LIVER ABSCESS &

TUMORS

Gopinath
Asyraf
Ahdiah
LIVER
ABCESS
• Def : pus-filled mass in liver that can develop from injury to the liver or intrabdominal infection
disemminated from portal circulation.
• Majority of these abscesses are categorized into pyogenic / amoebic, although minority caused
by fungus.

Epidemiology
• Annual incidence rate is around 2.3 cases per 100,000 people.
• Males more affected than female.
• People aged 40-60 years are more vulnerable to develop abscess that does not result from
trauma.
• Significant number of cases are reported to be pyogenic In middle East.
ETIOLOGY
• Biliary tract disease: biliary stone, strictures, malignancy, and some
congenital anomalies are major cause of pyogenic liver abscess.
• Half of bacterial cases developed by cholangitis, the most common
organism include E.Coli, Klebsiella, Streptococcus, Staphylococcus
and anaerobic organisms but are generally polymicrobial.
• If source is anaerobe, most common one is Entamoeba Histolytica,
it affects by first causing amoebic colitis, and migrating to liver and
portal system.
• Another rare but important parasitic organism is Echinococcus
Granulosus, which causes hydatid cyst of liver.
HISTORY,
PHYSICAL
EXAMINATION
AND
COMPLICATION OF
LIVER ABSCESS
AHDIAH SAYUTY
 PYOGENIC LIVER ABSCESS
HISTORY
 Clinical signs of PLAs are often nonspecific and include fever, chills,
malaise, weight loss and abdominal pain located in the upper
right quadrant. The onset may be occult in the elderly.
 Symptoms of a primary infection may appear first, e.g. diverticulitis.
Often, especially solitary PLAs are asymptomatic for a long time or cause
no characteristic symptoms. Multiple abscesses are associated with an
acute systemic inflammatory reaction. Sometimes, the sole symptom is
fever of an unknown origin.
 PYOGENIC LIVER ABSCESS
PHYSICAL
EXAMINATION
 On physical examination, the
liver is usually enlarged
and tender.
Jaundice is a late symptom of
liver abscess unless there is
purulent cholangitis.
 PYOGENIC LIVER ABSCESS
COMPLICATION  PLAs caused by Klebsiella
pneumoniae are associated with
septic metastatic complications
affecting the eye
(endophthalmitis), brain
(meningoencephalitis), and
fascia (necrotizing fasciitis).
Unfortunately, they may persist even
after successful topical treatment of
the abscess.
 AMOEBIC LIVER ABSCESS
HISTORY

 Most acute patients report fever with

chills and pain in the right
upper abdomen, cough, weight loss and jaundice. Less common
are diarrhea, nausea, vomiting, and loss of appetite.
 Prolonged diarrhea occurs in 20-50% of cases. About 80% of patients with
ALA will develop symptoms within a few weeks of infection. The
incubation period is usually 2-6 months, although cases of ALA have been
reported even several years after staying in the endemic region.
 AMOEBIC LIVER ABSCESS
PHYSICAL
EXAMINATION
 During palpation, we can find liver enlargement, tenderness in the
right hypochondrium, radiating pain to the right shoulder, and pain in
the right side of the chest.
 An abscess in the form of a single lesion is most often located in the right
liver lobe, while in the case of multiple lesions, the clinical course is more
severe, with symptoms of increased toxemia.
 AMOEBIC LIVER ABSCESS
COMPLICATION  Pulmonary-pleural form of
amoebiasis
 Secondary lesions in the peritoneal
cavity and pericardium
 Hepato-intestinal fistula
 Bacterial coinfections
 Biliary dysfunction
 Hepatic vein thrombosis and portal
vein thrombosis are rare.
 FUNGAL LIVER ABSCESS
CLINICAL FEATURES

 History of immunosuppression.
 The most common symptoms: the loss of appetite, worsening
malaise, tenderness in the RUQ abdomen.
 Clinical symptoms: fever of unknown origin, especially in the
absence of response to antibiotics, enlargement of the liver and/or
spleen, and jaundice.
 FUNGAL LIVER ABSCESS
COMPLICATION

