R E V I E W

A R T I C L E

JIACM 2002; 3(4): 367-73

Clinical Profile of Amoebic Liver Abscess

Shyam Mathur*, RS Gehlot**, Alok Mohta***, Narendra Bhargava****

Introduction
Amoebiasis is an infection by the intestinal
protozoan Entamoeba histolytica. About 90% of
the infections are asymptomatic and the remaining
10% produce a spectrum of clinical syndromes
ranging from dysentery to abscess of liver or other
organs1. Amoebic liver abscess (ALA) is the
commonest extra-intestinal manifestation of
amoebic infection, possibly because of portal
circulation. Often starting with non-specific
complaints, ALA must be excluded in all patients
presenting with right sided upper abdominal pain,
or right lower thoracic pain, with or without fever2.
Fortunately, ALA is a readily treatable form of
hepatic infection and mortality is negligible, if
diagnosed and treated in its early course. However,
if left untreated it may lead to serious lifethreatening complications like rupture into the
pleural, peritoneal, or pericardial cavities.
A prospective study was undertaken at our institute.
We have evaluated 100 cases of ALA prospectively
over a period of 3 years with emphasis on clinical,
serological, and radiological profile alongwith the
presence of complications and overall
management of these cases. The observations
from our study have been incorporated at relevant
places in this review article.

Epidemiology
Amoebic infection is common throughout the
world; about 10% of the worlds population is
infected with E. histolytica1. Among all cases of
amoebiasis, the incidence of ALA has been
* Assistant Professor
** Professor
*** Resident
**** Associate Professor
Department of Medicine,
Dr. S.N. Medical College and
M.G. Hospital, Jodhpur (Rajasthan State).

reported to vary between 3-9%. Despite improved

sanitation and advances in treatment, ALA has
the highest rate of incidence in developing
countries of the tropical regions, including India,
where it is endemic. In developed countries, the
main groups at risk are travellers, recent
immigrants, homosexual men, and inmates of
institutions.

Age and sex distribution

ALA characteristically occurs in adults and only
rarely appears in children. ALA occurs most
commonly in the age group of 20-45 years. It is
seven to nine times more common in males than
females3. ALA may commonly be seen in chronic
alcoholics and individuals who have diabetes
mellitus.
Moazam et al retrospectively reviewed incidence
of ALA in 48 paediatric patients with age ranging
from 3 weeks to 14.5 yrs. ALA was confirmed with
ultrasound scan together with elevated indirect
haemagglutination titres4. Katzenstein et al5 in a
study of 69 patients observed that ALA occurred
predominantly in patients in the age group 1660 years. Eighty five percent patients were males,
twenty five percent patients were reported chronic
alcoholics, and 3% were diabetics. In our study of
100 patients, we observed that 86% patients were
males and 14% patients were females; and the
common age group was 30-50 years. We also
observed that alcohol intake and diabetes mellitus
were seen in a significant number of patients. The
study revealed that 70% of male patients were
alcoholics and 21% of patients were having
diabetes mellitus, among them 19% were old
diabetics and 2% were newly diagnosed diabetic
individuals.

Clinical presentation
The main presenting symptoms are fever and

abdominal pain. Fever is the most common

complaint seen in 70% of the patients2,6. The acute
cases may present with moderate fever and rigors,
while high fever with chills may be suggestive of
secondary bacterial infection. Patients with chronic
illness are more likely to present with low grade
fever and sweating. Abdominal pain is usually
moderate and localised to right upper quadrant
or right lower thoracic region. Radiation to right
shoulder is not uncommon. Epigastric pain is
usually seen in left lobe abscess.
Other symptoms include cough which may be seen
in 10-15% of the patients associated with or
without expectoration. Pleuritic chest pain may also
be present. Gastro-intestinal symptoms of ALA are
much less prominent than pain and fever. Nausea,
vomiting, and anorexia are present in about onethird of patients. Diarrhoea and weight loss are
seen in only a minority of patients.
On abdominal examination, tender hepatomegaly
is detected in 80% of the patients. The liver surface
is generally smooth and upper abdominal
guarding and rigidity is seen in a minority of the
cases having features of generalised peritonitis3.
Point tenderness over the right costal margin
(anteriorly, laterally, or posteriorly) and a bulging
of right hemithorax, or right hypochondriac region
is common, while bulging of epigastrium may
occasionally be noted7.
Sharma et al3 in a prospective study, observed that
the patients with left lobe abscess may present
with long duration of symptoms and with an
epigastric lump. Multiple abscesses may manifest
as toxaemia, deep jaundice, and encephalopathy.
Ascites developing in a patient with ALA suggests
development of inferior vena cava obstruction, and
cough with copious expectoration of anchovy
sauce pus suggests rupture into right lower lobe
bronchus. During the course of illness 1/3 of
patients may develop clinical jaundice. Severe
icterus may be due to a large abscess, or multiple
abscesses, or an abscess situated at porta hepatis.
Our prospective study observed that fever occurred

