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Pyogenic liver abscess

Authors
Joshua Davis, MBBS, FRACP
Malcolm McDonald, PhD, FRACP, FRCPA
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Allyson Bloom, MD
Disclosures: Joshua Davis, MBBS, FRACP Nothing to disclose. Malcolm McDonald,
PhD, FRACP, FRCPA Nothing to disclose. Stephen B Calderwood, MD
Consultant/Advisory Boards: Pulmatrix [Inhaled antimicrobial products (Not currently
released)]. Patent Holder: Vaccine Technologies [Cholera (Cholera vaccines)]. Equity
Ownership/Stock Options: PharmAthene [Biodefense (Anthrax)]. Allyson Bloom, MD
Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When
found, these are addressed by vetting through a multi-level review process, and through
requirements for references to be provided to support the content. Appropriately referenced
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Conflict of interest policy
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: May 2014. | This topic last updated: Jan 21, 2014.
INTRODUCTION Pyogenic liver abscesses usually develop following peritonitis due to
leakage of intraabdominal bowel contents that subsequently spread to liver via the portal
circulation or via direct spread from biliary infection. They may also result from arterial
hematogenous seeding in the setting of systemic infection.
The clinical approach to pyogenic liver abscess will be reviewed here. Amebic abscesses
are discussed separately. (See "Extraintestinal Entamoeba histolytica amebiasis".)
EPIDEMIOLOGY
Prevalence Liver abscesses are the most common type of visceral abscess; in a report of
540 cases of intraabdominal abscesses, pyogenic liver abscesses accounted for 48 percent
of visceral abscesses and 13 percent of intraabdominal abscesses [1]. The annual incidence
of liver abscess has been estimated at 2.3 cases per 100,000 populations and is higher
among men than women (3.3 versus 1.3 per 100,000) [2-4]; substantially higher rates have
been reported in Taiwan (17.6 cases per 100,000) [5].
Risk factors Risk factors include diabetes, underlying hepatobiliary or pancreatic
disease, and liver transplant [2,3,6,7]. Geographic and host factors may also play a role; for

example, a primary invasive liver abscess syndrome due to K. pneumoniae has been
described in East Asia. This is discussed separately. (See "Invasive liver abscess syndrome
caused by Klebsiella pneumoniae".)
Association with colorectal neoplasia Several studies from Asia, where K. pneumoniae
is the primary cause of pyogenic liver abscesses, have suggested an association with
underlying colorectal cancer [8-13]. It is unclear whether these findings can be applied to
other parts of the world.
In a large retrospective analysis of claims data from the universal insurance program in
Taiwan, the incidence of any subsequent gastrointestinal malignancy diagnosis among
14,690 patients who had been diagnosed with pyogenic liver abscess was fourfold higher
than that among 58,760 controls matched for age, sex, and underlying diabetes mellitus
(10.8 versus 2.5 cases per 1000 person years) [13]. Colorectal carcinoma was the most
common malignancy in both cohorts but was more frequent among liver abscess patients
(7.3 versus 1.6 cases per 1000 person years). In a separate retrospective study from Taiwan,
in which 1257 patients with pyogenic liver abscess were observed to have a high risk of
subsequent liver or colorectal carcinoma, the greatest excess risk of a cancer diagnosis was
in the first three months after the abscess diagnosis [9]. In most studies that evaluated for
causative pathogens, liver abscesses caused by K. pneumoniae appear to have a stronger
association with colorectal cancer than those caused by other organisms [10-12], probably
because most other organisms came from biliary tract diseases. The long-term follow-up
prevalence of colorectal cancer among pyogenic liver abscess patients remained 2.3 to 3.2
percent [8,12]. Despite the limitations of these retrospective studies, the findings suggest
the possibility of an occult colorectal neoplasia among patients diagnosed with pyogenic
liver abscess, particularly due to K. pneumoniae, in the absence of apparent underlying
hepatobiliary disease.
Prognosis The mortality rate in developed countries ranges from 2 to 12 percent [3,14].
Independent risk factors for mortality include need for open surgical drainage, the presence
of malignancy, and the presence of anaerobic infection [15,16].
PATHOGENESIS A considerable proportion of pyogenic liver abscesses follow one or
more episodes of portal vein pyemia, usually related to bowel leakage and peritonitis.
Another important route is direct spread from biliary infection. Underlying biliary tract
disease such as gallstones or malignant obstruction is present in 40 to 60 percent of cases
[2,14,17]. Occasionally, abscesses arise from surgical or penetrating wounds [18].
Liver abscesses may also result from hematogenous seeding from the systemic circulation.
A monomicrobial liver abscess due to a streptococcal or staphylococcal species should
prompt evaluation for an additional source of infection.
Liver abscesses most commonly involve the right lobe of the liver, probably because it is
larger and has greater blood supply than the left and caudate lobes. Liver abscess may also
be accompanied by pylephlebitis [19]. (See "Pylephlebitis".)

