Benign Neoplasms of Liver This document provides an overview of benign liver tumors, including their epidemiology, etiology, classification, clinical features, diagnosis and treatment. The main benign liver tumors discussed are hepatocellular adenoma, cavernous hemangioma, and focal nodular hyperplasia. Hepatocellular adenoma is more common in females using oral contraceptives and can present with pain or rupture. Cavernous hemangioma is the most common benign liver tumor and often asymptomatic. Larger hemangiomas can cause pain, jaundice or complications. Imaging such as MRI is used for diagnosis, while treatment depends on size and symptoms, and may include resection, ablation or e

1. Benign Neoplasms of
Liver
Presented by: Dr. Nihar Chandak

2. Synopsis
• Introduction
• Anatomy
• Understanding the phases
• WHO classification of benign
liver tumors
• Hepatocellular adenoma
• Cavernous hemangioma
• Infantile hepatic hemangioma
• Focal Nodular Hyperplasia
• Hepatic Angiomyolipoma
• Hepatobiliary cystadenoma
• Bile duct adenoma
• Liver Resection
• Radiofrequency ablation (RFA)
• Hepatic Artery Embolization
(HAE)

3. Introduction
• Benign liver tumors is estimated to be present in approximately 10%
to 20% of the population.
• With the increasing use of rapidly improving radiologic examinations,
these entities have been encountered more frequently.
• The definitive diagnosis of a liver tumor is based primarily on accurate
examination and interpretation of histologic material.
• According to their histogenesis, primary intrahepatic tumors are
classified into three main categories—hepatocellular, biliary, and
mesenchymal tumors.

4. Anatomy
• Each lobule is made up of numerous individual liver cells i.e. hepatocytes.
• The biliary tree is formed from canaliculi (the smallest branches of the bile
collecting system, the canals of Hering and the slightly larger intrahepatic bile
ductules.
• The liver is divided into about one
million small units called lobules
that measure 0.7 to 2 mm in
diameter.
• These lobules are surrounded by
sheets of connective tissue called
septae in which run the vascular and
biliary vessels.

5. Hepatic Lobule
• Arranged as series of hexagonal
lobules.
• Each composed of series of
hepatocyte cords (plates)
interspersed with sinusoids.
• Hepatocytes are in single-cell
sheets with sinusoids on either
end aligned radially toward a
central hepatic venule.
• And is bounded by 6 peripheral
portal triads.

6. • The blood-containing sinusoids are lined by discontinuous endothelial cells and
scattered flat Kupffer cells belonging to the reticuloendothelial system.
• The space of Disse is the space between hepatocytes and sinusoidal lining
endothelial cells.
• A few scattered fat storing Ito cells lie within the space of Disse.

7. Understanding the phases
• Liver -dual blood supply
80% portal vein
20% hepatic artery
• All liver tumors blood supply comes
from hepatic artery
• Hence, tumors enhance in arterial
phase & liver will enhance in the
portal venous phase

8. Arterial Phase
• 20- 40 sec
• Hypervascular tumors enhance via the
hepatic artery
• Normal liver parenchyma not yet enhanced
• Hypervascular tumors enhance optimally at
35 sec
• Will be visible as hyperdense lesions in a
relatively hypodense liver
Portal Venous Phase
• 60- 80 sec
• To detect hypovascular tumors
Delayed Phase
• Begins at about > 180 sec
• Best done at 10 minutes

9. WHO Classification of benign liver tumors
Epithelial Non Epithelial
HEPATOCYTES 1. Hepatocellular adenoma (liver
cell adenoma)
MESENCHYMAL 1. Hemangioma
2. Focal nodular hyperplasia 2. Lymphangioma &
lymphangiomatosis
BILIARY CELLS 1. Intrahepatic bile duct
adenoma
3. Angiomyolipoma
2. Intrahepatic bile duct
cystadenoma
4. Infantile Hepatic
hemangioma
3. Biliary papillomatosis

10. Hepatocellular Adenoma
(HCA)

11. Epidemiology & Etiology
• Are rare (0.1 per year per 100,000 in non-OC users, 3 to 4 per
100,000 in long-term OC users)
• Occur predominantly in women (9:1)
• In the 2nd to 5th decades of life (child bearing)
• Usually solitary (70-80% of cases)
Commonly associated with
1. Use of estrogen, including exogenous estrogens in
OC Pills.
OCP use for more than 5 years, older age, and use of high
potency hormones all appear to increase the risk.
Cessation of estrogens often leads to regression of an
adenoma, adding support to their role in the pathogenesis.

