Summary![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Pyogenic liver abscess (PLA) is an uncommon condition characterized by solitary or multiple collections of pus within the liver. The infection is caused by bacteria and is often polymicrobial, with Escherichia coli, Streptococcus spp. and Klebsiella pneumoniae being common causative organisms. The majority of cases are caused by ascending infection from a biliary tract pathology (e.g., cholangitis due to choledocholithiasis or biliary strictures). Infection in the gastrointestinal tract or bacteremia can expose the liver to high bacterial loads because of the liver's dual blood supply from the portal vein and hepatic artery. Patients may present with nonspecific symptoms, such as fever, malaise, and weight loss. Right upper quadrant pain and tender hepatomegaly are specific features of a liver abscess but are not seen in all cases. Diagnosis is confirmed on abdominal imaging (ultrasound or CT), which would typically show intrahepatic fluid-filled lesions with surrounding edema. Broad-spectrum IV antibiotics and percutaneous or surgical drainage of the abscess cavity are the mainstays of treatment. Complications include sepsis, pneumonia, and abscess rupture into the peritoneum or thorax. Advances in diagnostics and treatment have reduced the complications and mortality rates of PLA.
Epidemiology![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Etiology![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Risk factors for PLA [2][4][5]
- Diabetes mellitus
- Liver surgery, e.g., liver transplant
- Hepatic disease, e.g., liver cirrhosis
- Malignancy, especially gastrointestinal malignancies
- Immunosuppression
- Chronic use of proton pump inhibitors
- Advanced age
- Male sex
Etiology by source [1][2][4][6]
The source of infection often remains unclear, but if an etiology is identified, the cause is most often found in the biliary tract. Other routes of infection include hematogenic spread via the portal vein or hepatic artery and direct extension.
Common causes of PLAs | ||
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Source | Etiology | Pathogenesis |
Biliary tract: most commonly identified cause (24–60%) [6][7] |
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Hepatic artery (∼ 10%) [6] |
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Portal vein (∼ 7%) [6] |
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Contiguous area (< 5%) [6] | ||
Others |
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Common pathogens [1][2][3][5][6][9]
- Often polymicrobial
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Most commonly isolated organisms
- E. coli
- K. pneumoniae [5][10]
- Streptococcus spp. [2][3][7]
- Other causative bacteria include Enterococcus spp., Staphylococcus aureus, and anaerobes. [6]
Clinical features![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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Classic triad of PLA
- Fever (with/without chills and rigors)
- Malaise
- Right upper quadrant pain
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Other symptoms
- Anorexia and weight loss
- Nausea and vomiting
- Symptoms of diaphragmatic irritation
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Physical examination
- Jaundice
- Tender hepatomegaly
- Intercostal tenderness
- Epigastric tenderness
- Decreased breath sounds in right lower lobe of the lung
- Features of sepsis
The symptoms of PLA are often non-specific (e.g., fever, weight loss, nausea).
References:[1]
Diagnostics![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
General principles
- Abdominal imaging (preferably ultrasound or CT) is required to confirm a diagnosis of PLA.
- Laboratory studies only provide supportive evidence of an underlying infectious process (i.e., leukocytosis, altered liver chemistries, positive blood culture).
- Once PLA is confirmed (or strongly suspected), an image-guided percutaneous aspiration of the lesion with Gram stain and culture of the aspirate should be obtained.
Laboratory studies [1][6][7][11]
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Routine studies: Obtain the following in all patients with suspected PLA.
- Complete blood count: neutrophilic leukocytosis, normocytic normochromic anemia
- Liver chemistries: ↑ alkaline phosphatase; (67–90%), ↑ AST and ALT, hypoalbuminemia, hyperbilirubinemia
- Inflammatory markers: ↑ ESR and CRP
- Other findings: ↑INR, ↑LDH
- Blood cultures: positive in up to 60% of cases [1][6]
- Serology (e.g., antibodies against amebiasis or echinococcosis): Consider to rule out differential diagnoses of PLA.
Blood cultures should preferably be obtained before initiating empiric antibiotic therapy for PLA.
Imaging [1][4][6][12]
- Indications: all patients with suspected PLA to confirm the diagnosis and possibly identify the underlying etiology (e.g., choledocholithiasis, biliary strictures)
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Characteristic findings
- Solitary; (more common) or multiple intrahepatic lesion(s) usually within the right lobe [1][6]
- Lesions may be fluid-filled or solid, or contain gas, debris, or septations/loculi
- Surrounding parenchyma appears edematous and hyperemic
- See individual modalities below for additional findings.
Abdominal ultrasound (preferably duplex scan) [13]
- Indication: first-line imaging modality for suspected PLA
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Findings
- Typically hypoechoic but may also be hyperechoic
- Early lesion(s) may be poorly demarcated; advanced PLAs may appear spherical with central necrosis
CT abdomen (preferably with IV contrast) [12]
- Indication: alternative first-line imaging modality for suspected PLA
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Findings
- Hypodense lesions that do not take up IV contrast [7]
- Peripheral rim enhancement on IV contrast administration
- Double target sign: a concentric appearance of the peripheral rim on CT with IV contrast, composed of an inner hyperdense layer surrounded by an outer hypodense layer
MRI abdomen/liver [12]
- Indication: Consider if US or CT findings are inconclusive but the index of suspicion for PLA is high.