MICROBIOLOGY Many pathogens have been described; this variability reflects the
different causes, types of medical intervention (such as biliary tree stenting, or
immunosuppression due to cancer chemotherapy) and geographic differences. Most
pyogenic liver abscesses are polymicrobial; mixed enteric facultative and anaerobic species
are the most common pathogens. Anaerobes are probably under-reported because they are
difficult to culture and characterize in the laboratory. For example, in one series of 233
cases, mixed facultative and anaerobic species were implicated in one-third of patients, and
bacteremia was documented in 56 percent of cases [2].
The highly variable microbiology justifies pursuing a microbiological diagnosis in virtually
every case. Potential pathogens include:
The Streptococcus milleri or S. anginosus group (including S. constellatus and S.
intermedius) is an important cause of liver abscess. When implicated, it should prompt a
search for simultaneous metastatic infections at other locations. (See "Infections due to the
Streptococcus anginosus (Streptococcus milleri) group".)
S. aureus, S. pyogenes, and other Gram positive cocci are recognized pathogens in
specific circumstances [20]. For example, in a report of liver abscesses in patients who
underwent transarterial embolization for hepatocellular carcinoma, they accounted for 60
percent of pathogens. (See "Nonsurgical therapies for localized hepatocellular carcinoma:
Transarterial embolization, radiotherapy, and radioembolization", section on
'Complications'.)
Candida species have also been implicated in pyogenic liver abscess and accounted for 22
percent of liver abscesses in one series [2]. Hepatosplenic candidiasis can occur in patients
who have received chemotherapy and presents with recovery of neutrophil counts
following a neutropenic episode. (See "Chronic disseminated candidiasis (hepatosplenic
candidiasis)".)
Klebsiella pneumoniae is an important emerging pathogen. This syndrome is discussed in
detail separately (see "Invasive liver abscess syndrome caused by Klebsiella pneumoniae").
Tuberculous liver abscesses are uncommon but should be considered when typical
pyogenic organisms are not recovered from cultures [21,22]. (See "Clinical manifestations,
diagnosis, and treatment of extrapulmonary and miliary tuberculosis".)
Burkholderia pseudomallei (the agent of Melioidosis) should be considered in patients
from endemic areas (Southeast Asia and Northern Australia). (See "Epidemiology, clinical
manifestations, and diagnosis of melioidosis".)
Amebiasis should be considered as a cause of primary liver abscess, especially in patients
who are from or have traveled to an endemic area within the past six months. The clinical
course and appearance may be difficult to distinguish from pyogenic liver abscess; this is
discussed in detail separately. (See "Extraintestinal Entamoeba histolytica amebiasis".)