12. 2. Anabolic androgenic steroid use (e.g Danazol therapy)
 Male predominance
Usually multiple
3. FAP (causes childhood hepatic adenomas)
4. Glycogen storage disease
Type I (frequency of approx. 25 to 75 %)
Type III ( frequency of approx. 25 %)
Male predominance
Diagnosis usually made in the childhood
• The designation liver adenomatosis is usually applied to cases with multiple
hepatocellular adenomas. (> 10 as in Sabiston/ >3 as in Blumgarts)
• The risk of malignant transformation (5 – 20%) is strongly associated with
male gender,
β-catenin activation,
tumor diameter larger than 5 cm.

13. Gross Morphology & Histology
• Relatively soft, light brown to yellow
tumor
• Sharply circumscribed but does not
have a true capsule, although a
pseudocapsule is formed by
compression of the surrounding liver
tissue
• Areas of necrosis and haemorrhage
• Consists of thick liver plates of regular,
larger than normal, and usually glycogen-
rich tumor cells
• Areas of focal necrosis and hemorrhages
• Kupffer cells fewer in no. than normal
• with regular nuclei
• not particularly prominent nucleoli
• usually without mitotic figures

14. Pathogenesis • HNF-1α (Hepatocyte Nuclear
Factor) is implicated in hepatocyte
differentiation and liver
development.
• Mature-onset diabetes of the
young (MODY3), an autosomal
dominant form of non-ketotic
diabetes mellitus presenting
before age 25, are common in
patients with liver adenomatosis.
• β-Catenin activation causes
formation of truncated proteins &
is associated with a higher risk of
malignant transformation along
with glycogen storage disease and
adenomas in male patients.
TCF1- T Cell Factor; HNF- Hepatocyte nuclear factor

15. Depending on the pathogenesis, HCA are divided in 4
sub-types:
No. Type
1. Inflammatory HCA Most Common
Highest rate of
bleeding
2. HNF-1α mutated
HCA
Second most common
Multiple
3. β-Catenin mutated
HCA
 Least common
 Highly malignant
 Men on anabolic
steroids
 Glycogen storage ds
 FAP
4. Unclassified

16. Clinical Features
• Mostly found incidentally.
• Approx. 25% experience pain in the right hypochondrium or
epigastrium –
• mild and ill defined
• may be severe as a result of bleeding into or infarction of the tumor.
• Hepatic adenomas are highly vascular tumors.
• Hence, the most alarming presentation is following rupture of an
adenoma presenting with severe abdominal pain and hypotension
from acute hemoperitoneum. (hypovolemic shock)
• Rupture is seen more commonly in
Tumor size more than >5cm
Superficial location

17. Diagnosis
• Sr. AFP- normal
• CRP level and WBC count may be elevated with inflammatory adenomas.
• FNA- useless as HCA mimics normal hepatocytes microscopically.
• Core needle biopsy has also been of limited diagnostic value
• definitive diagnosis can be made at expert centers with the use of IHC
markers.
• Markers of following 4 antibodies (AB) are used:
1. anti-liver-fatty acid binding protein (L-FABP),
2. anti–β-catenin,
3. anti-glutamine synthetase (GS),
4. anti-serum amyloid A (SAA)

18. Radiological
• Imaging modality of
choice: Dynamic MRI
with a hepatocyte-
specific contrast agent
such as gadobenate
dimeglumin.
• Imaging findings:
• Hypervascular
• Homogenous or
Heterogenous
• Lipid accumulation
(hypodense CT /
hyperintense MRI)
• Haemorrhage
• Capsule in approx. 30%

19. Treatment
Conservative
Smaller lesions less than 5cm
Asymptomatic females
Females on OCPs –
discontinuation is advised
 In Inflammatory HA
• Long term follow-up (yearly) for
at least 20yrs
Resection
Solitary lesion
lesions larger than 5 cm
those with evidence of
hemorrhage or other symptoms
in males (increased chances of
malignancy)
In β-Catenin mutated HA
(increased chances of malignancy)
Preoperative core biopsy in patients with large (>5 cm) is advised for sub-typing.

20. Ruptured HCA
• Should be treated electively
• Firstly stabilization of the patient
• Selective hepatic artery embolization
Transarterial embolization
RFA
• Patient observed for several months, until resorption of the
hematoma surrounding the tumor occurs. (Terkivatan et al, 2001; Marini et al,
2002)
• The absorption of the hematoma allows an easier and parenchyma-sparing
elective liver resection with a low risk of transfusion.
• Few hemorrhagic HAs, have decreased dramatically in size and even
disappeared after embolization.

