Liver Abscess

• Pyogenic liver abscesses (PLAs): These are the most common, especially in developed countries, accounting for approximately 80% of cases. They are typically polymicrobial and arise from biliary tract infections, portal vein seeding from intra-abdominal sources, or haematogenous spread through the hepatic artery. Other causes include direct extension from contiguous infections and trauma.
  
  
• Amoebic liver abscesses (ALAs): These are caused by Entamoeba histolytica, and account for around 10% of cases globally. They are more common in tropical and subtropical regions and are typically solitary and located in the right hepatic lobe. ALAs result from the haematogenous spread of trophozoites from the colon via the portal circulation.
  
  
• Fungal liver abscesses: These are rare and mostly occur in immunocompromised individuals, especially those with neutropenia or undergoing chemotherapy. The most common fungal agent is Candida species.
  
  

Pyogenic Liver Abscess (PLA)

• Polymicrobial nature: Most PLAs are polymicrobial. Common aerobic bacteria include:
  • Escherichia coli
  • Klebsiella pneumoniae – increasingly prominent globally, particularly in Southeast Asia, and strongly associated with monomicrobial infections, diabetes mellitus, and colorectal cancer. Hypervirulent strains are linked to metastatic infections such as endophthalmitis and central nervous system involvement.
  • Streptococcus species, especially the Streptococcus anginosus group (S. constellatus, S. anginosus, S. intermedius)
  • Enterococcus species
  • Staphylococcus aureus – typically associated with haematogenous spread, such as in endocarditis.
  • Pseudomonas species – less frequently encountered.
    
    
• Anaerobes: Historically under-recognised, anaerobic bacteria are now known to play a significant role in pyogenic liver abscesses due to improved culturing methods. Common anaerobes include:
  • Bacteroides fragilis
  • Fusobacterium necrophorum
  • Anaerobic and microaerophilic Streptococcus species
    
    
• Unusual bacterial pathogens:
  • Salmonella typhi – particularly in patients with recurrent pyogenic cholangitis
  • Yersinia enterocolitica, Actinomyces species, Eikenella corrodens, and Brucella melitensis – occasionally reported
  • A small case series from Taiwan linked PLA as a presenting feature of hepatocellular carcinoma, especially in endemic regions.
    
    
• Sources of infection:
  • Biliary tract disease (e.g. stones, strictures, malignancy, congenital anomalies) is now the most common cause.
  • Cholangitis is implicated in around half of pyogenic liver abscess cases.
  • Other routes: portal vein seeding from abdominal infections (e.g. diverticulitis, appendicitis), hepatic artery bacteraemia, direct extension from nearby infections (e.g. cholecystitis), and penetrating trauma.
  • Cryptogenic abscesses: Some cases have no identifiable source.
    
    

Amoebic Liver Abscess (ALA)

• Caused by Entamoeba histolytica, a protozoan parasite.
• Infection initiates in the colon, leading to amoebic colitis, with trophozoites migrating to the liver via the portal system.
• ALAs are usually solitary and located in the right lobe.
• While rare in developed countries, they are frequently observed in immigrants or travellers from endemic regions such as South Asia, Africa, and Central/South America.
  
  
  

Fungal Liver Abscess

• Primarily due to Candida albicans, with rare involvement by Aspergillus species.
• Typically occurs in immunocompromised individuals:
  • Prolonged antibiotic use
  • Haematologic malignancies
  • Solid-organ transplant recipients
  • Congenital or acquired immunodeficiency
    
    

Parasitic Liver Abscess – Hydatid Disease

• Caused by the larval stage of Echinococcus granulosus, a cestode (tapeworm) of the Taeniidae family.
• Transmitted via the faecal-oral route from infected dogs.
• The liver is the most common site of hydatid cyst formation.
• Patients may present with hepatomegaly, abdominal discomfort, or incidentally discovered cysts. These cysts grow slowly and often become symptomatic in the later stages of disease.
  
  

Routes of Infection and Mechanisms of Spread

1. Biliary Tree (Most Common Route)
   • Biliary obstruction—due to gallstones, malignancy, strictures, or congenital anomalies—can cause ascending infection.
   • Indwelling biliary stents or post-surgical complications may act as sources for solitary abscesses.
   • Stasis of bile flow permits bacterial proliferation and translocation into hepatic parenchyma.
     
     
2. Portal Vein
   • Infections from intra-abdominal organs such as the bowel, pancreas, or gallbladder can lead to septic thrombophlebitis.
   • Conditions like appendicitis, diverticulitis, or inflammatory bowel disease may trigger pylephlebitis, releasing septic emboli into the portal circulation.
   • These emboli are filtered by hepatic sinusoids and act as foci for microabscess formation, which may coalesce into solitary lesions.
     
