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| CASE REPORT |
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| Year : 2000 | Volume
: 46
| Issue : 2 | Page : 108-9 |
Isolated tuberculous hepatic abscess in a non-immunocompromised patient.
DD Balsarkar, MA Joshi
Department of Surgery, Division of Surgical Gastroenterology, L. T. M. Medical College, Sion, Mumbai - 400 022, India., India
Correspondence Address:
D D Balsarkar
Department of Surgery, Division of Surgical Gastroenterology, L. T. M. Medical College, Sion, Mumbai - 400 022, India.
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 0011013479 
A 38 years old female presented with pain in the epigastrium, jaundice and fever since one and half month. The computerised tomographic scan of the abdomen revealed a multiloculated abscess of the left lobe of liver. The pus drained from the liver abscess at laparotomy showed acid fast bacilli on microscopy. A detailed search failed to identify any other focus of tuberculous infection. The case has been reported for the rarity of isolated hepatic tuberculous abscess and its presentation with jaundice, a rare feature, and to highlight the importance of microscopic or culture diagnosis in a suspected case of pyaemic abscess.
Keywords: Adult, Case Report, Female, Human, Liver Abscess, diagnosis,microbiology,Tomography, X-Ray Computed, Tuberculosis, Hepatic, diagnosis,
How to cite this article:
Balsarkar D D, Joshi M A. Isolated tuberculous hepatic abscess in a non-immunocompromised patient. J Postgrad Med 2000;46:108 |
Tuberculous liver abscess is rare and when present is usually associated with the focus of infection in the lung or in the gastrointestinal tract[1] or is associated with an immunocompromised state. Isolated hepatic tuberculous abscesses are very rare[2]. The diagnosis has been difficult in most instances and usually made at post-mortem[1]. In this report, we describe a rare case of isolated tuberculous liver abscess.
A 38-year-old woman presented with history of pain, swelling in the epigastrium, associated with low grade fever, anorexia, weight loss and jaundice since six weeks. A computerised tomographic (CT) scan of abdomen revealed a 10 cm X 10 cm multiseptate abscess in the left lobe of liver for which a CT guided aspiration of 400 cc of yellow coloured pus was done. The patient was started on third generation cephalosporin and aminoglycoside with the provisional diagnosis of pyaemic liver abscess. Despite this treatment, the patient’s symptoms worsened. A repeat CT scan of the abdomen showed a refilling of left lobe liver abscess. With this the patient was referred to us. There was no positive history of tuberculosis or contact with patient with tuberculosis.
On examination, there was a 5 cm X 4 cm tender epigastric lump. The routine haematology investigation showed haemoglobin of 9.4 gms%, white blood cell count of 13000 cmm and an erythrocyte sedimentation rate of 61 mm at the end of one hour. The liver functions were deranged showing a total bilirubin of 4.2 mg%, direct bilirubin of 2.6 mg%, serum glutamic oxaloacetic acid transaminase value of 780 IU, serum glutamic pyruvate transaminase value of 1020 IU, serum alkaline phosphatase 123 IU, and the prothrombin time of 13.6 seconds with a control of 10.1 seconds. ELISA for HIV and hepatitis B surface antigen tests were negative. Chest skiagram and abdominal CT scan did not reveal lesions suggestive of tuberculosis. The prothrombin time was corrected by administration of vitamin K.
In view of the patient’s general condition and the refilling of the multi-septate abscess cavity, a decision of laparotomy was taken. At laparotomy, a multi-septate intraparenchymal liver abscess was seen in the left lobe with no other positive abdominal findings, which drained 800 cc of thick yellow coloured pus, after breaking of all the loculi. The liver cavity was closed over a tube drain. The drain output in the initial period was about 400 cc, which then decreased after one week. The drain was removed on eight post-operative day.