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in 87% of patients and pain at right upper

abdominal quadrant in 83% of patients, as main
presenting complaints. Seven percent patients
presented with epigastric pain. Diarrhoea was
seen in only 7% of patients. Seventy three percent
had point tenderness, with 91% having tender
hepatomegaly.

Amoebic liver abscess versus pyaemic

liver abscess
Liver abscesses account for 48% of all the visceral
abscesses. Pyogenic liver abscess may be solitary
or multiple and may arise from haematogenous
spread of bacteria, or from local spread from
contiguous sites of infection within the peritoneal
cavity.
Amoebic liver abscesses are most commonly
solitary, though in 16% of the cases may be
multiple. Secondary bacterial infection is common
in multiple liver abscesses.
Fever and abdominal pain may be present in both
types of abscess, though fever with chills may be
a prominent symptom in pyogenic abscess. Only
50% of the patients of pyaemic abscess have right
upper quadrant tenderness with hepatomegaly
whereas 80% of the ALA patients may have such
findings.
S. alkaline phosphatase may be raised in both
types of abscess, whereas rise of S. bilirubin is
more common in pyogenic abscess (seen in 50%
of the patients) than ALA (seen in 30% of the
cases).
Imaging studies show similar observations in
both groups. Aspiration of pyogenic abscess
with subsequent microscopic examination shows
presence of neutrophils. On laboratory culture,
the abscess may yield bacterial flora. Amoebic
liver abscess does not show neutrophils, as there
is no pus, and amoebae are rarely isolated from
the abscess. Patients with pyogenic abscess are
typically older and have a history of underlying
bowel disease or recent surgery. Amoebic
serology is helpful, but aspiration of the abscess,

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with Grams staining and culture of the material

may be required for differentiation of the two
diseases.

of human ALA, revealed the extensive tissue

necrosis in hepatic amoebiasis, a key
pathophysiological mechanism.

Pathogenesis and pathology

Laboratory findings

Amoebic liver abscesses are always preceded by

intestinal colonisation of the protozoan. There may
be presence of compromised blood vessels by lysis
of wall and thrombus formation. Trophozoites
invade veins to reach the liver through portal
venous system. Pathogenic isolates are resistant
to complement - mediated lysis, a property critical
for survival in the blood stream. In contrast, the
non-pathogenic strain such as Entamoeba dispar,
which is a non-invasive strain, is rapidly lysed by
complement, and is therefore restricted to bowel
lumen.

Blood counts : Majority of the patients of ALA

show leucocytosis. The counts above 20,000 may
be associated with an acute disease or secondary
infection in ALA9. ESR is raised in 2/3 of the
patients. Differential counts show predominance
of polymorph leucocytes with toxic granulation.
Alcoholics who are having suspected folate
deficiency may present with low counts5. Mild
anaemia may be seen. Haemoglobin values less
than 10 gm/dl are usually confined to patients
with chronic ALA.

