Amoebic 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.

Incidence
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 Guerin.⁶
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

Mortality
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-

1. Suppurative or purulent type - this can further be subdivided into (a) with acute onset, and (b) with gradual onset.

11. Sympathetic or non-suppurative type - this can be subdivided into that with (a) acute onset, and (b) gradual onset.

111. Constrictive amoebic pericarditis.

IV. Amoebic hydropneumopericardium.

All four types can be further subdivided into-

1. with associated left pleuropulmonary amoebiasis ^9,14
2. without associated left pleuropu!monary amoebiasis.

1. Suppurative or purulent amoebic pericarditis
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 pericardiectomy.¹⁰
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 shock.¹

(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 be present.
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 pericardium.
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 etiology:

1. 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).
2. Presence of a lump in the epigastrium in the enlarged left lobe of the liver.
3. 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.
4. Presence of icterus is a useful sign. This would also be the case when patient harbours two abscesses.
5. 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
6. Unfortunately, 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

Treatment
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 tissue amoebicide.
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 lobe.
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, if necessary.

11. Sympathetic 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 sequela.
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 management.¹

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.'

In conclusion, 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

References

1. Adams, E B. Proc. Internat. Conf. on Amoebiasis, 1975, 830 Ed. by Sepulveda, B. and Diamond, L S. Instituto Mexicano Del Seguro Social, Mexico, 1976.
2. Eguia y Moro, J P. Disertacion sobre Las obstruociones inflamatorias del higado, Mexico, 1972, as quoted by (10).
3. Rouis (1860) as quoted by Vergoz, P. and Hermanjat-Guerin, R P. 1932.
4. Germilton, W. (1899) as quoted by Fiegal (1959).
5. Jimenez, M F. Clinicia Medica, Abscecso del higado Union Medica de Mexico, 1859, 2, 10.
6. Vergoz, P. and Hermanjat-Cuerin, R P. (1932), as quoted by Wilmot, A J. 1962.
7. Carter, M G. and Korones, S B. New Eng. J. Med., 1950, 242, 390.
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11. Kulpati, D D, Venkatachalam C G. et al, J. Ass. Phys. Ind., i976, 24, 119.
12. Watson, R B. Am J. Trop. Med. Hvg.. 1972.
13. Tyagi, S K, Anand, I S. et al, Paper read at XXXIXth Annual Conference of Association of Physicians of India, Madras, Jan. 1979
14. Divekar, D V, Poornachandra Rao, Y. et al, as quoted by 15.
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21. Datey, K K, Parikh, C S. et al, Bom Hos J., 1978 20, 34
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