Abnormal liver blood test results are often the first indicator of hepatobiliary disease and a common indication for abdominal imaging with US, CT, or MRI. Most of the disease entities can be categorized into hepatocellular or cholestatic patterns, with characteristic traits on liver blood tests. Each pattern has a specific differential, which can help narrow the differential diagnosis when combined with the clinical history and imaging findings. Overall, integrating liver blood test patterns with imaging findings can help the radiologist accurately diagnose hepatobiliary disease, especially in cases where imaging findings may not allow differentiation between different entities.

1. Beyond LFT: A
Radiologist’s Guide to
the Liver Blood Tests
DR ABHINEET DEY
DEPARTMENT OF RADIOLOGY, SILCHAR MEDICAL COLLEGE & HOSPITAL (SMC H)

2. Radiographics Volume 42, Issue 1 / January-February 2022
Metra, B. M., Guglielmo, F. F., Halegoua-DeMarzio, D. L., Civan, J. M., & Mitchell, D. G. (2022). Beyond the Liver Function Tests: A
Radiologist's Guide to the Liver Blood Tests. RadioGraphics, 42(1), 125-142. https://doi.org/10.1148/rg.210137

4. Introduction
Acute and chronic liver disease each have many causes, some of which have high morbidity
and/or mortality.
Liver disease often progresses asymptomatically, with clinical symptoms beginning only after
development of advanced liver fibrosis.
Thus, a series of serum markers, often referred to as liver function tests are often used to screen
for liver disease.

5. Liver function test (LFT)
THE LIVER BLOOD TESTS ARE INDIRECT SERUM MARKERS OF
HEPATOBILIARY DISEASE.

6. General approach
Pattern of
Abnormality
Liver function test Role of Imaging
Hepatocellular
pattern
Elevated AST and ALT
levels
US to rule out structural lesions
US or MR elastography for staging of fibrosis
US with or without MRI for screening of hepatocellular
carcinoma in known chronic liver disease
Cholestatic pattern Elevated ALP or bilirubin
levels
US to assess for biliary obstruction
ERCP or MRCP if ductal dilatation found at US
Acute liver failure Decreased albumin level
or increased
prothrombin time
US plus Doppler imaging to assess hepatic vasculature
and rule out preexisting cirrhosis or malignancy;
possible liver biopsy to determine cause
Isolated
hyperbilirubinemia
Elevated bilirubin level
with normal ALP and
transaminase levels
US to assess for biliary obstruction
ERCP or MRCP if ductal dilatation found at US

7. Common liver blood tests
Test Normal range Hepatic Implication of Abnormal Result
AST (IU/L) <40 (0.67 μkat/L) Increased with hepatocellular injury; extrahepatic causes include cardiac and muscle disease
ALT (IU/L) <29–33 (0.48–0.55 μkat/L) in men
<19–25 (0.32–0.42 μkat/L) in women
Increased with hepatocellular injury (more specific than AST level)
ALP (IU/L) 30–130 (0.50–2.17 μkat/L) Increased with cholestasis (also elevated in bone disease, pregnancy, or childhood)
GGT (IU/L) <30 (0.50 μkat/L) Increased with cholestasis; confirms liver injury as cause of elevated ALP level
Direct bilirubin
(mg/dL)
<0.3 (5.1 μmol/L) or <30% of total
bilirubin level
Increased with cholestasis
Total bilirubin
(mg/dL)
<1.1 (18.7 µmol/L) Increased with hemolytic processes (if direct bilirubin level is not elevated) or cholestasis (if direct
bilirubin level is also elevated)
Albumin (g/dL) 3.5–6 (35–60 g/L) Decreased with impaired hepatic synthesis (>3 wk); also decreased in nonspecific severe systemic
illness or chronic inflammation
Prothrombin time
(sec), INR
10.9–12.5; INR < 1.1 Increased with impaired hepatic synthesis (>24 h); more time sensitive than albumin level in acute
liver failure
Platelet count
(cells/µL)
<150 000 (150 3 109/L) Decreased with advanced liver disease

8. Hepatocellular injury pattern
Suspected Cause Further Testing
Nonalcoholic fatty liver disease
(NAFLD)
Hemoglobin A1c test, lipid panel, US/MR elastography, exclusion of excessive alcohol consumption or
coexisting causes of chronic liver disease
Alcohol-related liver disease
(ARLD)
Assessment of alcohol use disorder or harmful alcohol consumption (>210 g/wk in men, >140 g/wk in women)
Viral hepatitis (A, B, C, D, E) Hepatitis A IgM, hepatitis B surface antigen, hepatitis C antibody with/without PCR, HEV IgM & IgG
Hepatitis from other viruses EBV antibody, HSV antibody, CMV antibody
Drug-induced liver injury Pharmacologic history, toxicology
Autoimmune liver disease AMA, ASMA, ANA, serum immunoglobulins, ALKM antibody
Celiac disease Anti–tissue transglutaminase/endomysial antibody
Iron overload Ferritin, transferrin, HFE mutation (if suspicion for hereditary hemochromatosis)
Wilson disease Ceruloplasmin, 24-hour urinary copper excretion
α1-antitrypsin deficiency α1-antitrypsin phenotype or level