Inoculation of amoebae into the portal system

results in an acute cellular infiltrate which
predominantly contains polymorphs; subsequently,
polymorphs are lysed by contact with amoebae
and the release of neutrophil toxins contribute to
necrosis of hepatocytes. The liver parenchyma is
replaced by necrotic material that is surrounded
by a thin rim of congested liver tissue. These
necrotic contents of liver abscess are classically
described as anchovy sauce or chocolate paste.
Though fluid is variable in colour and
bacteriologically sterile with little or no cells,
amoebae if found, tend to occur at the periphery
of the abscess.
Ventura et al8 described the liver invasion by E.
histolytica with resultant hepatic damage
characterised by the presence of extensive tissue
necrosis. The parasites interact with sinusoidal
endothelial cells, as a consequence of amoebaendothelial cells interaction, there is expression
of pro-inflammatory factors which lead to tissue
destruction. The immuno-histochemistry
observations regarding the localisation of
antigenic molecule of E. histolytica trophozoites
and of molecules such as intercellular adhesions
molecule 1. (ICAM-1), ICAM-2, and vonWillebrands factor in activated endothelial cells

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Liver function tests : Abnormally high alkaline

phosphatase levels may be seen in 60-80% of the
cases. Thus, alkaline phosphatase level is the most
reliable and consistent biochemical indicator of
ALA. The rise is usually 2-4 times. Katzenstein et
al suggested that the value of alkaline phosphatase
is correlated with duration of the disease. It is
normal in acute cases and patients with a chronic
history may have an abnormal alkaline
phosphatase, usually more than twice the normal
serum level. Serum bilirubin is raised mildly and
transiently in small number of patients. Severe
hyperbilirubinaemia though unusual, carries a
grave prognosis. The SGOT and SGPT levels are
mildly elevated and their abnormal values are
related to the severity of disease. The levels of
serum proteins may be altered with
hypoalbuminaemia as a consistent finding (serum
level < 2 gm/dl) in chronic cases.
Serological tests : Serology for antibodies to E.
histolytica is an useful adjunctive test for invasive
amoebiasis. These antibodies may be detected in
90-95% of patients with ALA. Indirect
haemagglutination, agar gel preciptin, and ELISA
are well established and readily available. ELISA
for the demonstration of anti-amoebic antibody
in titres greater than 1:400 is considered strong
evidence of ALA.

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The serum antibodies to E. histolytica become

positive after one week of onset of symptoms
and may remain positive for upto 6 months or
more. Positive results in conjunction with the
appropriate clinical syndrome suggest active
disease because serological findings usually
revert to negative within 6 to 12 months. Upto
10% of the patients with acute ALA may have
negative serological findings. In contrast to
carrier of E. dispar, most asymptomatic carriers
of E. histolytica develop antibodies, thus
serological tests are helpful in assessing the risk
of invasive amoebiasis in asymptomatic cyst
passers in an endemic area. In our prospective
study we performed serological test in 82
patients, out of which 79 were detected positive.
There is a high background level of seropositivity
for amoebiasis (owing to previous infection with
E. histoloytica) which may complicate the
interpretation of a positive serological test.
Recently, Stanley et al10 reported that a serological
test based on recombinant E. histolytica antigens
might offer improved diagnosis of current invasive
amoebiasis because they apparently differentiate
active infection from past exposure to the parasite.
Serum antibodies to 170 KD subunit of galactose
inhabitable adherence lectin is highly specific for
differentiating acute phase serum for convalescent
phase serum in endemic zones. Though some
authors have described counter immunoelectrophoresis for detecting circulating antigens
in ALA, the ELISA method proved to be the most
sensitive method for diagnosing ALA.
The patients of ALA from an endemic area who
present with history of weight loss, anorexia, and
a history suggestive of suspected HIV infection
should undergo serological test to confirm the HIV
infection. In this context, Fang et al11 have reported
in a study that invasive amoebiasis is an emerging
parasitic disease in patients infected with HIV in
an area endemic for amoebic infection.
Demonstration of E. histolytica in the aspirated
pus is rare, but trophozoites may be present in
the last few milliliters of the pus.

