Fulminant hepatic failure: correlation among different aetiologies, MDCT findings and histopathology in adult transplanted patients.

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1 Fulminant hepatic failure: correlation among different aetiologies, MDCT findings and histopathology in adult transplanted patients. Poster No.: C-0408 Congress: ECR 2013 Type: Authors: Keywords: DOI: Scientific Exhibit A. Pecchi, D. Corniani, M. De Santis, L. Maccio, N. De Ruvo, F. Di Benedetto, P. Torricelli; Modena/IT Abdomen, CT, Diagnostic procedure, Tissue characterisation, Transplantation, Pathology /ecr2013/C-0408 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 12

2 Purpose Some work reported in literature described the MDCT principal findings of fulminant hepatitis [1-9], however few authors correlated the imaging findings with the hystopathological examination performed on biopsy or explanted liver [3, 5, 7, 10] and these works are restricted to some particular aspect [5, 7] or have taken into account a small number of cases [3] or are only related to pediatric population [10]. The first aim of our work has been to review CT examinations of adult patients with fulminant hepatic failure of different aetiology (exotossic, viral or vascular) that underwent liver transplantation. Secondly, we planned to describe the main morphological and density findings gathered with MDCT and to correlate them with histopatological examination on explanted liver. Finally the correlations were critically evaluated in relation to hepatitis aetiology. Methods and Materials The MDCT examinations of 11 patients (4 men and 7 women, median age 44,5 years, age range years), who underwent OLT due to fulminant hepatic failure between 2003 and 2012 in our liver and multiorgan transplantation department, were retrospectively evaluated. These patients were grouped according to the etiology of the acute liver failure: 4 toxic hepatitis (Table 1) (2 from paracetamol, 1 from alcohol and 1 related to drugs used for tuberculosis therapy), 3 hepatitis B, 1 had a mixed etiology by HBV and alcohol (Table 2) and 3 had a vascular etiology (Table 3) (1 thrombotic thrombocytopenic purpura, 1 related to anti-platelets autoantibody syndrome in a patient with Budd-Chiari in heparin therapy for polycytemia vera and 1 ischemic hepatitis). Abdominal MDCT examinations were performed with 16-channel MDCT scanner (LightSpeed 16, General Electric Medical System, Milwaukee, WI, USA) or 64 channel (VCT LightSpeed, General Electric Medical System, Milwaukee, WI, USA) before and after intravenous injection of 2 ml/kg of non ionic iodinate contrast (Iomeron 300, 300 mg/ ml, Bracco, Milan, Italy) at a rate of 2-3 ml/s using a power injector and bolus tracking. Precontrast and arterial phase images of the upper abdomen and whole abdomen portal phase images with 2,5 mm slice thickness and 1,25 mm interval were obtained. Page 2 of 12

3 The timing between the onset of clinical symptoms leading to hospitalization and abdominal MDCT examination was about 1,4 days (range 1-3 days). The interval between abdominal MDCT examination and liver transplantation was 2,8 days (range 1-9 days). The MDCT examinations were evaluated by 2 radiologists with 15 and 5 years of CT scan experience respectively, searching the main alterations described in literature [3-6, 10]: hepatic volume variations, smooth or nodular liver contours, hepatic and periportal density, THAD (Transient Hepatic Attenuation Differences), morphology of hepatic veins, morphology of gall bladder wall (thickness and density), ascites, splenomegaly, colic wall (thickness and density). These morphology and density alterations were correlated with their corresponding histopathologic findings found in explanted liver by two pathologists with 18 and 5 years experience in liver pathology. Images for this section: Table 1: Patients with toxic acute hepatitis. Page 3 of 12

4 Table 2: Patients with viral acute hepatitis and mixed etiology (HBV + alcohol). Table 3: Patients with vascular acute hepatitis. Page 4 of 12