     
3. Hepatic Artery
   • Haematogenous dissemination from systemic infections (e.g. endocarditis, pyelonephritis) may result in microabscesses.
   • This is more common in immunocompromised individuals and patients with bacteraemia.
     
     
4. Contiguous Spread
   • Infections from adjacent structures (e.g. perforated bowel, subphrenic abscess) can directly invade liver tissue.
     
     
5. Penetrating and Blunt Trauma
   • Penetrating injuries may directly introduce pathogens into the liver.
   • Blunt trauma can result in haematoma, necrosis, and bile leakage, creating an environment conducive to secondary infection.
     
     
6. Procedural and Iatrogenic Sources
   • Liver abscess may arise after procedures such as:
     • Percutaneous ablation or chemoembolisation of hepatic tumours
     • Liver transplantation
     • Endoscopic biliary sphincterotomy
     • Hepatic cryotherapy
   • Instrumentation of the biliary tract is an increasingly recognised risk factor.
     
     

Anatomical Considerations

• The right hepatic lobe is affected more frequently than the left, in approximately a 2:1 ratio. This may be due to:
  • Greater volume of hepatic tissue
  • Richer blood supply via the superior mesenteric and portal veins
  • Denser network of biliary canaliculi
  • Proposed ‘streaming effect’ of portal blood flow directing pathogens preferentially to the right lobe
• Bilateral involvement is seen in approximately 5% of cases.
  
  

Host Factors and Underlying Conditions

• Immunocompromised states (e.g. diabetes mellitus, haematologic malignancy, chronic granulomatous disease, cirrhosis)
• Previous liver transplant
• Hepatic neoplasms (both primary and secondary)
• Cardiopulmonary disease
• Poor dental hygiene, possibly linked to cryptogenic bacteraemia
  
  

Other Contributing Factors

• Approximately 40% of liver abscesses are considered cryptogenic, where no definitive source of infection is found despite investigation.
• Secondary infection of existing hepatic lesions (e.g. amoebic abscesses, hydatid cysts, tumours) may also lead to pyogenic liver abscess.
• Rare causes include foreign body ingestion leading to perforation and migration into the liver.
  
  

Historical Perspective

• Historically, appendicitis was the predominant cause of liver abscess, but its incidence has significantly declined with advances in early diagnosis and management.
• In contemporary settings, biliary tract pathology is the most common identifiable aetiology.
  
  

Global Incidence and Regional Variation

• Overall Incidence:
  • In the United Kingdom and the United States, the estimated annual incidence is approximately 2.3 to 3.6 cases per 100,000 population.
  • The frequency among hospitalised patients ranges from 8 to 20 cases per 100,000 hospital admissions, with some studies noting a modest but steady increase in incidence.
    
    
• Regional Differences:
  • Higher incidence rates have been reported in East and Southeast Asia, particularly Taiwan, where the annual incidence has reached 15–17.6 per 100,000.
  • This elevated rate has been attributed to the rise in pyogenic abscesses due to Klebsiella pneumoniae, often in association with diabetes and hepatobiliary infections.
    
    
• Amoebic Abscesses:
  • Entamoeba histolytica infection, the cause of amoebic liver abscess, is endemic in Central and South America, Africa, and Asia.
  • In developed countries, amoebic abscesses are primarily observed in immigrants and travellers from endemic areas.
    
    

Demographics and Risk Stratification

• Age:
  • The incidence of liver abscess increases with advancing age, with most cases now occurring in individuals in their sixth and seventh decades.
  • Historically, abscesses were more prevalent in the fourth and fifth decades, especially as complications of appendicitis.
  • A small peak in incidence is seen during the neonatal period, usually associated with umbilical vein catheterisation and sepsis.
  • In children and adolescents, liver abscesses are rare and often linked to underlying immunodeficiency, trauma, or severe malnutrition.
    
    
• Sex:
  • While some data suggest a higher prevalence in males, particularly for pyogenic liver abscesses, more recent studies indicate that sex predilection has diminished.
  • However, males may have a poorer prognosis once hepatic abscesses develop.
    
    

Trends Over Time

• Historical Data:
  • Autopsy series from the late 19th to mid-20th century show consistent findings: 0.7% (1896–1933), 0.45% (1934–1958), and 0.57% (1959–1968) of autopsies revealed liver abscesses.
  • Despite stable or slightly rising incidence rates, mortality has declined, likely due to better imaging, earlier diagnosis, percutaneous drainage techniques, and improved critical care.
    