9. Cholestatic pattern
Suspected Cause Further Testing
Primary biliary cholangitis (PBC) (intrahepatic) Presence of antimitochondrial autoantibodies; more common in women
Primary sclerosing cholangitis (PSC)
(intra/extrahepatic)
Association with inflammatory bowel disease; more common in men; unresponsive to
corticosteroids
IgG4-associated cholangiopathy (intra/extrahepatic) Somewhat similar to PSC in terms of clinical presentation and imaging; responsive to
corticosteroids
Hepatocellular carcinoma (intrahepatic) Elevated α-fetoprotein (AFP) level
Hepatic sarcoidosis (intrahepatic) Isolated elevated ALP level; elevated angiotensin-converting enzyme (ACE) level;
responsive to corticosteroids
Hepatic abscess (intrahepatic) Elevated AFP level; clinical picture helps with distinction from neoplastic entities
Drug-induced cholestasis (intrahepatic) Distinguished from hepatocellular drug-induced injury with R-factor
Benign or malignant biliary strictures (extrahepatic) CT, MRI, or MRCP to characterize biliary strictures and assess for mass
Acute extrahepatic biliary obstruction Elevated ALP and GGT levels allow identification of patients at high risk for obstruction,
who warrant further imaging

10. Acute liver failure pattern
Causes of Moderate or Severe Transaminase Level Elevation: Potential Causes of Acute Liver
Failure
Acute viral hepatitis (whether from hepatitis A–E or other viruses)
Acute ischemia
Severe drug-induced liver injury
Acute hepatic outflow obstruction
HELLP syndrome of pregnancy
Rhabdomyolysis

11. Entities causing
hepatocellular pattern
IMAGING IS AN ESSENTIAL PART OF THE DIAGNOSTIC EVALUATION
OF HEPATOBILIARY DISEASE ONCE AN INJURY PATTERN HAS BEEN
RECOGNIZED.

12. Acute Viral Hepatitis
Acute viral hepatitis can develop from hepatitis viruses A–E, as well as Epstein-Barr virus,
cytomegalovirus, and herpes simplex virus.
Most cases of viral hepatitis present asymptomatically or with right upper quadrant pain. In rare
cases, fulminant hepatitis may develop, manifesting as hepatic encephalopathy and acute liver
failure.

13. Acute Viral Hepatitis
SEROLOGY
Marked transaminase level elevation (> 1000
IU/L); further serologic and virologic testing is
necessary to determine specific cause and
treatment
Mild to moderate elevation of ALP & GGT
levels (due to a component of intrahepatic
cholestasis, this is less severe than that of the
transaminases)
AST/ALT ratio < 1.0 (most cases)
AST/ALT ratio ≥ 2.0 (fulminant cases)
RADIOLOGY
US findings:
◦ Hepatomegaly
◦ Nonspecific “starry sky” appearance: Increased
periportal echogenicity
◦ Gallbladder wall thickening
CT or MRI findings:
◦ Periportal edema
◦ Hepatomegaly
◦ Gallbladder wall edema
◦ Ascites

14. Acute viral hepatitis B
infection in a 58-year-old
man with right upper
quadrant pain and scleral
icterus.
Liver blood test results show a
hepatocellular pattern of injury, with
marked elevation of AST and ALT
levels, as well as lesser elevations of
ALP and total bilirubin levels and
international normalized ratio (INR).
(A) Abdominal US image shows diffuse
gallbladder wall thickening (arrows).
The liver was also mildly enlarged,
measuring up to 15.6 cm.

15. Acute viral hepatitis B
infection in a 58-year-old
man with right upper
quadrant pain and scleral
icterus.
Liver blood test results show a
hepatocellular pattern of injury, with
marked elevation of AST and ALT
levels, as well as lesser elevations of
ALP and total bilirubin levels and
international normalized ratio (INR).
(B) Axial fat-saturated T2-weighted MR
image shows periportal edema
(arrowhead) and marked gallbladder
wall thickening and edema (arrow).
There was no biliary duct dilatation.

