Giant liver abscess with bilateral pleural effusion: An unfamiliar association.

Amoebic liver abscess is a common problem in tropical countries. However, its protean manifestations sometimes pose diagnostic dilemma leading to delay in starting appropriate therapy. We report here one interesting case of an amoebic liver abscess where the patient developed some uncommon features like bilateral pedal edema and bilateral pleural effusion. Although unilateral effusion is well known in such patients, the cause of bilateral involvement of pleura in this patient remained largely unknown. The cause of edema turned out to be compression of inferior vena cava by the large-sized abscess, rather than any cardiopulmonary abnormality. This case has global relevance because many of the migrant populations from tropical countries are settled all over the world, particularly in Europe and America. It would only be appropriate that the treating physicians are aware of this unfamiliar association.

INTRODUCTION

Infection by Entamoeba histolytica is common in tropical countries like India and its manifestations may be limited primarily to intestine or sometimes involves other organs like liver, pleura, or pericardium. The mechanism involved in the involvement of pleura has been invariably described as a result of leakage of pus from the liver or sometimes due to sympathetic stimulation. This results in a right side pleural effusion. We report here one interesting case of an amoebic liver abscess where the liver abscess was unusually large and it resulted in some unfamiliar complications like pleural effusion which was bilateral and also the posterior location of the abscess compressed inferior vena cava (IVC) which led to pedal edema.

CASE REPORT

A 42-year-old male, an occasional alcoholic, presented with dry cough, fever, pain in the lower back, severe vomiting and swelling of both feet since 5-6 days. His clinical signs of vital functions were stable and general physical examination was unremarkable except tachypnea and pitting pedal edema. Chest examination revealed woody dullness, decreased breath sounds, crepitations, and a pleural rub at right infrascapular region. Liver was two fingers enlarged and tender below the costal margin. Cardiovascular examination was essentially normal. A provisional diagnosis of right-sided pleural effusion along with consolidation was kept and a probability of liver abscess was kept. His investigations revealed the following: Hemoglobin (Hb), 12.6 g/dL (15.5 ± 2.5); total leukocyte count (TLC), 24,000/mm3 (400011,000); Erythrocyte Sedimentation Rate (ESR), 70 mm/fall 1st hour (0–10 by Westergreen's method); S. bilirubin total, 0.9 mg/dL (0.2-1.0); serum glutamic oxaloacetic transaminase (SGOT), 104 U/L (8-40); serum glutamic pyruvic transaminase (SGPT), 127 U/L (10-50); alkaline liver phosphatase (ALP), 600 U/L (78-220); S. protein, 6.8 g/dL (6-8); albumin, 3 g/dL (3.4-5); HIV, negative, and HBs Ag, negative. X-ray chest showed raised right half of the diaphragm and mild right-sided effusion. USG abdomen showed liver abscess with around 400 ml of fluid in it. The patient was started on antiamoebic drug metronidazole and antibiotic ceftriaxone on day 1, but pain, breathlessness, and swelling in his feet were not relieved even after 48 h. In view of the persistent symptoms, the abscess was aspirated and about 300 ml of chocolate brown colored pus (anchovy sauce type) was drained out. Microscopic examination of the pus revealed trophozoites of E. histolytica. Despite aspiration and intensive antiamoebic therapy, patient remained breathless and toxic. This prompted us to ask for CT scan of chest and abdomen to find out the extent of abscess and ascertain the presence of any hepatopulmonary complication. CT showed presence of giant liver abscess of the size of about 98 × 108 mm, occupying the segments VI and VII of the liver [Figure 1]. Repeat X-ray showed large amount of fluid now occupying both the pleural cavities. A repeat aspiration was done and around 200 ml pus was tapped. The pleural fluid was also tapped from the right side which was exudate in nature. Serum IgG serology for E. histolytica was strongly positive. Polymerase chain reaction (PCR) was negative for Mycobacterium tuberculosis. Following repeat aspiration of pus and intensive antiamoebic therapy, patient started improving. Pain in abdomen decreased and swelling in the feet disappeared. The initial gastritis remained unexplained but resolved in 2 weeks. Patient became afebrile and regained his appetite. Patient was discharged on maintenance antiamoebic therapy.

Figure 1

CT scan of the abdomen showing a large hypodense irregular margin lesion measuring 98 × 108 mm in the subscapular region of segments VI and VII, abutting part of the diaphragm

DISCUSSION

Amoebic liver abscess is a common problem in tropical countries.[1] However, its protean manifestations sometimes pose diagnostic dilemma leading to delay in starting appropriate therapy. This case presented with some unusual clinical features pointing to predominantly respiratory involvement rather than liver disease. However, the presence of bilateral pedal edema and tender liver prompted us to rule out the liver pathology in this case. This was confirmed by a CT scan which revealed a large giant size liver abscess of about 10 cm. The mechanism of bilateral pleural effusion in this case remained difficult to explain.[2] Usually effusion associated with amoebic liver abscess is on the right side. The effusion in such cases is either due to sympathetic stimulation when it is an exudate or due to rupture of the abscess when it could be anchovy sauce type of fluid.[3] Presence of bilateral pedal edema was another puzzle. As there was no other feature of cardiac decompensation, urine being normal without evidence of protein in it and serum proteins in normal range, it was speculated that the bilateral pedal edema was possibly because of pressure of posteriorly located large liver abscess on IVC, and this explanation was further strengthened by the fact that pedal edema disappeared after aspiration of the liver abscess.[4]

CONCLUSION

Unilateral pleural involvement is a well-known complication of liver abscess, but this case was interesting as there was involvement of both the pleura without any other associated pulmonary pathology. Also, our case presented with pedal edema without any associated cardiopulmonary disease and with normal serum proteins. Hence, we suggest that in such patients with pedal edema and no underlying cause, a compressive pathology of IVC should be actively searched for to reach the correct diagnosis. Further, this case has global relevance because many of the migrant populations from tropical countries are settled all over the world, particularly in Europe and America.[5] It would only be appropriate that the treating physicians are aware of this unfamiliar association.