Abses of Liver


•          Intraabdominal infection

•          Middle to older age (median age 51)

•          M = F


•          35 % : Biliary tract diseases cholangitis or acute cholecystitis

•           30 %  : diverticulitis, crohn’s, ulcerative colitis, bowel perforation

•           15% direct extension from a contiguous source : subphreric abscess or empyema of the gallbladder

•           Intraabdominal infections : bacterial seeding via portal vein can occur dental disease, endocarditis ; Other Causes  : Malignancy


•          Organism : gram (-) E.Coli 50-70%, gram (+) 25% & anaerob 50%

•           Abscess from biliary tend to be multiple & small, both lobes

•           Septic emboli via portal vein & contigous source tend to solitary


•          Colonic infection with invasive Entamoeba histolytica

•          Younger population (30-40 years)

•          M  > F


Bile is lethal to amebas, thus infection of gall bladder & bile duct do not occur


•          Usually arise from colonic infection w. invasive E.histolytica

•         Solitary & large, most common right lobe

•         Bile is lethal to amebas ? infection of gallbladder or bile duct do not occur


•         Ingestion contaminated water or food containing E. histolytica cysts –

•         infective cyst form of the parasite survives passage through the stomach and small intestine.

•         Excystation occurs in the bowel lumen, where motile and potentially invasive trophozoites are formed.

•         In most infections the trophozoites aggregate in the intestinal mucin layer and form new cysts, resulting in a self-limited and asymptomatic infection.

•         In some cases, adherence to and lysis of the colonic epithelium, mediated

•         by the galactose and N-acetyl-D-galactosamine (Gal/GalNAc)–specific lectin, initiates invasion of the colon ? neutrophils responding to the invasion contribute to cellular damage.

•          Once the intestinal epithelium is invaded, extraintestinal spread to the peritoneum, liver, and other sites may follow.

Clinical Manifestation

Nonspesific, fever (absent in 30%), chills, RUQ pain (45%), malaise, weight lose More severe RUQ pain, fever 90% cases
Dominate by underlying disease : appendicitis, diverticulitis, biliary disease Recent travel to endemic area, but maybe remote
Comorbid common : DM, malignancy, alcholism, cardiovascular, chronic renal disease Previous colonic amebiasis (only 5-15%), concurrent hepatic abcess & amebic dysenteri are unusual
Eosinophilia, high bilirubin, blood culture + 50%, aspirates + bacteria 75-90% Most aspiration does not yield an organism (tropozoite < 20%); odorless, serologic + only invasive amebiasis, negative asymptomatic carrier, gel diffusion precipitin (best test)
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Laboratory And Diagnostic
• Routine lab not diagnostic for both abcess : WBC (?), anemia (normocytic normochromic), sed rate (?)
• LFT nonspesific : 90% high AP, AST/ALT ? but to a lesser degree, low albumin (<2mg%) poor prognostic
• CXR : 50-80% abnormal (RLL atelectasis, R pleural eff, R hemidiaphragm elevation)


•          U/S initial test of choice : noninvasive, high sensitivity 80-90%; to distinguish cyst from solid lesion/visualizing biliary tree

•          CT (IV contrast) : smaller abcess, asses peritoneal cavity


•          Amebic aspiration : pyogenic can’t be roled out, respond to amebic therapy has not occurred within 24-48 hours, abcess is large (size greater than 5 cm) & painful

•          Surgical drainage of amebic abcess : located in left lobe, respon therapy is not dramatic in 4-5 days




•          Antibiotic : aminoglicoside/ cephalosporin (gram -), clindamycin/metronidazole (anaerobes), penicillin/ampicillin (enterococci)

•          Surgery percutaneus drainage : conservative measure fail, to treat primary intraabdominal lesion

76% cure rate, 60% either alone


•          Metronidazole drug active against extraintestinal form of amebiasis : 750mg TID x 10 days

•          Eradicates intestinal form : iodoquinol 650mg TID x 20 days

•          Consider aspiration if failing therapy

Complication And Prognosis

Untreated 100% mortality Rapid clinical improvement is observed in less than 1 week with antiamebic drug therapy alone
Ruptur into peritoneal cavity : subphrenic, perihepatic, subhepatic abscesses or peritonitis; metastatic ruptur emboli (lung, brain) similar
Left lobe abscess : cardiac tamponade, pericarditis Abscess in dome of liver or complicated by bronchopleural fistula
Depends on rapidity diagnosis & underlying illness Generally do well with treatment
Morbidity high (50%), mortality 5-10% (prompt recognation & adequate AB) higher in multipel abscesses Morbidity 4.5%, mortality 2.2%