In a patient with an amoebic liver abscess, a sympathetic effusion can occur in any of the serous cavities-pericardial, pleural or peritoneal. Usually, this effusion is in the form of a clear straw coloured fluid. On chemical analysis, it has the composition of an exudate, though at other times, it may be a transudate. The importance of this effusion is that it serves as a warning of the proximity of the abscess to a serous cavity and the possibility of its rupture into that particular serous cavity. Till the tapping of the serous cavity is done, it is not possible to differentiate effusion from a ruptured abscess. These effusions occur more often with superficial abscesses. Also the word "sympathetic" presumably implies a reflex vasodilatation and increased capillary permeability but it seems more reasonable to suppose that in most cases the serous cavity is involved by the periphery of the inflammatory process surrounding the abscess.
Pericardial sympathetic effusion has already been discussed in the chapter on pericarditis. Wilmot¹ and others, who described such effusions in the pericardial sac, termed them as "sympathetic", because they were considered harmless and did not call for any special treatment. Usually the fluid clears up with the usual line of therapy for the liver abscess. As discussed in an earlier chapter on amoebic pericarditis, it is not always so and this sympathetic effusion in a pericardial cavity can prove fatal in an occasional patient.
Pleural effusion occurs quite commonly in either of the pleural cavities. It is a sympathetic reaction due to diaphragmatic inflammation and irritation by a superior surface abscess. On three occasions, we saw this type of an effusion in the right pleural cavity with a very small superficial superior surface abscess of the right lobe, which did not even produce a clear cut cold area on the liver scan. Figures 16 a,b,c show a case who had to be operated upon to arrive at a correct diagnosis. Although these effusions respond well to medical treatment, I prefer to tap them dry, while diagnostic aspiration is being performed. Ibarra Perez et al² have reported 161 cases of sympathetic pleural effusion. Most of them responded to medical treatment with a combination of amoebicidal drugs. Deaths were more frequent among patients with associated bronchial or pericardial rupture.
Effusion in the peritoneal cavity-Two of my patients, who had inferior surface abscesses and developed acute abdomen, were operated upon. Straw coloured fluid was found in the peritoneal cavity (Fig. 17). The abscess had still not ruptured. These patients do not differ much from those presenting with pre-rupture syndrome described by Ramachandran .³
Following are the other causes of free fluid in the peritoneal cavity which we have observed in patients with amoebic liver abscess:

1. Gradual leak from the liver abscess
2. Leak from a colonic ulcer.
3. In patients, in whom the ascitic fluid is a transudate, following are the likely causes which are responsible alone or in combination:

1. low serum albumin level, which is quite common in patients having an amoebic Iiver abscess.
2. temporary obstruction (very rarely thrombosis) of the inferior vena cava seen in some patients having an amoebic liver abscess (Refer Section IV).
3. pressure on, or thrombosis of, branches of hepatic vein⁴ is a likely aetiological factor.
4. portal hypertension might have some part to play in a few patients

References

1. Wilmot AJ Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962
2. Ibarra Preez C and Selmanlama M Proc Internat Conf on Amoebiasis, 1975, 800 Ed by Sepulveda B and Diamond LS Instituto Mexicano Del Seguro Social, Mexico, 1976
3. Ramachandran S. Brit J Surg, 1974, 61, 353
4. Aikat B K Personal Communciation