- Findings: intrahepatic hypointense (T1) or hyperintense (T2) lesions
Contrast-enhanced ultrasound (CEUS)
- Indication: Typically performed to evaluate indeterminate hepatic lesions [14]
- Findings: peripheral rim enhancement and late phase washout [4]
X-ray abdomen
Not routinely indicated but, if performed to rule out differential diagnoses of PLA, may show the following:
- Gas bubbles within an ill-defined intrahepatic lesion
- Elevated right hemidiaphragm
- Lower lobe atelectasis of the right lung with/without pleural effusion
Percutaneous aspiration with Gram stain and culture [4][7]
- Allows for identification of the causative pathogen and its antibiogram [11]
- Positive in 70–80% of cases [1]
- See “Treatment” for further details on this procedure.
Differential diagnoses![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
PLA needs to be differentiated from nonpyogenic abscesses and other space-occupying lesions of the liver. [6]
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Nonpyogenic liver abscess [15]
- Amebic liver abscess; (∼ 10% of all liver abscesses) caused by Entamoeba histolytica [6]
- Fungal infection (< 10% of all liver abscesses) most commonly caused by Candida spp. [11][16]
- Hepatic echinococcosis (hydatid cyst of the liver)
- Hepatic cysts
- Benign liver tumors
- Hepatocellular carcinoma
- Liver metastases
The differential diagnoses listed here are not exhaustive.
Treatment![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
General principles [1][4][6]
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Empiric antibiotic therapy with broad-spectrum IV antibiotics is indicated in all patients with PLA.
- Obtain blood cultures before treatment if possible. [4]
- Initiate treatment as soon as possible; do not delay treatment until after percutaneous aspiration, especially in unstable patients.
- Conservative management with IV antibiotics alone may be considered in abscesses < 3–5cm. [12]
- Most patients also require percutaneous abscess drainage.
- Surgical drainage may be required for patients with complicated abscesses.
- The underlying cause should be evaluated for and managed accordingly (e.g., ERCP for biliary obstruction or cholecystectomy for cholecystitis).
Empiric antibiotic therapy [1][6]
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General principles
- There are no specific recommendations regarding preferred antibiotic regimens.
- Select an empiric regimen based on suspected infection route, suspected pathogen, and local resistance patterns.
- Switch to culture-specific antibiotics once culture results are available; deescalate if possible.
- Continue IV antibiotics for ≥ 2 weeks before switching to oral antibiotics. [1][4]
- Total duration of therapy: typically 4–6 weeks
- Coverage required: anaerobes, gram-negative bacteria, and gram-positive cocci
Empiric antibiotic therapy for PLA [17][18] | |
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Single-agent regimens (any of the following) |
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Combination therapy regimens |
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Drainage of the abscess cavity [7]
Indications
- Abscesses > 3–5 cm [4][12]
- Smaller abscesses with an inadequate response to antibiotic therapy [1]
- Radiological signs of impending perforation [1]
Image-guided percutaneous drainage [1][4][6]
- Indication: standard procedure in solitary, interventionally accessible abscesses
- Contraindication: coagulopathy (INR > 1.5; platelets ≤ 50.000/mm3) [19][20]
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Procedure: performed under ultrasound or CT guidance
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Percutaneous catheter drainage: generally preferred [12]
- An intracavitary catheter is placed and irrigated with saline every 8 hours
- Serial imaging is typically required to confirm adequate drainage and catheter placement.
- The catheter is typically removed when drainage is < 10 mL per day and the white blood cell count has normalized.
- Percutaneous needle aspiration: Consider in patients with smaller PLAs or in those with coagulopathy. [21]
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Percutaneous catheter drainage: generally preferred [12]
Correct coagulopathy before attempting percutaneous drainage of a PLA.
Ensure decreased catheter output is not due to catheter blockage or malposition before catheter removal.
Surgical drainage [1][4][6]
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Indications
- Complications requiring urgent surgical treatment (e.g., ruptured abscess, peritonitis)
- Underlying pathology that requires surgical intervention (e.g., cholecystitis, appendicitis)
- Abscess not amenable to percutaneous drainage, e.g., because of the location of the abscess or if abscesses are very large, multiple, or loculated
- Failed percutaneous drainage, e.g., due to thick viscous pus or necrotic tissue
- Procedure: open or laparoscopic [6][22]
The underlying etiology (e.g., choledocholithiasis, biliary stricture) should also be treated to prevent recurrent PLAs.
Complications![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Rupture
- Into the abdomen → peritonitis
- Into the chest → empyema
- Into the retroperitoneum → retroperitoneal abscess
- Sepsis
- Pneumonia
- Pleural effusion
References:[23][24]
We list the most important complications. The selection is not exhaustive.
Prognosis![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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Mortality rates
- Untreated PLA: 100%
- With treatment: ∼12 %
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Poor prognostic factors
- Pyogenic abscess with sepsis
- Advanced age (> 70 years)
- Multiple abscesses
- Polymicrobial infection; anaerobic infection
- Immunosuppression (e.g., malignancy, diabetes)
- Need for surgical drainage
References:[25]