16. Budd-Chiari syndrome
BCS is characterized by hepatic venous outflow obstruction, with venous congestion leading to
portal hypertension and ischemic parenchymal injury.
The most common cause of BCS is a hematologic abnormality, particularly myeloproliferative
disorders. BCS may manifest acutely with ascites, abdominal pain, and hepatomegaly; however,
subacute presentations with minimal ascites, hepatic necrosis, and outflow tract
collateralization are more common
Both acute and subacute presentations may manifest with a hepatocellular pattern.

17. Budd-Chiari syndrome
ACUTE BCS
Marked increase in transaminase levels (5x
elevation of ALT levels) due to parenchymal
ischemia
Varying increases in ALP and bilirubin levels
may also be seen, as well as prolonged
prothrombin time in acute cases with hepatic
insufficiency.
SUBACUTE BCS
Milder increase in ALT levels

18. Budd-Chiari syndrome
ACUTE BCS
Doppler US: Reduced/absent flow in hepatic
veins
CT/MRI: Features of hepatic congestion
(hepatomegaly and heterogeneous contrast
enhancement favoring central parenchyma)
CHRONIC BCS
Outflow collaterals
Sequelae of fibrosis
Caudate lobe hypertrophy
Regenerative nodules

19. Acute BCS in a 58-year-
old woman with
abdominal pain and
nausea.
Liver blood test results show a
hepatocellular pattern, with severe
elevation of AST & ALT levels and
milder elevation of ALP & bilirubin
levels.
(A) USG: Narrowed IVC (arrowhead)
and only limited color Doppler signal
in the expected regions of the right
and middle hepatic veins (arrows).
Color Doppler signal could not be
followed to the insertion at the IVC,
consistent with hepatic vein occlusion.
The patient was diagnosed with
polycythemia vera during admission.
Her clinical condition improved after
the transjugular intrahepatic
portosystemic shunt procedure.

20. Acute BCS in a 58-year-
old woman with
abdominal pain and
nausea.
Liver blood test results show a
hepatocellular pattern, with severe
elevation of AST & ALT levels and
milder elevation of ALP & bilirubin
levels.
(B) Axial postcontrast T1W MR:
Marked narrowing of the IVC
(arrowhead), caudate lobe
hypertrophy, and decreased
peripheral parenchymal enhancement
(*); the hepatic veins were not
visualized.
The patient was diagnosed with
polycythemia vera during admission.
Her clinical condition improved after
the transjugular intrahepatic
portosystemic shunt procedure.

21. Iron overload
Iron overload can occur from multiple causes, including primary entities such as HFE-associated
hereditary hemochromatosis or secondary to pathologic conditions such as ineffective
erythropoiesis or frequent blood transfusion.
While advanced hereditary hemochromatosis can manifest as cirrhosis, diabetes, and skin
pigmentation, most cases of primary or secondary iron overload manifest as asymptomatic
abnormal serum test results, such as mild transaminase level elevation.
Iron panel: Elevated serum ferritin level or increased transferrin saturation (> 45%)
◦ Although ferritin level may also be falsely positive owing to inflammation. Additionally, markedly
elevated serum ferritin level (>1000 μg/L [2247 pmol/L]) is predictive of cirrhosis, especially if combined
with elevated transaminase levels and thrombocytopenia

22. Iron overload
MRI: Best noninvasive method for detecting hepatic iron
Loss of signal intensity, proportional to iron deposition
◦ Accumulated iron shortens T1, T2, and T2* relaxation times
Demonstrate iron deposition pattern
◦ Deposition is primarily in the liver & pancreas in primary hemochromatosis compared with in the liver,
spleen, and bone marrow in transfusional overload
T2* relaxometry techniques: Quantification of hepatic iron levels, which highly correlate with
biopsy
Thus, MRI may replace the need for repeated liver biopsies in long-term surveillance of iron
overload and effects of treatment.

23. Secondary iron overload
in a 65-year-old man with
a history of AML requiring
frequent transfusion.
Liver blood test results show a
hepatocellular pattern, with moderate
elevation of AST level, mild elevation of
ALT level, and normal ALP and bilirubin
levels. Ferritin level is also severely
elevated (normal < 400 ng/mL [899
pmol/L]).
Out-of-phase (A) and in-phase (B) dual
gradient-echo T1-weighted MR images
(echo time = 2.1 msec and 4.2 msec,
respectively) show decreased signal
intensity in the liver, spleen, and
vertebral marrow on the in-phase image,
compared with the reference of
paraspinal muscle.
Results of R2* relaxometry corresponded
to approximately 7.2 mg of iron per gram
of liver, indicating moderate iron
overload.