21. Cavernous Hemangiomas

22. Epidemiology
• Most common benign liver tumor (1% to 20% of the general
population)
• More common in females (5:1)
• Mean age – 50yrs
• Found equally in both lobes
• Usually solitary (10% presenting as multiple)
• Majority are of size less than 5cms
• Giant Hemangiomas- those larger than 10cms (Blumgart)
• Are more common in multiparous than in nulliparous women.
• Malignant transformation has not been reported.

23. Etiology
• Cavernous hemangiomata have been associated with
1. Hormonal therapy
• Some of these tumors have estrogen receptors,
• accelerated growth has been observed with high-estrogen states, like
a/w
puberty,
pregnancy,
oral contraceptive use,
androgen treatment.
2. A/w Focal Nodular Hyperplasia (in approx. 25% cases)
3. Congenital vascular malformations

24. Clinical Features
• Usually asymptomatic. Hence, discovered incidentally
• Larger or multiple lesions produce symptoms
• Upper abdominal pain is the most common complaint associated
with giant cavernous hemangiomas and results from
partial infarction / thrombosis of the lesion or
pressure on adjacent tissues.
• Jaundice as a result of compression of bile ducts by giant
hemangioma has also been observed, but this is rare.

25. Complication
• Mostly observed in large hemangiomas. Can be divided as-
1) Alterations of internal architecture, such as with inflammation;
• Some cases of inflammatory processes complicating giant hemangioma have been
reported (Bornman et al, 1987; Takayasu et al, 1990)
• Present with- low-grade fever, weight loss, abdominal pain, accelerated ESR, normal
white cell count, anemia, thrombocytosis, and increased fibrinogen level.
2) Coagulation abnormalities, which could lead to systemic disorders such as
hemorrhage and subsequent haemoperitoneum;
1) Kasabach-Merritt syndrome
2) Spontaneous rupture (very rare)
3) Compression of adjacent structures

26. Kasabach-Merritt syndrome
• Rare complication of hepatic hemangioma in adults. (mortality-
10 to 37%)
• Consists of-
intravascular coagulation,
clotting,
fibrinolysis (sequestration of platelets) within the hemangioma.
• It progresses to secondary increased systemic fibrinolysis and
thrombocytopenia.
• Increases risk of bleeding complications including intracranial
hemorrhage.
• May lead to DIC.
Management:
• Definitive- The syndrome is reversible after removal of the
hemangioma.
• Supportive- platelet transfusions and FFPs
• In non- resectable cases- Arterial embolization, corticosteroids,
alpha-interferon, chemotherapy.
Giant hemangioma in 44yr old pt
with prolonged clotting time
KMS usually found in children
with congenital hemangiomas

27. • composed of blood-filled vascular
channels of varied size
• Lined by a single layer of flat endothelial
cells supported by fibrous tissue.
• Thrombi in various stages of organization
• areas of infarction
• dense fibrosis and calcification- in older
lesions
Gross Morphology & Histology
• well-delineated, flat lesions of red-
blue color.
• partially collapse on sectioning due to
escape of blood.
• Some degree of fibrosis, calcification,
and thrombosis may be observed,
mostly in the large lesions.

28. Diagnosis
• Lab investigations- usually normal.
• Increased fibrinogen level and
thrombocytosis- seen in inflammatory
hemangiomas.
• Core needle biopsy- C/I due to risk of
rupture.
• Diagnosed accurately on imaging studies.
• On US- classic appearance is a homogeneous
hyperechoic mass with acoustic
enhancement and sharp margins.
• No vascular pattern is usually identified on
Color Doppler.
• Hence other investigations are required
when US does not show typical patterns.
Hyperechoic liver lesion with
peripheral puddling followed by
complete and delayed enhancement.

29. • Imaging modality of choice- Magnetic
resonance (MR) imaging
• The classic appearance-
a hypointense lesion on T1-weighted
sequences,
a strongly hyperintense on T2-weighted
sequences, with a “lightbulb” pattern.
Hemangioma. T2-weighted MR imaging
showing typical bright signal

30. Treatment
• Whatever the size, there is no treatment for asymptomatic hemangioma.
• Allowing pregnancy or use of estrogen-containing medications in patients
with a cavernous hemangioma is considered safe.
• Indication of surgery- In symptomatic patients
• For giant hemangiomas- reduction in size is achieved with irradiation,
arterial ligation, arterial embolization, or systemic glucocorticoids.
• The choice between enucleation and resection requires consideration of the
size and anatomic location of the lesion.
• Enucleation- Hemangioma located in the peripheral liver area
• Liver Resection- Tumors which are deeply located
• Ruptured hemangiomas- (exceedingly rare) embolize or clamp the hepatic
artery to stop bleeding before proceeding with resection.