CLINICAL MANIFESTATIONS The typical clinical manifestations of pyogenic liver


abscess are fever and abdominal pain. Other common symptoms include nausea, vomiting,
anorexia, weight loss, and malaise.
Fever occurs in approximately 90 percent of patients, and abdominal symptoms occur in 50
to 75 percent of patients [2,3,14,23]. Abdominal symptoms and signs are usually localized
to the right upper quadrant and may include pain, guarding, rocking tenderness (pain
caused by gently rocking the patient's abdomen), and even rebound tenderness. About onehalf of patients with liver abscess have hepatomegaly, right upper quadrant tenderness, or
jaundice [23]. The absence of right upper quadrant findings does not exclude liver abscess.
DIAGNOSIS The diagnosis of pyogenic liver abscess is made by history, clinical
examination, and radiographic imaging followed by aspiration and culture of the abscess
material.
Imaging Computed tomography (CT) scan and ultrasound are the modalities of choice
(image 1) [18]. CT usually shows a fluid collection with surrounding edema. There may
also be stranding and loculated subcollections. Pyogenic liver abscess cannot be reliably
distinguished from amebic abscess by imaging studies [21]. (See "Extraintestinal
Entamoeba histolytica amebiasis", section on 'Amebic liver abscess'.)
Abscesses must be distinguished from tumors and cysts. Tumors have a solid radiographic
appearance and may contain areas of calcification. Necrosis and bleeding within a tumor
may lead to a fluid-filled appearance; in such circumstances radiographic differentiation
from abscess can be challenging. Cysts appear as fluid collections without surrounding
stranding or hyperemia.
An elevated right hemidiaphragm, right basilar infiltrate, or right-sided pleural effusion can
be seen in 25 to 35 percent of cases [24]; these findings should prompt further investigation
of the right upper quadrant with CT or ultrasonography. Magnetic resonance imaging and
tagged white blood cell scans are less useful for distinguishing abscess from other causes of
liver mass.
Microbial cultures Material obtained from CT or ultrasound-guided aspiration should be
sent to the laboratory for gram stain and culture (both aerobic and anaerobic). Anaerobic
culture should be specifically requested on the laboratory requisition.
Blood cultures are essential; they are positive in up to 50 percent of cases [25].
Cultures obtained from existing drains are NOT adequate for guiding antimicrobial therapy,
since they are often contaminated with skin flora and other organisms. This was
demonstrated in a study of 66 cases of liver abscess; cultures results obtained via
radiographic guidance were compared with cultures obtained from a drain that had been in
place for at least 48 hours [22]. Cultures from percutaneous specimens correlated with
cultures from drainage catheters in only one-half of cases. Treatment based upon drainage
culture results alone would have led to inappropriate therapy for the remaining patients.

Laboratory findings Laboratory abnormalities may include elevated bilirubin and/or


liver enzymes. Serum alkaline phosphatase is elevated in 67 to 90 percent of cases and
serum bilirubin and aspartate aminotransferase concentrations are elevated in about onehalf of cases [2,14,23].
Other laboratory abnormalities may include leukocytosis, hypoalbuminemia, and anemia
(normochromic, normocytic).
TREATMENT Treatment of pyogenic liver abscess should include drainage and
antibiotic therapy.
Drainage Drainage techniques include CT-guided or ultrasound-guided percutaneous
drainage (with or without catheter placement), surgical drainage, or drainage by endoscopic
retrograde cholangiopancreatography (ERCP).
For single abscesses with a diameter 5 cm, either percutaneous catheter drainage or needle
aspiration is acceptable [26-29]. Drainage catheters should remain in place until drainage is
minimal (usually up to seven days). Repeat needle aspiration may be required in up to half
of cases if a catheter is not left in situ [26,27].
For percutaneous management of single abscesses with diameter >5 cm, catheter drainage
is preferred over needle aspiration. These principles were illustrated in a trial of 60 patients
with pyogenic liver abscess treated with antibiotics and percutaneous drainage via catheter
or needle aspiration [29]. Among patients with an abscess diameter >5 cm, treatment was
successful in 100 percent of patients treated with catheter drainage compared with 50
percent of patients with needle aspiration. Successful outcomes were observed for all
patients with abscess 5 cm, regardless of drainage modality.
For single abscesses with diameter >5 cm, some favor surgical intervention over
percutaneous drainage [30,31]. The efficacy of this approach was suggested in a
retrospective study of 80 patients with abscess >5 cm managed with percutaneous or
surgical drainage; there was no difference in mortality, morbidity, duration of fever or
complication rates. However, the rate of treatment failure was lower with surgical drainage
(7 versus 28 percent).
Surgical drainage is also appropriate in the following circumstances:
Multiple abscesses
Loculated abscesses
Abscesses with viscous contents obstructing the drainage catheter
Underlying disease requiring primary surgical management
Inadequate response to percutaneous drainage within seven days

