amoebiasis has been cited with evidence as far back as
1903.1 Since then, thoracic complications
of amoebiasis are being diagnosed more often and reported
with impressive frequency.
Pleuropulmonary amoebiasis is the third most common
manifestation of amoebiasis in the body after amoebic
colitis and liver abscess. It is probably the most
important complication of amoebic liver abscess. The data
on the incidence according to some authors is as follows
(before hepatic scintigraphy and serological tests were
||% of pleuro pulmonary
|Ochsner and DeBakey2,3
|Hughes and Westphal4
|(a) Autopsy proved cases
|(b) Patients with hepatic
explanation for the marked difference in observations by
different authors may be because:
- the cases
selected were from clinical series only,
post-mortem series only or both.
- the criteria
for diagnosis of pleuropulmonary amoebiasis were
different in all series.
Pathology and pathogenesis
Pleuropulmonary amoebiasis may be primary or
At present, the term 'primary' lung involvement simply
denotes the absence of liver amoebiasis. This could
result from haematogenous7-9 or Iymphatic
spread directly from the storehouse of intestinal
'Secondary' pleuropulmonary amoebiasis always follows
manifest or occult amoebic liver abscess.
Strictly speaking, a 'primary' lung lesion should imply
infection of the lung by E. Histolytica in the absence of
either hepatic or even an intestinal lesion caused by the
same strain of the organism.8 This is a matter of dispute
and according to DeBakey10 and Wilmot8 such a concept is difficult
to prove. (If it does exist, then the term 'primary' used
currently should be labelled as 'secondary' and the term
'secondary' as 'tertiary' pleuropulmonary amoebiasis.)
Since this monograph is restricted to amoebic liver
abscess and its various manifestations, the discussion
which follows is almost exclusive of secondary
Mode of spread
How does E. Histolytica travel from a liver abscess
to involve the lung and the pleura? An embolic origin has
been suggested.11,12 This would explain patients
with bilateral lung lesions. Takaro13 has suggested invasion of
the lung by Iymphatics from a focus beneath the
diaphragm. These methods of spread, if they do occur,
must be rare. The most common mode of spread appears to
be direct by rupture through the diaphragm.14 'Erosion' with migration of
E. Histolytica along the adhesions has also been
Rogers14 suggested rupture of
amoebic Iiver abscess as a probable method of spread (Fig. 38). Whether an abscess ruptures into
the pleural space or directly into the lung depends on
the extent of adhesions between the lung, pleura and
Although a subphrenic amoebic abscess rupturing through
the diaphragm to involve the lung and pleura has been
described,15 this must be very rare as
usually extension of an abscess through the capsule of
the liver is preceded by the formation of adhesions
between the liver (Fig. 39) and the diaphragm. Thus,
local or general peritonitis is avoided and the chances
of a superior surface abscess rupturing into the
subphrenic space to cause a subphrenic abscess become
In other cases frank perforation may riot be present7 and the diaphragm is firmly
adherent to the under surface of the lung. The abscess
may slowly erode these adhesions. Here, by virtue of the
cytolytic and histolytic properties amoebae may set up
new lesions-giving rise to the 'collar stud'7 or 'collar button'
abscesses in the lung. These may occasionally occur at a
surprisingly long distance from the diaphragm. Figure 40 shows a lung abscess at a
considerable distance from the hepatic shadow an attached
to it by a linear strand.16
A superior surface liver abscess is one, which is
most prone to cause pleuropulmonary involvement. As the
abscess extends- upwards the inflammatory process
involves the diaphragm and later the overIying pleura to
cause pleuritis. This is followed by a sympathetic
pleural effusion.17,18 Adhesions between the two
pleural surfaces may form later. The underlying amoebic
liver abscess may rupture into the pleural space to cause
an empyema.18,19 This is especially true if
rupture takes place before extensive adhesions between
the two pleural surfaces have occurred (Fig. 41). Since some adhesions have
invariably formed, the empyema is often localised. It
extends more vertically and laterally than along the base16 (Figs. 42 a,b). This empyema may secondarily
involve the underlying lung or empty into a bronchus
forming a broncho-pleuro-hepatic fistula.2,20,21 Pyopneumothorax,
Pneumothorax and even haemothorax may also rarely occur.
On the other hand, when the two surfaces of the
diaphragmatic pleura are extensively adherent, the liver
abscess may either rupture directly into the lung (Fig. 43) or a bronchus,22.214.171.124.22 or E. Histolytica may
migrate along the adhesions as described earlier.
