pericarditis, although less common, is the most dangerous
complication of amoebic liver abscess.1 In 1790 Joaquin Pio Eguia y
Moro2 of Mexico City, by describing
"a pericardial cavity which was full of pus coming
from the liver abscess" was the first to report the
necropsy finding of this condition. Much later in 1860
Rouis3 also described the
necropsy finding of a similar case and this is
erroneously considered to be the first case.
Similarly although Germilton4 in 1899 is credited with
having made the first clinical diagnosis, it was Miguel
Jimenez5 also from Mexico, who in 1859 made
the first clinical diagnosis of a liver abscess rupturing
into the pericardium which was confirmed at autopsy.
In majority of the cases, this is a complication of
the left lobe superior surface amoebic liver abscess.1 Its occurrence is so rare
that it accounted for only 2.8% of 689 cases of ruptured
amoebic liver abscesses reported by Vergoz and Hermanjat
Carter and Korones7 reported a case in 1950 and
could find only 58 published case reports since 1885.
Macleod et al8 found 34 additional cases reported
from 1950 to 1965. To these they added 25 cases of their
own, diagnosed over a period of 3 years in South Africa,
where they treated 500 cases of amoebic liver abscess
every year. Carter and Korones7 analysed 44 proven cases
from the literature and found that only in two was a
correct diagnosis made prior to autopsy. In 1972, we9 reported six cases which
did not include any case from post-mortem series. Adams,1 in 1975,
presented 27 cases at the International Conference on
Amoebiasis in Mexico. Quijano Pitman et al,10 in the same conference,
presented 35 proved cases, 25 of the suppurative, while
the others of non-suppurative variety.
Till 1976, only 132 patients with amoebic pericarditis
had been reported in the published literature; of these
109 were suppurative and 23 non-suppurative.11
Although amoebic pericarditis can occur at all
ages, patients in the first,10 fourth and fifth decades
are the most vulnerable. As in amoebic liver abscess,
here too there is a clear predominance in males.
Watson et al12 quoted 5 cases
of amoebic pericarditis as a complication of the right
lobe amoebic liver abscess and added a sixth case of
their own. On careful analysis of all above cases and
based on my experience, I strongly feel that in most of
these cases, there were two abscesses-one in the right
lobe and the other in the left lobe. So common is this
occurrence that in our series of pericardial amoebiasis,
we found 33% of patients having a second abscess in the
right lobe.9 Thus, we conclude that in their
series the right sided thoracic complications were due to
a right lobe abscess and the pericardial complication due
to a left lobe abscess. It is obvious that in the above
cases, liver scanning was not done. It was also not well
recognised in the past that if one abscess is aspirated,
the second may not need aspiration and may respond to the
drugs only. Therefore, though it is not impossible for a
huge "right lobe" abscess, 1 or a junctional superior
surface abscess (as described in an earlierchapter), to
produce a pericardial complication, it is quite a rare
occurrence. In the series of amoebic pericarditis of
Tyagi et al, 13 two cases at autopsy had
non-suppurative sympathetic pericardial effusion, with
amoebic abscess occupying the whole of the right lobe of
the liver. In fact very rarely the infection can spread
from an amoebic lung abscess or an empyema into the
pericardium to produce amoebic pericarditis.1,14,15
Of 47 cases of amoebic suppurative pericarditis
reported by Takaro and Bond16 only two survived. Norris
and Beemer17 collected 47 examples of
suppurative pericarditis with only two survivors. In
Lamont and Pooler's series, five out of seven patients
with pericarditis died.18 Paulley19 reported mortality rate of
67%. In our series, of 6 cases reported in 1972, 2 died
(33%).9 Adams' reports fatality
rate of 29.6%. Thus, this complication still carries a
very high mortality rate, often because of delay in the
diagnosis. Of eleven cases of Carlos Ibarra Perez et al,20 eight patients died. In six
of these patients, the diagnosis was made at post-mortem.
In the series of Tyagi et al13 fifty percent cases were
diagnosed at autopsy.
Inspite of the patients being diagnosed and treated in
time and pericardial aspiration also being undertaken,
some patients still die for no obvious reason.14 In one of the
patients of Kulpati et al,11 where more than 800 ml. of
amoebic pus was aspirated from the pericardium on four
occasions, only 200 ml. more of thick fluid was found in
the pericardial cavity at autopsy. It is thus not
surprising that they postulated ultra-microscopic changes
in the myocardium resulting in sudden death from cardiac
arrythmia as a possibility. In the case reported by Datey
et al,21 varieties of tachy and
brady-arrythmias were recorded in the intensive care unit
before the patient died of ventricular fibrillation at a
time when he seemed otherwise to be progressing well.
However, the most common cause of death is acute
pericardial tamponade which could occur due to sudden
rupture of the liver abscess. In such an event the
diagnosis is usually missed.
TYPES OF AMOEBIC PERICARDITIS
There are four types of amoebic pericarditis-
or purulent type - this can further be subdivided
into (a) with acute onset, and (b) with gradual onset.
or non-suppurative type - this can be subdivided into
that with (a) acute onset, and (b) gradual onset.
