AMOEBIC LIVER ABSCESS: REVISITED

Jesus Y Perez Jr

Section of Gastroenterology, Department of Medicine,University of Santo Tomas Hospital, Manila, Philippines

Phil J Gastroenterol 2006; 2: 11-13

Amoebiasis is common in Asia, Africa, and SouthAmerica, and is endemic in many regions of thePhilippines1-4. Hepatic involvement is a frequentextra-intestinal complication which is encounteredin 3 to 9% of the cases of amoebiasis. In Africa,over a period of 20 years, the King Edward VIIIHospital reported 2,074 cases of hepatic abscess,while in New York City at the Mt. Sinai Hospitalonly 11 cases were seen in approximately 500,000admissions2,3. The Santo Tomas UniversityHospital in Manila had an incidence of one hepaticamoebic abscess per thousand admissions over aten-year period4,5.

Despite the advances in diagnostic tests andmanagement, amoebic liver abscess remains tobe a health problem in many parts of the world,where hygiene is not properly observed.

ETIOLOGY AND PATHOGENESISAmoebic liver abscess is a protozoal infestation

that starts in the colon. The etiologic agent isEntamoeba histolytica. The protozoa was discoveredby Losch in St. Petersburg, but named later on byProf. Shaudinn in 19031-3. Its transmission isthrough contaminated water or vegetables.Amoebic infestation is initiated by swallowingthe cysts. The cysts are spherical, 10 to 20um indiameter which rupture in the intestinal tractlumen into four metacystic trophozoites6,7.

It is through the trophozoites that the diseaseevolves, often in the cecum and the ascendng colon.The amebic protozoa may exist in its commensalstate for years before becoming invasive. Theinvasiveness of the infestation is possibly related tothe following: diet, host resistance, virulence of theprotozoa, humoral and the cell mediated immunity.It is the protective cell mediated immunity thatmay be vital in restricting tissue invasiveness, aswell as in aiding tissue resolution6.

PATHOLOGYThe typical amoebic abscess is due to necrotic

lysis of the liver tissue, which vary in size from afew centimeters to a large lesion. It is often single,usually in the posterior superior aspect of the rightlobe8,9. The abscess is well-demarcated that consistsof the chocolate brown “anchovy-like” materialof necrotic liver tissue, bile, fat and otherproducts4. It is usually sterile but may besecondarily infected.

Seen externally, the hepatic surface is smooth,swollen, and tender to touch. If untreated, it mayrapidly progress to form fibrous reactions on thehepatic surface and the surrounding tissues5. Itssuperior extension can lead to rupture into the pleuralcavity. Its rupture inferiorly can lead to fatalperitonitis. The left-sided lesions, though infrequent,can lead to cardiac tamponade. The present studyshowed complete resolution with almost little residualscarring with successful nonsurgical management.

CLINICAL FEATURESThe duration of the illness that denotes hepatic

involvement vary from a few days to several weeks.It is usually gradual in onset, with fever andprogressive right hypochondriac pain. The febrileepisode is intermittent, which later may beaccompanied by chills. The pain may later on radiateto the epigastrium, chest and shoulders. In somecases, it may be associated with coughing butdiarrhea is infrequent and loss of weight may notbe significant.

An enlarged liver is usually palpable, smoothand tender. Its upward enlargement may push theright hemidiaphragm, which may be associatedwith breathing difficulties. Tenderness over theintercostal spaces on the right side might indicatean impending rupture of the hepatic abscess,particularly when associated with skin discolora-tion over a localized area. If the abscess extendsdownwards, there might be a bulge below the right

12 Perez J

subcostal area, which when associated with exquisitetenderness, might indicate an unusually large abscesswith impending rupture into the peritoneal cavity.An enlarged and exquisitely tender left hepatic lobeis an indication of a possible rupture towards thepericardial cavity. Jaundice which is relativelyinfrequent is obstructive in nature10. It is importantto auscultate the hepatic area for possible frictionsound of hepatic amoebic abscess and differentiateit from the vascular sound of a neoplastic mass11,12.