Multiple or loculated abscesses may be successfully managed by percutaneous drainage;


this was illustrated in a retrospective study of patients with pyogenic liver abscess [32].
Successful percutaneous drainage was achieved in the setting of multiple abscesses (22 of
24 patients) and multiloculated abscesses (51 of 54 patients) [32].
Endoscopic retrograde cholangiopancreatography (ERCP) can be useful for drainage of
liver abscesses in patients with previous biliary procedures whose infection communicates
with the biliary tree [17,33].
Antibiotics No randomized controlled trials have evaluated empiric antibiotic regimens
for treatment of pyogenic liver abscess. Treatment recommendations are based upon the
probable source of infection and should be guided by local bacterial resistance patterns, if
known. (See 'Microbiology' above.)
Empiric broad-spectrum parenteral antibiotics should be administered pending abscess
gram stain and culture results. We suggest one of the regimens outlined in the table (table
1).
Regardless of the initial empiric regimen, the therapeutic regimen should be revisited once
culture and susceptibility results are available. Recovery of more than one organism should
suggest polymicrobial infection including anaerobes, even if no anaerobes are isolated in
culture. In such circumstances, anaerobic coverage should be continued.
Duration of therapy There are no randomized controlled trials evaluating the optimal
duration of therapy. This is typically determined by the extent of infection and the patient's
clinical response to initial management. Patients with abscess(es) that are difficult to drain
or slow to resolve on follow-up imaging usually require longer courses of therapy.
Useful clinical indicators to follow are temperature, white blood cell count and serum Creactive protein. Follow-up imaging should only be performed in the setting of persistent
clinical symptoms or if drainage is not proceeding as expected; radiological abnormalities
resolve much more slowly than clinical and biochemical markers. Among 102 pyogenic
liver abscess patients in Nepal, the mean time to ultrasonographic resolution of abscesses
<10 cm was 16 weeks; mean time to resolution for abscesses >10 cm was 22 weeks [34].
Drainage catheters should remain in place until drainage is minimal (usually up to seven
days). If percutaneous needle aspiration was performed without catheter placement, repeat
aspiration may be required in up to one-half of cases [26,27].
Antibiotic therapy should be continued for four to six weeks [35]. Patients who have had a
good response to initial drainage should be treated with two to four weeks of parenteral
therapy, while patients with incomplete drainage should receive four to six weeks of
parenteral therapy. The remainder of the course can then be completed with oral therapy
tailored to culture results [28,29]. If culture results are not available, reasonable empiric
oral antibiotic choices include amoxicillin-clavulanate alone or a fluoroquinolone
(ciprofloxacin or levofloxacin) plus metronidazole.

SUMMARY AND RECOMMENDATIONS


The clinical manifestations of pyogenic liver abscess usually include fever and abdominal
pain; other symptoms may include nausea, vomiting, anorexia, weight loss and malaise.
(See 'Clinical manifestations' above.)
The diagnosis of pyogenic liver abscess is confirmed by radiographic imaging (computed
tomography or ultrasound) followed by aspiration and culture of the abscess material. (See
'Diagnosis' above.)
Most pyogenic liver abscesses are polymicrobial. Amebic abscess is best distinguished
from pyogenic liver abscess by serology. (See 'Microbiology' above.)
We recommend draining liver abscesses (Grade 1B). For drainage of abscesses 5 cm in
diameter, we suggest needle aspiration rather than percutaneous catheter drainage (Grade
2C). Repeat needle aspiration may be required. (See 'Drainage' above.)
For drainage of abscesses >5 cm in diameter, we suggest percutaneous catheter drainage
rather than needle aspiration (Grade 2B). Drainage catheters should remain in place until
drainage ceases (usually up to seven days). (See 'Drainage' above.)
We suggest surgical drainage (rather than percutaneous drainage) in the following
circumstances (Grade 2C). (See 'Drainage' above.):
Multiple abscesses (depending on number, position, and size)
Loculated abscesses
Abscesses with viscous contents obstructing drainage catheter
Underlying disease requiring primary surgical management
Inadequate response to percutaneous drainage within seven days
We recommend empiric parenteral antibiotic therapy pending culture and susceptibility
results (Grade 1C). Suggested regimens are outlined in the table (table 1). (See 'Antibiotics'
above.)
When there is a clinical response to therapy, oral antibiotics may be substituted for
parenteral therapy (with the guidance of susceptibility testing) to complete a four to six
week course of treatment. (See 'Duration of therapy' above.)
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