Abses Liver
Abses Liver
Liver Abscess
Updated: Jun 20, 2016
Author: Ruben Peralta, MD, FACS; Chief Editor: John Geibel, MD, DSc, MSc, AGAF more...
Background
Pathophysiology
The liver receives blood from both systemic and portal circulations.
Increased susceptibility to infections would be expected given the increased
exposure to bacteria. However, Kupffer cells lining the hepatic sinusoids
clear bacteria so efficiently that infection rarely occurs. Multiple processes
have been associated with the development of hepatic abscesses (see the
image below).
Table 4: Underlying etiology of 1086 cases of liver abscess compiled from
the literature.
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Biliary tract disease is now the most common source of pyogenic liver
abscess (PLA). Obstruction of bile flow allows for bacterial proliferation.
Biliary stone disease, obstructive malignancy affecting the biliary tree,
stricture, and congenital diseases are common inciting conditions. With a
biliary source, abscesses usually are multiple, unless they are associated
with surgical interventions or indwelling biliary stents. In these instances,
solitary lesions can be seen.
The right hepatic lobe is affected more often than the left hepatic lobe
by a factor of 2:1. Bilateral involvement is seen in 5% of cases. The
predilection for the right hepatic lobe can be attributed to anatomic
considerations. The right hepatic lobe receives blood from both the superior
mesenteric and portal veins, whereas the left hepatic lobe receives inferior
mesenteric and splenic drainage. It also contains a denser network of biliary
canaliculi and, overall, accounts for more hepatic mass. Studies have
suggested that a streaming effect in the portal circulation is causative.
Etiology
Polymicrobial involvement is common, with Escherichia
coli and Klebsiella pneumoniae being the two most frequently isolated
pathogens (see the image below). Reports suggest that K pneumoniae is an
increasingly prominent cause. [3]
Table 2: Microbiologic results from 312 cases of liver abscess compiled
from the literature.
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Epidemiology
United States statistics
The incidence of pyogenic liver abscess has essentially remained
unchanged by both hospital and autopsy data. Liver abscess was diagnosed
in 0.7%, 0.45%, and 0.57% of autopsies during the periods of 1896-1933,
1934-1958, and 1959-1968, respectively. The frequency in hospitalized
patients is in the range of 8-16 cases per 100,000 persons. Studies suggest
a small, but significant, increase in the frequency of liver abscess.
Age-related demographics
Prior to the antibiotic era, liver abscess was most common in the fourth
and fifth decades of life, primarily due to complications of appendicitis. With
the development of better diagnostic techniques, early antibiotic
administration, and the improved survival of the general population, the
demographic has shifted toward the sixth and seventh decades of life.
Frequency curves display a small peak in the neonatal period followed by a
gradual rise beginning at the sixth decade of life.
Prognosis
Untreated, pyogenic liver abscess remains uniformly fatal. With timely
administration of antibiotics and drainage procedures, mortality currently
occurs in 5-30% of cases. The most common causes of death include sepsis,
multiorgan failure, and hepatic failure. [5]
History
The most frequent symptoms of hepatic abscess include the following (see
the image below):
Fever (either continuous or spiking)
Chills
Right upper quadrant pain
Anorexia
Malaise
Table 1: Presenting symptoms and signs in 715 patients diagnosed with
liver abscess.
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Physical Examination
Fever and tender hepatomegaly are the most common signs. A
palpable mass need not be present. Midepigastric tenderness, with or
without a palpable mass, is suggestive of left hepatic lobe involvement.
Decreased breath sounds in the right basilar lung zones, with signs of
atelectasis and effusion on examination or radiologically, may be present. A
pleural or hepatic friction rub can be associated with diaphragmatic irritation
or Glisson capsule inflammation.
Differential Diagnoses
Acute Gastritis
Bacterial Pneumonia
Biliary Disease
Cholecystitis
Hepatocellular Carcinoma
Hydatid Cysts
Parapneumonic Pleural Effusions and Empyema Thoracis
Laboratory Studies
Laboratory studies may include a complete blood count (CBC) with
differential (to identify anemia of chronic disease or neutrophilic leukocytosis)
and liver function studies (hypoalbuminemia and elevation of alkaline
phosphatase are the most common abnormalities; elevations of
transaminase and bilirubin levels are variable.
Imaging Studies
Advances in radiologic techniques has been credited with the
improvement in mortality. The various radiologic techniques have differing
benefits and limitations with regard to their diagnostic utility (see the image
below).
Table 3: Comparison of the radiologic procedures used in the diagnosis of
liver abscess.
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Computed tomography
Computed tomography (CT) with contrast and ultrasonography remain
the radiologic modalities of choice as screening procedures and also can be
used as techniques for guiding percutaneous aspiration and drainage.
