Diffuse hepatic diseases are difficult to detect as they minimally affect liver architecture. Hepatic steatosis involves increased triglyceride storage in hepatocytes and is caused by conditions like obesity, diabetes, and malnutrition. MRI is the most sensitive technique for detecting steatosis using Dixon-based chemical shift imaging. Cirrhosis is the end-stage of liver disease and causes nodular regeneration and lobar atrophy visible on ultrasound, CT, and MRI. Focal lesions like haemangiomas, cysts, and abscesses can also be identified and characterized using their specific imaging features on ultrasound, CT, and MRI.

2.  Diffuse hepatic diseases are more difficult to detect than
focal lesions as their effect on normal liver architecture is
minimal.

3.  HEPATIC STEATOSIS.
Increased triglyceride loading of hepatocytes.
Causes-acute and chronic alcoholic abuse, obesity, DM, insulin
resistance, cystic fibrosis, malnutrition, total parenteral nutrition.
USG:-
Increased parenchymal reflectivity which obscure portal vein
margins.
Further imaging is required as fibrosis can also cause increased
reflectivity.

4. CT:-
Demonstrate and quantify hepatic steatosis as attenuation
decreases.
Liver architecture is preserved.

5. MRI:-
MRI is the most sensitive and specific technique for demonstrating hepatic steatosis. Dixon-based
‘chemical shift’ or ‘in- and out-of-phase’ imaging allow accurate diagnosis.

6.  Cirrhosis
Cirrhosis is the end stage of a wide variety of hepatic disease processes
that cause hepatocellular inflammation and necrosis leading to hepatic
fibrosis and nodular regeneration.
commonest anatomical finding in advanced cirrhosis is atrophy of the
posterior segments (VI, VII) of the right lobe.
USG:-
Demonstrate nodularity of the liver margin in advanced cirrhosis.
Pure hepatic fibrosis increases reflectivity, resulting in loss of the margins
of the portal vein branches.
The liver texture becomes coarser or more heterogeneous as cirrhosis
Progresses.
DOPPLER:-
 damping of the normal right heart waveforms in the hepatic veins,
reduced main portal vein blood flow (<10 cm/s mean peak) or
hepatofugal flow.

7. CT:-
insensitive to early fibrosis changes but demonstrates the nodular margin and
lobar atrophy changes of advanced disease.

8. MRI:-
 insensitive to early fibrosis changes and there are no specific
changes of parenchymal signal intensity on T1w or T2w imaging,
although parenchymal heterogeneity.
 MR elastography is a relatively new technique quantifying liver
stiffness in a similar fashion to US methods
On MRI marked heterogeneity may occur in cirrhotic livers on (A) multi-shot
T2w FSE imaging due to the combination of increased signal from fibrosis
and reduced signal from iron accumulation within nodules and for similar
reasons on delayed post-gadoliniumT1w imaging (B)

9.  Viral hepatitis
Diagnosis and monitoring based on serological tests and imaging is
relatively non-specific.
USG:-
Non-specific decreased reflectivity occurs in acute viral hepatitis,
although the majority of cases have normal parenchyma.
Gallbladder wall thickening is a common non-specific finding in
acute hepatitis.
 In acute hepatitis imaging excludes obstructive causes of jaundice.
 In chronic hepatitis with cirrhosis, imaging helps monitor disease
progression, development of portal venous hypertension and
complications such as hepatocellular carcinoma (HCC).

10.  Haemochromatosis and Iron Overload
Haemochromatosis and multiple transfusions may both result in iron
deposition in the liver.
MRI:-
Most specific imaging technique, as intracellular iron exerts a local
susceptibility effect on SWI.
The liver signal is abnormally reduced (to less than that of adjacent
muscle).
T2w MRI
image demonstrating abnormally low liver signal parenchyma compared to adjacent muscle with linear fibrotic
increased signal regions, nodular margins and moderate ascites

11. CT:-
Unenhanced CT demonstrates hepatic iron deposition through an increase in HU value (>75
HU).
USG:-
US may demonstrate increased parenchymal reflectivity but there are no specific features
that characterise iron deposition

12. Wilson’s Disease
 It is an autosomal recessive disorder in which copper is deposited in the
liver.
 Copper is hepatotoxic and triggers inflammation that progresses to
cirrhosis. Imaging demonstrates the generalised cirrhotic changes.
 CT:-
Increase in hepatic attenuation on CT
 MRI:-
there may be a subtle increased signal on T1w with a decrease on T2w
images.
 USG:-
There are no specific features on US studies.