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Imaging techniques
Chest X-ray may reveal an elevated right hemidiaphragm and discoid atelectasis of the right
basal pulmonary parenchyma. Less often the chest
roentgenograms demonstrate a right pleural
effusion, pneumonitis, or frank pneumonia.
A liver scan (Gallium scan) may be helpful. Since
ALA is not a true abscess, there is no pus
(neutrophils), therefore Gallium scan of the lesion
reveals a cold spot of a decreased uptake with a
bright rim, while a pyogenic abscess demonstrates
increased uptake of Gallium12.
Ultrasound is the mainstay in the diagnosis of ALA.
It is the easiest and most cost effective way of
diagnosing liver abscess by considering its typical
site, appearance, internal echotexture, and most
importantly, its clinical presentation. More than
80% of the patients who have had symptoms of
more than 10 days duration have a single abscess
of the right lobe of liver. The more acute
presentation with symptoms of less than 10 days
duration have multiple abscesses13. Moreover,
ultrasound is helpful in the long term follow-up of
patients. Sonographic follow-up is assessed by
patterns of resolution of the abscess cavity.
ALA is the most commonly encountered entity in
daily ultrasound practice in the Indian
subcontinent. However, its ultrasound appearance
may be variable leading to wrong diagnosis such
as tumour, haemangioma, etc. Final diagnosis can
be obtained by FNAC or therapeutic drainage
guided by USG and follow-up response to antiamoebic treatment.
The ALA should also be differentiated from an
infected cyst in the region of right hypochondrium
as clinically both may exhibit rebound tenderness
and referred pain to the right shoulder and have
sub-acute course of illness. USG may reveal, in
such cases, a subdiaphragmatic lesion with typical
features of an abscess.
An abscess size > 10 cm in the superior part of
the right lobe may be associated with
complications (rupture in pleural space or right

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lower lobe bronchus). The left lobe abscess may

rupture in pericardium or may extend in perisplenic
space and pouch of Douglas region14.

day (deep intra-muscular injections) for 10

days with regular BP and ECG monitoring. Our
study showed excellent results with
metronidazole therapy, and in resistant cases
our experience of using DHE was satisfactory.

Computed tomography and MRI are also useful

for detection of ALA with or without complications.
Colonoscopy : Only 15 30 % patients of ALA
have diarrhoea. The use of colonoscopy may be
helpful in such patients. Sachdev et al14 observed
that colonic involvement is common in ALA as
confirmed by colonoscopy, but most patients do
not suffer from diarrhoea possibly because of very
limited extent of the pathology that is confined
mainly to right side of colon. He observed that
50% of ALA patients had few discrete, small ulcers
restricted to right side of colon. Seven percent of
patients had large and more numerous ulcers with
inflammation of the surrounding mucosa of the
left colon.

Studies in South Africans with liver abscess

showed that 72% of the patients of ALA without
intestinal symptoms were colonised by
pathogenic strains asymptomatically, therefore
a luminal agents (Diloxanide furoate 500 mg
TID) should be added, to eradicate cysts and
prevent further transmission.
2. Aspiration or drainage of abscess : Routine
aspiration of ALA is not indicated either for
diagnostic or therapeutic purposes. The
indications for aspiration are :
a. Lack of improvement with subsidence of
symptoms and signs in 48 to 72 hrs.
b. Left lobe abscess

Management

c. Abscess size > 10 cm.

1. Medical : The medical therapy of ALA includes

administration of either a single agent or
combination of drugs. A nitroimidazole, such
as metronidazole, is the drug of choice for ALA.
It is effective in 90% of the cases; the therapy
should be given for 10 days. In some cases
with relapse, it may be extended for a period
of 3 weeks. The dose of metronidazole is 40
mg/kg/day in divided doses. Tinidazole is an
alternative drug in a dose of 1.2 gm/day for 7
days.

d. Compression lesion A posteriorly located

ALA may present with inferior vena cava
obstruction.

The newer imidazoles have also been tried in

the treatment of ALA. In a randomised
double blind trial of metronidazole versus
secnidazole, Bhatia et al proved that
secnidazole is as effective in treating ALA as
metronidazole.

Percutaneous catheter drainage (PCD) is

presently becoming more popular with
growing interest in the management of ALA.
Hanna et al reported in his study of drug
resistant ALA that when PCD is combined with
anti-amoebic therapy, it expedites the recovery
and it is also curative in such cases15.

