Indian Journal of Medical Case Reports ISSN: 2319–3832(Online) An Open Access, Online International Journal Available at http://www.cibtech.org/jcr.htm 2014 Vol.3 (1) January-March, pp. 50-52/Bhattacharya et al. Case Report © Copyright 2014 | Centre for Info Bio Technology (CIBTech) 50 ANAESTHETIC MANAGEMENT OF A CASE OF TUBERCULAR CONSTRICTIVE-EFFUSIVE PERICARDITIS WITH BILATERAL PLEURAL EFFUSION POSTED FOR PERICARDIECTOMY *Dipasri Bhattacharya 1 , Rajkalyan Chakrabarty 2 , Sudev Saha 3 and Saswati Pal 4 1 Department of Anaesthesiology, R.G. Kar Medical College, Kolkata, West Bengal 2 Consultant Anaesthesiologist 3 Department of Surgery, NRS Medical College, Kolkata 4 Department of Anaesthesiology, NRS Medical College, Kolkata *Author for Correspondence ABSTRACT Perioperative management of tuberculous constrictive-effusive pericarditis (TBCEP) is always a challenge for the anaesthesiologist. Constriction develops initially, followed by effusion and may produce clinical findings typical of cardiac tamponade. Our patient had bilateral pleural effusion along with TBCEP. He was a drug nonresponder. Many intraoperative and postoperative problems were encountered during anaesthesia for pericardiectomy. Finally, recovery was total and uneventful. Keywords: Constrictive Effusive Pericarditis, Pleural Effusion, and Tuberculosis INTRODUCTION Tuberculous pericarditis occurs in 1 to 2% of patients with pulmonary tuberculosis (Brien and Pennington, 2005). The incidence has clearly declined with concomitant decline in prevalence of tuberculosis (Brien and Pennington, 2005) in developed countries but it is still common in our country. Pericardial infection occurs via extension of infection from lung, tracheobronchial tree, adjacent lymph nodes, spine or sternum or by miliary spread (Brien and Pennington, 2005). Inflammation affects both parietal and visceral pericardium. Fluid and fibrinous deposits are found in the pericardial space, eventually both layers of pericardium fuse affecting diastolic filling resulting in low cardiac output CSTnet [No Date]. CASES A 17 year old male patient was admitted to our hospital with progressive dyspnoea, precordial pain, bilateral pedal oedema, ascites, fever and a history of significant weight loss. He was taking isonicotinic hydrazide (INH) 300mg, rifampicin (RMP) 450mg and ethambutol (ETM) 800mg daily for the last two months for pulmonary tuberculosis diagnosed by chest x-ray and sputum examination. On examination he had pallor, bilateral pleural effusion, muffled heart sounds, hepatomegaly, ascites, pedal oedema, palpable cervical lymph nodes (bilateral – posterior triangle) and increased jugular venous pressure. Investigations: Blood- Haemoglobin 7gm%, neutrophil 60%, lymphocyte 35% with normal blood sugar, urea and creatinine; Liver Function Tests- Total protein 4.5gm/dl, albumin 3gm/dl, INR 1.66, marginally raised alanine transaminase and aspartate transaminase; Chest x-ray- Revealed bilateral pleural effusion and pericardial effusion as evidenced by flask shaped heart (X-ray 1); E.C.G.- Low voltage complex; USG- Bilateral pleural effusion, hepatomegaly, mild ascites. Fluid was drained by pleurocentesis – 500- 800 ml/day, 1.5 liter was removed to relieve respiratory distress. Pleural fluid sent for biochemical and cytological examination – was found to be exudative with predominant lymphocytes; Echo- Moderate pericardial effusion. Pericardium thickened with fibrinous bands. No features of cardiac tamponade; Lymph node (neck) biopsy and pleural biopsy- Histopathology confirmed tuberculosis. Treatment started with digoxin 0.25mg once daily (OD), frusemide 40 mg OD and deriphylline 100mg three times daily along with anti tuberculous drugs (ATD) which he was taking previously. He developed jaundice (total bilirubin 8 mg), two weeks later for which ATD was stopped and prednisolone 30 mg