13.  Calcification
Benign parenchymal calcification may occur following focal insults
such as tuberculosis, Pneumocystis infection, sarcoidosis, pyogenic
abscess and parenchymal haematoma.
CT:-
unenhanced CT is more sensitive and detects subtle calcification,
e.g. metastases.
Plain radiographs demonstrate gross calcification.

14. USG:-
clearly demonstrates focal calcification, with increased
reflectivity and a posterior acoustic corridor, but this feature
alone does not always allow distinction from focal gas.

15.  Pneumobilia
Gas in the biliary tract may occur as a result of a sphincterotomy,or Roux
loop procedure allowing reflux of intestinal gas into the biliary tree.
Identified by the linear distribution radiating from the hilum and gravity
dependence with air predominantly in the nondependent parts of the
biliary tree.
USG:-
 Ducts are increased echo-reflectivity linear structures that may be
differentiated from calcification by the pattern and movement of the
gas related to respiration, bowel peristalsis or patient position.

16. CT:-
presence of gas is easily demonstrated and localised.

17.  Portal Vein Gas
Portal vein gas is always abnormal and occurs when intestinal
permeability increases and/or there is an increase in intestinal
luminal pressure.
USG:-
 US sensitively detects moving gas bubbles in the main portal vein
which can be visualised on B-mode images and detected by
spectral Doppler as the gas bubbles reflect the sound beam
overloading the system receivers giving rise to a characteristic
high-pitched random bubbling sound with focal aliasing artefacts
on the spectral display

18. CT:-
If sufficient gas accumulates it may become visible on CT peripherally in the portal vein
branches

19.  Parenchymal Gas.
Results from a gas-forming organism in an abscess or infarct, or occasionally
following trauma or hepatic arterial thrombosis following liver transplantation.
CT:-
 Best delineates parenchymal gas collections and any related pathological
changes.
USG:-
 demonstrate gas collections but defining their extent may be difficult when
they are large or peripheral

20.  Cysts
True hepatic cysts arise from abnormal development of bile duct precursors (Meyenburg’s
complexes) and are lined by cuboidal epithelium.
Multiple cysts occur as part of adult polycystic disease.
USG:-
Hepatic cysts are spherical homogeneous structures with an imperceptible wall, posterior acoustic
enhancement, lacking internal echoes and internal flow on Doppler.
Differential diagnosis includes haemorrhage, abscess, cystic metastasis (e.g. ovarian), biliary
cystadenoma or cystadenocarcinoma and hydatid disease.

21.  CT:-
CT demonstrates cysts as homogeneous structures,
with imperceptible walls, attenuation of 0–10 HU,
and no enhancement following IV contrast medium.
MRI:-
Fluid content of a cyst results in low signal on T1w
imaging and very high signal on T2w imaging.
Cysts may be indistinguishable from haemangiomas
on conventional T2w MRI but heavily T2w imaging (as
used for MRCP) may help separate them.

22. Hydatid Disease.
This is a hepatic infection with Echinococcus granulosus.
Larvae migrate from the gut and embed in the liver, where they
encyst and develop, slowly provoking a surrounding inflammatory
reaction.
On imaging there is a wide range of appearances, from a simple cyst
indistinguishable from a true hepatic cyst to a complicated cyst with
any or all of the following features: debris (hydatid ‘sand’ made up
of dead scolices, which may calcify), daughter cysts, membrane
separation, and wall calcification.

23.  USG:-
US demonstrates clearly not only the simple cyst form but also the
more complex cyst features, such as the dependent debris, daughter
cysts (cyst within a cyst appearance), membrane separation and wall
calcification.