    
• Pyogenic Liver Abscess (PLA):
  • PLAs represent a major proportion of liver abscesses in developed regions, accounting for approximately 50% of all visceral abscesses and 13% of intra-abdominal abscesses.
  • In one Middle Eastern cohort of 67 liver abscess patients, 56 cases were pyogenic, and 91% occurred in males—highlighting both the predominance of PLA and male susceptibility in certain regions.
    
    

Key Components of the History

1. Demographic and Epidemiological Background
   • Age: Risk increases with advancing age, particularly beyond 50 years.
   • Sex: Male patients are at greater risk, with studies showing a relative risk of 2.6.
   • Travel History: Important in suspected amoebic liver abscess; infection with Entamoeba histolytica is endemic in South and Central America, Africa, and Asia.
   • Place of Origin or Immigration Status: Consider amoebic infection in immigrants from endemic areas.
     
     
     
2. Risk Factor Assessment
   • Underlying medical conditions:
     • Diabetes mellitus (odds ratio 3.6)
     • Malignancy (particularly gastrointestinal)
     • Cirrhosis (15-fold increased risk)
     • Cardiopulmonary disease
     • Immunosuppression (e.g. HIV/AIDS, chemotherapy, organ transplantation)
       
       
   • Medication and Procedure History:
     • Recent use of proton pump inhibitors
     • Invasive hepatobiliary interventions (e.g. biliary stenting, sphincterotomy, TIPS, percutaneous tumour ablation)
     • Recent chemotherapy or immunosuppressive therapy
       
       
   • Surgical or procedural history:
     • Recent abdominal trauma (blunt or penetrating)
     • History of liver transplantation
     • Recent dental infections or poor dentition (source of bacteraemia)
       
       
3. Presenting Symptoms
   
   
   • Constitutional symptoms:
     • Fever (continuous or spiking; occurs in >90%)
     • Chills, night sweats
     • Malaise, fatigue
     • Unexplained weight loss
       
       
   • Gastrointestinal and abdominal complaints:
     • Right upper quadrant abdominal pain (50–75% of cases)
     • Anorexia, nausea, vomiting
     • Dark urine (may mimic viral hepatitis)
       
       
   • Respiratory symptoms:
     • Cough, dyspnoea, chest pain (may reflect diaphragmatic irritation or pleural involvement)
     • Right shoulder pain (referred pain via phrenic nerve)
       
       
4. Pattern of Disease Onset
   • Pyogenic liver abscess often has an insidious onset.
   • Amoebic abscess tends to present more acutely.
   • Solitary lesions may be associated with chronic constitutional symptoms, mimicking malignancy.
   • Multiple abscesses are usually more acute and severe, often with systemic toxicity.
     
     
5. Specific Pathogen-Associated Features
   • Klebsiella pneumoniae: May lead to metastatic complications (endophthalmitis, meningitis, brain abscess); systemic symptoms may persist even after drainage.
   • Echinococcus granulosus (hydatid disease):
     • Often has an initial asymptomatic phase in childhood.
     • Symptomatic progression occurs over years as cysts enlarge (1–5 cm/year).
     • Liver involvement is common (≈66% of cases).
     • Symptoms arise from compression (e.g. biliary colic, obstructive jaundice, portal hypertension, Budd-Chiari syndrome) or rupture (peritonitis, anaphylaxis).
       
       
6. Rare or Context-Specific Clues
   • Fever of unknown origin (FUO): Liver abscess may be an underlying diagnosis in indolent presentations.
   • Anaemia and weight loss: Consider especially in solitary abscesses or elderly patients, where malignancy is a differential.
   • History of bacteraemia, endocarditis, or intravascular infection may suggest haematogenous spread to the liver.
   • Gastrointestinal inflammation (e.g. appendicitis, diverticulitis, pancreatitis): Can lead to portal vein pylephlebitis and seeding of the liver.

Common Examination Findings

1. Fever
   • Present in up to 90% of cases.
   • May be continuous or spiking.
   • Often accompanied by chills and sweating.
     
     
2. Hepatomegaly
   • Liver enlargement is a frequent finding and may be tender on palpation.
   • A palpable liver edge or mass may be noted in the right upper quadrant (RUQ) or epigastrium, especially in abscesses involving the left hepatic lobe.
     
     
3. Abdominal Tenderness
   • RUQ or midepigastric tenderness is common and correlates with hepatic involvement.
   • More than 50% of patients exhibit abdominal tenderness on examination.
   • Tenderness may be diffuse in cases of peritonitis or large abscess rupture.
     