31. Infantile Hepatic
Hemangioma

32. Introduction
• Previously referred to as hepatic infantile hemangioendotheliomas
• Have been reclassified by ISSVA. (International Society for the Study of Vascular
Anomalies )
• Are the liver lesion composed of large endothelial-lined vascular
channels seen in fetuses and neonates.
• It is the most frequent liver mass in infants <6 months.
• Detected in utero as early as at 16 weeks of gestation.
• Twice as common in girls than in boys

33. Clinical Presentation
• have substantial AV shunting- may lead to fetal cardiovascular
compromise and hydrops fetalis.
• In most cases entire liver is involved- hepatomegaly
• May also develop hemolytic anemia, thrombocytopenia, and
coagulopathies (Kasabach-Merritt sequence).
• If these tumors are not detected prenatally, neonates may present
with unexplained congestive heart failure.

34. Diagnosis
• On CT-
typical peripheral enhancement with gradual
filling in.
reduction in the aortic caliber (mid-aortic
syndrome) below the level of coeliac branch
(because of the important vascular distribution toward the liver)
Solitary
Multifocal
Management
• If asymptomatic- no treatment
• If symptoms of high output cardiac failure-
first line treatment is propranolol.
• If medical therapy fails- embolisation to
control any AV shunting.

35. Focal Nodular Hyperplasia

36. Introduction
• Second most common benign liver neoplasm (after hemangioma)
• Predominantly diagnosed in women (9:1)
• Occurs at all ages predominantly at 30 to 50 years of age
• not influenced by oral contraceptives
• Rarely grows or bleeds
• Has no malignant potential
• Mainly solitary (multiple FNH lesions observed in 20% of cases)
Pathogenesis:
• Is a hyperplastic reaction resulting from arterial malformation (Wanless et al,
1985).
• Increased arterial flow hyperperfuses the local liver parenchyma and leads to
secondary hepatocellular hyperplasia.

37. • This explains the occurrence of this lesion in patients with vascular
disorders of the liver, including
Budd-Chiari syndrome (Cazals-Hatem et al, 2003),
Thrombosis of hepatic vein (triad- abdominal pain, ascites, liver enlargement)
Hereditary hemorrhagic telangiectasia (Gincul et al, 2008),
Also k/a Osler–Weber–Rendu disease
Autosomal dominant disorder that causes abnormal angiogenesis
Congenital absence of portal flow (Kim T, et al, 2004),
Portal thrombosis with subsequent hepatic arterialization
Clinical Features
• Mostly asymptomatic.
• Diagnosis- incidentally (during surgery, autopsy or imaging procedures for others
symptoms)
• Patients may experience mild pain.
• The lesion may be felt when it is pedunculated, and it can be responsible for
acute episodes of pain because of torsion on the pedicle.

38. • well-circumscribed
• Un- encapsulated
• usually solitary
• characterized by a central fibrous scar
that radiates into the liver
parenchyma
• benign-appearing hepatocytes with increased
thickness
• arranged in nodules, delineated by fibrous septa
that originate from the central scar.
• The main diagnostic feature- presence of large
and dystrophic vessels in the fibrous septa,
accompanied by several degrees of ductular
proliferation and inflammatory cells.
Gross Morphology & Histology

39. Diagnosis
• Lab results- normal in nearly 80% of cases
• elevation of GGT (gamma glutamyl
transaminase) and alkaline phosphatase in
patients with a large FNH causing extrinsic
compression of intrahepatic biliary ducts
• Diagnosed easily on imaging modalities:
• In Color Doppler-
presence of a central feeding artery
with a stellate or spoke-wheel pattern
(corresponds to the artery running from the central
scar to fibrous septa) Color Doppler of FNH

40. • On CT scans-
lesion enhances rapidly at the arterial phase
decreases at the portal venous phase
central scar,
• observed more often in large lesions than in
small ones,
• enhances over time.
lobulated contour,
absence of a capsule

41. Management
• Whatever the size and number of lesions, no
treatment is necessary for asymptomatic FNH.
• regenerative procedure rather than a tumor
• no malignant potential
• Surgical resection- in symptomatic patients
• Enucleation not advised, as large veins often
surround FNH, which renders enucleation
difficult.
• Transarterial embolization done in-
symptomatic pts
Large FNH
Located in segment I
size decrease and complete devascularization of FNH after embolisation
risky resection

