US revealed the presence of an inhomogeneous area within the hepatic segment V (Fig. 1). After contrast agent administration, this lesion appeared as a large (approximately 6 cm) mass with a central anechoic area, expanding from segment V to the caudal portion of segment VI, and was associated with a hyperechoic rim in arterial phase. The central portion of the mass did not enhance (Fig. 2). A hepatic abscess was suspected and the patient underwent a Magnetic Resonance (MR) examination. The MR study was performed without intravenous contrast agent administration because of allergic diathesis of the patient, and confirmed the presence of a large subcapsular lesion in the segments V and VI.
The central component of the lesion was hyperintense on T1w and T2w secondary to necrotic hemorrhage. The surrounding rim was hypointense on T1w and hyperintense on T2w, compatible with an infectious reaction (Fig. 3-5).
A cytologic examination of the subsequent fine needle aspiration showed the presence of Escherichia coli infection, associated to necrosis, fibrin-leukocytes exudate, and cellular atypia.
Although antibiotic therapy was initiated, the fever persisted.
The patient was then subjected to exploratory laparotomy and wedge resection of the lesion.
Histology stated the diagnosis of a poorly differentiated HCC with necrotic exudate fibrin-leukocyte and intense desmoplastic reaction.
Patients with chronic hepatitis are at high risk of progression to liver cirrhosis and to malignant nodular progression to hepatocellular carcinoma (HCC).
HCC in association with liver abscess is very rare. Without treatment, advanced HCC usually causes death within months, and long-term survival is rare [1]. Pyogenic liver abscesses usually occur in patients with diabetes mellitus and malignancy [2]. Possible causes include hematogenous dissemination, ascending cholangitis, and superinfection of necrotic tissue [3]. Escherichia coli is the most common bacterium worldwide, but now Klebsiella pneumoniae surpasses E. coli as the predominant isolate in patients with hepatic abscess [2-4].
HCC manifests as a liver abscess either because of spontaneous liquefied necrosis of the tumour or because of biliary obstruction caused by a tumour fragment, which is a very rare condition [5].
Patients with liver abscess usually present with fever, chills, anorexia, fatigue, or other symptoms such as nausea, vomiting, right-upper-quadrant pain, diffuse abdominal pain, pleuritic chest pain, and jaundice [6]. The most common laboratory findings in these patients are leukocytosis (70–82% of patients), alkaline phosphatase levels (ALP) increased 2–3 times the upper limit of normal, elevated transaminase levels and hypoalbuminemia.
Clinically, in presence of necrotic tumour tissue, HCC can present like an abscess [6]. An explanation is the presence of neoplasm-associated granulocytosis, resulting from granulopoietin production by tumour cells as well as by pyrogen production by neoplastic cells or by macrophages followed by tumour necrosis [6].
For early diagnosis and differential diagnosis of liver abscess, imaging plays an essential role. At US, a liver abscess usually is visualized as a hypoechoic or mixed-echoic lesion, whose margins may be blurred or irregular, because of the inflammation of surrounding areas [7]. At MR, a liver abscess may appear as a round or irregularly shaped hypointense mass, with a peripheral capsule that exhibits contrast enhancement.
On baseline acquisitions different signal intensities within the lesion and in the surrounding tissue can be detected, because of the presence of different histologic components.
On T1w images the central portion of the abscess may appear hypointense, in case of colliquate necrosis, as well as slightly hyperintense in case of coagulative necrosis because of the presence of necrotic proteinaceous material. On T2w images the central portion is always hyperintense. A surrounding transition zone of slightly decreased signal intensity on T1w images and slight hyperintensity on T2w images may be appreciable secondary to an inflammatory reaction. T1w post-contrast sequences may demonstrate the "target sign", consisting of different signal intensities from the center to the periphery of the lesion: a hypointense, non-enhancing central area, surrounded by a hyperintense rim, which is in turn surrounded by a hypointense area, thought to correspond to localised edema.
A differential diagnosis is epitheloid hemangioendothelioma, which can mimic signal intensities in different acquisitions (both baseline and contrast-enhanced). The main diagnostic clue is the complete lack of clinical symptoms referring to an infective disease.
