In most of the standard text books of medicine, it is stressed that amoebic abscess of the liver is usually solitary.¹ Rogers² in 1913 first reported "fulminant multiple amoebic abscesses of liver" associated with severe dysentery. Later a few other authorities have also recognised this entity although the reported incidence was higher in autopsy cases than in the clinical series.^3-8 Table I shows the incidence of multiple amoebic liver abscesses in a few series.

TABLE I

In the past it was stressed that diagnosis of multiple amoebic liver abscesses can be made only at autopsy.¹⁰ In 1972, we analysed 98 autopsies of amoebic liver abscess and found 58 cases having multiple liver abscesses. When we made a retrospective analysis of the clinical picture of these autopsy cases, we came to the conclusion that multiple large amoebic liver abscesses could be diagnosed at the bedside.⁸ We had then suggested that in a case of amoebic liver abscess, presence of jaundice, abdominal distention, symptoms of early hepatic coma, presence of ascites or oedema of feet call for a diagnosis of multiple large amoebic abscesses (Table II). Although this would still often hold true today, our views have changed after our experience with liver scanning in cases of amoebic liver abscess. In one of my studies in collaboration with Ganatra,¹¹ out of 153 cases of amoebic liver abscess in whom liver scans were done, 108 showed a single abscess and 45 showed multiple abscesses (defined by us as more than one). Table III shows comparison of clinical picture of this latter group with the former having a single abscess. (Both groups clinical-no autopsy included). Thus, we realised that many patients whom we had diagnosed and treated as a single amoebic liver abscess often had a second amoebic liver abscess, which produced no extra physical signs and responded to medical treatment without any aspiration. These patients with multiple abscesses did not have the clinical criteria described by us earlier. But then in this latter series, the second abscess seen on scan was often very small. We had earlier described the clinical picture of multiple large abscesses where at least two abscesses were large .
With the present knowledge, I would divide multiple amoebic liver abscesses into the following five groups:

TABLE II

Signs and symptoms of 26 cases⁸ of multiple large abscesses compared with a published series of 103 cases of solitary amoebic liver abscesses (Subramaniam et al)¹²

TABLE lIl

Group I-Patient having one amoebic liver abscess on the superior surface and the second on the inferior surface of the right lobe of the liver
This presentation is commonly observed at autopsy (Figs. 95 a,b,c). A patient having a marked downward enlargement of the right lobe below the costal margin and also an elevated immobile right dome of the diaphragm with other radiological changes, most probably, belongs to this group. The right lobe is so voluminous that it is not possible for a superior surface abscess to extend upto the inferior margin of the liver. (I have seen only two cases at autopsy where the whole right lobe was replaced by the amoebic abscess. In both cases the liver was not enlarged but the right lobe was left as a thin rim of liver tissue around the pus).
Therefore, in all patients with a marked downward enlargement of the right lobe, an elevated immobile right dome may be due to a second abscess sitting on top. If the other radiological signs like a hazy right dome and obliteration of costophrenic angle are present,- there are more chances of a second abscess being present. On other occasions an elevated right dome of the diaphragm, often upto 2.5 cms. with minimal restriction of the movements can be produced by a huge inferior surface right lobe abscess. Presence of jaundice (mentioned earlier) should increase the suspicion. Liver scan if available, clinches the diagnosis (Figs. 96 a,b,c). In its absence, instillation of air into the abscess after tapping at both the tender spots would prove the existence of two abscesses (Fig. 97).
At other times if the air level is quite low down and the right dome is markedly elevated (Fig. 98) in an X-ray taken after aspiration, it should make one think of a second abscess situated on the superior surface.
Unawareness of this simple association of physical signs has led to many fatalities. In our own early series, while going through the notes of 13 autopsies where the patients were operated upon for an inferior surface liver abscess, we were impressed by the fact that the patients died because the second superior surface abscess seen at autopsy was missed and not explored, though the right dome was markedly elevated .
Hazra et al¹³ described the detailed histories of four cases of amoebic liver abscess with jaundice. Going through these cases, it is very apparent that the two patients who died but in whom autopsy was not performed, had typical signs and symptoms of multiple liver abscesses. Again, although in both these patients, the right dome of the diaphragm was very much elevated, at laparotomy only an inferior surface abscess was drained.

Group II-Left lobe abscess associated with a right lobe abscess
This is the second common type of combination of amoebic liver abscesses (Fig. 99). This group should be suspected in all cases of left lobe amoebic abscesses. If a patient having a left lobe abscess, shows a marked upward (elevated right dome or a hump in the right dome) or downward enlargement of the right lobe of the liver, a second amoebic liver abscess in the right lobe should be suspected. This is especially more likely if the patient has jaundice. Since this combination has not been appreciated, some authorities in the past have diagnosed pericardial amoebiasis following an abscess in the right lobe. Of course, in centres where liver scan facility is now available, there are no problems in picking up such cases (Fig. 100). The following case illustrates my point: On one of the days, when the isotope was not available in our nuclear medicine department, patient was sent to me for a liver scan. Twice before the abscess in the right lobe had been aspirated without any dramatic improvement. Figure 101a shows that this patient of right lobe amoebic liver abscess also had an obvious swollen left lobe in the epigastrium. This was tapped and air instilled (Fig. 101b) to show the presence of a second abscess for which scanning was not really necessary.