     
4. Jaundice
   • Occurs in up to 25% of patients, more frequently when:
     • Biliary tract obstruction is present
     • Multiple abscesses coexist
     • There is underlying cholangitis
       
       
5. Signs of Respiratory Involvement
   • Decreased breath sounds in the right lower lung zone, possibly due to:
     • Atelectasis
     • Reactive pleural effusion
     • Diaphragmatic irritation
   • Pleural or hepatic friction rubs may be heard if the Glisson capsule or diaphragm is inflamed.
   • Some patients experience pleuritic pain or referred pain to the right shoulder.
     
     
6. Signs of Sepsis or Shock
   • Tachycardia, hypotension, and clinical features of septic shock may be evident in severe cases.
   • A small subset of patients, particularly those with ruptured hydatid cysts, may present with anaphylactic shock.
     
     

Uncommon or Specific Signs

• Ascites: Rare, but may occur with extensive peritoneal irritation or advanced disease.
• Charcot Triad (fever, RUQ pain, jaundice): Typically associated with cholangitis but may be seen in liver abscess as part of the differential diagnosis.
• Signs of extrahepatic complications:
  • In Klebsiella pneumoniae liver abscess, ocular (endophthalmitis), neurological (meningitis), and cerebral signs may follow systemic embolisation.
  • In Echinococcus granulosus (hydatid disease), compression signs develop as cysts enlarge (>10 cm), including:
    • Biliary colic, obstructive jaundice
    • Portal hypertension, Budd-Chiari syndrome
    • Bronchial fistula
  • Ruptured cysts may result in peritonitis or anaphylaxis.
    
    
    

Laboratory Investigations

1. Full Blood Count (FBC)
   • Findings: Neutrophilic leukocytosis and anaemia of chronic disease.
   • Suggests an infectious or inflammatory process but is non-specific.
     
     
2. Liver Function Tests (LFTs)
   • Alkaline phosphatase: Elevated in approximately two-thirds of cases.
   • Transaminases (ALT/AST) and bilirubin: Mildly elevated unless there is significant biliary involvement or advanced disease.
   • Albumin: Often reduced (hypoalbuminaemia) in chronic or severe cases.
     
     
3. Coagulation Profile
   • Prothrombin time (PT) and activated partial thromboplastin time (aPTT): Performed before any aspiration or intervention to rule out bleeding risk.
   • Note: Coagulopathy must be corrected before invasive procedures.
     
     
4. Blood Cultures
   • Positive in ~50% of cases.
   • Sensitivity decreases if antibiotics are administered prior to sampling.
     
     
5. C-Reactive Protein (CRP)
   • Non-specific marker of inflammation; can be used to monitor treatment response.
     
     
6. Serological and Stool Antigen Testing for Entamoeba histolytica
   • Serum IgG antibody test: Positive in amoebiasis; remains positive for years.
   • Stool ELISA or PCR: Useful in patients with diarrhoea.
   • Antigen or DNA detection in aspirated pus: Diagnostic for amoebic liver abscess; aspirate classically resembles "anchovy paste".
     
     

Imaging Studies

1. Contrast-Enhanced Computed Tomography (CT)
   • Sensitivity: >95%.
   • Findings:
     • Well-defined, hypodense lesions with peripheral contrast enhancement.
     • Gas within the lesion (seen in ~20%) suggests pyogenic infection.
     • Useful in identifying small (<1 cm) abscesses and evaluating for intra-abdominal spread or underlying malignancy.
   • CT also guides percutaneous aspiration and drainage.
     
     
2. Ultrasonography (US)
   • Sensitivity: 80–90%.
   • Findings:
     • Hypoechoic, irregularly bordered lesions.
     • Internal septations or debris may be seen.
   • Benefits: Portable, no contrast needed, useful in critically ill patients, and allows real-time guidance for aspiration or catheter placement.
   • Limitations: Operator-dependent and less sensitive for small lesions.
     
     
3. Radionuclide Scanning
   • Includes technetium, gallium, and indium-labelled WBC scans.
   • Sensitivity varies: indium (90%) > technetium (80%) > gallium (50–80%).
   • Now largely replaced by CT and US due to slower diagnostic timelines and limited utility.
     
     
4. Chest Radiography (CXR)
   • May show:
     • Right-sided pleural effusion
     • Elevation of right hemidiaphragm
     • Basilar atelectasis
   • Typically supportive, used in presence of respiratory symptoms.
     
     
5. Magnetic Resonance Imaging (MRI)
   • More sensitive than CT for small abscesses.
   • Shows:
     • Low signal intensity on T1-weighted images
     • High signal intensity on T2-weighted images
   • Limited by cost and availability; requires gadolinium contrast.
     
