Study of characteristic of pericardial effusion and to analyze pericardial fluid in various etiologies

Background: Pericardial effusion in clinical practice is commonly under diagnosed or missed especially minimal to moderate effusion. Aim and objectives: To study the clinical and etiological profile of pericardial effusion and to recognize radiological, electrocardiographic and echocardiographic features that are characteristic of pericardial effusion and to analyze pericardial fluid in various etiologies. Materials and methods: It was prospective study in patients presenting with pericardial effusion in department of Medicine and Cardiology. Total of 30 patients who presented with pericardial effusion based on clinical criteria and confirmed by echocardiography were included in the study. Results: The causes of pericardial effusion in this study were Tuberculosis (33.33%), Uremia (20%), Viral /Idiopathic (16.67%), Bacterial (10%), Malignancy (10%), Hypothyroidism (3.33%), and post MI with ischemic cardiomyopathy (3.33%), SLE (3.33%). 3 cases (10%) were HIV positive among viral causes,1 patient had tuberculous pericarditis. ECG findings of low voltage complexes were present in 90% of patients and electrical alternans was seen mainly in tamponade cases. Chest X-ray finding of cardiomegaly was present in 90% patients with pleural effusion in 13.3% patients. ADA levels elevated in all 10 patients of tuberculous effusion with 100% sensitivity and among them smear for AFB was positive in 3 patients. Increased levels of ADA>60U/L was associated with increased incidence of effusive constrictive pericarditis in TB effusion. Pericardial fluid IFN-ᵞ increased greater than 200 pg/L, tuberculous etiology showed 100% sensitivity and specificity. In all 10 patients of 2Dimensional echocardiographic findings of right atrial, right ventricular collapse and left atrial collapse was seen predominantly in tamponade cases. Pericardiocentesis showed hemorrhagic effusion in malignancy and uremia, serous and serofibrinous in tuberculosis and purulent in pyogenic effusion. In 3 cases of pyogenic effusion, culture revealed Staphylococcus aureus in 2 patients and Klebsiella pneumonia in 1 patient. Among 3 cases of HIV, one patient had ADA >40 and smear for AFB positive suggesting tuberculous etiology and other 2 cases were directly due to HIV. In HIV with tubercular effusion the patient presented with cardiac tamponade. Conclusions: ADA>40U/L is diagnostic of tuberculous effusion which showed 100% sensitivity and specificity. Increase of ADA>60 U/L is associated with effusive constrictive pericarditis which has poor prognosis. IFN-ᵞ is increased >200pg/l in all patients of tuberculous etiology showing 100% sensitivity and specificity.