This document discusses the approach to evaluating and diagnosing liver masses. It defines a liver mass and explains how imaging techniques are used in the diagnosis. The differential diagnosis for liver masses can range from benign to malignant lesions. Cystic lesions discussed in detail include pyogenic and amoebic liver abscesses. Solid lesions include inflammatory conditions like abscesses as well as benign and malignant tumors. Treatment options for different lesions are outlined.

1. Approach to
Liver Mass
DR. SAURAV MAJUMDAR
DR. H.R. RAVISHANKAR

2. What is a liver mass?
❖Defined as a focal solid or cystic lesion that can be differentiated from the surrounding liver
parenchyma by imaging techniques.
❖Detection has dramatically increased in recent years due to the widespread use of imaging
techniques for evaluation of the abdomen
❖The differential diagnosis may range from benign asymptomatic lesions to malignant neoplasms
❖The correct characterization of a liver mass is a diagnostic challenge
❖The diagnosis of a focal liver lesion is based on clinical background, imaging findings and, in
some cases, on pathologic analysis.

3. ❖The clinical background may also suggest a diagnosis.
❖Imaging techniques show whether the tumour has a liquid or solid content.
❖The vascularization profile after contrast administration may also suggest its possible diagnosis.
❖Contrast-enhanced ultrasound, dynamic CT, and dynamic MRI may strongly suggest the
diagnosis.
❖Nevertheless, in a relevant number of cases the final diagnosis will be established solely by
pathological analysis obtained by biopsy

4. Classification of Liver Mass
Liver Lesions
Cystic
Parasitic Hydatid Cyst
Non Parasitic
Simple cyst
Polycystic disease
Biliary cystadenoma
Solid
Inflammatory
Abscess
(Pyogenic/ Amoebic)
Tumors
Benign
Haemangioma
Adenoma
FNH
Malignant HCC, Secondaries

5. PART I - Cystic
Lesions

6. PYOGENIC LIVER ABSCESS
Aetiology
1) Diseases of the biliary tract,
2) Infectious gastrointestinal disorders spreading via the portal vein (appendicitis/ diverticulitis)
3) Hematogenous spread via the hepatic artery,
4) Direct extension from an intraabdominal infection
5) Trauma
6) Cryptogenic

7. Predisposing factors
❖Diabetes mellitus
❖Cirrhosis
❖Chronic pancreatitis
❖Peptic ulcer disease
❖Inflammatory bowel disease
❖Jaundice
❖Pyelonephritis
❖Malignancy
❖ Chronic granulomatous disease
❖ Compliment deficiencies
❖ Leukaemia
❖ Sickle cell anaemia

8. Category of organism

9. Symptoms
❖Fever
❖Chills
❖Right upper quadrant abdominal pain
❖Jaundice
❖Weight loss
❖Nausea and vomiting
❖Rupture of the abscess with peritonitis (Rarely)
❖Sepsis
Most Common

10. Lab Findings
❖Leucocytosis
❖Hyperbilirubinemia
❖Hypoalbuminemia
❖Elevated serum alkaline phosphatase – M.C
❖AST may also be mildly elevated.

11. Investigations
PLAIN CHEST X RAYS
❖Abnormal In 50% Of Patients.
❖Elevated Right Hemidiaphragm,
❖Right Pleural Effusion,
❖Right Lower Lobe Atelectasis
ABDOMINAL FILMS
❖Hepatomegaly
❖Air-fluid Levels In The Presence Of Gas-forming Organisms within
the abscess cavity
❖Elevated hemidiaphragm

12. ULTRASONOGRAPHY
❖Demonstrate irregular margin and a hypoechoic
lesion
❖Gas within the cavity is detected by the presence of
microbubbles or diffuse hyperechoic spots with
reverberation
❖80–95% Sensitive
❖Cost Effective
❖Portable.