5 Results 6/11 patients (3/4 with toxic hepatitis and all with vascular etiology) were found to have hepatomegaly through the MDCT examination. Macroscopic evaluation of the explanted liver confirmed the hepatomegaly in five of them but not in one patient affected by vascular hepatitis. All patients with hepatitis B and the patient with mixed etiology (HBV + alcohol) had normal or small liver volume according to both MDCT and to pathologic examination. MDCT scan showed smooth liver contours in all our patients (11/11), while pathologic examination agreed only for 8/11 of the cases; in the remaining three patients with hepatitis B, the macroscopic examination did not report alteration of hepatic contours while the microscopic evaluation revealed a diffused micronodular structure. MDCT scan, especially in precontrast images, revealed a diffused hepatic hypodensity in 10/11 patients (Fig. 1a, b, c), while in the patient with ischemic hepatitis there was a heterogeneous density. The diffuse hypodensity of liver parenchyma, also less evidently observable in post-contrast images, corresponded to a diffused and massive hepatocyte necrosis on histopathologic specimen (Fig. 1d) while the heterogeneous density in the ischemic hepatitis, observed in the MDCT scan, correlated with patchy areas of hepatocyte necrosis. A characteristic aspect found in all patients (11/11) through MDCT scan, was the periportal hypodensity in the portal venous phase, as well as low-density tissue around the intra-hepatic course of the main branches of the portal vein (Fig. 2a, b, c). In histopathologic evaluation a periportal edema and inflammatory cell infiltration, mainly lymphocyte was observed (Fig. 2d). In the remaining two patients affected by vascular hepatitis, only periportal edema without inflammatory cell infiltration in relation to the rapid evolution of the hepatitis was found. The patients had been immediately transplantation and immune-mediated response had consequently less time to manifest. MDCT revealed narrow hepatic veins in 5/11 patients: 3 affected by toxic hepatitis, 1 by viral hepatitis and 1 by vascular hepatitis (Budd-Chiari syndrome). This finding, confirmed by macroscopic evaluation of the explanted liver, didn't have a specific histopathologic cause, and it was probably related to parenchymal alteration due to necrosis. Peribiliary THAD (Transient Hepatic Attenuation Differences) were identified in MDCT examination of 7/11 patients (Fig. 3a, b, c): 1 suffering from toxic hepatitis, 3 from Page 5 of 12

6 viral hepatitis, the patient affected by mixed viral and toxic etiology and 2 by vascular hepatitis. The histopathologic specimen showed biliary ductular proliferation in all these patients (7/11), more evident in those with viral hepatitis, associated with periportal inflammatory cell infiltration. In 1 case we reported THAD in MDCT examination without ductular proliferation or periportal inflammatory cell infiltration and in the remaining 3 cases these elements were present in the histopathologic specimens but MDCT images didn't revealed THAD. MDCT post contrast examination revealed in all patients, except one patient who had previously underwent cholecystectomy, gall-bladder hypodense wall thickening (>3 mm) and mucosa and submucosa hyperenhancement (Fig. 4a, b, c). In all these patients the histopathologic findings were inflammatory cell infiltration of the gall bladder wall, mainly by lymphocyte (Fig. 4d). Ascites was found in 9 out of 11 patients: among them four patients were suffering from toxic hepatitis, one was affected by hepatitis B, one by mixed etiology (HBV + alcohol), and the remaining three were suffering from vascular hepatitis. Splenomegaly was seen in 6 out 11 patients (one patient had previously surgically removed the spleen): 2 affected by toxic hepatitis, 2 by viral hepatitis and 2 by vascular ones. The MDCT examination of 3/11 patients with toxic etiology, revealed in the colonic wall the same alterations described just above for the gall bladder wall: thickened, low density wall, mucosa and submucosa hyperenhancement (Fig. 5). We didn't have histopathologic specimen about this because no colic wall biopsy or resection were needed, even though the similarity with the alterations of the gall bladder wall made us to suppose the presence of an inflammatory cell infiltration of colic wall. These alterations disappeared in post-olt MDCT examinations. Images for this section: Page 6 of 12

7 Fig. 1: Precontrast MDCT images show a diffuse low density liver parenchyma in patients with acute hepatitis of different etiology: toxic hepatitis (a), viral hepatitis (b) and vascular hepatitis (c). Photomicrograph of histopathologic specimen (EE 4x) shows diffuse hepatocyte necrosis (d). Page 7 of 12