Radionuclide scanning
The initial studies are used in diagnosis. [9] Gallium and technetium
radionuclide scanning use the fact that the radiopharmaceuticals share the
same uptake, transport, and excretion pathways as bilirubin and, thus, are
effective agents in evaluating liver disease. Sensitivity varies with the
radiopharmaceutical utilized, technetium (80%), gallium (50-80%), and
indium (90%). Limitations include a delay in diagnosis and the need for
confirmatory procedures; thus, they offer no benefit over other imaging
modalities.
Chest radiography
Chest radiographic findings of basilar atelectasis, right hemidiaphragm
elevation, and right pleural effusion are present in approximately 50% of
cases; before advancements in radiologic technique, these served as
diagnostic clues. Pneumonias or pleural diseases often are initially
considered because of the radiographic findings.
Medical Care
An untreated hepatic abscess is nearly uniformly fatal as a result of
complications that include sepsis, empyema, or peritonitis from rupture into
the pleural or peritoneal spaces, and retroperitoneal extension. Treatment
should include drainage, either percutaneous or surgical.
Surgical Care
Surgical drainage was the standard of care until the introduction of
percutaneous drainage techniques in the mid-1970s. With the refinement of
image-guided techniques, percutaneous drainage and aspiration have
become the standard of care.
Current indications for the surgical treatment of pyogenic liver abscess
are for the treatment of underlying intra-abdominal processes, including
signs of peritonitis; existence of a known abdominal surgical pathology (eg,
diverticular abscess); failure of previous drainage attempts; and the
presence of a complicated, multiloculated, thick-walled abscess with viscous
pus.
Consultations
Obtain an interventional radiology consultation as soon as the
diagnosis is considered to allow rapid collection of cavity fluid and the
potential for early therapeutic drainage of abscess.
Long-Term Monitoring
Aggressively seek an underlying source of the abdominal pathology.
Perform weekly serial computed tomography (CT) or ultrasound
examinations to document adequate drainage of the abscess cavity.
Continue radiologic evaluation to document progress of therapy after
discharge.
Drain care may be required. Maintain drains until the output is less
than 10 mL/day.
Medication Summary
Until cultures are available, the choice of antimicrobial agents should
be directed toward the most commonly involved pathogens. Regimens using
beta-lactam/beta-lactamase inhibitor combinations, carbapenems, or
second-generation cephalosporins with anaerobic coverage are excellent
empiric choices for the coverage of enteric bacilli and anaerobes.
Metronidazole or clindamycin should be added for the coverage
of Bacteroides fragilis if other employed antibiotics offer no anaerobic
coverage.
Antibiotics
Class Summary
Empiric antimicrobial therapy must be comprehensive and should
cover all likely pathogens in the context of the clinical setting.
Meropenem (Merrem)
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Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-
wall synthesis. Effective against most gram-positive and gram-negative
bacteria.
Cefuroxime (Ceftin)
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Second-generation cephalosporin maintains gram-positive activity that
first-generation cephalosporins have; adds activity against Proteus
mirabilis, Haemophilus influenzae, Escherichia coli, Klebsiella pneumoniae,
and Moraxella catarrhalis. Condition of patient, severity of infection, and
susceptibility of microorganism determine proper dose and route of
administration.
Cefotetan (Cefotan)
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Second-generation cephalosporin indicated for infections caused by
susceptible gram-positive cocci and gram-negative rods.
Cefoxitin (Mefoxin)
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Second-generation cephalosporin indicated for gram-positive cocci
and gram-negative rod infections. Infections caused by cephalosporin-
resistant or penicillin-resistant gram-negative bacteria may respond to
cefoxitin.
Cefaclor (Ceclor)
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Second-generation cephalosporin indicated for infections caused by
susceptible gram-positive cocci and gram-negative rods.
Determine proper dosage and route based on condition of patient, severity
of infection, and susceptibility of causative organism.
Clindamycin (Cleocin)
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Lincosamide for treatment of serious skin and soft tissue
staphylococcal infections. Also effective against aerobic and anaerobic
streptococci (except enterococci). Inhibits bacterial growth, possibly by
blocking dissociation of peptidyl t-RNA from ribosomes causing RNA-
dependent protein synthesis to arrest.
Metronidazole (Flagyl)
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Imidazole ring-based antibiotic active against various anaerobic
bacteria and protozoa. Used in combination with other antimicrobial agents
(except for Clostridium difficile enterocolitis).
Antifungal agents
Class Summary
Their mechanism of action may involve an alteration of RNA and DNA
metabolism or an intracellular accumulation of peroxide that is toxic to the
fungal cell.
Amphotericin B (AmBisome)
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Produced by a strain of Streptomyces nodosus; can be fungistatic or
fungicidal. Binds to sterols, such as ergosterol, in the fungal-cell membrane,
causing intracellular components to leak with subsequent fungal-cell death.
Fluconazole (Diflucan)
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Synthetic oral antifungal (broad-spectrum bistriazole) that selectively
inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.