13. CT SCAN
❖Can detect intrahepatic collections as small as 0.5 cm
❖Hypoechoic on plain CT
❖Peripheral rim enhancement on contrast study
❖Double target sign

14. Management
❖An untreated hepatic abscess is nearly uniformly fatal due to complications
❖Complications- Sepsis, empyema, or peritonitis from rupture into the pleural or peritoneal spaces, and
retroperitoneal extension
❖Treatment options:
1. Antibiotics
2. Aspiration
3. Percutaneous drainage
4. Surgical drainage.
5. Percutaneous drainage plus i.v antibiotics treatment of choice

15. ANTIBIOTICS REGIMEN
1. Broad spectrum synthetic penicillin
2. Aminoglycoside/3rd gen cephalosporin
3. Metronidazole
➢Aminoglycoside toxicity-aztreonam, imipenem
➢Penicillin allergy-imipenem
❖Duration of treatment must be individualised
❖Multiple abscesses are more problematic and can require up to 12 weeks of therapy
❖Both the clinical and radiographic progress of the patient should guide the length of therapy

16. ASPIRATION
➢Useful in young , otherwise healthy patients with solitary abscess and no co-existing intra-abdominal pathology
➢Pus can be collected for C & S
➢Must be radiologically guided
PERCUTANEOUS DRAINAGE
➢Must be radiologically guided
➢Most useful for critically ill patients who cannot undergo surgery
➢Best for solitary, uniseptate abscess
➢Contraindications – associated biliary or intraabdominal pathology, coagulopathy, multiple abscesses and
generalised ascites

17. SURGICAL DRAINAGE
EXPLORATORY LAPAROTOMY
❖For diagnosing intra-abdominal pathology
❖Provides concurrent diagnosis of both abscess and its source
❖Best for multiple abscesses and those inaccessible to PCD or co-existing biliary pathology
EXTRA PERITONEAL APPROACH
❖Subcostal, transpleural, retroperitoneal
❖Used only for selected abscesses located superiorly in liver dome

18. Amoebic Liver Abscess
❖Amebiasis has the highest incidence in subtropical and tropical
climates and in areas with poor sanitation.
❖Immunocompromised host are more prone to develop amebic liver
abscess
❖The disease is secondary to infestation with Entamoeba
histolytica.

19. Life cycle
❖The cystic form of E. histolytica gain access to the
host by oral ingestion of contaminated food or water.
❖The trophozoites are released into the
gastrointestinal tract, where they may reach the liver
via the portal system
❖The trophozoites cause cellular necrosis with the
development of abscess in the liver.
❖The amebic liver abscesses are usually solitary and
surrounded by a thin walled granulation tissue.

20. PATHOLOGY
Abscess usually large, single and superficial
Right lobe usually affected
Abscess fluid resembles “anchovy sauce” - Reddish brown
due to digested liver tissue and RBC
Sterile and odourless
Inner wall contains trophozoites

21. Symptoms and Signs
❖Pain
❖Fever
❖Diarrhoea
❖Nausea and vomiting
❖Anorexia
❖Weight loss
❖Malaise
❖Cough and pleurisy
❖Hepatomegaly
❖Right upper quadrant tenderness
❖Pleural effusion or rub
❖Right upper quadrant mass
❖Ascites
❖Jaundice

22. The diagnosis is mainly on clinical and serological
assessment
Cysts found in the stool in 1/4th of the patients
Indirect hemagglutination and gel diffusion precipitation are
the most commonly used serology tests
Ultrasound
❖Hypoechoic round to oval lesion located near the liver
capsule
❖Show low level internal echoes and posterior acoustic
enhancement with poor rim

23. CT scan
❖Hypodense lesions
❖Peripheral rim is non enhancing but show edema
❖Internal inhomogeneity
MRI
❖Central portion is cystic
❖Ring exhibits variable intensities
MRI T2
weighted
images
CT Scan

24. TREATMENT
ANTIBIOTICS
❖ Most uncomplicated amebic liver abscesses can be treated successfully with amebicidal drug
therapy alone.
❖After completion of treatment with tissue amebicides, luminal amebicides(diloxanide furoate) for
eradication of the
❖asymptomatic colonization state is necessary
❖Failure to use luminal agents can lead to relapse of infection in approximately 10% of patients.
❖Metronidazole drug of choice for amebic liver abscess (750 mg 3 times a day orally for 10 days)