8 Fig. 2: Portal venous phase MDCT images show perportal hypodensity in patients with acute hepatitis of different etiology in all etiologies: toxic hepatitis (a), viral hepatitis (b) and vascular hepatitis (c). Photomicrograph of histopathologic specimen (EE 20x) shows periportal edema, inflammatory cell infiltration and ductular proliferation (d). Page 8 of 12

9 Fig. 3: a) In 7/11 patients with acute hepatitis of different etiology we found diffuse peribiliary THAD. b) Photomicrograph of histopathologic specimen (CK7 20x) shows ductular proliferation associated with periportal inflammatory cell infiltration. Fig. 4: MDCT images show thickened low density gall bladder wall in patients with acute hepatitis of different etiology: toxic hepatitis (a), viral hepatitis (b) and vascular hepatitis (c). Photomicrograph of histopathologic specimen (EE 10x) shows inflammatory cell infiltration of the gall baldder wall (d). Page 9 of 12

10 Fig. 5: In 3 patients with toxic hepatitis with oral ingestion of the toxic agent MDCT shows thickened low density colic wall. Page 10 of 12

11 Conclusion The main histopathologic alterations in fulminant hepatitis are the liver inflammatory cell infiltration and the diffuse hepatocyte necrosis. The correspondent elements in MDCT examination are: low density liver parenchyma, periportal low density, thickened low density gall bladder wall and variations of liver volume. Regenerative phenomena in the parenchyma could be at the basis of the parenchimal heterogeneous density, like THAD, and nodular liver contours. Other frequent findings are splenomegaly, ascites and thickened low density colic wall in case of toxic hepatitis. With the limitations of a small number of patients, we observed that the main MDCT alterations don't change among hepatitis of different etiologies but these were the expression of an aspecific acute inflammation of the liver. In acute hepatitis B there was less tendency to hapatomegaly and we found micronodular remodeling only at microscopic evaluation. Only in some toxic hepatitis with oral ingestion of toxic agents we found alterations of the colic wall, which were reversible after liver transplantation. References 1. Muto, Y., Present status of fulminant hepatitis in Japan ( ). Gastroenterol Jpn, Suppl 4: p Sekiyama, K., et al., Prognostic value of hepatic volumetry in fulminant hepatic failure. Dig Dis Sci, (2): p Murakami, T., R.L. Baron, and M.S. Peterson, Liver necrosis and regeneration after fulminant hepatitis: pathologic correlation with CT and MR findings. Radiology, (1): p Itai, Y., et al., Fulminant hepatic failure: observation with serial CT. Radiology, (2): p Shakil, A.O., et al., Prognostic value of abdominal CT scanning and hepatic histopathology in patients with acute liver failure. Dig Dis Sci, (2): p Cakir, B., et al., Unusual MDCT and sonography findings in fulminant hepatic failure resulting from hepatitis A infection. AJR Am J Roentgenol, (4): p Poff, J.A., et al., Frequency and histopathologic basis of hepatic surface nodularity in patients with fulminant hepatic failure. Radiology, (2): p Kim, S.W., H.C. Shin, and I.Y. Kim, Diffuse pattern of transient hepatic attenuation differences in viral hepatitis: a sign of acute hepatic injury in patients without cirrhosis. J Comput Assist Tomogr, (5): p Page 11 of 12

12 9. Yasui, S., et al., Importance of computed tomography imaging features for the diagnosis of autoimmune acute liver failure. Hepatol Res, (1): p Cakir, B., et al., Fulminant hepatic failure in children: etiology, histopathology and MDCT findings. Eur J Radiol, (2): p Personal Information A. Pecchi, D. Corniani, M. De Santis, P. Torricelli * Department of Radiology, University of Modena and Reggio Emilia, via del Pozzo 71, Modena, Italy anna_pecchi@yahoo.com dario.corniani@libero.it torricelli.pietro@unimore.it L. Maccio Department of Pathology, University of Modena and Reggio Emilia, via del Pozzo 71, Modena, Italy N. De Ruvo, F. Di Benedetto ^ Department of Liver and Multiorgan Transplantation, University of Modena and Reggio Emilia, via del Pozzo 71, Modena, Italy Page 12 of 12