     

Microbiological and Percutaneous Diagnostic Procedures

1. Aspiration and Culture of Abscess Material
   • Best obtained under CT or US guidance.
   • Culture is positive in ~66% of cases.
   • Direct aspiration yields better microbiological yield than fluid collected via drainage catheter.
   • Contraindicated in:
     • Coagulopathy
     • Suspected hydatid cyst (risk of anaphylaxis)
       
       
       
2. Percutaneous Drainage
   • Standard of care for most pyogenic abscesses.
   • Techniques: Seldinger or trocar method under imaging guidance.
   • Catheter maintenance: Flushed daily; removed when output is <10 mL/day or cavity collapse is seen.
   • Preferred for:
     • Abscesses >5 cm
     • Multiloculated or ruptured lesions
   • Contraindications: Difficult access, peritonitis, uncorrected coagulopathy, viscous pus, or multiloculated abscesses.
   • Failure to improve may warrant surgical drainage.
     
     
     
     

Hepatobiliary and Intra-abdominal Differentials

1. Acute Cholecystitis
   • Presents with RUQ pain, fever, and leukocytosis.
   • Murphy’s sign may be positive.
   • Ultrasonography shows gallbladder wall thickening, stones, and pericholecystic fluid.
   • No hepatic lesions on imaging.
     
     
2. Ascending Cholangitis
   • Classically presents with Charcot's triad (fever, RUQ pain, jaundice); may progress to Reynolds’ pentad with hypotension and confusion.
   • Ultrasound or MRCP/ERCP shows biliary dilation or obstruction.
   • Biliary sepsis without hepatic parenchymal involvement distinguishes it from liver abscess.
     
     
3. Viral Hepatitis
   • Presents with malaise, jaundice, and hepatomegaly.
   • Fever may be present but is typically low-grade.
   • Transaminases are markedly elevated; imaging shows diffusely hypoechoic or normal liver without focal lesions.
     
     
4. Drug-Induced or Autoimmune Hepatitis
   • Can mimic acute hepatic inflammation.
   • Pain is often absent, unlike the localised discomfort seen in liver abscess.
   • Serological markers and drug history are key to diagnosis.
     
     
5. Hydatid Cyst (Echinococcus granulosus)
   • Common in endemic regions.
   • Presents with slowly enlarging RUQ mass, sometimes with compressive symptoms.
   • Imaging shows well-defined cysts with daughter cysts or calcifications.
   • Risk of anaphylaxis on rupture; aspiration contraindicated.
     
     
6. Cystadenoma or Cystadenocarcinoma
   • Insidious onset of abdominal fullness or discomfort; fever and chills are absent.
   • CT or ultrasound reveals complex cystic lesions with irregular walls and septations.
   • Diagnosis confirmed via histopathology.
     
     
7. Inflammatory Pseudotumour
   • Rare benign lesion, often in young men with prior infection or autoimmune conditions.
   • Clinical features overlap with liver abscess, including fever and RUQ pain.
   • Histological confirmation shows fibrous tissue with inflammatory cell infiltration.
     
     
8. Hepatocellular Carcinoma (HCC)
   • May present with RUQ pain and hepatomegaly.
   • Fever is typically absent.
   • Imaging may reveal arterial enhancement with washout on venous phase.
   • Confirmed by biopsy and tumour markers (e.g. AFP).
     
     
9. Secondary Liver Metastases
   • Often asymptomatic or with systemic symptoms referable to the primary tumour.
   • Fever uncommon, and laboratory markers less inflammatory.
   • Requires full body imaging and biopsy for confirmation.
     
     
     

Thoracic and Other Differentials

1. Right Lower Lobe Pneumonia or Empyema Thoracis
   • May present with pleuritic chest pain, cough, dyspnoea, and referred shoulder pain.
   • Chest X-ray or CT thorax shows consolidation or pleural fluid.
   • Diaphragmatic irritation may mimic hepatic pain.
     
     
2. Parapneumonic Pleural Effusion
   • Presents similarly to pneumonia with dullness to percussion and decreased breath sounds at the lung base.
   • May occur alongside or be mistaken for subphrenic or hepatic processes.
     
     
3. Appendicitis
   • Particularly if retrocaecal or complicated, it may mimic RUQ pain.
   • Differentiated by tenderness in the right lower quadrant, migration of pain, and classic gastrointestinal symptoms.
     
     

General Principles

• Prompt diagnosis and early empirical treatment are crucial.
• Most patients require a combination of antibiotics and drainage.
• The choice of antibiotics and method of drainage depends on clinical status, abscess size and complexity, and suspected pathogen.
  
  

Antibiotic Therapy

• Empirical broad-spectrum coverage is started immediately in unstable patients.
• Targets gram-positive, gram-negative, and anaerobic organisms.
• Anaerobic coverage (e.g. metronidazole) should be continued throughout treatment.
  