25. THERAPEUTIC ASPIRATION
INDICATIONS :
1. High risk of abscess rupture
2. Left lobe liver abscess
3. Treatment failure in which pain and fever persists despite 3 days of antibiotics.
4. When metronidazole is CI – pregnancy
5. To relieve pressure symptoms

26. Surgical drainage-Indications
1. Left lobe abscess not amenable to percutaneous drainage
2. Life threatening hemorrhage with or without intraperitoneal rupture of abscess.
3. Amoebic abscess eroding into neighboring structures
4. Septicaemia from secondary infection
5. Failure of response to conservative therapy

27. COMPLICATIONS
❖Complications from amebic abscesses occur secondary to rupture of the
abscess into the peritoneum, pleural cavity, or pericardium
❖Mortality rates between 12% and 50%.
SEQUELAE
❖Thoracic amebiasis (empyema, bronchohepatic fistulas, and
pleuropulmonary abscess) is the most common complication
❖Pericardial amebiasis (acute pericarditis with tamponade).
❖Pleural cavity
❖Bronchi,
❖Cerebral amebiasis - seizures.

28. HYDATID LIVER CYST
❖E. granulosus and E. multilocularis
❖Zoonosis
❖Humans are accidental intermediate hosts, whereas animals can be both intermediate hosts
and definitive hosts.
❖In humans, 50–75% of the cysts occur in the liver,
❖Asymptomatic in most cases and discovered accidentally on a routine abdominal ultrasound

29. Life Cycle
❖Echinococcus granulosus a cestode
❖Lives in the small intestine of dogs and other canines
❖Eggs are eliminated in the feces and when ingested,
liberate their larvae in the duodenum of an intermediate
host.
❖The intermediate host can be sheep/goat (pastoral
hydatidosis) or reindeer/moose/caribou (sylvan
hydatidosis).
❖Humans are accidental intermediate hosts.

30. Majority are single cysts which occur in the right lobe of the liver and half of them has daughter
cysts and are multiloculated
The typical hydatid cyst has a three-layer wall surrounding a fluid cavity
1. Pericyst is the outer layer composed of modified host cells that form a dense and fibrous
protective zone
2. Ectocyst, the middle laminated membrane, which is acellular and allows the passage of
nutrients
3. Encocyst, the inner germinal layer, where the scolices (the larval stage of the parasite) and the
laminated membrane are produced

31. Clinical Features
❖Theoretically, echinococcosis can involve any organ.
❖Organs affected by E granulosus are the liver (63%), lungs (25%), muscles (5%), bones (3%),
kidneys (2%), brain (1%), and spleen (1%).
❖Bacterial superinfection of a hydatid cyst can occur and present like a pyogenic abscess.
❖Rupture of the cyst into the biliary tree.
❖ Free ruptures can result in disseminated echinococcosis and a potentially fatal anaphylactic
reaction.

32. Symptoms and Signs
❖Asymptomatic
❖Abdominal pain
❖Dyspepsia
❖Fever and chills
❖Jaundice
❖Right upper quadrant mass
❖Right upper quadrant tenderness

33. Investigations
❖Elevated bilirubin
❖Increased alkaline phosphatase level.
❖Leukocytosis may suggest infection of the cyst.
❖Eosinophilia is present in 25% of all persons who are infected, while hypogammaglobinemia is
present in 30%.
❖The indirect hemagglutination test and the enzyme-linked immunosorbent assay (ELISA) have a
sensitivity of 90% and are the initial screening tests of choice.
❖Immunodiffusion and immunoelectrophoresis demonstrate antibodies to arc 5 and provide
specific confirmation

34. Plain X-RAY Films
nonspecific and non revealing.
A thin rim of calcification delineating a
cyst is suggestive of an echinococcal
cyst

35. ULTRASONOGRAPHY
❖Specificity- approx 90%
Findings can include:
❖Solitary Cyst with anechoic univesicular cyst with well
defined borders and enhancement of back wall echoes.
❖Dependent debris (hydatid sand) moving freely with
change in position
❖Separation of membranes (ultrasonic water lily sign)
❖Daughter cysts- cartwheel or honeycomb cyst