42. Hepatic Angiomyolipoma

43. Introduction
• Rare, benign mesenchymal tumor
• Composed of in various combinations
proliferating blood vessels (angioid),
smooth muscle cells (myoid) &
adipose tissue (lipoid)
• Belongs to the group of PEComas (perivascular epithelial cell tumors)
• Occurs frequently in the kidney but rarely in liver.
• May occur as a solitary mass
• Or as an associated finding with tuberous sclerosis (Hooper et al, 1994), which is
present in about 15% of cases
are usually multiple
• Predominantly affects women between 30 and 50 years of age.
• Lesions are often larger than 5 cm in diameter and can increase in size

44. Clinical Features
• Patients usually have no symptoms, and liver tests are normal.
• found incidentally on routine imaging studies.
• Epigastric discomfort and other symptoms may be related to the
increased tumor mass that leads to elevated tension in liver capsule
and increased compression towards the surrounding tissue, etc.
• This tumor was once considered benign, but malignant
transformation has been reported. (Zhou et al, 2008; Rouquie et al, 2006; Dalle et
al, 2000)

45. • Un-capsulated
• vascular, smooth muscle and
mature fat components
• Fat content can vary from less than
10% to more than 95%.
• Epithelioid smooth muscle cell,
proliferating blood vessels & adipose
tissue are visible.
• Classified histologically according to the
amount of fat content into :
1. mixed
2. lipomatous (>70% fat)
3. myomatous (<10% fat)
4. angiomatous
Gross Morphology & Histology

46. Diagnosis
• On CT-
enhanced on the arterial phase
with central vascular opacification.
large central vessels
(macroaneurysms) within the
lesion is characteristic
• On MRI-
marked hypersignal in T1-weighted
images,
which drops on fat-suppressed
sequences.

47. • AML with a prominent epithelioid myoid component may mimic HCC.
• Hence, a needle biopsy is reinforced with IHC by using the antibody anti–
HMB-45 (Human Melanoma Black), which stains the myoid component.
(Arblade et al, 1996)
• The positivity of this antibody in the cytoplasm of smooth cells is
characteristic of Angiomyolipoma.
Management:
• In asymptomatic patients with lesions less than 5 cm- careful observation
with serial follow-up
• Indication of Resection:
Hepatic AML larger than 5cm
Symptomatic patients

48. Hepatobiliary Cystadenoma

49. Introduction
• Extremely rare
• Primary cystic tumors of the liver
• Being of biliary origin, can occur anywhere along the biliary tree, including the
common hepatic duct, cystic duct, or gallbladder.
• Liver is the most frequent location (83% to 94% of the patients)
• Inherent risk of malignant transformation. (approx. 10% cases)
• Very high proportion of these tumors occur in the left paramedian section
(segment IV).
• Exclusively observed in women 40 to 60 yrs of age.
• Origin: Derived from embryonal tissue destined to form gall bladder.
• During embryonic development, ectopic ovarian cells migrate to the liver, release
hormones and growth factors, and cause endodermally derived epithelium to
proliferate and finally to form a tumor. (embryonal tissue sequestered in liver)

50. Gross Morphology
• lobulated and multiloculated
• contain clear to mucinous fluid in large
volumes.
• Hemorrhagic fluid may be present
very rare
should raise the suspicion of malignancy.
• A bilious content is very unusual, as lack of
communication with the biliary tree is a
distinctive feature.
• Fistulization of cystadenoma in the biliary tree has
been reported.

51. Histology
• Internal lining has three distinct layers:
1. Epithelial layer
1. glandular, nonciliated cells in single flat row
2. With polypoid projections
3. shows strong and diffuse cytoplasmin staining with antibodies
against CEA and CA19-9
4. also stains positive for CK-7, CK-19, CK-8, and CK-18, which
supports a biliary origin
2. Mesenchymal stroma
1. consists of a compact arrangement of bland, spindle-shaped cells
with round to oval nuclei
2. expresses estrogen and progesterone receptors
3. Hence the name given HBCA with Ovarian Stroma
3. Outer layer of collagen connective tissue (hyalinized
pseudocapsule)
1. separates it from the adjacent liver parenchyma
2. explains how these tumors can be enucleated

52. Clinical Features
• The onset of symptoms tends to be insidious because of the slow
progression of the neoplasm.
• Presents as vague abdominal complaints that include abdominal
discomfort or swelling.
• Compressive symptoms :
Compression of the biliary confluence
• can cause cholestasis, jaundice with acute pain (in 35 %)
• Is transient and jaundice tends to resolve spontaneously
compression of the stomach or duodenum
caval compression
• tumor rupture, superinfection & bleeding (are rare)