24. Entities causing
cholestatic pattern
MANY ENTITIES CAUSING A HEPATOCELLULAR OR CHOLESTATIC PATTERN
HAVE CHARACTERISTIC FINDINGS AT FURTHER SERUM TESTING OR
IMAGING, WHICH ARE CRITICAL TO RECOGNIZE FOR PROPER WORKUP
AND DIAGNOSIS.

25. Pyogenic abscess
Hepatic pyogenic abscesses can occur from hematogenous dissemination, ascending
cholangitis, or necrotic superinfection; many cases are polymicrobial or cryptogenic.
The ALP level is elevated in most patients to a greater degree than the other liver blood tests,
with transaminase and bilirubin levels being normal or mildly elevated in the absence of
underlying biliary tract disease. Leukocytosis is also present in most patients. Owing to the
nonspecific nature of these test abnormalities, imaging is essential for diagnosis and
interventional planning
CT & US allow detection of more than 90% of pyogenic abscesses:
◦ Complex hypoechoic lesions at US and hypoattenuating lesions at contrast-enhanced CT, with a “double
target” appearance of early inner wall arterial enhancement and progressive outer wall enhancement
◦ “Cluster sign” of multiple small hypoattenuating lesions may also be seen, eventually coalescing into a
large cavity
MRI: Signal intensity characteristics vary on the basis of protein content.

26. Pyogenic hepatic abscess
in a 75-year-old man with
a history of pNET
requiring biliary stents
who presented with
lethargy and fever.
Liver blood test results show a
cholestatic pattern, with greater
elevation of the ALP level than of the
AST, ALT, or bilirubin level.
(A) Coronal portal venous phase
contrast-enhanced CT image shows a
large complex multiseptated
hypoattenuating mass (arrow)
occupying the right hepatic dome,
indicative of the cluster sign of
coalesced microabscesses. Additional
smaller abscesses (arrowheads) are
scattered throughout the right lobe.

27. Pyogenic hepatic abscess
in a 75-year-old man with
a history of pNET
requiring biliary stents
who presented with
lethargy and fever.
Liver blood test results show a
cholestatic pattern, with greater
elevation of the ALP level than of the
AST, ALT, or bilirubin level.
(B) Axial CT image shows
communication of some of the
hypoattenuating lesions with dilated
intrahepatic bile ducts (arrowheads),
as well as a biliary stent (arrow),
indicating pyogenic cholangitis as the
most likely underlying cause.

28. Primary biliary cholangitis (PBC)
Primary biliary cholangitis (PBC) is an autoimmune disorder of progressive chronic injury to the
interlobular bile ducts, most common in middle-aged women.
Liver tests:
◦ Elevated ALP level and possible hyperbilirubinemia (related to the severity of ductopenia and biliary
inflammation in patients without cirrhosis)
◦ Mildly elevated transaminase levels & elevated IgG level (correlate with the degree of periportal
necrosis)
◦ The rise in serum bilirubin and immunoglobulin levels, together with decreased albumin levels and
thrombocytopenia, indicate development of cirrhosis and portal hypertension.
Nearly all patients with PBC have antimitochondrial antibody, and anti-gp210 or anti-sp100
antibodies may also be present.

29. Primary biliary cholangitis (PBC)
Imaging is recommended for all patients with
suspected PBC to allow exclusion of other
biliary tract disease via MRCP
Elastography allows assessment for advanced
fibrosis, predictive of poor clinical outcome
IMAGING CHARACTERISTICS
Early stages: Hepatomegaly and reticulated
lacelike fibrosis
Advanced stages:
◦ Progression to cirrhosis
◦ Characteristic “periportal halo” appearance:
Consisting of focal fibrosis surrounding the
portal venous triads

30. Controlled PBC in an
asymptomatic 58-year-
old woman who
presented for MRI for
screening of HCC
Liver blood test results show a
cholestatic pattern, with elevation of
ALP level, borderline elevation of AST
and ALT levels, and normal bilirubin
level.
Axial fat-saturated T2-weighted (A)
and postcontrast T1-weighted (B) MR
images show diffuse lacelike fibrosis
with T2-hyperintense septa
(arrowheads in A), as well as T1- and
T2-hypointense parenchymal signal
intensity surrounding portal vein
branches (black circle), indicating the
periportal halo of fibrosis.

31. Controlled PBC in an
asymptomatic 58-year-
old woman who
presented for MRI for
screening of HCC
Liver blood test results show a
cholestatic pattern, with elevation of
ALP level, borderline elevation of AST
and ALT levels, and normal bilirubin
level.
Axial fat-saturated T2-weighted (A)
and postcontrast T1-weighted (B) MR
images show diffuse lacelike fibrosis
with T2-hyperintense septa
(arrowheads in A), as well as T1- and
T2-hypointense parenchymal signal
intensity surrounding portal vein
branches (black circle), indicating the
periportal halo of fibrosis.

