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The “crude annual incidence” of liver abscesses was reported from a retrospec-
tive study from the United Kingdom to be 2.3 per 100,000 per year [25].
Fever and abdominal pain, usually localized to the right upper quadrant, are the
most common clinical manifestations in liver abscesses [26, 27]. An abnormal liver
prole is common, with increased serum alkaline phosphatase activity being the
most notable abnormality due to a space-occupying lesion.
Abdominal ultrasound and computed tomography (CT) are diagnostic in the
majority of the cases [25, 28].
Aspiration of abscess content yields the pathogen(s), which tend to be enteric
Gram-negative bacilli, Streptococci, and Staphylococcus aureus. Liver abscesses
Fig. 13.3 Coronal images from gadolinium enhanced magnetic resonance images (top row) and
unenhanced computed tomography (bottom row) show two large complex cystic non enhancing
masses in the right hepatic lobe compatible with echinococcal cysts (arrows).
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from which Klebsiella pneumoniae is isolated tend to be associated with a syn-
drome described in Asia; in this context, a publication from NewYork City reported
that Klebsiella pneumoniae was identied in 41% of cases, which included 50% of
the patients of Asian ethnicity [29]; this type of abscess has been reported in asso-
ciation with colorectal cancer in Asia.
Treatment consists of percutaneous drainage with needle aspiration or catheter
insertion, especially for large abscesses (i.e., >5cm). Large abscesses may require
surgical drainage, a decision that should be made when the size does not decrease in
association with nonsurgical treatment or when there is no clinical improvement.
The aspirate should be sent for Gram stain and culture. Drainage is used concomi-
tantly with intravenous antibiotics, beta-lactams being preferred, based on a study
that documented an increase in the proportion of patients that was readmitted within
30days post discharge when patients were transitioned to oral antibiotics for move-
ment from inpatient to outpatient care [30]; metronidazole should be included to
cover empirically for ameba until serology conrms its absence. The duration of
antibiotics is 4–6weeks; the radiographical resolution was reported within 18weeks
of diagnosis and treatment [31].
Hepatic Hemangiomata
Hepatic hemangiomata are the most common benign tumors of the liver, reported to
have a prevalence that ranges from 0.4% to 24% [32, 33]. They are more common
in women than in men [34, 35], tend to be asymptomatic, and are diagnosed inci-
dentally by the use of abdominal imaging. They are usually found in the right lobe
of the liver and are generally solitary, although more than one hemangioma can be
found. The liver prole is normal.
Giant hemangioma is a term reserved for tumors greater than 10cm, which can
be associated with symptoms, which tend to be right upper quadrant pain and early
satiety. Pain secondary to thrombosis [36] and hemobilia due to the rupture of the
tumor into the bile ducts has been documented [37] in cases of large
hemangiomata.
Vascular malformations are considered to be the etiology of these lesions, which,
histologically, have been described as tumors having an irregular interface with the
liver parenchyma. Collagen, elastic bers, and smooth muscle comprised the ves-
sels’ walls, with low proliferation rate and absence of estrogen or progesterone
receptors [38]. However, an increase in size in association with exposure to female
hormones has been reported [39].
Radiographically, liver hemangiomata appear like well-dened hyperechoic
lesions on ultrasound [40]. In contrast-enhanced computed tomography and
MRI studies contrast material lls the lesion irregularly from the periphery
(Fig.13.1).
Tumors with the typical appearance of hemangiomata by radiographic studies
that are not associated with symptoms do not require intervention [32]. A giant
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hemangioma may require surgical treatment. Enucleation was reported to be associ-
ated with fewer complications than surgical resection [41, 42]. Institutional exper-
tise is fundamental in the management of patients who required surgery [36].
Focal Nodular Hyperplasia
Focal nodular hyperplasia (FNH) is a benign tumor of the liver, reported as having
a prevalence that ranges between 0.4% and 3% in the general population [32, 43].
FNH is mostly diagnosed in individuals aged between 20 and 50years, with a
higher prevalence in women than men. The lesions are single in 80% of the cases
and range between 0.5 and 8cm in diameter [32, 43, 44].