HCC in association with liver abscess is very rare. Without treatment, advanced HCC usually causes death within months, and long-term survival is rare [1]. Pyogenic liver abscesses usually occur in patients with diabetes mellitus and malignancy [2]. Possible causes include hematogenous dissemination, ascending cholangitis, and superinfection of necrotic tissue [3]. Escherichia coli is the most common bacterium worldwide, but now Klebsiella pneumoniae surpasses E. coli as the predominant isolate in patients with hepatic abscess [2-4].
HCC manifests as a liver abscess either because of spontaneous liquefied necrosis of the tumour or because of biliary obstruction caused by a tumour fragment, which is a very rare condition [5].
Patients with liver abscess usually present with fever, chills, anorexia, fatigue, or other symptoms such as nausea, vomiting, right-upper-quadrant pain, diffuse abdominal pain, pleuritic chest pain, and jaundice [6]. The most common laboratory findings in these patients are leukocytosis (70–82% of patients), alkaline phosphatase levels (ALP) increased 2–3 times the upper limit of normal, elevated transaminase levels and hypoalbuminemia.
Clinically, in presence of necrotic tumour tissue, HCC can present like an abscess [6]. An explanation is the presence of neoplasm-associated granulocytosis, resulting from granulopoietin production by tumour cells as well as by pyrogen production by neoplastic cells or by macrophages followed by tumour necrosis [6].
For early diagnosis and differential diagnosis of liver abscess, imaging plays an essential role. At US, a liver abscess usually is visualized as a hypoechoic or mixed-echoic lesion, whose margins may be blurred or irregular, because of the inflammation of surrounding areas [7]. At MR, a liver abscess may appear as a round or irregularly shaped hypointense mass, with a peripheral capsule that exhibits contrast enhancement.
On baseline acquisitions different signal intensities within the lesion and in the surrounding tissue can be detected, because of the presence of different histologic components.
On T1w images the central portion of the abscess may appear hypointense, in case of colliquate necrosis, as well as slightly hyperintense in case of coagulative necrosis because of the presence of necrotic proteinaceous material. On T2w images the central portion is always hyperintense. A surrounding transition zone of slightly decreased signal intensity on T1w images and slight hyperintensity on T2w images may be appreciable secondary to an inflammatory reaction. T1w post-contrast sequences may demonstrate the "target sign", consisting of different signal intensities from the center to the periphery of the lesion: a hypointense, non-enhancing central area, surrounded by a hyperintense rim, which is in turn surrounded by a hypointense area, thought to correspond to localised edema.
A differential diagnosis is epitheloid hemangioendothelioma, which can mimic signal intensities in different acquisitions (both baseline and contrast-enhanced). The main diagnostic clue is the complete lack of clinical symptoms referring to an infective disease.
References
[1] Chan KS, Chen CM, Cheng KC, et al (2005) Pyogenic liver abscess: a retrospective analysis of 107 patients during a 3-year period. Jpn J Infect Dis 58:366-8 (PMID: 16377869)
[2] Branum GD, Tyson GS, Branum MA, Meyers WC. (1990) Hepatic abscess. Changes in etiology, diagnosis, and management. Ann Surg 212:655-62 (PMID: 2256756)
[3] Wong WM, Wong BC, Hui CK, et al (2002) Pyogenic liver abscess: retrospective analysis of 80 cases over a 10-year period. J Gastroenterol Hepatol 17:1001-7 (PMID: 12167122)
[4] Yeh TS, Jan YY, Jeng LB, et al (1998) Hepatocellular carcinoma presenting as pyogenic liver abscess: characteristics, diagnosis, and management. Clin Infect Dis 26:1224-6 (PMID: 9597257)
[5] Lederman ER, Crum NF (2005) Pyogenic liver abscess with a focus on Klebsiella pneumoniae as a primary pathogen: an emerging disease with unique clinical characteristics. Am J Gastroenterol 100:322-31 (PMID: 15667489)
[6] Saar B, Kellner-Weldon F (2008) Radiological diagnosis of hepatocellular carcinoma. Liver Int 28:189-99 (PMID: 18251978)
[7] Mortele KJ, Segatto E, Ros PR (2004) he infected liver: radiologic-pathologic correlation. Radiographics 24:937-55 (PMID: 15256619)
Case information
| URL: | https://www.eurorad.org/case/8177 |
| DOI: | 10.1594/EURORAD/CASE.8177 |
| ISSN: | 1563-4086 |
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