This document summarizes infectious diseases of the liver, focusing on pyogenic liver abscess and amebic liver abscess. Pyogenic liver abscess is usually polymicrobial, with risk factors including biliary tract disease, cirrhosis, and diabetes. Clinical features include fever, right upper quadrant pain, and jaundice. Treatment involves antibiotics and drainage of large abscesses. Amebic liver abscess is caused by Entamoeba histolytica and presents with nonspecific symptoms. Serology and imaging can help with diagnosis, and metronidazole is the treatment. Complications of liver abscesses include rupture, fistula formation, and spread to other organs.

1. Infectious diseases of liver
Nabin Paudyal

2. Pyogenic abscess
Epidemiology
• Seen in patients are 50-60 years of age
• Related to biliary tract disease or is cryptogenic
• In USA recent trends show annual incidence of 3.6 cases / 100k
population
• M:F = 1.5:1
• Patients with cirrhosis, diabetes, chronic renal failure and history of
malignancy have increased association

3. Pathogenesis
• Pyogenic abscess develops when the inoculum of bacteria, regardless of the
route of exposure exceeds liver’s ability to clear it.
• Resultant tissue invasion, neutrophil infiltration and abscess formation
occurs.
• Routes of invasion
• Biliary tree
• Portal vein
• Hepatic artery
• Direct extension of nearby nidus of infection
• Trauma

4. Events
• Biliary obstruction Bacterial colonization, infection, Ascension into the
liver by ascending through biliary tree Ascending suppurative
cholangitis
• In Asian countries Intrahepatic stones and cholangitis (recurrent
pyogenic cholangitis [RPC])
• In Western countries Malignant obstruction
• Other causes:
• Caroli disease
• Biliary ascariasis
• Biliary tract surgery

5. • Portal venous system drains Gastrointestinal tract any infectious
disorder of the GIT can result in ascending portal vein infection
(Pyelophlebitis) Expose liver to large amount of bacteria
• MCC of Pyelophlebitis Diverticulitis, appendicitis, pancreatitis, IBD, PID,
perforated viscus and omphalitis (in newborn).
• Hepatic abscess has also been associated with colorectal malignant
disease.
• In a case-control study of Taiwan GI cancers were associated with
fourfold among patients with pyogenic liver abscess.

6. • Any systemic infection  result in bacteremia infection of the liver through
hepatic artery.
• Micro abscess formation is a relatively common finding at autopsy in patients
dying of sepsis.
• Hepatic abscess from systemic infection may also reflect an altered immune
response (e.g. in patients with malignancy, AIDS, disorders of granulocyte
formation)
• Hepatic abscess can arise from  direct extension of an infectious process as in
suppurative cholecystitis, subphrenic abscess, perinephric abscess, perforation
of bowel.
• Trauma  Intrahepatic hematoma Abscess may manifest several weeks
after injury.
• Cryptogenic abscess Sometimes may be seen. Possible explanation include
Undiagnosed abdominal disease, resolved infectious process at the time of
presentation, host factors (diabetes, malignancy)

8. Pathology and microbiology
• Usually involves right hemi liver (75%) of cases  because of LAMINAR
FLOW of blood to right side of the liver
• Left liver (20%) and caudate lobe (5%)
• 50% of abscess is solitary
• Hepatic abscess can be classified on the basis of
• Size 1mm to 4 cm and > 4 cm
• Locules Unilocular and multilocular
• At abdominal exploration hepatic abscess can be tan and fluctuation.
Deeper abscess may not be palpable
• Culture reports have been variable in demonstrating the type of bacteria

9. • In early series sterile abscess were reported
• In modern series Heterogeneity of routes of infection makes
microbiology variable
• Pyelophlebitis or cholangitis Polymicrobial with high preponderance to Gram-ve
bacilli. Total 40% of hepatic abscess are polymicrobial.
• Systemic infections as source Single organism
• USUALLY SOLITARY LIVER ABSCESS ARE POLYMICROBIAL
• Anaerobic organisms are involved approximately 40-60% of the time.
• Organisms isolated
• E coli
• Klebsiella pneumoniae
• Staph.
• Enterococcus sp.
• Viridans strep.
• Bacteroides

10. • Following high yield points needs to be noted
• Gas forming abscess Klebsiella
• Polymicrobial Enterococci and viridans streptococci
• Monomicrobial Staphylococcus
• Blood cultures are positive in approximately 50-60% of cases.
• Highly resistant organisms are seen in patients with indwelling biliary
catheters, multiple episodes of cholangitis and repeated antibiotics use
• Fungal and mycobacterial hepatic abscess are seen in patients with
chemotherapy.

