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Tuberculous pericarditis leading to cardiac tamponade: importance of screening prior to immunosuppression.

ABSTRACT: Mycobacterium tuberculosis (TB) presenting with pericardial disease complicated by cardiac tamponade is rare in the developed world, although it occurs more frequently in the context of immunosuppression. In this report, a 74-year-old man on methotrexate for rheumatoid arthritis presented with fever, productive cough and cough-induced syncope. During his admission, he developed clinical signs of cardiac tamponade confirmed on an echocardiogram, which showed a massive pericardial effusion. He was treated with an urgent pericardiocentesis and a pericardial window. Subsequently, TB polymerase chain reaction of pericardial fluid unexpectedly returned positive, and he was commenced on standard quadruple therapy for TB, as well as high-dose prednisolone. Notably, the patient did not have a history suggestive of previous TB exposure, and no screening investigations had been performed prior to initiation of methotrexate. This case highlights the importance of TB screening prior to immunosuppressive therapy, even in populations considered low risk for latent disease.

SUBMITTER: Wee E

PROVIDER: S-EPMC4694605 | biostudies-other | 2015 Dec

REPOSITORIES: biostudies-other

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Project description:BackgroundPurulent bacterial pericarditis (PBP) is a highly lethal infection of the pericardial space that arises as a complication of infective illnesses. Purulent bacterial pericarditis remains a diagnostic challenge given its non-specific clinical and investigative features and carries exceedingly high mortality rates due to fulminant sepsis and morbidity including constrictive pericarditis in survivors. We present our management of cardiac tamponade and subsequent constrictive pericarditis due to Actinomyces meyeri PBP.Case summaryA 53-year-old Caucasian male presented with acute New York Heart Association Class IV dyspnoea and chest discomfort, in the context of multiple hospital presentations over the preceding 8 weeks due to presumed recurrent viral pericarditis. On this admission, initial transthoracic echocardiography (TTE) demonstrated a large asymmetric pericardial effusion for which he underwent urgent pericardiocentesis. Serial TTE post-pericardiocentesis, however, demonstrated effusion re-accumulation and effusive-constrictive pericarditis, confirmed on cardiac magnetic resonance imaging. Fluid culture was positive for A. meyeri. He was diagnosed with PBP, but his condition deteriorated despite appropriate intravenous antibiotic therapy, necessitating semi-urgent surgical pericardiectomy. He recovered well and was discharged on Day 10 post-operatively.DiscussionUnlike uncomplicated acute viral or idiopathic pericarditis, PBP portends a very poor prognosis if unrecognized and untreated. Diagnostic challenges persist given its rarity in modern clinical practice; however, PBP should be considered in cases of seemingly recurrent pericarditis. Multi-modal cardiac imaging and careful analysis of pericardial fluid including cultures and lactate dehydrogenase/serum ratios may assist in earlier recognition. In this case, source control and symptom relief were achieved only with combined intravenous antibiotics, surgical evacuation, and pericardiectomy.

Project description:BACKGROUND:Tuberculous pericarditis is associated with high morbidity and mortality even if antituberculosis therapy is administered. We evaluated the effects of adjunctive glucocorticoid therapy and Mycobacterium indicus pranii immunotherapy in patients with tuberculous pericarditis. METHODS:Using a 2-by-2 factorial design, we randomly assigned 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or placebo for 6 weeks and to either M. indicus pranii or placebo, administered in five injections over the course of 3 months. Two thirds of the participants had concomitant human immunodeficiency virus (HIV) infection. The primary efficacy outcome was a composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. RESULTS:There was no significant difference in the primary outcome between patients who received prednisolone and those who received placebo (23.8% and 24.5%, respectively; hazard ratio, 0.95; 95% confidence interval [CI], 0.77 to 1.18; P=0.66) or between those who received M. indicus pranii immunotherapy and those who received placebo (25.0% and 24.3%, respectively; hazard ratio, 1.03; 95% CI, 0.82 to 1.29; P=0.81). Prednisolone therapy, as compared with placebo, was associated with significant reductions in the incidence of constrictive pericarditis (4.4% vs. 7.8%; hazard ratio, 0.56; 95% CI, 0.36 to 0.87; P=0.009) and hospitalization (20.7% vs. 25.2%; hazard ratio, 0.79; 95% CI, 0.63 to 0.99; P=0.04). Both prednisolone and M. indicus pranii, each as compared with placebo, were associated with a significant increase in the incidence of cancer (1.8% vs. 0.6%; hazard ratio, 3.27; 95% CI, 1.07 to 10.03; P=0.03, and 1.8% vs. 0.5%; hazard ratio, 3.69; 95% CI, 1.03 to 13.24; P=0.03, respectively), owing mainly to an increase in HIV-associated cancer. CONCLUSIONS:In patients with tuberculous pericarditis, neither prednisolone nor M. indicus pranii had a significant effect on the composite of death, cardiac tamponade requiring pericardiocentesis, or constrictive pericarditis. (Funded by the Canadian Institutes of Health Research and others; IMPI ClinicalTrials.gov number, NCT00810849.).

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Tuberculous pericarditis leading to cardiac tamponade: importance of screening prior to immunosuppression.

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