32. Sclerosing cholangitis
PRIMARY SCLEROSING CHOLANGITIS (PSC)
Primary sclerosing cholangitis (PSC) is a
disorder of chronic progressive bile duct
fibrosis, leading to biliary strictures and
eventual cirrhosis.
Commonly associated with inflammatory
bowel disease, patients with PSC have higher
risk for cholangiocarcinoma, gallbladder
cancer, colorectal cancer, and hepatocellular
carcinoma.
IGG4–ASSOCIATED SCLEROSING CHOLANGITIS
(ISC)
IgG4–associated sclerosing cholangitis (ISC), a
biliary manifestation of systemic IgG4-related
disease, manifests with similar clinical and
imaging features to PSC; it may be associated
with autoimmune pancreatitis and responds
well to steroids, unlike PSC.

33. Sclerosing cholangitis
PRIMARY SCLEROSING CHOLANGITIS (PSC)
Early PSC:
◦ Cholestatic pattern (ALP elevation) & elevated
antineutrophil cytoplasmic antibody (ANCA)
level
◦ Transaminase and IgG serum levels may also be
mildly elevated, but the bilirubin level is normal
in most patients at diagnosis.
Advanced stages: Persistent inflammation
leads to further bile duct loss and generalized
hepatic fibrosis
IGG4–ASSOCIATED SCLEROSING CHOLANGITIS
(ISC)
On serum tests, the presence of a specifically
elevated IgG4 level and absence of ANCA can
hint toward ISC over PSC.

34. Sclerosing cholangitis
PRIMARY SCLEROSING CHOLANGITIS (PSC)
MRCP: Modality of choice
◦ Early PSC: Multifocal short segmental biliary
strictures with intrahepatic biliary dilatation
◦ Advanced disease: “Pruned tree” appearance
◦ Advanced PSC with cirrhosis: Unique hepatic
morphology (hypertrophy of caudate and central
segments and atrophy of the left lateral and
right posterior segments)
◦ Gallbladder abnormalities: Cholelithiasis,
polyps, and gallbladder carcinoma are also
common.
IGG4–ASSOCIATED SCLEROSING CHOLANGITIS
(ISC)
Distinction of ISC from PSC:
◦ Long continuous biliary strictures
◦ Lack of hepatic parenchymal changes
◦ Smooth appearance of biliary wall thickening
◦ Association with autoimmune pancreatitis

35. PSC in a 65-year-old
woman with a history of
ulcerative colitis.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level, borderline
elevation of AST level, and normal ALT
and bilirubin levels.
(A) Maximum intensity projection
image from three-dimensional MRCP
shows a multifocal beaded
appearance of strictures and
dilatation along the left intrahepatic
ducts (arrowheads), as well as an
abrupt stricture at the biliary
confluence (arrow).

36. PSC in a 65-year-old
woman with a history of
ulcerative colitis.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level, borderline
elevation of AST level, and normal ALT
and bilirubin levels.
(B) Axial fat-saturated T2-weighted MR
image shows a cirrhotic liver with
hypertrophy of the caudate lobe (*),
as well as hyperintense signal and
atrophy of the posterolateral
peripheral right lobe (arrowheads).

37. IgG4-associated
sclerosing cholangitis
(ISC) and autoimmune
pancreatitis in a 55-year-
old man with pruritus and
jaundice 10 months after
an episode of acute
pancreatitis.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level, severely
elevated bilirubin level, and mild
elevation of AST and ALT levels.
(A) Axial postcontrast T1-weighted MR
image obtained during an episode of
acute pancreatitis shows diffuse
enlargement of the pancreatic body
and tail, with loss of normal
lobulation and a hypointense
peripheral capsule (arrowheads),
consistent with autoimmune
pancreatitis.

38. IgG4-associated
sclerosing cholangitis
(ISC) and autoimmune
pancreatitis in a 55-year-
old man with pruritus and
jaundice 10 months after
an episode of acute
pancreatitis.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level, severely
elevated bilirubin level, and mild
elevation of AST and ALT levels.
(B) MRCP image obtained during
workup of jaundice shows a relatively
long primarily extrahepatic stricture
(arrow) of the common hepatic duct
and proximal common bile duct with
upstream intrahepatic biliary duct
dilatation.

39. IgG4-associated
sclerosing cholangitis
(ISC) and autoimmune
pancreatitis in a 55-year-
old man with pruritus and
jaundice 10 months after
an episode of acute
pancreatitis.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level, severely
elevated bilirubin level, and mild
elevation of AST and ALT levels.
(C) Axial postcontrast T1-weighted MR
image from the same study shows
circumferential wall thickening with
enhancement (arrows) surrounding
the biliary stricture.
Further serologic testing
demonstrated elevated IgG4 serum
levels, and the patient improved with
administration of corticosteroids.