  

• Critically ill / ICU patients:
  • Piperacillin/tazobactam
  • Imipenem/cilastatin or meropenem
  • Cefepime or levofloxacin plus metronidazole
  • Consider adding vancomycin if MRSA or resistant enterococci suspected
    
    
• Stable patients:
  • Ceftriaxone or cefotaxime plus metronidazole
  • Ciprofloxacin, levofloxacin, or moxifloxacin plus metronidazole
  • Avoid fluoroquinolones where local resistance >10%

• Fungal infection (e.g. Candida): Amphotericin B or fluconazole in immunocompromised patients
• Suspected ESBL-producing organisms: Use carbapenems
• Amoebic abscess:
  • Treated with metronidazole or tinidazole
  • Follow with luminal agents (e.g. paromomycin) to eradicate colonisation
    
    
    

Drainage Procedures

• Most abscesses >3 cm require drainage
• Urgent drainage if the patient is in shock or has multi-organ dysfunction
  
  

• Percutaneous Needle Aspiration:
  • For small or accessible lesions
  • Provides material for culture

• Percutaneous Catheter Drainage (Preferred for moderate/large abscesses):
  • Preferred for >5 cm, multiloculated, or non-ruptured lesions
  • Drain maintained until output <10 mL/day

• Surgical Drainage:
  • Indicated if:
    • Percutaneous drainage fails
    • Abscess is ruptured or multiloculated
    • Patient has APACHE II score ≥15
    • Concomitant surgical pathology exists (e.g. diverticular abscess)
  • Can be open or laparoscopic
    
    
• Endoscopic Drainage:
  • ERCP with stenting in biliary-source abscesses
  • Endoscopic ultrasound-guided drainage described in selected patients
    
    

• Usually not required unless:
  • Abscess is >5 cm or in the left lobe
  • No clinical response within 3–5 days
  • Diagnosis remains uncertain
    
    

Duration of Therapy

• Pyogenic abscess: Typically 2–6 weeks (longer for multiple abscesses, K. pneumoniae, or poor drainage)
  • Begin with IV antibiotics, then transition to oral once clinically improving
  • Normalisation of CRP and resolution of fever guide therapy duration
• Amoebic abscess: 7–10 days of nitroimidazole, followed by a luminal agent to prevent recurrence
  
  

Follow-up and Long-Term Monitoring

• Serial imaging (CT or ultrasound) to confirm drainage and monitor response
• Persistent fever after 2 weeks may suggest inadequate drainage or superinfection
• Monitor for recurrence, especially in those with biliary pathology (25% recurrence rate)
• Nutritional support, medication toxicity monitoring, and renal function checks are essential
• Multidisciplinary approach:
  • Radiology for guided drainage
  • Surgery for failed drainage or ruptured abscesses
  • Gastroenterology for evaluation of underlying disease
  • Infectious diseases for complicated or resistant infections

Consultations

• Interventional radiology: Early involvement for diagnostic and therapeutic drainage
• General surgery: For failed percutaneous drainage or concurrent intra-abdominal pathology
• Gastroenterology: To assess for underlying gastrointestinal or biliary disease (colonoscopy, ERCP)
• Infectious diseases: For complex cases, fungal infections, or multidrug resistance

General

• Untreated liver abscess is universally fatal, due to risks of rupture, sepsis, and multiorgan failure.
• With timely treatment, mortality ranges between 2.5–30%, depending on the setting, population studied, and presence of complications.
• A large US population-based study reported an in-hospital mortality of 5.6%, which remained stable over a 10-year period despite rising incidence.
  
  
  

Factors Associated with Poor Prognosis

1. Host-related Factors
   • Age >65 years: Associated with increased morbidity and mortality, though outcomes may be comparable to younger patients if aggressively managed.
   • ICU admission or septic shock at presentation
     Comorbid conditions:
     • Cirrhosis
     • Chronic renal failure
     • Malignancy (hepatic or extrahepatic)
     • Diabetes mellitus
     • Alcoholism
   • Immunocompromise: Particularly relevant in fungal liver abscess
     
     
2. Disease-specific Factors
   • Multiple abscesses or multiloculated collections
   • Biliary origin of the abscess
   • Delayed diagnosis or treatment initiation
   • Fungal infection
   • Inadequate or delayed drainage
   • Acute respiratory failure
     
     
3. Laboratory and Scoring Indicators
   • APACHE II score ≥15 is strongly predictive of mortality
   • Hypoalbuminaemia (<2 g/dL)
   • Hyperbilirubinaemia (>3.5 mg/dL)
   • Encephalopathy
     
     
4. Microbiological Features
   • Infections with Klebsiella pneumoniae may be associated with a hypervirulent phenotype, especially in cryptogenic or metastatic cases.
   • Fungal infections (e.g. Candida) are associated with higher mortality rates.
     
