[Amoebic Liver Abscess][Dr. O.P. Kapoor]
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SILENT ABSCESS

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Silent amoebic liver abscess can be compared to a silent myocardial infarction. A patient having a "true' silent myocardial infarction is very rarely seen ir clinical practice. Often while questioning the patient in detail a history of mild discomfort in the ches or sweating can be obtained. Similarly, since fever pain in the liver area and hepatic tenderness are the most important clinical features of an amoebic live abscess, strictly the term "silent" amoebic abscess should be used when all these clinical features are absent.
It is well known that in a few cases of amoebic liver abscess one or two of these features may be absent.
1 These patients have been then loosely labelled as cases of "silent" amoebic abscess. Thus Vakil et al 2 have labelled three cases with fever but without pair and hepatomegaly as silent abscesses.
A liver abscess in a patient presenting with severe amoebic dysentery has also been called "silent". As many as one third of acute amoebic dysentery patients have single or multiple abscesses. These can be picked up only on a strong index of suspicion.
A patient of amoebic liver abscess, having been treated with apparent success (with or without aspiration) may become symptomless or 'cold' for a variable period of time. Days or weeks later the symptoms may recur. Some authors have considered the above abscess as having been "silent" in this intervening period.
If a patient of amoebic liver abscess having a lump in the liver has no pain or tenderness, it can be mistaken for a hydatid cyst as reported by Cohen et al
3. Such an abscess may also be termed as "silent".
Verdon et al
4 while doing liver scans on patients returning from South-East Asia, found some having large abscesses in the liver. They ranged from severely ill and moribund to totally asymptomatic patients. The latter are true examples of "silent" abscesses. This fact may be important in case of returning military and peace corps personnel, most of whom will have been exposed to amoebic infection and many may harbour the disease within the liver in the subclinical state. Thus, in two of such cases reported by Abbruzzese,5 the liver abscess was possibly silent for months or years.
Patients of amoebic liver abscess who present straightaway with an acute abdomen may also be labelled as having had a "silent" abscess. Mallory's
6 case fits into this group.
Patients with a "silent" amoebic liver abscess may also present with symptoms of loss of weight and on examination, have a gross hepatomegaly. Thus, the clinical presentation is more like a hepatoma.

The following case illustrates this point:
I had advised weight reduction to one of my patients, who had hypertension. On a routine check up at the end of the second year, I discovered that he had lost 8 kgs. of weight. On examination, an enlarged non-tender liver was felt 8 cms. below the right costal margin. When questioned, he had no complaints and was feeling fine.
Figure 22 shows a large cold area detected on the liver scan. While attempting a diagnostic liver biopsy to confirm the clinical suspicion of a hepatoma, to our great surprise, chocolate coloured pus was obtained. Soon after he was discharged from the hospital, he put on 6 kgs. of weight. In retrospect I realised that the loss of weight was due to amoebic abscess and not the weight reduction measures that I had advised.
Finally patients have been labelled as having a "silent abscess" because of a large cold area persisting on a liver scan even after the patient has no abnormal clinical, radiological or laboratory findings of a residual amoebic liver abscess.7 Are we justified, in calling them as abscesses, because these cold areas may be scars or cysts occurring as sequelae of healed liver abscesses?

References

  1. Anderson, N H. Bostick, W J, et al, Amoebiasis- Pathology, Diagnosis and Chemotherapy, Charles C. Thomas Publications, Springfield, 1953, 131.
  2. Vakil, B J, Mehta, A J, et al, J Trop. Med. Hyg., 1970, 73, 63.
  3. Cohen, S S. and Gibbon, J H. Am J. Med. Sci., 1903, 125, 210.
  4. Verdon, T A, Hamilton, G D, et al, J Nucl. Med., 1967, 8, 402.
  5. Abbruzzese, A A, Am. J. Gastroent., 1970, 54, 464.
  6. Mallory, W J, J. Am. Med. Ass., 1920, 75, 1774.
  7. Sharma, B N. J. Ass. Phvs. Ind.. 1972. 20. 519