11. Clinical features
• Fever, Jaundice and RUQ pain with tenderness to palpation
• Chills and abdominal pain are the most common presenting
complains
• Malaise
• Vomiting
• Cough and dyspnea
• Pleural/pericardial fistula

12. • Can be acute/ chronic
• Acute abdominal pain chronic Cryptogenic abscess
• In diabetic patients endogenous endophthalmitis secondary to Klebsiella
hepatic abscess is seen
• On P/E of pyogenic liver abscess
• Fever, RUQ tenderness, Jaundice
• Chest findings (25% of people)
• Hepatomegaly (50%)
• Blood tests
• Leukocytosis
• Anemia
• LFT
• Mild elevation in ALP
• Elevation of Total. Bilirubin
• Elevation of Transaminases

13. • Radiographic imaging
• CXR Abnormal in approximately 50% of time
• Findings reflect subdiaphragmatic disease
• Elevated right hemidiaphragm
• Right pleural effusion
• Atelectasis
• Abdominal X-ray
• Air-fluid level OR portal venous gas may be seen
• Ultra-sonography and CT form mainstay of diagnosis
• USG
• Round or oval area that is less echogenic than liver parenchyma
• Can distinguish solid from cystic lesion
• Limitations:
• Inability to visualize lesions in the dome of the liver
• User dependent
• CT scan
• Lesions are lower attenuated than surrounding parenchyma
• Very small abscess and multiple small abscess can be demonstrated
• Abscess wall has intense enhancement on contrast-enhanced CT. (sensitivity 95-100%)

14. • MRI
• Can be used to identify Cause of hepatic masses, biliary tree for pathologic
changes.
• Differential diagnosis
• Amebiasis
• Echinococcal cyst

16. Treatment
• Board spectrum antibiotics immediately just even when suspected
• Blood and abscess used for C/S. In immunocompromised considered fungal/
mycobacterial culture
• Amebic serology also needs to be sent
• Start patient on
• Combination therapy Ampicillin/ aminoglycoside/third gen. cephalosporin with
metronidazole
• Duration is individualized depending upon success of drainage
• Leukocytosis is an indication to continue antibiotics
• Recommended duration is at least 2 weeks.

17. • Drainage
• Per-cutaneous drainage (PCD)
• Treatment of choice for most patients
• Success rates 66 to 90%
• Relative contraindication for PCD include presence of ascites, coagulopathy, proximity to vital
structures.
• Usually PCD is useful for abscess > 5cm
• Surgery is reserved for patients who require surgical treatment of primary pathology
(eg appendicitis) or failed PCD
• Catheter drainage is treatment of choice rather than aspiration.
• Liver resection
• Infected malignant neoplasm
• Hepatolithiasis
• Intrahepatic biliary stricture.
• Severe hepatic destruction due to infection

18. Outcomes
• Mortality has improved during the last 70 years.
• Mortality in recent publications (Memorial Sloan-Kettering Cancer Center)
show as less as 3%
• Factors associated with poor outcomes
• Presence of malignant disease
• Signs of sepsis
• Hypoalbuminemia
• Leukocytosis, APACHE II score, abscess rupture, bacteremia and shock

19. Amoebic liver abscess

20. Epidemiology
• Disease of tropical and developing country
• Endemic in India, Mexico, Africa, Central and South America
• E. dispar needs to be differentiated from E histolytica because it is a
non-pathogenic form of Entamoeba and presents as diarrhoea in
homosexuals
• 55% of the people in endemic areas get affected
• Hispanic men, 20-40 years age, Travel to endemic area (or originating
from)
• Poverty and cramped living conditions are a/w increased risk of
disease infection.