36. GHARBI’S CLASSIFICATION
❖Type I has a pure fluid collection
❖Type II has a fluid collection with a split wall (floating
membrane)
❖Type III reveals a fluid collection with septa
(honeycomb image)
❖Type IV has heterogenous echographic patterns
❖Type V has reflecting thick walls(dead calcified wall)

37. ❖Computed tomography (CT) is indicated in cases in which
USG fails due to patient-related difficulties (e.g. obesity,
excessive intestinal gas, abdominal wall deformities and
previous surgery)
❖CT has a high sensitivity and specificity
❖It may provide clue to presence of complications such as
infection, and intrabiliary rupture
❖Sharply marginated single or multiple rounded cysts with
thin dense rim and floating membrane

38. ❖Direct cholangiography – (Endoscopic or percutaneous) may be required in suspected intrabiliary
rupture and bile duct obstruction.
❖ERCP is also a valuable method for detecting post-operative complications involving the biliary
tree following surgical intervention
❖Magnetic resonance Imaging (MRI scan) Images show the cysts adequately, but MRI offers no
real advantage over CT scan.

39. TREATMENT
PRINCIPLES
(1) Eradication Of The Parasite Within The Cyst
(2) Protection Of The Host Against Spillage Of Scoleces,
(3) Management Of Complications.
METHODS
• Medical
• Percutaneous
• Surgical

40. ❖Medical treatment
❖Success rate of 30%
❖Albendazole (10-15mg/kg/day) is drug of choice/ Mebendazole (50mg /kg)& Praziquantel ( 50mg/kg)
1. Inoperable cases - as primary treatment - 3 cycles (28 days followed by 2 weeks gap)
2. Pre-operatively – to reduce the risk of recurrence 6 weeks continuous treatment
3. Post-operatively to prevent recurrence in cases of intraoperative cyst spillage – 3 cycles
Indications: Small cysts (<4 cm) located deep in the parenchyma of the liver and is inoperable
Contraindications: Early pregnancy, bone marrow suppression, chronic hepatic disease, large cysts with
the risk of rupture, and inactive or calcified cysts

41. PERCUTANEOUS ASPIRATION
AND DRAINAGE (PAIR)
PAIR technique stands for puncture of the cyst wall, aspiration of cyst content, injection, and r
aspiration of a scolecidal agent
FREQUENTLY USED PROTOSCOLICIDAL AGENTS
1. 15–20% Saline
2. 95% Ethanol
3. A Combination Of 30% Saline And 95% Ethanol,
4. Mebendazole Solution.
This technique, performed using either ultrasound or CT guidance

42. ❖Involves aspiration of the contents via a special cannula,
❖Injection of a scolicidal agent for at least 15 minutes
❖Reaspiration of the cystic contents.
❖This is repeated until the return is clear.
❖Perioperative treatment with a albendazole is necessary
❖The cysts should be larger than 5 cm in diameter and type I or II according to the Gharbi classification,
Type III without honeycombing
❖CONTRAINDICATION- Inaccessible, Inactive, communication with biliary tree or peritoneum

43. Surgery
Indications:
1. Large liver cysts with multiple daughter cysts
2. Superficially located single liver cysts that may rupture (traumatically or spontaneously)
3. Liver cysts with biliary tree communication or pressure effects on vital organs or structures
4. Infected cysts.
Contraindications:
1. General contraindications to surgical procedures (eg, extremes of age, pregnancy, severe preexisting medica
conditions)
2. multiple cysts in multiple organs
3. cysts that are difficult to access
4. dead cysts, calcified cysts and very small cysts are contraindications

44. Surgery
Preparation
• Give 4-6 week of albendazole tablet before surgery
• Pre operative visualization of biliary tract by ERCP.
• Anesthetist warned of sudden anaphylactic shock in case of spillage
Surgery
Marsupialisation, partial pericystectomy+ omentopexy, partial pericystectomy+ capittonage
Pericystectomy, Lobectomy, Partial hepatectomy
ELISA or indirect hemagglutination tests and imaging are usually performed at 3-, 6-, 12-, and 24-
month intervals as screening for recurrence

45. Hepatic Cysts
❖Most commonly encountered hepatic lesion
❖Deranged development of the biliary tree (i.e., a hamartoma of biliary origin or so-called “von
Meyenburg complex”
❖No communication with the biliary tree
❖They are usually asymptomatic but can sometimes be associated with serious complications
❖Larger cysts are more likely to result in symptoms from complications such as hemorrhage,
rupture, infection, or compression of the biliary tree

46. Epidemiology
❖Hepatics cysts are most prevalent in the female population.
❖Incidence also tends to increase with age.
❖Ciliated hepatic foregut cysts occur more commonly in men.
❖Biliary cysts can present in infants due to congenital abnormalities.