40. Extrahepatic biliary obstruction
ACUTE BILIARY OBSTRUCTION
Acute biliary obstruction
◦ CBD disease: Choledocholithiasis or cholangitis
◦ CHD obstruction: Mirizzi syndrome
Malignant biliary obstruction
MALIGNANT BILIARY OBSTRUCTION
Cholangiocarcinoma (arises from biliary
epithelium, with a varied manifestation
including perihilar mass, intrahepatic mass, or
intraductal tumor)
Pancreatic cancer
Gallbladder cancer
Papillary tumor
Extrinsic compression by adjacent
lymphadenopathy or metastasis
A variety of entities may cause extrahepatic
biliary obstruction, including acute and
malignant causes.

41. Extrahepatic biliary obstruction
SEROLOGY
Cholestatic pattern: Elevated ALP, bilirubin, or
GGT levels
◦ Allows identification of patients at high risk for
choledocholithiasis, with a GGT threshold of
more than 90 U/L (1.50 μkat/L) being most
sensitive.
Liver blood tests can gauge the pretest
likelihood of biliary obstruction when
considering further testing.
IMAGING
US may reveal certain entities, such as acute
cholecystitis; CT or MRI can aid if US findings
are equivocal or if more detailed evaluation of
the biliary tree is warranted.
Compared with benign strictures, malignant
strictures exhibit features such as:
◦ Ductal wall thickening
◦ Long segmental morphology
◦ Hyperenhancement compared with liver
parenchyma in the portal venous phase

42. Entities causing
extrahepatic biliary
obstruction.
(A) Obstructive cholangitis in an 83-year-
old woman with fever and abdominal
pain.
Liver blood test results show a mixed
pattern, with marked elevation of AST
and ALT levels, as well as elevated ALP
and bilirubin levels; the patient also had
leukocytosis concerning for cholangitis.
Coronal contrast-enhanced CT image
shows a distended gallbladder with
calculi and pericholecystic fluid. The
common bile duct (gold arrowhead) is
dilated upstream of a distal obstructing
calculus (white arrowhead).
The patient improved after endoscopic
retrograde cholangiopancreatography
(ERCP) and sphincterotomy.

43. Entities causing
extrahepatic biliary
obstruction.
(B) Mirizzi syndrome in a 70-year-old
woman with right upper abdominal
pain. Liver blood test results show a
cholestatic pattern, with severe
elevation of ALP level and direct
hyperbilirubinemia, as well as mild
elevation of AST and ALT levels.
MRCP image shows a large calculus in
the gallbladder neck (*) compressing
the common hepatic duct with
upstream dilatation of the
intrahepatic ducts (arrow), consistent
with Mirizzi syndrome.
The patient improved after open
cholecystectomy.

44. Entities causing
extrahepatic biliary
obstruction.
(C) Cholangiocarcinoma in a 69-year-
old man with jaundice. Liver blood test
results show a cholestatic pattern,
with marked elevation of ALP level,
direct hyperbilirubinemia, and severe
elevation of AST and ALT levels. Left:
Coronal T2-weighted MR image shows
an abrupt stricture (arrowheads) at
the common hepatic duct with
upstream intrahepatic biliary duct
dilatation. Right: Axial postcontrast T1-
weighted MR image shows an
enhancing soft-tissue mass around the
stricture (arrowheads).
ERCP-guided biopsy demonstrated
intraductal cholangiocarcinoma.

45. Acute liver failure
ACUTE LIVER FAILURE IS RARE COMPARED TO CHRONIC LIVER
DISEASE AND CAN OCCUR FROM A VARIETY OF CAUSES, WITH THE
MOST COMMON CAUSE BEING ACETAMINOPHEN TOXICITY.

46. Acute liver failure
Acute liver failure is a medical emergency
requiring stabilization in the intensive care unit
and often liver transplant, and diagnostic
workup including specific serologic tests and
imaging is critical in establishing the cause and
guiding specific management.
R-FACTOR
R-factor: Allows further assessment, as certain
agents have well-described patterns of
abnormality
Calculation: (ALT level/ULN of ALT level)/(ALP
level/ULN of ALP level)
◦ Hepatocellular pattern: R-factor > 5
◦ Cholestatic injury: R-factor < 2