INVESTIGATIONSDetermination of the white blood count can

be helpful and usually ranges from 10,000-20,000/cu.mm. The serum bilirubin is predominantlyconjugated, associated with elevated serum alkalinephosphatase. On the other hand, the hepaticenzymes are often not significantly elevated.

The chest x-ray is important to show theunusual elevation of the right hemidiaphragm,particularly in the right lateral position, whichsuggests upward hepatic enlargement that maybe associated with pleural effusion.

With the advent of hepatic imaging by meansof the sonogram and the CT scan, the confirmationof hepatic abscess has been made relatively easy,showing its location, size, number and extent of thehepatic enlargement. Through these means, it iseasier to rule out hepatic cysts, granulomas, neoplasticdisease and hepatic enlargements of other causes5.

Hepatic angiography as a means to differentiateproblematic cases from granulomatous andneoplastic lesions has been proven to be useful instudies done at the Sto. Tomas University Hospital5.Stool examinations should be done to determinethe presence of the parasite. Short or long endoscopicexaminations may likewise be considered to assessthe extent of possible associated intestinal disease6,7.

NEEDLE ASPIRATIONThe availability of imaging techniques makes

needle aspiration a relatively simple procedure4,9.Aspiration may be advised in certain lesions as partof the treatment as well as for the histologicconfirmation of the lesion, particularly in placeswhere liver cancer and hepatobiliary tuberculosisare common. If the abscess is large or a point ofexquisite tenderness is elicited externally, aspirationis mandatory to preempt rupture. Aspiration isdone using a medium bore needle about 1.5 mm.in diameter attached via a three-way stop-cock to a

50 ml. syringe. The selected site for aspiration isthe point of localized tenderness between theintercostal spaces with dullness on percussion. Left-sided lesions should be aspirated only if they aresuperficially located. Sonographic monitoring isrecommended whenever available. Surgicaldrainage is recommended when the abscess isunusually large, there are impending signs ofrupture or when rupture has occurred.

Examination of the aspirated material is impor-tant to confirm or exclude the diagnosis of amoe-biasis. However, the E. histolytica is usually difficultto demonstrate in the aspirated material, which mayrequire immunofluorescent techniques followedby conjugated anti-human globulin examination13.

SEROLOGYObviously, the traditional and reliable method

for the diagnosis of amoebiasis is the microscopicidentification of E. histolytica. Unless propertechnique is followed, the isolation of the protozoacan be frustrating.

To confirm the diagnosis of amoebiasis withcertainty, there are serologic tests which includeindirect immunofluorescence, indirect hemagglu-tination, enzyme-linked immunosorbent assay,and counter-immunoelectrophoresis13. Theindirect hemagglutination assay is widely used forits sensitivity in recognizing the invasiveness ofthe disease. Factors that may affect the result ofthe serologic test would include the length ofexposure, severity of infestation and immunologiccompetency. There are, however, simpler tests thatcan be done by the bedside, like the gel diffusionin capillary tubes and the slide agglutination ofantigen-coated latex particles. These tests havebeen found to show a positive result in more than95% of the patients with amoebic liver abscess.

DIFFERENTIAL DIAGNOSISAmoebic liver abscess should be differentiated

from pyogenic liver abscess in view of theirsimilarities in clinical behavior. Amoebic liverabscess is usually seen in the 2nd to 5th decade oflife, as a tender, smooth hepatic mass withassociated pulmonary symptoms. In large righthepatic lobe abscesses, localized points oftenderness along the intercostal spaces might beelicited. A third of these patients may have a historyof bloody diarrhea. Chest x-ray findings arecommon, manifesting as elevated right

Amoebic Liver Abscess 13

hemidiaphragm, effusion or atelectasis. Thehepatic sonogram and the CT scan are oftenclassic. The serologic tests are mandatory todifferentiate lesions from pyogenic abscesses withutmost care in interpreting the results in endemicareas

5,13.

Pyogenic abscess is more common in theelderly with known predisposing diseases, suchas biliary disorders, immunosuppressiveconditions, diabetes and malignancies. It has aninsidious onset of malaise, epigastric pain, feverand chills. Often the abscesses are multiple, thejaundice more obvious and the fever spiking. Thegeneral appearance of the patient is more toxic asa rule. Often, blood culture is necessary to showthe presence of bacterial infection, usually E. colior Klebsiella, to confirm the etiology of the disease.

