Gross examination
The liver is usually enlarged^1_10 and weighs more than normal. Sometimes its weight may be normal.³ However, Kean³ reported than in 28 of his cases, the liver weighed less than normal (2,000 gm taken as normal weight).
By and large the lobe which is the seat of abscess formation is enlarged. However, the enlargement of the unaffected lobe has also been reported in literature.^1,6,11 This generalised enlargement may be due to oedema and congestion^1,12,13 produced by pressure on the draining venous channels. Lamont and Pooler¹ feel that the congestion of the liver as a whole could be due to some unexplained neurovascular phenomenon.
When the abscess is superficial, it forms a bulge on the surface of the organ (Fig.3). Sometimes there may be thin strands of adhesion on the surface^3,14_16 even in the absence of a rupture.
For some unknown reasons the right lobe is affected more commonly as compared to the left.^17_23 Some^21,24 authors explain this on the basis of the larger size of that lobe. Still others^21,25 feel that it is because the right lobe receives the blood from the caecum, ascending colon and the right half of transverse colon, where the amoebic involvement is more common.^3,26 However, by the use of radioisotopes it has not been proved that there is no such stream-lining of the blood supply.
Paul et al²⁷ and Ribaudo²⁸ believe that amoebic liver abscess is not an abscess in the true sense of the word. The contents of this type of an abscess cannot be labelled as ‘pus’ because it is nothing but liquefied liver tissue.
The appearance of a cut section of a liver abscess varies according to the stage in which the abscess is seen.

1. Very early stage
2. Recently formed amoebic abscess
3. Chronic abscess
4. Healing stage

1. In the initial stage, cell death occurs but entire dissolution and liquefaction is not complete. Hence the affected area appears dark coloured, softened and well demarcated from the surrounding normal tissue.¹⁸. As the contents are not liquid, these may be termed as solid abscesses. Lesions of similar description can be found just beyond the spreading border of a well established amoebic abscess.²⁹ Carrera³⁰ found a leaf shaped area of similar description in his experimental animals while injecting amoebae in the portal radicle.

2. An abscess of recent onset has a distinct central liquefied area. The cavity may be round, oval or branching.²¹ The wall of the abscess may be shaggy, i.e. shreds of non-viable tissue are seen to hang loose from the walls^14,17,31 (Fig.4). Just outside this wall is a rim of dark coloured congested liver tissue (Fig.5). This area slowly merges with the normal tissue without any capsule to separate the two parts.

3. The only distinct difference between acute and chronic abscess is that in the latter the body has had time to wall off the lesion by producing a layer of fibrous tissue around it.^14,32_34 This wall may be a few millimetres to two centimeters thick (Fig.6)

4. If an abscess heals without being aspirated the liquid contents may dry up and are described to look like ‘putty’,^15,35 Rarely, these lesions may get calcified.

Microscopic examination
The microscopic details also differ depending on the age of the lesion.

Very early lesion
These lesions still have semblance to the liver architecture. The connective tissue may not be completely destroyed, but the hepatocytes show all signs of death. The affection of the liver cells is more marked towards the centre of the lobule as compared to the periphery.³⁰

Recently formed and/chronic abscess
In a well formed abscess the central zone is a cavity filled with thick liquid which is not true pus. Surrounding this necrotic area is a layer in which the hepatocytes are compressed, and tend to lie in cords, parallel to the wall of the abscess cavity.^29,32,36 Sinusoids may appear congested and hypercellular (Fig.7).
There are few changes at the portal triad. The portal vein radicles are maximally affected. Some of them show slight inflammatory changes in their walls.³⁰ Others show thrombosis^12,14,30 with E. Histolytica caught in the thrombus.^32,37 Occasionally some portal vein radicles are totally necrosed^12,29 (probably by the enzymatic action of E. Histolytica). The branches of hepatic artery are normal.^12,29 In some cases specially those with jaundice, inspissation of bile is note.^36,38,39 Periductal fibrosis and the bile duct proliferation have also been recorded.^36,38
In general there is paucity of inflammatory cells. When present they are in maximum numbers at the portal triad.^40,41 Monocytes and lymphocytes^{30,33,38,42,43} are observed more commonly than the polymorphs. Whenever there is secondary infection, the polymorphs dominate the scene.
Beyond this area, there is a lot of spreading activity, the extension occurring radially. In this region there are a log of trophozoites^{12,14,32,33,38,44} of E. Histolytica with evidence of multiplication of the parasite.
The older lesions are walled off from the surrounding normal tissue by a distinct fibrous band. The thickness of this wall probably depends on the age of the lesion. The wall is composed of reticulin fibres, fibroblasts and collagen fibres^32,36 (Fig.8). The thicker wells have thick bands of collagen.
Beyond the fibrous wall, the liver appears normal.²⁷ Some workers have noticed fatty changes³⁶ and altered staining pattern much beyond the site of the abscess (Fig.9). Whether the altered liver function tests^45_48 are due to hepatolysis in the localised area (the abscess) or hepatic damage in general is not easy to say.
Multiple small satellite abscesses are also found in this region.^12,37,49
Finally compression of the intrahepatic duct has been observed.^50,51 Thrombosis of small branches of hepatic veins has been recorded.⁵² This may also be responsible for congestion around the amoebic liver abscess.

Repair and healing
The abscess cavity may shrink within 2-3 days.⁵³ Complete resolution of the abscess takes 2 weeks^54-55 to 8 months.^55-59
Active regeneration is noted and can be seen even during the acute phase.^38,60 Periportal fibrosis of various degrees is also observed.⁶¹ For some unexplained reasons fibrosis seems to be a self limiting process in patients with amoebic liver abscess.³⁸ Rarely does the fibrous tissue undergo calcification.
Multiple amoebic liver abscesses have been discussed elsewhere.

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