 Initially, the invasion of Candida spp. and Aspergillus spp. affects the
mucous membranes, but further progression of the disease through the
circulatory system (fungemia) involves subsequent internal organs,
including the liver, leading to the formation of micro-abscesses.
 Sepsis is a rare form of trichosporosis and coccidioidomycosis when liver
granulomas and micro-abscesses may be formed.
 Hepatic mucormycosis is rare.
PYOGENIC LIVER ABSCESS
LAB RESULTS

 FBC will reveal two thirds of patients have leukocytosis with anemia
 Higher C-reactive protein (CRP) and procalcitonin concentrations are markers
of bacterial infection
 Alkaline phosphatase (ALP), bilirubin and aminotransferases (ALT, AST)
activities are raised
 Albumin level is decreased
PYOGENIC LIVER ABSCESS
IMAGING

 Chest X-ray can show a fluid level in the abscess cavity, fluid in the right pleural cavity or
elevation of the right diaphragm dome
 Abdominal USG remains the preferred initial method of imaging. CT scan is helpful to
identify other intra-abdominal abscesses
 MRCP and ERCP are used to define the localization of biliary obstruction and to allow
biliary stenting and drainage
 Colonoscopy is useful in detection of large bowel infections and colorectal neoplasms.
PYOGENIC LIVER ABSCESS
Tx & Mx
Empirical broad spectrum parenteral antibiotic therapy:
 Initiated immediately upon suspicion of infection

 Modified based on pus/blood culture results

 Consider potential sources of infection and target aerobic Gram-negative bacilli and Gram-positive cocci

 First-line therapies:
 Piperacillin/tazobactam
 Amoxicillin/clavulanic acid
 3rd generation cephalosporins (cefotaxime, ceftriaxone)
 Monotherapy or in combination with gentamicin (aminoglycoside)

 Anaerobic antibiotics (e.g., metronidazole) used if initial treatment is ineffective or suspicion of amoebic abscess

 In elderly or those with impaired renal function, use 3rd generation cephalosporin
PYOGENIC LIVER ABSCESS
Tx & Mx

 Antibiotic resistance considerations:

 Enterobacteriaceae family may show resistance to empirical antibiotics
 Early identification of microorganism based on abscess aspirate and/or blood culture crucial for modifying therapy

 Duration of treatment:
 Antibiotics administered for minimum 2 to 6 weeks
 Initial intravenous therapy followed by oral form in most cases to complete therapy

 Additional treatments:
 Ultrasound or computed tomography (CT)-guided percutaneous aspiration or catheter drainage often required
 Complete cure with antibiotic treatment possible in patients with small abscesses (size not exceeding 3-5 cm)
 Most patients require antibiotics in addition to drainage procedures.
AMOEBIC LIVER ABSCESS
LAB RESULTS

 FBC will reveal anemia, increased leukocytosis, usually up to 20,000/mm3

 Increased CRP concentration
 Increased ALP, AST,ALT, and γ-glutamyltranspeptidase (GGT).
 Puncture of the abscess with aspirate collection is of diagnostic and therapeutic importance.
The high density and chocolate color of the obtained aspirate are characteristic. Culture both
of blood and aspirate for bacterial infections with aerobic and anaerobic flora and fungi are
necessary.
AMOEBIC LIVER ABSCESS
IMAGING

 Abdominal imaging examinations are used in diagnosis and

monitoring of the treatment effect.
 Abdominal USG imaging shows hypoechoic liver changes
 Contrast enhanced CT shows a heterogeneous low-density mass
with fluid content and peripheral enhancement.
 Liver MRI shows low signal intensity (black/gray) of the mass
in the T1-weighted image and high signal intensity (white) with
perifocal edema in the T2-weighted image.
AMOEBIC LIVER ABSCESS
MICROBIOLOGY