47. Pathophysiology
❖They contain a clear fluid
❖Great variation in size.
❖Primary squamous cell carcinoma can arise in hepatic cysts.
❖Liver metastases, which originate from organs such as the ovaries, kidneys, colon, or pancreas,
may appear as hepatic cysts
❖Biliary cysts arise from the biliary ductal system and can be congenital in origin

48. History and Physical Examination
1. Mostly asymptomatic
2. Large cysts may become symptomatic
3. abdominal pain
4. nausea and anorexia.
5. Significantly large cysts may even be palpable on abdominal examination.
6. Biliary cysts may present as triad of pain, jaundice, and abdominal mass

49. ULTRASOUND
❖well-marginated , anechoic round to ovoid structure with an
imperceptible wall
❖enhancement of the posterior wall and posterior acoustic shadow
❖No septations or papillary projections
CT and MRI
❖simple cysts have attenuation (0–15 HU) and signal intensity (T1
hypointensity, T2 hyperintensity) similar to water
❖Simple cysts do not show enhancement even after contrast; can
rarely become complex

50. Treatment
❖Asymptomatic single liver cysts, do not require treatment or surveillance
❖Cysts >4cm require surveillance at 6mo/1 yr upto 2 years
❖In symptomatic patients requiring intervention hydatid cyst should be ruled out in all cases before the
operation
❖Surgical management include percutaneous aspiration, laparoscopic deroofing, and complete cyst
excision
❖Percutaneous aspiration can be performed on its own or alongside sclerosing agents such as alcohol
or minocycline hydrochloride
❖Laparoscopic deroofing
❖ Complete cyst excision or hepatectomy is the last line of treatment

51. Polycystic Liver Disease
❖PCLD is a genetic disease responsible for the development of multiple hepatic cysts.
❖It presents in two forms, with or without autosomal dominant polycystic kidney disease (ADPKD)
❖Both have an autosomal dominant transmission and similar clinical presentation.
❖PCLD associated with ADPKD is linked with mutations in the PKD1 (short arm of chromosome 16,
encoding polycystin-1) or PKD2 gene (chromosome 4, encoding polycystin-2),
❖Isolated PCLD is associated with heterozygous mutation in PRKC-SH or SEC63 genes
❖Overall prevalence is the same in gender, but female population is associated with more severe liver
disease
❖Pregnancy, multiparity, and use of steroids further increase the risk for severe hepatic cystic disease

52. ❖In most patients, cysts are small and asymptomatic
❖When present, symptoms are related mainly to the volume of enlarged liver rather than the volume of
a specific cyst
❖abdominal distension
❖Dyspnea
❖Pain
❖Early satiety
❖“Pseudo” Budd-Chiari syndrome
❖Cystic carcinoma- rare

53. USG
❖Multiple, fluid-filled, round or oval cysts with sharp
margins.
❖It may be difficult to identify vascular and biliary
structures adjacent to the cysts.
CT scan
❖Fluid attenuation with no contrast enhancement
Magnetic resonance imaging (MRI)
❖Hyperintense on T2-weighted and hypointense on T1-
weighted images.

54. Gigot’s classification
Used for staging based on CT findings:
❖typeI- less than 10 large cysts;
❖type II- diffuse involvement of liver
parenchyma, but with remaining large
areas of noncystic liver parenchyma
❖type III- massive, diffuse involvement of
liver parenchyma with only a few areas of
normal tissue between cysts.

