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.
especially in precontrast images,
revealed a diffused hepatic hypodensity in 10/11 patients (Fig.
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.
In histopathologic evaluation a periportal edema and inflammatory cell infiltration,
mainly lymphocyte was observed (Fig.
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).
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.
c): 1 suffering from toxic hepatitis,
3 from 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.
In all these patients the histopathologic findings were inflammatory cell infiltration of the gall bladder wall,
mainly by lymphocyte (Fig.
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.
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.