[Amoebic Liver Abscess][Dr. O.P. Kapoor]
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UNCOMMON COMPLICATIONS

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CHAPTER CONTENTS

The complications of an amoebic liver abscess can be so widespread that it can involve any part of the body. The following complications are encountered less often than those which have already been discussed. Evidently the surgeons and pathologists are more familiar with the rare type of complications.
Involvement of organs distant from the liver, beyond doubt, is due to the blood-borne infection. Such a distribution does not follow any set pattern as regards the frequency, site, number of lesions and their severity. Post-mortem studies have enlightened us to a great extent as to the site, number and frequency of the rare types of the lesions.
The complications of an amoebic liver abscess can be divided into

AA) General complications

(B) Local complications. (Refer Table 1 )

(C) Complications of silent colon lesions.

(D) latrogenic complications.

(A) General Complications

Grouped under this heading are the following:

  1. Cerebral lesions.
  2. Renal lesions.
  3. Myocardial abscess.
  4. Skin involvement.
  5. Hepatic coma.
  6. Hepatorenal failure.
  7. Ocular involvement.
  1. Cerebral lesions. Infection reaches the brain through the blood stream. The organism may enter the circulation in one of the following ways:
  1. through the intrahepatic portocaval anastomosis,
  2. as a result of trauma to blood vessels while aspirating a liver abscess,
  3. by extension to the lung or pleura and from the lung into the systemic circulation.

Amoebic abscess of the brain is generally single and relatively smaller in size.8,10 The lesion is fairly vascular. However, cases of multiple abscesses have been reported by Hughes et al.11
The symptoms of an amoebic cerebral abscess simulate a pyogenic cerebral abscess, differing only in the-severity and the rapid progress often seen in former. The course seems to be rapid and terminates within a matter of 10-14 days.
3 It has a poor prognosis and a mortality of nearly 100 percent. Hughes et al11report 3 survivals out of 97 cases. Huard collected 59 cases of amoebic cerebral abscess all of which terminated fatally. Only 4 were operated upon. In 6 there was rupture into the ventricle which resulted in death in a few hours.

  1. Renal lesions. These are descrebed later under local complications and can rarely be metastatic.
  2. Myocardial abscess. Myocardial metastatic abscess has been described.12
  3. Skin involvement. Granulomatous ulcerative lesions have been reported at the drainage sites of an amoebic liver abscess, amoebic empyema and post-operative abdominal wounds. These ulcers have elevated margins, indurated bases, undermined edges and the floors are covered with adherent dirty greyish slough. The discharge, teeming with E. Histolytica, is frequently blood stained.
  4. Hepatic coma and
  5. Hepatorenal failure. Haemorrhage, peritonitis, cardiac tamponade, congestive cardiac failure, etc.3,8 lead to reduced renal blood flow. These are probably the cases which present with hepato-renal failure13 and the onset of ensuing coma may be so rapid that it is difficult to distinguish the sequence of events. We have also seen the onset of hepatic coma coming on without any of the above mentioned associated complications.
  6. Ocular involvement. A variety of ocular complications such as conjunctivitis, iridocyclitis. thrombophlebitis and haemorrhage into retina have been described. I have never come across any of these complications.

(B) Local complications
Local extension by rupture and perforation into an adjacent organ can occur.
An upward rupture may rarely involve the following structures:

  1. Diaphragm-Subphrenic abscess.
    -Paralysis of diaphragm.
  2. Mediastinum-Mediastinitis.
  3. Heart-myocardial abscess.
  4. Thoracic wall-ribs, scapula-erosion.
  5. Oesophagus-Obstruction.