55. Complications
❖Bleeding
❖Rupture
❖Infection of cysts
❖The most severe complication is bacterial infection, especially those under dialysis for ADPKD or
in immunosuppressed patients after renal transplantation
❖Cholestasis secondary to compression of adjacent biliary duct

56. Management
❖Surgical removal or emptying of cysts aiming at decompression and reduction of the liver size.
❖Medical management has been proposed in advanced PCLD with diffuse disease
❖Two recent RCT have demonstrated that lanreotide, a long-acting somatostatin analogue, was
associated with a limited reduction of liver volume in both types of PCLD
❖Sclerotherapy and laparoscopic fenestration showed ineffective in the management of PCLD
van Keimpema L, de Man RA, Drenth JP. Somatostatinanaloguesreduce liver volume in polycysticliver disease.Gut. 2008 Sep 1;57(9):1338-9.

57. ❖Current surgical options include: open fenestration, liver resection, or liver transplantation
❖The appropriate surgical option may be defined based on Gigot’s classification;
1. typeI - laparoscopic fenestration is recommended as first option
2. type II, open fenestration is usually implemented
3. type III is a contraindication to fenestration and requires resection or liver transplantation in
symptomatic cases

58. Research Drugs in development
❖Vaso-pressin-2—receptor antagonists - Studies of an animal model of polycystic kidney disease
have demonstrated tolvaptan can reduce cyclic AMP secretion. Trial on PCLD is being attempted
❖Somatostatin receptor antagonists such as octreotide have demonstrated that it may slow down
the progression of liver cysts. Accordingly, investigators are currently conducting a multicenter trial
of octreotide therapy in patients with polycystic liver disease
❖mTOR is inappropriately activated in cystic epithelium, and this activation is thought to be
responsible, at least in part, for the dysregulated proliferation of cystic epithelium. The mTOR
inhibitor sirolimus has been demonstrated to block the
Everson GT. Polycysticliver disease. Gastroenterology& hepatology. 2008 Mar;4(3):179.

59. Hepatic Cystadenoma
❖Mucinous cystic neoplasm includes the subgroup of mucinous cystic neoplasm, also referred to as
biliary cystadenomas (BCA) and cystadenocarcinomas (BCAC)
❖comprise less than 5% of all cystic liver diseases
❖The exact cause of BCAs remains undetermined.
❖One current theory suggests that BCAs may arise from endodermal precursors to the local biliary
epithelium.
❖Other theory says it is secondary to implantation explaining the ovarian like subepithelial stroma,
expression of estrogen and progesterone receptors, predilection to be located in segment IV of the liver
❖Predominantly in middle-aged women
❖They are slow-growing lesions

60. History and Physical Examination
❖Asymptomatic.
❖Incidentally detected.
❖Abdominal pain
❖Distension
❖Nausea, and vomiting.
❖Rarely, present from symptoms secondary to obstructive jaundice, cholangitis, intracystic
hemorrhage, or cyst rupture.

61. INVESTIGATIONS
Sonography
❖Well defined, anechoic lesion surrounded by an echogenic
capsule
❖Contain multiple intrinsic septations.
CT scan
❖Fluid attenuating cystic mass with a soft tissue attenuating
rim, internal septa, and capsular calcifications
MRI
❖Signal characteristics are typical for fluid containing cystic
lesion
❖These lesions demonstrate mild capsular and septal
enhancement on postcontrast imaging at CT and MRI

62. Treatment / Management
❖BCA is considered a premalignant lesion.
❖Although imaging findings may be suggestive, they often are overlapping and nonspecific.
❖No published guidelines on appropriate therapy of BCAs currently exist due to the limited number
of reported cases.
❖Percutaneous ablation and unroofing techniques of BCAs are ineffective (high recurrence)
❖Complete surgical resection is the management of choice given the risk of malignant
transformation and recurrence

63. Treatment Algorithm of Hepatic
Cyst

64. THANK YOU

65. PART II- Solid
Lesions

66. Hepatic Adenoma
❖Liver cell adenoma is the most important benign epithelial tumour of the liver
❖Estimated incidence of 3 per 1 000 000 per year
❖The annual incidence is substantially higher with long-term oral contraceptive use, estimated at 3–4
per 100 000
❖Regression of the tumour may occur after cessation of oral contraceptive usage
❖Reports of progression to hepatocellular carcinoma many years after stopping oral contraceptives
❖Pregnancy appears to stimulate rapid growth in these lesions with risk of potentially fatal spontaneous
rupture
❖May also be associated with use of clomiphene, methyl testosterone, danazol, Klinefelter's syndrome,
Types I, III and IV glycogen storage disease, and familial adenomatous polyposis