Invasion of lung-parenchyma by E. Histolytica leads to
the development of interstitial pneumonitis. With the
formation of inflammatory exudate and migration of E.
Histolytica into the spaces, consolidation of that part
of the lung soon follows. The organisms, exerting their
histolytic action cause liquefaction resulting in the
formation of a lung abscess.7-9,23 This abscess may rupture
into a bronchus thus establishing a broncho-hepatic
A broncho-hepatic fistula may, therefore, occur in one of
the following ways:
- Rupture of an
amoebic empyema into a bronchus.
- Rupture of a
liver abscess directly into a bronchus.
- Rupture of a
resultant amoebic lung abscess into a bronchus.
Often the abscess
and/or empyema have been emptied of their contents by
coughing 2,18,20,21 Bilious fluid is sometimes
expectorated. This is due to formation of a rare
bilio-bronchial fistula where a connection between the
broncho-hepatic fistula and the biliary system of the
liver is established.
The fate of
With prompt and adequate treatment resolution of the
lesion is the rule. In other cases sequelae may occur.
Formation of diaphragmatic adhesions has been described.
Residual persistent fibrosis, cavity formation etc.,
which at a later stage may result in bronchiectasis in
the affected segment8,12 have also been documented.
A granulomatous mass may form-known as amoeboma of the
lung.23 It may present as a coin
shadow. Thickened pleura often follows pleural
To sum up, pleuropulmonary amoebiasis can be classified
pulmonary abscess without liver involvement;
pulmonary abscess and independent liver
involvement (Figs. 44, 45a,b,c);
abscess from liver abscess;
fistula with minimal pulmonary involvement; and
extending from a liver abscess.
Clinical features of
'right' sided pleuropulmonary amoebiasis
In the following discussion only those criteria by
which one suspects an amoebic etiology and the method of
establishing the diagnosis are presented. No attempt is
made to give detailed accounts of the clinical
manifestations of pleural effusion, lung abscess or any
of the numerous forms of amoebic involvement of the lung
and pleura. Left sided pleuropulmonary amoebiasis is
discussed in a later chapter.
The patients with pleuropulmonary amoebiasis are
predominantly in the third or fourth decade although
other ages are not exempt.12,20 In keeping with the sex
incidence of amoebic liver abscess, this condition also
occurs predominantly in males who account for about
85-95% of the patients.18
It is easy to suspect and diagnose pleuropulmonary
involvement in known cases of amoebic liver abscess when
they complain of pain in the right lower chest or right
shoulder. The same holds true for such patients if they
start getting a dry cough, or associated expectoration of
chocolate coloured sputum with or without preceding
haemoptysis. The sputum may sometimes be greenish yellow
and foul smelling.16 These patients usually show
other symptoms of infection such as a septic type of
fever with or without chills, anorexia, malaise, weakness
and loss of weight. On examination the right side of the
chest may show signs of fluid in the pleural space.
Tracheal shift, however, is minimal, probably because of
adhesions. In others, signs of consolidation with or
without colIapse may be present.
The difficulty in establishing amoebic etiology, however,
arises in patients who neither have symptoms suggesting
amoebic liver abscess nor a tender palpable hepatomegaly.
The most important prerequisite in the diagnosis of such
cases is a high index of suspicion. This is especially
true in countries where amoebiasis is endemic. The
physician should always be aware of a possible amoebic
etiology in a wide spectrum of respiratory illness. In
fact pleural effusion or lung abscess at the right lung
base should be looked upon with suspicion in our country.
Based on my experience, the criteria which aid in
establishing a possible amoebic etiology, are as follows:
- Past history
of dysentery or diarrhoea should make one highly
suspicious of a probable amoebic etiology.
However, absence of such a history does not
exclude pleuropulmonary amoebiasis. 16
- Localised pain
and tenderness over the liver area, however
minimal or insignificant, is also highly
suggestive. If the patient also complains of
right shoulder pain25,26 or hiccough
suggesting diaphragmatic irritation, one should
keep in mind the possibility of amoebiasis.
sputum (Fig. 46) especially in a
patient with clinical evidence of pathology in
the right lung base should always suggest the
diagnosis.6 Initial haemoptysis
often precedes expectoration of dark reddish
brown sputum in which E. Histolytica may
sometimes be demonstrated.8 Sometimes sputum
becomes greenish yellow and foul smelling because
of secondary infection by aerobic or anaerobic
organisms, as well as admixture with bile
(biloptysis). D'Abrew27 has observed
typhoid bacilli to be the most common organism
causing secondary infection in pleuropulmonary
- In pleural
effusion, especially of the right side, an
aspirate may show high protein content with
innumerable pus cells, but without organisms.