21. • M:F 10:1
• Pregnancy and menstruation Protective
• Alcohol increases risk
• Patients with impaired host immunity  increased risk of infection and higher
risk of mortality

22. Pathogenesis
• A protozoan that exists as cyst or trophozoite
• Ingestion of E histolytica cyst through feco-oral route is the main cause of
amebiasis
• Humans: Principal host
• Source of infection: Human contact with cyst-passing carrier
• Ingested cyst pass into intestine become trophozoite colonic mucosa
invasion entry into Portal-venous system Lodge into tissue tissue
reaction (lysis) formation of liver abscess

23. • Tissue events during pathogenesis
• Cell adherence
• Cell activation
• Subsequent release of enzymes
• Necrosis

24. Pathology
• Liquefactive necrosis of liver
• Cavity filled with blood and pus (liquified liver tissue)
• Progressive hepatic necrosis occurs and continues extending
up to Glisson capsule
• Because of this resistance by capsule, often the abscess is
crisscrossed by portal triads
• Early cavity is ill defined
• Late Chronic abscess ultimately develop a fibrous capsule
and may even calcify

25. Clinical features

26. • 80% of patients have symptoms lasting few days to 4 weeks
• Onset is usually less than 10 days
• On the basis of duration features may be divided as
• Acute presentation : < 10 days
• Chronic presentation: > 2 weeks
• A complicated course tends to ensue in acute presentation, but response to therapy is
similar in both groups.

27. Laboratory findings
• Mild to moderate Leukocytosis (no eosinophilia)
• Anemia
• Low albumin
• Deranged LFT. MC deranged LFT is abnormal PT-INR
• Serology:
• EIA
• E histolytica specific lectin antigen

28. Radiological findings
• CXR abnormal in 50% of cases. Usually demonstrate elevated right
diaphragm, pleural effusion, atelectasis
• Abdominal USG USG shows rounded lesion abutting liver capsule without
significant rim echoes. Usually the abscess is hypoechoic and
nonhomogeneous
• CT scan helps in differentiating amoebic liver abscess from pyogenic liver
abscess (PLA). In PLA, PERIPHERAL RIM ENHANCEMENT is seen.
• MRI scan Helps in differentiating atypical lesions
• Nuclear medicine scans Gallium scanning and Tc 99m liver scans helps
differentiate amoebic liver abscess from PLA. In amoebic liver abscess, no
leukocytes are not present. Therefore, ALA do not light up in nuclear
medicine scans

30. What is still not diagnosed?
• 2 options are to be considered
a. Therapeutic trial of anti amoebic drug
b. Diagnostic aspiration
CULTURE OF ANCHOVY SAUCE PUS IS STERILE
NEVER ASPIRATE IF HYDATID DISEASE IS SUSPECTED

31. Differential diagnosis
• Viral hepatitis
• Echinococcal disease
• Cholangitis
• Cholecystitis
• Inflammatory abdominal disorders (Appendicitis)
• Primary pulmonary disorders

32. Treatment
• Metronidazole 750 mg PO TDS for 10 days
• Improvement is seen within 3 days
• If metronidazole is not tolerated other nitroimidazoles can be used like
Secnidazole, Tinidazole
• Along with metronidazole, luminal agents like diloxanide furoate,
iodoquinol, paromomycin is used.

33. When to aspirate amebic liver abscess?
• Diagnostic uncertainty
• Failure to respond to metronidazole therapy in 3-5 days
• Larger abscess at the risk of rupture
• Abscess size > 5 cm

34. Complications
• Rupture Intraperitoneal, pleural, pericardial
• Manifested as pain, peritonitis, generalized distention
• Treated using percutaneous drainage
• Laparotomy in cases of doubtful diagnosis, hollow viscus perforation, fistula
formation resulting in hemorrhage and sepsis
• If pleural rupture Thoracocentesis
• Bronchial rupture Self-limited, postural drainage and bronchodilators
• Left-sided rupture Aspiration / drainage through pericardial window.
• Fistulation
• IVC abscess/ brain abscess.

35. Factors associated with poor
outcome
• Elevated bilirubin level > 3.5
mg/dl
• Encephalopathy
• Hypoalbuminemia < 2.0 g/dl
• Multiple abscess cavity
• Abscess volume > 500 ml
• Anemia
• Diabetes
• 3 to 9 months
• In 90% people resolution occurs
completely and lesions
disappear radiologically
Time for radiological
resolution