CLINICAL MEDICINE JIACM 2003; 4(2): 107-11
Amoebic Liver Abscess
MP Sharma*, Vineet Ahuja**
The intestinal protozoa have gained importance during
recent years as a result of increasing world travel,
economic globalisation, and the growing number of
chronically immunosuppressed people. AIDS and the
increasing use of organ transplants have led to a new
population at risk for protozoal infection. Protozoa that
infect the gastrointestinal tract include the parasite
Entamoeba histolytica, Giardia lamblia the most common
cause of waterborne disease outbreaks, and the large
group of spore forming parasites (Cryptosporidia,
Cyclospora, Isospora, and Microsporidia) that share a green
algae symbiont and a predilection for causing chronic
diarrhoea in immunocompromised persons. Of these
intestinal protozoa, Entamoeba histolytica is one of the
most prevalent intestinal protozoa in developing
countries.
Amoebiasis is the infection of the human gastrointestinal
tract by Entamoeba histolytica, a parasite that is capable
of invading the intestinal mucosa and may spread to other
organs, mainly the liver. Entamoeba dispar, an amoeba
morphologically similar to E. histolytica also colonises the
human gut and has been recognised recently as a separate
species with no disease potential1-4. The acceptance of E.
dispar as a distinct but closely related protozoan species
has had a major implication in the epidemiology of
amoebiasis, since most asymptomatic infections are now
attributed to this non-invasive amoeba. E. histolytica
infection may have intestinal as well as extra-intestinal
manifestations (Table I).This review shall address amoebic
liver abscess which is the commonest extra-intestinal
manifestation.
Amoebic liver abscess
It is an inflammatory space- occupying lesion of the liver
caused by Entamoeba histolytica. The incidence of ALA has
been reported to vary between 3% and 9% of all cases of
amoebiasis5. In India ALA is endemic. The diagnosis of this
* Professor, ** Assistant Professor, Department of Gastroenterology,
All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110029.
condition has undergone major changes after the advent
of advances in imaging and molecular biology techniques.
This has also enabled a reappraisal of the disease with
recognition of the wide variety of clinical presentations
and multitude of complications.
Table I : Clinical syndromes associated with E.
histolytica infection.
Intestinal amoebiasis
Asymptomatic cyst passers
Acute amoebic colitis
- Mucosal disease
- Transmural disease
- Ulcerative postdysentric colitis
Appendicitis
Amoeboma
Amoebic stricture
Extraintestinal amoebiasis
Amoebic liver abscess
Perforation and peritonitis
Pleuropulmonary amoebiasis
Amoebic pericarditis
Cutaneous amoebiasis
It has been observed that the classical description of an
ALA needs to be modified due to a large number of
patients who present with variants6,7. This may be due to
a better understanding of the pathogenesis and
presentation of the disease or changing patterns of the
disease. Long-term follow up of patients has helped in
identifying the factors affecting the healing pattern.
Separation of patients at high risk is of clinical relevance
so that more aggressive treatment can be instituted.
Clinical presentation
Amoebic liver abscess occurs most commonly in the age
group of 20 to 45 years. It has been noted infrequently at
the extremes of age and is seven to nine times more
common in males. ALA may present as an acute process
or as a chronic indolent disease. It has been classified by
the duration of illness and severity into :
i. Acute Acute benign
Acute aggressive
ii. Chronic Chronic benign
Chronic accelerated
Most patients present with an acute illness and duration
of symptoms less than 2 weeks. The main presenting
features are abdominal pain, fever, and anorexia.
Abdominal pain is usually moderate and localised to the
right upper quadrant or to the epigastrium. Diffuse
abdominal pain, pleuritic chest pain, and radiation of right
upper quadrant pain to the right shoulder are not
uncommon. Epigastric pain is commonly seen in left lobe
abscesses. Fever is of moderate degree in most instances,
while high fever with chills is suggestive of secondary
bacterial infection. Cough with or without expectoration
and pleuritic chest pain is also seen in ALA.
During the course of illness one-third of patients may
develop clinical jaundice. Severe icterus is usually due to
a large abscess or multiple abscesses, or to an abscess
situated at the porta hepatis8. Jaundice raises diagnostic
problems and brings in the possibilities of intra-hepatic
obstruction or viral hepatitis. Diarrhoea and weight loss
are not commonly seen. Unfortunately diarrhoea is such
a common complaint in the tropics that it may not be
given adequate consideration by the patient. Tender
hepatomegaly is detected in upto 80% of patients. The
liver surface is generally smooth. Upper abdominal
guarding and rigidity is seen in a minority of cases with
features of generalised peritonitis. Toxaemia and
septicaemia may be present.
However, it is the protean manifestations of the variants
that may be a source of consternation to the clinician. A
left lobe abscess may manifest as toxaemia, deep jaundice,
and encephalopathy. Ascites developing in a patients with
ALA suggests development or presence of inferior vena
cava obstruction, and cough with copious expectoration
suggests rupture into the communication with the right
lower lobe bronchus.
108 Journal, Indian Academy of Clinical Medicine
Variants9
ALA usually occurs in the right lobe of the liver and is
solitary (30% - 70%). Unusual presentations include
multiple abscesses, left lobe abscesses, abscesses
presenting as compressive lesion, and abscesses rupturing
into viscera. These are clinically important due to the
curable nature of this disease and potentially fatal
outcome in untreated abscesses.
Multiple liver abscesses : Fifteen per cent of patients may
have multiple abscesses.They present with fever, toxaemia,
deep jaundice, and encephalopathy. Toxaemia is
suggestive of an added bacterial infection leading to a
more severe disease. E.coli and Klebseilla are the
commonly cultured organisms. These patients present
with a clinical picture indistinguishable from hepatic
encephalopathy due to acute hepatocellular failure.
Hepatic encephalopathy in ALA patients possibly results
from combination of right hepatic vein occlusion,
pylophlebitis, and occlusion of several portal vein
radicles10,11.
Left lobe abscess : Thirty-five per cent of patients present
with a left lobe abscess. Half of these have associated
lesions in the right lobe while the remaining have solitary
left lobe abscess12. These patients have longer duration of
symptoms (3-4 weeks) and fever is less commonly
observed as compared to right lobe abscesses. It may
present as a large epigastric mass with minimal movement
with respiration. Often, to the clinicians despair, it has been
confused with pseudocyst of pancreas. These patients also
have weight loss with poor hepatic localisation of
symptoms. Complications like peritonitis and toxaemia are
significantly more common in left lobe abscess. Needle
aspiration may be more rewarding in combination with
anti-amoebic drugs. A high index of suspicion and early
diagnosis are important for proper management.
Compression lesions : A posteriorly located ALA in the
right lobe may present as inferior vena cava
obstruction or hepatic outflow obstruction13. This is
suggested by bilateral pedal oedema, ascites, visible
veins on anterior and posterior abdominal wall, along
with clinical, radiological, and serological features of
ALA. These features disappear after aspiration of the
abscess.

