Left ventricular pseudoaneurysm as a fatal complication of purulent pericarditis Bharath Sunkara, MD, Alexandros Briasoulis, MD, Luis Afonso, MD, FACC, Preeti Ramappa, MD, FACC * Division of Cardiology, Veterans Affairs Medical Center, Wayne State University, Detroit, MI 48201, USA article info Article history: Received 3 April 2015 Received in revised form 13 May 2015 Accepted 3 June 2015 Available online 8 July 2015 Keywords: Left ventricle Pseudoaneurysm Purulent pericarditis Streptococcus viridans Pericardial disease abstract We report a case of a 48-year-old man with purulent pericarditis by Streptococcus viridans, despite aggressive treatment with antibiotics and partial pericardiectomy was complicated by left ventricle pseudo-aneurysm resulting in a fatal outcome. The case highlights the course of complicated purulent pericarditis and the use of noninvasive imaging for assessing early signs of pseudoaneurysm and its typical progression. Published by Elsevier Inc. Introduction Left ventricular pseudo-aneurysm (LVPA) occurs as a result of ventricular free wall rupture with adherent pericardium or fibrous tissue. It commonly occurs following myocardial infarction (MI) but it can infrequently complicate cardiac surgery, trauma, or pericar- ditis. 1 LVPA as a result of purulent pericarditis in adults is extremely rare 2 and limited to case reports. The typical etiological agent in all of these cases has been reported as Staphylococcus aureus. We report a rare case of purulent pericarditis by Streptococcus viridans, complicated by LVPA that led to a fatal outcome despite aggressive medical and surgical therapy. Case A 48 year-old diabetic, hypertensive male with history of alcohol dependence and chronic pancreatitis, presented with fatigue and poor appetite and was found to be in diabetic ketoacidosis (DKA). He had a recent history of multiple decayed tooth extraction and teeth abscesses 3 months prior to presentation. DKA resolved but he subsequently developed chest pain and dyspnea and was noted to have clinical and echocardiographic evidence of pericardial effusion, which was initially a minimal accumulation along the posterobasal area and within 48 h, progressed to a large sized circumferential pericardial effusion with signs of cardiac tampo- nade (Fig. 1A and B). On presentation the patient appeared ill and cachectic and was afebrile, normotensive but in moderate respi- ratory distress with sinus tachycardia at a rate of 100 bpm, leuko- cytosis of 26,400 white blood cells/microliter with toxic granulation and elevated erythrocyte sedimentation rate (ESR) of 135 mm/h. No new electrocardiographic ST-T changes were observed and serial sets of cardiac biomarkers (Troponin I and creatine kinaseeMB subform) were negative, thus excluding the possibility that the initial presentation was ischemic in origin. He underwent emergent pericardiocentesis and 1 L of muddy brown, purulent fluid was drained which was positive for Streptococcus viridans. In spite of initial symptomatic improvement, his clinical condition deteriorated over the next 24 h and a repeat trans- thoracic echocardiogram (TTE) revealed thickened pericardium with moderate loculated pericardial effusion around the right ventricular (RV) free wall with signs of effusive constrictive peri- carditis. Emergent pericardial window was performed. The peri- cardial tissue also grew streptococcus viridans. Initially, the patient was treated with an empiric antibiotic combination consisting of ceftriaxone 2 g IV once daily and vancomycin 20 mg/kg every 12 h with a serum trough level goal of 15 mcg/mL or greater. After Funding: None. No ethical approval needed. Conflicts of interest: None. * Corresponding author. Tel.: þ1 313 576 3221. E-mail address: Preeti.Ramappa@va.gov (P. Ramappa). Contents lists available at ScienceDirect Heart & Lung journal homepage: www.heartandlung.org 0147-9563/$ e see front matter Published by Elsevier Inc. http://dx.doi.org/10.1016/j.hrtlng.2015.06.002 Heart & Lung 44 (2015) 448e450