67. Pathology
❖Composed of cords of benign hepatocytes containing
increased glycogen and fat, without bile ductules, fibrous
septa, portal tracts or central vein
❖Normal architecture of liver not seen in this case
❖Large plates of hepatocytes separated by dilated sinusoids
which are perfused solely by peripheral arterial feeding
vessels(lacks portal venous supply) under arterial pressure

68. Clinical Features
Upper abdominal pain in 50-75 % cases
Tumor markers- AFP is normal
Risks- Rupture or malignant transformation

69. Diagnosis
MRI-Well demarcated heterogenous mass containing fat
or haemorrhage
CT- Hypervascular and heterogenous on arterial phase
and becomes isodense or hypodense on portal phase as
a result of arteriovenous shunting
Distinctive findings from FNH: Smooth Surface, presence
of necrosis and haemorrhage and tumor capsule
Angiography: Hypervascular well circumscribed tumor
supplied by peripheral arteries

70. Treatment
• Acute Hemorrhage: Hepatic artery embolization
• Resection of symptomatic masses

71. Focal Nodular Hyperplasia
❖Second most common benign tumor of the liver
❖Seen in young women associated with ocp use
❖Usually a small (<5cm)nodular mass arising in a
normal liver, involves right and left liver equally

72. Pathology
Central fibrous scar with radiating septa in the mass
Microscopically- Cords of benign appearing hepatocytes
divided by multiple fibrous septae originating from a
central scar
Typical hepatic vascularity is not seen with atypical biliary
epithelium
Central scar contains large artery that branches out into
multiple small arteries in a spoke wheel pattern ( on
angiography)

73. Clinical Features
• Vague abdominal pain in symptomatic cases
• Normal AFP levels

74. Diagnosis
• Homogeneous mass with a central scar that rapidly enhances during
arterial phase of contrast administration

75. Treatment
• No treatment in asymptomatic cases
• Resection in cases of diagnostic uncertainty for histologic confirmation

76. Liver Hemangioma
❖MC benign tumor of liver
❖Mainly seen in women aged 45 years
❖Usually single, and <5cm in diameter occurs equally in right and left liver
❖Giant hemangioma lesions>5cm

77. Pathology
• Microscopically- Endothelium lined, blood filled
spaces that are separated by thin fibrous septa
• Enlargement are by ectasia rather than neoplasia

78. Clinical Features
❖Mostly asymptomatic and usually incidentally found
❖ Large compressive masses may cause vague upper abdominal symptoms
❖Kasabach-Merrit Syndrome- Syndrome of thrombocytopenia and consumptive coagulopathy
rarely seen
❖LFT and tumor markers normal

79. Diagnosis
CT and MRI are diagnostic if typical peripheral nodular
enhancement pattern is seen
Percutaneous biopsy is dangerous and not recommended

80. Treatment
• Observation for asymptomatic cases
• Enucleation with inflow control is TOC for symptomatic cases

81. Hepatocellular carcinoma
❖Primary malignancy of liver
❖Highest incidence in Asia and Africa – Hepatitis infection
❖Incidence in developing nations is >2x developed countries
❖Increases with age
❖Predominantly in patients with underlying chronic liver disease and cirrhosis

82. Etiology
❖Modifiable
1. Hepatitis C & B
2. Alcoholism
3. NASH
4. Aflatoxin
❖Non-modifiable
1. Alpha-1-antitrypsin deficiency
2. Haemachromatosis

83. Pathophysiology

84. Work-up
❖Confirm diagnosis (cirrhosis + characteristic imaging studies + elevated AFP)
❖Multiphase liver CT scan/MRI
❖AFP
❖Biopsy
❖Staging
❖Disease severity
❖Etiology of HCC

85. Multiphase liver CT scan
❖Accurate diagnosis, staging & surgical planning
❖Plain, early & late arterial, portal venous &
delayed phases
❖Hypervascular pattern with arterial enhancement
and rapid washout during portal venous phase
❖Tumor capsule, internal mosaic from variable
attenuation within the tumor and PV
thrombosis/invasion