Vol. 4, No. 2
April-June 2003
Extension of the abscess : Leakage of the abscess may
occur into the pleural cavity, with empyema thoracis. Intra-
abdominal extension following perforation into the
peritoneal cavity is usually associated with shock and
generalised peritonitis and may occur in upto 7% of cases.
Rupture into the colon and biliary tree has also been
reported. A subhepatic collection may also be localised
and walled off. Such presentations have however been
rare and form a small number of cases in any series in ALA.
The above clinical patterns have been described more
frequently with the routine availability of ultrasound and
serological assays. These clinical variants are important
because of their therapeutic and prognostic significance
with the best outcome occurring in patients with solitary
abscess.
Diagnosis
Ultrasound is very useful for diagnosis of amoebic liver
abscess. The classic appearance is a non-homogeneous,
hypoechoic, round or oval mass with well defined borders.
Complete resolution of an amoebic liver abscess may take
upto two years. Occasionally, percutaneous diagnostic
needle aspiration may be needed to differentiate between
amoebic and pyogenic liver abscess.
Serology : Serum antibodies to amoebae develop only
during E. histolytica infection and not during E. dispar
infection.The absence of serum antibodies to E. histolytica
after 1 week of symptoms is strong evidence against the
diagnosis of invasive amoebiasis of the colon or liver.
Serum antibodies to amoebae are detected in 85-95% of
all patients who present with invasive amoebiasis or liver
abscess. However, as antibodies persist for many years,
ELISA or IHA cannot differentiate acute from remote
infection in areas of high endemicity. Purified native and
recombinant parasitic antigens have been utilised in
serological studies with good results. More than 95% of
the patients with amoebic liver abscess have serum
antibodies to the 170 KD subunit of the galactose
inhibitable adherence lectin.This antigen is highly specific
for differentiating acute phase serum from convalescent
phase serum in areas of high endemicity.
Newer methods : Newer diagnostic strategies involve
detection of protein antigens in faeces or serum by
Journal, Indian Academy of Clinical Medicine
Vol. 4, No. 2
monoclonal antibodies and detection of parasitic DNA by
use of nucleotide probes and PCR amplification. A
commercial ELISA kit that uses monoclonal antibodies
directed against an amoebic adherence lectin and
accurately differentiates the true pathogen E. histolytica
from E. dispar has recently been developed for clinical
use14. Detection of amoebic lectin antigen in serum
samples from patients with amoebic liver abscess is also
more than 95% sensitive if used prior to treatment with
metronidazole.
Medical therapy
Medical therapy may be instituted using either a single
agent or a combination of drugs for the extra-luminal
parasite. Amoebicidal drugs(Table II) may be classified into
3 groups : luminal, tissue, and mixed amoebicides.
Duodohydroxyquin, diloxanide furoate, and paromomycin
are luminal amoebicides. The amoebicides effective in
tissues are emetine and dehydroemetine, which act in the
liver, intestinal wall; alongwith chloroquine which acts only
in the liver. Emetine and dehydroemetine because of their
cardiotoxicity are currently not used. Amoebicides
effective in both tissues and the intestinal lumen include
nitroimidazole derivatives-metronidazole, tinidazole, and
ornidazole. They are the drugs of choice in invasive
amoebiasis. Oral or intravenous metronidazole or
tinidazole also leads to rapid clinical improvement of
amoebic liver abscess15. This drug should be followed by
a luminally active drug.
Table II : Pharmacotherapy for E. histolytica infection
in adults.