Chloroquine may be an alternative and

judicious choice in a dose of 600 mg on day
one followed by 300 mg per day for 20 days
(a 21 days course in all). DHE (Dehydroemetine) may be tried in cases resistant to
metronidazole therapy in a dose of 1 mg/kg/

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e. Multiple liver abscesses.

f. Presence of jaundice due to a large abscess
or abscess at porta hepatis.
When ALA is uncomplicated, metronidazole
alone as monotherapy is as effective as routine
needle aspiration combined with
metronidazole in management of ALA.

3. Role of surgery : Surgical intervention is

required in case of large abscess with poor
yield on needle aspiration and in complicated
ALA. Open surgical drainage carries a
significant mortality, hence it should only be

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371

used when the abscess has ruptured into the

adjacent viscera, particularly in bowel or
pericardium.

Complications
Inspite of the availability of highly effective drugs
to treat an ALA, complication(s) are frequently
encountered. The morbidity and mortality is high
in complicated ALA. Common sites for perforation
include pleuro-pulmonary (72%), subphrenic
space (14%), peritoneal cavity (10%), and
pericardial space.
Pericardial rupture, a dangerous complication of
ALA, is typically seen with left lobe abscess and
very rarely with right lobe abscess. It may cause
pericardial tamponade. The treatment consists of
prompt drainage of pericardial cavity through
subxiphoid route under USG guidance. Sometimes
surgical pericardiectomy may be required.
Peritoneal involvement can either be in the form
of free perforation with generalised peritonitis or
a localised perforation in the subhepatic area. The
best method of dealing with this problem is to do
laparotomy, peritoneal toilet, and drainage.
Though some authors have described good results
with conservative therapy with PCD of peritoneal
cavity.
Other less common complications are intra-biliary
rupture, rupture in stomach, duodenum, or colon.
Involvement of the hepatic veins and IVC either
by direct rupture or compression or thrombosis is
also described. In fact the ALA has been emerging
as an important cause of Budd Chiari syndrome
in reports originating from the Indian subcontinent.
The abscess can rupture through the parietal wall
on the abdominal skin and gives rise to chronic
granulomatous involvement of skin called
Amoeboma cutis. Metastatic abscess to brain are
also reported from ALA through blood stream.

Some unusual presentations of ALA

Many of the investigators have reported some
unusual presentations of this disease which must

372

be borne in mind. ALA may co-exist with hepatitis

A and hepatitis E infection, since all these diseases
are water borne and mode of transmission is
faeco-oral with similar epidemiology. Jain et al16
reported a case with simultaneous ALA and
hepatitis E. Incidentally, the patient was also an
HbsAg carrier. Schwartz et al17 observed two cases
of hepatitis A with ALA, thus emphasising the role
of dual infection in patients from endemic area.
ALA may present alongwith pregnancy. Though a
very rare occurrence, it carries significant morbidity
due to frequent delay in the diagnosis. Mabina et
al18 reported two cases of pregnancy with ALA.
Though jaundice is present in minority of the
patients of ALA, its presence creates a diagnostic
problem, and brings the possibilities of viral
hepatitis and intrahepatic obstruction. Sarda et
al19 reported a middle aged person who presented
with ALA in both lobes of liver, had obstructive
jaundice due to pressure on the porta hepatis with
stasis of the bile in intra-hepatic biliary radicals.

Summary and conclusion

It is evident from the above discussion that ALA is
emerging as the commonest extra-intestinal
manifestation of amoebiasis particularly in
endemic areas. The disease has its acute (benign
and aggressive) or chronic (benign and
accelerated) course as far as the duration and
severity is concerned. Patients who present with
fever, right upper quadrant pain, and are
immigrants from an endemic area, have a history
of alcohol intake and diabetes mellitus, warrant a
high degree of vigilance. The modern day
ultrasound and other non-invasive imaging
techniques alongwith serology have greatly
revolutionised the diagnosis of ALA and its long
term follow up. Despite advances in surgical
techniques, the entity is still largely managed
medically with metronidazole which is the drug of
choice.
The prognosis of ALA may be categorised as good
or poor, based on clinical, biochemical, and
sonographic parameters. A bilirubin level of >

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3.5 mg/dl, encephalopathy, a large volume of the

abscess cavity with hypoalbuminaemia (serum
level < 2gm/dl) are independent risk factors for
mortality.

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