24. CT:-
CT defines all these features as well and is helpful where wall calcification obscures the view on
US.

25.  Abscess
Hepatic pyogenic abscesses usually arise from portal pyaemia.
An initial local inflammatory reaction is followed by progressive
central liquefaction with a surrounding inflammatory margin or
‘wall.
USG:-
On US studies an early pyogenic abscess appears as a solid spherical
lesion with an ill-defined margin and low reflectivity.
As the abscess liquefies, a thickened and irregular wall appears and
the necrotic centre contains sparse echoes from the debris.

26.  CT:-
abscesses are typically ill-defined, low attenuation and following IV
contrast medium demonstrate rim enhancement.
MRI:-
The MRI findings also overlap with necrotic metastases with an ill-defined
lesion on low signal on T1w and high signal on T2w, often with a higher
signal outer margin.

27. Haemangioma.
Haemangiomas are the commonest benign hepatic tumours.
They are composed of vascular channels of varying size (cavernous to
capillary), lined with endothelium, often with intervening fibrous
tissue.
MRI is the most sensitive and specific imaging examination for the
diagnosis of haemangioma.

28.  MRI:-
Using extended echo time (e.g. TE of 120 to 160 ms) T2w spin-echo
sequences at 1.5 T, haemangiomas appear as well-defined lesions
with a lobular outline and homogeneously high signal on T2w.

30.  CT:-
well-defined, lobulated lesion with attenuation close to blood values
before enhancement.
The pattern of enhancement follows centripetally infilling and
eventually merging with the background parenchyma.

32.  USG:-
US capillary haemangiomas are typically well-defined, lobular,
homogeneous lesions with increased echo reflectivity .
There is usually no detectable Doppler signal within the lesion due to
the slow flow.

33. Focal Nodular Hyperplasia.
This benign tumour occurs most commonly in women aged 20–50 years.
Focal nodular hyperplasia (FNH) is usually asymptomatic although rarely
patients present with pain or hepatomegaly.
It arises from an underlying congenital vascular malformation and enlarges
in response to hormone stimulation, for example by oral contraceptives.
FNH is composed of normal liver elements including hepatocytes, bile
ducts, Kupffer cells and intervening fibrous septa.
In FNH the biliary elements are not connected with the normal biliary
tree; this characteristic aids discrimination from adenoma.
Up to 50% of FNH lesions have a typical central stellate fibrovascular scar,
visible on at least one imaging technique.

34. USG:-
US findings are usually non-specific with subtle lesions of similar
reflectivity to adjacent liver detectable mainly by their mass effect.

35.  CT:-
On unenhanced CT studies FNH are subtle and well defined and
may exhibit mass effect, displacing adjacent vessels.
They demonstrate marked homogeneous enhancement in the
arterial phase of IV contrast enhancement, with the exception
of the central scar and large feeding vessels may be visible at
the periphery.

36.  MRI:-
On MRI the lesions are also subtle, being either isointense or of
minimally reduced signal on T1w and increased signal on T2w
images.
The central scar is hypointense on T1w and hyperintense on T2w
images, and may be visible on MRI .
On single-shotT2w FSE imaging the lesion is barely visible (A) but better demonstrated
(arrowheads) on fat-suppressed multi-shotT2w FSE (B).

37. There is avid arterial phase enhancement (C), becoming isointense in the portal (D) and delayed phases (E). A
central scar is evident on some of the images (arrowhead), which enhances on the delayed image (E).

38. Hepatic Adenoma.
Adenomas are rare benign tumours that may arise spontaneously or
in association with anabolic steroid use, glycogen storage disease
type 1, maturity-onset diabetes of the young and Klinefelter’s
syndrome when multiple lesions are commonly present.
They are vascular lesions composed primarily of hepatocytes, with
no portal tracts or bile ducts and no bilirubin excretion.

39.  CT:-
On CT adenomas may be isointense with adjacent liver, or of
slightly increased or decreased attenuation. This depends on
both the amount of fat in the background liver.