47. Acute-on-chronic liver failure (ACLF)
Acute-on-chronic liver failure (ACLF) is a
separate entity from acute liver failure,
manifesting as acute severe hepatic insult in a
patient with underlying chronic liver disease or
cirrhosis; similarly to acute liver failure, ACLF
has high short-term mortality, with liver
transplant being the definitive treatment.
ETIOLOGY
Specific insults that may trigger ACLF include:
Acute viral hepatitis (often distinguished from
acute liver failure by absence of
encephalopathy)
Alcoholic hepatitis (AST/ALT ratio >2.0)
Wilson disease (encephalopathy, but with
preexisting neurologic symptoms)

48. Acute liver failure
IMAGING: ACUTE PHASE (≤ 1 WEEK)
Periportal edema
Parenchymal necrosis
Marked parenchymal hypoechogenicity at US
or hypoattenuation at CT
IMAGING: SEVERE LIVER INJURY
Extensive necrosis and parenchymal collapse
can lead to a radiologic appearance mimicking
that of cirrhosis
◦ Requiring biopsy to differentiate between the
two entities and determine proper treatment.
For example, surface nodularity can be seen in
cases of acute liver failure without preexisting
cirrhosis

49. Acute liver failure
(A) A 22-year-old woman with
acetaminophen overdose.
Liver blood test results show an acute
liver failure pattern, with severe
elevation of AST and ALT levels,
elevation of the international
normalized ratio (INR), and normal ALP
and bilirubin levels. The R-factor was
greater than 5, indicating a
hepatocellular pattern of drug-induced
injury.
Axial portal venous phase contrast-
enhanced CT image shows periportal
edema (arrowhead) and
heterogeneous parenchymal
enhancement (*)

50. Acute liver failure
(B) A 72-year-old woman with
jaundice.
Liver blood test results show a mixed
pattern of injury, with elevated AST,
ALT, ALP, and bilirubin values and
increased INR.
US image shows heterogeneous
parenchyma, nodular contour
(arrowheads), and ascites. Results of
CT 2 months before admission were
normal.
Biopsy showed confluent hepatic
necrosis without fibrosis or cirrhosis.
No definite cause was found.

51. Post-transplant
complications
LIVER TRANSPLANT COMPLICATIONS CAN BE CATEGORIZED INTO BILIARY,
VASCULAR, OR OTHER CAUSES, WITH ABNORMALITIES IN LIVER BLOOD
TESTS OFTEN BEING THE FIRST SIGN OF DYSFUNCTION.

52. Post-transplant complications
While AST/ALT elevation is nonspecific, regular transaminase level monitoring is recommended
throughout the posttransplant period (43)
Normal range of AST and ALT levels may be higher in posttransplant patients, up to 54–57 IU/L
(0.90–0.95 μkat/L) (44).

53. Biliary complications (first 3 months)
ETIOLOGY
Biliary complications occur primarily in the
first 3 months and include:
◦ Anastomotic strictures
◦ Bile leak
◦ Nonanastomotic obstruction from biliary
casting or stones
◦ Ischemic cholangiopathy
A significant elevation in the ALT or ALP level
from the pretransplant baseline may allow
prediction of biliary strictures
IMAGING
MRCP: Modality of choice for detecting biliary
disease, but it still may not demonstrate up to
about 20% of strictures seen with endoscopic
retrograde cholangiopancreatography (ERCP)
CT, cholescintigraphy, or direct
cholangiography may demonstrate biliary
leaks.

54. Vascular complications
Vascular complications include hepatic arterial
thrombosis, stenosis, or occlusion
Elevated transaminase levels may occur from
hepatocellular injury, as well as a rise in ALP or
bilirubin level due to associated biliary
compromise (eg, ischemic cholangiopathy).
IMAGING
Doppler US features of hepatic artery
occlusion:
◦ Vessel non-visualization in occlusion or low
resistive index (<0.55)
◦ Long systolic acceleration time
◦ Distal tardus-parvus waveform in stenosis
Contrast-enhanced CT angiography is
warranted to localize the disease and guide
intervention

55. Long-term (>3 months) posttransplant
complications
Long-term (>3 months) posttransplant
complications include:
◦ Infection
◦ Allograft rejection
◦ Recurrence of primary disease
DIAGNOSIS
Like in the acute period, transaminase level
elevation is often the first sign of dysfunction
Doppler US allows screening for vascular or
biliary structural abnormalities
Additionally, imaging allows confident
identification of some pathologic conditions,
like hepatic abscess or tumor recurrence.
However, many cases require liver biopsy for
definitive diagnosis and to exclude allograft
rejection.

56. Posttransplant biliary
stricture in a 61-year-old
man with low-grade fever
and elevated bilirubin
level 6 months after
transplant for HCC and
NASH.
Liver blood test results show a
cholestatic pattern, with moderate
elevation of ALP level and direct
hyperbilirubinemia, as well as mild
elevation of AST and ALT levels.
Maximum intensity projection image
from three-dimensional MRCP shows
abrupt caliber change (arrowhead) at
the biliary anastomosis with
upstream dilatation.