 The detection of parasites in stools confirms the diagnosis, but it

is positive only in 20% of ALA cases
 Direct microscopy has limited sensitivity and specify (60% and
50%) and cannot distinguish Entamoeba histolytica from non-
pathogenic E. dispar
 Serological assay is used to detect Entamoeba coproantigen
 Serological tests detect antibodies to Entamoeba antigens with a
sensitivity of 65-92% and a specificity of > 90%.
AMOEBIC LIVER ABSCESS
Tx
Treatment for amoebiasis, including amoebic liver abscess (ALA):
 Nitroimidazole derivatives with activity against invasive trophozoites and an active drug against cysts in the
intestinal lumen are essential.
 Recommended regimen:
 Metronidazole 750 mg orally three times daily for 10 days, or
 Tinidazole 2.0 g daily for 5 days
 Severe cases or intolerance to oral treatment:
 Intravenous metronidazole 500 mg three times daily, or
 Paromomycin 25-35 mg/kg/day
 Antiparasitic treatment is usually initiated before confirming the etiology under strong epidemiological
conditions, often in conjunction with broad-spectrum antibiotic therapy.
AMOEBIC LIVER ABSCESS
Tx

 Abscess drainage:
 Considered if no improvement occurs within 72 hours of antiparasitic treatment, suspicion of bacterial co-
infection, large lesions (> 5-10 cm), or presence of abscess in the left lobe due to risk of perforation and
involvement of pleura, peritoneum, and pericardium.
 Post-treatment observations:
 After completion of causal treatment, slow regression of liver lesions is observed.
 Residual cavernous lesions may persist for up to 6 months.
FUNGAL LIVER ABSCESS
LAB Ix

 Integration of ultrasound findings with clinical and laboratory data:

 Abnormal values of C-reactive protein (CRP), aminotransferases, alkaline phosphatase (ALP), and bilirubin.

 Eosinophilia may be present in coccidioidomycosis.

 Additional diagnostic tools:
 US-guided fine-needle aspiration biopsy for microbiological examination.
 Contrast-enhanced CT or MRI examinations for further evaluation.
FUNGAL LIVER ABSCESS
IMAGING
 Diagnosis of fungal liver abscesses: Abdominal
ultrasound (US), computed tomography (CT), and
magnetic resonance imaging (MRI) are particularly
important.
 US findings:
 Numerous tiny lesions often detected as hypoechoic areas.
Convex probe greyscale ultrasound shows
 Characteristic images include: heterogeneous liver parenchyma with small
hypoechoic areas. It is difficult to tell if these are
 "Circle in a circle": hypoechoic center containing necrotic
lesions or not. Linear higher frequency probe
tissues surrounded by a hyperechoic layer of inflammatory helps to identify a few focal hypoechoic lesions
cells. (one is shown). Contrast-enhanced ultrasound
 "Shield" symptom. depicts many small non-enhancing round lesions,
suggestive of abscesses.
FUNGAL LIVER ABSCESS
Tx

 Pharmacotherapy for fungal liver abscesses: Primary drug: Liposomal amphotericin B

 Dosage: 5 mg/kg for at least 2 weeks

 Possible combination therapy:

 5-fluorocytosine: 100 mg/kg
 Fluconazole: Initially 800 mg, followed by 400 mg daily
 Itraconazole: 3 doses of 200 mg each, continued for 2-5 months
HEPATOCELLULAR
CARCINOMA

AHDIAH SAYUTY
TABLE OF CONTENTS
EPIDEMIOLOGY LAB
ETIOLOGY INVESTIGATION
STAGING
IMAGING
CLINICAL
FEATURES TREATMENT

COMPLICATION
 EPIDEMIOLOGY
 Liver cancer is the 5th most common cancer and the 4th leading
cause of cancer-related deaths worldwide.
 HCC accounts for more than 80% of primary liver cancer cases
worldwide.
 It’s the 4th most frequent cancer in male and 9th in women and the
2nd leading cause of cancer-related deaths in men and 4th in
women.
 Men are at a higher risk of developing liver cancer compared to
women with ratio of men to women is 2.8:1.
ETIOLOGY
Hepatitis B
Hepatitis C
Alcoholic liver disease
Non-alcoholic liver steatohepatitis/non-
alcoholic fatty liver disease
Autoimmune Hepatitis
Other risk factors include iron overload, Glycogen storage disease, Wilson disease, alpha one antitrypsin
disease, hypercitrullinemia, Alagille syndrome, and acute intermittent porphyrias
ETIOLOGY
CLINICAL FEATURES
Cirrhotic-related HCC patients may present
with symptoms of decompensated liver failure:

worsening jaundice, pruritus, hepatic

encephalopathy, ascites, palpable mass in the
upper abdomen, fever, malaise, weight loss,
early satiety, abdominal distension, and
cachexia. Abdominal pain is the commonest
presentation for HCC.
C L IN IC A L FE ATU R ES

Paraneoplastic syndrome in HCC patients

may present with hypoglycemia,
erythrocytosis, hypercalcemia, diarrhea, and
cutaneous findings such as pemphigus
foliaceous, pityriasis rotunda,
dermatomyositis, and Leser-Trelat sign.
Barcelona Clinic Liver Cancer
(BCLC) Staging
 LAB INVESTIGATIONS
 LFT including bilirubin, ALT, AST, ALP, and albumin may be elevated on the
initial evaluation.
 Coag profile: Elevated INR, PT, thrombocytopenia, anemia, hyponatremia, or
hypoglycemia.
 Patients with early non-cirrhotic-related HCC may present with normal LFTs on
the initial encounter.
 Patients with paraneoplastic features of HCC could present with
hypoglycemia, hypercalcemia, erythrocytosis.
 Serum Alpha-Fetoprotein (AFP). Elevated levels of AFP are typical for advanced
HCC.
 Other ix include hepatitis B surface antigen, anti-HCV antibody, alpha
antitrypsin level, copper levels, and iron saturation.
 ULTRASOUND
• Ultrasound with or without serum
alpha-fetoprotein is recommended
every six months for HCC surveillance
in high-risk patients.
 Non-contrast US determines the size, morphology, location, and
vascular invasion of HCC.
 HCC demonstrates increased blood flow and neovascularity.
 USG is limited for the detection of tumors less than 2 cm.
 Contrast-enhanced ultrasound (CEUS) is used for the
characterization of lesions detected on non-contrast ultrasound.
 OTHER IMAGING
 CT scan: Diagnostic imaging criteria for detecting HCC with triphasic
CT scan include hyperenhancement in the arterial phase and rapid
washout during the portal venous phase relative to the liver
background.
 MRI: T1-weighted images may be isointense to hyperintense
depending on the degree of fibrosis, fat, and necrosis. Hyperintense
images on T1 are mostly well-differentiated tumors and appear as
isointense on T2 images. Poorly or moderately differentiated tumors
appear as isointense on T1 images and hyperintense on T2 images.
 CT
SCAN

