Amoebic peritonitis is considered to be the second most common complication of amoebic liver abscess after pleuropulmonary amoebiasis.¹ The incidence varies from 5-10%.^2-4 Vergoz and Hermanjat Guerins found it to be the most common form of rupture into the serous cavities. Manson-Bahr⁶ reported that the highest percentage (26%) of ruptures occurred into the peritonium. (Table I in Chapter I, Section Vl gives further data on the relative frequency of this condition.)
Rogers⁷ found that this complication occurred more frequently in the left lobe abscesses (7.14%) than in the right (3.7%). Out of the seven cases of frank rupture of the abscess with generalized peritonitis, Ramchandran et al⁴ found that the abscess was situated in the left lobe in three. Alkan et al⁸ in 1961 noted that 4 out of 8 cases of perforation into the peritoneal cavity were associated with a left lobe abscess. This could probably be explained by the smaller bulk of the left lobe and its consequent inability in containing the rapidly expanding abscess. Moreover the anatomical relations of the left lobe reduce the chances of the formation of firm adhesions. The right lobe can easily accommodate an expanding abscess due to its larger volume. Leakage of the abscess appears to be as frequent a cause of peritonitis in right lobe abscesses as a frank rupture.

Acute peritonitis
When an abscess ruptures suddenly the natural restrictive factors like adhesions and paralytic ileus do not come into play early enough to restrict the spread of the pus. Thus, acute generalised peritonitis occurs.
Very rarely in a case of liver abscess, an associated silent amoebic ulcer of the colon may perforate causing acute peritonitis. This complication is more likely in patients who also complain of associated diarrhoea or dysentery and whose colon is extensive studded with amoebic ulcers.

ClINICAL FEATURES
The initial picture is similar to that of any peritonitis caused by perforation of a hollow viscus acute pancreatitis. 'Shock' is often considerable and the classical signs of an 'acute abdomen' are present. Death may occur at this stage. However, if the patient survives, abdominal distension and signs of free fluid in the abdomen, very soon replace those of generalised guarding and board-like rigidity of the abdominal wall. At this stage perforation of a typhoid or tuberculous ulcer of the small bowel would be a very close differential diagnosis.
The diagnosis depends upon a high index of suspicion. In the tropical countries every case of acute abdomen should be scrutinised for evidence of amoebic liver abscess by looking for intercostal tenderness, hepatomegaly, lump in the upper abdomen, presence of icterus, and suggestive investigations.

INVESTIGATIONS
Acute abdomen being an emergency, at the slightest suspicion of amoebic liver abscess it is prefers to institute the appropriate treatment even bed diagnostic confirmation becomes available. It must be emphasized here that every effort should be m to confirm the diagnosis of amoebic peritonitis when suspected, in view of the reports of reduced mortality in cases diagnosed early.^9,10 in plain X-ray of abdomen elevation of right dome of diaphragm should be looked for. It is a common observation that often in cases of acute abdomen duff amoebic liver abscess, a plain X-ray of the abdomen does not show air under the diaphragm. Proctoscopic and sigmoidoscopic demonstration of amoebic ulcers in the bowel (observed in 30-40% cases) would aid the diagnosis. Liver scan and serological tests should be done if time and the patient's condition permit. Elevated serum alkaline phosphatase and serum bilirubin levels if already done in the early part of the illness, may help in the diagnosis.
Finally, diagnostic tapping in all the four quadrants of the abdomen with a de Verres spring loaded needle should be tried. Detection of brownish pus would indicate the diagnosis of an amoebic liver abscess.

TREATMENT
The treatment of acute generalised peritonitis is surgical. This constitutes one of the most serious abdominal emergencies in tropical countries. Careful peritoneal toilette, drainage of the peritoneal cavity, drainage of the abscess cavity (if possible, through an extra-peritoneal route), careful aspiration of the subdiaphragmatic spaces and exclusion of multiple abscesses, must all be meticulously, yet speedily carried out.
Pre- and post-operatively a course of emetine must be started together with parenteral tetracycline. When the patient can take drugs orally, chloroquine and a luminal amoebicide should be added.²

Chronic generalised peritonitis
This is a very rare presentation. The pus leaking out of an abscess may spread slowly to cause chronic generalised peritonitis. In this case, the peritoneal cavity is a mass of adhesions and there are multiple small pockets of greyish yellow pus.²
The main features are abdominal discomfort and distension and a progressive loss of weight. The abdomen, on palpation feels doughy. We have seen such patients but we could never make up our mind whether a colonic ulcer or a leak from an associated liver abscess had led to amoebic peritonitis. Yet again differentiating a perforated typhoid or tuberculous ulcer would be very problematic.
Serological tests more than liver scanning could be of help in these cases. Peritoneal aspiration of brownish pus, and the demonstration of E. Histolytica in the same, may at times afford a clue to the diagnosis.
As in acute peritonitis, laparotomy with meticulous peritoneal toilette is very essential although some authorities¹¹ consider it to be indicated only for the establishment of a diagnosis.
Moreover, in the past, conservative drug therapy with emetine and chloroquine had been found to result in slow improvement and eventual recovery.¹¹ Some authorities consider the above entity to be hypothetical .