Cystic liver disease, including those due tohydatid cysts, should be considered in patientsfrom the tropics. Indirect hemagglutination andcomplement fixation tests for antibodies arepositive in at least 80%.

Of course, in regions where hepatocellularcarcinoma and other granulomatous diseases areprevalent, the histologic confirmation by meansof percutaneous or open biopsy may be necessaryas its clinical manifestation may simulate that seenin hepatic amoebic abscess

4,5,8,9.

MANAGEMENTAs late as in the ’70s, the treatment of amoebic

liver abscess remained debatable. There was nounanimity as to what was best, whether treatmentshould be with the use of anti-amoebic drugs aloneor should it be combined with aspiration. When theabscess is very large or is showing signs of possiblerupture, needle aspiration is deemed mandatory.

Currently, the most commonly used agent foramoebic liver abscess is metronidazole at a doseof 500 to 750 mg orally, three times a day for 7 to10 days, providing a cure rate of more than 90%.

Metronidazole is well absorbed from thegastrointestinal tract and the use of the parenteralform offers no significant advantage. If the patientshows slow response or relapse after treatment,aspiration and/or a prolonged course of metronida-zole may be considered. Metronidazole-resistant E.histolytica trophozoites had not been reported

8,9.

In some places, where tinidazole and/ornidazole are available, they can be considered asalternative agents, administered only for a few

days, with a reported success rate of 94%.Other alternatives for eradicating liver

trophozoites include chloroquine, at 600 mg dailyfor 2 days, then 300 mg daily for 2-3 weeks.Dihydroemetine and emetine are no longerrecommended in view of their significant potentialside effects including cardiac toxicity and shouldonly be administered in hospitalized patients14,15.

The use of luminal agents are recommendedfor the possible associated intestinal infestation,even if the stool is negative for the organism. Oneof the following may be used: paromomycin, at30 mg/kg/day orally in three divided doses for 10days; diiodohydroxyquin at 650 mg orally threetimes a day for 20 days; or diloxanide furoate at500 mg orally three times daily for 10 days11,15.

Uncomplicated amoebic liver abscess has a mor-tality rate of <1% if diagnosed early. However, forthe complicated disease, the mortality can be as highas 17 to 20%. Untreated, the mortality is 100%4.

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345:1565.3. Stanley, SL, et al, Amoebiasis. Lancet 2003; 361:1025.4. Perez,J, et al, Amebic liver abscess at Sto. Tomas

University Hospital; Proc. of 4th Asian-Pacific Cong. OfGastro; Manila 1972; 130-140.

5. Perez, J, et al. Accuracy of diagnostic teast inhepatic diseases using scintiscan, angiography andlaparoscopy. Journ of Phil Med Ass.1978, 367-372.

6. Aucott JN, et al, Amebiasis and nonpathogenicintestinal protozoa. Infect Dis Clin North Am 1993; 7:467.

7. Liboro, A; Entameba histolytica. Proc. Of 4th

Asian-Pacific Cong. of Gastro; Manila 1972; 657-663.8. Sharma, MP; Amebic liver abscess. Trop

Gastroenterol 1993; 14: 3.9. Petri WA, et al, Diagnosis and management of

amebiasis, Clin Infect Dis 1999; 29:1117.10. Vakil, B, et al, Jaundice in amebic liver abscess. Proc.

of 4th Asian-Pacific Cong. of Gastro; Manila 1972; 652.11. Thorsen, S, et al, Extraintestinal Amebiasis.

Scand J Infect Dis 1993; 25:747.12. Adams, EB, et al. Invasive amebiasis, part II,

Amebic liver abscess and its complications. Medicine,1977: 56-315.

13. Patterson, M, Serologic testing for amebiasis.Gastro 1980; 78:136.

14. Perez, J, Management of amebic hepatic abscess;Drugs. 1978; 49-52

15. Khukhani, RC, et al, Treatment of amebic liverabscess with tinidazole and metronidazole. Drugs 1978;15 Suppl 1:23.