presentation title 40
presentation title 41
 LIVER BIOPSY
Liver biopsy is not routinely done for
HCC as the procedure is associated
with the risk of tumor seeding and
bleeding, and false negative on
failure to obtain tissue from the
appropriate site.
 SURGICAL RESECTION
 Patients with Barcelona-clinic liver cancer (BCLC) classification of very
early (0) and early-stage (A) are ideal candidates for surgical resection.
 Patients with Child–Turcotte–Pugh A and without clinically significant
portal hypertension have favorable surgical resection outcomes.
 Patients with small HCC (tumors less than 5 cm) and Child-Pugh A
have survival rates of 70% and 35% at 5 and 10 years, respectively,
and recurrence-free survival rates of 36% and 22%.
 LIVER TRANSPLANTATION
 Liver transplantation is associated with the removal of tumors and the
potential for cure.
 Milan criteria for liver transplantation is a single nodule less than or
equal to 5 cm in diameter or not more than three nodules, with none
larger than 3 cm in diameter without macrovascular invasion and
extrahepatic spread.
 A patient who meets Milan criteria for liver transplantation is associated
with a 60%-80% and 50% survival rate at 5 and 10 years, respectively.
 Post-transplantation recurrence of HCC is less than 15%.
 TUMOR ABLATION
 Patients with BCLC classification of very early (0) and early-
stage (A) who do not meet surgical resection criteria are
appropriate for ablation.
 Ablation is by modifying the local tumor temperature by using
either radiofrequency ablation (RFA), cryotherapy, microwave,
or laser therapy or injection of chemical substances (ethanol,
boiling saline, and acetic acid).
 Radiofrequency ablation has been shown to have superior
ablative therapy in patients with tumors >2 cm as compared to
percutaneous ethanol and acetic acid injection.
 COMPLICATIONS
 Hepatic encephalopathy, portal vein thrombosis, worsening ascites,
variceal bleeding, obstructive jaundice, and pyogenic liver abscess
are common cx.
 Intraperitoneal bleeding is a life-threatening cx of HCC. Patients
present with worsening ascites and pain, hypotension, and anemia.
 Emergency OGDS or surgery for control of bleeding. CT abdominal
scan non-contrast is required for diagnosis.
 The most common extrahepatic metastasis of HCC is to the lung,
intra-abdominal lymph node, bone, and adrenal, respectively. The
brain tumor is a rare extrahepatic manifestation of HCC.
HEPATIC
HEMANGIOMA
• Mesoderm derived tumor consisting of blood-filled space, supplied by hepatic
arterial circulation, and lined by flat endothelial cells.
• Most common benign liver tumor, presenting as a well circumscribed
hypervascular lesion
• More commonly found in women.
• Commonly presents as incidental finding during radiological imaging
• Classified by their nature as cavernous, capillary and sclerosing hemangioma,
which can be misdiagnosed as malignant tumor
PATHOGENESIS
• Not completely known, in some cases genetic predisposition has been described.
• arises from a vascular malformation with a growing pattern secondary to dilation
rather than hypertrophy or hyperplasia.
• One hypothesis suggest HH results from abnormal angiogenesis and an increase
in pro-angiogenic factors
• Hormones such as estrogens play a role in HH growth, as they are seen more
frequently among women and their size increase after hormone replacement
therapy (HRT), oral contraceptive pills (OCPs), and pregnancy
• The direct mechanisms of hormone effects are unknown, as HH are negative for
estrogen and progesterone receptors and current evidence does not support a
contraindication of OCPs / HRT/ anabolic steroids in patients with HH
Symptoms
• HH are usually asymptomatic, however symptoms may present when a HH is larger
than > 5 cm
• patients usually describe abdominal pain, discomfort and fullness in the right
upper quadrant, secondary to stretching and inflammation of the Glisson’s capsule
• Tumors > 10 cm present with abdominal distention.
• Liver mass may cause pressure and compression of adjacent structures causing
other symptoms such as nausea, early satiety, and postprandial bloating.
DIAGNOSIS
• HH unique features by imaging , the presence of peripheral nodular
enhancement and a progressive centripetal fill-in. Ultrasound (US), computed
tomography (CT), and magnetic resonance imaging (MRI) are the most common
imaging tests.
• US is usually the first diagnostic imaging test due to its availability, appears as a
well-defined, homogeneously hyper echoic mass with posterior acoustic
enhancement .
• US has a sensitivity of 96.9% and a specificity of 60.3%.
• Some malignant hepatic lesions (Hepatocellular carcinoma and hepatic
metastases) may produce similar acoustic patterns and other imaging modality
must be used to confirm diagnosis.

Contrast-enhanced US (CEUS)
• peripheral nodular contrast enhancement in the early phase (arterial) with
centripetal filling in later phases.
Computed Tomography
• has a sensitivity of 98.3% and a specificity of 55%
• described as well-demarcated hypodense masses, when contrast used,peri-
ripheral nodular enhancement with centripetal homogeneous filling is expected,
however small lesions and HH with cystic areas, fibrosis or thrombosis may
show an atypical pattern.
MRI
• best imaging method for HH with a sensitivity of 90%-
100% and a specificity of 91%-99%
• well-defined, smooth, homogenous lesion, hypointense on
T1 and hyperintense on T2 weighted images.