57. Posttransplant hepatic
artery occlusion in a 62-
year-old man with
lethargy and fever 2
months after transplant
for HCC and NASH.
Liver blood test results show a mixed
pattern of injury, with marked
elevation of transaminase levels, as
well as severe direct
hyperbilirubinemia and mildly
elevated ALP level. Doppler US could
not demonstrate the hepatic arteries.
(A) Axial arterial phase CT angiogram
shows abrupt cutoff (arrowhead) of
the common hepatic artery.

58. Posttransplant hepatic
artery occlusion in a 62-
year-old man with
lethargy and fever 2
months after transplant
for HCC and NASH.
Liver blood test results show a mixed
pattern of injury, with marked
elevation of transaminase levels, as
well as severe direct
hyperbilirubinemia and mildly
elevated ALP level. Doppler US could
not demonstrate the hepatic arteries.
(B) Image from arteriography of the
celiac trunk shows the common
hepatic artery occlusion (arrowhead).
Attempted catheter-directed
thrombolysis and angioplasty were
unsuccessful, and the patient required
surgical revision of the hepatic artery
anastomosis.

59. Chronic liver disease
(CLD)

60. Chronic liver disease (CLD)
Most common causes of chronic liver disease:
◦ NAFLD (increasing prevalence with obesity epidemic)
◦ Alcohol-related liver disease (ARLD)
◦ Chronic hepatitis B (decreased prevalence decreased owing to vaccination and antiviral regimens)
All three entities often manifest asymptomatically, either with mild transaminase level elevation
or incidentally noted hepatic steatosis at imaging.

61. Chronic liver disease (CLD)
Borderline/mild elevation in AST and ALT levels
Borderline/mild elevation in transaminase
levels
NAFLD: Elevation in GGT and low titers of serum
autoantibodies or mildly elevated serum ferritin
or transferrin level, even in the absence of
autoimmune disease or iron overload
Chronic viral hepatitis: AST/ALT ratio > 1 is
correlated with poorer prognosis and is
predictive of progression to cirrhosis.
Another possible indication of possible chronic
liver disease is the incidental finding of hepatic
steatosis at imaging.
In either scenario, further diagnostic testing is
warranted to narrow the differential, including
exclusion of other causes of chronic liver disease
in cases of suspected NAFLD

62. Spectrum of
chronic liver
disease.
(A) A 36-year-old woman with
asymptomatic chronic hepatitis B virus
(HBV) infection. Results of liver blood
tests were all within normal limits,
with a FIB-4 score of 0.55, below the
threshold for fibrosis. US image shows
normal echogenicity, echotexture, and
contour of the liver.

63. Spectrum of
chronic liver
disease.
(B) A 41-year-old woman with
incidentally noted AST level elevation
and suspected NAFLD. Liver blood test
results show borderline elevation of
transaminase levels, with a FIB-4 score
of 1.40, in the indeterminate range. US
image shows increased hepatic
echogenicity in comparison with the
kidney (*) and increased attenuation,
consistent with hepatic steatosis. MR
elastography showed stiffness of 4.4
kPa, consistent with stage 3 or 4
fibrosis.

64. Spectrum of
chronic liver
disease.
(C) A 58-year-old man with cirrhosis
secondary to NAFLD. Liver blood test
results show mild elevation of
transaminase levels, with a FIB-4 score
of 4.05, above the cutoff for advanced
fibrosis. Axial portal venous phase
postcontrast T1-weighted MR image
shows nodular contour (arrowheads)
and morphology consistent with
cirrhosis, as well as a recanalized
paraumbilical collateral (arrow),
suggestive of portal hypertension. MR
elastography showed stiffness of 8.63
kPa, consistent with cirrhosis.

65. Cancer
LIVER BLOOD TESTS PLAY AN IMPORTANT ROLE IN SURVEILLANCE
FOR HEPATOBILIARY MALIGNANCY.

66. HEPATOCELLULAR CARCINOMA (HCC)
α-Fetoprotein (AFP): Important marker for
HCC, with a positive threshold of 20 ng/mL (20
μg/L),
AFP testing is recommended along with US
every 6 months in patients at risk
Albumin-bilirubin (ALBI) score: Determine
liver function and prognosis in diagnosed cases
PANCREATIC AND BILIARY TRACT CANCERS
CA 19-9: Tumor marker used for detection but
significant level elevations may occur with
benign obstructive jaundice as well as
malignancy; therefore, CA 19-9 level should be
interpreted in the clinical and imaging context

67. Thank you