Localised peritonitis
Sometimes, when slow leakage occurs from a liver abscess, adhesions of the intestines and omentum to the site of the leak, restrict the spread of the pus and a mass is formed.
An intra-abdominal mass in a patient suffering from amoebic liver abscess should suggest a localised intraperitoneal collection of pus. When the leak is into the lesser sac, initial acute epigastric pain and tenderness are marked. These may settle down after few days if the infection is walled off, the patient then presenting with "pyrexia of unknown origin" When the leak is posterior, the diagnosis of perinephric suppuration is often made, the amoebic pathology in the liver being diagnosed at the operation table. A 'leak' from an amoebic abscess may similarly be walled off in any of the subphrenic spaces leading to "pyrexia of unknown origin".
A localised collection of pus, calls for surgical drainage which, however, is not urgent.²

Superimposed local and generalised peritonitis
In such a presentation, the signs may be predominantly local, but there is some evidence of a wider peritoneal spread. Ileus and abdominal distension may develop.
As the etiology is uncertain such a case would warrant early surgery with subsequent drainage, if necessary.¹² However, the choice between the two lines of management remains a matter of individual preference. Gaseous abdominal distention calls for decompression by intermittent or continuous suction.

Bile peritonitis
Sometimes pure bile may seep into the abscess cavity from exposed biliary canaliculi in the absence of significant fibrous tissue reaction in the wall of the abscess.¹³ When such an abscess ruptures, bile peritonitis occurs.
This is a particularly severe form of peritonitis.¹³ Bile laden peritoneal fluid is an excellent culture medium for the growth of gram-negative organisms. Thus, the risk of developing secondary bacterial infection and consequent gram-negative septicaemia is quite high.¹⁴
The treatment of bile peritonitis is particularly urgent though in no way different from that of acute generalised peritonitis. A broad spectrum antibiotic must always be added. Culture and sensitivity of the organism, if isolated should guide the institution of specific antibiotics.

Mortality
Peritonitis is one of the dreaded complications of amoebic liver abscess.^10,11 and has been associated with a high mortality in the past. Earlier workers like Manson-Bahr⁶ and Rogers⁷ regarded this complication as most serious and likely to terminate fatally.¹⁵ (Table I)
Lamont and Pooler¹⁶ feel that provided the patient survives the initial effect of rupture, the prognosis seems favourable and the after effects are slight. Recently, more reports of timely diagnosis and good recovery from this condition are being published.³ Biliary peritonitis has a graver prognosis. Septicaemia and secondary bacterial peritonitis would appreciably
increase morbidity and mortality.¹³ If on opening up the abdomen, the surgeon finds the abscess intact, but sees a perforation of an acutely inflamed amoebic colon, the prognosis of the patient would be grave, as even handling this colon, which is like a wet blotting paper, is hazardous.

TABLE I

References:

1. Ochsner, A, and DeBakey, M E, Surg. Gyn. Obst. (I A S. ), 1951,92, 209
2. Wilmot, A J, Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962.
3. Archampong, E Q. and Clark, C G. Ann. Roy. Coll. Surg. Eng., 1973, 52, 36.
4. Ramachandran, S. and Coonatillake, H D, Brit.J. Surg., 1974, 61, 353
5. Vergoz, P. and Hermanjat Guerin, R P. Rev Chir., 1932, 70, 680.
6. Manson-Bahr, P. Lancet, 1923, 1, 941
7. Rogers, L, Lancet, 1922, 1, 463.
8. Alkan, W I, Kalmi, B. et al, Ann Int Med., 1961, 55, 800.
9. Sherlock Sheila, Diseases of the Liver and Biliary System, Blackwell Scientific Publications, Oxford,1975. 613
10. Macleod, J, Davidson's Principles and Practice of Medicine, Churchill Livingstone, Edinburgh, 1974.
11. Wilmot AJ, DM Thesis, University of Oxford, 1949.
12. McCarty, R B. and Schnedorf, I G, Am J Surg, 1946, 71, 401
13. Ramachandran, S. Induruwa, P A C, et al, J Trop Med Hyg., 1975, 78, 236
14. Miles, R M, and Jack, M S. Surgery, 1953, 34,445.
15. DeBakey M E and Jordan G L Surg Clin N.Am, 1977, 57, 325
16. Lamont, N M, and Pooler N R. Quart. J Med. 1958, 27, 389