Rupture of the liver abscess resulting in sub-diaphragmatic abscess has been proved by several investigators.1,4,14,15 The latter being difficult to detect and diagnose, leads to further complications by opening into the thoracic cavity.
Following an analysis of 169 records of autopsies of the amoebic liver abscess, Gharpure and Saldhana
1 observed that 4% of these cases had developed mediastinitis, as a consequence of the liver abscess having burst through the diaphragm. Myocardial abscess as a result of extension from a liver abscess has been reported by Madangopalan.16 Occasionally oesophageal obstruction can occur in a case of an amoebic liver abscess.16a A large neglected abscess may, by pressure, erode a rib.17 Bell et al18 have described a patient in whom extra-peritoneal spread of a liver abscess caused destruction of the scapula.
A liver abscess in the downward direction can rarely rupture into or affect the following organs:

1. Solid organs

    1. Spleen.
    2. Kidney.
    3. Right supra-renal gland.
    4. Rectus sheath .
    5. Lumbar region.
    6. Retroperitoneal muscles.

2. Hollow organs

  1. Stomach .
  2. Small intestine.
  3. Large intestine.
  4. Right renal pelvis and ureter.
  5. Common bile duct and gall bladder.

3. Vascular system

    1. Obstruction of l.V.C.
    2. Ruture into l.V.C.
    3. Portal vein thrombosis.

Occurrence of a splenic abscess either following a rupture or metastasis has been reported.19 Many cases of renal involvement have been reported.3,14 Pyelographic deformities and calycial displacement20 can be produced by large hepatic abscesses.21,22 Ramachandran et al have described two cases, which presented as renal or perirenal infection having fever, chills, rigors and tenderness of right loin with pyuria and albuminuria. Later on the classical picture of amoebic liver abscess in postero-inferior part of the right lobe developed suggesting an amoebic etiology.23 A hepato renal abscess affecting the upper pole of the right kidney has caused destruction of the right suprarenal gland and death in one patient due to adrenocortical failure.1, 13
Inferior vena cava in its passage through the groove in the right lobe may be obstructed by an adjacent abscess,
24 more so, if the abscess is of a giant size of six litres capacity as the one described by Islam.25 However, as mentioned elsewhere, obstruction of l.V.C. as seen on nuclear venography appears to be more common than judged by autopsy evidence. Rupture of a liver abscess directly into the inferior vana cava has been reported. Obstruction of the portal vein has been noted by Gulati et al.25 There have been many reports of an amoebic liver abscess obstructing or rupturing into the common bile duct.13 Adams et al have reported a case of haemobilia as a complication of amoebic liver abscess 8
Rupture into the stomach and colon has been found to be more common.
1,26,27 Hepato-colic fistula formation has been described by Madangopalan.28 Rupture into the duodenum was observed by Gharpure.1 If an abscess ruptures into a hollow viscus, pus is often efficiently drained and the fistulous opening may close on conservative treatment. However, quite often this complication is fatal.27 Severe bleeding may accompany or follow rupture of an abscess into the stomach or gut and haematemesis or melaena may be one of the most prominent symptoms. If an early diagnosis is not made a progressive severe anaemia develops in such patients. Sometimes fistulae persist and many bizarre examples, such as gastro-hepatico-pericardial or gut pleural via liver have been described. Caecal involvement by extra-intestinal spread due to rupture into the peritoneal cavity has been described by Theron.29
Finally rupture of the liver few months after the healing of an abscess, resulting in haemorrhage into the peritoneal cavity, has been described.
12
It will be noticed that most of the above rare general and local complications were seen more often in the past. Now-a-days with early diagnosis and the use of modern amoebicidal drugs, these complications have become still more rare.

(C) Complications of associated colon lesions
Often patients of an amoebic liver abscess have ulcers in the colon with or without accompanying symptoms of diarrhoea or dysentery. Colonic ulcers may rarely bleed profusely causing a massive rectal bleed. I had a female patient who presented with severe melaena. Initially, because of the associated fever, the diagnosis of 'enteric' was made. A routine plain X-ray abdomen taken for a suspected perforation of a typhoid ulcer showed an elevated right dome of the diaphragm. There was an opacity at the right base, suggestive of fluid. This patient had a right lobe superior surface amoebic liver abscess which had ruptured into the right pleural cavity. The rectal bleeding from the colonic amoebic ulcers was so massive that the patient needed eight pints of blood.
A colonic ulcer may perforate causing peritonitis which may be mistaken for the rupture of a liver abscess. Such patients often complain of associated diarrhoea or dysentery.