Angiography
• best option for atypical HH that are difficult to diagnose
with other imaging test.
• appears as a “snowy-tree” or “cotton wool” with a large
feeding vessel and diffuse pooling of contrast that
continues during delayed phase
Complications
• Giant HH may cause a life-threatening coagulation disorder
known as Kasabach-Merrit syndrome (thrombocytopenia,
disseminated intravascular coagulation, and systemic bleeding)
presenting with coagulopathy secondary thrombocytopenia,
anemia, hypofibrinogenimia, a decrease in prothrombin time,
and increase in D-dimer.
• Another serious complication is bleeding from spontaneous or
traumatic rupture (in peripherally located and exophytic giant
lesions), however the risk is extremely low (0.47%)
Management
• Small, asymptomatic HH do not require treatment or follow up.
• follow-up in HH > 5 cm at 6-12 mo to asses for rapid growth
with the same imaging test used at diagnosis
• Treatment should be restricted to symptomatic patients, with
continuous mass growth, compression of adjacent organs
(gastric outlet obstruction, Budd-Chiari syndrome) or
complications such as rupture with intraperitoneal bleeding or
Kasabach-Merrit syndrome.
Surgery
• most common treatment for HH. Surgical management
includes liver resection, enucleation, hepatic artery ligation
and liver transplantation.
• most common procedures worldwide are liver resection and
enucleation (open surgery, laparoscopy )
• Liver transplantation is reserved for unresectable giants HH
causing severe symptoms (respiratory distress, abdominal
pain), failure of previous interventions or life-threating
complications such as Kasabach Merrit syndrome
Non Surgical
• Transcatheter arterial embolization (TAE) is used to control
acute bleeding or shrink HH prior to surgery with metallic
coils, gelform particles, polyvinyl alcohol and liquid agents.
• Radiofrequency ablation (RFA) can be used percutaneously,
laparoscopically or by open surgery.
FOCAL
NODULAR
HYPERPLASIA
FOCAL NODULAR HYPERPLASIA
Focal nodular hyperplasia (FNH):
 Second most common benign liver tumor after hepatic hemangioma
 Estimated incidence: 3-5%.
 Predominantly affects women in the third through fifth decades of life
Liver regenerative ability:
 Liver is the only self-regenerative internal organ
 Regenerative ability increases risk for development of atypical masses
FOCAL NODULAR HYPERPLASIA
The etiology of focal nodular hyperplasia has not been definitively established.
However, it is thought to be caused by arterial malformations within the liver.
These malformations, coupled with changes in perfusion, cause a regenerative,
hyperplastic response of the normal hepatocyte
The origin of focal nodular hyperplasia is thought to be due to a hyperplastic growth
of normal hepatocytes with a malformed biliary drainage system, possibly in
response to a pre-existent arteriovenous malformation
 The arterial supply is derived from the hepatic artery whereas the venous drainage
is into the hepatic veins. Focal nodular hyperplasia does not have a portal venous
supply
FOCAL NODULAR HYPERPLASIA
FOCAL NODULAR HYPERPLASIA
Characteristics of focal nodular hyperplasia (FNH):
 Majority of patients present with solitary lesions, typically between 4 and 8 centimeters in diameter
 Only 3% of cases have lesions larger than ten centimeters
 Grossly evident hallmark feature: "central scar."
Histological features:
 Central scar composed of mature collagen surrounded by aberrant arteries, draining veins, and fibrous
septae forming a pseudocapsule
 Differentiates FNH from hepatocellular carcinoma, hepatocellular adenomas, and fibrolamellar
hepatocellular carcinoma
 Biopsy of central scar essential for diagnosis and ruling out malignancy
 FNH lesions may contain bile ducts and reticuloendothelial hepatic macrophages (Kuppfer cells)
 Cytologically, hepatocytes from FNH lesions are unremarkable, confirming benign origin
FOCAL NODULAR HYPERPLASIA
Typical FNH (80%): Atypical FNH (20%):
Macroscopic characteristics: Lacks central scar and central artery, making it
 Often large mass with well-circumscribed margins but harder to distinguish from other lesions.
poorly encapsulated
 Prominent central scar present in less than 50% of Abnormal nodular architecture and
cases cholangiolar proliferation.
 Large central artery with spoke wheel-like centrifugal
flow
Additional atypical features:
 Absence of portal veins  Pseudocapsule, lesion heterogeneity (more commonly
seen in adenoma), non-enhancement of central scar, and
intralesional fat.
Microscopic features:
 Abnormal nodular architecture, malformed vessels, Nodules can grow, disappear, and new nodules
and cholangiolar proliferation. can appear even after resection
 Nearly normal hepatocytes arranged in one to two
cell-thick plates.
 Bile ductules typically found at interface between
hepatocytes and fibrous regions.
 Presence of Kupffer cells.