Constrictive amoebic pericarditis.
All four types can
be further subdivided into-
associated left pleuropulmonary amoebiasis 9,14
associated left pleuropu!monary amoebiasis.
1. Suppurative or purulent
This term is a misnomer. It should ideally be termed
as pericardial amoebiasis with secondary infection. The
latter follows pericardial tapping where the first
aspirate is odourless chocolate coloured pus and the
second aspiration shows change in colour either to
yellowish white or green and it may also be foul
smelling. The importance of diagnosing such cases is to
give them additional antibiotics for secondary infection
(preferably selecting the right antibiotic after doing
the culture and sensitivity of the pus). Such patients
should always be advised open pericardial drainage or
The usual suppurative amoebic pericarditis is the one
which I would label as pericardial amoebiasis rather than
amoebic pericarditis. The latter term implies
inflammation of the pericardium. Often amoebic abscess of
the left lobe empties its chocolate coloured pus into the
pericardial sac (Figs. 86 a,b). There is no true inflammation.
(a) Acute onset type. Here sudden rupture
of an amoebic liver abscess into the pericardium may
result in a very severe shock and death within hours.
Such cases can present with sudden retrosternal pain and
shock with a previous history of epigastric pain and
fever of few days' duration. Miguel Jimenez described
such a clinical picture in his original case.5 Rarely the chest symptoms
are the first to appear. 21 Unless shock is
treated well and a quick pericardial tapping is done,
most of these patients die of pericardial tamponade and
(b) Gradual onset type. This is a more
frequent presentation10 wherein patients come with
symptoms similar to tuberculous pericarditis.1 Often a
fistulous tract between the liver abscess and the
pericardium is formed. Rarely the fistulous tract may not
Fever is a common symptom and often the patient is
thought to have P.U.O. In addition the patient has a
combination of symptoms of left lobe amoebic liver
abscess, pericardial effusion and often symptoms of left
pleuropulmonary amoebiasis. History of pain in the left
shoulder at the time of admission or a few days earlier
must be elicited. In patients with symptoms of left chest
pain and cough with expectoration, history of chocolate
coloured sputum may assist in the diagnosis. On
examination, in addition to usual signs of pericardial
effusion, such as pulsus paradoxus, increased cardiac
dullness, distant heart sounds, engorged neck veins,
enlarged tender liver, etc., presence of a lump in the
enlarged left lobe may be a pointer to the diagnosis.
However, often the lump is not seen and the bulging left
lobe is flattened after the abscess has ruptured into the
In a patient diagnosed as pericarditis with effusion with
positive E.C.G. and X-ray appearances, one or more of the
following features may help in pointing to its amoebic
- Presence of
unusual tenderness in the right lobe or an
elevated immobile right dome of the diaphragm.
(These signs are due to presence of a second
abscess which is not uncommon in patients with
left lobe abscesses).
- Presence of a
lump in the epigastrium in the enlarged left lobe
of the liver.
- Pain in the
left shoulder with or without an elevated
immobile left dome of the diaphragm. This finding
on X-ray chest has been recorded in a case report
as early as 1946.22 Chest X-rays taken
earlier during the illness (P.U.O.) must be
scrutinised. Often the left dome is elevated in
earlier X-rays (Figs. 87 a,b) and may get flattened after
the abscess ruptures into the pericardium.
- Presence of
icterus is a useful sign. This would also be the
case when patient harbours two abscesses.
- Ideally liver
scan and serological tests for amoebiasis should
be done in all suspected cases. With these two
investigations, diagnosis should be easy. I.H.A.
test, if done, is almost invariably positive.
Rarely, it can be negative as in one of the cases
reported by Kulpati et al.11
there are some patients whose general condition
may be so poor that one is unable to wait for the
above investigations. In such an emergency,
urgent therapeutic pericardial tapping should be
done. The condition should be suspected if,
instead of straw coloured fluid of tuberculous
pericarditis, a chocolate coloured or brownish
fluid is aspirated. Blood stained fluid if
aspirated is more in favour of tuberculous or
malignant etiology, though it has been reported
in amoebic pericarditis as well.21 The patient should
at once be put on injection emetine and
metronidazole. Although Pitman et al10 state that it is
possible to identify trophozoites in about half
the cases, E. Histolytica cannot commonly be
demonstrated in the pericardial fluid. Upto now
these have been seen in 9 cases.22
Adams' recommends the use of atleast two amoebicides
in combination. In his series, patients treated with a
combination of amoebicidal drugs had a much lower
mortality as compared to those treated with only one
In addition to medical treatment, frequent pericardial
aspirations should be done and as much pus as possible
should be removed.
Tapping of the left lobe is not always necessary. This is
because the left lobe abscess has more or less emptied
its contents into the pericardial sac. However, if any
bulging is seen or an enlarged left lobe is felt in the
epigastrium, no time should be lost in tapping the left
If there is associated left pleural amoebiasis, left
pleural cavity should also be tapped. If there is
additional tenderness of the right lobe, needling of the
right lobe should also be done, the site depending on
whether right dome of the diaphragm is markedly raised or
not. These are not major problems if liver scanning
reports are at hand. At times the pus in the pericardial
cavity is so thick that very little or none can be
aspirated. In these cases one should at once resort to
open drainage of the pericardium and left lobe abscess,
non-suppurative amoebic pericarditis
As discussed elsewhere, an amoebic abscess can
produce sympathetic effusions in pleural, pericardial or
peritoneal cavities depending on the site of the abscess.