53. Imaging
• MRI – Imaging modality of choice
• HBCA are typically seen as a fluid-containing
multilocular cyst.
homogeneous hyperintense on T2-weighted images
homogeneous hypointense on T1-weighted images
with visible septae
With varying signals depending on the content of the
cystic fluid
Mucinous fluid will appear with an isosignal,
serous fluid with a hyposignal,
hemorrhagic fluid with an hyperintense signal that can only
be seen in the lower part of a fluid-fluid level.
• On CT- may appear wrongly as unilocular. Hence, less
reliable.
Tumor is hyperintense on T2-weighted
images
Septa are visible on T1-weighted images

54. Treatment
• Partial excision, aspiration, and external or internal drainage are ineffective
as it causes very early recurrences.
• Hence require complete excision.
• Surgery can consist of partial hepatectomy or enucleation, as there is a
dissection plane between the cystadenoma and the adjacent parenchyma.
• Care should be taken when the cyst lies in segment IV so as not to injure the
biliary bifurcation.
• IOC (Intraoperative cholangiography) should be performed to document a
potential biliary communication and exclude the presence of mucus or
tumor material in the bile duct.

55. Bile Duct Adenoma

56. Introduction
• Rare benign intrahepatic tumor. (1.3% of primary liver tumors)
• Is a type of proliferative lesion originating from the damaged
intrahepatic bile duct epithelium.
• Between the age of 20 to 70 years old (average 55yrs)
• No significant gender difference
• Often do not present with any clinical symptoms.
• Hence, discovered incidentally.
• These lesion are comparatively small, (diameter between 1 to 20 mm)

57. Pathology
• Detected under the hepatic capsule (Sub-capsular)
• Usually solitary.
• Proliferated bile ducts (well differentiated without atypia)
• with plenty of chronic inflammatory cell infiltration.
• As the disease progresses, the number of proliferated bile ducts and the
infiltrated inflammatory cells gradually decreases, while that of fibrous
tissues increases.
• In the late stage, the hyaline-degenerated collagen fibers occupy the
region.
• IHC stains for CK7, CK19, and CD56 are positive.

58. Diagnosis
• Shows Hypervascular- prolonged enhancement on dynamic contrast-
enhanced CT, MRI & hepatic artery angiography.
Management
• No relationship between this tumor and cholangiocarcinoma has
been shown, and resection is unnecessary.
• Its only clinical significance lies in the possible confusion with
metastatic carcinoma during surgery.

59. Hepatic Resection

60. Introduction
• Hepatic resection for removal of lesions of the liver may be necessary for a
wide variety of conditions like-
1. Primary benign lesions of liver
2. Symptomatic cystic disease of liver
3. Malignant growths of the liver and biliary tract
4. Metastatic tumors (Most Common indication)
5. Ca Gall Bladder
6. Intrahepatic biliary stricture
7. Caroli’s Disease
• A healthy, non-cirrhotic liver may tolerate a resection of up to 80% of its
volume because liver’s enormous regenerative capacity enables functional
compensation within a few weeks.

61. Relevant Anatomy
• The anatomic division
between the right and
left liver is not at the
falciform ligament, but
rather follows a line
projected through a
plane—the principal
plane or Cantlie’s line -
running from the medial
margin of the gallbladder
bed to the left of the IVC
posteriorly.
• According to the
Brisbane terminology,
hepatic veins form the
boundaries between the
various sectors of the
liver.

62. Pre-Op Assessment
• Pre-operative imaging and volumetry
High resolution triphasic CT - to delineate the portal anatomy, biliary anatomy and
hepatic venous anatomy.
Urata formula is used to estimate the liver volume.
Functional volume of liver must be more than 30% for hepatic resection.
More than 40% for cirrhotic patients
Clinical & Lab
Criteria
Point 1 Point 2 Point 3
Encephalopathy None Mild to moderate
(Grade 1 or 2)
Severe
(Grade 3 or 4)
Ascites None Mild to moderate
(Diuretic responsive)
Severe (Diuretic
Refractory)
Bilirubin (mg/dL) <2 2-3 >3
Albumin (g/dL) >3.5 2.8-3.5 <2.8
Prothombin time
Seconds prolonged <4 4-6 >6
INR <1.7 1.7-2.3 >2.3
Class A= 5 to 6 points; Class B= 7 to 9 points; Class C= 10 to 15 points
• CTP (Child-Turcotte- Pugh) score
Class A- Fit for resection
Class B- reassessed with ICG
(Indocyanine Green) clearance test
Minimum clearance of 10% is required
for patients undergoing major
resection.
Class C- not fit for any type of
resection

63. Positioning and Incision
• To prevent air embolism, the dissection can be
performed with the patient in a 15-degree
Trendelenburg position.
• There must be a wide exposure of the abdomen
and chest.
• The cross bar should be fitted on table to hold
large retractor, used to elevate the costal margin.
• Incisions used for partial hepatectomy.
Rooftop incision- ABC
With vertical extension-
• Median sternotomy- DE
• Right thoracic extension- F
Most often an extended right subcostal incision
(ABD) is adequate.