Group lll-One large and one or two small abscesses (Fig. 102).
This group is only of academic significance. To a clinician, it is of very little importance. The patient here presents with a straight forward single amoebic liver abscess which can be localised by the site of maximum tenderness. If a routine liver scan is not asked for, the clinician might be surprised to final two or more cold areas. In such cases, of course, the tender area would need tapping to confirm the diagnosis. Once this is done and the patient is responding very well to the treatment, it is not necessary to tap the other areas. Often these resolve without aspiration.

Group IV-Multiple (more than 3 or 4) large amoebic liver abscesses
These patients would most likely show presence of jaundice, altered mental state (drowsiness, abnormal behaviour, irrelevant talking, rowdiness or semiconsciousness or coma), generalized abdominal distension or oedema of feet. Any one of these features in a case diagnosed as amoebic liver abscess should make one suspect the presence of multiple large abscesses. Presence of three or four of these features would make the diagnosis almost certain (since any one of these features can rarely be seen in a patient having a single large abscess). Before the days of scanning, these cases proved invariable fatal (Figs. 103 a,b,c). Recently, I have seen three patients with a positive liver scan, who recovered ( completely (Fig. 104). Tapping was done only a the most tender spots. Other cold areas were no aspirated. Pai¹⁴ has saved the lives of such patient by tapping as many as 6 or 7 abscesses, at different sites under ultrasonic guidance.

Group V-Multiple (more than 3 or 4 small amoebic liver abscesses.
These are the types of abscesses which Rogers² in 1913 reported as "fulminant multiple amoebic abscesses of liver". These are difficult to diagnose during life. Wilmot¹⁰also mentioned that they can be diagnosed only at autopsy. In our experience, even in the scan age, the diagnosis of this group has not improved. Unfortunately since these abscesses are often less than 2 cms. in diameter, they do not produce cold areas on the liver scan. At other times one big abscess produces a definite cold area and the small abscesses present as "diffuse patchy uptake of the isotope" on the liver scan.
These types of abscesses often accompany an attack of fulminating amoebic colitis. Because of the nature of these lesions in the liver (Figs. 105 a,b), localising signs are absent. Even the slightest discomfort in the right hypochondrium, presence of fever, leucocytosis, icterus in a patient suffering from acute amoebic dysentery should make one suspicious. In our experience, these patients die in spite of full treatment. Many of them look very toxic. Usually no pus or only a few millilitres of pus can be obtained on tapping such patients.

Mortality
Sambue¹⁵ as early as 1913 reported the mortality rate for single abscess as 23%, for two abscesses 45%, for three abscesses 90% and for those with four or more abscesses as 100%. Today the picture is not so bleak. Patients in Groups I, II and lIl can all be cured. Prognosis of patients in Group IV depends on the availability of modern investigations like nuclear or ultrasonic liver scans. Unfortunately patients in Group V cannot be saved even to-day. Is it that the strain of E. Histolytica in these patients is very virulent or the immunity is very poor? Further work in this field would throw more light.

References

1. Cecil, R L, and Loeb, R F. Textbook of Medicine W B Saunders & Co., Philad., 1963.
2. Rogers, L, Brit. Med. J., 1913, 2, 1246.
3. Clark, C, J. Roy. Army Med. Corp., 1910,15, 486
4. Craig, C F. The Etiology, Diagnosis and Treatment of Amoebiasis, Williams & Wilkins Co. Baltimore, USA, 1944.
5. Huard-Mayer, M, Ind Med. Gaz., 1940, 75, 262
6. Manson-Bahr, P H. Manson's Tropical Diseases Cassell & Co. Publications, London, ELBS, 1967
7. Ochsner, A, and DeBakey, M E, Surgery, 1943, 13, 460.
8. Kapoor, O P. and Joshi, V R. J. Trop. Med. Hyg., 1972, 75, 7.
9. Reddy, D C, Ind Med. Gaz., 1945, 80, 501
10. Wilmot, A I, Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962.
11. Kapoor, O P. and Canatra, R D, Paper read at Bombay Medical Congress, Bombay, Oct. 1974.
12. Subramaniam, R J. J. Ass. Phys. Ind., 1970, 18,729.
13. Hazra, D K, Seth, H C, et al, J Ind. Med. Ass., 1970, 55, 244.
14. Pai, R R. Personal Communication.
15. Sambue, 1913, as quoted by Wilmot (10).