(D) Iatrogenic complications

  1. complications due to drugs-like emetine myocarditis, and
  2. complications of aspiration, open drainage or other surgical procedures.

These have been discussed in detail elsewhere.

References

  1. Gharpure, P V, and Saldhana, J M, Ind. Med. Gaz., 1931, 66,132.
  2. Ochsner, A, and DeBakey, M E, Surg Gyn. Obst. (I. A. S. ), 1939, 96, 392.
  3. Craig, C F Etiology, Diagnosis and Treatment of Amoebiasis; Williams & Wilkins Co., Baltimore, USA, 1944
  4. DeBakey, M E, and Ochsner, A, Surg Gyn. Obst. (I A.S.), 1951, 92, 209.
  5. Lamont, N M, and Pooler, N R. Quart. J. Med., 1958, 27, 389.
  6. Mehta, A, and Vakil, B J, Ind J. Med. Sci., 1970, 24, 478.
  7. Joshi, V R. Kapoor, O P. et al, J. Ass. Phys. Ind., 1972, 20, 761.
  8. Adams, E B. and Macleod, I N. Medicine, 1977, 56, 375.
  9. Ramachandran, S. Goonatillake, H D, et al, Brit. J. Surg., 1976, 63, 220.
  10. Plorde, J J, Harrison's Principles of Internal Medicine, McGraw-Hill Kogakusha Publication, Tokyo, 1977.
  11. Hughes, F B. Faehhle, S T. et al, J. Pediat., 1975, 86, 95.
  12. Vakil, R J. and Udwadia, F E, Diagnosis and Management of Medical Emergencies, Oxford Medical Publications, Delhi, 1975.
  13. Rab, S M, Alam, N. et al, Am. J. Med., 1967, 43, 811.
  14. Ramachandran, S. and Goonatillake, H D, Brit. J. Surg., 1974, 61, 353.
  15. D'Abrew, A L, In: Practice Cardiothoracic Surgery, 4th Edition, Edward Arnold Publications, London, 1976, 667.
  16. Madangopalan, N. J Ass. Phys. Ind., 1963,18, 72.
    16a Baker, H M, and Murray, J A, Cent. Afr. J. Med., 1969, 51, 129.
  17. Wilmot, A J. Clinical Amoebiasis, Blackwell Scientific Publications, Oxford, 1962.
  18. Bell, L G. 1959, as quoted from Wilmot, 1962, 8.
  19. Bockus, H L, Gastroenterology, Vol. IV, 3rd Edition, W B Saunders & Co., Philad., 1976.
  20. Coppridge, W M, and Roberts, L C, J. Am. Med. Ass, 1951, 146. 107.
  21. Ramakrishnan, A S. Am. J. Surg., 1971, 37, 756.
  22. Saratchandra, and Gajraj, Personal Communication, 1973.
  23. Ramachandran, S. Goonatillake, H D, et al Brit. J. Surg., 1976, 63, 220.
  24. Dhariwal, R K S. Singh Verma, N P. et al, Ind. J. Med. Sci., 1963, 17, 63.
  25. Islam, N. J. Trop. Med., 1967, 70, 68.
  26. Gulati, P D, Gupta, D N. et al, Am. J. Med., 1967, 42, 852.
  27. Roy-Choudhury, D K, Bhattacharya, A K, et al, J. Ind. Med. Ass., 1975, 64, 210.
  28. Madangopalan, N. Progress in Clinical Medicine in India, Arnold Heinemann, India, 1976.
  29. Theron, P. Brit. Med. J., 1947, 2, 123.