     
     

Prognosis in Specific Subtypes

• Amoebic Liver Abscess
  • Generally excellent prognosis with medical therapy alone.
  • Risk factors for worse outcome include:
    • Bilirubin >3.5 mg/dL
    • Serum albumin <2 g/dL
    • Encephalopathy
    • Multiple abscesses
      
      
• Hydatid Cyst (Echinococcal Abscess)
  • Typically has a benign course.
  • Around 57% remain stable, and 76% of untreated cases remain asymptomatic for years.
  • Surgical intervention is required in approximately 15%, often delayed years after initial diagnosis.
    
    

Risk of Recurrence

• Recurrence is most common in patients with biliary tract abnormalities (≈25% recurrence rate).
• Underlying fistulous communications or incomplete source control should be investigated, typically via ERCP or MRCP.
• Cryptogenic liver abscess, particularly those caused by K. pneumoniae, has been associated with an increased risk of colorectal cancer, especially in East Asian populations—prompting some experts to recommend colonoscopy in selected patients.
  
  

Immediate and Short-Term Complications

1. Sepsis and Multiorgan Failure
   • A common and serious complication contributing significantly to mortality.
   • Requires broad-spectrum antimicrobial coverage and aggressive supportive care.
   • Risk is increased in elderly, immunocompromised patients, or those with delayed treatment initiation.
     
     
2. Abscess Rupture
   • Although rare, rupture can lead to pneumoperitoneum or generalised peritonitis.
   • Emergent surgical intervention is typically required.
     
     
3. Subphrenic Abscess
   • Occurs due to upward spread of infection beneath the diaphragm.
   • Symptoms include referred right shoulder tip pain, cough, or hiccups due to diaphragmatic irritation.
     
     
4. Pleuropulmonary or Hepatobronchial Fistula
   • Fistulisation into the bronchial tree presents with productive cough, often of foul or metallic-tasting sputum.
   • Can also cause recurrent respiratory infections or empyema.
     
     
5. Hepatic Artery Pseudoaneurysm
   • Results from erosion of the abscess into the hepatic arterial wall.
   • Diagnosed via CT angiography.
   • Requires urgent surgical or endovascular repair.
     
     
6. Abdominal or Hepatic Venous Thrombosis
   • Can affect the portal vein, hepatic veins, or both.
   • In one study, 42% of patients had venous thrombosis: 24% in portal veins, 22% in hepatic veins, and 4% in both.
     Best visualised using contrast-enhanced CT scans.
   • May lead to complications such as portal hypertension or Budd-Chiari syndrome.
     
     
7. Liver Failure
   • More frequent in those with pre-existing liver disease or large-volume abscesses.
   • May accompany sepsis-induced multiorgan dysfunction.
     
     
8. Acute Pancreatitis
   • A rare consequence; likely due to contiguous spread of inflammation.
   • Presents with epigastric pain and vomiting, and confirmed by elevated pancreatic enzymes and imaging.
     
     
9. Metastatic Infectious Complications
   • Especially common with hypervirulent Klebsiella pneumoniae infections.
   • May cause:
     • Endophthalmitis
     • Central nervous system septic emboli
     • Septic pulmonary embolism
   • Early recognition is critical as these may develop before or after liver abscess diagnosis.
     
     
     

Delayed or Variable-Onset Complications

1. Abscess Recurrence
   • Common in patients with underlying biliary pathology (up to 25%).
   • May indicate:
     • Incomplete source control
     • Presence of biliary-enteric fistula
   • Requires repeat imaging and evaluation with ERCP or MRCP for definitive diagnosis and management.
     
     
2. Fistula Formation to Adjacent Organs
   • Rare but serious; may involve:
     • Colon
     • Stomach
     • Small intestine
     • Kidneys
   • Diagnosed with CT abdomen, with further confirmation by contrast studies or fistulography.
     
     
     

Preventive and Follow-up Measures

• Post-drainage antibiotic therapy for 4–6 weeks significantly reduces complication risk.
• Prophylactic antibiotics during procedures such as chemoembolisation or ERCP in high-risk patients may reduce future abscess formation.
• Close follow-up with imaging (typically CT or ultrasound) is necessary to confirm resolution.
• Persistent radiological abnormalities may linger even after clinical and laboratory resolution—imaging should be delayed unless new symptoms appear.
• Recurrent abscess warrants a thorough search for anatomical defects or unresolved infection source.
  