The etiology of FNH is considered to be a proliferative cell response to an aber-
rant dystrophic artery [44]. Conditions of vascular etiology that can be associated
with FNH are hereditary hemorrhagic telangiectasia or previously treated solid
tumors in children, suggesting that a disturbance in blood ow may be relevant in
the pathogenesis of FNH [32]. The nodule is not encapsulated. Macroscopically, it
is characterized by a central, stellate brovascular zone comprised of dystrophic
arterial vessels, making the diagnosis by radiographic means possible [45]. However,
a histological study documented scars in 49% of cases [46], which has suggested
that mechanisms different from vascular processes may play a role in the formation
of FNH; in this regard, the idea of clonality as an etiological factor was supported
by a study that showed a uniform pattern of X chromosome inactivation [45]. It has
also been documented that signaling pathways mediated by transforming growth
factor β and Wnt/β-catenin are overexpressed [47]. The overexpression of Wnt/β- -
catenin results in the activation of the genes it targets, including GLUL, coding for
glutamine synthase, which results in a typical glutamine synthetase expression by
immunostaining described as a “map-like” pattern in the hepatocytes that comprise
the lesion, usually located around hepatic veins [48].
Patients with FNH tend not to have symptoms from the tumor. Physical examina-
tion does not provide any diagnostic clues.
On liver ultrasound, FNHs have been described as inhomogeneous nodules with
poorly delineated borders, as isoechoic lesions, in reference to the surrounding
parenchyma, and as having a rim surrounding the mass and displaying a central
brous scar. The use of conventional, color, and power Doppler may highlight the
presence of arteries that radiate toward the periphery in a spoke-wheel pattern, and
that of a hypertrophic hepatic artery consistent with the feeding vessel [49]. MRI
offers the best diagnostic option [50].
On computed tomography, the typical FNH tends to have a lobulated contour,
hypoattenuated or isoattenuated with respect to the surrounding liver tissue. In asso-
ciation with intravenous contrast, the lesion becomes hyperattenuated in the arterial
phase, except for the central scar. In the portal and following phases, there is isoat-
tenuation, compared to the parenchymal contour, and central scar enhancement may
be appreciated [51].
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On MRI, FNH is isointense or hypointense on T1-weighted images, with hyper-
intensity in T-2 with a hyperintense central scar in 80% of the cases [52]. In associa-
tion with gadolinium, FNH exhibits intense homogeneous enhancement in the
arterial phase, enhancing the central scar in subsequent phases [51].
Patients in whom a diagnosis of FNH is conrmed, as described above, do not
require diagnostic interventions [53]. If imaging studies cannot ascertain the diag-
nosis of FNH, referral to a center with expertise in biopsy and resection is recom-
mended [32].
Hepatocellular Adenomata
Hepatocellular adenomata (HCA) are rare tumors with a reported prevalence of
0.001 and 0.004%, more common in women than in men, usually diagnosed between
35 and 40years [32, 54]. There is an association between oral contraceptive pill use
(OCP) and anabolic steroids use and a reported increase in their incidence in rela-
tionship with obesity [54]. Other rare associations include familial HCA associated
with maturity-onset diabetes type 3 (MODY3), iron overload disorders, McCune–
Albright syndrome, and glycogen storage disease [32].
Mutations characterize specic subtypes of HCA: (i) HNF1α mutated (HA-H),
with somatic mutations of TCF1 (HNF1A) gene and heterozygous germline muta-
tions of CYP1B1 gene, which lead to increase in lipogenesis by enhancement of
fatty acid synthesis and by downregulation of liver type fatty acid-binding protein
[55]; (ii) β catenin mutated hepatocellular adenoma (HA-B), with mutations in the
β catenin gene and increased or transient activation of the Wnt /β catenin signaling
pathway, reported to have an increased risk of malignant transformation [56]; (iii)
inammatory hepatocellular adenoma (HA-I), with gain of function mutations of
the IL6ST gene, activation of STAT3 signaling pathway, and acute-phase inam-
matory response [57]; and (iv) sonic hedgehog (SHH) hepatocellular adenoma
(HA- sh), associated with activation of the sonic hedgehog pathway via fusion of
promoter of INHBE with GLI1 [58], and by upregulation of argininosuccinate
synthase 1, which were reported in association with increased risk of bleeding
[59, 60].
