5. Pathogenesis
• Occurs when an inoculum of bacteria regardless of the
route of exposure, exceeds the ability of liver to clear it.
• Organism invades tissue-> neutrophil infiltration and
formation of organized liver abscess.
6. Routes of infection.
1. Via biliary tree.( obstruction –stasis –infection= ascending
suppurative cholangitis)
2. Via portal vein:( drains GI tract- infections /malignancies=
pyelophlebitis)
3. Via hepatic artery( any systemic infections- endocarditis/ immune
compromised conditions.)
7. 4. Via direct extension:-
from suppurative cholecystitis, subphrenic abscess, perinephric abscess, perforation
peritonitis
5. Traumatic – penetrating /blunt trauma – direct inoculation of organisms
6. Cryptogenic :- no specific cause.
( possible explanations- undiagnosed abd. Pathology/diabetes/ malignancy)
8.
9.
10. Sites
• Most c’mon sites –RIGHT HEMILIVER -75%
-LEFT LIVER -20%
-CAUDATE LOBE – 5%
75%
25%
5%
LIVER
RIGHT LIVER LEFT LOBE
CUADATE LOBE
11. • 50% of liver Abscess is solitary
• Size varies from 1mm to 4/5 cm in diameter.
• Can be multi loculated/ single cavity
25. TREATMENT
MEDICAL
• BROAD SPECTRUM IV ANTIBIOTICS COVERING G+, G-,
ANEROBES(PENCILLIN +
AMINOGLYCOSIDES+METRONIDAZOLE)
• 3 RD GEN. CEPHALOSPORIN + METRONIDAZOLES
• SPECIFIC ANTIBIOTICS AS PER CULTURE AND SENSITIVITY
• TREATMENT FOR MIN. 2 WEEKS/ TILL SYMPTOMS SUBSIDES.
27. INVASIVE
• PERCUTANEOUS DRAINAGE
1. Abscess size < 5 cm- needle aspiration ( 60% success rate)/ catheter
drainage(~100% success rate)
2. Abscess size >5cm- catheter drainage
3. Percutaneous catheter drainage is the treatment of choice now a days
4. Surgery should be reserved for patients who require sxical treatment for
primary pathological process
28. • Similar success / mortality rate is seen in percutaneous and surgical
management.
• Mortality rate is 50-100% if
treated with antibiotcs with out any drainage
29. COMPLICATIONS
• RUPTURE OF ABSCESS
To pleural cavity-empyma pleuroperitoneal
fistula
To peritoneum –peritonitis
To pericardial cavity- tamponade/ effusion
To bronchi-
32. • Caused by entemoeba hystolytica, a protozoan
• Seen mainly in tropical and developing countries
• Endemic in India, Mexico, Africa and S. America
• ~40,000 to 100,000 deaths every year.
39. Pathology
• Due to liquefactive necrosis of liver– a cavity of blood +
necrotic tissues
• Necrosis continues until Glissons capsule– so cavity is
typically crisscrossed by portal triads
40.
41.
42. Clinical features
• ~ 80% of patients presented with prolonged symptoms <10 days
• Abdominal pain -92%
• Fever-90%
• Abdominal tenderness- 78%
• Hepatomegaly-50%
• anorexia-, diarrhoea, jaundice, wt. loss., symptoms of complicatns
43. • Acutely (<10 days)- 50% have multiple lesions
• Patients presents
• Chronic(>2 weeks)- 80% single right sided lesion
49. Treatment
TISSUE AMEBOCIDES
1. METRONIDAZOLE 750MG PO/IV Q8H X 10 DAYS( Curative in
> 90%)
2. TINIDZOLE/ORNIDAZOLE
3. EMETINE HYDROCHLORIDE- more effective but cardiac SE.
4. CHLOROQUINE- less effective.1GM(600MG base )OD X 3 DAYS
then 500mg( 300mg base) OD FOR 2-3 weeks
50. LUMINAL AMEBOCIDES
• IODOQUINOL 650MG TID X 20 DAYS OR
• PARAMOMYCIN 500MG TID X 10 DAYS OR
• DILOXAANIDE FUROATE 500MG TID X 10 DAYS
51. • SURGICAL INTERVENTIONS
• Indications for aspiration
• Size >5cm
• Impending rupture
• Left lobe abscess – pericardial rupture
Indications for laparotomy- intestinal perforation, pericardial
rupture
52.
53. COMPLICATIONS
• RUPTURE OF ABSCESS
To plueral cavity-empyma pleuroperitoneal
fistula
To peritoneium –peritonitis/intestine fistula
To pericardial cavity-tamponade/ effusion
To bronchi-fistula
Death in 5-50% in ruptured cases