The microscopy of pus showed the presence of acid-fast bacilli. The patient was started on O-floxacillin in the beginning, as it is one of the least hepatotoxic anti-tubercular drug. After the normalisation of the liver functions, four drugs anti-tubercular therapy was started. Patient had an uneventful postoperative therapy. The repeat sonography of abdomen at 4 months showed a complete resolution of the abscess cavity.
Bestowe first described tuberculous liver abscess in 1858[3]. Since 1930, 444 cases have been described[4]. Three forms of tuberculous liver involvement are described: diffuse involvement associated with miliary or pulmonary tuberculosis; diffuse parenchymal involvement without any evidence of existing tuberculosis anywhere (primary miliary tuberculosis of liver); and focal or nodular lesion in the liver which may be multiple or solitary and present as tuberculoma or abscess.
Tuberculous liver abscess is usually secondary to primary pulmonary or gastrointestinal involvement[5]. When there is no gut involvement, the route by which mycobacterium reach the liver could be hepatic artery during systemic mycobacteraemia from the lung[3]. High fever, weight loss, right hypochondriac pain and hepatomegaly are the most frequently observed clinical findings[5]. Jaundice is a very rare manifestation of tuberculous liver abscess and may be caused by extra or intra hepatic obstruction[5]. No clear relationship exists between the degree of liver involvement and jaundice[6]. Tuberculous liver abscess is frequently confused with hepatoma, pyogenic and amoebic liver abscess[1].
Clinical findings are non-specific; the diagnosis of hepatic abscess is often made at autopsy or at laparotomy. Ultrasonography (USG) and CT scan findings show multiseptate live abscess[1],[4],[7]. Ultimate diagnosis confirmation is by demonstration of acid-fast bacilli in the aspirated pus or in the necrotic tissue. When this is not successful, histological examination of the abscess wall may be required for confirmation of diagnosis.
Medical treatment of tuberculous liver abscess is still a subject of debate. On interest is the formation of liver abscess even after starting the chemotherapy[1],[5]. Gracey postulates that thick fibrous tissue around the abscess and their large size may prevent antibiotics from reaching the target[2]. Drug related hepato-toxicity may also contribute to failure of treatment[1]. Direct infusion of anti-tuberculous agents has more direct effects in the treatment of an abscess than systemic chemotherapy alone. Therefore, if a percutaneous catheter can be safely placed use of transcatheter infusion of antituberculous drugs can be considered[8]. CT and USG guided drainage has been found to be good for the successful drainage, although the surgical drainage, which was used early may be required[5] as was done in this patient successfully.
Though rare, tuberculous abscess should be ruled out in a case of suspected pyaemic abscess before starting antibiotics to avoid delay in treatment.
| :: References | |  |
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| 2. | Nampoory MR, Halim MM, Shreedharan R, al-Sweih NA, Gupta RK, Costandi JN. Liver abscess and disseminated intravascular coagulation in tuberculosis. Postgrad Med J 1995; 71:490-492. |
| 3. | Gracey L. Tuberculous abscess of liver. Br J Surg 1965; 52:442-443. |
| 4. | Stevens A, Little JM. Isolated tuberculous hepatic abscess. Aust N Z J Surg 1987; 57:409-411. |
| 5. | Wilde CC, Kueh YK. Case Report. Tuberculous hepatic and splenic abscess. Clin Radiol 1991; 43:215-216. |
| 6. | Reed DH, Nash AF, Valabhji P. Radiological diagnosis and management of solitary hepatic abscess. Br J Radiol 1990; 63:902-904. |
| 7. | Spiegel CT, Tuazon CU. Tuberculous Liver abscess. Tubercle 1984; 65:127-131. |
| 8. | Jain R, Sawhney S, Gupta RG, Acharya SK. Sonography appearances and percutaneous management of primary tuberculous liver abscess. J Clin Ultrasound 1999; 27:159-163. |
| 9. | Kubota H, Ageta M, Kubo H, Wada S, Nagamachin S, Yamanak T. Tuberculosis liver abscess treated by percutaneous infusion of antituberculous agents. Intern Med 1994; 33:351-356. |
Figures
[Figure - 1]
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