No malignant potential
FOCAL NODULAR HYPERPLASIA
Discovery of focal nodular hyperplasia (FNH):
 Most often incidental finding after imaging performed for unrelated abdominal
complaint
Clinical presentation:
 Typically asymptomatic
 May present as palpable abdominal mass
 Palpable mass more likely to be tender when lesion's diameter exceeds 10 centimeters
 Hepatomegaly uncommon due to solitary nature of lesions.
Complications:
 Spontaneous rupture extremely rare.
FOCAL NODULAR HYPERPLASIA
Diagnosis of focal nodular hyperplasia (FNH):
Consists of biopsy or imaging consistent with FNH and exclusion of other similar
lesions.
Lab work typically unremarkable, with alpha-fetoprotein (AFP) levels within
reference range, supporting benign clinical course.
Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline
phosphatase (ALP), and gamma-glutamyl transpeptidase (GGT) levels may display
minor elevations, but not specific to FNH.
FOCAL NODULAR HYPERPLASIA
Imaging modalities:
Ultrasonography:
 Often first-line imaging.
 Limited sensitivity (20%), but may reveal isoechoic or hypoechoic mass with hyperechoic central
scar.
 Contrast-enhanced ultrasonography can aid in distinguishing FNH from hepatocellular adenoma.
Triphasic helical computed tomography (CT):
 Cheap and reliable
 FNH appears hypodense or isodense pre-contrast, hyperdense during arterial phase, and isodense
during portal venous phase
Magnetic resonance imaging (MRI):
 FNH lesions appear isointense to hypointense on T1-weighted images and isointense to hyperintense
on T2-weighted images.
 Enhanced arterial phase and relatively obfuscated on venous and delayed phase images.
 Hepatobiliary contrast media with MRI provides high sensitivity and specificity (99% and 100%
respectively) and is considered the best test for FNH diagnosis.
FOCAL NODULAR HYPERPLASIA
Management approach for focal nodular hyperplasia (FNH):
 Close observation with serial imaging every three to six months is recommended due to procedural
risks associated with biopsy and surgical resection, as well as the indolent nature of FNH.
 Biopsy or resection may be pursued in symptomatic patients, inconclusive biopsy results with
concern for underlying malignancy, or if lesion displays continued growth.
 Definitive therapy remains surgical resection.
Relationship with oral contraceptive pills (OCPs):
 FNH was first described before widespread use of OCPs.
 No proven increase in incidence of FNH with OCP use.
 Almost all documented cases of hemorrhage or rupture associated with FNH have occurred in
patients taking OCPs.
 Discontinuation of OCPs not necessarily indicated, but follow-up imaging advised for patients on
estrogen therapy to monitor for growth.
Pediatric considerations:examination of patient's risk factors for underlying malignancy or liver
disease
 Thorough warranted in pediatric population.
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