64. Commonly performed Hepatic Resections
• Partial hepatectomy involves
removal of one or more segments by
isolation of the relevant portal
pedicle,
removal of the relevant hepatic veins
and biliary drainage channels,
removal of the associated liver tissue.
• Five types of major anatomic
resections are practiced (Couinaud
Nomenclature of Hepatic Resection)
Right Hepatectomy
(Seg- 5, 6, 7, 8)
Left Hepatectomy
(Seg- 2, 3, 4)
Right Lobectomy
(Seg- 4, 5, 6, 7, 8, sometimes 1)
Left Lobectomy
(Seg- 2, 3)
Extended Left Hepatectomy
(Seg- 2, 3, 4, 5, 8, sometimes 1)

65. • A minimum of 30% of functional liver must
be left behind (FLR—future liver remnant) for
adequate recovery of the patient.
• In cirrhotic patients, pre-operative portal vein
embolization (2 weeks prior) is done to
induce compensatory hypertrophy of remnant
liver in order to increase the FLR.
• The inflow to the liver can be controlled using
the Pringle manoeuvre.
The whole hepatic pedicle including the artery lies
in the free border of hepatoduodenal ligament.
Here it can be encircled using an umbilical tape or
vascular tape by making a window in the lesser
omentum.
Pringle manoeuvre

66. • The ligamentum teres is secured, and division
of the falciform ligament is begun.
• The falciform ligament is divided backward to
expose the suprahepatic IVC.
IVC ligament & Rt. triangular ligament is divided for
exposure of Rt. Lobe.
• Lt. triangular ligament is exposed and divided with cautery.
• Care should be taken not to injure the left phrenic vein.
Exposure & mobilization
of liver

67. Complications
1. Biliary leakage mostly in patients in whom biliary reconstruction is
necessary.
2. Bleeding from the hepatic veins and the inferior vena cava (IVC)
More likely-
i. during major resection of superiorly and posteriorly placed
tumors,
ii. or when tumors are closely adherent or adjacent to the IVC with
minimal clearance.
3. Post-op liver failure
P.T.O..

68. Post operative Liver Failure
• Is minimal if most of the specimen volume has been replaced by an
extensive tumor mass.
• B’coz in such pts, compensatory hypertrophy of the unaffected residual
liver has already occurred preoperatively.
In the cirrhotic liver,
• Liver failure is the most common cause of postoperative death after liver
resection
liver regeneration is much less effective;
impairment of liver function after resection is greater & may last longer
result in terminal liver failure.
• May be precipitated by intraoperative bleeding, abdominal infection.

69. Radiofrequency Ablation

70. Introduction
Principle of action:
• Deposition of energy into tumors induces
thermal injury resulting in a tumoricidal effect.
• RFA is a percutaneous, image-guided tumor
ablation methods involving flow of electrical
alternating current through tissue.
• RFA has been used as a treatment modality for
various benign neoplasms of liver.
• Also been used for the treatment of various
neoplasms, including metastases from a variety of
primary tumors, such as
hepatocellular carcinoma (HCC),
renal cell carcinoma (RCC),
non-small cell lung cancer (NSCLC),
osteoid osteoma

71. RFA System
• RF ablation system requires a closed-loop
circuit & comprises of
an electrical generator,
a needle electrode,
a patient (a resistor),
large dispersive electrodes (or “grounding
pads”)
• Different types of electrodes are
available.
• Some electrodes are internally cooled that
pump cooled saline in order to
minimize charring
permit optimal energy deposition
deeper tissue heating
Single needle electrode
Multi-tined electrode

72. Effective Ablation
• Can be achieved by
optimizing heat production-
depends upon tissue
temperature and duration of
the RF energy deposited
minimizing heat loss- depends
on blood flow within adjacent
blood vessels (Heat Sink Effect)
Heat Sink Effect

74. • Ablation margin should be minimum of around 1cm.
• Adjacent visceral organs, such as small bowel or colon, or diaphragm can be
displaced away from the tumor through patient positioning or
hydrodissection.
• Hydrodissection should be performed with sterile water or 5% dextrose
rather than saline because the latter conducts electricity.
• Effective RFA decreases when charring of tissue occurs.
Follow-up:
• Within a month and then at 3-month intervals after RFA with a repeat CT.
Complications:
1. hemorrhage,
2. biliary leakage or obstruction,
3. infection,
4. pneumothorax,
5. injury to adjacent organs