  

1. Abbas MT, Khan FY, Muhsin SA, et al. Epidemiology, clinical features and outcome of liver abscess: a single reference center experience in Qatar. Oman Med J. 2014;29(4):260–3.
2. Blessmann J, Ali IK, Nu PA, et al. Longitudinal study of intestinal Entamoeba histolytica infections in asymptomatic adult carriers. J Clin Microbiol. 2003;41(10):4745–50.
3. Brook I. Microbiology and management of abdominal infections. Dig Dis Sci. 2008;53(10):2585–91.
4. Chou FF, Sheen-Chen SM, Chen YS, et al. Prognostic factors for pyogenic liver abscess: a retrospective study of 162 cases. Am J Surg. 1995;170(6):556–60.
5. Chou FF, Sheen-Chen SM, Chen YS. Surgical treatment of pyogenic liver abscess: 15-year experience. J Gastrointest Surg. 1997;1(3):236–40.
6. Chou FF, Sheen-Chen SM, Lee TY, et al. Factors affecting the outcome of patients with pyogenic liver abscess: the importance of early diagnosis and effective drainage. Hepatogastroenterology. 1997;44(13):112–7.
7. Chen SC, Lee YT, Lai KC, et al. Risk factors for developing metastatic infection from pyogenic liver abscesses. J Intern Med. 2008;263(3):366–73.
8. Ferraioli G, Garlaschelli A, Zanaboni D, et al. Percutaneous and surgical treatment of pyogenic liver abscesses: observation over a 21-year period in 148 patients. Dig Liver Dis. 2008;40(8):690–6.
9. Fung CP, Chang FY, Lee SC, et al. A global emerging disease of Klebsiella pneumoniae liver abscess: is serotype K1 an important factor for complicated endophthalmitis? Gut. 2002;50(3):420–4.
10. Haque R, Huston CD, Hughes M, et al. Amebiasis. N Engl J Med. 2003;348(16):1565–73.
11. Huang CJ, Pitt HA, Lipsett PA, et al. Pyogenic hepatic abscess: changing trends over 42 years. Ann Surg. 1996;223(5):600–9.
12. Johannsen EC, Sifri CD, Madoff LC. Pyogenic hepatic abscesses. Infect Dis Clin North Am. 2000;14(3):547–63.
13. Kaplan GG, Gregson DB, Laupland KB. Population-based study of the epidemiology of and the risk factors for pyogenic liver abscess. Clin Gastroenterol Hepatol. 2004;2(11):1032–8.
14. Lin YT, Liu CJ, Chen TJ, et al. Pyogenic liver abscess as the initial manifestation of underlying hepatocellular carcinoma: a population-based study. Liver Int. 2011;31(3):326–33.
15. McManus DP, Zhang W, Li J, et al. Echinococcosis. Lancet. 2003;362(9392):1295–304.
16. Meddings L, Myers RP, Hubbard J, et al. A population-based study of pyogenic liver abscesses in the United States: incidence, mortality, and temporal trends. Am J Gastroenterol. 2010;105(1):117–24.
17. Moro P, Schantz PM. Echinococcosis: a review. Int J Infect Dis. 2009;13(2):125–33.
18. Ng DC, Chan MK, Cheung YC, et al. Clinical spectrum of pyogenic liver abscess: a review of thirty-one cases. J Microbiol Immunol Infect. 2005;38(6):421–6.
19. Ochsner A, DeBakey M, Murray S. Pyogenic abscess of the liver. Am J Surg. 1938;40:292–319.
20. Sharma MP, Ahuja V. Management of amoebic liver abscess. Arch Med Res. 2000;31(4 Suppl):S4–9.
21. Tsai FC, Huang YT, Chang LY, et al. Pyogenic liver abscess as endemic disease, Taiwan. Emerg Infect Dis. 2008;14(10):1592–600.
22. Wang JH, Chen KY, Yang YJ, et al. Pyogenic liver abscess with and without diabetes mellitus: clinical characteristics, laboratory findings, and management. Arch Intern Med. 1996;156(5):556–60.
23. Wang JH, Liu YC, Lee SSJ, et al. Primary liver abscess due to Klebsiella pneumoniae in Taiwan. Clin Infect Dis. 1998;26(6):1434–8.
24. Yeh TS, Jan YY, Jeng LB, et al. Pyogenic liver abscess in diabetic patients: association of gas-forming liver abscess with high mortality. Arch Surg. 1997;132(4):408–12.
25. Yang CC, Chen CH, Lin XZ, et al. Pyogenic liver abscess in Taiwan: emphasis on gas-forming liver abscess in diabetics. Am J Gastroenterol. 1993;88(11):1911–5.