An abscess in the superior surface of the left lobe can
produce sympathetic effusion in the pericardial cavity.
Most of the authorities23 with experience in this
field hold the view that these effusions are harmless.
Wilmot,24 Lamont and
Pooler18 and Laha23 have well documented the
above entity of non-purulent pericardial effusion with
E.C.G. changes. According to them the importance of this
clinical sign is that it serves as a warning of the
proximity of the abscess to the pericardium and
possibility of a frank rupture of the former into latter.
Most of these effusions disappear with the management of
the liver abscess. In my experience, although this is the
usual outcome, I have encountered a case where cardiac
tamponade was produced by a huge sympathetic pericardial
effusion and the patient would have died if timely
pericardial tapping had not been done (Figs. 88 a,b). In the series of Tyagi et al,13 two patients at autopsy had
non-purulent amoebic pericarditis. Therefore, though the
term "sympathetic" implies this complication to
be benign, it is not always safe to treat these patients
with any less enthusiasm.
In fact one cannot diagnose sympathetic pericardial
amoebiasis without aspirating the pericardia cavity. (We
have also seen patients where we have confirmed in
retrospect that there was pericarditis which disappeared
with treatment of the abscess.)9 We have also observed at
operation one part of the pericardial cavity having
sympathetic effusion and the other part having amoebic
pus (Fig. 89).
The aspirated pericardial fluid is clear and straw
coloured. On chemical analysis it is usually an exudate.
No centre in the world has had enough experience in
judging the management and the prognosis of this
condition. However, I feel that if this fluid remains
long enough in the pericardial cavity, it could lead to
constrictive pericarditis due to its high content of
proteins and fibrinogen. Therefore, it is hazardous to
wait too long for its resorption.
III. Constrictive amoebic pericarditis
We have not seen a single case of constrictive
amoebic pericarditis, although we have followed up a case
of amoebic pericarditis for seven years. Davis,25 who has followed up a case
for 11 years doubts the existence of this entity.
However, Lamont and Pooler18 have described such cases
which developed constriction over a period of few weeks
to few months. Wilmot24 has also
detected identical cases. He concludes that constrictive
pericarditis may follow amoebic suppurative pericarditis,
but it is yet uncertain whether secondary bacterial
infection of the amoebic pus is necessary for it to be a
When constriction has occurred, surgery should be delayed
as long as possible, for it is not a true fibrosis and
resolution is sometimes possible with conservative
IV. Amoebic hydropneumopericardium
We have seen two such cases upto date. In one case it
was not significant (Fig 90) because it fol|owed a
pericardial tapping In the other case, it occurred as a
complication of gastropericardial fistula (Fig 91 ) resulting from a huge left lobe
liver abscess This patient died. Thus, this is a dreaded
complication of !eft lobe liver abscess Such a case has
also been described by Adams.'
it may be stated that good results can be achieved by
being aware that amoebic pericarditis may masquerade as
pericarditis, heart failure or both together with
inconspicuous signs related to the liver. Vigilance with
regard to the onset of pericardial complication, use of
diagnostic aids such as serological tests and liver
scanning and relief from cardiac tamponade, preferably by
needle aspiration, have markedly reduced the mortality
rate in the recent years1
E B. Proc. Internat. Conf. on Amoebiasis, 1975,
830 Ed. by Sepulveda, B. and Diamond, L S.
Instituto Mexicano Del Seguro Social, Mexico,
y Moro, J P. Disertacion sobre Las obstruociones
inflamatorias del higado, Mexico, 1972, as quoted
(1860) as quoted by Vergoz, P. and
Hermanjat-Guerin, R P. 1932.
W. (1899) as quoted by Fiegal (1959).
M F. Clinicia Medica, Abscecso del higado Union
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P. and Hermanjat-Cuerin, R P. (1932), as quoted
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M G. and Korones, S B. New Eng. J. Med., 1950,
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O P. and Shah, N A, J. Trop. Med. Hyg,, 1972, 75,
Pitman, F. Flamand, E, et al, Proc. Internat
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D D, Venkatachalam C G. et al, J. Ass. Phys.
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R B. Am J. Trop. Med. Hvg.. 1972.
S K, Anand, I S. et al, Paper read at XXXIXth
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D V, Poornachandra Rao, Y. et al, as quoted by
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T. and Bond, W M, Surg Gyn. Obst. (l A S. ),
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D L, and Beemer, A M, J. Trop. Med. Hyg., 1956,
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Ibarra Perez, Leon Greens, et al, J. Thor C V S.
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K K, Parikh, C S. et al, Bom Hos J., 1978 20, 34
Singh, Ind. Med. Gaz., 1946, 81, 299.
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F W. Trans Fifth Surg Ass, 1948, 60, 344