Histologically, HCAs are characterized by thickened plates of hepatocytes with
preserved reticulin network and arteries not accompanied by bile ducts. Other fea-
tures include steatosis, inammatory cells, and dilated sinusoids. Fat can be appre-
ciated [61].
HCAs can be complicated by hemorrhage, especially from lesions greater than
5cm, and those protruding from the liver surface, and by malignant transformation.
In men, regardless of the adenoma size, resection is recommended because of the
risk for malignant transformation [32]. In women, lesions less than 5cm tend not to
rupture or convert into malignant tumors; however, it is recommended to discon-
tinue OCP and implement behavior modication in obese subjects [62].
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In contrast-enhanced ultrasound (CEUS), HCA demonstrates homogeneous con-
trast enhancement in the arterial phase, associated with rapid centripetal lling.
HCAs become isoechoic in reference to the surrounding liver parenchyma in the
early portal phase, although in some cases, there may be hyperechogenicity [63].
OnCT scan, tumors are well demarcated and isoattenuating with respect to the sur-
rounding liver parenchyma, and after contrast administration, they exhibit transient
homogenous enhancement with a return to baseline isodensity in the portal and
delayed phases [64]. HCAs appear hyperattenuating in association with recent hem-
orrhage, and hypoattenuating if they contain fat. On magnetic resonance imaging,
HCAs are bright on T1-weighted images and hyperintense, versus the surrounding
liver tissue, on T2-weighted images [64]; MRI is the preferred diagnostic modality.
Follow-up of patients with HCAs is recommended with a contrast-enhanced
MRI at 6months after the diagnosis. A lesion greater than 5cm and those that grow
20% of its diameter should be considered for resection because of the risks of hem-
orrhage and malignant transformation. A biopsy is recommended only for lesions
that cannot be characterized radiologically or for those in which malignancy cannot
be excluded [32].
Follow up with annual liver ultrasound up to 10years from diagnosis, and twice
a year beyond 10 years is recommended to assess growth and decide on denitive
treatment [32].
Special attention is required for pregnant women with HCAs, with liver sono-
grams recommended every 6–12 weeks to assess growth. Lesions smaller than
5cmin size, not protruding, nor growing do not require that a cesarean section at
the time of delivery be performed [32]. In women with large tumors, surgical resec-
tion may be recommended [32, 65]. Management, in collaboration with the obstetri-
cal team, is required [32, 65].
Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) is a malignant tumor of the liver. Cirrhosis is a
risk factor for HCC secondary to several types of liver diseases, including chronic
hepatitis C and B, and those with genetic diseases including porphyria [66], iron
overload in association with hemochromatosis [67], and alpha-1 antitrypsin de-
ciency [68]. Patients with chronic hepatitis B, in the absence of cirrhosis, are also at
risk of developing this type of cancer. Exposure to aatoxin B1 through contami-
nated foodstuff via mutations in tumor-suppressor gene p53 is a risk factor for HCC
[69–71]. The mortality from liver cancer was reported to have decreased in women
and to be stable in men [72]. Most cases of HCC are in Africa and East Asia; how-
ever, the incidence of HCC in the United States and Europe has increased. In gen-
eral, viral hepatitis has been the driving cause of liver disease; however, it is reported
that cirrhosis from nonalcoholic fatty liverdisease has become an important risk
factor for this type of cancer [73].
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The tumor is more prevalent in men than in women [74], with estrogens being
proposed as protective in the latter [75].
HCC is a vascular tumor. The physical examination may reveal a bruit on an
enlarged liver or one in which a mass can be palpated. The rest of the physical exam
may be notable for stigmata of chronic liver disease. Many times, the exam is non-
contributory; hence, the importance of imaging studies as part of a surveillance
program or as part of the liver disease workup initiated in a patient referred for
evaluation of possible liver disease.
The liver prole can be predominantly cholestatic or mixed. Serum concentra-
tion of alfa-fetoprotein (AFP) can be in hundreds or thousands.
Imaging studies reveal a mass, which, in a cirrhotic liver, HCC has to be consid-
ered. On liver sonogram, the mass is hypo or hyperechoic. The characteristic fea-
tures of HCC on CT scan or MRI are arterial enhancement versus the surrounding
liver tissue, and hypodensity also compared to the surrounding liver tissue, known
as wash out in the venous phase [76].
