This study shows that tuberculosis is the commonest cause of infectious pericardial effusion in this part of the world. Importantly the outcome of pericardial effusion of infectious etiology in the current era appears favourable with low mortality and low occurrence of constrictive pericarditis. The etiology of pericardial disease varies in different regions of the world. Publications from high income countries have limited information on infectious pericardial effusion in children. This is one of the largest single centre studies on infectious pericardial effusion in children and exemplifies the difficulties in diagnosing definite tuberculosis in the pediatric population.11 TBPE in children is a pauci-bacillary disease. It is considered to be an inflammatory response to the low concentration of tubercle bacilli in the pericardium accounting for the low isolation rate. Definite tubercular effusion was seen in only 21 % (4/19) in our study. Low yield of tubercle bacilli from pericardial fluid and biopsy of pericardium has been reported in children.7,8
Elevated pericardial ADA levels (> 35 U/L sensitivity and specificity of 90% and 74%, respectively), is a useful test for the diagnosis of tubercular effusion,14 it was positive in 86.9% (n = 20/23) of our cases. High ADA in tuberculosis appears to be indirectly related to the subsets of activated T cell lymphocytes involved in the antigenic response to tuberculous bacilli.15
CECT chest was particularly helpful in doubtful cases. 20 patients underwent CECT chest as a part of diagnostic evaluation, especially when it was difficult to differentiate between tubercular and pyogenic effusion.19 out of 20 had features suggestive of tuberculosis in the form of necrotic mediastinal lymph nodes or lung involvement suggestive of tuberculosis. In 6/20, there was no other evidence of tuberculosis apart from CT chest. In additional 6 patients, mantoux positivity was the only additional clue for tuberculosis apart from CT. Thus in 12/20 (60%) cases when there was doubt about the etiology, CT was helpful in establishing diagnosis. In a previous study, Cherian et al reported presence of enlarged mediastinal lymph nodes > 10 mm in all 22 patients of tubercular pericardial effusion and in none of the patients of a control group with large viral/idiopathic or postoperative pericardial effusion.16 We believe there is a role of CT in the diagnosis of tubercular pericardial effusion especially where microbiological diagnosis has not been made and pericardial fluid ADA is not elevated.
Pyogenic effusions occurred at a lower age with more respiratory distress, more pleura-pulmonary involvement, more tamponade and they had a longer hospital stay compared to tuberculous effusions.Similar to that reported previously, we also found pleural /pulmonary infection to be the focus in the majority of our patients, other foci were bone, soft tissue and liver.9,10,13 Most patients had received iv antibiotics prior to presentation which may be the cause of low culture positivity.
Overall 10 % (7/70) (5 tubercular and 2 pyogenic) had thrombus formation. Thrombosis was seen in jugular vein, inferior vena-cava, lung and left ventricle. Infection associated with venous stasis could be the contributory factor. This has not been reported in previously. Does it entail a chance association or a complication needs to be looked into and is worth observing in future studies.
Procedure related complication occurred in four patients. Myocardial perforation by needle, bradycardia and vasovagal syncope while removing pigtail, difficulty in removing pigtail due to knot in the pigtail and pneumothorax occurred in one patient each. Two patients had dry tap.
During the first hospital stay there was no mortality. Follow up information after discharge was available for 70.2 % (53/74) patients.Mortality occurred in 3.7% (2/53), both occurring in follow up in those with tubercular effusion. Both patients had undergone successful drainage and came back within a week after discharge, with re-accumulation of effusion and succumbed to tamponade.
Low mortality rates have been observed with the use of modern anti-tubercular treatment in pediatric patients.7,8 This is in contrast to adult studies where higher mortality has been observed (17–40%) despite 6 months of ATT.18 Higher mortality in adult studies are probably due to HIV, older age and concomitant pulmonary tuberculosis. It is also probably related to the higher bacillary load in adults compared to children, where it has been seen that bacillary load determines mortality.19
Chronic constrictive pericarditis (CCP) occurred in 3.7% (2/53) of the patients. Both cases were seen in those with tubercular effusion. This low rate of constrictive pericarditits is consistent with that seen in the current era in both adults and children.8,17
Steroid may have a role in decreasing the incidence of CCP compared to historical cohort. Hugo hamaman et al reported that, 14% children with pericardial effusion developed constrictive pericarditis.7 None of these patients who developed CCP were given steroids whereas all our patients were given steroids. The large IMPI trial also suggested that there is a role of steroids in preventing CCP.17 However, the effect of steroid on development of CCP is confounded by fact that previous studies have varied on HIV positivity rates, time of starting therapy and most importantly timing and effectiveness of drainage of pericardial fluid.16,20
In our study, 13 /54 (2 pyogenic and 11 tubercular) patients had organized/partially organized effusion with features of sub acute constriction at presentation. Besides medical management, eight underwent pericardial tap and 2 underwent immediate surgery.CCP developed in the remaining 2 out of 3 patients in whom neither tap nor surgical intervention was done. None of the patients who underwent drainage developed CCP. This may indicate that if the effusion needs to be drained especially where it is organized, in order to prevent CCP.
Strang et al in a factorial design randomized trial, allocated patients with tuberculous effusion to open drainage vs percutaneous drainage and prednisolone vs placebo and followed them for over 10 years. In their study lowest mortality and adverse events occurred in those with open drainage and steroids.20 Similar observations were made by Cakir et al in children with pyogenic effusions, wherein pericardiocentesis and sub-xiphoid tube placement followed by pericardial window and or primary pericardiocentesis in patients with thick exudates resulted in no constrictive pericarditis in their series.10 Future studies should study the effect and timing of surgical drainage in patients with organized effusions which cannot be drained percutaneously.
Limitations of the study
The major limitation of our study is that it is a retrospective review of data and a single institution study. Definite tubercular, pyogenic or viral pericardial effusion was present in a minority of patients. There was incomplete data and lack of follow up data in many cases.