86. Hepatic MRI
❖Hepato-specific paramagnetic gadolinium-based contrast
(Primovisttm)
❖Arterial, portal venous, late dynamic & hepatobiliary phases
❖HCC appears darker than background liver on T1- weighted
images
❖Superior sensitivity & specificity vs. CT for lesions <1cm3

87. Biopsy
– Controversial
– Depending on lesion size & institutional practice
<1cm <50% malignant, high false-negative. For
conservative management with close
follow-up and no biopsy
1 – 2cm Imaging usually inconclusive, need to biopsy
or MRI with gadoxetate contrast
>2cm Usually can be diagnosed without biopsy.
Risk of tumour seeding must be taken into
account

88. ❖Staging
CT scan/PET scan
❖Disease severity
Anaemia, leucocytosis (infected HCC), thrombocytopenia (portal HPT) , LFT – metabolic &
synthetic functions of liver, PT/PTT – synthetic function of liver, AST/ALT – active hepatitis
Hypogycaemia – end-stage liver disease (no glycogen)
❖Etiology
HBV/HCV serology

89. Treatment options
❖Surgery- Resection, Liver transplant
❖Ablative therapy- Thermal, Chemical, Electrical
❖Regional liver therapy- TACE, SIRT
❖Radiotherapy- Stereotactic radiosurgery
❖Systemic- Multikinase inhibitors

90. Surgery
Irresectable
– Child-Pugh score C
– Distant metastases
– Extrahepatic disease present – e.g. extensive lymphadenopathy or peritoneal deposits
– Extensive bilobar disease
– Hilar tumour involving major blood vessels not amenable to repair
– Inadequate functional liver residue predicted postoperatively (FLR < 40% if cirrhotic, <30% if
noncirrhotic, ICG15 >14%)

91. Resections
– Non-anatomic (wedge)- Limited resections of a small portion of liver without adhering to
segmental biliary ducts & vascular supply
– Anatomic- Removing 1 or more of the 8 segments of the liver
To improve resectability
– Contralateral portal vein embolization (for parenchymal hypertrophy) ± TACE (minimise
resected parenchymal mass)
• Liver transplantation
– Significant cirrhosis and limited tumour burden
– Milan criteria (determines candidacy for transplantation)

92. Ablative therapy
Best for tumours <3cm
• Indications
– Bridge to transplant by reducing the risk of tumor progression
– Palliative procedure to extend DFS
• Percutaneous, laparoscopic or open surgery

93. Options
❖Thermal
❖Radiofrequency ablation
❖Microwave ablation
❖High intensity focused ultrasonography (HIFU)
❖Cryoablation
❖Chemical
❖Electrical

94. Regional liver therapy
Generally considered non-curative
• Options
– Transarterial chemoembolization (TACE)
– Selective internal radiotherapy (SIRT)
Radiotherapy
• Stereotactic radiosurgery

95. Systemic therapy
• Multikinase inhibitors
• Indications
– Child’s A
– Metastatic disease
– Irresectable but failed/unsuitable for regional therapy
• Sorafenib, sunitinib

96. Screening
• All cirrhotic patients
• 6 monthly USG & AFP*
– No extra benefit with 3 monthly screen
• Reason
– Increased detection of early HCC
– Increased detection of single HCC <5cm
– Increased surgery for HCC
– Increased survival
– Increased cost effectiveness

97. USG
– Low cost, low risk, non-invasive, acceptable to patient
– Have a range of echogenicity
– Significant arterial blood supply and neovascularization
– Might miss nodules on cirrhotic background & SVII or VIII small lesions near diaphragm
– Does not provide sufficient anatomic detail for planning surgical resection or ablation
– No data to support CT/MRI for screening

98. AFP
– The result of production by the tumor or regenerating hepatocytes
– Suboptimal as a screening tool, therefore never performed alone
– Only 40-64% sensitive
– Only 20% of early HCC have abnormal AFP
– Fluctuates in flares of hepatitis or exacerbations of liver disease

99. THANK YOU