Aspiration if repeated after a few days may often
be rewarded with appearance of brown or
greenishyellow pus, diagnostic of a liver abscess
rupture resulting in an empyema.16 Examination of the
purulent material may show vegetative forms of E.
- Presence of
liver cells in the pleural aspirate or in the
sputum is a valuable indirect evidence of amoebic
- In a chest
X-ray of a case with right sided pleural effusion
or other lung pathology, if the right dome of the
diaphragm is raised or has any of the
characteristics described in Chapter 3, Section
IV, it is highly suggestive of amoebic liver
- Lastly, if a
case with effusion on the right side diagnosed as
tuberculous, does not respond to the usual
anti-tuberculous drugs, amoebiasis should always
be ruled out.16,28
However, in spite
of all this, sometimes the diagnosis is so difficult that
the real pathology is revealed only on the operation
table. This happened in four of our cases i n the days
when liver scan and serological tests were not available.16
As most investigations done are the same as in
amoebic liver abscess only a few pertinent points need to
be mentioned below.
Demonstration of E.
This, although diagnostic, is demonstrable only in
one fourth of the patients.9 The sputum,
aspirated fluid and also the stools should be examined.
Often the aspirate does not show the parasite. In the
sputum, E. Histolytica has to be distinguished from E.
Gingivalis, the latter being an oral commensal. For
positive identification, iron haematoxylin stained
preparations should be examined especially for
In a lung abscess bronchoscopic aspirates should be
examined. Rarely a lung biopsy may be done to look for E.
Histolytica in tissue sections.13
Since the lung is adherent to the diaphragm the
collection of pleural exudate may be more lateral than
basal (Fig. 42a & 42b) or the fluid may be
loculated only in the supradiaphragmatic region (Fig. 47). A massive pleural effusion may be
present without a significant tracheal shift16 (Fig. 48).
A lung abscess will show as a typical shadow (Figs. 49 a, b) with or without a fluid level
depending on whether or not the abscess has ruptured into
Schorr29 has also described a string
like shadow proceeding from a localised bulge of the
diaphragm to a pneumonic shadow in the lung. This was
seen in one of our cases (Fig. 50).
Obliteration of the costophrenic angle due to pleural
reaction (Fig. 51) and a triangular shadow from the
hilum of the lung8,13 extending upwards (Figs. 52a, b, c) are quite common.16
Pneumoperitoneum may be useful; at times the track from
the liver to the lung can be demonstrated (Fig. 53)16
Rarely a bronchogram, if done, may show a
supradiaphragmatic abscess (Fig. 54). Pyopneumothorax may be seen if the
lung abscess has burst into the pleural space'6 (Fig. 55).
Liver scan and serology
Now-a-days the diagnosis of pleuropulmonary
amoebiasis has been made easy by investigations such as
liver scan and serological tests for amoebiasis. If liver
scan shows a cold area and the serological tests are
positive, the lung or pleural pathology under
investigation is most likely to be amoebic in origin.
Lastly, if any lung or pleural pathology responds
rapidly to anti-amoebic treatment, it must in all
probability be pleuropulmonary amoebiasis.
Prognosis and mortality
The prognosis, at present, for a patient with
pleuropulmonary amoebiasis is very good. With prompt
diagnosis and speedy institution of adequate therapy, no
patient should be allowed to succumb to the disease.
Recovery is rapid in patients with a bronchohepatic
fistula as parenchymal involvement is minimal.12 However, when the lung is
involved, recovery may be protracted. Secondary
infection, by causing persistent irreversible pulmonary
lesion may worsen the prognosis.
In 1939, Oshsner and DeBakey25 reported a mortality of
77.7% in amoebic empyema, 43.2% in lung amoebiasis and
10% when a bronchopleurohepatic fistula occurred. Years
later in 1958, Takaro and Bond9 found the overall mortality
to be 19%. Thus, it is obvious that with a better
understanding of the disease on the part of clinicians
and advent of better facilities for diagnosis and
treatment, the mortality has decreased considerably.
The mortality rate in cases requiring surgery varies in
different series. Takaro and Bond9,13 in 1976 found no further
reduction in the mortality rate of 33% as observed in
1958. However, Bautista O'Farrill reporting a large
series found that the mortality had fallen from 14% to
8.7% after 1970.30
The treatment is discussed in a later section.
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