The treatment of HCC includes resection, local ablation, liver transplantation, or
a combination of the three, depending on the characteristics of the tumor and the
patient’s comorbidities. Systemic therapy is an alternative for patients who are not
eligible for invasive and surgical interventions or who progressed after local therapy
and includes sorafenib, regorafenib, nivolumab, and lenvatinib [77].
Screening measures are pivotal in managing patients at risk for HCC with a liver
sonogram and AFP every 6months, as suggested by the guidelines [78].
Fibrolamellar Carcinoma
Fibrolamellar carcinoma (FLC) is an uncommon malignant tumor most prevalent in
teenagers and patients in their 30s, with no gender preference [79].
FLC is associated with activation of protein kinase A, reported to occur from a
DNAJB1-PRKACA fusion transcript, secondary to somatic intrachromosomal
deletion on chromosome 19 [79].
Patients may present with weight loss, abdominal pain, and a palpable liver mass
[80], conrmed by imaging studies (see HCC above). The liver prole may be sug-
gestive of cholestasis or mixed, and an AFP is usually normal and rarely over
200ng/ml [81]. Histologically, the neoplastic hepatocytes are deeply eosinophilic,
associated with brosis arranged in a lamellar fashion, which gives it its name,
around the neoplastic hepatocytes [80].
In regards to enhancement features on CT scans, a retrospective study of 37
patients indicated arterial enhancement in 81%, with 96% exhibiting heterogeneity.
On MRI, 62% of the tumors were hypointense on T1-weighted imaging and hyper-
intense on T2-weighted imaging [82].
Treatment of FLC is resection or liver transplantation [83]. Chemotherapy with
a combination of cisplatin, epirubicin, and uorouracil has not been associated with
substantial benets [84]. Sorafenib similarly has not been associated with favorable
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response [84, 85]. A clinical trial that included mTOR inhibitors was not associated
with a therapeutic advantage [86]. The reader is referred to clinicaltrials.org for
information regarding study availability.
A retrospective review that identied 95 patients from three institutions identi-
ed female gender, macroinvasion, lymph node involvement, advanced stage, and
unresectability as poor prognostic features [84].
Intrahepatic Cholangiocarcinoma
Intrahepatic cholangiocarcinoma (ICC) originates from the intrahepatic biliary epi-
thelial cells, comprising 20% of the cholangiocarcinomas, which most commonly
emerge from extrahepatic bile ducts [87]. The risk factors that have been identied
in association with ICC include primary sclerosing cholangitis, hepatobiliary ukes,
hepatolithiasis, and biliary malformations, or patients may not have risk factors
for ICC.
Patients may be asymptomatic or present with right upper quadrant pain and an
associated mass. The liver prole is suggestive of cholestasis [88]. Cancer antigen
19–9 (CA 19–9), with a value greater than 1000 U/ml, suggests metastatic dis-
ease [89].
Radiographically, peripheral tumors tend to be associated with bile duct dilata-
tion, with retraction of the liver capsule noted in 36% of cases in a series of 24
patients, which included 25 tumors. In the portal phase, the tumors were hypodense,
with hyperattenuation in delayed phases. It was noted that rim-like contrast enhance-
ment was the most common feature in the arterial or portal phases, with portal
encasement in 40% of the cases [90, 91]. However, the denitive diagnosis is made
histologically.
The treatment of choice is the resection of the tumor [92]. Liver transplantation
has not been associated with a favorable prognosis because of the high recurrence
rate [93]. For patients with unresectable tumors, locoregional therapies are pro-
posed and include transarterial chemoembolization, radioembolization, and high-
dose, conformal external-beam radiation [94].
Hepatic Angiosarcoma
Hepatic angiosarcoma is uncommon. It originates from the sinusoidal lining. It
tends to be more common in men than in women at least 50years old [95]. The risk
factors identied in this type of tumor are thorium dioxide, vinyl chloride, arsenic,
and radiation exposure [96]. In addition, hemochromatosis and von Recklinghausen
disease have been reported in association with hepatic angiosarcoma [96].
Patients tend to present with fatigue, abdominal pain, hepatomegaly, ascites, and
hemoperitoneum from tumor hemorrhage [97].