40.  MRI:-
The lesions are well-defined isointense or slightly hyperintense
lesions on T2w and T1w images.
They typically enhance markedly and uniformly during the arterial
phase and disappear in the portal phase following gadolinium
enhancement on T1w imaging.

41.  USG:-
On US the lesions may be isoreflective with adjacent
parenchyma or, if they accumulate fat, are well-defined
increased echo-reflectivity lesions that mimic haemangiomas.

42.  Focal Fat
Regional or focal variations (increase or decrease) of fat occur
commonly and cause diagnostic confusion with tumours.
Focal fat have angular margins and a ‘geographic’ appearance that
when combined with the lack of mass effect and preservation of the
vascular architecture.

43. MRI using Dixon methods (otherwise known as ‘chemical shift’ or‘in- and out-of-phase’ imaging) is
the most accurate noninvasive diagnostic test.
This detects the presence of fat and water within the same image voxel as the water and fat
signal combine on the in-phase image but cancel on the out-of-phase image.

44.  Biliary Hamartomas.
Solitary and multiple biliary hamartomas occur and are typically
small lesions of 3–5 mm with a combination of solid and cystic
elements.
They may be indistinguishable from small metastases on both US and
CT .

45.  USG:-
they are not clearly visualised as discrete lesions on US and often
misinterpreted as diffuse malignant infiltration.
 CT:-
Reveals relatively cystic nature of lesion but as the lesions may have
a solid component they can still masquerade as metastases.

46. MRI:-
Demonstrates more clearly the small irregular-shaped cystic components.
Confident diagnosis may require biopsy and histological examination.

47.  Hepatocellular Carcinoma.
HCC or hepatoma is the commonest primary malignant neoplasm of
the liver.
HCC can be solitary, multifocal or, rarely, diffuse.

48.  USG:-
US is widely used as a screening technique small hepatomas may be
of increased or decreased reflectivity in relation to the adjacent
parenchyma.
Any new solid lesion on US in a high-risk patient is considered a
potential HCC.
Large lesions may show internal heterogeneity, due to haemorrhage,
necrosis, or fat and often cause portal vein thrombosis or tumour
thrombus, which can expand the vein.

49. CT:-
Unenhanced CT may demonstrate focal or multifocal HCC as ill-
defined low-attenuation lesions.
Fat accumulation may also occur in HCC.
Most HCCs are hypervascular and enhance during the late arterial
phase, with the majority demonstrating ‘washout’ in the portal
phase and later phases.

50.  MRI:-
MRI is considered the most sensitive technique for HCC
detection.
On contrast-enhanced T1w images the enhancement patterns
with Gd-DTPA parallel those for enhanced CT examination,
with typical lesions enhancing in the late arterial phase and
demonstrating washout in the portal and/or delayed 5- to 10-
min phases.
Features of portal venous invasion include the development of
thrombi and dilatation of the main portal vein or its branches.

51.  Fibrolamellar Carcinoma (FLC)
This lesion is now considered a separate entity to HCC that occurs in
the 5–35 years’ age group
FLC usually presents as a solitary, lobulated, well-defined large
tumour containing a central fibrous scar.
Punctate calcification is present in the scar in more than 50% of
cases, which may aid diagnosis as calcification is relatively rare in
HCC or FNH.

52.  CT:-
Unenhanced CT examination demonstrates a well defined
lobulated mass of low attenuation with an even lower
attenuation central scar with radial linear components and,
frequently, punctate calcification.
The lesion demonstrates non-specific enhancement and
delayed enhancement of the scar may occur, making
differentiation from FNH difficult.

53.  MRI:-
MRI reveals a low signal scar on T1w and T2w (in contrast to
FNH, where the scar is typically high signal on T2w).
 USG:-
lesion is commonly increased reflectivity and the central scar
and calcification may be evident

54. The large heterogeneous lesion with a fibrous central region with limited enhancement post
contrast medium is demonstrated on CT pre (A), arterial (B) and delayed phase (C).
MR single-shot T2w FSE (D), arterial phase T1w (E) and on DWI b500 imaging (F)

55. Thank you !