Intraluminal Diloxanide furoate 500 mg tid X 20 days
infection Paromomycin 30 mg/kg/day X 10 days
(in 3 divided doses)
Iodoquinol 650 mg tid X 20 days

Invasive Metronidazole 800 mg tid X 5 days
colitis Tinidazole 1 gm bd X 3 days

Amoebic Metrinidazole 800 mg tid PO X 10 days
liver abscess (500 mg qid IV)
Nitroimidazoles (including metronidazole) are effective
in over 90% of cases. Therapy should continue for at least
10 days. Relapses have been reported with this duration
of therapy and the drug may be administered for upto 3

April-June 2003 109
weeks. The dose of metronidazole is 40 mg/kg/day in
divided dosages. Tinidazole has been used in a dosage of
1.2 g per day for 7 days , but this dosage has not been
firmly established. Chloroquine, emetine, and
dehydroemetine may also be used. Single-agent therapy
with metronidazole yields excellent results and the
alternative toxic drugs are indicated rarely and used
mostly in seriously ill patients when the risk of failure of
therapy is unacceptable. The response to anti-amoebic
drugs is usually evident within 48-72 hours with the
subsidence of toxaemia, abdominal pain, anorexia,
jaundice, guarding, and tenderness in the right
hypochondrium, and hepatomegaly.
Aspiration or drainage of abscess
Routine aspiration of liver abscess is not indicated for
diagnostic or therapeutic purpose16. A combination of
ultrasonographic finding with a positive serology in the
appropriate clinical setting is adequate to start drug
therapy. Aspiration has been indicated in the following
circumstances: lack of clinical improvement in 48-72 hours,
left lobe abscess, thin rim of liver tissue around the abscess
(< 10 mm) and seronegative abscesses17. The aspirate is
anchovy sauce type in half of the patients. The chocolate
colour is due to admixture of blood with liver tissue.
Anti-amoebic therapy alone is as effective as routine
needle aspiration combined with anti-amoebic therapy
in the treatment of patients with uncomplicated amoebic
liver abscess18,19.
Surgical intervention
Open surgical drainage is rarely indicated and may be
required in the setting of a large abscess with a poor yield
on needle aspiration or clinical deterioration despite
attempted needle aspiration, and in complicated ALA.
Surgical mortality is, however, very high. Hence, it should
only be used when the cavity has ruptured into adjacent
viscera or peritoneum.
Long term follow-up
After clinical cure, patients show few symptoms and
sonographic follow-up demonstrates evidence of
persistent hypoechoic lesion 20 . The mean time for
110 Journal, Indian Academy of Clinical Medicine
disappearance of the sonographic abnormality is 6-9
months. Relapses are very uncommon and the
sonographic abnormality does not warrant continued
therapy. The patterns of resolution that have been seen
on sonographic follow-up include: type I, where complete
disappearance of the cavity occurs within 3 months
(29.8%); type II, where a rapid reduction till 25% of the
original cavity size and then a delayed resolution occurs
(5.9%).
Factors influencing healing time include the size of
abscess cavity at admission, hypoalbuminaemia, and
anaemia. The type of clinical presentation, nature of
therapy, number or location of abscesses, and time for
clinical resolution of multiple liver abscesses are similar
to those of solitary abscess and the number of abscesses
does not significantly influence the healing patterns or
rates. The total abscess volume of all the cavities is the
most important factor that influences resolution time in
multiple abscesses. As clinical resolution does not
correlate with ultrasonographic resolution, therefore
clinical criteria, rather than ultrasonography, should
monitor the result of therapy.
Prognostic markers
There are two major categories of patients with ALA: those
with a good prognosis and those with a poor prognosis.
These groups can be easily identified by evaluation of
clinical, biochemical, and sonographic criteria. Bilirubin
level > 3.5 mg/dL, encephalopathy, volume of abscess
cavity, and hypoalbuminaemia (serum albumin level < 2.0
g/dL) are independent risk factors for mortality21. The
duration of symptoms and the type of treatment do not
influence mortality.
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