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Histologically, the tumor is comprised of dilated cavernous vascular spaces lined
by pleomorphic neoplastic cells and spindle cells [98]. It is a highly aggressive
tumor at risk for spontaneous bleeding and in association with biopsy.
Imaging studies with CT and MRI are reported to exhibit tumor enhancement in
different phases of the dynamic post-contrast study, with heterogeneous hyperen-
hancement on the rst post-contrast phase that progressively expands on the subse-
quent phases, and typically follow blood pool with regards to CT attenuation and
magnetic resonancesignal intensity [99].
The prognosis of hepatic angiosarcoma is dismal, with a reported survival period
of 5 months [100]. Surgical resection is the optimal treatment for patients with
localized disease [101]. Several chemotherapeutic regimens have been used, but a
therapeutic benet has not been demonstrated [101]. Hepatic angiosarcoma is an
aggressive liver tumor for which treatment is suboptimal in the absence of curative
resection [102].
Hepatic Epithelioid Hemangioendothelioma
Hepatic epithelioid hemangioendothelioma (HEHE) is a hepatic tumor of endothe-
lial origin characterized by an unpredictable behavior [103], more common in
women, and reported to occur in 1 per one million persons [104].
Patients present with abdominal pain associated with a mass, or masses, and
weight loss [105]. The liver prole tends to be mixed, with a predominance of cho-
lestasis, reecting the space-occupying effect of the liver masses.
Histologically, the tumors have dendritic and epithelioid cells with vacuoles that
represent intracellular lumina. The stroma is brous. The tumorous cells are posi-
tive for endothelial markers, including factor VIII-related antigen, CD34, and/or
CD31 [106].
Radiographic ndings from contrast-enhanced CT and MRI include multiple
hypoattenuating lesions in both hepatic lobes that merge into large hypoattenuating
regions in a peripheral or subcapsular distribution, with a halo or target pattern of
enhancement in large lesions. There may be capsular retraction associated with
peripheral lesions. A typical nding known as lollipop sign is the tapering of hepatic
or portal veins to terminate at the end or within the masses’ edge. MRI reveals
hypointense lesions versus the surrounding parenchyma on unenhanced T1 with
heterogeneously increased signal intensity on T2-weighted images. Contrast
enhancement with gadolinium shows a peripheral halo or what has been described
as a target-type enhancement pattern with a peripheral hypointense rim [107].
The treatment of HEHE depends on the clinical status of the patient and includes
liver transplantation, resection, and chemotherapy with agents that include doxoru-
bicin, vincristine, interferon-α, 5-uorouracil, thalidomide, and monoclonal anti-
bodies against vascular endothelial growth factor, with the rst two being associated
with the best prognosis. After liver transplantation, the 5-year survival rate is 55%
to 75%, and with resection, 75% [108].
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Hepatic Mucinous Cystic Neoplasm
Hepatic mucinous cystic neoplasms comprise less than 5% of hepatobiliary
tumors [109].
The tumors have been reported mostly in middle-aged women, in the case of
cystadenomata, and in men, cystadenocarcinoma, with associated right upper quad-
rant pain, usually in association with large masses [110, 111].
In a study that characterized this type of tumor, the lesions were identied radio-
logically as measuring 25–250mm in diameter, the majority intrahepatic inloca-
tion, unilocular, multicystic, and multilocular, the latter being the most common,
with the absence of papillary mural nodule in 25 of 26 tumors [112].
Cystadenocarcinomas are characterized by cellular pleomorphism, anaplasia,
and inltration of brous stroma. It has been suggested that cystadenocarcinomas
evolve from cystadenomata [110]. The tumors are now dened as cyst-forming epi-
thelial neoplasms that usually do not communicate with the bile ducts, character-
ized by cuboidal to columnar epithelial cells, with various degrees of mucin
production, and associated with ovarian-type subepithelial stroma [112].
It is difcult to determine the nature of these tumors [113]; thus, malignancy
must be considered when the tumors appear as described above. In those cases,
surgical resection is a denitive treatment, associated with good outcomes [113].
We recommend referral to centers with expertise in hepatobiliary surgery for an
optimal approach.
Acknowledgments The author acknowledges Dr. Anatole Sladen for having contributed
Fig.13.1.
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