75. Contraindications
1. Bile duct or major vessel invasion
2. Significant extrahepatic disease
3. Child class C cirrhosis
4. Decompensated liver disease
5. Difficult to reach with electrodes
6. Lesions larger than 5 cm
7. More than 3 tumors High rate of recurrence

76. Hepatic Artery Embolization
(HAE)

77. Introduction
Principle of action:
• Is a procedure that injects substances to block or reduce the blood flow
to cancer cells in the liver.
• In HAE, a catheter is used to inject embolic material into the hepatic
arteries that provide nourishment for the tumors (feeding arteries),
resulting in obstruction of the feeding arteries and consequent ischemic
necrosis of the tumor.
• Normal liver is spared as most of its supply comes from portal vein.
Pre-requisite: Multiphasic CT or MRI
for accurate segmental localization of the tumor
 to know anatomic variations of celiac trunk and hepatic arteries
Most common hepatic artery variations are
right hepatic artery arising from the superior mesenteric artery & left hepatic artery arising from the left
gastric artery

78. Embolic Materials
• Must be of proper size.
• The optimal size should be small enough to reach and
occlude the capillaries to the tumor but bigger than
the arteriovenous shunt and peribiliary plexus, to
avoid the risk of pulmonary embolization and bile
duct necrosis.
• To date, gelatin sponge particles (Gel-foam) have
been the most frequently used agent.
used as 500- to 1000-μm cubes,
occludes the artery temporarily, with
recanalization taking place within 2 weeks
does not cause serious hepatic damage
Other embolic materials used
 Polyvinyl alcohol (PVA)
particle
 Absolute ethanol
 Starch microspheres
 Cyanoacrylate
 Autologous blood clot

79. Procedure
• After infiltration of local anesthetic,
Seldinger technique is used to gain access to
the common femoral artery.
• Initial diagnostic visceral arteriography is
performed to determine arterial anatomy to
the liver and patency of the portal vein.
• After the catheter is positioned
appropriately, embolic agent is used for
segmental arterial embolization.

81. Contraindications
Absolute
1. Patients with poor hepatic
function
• b’coz their livers are more
dependent on arterial blood
supply than normal liver
2. Extensive tumor involvement
of more than 50% to 75% of
the liver
3. Class C cirrhosis
Relative
1. active GI bleeding,
2. refractory ascites,
3. extrahepatic spread,
4. hepatic encephalopathy,
5. biliary obstruction,
6. Coagulopathy,
7. renal insufficiency

82. Complications
1. Postembolization syndrome (PES)
• occurs in approximately 80% of patients
• consists of pain, fever, nausea, and vomiting.
• Abrupt tumor cell death by ischemic damage causes release of intracellular toxins
into circulation.
• Possible causes of pain are
• acute ischemia of liver parenchyma,
• distension of the liver capsule,
• gallbladder ischemia secondary to inadvertent embolization of the cystic artery.
• T/T: supportive management that includes antiemetics, analgesics, and antipyretics;
it typically subsides after 1 to 3 days.
2. Liver Failure – most serious complication
3. Liver Abscess – is rare (0.5 to 2%)

83. 4. Bile Duct Injury
• relatively common (2% to 12.5%)
• may be injured as they are supplied by peribiliary capillary plexus from the
hepatic artery
• Manifests as intrahepatic biloma, focal stricture of the common bile duct, or
diffuse dilatation of intrahepatic bile duct
5. Extrahepatic Nontargeted Embolization
• Less common if diagnostic angiogram has been carefully performed
• Gallbladder- MC nontarget organ-
cystic artery is often not opacified on arteriogram.
Can give rise to symtoms of cholecystitis.
• Gastroduodenal ulcer can occur as a result of inadvertent embolization of the
accessory left gastric arteries (arising from Lt. hepatic artery) & Rt. Gastric artery (arising
from proper or left hepatic artery).

84. References
• Grant’s Atlas of Anatomy, 13th Ed.
• Sobotta’s Atlas of Anatomy, 15th Ed.
• Love and Bailey Textbook of Surgery, 26th Ed.
• Fischer’s Master of Surgery, 6th Ed.
• Blumgart: Surgery of the Liver, Biliary Tract and Pancreas, 4th Ed.
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 10 Ed.
• Schwartz Principles of Surgery, 10th Ed.
• Internet